Advances in Psychology Volume 62 Volitional Action Conation and Control

VOLITIONAL ACTION Conation and Control

ADVANCES

IN PSYCHOLOGY 62 Editors:

G. E. STELMACH

P. A. VROON

NORTH-HOLLAND AMSTERDAM. NEW YORK OXFORD. TOKYO

VOLITIONAL ACTION Conation and Control

Edited by

Wayne A. HERSHBERGER

1989

NORTH-HOLLAND AMSTERDAM. NEW YORK . OXFORD TOKYO

ELSEVLER SCIENCE PUBLISHERS B.V. Sara Burgerhartstraat 25 P.O. Box 21 1, 1000 AE Amsterdam, The Netherlands

Distributors for the United States and Canada: ELSEVIER SCIENCE PUBLISHING COMPANY, INC. 655 Avenue of the Americas New York, N.Y. 10010, U S A .

ISBN: 0 444 88318 5

0ELSEVIER SCIENCE PUBLISHERS B.V., 1989 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior written permission of the publisher, Elsevier Science Publishers B.V. / Physical Sciences and Engineering Division, P.O. Box 1991, 1000 BZ Amsterdam, The Netherlands. Special regulations for readers in the U.S.A. - This publication has been registered with the Copyright Clearance Center Inc. (CCC), Salem, Massachusetts. Information can be obtained from the CCC about conditions under which photocopies of parts of this publication may be made in the U.S.A. All other copyright questions, including photocopying outside of the U.S.A., should be referred to the copyright owner, Elsevier Science Publishers B.V., unless otherwise specified. No responsibility is assumed by the Publisher for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions or ideas contained in the material herein. Printed in The Netherlands

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PREFACE During the last several decades the behavioral sciences have been undergoing what is arguably a Kuhnian scientific revolution, with radical behaviorism giving way to considerations of cognition and conation. Although cognition is perhaps the more familiar of these two terms, conation (concerning the inclination to act purposively) is equally a hallmark of the times. Indeed, the past few years has seen a resurgence of interest in the psychology and physiology of volition that is unparalleled in this century. Not since William James published his Princ@les of psychology in 1890 has so much careful attention been devoted to a consideration of the will. The present book comprises a significant sample, or distillation, of the observations, both rational and empirical, of individuals from diverse disciplines who are contributing to the present renaissance in conation. The book was designed to serve a threefold purpose: (a) to consolidate the gains of the various scholars, relatively isolated in their respective disciplines, (b) to foster and help focus future research on conation and self-control, and (c) to provide practitioners in applied psychology with a broad-based tutorial. William James noted that there are two fundamental things to be understood about voluntary action: First, volitional actions, being desired and intended beforehand, are done with full prevision; that is, they are preceded by anticipatory images defining what those actions are to be. Secondly, these anticipatory images are representations of the intended sensory consequences of the necessary muscular innervation and not representations of the muscular innervation itself. (James’ putative image is not to be confused with von Holst and Mittelstaedt’s efference copy.) The chapters in this book have been authored by individuals with something further to contribute to our understanding of one or both of James’ observations. For example, some authors have been investigating the neurological signals which precede voluntary movements (e.g., Georgopoulos; and, Kornhuber, Deecke, Lang, Lang, & Kornhuber) whereas others (e.g., MacKay & Crammond) have been concerned primarily with the sensory feedback from the effectors involved in such

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Preface

movements. And still others, such as those with systems approaches (e.g., Bullock & Grossberg) are concerned with both aspects. The theoretical flavor of the book is largely cybernetic or control theoretic. That is, most of the authors are committed to the proposition that voluntary actions are intentional, self-controlled inputs or sensations (including, in some cases, the sensed corollary discharges of efference), just as James implied. The principal champion of this notion today is William Powers (see Chapters 2 & 13), who used the idea as the title of his influential 1973 book, Behavior: the control of perception. William James also noted that the sensory consequences which define a particular voluntary action may be resident or remote. Sensations arising from muscle spindles are resident sensations; those arising from exteroceptors are remote. A person driving an automobile, for example, is controlling the remote visual consequences of his or her effector activity. The driver is also controlling his or her destination, another remote sensory consequence. Some of the authors, particularly those with a psychological or sociological perspective (e.g., Hyland) are concerned primarily with the control of remote sensory consequences, whereas others, particularly those with a physiological perspective (e.g., Pavloski), focus more upon resident sensory effects. This, of course, is as it should be. The two perspectives are complementary. Volition is a phenomenon of immense practical as well as theoretical significance, and several chapters (e.g., Lord & Kernan) address the applied aspect. Professional psychology is in need of a broader scientific foundation than that provided by 20th century behaviorism. Conative science is a veritable cornerstone for such a new scientific foundation. I believe practitioners will find the observations in this book (even the esoteric ones) uncommonly stimulating, informative, and professionally relevant. The chapters are grouped according to the methodological approach of the author(s) into 5 sections: theoretical, neurophysiological, mathematical, psychological, and practical, in that order. Within each section the chapters are ordered alphabetically, by author. Wayne A. Hershberger DeKalb, Illinois June 1989

vii

CONTENTS Preface List of Contributors

V

xi

GENERAL THEORETICAL PERSPECTIVE 3

1.

The Synergy of Voluntary and Involuntary Action Wayne A. Hershberger

2.

Volition: a Semi-scientific Essay William T. Powers

21

On the Will: An Historical Perspective

39

3.

Eckart Scheerer

PHYSIOLOGICAL PERSPECTWE 4.

Volitional Eye Movements and their Relationship to Visual Attention Burkhart Fischer and Rolf Boch

5.

The Cerebral Correlates of Reaching Apostolos P, Georgopoulos

6.

Will, Volitional Action, Attention and Cerebral Potentials In Man: Bereitschaftspotential, Performance-Related Potentials, Directed Attention Potential, EEG Spectrum Changes H. H. Kornhuber, L. Deecke, W. Lang, M. Lang, and A. Kornhuber

63

73

107

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7.

8.

Contents

Cortical Modification of Sensorimotor Linkages in Relation to Intended Action Wlliam A. Macand Donald J. Crarnmond

169

Cerebral Correlates of Auditory Attention

195

R. Naatanen 9.

The Physiological Stress of Thwarted Intentions Raymond P. Pavloski

215

SYSTEMS-MODELING PERSPECTWE 10.

11.

A Control-Theory Analysis of Interference During Social Tracking W Thomas Bourbon

235

VITE and FLETE. Neural Modules for Trajectory Formation and Postural Control Daniel Bullock and Stephen Grossberg

253

12.

Behavior In the First Degree Richard S. Marken

299

13.

Quantitative Measurement of Volition: a Pilot Study W a r n T. Powers

315

PSYCHOLOGICAL PERSPECTIVE 14.

Some Experimental Investigations of Volition George S. Howard and Paul R Myers

15.

Control Theory and Psychology: a Tool for Integration and a Heuristic for New Theory Michael E. Hyland

335

353

Contents 16.

17.

ix

The Behavioral Illusion: Misperception of Volitional Action J. Scott Jordan and Wayne A. Hershberger

371

Volition and Self-Regulation: Memory Mechanisms Mediating the Maintenance of Intentions Julius f i h l and Miguel &Zen-Saad

387

18.

Levels of Intention in Behavior Richard S. Marken and William T. Powers

409

19.

Involuntary Learning of Voluntary Action Richard J. Robertson

43 1

APPLIED PERSPECTM 20.

A Paradigm Shift in Behavior Therapy: From External Control to Self-Control Dennk J. Delprato

449

21.

Fostering Self-Control: Comments of a Counselor Edward E. Ford

469

22.

Control Theory Applied to Stress Management David M. Goldstein

481

23.

Application of Control Theory to Work Settings Robert G. Lord and Mary C. Keman

493

24.

Effective Personnel Management: An Application of Control Theory James Soldani

515

The Giffen Effect: A Control Theory Resolution of an Economic Paradox William D. Williams

531

25.

Contents

X

Author Index

549

Subject Index

563

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CONTRIBUTORS Rolf Boch, Department of Clinical Neurology & Neurophysiology, University of Freiburg, D-7800 Freiburg, Federal Republic of Germany Thomas Bourbon, Department of Psychology, Stephen F. Austin University, Nacogdoches, TX 75962-3046, U.S.A. Daniel Bullock, Center for Adaptive Systems, Department of Mathematics, Boston University, Boston, MA 02215, U.S.A. Donald J. Crammond, Center for Research in Neurological Sciences, University of Montreal, Montreal, Quebec, Canada H3C 3J7 Liider Deecke, Neurological Clinic, University of Vienna, A-1090 Vienna, Austria Dennis J. Delprato, Department of Psychology, Eastern Michigan University, Ypsilanti, MI 48197, U.S.A. Burkhart Fischer, Department of Clinical Neurology & Neurophysiology, University of Freiburg, D-7800 Freiburg, Federal Republic of Germany Edward E. Ford, 10209 N. 56th St., Scottsdale, AZ 85253, U.S.A. Apostolos P. Georgopoulos, Philip Bard Laboratories of Neurophysiology, Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A. David M. Goldstein, 801 Edgemoor Road, Cherry Hill, NJ 08034, U.S.A. Stephen Grossberg, Center for Adaptive Systems, Department of Mathematics, Boston University, Boston, MA 02215, U.S.A. Wayne A. Hershberger, Department of Psychology, Northern Illinois University, DeKalb, IL 60115, U.S.A.

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Contributors

George S. Howard, Department of Psychology, University of Notre Dame, Notre Dame, IN 46556, U.S.A. Michael E. Hyland, Department of Psychology, Plymouth Polytechnic, Plymouth, Devon, PLA 8AA, England J. Scott Jordan, Department of Psychology, Northern Illinois University, DeKalb, IL 60115, U.S.A. Miguel Kazen-Saad, Department of Psychology, University of Osnabruck, D-4500 Osnabruck, Federal Republic of Germany Mary C. Kernan, Department of Business Administration, University of Delaware, Newark, DE 19716, U.S.A. Anselm W. Kornhuber, Neurological Clinic, University of Ulm, D-7900 Ulm, Federal Republic of Germany Hans H. Kornhuber, Neurological Clinic, University of Ulm, D-7900 Ulm, Federal Republic of Germany Julius Kuhl, Department of Psychology, University of Osnabriick, D-4500 Osnabruck, Federal Republic of Germany Michael Lang, Neurological Clinic, University of Ulm, D-7900 Ulm, Federal Republic of Germany Wilfried Lang, Neurological Clinic, University of Vienna, A-1090 Vienna, Austria Robert G. Lord, Department of Psychology, University of Akron, Akron, OH 44325, U.S.A. William A. MacKay, Department of Physiology, University of Toronto, Toronto, Ontario, Canada M5S 1A8 Richard Marken, Aerospace Corporation, Los Angeles, CA 90009-2957, U.S.A.

Contributors

xiii

Paul R. Myers, Department of Psychology, University of Notre Dame, Notre Dame, IN 46556, U.S.A.

R. Naatanen, Department of Psychology, University of Helsinki, 00170 Helsinki, Finland Raymond Pavloski, Department of Psychology, Indiana University of Pennsylvania, Indiana, PA 15705-1068, U S A . William T. Powers, 1138 Whitfield Road, Northbrook, IL 60062, U.S.A. Richard J. Robertson, Department of Psychology, Northeastern Illinois University, Chicago, IL 60625, U.S.A. Eckart Scheerer, Institute of Cognitive Science, University of Oldenburg, D-2900 Oldenburg, Federal Republic of Germany James Soldani, 13849 N. 64th Street, Scottsdale, AZ 85254, U.S.A. William D. Williams, 1850 Norwood, Boulder, CO 80304, U.S.A.

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GENERAL THEORETICAL PERSPECTIW

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VOLITIONAL ACTION, W.A. Hershberger (Editor) 0 Elsevier Science Publishers B. V. (North-Holland), 1989

3

CHAPTER 1 THE SYNERGY OF VOLUNTARY AND INVOLUNTARY ACTION Wayne A. Hershberger The first point to understand about the psychology of volition, according to William James (1890), the preeminent American psychologist at the turn of the century when conative psychology was last in vogue, is that voluntary acts "being desired and intended beforehand, are of course done with full prevision of what they are to be" (Vol. 2, p.487). In turn, the most important point to understand about this prevision or anticipatory image is that it represents an intended sensory consequence of muscular activity and not the muscular activity itself. As James put it,

I trust that I have now made clear what that "idea of a movement" is which must precede it in order that it be voluntary. It is not the thought of the innervation which the movement requires. It is the anticipation of the movement's sensible effects, resident or remote, and sometimes very remote indeed (Vol. 2, p. 522). To illustrate James' meaning, consider the process of emptying a cup of coffee with a series of successive sips each requiring a different muscular effort, the sensible effects of which are all essentially the same: a sip of coffee. Since the voluntary act of taking a sip is literally defined by this common sensory consequence, the act itself must be precipitated by an anticipatory image of that particular sensory consequence which alone defines the voluntary act. In brief, James was suggesting that volitional actions are intended selfcontrolled inputs rather than emitted or elicited outputs.

Volitional Actions Are Not Emitted Contemporary, behavioristic psychologists such as B. F. Skinner (Catania & Harnad, 1988), who define overt behavior as comprising only

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Wayne A. Hershberger

emitted and elicited outputs cannot, perhaps, legitimately be faulted for failing to find any intentional responses or volitional actions within the scope of human conduct given their definition of overt behavior. But they certainly can and should be faulted for their narrow definition of behavior, which excludes precisely that type of overt behavior which James had previously recognized as comprising volitional action, namely, intended, self-controlled input (Hershberger, 1987a, 1988a, 1988b). Man-made mechanisms that control their input, keeping the value of a monitored variable equal to an intended reference value by means of negative feedback, are called control systems, or closed-loop control systems. The household thermostat and furnace system is a commonplace example. Setting the thermostat of such a system specifies the temperature its thermocouple is intended to sense, not the amount of heat the furnace is going to emit. Having set the thermostat, one can predict the indoor temperature but not the fuel bill. The latter varies with the weather. The indoor temperature, however, is the mechanism’s doing. What these mechanisms do at our command is control the value of their own sensed input, which, of course, is also one of ours: sensed room temperature. Their response to our command is, hence, a particular, self-controlled value of input rather than any particular value of output, either emitted or elicited. This is not to say that the furnace does not emir heat nor that cold weather does not elicit compensatory emissions of heat from the furnace, but only that the control system does not itself control those heat emissions. That is not what it does! What it does, at our command, is control sensed temperature (Hershberger, 1988b, p. 107). In order to avoid confusion later, I draw the reader’s attention to a second example which illustrates several points that tend to be obscured by the furnace and thermostat example. Consider, if you will, the control system, known as power steering, commonplace in modern automobiles.1 Steering provides an historically apt example of control. When Norbert Wiener (1948) coined the term Cybernetics to name a new discipline concerned with control and communication in the animal and the machine, he derived the name from the greek word kubemetes, meaning steersman.

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This control system effectively monitors the value of a variable corresponding to the orientation of the front wheels and keeps that value equal to one expressed in terms of the orientation of the steering wheel. Although much more energy is required to turn the front wheels when the vehicle is at rest than when it is moving, this is of little concern to the driver who uses the steering wheel essentially as a means of communicating intentions about the desired orientation of the front wheels. The forces necessary to actualize an intended orientation under various driving conditions is left to the control loop which realizes or actualizes expressed intentions even as the driver is communicating them through the steering wheel. This example illustrates three important points that the furnace and thermostat example obscures: First, control systems are not necessarily homeostatic; a reference value in a control system may vary, or be varied, continuously. Second, the value of a controlled variable may "track" the value of a rapidly varying reference signal so precisely that they covary almost as if they were one and the same. And finally, control systems may employ proprioceptors, or the like, to control variables such as posture, just as they employ exteroceptors to control the value of variables in an external environment. The operating principle remains the same: the control of input through negative feedback. The principal relevance of these two examples of man-made control systems is that they illustrate graphically the very point which James considered to be of the first importance in understanding the nature of volition or volitional action. In organisms, as in man-made control systems, volitional action is essentially an image + input process, not an organism output process. Nor is volitional action, as described herein, to be regarded as an efference + reafference process. That is, a reference signal, such as James' anticipatory image, is not to be confused with von Holst and Mittelstaedt's (1950) efference copy. I have previously referred to reference signals, such as James anticipatory image, as aflerence copies in order to sharply contrast the concept with von Holst and Mittelstaedt's efference copy hypothesis (Hershberger, 1976, 1983, 1987b). The two notions are readily confused and were confused by von Holst and Mittelstaedt themselves, at least initially. Mittelstaedt acknowledged this in a subsequent paper (1958; also see MacKay & Mittelsteadt 1974) in which he presented a control-systems analysis of their original "functional schemata" and found, in addition to the efference copy they had originally posited, a higher order "command signal" which Mittelstaedt labeled simply "C." Upon analysis (see Hershberger 1976), C proved to --+

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Wayne A. Hershberger

be a reference signal, or afference copy, which is not surprising given that von Holst and Mittelstaedt were attempting to model volitional action in the first place, among other things.

Old Language Habits Die Hard James notion that volitional action is essentially an image -,input process rather than an organism output process, is, at once, both very simple and very difficult to understand. Although the idea appears to have been shared by other turn-of-the-century psychologists, including many American functionalists, it is not clear that any one of them, James included (see below), fully understood the idea or grasped its remarkable implications. The idea itself is simple enough. The difficulty lies in the fact that the notion is contrary to our traditional Cartesian habits of speech, and that, therefore, understanding the idea involves breaking the grip of the dead hand of habit, something that normally requires drill and practice as well as insight. As it turned out, these early American functionalists did not manage to escape their Cartesian language habits, although it was not entirely for lack of trying. John Dewey's classic critique of the reflex arc concept (Dewey, 1896) was a self-conscious attempt to identify and exorcise whatever vestiges of Cartesian interactionism remained in the new scientific psychology's behavioristic lexicon. Dewey's analysis focused primarily upon the primitive terms stimulus and response. Dewey warned that the reflex arc lacked unity and argued that behavior involves an entire loop or circle. As he put it, "The circle is a coordination, some of whose members have come into conflict with each other" (p. 370). Although he did not achieve a full understanding of closed-loop control, it is apparent that he was on the right track. Dewey's thought-provoking analysis is relevant and worth reading even today, but it is difficult to understand. The difficulty reflects, in part, the mind-bending paradoxes or apparent contradictions that seem inevitably to erupt when one attempts to describe voluntary behavior in the traditional terminology of response and stimulus. --+

For example, consider the following bizarre statement: The response of the furnace and thermostat system is a stimulus, not a response, but this stimulus is a response, not a stimulus. Although this grammatical statement is reasonably correct semantically (see below), it is gibberish, nonetheless. The

Synergv of Action

7

problem is that the terms stimulus and response have two distinctly different pairs of yoked meanings, among others: On the one hand, the two terms refer to receptor input and effector output, respectively $e., to sensory and motor variables). On the other hand, the two terms refer to cause and effect, respectively (i.e., to prod and product, or technically speaking, to independent and dependent variables). This confuses sensory input with cause and motor output with effect, a confusion that lends a specious legitimacy to the tenets of radical behaviorism, but that adds nothing to our understanding of control systems [or volitional action] but confusion itself, as the statement above amply illustrates. Deciphered, the statement reads as follows: The response of the furnace and thermostat system (i.e., what it produces or does) is a stimulus (i.e., a particular value of sensed temperature), not a response (or particular amount of heat output), but this stimulus (or sensed temperature) is a response (Lea, the dependent variable controlled by the system), not a stimulus (i.e., it does not control or cause the temperature being produced) (Hershberger, 1988a, p. 824). In retrospect, it is hardly surprising that the psychology of volition and volitional action languished as stimulus-response psychology flourished, or that functionalism gave way to behaviorism. That is, inasmuch as American functionalists routinely utilized the expressions motor response and sensory stimulus in their analyses of psychological phenomena-including Dewey (1896) himself in spite of his own implicit caveat to the contrary4 was, perhaps, inevitable that one of their number (it happened to be John B. Watson) would conclude that there is nothing scientific that can be said about volition or volitional action? In other words there are good pragmatic reasons why volitional action became an anathema to scientific psychology. However, good reason was not among them. Watson’s conclusion, which Skinner still champions (Catania & Harnad, Bergman (1956) called John B. Watson the “greatest...of the Functionalists” (p. 268). Watson, the founder of behaviorism, went to the University of Chicago to study with Dewey, a founder of functionalism, but as Watson (1936, p.274) acknowledged later he never quite understood what Dewey had to say. We cannot argue with that; he clearly missed the point of Dewey’s critique of the reflex arc concept. Of course, he was not alone in that respect.

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Wayne A. Hershberger

1988, pp.108-109) is specious; it follows from the mischievous habit of speech noted above, not from a logical train of thought. When behaviorists assert that volitional actions are incompatible with scientific psychology, they also imply that volitional actions are incompatible with those types of behavior that behaviorists have recognized as being scientific, that is, with elicited and emitted outputs. This notion, not surprisingly, is as specious as the fallacy that implies it. The terms voluntary and involuntary denote mutually exclusive categories of behavior, but they do not denote mutually exclusive behaviors! On the contrary, voluntary and involuntary behaviors are always found to go hand in hand in any system that controls its own input. Voluntary behavior actually presupposes involuntary behavior. For example, the flight path of an airplane is the pilot’s (or autopilot’s) doing only to the degree that the pilot’s (or autopilot’s) actions automatically offset any would-be aerodynamic disturbances to the intended flight path. Otherwise, he or she (or it) is merely along for the ride. The two types of behavior comprise a synergistic couple. They are complementary in the strong sense of the term: Like husband and wife, the existence of each type of behavior is distinct from but dependent on the nature of the other. Each has its mate. For every self-controlled input there is a corresponding, disturbance-driven output. And, the relationship is always synergistic (Hershberger, 1987a, p. 1032).

Canonical Self-Control Although control systems can be extremely complex, any system controlling a given parameter appears relatively simple when reduced to its basic canonical form, as is possible, in principle, with any such system, however complex. In its canonical form, the flow chart of any such system is a single negative feedback loop. The flow chart in Figure 1 is a canonical loop mapped onto the interface between an organism (or mechanism) and its environment. Everything above the dotted line is part of the organism (or mechanism). Everything below the dotted line is part of the environment. Note that although the organism (or mechanism) has only one input, the

Synergy of Action

9

(organism or mechanism)

- - - - - - - -(input) - 1 ~ - - - - - - - - - - - - - - \ f -(output)- - - - - (environment)

--

- A

Figure 1. A canonical control loop mapped onto the interface (dashed line) between an organism (or mechanism) and its environment.

control loop has two inputs. One input to the control loop is the reference value specifying the organism’s (or mechanism’s) intended input. The other input to the loop comprises all the environmental factors which potentially disturb the organism’s (or mechanism’s) input. The polarity of the feedback loop is negative. That is, discrepancies between the organism’s (or mechanism’s) intended and actual inputs constitute error signals which negate themselves by driving output so as to offset environmental disturbances and thereby keep the controlled input in close correspondence with the reference value. A coupling of two types of behavior is apparent, one involving controlled input and one involving elicited output. Consider first the

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Wayne A. Hershberger

controlled input. Inasmuch as the feedback loop keeps the controlled input equal to the reference value, the controlled input is to the reference input as an effect is to its cause or as a response is to its stimulus. And since this stimulus is an intention or intended value, the corresponding response is an intentional or voluntary behavior. This volitional action is represented by the large blocked arrow labeled Intentional actions. The error-driven output is another matter. Inasmuch as the organism (or mechanism) controls its input largely by offsetting environmental disturbances to that input with compensatory output, that compensatory output is to its eliciting disturbance as an effect is to its cause or as a response is to its stimulus. And since this stimulus is an unanticipated, unintended environmental disturbance, the elicited output is in the nature of a Cartesian reflex; that is, it is an involuntary reaction to an environmental stimulus. Note, incidentally, that this stimulus is not an input to the organism (or mechanism). It is an input only to the control loop (I will return to this point later). This involuntary action is represented by the large blocked arrow labeled Compensatory reactions. Note that the two blocked arrows point in a clockwise direction exactly opposite that of the solid arrows comprising the negative feedback loop. The two blocked arrows represent emergent properties of the system. Each represents a lineal cause and effect relationship that emerges from the underlying circular feedback process. To say that they are emergent is not to imply that they are merely putative properties. The blocked, counterclockwise arrows represent immanent and essential aspects of the control process. Nor is the counterclockwise orientation of the blocked arrows to be regarded as whimsical or accidental. That is, it is a mistake to suppose that the two counterclockwise arrows represent two lineal cause-effect arcs comprising the feedback loop itself (ie., two overlapping clockwise arcs). Closed-loop control systems do not control their input by controlling their output. Nor do disturbances elicit compensatory reactions by being sensed (e.g., the outdoor temperature that disturbs the thermostat and furnace system is not monitored by the system’s sensor; the thermocouple senses the temperature indoors not outdoors). In other words, closed-loop control does not involve reciprocal determinism. The feedback loop of a closed-loop control system involves reciprocal influence, not reciprocal control. The control process itself is an emergent property of the feedback loop, and this emergent control, or determinism, is lineal, not reciprocal: The value of the reference signal determines the value of the controlled input, but the opposite is certainly

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not true; ordinarily, the value of the controlled input does not even influence the reference value, let alone determine it. Similarly, the magnitude of the disturbance determines the magnitude of the system's output, but the opposite is certainly not true; ordinarily, the output does not even influence the disturbance, let alone determine it.

William James' Will: Right and Wrong In his chapter entitled "Will," James (1890) argued that the necessary and sufficient antecedent of any voluntary act is the anticipatory image defining the intentional action in question. He wrote, "We may consequently set it down as certain that, whether or no there be anything else in the mind at the moment when we consciously will a certain act, a mental conception made up of memory-images of these sensations, defining which special act it is, must be there!' (vol. 2, p. 492). He also asserted that this anticipatory image "is the only psychic state which introspection lets us discern as the forerunner of our voluntary acts" (vol. 2, p. 501). These two remarks are entirely consistent with the control process described in the paragraphs immediately above. However, James had not conceived the control process illustrated in Figure 1. He did not understand the feedback process by which a control system's reference signal (i.e., anticipatory image) determines the sensory consequences of the system's output (i.e., the system's input). Indeed, it is clear from a reading of James' description of the putative neural processes involved in volitional action that he was thinking of a calibrated input + output system rather than a control system. James neural model was functionally equivalent to any one of a number of more recent stimulus-response theories, such as Greenwald's (1970) ideo-motor theory of performance, based on James' own ideas, or Held's (1961) correlation store hypothesis, based on the reafference principle of von Holst and Mittelstaedt (1950), both of which suppose that neuromuscular outputs are centrally (i.e., neurally) coded in terms of their respective sensory consequences. A complication in all such theories is the fact that neuromuscular outputs do not each have just one particular sensory consequence; rather, for any given output the consequence varies with the circumstance, and circumstances vary endlessly. To paraphrase Heraclitus, one never encounters the same circumstance twice. This implies that an effective neural inventory of all such output/circumstance combinations and their attendant sensory consequences would be exceedingly complex; indeed, an exhaustive inventory would amount

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virtually to a neural model of the world. The informational load that the organism is expected to bear is staggering. By thus balancing the theoretical burden on the backs of the systems whose functioning they purport to explain, these theories project a specious appearance of parsimony. All things considered, they are anything but simple. However, what is more to the point, neither are they essentially volitional (see Kimble & Perlmuter, 1970). If volition involves merely the selection of an output according to its labeled consequence, wherein lies the distinction between voluntary and involuntary output? Only in the label. The output is the same, whatever one calls it, or however it is labelled or coded. Therefore the distinction is merely semantic. In summary, James’ neurological theorizing does not support the implications of his introspective observations. In this respect, James, like so many others, seems to have been unable to break the Cartesian habit of speech equating actions (including voluntary ones) with neuromuscular outputs. He seems, at once, both to have recognized and ignored the fact that a voluntary movement not only has sensible consequences, but is itself, a sensible consequence of neuromuscular output. James called the sensory consequences registered by receptors in the muscles, tendons and joints, resident effects, and those registered by exteroceptors, remote effects. The control of resident effects is considered in the next paragraph. The control of remote effects, is the process illustrated in Figure 1 above. In Figure 1, the control loop straddles the interface between the organism, or mechanism, and its environment. The controlled input is, therefore, an environmental variable monitored by an exteroceptor such as an eye or a thermocouple. That is, Figure 1 represents the canonical control process involved in such intentional behavior as that of a motorist keeping an automobile, buffeted by variable crosswinds, rolling straight down the highway, or a thermostat and furnace system keeping the temperature indoors at 72 degrees Fahrenheit as the temperature outdoors ranges from, say, 20 to 60 degrees. Resident effects comprise such voluntary actions as movements and postures. Consider, for example, a person lifting a cup to her lips or a power steering system turning the front wheels of an automobile to a desired orientation. In both cases, the intentional behavior involves compensation for variable environmental loads, because the cup may be full or nearly empty, and the automobile may be moving or stationary. However, in neither case is the controlled variable essentially environmental. Rather, in both cases the controlled variable is essentially a parameter of the organism, or mechanism, involving the articulation of

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several of its various parts. Consequently, Figure 1 would need to be modified slightly in order to accurately represent the canonical control of resident effects: Specifically, the dashed line representing the interface between the organism, or mechanism, and the environment should be located coincident with the bottom edge of the control loop. Posture or bodily motion is an environmental variable in the sense that it is publicly observable by others. I can, and often do, observe the orientation of the front wheels of a car facing me at an intersection, just as I can, and daily do, watch my wife across the dinner table lift a cup unerringly to her lips. I see these things, but the control systems need not, because they--the automobile's power steering and my wife's nervous system--are not controlling visual inputs from remote environmental sources. They are controlling the articulation of certain body parts, which are registered either by receptors resident in those body parts, or by corollary discharges of neural efference (or the like), or by both. Corollary discharges of efference (Sperry, 1950), or efference copies (von Holst & Mittelstaedt, 1950) need not be controlled inputs (controlled feedback), but they may be. When they are, any disturbance introduced upstream of the corollary discharge would be offset by compensatory adjustments of output, thereby controlling the value of the feedback signal. Robinson's (1975) model of the saccadic oculomotor control system involves this type of controlled input, or controlled feedback. His model "consists of a single negative feedback system whose forward [efferent] path contains a high gain saturating amplifier with a dead zone (so it is either on or off) and an integrator" (p. 369). The output of the integrator, which corresponds to eye orientation, is the feedback signal that is controlled. The expression "high gain saturating amplifier with a dead zone" means that the system operates in a "bang-bang" fashion exactly analogous to that of a furnace and thermostat system. Bullock and Grossberg (1988) claim that the control of such neural feedback signals is also an integral part of voluntary arm movements. See also their chapter in this volume. Interoceptors, which monitor such controlled variables as body temperature, may be regarded as measuring either resident or remote effects, depending upon the frame of reference assumed. If the organism as a whole is the assumed frame of reference, then interoceptors may be said to monitor resident effects. However, if one takes the control mechanism inside the organism to be the frame of reference, then interoceptors may be said to monitor environmental (i.e., remote) effects. For instance, Cannon (1932) described the control of vital signs such as

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body temperature as the control of environmental parameters, with the term environment referring to Bernard’s milieu intkrier (1878/1973).

The Involuntary Aspect of Self-Control Whether resident or remote, the consequences controlled by organisms, or mechanisms, are always the joint effects of two antecedents, only one of which is the organism’s, or mechanism’s, output. The other factor comprises all the various influences of the organism’s, or mechanism’s, environment. A closed-loop control system works by pitting these two factors against each other. The environmental factor is customarily called an environmental dkturbance, not only because it has the potential of disturbing the system’s controlled input, but also because it actually elicits compensatory output from the system. Closed-loop control systems control their own input by forfeiting control over their output, which is determined in large part by their environmental disturbances. For example, the amount of heat generated by the furnace of a system controlling indoor temperature depends upon a host of environmental variables all of which tend to influence the air temperature being controlled. These include, but are not limited to, the temperature outdoors, the intensity and direction of the wind, the number and types of windows in the house, the thermal insulation in the external walls and attic, the elevation and azimuth of the sun, the amount of cloud cover, the color of the shingles on the roof, the number of people going in and out, the wattage of incandescent lamps in use, the number of pots cooking on the stove, and the amount of laundry being tumbled in the drier. The thermostat and furnace system responds automatically to all these environmental disturbances with just the right amount of heat to keep the indoor temperature at the reference level, and does so without even measuring these disturbances, either individually or collectively. (It is almost enough to drive a Cartesian mechanist to thoughts of divine intervention.) When we observe an organism or mechanism’s output covarying systematically with an environmental variable, our Cartesian habits of speech (read thought) incline us to suppose that the form of the observed relationship somehow reflects the form of the mediating mechanism. But it should be obvious from the present example of the furnace and thermostat system that this does not hold for control systems. In control systems, output is error-driven, and relatively small errors (i.e., small departures of the controlled variable from the reference value) drive

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relatively large compensatory outputs which serve to nip disturbances in the bud, so to speak. Therefore, the effect of an environmental disturbance upon a control system's output depends entirely upon the influence of that would-be disturbance upon the variable being controlled. That is, it depends entirely upon the relationship obtaining between these two environmental variables, and has nothing to do with the .particulars of the control mechanism involved. For example, if one plotted a furnace's output as a function of outdoor wind speed (holding all other factors constant), the relationship observed would simply reflect the chilling effects of the wind on the house and the air inside, that is all. The function would reflect a law of physics, not a law of behavior. The behavioral law in question is so simple that it drops out of the equation. That law is this: in an ideal control system, a disturbance elicits output whose effects on the controlled variable are equal and opposite to its own; simply put, the output nulls the error signal. For an elegant mathematical exposition of these points, among others, see Powers' (1978) quantitative analysis of purposive systems. To say that the output nulls the error signal is to imply that two essential things need obtain, and essentially only two things. The control loop's output must be able to outmuscle its disturbances, and the polarity of the feedback must be negative. (The system, to be stable, must also be able to detect changes in the controlled variable as it is producing them; hence, a change-slowing factor is sometimes incorporated in man made systems: Chapter 13.) In the example of the furnace and thermostat system, the rate at which the furnace generates heat when it is on must be greater than the maximum rate at which heat is dissipated to the outdoors--however, the control process does not require any particular rate of heat production; that is, the output does not have to be calibrated to the conditions. Further, the polarity of the feedback loop is crucial: the furnace must be switched on or off when the sensed temperature is, respectively below or above the reference temperature. (If the polarity of the switch were reversed, the feedback would be positive and the sensed temperature would "run away" to one of its limits: extremely hot or cold.) Providing that these two conditions are met, a closed loop system will blindly dance to a disturbance's tune and thereby control its own input, keeping it virtually equal to the reference value. Although the system does not detect the disturbances to which it responds, those disturbances are nevertheless mirrored in the system's output (e.g., the weather is mirrored in the fuel bill). A system may thus appreciate the

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magnitude of a disturbance by recognizing the magnitude of its own output. This perception of the disturbance is entirely a posteriori, however; it comes after, not before, the elicited output. Obviously, this phenomenon provides a firm basis for at least some motor theories of perception (see Coren, 1986; Hershberger, 1983, 1987b). These observations also imply that sensations of innervation, in the form of efference copies or the like, are sometimes reflections of exafference (read environmental disturbance), contrary to what von Holst and Mittelstaedt (1950) initially supposed. Because the polarity of a control loop's feedback must be negative for the system to function properly, environmental factors which disturb that polarity, either neutralizing it or reversing it, are not automatically corrected by that control loop. In order for the polarity of a feedback loop to be controlled against such disturbances of polarity, a higher order control loop is required whose output would reorganize the subordinate loop. Ashby's (1952) classic Design for u Brain treats such self-reorganizing processes at length (also see Campbell, 1956, and Powers, 1953, Chapter 14). Although I do not wish to dwell on the topic of "selfreorganization" here, it is important to note that animal experiments in which the polarity of sensory feedback has been reversed, either optically or surgically, have invariably found evidence of positive feedback in the form of forced circus movements, run-away output or the like. The experiments have used a variety of species, including insects (von Holst & Mittelstaedt, 1950), fish, amphibians, rodents (Sperry, 1951), 4-day-old chickens (Hershberger, 19861, and the oculomotor control system of man (Smith & Molitor, 1969; Yarbus, 1962). In these experiments very little, if any, recovery of function has been observed to result from practice, suggesting that the polarity of some control loops are not readily altered by experience. That is, in animals, some control loops, particularly those already in evidence at birth, may be well-fixed genetically (i.e., "hardwired") and relatively inflexible to change. However, much of the intentional behavior of animals, particularly humans, appears to be mediated by control mechanisms that evolve with experience. For example, when driving a car, one controls the direction of locomotion with the hands not the feet, as evolution would have us do. Also, it is possible for one to steer an automobile while holding either the top or bottom rim of the steering wheel, despite the fact that a rightward motion of the hand has opposite remote effects in the two cases. Not only are these control mechanisms, at least in part, acquired, the latter example involves polarity reversals as well.

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Volition and Hierarchical Intentions Volitional actions are self-controlled, but not all self-control is volitional action. The control processes which regulate the parameters of the milieu int6rier are intentional inasmuch as they involve the maintenance of implicit reference values, but they are not considered voluntary because those reference values are fixed. In order for self-control to fully qualify as being voluntary, the reference value in question must not be fixed, either genetically or environmentally. A consideration of what this implies for hierarchical control mechanisms, such as those comprising complex organisms, merits attention here (also see Marken & Powers’ chapter in this volume). When two loops are joined hierarchically, so that the controlled input of the subordinate loop is the output of the superordinate loop, the controlled input of the subordinate loop, although intentional, is not fully volitional, because, ideally, the intentional actions of the subordinate loop are entirely at the service of two masters, namely, the superordinate intention and its disturbance. The only volitional actions available at the level of the subordinate loop are those which are orthogonal to the intention in question. For instance, if I wish to see either of my arms visibly outstretched at eye level (a superordinate intention controlling a remote effect), the intended posture of my arm (a subordinate intention controlling a resident effect) is fixed with respect to its elevation. Only the arms’ azimuth and its roll (palm up or down) remain optional parameters. Of course, there is also the choice of right or left arm. Our actions order themselves hierarchically in terms of the controlled variables involved. For instance, steering an automobile involves controlling the orientation of the front wheels. But the orientation of the front wheels is determined by the orientation of the steering wheel, and the orientation of the steering wheel is determined by the position of the driver’s arms. Therefore, steering an automobile involves a hierarchy of control. If the car is equipped with power steering, there are at least three hierarchical intentions, or reference signals involved: (a) the driver’s intended direction of visual locomotion, (b) the intended orientation of the driver’s arms, and (c) the intended orientation of the front wheels. Note that I have made proprietary reference only to the first of these three intentions. That is, the reference signal controlling the direction of visual locomotion is the only intention which is uniquely the driver’s. The intention listed last is the reference signal for the power

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steering. Although the driver is communicating this intention to the power-steering system, it is the power steering’s reference signal not the driver’s; it is not a reference signal for any control loop in the driver. The intended orientation of the driver’s arms is a reference signal for a control loop in the driver, but the value of that intended orientation is dependent in large part upon environmental disturbances. If the driver chooses to drive straight down the highway through a steady crosswind, he or she has no option but to crab the wheel just enough to offset the effects of the wind. So although the driver may have provided the muscle to turn the wheel, the intention to do so was not of his or her choosing; it derives almost entirely from two considerations, (a) the driver’s intention to stay on the road, and (b) the crosswind. If the wind is very gusty the driver will involuntarily be very busy at the wheel without voluntarily intending to do anything but stay on the road. Learning to drive or pilot a vehicle involves the development of control systems in which the control of resident sensory effects are subordinated to the control of remote visual effects (for a discussion of visual locomotion, see Gibson 1966; also see Owen & Warren, 1982). Initially, the novice driver controls the orientation of the steering wheel without effectively controlling the direction of the car. In contrast, the proficient driver has learned to control the car by allowing the environmental circumstances to dictate the orientation of the steering wheel. Inevitably, the more volitional the car trajectory becomes, the less volitional the hand motions become. There is a conservation principle at work. The development of hierarchical control serves to centralize choice or volition, but does not increase it. The amount of will which may be marshalled, or mustered, or brought to a focus is thus limited by the control system’s ordinal size, that is, by the number of orthogonal inputs (or variables) the system is able, in principle, to control. There is no will to be found lying around free.

References Ashby, W. R. (1952). Design for a brain. New York: Wiley. Bergman, G. (1956). The contribution of John B. Watson. Psychological Review, 63, 265-276. Bernard, C. (1973). Lectures on thephenomena of life common to animals and plants. (H. E. Hoff, R. Guillemin, & L. Guillemin, Trans.) Springfield, Illinois: Thomas. (Original work published 1878).

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Bullock, D., & Grossberg, S. (1988). Neural dynamics of planned arm movements: Emergent invariants and speed-accuracy properties during trajectory formation. Psychological Review, 95, 49-90. Campbell, D. T. (1956). Adaptive behavior from random response. Behavioral Sciences, I , 105-110. Cannon, W. B. (1932) Wisdom of the body. New York: Norton. Catania, A. C., & Harnad, S. (Eds.), (1988). The selection of behavior, New York Cambridge University Press. Coren, S. (1986). An efferent component in the visual perception of direction and extent. Psychological Review, 93, 391-410. Dewey, J. (1896). The reflex arc concept in psychology. Psychological Review, 3, 359-370. Gibson, J. J. (1966). The senses considered as perceptual system. Boston: Houghton Mifflin. Greenwald, A. G. (1970) Sensory feedback mechanisms in performance control: With special reference to the ideo-motor mechanism. Psychological Review, 77, 73-99. Held, R. (1961). Exposure-history as a factor in maintaining stability of perception and coordination.Journal of nervous and Mental Diseases, 132, 2632. Hershberger, W. A. (1976) Afference copy, the closed-loop analogue of von Holst's efference copy. Cybernetics Forum, 8, 97-102. Hershberger, W. A. (1983). A conditioned weight illusion: Reafference learning without a correlation store. Perception & Psychophysics, 33, 391-398. Hershberger, W. A. (1986). An approach through the looking-glass. Animal Learning & Behavior, 14, 443-451. Hershberger, W. A. (1987a). Of course there can be an empirical science of volitional action. American Psychologist, 42, 1032-1033. Hershberger, W. A. (1987b). Saccadic eye movements and the perception of visual direction. Perception & Psychophysics, 41, 35-44. Hershberger, W. A. (1988a). Psychology as a conative science. Arnen'can Psychologist, 43, 823-824. Hershberger, W. A. (1988b). Some overt behavior is neither elicited nor emitted. In A. C. Catania and s. Harnad (Eds.), The selection of behavior (pp. 107-109). New York: Cambridge University Press. James, W. (1890). The principles ofpsychology (Vol. 2). New York: Henry Holt. Kimble, G. A., & Perlmuter, L. C. (1970). The problem of volition. Psychological Review, 77, 361-384.

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MacKay, D. M., & Mittelstaedt, H. (1974). Visual stability and motor control (reafference revisited). In W. D. Keidel (Ed.), cybernetics and bionics. Munich: Oldenbourg. Mittelstaedt, H. (1958). The analysis of behavior in terms of control systems. In B. Schaffner (Ed.), Groupprocesses, Transactionuf the Fifth Conference. New York Josiah Macy, Jr., Foundation. Owen, D. H., & Warren, R. (1982). Optical variables as measures of performance during simulated flight. Proceedings of the Human Factors Society 26th Annual Meeting, 312-315. Powers, W. T. (1973). Behavior: The control of perception. Chicago: Aldine. Powers, W. T. (1978). Quantitative analysis of purposive systems: Some spadework at the foundations of scientific psychology. Psychological Review, 85, 417-435. Robinson, D. (1975). Oculomotor control signals. In G. Lennerstrand, P. Bachy-Rita, C. C. Collins, A. Jampolsky, & A. B. Scott (Eds.), Basic mechanisms of ocular motility and their clinical implications. New York: Pergamon Press. Smith, K. U., & Molitor, K. (1969). Adaptation to reversal of retinal feedback of eye movements. Journal of Motor Behavior, I , 69-87. Sperry, R. W. (1950). Neural basis of the spontaneous optokinetic response produced by visual neural inversion. Journal of Comparative & Physiological Psychology, 43, 482-489. Sperry, R. W. (1951). Mechanisms of neural maturation. In S. S. Stevens (Ed.), Handbook of experimental psychology. New York: Wiley. Watson, J. B. (1936). J. B. Watson. In C. Murchison (Ed.), A history of psychology in autobiography, Vol. 3. Worcester, Massachusetts: Clark University Press. Wiener, N. (1948). Cybernetics: Control and communication in the animal and the machine. New York: Wiley. von Holst, E. & Mittelstaedt, H. (1950). Das Reafferenzprinzip. Natuwksenshafen, 37, 464-476. Yarbus, A. L. (1962). Eye movements and vision. (Trans. by B. Haigh) New York Plenum Press.

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0 Elsevier Science Publishers B. V. (North-Holland). 1989

CHAPTER 2 VOLITION: A SEMI-SCIENTIFIC ESSAY William T.Powers Every child wonders, sooner or later, how it is that simply wanting one’s hands, arms, legs, body, head, or eyes to move suffices to create the wanted result. The sense of willing that one’s own body do something is at the same time unmistakable and unexplainable, being unlike any other mental or physical experience. While willing an act seems to suggest that we are masters of our own behavior, experiences of other kinds suggest just the opposite. As children we do as we will when it is playtime, but from the very beginning we find that we also do as we must, when people and events decree that playtime is at an end. Even the passive physical world forces us into action in ways that can seem to push the will aside. With growing force, necessity makes itself known in many forms. The demands of our bodies, saying that we must breathe, eat, drink, stay warm, seek love, and avoid pain, override the will more and more often; one demand leads to another, until by the time we are adults it can seem that we no longer have any freedom to will except as a momentary act of useless defiance. When the rat-race is at its worst, there seems to be an external reason for every slightest act from rising in the morning at the alarm clock’s buzz to swallowing the final nightcap so we can sleep, only to rise, too soon, again. To indulge in any extended period of purely volitional action would be to put unacceptable stresses on the network of behaviors we are forced to adopt, stresses that seize control again and bring us back into the daily groove, will we or nil we. The transition from childhood to adulthood is unpleasant largely because of the sense of steadily diminishing freedom to will. On the one hand, adulthood promises immense freedoms -- driving a car, getting out of school, having one’s own money, going to bed when one pleases, being listened to, understanding how things work, owning and managing things and events. On the other hand, adults obviously do not seem to enjoy these freedoms as much as they ought to. In fact, they seem to act as if they have no great amount of freedom. Every child must at some time

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vow not to become like that -- not to give up control of one’s own life. And every child inevitably ends up breaking the vow, perhaps raging but in almost every instance succumbing to all the controlling influences that prove unavoidable. The traditional scientific view of behavior is the adult’s view, not the child’s. But this is not the view of a wise adult; only of an adult who has decided that the sense of will that was given up must somehow have been an illusion. Opponents of the objective, dispassionate analysis of causation that is traditional in science, on the other hand, maintain the child’s view, insisting on the essential freedom of the mind with a child’s faith -- with the same amount of influence on science that children usually have on adults. The puzzle of the will is central in our attempts to understand human behavior. Insisting that creative will is all, the naive child’s view, is neither more nor less correct than insisting that it is impotent or nonexistent, the cynical adult’s view. To understand both will and necessity, we must avoid siding with either view, and try to define the terms of this puzzle in a way that gives us a chance at solving it.

Internal vs. External Causation To speak of volition as a sense of willing is to use one word in place of another, illuminating nothing. While only the individual can sense volition when it is occurring, the ability to sense it confers no particular understanding of it. If sensing it were enough, we would not have these problems. What we must do is find a place for volition in our general understanding of both private and public, but most importantly public, phenomena. Volition can be defined as a cause of behavior that is internal to the behaving system. Speaking generally instead of personally, we can see that human behavior seems to have two kinds of causes. One kind we can easily see, as when a gust of wind makes a man struggle to stand up, or an unexpected sound makes someone jump, or a worker tries harder when the boss threatens to fire her. The other kind is harder to see, because the cause is located where it can’t be observed; the identification of a volitional act always seems weak because all we can say is that there was no apparent external cause. Few of us would dare to claim that we have noticed every possible cause and ruled it out. The weakness of the identification would seem to leave external cause as the most rational choice.

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On the other hand, a careful consideration of human behavior, our own or that of others, makes it quite clear that we cannot identify many external causes. While we can pick out salient events such as an explosion or the offer of food and make a case that the ensuing behavior was the result, it is much harder to extend these connections to all behaviors and all events. Given any event chosen from the ongoing stream at random, we normally have no way of predicting what behavior will follow it in any given person. And if we really pay attention to behavior, we must admit that behavior is going on every moment of a person’s life, in an unending continuous flow. It isn’t just that our knowledge of external causes of behaviors is incomplete: it is nearly nonexistent. In sheer quantity, the amount of behavior that has been connected to prior causes is only an infinitesimal fraction of all the behavior that goes on every day. Scientists who have given up completely on internal causation have done so not because of the evidence, but because of an urge to simplify. It is much easier to assert that all behavior is externally caused than it is to envision trying to sort out one class of causes from another. In support of external causation, it has been claimed that in a physical universe, all material objects are caused to behave by the confluence of all current influences on them. But this physical principle is not a premise from which we can conclude that all behavior is externally caused: it is simply a restatement of the assertion in different words. And it is a restatement that ignores all the ways in which organisms differ from the simple point-masses to which the original Newtonian principle was applied. The principle difference is complexity: there is a great deal more going on inside an organism than inside any piece of matter that a physicist or a chemist studies. Most pieces of matter that a physicist studies do not stand up and try to get away. This complexity means not only that there are important processes going on inside the organism at all times, but that these processes may arise from sources that existed at unknown and unknowable times in the past. When a person speaks, the grammar and syntax that shape the speech may have originated in the outside world, but they certainly did not originate just before the utterance. As far as any present-time observer is concerned, the causes of grammar and syntax now are carried in the brain of the speaker, and cannot be traced to anything happening in the current environment. This gives us the first wedge with which to pry open the puzzle. We must admit at least that large parts of the behavior we observe have

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origins that are unconnected with the current environment. On this basis we may still claim that some behaviors amount to responses to current stimuli, but we must allow that even more of the behaviors, perhaps most of them, must be under control of processes that are not altered by any present stimuli.

The Logic of Causation Another route we can take involves a closer look at what is supposedly caused, behavior itself. What is behavior? The naive view, which is shared by scientist and laymen alike, is that behavior is whatever organisms do. But what do we mean by "doing?" The two-letter word "do" takes up four column-inches in an old Collegiate dictionary, and far more in an Unabridged. This primitive grunt refers to causing essentially any occurrence that can be named. It asserts agency, but reflecting our ignorance it skips over process. The doer does, but how the doer does it is not mentioned. How does one open a door? Not, we can be sure, by opening it -that is not an answer to a "how" question, but a reassertion of agency in more obscure form. Normally, one opens doors by pushing on them or pulling on them. Opening a door would surely be classed as a behavior, but in fact this behavior is carried out by an organism that is doing something distinctly different from ''opening." It is the door, not the organism, that opens. What the organism does is to apply a force with its muscles: the consequence of this effort is, usually, that the door opens. Most of us will open a sizable number of doors in one day, some familiar and some unfamiliar. We open bedroom doors, bathroom doors, front doors, car doors, supermarket doors, refrigerator doors, cupboard doors, and the doors where we work. There is no linguistic problem with calling all these activities "opening doors," but in terms of the motor actions we carry out, not only are the actions very different over all these instances of the "same behavior," but they are quantitatively different each time we open the same door. What we call behavior is really some repeatable recognizable consequence of our motor actions. Almost 100 years ago, William James pointed out the uncomfortable fact that while these consequences repeat, the actions that bring them about do not repeat. Had James gone on to analyze this observation in more detail, he would have realized that the actions do not repeat for the simple reason that if they did repeat, their consequences would vary. If you turn left to enter a cafeteria, you will

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be able to buy your lunch. But if you enter the building by a different door, or if someone is standing in the way, or if the cafeteria is locked, you will not get lunch by turning left. Something else will happen. This is the story of essentially every behavior of any amount of complexity. Circumstances change. The surrounding world influences the outcomes of actions, and those independent influences can change greatly from moment to moment. Sometimes they don’t change, so the same action will have nearly the same result as before. But organisms must produce behavior in the worst-case world, too, and they do. When external influences change, organisms alter their actions to compensate, even to the extent of reversing them or substituting a totally different action. This is a commonplace fact of life: regular behavior is nut brought about by regular motor actions, and regular motor actions would not normally produce regular results. That fact, as simple and obvious as it is, spells great difficulty for the concept of external causation. For external causation to work, the causal chain must remain predictable from beginning to end. There must not be any other causes that contribute to the outcome downstream from the initial cause -- otherwise, anything could happen. If the principle of external causation worked as it is supposed to work, we would predict that disturbing the outcome directly would cause the outcome to change, in exact proportion to the disturbance. What does happen is that an immediate change in the action just cancels the effect of the disturbance. This is the only way in which organisms can possibly continue to produce recognizable behavior. The patterns that result from their motor actions are ordinarily under continuous disturbance, the disturbances arising partly from independent sources in the environment and partly from the varying relationships of the organism to its environment. We see stable patterns; it follows that the actions of the organism cannot be correspondingly stable. This analysis would seem to rule out external causation altogether, but that is not quite the result. What happens instead is that we are made to focus on something outside the purview of the causal hypothesis -- not what changes when stimuli and disturbances occur, but what does not change.

The Logic of Control We do not normally pay attention to the motor acts by which familiar patterns of behavior are created; for one reason, they are hard

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to observe. It is not action, but the consequence of action, that is made to repeat by a behaving organism. To understand just how variable those acts must be, we have to understand something about the workings of the physical world. When we see a person reaching out toward the floorselector button in an elevator carriage, we see what seems to be a motion of the arm directed by its muscles toward the button. With a little reflection, we realize that the muscle forces are not aimed in the direction the hand is moving. They are aimed primarily straight up, countering the force of gravity and whatever accelerations of the elevator carriage are occurring. Even an act like reaching out toward something, which seems a direct expression of muscle action, is several steps removed from the actual motor behavior that is going on. The ends and the means are almost never related in any simple straightforward way. Clearly, we do not simply "doll behaviors. That description is just too sketchy. A more accurate description would be that we -- and other organisms -- act in such a way that certain consequences are brought about and maintained. The phrase "in such a way'' has a specific meaning: the way in question can be deduced from observing the consequence and knowing what independent forces are acting to alter the consequence. For instance, if we observe a car being steered straight down a level flat road, and we know that a crosswind is exerting 75 pounds of force on the car to the left, we can be quite sure that the driver is exerting a force on the steering wheel that, relayed through the power steering, the linkage, and the front tires, pushes the car to the right with a force of just 75 pounds. If that were not so, the car could not go straight. When more than one influence adds a sideward force to the car -- the camber of the roadbed, for instance, adding its effects to those of the crosswind -- we can be quite sure that the driver's effort, translated into an effect on the car, is equal and opposite to the sum of all those disturbing forces. That is simply a matter of applying Newton's laws of motion, and observing that the car continues in a straight line. When we see consistent behavior in the presence of independent disturbances, we can deduce that the actions of the organism must be varying so that the resultant is right for producing what we see. This is the basic logic of the phenomenon we know as control. A disturbance that tends to alter the final pattern results immediately in a change of motor action that tends to alter it by the same amount in the opposite direction. The net result is no change, or almost none. It is this lack of change, under circumstances where change is to be expected, that tells us control is occurring.

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This concept of behavior clearly does not fit the conventional causal model. As expressed so far, it seems to rely on variations in actions that are fortuitously just right to prevent disturbances from having disturbing effects. To implicate external causation in this kind of situation, we would have to imagine that the external cause varied in just the way needed (taking the organism’s properties into account) to make behavior change to preserve a particular outcome. We would have to imagine stimuli that act on the driver so as to keep the car exactly in its lane for, say, 100 miles despite the myriad disturbances, mostly invisible, that come and go during the trip. But the driver’s environment doesn’t care whether the car stays on the road or goes wandering off among the sagebrush. The causal explanation requires us to believe not just in one incredible coincidence, but in a never-ending stream of incredible coincidences. To define behavior as a process of control does not require us to explain how this process is brought about: first we define the phenomenon; then we try to understand how it is created. The phenomenon is this: by varying their actions, organisms stabilize certain outcomes of those actions, outcomes that would otherwise change with every change in environmental influences on the same outcome.

The Mechanism of Control The development now turns somewhat technical. The question before us is now how an organism must be organized to produce the control phenomena we observe. The answer to this question has, in fact, been known for some 50 years. If independent external causes cannot account for behavioral changes that control consequences, we must look for the causes elsewhere. The solution of this problem was found by engineers who studied certain types of human behavior in order to replicate it in a machine. The resulting machines were called control systems. The missing factor, these engineers discovered, was that the control system must sense the very consequence or outcome that is to be placed under control. The external cause of control behavior is the outcome itself -- the effect. The cause and the effect are identical. The cause is not independent of the effect. The basic arrangement of a control system is simple. A sensor reports the state of the controlled variable as a correspondingly variable signal, inside the control system. This signal is compared against a

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reference signal carried inside the system, and the discrepancy is represented by still another signal, the error signal. The error signal is amplified to produce a physical output, which in turn acts on the same controlled variable. This is the famous feedback loop, the feedback being negative in that any change anywhere in the loop propagates all the way around the loop to arrive at the starting point with the opposite effect. Properly speaking, feedback is a property of the entire closed loop, not of any one part of it. When such a system is properly designed (not a particularly difficult task if the system is simple), the result is not quite what may have been expected. The basic effect is that the sensor signal is held very actively in a match with the internal reference signal. If the controlled variable is disturbed, the beginning of the change due to the disturbance causes a slight departure of the sensor signal from the reference signal; an error develops, which, highly amplified, produces action. The action, simply because of the way the negative feedback loop is arranged, tends to force the controlled variable back toward its undisturbed state, and thus tends very strongly to force the sensor signal back toward a match with the reference signal. Almost as an afterthought, this action opposes the effect of the disturbance. The only generally correct way to describe the action of a control system is as a system in which all influences are in continuous equilibrium all around the closed loop. Applying a disturbance to the controlled variable results in an immediate rebalancing of the equilibrium, the action changing as the disturbance changes, so that the sensor signal is never allowed to depart much from the setting of the reference signal. Intuitively, we want to think of this circle as a sequence of events going around and around. Intuition, in this case, is simply wrong: it is attempting to treat the closed loop as if it were a lineal temporal sequence, and that does not work. Only the mathematics of control theory (or hands-on experience with control systems) can show the essentially simultaneous action of all parts of the system. Intuition must be retrained. If anyones intuition objects to the idea that mathematics can help it, the proof that it can is to be found in a basic property of control systems called "loop gain." Loop gain is the amount by which any variation is amplified as its effects make one complete trip around the loop. Real control systems normally have loop gains amounting to a factor anywhere between 10 and one million. In other words, the effect of a small change in a variable upon itself (via the closed loop) is a

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change from ten to a million times as large as the original, and in the opposite direction. Intuition, of course, predicts disaster. Instead, there is control. One must simply learn control theory to understand how this result can occur. Nothing in our intellectual training has prepared any of us to reason out, unaided, how control systems work. The principles involved, although 50 years old, are unknown to almost everyone but engineering specialists. Using the principles of control theory, engineers have built machines that behave exactly in the way organisms behave. They automatically vary their actions to bring about and maintain specific predetermined consequences of those actions, counteracting disturbances without any specific instructions to do so. They produce consistent outcomes by variable means: they behave just as William James said organisms behave. That is no coincidence: they were modeled on the behavior of organisms, and the engineers who invented them succeeded, serendipitously,in finding the first workable model of a behaving organism.

The Appearance of Control Behavior When an engineer builds a control system, providing a reference signal for it is just a matter of introducing a signal generator into the system. The source of reference signals in organisms is not quite that easy to explain, but we do not need to account for the presence of reference signals to understand their effects. For all practical purposes, reference signals function exactly as intentions are supposed to function. The reference signal specifies an intended state of the sensory input. Action is based at all times on the difference between the sensory input and the reference signal. The action, having a polarity opposite the detected difference, serves to reduce or negate that difference. This negative feedback first brings the external variable to the specified state, and then keeps it there, all the while creating actions that oppose any disturbances that might also act on the variable. Thus completely without any predictions and certainly without any influence of the future on the present, the control system’s reference signal determines the outcome of action. The action of a control system makes its sensory representation of an external variable match its internal reference signal. If that internal reference signal changes, the same organization will force the sensed variable to change in the same way, maintaining the match between sensory representation and reference signal. Thus whatever can vary the

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reference signal can cause the external variable to vary in the same way. The behavior of the external variable is then no longer what it would have been with the control system, the organism, absent. Normal physical influences are treated as disturbances, and cancelled by variations in the output actions of the control system. The external variable affected by the action behaves as the reference signal specifies, not as the environment otherwise would make it behave. Reference signals clearly have something to do with the phenomenon we intuitively recognize as volition. The simple alteration of a signal inside the system causes an external variable to behave in a corresponding way. But this causal connection is anything but straightforward, because the motor outputs that appear not only must bring the variable to the right state, but must show added variations that are needed to counteract the effects of unpredictable disturbances. In a great many situations, the outputs required to keep a variable under control are small and even trivial -- or would be, if disturbances were not present. Disturbances, however, are almost always present, and even in perfectly normal environments they have large influences on the variables we are controlling. A driver in a precisely-made car in perfect condition on an absolutely level road would scarcely need to steer at all -- the efforts involved would be miniscule. But if the road tilts and the crosswind blows, or if the car pulls spontaneously to one side, the driver must start exerting significant efforts, efforts that are needed simply to oppose disturbances. Because these efforts do occur, the controlled variable is kept from changing; it obeys the intention, not the disturbances. The logic of control shows us that there are really two major kinds of relationships going on at the same time. One is the relationship between the reference signal and whatever it is that is being controlled. The behavior of the reference signal determines, through feedback effects, the behavior of the controlled variable. At the same time, however, there is another relationship between the system’s actions and independent environmental disturbances. Every disturbance calls forth a change of action that is quantitatively equal and opposite to it, in terms of effect on the controlled variable. We know that this apparent relationship is really the result of small errors induced by the disturbances, errors that are highly amplified to become opposing actions. If we did not have that model of a control system in mind, the appearance would be that the disturbances are directly causing the actions, and the stability of the controlled variable would be just a lucky break for the organism.

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We therefore have a dual causal relationship that is seen in the behavior of every control system. The actions of the system appear to be determined largely by external forces that disturb the controlled variable. At the same time, the state of the controlled variable appears to depend only on the will of the control system, which we now recognize to mean on the setting of a reference signal inside the system. The controlled variable remains close to the state specified by the reference signal. We see the arms of the driver urging the steering wheel continuously to the left and right in an apparently random pattern, a pattern we could eventually trace to crosswinds and other variable influences on the car. But the car itself continues its course undisturbed, remaining on the line that the driver intends. What the car is doing seems to be almost unrelated to what either the crosswind or the driver’s arms are doing. These two seemingly different kinds of causal relationship are really just aspects of the way one system behaves in relationship to its environment. Control theory removes the duality, showing us what is really going on. But while it does that, it also explains why we see two different kinds of causation in behavior, external causes and, less obviously, internal causes. The reference signal is the internal cause, and what it causes is the outcome of behavior. The sum of all disturbances is the external cause, and what it causes is the action, or most of the action, that stabilizes the outcome. Control theory thus shows us how it is that outcomes can be voluntary while actions are involuntary ( a nice summing-up that is due to Wayne Hershberger). Once we have this picture clear, we can understand how the driver can intend for the car to stay on the road, and carry out that intention, while being unable to predict or choose the forces his own muscles apply to the steering wheel while bringing about the intended result. When the driver elects to control the position of the car, by that very choice he elects to let the wind and a dozen other invisible disturbances determine his motor actions.

A Hierarchy of Control Motor behavior involves the operation of hundreds of control systems, each associated with controlling the force applied at the attachments of a muscle. Many others sense and control muscle length. But these elementary control systems are not the end of the story: they are used in turn by systems of higher level, which control variables much farther removed from the nervous system. In the example of the driver,

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the muscle-force control systems are employed in the larger control loop that involves the steering forces applied to the car, the position of the car on the road, and the visual images that tell the driver about that position. In order to control the appearance of the scene in the windshield, the driver’s primary way of sensing the car’s position, the driver’s brain must compare the scene as it actually is with a reference image (or, if not literally an image, some internal information relating to the visual field). The mismatch between what is sensed and what the internal reference specifies is the basis for exerting forces to the left or right, or for not exerting forces on the steering wheel. The higher-level control loop does not operate the muscles directly; instead it varies reference signals sent to the muscle- force controlling systems (according both to this control-system model and to neuroanatomy). Those control systems automatically make the sensed forces match the reference signals, in the process generating physical forces on the steering wheel. There are probably more than just these two layers of control involved in steering a car, but these two will get us started. The reference signal specifying the car’s intended position is itself variable: the driver is not stuck forever in his lane. When the driver overtakes a slower vehicle, we observe that at some point the car veers left and takes up a new path in the adjacent lane until the vehicle is passed; then it swings back and resumes its former position. In a stiff crosswind this can be an exciting encounter as the car passes into the lee of the other vehicle; at that point the steering effort that has been counteracting the crosswind suddenly makes the car lurch toward the other vehicle, and the steering effort has to be relaxed -- and then proves insufficient as the driver’s car pulls ahead, into the crosswind again. But most drivers manage to pass another car or a truck in a way that seems effortless to an onlooker who does not feel the fluctuations in steering efforts. This passing-event required that the reference position for the visual-motor steering control system be changed for a while, and then changed back. But following the logic of control, we do not ask so much about these changes as about what remained constant because of them. What remained constant was the car’s progression toward its destination. There is no one generic answer to the question of what remains constant -- the driver might be trying to maintain a constant estimated time of arrival, or might just be trying to maintain a good average speed for some unexamined reason. Keeping the speedometer at a certain reading would

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be part of maintaining an average speed, but going around a truck instead of ploughing into its rear is also necessary. Voluntary and involuntary aspects of the behavior shift their roles as we consider higher levels of control. If the driver chooses to exert a specific sensed force on the steering wheel, he has no choice but to create a certain amount of contraction in his muscles. If he chooses to keep the car in a specific position on the road, he has no choice but to set the muscle-force reference signal at whatever level is required by disturbances of the car’s path. In effect the crosswind and other disturbances are determining the setting of the effort reference signal, given the intention to stay in the lane. And now the intention regarding the car’s position relative to the road has to be changed if the forward progress is to remain the same: the presence of the other vehicle makes the changed position mandatory, given the intention to maintain forward progress. Again we ask, what is this forward progress for? Presumably, the driver is not astonished to find himself driving a car down a road: he is going somewhere, perhaps intending to arrive in time to meet someone for lunch. The intention of arriving at a particular place at a particular time has put him on this road, in this car, going at this speed. However, if the perception of arriving in space and time as intended is to be maintained, the reference signal specifying forward progress has to be varied: it must have varied in order to get the car onto this road in the first place, and sooner or later it must vary in order to enter the driveway of the restaurant. To maintain the pattern of the whole trip in the intended form, the driver must periodically vary the intention regarding forward progress, and in the precise way dictated by the starting point, the time on the dashboard clock, and the location of a free parking slot at the destination. The reason for having made and now having kept this lunch date is for the driver to sell a house to the person waiting for him. The driver intends to sell this house. If someone else had called him to ask about it, he would have made a different trip, perhaps not even in a car, and he would have gone to a different destination, perhaps not for lunch. That is because once he has selected the reference condition of selling a house, he has to go wherever a buyer can or will meet him. There is no other way to give his pitch to the prospective buyer: he has no choice. As it happens, our driver was trained as a physicist specializing in nuclear power plant design. Why is he so intent on selling this house? And why was he so intent last week, and why will he be the same next

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week? Because selling houses is now his only means of making money, the demand for new nuclear power plants having slackened dramatically. This means of making money presented itself, and as he intended to make a reasonable living and no comparable opportunity was found, he had no choice but to take the job. This was the only available occupation that promised to provide the amount of money he intended to make. The intention to make $50,000 per year instead of, say, $25,000, can be traced to the fact that when he lost his job as a power plant designer, he consoled himself in a foolish manner and is now required to pay $25,000 per year in alimony. Actually, his simple needs would be met quite well on $25,000, but the negative $25,000 disturbance due to the alimony required him to set his salary goals correspondingly higher, so he can net enough to provide a sufficient living for himself. Obviously, he intends to make a sufficient living, as he thinks of it, but that intention, plus the disturbance, leaves him no choice but to earn twice as much as he needs. We can now see that it is the alimony disturbance of the driver’s income that explains why, at 11:48:37 this morning, he was exerting a 1.2 kilogram-meter torque to the left on the steering wheel, steering the car to the right around a curve in that ubiquitous crosswind. The highestlevel goal -- plus dozens of external disturbances at several intervening levels of abstract intentions -- required that effort at that time. If we were to carry out this sort of analysis with a real person, we would arrive eventually at levels of intention that would be very hard to trace any higher. Perhaps there is a highest level, having to do with control of abstract concepts like a self, relationships to a society or a family, loyalties to knowledge or culture or religion. Where the highestlevel reference signals come from is an interesting question, but not germane here. The central point of this imaginary excursion up the levels of control is that volition and necessity are not simple matters. It is rather arbitrary to select a momentary intention and treat it as if it came from nowhere and served no higher purpose. It is especially risky, in talking of the will, to talk of free will. What seems free will at one level of analysis is a necessary adjustment to external disturbances at another level. There is nothing wrong with identifying the sense of volition with reference signals in a hierarchical control-system model of the brain. That may well be a correct identification; it is certainly functionally and scientifically plausible. But in order to understand how voluntary and

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involuntary behavior interact, we must think of the entire hierarchy, not just one slice out of its middle.

The Web of Intention Even at the lowest level in the human behavioral hierarchy there are control systems, systems that maintain muscle forces, as sensed in the tendons, at levels specified by signals descending the spinal cord from the brain. Those descending signals, while acting as first-order reference signals, are also the actions of higher-level control systems concerned with controlling more abstract or general variables. There must be many major levels of control, perhaps ten or more, in the human nervous system and brain. At the lower levels we have systems that sense and control effort vectors in space, that employ these vectors to control bodily configuration, that vary congifuration reference signals to control movements or transitions. At still higher levels the configurations and movements become the familiar events we recognize as acts, and those acts are maintained in relationships involving many acts and many external objects and events. On top of these levels are all the cognitive levels, in which the world of experience is classified, analyzed symbolically and logically, abstracted to become principles and generalizations, and finally made into coherent concepts like the concept of a self, a society, a science, a material world. Control occurs at all of these levels, each level acting to control its own kind of perception by means of varying the reference signals, which we experience as volition, reaching lower systems. While it may be that human beings control what they experience in terms of certain broadly shared types of perception, the variety of human experiences, circumstances, preoccupations, and problems tells us that within these broad classes, the structures of control that individuals build up as they mature are highly idiosyncratic. It is no simple matter to manage a world that begins as millions of identical sensory signals, and is then subject to multiple levels of interpretation that must, for the most part, be worked out in private and without the aid of an instruction manual. It is no simple matter to discover how one part of this world can be controlled without negating the control of another part of it, at the same or a different level. The high-school senior understands that by going to college and submitting to at least four more years of school, he will be able to enhance his personal power and self-respect, to raise children in comfort, to feel a part of his conception of a larger world.

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But if he chooses that intention, he will have to tolerate continued supervision by his parents and others, he will have to leave behind the girl he loves, and who will take care of his cat? The loss of volition sensed by the adolescent -- and many who are much older -- is not really a loss of volition, but a gradually expanding network of self-contradictions, a consequence of ignorance about how we work. The physical world and the society into which we are born only set the stage on which our lives are played out: they do not limit our freedom, but simply constitute the means available to us for doing whatever we can make sense of doing. It is up to each of us to learn how to act on and in that world, to learn to perceive its possibilities, and to learn how to organize our intentions regarding that world. Through the miracle of communication each person can learn from the others, but if there are no others who understand human organization, the amount of help available is going to be small. People are very free with advice, but as advisors tend to contradict each other, the useful residue is not as useful as it might be. Look before you leap -- or nothing ventured, nothing gained? Beneath the fuzziness of personal experience there lurk some hard natural laws. The process of control itself, at any level, requires that certain mathematical relationships in space and time be properly established. Fortunately we seem to have the capacity to reorganize until we achieve skillful control. But there are even harder laws. Given a body containing about 800 muscles (depending on how they are counted), it is mathematically impossible to establish control of more than 800 independent variables of experience at the same time. The degrees of freedom of control cannot exceed the degrees of freedom to act. And actually to be able to control that many variables at once, one would have to solve 800 nonlinear differential equations in 800 unknowns. It is unlikely that the nervous system -- even the nervous system of an engineering mathematician -- would be able to realize anything near that potential. And that takes into account only the second level of control. Now we must consider that the variables of the second level, already abstracted once from raw sensory inputs, are abstracted again to yield a new type of experience, and thus a whole new set of potentially controllable experiences. And this adding of new modes of control at new and ever more abstract levels must continue for at least some respectable number of levels. In every case, at every level, the same mathematical problem

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exists: how to partition the universe of experience so that its parts can be independently controlled without self- contradiction; without conflict. This whole hierarchy of control contains a network of intentions that represent the actions of the control systems above the first level. When, inadvertently, the intentions cancel each other before they can produce any action, we feel a loss of volition, a paralysis of the will. At the highest levels our intentions are reasonably clear, but the the lower levels they may demand contradictory intentions, and so produce none at all, or only an unsatisfactory compromise. We easily become lost in the complexities of managing this physically compact but functionally gigantic structure, the human brain. How many of us could sit down and draw a map of our structures of intentions? Most of us could probably explain fragements of the structure here and there: this act serves that purpose, which in turn was selected as part of satisfying a higher-level intention, and so on for perhaps three or four levels at the most. A few of us might be able to show how the goals we seek at work relate to those we seek on weekends, or how our relationship to our parents interacts with our relationships to our wives and children. It is unlikely that any person alive could draw the whole map, even considering just the parts of it that are actually available to inspection. When we consider our own lives, we see them as if through a moving peephole that limits the size of the picture visible at a given moment, or as if we are shining a penlight around in a dark cathedral, trying to build up a picture of the whole huge room out of images that pass through the small circle of light. The sciences of life, being founded primarily on the old causal model, have little to tell us about understanding the vast structure of the mind. Having long ago dismissed the importance of phenomena such as volition, they have produced essentially nothing that would help us to map out our own organizations, either to understand or to improve them. Control theory, on the other hand, seems to show us the way toward doing something useful in this direction.

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CHAPTER 3

ON THE WILL: AN HISTORICAL PERSPECTIVE Eckart Scheerer Why did the will depart from modern psychology, to be resurrected, in this volume, under the title "volitional action"? Howard and Conway (1986) claim that the demise of the will was caused by the principles of extrospection, rational objectivity, and determinism, taken over by psychology from the physical sciences as a result of the "Baconian revolution." If volitional action is identified with the "free will" as postulated in ethics and theology, then it comes, indeed, into conflict with the principle of determinism and perhaps also of objectivism. From a psychological viewpoint, though, volition can be studied independently of the free will concept, and, in fact, it continued to be a subject of psychological study long after psychology had taken over the methodological standards of the physical sciences. Consequently, the story of the will's demise has to be told in different terms than those chosen by Howard and Conway, the more so because it was a tragedy with dramatic peripeties rather than a simple though perhaps protracted "decline and fall." In approaching the topic of volition from an historical perspective, we are struck by the variety of meanings attached to the term and its derivatives in the Western languages. As far as I see, at least three different basic meanings can be discerned. First, there is a class of movements that are conventionally called "voluntary," to distinguish them from "involuntary" movements such as reflexes or instincts. Second, we have a class of actions mediated by processes such as deliberation, decision, and choice, and opposed to more "impulsive" actions. And third, we have a mental faculty or subsystem called "the will" which is presumed to subserve voluntary movements and volitional actions, and may occur in various degrees of intensity or "will power." In order to understand the heterogeneity of the phenomena (or constructs) subsumed under the category of volition, we need to have a brief look at the philosophical antecedents of the concept.

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The Concept of Will: Its Philosophical Background Consider a student in one of the old European universities taking an exam at any time between the 13th and the 18th centuries. His professor confronts him with some easy questions. How many basic mental faculties or "powers" are there? Two, of course, cognition and desire (or appetite, or conation). What is the will? Rational desire. M a t is more important, the intellect or the will? The intellect, because willing occurs only in creatures that have an intellect; also, because volition depends on cognition but not the other way round. To what province of philosophy does the study of the will belong? To natural philosophy (physics) as well as to ethics; in physics we study the movements subserved by the will; in ethics we study the means and ends of volitional (i.e., purposeful and rational) actions. Our fictitious dialogue reflects the core of the received opinions about volition in the West, beliefs that were in a large measure due to Aristotle; that is, beliefs that outlived the Aristotelianism of the middle ages, even after it had been superseded by the "modern," experimental, mathematically oriented science of Descartes, Galilei, Kepler, and their followers. Aristotle had written about volition in his ethical works, but also from a perspective we would today call "biological," in his work On the Soul and in his little book On the Movements of Animals (Nussbaum, 1978). He said more about volition than was sketched in our dialogue. For instance, he was the first to distinguish clearly between voluntary and involuntary actions. Actually, he had even a tripartite division; involuntary movements (e.g., of the heart and of the genitals) were under the control of sense perception but not of thought, while non-voluntary movements (such as sleep/waking and respiration) were devoid of any such control. As far as the will was concerned, its assignment to a mental faculty different from cognition was motivated by its affinity to movement, its dynamic character, and its dependence on practical as opposed to theoretical reasoning. Aristotle also gave much attention to the cognitive processes involved in volitional action. His most influential ideas were the distinction between deliberation (in which we can wish impossible things) and choice (which pertains to the possible only), the assignment of freedom to the act of choice, and the conception of the "practical syllogism," which contains two premises (a general rule and a specific case) and the action itself as the conclusion. From late antiquity on, and for more than a millennium, Aristotle's analysis of volition remained a model to be improved and filled in with

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more detail, but not to be repudiated in its general outline. In Thomas of Aquinas we find an elaborate scheme of the "top-down" control in volitional action, encompassing judgment, will in the narrow sense, intention, deliberation, consent, choice, and even some kind of anticipated reinforcement; at the bottom of the hierarchy stands a simple "command" to the body, which then utilizes this command on its own account. To be sure, there were controversies around the will in the scholastic period. For instance, Duns Scotus assigned priority to the will rather than to the intellect, and he thought that the will intensifies and clarifies ideas which are in the background of consciousness; but he considered the will to be a rational faculty (Wolter, 1986), and so he stayed in the traditional "cognitivist" perspective on volition, despite his "voluntarism." The philosophers of the scientific revolution and the empiricists and sensualists of the 18th centuries may have ridiculed Aristotle, but they did not doubt his basic presuppositions such as the duality of cognition and volition, the rationality of volition, and the power of the will to move the body. Fundamentally new perspectives on the will arose only in the second half of the 18th and in the first half of the 19th century. One of these was the replacement of the dichotomous classification of mental processes by what Hilgard (1980) has called the "trilogy of mind," that is, cognition, affection, and conation, or thinking, feeling, and willing. The trilogy of mind was "dogmatized" by Immanuel Kant (1781) who drew upon developments in English philosophy and German empirical psychology which had resulted in the introduction of feeling as an independent class of mental phenomena. (In the Aristotelian scheme, feeling had been a concomitant of every mental process). In itself, the trilogy did not mean a deposition of the will; for instance, Kant himself still accepted the traditional definition of willing as an "appetitive faculty based on reason" (1781, p. 38). But it carried the potentiality of assimilating the will into the affective, emotional side of mental life. In turn, this could mean that the will was separated from reason and turned into an irrational factor of mental life. Another development was the emergence of a new voluntarism around the turn of the centuries. Maine de Biran, subsequently called the "Kant of France,'' conceived of the will as the basic force in mental life responsible for the emergence of the dualism between subject and object, or Ego and Non-Ego. In "immediate apperception" (i.e., introspection), on which Maine de Biran founded his psychology, the will is represented as a feeling of effort, which in turn is signalled by the muscle sense (sens musculaire). Like the German philosopher J. J. Engel, who

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had introduced the term "muscle sense" in 1802 (the priority usually given to Charles Bell or Thomas Brown is wrong; see Scheerer, 1987a) Maine de Biran appealed to the muscle sense in order to explain the formation of the concept of force through the resistance we encounter in the active handling of objects. Neither Engel nor Maine de Biran were concerned with the question whether the muscle sense was efferent or afferent. However, their descriptions permit the inference that they were primarily concerned with a correlate of the "effort of the will" and thus with an efferent impulse, although James (1880/1983, footnote 22) believed that Maine de Biran was referring to afferent impulses. Actually, James was projecting back a distinction not relevant to these earlier thinkers because the afferent/efferent distinction became obligatory only as a result of Charles Bell's (1826) work resulting in the law named after him and Magendie. Maine de Biran was not the only voluntarist in the first half of the 19th century. Apparently independent of him, the German philosopher J. G. Fichte derived the Ego/Non-Ego dichotomy from the experience of activity, but unlike Maine de Biran he did not consider himself a psychologist and was not interested in physiological or anatomical questions. A similar comment pertains to the metaphysical voluntarism of Schopenhauer. While important in the history of philosophy, these thinkers had little influence on empirical psychology. Concepts like "feeling of effort" and "muscle sense," on the other hand, had a profound influence on the emergent scientific psychology of the 19th century, and though they were initially formulated in the context of voluntarism, eventually they led to the demise of the will as an independent category of psychology.

Spontaneity, Innervation Sensations, and Reaction Times: The Will in Early Experimental Psychology It is well known that experimental psychology started with the investigation of sensations. However, this choice had primarily methodological reasons--among all mental processes, sensations were most easily amenable to experimentation--and did not necessarily imply a philosophical orientation toward sensualism and empiricism. In Germany, where experimental psychology originated, British empiricism and French sensualism generally were held in slight regard; neither philosophy belonged to the philosophical presuppositions of, for instance, Fechner and Wundt. Even Helmholtz, the one pioneer who had a high opinion

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of British philosophy, had a place for the will in his theory of perception. This is perhaps not so surprising if we consider that Alexander Bain, the chief systematizer of British association psychology, wrote a book entitled The Emotions and the Will and accepted the Kantian tripartite division of the mind. Until around 1880, the 'hew psychology" still accepted the concept of the will. Let us look at some details. One component of the will concept is that it is an inner determinant of behavior. In order for an impulse of the will to be generated from within, there must be some spontaneous activity of the nervous system. In the middle of the 19th century, the concept of spontaneous activity was not considered to be incompatible with a scientific outlook on psychology. Three examples will suffice. In 1859, Bain drew up a list of evidence for the spontaneity of movement, encompassing awakening (where movement was supposed to precede sensation), the activity of young animals in general, and certain temperaments where activity was stronger developed than sensibility. In 1888, he still summarized his position thus: "Movement precedes sensation, and is at the outset independent of any stimulus from without" (Bain, 1883, p. 303). In 1860, Fechner built his psychophysics on the notion of oscillatory "psychophysical excitation," which he conceptualized as being endogenous and modulated, rather than elicited, by external stimulation (Scheerer, 1987 b). And in 1863, Wundt declared that (spontaneous) drives were the primordial form of mental activity and the base from which both representation and volition were derived. During the same period it was generally assumed that at least some perceptual phenomena required the participation of efferent processes. The idea was a logical continuation of the "feeling of effort" concept developed within the framework of philosophical voluntarism, but it was now applied to the explanation of phenomena observed and occasionally measured in the laboratory and under clinical conditions. Efferent impulses subserving perception were called by Wundt, in 1863, "innervation sensations" or "innervation feelings"; other authors (e.g., Helmholtz) linked them more explicitly to the will by using terms like "effortloor "impulse of the will". Unfortunately, for the sake of terminological clarity, many French authors had a tendency to apply the term "muscle sense'' to efferent processes. Bain (1855) spoke of "outgoing1' (as opposed to "ingoing," i.e., afferent) impulses, a usage quite near to the current "outflow" vs. "inflow" terminology. Innervation sensations (see Scheerer, 1987a, for a fuller treatment) were invoked in four different contexts: (a) the stability of the visual

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world despite a moving retinal image produced by active eye movements, (b) differences between active and passive appreciation of weights, (c) clinical data from anaesthesia, paralysis, and amputation, and (d) the effects of paresis of eye muscles. Despite wide variations of individual viewpoints, the theoreticians of innervation sensations shared two common assumptions: The motor impulse originating in the brain (a) is available to consciousness, and (b) it somehow combines with afferent impulses to produce a given perceptual phenomenon. The need to postulate innervation sensations arose whenever the afferent excitation pattern was ambiguous and its perceptual effect depended on the absence vs. presence of voluntary movements (or the intention to produce them) on the part of the observer. Let us clarify this statement by adducing a classical example--egocentric visual localization. How do we determine, on the basis of the retinal image, whether seen objects are in movement or at rest? Johannes Miiller (1838) formulated three rules: (a) Movement of the retinal image results in perceived movement when our eyes and our body are at rest. (b) When we follow a moving object with our eyes and as a consequence its retinal image does not move, then we use "either the sensations from the moving eye muscles or the impulses sent to the eye muscles from the sensorium" (p. 363), to judge that the object moves. (c) When both the retinal image and the eye muscles move in correspondence with each other, then we judge that the object is at rest. Thus, Miiller accorded the centrifugal impulse a role in egocentric visual localization, but not to the extent of excluding the afferent impulses originating from eye movements, The scale tipped in favor of an efferent explanation (i.e., by means of innervation sensations) when it became clear that passive movements of the eye (produced by applying pressure to the eye ball) and the mere intention to move the eyes in the absence of actual eye movements (in cases of eye muscle paresis) resulted in perceived visual movement, albeit in a direction opposite to each other. The relevant observations had been made briefly after 1850, and for about a quarter of a century everybody (e.g., Wundt, 1863; Helmholtz, 1867; and Mach, 1886) was convinced that active (voluntary) and passive movements differ from each other with respect to their perceptual effect, and that these differences can and must be explained by the match or mismatch between the efferent impulse (i.e., innervation sensations) and its reafferent effect (e.g., the movement of the retinal image). A final research domain in which the will figured prominently was the fractionation of reaction times into stages, a practice that had been

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started by Donders in 1865 (Brozek, 1970). Among the mental operations that were "timed" in this way we regularly find included such traditional components of volition as choice and decision. Wilhelm Wundt considered the reaction time method as a useful technique for measuring the temporal dynamics of the "apperceptive" level of mental functioning. Because apperception to him was an internal act of volition, he assigned the study of reaction times to the section on the will in his Grundziige der physiologischen Psychologie of 1874.

The Demise of the Will: Reflex Physiology, Evolution Theory, and Neurology It may be said that the pioneers of experimental psychology took the will for granted. That is, they used the will in their explanations of other mental phenomena, rather than analyzing it in its own right. The downfall of the will began when it was converted from an explanatory concept into a subject matter of independent investigation. This development was not intrinsic to psychology but depended on the ascendancy of reflex physiology, evolution theory, and clinical neurology. The contributions of these disciplines may be briefly summarized as follows. For methodological reasons, the study of reflexes was for a long time restricted to spinal animals, particularly the decapitated frog. However, around 1860 a breakthrough was made in that the effects of brain stimulation on spinal reflexes were studied. The Russian physiologist Sechenov, who was one of the first to work along this line, in 1866 published a monograph entitled The Reflexes of the Brain, in which he asked for the application of the reflex arc model to all kinds of mental phenomena and, inter uliu, described volition as a reflex arc where the first, afferent, part was inhibited. Sechenov was perhaps the most vociferous spokesman of a general trend toward assimilating psychology into reflex physiology, a trend which tended to relativize the distinction between the brain (as the seat of voluntary action) and the rest of the central nervous system, and asked for an analysis of voluntary action in terms of its sensory antecedents. Traditional boundaries were also washed out by evolution theory. Ever since Aristotle had tied volition to intellect, creatures lacking reason were supposed to be incapable of volitional action. The very notion of instinct originally conveyed the idea that God or Providence had provided animals with special gifts for purposeful action in order to make up for

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their lack of reason. In the Cartesian tradition, where animals were even denied a soul, they were a fortiori devoid of volition. Stressing the continuity between brute and man, Darwin and his followers did away with the assignment of instinct to animals and of volition to people. Rather, the task was now to derive volition from various forms of involuntary actions (reflexes, drives, instincts) by means of a genetic analysis. Finally, clinical neurology (and psychiatry; the two disciplines were not separated in the period) tended in various ways to obliterate the clear demarcations contained in the traditional picture of the mind and its bodily substrate. Two somewhat disparate instances were particularly important. The first pertains to the interrelations between sensation and movement as revealed by neurological disorders (see Scheerer, 1987a, for more details). Motor disturbances were shown to have sensory causes; for instance, ataxia (on the face of it a purely motor disorder) was shown to result from damage to the sensory tracts of the spinal cord, and thus the importance of sensory feedback from the muscles for the control of movement was stressed. The second line of attack arose from the preoccupation of neurologists with hypnotism (or "somnambulism," as it still was called by some). Either during trance or as a consequence of post-hypnotic suggestions, hypnotic subjects displayed voluntary behavior in the absence of the subjective experience of volition. Once again, the dividing line between "voluntary" and "involuntary" seemed to become fuzzy. Taken together, these developments resulted in a "paradigm shift" in the psychology of volition. The beginning of the shift is indicated by publications such as G. E. Muller (1878), Ribot (1879), James (1880/1983), and Schneider (1880; 1882), and its consummation by Munsterberg (1888; 1889) and James (1890). It comprised a genuine shift of perspective; the will was now seen as a result of sensations and images, while before sensations and images had been made dependent on the will. As a result, the will lost its status as an independent element of mental life. Let us briefly look at some details in terms of the concepts introduced in the previous section. How could voluntary actions fall under the control of sensations or images? The detailed answers to this question varied somewhat among the proponents of the paradigm shift, but the general outline was always the same (Hildebrandt, 1985). It appealed to a "forward movement'' of the sensory consequences of actions. Suppose that the original motor equipment of the mind consists either in reflexes or in spontaneous

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movements. In either case, the execution of the movements will give rise to movement sensations. The movement sensations are associated with the conditions under which the movement was made, and, if these conditions are reinstated, they elicit the movement sensations but now in the form of an image of the movement, which in turn elicits the movement itself. Thus, consequences of actions became antecedents of actions, and movement sensations were converted into images, representations, or expectations of past movements. As a result, volitional action was no longer spontaneous or inner-directed but depended on the previous occurrence of some sensory or imaginal event; and the will was assimilated into the associative network of mental life. The process just described bears surprising similarity to modern accounts in terms of Pavlovian or operant conditioning, but it was a theoretical construction and did not rest on laboratory evidence on the learning process. Consequently, it was confronted with the factual question of whether movement images had, indeed, the power to elicit movements. An affirmative answer to this question was provided by the principle of ideomotor action. Introduced by Carpenter in 1852, the principle initially was meant to provide a naturalistic explanation for seemingly paranormal phenomena such as table lifting. Carpenter made it clear that ideomotor action was involuntary and under normal conditions was inhibited by the will. However, also in 1852, Lotze drew attention to everyday phenomena such as the involuntary imitation of seen movements and the automatic nature of many everyday actions such as walking. Such movements, he thought, were initiated by motor images, and he ventured the suggestion that "more complicated series of movements (even those comprising the content of a crime)" were initiated in this way (Lotze, pp. 294-296). Volitional action was reduced to the voluntary combination of involuntary elements. Subsequently, among psychologists and psychiatrists the conviction that "every representation of a motion awakens the actual motion which is its object, unless inhibited by some antagonistic representation simultaneously present to the mind" (James,1880/1983, p. 103) became so widespread that James could use it as one of the cornerstones of his theory of the will. What became of innervation sensations once motor images had been recognized as antecedents of voluntary action? They were no longer needed and fell victim to Occam's razor; or, to paraphrase William James (1880/1983), on a priori grounds alone they were a "pure encumbrance'' (p. 88). On the other hand, even James felt the need to base his argument against them on a posteriori evidence also. Two basic lines of

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reasoning were put forth by him and others, such as G. E. Muller (1878). First, given that innervation sensations were needed to disambiguate afferent input patterns, they would become superfluous if, under conditions in which they were invoked, the afference in fact was not ambiguous. Thus, in semiparesis of the eye muscles the healthy eye was still able to move, and it did so even when it was occluded. Consequently, the afferent situation was not ambiguous and evaluation of eye position could be done on the basis of the healthy eye. In modern terms, there is a mismatch not between efference and retinal re-afference but between two sources of afference (retinal and proprioceptive). Second, in cases where afferent information was lacking altogether or no sensory source for disambiguation could be found, appeal was made to expectations concerning the movement. Thus, paralytics felt that their paralyzed limbs were heavy because they expected them to move when they wanted to move them. Expectations were different from innervation sensations because they were based on memory images or traces of earlier afferent impulses. The fractionation of reaction times (a topic which James did not touch in his discussion of the will) was the last stronghold of the will as an independent mental element. Ironically, their downfall was initiated in Wundt's own laboratory, when his student L. Lange showed, in 1888, that simple reactions were faster when attention was paid to the movement ("muscular reactions") rather than to the stimulus ("sensorial reactions"). Muscular reactions were interpreted as brain reflexes, but sensorial reactions and choice reactions certainly reflected the dynamics of representations under voluntary control. This, at least, was the opinion of Wundt himself. Not so, argued Munsterberg (1889). He demonstrated that "muscular" reactions could be produced even under conditions of choice and semantic categorization and concluded that the consciously experienced impulse of the will followed rather than preceded the reaction. His general conclusion was that there was no difference between the involuntary and the voluntary dynamics of cognitive processes, and that the experience of volition consisted in stimulusspecific and generalized ("expectation") sensations of tension and strain.

Three Perspectives on the Will: Miinsterberg, James, and Wundt Around 1890 the case of innervation sensations "was not open and shut" (Boring, 1942, p. 528). Some authors retained the term but

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reinterpreted it such that it now meant the afferent sensations underlying the "feeling of effort." More commonly, it was dropped and replaced by "kinesthesis," introduced in 1880 by Bastian as a blanket term covering motor sensations and images of peripheral origin. Nevertheless, even after the will had lost the status of an independent mental element, there was still the need to explain volitional action in terms of other mental processes. The three main types of "theory of the will" are exemplified by the names of Munsterberg, James, and Wundt. All of them pointed to further developments in the psychology of volition, though later authors were rarely aware of their historical predecessors. The most "radical" (in the sense of reductionist) theory was Munsterberg's (Scheerer, 1984). His initial theory of the will, which earned him his early fame and the call to Harvard, was strictly associationist and "dissolved" the experience of volition into a complex of peripherally excited sensations. In 1900, he switched to a "centralist" theory (the "action theory") in which sensations were supposed to gain access to consciousness only if they were accompanied by a central motor discharge; yet the discharge in question was still instigated by afferent processes, and the whole scheme may be said to antedate the stimulusresponse bond of the behaviorists. More importantly, Munsterberg adhered to a strict epistemological division between scientific psychology and the humanities. All aspects of human experience that relate to active striving and the realization of values were to be dealt with by the humanities; scientific psychology was restricted to the study of conscious contents, as registered by a passively onlooking Ego. Insofar as volition encompassed the experience of an actively striving subject, it could, as a matter of principle, not be studied by a psychology adhering to the methods of the natural sciences. Volition, in the proper sense, was an exclusive subject-matter of the humanities. William James's (1890) chapter on the will is too well known to need a summary here. James succeeded in steering a middle course between abolishing the will altogether and treating it in a speculative and constructive manner, after the fashion of the old arm-chair psychology. The first strand of his thinking is represented by his polemics against innervation sensations and his adoption of the ideomotor principle, the second strand by his mental fiat and his discussion about different types of decision. Moreover, he indulged in the type of theorizing about the "neural machinery" that was so dear to his contemporaries and rendered his theory of the will scientifically respectable. The newly coined term "kinesthesis" allowed him to keep clear of the trappings of the ''muscle

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sense" concept and to subsume all kinds of reafferent sensations under one unitary label. On the other hand, he was probably the first to make a distinction between proprioceptive (Ikesident") and exteroceptive ("remote") reafference and to point out the importance of the latter. Another distinction he made proved to be prophetic. Volition, so he wrote in 1880 in referring to his mental fiat, ''is a psychic or moral fact pure and simple," and 'the supervention of motion upon its completion" belongs "to the department of physiology exclusively" (p. 107). In fact, he himself was perhaps the last to bring about a synthesis of the mental and the physiological aspects of volition, and, after him, the psychology of the will was destined to be either physiological and reductionist or outrightly mentalistic. Wilhelm Wundt's theory of volition presents a paradox. Before pointing out the paradox, it must be said that Wundt was not immune to the criticism of the innervation sensation concept. Although he did not abandon the term, after 1883 he reinterpreted it to bring it more in line with the thinking of his contemporaries. In the final version of his theory (Wundt, 1910, pp. 37-41), and in almost literal anticipation of Teuber's (1966) notion of "corollary discharge," he maintained that there were ''movement sensations of central origin" but interpreted them as resulting from the collateral discharge of motor impulses into neighboring sensory areas of the cortex. At the same time, he denounced James for appealing to some "transcendent, abstract will" in his fiat conception (Wundt, 1911, p. 272). And herein lies the paradox, for Wundt applied the label "voluntarism" to his own psychology. The paradox is dissolved when we notice that he did not consider the will as a particular type of mental element but rather as the prototype of all mental activity. More specifically, he assimilated willing into affective processes, which displayed a typical pattern of build-up and release of tension. Depending on whether relaxation was brought about by muscular movements or by changes in the course of ideas and emotions, Wundt distinguished between outer and inner voluntary actions. Somewhat surprisingly, he assigned genetic priority to inner voluntary action, that is, apperception, where relaxation resulted from bringing ideas into the focus on consciousness by means of inhibitory processes generated in the frontal lobes. From the standpoint of motives, Wundt distinguished between drives (one motive only), voluntary actions in the strict sense (several motives but one gains ascendancy) and choice (consciously experienced conflict between motives). Again, all forms of volitional activity, when analyzed introspectively, dissolved into sensations and emotions; the specificity of the will

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consisted not in the elements, but in their combinations and above all in their time course. Before discussing the continuation of the themes adumbrated by Munsterberg, James, and Wundt, we must briefly look at the final act in the downfall of the will, which proves to be an American tragedy.

How the Will Disappeared from American Psychology When John B. Watson (1913) supplemented his behaviorist manifesto by the analysis of some current psychological concepts, he chose "image and affection" and did not deem it necessary to discuss volition in behaviorist terms. This was no coincidence. The will had already departed from American psychology, and its exile was prolonged but not caused by behaviorism. Watson wanted to open "a free passage from structuralism to behaviorism," and so it is appropriate to look at Titchener's psychology first. Although Titchener posed as a spokesman of Wundt in the United States, he had little use for the latter's psychological voluntarism. In fact, he restricted apperception--the key concept of his master's system--to "attributive clearness" and disposed of the idea that it was an internal act of volition. Furthermore, he was a strict champion of kinesthetic sensations and images which invariably were reported by his introspective observers; and finally, he opposed Wundt's three-dimensional theory of feeling and thus the tension/relaxation dimension on which Wundt's affective theory of the will was based. In sum, in his system of psychology, which in its final version reduced the subject-matter of psychology to sensation, there was as little place for volition as in the behaviorism of Watson. Whatever their differences on other scores, they were united in favor of a strict peripheralism. There was, however, outside of Titchener's structuralism, a more specific development which tended to eliminate essential ingredients of James's theory of the will. First, the "idea of movement" had to go, when Woodworth (1906) concluded, from experiments involving the introspection of the "immediate antecedents" of voluntary movements, that an act may be thought of without any representative or symbolic image. Furthermore, when "kinesthetic images" were reported, they were often quite unlike the movement to which they referred. Woodworth started his work independently of the Wurzburg school in Germany, but when the latter became known to him, he pointed out that he had discovered "imageless thought" in the sphere of volition (Woodworth, 1907). The

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second phase consisted in Thorndike's (1913) attack on the principle of ideomotor action. Thorndike felt that belief in the principle was a mere superstition. In his view, the ability of an idea to produce a movement depended on the laws of habit formation rather than on the "amount of likeness between the members of the pair" (Thorndike, 1914). Woodworth and Thorndike were no behaviorists, inasmuch as they accepted the testimony of introspection. However, even if introspection was not rejected, the "imageless thought" doctrine, as applied to volition, did away with all antecedents of action except habits and current stimulation; and, the demise of the ideomotor principle meant that the relation between action and its antecedents was entirely arbitrary. Behaviorism rested on the rejection of cognitive mediators and maintained the essential arbitrariness of stimulus-response connections; and, in both respects, Watson's "principal contentions" had been prepared by "tendencies initiated by the psychologists themselves" (Watson, 1913, p. 423).

The Resurgence of the Will in European Psychology In the first half of the 20th century European and American psychology drifted apart. There was no behaviorist revolution in Europe, and new theoretical developments were largely indigenous. One symptom of this is that there was a fresh interest in volition that did not have a parallel in the United States. One characteristic feature of German psychology between the two world wars was the emergence of a new psychology based on the humanities @ezkteswissenschafilichepsychologie). Miinsterberg's conception of a bipartite psychology came true in the Weimar period (1918-33), which witnessed a 'krisis" resulting from the conflict between a scienceoriented and a humanities-oriented outlook on psychology. The ''humanistic'' psychologists were not really interested in the classification of mental phenomena, and so they did not discuss the question of the will's independent status. But Wilhelm Dilthey, from whom they derived their inspiration, had endorsed the "trilogy of the mind," and reference to the will was not considered problematic by the humanistic psychologists. Like Munsterberg, they linked the will to the concept of value; volitional action was seen as the "realization" of values which were defined in terms of objectively existing mental structures. Particular emphasis was laid on the typology of value systems, such as the "economic"versus the "aesthetic form of life" (Spranger, 1927), and on the conflict of values in mental development (Spranger, 1928). By stressing the real-life qualities and the

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supra-individual determinants of volitional action, the new psychology based on the humanities provided an important corrective to laboratory investigations of volition. Such investigations were conducted in great number during the Weimar period in continuation of work started before World War I. The protagonist of the flourishing experimental study of 'the will was Narziss Ach. Outside of Germany, he is known best for his first work (Ach, 1905) in which he used the method of systematic introspection in the context of reaction time experiments. One result--the ''presence of impalpably given knowledge," named "awareness" by Ach--belonged to the pioneer demonstrations of "imageless thought" by the Wurzburg school. But Ach was more interested in volition than in cognition, and he spent most of his subsequent career investigating its phenomenological and functional properties (Ach, 1935). To Ach, evidence for a volitional element of mental life rested, in the main, on his demonstration of "determining tendencies," which were supposed to derive from the internal representation of a goal and to direct the course of mental processes in accordance with the goal representation. Initially, Ach described the experience of willing, in somewhat Jamesian terms, as the "mental assent" to responding in consonance with some previously acquired determining tendency. In 1910, he devised an ingenious method for the study of volition: subjects were first given extensive practice with pairs of meaningless syllables and then were required to perform some other activity, such as rhyming or vowel substitution, on the stimulus terms of the previously acquired paired associates. When subjects were switched to the rhyming tasks, there was a strong tendency for the previous learned responses to be emitted, and in order to overcome these (associative) reproduction tendencies, the subjects deployed what Ach called a "primary act of the will." Primary, "energetical" volition was, in Ach's (1910, 1935) view, an irreducible mental state with unique structural and functional qualities. Structurally, it was defined by four "moments": relation to the task, experience of "I really want to do this," pronounced strain sensations, and an effortful attitude. Functionally, it was defined as a means to attain the goal by overcoming inhibitory conditions. The strength of the determining tendencies set up by a primary act of volition could be measured by their "associative equivalent," that is, by determining the maximum number of paired-associate learning trials which did not produce intrusions or prolonged reaction times after switching to the second task. In the final version of his theory, Ach stressed the largely unconscious nature of

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determining tendencies; once a certain task had been adopted by the subject, the selection and control of subsidiary mental processes is performed at an unconscious level. Even the act of willing could become automatized by frequent repetition; automatization was indicated by the lack of interference from a concurrent secondary task. Ach also formulated quite a few quantitative laws of volition; for instance, the ''law of specific determination" (determinations are realized more quickly and safely the more specific they are) and the "law of motivation from difficulty" (increased difficulty results in a spontaneous increase of effort of the will). Ach used to refer to his theory of the will as the "psychology of determination," and this alone is an indication that he did not consider the will to be free. In fact, he contrived an experimental procedure, known as the "prediction method," which allowed the experimenter to correctly predict the choices of subjects under conditions where the subjects themselves stated that they were totally free in their choices. The "feeling of freedom" was a dependent, not an independent variable in his theory. Ach was the most active, but by no means the only psychologist of the will in Weimar Germany. In 1911, the Belgian psychologist Michotte had suggested another method for the investigation of volition, where subjects were given a choice between performing different arithmetical operations; he reported that their decisions sometimes where reached without any sensory or imaginary content (Michotte & Prum, 1911). Subsequently, many German experimental psychologists (including Lindworsky, 1923, the author of a much-read monograph on the will) defined the will in terms of an activity which is experienced as originating from the Ego. From this perspective, Ach was criticized for having introduced extrinsic elements in the theory of the will; the phenomena on which his theory was based could arise from purely associative factors. Another line of criticism centered on Ach's reliance on meaningless materials and strict laboratory experimentation; for instance, Rohracher (1932) collected introspective reports while his subjects were refraining from food intake for a whole day and concluded that in volition, as opposed to drive, the Ego is active. More consequential was the criticism of Ach's methods and theories with which Kurt Lewin (1917, 1922) started his scientific career, for it gave rise to a theory of the will which stressed--like Wundt's theory, but in very different terms--the affective side of volition. Lewin initially was interested in the measurement of will power as proposed by Ach.

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Accordingly, he repeated Ach's experiments with a slight modification: after having thoroughly memorized pairs of syllables, subjects were required to read them and to refrain from attempts at reproduction; there were no intrusions or lengthened reaction times as required by Ach's theory. Other experiments showed that Ach's results could either be replicated or not be replicated on the same previously learned syllable pairs, depending on whether or not they were embedded in a context of neutral syllables. Lewin concluded that neither the "law of association" nor a conflict between reproductive and determining tendencies were operative in Ach's experiments. Instead, the results depended on the dynamics of task-specific sets (such as a recall set or a rhyming set) and the subject's spontaneous adoption of the easier activity when one and the same result could be attained by different activities. Thus, the will seemed to be gone once more, but it was resurrected in Lewin's classical Berlin work on the psychology of affect and action. In the introduction to the well-known series containing the work by Zeigarnik, Ovsiankina, Dembo and others, Lewin (1926) expressed the opinion that the psychology of the will should be approached from a causal-dynamical point of view, instead of focussing on the experiential qualities of volitional acts such as decision and resolve. The central concern was to be the problem of self-control, and this would mean a new approach to the experimental investigation of drive and affect, which were intimately connected with the problem of self-control. The "dominant theory of the will''--Lewin here referred to Ach, of course-was wrong in assigning central importance to the coupling between goal representations and the occasions for the execution of actions corresponding to them. Such a coupling should increase in strength upon repeated occurrence of the occasion; but once I have thrown a letter into a letterbox, I will not repeat this action when a second letter-box comes into sight. Thus, intentions function rather like needs in that they generate a tension state and are satisfied when they are acted on; they are quasineeds. Another divergence with Ach concerned the relationship between the strength of an intention and the likelihood of overcoming inhibitory influences; according to Lewin, very strong intentions often resulted in poor performance. Given that intentions are quasi-needs, do they still qualify as acts of the will? No, said Lewin; the defining characteristic of volitional actions is that they are "controlled," that they occur in opposition to some real need or quasi-need. In other words, they are relatively free from the dynamics of the psychological field, while instinctual and impulsive actions

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are completely determined by the field. Intentions, on the other hand, are defined by foresight and preparation; they set up a psychological field which without them would not exist or would exist in another form. Thus, we arrive at a fourfold classification of actions (field vs. controlled, intended vs. non-intended), where the combination "volitional action without intention" is not self-contradictory but corresponds to actually existing cases, such as the spontaneous act of saving somebody from a fire (against field forces but without preparatory intention). In reading Lewin's (1926) paper, one is struck to find quite friendly references to psychologists working in the humanities tradition. It seems that Lewin, like other Gestalt psychologists of the time, looked at his work as overcoming the crisis of psychology in the sense that he accepted the general aims of the psychological humanists but differed from them as far as scientific methodology was concerned. To the extent that he succeeded in integrating the divergent trends prevalent at his time, his work can be considered as the culminating point that the investigation of the will could reach in German interbellurn psychology. When he went to the United States, his interests shifted toward group dynamics and social psychology and lost their specifically German flavor, not only linguistically but in terms of the basic presuppositions guiding them. This meant that the will was again lost, and in fact the most accessible source on Lewin's contribution to the psychology of volition is Koffka's (1935) Principles of Gestalt Psychology, more so than Lewin's own writings in the English language.

Concluding Remarks The "cognitive revolution" in psychology was precipitated by developments occurring outside of psychology, such as communication theory and computer science (Scheerer, 1988). Once psychologists had convinced themselves that cognitive theorizing was not incompatible with scientific methodology, they started to look back at the history of their field and discovered that pre-behaviorist psychology had been cognitive all along. A similar constellation is to be expected in the impending "volitional revolution." The development was initiated by outside influences, in this case control theory, and it has to struggle with presuppositions that the will, by its very definition, is not amenable to scientific study. As far as these apprehensions are based on the supposed freedom of the will, the present essay has, I think, dispersed them; at no point in the history of psychology has the investigation of the will been

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prevented by a "freedom of the will." But history may point to another obstacle for the scientific study of the will. Perhaps the will is not entirely of a "natural kind" and will have to be dissected when we start to *'carve nature at the joints.'' This has been argued for the concept of consciousness (e.g., Wilkes, 1988) and it might equally well be argued for the concept of the will.

References Ach, N. (1905). h e r die Willenstatigkit und das Denken. Gottingen: Vandenhoeck & Ruprecht. Ach, N. (1910). h e r den willensakt und das Temperament. Leipzig: Quelle & Meyer. Ach, N. (1935). Analyse des Willens. Berlin, Wien: Urban & Schwarzenberg. Bain, A. (1855). The senses and the intellect. London: Parker. Bain, A. (1883). The emotions and the will (3rd ed.). London: Longmans, Green & Co. Bastian, C. (1880). The brain as an organ of the mind. London: Kegan Paul. Bell, C. (1826). On the nervous circle which connects the voluntary muscles with the brain. Philosophical Transactions of the Royal Sociev, 116(1), 163-173. Boring, E. G. (1942). Sensation and perception in the history of experimental psychology. New York: Appleton-Century-Crofts. Brozek, J. (1970). Wayward history: F. C. Donders (1818-1889) and the timing of mental operations. Psychological Reports, 26, 563-569. Carpenter, W. B. (1852). Electro-biology and mesmerism. Quarterly Review, 93, 501-557. Engel, J. J. (1802). Uber den Ursprung des Begriffs der Kraft. Quoted after: J.J. Engel, Schrifien, Vol10 (2nd ed.) (pp. 101-122). Berlin: Mylius 1844. Helmholtz, H. (1867). Handbuch der physiologischen Optik Leipzig: Voss. Hildebrandt, H. (1985). Ideomotorik: Ein neues Paradigma fur ein altes Problem? Perception & Action, Report # 65. Universitiit Bielefeld: Zentrum fur Interdisziplinare Forschung. Hilgard, E. R. (1980). The trilogy of mind: cognition, affection, and conation. Journal of the History of the Behavioral Sciences, 16, 107-117. Howard, G. S., & Conway, C. G. (1986). Can there be a science of volitional action? American Psychologist, 41, 1241-1251. James, W. (1890). The principles of psychology. New York: Holt.

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James, W. (1983). The feeling of effort. In F. H. Burkhardt, F. Bowers, & I. K. Skrupskelis (Eds.), The works of WilliamJames: Essays in psychology (pp. 83-124). Cambridge, MA: Harvard University Press. (Original work published in 1880) Kant, I. (1781). f i t & der reinen Vernunfl. Riga: Hartknoch. Koffka, K. (1935). Principles of gestalt psychology. London: Routledge & Kegan Paul. Lange, L. (1888). Neue Experimente uber den Vorgang der einfachen Reaktion auf Sinneseindriicke. Philosophische Studien, 4, 479-510. Lewin, K. (1917). Die psychische Tatigkeit bei der Hemmung von Willensvorgangen und das Grundgesetz der Assoziation. Zeitschn’ftfiir Psychologie, 77, 212-247. Lewin, K. (1922). Das Problem der Willensmessung und das Grundgesetz der Assoziation: I. Psychologische Forschung, 1, 191-302. Lewin, K. (1926). Vorsatz, Wille und Bedurfnis. Psychologische Forschung, 7, 330-385. Lindworsky, J. (1923). Der WilEe (3rd ed.). Leipzig: Barth. Lotze, R. H. (1852). Medicinische Psychologie oder Physiologie der Seele. Leipzig: Weidmannsche Buchhandlung. Mach, E. (1886). Beitruge zur Analyse der Empfindungen. Jena: G. Fischer. Maine de Biran, F. P. (1807). De l’apperception immediate (MCmoire de Berlin), J. Echevierra (ed.), Paris: Vrin 1963. Michotte, A., & Prum, E. (1911). etude experimentale sur le choix volontaire et ses antkctdents immediates. Archives de Psychologie, 10, 113-320. Miiller, G. E. (1878). Zur Grundlegung der Psychophysik Berlin: Hoffmann. Miiller, J. (1838). Handbuch der Physiologie des Menschen, 2. Band, Coblenz: Holscher. Munsterberg, H. (1888). Die Willenshandlung:Ein Beitrag zurphysiologischen Psychologie. Freiburg: Mohr. Munsterberg, H. (1889). Willkiirliche und unwillkurliche Vorstellungsverbindung. In H. Munsterberg (Ed.), Beitriige zur aperimentellen Psychologie, (pp. 64-188). Heft 1. Freiburg: Mohr. Miinsterberg, H. (1900). Grundzuge der Psychologie. Leipzig: Barth. Nussbaum, M. (1978). Ahtotle’s De Motu Animalium. Princeton: Princeton University Press. Ribot, T. (1879). Les mouvements et leur importance psychique. Revue Philosophique, 8, 371-386. Rohracher, H. (1932). Theorie des Wllens auf qerimenteller Grundlage. Leipzig: Barth.

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Scheerer, E. (1984). Motor theories of cognitive structure: A historical review. In W. Prinz & A. F. Sanders (Eds.), Cognition and Motor Processes (pp. 77-98). Berlin, Heidelberg, New York, Tokyo: Springer-Verlag. Scheerer, E. (1987a). Muscle sense and innervation feelings: A chapter in the history of perception and action. In H. Heuer & A. F. Sanders (Eds.), Perspectives on Perception and Action (pp. 171-194). Hillsdale, N.J.: Lawrence Erlbaum. Scheerer, E. (1987b). The unknown Fechner. Psychological Research, 49, 197202. Scheerer, E. (1988). Towards a history of Cognitive Science. International Social Science Journal, 40(1), 7-20. Schneider, G. H. (1880). Der thierische wille. Leipzig: Abel. Schneider, G. H. (1882). Der menschliche Wile vom Standpunkte der neueren Entwicklungstheorien (des "Danuinismus").Berlin: Diimmler. Sechenov, I. M. (1956). Reflexes of the brain. In I. M. Sechenov, Selected physiological and psychological works (pp. 31-139). Moscow: Foreign Languages Publishing House. (Original work published 1866) Spranger, E. (1927). Lebensfomzen (6th ed.). Halle: Niemeyer. Spranger, E. (1928). Psychologie des Jugendalters (10th ed.). Leipzig: Quelle & Meyer. Teuber, H. L. (1966). Alterations of perception in brain injury. In J. Eccles (Ed.), Brain and conscious experience (pp. 182-216). Berlin, Heidelberg, New York: Springer-Verlag. Thorndike, E. L. (1913). Ideo-motor action. Psychological Review, 20, 91-106. Thorndike, E. L. (1914). Ideo-motor action: A reply to Professor Montague. Journal of Philosophy, Psychology and Scientific Methods, 12, 32-37. Watson, J. B. (1913). Image and affection in behavior. Journal of Philosophy, Psychology and Scientific Methods, 10, 421-428. Wilkes, K. (1988). ---,yishi, dum, and consciousness. In A. J. Marcel & E. Bisiach (Eds.), Consciousness in contemporary science (pp. 16-41). Oxford: Clarendon Press. Wolter, A. B. (1986). Duns Scotus on the will and morality. Washington, D.C.: Catholic University Press. Woodworth, R. S. (1906a). The cause of a voluntary movement. In: Studies in philosophy and psychology, Garmun memorial volume (pp. 35 1-392). Boston: Houghton-Mifflin. Woodworth, R. S. (1906b). Imageless thought. Journal of Philosophy, Psychology and ScientiJic Methods, 3, 701-709. Wundt, W. (1863). Vorlesungen iiber die Menschen- und Thierseele. Leipzig: voss.

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Wundt, W. (1874). Grundziige der physiologischen Psychologie (1st ed.). Leipzig: Engelmann. Wundt, W. (1910). Grundzuge der physiologischen Psychologie: Vol. 2 (6th ed.). Leipzig: Engelmann, Wundt, W. (1911). Grundzuge der physiologischen Psychologie: Vol. 3 (6th ed.). Leipzig: Engelmann,

PHYSIOLOGICAL PERSPECTIVE

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CHAPTER 4 VOLITIONAL EYE MOVEMENTS AND THEIR RELATIONSHIP TO VISUAL ATTENTION Burkhart Fischer and Rolf Boch The eyes are moving virtually all the time (even during sleep), although rarely are we aware of these movements. Conversely, we can also consciously move our eyes. Therefore, a movement of the eyeball (defined by its rotational position in the orbit as a function of time) may be either (a) the consequence of our own decision, (b) the effect of a reflex, or (c) a superposition of both. For example, although eye movements are largely involuntary movements, they generally can be generated or suppressed voluntarily. However, this generalization needs qualification, because certain types of eye movements occurring under certain conditions are never under our voluntary control. The question of which types of eye movements are to be regarded as voluntary presupposes a prior classification of the types of eye movement to be considered. Therefore, in our attempt to answer the question of volition, we start from a classification of eye movements based upon the physical parameters of the movements and on the physical conditions under which these movements occur. This classification is illustrated in Figure 1. Then, in a second step we (a) try to identify those types and aspects of eye movements that are under volitional control, and (b) discuss their relationship to visual attention.

Classification of Eye Movements Eye movements are ordinarily distinguished or classified in terms of their velocity, as being either fast, slow (say, below 2Oo/s), or essentially zero (stationary). The three circles in Figure 1 represent the three velocity domains: fast, slow, and close to zero.

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MOVEMENTS of the EYE fast eye movements unvoluntary movements\ spontaneous eye movements self paced saccades anticipated saccades resting

eye

fixating

visual1y guided saccades corrective saccades

long

Figure 1. Diagram classifymg the different types of eye movements referring to their velocities. Fast eye movements are shown on the outer, slow movements on the middle, and no movement on the inner circle. Nystagmic eye movements break down into slow and fast phases, belonging to those eye movements collected on the middle and outer circle, respectively. An imaginary vertical midline divides the concentric circles into two halves with involuntary eye movements in the left and eye movements under at least some voluntary control in the right half. The thin horizontal line corresponds to the fact that drifts and microsaccades occur in the state of resting and fixating eyes, respectively. With respect to their reaction times, visually guided saccades are subdivided into express, regular, and long latency saccades (lower right). For details see text.

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Fast Eye Movements Fast eye movements are called saccades. They occur when the direction of gaze is suddenly shifted from one object at one position in space to another object at another position. Saccades can be subdivided into a number of different types depending on the conditions under which they occur: Spontaneous saccades are made in total darkness. Anticipated and corrective saccades occur under laboratory conditions; the former occurs when a subject being asked to respond to a sensory stimulus with a saccade initiates the eye movement prior to the stimulus; the latter occurs as a result of the eye missing the position of a target to which a subject is saccading. Anticipated saccades are slower in velocity than normal saccades of the same size and they often fail to reach the target position. Instead they undershoot and then are followed by corrective saccades. Selfpaced saccades are--by definition--voluntary saccades that a subject makes (without an external signal) on his own decision. fisually guided saccades are the most common eye movements we make. Every 200 - 300 ms the eye jumps from one position to the next if we are free to look at our visual surroundings. Under laboratory conditions visually guided saccades are typically initiated in response to the onset of a light stimulus. In this case one can classify the saccades as express, regular, or long on the basis of their reaction time (latency) being either extremely short (ca. 100 ms), intermediate (ca. 150 ms), or long (ca. 220 ms), respectively.

Slow Eye Movements Slow eye movements are made when we try to follow an object that moves relative to the head regardless of whether this relative movement is a consequence of our own body movements, or the consequence of a movement of the object, or both. These slow movements are therefore called pursuit eye movements. Vergence eye movements (counterrotating the two eyes) are also of slow velocity even when they are made to shift the gaze as quickly as possible from a near to a far object or vice versa.

No Eye Movements Tiny eye movements occur during time periods when we try to keep the image of a (small) resting object on our fovea. That is, during periods of fixation, the eye is not always at rest (no eye movement); rather, during these "fixation" periods the eyes also can move by slow drifts and fast microsaccades.

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Combinations of Fast and Slow Eye Movements Complex combinations of eye movements occur reflexively when the head moves. These reflexes, distinguished on the basis of the receptor detecting the motion, are of two types: vestibular and optokinetic. Both consist of slow phases when the eyes pursue a target and quick phases that look like saccades that bring the eyes back into an appropriate operating position in the orbit. Under laboratory conditions these reflexes lead to sequences of alternating quick and slow phases, called nystagmus.

Eye Movements and Volition

As pointed out already, movements of the eyes may be generated voluntarily. This, however, is a generalization which holds true only for certain types of eye movements and only for certain aspects of them. In this section we will go through the classification scheme represented in Figure 1 in an attempt to assign the attribute "volitional" or 'hot volitional" to each type of eye movement, or at least to some aspect thereof. Both slow and fast eye movements, as well as the state of "no movement,'' can be achieved by volition: we can decide to pursue a moving object, we can decide to keep the eyes still, and we can decide to initiate a saccade. However, we have no voluntary control over the velocity of the smooth pursuit movement, we have no voluntary control over the occurrence or suppression of slow drifts, we cannot initiate microsaccades voluntarily (but they may be suppressed by instruction; Steinman, Haddad, Skavenski, & Wyman, 1973), and we have no voluntary control over the velocity of saccades; instead there exists a fixed relationship between size and duration of saccades (Fuchs, 1967), the so-called ''main sequence." Nystagmus is a combination of eye movements almost completely controlled by reflexes (vestibular and/or optokinetic) and therefore--by definition-will be assigned as "not volitional". Among the various types of saccadic eye movements, self-paced saccades are "volitional" and spontaneous saccades are Ifnot volitional", both by definition. Furthermore, anticipatory saccades are also "not volitional," again by definition. Corrective saccades occur only after visually guided saccades that have missed the target. Most of the time the observer is unaware of his mistake in amplitude, and corrects the error involuntarily. All the remaining types of saccades are correct, visually guided, fast changes of the direction of gaze distinguished only on the basis of their reaction time (express, regular, long), Even though these eye movements are volitional, because they can all be initiated or suppressed by the subject's own decision,

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one cannot decide to initiate a certain type and not another. For example, a subject who usually produces a high percentage of express saccades cannot decide on a given trial to generate a regular saccade. In other words, he has no voluntary control over his reaction time other than to make it extremely long, that is, to suppress the saccade proper and to make another one some time later. In conclusion, not a single type of eye movement is generated and controlled completely by our will. Even self-paced saccades have a velocity which we cannot select independently from its size. Nevertheless we allocated the term "voluntay" to the types of eye movements at the right side of Figure 1 and "involuntary1'to those at the left side. What is meant is only that these types of eye movements are under at least some voluntary control whereas the others are completely involuntary. The volitional control of eye movements is restricted to certain types of movement and it is restricted to the initiation (in some cases) or to the suppression (in other cases) of the movement. This is a basic difference from the control of movements of the limbs, for example, of reaching movements (see chapter by Georgopoulos). Whether or not this difference is related to the fact that there exists no oculomotor cortex but a motor cortex is an interesting but open question.

Eye Movements and Attention Objects that draw our attention are usually the ones we look at. In terms of eye movements this means that we make a saccade to bring the image of the object to the fovea and than we fixate or pursue it. In other words: in everyday life eye movements can be regarded as more or less direct expressions of our attention. (Yet, this is not a fixed relationship because we can pay attention to things we are not looking at.) It is therefore not surprising that the studies of eye movements have been used to study mechanisms of visual attention (for review see Fischer & Breitmeyer, 1987). This is true in particular for the study of visually guided saccades, whereas-interestingly--the study of fixation has been neglected. The close relationship between fixation, attention, and saccades became clear only recently after the discovery of the express saccade defined by its extremely short reaction time of about 70 ms in monkeys (Fischer & Boch, 1983) and around 100 ms in man (Fischer & Ramsperger, 1984). Attempts to understand the conditions under which this type of saccade occurs have shown, that all saccades (except microsaccades perhaps) are arrested by directed or engaged visual attention. This is almost trivial as long

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as the direction of gaze and that of attention are coincident in space. If, however, attention is directed to an object in the periphery of the visual field one expects a shorter reaction time of a saccade directed to that object. The opposite is true (Mayfrank, Mobashery, Kimmig, & Fischer, 1986): Saccadic reaction times are extremely long when--at the time a saccade target occurs in the field of view--the subject still maintains fixation or pays attention to something in the periphery including the saccade target. On the other hand saccadic reaction times become extremely short (express saccades) when the subject has already disengaged his attention from wherever it has been engaged before. This notion of two states of the attentional system--one "engaged'' with saccades inhibited, the other "disengaged" with saccades permitted--leads to the question of what really happens when we make a voluntary saccade. Is it, for example, possible that, what we experience as a volitional saccade, is preceded by an internal switch from engaged to disengaged attention?

Neural Events Related to Saccadic Eye Movements and Attention Several brain structures--cortical and subcortical--have been investigated during the last 25 years using microelectrode, single-cell recording techniques in monkeys who have been trained to perform specific visuo-oculomotor tasks. The main result is that the visual responses of the cells (in the superior colliculus (Goldberg & Wurtz, 1972), the prestriate cortical area V4 (Fischer & Boch, 1981), the inferior parietal cortex (Robinson, Goldberg, & Stanton, 1978), the frontal eye fields (Wurtz & Mohler, 1976b), the prefrontal area 46 (Boch & Goldberg, in press) are enhanced when the visual stimuli that elicit the responses become targets of saccades. Whereas this enhancement is very closely related to the occurrence of the saccade for the cells in the colliculus (Wurtz & Mohler, 1976a) and in the frontal eye fields (Goldberg & Bushnell, 198l), response enhancement can be observed without saccades for cells in the parietal cortex (Bushnell, Goldberg, & Robinson, 1981) and in the prestriate cortex (Fischer & Boch, 1985) when the monkey just disengages his attention from the fixation point and moves it to the peripheral target. In fact, one can modulate the activity of a prestriate cortical cell by switching the fixation point on and off while the monkey's eyes stay still all the time and a constantly illuminated stimulus is projected into the cell's receptive field (Fischer & Boch, 1985). This occurs after the monkey has learned that the stimulus may change its luminance during the time the fixation point is invisible and that he has to detect this change to receive a reward. It has been argued, therefore, that this type of response modulation reflects the

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animal's visual attention moving back and forth from the fixation point to the peripheral stimulus. In the frontal eye fields--by contrast--there are cells which become active before saccades even though the monkey has no visible target. But the saccade must be part of a behavioral task, otherwise the cells remain silent (Goldberg & Bruce, 1986). This experiment shows that the question of whether or not a particular saccade, or aspect thereof, is indeed purposive, and therefore voluntary, is clearly distinguished by cells in the frontal cortex. Patients with frontal lesions lose, to some extent, their voluntary control over saccades in the sense that they are unable to suppress a saccade to a stimulus appearing in the part of the visual field affected by the lesion (Guitton, Buchtel, & Douglas, 1985). Instead they make reflex-like saccades about 100 ms after stimulus onset, which are probably express saccades. The intimate relation of frontal and parietal cortex to the generation and suppression of saccades as a function of fixation and directed attention is further emphasized by the results of electrical stimulation experiments. Saccades usually elicited by electrical microstimulation of these cortical areas are abolished when the stimulation is applied while the animal performs a fixation task (Goldberg, Bushnell, & Bruce, 1986; Shibutani, Sakata, & Hyvaerinen, 1984). Both experiments show that during fixation, pathways that mediate the generation of saccades are inhibited. This of course makes sense, because the decision to fixate contradicts the decision to make a saccade. If one assumes that fixation is the combination of a resting eye and attention being engaged to a foveal stimulus one predicts that engaged attention alone inhibits saccades. It is exactly this conclusion that has been reached by Mayfrank et al. (1986), and by Fischer (1987). A summary of the cortical control of eye movements is given by Fischer and Boch (in press). In conclusion, the attentional processes that usually precede voluntary saccades appear to take place in the prestriate and parietal areas, whereas the volitional aspect comes into play by frontal and prefrontal cortical mechanisms. However, these parts of cortex are intimately and mutually connected and the complex anatomical situation (see Fischer & Boch, in press, for an overview) suggests that the terms "voluntary" and "attentional" may not have simple neural correlates located in different small and well defined cortical areas.

Modification of Saccadic Eye Movements Some eye movements, or aspects thereof, are subject to modification as a function of practice. For example, when learning to read as a child, one

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learned to make saccades regularly and repetitively. Even as adults our saccadic system, or at least a mechanism which controls the generation of saccades, can be modified by daily practice. This applies mainly to the reaction time of visually guided saccades. It is not just that these reaction times may be reduced by training, but more specifically, and interestingly, that the occurrence of one type of saccade--the express saccade--can be increased in frequency of occurrence from close to zero in untrained subjects (Fischer & Ramsperger, 1986) or monkeys (Fischer, Boch, & Ramsperger, 1984) to almost 100 %. This means that the subject has learned to voluntarily control one or more processes which must be completed before a saccade can be made. Most probably these processes have to do with a change in the attentional system being switched from the engaged to the disengaged state (Fischer & Breitmeyer, 1987). Here we have an intriguing situation in that what would seem to be a prerequisite for successful learning--namely attention--is itself being modified by practice. So far, not a lot is known about the changes that occur in the neural activity of different brain structures during periods of practice. We do know, however, that a certain type of presaccadic activity in prestriate cortex is reduced as monkeys practice visually guided saccades thereby reducing their reaction times drastically (Fischer & Boch, 1982).

Conclusion Although we are intimately and immediately aware (i.e., conscious) of our own "will" and "attention," neither phenomenon, considered as an objective event or process, has directly measurable parameters. That is, although we know about their existence directly by introspection, this subjective "method is not accepted in science. Therefore, we try to get a scientific grip on these phenomena indirectly, by looking at their objective consequences in behavioral or neurophysiological terms. It is only natural, therefore, that attempts to understand such a simple thing as an eye movement should foster philosophical considerations of the essential nature of volition and attention. Or, to put it the other way around, a thorough investigation of the generation and control of voluntary saccades may well be expected to provide objective insights into the neurobiological aspects of volition and attention, terms usually discussed in philosophy and psychology.

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References Boch, R., & Goldberg M. E. (in press). The participation of prefrontal neurons in the preparation of visually guided eye movements in the rhesus monkey. Journal of Neurophysiology. Bushnell, M. C., Goldberg, M. E., & Robinson, D. L. (1981). Behavioral enhancement of visual responses in monkey cerebral cortex. I. Modulation in posterior parietal cortex related to selective visual attention. Journal of Neurophysiology, 46, 755-772. Fischer, B. (1987). The preparation of visually guided saccades. Review of Physiology and Biochemical Pharmacology, 106, 1-35. Fischer, B., & Boch, R. (1981). Enhanced activation of neurons in prelunate cortex before visually guided saccades of trained rhesus monkeys. Experimental Brain Research, 44, 129-137. Fischer, B., & Boch, R. (1982). Modifications of presaccadic activation of neurons in the extrastriate cortex during prolonged training of rhesus monkeys in a visuo-oculomotor task. Neuroscience Letters, 30, 127-131. Fischer, B., & Boch, R. (1983). Saccadic eye movements after extremely short reaction times in the monkey. Brain Research, 260, 21-26. Fischer, B., & Boch, R. (1985). Peripheral attention versus central fixation: modulation of the visual activity of prelunate cortical cells of the rhesus monkey. Brain Research, 345, 111-123. Fischer, B., & Boch, R. (in press). Cerebral cortex. In R. H. S. Carpenter (Ed.), Vision and visual dysfunction: Vol. 9. New York: Macmillan Press. Fischer, B., Boch, R., & Ramsperger, E. (1984). Express saccades of the monkey: effects of daily training on probability of occurrence and reaction time. Experimental Brain Research, 55, 232-242. Fischer, B., & Breitmeyer, B. (1987). Mechanisms of visual attention revealed by saccadic eye movements. Neuropsychologia, 25, 73-83. Fischer, B., & Ramsperger, E. (1984). Human express-saccades: extremely short reaction times of goal directed eye movements. Experimental Brain Research, 57, 191-195. Fischer, B., & Ramsperger, E. (1986). Human express saccades: effects of randomization and daily practice. Experimental Brain Research, 64, 569-578. Fuchs, A.F. (1967). Saccadic and smooth pursuit eye movements in the monkey. Journal of Physiology, 191, 609-631. Goldberg, M. E., & Bruce, C. J. (1986). The role of the arcuate frontal eye fields in the generation of saccadic eye movements. In H. -J. Freund, U. Bittner, B. Cohen, & J. Noth (Eds), Progress in brain research: Vol. 64 S. (pp. 143-154).Amsterdam: Elsevier Science Publishers B.V. (Biomedical Division).

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Goldberg, M. E., & Bushnell, M. C. (1981). Behavioral enhancement of visual responses in monkey cerebral cortex. 11. Modulation in frontal eye fields specifically related to saccades. Journal of Neurophysiology, 46, 773-787. Goldberg, M. E., Bushnell, M. C., & Bruce, C. J. (1986). The effect of attentive fixation on eye movements evoked by electrical stimulation of the frontal eye fields. Experimental Brain Research, 61, 579-584. Goldberg, M. E., & Wurtz, R. H. (1972). Activity of superior colliculus in behaving monkey: II. The effect of attention on neuronal responses. Journal of Neurophysiology, 35, 560-574. Guitton, D., Buchtel, H. A., & Douglas, R. M. (1985). Frontal lobe lesions in man cause difficulties in suppressing reflexive glances and in generating goal-directed saccades. Experimental Brain Research, 58, 455-472. Mayfrank, L., Mobashey, M., Kimmig, H., & Fischer, B. (1986). The role of fiation and visual attention on the occurrence of express saccades in man. European Journal of Psychiatiy and Neurological Science, 235, 269-275. Robinson, D. L., Goldberg, M. E., & Stanton, G. B. (1978). Parietal association cortex in the primate: sensory mechanisms and behavioral modulations. Journal of Neurophysiology, 41, 910-932. Shibutani, H., Sakata, H., & Hyvaerinen, J. (1984). Saccade and blinking evoked by microstimulation of the posterior parietal association cortex of the monkey. Experimental Brain Research, 55, 1-8. Steinman, R. M., Haddad, G. M., Skavenski, A. A., & Wyman, D. (1973). Miniature eye movement. Science, 181, 810-819. Wurtz, R. H., & Mohler, C. W. (1976a). Organization of monkey superior colliculus: enhanced visual response of superficial layer cells. Journal of Neurophysiology, 39, 745-765. Wurtz, R. H., & Mohler, C. W. (1976b). Enhancement of visual responses in monkey striate cortex and frontal eye fields. Journal of Neurophysiology, 39, 766-772.

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CHAPTER 5

THE CEREBRAL CORRELATES OF REACHING Apostolos P. Georgopoulos Reaching to objects of interest in immediate extrapersonal space is an important motor activity of primates in everyday life. Recent studies of the activity of single cells in various brain regions of behaving primates have provided new insights into the brain mechanisms underlying reaching. These studies are discussed below with emphasis on parametric studies of the relations of the neuronal activity to the direction of reaching. Several brain areas are involved in the initiation and control of reaching. The study of the role of the various areas in this function was made possible by the advent of a technique that allowed the recording of the activity of single cells in the brain of behaving animals during reaching. This technique (Lemon, 1984) is indispensable for the study of neural mechanisms underlying motor aspects of behavior. Typically, monkeys are trained to perform various motor tasks and then microelectrodes are inserted through the dura into the brain area of interest to record extracellularly the electrically isolated action potentials of single cells. This combined behavioral-neurophysiological experiment provides a direct tool and one with fine-grain by which the brain mechanisms underlying performance can be studied.

Posterior Parietal Cortex and Reaching An important finding from such studies has been that several brain areas are involved in reaching, including areas of the cerebral cortex and various subcortical structures. The first cortical area investigated was the posterior parietal cortex (Hyvarinen & Poramen, 1974; Mountcastle, Lynch, Georgopoulos, Sakata, & Acuna, 1975). This cortical region was chosen because posterior parietal lesions in human subjects and monkeys result in motor defects in reaching (see Georgopoulos, 1986, in press, for reviews). Indeed, cells were identified in the superior and inferior parietal lobules (Brodmann’s areas 5 and 7, respectively) that changed activity with reaching in the absence of any peripheral somesthetic driving. These

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Figure 1. Drawing of a monkey reaching towards a lighted target in an apparatus used by Mountcastle et al. (1975) for studies of the posterior parietal cortex. The animal has just released the key and reached out to touch the lighted switch mounted on the moving carriage. The head fixation apparatus, implanted microdrive, cathode follower, and reward tube are also shown. (From Mountcastle et al., 1975; reproduced with permission). changes in cell activity were studied quantitatively using a behavioral apparatus that allowed 3-dimensional (3-D) reaching to stationary or moving visual targets. This apparatus is illustrated in Figure 1. A trial started when the monkey depressed a key at lap level. As soon as the key was depressed, a red light was lit on a push-button mounted on a semicircular rail in front of the monkey at shoulder level. After a variable period of time the light dimmed which signalled to the monkey to release the key and reach towards and push the lighted button. In some trials the button was stationary whereas in others it moved and then dimmed after a period of time while in motion. Therefore, the task comprised

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DETECT

MEAN RESPONSE

Figure 2. Impulse activity of an area 5 neuron during repeated reaching movements. The cell never responded to any passively delivered mechanical stimulus to the arm, to visual or auditory stimuli, or during passive-aversive movements of the contralateral arm. "Detect" indicates key release (see Figure l), and "response" indicates contact with the lighted switch. The arrow is mean response time & 1 SD. (From Mountcastle et al., 1975; reproduced with permission.) reaching to both stationary and moving targets. A typical result from reaching to a stationary target is shown in Figure 2. It can be seen that the activity of the cell changed appreciably during reaching. Although the changes in cell activity associated with reaching could be observed in the absence of visual guidance (Hyvarinen & Poramen, 1974; Mountcastle, Motter, & Andersen, 1980), cell activity was usually modulated more strongly when the animal reached with the eyes open. Indeed, a particular class of cells could qualify for an "eye-hand coordination" function because the changes in their activity was most intense when the monkey tracked a moving visual target with both the eyes and the hand (Mountcastle et al., 1975).

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Premotor Cortex and Reaching It is reasonable to assume that the planning and execution of reaching involves the concurrent or sequential activation of several brain regions. It is well documented that visually guided reaching may be disturbed following damage to the parietal lobe ("optic ataxia"; see Perenin & Vighetto, 1988, for a review) but it is not known how this disturbance is brought about. One idea is that visuospatial information is transmitted from the parietal to the frontal lobe, so that defects in visually guided reaching can be thought of as resulting from a disconnection between these two lobes (see Ferro, Bravo-Marques, Castro-Caldas, & Antunes, 1983, for a succinct discussion, and also Haaxma & Kuypers, 1975). The main recipients of posterior parietal projections are areas located anterior to the motor cortex, i.e., premotor cortical areas (reviewed in Humphrey, 1979), although area 5 also projects directly to the motor cortex (Strick & Kim, 1978; Caminiti, Zeger, Johnson, Urbano, & Georgopoulos, 1985). The premotor areas comprise a number of different sub-areas in both the lateral and medial surface of the hemisphere and project to the motor cortex (Muakkassa & Strick, 1979; Barbas & Pandya, 1987). In fact, these areas seem also to project directly to subcortical structures, including the red nucleus (Humphrey, Gold, & Reed, 1984) and the spinal cord (Hutchins & Strick, 1987), which means that their influence on the motor function need not be exerted exclusively through the motor cortex. Reaching movements pointing to visual or auditory targets were used to study the activity of cells in the premotor cortex of the monkey (Weinrich & Wise, 1982). Three basic classes of cells (n = 205) were distinguished based on the changes of their activity in the task. Movement-related cells (45%) changed activity in relation to the movement. These changes were temporally correlated better with the onset of the movement than with the onset of the stimulus, and were the same whether the stimulus was visual or auditory. Signal-related cell (43%) responded phasically to the presentation of the visual (87/89 cells) or the auditory (2/89 cells) stimulus. Finally, set-related cells (29%) showed changes in activity during an instructed delay period, that is between the onset of a "ready" cue and a "go" signal. These changes in activity were maintained throughout the delay period in most (52/59) of these cells. Many movement-related (57/149) and set-related (36/59) cells showed changes in activity that differed for the two directions of movement (side-to-side) used. Wise, Weinrich, and Mauritz (1986) have argued convincingly that changes in cell activity in the premotor and

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motor cortex are related to the upcoming movement rather than to visuospatial cues themselves. Godschalk, Lemon, Kuypers, and van der Steen (1985) provided direct evidence for this idea by dissociating the direction of a reaching movement from the location or configuration of the visual stimulus that triggered the movement: under these conditions, the changes in the activity of premotor cells in the postarcuate area during a waiting period were related to the upcoming movement than to the visuospatial cue itself. However, Vaadia, Benson, Hienz, and Goldstein (1986) described cells in more anterior frontal regions which

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changed activity only when the monkey reached for an illuminated or a loud target but not when the same movement was made in the absence of such a target. The results of the studies above underscore the fact that several cortical areas are involved in preparation for and execution of reaching, as pointed out by Humphrey (1979) on grounds of anatomical connectivity. The different roles of various premotor areas in the initiation and control of reaching remain to be elucidated although there is clear evidence for their involvement in preparation for and anticipation of movement (see reviews by Wise, 1985, and by Tanji, 1984). The latter was observed clearly in premotor cell activity in studies by Mauritz and Wise (1986). A visua! pointing task was used. Events occurred in a fixed-timing sequence, as outlined in Figure 3, although the events themselves and some of the times involved were uncertain. A trial was initiated when the monkey pressed the central of three illuminable keys. (One of the two other keys was to the left and the other to the right of the central key.) After 1 s either the left or the right key (randomly selected) became illuminated. This key became the next target and illumination of the target key served as the instruction stimulus (IS). The IS was followed by an instructed delay period during which the monkey withheld its movement pending a subsequent cue. However, before that cue and 1 s after the onset of IS, one of the following three events happened with equal probability: (a) the target light remained on ("target on" condition, Figure 3), (b) the target key illumination was turned off ("target off'' condition), or (c) the target changed from one side to the opposite side ("target change" condition). After an additional 0.5, 1.25, or 2 s delay (randomly chosen) a light emitting diode over the target key was turned on. This served as the trigger stimulus (TS) for the monkey to move its arm and depress the target key to obtain a liquid reward. Figure 4 shows an example of anticipatory premotor cell activity in this task. These anticipatory changes in activity can be seen in both the left and right columns, corresponding to leftward and rightward trials. As described above, following the instruction stimulus there was a fixed 1 s delay after which different events could happen, and the trigger stimulus did not occur until after an additional 0.5, 1.25, or 2 s time period; thus, the three possible trigger-stimulus times were at 1.5, 2.25, or 3 s following the onset of the instruction stimulus. It can be seen in Figure 4 that clear changes in cell activity occurred at and around these three latter times, as shown in the rasters and the three peaks of the histograms following the instruction stimulus. Now, it is remarkable that even when

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Cerebral Correlates of Reaching

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Figure 4. Impulse activity and peri-event time histograms of a premotor neuron showing anticipatory activity before the trigger stimulus (TS). Six raster and peri-event time histograms are shown, 3 for leftward trials and 3 for rightward trials in each for the conditions of the fixed-timing task outlined in Figure 3. Left and right columns have the same format. Each histogram binwidth is 40 ms. The heavy mark on each rater line indicates the time of occurrence, on that trial, of the trigger stimulus (TS). The first two activity peaks at the left of each histogram indicate activity from preceding trials. 0, target removal; A, target change. Scale is in impulses/s. (From Mauritz & Wise (1986); reproduced with permission.)

the trigger stimulus did not appear until a later time (e.g., at 3 s following the instruction stimulus) the changes in cell activity were still present at the other times in which the trigger stimulus was expected (i-e,, at 1.5 and 2.25 s following the instruction stimulus). These results show that the premotor cortex is intimately involved in the monitoring of anticipated

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external events that have been associated with the elicitation of arm movements.

Figure 5. Schematic drawing of the apparatus used to study free reaching movements in 3-D space. A, monkeys reached towards and pushed lighted buttons mounted at the end of metal rods threaded through a heavy metal plate. The movement trajectory was monitored using an ultrasonic system. B, Schematic diagram of the location of the 9 buttons used. Dotted lines indicate directions of movements. (From Schwartz et al., 1988; reproduced with permission. Copyright by Society for Neuroscience.)

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Motor Cortex and Reaching Porter and Lewis (1975) studied the changes in activity of motor cortical cells while monkeys reached out and manipulated a handle in front of them. It was found that single cells changed their activity during the task and that the latency of activation of different cells shifted to later times as more distal parts of the limb became involved in the motor act. This question of the sequential activation of motor cortical populations in reaching and grasping was investigated in more detail by Murphy, Wong, and Kwan (1985). The activity of single cells in the forelimb area of the motor cortex was recorded in a task in which monkeys pointed to targets in front of them. The functional relation between the recording locus and the joint of the arm was determined by intracortical microstimulation. Thus a cell could be classified as relating mainly to movements at the shoulder, elbow, hand or fingers. It was found that in the pointing task cells were generally activated sequentially, from proximal to distal, reflecting the sequential engagement of successively more distal parts of the arm. Murphy, Kwan, MacKay, and Wong (1982) also investigated the possible relations between motor cortical cell activity and joint motion and electromyographic (EMG) activity in muscles of the forelimb during reaching. There were three main findings of this study. First, no simple relation was observed between single cell activity and the EMG, even when the muscle from which the EMG was recorded was activated by intracortical microstimulation. Second, single cells related to motion about the shoulder or elbow joints behaved similarly in the task, although the motions produced about these joints could be quite different. And third, the discharge of shoulder-related cells seemed to vary systematically with the movement trajectory. These results indicate that the relations between single cell activity in the motor cortex and components (joint rotation, EMG activity) of reaching are complex.

Parametric Studies of the Direction of Reaching

Motor Cortex Direction of reaching and single cell activity. Reaching movements possess two spatial components, namely direction and amplitude. The relations between the direction of reaching and the activity of single cells in the motor cortex were studied recently

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(Georgopoulos, Schwartz, & Kettner, 1986; Schwartz, Kettner, & Georgopoulos, 1988; Georgopoulos, Kettner, & Schwartz, 1988; Kettner, Schwartz, & Georgopoulos, 1988). The behavioral apparatus used in these studies is illustrated in Figure 5. It consisted of 9 buttons of which 8 were at the corners and 1 at the center of an imaginary cube in front of the monkey. In a typical trial, the center button was lighted first; the animal was required to push it for a period of time after which it was turned off and one of the peripheral lights was turned on; the monkey then moved towards and pushed the lighted button to receive a liquid reward. Different peripheral lights were turned on in a randomized block design; thus, reaching movements were made which were of the same amplitude but which differed in direction. In fact, the experiment was designed to study the relations between the cell activity and the direction of reaching. Cells were selected for study that changed activity with spontaneous or evoked arm movements outside the behavioral task. Recordings of cell activity were made in the motor cortex contralateral to the performing arm. A salient finding of these studies was that the activity of single cells was broadly tuned to the direction of movement: cell activity was most intense for movements in a particular direction (the cell's "preferred direction") and decreased progressively for movements made farther away from the preferred direction. An example is shown in Figure 6A. The crucial variable on which cell activity depends is the angle formed between the direction of the movement and the cell's preferred direction (Figure 6B); in fact, the intensity of cell activity is a linear function of the cosine of this angle, as shown in Figure 7B. The directional tuning equation, then, is

where di(M) is the discharge rate of the ith cell with movement in direction M, bi and ki are regression coefficients, and O C ~ Mis the angle formed between the direction of movement M and the cell's preferred direction Ci. A directional tuning volume constructed using Equation 1 above is shown in Figure 7C for the cell whose data were illustrated in Figures 7A and 7B. The preferred directions differed for different cells and were distributed in the whole 3-D directional continuum. The data discussed above were obtained using 3-D reaching movements. Very similar results were obtained when a 2-D reaching task was used in which the monkey was trained to move a handle on a planar working surface and point with it towards lighted targets on that surface

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Figure 7. A, impulse activity of a different directionally tuned cell. B, mean discharge rate (+ SD) during total time (from onset of target to end of movement) is plotted against the cosine of the angle 0 formed between the direction of the movement and the cell's preferred direction. C, directional tuning volume. The origin of the coordinate axes is at the origin of the movement and the arrow points in the cell's preferred direction. (From Schwartz et al., 1988; reproduced with permission. Copyright by Society for Neuroscience.) (Figure 8; Georgopoulos, Kalaska, & Massey, 1981; Georgopoulos, Kalaska, Caminiti, & Massey, 1982; see also Kalaska, Cohen, Hyde, & Prud'homme, in press). An example of a directionally tuned cell recorded in the motor cortex is shown in Figure 9. The directional tuning function plotted in Figure 9B is of the same form as that described by Equation 1 above. Finally, it is remarkable that the changes in cell activity relate to the direction of the reaching movement and not to its endpoint (Georgopoulos, Kalaska, & Caminiti, 1985). This is illustrated in Figure 10. Some possible implications of the directional tuning of motor cortical cells for circuits of the spinal cord related to reaching movements have been discussed elsewhere (Georgopoulos, 1988).

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Figure 8. Left: schematic drawing of the 2-D apparatus used to study "drawing" movements of monkeys. The monkey sat at A, in front of the working surface, B. The numbered light emitting diodes (LED) were placed on a circle of 8 cm radius. The monkey held the articulated manipulandum at its distal end (C) and captured a lighted LED within a 10 mm diameter transparent plexiglass circle (D). X-Y motion of the center of that circle was monitored every 10 ms with a resolution of 0.125 mm. Right: a monkey performing the task (side view). Insert shows two trajectories. (From Georgopoulos et al., 1981; reproduced with permission.)

Direction of Reaching and Neuronal Populations The data discussed above focus on the question of the neural representation and coding of the direction of reaching. They indicate that a given cell participates in movements of various directions and that, conversely, a movement in a particular direction will involve the activation of a whole population of cells: how, then, is the direction of reaching represented in a unique fashion in a population of neurons each of which is directionally broadly tuned? To answer this question it was hypothesized that the motor cortical command for the direction of reaching can be regarded as an ensemble of vectors (see Figure 11; Georgopoulos, Caminiti, Kalaska, & Massey, 1983; Georgopoulos e t al., 1986). Each vector represents the contribution of a directionally tuned cell. A

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Figure 9. Broad directional tuning in 2-D space of a cell recorded in the arm area of the motor cortex. Top, impulse activity during five trials with movements in the directions indicated in the drawing at the center. Short vertical bars indicate the occurrence of an action potential. Rasters are aligned to the onset of movement (M). Longer vertical bars preceding the onset of movement indicate the onset of the target (T); those following the movement indicate the entrance to the target window (see Figure 9) and the delivery of reward. Bottom, average frequency of discharge (-t SEM) from the onset of the stimulus until the entry to the target window are plotted against the direction of movement. Continuous curve is a cosine function fitted to the data using multiple regression analysis (see Georgopoulos et al., 1982 for details). (From Georgopoulos et al., 1982; reproduced with permission. Copyright by Society for Neuroscience.)

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particular vector points in the cell's preferred direction and has length proportional to the change in cell activity associated with a particular movement direction: then the vector of these weighted cell vectors (the "neuronal population vector") points at or near the direction of the movement (Georgopoulos et al., 1983; Georgopoulos et al., 1986). This

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is illustrated in Figure 12 for eight 2-D reaching directions. Some findings regarding the neuronal population vector are summarized below. The neuronal population vector predicts the direction of reaching during the reaction time. In the paradigms used in the studies described above, a reaction time of approximately 300 ms intervened from the onset of the stimulus to the beginning of the movement. Given that the changes in cell activity in the motor cortex precede the onset of movement by approximately 160-180 ms, on the average (Georgopoulos et al., 1982), it

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Figure 12. Neuronal population vector (heavy dashed lines with arrow) calculated for 8 movement directions. All clusters represent the same neuronal population composed of individual cell vectors (thin lines, N = 241 cells). The dotted lines in the center indicate the direction of movement. (From Georgopoulos et al., 1983; reproduced with permission.) is of interest to know whether the population vector predicts the direction of the upcoming movement during the reaction time. Indeed, this was found to be the case both for 2-D and 3-D reaching movements (Georgopoulos, Kalaska, Crutcher, Caminiti, & Massey, 1984; Georgopoulos et al., 1988). An example from two movement directions is illustrated in Figure 13. The neuronul population vector predicts the direction of reaching during an instructed delay period. In the experiments yielding this finding, monkeys were trained to withhold a visually cued movement for a period of time after the onset of the visual (i.e., directional) cue and to move later in response to a "go" signal. During this instructed delay period the population vector in the motor cortex computed every 20 ms gave a reliable signal concerning the direction of the movement that was to be

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triggered later for execution (Georgopoulos, Crutcher, & Schwartz, 1989). This finding suggests that the motor cortex is involved in processing information about the direction of the upcoming movement in space even in the absence of an immediate movement. The neuronal population vector predicts the direction of reaching for movements of different origin. In the experiments yielding this finding, monkeys made movements that started from different points, were in the same direction but described parallel trajectories in 3-D space. Under these conditions, the population vector in the motor cortex predicted well the direction of the reaching movement (Kettner et al., 1988). The neuronul population coding of the direction of reaching is resistant to loss of cells. The population coding described above is a distributed code and as such does not depend exclusively on any particular cell. This robustness was evaluated by calculating the population vector from progressively smaller samples of cells randomly selected from the original

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Figure 14. The variability of the estimated 3-D direction of the population vector is plotted as a function of the number of cells in the population. The units on the ordinate are half-angles (in degrees) at the apex of a directional confidence cone computed for the population vector using statistical bootstrapping techniques. (From Georgopoulos et al., 1988; reproduced with permission.) population (Georgopoulos et al., 1988). It can be seen in Figure 14 that the direction of the population vector can be reliably estimated from as few as 100-150 cells. The neuronal population vector transmits directional information comparable to that transmitted by the direction of movement. The information transmitted by the direction of the population vector was calculated using an information-theoretical analysis and compared to the information transmitted by the direction of 2-D reaching movements (Georgopoulos & Massey, 1988). It was found that both the neuronal population vector and the reaching movement transmitted comparable amounts of direction-

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Figure 15. Comparison of information transmitted by the direction of the neuronal population vector in the motor cortex ("Neural") and the direction of 2-D reaching movements (best human performance, "Human"). (From Georgopoulos & Massey, 1988; reproduced with permission.) a1 information at various levels of input information but the information transmitted by the population vector was consistently higher than that transmitted by the movement by a constant amount of approximately 0.5 bits (see Figure 15). These results, of the metric-free informationtheoretical analysis, reinforce the usefulness of the population vector as a meaningful measure of the directional tendency of neuronal ensembles and suggest that there is a loss of information following the processing by the motor cortex. The neuronal population vector can provide insight into the brain mechanisms underlying mental transformations. The fact that the population vector calculated post hoc during the reaction time or during an instructed delay period (see above) points in the direction of the upcoming movement has important implications and potentially significant applications for tasks that require spatial transformations because it provides an accurate and robust monitor of the directional tendency of

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a neuronal ensemble as this tendency evolves and changes in time. We utilized this feature to gain an insight into the brain correlates of a mental transformation. The task required the making of 2-D reaching movements in a direction that was at an angle from a stimulus direction. Under these conditions the reaction time of human subjects increases in a linear fashion with the angle (Georgopoulos & Massey, 1987) suggesting that a mental rotation of the stimulus direction to the movement direction (like the hand of a clock) might underlie performance in this task. This hypothesis could be tested because the directions above could be visualized as the neuronal population vector. Indeed, a monkey was trained to perform in a conditional 2-D reaching task which required that the monkey move towards a light when the light came on dim, or move in a direction perpendicular and counterclockwise from the light when it came on bright. The position of the light on a circle and the d i m r i g h t condition were combined (8 positions, at 45" intervals, X 2 conditions = 16 combinations) and presented in a pseudo-random sequence. Recordings in the motor cortex revealed that, during the reaction time, the neuronal population vector pointed in the direction of the movement when the monkey was moving towards the light (Figure 16, left panel). However, when the monkey moved in a direction perpendicular and counterclockwise from the light, the neuronal population vector pointed first in the direction of the stimulus and then rotated counterclockwise for approximately 90", and stabilized pointing in the direction of the movement. These findings provide evidence for the mental rotation hypothesis above and underscore the usefulness of the population vector as a meaningful tool for analysis and interpretation of brain events related to cognitive motor transformations.

Parietal Cortex (Area 5 ) Two-dimensional reaching tasks have been used to study the activity of cells recorded in area 5 (Kalaska, Caminiti, & Georgopoulos, 1983; Kalaska, 1988). The results obtained in these studies were very similar to those obtained in the motor cortex. An example of a directionally tuned cell in area 5 is shown in Figure 17. Moreover, the neuronal population vector in area 5 predicted well the direction of reaching (Kalaska et al., 1983; Georgopoulos, 1987). The similar directional properties of area 5 cells and the population coding of the direction of reaching by these cells are important because these two areas may relate to different aspects of the movement, namely the motor cortex to its initiation and area 5 to its

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Figure 16. Left panel: A, direction of required movement (M) was in the direction of the dim stimulus ( S , open circle). Direction is indicated in polar angles. B, neuronal population vector calculated every 10 ms from stimulus onset ( S ) points in the direction of upcoming movement (180") which started at M. C, population vectors during the reaction time from the moment it is lengthening until the onset of movement. D, direction of population vectors identified in C. above, is plotted against time elapsed from stimulus onset. (Direction is in polar angles). Right requiredA,movement panel: direction(M) of

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monitoring (Kalaska et al., 1983; Kalaska, 1988). Therefore, the similar relations observed between cell activity in these structures and the direction of movement may reflect a common "language" of communication in the spatial domain, given that these areas are anatomically interconnected (Strick & Kim, 1978; Caminiti et al., 1985). The main difference found between the two areas related to onset times of the changes in cell activity, with motor cortical cells being engaged approximately 60 ms before those of area 5 (Figure 18). This finding is in accordance with the different roles postulated above for these two areas.

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Cerebellum A broad directional tuning has also been observed in the cerebellum (Fortier, Kalaska, & Smith, in press). Figure 19 shows an example of a directionally tuned Purkinje cell in the cerebellar cortex, and Figures 20 and 21 show examples of directionally tuned cells in the cerebellar nuclei, interpositus (Figure 20) and dentate (Figure 21). Similarly to the motor cortex, the neuronal population vector in the cerebellar structures mentioned above predicted well the direction of reaching (Fortier et al., in press). This is significant because a major part of the cerebellar output is directed to the motor cortex via the thalamus; therefore, the similarity in the directional properties of the motor cortex and cerebellum may

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reflect the cooperation of these structures in the specification of the direction of reaching, and the use of a common "language" for communication.

Spinal Cord and Reaching Reaching involves motion at the shoulder and elbow joints. Behaviorally, there is little doubt that these two joints are controlled as one functional unit (Soechting & Lacqaniti, 1981), and that this control is separate from that of the wrist (Lacquaniti & Soechting, 1982; Soechting, 1984). Descending motor commands from the motor cortex and other brain areas influence the proximal arm motoneurons, i.e., those innervating muscles acting on the elbow and/or shoulder, through a set of interneurons located at the C3-C4 spinal segments, that is above the segments of the proximal motor nuclei. These interneurons ("C3-C4 propriospinal neurons", Lundberg, 1979) have been studied extensively in the cat. They receive monosynaptic inputs from several supraspinal sources (Illert, Lundberg, Padel, & Tanaka, 1978) including the pyramidal (i.e., corticospinal), rubrospinal, reticulospinal and tectospinal tracts; they distribute their axons to several proximal motoneuronal pools (Alstermark, Kummel, Pinter, & Tantisira, 1987); and, they also send an ascending collateral to the lateral reticular nucleus (Alstermark, Lindstrom, Lundberg, & Sybirska, 1981). Selective section of the output from these propriospinal neurons to their target motoneurons results in abnormal reaching with normal grasping, and similar effects are observed when the corticospinal input to the propriospinal neurons is removed (Alstermark, Lundberg, Norrsell, & Sybirska, 1981). Moreover, propriospinal neurons seem to be selectively engaged during reaching movements (Alstermark & Kummel, 1986). These results indicate that the C3-C4 propriospinal system is concerned with the neural integration of the reaching movement at the spinal level and that the motor cortex and other areas control reaching most probably through that system. This motor cortical control is also exerted at other levels within the propriospinal system; for example, there is direct corticospinal input on a key inhibitory interneuron which mediates inhibition from afferent fibers to propriospinal neurons (Alstermark, Lundberg, & Sasaki, 1984). This peripherally initiated inhibition of the propriospinal neurons is important in limiting the reaching movement, for lack of peripheral input results in consistent hypermetria in reaching (Alstermark, Gorska, Johannisson, & Lundberg, 1986).

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The results summarized above indicate that a large part of neural integration of the reaching movement is accomplished in the spinal cord. In a way, this is qualitatively similar t o the sophisticated integration observed in spinal circuits underlying locomotion (Grillner, 1981): both cases involve the production of complicated motor outputs, complicated in the sense of involving the time-varying control of several muscles ahd of more than one joint. It is possible, and even probable, that the detailed organization and the neural integration of the reaching movement need not be the concern, or the burden, of the motor cortex or other motor areas. These various areas could be concerned, instead, with the initiation and ongoing control of reaching according to internally generated goals, as, for example, in drawing, or according to information from exteroceptors, as, for example, in reaching towards a visual or auditory target. These functions would then be accomplished by the activation of neuronal populations in different brain areas, including the motor cortex, which, in turn, would engage the spinal "reaching" circuits.

Acknowledgement: This work was supported by USPHS Grant NS17413.

References Alstermark, B., Gorska, T., Johannisson, T., & Lundberg, A. (1986). Hypermetria in forelimb target-reaching after interruption of the inhibitory pathway from forelimb afferents to C3-C4 propriospinal neurones. Neuroscience Research, 3, 457-461. Alstermark, B., & Kummel, H. (1986). Transneuronal labelling of neurones projecting to forelimb motoneurones in cats performing different movements. Brain Research, 376, 387-391. Alstermark, B., Kummel, H., Pinter, M. J., & Tantisira, B. (1987). Branching and termination of C3-C4 propriospinal neurons in the cervical spinal cord of the cat. Neuroscience Letters, 74, 291-296. Alstermark, B., Lindstrom, S., Lundberg, A., & Sybirska, E. (1981). Integration in descending motor pathways controlling the forelimb in the cat. 8. Ascending projection to the lateral reticular nucleus from C3-C4 propriospinal neurones also projecting to forelimb motoneurones. Experimental Brain Research, 42, 282-298. Alstermark, B., Lundberg, A., Norrsell, U., & Sybirska, E. (1981). Integration in descending motor pathways controlling the forelimb in the cat. 9. Differential behavioral defects after spinal cord lesions interrupting defined pathways from higher centres to motoneurones. Experimental Brain Research, 42, 299-318.

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Alstermark, B., Lundberg, A., & Sasaki, S. (1984). Integration in descending motor pathways controlling the forelimb in the cat. 11. InhibitoIy pathways from higher motor centres and forelimb afferents to C3-C4 propriospinal neurones. Expenmental Brain Research, 56, 293-307. Barbas, H., & Pandya, D. N. (1987). Architecture and frontal cortical connections of the premotor cortex (area 6) in the rhesus monkey. Journal of Comparative Neurology, 256, 211-228. Caminiti, R., Zeger, S., Johnson, P. B., Urbano, A., & Georgopoulos, A. P. (1985). Cortico-cortical efferent systems in the monkey: a quantitative spatial analysis of the tangential distribution of cells of origin. Journal of Comparative Neurology, 241, 405-419. Ferro, J. M., Bravo-Marques, J. M., Castro-Caldas, A., & Antunes, L. (1983). Crossed optic ataxia: possible role of the dorsal splenium. Journal of Neurology, Neurosurgety, and Psychiatry, 46, 533-539. Fortier, P. A., Kalaska, J. F., & Smith, A. M. (in press). Cerebellar neuronal activity related to whole-arm reaching movements in the monkey. Journal of Neurophysiology. Georgopoulos, A. P. (1986). On reaching.-Annual Review of Neuroscience, 9, 147-170. Georgopoulos, A. P. (1987). Cortical mechanisms subserving reaching. In: Motor areas of the cerebral cortex, CIBA Foundation Symposium No. 132 (pp. 125-132). New York John Wiley. Georgopoulos, A. P. (1988). Neural integration of movement: role of motor cortex in reaching. The FASEB Journal, 2, 2849-2857. Georgopoulos, A. P. (in press). Visual control of reaching. In G. M. Edelman, W. E. Gall, & W. M. Cowan (Eds.), Signal and sense: local and global order in perceptual maps. New York: John Wiley. Georgopoulos, A. P., Caminiti, R., Kalaska, J. F., & Massey, J. T. (1983). Spatial coding of movement: a hypothesis concerning the coding of movement direction by motor cortical populations. Experimental Brain Research Supplement, 7, 327-336. Georgopoulos, A. P., Crutcher, M. D., & Schwartz, A. B. (1989). Cognitive spatial-motor processes. 3. Motor cortical prediction of movement direction during an instructed delay period. Experimental Brain Research, 75, 183-194. Georgopoulos, A. P., Kalaska, J. F., & Caminiti, R. (1985). Relations between two-dimensional arm movements and single cell discharge in motor cortex and area 5: movement direction versus movemeRt endpoint. Expenmental Brain Research Supplement, 10, 176-183.

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Georgopoulos, A. P., Kalaska, J. F., Caminiti, R., & Massey, J. T. (1982). On the relations between the direction of two-dimensional arm movements and cell discharge in primate motor cortex. Journal of Neuroscience, 2, 1527-1537. Georgopoulos, A. P., Kalaska, J. F., Crutcher, M. D., Caminiti, R., & Massey, J. T. (1984). The representation of movement direction in the motor cortex: Single cell and population studies. In G. M. Edelman, W. E. Gall, & W. M. Cowan (Eds.), Dynamic aspects of neocortical function (pp. 501-524). New York: John Wiley. Georgopoulos, A. P., Kalaska, J. F., & Massey, J. T. (1981). Spatial trajectories and reaction times of aimed movements: effects of practice, uncertainty, and change in target location. Journal of Neurophysiology, 46, 725-743. Georgopoulos, A. P., Kettner, R. E., & Schwartz, A. B. (1988). Primate motor cortex and free arm movements to visual targets in three-dimensional space. 11. Coding of the direction of movement by a neuronal population. Journal of Neuroscience, 8, 2928-2947. Georgopoulos, A. P., Lurito, J. T., Petrides, M., Schwartz, A. B., & Massey, J. T. (1989). Mental rotation of the neuronal population vector. Science, 243, 234-236. Georgopoulos, A. P., & Massey, J. T. (1987). Cognitive spatial-motor processes. 1. The making of movements at various angles from a stimulus direction. Experimental Brain Research, 65, 361-370. Georgopoulos, A. P., & Massey, J. T. (1988). Cognitive spatial-motor processes. 2. Information transmitted by the direction of two-dimensional arm movements and by neuronal populations in primate motor cortex and area 5. Experimental Brain Research, 69, 315-326. Georgopoulos, A. P., Schwartz, A. B., & Kettner, R. E. (1986). Neuronal population coding of movement direction. Science, 233, 1416-1419. Godschalk, M., Lemon, R. N., Kuypers, H. G. J. M., & van der Steen, J. (1985). The involvement of monkey premotor cortex neurones in preparation of visually cued arm movements. Behavioural Brain Research, 18, 143-157. Grillner, S. (1981). Control of locomotion in bipeds, tetrapods, and fish. In J. M. Brookhart, & V. B. Mountcastle (Eds.), Handbook of Physiology. The Nervous System IZ (pp. 1179-1236). Bethesda, MD: American Physiological Society. Haaxma, R., & Kuypers, H. G. J. M. (1975). Intrahemispheric cortical connexions and visual guidance of hand and finger movements in the rhesus monkey. Bruin, 98, 239-260.

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Humphrey, D. R. (1979). On the cortical control of visually directed reaching: contributions by nonprecentral motor areas. In R. E. Talbott & D. R. Humphrey (Eds.), Posture and movement (pp. 51-112). New York Raven Press. Humphrey, D. R., Gold, R., & Reed, D. J. (1984). Size, laminar and topographic origin of cortical projections to the major divisions of the red nucleus in the monkey. Journal of Comparative Neurology, 225, 75-94. Hutchins, K. D., & Strick, P. L. (1987). Origin of corticospinal projections to the ipsilateral spinal cord. Society for Neuroscience Abstracts, 13, 243. Hyvarinen, J., & Poramen, A. (1974). Function of the parietal associative area 7 as revealed from cellular discharges in alert monkeys. Bruin, 97, 673-692. Illert, M., Lundberg, A., Padel, Y., & Tanaka, R. (1978). Integration in descending motor pathways controlling the forelimb in the cat. 5. Properties of and monosynaptic excitatory convergence on C3-C4 propriospinal neurones. Experimental Brain Research, 33, 101-130. Kalaska, J. F. (1988). The representation of arm movements in postcentral and parietal cortex. Canadian Journal of Physiology and Phumcolo&v, 66, 455-463. Kdaska, J. F., Caminiti, R., & Georgopoulos,A. P. (1983). Cortical mechanisms related to the direction of two-dimensional arm movements: relations in parietal area 5 and comparison with motor cortex. Experimental Brain Research, 51, 247-260. Kalaska, J. F., Cohen, D. A. D., Hyde, M. L., & Prud’homme, M. (in press). A comparison of movement direction-related vs. load direction-related activity in primate motor cortex, using a two-dimensional reaching task. Journal of Neuroscience. Kettner, R. E., Schwartz, A. B., & Georgopoulos, A. P. (1988). Primate motor cortex and free arm movements to visual targets in three-dimensional space. 111. Positional gradients and population coding of movement direction from various movement origins. Journal of Neuroscience, 8, 2938-2947. Lacquaniti, F., & Soechting, J. F. (1982). Coordination of arm and wrist motion during a reaching task. Journal of Neuroscience, 2, 399-408. Lemon, R. N. (1984). Methods for neuronal recording in conscious animals. Chisester: John Wiley & Sons. Lundberg, A. (1979). Integration in a propriospinal motor centre controlling the forelimb in the cat. In H. Asanuma & V. J. Wilson (Eds.), Integration in the Nervous System (pp. 47-69). Tokyo: Igaku-Shoin.

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Mauritz, K. -H., & Wise, S. P. (1986). Premotor cortex of the rhesus monkey: neuronal activity in anticipation of predictable environmental events. @enmental Brain Research, 61, 229-244. Mountcastle, V. B., Lynch, J. C., Georgopoulos, A. P., Sakata, H., & Acuna, C.(1975). Posterior parietal association cortex of the monkey: command functions for operations within extrapersonal space. Journal of Neurophysiology, 38, 871-908. Mountcastle, V. B., Motter, B. C., & Andersen, R. A. (1980). Some further observations on the functional properties of neurons in the parietal lobe of the waking monkey. Behavioral and Brain Sciences, 3, 520-522. Muakkassa, K. F., & Strick, P. L. (1979). Frontal lobe inputs to primate motor cortex: evidence for four somatotopically organized "premotor" areas. Brain Research, 177, 176-182. Murphy, J. T., Kwan, H. C., MacKay, W. A., & Wong, Y. C. (1982). Precentral unit activity correlated with angular components of a compound arm movement. Brain Research, 246, 141-145. Murphy, J. T., Wong, Y . C., & Kwan, A. C. (1985). Sequential activation of neurons in primate motor cortex during unrestrained forelimb movement. Journal of Neurophysiology, 53, 435-445. Perenin, M. -T., & Vighetto, A. (1988). Optic ataxia: a specific disruption in visuomotor mechanisms. Brain, 111, 643-674. Porter, R., & Lewis, M.Mc. (1975). Relationship of neuronal discharges in the precentral gyrus of monkeys to the performance of arm movements. Brain Research, 98, 21-36. Schwartz, A. B., Kettner, R. E., & Georgopoulos, A. P. (1988). Primate motor cortex and free arm movements to visual targets in three-dimensional space. I. Relations between single cell discharge and direction of movement. Journal of Neurocsience, 8, 2913-2927. Soechting, J. F., & Lacquaniti, F. (1981). Invariant characteristics of a pointing movement in man. Journal of Neuroscience, 1, 710-720. Soechting, J. F. (1984). Effect of target size on spatial and temporal characteristics of a pointing movement in man. Experimental Brain Research, 54, 121-132. Strick, P. L., & Kim, C. C. (1978). Input to primate motor cortex from posterior parietal cortex (area 5). I. Demonstration by retrograde transport. Brain Research, 157, 325-330. Tanji, J. (1984). The neuronal activity in the supplementary motor area of primates. Trends in Neuroscience, 7, 282-285. Vaadia, E., Benson, D. A., Hienz, R. D., & Goldstein, M. H. Jr. (1986). Unit study of monkey frontal cortex: active localization of auditory and of visual stimuli. Journal of Neurophysiology, 56, 934-952.

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Weinrich, M., & Wise, S. P. (1982). The premotor cortex of the monkey. Journal of Neuroscience, 2, 1329-1345 Wise, S. P. (1985). The primate premotor cortex: past, present, and preparatory. Annual Review of Neuroscience, 8, 1-19. Wise, S. P., Weinrich, M., & Mauritz, K. -H. (1986). Movement-related activity in the premotor cortex of rhesus macaques. Progress in Brain Research, 64, 117-131.

VOLITIONAL ACTION, W.A . Hershberger (Editor) B. V. (North-Holland), 1989

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CHAPTER 6 WILL, VOLITIONAL ACTION, ATTENTION AND CEREBRAL POTENTIALS IN MAN: BEREZTSCHAFTSPOTENTL4L, PERFORMANCE-RELATED POTENTIALS, DIRECTED ATTENTION POTENTIAL, EEG SPECTRUM CHANGES H. H. Kornhuber, L. Deecke, W. Lang, M. Lang and A. Kornhuber This chapter is dedicated to Vernon B. Mountcastle

Contents 1. Introduction 2. Methods 2.1. Performance-related DC shifts 2.2. Event-related EEG spectrum 2.3. Regional cerebral blood flow by Tc-99m-HMPAO brain SPECT 2.4. Magnetoencephalography 2.5. Methodological considerations 3. Results and Comments 3.1. The initiation of volitional actions: When to do 3.1.1. Human pathophysiology 3.1.2. Human voluntary movement physiology: The Bereitschaftspotentid 3.1.3. Centralization of the starting function in volitional actions 3.1.4. Selecting the "right" moment to start a movement 3.1.5. After the starting signal has been released 3.1.6. Basal ganglia and cerebellum in the initiation of volitional actions 3.1.7. SMA and the temporal organization of motor sequences 3.2. Physiological signs of anticipatory, task-specific planning 3.3. Resoluteness: ability to maintain goals and adjust behavior 3.4. Cognitive information processing 3.5. Directing attention toward forthcoming, relevant, sensory events 3.5.1 Directed attention potential (DAP) 3.5.2 Anticipation of the right moment to act

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H. H. Komhuber et al. Volition in the sense of setting priorities General discussion The utility of a centralized starting function for movements Frontal lobe and volition Attention, the parietal lobe, and the directed attention potential Will and freedom

1. Introduction The concept of will did not originate within the science of neurophysiology. Neither did it come from comparative research on the behavior of animals and men, although it could have, because man and beast differ in the automaticity of their actions. Man acts more deliberately. Man usually considers various needs, duties, and stimuli, makes reasoned decisions, and even engages in creative planning, before acting, whereas in most animal species there is a more direct transfer from drives and stimuli into behavior. But the concept of will did not originate within the science of behavior. Indeed, it came from the forerunner of science, from ancient philosophy. It is an old observation that man has mind, different cultures, and a behavior more influenced by culture than by instinct. In the history of philosophical thought, it gradually became clear that without will, reasoning can not be transduced into behavior. It is only by means of a will with goals beyond our ego, that reason, conscience and good plans are able to determine priorities among needs and actions. Man does not become humane without possessing reason and good will -- at least this is the belief of most people who have thought profoundly about such matters since the time of Plato, including Aristotle, Zen0 from Kition, Thomas Aquinas, Duns Scotus, Descartes, Erasmus, Leibniz, Kant, and in our century Wundt, Pfander, Jaspers, H. Reiner, Nicolai Hartmann, Kurt Schneider, and Ricoeur. A regressive step towards a belief in the impotence of will came from determinism which entered physics from the apocalyptic branch of theology. Then, in the present century, because of the moral degeneration of the under-challenged upper class in the Europe of 1900, the teaching of Schopenhauer (who, perhaps for personal reasons, did not believe in free will) began to have an impact. Schopenhauer tried to eliminate the concept of will by overextending it in such a way that will became identical with drive. Freud then elaborated and explained what drive is supposed to be all about: He claimed that man is driven by a

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search for pleasure, with will being a narcissistic illusion. Subsequently, the theoretical significance of the will steadily declined, and, by the midsixties of our century, the term will no longer appeared in the Psychologicul Abstracts. Neither will nor volition is to be found in the 1983 edition of the Encyclopaedia Britunnica -- except, of course, for will in the sense of the last will (Le., testament). The impact of hedonism was not confined to academic abstractions. In 1968, there was a "cultural revolution" in Europe, with hedonism ("Freudo-Marxism") as the leading ideology. This new hedonism was marked by a sharp increase in the consumption of alcohol, cigarettes and drugs by the young European generation. As a consequence, alcoholic embryopathy, having been so rare that it was unknown to the medical world, became so common within a few years that it is now twice as common as the usually commonest inborn CNS disturbance, Down's syndrome (H. H. Kornhuber, 1984~). Thus, when our investigation of volition started (H. H. Kornhuber & Deecke, 1964, 1965) it was in opposition both to the morality and the academic mentality of that time. Our research was in part a consequence of the experience that will is important for human behavior under difficult circumstances (H. H. Kornhuber, 1961). We began our investigation of volition with experiments on voluntary movements. At that time nearly nothing was known about the mechanisms of will underlying voluntary movement (Eccles & Zeier, 1980).

2. Methods In our research, four parameters of brain activation have been measured: (a) performance-related shifts of the cortical steady (DC) potential, (b) event-related EEG-spectrum, (c) regional cerebral blood flow (rCBF), and (d) event-related changes of neuromagnetic fields (magnetoencephalography, MEG).

2.1. Performance-related DC shifls Changes of cortical activation are associated with changes of the cortical steady (DC) potential. Increasing levels of cortical activation (changes from sleep to wakefulness, increased awareness, seizure activity, etc.) lead to a rise of surface negativity that is caused by the augmentation of excitatory postsynaptic events at dendrites of superficial cortical layers (for reviews see Caspers, Speckmann, & Lehmenkuhler 1980; Creutzfeldt, 1983). This is true for both global and regional changes:

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Activations of circumscribed cortical areas cause local shifts of the cortical DC potential of those areas as demonstrated by (a) recordings of field potentials between surface and depth in animals (e.g., Sasaki & Gemba, 1982), or (b) by recordings from subdural electrodes paired with a distant reference electrode (Neshige, Luders, & Shibasaki, 1988). The conductivity of the skull for currents enables the recording of cortical DC shifts even through scalp electrodes. Since conductivity of the skull is low as compared to brain tissue, there is a filtering effect, in that spatial resolution is diminished in scalp recordings as compared to epicortical recordings. In all our experiments, brain potentials have been measured from 10 to 13 positions of the scalp with linked-ears serving for reference. Performance-related cortical DC shifts, as measured by scalp recordings, are usually small, although amplitudes exceeding 30 pV are possible. In order to achieve the required signal to noise ratio, many trials have to be collected and averaged (48 to 128 trials or more) in a time-locked manner, with each trial triggered by an experimental event. In our experiments, electrodes have been placed according to the 10-20 system recommended by Jasper (1958). The following spatial relations between electrode positions and cortical gyri have been found by Homan, Herman, and Purdy (1987): Fp l F p2 (rostra1 limit of superior frontal gyrus); F3F4 (middle frontal gyrus); C3/C4 (precentral gyrus, shoulder to wrist area); P3P4 (superior parietal lobule near intraparietal sulcus, superior to posterior portion of supramarginal gyrus); T3/T4 (overlapping middle and superior temporal gyri); 0 1 / 0 2 (occipital lobe). Some additional electrode positions have been used: FCz (midway between Fz and Cz), C1 (midway between Cz and C3), and C2 (midway between Cz and C4). The odd-numbered sites lie above the left hemisphere, the even numbered sites lie above the right; the z sites are located along the midline. In all experiments, great care has been taken to eliminate artifacts caused by eye movements: During the analysis period, subjects had to fiiate on a point straight ahead and had to prevent blinks and other eye movements. Trials contaminated by eye movements or blinks were excluded from the average. For this purpose, the electro-oculogram (EOG) has been recorded. Recent experiments introduced true DC recordings (M. Lang, Lang, Uhl, et al., 1987; W. Lang, Lang, Podreka, et al., 1988; W. Lang, Lang, Uhl, Koska, et al., 1988; W. Lang, Zilch, Koska, Lindinger, & Deecke 1989). In one experiment, the radial current density into the scalp was calculated and mapped (Lindinger, Lang, Obrig, Kristeva, & Deecke, in

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press). This procedure, as suggested by Hjorth (1975), Nunez (1981), and Perrin, Bertrand, and Pernier (1987), has the advantage of being reference-free and of decreasing the effect of volume conduction. To estimate radial current density, the scalp distribution of DC potentials was interpolated between electrode positions by use of polynomial cubic splines. Based on this continuous surface, the radial current density was estimated by applying the 2-dimensional Laplacian operator. The influence of the amplitude at an electrode position to the shape of the potential-surface can be weighted by spline functions, a procedure that is important for estimating potentials at the boundaries of the map (see also Koles, Kasmia, Paranjape, & McLean, 1989). For calculations and display of images, a simple head model is used: The scalp is assumed to be a square with left/right boundaries at T 3 n4 and anterior/posterior boundaries at Fpl,Fp2/01,02. Each side of the square is subdivided in 20 sections; this results in a spatial map-resolution of 400 points. For boundary estimation it is assumed that potentials decrease continuously to zero outside the square.

2.2. Event-related EEG spectrum In our experiments, EEG data have been filtered (32 Hz, 48db/octave low pass) and digitized at a sampling rate of 100 data points per second. Event-related EEG spectra have been calculated in periods of 1 to 1.28 s each using the Fast Fourier Transformation (FFT). For each spectrum, 30-50 sweeps have been averaged and Bartlett’s smoothing method has been used to reduce the cut off errors caused by the short epoch length (Diekmann, 1985). Data have been strictly edited off-line; eye, lid, and muscle artifacts have been rejected. Mean power density (MPD) has been computed for the classical frequency bands: (Delta, Theta [e; 3-7 Hz], Alpha [a; 7-14 Hz], and Beta) and for the total spectrum. Two parameters are of particular interest in our experiments, (a) the performance-related increase of the e-MPD, called IN-e-MPD and (b) the performance-related attenuation of the a-MPD, called AT-a-MPD. IN-e-MPD and AT-a-MPD have been calculated relative to the resting state, which is taken from a period that precedes volitional task initiation by 3 to 4 s. MPDs of performance-related epochs show considerable inter-individual variation. The calculation of changes between resting state and performance-related epochs minimizes the effects of this interindividual variability. So far, the a-rhythm has been widely investigated in humans, but little is known about the origin and physiological significance of the

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e-rhythm. In lower primates, as well as in humans, the "cortical" e-rhythm (as recorded directly from the cortex or by scalp electrodes) is related to effort in information processing and learning (Doyle, Ornstein, & Galin, 1974; Ahern & Schwartz, 1985; Dolce & Waldeier, 1974; Haslum & Gale, 1973; Ishihara & Yoshi, 1972; Gale, Christie, & Penfold 1971; Otto, Gruner, & Weber, 1983a, 1983b; Rugg & Dickens, 1982; M. Lang, Lang, Diekmann, & Kornhuber, 1987; W. Lang, Lang, Kornhuber, Diekmann, & Kornhuber, 1988). Little is known about the relationship between the "cortical" e-rhythm and the hippocampal e-rhythm; the latter is well investigated in primates and has also been found in humans (Arnolds, Lopes da Silva, Aitinik, Kamp, & Boeijinga 1980; Lesse, Heath, Mickle, Monroe, & Miller, 1955). In primates, hippocampal e-activity has been found to be linked to cognitive behavior such as learning (Crowne, Konow, Drake, & Pribram 1972; Crowne & Radcliffe 1975). Indirect evidence for a relation between limbic e-rhythm and "cortical" e-rhythm has been found in epileptic patients (Talairach, et al., 1973): Stimulation of the anterior cingulate was associated with a spread of excitation to the adjacent frontomedial cortex (including the SMA), and a steady 3-8 Hz rhythm developed in the EEG during stimulation, which was maximum at the vertex. Topographical analyses of the e-rhythm in scalp recordings point to an origin in the fronto-mesial cortex (Koles et al. 1989). For all these reasons, a functional relationship between the limbic system and the frontomesial e-rhythm in humans is assumed.

2.3. Regional cerebral blood flow by Tc-99m-HMPAO brain SPECT Single Photon Emission Computerized Tomography (SPECT) using

Tc-99m-Hexamethylpropyleneamineoxime(Tc-99m-HMPAO) makes it possible to visualize the distribution of regional cerebral blood flow (rCBF) of the brain. Tc-99m labelled HMPAO crosses the blood brain barrier with a high first pass extraction fraction. The tracer is deposited in brain tissue within the first two minutes after intravenous injection and is distributed there proportional to the cerebral blood flow. Within the immediately subsequent 2-hour period, redistribution of the tracer has not been measurable (Neirinckx et al., 1987; Podreka et al., 1987; W. Lang, Lang, Podreka, et al., 1988). Dosages of 0.2 mCi/ kg body weight have been applied in our studies. Local radioactive count rates (gamma-ray) have been measured by means of a dual-head, rotating, scintillation (gamma) camera. A parallel-hole collimator of high resolution (FWHM: 12 mm in the horizontal plane) has been used and 60 (2 x 30) projections have been achieved within 30 min (60 s per angle) with a linear sampling

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distance of 3.125 mm. Projections have been filtered before reconstruction and corrected for tissue absorption. Seven 3.125 mm thick slices have been summed up consecutively to achieve a set of transverse slices 21.9 mm thick covering the entire organ for final evaluation. Guided by anatomical templates, regions of interest (ROI) have been defined within five consecutive 21.9 mm thick transverse slices. ROIs are not necessarily congruent with anatomical boundaries, but it is assumed that the proportion of Tc-99m-HMPAO deposition in the respective anatomical structure is a major source for variation of the count rate of the whole region (Goldenberg, Podreka, Steiner, & Willmes, 1987). An absolute quantification of Tc-99m-HMPAO SPECT studies is not yet possible. For that reason, a relative local count rate (RI, regional index) has been obtained by referring the tracer concentration within each ROI to the mean count rate across all regions. It is important to note that only relative patterns of perfusion and their task-induced changes can be described. No information is available about absolute level of perfusion and task-induced changes of this parameter.

2.4. Magnetoencephalography Moving charges are associated with magnetic fields. In the nervous system, excitations of neurons cause intracellular and extracellular currents. Assuming a spherical model of the brain, magnetic fields as caused by extracellular currents cancel each other because of the symmetrical spreading of currents within the surrounding brain tissue. It is, therefore, the intracellular current that contributes to magnetic fields at the scalp surface. If particular areas of the cortex become activated, for example, by afferents from the periphery, intracellular currents of activated cortical neurons have an orientation that is perpendicular to the cortical surface. The reason for that orientation of intracellular currents lies in the fact that neurons together with most of their dendrites and neurites are oriented parallel to each other, and perpendicular to the cortical surface. The summation of intracellular currents within a certain cortical area is described by "current dipoles." Since the cortex is folded into gyri, dipoles have either tangential (two tangential directions in the three-dimensional space) or radial orientations with respect to the scalp surface. Dipoles having oblique directions can be decomposed geometrically into tangential and radial vectors. To sum up, magnetoencephalography (MEG) measures changes of the magnetic flux caused by tangential components of current dipoles which vary its strength over time.

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At the neurological clinics of Ulm and Vienna multi-channel MEG devices have been built. MEG is recorded in a magnetically and electrically shielded room, in Vienna, with two seven-channel, secondorder gradiometers using dc-SQUIDS (Superconducting Quantum Interference Device) with coils having a diameter of 1.8 cm (coil baseline 4.0 cm; Biomagnetic Technologies, Inc., San Diego, CA), whereas in Ulm a 24-channel system is used. MEG system noise is reducible by shielding to 10 femtoTesla/Hz’’2 .

2.5. Methodological considerations Physiology and informative content differ between electrophysiologic and circulatory-metabolictechniques: Electrophysiologic techniques (EEG, MEG) measure neuronal activity with high temporal resolution that is only limited by the setup of the data acquisition system. The ability to localize neuronal activity in the brain is different in EEG and MEG. In MEG, the present use of gradiometers and limitations of sensitivity restrict this method to investigations of neuronal activities which are close to the surface. Magnetic flux diminishes rapidly when increasing the distance of the sensing system. But this neuronal activity closely related to the surface can be localized with remarkable precision. For example, it is possible to demonstrate in humans the somatotopic organization of the primary motor cortex (MI; Cheyne, Kristeva, Lang, Lindinger, & Deecke, in press) or of the somatosensory cortex (Okada, Tanenbaum, Williamson, & Kaufman, 1984). Even the tonotopic organization of the primary acoustic cortex has been demonstrated with this method (Romani, Williamson, Kaufman, & Brenner, 1982). In the EEG, the ability to localize neuronal activity is limited. This is because extracerebral tissues (in particular the skull) have remarkable smearing effects on the scalp potentials generated by extracellular currents. There is no smearing effect of extracerebral tissue on magnetic fields. The EEG and the MEG delineate two aspects of neuronal activity and complement each other. For both EEG and MEG, considerable progress is going on in two directions, one localizing dipoles, and the other decomposing dipoles which become active simultaneously in different cortical areas. The combination of multi-channel EEG and MEG devices, coupled with realistic models for dipole decomposition and dipole fitting, along with magnetic resonance imaging (MRI), provides the possibility of assessing neuronal activity with high resolution in time and space. Circulatory-metabolic methods like SPECT do not measure neuronal activity directly. Rather, these techniques measure regional cerebral blood

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flow or metabolic parameters such as the regional glucose utilization in the brain. Close connections between neuronal activity and blood flow and metabolism are assumed. The temporal resolution of these techniques is limited; 20 s seems to be the best resolution at present for PET (in the Tc-99m-HMPAO SPECT technique between 90 and 120 s). The spatial resolution is high, in PET (positron emission tomography) resolution of 4 to 6 mm in the horizontal plane have been achieved (resolution of the Tc-99m-HMPAO SPECT technique is about 10 mm, but could be improved).

3. Results and Comments 3.1. The initiation of volitional actions: When to do 3.1.1. Human pathophysiokiigy. Real volitional action is spontaneous, that is, it is triggered by internal events. This is in contrast to re-actions triggered by external cues from the environment. In Parkinsonian patients, the clinical phenomenon of kinesia paradoxica points towards an impairment of the internal trigger and a dependency on external cues: the otherwise frozen individual may move briskly when a loud verbal command is given or when an accompanying person makes a step forward. The symptom of kinesia paradoxica, therefore, suggests that, while motor plans and motor programs are maintained, the trouble is a matter of access: the internal access is disrupted, the external one is partially preserved. Acute, unilateral lesions of the supplementary motor area (SMA) produce a transient l'akinesia'' or a lack of spontaneous activity on the contralateral side (Penfield & Welch, 1949; Laplane, Talairach, Meininger, Bancaud, & Orgogozo, 1977) or a transient inability to initiate speech (Masdeu, Schoene, & Funkenstein, 1978; Jonas, 1981). Selective impairments of volitional movements with preserved ability to react to external cues have been described in patients with lesions of the frontomesial cortex by Beringer (1944) and by Goldenberg, Wimmer, Holzner, and Wessely (1985). A patient with an infarction in the territory of the right anterior cerebral artery was unable to voluntarily move his left arm, but did so when grasping objects with his left hand which were moved towards him (authors' observations). The so-called "alien hand sign" (Brion and Jedynak 1972) has also been observed in patients with lesions of the SMA (Goldberg, 1985). The "alien hand sign" describes the phenomenon in which patients start to perform apparently purposeful actions but experience them as not being started by their own will. This

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symptom seems to be compatible with a role of the SMA in the initiation of volitional movements. 3.1.2. Human voluntary movement physiology: The Bereitschaftspotential. Research on movement-related brain potentials in humans started in 1964 by investigating brain potentials preceding self-initiated rapid flexion of the index finger (H. H. Kornhuber & Deecke, 1964, 1965). A slow, surface negative potential shift started about one second before the initiation of the movement, as defined by the first EMG response (Figure 1). It has been called Bereitschafrspotential (BP) or readiness potential. The BP has a rather consistent temporo-spatial distribution over the scalp: It starts in leads of the frontocentral midline, namely in Cz or FCz (Deecke, Grozinger, & Kornhuber 1976; Kristeva, Keller, Deecke, & Kornhuber 1979; Grozinger, Kornhuber, & Kriebel 1979; Boschert, Hink, & Deecke 1983; Deecke, Heise, Kornhuber, Lang, & Lang 1984; W. Lang, Lang, Heise, Deecke, & Kornhuber, 1984). It is important to note that even in unilateral movement, the BP starts bilaterally symmetrical in central and parietal recordings. In finger movements, BP becomes lateralized in central regions about 500 ms prior to movement onset, with the larger amplitudes contralateral to the performing hand (Deecke, Scheid, & Kornhuber, 1969; Deecke et al. 1976). BP maxima at movement onset have a characteristic pattern as well: maxima have been found in FCz and Cz, or C1 for right sided finger movements (C2 for left). Changes of BP topography associated with movements of different parts of the body (fingers, toes, hip, etc.) have demonstrated that the primary motor cortex (MI) is activated, starting between 200 and 500 ms prior to movement onset. Fingers and toes, for instance, have different representation areas in MI, with toes being located in mesial parts and fingers in lateral parts of the precentral gyrus. Comparing finger and toe movements, changes of BP topography at the scalp surface can be predicted by current dipoles arising in the particular representation area of the MI cortex (Boschert & Deecke, 1986). With magnetoencephalographic recordings (MEG) the current dipole in the MI cortex prior to self-paced movements could be localized (Deecke, Weinberg, & Brickett 1982, Deecke, Boschert, Weinberg, & Brickett 1983; Cheyne & Weinberg, 1989; Cheyne et al., in press). Recent MEG measurements in unilateral finger movements have provided evidence that not only the contralateral MI cortex becomes active prior to movement onset but also the ipsilateral one (Cheyne & Weinberg, 1989), confirming what Kornhuber and Deecke

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Figure 1. Slow shifts of the cortical DC potential (Bereitschaftspotential, BP) preceding volitional, rapid flexions of the right index finger a t time t = 0 s (vertical line). Recording positions were precentral left (L prec, C3), precentral right (R prec, C4), mid-parietal (Pz). Recordings were unipolar, with linked ears as reference. The difference between the BP in C3 and in C4 is displayed in the lowest graph (UR prec). Superimposed are the results of eight experiments with the same subject on different days. From Deecke et al., 1976.

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had already reported in 1965. But the signs of MI activation appear late (within the last 500 ms before movement onset) in the chain of cortical activation preceding self-paced movements. What then generates the early BP? BP is already in evidence 1 to 2 s prior to movement onset in recordings over the fronto-central, mesial cortex (FCz and Cz) and has its clear maximum there. These two characteristic features are present in various movements such as speech production (Grozinger et al. 1979; Deecke, Engel, Lang, & Kornhuber 1986), saccadic eye movements (Becker, Hoehne, Iwase, & Kornhuber, 1972) or limb movements, and thus point to a common cortical structure which seems to be involved in the initiation of all kinds of volitional movements. In 1978, recordings of the BP in patients with Parkinson’s disease (Deecke & Kornhuber, 1978) and measurements of the regional cerebral blood flow (Lassen, Ingvar, & Skinhoj, 1978; Roland, Larsen, Lassen, & Skinhoj, 1980) led to the following hypotheses: (a) The mesial, fronto-central cortex, including the supplementary motor area (SMA) becomes active in volitional movements. (b) It is this cortical area whose activation causes the early component of the BP in FCz and Cz. (c) BP maximum in the midline (Cz and FCz) is not due to a summation from more lateral potentials on both sides. MEG studies have supported the concept that at least two cortical areas become activated prior to volitional finger movements: Initial activity can be picked up from the SMA, subsequently the MI cortex is additionally activated (Deecke, Boschert, Brickett, & Weinberg, 1985). 3.1-3. Centralization of the starting function in volitional actions. Studies of the Bereitschafspotential, and observations in patients, give consistent evidence that the supplementary motor area (SMA) is the central key structure transducing the will-to-move into effective actions. In other words, the Sh4A has a common starting function for the various kinds of volitional actions such as movements of eyes, limbs or tongue (H. H. Kornhuber & Deecke, 1985). The centralization of the starting function is all the more remarkable for the fact that execution and control of different kinds of movements are widely decentralized in the human brain. For example, the musculature of tongue and mouth is innervated when speaking or chewing in a very precise way. But different parts of the cortex are involved when coordinating tongue and mouth during chewing on the one hand and speaking on the other. In speech production, the area of Wernicke in the temporal lobe and the basal ganglia seem to be important in creating and acoustically controlling the various phonemes (Brunner, Kornhuber, Seemiiller, Suger, & Wallesch,

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1982; H. H. Kornhuber, 1984a,b; Wallesch, Henriksen, Kornhuber, & Paulson, 1985). Motor systems for eating and chewing developed early in evolution, long before the production of speech. In rodents, the primary motor cortex developed along with the necessity of tactually controlling movements of tongue and mouth. In humans, the primary motor cortex not only controls movements of tongue and mouth but also has the function of tactually and proprioceptively controlling movements of limbs and fingers (particularly, in precision movements; H. H. Kornhuber, 1971, 1974, 1984a,b; Aschoff & Kornhuber, 1975). Furthermore, movements of the eyes are not represented in the primary motor cortex. Saccadic eye movements are organized in the pontomesencephalic region, the parieto-occipital cortex and under certain circumstances in the frontal eye field (Bruce & Goldberg, 1985). Although the motor system is decentralized and widely distributed in the brain, the Bereitschaftspotentialpoints towards a common structure, the SMA, which is involved in the volitional initiation of actions. Meanwhile, positron-emission-tomography and animal experiments have substantiated the activation of the SMA in voluntary saccadic eye movements (Fox, Fox, Raichle, & Burde 1985; Schlag & Schlag-Rey, 1985). SPECT (Single Photon Emission Computerized Tomography) data support SMA activation in speech production (Ingvar, 1983). The SMA is hypothesized to transduce the will-to-move into effective actions (H. H. Kornhuber, 1980). This process requires input from the motivational system to the Sh4A which has been demonstrated anatomically. There is direct or indirect (via the thalamus) input from hypothalamus, amygdala, inferior temporal cortex and prefrontal cortex (Jones, 1983; Wiesendanger & Wiesendanger, 1985). Patients with lesions of the SMA have and experience their will to move; they are able to select between motives and drives (what to do), but the transduction of their intentions into actions is disrupted. 3.1.4. Selecting the "right"moment to start a movement. The hypothesis that the starting function of volitional actions is centralized and organized within the SMA has implications for the motor system. For instance, consider a person performing a rapid reaching movement while walking. Movements of this kind have consequences for posture and have to be embedded into the ongoing motor behavior. Therefore, anticipatory mechanisms for postural adjustment and for the temporo-spatial integration of ongoing and intended actions are necessary. The "right" time to start the reaching movement cannot be settled by the person without having the knowledge that anticipatory adjustments are being prepared.

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Neuro-anatomical data would substantiate this view: The SMA has input from the sensorimotor cortex, from the cerebellum and basal ganglia via the thalamus, and from the motivational system (from hypothalamus, amygdala, inferior temporal cortex and prefrontal cortex). Because of these circuits linking SMA to other brain structures, the function of the SMA should not be studied in isolation. Indeed, the SMA seems to play a central role (both anatomically and functionally) in the critical decision of when to start a movement. The SMA has been linked to several functions such as anticipatory adjustments of posture (Massion, Viallet, Massarino, & Khalil, in press) instruction-induced preadjustments of sensorimotor behavior (Tanji, 1984), and the "programming" of action sequences which are "projectional" in that they rely on model-based predictions (Goldberg, 1985). According to the present concept these data and hypotheses have to be re-interpreted and integrated: (a) Anticipatory adjustment and integration of ongoing and intended behavior have to be settled before volitional actions can be started. (b) The starting function of volitional actions is centralized in the SMA. (c) In order to select the "right" time to start the movement, the SMA must have, at least, some information about, or some kind of control over, anticipatory mechanisms. (d) It is not reasonable to assume that all anticipatory mechanisms are organized by the SMA itself. Rather, it is likely that other brain structures get involved. However, the heavy interconnection of the SMA with other brain structures is entirely consistent with the hypothesized key role of initiation and coordination. In a recent experiment, movement-related potentials were recorded during an ongoing performance when an additional action, having strong tendencies to interfere with the ongoing performance, was initiated. Four conditions were investigated (W. Lang, Obrig, Lindinger, Cheyne, & Deecke, 1989): (a) Subjects started to flex and extend repetitively their two index fingers. Frequency of finger flexions was about 2/s. Subjects were instructed to start synchronous movements of the left index finger after some time (about 4 to 6 s after having started the right finger). This task has been called RH-SI (the right hand started, and the task was simple in nature). In (b) the left index finger started the simple task (LH-SI). In (c) the right finger started as in RH-SI with flexions at a frequency of 2/s. But now subjects had to perform flexions at a rate of 3/s with the left hand (RH-COM; right hand, complex situation). As in all tasks, subjects were free to determine the onset of left and right finger movements (in RH-COM the left finger usually started with a delay of 4 to 6 s after the right one). Task (d) corresponded to (c) but now the left

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finger started to move and the right one followed (LH-COM). Only music students participated in these experiments. They were well trained to perform dissociative rhythms with their index fingers but stated that it took a high degree of effort and concentration to start the 3/s rhythm when already moving the other finger at 2/s. The main point of interest was whether brain potentials preceding movement onset of the second finger (at time t*) would differ between complex (COM) and simple (SI) tasks. Consequently, movement-related, negative, DC shifts were averaged, time-locked to t*. Amplitudes were referred to a baseline taken in the resting state (4 to 3 s before initiating the whole task by moving the first finger). When preparing to start the 3/s rhythm with the second hand, negative potential shifts were larger than they were in the simple task (Figure 2). This difference (Nd: difference of negativity; i.e., extra negativity for the complicated rhythm) developed early -- about 4 s before t*-- and rendered large and significant differences over the central midline (Cz, C1, C2) and in Pz. For statistical comparisons, mean negativities across intervals of one second (N,: between t = 4 s and t = 3 s before t*; N3; N,; Nz) were calculated. Effects of the within-subject factors, "complexity" and "performing hand", on mean negativities were calculated by repeated MANOVAs. In C1, C2, Cz, P3, P4, and Pz, task complexity had a significant effect in all 4 intervals, N, to N4 (e.g., in Cz: F = 1 . 8 , ~< .004 for N,; F = 1 1 . 0 , ~< .005 for N3; F = 1 6 . 9 , ~< .001 for N2; and, F = 2 4 . 8 , ~< .0001 for Nz). Studies concerning inter-limb coordination point to limitations when executing movements simultaneously. Simultaneous movements can be performed accurately as long as they are harmonically related, either in phase or in alternation. Movements that are not harmonically related display interference when performed together (e.g., Klapp, 1979). Kinematic analyses indicate a common time scaling when coordinating bimanual movements (Kelso, Putnam, & Goodman 1983). Bimanual sequences at different rhythms, as investigated in the present study, create tendencies of mutual interference. Although subjects were trained musical students, effort was needed to overcome these interference tendencies . One result of the present study was that interference tendencies are effective not only when performing the task but also long before, in clear anticipation of the task (as evidenced by the DC negativity recorded). Any control mechanism that might, hypothetically, offset interference during task performance might also be too late to be fully effective. Effective coordination would appear to require a control mechanism capable of anticipating impending interference, such as that suggested by

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Figure 2. Slow DC-potential shifts preceding the time (t*: vertical line) at which the second hand (here, right hand) starts to move. There is already an ongoing performance of the other hand (here, left hand) with finger movements at a frequency of about 3s. Thin lines: The right finger (second hand) is brought in with the 3/s rhythm at t*. Thick lines: The right finger joins in with the 2/s rhythm at t*. Baseline was taken from the resting period before movement onset of either hand. Averages across all subjects, negativity up. Abscissa: time (s). Ordinate: amplitude (scaled in 20 pV).

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the early Nd. Nd may indicate increased motivational and intentional involvement when subjects prepare to act in a conflicting task. In other words, in order to get ready to start the movement, information about ongoing and intended actions has to be integrated by sensory input or by memory-based models of movement outcome and consequences. This integration requires effort and motivation. Nd appears over the central midline (Cz, C1, C2) and parietally (Pz). In view of this topography it is reasonable to assume that the mesial cortex, including the SMA, is involved in this process. Interestingly, at times, subjects did not reach the state of readiness in the complex task, and in these instances were not able to initiate the 3/s sequence. 3.1.5. Afer the starting signal has been released. Systematic analysis of the potential’s time course reveals that in approximately 85% of all subjects the BereitschufspotentiaZ reverses to a positivity about 90 ms prior to movement onset (pre-movement positivity, PMP; Deecke et al., 1969; Deecke et al., 1976). About 50 ms prior to movement onset, a sharp

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negative potential shift arises in the recording over the contralateral MI cortex. This negative potential has been called motor potential (MP; Deecke et al., 1969). It does not reflect the first activation of the MI cortex. As described above, the contralateral and, to a lesser degree, the ipsilateral MI cortex become activated 500 ms before movement onset. MP may correspond to synaptic events in conjunction with the pyramidal cell firing in area 4 (MI cortex) as the activity in the final motor pathway to alpha motoneurons in the spinal cord. 3.1.6. Basal ganglia and cerebellum in the initiation of volitional actions. The latency of about 40 ms between PMP and MP led to the hypothesis that the decision to move is not transferred in a direct way to the MI cortex, but, rather, via a subcortical loop including basal ganglia and the cerebellum (H. H. Kornhuber, 1971, 1974). Recordings of single neurons have supported such a view (Lamarre, Spidalieri, Busby, & Lund 1980; Melnick, Hull, & Buchwald, 1984). Recordings in Parkinsonian patients during stereotactic operations suggested the existence of slow negative potential shifts in the thalamus prior to uncued, self-paced movements (Knapp, Schmid, Ganglberger, & Haider 1980; Straschill & Takahashi, 1980). A recent study in monkeys demonstrated slow negative potential shifts arising about 500 ms before movement onset in several subcortical nuclei such as substantia nigra, red nucleus, midbrain reticular formation and caudate nucleus (Bauer & Rebert, in press). Therefore, regarding volitional action, theories about "preparatory set" should include circuits linking basal ganglia, cerebellum and cortex. 3.1.7. SMA and the temporal organization of motor sequences. In the preceding section, a theory has been presented in which the selection of the time to start a movement (when to start) is made by the SMA, with its multiple afferents from motivation and sensorimotor systems. This theory separates the decision when to do from other activities involved in volitional movements such as what or how to do. In order to make this functional separation clear, it is important to contrast it against an alternative theory of SMA function put forward by Roland et al. (1980) and Goldberg (1985). In his 1985 review article, Goldberg suggested that: the SMA has an important role to play in the intentional process whereby internal context influences the elaboration of action. It may be viewed as phylogenetically older motor cortex, derived from anterior cingulate periarchicortical limbic cortex, which, as a key part of the medial premotor system, is

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H. H. Komhuber ef al. crucial in the "programming" and fluent execution of extended action sequences which are "projectional" in that they rely on model-based prediction .... the SMA plays an important role in the development of the intention-to-act and the specification and elaboration of action through its mediation between medial limbic cortex and primary motor cortex. (p. 567)

Roland (1984) proposed that the SMA either elaborates or retrieves from memory the necessary information to form a short sequence of motor commands in which the elementary movements to be executed are specified exactly. With an example from the motor sequence test one could say that the SMA specified: (1) the fingers to be moved in the near future, (2) which were the movements of the individual fingers (i.e., opposition, flexion, extension) and (3) the sequence of (1) and (2). (pp. 209-210) Goldberg and Roland propose that the SMA forms and specifies subroutines in motor sequences during preparation and execution. According to their view, the SMA does not serve to transduce the willto-move into effective action, that is, to give the starting signal, but is involved in the process of determining how to perform the movement. In one experiment, subjects were asked to simulate internally the performance of the motor sequences without actually executing them (Roland et al., 1980). It was found that the SMA was still activated, while the primary motor cortex was not. The following three experiments were designed to test our theory against the one of Roland and Goldberg: Experiment I (W. Lang, Lang, Uhl, Koska, et a]., 1988): In this study 20 young, healthy human subjects performed four different kinds of motor sequences. In all tasks, subjects held their index fingers in an intermediate position during the resting period and started to move the fingers in order to repeatedly reach three positions, a flexed, an intermediate and an extended one. In SI-S, movements were performed simultaneously in the same direction. In SE-S, the right index finger started, the left finger followed with a delay of one movement (sequential). In SI-D, the sequence was initiated by flexing the right finger while simultaneously extending the left. Thus, the two index fingers moved simultaneously but in different directions. In SE-D, movements were

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performed sequentially and in different directions. Since it was our goal to study the planning and execution of learned movement sequences, subjects practiced each sequence thoroughly in pre-experimental sessions. In the experiment, subjects started the motor sequence at their own volition and performed the task for at least 6 s. An epoch of 5 s prior to movement onset and 6 s thereafter was analyzed. Two parameters were taken to describe negative DC shifts: N-BP (mean negativity over the last 250 ms prior to the volitional initiation) in order to describe the Bereitschafs~otentl,and N-P (mean negativity measured between 2 and 4 s after movement onset) to describe performance-related negative DC shifts. In this experiment, effects of the within-subject factors, "temporal organization" (simultaneous or sequential) and "spatial organization" (same or different directions), were tested by MANOVA. The results were that during the two sequential tasks, SE-S and SE-D, there was a large and sustained negative DC shift in recordings over the mesial fronto-central cortex. In contrast, in the two simultaneous tasks, SI-S and SI-D, performance-related negativity (N-P) declined rapidly over the epoch. This difference between SE and SI tasks was restricted to recordings of the mesial fronto-central cortex and had its maximum in Cz (F = 18.9, p < .0001; see Figure 3). Performancerelated DC shifts did not vary as a function of "spatial organization"; that is, there was no difference whether subjects moved their index fingers in the same or in different directions (for Cz: F = 2.2). Using the Wilcoxon, matched-pairs, signed-rank test, the Bereitschafs~otentialin Cz was significantly larger (p < .017, two-tailed) in SE-S as compared to SLS. Topographical differences of N-BP and N-P between SE-S and SI-S are displayed chromatically in Figure 14 on page 152. This color figure demonstrates the additional activation of the mesial frontocentral cortex in SE-S as compared to SI-S when preparing and executing these tasks. According to Roland's view, the way in which the finger had to be moved (same or different directions) should have had an effect on SMA activity and on performance-related DC shifts in recordings of the frontocentral midline. But such an effect was not found in our experiments. Note the large differences between SE and SI tasks, and the localized appearance of Nd (difference of negativity) in recordings from the frontocentral midline (which is likely to pick up the activity of the SMA). In SI-tasks, performance-related negativity decreases, perhaps reflecting automation of the motor sequence when the two index fingers act in phase. The situation is different in SE tasks. There is a sustained, and rather localized negative DC potential in Cz, C1 and C2. The reason

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Figure 3. Grand means averaged across all 20 subjects for each of 4 conditions: SI-S (simultaneous, same direction), SE-S (sequential, same direction), SE-D (sequential, different directions) and SI-D (simultaneous, different directions). Movement onset at t = 0 s (first activity of the right flexor indicis). The Bereitschaftspotential precedes the voluntarily initiated motor performance; task execution is accompanied by a negative DC potential shift (performance-related negativity). Data from W. king, Lang, Uhl, Koska, et al., 1988. may be that in SE-tasks, movement initiation is dissociated between the two index fingers. This situation is demanding for the central structure (SMA) responsible for starting the movement, and it is known that the two SMAs act in accord (i.e., even in unilateral movements the SMA of either hemisphere is activated, Brinkman & Porter, 1979; Roland, Meyer, Shibasaki, Yamamoto, & Thompson, 1982). Thus, the starting signal to move the index finger of one side can only be given when control mechanisms ensure that a movement of the other side is inhibited. However, this does not imply that the SMA also has to organize this inhibition. Rather, it implies that the SMA must have information that contralateral inhibition is settled when giving the starting signal. The increased activation of the SMA in the SE task, as compared to the SI

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task, has recently been substantiated in an experiment using the Tc-99mHMPAO SPECT technique (W. Lang, Podreka, & Deecke, unpublished data). Experiment II (W. Lang, Oldenkott, Goldenberg, Reisner, & Deecke, 1988): A total of 15 patients with chronic unilateral lesions of the SMA were examined using the SE and SI tasks. Latencies between the acute state of SMA lesion and date of examination ranged between 8 and 84 months (mean: 34). Eight patients had the lesions in their right, 7 in their left hemisphere. They had no paresis and performed at normal rates in a unilateral tapping test. In the study, they performed 64 trials of two different movements: Simultaneous flexions and extensions of the two forefingers (SI task), and sequential movements of the two forefingers (SE task: extension on the right side, extension left, flexion right, flexion left, etc.). Trials were voluntarily initiated and lasted 6 s. Movements were measured using a splint with potentiometers at the proximal finger joint. The following symptoms were observed: (a) Bradykinesia contralateral to the lesion in SI and SE, (b) marked deceleration of initial movement, (c) switching from sequential performance into simultaneity and (d) frequent failure to initiate or inhibit a movement on one side or the other (as demonstrated in Figures 4 and 5). Experim.ent III (M. Lang, Lang, Kornhuber, Groger, & Kornhuber, 1988): Eight right-handed subjects performed flexions of their right index finger in three different conditions. In one situation, subjects had to initiate single movements according to a precise timing structure which was defined by four intervals, for example 3, 7, 5, and 2 s. In this task, the Bereitschufispotentil was significantly larger in fronto-medial electrodes than in conditions involving either rhythmic, repetitive movements (at about 3/s) or movements which were performed at irregular intervals (see Figure 6). In addition to these experiments, clinical symptoms such as kinesia paradoxica in Parkinsonian patients and the inability to initiate speech and limb movements in acute unilateral SMA lesions can also be taken as evidence that the decision when to do is a process per se and has to be separated from other aspects of volitional actions. Recently, experiments were conducted to compare movement related DC shifts during SE and SI tasks as subjects either moved or imagined moving (mental rehearsal). Preliminary results (in 12 subjects) indicate that in the imagery task, retrorolandic areas are activated during SE and SI, but not the frontocentral midline. In Tc-99m-HMPAO SPECT studies on imagery of motor performances, activation of the SMA could not be found (Goldenberg,

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Figure 4. Finger movements of the right (RH) and left (LH) hand were measured by goniometers. Patients had to perform extensions and flexions in a sequential manner starting with an extension of the right index finger. Examples of omissions of movements of the left finger in various patients (disturbance of movement initiation). Omissions are indicated by a bold horizontal line. In the lower traces, the left finger is not moved at all (left side) or stops moving (right side). As shown, the degree of the symptom "omission of movement" varies. Podreka, Steiner, Suess, & Deecke 1988; W. Lang, Lang, Podreka, Goldenberg, & Deecke, 1989). Results of Experiment I1 are supported by other clinical findings: Patients with unilateral lesions of the SMA not only have difficulty voluntarily initiating single movements but also have difficulties initiating motor elements in a sequence. Jonas (1981) examined speech and found the following symptoms: disturbances to the initiation of propositional speech, hesitations, explosive speech, running of words together, variability in rate of speech emission and speech arrest. Forster (1936) in his remarkable clinical handbook of neurology described the following symptomatology when examining 40 patients who had lesions of the SMA (area 6aB) after surgical treatment for partial epilepsy:

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Figure 5. Finger movements of the right (RH) and left (LH) hand were measured by goniometers. Patients had to perform extensions and flexions in a sequential manner starting with an extension of the right index finger. Examples of the tendency to continue movements on one side (lack of movement inhibition) instead of alternating between left and right are indicated by arrows.

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I have operated area 6aS [corresponding to the supplementary motor area, SMA] in about 40 patients. Immediate consequences consisted in minor weakness and bradykinesia when moving limbs of the contralateral side or when turning and inclining either head or trunk to the contralateral side....Single, proximal and even distal movements can be performed by the limbs of the contralateral side within the normal scale. Composited movements, however, exhibit a loosening of its structure. There is a disruption of the fluent continuity by which single motor elements are spatially and temporally linked into composited movements. Single motor elements are performed separately, there are delays between them, one element can be omitted for a while and sometimes, an additional and "extra" impulse of will must be given for its initiation. (p. 279; translated into English by authors; for original text, see the Appendix.)

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3.2. Physiological signs of anticipatory, task-specific planning Intentionality in action is closely linked to the direction of an action toward a goal, that is, the achievement of a particular outcome. A volitional action is guided by abstract representations of its outcome. As described by Bernstein (1984), an individual has a "model of the future" that includes representations and motor plans of the outcome of an action (the knowledge of how to do). This "model of the future" stems from experience which is acquired by continuous interactions between the individual and its environment. Utilization of this memory-based "model of the future" supports the capacity to prospectively control behavior and to successively improve desired outcomes (Bernstein, 1984). Introspectively, task-specific planning prior to movement onset is a self-evident matter. Many observations are compatible with this assumption: Complex sequences of learned movements can be executed at a rate too fast to be guided by sensory feedback or for the individual components to be each under conscious control (Keele, 1968; Sternberg, Monsell, Knoll, & Wright, 1978). In speech production, one realizes that whole sentences are prepared in advance when observing anticipatory phonematic paraphasias in speech (e.g., "I sope so" instead of "I hope SOt1).

An example for a rather elementary kind of anticipatory, taskspecific "planning" has been given in section 3.1: When different parts of the body perform simple, rapid movements BP topography varies. The analysis of this variation revealed two BP components: A first component could be attributed to an activation of the SMA and remained invariant. A second component was specific for the part of the body moving. It developed at about 500 to 200 ms before movement onset and reflected activation of the primary motor cortex (MI). The question is whether the term "planning" is appropriate for this activation. For a long time it has been believed that the MI cortex is able to initiate and program volitional movements by itself. But it now seems evident that the MI cortex needs either direct or indirect input from basal ganglia, limbic systems, cerebellum, somatosensory association areas, and SMA in order to initiate movements (H. H. Kornhuber, 1971, 1974, 1984a,b). Pre-movement activation of the MI cortex may reflect final steps in the translation of motor programs into patterns of muscular activation. Amplitudes and topography of the Bereitschafspotential depend on structure and/or complexity of forthcoming tasks. Complex movements such as writing or drawing have BPs which are large, particularly early and widely distributed, even appearing in fronto-lateral recordings

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Figure 6. Left: Topography of the difference in Bereitschafispotential (BP) between "timed" and "irregular" flexion movements (cf. Exp. III in section 3.1.7). Mean values are taken from 130 ms to 30 ms prior to movement onset. Vertical line in each bar indicates k 1 standard error of the mean. The asterisk indicates a p < .05 in the one-tailed, Mann-Whitney U test. Right: The BP (cortical negativity vs. time, averaged over 8 subjects, movement onset at t = 0) in the "timed" (upper trace) and the "irregular" (lower trace) flexion movement over FCz. Since the experimental condition lacks a resting period, the baseIine was taken from 200 rns to 500 ms after movement onset. Recordings were unipolar, with linked ears as reference. (Schreiber et al., 1983). A sequence of two complex movements has a larger BP than one movement alone (Benecke, Dick, Rothwell, Day, & Marsden, 1985). Complex spatio-temporal sequences are preceded by larger BPs than simple and repetitive finger movements (W. Lang, Zilch, et al., 1989). Taylor (1978) studied the BP during the acquisition of a motor skill. A series of six button presses in a specified pattern constituted the motor task. The BP increased steadily at all electrodes as performance improved, that is, as response time decreased. This close correlation between BP increase and the acquisition of motor skill was taken as evidence that BP reflects task-preparation. After performance

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time reached asymptote, BP decreased in the frontal recording, Fz, but remained relatively constant in Cz. Large changes of BP topography take place in situations in which a voluntarily initiated simple finger movement triggers the presentation of stimuli (Deecke et al., 1984; W. Lang et al., 1984). Here the preparation of movement initiation is associated with other processes such as directing attention towards the forthcoming stimuli and preparing for its response. In such situations, BP is overlapped by another slow negative potential shift that has been called directed attention potential, DAP (see section 3.5). In summary, physiological signs of anticipatory, task-specific planning can be studied by the BP technique. Variations of BP topography indicate that various parts of the cortex (frontal, central, parietal) are involved in preparatory processes. As already described above, it turns out to be an oversimplification to contribute such planning functions to the SMA, as proposed by Goldberg (1985). Furthermore, variations of task complexity and structure not only require different amounts of programming but also different levels of motivational and intentional involvement, making it difficult to tear apart these preparatory processes of volitional actions. In order to investigate "preparatory set" neurophysiological techniques are necessary. Measurements of regional cerebral blood flow (rCBF) or metabolism do not posses the temporal resolution to separate states of preparation and those of performance. Some rCBF studies claimed that such a separation would be possible by measuring two separate states, (a) during task performance and (b) when "internally" performing the task without movement. But such argumentation may be erroneous. The "preparatory set" of volitional actions includes the transduction of the will to act into effective movements. The will to act includes the tendency towards its realization. When only imagining a task, that aspect of volition concerfied with the realization of intentions is missing and cannot be investigated.

3.3. Resoluteness: ability to maintain goals and adjust behavior Volitional actions are goal-directed. At times, goals can only be achieved in the distant future. But still, long term goals are maintained, a phenomenon that constitutes a basis for self-continuity during one's life. In the following experiments, subjects had instructions to reduce the error of performance in a conflicting-response-selection task across a series of trials. Maintaining this aim, subjects had to adjust their behavior to resist interference from inadequate stimulus-response patterns and to suppress shifts of attention and thought (M. Lang, Lang, Diekmann, & Kornhuber

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Figure 7. Subjects tracked a visual target (vt: circle) with a stylus held in their right hand. Horizontal and vertical coordinates [ x(t) and TV-SCREEN y(t) ] of tracking movements were transmitted to the TV screen in a linear ratio and I I displayed as a light spot (f: I feedback). In the learning I task, transmitted coordinates, I either of the horizontal (as PHOTO DETECTOR in the SPECT study) or the vertical (as in the DC-potential study) direction, were IOG multiplied by the factor (-1). In the DC-potential study, subjects fixed their gaze on a fixation point (FIX) in order to prevent artifacts in the EEG recordings. caused by eye movements. Thus, the stimuli were given in the lower field of vision. Subjects were not able to watch movement of the right hand. From W. Lang, et al., 1986.

1987; W. Lang, Lang, Kornhuber, Deecke, & Kornhuber, 1983; W. Lang, Lang, Kornhuber, & Kornhuber, 1986; W. Lang, Lang, Podreka, et al., 1988). In a recent experiment, two parameters of brain activity, performance-related D C shifts and Tc-99m-HMPAO uptake (SPECT, see 2.3) were measured. A total of 17 subjects participated in the SPECT study; in 16 of them, performance-related D C shifts were measured as well. Each subject performed two tasks. The order of tasks was balanced across subjects. Subjects held a stylus equipped with a pressure contact in their right hand (Figure 7). When a subject voluntarily lowered the stylus onto a pressure plate, a visual target (small circle) started moving across a CRT screen at constant speed in three successive steps of 1.5 s each; the direction of each step was randomly determined. Thereafter, the target jumped back to the center of the screen. Subjects had t o track

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I

Figure 8. Topographical distribution of performance-related DC-potential shifts, averaged across all subjects. The vertical line indicates the onset of the stimulus program (t = 0). Stimulus directions changed at t = 1.5 and t = 3 s, with the end of the stimulus program at t = 4.5 s. Upper row: Inverted Tracking (IT). Lower row: Tracking (T). Negativity up. The volitional initiation of stimulus onset is preceded by a Bereitschaftspotential (BP); task performance is accompanied by a slow negative potential shift, the performance-related negativity. From W. Lang, Lang, Podreka, et al., 1988. the target by moving the stylus with their right hand. This experimental design provided a continuous tracking performance. The position of the moving right hand was coupled back as a light spot on the TV screen. Accuracy of tracking was determined by the difference between target and light spot. In a visuomotor learning task (Inverted tracking, IT), subjects had to track horizontal movements of the stimulus in an inverted manner, that is, movements of the target to the right required hand movements to the left and vice versa; movements up and down were not inverted. In a control task (Tracking, T), subjects had to track the target in a normal, non-inverted manner. For further details of experimental procedure see W. Lang, Lang, Podreka, et al., 1988. Performance-related DC shifts: Tasks were performed four months after the rCBF measurements. It was assumed that the temporal delay

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would reduce memory effects and would therefore provide comparability between the two tasks. In order to avoid familiarity, the IT-task was modified in the brain potential study: now vertical movements of the target had to be tracked in an inverted manner, whereas left and right remained unchanged. After the 4.5 s of tracking, subjects moved the stylus to the starting position and had a resting period before starting the task again. Inter-trial intervals ranged between 8 to 12 s. Performance-related DC shifts are shown in Figure 8. The volitional initiation of the stimulus program was preceded by a Bereitschaflspatential (BP); visuomotor performance was associated with a slow negative DC-potential shift with larger amplitudes in IT as compared to T. Differences of amplitudes (Nd) had a clear fronto-central distribution (Figure 9) and were significant in frontal recordings, C3 and Cz. In these recordings, Nd was correlated with the success of a subject’s visuomotor learning; the coefficients of correlation, r, ranged between .6 and .8. The electrophysiological findings of previous experiments (W. Lang et al., 1983, 1986) were replicated. The conclusion of the DC-potential study, that frontal lobes are critically involved in visuomotor learning, was confirmed by the results of the SPECT study: In IT, as compared to T, there was an increased relative tracer uptake in frontal areas (in particular middle frontal gyrus of both sides, and fronto-mesial cortex) as compared to T dorsolateral parts. In addition, the SPECT study showed

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increased relative tracer uptake in basal ganglia and cerebellum (see color Figure 15 on page 152). Performance-related DC shifts and EEG spectra were analyzed in another experiment on visuomotor learning (M. Lang, Lang, Diekmann, & Kornhuber 1987). In agreement with findings reported above, performance-related, negative DC shifts in frontal recordings were larger in IT as compared to T. In visuomotor learning, e-MPD (mean power density of the e frequency band) was significantly larger during task performance than it was in the resting state. This IN-e-MPD (increase of e-MPD, see 2.2) was not present in T. In frontal recordings, differences of IN-e-MPD between IT and T were larger in good learners than in those who performed less efficiently. But differences were significant for the whole group of subjects (M. Lang, Lang, Diekmann, & Kornhuber 1987). In another visuomotor learning task (W. Lang et al., 1986) the feedback signal to the TV screen was distorted by imposing a sine wave when the subject started to track the target (DT; distorted tracking). This manipulation created a rather complex distortion which had to be compensated during tracking. In contrast to the other experiments, a simple cognitive strategy such as the inversion of horizontal and/or vertical direction could not be used. Subjects were still able to significantly reduce the error of tracking although they could not verbalize, and were not consciously aware of, the strategy they used. Amplitudes of negative DC shift were larger in DT as compared to a simple tracking control (T). This difference (Nd) was again significant in frontal recordings and correlated with the success of learning in Fz, FCz and F4 (r ranging between .5 and .6). A correlation between cortical negative shifts and success in learning could not be found in F3 (as it had been in the inverted learning tasks; see Figure 10). In another experiment, the question was raised whether there are differences between mentally and actually performing a visuomotor learning task using inversion of horizontal directions (Lang, Uhl, Koska, Lindinger, & Deecke unpublished data). The following significant differences were found: (a) When actually tracking, cortical DC shifts had their maxima in recordings from the fronto-central midline, whereas in the imagery situation, maxima were found parietally. (b) In general, amplitudes of performance-related DC shifts were larger during actual tracking as compared to mere imagining. (c) In the imagery task, DC shifts were significantly lateralized with the larger amplitudes occurring over the left hemisphere (in frontal, central and parietal recordings). The interpretation of this lateralization was ambiguous since it could be

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Figure 10. Topography of the correlation of subjects’ Nd (the difference, i.e., extra negativity, between the amplitudes of the performance-related negativity during the visuomotor learning task and the visuomotor control task) with the success of subjects’ visuomotor learning. The diameters of the circles are proportional to the correlation coefficients, r, for the respective electrodes. Left side: correlations in an inverted-tracking task (inversions of horizontal directions). Right side: correlations in a distorted-tracking task. due to the fact that subjects imagined acting with the contralateral right hand. Therefore, in a control experiment, 12 subjects were instructed to track the target with their left hand either mentally or actually. The lateralization of negativity towards the left hemisphere remained only in the imagery situation and was significant in frontal recordings. In conclusion, the frontal lobes are critically involved in visuomotor learning tasks. Such tasks require subjects to rely on an inner representation of the goal, to maintain it against interference of other thoughts and to develop adequate response patterns in order to achieve the goal. When developing these new stimulus-response patterns, interference from old associations has to be overcome. Possibilities of using cognitive

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concepts and predictive strategies varied between the tasks: Visuomotor learning involving horizontal and/or vertical inversions enabled subjects to use a verbal strategy in their prediction of trajectories, whereas learning in the distorted tracking situation was mainly based on feedback recognition and utilization (which could not be verbalized and experienced). This is why distorted tracking was associated with right frontal activation, whereas inverted tracking caused a more bilateral frontal activation. When imagining tracking in an inverted manner without actually moving, the left frontal lobe, but not the right one, became activated (in this context see section 3.5). Patients with frontal lesions become distractable (Luria, 1966). They still have long term goals but have problems in maintaining them. Susceptibility to interfering Stimuli has often been described; instead of continuing an action they tend to compulsively utilize presented objects or to imitate actions of the examiner (Lhermitte, Pillon, & Serdaru, 1986a,b). These patients have a loss of active and intentive elements in their behavior which are essential for pursuing prospective goals (Kleist, 1934; Fuster, 1980). Similar disorders have been found in animals after lesions of the prefrontal cortex: Those of the prearcuate cortex disturb performance in tasks that require a choice of action depending on the special attribute (including temporal or spatial discontinuities) of a recent stimulus (for review see Brody & Pribram, 1978; Fuster, 1980; H. H. Kornhuber, 1987). The importance of the frontal cortex for flexible, goaldirected behavior is also supported by anatomical data demonstrating a convergence in the frontal cortex of sensory inputs from the outer world, via the sensory projection and association areas of the posterior cortex, and of motivational impulses from the limbic system and the hypothalamus (Nauta, 1972; Kievit & Kuypers, 1975). Negative DC-potential shifts and Tc-99m-HMPAO uptake of the frontal cortex during visuomotor learning may indicate cortical activation. Increased performance-related e - W D may indicate activation of the frontal limbic system.

3.4. Cognitive information processing Verbal cognitive learning in associative learning or concept formation tasks has consistently been found to be associated with negative DC-potential shifts in left frontal recordings, indicating an activation of this area (M. Lang, Lang, Uhl, et al., 1987; W. Lang, Lang, Uhl, Kornhuber, et al., 1988; Uhl, Lang, Lindinger, & Deecke, 1989; Uhl, Franzen, et al., 1989). This left frontal activation remains rather constant when varying material (nonsense syllables, meaningful words) and learning

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strategies (creating a meaningful sentence with two items, imagery; W. Lang, Lang, Uhl, Kornhuber et al., 1988; Uhl, Lang, et al., 1989). When presenting pairs of words with pre-established, habitual associations (control tasks), the left frontal activation is not present. In a recent experiment two different conditions of verbal cognitive learning were investigated (Uhl, Franzen, et al., 1989): In one condition each trial contained a new pair of words that had to be associated by creating a meaningful sentence. In the second condition 8 pairs of words had to be associated in a first run. The following 7 runs (each run consisting of 8 trials) used the same words but each time in a different combination. This design caused proactive interference; that is, subjects had to prevent interference by prior habits when learning new ones. In both conditions, the negative DC-potential shift in left frontal recordings appeared. However, in the task with proactive interference an additional negativity occurred, particularly in frontopolar recordings (Fpl and Fp2; overlying the rostra1 limit of the superior frontal gyrus). During concept formation and associative learning, subjects perform creative operations by using cognitive strategies. It is interesting to note that associative learning with imagery techniques causes activation of the left fronto-lateral cortex, whereas imagery of non-verbal materials (colors, maps or faces), without the necessity of transforming, processing, or encoding the items, causes an activation not of the frontal lobes but of the occipito-parieto-temporal regions, with a significant lateralization towards the left hemisphere (Uhl, Goldenberg, et al., 1989). EEG spectra have been calculated in the concept formation task and in one of the associative learning experiments (M. Lang, Lang, Diekmann, & Kornhuber 1987, W. Lang, Lang, Kornhuber, et al., 1988). In these experiments, IN-e-MPD was significantly larger in frontal recordings (F3, FCz) during cognitive learning than in the control task. The frontal e-rhythm differed not only between learning task and control but also between successful learners and those who performed less efficiently. The a-rhythm did not differ between tasks or groups of subjects. In frontal recordings, the difference of IN-e-MPD between learning task and control was correlated with the difference of the performance-related negativity, Nd, between the two tasks. In summary, the left frontal lobe, and the limbic and paralimbic systems are activated when subjects perform cognitive learning tasks in which verbal material has to be processed. Performance is guided by a goal, namely, to learn the associations in order to perform efficiently in subsequent retrieval tasks. Direction of behavior toward a future goal

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requires drives, motives and will. Parallels to the visuomotor learning tasks are obvious and, again, we found similar physiological signs, increased frontal negativity and e-MPD. Measurements of the regional cerebral blood flow have also given evidence for an activation of the frontal cortex in verbal cognitive learning (Goldenberg et al., 1987; W. Lang, Lang, Goldenberg, Podreka, & Deecke, 1987; Maximilian, Prohovnik, Risberg, & Hakansson, 1978).

3.5. Directing attention toward forthcoming, relevant, sensory events 3.5.1. Directed attention potential (DAP). In this section evidence will be given that the parietal lobe is involved in the anticipatory process of directing attention towards stimuli having relevance for a forthcoming action. In the following experiments (for details see Deecke et al., 1984 and W. Lang et al., 1984) cortical DC shifts in self-initiated, sensory-guided tracking movements were investigated. Subjects fixed their gaze on a fixation point straight ahead. When lowering a stylus with their right hand onto a plate, a light spot in the left hemi-field of vision started moving for 1 s in a first random direction, and subsequently for 1 s in another random direction. Thus, sensory information was primarily projected to the sensory areas of the right hemisphere. Predominant events such as the start of a stimulus program and the change of stimulus direction were predictable in time, but unpredictable in direction. Subjects had to track the light spot that moved at a constant speed. Similarly, tactile stimuli were applied to the subject’s left palm by a modified XY-plotter and had to be tracked in a similar manner. Figure 11 compares corresponding recordings of the two hemispheres in the visual and the tactile task. As can be seen, the volitional initiation of the stimulus program at t = 0 was preceded by a BereitschafspotentiaE. Change of stimulus direction (t = 1 s) and the end of the stimulus program (t = 2 s) were preceded by slow negative potential shifts of an expectancy wave (CNV) kind. The BP contained a very striking feature: As predictable, in unilateral (right-sided) self-paced movements, BP had larger amplitudes over the contralateral (left-sided) primary motor cortex (C3) as compared to the ipsilateral one (C4). But in parietal recordings, an opposite lateralization effect occurred; that is, BP amplitudes were larger in P4 than in P3. In studies of unilaterally performed rapid finger movements, such an ipsilateral preponderance of the BP has never been observed. But the situation in the present experiment was different, because either a visual or a tactile stimulus of

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Figure 11. Hemispheric differences for the visual tracking experiment. Grand means averaged across 16 subjects. Dotted lines indicate recordings from the left, solid lines indicate recordings from the right hemisphere. Intervals with significant differences between single pairs of data points are marked (two-tailed t tests, p c .05). Modified, from Lang W et al., 1984.

task-relevance was triggered by the initiating movement, and appeared in the left hemi-field of vision or the left palm. The additional activation of the right parietal cortex can thus be interpreted as sign of directing attention towards a forthcoming task-relevant sensory cue which was predictable in time. It has, therefore, been called "directed attention potential, DAP" (Deecke et al., 1984; Kornhuber,l984a; W. Lang et al., 1984). In an additional control experiment naive subjects were instructed to initiate the same stimulus program but without tracking the target. Thus, movement initiation with the right hand was again associated with the occurrence of a visual target on the left side, but now the target had

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no behavioral relevance for the subject; a directed attention potential was absent. Therefore, directed attention can be characterized as an active and selective process that is based on the goals of an action. We propose that intentionality in actions includes not only representations of desired goals and motor planning but also the anticipation of behavior-relevant sensory events. To the extent that (a) unanticipated events are startling experiences for us, and (b) we are startled only infrequently, it appears that we actually anticipate virtually every voluntary act and its related sensory messages, at times without being conscious of it. In another experiment, the effect of pre-information on the parietal directed attention potential was tested (M. Lang, Lang, Kornhuber, Bunz, & Kornhuber, in press). Pre-information was given by a signal, S1. Subjects had to track a visual target that moved for 3 s, starting at signal S2, 3.5 s after S1. Eight experimental conditions were given in random order (A,B,C,D,E,F,G,H). A,C,E,G conditions required normal right handed tracking of a polygon. A warning stimulus Sw was given 0.5 s prior to S2. In the B,D,F,H conditions, subjects had to track the visual target in an inverted manner (horizontal and vertical inversion of subject’s hand tracking coupled back to the screen). In the sequence of conditions A,C,E,G (normal tracking, T) and B,D,F,H (inverted tracking, IT) the amount of pre-information provided by S1 increased; that is, A and B included no pre-information, whereas G and H contained maximum preinformation (presentation of the target and the information about normawinverted tracking). These two parameters, pre-information and tracking mode were treated as factors for statistical analysis. ANOVA revealed a significant influence of the pre-information factor on the negative amplitude prior to Sw at parietal recordings and on the difference between left and right hemisphere. Negative DC shifts increased slowly towards the presentation of S2. Amplitudes increased with increasing amounts of pre-information delivered by S1. Lateralization towards the left parietal (contralateral to the moving right hand) electrode was found, although the stimulus was projected in the subject’s central field of vision. In the tracking epoch, the frontal e-rhythm was significantly larger in the IT than in the T conditions. In the epoch between S1 and Sw, the a-rhythm in parietal and occipital recordings was attenuated, with this attenuation decreasing with increasing pre-information. Changes of the e-MPD in the tracking epoch were consistent with previous studies (section 3.3): IN-e-MPD was larger in IT than in T. Performance-related a-attenuation and DC-potential shifts are considered to be signs of

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cortical activation. However, in the epoch between S1 and Sw, "preinformation'' had contrary effects on these two parameters: Amplitudes of DC shifts in parieto-occipital recordings increased with increasing preinformation, whereas a-attenuation decreased in the same recordings. DC-potential data may indicate that the process of directing attention towards S2, increases with increasing pre-information delivered by S l , which renders the possibility of information processing in anticipation. a-attenuation may be more susceptible to arousal: In a situation of uncertainty, as created by little pre-information, arousal may be larger than in situations with more pre-information. In their animal studies, Mountcastle, Lynch, Georgopoulos, Sakata, and Acuna (1975) and Lynch (1981) showed that neurons in the parietal lobe become active when monkeys detect, look at or reach towards a motivationally relevant object or event within their extra-personal space. Input from the limbic system to the parietal lobe has been demonstrated by Mesulam (1983). Mountcastle et al. (1975) propose that "several abnormalities of function that occur in humans and monkeys after lesions of the parietal lobe can be understood as deficits of volition, of the will to explore with hand and eye the contralateral half-field of space, a deficit caused by the loss of the command operations which exist in the parietal association cortex" (p. 905). Clinical symptoms of parietal lesions have been described since B a h t (1909) and are called neglect to the contralatera1 half-field of space (Brain, 1941; Semmes, Weinstein, Genth, & Teuber, 1963). 3.5.2. Anticipation of the right moment to act. In the sensory-guided tracking task described above (see 3.5.1), the two dominant events, the onsets of the first and the second trajectories of the target at t = 0 s and t = 1 s, respectively, are predictable in time. The right moment to start the tracking movement is not selected by the subject but is given by external cues. This gives rise to the following considerations: The frontomedial cortex including the SMA has been described as playing a responsible role when subjects have to select and start a movement on their own (see section 3.1). Is this process "switched off' if no longer needed? Figure 12 demonstrates that fronto-mesial cortex and sensory areas have different temporal patterns of cortical activation: In FCz (over the mesial, fronto-central cortex including the SMA), the Bereitschaftspotential decreases about 150 ms before movement onset (PMP) whereas recordings from the occipital right cortex, 0 2 , show a sustained negativity which declines only 200 ms after the onset of movement. Even more striking is

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v i s . stim. midline, mOl. suppl. a r e a

Figure 12. Recordings in FCz (midline, supplementary motor area) and 0 2 (occipital right) are compared. Grand means averaged across 16 subjects. Dotted lines bounding the average indicate 2 1 standard error of the mean. Onset of voluntarily initiated stimulus occurred at t = 0 s, change of stimulus direction at t = 1 s, end of the stimulus program at t = 2s.

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the difference at the onset of the second trajectory. Now, the preceding negative potential shift in FCz ends already about 300 ms before this event, whereas in the sensory areas the negative potential shift continues for 200 ms after the onset of the trajectory. It is to be concluded that the sensory cortical areas remain activated in order to attend to and analyze the trajectories of the targets that have to be tracked. Primary sensory and association areas (including the parietal lobe) may now trigger the tracking performance themselves. Fronto-medial structures show an early decline of surface-negativity, probably delegating the function of movement initiation to the posterior primary sensory and association areas (H. H. Kornhuber, 1984a).

3.6. Volition in the sense of setting priorities In volitional actions, a stimulus or a drive is not immediately transferred into action. Rather, there is a moment of consideration before acting in which the present and forthcoming situations are evaluated in the context of duties, long term goals, etc. These reflections

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are associated with decisions about what to do, and are fundamental for the experience of volition in our actions. Any direct response to an internal (drive) or external stimulus is inhibited. If certain motives and drives become overwhelming, selectivity of behavior and volition in action is reduced, as in patients suffering from obsessive and compulsive disorders. These patients experience and complain that their behavior is not under control of their will any more. Lesions of the orbito-frontal cortex lead to disinhibition of primitive drives and to moral depravation as originally described by Kleist (1934; for review see Fuster, 1980; Stuss & Benson, 1986; H. H. Kornhuber, 1987). The self-perception regarding their behavioral disturbance is obviously reduced in these patients. An experiment has been performed in which subjects were asked to withstand self-administered aversive stimulation (pain and fatigue), by pressing on a button for as long as possible (A. Kornhuber, Lang, Lang, Kure, & Kornhuber, in press). Painful electrical stimuli with intensities of 25% or 75% of the subjective maximum pain level were applied either to the left or the right index finger. Pain was applied by self-paced button pressing, and disappeared when the index finger was lifted from the button. In another set of 4 conditions the same subjects had to press down on the button with 25% or 75% of a predetermined maximum of force, either with the left or the right index finger. Payment depended on the level of task performance, that is, how long subjects were able to tolerate the pain or the fatigue of pressing the button. This experimental design led to a conflict of motives: a conflict between a desire to earn wages (by withstanding pain or fatigue) on the one hand, and a desire to escape or relax on the other. The following main results were found when analyzing the EEG spectrum: During task performance frontal and central medial e-MPD was larger than during the preceding resting state (IN-e-MPD). When subjects stopped the performance, e-MPD decreased again (DE-e-MPD). Task-induced IN-e-MPD and relaxation-induced DE-e-MPD were significantly larger in the conditions with higher loads (with pain and force at the 75% level) as compared to those with lower ones. IN-e-MPD and DE-e-MPD (Figure 13) had a clear frontal distribution with a maximum in recordings from the fronto-central midline. Will is needed to select between motives and drives. Selection and maintenance of this choice during the action are important in these tasks. The choice in the present experiments involved the decision what to do and not (as in previous studies on visuomotor and cognitive learning) on the decision how to do. In spite of these differences one physiological parameter remained invariant: The frontomedial e-MPD increases with

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increasing difficulty of choice of what or how to do. We suggest that all deliberately and consciously-controlled decisions on aspects of voluntary actions require motivational input and will. The frontal e-rhythm may reflect input from the limbic system to the frontal convexity.

4. General discussion

4.1. The utility of a centralized startingfinction for movements There is an important feature in voluntary movements as opposed to voluntary thoughts: the movements interfere with the external world and might endanger the safe posture of the body in the field of gravity. Motion interferes with other living beings and is a potential signal for enemies. Therefore, the initiation of a voluntary movement needs more control than the initiation of a thought. Before a voluntary action is started, the position of body and limbs, as well as ongoing movements and signals from the environment, need to be considered. That is, signals from all sensory and motor systems and those from the motivation system have to be coordinated, in order to select the best starting time. The numerous afferents to the SMA are in accord with such a function. The SMA receives information from the precentral motor cortex, from the somatosensory and parietal areas, from the cerebellum and basal ganglia via thalamic nuclei, from the claustrum, and from various stages of the motivational system such as the hypothalamus (via the mediodorsal thalamic nucleus), the amygdala, the prefrontal cortex, etc. (Jones, 1983; Wiesendanger & Wiesendanger, 1985). The SMA is active prior to all kinds of voluntary movements including those which are not represented in the precentral motor cortex such as eye movements (Deecke et al., 1969; Deecke et al. 1976, Deecke & Kornhuber 1978, Becker et al., 1972, Grozinger et al. 1979). Regional cerebral blood flow measurements (Roland et al., 1980) are in agreement with our conclusion, although the time resolution of this method by itself is insufficient to even distinguish between changes before and after movement onset. The principle of centralization as realized in the SMA is particularly interesting in view of the fact that the motor system is much more decentralized in the brain than our present textbooks are advertising. For instance, the motor cortex for speech is in the temporal lobe (H. H. Kornhuber, 1984b). The same tongue movements which during chewing are controlled by the motor cortex and its tactile afferents (the motor cortex having features of a somatosensory association area; H. H. Kornhuber, 1974) need an entirely different control during speech production in which the upper

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Force

Figure 13. Topography of the difference between 75% and 25% of maximum tolerance in the "pain" and the "force" tasks (cf. section 3.6) in terms of the relative decrease of Theta mean power density (9-MPD) due to relaxation. There is a larger relative decrease over the frontal areas. temporal lobe and its auditory afferents are taking part. The relationship of the SMA with the motor cortex and the basal ganglia are in agreement with its proposed starting function. Neurons of the pallidum (Melnick et al., 1984) often start to discharge several hundred milliseconds prior to the onset of a voluntary movement, similar to the early beginning of the Bereitschuftspotential (H. H. Kornhuber & Deecke, 1965; Deecke et al., 1969, 1976; Deecke, Kornhuber, Lang, Lang, and Schreiber, 1985; Deecke and Kornhuber, 1977, 1978; W. Lang, Lang, Uhl, Koska, et al., 1988; W. Lang, Zilch, et al. 1989). Both the basal ganglia and the cerebellum are necessary for the preparation of an aimed voluntary movement (H. H. Kornhuber, 1974; Lamarre et al., 1980). The coordination of serial movements is just a special case of starting movements at the right moment (timing). As our data show, the SMA is likewise involved in single as in serial voluntary movements (H. H. Kornhuber & Deecke, 1965; Deecke et al. 1976; Deecke and Kornhuber, 1978; M. Lang et al., 1988; W. Lang, Lang, Uhl, Koska, et al., 1988; W. Lang, Zilch, et al., 1989).

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4.2. Frontal lobe and volition The first theory of voluntary movements was Liepmann's explanation of apraxia (Liepmann, 1900). In his theory he postulated an "imagination" (Vorstellung) between sensation and motion, but no volition. According to Liepmann, the posterior cerebral lobes and the motor cortex were involved, but not the frontal lobe, Since Walter Rudolf Hess found mechanisms of different drives, such as hunger, thirst, aggression, etc., within the diencephalon and limbic system (Hess, 1949), motivation was usually thought to be localized in subcortical systems, whereas the cortex was considered to supply merely cognitive information. The views of Feuchtwanger's (1923) and Kleist's (1934), who treated frontal lobe symptoms in terms of a psychology of will, were usually neglected by most psychologists. Even Teuber (1964), who knew the old German literature, did not seriously consider this tradition. His interpretation of frontal lobe function restricted itself to the concept of corollary discharge (i.e., feedback information from motor to sensory systems), without realizing the fundamental importance of volition in human motor action and behavior. In the psychological abstracts, will and volition had disappeared by 1965. Attempts to compensate for this deficit came from neurophysiology (H. H. Kornhuber, 1984a,c, 1987, 1988). It was Karl Kleist (1918, 1934), who distinguished between two different frontal-lobe syndromes in man: The syndrome of the lateral convexity of the frontal lobe, on the one hand, characterized by a reduction of spontaneity, indifference and apathy, and the syndrome of the orbito-frontal cortex, on the other hand, consisting of lack of endurance, deficits in moral behavior and disinhibition of drives. In our opinion, the inability of the patient with frontolateral lesions to develop new sorting strategies in the Wisconsin card sorting test as described by Brenda Milner (1963, 1964) and confirmed by us (Bechinger, Kornhuber, Jung, & Sauer, 1986) agrees well with Karl Kleist's statement. As was pointed out earlier (H. H. Kornhuber, 1973), the deficits in the delayed response task of monkeys having fronto-lateral lesions (Jacobsen, 1935, 1936; Jacobsen & Nissen, 1937) is also in good agreement with this dimension of frontal lobe function: There has to be a selection of the important events during the transfer from short term to long term memory prior to long term storage, and the motivation system is crucially involved in this evaluation. A classification of volitional functions into three stages has been proposed by Kornhuber (1984a, 1987): The first stage involves setting priorities among the needs, that is to say, to determine what shall be done

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(what to do). The second stage involves developing abilities, making plans and decisions about the way to do it (how to do), and the third involves the selection of the right moment when the action is to be started (when to do). As Karl Kleist (1934) had concluded earlier, the orbital cortex seems to be important for the first stage: The single unit data of Rolls (1983) and Thorpe, Rolls, and Maddison (1983) agree well with Kleist’s concept. For the second stage, the fronto-lateral cortex seems to be important. It is only the cortex of the frontal lobe convexity that exhibits significant correlations between an increase in the cortical DC potential and subjects’ success in learning a new performance, as demonstrated by human learning experiments (W. Lang et al., 1983, 1986, W. Lang, Lang, Podreka, et al., 1988). Furthermore, the observations of Kleist (1934), Jacobson (1935), Freeman and Watts (1942), Milner (1963, 1964), and Fuster (1973) are compatible with this interpretation. Additionally, the fact that the monoaminergic neuronal systems project mainly to the frontal lobe is in line with the lobe’s putative role in the second-stage process determining how to do (Lindvall & Bjorklund, 1983). For the third stage, mesial cortical areas of the frontal lobe, more specifically the SMA, seem to play the main role as pointed out at the beginning of this discussion. The function of acting at the right moment had previously escaped the attention of scientific research. That is, the right time for action (which is so important in education, sports, hunting, therapy, policy, business etc.) became a subject of neurophysiological interest only recently (Kornhuber, 1984a). This was probably because psychologists and philosophers had regarded psychological time as being a personal experience which was either too subjective or too abstract to afford the possibility of scientific investigation. Of course, the motionand-time studies of industrial psychology and engineering were realistic, but they were tied into the stimulus-response paradigm of machine-maninteractions. The problem of the right time, in our context, becomes sharper when the right time is not predetermined by a machine (or where the question is just whether a man is able to respond quickly enough), but, rather, when the individual is free to choose the right moment to start. The ancient Greeks intuitively knew the importance of the right moment; they had a word for it, Kairos. (Kairos, the youngest son of Zeus, was also the god of the right measure, in the sense of moderation.) The data on theta-enhancement over near-midline cortex under conditions of effort generally agree with the enhancement of the cortical DC potential. There is a significant correlation of both, theta-power and

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negative DC-potential shifts in the learning of a performance (M. Lang, Lang, Diekmann, & Kornhuber 1987; W. Lang, Lang, Kornhuber, et al., 1988). On the other hand, the relationship between the DC-potential shift and attenuation of the alpha-rhythm is less clear.

4.3. Attention, the parietal lobe and the directed attention potential At the same time that will and volition fell into disrepute and disappeared from psychology, attention gained a favorable reputation. Attention has a function in perception that is similar to the one volition has in action, but it was easier to think of attention as being stimulusdependent; the thought of volition appeared to imply freedom, which was a banished idea. In contrast to the importance of the frontal lobe for voluntary action, the maximum attention potential is over the parietal lobe, contralateral to the side of the visual or tactile stimuli (H. H. Kornhuber, 1984a; W. Lang et al., 1984). This is in agreement with the convergence of the sensory afferents from different senses (vision, audition and touch) in the posterior parietal area (Jones & Powell, 1970; H. H. Kornhuber, 1983), with clinical findings of disturbed attention (syndrome of neglect) following lesions of the parietal lobe (Brain, 1941; Semmes et al., 1963) and, most of all, with the single-unit (monkey) data of Mountcastle and his group (Mountcastle, Andersen, & Motter, 1983; Mountcastle, 1979, 1989).

4.4. Will and fieedorn Let us, finally, look at the reason why scientists repressed the concept of the will. It was probably because will belongs to freedom in the sense of free will and good will. Many scientists of today consider the idea of freedom an illusion. However, we must realize that there are two kinds of freedom: (a) freedom porn something (independence), and (b) freedom to or for something (ability, performance). This was clearly expressed by Nietzsche 1883; the roots of this distinction came from Nicolaus Cusanus, Pic0 della Mirandola, Leibniz, and Kant. Unfortunately, this distinction had little impact on the mentality of our civilization, for the causal connection of the two kinds of freedom was not considered -- perhaps because of the prejudice that freedom should not have a cause. Freedom from, however, is invariably based on freedom to (H. H. Kornhuber, 1984~). For instance, freedom from robbery is based on the ability of the state to maintain order, on parents’ ability to educate their children, etc.; freedom from illusion is based on the ability to reason, on the ability of the brain to function normally, etc. This positive freedom,

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freedom to or for, is a relative freedom; it is not contrary to nature. Many abilities contribute to it, but will has a central position among them. This relative freedom of will is reflected in the various ways we maintain our psychic balance, for example, avoiding dehydration by drinking water, avoiding exhaustion by sleeping, avoiding disinhibition by abstaining from alcohol, etc. When we become ill, we may try to maintain our freedom by seeking help from physicians. For example, physicians are obliged to prevent cretinism by early diagnosis of hypothyroidism in newborn infants and by treatment with thyroxine. Parents, teachers, psychologists, and doctors take on the task of helping others to become more free; indeed, that task is a challenge we all face. As Aristotle asserted in his Nicomachean Ethics, "virtues arise in us neither by nature nor contrary to nature; but by our nature we can receive them and perfect them by habituation ...We become just by doing what is just, temperate by doing what is temperate, brave by doing brave deeds" (Apostle, 1984, p. 21). What Aristotle called virtue is about the same as what we call positive freedom, or freedom for. Chance events in our brain may contribute to freedom via phantasy when creativity matters. Chance events alone, however, do not constitute freedom. It is by higher mental functions, by intelligence, reasoning, conscience, authenticity, by learning, practice, creativity, constructive cooperation and training of will that we become more free (H. H. Kornhuber, 1984c, 1987, 1988). If we compare the brains of different animals, it is obvious that the older parts of the motivation system, the hypothalamus and the limbic system are rather conservative. What makes the difference between a chimpanzee and a rat, and again between homo sapiens and a chimpanzee, is the larger development of the cortical association areas, almost half of which (the frontal, orbital, and anterior medial cortex) subserve volitional functions. This corresponds to the importance of consideration, planning, reasoning and associated volitional functions involved in responsible human behavior. While hedonism tries to make the whole brain serve a minor diencephalic function, a more humane philosophy (which reminds us that our reasonable will has higher goals, goals beyond our ego) is obviously in better agreement with human brain physiology. Human cerebral anatomy and physiology also leave open vast possibilities for the development of different modes of conduct, through cultural evolution, education, and learning. The more mind, the more good will is necessary to make mind effective for constructive and responsible behavior. In this endless task of mental and volitional development, more than intelligence matters, for mankind is always in

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Figure 14, upper photograph on facing page: (see Experiment I of section 3.1.7.) Comparison between SE-S and SI-S. Differences of amplitudes have been calculated for the Bereifschafspotentiual (Nd-BP, left side) and the performance-related negativity (Nd-P, right side). Based on Nd-BP and Nd-P, topographical distributions of current density at the scalp surface were calculated and displayed. Current flowing into the scalp is indicated in colors of yellow and red, current flowing out of the scalp in colors of green and blue. Note, current flowing into the scalp in the area of the central midline (overlying the SMA) indicating increased negativity of the mesial central cortex in SE-S as compared to SI-S.

Figure 15, lower photograph on facing page. (Compare with Figure 9 of secion 3.3.) Tc-99m-HMPAO brain SPECT of one subject. Four axial slices from cranial (left) to caudal (right). Upper row: Inverted Tracking (IT). Middle row: Tracking (T). Lower row: subtraction (IT minus T) after normalization of count rates. The relative tracer distribution is displayed in colors ranging from blue (low) to white (high concentration). In the lower row, colors of red and white display areas having a higher relative tracer concentration in IT as compared to T. This is particularly true in the mesial, fronto-central cortex, the dorso-lateral cortex of both hemispheres (mainly congruent with the middle frontal gyrus), basal ganglia and cerebellum. From W. Lang, Lang, Podreka, et al., 1988.

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danger of drifting away from those ideals that hold the greatest promise for humanity. Because of human creativity, man needs moral education by educated persons.

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Appendix Excerpt from Forster (1936): Ich habe das Feld 6aD in nahezu 40 Fallen excidiert. Die unmittelbaren Folgen bestehen erstens in einer geringen Schwache und Verlangsamung aller Bewegungen der kontralateralen Extremitat und der Neigung und Wendung des Kopfes und Rumpfes nach der Gegenseite. ... Alle Einzelbewegungen der einzelnen Extremitatenabschnitte einschliefilich der Bewegungen der Zehen, der einzelnen Finger und des Daumens bleiben aber in vollem Umfang erhalten. Hingegen erleiden die zusammengesetzten Bewegungen ... eine mehr oder weniger deutliche Lockerung des Gefiiges. Die fliefiende Kontinuitat, in welcher die einzelnen Komponenten der zusammengesetzten Bewegungen

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Die einzelnen Komponenten laufen mehr getrennt ab, eine hinkt der anderen her, eine Einzelkomponente kann zunlichst ganz ausbleiben und bedarf unter Umstanden zu ihrem Zustandekommen eines ad hoe erteilten besonderen Willensimpulses. (p. 279)

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CHAPTER 7 CORTICAL MODIFICATION OF SENSORIMOTOR LINKAGES IN RELATION TO INTENDED ACTION William A. MacKay and Donald J. Crammond The extent to which volition may be found in "voluntary" movement is a moot point, nowhere better discussed than in the writings of William James (1890), the source of the quotations which follow. Volition implies conscious thought, which in normal habitual action is needed only to prepare a chain of automatic processes, what we now call a motor program. In James' scheme, sensory signals generated by execution of a movement (reafference) play a major role in triggering each element of a motor sequence. This hardly constitutes volitional action if "a strictly voluntary act has to be guided by idea, perception, and volition, throughout its whole course". But "these immediate antecedents of each movement of the chain are at any rate accompanied by consciousness of some kind. They are sensations to which we are usually inattentive, but which immediately call our attention if they go wrong." In other words, the habitual level of motor control is subconscious: the neural signals eliciting motor responses are not strictly volitional. '"The will, if any will be present, limits itself to apemission that they [the neural signals] exert their motor effects." Indeed the central idea of the motor program is that a plan of action can unfold automatically as a computer program, in sequential flows of information without conscious intervention. Libet (1985) has ingeniously demonstrated that even the neuronal initiation of a self-willed movement is an unconscious event: awareness comes after a delay of about 300 ms. In the global scheme of things, however, the conscious element always comes first, even if it does not actually trigger action. Just as the computer's programmer must set up an algorithm to process information, consciousness prepares the CNS to produce a specific action when the appropriate inputs arise. Marcel (1980) has eloquently argued that consciousness provides the link between perception and action. Its purpose is to select between possible alternatives to give action a unitary goal. The links between

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perception and action can occur, of course, at many levels from the reflexive to the highly considered. These could correspond to the different levels of consciousness if consciousness is an ubiquitous property of voluntarily active systems. Concomitant levels of volition or "permission" would solve the problem encountered by James. In neurophysiology the closest that one normally ventures to the concept of consciousness is the recognition of motor "set", the state of preparedness for a particular action. But if Marcel is right, perhaps this is close to the mark. Our thesis here will be that the processes of selection of sensorimotor linkages which underlie production of intended movements, are a general model of the characteristic operations of the nervous system, at all levels, to effect volitional action in the broadest sense. The definition of a goal sets the volitional drive to act, a will which is essentially permissive, as James argued. That is, it enables a family of action sequences, any one member of which could achieve the goal depending on current peripheral conditions. The last point is both significant and ironic. Volitional actions can only be given general plans a priori within the CNS. Ultimate determination of detail originates from outside. The facilitation of interaction between the inside and outside such that required information is available when needed, is the key to successful voluntary action. We will establish this thesis in broad outline by reviewing pertinent neurological, physiological and anatomical studies, including our own work on modulation of somatosensory responses in cerebral cortex during volitional arm movement.

Frontal Syndromes Cortical lesions anterior to the motor region result in the release of reflexes, or more complex naturally conditioned responses, from their normal constraints. The sensory trigger signal, whenever it may occur, drives the motor response whether the response is behaviorally appropriate or not. Hence there is a loss of volitional control such that the program fails to direct incoming signals to serve the intended goal. One classic sign of premotor damage is forced grasping: tactile stimulation of the volar surface of the hand automatically elicits grasping (Denny-Brown & Botterell 1947). Smith, Bourbonnais, & Blanchette, (1981) have shown that ablations limited to the supplementary motor area (SMA), the medial end of the premotor strip (see Figure 2), are sufficient to produce this syndrome in monkeys. Similarly, surgical ablation of the frontal eye field region (FEF) prevents patients from making eye saccades

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away from a visual stimulus (Guitton, Buchtel, & Douglas, 1985). In effect, the patients lose the choice of alternatives to the '"visual grasp" response, and are compelled to foveate. Denny-Brown's (1958) hypothesis of frontal lobe inhibitory regulation of parietal lobe (sensory) input to motor centers, has been extended by the recent work of Lhermitte. He has demonstrated characteristic "'utilization" or "imitation behavior'' (Lhermitte, Pillon, & Serdaru, 1986) in patients with frontal lobe lesions, generally in the inferior half of the frontal cortex. Tactile, visuotactile or visual presentation of a useable object compels the patient to grasp and use that object. Gestures made by the examiner or postures assumed are also spontaneously mimicked by the patient. Perhaps the most dramatic examples of utilization behavior have been reported by Goldberg, Mayer, and Toglia (1981). Some of their patients with medial frontal lesions have involuntarily reached for door knobs, pencils, etc., with the arm contralateral to the lesion. The patients complained, that the arm would "not do what I want it to do". They could not voluntarily initiate movements with the affected arm, although a verbal command from someone else instantly set it off, correctly. Evidently the frontal lobe damage in these cases is revealing a sensorimotor connection which always exists, but normally is suppressed until conditions are appropriate for it to be expressed. The missing neuronal tissue helped to implement goals by selecting those sensorimotor linkages which would facilitate the intended action, and by inhibiting the rest. Without such an interface, motor output tends to be both dictated by randomly occurring external events, and limited to the most common patterns. The clinical evidence forces the additional (and very Jamesian) conclusion that the internal initiation of movement uses an anatomical base which is substantially distinct from that used by external triggering processes, and also distinct from that mediating the automatic information flow which sustains a motor program once started. On a general level frontal lobe dysfunction results in an inability to organize and plan a series of acts (Milner & Petrides 1984). Sequential ordering, both retrospectively of events in recent memory and prospectively for the preparation of future events, is badly muddled. Thus there is a tendency to perseveration, repeating the same stereotyped act again and again although it does not accomplish the goal. Alternative strategies cannot be worked out because of the inability to keep track of how individual elements relate to one another. Possibly prefrontal areas serve

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and Donald J. Crammond

CONSTRUCT r e p r e s e n t a t i o n

to a c t

to p e r c e i v e

STRATEQY

INTERMODAL

SELECTION

SCHEMAS

ACTION PLAN

SYNERGY ASSEMBLY

EFFECTORS

SENSORY MAPS

R E F L E X LINKS

PERIPHERAL INPUT

Figure 1. Schematic diagram of the interactions between the frontal and parietal lobes. A anatomical outline of monkey cerebrum which summarizes some of the connections discussed by Goldman-Rakic (1988). B: the hierarchical cascade emphasizes the frontal function of selecting appropriate sensorimotor links to effect a desired action. Abbreviations: cs, central sulcus; ips, intra-parietal sulcus; ps, principal sulcus; sts, superior temporal sulcus. to construct associations between specific action elements. When one element occurs, the next in order is appropriately facilitated (and all others are suppressed). Strokes which disable the motor and premotor cortex result in paresis for obvious reasons and spasticity from unregulated spinal reflexes. Furthermore, motor sequencing within a program can be affected, as noted in Alf Brodal’s (1973) account of his own convalescence after a stroke (right internal capsule infarct producing pure motor hemiplegia). He could readily start to tie a bow but then “his fingers did not know the next move”. Breaks in “the succession of movements (due to pareses and

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spasticity) interrupted a chain of more or less automatic movements. Consciously directing attention to the finger movements did not improve the performance; on the contrary it made it quite impossible.” Thus precentral cortex may facilitate the tight sensorimotor links which keep a motor sequence proceeding to completion, The extensive anatomical studies summarized by Goldman-Rakic (1988) have revealed strong and precisely organized interconnections between the prefrontal and posterior parietal cortex, and a large number of common target areas, some of which are depicted in Figure 1A. This framework provides an example of a physical substrate for the selection processes described above. Goldman-Rakic (1988) postulates that the parietal lobe is instrumental in constructing representations of the periphery and environment, whilst the frontal lobe puts these representations to use in order to effect actions. The selection of sensory constructions for motor use is depicted as a repeating cascade in Figure 1B to emphasize our belief that essentially the same types of interaction occur at all levels of the neuronal hierarchy. Frontal cortex may facilitate some feedforward paths and inhibit others, possibly through extensive connections to the parietal and temporal lobes. Without this anticipatory activity there is a failure to adequately prepare the next elements in a sequence, so that they are not triggered by the relevant cues.

Frontal Metabolism During Voluntary Behavior More insight into the role of frontal zones has been provided by studies of cerebral blood flow in humans (summarized in Roland 1985). Roland has distinguished 17 functional zones anterior to motor cortex. It will suffice here to describe only a few because a common theme permeates the entire lobe. Roland divides the superior frontal region (anterior to SMA) into three general zones, anterior, middle and posterior superior prefrontal cortex (Figure 2). For the anterior zone, blood flow increases in all tasks in which a primary instruction is given containing conditional directives for future processing. This area appears to participate in the recruitment of other cortical fields necessary to implement the actions required by the instruction. Simple direct commands (“open fist”) do not elicit metabolic changes in the anterior zone. The posterior portion is metabolically activated by tasks that require the analysis of sensory information or information retrieved from memory as a prior condition for further processing. The most intense increases

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Figure 2. Outline of human cerebrum showing some of the functional zones described by Roland. Abbreviations: cs, central sulcus; M1, primary motor cortex; FEF, frontal eye field; PM, premotor cortex; SMA, supplementary motor area; SPF, superior prefrontal cortex.

occur for communication between different sets of cortical fields in rapid succession, e.g., describing from memory the furniture layout of your living room. Thus frontal zones may select a set of other cortical areas appropriate to handling the demands of the task. Presumably more anterior zones function at a higher, more general level, while posterior zones become increasingly particular. Areas closest to the motor cortex manipulate sensorimotor triggers actually driving movement elements. The region immediately anterior to the motor cortex is divided into two functional zones by Roland, the premotor cortex and more medially the supplementary motor area (SMA). SMA has increased blood flow during the preparation and performance of complex motor sequences, including speech. SMA is not activated during simple repetitive motions (tapping a finger) to which the subject pays no attention. Nor is the premotor cortex significantly activated in such cases. The premotor region is particularly involved in exploratory limb movements carried out under sensory guidance. It must be remembered that the frontal lobe and basal ganglia are interdependent. The output of the basal ganglia is largely directed at the frontal lobe and thus may be used as a critical selector of frontal regions. Indeed, the striatum could provide a key path by which volition at a high level could access specific frontal "organizers." Regardless of the likely involvement of the basal ganglia, Roland (1985) has drawn some general conclusions about the hierarchy of steps underlying the generation of voluntary movement which are worthy of note. Firstly, before the execution of voluntary behavior, the brain ''tunes the cortical fields that are expected to participate in the processing of the

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task-related information." Secondly, "when the fields are tuned, they are recruited for the task and subsequently participate in the processing of the task-related information. However, since the brain has to estimate beforehand which cortical areas might be necessary for the task, some areas might be recruited in certain cases which actually do not participate in the processing of the task-related information." In an interactive model of volitional action, the final selection of output processors depends ultimately on current conditions. The preparatory process which Roland calls Yuning" might be likened to the creation of a dynamic attractor toward which subsequent input signals are drawn, just as a ball rolls toward the bottom of a basin (Kwan 1988).

Sensory Transmission During Purposeful Movement To account for the selective use of sensory inputs in motor programs, physiologists have proposed that gating or modulatory processes alter responses to sensory inputs according to a motor "set", specific for the intended movement. The gating can occur at all levels of the neuraxis, from the segmental to the cortical. The mechanisms by which cerebral cortex can regulate its own somatosensory inputs have been studied in some detail. Both via the corticospinal tract and corticobulbar-reticulospinal tracts, the cortex influences transmission within the dorsal horn and dorsal column nuclei (DCN). The dominant effect is one of inhibition of sensory transmission (Towe & Jabbur 1961), an inhibition which arises from somatosensory, motor and premotor cortex (Felix & Wiesendanger 1970). Nevertheless, significant excitatory effects are also present, especially from motor cortex. In general, motor cortex appears to have a net excitatory effect on the dorsal horn, including spinothalamic projection neurons (Yezierski, Gerhart, Schrock, & Willis, 1983). Giuffrida, Sanderson, and Sapienza (3 985) have shown that motor cortical facilitation of DCN transmission occurs only for afferent input from the vicinity of the activated muscle, and only for the duration of the motor cortex outflow. Other DCN cells with receptive fields remote from the activated muscle are inhibited. This work was done in rats, however, and may not be generally applicable to other species. In monkeys, for example, Jiang, Chapman, and Lamarre (1988) found that microstimulation of the motor cortex inhibited air puff responses in primary somatosensory cortex when the receptive field

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overlapped or was distal to the activated muscle: more proximal fields were not affected. By means of layer VI efferents, each cortical area regulates its own thalamic inflow. The corticothalamic projection from somatosensory cortex appears to have a mainly excitatory effect on thalamocortical neurons (Yuan, Morrow, & Casey, 1986). Thus the thalamocortical circuit offers a mechanism for amplifying particular somatosensory signals. This mechanism may be used, however, only in selected circumstances. Because of the dominant descending inhibition of DCN, voluntary movement of a limb significantly reduces evoked potentials in the medial lemniscus due to cutaneous stimulation of that limb, starting up to 200 ms before the movement (Ghez & Pisa 1972; Coulter 1974). Passive movements have no effect. At the thalamocortical level, Chapman, Jiang, and Lamarre (1988) have found that additional inhibition is imposed. It is, however, strictly limited to the time of actual limb displacement and appears to be associated with the arrival of reafferent input. At the thalamocortical level, passive and active movements produce the same suppressive effect on cutaneous responsiveness. The modulation of sensory transmission appears to be graded in proportion to the level of motor output (Coulter 1974; Ghez & Pisa 1972). It may be misleading, however, to say that sensory inflow is reduced in proportion to movement speed. The gating process is probably a very necessary measure to maintain a meaningful flow of information without saturation. The faster the movement, the greater the barrage of activity bombarding the sensorimotor regions and the greater the necessity to set limits on what gets through so that it can be effectively processed. A general homeostatic rule of sensory regulation could be postulated as follows: sensory responsiveness of the cerebral cortex is reduced in proportion to the total instantaneous afferent activity to that cortical region. For example, responses of motor cortical cells to paw stimulation are suppressed just prior to and during the stance phase of locomotion (Palmer, Marks, & Bak, 1985), i.e., when paw receptors would be most activated. In somatosensory cortex of rats, Chapin and Woodward (1982) found that responses to paw tactile stimulation during the step cycle of locomotion were modulated in one of two patterns. Responsiveness to paw stimulation was either reduced throughout the step cycle except for brief instants during the swing phase, or it was reduced throughout most of the cycle but disinhibited just prior to footfall. The latter case is an example where the general rule was broken and cortical neurons showed

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t e s t pulse times

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Figure 3. Paradigm to test cortical proprioceptive responsiveness during a cyclic forearm movement of alternating flexion and extension. The monkey tracked a stepping visual target (dotted line). In any one cycle a test pulse perturbation could be delivered at one of the times indicated by the arrows, to stretch either the flexor or extensor muscles. Test pulses were given in random order at 5 different phases of the active flexion and the same 5 phases of extension. The forearm displacement is a grand mean from all unperturbed trials in one monkey and has error bars marking the standard error at the time of test Dukes. relatively high responsiveness at a time when receptors were most active. Moreover, Iwamura, Tanaka, Sakamoto, and Hikosaka (1985) have reported neurons in areas 1 and 2 which were responsive to cutaneous stimulation of the hand only during active manipulation of objects. Such "active touch" cells provide evidence that the CNS, probably the cerebral cortex itself, can and does augment specific signals during the course of voluntary movements. The amplified signals are of potential use in guiding or controlling the movement performed. To demonstrate this point, Hikosaka, Tanaka, Sakamoto, and Iwamura (1985) showed that reversible lesions of discrete regions of the area 2 finger representation led to a loss of finger coordination during natural manipulative behaviors.

Cortical Responsiveness During Movement The studies discussed above were chiefly concerned with cutaneous inputs. Proprioceptive signals, which provide particularly important cues for the control of ongoing limb movements, could be treated differently

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within the CNS. However, Evarts and Fromm (1977) have shown that some corticospinal tract cells in motor cortex are insensitive to hand perturbations during very fast supination/pronation movements of the hand, whereas comparable perturbations during slow movements elicit strong responses, i.e., the general rule of afferent regulation seems to be obeyed. To examine the gating of proprioceptive input from the moving arm in more detail, we studied the responsiveness of sensorimotor cortex to a test pulse (forearm perturbation) delivered during the course of active movement. We gave test pulses at different phases of a normalspeed voluntary elbow movement, to look for changes which might reveal when the proprioceptive signal was most useful to motor control processes at the cortical level. In two macaque monkeys trained to perform alternating flexions and extensions of the forearm, the responsiveness of cortical neurons in the sensorimotor region (areas 4,3a,1,2,5) to a uniform torque perturbation was tested at 10 phases in the movement cycle (Figure 3), 5 in each direction of movement. When cells were selected such that their receptive field was proprioceptive input from the elbow, i.e., the test stimulus, then specific patterns of modulation were observed over the movement cycle. Responsive neurons with non-elbow receptive fields tended to conform to a standard modulation pattern of minimal responsiveness at peak velocity of movement in either direction. In almost all cases neuronal responsiveness was significantly reduced during the movement cycle compared to the same test stimulus delivered to the "resting" forearm. Thus the data presented here reveal relative changes in responsiveness over the flexion-extension movement cycle. For the elbow proprioceptive cells, the majority of neurons showed a modulated responsiveness in all cortical areas studied. The responsiveness of area 4 (motor cortex) neurons showed the least reduction of all areas at the onset of agonist muscle activity, a phase when responsiveness is most commonly reduced among neurons responding to deep elbow inputs. Of all the cells sampled, area 4 neurons were found to be the most responsive to deep elbow inputs during the agonist half of the movement cycle. That is to say, area 4 cells receiving input from the elbow flexor muscles (and generally evoking elbow flexion when stimulated) were most responsive prior to and during active flexion of the forearm. An example of just such a cell is illustrated in Figure 4A. Perturbation-evoked field potentials from the deep layers of motor cortex showed the same property (Figure 4B). The early negativity was well maintained throughout the agonist (flexion) phase but was greatly

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FLEXION

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Figure 4. Responsiveness of motor cortex to a forearm perturbation stretching the elbow flexor muscles, tested at the 5 phases of active flexion and extension shown in Figure 3. A: post stimulus time histograms from a representative neuron, localized by the filled circle on diagram of electrode track at left. All histograms are scaled to the number of trials which is indicated. Vertical dotted lines mark the onset of significant increases in firing rate. Vertical calibration provides probability of firing. B: local field potential recorded in the deep layers of motor cortex (filled circle). Vertical scale is 0.5 mV, positive upwards. CS: central sulcus. attenuated during the antagonist (extension) phase. Responses of neurons in area 3a were, on the whole, rather similar to those of motor cortical cells, with maximum reduction during the antagonist half of the cycle. But many cells (32%) in this primary sensory region showed no phase-dependent changes. In area 1, however, a remarkable contrast was noted. The responsiveness of area 1 neurons during the antagonist half of the cycle, was consistently greater than that

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Figure 5. A: Responsiveness of a neuron in area 1 to test pulses in phase 3 (peak velocity) of flexion and extension. B: Discharge of same cell during active flexion and extension without test pulses. Vertical calibration indicates 10" displacement and 0.5 probability of discharge.

of cells in other cortical areas responding to elbow stimuli. Thus an area 1 cell responding to elbow extensor muscle stretch was most responsive to extensor inputs during active flexion, when the extensor muscle was in fact being stretched (Figure 5A). Consequently this neuron increased its discharge during active flexion and decreased it during extension (Figure 5B). This is an important observation for several reasons. Firstly, it underscores the point that generalizations such as reafferent input being suppressed at times when it is most intense may not be universally applied. Secondly, it shows that a specific region in the somatosensory cortex appears to monitor input from the antagonist muscle as it is stretched. This complements the existing evidence that proprioceptive information from the stretched antagonist is used in regulating movement amplitude (Capaday & Cooke 1983). In posterior parietal area 5, neurons could show a similar pattern to area 1 (e.g., Figure 6), or the area 4-3a pattern. Generally, however, responsiveness was strongest at the end of the agonist phase of movement and prior to the antagonist phase. In other words, cells responding to

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Figure 6. Responsiveness of a neuron in area 5 to the test pulses at 5 phases of flexion and extension. IPS: intraparietal sulcus.

elbow extensor muscle stretch were most responsive in advance of the time when the extensor muscle would be stretched, i.e., prior to active flexion (Figure 6). Many of the studied neurons in all cortical regions, failed to show drops in responsiveness during the peak velocity agonist phase of movement. Again this shows the danger of drawing conclusions from generalizations about reafferent signals. The sensorimotor cortex is clearly responsive to potential inputs from a muscle throughout its period of active contraction. Note that motor cortex cannot be slavishly driven by incoming sensory signals, but carefully selected and controlled sensory signals do get access to the motor apparatus where they perform an important function. For example, transcortical loops could mediate aspects of load compensation (Phillips, 1969) during a movement. In our experiments we were able to monitor the late stretch reflex (latency 50-60 ms) elicited by the test pulses. On the assumption that this reflex is at least partly transcortical (Cheney & Fetz 1984), it was of interest to determine whether changes in reflex amplitude for different testing times during the movement cycle paralleled changes in cortical unit responsiveness. The reflex showed a very consistent pattern: it was largest

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at the onset of agonist contraction (cf. MacKay et al. 1983). Although most single cortical units did not show the same modulation pattern, the pattern was reasonably similar to that of the entire sampled population of elbow-related motor cortical neurons, which showed maximum responsiveness in phase 1 of agonist contraction, and a significant loss of responsiveness for the remaining 4 phases. The onset of contraction is normally when the greatest inertial load is encountered by the agonist muscle. It is therefore to good purpose that the motor cortex is prepared at this instant to trigger motor reinforcement if muscle spindle input indicates resistance. This is an example of the simplest and most direct (reflexive) triggering of action.

Movements Cued by a Sensory Stimulus When movements are cued by the occurrence of a sensory stimulus, neuronal responsiveness to the stimulus is enhanced in some cortical areas. For example, in a monkey conditioned to rapidly move his hand upon receipt of a vibrotactile stimulus, responses to the stimulus in areas 3a and 1 were increased compared to those when no movement was made (Nelson 1984). Cortical area 3b, however, showed little response modulation. It appears that primary sensory zones may faithfully monitor peripheral conditions regardless of the motor set, while other areas which provide an interface for sensory signals with the motor apparatus are greatly modified by motor preparation. One such interface is somatosensory association area 5, where Chapman, Spidalieri, and Lamarre (1984) have found movement-dependent modulation of responses to forearm perturbations. For many cells, responses to forearm perturbation were small or absent when the associated movements were not subsequently made. Similarly, in motor cortex itself many cells respond to a vibrotactile stimulus if it cues a movement, but the response is usually attenuated or blocked if the movement is to be withheld (Kurata & Tanji 1985). Motor cortical responses to somatic cues are frequently bimodal with a short-latency component coming directly from somatosensory cortex or thalamus and a later component linked to the intended movement. The latter is always suppressed if no movement is made: the former is only partly blocked (Kurata & Tanji 1985). Visual and auditory signals do not share the same tight coupling to motor cortical neurons that somatic inputs possess (Lamarre, Busby, & Spidalieri, 1983). In motor (and premotor) cortex, responses to visual

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Figure 7. Responses in area 7a of parietal lobe to task-related events. A: Peri-event time histogram with 3 sample trials below showing a cell's firing pattern related to appearance of target on the video monitor (see inset), to the movem,ent of the square cursor indicating hand movement, and to anticipation of the reward given at the end of each trial. Discharge was not correlated to eye movements monitored in EOG records. B: Two trials of the forearm visual tracking task showing discharge of a neuron during the time that the cursor is within the target window. The stepping target is indicated by the broken line, and the arrows mark the times when torque perturbations were given. stimuli are only observed if the stimulus serves as a cue for action (Kwan, MacKay, Murphy, & Wong, 1985). When that action is not fully specified in advance, the visual cue activates a rather diverse population of neurons, many of which are not needed for the subsequent movement. In this regard, Riehle and Requin (1989) have found precentral cells that respond much more strongly to a visual cue when the motor reaction is not known in advance compared to when it is known. In prefrontal cortex (principal sulcus), visual (or other) stimuli excite large numbers of neurons provided the stimulus serves as a behavioral cue, e.g., for a conditioned motor response (Fuster 1984). The frontal eye fields (FEF) may be the only frontal region where visual responses

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per se can be found. Yet, even here, about half of the visual responses are highly dependent on the occurrence of a saccade which moves gaze onto the neuron’s receptive field (Bruce & Goldberg 1984). In area 7 of parietal lobe, responses to visual stimuli are also highly dependent on motor set (Bushnell, Goldberg, & Robinson, 1981; Mountcastle, Andersen, & Motter, 1981). In monkeys performing the same flexion-extension tracking paradigm mentioned earlier (either wrist or elbow movement), we have found within area 7a some rather complex visual responses (Figure 7). Cells respond to the cue to start (the appearance of the target on a video monitor), and to the moving cursor (on the video monitor) as the tracking movement is performed. Occasional cells respond to the placement of the cursor correctly within the target window (Figure 7B). Such types of responses would be disastrous if they directly commanded a fixed motor output, as in a reflex. But given an appropriately prepared motor pattern, these responses could serve useful functions as temporal triggers. The enhancement of sensory responses when they are to be used to guide or trigger action, provides a selection mechanism. But in the case of visual or auditory triggers especially, specific connections to effectors cannot be made without losing adaptability. Therefore, a process of preparation must precede the trigger volley so that it may be functionally focused onto the appropriate motor output zones. Moreover, any sensory cue to prompt a movement will not actually trigger it unless the movement is specified in advance. Thus when the movement is not known in advance, a level of interpretative processing intercedes between sensory cue and triggering of motor output. The source of the actual trigger is embedded in the CNS.

Sensory Representation Before Movement There is a natural tendency to expect activity in somatosensory cortex after movement onset when the great barrage of reafferent input arrives. Indeed such is the case (Bioulac & Lamarre 1979). But from foregoing arguments regarding the preparatory facilitation of sensorimotor links, a logical outcome would be the occurrence of parietal discharge before movement. In fact there are now many reports of parietal activity preceding movement onset, usually in neurons which are also activated during the movement. Precocious discharge is most conspicuous in posterior parietal cortex, but it can also be found in somatosensory areas

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3a, 1 and 2 of the postcentral gyrus (Fromm & Evarts 1982; Nelson 1987; Soso & Fetz 1980). In area 5, Seal, Gross, Doudet, & Bioulac, (1983) identified 2 populations of cells. The first discharged up to 280 ms before movement onset and did not have clear peripheral input: discharge persisted after deafferentation. The other population responded to peripheral stimuli and discharged after the onset of movement, unless the animal was deafferented. One may postulate that the first population functioned to modulate the responsiveness of the second during the movement. However, MacKay, Kwan, Murphy, and Wong (1978) observed area 5 cells with a tonic relationship to wrist angle and clear sensory input from passive bending of the wrist, which changed their discharge rate to correspond to the intended final angle immediately before the commencement of the movement. The results of Favorov, Sakamoto, and Asanuma (1988) indicate that much of the premovement discharge in motor cortex and in area 2 is due to minute changes in muscle tone and consequent afferent feedback to sensory and motor cortex. Furthermore, the corticoperipheral loop is necessary for skilled execution of a task involving picking up food from a revolving wheel. Dorsal column section abolished both cortical premovement discharge and performance skill. In other words, somatosensory inputs can play a major role in the preparatory process for action (cf. Dubrovsky & Garcia-Rill 1973). A peripheral loop, however, does not explain the premovement discharge which survives deafferentation (Seal et al. 1983). Very recently, Crammond and Kalaska (in press) recorded area 5 unit discharge during a preparatory waiting period: the monkey had full information about where he was to move his hand when the GO signal appeared (change of target lamp color). During the preparatory period the discharge rates of over half of the sampled cells changed. Moreover, these changes were predictive of the activity during the subsequent movement. The preferred direction for preparatory discharge was similar to that for movement-related discharge. In area 2 neurons, however, preparatory discharge showed no directional preference. The preparatory discharge of the area 5 cells would appear to be an excellent example of what Roland (1985) has called "tuning" of cortical fields which are to be used to control the motor performance. The tuning is direction-specific, and since the intended movement is guided by sensory inputs, it is likely that premotor cortex may be critically involved in the tuning process. Certainly Riehle and Requin (1989) and Weinrich, Wise, and Mauritz

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(1984) have found direction-specific preparatory activity within the premotor area. Batuev, Shaefer, and Orlov (1985) have also observed spatially selective preparatory activity in both prefrontal cortex (principal sulcus) and in the intraparietal sulcus. Source localization of scalp potentials in humans during pre-cued preparatory periods in which either force or direction (or both) of an upcoming elbow movement was known, have revealed that the major locus of developing negativity (CNV) was in the parietal lobe, especially when direction was cued in advance (Bonnet & MacKay, 1989). Since many, if not most, parietal neurons have demonstrable receptive fields, it is not unreasonable to consider pre-movement parietal activity a form of sensation, or at least specific sensory facilitation. We have encountered a number of cells in areas 5 and 7 which discharge in anticipation of receptive field contact by the examiner (MacKay & Crammond 1987; cf. Hyvarinen 1982). The discharge is triggered by sight of the examiner's hand approaching the receptive field, and is reinforced at the moment of contact. Such discharge may correspond to anticipatory sensation from the target zone. When contacting one's own body, anticipatory sensation from the target region may involve the cerebellum. Sasaki (1985) reported a case study of a patient who suffered a localized left cerebellar infarct. Whenever the patient attempted to touch some part of his body with the left hand, the intended target dropped out of his body perception: he felt as though he was groping in "a sea of clouds". It appears that afferent inflow from the intended target region was subjected to the same movement-related suppression which affects the moving limb at the level of the cord and brainstem. Sasaki postulated that compensation for loss of input to the target representation may normally be mediated by dentate nucleus facilitation of parts of the prefrontal and premotor cortex. This possibility does fit with Roland's characterization of frontal areas. The preparation for action involves not only regulation of the input channels to be used, but an initial construction of the internal representation of the action. Thus when a voluntary movement is learned, "the idea of the movement's sensory effects will have become an immediately antecedent condition to the production of the movement itself' (James 1890). Such anticipatory representation may prepare the way for motor triggers to activate specific neuronal groups. Anticipation of non-somatic events (e.g., visual cues) occurs in premotor cortex (Mauritz & Wise 1986), and may similarly serve to set up reactions to the anticipated events.

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Cortical Preparatory Mechanisms Evarts (1984) postulated that set-dependent premotor cortex activity may alter motor cortical responses to sensory trigger stimuli. The available data are in accord with this idea, although direct evidence is not abundant. Microstimulation of the supplementary motor area (SMA) can suppress motor cortical responses to muscle afferent inputs (Hummelsheim, Wiesendanger, & Bianchetti, 1986). However, the key word in Evarts' postulate was "set-dependent": effects on sensory responses must be tested within a specific action context. Tanji, Kurata, and Okano (1985) locally cooled SMA while monkeys performed a key-press to a sensory cue or withheld responses for a different cue. During cooling frequent errors were made, with motor cortical responses to the nontrigger cue always preceding the erroneous key-presses. A population of SMA cells responded specifically to the nontrigger cue (Kurata & Tanji 1985): silencing these cells by cooling may have allowed the erroneous motor cortical responses. Inhibition seems to be the dominant effect of SMA on cortical sensorimotor connections. The use of delay or preparatory periods in behavioral paradigms for cortical unit recording has revealed the existence of a continuous ordering of neuronal activities from cue-related to delay-related to movementrelated, all within the same functional region. This is true within prefrontal (principal sulcus) cortex (Fuster 1984), the frontal eye fields (Bruce & Goldberg 1984), premotor cortex (Riehle & Requin, 1989; Weinrich et al. 1984), motor cortex (Lecas, Requin, Anger, & Vitton 1986; Riehle & Requin, 1989), and posterior parietal cortex (Batuev et al. 1985; Seal & Commenges 1985). One may therefore postulate that functional zones are structured as internal cascades, with cue responses in some way facilitating delay-related activity which in turn prepares movement-linked discharge (Requin, Riehle, & Seal, 1988). Such local cascades would be in addition to the interactions schematized in Figure lB, and would necessarily be closely interwoven with them. Thus flow of activity along a local cascade would be critically dependent on the receipt of external signals from other regions. This feature of cortical information flow is sketched in Figure 8. Extrinsic preparatory facilitation of a cortical region initiates local interactions between cue-, delay- and actionrelated clusters (labelled 1, 2 and 3, respectively in Figure 8). The net effect is to create a potential well as it were, which serves as an "attractor" for the final motor trigger. Thus the trigger does not require restricted anatomical connections.

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Figure 8. Highly abstracted model of preparatory facilitation of a cortical area to create an attractor for a trigger signal. Local interactions between adjacent clusters (arrows) receiving preparatory facilitation, intensify the attractor structure. Clusters are classified as 1: cue-related, 2: delay-related, or 3: movement-related. The true anatomical relationships of the functional groups may vary among cortical areas. The different task-related clusters may be layered in specific cortical laminae. In prefrontal cortex, cue responses are found mainly in layer IV, delay activity in layers 11-111 and action-related activity in layers V-VI (Sawaguchi, Matsumura, & Kubota, 1989). Delay-related activity may be in part involved in the computational processing interposed between cue and movement. It continues even when the sensory cue is circumvented. For example, "visual cells" in FEF are silent during saccades made to memorized targets in the dark. Only the "visuomovement" (or delay-related) and "movement" cells are activated (Bruce & Goldberg 1984), the former to a lesser extent than the latter. Thus the information for spatial guidance can come either from the periphery or from cognitive memory. Where the trigger signal comes

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from to ignite the movement cells remains a mystery: perhaps it is released by basal ganglia disinhibition. Except for the simplest of reflexes, no movement is performed unless it is prepared in advance. Particular sensory channels are facilitated, others suppressed, and specific internal representations necessary to guide the movement are activated. As a result of volitional setting up, motor triggers, whether they arise from filtered external stimuli or internal signals, initiate a prepared sequence of events. A motor trigger itself need have no motor relevance other than time: it is led inexorably to the correct target.

Acknowledgements Many thanks are due Drs. Alexa Riehle and Hon Kwan for suggesting improvements to drafts of the text. The experimental studies were supported by MRC of Canada.

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Chapin, J.K., & Woodward, D.J. (1982). Somatic sensory transmission to the cortex during movement. 11. Phasic modulation over the locomotor step cycle. Experimental Neurology, 78, 670-684. Chapman, C.E., Spidalieri, G., & Lamarre, Y. (1984). Discharge properties of area 5 neurones during arm movements triggered by sensory stimuli in the monkey. Brain Research, 309, 63-77. Chapman, C.E., Jiang, W., & Lamarre, Y. (1988). Modulation of lemniscal input during conditioned arm movements in the monkey. Expenmental Brain Research, 72, 316-334. Cheney, P.D., & Fetz, E.E. (1984). Corticomotoneuronal cells contribute to long-latency stretch reflexes in the rhesus monkey. Journal of Physiology, 349, 249-212. Coulter, J.D. (1974). Sensory transmission through lemniscal pathway during voluntary movement in the cat. Journal of Neurophysiology, 37, 831-845. Crammond D.J., & Kalaska, J.F. (In press). Neuronal activity in primate parietal cortex area 5 varies with intended movement direction during an instructed delay period. Experimental Brain Research. Denny-Brown, D. (1958). Nature of apraxia. Journal of Nervous and Mental Disease, 126, 9-32. Denny-Brown, D., & Botterell, E.H. (1947). The motor functions of the agranular frontal cortex. Research Publications Association for Research In Nervous and Mental Disease, 27, 235-345. Dubrovsky, B, & Garcia-Rill, E. (1973). Role of dorsal columns in sequential motor acts requiring precise forelimb projection. Experimental Brain Research, 18, 165-177. Evarts, E.V. (1984). Neurophysiological approaches to brain mechanisms for preparatory set. In S. Kornblum & J. Requin (Eds.), Preparatoy States and Processes (pp. 137-153). Hillsdale NJ: Erlbaum Assoc. Evarts, E.V., & Fromm, C. (1977). Sensory responses in motor cortex neurons during precise motor control. Neuroscience Letters, 5, 267-272. Favorov, O., Sakamoto, T., & Asanuma, H. (1988). Functional role of corticoperipheral loop circuits during voluntary movements in the monkey: a preferential bias theory. Journal of Neuroscience, 8, 3266-3277. Felix, D., & Wiesendanger, M. (1970). Cortically induced inhibition in the dorsal column nuclei of monkeys. Pjliigers Archiv, 320, 285- 288. Fromm, C., & Evarts, E.V. (1982). Pyramidal tract neurons in somatosensory cortex: central and peripheral inputs during voluntary movement. Brain Research, 238, 186-191. Fuster, J.M. (1984). Behavioral electrophysiology of the prefrontal cortex. Trends in Neurosciences, 7, 408-414.

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Ghez, C., & Pisa, M. (1972). Inhibition of afferent transmission in cuneate nucleus during voluntary movement in the cat. Brain Research, 40, 145-151. Goldberg, G., Mayer, N.H., & Toglia, J.U. (1981). Medial frontal cortex infarction and the alien hand sign. Archives of NeuroZogy, 38, 683-686. Goldman-Rakic, P.S. (1988). Topography of cognition: parallel distributed networks in primate association cortex. Annual Review of Neuroscience, 11, 137-156. Giuffrida, R., Sanderson, P., & Sapienza, S. (1985). Effect of microstimulation of movement-evokingcortical foci on the activity of neurons in the dorsal column nuclei. Somtosensory Research, 2, 237-247. Guitton, D., Buchtel, H.A., & Douglas, R.M. (1985). Frontal lobe lesions in man cause difficulties in suppressing reflexive glances and in generating goal-directed saccades. Experimental Brain Research, 58, 455-47. Hikosaka, O., Tanaka, M., Sakamoto, M., & Iwamura, Y. (1985). Deficits in manipulative behaviors induced by local injections of muscimol in the first somatosensory cortex of the conscious monkey. Brain Research, 325, 375-380. Hummelsheim, H., Wiesendanger, M., & Bianchetti, M. (1986). The supplementary motor area modulates perturbation-evoked discharges of neurones in the precentral motor cortex. Neuroscience Letters, 67, 119-122. Hyvarinen, J. (1982). The parietal cortex of monkey and m n . Berlin: Springer-Verlag. Iwamura, Y., Tanaka, M., Sakamoto, M., & Hikosaka, 0. (1985). Vertical neuronal arrays in the postcentral gyrus signalling active touch: a receptive field study in the conscious monkey. Experimental Brain Research, 58, 412-420. James, W. Principles of Psychology. 1890, New York: Holt. Jiang, W., Chapman, C.E., & Lamarre, Y. (1988). The topographical modulation of somatosensory transmission to SI cortex produced by microstimulation of MI cortex in the monkey. Society for Neuroscience Abstracts, 14(1), 509. Kurata, K., & Tanji, J. (1985). Contrasting neuronal activity in supplementary and precentral motor cortex of monkeys. 11. Responses to movement triggering vs. nontriggering sensory signals. Journal of Neurophysiology, 53, 142-152. Kwan, H.C. (1988). Network relaxation as behavioral action. Research in Biological and Computational Vision Technical Report, RBCV-TR-8826, Dept. of Computer Science, University of Toronto. Kwan, H.C., MacKay, W.A., Murphy, J.T., & Wong, Y.C. (1985). Properties of visual cue responses in primate precentral cortex. Brain Research, 343, 24-35.

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Lamarre, Y., Busby, L., & Spidalieri, G. (1983). Fast ballistic arm movements triggered by visual, auditory, and somesthetic stimuli in the monkey. I. Activity of precentral cortical neurons. Journal of Neurophysiology, 50, 1343-1358. Lecas, J.-C., Requin, J., Anger, C., & Vitton, N. (1986). Changes in neuronal activity of the monkey precentral cortex during preparation for movement. Journal of Neurophysiology, 56, 1680-1702. Lhermitte, F., Pillon, B., & Serdaru, M. (1986). Human autonomy and the frontal lobes. Part I: Imitation and utilization behavior: a neuropsychological study of 75 patients. Annals of Neurology, 19, 326-334. Libet, B. (1985). Unconscious cerebral initiative and the role of conscious will in voluntary action. Behavioral and Brain Sciences, 8, 529-566. MacKay, W.k, & Crammond, D.J. (1987). Neural correlates in posterior parietal lobe of the expectation of events. Behavioral Brain Research, 24, 167-179. MacKay, W.A., Kwan, H.C., Murphy, J.T., & Wong, Y.C. (1978). Responses to active and passive wrist rotation in area 5 of awake monkeys. Neuroscience Letters, 10, 235-239. MacKay, W.A., Kwan, H.C., Murphy, J.T., & Wong, Y.C. (1983). Stretch reflex modulation during a cyclic elbow movement. Electroencephalography and Clinical Nerophysiology, 55, 687-698. Marcel, A.J. (1980). Explaining selective effects of prior context on perception: the need to distinguish conscious and pre-conscious processes. In J. Requin (Ed.), Anticipation and Behaviour (pp. 411-432). Paris: C.N.R.S. Mauritz, K. H., & Wise, S.P. (1986). Premotor cortex of the rhesus monkey: neuronal activity in anticipation of predictable environmental events. Experimental Brain Research, 61, 229-244. Milner, B., & Petrides, M. (1984). Behavioural effects of frontal-lobe lesions in man. Trends in Neurosciences, 7, 403-407. Mountcastle, V.B., Andersen, R.A., & Motter, B.C. (1981). The influence of attentive fixation upon the excitability of the light-sensitive neurons of the posterior parietal cortex. Journal of Neuroscience, I, 1218-1235. Nelson, R.J. (1984). Responsiveness of monkey primary somatosensory cortical neurons to peripheral stimulation depends on "motor set." Brain Research, 304, 143-148. Nelson, R.J. (1987). Activity of monkey primary somatosensory cortical neurons changes prior to active movement. Brain Research, 406, 402-407. Palmer, C.J., Marks, W.B., & Bak, M.J. (1985). The responses of cat motor cortical units to electrical cutaneous stimulation during locomotion and during lifting, falling and landing. Experimental Brain Research, 58, 102-1 16.

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Phillips, C.G. (1969). Motor apparatus of the baboon’s hand. Proceedings of the Royal Society, Series B, 173, 141-174. Requin, J., Riehle, A., & Seal, J. (1988). Neuronal activity and information processing in motor control: from stages to continuous flow. Biological Pychology, 26, 179-198. Riehle, A., & Requin, J. (1989). Monkey primary motor and premotor cortex: single-cell activity related to prior information about direction and extent of an intended movement. Journal of Neurophysiology, 61, 534-549. Roland, P.E. (1985). Cortical organization of voluntary behavior in man. Human Neurobiology, 4, 155-167. Sasaki, K. (1985). Cerebro-cerebellar interactions and organization of a fast and stable hand movement: cerebellar participation in voluntary movement and motor learning. In J. Bloedel, J. Dichgans & W.Precht (Eds.), Cerebellar Functions (pp. 70-85). Berlin: Springer-Verlag. Sawaguchi, T., Matsumura, M., & Kubota, K. (1989). Depth distribution of neuronal activity related to a visual reaction time task in the monkey prefrontal cortex. Journal of Neurophysiology, 61, 435-446. Seal, J., & Commenges, D. (1985). A quantitative analysis of stimulus- and movement-related responses in the posterior parietal cortex of the monkey. Experimental Brain Research, 58, 144-153. Seal, J., Gross, C., Doudet, D., & Bioulac, B. (1983). Instruction-related changes of neuronal activity in area 5 during a simple forearm movement in the monkey. Neuroscience Letters, 36, 145-150. Smith, A.M., Bourbonnais, D., & Blanchette, G. (1981). Interaction between forced grasping and a learned precision grip after ablation of the supplementary motor area. Brain Research, 222, 395-400. Tanji, J., Kurata, K., & Okano, K. (1985). The effect of cooling of the supplementary motor cortex and adjacent cortical areas. Experimental Brain Research, 60, 423-426. Towe, A.L., & Jabbur, S.J. (1961). Cortical inhibition of neurons in dorsal column nuclei of cat. Journal of Neurophysiology, 24, 488-498. Weinrich, M., Wise, S.P., & Mauritz, K.-H. (1984). A neurophysiological study of the premotor cortex in the rhesus monkey. Brain, 107 385-414. Yezierski, R.P., Gerhart, K.D., Schrock, B.J., & Willis, W.D. (1983). A further examination of effects of cortical stimulation on primate spinothalamic tract cells. Journal of Neurophysiology, 49, 424-441. Yuan, B., Morrow, T.J., & Casey, K.L. (1986). Corticofugal influences of S1 cortex on ventrobasal thalamic neurons in the awake rat. Journal of Neuroscience, 6, 361 1-3617.

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CHAPTER 8 CEREBRAL CORRELATES OF AUDITORY ATTENTION R. Naatanen One of the clearest, if not oldest, distinctions made within the attention literature is that between active and passive attention, a distinction proposed by William James a century ago (1890). Active attention refers to a selective state of our information-processing system (and to the ensuing selective processing) which we ourselves develop, according to our momentary interests and motives. Passive attention, in contrast, is initiated by environmental events, and this occurs irrespective of our will. Passive attention is even elicited when it is clearly harmful to the ongoing performance. Here, apparently, we are facing a mechanism of vital significance capable of generating high-priority interrupt signals that secure the eliciting stimulus's access to the limited-capacity system. These two complementary mechanisms central to information processing, conscious perception and experience, as well as to behavior, are currently intensely investigated in cognitive psychology and related fields. Despite this massive work, however, most centraI issues still await a solution. The best-known of these controversies involves the level of information processing at which attentional selection takes place in a typical selective-attention situation such as selective dichotic listening ("the filtering paradigm"; Kahneman & Treisman, 1984). The so-called earlyselection theories hold that in certain conditions, little or no semantic processing occurs to the unattended input, whereas the opposite type of theories, the late-selection theories, maintain that all sensory information is automatically processed to the semantic level. The latter type of theory describes attention only as selecting input to consciousness, memory, and response. Because behavioral research on attention has not been able to provide conclusive answers to central issues such as that mentioned above, despite their utilization of ingenious paradigms, more and more research interest has been directed to the underlying physiology. Physiological processes initiated by stimuli under different attentional instructions have

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been studied, the purpose being to map the attentional influences on these processes. It was hoped that this might enable construction of putative mechanisms of attentional selection operating between the stimulus and the response, hidden from behavioral attention research by the "Black Box". This optimism has been reinforced by the rapid development of new technology for cognitive brain research. In the present chapter, my purpose is to review some central lines of physiological research on human auditory attention, both passive and active attention. Most of this work was conducted by recording eventrelated brain potentials (ERP) from the scalp of healthy human subjects but important complementary information was provided by related magnetoencephalographic (MEG) and regional cerebral blood-flow (rCBF) work. ERPs or evoked potentials (EP) are discrete and minute electrical potentials which appear in the electroencephalogram (EEG). They are usually caused by and time-locked to sensory stimuli. These small changes in the EEG are normally obscured by much larger spontaneous brain waves and rhythms. However, if brief EEG epochs are summed and averaged over many presentations of the same stimulus, the EEG activity time-locked to the stimulus is enhanced whereas the randomly occurring spontaneous waves are reduced, leaving distinct ERP waveforms for study. The ERP consists of a sequence of positive and negative waves or peaks. Although these deflections in the waveform provide a convenient point for measurement, they are not necessarily generated by individual cerebral events. At any point in time, multiple cerebral processes may contribute to the ERP waveform. In this chapter, an ERP component will be taken to be "the contribution to the recorded waveform of a particular generator process, such as the activation of a localized area of cerebral cortex by a specific pattern of input .... Whereas the peaks and deflections of an EP can be directly measured from the averaged waveform, the components contributing to these peaks can usually be inferred only from the results of experimental manipulation" (Naatanen & Picton, 1987, p. 376; see also Donchin, Ritter, & McCallum, 1978). Thus, by recording ERPs, it appears that we might be able to follow some aspects of the processing initiated by a stimulus in the brain. Further, if we are able to disentangle the overlapping components of the ERP and to localize their sources, we could trace a substantial part of the spatio-temporal activation pattern associated with stimulus processing. Source localization on the basis of ERPs recorded in parallel from numerous scalp sites is, however, rather problematic, but nevertheless

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some relatively safe conclusions can be made when ERP information is interpreted in the light of the known brain anatomy and physiology (see Wood, et al., 1984). Recording stimulus-induced changes in the magnetic fields surrounding the head (produced by the brain's electrical activity) provides, in general, a better means for localizing event-related electrical activity in the brain (for reviews, see Hari, in press; Kaufman & Williamson, 1988), but due to certain limitations of the MEG, a parallel recording of the ERP and the MEG is advisable in many types of studies (see, e.g., Hari, Kaila, Katila, Tuomisto, & Varpula, 1982). Further, complementary information may be obtained by recording regional cerebral blood flow, or rCBF, and regional metabolic changes, the latter usually by means of positron emission tomography (PET). Thus, modem technology has opened ample opportunities for noninvasive research on the physiological basis of information processing as well as on attentional manifestations in, and effects on, these physiological events. Consequently, some of the physiology underlying human attention is already rather well known. The import of these data to cognitive theories of attention is, however, in most cases rather unclear, due to the lack of understanding of what the physiological processes measured mean in terms of actual information extraction, transfer, and use (Naatanen, 1988). In the next section, some central aspects of these physiological data, involving auditory attention, are reviewed and discussed with a view to clarifying not only the mechanism of auditory attention but also that mechanism's role in auditory information processing.

Passive Attention and Its PhysioIogy in Audition Passive attention was described above as a form of attention which is involuntarily caught by stimuli, rather than initiated by ourselves. Two broad classes of stimulus events can be separated here, again as previously recognized by William James (1890): (a) stimuli which elicit attention due to their physical properties, and (b) stimuli which elicit attention due to their psychological or semantic properties (i.e., what James called "derived" properties). As to these physical properties, the onset of a stimulus tends to capture attention, especially when the stimulus is delivered after a long silent interval. According to Newstead and Dennis (1979), it is impossible not to become aware of discrete stimuli occasionally presented to the otherwise "silent" unattended ear while listening to stimuli delivered to the opposite ear. The offset of a long-duration sound also is an attention-

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capturing event. Similarly, we tend to become aware of the occurrence of occasional changes in a repetitive or continuous stimulus in our acoustic environment. The effectiveness of a stimulus onset in catching our attention apparently depends on various factors such as the loudness and rise time of the stimulus as well as the length of the preceding silent interval. Similarly, a stimulus offset is, apparently, more attentioncatching, the louder the stimulus, the longer the duration, and the shorter the fall time. Now, the question arises whether the auditory ERP includes any components which are generated by mechanisms underlying shifts of attention to physical stimulus events. For instance, with regard to stimulus onsets, such a mechanism would be one which is particularly sensitive to stimulus onsets, especially to abrupt onsets of loud stimuli after long silent periods, but does not belong to neural mechanisms encoding any particular stimulus attribute such as frequency. Consider the various components comprising the auditory ERP. A discrete auditory stimulus, such as a brief tone pip, first elicits cochlear and brainstem potentials recordable from the scalp. These deflections are of very low amplitude, however, and must be averaged over many hundreds or even thousands of stimuli in order to be resolved clearly. The brainstem response consists of seven small deflections, all occurring within the first 10-12 ms from stimulus onset (Picton, Stapells, & Campbell, 1981; Starr & Don, 1988). These deflections probably reflect the arrival of sensory input to the various auditory nuclei in the cochlea and brainstem. The brainstem responses are followed by the middle-latency responses occurring from about 10 to 50 ms from stimulus onset. These comprise a sequence of low-amplitude, fast deflections, some of which are myogenic (muscular) in origin; those of cerebral origin are probably generated at the thalamic and cortical levels (Picton, Hillyard, Krausz, & Galambos, 1974). The arrival of the auditory input to the primary auditory cortex occurs, according to Vaughan and Arezzo (1988), at about 9 ms after stimulus onset and is reflected by the No wave of the middlelatency responses. According to Celesia (1976), auditory input arrives at the primary auditory cortex in 10-12 ms from stimulus onset. The middle-latency responses are followed by a large wave complex Nl-P2, with peak latencies at about 100 and 200 ms, respectively, usually preceded by a small P1 peaking at about 50 ms. These waves reach their maximal amplitudes at, or slightly anterior to, the vertex of the scalp (Picton et al., 1974). The N1 wave can be decomposed into at least three

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different "genuine" components which, according to Naatanen and Picton (1987), are as follows: (1) The frontocentral negativity generated by bilateral, vertically-oriented dipole planes in the auditory cortices on the superior aspect of the temporal lobe (Vaughan & Ritter, 1970); (2) the T complex, with a positivity peaking at 90-100 ms and a negativity at 140-150 ms, probably originating in the auditory association cortex on the lateral aspect of the superior temporal gyrus (Wolpaw & Penry, 1975); (3) the nonspecific component, maximal at the vertex, at a latency of 100 ms (Hari et al., 1982), with an unknown locus of origin (which probably is outside the auditory cortex, however). The above-listed ERP components are characterized as exogenous (Donchin et al., 1978) or "obligatory" (Naatanen, 1987) for they are mainly determined by physical and temporal features of stimulation and are, within a very wide range of variation in the organism's state, obligatorily elicited by appropriate stimulation. Most of these components seem to reflect the operations of mechanisms with other than attentional functions, judging from the very short recovery times of these components after a stimulus (e.g., Picton et al., 1981; Starr & Don, 1988). These functions probably belong to the processing of specific stimulus information, and this processing occurs both at the subcortical and cortical levels. The components forming the large N1 wave, however, at least the supratemporal component, might express the operation of a mechanism somehow related to passive attention. The recovery time of this component is of the order of 10 s, judging from MEG recordings (Makela, Hari, & Leinonen, 1988); MEG permits measurement of this component which is difficult to accomplish by means of the ERP. (The recovery time of the nonspecific N1 component is too long for a principal mechanism of passive attention elicited by stimulus onset; see Fruhstorfer et al., 1970.) Naatanen (1986) proposed that the function of the neuronal population that generates the supratemporal component is to summon attention to the eliciting auditory stimulus, whose specific features might be analyzed by neuronal events that are earlier and faster but subjectively "silent", and in part subcortical. It appears impossible that events of this processing level per se could underlie conscious perception or trigger attention in view of the large number of parallel processes occurring in the different sensory systems of different modalities. Moreover, in that case, concentrated task performance, probably even sleep, would be either impossible or very difficult, at least much more difficult than they are in fact. Therefore a separate mechanism is needed which (a) selects stimuli

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for entry into the limited-capacity system and thus protects it from sensory overload, and (b) controls the threshold of this entry. The brain mechanism generating the supratemporal N1 component might serve as such a mechanism within the auditory modality. As already mentioned, this suggestion is supported by the relatively long recovery times of the supratemporal component. This component is considerably larger for longer ISIs (Figure 1). It is very large in response to the first stimulus and attenuates thereafter, reaching some constant level by the 5th stimulus or so, as illustrated in Figure 1, depending on the inter-stimulus interval (ISI) used (see Ritter, Vaughan, & Costa, 1968). These facts roughly correspond to the subjective "obtrusiveness" of a stimulus when it is presented as the first stimulus of a stimulus block, or at long ISIs, and might also explain the attention-catching character of stimuli delivered at long ISIs to the ''unattended" ear in dichotic listening (Newstead & Dennis, 1979); this is also consistent with the fact that we usually perceive even repetitive stimuli consciously. Moreover, the supratemporal component does not fully disappear even with very short ISIs, which agrees with the fact that we tend to perceive even these stimuli perfectly well. Consistently with this, experiments conducted at the auditory detection threshold (e.g., Parasuraman, Richter, & Beatty, 1982) have shown that the detection of weak auditory stimuli correlates strongly with the N1 amplitude. Further, whereas the N1 is especially sensitive to transient aspects of stimulation, that is, to energy change per unit time during stimulus onsets and offsets (Naatanen & Picton, 1987; see also Graham, 1979)), it seems to be associated with no more specific aspect of perception than with mere detection. For example, a dissociation between N1 amplitude and subjective loudness has been demonstrated in several ways (for a review, see Naatanen & Picton, 1987). Butler (1972) in turn found a dissociation between the frequency-specificity of the neuronal populations generating the N1 and perceived pitch. Davis and Zerlin (1966) suggested that "the mechanisms that generate the potential and determine its magnitude do not lie on the direct path, so to speak, to psychological sensation but rather on a parallel path with other functions" (Davis & Zerlin, 1966, p. 116). Consistent with this, very similar N1 responses are elicited by a wide variety of acoustic stimuli such as clicks, tones, speech and animal sounds (Gaillard & Lawson, 1984; Woods & Elmasian, 1986; Hari, in press). Finally, the N1 wave is reduced as sleep becomes deeper and finally disappears at Stage 4, recovering to half the waking amplitude during REM sleep (see Figure 13 in Naatanen & Picton, 1987). Judging from the IS1 in that study, this N1

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NON-SPECIFIC COMPONENT SUPRATEMPORAL COMPONENT

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A schematic illustration of the effect of the serial posi1.m of a stimulus in a stimulus train on the vertex N1 wave (top row) and on its two components, the nonspecific (second row) and the supratemporal (third row) ones. In the bottom of the figure, the differential IS1 sensitivity of these two components is schematically illustrated.

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wave was mainly composed of the supratemporal component. Thus, under the present hypothesis, the obtrusiveness of discrete auditory stimuli is reduced during sleep, which is consistent with behavioral data. Such a reduction may be important for maintaining the sleep state. In the foregoing, I have reviewed evidence that suggests, or is consistent with, the hypothesis that the supratemporal N1-generator process acts as an internal attentional trigger, choosing auditory stimuli for conscious perception. The evidence for the specific relation of N1 to energy onset and offset suggests that the underlying neuronal population detects a stimulus or its termination but does not provide specific perceptual contents. Consequently, the process informs that some stimulus is occurring without indicating what the stimulus is or what its precise features are. Although the generator is organized with at least some stimulus-specificity, the numerous dissociations between the N1 and the specific contents of perception suggest that perception is not based on the stimulus-specificity of this generator, but, rather, probably on that of earlier mechanisms of sensory analysis. The nonspecific component of the N1 wave is associated with a transient arousal burst caused by the stimulus (for a review, see Naatanen & Picton, 1987). Probably, this arousal burst, or the activation of the generator mechanism of the component itself, together with the associated proprioceptive and other internal feedback, also possesses an attentioncatching property. Because of the long refractory period (see Figure l), the component is elicited mainly at the onset of a stimulus sequence, and by subsequent stimuli only when ISIs are long. Hence this generator process cannot provide the principal mechanism for conscious perception of auditory stimuli. In reality, acoustic stimulation (e.g., speech) is often continuous rather than discrete, with changes occurring in the absence of any "empty" ISIs. Even minor frequency or intensity changes in a continuous tone elicit large N1 types of waves. Such a wave in response to a brief change from a continuous 600-Hz tone to 625 Hz is illustrated in Figure 2. Further, Arlinger, et al. (1982) recorded magnetic fields evoked by brief changes in the frequency of a continuous tone. Like the N1 type of response to tone onset, the response to a frequency glide was generated in the supratemporal plane. On the basis of this and further similar evidence, Naatanen (1988) suggested that the inherent attention-catching property of any changes in a continuous stimulus is based on the high sensitivity of the mechanism generating the supratemporal N1 component to these changes.

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Figure 2. Across-subject ERPs to a transitory frequency modulation (onset at 'IS") of a 600-Hz continuous tone to 625 Hz for a duration of 50 ms. The mean interval between successive frequency modulations was 3.1 s. The trace length is 300 ms. (From Naatanen, Paavilainen, Alho, Reinikainen, & Sams, 1987. Reproduced with permission; see acknowledgements.)

ERP studies also suggest a mechanism for switching attention in response to a change in a repetitive homogeneous sequence of discrete stimuli. In these studies, the subject's attention is directed elsewhere while he/she is presented with a long sequence of auditory "standard" stimuli, one of which is occasionally replaced by a "deviant" stimulus. The two stimuli elicit quite similar N1 and P2 components which may, however, be slightly larger in response to the deviant stimuli, at least when the stimulus difference is not small. On the other hand, the deviant stimuli elicit a new component called the mismatch negativity (MMN) which is not elicited by the standard stimuli (Naatanen, Gaillard, & Mantysalo, 1978). The MMN can be derived from a difference wave obtained by subtracting the standard-stimulus ERP from that to the deviant stimulus. The negativity of the difference wave usually yields a rather good estimate of the MMN component because, as already mentioned, the N1 and P2 components elicited by the deviant stimuli are quite similar to those elicited by the standard stimuli when the magnitude of stimulus deviation is not large (Sams, Paavilainen, Alho, & Naatanen, 1985). This subtraction procedure, as well as a MMN in response to a change in tonal frequency, are illustrated in Figure 3 (Sams et al., 1985). Each stimulus block was composed of 80% standard stimuli of 1000 Hz and 20% deviant stimuli, differing in frequency from the standards, delivered in a random order and at constant ISIs of 1 s. The frequency

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of the deviant stimulus was, in separate blocks, either 1004, 1008, 1016, or Deu i ant FZ CZ 1032 Hz. The subject was instructed to ignore the auditory stimuli and to concentrate on reading a book. The N1 wave in response to the various deviant stimuli is similar to the one evoked by the standard stimulus, and does not vary in amplitude or latency with the degree DIFFERENCE of deviance. As shown by 1004 Hz the difference waveforms, a clear MMN is elicited by deviant stimuli with fre1008 HZ , quencies higher than 1008 Hz. (In a control experi1016 Hz Avr ment, a MMN was elicited when the subject instead of reading, performed a 1032 Hz difficult visual computer game.) In a separate condition, the subjects were found to be able to discriminate these stimuli from the standards. Even Figure 3. Top: Across-subject ERPs to 1000the 1008-Hz stimuli, which Hz standards (thin line) and to deviants (thick were found to be near the line) of different frequencies, as indicated on discrimination threshold, the left side. Bottom: The respective difference elicited a MMN although waves obtained by subtracting the standardstimulus ERP from the respective deviant-stimua very small one. The lus ERP. (From Sams et al., 1985). MMN peak is earlier for larger deviations in pitch. When the magnitude of deviation is further increased, the decreased MMN latency results in an increasing overlap between the MMN and N1 components (Naatanen & Gaillard, 1983).

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The MMN seems to be elicited by any physical or temporal deviance in the auditory stimulus sequence. Even intensity and duration decrements elicit the MMN, and this occurs independently of attention (for a review, see Naatanen, in press). These and some further data indicate that the MMN cannot be explained by new afferent elements activated by deviants but not standards. Therefore the MMN appears to be generated when an input from a deviant stimulus encounters the neural representation or memory trace of the standard stimulus (see Naatanen, in press). The biological function of the process generating the MMN might be to initiate a sequence of further brain processes leading to an attention switch to a change in an unattended auditory input (Naatanen, 1985). Some of these further processes might be reflected by the P3a component of the ERP, a frontocentral positivity peaking at 250-300 ms (see Squires, Squires, & Hillyard, 1975). James (1890) and his followers assumed that an attention switch can also occur due to the semantic meaning of an unattended stimulus. This brings us into the middle of one of the central issues of attention research to date, that concerning the degree of automaticity of semantic processing mentioned. ERP data might be interpreted as suggesting that semantic processing does not have to be fully automatic (in the sense of being independent of attention). In the foregoing, we have examined ERP data suggesting attention-switching mechanisms which are frequently activated by certain physical events in the unattended input. Apparently, these mechanisms cause frequent momentary attention switches to this input (see Lyytinen, Blomberg, & Naatanen, 1989). According to MMN data, this input is fully processed with regard to its physical and temporal properties and stored for a few seconds in a memory system probably corresponding to cognitive psychologists' notion of sensory or precategorical memory. It is, presumably, this information store that is looked at by the attentional focus while momentarily caught by the "wrong" input, rather than the ongoing sensory processing per se. Such frequent attention switches to such fully processed representations of the physicaltemporal features of the auditory stimuli might well serve to introduce these representations into long-term memory and thus explain data interpreted in terms of attention-independent semantic processing (Naatanen, in press).

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Selective Attention and its Physiology in Audition Research on ERP correlates of auditory selective attention was initially centered around the N1 wave. The first demonstration of a selective-attention effect on the N1 wave, which could not be questioned on methodological grounds, was the one reported by Hillyard, Hink, Schwent, & Picton, (1973) (for a review, see Naatanen, 1982). In Hillyard et al.'s dichotic-listening task with very short irregular ISIs, the left-ear tones were of a considerably higher pitch than the right-ear tones. Both sequences included occasional, randomly placed, slightly higher tones. The task was to count the deviants among the standards in a designated ear and to ignore all the input to the other ear. The vertex N1 deflection was larger in response to the attended than to the ignored stimuli. The authors regarded their "N1 effect" as an enhancement of the exogenous "N1 component" and suggested that it reflects Broadbent's (1971) stimulus-set mode of attention. Since this pioneering study, considerable research effort has been expended to clarify the conditions and limits of the N1 effect (for reviews, see Hillyard & Picton, 1979; Naatanen, 1982). Naatanen, et al. (1978), however, described a different kind of selective-attention effect on the ERP, which they called the processing negativity (PN). The effect was not produced by any exogenous ERP component but was rather a new component emerging during selective attention. The dichotic-listeningtask used differed from that of Hillyard et al. (1973) in having, among other things, a considerably longer and constant IS1 (800 ms). The peak amplitude of the N1 deflection was not affected, but the N1 peak was followed by a low-amplitude negative displacement of the ERP to the attended standards relative to the unattended standards. This displacement began at 150 ms, during the descending limb of the N1 deflection, and persisted for at least 500 ms. The authors proposed that the PN is an endogenous component generated by a cerebral mechanism different from that of the N1 component and, further, that even the N1 effect reported by Hillyard et al. (1973) might have been caused by a PN rather than by an intensification of the generator process of the N1 component. The considerably shorter ISIs used by Hillyard et a1.(1973) might have shortened the PN latency so that the PN overlapped the N1 component, causing an artificial increase in its measured amplitudes. Even to date, it is not entirely clear whether all ERP effects of auditory selective attention are due to the PN or whether an enhancement of some N1 component may also occur in some conditions (Woldorf

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et al., 1987; Hackley, Woldorff, & Hillyard, 1987; Naatanen, Teder, & Alho, in preparation). The PN has been verified by many studies (e.g., Okita, 1979; Parasuraman, 1980) and has also been observed by Hillyard and his colleagues (Hansen & Hillyard, 1980). Hansen and Hillyard's.data suggest that the onset latency of the attention effect depends on the difference between relevant and irrelevant stimuli. The subjects in this study were presented with a binaural sequence of equiprobable "high-pitch" and "lowpitch'' tones. The frequency of the high tones was, in separate blocks, either 350, 400, or 700 Hz, the low tones always being 300 Hz. Thus pitch separation between the two tones in a block was either 50, 100, or 400 Hz. In different blocks, either the low or high tones were designated as task-relevant, the subject's task being to discriminate occasional longerduration tones among the task-relevant tones. The right side of Figure 4 presents the attention effect called the "Nd" (negative difference) by the authors, obtained by subtracting the ERP to the unattended stimuli from that to the attended stimuli. With greater pitch separation, both onset and peak latencies of the Nd were shorter and the Nd duration longer. The late portion of the Nd had a topography anterior to that of the earlier portion, suggesting that there are in fact two partially overlapping components in the attention effect. Subsequent studies showed, among other things, that (a) the PN onset latency is shorter when the mean IS1 in studies using irregular ISIs is shorter (Parasuraman, 1980); (b) the PN is elicited even by complex stimuli, e.g., by speech sounds (Woods, Hillyard, & Hansen, 1984); (c) even (slowly) moving attended stimuli can elicit a PN (Okita, 1979); (d) at least some of the PN is, according to MEG recordings, generated in the supratemporal auditory cortex (Hari et al., in press; Arthur, Lewis, Medvick, & Flynn, 1989); (e) a few relevant stimuli must be delivered before the PN can be elicited (Hansen & Hillyard, 1988; see also Donald & Young, 1982). Naatanen (1982) proposed that the first PN component, probably generated in the auditory cortex, expresses selection of the to-be-attended stimuli among irrelevant stimuli. According to him, selective attention to one class of stimuli physically differing from the other stimuli is based on maintaining a neuronal representation of the physical feature(s) defining the relevant stimuli. This representation would be based on the presence of a corresponding stimulus representation in sensory memory, explaining why a few stimuli are needed before attention can be "tuned" to a particular stimulus. (For consistent behavioral results, see Treisman,

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Figure 4. Across-subject ERPs to standard tones at three different frequency separations in a binaural durationdiscrimination task. ERPs at left are to 300 Hz (low) tones and at center to 350, 400, or 700 Hz (high) tones, according to condition. ERPs to attended tones (solid lines) and unattended tones (dotted lines) are overlapped. Tracings at right are superimposed difference waves between ERPs to attended and unattended tones. (From Hansen & Hillyard, 1980).

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Squire, & Green, 1974). This voluntary neuronal representation, proposed to be located in the auditory cortex, was called the attentional trace. It was further suggested that the attentional trace is maintained by a frontallobe mechanism which might account for the later, frontal PN component. Some rCBF data of Roland (1981, 1982) support this proposal. During selective attention, each auditory input is, on this theory, compared with the attentional trace and, further, this comparison process lasts longer the more similar the stimulus is to that represented by the attentional trace. Thus the relevant stimulus generates the longest and largest PN but even irrelevant stimuli generate some PN. Hence selective attention in these kinds of situations would be based on a self-terminating matching or comparison process which selects, for further processing, stimuli meeting the criteria represented by the attentional trace and rejects all other stimuli. These predictions have recently been verified by Alho et al. (e.g., Alho, Sams, Paavilainen, & Naatanen, 1986; Alho, Tottola, Reinikainen, Sams, & Naatanen, 1987). Their results imply that the Nd obtained by subtracting the irrelevant-stimulus ERP from the relevant-stimulus ERP (see Figure 4) does not yield the whole PN, for the common initial PN elicited by both stimuli at the same onset latency is cancelled. This cancellation effect accounts for the later Nd onset with smaller separations (Figure 4), i.e., the later separation of the traces for the relevant and irrelevant stimuli. This later Nd onset is hence not due to a later PN onset to relevant stimuli. For details of the attentional-trace theory and results of further studies testing its predictions, see Naatanen (1982; and in press). In conclusion, ERP studies on auditory attention suggest that selective attention to a class of stimuli defined by some physical feature is realized via a matching type of process. This process expresses comparison of each auditory input with a voluntarily maintained representation of the physical features defining the relevant stimulus class. Further, in contrast to filtering or gating types of theories, the processing of physical features of irrelevant stimuli is not blocked or attenuated, but these stimuli are rejected from further processing following initial selection. Therefore these data tend to support early-selection rather than late-selection types of attention theory (see Naatanen, in press). The above-mentioned filtering or gating types of theories in turn would be supported by results suggesting that selective attention enhances exogenous ERP components. As already mentioned, such evidence should still be considered inconclusive with regard to the N1 component. Very

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recent research (Woldorf et al., 1987; Hackley et al., 1987), however, suggests that under certain specific conditions, attended stimuli elicit a small positivity at a latency as short as 30-50 ms preceding the negative attention effect. The significance of this finding should be determined by future research.

Summary Physiological studies on human auditory attention were reviewed. These studies mainly involve event-related brain potentials (ERP) but some magnetoencephalographic (MEG) and regional cerebral blood-flow (rCBF) studies have also been performed. ERP studies on passive attention suggest cerebral mechanisms of attention switch to certain physical events in the unattended auditory input. These events include stimulus onsets and offsets as well as changes in continuous or discrete stimuli. MEG studies provide information on cerebral locations of these mechanisms. ERP studies on auditory selective attention reveal a specific ERP component, the processing negativity, which permits certain conclusions regarding the nature and mechanisms of attentional stimulus selection.

Acknowledgments The preparation of this article was supported by the Wissenschaftskolleg zu Berlin (Institute of Advanced Study Berlin) and the Academy of Finland. Figure 2 reproduced, with permission, from R. Naatanen, et al., (1987). "Interstimulus interval and the mismatch negativity. In C. Barber and T. Blum (Eds.), Evoked potentials 111: The third international evoked potentiah symposium. Stoneham, M A Butterworth Publishers.

References Alho, K., Sams, M., Paavilainen, P., & Naatanen, R. (1986). Small pitch separation and the selective-attention effect on the ERP. Psychophysiology, 23, 189-197. Alho, K., Tottola, K., Reinikainen, K., Sams, M., & Naatanen, R. (1987). Brain mechanisms of selective listening reflected by event-related potentials. Electroencephalography and clinical Neurophysiology, 68, 458-470.

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Arlinger, S., Elberling, C., Bak, C., Kofoed, B., Lebech, J., & Saermark, K. (1982). Cortical magnetic fields evoked by frequency glides of a continuous tone. Electroencephalography and clinical Neurophysiology, 54, 642-653. Arthur, D. L., Lewis, P. S., Medvick, P. A., & Flynn, E. R. (1989). A neuromagnetic study of selective auditory attention. Manuscript submitted for publication. Broadbent, D. E. (1971). Decision and Stress. New York: Academic Press. Celesia, G. G. (1976). Organization of auditory cortical areas in man. Brain, 99, 403-414. Davis, H., & Zerlin, S. (1966). Acoustic relations of the human vertex potential. Journal of Acoustical Society of America, 39, 109-116. Donald, M. W., & Young, M. J. (1982). The time course of selective neural tuning in auditory attention. Experimental Brain Research, 46, 357-367. Donchin, E:, Ritter, W., & McCallum, W. C. (1978). Cognitive psychophysiology: The endogenous components of the ERP. In E. Callaway, P. Tueting, & S. H. Koslow (Eds.), Event-related brain potentials in man (pp. 349-441). New York: Academic Press. Gaillard, A. W. K., & Lawson, E. A. (1984). Evoked potentials to consonantvowel syllables in a memory-scanning task. In R. Karrer, J. Cohen, & P. Tueting (Eds.), Brain and information: Event-relatedpotentials. Annals of the New York Academy of Sciences, 425, 204-209. Graham, F. K. (1979). Distinguishing among orienting, defence and startle reflexes. In H. D. Kimmel, E. H. van Olst, & J. F. Qrlebeke (Eds.), The orienting reflex in humans (pp. 137-167). Hillsdale, N.J.: Erlbaum. Hackley, S. A., Woldorff, M., & Hillyard, S. A. (1987). Combined use of microreflexes and event-related brain potentials as measures of auditory selective attention. Psychophysiology, 24, 632-647. Hansen, J. C., & Hillyard, S. A. (1980). Endogenous brain potentials associated with selective auditory attention. Electroencephalography and Clinical Neurophysiology, 49, 277-290. Hansen, J. C., & Hillyard, S. A. (1988). Temporal dynamics of human auditory selective attention. Psychophysiology, 25, 316-329. Hari, R. (In press). The neuromagnetic method in the study of human auditory cortex. In F. Grandori, G. L. Romani, & M. Hoke (Eds.), Advances in

Audiology. Hari, R., Hamalainen, M., Kaukoranta, E., Makela, J., Joutsiniemi, S.-L., & Tiihonen, J. (In press). Selective listening modifies activity of the human auditory cortex. Expenmental Brain Research.

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Hari, R., Kaila, K., Katila, T. Tuomisto, T., & Varpula, T. (1982). Interstimulus interval dependence of the auditory vertex response and its magnetic counterpart: Implications for their neural generation. Electroencephalography and clinical Neurophysiology, 54, 561-569. Hillyard, S. A., & Picton, T. W. (1979). Event-related brain potentials and selective information processing in man. In J. E. Desmedt (Ed.),

Cognitive components in cerebral event-related potentials and selective attention. Progress in Clinical Neurophysiology, 6 (pp. 1-52). Basel: Karger. Hillyard, S. A., Hink, R. F., Schwent, V. L., & Picton, T. W. (1973). Electrical signs of selective attention in the human brain. Science, 182, 177-180. James, W. (1890). The principles ofpsychology. New York: Holt. Kahneman, D., & Treisman, A. (1984). Changing views of attention and automaticity. In R. Parasuraman, & D. R. Davies (Eds.), Varieties of attention (pp. 29-61). London: Academic Press, . Kaufman, L., & Williamson, S. (1988). Recent developments in neuromagnetism: Implications for imaging. In G. Pfurtscheller, & F. H. Lopes da Silva (Eds.), Functional brain imaging (pp. 11-29). Bern: Hans Huber Publishers. Lyytinen, H., Blomberg, A-P., & Naatanen, R. (1989). Autonomic concomitants of event-related potentials in the auditory oddball paradigm. Submitted for publication. Makela, J. P., Hari, R., & Leinonen, L. (1988). Magnetic responses of the human auditory cortex to noisehquare wave transitions. Electroencephalography and clinical Neurophysiology, 69, 423-430. Naatanen, R. (1982). Processing negativity: An evoked-potential reflection of selective attention. Psychological Bulletin, 92, 605-640. Naatanen, R. (1985). Selective attention and stimulus processing: reflections in event-related potentials, magnetoencephalogram and regional cerebral blood flow. In M. I. Posner, & 0. S. Marin (Eds.), Attention and Performance X I (pp. 355-373). Hillsdale, N.J.: Erlbaum. Naatanen, R. (1986). The orienting response theory: An integration of informational and energetical aspects of brain function. In R. G. J. Hockey, A. W. K. Gaillard, & M. Coles (Eds.);Adaptation to stress and task demands: Energetical aspects of human infomtion processing (pp. 91 111). Dordrecht: Martinus Nijhoff. Naatanen, R. (1987). Event-related brain potentials in research of cognitive processes -- a classification of components. In E. van der Meer, & J. Hoffmann (Eds.), Knowledge Aided Information Processing (pp. 241273). Amsterdam: Elsevier. Naatanen, R. (1988). Implications of ERP data for theories of attention. Biological Psychology, 26, 117-163.

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Naatanen, R. (In press). Role of attention in auditory information processing revealed by event-related brain potentials. Behavioral and Brain

Sciences. Naatanen, R., & Gaillard, A. W. K. (1983). The N2 deflection of ERP and the orienting reflex. In A. W. K. Gaillard, & W. Ritter (Eds.), EEG correlates of information processing: Theoretical issues (pp. 119-141). Amsterdam: Elsevier. Naatanen, R., & Picton, T. W. (1987). The N1 wave of the human electric and magnetic response to sound: A review and an analysis of the component structure. Pvchophysiologv, 24, 375-425. Naatanen, R., Gaillard, A. W. K., & Mantysalo, S . (1978). Early selective attention effect on evoked potential reinterpreted. Actu Pychologica, 42, 313-329. Naatanen, R., Paavilainen, P., Alho, K., Reinikainen, K., & Sams, M. (1987). Inter-stimulus interval and the mismatch negativity. In C. Barber, & T. Blum (Eds.), Evoked potentials 111 (pp. 392-397). London: Butterworths. Naatanen, R., Teder, W., & Alho, K. (In preparation). Processing negativity and the "Nl effect": One or two selective-attention effects on the

auditory event-related brain potential. Newstead, S . E., & Dennis, I. (1979). Lexical and grammatical processing of unshadowed messages: A reexamination of the MacKay effect. Quarter& Journal of Experimental Psychology, 31, 477-488. Okita, T. (1979). Event-related potentials and selective attention to auditory stimuli varying in pitch and localization. Biological Psychology, 9, 271-284. Parasuraman, R. (1980). Effects of information processing demands on slow negative shift latencies and NlOO amplitude in selective and divided attention. Biological Psychology, 11, 217-233. Parasuraman, R., Richter, F., & Beatty, J. (1982). Detection and recognition: Concurrent processes in perception. Perception and Pychophysics, 31, 1-12. Picton, T. W., Hillyard, S . A., Krausz, H. I., & Galambos, R. (1974). Human auditory evoked potentials. I. Evaluation of components. Electroencephalography and clinical Neurophysiology, 36, 179-190. Picton, T. W., Stapells, D. R., & Campbell, K. B. (1981). Auditory evoked potentials from the human cochlea and brainstem. The Journal of Otolaryngology, 10, 1-41. Ritter, W., Vaughan, H. G., & Costa, L. D. (1968). Orienting and habituation to auditory stimuli. A study of short term changes in average evoked responses. Electroencephalography and clinical Neurophysiology, 25, 550-556.

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Roland, P. E. (1981). Somatotopical tuning of postcentral gyrus during focal attention in man. A regional cerebral blood flow study. Journal of Neurophysiology, 46, 744-754. Roland, P. E. (1982). Cortical regulation of selective attention in man. A regional cerebral blood flow study. Journal of Neurophysiology, 48, 1059-1077. Sams, M., Paavilainen, P., Alho, K., & Naatanen, R. (1985). Auditory frequency discrimination and event-related potentials. Electroencephalographyand clinical Neurophysiology, 62, 437-448. Squires, N. K., Squires, K. C., & Hillyard, S. A. (1975). Two varieties of longlatency positive waves evoked by unpredictable auditory stimuli in man. Electroencephalography and clinical Neurophysiology, 38, 387-401. Starr, A., & Don, M. (1988). Brain potentials evoked by acoustic stimuli. In T.W. Picton (Ed.), Human event-related potentials. EEG handbook (revised series, Vol. 3) (pp. 97-157). Amsterdam: Elsevier. Treisman, A. M., Squire, R., & Green, J. (1974). Semantic processing in dichotic listening? A replication. Memory and Cognition, 2, 641-646. Vaughan, H. G., & Ritter, W. (1970). The sources of auditory evoked responses recorded from the human scalp. Electroencephalography and clinical Neurophysiology, 28, 360-367. Vaughan, H. G., & Arezzo, J. C. (1988). The neural basis of event-related potentials. In T. W. Picton (Ed.), Human event-relatedpotentials. EEG handbook (revised series, Vol. 3) (pp. 45-96). Amsterdam: Elsevier. Wolpaw, J. R., & Penry, J. K. (1975). A temporal component of the auditory evoked response. Electroencephalographyand clinical Neurophysiology, 39, 609-620. Wood, C. C., McCarthy, G., Squires, N. K., Vaughan, H. G., Woods, D. L., & McCallum, W. C. (1984). Anatomical and physiological substrates of event-related potentials. Two case studies. In R. Karrer, J. Cohen, & P. Tueting (Eds.), Brain and information: Event-related potentials. Annals of the New York Academy of Sciences, 425, (pp. 681-721). Volume in the N.Y. Academy Series of Publications. Woods, D. L., & Elmasian, R. (1986). The habituation of event-related potentials to speech sounds and tones. Electroencephalography and clinical Neurophysiology, 65, 447-459. Woods, D. L., Hillyard, S. A., & Hansen, J. C. (1984). Event-related brain potentials reveal similar mechanisms during selective listening and shadowing. Journal of Experimental Pychology: Human Perception and Pe$omurnce, 10, 761-777.

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CHAPTER 9 THE PHYSIOLOGICAL STRESS OF THWARTED INTENTIONS Raymond P. Pavloski This chapter examines a conception of physiological stress derived from control theory. Physiological activity is modulated by neural processes that are tightly linked to the generation and control of behavior (e.g., Brener, 1987). Consequently, changes in physiological activity, including those changes commonly regarded as being stress related, necessarily involve the control mechanisms by which behavior itself is generated. In other words, physiological stress is a theoretical concept which derives its scientific meaning from its larger theoretical context, that is, from its position within a general theory of behavior. Only from within the context of a general theory of behavior can we precisely specify what is meant by the expression physiological stress, in the same way that something precise is meant by the terms stress and strain in the context of Newtonian mechanics (Gartenhaus, 1977, Chapters 1-12).

Defining Stress Requires a Theory of Behavior The general theory of behavior from which the present conception of physiological stress is derived is the theory that human beings are control systems employing negative feedback (for a detailed control-system analysis of human behavior, see Powers, 1973a, 1973b). A negative-feedback control system produces a behavior reliably by varying its output so that the monitored value of a controlled variable (a representation of what is--an input to the system) matches the system’s reference level (a representation of what is intended-the value of the reference signal for the system). Both artificial control systems and those natural systems that have been investigated maintain a near-zero difference between these two representations over time (see review in Pavloski, in press). A thwarted intention exists when the two representations do not closely match. Physiological stress is defined here as the physiological consequence of thwarted intentions; that is, of non-zero error in the operation of negativefeedback control systems. Defined in this way, physiological stress appears

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to be related to the psychophysiologist's concept of physiological reactivity-enhancement of a physiological activity that would in certain circumstances have functional behavioral significance. Two examples are a pounding heart and sweaty palms. The pounding heart refers to increased cardiac performance that would meet the metabolic demands of increased striate muscle activity, but is metabolically inappropriate in an individual not experiencing any increased metabolic load (Brener, 1987; Obrist, 1981; Sherwood, Allen, Obrist, & Langer, 1986). Optimal activity of the eccrine sweat glands has been proposed to aid in manipulation by increasing friction, to increase tactile discrimination, and to make it more difficult to tear the skin, but is inappropriate when excessive and in the absence of hand-environment interactions (Edelberg, 1972). I shall concentrate on cardiovascular reactivity, which has been the focus of my research (e.g., Pavloski, 1988).

The Control-System Analysis of Person-Environment Transactions: Intentional Behavior Motor Equivalence is a Helpfil Observation The problem of motor equivalence posed by Lashley (1930) provides a nice point of introduction to a control-system mode of analysis. Lashley viewed motor equivalence as a problem. He wondered what type of mechanism the nervous system embodies that allows it, on different occasions of the same behavior, to provide suitably different outputs in order to achieve the same behavioral result. That is, how can a consistent behavior be produced when that behavior is only partially determined by the outputs of the nervous system, and is also partially determined by outside influences that (a) are different on different occasions of the behavior's occurrence, (b) are not necessarily influenced by the outputs of the nervous system, and (c) may not even be represented in the nervous system? In other words, what type of mechanism must the nervous system embody so that, without knowing beforehand the particular time course and constellation of outside influences, the nervous system produces the necessary, properly timed, outputs that combine with those outside influences to produce a given behavior and to produce it reliably? The phenomenon of motor equivalence poses a significant theoretical problem, one that has been recognized by cognitive psychologists (Bruner & Bruner, 1968, pp. 251-255), by behaviorists (Brunswick, 1952), and by psychologists studying motor behavior (Turvey, 1977, pp. 2 15 -216). The phenomenon of motor equivalence is clearly evident in our experiences of what might be called "high-level" behaviors. Consider what occurs

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when we say that a woman leads or facilitates a group discussion. The behavior in this case is the discussion. Clearly, the behavior is the result of the actions of all of the participants, and not just those of the leader. Yet, a "good" leader or facilitator reliably sees to it that a good discussion occurs. Furthermore, she does so in very different ways on different occasions, and consistently good discussions result. The same phenomenon occurs in what might be called "low-order" behaviors. Consider what occurs in creating and maintaining a particular position of a limb--an arm, say. The nervous system outputs volleys of motor neuron impulses that arrive at neuromuscular junctions. The volley of motor neuron impulses is the only thing that the nervous system can be sure will occur (see Milner, 1970, pp. 59-67). A given volley of impulses will result in a release of neurotransmitter that will change from occasion to occasion; a given amount of neurotransmitter will result in different amounts of change in muscle tension from occasion to occasion that depend on the initial length and state of fatigue of the muscle fibers; and the change in position of the limb will vary from occasion to occasion with a given change in tension, depending on the actions of other muscles and on acceleratory forces that depend on dynamic changes in posture (McMahon, 1984). Despite the existence of influences that are uncontrolled by the nervous system, some of which are not even represented in the nervous system, it is clearly possible and in fact trivially easy to produce a certain limb position reliably. Finally, consider the behavior of keeping a motor vehicle centered on a road lane. Even if we assume that it is no problem to produce a given motion of the steering wheel, the effects of this motion combine with the influences of roadbed tilt, of acceleratory forces that change with the motion of the vehicle, of wind forces, and of forces produced by imperfections in the road to determine the actual position of the vehicle. It is commonplace to observe a driver continuously moving the steering wheel from side to side in an apparently random fashion that produces just those effects necessary, in combination with the other influences, to keep the car centered in the appropriate lane. Those who would "explain" these behaviors by appealing to operant conditioning, to maturation, to skill-learning, or to schema-driven outputs that are modified on the basis of existing inputs should become aware of the physics of behavior. Such an awareness provides a sobering perspective on the nature of such "explanations." An awareness of the mechanics of even the simplest movements (e.g., Hobbie, 1978, pp. 252-255; Turvey, 1977) reveals that such statements merely beg the question of the mechanism that produces the behavior. Physics describes the environment of the nervous

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system. It shows us how the physical properties of the components of an organism and its surrounds are described as functions of time, and it explains how physical quantities affect one another. Explaining behavior means understanding what physical quantities must affect and be affected by the nervous system, and the forms of the relationships involved, so that behavior is produced. Motor equivalence actually makes this understanding easier, since it indicates that the mechanism involved must reliably produce certain effects in this physical world, even though at any moment in time those effects are only partially the result of the outputs of the nervous system. The observation of motor equivalence thereby puts stringent constraints on the type of theoretical mechanism or model deserving serious consideration. Control theory suggests that a single mechanism underlies all of the above examples, as well as countless other instances of motor equivalence. This mechanism is called a control system. The mechanism comprises one or more negative-feedback loops, and operates as follows.

The Continuous Realization of Intention: Near-Zero Error as the Hallmark of Control-System Operation Figure 1 shows the essential elements of a negative-feedback control system and its immediate environment. Two classes of time-dependent quantities are shown in this diagram. The physical quantities of the environment are called variables, while those within the system are called signals. Both are, in general, continuous functions of time. Beginning at the input end of the system, physical energy is transmitted from the controlled variable to the control system according to physical laws, and is transduced by an input function into a perceptual signal. The timedependent difference between the perceptual signal and a reference signal, generated outside the feedback loop, is called error. An output function transduces the error signal into an oytput variable. We are now back in the system’s environment. The feedback function represents those physical properties of the environment that determine how the output variable affects the controlled variable, again as a function of time. The controlled variable is, in general, also affected by influences that are independent of the system. These influences together provide a disturbance, an independent variable that affects the controlled variable according to physical properties of the environment; this is depicted in Figure 1 as the disturbance function, The system shown cannot affect these influences, and they are not even represented within the simple control system depicted here (i.e., there is no mental, neural, or other representation of them within the system).

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Figure 1. General model of a negative-feedback control system and its irnmediate environment. Reprinted with permission of the publisher (The Society for Physiological Research, Copyright 1989) from "A control system approach to cardiovascular reactivity: Behavioral models that behave," by R. Pavloski, in press, Psychophysiology; adapted with permission from William T. Powers, Behavior: The Control of Perception (New York Aldine-DeGruyter). Copyright 0 1973 by William T. Powers. @

It is difficult to grasp intuitively how a control system operates, because our intuition readily neglects physical time. Physics tells us that it takes time for any physical quantity to affect a second quantity, and this means that physical time must be properly included in any adequate description of the

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system’s operation. A differential equation is required to describe the timedependent cause-effect relationship between any two physical quantities (variables and signals) whose values are continuous functions of time. An intuitive grasp is also likely to be based on a sequential description of the system’s operation. But a sequential description cannot be correct, since both members of any given pair of quantities in the loop are continuously exerting influences on each other. In pictorial terms, the arrows in Figure 1 depict physical relationships that are always in effect--for example, the effect of the value of the controlled variable on the output variable is not suspended temporarily while the value of the output exerts an effect on the controlled variable. The output variable continues influencing the controlled variable at the same time as the controlled variable is influencing the output. This is not mysterious as some believe (Bandura, 1983); the value of the controlled variable at time t is a function of the value of the output variable, and the reverse is also true. This simply shows that a simultaneous pair of equations is required to describe the interactions between the system and its environment. We can choose two quantities in the loop (the output and controlled variables, say), and write 1 equation that describes the output as a function of the controlled variable, and a second that describes the controlled variable as a function of the output. These equations can then be solved for either the controlled variable or the output variable as a function of time. Certain choices for the functions within the system will keep the values of the time-dependent perceptual and reference signals approximately equal over time. A system with such functions produces a continuously varying output variable whose continuously varying effects on the controlled variable almost exactly cancel any outside influences on the controlled variable that would cause the perceptual and reference signals to differ in value. Negativefeedback control systems embody such functions and thereby maintain the error signal near zero. If we call the reference level (value of the reference signal) the intention of the control system, then it follows that by cancelling the effects of influences on the controlled variable that would produce deviations between the values of the perceptual and reference signals, the system continually realizes its intention. The intention will in general vary over time, and its variation can result in the production of behavior. For example, changes in the value of a certain reference signal over time can have effects on a controlled variable whose value indexes the changing length of a muscle so that an object is picked up. Changes in the value of another reference

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signal can have effects on another controlled variable whose value indexes progress in a group discussion.

Hierarchies of Control Systems-A view of Human Performance I have called the maintenance of error near zero a hallmark of controlsystem operation. It adds to the view of intentional behavior the notion that those intentions are satisfied in a quantitative sense over time. A hallmark of human behavior is that many intentions are being satisfied simultaneously, some of them by systems operating on one and the same time scale, and others by systems operating at different time scales. Consider a subject who is complying with an experimenter’s request to maintain a cursor in the center of a video screen by manipulating the position of a stick connected to a potentiometer while a computer simultaneously influences the position of the cursor with a disturbance that varies randomly over time. A great many intentions can be discerned here. The subject is intentionally maintaining the position of the cursor at a reference level by changing the position of the stick in just the manner required to cancel the effects of the unseen and unpredictable disturbance. Intentions operating on a faster time scale can be seen by asking how the cursor-position control system keeps the cursor in the center of the screen. The subject does this by moving a stick. Might not the position of the stick be a controlled variable, with its reference signal provided by the output of the cursor-position control system? And how does the stick control system achieve a given stick position--are muscle tensions controlled variables with reference signals provided by the stick control system? Clearly, the muscle-tension control systems must operate on a time scale faster than the stick control system, which operates on a scale faster than the cursor-position control system. If this were not so, then non-zero error in stick position, for example, would be counteracted not only by the stick system but also by the cursor control system; the reference to the stick control system would be modified even though its operation was faultless, and the hierarchy would be a dynamically unstable system, creating its own errors. More slowly operating systems can be found by asking why the subject is controlling the position of the cursor. Where does the reference signal for cursor-position control originate? The subject is controlling the position of the cursor because his professor asked him to. The cursor-position control system receives a reference signal from a higher order system, or perhaps a reference signal that is a weighted combination of the outputs from many higher order systems. These higher order systems control their input signals

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by setting values for reference signals such as the one to the cursor position system. This process of asking, how and why, can be used to move up and down a hierarchy of control systems, as Powers (1973b) has done. It results in the view of a human being as continually satisfying intentions at many levels by controlling variables on different time scales related to different levels of intention.

Physiological Stress as the Result of Thwarted Intentions The Control-System-Error Theory of Cardiovascular Reactivity A proposal for a connection between the operation of human control systems and physiological activity follows easily once the basic principles of control-system operation are understood. Consider the problem of explaining how the activity of the heart is related to the production of behavior. We have evidence that cardiac performance is (appropriately) integrated with the metabolic demands of behavior under a variety of experimental conditions, and is (inappropriately) greater than metabolic demands warrant under others (Brener, 1987; Obrist, 1981; Sherwood et al., 1986). How might the production of behavior be related to both appropriately and inappropriately enhanced cardiac activity? The control-system-error theory of cardiovascular reactivity states that error in the operation of behavioral control systems is the modulator of cardiac performance in both types of situation. In the case of metabolicallyappropriate increases, we might suppose that error departs significantly from the zero value that it would have if control were perfect, and that it does so because the physical load placed on the muscles that form the output function of the control system is near the capacity of those muscles. Since we are assuming that we have convincing evidence that the behavior is produced by the operation of a control system, and since skeletal muscles form the output functions of such systems, we expect muscular effort to increase as the system tries to reduce the error. We know that cardiac performance increases in such situations (e.g., Brener, 1987), but are in need of a mechanism to link behavior to the increased cardiac performance. From the perspective provided by control theory, we are led to hypothesize that it is the error in the operation of the control system that signals the increased cardiac performance that we observe. Now consider another situation in which error departs significantly from zero, and in which the error signal is not converted into muscular efforts of proportional magnitude. This might occur for a variety of reasons. For

Stress of Thwarted Intentions

223

instance, it will occur if the rate of change of environmental influences on the controlled variable exceeds the speed of response of the control system (see Figure 2). In such a situation error will be changing faster than the system can respond. Other reasons are explored below.

Initial Tests of the Control System Error Theory My students and I have carried out several initial tests of the control system error theory. The results of completed experiments are summarized here. Rotated I/isual Image Task. We have carried out 1 experiment using this procedure (Pavloski, 1988). Subjects attempt to trace a line drawing on a sheet of paper while viewing a video image of the drawing surface (showing the sheet of paper with the drawing and the subject’s hand holding a pen). Control- system error can be increased from normal values near zero by rotating this visual image through an angle about the central axis of the lens of the video camera. A group of 27 subjects traced line drawings under 7 different angles of rotation, with the expectation that at least some of these would lead to large error values. Based on previous research using a similar procedure (Smith & Smith, 1962), it was expected that there would be large individual differences in control-system-error values that would permit an initial between-subjects test of the control-system-error hypothesis. Since we had available a group of subjects participating in a study of the relationship of cardiorespiratory fitness to heart rate (HR) reactivity (Arbitell & Pavloski, 1987), we were able to determine the relationship of both fitness and error to HR reactivity. Wide ranges of fitness and HR reactivity were obtained. Maximum oxygen consumption (VO, Max) (treadmill test) ranged from 35.5 ml/min/kg (poor) to 62.3 ml/min/kg (very fit), and HR reactivity ranged from 2 to 58 beats per minute. The rotation of the image was associated with increased error [F(6,138) = 16.99, p < .OOOS] and with increases in HR from baseline values [F(6,138) =7.19, p < .0005]. Multiple regression analysis with error, VO, Max and their interaction entered in that order revealed a significant between-subjects correlation between error and HR reactivity [r=.54, F(1,22)=9.20,pc.007]. VO, Max did not account for a significant proportion of the variance in HR reactivity, and was unrelated to error @>.05). Cursor-Position Control Tusk. Two subsequent experiments (Pavloski, 1988) employed a computer-controlled task in which a subject is asked to keep a cursor at a particular position on a video display. The position of the cursor is determined by the time-dependent values of two variables: the position of a handle that can be moved in 1 plane by the subject, and a

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Raymond P. Pavloski

Figure 2. (to the right) Plots of slow- (a), medium- (b), and fast(c and d) rate-of-change disturbance functions shown together with the representative performances of a subject instructed to keep the cursor at the center of the screen. The subject moves the handle in such a way as to counteract the effect of the disturbance to cursor position. Both disturbance function and handle position are expressed in terms of their independent effects on cursor position. Error is the deviation of the cursor from the center of the screen. If the disturbance function and handle position were symmetric, error would remain at zero. When the disturbance’s rate of change is fast (plot c), error is so large that it must be shown separately (plot d) for clarity of presentation.

disturbance function produced by smoothing the output of a random number generator over time. Performance in this task has been simulated with great accuracy by control- system models (Marken, 1986; Powers, 1978). It was expected that increasing the rate of change of disturbance would increase control-system error and, by hypothesis, H R reactivity. In two experiments employing a total of 60 subjects, each subject was exposed to 5 final test trials at each of 3 rates of change of disturbance (slow, medium, fast). Each of 3 groups of subjects received 0, 1, or 2 15-minute training sessions prior to the test session. The slope and intercept of the regression line relating handle position to disturbance value for the test-session trials showed that subjects controlled cursor position as requested during the slow- and medium-rate-of-change trials, but may not have done so for the fast trials. Training had no significant effects on performance or reactivity. The rate of change of disturbance had a highly significant effect (for both experiments combined) on error, [F(2,114)=650.7, pO 0 if 050.

Because active contraction can lower the threshold, (8) is replaced by

F = g([L -(r -C)]+)

(9)

or equivalently

where C measures the amount of contraction. Note that active contraction does not result in muscle shortening if another force--such as that developed by an opponent muscle--counteracts the contractive force. For the subsequent discussion it is very important to remember that muscles often actively contract without changing their length, as measured from origin to insertion. Suppose that two opponent muscles exert forces FI and F2 from opposite sides of a rotating limb segment (Figure 9) and that the outputs from antagonistic PPC stages in a VITE circuit (Figure 2) are sent to a stage capable of directly adjusting C, and C2 in the following equations for F1 and F2: (11) FI = g([LI -r, +c11+)

where the ri are constant thresholds. If initially F, = F2, then reducing C, and increasing C2 by AC creates a force imbalance such that F2

'F1

275

VITE and FLETE: Neural Modules

Figure 9. Equilibrium joint angle depends on the balance of forces developed by opponent muscles. Each muscle’s force depends on its length L , its resting length ri,and its active contractile state, Ci.

Rotation occurs until

[LI +AL

-rI +CI -AC]+

=

[L2 -M

-r2 +C2

+AC]+

(14)

and a force balance is once again restored. In vivo, the alpha-motoneurons transiently activate contractile fibers from a finite population of fibers. As in equations (11) and (12), let Ci be the degree of contraction, and let Mi be the output signal of the motoneuron pool in channel i, i = 1,2. Then a simple law for change in contraction in a finite population is:

This says that M iincreases Ci by activating unactivated fibers, which number (Bi-Ci),from a population of size Bi,and that contraction spontaneously decays at rate 6.

276

Daniel Bullock and Stephen Grossberg

However, it is known that contracted fibers yield, or decontract, when the force acting to stretch them is sufficiently large. Thus (15) is replaced by

where

o< pi < l a

In equation (16), when the force exceeds the threshold level, TF,it acts to reduce contraction. Inequality (17) acknowledges that any active contraction caused by neural input Mi is slow relative to the fast decontractive effect of suprathreshold forces. The simple model (16) provides a new perspective for understanding the functional role of a widely observed, but imperfectly understood, physiological law. At equilibrium, $Ci = 0 in (16), so that the equilibrium value of Ci is

Given (18), how is it possible to generate and sustain forces much larger than rF at a fired muscle length? Because

F~ = &Li

-ri +ci]+)

(19)

in (11) and (12), where ri is a constant, greater force at a fixed length Li can be generated only by increasing Ci . However, if pi is constant and less than 1, then (18) shows that the negative force feedback will cancel the effects of increasing Mi, and Ciwill not be able to increase, at least if a near linear or faster-than-linear g ( o ) is assumed. To overcome this deficiency within the constraints imposed by equation (16), let the contraction rate parameter pi and the number of sites Bi increase with Mi. Such a relation is well documented empirically and is often called "Henneman's size principle" (Henneman, 1957; 1985): As total excitatory input to the alpha motoneuron population grows, it recruits additional, progressively larger motoneurons which have faster

MTE and FLETE: Neural Modules

277

conducting axons, whose collaterals reach many more motor fibers and whose potentials evoke more rapid muscle contractions. Prior treatments of the function of the size principle have focused on either the contraction-time effects or the force-magnitude effects seemingly implied by activation of cells that project to larger numbers of motor fibers. The present analysis suggests that both aspects of the size principle help realize a large force range at any fixed muscle length. In particular, merely making Bi increase with Mi is not enough. The contraction rate parameter pi also needs to increase with Mi . Thus contractile rate is as critical a component of the system for yielding compensation as the more frequently cited reflex circuits (Houk & Rymer, 1981). Assuming that g(o) is slightly faster than linear, e.g.,

then the system

-ri +ci]+>a

Fi = ( [ L ~

generates a family of curves like those shown in Figure 10 where equilibrium force is plotted as a function of muscle length for four different values of Mi with Pi and Bi constant. Data from experiments in which equilibrium muscle tension (in areflexive muscle) was measured as a function of length and frequency of electrical stimulation have the same form with one difference: the higher stimulation rates lead to slightly larger slopes and higher asymptotic tensions (Rack & Westbury, 1969). From the above analysis, both the slope change and the raised peak tension can be attributed to the size principle: higher stimulation rates evoke faster-contracting fibers, which leads to a higher equilibrium Ci and Fi, and a higher multiplier of Li .

10. Size Principle With Co-Contraction Poses A Threat To Invariant Position Coding The above analysis suggests that the size principle plays a major role in generating a wide range of forces at each fixed muscle length. This

278

Daniel Bullock and Stephen Grossberg

f

SHIFT AS C i INCREASES

Figure 10. In first approximation, the effect of increased muscle stimulation is a shift in the threshold length for force development.

property is important both during high co-contraction conditions when the arm resists changes in position due to variable external forces (e.g., Humphrey & Reed, 1983), and in carrying out planned arm movements wherein the arm undergoes a continuous change of position. In the latter situation, the ability to generate a wide range of forces at each position of a movement trajectory is needed to enable the arm to accurately track the PPC commands that are continuously read-out at variable rates by central circuits. During trajectory formation, a wide range is also needed to compensate for variable forces due either to external perturbations of the arm or to variable arm inertias caused by variable velocities or trajectories of variable shape (e.g., Lestienne, 1979). However, we now show that the size principle, while extending the force range, can also pose a threat to invariant position coding. In particular, we describe an example that shows how the size principle could prevent any simple PPC code from being realized by the arm, such as one based upon adjusting the relative sizes of PPC commands to agonistantagonist muscle groups. We then present the additional neural circuit needed to negate this threat.

K'TE and FLETE: Neural Modules

279

As illustration of the invariance problem, suppose that a limb segment is initially at equilibrium, such that FI = F2

.

where CI(AI)denotes the equilibrium value of Cl when MI = f(A,) in (16). Now suppose that we attempt to hold the limb at the same position, but more rigidly, by increasing the level of muscle contraction on both sides of the joint. The simplest way to do this is by adding a constant, P, to each motoneuron input. Thus M I = f(A,+P) and M2. = f(A2+P). However, in a system that obeys the size principle, equation (23) implies

for arbitrary values of P and the same initial values of L, only if A , = A2 (see explanation in Figure 11). In other words, sending the same cocontractive input P to both motoneuron pools in an attempt to further stabilize current limb position could instead cause a limb rotation. This is a prime example of a failure of factorization of length and tension: an attempt to change only tension inadvertently changes length. Because the motor cortex appears to follow the simplest strategy (adding a constant P ; see section 14), some mechanism must exist to prevent unwanted limb rotations. In the light of this problem, many researchers have proposed that Ciand Li should interact multiplicatively to produce force. Though this would reduce the problem, the proposal amounts to a claim that the primary effect of changing Mi is a change in the stiffness (AF/AL) of areflexive (deafferented) muscle. However, experimental data show that stiffness changes relatively little as Mi changes; the primary effect of changing Miis a change in the threshold length for force development, as suggested in Equation (9) and Figure 10 (Feldman, 1986; Rack & Westbury, 1969).

280

Daniel Bullock and Stephen Grossberg

'Figure 11. When opponent motoneuron populations obey the size princiMOTONEURON POOL (A) ACTIVATION LEVEL ple, a co-contractive sigBIG CELL nal P sent in parallel to ZONE both populations can RECRUITMENT THRESHOLD disrupt the joint position SMALL CELL code. (A) Signals A, and ZONE A1 A, supraliminally activate only small cells in opposing channels and their relative sizes determine BIG CELL the balance of muscular ZONE forces and thus the equiRECRUITMENT THRESHOLD librium joint position. (B) SMALL CELL With A, > A,, co-conZONE tractive signal P causes *1 P the total input A, + P to exceed the big cell threshold while input A, + P remains below the big cell threshold. Thus part of the signal P is subjected to greater amplification in channel 1 than in channel 2. Unless compensated, this would create a new balance of forces and cause an unwanted joint rotation.

11. Compensatory Properties Of Renshaw-Ia Pathway An alternative solution may be sought in known neural circuits. Is there any neural site that is sensitive to the amplification factor (Figure 11) introduced by progressive recruitment within an alpha-motoneuron population? The alpha-gamma system cannot provide the type of compensation desired because gamma motoneurons are not sensitive to the amplification. However, inspection of Figure 8 reveals the Renshaw cells as sole neural targets of a-MNaxon collaterals, and that a-MN cells receive feedback signals from Renshaw cells. Thus Renshaw cells are well situated to measure and modify the final output of the motor channel. Moreover, it is known that collaterals of larger, later recruited motoneurons make many more synaptic contacts with Renshaw cells than smaller, earlier recruited motoneurons (Cullheim and Kellerth, 1978). These properties are consistent with the hypothesis that Renshaw cells

VlTE and FLETE: Neural Modules

281

play the required compensatory role. We now present computer simulations of the system in Figure 8 which show how model Renshaw cells can compensate for position code distortions that would otherwise be generated when co-contraction is combined with the size principle of motoneuron recruitment. This property depends upon how,the feedback pathways in the circuit are organized into opponent, or antagonistic, muscle channels.

Table 1 Major FLETE Model Variables

Descending reciprocal input to alpha motoneuron and Ia interneuron population i, i = 1,2 Descending co-contractive input to both alpha motoneuron populations Force developed by muscle i, i = 1,2 Contractile state of muscle i, i = 1,2 Origin-to-insertion length of muscle i, i = 1,2 Alpha-MN population activity, i = 1,2 Renshaw population activity, i = 1,2 IaIN population activity, i = 1,2 Composite signal from spindle organs, i = 1,2

The compensation occurs as follows. Opponent Renshaw populations R, and R, measure the output of their respective alpha-motoneuron populations, a-MN,, and a-MN,, and compare those outputs via mutually inhibitory signals (Figure 8). A consensus emerges regarding which MN channel to inhibit via Renshaw feedback, and which to disinhibit via feedback from the Ia interneuron (IaIN) pathway. Suppose that a cocontractive input, P, to a-MN, and a-MN2 occurs when input A, exceeds Suppose that the activity of a-MN, is consequently multiplied by a larger factor than that of a-MN, due to the size principle (Figure 11). Then R, also becomes much more active due to the size-correlated synaptic weighting on a-MN, axon collaterals to R,. Because the opposing R, has not experienced as large an input increment, R, will transiently become more active than R , by an amount that scales with the

A,.

282

Daniel Bullock and Stephen Grossberg

diflerence between the a-MN output increments due to the change in P. Thus this system calculates an error due to unequal amplifications of cocontractive inputs. This error signal then directly inhibits a-MN1 and, by inhibiting laIN1, indirectly activates a-MN,. Both actions work to zero the error without negating either the shared increment in a-MNi activation required to increase joint stiffness, or the joint angle setting determined by the difference in descending inputs, exclusive of P, to opponent a-MN and IaIN populations. Readers not interested in the details of the simulations should skip ahead to the Results subheading. Others may consult Table 1 for definitions relevant to equations (25)-(37). As in Figure 9, we assumed a rotary joint affected by two opponent muscles, each of which is inserted in the moving segment one unit from the axis of rotation. The distance from muscle origin to the axis of rotation was 20 units, and the midpoint of the limb's 180" excursion was stipulated to be at joint angle 0 = 0". Origin-to-insertion muscle lengths, L , were thus functions of 0:

In the simulations reported here, we were interested only in large-scale effects on equilibrium joint angle. Thus we ignored moment-arm and force-velocity effects and chose the simple force law

Fi = k[Li -ri +CJ+ where k = .5, ri = 20.9 and i = 1,2. Limb dynamics were governed by equation

zd2G0 = -m1 (F1 -F2 - n dx0 ) where rn represents mass and n is a damping coefficient. Cbntradle state Ciwas governed by

U T E and FLETE: Neural Modules with 6 = 1, and ,?I

= 0. Variables pi and

pi = .05

+ .02(Ai

283

Biwere defined by:

+P)

(29)

Both variables grow as a function of total descending input Ai+P to the MN pools in channel i, but pi grows with a smaller slope. Equations (16), (29), and (30) use parameters pi and Bi to approximate a-MN recruitment effects that occur in viva Which a-MNs exceed threshold may depend not only on the total descending drive, Ai+P, as in (29) and (30), but also on inhibitory inputs from IaINs and Renshaw cells as well as on inputs arising from sensory organs in the muscle. In this lumped model, sensory feedback was omitted to isolate the potential compensatory effect of the Renshaw pathway. The lumped model does, however, include the critical assumptions that Renshaw populations associated with opponent muscles are mutually inhibitory, and that each Renshaw populations’s activity be sensitive to the amplification factor introduced by recruitment of larger motoneurons. Such sensitivity requires that growth in a Renshaw population’s activity not saturate prior to saturation of growth in a-MN population activity, and that the input to the Renshaw population scale with the net amplification due to recruitment. As noted above, there is evidence that this scaling is effected in vivo by increasing the synaptic weighting factor associated with Renshaw-directed axon collaterals from larger a-MNs. In our lumped model, this effect was absorbed into a single variable coefficient, zi, which was made a function of recruitment extent, as approximated by A,+P. The lumped equations for opponent Renshaw populations were thus

$ R, = (lB1 -Rl)z1Ml

-R1(1 +R2)

with 1 = 5 and

zi = .2

+ .8 (Ai+P)

(33)

284

Daniel Bullock and Stephen Grossberg

for i = 1,2. Parameter Bi in (31) and (32) approximates the property that the Renshaw population has a continuum of recruitment thresholds similar to the a-MN population, and that the number of suprathreshold Renshaw sites increases as more a-MNs are recruited (with increasing Ai+P). We modeled the opponent alpha-motoneuron populations via

where 9 = .2, x = 0, and 52 = 0 or 1. The inhibitory Zi inputs represent signals from the IaINs (see Figure 8) and the excitatory El inputs represent signals from the muscle spindles. We assumed that IaINs were not subject to any recruitment effects. Thus their dynamics were modeled without a direct dependence on BP and without a co-activating input P:

3

I = @(lo -Z2)(A2 +xE2) -Z2(1 2

+m, +I,)

(37)

Composite spindle feedback signals E, and E2 (in Equations 3437) were gated off in our simulations by setting x = 0. This corresponds to destroying the stretch reflex via deafferentation, and it allowed us to test the ability of the Renshaw-Ia-MN feedback circuit to achieve position code invariance. The Renshaw feedback signals were gated on or off, respectively, by setting parameter C2 (in Equations 34-37) equal to 1 or 0.

Results Table 2 shows representative numerical results. Variables A l , A,, and P (see Equation 24) represent constant inputs and variables L,, F,, and 0 represent equilibrium values of dependent variables. Because L, and L, are complements and F, = F2 at equilibrium, L2 and F2 are omitted from the table. Because small length changes can imply large joint rotations, the most informative column in Table 2 is that showing

285

U T E and FLETE: Neural Modules

0,the equilibrium joint angle. When Renshaw feedback was absent (Q = 0), changing P while A , and A, remained fixed led to large undesirable rotations (10" in block 1, 22" in block 3). However when Renshaw feedback was present (Q = l),rotations due to changing P with fixed A, and A, were extremely small ( < l o in block 2 and 0 THEN M = M

-

+

.01

"PREFERENCE LOOP*v:GOTO 360

Appendix B Derivation of the conditions for observing the Giffen Effect Let: m = meat consumed; b = bread consumed; Cm = calories per unit of meat; c b = calories per unit of bread; Pm = price per unit of meat; Pb = price per unit of bread; I = income available for food; C = caloric requirement; 1:

Total calories consumed

2

Total cost, fixed at budget

3:

from 2:

4:

Substitute for m into 1: and expand:

5:

C C C = I 3 -b(Pb)L Pm Pm Collect terms

6:

Results:

+ b(Cb)

The Giffen Effect

547

The Giffen Effect occurs when the following conditions hold:

I(Cm)/(Pm) is the number of calories obtained if the whole budget is spent on meat. Condition (a) states that this number is less than or equal’to the caloric requirement C. (b)

cb

’pb(cm)/(p,),

Or

cb/pb > cm/pm.

Condition (b) states that the calories per unit price obtained from bread are greater than the calories per unit price obtained from meat. Derived by William Powers

This Page Intentionally Left Blank

549

AUTHOR INDEX

Accornero, N. 264, 292 Ach, N. 53-55, 57, 400, 405 Ackerman, P.L. 406, 506, 511 Acuna, C. 73, 105, 143, 164 Adler, S. 507, 514 Adolph, E.F. 455, 463, 464 Agarwal, G.C. 319, 332 Ahern, G.L. 112, 155 Aitinik, J.W. 112, 155 Albus, J. 409, 429 Alho, K. 203,207, 209, 210 Allen, A. 365, 366, 368 Allen, M.T. 216, 232 Allen, R.G.D. 532, 543 Alstermark, B. 97, 101, 102 Andersen, R.A. 75, 105, 150, 164, 184, 192 Anderson, M.E. 265-269, 292, 295 Anderson, J.R. 395, 405 Andrasik, F. 487, 491 Anger, C. 187, 192, Anliker, J. 462, 464 Ansell, S.D. 462, 464 Antunes, L. 76, 102 Apostle, H.G. 151, 155 Appelbaum, K.A. 487, 491 Apter, M.J. 361, 362, 364, 365, 367 Arbib, M. 409, 429 Arbitell, M. 223, 230 Archabold, G.C. 534, 543 Arezzo, J.C. 198, 214 Arlinger, S. 202, 211 Amolds, D.E. 112, 155 Arthur, D.L. 207, 211 Asano, T. 542, 544 Asanuma, H. 103, 185, 190 Aschoff, J.C. 119, 155 Ashby, W.R. 16, 18

Ashford, S.J. 499, 511 Atkeson, C.G. 260, 295 Atkinson, J.W. 357, 358, 361, 363, 367, 368 Austin, J.T. 249, 503, 511, 544 Bain, A. 43, 57 Bak, M.J. 176, 192 Bak, C. 211 Baker, F.H. 232, 267, 296 B a h t , R. 143, 155 Ball, G. 44, 175, 470, 475, 486, 491 Bancaud, J. 115, 163, 166 Banchard, E.B. 491 Bandura, A. 220, 230, 460, 461, 464, 501, 508, 511 Barbas, H. 76, 102 Barrett, G.V. 502, 511 Bastian, C. 49, 57 Batuev, AS. 186, 187, 189 Bauer, H. 123, 155 Baum,, W.M. 231, 460, 464 Beatty, J. 200, 213, 464 Beaubaton, D. 269, 297 Bechinger, D. 148, 155 Becker, W. 118, 146, 155 Beckmann, J. 394, 397, 405-407, 513 Beggs, W.D.A. 264, 292 Bell, C. 42, 57, 458 Bem, D.J. 365, 366, 368 Benecke, R. 131, 155 Benson, D.F. 145, 166 Benson, D.A. 77, 105 Bentley, A.F. 450, 461, 465 Bergen, A. van, 395, 405 Berger, P.L. 350, 351 Bergman, G. 7, 18

550

Author index

Beringer, K. 115, 155 Berkinblit, M.B. 290, 292 Berlyne, D. 388, 405 Bernard, C. 14, 18 Bernstein, N. 130, 155 Bertalanffy, L. V. 453, 464 Bertrand, 0. 111, 165 Bianchetti, M. 187, 191 Bioulac, B. 184, 185, 189, 193 Birch, D. 357, 363, 367, 368 Bizzi, E. 264, 292 Bjorklund, A. 149, 164 Black, A.H. 196, 299, 306, 461, 464 Blanchard, K. 487, 520, 529 Blanchette, G. 170, 193 Blaney, P.H. 509, 511 Blomberg, A.P. 205, 212 Bobko, P. 503, 511 Boch, R. 63, 68-70, 72 Bock, M. 397, 405 Boeijinga, P. 112, 155 Bonis, A. 166 Bonnet, M. 186, 189 Bordas-Ferrer, M. 166 Boring, E.G. 48, 57 Boschert, J. 116, 118, 155-157 Botterell, E.H. 170, 190 Boulding, K. 532, 543 Bourbon, W.T. 235, 236, 246, 247, 249 Bourbonnais, D. 170, 193 Brain, W.R. 143, 150, 156 Bravo-Marques, J.M. 76, 102 Breitmeyer, B. 67, 70, 72 Brener, J. 215, 216, 222, 223, 230, 462, 464 Brenner, D. 114, 166 Brickett, P. 116, 118, 157 Brinkman, C. 126, 156 Brion, S. 115, 156 Broadbent, D.E. 206, 211 Brodal, A. 172, 189 Brody, B.A. 138, 156

Brooks, J. 352, 541, 543 Brown, E.R. 419, 430 Brown, S.H. 291, 293 Brozek, J. 45, 57 Bruce, C.J. 69, 71, 72, 119, 156, 184, 187-189 Briicke, T. 165 Bruner, J.S. 216, 230 Bruner, B.M. 216, 230 Brunner, R.J. 118, 156 Brunswick, E. 216, 230 Buchtel, H.A. 69, 73, 171, 191 Buchwald, N.A. 123, 164, 267, 296 Buckley, W. 454, 464, 467 Budingen, H.J. 264, 293 Bullock, D. 13, 19, 253-255, 263-266, 268, 272, 287, 291-293 Bum, J. 142, 162 Burde, R.M. 119, 158 Busby, L. 123, 161, 182, 192 Bushnell, M.C. 68, 69, 72, 73, 184, 189 Buss, A.H. 508, 512 Butterfield, E.C. 395, 405 Caminiti, R. 76, 84, 85, 89, 93, 95, 102-104, 264, 294 Campbell, K.B. 198, 213 Campbel1,D.T. 16, 19 Campion, M.A. 495, 497, 498, 511 Canning, L.R. 165 Cannon, W.B. 13, 19 Capaday, C. 180, 189 Carpenter, G.A. 47, 57, 72, 253, 287, 292, 293 Carver, C.S. 363, 368, 463, 464, 505, 507-509, 511, 512 Casey, K.L. 176, 193 Caspers, H. 109, 156 Castro-Caldas 76, 102 3, 7, 19, 460, 464

Author Index Cavender, J.W. 501, 514 Celesia, G.G. 198, 211 Cervone, D. 508, 511 Chapin, J.K. 176, 189 Chaplin, S.B. 165 Chapman, C.E. 175, 176, 182, 190, 191, 292 Chapple, W. 264, 292 Charng, H. 508, 514 Cheney, P.D. 181, 190 Cheyne, D. 114, 116, 120, 156, 163 Chi, M.H. 377, 379, 506, 512 Chong, E. 236, 249 Christie, B. 112, 158 Clark, R.K. 20, 235, 250, 409, 430 Cohen, D.A.D. 72, 84, 104, 211, 214, 297 Collins, R.L. 20, 494, 513 Commenges, D. 187, 193 Conway, C.G. 39, 57, 341, 343, 344, 347, 352 Cook, T.D. 343, 352, 505 Cooke, J.D. 180, 189,264,269,271, 291, 293, 296 Coren, S. 16, 19 Costa, L.D. 200, 213 Cott, A. 461, 464 Coulter, J.D. 176, 190 Crammond, D.J. 169, 185, 186, 190, 192 Creutzfeldt, 0. 109, 156 Cronbach, L.J. 340, 341, 351 Crowne, D.P. 112, 156 Crutcher, M.D. 89, 90, 102, 103 Cullheim, S. 280, 286, 293 Cummings, L.L. 499, 511, 514 Curtin, T.D. 341, 348, 351, 352 Daft, R.L. 506, 512 Davis, H. 200, 211 Davis, W.J. 409, 429 Davisson, W.I. 243, 249 Day, B.D. 131, 155 Deci, E.L. 508, 512

551

Deecke, L. 107, 109, 110, 114, 116-118, 120, 122, 123, 127, 128, 132, 133,l 3 6 , 138, 140, 141, 146, 147, 155-158, 160-167 DeGood, D.E. 487, 491 DeLong, M.R. 267, 296 Delprato, D.J. 449, 453, 464, 467 Dembroski, T.M. 228, 230 Denenberg, V.H. 453, 464 Dennis, I. 197, 200, 213, 449 Denny-Brown 170, 171, 190 409, 430 Dewey, J. 6, 7, 19, 450, 461, 465 Dick, J.P.R. 131, 155 Dickens, A.M. 112, 166 Diekmann, V. 111, 112, 132, 136, 139, 150, 157, 162 DiGangi, M.L. 341, 344, 347, 352 Dolce, G. 112, 157 Don, M. 25, 198, 199, 214, 307, 309, 342, 361, 439-441, 474, 477, 478, 488, 526 Donald, M.W. 169, 207, 211 Donchin, E. 196, 199, 211 Dorner, D. 388, 405 Doudet, D. 185, 193 Douglas, R.M. 69, 73, 171, 191 Doyle, J.C. 112, 158 Dubrovsky, B. 185, 190 Dworkin, B.R. 461, 465 Eccles, J.C. 59, 109, 158, 164, 165, 287, 293, 433, 443-445 Edelberg, R. 216, 230 Eichner, A. 542, 543 Einstein, A. 450, 451, 465 Elberling, C. 211 Elmasian, R. 200, 214 Engel, M. 118, 157

552

Author index

Engel, J.J. 41, 42, 57 Enoka, R.M. 286, 294 Erdelyi, M.H. 388, 405 Erez, M. 496, 497, 512, 513 Evarts, E.V. 178, 185, 187, 190, 263, 293, 294 Farr, M.J. 506, 512 Fatt, P. 287, 293 Favorov, 0. 185, 190 Feigl, H. 452, 465, 467 Feinstein, M.H. 232 Feldman, A.G. 279, 288, 290, 292, 293 Felix, D. 175, 190 Fenigstein, A. 507, 512 Ferro, J.M. 76, 102 Ferrell 430 Fetz, E.E. 181, 185, 190 Feuchtwanger, E. 148, 158 Fischer, B. 58, 63, 67-70, 72, 73, 160 Fishbein, S.S. 341, 352 Fisher, A. 529 Fisher, C.D. 494, 499, 503, 513, 514 Fisk, J.D. 271, 293 Fitts, P.M. 264, 293, 419, 429 Flynn, E.R. 207, 211 Ford, M.R. 486, 491 Ford, E.E. 248-250, 474, 479, 490, 491 Forster, A.M. 165 Forster, 0. 128, 158, 165, 167 Fortier, P.A. 96, 98-100, 102 Fox, J.M. 119, 158 Fox, P.T. 119, 158 Frank, P. 451, 465 Franzen, P. 138, 139, 167 Freeman, W. 149, 158 Freud, S. 299, 314, Freund, H.J. 72, 264, 293, 297 Frijda, N.H. 389, 405, 406 Fromm, C. 178, 185, 190, 263, 286, 293, 346

Fuchs, A.F. 66, 72 Fubon, 0.1. 290, 292 Funkenstein, H. 115, 164 Furukawa, K. 287, 291, 295 Fuster, J.M. 138, 145, 149, 158, 183, 187, 190 Gahery, Y. 267, 268, 294 Gaillard, A.W.K. 200, 203, 204, 211-213 Galambos, R. 198, 213 Galanter, E. 409, 430 Gale, A. 112, 158 Galin, D. 112, 158 Ganglberger, J.A. 123, 160 Garcia-Rill 185, 190 232 Gartenhaus, S. 215, 231 Geier, S. 166 Gemba, H. 110, 166 Genth, L. 143, 166 Georgescu-Roegen, N. 532, 543 Georgopoulos, A.P. 67, 73, 76, 82-94, 102-105, 143, 164, 264, 265, 269, 271, 289, 294, 297 Gerhart, K.D. 175, 193 Ghez, C. 176, 190, 264, 291, 294 Gibson, J.J. 18, 19 Gielen, C.C.A.M. 255, 264, 272, 294, 297 Giuffrida, R. 175, 191 Glaser, J. 506 Glasser, W. 488, 491, 541, 543 Glazer, R. 512 Glines, L.A. 434, 445 Godschalk, M. 77, 103 Gold, R. 76, 104 Goldberg, G. 115, 120, 123, 124, 132, 158, 171, 191 Goldberg, M.E. 68, 69, 72, 73, 119, 156, 184, 187-189

Author Index Goldenberg, G. 113, 115, 127, 128, 139,140,158,162,163,165,167 Goldiamond, I. 460, 465 Goldman-Rakic, P.S. 172, 173, 191 Goldstein, D.M. 442, 445, 481, 482, 484, 489-491 Goldstein, M.H. Jr. 77, 105, Goodale, M.A. 271, 293, 294 Goodman, D. 121, 159 Gordon, J. 264, 291, 294, 346, 433 Gorska, T. 97, 101 Goschke, T. 395, 405 Gottlieb, G.L. 319, 332 Graham, F.K. 200, 211 Green, J. 57, 152, 209, p14 Greenberg, J. 508, 514 Greenwald, A.G. 11, 19 Grignolo, A. 231 Grillner, S. 101, 103, 429 Groger, P. 127, 162 Gross, C. 160, 185, 193, 351 Grossberg, S. 13, 19, 253-255, 261, 263-266, 268, 269, 272, 287, 290, 291, 292-294 Grozinger, B. 116, 118, 146, 157, 158 Gruner, P. 112, 165 Guitton, D. 69, 73, 171, 191 Haase, J. 286, 293 Haaxma, R. 76, 103 Hackley, S.A. 207, 210, 211 Haddad, G.M. 66, 73 Haider, M. 123, 160 Hakansson, K. 140, 164 Hamalainen, M. 211 Handy, R. 450, 465 Hanges, P.J. 248, 249, 493, 498-500, 503, 513 Hann, D.H. 453, 467 Hansen, J.C. 207, 211, 214 Hansen, N.R. 340, 352 Harcourt, G.C. 534, 543

553

Hari, R. 197, 199,200,207,211, 212

Harnad, S. 3, 7, 19 Harrell, J.P. 228, 230 Harris, A. 459, 465 Harwood, E.C. 450, 465 Hasan, Z. 286, 294 Haslum, M.N. 112, 158 Hastrup, J.L. 231 Hayes, S.C. 343, 344, 352 Heath, R.G. 112, 163 Heider, F. 384, 385 Heimann, B. 498, 513 Heise, B. 116, 157, 162, 166 Held, R. 11, 19, 28, 42, 85, 124, 133, 159, 254, 268, 346, 438, 519, 522, Helle, L. 403, 406 Helmholtz, H. 42-44, 57 Henatsch, H.D. 287, 288, 295 Henneman, E. 255, 276, 295 Henriksen, L. 119, 167 Herman, J. 110, 159, 429 Herold, D.M. 499, 512 Hermstein, R.J. 460, 465 Hershberger, W.A. 3-5, 7, 8, 16, 19, 31, 371, 385, 432, 445 Hess, W.R. 148, 159 Hicks, J.R. 532, 534, 543 Hienz, R.D. 77, 105 Hikosaka, 0. 177, 191, 269, 297 Hildebrandt, H. 46, 57 Hilgard, E.R. 41, 57 Hillyard, S.A. 198, 205-207, 211-214 Hink, R.F. 116, 155, 206, 212 Hjorth, B. 111, 159 Hobbie, R.K. 218, 231 Hoehne, 0. 118, 155 Hogan, N. 264, 292 Hollenbeck, J.R. 493, 497, 498, 507, 512 Hollerbach, J.M. 260, 295

554

Author index

Holmes, R.A. 165, 433 Holton, G. 451, 452, 458, 465 Holzner, F. 115, 158 Homan, R.W. 110, 159 Horak, F.B. 265-269, 292, 295 Houk, J.C. 255, 272, 277, 294, 295 Howard, G.S. 39, 57, 335, 341, 343-348, 351, 352 Howarth, C.I. 264, 292 Hoy, S.L. 503, 512 Hudgins, C.V. 458, 459, 465 Hull, C.D. 123, 164, 267, 296, Hull, C.L. 354, 363, 368 Hultborn, H. 255, 287, 288, 295 Hummelsheim, H. 187, 191 Humphrey, D.R. 76, 78, 104, 278, 289, 295 Hunter, W.S. 458, 459, 465 Hutchins, K.D. 76, 104 Hyde, M.L. 84, 104 Hyland, M.E. 353-355, 360, 361, 364, 368, 463, 465, 493, 508, 512 Hyvarinen, J. 73, 75, 104, 186, 191 Iaffaldano, M.T. 501, 512 Ilgen, D.R. 494, 499, 500, 503, 513, 514 Illert, M. 97, 104 Infeld, L. 450, 451, 465 Ingvar, D.H. 118, 119, 159, 163 Inoshita, 0. 497, 514 Ishihara, T. 112, 159 Ito, M. 291, 295 Iwamura, Y. 177, 191 Iwase, K. 118, 155 Jabbur, S.J. 175, 193 Jackson, L.F. 533, 543 Jacobsen, C.F. 148, 159 James, W. 3-6, 11, 12, 19, 42, 46-51, 57, 58, 169, 170, 186, 191, 195, 197, 205, 212, 449, 465 Jankowska, E. 287, 295 Jareen, L. 544

Jasper, H.H. 108, 159 Jay, M.F. 269, 297 Jedynak, C.P. 115, 156 Jiang, W. 175, 176, 190, 191 Johannisson, T. 97, 101 Johnson, A.J. 341, 344, 347, 348, 351, 352 Johnson, P.B. 76, 102 Johnson, S. 529 Jonas, S. 115, 128, 159 Jones, E.G. 119, 146, 150, 159 Jordan, L.M. 288, 296 Jordan, S.J. 385 Joutsiniemi, S.L. 211 Jung, H. 148, 155, 160, 346 Kahneman, D. 195, 212 Kaila, K. 197, 212 Kalaska, J.F. 84, 85, 89, 93-96, 102-104, 185, 190, 264, 294 Kamp, A. 112, 155 Kanfer, F.H. 406, 460-462, 465, 466 Kant, I. 41, 58, 108, 150 Kantor, J.R. 449-455, 457, 458, 462, 463, 466 Kasmia, A,. 111, 160 Katila, T. 157, 197, 212 Kaufman, L. 114, 165, 166, 197, 212 Kaukoranta, E. 211 Kawato, M. 287, 291, 295 Kazen-Saad, M. 387, 398, 403, 406 Keele, S.W. 130, 159, 419, 429 Keidel, M. 20, 166 Kellerth, J.O. 280, 286, 293 Kelley, H.H. 384, 385 Kelso, J.A.S. 121, 159, 292 Kenny, S.B. 409, 430 Kernan, M.C. 493, 497, 498, 501, 504, 505, 510, 513

Author Index Kettner, R.E. 82, 90, 103-105, 264, 297 Keynes, J.M. 534, 543 Khalil, R. 120, 164 Kievit, J. 138, 159 Kim, C.C. 76, 95, 105 Kimble, G.A. 12, 19 Kimmig, H. 68,73 Kinerson, K.S. 463, 466 Klapp, S.T. 121, 160 Klein, R. 355, 358, 368, 409, 429, 493, 497, 498, 507, 512, 513 Kleist, K. 138, 145, 148, 149, 160 Klinger, E. 397, 405 Knapp, E. 123, 160 Knoll, R.L. 130, 166 Koepke, J.P. 231 Koffka, K. 56, 58 Kofoed, B. 211 Koketsu, K. 287, 293 Koles, Z.J. 111, 112, 160 Komaki, J.L. 494, 513 Kondrasuk, J.N. 498, 513 Kornai, J. 533, 543 Kornhuber, A. 112,116,118, 127 133, 138, 139, 142, 145, 147, 150, 160-163, 166, Kornhuber, H.H. 109, 112, 116, 118, 119, 123, 127, 130, 132, 133, 136, 138, 139, 141, 142, 144-151,155-158,160-162,166, 167, 444, 445 Koska, C. 110, 124, 126, 136, 147, 162, 163 Kotovsky, K. 417, 430 Krantz, D.S. 225, 229, 231 Kraska, K. 388, 389, 406 Krasner, L. 457, 466 Krausz, H.I. 198, 213 Kriebel, J. 116, 158 Kristeva, R. 110, 114, 116, 161, 164 Kubota, K. 188, 193 Kuenne, R.E. 533, 543

555

387-389, 393-395, Kuhl, J. 397-399,403,405-407,508, 513 Kuhn, T.S. 340, 352 Kummel, H. 97, I01 Kuperstein, M. 261-263, 269, 287, 290, 291, 294, 295 Kurata, K. 182, 187, 191, 193 Kure, W. 145, 160 Kuypers, H.G.J.M. 76, 77, 103, 138, 159 Kwan, H.C. 81, 105, 175, 183, 185, 189, 191, 192 Lacquaniti, F. 97, 104, 105 Lamarre, Y. 123, 147, 161, 175, 176, 182, 184, 189-192 Lancaster, K.J. 532, 534, 543 Lang, M. 110, 112, 116, 124, 126-128, 132-136, 138-142, 145, 149, 150, 152, 157, 160-163, 166 Lang, W. 110, 112, 114, 116, 118, 120, 124, 126-128, 131-136, 138-142, 145, 147, 149,150, 152,156, 157, 160167 Lange, L. 48, 58 Langer, A.W. 216, 231, 232 Laplane, D. 115, 163 Larsen, B. 118, 165 Lashley, K.S. 216, 231, 409, 430 Lassen, N.A. 118, 163, 165 Latham, G.P. 368, 494,496, 513 Lawson, E.A. 200, 211 Lazarick, D.L. 341, 347, 348, 352 Leathemood, M.L. 499, 512 Lebech, J. 211 Lecas, J.C. 187, 192 Legallet, E. 269, 297 Lehmenkiihler, A. 109, 156 Leibenstein, H. 541, 543 Leinonen, L. 199, 212

556

Author index

Lemon, R.N. 73, 77, 103, 104 Leslie, A.M. 396, 406 Lesse, H. 112, 163 Lestienne, F. 278, 290, 295 Lewin, K. 54-56, 58, 354, 358, 368, 395, 406, 453, 454, 466 Lewis, P.S. 207, 211 Lewis, M.Mc. 81, 105 Lhermitte, F. 138, 163, 171, 192 Li, C.L. 267, 275-277, 279, 281, 282, 297 Libet, B. 169, 192 Liden, R.G. 499, 512 Lieberman, P. 291, 296 Liebhafsky, H.H. 532, 543 Liepmann, H. 148, 163 Light, K.C. 37, 65, 74, 78, 85, 93, 133, 134, 140, 164, 192, 197, 228, 231, 255, Lindinger, G. 110, 114, 120, 136, 138, 156, 163, 164, 167 Lindstrom, S. 97, 100, 255, 287 Lindvall, 0. 149, 164 Lindworsky, J. 54, 58 Lipsey, R.C. 532, 544 Locke, E.A. 358, 368, 494-497, 502, 510, 513 Loiello, M.J. 341, 352 Lopes da Silva, F.H. 112, 155, 163, 212 Lord, R.G. 248, 249, 493, 495, 497-501, 503-506, 510, 511, 513 Lotze, R.H. 47, 58 Luchins, A.S. 463, 466 Luders, H. 123, 161 Lundberg, A. 97, 101, 102, 104 Luria, A.R. 138, 164, 459, 466 Lurito, J.T. 94, 103 Lushene, R. 228, 230 Lynch, J.C. 73, 105, 143, 164 Lyytinen, H. 205, 212 MacDougall, J.M. 228, 230

Mach, E. 44, 58, 465 MacKay, D.M. 5, 19 MacKay, W.A. 81, 105, 169, 182, 183, 185, 186, 189, 191, 192 Maddison, S. 149, 167 Maher, K. 501, 506, 513 Mahoney, M.J. 346, 352 Maine de Biran, F.P. 41, 42, 58 Makela, J.P. 199, 211, 212 Mandler, G. 228, 231 Mbtysalo, S. 203,213 Manuck, S.B. 225, 229, 231 Marcel, A.J. 59, 169, 170, 192, 296 Marken, R.S. 17, 224, 231, 236, 246, 247, 249, 299, 300, 314, 315, 332, 409, Marks, W.B. 176, 192, 315, 316, 321, 323, 429 Marmor, J. 453, 466 Marriot, J.A. 165 Marsden, C.D. 131, 155 Marshall, A. 531, 532, 538, 540, 544 Marteniuk, R.G. 264, 296 Martin, J.G. 417, 430 Masdeu, J.C. 115, 164 Massarino, R. 120, 164 Massey, J.T. 84, 85, 89, 91-94, 101, 102, 264, 294 Massion, J. 120, 164, 166, 267, 268, 294 Masuda, E. 532, 544 Mateer, C. 267, 296 Matsui, T. 497, 514 Matsumura, M. 188, 193 Matus, I. 486, 491 Mauritz, K.H. 76-79, 104, 106, 185, 186, 192, 193 Maximilian, V.A. 140, 164 May, R. 229, 231 Mayer, N.H. 160, 171, 191

Author Index Mayfrank, L. 68, 69, 73 McCallum, W.C. 196, 211, 214 McCarthy, G. 214 McClelland, D.C. 357, 368 McCubbin, J.A. 231 McFarland, R.I. 235, 250, 409, 430 McGee, G.W. 501, 514 McKenzie, R.B. 531, 544 McLean, D.R. 111, 160 McMahon, T.A. 217, 231, 272, 288, 296 McPhail, C. 248, 249 Medvick, P.A. 207, 211 Meichenbaum, D. 459, 466 Meininger, V. 115, 163 Melnick, S.A. 123, 147, 164 Meltzer, A.S. 463, 466 Mermel, M. 442, 445, 482, 491 Mesulam, M.M. 143, 164 Meyer, E. 57, 59, 126, 165, 287, 295, 405, 479, 491 Meyer-Lohmann, J. 295 Michotte, A. 54, 58 Mickle, W.A. 112, 163 Miller, N.E. 461, 465 Miller, W.H. 112, 163 Miller, G.A. 409, 430 Miller, S. 286, 288, 296 Milner, B. 148, 149, 164, 171, 192 Milner, P.M. 217, 231 Mischel, H.N. 388, 406 Mischel, W. 362, 365, 368, 388, 406 Mishan, E.J. 534, 544 Mitchell, S.J. 267, 296 Mittelstaedt, H. 5, 6, 11, 13, 16, 19, 20 Mobashery, M. 68, 73 Mohler, C.W. 68, 73 Molitor, K. 16, 20 Monroe, R.R. 112, 163 Monsell, S. 130, 166 Moore, S.P. 260, 264, 295, 296 Morin, C. 256, 296

557

Morrow, T.J. 176, 193 Motter, B.C. 75, 105, 150, 164, 184, 192 Mountcastle, V.B. 73-75, 103, 105, 143, 150, 164, 165, 184, 192 Muakkassa, K.F. 76, 105 Muchinsky, P.M. 501, 512 Muller, G.E. 46, 58 Muller, J. 44, 58 Muller, C. 162, 163, 165 Munhall, K.G. 264, 296 Munsterberg, H. 46, 48, 49, 51, 52, 58 Murphy, J.T. 81, 105, 183, 185, 191, 192, Murphy, P.E. 236, 247, 249 Murray, H.A. 354, 357,358, 369 Musgrave, M. 442, 445, 482, 491 Mycielska, R 299, 314 Naatanen, R. 195-197, 199, 200, 202-207, 209, 210, 212-214 Nauta, W.J.H. 138, 165 Neafsey, E.J. 267, 296 Neirinckx, R.D. 112, 165 Nelson, R.J. 182, 185, 192 Neshige, R. 110, 165 Neumann, 0. 388,390,406,407 Newman, P. 532, 544 Newstead, S.E. 197, 200, 213 Nieoullon, A. 269, 297 Nietzsche, F. 150, 165 Nissen, H.W. 148, 159 Norman, D.A. 299, 314, 388, 391, 394, 407 Norrsell, U. 97, 101 Nowotnik, D.P. 165 Nunez, P. 111, 165 Nussbaum, M. 40, 58 O’Neill, W.D. 319, 332 Obrig, H. 110, 120, 163, 164

558

Author index

Obrist, P.A. 216, 222, 225, 231, 232, 464 Ojemann, G.A. 267, 297 Okada, A. 114, 165, 497, 514 Okano, K. 187, 193 Okita, T. 207, 213 Oldenkott, B. 127, 163 Orgogozo, J.M. 115, 163 Orlov, A.A. 186, 189 Ome, M.T. 343, 352 Ornstein, R. 112, 158 Osafa-Charles, F. 319, 332 Ostry, D.J. 264, 2% Otto, E. 112, 165 Owen, D.H. 18, 20 Paavilainen, P. 203, 209, 210, 213, 214 Padel, Y. 97, 104 Palmer, C.J. 176, 192 Pandya, D.N. 76, 102 Paranjape, R.B. 111, 160 Parasuraman, R. 162, 200, 207, 212, 213 Parsegian, V.L. 463, 466 Parsons, C.K. 499, 512 Passingham, R.E. 268, 296 Paulson, O.B. 119, 167 Pavloski, R.P. Pavloski 215, 216, 219, 223, 224, 230, 231, 461, 464, 481, 483, 491 Pelisson, D. 271, 294 Pelitto, J. 228, 230 Penfield, W. 115, 165 Penfold, V. 112, 158 Penn, P. 494, 513 Penney, J.B. 267, 296 Penry, J.K. 199, 214 Perenin, M.T. 76, 105 Perlmuter, L.C. 12, 19 Pernier, J. 111, 165 Perrin, F. 111, 165 Peters, T.J. 516, 529

Petrides, M. 94, 103, 171, 192 Petty, M.M. 501, 514 Pew, R.W. 409, 430 Phillips, C.G. 181, 193, 230 Piaget, J. 250, 262, 271, 296 Pickett, R.D. 165 Picton, T.W. 196, 198-200, 202, 206, 212-214 Pierrot-Deseilligny, E. 256, 296 Piliavin, J.A. 508, 514 Pillon, B. 138, 163, 171, 192 Pinter, M.J. 97, 101 Piper, I.M. 165 Pisa, M. 176, 190 Plooij, F.X. 248, 250 Podreka, I. 110, 112, 113, 127, 128, 133-135, 140, 149, 152, 158, 162, 163, 165 Pollack, M.H. 231 Pompeiano, 0. 286, 287, 296, 297 Popper, K.R. 433, 443-445 Poramen, A. 73, 75, 104 Porter, R. 81, 105, 126, 156 Posner, M.I. 212, 388, 407, 419, 429 Powell, A. 366, 369 Powell, T.P.S. 150, 159, Powers, W.T. 15-17, 20, 21, 40, 215, 219, 222, 224, 229, 232, 235, 236, 247, 248-251, 291, 296, 299, 305, 307, 308, 313-315, 371, 373, 385, 409, 416, 417, 421, 429-431, 443, 445, 449, 450, 452, 454, 466, 469, 470, 479, 481-487, 491, 505, 514, 517, 518, 529, 531, 544, 547 Prablanc, C. 271, 294 Pratt, C.A. 288, 296

Author I d a Pribram, K.H. 112, 138, 156, 409, 430 Prinz, W. 59, 161, 390, 407 Prohovnik, I. 140, 164 Prud'homme, M. 84, 104 Prum, E. 54, 58 Purdy, P. 110, 159 Putnam, C.A. 121, 159 Pyszczynski, T. 508, 514 Rachlin, H. 460, 466 Rack, P.H.M. 277, 279, 296 Radcliffe, D.D. 112, 156 Raichle, M.E. 119, 158 Ramsperger, E. 68, 70, 72 Rapoport, A. 453, 467 Ray, R.D. 112, 453, 467 Reason, J. 7, 21, 24, 25, 29, 32, 33, 41, 45, 46, 108, 113, 125, 150, 299, 313, Rebert, C. 123, 155 Reed, D.J. 76, 104, 278, 289, 295 Reinikainen, K. 203, 209, 210, 213 Reisner, T. 127, 163 Renshaw, B. 255, 256, 272, 273, 280, 281, 283-290, 295-297 Requin, J. 183, 185, 187, 190, 192, 193, 293 Restle, F. 417, 419, 430 Ribot, Th. 46, 58 Richardson, R.T. 267, 296 Richter, F. 200, 213 Riehle, A. 183, 185, 187, 189, 193 Risberg, J. 140, 164 Rissland, E.L. 232 Ritj-Plooij, H.H.C. van de 248, 250 Ritter, W. 196, 199, 200, 211, 213, 214 Robertson, R.J. 434, 442, 415 Robinson, D.L. 68, 71, 72, 73, 184, 189 Robinson, D. 13, 20 Robinson, J. 538, 544 Rodin, J. 363, 369

559

Rohracher, H. 54, 58 Roland, P.E. 118, 123-126, 146, 165, 166, 173-175, 185, 186, 193, 209, 214 Rolls, E.T. 149, 166, 167, 175 Romani, G.L. 114;166 Rosenbaum, D.A. 232, 409, 429, 430 Rosenberg, A. 542, 544 Rothwell, J.C. 131, 155 Royce, J.R. 366, 369 Ruben, D.H. 453, 467 Rugg, M.D. 112, 166 Russell, B. 452, 467 RUSU,M. 166 Ryall, R.W. 287, 297 Ryan, R.M. 508, 512 Rymer, W.Z. 277, 295 Saan, L.M. 358, 368, 494, 513 Saermark, K. 211 Sakamoto, T. 190, 185 Sakamoto, M. 191, 177 Sakata, H. 69, 73, 105, 143, 164 Sameroff, A.J. 453, 467 Sams, M. 203, 204, 209, 210, 213, 214 Samuelson, P.A. 534, 544 Sanderson, P. 175, 191 Sapienza, S. 175, 191 Sasaki, K. 110, 166, 186, 193 Sasaki, S. 97, 102 Sauer, E. 148, 155 Saunders, D.R. 232, 484, 491 Sawaguchi, T. 188, 193 Schacter, D.L. 390, 407 Schacter, S. 363, 369 Schaub, H. 388, 405 Scheerer, E. 39, 42, 43, 46, 49, 56, 58, 59 Schefft, B.K. 461, 462, 466 Scheid, P. 116, 157

560

Author index

Scheier, M.F. 363, 368, 463, 464, 505, 507-509, 511, 512 Schlag, J. 119, 166 Schlag-Rey 119, 166 123, 160 Schmidt, R.A. 264, 297 Schmidt, J. 295, 287 Schneider, G.H. 46, 59, 108 Schoene, W.C. 115, 164 Schreiber, H. 131, 147, 157, 166 Schrock, B.J. 175, 193 Schultz, D. 166, 346, 352 Schiirmann, M. 398, 408 Schwartz, G.E. 112, 155 Schwartz, A.B. 80, 82, 84, 90, 94, 102-105, 264, 297 Schwent, V.L. 206, 212 Scott, P.D. 20, 286, 288, 296, 371 Seal, J. 185, 187, 193 Sechenov, I.M. 45, 59 Seemueller, E. 156 Semmes, S. 143, 150, 166 Serdaru, M. 138, 163, 171, 192 Serles, W. 167 Shaefer, V.I. 186, 189 ShaIIice, T. 388, 391, 394, 407 Shaw, K.N. 232, 358, 368, 494, 513 Shepherd, G.M. 288, 297 Sheridan, T.B. 412, 430 Sherrington, C.S. 286, 297 Sherwood, A. 216, 222, 232 Shibasaki, T. 126, 166 Shibasaki, H. 110, 165 Shibutani, H. 69, 73 Shields, J.L. 228, 230 Siatczynski, A.M. 341, 343, 352 Silberberg, A. 542, 544 Simon, H.A. 291, 297, 417, 430, 465, 467, 501, 514 Skavenski, A.A. 66, 73 Skinhoj, E. 118, 163, 165 Skinner, B.F. 371, 386, 457, 459, 460, 467

Smith, K.U.16,20,223,232,247, 250, 449, 454, 455, 456, 462-464, 467 Smith, T.J. 247, 250, 454, 455, 456, 462, 463, 467 Smith, N.W. 451, 466 Smith, A.M. 96, 102, 170, 193, Smith, W.M. 223, 232, Smith, M.F. 449, 454, 467 molensky, P. 396, 407 Soechting, J.F. 97, 104, 105 Soldani, J.C. 248, 250, 515 Sparks, D.L. 269, 297 Speckmann, E.J. 109, 156 Speny, R.W. 13, 16, 20 Spidalieri, G. 123, 161, 182, 190, 192 Spranger, E. 52, 59 Squires, K.C. 205, 214 Squires, N.K. 205, 214 Stahelski, A.J. 384, 385 Stanton, G.B. 68, 73 Stapells, D.R. 198, 213 Starr, A. 198, 199, 214 Staudel, T. 388, 405 Steibe, S.C. 341, 348, 352 Steiner, P.O. 532, 544 Steiner, M. 113, 128, 158, 162, 165, 167 Steinman, R.M. 66, 73 Steinsmeyer-Pelster, J. 398, 407 Sternberg, S. 130, 166 Stillings, N.A. 229, 232 Stilson, D.W. 486, 491 Straschill, M. 123, 166 Strick, P.L. 76, 95, 104, 105 Strohschneider, S. 388, 405 Stuss, D.T. 145, 166 Suess, E. 128, 158, 162, 163, 165 Suger, G. 118, 156 Suzuki, R. 287, 291, 295 Sybirska, E. 97, 101

Author Index Szikla, G. 166 Takahashi, I. 123, 166 Talairach, J. 112, 115, 163, 166 Tanaka, R. 97, 104 Tanaka, M. 177, 191 Tanenbaum, R. 114, 165 Tanji, J. 78, 105, 120, 166, 182, 187, 191, 193 Tantisira, B. 97, 101 Taylor, M.J. 131, 166 Taylor, M.S. 494, 499, 503, 513, 514 Teder, W. 207, 213 Teuber, H.L. 50, 59, 143, 148, 166, 167 Thompson, C.J. 126, 165, 464 Thoresen, C.E. 346, 352 Thorndike, E.L. 52, 59 Thorpe, S.J. 149, 167 Tiihonen, J. 211 Toda, M. 389, 407 Toglia, J.U. 171, 191 Tolman, E.C. 354, 363, 369, 457 Tottola, K. 209, 210 Towe, A.L. 175, 193 Treisman, A. 195, 207, 212, 214 Trouche, E. 269, 297 Tucker, W.T. 541, 544 Tullock, G. 544 Tulving, E. 391, 397, 407 Tuomisto, T. 197, 212 Turvey, M.T. 217, 218, 232 Uhl, F. 110, 124, 126, 136, 138, 139, 147, 161, 162, 167 Uhran, J.J. 243, 249 Urbano, A. 76, 102 Vaadia, E. 77, 105 Vallacher, R.R. 506, 514 Van Buren, J.M. 267, 297 van Inwagen, P. 349, 352 van der Steen, J. 77, 103 Varpula, T. 197, 212 Vaughan, H.G. 198-200, 213, 214 Veblen, T.B. 531, 532, 541, 544

561

Viallet, F. 120, 164, 269, 297 Vighetto, A. 76, 105 Vitton, N. 187, 192 Volkert, W.A. 165 von Holst, E. 5, 6, 11, 13, 16, 19, 20 Vroom, V.H. 361, 369 Vygotsky, L.S. 459, 467 Wahler, R.G. 453, 467 Waisbrot, A.J. 462, 464 Waldeier, H. 112, 157 Waldhauer, F.D. 299, 314 Wallesch, C.W. 118, 119, 156, 167 Wand, P. 286, 296, 297 Warren, R. 18, 20, 164, 167, 542, 544 Warren-Boulton, F.R. 542, 544 Waterman, R.H.Jr. 516, 529 Watson, J.B. 7, 18, 20, 51, 52, 59, 351, 443, 452 Watt, K.E.F. 243, 251 Watts, J.W. 149, 158 Weber, H. 112, 165 Weber, S.3. 343, 352 Wegner, D. 506, 514 Weick, K.E. 506, 512 Weinberg, H. 116, 118, 156, 157 Weiner, B. 359, 369 Weinrich, M. 76, 106, 185, 187, 193 Weinstein, S. 143, 166 Weisner, P.S. 165 Weiss, H.M. 507, 514 Welch, K. 115, 165 Wessely, P. 115, 158 Westbury, D.R. 277, 279, 296 White, J.M. 152, 248, 250, 251, 306 Wiener, N. 4, 20, 354, 369, 531, 544

562

Author index

Wiesendanger, M. 119, 146, 166, 167, 175, 187, 190, 191 Wigstrom, H. 255 Wilkes, K. 57, 59 Williams, C.R. 507, 512 Williams, E.M. 487, 491 Williamson, S.J. 114, 165, 166 Williamson, S. 197, 212 Willis, W.D. 175, 193 Wimmer, A. 115, 158 Windhorst, U. 287, 295 Wise, S.P. 22, 76-79, 104, 106, 185, 186, 192, 193, 294, 296 Wohlstein, R.T. 248, 249 Woldorff, M. 207, 211 Wolf, E. 286, 293 Wolpaw, J.R. 199, 214 Wolter, A.B. 41, 59 Wong, Y.C. 81, 105, 183, 185, 191, 192 Wood, C.C. 197, 214, 361 Woods, D.L. 200, 207, 214 Woodward, D.J. 176, 189 Woodworth, R.S. 51, 52, 59, 264, 297 Would, H. 533, 544

Wright, C.E. 130, 166 Wundt, W. 42-45, 48-51, 54, 59, 60,108 Wurtz, R.H. 68,73, 269, 297 Wyman, D. 66, 73 Yamamoto, Y.L. 126, 165 Yarbus, A.L. 16, 20 Yezierski, R.P. 175, 193 Yoshi, N. 112, 159 Young, L.R. 416, 430 Young, M.J. 207, 211 Young, A.B. 267, 296 Youngs, W.H. 341, 343, 345, 352 Yuan, B. 176, 193 Zeger, S. 76, 102 Zeier, H. 109, 158 Zeigarnik, B. 55, 395, 407 Zeitlhofer, J. 163 Zelaznik, H.N. 264, 297 Zerlin, S. 200, 211 Zidon, I. 496, 497, 512 Zilch, 0. 110, 131, 147, 163 Zivin, G. 459, 465, 468

563

SUBJECT INDEX

Accidental effects 10, 249, 299-301, 303, 314, 332 Action control 368, 387, 397, 401, 405, 406, 508, 513 Afference copy 6, 19 Alcohol 109, 151,345,348,349,351 Alien hand sign 115, 191 Alpha-motoneurons 280, 282-284, 286 111, Alpha mean-power-density 136, 138-140, 142, 145, 147 Alpha rhythm 111, 112, 139, 142, 146 Amygdala 119, 120, 146, 268 Anticipatory image 3, 5, 11, 432 Anticipatory premotor cell 78 Aristotle 40, 41, 45, 58, 108, 151, 155 Arm 13, 17, 19, 26, 49, 75, 78, 80-82, 86, 97, 101-104, 115, 161, 166, 170, 171, 178, 190, 192, 217, 256, 260-262, 264-268, 270, 271, 278, 282, 286, 290-293, 295-297, 381, 382, 434 Association cortex 73, 104, 143, 164, 191, 199 Attention 4, 17, 23, 25, 40, 47, 48, 63, 67-73, 107, 108, 132, 140-143, 149, 150, 157, 161, 162, 164, 169, 173, 174, 189, 195, 196-200, 202, 203, 205-207, 209-214, 361, 368, 390, 393, 394, 397, 404, 406, 407, 431, 432, 434, 439, 442, 449, 459, 463, 476, 477, 503-512, 521, 532 auditory 195-197, 209-211

directed (see directed) passive 195, 197, 199, 210 selective 206-214, 390, 394, 404 trigger 202 Attractor 175, 187, 188 Attribution 384, 385, 512 Auditory attention (see attention) cortex 166, 198, 199, 207, 209, 211, 212 modality 150, 197, 200, 206 nuclei 198 stimuli 200, 214 stimuli, dichotic 195, 200, 214 Axon collaterals 280, 281, 283, 293, 297 Baboon 193 Ballistic 160, 161, 192, 294 Basal ganglia 107, 118, 120, 123, 130, 136, 146, 147, 152, 155, 156, 160, 165, 174, 189, 265, 267-269, 296, 297, 445 see also: globus pallidus, internal capsule, putamen, substantia nigra Behaviorism 7, 51, 52, 232, 250, 353, 445, 457-460, 464-466 Bereitschafspotent~a 1 107, 116-119, 122, 125-127, 130-135, 140, 143, 147, 152, 155-157, 161-163, 166 Bradykinesia 127, 129 Brainstem 186, 198, 213

564

Subject Index

Cardiac performance 216, 222, 223, 225, 229 Cardiovascular reactivity 216, 219, 222, 225, 230, 231, 491 Cat 36, 97, 100, 101, 103, 190-193, 267, 293, 295, 296, 356 Caudate nucleus 123 Cause (see also: determinism, control) and effect 7, 10, 220, 243, 372, 452, 517 external 22, 23, 25, 27 internal 23 lineal 10, 452 mechanistic 450 open sequence (open-loop) 417-420, 450 Cerebellum 96, 107, 120, 123, 130, 136, 146, 147, 152, 155, 160, 186, 261, 290, 291, 295, 433, 445 Cerebral blood flow 107, 109, 112, 114, 118, 132, 134, 140, 146, 158, 162, 164, 165, 167, 173, 196, 197, 209-214 Cerebral cortex (see cortex) Chewing 118, 119, 146 Cochlea 198, 213 Cognition 40, 41, 53, 57, 59, 160, 161, 191, 214, 294, 369, 389, 393, 405, 406, 407, 467, 513 Commitment 390, 393, 398, 399, 401, 403, 404, 473, 479, 495, 497, 498, 499, 507-509, 512, 513, 526, 528 Comparator 248, 318, 319, 355, 494 Compensatory reactions 10, 372, 373, 378, 432 Computer 56, 158, 169, 191, 204, 221, 224, 236, 237, 244, 245, 256, 272, 281, 290, 293, 300, 302, 304, 306, 307, 309, 313, 315, 316, 318, 320, 322, 331, 373-376, 378, 379, 382, 383,

385, 394, 399, 400, 410, 413, 431, 434-439, 464, 518, 537 Conation 40, 41, 57 Conscious 6, 49, 59, 70, 103, 130, 142, 169, 191, 192, 195, 199, 202, 254, 346, 350, 390, 395, 442, 443, 490 Consciousness 41, 44, 49, 50, 57, 59, 169, 170, 195, 228, 390, 407, 431, 432, 433, 443, 507, 512, 514 Control closed-loop 4, 6, 10, 14, 19, 293, 322, 417, 419, 453-455, 461-463 complex 469, 495, 500, 509 non-specific 254 of input 4, 8-14, 17, 315, 371-373 of perception 429, 434, 517 of variable 5, 12, 14, 15, 27, 28, 30, 31, 215, 218-221, 223, 305, 307-313, 315, 385, 434, 490 superordinate 356 Control system 4, 5, 10, 11, 13-16, 18, 27-32, 215, 218-223, 225, 228, 231, 248-250, 287, 293, 308, 357, 371-373, 411, 421, 427, 429, 433, 443, 445, 454, 455, 462, 466, 469, 470, 482, 485, 490, 491, 494, 497, 502, 503, 507 Control theory 28, 29, 31, 37, 56, 215, 218, 223, 228-230, 235, 247, 249, 299, 314,

Subject Index 315, 332, 353-356, 358-360, 362, 364, 367, 368, 397, 417, 461, 463-465, 469, 471, 473, 474, 478, 481, 483, 484-486, 488-491, 493-496, 499, 501, 502, 504, 507, 509, 511-515, 517, 521, 523, 524, 526, 529, 531-533, 535, 540, 541-543 Coordination 6, 19, 75, 103, 120, 121, 147, 159, 164, 177, 292, 295 Corollary discharge 13, 50, 148, 257 see also: Efference copy Cortex 50, 67-70, 72-74, 76, 77, 79, 81, 82, 84, 86, 88-90, 92, 93, 96, 97, 98, 100-105, 112-116, 118-120, 122-125, 130, 132, 135, 138, 139-141, 143, 145-149, 151, 152, 155-160, 162, 164-167, 170-193, 196, 198, 199, 207, 209, 211, 212, 264, 265, 268, 279, 289, 290, 294, 296, 297, 445 (for specific cortical area or function see specific headings) Corticospinal 97, 103, 175, 178 Counseling 248, 346, 352, 469, 470, 474, 478, 479 Cuneate nucleus 191 Cursor 183, 184, 221, 222, 224, 225, 236-246,315-318,320-330,373, 410, 41 1-418, 420-429 Cutaneous 176, 177, 192 Cybernetics 4, 19, 20, 155, 157, 249, 250, 294, 295, 315, 332, 369, 453-456, 462-469, 491, 501, 506, 531, 544 Damping 282, 287 DC potential shifts 107, 109, 110, 117, 121, 125-127, 133-136, 140, 142, 143, 149, 162, 163 Deafferentation 185, 189, 279

565

Delay 76-78, 89, 92, 101, 120, 124, 134, 169, 187, 188, 190, 319, 322, 410, 417, 419, 421, 444, 486 Demand curve 531-534, 542 Dentate nucleus 186 Descartes 40, 108, 443, 463 Cartesian 6, 10, 12, 14, 46, 433, 443, 453, 457, 517 Descending motor pathways 100, 101, 103 Determining tendencies 53-55 Determinism 10, 39, 108, 230, 335-337, 349, 451, 452, 460, 517 Difference of negativity 121, 122, 125, 135-137, 139, 152, 207, 209 Directed attention potential 107, 132, 140-142, 150 Directional tuning 82-84, 86, 96 Directionally tuned cell 84, 85, 93 Disturbance 8, 10, 11, 13-17, 25, 26, 28, 30, 34, 76, 109, 128, 145, 177-179, 182, 183, 191, 219, 221, 224, 225, 228, 229, 235, 270, 278, 289, 293, 302, 305-308, 310-312, 315-317, 320, 321, 325, 329, 354, 371-374, 376, 385, 410, 424-428, 442, 483, 484 Dorsal column nuclei 175, 176, 190, 191, 193 Dorsal columns 190 Dorsal horn 175 Drug therapy 481, 483, 487 Economic theory 531-544 Efference copy 5, 19, 257 see also: Corollary discharge

566

Subject Index

Effort of the will 42, 54 see also: muscle sense, innervation sensations Ego 41, 42, 49, 54, 108, 151, 499 Elbow 81, 97, 178-182, 184, 186, 192, 264, 266, 294 Electro-oculogram 110, 183 Electroencephalogram 107, 109, 111, 112, 114, 133, 136, 139, 145, 155, 157-160, 162, 165, 196, 213, 214, 485 see also: Alpha, Theta Electroencephalographic (see specific potential, e.g., DC, evoked, negative) Electromyogram 81, 116, 189, 266-268, 290, 484-487, 491 Epilepsy 112 Equifinality 269 Error sensitivity 355, 356, 358-366, 484 Error signal 15, 28, 218, 220, 223, 282, 319, 324, 327, 371, 432, 442, 444, 482-484 Essential substance 450 Ethics 39, 40, 151, 155 Event-related brain potentials 162, 1%-199, 203-207, 209-214 Evoked potentials 176, 196, 210, 211, 213, 444 Eye movements 13, 16, 19, 20, 44, 63-73, 110, 118, 119, 146, 183, 269, 292, 294, 297, 301 optic ataxia 76, 101, 104 saccadic 13, 19, 64-73, 118, 119, 156, 158, 160, 170, 184, 188, 191, 269, 270, 291 corrective 65, 66 express 67-69, 72, 73 microsaccades 64-68 Factorization 253-255, 269, 270, 272, 279, 292, 293

Feedback biofeedback 461, 462, 464, 481, 483-487, 490, 491 internal 202 loop 8-10, 15, 16, 28, 218, 267, 371, 372 negative 4, 5 , 8, 10, 13, 28, 29, 215, 247, 371, 372, 481, 486 positive 16, 267 self-delivered 499 sensory 16, 19, 46, 130, 283, 456 spindle afference (Ia) 290, 291 Feedforward 173, 261, 287, 290 Fiat 49, 50 Finger 102, 116-118, 120-122, 124-129, 131, 132, 140, 145, 155-157, 161, 162, 167, 173, 174, 177, 300, 432, 434 Fixation 65, 67-69, 72-74, 133, 140, 164, 166, 192 F E T E 253,255, 261, 265, 272, 273, 281, 285, 287, 289-291 Force 21, 24, 26, 28, 29, 31-33, 41, 42, 145, 147, 186, 189, 253, 265, 271, 272, 274-279, 281, 282, 285, 293, 294, 332, 336, 342, 343, 349, 354, 363, 428, 450, 451, 532 Forelimb 81, 100, 101, 103, 104, 190, 269 Free will 34, 39, 108, 150, 335-337, 342, 348-350, 352 Freedom 21, 22, 36, 40, 54, 56, 57, 108, 150, 151, 161, 249, 337, 339, 345, 349,

Subject Index 350, 352, 386, 478, 479, 491 Freud 108, 299, 314, 395, 452 Frog 45 Frontal eye fields 68, 69, 72, 73, 119, 156, 170, 174, 183, 187-189 Frontal lobes 50, 73, 76, 104, 108, 135-139,148-150,158-163,166, 192, 167, 171, 173, 174, 191 Frontocentral midline 116 Frontocentral negativity 199 Frustration 230, 470, 474, 477, 478 Galilei 40 Gating 175, 176, 178, 209, 262, 263, 267, 269 Genetic 46, 50, 337, 351, 455, 461 Gestalt 56, 58 Giffen 531-538, 540-542, 544-547 Globus pallidus 263, 265-268, 292, 295, 296 GO (or "go1') signal 76, 89, 185, 254-257, 259, 260, 263-270, 291 Goals future 139 internal 515, 519 multiple 387, 404, 495, 501, 503-505, 509, 510, 512 Habituation 151, 213, 214 Heart rate 223-225, 229, 231, 236, 245, 246 Heart rate reactivity 223, 224 Hierarchy 17, 18, 31, 34, 35, 37, 41, 172-174, 221, 222, 225, 227, 231, 249, 295, 313, 330, 355364, 409, 416-421, 427-431, 434, 435, 444, 469, 470, 471, 478, 482-485, 489, 490, 505, 506, 517, 519, 536 Homeostasis 5, 176, 483 Humanities 49, 52, 53, 56, 335 Hypermetria 97, 100 Hypertension 231

567

Hypothalamus 119, 120, 138, 146, 151 Ia feedback 290, 291 Ia interneuron 273, 281, 282, 286, 287, 290 Ideomotor 11, 19, 47, 49, 52, 59 Illusion 19, 22, 109, 150, 371, 373, 374, 378, 381, 383-385, 433, 442, 443 Imitation 47, 163, 171, 192 Impulsivity 391, 393 Individual differences 223, 225, 357, 358, 361, 362, 369, 397, 405, 406, 493, 495, 506-511 action oriented 508 state oriented 361 Inertia 254, 427 Infarction 115, 164, 191 Inferior temporal cortex 119, 120 Innervation sensations 42-44, 47-49 Integrated-field 450, 453-455, 462 Integration 97, 100, 101, 103, 119, 120, 122, 212, 244, 245, 254, 319, 322, 323, 324, 326, 353, 355, 368, 413, 416, 419, 465, 511, 512 Integration factor 244, 245, 322-324, 326, 416 Interference 54, 114, 121, 132, 137, 139, 167, 235, 236, 242, 247, 401 Internal capsule 172 Interneurons 97, 265, 273, 281, 296 Interpositus 96 Introspection 11, 12, 41, 51-54, 70 Intuition 28, 29, 220, 304

568 Joint

Subject index

14, 81, 100, 127, 163, 253, 257, 273, 275, 279, 280, 282, 284, 2.85, 287, 289, 291, 295, 308, 309, 359, 380, 381, 481, 516 Kant 41, 58, 108, 150 Key press 187, 438 Kinematic 121, 265, 271, 296, 297 Kinesia paradoxica 115, 127 Kinesthesis 49 Language 6, 56, 95, 97, 156, 159, 164, 167, 296, 318, 319, 354, 355, 360, 362, 364, 367, 421, 451, 452, 467, 540 Latency 64, 65, 81, 96, 123, 127, 159, 166, 181, 182, 190, 198, 199, 204, 206, 207, 209, 210, 213, 214, 419 also see: Reaction time Lateral inhibition 387-389, 404 Lateralization 136, 137, 139, 140, 142, 155 left hemisphere 110, 127, 136, 137, 139 right hemisphere 140-142 Learning 18, 19, 47, 53, 70, 112, 133-140, 145, 149-151, 157, 161-164, 166, 167, 193, 217, 250, 260, 262, 263, 268, 290, 294, 295, 296, 320, 354, 405, 407, 430-432, 436, 438, 441, 457, 461, 464, 465, 467, 483, 485, 486, 493, 501, 505, 506, 510, 511, 524 Lesions 69, 73, 100, 115, 119, 127, 128, 138, 143, 145, 148, 150, 155, 156, 159, 163, 164, 170, 171, 177, 191, 192, 265, 266, 269, 295, 297, 433 Levels of control 33-36, 227, 404, 442, 469, 489, 490 Limbic cortex 123, 124

Limbic system 112, 138, 143, 146, 148, 151, 160 Locomotion 16-18, 100, 102, 176, 192, 231, 248, 249, 296, 429 Loop gain 28 Magnetic resonance imaging 114 Magnetoencephalogram 109, 113, 114, 116, 118, 157, 196, 197, 199, 207, 210, 212 Management 248,368,387,475, 481, 485, 490, 493, 494, 512-519, 528, 529, 534 Manager 474, 500, 517, 518, 520-522, 524, 528, 529 Mass-spring 264 Mental faculties 39, 40 Mesial, fronto-central cortex 118, 143, 152 Meta-volition 345 Metabolic load 216 Microstimulation 69, 73, 81, 175, 187, 191, 289 Mind 6, 11, 22, 30, 37, 41, 43, 46, 47, 52, 57, 108, 151, 228, 231, 294, 304, 307, 314, 332, 352, 406, 407, 441-443, 450, 453, 457, 469, 473, 491, 498, 521, 525 Mind reading 307, 314, 332 Mismatch negativity 203-205, 210, 213 Mode theory 355, 362-367 Modulation 69, 185, 229, 262, 350 Monkey 69, 72-78, 82, 85, 88, 93, 101-105, 150, 155, 156, 159-161, 164, 166, 167, 172, 177, 182, 185, 189-193, 266, 293, 544

Subject Index Motivation 54, 122, 123, 146, 148, 151, 156, 160-162, 249, 338, 354, 355, 356, 359-363, 367-369, 394, 395, 400, 405, 406, 493, 494, 495, 496, 498, 501, 502, 505, 507-509, 511-513, 516, 517, 519 Motor commands 97, 124, 260 Motor cortex 67, 76, 77, 81, 82, 84, 86, 88-90, 92, 93, 96, 97, 100, 101, 102-104, 114, 116, 119, 123, 124, 130, 140, 146-148, 155-157, 159, 173-175, 178, 179, 181, 182, 185, 187, 190, 191, 193, 264, 265, 279, 289, 290, 294, 296, 297 Motor cortical population 88 Motor equivalence 216-218, 229 Motor pathways 100, 101, 103 Motor sequencing 172 Motor trigger 187, 189 Motor unit 289 Movement-related cells 76 Multiple personality 482 Muscle agonist 178, 180-182, 256, 257, 273, 278, 293 antagonist 179, 180, 256, 257, 273, 278, 295 extensor 177, 180, 181, 266, 290, 293 flexor 126, 177-179, 266, 290 isometric 264, 291, 294, 296 sense 41-43, 50, 59 spindle 182 striate 216 No component 198 N1 component 198-202, 204, 206, 209, 213 Needs 34, 55, 63, 108, 130, 146, 148, 152, 268, 277, 321, 350, 357, 387, 390, 395, 494, 508-511

569

Negative potential DC shift 116, 123, 125, 132, 134, 136, 142, 144 Negative reinforcement 516, 520 Neural circuit 264, 265, 278 Neural model 11, 12 Neuronal population coding 88, 90, 102 Neuronal population vector 87-94, 96, 102 Neurotransmitter 217 Newton 26, 450, 451 Organizational systems 249, 313, 346, 368, 409, 429, 493, 499, 500, 507, 510, 511, 512-514, 518 Overcommitment 402 Oxygen consumption 223 P1 component 198, P2 component 198, 203 Pain 21, 145, 147, 487 Paralysis 37, 44, 172, 189 hemiplegia 172 paresis 44, 127, 172 Parietal lobe 68, 69, 72-76, 93, 103, 104, 108, 140-144, 150, 156, 164, 165, 171, 173, 183-193 paneto-occipital cortex 119 posterior parietal cortex 72-74, 104, 164, 173, 184, 187, 189, 192, 193 Parkinsonism 164 Pars reticulata 269 Pavlov 443 Pavlovian conditioning 458-460 Performance-related DC 107, 109, 125, 133-136

570

Subject Index

Performance-relatednegativity 125, 126, 134, 135, 137, 139, 152 Perseveration 171, 514 Personality 338, 352, 355, 357, 358, 360-363, 365, 367-369, 394, 398, 399, 400, 404-407, 464, 482, 486, 507, 508, 511, 512, 514 Perturbation (see disturbance) Physiological reactivity 216, 229 Plat0 108 Pleasure 109, 360, 361, 364 Population vector 87-94, %, 102 Positive reinforcement 5 18 Positron emission tomography 115, 197 Postarcuate area 77 Postcentral gyrus 185, 191, 214 Posture 5, 13, 17, 103, 119, 120, 146, 164, 217, 253, 255, 261, 262, 288, 292, 294, 485 Practice 6, 16, 44, 53, 70, 72, 102, 151, 248, 294, 320, 346, 352, 421, 443, 458, 485, 490, 493, 513, 516 Precentral gyrus 104, 110, 116, 156 Premotor cortex 76,77,79, 101-103, 105, 172, 174, 175, 185-187, 192, 193 Preparatory activity 186 Preparatory set 123, 132, 190 Primate 73, 102-105, 156, 159, 190, 191, 193, 296, 297 Processing negativity 206, 207, 209, 210, 212, 213 Program 130, 134, 135, 140, 141, 144, 160, 164, 169-172, 247, 318, 319, 320, 321, 324, 325, 351, 376, 378, 379, 410, 416, 431, 432-434, 445, 473, 489, 490, 505, 517, 526, 528, 537, 538, 539, 540, 545

Proprioception 48, 50, 177, 178, 180, 202, 271 Psychophysics 19, 43, 213 Psychotherapy 344, 346, 481, 483, 488-490 PUP 261-263 Putamen 266 Pyramidal 97, 123, 190, 293 Reaching 2-D reaching 82, 88, 91-94, 98 3-D reaching 82, 89 Reaction time 42, 44, 45, 48, 53, 55, 64, 65, 67, 68, 70, 72, 88, 89, 92-94, 102, 193, 266, 294, 396, 419, 442, 432 also see: Latency Reactivity 216, 219, 222-225, 227, 229-231, 490, 491 Reafference 5, 11, 19, 20, 48, 50, 169 Receptive field 69, 175, 178, 184, 186, 191 Red nucleus 76, 103, 123, 287, 295 Reference criterion 355-364, 366 Reference level 14, 215, 220, 221, 245, 308-311, 411, 429, 484, 535 Reference signal 5, 6, 10, 11, 17, 18, 28-33, 215, 218, 220-222, 228, 315, 319, 321-330, 414, 417, 443, 444, 462, 473, 482 Reflex 6, 7, 10, 19, 39, 45, 46, 48, 59, 63, 66, 69, 170, 172, 181, 184, 189, 190, 192, 211, 213, 255, 263, 272, 277, 284, 286, 288,

Subject Index 289, 296, 297, 458, 460, 463, 465 Regional cerebral blood flow (see cerebral blood flow) REM sleep 200 Renshaw 255, 256, 272, 273, 280, 281, 283-290, 295-297 Reorganization 16, 445, 483, 485, 488 Resoluteness 107, 132 Reticular formation 123 Retinal image 44 Reward 69, 74, 77, 78, 82, 86, 183, 461, 503, 518, 519 Robot 407 Schema 217, 228, 388-391, 393, 394 Schopenhauer 42, 108 Script 395-397, 505, 506, 510 Self-determination 335, 336, 339, 341, 345, 346, 349-351 Self-regulation 387, 390, 405-407, 449, 450, 454, 457-459, 461, 465, 468, 491, 511 Sensorimotor 120, 123, 169-174, 176, 178, 181, 184, 187 Sensorimotor area 5 75, 76, 93-96, 101-104, 180-182, 185, 190, 192, 193 Set-related cells 76 Shoulder 74, 81, 97, 110, 264, 266, 518 Single cell 81, 101, 102, 104, 294, 297 Single photon emission computerized tomography (see SPECT) Size principle 255, 272, 276-281, 286, 289, 292 Skill 131, 185, 217, 330, 430, 511 Skinner 3, 7, 371, 386, 443, 457, 459, 460, 467 Slowing factor 15, 318, 322

571

Somatosensory cortex 114, 165, 175, 176, 180, 182, 184, 190, 191 Somatosensory inputs 175, 182, 185 Somesthesis 73, 192 Soul 40, 46, 443, 450, 453, 463 SPECT 107, 112-115, 119, 127, 133, 135, 152, 163, 165 Speech 6, 8, 12, 14, 23, 115, 118, 119, 127, 128, 130, 146, 157-159, 166, 174, 200, 202, 207, 214, 267, 291, 296, 430, 443, 465, 466, 468, 483 Spinal circuits 100 Spinal cord 35, 46, 76, 84, 97, 100, 103, 123, 253, 295, 296 Stability 19, 30, 43, 255, 291, 305-307, 313, 483, 519, 533, 534, 537 Stiffness 269, 279, 282, 295 Stimulus-response 7, 11, 49, 52, 132, 137, 149, 454, 483, 515, 517 Stress 211, 212, 215, 216, 222, 229-232,467,479,481-485, 488, 490, 491, 497, 520 Stretch 177, 180, 181, 190, 192, 255, 272, 276, 284, 286-289, 297 Stretch reflex 181, 192, 255, 272, 284, 286, 288 Striate cortex 73 Stroke 172, 189 Substantia nigra 123, 269, 297 Superior colliculus 68, 73, 269, 297 Superior prefrontal cortex 173, 174 Superior temporal gyrus 199

572

Subject Index

Supplementary motor area 104, 107, 112, 115, 116, 118-120, 122-129, 130, 132, 143, 144149, 152, 155-158, 161, 163167, 170, 173, 174, 187, 191, 193 Supratemporal component 199,200, 202 Synchronous movements 120 Systems analysis 5, 251, 467 T complex 199 Tactile 140, 146, 150, 170, 171, 176, 216 Teamwork 517, 524, 526, 528, 529 Ten-twenty system 110, 159 Thalamus 146, 176, 193, 198, 296 Theta mean-power-density 111, 136, 138-140, 142, 145, 147, 178 Theta rhythm 111, 112, 139, 142, 146 Thresholds 200, 204, 272, 274, 276, 278-280, 283, 414, 421 Timing (see: when to do) Tongue 118, 119, 146 Tracking 133-138, 140-144,152, 157, 162, 183, 184, 235-237, 242, 245, 246, 247, 249, 250, 290, 300, 304, 315, 330, 410, 411, 417, 419-421, 423 compensatory 315 inverted 134, 138, 142, 152, 424 pursuit 235, 236, 411

Tracts 46, 97, 175 Trajectory 18, 19, 80, 81, 144, 253-256,258,261-264,266, 269-271, 278, 292, 294 Trigger 77-79, 115, 144, 169, 170, 182, 184, 187-189, 199, 202, 484, 504 Trilogy of the mind 52 Unconscious 53, 54, 169, 192, 405, 490 Vertex 112, 198-201, 206, 211, 212 Vibration 189, 297 Video 183, 184, 221, 223, 224 Visual control 101 Visual localization 44 Visual stimulus 77, 171 Visual target 75, 133, 141, 142, 177 VITE 253-257, 259-266, 269, 271, 274, 289-292 Watson 7, 18, 20, 51, 52, 59, 351, 443, 452 When to do 107, 115, 123, 127, 149 Will power 39, 54 Wrist 97, 103, 110, 184, 185, 192, 266, 289, 290 Wundt 42-45, 48-51, 54, 59, 60, 108 Wiirzburg school 51, 53