Colour Atlas of the Anatomy and Pathology of the Epitympanum

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Author: T. Palva | Hans Ramsay | Clarinda Northrop

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Color Atlas of the Anatomy and Pathology of the Epitympanum

T. Palva In collaboration with H. Ramsay, C. Northrop

Color Atlas of the Anatomy and Pathology of the

Epitympanum 171 figures, 166 in color, 2001

Basel 앫 Freiburg 앫 Paris 앫 London 앫 New York 앫 New Delhi 앫 Bangkok 앫 Singapore 앫 Tokyo 앫 Sydney


Tauno Palva, MD Professor Emeritus of Otolaryngology University of Helsinki, Finland In collaboration with

Hans Ramsay, MD Associate Professor of Otolaryngology University of Helsinki, Finland and

Clarinda Northrop, B.A. Director of Research Temporal Bone Foundation, Boston, Mass., USA

The Temporal Bone Foundation has generated a 3D video model of one of the temporal bones described in Chapter 2. This model is available on a CD, which can be obtained by contacting: The Temporal Bone Foundation, Inc. 9 Brimmer Street Boston, MA 02108 (USA) Phone: +1 617 742 5927, Fax: +1 617 742 4666 E-Mail: [email protected] Offer good until September 1, 2002

Library of Congress Cataloging-in-Publication Data Palva, T. (Tauno) Color atlas of the anatomy and pathology of the epitympanum / Tauno Palva, Hans Ramsay, Clarinda Northrop. p. ; cm. Includes bibliographical references. ISBN 3805572271 1. Middle ear--Anatomy--Atlases. 2. Middle ear--Histology--Atlases. I. Ramsay, Hans. II. Northrop, Clarinda. III. Title. [DNLM: 1. Ear, Middle--anatomy & histology--Atlases. 2. Ear, Middle--anatomy & histology--Case Report. 3. Ear, Middle--pathology--Atlases. 4. Ear, Middle--pathology--Case Report. WV 17 P184c 2001] RF220 .P25 2001 617.8)4--dc21 2001029653

Bibliographic Indices. This publication is listed in bibliographic services, including Current Contents® and Index Medicus. Drug Dosage. The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.

All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. © Copyright 2001 by S. Karger AG, P.O. Box, CH–4009 Basel (Switzerland) Printed in Switzerland on acid-free paper by Reinhardt Druck, Basel www.karger.com ISBN 3–8055–7227–1


Contents

IX

Preface Part 1

1

3 3 4 7 8 8 8 8 9 9 9 10 11 11 12 12 12 13 15 15 15 16 17 18 20 21 26 27 28 28 28 30 31 31 32 33 36

Anatomy and Pathology of the Epitympanum Introduction and General Review Development of the concept of epitympanum Early data of the soft tissues in the epitympanum Fetal development of epitympanic folds and compartments Tensor Fold Lateral Incudomalleal Fold Chordal Fold Other Duplicate Folds Tympanic Isthmus Development of Prussak’s Space Contemporary Concepts of the Anatomy of the Epitympanum Material and Methods Anatomy and Pathology of the Epitympanum and Supratubal Recess Epitympanic Diaphragm Normal Anatomy of Prussak’s Space (with the Lateral Malleal Space) Microdissection Lateral Malleal Space Prussak’s Space Serial Sections Floor of the Lateral Malleal Space (Roof of Prussak’s Space) Shrapnell’s Membrane Anterior Membrane of Prussak’s Space Aeration Pathways to Prussak’s Space Pathology of Prussak’s Space and the Lateral Malleal Space Microdissection Serial Sections Cholesteatoma in Prussak’s Space Large Epitympanic Compartments Posterior Epitympanum Normal Anatomy by Microdissection Lateral Incudomalleal Fold Posterior Incudal Ligamental Fold Superior Malleal Ligamental Fold Tympanic Isthmus Normal Anatomy by Serial Sections Pathology as Seen in Microdissection Pathology as Seen in Serial Sections

36 38 38 39 41 42 42 43 45 45 48 48 51 52

Anterior Epitympanum Normal Anatomy by Microdissection Transverse Crest Tensor Fold Other Folds in the Anterior Epitympanum Normal Anatomy by Serial Sections Pathology as Seen in Microdissection Pathology as Seen in Serial Sections Supratubal Recess (Space) Normal Anatomy by Microdissection Normal Anatomy by Serial Sections Pathology as Seen in Microdissection Pathology as Seen in Serial Sections References

Part 2

VI

53

Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection

55 57 61 61 61 62 62 64 64 64 66 66 66 67 67 69 69 70 72 73 73 73 73 74 75 76 77 79 82 82 84 85 86 86 86 87 88 89

Introduction and Short Review of the Literature on Amniotic Fluid Cellular Content Short Review of Mastoid Pneumatization Amniotic Fluid Cellular Content-Related Middle Ear Pathology as a Function of Age in Serial Sections Temporal Bones from Neonates Superior and Anterior Epitympanum and Antrum Tensor Fold and Supratubal Recess Lateral Incudomalleal Fold and Lateral Attics Lateral Malleal Space and Prussak’s Space Medial Attic and Tympanic Isthmus Tympanic Cavity Eustachian Tube Mastoid Pneumatization Comment Temporal Bones from 2- to 4-Month-Old Infants Compartments above the Epitympanic Diaphragm and the Mastoid Antrum Tensor Fold and Supratubal Recess Lateral Malleal Space and Lateral Attics Prussak’s Space and Its Aeration Pathways Tympanic Isthmus and Posterior Tympanum Tympanic Sinus and Round Window Niche Eustachian Tube Elements Specific to Amniotic Fluid Cellular Content Mastoid Pneumatization Comment Temporal Bones from 5- to 23-Month-Old Infants Case 1 Case 2 Case 3 Case 4 Case 5 Elements Specific to Amniotic Fluid Cellular Content Mastoid Pneumatization Comment General Comments Histological Considerations regarding Amniotic Fluid Cellular Content-Associated Pathology Mastoid Pneumatization Clinical Considerations References

Contents

Part 3 91 Microsurgical Approaches to Inflammatory Ear Disease 93 94 94 94 95 97 98 98 99 99 100 100 101 102

Introduction Early Attempts to Improve Epitympanic Aeration Microsurgical Methods in Surgery for Retraction Pockets Surgery for Incipient Retraction Pocket Surgery for Established Retraction Pockets Frontolateral Atticotomy Extensive Attic and Mesotympanic Disease in Chronic Otitis media Spread of Cholesteatoma from Prussak’s Space Posterior Route Inferior Central Route Superior Route Anterior Route Final Remarks References

103 Subject Index

Contents

VII


Preface

In many different fields of research progress has been made so rapidly that the most advanced knowledge of today may be old-fashioned in a few year’s time, and the established procedures and techniques need constant modernization. This fast progress is also obvious in many areas of medicine where, for example molecular biology and gene research have opened entirely new horizons for both diagnosis and treatment. On the other hand, notably in macroanatomy, previous generations have already done the basic studies, and their results can rarely be fundamentally improved upon. The knowledge of human anatomy and pathology, obtained at autopsies and complemented by light-microscopic examination, has remained essentially unchanged for many decades, even if at a molecular level many new discoveries are being made. In modern otology, after the Second World War, clinicians have been able to take advantage of the superb magnification of the surgical field provided by the operation microscope, which has increased the knowledge of the anatomy based solely on the naked eye. The magnified view, nevertheless, has not rendered conventional microscopic anatomy redundant for those who wish to understand the nature of the structures they are dealing with. In this area the work of the early anatomists, even without our sophisticated tools for magnification, still contains many valuable observations. Especially in the latter part of the 19th century the anatomy and pathology of the ear was a topic favored by many prominent scientists and clinicians. During the latter part of my 40 active clinical years, ending in the early 1990s, I became more and more dissatisfied with the articles discussing the anatomy of the epitympanum and was convinced that some of the described features did not reflect the facts. The contemporary authoritative descriptions, for example, of the anatomy and aeration of Prussak’s space, and of the structure of the

major epitympanic compartments, contained features that I was at a loss to understand. Some sketches of the epitympanic folds were so elaborate that they appeared to preclude all effective aeration and drainage. I finally went back to the original writing of Prussak and this experience made me reread other related original works, for example, by von Tröltsch, Politzer, Wittmaack and many others. However, only after a perusal of Hammar’s study of the fetal development of epitympanic folds did I feel close to understanding the epitympanic compartments and their origin. This was followed by going personally back to the dissection laboratory and beginning with the microdissection of temporal bones in an effort to verify the folds and basic compartments that Hammar had described. These data obtained by microdissection have during the last 10 years been published in otological periodicals and have helped to clear up many earlier misconceptions, the epitympanic anatomy has emerged as a sensible and logical arrangement. I had enormous help in elaborating and deepening of the knowledge I obtained through microdissection by having the continuing cooperation with Clarinda Northrop of the Temporal Bone Foundation in Boston who permitted me to use their magnificent collection of serially sectioned newborn and infant temporal bones. Hans Ramsay, my former resident, who has now taken over my surgical work in the Department of Otolaryngology in Helsinki, made the material and facilities for microdissection available to me. After my retirement from clinical activity we have continued to enjoy fruitful joint research activity, now over a period of 10 years. During the last decade I have led the department seminars of anatomy, pathology and surgery of the ear. It appeared that the initial level of knowledge of the residents regarding epitympanic anatomy and pathology was not sufficient for a future ear surgeon. It also became clear

IX

that for self-education there were no reliable books which would cover the entire area without the need to peruse individual reports from periodicals. Furthermore, it appeared that the earlier literature did not contain anatomic documents but showed mostly sketches which often did not conform with reality. For these reasons I decided to write the present atlas which summarizes the work of our research groups during the last decade. In order to obtain maximal clarity it was decided to use only colored photographs for the description of the anatomy and pathology. Part 1 of this atlas was compiled in the hope that it would, by ample documentation, help both the younger people in training as well as experienced specialists to have in one volume all data necessary for an understanding of the mysteries of the epitympanum. We hope that reading it would stimulate the otologists to go personally to the dissection laboratory and practise the microdissection approaches we have advocated, to become familiar with the structures forming the epitympanic compartments. We are convinced that afterwards work in the operation theater becomes even more interesting, when structures discovered and understood as a result of microdissection are once again encountered. The procedures for improving aeration and drainage we have outlined in Part 3 are not difficult and are likely to lead to better functional results once the surgeon becomes accustomed to them.

X

Preface

In Part 2 of this atlas we present in compact form the present knowledge of the spread of the amniotic fluid cellular content into the different compartments of the middle ear. We also present a great deal of documentation of the intensive foreign body-type tissue reaction caused by amniotic fluid cellular content, at times combined with infection, on the soft tissue structures of neonates and infants. These sometimes massive reactions were already well known to the investigators at the end of the 19th century, and both Aschoff and Wittmaack produced voluminous documents, the contents of which are still valid today. We believe that part of the long-standing problem of middle ear infection in infancy is initially related to this forgotten cause. The photographs of serial sections shown in the atlas were made by Mauri Laakso, Ari Aalto and Richard Cortese. The Ear Research Foundation, Helsinki, the Department of Otolaryngology, University of Helsinki, and the Temporal Bone Foundation, Boston, Mass. with their generous financial support have made the publication of this atlas possible. December 2000

Tauno Palva

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Anatomy and Pathology of the Epitympanum

1


Anatomy and Pathology of the Epitympanum

Introduction and General Review Development of the Concept of Epitympanum The division of the middle ear spaces into different anatomic subcompartments was established during the latter part of the 19th century, and initially there was some confusion which name should be used for the portion superior to the main tympanic cavity. In his concise chapter entitled ‘Mittelohr und Labyrinth’ in Karl von Bardeleben’s Handbuch der Anatomie des Menschen, Siebenmann [1] still referred to this superior segment as ‘aditus (ad antrum)’ but admitted there was additional usage in the form of ‘recessus epitympanicus’, ‘epitympanum’ and in the German ‘Kuppelraum’. Siebenmann pointed out that most of his contemporary authors still considered this area to be part of the tympanic cavity (Paukenhöhle) but von Tröltsch, Eysell and Schwartze, all well known researchers, started to use the name ‘aditus’ for this superior region, and that it was Bezold who described its anatomic limits. Siebenmann was horrified that the Americans referred to the recessus epitympanicus by the name of ‘attic’ since he argued that this term ‘was used in architecture to describe a half story adnex on top of the house proper’ and did not like the emerging French usage of ‘attique’. He warned his colleagues about adopting ‘this barbaric word, even if latinized into the form of “atticus”, into the German language but one should continue to use the established word of “aditus”’. He also criticized the recently established nomenclature commission for recommending the ‘difficult concept of recessus epitympanicus’ because the word recess implies a blind extension of a certain space which ‘aditus’ is not. Siebenmann then went on to describe exactly the limits of the ‘aditus’, which we nevertheless, with due respect to

him, from now on will call either epitympanum or attic. The word aditus has become established as indicating the posterior open portion of the epitympanum connecting it to the mastoid antrum. Siebenmann’s criticism has been accepted in that the word ‘recess’ has been dropped in the context of the epitympanum and is presently used in connection with the supratubal recess which indeed usually is a blind space as the word implies. Siebenmann cited the measurements of Bezold for the dimensions of the epitympanum, which are still valid today: just behind the level of the malleus head, the breadth had a mean of 6.6 mm (range 5.3–8.0 mm). The height from the tip of the short process of the incus to the superior wall was 5.7 mm (range 5.0–6.3 mm). The inferior limit of the attic anteriorly was formed by the tensor tendon, from which the folds originated directed upwards in form and direction (plicae transversae), attaching superiorly to the transverse crest. Siebenmann observed that there was often a defect in this fold, varying in structure, which then connected the epitympanum to the protympanic spaces. The area in front of the fold formed a ‘large pneumatic cell’, a portion of the tympanic cavity. The roof of the epitympanum or the floor of the middle fossa was medially part of the petrous bone, the lateral portion being part of the squamous bone, the suture line running lateral to the midline making the medial portion larger. The anterior portion of the tegmental bone, towards the eustachian tube, showed a downwards sloping form while the posterior portion remained horizontal. The lateral limit of the epitympanum was formed superiorly by a very hard bone, lacking air cells, extending in a curved form to the notch of Rivinus, the edges allowing an insertion ring for the lateral inferior portion, Shrapnell’s membrane. The medial wall was formed by the labyrinth capsule and posteriorly the space was open to the mastoid antrum.

3

The bony limits of the epitympanum have thus been established for already well over 100 years. Analyzing them again and writing a new atlas of the anatomy of the epitympanum would only be a repetition of known facts and a waste of time. However, the soft tissue structures inside the epitympanum, or bordering it, have remained obscure to most contemporary writers even if much of their basics had been worked out satisfactorily at the end of the 19th century. As we did microdissection and histopathological studies in the 1990s we also became familiar with the considerable knowledge available in the old writings. We were astonished by the concise description of the anatomic details and can but admire the quality of the work the pioneers did with simple tools. There were other authors who have contributed significantly to the knowledge of the epitympanum as we will see later on. Of the many we would like to mention several here: von Tröltsch [2] who established the concepts of the anterior and posterior pouches as common knowledge, Prussak [3] who described the superior pouch, Helmholtz [4] who described the malleal ligaments, particularly the posterior, and Hammar [5] whose contribution to the fetal development of the middle ear remains to be surpassed. As far as the histology of the epitympanum is concerned, Wittmaack’s work [6, 7] has been colossal and much of it is still valid today. Many other research workers made significant contributions at the turn of the 19th century and we will refer to them during the discussion of specific chapters.

Early Data of the Soft Tissues in the Epitympanum The anterior and posterior pouches became known in the first half of the 19th century. In his textbook (in German) on anatomy and diseases of the ear from 1881 von Tröltsch [2] reviewed the then current knowledge and found that Wildberg already in 1795 was aware of these ‘duplicates of the tympanic membrane’ but erroneously considered them as malleal muscles. The dissertation of Cornelius from Dorpat in 1825 suggested, according to von Tröltsch, the right idea of the folds forming the pouches but he failed to note the connection the folds had with the tympanic membrane. Arnold in 1839 had depicted the folds correctly both in writing and figures but von Tröltsch thought he made a mistake by describing them as mucosal folds, and not as duplicates of the tympanic membrane. A further mistake was that Arnold considered the folds not constant and left them out of several figures which showed the medial side of the tympanic

4

membrane. The conviction of von Tröltsch that especially the posterior pouch was a duplicate of the tympanic membrane was based on the observation that both of them started from the same site in the annular bone and that their fibrotic layers were identical. Von Tröltsch believed that this pouch membrane, thanks to its fibrotic layer, increased the elasticity and vibrations of the tympanic membrane. The name of von Tröltsch has since been attached to these pouches. In his textbook von Tröltsch [2] gave a detailed description of the structure forming the posterior pouch. Its dimensions, measured after removal of the incus, were 3– 4 mm in height and up to 4 mm in width. It was irregularly triangular and extended from the annular bone to the handle of the malleus. The fold was superiorly attached to the tympanic membrane but deviated inferiorly from it forming the pouch, open to the posterior mesotympanum. The chorda tympani nerve became connected to the medial surface of the posterior portion of the membrane before entering its bony canal. He definitely rejected Henle’s observation from 1875 that the fold contained distinct stiff bundles of ligamental fibers of connective tissue. The medial border of the anterior pouch, on the other hand, was no longer considered [2] as a duplicate tympanic membrane. The pouch formed between the tympanic membrane and a composite structure, consisting of the long process of the malleus (processus gracilis), the anterior malleal ligament, the chorda tympani nerve and the inferior tympanic artery, enveloped by mucous membrane. We may say even now that this observation has stood the test of time whereas, as we shall see later, the concept of the posterior pouch has not. Several of the critical remarks that von Tröltsch made on the work of others, referred to above, were unfounded. The next step forward was made in St. Petersburg by the Russian otologist Prussak [3] who in 1867 described the superior pouch of the tympanic membrane. Prussak’s study testifies that astute anatomical observations with limited tools can lead to new, lasting discoveries. His description of the superior pouch, now known as Prussak’s space, essentially holds true today. Although Prussak accepted the concept of von Tröltsch [2] that the membrane forming the posterior pouch represented a duplicate of the fibrotic layer of the tympanic membrane, he questioned the idea of an anterosuperiorly blind pouch and started to search for an opening either into the tympanum, or over the malleus neck to the anterior pouch. His starting point was the observation that Shrapnell’s membrane was not fixed to the neck of the malleus but


that there was an air filled space between the two, which he then found to communicate with the posterior pouch. Prussak’s description of this superior pouch was very accurate as judged today. He described its limits as follows: (1) outwards as Shrapnell’s membrane, (2) inwards as the entire lateral surface of the neck of the malleus, (3) downwards as the upper surface of the short process of the malleus, (4) upwards as a ligament-like structure from the spina capitis malleis to margo tympanicus, (5) forward as a transverse, thin duplicate membrane from the malleus to the tympanic membrane while (6) posteriorly the space was open to the posterior pouch. A round-tipped probe could be introduced via the end portion of the posterior pouch and its progress followed into the superior pouch. Prussak was quick to find out that his discovery was not only important theoretically but that it also had clinical significance. Studying the temporal bones he noted that the superior pouch was full of thick mucus in many instances. If the mucus also filled the posterior pouch he noticed that it was much easier to remove the material from the posterior than from the superior pouch. As to its importance he theorized that if the mucus in the posterior pouch is disadvantageous to the movements of the tympanic membrane, it must be even more harmful to these vibrations if present in the superior pouch. Prussak’s description of the superior limit of the space was amplified in 1868 by Helmholtz [4], who gave a good description of the ligaments which serve to keep the malleus in position (fig. 1). The structure extending from the malleal spine to the lateral attic bone was shown to be a ligamental membrane as was suggested by Prussak. Helmholtz agreed that the superior pouch was in open connection with the posterior pouch and even pointed out that a defect in the lateral malleal ligamental fold would lead to a space we now call the lateral malleal space [8]. Furthermore, Helmholtz gave the name ‘posterior malleal ligament’ to the strong bundles of fibers leading fanwise from the neck of the malleus to the posterior tympanic spine, accompanied medially by the chorda tympani nerve. Touching the tough fibers with a needle caused a clear movement of the malleus whereas touching the soft fold portion along the chorda tympani nerve had no effect. It became thus clear that the criticism of von Tröltsch [2] of the work of Henle was unfounded, but it in no way affected his convictions. Prussak’s descriptions of the superior pouch gave rise to several comments by contemporary authors. In 1870, Politzer [9] observed connections not only from the superior pouch but also to the anterior pouch and in two temporal bones there was a connection superiorly, to a space

Fig. 1. Original sketch of the malleal ligaments by Helmholtz [4] from 1868. m = Malleus head; i = Incus; bi = tip of the incus short process; Tu. = tubal orifice; St. = stapes; M.st. = stapedius tendon; Ch.T = chorda tympani; T.t. = tensor tympani tendon and processus cochleariformis; f = superior bundles of the anterior malleal ligament; Sp.t. = anterior tympanic spine; e = anterior end of the lateral malleal ligament; g = the most posterior bundle of the same ligament, inserting to the posterior tympanic spine. Our major objection to this sketch is that the lateral malleal ligament is strong only anteriorly. The middle and posterior portions show separate, individual bundles and there thus appears a weak spot, at times even a membrane defect in the fold.

above the lateral malleal ligament. These observations were later confirmed by Hammar [5] in 1902 in a study of developmental histology of the middle ear compartments. Politzer [10] later proved the existence of the two different aeration pathways by pouring liquid mercury into Prussak’s space and observed it coming regularly out from the posterior pouch but occasionally also from the anterior pouch. In his initial publication concerning the superior pouch of Prussak, Politzer [9] reported upon ‘a system of spaces between the tympanic membrane and the neck of the malleus’ and presented a sketch of an elaborate network both inside Prussak’s space and superior to it, extending to the level of the malleus head. This picture (fig. 2) was based on a child’s temporal bone in which the superior pouch as well as the space above were noticed to have been filled with a yellow fluid. Politzer did not refer to this finding as pathological but we of course now recognize the condition as representing a secretory otitis media in which the organization of secretion in Prussak’s space was ongoing. Even if Politzer [10] in his textbook of 1908, in addition to this picture distorted by inflammation, presented two other,

1 Anatomy and Pathology of the Epitympanum

5

Fig. 2. Original sketch by Politzer [9] from 1870, showing Prussak’s space in a child. k = Processus brevis of the malleus; s = Shrapnell’s membrane from which a curved membrane arises crossing the space to the neck of the malleus; r = space arising inferior to the membrane, above which a network of spaces is situated, containing yellow fluid, up to the lateral malleal ligamental fold (m); t = anterior tympanic spine; f = inconstant folds lateral to the head of the malleus. This sketch in reality shows an organization process in the upper portion of Prussak’s space, apparently due to secretory otitis media, erroneously interpreted as normal Prussak’s space.

Fig. 3. A sketch on Prussak’s space by Politzer [10] from 1908. h = Head of the malleus; te = annulus tendinosus; b = processus brevis; u = umbo; t = chorda tympani; s = Shrapnell’s membrane; e = external (lateral) malleal ligament; ae = external attic; P = Prussak’s space; l = superior malleal ligament; c = vascular channel. The anatomical structures are correct but the dome of Prussak’s space is too low and the lateral malleal ligament too short.

normal pictures (fig. 3, 4), it is the picture representing pathological changes that many of our contemporary authors have reproduced as the sketch for Prussak’s space. This was seen e.g. in the book by Wullstein and Wullstein [11] who speculated on the important role of these ‘air cushions’, actually sequelae of inflammation in the lateral malleal space, in the mechanics of the middle ear. In 1995, Tos [12] no longer gave it a place in his manual, but several of his other sketches do not conform with Prussak’s original description.

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Fig. 4. Another sketch by Politzer [10] also from 1908 was based on his collection of temporal bones. ls = Superior malleal ligament; le = lateral malleal ligament; s = pars flaccida; o = Prussak’s space; t = tensor tympani tendon; r = network of spaces between the malleus head and the lateral attic bone. This sketch is accurate. Note that the network of spaces inside Prussak’s space is no longer present in figure 3 and here. In the lateral malleal space it has been reduced to one tissue strand, apparently a postinflammatory change.

In 1897 Siebenmann [1] summarized the main epitympanic compartments and presented two alternative pictures of the somewhat varying relationships. Figure 5 shows a still accurate representation of the posterior, superior and anterior pouches in relation to the lateral surface of the tympanic membrane. It is remarkable that he also presented here the anterior limit of the epitympanum, the tensor fold, even if it was drawn in both sketches as a vertical fold between the tensor tendon and the transverse crest. He thus also had a clear representation of the


Fig. 5. Siebenmann’s drawing [1] from 1897 of the compartmental anatomy of the attic and of the posterior, superior and anterior pouches (hintere, obere, vordere Trommelfelltaschen), and of the upper and lower lateral attics (oberer and unterer Hammer-Amboss-Schuppenraum). The tensor fold (horizontal arrow) between the anterior epitympanum and supratubal recess was named as plica transversa. Note that the transverse crest, the superior insertion of the fold, is correctly shallow, and that the web (oblique arrow) at the recess base is discontinuous, the supratubal space being part of the mesotympanum. The arrows were added by us.

supratubal recess, open to the mesotympanum and part of it. The discontinuous fold he showed near the tubal orifice appears to represent an inflammatory fold, probably arising due to a, at that time common, diphtheric infection in this ‘pneumatic cell’.

Fetal Development of Epitympanic Folds and Compartments The only study recording different phases of the development of the various soft tissue structures in the epitympanum, from a 3-mm embryo to the term fetus, was done in 1902 by Hammar [5] in Uppsala. He sectioned the temporal bone sagittally or frontally in 26 fetuses and made a model of each, recorded the findings in great detail and illustrated them by 67 drawings. This study is one of the classics in otology but a great deal of effort and concentration are necessary to read it, and being written in the German language it is unfortunately not available to the English-speaking research community. The discussion important for a clinician starts with the 190-mm embryo when Hammar described 4 air sacs, the anterior, medial, superior and posterior, which begin to replace the mesenchyme, starting anteriorly in the upper portion of the medial wall of the middle ear. Up to this stage of fetal development the bony middle ear space is filled only with the ossicles and mesenchyme, the embryonic connective tissue, except for a slit running from

the eustachian tube to the inferior part of the tympanic membrane. As the air sacs expand, more and more of the meso- and epitympanic bony cavities open until finally most of the embryonal tissue has disappeared and the epitympanic subcompartments formed. In this context we will not follow these processes in detail but first limit ourselves to single out one essential point. When the air sacs expand, the epithelium from the eustachian tube orifice expands covering the sac walls but loses its cilia and becomes thinner, endothelium-like with one cell layer. When a sac meets a fixed structure it provides it with mucosa and this is how the position-fixed structures, e.g. ligaments, are coated by epithelium. When an air sac meets a position-fixed structure of another type, e.g. the long process of the incus or the chorda tympani nerve, which can be passed on both sides, the sac divides into two, one portion continuing over the lateral, the other over the medial side of the obstacle. Having passed it the connective tissue surfaces of both sacs merge, the epithelium remaining on both sides of the common central layer. This is one of the ways in which the position-changing duplicate folds arise and during the fetal development they initially arise every time a structure is passed by two sides. The other way is when two air sacs approach each other from different directions: the meeting connective tissue sides merge, and the epithelium prevails on both sides. Large duplicate folds are likely to persist even if they sometimes show membrane defects. Small duplicate folds, however, may remain slender and


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tend to atrophy, due both to their thinness and to a loss of sufficient blood circulation. In a term fetus the number of duplicate folds becomes then less than that during the fetal development. We will, therefore, review Hammar’s work and his findings on the origin of the folds by discussing the final situation he described in his two models for term fetuses. We will limit ourselves only to reviewing those folds which at the same time have a major role in the compartmentalization of the attic. Those interested in the gradual development and atrophy of all different folds are referred to Hammar’s original publication [5]. There are two major duplicate folds that are present in neonates as well as in adults at nearly 100%, that is the tensor fold and the lateral incudomalleal fold. They both form important limiting structures in the epitympanum, the tensor fold separating the anterior epitympanum from the supratubal recess. The lateral incudomalleal fold divides the lateral attic into two subcompartments, the upper and lower lateral attics. The other duplicate folds show more variation in structure and have limited clinical importance. Tensor Fold The tensor fold results from the fusion of the anterior and medial air sacs when they have advanced sufficiently far to meet one another, the anterior air sac from the anterior direction and the medial air sac from the posterior direction. The anterior air sac, while enlarging, provides first the epithelium for the anterior malleal ligament which, as pointed out above, forms the medial border of the anterior pouch. The sac expands further, covers the tensor tendon and proceeds upwards and medially, replacing the embryonal mesenchyme. During this time the medial air sac has grown more posteriorly and its superior portion advances between the tensor tendon and the body of the long process of the incus. The space thus opening proceeds in two directions, one branch posteriorly and another superiorly. The latter provides the body of the incus and a portion of the malleus with epithelium and while advancing further, it meets the anterior air sac, merging with it and forming the tensor fold. The epithelium also covers the connective tissue between the medial side of the processus brevis of the malleus and the chorda tympani nerve which becomes embedded in the lateral border of the tensor fold. Lateral Incudomalleal Fold The structure that separates the upper and lower lateral attics differs from the tensor fold in that it combines the characteristics of both the ligamental and duplicate folds.

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Consequently, its posterior portion, consisting of the lateral portion of the posterior incudal ligamental fold, is much thicker than the larger anterior portion, the lateral incudomalleal fold. This is also the reason why the posterior ligamental portion is always present and has a constant position whereas the thin anterior portion is subject to changes typical of position-changing duplicate folds. The lateral incudomalleal fold is the result of a fusion of an upper and lower subexpansion of the medial air sac and normally the upper and lower lateral attics remain totally separate. The anterior portion of the fold, however, may be subject to some changes. If it is short and ends with a free edge, both lateral attics communicate anteriorly. If it turns upwards and inserts into the attic roof, it makes the upper lateral attic short and allows the lower lateral attic to communicate with the superior attic via the lateral malleal space. Chordal Fold The chordal fold is always present but may be very small and only envelopes the nerve. In the anterior tympanum the nerve is part of the major structure, the anterior malleal ligamental fold, and receives its mucosa from the advancing anterior air sac. In the posterior tympanum, specifically in the lower lateral attic, the advancing medial air sac provides the nerve with its fold which posteriorly could show a free edge or continue to the annular bone. Hammar [5] was, however, inclined to consider the chordal fold to be identical with the fold forming the posterior pouch because in a 330-mm fetus the formation of the posterior pouch fold and its union medially with the chordal fold seemed to occur simultaneously. Other Duplicate Folds All other folds have much less importance and most of them in Hammar’s study showed great variations and they were frequently absent in the term fetus. Thus for example the initial portion of the duplicate fold, arising when the long process of the incus was passed on both sides (forming ‘plica cruris longi incudis’) mostly disappeared before birth because the superior and medial air sacs ended, after the merge, with atrophy. Of the continuing end portions of the initial expansion of this branch of the medial and superior air sacs, the anterior, superior and posterior stapedial folds disappeared during the final period of fetal development while the fourth, the obturator fold, between the crura was sometimes present. The fold trailing after the superior malleal ligament also remained insignificant.


Tympanic Isthmus In a fetus of 285 mm length the expansion of both the medial and superior air sacs through the tympanic isthmus was distinct, both becoming narrow at this site and expanding again more superiorly. Discussing the 330mm-long fetus Hammar stressed that of the various epitympanic main compartments it was only the medial attic which via the tympanic isthmus is in direct communication with the tympanic cavity. Even if during the earlier stages the fold of the long process of incus and the stapedial folds appeared in the lateral portion of the isthmus, in the 360-mm fetuses only remnants were present and in the two term fetuses they all had atrophied leaving the isthmus fully open. Development of Prussak’s Space Prussak’s space appeared in the 330-mm fetus when a small opening continued anteriorly from the narrow superior end of the posterior pouch, starting the formation of the superior pouch. In a 360-mm fetus Prussak’s space was larger but it had originated from a different direction, a narrow passage from the anterior pouch. In two term fetuses the space was still small, originating in both from the posterior pouch, this time with a relatively large pathway.

Contemporary Concepts of the Anatomy of the Epitympanum We have reviewed the early studies at length because we would like to show that the pathways for the aeration and drainage of the epitympanic compartments were quite accurately known at the end of the 19th century. First, the wide route from the medial mesotympanum via the tympanic isthmus was known to aerate the large epitympanic compartments. Second, the separate narrow route from the lateral mesotympanum formed the aeration and drainage pathway via the posterior pouch to the small space of Prussak. Hammar [5] even stressed, commenting upon Siebenmann’s [1] finding of a membrane defect in the tensor fold, that through this defect the air spaces of the epitympanum and the mesotympanum became united with another aeration route, fully independent of the tympanic isthmus. The basic data on Prussak’s space, so accurately described by Prussak himself, became largely forgotten during the latter part of the 20th century and the contemporary detailed anatomic knowledge has not remained at the level set by the pioneers. Responsible for this was a publi-

cation by Proctor [13] in 1964 in which beautiful art work drawings beguiled the reader for decades into believing that the text on which they were based was of equal quality. Regarding the aeration of Prussak’s space Proctor states: ‘The entrance into Prussak’s space is usually located between the lateral malleolar fold and the lateral incudal fold.’ The basic mistake here is that Proctor did not seem to understand that the lateral incudomalleal duplicate fold and the lateral malleal ligamental fold are two different entities at different levels and not just one, as he instructed the artist to draw. In addition, he combined the qualities of a duplicate thin fold and those of a thicker ligamental fold to this single ‘lateral malleolar fold’. This led to another erroneous conclusion that the anterior limit of Prussak’s space would be formed by a ligamental fold instead of the thin duplicate membrane already observed by Prussak [3]. His sketch [14] in figure 108 implies that the aeration pathway would go from the upper lateral attic through the lateral incudomalleal fold which is superior to Prussak’s space and not in contact with it. In reality the floor of the lateral malleal space, consisting of the lateral malleal ligamental fold, is the intact roof of Prussak’s space. Even if the posterior pouch was accurately placed between the posterior malleal ligamental fold and the tympanic membrane, its role as the aeration pathway to Prussak’s space was not appreciated. Another misconception was, as mentioned above, the drawing of the roof of Prussak’s space as a half circle, the thick anterior end of the ‘lateral malleolar fold’ closing Prussak’s space anteriorly. This misconception was unfortunately also adopted from Proctor by Schuknecht and Guluya [15], who suggested that Prussak’s space is anteriorly closed by the lateral malleal ligament. However, as appears from the above review, from the days of Hammar [5] the frontal membrane of Prussak’s space is known to arise when the medial (or at times superior) air sac aerating Prussak’s space meets and merges with the advancing wall of the anterior air sac aerating the anterior pouch. It is thus a thin duplicate fold which can be verified as well during microdissection as from serial sections. Only the superior portions of Prussak’s space are anteriorly limited by the thick anterior and lateral malleal ligamental folds. We have earlier [16–21] pointed out several other erroneous statements in Proctor’s text regarding the major epitympanic compartments, but restrict ourselves here to stressing another major one regarding the tympanic isthmus. Proctor suggested that the isthmus should be anatomically divided into two portions, the ‘isthmus tympani anticus’ and ‘the isthmus tympani posticus’. The anterior


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isthmus was to be the larger and the fully open one, extending from the tensor tympani tendon to the stapes, while the smaller one in a large part closed posterior isthmus extended from the stapes to the pyramidal process. In plate 1 [13], a sketch of the normal arrangement of the floor of the attic as viewed from above, he instructed the artist to draw imaginary folds which blocked most of the ‘posterior isthmus’, leaving only a small opening near the tip of the incus. The legend states that ‘The mesotympanum is almost completely separated from the attic by the ossicular chain and mucosal folds’. This erroneous arrangement has been quoted over and over again in many later studies. If this nearly complete separation of the posterior portion of the tympanic isthmus were to be the case, nature would indeed have been a poor planner. In our temporal bone microdissections in mostly adult normal bones the tympanic isthmus appeared regularly as one large opening, without any blocking folds, from the tensor tendon to the anterior border of the medial portion of the posterior incudal ligament [16–21]. The stapes does not come to the level of the opening itself, and its articulation to the lenticular process of the incus is more inferior. Also Aimi [22, 23], who has done a large amount of microdissections and has tried to interpret his findings to agree with Proctor’s concepts, here deviated from them and suggested that the isthmus be regarded as one single open entity.

Material and Methods This atlas is based on the experience gained on temporal bone microdissection and serial sectioning. 125 microdissections were made at the Department of Otolaryngology, University of Helsinki, on temporal bones ranging from neonates to 80-year-olds. The temporal bones were removed with permission granted by the State Council of Patients’ Rights, allowing the use of the bones for research purposes. The major portion was obtained from the Forensic Institute of the university, which unfortunately meant that no data other than the persons’ age was allowed to be used. A smaller portion was obtained from the autopsies performed at the Subdivision of the University Department of Pediatric Pathology with access to the hospital records. The majority of bones were preserved in a deepfreezer and thawed in temperate water immediately before processing. A small portion was dissected fresh, directly from autopsy, and another small number was preserved in formalin until dissected. There was absolutely no difference between the methods in the preservation of the delicate thin folds and strands. Preservation in formalin, however, had caused the tissue to lose all of its natural color and luster and, therefore, was not used except in some badly infected ears. The basic method initially was the common horizontal dissection starting from the floor of the middle fossa, later complemented by anterior and lateral approaches. Documentation in each case was done by black

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and white or color photography, or both, using the operation microscope. For the actual microdissection of the temporal bone we currently use the following order of dissection. Anterior Dissection. After location of the anterior sulcus of the tympanic membrane, a frontal saw cut is made so that the cutting line goes across the bony eustachian tube a few millimeters anterior to the sulcus. The tubal opening, lateral to the large bony depression for the carotic artery, is enlarged by drilling until it makes possible a good evaluation of the structures in the mesotympanum, inferior to the epitympanic diaphragm, by the operation microscope. The specimen is then tilted to permit a view superiorly towards the supratubal recess. Observations and documentation can now be made of the anterior pouch up to the anterior membrane of Prussak’s space, medially to it of the bulk of the anterior malleal ligamental fold, and further medially of the supratubal recess and the tensor fold. If one wishes to proceed with a combined anterosuperior approach, careful bone removal by drilling is continued further along the tegmen over the insertion of the tensor fold to expose the anterior epitympanum, and if so decided, to uncover the entire epitympanum until the aditus ad antrum. Superior Dissection. After having completed the anterior approach the bone block is turned 180° so that an opening can be drilled on the middle fossa floor over the antrum, or aditus ad antrum, which offers an initial view of the posterior epitympanum. If the area around the tip of the short process of the incus appears normal, an island flap of bone is formed by drilling along the medial and lateral margins of the epitympanic cavity until the level of the head of the malleus is reached. A transversal drilling of bone is then made thinning it until its periosteum, when the bony flap can be gently lifted superiorly with a small hook under its posterior edge. The opening view is scrutinized to note any folds or strands that might unite the short process of the incus to the tegmental roof, and if so, documentation is made before disrupting them. If the initial view discloses signs of inflammation, the removal of the tegmental roof can be carried out in stages. Having examined and documented the structures in the posterior epitympanum in detail, drilling is carefully continued over the head of the malleus to expose the anterior epitympanum. This must proceed slowly so as not to disrupt the delicate folds often running from the superior malleal ligament, or from the medial side of the malleus, towards the transverse crest and the tensor fold. Here again the structures are observed and documented as they appear before removal of the bone and its periosteum would possibly distort the anatomy. The entire tensor fold with its insertion, and the position of the transverse crest can now be ascertained. Finally, after full removal of the tegmental bony roof, the soft tissue insertion ring of the tensor fold and the fold itself can be viewed as the only remaining structures between the anterior epitympanum and the supratubal recess. Lateral Posterior Dissection. The specimen is turned to the usual surgical position for tympanoplasty, a transverse cut is made to the ear canal skin 5 mm lateral to the annulus and the lateral canal skin removed. Together with the remaining skin of the ear canal, the tympanic membrane is lifted anteriorly until it is turned over the malleus handle and Shrapnell’s membrane displaced fully. Prussak’s space can now be observed and documented for the presence of fluid, mucosal strands and adhesions. The details of the anterior membrane are recorded when it is observed over the short process and neck of the malleus, even if a full view cannot be obtained from this direction. Whenever in doubt, a needle is put through the membrane


and its tip observed from the anterior approach. Anterior observation following a simple short incision is not sufficient because in membranes thicker than normal the incision edges become almost immediately approximated and the membrane may appear intact. The tensor tendon, running from the neck of the malleus, is next looked for, but it remains mostly hidden and only its insertion near the cochleariform process may be seen. The malleus head is then cut with the malleus head nipper which is gently introduced sideways between the long process of the incus and the handle of the malleus and then turned 90° to allow the lower jaw to slip under the malleus neck. The line of cutting is medial to the tensor tendon which remains attached to the malleus handle. A portion or all of the anterior malleal ligament should be left attached to the head of the malleus to allow it to keep its position. Using a pick to turn the handle of the malleus and the tendon laterally exposes the tensor fold which now can be removed by sickle knife and/or microforceps, to simulate clinical removal by laser evaporation. If the malleus head keeps its place, the cut edge of the handle is approximated with the malleus head and the tympanic membrane repositioned. If the malleus head becomes dislodged by lifting the malleus handle laterally, when the anterior malleal ligament remained attached partially to both, the head is removed with microforceps and refashioned to be placed on the long process of the incus as a riding columella [24]. This gives good practise for teaching purposes in simulating the clinical procedure. Initially [20] we also used the lateral anterior dissection which was based on the anterior tympanotomy used in the early 1960s for enlarging the anterior mesotympanic air space in ears with an adhesive otitis media [25], and later for repairing anterior perforations of the tympanic membrane [26]. This approach in its extended form is started by a canal skin incision 5 mm lateral to the sulcus and the anterior half of the tympanic membrane is dissected free and together with the canal skin turned over the malleus handle. For greater freedom of anatomic evaluation in microdissection, the anterior ear canal bone and lateral skin can be removed at the beginning, allowing a good view of the anterior half of the tympanic membrane. This exposure gives a direct view of the tensor tympani tendon and of a low portion of the tensor fold. Bone removal at the lateral attic margin opens the anterior epitympanum and discloses the anterior portion of the head of the malleus superior to the anterior malleal ligament. A portion of the shallow transverse crest of the tegmen can always be made visible. Further removal of bone anteriorly opens the supratubal recess, but the anterior tympanic spine and the anterior malleal ligament with structures within obscure the upper portion of the tensor fold and its insertion. Their removal destroys the anatomy and we no longer include this approach in the regular microdissections. Nevertheless, the first steps of this approach, when applied as a regular anterior tympanotomy, give a surgeon under training the ability to repair anterior tympanic membrane perforations with confidence. The majority of the material for serial sections derives from the collection of the Temporal Bone Foundation, Boston, Mass. consisting totally of 256 serially sectioned temporal bones from neonates and infants. A smaller sample of 28 temporal bones was available at the University of Helsinki. The preparation of temporal bones for horizontal serial sectioning after fixation in 10% formalin was done in a routine fashion and described earlier [27]. The sections were cut to 20 Ìm thickness, every 10th section saved, and stained by hematoxylin-eosin, alternately by van Gieson’s, and a few specimens with Masson’s trichrome. All sections were studied by microscopy and

alterations in various compartments recorded. Additionally, in the Temporal Bone Foundation material, scanned colored images, using a Polaroid Sprintscan 35 Plus, were printed out and allowed easy side by side recognition of the magnified compartment boundaries. The height of various spaces and structures was determined from the numbered sections, each 20 Ìm with an interval of 0.2 mm. Horizontal and vertical widths of a single section were measured directly from the microscope by using a measure (Graticules, Tonbridge, UK), divided into 100 lines, in one of the oculars. We [16–20, 27] have earlier used varying ways of presenting the printed serial sections and in this Atlas we follow the method adopted in our two latest publications [28, 29]. We view the left and right sides similarly to an otologist examining the tympanic membrane. The lateral side of the temporal bone section of either ear is thus the lower side of the picture, in the right ear the anterior portion is pointing to the right and in the left ear the anterior portion is pointing to the left. In addition to the figures given for magnification, several photographs contain also a horizontal 1-mm bar which makes, if so desired, an immediate measuring of the size of the structures rapid.

Anatomy and Pathology of the Epitympanum and Supratubal Recess Epitympanic Diaphragm In 1946 Chatellier and Lemoine [30] published a histological study of the newborn and introduced the term interatticotympanic diaphragm, which we simply called the epitympanic diaphragm [8]. They studied it from frontal serial sections and found that it consists, in addition to the thin tensor and lateral incudomalleal folds, of the thick structures formed by the malleal and incudal ligamental folds and of the ossicles themselves. It was also stated that Prussak’s space is situated inferiorly to the diaphragm, its roof, the lateral malleal ligamental fold, being the dividing structure. Chatellier and Lemoine linked their anatomic study to clinically important aspects encountered in treating patients with complications of acute otitis media. We presented earlier [8] a sketch of the epitympanic diaphragm that was based upon serial sections of temporal bone. In addition to the ligamental folds it included only two major duplicate folds, the tensor fold and the lateral incudomalleal fold, and this sketch was later found to be consistent with the findings in microdissection. We make, however, two alterations to the nomenclature and to the concepts based on subsequent work. We called, according to the then prevailing literature, the space anterior to the malleus head ‘protympanic recess’ but later, when our detailed microdissection work progressed, we adopted the natural term ‘anterior epitympanum’ as the correct one. The anterior epitympanum is fully open to the medial attic, the head of the malleus being the struc-


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Normal Anatomy of Prussak’s Space (with the Lateral Malleal Space)

Fig. 6. Sketch of the epitympanic diaphragm of the right ear. 1 = Anterior attic bone; 2 = tensor fold; 3 = petrotympanic fissure; 4 = chorda tympani nerve; 5 = anterior malleal ligament; 6 = anterior tympanic spine; 7 = strong portion of the lateral malleal ligament; 8 = tensor tympani tendon; 9 = weak portion of the lateral malleal ligament; 10 = neck of the malleus; 11 = lateral incudomalleal fold; 12 = incus; 13 = stapes; 14 = tympanic isthmus; 15 = posterior incudal ligament; 16 = inconsistent aeration pathway via the incudal fossa.

ture that narrows the space posteriorly. The posterior epitympanum, the larger compartment, houses both the medial attic as well as the upper and lower lateral attics. Its superior subcompartment, between the upper surface of the ossicles malleus and incus, and the tegmental roof, is an open space up to the mastoid antrum. As we strongly objected to Proctor’s concept [13] of dividing the tympanic isthmus into two portions, the anterior and posterior isthmus, and considered the tympanic isthmus to be one single entity calling it the ‘anterior tympanic isthmus’, we gave the name ‘posterior tympanic isthmus’ to a pathway behind the tip of the incus. Later we dropped the word ‘anterior’ from the main aeration pathway to the attic and called it, as the 19th century authors did, the tympanic isthmus. The posterior tympanic isthmus behind the incus tip proved to be so inconstant and small that we will refer to it now as an inconsistent auxiliary aeration pathway via the incudal fossa. Figure 6 shows the modified sketch of the epitympanic diaphragm which is now turned 180° in order to conform with the presentation of serial sections. Actual documents on which this sketch is based are seen among the figures dealing with superior microdissection and horizontal serial sections (for example fig. 33, 44 and 46).

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Even if Prussak’s space forms an inseparable part of the epitympanum, from the aeration and drainage point of view it is an independent unit. It can be blocked or obliterated without any influence as such on the workings of the major compartments superior to the epitympanic diaphragm, the anterior and posterior epitympanum, aditus ad antrum, and the mastoid air cell system. On the other hand, a blockage of the tympanic isthmus causes extensive pathology in all the above-mentioned compartments and seriously impairs the middle ear function. In the discussion of the anatomy of Prussak’s space, however, we also comment on one portion of the posterior epitympanum, namely the lateral malleal space since its floor is also the roof of Prussak’s space. Microdissection Lateral Malleal Space. In our initial discussion of the epitympanic compartments [8] we gave the name ‘lateral malleal space’ to a distinct anatomic area well separable from the other subcompartments of the epitympanum. When the island bone flap is lifted in the superior microdissection, it reveals the lateral incudomalleal fold and the tympanic isthmus, but not yet the lateral malleal space. When bone is removed over the head of the malleus, a view opens to the lateral malleal space. The space is limited medially by the malleus head and neck and laterally by the lateral attic bony wall. Anteriorly its boundaries are formed by the inconstant anterior malleal suspensory ligament and inferior to it, by the anterior malleal ligamental fold, described already by von Tröltsch [2]. Its ligamental portion, originating in the malleus neck, contains, in addition to the strong ligament, the long process of the malleus, the chorda tympani nerve and the inferior tympanic artery. The structure broadens inferiorly and leads to the anterior tympanic spine and towards the petrotympanic fissure. The posterior limit is formed superiorly by the downturning anterior end of the lateral incudomalleal fold and the posterior malleal ligamental fold. As the latter fold also becomes broader inferiorly, the lateral malleal space becomes bowl-shaped near its floor, which is formed by the lateral malleal ligamental fold, posteriorly frequently devoid of ligamental bundles (fig. 7). The lateral malleal space is regularly open superiorly to the upper lateral attic, but in rare cases the incudomalleal fold may extend over the entire space. As the fold in such cases does not turn down and unite with the posterior


Fig. 7. Series G, adult case 55, right ear. Superior view of the lateral malleal space between the malleus head (M) and the lateral attic bone (B). The space is anteriorly limited by the anterior malleal ligamental fold (horizontal arrow). The downgoing portion of the lateral incudomalleal fold (vertical arrow) forms the superior portion of the posterior limit. The anterior portion of the floor is thick, the posterior portion is thin and contains a weak spot (curved arrow) limited by separate, whitish ligamental bundles. I = Incus.

Fig. 8. Series G, adult case 14, right ear. Superior view of the lateral malleal space after removal of the lateral incudomalleal fold, uniting the lateral attics (curved arrow). The anterior limit, the anterior malleal ligamental fold (A), inserts into the anterior tympanic spine (S); the low posterior limit is formed by the posterior malleal ligamental fold (vertical arrow). The strong lateral malleal ligamental fold (oblique arrow) forms the larger portion of the floor which posteriorly has a membrane defect (horizontal arrow). The inner blade of the posterior pouch (open arrow) is inferiorly united with the chorda tympani nerve (C). M = Malleus; I = incus; B = lateral attic bone; T = tensor tendon.

malleal ligamental fold, the lateral malleal space remains in direct communication with the lower lateral attic. As already pointed out by Hammar [5], the interconnections of the lateral malleal space and the upper and lower lateral attics show considerable variation. In no case, however, is the lateral malleal space entirely closed because it receives aeration from one of the adjoining spaces. The mucosa of the lateral malleal space, while descending towards the floor, becomes often thicker and undulating and does not seem to cover the structures tightly as is more the case at the superior portions. This apparently is related to the necessity of the mucosa to move freely, together with the nearly continuous movements of the malleus. The floor is not even but shows local areas that extend deeper towards Prussak’s space than the adjacent portions (fig. 7). The floor of the lateral malleal space, the roof of Prussak’s space, is subject to great variations in thickness. In all dissected bones the anterior portion has always been the thickest due to the thick bundles of the lateral malleal ligament. More posteriorly the ligament is much weaker and individual separate bundles may be seen as transparent whitish structures through the covering epithelium. The floor often shows a weak area posteriorly (fig. 7) and

in about 6% of our total material a membrane defect connected the lateral malleal space to Prussak’s space (fig. 8, 9). The lateral malleal ligamental fold, the roof of Prussak’s space, is not a curved half circle-type structure as indicated by Proctor [13, 14] but more or less horizontal, as shown already by Helmholtz (fig. 1). Prussak’s Space. Part of the walls of Prussak’s space are bone, like the neck and the short process of the malleus, forming medial and inferior walls, respectively. The soft walls show some variability in size and shape, even if the structures are basically similar. The roof, discussed already above, shows a similar unevenness as the floor of the lateral malleal space, so that a certain portion of the roof extends in a dome-like form more superiorly than the main roof. When the roof of Prussak’s space is opened from above, or if a membrane defect allows a view of the inside of the space, the first structure seen is the round horizontal portion of the neck of the malleus (fig. 9). By viewing anterosuperiorly past the neck of the malleus, and turning the anterior end of the specimen slightly medially, a portion of the thin anterior membrane of Prussak’s space is revealed (fig. 10). However, this approach does not allow a full view of its inferior portion. Viewing along the neck


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Fig. 9. Series G, adult case 11, left ear, superior view. A central membrane defect in the floor of the lateral malleal space allows a view of Prussak’s space, where the neck (horizontal arrow) of the malleus (M) is seen. The anterior malleal ligament (A) leads to the petrotympanic fissure, the chorda tympani nerve (C) emerges to join the ligament. The thin tensor fold anterior to the tensor tendon (T) has a membrane defect. The oblique arrow points to the superior portion of the posterior malleal ligamental fold. I = Incus; S = stapes, on both sides of it is the tympanic isthmus.

Fig. 11. Series A, adult case 19, left ear, superior view after removal of the incus. A probe has been inserted through the floor of the lateral malleal space to Prussak’s space and along the posterior pouch, between the posterior malleal ligamental fold (horizontal arrow) and the tympanic membrane, down to the mesotympanum. The chorda tympani nerve (C) runs along the inferior edge of the posterior pouch. M = Malleus head.

in the posterior direction makes the regular aeration pathway via the posterior pouch visible. However, if one wants to see the entire aeration pathway to the posterior pouch, some tissue destruction is bound to occur. A round probe can be passed via the posterior upper portion of Prussak’s space and it becomes visible at the lowest por-

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Fig. 10. Series A, adult case 13, right ear, superior view. A large portion of the roof of Prussak’s space and the incus have been removed, the neck (horizontal arrow) of the malleus (M) appears. The upper portion of the anterior membrane of Prussak’s space (oblique arrow) is seen inferior to the anterior malleal ligamental fold (A). The superior portion of the aeration pathway (open arrow) leads to the posterior pouch, formed medially by the posterior malleal ligamental fold (vertical arrow) and laterally by the tympanic membrane

tion of the pouch, between it and the tympanic membrane (fig. 11). The anterior membrane of Prussak’s space can best be viewed with the anterior microdissection approach. The translucent membrane, a distinct oval structure around 1 mm in diameter, appears in the superior aspect of the anterior pouch (fig. 12). It is inserted laterally to the tympanic membrane and medially to the anterior portion of the malleus neck. In teaching the anterior approach we have noted how effectively this view, hitherto unused, helps both the training surgeon as well as the specialist to understand Prussak’s space better. Rarely there is no anterior membrane (fig. 13), and Prussak’s space in such cases has developed embryologically from the anterior pouch, which then functions as the aeration and drainage pathway. This infrequent occurrence, as may be remembered, was already observed by Hammar [5] and by Politzer [10]. Both the lateral anterior and posterior dissections give an excellent view of Shrapnell’s membrane and allow one to ascertain its thickness as well as the presence of secretion and possible adhesions to the neck of the malleus. A portion of the roof of Prussak’s space superiorly can be observed, and in the lateral anterior dissection the inferior portion of the tensor fold is also seen (fig. 14). The posterior approach allows a limited view of the anterior mem-


Fig. 12. Series P, case 11, a child aged 2 years, left ear, anterior microdissection. The thin, translucent anterior membrane (vertical arrow) of Prussak’s space appears superior to the handle of the malleus (M) and medial to the tympanic membrane (TM). The membrane contains no ligamental fibers which sometimes extend to it from the tensor tendon.

Fig. 13. Series A, adult case 22, right ear, anterior microdissection. The anterior membrane of Prussak’s space above the handle of the malleus (M) is absent (vertical arrow). This route rarely serves as the aeration and drainage pathway to Prussak’s space. TM = Tympanic membrane; A = anterior malleal ligamental fold; C = chorda tympani nerve. A horizontal arrow points to the supratubal recess.

brane. In the lateral posterior dissection the posterior pouch gets turned away together with the tympanic membrane and cannot be observed in its natural position. Serial Sections Floor of the Lateral Malleal Space (Roof of Prussak’s Space). In a section across the superior portion of the lateral malleal space well above its floor, the anterior wall consisting of the upper portion of the anterior malleal ligamental fold is relatively thin but thicker than the upper portion of the posterior wall which consists only of the downward turning thin lateral incudomalleal fold (fig. 15a). Sections further down show stronger bundles of the anterior malleal ligamental fold while the posterior wall remains thin or may, as in the ear shown, end before reaching the posterior malleal ligamental fold (fig. 15b). Thus in this case the lower lateral attic and the lateral malleal space became united. Further sections showed the weaker bundles of the lateral malleal ligament, adjacent to the strong anterior malleal ligament, to spread from the malleus neck to the opposite lateral attic wall, thus forming the resistant anterior half of the floor. When the dome of Prussak’s space made its appearance the lateral malleal ligamental bundles were still present anteriorly (fig. 15c). Shrapnell’s Membrane. We limit ourselves in this connection only to the observation that Shrapnell’s membrane (fig. 15d) is also subject to a considerable variation in size and in structure. It may be very small when most

Fig. 14. Series A, adult case 7, left ear. Lateral anterior approach. The tympanic membrane (TM) has been detached from the anterior sulcus and turned posteriorly together with Shrapnell’s membrane. Prussak’s space (horizontal arrow) appears superior to the short process of the malleus (M) and extends superiorly past the rim of the lateral attic bone (B). This lateral anterior approach provides a view of the low portion of the tensor fold (curved arrow).

parts of Prussak’s space are situated above the bony rim of the attic bone where the membrane has its insertion. At times it is large, covering a sizeable Prussak’s space under the bony rim. Both these situations were well illustrated also by Politzer [10] in 1908 (fig. 3, 4). Even normally the covering epidermis may show distinct changes, the papil-


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Fig. 15. Adult patient, otosclerosis, right ear. Sections across the lateral malleal space (L) and Prussak’s space (P). a Upper portion of the lateral malleal space is limited by the anterior malleal ligamental fold (oblique arrow), the downgoing portion of the lateral incudomalleal fold (horizontal arrow), the malleus (M), and the lateral attic bone (B). b The middle portion shows a membrane defect (horizontal arrows) which connects the lateral malleal space with the lower lateral attic (LL). The first bundles of the lateral malleal ligament (oblique arrow) appear. c The strong lateral malleal ligament from malleus to the anterior tympanic spine (AS) forms the anterior portion of the

roof of Prussak’s space. Posteriorly the section goes across the dome of Prussak’s space. A vertical arrow points to the upper portion of Shrapnell’s membrane, its epidermal layer is artifactually absent. d The low portion of Prussak’s space is continuous with the wide open posterior pouch (PP). The posterior malleal ligament (vertical arrow) goes from the neck of the malleus to the posterior tympanic spine (PS). A horizontal arrow points to the anterior membrane of Prussak’s space. TM = Tympanic membrane; I = incus; T = tensor tendon; C = chorda tympani nerve. Hematoxylin-eosin stain. Magnification !28 (a–c), !12 (d).

lae at times being short and inactive, sometimes long and active, looking capable of deeper invasion towards the basal cell layer. Anterior Membrane of Prussak’s Space. This frontal wall, limiting Prussak’s space anteriorly, arises as a duplicate fold when the anterior air sac, advancing posteriorly, meets the expanding projection of either the medial or superior air sac, advancing anteriorly and forming Prussak’s space. The membrane fastens laterally to the tympanic membrane and medially regularly to the anterior portions of the malleus neck, or anterior to it, to the tensor

tendon. Being a duplicate fold it is thin, consisting of a tiny connective tissue core with the surface constituted by a one-cell layer epithelium on both sides. Sometimes it extends past the neck of the malleus to the tensor tendon (fig. 15d, 16) and in such cases a few collagen fibers from the tensor tendon may extend even up to the tympanic membrane. It should be stressed once more that this anterior membrane is a separate structure of its own and in no way part of the lateral malleal ligamental fold as indicated in Proctor’s sketches [13, 14].

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Fig. 16. The anterior membrane of Prussak’s space shown at a lower level of magnification in figure 15d. Laterally the membrane is thin with a flat one-cell layer epithelium, medially a collagen bundle (arrow) from the tensor tendon fortifies the membrane. P = Prussak’s space, A = anterior pouch, TM = tympanic membrane, M = malleus. Hematoxylin eosin stain. Magnification !80.

Aeration Pathways to Prussak’s Space. Examination of the histological slides depicting Prussak’s space and its adjacent tissues section by section is the only way of defining the aeration and drainage pathways satisfactorily. Initially we [16] thought that the posterior pouch is the highly dominant pathway, as initially noted by Prussak [3] and by Politzer [9], but later found out [31, 32] that aeration and drainage pathways could also go directly to the lower lateral attic and mesotympanum. Therefore, we recently analyzed 55 temporal bones to obtain an idea of the importance and frequency of different pathways in the aeration and drainage of Prussak’s space [29]. It appeared that the posterior pouch as a definite structure was present in all examined ears. However, it functioned as the aeration and drainage pathway to Prussak’s space only in 62% of the ears and in 38% of the ears it formed a superiorly blind space. In the latter group it thus did not communicate with Prussak’s space. Before ending superiorly it became a slit which further inferiorly opened up to form a shorter or longer pouch between the tympanic membrane and the posterior malleal ligamental fold. In both groups it showed a considerable variation as to its height and width and to its relation to the chorda tympani nerve. Figure 17 shows a composite picture of the regular type of Prussak’s space aeration via the posterior pouch. Prussak’s space (fig. 17a) moves first posterior to the malleus, becoming the superior portion of the posterior pouch

(fig. 17b). This roundish space widens after a few sections to its full size occupying the entire area from the malleus to the posterior tympanic spine (fig. 17c). The height of the pouch varied [29] from 0.5 to 2.4 mm and the greatest width anteroposteriorly, towards the posterior tympanic spine, from 1.6 to 3.2 mm. The tympanic membrane inserted in most instances into the lateral edge of the spine, or into the bony annulus, continuing directly as the skin of the ear canal (fig. 17c). The pouch in the case shown ended in the mesotympanum a few sections later (fig. 17d). In some cases the pouch extended even 1.5 mm past the annular rim, the tympanic membrane joining there the skin of the ear canal (in fig. 23d). The chorda tympani nerve was generally separate of the pouch in the anterior half but posteriorly joined it frequently (fig. 17d) and entered its bony canal adjacent to the insertion of the fold. In some cases the chorda with its fold was separate from the fold during its entire course across the tympanum [29]. Fig. 18 shows a composite picture of the direct aeration pathway from Prussak’s space to the lower lateral attic and mesotympanum, found in 32% of the specimens [29]. This route is short, Prussak’s space has just moved posterior to the malleus (fig. 18a) when in the next sections it opens to the large lower lateral attic and mesotympanic space adjacent to the handle of the malleus (fig. 18b). The blind posterior pouch started more inferiorly (fig. 18c), accompanied by the chorda tympani nerve. The short pouch opened a few sections later to the mesotympanum (fig. 18d). In a few ears we have seen a combination of the above described two main arrangements [29]. There was a defect in the membranous section of the posterior pouch, leading to the lower lateral attic and mesotympanum, even if the regular posterior pouch also continued as far as the mesotympanum. This defect measured 0.6 mm and clearly functioned as part of the drainage route. The most infrequent type of aeration pathway from Prussak’s space leads to the anterior pouch. In the serial sections we have once also observed a communication through the roof of Prussak’s space to the lateral malleal space. Examples of these are presented in figures 25 and 26 in the section of pathological changes in the aeration pathways of Prussak’s space. Our finding of the occurrence of the superiorly blind posterior pouches might be the reason why von Tröltsch [2] never discovered the superior pouch. There is no mention of the number of cases he had studied, but they probably were not very many as he referred to his initial 1856 congress report as the only data of the pouch in the text-


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Fig. 17. Series P, a child aged 4 years, left ear. Sections across Prussak’s space (P) and posterior pouch (PP). a Prussak’s space at the level of the superior portion of Shrapnell’s membrane (SM). The posterior malleal ligament (oblique arrow) connects malleus (M) to the posterior spine (S). The anterior pouch (AP) contains secretion devoid of cells. b The posterior pouch (oblique arrow) appears behind the malleus, the chorda tympani nerve (C) is medial to it. The thick ligament (vertical arrow) is united with the tympanic mem-

brane. c The pouch is fully open between the malleus and the spine. The ligament (vertical arrow) is thin. Chorda tympani nerve (oblique arrow) is posterior to the malleus separate from the pouch. d The pouch is open to mesotympanum, the chorda has joined the medial surface of the pouch. Pars tensa fastens to the annular bone, slightly past the spine. I = Long process of the incus. The height of the aeration pathway was 1.4 mm. Hematoxylin-eosin stain. Magnification !20.

book from 1881. It might be that all of them happened to be those in which the pouch ended blindly and von Tröltsch thus had no chance of finding the connection. The documents shown of the normal aeration and drainage pathways of Prussak’s space by both microdissection and by serial sections leave no place for speculation. The two pathways, one via the posterior pouch and another directly to the lower lateral attic and mesotympanum, are the norm and slight deviations along these routes may occur. The routes to the anterior pouch, or through the lateral malleal ligamental fold are rare, facts already noted by the early investigators [4, 5, 10]. The misconception that Prussak’s space is aerated from be-

tween the ‘lateral incudal and lateral malleolar folds’ advocated by Proctor [13, 14] has not been documented and is not realistic.

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Pathology of Prussak’s Space and the Lateral Malleal Space Inflammation of the middle ear, be it caused by viruses, bacteria or foreign body-type noninfectious agents, spreads to all spaces interconnected by the aeration pathways. There is no anatomic obstacle between the upper mesotympanum, the lower lateral attic and the orif-


Fig. 18. Case A89-295, Temporal Bone Foundation, a child 15 months of age, left ear. Aeration pathway to Prussak’s space from the mesotympanum directly via the lower lateral attic. a Section 211. The pathway from a 0.8-mm-high Prussak’s space has moved posterior to the malleus (M) where it measures 0.8 ! 1.1 mm and is inferiorly open to the lower lateral attic (L) and mesotympanum. The chorda (C) is connected to the posterior malleal ligamental fold (oblique arrow) . b A section 0.3 mm inferior to a. The pathway is also medially open to the mesotympanum (vertical arrow), the chorda remains

connected to the tympanic membrane. The height of the aeration pathway is only 0.4 mm. c A section 0.8 mm inferior to b. A slit-like posterior pouch appears in the tympanic membrane, measures 1.6 ! 0.1 mm, the pouch wall contains a ligament bundle (oblique arrow), the chorda is connected to it with a short pedicle. d A section 0.1 mm inferior to c. Anterior portion of the pouch is open (vertical arrow) to the mesotympanum, the chorda remains posteriorly connected to it. The pouch height was only 0.5 mm. I = Long process of incus; T = tensor tendon. Hematoxylin-eosin stain. Magnification !10.

ice of the posterior pouch, and thus the route is open via these regular aeration pathways to Prussak’s space. Similarly, if Prussak’s space is aerated from the anterior pouch, the route for the spread of infection is both short and wide. If there is an open communication between Prussak’s space and the lateral malleal space, inflammatory agents can spread in either direction. In acute otitis media the congested mucosa may temporarily occlude these communications, leading to absorption of air from Prussak’s space. In acute infection, changes in the pars tensa are so marked that they often mask those occurring in the small Shrapnell’s membrane. There are no generally applicable

data of the frequency of these changes which occasionally are noted either as indrawing or bulging of the membrane. Perforation of Shrapnell’s membrane due to severe infection in Prussak’s space is very rare as a result of the escape route for pus via the posterior pouch or even easier via the lower lateral attic. Even if these routes were blocked, the thin limiting anterior membrane, or the weak point in the lateral malleal ligamental fold, would be much more likely to break than the relatively thick Shrapnell’s membrane, conducting pus from Prussak’s space into either the anterior pouch or the lateral malleal space.


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Fig. 19. Series P, case 2, a child aged 2 years, left ear, superior lateral view. The mucosa of the lateral malleal space (L) is edematous and red, similarly to the downgoing portion of the lateral incudomalleal fold (vertical arrow). There is granulation tissue on the anterior malleal ligamental fold (A). The tympanic isthmus (horizontal arrow) contains secretion and inflammatory strands. T = Tensor tendon; M = malleus; I = incus; B = lateral attic bone.

Fig. 20. Series G, adult case 17, right ear, superior view. The entire epitympanum contained blood-stained secretion which is still present in the tympanic isthmus (horizontal arrows) on both sides of the stapes (S). The large thin floor of the lateral malleal space (oblique arrow) is retracted, and secretion around the neck of the malleus is dimly seen through the membrane. The lateral incudomalleal fold (curved arrow) is thin and intact. M = Malleus; I = incus; A = anterior tympanic spine; T = tensor tendon.

Fig. 21. Series G, adult case 12, right ear, superior view after removal of the incus. The roof of Prussak’s space lateral to the head of the malleus (M) has been opened, revealing slimy secretion with a few strands of granulation tissue (horizontal arrow). The sucker touches the anterosuperior edge of the posterior malleal ligamental fold which shows both ligament bundles and thin membranous areas (oblique arrow) and is united with the chorda tympani nerve (C). A small portion of the anterior membrane of Prussak’s space (curved arrow) appears in front of the neck of the malleus. S = Stapes.

Fig. 22. Series G, adult case 16, left ear, superior view after removal of the incus. Prussak’s space (horizontal arrow) is filled with secretion and granulation tissue. The posterior malleal ligament bundles (asterisks) show a fanwise spread, starting from the malleus (M) and inserting into the annular bone (B) and the posterior tympanic spine. The membrane between the bundles is thin, the chorda tympani nerve (C) runs in the inferomedial edge of the ligamental fold. A large inflammatory web partly obstructing the tympanic isthmus extends to various directions from the head of the stapes (S). A = Anterior malleal ligamental fold; T = tensor tendon.

Microdissection In superior microdissection the lateral malleal space frequently shows secretion on its floor, with a resulting inflammation of the covering mucosa (fig. 19). Changes in its basic structure do not appear as neither under- nor

overpressure can change the position of the three strong position-fixed malleal ligamental folds forming its borders. What can be observed frequently is a marked retraction of the lateral incudomalleal fold drawing its inferiorly directed anterior portion even below the level of the floor

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Fig. 23. Case A91-01, Temporal Bone Foundation, a child aged 23 months, left ear. Aeration pathway to Prussak’s space (P) via a large posterior pouch (PP). a Section 262. Prussak’s space, 0.9 mm high, measures 1.1 ! 0.9 mm, the anterior membrane separates it from the secretion-filled anterior pouch (AP). A thin membrane (oblique arrow) limits the changeover to the upper portion of the posterior pouch. The 1.8-mm-long posterior malleal ligamental fold starts from the malleus neck (M) towards the posterior tympanic spine. The chorda (C) is medial to the malleus. b A section 0.9 mm inferior to a. The posterior pouch measures 2.2 ! 1.3 mm, its medial wall is without ligamental fibers (oblique arrow) and inserts to the spine (S) and

past it. c A section 1 mm inferior to b. The pouch measures 2.8 ! 0.7 mm and extends for 1.3 mm on the annular bone (B). A ligament bundle (vertical arrow) is seen in the posterior portion of the fold, the chorda is united with it. d A section 1 mm inferior to c. The pouch is open to the mesotympanum (oblique arrow), a space remains between the tympanic membrane and the annular bone. The chorda enters its bony canal. The height of the pouch was 2.4 mm. This regular aeration pathway was filled throughout with secretion and a few clusters of round cells. Hematoxylin-eosin stain. Magnification !20.

of the lateral malleal space. If the floor contains a larger weak area, this thin portion is in such cases retracted towards the neck of the malleus into Prussak’s space (fig. 20). When the entire epitympanum shows granulation tissue the lateral malleal space shows similar involvement. In chronic infections, as soon as the roof of Prussak’s space is opened, a mucoid fluid is frequently seen (fig. 21). In the secretion there may be strands of granulation tissue crossing and partially filling the space (fig. 22). These changes are observed similarly in the lateral approach via the posterior tympanotomy. If a full obliteration of Prus-

sak’s space has occurred, Shrapnell’s membrane being united with the neck of the malleus, this can be ascertained by microdissection, but the information is meagre as compared to serial sections. Serial Sections In our entire temporal bone material with chronic inflammatory pathology there has been one constant finding both in adults and children, that is the accumulation of inflammation products in the lower lateral attic. The latter together with the superior and posterior mesotympanum attracts both amniotic fluid cellular content


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Fig. 24. Case A89-120, Temporal Bone Foundation, an infant 5 months of age, right ear. Aeration pathway from the lower lateral attic (L). a Prussak’s space (P) contains secretion and an end portion of an epithelialized polyp (oblique arrow). The inflamed anterior membrane (horizontal arrow) separates Prussak’s space from the anterior pouch (AP) which contains a nonepithelialized polyp (vertical arrow). b Section 0.4 mm inferior to a. Prussak’s space opens with a large pathway to the lower lateral attic, the central portion of the epithelialized granulation tissue (horizontal arrow) extends along the

malleus (M) to Prussak’s space. c Section 1.4 mm inferior to b. The large, superiorly blind posterior pouch (PP) contains secretion and fills the entire area between malleus and the posterior tympanic spine (S), ligamental bundles (vertical arrow) appear. The chorda (C) is separate from the medial pouch wall. d Section 0.4 mm inferior to c. The posterior pouch opens (oblique arrow) to the mesotympanum, large epithelialized granulation tissue surrounds the chorda, separate from the pouch until the end. Hematoxylin-eosin stain. Magnification !20.

(AFCC) in the neonates [31] as well as sticky mucus with inflammatory cells in older children and adults [8, 31– 33]. The early authors, including Prussak [3] and Politzer [9] already noted that Prussak’s space may be filled with the same thick mucus that was seen in the lower lateral attic and in the posterior pouch. A permanent block of aeration to Prussak’s space results in a retraction of Shrapnell’s membrane and organization of the secretion starts, fibrocytes and capillaries entering the secretion via portals developing in the areas of epithelial breaks. We start this section by showing a documentation of the different modes of aeration and drainage pathways in the presence of inflammation. The regular aeration path-

way via the posterior pouch can be seen in figure 23. Prussak’s space contains much secretion with round cells (fig. 23a) which continue to be present when the space has moved behind the malleus (fig. 23b). More inferiorly, the pouch has become longer and narrower, contains secretion, and the chorda tympani nerve has joined the medial pouch wall (fig. 23c). Finally, when the pouch opened to the mesotympanum, it continued for 1.5 mm on the lateral side of the annular bone (fig. 23d). Even if the short and generally wide aeration pathway from the lower lateral attic seems likely to provide a generous pathway for drainage of secretions (fig. 18), extensive inflammatory processes in the lower lateral attic may

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Fig. 25. Case A80-126, Temporal Bone Foundation, an infant 5 months of age, left ear. Aeration pathway from the anterior pouch (AP). a Section level 121. The 1-mm-high Prussak’s space (P) measures 1.5 ! 0.9 mm, is anteriorly limited by the anterior and lateral malleal ligaments (A) around the long process of the malleus (M). b A section 0.4 mm inferior to a. Prussak’s space is aerated from the anterior pouch, secretion drains into it through a large pathway. A vertical arrow points to a superiorly blind extension of the lower lateral

attic (L) towards Prussak’s space. c Section 0.8 mm inferior to b. The blind pathway in b opens (vertical arrow) via the lower lateral attic to the mesotympanum. The superior portion of the posterior pouch (oblique arrow) appears as a slit in the tympanic membrane. d A section 0.6 mm inferior to c. The short posterior pouch is open to the mesotympanum (vertical arrow). T = Tensor tendon, C = chorda tympani nerve. Hematoxylin-eosin stain. Magnification !20.

also spread to Prussak’s space. In this type of a process Prussak’s space can be invaded by granulation tissue arising from the lower lateral attic and advancing to Prussak’s space (fig. 24a, b). The more inferiorly situating blind posterior pouch was relatively free of pathology even if there was much inflammatory tissue around the chorda tympani nerve and its fold (fig. 24c, d). In serial sections we have seen the aeration pathway to the anterior pouch in both ears of one case. There was a normal Prussak’s space which contained a small amount of secretion with round cells (fig. 25a). The communication with a large pathway opened early to the anterior pouch when Prussak’s space still was present lateral to the malleus

(fig. 25b). A blind extension from the lower lateral attic towards Prussak’s space testified of a disturbed attempt towards the development of a normal aeration pathway (fig. 25b, c). Here a small posterior pouch had also developed and the ligamental fibers spread to the posterior tympanic spine both along the pouch wall and partly in the medial surface of the tympanic membrane. This made the tympanic membrane much thicker than the regular tympanic membranes, until the pouch opened (fig. 25d). The superior pathway through the roof of Prussak’s space is shown in figure 26 and we have observed it only once in serial sections. It appeared to be an auxiliary aeration route as the regular aeration pathway went normally


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Fig. 26. Case A91-01, Temporal Bone Foundation, a child aged 23 months, left ear, section 223. An auxiliary aeration pathway from the lateral malleal space to Prussak’s space. A membrane defect (P) connects the two spaces and measures 0.8 ! 1 mm. Sections both superior and inferior to this level showed increasing dimensions. A strong bundle of the lateral malleal ligament appears anterior to the defect

(oblique arrow), a weak bundle (horizontal arrow) outlines its posterior margin. Secretion with clusters of round cells is seen in both the defect area and in the lower lateral attic (L). M = Malleus; I = incus; A = anterior malleal ligament; C = chorda tympani nerve; S = anterior tympanic spine; B = lateral attic bone. Hematoxylin-eosin stain. Magnification !40.

Fig. 27. Series P, case 9, a child aged 18 months, right ear. Prussak’s space (P) contains only a short stretch of flat epithelium laterally; there is connective tissue ingrowth from all directions. A vertical arrow points to one of the several organizing tissue strands with capillaries. The cells in Prussak’s space are mostly fibrocytes with some round cells. A tissue strand (oblique arrow) has separated a small air-filled corner off the main space. Shrapnell’s membrane (S) is separated from Prussak’s space by a thick connective tissue layer infiltrated by round cells. A change of this kind leads to obliteration of Prussak’s space. AP = Anterior pouch; LL = lower lateral attic. M = malleus. Hematoxylin eosin stain. Magnification !54.

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Fig. 28. Case A92-168, right ear, Temporal Bone Foundation. The inferior portion of the posterior pouch (PP), measuring 2.8 ! 0.9 mm, is open to the mesotympanum (oblique arrow) which is filled with secretion and granulation tissue. The posterior malleal ligamental fold near the malleus (M) has an epithelial defect in its contact point with the secretion mass (vertical arrow), indicating a beginning organization. A horizontal arrow points to a cross section of a granulation tissue polyp. The chorda (C) is separate from the posterior pouch membrane. I = Long process of the incus. Hematoxylin-eosin stain. Magnification !35.

from Prussak’s space via the posterior pouch to the mesotympanum. One might speculate that because the sections are 0.2 mm apart, the intervening sections could in many other cases easily have shown a similar defect. However, experience in microdissection, during which a membrane defect can always be seen, testifies that the frequency of such an occurrence is low. The filling of Prussak’s space with cell-rich secretion leads to the initial organization from portals which develop through epithelial breaks in the mucous membrane. Organization may occur in Prussak’s space itself (fig. 27) or anywhere along the aeration pathways (fig. 28). If the pathway is sufficiently large an infection need not block the routes fully even if some organization of secretion appears through the entire pathway (fig. 29a–d). Some of these processes, when intense, totally block the posterior pouch, causing absorption of air from Prussak’s space and leading to obliteration of Prussak’s space, without or with

severe retraction of Shrapnell’s membrane (fig. 30). Restoration of an air filled Prussak’s space is no longer possible [33]. This retraction can result in two other different end stages. One is the invagination of Shrapnell’s membrane forming so deep a retraction that the horizontal migration may soon be incapable of removing the keratin layer out of the pocket (fig. 31). This is a nonreversible stage and will lead to the development of a retraction pocket cholesteatoma. Another possibility is the filling of Prussak’s space with abundant granulation tissue which finally, after maturing, fills the entire space allowing even considerable retraction but no pocket formation, the keratin transport being unimpaired (fig. 32). Such ears, even if Shrapnell’s membrane is retracted and nonmobile, are stable and the papillae do not advance to the dense connective tissue.


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Fig. 29. A patient with a long-standing chronic otitis media. Sections through Prussak’s space (P) and a large posterior pouch (PP). a Middle portion of Prussak’s space. A network of capillaries (oblique arrow) has developed from organization portals in the epithelium. The anterior membrane (horizontal arrow) is thin, the anterior pouch (AP) contains scant secretion. Shrapnell’s membrane (S) is thick and shows large capillaries. The posterior malleal ligamental fold connects the malleus (M) to the annular bone (B). b Low portion of Prussak’s space with the beginning of a large posterior pouch. The space contains a few capillaries and secretion. The posterior malleal ligament (oblique

Cholesteatoma in Prussak’s Space As appears above, cholesteatoma in Prussak’s space develops in two basically different forms. Retraction pocket cholesteatoma presupposes absorption of air from Prussak’s space due to blocked aeration pathways, the posterior pouch and the lower lateral attic. This is followed by retraction of the posterior portion of the pars tensa and of Shrapnell’s membrane, and by gradual retention of keratin and bone resorption at the posterior retraction edge. The disease progresses relentlessly but the

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arrow) is thick, the anterior membrane of Prussak’s space thin (horizontal arrow). Secretion with round cells of varying sizes fills the lower lateral attic (LL). c The posterior pouch has moved posterior to the malleus. Capillaries deriving from an organization portal (oblique arrow) are seen in the secretion. The epidermal papillae, similarly as in b, show active prolongation (vertical arrows) but remain lateral to the inner mucosal lining. d The posterior pouch has opened (vertical arrow) to the mesotympanum which contains granulation tissue and secretion. Portals for organization are present (oblique arrows). Masson’s trichrome stain. Magnification !25.

advantage is that it can be diagnosed and treated already in the early stages. The second form is the development of cholesteatoma from Shrapnell’s membrane by papillary ingrowth, the start of which was already demonstrated by Wittmaack [6, 7]. This form, in addition to a destruction of the lining epithelium of Prussak’s space, also presupposes a break in the basement membrane of Shrapnell’s membrane. If the inflammation continues the papillae become longer and thicker (fig. 29). An ingrowing papilla passes through an area of mucosal damage and gradually its advancing tip


Fig. 30. A patient with a long-standing secretory otitis media treated for 7 years with a tympanostomy tube, left ear. Section across the neck of the malleus (M) shows a tiny remnant of Prussak’s space (vertical arrow), filled with cholesterol crystals. The epidermis of Shrapnell’s membrane (oblique arrow) is very thin, without papillae and adherent to the malleus. There is hemorrhage between the artifactually separated tympanic membrane (TM) and the posterior malleal ligament (L). C = Chorda tympani nerve; T = tensor tendon. Masson’s trichrome stain. Magnification !25.

forms a keratin-containing small cyst which, not having any outlet, becomes larger and finally forms the typical ball-type cholesteatoma in Prussak’s space. The direction of growth of this type of cholesteatoma varies, the easiest route being via the open aeration pathway into the posterior pouch and to the posterior tympanum. If the aeration comes via the direct route from the lower lateral attic, the cholesteatoma sac arrives centrally, adjacent to the short process of the malleus, to the mesotympanum. If the aeration pathway leads to the anterior pouch, the spread occurs straight to the supratubal recess. A fourth route for extension is through a defect, or the frequently present weak area in the roof to the lateral malleal space and once there, the way is open in all directions. These routes are discussed in detail in Part 3.

Large Epitympanic Compartments Leaving aside Prussak’s space, the epitympanum can be conveniently divided into two major portions, the large posterior and the smaller anterior epitympanum. The borderline between the two is formed by the head of the malleus which blocks much of the direct communication but

Fig. 31. Series P, case 6, a child aged 6 years, left ear. The retracted portion of the posterior pars tensa (vertical arrow) is adherent to the posterior malleal ligament (L). Shrapnell’s membrane is retracted and forms a deep pocket (oblique arrow) attached to the neck of the malleus (M). The anterior membrane of Prussak’s space (horizontal arrow) still has its normal position and thickness. It is attached to the indrawn anterior portion of Shrapnell’s membrane, its covering epidermis (curved arrow) is displaced laterally at sectioning. The anterior pouch (AP) contains cell-rich secretion. C = Chorda tympani nerve with its fold; S = posterior tympanic spine. A change of this kind is a forerunner of a retraction pocket cholesteatoma. Hematoxylin-eosin stain. Magnification !12.

Fig. 32. Series P, case 5, a child aged 11 years, left ear. The remaining open area of Prussak’s space (vertical arrow) measures 0.1 ! 0.2 mm and contains secretion. The anterior membrane of Prussak’s space (horizontal arrow) and Shrapnell’s membrane cover a thick, flat mass of obliterating connective tissue. The squamous epithelium shows no papillae. The lower lateral attic (LL) contains cellular secretion. The posterior malleal ligamental fold (L), starting from the malleus (M), is thick and adherent to tympanic membrane (oblique arrow). C = Chorda tympani nerve with fold; T = tensor tendon. A condition of this kind, similarly to that seen in figure 30, is likely to remain stable, with no development of cholesteatoma. Hematoxylin-eosin stain. Magnification !25.


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Fig. 33. Series G, adult case 3, right ear, superior view. The lateral incudomalleal fold continues directly from the lateral portion of the posterior incudal ligament (oblique arrow). It closes the space between the incus (I) and the bony lateral attic wall (B), and regularly turns downwards anteriorly (horizontal arrow). The large open tympanic isthmus appears on both sides of the long process of the incus between the tensor tendon (T) and the medial portion of the posterior incudal ligament (curved arrow). M = Malleus; TF = tensor fold.

Fig. 34. Same ear as in figure 33, anterosuperior view. The downgoing portion (horizontal arrow) of the lateral incudomalleal fold forms the superior portion of the posterior limit of the lateral malleal space (oblique arrow), the anterior malleal ligamental fold (A) forms its massive anterior border. The tympanic isthmus extends anteriorly up to the tensor tendon (T), its superoposterior border is formed by the medial edge of the posterior incudal ligament (curved arrow), the posteroinferior limit by the pyramidal process. The tensor fold shows a membrane defect (vertical arrow). M = Malleus; I = incus.

allows aeration and drainage to occur predominantly on its medial side and superiorly. The connection between the spaces formed by the upper lateral attic and the lateral malleal space to the anterior epitympanum is narrow and may be fully closed by the suspensory malleal ligament and the anterior malleal ligament with their folds. The medial portion of the posterior attic has normally a large communication with the anterior attic from the tensor tendon to the attic roof.

air space without any limiting borders. Above the superior surface of the ossicles the upper lateral attic, together with the medial attic, forms the superior attic, which normally extends from the lateral to the medial attic bony wall, separated only by the superior malleal ligament and by its generally short anteriorly trailing, mostly absent fold [18] . The superior attic changes into the medial attic without any borders at the level of the ossicles, and communicates with the mesotympanum via the large tympanic isthmus.

Posterior Epitympanum A substantial proportion of the volume of the posterior epitympanum is taken up by the body and the short process of the incus together with the head of the malleus. In adults the distance from the anterior portion of the head of the malleus to the tip of the incus is around 8 mm. The malleus head is superiorly close to the attic roof but from the tip of the incus the distance is larger, around 6 mm. The lateral portion of the posterior epitympanum is narrower and the thin incudomalleal fold divides it into two separate compartments which overlie each other. The lower lateral attic, between the short process and the body of the incus, and the lateral attic wall are thus below the epitympanic diaphragm and go over to the mesotympanic

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Normal Anatomy by Microdissection Superior microdissection is by far the best method for getting an idea of the normal subcompartments within the posterior epitympanum because it gives at one glance a 3-dimensional view of all spaces and structures. The indepth perception is especially important in the evaluation of the tympanic isthmus, through which in normal cases one can see deep down to the medial portion of the mesotympanum without any obstruction. Structures and subcompartments which are usually present are discussed individually below. Lateral Incudomalleal Fold. This thin fold starts posteriorly from the lateral portion of the posterior incudal ligamental fold and continues directly anteriorly between the incus short process and the lateral attic wall up to the


Fig. 35. Series G, adult case 11, left ear, superior view. An oblique strong bundle appears in the middle portion of the lateral incudomalleal fold (horizontal arrow) allowing for slightly different sloping of the anterior and posterior halves of the fold. Another ligamental bundle starting from the malleus (oblique arrow) appears at the downward turn of the fold towards the lateral malleal space (L). The tympanic isthmus (TI) is fully open. M = Malleus; I = incus; A = anterior malleal ligamental fold.

posterior edge of the malleus head (fig. 33). Here it regularly turns downwards to become united with the posterior malleal ligamental fold, forming with it the posterior border of the lateral malleal space (fig. 34), closing completely the lower lateral attic. At times 1 or 2 stronger transverse bundles cross the fold allowing a slight change in its horizontal orientation (fig. 35). In some ears it courses inferiorly along the low border of the incus directly to the posterior malleal ligamental fold (fig. 36). Rarely the space can in fact be quite narrow, with the attic wall being close to the lateral surface of the incus. The incudomalleal fold rarely continues directly anteriorly, without turning down, along the malleus head and forms a thin roof for the lateral malleal space (fig. 37). It still remains the same thin duplicate fold and should not be confused with the lateral malleal ligamental fold that more inferiorly forms the floor of the lateral malleal space. The aeration of the lateral malleal space in such cases comes from the lower lateral attic. At times there may be a short open space towards the lateral incudomalleal fold and the lateral malleal fold continues as a separate narrower or broader strip, crossing from the malleus head to the lateral attic wall, forming a partial roof for the lateral malleal space. The anterior portion of the fold is subject to large variations. The fold may end short of the posterior malleal

Fig. 36. Series G, adult case 55, right ear, superoposterior view. The thin lateral incudomalleal fold (horizontal arrow) runs anteriorly in a steadily descending slope along the inferior border of the incus (I) short process and body towards the lateral malleal space (oblique arrow). The head of the malleus (M) is close to the attic roof and the superior malleal ligament is short (vertical arrow). T = Tensor tendon; TF = tensor fold.

Fig. 37. Series A, adult case 14, left ear, superior view. The lateral incudomalleal fold (horizontal arrow) is thin and there is a curved tissue strand (oblique arrow) in its anterior portion. Anterior to it a thin lateral malleal fold (curved arrow) covers the lateral malleal space. M = Malleus; I = incus; A = anterior malleal ligament.

ligamental fold and thus leave the lower lateral attic to communicate freely with both the upper lateral attic and the lateral malleal space (fig. 15, 38). In such cases a rare view to the lower lateral attic under the lateral incudomalleal fold may be obtained from the anterior direction [18].


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Fig. 38. Series A, adult case 16, right ear, a medial view. The lateral incudomalleal fold ends (horizontal arrow) near the incus (I) body, the anterior portion is absent. The lower lateral attic (curved arrow) communicates freely with the upper lateral attic. A small area of the lateral malleal space (oblique arrow) appears lateral to the malleus (M). TI = Tympanic isthmus.

Fig. 40. Series G, adult case 16, left ear, superior view. An auxiliary aeration pathway (vertical arrow) via the incudal fossa appears posterior to the tip of the incus short process (I). Application of a suction tip to this opening emptied rapidly the tympanic cavity filled with water. An oblique arrow points to the tympanic isthmus, a curved arrow to the lateral incudomalleal fold.

Infrequently the fold turns superiorly ending up in the attic roof, closing then the anterior portion of the upper lateral attic, the lower lateral attic retaining a large communication to the lateral malleal space. Membrane defects appear in the lateral incudomalleal fold in around 15% (fig. 38, 39); therefore, in such cases

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Fig. 39. Series G, case 18, right ear, lateral view. A membrane defect in the horizontal portion of lateral incudomalleal fold, starting from the posterior incudal ligament (horizontal arrow). The lateral malleal space (vertical arrow) is normal between the head of the malleus (M) and the lateral attic bone (B). The posterior malleal ligamental fold (between oblique arrows) shows again the fanwise spread of the ligamental bundles. I = Incus.

this auxiliary aeration pathway lateral to the incus assists the normal pathway, the tympanic isthmus on the medial side of the incus. Posterior Incudal Ligamental Fold. The tip of the incus short process is firmly fixed to the adjacent attic bone laterally and medially by the posterior incudal ligament, which spreads fanwise at an angle of 90° from the incus tip portion. The ligament is much stronger laterally than medially, and the lateral incudomalleal fold continues immediately anteriorly from this portion of the ligament. Initially, behind the tip of the incus short process we [8, 18] found a relatively large opening (fig. 40), connected via the incudal fossa with the posterior tympanum, and started to call this aeration route the posterior tympanic isthmus. In addition, large neighboring air cells (fig. 41) turned out to have often a workable communication with the mesotympanic air spaces since the application of a suction tip to the air cells rapidly emptied the middle ear filled with fluid. In the entire series it has become apparent, however, that these routes are open in around 25% of the cases and in the majority the isthmus is closed by the posterior incudal membrane, continuing directly from the posterior incudal ligamental fold (fig. 42). We have, therefore, dropped the term posterior tympanic isthmus and prefer to call it an auxiliary aeration route via the incudal fossa. The entrance to the open incudal fossa below the incus tip portion can be seen looking towards it from the ante-


Fig. 41. Series S, adult case 10, left ear, superior view. An auxiliary aeration pathway via open air cells (vertical arrow) posterior to the tip of the incus short process connects the antrum through the incudal fossa to the mesotympanum. Suctioning rapidly evacuated water from the tympanum.

romedial direction [18] in microdissection but serial sections are more accurate in the description of pathological changes in this area. Superior Malleal Ligamental Fold. The head of the malleus is fastened superiorly to the attic roof by a narrow ligament. In the fetal process of the aeration of the epitympanum, the anteriorly advancing medial air sac, when passing this structure, leaves a trailing fold. It is generally thin and short and only occasionally may extend forward to the attic roof in front of the head of the malleus, and mostly it is absent (fig. 43). The elaborate superior malleal and incudal sagittal and frontal folds included in the sketches of Proctor [13, 14], and reproduced by Wullstein and Wullstein [11], are pure fantasy in normal ears. Only inflammatory webs often cross the superior attic air space in a haphazard manner. Tympanic Isthmus. This regular large aeration pathway serving the entire epitympanum, except Prussak’s space, extends from the tensor tendon anteriorly to the pyramidal process inferoposteriorly, and to the medial portion of the posterior incudal ligament superoposteriorly (fig. 33–36). Medially it is limited by the attic bone and laterally by the body and short process of the incus and the head of the malleus. The space limited by these structures is the medial attic, which inferior to the incus body becomes the mesotympanum. The anterior portion of the tympanic isthmus, superior to the level of the tensor tympani tendon, is in large open communication with the

Fig. 42. Series G, adult case 18, right ear, superior view. A large opening posterior to the tip of the incus short process (I) is covered by a posterior incudal fold (horizontal arrow), which blocks the auxiliary aeration route. This finding is more frequent than the two states shown in figures 40 and 41. A vertical arrow points to the posterior portion of the tympanic isthmus, an oblique arrow to the lateral incudomalleal fold.

Fig. 43. Series G, adult case 52, left ear, superoposterior view. The superior malleal ligament (vertical arrow) connects the head of the malleus (M) to the attic roof. There is no trailing fold, a general finding. The space between the malleus and attic bone is narrow and there is one narrow tissue strand across the space (horizontal arrow). The oblique arrow points to the medial portion of the transverse crest.

anterior epitympanum. In adults, the breadth of the medial attic at the middle of the short process of the incus is around 1.3 mm, the narrowest width at the level of the body of the incus may be less than 1 mm. The anteroinferior portion of the tympanic isthmus between the tensor tendon and the inferior surface of the malleus head is larger, around 3 mm (fig. 34). The distance from the tensor tendon to the anterior edge of the posterior incudal liga-


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Fig. 44. A patient with a long-standing secretory otitis media, left ear, normal upper portion of the epitympanum. The medial attic (MA), part of the tympanic isthmus, communicates fully with the anterior attic (AA) and is inferiorly open to the mesotympanum. The lateral malleal space (L) makes a compartment of its own, open superiorly. The lower lateral attic (LL) is in direct communication with the lateral mesotympanum. M = Malleus; I = incus; T = composite tissue insertion ring for the tensor fold. Masson’s trichrome stain. Magnification !7.

Fig. 45. Same ear as in figure 44. The lateral half of the horizontal portion of the thin lateral incudomalleal fold appears in this section, the medial half was seen in the next. There is some irritation in the form of an increased size of capillaries in the posterior portion of the fold due to the overlying scant secretion (oblique arrow). B = Lateral attic bone; PL = lateral portion of the posterior incudal ligament. Masson’s trichrome stain. Magnification !60.

ment is around 6 mm. In the middle of it, but 1–2 mm inferior to the level of the isthmus, is the incudostapedial articulation (fig. 33, 34). Even if it serves as an area providing insertion points for inflammatory folds which may seriously restrict the passage to the isthmus itself, the isthmus in normal ears is clearly one single unit without obstacles for aeration. In our entire series of microdissections of normal ears, the tympanic isthmus has been fully open and free of folds. This applies to neonates as well as to children and adults and conforms with Hammar’s [5] finding of the atrophy of the composite fold affecting the medial attic during the fetal stages. As will be remembered, this is the fold deriving from passing of the air sacs over both sides of the incus long process and of its continuation posteriorly as the three stapedial folds. They may continue also anteriorly for a limited distance, and we have earlier called them the incus intercrural fold or the medial malleal fold [18]. To make matters more simple, we have recently [32] suggested that this structure be called the medial ossicular fold which would allow its presence as a long fold or folds limited to short stretches along the medial side of the entire ossicular chain. In some ears of neonates and infants in the material of the Temporal Bone Foundation shorter or longer stretches of this vertically oriented medial ossicular fold

have unquestionably been seen in serial sections. They usually start from the incus, do not always reach the opposite medial attic bone and it is likely that they atrophy with the growing of the child, hence their general absence in older children and adults. There are no grounds for ascribing them a prominent role by normally obstructing the posterior portion of the tympanic isthmus as was done in the undocumented sketches of Proctor [13, 14]. Nevertheless, as we will see later in connection with the AFCC-induced sterile otitis media of the neonate, their remnants may have a definite role in that they provide fixation points for AFCC in the tympanic isthmus.

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Normal Anatomy by Serial Sections In the absence of inflammatory changes, microdissection can instantly provide an idea of the compartments compared to serial sections (fig. 44), necessitating examination of a large number of slides. The lateral incudomalleal fold, being largely horizontal and thin, less than 0.2 mm in thickness, generally can be seen only partially in one single serial section in adults (fig. 45). In neonates and infants larger areas and thicker portions are seen because the formation of the fold has not yet been finalized, embryonal tissue remaining between the upper and lower lateral attics. The anterior portion of the fold, on the other hand, because as a rule it becomes directed inferi-


Fig. 46. Same ear as in figure 44, section 0.8 mm more inferior. Medial attic (MA) still communicates fully with the anterior attic (AA) which in turn is separated by the thin tensor fold (horizontal arrow) from the supratubal recess (R). The incudal fossa is inferior to the tip (I) of the incus short process (curved arrow). M = Malleus; LL = lower lateral attic. At a level 0.4 mm inferior to this, only cross sections of the long process of the incus remain and the epitympanum changes without borders into the mesotympanum. Masson’s trichrome stain. Magnification !7.

Fig. 47. Series G, adult case 2, right ear. a A superior view of the epitympanum discloses a few postinflammatory tissue strands in the anterior portion of the tympanic isthmus (horizontal arrow), the posterior portion (oblique arrow) appears free. The lateral incudomalleal fold is intact but indrawn and contains a few thicker areas (curved arrow). The lateral malleal space (vertical arrow) is normal and a posterior incudal fold closes the auxiliary aeration pathway via the incu-

dal fossa (open arrow). M = Malleus; I = incus. b Removal of the incus discloses a large thin postinflammatory web which contains many thicker fibrotic strands and only small defects (oblique arrow) allow for aeration. The medial wall of the posterior pouch, the posterior malleal ligamental fold (between horizontal arrows), is distinct. The floor of the lateral malleal space is intact (curved arrow). T = tensor tendon.

orly towards the posterior malleal ligamental fold (fig. 15a) is well visible at thin cross sections. The majority of the sections further inferiorly show the air-filled large compartments of the medial attic down to the tympanic isthmus on one side, and either the upper or the lower lateral attic on the other side of the incus (fig. 46). In the area of the incudal fossa the serial sections show the relatively spacious area underneath the incus tip, bordered by the air cells, while the larger posterior incudal aeration pathway route appears behind the tip.

Pathology as Seen in Microdissection The mild forms of inflammatory pathology causing soft tissue sequelae appear in the form of mature tissue strands and narrow or broader webs crossing the tympanic isthmus (fig. 47a). In such cases microdissection may make an instantaneous evaluation still possible, by allowing a look between the strands to the changes deep down in the mesotympanum. However, sometimes quite unexpectedly the removal of the incus may reveal in the inferior portion of the isthmus postinflammatory thin webs which may greatly obstruct the air flow through it (fig. 47b). One of the very frequent, almost routine find-


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Fig. 48. Series G, adult case 16, left ear, superior view. Many crossing postinflammatory tissue strands appear across the tympanic isthmus, anterior and posterior to the stapes (S). More webs appear deeper down in the posterior portion of the isthmus (oblique arrow). The lateral incudomalleal fold is deeply retracted on top of the posterior pouch wall (horizontal arrow), obliterating the lower lateral attic. The posterior portion of the fold is thick with underlying scar tissue (curved arrow). The entire posterior portion of the floor of the lateral malleal space (vertical arrow) is retracted. M = Malleus; I = incus; A = anterior malleal ligamental fold; T = tensor tendon.

Fig. 50. Same ear as in figure 49 after removal of the lateral attachments of the inflammatory network in the tympanic isthmus. Portion of the web remains (oblique arrow) adherent to the medial side of the malleus (M) and incus (I). The tympanic isthmus (horizontal arrows) now opens up to the tensor tendon (T). L = Lateral malleal space, A = anterior malleal ligamental fold; C = chorda tympani nerve.

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Fig. 49. Series P, case 12, a child aged 6 years, left ear, superior view. This patient had a tympanostomy tube in place with a clinically symptomless mesotympanum. There was thick mucus in the epitympanum, after suctioning small cholesterol cysts (oblique arrows) remain on the tip of the incus (I) and on the head of the malleus (M). The lateral incudomalleal fold is thin (horizontal arrow). A multilayered inflammatory network (curved arrows) closes the major portion of the tympanic isthmus, the small remaining open area did not allow outflow of the sticky secretion.

ings in chronic inflammation is the deep indrawing of the lateral incudomalleal fold, which in certain areas may be retracted below the level of the roof of Prussak’s space (fig. 48). This is due to a gradual change of immature granulation tissue to mature constricting scar tissue with a full disappearance of the lower lateral attic air space. In long-standing cases of secretory otitis media and apparently innocent looking mesotympanum, the epitympanum may show ongoing active inflammatory changes even in the presence of a tympanostomy tube. Immature granulation tissue, thick inflamed webs and occasional cholesterol cysts may partially block the tympanic isthmus (fig. 49, 50).Without surgical interference such cases lead to a prestage of an adhesive otitis media, with recurrent bouts of infection and with a continuing increase of the granulation tissue. The blocking tissue in the tympanic isthmus may present itself in less inflamed cases as web-type layers of connective tissue and in cases of longer duration as immature or mature connective scar tissue (fig. 51) or as a continuous mass of granulation tissue for the entire depth of the isthmus. In an ongoing chronic inflammation the granulation tissue appears already between the incus and the attic roof (fig. 52); it may continue down to the isth-


Fig. 51. Series A, adult case 17, left ear, superior approach, medioposterior view. The tympanic isthmus posterior to the stapes (S) and medial to the incus (I) is blocked by a multilocular inflammatory tissue network filled with secretion. The anterior portion of the isthmus (horizontal arrow) was open but showed a few separate tissue strands. B = Medial attic bone.

Fig. 52. Series A, adult case 12, right ear, superoposterior view. Granulation tissue fills the space between the attic roof and the malleus (M) and incus (I), and the posterior portions of the upper lateral attic (vertical arrow) and the tympanic isthmus (horizontal arrow). Similar tissue appeared deep down in the anterior portion of the isthmus, and on top of the lateral malleal space (curved arrow).

Fig. 53. Series A, adult case 11, left ear, the entire epitympanum blocked by granulation tissue, a view after removal of the attic roof and some granulation tissue from the top of the ossicles. a Granulation tissue fills all spaces and it extends inferiorly around the ossicles as far as the hypotympanum. b Removal of the incus left a cast in the mesotympanic granulation tissue. The horizontal arrow marks the place occupied by the incus long process.

mus and a direct view to the tympanic isthmus becomes obscured due to a full blockage (fig. 53a). In microdissection layer after layer of the webs and granulation tissue must be removed to arrive at the deeper spaces. It may be necessary to remove the entire incus to get an idea of the deepest layers at the low border of the tympanic isthmus and around the incudostapedial articulation. Even then

the granulation tissue may be so extensive that only a cast of the incus remains after its removal (fig. 53b). A biopsy of such a mass may show various stages of maturation in the granulation tissue (fig. 54), the final stage of which appears years later when the tissue mass has become dense scar tissue with full ossicular fixation and obliteration of the middle ear spaces.


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Fig. 54. Granulation tissue removed from the posterior epitympanum of case A 11 shown in figure 53. A patchy one-cell layer epithelium covers the superior surface of the specimen. Much of the biopsy consists of connective tissue undergoing maturation, but there are regions with round cell clusters (vertical arrows). The trapped epithelium (oblique arrow) appears in many areas as well as hemosiderin pigment (horizontal arrows). Hematoxylin-eosin stain. Magnification !60.

Pathology as Seen in Serial Sections While the serial sections in normal ears were not as quickly informative as microdissection, in the presence of pathology they are invaluable in giving information about the exact location and histological nature and phase of the disease. The presence of secretion, either serous or mucinous together with its cellular content, and the appearance of the epitympanic mucosa make it possible to draw conclusions of the duration and activity of the process. When organization phenomena are ongoing, the maturity of the granulation tissue, epithelialization of its surface and the formation of pseudocysts are important markers of the severity and duration of the process. Chronic inflammation, even if mild, causes many changes some of which appear in figure 55. The duplicate folds become thicker with a distinct increase of capillaries combined with a slight infiltration by the inflammatory cells (fig. 55a). The air cells in the attic walls may be filled with secretion containing round cells, some cells are obliterated by connective tissue and some by cholesterol crystals. Round cells containing secretion also appear in the major air compartments (fig. 55b), the amount depending upon the available open drainage pathways. The tympanic isthmus may become partially blocked by inflammatory webs or by polypoid tissue at times covered by advancing squamous epithelium from the mesotympanum (fig. 55c). These changes become also well apparent around the incudal fossa where the ligamental fold epithe-

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lium becomes edematous and filled with large capillaries, and cell-rich secretions appear on all sides of the posterior incudal ligamental fold (fig. 55d). We have found that the incudal fossa itself is free of granulation tissue and some aeration of the mastoid cells may occur in children suffering from secretory otitis media even if the main pneumatization process remains halted. Extensive development of granulation tissue in the posterior epitympanum occurs, even during the era of antibiotics and disappearance of florid mastoid infections, since the process of organization involves the nonremoved masses of mucoid secretion filling the attic. This may be seen in association with an undiagnosed AFCClinked foreign body otitis media of neonates and infants, especially in cases with superimposed low grade bacterial infections of longer duration As both these processes often go hand in hand we will discuss this type of pathology seen in serial sections in Part 2 of this atlas in connection with AFCC-related pathology. Anterior Epitympanum The anterior attic is one of the major epitympanic compartments which has been subject to a considerable confusion. The early scientists like Siebenmann [1] at the end of the 19th century already had an accurate idea of this space, defining it as a forward continuation of the medial attic past the head of malleus. Its inferior limit was formed by the tensor tendon and anteriorly and upwards


Fig. 55. A patient with a long-standing chronic otitis media with a migration cholesteatoma of the mesotympanum, right ear. a Section through a remnant of the lateral incudomalleal fold (horizontal arrow) shows dominant capillaries but only a few inflammatory cells. The downgoing portion of the fold (oblique arrow) is slightly edematous. Scant secretion appears in the lower lateral attic (LL) and in the lateral malleal space (L). M = Malleus; I = incus; B = lateral attic bone. b The dome of Prussak’s space (P) contains secretion, similarly to the lower lateral attic (LL) and the supratubal recess (R). The medial (MA) and anterior attics (AA) are open and free of secretion. Vertical arrow points to low portion of the anterior malleal liga-

mental fold. c The low portion of the tympanic isthmus is partially blocked by an inflammatory fold (horizontal arrow), part of which has as its surface the migrating squamous epithelium. The lower lateral attic, together with Prussak’s space, contains secretion with round cells. The anterior attic and the supratubal recess show scant secretion. d An inflammatory fold (horizontal arrow), with large capillaries and inflammatory cells, adjoins the tip of the incus overlying the fossa incudis. There is secretion in the posterior tympanum (T) and in the antrum (A). Note that the posterior incudal ligaments (vertical arrow) go directly lateral and medial from the incus. Masson’s trichrome stain. Magnification !25 (a, d), !7 (b, c).

it was closed by the vertically rising tensor fold, the insertion of which was into the transverse crest in the attic tegmen (fig. 5). The writers of that period defined the space anterior to the fold as a ‘pneumatic cell’ which was partially limited at its low portion by a free fold-like structure arising from the tegmen tubae. Siebenmann noted that this ‘pneumatic cell’ harbored trapped disease, but he specifically pointed out that it is part of the mesotympanum, not the epitympanum. His description differs from our

concepts [19, 20] of the anterior epitympanum concerning the superior insertion of the tensor fold. As to the pneumatic cell limited inferiorly by an incomplete fold we have proposed tentatively that the fold was simply an inflammatory web arising during the long-standing chronic diphtheric disease. We have previously discussed the current chaotic and confused concepts of using many different names for the anterior epitympanum, also regarding it as the pneumatic


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Fig. 56. Series G, adult case 56, left ear, a posterosuperior view of the anterior epitympanum. a Laterally, the anterior attic continues only a short stretch past the lateral malleal space (L). The space between the malleus head (M) and the attic roof (B) is short with no open space. Medially the tensor tendon (T) and the tensor fold (TF) form the frontal border of the anterior attic. The superior attachment of

the tensor fold is anterior to the transverse crest (vertical arrow). b The transverse crest (between horizontal arrows) has been removed together with the roof of the anterior attic. The superior insertion of the tensor fold (vertical arrow) is anterior to the crest, and an extension of the anterior attic appears when normal large air cells have been opened towards the supratubal recess tegmen (oblique arrows).

cell of Siebenmann, and confusing it with the supratubal space in front of it [19, 20, 24], and will not repeat them here. Suffice it to say that even in the year 2000, as an answer to our letter [34] to the editor of the American Journal of Otology concerning the ideas of supratubal recess and pathways to Prussak’s space in epitympanic endoscopy [35], the authors still sought to backup their argument by referring to the erroneous writings of Proctor [13, 14]. Among other unfounded claims they maintained that the anterior epitympanum was the supratubal recess and continued that: ‘By definition, supratubal recesses and intact plicae tensoris are mutually exclusive’! The truth of course is the opposite: when the tensor fold is intact, the anterior epitympanum and the supratubal recess form two separate compartments.

tinctly shorter than the medial portion which extends anteriorly until the tensor fold (fig. 56a). The bony walls of the anterior epitympanum generally showed good pneumatization, sometimes it was extensive and extended a long distance anteriorly above the tubal tegmen (fig. 56b). In a few cases a major sinus-like formation appeared superior to the insertion of the tensor fold, extending for more than 10 mm anteriorly (fig. 57, 58). Transverse Crest. The position and extent of this structure have been misunderstood by most of the contemporary writers even if Siebenmann already in 1897 published an accurate drawing depicting its dimensions. The crest starts from the anterior tympanic spine and crosses the tegmen transversely 1–2 mm in front of the malleus head (fig. 5), while its medial leg may continue until the cochleariform process. This portion, which may be independent and without any continuity with the transverse portion, was called a ‘cog’ by Sheehy [36] as it looks like a cog of a wheel. As a rule the crest is low, around 0.5 mm, and only in very rare cases, in our series 2%, has it exceeded a height of 1 mm. Its lower edge is sharp generally with an uneven curve with many bony ridges and tags. Siebenmann believed that the tensor fold attached to the transverse crest and therefore the tensor fold drawn by him was vertical and the anterior epitympanum rather small in size. This insertion, however, is not the regular one but appeared only in 10% of our microdissections. The tensor fold insertion is regularly anterior to the trans-

Normal Anatomy by Microdissection The medial attic continued in all dissected bones unobstructed, superior to the tensor tendon and medial to the head of the malleus, and became the anterior epitympanum. Superiorly the connecting space is narrower and somewhat obstructed by the superior malleal ligament and its variable short fold (fig. 43). Connections from the lateral portion of the anterior attic with the posterior compartments, the upper lateral attic and the lateral malleal space are often narrow and may be closed by a short fold between the malleal ligaments and the attic roof. The lateral portion of the anterior epitympanum is as a rule dis-

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Fig. 57. Series P, case 11, a child aged 2 years, left ear, superoposterior view. The anterior attic has an extension in the superior direction (between horizontal arrows). The tensor fold is very thin and contains a membrane defect (oblique arrow). M = Malleus; TI = tympanic isthmus; A = anterior malleal ligamental fold; T = tensor tendon.

Fig. 58. Series G, adult case 49, left ear, superoposterior view. This is the largest bony sinus seen in the anterior epitympanum in the present series. The oblique arrow points to the superior insertion of the tensor fold (TF). M = Malleus head.

Fig. 59. Series A, adult case 14, left ear. a Superoposterior view through the anterior attic to the supratubal recess after removal of the tensor fold. The vertical arrow points to the transverse crest. L = Lateral malleal space; M = malleus; I = incus; S = stapes. b Anterior view of the transverse crest (vertical arrow) from the supratubal recess. Horizontal arrows mark the soft tissue insertion ring of the removed tensor fold. Tensor fold removal creates a large direct aeration and drainage pathway from the epitympanum to the eustachian tube orifice.

verse crest into a thinner or thicker ring of a composite tissue, fixed with a broad base to the tegmen. One major misconception is, as the transverse crest is situated in the tegmental roof, that it forms the frontal border of the anterior epitympanum and the space in front of it is the supratubal recess. However, the crest only divides the anterior epitympanum into two portions, anterior and posterior, both of which merge inferior to the crest and form one common space. Another, even more major misconception by contemporary writers is that the transverse crest would form a bony separation between the anterior epitympanum and the supratubal recess. This has been suggested especially by Japanese workers [37, 38] and even new surgical tech-

niques have been proposed for removing this ‘bony obstruction’ to provide epitympanic aeration directly from the supratubal recess. The error in this reasoning can be shown very simply by the removal of the tensor fold: a large communication between the anterior epitympanum and the supratubal recess appears between the transverse crest and the tensor tendon (fig. 59a, b). In our series of 125 microdissections the crest has only twice taken up the upper half of the separating wall while the thin tensor fold formed the lower half. In all others the crest played an insignificant role in the separation of these two major compartments. Tensor Fold. As already emphasized, this duplicate fold has a highly important strategic position as it normal-


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Fig. 60. Series G, adult case 15, left ear, superoposterior view. The tensor fold (TF) contains large thin areas with a few stronger connective tissue strands across the fold. The thin fold from the malleus (M) to the tensor fold (oblique arrow) was present in 40% of microdissections. The chorda tympani nerve (C) is always positioned at the lateral edge of the tensor fold. A = Anterior malleal ligamental fold; T = tensor tendon. The tensor fold separates the anterior epitympanum from the supratubal recess, the regular state.

Fig. 61. Series G, adult case 2, right ear, superoposterior view. A small portion of the tensor fold is present, attached to the tensor tendon (T), while the major portion shows a membrane defect (horizontal arrow). M = Malleus; TI = anterior portion of the tympanic isthmus. A membrane defect of this size provides a large and effective auxiliary aeration and drainage pathway from the anterior epitympanum to the supratubal recess (R) and eustachian tube.

ly prevents communication between the supratubal recess, part of the mesotympanum, and the anterior epitympanum (fig. 56, 57, 60). This means that the only aeration and drainage pathway in the majority of ears is through the tympanic isthmus. We have found a membrane defect in this fold, allowing for direct attic aeration from the supratubal recess, in around 25% of microdissections (fig. 61). Siebenmann’s finding [1] of a defect in the majority of cases probably depended upon the corrosive methods used at that time in the handling of the specimens, which were likely to destroy the thin fold portions looking like a pseudomembrane. Hammar [5] did not observe it in his fetal series but considered Siebenmann’s finding possible because of a secondary fold atrophy. Aimi’s [22, 23] figure for tensor fold membrane defects was 10%. The tensor fold starts from the tensor tendon upwards in a slightly concave fashion and may have a greatly varying further course. If the insertion is to the transverse crest, then the direction is nearly vertical, when the insertion is to the tubal tegmen, the fold is nearly horizontal. In most cases the angle is around 45° and the insertion ring situated halfway between the downsloping combined anterior epitympanic-supratubal tegmen. The fold appears generally thicker close to its borders and may have crossing strands, while the central portion is thin like a pseudomembrane (fig. 60). Nevertheless it is a tough structure

that does not break even if subjected to vigorous movement after deliberate filling of the entire middle ear with water and sucking it out with force. Removal of bone from the epitympanic and supratubal space tegmen reveals the soft tissue insertion ring and a relatively thin mucosa on either side. Cutting through the soft tissues superiorly shows the thick insertion ring which even by gross examination is seen to contain varying amounts of fat (fig. 62, 63). These views, and fig. 61, demonstrate well how the removal of the fold connects the two big compartments, the anterior epitympanum and the supratubal recess, with a large aeration and drainage route continuing unobstructed to the eustachian tube. The insertion of the tensor fold anterosuperiorly can well be studied in separate biopsies obtained during microdissection. The thin insertion rings consisted of dense collagenic fibrous tissue with small bone fragments but without adipose tissue (fig. 64). The thicker insertion rings showed a pronounced broader base with many bone fragments, with collagenic fibrous tissue and many islands of adipose cells (fig. 65). The fat-specific Sudan black staining in fresh specimens was always positive for the areas which in the normally processed specimens with the hematoxylin-eosin stain showed only the cell outlines. Maximally the insertion ring, measured from successive sections, was found to extend even to 4 mm in the inferior-superior direction in the tegmental bone.

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Fig. 62. Series G, adult case 52, left ear, superior view. The tensor fold has been removed and the thin soft tissue insertion ring (between horizontal arrows) cut. Through the supratubal recess (R) the route is free to the eustachian tube. The tympanic isthmus is open between the tensor tendon (T) and the posterior incudal ligamental fold (oblique arrow). M = Malleus; I = laterally displaced incus.

Fig. 63. Series G, adult case 54, left ear. Thin low portion of the tensor fold (TF) remains inferior to the membrane defect. The thick soft tissue insertion ring (vertical arrow) has been cut, showing much fatty tissue. R = Supratubal recess.

Fig. 64. Thin soft tissue insertion ring and portion of the tensor fold (vertical arrow) removed during microdissection. A thin slice of bone (B) remains at the insertion surface of the attic roof, otherwise the block consists of connective tissue with only little fat. Hematoxylineosin stain. Magnification !21.

Other Folds in the Anterior Epitympanum. The fold arising when the superior malleal ligament is passed by the medial air sac may rarely extend in the lateral portion of the anterior epitympanum up to the bony anterior attic wall. Generally it ends with a free edge and is as a whole infrequent and generally missing (fig. 43). Another trail-

Fig. 65. A broad composite tissue insertion ring removed during microdissection. The bone at the insertion surface (B) of the attic roof extends deeper into the ring itself which consists of loose connective tissue and a lot of dissolved fatty tissue. Hematoxylin-eosin stain. Magnification !21.


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Fig. 66. Series P, a neonate, left ear. The anterior attic (AA) is empty and connected to the medial attic (MA) which is partially divided into two portions by a 1.5-mm-high vertical medial ossicular fold (horizontal arrow). M = Malleus; I = incus; L = lateral malleal space; LL = lower lateral attic. Hematoxylin-eosin stain. Magnification !12.

ing fold, present in around 40%, starts from the medial edge of the superior portion of the malleus neck and spreads fanwise anteriorly to attach either to the anterior attic wall or to upper portion of the tensor fold, or both (fig. 60). It sometimes gives the impression of a multilayered structure obscuring the view of the tensor fold and represents probably the ‘coulisse’ that Siebenmann [1] described as part of the anterior soft tissue wall of the anterior epitympanum. Normal Anatomy by Serial Sections Serial sections add only little to the general concept of the anterior epitympanum which in normal cases, similar to the posterior epitympanum, can again instantaneously be evaluated. At the superior levels (fig. 66) the space in front of the head of the malleus is normally empty and may or may not contain the anterior malleal trailing fold [19]. At lower levels the anterior attic remains free and is widely connected to the medial attic. The thinness of the tensor fold and the thickness of the soft tissue insertion ring appear clearly, again demonstrating the role of the tensor fold in the separation of the anterior attic from the supratubal recess (fig. 46).

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Normally in cases with a shallow transverse crest the upper portions of the anterior epitympanum remain small and they are easily recognized as upward extensions of the common air space for the anterior attic. If the crest is higher, the posterior portion may remain small while the anterior portion is much larger and an inexperienced observer may believe it to be the supratubal recess separated by a bony wall from the recess (fig. 67). However, when the sections are followed further inferiorly, the merging of the spaces to just one anterior epitympanic compartment becomes obvious. The final proof is provided by an investigation of the dome of the supratubal recess at still more inferior sections. In those ears in which the tensor fold adheres directly to the crest, the dome of the supratubal recess can extend distinctly more superiorly than the low border of the crest [31–33]. The bony walls of the anterior epitympanum appeared smooth in half of the specimens whereas the other half had numerous tags and ridges, often starting from the transverse crest itself (fig. 67). The air cells were equally well developed in the entire anterior bony tegmen as in the posterior epitympanum. The tensor fold in serial sections can be followed from its uppermost portion, the dome of the supratubal recess, to its insertion at the tensor tendon. It is a thin structure, normally around 0.1 mm, the superior and inferior cross sections may appear wider because of the more horizontal slope of these portions of the fold. The chorda tympani nerve, enveloped by its own fold, runs always at the lateral edge of the tensor fold, medial to the anterior malleal ligamental fold, towards the petrotympanic fissure. In adults the general width of the tensor fold near its tendon is around 2.5–3 mm. Its height as measured on the basis of the number of sections from the dome to the tensor tendon is around 3 mm, but shows much individual variation, also due to the different fold angles. In children the measures are slightly smaller [39]. Pathology as Seen in Microdissection Inflammatory changes in the anterior epitympanum are generally somewhat less pronounced than those seen in the posterior attic. The most frequent form was the appearance of inflammatory strands and webs of varying thickness and width posterior to the tensor fold, together with secretion and mucosal edema (fig. 68). In a more extensive blockage of the tympanic isthmus but in the absence of major infection, the anterior epitympanum was also filled with a space-taking network of fibrotic tissue [18]. In active chronic inflammation granulation tissue either obscured the details of the space (fig. 68) or


Fig. 67. Adult patient, otosclerosis, left ear. The posterior portion of the anterior attic (AA) is narrow between the malleus (M) and the transverse crest (horizontal arrow), while its major anterior portion is situated between the crest and the anterior attic bony wall (B). The spaces merged fully in a section 1 mm more inferior. The walls of the well-pneumatized anterior attic as well as the crest itself show an unusual amount of bony ridges and tags. Hematoxylin-eosin stain. Magnification !12.

Fig. 68. Series A, adult case 12, left ear, superoposterior view. Thick mucosa and granulation tissue mask the details of the anterior attic. Vertical arrow points to the area of the tensor fold covered by granulation tissue and webs, horizontal arrow to the place of the tensor tendon. There is similar tissue on top of the lateral malleal space (oblique arrow). M = Malleus.

Fig. 69. Series A, adult case 15, left ear, superior view. a The anterior attic is full of immature granulation tissue and no details can be discerned. b Same region after removal of much of the granulation tissue. The head of the malleus (M), the anterior malleal ligamental fold (A) and the lateral malleal space (L) can now be identified. Granulation tissue still fills the upper portion of the anterior attic, a narrow route (oblique arrow) has been opened towards the intact tensor fold. A horizontal arrow points to the blocked tympanic isthmus.

filled the entire anterior epitympanum (fig. 69a, b). When the entire tegmen was removed, revealing the soft tissue insertion ring, the tensor fold was seen to effectively limit the disease to the anterior epitympanum (fig. 70). In one case, however, we have seen the granulation tissue progress by bone destruction to the supratubal recess. Pathology as Seen in Serial Sections Inflammation in the anterior attic appeared as the presence of cell-rich secretion and mucosal edema at var-

ious levels of the sections (fig. 71, 72) and inflammatory webs with trapped secretion going across the space (fig. 73). Also, the air cells around the anterior attic space showed signs of mucosal edema, round cell secretion or total obliteration of their lumen. Some air cells contained cholesterol crystals. Further examples associated with active inflammation and development of granulation tissue in the anterior epitympanum are shown in Part 2 dealing with the AFCC-associated pathology.


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Fig. 70. Series A, adult case 16, right ear. The entire bony tegmen of the anterior attic (A) and of the supratubal recess (R) has been removed revealing the soft tissue insertion ring (between horizontal arrows). The tensor fold (TF) is thick with a granulating surface. Granulation tissue (oblique arrow) and inflammatory webs fill the space between the head of the malleus (M) and the tensor fold.

Fig. 71. A patient with a long-standing chronic otitis media, right ear. The anterior attic (AA), partly divided into two spaces by a bony ridge (horizontal arrow), contains secretion with round cells and a few multinucleated cells. Mainly cell-free secretion appears in the lateral malleal space (L). A partially blocked air cell shows a small lumen half-filled with secretion (vertical arrow). Another air cell is obliterated (oblique arrow). M = Malleus; A = anterior malleal suspensory ligament. Masson’s trichrome stain. Magnification !12.

Fig. 72. Case A92-168, an infant aged 8 months, left ear, Temporal Bone Foundation. Thick mucoid secretion appears in the anterior attic (A) and in the supratubal recess (R). The tensor fold (horizontal arrow) is slightly edematous and polypoid structures appear in the mucosa (vertical arrows). M = Malleus; I = incus; P = Prussak’s space. Hematoxylin-eosin stain. Magnification !25.

Fig. 73. Case A89-195, an infant aged 15 months, left ear, Temporal Bone Foundation. The anterior attic (AA) forms a compartment with trapped secretion and is divided into smaller spaces by inflammatory folds (vertical arrows). The anterior malleal ligament, the superior portion of which is present (A), forms the border towards the empty lateral malleal space (L). An inflammatory web (horizontal arrow) closes the route to the medial attic (MA). M = Malleus; I = incus. Hematoxylin-eosin stain. Magnification !15.

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Fig. 74. Series A, adult case 13, right ear, anterior approach, oblique view from the protympanum to mesotympanum. The malleus handle (M) and the tympanic membrane (TM) appear on the left, the tensor tympani tendon (T) is directed to the right. Long process of the incus (I) articulates with the stapes (S). Between them and the tensor tendon is the anterior portion of the tympanic isthmus.

Fig. 75. Series P, case 11, a child aged 2 years, left ear, anterior approach. Direct view onto the ossicles in the mesotympanum. M = Malleus handle; T = tensor tendon; I = long process of the incus; S = stapes. Vertical arrow points to hypotympanum, horizontal arrow to the low lateral portion of the supratubal recess.

Supratubal Recess (Space) The supratubal recess is a mediosuperior extension of the protympanum and anterior mesotympanum, a space in front of the tensor fold. The size of the recess is mainly related to the degree of the angle of the tensor fold being largest in ears with more vertically oriented folds and smallest in more horizontally oriented folds. We have observed that the shape and size of the supratubal recess existed in a nearly similar form in both temporal bones in a newborn [39] as well as in normal adult ears [20].The formation of the supratubal recess during the fetal period was already described by Hammar [5]. As reviewed above (pages 6, 7), the early authors [1, 5] often called this area the ‘pneumatic cell’ and clearly understood it to be part of the mesotympanum, outside the borders of the epitympanum. In the conventional superior microdissection removal of the tensor fold made a reasonable evaluation of a normal supratubal recess possible (fig. 59). It also allowed evaluation of the soft tissue insertion ring after removal of the tegmental bone and incising the ring (fig. 62, 63). Pathological changes, however, were found difficult to evaluate properly, because removal of the tensor fold destroyed much of the anatomy of the inflammatory tissues, fixed to the anterior surface of the fold. We, there-

Fig. 76. Series P, case 3, an infant aged 3 months, left ear, anterior approach. The saw cut has been made across the anterior sulcus and the tensor fold (TF) has been partly destroyed, creating a large opening to the anterior epitympanum (between horizontal arrows). TM = Tympanic membrane; M = handle of the malleus; S = stapes; P = promontory; T = tensor tendon. Oblique arrow points to the area of the anterior membrane of Prussak’s space.

fore, developed the anterior approach for microdissection which allowed evaluation of the entire supratubal recess without disturbing any of the normal or pathological structures in the region [20]. It also makes possible the evaluation of a large portion of the mesotympanum and of the anterior portion of the tympanic isthmus. Normal Anatomy by Microdissection The anterior approach gives initially a very limited view, depending upon how near the saw cut is to the anterior sulcus of the tympanic membrane. Usually a good deal of enlargement must be done with a drill to give adequate light for documentation of the structures deep inside. Once near the sulcus, a full view opens to the mesotympanum (fig. 74, 75) of which even the regions past the stapes can be evaluated. The anterior portion of the tympanic isthmus can also be visualized well and the area examined for the presence of blocking folds between the incudostapedial articulation and the tensor tendon. If the saw cut is made too much posteriorly and across the anterior portion of the tympanic membrane, the tensor fold becomes partly destroyed but at the same time the excellent communication to the anterior epitympanum can instantly be seen (fig. 76).


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Fig. 77. Series S, adult case 10, right ear, anterior approach. The tympanic membrane (TM), the malleus handle (M) and the open route towards the tympanic isthmus (curved arrow) form the anterior portion of the mesotympanum. The anterior membrane of Prussak’s space (horizontal arrow) in the anterior pouch and the low portion of the supratubal recess (oblique arrow), superior to the tensor tendon (T), are in full communication with the mesotympanum. The anterior malleal ligamental fold (A), housing also the chorda tympani nerve (C), separates the anterior pouch from the supratubal recess.

Fig. 78. Series S, adult case 12, right ear, anterior approach. Direct view onto the anterior membrane of Prussak’s space (between vertical arrows) showing its typical oval form, the horizontal diameter being longer than the vertical. The anterior malleal ligamental fold (A), housing the chorda tympani nerve (C), separates the anterior pouch and the supratubal recess (horizontal arrow); of the latter only the lateral portion can be seen. M = Malleus handle; T = tensor tendon.

Looking more superiorly along the malleus handle, in addition to the superior mesotympanic structures, the view includes the anterior pouch, the anterior malleal ligamental fold and the lateral lower portion of the supratubal recess (fig. 77). The anterior membrane of Prussak’s space, its anterior wall, appears as a truly delicate duplicate membrane, inferior to the lateral malleal ligamental fold (fig. 78). The reason why Proctor [13, 14] described the anterior wall as being a curved portion of the lateral malleal ligamental fold is apparently due to the fact that he never saw the membrane, neither from Prussak’s space nor from the supratubal recess side. With a mediosuperior view the size and shape of the entire supratubal recess and the tensor fold (fig. 79, 80) can be evaluated in minute detail. Similarly to a view from the anterior epitympanum in the superior approach, a look from the supratubal recess side shows varying textures in the tensor fold. Intact folds had at least portions of thin and smooth surfaces and in some specimens the surfaces were undulating with crossing thicker strands. The fold margins generally appeared thicker and could contain whitish strands resembling

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Fig. 79. Series S, adult case 4, left ear, anterior approach. An oblique view more medially makes a large part of a shallow supratubal recess visible. The central portion of the tensor fold (horizontal arrow) is very thin, the edges are whitish and distinctly thicker and it attaches to the transverse crest (vertical arrow). The oblique arrow points to the anterior membrane of Prussak’s space. M = Malleus handle; TM = tympanic membrane; A = anterior malleal ligamental fold; C = chorda tympani nerve.

fibers seen in the thin portions of the lateral malleal ligamental fold [16]. The membrane appeared resistant to movement but even a slight touching with the suction tip produced an opening, testifying to the fold’s tension. In the entire series of microdissection we have only once noted an anomaly when neither the tensor tendon nor the fold had developed, even though the tensor muscle was in its canal (fig. 81, 82). The anterior approach, similarly to the superior approach, usually reveals the insertion of the tensor fold into the soft tissue ring, while in a few ears it is inserted into the transverse crest. Membrane defects in the tensor fold, as seen already from the superior approach (fig. 61), demonstrated the large size of this new aeration route. Seen from the recess side (fig. 83) it appears convincing that a full removal of the tensor fold will provide an adequate auxiliary pathway for aeration and drainage of the epitympanum in cases where the tympanic isthmus posterior to the tensor tendon does not function at full capacity. The supratubal recess has a rounded dome anterior and slightly superior to the insertion of the tensor fold (fig. 79, 80, 83). Its anterior wall, the recess tegmen,


Fig. 80. Series S, adult case 10, right ear, anterior approach. Direct view medially into a broad and high supratubal recess, the anterior membrane of Prussak’s space is no longer visible. The tensor fold (TF) is centrally thin with thicker whitish strands laterally and superiorly. Chorda tympani nerve (C) runs in the lateral border of the tensor fold. The curved arrow points to the anterior portion of the tympanic isthmus, posterior to the tensor tendon (T). CP = Cochleariform process.

Fig. 81. Series A, adult case 14, left ear, anterior approach. Total absence of both the tensor fold and the tensor tendon. This has been observed only once and it was unilateral in the present case. The vertical arrow points to a small interossicular fold. TM = Tympanic membrane; M = malleus handle; I = long process of the incus.

steadily descends with a convex slope to join the tubal tegmen. The bony walls are generally smooth, but even marked bony tags and ridges may appear especially in the medial bony wall. As a rule, marrow bone adjoined the tegmen bone plate, but in the temporal bones with extensive pneumatization, air cells also extended to the supratubal tegmen. The size of the supratubal recess was generally related to the angle of the tensor fold being large in cases with an upward directed tensor fold [20]. There were, however, exceptions to this rule because the distance of the tensor tendon from the supratubal tegmen could be small. The height of the recess in a few adult specimens, measured from the level of the superior edge of the tensor tendon to the dome of the space, varied between 1 and 5 mm. The dome as a rule extended only to a slightly higher level than the tensor fold insertion ring, with the exception of 2 ears with the fold insertion into a long transverse crest when the upward extension was 2–2.5 mm. The width from the tensor tendon to the eustachian tube tegmen varied from 1.5 to 4 mm. At the midpoint the tensor fold width measured around 2.5–3 mm. The length of the tensor tendon


Fig. 82. Same ear as in figure 81, superior approach. Neither the tensor tendon nor the tensor fold is present and the anterior epitympanum communicates directly with the supratubal recess (R). The lateral incudomalleal fold (horizontal arrow) and the lateral malleal space (vertical arrow) are normal. The oblique arrow points to the transverse crest, the curved arrow to an open aeration pathway via the incudal fossa. M = Malleus; I = incus; S = stapes; TI = posterior portion of the tympanic isthmus.

Fig. 83. Series A, adult case 13, right ear, anterior approach. A membrane defect (between horizontal arrows) appears in the upper portion of the tensor fold. The oblique arrow points to the more posterior transverse crest. The curved arrow points to the anterior portion of the tympanic isthmus, the regular pathway of aeration of the epitympanum. T = Tensor tendon.

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Fig. 84. A patient with a long-standing chronic otitis media, right ear. The tensor tendon (T) is normally the superior border for aeration of the entire middle ear from the eustachian tube (ET). The medial widening (vertical arrow) of the low border of the supratubal recess appears. Anteromedially to it there is much connective tissue and fat between the tensor tympani muscle (TM) and the lateral bony lamella (B) of the muscle canal. M = Malleus; ET = eustachian tube; E = external ear canal. Masson’s trichrome stain. Magnification !12.

Fig. 85. Series A, adult case 21, left ear, anterior approach. The view of the mesotympanum reveals inflammatory webs (horizontal arrow), starting from the stapes (S) and spreading fanwise towards the tympanic isthmus and the tensor tendon (T), causing a partial block of the anterior portion of the isthmus. M = Malleus handle; TM = tympanic membrane.

measured from the malleus handle to the medial leg of the transverse crest varied between 2.5 and 3.5 mm.

Pathology as Seen in Microdissection The anterior approach also allows a good view of the pathological changes in the anterior portion of the tympanic isthmus. These ranged from mature tiny tissue strands from the stapes towards the long process of the incus and the tensor tendon (fig. 85) to webs completely closing the anterior portion of the isthmus, from the stapes to the tensor tendon (fig. 86). In some cases these webs also extended to both sides of the stapes and its tendon, the medial ones partly blocking the posterior portion of the isthmus (fig. 87). Removal of the entire tegmental bone together with the tensor fold gives a particularly good view of the webs closing the anterior portion of the tympanic isthmus (fig. 88). If the entire supratubal and epitympanic bony tegmen is removed and the mucosa incised, microdissection gives a full general view of the eustachian tube lumen, the supratubal recess, the soft tissue insertion ring, the head of the malleus and epitympanum. Pathological changes in different compartments become obvious and can be studied in detail. Pathological changes in the supratubal recess itself were clearly less frequent than those seen in the epitympanum. Chronic changes in the anterior pouch appeared as mature inflammatory strands and webs attached to the frontal membrane of Prussak’s space and to its margins

Normal Anatomy by Serial Sections The supratubal recess extends to levels superior to the highest point of the anterior pouch, hence a large portion of the anterior wall of the recess is seen only in serial sections. Along the tegmen the ongoing composite tissue insertion ring appears clearly in each section (fig. 44, 46). The largest insertion ring observed measured 4 mm in height on the tegmental bone, the narrow ones were around 1 mm. At lower levels the anterior pouch and the recess are separated by the anterior malleal ligamental fold (fig. 55b) until its lowest mucosal surface is passed when the pouch and the recess merge to one large single compartment (fig. 55c). At the level of the tensor tendon the sections usually show also the eustachian tube lumen, laterally there is the anterior sulcus of the tympanic membrane, medially the lowest portion of the supratubal recess with the tensor tympani muscle (fig. 84). The detailed structure of these tissues is apparent only in serial sections but as with the superior microdissection in normal ears, a single observation in microdissection from the tubal orifice mediosuperiorly reveals the entire normal gross appearance of the supratubal recess.

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Fig. 86. Series P, case 9, a child aged 18 months, right ear, anterior approach. The handle of the malleus (M) and the tympanic membrane (TM) are retracted. An inflammatory fold (horizontal arrow) blocks completely the anterior portion of the tympanic isthmus between the incudostapedial articulation (S) and the tensor tendon (T).

Fig. 87. Same ear as in figure 86, an oblique anterior view. An inflammatory web forms a closed space between the stapedius muscle tendon (ST) and promontory (P). Another web (vertical arrow) spreads medially towards the posterior portion of the tympanic isthmus. I = Long process of the incus; S = stapes; PP = pyramidal process.

(fig. 89) or covering the entire membrane by dense scar tissue (fig. 90). The membrane could be indrawn into obliterative processes of Prussak’s space, and hemorrhagic fluid inside the space appeared as a reddish coloring of the membrane. The inflammatory tissue sheets appeared to spread inferior to the tensor tendon near the malleus to the supratubal space whenever the granulation tissue formation in the epitympanum was excessive. First the entrance to the anterior pouch became obliterated and the changes spread further towards the tensor fold. Horizontal scar tissue webs at times appeared at the level of the tubal tegmen (fig. 91), resembling the inflammatory web in Siebenmann’s drawing [1] (fig. 5). Thick soft granulomatous tissue or extensive, more mature tissue webs could fill the entire space (fig. 92). In the early stages they could easily be peeled off from the surface of the tensor fold, in later stages of organization this process was very tedious. At the end, however, the thin intact tensor fold could generally be dissected free, testifying to the spread not through the membrane but around the tensor tendon (fig. 93). Biopsies taken during microdissection of the pathologic changes showed most frequently abundant amounts of collagenic scar tissue with areas of varying maturity. The low portion of the tympanic cavity connecting to the eustachian tube remained singularly unaffected.


Fig. 88. Series A, adult case 15, left ear, anterior approach. The entire tegmental roof is removed. A thick inflammatory web (horizontal arrow) closes the anterior portion of the tympanic isthmus, cutting off half of the entire aeration pathway. The tensor fold has been removed, revealing fully the anterior epitympanum with the head of the malleus (M) and an open route to the medial attic (MA). H = Handle of the malleus; T = tensor tendon.

Fig. 89. Series A, adult case 21, left ear, anterior approach. Mature, thin postinflammatory webs (oblique arrow) crossing the thickened anterior face of the anterior membrane of Prussak’s space (vertical arrow) M = Malleus handle; TM = tympanic membrane; A = anterior malleal ligamental fold.

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Fig. 90. Series A, adult case 11, lef ear, anterior approach. An oblique view shows a thick, mature scar tissue (horizontal arrow), which obscures the entire anterior membrane of Prussak’s space. M = Handle of the malleus; I = long process of the incus.

Fig. 93. Same ear as in figure 91. The central block of the fibrotic mass has been removed, disclosing a thin tensor fold membrane (TF) superior to the tensor tendon (T). On both sides (horizontal arrows) portions of the fibrotic mass remain. The soft tissue insertion ring of the tensor fold is between oblique arrows. Removal of the granulation tissue has opened the route to the anterior epitympanum (curved arrow). M = Head of the malleus; TC = transverse crest.

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Fig. 91. Series A, adult case 12, right ear, anterior approach. The malleus handle (M), the tympanic membrane (TM) and the entrance to the eustachian tube (vertical arrow) are normal. The supratubal recess contains a mass of fibrotic scar tissue (between horizontal arrows), the low border is crossed by a thick strand of scar tissue (oblique arrow), resembling the structure described at this site by Siebenmann [1] (see fig. 5).

Fig. 92. Same ear as in figure 91. A direct view of the supratubal recess shows a thick fibrotic scar tissue superior to the tensor tendon (T), blocking the view to the tensor fold. The horizontal arrow points to an area of granulation tissue which continued through the bone to the anterior attic. M = Malleus handle; I = incus; S = stapes; TM = tympanic membrane.

Fig. 94. Case A89-13, right ear of a neonate, Temporal Bone Foundation. AFCC is concentrated in the medial attic (MA), a lesser amount appears in the anterior attic (AA) and in Prussak’s space (P), already posterior to the malleus (M). The section goes through the superior portion of the supratubal recess (R) which shows three separate spaces, all containing acellular fluid. The surface of the tensor fold on the recess side (vertical arrow) is covered by secretion containing round cells. The anterior pouch (AP) shows mainly acellular fluid and one cell cluster. A = Inferior mucosal surface of the anterior malleal ligamental fold. In more inferior sections the two spaces merged. Hematoxylin-eosin stain. Magnification !12.


Fig. 95. Case A89-295, right ear of an infant aged 15 months, Temporal Bone Foundation. The tensor fold (oblique arrow) is infiltrated by round cells, similarly to the soft tissue walls of the supratubal recess (R). Organization of the secretion is beginning from an epithelial portal (vertical arrow). The highest point of the anterior pouch (horizontal arrow) appears lateral to the anterior malleal ligamental fold (A). M = Malleus; C = chorda tympani nerve. Hematoxylin-eosin stain. Magnification !25.

Fig. 97. Case A80-126, left ear of an infant aged 5 months, Temporal Bone Foundation. Cell-rich mucus is passing from the anterior attic (AA) through a membrane defect (horizontal arrow) in the tensor fold (TF) to the supratubal recess (R). The inflamed and thick end of the tensor fold shows an epithelial defect (oblique arrow) from which the organization process has started and transformed part of the secretion into polypoid granulation tissue (vertical arrow). Free secretion posterior to it in the anterior attic contains round cells of different sizes and giant cells. Hematoxylin-eosin stain. Magnification !120.

Fig. 96. Case A92-168, right ear of an infant aged 8 months, Temporal Bone Foundation. The anterior attic (AA) is filled with thick cellular secretion part of which has entered the supratubal recess (R) through a defect in the tensor fold (between arrows). The secretion fills the recess and part of it is undergoing organization. Prussak’s space (P) is filled with secretion containing round cells. M = Malleus; C = chorda tympani nerve, E = external ear canal. Hematoxylin-eosin stain. Magnification !25.

Pathology as Seen in Serial Sections We have not had cases among our serial sections showing large, mature granulation tissue masses in the supratubal recess, comparable to those shown in figures 90–93. Among the infants with pathology related to an influx of AFCC into the middle ear, there are many temporal bones showing changes from acute to subchronic inflammation also in the supratubal recess but not diseases of really long duration. The initial spread of AFCC into the supratubal recess remained generally less than the amount seen in the epitympanic compartments (fig. 94), together with the area of the stapes. In cases with a chronic inflammation with an acute phase, the supratubal recess could show both mucosal edema and cellular infiltration as well as secretion with leukocytes in the lumen, with signs of an early organization process (fig. 95). In cases with a membrane defect in the tensor fold, secretion was seen to pass from the anterior attic through the defect into the supratubal recess, from where the drainage continued to the eustachian tube (fig. 96, 97). This pathology is more extensively discussed in Part 2 of this atlas, dealing specifically with AFCC and chronic inflammation.


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References 1 Siebenmann F: Mittelohr and Labyrinth; in Bardeleben K von (ed): Handbuch der Anatomie des Menschen. Jena, Fischer, 1897, vol 5, Abt. 2, pp 244–287. 2 von Tröltsch A: Lehrbuch der Ohrenheilkunde mit Einschluss der Anatomie des Ohres, ed 7. Leipzig, F.C.W. Vogel, 1881. 3 Prussak A: Zur Anatomie des menschlichen Trommelfells. Arch Ohrenheilkd 1867;3:255– 278. 4 Helmholtz H: Die Mechanik der Gehörknöchelchen und des Trommelfells. Pflügers Arch Ges Physiol 1868;1:1–25. 5 Hammar JA: Studien über die Entwicklung des Vorderdarms und einiger angrenzenden Organe. 1. Allgemeine Morphologie der Schlundspalten beim Menschen. Entwicklung des Mittelohrraumes und des äusseren Gehörganges. Arch Mikrosk Anat 1902;59:471–628. 6 Wittmaack K: Über die normale und pathologische Pneumatisation des Schläfenbeines. Jena, Fischer, 1918, pp 37–56, 295–296. 7 Wittmaack K: Die entzündlichen Erkrankungsprozesse des Gehörorgans; in Henke F, Lubarsch O (eds): Handbuch der speziellen pathologischen Anatomie und Histologie. Berlin, Springer, 1926, pp 102–379. 8 Palva T, Johnsson L-G: The epitympanic compartments, surgical considerations: A re-evaluation based on findings in a pair of temporal bones and a literature review. Am J Otol 1995; 16:505–513. 9 Politzer A: Über die Höhlensysteme zwischen Trommelfell und Hammerhals. Med Wochenschr (Wien) 1870;20:252–253. 10 Politzer A: Lehrbuch der Ohrenheilkunde, ed 5. Stuttgart, Enke, 1908, pp 24–28. 11 Wullstein HL, Wullstein SR: Tympanoplasty, Osteoplastic Epitympanotomy. New York, Thieme Medical, 1990. 12 Tos M: Mastoid Surgery and Reconstructive Procedures, vol 2: Manual of Middle Ear Surgery. Stuttgart, Thieme, 1995.

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13 Proctor B: The development of the middle ear spaces and their surgical significance. J Laryngol Otol 1964;78:631–648. 14 Proctor B: Surgical Anatomy of Ear and Temporal Bone. New York, Thieme, 1989. 15 Schuknecht HF, Guluya AJ: Anatomy of the Temporal Bone with Surgical Implications. Philadelphia, Lea & Febiger, 1986. 16 Palva T, Ramsay H, Böhling T: Prussak’s space revisited. Am J Otol 1996;17:512–520. 17 Palva T, Ramsay H: Prussak’s space in health and disease; in Tos M, Thomsen J, Balle V (eds): Otitis media Today. The Hague, Kugler, 1999, pp 301–306. 18 Palva T, Ramsay H: Incudal folds and epitympanic aeration. Am J Otol 1996;17:700–708. 19 Palva T, Ramsay H, Böhling T: Tensor fold and anterior epitympanum Am J Otol 1997;18: 307–316. 20 Palva T, Ramsay H, Böhling T: Lateral and anterior approach to supratubal recess and tensor fold. Am J Otol 1998;19:405–414. 21 Palva T, Ramsay H: Mucosal pathology of the attic; in Tos M, Thomsen J, Balle V (eds): Otitis media Today. The Hague, Kugler, 1999, pp 307–314. 22 Aimi K: The clinical significance of epitympanic mucosal folds. Arch Otolaryngol 1971; 94:499–508. 23 Aimi K: The tympanic isthmus: Its anatomy and clinical significance. Laryngoscope 1978; 88:1067–1081. 24 Palva T, Ramsay H: Chronic inflammatory ear disease and cholesteatoma. Creation of auxiliary attic aeration pathways by microdissection. Am J Otol 1999;20:145–151. 25 Palva T: Surgical treatment of adhesive tympanum. Acta Otolaryngol Suppl 1964;188:70– 74. 26 Palva T, Ramsay H: Myringoplasty and tympanoplasty – Results related to training and experience. Clin Otolaryngol 1995;20:329–335. 27 Northrop C, Piza J, Eavey R: Histological observations of amniotic fluid cellular content in the ears of neonates and infants. Int J Pediatr Otorhinolaryngol 1986;11:113–127.


28 Palva T, Northrop C, Ramsay H: Middle ear pathology in infants. Am J Otol, in press. 29 Palva T, Northrop C, Ramsay H: Aeration and drainage of Prussak’s space. Int J Pediatr Otorhinolaryngol 2001;57:55–65. 30 Chatellier HP, Lemoine J: Le diaphragme interattico-tympanique du nouveau-né. Ann Otolaryngol Chir Cervicofac (Paris) 1946;13: 534–566. 31 Palva T, Northrop C, Ramsay H: Spread of amniotic fluid cellular content within the neonate middle ear. Int J Pediatr Otorhinolaryngol 1999;48:143–153. 32 Palva T, Northrop C, Ramsay H: Effect of amnion fluid cellular content to attic aeration pathways. Histological observations of infants aged 2 to 4 months. Am J Otol 2000;21:62–71. 33 Palva T, Johnsson L-G, Ramsay H: Attic aeration in temporal bones from children with recurring otitis media. Tympanostomy tubes did not cure disease in Prussak’s space. Am J Otol 2000;21:485–493. 34 Palva T, Ramsay H: Endoscopy of the middle ear (letter). Am J Otol 2000;21:288–289. 35 Klug C, Fabinyl B, Tschabitcher M: Endoscopy of the middle ear through the eustachian tube. Anatomic possibilities and limitations. Am J Otol 1999;20:299–303. 36 Sheehy JL: Surgery of chronic otitis media; in English G (ed): Otolaryngology. Hagerstown, Harper & Row, 1977. 37 Morimitsu T: Cholesteatoma and Anterior Tympanotomy. Tokyo, Springer, 1997, pp 1– 114. 38 Tono T, Schachern P, Morizono T, et al: Developmental anatomy of the supratubal recess in temporal bones from fetuses and children. Am J Otol 1996;17:99–107. 39 Palva T, Northrop C, Ramsay H: Supratubal recess in neonates and infants. Int J Pediatr Otorhinolaryngol 1999;50:99–107.



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Introduction and Short Review of the Literature on Amniotic Fluid Cellular Content Towards the end of the 19th century the scientific literature contained numerous publications on the ‘otitis media neonatorum’, a condition that had repeatedly been seen in the autopsies of neonates. Secretion, or frank pus had been found in the middle ear compartments and a lively controversy arose as to whether or not this finding should be considered as a physiological phenomenon or whether it was due to infection. The great authorities of the period took part in the debate and the advances made by the development of bacteriology were initially thought to resolve the question. However, the discovery of saprophytic bacteria in the cultures, associated with the delay in the autopsies, kept the battle lines intact. In 1897 Aschoff [1] published an article which can be regarded as a cornerstone in the discussion of the newborn middle ear dilemma. His neonate autopsy material was transported from the obstetrical hospital in Hanover to the Institute of Pathology in Göttingen, a delay that made the bacteriological investigations futile. Instead, he decided to concentrate on studying the cellular composition of the middle ear secretion by microscopy and on evaluating the degree of inflammation of the middle ear mucosa in the sections. During a 2-year period he managed to evaluate 85 stillborns and neonates, presenting the essential individual data in a detailed table. He concluded that the gross nature of the secretion varied considerably but that the mucoid element was generally prominent. In microscopy the findings included the presence of round cells, polymorphonuclear leukocytes, nuclei-containing or nonnucleated cells of the squamous epithelium, hairs, larger particles of meconium, and cholesterol crystals. His first conclusion was that in all children the middle ear contains at birth secretion which varies from clear fluid to

thick mucus mixed with pus and that an amniotic fluid cellular content (AFCC) is present in a great percentage of the specimens. Aschoff’s next observation was that of the 33 ears which showed a diseased middle ear with mucoid secretion and inflammatory cells, 19 showed a large amount of AFCC in the middle ear whereas of 39 ears with a healthy middle ear only 2 showed some AFCC. Based on these data he concluded that it is the AFCC that is responsible for the presence of the leukocytes. In additional studies of 9 fetuses of 11–27 cm in length, 2 were found to show squamous epithelial cells in the ear fluid. In one case, delivered to him with an intact amnion sac after the fourth gestational month, he found exactly similar cells in the amnion fluid as were present in the middle ear. He felt the evidence was conclusive in showing that the inflammatory cell response in the middle ear secretion was due to the presence of AFCC. The inflammatory changes in the neonate were not physiological but a response to the aspirated or swallowed AFCC. The ‘otitis media neonatorum’ thus was a typical reaction against this foreign material. The histological studies were in accordance with the findings based on the above conclusions from the cellular analysis of the secretions. The mucosa showed infiltration of the subepithelial layer with inflammatory cells, increasing with increasing amounts of AFCC present. In the ears with no or only a small amount of AFCC the mucosa was normal. Even in the presence of large contamination, however, the leukocytic infiltration of the subepithelial tissue never reached the amount generally seen in severe cases of otitis media of infectious origin. The data and conclusions of Aschoff and of other prominent scientists were elaborated on by Wittmaack [2, 3], an outstanding authority in ear pathology. In 1925 [3] he considered the battle between the two camps to be over

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and it was universally accepted that the filling of the neonatal middle ear with a mucoid secretion is definitely pathological. The process is sterile and develops because of the presence of AFCC in the middle ear causing the foreign body-type inflammation. He went an important step further by developing the notion that the AFCC is responsible for the infant otitis media, seen most often at the age of 4–5 months, but often continuing much longer. It is a condition marked by a strong hyperplastic reaction of the mucosa that, together with secretion, may fill all middle ear spaces. Wittmaack’s histological figures demonstrated the continuing process in the infant otitis media, starting from the clusters of AFCC inside a granulation tissue and leading through the organization process of the secretions to large hyperplastic tissue masses in the middle ear compartments. These processes were particularly severe in the epitympanum while the mucosal polyps were more marked in the meso- and hypotympanum. Wittmaack considered that nature could remove the thick tissue-fixed secretion only by resorption or by the process of organization. The open space lost to granulation tissue could be partly regained by its maturation and subsequent shrinkage. However, Wittmaack observed that there was a variation in this future development of the organizing tissues. If the organization process had completely eliminated the foreign bodies, the process calmed down, the granulation tissue matured and formed postinflammatory scar tissue and webs crossing from one compartment wall to the other. If the child suffered, for example, from periods of vomiting, new foreign bodies could be introduced into the ears and the process would start anew. During the course of months it could be accompanied by secondary, low grade bacterial invaders and a latent fight between the mucosa and the invader would continue, in some cases over many years. During certain periods the invaders may become more virulent and an exudative phase with secretion and signs of inflammation developed. An infection with virulent bacteria would cause symptoms of an acute process. When the cases were of longer standing the process would prevent pneumatization of the mastoid bone. During the following decades the presence of AFCC in neonate and infant ears was confirmed by several investigators. Benner [4] in 1940 in a study of 70 neonates not only examined the temporal bones but also the paranasal sinuses and lungs and found 44 cases to be essentially normal while 26 (37%) showed an inflammatory reaction. It is interesting to note that in her extensive bacteriological portion of the study she came to the same conclusion as

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Aschoff [1], namely that the results do not correlate with the findings of pathology. Nevertheless, even if she speculated that the pathological process could be due to a foreign body-type reaction, she was more inclined to think that the inflammatory condition in the ears resulted from an aspiration of infected amniotic fluid. Similar reasoning can also be found in a study by McLellan et al. [5] who found an inflammatory reaction in 19 of 28 middle ears of premature infants. Buch and Jörgensen [6] reviewed serial sections of 135 temporal bones of neonates and found AFCC in 77% in ample or moderate amounts. They felt that conclusions of the etiology of the infant otitis media would be possible only after bacteriological investigations. In 1973 de Sa [7] reported a series of 130 cases, 36 stillbirths and 94 neonatal deaths. In 56 cases the middle ear cavities were considered as normal, in 55 AFCC was present, and in 17 cases otitis media was found to be present. In 2 cases there was mucoid debris but AFCC could not be found. AFCC was seen in the stillbirths in infants of over 28 weeks of gestation who had suffered intrapartum asphyxia and also had AFCC in the pulmonary airways. While the second group with AFCC in the middle ears conforms well with the findings of Aschoff [1] and Wittmaack [2, 3], the third group of 17 ears with frank otitis media deserves attention. These children lived from 12 h to 27 days after birth, 15 over 4 days. 11 of them had AFCC present but all had evidence of infection elsewhere, particularly with septicemia, pneumonia and meningitis, the principal invaders being Escherichia coli and Pseudomonas. They thus can be set apart from the group of pure infant otitis media but represent ears of generalized infection independent of AFCC. In a subsequent study de Sa [8] reported on histological findings in 72 infants of varying periods of gestation and ages, all of whom died after receiving ventilatory support and oxygen for longer than 14 days. Only 5 of these infants showed normal middle ear histology. In the remainder a wide range of changes were observed, from glandular metaplasia, retained squamous debris, squamous polyps, otitis media signs to destruction of ossicles. None of the middle ear problems was diagnosed before autopsy, all were associated with pneumonia. De Sa drew the important conclusion that similar changes, possibly of lesser severity, could be present in the survivors in whom otitis media with conductive hearing losses could be expected. During the last two decades the Boston-Costa Rican research group has reinvigorated the concept of the


AFCC-related infant otitis media. In a study of 63 children aged from 10 min to 70 days, 39 of 43 bones of neonates had AFCC present, and in children aged 31–70 days AFCC was found in 11 of 20 bones [9]. Keratinized cells and lanugo hair appeared in the early stages free in the lumen without a mucosal reaction, later phagocytosis and the development of granulation tissue could be observed, the most involved types showing large, completely epithelialized masses of granulation tissue still containing AFCC. Mucosal reaction appeared in the form of mononuclear leukocytes subepithelially in the areas in contact with AFCC and bridges had formed from the mucosa to the organizing mass of AFCC and inflammatory cells. Clinical relevance was discussed on the basis of formation of middle ear adhesions, a tendency to develop recurring otitis media infections and of a possible development of cholesteatoma from the inoculated squamous cells. The importance of the amount of AFCC contamination was further evaluated by comparing the temporal bones of 9 patients born through meconium-contaminated amniotic fluid with 10 children born through clear amniotic fluid [10]. All bones came from neonates less than 17 days of age and altogether 37 bones could be evaluated. As can be expected, greater volumes of AFCC were found in children born through thick meconium and it was thought that these children would be at greater risk of developing otitis media due to this preexisting inflammatory foreign body reaction. Of this same group, Eavey [11] published a comprehensive report of the abnormalities in a neonate ear. Otoscopic observations in 44 neonates of 1–24 days of age showed that nearly all (97.7%) of the tympanic membranes were abnormal as to their color, luster, vascularity and mobility. However, it was not possible to determine the middle ear status as myringotomy and aspiration was not performed because this was thought to create ethical problems in an asymptomatic child. Instead, the 56 temporal bones of the Costa Rican material were used to give an idea of the middle ear contents in the newborn. This examination, as noted above [9], provided ample confirmation of the presence of AFCC in the middle ears. Finally, Eavey collected minced hair and epithelium from the abdomen of a gerbil and in seven animals injected it to the right tympanic bulla. The animals were sacrificed from 0 to 63 days later and the temporal bones serially sectioned. By 7 days there was granulation tissue, blood vessel formation and mucosal thickening which increased in 14 days and showed also some osteogenesis. These alterations increased further in severity and cholesterol granu-

lomas were met at 42 days. At 63 days much hair was still present embedded in granulation tissue but also trapped inside new bone formation. Bacterial infection did not appear in any of the ears. The article by Eavey provides an ample bibliography for various aspects of the neonatal ear. As an evaluation of all these aspects with reference to these articles is beyond the scope of this atlas, a reader further interested in some of the details is referred to Eavey’s bibliography. Northrop et al. [12] discussed the future problems possibly caused by AFCC on the basis of an increased series of 261 temporal bones, 155 neonate and 106 infant ears. Foreign material was found in all neonate ears except 3 with Potter’s sequence. Of 38 ears of neonates born through thick meconium 12 had abundant epithelial cells, many with lanugo hair, 17 ears showed a moderate amount and 2 a sparse one. Seven could not be evaluated due to damage during removal of the bones. In infants, 28 of 106 temporal bones showed massive reactive polyps, 46 had moderate reactivity and 14 (13%) showed completely clear middle ear spaces. Only 3 had been born through thick meconium indicating that heavy contamination would not be a prerequisite for the presence of AFCC in the middle ear. It was thought that the changes demonstrated make the infant prone to otitis and indicate that the circumstances of their birth should be investigated for possible clues as to the etiology of the bouts of recurrent otitis media.

Short Review of Mastoid Pneumatization Even if our observations of mastoid pneumatization form only a sidetrack in the present analysis of neonate and infant temporal bones and must await a more extensive treatise, we will nevertheless review the relevant literature at this stage because AFCC has been shown to play an important role in arrested pneumatization [2, 3]. Numerous recent studies published on this subject speculate, mostly with irrelevant data, which ‘theory’ is correct, the genetic ones suggesting that the genetic factors determine the size of the mastoid pneumatization, even up to full absence of mastoid air cells, making the ear susceptible to infections, or the ‘environmental’ ones suggesting that inflammation caused by various agents leads to the observed arrested pneumatization. These questions can only be approached by first studying the early basic documents of the histology of mastoid pneumatization, such as Wittmaack’s book [2] published in 1918, and his articles in the handbook on the histopathology of the ear [3] and

2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection

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by Eckert-Möbius [13] who gave a short version of Wittmaack’s data [2, 3] of the pneumatization in a normal healthy ear. The first phase of a normal pneumatization was found to extend from birth through the first year of life. The middle ear spaces and the mastoid antrum are usually well formed in the neonate even if a substantial amount of embryological tissue is present especially in the posterior hypotympanum, anterior attic and mastoid antrum. The mastoid process at this stage consists of spongy bone. The main change in the growing bone towards the end of the first year of life was the enlargement of the mastoid antrum posteriorly, inferiorly and medially due to partial resorption of bone and thinning of the subepithelial mesenchyme. The basic process involved invasion of the vascular subepithelial connective tissue through the bone defects, caused by resorption, to the open marrow spaces. The cuboid or flat epithelium followed into the depths covering the developing spaces connected to the antrum. The walls of the antrum at 6 months of age remained still mostly even, with the exception of the posterior ear canal bone where the trabeculae could be more prominent. The second phase of normal pneumatization involved the development of the pneumatic cell system and continued until the age of 3 years. Towards the end of the first year the histological picture started to show a major continuous change in the form of a more rapid bone resorption and advancement of the connective tissue into the receding marrow spaces. The covering cuboid epithelium formed the surface of the bone ridges that projected towards the antral lumen and followed the connective tissue into the depths to line the developing bony network of air cells communicating with the antrum. Simultaneously with this process, pneumatization proceeded also from the low posterior tympanic cavity independent of the antral pneumatization, and provided aeration for the mastoid tip area. From the anterior portions of the middle ear pneumatization proceeded towards the bone surrounding the tubal orifice. At the end of the second period the mastoid bone showed a mixed picture of pneumatization combined with more or less marrow bone present especially in the mastoid tip area. Generally at the end of the third year, and latest at the end of the fourth year, the pneumatization of the mastoid bone was completed. If this was not true at the end of the fifth year, there had been a disturbance of the pneumatization process. The third period of normal pneumatization involved a slow enlargement towards the compact labyrinthine bone and in remodelling the existing air cells around the blood vessels. However, as far as the area of pneumatization is

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concerned, these changes did not essentially change the picture seen at the end of the fifth year of life. Pathological pneumatization was divided by Wittmaack [2, 3] into two forms, the most important being associated with a grossly hyperplastic mucosa, the other being due to mucosal fibrosis. The hyperplastic form generally followed the ‘infant otitis media’, resulting from aspiration of AFCC, but he considered also the aspiration of gastric contents during vomiting as an additional cause especially at the age from 2 to 4 months. This foreign material led to the development of mucosal hyperplasia, and to the presence of generally sterile mucoid secretion; if there was a growth it was by low-virulence bacteria. The development of granulation tissue led to a protracted course continuing possibly over several years. The process did not cause a perforation of the tympanic membrane, which looked more or less normal. Even with the naked eye in the temporal bones very sticky mucus could be seen in the middle ear compartments with tissue masses fastened by many bridges to the mucosa. The hyperplastic otitis media of the neonate was found to have only a small effect on the first phase of normal pneumatization. Thus the marrow bone adjacent to the antrum showed a beginning of a slight invasion by connective tissue with numerous blood vessels, similarly to normal pneumatization. However, the second and third phases became disturbed, the final effect depending upon the degree of the hyperplastic changes in the middle ear and mastoid antrum. The most serious end result in the second phase was a full absence of mastoid pneumatization and it was associated with the filling of the antrum by a large mass of organizing granulation tissue. Even if the nearest marrow bone areas became filled with the connective tissue from the highly hyperplastic antral mucosa, the epithelial invagination did not occur and the bone gradually started to ossify and in time changed to fully compact sclerotic bone. The tympanum remained filled with mucoid secretion which together with the granulation tissue was particularly marked in the epitympanum. Moderate arrest of pneumatization occurred in cases with less intensive mucosal hyperplasia and with less marked development of granulation tissue in the large middle ear compartments and the antrum. The peripheral mastoid areas showed sclerotic changes, while the areas around the antrum showed a replacement of red bone marrow with connective tissue, followed by the development of air cells that remained smaller than usual, with thick bony walls. Microscopically these air cells often showed mucosal cystic formations, and at times there was


the same organization process in the secretion which appeared in the main compartments. The third form, following a slight mucosal hyperplasia, affected the pneumatization process only slightly. All middle ear compartments appeared macrosopically wide with less secretion than in the two preceding models. The structure of the pneumatized air cells differed from normal by their irregular form and by the thicker than normal bony septa. Some of the air cells were filled with connective tissue. Often the middle portion of the mastoid showed a larger irregularity with small air cells lined by thick mucosa, while the terminal air cells in the mastoid tip, connected to the posterior tympanum, occasionally were large and intact. The extent of the pneumatized bone could be as large as seen in normal cases. Wittmaack [2, 3] found the second form of arrested pneumatization to be associated with exudative processes due to virulent infections occurring at any age. He found in such ears a very thin mucosa with a fibrotic, nearly absent subepithelial layer. This mucosa was not able to continue the pneumatization process and the mastoid air cell formation halted at the stage it had reached when the exudative process started. He also described a combined hyperplastic-fibrotic type in which pneumatization could continue from the regions containing active, thicker subepithelial tissue rich in capillaries on top of the marrow bone. Wittmack’s strong dependence on the two types of mucosa leading to arrested pneumatization was already criticized by some of his contemparies and can be found, for example, in the investigations by Rüedi [14, 15]. He pointed out that normal pneumatization is a combination of two different occurrences, of a preformation of the bony spaces and of a growing of the epithelium from the eustachian tube to prepare for the filling of these spaces with air. At birth the preformed open spaces limited by bone include the entire middle ear, the mastoid antrum and at times a few air cells while the epithelium-lined air space is much smaller. The intervening tissue between the two, the embryonal mesenchyme, has areas of a widely varying thickness and could be thought of as filling material. Further growth of bone and its preformation continues guided by hereditary factors, leading to the development of bone spaces filled with connective tissue. Simultaneously with this process the mesenchyme becomes thinner, and at the end of 1 year all bone surfaces are normally covered by a thin layer of mucoperiosteum. Thus during the first months of life, due to the thick embryonal mesenchyme, every infant in Wittmaack’s terminology could be said to have a hyperplastic mucosa. The thinning

process occurs when there is a physiological equality of pressure between the enlarging lumen and the living tissues. Neonate otitis media with underpressure and associated changes disrupts this normal mucosal alteration and even if the preformation of bone space continues, there is no receding of the mesenchyme which may even increase in thickness and the mucosa becomes highly hyperplastic. This will put an end to the pneumatization process and the dissociation between the two processes may prevail for a long time and may finally lead to adhesive processes or chronic middle ear infections. The above described views, based on documented histology of pneumatization, prevailed as the main concepts and their essential message was that every normal ear is subject to mastoid pneumatization the extent of which may show individual variation. Arrested pneumatization is always due to external factors having their basic influence during the first 3 years of life. This notion was challenged in 1940 especially by Diamant [16] and later amplified by Dahlberg and Diamant [17] and by Diamant [18] with a thesis that the pneumatization process was governed only by genetic factors and that the postpartum environmental factors did not play an appreciable role in it. Diamant’s concepts [16] were based on measurements of the pneumatized areas in a series of 320 ears, termed as normal material, consisting in the main of patients admitted to hospital because of scarlet fever. Further groups were formed of patients with acute or chronic otitis media, to which later studies [17, 18] of the pneumatized areas measured from monovular and binovular twins were added. The measurements were made with a planimeter from an X-ray film taken in a modified lateral projection. The data showed that in the studied groups the areal figures became progressively smaller with increasing severity of middle ear disease. After a statistical assessment of the results [16–18] it was proposed that mastoid pneumatization was determined by genes and that the environmental factors had their effect only in utero and were definitely nonpathological. What these environmental factors were was not clarified, even if the presence of amniotic fluid in the ear during the fetal period was considered to possibly form a small portion of them. Nothing that happened at the time of delivery or postpartum, even the massive aspirations of AFCC reported by Aschoff [1], could in his opinion [18] appreciably alter the pattern of the predetermined size of mastoid pneumatization. The small areal figures in diseased ears were explained away by a claim that the acellular or hypocellular mastoid was prone to otitic infections, hence the association of arrested pneumatization with chronic otitis media.


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Diamant’s claim [16] that the mastoid pneumatization was determined only by genetic and intrauterine factors was opposed by Ojala [19] in a histological study of 10 infant and 89 adult human temporal bones. In the infant bones pneumatization was seen to start at the end of the fetal period but its amount varied from case to case, being similar bilaterally. He confirmed Rüedi’s concept [14, 15] of the normal association of the continuing preformation of the growing periosteal bony walls of the mastoid cavity with simultaneous thinning of the mucous membrane. In an infant otitis media the latter remained hyperplastic, showing what Rüedi considered to be a dissociation of the two processes, leading to an arrest of pneumatization. He stressed that the ‘hyperplastic mucous membrane constitution’ is not pathognomonic to otitis media in infancy alone but may occur at any age under the same conditions, essentially providing evidence for an inflammation or a postinflammatory state. The basic requirement for air cell formation is that the pressure in the growing air space remains continually equal to the tissue pressure, for its maintenance it is of no consequence whether this is achieved with the aid of air or with amniotic fluid during the fetal period. Sclerosis of the mastoid was attributed to recurrent or chronic otitis media processes. Tumarkin’s series of studies [20–22] published in 1957 should be read by all interested in mastoid pneumatization. He did not accept the conclusions drawn by the Swedish investigators [16–18] and took pains to reexamine their statistics. He presented arguments which point by point revealed the fallacies in the statistical treatment of the data employed to support the genetic theory. When properly examined the data supported a different conclusion, namely that the chronic otitis media was the cause for arrested pneumatization. In addition, he also pointed out that the above-reviewed Wittmaack concept was marred by the speculation on the dominant role of the mucous membrane, the hyperplastic mucosa arising from the prenatal foreign body inflammation and the hypoplastic mucosa resulting from fibrosis following exudative postnatal infections. Tumarkin felt that this complicated histological speculation obscured the true value of Wittmaack’s great contribution, namely that the hypocellular mastoid is the end result of arrested normal pneumatization and that it occurs as a result of an aseptic phenomenon or a severe infection. He felt that the evidence for or against the prenatal aseptic (AFCC) inflammation was inadequate and thought that the aseptic type of inflammation was due to the middle ear process in children we now call secretory otitis media.

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Tumarkin’s own data derived from planimetric measurements similar to those used by Diamant [16] of the size of the mastoid pneumatization in groups of workingclass children from Liverpool slums with frequent infections in contrast to middle-class children with much better living standards, with a smaller number of infections and better access to medical care. The results were clearcut, the working-class group showing poorer pneumatization than the middle-class children. He concluded that normal mastoids are always pneumatized, and that the hypocellular mastoid is caused primarily by the inhibition of pneumatization due to pathological forces which may play a part during infancy and childhood. Such hypocellular mastoids, affected by persistent chronic inflammation, gradually sclerosed and became ultimately acellular. These results are the same as the histological ones presented by Wittmaack [2, 3] with the difference that Wittmaack stressed the type of mucous membrane determining the course while Tumarkin stressed the underpressure in the middle ear and infections from birth to puberty as the causes leading to different degrees of arrested pneumatization. Because of these differences to Wittmaack’s thesis Tumarkin considered himself a neo-Wittmaackian. The remodelling of bone and sclerosis of the mastoid, shown to occur in infants both in aseptic and infected ears by Wittmaack [2, 3] and Ojala [19], was found to occur in animal experiments on guinea pigs by Friedmann [23]. Especially in the chronic type of suppuration, following an inoculation of various strains of bacteria, there was a depositing of fresh bone resulting, with pyocyaneus and proteus strains, in a complete obliteration of the bulla. In human clinical material, in acute and chronic mastoiditis in children, the surgically removed bone chips showed that the mastoid bone was involved early in the course of the disease. There was repeated absorption and deposition of bone leading to a reconstruction of the normal pattern, and in extensive disease the depositing of new bone led to partial or total obliteration of the air cell system [24, 25]. Evidence of the role of blocked aeration on pneumatization was obtained from the animal experiments of Ojala [26] and Beaumont [27]. Both used the chick humerus as a model because this bone is pneumatized through the foramen pneumaticum which can be blocked either temporarily or permanently. Ojala reported that a temporary blockade of 2–4 weeks’ duration delayed but did not arrest pneumatization while a permanent occlusion was followed by an inflammatory process in the humerus comparable to the long-standing occlusion of the eusta-


chian tube. Such pathological conditions arrested the air space formation in the chick humerus. Beaumont’s study employed 24 cockerels with full pneumatization and 20 who initially showed partial pneumatization of the humerus. After occlusion of the foramen pneumaticum serial sacrifice was carried out weekly over 4 weeks, and monthly over a period from 5 to 8 months. Early changes involved initial rounding of the epithelial cells followed by the cytoplasm becoming foamy and laden with fat. The subepithelial tissue initially showed marked congestion of blood vessels, followed by tissue edema with protein-rich fluid collection. Mesenchymal proliferation formed polyps accompanied by an outgrowth of blood vessels. After 6–8 weeks the mesenchymal cells showed intracellular deposits of lipoid material, some areas changed to true fat cells. After 4–5 months two patterns of new bone formation appeared, one in the midst of the masses of vascular mesenchyme, another immediately deep to and parallel to the lining epithelium and the dilated network of blood vessels. Cholesterol granuloma tissue appeared after 2–3 months, scattered throughout all regions of the obstructed pneumatic system, increasing in animals sacrificed later. New bone was also deposited in this tissue, appearing finally as cleft-like spaces encased in a block of new bone. The bone marrow already present prior to blockage did not undergo any significant alterations. No specimen in the series showed total histological obliteration of all areas of the original pneumatic system. The investigations reviewed above strongly suggest that arrested pneumatization is associated either with an aseptic inflammation, generally caused by AFCC, or follows long-standing middle ear infections [2, 3, 19–25], even if Wittmaack’s original idea of the mucous membrane dependence as such is outdated. A lack of aeration alone, without infection, can convert an already pneumatized system into an obliterated state with new bone formation and sclerosis [26, 27]. It can be said that the general process of arrested pneumatization is well known, but detailed data of the normal speed and extent of undisturbed air cell development month by month during the first year of life are not available. Such additional data would still be of great interest and they can be obtained only from histological analyses of sufficiently large numbers of serially sectioned temporal bones from neonates and young children.

Amniotic Fluid Cellular Content-Related Middle Ear Pathology as a Function of Age in Serial Sections Temporal Bones from Neonates We started the joint project between the Temporal Bone Foundation in Boston, Mass. and the Department of Otolaryngology in Helsinki with an analysis of the spread of AFCC into various compartments of the middle ear, the development and definition of which had been one of the principal interests of the Helsinki group. For this, both temporal bones from four neonate autopsies were available. Cases 1, 2 and 4 had been born full term through thick meconium while the records contained no mention of meconium in case 3. Cases 1 and 2 died within 24 h after birth of respiratory distress due to meconium aspiration. Case 3 died at 3 days of age due to associated congenital heart defects and case 4 survived the pulmonary aspiration of AFCC for 9 days [28]. In the three cases with meconium colored amniotic fluid AFCC was found in the whole middle ear area from the superior attic to the hypotympanum whereas in case 3 the main amount appeared in the antrum and posterior tympanum. The mucosal reaction was manifested in all cases in subepithelial local round cell collections without signs of an infectious process. There were many areas with retained fetal tissue, the amount of which differed considerably between the specimens. The entire material in Part 2 of this atlas, with the exception of case 4 of the temporal bones of the neonates, is from the collection of the Temporal Bone Foundation. The methods used to prepare the serial sections were described earlier (p. 11). The staining method used in all figures shown in this section is hematoxylin-eosin. Superior and Anterior Epitympanum and Antrum In all temporal bones the sections inferior to the epitympanic bony roof showed a common air space extending from the anterior bony wall to the antrum. The AFCC clusters in cases 1 and 2 floated partly free in the fluid and were partly adjacent to the epithelial surfaces and niches formed by the numerous ridges of the squamous bone (fig. 98). In case 3 the superior and anterior attics were free of amniotic cells but this material filled the antrum. In case 4 the main bulk of AFCC was in the posterior tympanum and in the mastoid antrum. Cell clusters in the anterior attic in cases 1 and 2 had contact surfaces with epithelium with a beginning development of portals for subsequent organization (fig. 99), while in the 9-day-old


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Fig. 98. Case 1 (A87-213), 1 day of age, right ear, section 12. General view of the superior epitympanum and mastoid antrum (A). A moderate amount of AFCC is concentrated posterior to the head of the malleus (M) and to the peripheric portions of the fluid lining the mucosa of the antrum. Fetal mesenchyme is present in front of the malleus and between the trabeculae (oblique arrows) of the preformed thin squamous bone. A horizontal arrow points to its merging with the thick medial wall of the antrum, the petrous bone, which contains hemopoietic bone marrow, with multiple connections to the mucosa (vertical arrow). Magnification !7.

Fig. 99. Case 1, right ear, section 81. The anterior attic (AA) is filled with amniotic fluid containing a larger cluster of AFCC. The cells also line the anterolateral mucosa (horizontal arrow). Epithelial breaks form portals for organization (oblique arrows). Fetal tissue surrounds the superior portion of the anterior malleal ligament (A) and shows vacuolization. UL = Superior portion of the upper lateral attic; M = malleus. Magnification !25.

case 4 organization of a large AFCC cluster was under way via a portal through the mastoid epithelium (fig. 100).

Fig. 100. Case 4, series P, a neonate of 9 days, right ear, section 20. An epithelial break in the mucosa (vertical arrow) provides a portal for organization of the large mass of AFCC which fills the mastoid antrum. Most of the inflammatory cells are round cells, many of them show signs of degeneration. The oblique arrow points to a larger cluster of squamous epithelial cells. B = Medial bony wall of antrum. Magnification !150.

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Tensor Fold and Supratubal Recess Different amounts of AFCC clusters adhered to the posterior surface of the tensor fold in both ears of case 1 (fig. 101, 102). In cases 2 and 3 the fold surfaces showed only thin films of amniotic fluid and cells. In case 4 the fold was thin and had a location more posterior than normally. Its surface was free of cells but cell clusters were present in both the anterior attic and the supratubal recess (fig. 103). None of the folds showed membrane defects and there was a full separation of the anterior attic from the supratubal recess. The supratubal recesses in cases 1 and 3 contained practically cell-free amniotic fluid. In case 2 some AFCC was seen in the lower sections at the level of the anterior malleal ligamental fold. Lateral Incudomalleal Fold and Lateral Attics In all ears there were fluid columns in both the upper and lower lateral attics, while the cell clusters were mainly found in the latter, in cases 1–3 generally floating freely (fig. 104) but there were a few areas with slight epithelial damage when the AFCC was in direct contact with the epithelium. In case 4 portals through the epithelium were forming to begin the organization process.


Fig. 101. Case 1, left ear, section 81. In several sections across the dome of the supratubal recess, this large cluster of AFCC adhered to the lateral portion of the posterior surface of the edematous tensor fold (TF). The underlying epithelium is destroyed. AA = Anterior attic; R = supratubal recess. Organization of clusters of this type on the tensor fold would later show fibrotic scar tissue strands of varying dimensions. Magnification !150.

Fig. 102. Same case as in figure 101, a 1.4 mm more inferior section. The tensor fold (TF) is of normal thickness and only a thin layer of AFCC adheres to the lateral portion of the fold (oblique arrow) towards the anterior attic (AA). Amniotic fluid in the supratubal recess (R) contains a few small clusters. Fluid in Prussak’s space (P) is cell free. M = Malleus; A = anterior malleal ligamental fold; C = chorda tympani nerve. Magnification !25.

Fig. 103. Case 4, right ear. The tensor fold (oblique arrow) is thin and has an unusually posterior location. A small amount of secretion, containing round cells, appears in the anterior attic (AA) and a larger cluster is seen in the supratubal recess (R). Fetal mesenchyme appears both medially and laterally. A vertical medial ossicular fold of a height of 9 mm (horizontal arrow) divides the medial attic partly into two portions. M = Malleus; I = incus. Magnification !12.

Fig. 104. Case 1, left ear, section 111. The lower lateral attic (LL) is filled with fluid with an AFCC cluster anteriorly. A few cells appear in the fluid lining the medial surface of the incus (I) and the posterior surface of the tensor fold (TF) in the anterior attic (AA). The supratubal recess (R) is filled with acellular fluid. The roof (P) of Prussak’s space lateral to the malleus (M) contains vacuolated fetal tissue. C = Chorda tympani nerve; A = anterior malleal ligament; L = lateral malleal ligament; MA = medial attic. Magnification !12.


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Fig. 105. Case 2 (A89-13), section 361, right ear. Prussak’s space (P) contains a small amount of AFCC, the anterior membrane (horizontal arrow) is thin, some AFCC is present in the anterior pouch (oblique arow). Cell-free material is present in the anterior attic (AA). The submucosa shows moderate round cell infiltration. M = Malleus; A = anterior malleal ligamental fold; SM = Shrapnell’s membrane. Magnification !25.

Fig. 106. Case 2, section 401, right ear. A large amount of AFCC is concentrated in the posterior tympanum around the long process of the incus (I). The posterior pouch (P) contains some AFCC. The anterior mesotympanum (AM) in front of the tensor tendon (oblique arrow) contains mainly cell-free fluid. M = Malleus; E = ear canal. Magnification !12.

sional cells. Prussak’s space was small and slit-like in case 1, and in case 3 its site contained only fetal tissue. In case 2 Prussak’s space was well developed and contained a small amount of AFCC (fig. 105). The aeration pathway through the posterior pouch, or directly to the lower lateral attic, was empty in case 4 and in the others showed insignificant amounts of AFCC (fig. 106) or was filled with nearly cell-free fluid (fig. 107).

Fig. 107. Case 1, section 221, left ear The posterior pouch (P) is filled with fluid showing scant AFCC laterally. More AFCC is present medial to the pouch, partly fixed to the mucosa (vertical arrow). Some AFCC-containing fluid is present in the anterior mesotympanum (oblique arrows). The horizontal arrow points to a remnant of the vertical medial ossicular fold. M = Malleus; I = long process of incus; C = chorda tympani nerve; S = posterior tympanic spine. Magnification !20.

Lateral Malleal Space and Prussak’s Space In both ears of cases 1 and 3 the inferior portion of the lateral malleal space contained fetal tissue. In cases 2 and 4 the lateral malleal spaces were well formed and contained only small amounts of amniotic fluid with occa-

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Medial Attic and Tympanic Isthmus In case 1 the amniotic fluid filling the space contained a few AFCC clusters which adhered to the epithelial surfaces. In case 2 both ears contained massive amounts of floating AFCC clusters (fig. 108–110), contacting especially the remnants of the medial ossicular (incudal) fold. In case 3 AFCC appeared in the fluid in the posterior half of the tympanic isthmus, with round cells of various size, multinucleated giant cells and also polymorphonuclear leukocytes, continuing to the mastoid antrum. In the right ear of case 4 AFCC appeared principally in the anterior portions of the isthmus without contact to the mucosa while the left ear still contained a large amount of embryonal tissue. Tympanic Cavity In all 8 temporal bones the hypotympanum and lower portion of the mesotympanum contained only little AFCC and the mucous membrane was thin. The presence


Fig. 108. Case 2, section 331, left ear. A large cluster of AFCC (horizontal arrow) appears in the medial attic. AFCC-containing fluid also appears in the mastoid antrum (MA), lower lateral attic (LL), anterior attic (AA) and in the supratubal recess (R). The tensor fold (oblique arrow) is thin. E = Ear canal; I = incus; M = malleus. Magnification !8.

Fig. 109. Case 2, section 336, left ear. A polypoid remnant of the vertical medial ossicular fold contains many capillaries and is infiltrated by round cells. It is surrounded by a large cluster of AFCC which contacts the epithelium at several sites preliminary to the developement of portals for organization. Magnification !125.

Fig. 110. Case 2, left ear, section 371. A magnified view of the continuing AFCC cluster in the medial attic, 0.8 mm more inferior to that shown in figure 108. A large number of squamous epithelial cells and some lanugo hair appear surrounded by round cells and multinucleated cells. Magnification !200.

Fig. 111. Case 2, section 391, left ear. The entire mesotympanum around the long process of the incus (I) contains fluid with AFCC clusters. Fluid with few cells fills the anterior mesotympanum (AM). The footplate area is free (vertical arrow), the posterior pouch (oblique arrow) contains scant fluid. E = Ear canal; F = facial nerve; M = malleus. Magnification !12.

of the cell clusters was particularly noticeable around the incus long process (fig. 111) and the stapes (fig. 112) and there were many areas with small epithelial breaks forming future portals from the subepithelial space to the mucus. In case 3 there were several multinucleated giant cells, some of which had ingested fragments of squamous epithelial cells (fig. 113). The round window membrane

was normal in all temporal bones, but there was some AFCC posterior to it together with prominent capillaries and polypous mucosa in case 2. In all ears the tympanic sinus contained fluid with a varying amount of AFCC and distinct areas of contact with the epithelium for the development of portals for organization.


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Fig. 112. Case 2, section 451, left ear. There is fluid on the footplate and AFCC clusters nearby. Between the crura there is fluid with a smaller number of cells, the mucosa shows some tendency to polyp formation (oblique arrow). One multinuclear cell appears near the footplate (vertical arrow). AFCC clusters appear also posterior to the stapes crura (horizontal arrow). Magnification !40.

Fig. 113. Case 3, section 291, left ear. Many macrophages and two multinucleated cells in the space between the stapes and the facial nerve. One of the large cells contains phagocytized material (horizontal arrow). Magnification !200.

Eustachian Tube In all temporal bones the lateral portion of the protympanum and the bony eustachian tube contained moderate numbers of amniotic cells and fluid, not attaching to the walls.

cells were filled with AFCC. The inferior portions of the antrum, separated already by thick bone from the middle ear spaces, were surrounded by smooth-walled red marrow bone.

Mastoid Pneumatization The mastoid antrum was well formed in all 8 specimens, open for the most part except in one ear which showed a large antrum still filled with mesenchyme The petrous bone, making its thick posteromedial wall, was typically red marrow bone containing hemopoietic tissue throughout. It even showed smooth contours with occasional short trabeculae projecting to the antral lumen and was lined by mucosa which contained some embryological mesenchyme. The squamous bone, the smaller anterolateral portion of the mastoid bone, was much thinner and showed evidence of a marked preformation extending close to the lateral periosteum. Numerous short and long trabeculae projected towards the antral cavity with embryonal mesenchyme, generally rich in capillaries, between them (fig. 98). The marrow spaces close to the periosteum contained no hemopoietic tissue, only connective tissue and a few capillaries. The bone preformation continued from the attic roof until the fossa incudis. In several specimens there was a marked lateral formation of air cells with spaces lined by epithelium, the subepithelial tissue still containing thick mesenchyme. Many such air

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Comment A varying amount of embryonic tissue remained in all these neonatal ears. It made the incudomalleal fold areas thick between the lateral attics. In 3 bones it was present in large amounts in the lateral malleal and in Prussak’s spaces and only in case 2 was Prussak’s space fully open and comparable to the adult. In case 4 in the left ear the large attic compartments were also only partially open. The fetal mesenchymal tissue in the lower lateral attic and around the posterior pouch clearly protected Prussak’s space from AFCC contamination. The anterior membrane of Prussak’s space, the anterior malleal ligament and an intact tensor fold form a dead end for a superior air flow. This is in accordance with the presence of generally only little or no AFCC in the supratubal recess, apart from the main flow of air to the middle ear inferior to the tensor tympani tendon. An exception was made in the right ear in case 4 where the recess was posteriorly unusually deep (fig. 103). Due to the direct aeration route from the eustachian tube to the incudostapedial articulation and to the lower lateral attic, these areas constantly showed varying amounts of AFCC. From the upper mesotympanum and the lower lateral attic


AFCC may reach Prussak’s space if its aeration pathways are well open. Other main sites for AFCC were the stapes region and the sinus tympani, and the tympanic isthmus especially if remnants of the vertical medial ossicular fold were present. The ciliated epithelium in the eustachian tube definitely propels much of the freely floating meso- and hypotympanic AFCC to the pharynx but AFCC became fixed to other areas, for example, around the stapes, tympanic isthmus, the attic and mastoid where they cannot be removed. On the basis of these findings it appeared that small numbers of cell clusters in the protympanum, supratubal recess, Prussak’s space, hypotympanum and the mastoid would later result in local soft tissue thickening and postinflammatory folds, but would not create functional problems. On the other hand, massive cell clusters in the tympanic isthmus and around the stapes would be likely to cause a development of large masses of granulation tissue and lead to a partial or even a full block of the tympanic isthmus. Organization of cell clusters in the posterior pouch might lead to obstruction of aeration and to obliteration of Prussak’s space.

Temporal Bones from 2- to 4-Month-Old Infants Five temporal bones were available in this age range and the AFCC contamination of the middle ears was comparable to the moderate or massive involvement seen in the above-discussed newborns. Case 1 (A86-055) died at the age of 113 days as a result of severe diarrhea, anemia and metabolic acidosis. Case 2 (A89-105) died at the age of 67 days of septic shock and multifocal hepatic necrosis. Case 3 (88-022) died at the age of 84 days after 10 days’ treatment in hospital with a final diagnosis of diarrhea associated with vomiting, mixed shock and severe dehydration [29]. Compartments above the Epitympanic Diaphragm and the Mastoid Antrum Case 1. In the right ear all sections through the antrum showed a large block of pseudocystic granulation tissue covered by flat epithelium and connected with many bridges to the mucosa (fig. 114). Many air cells adjoining the attic space contained mucus and inflammatory cells. The anterior attic posterior to the shallow 0.4-mm-high transverse crest contained a meshwork of granulation tissue. In the left ear the findings were close to those seen on the right side.

Fig. 114. Case 1 (A86-055), right ear, section 170, general view. A granulation tissue mass with pseudocysts in the mastoid antrum (vertical arrow) is covered by flat epithelium and connected to mucosa with tissue bridges. The red bone marrow of the petrous bone is in contact with the mucosal lining (oblique arrow). The trabecular squamous bone has some air cells still containing mesenchyme (horizontal arrow). The lower lateral attic (LL) contains a secretion-covered sheet of granulation tissue. The lateral malleal space (L) contains secretion, the anterior attic is filled with pseudocystic tissue (curved arrow) which continues along the medial surface of the incus (I). The portion of the anterior attic in front of the transverse crest (open arrow) contains thick mucosa and secretion with round cells. The main portion of the tympanic isthmus (TI) is free. M = Malleus; A = anterior malleal ligament. Magnification !7.

Case 2. In the right ear the superior epitympanum contained an epithelialized granulation tissue sheet measuring 11 mm in length, extending from the anterior attic to the mastoid antrum (fig. 115). It involved all attic and antral sections and was thin in the medial attic and broad in the antrum, where it was united with many tissue bridges to the mucous membrane. Additionally there was thick secretion which was also present in the lateral malleal space and both lateral attics. The mucosa was edematous and thick, also in the neighboring attic air cells, but only a few inflammatory cells were present. Case 3. The superior attic in the left ear showed large amounts of mucus and the mucosa was edematous and infiltrated by inflammatory cells. The same findings continued in the more inferior sections. In the right ear the pathological changes were less intense. Secretion lined the superior attic walls and abundantly appeared only in the mastoid antrum. Many attic air cells contained mucus and showed organization processes.


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Fig. 115. Case 2 (A89-105), right ear, section 71, general view. The petrous bone shows short bone ridges and the bone marrow is in contact with the thick mesenchyme of the mucosal lining (open arrow). The lateral squamous bone shows deep trabeculation, medially the preformed air cells are lined by thick mucosa. An 11-mm-long epithelium-covered granulation tissue strand (vertical arrows) extends from a nearly obliterated anterior attic (AA) to the mastoid antrum. Secretion medial to it in the isthmus (oblique arrow) contained round cells, capillaries and portals for organization. The upper portion of the lower lateral attic (curved arrow) and the lateral malleal space (horizontal arrow) contain secretion with round cells and giant cells. M = Malleus; I = incus; A = anterior malleal ligament. Magnification !7.

Fig. 116. Case 1, right ear, section 200. The pseudocystic granulation tissue in the anterior attic (AA) extends around the remaining lateral portion of the tensor fold (curved arrow) into the supratubal recess dome (R). Strands of secretion (oblique arrows) contain round cells. Prussak’s space (P) contains a small amount of secretion. The lower lateral attic is divided by pseudocystic tissue (horizontal arrows) into several compartments, the secretion contains both round cells and multinucleated cells. M = Malleus; I = incus; A = joint portion of the anterior and lateral malleal ligaments. Magnification !12.

Fig. 117. Case 1, right ear, section 210. The pseudocystic granulation tissue mass (horizontal arrow) adheres to the margins of the tensor fold membrane defect (oblique arrows) and shows posteriorly large connecting strands (vertical arrows) to the malleus (M) and incus. A = Anterior malleal ligament; R = supratubal recess. Magnification !25.

Fig. 118. Case 1, left ear, section 132. A long secretion mass fills half of the tympanic isthmus (TI) and continues to the anterior attic (AA) where part of it drains into the dome of the supratubal recess (R) via a defect (oblique arrow) in the superior portion of the tensor fold. The lateral malleal space (L) and the lower lateral attic (LL) contain secretion with round cells. M = Malleus; I = incus. Magnification !12.

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Fig. 119. Case 3 (A88-022), left ear, section 230. Thick mucus, containing round cells, appears in the supratubal recess (R), in the entrance to the tympanic isthmus (TI) and in the lower lateral attic (LL). The tensor fold is edematous and shows a medial membrane defect (horizontal arrow) while the supratubal recess is divided into subcompartments by inflammatory folds (oblique arrow). Many cross sections of granulation tissue polyps appear (vertical arrows), the mucosa is edematous and shows moderate or extensive numbers of inflammatory cells. Prussak’s space (P) is filled with mucus and contains a polyp posteriorly. The anterior pouch (AP) is full of mucus. M = Malleus; I = incus. Magnification !12.

Fig. 120. Case 3, right ear, section 181. The tensor fold (horizontal arrow) is edematous and the dome of the supratubal recess (R) contains mucoid secretion with a few cells. Prussak’s space (P) is partially obliterated by organizing secretion. The lower lateral attic (LL) shows secretion containing round cells and a cross section of a granulation tissue polyp; a similar polyp (vertical arrows) appears in the anterior attic (AA). The mucous membrane is infiltrated by round cells. M = Malleus; I = incus; C = chorda tympani nerve. Magnification !12.

Tensor Fold and Supratubal Recess Case 1. Organized granulation tissue and strands of secretion appeared in the anterior attic and around the tensor fold which had a 0.4-mm-high membrane defect in the superior portion of the deformed fold (fig. 116). In the following section the defect became patched with the increasing size of granulation tissue (fig. 117) and further sections showed an intact fold drawn posteriorly by contracting tissue bridges. Excluding its upper portion the supratubal recess was free of pathological changes. In the left ear the membrane defect in the superior portion of the tensor fold was smaller but still provided a tiny passage for secretion from the anterior attic to the supratubal recess (fig. 118). Case 2. The tensor fold was intact in the right ear and the supratubal recess contained acellular secretion. Case 3. In the left ear the tensor fold showed a defect 0.2 ! 0.5 mm in width and 0.3 mm high in its medial portion (fig. 119), the fold was thick and infiltrated by round cells. In some sections mucus was seen to go through the defect. The supratubal recess contained large polypous epithelialized tissue strands which divided it into several compartments, the mucosa being severely infiltrated. In the right ear near the recess dome the tensor

fold was intact but thick and invaded by inflammatory cells. The supratubal recess contained cell rich secretion (fig. 120). Lateral Malleal Space and the Lateral Attics Case 1. In the right ear the lateral malleal space and the lower lateral attic contained cellular mucus and in the latter there was also epithelialized granulation tissue, but the downturning anterior edge of the lateral incudomalleal fold remained thin (fig. 114). Further inferiorly the lower lateral attic contained increasing amounts of pseudocystic granulation tissue (fig. 116). In the left ear the upper and lower lateral attics contained thick mucoid secretion with round cells and many giant cells. Case 2. The lateral incudomalleal fold was thick in the right ear, rich in capillaries, and slightly infiltrated by round cells. Several polypoid formations and crossing strands appeared in the lower lateral attic together with secretion (fig. 121). Case 3. The lower lateral attic, the lateral malleal space and the anterior attic contained in both ears secretion with round cells and giant cells with a few mucosal polyps (fig. 122).


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Fig. 121. Case 2, right ear, section 166. Prussak’s space has been passed and a superior portion of the posterior pouch appears (horizontal arrow). The lower lateral attic (LL) contains cellular secretion and is crossed by inflammatory strands and polyps (oblique arrows). The tissue strand in the tympanic isthmus (vertical arrow) close to the incus (I) and the strand of secretion (curved arrow) appeared already in figure 115, a section 2 mm more superior. The anterior mesotympanum in front of the tensor tendon (T) contains acellular secretion. M = Malleus; S = posterior tympanic spine; C = chorda tympani nerve. Magnification !12.

Prussak’s Space and Its Aeration Pathways Case 1. In the right ear Prussak’s space contained a small amount of secretion and opened directly to the lower lateral attic, partially filled with a meshwork of granulation tissue (fig. 123). The posterior pouch was separate from Prussak’s space and except its mucus-filled dome free of pathology. In the left ear thick mucus from Prussak’s space drained through a large pathway to the mucusfilled lower lateral attic (fig. 124), similarly to the right ear. Also, here the posterior pouch was separate from Prussak’s space but in contrast to the opposite ear, it was almost completely filled with thick secretion (fig. 125). Case 2. The right ear still contained embryonal tissue in Prussak’s space and in the lumen there was nearly acellular secretion. Posterior to the neck of the malleus there was a normal-sized aeration pathway via the posterior pouch which contained mucoid secretion with round cells and giant cells (fig. 126). Case 3. In the left ear Prussak’s space was shallow, only 0.3 mm in height. The posterior pouch contained thick secretion with round cells and also polyp formations (fig. 127). The pouch opened to the upper lateral mesotympanum where mucus and a thick polypous mucosa surrounded the chorda tympani nerve and the incus long process. In the right ear the lumen of the 1-mm-high

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Fig. 122. Case 3, right ear, section 130. Secretion containing a moderate number of round cells of various sizes appears in the lower lateral attic (LL), lateral malleal space (L), and in the anterior attic around the tip of a granulation tissue polyp (vertical arrow). The medial attic (MA) is empty. The edematous mucous membrane shows marked infiltration by round cells and two small polyps (oblique arrows) appear medially in the lower lateral attic. M = Malleus; I = incus. Magnification !12.

Fig. 123. Case 1, right ear, section 250. Prussak’s space (P) opens directly to the lower lateral attic (LL) which contains both secretion with round cells and epithelialized granulation tissue (oblique arrows). The anterior pouch (AP) and the supratubal recess (R) are free of pathology, the lowest portion of the anterior malleal ligamental fold (vertical arrow) still separates the two spaces. The posterior pouch, the dome of which appears (curved arrow), is separate from and inferior to Prussak’s space. Its walls are covered by thick mucus with a moderate number of round cells; further inferiorly it was free of pathology for its whole length of 1.4 mm. The horizontal arrow points to the anterior membrane of Prussak’s space. M = Malleus; I = long process of incus; C = chorda tympani nerve. Magnification !12.


Fig. 124. Case 1, left ear, section 203. Prussak’s space (P) is half filled with mucoid secretion which contains round cells, giant cells and cholesterol clefts. Its 0.4-mm-long aeration and drainage pathway (oblique arrow) leads directly to the lower lateral attic (LL) which contains an abundant amount of mucoid secretion with beginning organization. The anterior membrane of Prussak’s space (horizontal arrow) is thin and receives some fibers from the tensor tympani tendon (T). The anterior pouch (AP) has fully joined the supratubal recess and both were free of secretion. M = Malleus; I = incus; C = chorda tympani nerve. Magnification !40.

Fig. 125. Same ear as in figure 124, section 259. The separate posterior pouch (PP) contains thick secretion which posteriorly is dense and starts to undergo organization. The chorda tympani nerve (C) has joined the inner blade of the pouch. The posterior tympanum contains both epithelialized granulation tissue (oblique arrow) and thick mucoid secretion. M = Malleus; S = posterior tympanic spine. Magnification !40.

Fig. 126. Case 2, right ear, section 221. The posterior tympanum shows a large epithelium-covered granulation tissue mass around the long process of the incus (I). Secretion contains both round cells and giant cells in all areas, also in the posterior pouch (horizontal arrow). The chorda tympani nerve (C) is surrounded by granulation tissue. One continuous bundle (vertical arrow) of the posterior malleal ligament appears. S = Posterior tympanic spine; M = malleus. Magnification !12.

Fig. 127. Case 3, left ear, section 260. The posterior pouch (oblique arrow) contains dense clusters of round cells. The fold around the chorda tympani nerve (C) is infiltrated by round cells and the mucosa in the posterior tympanum is polypous throughout. Epithelialized granulation tissue (horizontal arrows) adheres to the tensor tendon (T) and the anterior mesotympanum contains secretion with round cells (vertical arrow). M = Malleus; I = long process of incus. Magnification !12.


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Fig. 128. Case 3, right ear, section 211. Aeration pathway to Prussak’s space posterior to the neck of the malleus (M) shows round cell infiltrated mucus and a granulation tissue polyp (curved arrow). Similar polyp formation and secretion appears in the lower lateral attic (oblique arrow). The tensor fold adjoining the tendon (T) is edematous and infiltrated by round cells, similarly to the mucosa surrounding the malleus. The anterior mesotympanum shows cell free secretion (vertical arrow). I = Incus; C = chorda tympani nerve; S = posterior tympanic spine. Magnification !25.

Fig. 129. Case 3, right ear, section 270. The end portion of the posterior pouch in the lateral mesotympanum shows cellular secretion (vertical arrow) and polypoid mucosa. An epithelialized polypous granulation tissue sheet extends from the malleus (M) via incus (I) to the stapes (S). Numerous pseudocysts appear in the polypous mucosa and in the granulation tissue. Air cells in the facial recess contain secretion and the mucosa is swollen, up to disappearance of the air space. C = Chorda tympani nerve; F = facial nerve. Magnification !25.

Prussak’s space was reduced because of polyps and organizing secretion which continued to the superior portion of the posterior pouch (fig. 128). The pouch full of mucus continued to the mesotympanum where inflammatory folds surrounded the chorda tympani nerve and the short process of the incus (fig. 129).

Fig. 130. Case 1, right ear, section 300. A large epithelium-covered granulation tissue mass, with an abundant amount of capillaries and a few pseudocysts, surrounds the head and crus portion of the stapes. Part of the mass is covered by secretion (oblique arrow) containing round cells and undergoing organization. A separate secretion-lined granulation tissue mass (vertical arrow) appears closer to the footplate (S). Magnification !40.

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Tympanic Isthmus and Posterior Tympanum Case 1. In the right ear the tympanic isthmus was practically free of secretion but contained thin inflammatory tissue strands (fig. 114, 116). There were similar strands with secretion in the posterior tympanum between the malleus, incus and tympanic membrane, extending towards the incudostapedial articulation and facial recess and an extensive granulation tissue surrounded the stapes (fig. 130). In the left ear the changes were less marked with only some granulation tissue and tissue strands. Case 2. The right ear showed large amounts of organized tissue in the posterior tympanum around the incus long process (fig. 126). The stapes was buried in a mass of granulation tissue with many tissue bridges to the mucosa and formation of pseudocystic cavities (fig. 131). Case 3. In the left ear there were relatively thin organized tissue sheets close to the medial surfaces of the incus and malleus but the main portion of the tympanic isthmus


Fig. 131. Case 2, right ear, section 281. The stapes (S) is buried in a multicystic mass of granulation tissue with marked round cell infiltration. Several tissue bridges appear and organization of the remaining secretion is in progress. A large polypoid granulation tissue sheet (vertical arrow) extends towards the facial recess. Magnification !25.

Fig. 132. Case 3, left ear, section 461. The round window niche is half filled with epithelialized granulation tissue. The mass is fixed to the window membrane (horizontal arrow) as well as to the niche walls and shows many pseudocysts. The mucous membrane in the hypotympanum is edematous and polypous (oblique arrow), contains pseudocysts and shows marked round cell infiltration. Magnification !40.

was free. The stapes was surrounded by heavily infiltrated thick, polypous mucosa. In the right ear the whole posterior tympanum and facial recess presented polypous mucosa and there was a long organized pseudocystic tissue sheet starting from the malleus via the long process of the incus to the stapes (fig. 129).

contained scant secretion and there was slight infiltration of the subepithelial tissue with round cells. In the left ear of case 3 inferior and anterior to the level of umbo the mesotympanic spaces were nearly empty. It was observed that some mucus had been transported to the intact eustachian tube.

Tympanic Sinus and Round Window Niche Case 1. In the right ear there was a small amount of granulation tissue in the round window niche but the membrane itself was normal. Case 2. In the right ear the round window niche showed both secretion and mucosal polyps. The membrane itself was normal and not affected by inflammatory changes. Case 3. In the left ear the sinus tympani was full of mucus and the mucosa was infiltrated by round cells. An organized pseudocystic tissue mass filled the round window niche and the membrane was firmly connected to the mucosal surfaces of the niche (fig. 132). In the right ear the changes were slightly less intense and the window membrane itself was still free of the organizing tissue mass present in the niche.

Elements Specific to Amniotic Fluid Cellular Content In the right ear of case 1 fragments of hair were seen in the granulation tissue surrounding the incus body and the stapes, and in the mastoid antrum. In the left ear similar fragments appeared in the anterior attic. In the right ear of case 2 fragments of hair were frequently seen the granulation tissue, exceptionally also in the free space, in all compartments apart from Prussak’s space and posterior pouch. Macrophages or giant cells were a frequent finding surrounding portions of hair, around one end of a hair (fig. 133, 134) or engulfing a fragment. Some areas were surrounded by clusters of activated lymphocytes. In case 3 only a few small fragments of hair were found.

Eustachian Tube In case 1 both eustachian tubes had normal mucosa and practically no secretion. In case 2 the eustachian tube

Mastoid Pneumatization The petrous bone in 4 specimens showed similar characteristics as in the neonate series. Distinct embryonal mesenchyme was still present subepithelially, and the bone surface facing the antrum was even or showed only short ridges (fig. 114, 115). At inferior portions of the


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Fig. 133. Case 2, right ear, section 246. Polypoid granulation tissue in the posterior tympanum contains a hair surrounded at one end by a multinucleated macrophage (horizontal arrow). The area close to the epithelium contains mostly fibrocytes while deeper layers show infiltration by round cells of varying sizes and numerous pseudocysts (vertical arrows) Magnification !200.

Fig. 134. Case 2, right ear, section 256. Hairs in the capillary-rich epithelialized granulation tissue between the long process of the incus and stapes crura. The crossing area of the longer hair by the shorter one is surrounded by a large multinucleated giant cell. Macrophages (oblique arrows) envelope the opposite end of the longer hair. Vertical arrow points to numerous pseudocysts in the granulation tissue. Magnification !200.

antrum the marrow bone surrounded the entire cavity and there was no sign of pneumatization. The squamous bone laterally varied in thickness and close to the periosteum contained marrow bone without hemopoietic tissue. Towards the antral cavity there was the preformed trabecular arrangement and distinct air cells had formed between the bone ridges medially, lined with a thick, mesenchyme-containing mucosa (fig. 115). Only in the right ear of case 3, showing smaller inflammatory changes, was there more advanced air cell formation especially in the squamous bone, less in the petrous bone. Several air cells were filled with mucus and showed signs of organization.

fragments appeared less frequently in case 1, aged 84 days, and only rarely in case 3, aged 113 days. It is obvious that the process of organization gradually eliminates AFCC by enzymatic breaking of keratin and phagocytosis by the activated macrophages. The presence in all studied ears of the still very cellular granulation tissue covered by epithelium made it possible to determine that the beginning of the process occurred during the period of birth. It must be remembered as pointed out in Ashoff’s study [1] that aspiration during delivery is not the only cause for the presence of AFCC in the middle ear cleft. In fact, he found that due to swallowing AFCC may appear in the middle ears from the 4th fetal month on. Thus asphyxia and aspiration must not be regarded as the only criteria indicating that a neonate can have AFCC present in the middle ear. In the present ears there were also associated factors which could have contributed to an inflammatory middle ear disease. In case 1 the nasogastric tube could have aided the development of signs of the secretory otitis media in the left ear, containing large amounts of not yet organizing mucoid secretion. In case 3 the associated vomiting might have forced contents of the mouth into the middle ears even if squamous, mouth-derived epithelial cells were not seen. The areas most affected both by collection of mucoid secretion and fresh granulation tissue proved to be the posterior tympanum and the lower lateral attic. These

Comment The hospital records of these 3 children contained neither data of the presence of meconium in the amniotic fluid nor information of a possible aspiration during delivery. It is apparent that there had been no massive pulmonary aspiration because the asphyxic state would have been obvious clinically. The focal pulmonary infiltrates in case 1 might indicate some aspiration even if diarrhea was the cardinal symptom. The initial presence of AFCC in the middle ears could, nevertheless, be ascertained by the identification of specific histology. Case 2, 67 days of age, had fragments of hair at several sites inside the granulation tissue, a finding in line with the earlier data reported in the age groups under 70 days [9]). These

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sites are directly connected with the pathways of aeration of Prussak’s space. As compared to the findings in the 8 temporal bones of the neonates with only a slight spread of AFCC to Prussak’s space, these infants all had mucoid secretion both in Prussak’s space and in the aeration pathways. This in time will lead to epithelial damage and mucus organization which may cause partial or total obliteration of Prussak’s space and its aeration pathways. Further changes will be the indrawing of Shrapnell’s membrane with a possible development of a retraction pocket, or a papillary ingrowth cholesteatoma. From the point of view of drainage, the less common shorter aeration route directly from the lower lateral attic would seem more favorable than the normal pathway via the posterior pouch. The fact that the aeration routes, and Prussak’s space itself filled early with mucus and granulation tissue seems to explain our observations [30] that tympanostomy tubes do not prevent varying pathological processes developing in the region of Shrapnell’s membrane. In infants the tympanic isthmus, when partially blocked by AFCC-derived granulation tissue, becomes more reduced in size by a superimposed secretory otitis media with secretion and underpressure in the attic. Early use of tympanostomy tubes in such ears may halt the attic process and help maturation of the granulation tissue to unimportant webs not restricting the ventilation via the isthmus. However, a nonresolved chronic attic and mastoid disease may remain as a source for repeated recurrences and necessitates more energetic methods of active treatment [31]. There is a great need for studies of temporal bones of older infants and young children for evaluation of late tissue changes both in the attic and mastoid, aerated via the tympanic isthmus, as well as in the limited regional entity of the posterior pouch and Prussak’s space. An extensive connective tissue network in the stapes area is likely to cause some restriction in the movements of the stapes and more importantly, the late tissue contraction may cause permanent indrawing of the posterior portion of the pars tensa. This in turn causes further narrowing of the already affected tympanic isthmus and leads to an irreversible attic aeration defect. Posterior retraction is a serious sign suggesting a need to create additional aeration pathways for safeguarding the attic ventilation. The process of organization destroys foreign substances from the middle ear when they have become fixed to the tissue and cannot be removed by ciliary beat. There is no evidence that the squamous epithelial cells of AFCC would escape this process and survive, leading to the development of cholesteatoma. The phagocytosis and for-

mation of granulation tissue in the present ears had annihilated all these cells except remnants of lanugo hair and the same trend was noted earlier with increasing infant age in the whole infant material [8].

Temporal Bones from 5- to 23-Month-Old Infants In the age group of children from 5 to 23 months 10 temporal bones from the Temporal Bone Foundation were available for study [32]. They were comparable to the slightly, moderately or massively contaminated middle ears discussed above for the neonates, and for the infants aged 2–4 months. Case 1 was a 5-month-old, previously healthy girl who became ill with diarrhea, vomiting and fever, progressing to septicemia. She died due to cardiorespiratory failure 20 days after the initial symptoms. The lungs showed desquamative pneumonia. Signs of a disseminated herpes infection were found in the liver, esophagus, oral cavity and skin. Case 2 was a 5-month-old girl with Goldenhar’s syndrome who after 3 months of age had respiratory symptoms, the final illness with fever, a cough and marked respiratory distress, diagnosed as bronchiolitis, starting 1 day before hospitalization. The child died in circulatory failure after 18 days of illness. The lungs showed large dense areas and the culture revealed coagulase-positive staphylococci. Case 3 was 8 months old and had been born through thick meconium and developed within 2 h a respiratory distress with severe cyanosis. Intubation with assisted ventilation was started 15 h later but all attempts of extubation failed and at the age of 4 months a tracheotomy was performed but she continued to need assisted ventilation. The principal cause of death was bronchopneumonia and cultures of the lung tissues grew Haemophilus influenzae. Case 4 was 15 months of age and had congenital agenesia of the left and dysplasia of the right kidney. The final illness had started with vomiting, followed by respiratory difficulties and dehydration and he died 4 h after admission to hospital. The blood cultures grew E. coli and coagulase-positive staphylococci. E. coli was also cultured from specimens from the right lung. Case 5, aged 23 months, had a congenital transposition of the large vessels and an interatrial communication. She received corrective vascular surgery but 3 days postoperatively had a cardiac arrest, was resuscitated but died 14 days later with signs of ischemia, hepatic necrosis and


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Fig. 135. Case 1 (A80-126), right ear, section level 00K. Superior epitympanum contains a 6-mm-long epithelialized granulation tissue mass (vertical arrow) with wide bridges (horizontal arrow) to the lateral attic mucosa. Prominent capillaries in its center (curved arrow) are surrounded by round cells which elsewhere are degenerate and the fibrocytes dominate. Mucus medially (open arrow) contained degenerating round cells and a few multinucleated cells. Organization portals to secretion appear (oblique arrow). M = Malleus; I = incus; A = antrum; U = upper lateral attic. Magnification !9.

Fig. 136. Case 1, right ear, section level 161. Tensor fold defect (vertical arrow) allows secretion to pass from the anterior epitympanum (A) to the supratubal recess (R). Prussak’s space (P) contains secretion and drains into the anterior pouch. Secretion also appears in the lower lateral attic (L) and through the entire tympanic isthmus (T) until the posterior tympanum. An epithelialized strand of granulation tissue in the anterior attic (horizontal arrow) extends towards the tympanic isthmus. Similar but more immature tissue appears in the posterior tympanum. A dense layer of bone separates the red bone marrow of the petromastoid bone from the mucosa. M = Malleus; I = long process of incus. Magnification !7.

multiple hemorrhagias. Culture from pulmonary tissues was negative. In the analysis of the serial sections the findings in cases 1–3 between 5 and 8 months of age were much more extensive than those in the infants over 1 year of age. Cases 4 and 5 were apparently exposed only to a small extent to an AFCC contamination.

was empty, the lower half contained secretion. Prussak’s space was half-filled with secretion and drained to the anterior pouch. The common posterior pathway from the lower lateral attic ended short of Prussak’s space. The posterior pouch was superiorly a blind space containing scant secretion. Mucoid secretion was present in the posterior hypotympanum and tympanic sinus. In summary, mucoid secretion in most compartments indicated recent changes. Long-standing changes appeared in the superior attic as an epithelialized block of granulation tissue, and as thinner strands in the tympanic isthmus and in the posterior tympanum.

Case 1 Right Temporal Bone The superior epitympanum contained epithelium-covered granulation tissue with wide bridges extending to the lateral attic wall (fig. 135). The mucosa was moderately invaded by round cells. The granulation tissue thinned progressively inferiorly and at the tympanic isthmus only strands remained, which formed a bridge to the medial mucosa. Mucoid secretion with round cells and some multinucleated cells was present in the attic compartments. A small portion of the tympanic isthmus and the posterior tympanum (fig. 136) contained mucoid cell-rich secretion and strands of connective tissue. The tensor fold had anteriorly a 0.7-mm-high membrane defect. The upper portion of the supratubal recess

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Left Temporal Bone The superior attic was devoid of secretion. Mucoid secretion with round cells and occasional multinucleated cells was present in all more inferior attic compartments. The mucous membrane showed a slight round cell invasion with occasional portals for organization. The tensor fold was invaded by round cells and had a small 0.2 ! 0.2 mm defect in the anterior portion, mucoid secretion passing through it to the supratubal recess (fig. 137). Prussak’s space was aerated from the anterior pouch (fig. 25b). Pos-


Fig. 137. Case 1, left ear, section level 101. Even a small defect in the tensor fold (horizontal arrow) allows secretion to pass from the anterior attic (AA) into the supratubal recess (R, a magnified view is shown in fig. 97). The lower lateral attic (L) and the posterior portion of the tympanic isthmus (T) contain secretion with round cells. There is also secretion in the mastoid antrum (A), its mucosa is thick with embryonal mesenchyme, and it is surrounded mainly with nonpneumatized red bone marrow. The vertical arrow points to the dome of Prussak’s space. M = Malleus; I = incus. Magnification !6.

teriorly there was a blind pouch as an extension of the lower lateral attic towards Prussak’s space (fig. 25b, c). The posterior pouch was a separate, superiorly blind space, containing secretion with cells. Adjacent to the stapes there was granulation tissue with many secretion-containing pseudocysts (fig. 138). Mucoid secretion appeared in the whole oval window region, in the round window niche and in the tympanic sinus, where there were portals for organization and a few small polyps. In summary, a slightly invaded mucosa with organization portals to cell-rich secretion indicated recent changes. Long-standing changes appeared around the stapes as epithelialized granulation tissue with pseudocysts. Case 2 Right Temporal Bone The superior epitympanum was filled with an epithelialized granulation tissue mass connected with numerous tissue bridges to the inflamed attic mucosa (fig. 139). At the superior level of the short process of the incus the mass still occupied half of the medial attic but more inferiorly it became thinner and filled only portions of the posterior

Fig. 138. Case 1, left ear, section level 221. An organization process of longer standing around the stapes. Pseudocystic epithelialized fibrotic tissue with trapped secretion appears between the crura and around them. Organizing mucus with round cells and multinucleated cells appears in the window niche. F = Facial nerve; E = ear canal. Magnification !9.

Fig. 139. Case 2 (A89-120), right ear, section 031, general view. A 14-mm-long epithelialized mass of granulation tissue extends from the malleus head (M) to the mastoid antrum and is connected with many bridges to the attic mucosa. Its edges are more pseudocystic, the central portion more fibrotic. The cortex of the squamous bone is thin and the preformed air cells are filled with secretion (vertical arrow) or connective tissue (horizontal arrow). The antral mucosa has direct contact with the bone marrow of the petrous bone (open arrow), with some bone resorption. The anterior attic (A) contains fluid with dispersed round cells and one cluster. Many organization portals (oblique arrow) indicate ongoing organization. I = Incus. Magnification !4.


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Fig. 140. Case 2, right ear, section level 161. An epithelialized tissue strand (vertical arrow) extends from the thick tensor fold to the incus (I). Mucosa of the supratubal recess (R) is heavily infiltrated by round cells. Prussak’s space (P) and the anterior pouch (curved arrow) contain fluid with round cells and granulation tissue. Pseudocystic granulation tissue adjoins the incus in the lower lateral attic (L) and in the tympanic isthmus (T). The mastoid antrum (A) shows secretion and epithelialized blocks of granulation tissue, forming bridges to the mucosa. The petromastoid bone contains red bone marrow with extensive mucosal contacts (oblique arrows) and shows some resorption. The squamous bone cortex is thin and the trabeculae show marked resorption. M = Malleus. Magnification !4.

portion of the isthmus (fig. 140). The antral mass persisted in all sections. The intact tensor fold was invaded by round cells and showed polypoid strands on its posterior surface. The supratubal recess was free of secretion but in the anterior pouch and in Prussak’s space there was mucoid secretion with clusters of round cells together with small polyps (fig. 141). In this section and more inferiorly, a thick strand of organized tissue entered the low portion of Prussak’s space from the lower lateral attic. The posterior pouch was a separate, superiorly blind space, free of secretion (fig. 24 a–d). The stapes was surrounded by pseudocystic granulation tissue with numerous bridges to mucosa. The promontory mucosa was hyperplastic with masses of round cells. In summary, more recent changes included cell-rich secretion in several compartments with hyperplastic, round cell-invaded mucosa. The long-standing changes were extensive in the form of attic and mesotympanic pseudocystic, epithelium-covered granulation tissue masses and a fibrotic invasion of Prussak’s space. Left Temporal Bone The ear canal and the tympanic membrane were absent, and only a deformed stapes was present. The footplate was intact and covered by embryonic tissue. Masses of round cells appeared in all open spaces. Early phases of

Fig. 141. Case 2, right ear, section level 181. The lowest portion of Prussak’s space (P) contains secretion with round cells. A large epithelialized and already fibrotic polyp (horizontal arrow) fills the aeration pathway to the lower lateral attic (L). The anterior membrane of Prussak’s space (oblique arrow) has normal mucosa towards the anterior pouch (AP) while the surface towards Prussak’s space is edematous. New portals of organization are developing from the edematous mucosa (vertical arrows). M = Malleus. The blind superior end of the posterior pouch appeared 1 mm inferior to this level. Magnification !36.

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Fig. 142. Case 2, left ear with Goldenhar’s syndrome, general view. The middle ear forms one common space from the eustachian tube (E) to the mastoid antrum (A), part of which is filled with fetal mesenchyme. The ossicles are missing. All spaces are filled partly with mucoid secretion (vertical arrow), partly with dense clusters of round cells (horizontal arrow). The mucosa is polypous, infiltrated by round cells which at some places form distinct follicles. Squamous cells appear solitary and in small clusters in the secretion. Magnification !5.

Fig. 143. Case 2, left ear, section 386. A cluster of squamous epithelial cells and round cells in the round window niche posterior to the membrane. Organization portals have not yet formed. Solitary squamous cells surrounded by macrophages show signs of disintegration. Magnification !90.

organization of the secretion were present, and remnants of squamous cells were seen in some mucosally connected round cell clusters. The low portion of the tympanic cavity was large, the mucosa was hyperplastic, and polypous on the promontory (fig. 142). A cluster of squamous and round cells, 0.8 mm in diameter, appeared in the round window niche (fig. 143). Remnants of squamous cells appeared in the secretion, also in the eustachian tube which had developed normally (fig. 142). In summary, only more recent changes appeared, showing subacute inflammation, massive secretion and hyperplastic polypoid mucosa and organization portals. Squamous epithelial cells appeared in the granulation tissue and as free clusters. Case 3 Right Temporal Bone A thick desiccated mucinous secretion undergoing organization filled the superior attic and the antrum (fig. 144). It contained areas with degenerated cells, macrophages, multinucleated cells and polymorphonuclear leukocytes and relatively few fibrocytes. Inside the mucinous mass there were nonepithelialized cross sections of granulation tissue and short stretches of epithelium appeared on the surface. The mass in the attic continued

Fig. 144. Case 3 (A92-168), right ear, section level 123, general view. Desiccated mucoid secretion in an early phase of organization with degenerate cells, macrophages, a few multinucleated cells and granulation tissue polyps (vertical arrow) fills all spaces from the anterior attic (A) via the tympanic isthmus (T) to the mastoid antrum (MA). Mucosa in the isthmus shows moderate round cell infiltration. The petromastoid bone contains red bone marrow with a dense layer of sclerotic bone parallel to the mucosa, making only minute contacts (oblique arrow) between the two possible. The cortex of the squamous bone is thin, many trabeculae are resorbed, and much of the loose mesenchyme is retained. M = Malleus; I = incus. Magnification !4.


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Fig. 145. Case 3, right ear, section level 168. Thick mucoid secretion undergoing organization continues from the tympanic isthmus (T) and the anterior attic (A) via a defect (between horizontal arrows) in the tensor fold to supratubal recess (R), a magnified view is shown in figure 96. Prussak’s space (vertical arrow) contains a thick cluster of degenerating cells and macrophages. The mastoid antrum (MA) contains organizing secretion and granulation tissue. Medially the dense plate of bone still separates the antral mucosa from the red bone marrow, laterally the squamous bone is thin and a few bone ridges project to the cavity. Posteriorly there is a slight invasion of bone marrow by connective tissue (oblique arrow). M = Malleus; I = incus; E = external meatus. Magnification !5.

Fig. 147. Case 3, right ear, section 248, the general view appears in figure 146. The posterior tympanum and the posterior pouch (P) are filled with thick organizing secretion. An epithelialized pseudocystic granulation tissue network surrounds the incus long process (I) and the chorda tympani nerve (C). The meshes are filled with secretion (oblique arrow) containing predominantly macrophages and degenerating cells. The vertical arrow points to a cross section of a granulation tissue polyp. M = Malleus. Magnification !25.

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Fig. 146. Case 3, right ear, section level 248, general view. Desiccated thick mucus with ongoing organization fills the entire middle ear up to the eustachian tube (E). Pseudocystic epithelialized granulation tissue envelopes the incus long process (I) and chorda tympani nerve (C). Vertical arrows point to cross sections of immature granulation tissue polyps. The posterior pouch (oblique arrow) contains secretion with degenerating cells, shows the beginning organization and opens to mesotympanum. The mastoid antrum (A) still contains granulation tissue and is walled by a similar type of bone as shown in figure 145. M = Malleus; S = stapes footplate; F = facial nerve. Magnification !4.

through the tympanic isthmus (fig. 145) as far as the hypotympanum (fig. 146). The subepithelial tissue showed a moderate round cell infiltration, some areas had embryonic tissue and there were polypoid changes. The thick secretion passed through a 0.4 ! 1 mm defect in the anterior portion of the tensor fold (fig. 96, 145) and filled the supratubal recess down to the orifice of the eustachian tube (fig. 146). Prussak’s space was half-filled with a cluster of degenerating cells, macrophages being dominant. The aeration pathway via the posterior pouch was partly filled with secretion which continued to the mesotympanum (fig. 147). Remaining embryonic tissue together with mucosal pseudocysts resulted in a thick mucosa and a narrow lower lateral attic. The anterior portion of the tympanic isthmus contained thick secretion with macrophages and cells undergoing degeneration. The posterior portion was blocked by a pseudocystic granulation tissue mass. It also filled the posterior tympanum and surrounded the long process of the incus and the stapes. Thick secretion filled the tympanic sinus and the round window niche with signs of incipient organization.


Fig. 148. Case 3, left ear, section 051, general view. The superior attic contains epithelialized granulation tissue (vertical arrows) with many bridges to mucosa which contains thick embryonic mesenchyme. Secretion with degenerative round cells is trapped in numerous smaller or larger compartments surrounding the granulation tissue and is undergoing organization. The petrous bone, filled with hemopoietic bone marrow, is walled off from the antrum (A) by a dense bone lamella with minute contacts (oblique arrow) to the mesenchyme. The preformed squamous bone shows prominent trabeculae, their interspaces are still filled with embryonal mesenchyme. M = Malleus. Magnification !5.

Fig. 149. Case 3, left ear, section 196. The intact tensor fold (horizontal arrow) separates the supratubal recess (R) from the anterior attic (A); both contain desiccated mucoid secretion with macrophages and multinucleated cells (a magnified view is shown in fig. 72). Prussak’s space (oblique arrow) contains similar secretion. Both the tympanic isthmus (T) and the lower lateral attic (L) are narrow due to the thick mesenchyme, and a network of trapped secretion and pseudocystic granulation tissue appeared in all sections. The low portion of the mastoid antrum (MA) shows granulation tissue with bridges to thick mucosa together with thick secretion and organization portals. The petromastoid bone contains red bone marrow which posteriorly shows wide mucosal contacts (vertical arrow). The trabecular squamous bone shows insignificant air cell preformation. M = Malleus; I = incus. Magnification !4.

In summary, changes due to ongoing infection included degenerating cells and all classes of inflammatory cells in desiccated secretion undergoing organization, with immature granulation tissue and a polypous, inflamed mucosa. Long-standing changes appeared as a pseudocystic network of epithelialized granulation tissue in the tympanic isthmus and in the posterior tympanum.

with a narrow passage showing polypoid changes. The tympanic isthmus was full of a network of epitheliumcovered pseudocystic granulation tissue (fig. 149). The intact tensor fold separated the supratubal recess from the anterior attic and showed sections of inflammatory thickening. The recess was nearly empty at its dome but the inferior sections were half-filled with secretion (fig. 149). Prussak’s space was superiorly empty, the low sections contained round cell secretion (fig. 149) which continued via the posterior pouch to the mesotympanum. The oval window area and the entire posterior tympanum were filled with secretion and granulation tissue (fig. 150). Secretion continued to the tympanic sinus and the round window niche. In summary, changes related to infection included cellrich secretion in the attic and in the tympanic sinus and round window niche. Extensive long-standing changes appeared as pseudocystic, epithelium-covered granulation tissue network which filled the superior and lateral attics, mastoid antrum, tympanic isthmus and posterior tympanum.

Left Temporal Bone The superior epitympanum and the antrum contained a central mass of epithelium-covered granulation tissue with pseudocysts and bridges to the mucosa (fig. 148). Outside this mass the adjoining open compartments contained secretion rich in macrophages. Embryonic tissue with a few round cells appeared in the subepithelial tissue. At lower levels the secretion masses and the granulation tissue were present in the entire area from the anterior attic to the antrum. The mucosa of the lateral attic contained partly embryonic tissue and partly old inflammatory pseudocysts, causing a thickening of the whole mucosal layer. The upper and lower lateral attics were connected


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Fig. 150. Case 3, left ear, section 256. The posterior tympanum close to the stapes footplate (S) is filled with thick organizing secretion (oblique arrow) and with a large network of epithelialized granulation tissue (vertical arrow) with numerous bridges to the inflamed mucosa. I = Long process of the incus; F = facial nerve. Magnification !25.

Case 4 Right Temporal Bone Recent changes appeared in the superior attic which was half-filled with secretion containing predominantly macrophages, a few multinucleated cells, and polymorphonuclear leukocytes. Similar secretion appeared in the supratubal recess (fig. 151), in the lower lateral attic, in the oval window niche, in the meso- and hypotympanum and in the sinus tympani. The mucosa was thin but there were large subepitelial clusters of round cells in areas lined by secretion. A few epithelial defects appeared with distinct portals for incipient organization. The long process of the incus and the stapes were enveloped by a thick mucosa containing round cells. The lateral portion of the mastoid process showed good pneumatization, with secretion in some of the air cells. Left Temporal Bone Both recent and long-standing changes were present in the left ear. The anterior portion of the superior attic showed secretion, continuing to the anterior attic, which was divided by mature tissue strands to separate compartments and contained cell-rich secretion with fresh portals for organization (fig. 152). At lower levels long and thin tissue strands crossed the medial attic. The postinflammatory sheets in the tympanic isthmus extended through the aditus to the mastoid antrum. Through the whole isthmus the sheet formed a row of pseudocysts with the medial

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Fig. 151. Case 4 (A89-295), right ear, section 191, general view. Secretion containing clusters of round cells and signs of early organization appears in the tympanic isthmus (T) and anterior attic (A). The tensor fold (oblique arrow) is inflamed and the supratubal recess (R) contains a large cluster of round cells and portals for organization (a magnified view is shown in fig. 95). The lower lateral attic (L) and the mastoid antrum (MA), lobulated by the bone trabeculae, contain scant secretion. The squamous bone is pneumatized but still contains connective tissue in many cells near the thin cortex. Also, the posterior portion of the petromastoid bone is pneumatized while the medial portion still contains red bone marrow. Some air cells contain secretion and thick mucosa. M = Malleus; I = incus; E = ear canal. Magnification !5.

mucosa. The tensor fold was heavily infiltrated by round cells. The supratubal recess was in its upper portion divided in 3 segments by 0.5-mm-high inflammatory webs. The scant secretion predominantly showed macrophages. Prussak’s space was empty, scant secretion appeared in the oval window niche, in the sinus tympani and in the round window niche. Also on this side the mastoid process showed good lateral pneumatization with secretion in many air cells. Case 5 Right Temporal Bone There were both recent and long-standing changes. An acellular fluid filled the superior and anterior attics, the antrum and the adjoining large pneumatized area as well as the anterior mesotympanum (fig. 153). Around the stapes there were thin fibrotic webs and the posterior tympanum contained secretion with a few cells. In the sinus tympani, and especially in the round window niche there were constricting webs predominantly of fibrocytes and epithelialized pseudocystic granulation tissue with secretion consisting of round cells and newly formed portals for organization (fig. 154).


Fig. 152. Case 4, left ear, section 116, general view. The main pathology appears in the anterior attic (A) which shows trapped secretion in a meshwork of inflamed inflammatory webs (a magnified view is shown in fig. 73). In the mastoid antrum (MA) many epithelialized thin postinflammatory connective tissue strands appear, one (vertical arrow) starting from the anterior portion of the tympanic isthmus (T). The lower lateral attic (L) contains scant secretion and small epithelial mucosal polyps in the incudal (I) mucosa. Pneumatization is similar to the right ear. M = Malleus. Magnification !7.

Fig. 153. Case 5 (A91-01), right ear, section 151, general view. A nearly cell-free secretion fills the supratubal recess (R), the tympanic isthmus (T) and a large part of the antrum (A). There is a good pneumatization around the antrum. The squamous bone laterally shows only the dense cortex (vertical arrow) and also much of the petromastoid bone is pneumatized, the remaining hemopoietic bone marrow being thin (oblique arrow). M = Malleus, I = incus. Magnification !4.

Fig. 154. Case 5, right ear, section 381. Epithelialized fibrotic tissue strands (oblique arrows) with a few pseudocysts and bridges to the mucosa appear in the round window niche. Fresh changes appear as new organization portals (vertical arrow) into the round cells in the secretion. One portal starts from the locally thickened round window membrane (horizontal arrow). Magnification !25.


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Fig. 155. Case 5, left ear, section 162, general view. Secretion containing occasional small clusters of round cells appears in all attic compartments from the anterior attic (A) to the mastoid cells (MC). The anterior attic is large, at the level of the inferior portions of the transverse crest (horizontal arrows) the distance from the malleus to the anterior wall is 3.8 mm. The mastoid is well pneumatized around the antrum but connective tissue fills many cells. Red bone marrow remains medially and posteriorly in the petromastoid bone. M = Malleus; I = incus; U = upper lateral attic. Magnification !5.

Left Temporal Bone Most changes were of recent origin. Acellular fluid appeared in the superior attic and in the aditus and antrum with normal mucosa (fig. 155). The supratubal recess was full of fluid with peripheral round cells similarly to Prussak’s space and its entire aeration pathway. The posterior tympanum contained mucoid secretion with round cells dispersed and in clusters. The stapes was enveloped by a thick mucosa with portals for organization and with strands of old organized tissue. The sinus tympani was full of round cells and mucus. The round window niche showed the ongoing organization process of the mucoid secretion. The mastoid process was well pneumatized around the antrum and the adjoining bone was already invaded by connective tissue, the marrow bone being present only peripherally. Secretion filled most of the open air cells. Elements Specific to Amniotic Fluid Cellular Content A tiny fragment of hair was found in the right ear in case 2, surrounded by macrophages and giant cells (fig. 156a, b). In case 3 solitary thin remnants of squa-

Fig. 156. Case 2, right ear, section 100. a The general view reveals a mass of epithelialized granulation tissue in the tympanic isthmus (T); a narrow strand (oblique arrow) extends to the anterior attic (A). Secretion containing round cells fills the anterior and lower lateral (L) attics. M = Malleus; I = incus. b The area boxed in a shows a remnant of a disintegrating hair, one end breaking into filaments (vertical arrow) surrounded by macrophages and giant phagocytes. Magnification !12 (a), !250 (b).

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mous epithelial cells appeared in the granulation tissue in both ears (fig. 157). In case 4, thin epithelialized tissue strands contained remnants of two, initially apparently AFCC-containing clusters (fig. 158a, b). Mastoid Pneumatization In cases 1–3 with severe inflammatory changes there were slight differences in the mastoid pneumatization as compared to the two younger age groups. The petrous bone generally showed a full arrest, the bone marrow still bordered the antrum (fig. 139, 144, 145) and only seldom showed longer bone ridges. In case 3 with the most extensive inflammation, the antral mucosa was separated from the bone marrow with a dense parallel layer of bone with minute contacts to the mucosa (fig. 144–148). The squamous bone in cases 2 and 3 showed distinct pneumatization with filling of the air cells with secretion or connective tissue, resulting in a slight lateral enlargement of the antrum (fig. 139, 140, 144, 145). On the other hand, in cases 4 and 5 with minor signs of old or recent inflammation, pneumatization was much more advanced. In case 4, 15 months of age, the entire squamous bone and the later-

Fig. 157. Case 3, right ear, section 123. A magnified view of a granulation tissue polyp marked with a vertical arrow in the mastoid antrum in figure 144. A disintegrating squamous epithelial cell (vertical arrow) is surrounded by macrophages and giant phagocytes. The cell remnant is so thin that the round cells shimmer through it. Magnification !250.

Fig. 158. Case 4, left ear, section 31. a The general view shows secretion in the anterior attic (A) and around the malleus (M) and incus (I). Fully epithelialized tissue strands (oblique arrows) cross the posterior attic and mastoid antrum and contained a few dense cell clusters (boxed area). The squamous bone shows medially air cells (horizontal arrow) while the bone near the cortex still contains connective tissue. Hemopoietic bone marrow appears in the petromastoid bone (vertical arrow). b A magnified view of the boxed area shows that the dense cell cluster consists of macrophages and giant phagocytes surrounded by a dense ring of round cells. They apparently represent an initial small cluster of AFCC, of which filament-like remnants of keratin are still present (oblique arrow). An unusually thick epithelium forms the surface of the tissue strand. Magnification !6 (a), !250 (b).


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al portion of the petromastoid bone were pneumatized. Some of the air cells were filled with secretion and showed mucosal thickening (fig. 151, 152). In case 5, 23 months of age, pneumatization was well advanced even if the cellfree secretion filled practically all compartments. In addition to pneumatized squamous bone the petromastoid bone also showed distinct receding of the bone marrow around the antrum (fig. 153, 155). Comment The specific elements of AFCC, squamous epithelial cells and lanugo hair generally disappear during the first months, being either removed via the eustachian tube or phagocytized during the organization process. The scar tissue which finally forms in this process does not disappear. The 8-month-old child (case 3) was born through thick meconium and was also subject to serious AFCC aspiration and remnants of squamous cells were still observed in the granulation tissue of both middle ears. A remnant of hair testified to an influx of AFCC in case 2 aged 5 months and there were still recognizable remnants of keratin squames in a fibrotic web in the right ear of case 4 aged 15 months. The presence of long-standing histological changes in case 1 aged 5 months suggests that their starting point occurred during the neonatal period. As found earlier the amount of contamination by AFCC in the ears of an individual may initially be unequal. In case 5, 23 months of age, the absence of acute middle ear infections in the history may or may not indicate that the long-standing pathology is related to AFCC. The initial causative agent cannot be determined histologically at this age because all specific elements possibly present initially have become phagocytized. Mature granulation tissue is similar whether it derives from an initial influx of AFCC or follows organization of fibrin and inflammatory cells in nondrained secretions in, for example, pain-free secretory otitis media. All squamous epithelium, however, does not derive from AFCC. The cell clusters (see fig. 142, 143) in the microtic left ear of case 2 cannot represent AFCC as only changes due to a recent infection were present histologically, with early stages of organization. Apparently they derived from the oral squamous epithelium, forced into the ear by vomiting [1, 2] or by maneuvers around the mouth to assist respiration. The reaction of the middle ear mucosa to these cells is similar to that against AFCC and only the stage of the process makes a distinction between the two possible. As observed in case 2, the ciliary beat can propel the loose cells back to the pharynx. However, the foreign

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material becomes fixed to tissue when contact with AFCC has caused a defect in the thin epithelium of the middle ear, releasing the organization process. The force of gravity becomes then ineffective, aided by many horizontally placed attic structures, and the cell clusters no longer descend to the hypotympanum and eustachian tube orifice. The thick respiratory epithelium of the eustachian tube is not subject to organization phenomena, which explains why the tube as a rule is intact despite serious changes in the entire middle ear.

General Comments Histological Considerations regarding Amniotic Fluid Cellular Content-Associated Pathology The changes in the specimens of infants aged 2–4 months as well as in the group of older infants and children testified to both recent and old processes. The regular appearance of secretion, with a distinct mucoid element and with varying numbers of round cells, multinucleated cells and giant cells, at times with polymorphonuclear leukocytes, indicates a relatively recent and an ongoing process. In many compartments there were only a few organization portals, as the mucosal damage was minimized by the intensive use of antibiotics during the terminal illness. In the ears with more severe changes the subepithelial tissue contained at times massive amounts of inflammatory cells. Had the child recovered from this process it would have led to the development of a substantial amount of new granulation tissue. The large granulation tissue blocks, covered by thin epithelium and containing numerous pseudocysts, are indicators of a process that has started several months ago. In younger infants this tissue was still immature containing, in addition to a large number of capillaries and round cells, a smaller number of fibrocytes. Shrinkage due to tissue maturation appears later, granulation tissue transforms to fibrous strands and sheets, fibrocytes becoming the dominating cells. This process starts peripherally and the central portions can contain for a long time both capillaries and round cells, together with occasional remnants of AFCC (fig. 156a, b, 157). Fibrotic thin sheets may retain remnants of the squamous cells and hairs an unexpectedly long time and the round cell follicles probably remained at the sites where AFCC clusters had been phagocytized (fig. 158a, b). Inflammatory cells in the pseudocysts and in the mastoid air cells may persist for years, may finally become phagocytized, or transformed into cholesterol granulomas.


In a shrinking process the cell content diminishes and small pseudocysts disappear resulting in connective tissue webs or dense scar tissue. If the granulation tissue initially bridges two surfaces the developing sheets or strands cross the compartments from one wall to the other. If the initial fixation was to one wall only, then the final outcome may only be a local mucosal thickening. These two types of the late development of scar tissue were apparent in many microdissection figures shown in Part 1 of this atlas. On the other hand, a superimposed infection will halt the maturation process and the granulation tissue blocks not only retain their size but increase their volume. Indeed, Wittmaack [2, 3] demonstrated that in a 10-year-old child with continuing disease the epithelialized blocks were massive without signs of constriction. A large tensor fold defect helps to keep the anterior attic free of secretion, allowing drainage via the recess to the eustachian tube. Even a small tensor fold defect, 0.4 mm in diameter, made the passing of secretion possible (fig. 116). When a thick, desiccated secretion filled all compartments including the supratubal recess, the transport via any of the drainage pathways seemed unsuccessful (fig. 144–146). Collection of AFCC in the posterior pouch and the lower lateral attic, leading to the development of granulation tissue, affects the drainage routes of Prussak’s space and may lead to its obliteration. None of the present cases has so far shown so advanced a pathology but there was organization of secretion inside the space as well as an advancement of granulation tissue from the lower lateral attic to Prussak’s space or from the mesotympanum into the posterior pouch (fig. 24a, b, 141, 146). Evidence of older children as well as of adults shows that Prussak’s space becomes obliterated in such a process, paving the way for the future development of either a papillary ingrowth or a retraction pocket cholesteatoma [25]. Several figures showing this are discussed in Part 1 of this atlas. The region of the stapes, one of the favourite places for collection of AFCC [9, 13], had the greatest frequency of both recent infectious and long-standing pathological changes. The latter ranged from pseudocystic thick mucosa enveloping the stapes (fig. 129, 131) to marked obliterating connective tissue extending superiorly and blocking the tympanic isthmus (fig. 149, 150). The recent changes in the same ears appeared in the form of thick mucosa, cell-rich secretion and beginning organization, which would be added to the preexisting changes of a longer standing. Similar changes, but generally less extensive ones, appeared in the round window niche and tympanic sinus (fig. 132, 154).

The above-observed coexistence of AFCC-caused old and infectious recent processes of organization applies also to cases of purely infectious recurrent otitis media. Each infection creates new granulation tissue and adds to the already existing pathology and increases the existing difficulty of drainage of the inflammatory exudate. The unfavorable effects accumulate and a circulus vitiosus of recurrent middle ear infections becomes established [30]. As suggested in early studies [1–3] it seems possible that infants with large amounts of AFCC-derived granulation tissue in the middle ear become prone to recurring infections. The start of this tendency, when related to AFCC, is obviously limited to the first year of life since maturation and shrinking of the initial granulation tissue (the foreign body removal process), lacking further irritants, reaches its end stage during a period of this length. Wittmaack [2, 3], Döderlein [33] and Ojala [34] already presented comprehensive histological analyses of ears as discussed above. These processes apply to cases developing initially from AFCC contamination as well as to those following recurrent bacterial infections filling the middle ear compartments with fibrin and cellular secretion. The histological phenomena in both etiological groups are similar, nature removes the irritating masses and stagnating secretion by organization if they are not removed by drainage. In long-standing or recurring cases of otitis media basic histological pathology behind an intact tympanic membrane needs to be considered to avoid irreversible damage to the hearing. Mastoid Pneumatization The above-analyzed material of 23 temporal bones represents less than one tenth of the total number of specimens in the Temporal Bone Foundation. The data presented on pneumatization was recorded in conjunction with the main study, a description of the middle ear pathology associated with AFCC. Even if the series is small for the time being, it, nevertheless, is one of the rare instances when neonate and infant temporal bones have been studied to relate the tissue changes in the middle ear and mastoid antrum with histological evidence of either normal or arrested pneumatization. The structure of the squamous bone, the anterolateral portion of the temporal bone bordering the middle ear and the mastoid antrum, appeared different from the posteromedial portion, the petrous bone. The latter is diploic and contains red bone marrow whereas the former is formed of trabecular bone without hemopoietic tissue. In all 8 neonate temporal bones the squamous bone showed considerable preformation towards a future formation of


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air cells, concerning both its lateral surface and the roof. The bone adjacent to the outer periosteum was thin and many variously shaped shorter or longer solitary trabeculae projected from it to the antral cavity and the superior epitympanum, their interspaces still containing embryonal tissue (fig. 98). In some specimens distinct air cells had already developed with an epithelial lining and a thick mesenchyme. Many such air cells were filled with AFCC. The connective tissue in the thicker squamous bones near the inner periosteum formed distinct borders with the embryonal mesenchyme between the trabeculae, the latter in the process of forming air cells. In young infants the continuing periosteal bone growth led to much thicker trabecular bone in some specimens (fig. 115) than that seen in the neonate but there was only little progress in pneumatization compared to the neonatal state. Because of inflammation, pneumatization of these preformed spaces continued slowly, and some of the developed air cells contained mucoid secretion with inflammatory cells. In others the medial trabeculae showed absorption and remodelling, the embryonal mesenchyme regressed and the epithelium advanced to the cells. Lateral enlargement of the antrum could thus also be seen in the presence of a middle ear disease (fig. 139, 144). The red bone marrow in the petromastoid bone remained generally unchanged but exceptionally showed a beginning pneumatization (fig. 139, 140). These data are in agreement with the histological evidence presented by Wittmaack [2, 3] and Rüedi [14, 15] on the first phase of mastoid pneumatization in infancy both normally and during inflammation. Rüedi’s notion of the dissociation between the preformation of bone and thickening of the mucosa, with an arrest of pneumatization, was apparent in cases 1–3 in our third group of children, infants aged 5–8 months. The dense bone plate around the antrum between the mucosa and the red bone marrow of the petrous bone, seen in extensively diseased ears (fig. 144), agrees with the observations of Beaumont [27] after the occlusion of the foramen pneumaticum in cockerels and would likely lead to the development of a sclerotic mastoid. On the other hand, in some inflamed ears the open contacts between the antral mucosa and the bone marrow (fig. 139, 140) suggest that the pneumatization process could continue provided that the inflammatory process came to an end, allowing the granulation tissue to mature and shrink. Similarly, the pneumatization in the children aged 15 and 23 months with minor signs of earlier inflammations is in line with the concepts presented above on the second phase of pneumatization, air cell formation also involving

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a good portion of the petromastoid bone in the four temporal bones. Our data concur with the notion of Wittmaack [2, 3], Rüedi [14, 15], Tumarkin [20–22] and Friedmann [23, 24] that normally all mastoids pneumatize and if there is an arrested pneumatization, it is due to a massive sterile inflammation post partum or chronic childhood infection. Detailed information on a monthly basis of a normal pneumatization during the first year of life must await the evaluation of the entire histological material of the Temporal Bone Foundation. A comparison of the extent of pneumatization in diseased ears to that in nondiseased ears will give irrefutable evidence of the natural and pathological course of the pneumatization process. It should be stressed that there are no methods other than histological studies of serially sectioned temporal bones that can clarify these events. Clinical Considerations One of the clinical problems is how to recognize the cases with massive AFCC contamination of the middle ears and how to treat them. The diagnosis is obvious if AFCC also enters the airways causing life-threatening pulmonary damage (case 3). We have suggested earlier [28, 29] that if a child is subjected to bronchoscopy and pulmonary lavage because of an AFCC aspiration, myringotomy should also be done and AFCC sucked out before it becomes fixed in the tissue. This period may last a couple of weeks but it would be ideal to perform it simultaneously with pulmonary aspiration. Difficulties arise in cases comparable to cases 1 and 2 in the oldest group, with extensive pathology without pulmonary aspiration. The departments taking care of newborns and infants should establish a database of children born through meconium-stained amniotic fluid and follow them closely during their first year of life. It could be established how often an AFCC-induced noninfectious foreign body otitis media turned into recurring otitis media if these children were compared to those born through clear amniotic fluid. The study could also clarify whether the at times massive granulation tissue could constrict to become inoffensive, mature connective tissue, or whether if untreated it would lead to a serious hearing impairment. The histology in cases 4 and 5 in the oldest group suggests that there is no need to worry about a slight contamination of the middle ear with AFCC. No matter whether the long-standing changes were caused by AFCC or by infection, the observed connective tissue webs and strands in the tympanic isthmus and oval and round win-


dow niches would not have caused an impairment of function. However, cases 4 and 5 suggest that limited long-standing changes may form foci where a recurrence of infection may cause a flare-up of the old dormant process. An early use of tympanostomy tubes may prevent the development of a chronic attic disease if the additional aeration renders the tympanic isthmus permanently open. However, the presence of tubes is no guarantee for a healing of the disease in the attic compartments when there is trapped cellular secretion especially in the anterior attic and when the tympanic isthmus has become closed by inflammatory webs [28]. More extensive surgery is at present seldom offered in the case of noncholesteatomatous ears because with the advanced use of antibiotics the mastoid and attic pathology has become dormant, old signs of serious disease having vanished. We believe that among the cases now treated for secretory or recurrent otitis media there is a small percentage who need surgery that is different from that which has been used so far. When evaluating recurring disease the facts known about the mastoid and attic drainage and aeration should be considered.

Looking at the histology in our cases 2 (right ear) and 3 in the oldest group, conservative treatment would have led to the development of an adhesive otitis media, the surgical treatment of which in adulthood has universally proved to be disappointing as regards an improvement of the hearing. In all ears in the present cases the eustachian tube was anatomically intact but in the infants the ciliary beat could not propel the thick mucoid secretion forward, not to mention the granulation tissue. As the massive pathology was limited to the attic, tympanic isthmus and stapes region, it is likely that surgery at this stage would be more successful. The problems are twofold: how to remove all granulation tissue safely from these areas when the ossicular chain is intact, and how to avoid bare bone surfaces which discourage the regeneration of normal mucosa? This issue will be discussed in Part 3 of this atlas.

References 1 Aschoff L: Die Otitis Media Neonatorum. Ein Beitrag zur Entwicklungsgeschichte der Paukenhöhle. Z Ohrenheilkd (Wiesbaden) 1897; 312:295–346. 2 Wittmaack K: Über die normale und pathologische Pneumatisation des Schläfenbeines. Jena, Fischer, 1918. 3 Wittmaack K: Die entzündlichen Erkrankungsprozesse des Gehörorgans; in Henke F, Lubarsch O (eds): Handbuch der speziellen pathologischen Anatomie und Histologie. Berlin, Springer, 1926, pp 102–379. 4 Benner M: Congenital infection of the lungs, middle ears and nasal accessory sinuses. Arch Pathol 1940;29:455–472. 5 McLellan M, Strong J, Johnson Q, Dent J: Otitis media in premature infants. J Pediatr 1962; 61:53–57. 6 Buch N, Jorgensen M: Leukocytic infiltration in the middle ear of newborn infants. Arch Otolaryngol 1964;80:141–148. 7 de Sa D: Infection and amniotic aspiration in stillbirths and neonatal deaths. Arch Dis Child 1973;48:872–880.

8 de Sa D: Mucosal metaplasia and chronic inflammation in the middle ear of infants receiving intensive care in the neonatal period. Arch Dis Child 1983;58:24–28. 9 Northrop C, Piza J, Eavey R: Histological observations of amniotic fluid cellular content in the ear of neonates and infants. Int J Pediatr Otorhinolaryngol 1986;11:113–127. 10 Piza J, Gonzales M, Northrop C, Eavey RD: Meconium contamination of the neonatal middle ear. J Pediatr 1989;115:910–914. 11 Eavey R: Abnormalities of the neonatal ear: Otoscopic observations, histologic observations, and a model for contamination of the middle ear by cellular contents of amniotic fluid. Laryngoscope 1993;103(suppl 58);1–31. 12 Northrop C, Piza J, Karmody C, Eavey R: The neonatal middle ear. Indicator for future problems? 3rd Extraordinary Symposium on Recent Advances in Otitis Media, Copenhagen, June 1–5, 1997. The Hague, Kugler, 1999, pp 321–325. 13 Eckert-Möbius A: Die pathologisch-anatomische Untersuchungstechnik und die normalhistologische Grundlage; in Henke F, Lubarsch O (eds): Handbuch der speziellen pathologischen Anatomie und Histologie. Berlin, Springer, 1926, pp 1–101.

14 Rüedi L: Die Mittelohrraumentwicklung vom 5. Embryonalmonat bis zum 10. Lebensjahr. Acta Otolaryngol 1937:(suppl 22):1–131. 15 Rüedi L: Mittelohrraumentwicklung und Mittelohrenentzündung. Z Ohrenheilkd 1939;45: 175–213. 16 Diamant M: Otitis and pneumatisation of the mastoid bone. A clinical-statistical analysis. Acta Otolaryngol 1940(suppl 41):1–149. 17 Dahlberg G, Diamant M: Inheritance of pneumatization of the mastoid bone. Hereditas 1945;31:441–456. 18 Diamant M: Chronic otitis. A critical analysis. Pract Oto-Rhino-Laryngol (Basel) 1952;14 (suppl 1):1–190. 19 Ojala L: Contribution to the physiology and pathology of mastoid air cell formation. Acta Otolaryngol 1950(suppl 86):1–134. 20 Tumarkin A: On the nature and vicissitudes of the accessory air spaces of the middle ear. I. Facts. II. Theories. J Laryngol Otol 1957;71: 65–99. 21 Tumarkin A: On the nature and vicissitudes of the accessory air spaces of the middle ear. III. Experiments. IV. Arguments. J Laryngol Otol 1957;71:137–161.


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22 Tumarkin A: On the nature and vicissitudes of the accessory air spaces of the middle ear. V. More arguments. VI. Conclusions. J Laryngol Otol 1957;71:211–248. 23 Friedmann I: The comparative pathology of otitis media – Experimental and human. J Laryngol Otol 1955;69:27–50. 24 Friedmann I: The pathology of otitis media (III) with particular reference to bone changes. J Laryngol Otol 1957;71:313–320. 25 Palva T, Friedmann I, Palva A: Mastoiditis in children. J Laryngol Otol 1964;78:977–991. 26 Ojala L: Pneumatization of the bone and environmental factors. Experimental studies on chick humerus. Acta Otolaryngol 1957(suppl 133):1–28.

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27 Beaumont G: The effects of exclusion of air from pneumatized bones. J Laryngol Otol 1966;80:236–249. 28 Palva T, Northrop C, Ramsay H: Spread of amniotic fluid cellular content within the neonate middle ear. Int J Pediatr Otorhinolaryngol 1999;48:143–153. 29 Palva T, Northrop C, Ramsay H: Effect of amniotic fluid cellular content on attic aeration pathways. Histological observations of infants aged 2 to 4 months. Am J Otol 2000;21:62–70. 30 Palva T, Johnson L-G, Ramsay H: Attic aeration in temporal bones from children with recurring otitis media. Tympanostomy tubes did not cure disease in Prussak’s space. Am J Otol 2000;21:485–493.


31 Palva T, Ramsay H: Chronic inflammatory ear disease and cholesteatoma. Creation of auxiliary attic aeration pathways by microdissection. Am J Otol 1999;20:145–151. 32 Palva T, Northrop C, Ramsay H: Middle ear pathology in infants. Am J Otol, in press. 33 Döderlein W: Die Organisationsvorgänge an den entzündlichen Exsudaten im Mittelohr. Z Ohrenheilkd 1920;79:1–56. 34 Ojala L: Pathogenesis and histopathology of chronic adhesive otitis media. Arch Otolaryngol 1953;57:378–401.


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Microsurgical Approaches to Inflammatory Ear Disease

Introduction The importance of the tympanic isthmus for aeration of the major compartments of the epitympanum, as well as that of the separate pathways for Prussak’s space have generally not been discussed in the treatment and healing process of recurring or chronic otitis media. The interests of the otologists have been focused on the eustachian tube function and on the mesotympanic aeration by means of the ventilation tubes. Clinical experience indeed shows that aeration via a ventilation tube generally normalizes the meso- and hypotympanic mucosa. Sixty-five percent of our patients remained free of disease after an average mean stay of the tube of 11 months during a follow-up period of 38 months [1]. In an uncured group of children each recurrence increases mucosal pathology and the adherent thick mucus starts to undergo organization. In some ears this process may lead to the development of granulation tissue masses blocking the tympanic isthmus and even filling the entire attic [2]. Therefore, despite repeated insertions of ventilation tubes, some or all the attic compartments may be affected by a deficient aeration, or may remain without aeration. As long as there is inflammation the process remains active and the forces of defense try to bring it to a standstill by organization and gradual tissue maturation. In the end this may finally mean arriving at an irreversible adhesive otitis media, possibly after several years. Such changes were seen to develop in 14% of the patients in a small group of children followed up for nearly 5 years [1]. In some children this process can already start at birth without preceding infection, following the presence of aspirated or swallowed amniotic fluid cellular content in the tympanum [3–5].

The narrow passage to Prussak’s space is likely to be often affected in chronic middle ear infections but histological evidence of this is only sporadic. Our first histologically analyzed adult case of secretory otitis media [6] had been treated with ventilation tubes by us for a period of 7 years before the patient’s death. The attic was aerated and the mucosa nearly normal, while Prussak’s space was obliterated and Shrapnell’s membrane retracted and fixed to the neck of the malleus. Nevertheless, there was no indication that the squamous epithelium was to start a cholesteatomatous process either by papillary ingrowth or by forming a retraction pocket (fig. 30). In the right ear of this same patient there was a chronic otitis media with a migration type ingrowth of squamous epithelium from a pars tensa defect (fig. 55). There was partial obstruction of the tympanic isthmus with an inflammatory polyp, but the drainage routes were still open. Even if the disease did not as such involve the epitympanic spaces, there were signs of uncured infection in the form of thick mucosa in the air cells, some of them being filled with round cell secretion while others showed cholesterol crystals. The mucosa was thicker than normal and showed patchy infiltration with inflammatory cells. To a lesser degree, these same changes also occurred in the left ear with secretory otitis media. Prussak’s space in the right ear was fully open but showed mucosal edema and secretion together with inflammatory tissue strands with capillaries, arising through epithelial portals (fig. 29). In a recent article we [7] described the findings in 8 temporal bones from 4 children with an inflammatory middle ear pathology. These 4 patients had suffered from recurring otitis media and had undergone one or several treatment periods with ventilation tubes. In each of them, unsuspected before histological examination, there were changes in Prussak’s space ranging from filling with secretion and beginning organization to full obliteration, in one

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case leading to the development of a papillary ingrowth cholesteatoma and in another to a prestage of a retraction pocket cholesteatoma (fig. 31). In one ear in this series [7], there was an absence of the tensor fold which provided the attic with a large direct drainage and aeration pathway to the supratubal recess and eustachian tube. The epitympanic pathology was slight and in marked contrast to the left ear with the tensor fold present. In many other cases, studied in serial sections, epitympanic secretion was seen to drain via a defect in the tensor fold membrane directly to the supratubal recess, and thus to the orifice of the eustachian tube. However, even this additional direct attic aeration route and the use of a ventilation tube did not prevent the destruction of the epithelium in Prussak’s space and its gradual fibrotic obliteration. These documented observations, arrived at by combining data obtained by microdissection with those obtained by studying serial sections of diseased temporal bones, made us search for new microsurgical approaches with a better guarantee of improving aeration and drainage to and from the epitympanic compartments than the currently used techniques [8]. Initially we tried to arrive at methods which would prevent the development of the serious disease processes behind Shrapnell’s membrane and in Prussak’s space, and later focused our attention on surgical methods for tensor fold removal.

Early Attempts to Improve Epitympanic Aeration In the late 1980s removal of the tensor fold had become a routine step in our canal-wall-down surgery with mastoid obliteration and there were no technical problems when the incus and the head of the malleus were removed. In retraction pockets without mastoid pathology, with an intact ossicular chain and still with normal hearing, no methods were available that allowed direct vision of the tensor fold. Only in spacious anterior attics with a good safety margin to the head of the malleus, bone could be removed to enter into the supratubal recess. However, because the working angle was not comparable to the superior approach in microdissection but was through the ear canal, the tensor fold remained hidden behind the neck of the malleus and had to be destroyed blindly with angled hooks. When the anterior attic was short, there was no safe way of excising the fold. At the same time, Morimitsu [9] started to use a basically similar approach that he called ‘anterior tympanotomy’. While we worked with limited disease through the

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ear canal, he used the canal-wall-up-type surgery for all forms of cholesteatoma. Bone removal from the lateral attic was continued until the zygoma so that the working axis towards the tensor fold became frontally parallel with the axis of the ear canal. This allowed nearly vertical drilling in front of the malleus head through bone, which was called the ‘attic plate’ and was described as the separating structure between the anterior attic and the supratubal recess. The misconception here was that the attic plate in reality is the transverse crest which from this lateral approach gave an illusory appearance as a dividing structure between the two compartments. From the two preceding parts of this atlas it is clear that the dividing structure that exists and matters is not the transverse crest but the tensor fold.

Microsurgical Methods in Surgery for Retraction Pockets Obstruction of the aeration pathway either via the posterior pouch, or from the lower lateral attic directly, may lead to gradual obliteration of Prussak’s space (fig. 24, 27, 141). If the tympanic isthmus functions normally the main attic remains aerated as shown in CT scans [10]. A deeply indrawn Shrapnell’s membrane may then appear as the only sign of this initially limited pathology. This state will remain resistant to all modes of conservative treatment. An indrawn membrane may remain inactive when there is a thick layer of mature connective tissue underneath, allowing no retraction to occur towards the neck of the malleus. The epidermis then becomes resting, loses its papillae and this condition does not indicate any interference (fig. 30, 32). Patients with a distinct indrawing of Shrapnell’s membrane with even minimal signs of retained keratin should have otomicroscopy once a year to provide a sufficiently early diagnosis of a permanent, increasing collection of keratin in the initially tiny pocket. Surgery at this stage is still a minor procedure and should be undertaken to prevent serious future problems. Surgery for Incipient Retraction Pockets Both the endaural and postauricular incisions can be used but we prefer the postauricular one because it gives a better angle to the anterior portions of Prussak’s space. Canal skin is cut transversely 5 mm above the annulus and the incision continued superiorly over the vascular strip to the anterior edge of the notch of Rivinus. Canal skin, superior portion of the posterior pars tensa and


Shrapnell’s membrane are then dissected free of bone and of the edges of insertion to the notch of Rivinus, and the entire skin flap is turned over the short process of the malleus. If there is already fixation to the malleus neck, we detach Shrapnell’s membrane from bone with argon laser, but this work can also be done gently with a sickle knife. After sucking out possible mucus and removing inflammatory organized tissue strands Prussak’s space is carefully scrutinized under sufficient magnification. The anterior membrane will be seen as a distinctly transverse structure of varying thickness, descending slightly inferiorly anterior to the curved neck of the malleus. The entire anterior membrane is next evaporated with laser producing an open connection with the anterior pouch. Thin, translucent membranes can be circumcised and removed with the sickle knife and microforceps. Thick, inflamed tissues always need laser destruction since the incision made to open it inevitably closes quickly afterwards. While the canal skin, the pars tensa portion and Shrapnell’s membrane were turned over the short process of the malleus, the connection with the posterior pouch becomes disrupted. In all probability the pouch is already occluded and a lumen leading inferiorly is no longer present. A large opening is now made with laser towards the lower lateral attic by evaporating the connective tissue mass of varying thickness between Prussak’s space and the chorda tympani nerve. In this area the use of laser is mandatory, the thick scar tissue masses cannot be removed manually without injuring the adherent nerve. At this stage Prussak’s space itself is fully open, possibly without a mucous membrane and a large pathway connects it to both the anterior pouch, and posteriorly to the lower lateral attic and mesotympanum. We prefer to fill the area of Prussak’s space with a tiny strip of cartilage, earlier with lyophilized dura when it was in general use, to keep Shrapnell’s membrane in its proper position. The cartilage prevents any contact between the generally epithelium-free medial surface of Shrapnell’s membrane and the bone surface of the malleus neck and does not resorb. We have seen no problems following the use of this procedure. Surgery for Established Retraction Pockets In ears of this type we use the postauricular incision for reasons given above, as well as to retain greater manipulative freedom in the event that the spread of the disease later necessitated more extensive surgery. Removal of the skin pocket is started posteriorly, separating it carefully from the underlying ear canal bone, incus and malleus.

Fig. 159. Surgical case, adult, left ear. The cholesteatoma had advanced to the anterior attic and the entire malleus was removed. Its healthy head (M) was shaped so as to sit as a riding columella on top of the incus long process (I). It raises the level of the ossicular chain laterally, allowing the tympanic membrane to assume its initial position while adhering to the malleus head.

The laser beam is again invaluable in the evaporation of the scar tissue fixing the skin to the ossicles. If the retraction around the neck of the malleus is not too deep, the whole skin pocket may be excised from the intact ossicles. The aeration routes to the anterior pouch and to the lower lateral attic are created with laser as described above. If preoperatively the mastoid and the major attic compartments had been aerated and the problem seems to be limited to the blocked separate aeration pathway to Prussak’s space, nothing further need be done. For cases in which there seemed to be also changes in the large epitympanic compartments which might not need major surgery but would benefit from improved aeration, we searched for various routes for a safe removal of the tensor fold with this limited surgical approach. One of the methods in the 1980s was to remove the head of the malleus and after the tensor fold removal, place the malleus head as a riding columella on the long process of the incus (fig. 159). At that time, we devised a new way of removing tympanic glomus tumors that extended past the malleus handle to the anterior tympanum. A perfect view of the whole tumor was obtained by cutting the neck of the malleus, making an upward lifting of the entire tympanic membrane possible with an elevator under the malleus handle. Repositioning of the cut edges of the malleus after tumor removal resulted in the preservation of a normal hearing [11]. This method was afterwards

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Fig. 160. Series P, case 12, a child aged 2 years, left ear. Posterior tympanotomy for tensor fold removal in microdissection. Yellow mucous secretion (horizontal arrow) filled the lateral side of the ossicles, and Prussak’s space was full of similar fluid (vertical arrow). M = Malleus handle; I = incus long process; C = chorda tympani nerve.

Fig. 162. Same ear as in figure 161. The malleus handle (H) is drawn laterally exposing the tensor tendon (oblique arrow) down to the cochleariform process (horizontal arrow). The tensor fold appears superior to the tendon (vertical arrow). M = Malleus head.

adopted for use in surgery for recurrent ear disease and cholesteatoma. After the creation of the meatal skin flap and the moving aside of Shrapnell’s membrane (fig. 160), the malleus head nipper is introduced parallel to the long process of the incus and turned 90° allowing the lower blade to go

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Fig. 161. Same ear as in figure 160. The malleus neck has been cut (vertical arrow) with a malleus head nipper, allocating the tensor tendon to the handle (H) portion and the anterior malleal ligamental fold to the malleus head portion (M).

under the inferior edge of the malleus neck. The neck is cut close to the short process with a steady hand and elbow support (fig. 161). The tensor tendon will then stay on the manubrium side and the superior to the tendon inserting anterior malleal ligament is left on the malleus head side. The head then keeps its original position, being fixed by the named ligament, the superior malleal ligament, and the incudomalleal joint. When withdrawn, the nipper is again turned parallel to the incus long process. A gentle lifting of the malleus handle makes the tensor tendon and the tensor fold instantly visible (fig. 162). Without stretching the tendon unnecessarily, a thin fold can be destroyed in a few seconds with a sickle knife (fig. 163), even if we prefer the laser which in thick folds is mandatory to avoid reclosure. The elastic tensor tendon pulls the malleus handle back to contact the head portion, and after a drop of tissue glue, the closing steps are as described above. When viewed from the superior aspect both the incus and the head of the malleus have retained their position and the tensor fold is absent (fig. 164). If the malleus head becomes dislodged, it should be cautiously removed and fitted, as shown in figure 159, as a riding columella on the long process of the incus. The incus will keep its position even if it loses its contact with the malleus because it is still fixed by the posterior incudal ligaments, by the lateral incudomalleal fold, and by the lenticular process. If bundles of the anterior malleal liga-


Fig. 163. Same ear as in figure 162. A hole (vertical arrow) has been made with a sickle knife in the tensor fold, part of which (oblique arrow) remains to be severed. H = Malleus handle; M = malleus head; T = tensor tendon.

Fig. 164. Same ear as in figure 163. The specimen has been turned and a superior microdissection carried out. Portion of the hole in the tensor fold appears (vertical arrow) in front of the tensor tendon (T). The anterior attic (A) shows granulating mucosa. The tympanic isthmus has inflammatory webs both anteriorly and posteriorly (horizontal arrows). Note that the malleus head (M) has kept its position despite the cutting of its neck. I = Incus.

ment remain fixed to both malleal fragments after cutting, sideward shifting of the manubrium fragment could pull the head laterally and dislodge it. A further division of the ligament on the malleus handle is then made with laser, or with a sharp sickle knife. The surgeon’s touch should be gentle in all phases, and a few temporal bones should be dissected in the laboratory before applying the method to actual surgery. If mastoidectomy is indicated, or the retracted skin envelopes the neck of the malleus, or the pocket extends superiorly, we regularly remove the incus and cut the head of the malleus. In our experience, whenever it is unclear whether or not the squamous epithelium has been removed totally, the procedure should be carried out. This exposure reveals the contents of the whole attic and allows removal of the diseased tissues. The view of the tensor fold becomes unobstructed, allowing its removal with a full examination of the supratubal recess. Reconstruction of the stapes is done with the patient’s own tissues, incus or cortical bone, following the established principles.

removal. We were initially perplexed by the term ‘attic plate’ used by their group [9, 12] which was said to separate the anterior epitympanum from the supratubal recess. Since the days of Siebenmann [13] and Hammar [14], more than a hundred years ago, it has been recognized that the separation is done by the tensor fold. We then understood that in the lateral approach the transverse crest of the tegmen gave the authors an illusion of a separation of the epitympanum and the recess by the transverse crest. In superior microdissections, and in horizontal serial sections, the transverse crest is seen to play no role except at times it divides the anterior epitympanum superiorly into two sections (fig. 67, 114). We use the frontolateral atticotomy in generalized cholesterol granulomatous mastoiditis and epitympanitis with a canal-wall-up surgery for excision of the tensor fold, combined with preservation of the ossicular chain. As Morimitsu [9] suggested, bone in the atticotomy has to be removed as far as the zygoma so that the approach allows for transversely continued drilling in front of the head of the malleus (fig. 165). At the end of the atticotomy we also break the lateral incudomalleal fold blindly, with a long right angle hook, by gentle movements of the hook between the incus short process and the lateral attic bone. This opens one additional aeration route to the attic combining the air spaces of the upper and lower lateral attics (fig. 39).

Frontolateral Atticotomy After having read Morimitsu’s manual [9] on what he called ‘anterior tympanotomy’ for cholesteatoma removal we thought the approach worth trying in tensor fold


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Fig. 165. Series A, adult case 9, left ear. An atticomastoidectomy has been made with exposure of the incus (I) and the malleus (M). A postinflammatory web appears in the tympanic isthmus (horizontal arrow). At this stage the lateral incudomalleal fold can be destroyed by a long right-angle pick moving it gently between the incus short process and the lateral attic bony wall (B). A = Mastoid antrum; E = ear canal.

Fig. 166. Surgical case, adult, left ear. The frontolateral atticotomy has been completed and the tensor fold (T) is visible medial to the head of the malleus (M). I = Incus; E = ear canal.

The actual approach to the tensor fold necessitates a small diamond drill in an angled handpiece for removing the lateral portion of the transverse crest in front of the malleus head. The anterior malleal ligament in front of the malleus head leads directly to the tensor fold which has the appearence of an oblique thin membrane anteromedial to the surgical route (fig. 166). Thin folds can be excised with a sickle knife but laser is generally preferred, and it is mandatory in thick folds (fig. 167). If a major portion of such folds is not evaporated, a simple incision quickly heals leaving no permanent membrane defect. If the tensor fold has become inserted into the crest itself, in around 10% of our cases, the surgical route through the crest also destroys the fold directly when the lateral portion of the crest is drilled away. Extensive Attic and Mesotympanic Disease in Chronic Otitis media In recurring inflammatory ear disease, both the epitympanum as well as the mesotympanum may present with an extensive amount of granulation tissue. In addition to the blockade of both the tympanic isthmus and the aeration pathway to Prussak’s space, granulomatous obliterating tissue and polyps may envelope the incus so that preservation of an intact ossicular chain becomes too risky (fig. 52, 53). In addition to the above-described proce-

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Fig. 167. Same ear as in figure 166, surgery completed and the tensor fold removed, exposing the supratubal recess (R). Chorda tympani nerve (horizontal arrow) is seen adjacent to the neck of the malleus (M). I = Incus.

dures for disease in Prussak’s space and removal of the tensor fold, all of the meso- and epitympanic polypoid granulation tissue should also be removed after early removal of the incus. The mucoperiosteum together with thin areas of mucosa should be conserved to allow epithelial regeneration from the remaining small stretches of a near-normal epithelium and to keep the development of granulation tissue formation on raw surfaces at a minimum. Much of the excision of the granulation tissues should be done with laser, especially around the stapes. In the absence of the incus columellization with the head of the malleus on the stapes is the best method for creating space as it leads to a large tympanoattic middle ear compartment with unhindered drainage and aeration. A short-term cortisone therapy with antibiotic cover during the postoperative period in such cases would contribute to quicker healing of the mucosal layer.

Spread of Cholesteatoma from Prussak’s Space There are four routes for the spread of cholesteatoma from Prussak’s space, the posterior, inferior, superior and anterior, and each gives a different type of involvement of the neighboring compartments. These cholesteatomas start from an epithelial papillary projection, penetrating


Fig. 168. Series P, case 8, a child aged 6 years, right ear. A case of granulomatous mastoiditis with a perforation (horizontal arrow) in the posterior portion of Shrapnell’s membrane. The anterior portion of Prussak’s space was filled with thick yellow mucus (oblique arrow). The tympanic membrane (TM) is retracted and fixed to the long process of the incus (I), shimmering through the tympanic membrane. M = Malleus handle.

Fig. 169. Same ear as in figure 168, anterior microdissection, a view of the tympanic cavity after removal of a loose keratin mass from the orifice of the eustachian tube and protympanum. The anterior mesotympanum is still full of contents of a disrupted cholesteatoma sac (horizontal arrows) until the perforation. M = Malleus handle; TM = tympanic membrane. This kind of spread of cholesteatoma, centrally and anteriorly, occurs when Prussak’s space is aerated from the lower lateral attic immediately posterior to the malleus neck.

the basal lamina, into adjacent granulation tissue in Prussak’s space. There the advancing front portion of the papilla becomes a minicyst and begins to enlarge due to trapped keratin and transforms into a typical ball-type cholesteatoma. Common to them all is the squamous epithelium in the inner lining of the cystic formation, connective tissue covering the outside. However, any granulation tissue adjacent to the connective tissue may contain papillae from the squamous epithelium, regardless of the type of cholesteatoma.

touch either the fold insertion ring or mucosa of the supratubal recess, which are well outside the area of cholesteatoma.

Posterior Route This is the common way of extension because the sac enlarges along the regular aeration pathway through the posterior pouch, gradually fills and expands it so that it occupies the entire space below the lateral incudomalleal fold. When it arrives at the mesotympanum, an early sign is a slightly bulging whitish area in the posterior upper segment of the pars tensa; in later stages this area extends to the lower posterior segment. Generally the sac has become so large that it reaches the long process of the incus and the stapes crura, necessitating partial ossicular resection. There is a good chance for total removal because the upper lateral attic and the superior attic are primarily intact. Excision of the membranous portion of the tensor fold is made routinely, but there is no need to

Inferior Central Route In around 36% of ears Prussak’s space is aerated directly from the lower lateral attic and the posterior pouch forms a superiorly blind sac without any connection to Prussak’s space [15]. In such ears the aeration pathway leads to the lower lateral attic and the superior mesotympanum immediately posterior to the short process of the malleus. From here the cholesteatoma sac has a tendency to enlarge into the anterior direction under the handle of the malleus and it is impossible to diagnose it at an early stage before perforation occurs in Shrapnell’s membrane. We recently studied a temporal bone with this type of involvement [7], combined with Shrapnell’s membrane perforation (fig. 168) and complicated during the terminal stage of septicemia with extensive mastoid granulomatous infection. When we started with the anterior microdissection we found that there had been a disruption of the cholesteatoma sac and the keratin mass had spread anteriorly as far as the bony eustachian tube (fig. 169).


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Fig. 170. Surgical case, adult, right ear, endaural approach. Cholesteatoma in Prussak’s space had spread to the anterior attic and the ball-type mass extended on top of the tensor fold. The macerated surface of the tensor fold (between horizontal arrows) appears after removal of cholesteatoma. A vertical arrow points to the anterior membrane of Prussak’s space, an oblique arrow to the tympanic cavity. M = Malleus, A = anterior malleal ligamental fold.

Fig. 171. Same ear as in figure 170. The entire tensor fold has been removed leaving a good-sized communication (between horizontal arrows) with the supratubal recess (R). Malleus head (M) shows erosion (oblique arrow). I = Incus long process.

Superior Route The roof of Prussak’s space may contain a membrane defect (fig. 8, 9) and even if intact, its posterior portion regularly offers easy penetration because of the thin portion of the lateral malleal ligamental fold which contains no ligamental bundles (fig. 7). The anterior portion of the lateral malleal ligament is always so strong that it entirely precludes the possibility of penetration into the lateral malleal space (fig. 8, 15c). Once there, the ball may grow in all directions: over the malleus head to the superior and medial attics, through a small communication between the malleus head and the lateral malleal ligamental fold to the anterior attic, or posteriorly to the direction of the aditus ad antrum on top of the lateral incudomalleal fold. If the disease remains limited to the attic, its most anterior extension is halted by the tensor fold. Even if this fold normally looks like a pseudomembrane, it can generally be found intact even if the connective tissue side of the cholesteatoma ball is united with the fold’s posterior surface. In cases with a large anterior attic cholesteatoma removal may be possible by keeping the ossicular chain intact (fig. 170, 171). However, generally the removal of the incus and the head of the malleus are essential, and dissection of the ball anteriorly should include the tensor fold and its insertion ring. The supratubal recess remains intact and no soft tissue removal is needed.

Anterior Route Prussak’s space has another weak wall inferoanteriorly (fig. 77–80) where the limiting membrane is thin, even if it contains fortifying fibers from the tensor tympani tendon which resist penetration (fig. 16). We have found this pathway for cholesteatoma spread to be uncommon. The enlarging mass expands, once in the anterior pouch, around the lateral portion of the tensor tympani tendon to the supratubal recess. We remove most, if not all, of the malleus together with the tensor tendon and the insertion ring of the tensor fold. In patients with advanced spread, all soft tissue from the supratubal recess tegmen must be excised down to the eustachian tube orifice. We use the canal-wall-down surgery to obtain a fully unobstructed view of the eustachian tube. The reconstruction with ossiculoplasty and repositioning and filling of the skin tube of the intact ear canal by a dense Merocel® tampon [16] is followed by obliteration. If the disease is diagnosed early and the anterior and posterior attics are free of disease, limited surgery may be possible and the incus can be left in place. This allows easy reconstruction with the riding columella (fig. 159) on top of the incudostapedial articulation.

100


Final Remarks We have suggested earlier [8] that the supervised microdissection training, including the lateral and anterior approaches, be incorporated into the temporal bone surgery teaching programs for acquiring the necessary anatomic knowledge. Surgical competence can only be achieved through personal work, combined with preceding seminars with documented figures of microdissections and of serial sections of temporal bones. Documented evidence is the only valid reference when seeking to understand anatomy, and sketches must always be accompanied by photographs of the anatomic structures on which they are based. The trainees will profit immediately from traditional superior microdissection, when done personally once they have obtained sufficient theoretical knowledge of the structures to be encountered. He or she can instantly recognize in the posterior epitympanum, medially to the incus short process, the large major aeration and drainage route, the tympanic isthmus. Lateral to the incus one can see the delicate incudomalleal fold and the upper lateral attic and will know that the lower lateral attic is immediately inferior to this fold. Posteriorly one sees how the posterior incudal ligaments go transversely to both sides, not along the long axis of the short process, and that the lateral ligament is clearly the stronger of the two. By following the lateral incudomalleal fold anteriorly one can see how it descends towards the posterior malleal ligamental fold and how the lateral malleal space forms between the three malleal ligamental folds. After further removal of the tegmen, the anterior epitympanum is fully visible, the shallow transverse crest crossing the tegmen, its medial leg possibly continuous with the cochleariform process. The pseudomembranous tensor fold finally gives a clear indication of the closed anterior borderline of the anterior epitympanum. Anterior dissection [17] gives the trainees a precise idea of the supratubal recess and the anterior pouch, both areas which they would normally not have seen before. One can immediately recognize that the anterior membrane of Prussak’s space is a thin duplicate membrane, not a ligamental fold, and appreciate that it can give way to expanding cholesteatoma from Prussak’s space. By viewing the tensor fold medially one notes that the supratubal space extends a good deal superior to the eustachian tube tegmen. By inserting an instrument through the fold one can see it approaching the anterior epitympanum and after removal of the entire thin fold one sees how the two spaces become one.

Finally, the lateral route via the regular posterior tympanotomy completes the picture of the anatomic arrangement of the structures which will confront the trainee surgeon in the operation theater. Moving aside Shrapnell’s membrane allows one to view the roof of Prussak’s space and the anterior membrane which is anteroinferior to the neck of the malleus. Cutting the head of the malleus as indicated above gives a greater sense of dexterity and safety in doing the same procedures in one’s daily work, in the creation of additional attic aeration pathways or in preparing adequate access for the removal of anterior glomus tumors. When the ear surgeon knows the detailed anatomy of the middle ear inside out it gives him great confidence in planning and executing successfully any type of surgery for inflammatory middle ear disease.


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References 1 Kokko E, Palva T: Clinical results and complications of tympanostomy. Ann Otol Rhinol Laryngol 1976;85:(suppl 25):277–279. 2 Palva T, Ramsay H: Mucosal pathology of the attic; in Tos M, Thomsen J, Balle V (eds): Otitis media Today. The Hague, Kugler, 1999, pp 307–314. 3 Northrop C, Piza J, Eavey R: Histological observations of amniotic fluid cellular content in the ears of neonates and infants. Int J Pediatr Otorhinolaryngol 1986;11:113–127. 4 Palva T, Northrop C, Ramsay H: Spread of amniotic fluid cellular content within the neonate middle ear. Int J Pediatr Otorhinolaryngol 1999;48:143–153. 5 Palva T, Northrop C, Ramsay H: Effect of amnion fluid cellular content to attic aeration pathways. Histological observations of infants aged 2 to 4 months. Am J Otol 2000;21:62–70. 6 Palva T, Johnsson L-G: The epitympanic compartments, surgical considerations: A re-evaluation based on findings in a pair of temporal bones and a literature review. Am J Otol 1995; 16:505–513.

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7 Palva T, Johnson L-G, Ramsay H: Attic aeration in temporal bones from children with recurring otitis media. Tympanostomy tubes did not cure disease in Prussak’s space. Am J Otol 2000;21:485–493. 8 Palva T, Ramsay H: Chronic inflammatory ear disease and cholesteatoma. Creation of auxiliary attic aeration pathways by microdissection. Am J Otol 1999;20:145–151. 9 Morimitsu T: Cholesteatoma and Anterior Tympanotomy. Tokyo, Springer, 1997, pp 1– 114. 10 Shiga T, Hozawa K, Adachi M, Takasaka T: Attic retraction as a sequel of otitis media with effusion; in Tos M, Thomsen J, Balle V (eds); Otitis media Today. The Hague, Kugler, 1999, pp 561–564. 11 Palva T: Glomus tympanicum tumors. Removal through the ear canal. Department of Otolaryngology, University of Helsinki, 1988: Video No. 78.


12 Tono T, Schachern P, Morizono T, Paparella MM, Morimitsu T: Developmental anatomy of the supratubal recess in temporal bones from fetuses and children. Am J Otol 1996;17:99– 107. 13 Siebenmann F: Mittelohr und Labyrinth; in Bardeleben K von (ed): Handbuch der Anatomie des Menschen. Jena, Fischer, 1897, vol 5, Abt. 2, pp 244–287. 14 Hammar JA: Studien über die Entwicklung des Vorderdarms und einiger angrenzenden Organe. 1. Allgemeine Morphologie der Schlundspalten beim Menschen. Entwicklung des Mittelohrraumes und des äusseren Gehörganges. Arch Mikrosk Anat 1902;59:471–628. 15 Palva T, Northrop C, Ramsay H: Aeration and drainage pathways of Prussak’s space. Int J Pediatr Otorhinolaryngol 2001;57:55–65. 16 Palva T: Cholesteatoma surgery today. Clin Otolaryngol 1993;19:405–415. 17 Palva T, Ramsay H, Böhling T: Lateral and anterior approach to supratubal recess and tensor fold. Am J Otol 1998;19:405–414.


Subject Index The subject index contains terms which are of major importance in finding the passages which deal with the term sought for. Due to the frequent appearance of some of the terms, all occurrences have not been printed; mainly those are included which contain additional information. Those page numbers which contain essential basic information of anatomy or pathology are printed in bold.

Aditus ad antrum 3, 10, 12, 100 Aeration pathway 9, 14, 17–19, 21–27, 30, 31, 40, 46, 66, 70, 75, 80, 93, 94, 99 Aimi 10, 40 Air sac – – anterior 7, 8, 16 – – medial 7, 8, 16, 31 – – posterior 7 – – superior 7, 16 Amniotic fluid 59, 61 – – cellular content 21, 61–66, 93 Animal model of pneumatization 60, 61 Annular bone 4, 8 Anterior attic → Epitympanum – membrane of Prussak’s space 13, 16, 19, 46, 95 – pouch 4, 23, 27, 46, 48, 95 – tympanic isthmus 12 Arnold 4 Aschoff 55, 56, 59 Attic → Epitympanum – bone 5, 15, 30, 31 – roof 8, 28, 30, 31 Atticotomy 97 Auxiliary aeration pathway 12, 30 von Bardeleben 3 Beaumont 60, 61, 88 Benner 56 Bezold 3 Buch 56 Chatellier 11 Cholesteatoma 26, 27, 37, 57, 94, 95, 98–100 Cholesterol crystals 27, 36, 43, 55, 93 – granuloma 57, 61, 86, 97 Chorda tympani nerve 4, 5, 8, 12, 17, 42, 72, 95 Chordal fold 8

Cochleariform process 38, 47, 96 Cog 38 Cornelius 4 Cutting of malleus neck 96 Dahlberg 59 Diamant 59, 60 Döderlein 87 Drainage pathway → Aeration pathway Duplicate folds 7 Eavey 57 Eckert-Möbius 58 Endaural incision 94 Epidermal papillae 26 Epitympanic diaphragm 11, 12 – folds → Folds – ligaments → Ligaments – sinus 38, 39 Epitympanum – anterior 11, 27, 28, 31, 36–44, 58, 61, 94, 97 – medial 9, 11, 12, 28, 31–33, 38, 42, 64 – posterior 12, 27, 28–36, 42, 101 – superior 8, 28, 31, 61, 62, 76, 77, 81, 88 Eustachian tube 7, 40, 48, 59, 66, 73, 93, 94 Eysell 3 Fetal development 7 Fibrosis 60 Folds (variable, position-changing) – chordal 8 – cruris longi incudis 8 – incus intercrural 32 – interossicular 47 – lateral incudomalleal 8, 11, 12, 15, 20, 28, 30, 32, 62 – medial ossicular 32

– – – –

obturator 8 posterior incudal 30 stapedial 8, 32 tensor 6–8, 11, 37, 38, 39, 40, 42, 43, 46, 47, 62, 66, 69, 94 – trailing medial surface of malleus to tensor fold 42 – trailing superior malleal ligament 8, 41 Foreign body 18, 56, 57, 60 Fossa incudis 30, 66 Friedmann 60, 88 Frontolateral atticotomy 97 Giant cells 69, 70, 73, 84, 86 Glomus tumor 95 Goldenhar’s syndrome 75, 79 Granulation tissue 21, 23, 25, 34–36, 42, 43, 56–58, 67, 69, 70, 72–74, 81, 85–87, 98 Guluya 9 Hammar 4, 5, 7–9, 13, 14, 32, 40, 45, 97 Hammer-Amboss-Schuppenraum 7 Helmholtz 4, 5, 13 Henle 5 Hypotympanum 35, 56, 61 Incudal fossa 30, 66 Incudostapedial articulation 32, 35, 66 Inferior tympanic artery 4, 12 Interatticotympanic diaphragm 11 Jörgensen 56 Kuppelraum 3 Labyrinth capsule 3 Labyrinthine bone 58 Lanugo hair 57, 75, 86

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Lateral attics 8, 12, 62, 69 – attic bone 5, 12 – incudomalleal fold → Folds – malleal space 5, 6, 8, 9, 12, 13, 15, 16, 18–21, 27–29, 38, 64, 66, 69 Lemoine 11 Ligaments (ligamental folds, position-fixed) – anterior malleal 4, 5, 8, 12, 15, 42, 46, 48 – anterior malleal suspensory 12 – lateral malleal 5, 9, 12, 13, 15 – posterior incudal 8, 10, 28, 30, 31, 36 – posterior malleal 5, 12, 13, 29 – superior malleal 28, 38 Lower lateral attic 8, 13, 15, 17, 21, 22, 28–30, 29, 63, 66, 74, 95 McLellan 56 Malleal ligaments 4, 5 – spine 5 Margo tympanicus 5 Mastoid antrum 3, 12, 59, 61, 62 Mastoidectomy 97 Mastoiditis 60 Meconium 55, 57, 61 Medial attic → Epitympanum – ossicular fold → Folds Mesotympanum 4, 17, 18, 21, 26, 28, 40, 45, 56, 98 Microsurgery 94–97 Morimitsu 94, 97 Mucosal fibrosis 58 – hyperplasia 58, 59 – polyps 56, 69, 73 Multinucleated cells 64, 79, 81, 82, 86 Northrop 57 Notch of Rivinus 3, 94, 95 Obturator fold → Folds Ojala 60, 87 Organization 74, 80–83, 87 Otitis media – – acute 5, 19, 59 – – adhesive 34, 89, 93 – – chronic 26, 37, 40, 48, 59, 60, 93, 98 – – hyperplastic 58

104

Subject Index

– – infant 56–58, 60 – – infectious 55 – – neonatorum 32, 55, 59 – – recurrent 87–89, 93 – – secretory 5, 6, 11, 27, 34, 36, 60, 93 – – sterile 32 Otosclerosis 43 Paukenhöhle 3 Periosteal bone 88 Petrotympanic fissure 12, 42 Petrous bone 3, 66, 73, 85–88 Plica cruris longi incudis 8 – transversa 3, 7 Pneumatic cell 7 Pneumatization 36, 38, 47, 57–61, 66, 73, 85–88 Politzer 5, 6, 14, 15, 17, 22 Portal for organization 26, 62, 68 Position-changing folds 7 Position-fixed folds 7 Postauricular incision 94, 95 Posterior attic → Epitympanum – pouch 4, 9, 17, 18, 21, 23, 25, 95 – tympanic isthmus 12, 30 – tympanotomy 21 – tympanum 12, 27, 30, 59, 61, 72, 74 Potter 57 Proctor 9, 12, 13, 16, 18, 31, 32, 38, 46 Protympanic recess 12 Prussak 4, 5, 9, 17, 22 Prussak’s space 5, 6, 9, 11–27, 46, 49, 63, 64, 66–70, 72, 93–95, 98 Pseudocystic granulation 67, 78–81, 84 Pyramidal process 10, 31 Recessus epitympanicus 3 Retraction pocket 25, 27, 75, 93–95 Riding columella 95 Round window membrane 65, 73, 84 – – niche 73, 79 Rüedi 59, 60, 68 de Sa 56 Schuknecht 9 Schwartze 3

Sheehy 38 Shrapnell 5 Shrapnell’s membrane 3–5, 14–16, 18, 19, 21, 24–27, 75, 93, 94 Siebenmann 3, 6, 7, 9, 37, 38, 40, 42, 49, 50, 97 Sinus tympani → Tympanic sinus Spina capitis mallei 5 Squamous bone 3, 61, 66, 74, 85–88 – epithelial cells 55, 75, 79, 85 Stapedial fold → Folds Stapedius tendon 5 Superior attic → Epitympanum – pouch 4, 9 Supratubal recess 3, 6–8, 27, 39, 40, 42, 43, 45–51, 62, 63, 66, 69, 94 Tensor fold → Folds – tendon 3, 6, 10, 16, 31, 36, 38, 40, 47, 48 Tos 6 Transverse crest 3, 6, 38, 39, 94 von Tröltsch 3, 5, 12, 18 Trommelfelltasche 7 Tubal orifice 5 – tegmen 38 Tumarkin 60, 88 Tympanic cavity 3, 9, 49, 58, 64, 79 – glomus tumor → Glomus tumor – isthmus 9, 10, 12, 28, 31–33, 34–36, 40, 48, 64, 67, 72, 93, 94 – membrane 4, 5, 17, 23, 57 – sinus 65, 67, 73 – spine – – anterior 5, 12, 38 – – posterior 5, 17, 23 Tympanostomy tube 27, 34, 75, 89, 93 Tympanotomy – anterior 11, 94 – posterior 11, 94, 95 Upper lateral attic 8, 12, 13, 28, 38, 62 Wildberg 4 Wittmaack 4, 26, 55–61, 87, 88 Wullstein 6, 31

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