The Neurobiology of Painting - International Review of Neurobiology Vol 74

International REVIEW OF Neurobiology Volume 74 International REVIEW OF Neurobiology Volume 74 SERIES EDITORS RONALD...

Author: Ronald J. Bradley | R. Adron Harris PhD | Peter Jenner

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International REVIEW OF

Neurobiology Volume 74

International REVIEW OF

Neurobiology Volume 74 SERIES EDITORS RONALD J. BRADLEY Department of Psychiatry, College of Medicine The University of Tennessee Health Science Center Memphis, Tennessee, USA

R. ADRON HARRIS Waggoner Center for Alcohol and Drug Addiction Research The University of Texas at Austin Austin, Texas, USA

PETER JENNER Division of Pharmacology and Therapeutics GKT School of Biomedical Sciences King’s College, London, UK EDITORIAL BOARD ERIC AAMODT PHILIPPE ASCHER DONARD DWYER MARTIN GIURFA PAUL GREENGARD NOBU HATTORI DARCY KELLEY BEAU LOTTO MICAELA MORELLI JUDITH PRATT EVAN SNYDER JOHN WADDINGTON

HUDA AKIL MATTHEW J. DURING DAVID FINK MICHAEL F. GLABUS BARRY HALLIWELL JON KAAS LEAH KRUBITZER KEVIN MCNAUGHT JOSE´ A. OBESO CATHY J. PRICE SOLOMON H. SNYDER STEPHEN G. WAXMAN

The Neurobiology of Painting EDITED BY

F. CLIFFORD ROSE Founding Director, Academic Unit of Neuroscience Charing Cross & Westminster (now Imperial College) Medical School Late Physician-in-Charge Department of Neurology Charing Cross Hospital London UK

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CONTENTS

Contributors......................................................................... Preface ...................................................................................

xiii xv

Evolutionary Neurobiology and Art C. U. M. Smith I. II. III. IV. V. VI. VII. VIII. IX.

Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Definitions . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Play . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. ‘‘Shock of the New’’. . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Neurophysiology . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Landscape . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Mate Selection. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Parts and Wholes. . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Imagination . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

1 2 3 4 4 6 8 10 12 13

SECTION I VISUAL ASPECTS Perceptual Portraits Nicholas Wade I. II. III. IV. V. VI. VII.

Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Medical Societies in London . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Anatomists of the Brain. . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Microscopists. . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Functions of the Brain . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Dysfunctions of Behavior . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Conclusions . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

v

17 19 21 24 28 33 36 36

vi

CONTENTS

The Neuropsychology of Visual Art: Conferring Capacity Anjan Chatterjee I. II. III. IV. V. VI.

Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Disposition to Produce Art. . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Visual Vocabulary. . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Descriptive Accuracy . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Enhanced Expressivity . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Conclusions . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . References . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

39 40 41 42 44 46 47

Vision, Illusions, and Reality Christopher Kennard I. II. III. IV.

Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Functional Specialization in the Visual Brain .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Face and Object Recognition. . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Recommended Reading .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

51 52 53 54

Localization in the Visual Brain George K. York I. II. III. IV. V.

Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . A Note on Localization. .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . The Painter at the Bedside . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . The Neurologist in the Picture Gallery . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Commentary: The Three Cultures. . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . References . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

55 56 58 60 62 64

SECTION II EPISODIC DISORDERS Neurology, Synaesthesia, and Painting Amy Ione I. II. III. IV.

Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Case of the Color-Blind Artist . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Normals and Synaesthesia. . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Metaphor and Synaesthesia . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . References . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

69 71 72 75 77

CONTENTS

vii

Fainting in Classical Art Philip Smith I. II. III. IV. V. VI. VII. VIII.

Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Blackouts in Paintings. . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Crucifixion Fainting . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Historical Fainting . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Genre Fainting . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Swooning . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Men Fainting . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Conclusions . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

79 80 80 81 83 84 85 87 87

Migraine Art in the Internet: A Study of 450 Contemporary Artists Klaus Podoll I. II. III. IV.

Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Methods . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Results . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Discussion . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

89 90 91 104 106

Sarah Raphael’s Migraine with Aura as Inspiration for the Foray of Her Work into Abstraction Klaus Podoll and Debbie Ayles I. II. III. IV. V.

Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Art Critics’ Notions on Sarah Raphael’s Migraine with Aura . . . . . . . . . .. History of Illness . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Impact of Sarah Raphael’s Migraine with Aura on Her Art. . . . . . . . . . . .. Conclusions . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

109 110 110 113 116 117

The Visual Art of Contemporary Artists with Epilepsy Steven C. Schachter I. Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. II. Background to the Collection . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. III. Artistic Themes in the Works of Contemporary Artists with Epilepsy. . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. IV. Conclusions . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

119 120 120 130 130

viii

CONTENTS

SECTION III BRAIN DAMAGE Creativity in Painting and Style in Brain-Damaged Artists Julien Bogousslavsky I. Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . II. Change in Creativity and Style in Artists after Brain Lesion. . . . . . . . .. . . . III. Change of Style in Artists . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . References . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

135 139 141 146

Artistic Changes in Alzheimer’s Disease Sebastian J. Crutch and Martin N. Rossor I. Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . II. Willem de Kooning (1904–1997) and Other Artists with Alzheimer’s Disease . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . III. William Utermohlen (b. 1933) . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . IV. Positive and Negative Cognitive Phenomena .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . V. Conclusions . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . References . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

147 150 152 156 160 160

SECTION IV CEREBROVASCULAR DISEASE Stroke in Painters H. Ba¨zner and M. Hennerici I. II. III. IV. V.

Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Case Studies of Painters with Right Hemisphere Stroke . . . . . . . . . . . . .. . . . Case Studies of Painters with Left Hemisphere Stroke. . . . . . . . . . . . . . .. . . . Other Cases . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Conclusions . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . References . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

165 166 180 186 187 189

Visuospatial Neglect in Lovis Corinth’s Self-Portraits Olaf Blanke I. Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . II. Mature Style–Late Style?.. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . III. Hospitalization . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

193 196 199

CONTENTS

IV. V. VI. VII. VIII.

Rehabilitation. . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Self-Portraiture . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Drawings. . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Paintings. . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Discussions . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

ix 199 201 201 204 209 212

Art, Constructional Apraxia, and the Brain Louis Caplan I. Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. II. Constructional Apraxia. . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. III. What Attributes are Customarily Needed to Make a Painting or Sculpture? . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. IV. The Frontal Lobes and Their Projections. . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. V. The Parietal Lobes and Their Projections . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

215 215 216 217 222 232

SECTION V GENETIC DISEASES Neurogenetics in Art Alan E. H. Emery I. II. III. IV.

Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. How Neurogenetic Disease AVected the Artist’s Work?. . . . . . . . . . . . . . . . .. Neurogenetic Disease Depicted in Art. . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Conclusions . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

235 235 237 239 239

A Naı¨ve Artist of St Ives F. Clifford Rose I. II. III. IV. V. VI.

Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Bryan Pearce . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. His Painting. . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. His Sister . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Phenylketonuria. . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Another Famous Case . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

241 241 243 246 249 251 252

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CONTENTS

Van Gogh’s Madness F. Clifford Rose I. II. III. IV. V. VI.

Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . His Art . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . His Illness. . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Ear Amputation. . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . His Attacks. . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . What Disorder Did van Gogh Have? . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . References . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

253 254 255 256 258 261 268

Absinthe, The Nervous System and Painting Tiina Rekand I. II. III. IV. V.

Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Art as a Reflection of Life. . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Medical EVects of the Absinthe . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . EVect of Absinthe on Artistic Expression . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Conclusions . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . References . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

271 272 273 274 276 278

SECTION VI NEUROLOGISTS AS ARTISTS Sir Charles Bell, KGH, FRS, FRSE (1774–1842) Christopher Gardner-Thorpe I. II. III. IV. V. VI. VII. VIII. IX. X. XI.

Introduction. . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Charles Bell’s Early Years. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . David Allan (1774–1796) . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Raphael Cartoons Studied by Bell . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Corunna Oils in 1809. . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . After Corunna in 1809 and Marriage in 1811 . . . . . . . . . . . . . . . . . . . . . . . . .. . . . Waterloo in 1815 and the Watercolors of 1836. . . . . . . . . . . . . . . . . . . . . . . .. . . . After Waterloo . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Italian Tour in 1840 . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . Death at Hallow Park in Worcestershire . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . After Bell. . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . References . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . .

281 282 282 283 284 284 284 285 287 287 287 288

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SECTION VII MISCELLANEOUS Peg Leg Frieda Espen Dietrichs I. II. III. IV. V. VI. VII. VIII.

Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Background . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Poliomyelitis . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. School . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Accident and Artist Debut .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Diego Rivera . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. SuVering and Painting . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Disease and Creativity . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

293 293 294 294 295 295 296 298

The Deafness of Goya (1746–1828) F. Clifford Rose I. II. III. IV. V. VI.

Introduction . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. The Duchess of Alba . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. What was Goya’s Illness? . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. DiVerential Diagnosis. . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Vogt-Koyanagi Syndrome . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. Black Paintings . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. References . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . ..

301 306 307 308 308 312 315

Index ...................................................................................... Contents of Recent Volumes................................................

317 323

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CONTRIBUTORS

Numbers in parentheses indicate the pages on which the authors’ contributions begin.

Debbie Ayles (109), Department of Psychiatry and Psychotherapy, RWTH Aachen University, Pauwelsstrasse 30, 52074 Aachen, Germany H. Ba¨zner (165), Department of Neurology, University of Heidelberg Universita¨tsklinikum Mannheim, 68135 Mannheim, Germany Olaf Blanke (193), Laboratory of Cognitive Neuroscience, Brain Mind Institute, Ecole Polytechnique Fe´de´rale de Lausanne (EPFL), Swiss Federal Institute of Technology, Station 15, 1015 Lausanne, Switzerland; and Department of Neurology, University Hospital, CH-1211 Geneva, Switzerland Julien Bogousslavsky (135), University Department of Neurology, Lausanne, Switzerland Louis Caplan (215), Harvard Medical School, Best Israel Deaconess Medical Center, Boston, Massachusetts 02215 , USA Anjan Chatterjee (39), Department of Neurology and the Center for Cognitive Neuroscience, The University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA Sebastian J. Crutch (147), Dementia Research Centre, Department of Neurodegeneration, Institute of Neurology, University College London, United Kingdom Espen Dietrichs (293), Department of Neurology, Rikshospitalet University Hospital/The National Hospital, University of Oslo, N-0027 Oslo, Norway Alan E. H. Emery (235), Green College, Oxford, United Kingdom Christopher Gardner-Thorpe (281), Exeter Neurosciences and Peninsula Medical School, Royal Devon and Exeter Hospital, Exeter, EX2 5DW, United Kingdom M. Hennerici (165), Department of Neurology, University of Heidelberg Universita¨tsklinikum Mannheim, 68135 Mannheim, Germany Amy Ione (69), The Diatrope Institute, Santa Rosa, California 95406, USA Christopher Kennard (51), Department of Clinical Neuroscience, Imperial College London, United Kingdom Klaus Podoll (89,109), Department of Psychiatry and Psychotherapy, RWTH Aachen University, Pauwelsstrasse 30, 52074 Aachen, Germany Tiina Rekand (271), Department of Neurology, Haukeland University Hospital and University of Bergen, 5021 Bergen, Norway xiii

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CONTRIBUTORS

F. CliVord Rose (241,253,301), Founding Director, Academic Unit of Neuroscience, Charing Cross & Westminster Medical School, London, United Kingdom Martin N. Rossor (147), Dementia Research Centre, Department of Neurodegeneration, Institute of Neurology, University College London, United Kingdom Steven C. Schachter (119), Harvard Medical School, Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA C. U. M. Smith (1), Vision Sciences, Aston University, Birmingham B4 7ET, United Kingdom Philip Smith (79), Department of Neurology, University Hospital of Wales, CardiV, United Kingdom Nicholas Wade (17), Department of Psychology, University of Dundee, Dundee DD1 4HN, Scotland, United Kingdom George K. York (55), Kaiser Permanente Stockton Medical Center and the Sa˚a Institute, Fiddletown, California 95629, USA

PREFACE

What does the Neurology of Painting mean? When the average gallery visitor is asked this question, after the initial pause of puzzled thought, a variety of individual answers are given. The response may be to wonder why, ever since the first caveman drew images of hunting on their walls, art has been a universal feature of human existence, and the first chapter attempts to answer this enigma with evolutionary neurobiology. The difference between sensation and perception is then explored in the second chapter that includes several neuroscientists with their discoveries. The visual brain is considered in depth with the difference between illusions and reality, how the mind works, and the parts of the brain involved in visual processes. Another response is that the subject deals with brain disorders of artists, either transient ones such as fainting, migraine, epilepsy, and synaesthesia (where one sensation, e.g., music, is associated with another, e. g., color). More permanent disorders include the effects of brain damage such as Alzheimer’s disease and stroke on the different parts of the brain concerned with creativity. There is also an overall view on inherited disorders and how these may affect the work of artists. A further response to the initial question is to consider eminent neurologists whose art was also professional. Since Frida Kahlo’s spinal cord damage so profoundly affected her painting, she is included in the penultimate chapter. As the cause of Goya’s deafness has puzzled many generations, the final chapter attempts a definitive answer, but this was an unknown condition in his lifetime. This volume is developed from the proceedings of the Mansell Bequest Symposium of the Medical Society of London. A previous book included music and literature,1 but it became clear that the subject of the neurology of painting merited this volume.

1 ‘‘The Neurology of the Arts: Painting, Music, Literature’’, Rose FC (ed.). London: Imperial College Press. 2004. xv

EVOLUTIONARY NEUROBIOLOGY AND ART

C. U. M. Smith Vision Sciences, Aston University, Birmingham B4 7ET, United Kingdom

I. II. III. IV. V. VI. VII. VIII. IX.

Introduction Definitions Play ‘‘Shock of the New’’ Neurophysiology Landscape Mate Selection Parts and Wholes Imagination References

I. Introduction

In his important book on evolutionary theory, Darwin’s Dangerous Idea, Daniel Dennett warns that Darwin’s idea seeps through every area of human discourse like a ‘‘universal acid’’ (Dennett, 1995). Art and the aesthetic response cannot escape its influence. So my approach in this chapter is essentially naturalistic. Friedrich Nietzsche writes of observing the human comedy from afar, ‘‘like a cold angel. . .without anger, but without warmth’’ (Nietzsche, 1872, p. 164). Whether Nietzsche, of all people, could have done this is a matter of debate. But we know what he means. It describes a stance outside the human world as if looking down on human folly from Mount Olympus. From this stance, humans, their art and neurology are all part of the natural world, all part of the evolutionary process, the struggle for existence. The anthropologist David Dutton, in his contribution to the Routledge Companion to Aesthetics, says that all humans have an aesthetic sense (Dutton, 2001). It is a human universal. Biologists argue that such universals have an evolutionary basis. Furthermore, many have argued that not only humans but also animals, at least the higher mammals and birds, have an appreciation of the beautiful and the ugly INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74001-6

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Copyright 2006, Elsevier Inc. All rights reserved. 0074-7742/06 $35.00

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(Eibl-Eibesfeldt, 1988).1 This again suggests that aesthetics has an evolutionary origin. In parenthesis here, I should perhaps say that I am well aware of the criticism leveled at evolutionary psychology. I am well aware that it has been attacked as just so many ‘‘just-so’’ stories. This is neither the time nor the place to mount a defense but simply just to say that I believe that a defense is eminently feasible.

II. Definitions

Before going any further it is important to be clear about what we mean by the term ‘‘aesthetics.’’ The Oxford Dictionary gives an instructive derivation. It says that the word derives from a Greek root meaning ‘‘to perceive by the senses’’ as opposed to ‘‘things thinkable or immaterial.’’ This sense was taken up by Leibniz in the early eighteenth century (Baumgarten, 1750, 1758) and thence by Baumgarten in his seminal Aesthetica of 1750/1758. Baumgarten went on to define the ‘‘beautiful’’ as ‘‘sensuous knowledge which gave satisfaction and/or pleasure.’’ The Penguin Dictionary provides a succinct definition: ‘‘Aesthetics is the study of beauty and ugliness.’’ All of these definitions help us home in on what we mean by the term. None of them seem to me fully adequate. What is it that makes us feel that one thing is ‘‘beautiful’’ and another thing ‘‘ugly.’’ Some have said that this ability constitutes a ‘‘seventh sense’’ (Kivy, 2003). If we go back to the beginning, we find Aristotle writing in the Poetics, (1450b20–1451a15) that: To be beautiful a living creature, and every whole made up of parts, must not only present a certain order in its arrangements of parts, but also be of a certain definite magnitude. Beauty is a matter of size and order and therefore impossible in a very minute creature, since our perception becomes indistinct as it approaches instantaneity; or, secondly, in a creature of vast size,—one say a thousand stadia long—as in that case, the object cannot be seen all at once and the unity and wholeness of it are lost on the beholder.

The proper relationship between parts in the formation of the whole is an important part of the aesthetic response. It is a theme running through the long history of aesthetic thought. Leibniz, Shaftesbury, Hutcheson all found it central. I shall return to it later. But it is not, of course, the only sensory experience that we find beautiful. Who would deny that the colors of sunset or sunrise, or the seaward view of a coral island at noon, are beautiful? Moreover, all the instances so far mentioned involve the visual sense. The auditory and the olfactory/gustatory 1 Charles Darwin indeed writes ‘‘Birds appear to be the most aesthetic of all animals, excepting, of course, man, and they have nearly the same sense of the beautiful that we have’’ (1871, The Descent of Man and Selection in Relation to Sex, London: John Murray, vol.2, xiii, 39).


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senses may also trigger this seventh sense. No one disputes the beauty of classical music, although tastes may vary, and we often speak of ‘‘beautiful’’ scents and flavors. It may be, as Erasmus Darwin (1802) remarked, that these uses of the term are derivative, or it may be as Ogden and Richards (1925) maintain that aesthetics does not form a unitary subject at all but a number of diVerent fields, which should be investigated separately or, finally, it may be, as Wittgenstein (1966) suggested, that there is no ‘‘core’’ meaning but, as in his famous example of games, only family resemblances. Evidently, in a short chapter I can only give the merest sketch of a corner of a subject that has spawned innumerable books and articles over several centuries. Returning to Aristotle, this time to the Metaphysics, we find him asserting that ‘‘. . .we take a delight in our senses; for even apart from their usefulness they are loved for themselves; and above all others the sense of sight’’ (Book 1, 980a). This gives an important clue. Modern students of aesthetics are prone to insist that ‘‘the aesthetic gaze terminates on the aesthetic object’’ by which they mean that the aesthetic response is suYcient unto itself, it is not directed to any utilitarian end. When we look at a great engineering artifact or a great piece of architecture, or when we look at some of the images of contemporary science, a great protein molecule, perhaps, or the intricate tracery of a Golgi-stained cortex, we may have the immediate feeling, ‘‘That is beautiful.’’ But this response has, it is said, nothing to do with function. It has, as Aristotle suggested, everything to do with the delight we take in the senses. Indeed, the pleasure derived from the use of the senses might be compared with the pleasure derived from the use of the neuromuscular system. Both sensory and exercise deprivation are used as forms of torture. Both are, moreover, related to that other human universal: play.

III. Play

Herbert Spencer, long ago, argued that ‘‘the aesthetic sentiments originate from the impulse to play . . . .the aesthetic character of a feeling is habitually associated with separateness from life-serving functions’’ (Spencer, 1872, paras 533 & 535). One can see what he means. It is related to the observation, already noted, that the aesthetic response ‘‘terminates’’ on the aesthetic object. Biologists, however, do not now regard ‘‘play’’ as having no biological function; rather the opposite: it is seen as of paramount importance in human development. It may not have immediate ‘‘life-serving functions,’’ but it provides endless opportunities for exploratory behavior—for testing out strategies and discovering the bounds of the possible. Sensory systems are used to the full, new situations and experiences are continually being chanced upon and old ones re-experienced and consolidated. The senses are stretched and challenged.

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IV. ‘‘Shock of the New’’

This stretching and challenging is continued by artists into the adult world. Sensory systems are every so often assaulted by what the Australian critic Robert Hughes called ‘‘the shock of the new’’ (Hughes, 1980). The famous paper by Lettvin et al. in 1959 with its provocative title ‘‘What the frog’s eye tells the frog’s brain’’ emphasized that it was predominantly a change in the visual scene that activated the mesencephalic visual centers. And so it is quite generally throughout sensory physiology (Smith, 2000). When there is little or no change in an animal’s sensory environment only minimal activity occurs in their sensory systems. This neurophysiological finding is paralleled by psychological investigation. After a number of repetitions, sensory systems become habituated and the stimulus is hardly noticed. Can this account for some trends in the history of art? Martindale, in particular, has examined a number of artistic traditions, ranging from French poetry to Gothic architecture and pre-Columbian sculpture and shows that there is a continuous development of devices designed to catch the attention (Martindale, 1990). In the twenty-first century, artistic forms seem to evolve at what often seems an absurd pace. The modern artistic palate seems far more easily jaded than in past times. It craves novelties, fresh perspectives, and fresh jolts. Indeed, Andrew Harrison in his interesting discussion of Philosophy and the Arts concludes that the primary function of art lies in ‘‘pushing the limits of what can be represented or conceived’’ (Harrison, 1997).

V. Neurophysiology

Turning from general features of all sensory systems to particular features of the visual system, we can take note of the well-known neurophysiology for which Hubel and Wiesel were awarded the 1981 Nobel Prize. The elements that Hubel and Wiesel discovered in the mammalian visual system were hierarchies of edge detectors responding optimally to lines of certain orientation, to ‘‘stopped’’ lines, to certain angles, and so on. Evolutionists adduce good reasons for this particular type of organization. They point out that the visual world is full of edges and discontinuities. These include, among many others, the outlines of objects moving across the field of vision, the vertical and diagonal lines of tree trunks and branches as the eye scans across them, the wrinkled edges of leaves, uneven contours of boulders, the moving shadows of animals, the long grasses of the savannah, the horizon, and so forth. It has been pointed out that many artists, particularly the post-Daguerre, postFox-Talbot, nonrepresentational artists, seem to have exploited this specialization


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of the visual system. The development of Piet Mondrian’s paintings provides an excellent example. As he strove toward ever greater concentration on the essence of what was ‘‘there,’’ toward, in other words, ever greater abstraction, the emphasis on edges increases. This can be seen when the tree pictures of 1908 and 1911 are compared and perhaps even more strikingly in the 1915 Pier and Ocean (Fig. 1). Not only do all except primary colors disappear, indeed, in the 1911 picture only grays are used but also the orientation detectors are stimulated by strongly emphasized edges. This investigation of what we ‘‘really’’ see was, of course, carried forward to the ‘‘bitter’’ end in the great works of Picasso, Braque, and others in early twentieth century cubism. Picasso is quite explicit about what he is doing: ‘‘I paint forms as I think them, not as I see them’’ (Gomez de la Serna, 1929). The visual system, however, is far more than a hierarchy of feature detectors, from simple orientation detectors to face detectors, and too much should not be made of edge detectors and so on in the analysis of nonrepresentational art. We shall return to this in the context of the ‘‘binding problem’’ later. In spite of centuries of research, we still know rather little about the way the visual system ‘‘works’’! Before leaving these neurophysiological considerations of the visual system, it is worth noting the far-from-intuitively-obvious nature of color vision. We all know, and have known since Thomas Young at the beginning of the nineteenth

FIG. 1. Piet Mondrian, 1915, Pier and Ocean. Courtesy of Haags Gemeentemuseum.

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century (Young, 1802), that the retina possesses three distinct types of color receptor, nowadays identified as cones, sensitive to long (red), medium (green), and short (blue) wavelengths. But this is very far from the end of the story. Ewald Hering at the beginning of the twentieth century and then Edwin Land toward the end of that century showed that the neurophysiology underlying our sensation of color was much more complex, indeed still only imperfectly understood (Hubel, 1995). Colour vision is, of course, of considerable evolutionary significance in many vertebrate lineages, although it appears somewhat sporadically in the animal kingdom and has possibly been lost and reinvented several times. Where it is present, it acts as an additional means of picking out predator and/or prey, or a suitable and suitably receptive mate. It is also of importance for many primates in finding ripe fruits and berries among the foliage of their arboreal environment. Painters have always been interested in color and, in post-Fox-Talbot times, many have attempted to abstract and emphasize the essentials of our color sense. This is seen in the increasingly bare yet vivid grid paintings of Piet Mondrian and perhaps, even more interestingly, in the pointillist works of Georges Seurat. In the latter case, the artist consciously sought to make use of a scientific account of color vision, which he had found in the book published by the French organic chemist and director of the Gobelin carpet manufactory, Euge`ne Chevreul. In The Law of Simultaneous Colour Contrast (1839), Chevreul showed that adjacent colors influence each other and, hence, that the brain played an active role in color perception (Chevreul, 1839). Once again, evolutionists adduce good reasons for the brain’s work in emphasizing color contrasts. The fact that Chevreul’s book was written long before our contemporary understanding of visual neurophysiology became available was of little moment to the painters who read him.2 This is quite clear from the marvelously shimmering works painted by Seurat in response to Chevreul’s revelation (e.g., Port of Gravelines Channel, La Grande Jatte, and so on). These explorations of color support Semir Zeki’s contention that artists and neuroscientists are engaged in a common endeavor: an investigation of the evolved strengths and weaknesses of the human visual system (Zeki, 1999).

VI. Landscape

The cubists and others emphasize that it is not the retina, hugely complex as it is, which generates aesthetic emotion but the visual brain. This is brought out by evolutionary analyses of landscape painting. Palaeoanthropologists point out that the major part of human experience has been of hunter-gathering on the 2 In fact both Leonardo da Vinci and Goethe had previously noticed the effect of adjacent colours on each other.


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African savannahs. No one knows how many generations passed their lives in this mode of existence. The earliest remains of our genus date back 2 or 3 million years, and our australopithecine forebears reach even further back into the past. Evolutionists maintain that this deep experience cannot but have left its trace upon the human psyche and with it on our aesthetic sense. This speculation receives some support from studies of the types of landscape painting preferred by contemporary humans. It seems that open, savannah-like environments are chosen, especially where there is water, large trees, semi-open space, changes in elevation, a clear view of the horizon, and moderate complexity (Orians and Heerwagen, 1992). In addition, many viewers respond to elements of mystery, elements that draw the spectator into the landscape and make him want to find out more about it: the winding path that disappears behind a clump of trees, perhaps, or proceeds over the horizon (Kaplan, 1992). Many of us derive aesthetic pleasure from what Edmund Burke (1757) called ‘‘the sublime’’: the bare landscapes of winter, the driving gales of the equinoxes, and the high mountains. Joseph Addison writes that ‘‘our imagination loves to be filled with an object or to grasp at anything that is too big for its capacity. We are flung into a pleasing astonishment at such unbounded views, and feel a delightful stillness and amazement in the soul. . .’’ (Addision, 1727). It need hardly be said that these are not the landscapes early humans inhabited—if they had the choice. The evolutionist would argue that they are culturally derived, noting that mountains and tumultuous seas were not well regarded before modern times. Only in the nineteenth century with the rise of the Romantics was Burke’s notion of the sublime with its equation between nature and the divine,3 with all its mysteries and terrors, accepted (Schlegel, 1797). It is only when the ‘‘sturm und drang’’ is safely behind glass that it is enjoyed—only then can we hope to experience ‘‘a delightful stillness in the soul’’! This reminds us, once more, that art serves no immediate purpose; the aesthetic vision terminates on the aesthetic object. It also reminds us that the aesthetic response, although having a neurobiological foundation, is channeled through powerful cultural filters. But whether looking at safely-caged, life-threatening views or entering into the mystery of peaceful landscapes, the aesthetic response is immediate; the intricately-balanced neural computation from which it emerges takes place ‘‘below’’ the level of consciousness. Where does this computation occur? In recent years, with the advent of powerful neuroimaging techniques, there has been a considerable amount of research aimed at identifying neural structures underlying the aesthetic response. Paradiso et al. (1999) have used PET to investigate cerebral blood flow changes to brain areas in response to pleasant, neutral, and unpleasant visual stimuli. Others have examined 3 Wackenroder (1797) writes: ‘‘There are only two languages which allow humans to comprehend the Divine, one of these is reserved for God, the other given to a few anointed favourites. The second language has two components ‘Nature and Art’.’’

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the brain’s response to the attractiveness of faces (Nakamura et al., 1998) and response to paintings (Vartanian and Goel, 2004). It was shown that brain areas displaying diVerential activity are largely in the frontal, limbic, and paralimbic areas and in the visual cortex. Present-day neuroimaging techniques are, of course, ‘‘broad-brush’’ approaches. They do not yet allow precise neural pathways to be delineated. The evolutionist would suggest that these pathways were laid down in the Pleistocene when, through countless generations, the human biotype was forged.

VII. Mate Selection

Turning from the subtleties of landscape appreciation to those of mate selection we find a similar, if not stronger, evolutionary element in our aesthetic response. The sexual strategies of the higher animals depend on the fine tuning of the sense organs. The magnificent color and rustle of the peacock’s tail is famous. It would seem that only sexual selection, on the grounds of aesthetic pleasure, could account for such an otherwise disadvantageous character. A similar explanation can be adduced for the magnificent, and magnificently cumbersome, plumage of male birds of paradise. In parenthesis, it is relevant to note that before the days of animal rights and environmental conversation, the gorgeous feathers of these birds were much in demand to enhance the allure of female members of Homo sapiens. Perhaps the most impressive (to human eyes, at least) of these avian eVorts to attract the opposite sex are the courtship arenas built by Bower Birds. Have humans escaped the power of sexual selection? It seems unlikely. Erasmus Darwin at the end of the eighteenth century writes that ‘‘when a babe, soon after it is born into this cold world, is applied to its mother’s bosom, it experiences its first pleasures (and consequently), when any object of vision is presented to us, which by its waving or spiral lines bears any similitude to the form of the female bosom, whether it is to be found in a landscape. . . or in the form of some antique vases . . .. we feel a general glow of delight’’ (Darwin, 1802, p.145). Can we see in Darwin’s thesis an evolutionary reason for the attractiveness of Hogarth’s famous ‘‘line of beauty’’? In the preface to The Analysis of Beauty (Fig. 2), Hogarth explains that the idea grew from his need to justify his commentaries on beauty in art. Lines with too shallow a curve are, he says, ‘‘mean and poor’’; lines with too generous a curve are ‘‘gross and clumsy.’’ Variety is symbolized by a wavy line in two dimensions and a serpentine line in three dimensions as opposed to unvarying geometrical shapes like straight lines and circles. ‘‘. . . the waving line, or line of beauty,’’ he writes, ‘‘. . . being composed of two curves contrasted, becomes still more ornamental and pleasing, insomuch as the hand takes a lively movement in making it with pen or pencil’’ (Hogarth, 1753). Can we see, perhaps, in this last quotation Darwin’s evolutionary foundation being supplemented by neuromuscular


FIG. 2. Title page of Hogarth’s, 1753, Analysis of Beauty.

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pleasure in the artist’s hand–eye coordination and its vicarious sharing by the spectator? Hogarth thought he saw the ‘‘line of beauty’’ everywhere in Nature: in flowers, in water, and especially in the human form. The human form is inescapable. Kenneth Clark in his great book, The Nude (Clark, 1956), argues that it glimmers behind much of our aesthetics—from the rhythm of breathing to the beat of heart; from the upright stance of our body, the set of the head, the proportions of torso and skull. All this is ingrained in us from our earliest experience and reinforced daily by the images that saturate our world. And not only the ‘‘human form divine,’’ but also the morphologies of the animal kingdom exhibit graceful symmetry expressing an indwelling, lithe energy. We are distressed when this ‘‘fearful symmetry’’ is upset—when some accident of birth, development, or genetic manipulation destroys this coherent proportionality. Root-Bernstein (2002) calls this inherent appreciation ‘‘aesthetic cognition,’’ a species of prelogical thinking that forms the substratum of all our thought. Nietzsche (1872) goes further: ‘‘All pleasure,’’ he writes ‘‘depends upon proportion: displeasure upon disproportion.’’ This brings me to the last aesthetic universal I have space for in this chapter: the interrelation of parts and wholes.

VIII. Parts and Wholes

You will remember the quotation from Aristotle at the beginning of this chapter. Sir Joshua Reynolds in his Discourses speaks of the ‘‘dilated pupil’’ by which he means the ability to take in the whole, appreciating the relation of all the parts. Roger Fry, who edited Sir Joshua’s Discourses in 1905, instances Rubens’ painting of the Virgin and Child Adored by Saints in the church of St. Augustine in Antwerp (Fig. 3). All the elements of the painting cohere to create the final eVect. Once more the aesthetic response is immediate yet must be based on complex cerebral computation (Zeki, 2004).4 This aspect of the aesthetic response is shared by the great mathematical physicists. Werner Heisenberg, for instance, remarks that ‘‘Beauty is the proper conformity of the parts to one another and the whole’’ (Heisenberg, 1959), and in A Mathematician’s Apology, G. H. Hardy writes that ‘‘The mathematician’s patterns, like the painter’s or the poet’s, must be beautiful; the ideas, like the colours or words, must fit together in a harmonious way. Beauty is the first test; there is no permanent place in this world for ugly mathematics’’ (Hardy, 1994). As this appreciation of the proper integration of parts to form a whole seems to be another aesthetic universal, it should have an evolutionary basis. I argue in 4 Zeki emphasizes the intricacy of the neurophysiological goings-on in the brain before even such an apparently ‘‘raw feel’’ as color emerges into consciousness.


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FIG. 3. Peter Paul Rubens (c.1630): Virgin and Child adored by Saints.

a paper published in Perspective in Biology and Medicine that this universal has been deeply embedded into the visual brain by the need to detect pattern and the breaking of pattern (Smith, 2005). Throughout the arms races of evolutionary history, predator and prey have sought to conceal themselves from each other, and all sorts of camouflage devices have accordingly evolved. Similarly, sensory systems have been subjected to intense selective pressure to ensure that they can detect pattern and disruption of pattern. Highly evolved brains, such as those found in the higher mammals and a fortiori in the primates, consist of layer upon layer of sensory analyzers. The cerebral cortex of the macaque contains more than 2 dozen visual areas. The whole interconnected system is ‘‘designed’’ to extract ‘‘meaningful’’ pattern from the cascade of data raining in along the optic nerves. This pattern recognition is what Immanuel Kant called ‘‘the synthetic unity of apperception.’’ In the Critique of Pure Reason, he writes that ‘‘synthesis (the process of joining diVerent representations to each other and of comprehending their diversity in one cognition) . . . is a blind but indispensable function of the

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soul, without which we should have no cognition whatever, but of which we are seldom even conscious’’ (Kant, 1787). Pattern recognition is deeply incorporated into our brains. The attempt to relate parts to make a coherent whole is an ‘‘indispensable function of the soul,’’ an essential part of the brain’s make-up. Only when it is achieved is our aesthetic sense satisfied. Once again, we see that the response is the outcome of a massive, and massively rapid, computation beneath the level of consciousness. The study of the aesthetic response brings us close to that major unsolved problem in neuroscience known as ‘‘the binding problem.’’ IX. Imagination

This brings me to the last of the major themes in aesthetics I have space for in this chapter: the role of the imagination. Aristotle writes that ‘‘Art completes what nature cannot finish. The artist gives us knowledge of Nature’s unrealized ends’’ (Clark, 1956, p. 9) and Joshua Reynolds says much the same in his thirteenth Discourse: ‘‘Upon the whole, it seems to me that the object and intention of all the arts is to supply the natural imperfection of things . . . to gratify the mind by realizing and embodying what never existed but in the imagination’’ (Reynolds, 1778, p. 369). Perhaps this is why the unfinished masterpieces of the great artists,

FIG. 4. Kanizsa’s triangle.


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one thinks of Michelangelo’s Prisoners or the Rondanini Pieta` on which he was working at the time of his death, the sketches of master draftsmen, those which fill Leonardo’s notebooks, for instance, or the mysterious last paintings of Rembrandt, are so compelling. For many, like Aschenbrenner, imagination lies at the root of the aesthetic response. We saw that Addison alluded to it in his discussion of the ‘‘sublime.’’ It is, of course, central to the mind’s operation and close to the pattern recognition we discussed earlier. The study of visual illusions, such as Kanizsa’s triangle, shows how ready we are to complete pattern by imagining what is not there (Fig. 4). To my mind it is the most important thing. In the Dejection Ode, Coleridge mourns above all else the loss of his ‘‘shaping spirit of the Imagination.’’ Imagination lies at the heart of the artistic endeavor and of the aesthetic response. In the Mansell Bequest Symposium of April 2001, Semir Zeki quoted Arthur Schopenhauer: ‘‘Something, and indeed the ultimate thing, must be left over for the mind to do’’ (Zeki, 2004, p. 31). I hope that this introductory chapter does indeed leave something for the mind to do, that it has started some intellectual hares and that it serves as a foretaste of the riches that follow.

References

Addision, J. (1727). ‘‘Spectator.’’ Baumgarten, A. G. (1750, 1758). ‘‘Aesthetica.’’ Trajecti cis Viadrum. Burke, E. (1757). ‘‘A Philosophical Enquiry into the Origin of our Ideas of the Sublime and the Beautiful’’ ( J. T. Bolton, Ed.), 1958. Routledge and Kegan Paul, London. Chevreul, M. E. (1839). ‘‘De la loi du contraste simultane´ des coleurs et de l’assortiment des objects colore´s.’’ Paris. Clark, K. (1956). ‘‘The Nude: A Study of Ideal Art.’’ John Murray, London. Darwin, E. (1802). ‘‘Zoonoma,’’ 3rd ed. J. Johnson, London. Dennett, D. C. (1995). ‘‘Darwin’s Dangerous Idea.’’ Allen Lane, Penguin Press, London. Dutton, D. (2001). Aesthetic universals. In ‘‘The Routledge Companion to Aesthetics’’ (B. Gaut and D. M. Lopes, Eds.), pp. 203–214. Routledge, London. Eibl-Eibesfeldt, I. (1988). The biological foundations of aesthetics. In ‘‘Beauty and the Brain: Biological Aspects of Aesthetics’’ (I. Rentschler et al., Eds.). Birkhau¨ser Verlag, Basel. Gomez de la Serna, R. (de la Serna 1929). Completa y veridical historia de Picasso y el cubismo. Rivista de Occidente 25( July), 100. Hardy, G. H. (1994). ‘‘A Mathematician’s Apology.’’ Cambridge University Press, Cambridge. Harrison, A. (1997). ‘‘Philosophy and the Arts: Seeing and Believing.’’ Thoemmes Press, Bristo. Heisenberg, W. (1959). ‘‘Physics and Philosophy.’’ George Allen and Unwin, London. Hogarth, W. (1753). ‘‘The Analysis of Beauty.’’ London. Hubel, D. (1988). ‘‘Eye, Brain and Vision.’’ Freeman, New York. Hughes, R. (1980). ‘‘The Shock of the New.’’ British Broadcasting Corporation, London. Kant, I. (1787). ‘‘Critique of Pure Reason,’’ 2nd ed. N. Kemp-Smith (trans.). Macmillan, London.

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Kaplan, S. (1992). Environmental preferences in a knowledge-seeking, knowledge-using organism. In ‘‘The Adapted Mind’’ ( J. H. Barkow, L. Cosmides, and J. Tooby, Eds.), pp. 581–598. Oxford University Press, Oxford. Kivy, P. (2003). ‘‘The Seventh Sense: Francis Hutcheson and eighteenth Century Aesthetics.’’ Oxford University Press, Oxford. Lettvin, J. H., et al. (1959). What the frog’s eye tells the frog’s brain. Proc. Inst. Radio Engineers 47, 1940–1951. Martindale, C. (1990). ‘‘The Clockwork Muse: The Predictability of Artistic Change.’’ Basic Books, New York. Nakamura, et al. (1998). Neuroanatomical correlates of the assessment of facial attractiveness. Neuroreport 9, 753–757. Nietzsche, F. (1872). The philosopher. In ‘‘Philosophy and Truth’’ (D. Breazeale, trans. and Ed. 1979). Harvester Press, Sussex. Ogden, C. K., and Richards, I. A. (1925). ‘‘The Foundations of Aesthetics.’’ 2nd ed. Allen and Unwin, London. Orians, G. H., and Heerwagen, J. H. (1992). Evolved responses to landscape. In ‘‘The Adapted Mind’’ ( J. H. Barkow, L. Cosmides, and J. Tooby, Eds.), pp. 555–579. Oxford University Press, Oxford. Paradiso, S., et al. (1999). Cerebral blood flow changes associated with attribution of emotional valence to pleasant, unpleasant and neutral visual stimuli in a PET study of normal subjects. Am. J. Psychiatry 156, 1618–1629. Reynolds, J. (1778). Chapter 7. In ‘‘Discourses’’ (R. Fry, Ed.), 1905. Seeley and Co., London. Root-Bernstein, R. S. (2002). Aesthetic cognition. Int. Stud. Phi. Sci. 16(1), 61–77. Schlegel, F. (1797). ‘‘Ideas about a Nature Philosophy.’’ Trans. Harns, E. E. & Heath, P. (1988): Cambridge University Press, Cambridge. Smith, C. U. M. (2000). ‘‘Biology of Sensory Systems.’’ John Wiley, Chichester. Smith, C. U. M. (2005). Evolutionary neurobiology and aesthetics. Perspect. Biol. Med. 48, 17–30. Spencer, H. (1872). ‘‘Principles of Psychology,’’ vol. 2. Williams and Norgate, London. Vartanian, O., and Goel, V. (2004). Neuroanatomical correlates of aesthetic preferences in paintings. Neuroreport 15, 893–897. Wackenroder, W. (1797), ‘‘Effusions of an Art-Loving Friar,’’ at . Wittgenstein, L. (1966). ‘‘Lectures and conversations on aesthetics, psychology and religious belief’’ (C. Barrett, Ed.). Blackwell, Oxford. Young, T. (1802). On the theory of light and colours. Phil. Trans. Roy. Soc. (Lon.) 92, 44. Zeki, S. (1999). ‘‘Inner Vision: An Exploration of Art and the Brain.’’ Oxford University Press, Oxford. Zeki, S. (2004). Neural concept formation and art: Dante, Michelangelo, Wagner. In ‘‘Neurology of the Arts’’ (F. CliVord Rose, Ed.). Imperial College Press, London.

SECTION I VISUAL ASPECTS


PERCEPTUAL PORTRAITS

Nicholas Wade Department of Psychology, University of Dundee Dundee DD1 4HN, Scotland, United Kingdom

I. II. III. IV. V. VI. VII.

Introduction Medical Societies in London Anatomists of the Brain Microscopists Functions of the Brain Dysfunctions of Behavior Conclusions References

I. Introduction

Perceptual portraits represent people in an unconventional style. The portraits themselves are not always easy to discern—the viewer needs to apply the power of perception in order to extract the facial features from the design that carries them. The aim of perceptual portraits is both artistic and historical. They generally consist of two elements—the portrait and some appropriate motif. The nature of the latter depends on the endeavors for which the portrayed person was known. In some cases the motif is drawn specifically to display a phenomenon associated with the individual, in others it is derived from a figure or text in one of their books, or apparatus that they invented. The portraits and motifs have themselves been manipulated in a variety of ways, using graphical, photographical, and computer graphical procedures. The illustrations often require some eVort on the part of the viewer to discern the faces embedded in them. I believe that such perceptual portraits both attract attention and engage the spectator’s interest to a greater degree than do conventional paintings, prints, or photographs. It is hoped that this visual intrigue will enhance the viewer’s desire to discover why particular motifs have been adopted and, in turn, to learn more about the persons portrayed: it is intended to be an instance of art serving science. Further examples can be found in Wade (1990, 1995).

INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74002-8

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Copyright 2006, Elsevier Inc. Illustrations copyright # Nicholas Wade 0074-7742/06 $35.00

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FIG. 1. (A) ‘‘Founder member.’’ John Coakley Lettsom (1744–1815) was a founder of the Medical Society of London. He is shown in a notice of its first meeting, listing those present and those elected to membership. The portrait is after an engraving in Hunt (1972), and the notice is derived from an illustration in Hunting (2004). (B) ‘‘Lettsom in the eyes of his teachers’’ William Fothergill (1712–1780) and George Fordyce (1736–1802). (# Illustrations by Nicholas Wade.)

Figure 1A provides an apposite example of a perceptual portrait. The person portrayed is one to whom we owe a great debt, and without whom we would not be meeting here—John Coakley Lettsom (1744–1815). His portrait is not easy to see, but it can be discerned by squinting the eyes, shaking the head from side to side, viewing the page from a distance, removing your spectacles if you wear them—in fact any procedure that reduces the sharpness of the fine lines in the pattern that make up the motif. The pattern is derived from a notice listing those attending the first meeting of the Medical Society of London on May 19, 1773 as well as those proposed and accepted for membership (Hunting, 2004). Artistic license has been taken with the notice for graphical reasons. The list of 10 members has been presented in triplicate, which is appropriate since the membership was initially set at 30 physicians, surgeons, and apothecaries; those of the proposed members are in duplicate so that the pattern would be a better carrier for the portrait. The portrait of Lettsom is derived from an engraving, which was in turn copied from an oil painting. The portrait has been reduced to its minimal elements and then combined with the notice so that the principal features—eyes, nose, and mouth—blend with the pattern of the text. A more conventional portrait of Lettsom is shown in the background of Fig. 1B. He is sharing his


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vision with his teachers, William Fothergill (1712–1780) and George Fordyce (1736–1802). The graphical history of neuroscience has been well documented (Clarke and Dewhurst, 1972; Finger, 1994), and I have drawn, in part, on this rich pictorial record. By means of perceptual portraits it becomes possible to combine the history of a subject with depictions of those who have charted the course over which the ideas developed. This perceptual purview can only be carried out in a very selective way here, but its flavor can be imparted. I will look at some aspects of brain anatomy, the methods and models that have been applied studying nervous function, and the benefits that achromatic microscopes provided in the nineteenth century. All these topics will be colored by my own particular area of interest—vision. Finally, the interface between neurology and abnormal behavior will be touched upon, with representations of some who have advanced psychopathology in its many guises. The neurology of painting does tend to focus on those who have reflected aspects of brain disorder through the art they produce, and so presenting perceptual portraits of those whose theories often inform such deliberations will be pertinent. First, however, a little will be said of the Medical Society of London and others that were formed at around the same time in this city.

II. Medical Societies in London

The Medical Society of London was not the only one to be founded in late eighteenth-century London. Indeed, medical societies blossomed then, largely as a consequence of obstacles raised by the College of Physicians regarding requirements for Fellowship (Clark, 1966). Many of the founders were Scots who did not qualify for Fellowship without a medical degree from Oxford or Cambridge. For example, in 1767, William Hunter (1718–1783) (Fig. 2A) and Fordyce collaborated to establish the Society of Licentiate Physicians in order to campaign for the rights of licentiates in the College. Fordyce was involved in the formation of another society in 1783 with John Hunter (1728–1793) (Fig. 2B); it was called the Lyceum Medicum Londinense and was principally concerned with encouraging medical students to present the results of original research at its weekly meetings. John Hunter ‘‘was always solicitous for some improvement in medical education’’ (Home, 1794, p. xxxii). While many small London medical societies blossomed, the blooms were usually short-lived, although some made lasting contributions to medicine. The Society for the Improvement of Medical and Chirurgical Knowledge was founded in 1783, by Fordyce and John Hunter. The initial membership of the Society was 9, and an upper limit of 12 was set. It met at dinner once a month

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FIG. 2. The Hunter brothers. (A) ‘‘Obstetrician’’ showing a gravid William Hunter (1718–1783). Portrait after an engraving in Chambers (1835), motif from his engraving of the gravid uterus. (B) ‘‘Torpedo Hunter’’; John Hunter (1728–1793) after an engraving in Knight (1834) enclosed within his illustration of the torpedo fish, with the electric organ exposed in the upper left. (# Illustrations by Nicholas Wade.)

(except during the summer) at Slaughter’s coVee-house in St. Martin’s Lane. The papers communicated were first read, then discussed, and corrected after dinner. The three volumes of Transactions of a Society for the Improvement of Medical and Chirurgical Knowledge appeared in 1793, 1800, and 1812 (Wade, 2003). Meetings of these early medical societies were not always sedate. This certainly applied to the Medical Society of London, as it did to the Society for the Improvement of Medical and Chirurgical Knowledge. An instance relates to a particular intense debate concerning the state of the brain in mania. Matthew Baillie (1761–1823) (Fig. 3A) and Andrew Marshal (1742–1813) (Fig. 3B) were members of the society, and both had an active interest in the morbid state of the brain. At two meetings in 1789, altercations took place between Hunter and Marshal. At first, Marshal noted that his dissections of the brains of those who had died insane were always abnormal. Hunter’s opposition to this opinion was vehement, and when he was asked to retract it at the next meeting he refused and a fight broke out! Both Hunter and Marshal had fiery temperaments, and their enmity continued. Prior to the altercation, they had been on good terms (Wade, 2005). It is not known precisely what Marshal said at the meeting of the Society that so incensed Hunter because he did not publish his observations. Some of


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FIG. 3. Brain pathologists. (A) ‘‘Morbid anatomist’’ Matthew Baillie (1761–1823) and the title page of his book on morbid anatomy (Baillie, 1793). (B) ‘‘Marshaling the facts’’ Andrew Marshal (1742–1813) and the title page of his book on the brain, published posthumously (Marshal, 1815). (# Illustrations by Nicholas Wade.)

Marshal’s unpublished papers were assembled and printed after his death by his former assistant, Solomon Sawrey (1765–1825) (Marshal, 1815). III. Anatomists of the Brain

The study of the brain was not restricted to examining disorders like mania. There was a long history of investigating its gross anatomy, although much less attention was paid to the brain than to the musculature. Within the nervous system, much more was known about the peripheral nerves than the brain. This is evident in the diagram of the nerves given by Ambroise Pare´ (1510–1590) (Fig. 4A): the structure of the brain is crudely represented. It was still the belief that the animal spirit flowed through the hollow nerves from the senses to the ventricles in the brain. Pare´ (1551) initiated medical interest in the intriguing phenomenon of phantom limbs. Evidence of loss of limbs through disease, accident, warfare, or ritual

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FIG. 4. (A) ‘‘Phantom limbs’’; two portraits of Ambroise Pare´ (1510–1590) in diagrams of the peripheral nerves from Pare´ (1649). (B) ‘‘The renaissance of anatomy’’; Andreas Vesalius (1514–1564) after a woodcut frontispiece portrait in Saunders and O’Malley (1950) and his illustration of the base of the brain from Vesalius (1543). (# Illustrations by Nicholas Wade.)

has been commented on since records began. With this legacy, it is remarkable that reports of phantom limbs entered so late into medical records. Perhaps this was because few of those who had limbs amputated survived to describe their experiences. Pare´ made great strides in the surgical treatment for amputation; he applied ligatures to the large vessels in the limbs to staunch the bleeding following amputation and applied tourniquets above the site of severance. Accordingly, it is appropriate to present his portrait in one of his diagrams with missing limbs. The renaissance of anatomy is associated with Andreas Vesalius (1514–1564) (Fig. 4B) who published his book De Humani Corporis Fabrica in 1543. It is taken to be a synthesis of science and art because of the high quality of its anatomical illustrations. The blocks from which the woodcuts were printed survived into the twentieth century, and they were reprinted in Saunders and O’Malley (1950). Vesalius presented an account of anatomy that was almost free from the legacy of Galen. While Vesalius could examine the structure of the brain with his own rather than Galen’s eyes, he did not pay too much attention to it. He was more accurate than Pare´ in his representation of the base of the brain. The convolutions are displayed, as are the cerebellums; the visual pathways are clearly shown, but Vesalius considered that the optic nerve fibers projected to the ipsilateral hemisphere. Vesalius represented the visual pathways as separate at the optic chiasm and with ipsilateral projection of the optic nerves to the brain. This was integrated into the analysis of vision by Rene´ Descartes (1596–1650) (Fig. 5). The diagrams


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FIG. 5. ‘‘Cartesian dualism.’’ The portraits of Rene´ Descartes (1596–1650) are after an engraving in Knight (1835), they are enclosed within diagrams of the brain from: (A) his Traite´ de l’Homme (1664) and (B) De Homine (1662). (# Illustrations by Nicholas Wade.)

in Descartes’ Traite´ de l’Homme (1664) retain the ipsilateral projection of the optic nerves to the brain, with union in the pineal gland where mind and body interact. Singleness of binocular vision is achieved by a single anatomical structure. It is instructive to compare it with the monocular representation made for De Homine (1662): both engravings were derived from essentially the same text, which does not mention stimulation of two eyes. A number of similar illustrations from De Homine all depict one eye only, whereas their corresponding figures from the Traite´ display two. It would seem that the illustration has played a greater role in historical interpretations than the text from which it was derived, and the credit should be placed with the artist as well as Descartes. It is particularly significant in this case because neither of the series of diagrams was produced by the author of the text (Hall, 1972). The Traite´ first appeared over a decade after his death, and two separate versions of it were printed. The first, in 1662, was translated into Latin (De Homine) and illustrated by Schuyl, who is said to have worked from a defective manuscript copy of the French. The French version (Traite´ de l’Homme) appeared in 1664: the text was given to two illustrators (van Gutschoven and La Forge), who each made a complete set of drawings independently of the other; van Gutschoven’s were the ones most generally printed, although some of La Forge’s were included, too. The whole set of La Forge’s illustrations can be found in Descartes (1677). Anatomy was pursued in Britain, most notably by Thomas Willis (1621–1675) (Fig. 6A) and his circle. In the context of vision, the old ideas about species were retained by some even if the species were carried by the optic nerve to the brain. In the same year in which Descartes’ Traite´ was published, Willis (1664) established that the optic nerves projected to the optic thalami, although the distinction between the thalami and the striate cortex had not been made at that time (Wade, 1998).

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FIG. 6. (A) ‘‘Circle of Willis’’; Thomas Willis (1621–1675) after a portrait in Birch (1743), enclosed within the drawing of the brain by Christopher Wren in Willis (1664). (B) ‘‘Visionary’’; Isaac Newton (1642–1727) after a portrait in Knight (1833), motif of the spectrum after a figure in Newton (1704), his account of the visual pathways after a figure in Brewster (1855). (# Illustrations by Nicholas Wade.)

A truly mechanistic interpretation of vision was given by Isaac Newton (1642–1727) (Fig. 6B): light produced vibrations in the retina, and these were conducted to the brain along the optic nerve. It would appear that Newton conducted experiments with cut sections of optic nerve and concluded that vision like hearing is mediated by vibrations, largely because of his lack of success in isolating the animal spirits: ‘‘tho’ I tied a piece of the optic nerve at one end, and warmed it in the middle, to see if any airy substance by that means would disclose itself in bubbles at the other end, I could not spy the least bubble; a little moisture only, and the marrow itself squeezed out.... And that vision is thus made, is very conformable to the sense of hearing, which is made by like vibrations’’ (Harris, 1775, p. 100). The concept of the hollow optic nerves, which had survived since Alcmaeon (ca. 500 BC), was gradually being replaced. It stimulated Newton’s interest in the visual pathways and in the ways in which messages from the two eyes could be combined. He made the first representation of partial decussation at the optic chiasm and proposed a theory of binocular single vision based on it in around 1682.

IV. Microscopists

The gross structures of the nervous system could be examined with the naked eye, but a new world was exposed by the microscope (Harris, 1999). However, this formerly unseen territory was not sharply resolved by its seventeenth-century


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FIG. 7. Early microscopes and microscopists. (A) Robert Hooke (1635–1703) derived from a portrait in Jardine (2003) and his compound microscope (Hooke, 1665). (B) Antonius van Leeuwenhoek (1632–1723) after a frontispiece engraving in Leeuwenhoek (1684) and his simple magnifier. (# Illustrations by Nicholas Wade.)

explorers due to the optical aberrations inherent in the relatively simple devices and the lack of techniques for preparing specimens for observation. While the microscopes of Robert Hooke (1635–1703) (Fig. 7A) and Antonius van Leeuwenhoek (1632–1723) (Fig. 7B) bared the cell before the human eye, they did little to expose its fine structure. This was to await the development of achromatic microscopes in the early nineteenth century. Cells were so named by Hooke (1665) when he observed the structure of sections of cork under the microscope. Leeuwenhoek (1674) gave accounts of several animal cells, including nerve fibers, when he directed his simple magnifier to animal tissue. Relatively little attention was paid to these observations because the resolving power of the microscopes was poor. Microanatomy was not advanced greatly in the eighteenth century, and the use of the microscope was often disparaged. The microscopic world was transformed by the introduction of powerful achromatic instruments in the 1820s, and rapid advances were made thereafter. The cell doctrine was most clearly articulated at the end of the next decade, but it was not until the end of the nineteenth century that the neuron doctrine began to be widely accepted. In 1832, Jan Evangelista Purkinje or Purkyneˇ (1787–1869) (Fig. 8A) obtained an achromatic microscope made by Plo¨ssl. He directed it at the large cells in the cerebellum, thereby identifying his eponymous cells. His microscopic observations were made before any adequate staining methods had been developed. Purkinje used alcohol to fix his preparations, and he made thin sections so that they could be examined microscopically.

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FIG. 8. Pioneers of the achromatic microscope. (A) ‘‘Purkinje cells’’; Jan Evangelista Purkinje or Purkyneˇ (1787–1869) after a portrait in Purkinje (1918) in his representation of cells in the cerebellum. (B) ‘‘Purkinje cell’’; Santiago Ramoń y Cajal (1852–1934) after a portrait in Finger (1994) in his drawing of a single Purkinje cell. (# Illustrations by Nicholas Wade.)

It is an irony of science that Purkinje was not able to resolve the amazingly detailed structure of the cells bearing his name. By the time Santiago Ramoń y Cajal (1852–1934) (Fig. 8B) was directing his microscope at neural structures, great strides had been made in both sectioning and staining specimens. A single Purkinje cell sprouted arborizations of astonishing complexity. Ramoń y Cajal expressed his artistry not only in observing the fine detail of neural structures but also in their depiction. His use of Golgi’s silver staining methods enabled him to see detailed structures that had otherwise been invisible or overlooked. He examined the structures of the retina, cerebellum, and spinal cord and made some improvements to the Golgi technique. He used his histological studies of the brain to lend support to the emerging neuron doctrine, which was enunciated by Wilhelm von Waldeyer (1836–1921) in 1891. Two views were entertained about the structure of the nervous system. On the one hand, it was argued that the nerves were connected in a vast reticulum. On the other hand, the argument was that the nerves were independent units that were not physically connected.


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FIG. 9. Microanatomists of the retina. (A) ‘‘Structure of the retina’’; Gottfried Reinhold Treviranus (1776–1837) in his diagram of the crow’s retina (Treviranus, 1837). (B) ‘‘Bowman’s bulbs’’; William Bowman (1816–1892) and his diagram of rods and bulbs (Bowman, 1849). (# Illustrations by Nicholas Wade.)

The retina was one of the many anatomical structures subjected to the new achromatic scrutiny, but as with the gross anatomy of the eye, the initial observations were not free from the received dogma. Descartes (1637) had suggested that the limits of visual resolution were a consequence of the dimensions of the receptive fibers in the retina. Receptors were not known about at that time, and Descartes assumed that the retina consisted of the endings of the fibers of the optic nerve. Since these were of a particular size, he argued that no object smaller than a fiber could be resolved. Descartes’ anatomical speculation possibly influenced the first detailed diagrams of the microscopic structure of the retina that were produced by Gottfried Reinhold Treviranus (1776–1837) (1837). He directed the nerve endings toward the lens rather than away from it (Fig. 9A). This anatomical error was soon corrected. The structure of the endings became more finely resolved, and it was evident that the endings were not all alike. William Bowman (1816–1892) (1849) provided a diagram of the retina, which distinguished between what he called rods and bulbs (Fig. 9B). Bowman drew attention to the disagreements about the interpretations of the terminal structures of the retina and to the diYculties of obtaining good specimens for microscopical study. Further refinements were due to Alfred Ko¨lliker (1817–1905), who also provided a numerical system for the layers that could be distinguished. The numbering sequence of the layers was extended from 8 to 10 and reversed in direction by Max Schultze (1825–1874). Not only did Schultze distinguish between rods and cones, but he also bestowed specific functions on each of them. Rods were active in low levels of illumination whereas cones required higher light levels and could distinguish between diVerent wavelengths of light.

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V. Functions of the Brain

With a growing understanding of the gross and fine anatomy of the brain, attention was directed to the functions it served. Some theories were fanciful, but even they sharpened the questions that were addressed and the tentative answers that were proposed. Franz Joseph Gall (1758–1828) (Fig. 10A) represents the emergence of medicine and physiology as sources of psychological speculation. From the early nineteenth century, anatomists dissected neural pathways in the brain with increasing precision, and these were related to the developing understanding of nerve transmission. These anatomical and physiological discoveries were applied to individual diVerences in the gross structure of the brain and to disorders of its function due to trauma or disease. Gall gained a reputation as one of the leading neuroanatomists in Europe; he was the first to draw a clear distinction between the gray matter of the cerebral cortex and the underlying white matter. In 1791, he advocated cortical localization of mental functions. However, it is for phrenology—assessing mental characteristics from the external shape of the skull—that Gall is best known. In the early nineteenth century, after losing his stipend in Vienna for publishing such novel ideas about brain function,

FIG. 10. (A) ‘‘Phrenological head of Gall’’; the sculpted head of Gall (from the Dundee Art Galleries and Museums) has phrenological markings on both sides, but those on the left of the original are colored as well as numbered. The sculpted head has been orientated to match that of a lithographic portrait of Gall (Polyak, 1957). A slide of the portrait was projected onto the head and photographed so that the facial details of the portrait were superimposed on the model. (B) ‘‘Extirpator’’; Marie Jean Pierre Flourens (1794–1867) after an engraving in Haymaker and Schiller (1970). His portrait is combined with the blades he wielded with such precision in conducting experiments on extirpation. (# Illustrations by Nicholas Wade.)


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he made an enormously successful tour of European capitals, together with Johann Gaspar Spurzheim (1776–1832), lecturing on and demonstrating phrenology. Marie Jean Pierre Flourens (1794–1867) (Fig. 10B) was a harsh critic of Gall’s phrenology, not so much in terms of its psychological speculations as its support of cortical localization based on anecdotal and clinical observation. Flourens provided experimental evidence questioning functional localization in the brain. He was trained in medicine and became renowned for his skill as an experimental physiologist. The technique he introduced was that of extirpation or ablation: the surgical removal of parts of the brain to examine how the remainder functions by studying postoperative behavior. Flourens’s most productive period was in the 1820s with his experiments on reptiles, birds, and mammals; he rarely made distinctions between the brains of these animals. He viewed the brain as having some degree of localized function, but it acted as a unit. Moreover, he demonstrated that there is considerable plasticity in the cerebral cortex. Deficits in behavior caused by cortical lesions could recover. Since it was known that brain tissue did not regenerate, this was taken to be evidence that the same functions can be controlled by diVerent parts of the brain. The debate between the localizers and the equipotentialists reverberated throughout the nineteenth century. Pierre Paul Broca (1824–1880) (Fig. 11A) provided evidence from clinical examination and autopsy to support cerebral localization of function. He was initially influenced both by comparative anatomy

FIG. 11. (A) ‘‘Broca’s area’’; Pierre Paul Broca (1824–1880) after an engraving in Polyak (1957). He is shown in a diagram of Broca’s area, taken from an illustration in one of his own books on the brain (Broca, 1888). (B) ‘‘L’arc de cercle’’; Jean-Martin Charcot (1825–1893) after frontispiece engraving in Charcot (1892). Motif after a drawing of a hysterical patient adopting l’arc de cercle in Charcot and Richer (1887). (# Illustrations by Nicholas Wade.)

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and Gall’s speculations on cortical localization. Such evidence was not new, but Broca’s views were treated with greater seriousness by the scientific community because he was not tainted by phrenology. In 1859, he was involved in founding the first Anthropological Society at Paris, and this was the platform from which his most noted work was delivered. At that time, Broca was treating a patient suVering from loss of speech, referred to as aphemia by Broca and later as aphasia. The patient was known as Tan since this was the only utterance he made, but he was able to understand speech. Tan died 1 week later, and his brain, which was exhibited at the next meeting of the Society, was found to have a cavity in the left frontal lobe. Despite disputes regarding the priority of Broca’s discovery and the extent of the lesions in his patients, the link forged between language and cortical location proved very fruitful, and led others, such as Carl Wernicke (1848–1905), to relate the receptive aspects of language to more posterior locations in the left hemisphere. Jean-Martin Charcot (1825–1893) (Fig. 11B) was a gifted teacher who demonstrated the art of diagnosis with patients in the presence of his students. His lectures became celebrated and attracted students from around the world. He was, with Broca, a staunch supporter of cerebral localization, and he dealt with aphasia at length in his lectures. Charcot related clinical symptoms to brain autopsies and developed the clinical-anatomical method. His portrait is shown together with a drawing of a hysterical patient in a classical posture—l’arc de cercle. It is the same hysterical crisis that is represented in the famous painting by Brouillet of ‘‘A clinical lecture at the Salpeˆtrie`re’’ in which Charcot demonstrates hypnosis to a group of students. Moreover, a painting in the background of the lecture room displays a patient in this same posture. The functions of the brain were investigated both theoretically and experimentally in Britain during the nineteenth century. Alexander Bain (1818–1903) (Fig. 12A) wrote two textbooks on psychology, which were to provide the prototypes for subsequent writers; he also founded the first journal, Mind, concerned principally with psychological issues in 1876. Bain integrated sensory physiology with philosophy to espouse an independent discipline of psychology ‘‘conceiving that the time has now come when many of the striking discoveries of Physiologists relative to the nervous system should find a recognized place in the Science of Mind’’ (Bain, 1855, p. v). The illustration reflects the importance of Bain’s Mind, which was initially edited by one of his former students; it also incorporates a model of a neural processing designed by Bain to give diVerential output with input of varied intensities. That is, he proposed a connectionist account of learning 70 years before Hebb (1949). Whereas Bain founded Mind, David Ferrier (1843–1928) (Fig. 12B) was a founding editor of the journal Brain in 1878. Ferrier electrically stimulated the brains of many species and mapped areas of the cortex: ‘‘the whole brain is regarded as divided into sensory and motor regions. . . a scientific phrenology


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FIG. 12. (A) ‘‘Mind reader’’; Alexander Bain (1818–1903) after a photograph in Bain (1904). Text motif after the title page of the first issue of Mind. Motif after a diagram of a neural network model in Bain (1873). (B) ‘‘Brain stimulator’’; David Ferrier (1843–1928) after a photograph in Haymaker and Schiller (1970). He is enclosed in a diagram of the human brain from Ferrier (1876). (# Illustrations by Nicholas Wade.)

is regarded as possible.’’ The long-held view that the brain was unaVected by direct stimulation had been overturned by Gustav Theodor Fritsch (1838–1927) and Eduard Hitzig (1838–1907) in 1870. They galvanically stimulated the exposed brains of unanaesthetized dogs and found specific precentral areas that resulted in muscular contractions: they divided the cortex into two parts—motor and not motor. The involvement of certain cortical regions in motor control had been proposed by John Hughlings Jackson (1835–1911) on the basis of his studies of epilepsy, and these, too, were the stimulus for Ferrier’s investigations. In 1873, he commenced a series of experiments on anaesthetized frogs, pigeons, guinea pigs, rabbits, cats, dogs, and monkeys in which he applied faradic stimulation to localized areas of the cortex; he also carried out ablations of the same areas. These demonstrated large species diVerences and pointed to the dangers of extrapolating broadly, as Flourens had done. Ferrier is represented in his illustration of the human brain that is marked with the motor map of monkey cortex: the numbers specify localized movements with the letters representing movement areas for the hand and wrist. Ferrier did much to shift the center of gravity of nineteenth century neuroscience toward the English language, and this movement was reinforced by

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FIG. 13. (A) ‘‘Scratch reflex’’; Charles Scott Sherrington (1857–1952) after an illustration in Eccles and Gibson (1979), tracing of the scratch reflex from Sherrington (1906). (B) ‘‘Alpha rhythm’’; Hans Berger (1873–1941) enclosed within a multiplied EEG pattern (derived from Berger, 1930). (# Illustrations by Nicholas Wade.)

Charles Scott Sherrington (1857–1952) (Fig. 13A). Electrical stimulation of the brain represented a novel technique that could disclose functions of the brain. Many others were based on the emerging concept of the nerve cell as the building block of the nervous system. The neuron doctrine was firmly established by evidence about the synapse, the term introduced by Sherrington, who proposed a mode of chemical transmission across the synaptic junctions. Sherrington’s early work was concerned with the knee jerk reflex and then the scratch reflex, and he found similar integrating principles in operation. In his Integrative Action of the Nervous System (1906), he mapped out what was known about reflex action and signed the way ahead. The portrait of Sherrington was made during his tenure in Liverpool, in 1901, a few years before publication of The Integrative Action (from which the motif of a tracing of the scratch reflex was taken). Sherrington dedicated his book to Ferrier ‘‘in token of recognition of his many services to the experimental physiology of the central nervous system.’’ Hans Berger (1873–1941) (Fig. 13B) recorded electrical potentials on the surface of the human scalp and plotted the EEG. His life-long search was for an objective index of subjective experience. He initially measured variations in


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brain circulation and temperature in an attempt to capture the essence of psychic energy, but he abandoned that approach. Small cortical potentials had been recorded from the exposed brains of rabbits, cats, and monkeys as early as 1875 by the Liverpool surgeon, Richard Caton (1842–1926), but no success had been achieved with recordings from humans. After many vain attempts on his patients, Berger achieved success with recordings from his teenage son and from himself, and he was able to report in 1929: ‘‘I believe I have indeed discovered the electroencephalogram in man’’; 13 more papers on the human EEG followed. They are examples of experimental rigor and cautious interpretation. Berger is shown together with the first tracing of the alpha rhythm published, in his second report of 1930. The record has been graphically multiplied and is accompanied by those for the heart rate and time base.

VI. Dysfunctions of Behavior

The link between neurology and painting tends to focus on the eVects of neurological dysfunction and representation. It is instructive, then, to look at those who have provided theories of abnormal behavior and who have suggested treatments for alleviating feelings of malaise or worse. Franz Anton Mesmer (1734–1815) (Fig. 14A) set in train a branch of fringe medicine that proved to be the motive force for later dynamic psychiatry. He was attempting to provide a scientific explanation for some remarkable cures he had eVected by requiring patients to grasp magnetized iron bars. He considered that this procedure resulted in restoring equilibrium between the patient’s state of animal magnetism and that prevailing in the environment. Later, cures were achieved without the use of magnetic bars, by rhythmic movements, fixating, and stroking the body. Despite his desire for academic respectability, Mesmer was ridiculed by his peers in Vienna and moved to Paris in 1778. Mesmer is represented in combination with a contemporary portrayal of a mesmeric seánce. He recommended treatment in seánces that were conducted with much theatricality: patients, connected to one another by cords, would sit round a tub, or bacquet, of ‘‘magnetized’’ fluid grasping iron rods that protruded from it. Mesmer and his assistants, called magnetizers, would pass among them occasionally stroking the body or the aZicted part. Patients often experienced convulsions during treatment, after which they were taken to a padded ‘‘crisis room,’’ where they usually passed into a trance before returning to their normal state. Philippe Pinel (1745–1826) (Fig. 14B) moved to Paris to practice medicine in the same year as Mesmer, but his concerns were quite diVerent. Rather than treating the well-to-do ladies of the city, he dealt with the destitute and dispossessed inhabitants of the asylums for the insane. Conditions in the asylums were

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FIG. 14. (A) ‘‘Animal magnetism’’; Franz Anton Mesmer (1734–1815) after an engraving in Hilgard and Hilgard (1975) and a mesmeric seánce after an engraving in Darnton (1968). (B) ‘‘Emancipator’’; Philippe Pinel (1745–1826) after a frontispiece engraving in Pinel (1818). The motif of text is after a case history by Pinel, and the embedded motif is after a detail in the painting by Robert-Fleury of Pinel unchaining the inmates of the Biceˆtre mental asylum. (# Illustrations by Nicholas Wade.)

appalling; one report recorded that there were four times as many patients as there were beds, and many of the patients were fettered. On his appointment as chief physician at the Biceˆtre in 1793, Pinel entered the hospital and ordered the patients’ chains to be removed. Pinel’s decision was questioned by the Revolutionary authorities, and he was required to defend it in front of the Commune. Following the accusation that he himself was mad ‘‘to unchain these animals’’ Pinel replied ‘‘it is my conviction that these mentally ill are intractable only because they are deprived of fresh air and of their liberty.’’ His example of treatment for mental patients and the organization of mental hospitals was followed initially in Britain and eventually throughout the world. Pinel’s act of unchaining the patients was of great symbolic significance. It has been celebrated in two paintings, details from one of which are incorporated in the portrait; the third element is a copy of a case history taken by Pinel. The treatment of most mental illnesses improved throughout the nineteenth century, and their classification became more detailed. A major change in theories of neuroses was set in train by Sigmund Freud (1856–1939) (Fig. 15A); he established psychoanalysis as a treatment and developed a theory of mind that emphasized unconscious motivation. As such, he challenged many of the intellectual icons of his day, particularly those associated with infantile sexuality and personality development. Freud devised numerous neologisms that are now


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FIG. 15. (A) ‘‘Ichonoclast’’; Sigmund Freud (1856–1939) after a frontispiece photograph in Freud (1955), motif after a model of mental motivation in Freud (1933). (B) ‘‘Yin-Jung’’; Carl Gustav Jung (1875–1961) after a photograph in Runes (1959) encompassed within the symbols he embraced. (# Illustrations by Nicholas Wade.)

part of the fabric of our language. His methods in psychopathology did not draw on his neurological training nor did his theoretical concepts reflect his exposure to the mechanistic neurophysiology of his day. Most concepts in Freudian theory have a long and well-defined heritage, but Freud assembled and reassembled them in novel ways. His portrayal is derived from a photograph taken at the same time (i.e., 1922) that his theory of mind was proposed, and he is enclosed within it. Carl Gustav Jung (1875–1961) (Fig. 15B) established an analytic psychology that emphasized the self—the achievement of harmony among the various strands of personality. He displayed an early ambivalence in his approach to psychology: on the one hand, he developed a method of determining emotionality from associative reaction times to words; on the other, he studied occult phenomena and alchemy. Jung was closely associated with Freud between 1907 and 1912, but thereafter Jung developed his analytic psychology, concentrating on individual diVerences in personality and cross-cultural comparisons. His system became increasingly complex and amorphous, in contrast to Freud’s more constrained model of personality. The collaboration ceased in 1914, when their disparate views on the importance of psychosexuality led to a bitter split. Following the schism Jung entered a depression and sought to express his feelings in paintings. Initially they were representational but became increasingly abstract—often in the form of circular, quartered designs. He was later struck

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by the similarity of his paintings to the symbols and myths used in all human cultures. In particular, the mandala was treated as a symbol of total unity. Even his graphical model of mind consisted of concentric circles, with sensations in the outermost annulus, progressing centripetally through thinking, feeling, intuition, and memory to the central core of the personal unconscious. Jung studied comparative religion and the occult throughout his life, and he placed particular significance on visual symbols, like the mandala, used in diVerent cultures. These included yin-yang—representing the union of opposites—and Jung is shown within a variant of this symbol made up of concentric circles.

VII. Conclusions

It is hoped that some flavor of the perceptual potential oVered by portrayals in this manner has been conveyed. The work of individuals can be represented in more than their visages. Indeed, their appearances can be subordinated to some signs of their contributions to human thought. Histories of medicine are replete with standard portraits of its pioneers. Perhaps it is time for them to be seen in a fresh light!

References

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Clarke, E., and Dewhurst, K. (1972). ‘‘An Illustrated History of Brain Function.’’ University of California Press, Berkeley. Darnton, R. (1968). ‘‘Mesmerism and the End of the Enlightenment in France.’’ Harvard University Press, Cambridge, MA. Descartes, R. (1637/1902). La Diotrique. In ‘‘Oeuvres de Descartes’’ (C. Adam and P. Tannery, Eds.), Vol. 6, pp. 81–228. Cerf, Paris. Descartes, R. (1662). ‘‘De Homine Figuris et Latinitate.’’ Schuyl, F. (trans). LeVen & Moyardum, Leyden. Descartes, R. (1662). ‘‘De Homine Figuris et Latinitate. Trans. F. Schuyl.’’ LeVen & Moyardum, Leiden. Descartes, R. (1664/1909). Traite´ de l’Homme. In ‘‘Oeuvres de Descartes’’ (C. Adam and P. Tannery, Eds.), Vol. 11, pp. 119–215. Cerf, Paris. Descartes, R. (1677). ‘‘Tractatus de Homine et de Formatione Foetus Illustrated by L. de la Forge.’’ Elsevier, Amsterdam. Eccles, J. C., and Gibson, W. C. (1979). ‘‘Sherrington. His Life and Thought.’’ Springer, Berlin. Ferrier, D. (1876). ‘‘The Functions of the Brain.’’ Smith, Elder, London. Finger, S. (1994). ‘‘Origins of Neuroscience. A History of Explorations into Brain Function.’’ Oxford University Press, New York. Freud, S. (1933). ‘‘Neue Folge der Vorlesungen zur Einfu¨hrung in die Psychoanalyse.’’ Internationaler Psychoanalytischer Verlag, Vienna. Freud, S. (1955).‘‘The Standard Edition of the Complete Psychological Works of Sigmund Freud.’’ Vol. 18, Strachey, J. (trans). Hogarth Press, London. Hall, T. S. (1972). ‘‘Treatise of Man. Rene´ Descartes’’ Harvard University Press, Cambridge, MA. Harris, J. (1775). ‘‘A Treatise of Optics: Containing Elements of the Science; in two Books.’’ White, London. Harris, H. (1999). ‘‘The Birth of the Cell.’’ Yale University Press, New Haven, CT. Haymaker, W. and Schiller, F. (Eds.) (1970). ‘‘The Founders of Neurology.’’ 2nd ed. Thomas, Springfield, Ill. Hebb, D. O. (1949). ‘‘The Organization of Behavior.’’ Wiley, New York. Hilgard, E. R., and Hilgard, J. R. (1975). ‘‘Hypnosis in the Relief of Pain.’’ Kaufmann, Los Altos, CA. Home, E. (1794). A short account of the author’s life. In Hunter, J. ‘‘Treatise on the Blood, Inflammation, and Gun-Shot Wounds’’, pp. xiii–lxvii. Nicol, London. Hooke, R. (1665). ‘‘Micrographia: Or some Physiological Descriptions of Minute Bodies made by Magnifying Glasses with Observations and Inquiries thereupon.’’ Martyn and Allestry, London. Hunt, T. (Ed.) (1972). ‘‘The Medical Society of London 1773–1973.’’ The Medical Society of London, London. Hunting, P. (2004). The Medical Society of London. Postgrad. Med. J. 80, 350–354. Jardine, L. (2003). ‘‘The Curious Life of Robert Hooke: The Man Who Measured London.’’ Harper Collins, London. Knight, C. (1833). ‘‘The Gallery of Portraits: With Memoirs.’’ Vol. 1. Knight, London. Knight, C. (1834). ‘‘The Gallery of Portraits: With Memoirs.’’ Vol. 3. Knight, London. Knight, C. (1835). ‘‘The Gallery of Portraits: With Memoirs.’’ Vol. 4. Knight, London. Leeuwenhoek, A. van. (1674). More observations from Mr. Leewenhook. Philos. Trans. R. Soc. 9, 178–182. Leeuwenhoek, A. van. (1684). ‘‘Ontledingen en Beschouwingen der Onsigtbare geschapene Waarheden.’’ van Gaesbeek, Leiden. Marshal, A. (1815). ‘‘The Morbid Anatomy of the Brain in Mania and Hydrophobia’’ (S. Sawrey, Ed.). Longman, Hurst, Rees, Orme, & Brown, London. Newton, I. (1704). ‘‘Opticks: Or, a Treatise of the Reflections, Refractions, Inflections and Colours of Light.’’ Smith and Walford, London.

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Pare´, A. (1551). ‘‘La Me´thode de Traicter les Playes Faictes tant par Hacquebutes que par Fleches.’’ de Brie, Paris. Pare´, A. (1649). ‘‘The Workes of that Famous Chirurgion Ambrose Parey.’’ Johnson, T. (trans). Clarke, London. Pinel, P. (1818). ‘‘Nosographie Philosophique, ou la Me´thode de l’Analyse Appliqueé a la Me´decine.’’ 6th ed. Brosson, Paris. Polyak, S. (1957). ‘‘The Vertebrate Visual System.’’ University of Chicago Press, Chicago. Purkinje, J. E. (1918). ‘‘Opera omnia’’ (K. J. Lhotak, Ed.), Vol. 1. Society of Czech Physicians, Prague. Runes, D. G. (1959). ‘‘Pictorial History of Philosophy.’’ Philosophical Library, New York. Saunders, J. B. de C. M., and O’Malley, C. D. (1950). ‘‘The Illustrations from the Works of Andreas Vesalius of Brussels.’’ World Publishing, New York. Sherrington, C. S. (1906). ‘‘The Integrative Action of the Nervous System.’’ Scribner, New York. Reprinted in Wade, N. J. (Ed.) (2000). ‘‘The Emergence of Neuroscience in the Nineteenth Century.’’ Vol. 8. Routledge/Thoemmes, London. Treviranus, G. R. (1837). ‘‘Beitra¨ge zur Aufkla¨rung der Erscheinungen und Gesetze des organischen Lebens.’’ Heyse, Bremen. Vesalius, A. (1543). ‘‘De Humani Corporis Fabrica.’’ Oporini, Basel. Wade, N. J. (1990). ‘‘Visual Allusions: Pictures of Perception.’’ Erlbaum, London. Wade, N. J. (1995). ‘‘Psychologists in Word and Image.’’ MIT Press, Cambridge, MA. Wade, N. J. (1998). ‘‘A Natural History of Vision.’’ MIT Press, Cambridge, MA. Wade, N. J. (2003). ‘‘Destined for Distinguished Oblivion. The Scientific Vision of William Charles Wells (1757–1817).’’ Kluwer Academic/Plenum, New York. Wade, N. J. (2005). Medical societies and insanity in late-eighteenth century London: The fight between Andrew Marshal and John Hunter. J. His. Neurosci. 14, 11–15. Willis, T. (1664). ‘‘Cerebri Anatome: cui accessit Nervorum Descriptio et Usus.’’ Martyn and Allestry, London.

THE NEUROPSYCHOLOGY OF VISUAL ART: CONFERRING CAPACITY

Anjan Chatterjee Department of Neurology and the Center for Cognitive Neuroscience The University of Pennsylvania, Philadelphia Pennsylvania 19104, USA

I. II. III. IV. V. VI.

Introduction Disposition to Produce Art Visual Vocabulary Descriptive Accuracy Enhanced Expressivity Conclusions References

I. Introduction

The eVects of brain damage on the capacity to produce visual art stand in sharp contrast to many other human capacities. Diseases of the brain can impair our ability to speak or comprehend language, coordinate movements, recognize objects, apprehend emotions, and make logical decisions. By contrast, while diseases of the brain can certainly alter the ability to produce art, in many instances it is not so clear that the results are ‘‘impaired.’’ Paradoxically, in some cases the art seems to improve. In what follows, I will review the ways in which neurological disorders can create a disposition to produce visual art, provide artists with a unique visual vocabulary, add to artists’ descriptive accuracy, and enhance their expressive powers. These alterations are, of course, predicated on the brain damage not producing the kind of motor weakness that would make graphic expression impossible. I am not claiming that artists, by dint of their special talents, are exempt from the ravages of brain damage. Elsewhere, I have reviewed ways in which brain-damaged artists manifest deficits, such as achromatopsia, unilateral spatial neglect, visual agnosias, and asymbolias, similar to nonartists, albeit more eloquently (Chatterjee, 2004a,b). INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74003-X

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II. Disposition to Produce Art

People with frontotemporal dementias (FTD) undergo profound changes in their personalities. They can be socially disinhibited and disorganized and can have problems with their language, attention, and ability to make decisions. Despite these alterations in comportment and cognition, some people with FTD develop a propensity to produce art for the first time. Miller and colleagues (1998) note that the art tends to be realistic rather than abstract or symbolic. The art is most often visual and highly detailed with an obsessive quality. The patients themselves are intensely preoccupied with their art. The disposition to produce visual art can even arise late in the course of FTD. Anterion and colleagues (2002) reported a patient who began to draw in an advanced stage of his disease, the point at which he was apathetic and did not follow verbal commands; although he responded to family members with appropriate emotional responses. Despite this severely compromised state, he would draw when pencils were placed in front of him. He produced landscapes, houses, figures of women, and self-portraits. The artistic output of people with FTD appears to be a consequence of the change in their personalities, for example, acquired obsessive–compulsive traits find expression graphically, and they produce striking visual images as a consequence of their repetition and attention to detail. Are there other instances of obsessive–compulsive traits brought on by neurological diseases predisposing individuals to produce art? Three examples are consistent with this hypothesis: a person with probably partial complex seizures, a person with a subarachnoid hemorrhage, and a subset of children with autism. Sacks (1995c) described the remarkable case of Franco Magnani, an Italian painter working in San Francisco. Magnani painted hundreds of realistic scenes of an Italian town, Pontito, where he had grown up. At the age of 31, Magnani had a febrile illness that was probably an encephalitic disease. Following that illness, he began to paint obsessively. Pontito was the only subject of his art, and he painted compulsively. His obsession with Pontito pervaded virtually all his conversations. Sacks speculates that he had partial complex seizures and was in part demonstrating the kind of obsessive ‘‘sticky’’ personality disorder that is sometimes associated with temporal lobe epilepsy (Waxman and Geschwind, 1975). However, instead of being hypergraphic verbally, as is more common among such patients, he was hypergraphic visually. More recently, Lythgoe and colleagues (2005) reported the case of a builder with a subarachnoid hemorrhage. He had no interest in art premorbidly but became an obsessive artist after recovery from the initial injury. After the hemorrhage, he had a normal verbal and performance IQ and normal behavior, except for some degree of verbal disinhibition. He did well on most neuropsychological


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tasks, except for those that involved task switching. He also began to draw hundreds of sketches, mostly faces. He then moved to large-scale drawings sometimes covering entire rooms but confined his art to a few themes. The authors emphasize his perseverative tendencies as critical to the emergence of his artistic skills. Finally, about 10% of autistic children have savant-like abilities (Rimland and Fein, 1988). A subset of these children produces striking visual images (Sacks, 1995a). The most detailed description of such a case was Nadia, reported by Selfe (1977). As a baby, Nadia did not respond to her mother, and as she got older she lacked social empathy. As a child, she had an obsessive concern with the presence of other children without establishing any substantial interactions with them. Her acquisition of language was delayed. Despite these developmental abnormalities, she had remarkable drawing skills. By the age of 3, she was drawing life-like horses. She drew intensively for a few moments at a time, always copying images. She also focused on specific kinds of images like horses, of which she drew hundreds of examples. While Nadia’s abilities were striking, she was not unique. Autistic children with these striking drawing skills seem to focus on specific subjects and draw them repeatedly. Thus, it appears that several neurological disorders that produce obsessive– compulsive traits can also dispose people to produce art. These artists seem to produce realistic images and tend to be preoccupied by specific themes. While the neural basis for obsessive–compulsive disorders is not completely understood, it is associated with dysfunction of the orbitofrontal and medial temporal cortices and frontostriatal circuits (Kwon et al., 2003; Saxena et al., 1999; Ursu et al., 2003). Notably, in the cases described, these regions could have been damaged, and posterior occipitotemporal cortices were presumably intact. The preservation of posterior cortices ensures that the neural substrate for recognizing and representing faces, places, and objects is preserved and, thus, available to be the subject of these patients’ obsessions.

III. Visual Vocabulary

Artists develop visual vocabularies that they use in their artwork. They acquire these vocabularies from a variety of sources, including formal training and other artists. Neurological disorders, such as migraine and epilepsy, can be associated with productive visual phenomena. People with these disorders may have another source of imagery to enrich their visual language. People with migraine experience various visual phenomena, including scotoma, phosphenes, scintillations, and fortification spectra. Wilkinson and Robinson (1985) analyzed the artwork submitted to the first National Art Competition

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sponsored by the British Migraine Association and WB Pharmaceuticals. Of over 200 entries, 70% showed spectral appearances, 48% showed fortifications, 16% showed areas of visual loss, and 2.5% showed mosaic visions (Chapters 8 by Klaus Podoll and 9 by Klaus Podoll and Debbie Ayles). The artist Ignatius Brennan, as reported by Podoll and Robinson (2000), eloquently expressed the idea that migrainous auras can inspire art. He had migraine since the age of 11, which he experienced as frightening episodes of visual loss, often with a zigzag cloud obscuring much of his visual fields. As he got older, he saw triangles and rounded forms as well as mosaics. He also experienced macroscopic and microscopic visual distortions. He described the eVects of migraine on his art as follows: ‘‘I started with pictures of my migraine experiences unconsciously rather than deliberately, when I was in art school. I used to do a lot of drawings of landscapes at that time and often found that I would be drawing clouds not just in the sky, but everywhere, which I think was a reference to the visual voids experienced during visual loss. I also used serrated zigzag shapes in my drawings, symbolizing the experience of a whole being broken up. . ..Clouds, zigzags and other imagery are part of my own personal visual vocabulary, but which certainly has come out of migraine experiences. I’m absolutely sure. I don’t tend to do that deliberately, but when it suits a particular subject, e.g. to represent a feeling or an emotion, I make use of these images in diVerent ways . . ..’’

IV. Descriptive Accuracy

For centuries visual artists have been preoccupied with rendering objects and the environment accurately. Underlying the problem of depictive accuracy in drawing and painting are the roles of knowing and seeing when apprehending objects. And here, patients with disorders of knowing and seeing might be informative. Since Lissauer’s (1890) classic descriptions of visual agnosias, object recognition deficits are recognized to lie on a continuum between perceptual and conceptual deficits. Perceptually based agnosias, called apperceptive agnosias, impair the ability to process the visual information into a coherent object. Conceptually based agnosias, called associative agnosias, involve a disconnection between semantic and visual representations or impairments of semantic representations themselves (Farah, 1990). One might infer that an inability to recognize objects would be accompanied by an inability to draw that object. This inference turns out to be not quite accurate. Wapner et al. (1978) described an artist with an apperceptive agnosia who had diYculty copying images despite being able to convey depth and shading in drawings that were otherwise fragmented. His preserved semantic


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system was of little help in guiding his artistic production. Thus, when asked to draw a telephone, he would construct images by reasoning. ‘‘It needs a base for it to stand on, a place to speak into, something to hear with, a wire to plug in for communication and a place to dial.’’ This verbal strategy was not particularly eVective in rendering accurate images. Thus, semantic knowledge by itself does not help render objects accurately. This patient contrasts with two people with associative agnosias (Franklin et al., 1992; Schwartz and Chawluck, 1990). Their agnosias were probably because of an underlying semantic dementia, but at the time this entity was not well recognized. In both cases, when asked to draw objects from verbal labels these people drew crude, simplified images similar to those drawn by a young child. However, with complex visual images, the results were strikingly diVerent. For example, one of these people could copy a portrait originally painted by Botticelli or draw a portrait of a staV worker beautifully (Franklin et al., 1992). These artists’ drawings also deteriorated dramatically if the model was taken away suggesting that a visual short-term memory deficit was part of the picture. However, for our purposes, the point is that semantic knowledge of an object is by no means necessary to render it accurately. Observations of a Polish aphasic artist are also consistent with this point (Kaczmarek, 1991). Profoundly influenced by the events of the World War II, his premorbid paintings were antiwar statements, which often included numbers, letters, and ideograms. Following his stroke, he was nonfluent and only produced a few words. Our semantic system at its core has the ability to abstract and generalize. On this view, the use of abstracted symbols could be considered a marker for a preserved semantic system. Although his semantic system was not tested in detail, one might infer that it was impoverished. His inability to make use of verbal symbols also extended to his artwork. He was no longer able to produce paintings in his previous style. However, he was still able to draw realistic landscapes and portraits quite well. Here again is an example of an individual able to depict scenes and people accurately despite having lost his ability to manipulate symbols. Does semantic knowledge of an object actually hinder artistic production? The art historian Gombrich (1960) observes that even trained artists bring a set of hypotheses of what they are looking at to bear on their depictions and that these hypotheses sometimes blind them to what they are seeing. It would follow that impaired knowledge of the object of one’s gaze, provided the rest of the visualmotor systems are intact, would aid in the ability to depict objects and scenes accurately. Perhaps this is what is happening in the cases of autistic children with savant-like artistic abilities. Autistic artists like Nadia and Wiltshire needed only to look at an object for a few minutes before drawing them rapidly and accurately (Sacks, 1995a; Selfe, 1977). Nadia’s abilities were not an accelerated version of other children’s

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drawing development. She did not first go through a phase of drawing simple schematic images before learning to draw realistically. Rather her skills were developed at the outset and did not change much over time. She made lines deftly and without hesitation. Nadia drew horses repeatedly. Two observations suggest that Nadia treated these images diVerently than most people. First, she would start the drawing anywhere on the page. Rather than trying to squeeze the image into the page, she terminated the drawing when she came to the paper’s edge, even if it meant only drawing part of the horse’s head. Second, most people draw horses by starting at the head. Nadia might start her drawing at the neck of the horse and seemed unaVected by critical features by which we might recognize an object. Her remarkable skill at drawing horses and pelicans appear to have emerged from the obsessive focus on specific objects that were at the same time not obscured by semantic associations that interfere with the ability to ‘‘see’’ the visual object. The history of her cognitive development and drawing skills is consistent with this speculation. As Nadia eventually acquired language, her drawings became more prosaic. Presumably, the acquisition of language reflected the development of a richer semantic system and detracted from her artistic skills.

V. Enhanced Expressivity

Visual art is, of course, not restricted to the task of descriptive accuracy. Perhaps driven by the advent of photography, visual art has diverged into many forms. Among the most intriguing eVects of brain damage on artists are a class of phenomena in which the inability to make accurate depictions results in surprisingly appealing stylistic changes in their art. These stylistic changes can occur in the use of color and form, and in the content of images. Sacks (1995b) described an artist with an acquired achromatopsia following a traumatic brain injury. Before the accident, his paintings were colorful and quite abstract. After the accident everything appeared ‘‘dirt gray’’ to him. His initial attempts to use color were haphazard, and he ultimately resigned himself to black and white paintings. Eventually, he introduced a limited set of colors to his paintings. After an initial sense of helplessness, he began to consider his new way of seeing as a strange gift in which he saw the world as pure form, uncluttered by color. This new way of seeing introduced him to a new range of expressions. For example, when driving he saw a sunrise in which blazing reds were seen as black. He described the scene as ‘‘The sun rose like a bomb, like some enormous explosion. Has anyone seen a sunrise like this before?’’ Inspired by this image, he produced a black and white painting called ‘‘Nuclear Sunrise.’’ Right hemisphere damage can produce left spatial neglect in which patients are unaware of the left side of space (Chatterjee, 2003). Artists with neglect omit


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the left side of images that they draw or paint (Blanke et al., 2003; Cantagallo and Sala, 1998; Halligan and Marshall, 1997; Jung, 1974; Marsh and Philwin, 1987; Schnider et al., 1993). As they recover from their neglect, their use of line may still be altered. Two examples show how this change in the use of line can produce art that comes to be regarded highly. Lovis Corinth, an important German artist, suVered a right hemisphere stroke in 1911. As he recovered, he resumed painting. His self-portraits and portraits of his wife showed clear changes in style, with details on the left sometimes left out and textures on the left blended with the background. Alfred Kuhn characterized this work as follows (quoted in Gardner, 1975) ‘‘He [Corinth] had become prescient for the hidden facets of appearance . . .. The contours disappear, the bodies are often as ript asunder, deformed, disappeared into textures . . . also the faithfulness of portraits had ceased almost entirely . . .. With wide stripes the person is captured in essence. Characterization is now exaggerated; indeed, often to caricature . . . Corinth always seems to be painting a picture behind the picture, one which he alone sees . . . at this point Corinth shifted from the ranks of the great painters into the circle of the great artists.’’ More recently, in the 1990s, Heller (1994) reported the experience of the artist Loring Hughes, who after a right hemisphere stroke had diYculty in coordinating the spatial relationship between lines. This forced her to abandon her premorbid style of depictive accuracy. Instead, she turned to her own imagination and emotions. Initially, she was too ashamed to display her paintings. Once she became comfortable with her new style, she began to show her work. To her surprise the artistic community responded well to these distorted images. The critic Eileen Watkins described her work as now delivering ‘‘an emotional wallop’’ that was not present previously. The stylistic changes, when they occur with left brain damage, appear to be quite diVerent than those observed with right brain damage. The specific changes are the introduction of more vivid colors and a change in content. These changes are exemplified in the Bulgarian painter, Zlatio Boiyadjiev, a Californian artist named Katherine Sherwood, and a Swiss painter reported recently by Annoni and colleagues. Boiyadjiev’s premorbid artistic style was natural and pictorial, and he tended to use earth tones in his paintings. Following the onset of his aphasia, Boiyadjiev’s paintings became richer, more colorful, and contained more fluid and energetic lines (Brown, 1977; Zaimov et al., 1969). The imagery in his work became more inventive and at times even bizarre and fantastical. Similarly, Katherine Sherwood suVered a left hemisphere hemorrhagic stroke, which left her with an aphasia and right-sided weakness (Waldman, 2000). She trained herself to paint with her left hand, and since then her career has flourished. Premorbidly, her images were described as ‘‘highly cerebral’’ incorporating a range of esoteric images such as cross-dressers, medieval seals, and spy photos. After her stroke she felt that she could not produce such images if she wanted. Her new style is

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described as ‘‘raw’’ and ‘‘intuitive,’’ with large irregular circular movements. She says her left hand enjoys an ease and a grace with the brush that her right hand never had and describes it as ‘‘unburdened.’’ Finally, Annoni and colleagues (2004) recently described a Swiss landscape painter whose art was described as being ‘‘figurative-impressionist.’’ He had a small stroke in the left thalamoperforant vascular distribution. His wife thought he had mild emotional dyscontrol after his stroke. He felt that he was more sensitive to the hidden beauty of images and used bolder colors. He switched from impressionist to more realistic images. He thought that he was less likely to use lines, contours, and perspective clearly and was more creative when he used his left than his right hand. A final stylistic change rendered by brain damage is a move toward simplicity. Annoni and colleagues (2004) also described a person with a left occipital lesion involving areas V1 and V2, resulting in a right superior quadrantanopsia with macular sparing. A month after his stroke he resumed drawing and painting. His new artwork was simplified, stylized, increasingly abstract, and confined to a limited use of colors. It is not known if damage to visual association cortices would consistently result in simplification and abstraction. However, a few artists with Alzheimer’s disease who have continued to paint (Crutch et al., 2001; Maurer and Prvulovic, 2004; Miller and Hou, 2004) seem to demonstrate a similar pattern.1 The most prominent of these is the expressionist Willem de Kooning (Storr, 1995). After the onset of his neurological disease, de Kooning’s ex-wife and some students provided the structure from which he could continue to work. They stretched his canvases and mixed his colors. He was noted to be generally apathetic except in his studio, where he was engaged and lively. Experts generally agree that this late period represents a new and coherent style for de Kooning. His paintings became successively simpler, and he confined his palette to primary colors. Traces of shapes from earlier works are evident, but these are pared down. Garrels (1995), the senior curator at the San Francisco Museum of Modern Art, thought ‘‘the vocabulary of forms was retained, but clarified . . . the results are paintings of an openness and freedom not seen before, paintings that are extraordinarily lyrical, immediately sensual, and exhilarating.’’

VI. Conclusions

I would like to conclude with a few comments about the nature of the evidence being discussed here. My speculations are based on anecdotes. Extracting 1 My own clinical experience is that such patients are often too disorganized to take an art project to completion. I have cared for several artist-patients that spend hours in their studio puttering around without producing much art.


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general principles from anecdotes is risky business. Undoubtedly, some of these claims will need to be modified as the number of such cases grows. The neuropsychology of art has not developed into an experimental science. Such a development will be diYcult, given the topic of inquiry, but it is necessary if we are to go beyond the cataloguing of fascinating anecdotes. These rich qualitative accounts need quantitative underpinnings. In my view, two things are needed. First, we need greater in-depth analyses of artists with brain damage in which both the art and components of their cognition are examined carefully. Such analyses would clarify the relevant questions. For example, the question of whether aphasia aVects art is probably ill formed. Art is quite varied and ‘‘aphasia’’ is itself too varied a syndrome to expect any direct mapping of one category on to the other. With analyses of the components of art, we could generate testable hypotheses about how brain damage might impair, alter, or improve art. Second, group studies are probably impossible (with perhaps the exception of artist with migraine) given the rarity of established artists who acquire neurological disorders. Thus, we will need meta analyses of the case series to generate general principles about the neuropsychology of art. However, such analyses are entirely dependent on the first point, that is, the need for adequately studied individual cases. Finally, in this chapter I have emphasized the enhancing eVects of brain damage on artistic production. These observations are subject to significant selection biases. It is likely that many more artists are devastated by their brain injury, and these cases are not reported. We simply do not know the base rate of the kinds of eVects I have outlined. And yet, these examples of improved art following brain damage do point to the multifaceted nature of art. Cases of improved artistic abilities fall into a general class of paradoxical functional facilitations produced by brain damage (Kapur, 1996). Other examples of such facilitation involve relatively simple sensory and motor abilities and automatic processes. The ability to produce visual art is striking in its complexity as compared to these other examples. Art is suYciently multifaceted that impairments in one component can be compensated by or facilitated by other components. These observations hint at the resilience of the creative spirit, which finds expression even when its habitual outlets are obstructed. References

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Blanke, O., Ortigue, S., and Landis, T. (2003). Color neglect in an artist. Lancet 361, 264. Brown, J. (1977). ‘‘Mind, Brain, and Consciousness: The Neuropsychology of Cognition.’’ Academic Press, New York. Cantagallo, A, and Sala, S. D. (1998). Preserved insight in an artist with extrapersonal spatial neglect. Cortex 34, 163–189. Chatterjee, A. (2003). Neglect: A disorder of spatial attention. In ‘‘Neurological Foundations of Cognitive Neuroscience’’ (M. D’Esposito, Ed.), pp. 1–26. MIT Press, Cambridge, MA. Chatterjee, A. (2004a). The neuropsychology of visual artists. Neuropsychologia 42, 1568–1583. Chatterjee, A. (2004b). Prospects for a cognitive neuroscience of visual aesthetics. Bull. Psychol. and the Arts 4, 55–59. Crutch, S., Isaacs, R., and Rossor, M. (2001). Some workmen can blame their tools: Artistic change in an individual with Alzheimer’s disease. Lancet 347, 1096–1098. Farah, M. J. (1990). ‘‘Visual Agnosia.’’ MIT Press, Cambridge, MA. Franklin, S., van Sommers, P., and Howard, D. (1992). Drawing without meaning?: Dissociations in graphic performance of an agnosic artist. In ‘‘Mental Lives. Case Studies in Cognition’’ (R. Campbell, Ed.), pp. 179–198. Blackwell, Cambridge, USA. Gardner, H. (1975). ‘‘The Shattered Mind: The Person After Brain Damage.’’ Alfred A. Knopf, New York. Garrels, G. (1995). Three toads in the garden: Line, color, and form. In ‘‘Willem de Kooning. The Late Paintings, The 1980s,’’ pp. 9–37. San Fransisco Museum of Modern Art and Walker Arts Center, Minneapolis. Gombrich, E. (1960). ‘‘Art and Illusion.’’ Princeton University Press, Princeton. Halligan, P. W., and Marshall, J. C. (1997). The art of visual neglect. Lancet 350, 139–140. Heller, W. (1994). Cognitive and emotional organization of the brain: Influences on the creation and perception of art. In ‘‘Neuropsychology’’ (D. Zaidel, Ed.), pp. 271–292. Academic Press, New York. Jung, R. (1974). Neuropsychologie und neurophysiologie des konturund formsehens in zeichnerei und malerei. In ‘‘Pyschopathologie Mususcher Gestaltungen’’ (H. Weick, Ed.), pp. 27–88. FK Shattauer, Stuttgart. Kaczmarek, B. (1991). Aphasia in an artist: A disorder of symbolic processing. Aphasiology 5, 361–371. Kapur, N. (1996). Paradoxical functional facilitation in brain-behavior research. Brain 119, 1775–1790. Kwon, J., Kinm, J., Lee, D., Lee, J., Lee, D., and Kim, M. (2003). Neural correlates of clinical symptoms and cognitive dysfunctions in obsessive-compulsive disorder. Psychiatry Res. 122, 37–47. Lissauer, H. (1890). Ein Fall von Seelenblindheit Nebst Einem Beitrage zur Theori derselben. Archiv fur Psychiatrie und Nervenkrankheiten 21, 222–270. Lythgoe, M., Polak, T., Kalmus, M., de Haan, M., and Khean Chong, W. (2005). Obsessive, prolific artistic output following subarachnoid hemorrhage. Neurology 64, 397–398. Marsh, G. G., and Philwin, B. (1987). Unilateral neglect and constructional apraxia in a right-handed artist with a left posterior lesion. Cortex 23(1), 149–155. Maurer, K., and Prvulovic, D. (2004). Paintings of an artist with Alzheimer’s disease: Visuoconstructive deficits during dementia. J. Neural. Transm. 111, 235–245. Miller, B. L., Cummings, J., Mishkin, F., Boone, K., Prince, F., and Ponton, M. (1998). Emergence of artistic talent in frontotemporal dementia. Neurology 51, 978–982. Miller, B., and Hou, C. (2004). Portraits of artists: Emergence of visual creativity in dementia. Arch. Neurol. 61, 842–844. Podoll, K., and Robinson, D. (2000). Migraine experiences as artistic inspiration in a contemporary artist. J. R. Soc. Med. 93(5), 263–265.


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VISION, ILLUSIONS, AND REALITY

Christopher Kennard Department of Clinical Neuroscience Imperial College London, United Kingdom

I. Introduction II. Functional Specialization in the Visual Brain III. Face and Object Recognition Recommended Reading

I. Introduction

Since vision is our primary sense, it is not surprising that a large part of the human brain is devoted to processing the image of our visual world to generate visual percept. However, it is wrong to consider that our visual brain always provides us with a percept that is true to the external visual world. Rather, it actively participates in constructing what we see. Our visual percept, obtained from the information it receives from the two eyes, may sometimes be distorted as a result of physiological interactions among neurons in the visual brain due to the pattern of their connections. This is best exemplified by the study of visual illusions, for example, in the Zo¨llner illusion parallel lines appear bowed or nonparallel when a series of short orthogonal lines are added due to lateral interactions between orientation columns (Fig. 1). Alternatively at other times, distortions arise from the generation of hypotheses by the visual brain about the visual world, for example, when the two-dimensional metastable illusion (Necker cube) is viewed it appears three-dimensional, but its forward face repeatedly changes between two alternatives (Fig. 2). As in the rest of science, these hypotheses may not always be correct and individuals may require other sensory inputs (e.g., tactile) to determine reality. The visual brain also has to restrict what we see since processing all the visual information received by our eyes would require a visual brain many times larger than available to us. We, therefore, focus attention and hence visual processing on a restricted region of the visual world. INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74004-1

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FIG. 1. (A) Zo¨llner illusion. Lines appear to diverge and converge depending on the angled cross hatching. (B) PoggendorV illusion. 2 segments appear displaced. (C) Hering illusion. Parallel lines that cross a set of radiations appear to bulge. These are examples of lateral interactions between orientation columns.

FIG. 2. The Necker cube. An ambiguous two-dimensional object interpreted by the visual brain as a three-dimensional cube. The structure is a metastable illusion, and the cube can be seen in two diVerent orientations. II. Functional Specialization in the Visual Brain

The visual world is made up of a number of visual attributes, such as orientation, color, motion, form, and stereopsis, which are eVortlessly identified by the visual brain. The use of electrophysiological recording in nonhuman primates and more recently the use of functional brain imaging in normal human subjects have

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helped to settle the long-standing debate concerning the functioning of the visual brain as to whether or not these diVerent visual attributes are each processed in separate areas or globally. Put more succinctly, is there functional specialization in the visual brain? However, despite the sophistication of these techniques that have clearly identified functional specialization, the neurological patient with a small focal cortical lesion (usually due to cerebral infarction) who shows a specific neurological deficit, as originally used by Paul Broca in the nineteenth century in relation to identifying the dominant speech area, is another required level of proof for deciding on the specific function of an area of the visual brain. Functional brain imaging has identified a region of occipital ventral cortex, in the fusiform gyrus, which is involved in color processing—area visual 4 (V4). Damage to this area gives rise to the main central disorder of color processing, achromatopsia, in which there is impaired color perception involving all or part of the visual field, with preservation of form and motion vision. Discrimination of wavelength diVerences, however, may be intact. Patients describe the world, for example, as drained of color, a collection of shades of grey or that brightly saturated colors look pale. Although during functional imaging several diVerent areas of the visual brain are activated by motion perception, the major site lies some way from V4 in the region of the lateral occipitotemporal junction—an area called V5 or middle temporal (MT). Only one patient has been well documented with bilateral lesions that aVected this region causing a disturbance of motion perception, akinetopsia. The disorder was highly specific for motion, the patient having no diYculty in seeing colors, form, or depth. She described how, for example, she experienced problems in crossing the road because the exact positions of moving cars were diYcult for her to judge, or pouring tea or coVee into a cup because the fluid appeared to be frozen. III. Face and Object Recognition

Face perception is the most developed visual perceptual skill in humans, playing a critical role in social interactions as well as enabling the recognition of the identity, background, and mood of people around us. In view of this, it is not surprising that regions of the visual brain have evolved to become devoted to face recognition. Neurons have been recorded electrophysiologically in the superior temporal sulcus of monkeys, which respond selectively to the presentation of the image of a face in their receptive fields. Functional imaging in man has similarly identified activation when viewing faces in the same region, as well as in the inferior occipital gyrus and the lateral fusiform gyrus, the latter located anterior to the color area V4. Damage to these areas results in a very specific disturbance—prosopagnosia, a term used to describe the inability to recognize faces or their representation. Although prosopagnosia can occur in isolation,

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it is often observed in association with other functional visual deficits such as achromatopsia and visual agnosia. Although the most obvious disturbance in such patients is impaired facial recognition, they may also show an inability to distinguish between objects belonging to other object categories, such as buildings, animals, or automobiles. Prospagnosia often occurs as a result of a lesion in the occipitaltemporal region, which damages or disconnects the inferior visual association cortex from the right temporal cortex. Although an inability to recognize objects visually—visual agnosia or visual object agnosia—is a relatively rare neuropsychological symptom, such cases have led to a considerable variety of theories concerning higher visual processing. A categorization, however, proposed by Lissauer (1889) over a century ago, still serves as a useful framework to understand the main types of visual agnosia. In apperceptive visual agnosia, there is a breakdown in high-level visual perception leading to an inability to generate a stable perceptual representation of an object. Such patients cannot name, copy, or recognize visually presented objects, but can do so with auditory or tactile cues. Tests of basic visual perception, for example, visual acuity, contrast sensitivity, line orientation discrimination, or color identification, are performed correctly. Lissauer also described associative visual agnosia, which occurs when there is a breakdown in retrieving stored knowledge about the object, which normally allows it to be recognized—a normal percept stripped of its meaning (Teuber). Other high-level visual processes, such as copying figures or written material, matching photographs taken from unusual views, or block design, are intact. Most cases have had bilateral lesions, due to stroke or tumor, advanced degenerative dementia, or carbon monoxide poisoning, which involve the ventral occipitaltemporal lobe. Recent functional imaging studies have identified areas in this region, which are specifically activated when diVerent categories of objects, such as houses or chairs, are viewed. Therefore, there is much evidence to suggest that there is marked functional specialization in our visual brain—indeed it is likely that there are over 30 diVerent areas interconnected and influencing each other in a very complex manner. It is no surprise, therefore, to conclude that the visual brain is not a mere chronicler of the external physical reality, but as a result of its own set of rules and programs, it actively participates in generating our visual percept. Recommended Reading Eagleman, D. M. (2001). Visual illusions and neurobiology. Nat. Rev. Neurosci. 2, 920–926. Gregory, R. L. (1998). ‘‘Eye and Brain: The Psychology of Seeing.’’ Oxford University Press, Oxford. Kennard, C. (Ed.) (1993). Visual perceptual defects. Bailliere. Clin. Neurol. 2(2), Bailliere Tindall, London. Sacks, O. (1985). ‘‘The Man Who Mistook His Wife for a Hat.’’ Picador, London. Trobe, J. D. (2001). ‘‘The Neurology of Vision.’’ Oxford University Press, Oxford. Zeki, S. (2003). ‘‘A Vision of the Brain,’’ 2nd ed. Blackwell, Oxford.

LOCALIZATION IN THE VISUAL BRAIN

George K. York Kaiser Permanente Stockton Medical Center and the Sa˚a Institute Fiddletown, California 95629, USA

I. II. III. IV. V.

Introduction A Note on Localization The Painter at the Bedside The Neurologist in the Picture Gallery Commentary: The Three Cultures References

I. Introduction

Contemplating a successful painting evokes a variety of responses, including amazement, passion, sympathy, anger, puzzlement, and admiration. If the viewer happens to be a neurologist, it might also evoke two scientific questions, namely where in the artist’s brain does the artistry come from and where in the art-lover’s brain does the painting’s impact reside? These questions lend themselves to systematic inquiry, if not scientific investigation, and the principles of classical neurology can inform the painter and the patron alike. A cornerstone of clinical localization is the assumption that the nervous system is an aggregate of diVerent anatomical elements, or organs, each with a single discrete function. This assumption originated in the pseudoscience of phrenology, which was debunked almost 200 years ago. The phrenological assumption, on the other hand, formed the basis of diagnostic neurology and has withstood the test of intense clinical and experimental scrutiny since Victorian times. The world has accepted that a careful analyses of signs and symptoms can lead the astute neurologist to determine the presence of pathology in the nervous system. Diagnostic localization requires the knowledge of the normal anatomy and physiology of the nervous system, a knowledge that might be useful in looking at paintings. Neurology involves paying attention to the structural and functional relationship between the various neurological organs, with the confidence that it will lead to tolerably consistent predictions about health and disease.


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Diagnostic neurology recognizes a number of anatomic divisions defined by their functions, including the auditory brain, the motor brain, and the visual brain. Close attention to vision reveals the presence of several discrete visual organs within the visual brain, including those responsible for color vision, form, and motion. These organs are contiguous but anatomically separate, and the careful neurologist can diagnose isolated lesions in each of them. This study aims to examine those visual functions that may be clinically localized in living human subjects, using the conceit of the painter at the bedside. It will then ask whether aesthetic sense or creativity is localized in the visual brain, taking the point of view of the neurologist in the picture gallery. Although the neurologist’s point of view is not necessarily privileged, the scientific validity of clinical localization does make his or her perspective worthy of attention. Furthermore, localization means diVerent things to diVerent people, so localization in the visual brain depends on who is doing the localizing. This issue is controversial, showing important diVerences between neurologists and other commentators on art, painting, and the visual brain (Edwards, 1989; Livingstone, 2002; Ramachandran, 1999; Solso, 1999; Zeki, 1999).

II. A Note on Localization

In keeping with the theme of localization in the visual brain, it is worth asking what counts as localization. In turn, this raises the question of just what functions, precisely, are localized. The advent of reliable medical physiology in the middle of the nineteenth century put a premium on the definition of the functions of nervous system, but there was no consensus about which neurological functions could be investigated in the laboratory or at the bedside. French physiologists looked for the localization of a set of faculties such as intelligence, memory, will, judgment, and insight. By contrast, physiologists and physicians in Englishspeaking countries did not accept the faculty view of neurological function. For them, the functions of the nervous system are exclusively aVerent and eVerent, sensory and motor. To further complicate matters, most neurophysiologists believed that the metaphysical soul resides in the cortex, and, therefore, the cortex must have a physiology diVerent from the lower, sensorimotor areas. The cortex was thought to be electrically inexcitable with no motor or sensory function whatever. This situation made the prospect of scientific neurophysiology and practical localization of function at the bedside much more diYcult (Harrington, 1987; Smith, 1982; York and Steinberg, 1993; Young, 1970). The solution to the dilemma emerged in London and Berlin. In 1868, John Hughlings Jackson observed that patients with cortical lesions may have the march of myoclonic jerks in focal epilepsy. He interpreted this to mean that


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the cortex is excitable, it follows the same physiological principles as the rest of the nervous system, and these principles are exclusively sensorimotor (Hughlings Jackson, 1968). Furthermore, he concluded that the motor cortex is somatotopically organized in the same way as the rest of the motor systems. These ideas did not excite much scientific interest until 1870, when Gustav Fritsch and Eduard Hitzig demonstrated somatotopically organized motor areas in the cortex of dogs (Fritsch and Hitzig, 1870) . This study, published in German, showed that galvanic stimulation of diVerent cortical areas evokes movement in diVerent parts of the body. Shortly thereafter, David Ferrier confirmed the existence of these cortical motor areas in primates (Ferrier, 1873). The confirmation of cortical motor regions opened the door for a unified neurophysiology, which applied to the entire nervous system and eliminated the scientific search for the workings of immaterial objects like the soul. In light of these findings, and with Darwinism in its ascendancy, Hughlings Jackson promulgated the physiological principle that the entire nervous system, including the cortex, is an exclusively sensorimotor mechanism governed by the laws of evolution and the conservation of energy. His motivation was to develop a practical diagnostic system, but he was aware of the scientific implications of his work. A practicing physician, he was also intimately aware of the power of the mind in health and disease. He, therefore, had to consider the medical implications of a philosophical conundrum, namely the mind-brain relationship. After considering the alternatives, he articulated his Doctrine of Concomitance, stating that the brain and the mind exist in parallel but have no cause-and-eVect relationship with each other. Under this doctrine, neurological illness and medical illness exist concomitantly but have no causal eVect on each other (Hughlings Jackson, 1884). The scientific discipline of Jacksonian localization was applied exclusively to the sensorimotor machine, leaving diagnosis and treatment of mental disease to psychiatry. Jacksonian concomitance allows neurologists to practice scientific medicine without concern for its philosophical significance, if any. Neurologists, as physicians, localize pathology by examination of a patient’s sensation and movement. We do not try to localize mental functions such as creativity, free will, morality, or aesthetic sensibility. In fact, we claim that such localization is impossible. Neurologists spend their days searching for pathology in the nervous system with techniques based on the assumption that stimulation and ablation are reciprocal processes, and that focal epilepsy and focal infarction produce reciprocal symptoms. When we analyze these symptoms in sensorimotor terms, we believe that we have identified some aspect of neurological function. The world accepts, and pays for, this type of scientific neurology for the simple reason that it is a consistent way to diagnose and treat illness. In general, the world is less concerned about any philosophical inconsistencies. Experimental devices and techniques, such as electroencephalography, magnetoencephalography, and imaging, provide information about neurological

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responses to various types of stimulation. When the evoked response occurs focally, the putative function is said to be localized. However, the task may involve some form of mental action, which conservation laws and Jacksonian concomitance say cannot cause a physical response. For example, tasks that require free will or moral judgment may illuminate the sensorimotor concomitant of the mental function, but they do not localize the mental function itself. Neurologists know this from experience because focal epilepsy does not evoke free will and stroke does not eliminate moral judgment. The Jacksonian neurologist is a practical physician whose prime concern is to diagnose and treat diseases of the nervous system. He or she is well aware of the scientific, psychological, and philosophical dimensions of the craft and sympathetic to the nuances of these disciplines. However, the neurologist is also mindful of the diYculties involved in trying to localize mental symptoms. Equating the mind and brain may suit the needs of speculation, but it does not help in taking care of patients. Commentators from other disciplines criticize this attitude, suggesting that neurologists pay insuYcient attention to aesthetics and theory (Zeki, 1999a,b). At the same time, these commentators are anxious to claim that they, too, are neurologists by virtue of their interest in neuroanatomy and neurophysiology. They are not as interested in medicine or therapeutics, and therefore, they ignore Jacksonian localization principles, including concomitance. Hence, they have diYculty with bedside localization, not that they care about it.

III. The Painter at the Bedside

A painter with a working knowledge of the visual brain may localize pathology in the nervous system by stimulating it in diVerent ways. For example, the painterly neurologist may present points to the patient’s visual field and discern the presence of focal pathology in the primary visual pathways. The distribution of visual loss tells our sophisticated painter about optic neuropathy, pituitary tumors, and occipitotemporal strokes. Creative painters at the bedside might devise amusing ways to stimulate the visual fields and would amaze their friends with the accuracy of their diagnosis. The neurologist Kandinsky presents points, lines, or planes to patients, asking them whether they see the object presented. He might also present colored points, moving objects, or faces, again asking what the patient sees. Our bedside Mondrian knows that the visual brain has a curious anatomical organization called retinotopic representation. Fibers originating in one part of the retina remain close to their neighbors, even after they have synapsed with other neurons. This means that images in a particular field are represented throughout the central pathways and lesions in those central pathways lead to symptoms


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located in the same field. Hence, lesions behind the optic chiasm produce homonymous quadrantanopsia or hemianopsia, with the more congruent field loss in more posterior lesions. The visual brain responds to stimuli other than points or lines in a plane. It also actively processes color, motion, depth, and form. Manipulating visual perception is a painter’s stock in trade, so the painter at the bedside may stimulate the visual brain in unusual ways and localize a pathological lesion in the brain. Our artistic neurologist knows that the perception of these elements occurs in diVerent parts of the visual brain, and so painting may tell us how the nervous system works and vice versa. The Bellini at the bedside can find patients who cannot perceive color, most of whom have degeneration of the color-sensitive cells in the retina. The astute neurologist knows that, in rare circumstances, color blindness may occur with lesions of the visual association cortex. The purest form occurs in damage to the right occipitotemporal gyrus, leading to achromatopsia in the left visual field (Damasio et al., 1980). Full-field cerebral achromatopsia requires bilateral lesions and is often associated with hemianopsia and visual agnosia. In cortical achromatopsia, patients have preserved ability to perceive form. The area involved corresponds to the visual area V4, as studied in experimental animals (Zeki, 1990). Cerebral achromatopsia has gained notoriety because of the curious case of a painter who developed achromatopsia after a head injury, as described by Oliver Sacks and Robert Wasserman (1987). These authors say that after his injury the painter refused to go to art galleries because he could not tolerate the unpleasant colors in the painting. Others have interpreted this to mean that the painter had lost his aesthetic sense, although Sacks and Wasserman noted that the patient continued to make art. The color-blind painter turned to drawing and monochrome painting with considerable success and personal satisfaction. Painting usually requires the application of pigment to a static surface, and moving pictures are usually considered a diVerent art form. In today’s world, the distinction between painting and motion picture is blurred, as a visit to the Tate Modern will attest. The clinical Caravaggio knows that lesions of the visual association cortex may produce a striking illness in which patients cannot perceive motion. Akinetopsia would not particularly incapacitate a visitor to the Courtauld Gallery in the Strand, but the Calder of the clinic would enjoy devising bedside tests in order to demonstrate it (Seki, 1991; Zihl et al., 1983). Our artistic neurologist can localize lesions that result in the inability to recognize a variety of forms, including faces. Patients with this symptom, which is known generically as visual agnosia, are able to perceive the color, shape, and size of objects and can even draw them, but cannot identify them. When patients recruit another cerebral organ, such as the tactile or the olfactory brain, they immediately recognize the object. The portraitist may be confronted with the symptom of prosopagnosia, in which the patient cannot recognize faces. Patients

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with prosopagnosia can identify a subject’s age, gender, and facial expression but cannot identify the individual (Tranel et al., 1988). The lesions are located in the mesial occipitotemporal regions, centered in the fusiform gyri and are functionally, if not anatomically, symmetrical (Cohn et al., 1977; Damasio et al., 1982). The landscape painter is particularly taken by the symptom of simultanagnosia, in which patients cannot perceive all the elements of a scene at the same time. When patients attend to one element of a scene, they cannot see other elements. As a result, they cannot interpret the composition. These patients may look at a scene but do not see it. Most investigators find that patients with simultanagnosia have lesions in both superior occipital lobes, in a watershed distribution, although Kinsbourne and Warrington describe a patient with a unilateral lesion (Kinsbourne and Warrington, 1963; Rizzo and Hurtig, 1987; Rizzo and Robin, 1987). This symptom is often part of the Balint syndrome, comprising gaze paraxial, optic agnosia, and diminished visual attention. The visual agnosias present a conceptual diYculty for the Klee of the neurological wards. To say that a patient has the inability to recognize faces, colors, scenes, and the like presumes that vision, language, and intellect are preserved. However, close inspection of these patients often reveals that these other functions are not completely intact. Memory, naming, or visual attention is often deranged to some degree, calling into question the purity of these symptoms. Of course, the painter is used to ambiguity, visual and otherwise, and recognizes that diagnostic consistency is more important than conceptual rigor. This resonates with artistic intent in which the practical eVect on the viewer trumps adherence to artistic movements or sociopolitical aims. The enterprising neurologist might want to test aesthetic sensibility or creativity at the bedside, but such testing is inherently impossible because there is no stimulus that reliably evokes an aesthetic experience in all subjects. Asking an Englishman whether Turner’s landscapes are beautiful might evoke a consistent response, but a Fijian or a Chinese would not necessarily have the same answer. By the same token, asking a Geordie whether a Papuan drawing is beautiful might lead to incomprehension or worse. Not only is beauty culturally defined, but so are ugliness, revulsion, and even perplexity. The claim that an iconic Renaissance painting evokes some essential human response ignores not only these cultural issues but also the social and political aims of the avant garde.

IV. The Neurologist in the Picture Gallery

The neurologist visits the picture gallery more often than the painter visits the bedside, and the questions that he or she asks in the Wallace Collection are a little bit diVerent. Like other viewers, the cultivated neurologist has transcendent


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feelings when looking at paintings. However, thinking neurologically imposes a certain structure to his or her musings, most notably the conviction that there is a diVerence between perception and aesthetic sensibility. Unlike those who believe that the brain and the mind are identical, for whom perception and aesthetic sensibility are also identical, Jacksonian neurologists distinguish between the two. Hence, Jacksonian neurologists believe that form, color, grouping, and motion are perceived in diVerent parts of the brain but creativity and aesthetic sense, as mental functions, are not. The transcendent feeling of making or viewing sublime pictures need not necessarily be pleasurable. Other aesthetic responses, like revulsion, anger, or perplexity, may emerge instead, as a visit to any of several galleries in central London shows. These feelings are indubitably mental responses, and Jacksonian neurologists deny that it is possible to localize mental functions. Instead, we say that the nervous system and the mind exist concomitantly and every mental state, including aesthetic experience, has a concomitant neurological state. Mental states occur concomitant to pathological as well as normal neurological states, but it does not follow that the mental states concomitant to focal lesions are located in that part of the nervous system. This view might be philosophically impoverished, but it has the distinct advantage of being scientifically consistent. Neurophysiologists and cognitive neuroscientists take a diVerent view. For example, the visual physiologist Semir Zeki (1999) has proposed a biological approach to aesthetics based on the assumption that the brain and the mind are identical. He asserts that advances in the neurobiology of visual perception allow a biological theory of aesthetics. He admits that it is diYcult to know where in the brain aesthetic experience arises and that the neurology of emotion is obscure. He also says that it is hard to say much about the perceptual neurophysiology of narrative and representational painting, the subject matter of Old Master paintings. Nevertheless he excoriates neurology for failing to address the localization of the mental functions involved in painting. Zeki also characterizes painters, writers, and composers as neurologists, at least unconsciously, because they aim to probe the human mind for aesthetic purposes. He says that these creative people have a superior understanding of the emotions, which makes them superior neurologists. Such claims are undeniably poetical, but they ignore the question of what it means to be a neurologist. As physicians, Jacksonian neurologists have practical aims, as Hughlings Jackson had himself. The claim that an understanding of the mind betokens an understanding of the brain might reflect the attitudes and practices of neuropsychologists, but it conflates the mind and brain in ways that Jacksonian neurologists reject. Jacksonian neurology uses a set of concepts, or principles, in order to organize its diagnostic observations. Calling these concepts ‘‘laws’’ is a bit of an overstatement, but they suYce to make a reasonably scientific discipline. The neurologist in the picture gallery might comment on the localization of form, or color, or

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composition, but he or she is agnostic about the localization of creativity and aesthetic experience. Manipulating perception, the province of the master painter, is not the same as manipulating the mind, which need not follow the electrophysiological principles of the experimental laboratory. Zeki (1999) claims that visual art must obey the experimental laws of the physiology laboratory or the imaging suite, and, therefore, any aesthetic theory that is not biologically based can be neither complete nor profound. The cognitive neuropsychologist V. S. Ramachandran echoes these claims, postulating eight laws of aesthetic experience (Ramachandran, 1999). These eminent biologists seem to deny Paul Klee’s expressionist credo, ‘‘Art does not reproduce the visible; rather it makes visible’’ (Klee, 1920). Sensitive Jacksonian neurologists, on the other hand, understand Klee despite his lack of logic, biology, or evolutionary rationale. Artistic creativity is also a mental function, existing concomitant to various neurological states. It makes no sense to say that we can localize or even lateralize creativity, that drawing is located on the right side of the brain. Artists who sustain focal neurological disease may well lose some sensorimotor function related to their art, such as the ability to use a paintbrush with their dominant hand, but they do not lose their creativity. The sensorimotor expression of that creativity may well change after a focal lesion, but the creativity itself is not lost (York, 2004). The neurologist in the picture gallery believes that beauty, aesthetics, and creativity occupy a diVerent realm than color, form, and motion. As practical people, they are unconcerned about the philosophical inconsistencies inherent in their point of view, an attitude that they share with most painters. They also pay no attention to the excoriations of experimentalists, since their work has both medical importance and social impact. Yet cultured neurologists have a place at the table, or in the bierstube, with painters, musicians, writers, and scientists, because of their attention to the human experiences of health and disease, youth and aging, science and art.

V. Commentary: The Three Cultures

C. P. Snow ignited a firestorm of controversy with his 1959 Rede Lecture entitled ‘‘The Two Cultures’’ (Snow, 1998). He contrasted the attitudes and beliefs of what he called ‘‘literary intellectuals’’ and physical scientists. He characterized the relationship between the two cultures as one of mutual incomprehension and conceptual hostility, notwithstanding the cordial relations between individuals. Snow asserted that professors of literature were natural Luddites responsible, in some ways, for the horrors of the world wars. This elicited a contemptuous response from F. R. Leavis, the University Reader in English at Cambridge, who pointed out that academic conflicts and jealousies hardly


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counted as a clash of civilizations (Leavis, 1962). Leavis also pointed out physical science’s important contribution to the death and destruction of the preceding half century. Both factions have seen their prominence diminish since then, but tension between science and the humanities persists in many parts of society. In many ways, experimental neuropsychologists and postmodernist painters recapitulate the tension of Snow’s, two cultures with dialogue between the two distinguished by dismissive comments from both camps (Commentaries on Ramachandran and Hirstein, 1999). Psychologists claim to understand the creative process, but their descriptions of it bear little resemblance to the aims and motivations of modern painters. The manifestos of postmodern painting make no sense to scientists. Today, this tension exists primarily in academe, with a strong element of academic moralizing in the bargain. Each culture continues to produce its particular science and art, barely recognizing the output of the other. The cultivated practice of neurology is a third culture, particularly when it occurs outside the confines of academic medical centers. Neurologists strive to be scientific and are grateful for any practical advance to come from the laboratory. At the same time, introspective neurologists are only too aware of the extrascientific components of their daily lives. It might be an exaggeration to call this artistry, but it does have a strong subjective flavor. Neurology, experimental neuropsychology, and painting are discrete cultures, occupying diVerent but complementary spheres of the human experience. The three cultures might appear distinct, even incompatible, and communication between them appears fraught with misunderstanding. Attempts to find common ground may be met with scorn or contempt from purists on both sides. Painters who look for neurological insight are called naı¨ve, scientists who study painting are called fuzzy-minded, and neurologists are caricatured as unreliable in both the laboratory and the studio. This criticism does not keep the painter from the bedside, still less the neurologist from the picture gallery. The scientific enterprise, the aesthetic experience, and the practice of neurology are rewarding to those who seek them, notwithstanding the rationale for doing so. Creative insight may come when we least expect it, and Nobel Prize-winning ideas may come in dreams. Much of what counts in the creative realm, whether art or science, is in a way accidental. The human element unites the cultures in ways that painters, experimentalists, and neurologists appreciate, to their collective satisfaction.

Acknowledgment

I am grateful to my colleague and friend David A. Steinberg for his discussion on many of the issues raised in this chapter.

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References

Cohn, R., Neumann, M. A., and Wood, D. H. (1977). Prosopagnosia: A clinicopathological study. Ann. Neurol. 1, 177–182. Commentaries on Ramachandran and Hirstein (1999). J. Conscious. Stud. 6, 52–75. Damasio, A. R., Damasio, H., and Van Hoesen, G. W. (1982). Prosopagnosia: Anatomic basis and behavioral mechanisms. Neurology 32, 331–341. Damasio, A., Yamada, T., Damasio, N., Corbett, J., and McKee, J. (1980). Cerebral achromatopsia: Behavioral, anatomic and physiologic aspects. Neurology 30, 1064–1071. Edwards, B. (1989). ‘‘Drawing on the Right Side of the Brain.’’ Jeremy P. Tarcher Inc., Los Angeles. Ferrier, D. (1873). Experimental researches in cerebral physiology and pathology. West Riding Lunatic Asylum Medical Reports 3, 30–96. ¨ ber die elektrische Erregbarkeit des Grosshirn. Archive fu¨r Anatomie, Fritsch, G., and Hitzig, E. (1870). U physiologie und wissenschaftliche Medicin, 300–332. Harrington, A. (1987). ‘‘Medicine, Mind and the Double Brain.’’ Princeton University Press, Princeton. Hughlings Jackson, J. (1868). Notes on the physiology and pathology of the nervous system. Medical Times Gazette 2, 696. Hughlings Jackson, J. (1884). Evolution and dissolution of the nervous system. Croonian Lectures delivered at the Royal College of Physicians, March 1884. Lancet 1, 555–558, 649–652, 739–744. Kinsbourne, M., and Warrington, E. K. (1963). The localizing significance of limited simultaneous visual form perception. Brain 86, 697–702. Klee, P. (1920). Scho¨pferische Konfession. (Kaisimir edschmid, Ed.). In ‘‘Tribune der Kunst und Zeit.’’ no. 13. Erich Reiss, Berlin. Translated as Klee, P. (1959). ‘‘The Inward Vision: Watercolours, Drawings and Writings,’’ pp. 5–10. Guterman, N. (trans.). Abrams, New York. Leavis, F. R. (1962). Two cultures? The significance of C.P. Snow. ‘‘The Spectator.’’ Reprinted in Leavis, F. R. (1962). ‘‘Nor Shall my Sword. Discourses on Pluralism.’’ Compassion and Social Hope, London. Livingstone, M. (2002). ‘‘Vision and Art: The Biology of Seeing.’’ Abrams, New York. Ramachandran, V. S. (1999). The science of art: A neurological theory of aesthetic experience. J. Conscious. Stud. 6, 15–51. Rizzo, M., and Hurtig, R. (1987). Looking but not seeing: Attention, perception and eye movements in simultanagnosia. Neurology 37, 1642–1648. Rizzo, M., and Robin, D. A. (1987). Simultanagnosia: A defect of sustained attention yields insights on visual information processing. Neurology 40, 447–455. Sacks, O., and Wasserman, R. (1987). The case of the colorblind painter. New York Review of Books 34, Accessed on May 2, 2005, at http://nybooks.com/articles/4601. Seki, S. (1991). Cerebral akinetopsia (visual motion blindress). Brain 134, 811–824. Smith, C. U. M. (1982). Evolution and the problem of mind: Part II Hughlings Jackson. J. Hist. Biol. 15, 241–262. Snow, C. P. (1998). ‘‘The Two Cultures.’’ Cambridge University Press, Cambridge. Solso, R. L. (1999). ‘‘Cognition and the Visual Arts.’’ MIT Press, Cambridge, MA. Tranel, D., Damasio, A. R., and Damasio, H. (1988). Intact recognition of facial expression, gender, and age in patients with impaired recognition of face identity. Neurology 38, 690–696. York, G. K. (2004). The cerebral localization of creativity. In ‘‘Neurology of the Arts’’ (F. C. Rose, Ed.), pp. 1–11. Imperial College Press, London. York, G. K., and Steinberg, D. A. (1993). Hughlings Jackson’s theory of cerebral localization. J. Hist. Neurosci. 3, 153–168.


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SECTION II EPISODIC DISORDERS


NEUROLOGY, SYNAESTHESIA, AND PAINTING

Amy Ione The Diatrope Institute, Santa Rosa, California 95406, USA

I. II. III. IV.

Introduction Case of the Color-Blind Artist Normals and Synaesthesia Metaphor and Synaesthesia References

I. Introduction

Although descriptions of cross-sensory experience abound, particularly in the arts, it is only recently that well-developed experiments have aimed to empirically evaluate them. The explosion of research that probes intersensory, subjective sensations has, no doubt, fostered the current fascination with these occurrences, often termed synaesthesia, which in part explains my choice of this topic. Admittedly, I am also drawn to it through many artists who have spoken of cross-modal sensations historically, frequently incorporating their responses into their projects. Relationships between art practice and synaesthesia will be the primary focus of this chapter. The specific condition we term synaesthesia occurs when an individual receives a stimulus in one sense modality and experiences a sensation in another. Historical diYculties of subjecting cross-modality to rigid scientific analysis, however, have led past commentators to cast the phenomenon in terms of abnormality, philosophy, and metaphor. Clearly discernable patterns of correspondence were not obvious, and the frequently contradictory historical data were composed of lists of stimuli and varied synaesthetic responses. This is due to the individual nature of synaesthete associations that are verifiable in a laboratory but not consistent from person to person. For example, Patricia DuVy and Carol Steen are both synaesthetes who see colored letters. Yet, strange as it might seem to the nonsynaesthete, they do not have matching alphabets. This means there is


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a qualitative similarity within their experience but not a direct correlation between them (DuVy, 2001). These kinds of idiosyncrasies resulted in the confusing and haphazard body of examples historically. This material is being revisited as researchers design studies capable of examining cross-modal sensation from a neural perspective. Exciting findings have reinvigorated synaesthesia research so that many of the documented accounts regarded as incoherent in earlier times now appear to be essentially correct in light of what laboratory experiments are revealing (Baron-Cohen and Harrison, 1997; Cytowic, 1983, 2002; Dann, 1998; Frith and Paulesu, 1997; Harrison, 2001; Marks, 1978; Mattingley et al., 2001; Ramachandran and Hubbard, 2000, 2001; Robertson and Sagiv, 2005). Moreover, the validation of older accounts complements a long historical literature on sensory interrelationships, which is robust and cross-cultural. The range is particularly thought provoking when contrasted with current research findings regarding the phenomena. In previous study I have discussed synaesthesia’s fascinating history and will not detail it here. SuYce to say that it was long seen as neurologically abnormal because it is at odds with the idea that we have five distinct senses, as codified by Aristotle (Ione, 2004, 2005). In other words, as the philosophical trajectory joined with that of science, the Aristotelian idea of distinct senses continued to hold, although we can identify many instances that speak of the senses as operating in tandem, even within Aristotle himself. Later figures who have spoken of synaesthetic experience have added to the renewed interest (Ione, 2005; Ione and Tyler, 2003, 2004). Some of them include Charles Baudelaire, Arthur Rimbaud, Alexander Scriabin, Vassily Kandinsky, Vladimir Nabokov, Sergei Eisenstein, David Hockney, and Richard Feynman, to name only a few. These attributions are based on some of the intriguing comments we find in their writings or remarks they have made about their own work. For example, in his book, What Do You Care What Other People Think?, Feynman claimed, ‘‘When I see equations, I see the letters in colors’’ (Feynman, 1988). To composer Alexander Scriabin, the key of F# major appeared violet in color (Myers, 1914). Writer Vladimir Nabokov noted in his autobiography Speak, Memory, ‘‘[t]he long ‘aaa’ of the English alphabet has for me the tint of weathered wood, but a French ‘a’ evokes polished ebony’’ (Nabokov, 1947). Since these figures can no longer be tested, their comments are unverifiable. What we can say is that the space between empirical verification and subjective reports is starting to narrow due to the way contemporary research has allowed us to look more closely at the brain. As a result, we are now better able to distinguish among experiences and to recognize that some can be equated with neurological disturbance, others are evident within the ‘‘normal’’ population and cases remain in which art and metaphor are mixed with the synaesthetic response. I look at examples of each in the following sections.


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II. Case of the Color-Blind Artist

Jonathan I, a color-blind artist made famous by the neurologist Oliver Sacks (1995), is one of the most thought-provoking cases of synaesthesia that we can directly relate to a neurological occurrence. This case also compels us to ask to what degree the history of an artist and an individual impacts how the brain develops and operates. Briefly, this artist became color-blind after a small accident in which his car was hit by a truck. Before this accident, Mr. I. had been a painter who had always relished color. We can appreciate the degree to which his vivid sense of color informed his work when comparing his later paintings with those completed shortly before the automobile accident after which he found he could not see color at all. While the preaccident expressions oVer some indication of how much his color sense influenced the emotive quality of his earlier work, it is through the postaccident projects that the extent of the neurological change becomes clear in relation to his art practice. After the trauma, Mr. I.’s initial impulse was to paint in color despite his inability to see this way, and he produced some rather unintelligible results. Eventually, this artist’s sense of helplessness led to a resolve to paint in black and white. This decision came about while looking at a brilliant sunset that was invisible to Mr. I. Realizing that no one else could see it the way he did, his determination to communicate the black and white world he saw strengthened. A photograph that simulates a sense of what he saw aids in conceptualizing the nature of his black and white experience. Viewing it, however, also reminds us of how diYcult it is to imagine an experience that is not at all comparable to our normal sense of the world in which we live. A black and white photograph aids in envisioning a world in which all the hues and color accents are totally gone but is unable to delete them from our mind. Once committed to sharing his new ‘‘perspective’’ on reality, Mr. I.’s focus shifted. Sometimes he turned to representational themes, although he had not worked in this way in years, and his eVorts to show his world to others are evident in his painting of leaden fruit, for example. He also performed tasks such as a rendition that compares a drawing of his with that of a red–green color-blind subject as well as a person with normal color vision. Particularly compelling are his experiments with adding colors he could not see to black and white paintings. These were not intended to share his vision as much as an experimental exercise through which he was able to ponder the mystery that he could manipulate elements, which he could no longer perceive. When comparing the monochromatic paintings he produced at this time with his earlier compositions, it is important to keep in mind that the accident only damaged the section of his brain specialized for color (designated as visual area V4 in the occipital lobe), and yet the depth of the overall change altered his entire

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way of being. Perhaps, of greatest importance to his life as a painter was that he did not lose just his perception of color, he also lost his sense of color imagery, the ability to dream in color, and even his memory of color. In addition, prior to the accident Jonathan I. experienced the form of synaesthesia in which one sees colors when presented with musical tones. After the accident, he lost his synaesthesia along with all other color experiences. In other words, he no longer had the ability to see color and lost the experience of color in response to musical tones. Let me stress that his synaesthesia did not return even when he began painting again. What I find most compelling about this case is the reaction of his audience. The gray-tone paintings produced at this time were highly successful, and people commented on his creative renewal when seeing this new ‘‘phase’’ that he had ‘‘moved’’ into. The excitement people felt when seeing his monochromes is perhaps most meaningful when we reflect on the fact that very few people knew that this new phase was anything other than an expression of his artistic development. They failed to recognize that it was brought about by a calamitous neural loss (Sacks, 1995). Two aspects of his case are particularly noteworthy neurologically. First, since he continued to paint, researchers were able to use his work to explore how a brain could adapt to radically new modes of expression and ways of seeing. Sacks believes that this kind of case allows us to assess how the cerebral ‘‘mapping’’ may be drastically reorganized and revised in cases of the special use or disuse of individual parts. In addition, while his brain did adapt, these adaptations did not bring color back into his memory or visual experience. In sum, he never recovered his synaesthesia or any sensation of color.

III. Normals and Synaesthesia

Artists who show no evidence of neurological disturbance raise other kinds of questions when we ponder synaesthesia. For example, might the possibility of lost (or acquired) synaesthesia in reaction to life-changing environmental conditions oVer insights that, while useful, limit our knowledge of normals? Is it possible that one question that cases of disturbance fail to advance is whether artists develop synaesthetic capabilities as they practice? Art practices certainly suggest this possibility. For example, Jack Ox is an intermedia artist who has been experimenting for over 20 years with how to combine diVerent media into one. She claims that now it is easy and natural for her to see sonic forms (Ox, 1999). As she has said, her capacity to combine her auditory and visual modalities might be compared to how we characterize pitch. Absolute pitch is


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generally characterized as the ability to recognize or sing a specific musical note independent of context. This ability is usually said to be innate. Relative pitch, on the other hand, is characterized as the ability to tell what a note is, only when given a starting note as a reference. It is a fundamental ability required for a musician, and it can be learned (Ox, 1999). Equally thought provoking in terms of learning, metaphor, and genetic proclivities are historical artists associated with synaesthesia. Vassily Kandinsky (1866–1944) is perhaps the best known, no doubt, because his study has a dynamic, musical feel to it, and his writings often speak about relationships between music and art. We also know of his interest in ‘‘colored hearing,’’ the most common form of synaesthesia. Briefly, Kandinsky was intent on developing means for people to expand cross-modal sensitivity. While his focus is elaborately explained in his writing, it is paradoxically due to his eVorts to explain his goals ‘‘scientifically’’ that the techniques he speaks about often fail to resonate with scientists. The ‘‘universals’’ he postulates in building a framework to ‘‘prove’’ his ‘‘spiritual science’’ are presented in a way that has a metaphorical feel since the science he presents to press his case is slim to nil (Ione, 2004, 2005; Ione and Tyler, 2003, 2004). Yet, on the other hand, evidence from his painting practice, comments oVered by some who knew his personal history, and his collaborative projects all suggest that he was a true sensory synaesthete. For example, Nina Kandinsky, his wife, wrote that he passionately loved colors from early childhood and claimed to distinguish a particular smell and musical sound for each color, a common synaesthetic trait (Kandinsky, 1947). A cellist and a violinist since childhood, Kandinsky had a well-developed sense of music and much experience with it, so his inclination to combine color and music seems as much a logical response as a synaesthetic one. On the other hand, while there is a metaphoric quality in his written statements, his words nonetheless clearly convey that his experiences are of concrete nature and seem to express something experienced directly. But, of course, as mentioned earlier, we have no proof. Another fascinating aspect of his history are the two events that led him to become an abstract painter, both appear to reveal how he endeavored to enhance his capabilities. The first, which was not directly related to synaesthesia, occurred when viewing an exhibition of French Impressionists in Moscow in 1896. During this visit a Monet Haystack painting led him to the realization that a picture can hold a viewer’s attention even if the subject cannot be immediately recognized. The second critical event was directly related to synaesthesia. This was a performance of Richard Wagner’s Lohengrin in Moscow, also in 1896. He later described the impact of this event, saying:

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The violins, the deep tones of the basses, and especially the wind instruments at that time embodied for me all the power of that pre-nocturnal hour. I saw all my colors in my mind; they stood before my eyes. Wild, almost crazy lines were sketched in front of me. Kandinsky, 1913/1982

This sensory unification of line, color, and music stimulated Kandinsky to systematically develop painted compositions in which one does not perceive a static representation. Rather they evoke a dynamic expression, captivated by a visceral language that entices colors to sway to unheard music. The viewer immediately senses that each point seen is moving toward the evocation of its counterpoint, just as each series of lines appears to correlate with a sonic form. Kandinsky’s writings support the viewer’s reaction, often stating his longing to provide painting with the independence from nature that he felt in music. Also in support of Kandinsky as a synaesthete is the evidence that he penciled notes in his books that spoke of exercises one could do to enhance synaesthesia. In addition, he desired to bring the essence of cross-modal experience to a wider audience. Toward this end, he frequently spoke of how an understanding of art and music can expand the value of using associative techniques aimed at enhancing sensory exchange. To reiterate, the idea that he developed his innate capabilities is supported indirectly by our knowledge of how he worked as well as the circumstantial evidence contained in his writings. Here, we find that he explored cross-modal sensory experience and asserted, ‘‘that one can feel the multi-sensory consonances and dissonances in simultaneously performed color movements, musical movements and dance movements.’’ (van Campen, 1997). Indeed, one well-known collaborative work on this theme was Kandinsky’s musical play ‘‘The Yellow Clang.’’ Conceived with the composer Thomas de Hartmann and the dancer Alexander SacharoV, this production may well have been a springboard of the modern dance movement, from Isadora Duncan to Serge Diaghilev (Ione and Tyler, 2003, 2004). Thus, although we are unable to test him, there is much to suggest that metaphor was an artistic device for this genuine synaesthete. Moreover, the urge to place him into a metaphorical context is enhanced by our knowledge of his community. When he lived, at the beginning of the twentieth century, there was a great interest in synaesthesia, partly enhanced by the publicity that Kandinsky and his colleagues gave it. As a result, even those who were not synaesthetes were eager to use cross-sensory metaphors in their artistic statements. Ironically, although it continues to be hotly debated whether Kandinsky was actually a synaesthete, the validity of synaesthetic experience itself is now broadly accepted due to recent research. In addition, and perhaps ironically, the foundational issues became somewhat moot with the advent of the hallucinogenic drug lysergic acid diethylamide (LSD) in the 1960s. Multimodal synaesthesia is experienced by many who take LSD, revealing that it is a latent facility that takes only the specific


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eVects of a miniscule dose of this drug to release (Marks, 1978). Such releasers imply a kind of neural plasticity in which the latent synaesthesia can be triggered and, presumably, developed by appropriate forms of stimulation. Cytowic (2002) points out, however, that the eVect is not universal and LSD does not produce synaesthesia every time the drug is ingested.

IV. Metaphor and Synaesthesia

Still the question of how artistic statements about synaesthesia will fare as we learn more remains an open one. For example, Marcia Smilack, who photographs reflections on water, is a synaesthete who calls herself a Reflectionist (Fig. 1). She uses the surface of the water as her canvas and the wind as her brushes, relying on the season and location to produce her palette. Smilack relates that she never manipulates the water or changes the pictures later. Instead, she taught herself photography by shooting whenever she hears a chord of color, one of her synaesthetic responses to what she sees. Her cello image (Fig. 2) shows how this works. After relating a recent dream, Smilack writes: In waking life, I had a similar experience the first time I photographed cello music . . . On the night I took the cello image, the setting sun, reflected on the water, turned the skin of the sea to a golden hue that, in combination with the wave formation, created for me the sound of cello though the actual instrument was no more a cello than the dreamed piano. The diVerence between the two experiences came to me when a scientist who attended an exhibit of mine explained that it was no surprise I heard cello music since I had captured on film the exact sine waves produced by cello strings—an insight I found fascinating since I had no idea I had done any such thing, though it gave me this idea: that the synaesthesia artists experience in their work operates like an internal sonar that takes them directly to the archetypal patterns we know exist in art as well as science; and that my images, which look like dreams from a collective unconscious, are evidence if not proof that the universe is dreaming. Smilack, 2005.

She adds that she hears cello every time she looks at the image today and has found that when she turned it upside down she discovered that it evokes violin music. I find the words and the image beautiful. In terms of the artistry, I am drawn to see the many lenses through which we can view the conjunction of the images and words. Initially, her ideas evoked a Jungian worldview in which ideas about a collective unconscious intersect with cross-cultural mythology and the often contradictory philosophical debates that engage with how we might characterize reality. Many of these discussions center around the question of whether we (and the universe) are dreaming. These, to my mind, are more philosophical than scientific. I am far from certain that synaesthesia research can resolve the issues. We could also see her words as a metaphorical statement of

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FIG. 1. Camera Girl (Self-Portrait) by Marcia Smilack. 2003, 11 inches 14 inches.

FIG. 2. Cello Music by Marcia Smilack. 1993, 11 inches 14 inches.

the commonalities of our neural responses to particular stimuli. From this perspective, we could say there is a vein of validity here insofar as we have the same brain structures, of which we are unconscious. Then her words might serve as a metaphorical statement of the commonalities of our neural responses to particular stimuli. In closing, to my mind, the integration of research data and theoretical assumptions in the words talented artists use to explain their creative contributions continues to suggest there is an ongoing need to carefully distinguish what we know from the many ways we can interpret all that remains unknown to us. Within this, it is clear, at least to me, that the boundary between the known and the unknown changes. I would propose that synaesthesia research in all of


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its phases oVers a thought-provoking example of how new empirical evidence revises historical ideas as our knowledge base evolves. Indeed, with the current explosion of techniques to explore the brain, synaesthesia, like other formerly misunderstood behaviors, is opening doors that allow us to reevaluate art, neural wiring, and sensory relationships. Thus, it seems fair to conclude that the cross-modal enrichment of synaesthesia is itself a metaphor for the crossdisciplinary interplay of ideas and techniques that enhance both neurological methodology and art.

References

Baron-Cohen, S., and Harrison, J. (1997). ‘‘Synaesthesia: Classic and Contemporary Readings.’’ Blackwell Publishers, Cambridge, MA. Cytowic, R. E. (1983). ‘‘The Man Who Tasted Shapes.’’ Putnam, New York. Cytowic, R. E. (2002). ‘‘Synaesthesia: A Union of the Senses.’’ MIT, Cambridge, MA. Dann, K. T. (1998). ‘‘Bright Colors Falsely Seen: Synaesthesia and the Search for Transcendental Knowledge.’’ Yale University Press, New Haven. DuVy, P. L. (2001). ‘‘Blue Cats and Chartreuse Kittens.’’ W. H. Freeman/Times Books/Henry Holt & Co, New York. Feynman, R. (1988). ‘‘What Do You Care What Other People Think?’’ p. 59. Unwin Paperbacks, London. Frith, C. D., and Paulesu, E. (1997). The physiological basis of synaesthesia. In ‘‘Synaesthesia: Classic and Contemporary Readings.’’ (S. Baron-Cohen and J. Harrison, Eds.), pp. 123–147. Blackwell, Oxford, England. Harrison, J. (2001). ‘‘Synaesthesia: The Strangest Thing.’’ Oxford University Press, Oxford. Ione, A. (2004). Polyphonic painting, chromatic chords and synaesthesia. J. Consciousness Stud. 11(3–4), 148–158. Ione, A. (2005). ‘‘Visualizing Innovation: Art, Science, Technology, and Visual Studies.’’ Rodopi, Amsterdam and New York. Ione, A., and Tyler, C. W. (2003). Was Kandinsky a synesthete? J. Hist. Neurosci. 12(2), 223–226. Ione, A., and Tyler, C. W. (2004). Synaesthesia: Is F-sharp colored violet? J. Hist. Neurosci. 13(1), 58–65. Kandinsky, W., and Kandinsky, N. (1947). Some notes on the development of Kandinsky’s painting. In ‘‘Concerning the Spiritual in Art.’’ pp. 9–11. Wittenborn Art Books, New York, Inc. Kandinsky, W. (1913/1982). Reminiscences. In ‘‘Kandinsky: Complete Writings on Art’’ (K. C. Lindsay and P. Vergo, Eds. and Trans.), p. 364. Faber & Faber, London. Marks, L. E. (1978). ‘‘The Unity of the Senses: Interrelations among the Modalities.’’ Academic Press, New York. Mattingley, J. B., Rich, A. N., Yelland, G., and Bradshaw, J. L. (2001). Unconscious priming eliminates automatic binding of colour and alphanumeric form in synaesthesia. Nature 41, 580–582. Myers, C. (1914). A case of synaesthesia. Brit. J. Psych. 6, 228–232. Nabokov, V. (1947). ‘‘Speak, Memory.’’ p. 21. Knopf, New York. Ox, J. (1999). Color me synaesthesia. Leonardo 32, 7–9.

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Ramachandran, V. S., and Hubbard, E. M. (2000). Psychophysical investigations into the neural basis of synaesthesia. In ‘‘Proceedings Royal Society of London B.’’ Ramachandran, V. S., and Hubbard, E. M. (2001). Synaesthesia—a window into perception, thought and language. J. Consciousness Stud. 8, 3–34. Robertson, L. C. and Sagiv, N. (Eds.) (2005). ‘‘Synaesthesia: Perspectives from Cognitive Science.’’ Oxford University Press, Oxford. Sacks, O. W. (1995). The case of the colorblind painter. In ‘‘An Anthropologist on Mars: 7 Paradoxical Tales,’’ pp. 3–41. Alfred A. Knopf, New York. Smilack, M. (2005). ‘‘Synesthetic Sonar between Artist and Archetype: Photographic Proof that the Universe Is Dreaming.’’ Presentation at the College Art Association 93rd Annual Conference, Panel title: Synaesthesia and Perception, Atlanta, GA. van Campen, C. (Campen 1997). Synaesthesia and artistic experimentation. PSYCHE 3(6).

FAINTING IN CLASSICAL ART*

Philip Smith Department of Neurology, University Hospital of Wales Cardiff, United Kingdom

I. II. III. IV. V. VI. VII. VIII.

Introduction Blackouts in Paintings Crucifixion Fainting Historical Fainting Genre Fainting Swooning Men Fainting Conclusions References

I. Introduction

Fainting (syncope) is a temporary loss of consciousness and posture. The commonest form is vasovagal syncope, something experienced by about 20% of the healthy population. Syncope typically happens in particular situations such as hot crowded environments, including restaurants or aeroplanes, in the doctor’s surgery, or in the bathroom at night; specific triggers include prolonged standing, emotional trauma, and pain. In susceptible individuals, coughing, swallowing, or micturition may provoke vasovagal syncope. Fainting without provocation, without warning, or for the first time in older individuals must be investigated for more serious underlying causes such as heart disease. The phases of syncope are the prodrome, the event itself, and recovery. The typical prodrome (light headedness, nausea, sweating, graying or blacking of vision, muZed hearing, and feeling distant) develops over 1–5 min. The index event is characterized by abrupt onset of unconsciousness usually lasting less than 1 min, and witnesses may describe pallor, sweating, cold skin, eyes open and *

Part of this paper is published and illustrated separately in Practical Neurology (2005); 5: 366–369.


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elevated, and sometimes limb stiVness, and brief convulsive jerks. Incontinence and injury are uncommon and lateral tongue biting rare. Recovery is prompt, and any postictal confusion is brief, typically a few seconds, unless there had been associated head trauma.

II. Blackouts in Paintings

Episodes of loss of consciousness are portrayed fairly frequently in art, particularly in situations of high tension and anxiety. Several good examples of epilepsy and art are shown on the German Art Museum web page (see references). The demonic implications of seizures were often emphasized in representations of epilepsy before the nineteenth century. This is well illustrated in Rubens’ (1577–1640) huge painting The miracles of St Ignatius of Loyola in which the exorcised demons are even seen to fly upward into the church, away from the man having a seizure in the foreground. A more sympathetic portrayal of epilepsy is Raphael’s (1483–1520) The Transfiguration, perhaps the most widely recognized portrayal of epilepsy in classical art, especially after it was featured on the cover of William Lennox’s classical treatise ‘‘Epilepsy and Related Disorders’’ (Lennox, 1960). This picture shows two consecutive events from St. Mark’s Gospel: the healing of the ‘‘lunatic and sore vexed’’ child and the miraculous Transfiguration of Christ on Mount Tabor. Janz (1986) made a fascinating interpretation of this painting, exploring the symbolic representation of the boy’s epileptic seizure as a metaphor of suVering, death, and resurrection (aura, blackout, and recovery), paralleling the transfiguration scene above him. Since syncope is actually more common than epilepsy (syncope prevalence 22%; epilepsy prevalence 0.75%), one might expect syncope would feature more often than epilepsy in classical paintings. However, this is not the case. Syncope is usually far less dramatic than a seizure and perhaps adds less drama to a scene. When syncope is portrayed, it is usually in the context of (and adding to) a scene of high drama and emotion. An obvious example is the witnessing of a crucifixion.

III. Crucifixion Fainting

Mary’s fainting at the foot of the Cross is by far the commonest depiction of fainting in classical art. This scene is most wonderfully illustrated in Rogier van der Weyden’s (c. 1399–1464) The Deposition, the central panel of an altarpiece triptych; sadly the two side panels are now lost. Van der Weyden was the most influential artist

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of the mid fifteenth century and a pioneer of the newly introduced medium of oil painting. The painting has a minuteness of realistic detail, including depiction of varied expressions of grief, something that had not been possible with fresco. Despite this, the composition is more symbolic than natural, with several figures closely crowded around Christ being lowered from an unrealistically small Cross. Mary’s posture mirrors the dead Christ, her right hand echoing his left and her left his right. The pallor of the collapsed Mary and the dead Christ is further emphasized by her headdress and his robes of pure white, the color of purity and innocence. Mary’s posture and plight highlight further her son’s physical and emotional agony (Cumming, 2000). As in Raphael’s Transfiguration, Mary’s collapse here symbolizes Christ’s Passion—prodromal suVering, collapsing, and lying still, pale, and unconscious, with recovery and resurrection to come. These parallels are reinforced by the almost unblemished appearance of Christ, who has only fine trickles of blood from his five wounds, as if he too has only fainted and will rise again. A similar altarpiece composition by the Master of the St. Bartholomew Altar (Fig. 1) displayed in London’s National Gallery was doubtlessly influenced by van der Weyden’s work. The Virgin is again pale and syncopal at the foot of the Cross, held partially upright by St. John, the Baptist. Rembrandt’s (1606–1669) Descent from the Cross is a darker but equally touching depiction of Jesus’s mother collapsing at the Crucifixion. The illuminated central figure of Jesus is flopping and largely unblemished, as if in a faint. His distraught mother, collapsed with emotional agony in the background darkness, again echoes her son’s physical state.

IV. Historical Fainting

Paintings of historical scenes were very popular in the eighteenth century because they provided not only beautiful decoration but also provided the owner the vehicle to impress friends with his education and knowledge of historical and legendary texts. Often, the family commissioning the painting would put themselves center stage of the scene. In Jean-Joseph Taillasson’s (1785–1809) Virgil reading the Aeneid to Augustus and Octavia, the Emperor Augustus and his sister Octavia listen to Virgil reading his twelve-book epic, The Aeneid. Octavia has apparently fainted with emotion at the reference to her dead son (Augustus’ adopted heir) Marcus Claudius Marcellus. The Emperor is moved but ignores her reaction. Octavia, the great niece of Julius Caesar, was a strong person for whom displays of emotion were of character. After her first husband’s death, she had agreed to marry Mark Antony to reconcile him to Augustus but Antony had abused her and left her for Cleopatra. Such was Octavia’s loyalty and virtue that, following Antony’s

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FIG. 1. Master of the St. Bartholomew Altarpiece (active 1470–1510). The Deposition. Oil on oak 74.9 cm 47.3 cm. National Gallery, London. Reproduced by permission.

death, she brought up not only Antony’s children by Fulvia, his first wife, but also those by Cleopatra. Acts of moral courage, such as these, enhanced her reputation as an ancient queen of people’s hearts. Probably the scene in this picture was invented to appeal to the neoclassical taste of late eighteenth century’s polite society, where simulated swooning (‘‘feinting’’) was an encouraged female behavior (Smith, 1999). Another example of fainting whilst witnessing an emotional historical scene is the faint of one of the attendants in Paul Delaroche’s painting of The execution of


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Lady Jane Gray (National Gallery, London), who was Queen of England for just nine days. The grief of her attendant contrasts starkly with the impassivity of her executioner. However probably, the most frequently painted historic scene of emotionally provoked fainting is of Esther, the Jewish Queen of King Ahasuerus. The story is taken from the apocryphal additions to the Bible in the Greek (Septuagintal) version of the Book of Esther 5:1–8. In a culture in which a wife could be killed for upsetting her husband, Esther approached the King and told him of a plot to massacre the Jews, thereby attempting to save her own people from persecution. On this occasion, Ahasuerus received the news gratefully and with good favor, causing her to faint with relief. A fine example of this scene is Antoine Coypel’s (1661–1722) The Swooning of Esther. A universal feature of all Esther fainting scenes, for example Lefevre’s Esther before Ahasuerus, Caucig’s Queen Esther Before King Ahasuerus, and Poussin’s Esther before Ahasuerus, is to have Esther always held upright by well-meaning courtiers, something that might clearly worsen the situation. In fact (if indeed the painting is of fact), the apparent syncope was likely to have been only a swoon (usually Esther is shown with a rosy glow in her cheeks), making her posture unimportant.

V. Genre Fainting

Genre painting usually refers to a style of painting popular in the seventeenthcentury Dutch and Flemish painting of domestic scenes. In general, intimate domestic scenes ranked higher than portraits or still lives but considerably lower than history paintings. However, small-scale, portable canvases appealed at this time to wealthy collectors who preferred to display in their homes meticulously painted still lives and genre scenes rather than large-scale history paintings. Fainting occasionally featured in such paintings, again usually in response to emotion, and with the strong suggestion of a psychological (swooning) component. Marguerite Ge´rard (1761–1837), a pioneer female artist, developed a sentimental style of domestic genre scenes, which greatly appealed to her contemporaries. Her Bad News is a small painting depicting a mother’s emotional agony on reading of her son’s death. As with Esther, her lack of pallor in fact suggests a swoon, reducing any concern about her remaining upright during the episode. The painting has Ge´rard’s signature style of painstakingly accurate detail, rendered with subtly blended brush strokes. Pietro Longhi (1702–1785) is best known for his intimate glimpses of Venetian upper-class social and domestic life in a period of refined decadence. He concentrated mainly on living room scenes of his well-to-do patrons at leisure. In The Faint, he shows a young woman who has apparently fainted, looking not particularly pale and evidently the center of attention. Her caring and concerned

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FIG. 2. William Hogarth (1697–1764). A Rake’s Progress. VII The Prison. Oil on canvas. Sir John Soane’s Museum, London. Reproduced by permission.

attendants support her upright on a pillow and administer smelling salts. Closer viewing shows her to be surprisingly gray haired, her eyes are closed and brimming with tears, and her right breast has become bared in the chaos. A tipped table on the left has spilt cards, coins, and an open purse to the floor. It is likely that she had been gambling and had conveniently pretended to faint and turn the table to cut her losses. Another example of fainting, increasing the drama of a scene, is in Hogarth’s ‘‘A Rake’s Progress’’ (Fig. 2). Tom’s hapless first love, Sarah, collapses in horror when visiting him in the Fleet prison for debtors, while his one-eyed but previously wealthy wife scolds him for gambling away her money. Sarah’s faint is managed unsympathetically and heavy handedly with smelling salts and slapping. VI. Swooning

Fainting among women was a recurrent theme in literature of the period: women would pretend to faint over trivia. The witnesses of such faints led to the misguided but widespread belief that fainting is where women fall, lie still with


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eyes closed, and then recover. However, in genuine vasovagal syncope, people feel ill beforehand, may fall with stiVness, sometimes shaking, and have their eyes open and usually elevated. In fact, actual fainting may have occurred more often in women at this time partly due to tight clothing and hunger. The weight of garments along with the fashionable tight lacing at the waist would have contributed. Furthermore, it was sometimes considered distasteful for women to eat in public and so many went without food.

VII. Men Fainting

Despite the earlier descriptions of women fainting in art, there are remarkably few examples of men depicted in similar situations. An isolated example of a man swooning is Isaac Cruikshank’s (1756–1811) A Dandy Fainting (Fig. 3). The delicate and eVeminate young male caricature has fainted at the divine singing of a castrato, while his friends flap around trying to revive him.

FIG. 3. Isaac Cruikshank (1756–1811). A Dandy Fainting or, An exquisite in fits. Scene a private box opera. 1818. Etching, hand colored. British Museum, London. Copyright of the Trustees of the British Museum.

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It seems that when men faint, or nearly faint, in classical paintings, there is (notwithstanding the ‘‘dandy’’ faint) almost always a very serious and near-fatal cause such as massive blood loss or heart disease. A well-known example is Benjamin West’s (1738–1820) The Death of General Wolfe in which the dying hero of Canadian independence gradually sinks into syncope through hemorrhagic blood loss at the decisive Battle of Quebec. West had been born in America but spent most of his life abroad and enjoyed the patronage of King George III. He later painted The Death of the Earl of Chatham, a scene from the House of Lords on April 7, 1778, when William Pitt, the Earl of Chatham, collapsed from a presumed myocardial infarction during a crucial debate about British policy in the American colonies. Despite the painting’s title, the Earl survived this immediate episode but died a month later. West has positioned the Earl and the surrounding peers in a structure almost identical to that in his Wolf picture. This painting is commonly used (unlabeled) to illustrate lectures on syncope. West’s pupil, John Copley (1738–1815), later repainted the scene in more detail (Fig. 4). The Earl is shown looking pale, with his eyes open and elevated (clearly not a

FIG. 4. John Copley (1738–1815). The Death of the Earl of Chatham. 1779–1781. Oil on canvas. 228.6 cm 307.3 cm. Tate (2006); on loan to the National Portrait Gallery, London. Reproduced by permission.


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‘‘swoon’’), with the other Lords managing the situation entirely appropriately by elevating his legs to improve venous return. Not so fortunate is the mayor ridiculed in William Hogarth’s (1697–1764) An Election Entertainment, a satirical picture aimed at criticizing political corruption. The Mayor on the right of the picture has collapsed from overindulgence at a banquet hosted by the Whig party. The pile of oyster shells in front of him and the plentiful ale in the foreground are the main sources of his indisposition. His attendant, probably a barber surgeon, is managing his faint by maintaining his upright posture, applying an upper arm tourniquet, and placing a bowl beneath his arm to begin bloodletting. A less appropriate management of syncope would be hard to conjure.

VIII. Conclusions

Fainting is far commoner than epilepsy, but in art, epileptic seizures are more commonly depicted than fainting. Emotional turmoil, particularly grief, usually causes the syncope shown in art; the common causes of syncope in real life, such as prolonged standing and being in hot environments, are rarely shown. Women in art are much more likely to faint than men, and typically are young, beautiful, and reacting to grief; in real life, the sex ratio only slightly favors women. When men are shown to faint in art, it is often through serious, even life threatening causes such as severe blood loss or terminal illness. Simple faints in art, particularly in women, often has overtones of a psychogenic component (‘‘swooning’’). Thus, the fainters are often painted with pink skin, eyes closed, and held upright, seemingly without coming to harm.

References

Cumming, R. (2000). ‘‘Annotated Art,’’ 16–17. Dorling Kindersley, London. Epilepsy and art. German epilepsy museum. http://www.epilepsiemuseum.de/alt/body_arsen.html (Accessed January 15, 2005). Janz, D. (1986). Epilepsy, viewed metaphysically: An interpretation of the biblical story of the epileptic boy and of Raphael’s transfiguration. Epilepsia 27, 316–322. Lennox, W. G. (1960). ‘‘Epilepsy and related disorders,’’ Vol. 2. Little, Brown and Co., Boston, Toronto. Smith, P. E. M. (1999). Neurology in the National Gallery. J. Roy. Soc. Med. 92, 649–652.

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Paintings Cited in the Text

Antoine Coypel (1661–1722). The Swooning of Esther. c. 1704. Oil on canvas, 105 137 cm. Museé du Louvre, Paris. Benjamin West (1738–1820). The Death of General Wolfe. 1770. Oil on canvas. 152.6 214 cm. National Gallery of Canada, Ontario. Benjamin West (1738–1820). The Death of the Earl of Chatham. 1778. Oil on canvas. 71.4 92.0 cm. Kimbell Art Museum, Texas. Francesco Caucig (1755–1828). Queen Esther Before King Ahasuerus. c.1815, Oil on canvas, 141.6 207 cm. University of Virginia Art Museum, USA. Jean-Joseph Taillasson (1785–1809). Virgil reading the Aeneid to Augustus and Octavia. 1787. Oil on canvas. 147 167 cm. National Gallery, London. Marguerite Ge´rard (1761–1837). Bad News. 1804. Oil on canvas. 63 50 cm. Museé de Louvre, Paris. Nicolas Poussin (1594–1665). Esther before Ahasuerus. 1640s. Oil on canvas. State Hermitage Museum, St. Petersburg. Paul Delaroche (1797–1856). The execution of Lady Jane Grey. 1833. Oil on canvas. 246 297 cm. National Gallery, London. Peter Paul Rubens (1577–1640). The Miracles of St. Ignatius of Loyola. c. 1615/16. Oil on canvas. 535 395 cm. Kunsthistorisches Museum, Vienna. Pietro Longhi (1702–1785). The Faint. c. 1744. Oil on canvas. 50 61.7 cm. Samuel H. Kress Collection, National Gallery of Art, Washington DC. Raphael (RaVaello Sanzio) (1483 1520). The Transfiguration. 1520. Oil on panel. 405 278 cm. The Vatican, Rome. Rembrandt van Rijn (1606–1669). The Descent from the Cross. 1634. Oil on canvas. 158 117 cm. Hermitage Museum, St. Petersburg. Rogier van der Weyden (c. 1399–1464). The Deposition. c.1435–40. Oil on panel 220 262 cm. Oil on panel. Museo del Prado, Madrid. Valentin Lefevre (1637–1677). Esther before Ahasuerus. Late 17th century. Oil on canvas. 100 121 cm. State Hermitage Museum, St. Petersburg. William Hogarth (1697–1764). An Election Entertainment. 1754. Oil on canvas. 100 127 cm. Sir John Soane’s Museum, London.

MIGRAINE ART IN THE INTERNET: A STUDY OF 450 CONTEMPORARY ARTISTS

Klaus Podoll Department of Psychiatry and Psychotherapy, RWTH Aachen University Pauwelsstrasse 30, 52074 Aachen, Germany

I. Introduction II. Methods A. Identification of Study Sample B. Assessed Variables C. Statistical Evaluation III. Results A. Characteristics of Study Sample B. Relationships Between Migraine and Art Making C. Participation in Migraine Art/Headache Art Contests D. Analysis of Artists’ Media and Representations of Migraine Symptoms IV. Discussion References

I. Introduction

Although its roots may be traced back to nineteenth century neurology, it was not until the inspiring example of an art teacher’s pictorial representations of her migraine attacks that the Migraine Art concept (Wilkinson and Robinson, 1985) was developed by Derek Robinson in the 1970s (Podoll, 2001); it served as the basis of four National Migraine Art Competitions and similar contests held in UK and USA, the results of which were presented in a number of exhibitions and publications in both the lay and medical press. The Migraine Art (1980–1987), Migraine Masterpieces (1988–2003), Headache Art (1989), and Migraine Images (1992) art contests have helped migraine suVerers to express themselves; other suVerers realize that they are not alone in what they see and feel and have helped doctors understand their patients a great deal better (Podoll and Robinson, 2002). The entries in those special art contests have also been used for comparative purposes in the study of migraine aura phenomena as source of artistic inspiration in famous painters, for example Georgia O’KeeVe (Cadenhead, 1885), Giorgio de INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74008-9

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Chirico (Fuller and Gale, 1988), and Sarah Raphael (Podoll and Ayles, 2002). However, the creative processes involved in the act of making a submission to a Migraine Art competition may be diVerent to those produced for the general art market, which may limit their use for a study of the neuropsychology of visual artistic production (Chatterjee, 2004). With the advent of the Internet in 1992, a new medium was formed, which has not only oVered migraine suVerers new opportunities to express themselves by means of art but also provided researchers with access to art designated as being migraine related by their makers without having been produced as entries to special art contests for migraineurs; this overcomes the previously mentioned possible limitation in studying relationships between migraine experiences and art-making activities (see examples provided from the Internet by Nicola and Podoll, 2003). This chapter (www.migraine-aura.org) describes the characteristics of a sample of 450 contemporary artists identified over a period of about 2½ years in the Internet.

II. Methods

A. IDENTIFICATION

OF

STUDY SAMPLE

The output of Google searches, performed every 4 months between August 1, 2002 and December 31, 2004, for images (‘‘migraine,’’ circa 4080 hits per search query; ‘‘Migra¨ne,’’ circa 650 hits; ‘‘migranã,’’ circa 120 hits; ‘‘jaqueca,’’ circa 110 hits; ‘‘emicrania,’’ circa 60 hits) and texts (‘‘migraine artist,’’ circa 12700 hits; ‘‘migraine painting,’’ circa 9410 hits; ‘‘migraine sculpture,’’ circa 1770 hits; ‘‘migraine collage,’’ circa 665 hits; and the same search terms in French, German, Spanish, and Italian) were screened for websites providing the names (or Internet pseudonyms) of artists who (1) were reported to suVer from migraine, (2) had participated in art contests for migraine suVerers, or (3) had used any of the aforementioned terms in the titles of their own artworks. B. ASSESSED VARIABLES Information on sex, age, and nationality of the artists identified was recorded when available. A contents analysis of the found texts from or about the identified artists was made, coding reports on (1) migraine experiences as source of artistic inspiration, (2) migraine experiences as impediment of art making, or (3) art making as a relief of headaches and migraine. Images of migraine-related artworks were coded, according to the year of production, title, used art media,


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genres, and representations of migraine symptoms identified by expert opinion on the grounds of phenomenal similarities between the features of the given images and the semeiology of migraine with aura (Podoll and Robinson, 2002). C. STATISTICAL EVALUATION Group diVerences of various ordinal or nominal scaled variables between the groups of participants and nonparticipants in art contests for migraine suVerers were assessed by Mann-Whitney U-tests and Chi2-analyses, respectively.

III. Results

A. CHARACTERISTICS

OF

STUDY SAMPLE

A total of 450 artists, 267 females (59%) and 183 males (41%), were identified. As shown in Fig. 1, several artists fulfilled more than one of the said three criteria of inclusion into the study sample. In a subset of 218 artists for whom

FIG. 1. Venn diagram showing the distribution of inclusion criteria encountered in 450 artists identified according to (A) self-reported diagnosis of migraine, (B) participation in art contests for migraine suVerers, or (C) reference to migraine in titles of artworks.

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NATIONALITY

OF THE

TABLE I 450 ARTISTS

OF THE

STUDY SAMPLE

Nationality

Number of artists

USA UK Canada France Germany Australia Sweden Belgium Netherlands South Africa Switzerland Brazil Mexico Armenia Egypt Finland Yugoslavia Korea Lebanon Malaysia New Zealand Peru Poland Russia Zimbabwe Unknown

347 32 13 10 9 5 5 3 3 3 3 2 2 1 1 1 1 1 1 1 1 1 1 1 1 1

information on the year of birth was available, the age ranged between 16 and 94 years (with a mean of 43.3 years). As regards nationality, a majority of 347 artists (77%) were US citizens, reflecting not only the bias introduced by the high degree of distribution of the Internet in the USA but also the fact that 156 artists were identified on the grounds of their participation in US art contests. The remaining 103 artists came from countries all over the world (Table I). B. RELATIONSHIPS BETWEEN MIGRAINE

AND

ART MAKING

Out of the 169 websites on artists with a reported diagnosis of migraine, 52 provided further information concerning relationships between migraine and their art.


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1. Migraine Experiences as Source of Artistic Inspiration In 33 cases, migraine experiences are explicitly described as a source of artistic inspiration. In May 1999, the Art Access Gallery, Salt Lake City, Utah, presented an exhibition entitled SuVering in Silence: Creativity and Migraine, ‘‘featuring migraineinspired artwork by Ed Dolinger, Bonnie Sucec, Susan Madden and Jennifer Martinsen.’’ The impetus for the exhibit came last year after Dolinger discussed his condition with a fellow migraine-suVering artist. For Dolinger, gathering his fellow migraine-suVering artists was a revelation. ‘‘The sharing and exchanging of war stories has been quite moving, with descriptions that rival poetry or literature,’’ he explained. The resulting exhibition uses art to bridge the myths surrounding migraine’s medical and scientific realities. ‘‘It is a cruel irony that the very gifts of sensitivity that enhance my work in the studio, provide the triggers for episodes of debilitating migraines,’’ Dolinger noted. ‘‘Slowly over the years I have used this very strange downtime to explore the diVerent mental landscapes that unfold while experiencing the classic migraine aura.’’ These mental landscapes provide the inspiration for his mixed-media creations. Along an expansive wall, Dolinger has assembled 14 works that subtly reveal the human torso and head in the throws of a migraine attack . . . . Migraine headaches have been a continual presence since childhood for Bonnie Sucec. ‘‘All of my paintings are migraine paintings, as they all reflect who I am and migraine is such a large part of my life,’’ she explains. (http://www.slweekly.com/editorial/1999/ae_990513.cfm, September 21, 2003)

On her personal website, Valerie Allard writes: ‘‘I have thought a lot in the last couple of years about the relationship between the migraine and the work I produce. Most of all, I think the migraine has created a certain drive—both to try to alleviate the state of pain and bewilderment it produces and also the desire to ‘‘make sense’’ of what I experience. I find most of the abstract work that I do is directly related to the perceptual experiences I have with the migraine—and most of the work lacks coherent form—is very colour orientated—and has a confused sense of space and time. With ‘‘Flocking,’’ I tried to find a more compositional and graphic sense of order within the movements of light I experience (now gratefully only every couple of weeks).’’ (http://karaab.blogspot.com/, July 12, 2003)

Linda Anderson paints ‘‘canvases of bold abstract composition, based on the moving patterns she sees during episodes of migraine headaches’’ (http://www.baruch.cuny.edu/mishkin/memory/, December 12, 2002).

Debbie Ayles ‘‘was inspired by the colours and eVects experienced during an attack and these are depicted in her paintings.’’ On the Axis website, she characterizes her art thus:

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Concepts, ideas and themes—I create abstract images of intricate shapes and colour to visualise some of the migraine phenomena I have experienced. Using my environment as source material—a conventional theme such as a still life is altered or fragmented. Still retaining something of the original, the image changes into something chaotic and confusing, the colour becomes stunning and overpowering. Shapes appear, disappear. Image, content and narrative are distorted. Nothing is quite as it seams. Farewell to M.R., Poole II and Mirosa 5 are images influenced by this. Slowly the familiar world has dislocated into mosaics. Beautiful coloured shapes flow into the visual plane, pulse forward, recede and move about. You are drawn into this kaleidoscope of strong greens and blues, reds, pinks oranges and yellow, finally subsiding into monochrome. A wonderful private picture show for just you to view. Processes and techniques—By overlaying and deconstructing images I investigate eVects of line and colour with the use of succulent acrylics. Computer manipulation of original drawings and photographs complements the physical and manual process of looking for an interpretation of shapes and images through these strange phenomena. Influences and aims—Out there, millions of people have diVerent experiences of migraine. I aim to show through my images that when the agony is over, energy, positiveness, enthusiasm and serenity return. This renewed spirit and clarity gives me inspiration.. . . (http://www.axisartists.org/artistid/9069, October 1, 2003)

Molly Barr records on her website: For over 30 years I’ve suVered from chronic migraines, and actually owe my art career to them as I’ve been forced to retire as a result of the condition worsening to that what is known as a ‘‘chronic daily’’ disorder. One night as I was awakening from a particular vicious one, I dreamed that I had put my head in a suitcase and was carrying it at my side to keep the pain contained. This image was the result of that dream. (http://www.monkeysdragon.net/dragontree/migraine.htm, August 14, 2002)

The artist’s migraine inspired a second painting for which she was credited an honorable mention in the fourth Migraine Masterpieces art contest: Beastly Migraine: Okay. So I had another migraine dream! As I was awakening in the pain of a migraine, in my dream, I sensed but didn’t actually feel tactically, that a creature was clinging to me. I got up (in the dream) and looked in the mirror. All I could see was the creature’s tentacle snaking through my hair and boring into my temple where the seat of the pain was. Capturing this scene was a new challenge for me—my first nude . . . and not one, but two! (http://www.monkeysdragon.net/dragontree/beastlymigraine.htm, January 10, 2003)

On a net forum devoted to scintillating scotoma (SS), Robert Buelteman writes: I have had SS for about 15 years now, with episodes occurring irregularly, sometimes years between episodes, but weekly over the last few months . . . I think my experience had deeply aVected my work as an artist. (http://www.edithfrost.com/archive/2001/01/28-scintillating scot.html, July 11, 2003) On his painting The Rising Sun, Mark Copeland relates ‘‘how he first painted the woman as a conventional nude, but felt that it did not quite work and that after a severe migraine he felt


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compelled to cover her body with woods and fields,’’ a description that suggests an impact of the migraine attack on his creativity. (http://www.art-network.co.uk/banca/copmar/, September 3, 2003)

Helen Donis-Keller, renowned both as a molecular biologist and an artist who explores the issue of genotype/phenotype in her series of Helen Heads, reports on her work in progress: I started a new series of very large charcoal drawings that are based on the migraine headaches I suVer from, as my grandmother did. As a part of the diagnostic procedure, I had CT scans and MRIs. These drawings that I’m working on now are a combination of the CT scans and a portrait of my head. I’m working them together, still following the idea of the Helen heads, but now with more interiority. (http://www.genart.org/genome-keller.htm, August 14, 2002)

Claire Fell records: Although my work is abstract, it is still quite controlled both in form and content. The work is cubic and can be likened to ceramic tiles. I am influenced by the structure of crystals, minerals and the texture of rocks, also by my memory of reticulated migraine aura. (http://www.foldgallery.co.uk/snowcase/artists/fell.html, October 16, 2003)

One of Rebecca J. Gill’s ‘‘ ‘pick-up-a-pen-and-go-with-it’ pictures’’ is titled Migraine Induced Art (http://elfwood.lysator.liu.se/loth/j/a/janyth/weirded.gif.html, November 6, 2003).

Self-taught artist Corine C. Glyzinski uses visions caused by a stroke from a migraine headache in 1991 (http://www.olympiaartleague.com/corineglyzinski/profile/index.htm, August 11, 2002).

Maura Hallowell’s triptych Anatomy of a Migraine is ‘‘aVected by the migraines she has suVered from since the age of 6.’’ She explains: In the past, I didn’t want to give them any more attention than I had to—they have been so debilitating and intrusive. But they are a large part of my experience, and they are very personal. In a way, these paintings have become my self-portraits. (http://www.skidmore.edu/studentorgs/skidnews/back/96–97/3–6–97/ae.html, November 20, 2002)

Enamelist William Harper reports: I cannot underestimate the role that migraine headaches play in the conception of some of my best work. I suVer migraines quite frequently, but during the recovery period, which is wretchedly painful, I think and conceptualize very clearly, and have often been inspired during these times with some of my deepest ideas for my work. (http://americanart.si.edu/collections/exhibits/whc/harper.html, July 11, 2003)

Tulsa artist A. Nigh Herndon has experienced severe migraine headaches throughout his life and attributes his artistic inspiration to coping with the pain. This exhibition of work was inspired ‘‘by an unconscious

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train of thought produced by dreams and an underlying tone of day-to-day life living with migraine headaches,’’ according to the artist. (http://www.rsu.edu/news/2003/01–07_RSUGalleryToFeatureWorkOfHerndon. html, November 17, 2003)

Commenting on his Radio Times Girl desktop image, Kevin Inskip notes that I’m a migraine suVerer, and I’ve designed the colours of the theme to be easy on the eye—it seems to work as I get less headaches with this theme than with others—although I doubt that it can be scientifically proved. (http://www.easytoremember.pwp.blueyonder.co.uk/Pages/freestuV.html, August 28, 2003)

Sheri L. Larrimer’s painting Vision Lost is Inspired by the National Headache Foundation’s Migraine Masterpieces and my own experiences with migraines. (http://www.deviantart.com/deviation/2512989/, July 25, 2003)

Sue Macarthur notes: My work is often monochromatic with subtle tones. I am not a user of strong colour, partly due to being a migraine suVerer and not being able to tolerate vivid hues. (http://embroidery.embroiderersguild.com/2001–3/macarthur.htm, August 23, 2003)

Janet McKenzie’s migraines have had a great impact on her art. Her images deal with women, isolation and loneliness, all associated with Migraines . . . In the words of the artist: ‘‘As a lifelong Migraine suVerer, and artist, I ponder just what role living with Migraines has played with regard to my work. I have always created imagery of women and it is clear to me that the figure is presented monumentally. She is massive and I wonder at my own need to create such an image of strength. Certainly, anyone who has experienced Migraines, or loved someone who suVers from them, knows how helpless you feel when they strike . . . . As I look at my work from the perspective of living with Migraines, I see imagery that appears impervious to many things. The subjects seem to be more than capable of preventing anything from hurting, altering or dominating them. Perhaps in some respects I’ve built them, whether in paint or clay, in the way I’d like to be, too powerful to be altered by many things, blinding ‘‘beats’’ of pain being one of them. (http://www.migraines.org/about/, December 31, 2002)

According to the artist, Creighton Michael’s series FIELD was partly inspired by the visual eVects of a migraine. (http://newtimes.rway.com/2004/041404/art.shtml, September 12, 2004) Jelene Morris writes, ‘‘I did make several paintings after I had a migraine,’’ her migraineinspired art featuring ‘‘Knife stabbing heads, twisted heads, and down right confusion.’’ (http://www.jelene.com/archives/2002_11_10_brainfizz_archive.html, November 14, 2002).


Serena Morrow created her art as a form of communication: ‘‘I’ve suVered from migraines since 1992,’’ she said of her art that depicts a visual model of a migraine. ‘‘My art allows an outlet for emotions and feelings otherwise diYcult to express. Some people say that’s art therapy, but it’s a form of communication to me.’’ (http://www.theshorthorn.com/archive/2004/spring/04–apr-13/n041304–05.html, May 15, 2004)

According to Terry Pond, Boy, some of the metaphors I’ve used for describing migraine pain would make good art. (http://www.ebsqart.com/cgi-bin/board/YaBB.pl? board¼desired;action¼display; num¼1045955413, March 26, 2003)

Up to his mid 20s, Eric Ringsby suVered ‘‘from migraines that were ruining his life . . . Roman Wilderness of Pain, 1990, was created by the artist in an eVort to ascertain the origin of his aZiction’’ (http://www.ericringsby.com/ roman.htm, September 17, 2002). Similarly, his sculpture Burn, Baby, Burn! ‘‘comes directly from the artist’s experience of migraines’’ (http://www.ericringsby.com/burnbaby.htm, September 17, 2002).

Suzanne Scott reports: Circles are my compulsion: I relate to the world through circles. I see them and am drawn into them in every day situations, whether it is through anatomy, light beams or even spiral staircases. I see them—beautiful and intense—in the fleeting moments before I lose my sight to migraine headaches. I feel they are the perfect figure to represent the metaphysical nature of Nature, and I use them to further abstract the already abstract elements of Nature. As I paint, I try to extract the energy of the circle in order to recreate it as a figural element, existing in various environments. In the process, they permit me to see myself and provide me with a sense of my own internal reality. My impulse is to paint the circle, and in so doing, the circle is subjected to my immediate emotions—traumas, celebrations, and temporal sense. Each brush stroke, each color, each work becomes a material manifestation of the emotional and metaphysical planes of my existence. (http://www.ezairgallery.com/S_Scott.html, October 8, 2003)

Mindy Smith found out about the 5th Baker’s Dozen International Collage Exchange only days before the mailing date. The next day I was struck by an awful two-day migraine. I decided to use the series as a way to work through the migraine. The flashes of light behind my eyes and intense pain in my head became the deliberate lines and deep resonating colors expressed in the collages. The pieces in this series could not have been created had I not been working through the migraine. My style comes through the pain, yet the influence of the migraine adds depth and a sense of mystery that otherwise would not exist. (http://outofsight.co.nz/Bakers5/exb88.htm, July 11, 2003)

Steven Stone’s pen and ink portrait of himself in the agonizing grip of a migraine is a reminder that muses are not always benevolent. (www.metroactive.com/papers/cruz/06.20.01/collective-0125.html, September 6, 2002)

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According to Elizabeth O’Hara, Sally Trueman’s renown will perhaps rest ultimately in her paintings and pastels depicting the French landscape and influenced by her migraines. These pictures are often disturbing and tantalisingly eye-catching showing the visual disturbances associated with migraine. Such magical skill, powerful enough to captivate, can make one feel uneasy: this artist can show us whatever she wants us to see! (http://www.sally-trueman.com/news.html, August 13, 2004)

‘‘The Evil Twin,’’ a female artist with an Internet pseudonym, writes: Before a migraine hits, I find myself doing more writing, or working on my fractal artwork and getting some really good pictures. However, I would toss this creative burst in a minute, if it meant release from migraine pain. (http://groups.google.de/group s?selm¼os5Q9.13187%24aV5.34047%40news-server. bigpond.net.au and oe¼UTF-8 and output¼gplain, November 12, 2003)

Commenting on his comic strip entitled Demented, ‘‘The hackartist’’ makes the following Disclaimers—This strip was prepared under the mind boggling influence of a migraine thanks to the sun . . . The hackartist, i.e. me thus disclaims any intention or knowledge of what has happened. There is no actus reus and mens rea and as such I AM INNOCENT I TELLYOU!!! (http://www.angelfire.com/hi5/kit/yami27.html, October 16, 2003)

Finally, children’s book illustrator Neil Waldman reported that one time he envisioned a whole book during a terrible migraine headache. (http://www.charlesbridge.com/waldman.htm, September 21, 2003)

2. Migraine Experiences as Impediment of Art Production The records on 13 websites consider migraine as an obstacle for the artists’ creativity. ‘‘Bryne’’ refers to a ‘‘very uninspirational migraine’’ preventing him from producing art. (http://www.charmattack.net, November 20, 2002). Rosemary Lucy Cosentino titles a commissioned painting that represents the experience of her recurring migraine attacks An Artist’s Impediment to Create (http://www.rosemary-cosentino.com, August 19, 2002).

Dana De Sors is an art Student who initially discovered her interest in art with a drawing class. Out of curiosity, she later looked in on a painting class in progress, but began to feel unwell after less than 10 minutes. Later that night she developed a migraine headache . . . she recognized the correlation between the symptoms and the . . . trigger, but returned to the class the following day to test her suspicion. Again, a few minutes exposed to the linseed triggered nausea, followed by a migraine that evening . . . Many potential art students would have given up at this point, but De Sors looked for a solution to the problem and discovered a willing ally in art instructor Noreen Naughton. In a solvent-free classroom located next to the room where Naughton teaches her classmates, De Sors works largely on her own. (http://166.122.11.5/news/kapio/10 12 99/feature/ desors.html, August 18, 2002)


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A female artist with the Internet pseudonym ‘‘eccentric artist’’ comments on having a Migraine again . . . I’m having a big war inside. Part of me is . . . get this . . . fighting against being creative! (http://juliasjournal.blogspot.com/, September 22, 2003)

Gerd Hardon made most of his Paintings at night at moments he wasn’t bothered by fits of migraine. (http://home.wxs.nl/zelde025.start english.htm, October 26, 2002)

‘‘Martha’’ tells of her experience that The migraine problem is a bit worse and there is nothing to do but shut the art down for a while and wait it out. After, when all is clear I go again and it makes me happy, happy, happy to be real all over. (http://www.painterskeys.com/clickbacks/gooddays.htm, August 14, 2002)

The website of Jelene Morris includes a diary entry entitled ‘‘another day, another migraine, my brain is jello.’’ On June 21, 2001, she noted: as I write this I have a migraine, earlier today, it was a migraine, which sucked. I couldn’t get any painting done. If I looked at a canvas too long, I would have gotten sick to my stomach . . . hopefully tomorrow will be productive with no headache worries. (http://www.jelene.com/headjello.html, October 29, 2002)

Larry Nelson records that Last Friday should have been a sculpture day but a migraine derailed that and I wound up working instead. (http://www.sandhands.com/library/sculplog/1999/cat99p10/99p10rpt.htm, November 17, 2002)

Kim Niles writes, ‘‘Came down with my monthly migraine by 1 pm yesterday and as I felt it coming on, I knew I’d better not attempt any more work on Sonny,’’ her current project, ‘‘or I’d muck it up.’’ (http://www. islandillusions.com/bjune.html, July 10, 2003).

Steve Perrault reports: When I’m suVering from a migraine, I can’t work, do errands or even pursue my passion for painting. (http://www.naplesnews.com/today/neapolitan/d326705a.htm, September 22, 2002)

Marlene Shuman looks back at the restrictions imposed by her migraines to her career as an artist. I’m a lifelong lover of Decorative Painting, she writes, ‘‘and have pursued my love in various ways for many years. Early on, I was mostly self-taught as I raised my children. In the early 80s, I spent several months studying oil painting . . . Then I developed a problem with

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migraine headaches every time I picked up oils and that’s when my fabric painting career began . . . I have recently begun to paint with oils again observing better safety measures for my health and have had no problems since. And since I lost all those years when I couldn’t paint with oils, I plan to live to be at least a 100 so I will have plenty of time left to practice. (http://members.aol.com/tinybrush/artist.htm, September 14, 2002)

Jim Stevens writes: In 1994, I suVered a migraine that caused a stroke which, in turn, took my eyesight. After losing my eyesight, I . . . lost the confidence to continue with my art . . .. In 2000, I began to produce art again . . .. I kept working and re-learning the craft—learning how to do my art without the eyesight an artist so desperately needs. It has been a long process but I finally remastered the skills—in a very diVerent way, out of necessity, of course, but the art and the quality are finally there again. (http://www.scrimshawstudio.com/about.html, February 7, 2003)

Finally, Wendi Strang-Frost reports: Tried to work on the comic when we got back, but got hit with a massive dose of fatigue and what I think might have been the beginnings of my first migraine. So I took drugs and fell asleep instead of accomplishing anything. (http://www.sfpro.com/blog/2003_03_01_archive.html, August 14, 2003)

3. Art Production as a Relief of Headaches and Migraines According to the records on seven websites, art making can lessen or alleviate migraine attacks. Christian Grossman relates that concentrating on his incredibly crafted and painted wood construction like ‘‘Salome’’ actually relieved his migraine headaches. (http://www.pacificoart.com/pacificoart2/. . .releases/Obsessing%20Press%20 Release.htm, August 14, 2002)

Tommy Hodges writes: 2 baby related concepts/sketches added. I’m pretty proud of these two drawn in the wee hours of night/morning. I had a migraine, drawing made it go away. (http://www.battlemonkey.com/FRONT_GATE.html, December 12, 2004)

Thomas C. Lolan says: Without doubt, art helps relieve headaches . . .. When I’m at the computer or doing photography, those are the times when I have the fewest headaches . . .. When I keep my mind focused on the subjects I can ignore the other things that might induce the headache. Stress—that triggers my headache. But when I have my camera in my hand, I’m in control. My work allows me to relax. (http://cssvc.health.webmd.compuserve.com/content/article/1728.81313, September 13, 2002)

Pat McInnes confirms: When I get into the artwork, I’m in another place, I get so absorbed . . .. Painting is a relief.


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(http://wysiwyg://54//http://my.webmd.com/content/article/11/1668 51197, December 16, 2002)

Linda O’Neill reports having used her artistic ability . . . as an expression, an outlet . . . it’s been very therapeutic for me. (http://www.dailycamera.com/bdc/health_and_fitness/article/0,1713, BDC_2431_2136493,00.html, September 5, 2003)

Marion Pruitt oftentimes uses painting as a therapeutic outlet. ‘‘It’s a great relaxer and temporarily puts my migraines on the backburner.’’ (www.headaches.org/consumer/presskit/MigraineMasterpieces2003/Announcement_ of_Winners.pdf, August 18, 2003)

Heather Roraback began painting as a teenager. Besieged by chronic migraine headaches, painting provided a release from the crippling pain. (http://www.fulcrumgallery.com/showArtist.aspx?name¼RORABACK, November 23, 2003)

C. PARTICIPATION

IN

MIGRAINE ART/HEADACHE ART CONTESTS

Of the 450 artists of the study sample, 161 or 36% have participated in several Migraine Art or Headache Art competitions held by various organizations in UK and USA since the 1980s. One artist, J. J. Ignatius Brennan (Podoll and Robinson, 2000a), has been a prizewinner in two contests (Table II). The two subgroups of participants versus nonparticipants in such contests diVered significantly in their distribution of sex (Chi2 ¼ 16.80, df ¼ 1, p < 0.001) and nationality (Chi2 ¼ 55.59, df ¼ 1, p < 0.001), the entrants to the said art competitions being more frequently females and US artists (Table III). TABLE II PARTICIPATION OF THE ARTISTS OF THE STUDY SAMPLE IN MIGRAINE ART/HEADACHE ART COMPETITIONS Competition

Number of artists

Fourth National Migraine Art competition 1989 Headache Art contest Through the Looking Glass 1989 Migraine Images art contest 1992 First Migraine Masterpieces art contest 1989 Second Migraine Masterpieces art contest 1999 Third Migraine Masterpieces art contest 2001 Fourth Migraine Masterpieces art contest 2003

1 41 5 30 24 25 36

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TABLE III COMPARISON BETWEEN 289 NONPARTICIPANTS AND 161 PARTICIPANTS MIGRAINE ART/HEADACHE ART COMPETITIONS Nonparticipants (n ¼ 289)

Variables Females Males Artists from USA Artists from other countries

52% 48% 66% 34%

(151/289) (138/289) (191/289) (98/289)

Participants (n ¼ 161) 72% 28% 97% 3%

(116/161) (45/161) (156/161) (5/161)

IN

Comparison (Chi2-test) p p p p

< < <
0,75) between self-reported diagnosis of migraine and diagnosis according to a clinical interview based on IHS criteria (Rasmussen et al., 1991, 1992, 1995). Migraine-related arts from nonparticipants and participants in contests for migraine suVerers diVer in the media employed, the pieces of art produced for the general art market encompassing virtually the complete range, including painting, drawing, digital art, photography, comic, book art, sculpture, installation, and performance (Table IV), a list to which can be added film (Darren Aronofsky, Pi, 1997; Joel Frenzer, Architecture of a Migraine, 2003; John Hudson, Of Art and Migraines, 2003) and video (Helen Donis-Keller, Migraine, 2001; Phyllis Baldino, mi-missing-GR-brain, 2002). This finding suggests, perhaps not surprisingly, that inspiring migraine experiences may be transformed by visual artists into arts in any possible medium. Almost the same spectrum of symptoms of the migraine attack and migraine aura can be discerned by neurological analysis in arts produced by nonparticipants as well as in entries to art contests for migraine suVerers (Table V). This demonstrates that such use of migraine experiences as artistic inspiration does not only occur, more or less deliberately, in the form of sophisticated medical illustration as requested by Migraine Art contests but also in the art produced for the general market. This finding bridges the gap that exists between the paintings and drawings from the semiclinical settings of Migraine Art and Headache Art contests and the migraine-inspired works of famous painters like Georgia O’KeeVe, Giorgio de Chirico, and Sarah Raphael. Far from being just relevant as an art-inspiring factor in the context of Migraine Art contests, migraine experiences can be shown to act as a source of artistic inspiration in a considerable number of contemporary artists, just like dreams, hypnagogic hallucinations, or drug-induced phenomena, the impact of which has been recognized for long in the history of art (Fischer and Scheib, 1971; McKellar, 1995; Stoll, 1995).

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Even more helpful in bridging the aforementioned gap between Migraine Art and the canonical works of the famous artists, it was shown that in a total of 21% of migraine-related art from nonparticipants as opposed to just 3% of the entries to art contests for migraine suVerers (p < 0.001) no representation of the semeiology of migraine with aura could be detected by the neurologist’s ‘‘clinical gaze.’’ This observation resolves the apparent contradiction between the claim that has been made in the case of Giorgio de Chirico, who is supposed to have used migraine aura experiences as a central source of his artistic inspiration (Nicola and Podoll, 2003), and the obvious fact that there exists a great number of paintings from his metaphysical period in which no traces of inspiring migraine symptoms can be identified. This suggests that in such cases the transformations occurring between migraine experiences and the making of migraine-inspired arts may have been so complex as to veil or render ‘‘invisible’’ the original sources of artistic inspiration, that is,, the signs and symptoms of migraine. To learn more about these techniques of veiling that may be operant (not necessarily consciously) in the creative process of making a migraine-inspired art, one can (1) make a follow-up inquiry allowing for direct interviews with the artists in question or (2) apply the art-historical method of establishment of iconographic chains through comparative methods; both of these strategies will be followed in future investigations.

References

Cadenhead, K. A. (1885). The art of migraine: An exploration of the alchemy of migraine headaches on the art and lives of artists/migraineurs. ‘‘Thesis,’’ Boston University School of Education, Boston. Chatterjee, A. (2004). The neuropsychology of visual artistic expression. Neuropsychologia 42, 1568–1583. Drake, M. E., Jr. (1983). Migraine as an organic cause of monocular diplopia. Psychosomatics 24, 1024–1027. Fiering, G. (1996). ‘‘Migraine Boy: Fair Weather Friends. With an Introduction by Michael Stipe.’’ St Martins Press, New York. Fischer, R., and Scheib, J. (1971). Creative performance and the hallucinogenic drug-induced creative experience or one man’s brain-damage is another’s creativity. Confin. Psychiat. 14, 174–202. Fuller, G. N., and Gale, M. V. (1988). Migraine aura as artistic inspiration. Brit. Med. J. 297, 1670–1672. Kalmbach, A. E., and Kellner, E. (1987). ‘‘My 9 Migraine Cures.’’ Women’s Studio Workshop. IHS (International Headache Society) (1988). Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 8(7), 1–96. McKellar, P. (1995). Creative imagination: Hypnagogia and surrealism. J. Mental Imagery 19, 33–42.


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Nicola, U., and Podoll, K. (2003). L’aura di Giorgio de Chirico. ‘‘Arte emicranica e pittura metafisica.’’ Mimesis, Milan. Podoll, K. (1998). Migraine art: The migraine experience from within. Cephalalgia 18, 376. Podoll, K. (2001). Derek Robinson’s audiovisual programme ‘‘In the picture—A personal view of migraine’’: The cradle of the migraine art concept. Neurol. Psychiat. Brain. Res. 9, 17–22. Podoll, K., and Ayles, D. (2002). Inspired by migraine: Sarah Raphael’s ‘‘Strip!’’ paintings. J. Roy. Soc. Med. 95, 417–419. Podoll, K., and Robinson, D. (2000a). Migraine experiences as artistic inspiration in a contemporary artist. J. Roy. Soc. Med. 93, 263–265. Podoll, K., and Robinson, D. (2000b). Illusory splitting as visual aura symptom in migraine. Cephalalgia 20, 228–232. Podoll, K., and Robinson, D. (2000c). Macrosomatognosia and microsomatognosia in migraine art. Acta Neurol. Scand. 101, 413–416. Podoll, K., and Robinson, D. (2001a). Splitting of the body image as somesthetic aura symptom in migraine. Cephalalgia 22, 62–65. Podoll, K., and Robinson, D. (2001b). The idea of a presence as aura symptom in migraine. Neurol. Psychiat. Brain Res. 9, 71–74. Podoll, K., and Robinson, D. (2002). Migraine art—The migraine experience from within. Neurol. Psychiat. Brain Res. 10, 29–34. Podoll, K., To¨pper, R., Robinson, D., and Saß, H. (2000). Wiederkehrende Traüme als Aurasymptome der Migra¨ne. Fortschr. Neurol. Psychiat. 68, 145–149. Rasmussen, B. K., Jensen, R., and Olesen, J. (1991). Questionnaire versus clinical interview in the diagnosis of headache. Headache 31, 290–295. Rasmussen, B. K., Jensen, R., and Olesen, J. (1992). Impact of headache on sickness absence and utilisation of medical services: A Danish population study. J. Epidemiol. Community Health 46, 443–446. Rasmussen, B. K., Jensen, R., and Olesen, J. (1995). Prevalence and sex-ratio of the subtypes of migraine. Int. J. Epidemiol. 24, 612–618. Stoll, R. T. (1995). Sleep and dreams in pictures. Schweiz. Rundsch. Med. Prax. 84, 432–439. Talbot, B. (1999). The heart of empire. ‘‘Dark Horse Comics,’’ Milwaukie, OR. Vick, R. M., and Sexton-Radek, K. (1999). Interplay of art making practices and migraine headache pain experience. Headache Quart. 10, 287–291. Wilkinson, M., and Robinson, D. (1985). Migraine art. Cephalalgia 5, 151–157. Wolberg, F. L., and Ziegler, D. K. (1982). Olfactory hallucination in migraine. Arch. Neurol. 39, 382.


SARAH RAPHAEL’S MIGRAINE WITH AURA AS INSPIRATION FOR THE FORAY OF HER WORK INTO ABSTRACTION

Klaus Podoll and Debbie Ayles Department of Psychiatry and Psychotherapy, RWTH Aachen University Pauwelsstrasse 30, 52074 Aachen, Germany

I. II. III. IV. V.

Introduction Art Critics’ Notions on Sarah Raphael’s Migraine with Aura History of Illness Impact of Sarah Raphael’s Migraine with Aura on Her Art Conclusions References

I. Introduction

Sarah Raphael (1960–2001) was one of the leading British artists of her generation. She died from septicemia following pneumonia at the age of 41. First known during the 1980s as a figurative and portrait painter, from the mid 1990s her artistic development moved from naturalism toward abstraction. This change in her work started with her Desert paintings series, inspired by her travels in the Australian outback, for which she won the £ 36,000 NatWest 90s Prize for Art in 1996. It culminated in her series of ‘‘Strip!’’ paintings presented in her 1998 exhibition at Marlborough Fine Art Gallery, London, featuring a comic-strip format with hundreds of tiny images of brightly colored shapes, devoid of meaning and narrative. Referring to Andre´ Malraux’s dictum ‘‘that people become artists not by looking at life but by looking at art,’’ Sarah Raphael’s father, novelist, and Oscar-winning film writer Frederic Raphael (2003) noted: ‘‘It is true that to be an artist requires attention to what art is, and what previous artists have done, but in Sarah’s case Malraux was only half right: she looked at art, with increasing keenness of perception and critical admiration, but she also looked—and with how keen an eye!—at life, at men and women, at things, at anything. Sarah may have feared many things, not least the pain which crowded the last years of her life, but she flinched from nothing. She looked the world in the face and depicted it, in the light of her genius, in ways that made it more visible.’’ Sarah Raphael certainly did not flinch from the pain and other INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74009-0

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experiences attributable to her long-standing migraine; as this chapter gathers together various sources of information and investigates the link between migraine experience and her inspiration (Podoll and Ayles, 2002) endeavoring to show another aspect of this artist who, so sadly, was unable to continue along the path she had begun. ‘‘In her painting,’’ as Frederic Raphael (2004) puts it, ‘‘one thing led to another, and sometimes to a new style, not least when the agony of her migraine headaches drove her to see a maelstrom of pigmented pain, and to find art (but not relief) in the radiant order in which chaos was made visible to her.’’ II. Art Critics’ Notions on Sarah Raphael’s Migraine with Aura

Several art critics have noted the similarity between the imagery of the ‘‘Strip!’’ paintings and certain types of universal visual perceptual experiences, the so-called phosphenes (Oster, 1970), which can occur in a great variety of conditions and are hence known, potentially, to everyone (for example from hallucinations seen in the twilight periods of approaching or ending sleep). According to Jennifer Hall (1998), the ‘‘Strip!’’ paintings ‘‘in vivid technicolour’’ are ‘‘Reminiscent of Herge´ on acid,’’ suggesting a resemblance between Raphael’s comic-strip patterns (her work being likened to Herge´’s Adventures of Tintin) and psychedelic hallucinations such as those induced by lysergic acid diethylamide (LSD). According to Andrew Motion (1998), their ‘‘unrecognisable shapes’’ are ‘‘like the shapes which appear when you rub your eyes too hard,’’ the so-called pressure-induced phosphenes (‘‘seeing stars’’). ‘‘Or maybe,’’ the Poet Laureate continued, ‘‘like the start of a headache, before the pain starts’’—a clear reference to the so-called migraine aura, characterized by a variety of neurological symptoms (mostly visual disturbances), which can herald the headache of a migraine attack. Similarly, Geordie Greig (1998) noted that ‘‘There is a blurring, a dizziness, an intensity, but no one single focus’’ in Raphael’s ‘Strip!’ images, suggesting that ‘‘This all brings us back to her migraine’’ (or more precisely, her visual migraine aura). We now know that migraine experiences have acted as a source of artistic inspiration both in the past (Fuller and Gale, 1988) and in contemporary artists (Podoll and Robinson, 2001), so the notion of the impact of Raphael’s migraine on her art merits consideration. III. History of Illness

The history of Sarah Raphael’s migraine can be reconstructed from a number of articles based on interviews given by the artist on the occasion of her said ‘‘Strip!’’ exhibition. At the age of 15 or 16, she ‘‘began to get unusually bad

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headaches,’’ but it was not until she was 21 that she experienced her first fullblown migraine. ‘‘I remember this friend coming round to see me, and, while she was talking, feeling myself close down, and this incredible pain take over,’’ she says. ‘‘After she’d gone, I lay on the ground in floods of tears banging my head on the floor. I phoned Paul, my brother, who came round with codeine, and eventually it went away.’’ Over the next 15 years, she began to learn what triggered the headaches, although headache is too mild a word for the ‘‘absolute revolt of the nervous system’’ she felt during an attack. In her case, she had to avoid alcohol, coVee, wheat, and cheese. She tried ‘‘every kind of alternative therapy: acupuncture, osteopathy, Chinese herbs, yoga.’’ Some eased the situation, but none cured her’’ (Gregson, 1998). ‘‘At Camberwell her terrible headaches were first diagnosed as migraine, a complaint that dogged her life as an artist, causing her such pain that she had to give up work for a couple of years both then, and later with the birth of her third daughter, Rebecca’’ (Barnes, 2001). ‘‘I basically had them non-stop,’’ she said, ‘‘which made me insane. I couldn’t see properly, couldn’t stand noise, bright lights or any kinds of movement. I didn’t stop painting straight away, but it slowed down till I was in bed in a blacked-out room, taking large amounts of Pethidine [a narcotic painkiller] and not having a life’’ (Petrovic, 1998). Thus, ‘‘A blinding migraine meant Sarah Raphael could barely leave her sick bed for almost eighteen months’’ (Greig, 1998). In summary, the available information strongly suggests a diagnosis of migraine with aura, although there is a sad lack of description of the visual aura phenomena experienced by the artist during her attacks of a ‘‘blinding migraine.’’ Sarah Raphael’s moving and instructive description of her ‘‘eighteen-month migraine,’’ and its impact upon her art, as recorded in the interview by Julia Gregson (1998), deserves to be cited in full. ‘‘It was when she was pregnant with her third daughter, Rebecca, in 1996, that the full force of the condition struck and Sarah experienced a terrifying continuous migraine which, for the first time in her life, stopped her from painting.’’ ‘‘I had a headache which basically didn’t go away for one-and-a-half years. During this pregnancy I had morning sickness 24 hours a day. I couldn’t remember what it was like not to be in pain. I might throw up three times on a simple trip to take the kids to school. I cherished simple memories such as going to Sainsbury’s without a headache. I just closed down. I didn’t see anyone apart from my children, who did their homework at the end of my bed, and my parents. I couldn’t speak on the phone. I’d lost it, and with two small children I was terrified.’’ In terrible pain and unable to take her usual doses of Imigran, which is contraindicated during pregnancy, she was prescribed the morphine-based drug, pethidine, in increasing quantities. At one point, she was taking it four times, day and night. ‘‘I kept thinking that if I was a proper mother I would survive this pain without drugs,’’ says Sarah, ‘‘but, for the first time, I was defeated by it.’’ Then, shortly after Rebecca’s birth, came the slow, terrible realisation that she was not only a migraine suVerer, but a pethidine addict. She still finds it diYcult to talk about that period of her life.

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‘‘I am a strong-willed person,’’ she says, ‘‘and I come from a hard-working, fairly abstemious family, who have lots of outlets for joy, so I’m not obvious addict material, or didn’t think I was. But on pethidine, the combination of the pain going at last, and the euphoria from the opiates themselves, was lethal.’’ One of the most insidious side eVects of pethidine was that it gave her a spurious imitation of the natural highs she gets from painting. ‘‘Pethidine, by killing all pain—whether physical, spiritual, or emotional—oVers a false promise,’’ Sarah explains. ‘‘It tells you that you’re a genius and that everything you do is fine, which is nonsense.’’ Sarah’s work had always been a fundamental part of her life, throughout adolescence and marriage (to Nick Dowell from whom she separated), through pregnancy and many travels. ‘‘Not being able to paint was a kind of death: I’m not much use to anyone when that line is cut,’’ she says. The worst point came in January last year [1997] when the pressures of dealing with a tiny baby, young daughters and no painting led her to a headache so severe that she was hospitalised for three days. It was then that she realised she was an addict. When she woke up in hospital, without her headache—or the pethidine—she started sweating and shaking uncontrollably. ‘‘I went through 24 hours of cold turkey,’’ she says. Four or five days later, just when she thought she had come through it, the pain returned. ‘‘I had a really bad migraine attack and I just didn’t know how I was going to go on.’’ During the next eight months, she tried to paint in spite of the headache until, finally, in despair, she checked into the Priory Hospital in London. She was treated with Valium for 10 days, and then she went into an addiction unit for three weeks, during which time she had counselling, hypnotherapy and rest. The headaches did not miraculously disappear but, for Sarah, it is enough of a miracle that she was drawing again as soon as she could see straight. ‘‘It was bizarre. I would wake up in hospital having been given amazing doses of Valium and when I started to draw, my hand would be just as sure. I felt like that bit of me was kept safe.’’ The drawings she did in hospital inspired the next phase of her work. ‘‘They are quite ordered and precise, but there is this exuberance about them, they were leading me out of a dark place,’’ she says. The price of this period has been high for her children, for herself and for her relationships. She refuses to discuss the break-up of her marriage last year. But good things have come out of the experience as well. ‘‘My baby Rebecca is a miracle. The first year of her life was mayhem and yet she is the sunniest, most wonderful child—it makes you wonder how much that is experienced in pregnancy does filter through.’’ It has also taught her that she has to work around her migraines rather than go at them with a battering ram. ‘‘One of the problems is that you get so angry and frustrated by all the false prophets oVering solutions. Lots of alternative therapies do make a lot of sense but some of their practitioners made me worse by saying: ‘‘No problem these migraines of yours, give me a couple of sessions and I’ll have them sorted. When they didn’t, I became furious and anger is not good for migraines. Crying is even worse.’’ ‘‘So you try and get better at avoiding getting tired or upset. That is a kind of discipline.’’ Sarah now paints in a light, airy studio oV her kitchen, breaking oV, when necessary, to help with homework, change a nappy or play with a child. She has painted more here in the past year than ever before, reminded of the pure enjoyment she experienced painting as a child. Picasso once said that painting is another way of keeping a diary. Her decision to tough out her migraines and never take mind-altering drugs, no matter how bad the pain, has led to a


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show which marks a departure from her earlier work. The risk she took by doing this is the very antithesis of addiction, where the rewards are measured out and arrive on time and in order. Critics have noticed the excitement in her work, the boisterous colour and the marvellous precision—what the writer, Andrew Motion calls, ‘‘the honesty of emotions that are prepared to admit what is possible as well as what is not.’’ (Gregson, 1998)

IV. Impact of Sarah Raphael’s Migraine with Aura on Her Art

According to John Russell Taylor’s (2001) obituary of Sarah Raphael, ‘‘Her struggles with ill-health of various kinds, all of them rooted in migraine, inevitably led to speculation about a connection between her artistic obsessiveness and her malady. Curiously, though, knowledge of her illness throws very little light on her painting itself.’’ However, Julia Gregson (1998) made a general claim that ‘‘The story of Sarah Raphael’s pain, and her addiction to pethidine, is told in her painting,’’ but she remained vague as to how exactly migraine was assumed to have influenced Raphael’s ‘‘Strip!’’ images. In more detail, Geordie Greig (1998) suggested that ‘‘Courageously and cleverly, she turned this [i.e., her blinding migraine] to her professional advantage by making comic-strip paintings on which she could work just a little bit at a time. She could manage only short periods of work before the pain became too much. This meant that large singleimage pictures were too demanding. Her new, detailed, and painstakingly constructed works constitute ‘Strip!’, her first exhibition at Marlborough Fine Art.’’ Rada Petrovic (1998) provided further information confirming that ‘‘Raphael devised a migraine-friendly working method. The hundreds of tiny, individual pictures that comprise these paintings lent themselves perfectly to working in staccato fashion—her only real option. ‘I was only able to do bite-sized sections, because I could do them one at a time.’ Raphael also had to give up her favourite medium, oil paint, as the smell of linseed and turps became a relentless trigger for new migraine attacks. In came flat, harsh but mercifully fragrance-free acrylic paints (some would say a much more appropriate medium for the pop-artish flavour of the new works, anyway).’’ These accounts emphasize the impact of migraine on Raphael’s art by means of the restrictions the illness may have imposed upon her choice of art media and art-making practices. Similarly, a Migraine Masterpieces competition organized in 1997 by the National Headache Foundation in the USA provided evidence to the eVect that migraine patients/artists often manage their pain by changing art materials and methods, for example, ‘‘switching from techniques that require high levels of precision and avoiding materials with noxious fumes’’ (Vick and Sexton-Radeck, 1999).

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However, a closer inspection of Sarah Raphael’s ‘‘Strip!’’ paintings indicates that her ‘‘blinding migraine’’ may have influenced her art also in a more direct way. ‘‘As ‘Strip!’ testifies,’’ wrote Rada Petrovic (1998), ‘‘migraines ain’t all bad. ‘This work should have been a lot more dark and interior than it is,’ says Raphael. ‘I painted these coming out of the most horrific period of my life, but ironically, they are more playful and eVervescent than anything I’ve done before.’’’ ‘‘. . . too often, in pain from persistent migraine,’’ recalled Frederic Raphael (2004), ‘‘she suVered cruelly (to the point of being ashamed of it), but I associate her with happiness. . . Sarah knew the pain, but also the comedy, and their fragile proximity.’’ In four ‘‘Strip!’’ pictures, the regular grids arranged by tiny boxes (Strip Pages 5, 7, and 9) or repetitive images of unrecognizable objects (Strip Page 8) are superimposed by large zigzags enclosing an oval-shaped area displaying some obscuration or alterations of color (e.g., Figs. 1 and 2), reminiscent of the form and other phenomenal features of the so-called fortification spectra (Fig. 3), which represent a common type of visual aura symptom in migraine, so named after its similarity to the map of the bastions of a fortified town as viewed from above. Perhaps such symptoms of Raphael’s ‘‘blinding migraine’’ were exploited as a source of artistic inspiration in her ‘‘Strip!’’ paintings produced during her 18-month migraine. Such action is by no means uncommon in migraine patients/artists. It can be seen from the aforementioned Migraine Masterpieces competition (Vick and Sexton-Radeck, 1999) in which about one quarter of those suVerers who experienced visual aura symptoms said they deliberately depicted these phenomena in their art. Not only the zigzags of star shapes but many other patterns of the geometric imagery encountered in Raphael’s ‘‘Strip!’’ paintings, for example, triangles, squares, rectangles, rhombuses, and rhomboids, crosses, arcs, circles, spirals,

FIG. 1. Sarah Raphael, Strip Page 7 (detail), 1998, acrylic on canvas with papier mache´ collage (72 inches 72 inches) # 2006 Estate of Sarah Raphael, Courtesy Marlborough Fine Art (London) Ltd.


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FIG. 2. Sarah Raphael, Strip Page 9 (detail), 1998, acrylic on canvas with papier mache´ collage (72 inches 72 inches) # 2006 Estate of Sarah Raphael, Courtesy Marlborough Fine Art (London) Ltd.

FIG. 3. Zigzag fortification spectrum illustrated in an entry in the national Migraine Art competition.

checkerboards, grids, lattices, can also be seen during visual migraine auras (Podoll and Robinson, 2002), so it is possible that the impact of her ‘‘blinding migraines’’ went much beyond their serving as a model for the said zigzag shapes. Whereas the ‘‘Strip!’’ paintings (1996–1998) concentrate on exploring the form and color dimensions (Siegel and Jarvik, 1975) of the various types of geometric imagery she depicted, some of the etchings from her series ‘‘Small Objects in Transit’’ (1999–2000) and the four paintings from the unfinished series ‘‘Time Travel for Beginners’’ (2000–2001) also deal with the issue of its movement dimension

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FIG. 4. Sarah Raphael, The Childhood Cube (detail), 1999. # 2006 Estate of Sarah Raphael, Courtesy Marlborough Fine Art (London) Ltd.

(Siegel and Jarvik, 1975), as represented not only by the artworks’ titles (with the notions of ‘‘Transit’’ and ‘‘Travel’’ both referring to movement), but also by the graphic symbols of arrows and interrupted lines suggesting trajectories. In addition to all the aforementioned dimensions of visual imagery, Raphael’s ‘‘Childhood Cube’’ (1999), which she did for the Millennium Dome in London, also conveys action patterns (Siegel and Jarvik, 1975), that is, the temporal sequence of diVerent images as implemented by the electric light installation of the Cube, illuminating its boxes in alternating colors. As a final reference of Raphael’s ‘‘Childhood Cube’’ to the artist’s recurring migraines, one of the tiny sculptures contained in some of the Cube’s boxes shows a child lying in bed with one hand held against the head and the other against the tummy, representing the headache and abdominal complaints of an acute migraine attack, suggested to be triggered by the chocolate and pizza, which can be seen on a desk standing nearby (Fig. 4).

V. Conclusions

According to Andrew Motion (1998), Sarah Raphael’s development had taken her ‘‘from naturalism to abstraction, from outward looking to inward gazing.’’ In 1998, the artist recorded, ‘‘I came to abstraction reluctantly. It was never my intention’’ (Greig, 1998). Indeed, critics of Raphael’s Desert paintings series have noted that these achieved a provocative synthesis of figurative and abstract art. ‘‘They are, on one level, works of brilliant hyper-realism. . . And, on another level, the paintings take on


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the eerie and quasi-mystical properties of colour field abstraction’’ (Boyd, 1995). Our study suggests that such synthesis can also be found at the heart of ‘‘Strip!’’ and her later groups of work, where figurative representations of geometric patterns of migrainous origin, subjected to the artist’s practice to ‘‘gaze upon an object and paint it as truthfully as I can’’ (Motion, 1998), are amalgamated with the abstract imagery of ‘‘stripped-down forms, objects with just a hint of familiarity but from which any immediate identity has been pared away’’ (Greig, 1998). Identifying Sarah Raphael’s migraine experiences as a source of her artistic inspiration does by no means demystify or etiolate her art in a reductionistic way but rather enriches our appreciation of its complexities and beauty. ‘‘I loathe the idea of art being a vomiting forth of one’s deepest miseries and neuroses’’ (Petrovic, 1998), she said in an interview, expressing a point of view, which is not at all at variance with the notion that she has spiritually transformed her migraine experiences in her art. As Frederic Raphael has put it in a personal communication to Debbie Ayles dated May 23, 2002: ‘‘. . . while Sarah was indeed a migraine suVerer (so was I in my earlier years, and still very occasionally), I do not accept that her work was the consequence of migraine, more that it was, at times, accompanied by migraine. Sarah was an artist of some power and rare imagination before she suVered from migraine. There are, somewhere, some drawings she did literally of her headaches, but I do not see a causal relation between her pain and the beauty she created. . . I mention this not to be disagreeable, but to clarify a point which, in the present world, where everything tends to be deemed the result of some psychological wound, or a response to it, is often missed: art is not, in my view, explained by its ‘sources,’ whatever they are. Many have migraine, not all turn into Sarah Raphael. . .,’’ who will be remembered not for her migraines but for her achievements as one of the outstanding artists of her generation. Acknowledgment

Figures 1, 2, and 4 are reproduced by permission of the Estate of Sarah Raphael and Marlborough Fine Art (London) Ltd. Figure 3 is reproduced by courtesy of the Migraine Action Association and Boehringer Ingelheim Ltd. Finally, we wish to thank for the permission to reprint parts of a paper published previously in the Journal of the Royal Society of Medicine (Podoll and Ayles, 2002).

References

Barnes, R. (2001). Sarah Raphael. Guardian, January 8. Boyd, W. (1995). Sarah Raphael. In ‘‘Raphael S: Desert Paintings and Other Recent Work.’’ Agnew’s and the Fitzwilliam Museum, London. Fuller, G. N., and Gale, M. V. (1988). Migraine aura as artistic inspiration. BMJ 297, 1670–1672.

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Gregson, J. (1998). My eighteen-month migraine: The story of Sarah Raphael’s pain, and her addiction to pethidine, is told in her painting. Weekend Telegraph, October 31. Greig, G. (1998). Empty speech bubbles: Sarah Raphael’s surprising foray into abstraction marks an about-turn by an artist easily bored by standing still. Mod. Painters 11(4), 82–84. Hall, J. (1998). Artist of the month: Sarah Raphael. Tatler 293(10), 70. Motion, A. (1998). Introduction. In ‘‘Raphael S: Strip!’’ pp. 4–5. Marlborough Fine Art (London) Ltd., London. Oster, G. (1970). Phosphenes. Sci. Am. 222, 82–87. Petrovic, R. (1998). Painting a picture of my pain: When agonising illness strucks artist Sarah Raphael, it wreaked havoc on her life, but it also transformed her work. Independent Sunday, October 18. Podoll, K., and Ayles, D. (2002). Inspired by migraine: Sarah Raphael’s ‘Strip!’ paintings. J. Roy. Soc. Med. 95, 417–419. Podoll, K., and Robinson, D. (2001). Visual migraine aura as source of artistic inspiration in professional painters. Neurol. Psychiat. Brain. Res. 9, 81–94. Podoll, K., and Robinson, D. (2002). Migraine Art—The migraine experience from within. Neurol. Psychiat. Brain. Res. 10, 29–34. Raphael, F. (2003). Sarah Raphael. In ‘‘Sarah Raphael 1960–2001. A Survey of Work from 1994– 2001,’’ pp. 5–7. Marlborough Fine Art (London) Ltd., London. Raphael, F. (2004). Introduction. In ‘‘Sarah Raphael Drawings,’’ pp. vii–xiii. Carcanet Press Limited, Manchester. Siegel, R. K., and Jarvik, M. E. (1975). Drug-induced hallucinations in animals and man. In ‘‘Hallucinations—Behavior, Experience, and Theory’’ (R. K. Siegel and L. J. West, Eds.), pp. 81–161. Wiley, New York. Taylor, J. R. (2001). Sarah Raphael: Talented painter whose restless urge to experiment took her from portraits and landscapes to patchworks of pure colour in an all too short career. Times, January, 17. Vick, R. M., and Sexton-Radeck, K. (1999). Interplay of art making practices and migraine headache pain experience. Headache Quart. 10, 287–291.

THE VISUAL ART OF CONTEMPORARY ARTISTS WITH EPILEPSY

Steven C. Schachter Harvard Medical School, Department of Neurology Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA

I. Introduction II. Background to the Collection III. Artistic Themes in the Works of Contemporary Artists with Epilepsy A. Seizure Experiences B. Psychiatric Comorbidity C. Psychosocial Aspects of Epilepsy D. Nonepilepsy Related IV. Conclusions References

I. Introduction

Epilepsy is one of the most common neurological disorders encountered in clinical practice, aVecting approximately 1 of 50 children and 1 of 100 adults in developed countries, with a higher prevalence in developing countries. Epilepsy is called a hidden disability because people with the condition usually appear normal between seizures. Yet, ironically, the appearance of someone having a seizure is anything but hidden from view and is often dramatic and frightening. Consequently, epileptic seizures have been depicted in art through the ages, colored by views on its medical, social, and psychological aspects. The history of epilepsy in pictorial art was reviewed during the last Mansell Bequest symposium (Engelsen, 2004) as well as elsewhere (Schachter, 1996) and will not be further explored in this chapter. Artists who themselves have epilepsy present a unique view of their condition. Over the years, I have collected the works of contemporary artists with epilepsy, compiling much of it along with the artists’ written comments in a book (Schachter, 2003). In addition to its pictorial qualities, the art is replete with insights into the experiences of having seizures and living with epilepsy. This chapter presents examples from my collection, organized by the apparent connection between


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the pictorial subject and epilepsy as currently understood from a medical perspective.

II. Background to the Collection

In 1992, Jennifer Hall, a gifted Boston artist with epilepsy, organized a show at her gallery (http://www.dowhile.org/) called ‘‘From the Storm’’ (http://www. dowhile.org/physical/overview/presentations/asci/storm.html). Her hope was that curating the show would help her to better understand herself through the collective voice of other artists with epilepsy ‘‘working under similar conditions’’ and would provide a guide to the ‘‘rich, randomly mapped terrain’’ of creativity and epilepsy (Hall, 1992). In assembling the show, she ‘‘found an abundance of creative people eager to share of themselves in an intimate and vulnerable way,’’ who were willing to share, through their art, ‘‘the problems of negotiating basic life and the cultural stigmas of having any form of epilepsy.’’ The collected works demonstrated to her the relationships between the art and seizures, the process of diagnosis, and the lifestyle of people with epilepsy, amplified by the personal statements of the artists that were displayed alongside their work and in the show’s catalogue. Based on a successful run in Boston, ‘‘From the Storm’’ toured USA, Canada, and Australia, where it was on display in conjunction with the 1995 meeting of the International League Against Epilepsy. I was pleased to help sponsor the show and its worldwide journey from its inception, and in doing so I came to appreciate the multifaceted significance of the collected works. Particularly aware of the value the art held for health care providers and the epilepsy community, I launched a series of calendars, initially featuring the art from the show, which were distributed to physicians, nurses, and epilepsy advocacy groups. Soon, dozens of artists with epilepsy from around the world, many encouraged by their physicians, began to send me photographs, digital files, and slides of their work, as well as canvases and prints, often with lengthy personal statements. Currently, there are approximately 1200 pieces in the collection from over 50 artists. I have featured selected works on the covers of books and issues of Epilepsy & Behavior (Academic Press).


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III. Artistic Themes in the Works of Contemporary Artists with Epilepsy

The art in the collection can be organized under four general themes: seizure experiences, psychiatric comorbidity, psychosocial aspects of epilepsy, and nonepilepsy related. A. SEIZURE EXPERIENCES Seizures are experienced variously by diVerent patients, and having a seizure is central to a number of the art pieces in the collection. As background to these works, there are two main types of seizures, generalized and partial. Whereas generalized seizures aVect both sides of the brain simultaneously, partial seizures aVect a restricted area of cortex. Symptoms that patients consciously experience with partial seizures are often called auras or warnings and are classified as simple partial seizures—‘‘simple’’ meaning consciousness is not impaired. Typical simple partial seizures include nausea, fear, jerking of one side of the body, or a metallic taste, although a wide variety of other cognitive, perceptual, and emotional auras have been described (Schachter, 1993). For example, some patients have visual symptoms, such as shown in Fig. 1, while others have complex distortions of body image (Figs. 2 and 3). If patients do not have conscious symptoms as the manifestations of their seizures, then they abruptly lose consciousness, often described as a fadeout or blackout. Patients are unconscious during these types of seizures, so they have

FIG. 1. Brainstorm #20, Craig GetzlaV, 2002, Acrylic, Dyptic 36 24 for each piece. Reprinted from (Schachter, 2003) with permission.

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FIG. 2. Transcending, Jennifer Hall, Computer graphic. Reprinted from (Schachter, 2003) with permission.

no memory of what happened and describe a gap of time for which they have no recollection. This interruption of time is shown dramatically in Fig. 4 as cracks in a bridge in which the bridge symbolizes a day in the life of someone with seizures. The complex partial seizure (known in the past as temporal lobe seizures and psychomotor seizures) is the most common type of seizure in adults with epilepsy. During complex partial seizures, patients typically appear awake but do not meaningfully interact with people around them or respond normally to instructions or questions. Generalized tonic-clonic seizures (also called grand mal seizures or convulsions) may begin with a loud scream. The limbs then stiVen (tonic phase), the patient falls to the ground, cyanosis ensues, and the extremities jerk (clonic phase). Bloody, frothy sputum may be seen. The termination of the clonic phase represents the onset of the postictal period. After complex partial or generalized tonic-clonic seizures, patients may appear to be in a deep sleep, or confused, and may complain of a headache. Other symptoms commonly experi-


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FIG. 3. Untitled, Todd Gieg. Reprinted with permission from the artist.

enced during the postictal period include shame, embarrassment, depression, loss of contact with reality, and visual perceptual distortions (Fig. 5). B. PSYCHIATRIC COMORBIDITY Depression, anxiety, and psychosocial aspects are the three most common psychiatric disorders that occur in people with epilepsy. Many of the pieces in the collection reflect an awareness of one or more of these disorders. Depression occurs in nearly one in five patients whose seizures are controlled and more than half of patients whose seizures continue despite treatment (Mendez et al., 1986; O’Donoghue et al., 1999). Depression, conveyed beautifully in Fig. 6, is underrecognized and, when diagnosed, usually undertreated (Kanner and Barry, 2003). It may arise from epilepsy-related brain dysfunction as well as social or vocational disabilities (Gilliam and Kanner, 2002). Neurologists do not appreciate well enough that depression negatively impacts on the quality of life, independent of seizure frequency (Hermann et al., 2000). Nearly one in four people with epilepsy have an anxiety disorder; higher rates have been reported in patients with medication-resistant seizures (Vazquez and Devinsky, 2003). Like depression, anxiety significantly impacts on the quality of life (Cramer et al., 2005). Anxiety disorders, most commonly present as a

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FIG. 4. Interruptions, Wolfgang Fehring, 1999, Oil, 70 100 cm. Reprinted from (Schachter, 2003) with permission.

generalized anxiety disorder, the degree and persistence of which may not correlate with seizure frequency (Goldstein and Harden, 2000). Some patients experience anxiety as a symptom of their seizures, as illustrated in Fig. 7 and described by another individual: ‘‘I experience a combination of de´ja` vu with extreme fear. Nothing I can do takes me out of it. Everything that happens becomes a part of it. The general feeling is like being in front of an oncoming train with no way to escape’’ (Schachter, 1993). Paradoxically, anxiety may develop after a patient attains seizure freedom and, therefore, when they take on, as Bladin and colleagues have described, the ‘‘burden of normality’’ (Wilson et al., 2004). Complete control of epilepsy may be anxiety provoking and requires, as stated by the sculptor Betsy Elliott Zukin, both medical and physical control, which she incorporates into her tightly woven self-portrait (Fig. 8).


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FIG. 5. Postictal, Jacqui Streeton, 1993, Ink (watercolor wash), 14 14 inches. Reprinted from (Schachter, 2003) with permission.

C. PSYCHOSOCIAL ASPECTS

OF

EPILEPSY

There are very few, if any, aspects of daily living not aVected by the diagnosis of epilepsy. Restrictions on independence can be the most socially disabling—in particular eVects on employment, driving an automobile, life insurance, and lifestyle. The majority of works in the collection that relate to epilepsy pertain to the day-to-day experiences, in between seizures, of living in society with a diagnosis of epilepsy. Common subthemes are isolation, stigma, and the impact of epilepsy treatments. Persons with epilepsy often feel isolated and alone, whether in their own home (Fig. 9) or out in social settings. Fear of and worrying about having a seizure in public are common among people with epilepsy. Nearly half of a sample of community-based people with epilepsy responding to a survey reported that fear was ‘‘the worst thing about having epilepsy’’ (Fisher et al., 2000a,b). Fear was further described by some respondents as fear that others would witness a seizure, with

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FIG. 6. Abstract Face, Jude Rouslin, 2001, Computer generated, 8.5 11 inches. Reprinted from (Schachter, 2003) with permission.

FIG. 7. Gray Abstract, 1999, Jude Rouslin, Computer generated, 8.5 11 inches. Reprinted from (Schachter, 2003) with permission.


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FIG. 8. Bound for Life, Betsy Elliott Zukin, 1991, Stainless steel rod, copper, patina, 30 30 62 inches. Reprinted from (Schachter, 2003) with permission.

FIG. 9. Separate, Wolfgang Fehring, 1998, Oils, pastels, and pencil, 12 12 cm. Reprinted from (Schachter, 2003) with permission.

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FIG. 10. Self Portrait after Surgery, David Thinger, 6 9 inches. Reprinted from (Schachter, 2003) with permission.

the embarrassment and humiliation of awakening from a fit with strangers peering down. Stigma aVects the quality of life of people with epilepsy at any age and in every country (Baker et al., 1997; Jacoby, 2002; MacLeod and Austin, 2003; Morrell, 2002). It results in discrimination in the course of everyday activities such as attending school, driving, and working (Jacoby and Jacoby, 2004). Persons with epilepsy may perceive stigma in connection with visible reminders of their epilepsy such as the need for brain surgery (Fig. 10) or taking pills (Fig. 11).


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FIG. 11. Imari and Orbs, Roxanne Hilsman, 2003; Oil on canvas. Reprinted from (Schachter, 2003) with permission.

FIG. 12. Springtime, Patricia Bernard, 2000, Acrylic, 16 30 inches. Reprinted from (Schachter, 2003) with permission.

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FIG. 13. The Coves, Klaas Verboom, Oil on board, 28 32 inches. Reprinted from (Schachter, 2003) with permission.

D. NONEPILEPSY RELATED The subject matter of the majority of the pieces in the collection is unrelated to specific aspects of epilepsy such as shown in Figs. 12 and 13. The importance of sharing this work with society and people with epilepsy and their families cannot be underestimated because it demonstrates that persons with epilepsy can be creative and productive, and can meaningfully contribute to society. This counters the stigma of epilepsy, that is, the notion that persons with epilepsy are defective in some way, with a spoiled identity (GoVman, 1963).

IV. Conclusions

The works of contemporary artists with epilepsy oVer insightful perspectives into the varied experiences of people with this disorder through the expression of epilepsy-related experiences and demonstration that people with epilepsy can contribute to culture. Interesting research questions are raised as well such as Are persons with epilepsy particularly likely to engage in artistic activities? If so, are there specific characteristics to the art or correlations with seizure focus, age of onset, other related


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cognitive/aVective factors, and so on? What testable hypotheses are suggested by the art regarding brain functions (e.g., visual perception, consciousness, aVect)?

Answering these questions with further study may bring us closer to a deeper understanding of the meaning of the art of contemporary artists with epilepsy. Even before the answers are forthcoming, however, physicians and the epilepsy community can learn much from the art and appreciate its beauty and value.

References

Baker, G. A., Jacoby, A., Buck, D., Stalgis, C., and Monnet, D. (1997). Quality of life of people with epilepsy: A European study. Epilepsia 38, 353–362. Cramer, J. A., Brandenburg, N., and Xu, X. (2005). DiVerentiating anxiety and depression symptoms in patients with partial epilepsy. Epilepsy Behav. 6, 563–569. Engelsen, B. A. (2004). Epilepsy in pictorial art. In ‘‘Neurology of the Arts: Painting, Music, Literature’’ (F. C. Rose, Ed.), pp. 141–152. Imperial College Press, London. Fisher, R. S., Vickrey, B. G., Gibson, P., Hermann, B., Penovich, P., Scherer, A., and Walker, S. (2000a). The impact of epilepsy from the patient’s perspective I: Descriptions and subjective perceptions [in process citation]. Epilepsy Res. 41, 39–51. Fisher, R. S., Vickrey, B. G., Gibson, P., Hermann, B., Penovich, P., Scherer, A., and Walker, S. G. (2000b). The impact of epilepsy from the patient’s perspective II: Views about therapy and health care. Epilepsy Res. 41, 53–61. Gilliam, F., and Kanner, A. M. (2002). Treatment of depressive disorders in epilepsy patients. Epilepsy Behav. 3, 2–9. GoVman, E. (1963). ‘‘Stigma: Notes on the Management of Spoiled Identify.’’ Prentice-Hall, Englewood CliVs, N J. Goldstein, M. A., and Harden, C. L. (2000). Epilepsy and anxiety. Epilepsy Behav. 1, 228–234. Hall, J. (1992). ‘‘From the Storm: Artists with Temporal Lobe Epilepsy,’’ p. 35. The Do While Studio, Boston. Hermann, B. P., Seidenberg, M., Bell, B., Woodard, A., Rutecki, P., and Sheth, R. (2000). Comorbid psychiatric symptoms in temporal lobe epilepsy: Association with chronicity of epilepsy and impact on quality of life. Epilepsy Behav. 1, 184–190. Jacoby, A. (2002). Stigma, epilepsy, and quality of life. Epilepsy Behav. 3, 10–20. Jacoby, K., and Jacoby, A. (2004). Epilepsy and insurance in the UK: An exploratory survey of the experiences of people with epilepsy. Epilepsy Behav. 5, 884–893. Kanner, A. M., and Barry, J. J. (2003). The impact of mood disorders in neurological diseases: Should neurologists be concerned? Epilepsy Behav. 4, 3–13. MacLeod, J. S., and Austin, J. K. (2003). Stigma in the lives of adolescents with epilepsy: A review of the literature. Epilepsy Behav. 4, 112–117. Mendez, M. F., Cummings, J. L., and Benson, D. F. (1986). Depression in epilepsy: Significance and phenomenology. Arch. Neurol. 43, 766–770. Morrell, M. J. (2002). Stigma and epilepsy. Epilepsy Behav. 3, 21–25. O’Donoghue, M. F., Goodridge, D. M., Redhead, K., Sander, J. W., and Duncan, J. S. (1999). Assessing the psychosocial consequences of epilepsy: A community-based study. Br. J. Gen. Pract. 49, 211–214. Schachter, S. C. (1993). ‘‘Brainstorms: Epilepsy in Our Words.’’ Raven Press, New York.


SECTION III BRAIN DAMAGE


CREATIVITY IN PAINTING AND STYLE IN BRAIN-DAMAGED ARTISTS

Julien Bogousslavsky University Department of Neurology, Lausanne, Switzerland

I. Introduction II. Change in Creativity and Style in Artists after Brain Lesion III. Change of Style in Artists References

I. Introduction

Creativity can be defined as the ability to (1) produce; (2) original material; (3) which responds to a motivational drive or need. It is not limited to art, as there are examples of creativity in virtually all domains. The question of the existence of a ‘‘creative personality’’ and the link between madness and genius has been raised by Aristotle; although psychological characteristics of creative persons have been suggested such as openness, being conventional, playful thinking, and risk taking (Barron and Harrington, 1981). These characteristics remain controversial. The fact is that most severe psychiatric patients are not creative at all and a certain coherence in mental activity is necessary for creativity. On the other hand, it is also striking that emotional instability, often with the need for strong aVective support by specific persons, is a very common feature in major artists. The New York abstract expressionists active in the 1940–1960s are a fascinating illustration of emotional psychopathology, with 12–13 out of 15 of them being aZicted by depressive disorders or alcohol abuse, with suicide attempts or psychiatric therapy (Schildkraut and Otero, 1996). Joan Miro´ also is an interesting example of creativity associated with unstable, depressive mood in the context of mild bipolar fluctuations (Schildkraut and Otero, 1996). Indeed, depression may be associated with incubation processes developing without avert expression, which may then be expressed in art works with subsequent mood fluctuations. Imagination and integration of dream memories into reality are often features, which may facilitate creativity. It has been suggested that modularity, that is, specificity for one domain, is characteristic of creativity and genius, but there INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74011-9

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are spectacular exceptions, for example, Leonardo da Vinci. The capacity to ‘‘disinhibit,’’ in a jacksonian sense, repressed, controlled mental processes is illustrated by the attempt of numerous artists to achieve a ‘‘low arousal’’ state, which may allow the emergence of more ‘‘spontaneous’’ expressions. The unique development of creativity in painting, which characterized the early twentieth century, is often put in parallel with a behavioral disinhibition of individuals, who associated with destructive activities (Dada performances, for instance) before renewed art forms emerged. This should be viewed as a major evolutionary step taken by art during the preceding century, without forgetting that nonreligious ‘‘art’’ itself is a rather recent development. While art obviously has a biological basis on brain activity (Bogousslavsky and Boller, 2005), it is unknown how the recent evolution in art corresponded to specific changes in mental processes. For instance, why did the classical anecdote referring to Kandinsky ‘‘inventing’’ abstract art after experiencing the shock of seeing one of his paintings placed upside-down not happen before ? Was this only due to previous social pressure and inhibition? Why did abstract, nonfigurative art subsequently become one of the major ways of expression in painting in the last century? The ability to produce something ‘‘beautiful’’ does not appear to be linked to emotional stability, as emphasized earlier, or to higher ethical standards, or superior intelligence. Although a minimal IQ is often required for dealing with the mental processes associated with creativity, this is not invariable. While nature is often perceived as intrinsically beautiful, processing by man is necessary for natural objects, places, and so on, to be considered beautiful works of art. The search for beauty is likely to correspond to the expression of a brain stereotype, which may however be largely modulated by culture influences. Besides its aesthetic value, an art work may have other, often contradictory, nonaesthetic values. One is monetary, while the other is more perceptible in the absence of a strong aesthetic value. The fascination exerted by ugly or strange works, such as Marcel Duchamp’s 1917 ‘‘fountain’’ readymade (Fig. 1), is actually questionable. Indeed, Duchamp’s readymade has become one of the most famous art works of the twentieth century, although it is just a urinal put upsidedown intentionally by the ‘‘artist.’’ Ambiguity, defined as the brain evoking several perceptions, interpretations, or solutions simultaneously, has been emphasized as the source of this fascination that goes beyond the aesthetic features of art works (Zeki, 1999). I personally prefer the notion and term of ‘‘mystery’’ or ‘‘openness’’ of an art work, which may include conflicting, ambivalent and ambiguous elements. Heironymus Bosch and more recently de Chirico, Magritte and surrealist painters have been great masters in this specific emphasis of this nonaesthetic value of their productions. More than the beauty of a work, these nonaesthetic features force the observer to reconstruct additional mental images


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FIG. 1. Marcel Duchamp’s readymade ‘‘Fountain’’ refused by the jury at the New York. Independent artists exhibit in 1917. Reprinted with permission from Prolitteris, Zurich.

of what they are looking at, justifying Matisse’s word that an active, creative process is a basic characteristic of looking at art. Art works that simultaneously elicit emotional (beauty) and intellectual (mystery, conflict) responses may achieve the strongest artistic stimulation, but the way how creation of works originates and develops in the brain remains a matter of speculation. Three main stages are displayed in Fig. 2: (1) perception processing; (2) extraction (delineating major features) and abstraction (synthesizing what has been extracted); and (3) execution. This complex combination of sensory, cognitive, and motor activities emphasizes the holistic functioning of the brain in creativity, while also showing that specific, focal brain lesions may alter or disrupt the process. In specific patients, such as autistic ‘‘idiots savants,’’ the lack of emotional or other interfering influences, together with a failure in the abstraction–extraction process may lead to pure reproductions of items (landscapes and so on) with full details and absence of any hierarchy between them. The importance of the frontal lobe in creativity is underlined by the earlier mentioned motor skills and the critical role of extraction–abstraction processes,

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FIG. 2. Schematic whole brain functioning in artistic creativity. Reprinted with permission from Prolitteris, Zurich.

which necessitate a particularly eVective relationship between tertiary sensory and prefrontal cortices. Table I summarizes frontal lobe functions that may play a critical role in creativity. The frontal cortex probably has both proactive and inhibitory roles in creativity processes, which necessitate sophisticated motivation, programming, internal representation, and interpretation abilities, being generated and maintained through frontal lobe activity. The extraction–abstraction abilities as well as the elaboration of works attended by outside aesthetic considerations also suggests that well functioning frontal systems are fundamental to artistic activities. But the role of frontal disinhibition also appears to be critical for allowing the emergence of the novelty prerequisite of creativity. The jacksonian concept of ‘‘unmasking’’ functions that are usually inhibited during day-to-day living seems crucial to various forms of creation, including poetry, jazz improvisation, the automatic writing of the surrealists, or the often quoted reference that artists are commonly attempting ‘‘to get back to infancy,’’ in order to eliminate acquired social and personal constraints that limit their creative power. A reverse example may be writer’s block in which increased mentalization and eVorts for inspiration induce a circulatory inhibition to creative thinking. Convincing clinical examples of increased creativity with decreased frontal lobe functioning are provided by several cases of frontotemporal dementia (FTD) (Miller et al., 2000; Tanabe et al., 1996), or more spectacularly, a start in


TABLE I FRONTAL LOBE AREAS POTENTIALLY INVOLVED

IN

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artistic painting activities in nonpainters. These surprising outbursts of creativity correspond well to a progressive decline in frontal performances associated with the evolving dementia. There are also some convincing examples of pathologyinduced changes of creativity in focal frontal or frontotemporal damage in famous artists or writers, such as Georges Braque and Guillaume Apollinaire, who both suVered from traumatic brain injury during the First World War. Braque dramatically modified his cubist style in 1917 after having been trepanned, while the poet Apollinaire started to paint colorful watercolors (Fig. 3) rather than writing poetry after his right-sided anterolateral head wound in 1916 (Bogousslavsky, 2003a).

II. Change in Creativity and Style in Artists after Brain Lesion

Diseases aVecting the brain have also been reported to influence creativity in famous painters, musicians, writers, and philosophers (Bogousslavsky and Boller, 2005). Dostoevsky’s and Flaubert’s epilepsy, Van Gogh’s illness, De Chirico’s

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FIG. 3. Example of a watercolor, which the poet Guillaume Apollinaire started to paint shortly after his head wound in 1916. Reprinted with permission from Prolitteris, Zurich.

migraine or epilepsy, or Ravel’s neurodegenerative disease have been repeatedly emphasized in relationship to their productions. Stroke cases have also been studied with reference to subsequent artistic activity, including Caspar David Friedrich, Arnold Bo¨cklin, Lovis Corinth, Otto Dix, Paul-Elie Gernez, and other less famous ones. In 24 professional painter cases from the literature, in whom changes in creativity could be assessed over a mean survival of 9 years (Hennerici and Baëzner, 2005), the chronological influence of stroke was definite in most of them (20/24), with a rather balanced involvement of both hemispheres (left: 9; right: 12; other: 3). A famous, recent, example in a nonpainter is the film director Federico Fellini, who produced interesting humoristic drawings after a right


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hemisphere stroke associated with left hemineglect and hemiplegia (Cantagallo and Della Sala, 1998). Although the role of whole-brain functioning behind creativity is emphasized earlier, it is interesting that various stroke locations have been associated with an association in creativity in artists. But in painters, there is a special emphasis on posterior circulation stroke, probably because of the common involvement of visual systems (Bogousslavsky, 2000, 2003b).

III. Change of Style in Artists

Since style is mostly involuntary and the most personal signature in artistic production corresponding to the uniqueness of each individual and his brain, it is not surprising that even subtle brain dysfunction can result in specific stylistic modifications in a given artist. Linking a change of style to a brain lesion is far from being easy for many reasons. First, evolution of style over an artist’s life is a natural phenomenon, which can be associated with ‘‘ageing’’ in its broadest sense, including maturation. Second, smooth or small stylistic changes may be diYcult to trace and identify. Finally, other factors apart from brain disease may trigger stylistic changes, which may not correspond to any specific, identifiable factor. Pablo Picasso is one of the twentieth-century artists whose style has evolved the most, renewing itself several times over the years, sometimes dramatically, in the absence of any brain disorder and usually without clear triggering factors. Francis Picabia, Wasily Kandinsky, and others also showed a changing style until their death at an advanced age, again without evidence of neurological disease. Marc Chagall provides an opposite example, since some of his works separated by over 50 years are very similar in style. Giorgio de Chirico developed a curious behavior to ‘‘fight’’ against his own, natural, stylistic evolution, by copying his older paintings up to 17 times for some works, which is a rare example of ‘‘authentic forgery’’! However, we do not know how his neurological problem (partial complex epilepsy or migraine with aura) (Bogousslavsky, 2000, 2005) influenced this unusual behavior. Recent concepts attached to brain plasticity are particularly attractive to this issue of stylistic evolution in artists (Blanke and Landis, 2005), whether or not in relation to brain lesion but no specific research is available. Apart from a few stroke cases, the most convincing examples of change in artistic style associated with a brain disorder is found in patients developing dementia. I mentioned earlier the reported cases with FTD, who either started artistic painting or changed their style of painting in connection with cognitive decay (Miller et al., 2000; Tanabe et al., 1996). A fascinating example in a famous

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artist is the case of Willem de Kooning, who developed progressive dementia (labeled ‘‘Alzheimer’s disease’’ with toxic factors related to alcohol intake) over nearly 2 decades (Espinel, 1998), corresponding to marked stylistic change while his previous style had little evolved in the preceding years (Fig. 4). While his late, ‘‘demented’’ works are quite striking and display a strong aesthetic value, it is obvious that they correspond to marked simplification of the previous painting’s structure. While it could be argued that de Kooning’s work kept the same

continues


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FIG. 4. Evolution of style before (A–D) or while (E–H) dementia developed in the famous painter Willem de Kooning. Reprinted with permission from Prolitteris, Zurich.

quality or sophistication standards, these may in fact reflect some progressive impoverishment of his brain abilities. Nevertheless, the indisputable aesthetic value of these late productions still support the point that creativity in dementia may be maintained even while being transformed or displaced. Interestingly, the reported stylistic changes in patients with FTD also display some form of

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impoverishment with increased tendency to reproduce images semiphotographically (landscapes . . .), rather than freely interpreting them, as this had been the case before dementia. Because strokes are focal and well defined in time, their brain lesion impact on creativity in artists is fascinating, but the stylistic changes in the painters who resume their activity after stroke may be subtle and diYcult to delineate beyond the acute phase. For instance, the well-known German artist, Lovis Corinth (1858–1925) had a right hemisphere stroke in 1911: while this has been claimed as the main trigger that made him evolve toward the vivid expressionism in his later years, it is not obvious to diVerentiate this evolution from that of his contemporary fellow painters without stroke. While Corinth’s early works after stroke display clear signs of left hemineglect and novel spatial distortions, these elements subsequently faded away or were integrated into Corinth’s general expressionistic evolution. Other cases of stroke in painters summarized in the Hennerici and Ba¨zner’s series (2005) are more convincing, including Daniel Vierge and Anton Ra¨derscheidt. Paul-Elie Gernez, ‘‘Alajouanine’s painter’’ (Bogousslavsky and Boller, 2005) was another example, who showed that severe aphasia was not an obstacle to successful resumption and development of artistic painting after stroke; his case also emphasized the interesting role of change in the painting hand in recovery from stroke. We studied a right-handed 71-yearold painter with left thalamic infarct and hypaesthetic hemiataxia, who became ambidextrous for painting as a consequence of stroke (Annoni et al., 2005); this corresponded to stylistic changes with an evolution from an impressionist manner to a more joyous, geometric, and simplistic art (Fig. 5). The patient claimed that when he wanted to use brighter, vivid colors, he was using his left hand, while the reverse was true for the right hand. Another patient, a well-known local painter, had a left occipital infarct involving part of V1 and V2 leading to hemianopia and recurrent flashes, which significantly modified his work, as he switched to a more stylized and symbolic art (Annoni et al., 2005). A third patient of ours, a painting teacher aged 78, had minor posterior circulation stroke involving the pons (with ataxia), which also modified her work toward more synthetic and symbolic output. Common features in these patients included: 1. Initial unwareness of stylistic change, which was noted by relatives and the public 2. Lack of obvious personality change 3. Latent emotionalism and mood instability 4. Minor executive dysfunction on test batteries 5. Absence of any other significant cognitive impairment. These illustrative cases of the impact on artistic output from stroke should be put in balance against cases in which repeated strokes did not seem to alter creativity or lead to any stylistic changes. Such an example among famous artists


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FIG. 5. Pre- (A) and poststroke (B) paintings in a professional painter, who developed a left thalamic infarct. Reprinted with permission from Prolitteris, Zurich.

is Balthus (Balthazar Klossowski de Rola), who little modified his artistic style over the last 50 years of his life, despite multiple subcortical strokes and bilateral internal carotid artery occlusions.

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Obviously, much remains to be reported and studied in the neurobiology of artistic activity, despite diYculties inherent by the apparent lack of formal rules in this domain. Our understanding of human creativity will be markedly improved when we are able to delineate better brain functioning during the genesis of an art work, both in healthy and brain-diseased painters.

References

Annoni, J. M., Devuyst, G., Carota, A., Bruggimann, L., and Bogousslavsky, J. (2005). Changes in artistic style after minor posterior stroke. J. Neurol. Neruosurg. Psychiatr. 76, 797–803. Blanke, O., and Landis, Th. (personnal communication, 2005). The metaphysical art of Giorgio de Chirico. Barron, F., and Harrington, D. M. (1981). Creativity, intelligence, and personality. Ann. Rev. Psychol. 32, 439–476. Bogousslavsky, J. (2000). Le cerveau et l’art, aux frontie`res de la neurologie. Me´d. Hyg. 2300, 1027–1029. Bogousslavsky, J. (2003a). L’amour perdu de Gui et Madeleine. Le syndrome e´motionnel et comportemental temporal de Guillaume Apollinaire. Rev. Neurol. (Paris) 15, 171–179. Bogousslavsky, J. (2003b). The neurology of art: The example of Giorgio de Chirico. Eur. Neurol. 50, 189–190. Bogousslavsky, J., and Boller, F. (Eds.) (2005). Neurological disorders in famous artists. ‘‘Frontiers of neurology and neuroscience.’’ Karger, Basel. Cantagallo, A., and Della Sala, S. (1998). Preserved insight in an artist with extrapersonal spatial neglect. Cortex 34, 163–183. Espinel, Ch. (1998). De Kooning’s late colours and forms: Dementia. Lancet. Hennerici, M. G., and Ba¨zner, H. (2005). Personal communication. Miller, B. L., Boone, K., Cummings, J. L., Read, S. L., and Mishkin, F. (2000). Functional correlates of musical and visual ability in fronto-temporal dementia. Br. J. Psychiat. 176, 458–463. Schildkraut, J. J., and Otero, A. (Eds.) (1996). ‘‘Depression and the spiritual in modern art.’’ John Wiley & Sons, Chichester. Tanabe, H., Nakagawa, Y., Ikeda, M., Hashimoto, M., Yamota, N., Kazui, H., Nishikawa, T., and Okuda, J. (1996). Selective loss of semantic memory for words. In ‘‘Brain Processes of memory’’ (K. Ishikawa, J. L. Mc Gaugh, and H. Sakata, Eds.), pp. 141–152. Elsevier Science B. V., Amsterdam. Zeki, S. (1999). ‘‘Inner vision: An exploration of art and the brain.’’ Oxford University Press, Oxford.

ARTISTIC CHANGES IN ALZHEIMER’S DISEASE

Sebastian J. Crutch and Martin N. Rossor Dementia Research Centre, Department of Neurodegeneration, Institute of Neurology University College London, United Kingdom

I. II. III. IV. V.

Introduction Willem de Kooning (1904–1997) and Other Artists with Alzheimer’s Disease William Utermohlen (b. 1933) Positive and Negative Cognitive Phenomena Conclusions References

I. Introduction

Examination of the relationship between artistic endeavor and neurological disease presents a number of fascinating opportunities and puzzling dilemmas. Exploring how aspects of human behavior may alter or remain stable in the context of damage to the central nervous system lies at the core of several scientific disciplines, including behavioral neurology and cognitive neuroscience. Painting and other acts of artistic creativity constitute behaviors that are both susceptible to change following neurological insult and amenable to scientific study, being dependent as they are upon a complex array of cognitive and emotional processes. However, it is this very same reliance upon multiple, concurrent strands of feeling and thought that makes alterations in artistic production so diYcult to assign to specific aspects of neural dysfunction. The scientific investigation of human cognitive disorders tends to favor situations in which component processes can be explored in isolation or in which the influence of concomitant variables or skills can be controlled for. Unlike tasks such as word reading, for which subcomponent processes like visual word processing, comprehension of meaning, and production of the word name can be assessed relatively independently, the act of painting cannot be divided so easily. Although healthy artists rely upon a number of cognitive tools, which can be subjected to quantitative assessment in order to perform their trade (e.g., appreciation of color, form, texture, and space), the coherent use of these skills to complete a portrait, scene, INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74012-0

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or sketch is dependent on a further set of much more elusive cognitive phenomena such as creativity and originality. While questions about how the brain supports such complex, multifactorial characteristics are of undoubted neuroscientific interest, the organization and localization of brain areas underlying artistic creativity and ingenuity are currently very poorly understood. As a consequence, painting remains an area in which scientists are often restricted to making qualitative judgments about the pertinence of neurological deficits to aspects of artistic production. In establishing a link between painting ability and a variety of neurological conditions, the most fundamental issue is whether or not a change has occurred in some aspect of the work produced by the aVected individual. The identification of putative change is in itself not necessarily easy to determine because of the variability of the themes expressed within each painting. Unlike formal neurological, physiological, or radiological assessments in which change is indicated by discrepant performance on a unitary sets of tests or questions administered at two points in time or compared to some normative standard, direct comparison of the structural or stylistic elements of paintings is made diYcult because successive paintings are rarely repeats of the previous creation. In those artists who do appear to exhibit some reliable alteration in their paintings, the much more controversial question that follows is whether this change is directly attributable to alterations in neurological state or whether it represents a stylistic change made deliberately to reflect symptoms, experiences, or feelings connected to the event. In some ways, attempting to distinguish between intentional stylistic changes in artwork and those enforced by disease may be a false distinction to draw, given the almost inevitable connection between the psychological and neurological states. However, in this chapter, the assumption is made that in addition to intentional expressive alterations to artistic production, individuals with neurodegenerative diseases inevitably experience cognitive dysfunction that has the potential to limit and impair the artist’s ability to realize their creative and expressive intentions through painting. Above and beyond these general issues relating to how and whether we should examine the links between painting and neurology, there are a specific set of concerns, which have to be addressed when considering artistic change following progressive neurodegenerative disease, which may not always apply to other more transient or monophasic forms of neurological illness. First, many neurodegenerative diseases exhibit an insidious onset with pathological changes occurring as much as several years before the earliest cognitive and behavioral symptoms. Therefore, unlike individuals who suVer a neurological insult which can be clearly temporally defined (e.g., major stroke, traumatic brain injury), assessing the point at which dementia may or may not have begun to influence the topic, style, or quality of an artist’s work may be severely hampered by uncertainty over the onset and speed of progression of the disease. Second,


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degenerative disease can result in contrasting patterns of cognitive deficits, which, particularly in the more advanced stages of the disease process, might aVect many aspects of function that were required to support premorbid artistic endeavor. Moreover, symptom complexes associated with diVerent degenerative diseases, such as Alzheimer’s disease (AD) and Pick’s disease, can vary widely and even within a single disease, such as AD, the clinical phenotypes of individuals with the same underlying pathology may diVer considerably. With the emergence of atypical presentations of AD in which the predominant early impairment can be in visual or linguistic processing rather than the more commonly described amnestic variant, it becomes clear that in some circumstances the disease may first impinge directly upon skills that are critical to the artistic process while in other circumstances the production of paintings consistent with the premorbid style may continue relatively unaVected for some time. Third, the onset of degenerative disease is frequently accompanied by symptoms of psychiatric illness, such as depression, which in itself may be suYcient to account for observed changes in artistic style. Indeed, depression independent of degenerative disease has been cited as a significant influence upon the work of a number of major artists, for example Mark Rothko (Ravin et al., 1978). Finally, any assessment of artistic changes must take account not only of the expression of the disease from which the individual suVers but also the speed or rate at which that condition progresses. Unlike individuals who suddenly acquire clear-cut deficits, artists with a slowly progressive dementia may for sometime retain suYciently preserved artistic skills to comment powerfully on their developing condition. Although all forms of neurodegenerative disease might reasonably be expected to encourage or dictate some form of alteration in the nature of paintings which an individual might produce, the focus of this chapter is on AD. Alzheimer’s disease is the most prevalent form of dementia, accounting for 40–60% of cases with a 10–12% overall lifetime risk of developing the condition. The hallmarks of the condition are senile plaques (largely consisting of the peptide -amyloid) and neurofibrillary tangles (aggregations of tau protein) in the cerebral cortex. Consequent dysfunction and demise of neurons result in cerebral atrophy and a developing pattern of widespread cognitive and behavioral impairment. While a decline in recent episodic memory is the most common presenting symptom and a central aspect of clinical diagnostic criteria, subtle disturbances in the multiple cognitive domains of language expression and comprehension, literacy and numeracy, perception, praxis, and executive function may all be present quite early in the disease course, along with more general disturbances of personality and intellectual reasoning. Independent functioning and activities of daily living tend to decline gradually, while routine or enjoyable activities or hobbies, such as painting, are often eventually abandoned.

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II. Willem de Kooning (1904–1997) and Other Artists with Alzheimer’s Disease

In the context of this progressive deterioration of higher order functions, the work of a number of professional and amateur artists with AD has been described and the diVerences between paintings completed before and after realization of disease onset considered. Perhaps foremost of the work considered in this light is that of the Dutch–American abstract expressionist Willem de Kooning. Originally trained at the Royal Academy of Arts in Rotterdam, de Kooning moved to USA in 1926 but did not start painting full time until 1935. His first solo exhibition was held in New York in 1948, and twice during his career, paintings by de Kooning became the most expensive works in history to be painted by a living artist. Over 4 decades, de Kooning gradually moved from producing realist portraits and advertising drawings to highly abstract washes of form and color designed to express raw emotions and psychological states. In 1989, de Kooning was given a diagnosis of probable AD from which he may have been suVering for up to 10 years, although the diagnosis was clouded by years of alcoholism and poor nutrition. Consequently, the work of the artist during the 1980s has been examined very closely to assess whether it reveals signs of the ongoing disease process (Espinel, 1996; Storr, 1995). The works that serve best as a reference point for his later productions are paintings, such as Untitled (1970–1977), which feature thick brushstrokes, heavy use of paint, complex combinations of color, and frequent repainting and scraping of the canvas. By contrast, many of the paintings produced by de Kooning in the 1980s, such as Untitled III (1986), were much simpler in style, with fewer overlapping forms, and a tendency to concentrate upon the colors red, white, and blue. Changes in the style were accompanied by alterations in working practice; whereas de Kooning had previously been notoriously slow to finalize paintings, often repainting sections again and again for up to 18 months, at times during the mid-1980s de Kooning produced a canvas per week with the help of his assistants. The quality of these later paintings was a subject which divided critics at the time and since. While some considered the paintings to be poor reflections of his former achievements with less impact, intensity, and inventiveness, others viewed the works as a summary of his career and cited a comparable tendency toward simplicity in the later works of other major artists such as Monet. What was agreed upon was that a change in artistic style had occurred, which was associated, at least temporally, with the development and progression of probable AD. Several other case reports of professional or amateur artists who went on to develop AD have been published in the medical literature. Although none of the artists featured has the renown or familiarity of de Kooning, each serves to highlight some aspect of the way in which artistic endeavor can be modified by disease. One artist, Carolus Horn (1921–1992), worked as a graphic artist for an


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advertising agency and also painted landscapes and still life scenes for pleasure (Maurer and Prvulovic, 2004). Symptoms of memory loss were first noted at the age of 58 and were followed by diYculties with temporal and spatial discrimination and a decline in language, calculation, and reasoning skills. Alterations in artistic ability are most clearly observable in a series of landscape scenes, one of the Eiserner Steg Bridge in Frankfurt and one of the Bridge of Sighs in Venice, which were painted on two separate occasions several years apart. With careful examination, subtle disturbances of perspective are observable in both the latter paintings relative to the former and the quality of representation is simpler with less shading and blending of colors. A series of later paintings completed around the age of 66 or 67 also appear to introduce a number of unrealistic and symbolic figures, which were untypical of previous work and have prompted speculation that the artist was incorporating aspects of visual hallucinations experienced as part of his dementia into his artistic works. The last pieces completed by Horn are free from both form and color and consist of scribbling in either horizontal or vertical sections. A more mild deterioration in artistic abilities appears to be demonstrated in the paintings of the Canadian artist Danae Chambers (b. 1941). An established portrait artist in Canada and abroad, Chambers was given a diagnosis of probable early onset AD in 1996 following up to 6 years of memory loss, disorientation, and increasingly poor self-care (Fornazzari, 2005). Although continuing to paint until her institutionalization in 1999, her paintings and in particular her self-portrait work reveal subtle disturbances of form and spatial arrangement. Although the overall composition and organization of the painting appears preserved, frequent attempts to repaint the face and a sense of disproportion between the facial features suggest that weakened perceptual and spatial skills may have contributed to a diYculty in realizing the artist’s creative intentions. Nonetheless, the artist’s continuing ability to complete a rather successful portrait despite progression to a state of severe AD is impressive and suggests that cognitive skills essential to the painting process remained relatively preserved in this individual until late in the disease course. Further evidence about the cognitive demands of painting has been obtained from studies of amateur and naı¨ve artists with and without dementia. For instance, Cummings and Zarit (1987) reported the case of a farmer who was an accomplished amateur artist and who regularly produced oil paintings of landscape scenes. At the age of 67, changes in personality, memory, and judgment were noted, and 3 years later a formal diagnosis of probable AD was made. As with the artist Carolus Horn, alterations in artistic style were observable most easily by comparison of a painting of a landscape scene completed around the time of diagnosis with three further eVorts at the same scene attempted 7, 8, and 9 years after diagnosis. The three pictures all demonstrate an increasing loss of perspective and detail with only the first being completed in oil paints. The latter

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two pieces were pencil sketches drawn not from the original scene but by copying earlier attempts. Cummings and Zarit argue that the mere completion of these attempts at complex figure drawing in the face of global and severe intellectual decline might indicate either resilience of the visuomotor and visuoperceptual skills required to create art or an asymmetric presentation of AD, which tended to spare the right hemisphere relative to the left. Nonetheless, it remains an empirical question as to whether the artistic skills of amateur artists might be less resilient than those of professional artists in the face of neurological insult. The landscape drawings of this amateur artist, like the scenes painted by Carolus Horn, also highlight the fact that paintings with such neutral themes might enable quantitative comparisons of structural elements of artistic works but make judgments of emotional content and personal expression very diYcult.

III. William Utermohlen (b. 1933)

As noted previously, one diYculty in assessing whether the progressive deterioration in cognitive function typical of AD is matched by a progressive alteration in artistic ability is the variability of thematic content of consecutive paintings. However, this concern was largely circumvented in the case of another professional artist who developed AD, William Utermohlen (Crutch et al., 2001). This artist provided the opportunity to assess directly whether a change in artistic ability had occurred because from around the time of his diagnosis onward he produced a series of self-portrait paintings. By their very nature, the thematic content of this series of artworks was held relatively constant. William Utermohlen was born in Philadelphia and studied at the Pennsylvania Academy of Fine Arts from 1951 to 1957. In 1957, he moved to England where he enrolled at the Ruskin School of Art in Oxford before settling in London. Much of his early work was characterized by linear expressionism, with frequent inclusion of Pop imagery and styles, including a use of strong colors. Utermohlen completed several major works, including murals at the Liberal Jewish Synagogue in St. John’s Wood and the Royal Free Hospital in Hampstead, and also produced many charcoal and pencil line-drawings of friends and nudes. Common themes for his painting include his wife, groups of friends, and aspects of human emotion and psychology, as particularly illustrated in a series of works known as the Conversation Pieces produced in 1980s and early 1990s (Fig. 1). However, in 1995 William Utermohlen was referred to a neurologist with suspected depression and cognitive impairment, and a diagnosis of probable AD was made. The earliest symptoms of the condition could be traced back approximately 4 years and involved diYculties with tying a necktie, calculating household finances, and memory for day-to-day events. Mood had also become rather suppressed


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FIG. 1. An example from the Conversation Pieces (c. 1985).

and subdued. Formal neuropsychological examination revealed a moderate degree of global cognitive deterioration, while MRI indicated generalized cerebral atrophy. Following the initial diagnosis at the age of 61, regular clinical assessments indicated a gradual decline in cognitive function, which was supported by a progressive fall in scores on the Mini-Mental State Examination (Folstein et al., 1975) and on subsequent neuropsychological assessment at the age of 65. At this latter assessment, the domains of cognition most severely aVected were verbal memory, visuoperceptual and visuospatial skills, and executive functioning. Thus, a progressive increase in disease severity was documented over the course of approximately 5½ years. Two reference points can be provided against which the style and form of self-portraits painted after the diagnosis of AD can be compared; one self-portrait from much earlier in his career and a second painting completed at the age of 60, before any discernible change in artistic abilities had been noticed by the artist or his wife (Figs. 2A and B). These images not only provide a technical reference point and demonstrate the ability of this artist but also illustrate the range of styles and modes in which William Utermohlen painted. It is with such stylistic variation in mind that any assertions regarding the intentionality of subsequent changes in brush technique and color scheme must be made with extreme caution. Although some observers might attribute any or all apparent shifts in

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FIG. 2. Self-portrait series. Painted at approximately age 40 years (A), at 60 (B), at 62 (C), at 63 (D), and at 64 (E). Pencil drawings at age 66 (F). Reproduced with permission from The Lancet.

the nature, quality, theme, or precision of productions to intentional artistic device, independent evidence of a decline in certain fundamental artistic skills was gathered from an analysis of drawing tasks, which were relatively free from


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FIG. 3. Pencil sketch of ‘‘a welcoming man’’ drawn at age 61. Reproduced with permission from The Lancet.

stylistic bias. In particular, simple figure-copying tasks (e.g., drawing two interlocking pentagons) were shown to be subject to spatial and organizational errors, while an attempt to produce a simple line drawing of a male figure resulted in an image containing an organizational error, which the artist knew to be present but was unable to correct (Fig. 3). The portraits painted after the diagnosis of AD appear to be characterized by less precise brushstrokes, more overlapping and reworking of lines, and qualitatively rawer, less clean surfaces. One portrait painted at the age of 62 appears to show the first signs of a diYculty in representing individual facial features (Fig. 2C). In particular, the quality of the leftmost eye and cheek shows clear similarities to the way in which facial features are represented in the self-portrait work of the artist Danae Chambers, with an apparent loss of sharpness and precision. Another point made strongly by this particular self-portrait by Utermohlen is the importance of timing and attitude when considering a specific artistic production. The artist himself highlights the inclusion of a saw on the right side of the portrait as a point of thematic significance, reflecting his recently acquired understanding from his physicians that AD remains a diagnosis which can only be confirmed by histopathological examination. In this way, this portrait provides not only a suggestion that AD

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had degraded aspects of Utermohlen’s artistic skill but also a comment by the artist upon his experience of and reaction to both the disease and the medical profession. The relatively subtle diYculties with the representation of facial features seen in Fig. 2C appear more pronounced in a further portrait painted at the age of 63 (Fig. 2D). Here, the sense of proportion has altered particularly with respect to the ear and the forehead and the spatial arrangement of the facial features appears somewhat disordered. The painting and repainting of the eyes, eyebrows, and lower forehead suggests that the unusual positioning of eyes in the portrait may not necessarily have been intended by the artist. This spatial disorganization is also seen in the portrait painted at the age of 64 in which the features appear either blurred or strangely disjointed (Fig. 2E). In commenting on this work, both the artist and his wife attributed the unusual form of the piece to a decline in painting ability rather than to an intentional change in artistic style. However, the strong usage of the color red in the area near the leftmost ear perhaps indicates that Utermohlen continued even at this stage of the disease to attempt an artistic interpretation rather than simply a faithful representation of the face in the mirror before him. Latterly, Utermohlen abandoned oil painting and resorted to pencil sketches in which only the most essential components of the face are recognizable (Fig. 2F). With a continued desire to express himself through his artistic activity, Utermohlen also embarked on a further but dramatically diVerent set of selfportrait pieces, using a much more abstract style (Figs. 4A–D). The paintings are all more primitive than the earlier self-portraits, not only in form and color but also in perspective, presenting a direct rather than oblique view. Despite the absence of the detail that identified the earlier pieces as self-portraits, these abstract works are among Utermohlen’s most dramatic and evocative, and they keenly express many of the emotions he experienced at the time of painting, including terror, sadness, anger, and resignation. Indeed, inscribed in a shaky hand on the reverse of one portrait (Fig. 4B) was the single word ‘‘fear.’’ The stylistic alteration engendered in these abstract paintings may reflect the artist’s appreciation that the realism of his earlier works was no longer attainable, but for all that, their mere production, let alone their quality and theme, clearly indicates a significant preservation of the creative urge, which had always underpinned Utermohlen’s artistic production.

IV. Positive and Negative Cognitive Phenomena

Studying the paintings of individuals with AD can provide a powerful and original insight into the experience of dementia. The work of the artists reviewed earlier, and in particular the manner in which their paintings changed or altered


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FIG. 4. Abstract self-portraits painted at the age of 65. Reproduced with permission from The Lancet.

over time, makes a powerful statement about the nature of the disease and, most importantly, about the person whom the disease was aVecting. Furthermore from an artistic perspective, such works have inherent value with respect to the skills and talents required to create them and their capacity to move, stimulate, and engage the viewer. From a purely scientific point of view, however, one might also ask what if anything can be learnt about the brain or its systems and

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processes by investigation of creative acts in the context of a neurological disease. For many, the answer to this question might be very little, given the unconstrained environment in which paintings are naturally created and the way in which the subject matter, style, and design of each piece are determined by the artist and not a scientific investigator. For these reasons, the investigation of the brain basis of visual artistic production has been limited largely to the drawing of shapes, lines, and simple scenes in individuals with static and progressive brain injury. On tasks involving the copying of simple figures, a clear relationship has been found between the quality of errors made and the location of brain lesion. Individuals with damage to the right cerebral hemisphere show a tendency to misrepresent the spatial relationships between parts of an image or to neglect entire sections of their drawing. By contrast, individuals with left hemisphere damage generally show maintenance of spatial relationships but often oversimplify the details of a picture (Arrigoni and De Renzi, 1964; Gainotti and Tiacci, 1970; Warrington et al., 1966). Assessments of the drawing abilities of individuals with AD appear to show a combination of these errors. More specifically, the drawings of AD patients tend to be characterized by fewer angles, more impaired perspective, greater simplification, and less accurate representation of spatial relations than healthy age-matched control subjects (Kirk and Kertesz, 1991). Drawing changes of this nature are held to be the consequences of negative cognitive phenomena, including visual apperceptive agnosia and visuospatial agnosia, and have in fact contributed to our understanding of how these functions are localized in the brain. Although the painting of individuals with dementia is undoubtedly prone to the influence of negative cognitive phenomena, such as the inability to accurately perceive and represent form and space, this medium of expression may oVer an invaluable insight into a number of less commonly or less easily studied cognitive consequences of brain atrophy and neural dysfunction. Whereas AD is associated with many negative cognitive phenomena (e.g., a lost or degraded ability to perceive form clearly), in some patients the condition can also produce or exacerbate certain experiences and sensations, which healthy individuals either do not have or are unaware of. These experiences can be labeled positive cognitive phenomena. One such phenomenon is that of abnormally prolonged color afterimages. It is well recognized that prolonged visual fixation upon a colored stimulus, followed by removal of the colored stimulus and fixation upon a neutral stimulus, can elicit the apparent perception of a color complimentary to that of the preceding stimulus. In healthy individuals, this eVect is short lived lasting approximately 2–6 s depending on stimulus duration and has been attributed by some researchers to the physiological properties of wavelength selective cells in occipital area V1, which display chromatic opponency characteristics, being excited by light of a certain wavelength and inhibited by light of a complementary spectral composition (Livingstone and Hubel, 1984; Zeki, 1983). However, it


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has been reported that the duration of color afterimages may be increased in the context of posterior cortical atrophy attributable to probable AD (Chan et al., 2001). Quantitatively, afterimages may endure for four times longer than in healthy individuals; while qualitatively such patients report abnormal washes of color across the visual environment and can experience the concurrent perception of a predominant color that is present in the visual environment and its complimentary but absent hue. Such distortions of color perception, even if not as pronounced as in the case reported by Chan et al. (2001), might well be expected to influence or confuse the color selection and mixing of an artistic individual when painting. Other positive visual phenomena include visual instability and visual hallucinations. Visual instability is most commonly reported in patients with an atypical, posterior presentation of AD (e.g., bi-parietal AD) (Galton et al., 2000; Ross et al., 1996) and refers to the perceived motion of static stimuli. Patients with visual instability report that elements in their visual environment ‘‘bounce around’’ or ‘‘move over one another’’ and often have great diYculty performing spatial tasks such as counting dots. This disorder is reminiscent of reports made by children with developmental dyslexia regarding the movement of letters and words, but it is unclear whether the experience reflects primary cortical dysfunction or a magnocellular impairment, which leads to unsteady binocular fixation (Stein, 2001). However, perhaps the most striking examples of positive cognitive phenomena are the visual hallucinations described by individuals with AD and more frequently by those with Dementia with Lewy Bodies. Visual hallucinations include linear distortions and disruptions (e.g., perceiving the edge of a table or a door frame to bend and flex) but most notably the perception of human and animal figures. Such figures are typically well formed, silent, and passive and may in some instances be triggered by environmental stimuli. However, visual hallucinations represent a good example of a positive cognitive phenomenon, which can influence the theme of artistic sketches and paintings. The most profound illustration of this influence is found in the work of the artist Mervyn Peake (1911–1968) who developed parkinsonian features and cognitive deficits consistent with Dementia with Lewy Bodies during his 5th decade (Sahlas, 2003). Aside from diYculties with visuospatial perception, attention, and memory, a number of Peake’s later works appear to reflect the visual hallucinations, which he was experiencing at the time of painting. Perhaps of principal interest is a series of sketches featuring figures with pointed heads. Such images are extremely compatible with multiple, independent anecdotal reports from other patients with Dementia with Lewy Bodies who describe hallucinating about figures with pointed hats or heads, often likened to characters such as ‘‘Coco the clown.’’ The recurring theme of misshapen heads both within Peake’s own works and in the verbal reports of other individuals appears to indicate some form of commonality either in the processes by which visual hallucinations are represented or

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by which they are triggered. Through works, such as those of Mervyn Peake, one can see how the examination of works painted by artists with dementia may serve to illustrate and highlight aspects of cognitive dysfunction, which otherwise would remain either undocumented or confined to verbal reports and descriptions.

V. Conclusions

In summary, in this chapter an attempt has been made to consider the opportunities and problems of studying and evaluating paintings produced by artists with neurodegenerative conditions such as AD. The diYculties of making controlled, empirical assessments of artisitic ability and how it may alter following neurological disease have been discussed. In particular, it has been noted that painting is in many ways too large and involved a process to be diluted down into a small set of component skills for which quantitative tests or measures can be conceived. It has been suggested that the works of artists, such as Willem de Kooning and William Utermohlen, demonstrate that it is possible to follow the evolution of artistic change in AD and analyzing the component parts of a painting can be informative about the specific cognitive influences upon visual artwork. However, an increase in the scientific understanding of the neural processes involved in the artistic process is by no means the only motivation for studying the paintings of individuals with degenerative conditions such as AD. On the contrary, painting can provide a means by which those with dementia who are blessed with artistic abilities can express their reactions to their circumstances and can provide for the viewer a powerful insight into both the disease and how we ourselves might respond to the experience of dementia.

Acknowledgment

We are grateful to Patricia Utermohlen and the Lancet for allowing us to reproduce the artwork of William Utermohlen. This article was written in loving memory of Ron Isaacs BA RGN RMN (1946–2003) who worked with William Utermohlen for many years.

References

Arrigoni, G., and De Renzi, E. (1964). Constructional apraxia and hemispheric locus of lesion. Cortex 1, 170–179.


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Chan, D., Crutch, S. J., and Warrington, E. K. (2001). A disorder of colour perception associated with abnormal colour after-images: A defect of the primary visual cortex. J. Neurol. Neurosur. Ps. 71, 515–517. Crutch, S. J., Isaacs, R., and Rossor, M. N. (2001). Some workmen can blame their tools: Artistic change in an individual with Alzheimer’s disease. Lancet 357, 2129–2133. Cummings, J. L., and Zarit, J. M. (1987). Probable Alzheimer’s disease in an artist. JAMA 258, 2731–2734. Espinel, C. H. (1996). De Kooning’s late colours and forms: Dementia, creativity, and the healing power of art. Lancet 347, 1096–1098. Folstein, M. F., Folstein, S. E., and McHugh, P. R. (1975). Mini-mental state: A practical method for grading the cognitive state of patients for the clinician. J. Psychiatr. Res. 12, 189–198. Fornazzari, L. R. (2005). Preserved painting creativity in an artist with Alzheimer’s disease. Eur. J. Neurol. 12, 419–424. Gainotti, C, and Tiacci, C. (1970). Patterns of drawing disability in right and left hemispheric patients. Neuropsychologia 8, 379–384. Galton, C. J., Patterson, K., Xuereb, J. H., and Hodges, J. R. (2000). Atypical and typical presentations of Alzheimer’s disease: A clinical, neuropsychological, neuroimaging and pathological study of 13 cases. Brain 123, 484–498. Kirk, A., and Kertesz, A. (1991). On drawing impairment in Alzheimer’s disease. Arch. Neurol 48, 73–77. Livingstone, M. S., and Hubel, D. H. (1984). Anatomy and physiology of a color system in the primate visual cortex. J. Neurosci. 4, 309–356. Maurer, K., and Prvulovic, D. (2004). Paintings of an artist with Alzheimer’s disease: Visuoconstructional deficits during dementia. J. Neural. Transm. 111, 235–245. Ravin, J. G., Hartman, J. J., and Fried, R. I. (1978). Mark Rothko’s paintings: Suicide notes? Ohio State Med. J. 74, 78–79. Ross, S. J., Graham, N., Stuart-Green, L., Prins, M., Xuereb, J., Patterson, K., and Hodges, J. R. (1996). Progressive biparietal atrophy: An atypical presentation of Alzheimer’s disease. J. Neurol. Neurosur. Ps. 61, 388–395. Sahlas, D. J. (2003). Dementia with Lewy bodies and the neurobehavioral decline of Mervyn Peake. Arch. Neurol. 60, 889–892. Stein, J. (2001). The magnocellular theory of developmental dyslexia. Dyslexia: Int. J. Res. Practice 7, 12–36. Storr, R. (1995). At last light. In ‘‘Willem de Kooning: The Late Paintings, the 1980s’’ ( J. Jenkins and S. Engberg, Eds.), pp. 39–80. Wallace Carlson, Minneapolis. Warrington, E. K., James, M., and Kinsbourne, M. (1966). Drawing ability in relation to the laterality of cerebral lesion. Brain 89, 52–82. Zeki, S. (1983). Colour coding in the cerebral cortex: The responses of wavelength selective and colour coded cells in monkey visual cortex to changes in wavelength composition. Neuroscience 9, 767–781.


SECTION IV CEREBROVASCULAR DISEASE


STROKE IN PAINTERS

H. Ba ¨ zner and M. Hennerici Department of Neurology, University of Heidelberg Universita ¨ tsklinikum Mannheim 68135 Mannheim, Germany

I. Introduction II. Case Studies of Painters with Right Hemisphere Stroke A. Anton Ra¨derscheidt B. Otto Dix C. Johannes Thiel D. Lovis Corinth E. Wolfgang Aichinger-Kassek F. Federico Fellini G. Reynold Brown H. Tom Greenshields I. Schnider et al. J. Vigouroux et al. K. Blanke et al. L. Guglielmo Lusignoli M. Kurt Schwitters III. Case Studies of Painters with Left Hemisphere Stroke A. Paul-Elie Gernez B. Daniel Urrabieta y Vierge C. Zlatyu Boijadjiev D. Ernst Oldenburg E. Beni Ferenczy F. Polish painter ‘‘R. L.’’ G. Afro Basaldella H. Arnold Bo¨cklin I. Caspar David Friedrich IV. Other Cases A. The Case of an 87-Year-Old Artist B. Tommy McHugh C. Jon Sarkin V. Conclusions References

I. Introduction

A stroke may befall anyone because brain lesions caused by cerebrovascular disease are common and can result in devastating disability. Improvements in modern neurophysiological, neurosonological, and continuously developing INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74013-2

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neuroimaging technology have led to precise lesion localization, giving a better understanding of pathophysiological mechanisms leading to stroke. Recent developments in neuropsychology have revealed certain irregularities as a consequence of stroke depending on lesion extent and localization. Although our knowledge is growing regarding the eVects of stroke on the majority of patients, when facing the specialized individual and highly developed skills of professional visual artists and lacking a reasonably large patient collective, few authors have aimed at analyzing systematically the consequences of stroke in such a group. On the other hand, some very interesting case reports have been produced, going back to the early twentieth century. A seminal article including the cases of four German professional artists with right hemisphere lesions has been published in 1974 by Richard Jung (1974) (Chapter 14 by Blanke in this volume). Prof. Jung, chairman of the department of Neurology and Clinical Neurophysiology at Freiburg University, was a clinical neurologist and researcher with a special interest in the neurophysiology of the visual system; he was also an amateur and collector of modern German artwork, and his study reported the cases of Anton Ra¨derscheidt, Lovis Corinth, Otto Dix, and Johannes Thiel. By reviewing the literature and adding several additional cases, totaling a number of 24 professional visual artists, we will try to comment on common features of right versus left hemisphere damage with an emphasis on artistic production. We are well aware of the limitations of our eVort, since the freedom of art rarely follows simplistic rules, and as artists and art historians will not always share the neurological point of view, we are obliged to interpret our observations with care.

II. Case Studies of Painters with Right Hemisphere Stroke

A. ANTON RA¨DERSCHEIDT Anton Ra¨derscheidt (October 11, 1892–March 3, 1970) started his artistic career in Cologne, the town of his birth. His portraits and figure paintings were shown in the famous ‘‘Neue Sachlichkeit’’ exhibition in Mannheim in 1925. He was a protagonist of the ‘‘magic realism’’ in which persons and their surroundings were painted close to photographic art, the emotional content being reduced to a minimum, as opposed to the contemporary expressionistic painters. He emigrated from Germany in 1934 to live in Switzerland, England, and France until 1949, when he returned to Cologne with his second wife. His artistic style changed after 1950, when he became inspired by cubism. On September 24, 1967, shortly before a large retrospective exhibition in Cologne, Ra¨derscheidt suVered a stroke with severe visual disturbances and a

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mild left hemisyndrome. He had a left homonymous hemianopsia with left-sided hemineglect, a disturbance of spatial orientation and an initially severe prosopagnosia. The problem of face recognition was so severe that he was unable to recognize even close relatives, a problem that persisted for several weeks. Beginning in December 1967 and continued over the period from January to June 1968, Ra¨derscheidt painted an enormously large series of self-portraits with the intention of compensating for his severe left-sided hemineglect. In Jung’s study (1974), the improvement of his neglect was illustrated using five of these selfportraits, set of four (Figs. 8B and 9A–C of Jung’s study) ones being later repeatedly published (Butter, 2004; Gardner, 1977). The change in artistic style in his late paintings displaying couples or nudes has already been discussed by Jung, who noticed a stronger aVective relationship. Ra¨derscheidt’s son Pascal, who runs a remarkable website (http://www.raederscheidt.com) presenting biographical data and a large collection of his father’s artwork, says that his father referred to these paintings as ‘‘Bo¨se Bilder’’ (nasty paintings). Ra¨derscheidt is cited with the following remark concerning his stroke, ‘‘Using all of my willpower, I intended to force my eyes to see correctly again. [. . .] A stroke has taken me away from the scene of life; oVstage the play is going on with me. I am no longer the director of this play. I have to take care, not to miss my entrance in the play. My requisites obey to tricks only. Moreover, I am missing my loud colours. [. . .] The reproduction of my surroundings is a damned diYcult thing. Nothing is staying in its place, nothing is keeping the shape. Perhaps I will be able to get hold of a credible shape now if I can use this permanent motion. [. . .] In the past it felt like hunting [shape], now it feels more like catching a trout in moving water using bare hands. [. . .] Painting is like taming beasts of prey’’ (Richter, 1972). Neurological examination was not repeated, and he died in March 1970, but Jung assumed that his hemianopsia was unchanged and that the painter learned to compensate for his neglect ( Jung, 1974). As to artistic expression, a total revolution occurred after his stroke: compared to his earlier grouped figures and couples, which are lacking any emotional content and avoid personal contact, his poststroke paintings are overloaded with wild colorful brushstrokes, display ecstatic scenes, often depicting couples in close personal contact (‘‘bo¨se Bilder,’’ Fig. 1A and B). Persons, who had previously been painted in a very realistic manner, are grossly deformed, the artist using brighter colors and a larger variety of colors. B. OTTO DIX Otto Dix (December 2, 1891–July 25, 1969) was born in Untermdorf near Gera, studied in Du¨sseldorf and Dresden, and became a professor of arts of the Dresden Academy of Arts in 1927. He was well known in his early years for his naturalistic-veristic style, and was painting large series of war scenes, having been

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FIG. 1 (A and B). Anton Ra¨derscheidt’s post-stroke paintings display ecstatic scenes, often depicting couples in close personal contact. Persons are grossly deformed, the artist using brighter colors and a larger variety of colors compared to his pre-stroke art. A moderate left sided hemineglect can be noted. Part A and B # VG Bild-Kunst, Bonn, 2006.

a soldier in the First World War. His portraits in 1920s were often over characterized and displayed ugly human figures close to caricature. His paintings were classified as ‘‘degenerate,’’ and he was forced to leave the academy of arts in 1933. He moved to the Bodensee, where he stayed over 30 years until his death in 1969 (Schubert, 1980). On November 13, 1967, Dix suVered a right hemisphere stroke with left-sided hemiparesis, left hemineglect, partial hemianopsia, and mild spatio-constructive disturbances. Moreover, a reduced proprioception and apraxia of his left arm were noted by his treating neurologist, Prof. Gunter Baumgartner of Zu¨rich. In the first 3 days following the stroke, Dix was unable to draw at all. On day four, after the onset of symptoms, he could draw a simple and small sketch of a tree, with a unilateral shadowing giving the tree a plastic appearance. The left part of the paper was left free indicating his neglect. One week later, the neglect seemed widely compensated in a second sketch of a tree (both sketches are documented in Dix’ patient chart in Zu¨rich University Hospital and are reproduced in Jung, 1974), but we cannot support Jung’s view of an unchanged drawing style. His drawing was altered noticeably at least in his last self-portraits; self-portrait with black collar (1968), small self-portrait (1968), self-portrait with a hand (1968), and self-portrait as a skull (1968) all share a missing resemblance to the painter. This is substantially diVerent from the self-portraits Dix painted in 1957 (Fig. 2B), 1964 (Fig. 2C), and 1967, whose similitude is very close to the photographs showing Dix at the

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FIG. 2. Otto Dix’ drawing style was altered noticeably in his last self-portraits. Self-portrait with black collar (1968, Fig. 2D), small self-portrait (1968, Fig. 2F), self-portrait with a hand (1968, Fig. 2E) and selfportrait as a skull (1968) all share a missing resemblance to the painter. This is substantially different from the self-portraits Dix painted in 1957 (Fig. 2B), 1964 (Fig. 2C), and 1967 whose similitude is very close to the photographs showing Dix at the respective dates (Fig. 2A). Part A–F # VG Bild-Kunst, Bonn, 2006.

respective dates (Fig. 2A). Self-portrait with black collar bears a certain resemblance to Dix, but spatial relations and facial structures are disturbing, with his closed right eye seemingly protruded (Fig. 2D). The painter’s face appears to be held upon the left side of the portrait by a frame-like band, seemingly preventing the painters head from falling forward. Small self-portrait has much of a caricature (Fig. 2F), and self-portrait with a hand shows the painter’s hand holding the pencil in the forefront of the drawing covering most parts of the lower face (Fig. 2E). On this right hand, we count more than five fingers; the same observation can be made with certitude in his last large self-portrait with Marcella (1969) in which Dix holds the little girl with both hands. At his right hand, six fingers can be diVerentiated. Dix continued to paint until his death, working mostly on lithographs. He died of a second stroke on July 25, 1969 in Singen.

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C. JOHANNES THIEL Johannes Thiel (September 11, 1889–September 31, 1962) traveled in Europe after studies at the academies of art in Munich and Stuttgart. He lived in Kirchzarten near Freiburg, producing landscape and figure paintings as well as book illustrations. His best artwork, according to Jung (1974), was his watercolor landscapes in which Thiel reached perfection in the 6th and 7th decades of his life. Thiel suVered two strokes with left-sided hemiparesis in 1959 (facial paresis on the left and mild weakness of the left hand with complete recovery) and 1960 (with a permanent left hand weakness) but recovered fairly well and was enormously productive until a third stroke in 1962 put an end to his life. Except for a portrait sketch done in the days following his first stroke, Jung was unable to notice any change in style or signs of neglect. Jung examined Thiel after his third and subsequently fatal stroke and described a left-sided hemiplegia and hemianopsia ( Jung, 1974). D. LOVIS CORINTH Lovis Corinth ( July 21, 1858–July 17, 1925) certainly has the most interesting patient history of this case series (Chapter 14 by Blanke). This German painter was one of the most important and innovative artists of the period and is nowadays represented in the major museums and galleries of Europe and USA (Schuster et al., 1996). After his study period at academies in Ko¨nigsberg and Paris, he lived in Munich for about 10 years. Then a ‘‘realistic naturalist,’’ he moved to Berlin, where he settled down in 1901, to work as a painter and teacher of arts. He founded the first women’s painting school of Berlin, and his first pupil, Charlotte Berend, became his preferred model and his wife in 1902 (Uhr, 1990). In Berlin, Corinth rapidly succeeded to become a leading member of the Berlin ‘‘Secession’’ with Liebermann and Slevogt to form the triad of German impressionism. Besides his paintings of landscapes, portraits, nudes, and still-lives, Corinth was dedicated to biblical, mythological, and literary subjects. Moreover, he produced large quantities of drawings, lithographs, etchings, and watercolors. Later, his style changed substantially, and he became a protagonist of expressive (or expressionist) realism. In November 1911, Corinth sustained a right hemisphere stroke with a leftsided hemiparesis and hemineglect and a subsequent severe depressive episode. After this, he limped when tired, his gait became shuZing, and his left hand no longer obeyed when he tried to perform intricate tasks (Berend-Corinth, 1958a, b). Later photographs show a spastic posture of his left arm and hand, but his wife states that he used his weak left hand to press the copper plate to his body while engraving (Schuster et al., 1996; Uhr, 1990). In the days immediately following the stroke, Corinth describes dream-like optical sensations and states further that

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he had come face-to-face with death (Corinth, 1923). According to Horst Uhr (1990), ‘‘in one form or another virtually all his subsequent works bear the mark of this experience.’’ Critics agree that Corinth’s works underwent a change of style, but they are unanimous in attributing this change to purely psychological factors such as depression and intensified awareness of the fragility of human life, increasing preoccupation with death, and heightened capacity to seize the essence of objects and experience. Alfred Kuhn, a contemporary critic who edited an early Corinth monograph in 1925, interpreted his late works as follows, ‘‘When Corinth arose from the sickbed, he was a new person. He had become prescient for the hidden facets of appearance . . .. The contours disappear, the bodies are often as if ript asunder, deformed, disappeared into textures . . . also the faithfulness of portraits had ceased almost entirely . . . all detailed execution came to nothing. With wide stripes the person is captured in essence. Characterisation is now exaggerated, indeed, often to caricature . . . models, no matter who they are, are now just objects to be painted . . .. Indeed, the models must suVer every deprivation. Corinth always seems to be painting a picture behind the picture, one which he alone sees . . . at this point Corinth shifted from the ranks of the great painters to the circle of great artists’’ (Kuhn, 1925). Other than might be expected, Corinth’s productivity was even growing after recovery. Close to 500 paintings, over 800 prints, and scores of watercolors and drawings—more than half of all his works date from this period (Uhr, 1990). However, he focuses on self-portraits, family portraits, and landscape and produces large series of lithographs and etchings, partly as illustrations to books. ‘‘My entire life passed before me, a life which in this lonely battle seemed more precious now than when I was young and strong. I was forced to reckon with myself. [. . .] But time seemed so very short’’ (Corinth, 1926). The first products after his stroke are very fascinating; while still on the sickbed, Corinth asked for pencil and paper and sketched a series of horrible monsters and strange ghost-like images of famous figures from history, apparently, none of these drawings has survived. When Charlotte accompanied him on returning to his studio for the first time, she watched as he gazed long in the familiar large mirror. In her diary-like memoirs, she writes ‘‘Again and again he moaned in despair, black thoughts attacked him [. . .]. I had no more ideas to console him. [. . .] Then suddenly, he reached for palette and paint, sat down and quickly dashed oV this first of a long series of sorrowful self-portraits’’ (BerendCorinth, 1958b). In fact, this self-portrait shows the painter wearing a coat over the pajama from his sickbed. The self-portraits following his stroke show a continuous process of confrontation with his declining physical constitution and were to focus on his physical frailty and mental anguish. In early February 1912, using the ‘‘vernis-mou’’ technique he made a small engraving showing the sick painter as ‘‘Job with his friends’’ (Fig. 3). His son, Thomas, remembered that Hermann Struck, a friend of Corinth, assisted with the preparation of the

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FIG. 3. Lovis Corinth’s self-portraits following his stroke show a continuous process of confrontation with his declining physical constitution and were to focus on his physical frailty and mental anguish. In early February 1912 he made a small engraving showing the sick painter as ‘‘Job with his friends.’’ # Kupferstichkabinett. Staatliche Museen zu Berlin.

printing plate (Corinth, 1979). In the print, Job is depicted while sitting on the floor with crossed legs, his right hand is placed on the right foot, the supinated and palmarflexed lame and atrophic left arm is resting on the floor, his right foot is supinated. Job is wearing a cape that Corinth had used in earlier self-portraits. The title of the etching contains a small mistake in the mirrored text with a twist of the character ‘‘&.’’ With Charlotte, he traveled to Bordighera on the Italian Riviera in spring 1912, which was intended to serve as a kind of rehabilitation stay. There he completed a small pencil self-portrait that hardly resembles the painter. Several similar studies at this time show a left-sided neglect with missing parts of right upper extremities. A pencil drawing of his wife also finished in Bordighera grossly lacks texture, her dress looks lifeless; the lack of plausible anatomical articulation results in a strong sense of compression, his wife appearing ill at ease (Schuster et al., 1996). In contrast, a very appealing balcony scene in Bordighera shows his wife on the balcony of the hotel at the moment she unfolds a small parasol. Following Horst Uhr, this painting lacks correct perspective with the vertical lines of the hotel’s facade not matching and the building appearing to lean to the left (Uhr, 1990). Later Bordighera paintings, however, seem to reflect his ongoing recovery. The first large painting of 1912 shows ‘‘Samson blinded’’ as a martyred and desperate figure, grasping in the direction of the observer, insecure, and not yet relying on his regained forces

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(Uhr, 1990). In a preparatory pencil study for ‘‘Samson blinded,’’ the biblical figure is grotesquely distorted (Schuster et al., 1996). Still in October 1912, 11 months after the stroke, a small pencil study of his wife still shows a marked neglect with missing contours of the left face (reproduced in Corinth’s autobiography in 1926). We agree with Jung (1974), who finds the neglect compensated after 1913 in landscape paintings but notices several occurrences of uncertainty in the reproduction of left-sided facial aspects in his self-portraits. Here, the artist has to fixate strongly on his face in a mirror. In doing so, a visual field defect focused in the parafoveal region might become apparent. Interestingly and other than famous colleagues, Corinth never corrected the mirror eVect in that, the right handed painter holds the pencil in the left hand in all of his self-portraits (however, this can be noticed also prior to his stroke!). (The detailed analysis of Corinth’s self-portraits is given in Chapter 14 by Blanke in this volume.) The sequelae of his stroke were reported by Corinth’s wife Charlotte, who described her husband’s anxiety and depression and the exhaustion following the slightest physical exertion (Berend-Corinth, 1958b). According to Uhr ‘‘she aided him as he struggled to summon up his strength. She laid out the colours before him, placed palette and brushes in his encumbered left hand, and removed them from his stiV and swollen fingers when he had finished painting. When his own hand failed to provide adequate support, she gently and tactfully helped to steady his sketchbook’’ (Uhr, 1990). Remarkably, Charlotte writes in her memoirs on several occasions of her husbands ‘‘first’’ stroke, although a definite description of a second stroke is never given. On the occasion of his 60th birthday, Corinth had a syncopal attack as far as can be gathered from his wife’s diary (Berend-Corinth, 1958b). Certainly, the judgment of an art critic or art historian will be diVerent from that of a neurologist familiar with the consequences of right hemisphere damage. Of course, the artist reacts to the ‘‘stroke attack’’ with thematic changes and may be obliged to paint stylistic variations. But as Gardner (1977) has pointed out, the specific features altered in Corinth’s work are striking: loss of contours (e.g., in the portrait of the painter Gro¨nvold, 1925 or in ‘‘Frauenraub,’’ 1918), misplacement of details (e.g., etching of ‘‘Knecht Franz,’’ 1919, with asymmetric arms), neglect and obscuring of texture (e.g., in ‘‘Susanna and the Elders,’’ 1923 and ‘‘Birth of Venus,’’ 1923), alteration of emotional nuance (e.g., portrait of his son Thomas with a hat in his hands, 1922), increased subjectivity (e.g., in ‘‘Carmencita,’’ 1924, compared with a prestroke painting of a similar subject, Woman with a black mask, 1908, Fig. 4), idiosyncrasy (e.g., in ‘‘Still Life with Flowers, Skull, and Oak Leaves,’’ 1920), obscurity (in several Walchensee paintings of 1924 and 1925). Further, we would add dissimilarity of familiar faces in portraits (e.g., in an engraving of his wife in 1920, compared to a prestroke portrait of 1911, Fig. 5A and B), lack of correct perspective (e.g., ‘‘On the Balcony in Bordighera,’’ 1912, ‘‘Berlin unter den Linden,’’ 1922), and lack of anatomical exactitude (e.g., study for ‘‘Samson

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FIG. 4. Lovis Corinth’s post-stroke paintings show a marked increase in subjectivity. A good example for this feature is the painting ‘‘Carmencita’’ (1924, Fig. 4B, by courtesy of Sta¨delsches Kunstinstitut, Frankfurt am Main, Sta¨delscher Museums-Vereine. V.), the last portrait of his wife Charlotte. In contrast, a prestroke painting of a similar subject, ‘‘Woman with a black mask,’’ dating from 1908 (Fig. 4A, ‘‘Die schwarze Maske’’, by courtesy of Staatliche Museen Kassel), is much more realistic.

FIG. 5. Corinth’s post-stroke portraits demonstrate a definite dissimilarity of familiar faces such as in a pencil drawing of his wife in 1920 (Fig. 5B, Lovis Corinth, German, 1858–1925, Portrait of Charlotte Berend-Corinth, 1920, graphite on ivory wove paper, 457 300 mm (max.), Gift of Dennis Adrian in memory of Charlotte Berend-Corinth, 1968.20, The Art Institute of Chicago. Photography # The Art Institute of Chicago. Detail) compared to a prestroke portrait of 1911 (Fig. 5A, # 2006 Museum Associates/LACMA).

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blinded,’’ 1912 and ‘‘Pieta,’’ 1920). These examples could be completed by a more thorough analysis of Corinth’s total oeuvre, but to be fair, large parts of his late work are simply superb products of a great artist and do not bear any ‘‘pathological features,’’ either from the point of view of a critical neurologist and ambitious pathographer. On the other hand, Corinth’s immense number of artwork allows a detailed study of some very subtle consequences of his cerebrovascular disease. E. WOLFGANG AICHINGER-KASSEK Wolfgang Aichinger-Kassek is an Austrian artist, who suVered a right hemisphere stroke on the basis of arterio-arterial embolism from a severe carotid stenosis in 1995 (Aichinger-Kassek, 1995). When he recovered slowly from his stroke, he noticed that he was unable to continue working on his sculptures that he had constructed using heavy materials, cut from metal welded iron. As a reaction to this drawback, he produced a series of ‘‘neurological folios’’ comprising 30 colored graphics. His daughter, a consultant in neurology, writes in the preface to this collection: ‘‘As soon as the acute stage of the apoplectic fit was over, it gave way to thoughts regarding his future artistic career. They all ended with the question of whether creative activity would still be possible. For many long months, the phases of depression and despair seemed to hold the upper hand and the paralysis of thought and inspiration outweighed all other problems. The artist’s dependency on his ideas obliged [him] to assume the role of waiting in uncertainty of his fate. But then, from one day to the next, feelings and inspirations forced their way to the surface. It became possible to represent pictorially the phases of depression, fear, of incursions into his own body, the hospital environment. Most of the works in this cycle were created within a few days (Fig. 6). The person W.A. now sees prospects for his future once again.’’ Aichinger-Kassek himself comments on his stroke as follows: ‘‘Apoplexy—that’s a stroke of lightning in life’s thunderstorm! It attacks you! And fells you like a blossoming tree. The stroke is the insidiousness of an unexpected menace. It’s danger and warning. The stroken [sic!] one is defeated by a depressive attack while his life is passing before his eyes like a trashy movie. Apoplexy—that’s also a determination of life-positions consisting in bygone past and uncertain future. In all, uncertainty is a serious component of insidiousness.’’ F. FEDERICO FELLINI The case of the famous Italian film director and skilled painter and cartoonist Federico Fellini (1920–1993) was reported extensively in 1998 by Cantagallo and Della Sala (1998), who followed the artist for 2 months after a CT-documented

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FIG. 6. Wolfgang Aichinger-Kassek, an Austrian artist suffered a right hemisphere stroke in 1995. As a reaction, he produced a series of ‘‘neurological folios.’’ According to the artist’s daughter, they represent ‘‘pictorially the phases of depression, fear, of incursions into his own body, the hospital environment.’’ (Private collection).

right temporo-parietal ischemic stroke that left the artist with a severe sensorimotor hemisyndrome and left inferior quadrantanopsia. Fellini was examined in detail for his left visuomotor hemineglect syndrome, including neglect dyslexia as well as some evidence of altered processing with neglected parts of the stimuli. The artist was aware of his motor and attentional deficits but unable to functionally compensate for them. The documents of visuomotor neuropsychological testing are reproduced in the paper and demonstrate besides the pure neuropsychological deficit a remarkable introspective analysis of the artist’s own situation, including some quite ironical and sometimes provocative though charming personalized ruminations. G. REYNOLD BROWN Reynold Brown (1917–1991) received his first art education in Alhambra High School in California. The following information was obtained through the website designed and maintained by his son Franz (http://www.geocities. com/chapulinas). He illustrated and drew a comic strip and produced illustrations for service manuals, several magazines, and pocket books. In 1950s,

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Brown decided to come back to freelance illustration and took a teaching position at Art Center College of Design, where he taught figure and head drawing for 26 years. At that time, he started a series of movie posters for the large film companies and for record jacket covers. From 1970s, Brown concentrated on fine art painting, with western themes as his preferred subject, and succeeded by selling about 250 oil paintings, including portraits, harbor scenes, and landscapes. In 1976, Brown suVered a severe stroke together with a myocardial infarction leaving him with a severe left-sided hemiparesis and hemineglect syndrome. Compared to his colleagues suVering from right hemisphere damage, Brown was hit by the stroke in even more devastating manner, since the paralyzed left arm was his ‘‘drawing arm,’’ and his doctors’ prognosis as to future artistic work was pessimistic. His doctors were wrong; similar to Corinth and his wife Charlotte, Brown was helped to retrain his physical abilities during his first steps back into art by his wife Mary Louise, who was an artist as well. She was working with him everyday so that he first started to draw and then paint again. Emphasis was put into the eVort of teaching the ‘‘good’’ right arm. Brown had to battle further a very dense left lower quadrantanopsia, which made him tend to leave the lower left portion of the canvas unpainted; he started each session on the right side of a painting, which resulted in canvasses heavily worked on the right and thinly painted on the left. His portraits were disorganized with a marked distortion of facial structures, similar to Corinth’s and Ra¨derscheidt’s (self ) portraits. Franz Brown comments on a stretching eVect present from upper right to lower left, which decreased with time. The same eVect can be seen in several of Corinth’s portraits and self-portraits and in the series of Ra¨derscheidt’s self-portraits. A further source of frustration was the limited use of his previously dominant left hand, due to a severe reduction of tactile sense. In summary, according to his son, he was subsequently unable to do the highly representational work of his prestroke years but ‘‘was nonetheless able to produce some powerful drawings and beautiful landscape paintings of Nebraska,’’ where he settled in 1983 and remained until his death in 1991. Franz Brown states that his portraits ‘‘for some [. . .] carry a greater emotional impact than the more realistic work of his earlier years. His landscapes became looser and more painterly,’’ and he ‘‘seemed to see the world on diVerent, more intense colours.’’ The cited homepage (http://www.geocities.com/chapulinas) contains a series of most remarkable drawings and paintings by Brown, done in the period after his right hemisphere stroke (Fig. 7). In a striking similarity to the early poststroke artwork by Lovis Corinth, Brown’s drawings show a severe left-sided hemineglect, which improves through the following years but is never perfectly resolved as far as can be assessed from the paintings exhibited.

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FIG. 7. Reynold Brown’s drawings and paintings produced in the period after his righthemisphere stroke resemble strikingly to the early post-stroke artwork by Lovis Corinth and Anton Ra¨derscheidt. His drawings show a severe left sided hemineglect, which is improving through the following years. Reproduced with permission of the Tejeda-Brown family.

H. TOM GREENSHIELDS Tom Greenshields (1915–1994), an accomplished and well-known painter and sculptor was 75 years old, when he had a right hemisphere stroke in August 1989 (Halligan and Marshall, 1997). His symptoms included a mild sensorimotor hemisyndrome on the left side, left lower quadrantanopsia, and left visual neglect. Eight years earlier, he had lost the use of his right painting arm in an accident. Therefore, he had learned to transfer his artistic skills to the left hand and continued to work as painter and sculptor and to sell and exhibit his artwork. After his stroke, despite good physical recovery of his left arm and hand function, he became frustrated because of poorly constructed and less elaborate drawings, compared to his prestroke creations. He concentrated on the right side of his drawings and sculptures and neglected the left parts; moreover, his artwork showed distorted, exaggerated or deformed figures. On neuropsychological examination, visuospatial neglect was confirmed. Similar to Reynold Brown, he would ignore food on the left side of the plate. A photograph of a sculpture in Halligan’s paper (Fig. 1 bottom) shows a clay sculpture with intact facial proportions on the right side of the face and very incomplete modeling of the left parts of the face. Similar disturbances can be noticed in Fig. 2, a drawing of a sitting man with missing left face, left shoulder, and left parts of the chair. According to Halligan, residual traces of neglect were still discernible until the death of the artist in 1994. This is the single case of a sculptor with a severe neglect described so far reflecting the diYculty of the right hemisphere damaged individual to detect and depict the third dimension.

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I. SCHNIDER

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ET AL.

Schnider et al. (1993) described the case of an unnamed Swiss artist in 1993 who suVered a CT-documented large ischemic infarct in the right temporoparieto-occipital region. Post-stroke drawings diVered markedly from prestroke ones with changes reflecting both behavioral and mood disturbances. This artist exhibited hemispatial neglect, hallucinations, hyperverbalization (he would include much text in his early post-stroke sketches), and rapid cycles of a bipolar disorder. His drawings became simplified, more sketch-like, although the technical characteristics seemed similar to the premorbid artwork. Remarkably, the severity of neglect expressed in his drawings was highly variable and could change within hours. J. VIGOUROUX

ET AL.

Vigouroux et al. (1990) published the case of an artist with right hemisphere stroke in 1990. This unnamed ‘‘well-known French painter’’ exhibiting a large variety of stroke risk factors, presented with a severe left-sided sensorimotor hemisyndrome, including a severe left homonymous hemianopsia. Shortly after the stroke, he experienced a severe depressive episode, apparently reflected in his drawings that, according to the authors, were of minor quality at that point, although particularly expressive at the same time. This period was followed by a phase of rich pictorial production. Remarkably, these drawings and paintings showed no alteration of figural shape or volume, no change in style, and unchanged artistic topics compared to the premorbid period, in spite of a variably severe hemineglect. K. BLANKE

ET AL.

Recently, Blanke et al. (2003) published the case of a 71-year-old artist with mild left neglect as the consequence of a right parietal hemorrhage. Within her post-stroke drawings, she used minimal color on the left, whereas she colored the right side completely and evenly. Thus, she was able to produce the correct forms of images in the left visual hemifield but not the colors. L. GUGLIELMO LUSIGNOLI Guglielmo Lusignoli (born in 1920) was aVected by a right hemisphere stroke in 1987 at the zenith of his creativity and artistic production (Mazzucchi et al.,

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1994). He suVered from hemineglect and left-sided paresis but resumed his work and was enormously productive after the stroke. M. KURT SCHWITTERS As far as can be told from his biography (Orchard et al., 1998), the famous German Dada artist Kurt Schwitters (1887–1948) suVered a right hemisphere stroke in 1944 with subsequent paresis of his left arm. A second stroke (presumably an hemorrhage) occurred in February 1946. In December 1945, he writes ‘‘I am [now] painting smaller formats and do some very small modelling, pocket format. My sculptures are a new experience for me, they are my best works now.’’ Further evidence for any alterations in artistic expression is scarce.

III. Case Studies of Painters with Left Hemisphere Stroke

A. PAUL-ELIE GERNEZ Paul-Elie Gernez (1888–1948) was recently identified by Boller (2005) as the painter in Alajouanine’s seminal paper published in 1948 in Brain (Bonvicini, 1929). Gernez was a prominent member of the French contemporary school, ‘‘because of the originality of matter, technical qualities of realisation and intense individualism of each of his works.’’ Many of his works can be seen in his home town of Honfleur (Normandy) in the ‘‘Euge`ne Boudin’’ museum. When he was only 23-years old, he obtained the post of ‘‘Professeur de dessin’’ at Honfleur high school, and thanks to his art, he was able to become financially independent shortly thereafter. He started with naturalistic paintings and drawings of still lives, nudes, boats, and landscapes, experimented with pointillism and was inspired by cubism toward 1920s. Alajouanine writes that his paintings create feelings of the ‘‘bitter and sensual poetry of Baudelaire’’ and the ‘‘delicious polyphonic music of Debussy’’ (Bonvicini, 1929). In 1940, when he was 52 years old, he was aVected by persistent aphasia after two short and transient episodes. Alajouanine describes the aphasia as of Wernicke type without any phonetic alteration or paresis but with a slight hemianopic defect and accompanied by transient apraxia. Spoken language was disturbed with anomia, severe paraphasia, and severe agraphia, comprehension was relatively preserved as judged from normal conversation and intellect was not altered. The painter was well aware of these deficits, saying that ‘‘there are in me two men, the one who paints, who is normal while he is painting, and the other one who is lost in the mist, who does not stick to life . . .. I am saying very

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poorly what I mean . . .. There are inside me the one who grasps reality, life; there is the other one who is lost as regards abstract thinking. When I am painting I am outside my own life; my way of seeing things is even sharper than before; I find everything again; I am a whole man. Even my right hand that seems strange to me, I do not notice it when I am painting. These are two men, the one who is grasped by reality to paint, the other one, the fool, who cannot manage words anymore’’ (Bonvicini, 1929). Gernez became depressed and irritable and ‘‘increased the isolation to which he was prone.’’ According to Alajouanine, the post-stroke artistic work was just as perfect as before, as he did not notice any changes in his artistic skills or style, and his working speed was unchanged. Connoisseurs believed that he had found even a more intense and acute expression, a view essentially shared by Boller (2005), who had been able to inspect preand post-stroke paintings by Gernez with the help of his family. However, Boller noticed a tendency to a more concrete and realistic style and a certain lack of the ‘‘almost oneiric poetry found in some of his previous paintings.’’ B. DANIEL URRABIETA Y VIERGE Daniel Urrabieta y Vierge (March 5, 1851–May 2, 1904) was born in Madrid to a noted illustrator. Vierge studied at the Madrid Academy and went to Paris at the age of 16 to become a painter and is often referred to as one of the founders of modern illustration. Due to the Franco–Prussian war he was obliged to interrupt his studies and started a career in 1870 as an illustrator for leading Paris magazines and several books, some by Victor Hugo. At the age of 25, he began to prepare for a new kind of illustrated book choosing Quevedo’s ‘‘Pablo de Segovia’’ as his subject. Using the new photo-engraving process for his illustrations, he became known to a broader public when the first edition of this book was published in 1882. However, after he had already finished 90 illustrations, the work on the complete edition of this book had almost been finished, his compellingly straight career was interrupted by a severe stroke on February 14, 1882, when he was just 30 years old (Alajouanine, 1948; Bonvicini, 1926). Charcot, who had been called, thought that he was lost, but he survived and recovered fairly well, although his right side was completely paralyzed and he had lost his speech. His only verbal expression consisted of the recurring word ‘‘paciencia’’ (Spanish for patience), later of repeated syllables such as ‘‘de-de-de.’’ Furthermore, he had a severe agraphia, while comprehension seemed to be well preserved. Over a period of 2 years, his right-sided paresis improved except for his right hand and wrist, which remained weak. Bonvicini (1926) reported that he was still able to roll a cigarette with his left hand on his right arm. The most remarkable aspect was that Vierge learned to draw and paint with his left hand in a period of 6 months. He was able to resume his previous work 2 years after the

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stroke. Interestingly, Vierge made two engravings, displaying the electrotherapy service at the Salpeˆtrie`re, which had been started by Vigouroux with the support of Charcot (Holcomb, 1967). Electrotherapy was a popular method of treatment for paralysis at that time, and Vierge must have hoped to get some improvement for his severe paresis after the stroke. While clearly less prolific as he had been, he completed the remaining 20 illustrations for ‘‘Pablo de Segovia,’’ which was published in the complete edition in 1892. His major achievement, the 257 illustrations for his Don Quixote were all done after his stroke using the left hand. This incredible eVort took him 10 years, before the four volume set was published in an edition of 1150 copies in 1906. Bonvicini comments on a certain change in artistic technical orientation after the stroke with a growing devotion to watercolors and even oil paintings in a realistic style (Bonvicini, 1926). Even though Bonvicini may be correct with regard to technical orientation, the post-stroke paintings that were available to us did not show any major stylistic change compared to the prestroke artwork. Vierge died in 1904 of a second stroke at the age of 53. C. ZLATYU BOIJADJIEV A further case of left-hemisphere stroke in a professional artist is reported of the Bulgarian painter Zlatyu Boijadjiev (October 22, 1903–February 2, 1976). This famous protagonist of contemporary Bulgarian art suVered a left hemisphere stroke, which, according to the 1969 paper by Zaimov and colleagues (Zaimov et al., 1969), may well have been a cerebral hemorrhage. The onset of symptoms was accompanied by a severe headache and a right oculomotor palsy. The artist was severely confused and bedridden but was able to leave hospital for rehabilitation at his home only 5 weeks later. Neurological examination showed a right-sided hemiplegia and a mixed but predominantly expressive aphasia together with the right oculomotor palsy. Only 5 months later, he was able to take a few steps and learned to use a cane; at that time his oculomotor palsy resolved. Neurological examination showed a residual spastic hemiparesis 2 years later, enabling him to walk on his own but with no function in the right distal upper extremity. He had a vocabulary of about 70–80 words and showed variable word comprehension, together with agraphia and alexia. He later developed symptomatic epilepsy. Regarding his artistic career, he had to learn painting and drawing with his left hand, which he tried to do for the first time 3 months after the stroke. Slowly his left hand drawings improved to the degree that enabled him to resume his previous creative output, totaling more than 500 paintings in the post-stroke era. The stylistic changes in these paintings are judged by critics as marking the birth of a new painter, as he now preferred bright colors, and the narrative and naturalistic character of his prestroke paintings were no longer present.

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In contrast, his paintings became richer, more colorful, although more simplified, similar to primitive art, demonstrating great vigor, and inventiveness. Much of the imagery was bizarre and fantastical. D. ERNST OLDENBURG Ernst Oldenburg ( January 8, 1914–January 9, 1992), a locally well-known German painter and sculptor, suVered a left hemisphere stroke at the age of 74 (1988) with a severe paresis of his dominant right arm (Pese and RamasOldenburg, 2004). The first sketch done after his stroke using his untrained left hand shows a very insecure outlining with nonetheless excellent figural composition, although the figures are placed on the left part of the paper, indicating certain neglect on the right. After being discharged from hospital, he resumed his artistic production beginning with a self-portrait that resembles the painter very much and bears no stylistic changes to previous self-portraits. Similar to a selfportrait finished a year later, except for a certain blurring of the left half of his glasses and the left eye, which cannot be diVerentiated from the surrounding texture, no signs of stroke can be inferred. His figural compositions are definitely unchanged to the prestroke paintings, so that we can state that Oldenburg as with Vierge, managed to continue his professional artistry with no significant alteration of painting style and only a mild right visuospatial neglect, despite being forced to transfer his artistic abilities from the right to the left hand. According to his daughter, he had no aphasic disturbance. E. BENI FERENCZY Kornyey reports the case of an artist (Kornyey, 1977) active in drawing and water painting but most prominent in sculpture, later identified as the Hungarian artist Beni Ferenczy ( June 18, 1890–June 2, 1967) (Marsh and Philwin, 1987), who suVered a left hemisphere stroke at the age of 66 years. Right hemiparesis and severe motor aphasia remained persistent in spite of modest progress in his writing performance. Some months after the insult, he resumed his artistic activity using the left hand and continued principally in the same manner as during his prestroke artistic career. His drawing and water painting were basically unchanged apart from some uncertainty of lines and a certain loss of perspective. His pieces of sculpture regained the quality of his earlier works, as proven by the first statue he made after the stroke. This is the single instance of a sculptor with left hemisphere stroke proving essentially unchanged three-dimensional perception and artistic output and contrasts nicely with the case of Tom Greenshields, who was no longer able to return to perfect sculptural production after a right hemisphere stroke.

184 F. POLISH

BA¨ZNER AND HENNERICI PAINTER

‘‘R. L.’’

Kaczmarek described the case of the Polish painter ‘‘R. L.’’ (Kaczmarek, 1991), who was an Associate Professor at the Faculty of Arts, the University of Lublin. R. L. may be the clearest example of an artist with a change in style due to an aphasic disturbance after stroke (Chatterjee, 2004). R. L. suVered a left hemisphere stroke with expressive aphasia. After the stroke, the production of skilled charcoal drawings, easily recognizable self-portraits, and landscapes were still possible, but the painter complained of the loss of his previous ability to paint highly symbolic paintings after his stroke. He was aware of the deficit and said that his mind was blank and he could not return to his premorbid style of symbolic painting. This case uniquely illustrates the need of verbal ‘‘symbolic’’ processing for visual ‘‘symbolic’’ output. G. AFRO BASALDELLA The Italian neurologist Anna Mazzucchi has collected a series of Italian and European painters (Mazzucchi et al., 1994) who had suVered a stroke. Among them, Afro Basaldella (March 4, 1912–July 24, 1976) had a left hemisphere stroke accompanied by profound aphasia in 1971. He reportedly returned to ‘‘neocubism’’ 2 years after his stroke. H. ARNOLD BO¨CKLIN Arnold Bo¨cklin (October 16, 1827–January 16, 1901) had first stroke aVecting his right side of the body in 1892. In an early biography from 1907, von Ostini (1907) comments on a strange case of a very annoying illness that was at its beginning not clear to the doctors, but the use of baths at the seashore brought a sudden recovery; he repeatedly went to San Terenzo near La Spezia. From autumn 1893 until spring 1895, he stayed in Florence with a scarcely restored constitution. The biographer described the paintings Bo¨cklin created at that time by commenting on the growing variety and diVerentiation in the use of colors. The two main final oeuvres were ‘‘The War (1897)’’ and the unfinished ‘‘The Plague (1898).’’ Both are horrifying depictions of the themes with an apocalyptic visionary character. In April 1895, Bo¨cklin settled down in a house near Fiesole. Von Ostini states that from his 70th birthday onwards, the ailments of impeding age brought his artistic production to an end. According to the biographer, his speech and gait were disabled through repeated strokes, and on January 16, 1901 Bo¨cklin died after a brief final illness. In summary, the right-sided paresis and speech disturbance of Bo¨cklin may be interpreted as due to repeated left

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hemisphere strokes, possibly on the basis of recurrent embolism from a left carotid stenosis. Alternatively, one may speculate about repeated minor (lacunar) strokes, as there was only minimal evidence for a true aphasic disturbance. I. CASPAR DAVID FRIEDRICH Caspar David Friedrich (September 5, 1774–May 7, 1840), a well-known German painter of realistic landscapes, suVered a left hemisphere stroke in his 61st year of life (Hinz, 1974; Jensen, 1974), which caused a right-sided hemiparesis. A long stay in Teplice, where he used the warm baths shortly after the onset of symptoms, allowed a fair recovery and enabled the painter to resume his profession. However, he was no longer able to produce large paintings but finished some smaller drawings often displaying desperate scenes such as ‘‘Landscape with Grave, CoYn, and Owl (1836/1837).’’ In a letter to his nephew dated September 1835, Friedrich writes: ‘‘In Teplice, I stayed for six weeks on the advice of my doctor, due to the known reason. Since the day before yesterday, I am back at home. I am fairly well and back on my feet, and hope that the eVects of the baths will continue to work, and will finally enable my hand to do some work. [. . .] Writing goes as bad as thinking today . . .’’ (Hinz, 1974). On November 19: ‘‘Sincerely, I have not the hope that I will fully recover from the paresis.’’ On December 12: ‘‘I have had so many visitors recently that due to my sick legs and the unfamiliar tongue, I felt so much under pressure that for nobody could I be the person; I would have liked to be.’’ This is the single occasion of a possible speech involvement in Friedrich’s stroke. On March 19, 1840, Shukowski noted in his diary after a visit to Friedrich: ‘‘Been visiting Friedrich. Sad ruin. He cried like a child’’ ( Jensen, 1974). Friedrich’s friend, Carl Gustav Carus, a doctor and painter, wrote about Friedrich: ‘‘Possibly as precedents of a developing brain disease Friedrich died of later, and along with his strange, always dark and often rude character, he had developed certain fixed ideas which began to undermine his existence at home: suspicious as he was, he martyred himself and his family with the idea of his wife being unfaithful, which was completely absurd, but was severe enough to absorb him completely from his family.’’ Kerner (1974) attributed his cerebrovascular insult to neurosyphillis, a diagnosis that he deduces from a self-portrait showing unequal pupils. Indeed, Friedrich’s self-portrait dating from 1810 shows a larger pupil on the left. But another evidence for this diagnosis is scarce, given the few hints to a severe chronic neurological illness until the stroke. Friedrich certainly experienced recurrent episodes of depression reflected in several reproductions of cemeteries or similar subjects. Similar to Bo¨cklin, a definite diagnosis in Friedrich’s case is not possible. Both left hemisphere strokes due to repeated embolism and, more plausibly, a lacunar syndrome with the subsequent development of subcortical vascular

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encephalopathy (including gait disturbance, depression, cognitive decline, and dysarthria) are possible explanations. IV. Other Cases

A. THE CASE

OF AN

87-YEAR-OLD ARTIST

Smith and colleagues (2003) report the case of an 87-year-old artist who experienced a top-of-the-basilar-artery embolic stroke with subsequent visual agnosia. She had painted scenes solely from her memory prior to her stroke. During recovery from stroke, her serial drawings and paintings revealed selective attention to the left lower quadrant, ‘‘with important aspects of the whole image ‘clipped’ as if missing from her internal representation of the whole object.’’ She made a good recovery over the following years with only minor diVerences in her artistic products from those prior to stroke. The authors interpret her problem as simultanagnosia—the inability to simultaneously process visual parts and synthesize meaning. Lesions able to produce such a disturbance may be uni- or bilateral in the posterior parietal lobes. B. TOMMY MCHUGH Recently, the remarkable case of Tommy McHugh (born in 1950) was reported by Lythgoe et al. (2005). This gentleman, who reported his personality as fiery temper and aggressive, suVered a subarachnoid hemorrhage from bilateral middle cerebral artery aneurysms. Subsequently, he experienced a depressive episode and complained of a ‘‘split-mind disorder.’’ Strikingly, after recovery from brain damage and depression, the former builder, who had never been active as an artist before, started to feel an insatiable need to create, from painting and drawing to writing and sculpting. His first drawings during recovery showed signs of a left hemispatial neglect. During early recovery, he began to compose poems and verse, describing his ‘‘split brain’’ altered perceptions and personality. Later, he started to draw large quantities of sketches, mainly of faces, all of them asymmetric, followed by large-scale drawings on the walls of his house. He claimed that the brain injury left him obsessed with making art, and he now spends most of his day painting and sculpting. C. JON SARKIN Comparably, the case of former chiropractor Jon Sarkin (born in April 27, 1953) provoked astonishment (Winner and von Karolyi, 1998). Sarkin was

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operated by a well-known vascular neurosurgeon with the intention to cure his tinnitus and vertigo, which was thought to be caused by a vascular compression of his left 8th cranial nerve. Apparently, a severe postsurgery hemorrhage led to a coma and necessitated an immediate craniotomy and removal of the hematoma and partial resection of his cerebellum. Sarkin recovered very slowly. When he was back at home, he was a diVerent person. He was now disorganized and chaotic, manic in energy, driven to philosophical ramblings and strange poetry, and intricate, humorous paintings. He became obsessed with color and declared that he could really see color. He had a very powerful urge to paint that he could not resist. His story was sold to a large Hollywood company in order to produce a film with the famous actor Tom Cruise depicting Sarkin.

V. Conclusions

This series of 25 visual arts professionals (13 right hemisphere strokes, 9 left hemisphere strokes, and 3 other) illustrates the large variability of the consequences of stroke for their artistic creation. This series of painters had a mean age of 63 at stroke onset and survived their first stroke for more than 8 years (Table I). a. Not surprisingly, the immediate reaction after a devastating and unexpected stroke ‘‘attack’’ is very often a period of depression and despair. Irrespective of the lesioned hemisphere, both left- and right-sided strokes lead sometimes to very severe episodes of depression and even to suicidal attempts. Valuable introspective comments on their disease can be found in Corinth’s, Aichinger-Kassek’s, and Tommy McHugh’s reports. b. Stroke influences paintings of the vast majority of artists to a significant degree. Whereas in some cases the (repeated) strokes ended artistic careers (Friedrich, Fellini), the majority reported resumed artistic production, although having to overcome various types and degrees of disability. c. Four of the artists suVering a left hemisphere stroke had to switch from their prestroke dominant right hand to the left hand (Vierge, Boiyadjiev, Oldenburg, case Kornyey), which was possible without a notable change in style, except for Boiyadjiev. Vice versa, Reynold Brown, a previously left-handed artist suVered a right hemisphere stroke and had to learn to use his previously nondominant right hand. His artwork was further altered by severe visual disturbances. d. Visuospatial neglect is far more common in right hemisphere stroke than in left hemisphere damage. Noticeable degrees of neglect can be deferred from the post-stroke artwork of virtually all of the right-hemisphere patient—artists. This severe problem for the visual artist is often compensated in paintings of the

TABLE I THE SERIES OF 25 VISUAL ARTS PROFESSIONALS ILLUSTRATES THE LARGE VARIABILITY OF THE CONSEQUENCES OF STROKE FOR THEIR ARTISTIC CREATION

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Author

Last name

First name

Date of birth

Date of death

Lythgoe, 2005 N.N. Kerner, 1974 N.N. Bonvicini, 1926 Alajouanine, 1948 Kornyey, 1977 Zaimov, 1969 Mazzucchi, 1994 N.N. Kaczmarek, 1991 Mazzucchi, 1994 Jung, 1974 N.N. Jung, 1974 Jung, 1974 Jung, 1974 Vigouroux, 1990 Franz Brown (www) N.N. Halligan, 1997 Cantagallo, 1998 Blanke, 2003 Schnider, 1993 Smith, 2003

McHugh Sarkin Friedrich Bo¨cklin Vierge Gernez Ferenczy Boiyadjiev Basaldella Oldenburg L. Lusignoli Corinth Schwitters Thiel Dix Ra¨derscheidt NN Brown Aichinger-Kassek Greenshields Fellini N.N. N.N. N.N.

Tommy Jon Caspar David Arnold Daniel Paul-Elie Beni Zlatyu Afro Ernst R. Guglielmo Lovis Kurt Johannes Otto Anton NN Reynold Wolfgang Tom Federico N.N. N.N. N.N.

1950 1953 1774 1827 1851 1888 1890 1903 1912 1914 Unknown 1920 1858 1887 1889 1891 1892 1906 1917 1932 1915 1920 1932 1936 1915

Alive Alive 1840 1901 1904 1948 1967 1976 1976 1992 Unknown Unknown 1925 1948 1962 1969 1970 1985 1991 Alive 1994 1993 Unknown Unknown Unknown

n ¼ 25

Date of 1st stroke 2001 1989 1835 1892 1882 1940 1956 1951 1971 1988 1991 1987 1911 1944 1959 1967 1967 1973 1976 1995 1989 1993 2003 1990 2002

June 26 May 14 Feb 14

Nov 8

Dec

Nov 13 Sep 24 Apr 15

August

Age at 1st stroke 51 46 61 65 30 52 66 48 59 78 Unknown 67 53 57 70 76 75 66 59 64 74 73 71 54 87 Mean: 62,7

Hemisphere Bilateral Cerebellar Left Left Left Left Left Left Left Left Left Right Right Right Right Right Right Right Right Right Right Right Right Right Right or bilateral 9l, 13r, 3 other

Years survived

Influence on painting

4 16 5 9 22 8 11 25 5 4 Unknown Unknown 14 4 3 1,5 2,5 12 15 Unknown 5 0,2 Unknown Unknown Unknown

Definite Definite Definite Uncertain Definite Uncertain Little Definite Definite Definite Definite Definite Definite Uncertain Definite Definite Definite Definite Definite Definite Definite Definite Definite Definite Definite

Mean: 8,7

Definite: n ¼ 21

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wider scenery of landscapes and large figural compositions but is commonly detectable in self-portraits due to the necessity of strong fixation in the center of the visual field. Ernst Oldenburg is the only left hemisphere stroke victim, who exhibited a mild neglect in his post-stroke self-portraits. e. The finding of facial distortion in at least six of the right hemisphere patients is hinting to the representation of both facial recognition and spatial organization in the right hemisphere. In addition, the striking loss of self resemblance in the self-portraits of Corinth, Dix, and Ra¨derscheidt points to a certain degree of prosopagnosia in these right hemisphere stroke victims. Facial construction is unaVected in all of the painters with left hemisphere stroke. The case of Tommy McHugh with hemispatial neglect to the left and asymmetrical portraits produced after subarachnoid hemorrhage and surgical repair of bilateral middle cerebral artery aneurysms suggest a predominantly right hemisphere damage. f. Spatial organization is disturbed in several of the right hemisphere painters with disturbances of perspective or of third dimension in sculptural creation. In the post-stroke artwork by Corinth, Ra¨derscheidt, Dix, Greenshields, and Brown, anatomical exactitude is altered, details are misplaced. This is not the case in painters with left hemisphere strokes. g. The remarkable case of Lovis Corinth illustrates further possible consequences of right hemisphere function to the artist: loss of contours, alteration of emotional nuance, increased subjectivity, idiosyncrasy, and obscurity. h. Hallucinatory episodes, delusions, and dream-like optical sensations can be found in the case histories of several of the right hemisphere stroke painters such as Ra¨derscheidt, Corinth, Aichinger-Kassek, and Schnider’s case. The cases of left hemisphere stroke victims, such as Friedrich and Bo¨cklin, show a predominance of symbols of death in their artistic realizations. i. Evidence for a direct impact of aphasia on artistic production is scarce in the reported cases, indicating that verbal and visual creative output may use separate output channels. The case of a Polish painter who lost his previous ability to paint highly symbolic paintings after left hemisphere stroke is unique in that it illustrates the need of verbal ‘‘symbolic’’ processing for visual ‘‘symbolic’’ output. j. Finally, as evidenced in the cases of Tommy McHugh and Jon Sarkin, stroke damage has apparently the potential to unmask artistic potential.

References

Aichinger-Kassek, W. (1995). ‘‘Neurological Folios.’’ Gorenjski Tisk, Kranj, Slovenia. Alajouanine, T. (1948). Aphasia and artistic realisation. Brain 71, 229–241. Berend-Corinth, C. (1958a). ‘‘Lovis.’’ Langen-Mu¨ller, Mu¨nchen.

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Berend-Corinth, C. (1958b). ‘‘Mein Leben mit Lovis Corinth.’’ Mu¨nchen. Blanke, O., Ortigue, S., and Landis, T. (2003). Colour neglect in an artist. Lancet 361(9353), 264. Boller, F. (2005). Alajouanine’s painter: Paul-Elie Gernez. In ‘‘Neurological Disorders in Famous Artists’’ ( J. Bogousslavsky and F. Boller, Eds.), pp. 92–100. Front Neurol and Neurosci. Basel, Karger. Bonvicini, G. (1926). Die Aphasie des Malers Vierge. Wien. Med. Wochenschr. 76, 88–91. Bonvicini, G. (1929). Sensorische Aphasie und Zeichnung. In ‘‘Die Sto¨rungen der Lautsprache bei Temporallappenla¨sionen. Handbuch der Neurologie des Ohres. II.2’’ (G. Alexander, O. Marburg, and H. Brunner, Eds.), pp. 1735–1746. Urban und Schwarzenberg, Berlin, Wien. Butter, C. M. (2004). Anton Raederscheidt’s distorted self-portraits and their significance for understanding balance in art. J. hist. Neurosci. 13, 66–78. Cantagallo, A., and Della Sala, S. (1998). Preserved insight in an artist with extrapersonal spatial neglect. Cortex 34, 163–189. Chatterjee, A. (2004). The neuropsychology of visual artistic production. Neuropsychologia 42, 1568–1583. Corinth, L. (1926). ‘‘Selbstbiographie.’’ Hirzel, Leipzig. Corinth, T. (1979). ‘‘Lovis Corinth. Eine Dokumentation.’’ Tu¨bingen. Gardner, H. (1977). The pathology of art. In ‘‘The Shattered Mind,’’ pp. 291–349. Routledge and Kegan Paul, London and Henley. Gardner, H., and Winner, E. (1981). Artistry and aphasia. In ‘‘Acquired Aphasia’’ (M. T. Sarno, Ed.), Chap. 12, pp. 361–384. Academic Press, New York. Halligan, P. W., and Marshall, J. C. (1997). The art of visual neglect. Lancet 350, 139–140. Hinz, S. (1974). ‘‘Caspar David Friedrich in Briefen und Bekenntnissen.’’ Henschelverlag, Berlin. Holcomb, H. S. 3rd. (1967). Electrotherapy. J. Hist. Med. 22, 180–181. http://www.geocities.com/chapulinas. http://www.raederscheidt.com. Jensen, J. C. (1974). ‘‘Caspar David Friedrich. Leben und Werk.’’ Dumont, Ko¨ln. Jung, R. (1974). Neuropsychologie und Neurophysiologie des Kontur- und Formsehens in Zeichnung und Malerei. In ‘‘Psychopathologie musischer Gestaltungen’’ (H. H. Wieck, Ed.), pp. 29–88. Schattauer, Stuttgart, New York. Kaczmarek, B. (1991). Aphasia in an artist: A disorder of symbolic processing. Aphasiology 5, 361–371. Kerner, D. (1974). Die Krankheit des Malers Caspar David Friedrich. Med. Welt 25, 2136–2138. Kornyey, E. (1977). Aphasie et realistion artistique. Encephale 3, 71–85. Kuhn, A. (1925). ‘‘Lovis Corinth.’’ Berlin. Lythgoe, M. F., Pollak, T. A., Kalmus, M., de Haan, M., and Chong, W. K. (2005). Obsessive, prolific artistic output following subarachnoid hemorrhage. Neurology 64, 397–398. Marsh, G. G., and Philwin, B. (1987). Unilateral neglect and constructional apraxia in a right-handed artist with a left posterior lesion. Cortex 23, 149–155. Mazzucchi, A., Pesci, G., and Trento, D. (1994). ‘‘Cervello e pittura: EVetti delle lesioni cerebrali sul linguaggio pittorico.’’ Fratelli Palombi, Roma. Orchard, K., Schulz, I., and Brogden, J. (1998). ‘‘Kurt Schwitters: Werke und Dokumente. Verzeichnis der Besta¨nde im Sprengel Museum Hannover.’’ Sprengel Museum, Hannover. Pese, C., and Ramas-Oldenburg, K. (2004). ‘‘Ernst Oldenburg 1914–1992.’’ Edition Braus, Wachter Verlag. Richter, H. (1972). ‘‘Anton Ra¨derscheidt.’’ Bongers, Recklinghausen. Schnider, A., Regard, M., Benson, D. F., and Landis, T. (1993). EVects of a right hemisphere stroke on an artist’s performance. Neuropsy. Neuropsy. Be. 6, 249–255. Schubert, D. (1980). ‘‘Otto Dix.’’ Rowohlt, Reinbek. Schuster, P. K., Vitali, C., and Butts, B. (1996). ‘‘Lovis Corinth.’’ Prestel. Mu¨nchen, New York.

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Smith, W. S., Mindelzun, R. E., and Miller, B. (2003). Simultanagnosia through the eyes of an artist. Neurology 60, 1832–1834. Uhr, H. (1990). ‘‘Lovis Corinth.’’ Berkeley, Los Angeles, Oxford. Vigouroux, R. A., Bonnefoi, B., and Khalil, R. (1990). Reálisations picturales chez un artiste peintre pre´sentant une he´mine´gligence gauche. Rev. Neurol. (Paris) 146, 665–670. von Ostini, F. (1907). ‘‘Bo¨cklin.’’ Velhagen und Klasing, Bielefeld und Leipzig. Winner, E., and von Karolyi, C. (1998). Artistry and aphasia. In ‘‘Acquired Aphasia’’ (M. T. Sarno, Ed.), pp. 375–411. Academic Press, New York. Zaimov, K., Kitov, D., and Kolev, N. (1969). Aphasie chez un peintre. Encephale 58, 377–417.


VISUOSPATIAL NEGLECT IN LOVIS CORINTH’S SELF-PORTRAITS*

Olaf Blanke Laboratory of Cognitive Neuroscience, Brain Mind Institute Ecole Polytechnique Fe´de´rale de Lausanne (EPFL), Swiss Federal Institute of Technology Station 15, 1015 Lausanne, Switzerland; and Department of Neurology, University Hospital, CH-1211 Geneva, Switzerland


Introduction Mature Style–Late Style? Hospitalization Rehabilitation Self-Portraiture Drawings Paintings Discussions References

The characteristics of styles vary continuously and resist a systematic classification into perfectly distinct groups. It is meaningless to ask exactly when ancient art ends and medieval begins. There are of course, abrupt breaks and reactions in art, but study shows that here too, there is often anticipation blending and continuity. Precise limits are sometimes fixed by convention for simplicity in dealing with historical problems or in isolating a type . . . . Through careful description and comparison and through formation of a richer, more refined typology adapted to the continuities in development, it has been possible to reduce the areas of vagueness and to advance our knowledge of styles. (Heinrich Wo¨lZin, ‘‘Principles of Art History: The problem of the development of style in later art,’’ 1915.)

I. Introduction

Lovis Corinth (1858–1925) is one of the great individualists in the history of painting who transcended both his own time and conventional classifications (Kuhn, 1925; Osten, 1955; Schro¨der, 1992; Uhr, 1990). Corinth’s productive years spanned nearly half-a-century (1876–1925), and he studied at the academies in Ko¨nigsberg, *In memoriam of the 10th anniversary of the death of Dr. Otto-Joachim Gru¨sser. INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74014-4

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Munich, and Paris (1876–1887). By 1901, he had emerged as one of the most eminent German painters and moved from Munich to Berlin. Art historical labels, however, are not easily applied to Corinth’s works (Kuhn, 1926; Osten, 1955; Schro¨der, 1992; Uhr, 1990). He painted naturalistic portraits, slaughterhouse scenes as well as interiors, still lifes, and landscapes that link him to Impressionism. At the same time, he produced historical paintings illustrating biblical and mythological scenes on which his reputation in the last decade of the nineteenth century was based. Although he rejected Expressionism, some of Corinth’s later works place him among the Expressionists (Schro¨der, 1992; Uhr, 1990). His work thus defies easy categorization, and most people have failed to categorize artist and his oeuvre. Schro¨der (1992) writes that ‘‘[t]here were no problems to distinguish the early works from the mature period of his first decade in Berlin [. . .]. The helplessness begins when trying to describe Corinth’s late works. Already where it belongs is debated. Is it expressionistic? Or did it remain to the end consequently impressionistic?’’ A way to avoid this diYculty has been to classify him as an outsider. Thus, two major periods have preoccupied art historians, Corinth’s mature, ‘‘impressionistic’’ period or style (1900–1911) (Figs. 1A–C) and his late ‘‘expressionistic’’ style (1912–1925) (Figs. 1D–F). A change of style has been recognized by several authors (Gardner, 1975; Kuhn, 1925; Schro¨der, 1992), but it has also been refuted by others (Jung, 1974; Zdenek, 1985) who argue for continuity of style.1 To complicate matters, the moment of change from Corinth’s mature to his late period coincides with a right hemispheric stroke that the artist suVered in December 1911. This event and its consequences have been discussed by art historians, but only with an emphasis on the relevance of psychological and motor-related eVects of the stroke on Corinth’s art (Kuhn, 1925; Schro¨der, 1992). Apart from discussing these latter factors, the neurologist Richard Jung (1974, 1975) has detected signs of visuospatial neglect in Corinth’s postmorbid drawings. Thus, Jung (1974, 1975) described left-sided omissions and deformities in Corinth’s drawings, especially in the first year after the stroke, in 1912. Despite these changes, Jung (1974) argued for continuity and a continuous evolution of Corinth’s style after his brain damage. Others have confirmed Jung’s observations but nonetheless arrived at the conclusion of a stylistic change (Gardner, 1975, 1981; Gru¨sser and Landis, 1991). As new material about Corinth has become available 1 For the sake of simplicity, we will speak of the mature or ‘‘impressionistic’’ Corinth and the late or ‘‘expressionistic’’ Corinth as units of style, although these periods signify no homogeneous production and, in particular, features of ‘‘expressionism’’ had begun to take shape long before the year 1912, just as, on the other hand, the features of ‘‘impressionism’’ long continued to aVect Corinth’s works after 1912. Our object is to compare type with type, the finished with the finished. Of course, in the strictest sense of the word, there is nothing ‘‘finished’’: all historical material is subject to continual transformation; but we must make up our minds to establish distinctions at a fruitful point (here 1912), and to let them speak as contrasts, if we are not to let the whole development slip through our fingers.

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FIG. 1. Mature and Late style of Lovis Corinth. (A) ‘‘Donna Gravida,’’ 1909 (Nationalgalerie, Berlin, Germany). (B) ‘‘Hymne fu¨r Michelangelo,’’ 1911 (Lenbachhaus, Munich, Germany). (C) ‘‘Die Nackheit,’’ 1908 (Niedersa¨chsisches Landesmuseum, Hannover, Germany). (D) ‘‘Portra¨t von Charlotte Berend,’’ 1912 (Germanisches Nationalmuseum, Nuremberg, Germany). (E) ‘‘Blumen und Tochter Wilhelmine,’’ 1920 (Kunstmuseum, Basel, Switzerland). (F) ‘‘Weihnachtsbescherung,’’ 1913 (Neue Galerie, Linz, Austria).

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(Corinth, 1979, 1990) and left-sided neglect has also been described in Anton Ra¨derscheidt and Otto Dix (Jung, 1974) as well as several other painters (Blanke et al., 2003; Cantagallo and Della Sala, 1998; Halligan and Marshal, 1997; Heller, 1994; Marshall, this issue; Mazzucchi et al., 1994; Schnider et al., 1993; Vigouroux et al., 1990), I have reanalyzed the drawings and paintings before and after 1912. As Corinth has produced more than 1200 paintings, several hundreds of aquarelles, and thousands of drawings and prints, I have here concentrated on the analysis of his self-portraits. This approach was adopted for several reasons. The first was Jung’s (1974) remark that ‘‘[a]n influence of the brain damage [. . .] can especially be seen in the series of his self-portraits.’’ The second was the particular and more constant situation between painter and painted object in self-portraiture (Blanke, 2005; Critchley, 1974; Pa¨cht, 1991). This was complemented by observations from Corinth’s family members (Berend-Corinth, 1958; Corinth, 1979, 1990) and friends (Kuhn, 1925) about his mental and physical state in 1912.

II. Mature Style–Late Style?

In 1925, Alfred Kuhn defined Corinth’s paintings carried out after 1911 as the ‘‘Altersstil [or late style] of the painter.’’ He commented that ‘‘the preponderance of the plastic and corporeal starts to disappear progressively’’ and ‘‘an essentially plane-like painterly seeing was appearing’’ (compare Figs. 1B and C with Figs. 1E and F). He noted that ‘‘the contours disappear, that the bodies are often as if pulled apart, deformed, their spatial relationships distorted, as if this would not be important anymore.’’2 Thus Kuhn’s (1925) account already mentions the major changes in Corinth’s late works that later art historians and neurologists redescribed. Schro¨der (1992) even describes the deformative elements as ‘‘unstable,’’ ‘‘tilting,’’ ‘‘vertiginous,’’ or ‘‘rotatory,’’ as paintings in which ‘‘the balance between horizontal and vertical seems disturbed.’’ This is opposed to Corinth’s mature style that was characterized by high levels of corporeality, richly nuanced flesh of the human body in figure and historical paintings (Figs. 1A and C) that made Corinth famous, as well as the importance of depth and spatial relations that were seen as the ‘‘Bravourelements’’ of his art (Kuhn, 1925; Schro¨der, 1992). Schro¨der (1992) adds that some of the elements of the late style ‘‘were present before 1911,’’ but ‘‘they were always hampered by mythological themes.’’ Kuhn (1925) explicitly mentions Corinth’s disease as an important factor in this artistic change. Osten (1955) describes Corinth’s late works as ‘‘another I (or self), deep inside, productive 2 Kuhn (1925) writes further that ‘‘the similarity of the portraits has almost stopped’’ and ‘‘all detailed carrying out has disappeared.’’ ‘‘The essential parts of a person are put together with broad strokes.’’ In addition, Corinth’s paintings are described as ‘‘pictures that only Corinth is able to see.’’


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and meditating’’ that ‘‘becomes more and more the real source of his art.’’ Yet, Osten (1955) disapproves of psychological and medical theories about Corinth’s art and rather stresses its natural evolution, although he also states that there is the mature and late style. Osten (1955) points out the singularity of Corinth’s art stating that he ‘‘discovered—at a late age, and independent from others—his own way of expressionism.’’ He adds that Corinth ‘‘does not belong to any of the groups that invented [expressionism],’’ and he ‘‘actually despised their appearance and habits quite often [. . .].’’ For Osten (1955)—as for Kuhn (1925) and Uhr (1990)— Corinth’s late style starts in early 1912.3 Uhr (1990) stresses the eVects of Corinth’s stroke by stating that ‘‘although Corinth recovered his physical strength within months, he never overcame the long-term consequences of his illness.’’ Yet, Uhr (1990) aYrms that ‘‘this infirmity did not fundamentally interfere with his ability to paint.’’ He also notes the occasional deformities and the diagonal hatchings (Fig. 1D), but sees them mainly as related to motor impairments consecutive to Corinth’s brain damage. He adds that these ‘‘technical peculiarities’’ rarely diminish the quality of Corinth’s paintings and graphics. On the contrary, Uhr (1990) argues that these peculiarities led a ‘‘new synthesis of content and form’’ characteristic of the late style. Others have underlined the psychological factors in the development of Corinth’s late style stating that ‘‘the life threatening event of the stroke in the Winter 1911 allow[ed] the artist to radicalize his artistry’’ making the ‘‘patch structures [. . .] coarser, freer, and more energized’’ (Gross, 1985; Uhr, 1990). Indeed, to my knowledge, only Zdenek (1985) and Jung (1974) do not see a distinct mature and late style in Corinth and argue for a continuous evolution of Corinth’s art and a thematic constancy throughout the artist’s life. The neurologist Richard Jung (1974, 1975) added essential and new information about Corinth. He described a number of classical signs of left-sided visuospatial neglect in several of Corinth’s drawings from 1912 and 1921. Neglect is a common neurological condition following generally right posterior brain damage. It is an attentional disorder that is characterized by failure to report, respond, or orient to left-sided information (Gru¨sser and Landis, 1991; Robertson and Marshall, 1993; Marshall, this issue). The drawings of patients with visuo-spatial neglect classically show left-sided omissions and left-sided spatial deformities whereas the right side of drawings is more completely carried out (graphic neglect; Halligan and Marshall, 2001). In addition, graphic neglect may be characterized by the loss of spatial contours, the appearance of spatial deformities, and in diYculties in appreciating depth and three-dimensional objects. These latter changes also predominate on the left side of the picture. Jung’s observation thus 3 To underline this, Osten (1955) discusses landscape paintings from 1912 and 1913, such as ‘‘In Bordighara’’ (1912), describing the ‘‘largely formdistorted face’’ of Charlotte Berend-Corinth (the artist’s wife), the ‘‘non-form of the balcony railing [. . .], ‘‘which floats somewhat tilted in front of the house’s wall’’ and the sky that is painted in the now ‘‘typical diagonal strokes.’’

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diVers with respect to previous disease-related theories in which changes in artistic style were attributed largely to stroke-related motor changes and/or purely psychological factors (Kuhn, 1925; Osten, 1955; Schro¨der, 1992; Uhr, 1990). Jung’s (1974) examination thus revealed a cognitive and spatial impairment, visuospatial neglect, which influences artistry at a ‘‘higher’’ and diVerent level than motorrelated impairments that have been predominantly discussed. Although Jung (1974) described the prominent left-sided graphic neglect in Corinth, he argued that this was compensated for from 1913 onwards in Corinth’s drawings and that neglect did not appear in his paintings. Jung (1974) writes that ‘‘Corinth took up his productive drawing and painting soon after his stroke, continued drawing and painting over the next 10 years and developed consequently his style [. . .]. In later drawings these left-right diVerences are not present anymore and apparently since 1913 mostly compensated.’’ Despite the signs of graphic neglect, Jung (1974) states that there is a ‘‘remarkable constancy of the drawing style. There is no change of style.’’ He adds that Corinth’s usage of ‘‘broader lines’’ and ‘‘contour-independent diagonal hatchings’’ was already present in earlier periods and rather increased through his graphic neglect. He concludes, based on his observations of graphic neglect in Anton Ra¨derscheidt and Otto Dix, that ‘‘even severe deficits of spatial vision and of the perception of symmetry in painters are compensated and only have a minor influence on the development of their style, which was established over a lifetime.’’ Jung (1974) describes the resulting deficit as ‘‘a formal increase in diYculty of drawing and painting, rather than a significant change in style.’’ Howard Gardner (1975, 1981) agrees with Jung’s observations concerning leftsided neglect and suggested that it diminished within several months after the stroke with only residual traces occasionally ‘‘discernible either in the overall placement of the subject toward the right side of the canvas or in a somewhat less careful execution of the left side of the work.’’ Gardner (1975) observes that the ‘‘style remain[s] at least recognizable after brain injury [with] a definite continuity’’ (Gardner, 1975). Yet, he concludes that there is a definite alteration in style that is ‘‘more directly expressive, more raw and sensuous.’’ Whereas Schro¨der (1992) would probably accept these latter neurological observations, he fails to concur with Jung’s (1974) conclusions (as do most scholars after 1974) about the influence of neglect in Corinth. He redescribes the classical signs of Corinth’s late style but does not include Jung’s (1974) observations on Corinth. In addition, in Corinth’s paintings from 1912, Schro¨der (1992) does not yet see the characteristic diagonal hatchings and broad strokes of his late style (i.e., ‘‘Portrait with Panama hat’’; ‘‘Lady with Head of Roses’’). He rather argues that the development of his late style cannot be related to Corinth’s stroke.4 4 Schro¨der (1992) rather finds the elements of the late style only in paintings from 1913, such as ‘‘Weihnachtsbescherung’’ and ‘‘Kegelbahn,’’ stating that only by then Corinth masters his new style and ‘‘has overcome and won against his new way of seeing’’: ‘‘he starts to change it in a grandiose way over the next years and liquidates German Impressionism.’’


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III. Hospitalization

In the night from the 12th to the 13th December 1911, Corinth suVered a stroke and was immediately hospitalized by his physician Dr. Strassmann. Although there seem to be no medical records, Jung (1974) has proposed—based on the probable symptoms of left hemparesis, left (parafoveal) visual field defect, and left-sided visuospatial neglect (as evident in Corinth’s drawings)—the diagnosis of an infarction in the distribution of the right middle cerebral artery. Jung (1974) also suggested that the impairment of left-sided finer movements and leftsided limping were long-lasting neurological motor signs. Thomas Corinth (1979) describes that his father already drew while still in bed in the hospital (as also observed for other painters with left-sided neglect; Blanke et al., 2003; Schnider et al., 1993), and he left the hospital on February 19, 1912. While still in his sickbed, it appears that Corinth sketched a series of horrible monsters and strange, ghost-like images of famous figures from history (Corinth, 1979; Uhr, 1990), which seemed to be part of his complex visual hallucinations (Jung, 1974).5 Yet, none of these drawings seems to have survived. Charlotte Berend-Corinth (1955) adds that ‘‘as soon as he had control over his hands, he already drew ‘‘Job’’ (Uhr, 1990, Fig. 117). He portrayed me with a pencil—while I, looking at him— was at the lower end of his bed. This [drawing] seems to me as one of the most beautiful of all that he dedicated to me.’’ (Berend-Corinth, 1958). Corinth only briefly comments on his stroke in his autobiography (Corinth, 1926): ‘‘In December 1911 I had to suVer a disease that brought me close to death. Often during the night my deceased [relatives] seemed to wave to me, while from above a force pressed upon me. [. . .] ‘‘This is it’’ I told the nurse. And the doctor, with whom I shared similar assumptions answered: With such a strong heart one does not yet die.’’ IV. Rehabilitation

After hospital discharge, Corinth left with his wife for Bordighera (Ligurian coast) after having painted a self-portrait (Fig. 6A). They stayed in Bordighera for 2 months. Berend-Corinth (1955) writes about the severe illness of Corinth and her exhausting days trying to comfort him as much as she could: ‘‘Now began a 5 This has also been documented by Alfred Kuhn (1925): ‘‘In the paralyzing hours of being half asleep or awake he was confronted with visions from hell such as Bosch and Breughel have shown to us. He saw monsters—half animal, half man—that devoured the dead; rapidly many diVerent people from the history of mankind appeared, especially Napoleon, mixed with family members and friends. In unpublished drawings that he carried out at the time, all this is testified.’’

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hard time. Corinth could not do anything without help. But as tired and disabled as he was he never complained.’’ He was able to walk several steps but only when supported by his wife and a walking cane. The trip to Bordighera exhausted Corinth’s wife enormously as she assisted her husband day and night. In a letter to her mother from February 1912, Charlotte Berend-Corinth writes ‘‘Lovis [. . .] is very tired, and the doctor [. . .] also told me, that his condition is alarming. [. . .] I cannot leave him alone.’’ Charlotte prepared all paintings and drawings that Corinth executed (and probably for a long period afterwards as well) stating that she even used to ‘‘put the palette and the brushs in Corinth’s left hand that was still not very mobile and did not obey him.’’ Paralysis of the left hand is also mentioned by Thomas Corinth (1990): ‘‘the left hand no longer obeyed when he tried to perform intricate tasks.’’ Several other authors have commented on the trembling of Corinth’s right hand and the eVect this might have had on his late style (especially the diagonal strokes and hatchings; Uhr, 1990). Thomas Corinth adds that ‘‘his right hand was aVected too and trembled severely.’’ Yet, Charlotte mentions that ‘‘the right hand carried the brush as surely as before and [that] he advanced quickly’’ and this seems to have been visible also in a film about Corinth ‘‘showing that the brush [in his right hand] grew steady the moment it touched the canvas’’ (Uhr, 1990). In Bordighera, Charlotte Berend-Corinth used to ‘‘prepare the color tubes on a small chair next to him, after having taken their lids oV, so he could use them easily.’’ She was also impressed with ‘‘how quickly he worked’’ and reports explicitly an episode of left-sided unawareness in Corinth while he was painting.6 The Corinths returned to Berlin on the April 4, 1912 and stayed until mid June when they left for the South of Germany (Bernried). They returned to Berlin for the rest of the year attending an important exposition of Corinth’s work. Thomas Corinth (1979) remembers that his father recovered quickly from his left-sided paresis, yet also mentions the rapid fatigue of left arm and left leg. In a letter to his painter-friend, Hermann Struck, from August 1912 Corinth writes: ‘‘As it is written in the newspaper that I have completely recovered, I don’t dare to say anything to the contrary’’ (Corinth, 1979). In 1914, Thomas Corinth describes his father as swimming in the Mediterranean Sea during their family summer vacation. From 1915 onward, he took long walks in Berlin and used the subway independently. His walking diYculties (as was probably the case with his graphic neglect) are described as increasing when the painter was tired (Corinth, 1955, 1979). 6 ‘‘[. . .] while sitting on the bank, to open his drawing book, it became apparent that his left hand was very unsure; the left hand could not hold the drawing book. I moved very closely to Corinth and tried to replace it [his left hand] by sliding in my hand and by holding the painting book at its corner as unconspicuously as possible. Corinth did not realize it or did not show that he had become aware of this so necessary help.’’


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V. Self-Portraiture

According to Brugger (1992), Corinth completed about 1200 paintings, several hundred aquarelles, and thousands of drawings and prints. In 1911, the year preceding his stroke, he produced 67 paintings. In 1912, this dropped to 24 paintings. In 1913, his productivity had already risen again to 53 paintings. From 1919 to 1925, Corinth completed over 250 paintings. Given this enormous amount of material, as mentioned earlier, I have here concentrated on an analysis of 54 self-portraits from his mature and late period that have been published in Kuhn (1925), Corinth (1926), Osten (1955), Uhr (1990), and Schro¨der (1992). Twenty-four of these were drawings of which six were carried out before the stroke (1873–1911) and 18 after the stroke (1912–1925). I analyzed 30 paintings; 12 were painted before the stroke (1887–1911) and 18 after the stroke (1912–1925). VI. Drawings

Several self-portraits from the period of the late style revealed left-sided omissions as described by Jung (1974). The central portrait in Fig. 2A depicts Charlotte to which Corinth has added two portraits—probably of himself ( Jung,

FIG. 2. Self-portraits after 1912 with left-sided omissions. Drawings from 1912 (reproduced with permission from Corinth, 1926).

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1974)—on each side of Charlotte’s portrait. Many instances of left-sided omissions can be seen in Charlotte’s face, her forehead, her hair. Also note that her left shoulder is not drawn and has been replaced by a small self-portrait. Although her left hand and arm are drawn, both show signs of spatial deformities and are less precisely drawn than the corresponding right body parts. Her left hemiface is less wide and drawn with less spatial detail and nuances. This can also be seen at the left eyebrow and left eye that seems to have been redrawn several times. All these signs suggest left-sided graphic neglect that is space-centered (or centered on the entire frame of the picture). Corinth’s self-portrait on the right side also shows left-sided neglect suggesting the presence of object-centered graphic neglect (Halligan and Marshall, 2001): despite placing his self-portrait in his preserved right spatial field, Corinth omitted left facial features, such as the eye and hair, as well as the left facial contour. Object-centered neglect has been described in works by Corinth (Jung, 1974) and other painters (Vigouroux et al., 1990). The left self-portrait also shows left-sided graphic neglect (the left eye and other left facial features are missing). Jung (1974) has argued that the oval structure in this small self-portrait that is placed at the position of the left eye is probably depicting Corinth’s left parafoveal visual field defect. In a later self-portrait from 1912, further left-sided omissions can be found (Fig. 2B). Here, the outer contour of the left arm is missing. The left arm is smaller than the right arm. In addition, the diagonal hatching of the left arm is missing whereas it is more complete for the right arm. Finally, the left hand is only roughly rendered without the depiction of individual fingers. This is not the case for the right hand, which is well modeled and completely drawn. Again, this bodily asymmetry has also been observed in a recently described professional painter (Blanke et al., 2003) in which it was found to be, in addition, independent of whether the artist drew herself from an imaginary front-view or an imaginary back-view perspective. With the exception of a self-portrait from 1921 (Fig. 4A), no further self-portraits with significant leftsided omissions were found (although Corinth seems to have partly omitted the left side of his moustache in several self-portraits; i.e., object-centered graphic neglect) suggesting that Corinth’s graphic neglect was mostly compensated 1 year after the stroke as also observed in other professional painters (Blanke et al., 2003; Jung, 1974; Schnider et al., 1993). Yet, in other instances spatial deformities located predominantly on the left side of the artworks can be found suggesting their relationship to visuospatial neglect. Thus, in Fig. 3, two self-portraits are shown in which the left eye is lower and of a diVerent size than the right. Also note that the spatial distance between the left eye and ear seems somewhat widened in both drawings with respect to Corinth’s physical appearance, but also with respect to Corinth’s ‘‘mature’’ self-portraits. Left hemifaces also appear somewhat flatter (without much three-dimensional modeling), whereas the corresponding right hemifaces (and the mature self-portraits; Figs. 4A–C) are three-dimensional, spatially nuanced, and finely shaded. In fact, an inspection of each hemiface separately reveals the faces of two diVerent persons for many late


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FIG. 3. Self-portraits after 1912 with left-sided deformities and flatness. Drawings from (A) 1922 and (B) 1923 (reproduced with permission from Corinth, 1926).

FIG. 4. Self-portraits after 1912 with diagonal hatchings. Drawings with (A) left-sided hatchings from 1921 and (B, 1921; C, 1922) generalized diagonal hatchings (reproduced with permission from Corinth, 1926).

self-portraits. In Fig. 4A, a further right-left diVerence can be found (Jung, 1974). Thus, the left lower side of the drawing (and thus the location where Corinth’s spatial as well as visual deficits can be assumed to have predominated) is filled by diagonal hatchings or lines—a phenomenon also observed in another painter (Blanke et al., 2003). Questioning of this latter painter revealed that she incorporated

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these lines or diagonal hatchings in the left lower part of her drawings to represent elementary visual pseudo-hallucinations that she experienced in that part of her visual field. It might therefore be suggested that the diagonal hatching in the left lower drawings of Corinth might have been related to similar experiences and mechanisms. Furthermore, based on inspection of other self-portraits (Figs. 4B and C), it may be suggested that Corinth used this (and probably other) pathological visual experiences as an artistic inspiration; an argument put forward by several authors in relation to painters with migraine, epilepsy, or focal brain damage (Blanke and Landis, 2003, 2004; Blanke et al., 2003; Chatterjee, 2004; Kuhn, 1925; Podoll and Robinson, 2001; Waxman and Geschwind, 1975). After 1913, the initial preponderance of left-sided spatial deformities can also be found on the right side of Corinth’s self-portraits.7 These left-sided omissions and spatial deformities are not observed in Corinth’s self-portraits prior to 1912 (Fig. 5). Finally, analysis of Corinth’s self-portraits shows that the relative size of his body that he drew decreased: self-portraits changed from 1/2 or 3/4 portraits to portraits representing head and shoulders (Kuhn, 1925). This change is accompanied by a change in posture of the portrayed Corinth. The mature Corinth depicted a turned head and body, whereas the late Corinth preferred a straight body and head that is thus positioned frontally and closer to picture plane and mirror (Kuhn, 1925; Schro¨der, 1992). These positional changes add to the flatness of Corinth’s self-portraits.

VII. Paintings

The painted self-portraits do not show significant left-sided omissions. This might be due to the longer time periods generally needed to produce paintings and thus greater control and less spontaneity in their making. Alternatively, greater physical distance and greater variety of distances while painting might account for the absence of omissions in paintings. Finally, greater assistance by his wife (who was a professional painter) might have played a role. Yet, spatial 7 A further sign that has been described in his late self-portraits (Schro¨der, 1992; Uhr, 1990) is that Corinth frequently inverted his right and left hand, thus drawing himself as a left-hander. Some have erroneously assumed that Corinth was a left-hander and have argued that Corinth’s left hemiparesis would provide an (motor) explanation for the development of his late style. This has been corrected by Corinth’s wife (Berend-Corinth, 1955), daughter (Corinth, 1990), and son (Corinth, 1979), who declared that Corinth was right-handed and his stroke-related motor deficits were only left-sided. Based on the observation that Corinth rarely drew himself as right-handed, some have even argued that he could paint equally well with both hands (Schro¨der, 1992). Right-left inversions of Corinth’s painting hand in postmorbid paintings and drawing are not neglect-related as they can also been found in most of his self-portraits before the stroke. This demonstrates that some painters are rather ‘‘visual’’ self-portraitist (Pa¨cht, 1991 on this issue in Rembrandt), whereas other painters rely more on nonvisual, body-related, and spatial information to draw their self-portrait (Blanke, 2005).


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FIG. 5. Self-portraits before 1912. Drawings from (A) 1887, (B) 1908, (C) 1911 (reproduced with permission from Corinth, 1926).

deformities and modified spatial organization, as described earlier for drawings, have also been described in Corinth’s paintings. Already in his first self-portrait, painted in February 1912 (Fig. 6A), a broadening of Corinth’s brushstrokes, as well as an increased flatness, several deformities, as well as a closeness of the portrayed Corinth have been described. Highlighting psychological factors, Kuhn (1925) writes that ‘‘rising from the sickbed, the artist has painted his selfportrait. Not anymore as a worldly adventurer with weapons, neither a young woman in his arm, nor exposing his naked body, but just plain and simple in a dark suit and hat, looking out of the picture with widely opened eyes. The body is weak [. . .] reduced to the upper part of the trunk and the right shoulder, while the head with its torn features [. . .] seems to occupy the whole canvas. A disappearance of the fleshly and corporeal elements in Corinth’s art has happened.’’ Similar, albeit less prominent changes can also be observed in his second self-portrait after the stroke (Fig. 6B). Note that although these characteristics of his late style do appear immediately after his stroke, they are not lateralized to the left side of this and most of the subsequent self-portraits. However, I would like to underline the following three additional observations that suggest that Corinth’s painted self-portraits of the late period have also been influenced by visuospatial neglect (although in a somewhat more indirect manner than his drawings). These are: (1) Corinth’s position in front of the mirror when painting himself, (2) the direction of light, and (3) the prominence of his signature (and other inscriptions) in his paintings. First, whereas in his mature self-portraits, Corinth depicts his body as turned rightwards (or straight ahead) with body (92% of all analyzed premorbid paintings) and head (92%), the late Corinth depicts himself mostly as turned leftwards (or straight ahead) with body (50% of all analyzed postmorbid paintings) and head (55%). The same analysis of 20 painted self-portraits of Rembrandt (who was right-handed as Corinth) also reveals that

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FIG. 6. The first painted self-portraits after 1912. From: February 1912 (A) ‘‘Selbstbildnis,’’ private collection, New Haven, USA; and August 1912 (B) ‘‘Selbstbildnis mit Panamahut,’’ Kunstmuseum Luzern, Switzerland.

Rembrandt positioned himself in front of the mirror as did Corinth before his stroke.8 The question must be asked as to why Corinth would change his position in front of the mirror, thus deviating both from his own customary stance and that of his much admired Dutch masters Frans Hals and Rembrandt (compare mature self-portraits, Figs. 7A–C, with late self-portraits, Figs. 7D–F)? I would like to suggest that this was due to the artist’s acute and chronic spatial (and probable visual) left-sided deficits. When—after the stroke—the rightward turning artist inspected himself in the mirror in his familiar way (as Corinth still did in the first two paintings after his stroke; Fig. 6) he was inspecting his mirror image in his left visual and spatial field and thus in the visuo-spatial field where his neurological impairments predominated. In order to circumvent this diYculty, I suggest that Corinth turned himself leftwards and could thereby inspect his mirror image in his preserved right visual and spatial field.9 This change in position and visuo-spatial field probably lead to a diVerential hemispheric implication in the visual and spatial assessment and appreciation of the inspected object. Second, the direction of light is diVerent in the mature and late selfportraits. Complementary to the positional changes, the direction of light changed 8 A similar analysis of posture in portraiture has been carried out previously for a number of artists across many centuries by Gru¨sser (1989) and Hufschmidt (1980, 1983). 9 Similar changes can also be observed in the self-portraits of Anton Ra¨derscheidt.


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FIG. 7. Positional change and light direction change in the self-portraits after 1912. The figure shows three self-portraits that were created before 1912: (A) 1887, ‘‘Selbstbildnis,’’ Museum, Schweinfurt, Germany; (B) 1901, ‘‘Selbstportra¨t mit Modell,’’ Kunstmuseum, Winterthur, Switzerland; (C) 1911, ‘‘Selbstbildnis mit schwarzem Hut und Stock,’’ Kunstmuseum, St Gallen, Switzerland; and after 1912: (D) 1913, ‘‘Selbstbildnis mit Tirolerhut,’’ Museum Folkwang, Essen, Germany; (E) 1918, ‘‘Selbstbildnis im weissen Kittel,’’ Walraf-Richartz-Museum, Cologne, Germany; (F) 1924, ‘‘Grosses Selbstportrait vor dem Walchensee,’’ Bayrische Staatsgema¨ldesammlungen, Munich, Germany.

from a ‘‘mature-style’’ light source that illuminates the face and body from the right, to a ‘‘late-style’’ left-sided light (Fig. 7) (Gru¨sser, 1989). Third, Schro¨der (1992) has commented on the heightened prominence of the artist’s signature in his late works arguing that that the signature progressively became part of the painting (Figs. 7D and 8). Corinth not only increased the size of the signature but also the number of words by often adding a title (i.e., Ego; Fig. 7D), as well as the town (i.e., Bernried; Fig. 7D) and state or country (i.e., Tirol; Fig. 7D) in which he had drawn the self portrait. In addition, he rendered these writings more prominent by using a diVerent color than in the background (this was only rarely the case in his mature

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FIG. 8. Hyperverbalization. ‘‘Orientalischer Teppichha¨ndler’’ 1913 (private collection; New York, USA).

style in which the signature blended in with the background). This can especially be seen in Corinth’s ‘‘Orientalischer Teppichha¨ndler’’ from 1913 (Fig. 8) in which he actually included nine lines of text that covered a significant portion of the painting. Interestingly, a similar tendency—termed hyperverbalization—has also been observed to diVerent degrees in other artists following right hemispheric brain damage and visuo-spatial neglect (Blanke et al., 2003; Schnider et al., 1993) suggesting its at least partial relation to the latter disorder, although others have observed that there seems to be, in general, a tendency to include longer inscriptions in self-portraiture than in portraiture or landscape painting (West, 2004).10 10 ‘‘Like documents, portraits often contain words. These words can appear on a scroll or piece of paper within the representation, or be written on the canvas itself or on the frame. The use of labels to indicate the age of the sitter, the date the portrait was produced, or other pieces of information was commonplace from the fifteenth century’’ (West, 2004). Yet, why would Corinth show this tendency especially after his stroke?


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VIII. Discussions

The present article corroborates and extends Jung’s (1974) diagnosis of leftsided graphic neglect in Lovis Corinth due to an obstruction of the right middle cerebral artery leading to damage in the right parietal and temporal lobes. In addition, hemianopia or lower quadrantanopia might have been present due to damage to the adjacent occipital lobe (Jung, 1974). Graphic neglect manifests in Corinth’s drawings as left-sided omissions and left-sided deformities and was especially evident in drawings of 1912, but continued to influence Corinth’s drawings and paintings until his death in 1925. Importantly, comparison with other painters that have also suVered from visuospatial neglect (Blanke et al., 2003; Halligan and Marshall, 1997; Heller, 1994; Mazzuchi et al., 1994; Schnider et al., 1993; Vigouroux et al., 1990) reveals that all examined painters—despite their diVerences in style prior to right hemispheric brain damage—showed similar left-sided omissions and deformities or style. The present analysis also suggests that Corinth’s paintings, and not only his drawings, were influenced by graphic neglect. Although in his paintings no significant left sided-omissions were found, Corinth’s productivity dropped (especially from January to June 1912) and early paintings reveal a broadening of brushstrokes, less spatial detail, and lack of depth or flatness. This was observed for his self-portraits (Fig. 5) (Kuhn, 1925), as well as paintings of his wife carried out from February to May 1912 (Uhr, 1990). Corinth’s left-sided graphic neglect in drawings was largely compensated for by 1913 (Jung, 1974), a finding that again has also been reported in other painters suVering from neglect (Blanke et al., 2003; Schnider et al., 1993). Yet, less prominent signs of graphic neglect, such as minor omissions and especially spatial deformities, flatness, and probably neglect-related diagonal hatchings, can be observed after 1912 in his drawings and paintings. Whereas these latter signs after 1913 may predominate on the left side of some pictures, Corinth has often employed them over the entire picture such as the diagonal hatchings characteristic for his late style (Kuhn, 1925; Osten, 1955; Schro¨der, 1992). Based on drawings like Fig. 4A, it might be suggested that the left-sided diagonal hatchings were depictions of Corinth’s visual pseudo-hallucinations that probably predominated in his left visual field. Thus, Corinth might have introduced these into his art as new style elements as suggested by recent observations in a contemporary painter with neglect (Blanke et al., 2003). This introduction of abnormal perceptions into his art seems quite probable since Kuhn (1925), Jung (1974), and Uhr (1990) have already suggested that Corinth introduced his more complex hallucinations involving scenes and figures (from his hospitalization) into his art works (Job series from 1911/1912). This seems also to accord with Corinth’s maxim that one should paint what one sees (Schro¨der, 1992). A continuing influence of visuospatial neglect on his art after 1913 is also suggested by Corinth’s positional change, the change in the direction of light, and hyperverbalization. It might thus

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be suggested that, although Corinth’s visuospatial neglect characterized by leftsided omissions was mainly compensated since 1913, it continued to influence his art at the following more subtle levels. First, Corinth seems to have introduced stroke-related experiences into his art and might have used some of these experiences as artistic inspiration (Blanke and Landis, 2003, 2004; Jung, 1974; Robinson and Podoll, 2001), such as described above for diagonal hatchings, but also more explicitly as in his ‘‘Samson Blinded’’ from 1912 in which one might argue that Corinth depicted his visual and motor impairments (Fig. 9). Second, Corinth seems to have explored and generalized neglect-related elements, such as spatial deformities, flatness, and diagonal hatchings, which initially predominated on the left side of his works to the entire picture. A more refined and detailed analysis will be necessary to examine the precise relationship of Corinth’s left-sided omissions, his positional change in front of the canvas, change in the direction of light, spatial deformities, flatness, diagonal hatchings as well as his hyperverbalization. This should ideally be done in a comparative fashion with respect to expressionists from Corinth’s time and other painters that have suVered from visuospatial neglect. As noted by Schro¨der (1992) and Uhr (1990) art historical labels do not easily fit Corinth’s output. The neurological art critic, an amateur in the field of art history and criticism, should thus be careful and only suggest potential links between Corinth’s art and his neurological aVection in order to encourage interest from

FIG. 9. Pathological experience as artistic inspiration? ‘‘Der geblendete Samson,’’ 1912 (Alte Nationalgalerie, Berlin, Germany).


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scholars in this fascinating field. Unfortunately until now most scholars have related the style change in Corinth to purely psychological factors or stroke-related motor impairments due to his illness (Kuhn, 1925; Osten, 1955; Schro¨der, 1992; Uhr, 1990). The present analysis shows that this is not suYcient and one should include knowledge about the clinical condition of visuospatial neglect (Gardner, 1975, 1981; Gru¨sser and Landis, 1991; Jung, 1974, 1975). To complicate matters, Jung (1974)—who initially showed that Corinth suVered from graphic neglect— argued that ‘‘there is no change of style’’ suggesting that the characteristics of the late style are related to a ‘‘strengthening’’ or ‘‘disinhibition’’ of Corinth’s mature style. He concluded (based on his concordant observations in Lovis Corinth, Anton Ra¨derscheidt, and Otto Dix) that ‘‘even severe deficits of spatial vision [. . .] are compensated and have only a minor influence on the development of [an artist’s] style which was established over a lifetime.’’ Style constancy, despite leftsided graphic neglect has also been suggested by Vigouroux et al. (1990) in a French painter. The present author agrees with Jung’s (1974) proposition of a constancy of style that was further developed by Corinth after his stroke in 1911. Yet, this is mostly true with respect to the left-sided omissions in Corinth’s late works. More subtle changes, such as the spatial deformities, flatness, diagonal hatchings, direction of light, positional change, hyperverbalization that are characteristic of his late style, have also been found in other artists with visuospatial neglect (Blanke et al., 2003; Jung, 1974; Schnider et al., 1993). This suggests that despite the constant recognition of the individual style of Corinth as such, right hemispheric brain damage might lead painters, independent of their premorbid styles, to an ensemble of style elements thought to be characteristic of the late Corinth. Schro¨der (1992) states that ‘‘a medical diagnosis would miss the artistic seriousness of Corinth’s new ambitions’’ and ‘‘they do not tell us much about an artist and his art.’’ The present observations show that on the contrary, neurological and neuropsychological observations might be useful for the art historian (Jung, 1971; Wo¨lZin, 1941), allowing diVerentiation between pictorial elements that are frequently neglectrelated (e.g., left-sided omissions and left-sided deformities), related to modified experiences of the visual world, as well as never neglect-related or related to the individual painter. Thus, neurological observation facilitates the ‘‘ruling out’’ that Corinth’s late style was due to a stroke-related motor impairment of his right hand and emphasizes the importance of cognitive and spatial impairments. Schro¨der (1992) adds that in his opinion ‘‘the liquidation of German Impressionism (as championed by Corinth, Liebermann, and Slevogt) by Corinth is too consequent and reflective in order to be related to a disease.’’ Alternatively, one might argue that only the great artist Corinth—confronted with the experience of a world that was altered by his neglect—was able to consequently develop his late style through a progressive modification or liquidation of his own Impressionism. The present observations were limited to self-portraiture, in which only a subset of visuospatial and perceptual mechanisms of painting are important

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(Blanke, 2005; Critchley, 1974; West, 2004). Corinth’s landscape and still life paintings might be less influenced by neglect as suggested by Jung (1974), but this awaits further, more detailed analysis of these works. As stated by Heinrich Wo¨lZin (1915) ‘‘the characteristics of styles vary continuously and resist a systematic classification into perfectly distinct groups.’’ It seems ‘‘meaningless to ask exactly when a certain style begins and when it ends.’’ ‘‘Precise limits are sometimes fixed by convention for simplicity in dealing with historical problems or in isolating a type.’’ Meyer Schapiro (1953) adds that ‘‘by considering the succession of works in time and space and by matching the variations of style with historical events and with the varying features of other fields of culture, the historian of art attempts with the help of common-sense psychology and social theory, to account for the changes of style.’’ With respect to the art of Corinth, it is hoped that ‘‘through careful description and comparison [. . .]’’ and through formation of a richer, more refined typology adapted to (Corinth’s) development and by the use of ‘‘common-sense’’ neurology and neurobiology (Gru¨sser, 1989; Gru¨sser et al., 1988; Jung, 1971), it will be possible to further advance our knowledge of Corinth’s style(s). Future art historical studies may therefore profit from including information from neurology and neurobiology to their variety of sources including history, sociology, psychology, and biography.

References

Berend-Corinth, C. (1958). ‘‘Lovis’’ A. Langen and G. Mu¨ller Verlag, Mu¨nchen. Blanke, O., and Landis, T. (2003). The metaphysical art of Giorgio de Chirico: Migraine or epilepsy? Eur. Neurol. 50, 191–194. Blanke, O., Ortigue, S., and Landis, T. (2003). Colour neglect in an artist. Lancet. 361, 264. Blanke, O., and Landis, T. (2004). Giorgio de Chirico: Intricate links between spiritual fevers, metaphysical art, and the interictal temporal lobe syndrome. Eur. Neurol. 51, 186–187. Blanke, O. (2005). Experience and perception of the self in autoscopic phenomena and self-portraits. Swiss. Arch. Neurol. Psychiatry. 156, 173–188. Brugger, I. (1992). Biographie. In ‘‘Lovis Corinth’’ (K. A. Schro¨der, Ed.), pp. 206–223. Prestel Verlag, Munich. Cantagallo, A., and Della Sala, S. (1998). Preserved insight in an artists with extrapersonal spatial neglect. Cortex 34, 163–189. Chatterjee, A. (2004). The neuropsychology of visual artistic production. Neuropsychologia 42, 1568–1583. Corinth, T. (1979). ‘‘Lovis Corinth. Eine Dokumentation.’’ Verlag Ernst Wasmuth, Tu¨bingen. Corinth, W. (1990). ‘‘Ich habe einen Lovis, keinen Vater.’’ Helga Schalkhaüser Verlag, Mu¨nchen. Corinth, L. (1926). Selbstbiographie. Hirzel Verlag, Berlin/Leipzig. Critchley, M. (1974). Ecce homo. Observations upon self-portraiture. In ‘‘The Divine Banquet of the Brain and Other Essays,’’ pp. 121–129. Raven Press, New York.


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Heller, W. (1994). Cognitive and emotional organization of the brain: Influences on the creation and perception of art. In ‘‘Neuropsychology’’ (D. Zaidel, Ed.), pp. 271–292. Academic Press, New York. Gardner, H. (1975). The pathology of art. In ‘‘The Shattered Mind: The Person After Brain Damage,’’ pp. 291–349. Vintage Books, New York. Gardner, H. (1981). Artistry after brain damage. In ‘‘Art, Mind, Brain: A Cognitive Approach to Creativity,’’ pp. 318–335. Basic Books, New York. Gross, F. (1985). Die Sinnlichkeit der Malerei Corinths. In ‘‘Lovis Corinth’’ (F. Zdenek, Ed.), pp. 39–54. Dumont Verlag, Cologne. Gru¨sser, O. J., Selke, T., and Zynda, B. (1988). Cerebral lateralisation and some implications for art, aesthetic perception, and artistic creativity. In ‘‘Beauty and the Brain’’ (I. Rentschler, Ed.), pp. 257–293. Birkhaueser, Basel. Gru¨sser, O. J. (1989). Gehirnvorga¨nge und bildnerische Kreativita¨t. Phylogenetische, historische und individuelle Bedingungen. In ‘‘Musik, Gehirn, Spiel’’ (H. Pestche, Ed.), pp. 53–90. Birkhaüser, Basel. Gru¨sser, O. J., and Landis, T. (1991). Visual hemineglect and related disorders. In ‘‘Visual Agnosias and Other Disorders,’’ pp. 431–466. MacMillan, London. Halligan, P. W., and Marshall, J. C. (2001). Graphic neglect—More than the sum of the parts. NeuroImage 14, S91–S97. Halligan, P. W., and Marshall, J. (1997). The art of visual neglect. Lancet 350, 139–140. Hufschmidt, H. J. (1980). Das Links-Rechts Profil im kulturhistorischen La¨ngsschnitt. Arch. Psychiatr. Nervenkr. 229, 17–43. ¨ ber die Linksorientierung der Zeichnung und die optische Dominanz der Hufschmidt, H. J. (1983). U rechten Hemispha¨re. Z Kunstgesch. 46, 287–294. Jung, R. (1971). Konttrastsehen, Kontourbetonung und Ku¨nstlerzeichnung. Studium Generale. 24, 1536–1565. Jung, R. (1974). Neuropsychologie und Neurophysiologie des Kontur und Formensehens in Zeichnerei und Malerei. In ‘‘Psychopathologie musischer Gestaltungen’’ (H. H. Wieck, Ed.), pp. 27–88. F. K. Schattauer, Stuttgart. Jung, R. (1975). Compensation of visual neglect of the left side in right hemispheric lesions. In ‘‘Cerebral Localization’’ (K. J. Zu¨lch, O. Creuzfeld, and C. J. Galbraidt, Eds.), pp. 302–305. Springer, Berlin. Kuhn, A. (1925). ‘‘Lovis Corinth.’’ Propylaën Verlag, Berlin. The eVects of brain damage on the works of amateur and professional artists. In ‘‘Neurology of Painting’’ (Rose, Ed.), (in preparation). Mazzucchi, A., Pesci, G., and Trento, D. (1994). Lovis Corinth. In ‘‘Cervello e Pittura,’’ pp. 171–211. EVeti delle lesioni cerebrali sul linguaggio pittorico. Fratelli Palombi Editori. Osten G von der (1955). ‘‘Lovis Corinth.’’ F. Bruckmann Verlag, Munich. Pa¨cht, O. (1991). Das Selbstbildnis. In ‘‘Rembrandt,’’ pp. 65–78. Prestel Verlag, Munich. Podoll, K., and Robinson, D. (2001). Visual migraine aura as a source of artistic inspiration in professional painters. Neurol. Psychiatr. Brain Res. 9, 81–94. Robertson, I. H., and Marshall, J. C. (1993). Unilateral neglect: Clinical and experimental studies Lawrence Erlbaum, Hove. Schapiro, M. (1953). Style. In ‘‘Anthropology Today’’ (Kroeber, Ed.), pp. 137–144. Chicago University Press, Chicago. Schnider, A., Regard, M., Benson, F., and Landis, T. (1993). EVects of a right hemispheric stroke on an artist’s performance. Neuropsychiatr. Neuropsychol. Beh. Neurol. 6, 249–255. Schro¨der, K. A. (1992). Na¨he und Ferne: Faktur und Ausdruck im SchaVen Lovis Corinths. In ‘‘Lovis Corinth’’ (K. A. Schro¨der, Ed.), pp. 8–35. Prestel Verlag, Munich. Uhr, H. (1990). ‘‘Lovis Corinth.’’ California University Press, Berkeley.

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Vigouroux, R. A., Bonnefoi, B., and Khalil, R. (1990). Reálisations picturales chez un artiste peintre pre´sentant une he´mine´gligence gauche. Rev. Neurol. 146, 665–670. Waxman, G. S., and Geschwind, N. (1975). The interictal behavior syndrome of temporal lobe epilepsy. Arch. Gen. Psychiatry. 32, 1580–1586. West, S. (2004). Self-portraiture. In ‘‘Portraiture,’’ pp. 163–185. Oxford University Press, Oxford. Wo¨lZin, H. (1915). Kunstgeschichtliche GrundbegriVe: Das Problem der Stilentwicklung in der neueren Kunst. Bruckmann, Munich. ¨ ber das Rechts und Links im Bilde. In ‘‘Gedanken zur Kunstgeschichte,’’ Wo¨lZin, H. (1941). U pp. 82–90. Schwabe, Basel. Zdenek, F. (1985). Der Werdegang eines Aussenseiters. In ‘‘Lovis Corinth’’ (F. Zdenek, Ed.), pp. 12–22. Dumont Verlag, Cologne.

ART, CONSTRUCTIONAL APRAXIA, AND THE BRAIN

Louis Caplan Harvard Medical School, Best Israel Deaconess Medical Center Boston, Massachusetts 02215, USA

I. II. III. IV.

Introduction Constructional Apraxia What Attributes are Customarily Needed to Make a Painting or Sculpture? The Frontal Lobes and Their Projections A. Nature of the Deficits B. Anatomy C. Testing at the Bedside V. The Parietal Lobes and Their Projections A. Left Parietal Lobe B. Right Parietal Lobe References

I. Introduction

Art is diverse. Painters, sculptors, and architects use diVerent media and often pursue their art in very diVerent ways. Painters can be as diVerent as Rembrandt, Turner, Mondrian, Klee, Miro, and Rothko, yet all share important attributes. In this volume, the various contributors also have very diVerent backgrounds, being engaged in diVerent artistic and medical disciplines. My perspective is that of a doctor, a neurologist who cares for individuals with brain diseases, mostly strokes and will comment on the dysfunction, labeled constructional apraxia, from a practicing physician’s viewpoint. After describing and defining the term, I reflect on important attributes needed to complete successful art. I then will turn to the regions of the brain that usually show lesions in patients with constructional apraxia and comment on bedside testing of the various disorders that contribute to this disorder, emphasizing my own approach.

II. Constructional Apraxia

Art is performed using many parts of the brain. Children love to build with blocks, make castles and bridges in the sand, draw and finger paint, and mold INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74015-6

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clay into objects. The brain regions involved in these functions are active early in life, very widespread, and distributed within much of the brain. Neurologists coined the term ‘‘constructional apraxia’’ to describe diYculties with functions that relate to art. The early definitions are diYcult to decipher. Macdonald Critchley (1969) wrote ‘‘constructional apraxia can be defined in simplest form as a diYculty in putting together one-dimensional units as to form two-dimensional figures or patterns.’’ Karl Kleist wrote that constructional apraxia describes ‘‘a disturbance in formative activities (arranging, building, drawing) in which the spatial part of the task is missed, although there is no apraxia of single movements’’ (Critchley, 1969). I find it easier to think of constructional apraxia simply as diYculty in drawing, copying, and arranging when elementary neurological functions, such as seeing, speaking, and using the limbs, are well preserved. After Critchley (1969) and his famous monograph on The Parietal Lobe, neurologists have tended to emphasize the parietal lobe, especially the inferior portion of the right parietal lobe, as being the epicenter in which lesions cause constructional apraxia. However, many brain lesions can result in constructional apraxia—each with very diVerent signatures and mechanisms. Herein, I analyze the three most common brain regions that relate to art—to drawing and copying, realizing at the same time that much of the rest of the brain is also involved in creative art.

III. What Attributes are Customarily Needed to Make a Painting or Sculpture?

An artist must have the initiative to begin the task. He or she must be motivated and energized in order to start preparing for the task. They then must consider what to depict in their work of art. This decision depends on weighing a number of factors, such as their own abilities, strengths, past successes and failures, the available tools and equipment (paints, colors, easels, canvas, and so on), and societal issues such as what might fit with the present norms of art, what patrons might support, what consumers might buy, and what galleries might display. Next, the artist must plan the work. Once the task has been decided and planned, the artist must be able to switch from one function to another and back to another during performance of the task. The artist must have the perseverance to complete the task and to do so timely enough to meet prespecified targets. The functions described so far are generally attributed to the frontal lobes of the brain and their aVerent and eVerent projections. The work of the artist diVers considerably, depending on whether the artist is creating the work without a model from their own memory, and must be able to revisualize and imagine the art that they will create or whether a picture is made by


217

copying in some fashion a scene, a landscape, actual objects, people, or animal life. Creating an image without a present object requires conceptualization of the object, a function usually assigned to the left cerebral parasylvian speech cortex, especially portions of the left inferior parietal lobe—the supramarginal and angular gyri. Revisualization of objects is attributed mostly to the inferior banks of the calcarine sulci—the lingual and fusiform gyri (lesions of which almost invariable are accompanied by a visual field defect); revisualization of directions is usually assigned to the visual tracts that course from the upper banks of the calcarine sulci—the cuneus— through the superior parietal lobes and are also mostly accompanied by visual field defects or with features of the Balint syndrome (Barton and Caplan, 2001). Copying and depiction of size, shape, proportions, and relationships of visual percepts are functions most often localized to the right inferior parietal lobe. Since the designation constructional apraxia is by definition limited to those individuals who have normal visual and limb functions, the usual distribution of lesions associated with constructional apraxia are the frontal lobes and their projections and the left and right parietal lobes, mostly their inferior portions. In the remainder of this chapter, I will discuss the anatomy of the lesions that are most often responsible for constructional apraxia and their clinical testing.

IV. The Frontal Lobes and Their Projections

A. NATURE

OF THE

DEFICITS

Individuals with frontal lobe lesions have a number of dysfunctions that limit their creative artistic abilities (Table I). Some relate to the quantity and timing of actions and behavior; the two most important of which in relation to art are abulia and motor impersistence. Abulic individuals have a paucity of spontaneous behavior, speech, and action. They tend to sit for long periods without taking the initiative to begin to draw or paint. When they are asked questions or given directions they often delay their replies. Often they must be asked or told something repeatedly before a response is forthcoming. They have diYculty in persevering with tasks, often performing one appropriate action or giving several responses when many are requested or required. Abulic artists would have diYculty initiating a work of art and would be quite unable to persist to complete the work. Individuals with motor impersistence often respond quickly to commands and queries, although they just as quickly terminate the activity or response (Fisher, 1956). When asked to hold their arms outstretched in front of them, they assume this posture quickly but then drop their arms failing to persist with the task. Miller Fisher was accustomed to define deficits operationally by describing the tests and responses that he meant (Fisher, 1956). Impersistence is translated in life into impulsivity and

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ABNORMALITIES

IN

TABLE I PATIENTS WITH FRONTAL LOBE LESIONS

Abnormal quantity and timing of behavior Abulia Slowness Motor impersistence (impulsivity and diYculty persevering with tasks) Hyperactivity ‘‘Executive Dysfunctions’’ Loss of planning capabilities DiYculty performing concurrent and sequential acts Perseveration DiYculty switching ideas and actions Loss of working memory Ignoring of lessons from past personal experiences, society norms, and mores in making decisions and actions

diYculty persisting with activities; these individuals often answer queries even before the question is finished and make rather hasty, impulsive decisions that are not appropriate because they were not thought through before action. They also leave tasks prematurely and cannot persist with tasks that were planned. The other important capabilities loosely attributed to the frontal lobe are usually bundled under the designation of ‘‘executive functions.’’ These include the initial planning of a task or project. In order to appropriately plan, an individual must be aware of their own past experiences and capabilities as well as a multitude of practical issues—money, salability, society norms and mores, and what is ‘‘en courant.’’ After planning the task, the artist needs to frequently switch activities during the actual task of creating the art work. This involves switching diVerent colors, diVerent techniques, and diVerent parts of the work. Patients with executive dysfunctions often have diYculty switching tasks and performing concurrent and sequential tasks. They often perseverate, continuing the same activity with delays in switching to a new direction. B. ANATOMY The deficits described are noted most often in patients with rather large frontal lobe lesions, often tumors. The precise anatomy within the frontal lobes, even left versus right versus bilaterality has not been well worked out. Most frontal lobe lesions that cause abulia and executive dysfunctions involve the lateral frontal convexal structures or areas near the frontal poles. Patients with strokes involving the caudate nucleus and the adjacent anterior limb of the internal capsule also show abulia, usually for a period that lasts up to


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FIG. 1. An MRI that shows an acute medial thalamic infarct (white arrow). The patient acutely became abulic.

6 months (Caplan et al., 1990). These areas have strong projection to the frontal lobes. The other main lesion that causes abulia and some executive dysfunction involves the medial thalamus on either side (Bogousslavsky and Caplan, 1993; Bogousslavsky et al., 1986). Infarcts within the territory of the thalamo-tubular arteries (also called the polar arteries) are most often responsible (Bogousslavsky and Caplan, 1993; Bogousslavsky et al., 1986). These arteries are usually branches of the posterior communicating arteries but occasionally branch from the thalamo-perforating arteries. Figure 1 shows an MRI of a medial thalamic infarct in an abulic patient. Like caudate lesions, the abulia that develops in medial thalamic infarct patients usually abates within the first 6 months after the stroke. C. TESTING

AT THE

BEDSIDE

The most important but oft-neglected first step is simple observation of the individual, noticing spontaneous behavior and conversation patterns. Abulic persons usually do not initiate conversations, reply belatedly or not at all to

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queries or directions, and speak in brief phrases or sentences. I recommend three tests: counting 20–0, cross oV all the A’s on a page, and name 10 articles of clothing. Ask the person to count quickly from 1–20, and then, if that task is performed accurately, to count backward from 20–1 without stopping. Abulic individuals can count forward indicating their understanding of the task and of the numbers involved. They, however, have great diYculty counting in reverse. They characteristically begin well and then pause, slow down, stop, or sometimes reverse directions and count forward. A typical example would be: 20–19–18– 17. . .. . .. . .16. . .. . .. . .15 (and then after they stop and you encourage) . . .14 . . .. . .13 . . .. . .. . .12 . . .. . .13 . . .14, and so on. Many never reach 0 or do so very slowly and only with encouragement and cues to continue. Next show the individual a text in a newspaper, magazine, or page of print. Ask them to cross oV with a pencil all of one letter, for example A. Abulic individuals usually cross oV a few As correctly and then become distracted and quit. The fact that they do the initial identification correctly shows that they understand the nature of the task and can recognize the letter A; their problem is an inability to persevere with the task. Another strategy for testing is to ask the individual to make a list (either verbally or on paper) of common items, for example, articles of clothing, colors, fruits, cities, means of conveyance, and so on. Ask them to give you 10 names. Abulics usually get 2 or 3 items in the category and then stop and rarely persist until 10 are named. Testing for impersistence again begins with behavioral observation, since these individuals are often restless and easily distracted, they answer questions very quickly, often before the query is finished; they perform tasks quickly but just as quickly discontinue, even when directed to continue. Directions to the patient might include: hold up your hands in front of you and keep them there or hold your tongue out until I say to withdraw it. Table II lists Miller Fisher’s (1956) criteria for motor impersistence; note that he defines the term operationally by their response to the tests enumerated. Executive functions can be tested in several ways. I often test planning by asking the individual to draw a floor plan of the first floor of a house in which they would like to live. This task requires thought. How many bedrooms? Where to TABLE II MOTOR IMPERSISTENCE (FISHER, 1956) Inability to maintain conjugate gaze steadily Inability to keep mouth open or tongue protruded Inability to maintain fixation on examiner’s nose during visual field testing Inability keeping eyes shut during sensory testing-peeking DiYculty holding breath or maintaining an ‘‘ah’’ sound DiYculty maintaining steady pressure during a hand grip


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place the dining room, kitchen, pantry, doors, hallway, entrance, bathrooms, and so on. The location, size, and relationship of the rooms must be considered. Usually this task requires considerable thought and planning. I also use the Porteus Mazes test—which involves the ability to plan a strategy for route finding using a paper—and pencil maze test (Mesulam, 2000; Porteus, 1965). Another rather good test is the Tower of London puzzle test which is shown in Fig. 2 (Mesulam, 2000; Shallice, 1982). Patients with frontal lobe lesions often have diYculty switching from one subject or task to another. There are a number of bedside tests useful in testing this ability and seeking preservations. I give the individual a pencil and paper and ask them to make repeatedly a series of two squares, one circle, two squares, one circle, two squares, and one circle; patients with frontal lobe disease may have diYculty in switching from square to circle and will write more than two squares. A similar task involves tapping with palm down twice, alternating with palm up once. The patient can be asked to alternate positions using one hand. The patient is told to hit the top of the desk, first with a fisted hand, then with the palm, then with the side of the hand; these alternate hand postures are continued for 20 s or more. Patients who perseverate will have diYculty inhibiting repetition of postures. Another test involves alternating actions of the two hands such as palm down with the left hand followed by palm up with the right hand then palm up with the left hand and palm down with the right hand. The Go–No-Go test is another rather simple investigation of the ability of the individual to switch that can be performed at the bedside. The directions for this test are: place your hand palm down on table then raise your index finger if I tap once (Go signal) but do not raise the index finger if I tap twice (No-Go signal). Individuals with executive dysfunctions have diYculty with sequential or concurrent performance and frequently perseverate the last response (Drewe, 1975; Mesulam, 2000).

FIG. 2. The tower of London puzzle (from Mesulam, 2000 with permission).

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V. The Parietal Lobes and Their Projections

A. LEFT PARIETAL LOBE 1. Nature of the Deficits The left parasylvian area is most well known for a specialization in language. Language in its simplest sense means words, but more complex is the issue of concepts, for example, what is a chair. There are innumerable examples of chairs all configured, constructed, and modeled diVerently (Fig. 3). Similarly the concept of a table is complex; an individual can picture a specific table, but the concept of what really defines or makes a table is quite diVerent (Fig. 4). Patients with left parietal lobe lesions have diYculty in revisualizing the nature of objects and their appearances (Barton and Caplan, 2001; DeRenzi et al., 1969; Gainotti, 1985; Hećaen and Assal, 1970; Piercy et al., 1960). Patients with left parietal damage often draw very simple rudimentary figures but do not omit one side of the drawing and generally estimate size, angles, and proportions well. They are able to copy well, greatly improving their spontaneous performance. Their problem is conceptualization of the abstract idea of the object, while patients with right parietal lobe damage have a normal concept of the object, they cannot

FIG. 3. A selection of various chairs taken from catalogue.


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FIG. 4. A selection of various tables taken from catalogues.

construct the visuospatial components of that percept (DeRenzi et al., 1969; Gainotti, 1985; Hećaen and Assal, 1970; Piercy et al., 1960). 2. Anatomy The major region that correlates with constructional dyspraxia is the inferior parietal lobe, the supramarginal and angular gyri. Individuals with lesions in this area also may have a number of other deficits that are listed in Table III. The most common language disorders involve written language. Patients act as if they are illiterate, that is, they become unable to read, write, and spell. They may also make speech sound-alike and mean-alike errors and have diYculty repeating spoken language associated with some diYculty in understanding spoken speech. They also may show some of the various components of the Gerstmann syndrome (agraphia, right–left confusion, finger agnosia, and constructional apraxia) (Critchley, 1969). Some patients with superior parietal lobe lesions, the precuneus and gyri posterior to the postcentral gyrus, may have diYculty drawing living things, especially people. They seem to have diYculty with body parts and with conceptualization of the human and animal forms. 3. Testing The major testing for constructional apraxia associated with left parietal lobe lesions is to ask the patient to draw a complex figure from memory. Familiar

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TABLE III LEFT INFERIOR PARIETAL LOBE CLINICAL DEFICITS Alexia Agraphia DiYculty spelling Conduction aphasia Acalculia Right–left confusion Finger agnosia Constructional apraxia

FIG. 5. Shows examples of spontaneous drawing and copying of houses by patients with left parietal lobe damage (from Piercy, 1960 with permission).

figures, such as a house, bicycle, daisy, or church, are requested, and patients with left parietal lesions usually draw very simple figures that are not elaborate. The sizes, proportions, angles, and relationships are usually drawn appropriately, and they are able to copy complex figures rather well, indicating that the main problem is conceptual with diYculty in the concept of the object drawn. Once a model is available, they can copy and imitate it well. Figure 5 shows examples of spontaneous drawing and copying of houses by patients with left parietal lobe damage. The spontaneous drawings are rudimentary, but the copies are improved over the spontaneous performance. I usually also ask them to copy complex objects, such as the Rey-Osterrieth Figure (Osterrieth, 1944; Rey, 1941) (Fig. 6), which they usually do quite well.


225

FIG. 6. The Rey-Osterrieth figure.

Ancillary testing of reading, writing, spelling, finger naming, and arithmetic functions is often useful in localizing the lesion to the left inferior parietal lobe. Asking the patient to draw a person is also useful. B. RIGHT PARIETAL LOBE While the left cerebral hemisphere is thought to be dominant for language and recall of language-related semantic information, the right cerebral hemisphere is considered dominant for visuospatial functions and recall of visual data (Barton and Caplan, 2001; Caplan and Bogousslavsky, 1995; Hier et al., 1983). Patients with right parietal damage usually copy very poorly. In their spontaneous figures, they often omit objects on the left. Size, angles, and proportions are often misjudged (DeRenzi et al., 1969; Gainotti, 1985; Hećaen and Assal, 1970; Piercy et al., 1960). Figure 7 shows examples of houses drawn by patients with right parietal lobe damage; copying does not improve their performance. They may also have diYculty in revisualizing the arrangements of things in their rooms at home, the relationships of one room to another, and directions within the city or town in which they live. Their deficits involve the visuospatial attributes of objects and places and involve revisualization, drawing, copying, and arranging. 1. Anatomy Most lesions that cause constructional apraxia are located within the inferior parietal lobe region—the supramarginal and angular gyri. Infarcts in this region are most often embolic, the donor source being the heart, aorta, or the ipsilateral

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FIG. 7. Shows examples of houses drawn by patients with right parietal lobe damage (from Piercy, 1960 with permission).

carotid artery. An agitated hyperactive state and a left superior quadrantanopia often accompany the constructional apraxia (Caplan et al., 1986). Large lesions that undercut these gyri, for example, large right posterior cerebral artery distribution infarcts, and posterior temporal–occipital hemorrhages can also aVect the function of the right inferior parietal lobe. 2. Testing The most common way to test for constructional apraxia is to ask the patient to draw objects such as a clock, house, daisy, bicycle, and so forth. Next, draw an abstract figure and ask the patient to copy it as exactly as possible. I suggest using a modern-art type figure that the patient cannot easily describe in words. If one asks the patient to copy a commonly recognized object, they will often see the object, give it a name (e.g., clock) and then draw a clock instead of slavishly copying the clock that you have asked them to reproduce. Visuospatial abnormalities can be further checked by having the patient copy the Rey-Osterrieth figure (Osterrieth, 1944; Rey, 1941) (Fig. 6). This can be done with the figure present to copy, or the figure can be removed and the patient asked to reproduce as much of the figure as they recall; this delayed reproduction tests visual memory ability. An alternate method of testing visuospatial functions is to ask patients to copy arrangements. Tongue blades, Q-tips (cotton topped sticks) with cotton removed (Fig. 8), or childrens’ building blocks (Fig. 9) can be


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FIG. 8. Sticks arrangements and their copies (from Critchley, 1969 with permission).

FIG. 9. Child building block arrangement and a patient’s copy (from Critchley, 1969 with permission).

arranged by the examiner in various patterns and the patient asked to reproduce the arrangement using a stack of the same materials. Drawing and then copying clocks, houses, daisies, and so on are the most important tests. Visuospatial capabilities are also readily tested at the bedside by asking the patient to construct mosaic patterns using Koh’s blocks (Fig. 10). Koh’s blocks are

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FIG. 10. Koh’s blocks.

small cubes that have surfaces that are red, blue, and white; red and white; blue and white; and red and blue. Diagrams of models of mosaics to be copied are available in WAIS-R testing kits, since testing with red and white Koh’s blocks is a standard part of this IQ test (Wechsler, 1981). Figure 11 shows some sample mosaics and attempts at copying by patients with right parietal lobe lesions. This subtest of the WAIS is easily administered in the oYce or at the bedside and is very useful in quantifying the severity of constructional, visuospatial deficits. Reading and writing can also show signs of left visual neglect. If patients are asked to read a paragraph, they may omit the most leftward words or phrases and have diYculty directing their gaze and attention to the left border of the page. Figure 12 shows an example of writing on the right side of a page ignoring the paper on the left side. Visual functions can be tested by showing pictures of scenes and individuals, specially those cut out from magazines such as the National Geographic or advertisements. The pictures chosen should have multiple persons or objects scattered on the left and right sides. Hold the picture in front of the patient for about 10 s. If the patient has poor visual acuity, give the picture to the patient to examine. After withdrawing the picture, ask the patient what they saw. After their general description, ask for specific details. When and where did the scene take place? How old are the individuals? How are they dressed, and so on? Much can be learned from the patient’s performance. Watch the patient’s eyes as they scan the picture. Do they search symmetrically? Have they seen the whole picture? Have they grasped the general gestalt of the picture or instead focused on a minor peripheral aspect? Patients with right cerebral hemisphere lesions often neglect


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FIG. 11. Sample mosaics and attempts at copying by patients with right parietal lobe lesions. (from Critchley, 1969 with permission).

figures on the left. Left visual neglect is often but not always accompanied by constructional apraxia (Osterrieth, 1944). Patients with frontal lobe disease often scan poorly and are satisfied with telling about the first feature that catches their eye and do not extract further information from the scene. DeRenzi and colleagues performed a series of three tests that illuminates the nature of the comparison of deficits between left and right parietal lobe damaged patients (DeRenzi et al., 1969). In the first test, patients were asked to match photographs that showed individuals’ faces in a frontal view with the same individuals shown in a profile or side view (Fig. 13); in the second test, patients were given an overlapping figure that contained various fruits (Fig. 14). The task was to select those fruits from the drawings of various fruits on the side of the overlapping figure that were contained within the overlapping figure. In the third test, patients were shown photographs of various objects and asked to match the photographs with actual objects, but the objects were not exactly the same as the pictures (Fig. 15). The actual objects diVered in form and color from the pictures.

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FIG. 12. Shows an example of writing on the right of a page ignoring the paper on the left side. (from Critchley, 1969 with permission).

FIG. 13. Matching of front-view photographs with side views. (from DeRenzi et al., 1969 with permission).

Patients with left parietal damage had no diYculty matching photographs of individuals (test 1) or identifying the fruits in the overlapping figure (test 2) but did poorly on test 3 matching nonidentical stimuli. The first two tests are purely visual; one does not need to know the names or identities of the people or fruits. These tests are visual matching tests and left parietal lobe damaged patients have no diYculty with visuospatial functions. The third test relates to categorization


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FIG. 14. The Ghent overlapping figures test. (from DeRenzi et al., 1969 with permission).

FIG. 15. An example of nonidentical matching of objects. (from DeRenzi et al., 1969 with permission).

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and left parietal lobe damaged patients have diYculty with this function, doing less well than right parietal damaged patients. In contrast, patients with right parietal lobe damage did poorly on the first two tests of visuospatial matching and did well on the third test of categorization (DeRenzi et al., 1969).

References

Barton, J. S., and Caplan, L. R. (2001). In ‘‘Cerebral Visual Dysfunction in Stroke Syndromes’’ (J. Bogousslavsky and L. R. Caplan, Eds.), 2nd ed., pp. 87–110. Cambridge University press, Cambridge, UK. Bogousslavsky, J., and Caplan, L. R. (1993). Vertebrobasilar occlusive disease: Review of selected aspects. Lll. Thalamic infarcts. Cerebrovasc. Dis. 3, 193–205. Bogousslavsky, J., Regli, F., and Assal, G. (1986). The syndrome of tuberothalamic artery territory infarcts. Stroke 17, 434–441. Caplan, L. R., and Bogousslavsky, J. (1995). Abnormalities of the right cerebral hemisphere. In ‘‘Stroke Syndromes’’ ( J. Bogousslavsky and L. R. Caplan, Eds.), pp. 162–168. Cambridge University press, Cambridge. Caplan, L. R., Kelly, M., Kase, C. S., Hier, D. B., White, J. L., Tatemichi, T., Mohr, J. P., Price, T., and Wolf, P. (1986). Infarcts of the inferior division of the right middle cerebral artery: Mirror image of Wernicke’s aphasia. Neurology 36, 1015–1020. Caplan, L. R., Schmahmann, J. D., Kase, C. S., Feldmann, E., Baguis, G., Greenberg, J. P., Gorelick, P. B., Helgason, C., and Hier, D. B. (1990). Caudate infarcts. Arch. Neurol. 47, 133–143. Critchley, M. (1969). ‘‘The Parietal Lobes.’’ Hafner Pub Co., New York. DeRenzi, E., Scotti, C., and Spinnler, H. (1969). Perceptual and associated disorders of visual recognition: Relationship to the side of the cerebral lesion. Neurology 19, 634–642. Drewe, E. A. (1975). Go No-go learning after frontal lobe lesions in humans. Cortex 11, 8–16. Fisher, C. M. (1956). Left hemiplegia and motor impersistence. J. Nerv. Ment. Dis. 123, 201–218. Gainotti, G. (1985). Constructional apraxia. In ‘‘Handbook of Clinical Neurology’’ (P. Vinken, G. Bruyn, and H. Klawans, Eds.), Vol. 45, pp. 491–506. Elsevier Science Publishers, Amsterdam. Hećaen, H., and Assal, G. (1970). A comparison of construction deficits following right and left hemisphere lesions. Neuropsychologia 8, 289–304. Hier, D., Mondlock, J. J., and Caplan, L. R. (1983). Behavioral defects after right hemisphere stroke. Neurology 33, 337–344. Mesulam, M.-M. (2000). In ‘‘Principles of Behavioral and Cognitive Neurology,’’ 2nd ed., pp. 121–173. Oxford University press, Oxford. Osterrieth, P. A. (1944). Le test de copie d’une figure complex. Archives de Psychologie 30, 206–356. Piercy, M., Hecaen, H., and De Ajuriaguera, J. (1960). Constructional apraxia associated with unilateral cerebral lesions, left and right sided cases compared. Brain 83, 225–242. Porteus, S. D. (1965). ‘‘Porteus Mazes Tests: Fifty Years Applications.’’ The Psychological Corporation, San Antonio Texas. Rey, A. (1941). L’examen psychologique dans les cas d’encephalopathie traumatique. Arch de Psychologie 28, 286–340. Shallice, T. (1982). Specific impairments of planning. Philos. Trans. R. Soc. London Biol. 298, 199–209. Wechsler, D. (1981). ‘‘WAIS-R. Wechsler adult intelligence scale – Revised.’’ Psychological Corporation, New York.

SECTION V GENETIC DISEASES


NEUROGENETICS IN ART

Alan E. H. Emery Green College, Oxford, United Kingdom

I. II. III. IV.

Introduction How Neurogenetic Disease AVected the Artist’s Work? Neurogenetic Disease Depicted in Art Conclusions References

I. Introduction

Much has been written about the relationship between art and disease. One excellent review concerning neurology and art considered illustrations of the nervous system and the portrayal of neurological diseases (McHenry, 1982). Here the emphasis will be on neurological disease with a hereditary basis: first, how this has sometimes aVected artists themselves and second, the portrayal of such diseases in works of art. Very few of these disorders, however, are in fact due to single genes (unifactorial) rather than to both genetic and environmental factors (multifactorial). This is understandable since most unifactorial neurological disorders are very rare and also seriously disabling and would usually, although not always, preclude any artistic work of merit.

II. How Neurogenetic Disease Affected the Artist’s Work?

Migraine can have a familial basis. It has aZicted a number of artists including in Britain, Sarah Raphael (1960–2001) and J. J. Ignatius Brennan (1949) and in Italy, the surrealist painter Giorgio de Chirico (1888–1978). All three frequently depicted their impressions of fortification spectra (Fuller and Gale, 1988; Podoll and Robinson, 2000). Although rare, early onset familial cases of Alzheimer’s disease have been shown to be due to mutations of the presenilin 1 and 2 and amyloid precursor protein (APP) genes, the commoner late onset cases appear to be multifactorial in INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74016-8

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causation. The disease has aVected several artists and is reflected in a gradual deterioration in their ability to depict representational imagery as the disease progressed. One of the earliest manifestations of the disease has been reported to be impairment of visual memory associated with atrophy of the hippocampus and medial temporal lobe structures (Panegyres, 2004). Willem de Kooning (1904–1997) developed the disease in his 60s, and as the disease advanced his work became more abstract. A contemporary artist, William Utermohlen, was diagnosed with the disease in 1996, and the progressive eVects of the disease on his art have been graphically reproduced (Crutch et al., 2001). Mervyn Peake (1911–1968), a brilliant if somewhat eccentric English artist and writer, suVered from a disease, which in retrospect may have been dementia with Lewy bodies (Sahlas, 2003). He often depicted in his work the visual hallucinations he experienced, but the hereditary nature of this disease is still far from clear. Certainly, Peake had no family history of the condition although, like sporadic Alzheimer’s of late onset, it can be associated with the ApoE4 polymorphism (Ritchie and Lovestone, 2002). Some cases of the disease are due to mutations of the -synuclein gene (Singleton and Gwinn-Hardy, 2004). Another recent professional artist developed frontotemporal dementia, and her paintings became progressively less conventional, freer, and more original (Mell et al., 2003). Rare familial cases of this disorder are caused by mutations of the tau gene (microtubule binding protein). Two other noteworthy neurological conditions that have occasionally aVected professional artists are multiple sclerosis and motor neuron disease (amyotrophic lateral sclerosis). Apart from a small proportion (2–4%) of the latter, which are due to mutations of the SOD-1 gene, the majority of cases of both these disorders are believed to be multifactorial in causation. Candidate gene studies have, however, firmly established the importance of the association of multiple sclerosis with the HLA haplotype DR 15 (DR B1 * 1501). A welldocumented case of multiple sclerosis is of Peter MacKarell, an English artist who died in 1988 (Emery, 1997). How it aVected his art is revealingly illustrated in his book, Depictions of an Odyssey, including the development of a central scotoma in his right eye (Fig. 1). John Paterson, a Scottish artist, developed a form of motor neuron disease in 1996. His later work illustrates the changing relationship with, and dependence on, his carers (Emery, 2004). Finally, Salvador Dali (1904–1989) developed parkinsonism in later life, like his father before him raising the possibility that a rare genetic cause may have been responsible. Roughly 15–20% of individuals with Parkinson’s disease have a positive family history, and to date mutations in nine so-called PARK genetic loci have been identified in aVected families (Feany, 2004; Hattori and Mizuno, 2004) and in some isolated cases as well (Brice, 2005). Mutations of the -synuclein gene (PARK 1) have been identified in families with Parkinson’s disease as well as in some families with dementia with Lewy bodies (Table I). But in all these progressive neurological disorders, especially motor neuron disease and parkinsonism, their physical eVects would seriously restrict any artistic

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FIG. 1. Self-portrait of Peter MacKarell with the eVects of a right central scotoma.

TABLE I GENETIC LOCI IMPLICATED IN PARKINSON’S DISEASE Locus PARK PARK PARK PARK PARK PARK PARK PARK PARK

1 2 3 4 5 6 7 8 9

Chromosome

Genetics

Protein

4q21 6q25 2p13 4q21 4p14 1p36 1p36 12p11–13 1p36

AD AR AD AD AD AR AR AD AR

-SYNUCLEIN PARKIN ? -SYNUCLEIN UBIQUITIN HYDROLASE MT PROTEIN KINASE DJ-1 (CHAPERONE) ? ?

endeavors. Writers, on the other hand, may continue with their creative work for many years despite severe physical limitations such as Joyce Cary (1888–1957). III. Neurogenetic Disease Depicted in Art

The commonest unifactorial neuromuscular disease is Duchenne muscular dystrophy. Since this disease, beginning in early childhood, is so obvious in its progressive nature resulting in death in late adolescence, it might be thought that it would have been noted and recorded. Although the problem has been carefully studied from early Egyptian art onward (Emery and Muntoni, 2003), the only

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convincing example is that of the Sick Boy (1915) by Karl Schmidt-Rottluf (1884–1976), a German expressionist painter. Myotonic dystrophy may have aVected the subject used by Botticelli in his painting of John the Baptist (1490), although this is purely speculative. A convincing and well-documented case of this autosomal dominant disorder, however, is portrayed in the head of Prince Alexandre Ypsilante, which was reproduced on a Greek stamp commemorating the country’s liberation in 1832 (Caughey and Myrianthopoulos, 1963). The marvelous portrait of Prof. Stephen Hawking, the acclaimed mathematician, by Yolanda Sonnabend in 1985 and now on display in the National Portrait Gallery, clearly illustrates the physical ravages of spinal muscular atrophy. The artist has also captured the subject’s mental alertness and penetrating gaze. Although there might be some question about the precise medical condition in many works of art, this is certainly not the case in which the artist is himself a doctor. This is well illustrated in the case of Sir Roy Calne’s Boy After a Liver Transplant (1989). The artist is also a renowned surgeon and tells us that the boy had Wilson’s disease (Fig. 2). This is an autosomal recessive condition causing neurological damage and cirrhosis of the liver due to defective copper metabolism. In this work, the artist has caught the relief the subject experienced

FIG. 2. Boy After a Liver Transplant (1989) by Sir Roy Calne (with kind permission of the artist).


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now as the procedure has been accomplished. But as one commentator has written, the work also ‘‘arrests the attention with an urgency and conveys a message of compassion, tolerance and understanding which is diYcult to escape’’ (Sheeran, 1991).

IV. Conclusions

Just a few examples have been discussed of neurogenetic conditions aVecting artists or portrayed in their art. But unless there is firm medical evidence of a diagnosis, there is a danger that such discussions can only be speculative. In some cases, the depiction of an apparent disorder may merely reflect the artist’s intention to convey an emotion or idea rather than a specific medical condition. This can certainly be the case in self portraits. An excellent example of this is the self portrait (1912) by Marc Chagall (1887–1985) in which he paints himself with seven fingers. But he did not have polydactyly. Apparently to be praised in Yiddish for doing something well is to do it with ‘‘seven fingers.’’ Like much of his art, it defies any superficial interpretation, which is also true of the work of many other notable artists.

References

Brice, A. (2005). How much does dardarin contribute to Parkinson’s disease? Lancet 365, 363–364. Caughey, J. E., and Myrianthopoulos, N. C. (1963). ‘‘Dystrophia myotonica and related disorders.’’ C. C. Thomas, Springfield, IL. Crutch, S. J., Isaacs, R., and Rossor, M. N. (2001). Some workmen can blame their tools: Artistic change in an individual with Alzheimer’s disease. Lancet 357, 2129–2133. Emery, A. E. H. (1997). Medicine, artists and their art. J. Roy. Coll. Phys. 31, 450–455. Emery, A. E. H. (2004). How neurological disease can aVect an artist’s work. Practical Neurology 4, 366–371. Emery, A. E. H., and Muntoni, F. (2003). ‘‘Duchenne muscular dystrophy,’’ 3rd ed. Oxford University Press, Oxford. Feany, M. B. (2004). New genetic insights into Parkinson’s disease. New Engl. J. Med. 351, 1937–1940. Fuller, G. N., and Gale, M. V. (1988). Migraine aura as artistic inspiration. Brit. Med. J. 297, 1670–1672. Hattori, N., and Mizuno, Y. (2004). Pathogenetic mechanisms of parkin in Parkinson’s disease. Lancet 364, 722–724. McHenry, L. C. (1982). Neurology and art. In ‘‘Historical Aspects of the Neurosciences’’ (F. CliVord Rose and W. F. Bynum, Eds.), pp. 481–519. Raven Press, New York.

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Mell, J. C., Howard, S. M., and Miller, B. L. (2003). Art and the brain: The influence of frontotemporal dementia on an accomplished artist. Neurology 60, 1707–1710. Panegyres, P. K. (2004). The contribution of the study of neurodegenerative disorders to the understanding of human memory. Q. J. Med. 97, 555–567. Podoll, K., and Robinson, D. (2000). Migraine experiences as artistic inspiration in a contemporary artist. J. Roy. Soc. Med. 93, 263–265. Ritchie, K., and Lovestone, S. (2002). The dementias. Lancet 360, 1759–1766. Sahlas, D. J. (2003). Dementia with Lewy bodies and the neurobehavioural decline of Mervyn Peake. Arch. Neurol. 60, 889–892. Sheeran, J. (1991). Sir Roy Calne: The paintings. In ‘‘The Gift of Life: Recent Paintings by Sir Roy Calne,’’ p. 37. Sheeran Lock Fine Art Consultants, Hebden Bridge, W. Yorks. Singleton, A., and Gwinn-Hardy, K. (2004). Parkinson’s disease and dementia with Lewy bodies: A diVerence in dose? Lancet 364, 1105–1107.

A NAI¨VE ARTIST OF ST IVES

F. Clifford Rose Founding Director, Academic Unit of Neuroscience Charing Cross & Westminster Medical School London, United Kingdom


Introduction Bryan Pearce His Painting His Sister Phenylketonuria Another Famous Case References

Naivete´ is simply the eruption of sincerity originally natural to Mankind. Emmanual Kant

I. Introduction

In 1971, my wife, Angela, went to the hairdresser in Sloane Street, London; it is no longer there, but when she came out there was an art gallery next door (again no longer there). Having been left a small sum of money by her recently deceased grandmother, she spent some of her inheritance (much to her father’s disappointment) on a naïve painting by an artist from St Ives, Cornwall (Fig. 1). His name is Bryan Pearce and at the time of writing (2006) he is still alive and painting. This chapter is about his life, my wife’s fondness for his paintings and the rare brain disorder from which he suVered.

II. Bryan Pearce

Bryan was born in St Ives, Cornwall in 1929; his birth weight was 8½ lbs, but he was a slow developer; he did not sit up until he was 9 months old and did not take his first steps until he was 2 years old. The most worrying feature was his INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74017-X

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FIG. 1. Angels (1971), 1973.

inability to communicate; he understood what was said to him but only slowly. In nursery school he was way behind his contemporaries in play and understanding. Because of his failure to speak, he was taken to a ‘‘speech specialist’’ in London, who attributed the problem to ‘‘some sort of phobia, possibly of a temporary nature’’ (Table I). At the age of 8½, Bryan went to a boarding school, where, because he held his head down in an odd manner, the headmaster’s wife recommended an osteopath. His general practitioner instead recommended a visit to a nerve specialist in London. When Bryan was 10 years old, he was assessed over a period of 1 week by three specialists who agreed that his intelligence was seriously impaired, either before or after birth, and he would never have normal intelligence. In the following years, he went to a school for the mentally handicapped, which, in the 1930s, was mainly custodial.


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TABLE I MILESTONES Birth weight Sits up First steps Speech specialists 8½ years 10 years

8½ lb 9 months 2 years ‘‘some sort of phobia, possibly of a temporary nature’’ osteopathy suggested Assessed by three specialists over 1 week whose diagnosis was: ‘‘Intelligence severely impaired, either before or after birth’’

Bryan, at the age of 16, left this boarding school and returned home so that his formal education, which was of necessity very limited, came to an end. At the age of 24, Bryan’s maternal grandmother, who had taken a Diploma in Drawing and taught before her marriage, suggested that one of the artists in St Ives, which was a center for art, might be encouraged to teach him to paint or draw; Bryan refused, hoping to improve his musical interest. In spite of this, his mother, who always herself wanted to paint, bought a child’s coloring book from Woolworths; this intrigued Bryan and his first eVort was coloring a picture of a musical instrument, the cornet, which he had seen being played. It was the same technique of painting that he continued in the following decades, namely, ‘‘meticulously in-filling of pure colour within a fixed framework’’ (Jones, 1976, p. 47). He later began to draw and paint objects of his own choice or which his mother suggested. A customer in his father’s butcher’s shop, Isobel Heath, invited Bryan to her studio, where he had weekly art lessons for 3 months. Armed with a letter from her, his mother took him to Leonard Fuller, the Principal of St Ives School of Painting, who accepted Bryan as a pupil; Bryan gave up his job at the family’s butcher’s shop in order to take up his new interest on four mornings a week.

III. His Painting

At the St Ives School, he used watercolors. His individual way of painting was to draw an outline in pencil on bare white board or canvas, first very lightly and then firmer, which was followed by yellow ochre (Fig. 2). He would then fill in using bright colors such as orange or yellow, or sometimes green if there were trees; this he found the enjoyable part, especially the details of stones, tiles, cobbles, and complex patterns (Whybrow, 1999,

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FIG. 2. Blue Jug and two primula pots (1998–99), Truro, 2003 (Conte´ drawing).

p. 24); all minor objects, such as these, windows, and flowers, had his intense concentration (Figs. 3–5). Particular yellow ochre was often used to outline stonework, possibly because of the lichen he saw on the roofs from his window. ‘‘Like Van Gogh, he could intensify the reality of simple household possessions and add a new significance to mundane things’’ ( Jones, 1976, p. 61). It was after 2 years of schooling with Mr Fuller that an exhibition of Bryan’s paintings was set up in their sitting room at home for the teachers of St Ives School; soon after this, Bryan made his first sale, which was of an old couch. His mother, Mary, was astonished when Mr Fuller told her that someone wished to know the price and she asked him whether half-a-crown would be too much, to which he replied, ‘‘I think we could ask five shillings’’ ( Jones, 1976 p. 58). The buyer was a lady artist who had returned from the Far East to St Ives and was delighted to discover a true ‘‘primitive.’’ It was after this that Bryan began


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FIG. 3. Pink Flowers in Glass Jug (1982).

working at home and Mary was pleased to give him her own studio, which she had begun to use.1 Bryan found oils easier to manipulate and mixes colors using several brushes but cleans them as he goes. His materials are oil on board, black ink on paper, and Conte´ crayons on tinted paper. In the early 1990s a gallery owner suggested to Bryan’s mother that Bryan might like to try the medium of Conte´ pencil on tinted paper, working on smaller pictures that could be completed in a shorter time. His subjects are St Ives and still life; harbor scenes were favorite subjects,

1 Bryan’s mother, Mary, now found time to have lessons from Mr Fuller on two mornings a week. Her technique proved peculiar to herself, for example, with portraiture, she would concentrate, without any preliminary drawing, on the upper third of the face, then the middle third, and finally the lower third. She obviously had artistic talent, and eventually, she did get her own studio at home. Mary Pearce died in 1997 at the age of 91.

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FIG. 4. DaVodils on Window Sill (1996).

particularly the blue sea and boats that showed his original color sense (Fig. 6). He will often sign his name but not at the bottom right or left hand corner. Recognizing his individual style, Bryan’s mother collected his paintings and eventually showed five of them at the annual Penwith Society’s Exhibition, which was intended to encourage new work that was diVerent and unconventional. His first one-man show was 5 miles from St Ives at Newlyn Gallery on Saturday, August 24, 1959, and several paintings were sold (Table II).

IV. His Sister

The parents were assured that the problem with Bryan would not occur if they had a second child, and his younger sister, Margaretta, was born in 1941. At the age of 7 months, her limbs suddenly become stiV, her eyes fixed, and the


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FIG. 5. Newlyn Harbour (2002).

whole body shook. Further fits followed, so teething and the changed diet were excluded as causes. At the age of 11 months, she was seen by a specialist, who told the parents it was petit mal and that many such children led normal lives, although some were retarded. The attacks became more severe, and 4 months later they were told, again by a specialist, that she would never walk or talk. Her brightness was now dulled by antiepileptic medication. At the age of 4½, she took her first steps and began to walk, albeit poorly. When Margaretta was 5 years old, she still needed continuous care since she did not learn to masticate food until well over this age and then learned to walk, run, dance, and sit and ride well on horseback. At about the age of 9, she began to have grand mal attacks (major epilepsy), which continued for the rest of her life. At one time Margaretta had a severe attack of acidosis requiring a diet of glucose and water, and for the following 6 years she had no attacks of epilepsy. The sedative drugs were stopped, and she began to use her arms and hands (Table III).

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FIG. 6. Porthleven (1967). ‘‘Outline painting’’.

TABLE II ARTISTIC DEVELOPMENT 1929 1953 1953–57 1959 1962 and 1964

Born in St Ives, Cornwall Begins drawing and painting Attends St Ives School of Painting First one-man exhibition at Newlyn Gallery St Martin’s Gallery, London

TABLE III MARGARETTA PEARCE—BRYAN’S SISTER Born First epileptic attack Diagnosis of petit mal First steps Grand mal attacks Died after nocturnal fit

1941 7 months 11 months 4½ years 9 years 19 years


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Margaretta’s nocturnal fits continued and one morning when she was 19, her mother discovered she had died, having suVocated in her sleep, an event long expected. Bryan took the death of his sister with calm, saying that although he missed her greatly, she had gone to heaven to be with Jesus. His paintings of three angels with golden haloes, rising from the clouds wore robes in fresco-bright colors. When asked about the presence of angels, he replied, ‘‘it just came into my mind—the church in the Holy Land with angels coming down from the sky’’ (Fig. 1).

V. Phenylketonuria

A cult called Divine Healers often visited the children and Mary wrote to a member, a medical man, who visited and said ‘‘diet is a most important factor in their lives.’’ This was later confirmed by the Mental Health visitor who told them that a rare disease, phenylketonuria, had been isolated. One of the specialists that Bryan Pearce saw was Dr Brian Kirman, who was a consultant psychiatrist at Queen Mary’s Hospital for Children at Carshalton, Surrey. He had a special interest in mental handicap and genetic disorders and was also an honorary consultant at the Maudsley and St Georges Hospitals. On Bryan’s paintings he said, ‘‘He has a natural talent set against a background of genetic hardship and he uses this talent with a natural, unsophisticated and appealing way.’’ Bryan Pearce was aged 44 when his parents were interviewed by the police because their son had been lost on the London underground railway. Because of his mental handicap, his mother doubted whether he would know to which station he was traveling. He was described as being 5 ft 9 inches, thickset, fair hair slightly thinning, blue eyes, and fresh complexion. They were in London for the opening of a Bryan Pearce exhibition at a Knightsbridge gallery, where for the first time a four-figure sum was paid for one of his paintings. It was in 1934 that the Norwegian biochemist and physician, Følling, described a metabolic disorder that caused severe intellectual impairment in addition to other features. He identified the condition by an abnormal excretion in the urine of phenylpyruvic acid. Følling was born near Trondheim, the ancient capital of Norway, in 1888. Unlike other farmers’ children, he went on to further education in Trondheim, where he majored in chemistry, but then went on to study medicine in Oslo, qualifying in 1922. In 1928, he won a Rockefeller Foundation Scholarship to study metabolic diseases in the United States. After returning to Norway, Følling was contacted by the parents of two children with mental deficiency. It was while routinely testing their urine with aqueous ferric chloride for ketones that he found the samples turned green and then faded. Normally, if no ketones are present, the

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wine turns red-brown; if they are present it turns purple, like burgundy, but to turn green was a new observation; the substance responsible was eventually shown to be phenylpyruvic acid. Følling then went on to test urine samples from 400 mentally defective children in institutions around Oslo and found eight individuals, including two additional sibling pairs, with the same reaction. They all had low IQ’s, spastic gait, and tended to be fair-haired. Although Følling initially called the condition imbecillitas phenylpyrouvica, it was named in 1983 phenylketonuria (PKU) by the English geneticist, Lionel Penrose, the name by which it is now known (Table IV). Phenylketonuria is a genetic disorder caused by a deficiency of an enzyme, phenylalanine hydrolase, which results in the failure to convert an amino acid, phenylalanine. Microcephaly (small head) and movement abnormalities are due to consuming food containing phenylalanine, which probably competes with such neurotransmitter precursors as tyrosine. Phenylketonuria is due to a deficiency of the enzyme phenylalanine hydroxylase, which helps in the conversion of phenylalanine to tyrosine, a normal amino acid in the blood. It is inherited as an autosomal recessive disorder but now all newborn infants are routinely tested; if the level of phenylketones is raised, then a specific diet prevents its toxic eVects on the central nervous system (Table IV). It was only in the 1950s that it was found that reducing the intake of phenylalanines during childhood and adolescence would prevent mental retardation. If the restriction of dietary phenylalanine is started before 3 weeks of age, this is eVectual in preventing brain damage. Although neonates are normal at birth, suVerers from PKU can show nonspecific developmental signs within 2 months, for example, vomiting; neurological deterioration is the prime feature, but does not occur until after 1 year of age. Every aVected child will show some degree of agitation, hyperactivity, movement disorder, or hypertonia. It is the consumption of phenylalanine in those with PKU that produces irreversible damage to the nervous system and untreated cases have an IQ of less than 60. Hypo-pigmentation with blue eyes and fair hair is often a feature, as is epilepsy. Urinary ferric chloride testing of the urine is not always adequate, so an estimation of PK is done when indicated; a TABLE IV PHENYLKETONURIA (PKU) Genetic disorder, autosomal recessive AVects 1 in 10,000 Fair hair, blue eyes, light skin Mental handicap Epilepsy Deficiency of phenylalanine hydroxylase


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level above 20 mg/dl with normal serum tyrosine and urinary excretion of phenylketones is diagnostic. There are, however, PKU variants. It is a rare condition occurring only once in 10,000 children (1:10,000). There is a slightly higher incidence in those of Irish and West Scottish blood. The fact that the Pearce family are Cornish and that these three areas are Celtic in origin may, therefore, be significant. It has been suggested (Christ, 2003, p. 44) that the higher than normal levels of phenylalanine may protect against the ‘‘negative health consequences associated with the consumption of mouldy foods’’ found in the wet climates of these areas; this explanation seems rather far-fetched. In the case of the Pearce children, the discovery was too late to be of benefit. Phenylketonuria has virtually ceased to present as a cause of mental handicap, such is the success of treatment. It is a classical example of an autosomal recessive mode of transmission, and, as is the case of similar conditions, alternative mutations provide a variation on the genetic theme (Kirman, 1979, p. 267). Bryan Pearce has a consuming interest in music, trains, and steamboats. He listens to classical music, mostly Beethoven, and the choir of King’s College Chapel. In his small library, he has a collection of illustrated books of steam trains. As Bryan enjoyed music, his mother bought him a glockenspiel that he played with a good sense of rhythm and timing. He is a regular churchgoer and sings all the hymns, reading from the hymn book; his reading of music notation is limited. With a large collection of classical records and tapes, he prefers to listen to classical music rather than watch television. When asked what he would like to have been if not a painter, he replied ‘‘a musician.’’ Bryan Pearce has been described as ‘‘a primitive painter in the sense that hardly an external cultural influence determined his art’’ (Whybrow, 1999, p. 89). After the death of his mother, and largely because of his age and a growing inability to control a shaky hand, Bryan’s painting took on another quality. The smooth application of oil paint was no longer possible, and the pictures showed a freer hand to their finish.

VI. Another Famous Case

Another famous case of PKU was the daughter of the Nobel Literature writer Pearl S Buck. In 1920, Carol, the daughter of Pearl S Buck (1892–1973) was born; she was nearly 3 years old when Pearl became aware that there was something wrong since she had not begun to talk and her movements were uncoordinated; it was later noticed that she had persistent eczema. At the age of 4, a psychologist pointed out how short was her attention span. By the age of 8 she was having ‘‘increasingly frequent behavioural outbursts’’ (Finger and Christ, 2004, p. 48). She became mentally retarded, and in order to pay for

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her institutionalized care, Pearl Buck wrote ‘‘The Good Earth,’’ for which she won the Pulitzer Prize in 1932; in 1938 she was the first American woman to win the Nobel Prize for Literature. It was not until the mid 1930s that Følling distinguished PKU from other forms of mental backwardness, much too late to help Carol Buck. Her illness was kept secret until Pearl published a book entitled ‘‘The Child who Never Grew’’ in 1950. References

Christ, S. E. (2003). Asbjorn Følling and the discovery of phenylketonuria. J. Hist. Neurosc. 12(1), 44–54. Finger, S., and Christ, S. E. (2004). Pearl S Buck and phenylketonuria (PKU). J. Hist. Neurosci. 3(1), 44–57. Jones, R. (1976). ‘‘The Path of the Son: A Biography of Bryan Pearce.’’ Sherlock Gallery Publications, Torpoint, Cornwall. Kirman, B. H. (1979). Mental handicap. In ‘‘Paediatric Neurology’’ (F. CliVord Rose, Ed.). Blackwell, Oxford. Whybrow, M. (1999). ‘‘The Innocent Eye: Primitive and Naı¨ve Painters in Cornwall.’’ Samson and Company Limited, Bristol.

VAN GOGH’S MADNESS



Introduction His Art His Illness Ear Amputation His Attacks What Disorder Did van Gogh Have? A. Epilepsy B. Schizophrenia C. Neurosyphilis D. Bipolar Disorder E. Substance Abuse F. Menieres Disease G. Acute Intermittent Porphyria References

I. Introduction

Historical Enquiry: L’art de choisir, entre plusieurs mensonges celui qui resemble le mieux a` la verite´ Rousseau

Vincent van Gogh (1853–1890), a vicar’s son, was a quiet boy, obstinate, secretive, a loner, but deeply religious. Although zealous as a missionary, he failed in this, as in previous attempts to find a career, (Table I), and it was then that his parents first thought that he began ‘‘to go to the bad’’ and considered putting him in a lunatic asylum, ‘‘en curatelle.’’ He stayed in London from the age of 22 for 2 years during which he fell in love with his landlady’s daughter, who was in love with someone else (Dunlop, 1974) and turned down his proposal of marriage. He later fell in love with his widowed cousin, whose father refused to let him see her, and it was after this rejection that he began to concentrate more on painting (Walther, 2000). INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74018-1

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TABLE I VINCENT’S LIFE BEFORE PAINTING The Hague, Goupil London, Goupil Paris England, clergyman Dordrecht, bookselling Amsterdam, divinity student Brussels, mission student Borinage, pastor

4 2 10 8 3 14 4 22

years years months months months months months months

TABLE II VAN GOGH’S ARTISTIC DEVELOPMENT 1864 1869 1880 1881 1884 1886 1886

Begins drawing Visits museums Sketches mines Starts landscapes; still life Teaches painting Takes painting course in Antwerp Paints 200 pictures in Paris in 2 years

II. His Art

It was at his brother Leo’s suggestion that he decided to become an artist. He was largely self taught (Table II). In the years 1882–1883, he made many mixed media drawings in the Hague, teaching himself to paint from a manual and books illustrating the old Masters. ‘‘Based in Paris during the years 1886–1888, van Gogh, after a unique five year apprenticeship, works with colour’’ (Tuchman, 2000). A review of his work (Reif, 1979) reported: ‘‘Van Gogh was 27 when he became an artist, having failed as an art dealer, teacher and minister. A thoughtful, well-educated man who was a fervent religious scholar and champion of the downtrodden, he sought to evoke the humanity and emotions in every day existence. His subjects were nature, peasants at work, and other ordinary people. Carefully and methodically following his vision, he produced over 2000 works in ten years. Van Gogh was a heavy smoker. He moved to Paris in 1886, discovering Japanese prints (Fig. 1) and the Impressionists’ bright colours. Travelling south to Arles in 1888, van Gogh, deriving inspiration from the bright sun and colour, painted with speed and intensity, determined to capture fleeting eVects and emotions.’’


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FIG. 1. Japonaiserie: Van Gogh museum, Amsterdam.

III. His Illness

In the winter of 1886, he was short of money, eating only bread, and smoking heavily. He developed dizzy spells and abdominal pain and consulted a doctor, as he feared ‘‘that I was not long for this world.’’ He found relief in painting, writing to his sister that ‘‘. . . it is a relief to paint a picture and, without it, I should be more miserable than I am’’ (De Lleuw, 1997; Roskill, 2000). Van Gogh left Paris for Arles in February 1888, where he produced his first Fauve painting with broad strokes and crushed paint. He felt he was ‘‘. . . now

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TABLE III VAN GOGH’S ILLNESS 1888 1889 1890

October 23 December May July May 27 July

Gauguin comes to Arles Cuts oV part of left ear Admitted to St Paul-de-Mausole, St Re´my-en-Provence Attacks after visiting Arles Auvers-sur-Oise (Dr Gachet) Shoots himself

bereft of control, or at the mercy of blind or mechanical forces . . ..’’ He was often tired and hungry and, in a letter to his brother, wrote ‘‘[t]he more ugly, old, vicious, ill and poor I get, the more I want to take my revenge by painting in brilliant colours, well arranged, resplendent.’’ In October 1888, the month that Gauguin arrived in Arles, he wrote to his brother, Theo, ‘‘I suVer from vertigo’’ (Pickvance, 1984, p. 28) (Table III).

IV. Ear Amputation

Gauguin lived with him for only 8 weeks, but they often argued. On the evening of the December 23, 1888, Gauguin and van Gogh drank some absinthe at a cafe´ when suddenly van Gogh threw a glass at Gauguin who dodged and then took Vincent, who looked like a sleepwalker, home by the arm. Back at the Yellow House, Vincent went to bed and fell asleep. On the next morning, Vincent had a swimming head and could not remember the previous night. This was all according to Gauguin (Cabanne, 1963, p. 155), who refused to return to their house and stayed that night in a hotel. Van Gogh, after going home, cut oV the lower lobe of his left ear (Fig. 2) by a diagonal incision beginning ‘‘posteriorly towards the top of the ear and cut anteriorly through the tragus (the prominence in front of the external opening)’’ (Lubin, 1975, p. 184). He had washed the ear, put it in an envelope and went to the brothel to present it to the prostitute (variously called Gaby or Rachel), saying, ‘‘Here is something to remember me by’’ (Druick and Zegers, 2001). The day following his ear amputation, having lost a good deal of blood, he was taken to hospital, where he was delirious with visual and auditory hallucinations. Under the care of Dr Felix Rey (1867–1932), (Fig. 3) who diagnosed acute mental derangement accompanied by generalized delirium, Theo was not allowed to see him. His illness cleared within 3 days, and he was discharged on


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FIG. 2. Self-portrait.

January 7, 1889. On leaving hospital, he began Dr Rey’s portrait, which (it is said) the doctor used to block a hole in a chicken coop.1 There have been various explanations for his ear amputation (Table IV), from being a phallic symbol to the influence of bullfighting in Arles, where a successful bullfighter would be presented with the dead bull’s ears—tauromachy (Lubin, 1975, pp. 186–187). Both these seem unlikely explanations. Even more far fetched is that, about the same period, Jack the Ripper was removing ears from Whitechapel prostitutes. A more recent suggestion is that Gauguin, who has been considered as a poor witness but the only observer of the incident, was responsible for the ear amputation as he was a fencer (Conradi, 2001). As the ear amputation occurred the day before Christmas, it may have been done in a fit of religious despair. Whatever the explanation, the ear amputation was perhaps the first unequivocal evidence of definite ‘‘madness.’’

1 Van Gogh painted three of his doctors, Covenaille, Rey, and Gachet (Park and Park, 2004). The first was in Antwerp in 1886 when being treated for dyspepsia by Dr Hubertus Amadeus Covenaille; instead of paying the doctor, van Gogh drew his portrait and presented it to him in lieu of a medical fee.

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FIG. 3. Dr Fe´lix Rey.

TABLE IV VINCENT’S EAR 1. 2. 3. 4. 5. 6.

Theo’s engagement Gauguin’s departure Tauromachy Jack the Ripper Religious Phallic symbol

V. His Attacks

On the January 7, 1889, the day of his hospital discharge, he writes ‘‘I hope I have just had simply an artists fit, and a lot of fever after very considerable loss of blood, as an artery was severed . . ..’’ Later that month he wrote ‘‘. . . the unbearable hallucinations have ceased, and are now getting reduced to a simple


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FIG. 4. St Paul-de-Marsule asylum, Hospital gardens.

nightmare, in consequence of my taking Bromide of potassium, I think . . .’’ (Pickvance, 1984, p. 29). In April 1889, he wrote ‘‘I have had in all four great attacks, during which I didn’t in the least know what I said, what I wanted and what I did. Not taking into account that I have previously three fainting fits without any plausible reason, and without retaining the slightest remembrance of what I felt’’ (Pickvance, 1984, p. 30). In the same letter (April 30, 1889) he wrote ‘‘[e]very day I take the remedy which the incomparable Dickens prescribes against suicide. It consists of a glass of wine, a piece of bread with cheese and a pipe of tobacco.’’ As van Gogh’s mental infirmities (diagnosed at the time as epilepsy) increasingly incapacitated him after 1888, he committed himself to the private asylum of St Paul-de-Mausole in St Re´my-en-Provence (Figs. 4 and 5), where he alternated between healthy outdoor painting and incoherent spells (Table V). He was there from May 1889 and left in May 1890.

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FIG. 5. Hospital ward, St Paul.

TABLE V 1889 7th January Early February Late February 8th May 7th July November December

Leaves Arles hospital Attack Further attack, readmitted Admitted St Paul-de-Mausole Further attack, depressed. In-patient 2 months Visits Arles Attack lasting one month

Van Gogh wrote that ‘‘. . . there is quite definitely something or other deranged in my brain . . ..’’ In July 1889, while settling down to paint, his orderly by his side, his eyes ‘‘suddenly became wild, his hand began to move convulsively, his body arched backwards.’’ This was undoubtedly an epileptic attack, which Dr Perynon, Director of the asylum, diagnosed. For 3 weeks he suVered attacks of confusion and prostration, after which he was remorseful and depressed. In


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September 1889, he noticed attacks came every 3 months and had another attack in December 1889, but this was less severe, lasting 1 week. The year 1890 is important in his disease progression. On January 23, he had an attack after visiting Arles. On the February 1, his nephew was born, and this may have aVected him as he would be a rival for Theo’s financial interests. On February 24, 1890, he visited a brothel and had another severe attack; he snatched lamp oil to drink, sank into a dazed state and only in April began to improve. During convalescence he suddenly kicked his orderly in the stomach and said: ‘‘forgive me, I’m not very clear what I’ve done. I thought I was at Arles being hunted by police.’’ During this time he was erratic and moody and again began to drink. He lost his temper with boys who teased him by putting salt in his coVee. In all, he had seven attacks in Arles and St Re´my. Four were ‘‘grandes crises’’ and three fainting spells, but he was amnestic for all of them; they were all sudden in onset and slow in resolution. He recovered from most within 1–2 weeks, but two lasted 2 months. While at St Re´my, three or four episodes occurred after going to Arles (Lubin, 1975, p. 217). The attacks were initiated by an ‘‘acute state of delirium and disorientation,’’ accompanied by visual and auditory hallucinations and paranoia. He was drinking turpentine, kerosene, and oil colors, so his tubes of color paints had to be removed. During these attacks he was unable to paint, did not always recognize people, and ‘‘complained of dizziness which was provoked by heights and he disliked climbing stairs’’ (Pickvance, 1986). In the year that Vincent was in St Re´my-en-Provence, he painted 150 oils, 100 drawings, 10 watercolors, and wrote 750 letters, which were all lucid (Walther and Metzger, 2001).

VI. What Disorder Did van Gogh Have?

There is no consensus as to the diagnosis of van Gogh’s illness, but Pennanen (1995), a surgeon in Washington, mentioned several possibilities that are discussed in the following sections. A. EPILEPSY In Arles, the house surgeon, Dr Rey, talked of epileptic crises and Dr Perynon, Director of the St Re´my asylum, of attacks of epilepsy. Weight was paid to the family history of epilepsy, and it was concluded that the cause of his illness was some form of epilepsy ‘‘whether exacerbated by absinthe, glaucoma, digitalis poisoning or Syphilis . . .. Between his breakdowns in the asylum he had long periods of absolute lucidity . . .’’ (Pickvance, 1986, p. 15). He had three

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blackouts without warning in April 1889. On other occasions, there was ‘‘prolonged loss of consciousness, often preceded by irrational behaviour’’ (Critchley, 1987, p. 157). The diagnosis of epilepsy would fit in with his complete recovery between attacks, and Prof Henri Gastaut of Marseilles, a famous epileptologist, diagnosed temporal lobe epilepsy. His attacks were controlled by bromides, then the only antiepileptic drug known, but this as a sole diagnosis would not explain prolonged attacks lasting weeks. There are two main types of epilepsy—primary and secondary. Primary epilepsy starts usually before the age of 20 and is familial. On his mother’s side, there were several with epilepsy, a maternal aunt reputedly dying from this condition. Secondary epilepsy, which includes epilepsy of late onset (i.e., after the age of 20), is symptomatic of an underlying cause. It may be due to a birth injury; he was the eldest of six surviving children and was born when his mother was 35; labor was prolonged, and, at birth, he had craniofacial asymmetry. More recently, some authorities label seizures that are secondary as not ‘‘full’’ epilepsy (Hughes, 2005). B. SCHIZOPHRENIA Schizophrenia was considered the most likely diagnosis by Karl Jaspers and the German School of neuropsychiatrists. His sister was diagnosed as schizophrenic, and some of his behavior, such as paranoia and suicidal thoughts, would support this diagnosis, but it does neither fit in with sudden complete recovery between episodes nor with his abdominal problems. C. NEUROSYPHILIS In 1882, he had an attack of gonorrhoea and could have contracted syphilis from his mistress, a prostitute in Antwerp, but the time interval was too short for the development of general paralysis of the insane (GPI), although not for meningo-vascular syphilis, the other type of tertiary neurosyphilis, which, however, would not explain his symptoms. At this time his teeth fell out, possibly due to mercury treatment of his supposed syphilis. D. BIPOLAR DISORDER Bipolar disorder (manic-depressive psychosis) has been diagnosed because of intermittent confusional episodes, with prolonged periods of hypomanic activity in between. In favor of this diagnosis was that his illness developed in his third, and lasted into his fourth, decade. When admitted to hospital in Arles, the


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diagnosis of the Director was acute mania with generalized delirium. There were periods in which he would gesticulate and talk wildly with great agitation. At other times these episodes were followed by prostration and calm. These sudden attacks could be provoked by trifling incidents, and he had no recollection of his attacks of hallucinations during which he had uncontrollable aggression and threatening behavior. His abdominal symptoms and epileptic attacks could not be explained by manic-depressive psychosis, and complete recovery in between attacks is against the diagnosis in van Gogh’s case. E. SUBSTANCE ABUSE 1. Alcohol His health suVered because of his excessive smoking and drinking. During the winter of 1887–1888 in Paris, he had problems with his ‘‘blood,’’ variously described as poor circulation or anemia as well as indigestion, nerves, and melancholy; the latter was made worse by attempts to reduce his alcohol intake and smoking. In Paris, he had a ‘‘tired brain’’ and ‘‘tired eyes’’ after painting and referred to a ‘‘stroke’’ and ‘‘breakdown.’’ Following withdrawal of alcohol,2 delirium tremens often ensues, which includes visual rather than auditory hallucinations. Tremor is almost invariable (hence the name), but it would be strange if this diagnosis had not been made at that time when it was a well-recognized condition. His attacks seem to be provoked after alcohol intake rather than its withdrawal as would be the case in delirium tremens. 2. Absinthe He talked of ‘‘bad wine’’ in Paris and brandy in Arles but did not mention absinthe, possibly because this was not specifically considered as a toxin at that time. A toxic psychosis consists of disorientation, hallucinations, delusions, feelings of terror, and violent behavior. He was said to have drunk absinthe excessively in Paris. It was Hemphill (1961), who first pointed out that van Gogh, was more sensitive than others (e.g., Gauguin) to the eVects of absinthe and he was ‘‘a manic-depressive who develop confusional periods and fits due to his addiction to the liqueur called absinthe.’’ Van Gogh’s crises were improved when 2 Another example of substance abuse in the case of an artist was Toulouse-Lautrec, who was an alcoholic; it was while being ‘‘dried out’’ in a clinic that he drew his famous circus scenes. He had many medical connections, for example, he spent Saturday mornings visiting hospitals, and his chosen profession if he had not become a painter was medicine; and his last paintings often had a medical association. He was said to have died of a stroke at the age of 37, the same age at which his friend van Gogh died.

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institutionalized, given bromides with restricted smoking. The Absinthe drinker was painted by Edgar Degas (1934–1917) showing that drug addiction was not an uncommon condition.3 Unlike the hallucinations of schizophrenia, which are usually auditory, absinthe can also cause visual hallucinations.4 The symptoms may present after drinking ceases. The consumption of absinthe was four times the national average in Bouches-des-Rhoˆne, which includes Arles and St Re´my. In excess, it gave seizures, vertigo, hallucinations, and delirium; its constituent, thujone, is a brain toxin, which is also found in cannabis. Van Gogh took excessive amounts of camphor to help him sleep, turpentine, which contains pinene, and was found in oil colors that he also took. Thujone and camphor induce convulsions in animals, which are relieved by bromides. 3. Digitalis Used now in cardiac conditions, van Gogh’s propensity for yellow and halo eVects has been claimed to be due to digitalis. On two occasions in 1890, he painted Dr Paul-Ferdenand Gachet; in both pictures there is ‘‘a foxglove flower of dark purple,’’ that is, Digitalis pupurea, the purple foxglove,5 from which digitalis is obtained. The Czech neuroscientist, Jan Evangelista Purkinje, experimented in 1825 with digitalis, which he reported produced circular concentric light and dark waves.

3 Degas’ ‘‘Absinthe drinker’’ can be seen in the Jeu de Paume, the Impressionist gallery adjoining the Louvre. It was unusual for Degas because he did not usually use models; he knew the couple portrayed well and asked them to pose in the Cafe´ de la Nouvelle-Atheńes on Place Pigalle. Painted in 1876, the man was Marcellin Desboutin, a painter and engraver, who introduced Degas to the cafe´; the woman Ellen Anfree, was an actress. While she is portrayed as innocent and youthful and fashionably dressed he is mature and worldly. They both sit with sad eyes staring distractedly in a state of apathy. Degas suVered from high grade myopia and for the last 20 years of his long life, was blind from myopic degeneration. This may be the reason why initially he drew from photographs and later took more to sculpture. 4 Toulouse-Lautrec and Modigliani also drank absinthe, as did the poets Baudelaire and Verlaine. Absinthe was popular in nineteenth-century France and was obtained from wormwood (Artemisia absinthium). It was thought to be a cure-all and was used by French soldiers in Algeria to reduce fevers. The first commercial producer was Henri Louis Pernod in 1797 who obtained the recipe from a Swiss GP: ‘‘The extract was prepared by steeping the pungent herb in alcohol and distilling the spirit.’’ Other herbs, such as fennel and licorice, were added to lessen the bitter taste. Its production was prohibited in France during the First World War in 1915 since absinthe was found to be addictive. Modern Pernod is an aniseed-flavored beverage. The ban has recently been lifted, and a less powerful absinthe is available, known as the ‘‘Green Fairy.’’ 5 In the nineteenth century it was used to treat epilepsy. Digitalis intoxication causes confusion, delirium, and hazy yellow vision.


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4. Lead Poisoning He could have inhaled lead from his paints, but his symptoms were not suggestive of lead poisoning, which more likely might have acted as a trigger. F. MENIERES DISEASE Although he complained of dizziness (possibly more likely to be unsteadiness rather than true vertigo, a rotatory sensation), there was no suggestion of episodic attacks or accompanying nausea or tinnitus nor would Menieres disease explain all the other symptoms of his disorder. G. ACUTE INTERMITTENT PORPHYRIA Acute intermittent porphyria (AIP) is a metabolic disorder in which there is an excessive production of porphyrins so that their concentration is raised in the body and the urine. The term acute in AIP is because of the rapid onset and cessation of the intermittent attacks with normal intervening periods. The typical age of onset is in the third decade (20–29 years), and the most common symptoms are gastrointestinal, that is, abdominal pain, vomiting, diarrhea, and constipation. The neurological abnormalities are due to the porphyrin precursors, and in AIP there are no skin problems, as in van Gogh’s case. Warnings of the attacks are irritability and restlessness.6 The weakness usually resolves within months after the attacks as do such psychiatric problems as delirium, agitation, depression, or paranoia. Epilepsy occurs in about 20% of patients (Table VI). Low calorie diets should be avoided such as, in van Gogh’s case, going without food; low protein and low carbohydrate diets are especially detrimental. Drinking alcohol precipitated his attacks; he was in remission when the triggers were obviated while an inpatient and also by bromide therapy. A single explanation for all these features in van Gogh would be acute intermittent porphyria (Loftus and Arnold, 1991) (Table VII). The first diagnosis of AIP was reported in the Dutch medical literature just before van Gogh’s death, so his attending doctors would not have been aware of 6 Porphyria is a disturbance of haem, the essential constituent of hemoglobin, contained in red blood cells. It results in a group of disorders, the chief of which are neuropsychiatric. Of the seven enzyme defects, three produce disturbances of the skin. Of the hepatic porphyrias, acute intermittent porphyria, which is the commonest, does not cause skin photosensitivity. Although it is inherited as an autosomal dominant, 90% are latent without any disease. Triggers that provoke attacks are drugs and poor nutrition.

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TABLE VI SYMPTOMS OF PORPHYRIA Abdominal Psychiatric

Nausea, vomiting, colic, constipation, diarrhea Anxiety, depression, confusion, coma, hallucinations, epilepsy

TABLE VII ATTACKS IN PORPHYRIA Age of onset Length of attacks Remissions Triggers

Adult years Days to months Weeks to years Fasting, alcohol (absinthe), fatigue, infections

this diagnosis. Transmission by an autosomal dominant gene would fit in with the fact that van Gogh had several relatives with neuropsychiatric disorders (Dean, 1971).7 Triggers included overwork and a proclivity for camphor and other terpenes. The reason why there has been no report of colored urine may be explained since ‘‘freshly voided urine is colourless, but on exposure to air and light it becomes dark or a wine red colour after several hours’’ (Loftus and Arnold, 1991). Since van Gogh did much of his painting out of doors, the urine would have been colorless. The cerebral features of porphyria include anxiety, agitation, and seizures, all of which van Gogh had. Behavioral disturbances, for example, irritability, confusion, mania, or depression, occur in 30% of cases and epilepsy in 20%. Drugs precipitate the attacks; especially alcohol, and this may be the reason why he often developed attacks after visiting Arles. As in van Gogh’s case, there may be 7

The word porphyria is derived from the Greek word meaning reddish-purple. The red pigment that gives a reddish urine does not contain iron. The porphyrias are inherited as autosomal dominant traits (except for congenital erythropoietic porphyria). They are due to abnormalities in the synthesis of haem and associated with excessive secretion of porphyrins (Green, 1976). Although porphyria variegata and acute intermittent porphyria are both genetically determined, they are two distinct inborn errors of metabolism. Both types occur in Holland. Patients may complain of abdominal pain, made worse by barbiturates, they may be unstable, neurotic, or mentally disorientated (Dean, 1971, p. 1). In the 1963 classification, porphyrias are broadly divided into hepatic and erythropoietic. The first includes: 1. 2. 3. 4.

acute intermittent porphyria porphyria variegata coproporphyria porphyria cutanae tarda.

The erythropoietic is divided into: 1. congenital porphyria 2. erythropoietic protoporphyria.


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FIG. 6. Dr Gachet.

no symptoms in between attacks. A thousand cases of porphyria in South Africa were all descended from two Dutch immigrants 3 centuries previously. After his year in the asylum of St Paul-de-Mausole in St Re´my-en-Provence, van Gogh moved to Auvers-sur-Oise, 20 miles to the northwest of Paris, where his brother Theo had arranged for Dr Paul Ferdinand Gachet (1828–1909) to look after him. Dr Gachet was said to be a specialist in nervous diseases and the role of occupational therapy in psychiatric disease. He was interested in art and had known the young Ce´zanne and Pissarro. In 10 weeks he stayed at Auvers-sur-Oise, van Gogh did an etching, the only one he ever did, and two oil paintings of Dr Gachet (Fig. 6). On the July 27, 1890, on a bright, hot day, Vincent, who was usually punctual, was not in time for dinner. ‘‘They found him in his second-floor room stretched out on his bed, lying in his own blood.’’ He had shot himself (Bonafaux, 1992, p. 126) and died at the age of 37 (Table VIII). The parish priest refused to give a funeral to a man who had committed suicide. He was buried on July 30, 1890; his brother, Theo, died a year later in Utrecht, and his ashes were

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TABLE VIII THE LAST 18 MONTHS 1888 1889 1890

October 23 December May

Gauguin comes to Arles Cuts oV part of left ear Admitted to St Paul-de-Mausole St Re´my-en-Provence Attacks after visiting Arles Auvers-sur-Oise (Dr Gachet) Shoots himself

July May 27 July

transferred to Auvers-sur-Oise in 1914 to lie beside his beloved brother (Bonafaux, 1992). It is not accurate that van Gogh ‘‘sold only one painting’’ because he sold ‘‘a drawing in The Hague, a few items sold in Paris, a self-portrait sold to a London dealer in 1888 and one sale from an influential Les Vingt exhibition (1890) in Brussels’’ (Arnold, 2004); these were apart from three commissions and acceptances of his art work in lieu of payment for services. Toward the end of his life, he was deeply disappointed in his lack of recognition—he believed in himself as a great artist and followed the example of such masters as Michelangelo (Buonarroti), Raphael (Santi), and Rembrandt (van Rijn) by signing his paintings with only his first name, Vincent. References

Arnold, W. N. (2004). The illness of Vincent van Gogh. J. Hist. Neurosci. 13(1), 22–43. Bonafaux, P. (1992). ‘‘Van Gogh: The Passionate Eye.’’ Thames and Hudson, London. Cabanne, P. (1963). ‘‘Van Gogh.’’ Thames and Hudson, London. Conradi, P. (2001). ‘‘Gauguin cut oV van Gogh’s ear.’’ Sunday Times, London. Critchley, E. M. R. (1987). ‘‘Hallucinations and Their Impact on Art.’’ Carnegie Press, Preston. Dean, G. (1971). ‘‘The Porphyrias.’’ Weidenfeld and Nicolson, London. De Lleuw, R. (1997). ‘‘The Letters of Vincent Van Gogh.’’ Penguin, London. Druick, D. W., and Zegers, P. K. (2001). ‘‘Van Gogh and Gauguin: The Studio of the South.’’ Thames and Hudson, London. Dunlop, I. (1974). ‘‘Van Gogh.’’ Weidenfeld and Nicolson, London. Green, M. (1976). ‘‘Porphyria in Handbook of Clinical Neurology’’ (P. J. Vinker and G. W. Bruyn, Eds.), Vol. 27, pp. 429–448. Oxford, North Holland. Hemphill (1961). The illness of Vincent van Gogh. Proc. Roy. Soc. Med. 54, 1083–1089. Hughes, J. R. (2005). A reappraisal of the possible seizures of Vincent van Gogh. Epilepsy Behav. (In Press). Loftus, L. S., and Arnold, W. N. (1991). Vincent van Gogh’s illness: Acute intermittent porphyria. Brit. Med. J. 303, 1589–1591. Lubin, A. J. (1975). ‘‘Strangers on the Earth: The Life of Vincent Van Gogh.’’ St. Albans, Parladin.


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Park, M. P., and Park, R. H. R. (2004). The fine art of patient-doctor relationships. Brit. Med. J. 329, 1475–1480. Pennanen, M. F. (1995). Vincent van Gogh: What do his letters suggest about the diagnosis. J. Med. Biog. 3, 43–49. Pickvance, R. (1984). ‘‘Van Gogh in Arles.’’ Harry N Abrams, New York. Pickvance, R. (1986). ‘‘Van Gogh in St Re´my and Auvers.’’ Harry N Abrams, New York. Reif, W. J. (1979). Van Gogh’s Van Gogh. Lancet 352, 1478. Roskill, M. (Ed.) (2000). ‘‘The Letters of Van Gogh.’’ Flamingo, London. Tuchman, P. (2000). Facing Van Gogh at the PMA. Lancet 356, 1529–1530. Walther, I. F. (2000). ‘‘Vincent Van Gogh 1853–1890.’’ Taschen, London. Walther, I. F., and Metzger, R. (2001). ‘‘Van Gogh: The Complete Paintings.’’ Taschen, London.


ABSINTHE, THE NERVOUS SYSTEM AND PAINTING

Tiina Rekand Department of Neurology, Haukeland University Hospital and University of Bergen 5021 Bergen, Norway

I. II. III. IV. V.

Introduction Art as a Reflection of Life Medical EVects of the Absinthe EVect of Absinthe on Artistic Expression Conclusions References

I. Introduction

Paris has been an important center of cultural events and bohemian life from the middle of the nineteenth century. Many prominent artists performed and were inspired by the cafe´-life in which the use of absinthe was an inseparable part of bohemian life in many years. Absinthe is a green strong liquor containing ethanol (70%–80%) and wormwood (Artemisia absinthium) (Lanier, 1995). In addition, several herbs, including anise, fennel, melissa, hyssop, juniper, angelica, nutmeg, star anise, and veronica, are ingredients that were used for flavor and aroma (Conrad, 1988). The harmful constituents of absinthe originate from wormwood (Lanier, 1995), which, historically, has been known as an eYcient remedy against intestinal worms and moths and was used as a medicine in ancient Greek and earlier Egyptian culture. In his compendium Historia Naturalis, Pliny the Elder described wormwood as a potent medicine against tapeworms and stomach pains (Conrad, 1988). Absinthe, however, was first produced much later, in 1792 with a recipe created by a French general practitioner, Pierre Ordinaire, in Switzerland and introduced as an all-purpose treatment (Berulfsen, 2001; Conrad, 1988). Five years later, Henri-Louis Pernod bought the recipe and opened the first absinthe distillery in Switzerland and later a larger one in Portarlier, France (Berulfsen, 2001; Conrad, 1988). Initially the drink was expensive and only used by the wealthy but, thanks to wars in the nineteenth century, the usage increased to INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74019-3

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become more common (Lanier, 1995). In the 1870s, l’heure verte (‘‘the green hour’’) became an established event in many cafe´s and clubs in Paris. The popularity of absinthe has several explanations: it is very bitter and has to be mixed with sugar; since the mixture should be made slowly, special equipment, such as spoons and water dispenser, are needed. The traditional absinthe ritual requires a flat spoon with tiny holes placed on the top of a special glass containing green absinthe, which is mixed with syrup by dripping water on sugar cubes. The drink then turns to a milky color because the essential herb oils are precipitated. Such an interesting ritual is well suited for social events (Arnold, 1989; Conrad, 1988; Rekand and Sulg, 2003).

II. Art as a Reflection of Life

In the beginning of the twentieth century, absinthe was a common part of social, bohemian, and artistic life in Paris. Many artists and poets did enjoy absinthe and portrayed their personal experiences as well as life around them. The lives and literary work of French poets and bohemians, such as Paul Verlaine (1844–1896) and Arthur Rimbaud (1854–1891), were influenced by absinthe abuse (Lanier, 1995). The English poet Oscar Wilde (1854–1900) used absinthe, one of his famous citations being: ‘‘After the first glass you see things as you wish they were. After the second, you see things as they are not. Finally you see things as they really are, and that is the most horrible thing in the world’’ (Conrad, 1988; Lanier, 1995). Absinthe drinking was depicted by several artists of that time. The impressionist Edouard Manet (1832–1883) painted The Absinthe Drinker in 1858–59 and submitted the painting to the French Salon for exhibition in 1859, but it was rejected as not appropriate. After this rejection, many paintings by innovative artists, later called the impressionists, were not accepted by the French Salon. The Salon de Re´fuses was established to let the public judge the rejected paintings (Lanier, 1995). Edgar Degas (1834–1917) painted his version of the absinthe drinking, L’Absinthe (often known as In a Cafe´) in 1876; this portrays two people at nearby tables whose isolation and loneliness are apparent, and it was widely criticized for its theme and composition, particularly in England (Lanier, 1995). French post-impressionist Henri Toulouse-Lautrec (1864–1901) is best known for his depiction of life in Paris in the 1880s and 1890s; he took an active part in nightlife and probably introduced local drinking habits to his many friends, including Vincent van Gogh. Toulouse-Lautrec used absinthe himself and was famous for his home-made drinks, his speciality being a mix of cognac and absinthe called ‘‘earthquake’’ (Lanier, 1995). His paintings, by Cafe´-life, depicts absinthe drinking in several of his works such as At the Moulin Rouge


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(1892–95), Monsieur Boileau at the Cafe´ (1893), At Grenelle, absinthe drinker (1886), and The absinthe drinker (1888). He portrayed his friend Vincent van Gogh with an absinthe glass in 1887 (Conrad, 1988; Lanier, 1995). The Spanish artist Pablo Picasso (1881–1973) moved to Paris in 1904 after frequent visits since 1900. Absinthe drinking and absinthe had been an inspiration for several of his works from the diVerent periods. He had a particular fascination of absinthe drinking women and created several diVerent paintings during 1901–1902, such as The absinthe drinker (1901 and 1902), The absinthe (1921), The absinthe lover (1901), Woman drinking absinthe (1901); the latter shows most clearly the personal degradation as a consequence of absinthe abuse. Later, Picasso became interested in absinthe as a theme: the paintings The glass of absinthe (1911) and Bottle of Pernod and Glass (1912) were followed by the bronze sculpture Absinthe Glass in 1914. He made six sculptures with the absinthe glass, spoon, and sculptured cube of sugar. Although similar in configuration, each one was painted diVerently (Lanier, 1995). There are several less known artists who were inspired by the absinthe theme, which was used in their artworks. Some of these paintings, for instance Albert Maignan’s The green muse (1895), have later been their best known artwork. The drinking of absinthe was not only associated with Paris at that time but was used among bohemians in several countries, for instance the Norwegian painter Edvard Munch painted his bohemian friend Hans Jaeger with an absinthe glass in 1898 (Rekand and Sulg, 2003).

III. Medical Effects of the Absinthe

The first medical studies on the eVects of absinthe were published around 1870 (Amory, 1868; Magnan, 1874). Magnan studied the eVect of absinthe both clinically and experimentally and concluded that abuse caused epileptic seizures, respiratory problems, and reddish urine. The identified epileptogenic agent was the oil of wormwood (Magnan, 1874). Cases of acute poisoning with wormwood oil are seldom mentioned, but The Lancet published a case of acute intoxication caused by essential oil of wormwood in 1997 (Weisbord et al., 1997), which was ordered via the Internet and was meant for aromatherapy but was consumed in the belief that he was drinking absinthe. Acutely hospitalized with epileptic seizures and agitation, disorientation, and lethargy, he developed hypernatremia, hypokalemia, hypobicarbinaemia, and later rhabdomyolysis with acute renal failure. After long abuse with absinthe, the syndrome absinthism includes auditory and visual hallucinations, sleeplessness, tremor, epileptic seizures, and paralysis. The visual eVects include xanthopsia, diplopia, and amblyopia (Arnold and Loftus,

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1991). In the beginning of the twentieth century, the public became more aware that absinthe may cause psychological disorders. In 1905, Jean Lafray, a peasant and regular absinthe drinker, in Switzerland, murdered his pregnant wife and two daughters without apparent cause (Lanier, 1995); investigation later revealed that he used various alcoholic drinks, including absinthe. Lafray was examined by a psychiatrist from the University of Geneva who concluded that his long-time abuse of absinthe contributed to his blind rage and the murders. The tragedy caused much attention and lead to later prohibition of absinthe in almost all of Europe, but the use of absinthe continued to be a part of the bohemian life, at least in Paris until the 1930s (Conrad, 1988). The exact mechanism of action of absinthe remained unclear for many years. The toxic ingredient of absinthe is thujone, a terpenic oil of wormwood. In 1974, Del Castillo reported with coworkers similar psychological reactions in users of absinthe and marijuana (Del Castillo et al., 1975). They hypothesized that both thujone and tetrahydrocannabiol, the toxic ingredient of marijuana, interact with a common receptor in the central nervous system. More detailed explanation was published in 2000 by Ho¨ld and coworkers (2000) who demonstrated in four diVerent ways that -thujone is a modulator and antagonist of -aminobutyric acid type A receptor channels. This mechanism explains why thujone has an excitatory eVect on brain function. In absinthe, however, two antagonistic eVects counteract each other namely the anxiolytic eVect of ethanol and the analeptic eVect of thujone (Olsen, 2000).

IV. Effect of Absinthe on Artistic Expression

The Dutch artist, Vincent van Gogh, was one of the most prominent postimpressionist painters. Born in 1853 in Zundert, the Netherlands, he was the eldest son of Theodorus van Gogh and Anna Cornelia Carbentus (van Goghs museum, 1996). At the age of 16, he started working in an art gallery but later tried several professions, including teaching and a religious career. In 1880s, he decided to become an artist, a decision supported by his brother, Theo. Van Gogh began his art studies in the Netherlands but in 1886 moved to live with his brother in Paris, where he lived and painted for 2 years. In 1888, he left Paris for Arles, a city in southern France, where he stayed for 15 months. During this period he had several attacks of illness and in one of them he cut oV his left ear lobe. In April 1889, he was voluntarily admitted at Saint-Paul-de-Mausole asylum. In 1890, he went to Paris for a few days and then to Auvers-sur-Oise, where he was examined and observed by Dr Paul Gachet. He stayed there from May 23 until July 27, 1890 when he shot himself in the chest and died 2 days later.


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There are several hypotheses regarding van Gogh’s illness including bipolar disorder, epilepsy, porphyria, and Meńiere’s syndrome (Arenberg et al., 1990; Loftus and Arnold, 1991; Meissner, 1998; Ravin and Anderson, 1998). In addition, there was a considerable abuse of absinthe. His portrait with an absinthe drink painted by Toulouse-Lautrec and van Gogh’s own Still life with Absinthe (1887) are evidence that absinthe was part of his lifestyle, probably also during his hospitalization at the asylum (Arnold, 1988), but he also abused several other substances such as alcohol, nicotine, and bromide (Arnold, 1988). Arnold and Loftus examined van Gogh’s yellow palette in his paintings between 1885 and 1890 (Arnold and Loftus, 1991). Of the 638 paintings during this period, some are so called ‘‘high yellow pictures’’ with a rich yellow color without blue, violet, and white. The lack of blue is as important as the presence of yellow for diagnosing xanthopsia. Among those high yellow paintings are one version of Sunflowers (painted in Paris, 1887), The Night Cafe (Arles, 1888), and Roses (St. Re´my, 1890). Although van Gogh abused several substances, the episodic changes to high yellow and sudden change of artistic expression may be explained by absinthe-related xanthopsia and visual hallucinations. The internationally known artist Eduard Wiiralt (1898–1954) was one of the most valued Estonian artists of the twentieth century. Between 1919 and 1921, he studied at the art school ‘‘Pallas’’ in Estonia. He won a scholarship to study in Dresden, Germany (1922–23) and returned to Estonia in 1924. In 1925, he moved to Paris where he stayed until 1939; during this period, he had his first exhibition in Paris and subsequently several others in Europe, which lead to his artistic breakthrough. Wiiralt returned to Estonia in 1939 but left in 1944 to Vienna but in 1946, settled in Paris until his death in 1954 (Levin, 1998). Wiiralt started his artistic career as a book illustrator but later became a graphic artist. His earlier pictures were characterized by a realistic artistic expression until 1933. In his first period in Paris, he achieved fame and took an active part in social events and bohemian parties. In 1930–1933, his artistic expression changed considerably and created his best known work The Hell (1930–1933) (Fig. 2), The Cabaret (1930), and The Preacher (1932). All these works have a new, mystic-hallucinatory theme with a confluent mixture of shapes and figures. In 1933, he painted The absinthe drinkers (Fig. 1). Two absinthe drinkers, presented in this picture, have double irises in their eyes. One interpretation of these faces may be that the drinkers experience diplopia, a common eVect of absinthe abuse. In 1933, Wiiralt collapsed because of his abuse and was hospitalized for rehabilitation. His health had considerably deteriorated, and he had to stop all use of alcohol, which he managed to do and continued his artistic career for 2 more decades until his death. However, the mystic expression disappeared, and he returned to a more realistic one. Retrospectively, Wiiralt admitted his long abuse of absinthe in the letters to his friends (Kangro, 1955). The Absinthe drinkers

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FIG. 1. E. Wiiralt. The absinthe drinkers, 1933.

indicate that he had knowledge of the eVects of absinthe on vision. The change of artistic expression to a more mystical one in 1930–1933 was probably caused by absinthe-related visual hallucinations since it stopped after his rehabilitation (Rekand and Sulg, 2003). V. Conclusions

In the past, the use of absinthe was common, particularly among bohemians and as part of the nightlife in Paris and generally in Europe in the nineteenth and twentieth centuries. Many artists, impressionist, and postimpressionist, in


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FIG. 2. E. Wiiralt. The hell. 1930–1933 (fragment).

particular, used absinthe drinking as a theme in their paintings; long abuse lead to changed perception so that subsequently artistic expression changes. The periodical yellow palette of Vincent van Gogh at the end of his life and the peculiar hallucinatory expression of Eduard Wiiralt in 1930–1933 may be a consequence of absinthe abuse. This does not in any way diminish the artistic value of these pictures. After many years of prohibition, absinthe is again available and may be obtained in several countries, even via the Internet; the current formula lacks its original toxic features because the upper limit of thujone concentration is lower than the original (0.26 g/l–0.01 mg/l) (Strang et al., 1999).

Acknowledgment

Thanks to Dr. Solveig Glad for the fruitful discussion and comments.

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References

Amory, R. (1868). Experiments and observations on absinth and absinthism. Boston Med. Surg. J. 1, 68–71, 83–85. Arenberg, I. K., Countryman, L. F., Bernstein, L. H., and Shambaugh, G. E. (1990). Van Gogh had Meniere’s disease and not epilepsy. JAMA 264, 491–493. Arnold, W. N. (1988). Vincent van Gogh and the thujone connection. JAMA 260, 3042–3044. Arnold, W. N. (1989). Absinthe. Sci. Am. 260, 87–91. Arnold, W. N., and Loftus, L. S. (1991). Xanthopsia and van Gogh’s yellow palette. Eye 5, 503–510. Berulfsen, T. (2001). ‘‘Edle dra˚per.’’ Cappelen, Oslo. Conrad, B., III (1988). ‘‘Absinthe. History in Bottle.’’ Chronicle Books, San Francisco. Del Castillo, J., Anderson, M., and Rubottom, G. M. (1975). Marijuana, absinthe and the central nervous system. Nature 253, 365–366. Guide to van Gogh Museum, Amsterdam (1996). Ho¨ld, K. M., Sirisoma, N. S., Ikeda, T., Narahashi, T., and Casida, J. E. (2000). -thujone (the active component of absinthe): -aminobutyric acid type A receptor modulation and metabolic detoxification. PNAS 97, 3826–3831. Kangro, B. (1955). ‘‘Eduard Wiiralt 1898–1954.’’ Lund, Eesti Kirjanike Kooperativ. Lanier, D. (1995). ‘‘Absinthe. The Cocaine of the Nineteenth Century.’’ JeVerson, McFarland, North Carolina. Levin, M. (1998). ‘‘Eduard Wiiralt 1898–1954.’’ Tallinn, Eesti Kunstimuuseum. Loftus, L. S., and Arnold, W. N. (1991). Vincent van Gogh’s illness: Acute intermittent porphyria? BMJ 303, 1589–1591. Magnan, V. (1874). On the comparative action of alcohol and absinthe. Lancet 2, 410–412. Meissner, W. W. (1998). The van Gogh family: A study in alienation. Psychoanal. Rev. 85, 269–299. Olsen, R. (2000). Absinthe and -aminobutyric acid receptors. PNAS 97, 4417–4418. Ravin, J. G., and Anderson, N. (1998). Vincent van Gogh and Felix Rey MD: The whereabouts of half an ear. J. Med. Biogr. 6, 49–52. Rekand, T., and Sulg, I. (2003). Absinthe and the artistic creativeness. Tiddskr Nor Lægeforen 123, 70–73. Strang, J., Arnold, W. N., and Peters, T. (1999). Absinthe: What’s your poison? BMJ 319, 1590–1592. Weisbord, S. D., Soule, J. B., and Kimmel, P. L. (1997). Poison on line—acute renal failure caused by oil of wormwood purchased through the internet. N. Engl. J. Med. 337, 825–827.

SECTION VI NEUROLOGISTS AS ARTISTS


SIR CHARLES BELL, KGH, FRS, FRSE (1774–1842)

Christopher Gardner-Thorpe Exeter Neurosciences and Peninsula Medical School Royal Devon and Exeter Hospital Exeter, EX2 5DW, United Kingdom

I. II. III. IV. V. VI. VII. VIII. IX. X. XI.

Introduction Charles Bell’s Early Years David Allan (1774–1796) Raphael Cartoons Studied by Bell Corunna Oils in 1809 After Corunna in 1809 and Marriage in 1811 Waterloo in 1815 and the Watercolors of 1836 After Waterloo Italian Tour in 1840 Death at Hallow Park in Worcestershire After Bell References

I. Introduction

In studying the neurology of painting, some have discussed the eVects of neurological disorder in artists, (Bogousslavsky and Boller, 2005) others the eVects of disease on the work of their patients (Fornazzari, 2005) and yet others the artwork of those whose primary skills lie in the so-called healing arts. Charles Bell falls into the last of these categories. Bell is best known for the variety of lower motor neuron facial palsy he described and for his skill in diVerentiating that form of weakness from the facial weakness which results from damage to the cortex of the brain. Previous biographical works have discussed features of his life, work, and times1 (Gardner-Thorpe, 2002, 2004; Gordon-Taylor et al., 1958). His artistic skills 1 Walls, E. W., and Gardner, D. L. Charles Bell 1774–1842. Surgeon, Physiologist, Artist and Author. A booklet prepared to accompany an exhibition from August 12th to August 31st 1996 at the Royal College of Surgeons of Edinburgh, of Sir Charles Bell’s books, drawings and 1809 ‘‘Corunna’’ oil paintings, together with photographic reproductions of his 1836 ‘‘Waterloo’’ watercolour drawings.

INTERNATIONAL REVIEW OF NEUROBIOLOGY, VOL. 74 DOI: 10.1016/S0074-7742(06)74020-X

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were not inconsiderable and his writing extensive, for he has left us some 69 publications. His painting, and surely his writing too, was undertaken for pleasure and to teach his students the craft of surgery. British painters before Bell have produced a rich array of images. Among those who preceded him are Nicholas Hilliard (c1547–1619), Sir Peter Lely (1618–1680), William Hogarth (1697–1764), Sir Joshua Reynolds (1723–1792), George Stubbs (1724–1806), Thomas Gainsborough (1727–1788), Johann ZoVany (1733–1810), James Gillray (1756–1815), Thomas Rowlandson (1756– 1827) and William Blake (1757–1827). Conspicuous by their absence are the medical practitioners. However, James Parkinson (1755–1824), best known in medical circles for his An Essay on the Shaking Palsy published in 1817 (Parkinson, 1817), was a medical artist but he drew the illustrations for his publications on fossils and, certainly outside London, he was best known for his geological publications (Parkinson, 1804–1811; 1822). Others have followed Bell.

II. Charles Bell’s Early Years

Charles Bell was born in 1774 in the Fountainbridge suburb of Edinburgh, the son of the Reverend William Bell (1704–1779) who had been ordained into the Episcopal Church of Scotland. William had come from the West to the Counties bordering the River Forth with his own father, John Bell (1676– 1708). Charles’ mother, Margaret Morice, was William’s second wife and the granddaughter of Bishop White, later Primus of Scotland. Both Margaret and her grandfather were good artists and so their and Charles’ skill resided at least in part in the genes.

III. David Allan (1774–1796)

One of Charles’ teachers was the artist David Allan, who encouraged Bell to copy the Raphael Cartoons. Allan was born in Alloa on the estate of Erskine of Mar, the son of a shoremaster, and studied in Glasgow at Robert Foulis’ (1707– 1776) Art Academy. Through the patronage of Erskine, Allan was able to travel to Rome in 1764 to study at the Academy of St Luke in Rome from 1767 to 1777 under Gavin Hamilton. He painted The Start of the Race in the Corse, Rome and Preaching in the Collosseum at Rome, and in 1776 he painted an album entitled A Collection of Dresses by David Allan Mostly from Nature. While in Rome, he won the history prize for painting.

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Allan moved to London in 1777 and, in 1779, painted the 3-year old James Abercromby (Lord Dunfermline) as an Infant. He then settled in Edinburgh in 1780 and was dubbed The English Hogarth for his paintings of French and Italian Peasants and of modern moral subjects. William Hogarth (1697–1764), the satirist and cartoonist, painted realistic portraits of modern moral subjects, comic-strip like pictures. In 1786, Allan became Director of the Edinburgh Academy of Arts, and in 1788 he prepared an Aquatint frontispiece for Allan Ramsay’s (1681–1758) The Gentle Shepherd, A Pastoral Comedy. Allan is buried in Old Calton Cemetery in Edinburgh.2

IV. Raphael Cartoons Studied by Bell

The cartoons were assembled in the 1690s. They are six preparatory designs for artwork in another medium; the Italian word cartone refers to a large piece of paper, and in this case the cartoons were preparatory works for tapestries, prepared on many small sheets glued together. Pope Leo X (reigned 1513–1521) commissioned designs for 10 tapestries for the lower walls of the Sistine Chapel to depict St. Peter and St. Paul as twin founders of the church. Raphael Sanzio (1483–1520) prepared the cartoons that were sent to Brussels in 1517, where several sets of tapestries were woven. After his return to Italy, King Charles I (reigned 1625–1649) purchased them for the tapestry factory at Mortlake in Surrey. They have remained in England and are on loan to the Victoria and Albert Museum from the Royal Collection. Seven cartoons are listed: The Miraculous Draught of Fishes, The Healing of the Lame Man, The Conversion of the Proconsul, Christ’s Charge to Peter, The Death of Ananias, The Sacrifice at Lystra and Paul Preaching at Athens. Charles’ brother, John Bell (1763–1820), and the anatomist Alexander Monro II (1773–1859) taught him Anatomy, and from their example Charles would have improved his drawing and painting skills; during the years 1798– 1803 he published A System of Dissections explaining the Anatomy of the human body, the manner of displaying the parts and their varieties in disease (Bell, 1798– 1803). In 1804 Charles left Edinburgh for London and there he worked as surgeon and teacher of anatomy until 1836. During his time in London he published

2 David Allan’s works may be found in the Aberdeen Art Gallery and Museums, the Courtauld Institute of Art in London, the Fine Arts Museum of San Francisco, The Tate Gallery in London and the University of Dundee Fine Art Collection. Perhaps he is best known for his portrait of Robert Burns and for his self-portrait that hangs in the National Gallery of Scotland.

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several important works. His principal contribution to the arts was his volume entitled Essays on the Anatomy of Expression in Painting, published in 1806 (Bell, 1806). In those years the study of anatomy was deemed essential for both artist and surgeon. It is said that Charles had an aYnity with the Scottish painter, Wilkie. Bell’s study of the cartoons probably influenced him in his depiction of the Genius of Michelangelo as drawn in his Anatomy of Expression. V. Corunna Oils in 1809

Soldiers who had fought in the Peninsular War at Corunna in the northwest of Portugal and secured victory there were sent back to Portsmouth in January of 1809. Details of the patients are scanty, but by the time of his later surgery after Waterloo he kept more detailed records. The wounds were terrible, and Bell oVered his services to the Medical Board. His help was accepted, and early in February he operated at Haslar for long hours each day. The experience gained there formed the basis for his 1814 A Dissertation on Gun-Shot Wounds (Bell, 1814). He undertook wax modeling too, and this is illustrated by his A Case of Hernia Cerebri. VI. After Corunna in 1809 and Marriage in 1811

In 1811, he published his anatomical and somewhat philosophical book entitled Idea of a New Anatomy of the Brain (Bell, 1811). In June 1811 he married Marion Shaw, but they did not have children. He sketched during the honeymoon in Scotland, the Lake District and Oxford, and his watercolors of these areas may well have been painted at that time. Bell’s Scottish scenes illustrate his landscape and character painting and do not include items of neurological interest. In 1814 he was appointed surgeon at the Middlesex Hospital but shortly afterward, the Peninsular War would engage his attention once again. VII. Waterloo in 1815 and the Watercolors of 1836

The Battle of Waterloo commenced on Sunday June 18, 1815, and on June 26 Bell set oV for the battlefield. There he climbed the scaVolding that had been erected some 65 ft above the battlefield by order of Napoleon. Bell was impressed by Napoleon’s mastery of the battle and wrote ‘‘the view was magnificent. I was only one-third up the machine, yet it was a giddy height. Here Buonaparte stood

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surveying the field.’’ But it seems unlikely Napoleon ever did actually ascend the structure (Editorial, 1912). Bell attended some 300 of the wounded and operated for 5 days. The French casualties suVered more serious injuries than the British. From June 29, 1815 he operated for at least 3 days, from 6 am to 7 pm, on French and British soldiers at Antwerp and Brussels, where he kept a sketchbook with outline sketches in black lead and careful notes. The Waterloo watercolors were painted for teaching purposes many years later, in 1836 in Edinburgh. The pictures are painted on paper sheets measuring some 30 by 22 inches. In 1867, Lady Bell presented these 17 watercolors together with Charles’ notebook to the Royal Hospital at Netley in Hampshire. Although several paintings depict limb injuries, and those patients must also have had severe damage to nerves, the neurological images are best represented by the severe wounds to the head, often with surprisingly little disability. However, the cognitive eVects may have been subtle and not readily recorded. Since many of the survivors had lain on the battlefield for several days, it is probable that the passage of time had in eVect triaged the wounded, and the more robust had survived anyway. One unknown soldier of the 1st Dragoons suVered a sabre wound to the head. He was not able to speak when admitted to the Hoˆpital de la Gendarmerie but recovered after bone fragments were removed. Domenic de Lorraine suVered a musket ball wound of the head and lay for 3 days on the battlefield. He complained of headache but could walk. The musket ball had passed through the brain; it was removed, and he remained well on the following day. Samuel Prichard suVered a gunshot wound of the head. The musket ball perforated the frontal bone and entered the left orbit and proptosis ensued. He was asymptomatic otherwise and survived to be sent home. Two soldiers suVered gunshot wounds of the face with loss of the sense of smell; one with loss of vision in both eyes from where the gunshot had passed, and the other lost vision just in the left eye. Soldier Wanstell of the 17th Regiment suVered a gunshot injury to the skull with fracture. He was found insensible on the battlefield 5 days after the battle. Some bone was removed, but he died within a few days. Only two soldiers of the many with tetanus survived. Other images depict mainly upper limb injuries, with some chest injuries and one injury to the lower limb. Several display bandaging to the head, implying trauma there too.

VIII. After Waterloo

Bell’s next major neurological work, published in 1821, was On the Nerves (Bell, 1821). In 1822, François Magendie (1783–1855) published his views on the

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function of the nerve roots that led to the famous controversy as to who had prior claim to the discovery that the anterior roots of the spinal cord were motor and the posterior sensory. To some extent the discussion continues, but a fair view that each contributed is that Bell made the prior observation but failed to publish this suYciently clearly—hence the Bell-Magendie Law. In 1826, Bell was elected a Fellow of the Royal Society (FRS). In 1830, he published The Nervous System of the Human Body, embracing the papers delivered to The Royal Society on the subject of the Nerves.3 In 1831, King William IV knighted him in The Royal Guelphic Order, an order instituted on August 12, 1815 by the Prince Regent who later became King George IV. It was discontinued as a British Order in 1837 but continued as a Hanoverian Order. Awarded for distinguished services to the United Kingdom or Hanover, there are three grades, in Civil and Military Divisions with post nominal letters GCH (Knight Grand Cross), KCH (Knight Commander) and KH (Knight). In 1833, he published his Bridgwater Treatise entitled The Hand, its mechanism and vital endowments as evincing design (Bell, 1833). The Bridgwater Treatises formed a series of twelve volumes published in 1833 and 1834 on scientific subjects by eight authors, four medical and four divines, each of whom was awarded 1000 pounds from the Will of the Earl of Bridgwater who had died in 1829. They were to provide scientific argument for the existence of God, at a time when the theory of Creationism was under threat. The Treatises were entitled On the Power, Wisdom, and Goodness of God as manifested in the adaptation of external nature to the moral and intellectual constitution of Man (Thomas Chalmers), On the adaptation of external nature to the physical condition of Man (John Kidd), Astronomy and general physics considered with reference to natural theology (William Whewell), The Hand: its mechanism and vital endowments as evincing design (Charles Bell), On animal and vegetable physiology (Peter Mark Roget), On geology and mineralogy (William Buckland), On the history, habits, and instincts of animals (William Kirby), and On chemistry, meterology, and the function of digestion (William Prout). In 1836, Bell returned to Edinburgh as Professor of Systematic Surgery and prepared his 17 watercolors. In addition to painting, Bell drew and published engravings and etchings to illustrate his clinical and research work, and he used his artistic skills to further both art and medicine in their broadest senses. Bell’s etchings and engravings, along with his other works, demonstrate his eclectic skills.

3 (2nd Edition), London, Longmans, 1830. Garrison Morton, 1258. This copy was Dr. Marshall Hall’s First Prize in the Theory and Practice of Physic 1835–1836 and was awarded to WF Barlow. It contains two oVprints, namely On the functions of some parts of the brain, and on the relations between the brain and nerves of motion and sensation, published in Philosophical Transactions part II for 1834; and On the relations between the nerves of motion and of sensation, and the brain; more particularly on the structure of the medulla oblongata and the spinal marrow, published in Philosophical Transactions, part II for 1835.

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IX. Italian Tour in 1840

In the Spring of 1840, Bell toured Paris, Nice, Genoa, and Rome where his elder brother John had died 20 years earlier, in 1820, and where he is buried. During this 3-month tour he sketched but complained of stomach pain, probably the beginning of the angina pectoris that a couple of years later would presage his death.

X. Death at Hallow Park in Worcestershire

Charles and his wife visited their friend Mrs Holland at Hallow Park near Worcester on April 27, 1842. Next day he sketched Pastoral Scene with the Malvern Hills in the Background. On the following day he died. The cause of death was recorded as Visitation of God, but the pathological diagnosis was ossification of the heart. He is buried in Hallow Churchyard. Jessie Wilson recorded ‘‘Daniel will be greatly grieved, I am sure, to learn of Sir Charles Bell’s death, and still more when he hears the circumstances: Sir Charles was on a visit to a friend, and during the night was seized with spasm in the stomach, to which he was subject. Lady Bell arose to get him some laudanum, but he hastily recalled her to his side, and leaned his head on her shoulder. She thought he was merely squeamish, and supported him in this position for threequarters of an hour, till the doctor came. When the doctor looked, he found he was dead, quite cold; his poor wife had mistaken her own breathing for his, and had been unconsciously supporting his corpse all the while. He must have died in a moment; his death resulted from ossification of the large arteries near the heart, which were found extensively diseased. One of his last acts on the evening before was to make a sketch of a yew in an old churchyard in the neighbourhood. He had been struck with the beauty of this churchyard and had said, that if asked to say where he should like to be laid, it would be there. There he now slumbers’’ (Wilson, 1860).

XI. After Bell

Many other well-known British painters overlapped in time with Bell or followed him, but none has contributed in similar fashion to our understanding of military surgery. Those painters at that time include Joseph Mallord William Turner (1775–1851), John Constable (1776–1837), John Martin (1789–1854), Jean-Baptiste-Camille Corot (1796–1875), John Everett Millais (1829–1896),

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E´douard Manet (1832–1883), James Abbott McNeill Whistler (1834–1903), Edgar Degas (1834–1917), Paul Ce´zanne (1839–1906), Claude Monet (1840– 1926), Pierre-Auguste Renoir (1841–1919) and Paul Gauguin (1848–1903). During the Crimea and the Boer War it seems that comparatively little was contributed toward the art of painting. Photography became available at that time yet images do not seem to be readily available. During the First World War images became popular again, although a major art contribution was in poetry (Gardner-Thorpe, 2004). Henry Tonks (1862– 1936) (Wildgoose, 2002) trained at the Royal Sussex County Hospital in Brighton in 1880 at a time when the provincial hospitals trained doctors on a regular basis. He became House Surgeon at The London Hospital in 1881 and then proceeded FRCS and joined Westminster School of Art. He wrote ‘‘You need to be a poet to produce a beautiful drawing, and that no man can impart to another man.’’ Using mainly pen and ink and pastels, Tonks drew the planning stages of the operations carried out in 1916–1917 by the plastic surgeon Harold Delf Gillies (1882–1960). Photography and the long written description became more popular during the Second World War. Wars continue more than once for each generation. As the media for portrayal of war becomes more sophisticated, the images become no less ghastly—they just change in nature. References

Bell, C. (1798–1803). ‘‘A System of Dissections Explaining the Anatomy of the Human Body, the Manner of Displaying the Parts, and Their Varieties in Disease.’’ Two volumes. Mundell and Son, Edinburgh. Bell, C. (1806). ‘‘Essays on the Anatomy of Expression in Painting.’’ Longman, London. Bell, C. (1811). ‘‘Idea of a New Anatomy of the Brain.’’ Strahan and Preston, London. Bell, C. (1814). ‘‘A Dissertation on Gun-Shot Wounds.’’ Longman, London. Bell, C. (1821). On the nerves, giving an account of some experiments on their structure and function, which lead to a new arrangement of the system. Philos. Trans. 111, 398–424. Bell, C. (1833). ‘‘The Hand, its Mechanism and Vital Endowments as Evincing Design.’’ Pickering, London. Bogousslavsky, J., and Boller, F. (2005). Neurological Disorders in Famous Artists ‘‘Frontiers of Neurology and Neuroscience,’’ Vol. 19. Karger, Basel. Editorial (1912). Sir Charles Bell and Waterloo. Br. Med. J. 8 June, 1327–1328. Fornazzari, L. R. (2005). Preserved painting creativity in an artist with Alzheimer’s disease. Eur. J. Neurol. 12, 419–424. Gardner-Thorpe, C. (2002). Charles Bell (1774–1842) and an early case of muscular dystrophy. The Third Meryon Society Lecture read at Worcester College, Oxford on 28 July 2000. Neuromuscular Disord. 12, 318–321. Gardner-Thorpe, C. (2004). ‘‘The Art of Sir Charles Bell. Chapter 6 in Neurology and The Arts: Painting, Music, Literature’’ (F. CliVord Rose, Ed.), pp. 99–128. Imperial College Press, London, ISBN 9 871860 368 3.

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Gardner-Thorpe, C. (2004). ‘‘The Poetry of Henry Head. Chapter 23 in Neurology and The Arts: Painting, Music, Literature’’ (F. CliVord Rose, Ed.), pp. 401–420. Imperial College Press, London, ISBN 9 871860 368 3. Gordon-Taylor, Sir Gordon, and Walls, E. W. (1958). Three volumes. ‘‘Sir Charles Bell. His Life and Times.’’ E&S Livingstone, Edinburgh. Parkinson, J. (1804–1811). ‘‘Organic Remains of a Former World.’’ Three Volumes. Sherwood, Neely and Jones, London. Parkinson, J. (1817). An Essay on the Shaking Palsy. Sherwood, Neely and Jones, London. Also reprinted in Medical Classics, Baltimore, 1938. 2, 964–997. Parkinson, J. (1822). ‘‘Outlines of Oryctology; or, An Introduction to the Study of Fossil Organic Remains.’’ Sherwood, Neely and Jones, London. Wildgoose, J. (2002). A surgeon’s art. Henry Tonks: Art and surgery. Report of an exhibition at University College, London. Lancet 360, 1993. Wilson, and Jessie Aitken (1860). ‘‘Memoir of George Wilson MD FRSE,’’ pp. 199–200. Edmonston & Douglas, Edinburgh.


SECTION VII MISCELLANEOUS


PEG LEG FRIEDA

Espen Dietrichs Department of Neurology Rikshospitalet University Hospital/The National Hospital University of Oslo N-0027 Oslo, Norway


Introduction Background Poliomyelitis School Accident and Artist Debut Diego Rivera SuVering and Painting Disease and Creativity

I. Introduction

The brain undergoes plastic changes throughout our lives. All our experiences participate in forming the brain, thereby also influencing our personality. The story of the famous Mexican painter, political activist, and woman’s liberationist Frida Kahlo shows that neurological disease may not only mark an artist but also her artistic creativity. But in her case it may even be the very reason why she became an artist. II. Background

Magdalena Carmen Frieda Kahlo y Calderoń was born outside Mexico City on July 6, 1907. Later, she always claimed to be born in 1910, wanting to be a child of the Mexican revolution (1910–1920). Her first two names were Christian names for her baptism, but she and her family only used Frieda (German for ‘‘peace’’). When the Nazis started the Second World War, she omitted ‘‘e’’ and started to spell her name ‘‘Frida.’’ Her mother was Mexican, partly of Spanish, partly of native Mexican heritage. Frida’s father was a Hungarian Jew, born in Germany. Originally, her


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father was a student at the University of Nu¨rnberg, but he had to leave his studies when he had a head trauma and developed posttraumatic epilepsy. He went to Mexico when his mother died and his father remarried to a woman he disliked. In Mexico he trained as a photographer and married a woman who suVered from poor health, and she had (psychogenic) fits that closely resembled her husband’s epileptic seizures. III. Poliomyelitis

Frida Kahlo contracted poliomyelitis when only 6 years old, causing severe paresis particularly of her right leg. She was confined to her own room for 9 months, and when she finally was back on her feet, her father encouraged her participation in all forms of sports (football, boxing, wrestling, swimming, rowing) as rehabilitation. This was unusual as at that time such activities were considered most inappropriate for a girl. Frida’s right leg remained weak and atrophic throughout her life, and for periods, she had to use a wooden brace on her leg. Other children bullied her, shouting ‘‘Frieda, pata de palo’’ (‘‘peg leg Frieda’’). Her feelings were deeply hurt by this, and she tried to camouflage her brace. At first, she started to use several pairs of socks, later in life she would choose costumes that covered her legs. She would wear long dresses inspired by the folk costumes from the Tehuantepec, a Mexican region with strong Indian and matriarchal traditions, but for some periods she even chose to wear men’s clothes. After her illness, Frida developed strong bonds with her father, often accompanying him when he went out, shooting photographs or painting landscapes. Her father taught her photography, painting, and retouching, and Frida also learnt how to cope with her father’s epileptic seizures. IV. School

Frida went to the German elementary school in Mexico, the Colegio Alemań. She was a bright pupil and passed the qualifying exam in 1922 for Mexico’s most prestigious high school, La Escuela Nacional Preparatoria. Among the 2000 pupils, only 35 were girls. Frida chose topics like biology, zoology, and anatomy, aiming to study medicine in the future. She was also a talented artist, making outstanding drawings but showed no interest in an art career. For a time, she earned some extra money copying paintings by the Swedish artist, Anders Zorn, for a friend of the family who ran a printing press.

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V. Accident and Artist Debut

On September 17, 1925 Frida was on her way home from school when her bus was involved in a collision with a tram car. Several people were killed, and Frida was thrown out and hit by an iron rod, which pierced her hip and perineum. In addition, she had several other wounds, including fractures and contusions of her already marginally functioning right leg. She was taken to the nearest hospital and operated on, but her condition remained critical for several days. She was discharged from hospital after a month but confined to bed at home for another 8 weeks. She was mobilized with good hopes of recovery but developed increasing pains in her back and right leg. One year after the accident, she was readmitted to hospital. Possibly by mistake, her spine had never been x-rayed after the accident, but x-rays now revealed three fractures in the lower part of her vertebral column. For the next 9 months, she had to wear corsets made of plaster. She was unable to sit, and for long periods she was again confined to bed. Since staying in bed was boring, to kill time she took up painting. She borrowed a palette, brushes, and oil colors from her father, and her mother hired a local carpenter to make a special easel that could be attached to the bed. With this easel, she could paint while lying flat on her back in bed. Her bed was a four-poster with a mirror above her, so that it was a natural choice to start painting self-portraits. Among about 150 paintings she made throughout her career, approximately one-third were self-portraits. Even though the traYc accident changed her life and its consequences influenced her entire artistic career, she never painted the actual incident. But around 20 years later, she came across a post card with a motif that strikingly resembled her own accident. She retouched the postcard to make the scene even more accurate also by adding her own features to the victim lying on the ground. She then put an inscription at the bottom of the card, expressing her parents’ gratitude for Frida’s survival from the accident. VI. Diego Rivera

Toward the end of 1927, Frida had recovered enough to be able to live a comparably normal life. Through renewed contact with her old schoolmates, she got in touch with a group of radical intellectuals and artists. She was an active participant herself and soon joined Mexico’s communist party. Through her friends she was also introduced to the famous painter and liberation activist Diego Rivera, her senior of 21 years. They soon became lovers and got married in 1929. By that time, Frida had been told that she was unable to give birth to

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children because of her extensive pelvic injuries. In spite of this, she had a strong wish to have her own children. She became pregnant three times over the next few years but, to her sorrow, all pregnancies resulted in abortions. The marriage was stormy. They stayed in USA for 4 years, where Diego Rivera painted murals, but then returned to Mexico. In Mexico City, they lived in one cubic house each. Frida had a small blue house, and Diego had a large red house next door, where he also had his studio. Diego had a series of lovers. When she found out that Diego had an aVair with her sister, Frida moved away for a short period in 1935. After this, she herself started to take lovers, of both sexes. Her most famous lover was Leo Trotsky. Expelled form the Soviet Union, Trotsky spent some months in Norway in 1935–1936 but was also expelled from there. With his wife Natalia, Trotsky then moved to Mexico, where they stayed for 2 years in the blue house as the guests of Frida and Diego. Frida and Diego divorced in 1939 on his initiative. They still kept in touch and continued going together to oYcial gatherings and arrangements. In spite of this, Frida’s feelings were deeply hurt by the divorce; she became depressed and began to drink. She also cut her long, black hair short and started wearing only men’s clothes. In addition, she had increasing pains from her back and right leg. Diego was very concerned about her increasing problems and several times proposed remarriage. Eventually, Frida accepted his proposals and got remarried in 1940, after Diego had accepted Frida’s special marriage clauses: she should provide for herself and pay exactly 50% of the household expenses and they should have no sexual intercourse. But it appears that after a while they returned to a marriage very similar to what they had had before.

VII. Suffering and Painting

Frida Kahlo’s art is a good example how life may influence artistic creativity. Not only was immobilization as part of her medical treatment the very reason why she started painting, her medical conditions and suVerings were central motifs for much of her artwork. Her accident accounts for the pains in her back and right leg as well as for her inability to bear a child. Other paintings reflect her stormy relations with Diego Rivera and the political situation in Mexico. But, in spite of numerous self-portraits, she avoided one particular motif, most likely since she was bullied as a child: she never painted her right leg as it really looked, small and atrophic after her childhood poliomyelitis. Since she spent long periods of her life in bed, many paintings were made on the small, special easel attached to her bed, which explains why the majority of her paintings have a small format. Eventually, she gained huge acceptance as an

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artist, especially after several exhibitions held from 1938 onward. She was first recognized in USA, but her popularity soon spread to Mexico. After this, she was awarded a national art grant and, in 1943, was appointed as a teacher in the School of Painting and Sculpture, run by the Ministry of Public Education. After some good years, the intensity of Frida’s pains started to worsen around 1939, as did her general health. Mexican doctors were of the opinion that she had tuberculosis in her spine and wanted to operate. Seeking second opinions from doctors in USA, she obtained other recommendations, as these doctors were unable to confirm the diagnosis and so discouraged operation. Following treatment for a kidney infection, she temporarily felt better, but her medical problems again increased. In 1944, she wore a steel corset to immobilize the spine, to avoid ‘‘irritation of the nerves,’’ but even after several months her problems continued to increase. From 1944 on, she was successively treated with not less than 28 diVerent corsets; in addition to the steel corset, three were made of leather; and remaining were made of plaster, some of which she decorated with paintings. She was also treated with various forms of traction, using steel rings, sand bags, and other attempt at straightening her vertebral column. Mexican orthopedic surgeons repeatedly recommended operation, and when a well-known American orthopedic surgeon supported this course, she was operated on in New York in 1946. This was a fixation operation, fusing four lumbar vertebrae with steel rods and with bone taken from the pelvic girdle. But neither this operation nor the subsequent 8 months of immobilization with corsets resulted in any improvement. Mexican orthopedic surgeons now suggested that fixation had been performed on the wrong vertebrae and began to discuss further operations. Frida had permanent problems with pains radiating from the lower part of her spine and into the right leg. She needed more and more, stronger and stronger, medication for pain relief and from 1950 onward was unable to paint without large doses of opiates. With these increasing problems, she spent 9 months continuously in hospital in 1950, during which year alone seven further operations were performed, among which was a new fixation operation with fusion of three more vertebrae, using bone from the pelvic girdle. She suVered from complications from several of these operations, namely, intestinal obstruction (paralytic ileus) and infections. From some of Frida’s letters, it appears that the inserted bone did not fuse and bone tissue in the operated region became infected (osteomyelitis). Scaring with infection after surgery caused continuous secretions that had to be drained by specially cut windows in her corsets, and these complications provoked several reoperations. In addition to the radiating pains, the toes on her right foot started to change color, becoming black, and she gradually developed gangrene. After 1950, Frida was mainly bedridden, but she could be taken around in a wheelchair as she could walk only a few meters on crutches. In 1953, her right leg

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was amputated at the knee, and an artificial limb tried to make her able to walk for short distances. She became very depressed after the amputation, and her condition continued to deteriorate. She still painted when she felt capable, but these later paintings were less precise and less thoroughly done, probably because of pains and the continuous use of opiates. In July 1954, Frida developed pneumonia. Against the advice from her doctors, she participated in a demonstration march, in which Diego Rivera pushed her wheelchair, after which the pneumonia worsened. She died at her home on July 13th, only 47 years old. Lung embolism was considered the most likely cause of death, and this is the diagnosis written on the death certificate. Later, some claimed that the real cause of death was an overdose of pain medication. The last entry in her diary was: I hope the exit is joyful—and I hope never to come back. Frida

VIII. Disease and Creativity

SuVering was a major part of Frida Kahlo’s life. By the age of 6, she was permanently marked by poliomyelitis and bullied because of her handicap. Aged 18, she was seriously hurt in the traYc accident that influenced the rest of her life. Without access to detailed medical information, it is reasonable to assume that she had fractures of several lumbar vertebrae with compression of several nerve roots supplying her right leg. She was more or less permanently troubled by lower back pain with radiating nerve root pains down the right leg (radiculopathy). She may have developed reflex sympathetic dystrophy in her right leg because of the chronic nerve root aVection and/or fractures. Critical review of her history invariably gives the impression that the medical treatment oVered was suboptimal. In the acute stages after the traYc accident, medical examinations were insuYcient and her vertebral fractures escaped recognition. Later, she went through orthopedic surgery at least 32 times, several of these procedures probably on doubtful indications. Many of these operations may have contributed to a further worsening of her already chronic problems. Frida obviously suVered from a heavy disease burden. After her death, several voices claimed that most of her problems had a psychiatric explanation, even Mu¨nchausen’s syndrome, i.e., she simulated symptoms that lead to hospitalizations and operations. The biographer Hayden Herrera claims in ‘‘Frida: A biography of Frida Kahlo’’ that her worsening of symptoms occurring at the

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same time as psychological trauma and marriage problems may be taken as evidence for an underlying psychiatric cause and suggested that Frida ‘‘used’’ her symptoms to force through her own wishes. This author finds it diYcult to accept such accusations. It is a common observation that a patient’s ability to withstand pain and suVering is impaired by life crises and worsening of a chronic disease often occurs in such situations. From the diseases and traumas in Frida’s life, it is obvious that she had considerable somatic sequels. It appears from several of her letters that Mexican orthopedic surgeons recommended operations, which she herself was reluctant to undertake until highly regarded American surgeons shared their view. This seems to indicate she was the victim of poor medical advice and, in addition, was unlucky contracting complications from many of the operations. The result was a life marked by disease and pain in which her suVering, in fact, both initiated and inspired her career as a painter. When we study her pictures, there is little doubt that her medical problems had a major impact both on the person, Frida Kahlo, and on her artistic creativity.


THE DEAFNESS OF GOYA (1746–1828)



Introduction The Duchess of Alba What was Goya’s Illness? DiVerential Diagnosis Vogt-Koyanagi Syndrome Black Paintings References I. Introduction

Goya was born in Fuentetodos1 40 miles away from the provincial capital of Aragon, Saragossa,2 where his family came from and returned when he was aged 4. His father worked as a gilder in Saragossa but, in Fuentetodos, probably worked on land belonging to his wife’s family. At school, Goya probably learned some Latin (from Virgil).3 He became interested in drawing from an early age and, by the time he was 14, had already painted frescoes in his local church. At this age, he became apprenticed to Jose´ Luzan4 with whom he spent 4 years, learning design and copying the best prints his teacher possessed. Determined to become a painter, Goya entered, at the age of 17, the competition for a bursary at The Royal Academy of Fine Arts of San Fernando in Madrid; he failed on that occasion and again when he tried 3 years later. As a teenager, he had a hasty and quick-tempered personality and, considered to be the best swordsman in Spain, was often involved in dueling. Because of this, he was sought by the Inquisition and left Spain for Italy, which was the 18

For example, the one of the New York Hispanic Society painted in 1797.

2 A corruption of Caesar Augusta, the Roman Emperor who named the town after himself in the first century AD. The Romans were displaced by the Goths in the fifth century AD, and they in their turn by the Moors 300 years later. It was recaptured by the Spaniards in the twelfth century under the leadership of Alfonso I of Aragon, who made it his capital. 3 A witchcraft scene in Los Caprichos was entitled Volvetverunt, meaning ‘‘they will have flown’’ although it is also a common domestic Spanish phrase (Hughes, 2004, p.32). 4 Luzan also trained Francisco Bayeu who was to become Goya’s brother-in-law.


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center for art at that time. Goya furthered his studies there, as had previously two other Spanish artists, Velazquez (1629–1631) and (1649–1651) and Ribera (1612–1652). The King, Charles III, was an Italophile who brought to the Spanish Court Anton Mengs, the German-born painter, from Naples in 1761 and, in the following year, Tiepolo, the Venetian painter, who spent the latter years of his life (1762–1770) in Madrid,5 where he painted ceilings in the royal palace and influenced Goya’s early Baroque paintings and luminous skies. Goya’s early career continued with religious subjects such as the ceiling of part of the Church of El Pilar in Saragossa in 1772; it was a fresco on plaster, a technique he learned in Italy. Goya studied and copied the paintings of Velasquez who, like the Spanish school in general, had a tendency to portray humble models and often invalids. Goya was a pupil of the Court painter Francisco Bayeu (Fig. 1) whose sister, Josefa, he married in 1772. After Tiepelo’s death in 1770, Goya’s brother-in-law Bayeu became more important, and it was through his influence with Mengs, first painter of the King, that Goya moved from Saragossa to Madrid in 1774 to work at the Royal Tapestry Factory at Santa Barbara, just outside Madrid. His job was to produce full scale paintings that were to be used as cartoons for weavers to reproduce in wool as tapestries. He completed his first set of paintings for the dining room of El Escorial, which included the two passions of Charles III, hunting and fishing. He worked there until 1792, during which he did more than 60 paintings for tapestries, all in a light-hearted genre. When Mengs died in 1779, he was replaced in the Royal Academy of San Fernando by Goya. In 1785, when he was elected Deputy Director of Painting at the Royal Academy, ‘‘Goya was already showing signs of being unwell’’ (Rapelli, 1999). In December 1788, Charles III died to be succeeded by Charles IV who reigned for nearly 20 years during which time Goya reached ‘‘his peak of material and social success—while being struck down with a crippling but unidentified illness that would immeasurably deepen his art’’ (Hughes, 2004, p. 145). Without explanation, he suddenly stopped working on tapestries and left Madrid for Cadiz to stay with his close friend Sebastian Martinez (Fig. 2). His departure from Madrid was partly dissatisfaction with the rules of the Academy of San Fernando, but he was unhappy with his work for tapestries, which did not extend his range to more serious subjects. Another reason to visit his close friend Sebastian Martinez was to paint his portrait. Goya traveled from Madrid in November 1792 and was due to make only a short visit, but because of his illness he did not return to Madrid until 5 Unlike Barcelona, Madrid was founded in the ninth century by the Muslims who set up a fortress overlooking the Manzanares River. It became a great city only in the mid-sixteenth century when the Hapsburg Emperor established his court there, because it was the geographical center of Spain, which did not favor regional provinces and was also away from ports and their foreign influence. In 1530, Madrid had a population of 4,000; within a century there were more than 150,000 inhabitants, much the same number as when Goya arrived in the late eighteenth century.


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FIG. 1. Francisco Bayeu.

the spring of 1793 (Waldemann, 1998, p. 30). Goya’s painting of Martinez was one of his finest portraits, which he must have painted before he became ill in the last weeks of 1792 (Waldemann, 1998, p. 20). Although he had been ill in Madrid, he recovered suYciently to travel, but after arriving in Cadiz he suddenly could not see, hear, or speak, or swallow food or drink. He had generalized cramps followed by ‘‘total paralysis that froze him into a protracted spasm of helplessness’’ (Blackburn, 2002, p. 32). He had a high fever with hallucinations, was totally confused, and disorientated with loss of memory of his own name, place of birth, and his occupation as a celebrated painter. Martinez thought that he was dying, as evidenced by the contents of the letters he wrote. After several months of illness, Goya slowly recovered but not his hearing. During this period, he wrote to Zapater, another close friend, ‘‘I am on my feet, but so bad I don’t know if my head is on my shoulders, with no desire to eat or anything else’’ (Blackburn, 2002, p. 40). ‘‘No one can say what laid him low and so nearly killed him. He heard loud and constant noises, buzzing and roaring and ringing in his head. But he had

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FIG. 2. Sebastian Martinez.

more and more diYculty hearing the sounds of the real world, and could hardly make out the syllables of ordinary speech. His balance was badly aVected; he could not go up and down stairs without feeling in danger of falling over. He had fainting fits and spells of semi-blindness, . . .. He often felt nauseated and ready to throw up. He also had weakness and delirium’’ (Hughes, 2004; Rose, 2004). Goya wrote that he had spent ‘‘two months in bed with painful colics.’’ In March 1793, he wrote to his friend Martinez, as he did to Zapater, ‘‘. . . I can stand on my own feet, but so poorly that I don’t know if my head is on my shoulders; I have no appetite or desire to do anything at all.’’ Zapater was informed on March 20, 1793 how serious his condition was and that Goya was likely to be deaf the rest of his life (Rapelli, 1999, p. 42). On the March 29, Zapater also received a letter from Martinez who wrote ‘‘the ringing in his head


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and the deafness have not yet lessened, but he is looking much better again and no longer suVers from disturbances of equilibrium. He can get up and down stairs very well and is doing things again he has been unable to do’’ (Waldemann, 1998, p. 28). He recovered from his initial illness ‘‘but again he collapsed and lay in bed for several months, half paralyzed, deafened, at times delirious’’ (Connell, 2004, p. 79). The paralysis was only temporary, but the deafness was permanent, and he had a persistent buzzing noise (tinnitus). Goya left Cadiz in the spring of 1793, but his continuing ill-health prevented him from working until the summer of 1793. In January 1794, he wrote to the Academy of San Fernando to state that he was painting again, this time a series of 11 or 12 portable paintings (‘‘cabinet pictures’’) 6 of which depicted bull fighting, the first he had done on this theme. Goya explained that the images were works of whimsy and imagination and could not have been done as commissioned works. Some of these were ‘‘a very long way . . . from the pastoral and sociable pleasures of the tapestry cartoons . . . it announces a thread of violence and fears that would henceforth run through his work—an important diVerence . . . from his previous work.’’ Such paintings included ‘‘In terror of a Prison’’; in this, seven men are chained and fettered in dejected misery; another was the ‘‘Yard with Lunatics’’ from a hospital in Saragossa (Fig. 3). On arrival back in Madrid, he was still weak and easily disorientated, but the series of cabinet paintings were done for himself ‘‘to occupy my mind mortified

FIG. 3. Lunatic asylum.

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by illness’’.6 Other work included a shipwreck with survivors on a rock, traveling players with masked faces and a coach held up by bandits who kill nearly all the travelers. After his illness, his paintings changed from establishment portraits to such pictures as a shipwreck, prison, lunatic asylum, or a fire at night. In addition to the usual crowds of Spaniards, he now drew demons, witches, and people with animal heads, which had been intended to be included in his later Caprichos. During 1797, he worked in a garret rather than his usual studio (Connell, 2004, p. 122). Goya returned to the South of Spain in 1796. Even 4 years after his illness he was still suVering from the aftereVects, walking with unsteady steps because of his imbalance and holding on to walls.

II. The Duchess of Alba7

In 1796, the Duchess of Alba’s 39-year-old husband died, and after his death she became one of Goya’s patrons. She went to Sanlucar de Barrameda for 6

He cut small rectangles of tin with scissors and on a brown underpainting built up figures. Goya painted the Duchess of Alba in 1795, but he first mentioned her to his friend Zapater in a letter, which was dated 5 years later in 1800; peculiarly the letter was dated London, although Goya never visited London (Connell, 2004, p. 5). In February 1797, the Duchess of Alba wrote her Will, one of the beneficiaries being Javier, Goya’s 12-year-old son who would receive 12 reales a day for the rest of his life. After Goya left her, she had aVairs with the bullfighter Pedro Romero, and Manuel Godoy, the Queens favorite, besides others, eventually marrying field marshal Antonio Cornel just before her death in July 1802 at the age of 39. Queen Maria Luisa was wearing her pearls and diamonds within a week of her death; Godoy lived in her Madrid palace and took possession of her paintings, which included the Rokeby Venus by Velazquez. It was nearly 40 years before her estate was distributed to the heirs named in her will, by which time most of them were dead. In one of the Caprichos, Goya did an etching of her floating through the air on the back of three crouching men, one of whom is recognized as the bullfighter Pedro Romero. Goya mourned her death with a drawing for a sepulchre that was never built. In 1845, her remains were exhumed and the size of the skeleton fitted with the proportions of the Naked Maja. It was revealed that her feet had been amputated when she was disinterred to move her to the San Isidoro Cemetery in Madrid as the new coYn was too short by 3½ inches. The idea that Goya had gone to a secret tryst with the Duchess of Alba is not supported by the evidence. 7

1. The summer palace of the Duchess of San Lucar de Barrameda was leased at that time to the Archbishop of Seville. 2. The Duchess was at her country house in Piediahita in September and October of 1792. She returned to Madrid on November 2 meeting her husband soon after this at the Escorial, returning by herself to Madrid in early December. The trigger to Goya’s case may have been coldness and over-exertion when he was trying to mend the axle of a coach in which he and the Duchess of Alba were traveling.


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traditional mourning, during which time Goya visited her, having applied for absence of leave, which was granted. His paintings of her were among the most beautiful of his works8 and he said of the Duchess ‘‘there was not a hair on her head that did not arouse desire’’ (Rapelli, 1999 p. 50). It is possible that he was in Seville about the time of death of his patron, the Duke of Alba and this is how he was invited by the newly widowed Duchess to stay in her farmhouse on the estuary of the Guadalquivir River, in the center of what is now the Donãna Nature Reserve. Goya painted her in 1797, and they may have lived together for several or more months (Blackburn, 2002, p. 61). When there, he drew a notebook of pen and ink drawings of his life. Goya left Donãna before the winter of 1796 and was back in Madrid by April 1, 1797 when he resigned from his teaching job at the Academy ostensibly because of his deafness. Goya spent several weeks at Sanlucar de Barrameda, the Duchess’s country estate, and it was here in southern Spain that they probably became lovers. On returning from Sanlucar to Madrid, he started working on an album of some 200 sketches.

III. What was Goya’s Illness?

A recent biography (Hughes, 2004, p. 127) asks ‘‘what was this illness? It is impossible to say, because no modern diagnosis can be made, there simply isn’t the evidence. Goya’s deafness is one of the insoluble mysteries of the art’s medical history, ranking with Vincent van Gogh’s madness and depression.’’ The conclusion made was ‘‘what Goya had been through in his sudden illness was not a fantasy, but it was a mystery. Neither he nor any of the doctors he might have consulted could possibly have diagnosed what was wrong with him, because such diagnosis was not within the reach of the medical knowledge of his time. (If it had been, we might have more chance of naming his aZiction ourselves). To fall badly ill, sustain grievous injury, yet not be able to name what the trouble is, know whether it is temporary or permanent, or, if the former, make any guesses how long it will last, whether it will ruin your career and your normal social relations or eventually sheathe its claws and let you alone—all that is an experience that verges on desperation’’ (Hughes, 2004, p. 137). It has been suggested that the thread that links his cabinet pictures of the 1790s was Goya’s depression. ‘‘He had just been stricken down into the depressive’s nightmare predicament: cut oV from the world and from intimate contact with others by a severe, undiagnosable and incurable illness; alienated lost within himself . . . (Hughes, 2004, p. 141). 8

For example, the one of the New York Hispanic Society painted in 1797.

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IV. Differential Diagnosis

Since his illness lasted nearly a year, it is not surprising many diagnoses have been oVered in the past. 1. Syphilis: This was to explain the deaths of many of his children, but there were no signs of this, and he lived to be 82 years of age 2. Lead poisoning, an occupational disease of painters: Exposure to white lead is now a recognized danger; as early as 1839 it was called encephalopathis saturnina. Before that, a 1762 Italian treatise on painting warned against using vermillion and ceruse, this being white lead. A visitor in the 1760s warned of pigments and such metals as lead and tin, the former from Spanish cooking pots and the latter when their tin lining had worn through (Connell, 2004, p. 78). Goya used 100 pounds of white lead in each of the 18 years that he worked on tapestry cartoons. ‘‘Any physical handling of the lead white or, even worse, inhaling its dust, could suYce to induce lead encephalopathy’’ (Connell, 2004, p. 79). The sperm count is reduced by lead in the blood, and this has also been invoked to explain Goya having only one surviving child 3. Menieres syndrome (auditory vertigo) 4. Neurolabyrinthitis (‘‘an inflammation of the nerves of the inner ear’’) 5. Botulism, typhoid fever, or poliomyelitis 6. Meningitis, as he hallucinated so much 7. Hepatitis Two recent biographies published in 2004 still called his illness a mysterious disease (Blackburn, 2004; Hughes, 2004).

V. Vogt-Koyanagi Syndrome

Goya’s sudden deafness can be explained by the diagnosis of the VogtKoyanagi syndrome, in which in addition to deafness there is uveitis (inflammation of the eye); there may also be loss of pigmentation of the skin and hair. The eye problem tends to clear up, but the deafness is permanent. Unknown in his day, this disease is now recognized as an autoimmune disorder aVecting melanin, the black pigment found in the inner ear (to give dizziness, tinnitus, and permanent deafness), the uveal tract (to give blurred vision), and sometimes the skin (to give vitiligo or depigmentation) and hair (to give poliosis or whitening). It is associated with a meningo-encephalitis, which explains the seriousness of his illness, vomiting, fits, and hallucinations. Each of these features can be present


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alone or in combination. His illness lasted nearly a year, and its many diVerent symptoms have been responsible for a large diVerential diagnosis. Vogt (1906) and Koyanagi (1929) first described the association of uveitis, deafness, and pigmentary changes in skin and hair. In 1926, Harada pointed out the more severe involvement of the central nervous system (CNS) (Manor, 1978). The Vogt-Koyanagi syndrome is in a group of autoimmune disorders that includes sarcoidosis and Behcet’s syndrome. The meningeal inflammation can cause cranial neuropathies and abnormal cerebro-spinal fluid (Bradley et al., 1996, p. 1820).9 Sudden sensorineural hearing loss is estimated at 20 cases per 100,000 inhabitants per year (Suckville et al., 2002). This may result from a circulatory disturbance of the inner ear (cochlea)10 or viral infection, but it is most likely that Goya’s disturbance was due to an immune disorder as evidenced by the addition to deafness of visual disturbance and a meningo-encephalitis giving fits, limb paralysis, and coma. If the deafness is one-sided, this is more likely to be circulatory in origin, which will aVect the immediate function. He finished his ‘‘Witchcraft’’ series for the Duke and Duchess of Osuna in June 1798, which followed on the Caprichos of the same period (1792–1798). Etchings on paper by metal has been used since the fifteenth century, and Goya used copper plates. The Academy was not keen on etchings, forcing Goya to withdraw them from sale. After this he painted characterizations of his friends who were liberal intellectuals. He was, however, in debt and so took on the commission to paint the Cupula of San Antonio de la Florida, which he completed within 4 months; this is where his remains are buried and the site of the Goya Museum (Fig. 4).11

9

I reported a possible case of the Vogt-Koyanagi Syndrome to the Section of Neurology of the Royal Society of Medicine nearly 50 years ago (Rose, 1960). This was a patient of Dr Denis Williams and was discussed at the annual clinical meeting of the section, which was held on December 3, 1959 at the National Hospital, Queen Square, where I was Resident Medical OYcer and, thus, responsible for organizing the session. 10 This is the site of the organ of Corti, the end organ of hearing. 11 St Anthony was born in Lisbon, the son of a Portuguese knight. He enrolled at the age of 15 with the Canons Regular of St Augustine but left after 2 years to become a Franciscan in 1220, an Order attempting to convert the Moors. He went to North Africa but became ill and returned to Europe landing in Messina; he then went to Assisi, where the Chapter General in session gave him the chance to speak in an ordination. His talent for preaching was recognized, and in 1226, Pope Puis XII gave him permission to preach in and around Padua, where he died at the age of 36. He was known for the miracle in Lisbon where his father was accused of murder. He immediately ‘‘flew’’ home from Italy, but the judges did not believe his claim of his father’s innocence. He asked that the corpse be brought to court where the dead man was asked if his father was the murderer. The corpse arose, declared the accused was innocent and then sank back in his bier; St Anthony was eventually canonized.

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FIG. 4. Goya’s portrait.

In 1799, Goya was very much in favor with the court and painted in September a portrait of the Queen as Maja and the King in hunting dress. He was appointed first painter to the Court in the following month with a salary of 50,000 reales a year.12

12 Charles IV had married his cousin, Maria Luisa of Palma, when he was 16 years and she 2 years younger. She bore 22 children of whom only six survived, the youngest rumored to be sired by Manuel Godoy. He had been a royal bodyguard, but after becoming the Queen’s favorite, he became the King’s right hand man, Commander-in-Chief of the army, Universal Minister, and was bestowed the title of Price of Peace. The painting of the family of Charles IV was done at the Aranjuez Palace with 13 members of the ruling Bourbon family, all of whom were delighted with the result. He made four trips to the Palace and did 10 studies of head and shoulders of the principal 10 personalities.


311

Goya stayed in Madrid when the Peninsular War started in 1807 and may have actually seen the events he later portrayed on May 2 and 3 (Figs. 5 and 6). In August 1808, he went to Zaragossa where there had been a siege for 3 months; 10,000 lives were lost, but in the second siege, beginning in November, there were 70,000 corpses. Goya had been invited there to paint a portrait of the defending General Jose´ de Palafax; often doing the preliminary sketches before the November siege, he went to his family house outside Fuentetodos to stay with his brother for a few weeks, returning to Madrid before April 1807. In 1808, Goya embarked on a series of prints called the Disasters of War, a portrayal of the insanity of conflict, his theme being that neither the Church nor the rulers cared for the ordinary people. At the same time, he also painted popular scenes and still life. The series consists of 22 prints that he produced from 1810 to 1820. In 1812–1830, Goya was short of money even though his wife had left him a small legacy. The relationship between father and son was not good, as evidenced by the fact that he left Moriano, his beloved grandson, the house in 1823 after finishing the Black Paintings.

FIG. 5. Peninsular war on May 2.

312

F. CLIFFORD ROSE

FIG. 6. Peninsular war on May 3.

In 1815, he met and began an aVair with Leocadia Zorilla (Fig. 7), who was the youngest daughter of wealthy parents of Basque origin, a relative of his daughter-in-law, and 42 years junior to him. In this year, he did a series of engravings in bullfighting of which there were at least 35 and another self portrait. In the same year, he had to attend a tribunal to prove, with help of friends, his loyalty to King Ferdinand. In the following year, he was meant to appear before the Inquisition to explain the meanings of some of his drawings, for example, a nude woman, but it is presumed, in the absence of any record, that this hearing was postponed indefinitely.

VI. Black Paintings

In 1819, Goya moved out of central Madrid to the Quinta del Sordo where he initially decorated the walls with his series of pleasant images, consisting of 14 art-on-plaster works. Initially he had planned joyous paintings, but when the Congress of Vienna returned the monarchy to Spain, he had a change of heart.


313

FIG. 7. Leocadia Zorilla.

In the Quinta del Sordo, he decorated the walls of two rooms one above the other. Modern x-ray techniques show that originally there were pleasant scenes, but he plastered over this and painted grimmer stories, for example, The Pilgrimage to San Isidoro, which showed a crowd following a blind guitarist, and Saturn with his insatiable appetite. There were 14 paintings in these two rooms, but he then went on to paint the panels of several smaller rooms and the staircase that connected the two floors. These Black Paintings were lifted from the walls, fixed on to canvas and are now exhibited in the Prado. He moved to this country house with Leocadia, oYcially his housekeeper, and their two youngest children. From this house he could see the Church of San Antonio de la Florida, where 20 years previously, he had spent 4 months with an assistant painting the arched ceiling, with the cupola featuring the story of St Anthony bringing a murdered man back to life to name his murderer.

314

F. CLIFFORD ROSE

FIG. 8. Self portrait with Dr Eugenio Garcia Arrieta (1820).

Toward the end of that year, he became ill and was delirious with diarrhea and jaundice, presumably due to an infection. Everyday he was visited by Dr Eugenio Garcia Arrieta of whom he painted an appreciative painting with himself when sick. Goya grasps his shirt as if clinging to life (Park and Park, 2004). Goya recovered and lived another 8 years. Dr Eugenio Garcia Arrieta (Fig. 8) was his friend, whom he trusted implicitly, and the double portrait of patient and doctor was painted in 1820 with a long inscription: ‘‘Goya in gratitude to his friend Arrieta for the skill and great care with which he saved his life in his acute and dangerous illness, suVered at the end of 1819, at the age of seventy-three years. He painted this in 1820.’’ The only suggestion of the nature of his illness was that Dr Arrieta was a specialist in infectious diseases, who visited North Africa in 1820 to research bubonic plague; yellow fever was transferred from there to Spain by Mediterranean shipping. In the painting, the doctor holds up a glass to him, presumably of medicine. Goya is


315

sitting up being held up by the doctor but looking as if he was at death’s door. His hands are plucking at bedclothes (Carphology),13 which occurs in typhoid. The image is very diVerent from his attitude to his earlier doctors as evidenced by ‘‘his Caprichos’’ when he called them killers of the healthy (Matasonos). Goya did not think much of doctors. His Capricho number 40 entitled ‘‘What illness did he die from?’’ (De que mal movira), shows a suited ass taking the pulse of a dying man with this hoof. It is clear the donkey, like a human doctor, cannot make a diagnosis, both being ill trained and ignorant. It may be that the failure of his doctors during his severe illness when he was aged 47 was the cause of his poor opinion of doctors. He, in fact, changed his mind when he was treated for the illness in 1819 by Dr Eugenio Garcia Arrieta (Hughes, 2004, p. 201). Goya’s entire oeuvre comprised almost 2000 paintings, drawings, etchings,14 engravings,15 and lithographs. In the 10 years after the age of 62, he produced over 700 paintings. Goya painted Los desastres de la Guerra between 1810 and 1814. These included scenes of terror from the Napoleonic invasion; he added 17 plates in 1814 on the restoration of Ferdinand VIII. Hating tyranny, social injustice and human stupidity, he went into exile in France toward the end of his life and died in Bordeaux in 1828, from a stroke. The follies (Disparates or the Proverbs) were done between 1816 and 1823 but not published until after his death. There were at least 25 but only 22 are known. Similar themes to the Caprichos are shown, for example, men as weak, foolish, and superficial. In these, his views became more critical of the church.

References

Blackburn, J. (2004). ‘‘Old Man Goya.’’ Jonathan Cape, London. Bradley, W. G., Danoff, R. B., Fenichel, G. M., and Marsden, C. D. (1996). Clin. Neurol. 1820. Connell, E. S. (2004). ‘‘Francisco Goya: A Life.’’ Counterpoint, New York. Hughes, R. (2004). ‘‘Goya London.’’ Harvill Press, London. 13 Carphology (OED). The movements of delirious patients, as if searching for imaginary objects or picking the bedclothes. 14 Etching is when a flat metal plate, usually copper as it is soft, is covered with thick acid-resistant coating (wax, resin, and asphalt). This is covered with black soot. This drawing is made using a sharp needle leaving unprotected copper, which is then ‘‘eaten away’’ by a mordant, for example, weak nitric acid. The ground is cleaned oV and wet ink applied, which stays in the grooves and damp paper pressed on. Nearly a quarter of the 80 Caprichos deal with witches, even more deal with sexual mores. Etching does not use cutting but an engraver does. 15 Aquatint is using a flat watercolor wash with tiny grains and speckles giving a variety of tints. Dusting areas of the copper plate with fine pulverized resin, which on heating sticks to the copper. This is then immersed in an acid bath.

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Koyanagi (1929). Klin Monatsbl Augenheilkd 82, 194. Manor, R. S. (1978). Vogt-Koyanagi Syndrome and related diseases. In ‘‘Handbook of Clinical Neurology’’ (P. K. Vinken and G. W. Bruyn, Eds.), Vol. 34, pp. 513–544. Park, M. P., and Park, R. H. R. (2004). The fine art of patient-doctor relationships. Br. Med. J. 320, 1475–1480. Rapelli, P. (1999). ‘‘Art Book, Goya.’’ Dorling Kindersley, London. Rose, F. C. (1960). Vogt-Koyanagi Syndrome. J. Roy. Soc. Med. 53, 137. Rose, F. C. (2004). Neurology of art: An overview. In ‘‘Neurology of the Arts: Painting, Music, Literature’’ (F. CliVord Rose, Ed.). Imperial College Press, London. Suckville, M. (2002). Fibrinogen and LDL. Apheresis in treatment of sudden hearing loss: A randomised multi-centre trial. Lancet 360, 1811–1817. Vogt (1906). Klin Monatsbl Augenheilkd 44, 228. Waldmann, S. (1998). ‘‘Goya and the Duchess of Alba.’’ Prestel, London.

INDEX

A Absinthe, 271–272 drinking of, 273 effect of, on artistic expression, 274–276 medical effects of, 273–274 toxic ingredient of. See Thujone Abstract images, 94 Abulia. See Abulic individuals Abulic individuals, 217, 219–220 Abusive substances used by Van Gogh absinthe, 263–264 alcohol, 263 digitalis, 264 lead poisoning, 265 Achromatopsia, 59 Acute intermittent porphyria (AIP), case study of Van Gogh, 265–268 AD. See Alzheimer’s disease ‘‘Aesthetic cognition,’’ 10 Aesthetics definition, 2 response, 3 Akinetopsia, 53, 59 Alzheimer’s disease (AD), 149 in artists, 235–236 artists, artistic changes in Carolus Horn, 150–152 Danae Chambers, 151 Willem de Kooning, 150 William Utermohlen, 152–156 patients, influence of negative and positive cognitive phenomena on, 156–160 Ancillary testing, 225 Anxiety, 122–124 Aphasia in artists, 144 Appreciative agnosias, 42 Aromatherapy, Internet for, 273 Art depiction of neurogenetic diseases in, 237–239 effect of neurogenetic diseases on, 235–237 relation of neurogenetic diseases and, 235, 239

Artistic changes in paintings by AD artists, 147–149 Carolus Horn, 150–152 Danae Chambers, 151 effect of positive and negative cognitive phenomena on, 156–160 Willem de Kooning, 150 William Utermohlen, 152–156 Artistic creativity, 62 in painting and style in brain-damaged artists, 135–139 role of frontal lobe areas in, 138–139 and style in artists after brain lesions, change in, 139–141 Artistic style, 45 in artists after brain lesions, change in, 141–146 in brain-damaged artists, 135–139 of Lovis Corinth, effect of visuo-spatial neglect on, 196–198 Artists for making sculpture or painting, attributes required by, 216–217 Associative agnosias, 42 Attentional disorder. See Visuo-spatial neglect Attractiveness of faces, brain’s response to, 7 Autistic artists, 43

B Balint syndrome, 60 Basaldella, Afro, 184 Bedside testing for patients with frontal lobe lesions, 219–221 Behavior, dysfunctions of, 33–36 Bell, Charles, 281, 288 after Corunna in 1809 and marriage in 1811, 284 after Waterloo, 285–286 Corunna oils in 1809, 284 David Allan, 282–283 death of, 287 317

318

INDEX

Bell, Charles (cont.) early years of, 282 influence of Raphael cartoons on, 283–284 Italian tour in 1840, 285–286 Waterloo in 1815 and the watercolors of 1836, 284–285 ‘‘binding problem,’’ 12 Bipolar disorder, case study of Van Gogh, 262–263 ‘‘Blinding migraine,’’ 113 Bo¨cklin, Arnold, 184–185 Boijadjiev, Zlatyu, 182–183 Brain anatomists of, 21–24 damage, effects of, 39 dysfunction in artistic style, role of, 141–146 electrical stimulation of, 32 functioning in artistic creativity, 137–138 functions of, 30 structures, 76 tissues, 29 Brain-damaged artists, artistic creativity in painting and style in change in, 140–146 introduction to, 135–139 Brain lesions change in artistic creativity and style in artists after, 139–141 change in artistic style in artists after, 141–146 Brown, Reynold, 176–178 C Cell doctrine, 25 Cerebral achromatopsia, 59 Cerebral cortex, 28 Chambers, Danae, artistic ability of, 150 ‘‘Childhood Cube,’’ 116 Clinical testing for constructional apraxia with frontal lobe lesions, 219–221 left parietal lobe lesions, 223–225 right parietal lobe lesions, 226–232 Cognitive dysfunction in artists, 148 Cognitive phenomena negative, 156–160 positive, 156–160 Color-blind artists, 71 ‘‘Colored hearing,’’ 73 Colour vision, 6 Complex partial seizure, 121

Constructional apraxia, 216 anatomy of, associated with frontal lobe lesions, 218–219 left parietal lobe lesions, 223 right parietal lobe lesions, 225–226 clinical testing for with frontal lobe lesions, 219–221 with left parietal lobe lesions, 223–225 with right parietal lobe lesions, 226–232 Corinth, Lovis case study of right hemisphere stroke, 170–175 case study of visuo-spatial neglect, 193–196 artistic style of, 196–198 discussions on, 209–212 drawings of, 201–204 hospitalization of, 199 paintings of, 204–208 rehabilitation of, 199–200 self-portraiture of, 201 Cortex, 56 Cortical motor regions, 57 Cross-modal sensory, 74 Crucifixion fainting, 80–81 D Dementia patients, 141–144 Depression, 122–123 in artists, 135 Disorder of color processing, 53 Dix, Otto, 167–169 Drawings, computer manipulation of, 94 Duchenne muscular dystrophy, 237–238 E ‘‘Earthquake,’’ 272 Electrophysiological recording, use of, 51 Emotional turmoil, 87 Epilepsy, artistis with, 119 artistic themes in works of, 120 nonepilepsy related, 128–130 psychiatirc comorbidity, 122–124 psychological aspects of, 124–128 seizures experiences, 121–122 collection of work of, background of, 120 Epilepsy, case study of Van Gogh, 261–262 Executive dysfunction, patients with, 218

INDEX

F Face perception, 53 Fainting (syncope), 79, 87 among women, 84–85 crucifixion, 80–81 historical, 81–83 Mary’s, 80–81 phases of, 80 Fellini, Federico, 175–176 Ferenczy, Beni, 183 ‘‘Figurative-impressionist,’’ 46 Fortification spectra, 114 Freudian theory, concepts in, 35 Friedrich, Caspar David, 185–186 ‘‘From the Storm,’’ 120 Frontal lobe areas in artistic creativity, role of, 138–139 Frontal lobe lesions abnormalities of patients with, 218 anatomy of, 218–219 clinical testing for constructional apraxia with, 219–221 nature of the deficits, 217–218 Frontotemporal dementias (FTD), 40 FTD. See Frontotemporal dementias Functional brain imaging, 53 Fuzzy-minded scientists, 63 G Genre painting, 83–84 Gernez, Paul-Elie, 180–181 Gerstmann syndrome, 223 Gogh, Van, 253 art of, 254–255 attacks of, 258–261 ear amputation of, 256–258 illness of, 255–256 possible disorders of abusive substances, 263–265 acute intermittent porphyria, 265–268 bipolar disorder, 262–263 epilepsy, 261–262 Menieres disease, 265 neurosyphilis, 262 schizophrenia, 262 Golgi technique, 26 Go-No-Go test, 221 Goya background, 301–306

319

Black paintings, 312–315 differential diagnosis, 308 the Duchess of Alba, 306–307 illness, 307 Vogt-Koyanagi Syndrome, 308–312 Graphic neglect effect on paintings and drawings of Lovis Corinth, 201–208 in painters, 197–198, 209 Greenshields, Tom, 178 H Hidden disability, 119 ‘‘Highly cerebral,’’ 45 ‘‘High yellow pictures,’’ 275 Historical fainting, 81–83 Hollow optic nerves, 24 Horn, Carolus, artistic ability of, 150–152 I Idiosyncrasies, 70 Imagination, 12–13 Imigram, 111 Impressionists, 273 J Jacksonian neurology, 61 K Kahlo, Frida accident and artist debut, 295 childhood sufferings, 293–294 disease and creativity, 298–299 marriage, 295–296 school, 294 suffering and painting, 296–298 Koh’s blocks, 227–228 Kooning, Willem de, artistic ability of, 150 L Left hemisphere stroke, case studies of painters with Afro Basaldella, 184 Arnold Bo¨cklin, 184–185 Beni Ferenczy, 183

320

INDEX

Left hemisphere stroke, case studies of painters with (cont.) Caspar David Friedrich, 185–186 Daniel Urrabieta y Vierge, 181–182 Ernst Oldenburg, 183 Paul-Elie Gernez, 180–181 Polish painter ‘‘R. L.’’, 184 Zlatyu Boijadjiev, 182–183 ‘‘literary intellectuals’’, 62 LSD. See Lsergic acid diethylamide Lusignoli, Guglielmo, 179–180 Lyceum Medicum Londinense, 19 Lysergic acid diethylamide (LSD), 74–75, 110

Neurogenetic diseases depiction of, in art, 237–239 effect of, on art, 235–237 relation of art and, 235, 239 Neurological disorders, 41 Neurological disturbance, artists, 72–73 Neuron(s), 53 doctrine, 32 Neurophysiology, 4–6 Neuroscience, graphical history of, 19 Neurosyphilis, case study of Van Gogh, 262 ‘‘Nuclear Sunrise,’’ 44 O

M Macaque, cerebral cortex of, 11 Magnetizers, 33 Manic-depressive psychosis. See Bipolar disorder Man swooning, 85 Mary’s fainting, 80–81 Mate selection, 8–10 Menieres disease, case study of Van Gogh, 265 Microanatomy, 25 Middle temporal (MT), 53 Migraine Art competition, 93 Migraine art in the Internet, 89, 93 methods assessed variables, 90–91 identification of study sample, 90 statistical evaluation, 91 results analysis of artists’ media, 102–104 characteristics of study sample, 91–92 participation in migraine art, 101–102 relationships between migraine and art making, 92–101 Migraine aura, 110 Migraine Masterpieces competition, 113 Modern artistic palate, 4 Monochromatic paintings, 71 Motor impersistence, 217–218, 220 clinical testing for, 220–221 Multiple sclerosis, 236 N Nave, 63 Nervous system, 55 gross structures of, 24

Occipital ventral cortex, 53 Occipito-temporal junction. See Middle temporal Oldenburg, Ernst, 183 P Painters, 6, 58 with AD, changes in artistic ability in, 147–149 Carolus Horn, 150–152 Danae Chambers, 151 Willem de Kooning, 150 William Utermohlen, 152–156 Painting blackouts in, 80 neurology of, 19 Parietal lobe lesions left anatomy of, 223 clinical testing for constructional apraxia with, 223–225 nature of the deficits, 222–223, 224 right anatomy of, 225–226 clinical testing for constructional apraxia with, 226–232 nature of the deficits, 225 Patients. See also Brain-damaged artists; Brain lesions common features in brain-damaged, 143 dementia, 141–144 with neurodegenerative diseases, 148 artistic changes in, 147–149 Pattern recognition, 11

INDEX

Pearce, Bryan, 241–243 art of, 243–249 Phenylketonuria in, 249–251 Perceptual portraits, 17–18 Pethidine, 111 Phenylalanine hydroylase, 250 Phenylketonuria (PKU), 250 case study of Bryan Pearce, 251 case study of Carol Buck, 251–252 symptoms of, 250–251 Phenylpyruvic acid, 249 Phosphenes, 110 Piet Mondrian’s paintings, 5 Pinel’s act, 34 PKU. See Phenylketonuria ‘‘Play,’’ 3 Portrait of Lettsom, 18 Postmodern painting, 63 Postsurgery hemorrhage, case study of, 186–187 Prosopagnosia, 53 symptom of, 59 Psychiatric disorders, 124 Psychoanalysis, 34 Psychosexuality, 35 R Ra¨derscheidt, Anton, 166–167 Raphael, Sarah, 12–13 ‘‘blinding migraine,’’ 114–115 development, 116 migraine, description of, 111 migraine experiences, 116–117 paintings, 110 Renaissance of anatomy, 22 Retina, 27, 58 Revisualization, 217 Right hemisphere stroke, case studies of painters with Aichinger-Kassek, Wolfgang, 175 Anton Ra¨derscheidt, 166–167 Blanke et al., 179 Federico Fellini, 175–176 Guglielmo Lusignoli, 179–180 Johannes Thiel, 170 Kurt Schwitters, 180 Lovis Corinth, 170–175 Otto Dix, 167–169 Reynold Brown, 176–178

321

Schnider et al., 179 Tom Greenshields, 178 Vigouroux et al., 179 Rods, 28 S Schizophrenia, case study of Van Gogh, 262 Schwitters, Kurt, 180 Scintillating scotoma (SS), 94 Seizures, demonic implications of, 80 Sensorimotor expression, 62 Sensory systems, 3 Sexual strategies of higher animals, 8 ‘‘Shock of the new,’’ 3 SOD-1 gene, 236 Spatial organization, 189 SS. See Scintillating scotoma Stroke in painters, 165, 189 case studies of painters with left hemisphere stroke Afro Basaldella, 184 Arnold Bo¨cklin, 184–185 Beni Ferenczy, 183 Caspar David Friedrich, 185–186 Daniel Urrabieta y Vierge, 181–182 Ernst Oldenburg, 183 Paul-Elie Gernez, 180–181 Polish painter ‘‘R. L.’’, 184 Zlatyu Boijadjiev, 182–183 case studies of painters with right hemisphere stroke Anton Ra¨derscheidt, 166–167 Blanke et al., 179 Federico Fellini, 175–176 Guglielmo Lusignoli, 179–180 Johannes Thiel, 170 Kurt Schwitters, 180 Lovis Corinth, 170–175 Otto Dix, 167–169 Reynold Brown, 176–178 Schnider et al., 179 Tom Greenshields, 178 Vigouroux et al., 179 Wolfgang Aichinger-Kassek, 175 case study of a 87-year-old artist with top-of-the-basilar-artery embolic stroke, 186 Jon Sarkin, case study of postsurgery hemorrhage, 186–187

322

INDEX

Stroke in painters (cont.) Tommy McHugh, case study of subarachnoid hemorrhage, 186 Stylistic changes, 45–46 Subarachnoid hemorrhage, case study of, 186 ‘‘Sublime,’’ 7, 13 Swooning, 84–85 Syncope. See Fainting Synaesthesia, 69, 71 ‘‘synthetic unity of apperception, 11 -Synuclein gene, 236 T Thiel, Johannes, 170 Thujone, 274 Tonic-clonic seizures, 121–122 Top-of-the-basilar-artery embolic stroke, case study of 87-year-old artist with, 186 U Utermohlen, William, artistic ability of, 152–156 V Vesalius, 22 Vierge, Daniel Urrabieta y, 181–182 Vision, 51 anatomy, 23–24

Visual agnosia(s), 42, 53, 59 Visual art, 39, 44 deposition to produce, 40–41 Visual association cortices, damage to, 46 Visual brain, 6, 59 localization in, 56–58 Visual functions, 56 Visual hallucinations, 159 Visual instability, 159 Visual perception, 59 Visual processings, 53 Visual-spatial functions testing, 226–229 Visual system, 5 Visual vocabularies, 41–42 Visuo-spatial neglect, 187–189 case study of Lovis Corinth suffering with, 193–196 artistic style of, 196–198 discussions on, 209–212 drawings of, 201–204 hospitalization of, 199 paintings of, 204–208 rehabilitation of, 199–200 self-portraiture of, 201 characteristics of, 197–198, 210 Vogt-Koyanagi syndrome, 308–312 W Wilson’s disease, 238

CONTENTS OF RECENT VOLUMES

Memory and Forgetting: Long-Term and Gradual Changes in Memory Storage Larry R. Squire

Volume 37 Section I: Selectionist Ideas and Neurobiology in

Implicit Knowledge: New Perspectives on Unconscious Processes Daniel L. Schacter

Population Thinking and Neuronal Selection: Metaphors or Concepts? Ernst Mayr

Section V: Psychophysics, Psychoanalysis, and Neuropsychology

Selectionist and Neuroscience Olaf Sporns

Instructionist

Ideas

Selection and the Origin of Information Manfred Eigen

Phantom Limbs, Neglect Syndromes, Repressed Memories, and Freudian Psychology V. S. Ramachandran

Section II: Populations

Neural Darwinism and a Conceptual Crisis in Psychoanalysis Arnold H. Modell

Development

and

Neuronal

Morphoregulatory Molecules and Selectional Dynamics during Development Kathryn L. Crossin

A New Vision of the Mind Oliver Sacks

Exploration and Selection in the Early Acquisition of Skill Esther Thelen and Daniela Corbetta

index

Population Activity in the Control of Movement Apostolos P. Georgopoulos

Volume 38

Section III: Functional Integration in the Brain

Segregation

and

Reentry and the Problem of Cortical Integration Giulio Tononi Coherence as an Organizing Principle of Cortical Functions Wolf Singerl

Regulation of GABAA Receptor Function and Gene Expression in the Central Nervous System A. Leslie Morrow Genetics and the Organization of the Basal Ganglia Robert Hitzemann, Yeang Olan, Stephen Kanes, Katherine Dains, and Barbara Hitzemann

Section IV: Memory and Models

Structure and Pharmacology of Vertebrate GABAA Receptor Subtypes Paul J. Whiting, Ruth M. McKernan, and Keith A. Wafford

Selection versus Instruction: Use of Computer Models to Compare Brain Theories George N. Reeke, Jr.

Neurotransmitter Transporters: Biology, Function, and Regulation Beth Borowsky and Beth J. Hoffman

Temporal Mechanisms in Perception Ernst Po¨ppel

323

Molecular

324


Presynaptic Excitability Meyer B. Jackson

Volume 40

Monoamine Neurotransmitters in Invertebrates and Vertebrates: An Examination of the Diverse Enzymatic Pathways Utilized to Synthesize and Inactivate Biogenic Amines B. D. Sloley and A. V. Juorio

Mechanisms of Nerve Cell Death: Apoptosis or Necrosis after Cerebral Ischemia R. M. E. Chalmers-Redman, A. D. Fraser, W. Y. H. Ju, J. Wadia, N. A. Tatton, and W. G. Tatton

Neurotransmitter Systems in Schizophrenia Gavin P. Reynolds

Changes in Ionic Fluxes during Cerebral Ischemia Tibor Kristian and Bo K. Siesjo

Physiology of Bergmann Glial Cells Thomas Mu¨ller and Helmut Kettenmann index

Techniques for Examining Neuroprotective Drugs In Vitro A. Richard Green and Alan J. Cross

Volume 39

Techniques for Examining Neuroprotective Drugs In Vivo Mark P. Goldberg, Uta Strasser, and Laura L. Dugan

Modulation of Amino Acid-Gated Ion Channels by Protein Phosphorylation Stephen J. Moss and Trevor G. Smart Use-Dependent Regulation Receptors Eugene M. Barnes, Jr.

of

GABAA

Synaptic Transmission and Modulation in the Neostriatum David M. Lovinger and Elizabeth Tyler The Cytoskeleton and Neurotransmitter Receptors Valerie J. Whatley and R. Adron Harris Endogenous Opioid Regulation of Hippocampal Function Michele L. Simmons and Charles Chavkin Molecular Neurobiology of the Cannabinoid Receptor Mary E. Abood and Billy R. Martin Genetic Models in the Study of Anesthetic Drug Action Victoria J. Simpson and Thomas E. Johnson Neurochemical Bases of Locomotion and Ethanol Stimulant Effects Tamara J. Phillips and Elaine H. Shen Effects of Ethanol on Ion Channels Fulton T. Crews, A. Leslie Morrow, Hugh Criswell, and George Breese index

Calcium Antagonists: Their Role in Neuroprotection A. Jacqueline Hunter Sodium and Potassium Channel Modulators: Their Role in Neuroprotection Tihomir P. Obrenovich NMDA Antagonists: Their Role in Neuroprotection Danial L. Small Development of the NMDA Ion-Channel Blocker, Aptiganel Hydrochloride, as a Neuroprotective Agent for Acute CNS Injury Robert N. McBurney The Pharmacology of AMPA Antagonists and Their Role in Neuroprotection Rammy Gill and David Lodge GABA and Neuroprotection Patrick D. Lyden Adenosine and Neuroprotection Bertil B. Fredholm Interleukins and Cerebral Ischemia Nancy J. Rothwell, Sarah A. Loddick, and Paul Stroemer Nitrone-Based Free Radical Traps as Neuroprotective Agents in Cerebral Ischemia and Other Pathologies Kenneth Hensley, John M. Carney, Charles A. Stewart, Tahera Tabatabaie, Quentin Pye, and Robert A. Floyd


Neurotoxic and Neuroprotective Roles of Nitric Oxide in Cerebral Ischemia Turgay Dalkara and Michael A. Moskowitz

Sensory and Cognitive Functions Lawrence M. Parsons and Peter T. Fox

A Review of Earlier Clinical Studies on Neuroprotective Agents and Current Approaches Nils-Gunnar Wahlgren

Skill Learning Julien Doyon

index

Volume 41

Section V: Clinical and Neuropsychological Observations Executive Function and Motor Skill Learning Mark Hallett and Jordon Grafman

Section I: Historical Overview

Verbal Fluency and Agrammatism Marco Molinari, Maria G. Leggio, and Maria C. Silveri

Rediscovery of an Early Concept Jeremy D. Schmahmann

Classical Conditioning Diana S. Woodruff-Pak

Section II: Anatomic Substrates

Early Infantile Autism Margaret L. Bauman, Pauline A. Filipek, and Thomas L. Kemper

The Cerebrocerebellar System Jeremy D. Schmahmann and Deepak N. Pandya Cerebellar Output Channels Frank A. Middleton and Peter L. Strick Cerebellar-Hypothalamic Axis: Basic Circuits and Clinical Observations Duane E. Haines, Espen Dietrichs, Gregory A. Mihailoff, and E. Frank McDonald Section III. Physiological Observations Amelioration of Aggression: Response to Selective Cerebellar Lesions in the Rhesus Monkey Aaron J. Berman Autonomic and Vasomotor Regulation Donald J. Reis and Eugene V. Golanov Associative Learning Richard F. Thompson, Shaowen Bao, Lu Chen, Benjamin D. Cipriano, Jeffrey S. Grethe, Jeansok J. Kim, Judith K. Thompson, Jo Anne Tracy, Martha S. Weninger, and David J. Krupa

Olivopontocerebellar Atrophy and Friedreich’s Ataxia: Neuropsychological Consequences of Bilateral versus Unilateral Cerebellar Lesions The´re`se Botez-Marquard and Mihai I. Botez Posterior Fossa Syndrome Ian F. Pollack Cerebellar Cognitive Affective Syndrome Jeremy D. Schmahmann and Janet C. Sherman Inherited Cerebellar Diseases Claus W. Wallesch and Claudius Bartels Neuropsychological Abnormalities in Cerebellar Syndromes—Fact or Fiction? Irene Daum and Hermann Ackermann Section VI: Theoretical Considerations Cerebellar Microcomplexes Masao Ito

Visuospatial Abilities Robert Lalonde

Control of Sensory Data Acquisition James M. Bower

Spatial Event Processing Marco Molinari, Laura Petrosini, and Liliana G. Grammaldo

Neural Representations of Moving Systems Michael Paulin

Section IV: Functional Neuroimaging Studies Linguistic Processing Julie A. Fiez and Marcus E. Raichle

325

How Fibers Subserve Computing Capabilities: Similarities Between Brains and Machines Henrietta C. Leiner and Alan L. Leiner

326


Cerebellar Timing Systems Richard Ivry

Volume 43

Attention Coordination and Anticipatory Control Natacha A. Akshoomoff, Eric Courchesne, and Jeanne Townsend

Early Development of the Drosophila Neuromuscular Junction: A Model for Studying Neuronal Networks in Development Akira Chiba

Context-Response Linkage W. Thomas Thach

Development of Larval Body Wall Muscles Michael Bate, Matthias Landgraf, and Mar Ruiz Gmez Bate

Duality of Cerebellar Motor and Cognitive Functions James R. Bloedel and Vlastislav Bracha Section VII: Future Directions Therapeutic and Research Implications Jeremy D. Schmahmann

Volume 42 Alzheimer Disease Mark A. Smith Neurobiology of Stroke W. Dalton Dietrich Free Radicals, Calcium, and the Synaptic Plasticity-Cell Death Continuum: Emerging Roles of the Trascription Factor NFB Mark P. Mattson AP-I Transcription Factors: Short- and LongTerm Modulators of Gene Expression in the Brain Keith Pennypacker

Development of Electrical Properties and Synaptic Transmission at the Embryonic Neuromuscular Junction Kendal S. Broadie Ultrastructural Correlates of Neuromuscular Junction Development Mary B. Rheuben, Motojiro Yoshihara, and Yoshiaki Kidokoro Assembly and Maturation of the Drosophila Larval Neuromuscular Junction L. Sian Gramates and Vivian Budnik Second Messenger Systems Underlying Plasticity at the Neuromuscular Junction Frances Hannan and Yi Zhong Mechanisms of Neurotransmitter Release J. Troy Littleton, Leo Pallanck, and Barry Ganetzky Vesicle Recycling at the Drosophila Neuromuscular Junction Daniel T. Stimson and Mani Ramaswami Ionic Currents in Larval Muscles of Drosophila Satpal Singh and Chun-Fang Wu

Ion Channels in Epilepsy Istvan Mody

Development of the Adult Neuromuscular System Joyce J. Fernandes and Haig Keshishian

Posttranslational Regulation of Ionotropic Glutamate Receptors and Synaptic Plasticity Xiaoning Bi, Steve Standley, and Michel Baudry

Controlling the Motor Neuron James R. Trimarchi, Ping Jin, and Rodney K. Murphey

Heritable Mutations in the Glycine, GABAA, and Nicotinic Acetylcholine Receptors Provide New Insights into the Ligand-Gated Ion Channel Receptor Superfamily Behnaz Vafa and Peter R. Schofield

Volume 44

index

Human Ego-Motion Perception A. V. van den Berg Optic Flow and Eye Movements M. Lappe and K.-P. Hoffman


The Role of MST Neurons During Ocular Tracking in 3D Space K. Kawano, U. Inoue, A. Takemura, Y. Kodaka, and F. A. Miles Visual Navigation in Flying Insects M. V. Srinivasan and S.-W. Zhang Neuronal Matched Filters for Optic Flow Processing in Flying Insects H. G. Krapp A Common Frame of Reference for the Analysis of Optic Flow and Vestibular Information B. J. Frost and D. R. W. Wylie Optic Flow and the Visual Guidance of Locomotion in the Cat H. Sherk and G. A. Fowler Stages of Self-Motion Processing in Primate Posterior Parietal Cortex F. Bremmer, J.-R. Duhamel, S. B. Hamed, and W. Graf Optic Flow Perception C. J. Duffy

Analysis

for

Self-Movement

Neural Mechanisms for Self-Motion Perception in Area MST R. A. Andersen, K. V. Shenoy, J. A. Crowell, and D. C. Bradley Computational Mechanisms for Optic Flow Analysis in Primate Cortex M. Lappe Human Cortical Areas Underlying the Perception of Optic Flow: Brain Imaging Studies M. W. Greenlee

327

Brain Development and Generation of Brain Pathologies Gregory L. Holmes and Bridget McCabe Maturation of Channels and Receptors: Consequences for Excitability David F. Owens and Arnold R. Kriegstein Neuronal Activity and the Establishment of Normal and Epileptic Circuits during Brain Development John W. Swann, Karen L. Smith, and Chong L. Lee The Effects of Seizures of the Hippocampus of the Immature Brain Ellen F. Sperber and Solomon L. Moshe Abnormal Development and Catastrophic Epilepsies: The Clinical Picture and Relation to Neuroimaging Harry T. Chugani and Diane C. Chugani Cortical Reorganization and Seizure Generation in Dysplastic Cortex G. Avanzini, R. Preafico, S. Franceschetti, G. Sancini, G. Battaglia, and V. Scaioli Rasmussen’s Syndrome with Particular Reference to Cerebral Plasticity: A Tribute to Frank Morrell Fredrick Andermann and Yuonne Hart Structural Reorganization of Hippocampal Networks Caused by Seizure Activity Daniel H. Lowenstein Epilepsy-Associated Plasticity in gammaAmniobutyric Acid Receptor Expression, Function and Inhibitory Synaptic Properties Douglas A. Coulter

What Neurological Patients Tell Us about the Use of Optic Flow L. M. Vaina and S. K. Rushton

Synaptic Plasticity and Secondary Epileptogenesis Timothy J. Teyler, Steven L. Morgan, Rebecca N. Russell, and Brian L. Woodside

index

Synaptic Plasticity in Epileptogenesis: Cellular Mechanisms Underlying Long-Lasting Synaptic Modifications that Require New Gene Expression Oswald Steward, Christopher S. Wallace, and Paul F. Worley

Volume 45 Mechanisms of Brain Plasticity: From Normal Brain Function to Pathology Philip. A. Schwartzkroin

Cellular Correlates of Behavior Emma R. Wood, Paul A. Dudchenko, and Howard Eichenbaum

328


Biosynthesis of Neurosteroids and Regulation of Their Synthesis Synthia H. Mellon and Hubert Vaudry

Mechanisms of Neuronal Conditioning David A. T. King, David J. Krupa, Michael R. Foy, and Richard F. Thompson Plasticity in the Aging Central Nervous System C. A. Barnes Secondary Epileptogenesis, Kindling, and Intractable Epilepsy: A Reappraisal from the Perspective of Neuronal Plasticity Thomas P. Sutula Kindling and the Mirror Focus Dan C. McIntyre and Michael O. Poulter Partial Kindling and Behavioral Pathologies Robert E. Adamec The Mirror Focus and Secondary Epileptogenesis B. J. Wilder Hippocampal Lesions in Epilepsy: A Historical Review Robert Naquet Clinical Evidence for Secondary Epileptogensis Hans O. Luders Epilepsy as a Progressive (or Nonprogressive ‘‘Benign’’) Disorder John A. Wada Pathophysiological Aspects of Landau-Kleffner Syndrome: From the Active Epileptic Phase to Recovery Marie-Noelle Metz-Lutz, Pierre Maquet, Annd De Saint Martin, Gabrielle Rudolf, Norma Wioland, Edouard Hirsch, and Chriatian Marescaux

Neurosteroid 7-Hydroxylation Products in the Brain Robert Morfin and Luboslav Sta´rka Neurosteroid Analysis Ahmed A. Alomary, Robert L. Fitzgerald, and Robert H. Purdy Role of the Peripheral-Type Benzodiazepine Receptor in Adrenal and Brain Steroidogenesis Rachel C. Brown and Vassilios Papadopoulos Formation and Effects of Neuroactive Steroids in the Central and Peripheral Nervous System Roberto Cosimo Melcangi, Valerio Magnaghi, Mariarita Galbiati, and Luciano Martini Neurosteroid Modulation of Recombinant and Synaptic GABAA Receptors Jeremy J. Lambert, Sarah C. Harney, Delia Belelli, and John A. Peters GABAA-Receptor Plasticity during LongTerm Exposure to and Withdrawal from Progesterone Giovanni Biggio, Paolo Follesa, Enrico Sanna, Robert H. Purdy, and Alessandra Concas Stress and Neuroactive Steroids Maria Luisa Barbaccia, Mariangela Serra, Robert H. Purdy, and Giovanni Biggio

Local Pathways of Seizure Propagation in Neocortex Barry W. Connors, David J. Pinto, and Albert E. Telefeian

Neurosteroids in Learning and Processes Monique Valleé, Willy Mayo, George F. Koob, and Michel Le Moal

Multiple Subpial Assessment C. E. Polkey

Neurosteroids and Behavior Sharon R. Engel and Kathleen A. Grant

Transection:

A

Clinical

The Legacy of Frank Morrell Jerome Engel, Jr. Volume 46 Neurosteroids: Beginning of the Story Etienne E. Baulieu, P. Robel, and M. Schumacher

Memory

Ethanol and Neurosteroid Interactions in the Brain A. Leslie Morrow, Margaret J. VanDoren, Rebekah Fleming, and Shannon Penland Preclinical Development of Neurosteroids as Neuroprotective Agents for the Treatment of Neurodegenerative Diseases Paul A. Lapchak and Dalia M. Araujo


Clinical Implications of Circulating Neurosteroids Andrea R. Genazzani, Patrizia Monteleone, Massimo Stomati, Francesca Bernardi, Luigi Cobellis, Elena Casarosa, Michele Luisi, Stefano Luisi, and Felice Petraglia Neuroactive Steroids and Central Nervous System Disorders Mingde Wang, Torbjo¨rn Ba¨ckstro¨m, Inger Sundstro¨m, Go¨ran Wahlstro¨m, Tommy Olsson, Di Zhu, Inga-Maj Johansson, Inger Bjo¨rn, and Marie Bixo Neuroactive Steroids in Neuropsychopharmacology Rainer Rupprecht and Florian Holsboer Current Perspectives on the Role of Neurosteroids in PMS and Depression Lisa D. Griffin, Susan C. Conrad, and Synthia H. Mellon index

329

Processing Human Brain Tissue for In Situ Hybridization with Radiolabelled Oligonucleotides Louise F. B. Nicholson In Situ Hybridization of Astrocytes and Neurons Cultured In Vitro L. A. Arizza-McNaughton, C. De Felipe, and S. P. Hunt In Situ Hybridization on Organotypic Slice Cultures A. Gerfin-Moser and H. Monyer Quantitative Analysis of In Situ Hybridization Histochemistry Andrew L. Gundlach and Ross D. O’Shea Part II: Nonradioactive In Situ Hybridization Nonradioactive In Situ Hybridization Using Alkaline Phosphatase-Labelled Oligonucleotides S. J. Augood, E. M. McGowan, B. R. Finsen, B. Heppelmann, and P. C. Emson

Volume 47

Combining Nonradioactive In Situ Hybridization with Immunohistological and Anatomical Techniques Petra Wahle

Introduction: Studying Gene Expression in Neural Tissues by In Situ Hybridization W. Wisden and B. J. Morris

Nonradioactive In Situ Hybridization: Simplified Procedures for Use in Whole Mounts of Mouse and Chick Embryos Linda Ariza-McNaughton and Robb Krumlauf

Part I: In Situ Hybridization with Radiolabelled Oligonucleotides In Situ Hybridization with Oligonucleotide Probes Wl. Wisden and B. J. Morris

index

Cryostat Sectioning of Brains Victoria Revilla and Alison Jones

Volume 48

Processing Rodent Embryonic and Early Postnatal Tissue for In Situ Hybridization with Radiolabelled Oligonucleotides David J. Laurie, Petra C. U. Schrotz, Hannah Monyer, and Ulla Amtmann

Assembly and Intracellular GABAA Receptors Eugene Barnes

Trafficking

of

Processing of Retinal Tissue for In Situ Hybridization Frank Mu¨ller

Subcellular Localization and Regulation of GABAA Receptors and Associated Proteins Bernhard Lu¨scher and Jean-Marc Fritschy D1 Dopamine Receptors Richard Mailman

Processing the Spinal Cord for In Situ Hybridization with Radiolabelled Oligonucleotides A. Berthele and T. R. To¨lle

Molecular Modeling of Ligand-Gated Ion Channels: Progress and Challenges Ed Bertaccini and James R. Trudel

330


Alzheimer’s Disease: Its Diagnosis and Pathogenesis Jillian J. Kril and Glenda M. Halliday DNA Arrays and Functional Genomics in Neurobiology Christelle Thibault, Long Wang, Li Zhang, and Michael F. Miles

The Treatment of Infantile Spasms: An Evidence-Based Approach Mark Mackay, Shelly Weiss, and O. Carter Snead III

index

ACTH Treatment of Infantile Spasms: Mechanisms of Its Effects in Modulation of Neuronal Excitability K. L. Brunson, S. Avishai-Eliner, and T. Z. Baram

Volume 49

Neurosteroids and Infantile Spasms: The Deoxycorticosterone Hypothesis Michael A. Rogawski and Doodipala S. Reddy

What Is West Syndrome? Olivier Dulac, Christine Soufflet, Catherine Chiron, and Anna Kaminski

Are there Specific Anatomical and/or Transmitter Systems (Cortical or Subcortical) That Should Be Targeted? Phillip C. Jobe

The Relationship Between Encephalopathy and Abnormal Neuronal Activity in the Developing Brain Frances E. Jensen

Medical versus Surgical Treatment: Which Treatment When W. Donald Shields

Hypotheses from Functional Neuroimaging Studies Csaba Juha´sz, Harry T. Chugani, Ouo Muzik, and Diane C. Chugani Infantile Spasms: Unique Sydrome or General Age-Dependent Manifestation of a Diffuse Encephalopathy? M. A. Koehn and M. Duchowny

Developmental Outcome With and Without Successful Intervention Rochelle Caplan, Prabha Siddarth, Gary Mathern, Harry Vinters, Susan Curtiss, Jennifer Levitt, Robert Asarnow, and W. Donald Shields Infantile Spasms versus Myoclonus: Is There a Connection? Michael R. Pranzatelli

Histopathology of Brain Tissue from Patients with Infantile Spasms Harry V. Vinters

Tuberous Sclerosis as an Underlying Basis for Infantile Spasm Raymond S. Yeung

Generators of Ictal and Interictal Electroencephalograms Associated with Infantile Spasms: Intracellular Studies of Cortical and Thalamic Neurons M. Steriade and I. Timofeev

Brain Malformation, Epilepsy, and Infantile Spasms M. Elizabeth Ross

Cortical and Subcortical Generators of Normal and Abnormal Rhythmicity David A. McCormick Role of Subcortical Structures in the Pathogenesis of Infantile Spasms: What Are Possible Subcortical Mediators? F. A. Lado and S. L. Moshe´ What Must We Know to Develop Better Therapies? Jean Aicardi

Brain Maturational Aspects Relevant to Pathophysiology of Infantile Spasms G. Auanzini, F. Panzica, and S. Franceschetti Gene Expression Analysis as a Strategy to Understand the Molecular Pathogenesis of Infantile Spasms Peter B. Crino Infantile Spasms: Criteria for an Animal Model Carl E. Stafstrom and Gregory L. Holmes index


Volume 50 Part I: Primary Mechanisms How Does Glucose Generate Oxidative Stress in Peripheral Nerve? Irina G. Obrosova Glycation in Diabetic Neuropathy: Characteristics, Consequences, Causes, and Therapeutic Options Paul J. Thornalley Part II: Secondary Changes Protein Kinase C Changes in Diabetes: Is the Concept Relevant to Neuropathy? Joseph Eichberg Are Mitogen-Activated Protein Kinases Glucose Transducers for Diabetic Neuropathies? Tertia D. Purves and David R. Tomlinson Neurofilaments in Diabetic Neuropathy Paul Fernyhough and Robert E. Schmidt Apoptosis in Diabetic Neuropathy Aviva Tolkovsky Nerve and Ganglion Blood Flow in Diabetes: An Appraisal Douglas W. Zochodne Part III: Manifestations Potential Mechanisms of Neuropathic Pain in Diabetes Nigel A. Calcutt Electrophysiologic Measures of Diabetic Neuropathy: Mechanism and Meaning Joseph C. Arezzo and Elena Zotova Neuropathology and Pathogenesis of Diabetic Autonomic Neuropathy Robert E. Schmidt Role of the Schwann Cell in Diabetic Neuropathy Luke Eckersley

331

Nerve Growth Factor for the Treatment of Diabetic Neuropathy: What Went Wrong, What Went Right, and What Does the Future Hold? Stuart C. Apfel Angiotensin-Converting Enzyme Inhibitors: Are there Credible Mechanisms for Beneficial Effects in Diabetic Neuropathy? Rayaz A. Malik and David R. Tomlinson Clinical Trials for Drugs Against Diabetic Neuropathy: Can We Combine Scientific Needs With Clinical Practicalities? Dan Ziegler and Dieter Luft index

Volume 51 Energy Metabolism in the Brain Leif Hertz and Gerald A. Dienel The Cerebral Glucose-Fatty Acid Cycle: Evolutionary Roots, Regulation, and (Patho) physiological Importance Kurt Heininger Expression, Regulation, and Functional Role of Glucose Transporters (GLUTs) in Brain Donard S. Dwyer, Susan J. Vannucci, and Ian A. Simpson Insulin-Like Growth Factor-1 Promotes Neuronal Glucose Utilization During Brain Development and Repair Processes Carolyn A. Bondy and Clara M. Cheng CNS Sensing and Regulation of Peripheral Glucose Levels Barry E. Levin, Ambrose A. Dunn-Meynell, and Vanessa H. Routh

Part IV: Potential Treatment

Glucose Transporter Protein Syndromes Darryl C. De Vivo, Dong Wang, Juan M. Pascual, and Yuan Yuan Ho

Polyol Pathway and Diabetic Peripheral Neuropathy Peter J. Oates

Glucose, Stress, and Hippocampal Neuronal Vulnerability Lawrence P. Reagan

332


Glucose/Mitochondria in Neurological Conditions John P. Blass Energy Utilization in the Ischemic/Reperfused Brain John W. Phillis and Michael H. O’Regan

Stress and Secretory Immunity Jos A. Bosch, Christopher Ring, Eco J. C. de Geus, Enno C. I. Veerman, and Arie V. Nieuw Amerongen Cytokines and Depression Angela Clow

Diabetes Mellitus and the Central Nervous System Anthony L. McCall

Immunity and Schizophrenia: Autoimmunity, Cytokines, and Immune Responses Fiona Gaughran

Diabetes, the Brain, and Behavior: Is There a Biological Mechanism Underlying the Association between Diabetes and Depression? A. M. Jacobson, J. A. Samson, K. Weinger, and C. M. Ryan

Cerebral Lateralization and the Immune System Pierre J. Neveu

Schizophrenia and Diabetes David C. Henderson and Elissa R. Ettinger

Behavioral Conditioning of the Immune System Frank Hucklebridge Psychological and Neuroendocrine Correlates of Disease Progression Julie M. Turner-Cobb

Psychoactive Drugs Affect Glucose Transport and the Regulation of Glucose Metabolism Donard S. Dwyer, Timothy D. Ardizzone, and Ronald J. Bradley

The Role of Psychological Intervention in Modulating Aspects of Immune Function in Relation to Health and Well-Being J. H. Gruzelier

index

index

Volume 52 Volume 53 Neuroimmune Relationships in Perspective Frank Hucklebridge and Angela Clow Sympathetic Nervous System Interaction with the Immune System Virginia M. Sanders and Adam P. Kohm Mechanisms by Which Cytokines Signal the Brain Adrian J. Dunn Neuropeptides: Modulators of Responses in Health and Disease David S. Jessop

Immune

Brain–Immune Interactions in Sleep Lisa Marshall and Jan Born Neuroendocrinology of Autoimmunity Michael Harbuz Systemic Stress-Induced Th2 Shift and Its Clinical Implications Ibia J. Elenkov Neural Control of Salivary S-IgA Secretion Gordon B. Proctor and Guy H. Carpenter

Section I: Mitochondrial Structure and Function Mitochondrial DNA Structure and Function Carlos T. Moraes, Sarika Srivastava, Ilias Kirkinezos, Jose Oca-Cossio, Corina van Waveren, Markus Woischnick, and Francisca Diaz Oxidative Phosphorylation: Structure, Function, and Intermediary Metabolism Simon J. R. Heales, Matthew E. Gegg, and John B. Clark Import of Mitochondrial Proteins Matthias F. Bauer, Sabine Hofmann, and Walter Neupert Section II: Primary Respiratory Chain Disorders Mitochondrial Disorders of the Nervous System: Clinical, Biochemical, and Molecular Genetic Features Dominic Thyagarajan and Edward Byrne


Section III: Secondary Respiratory Chain Disorders Friedreich’s Ataxia J. M. Cooper and J. L. Bradley Wilson Disease C. A. Davie and A. H. V. Schapira

333

The Mitochondrial Theory of Aging: Involvement of Mitochondrial DNA Damage and Repair Nadja C. de Souza-Pinto and Vilhelm A. Bohr index

Hereditary Spastic Paraplegia Christopher J. McDermott and Pamela J. Shaw Cytochrome c Oxidase Deficiency Giacomo P. Comi, Sandra Strazzer, Sara Galbiati, and Nereo Bresolin Section IV: Toxin Induced Mitochondrial Dysfunction Toxin-Induced Mitochondrial Dysfunction Susan E. Browne and M. Flint Beal Section V: Neurodegenerative Disorders Parkinson’s Disease L. V. P. Korlipara and A. H. V. Schapira Huntington’s Disease: The Mystery Unfolds? A˚sa Peterseń and Patrik Brundin Mitochondria in Alzheimer’s Disease Russell H. Swerdlow and Stephen J. Kish Contributions of Mitochondrial Alterations, Resulting from Bad Genes and a Hostile Environment, to the Pathogenesis of Alzheimer’s Disease Mark P. Mattson Mitochondria and Amyotrophic Lateral Sclerosis Richard W. Orrell and Anthony H. V. Schapira

Volume 54 Unique General Anesthetic Binding Sites Within Distinct Conformational States of the Nicotinic Acetylcholine Receptor Hugo R. Ariaas, William, R. Kem, James R. Truddell, and Michael P. Blanton Signaling Molecules and Receptor Transduction Cascades That Regulate NMDA ReceptorMediated Synaptic Transmission Suhas. A. Kotecha and John F. MacDonald Behavioral Measures of Alcohol Self-Administration and Intake Control: Rodent Models Herman H. Samson and Cristine L. Czachowski Dopaminergic Mouse Mutants: Investigating the Roles of the Different Dopamine Receptor Subtypes and the Dopamine Transporter Shirlee Tan, Bettina Hermann, and Emiliana Borrelli Drosophila melanogaster, A Genetic Model System for Alcohol Research Douglas J. Guarnieri and Ulrike Heberlein index

Section VI: Models of Mitochondrial Disease Models of Mitochondrial Disease Danae Liolitsa and Michael G. Hanna

Volume 55

Section VII: Defects of Oxidation Including Carnitine Deficiency

Section I: Virsu Vectors for Use in the Nervous System

Defects of Oxidation Including Carnitine Deficiency K. Bartlett and M. Pourfarzam

Non-Neurotropic Adenovirus: A Vector for Gene Transfer to the Brain and Gene Therapy of Neurological Disorders P. R. Lowenstein, D. Suwelack, J. Hu, X. Yuan, M. Jimenez-Dalmaroni, S. Goverdhama, and M. G. Castro

Section VIII: Mitochondrial Involvement in Aging

334


Adeno-Associated Virus Vectors E. Lehtonen and L. Tenenbaum Problems in the Use of Herpes Simplex Virus as a Vector L. T. Feldman Lentiviral Vectors J. Jakobsson, C. Ericson, N. Rosenquist, and C. Lundberg Retroviral Vectors for Gene Delivery to Neural Precursor Cells K. Kageyama, H. Hirata, and J. Hatakeyama

Processing and Representation of SpeciesSpecific Communication Calls in the Auditory System of Bats George D. Pollak, Achim Klug, and Eric E. Bauer Central Nervous System Control of Micturition Gert Holstege and Leonora J. Mouton The Structure and Physiology of the Rat Auditory System: An Overview Manuel Malmierca Neurobiology of Cat and Human Sexual Behavior Gert Holstege and J. R. Georgiadis

Section II: Gene Therapy with Virus Vectors for Specific Disease of the Nervous System

index

The Principles of Molecular Therapies for Glioblastoma G. Karpati and J. Nalbatonglu

Volume 57

Oncolytic Herpes Simplex Virus J. C. C. Hu and R. S. Coffin

Cumulative Subject Index of Volumes 1–25

Recombinant Retrovirus Vectors for Treatment of Brain Tumors N. G. Rainov and C. M. Kramm

Volume 58

Adeno-Associated Viral Vectors for Parkinson’s Disease I. Muramatsu, L. Wang, K. Ikeguchi, K-i Fujimoto, T. Okada, H. Mizukami, Y. Hanazono, A. Kume, I. Nakano, and K. Ozawa HSV Vectors for Parkinson’s Disease D. S. Latchman Gene Therapy for Stroke K. Abe and W. R. Zhang Gene Therapy for Mucopolysaccharidosis A. Bosch and J. M. Heard index

Volume 56 Behavioral Mechanisms and the Neurobiology of Conditioned Sexual Responding Mark Krause NMDA Receptors in Alcoholism Paula L. Hoffman

Cumulative Subject Index of Volumes 26–50

Volume 59 Loss of Spines and Neuropil Liesl B. Jones Schizophrenia as a Disorder of Neuroplasticity Robert E. McCullumsmith, Sarah M. Clinton, and James H. Meador-Woodruff The Synaptic Pathology of Schizophrenia: Is Aberrant Neurodevelopment and Plasticity to Blame? Sharon L. Eastwood Neurochemical Basis for an Epigenetic Vision of Synaptic Organization E. Costa, D. R. Grayson, M. Veldic, and A. Guidotti Muscarinic Receptors in Schizophrenia: Is There a Role for Synaptic Plasticity? Thomas J. Raedler


335

Serotonin and Brain Development Monsheel S. K. Sodhi and Elaine Sanders-Bush

Volume 60

Presynaptic Proteins and Schizophrenia William G. Honer and Clint E. Young

Microarray Platforms: Introduction and Application to Neurobiology Stanislav L. Karsten, Lili C. Kudo, and Daniel H. Geschwind

Mitogen-Activated Protein Kinase Signaling Svetlana V. Kyosseva Postsynaptic Density Scaffolding Proteins at Excitatory Synapse and Disorders of Synaptic Plasticity: Implications for Human Behavior Pathologies Andrea de Bartolomeis and Germano Fiore Prostaglandin-Mediated Signaling in Schizophrenia S. Smesny Mitochondria, Synaptic Plasticity, and Schizophrenia Dorit Ben-Shachar and Daphna Laifenfeld Membrane Phospholipids and Cytokine Interaction in Schizophrenia Jeffrey K. Yao and Daniel P. van Kammen Neurotensin, Schizophrenia, and Antipsychotic Drug Action Becky Kinkead and Charles B. Nemeroff Schizophrenia, Vitamin D, and Brain Development Alan Mackay-Sim, François Fe´ron, Darryl Eyles, Thomas Burne, and John McGrath Possible Contributions of Myelin and Oligodendrocyte Dysfunction to Schizophrenia Daniel G. Stewart and Kenneth L. Davis Brain-Derived Neurotrophic Factor and the Plasticity of the Mesolimbic Dopamine Pathway Oliver Guillin, Nathalie Griffon, Jorge Diaz, Bernard Le Foll, Erwan Bezard, Christian Gross, Chris Lammers, Holger Stark, Patrick Carroll, Jean-Charles Schwartz, and Pierre Sokoloff S100B in Schizophrenic Psychosis Matthias Rothermundt, Gerald Ponath, and Volker Arolt Oct-6 Transcription Factor Maria Ilia NMDA Receptor Function, Neuroplasticity, and the Pathophysiology of Schizophrenia Joseph T. Coyle and Guochuan Tsai index

Experimental Design and Low-Level Analysis of Microarray Data B. M. Bolstad, F. Collin, K. M. Simpson, R. A. Irizarry, and T. P. Speed Brain Gene Expression: Genomics and Genetics Elissa J. Chesler and Robert W. Williams DNA Microarrays and Animal Models of Learning and Memory Sebastiano Cavallaro Microarray Analysis of Human Nervous System Gene Expression in Neurological Disease Steven A. Greenberg DNA Microarray Analysis of Postmortem Brain Tissue Ka´roly Mirnics, Pat Levitt, and David A. Lewis index

Volume 61 Section I: High-Throughput Technologies Biomarker Discovery Using Molecular Profiling Approaches Stephen J. Walker and Arron Xu Proteomic Analysis of Mitochondrial Proteins Mary F. Lopez, Simon Melov, Felicity Johnson, Nicole Nagulko, Eva Golenko, Scott Kuzdzal, Suzanne Ackloo, and Alvydas Mikulskis Section II: Proteomic Applications NMDA Receptors, Neural Pathways, and Protein Interaction Databases Holger Husi Dopamine Transporter Network and Pathways Rajani Maiya and R. Dayne Mayfield Proteomic Approaches in Drug Discovery and Development Holly D. Soares, Stephen A. Williams,

336


Peter J. Snyder, Feng Gao, Tom Stiger, Christian Rohlff, Athula Herath, Trey Sunderland, Karen Putnam, and W. Frost White Section III: Informatics Proteomic Informatics Steven Russell, William Old, Katheryn Resing, and Lawrence Hunter Section IV: Changes in the Proteome by Disease Proteomics Analysis in Alzheimer’s Disease: New Insights into Mechanisms of Neurodegeneration D. Allan Butterfield and Debra Boyd-Kimball Proteomics and Alcoholism Frank A. Witzmann and Wendy N. Strother Proteomics Studies of Traumatic Brain Injury Kevin K. W. Wang, Andrew Ottens, William Haskins, Ming Cheng Liu, Firas Kobeissy, Nancy Denslow, SuShing Chen, and Ronald L. Hayes Influence of Huntington’s Disease on the Human and Mouse Proteome Claus Zabel and Joachim Klose Section V: Overview of the Neuroproteome Proteomics—Application to the Brain Katrin Marcus, Oliver Schmidt, Heike Schaefer, Michael Hamacher, AndrA˚ van Hall, and Helmut E. Meyer index

Volume 62 GABAA Receptor Structure–Function Studies: A Reexamination in Light of New Acetylcholine Receptor Structures Myles H. Akabas Dopamine Mechanisms and Cocaine Reward Aiko Ikegami and Christine L. Duvauchelle Proteolytic Dysfunction in Neurodegenerative Disorders Kevin St. P. McNaught Neuroimaging Studies in Bipolar Children and Adolescents

Rene L. Olvera, David C. Glahn, Sheila C. Caetano, Steven R. Pliszka, and Jair C. Soares Chemosensory G-Protein-Coupled Receptor Signaling in the Brain Geoffrey E. Woodard Disturbances of Emotion Regulation after Focal Brain Lesions Antoine Bechara The Use of Caenorhabditis elegans in Molecular Neuropharmacology Jill C. Bettinger, Lucinda Carnell, Andrew G. Davies, and Steven L. McIntire index Volume 63 Mapping Neuroreceptors at work: On the Definition and Interpretation of Binding Potentials after 20 years of Progress Albert Gjedde, Dean F. Wong, Pedro Rosa-Neto, and Paul Cumming Mitochondrial Dysfunction in Bipolar Disorder: From 31P-Magnetic Resonance Spectroscopic Findings to Their Molecular Mechanisms Tadafumi Kato Large-Scale Microarray Studies of Gene Expression in Multiple Regions of the Brain in Schizophrenia and Alzeimer’s Disease Pavel L. Katsel, Kenneth L. Davis, and Vahram Haroutunian Regulation of Serotonin 2C Receptor PREmRNA Editing By Serotonin Claudia Schmauss The Dopamine Hypothesis of Drug Addiction: Hypodopaminergic State Miriam Melis, Saturnino Spiga, and Marco Diana Human and Animal Spongiform Encephalopathies are Autoimmune Diseases: A Novel Theory and Its supporting Evidence Bao Ting Zhu Adenosine and Brain Function Bertil B. Fredholm, Jiang-Fan Chen, Rodrigo A. Cunha, Per Svenningsson, and Jean-Marie Vaugeois index


337

Volume 64

G-Protein–Coupled Receptor Deorphanizations Yumiko Saito and Olivier Civelli

Section I. The Cholinergic System John Smythies

Mechanistic Connections Between Glucose/ Lipid Disturbances and Weight Gain Induced by Antipsychotic Drugs Donard S. Dwyer, Dallas Donohoe, Xiao-Hong Lu, and Eric J. Aamodt

Section II. The Dopamine System John Symythies Section III. The Norepinephrine System John Smythies Section IV. The Adrenaline System John Smythies

Serotonin Firing Activity as a Marker for Mood Disorders: Lessons from Knockout Mice Gabriella Gobbi

Section V. Serotonin System John Smythies

index

index

Volume 66

Volume 65

Brain Atlases of Normal and Diseased Populations Arthur W. Toga and Paul M. Thompson

Insulin Resistance: Causes and Consequences Zachary T. Bloomgarden

Neuroimaging Databases as a Resource for Scientific Discovery John Darrell Van Horn, John Wolfe, Autumn Agnoli, Jeffrey Woodward, Michael Schmitt, James Dobson, Sarene Schumacher, and Bennet Vance

Antidepressant-Induced Manic Conversion: A Developmentally Informed Synthesis of the Literature Christine J. Lim, James F. Leckman, Christopher Young, and Andre´s Martin Sites of Alcohol and Volatile Anesthetic Action on Glycine Receptors Ingrid A. Lobo and R. Adron Harris Role of the Orbitofrontal Cortex in Reinforcement Processing and Inhibitory Control: Evidence from Functional Magnetic Resonance Imaging Studies in Healthy Human Subjects Rebecca Elliott and Bill Deakin

Modeling Brain Responses Karl J. Friston, William Penny, and Olivier David Voxel-Based Morphometric Analysis Using Shape Transformations Christos Davatzikos The Cutting Edge of f MRI and High-Field f MRI Dae-Shik Kim Quantification of White Matter Using DiffusionTensor Imaging Hae-Jeong Park

Common Substrates of Dysphoria in Stimulant Drug Abuse and Primary Depression: Therapeutic Targets Kate Baicy, Carrie E. Bearden, John Monterosso, Arthur L. Brody, Andrew J. Isaacson, and Edythe D. London

Perfusion f MRI for Functional Neuroimaging Geoffrey K. Aguirre, John A. Detre, and Jiongjiong Wang

The Role of cAMP Response Element–Binding Proteins in Mediating Stress-Induced Vulnerability to Drug Abuse Arati Sadalge Kreibich and Julie A. Blendy

Neural Modeling and Functional Brain Imaging: The Interplay Between the Data-Fitting and Simulation Approaches Barry Horwitz and Michael F. Glabus

Functional Near-Infrared Spectroscopy: Potential and Limitations in Neuroimaging Studies Yoko Hoshi

338


Combined EEG and fMRI Studies of Human Brain Function V. Menon and S. Crottaz-Herbette

W. Gordon Frankle, Mark Slifstein, Peter S. Talbot, and Marc Laruelle index

index

Volume 68 Volume 67 Distinguishing Neural Substrates of Heterogeneity Among Anxiety Disorders Jack B. Nitschke and Wendy Heller Neuroimaging in Dementia K. P. Ebmeier, C. Donaghey, and N. J. Dougall Prefrontal and Anterior Cingulate Contributions to Volition in Depression Jack B. Nitschke and Kristen L. Mackiewicz Functional Imaging Research in Schizophrenia H. Tost, G. Ende, M. Ruf, F. A. Henn, and A. Meyer-Lindenberg Neuroimaging in Functional Somatic Syndromes Patrick B. Wood Neuroimaging in Multiple Sclerosis Alireza Minagar, Eduardo Gonzalez-Toledo, James Pinkston, and Stephen L. Jaffe Stroke Roger E. Kelley and Eduardo Gonzalez-Toledo Functional MRI in Pediatric Neurobehavioral Disorders Michael Seyffert and F. Xavier Castellanos Structural MRI and Brain Development Paul M. Thompson, Elizabeth R. Sowell, Nitin Gogtay, Jay N. Giedd, Christine N. Vidal, Kiralee M. Hayashi, Alex Leow, Rob Nicolson, Judith L. Rapoport, and Arthur W. Toga Neuroimaging and Human Genetics Georg Winterer, Ahmad R. Hariri, David Goldman, and Daniel R. Weinberger Neuroreceptor Imaging in Psychiatry: Theory and Applications

Fetal Magnetoencephalography: Viewing the Developing Brain In Utero Hubert Preissl, Curtis L. Lowery, and Hari Eswaran Magnetoencephalography in Studies of Infants and Children Minna Huotilainen Let’s Talk Together: Memory Traces Revealed by Cooperative Activation in the Cerebral Cortex Jochen Kaiser, Susanne Leiberg, and Werner Lutzenberger Human Communication Investigated With Magnetoencephalography: Speech, Music, and Gestures Thomas R. Kno¨sche, Burkhard Maess, Akinori Nakamura, and Angela D. Friederici Combining Magnetoencephalography and Functional Magnetic Resonance Imaging Klaus Mathiak and Andreas J. Fallgatter Beamformer Analysis of MEG Data Arjan Hillebrand and Gareth R. Barnes Functional Connectivity Analysis in Magnetoencephalography Alfons Schnitzler and Joachim Gross Human Visual Processing as Revealed by Magnetoencephalographys Yoshiki Kaneoke, Shoko Watanabe, and Ryusuke Kakigi A Review of Clinical Applications of Magnetoencephalography Andrew C. Papanicolaou, Eduardo M. Castillo, Rebecca Billingsley-Marshall, Ekaterina Pataraia, and Panagiotis G. Simos index


339

Volume 69

Spectral Processing in the Auditory Cortex Mitchell L. Sutter

Nematode Neurons: Anatomy and Anatomical Methods in Caenorhabditis elegans David H. Hall, Robyn Lints, and Zeynep Altun

Processing of Dynamic Spectral Properties of Sounds Adrian Rees and Manuel S. Malmierca

Investigations of Learning and Memory in Caenorhabditis elegans Andrew C. Giles, Jacqueline K. Rose, and Catharine H. Rankin

Representations of Spectral Coding in the Human Brain Deborah A. Hall, PhD

Neural Specification and Differentiation Eric Aamodt and Stephanie Aamodt

Spectral Processing and Sound Source Determination Donal G. Sinex

Sexual Behavior of the Caenorhabditis elegans Male Scott W. Emmons

Spectral Information in Sound Localization Simon Carlile, Russell Martin, and Ken McAnally

The Motor Circuit Stephen E. Von Stetina, Millet Treinin, and David M. Miller III

Plasticity of Spectral Processing Dexter R. F. Irvine and Beverly A. Wright

Mechanosensation in Caenorhabditis elegans Robert O’Hagan and Martin Chalfie

Spectral Processing In Cochlear Implants Colette M. McKay index

index Volume 71

Volume 70 Spectral Processing by the Peripheral Auditory System Facts and Models Enrique A. Lopez-Poveda Basic Psychophysics Processing Brian C. J. Moore

of

Human

Spectral

Across-Channel Spectral Processing John H. Grose, Joseph W. Hall III, and Emily Buss Speech and Music Have Different Requirements for Spectral Resolution Robert V. Shannon Non-Linearities and the Representation of Auditory Spectra Eric D. Young, Jane J. Yu, and Lina A. J. Reiss Spectral Processing in the Inferior Colliculus Kevin A. Davis Neural Mechanisms for Spectral Analysis in the Auditory Midbrain, Thalamus, and Cortex Monty A. Escab and Heather L. Read

Autism: Neuropathology, Alterations of the GABAergic System, and Animal Models Christoph Schmitz, Imke A. J. van Kooten, Patrick R. Hof, Herman van Engeland, Paul H. Patterson, and Harry W. M. Steinbusch The Role of GABA in the Early Neuronal Development Marta Jelitai and Emlia Madarasz GABAergic Signaling in the Developing Cerebellum Chitoshi Takayama Insights into GABA Functions in the Developing Cerebellum Mnica L. Fiszman Role of GABA in the Mechanism of the Onset of Puberty in Non-Human Primates Ei Terasawa Rett Syndrome: A Rosetta Stone for Understanding the Molecular Pathogenesis of Autism Janine M. LaSalle, Amber Hogart, and Karen N. Thatcher

340


GABAergic Cerebellar System in Autism: A Neuropathological and Developmental Perspective Gene J. Blatt

A Systematic Examination of Catatonia-Like Clinical Pictures in Autism Spectrum Disorders Lorna wing and Amitta Shah

Reelin Glycoprotein in Autism and Schizophrenia S. Hossein Fatemi

Catatonia in Individuals with Autism Spectrum Disorders in Adolescence and Early Adulthood: A Long-Term Prospective Study Masataka Ohta, Yukiko Kano, and Yoko Nagai

Is There A Connection Between Autism, PraderWilli Syndrome, Catatonia, and GABA? Dirk M. Dhossche, Yaru Song, and Yiming Liu Alcohol, GABA Receptors, and Neurodevelopmental Disorders Ujjwal K. Rout Effects of Secretin on Extracellular GABA and Other Amino Acid Concentrations in the Rat Hippocampus Hans-Willi Clement, Alexander Pschibul, and Eberhard Schulz Predicted Role of Secretin and Oxytocin in the Treatment of Behavioral and Developmental Disorders: Implications for Autism Martha G. Welch and David A. Ruggiero Immunological Findings in Autism Hari Har Parshad Cohly and Asit Panja Correlates of Psychomotor Symptoms in Autism Laura Stoppelbein, Sara Sytsma-Jordan, and Leilani Greening GABRB3 Gene Deficient Mice: A Potential Model of Autism Spectrum Disorder Timothy M. DeLorey The Reeler Mouse: Anatomy of a Mutant Gabriella D’Arcangelo Shared Chromosomal Susceptibility Regions Between Autism and Other Mental Disorders Yvon C. Chagnon index

Section II: Assessment Psychomotor Development and Psychopathology in Childhood Dirk M. J. de Raeymaecker The Importance of Catatonia and Stereotypies in Autistic Spectrum Disorders Laura Stoppelbein, Leilani Greening, and Angelina Kakooza Prader–Willi Syndrome: Atypical Psychoses and Motor Dysfunctions Willem M. A. Verhoeven and Siegfried Tuinier Towards A Valid Nosography and Psychopathology of Catatonia in Children and Adolescents David Cohen Section III: Biology Is There A Common Neuronal Basis for Autism and Catatonia? Dirk Marcel Dhossche, Brendan T. Carroll, and Tressa D. Carroll Shared Susceptibility Region On Chromosome 15 Between Autism And Catatonia Yvon C. Chagnon Section IV: Treatment Current Trends in Behavioral Interventions for Children with Autism Dorothy Scattone and Kimberly R. Knight Case Reports with A Child Psychiatric Exploration of Catatonia, Autism, and Delirium Jan N. M. Schieveld

Volume 72 Section I: Classification Classification Matters Autism in Children Klaus-Ju¨rgen Neuma¨rker

Are Autistic and Catatonic Regression Related? A Few Working Hypotheses Involving GABA, Purkinje Cell Survival, Neurogenesis, and ECT Dirk Marcel Dhossche and Ujjwal Rout

ECT and the Youth: Catatonia in Context Frank K. M. Zaw for

Catatonia

and

Catatonia in Autistic Spectrum Disorders: A Medical Treatment Algorithm Max Fink, Michael A. Taylor, and Neera Ghaziuddin


Psychological Approaches to Chronic Catatonia-Like Deterioration in Autism Spectrum Disorders Amitta Shah and Lorna Wing Section V: Blueprints Blueprints for the Assessment, Treatment, and Future Study of Catatonia in Autism Spectrum Disorders Dirk Marcel, Dhossche, Amitta Shah, and Lorna Wing

341

Thomas J. Montine, David R. Goodlett, and Jing Zhang Hormonal Pathways Regulating Intermale and Interfemale Aggression Neal G. Simon, Qianxing Mo, Shan Hu, Carrie Garippa, and Shi-Fang Lu Neuronal GAP Junctions: Expression, Function, and Implications for Behavior Clinton B. McCracken and David C. S. Roberts

index

Effects of Genes and Stress on the Neurobiology of Depression J. John Mann and Dianne Currier

Volume 73

Quantitative Imaging with the Micropet SmallAnimal Pet Tomograph Paul Vaska, Daniel J. Rubins, David L. Alexoff, and Wynne K. Schiffer

Chromosome 22 Deletion Syndrome and Schizophrenia Nigel M. Williams, Michael C. O’Donovan, and Michael J. Owen Characterization of Proteome of Human Cerebrospinal Fluid Jing Xu, Jinzhi Chen, Elaine R. Peskind, Jinghua Jin, Jimmy Eng, Catherine Pan,

Understanding Myelination through Studying its Evolution Ru¨diger Schweigreiter, Betty I. Roots, Christine Bandtlow, and Robert M. Gould index

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International Review of Neurobiology Volume 38

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International Review of Neurobiology Volume 31

International Review of Neurobiology Volume 14

International Review of Neurobiology, Volume 23

International Review of Neurobiology Volume 1

International Review of Neurobiology Volume 13

International Review of Neurobiology Volume 5

International Review of Neurobiology, Volume 21

International Review of Neurobiology Volume 36

International Review of Neurobiology Volume 16

International Review of Neurobiology Volume 32

International Review of Neurobiology Volume 12

International Review of Neurobiology Volume 3

International Review of Neurobiology, Volume 48

International Review of Neurobiology, Volume 20

International Review of Neurobiology, Volume 73

International Review of Neurobiology Volume 29

International Review of Neurobiology, Volume 8

International Review of Neurobiology Volume 30

International Review of Neurobiology Volume 17

International Review of Neurobiology Volume 4

International Review of Neurobiology, Volume 63

International Review of Neurobiology Volume 2

The Neurobiology of Painting - International Review of Neurobiology Vol 74

The Neurobiology of Painting, Volume 74: International Review of Neurobiology

DNA Arrays in Neurobiology (International Review of Neurobiology, Vol 60)

INTERNATIONAL REVIEW NEUROBIOLOGY

The Neuromodulators, (International Review of Neurobiology)

International Review of Neurobiology, Volume 6

International Review of Neurobiology Volume 25

International Review of Neurobiology Volume 38

International Review of Neurobiology Volume 18

International Review of Neurobiology Volume 31

International Review of Neurobiology Volume 14

International Review of Neurobiology, Volume 23

International Review of Neurobiology Volume 1

International Review of Neurobiology Volume 13

International Review of Neurobiology Volume 5

International Review of Neurobiology, Volume 21

International Review of Neurobiology Volume 36

International Review of Neurobiology Volume 16

International Review of Neurobiology Volume 32

International Review of Neurobiology Volume 12

International Review of Neurobiology Volume 3

International Review of Neurobiology, Volume 48

International Review of Neurobiology, Volume 20

International Review of Neurobiology, Volume 73

International Review of Neurobiology Volume 29

International Review of Neurobiology, Volume 8

International Review of Neurobiology Volume 30

International Review of Neurobiology Volume 17

International Review of Neurobiology Volume 4

International Review of Neurobiology, Volume 63

International Review of Neurobiology Volume 2

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