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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
OOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOO

Tauno Palva, MD
Professor Emeritus of Otolaryngology
University of Helsinki, Finland
The Temporal Bone Foundation has generated a
In collaboration with 3D video model of one of the temporal bones
described in Chapter 2. This model is available on
Hans Ramsay, MD a CD, which can be obtained by contacting:
Associate Professor of Otolaryngology The Temporal Bone Foundation, Inc.
University of Helsinki, Finland 9 Brimmer Street
Boston, MA 02108 (USA)
and Phone: +1 617 742 5927, Fax: +1 617 742 4666
Clarinda Northrop, B.A. E-Mail: rindyn@aol.com

Director of Research Offer good until September 1, 2002

Temporal Bone Foundation, Boston, Mass., USA

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

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ISBN 3–8055–7227–1
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Contents

IX Preface

Part 1

1 Anatomy and Pathology of the Epitympanum

3 Introduction and General Review
3 Development of the concept of epitympanum
4 Early data of the soft tissues in the epitympanum
7 Fetal development of epitympanic folds and compartments
8 Tensor Fold
8 Lateral Incudomalleal Fold
8 Chordal Fold
8 Other Duplicate Folds
9 Tympanic Isthmus
9 Development of Prussak’s Space
9 Contemporary Concepts of the Anatomy of the Epitympanum
10 Material and Methods
11 Anatomy and Pathology of the Epitympanum and Supratubal Recess
11 Epitympanic Diaphragm
12 Normal Anatomy of Prussak’s Space (with the Lateral Malleal Space)
12 Microdissection
12 Lateral Malleal Space
13 Prussak’s Space
15 Serial Sections
15 Floor of the Lateral Malleal Space (Roof of Prussak’s Space)
15 Shrapnell’s Membrane
16 Anterior Membrane of Prussak’s Space
17 Aeration Pathways to Prussak’s Space
18 Pathology of Prussak’s Space and the Lateral Malleal Space
20 Microdissection
21 Serial Sections
26 Cholesteatoma in Prussak’s Space
27 Large Epitympanic Compartments
28 Posterior Epitympanum
28 Normal Anatomy by Microdissection
28 Lateral Incudomalleal Fold
30 Posterior Incudal Ligamental Fold
31 Superior Malleal Ligamental Fold
31 Tympanic Isthmus
32 Normal Anatomy by Serial Sections
33 Pathology as Seen in Microdissection
36 Pathology as Seen in Serial Sections
 36 Anterior Epitympanum
38 Normal Anatomy by Microdissection
38 Transverse Crest
39 Tensor Fold
41 Other Folds in the Anterior Epitympanum
42 Normal Anatomy by Serial Sections
42 Pathology as Seen in Microdissection
43 Pathology as Seen in Serial Sections
45 Supratubal Recess (Space)
45 Normal Anatomy by Microdissection
48 Normal Anatomy by Serial Sections
48 Pathology as Seen in Microdissection
51 Pathology as Seen in Serial Sections
52 References

Part 2

53 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection

55 Introduction and Short Review of the Literature on Amniotic Fluid Cellular Content
57 Short Review of Mastoid Pneumatization
61 Amniotic Fluid Cellular Content-Related Middle Ear Pathology as a Function of Age in Serial Sections
61 Temporal Bones from Neonates
61 Superior and Anterior Epitympanum and Antrum
62 Tensor Fold and Supratubal Recess
62 Lateral Incudomalleal Fold and Lateral Attics
64 Lateral Malleal Space and Prussak’s Space
64 Medial Attic and Tympanic Isthmus
64 Tympanic Cavity
66 Eustachian Tube
66 Mastoid Pneumatization
66 Comment
67 Temporal Bones from 2- to 4-Month-Old Infants
67 Compartments above the Epitympanic Diaphragm and the Mastoid Antrum
69 Tensor Fold and Supratubal Recess
69 Lateral Malleal Space and Lateral Attics
70 Prussak’s Space and Its Aeration Pathways
72 Tympanic Isthmus and Posterior Tympanum
73 Tympanic Sinus and Round Window Niche
73 Eustachian Tube
73 Elements Specific to Amniotic Fluid Cellular Content
73 Mastoid Pneumatization
74 Comment
75 Temporal Bones from 5- to 23-Month-Old Infants
76 Case 1
77 Case 2
79 Case 3
82 Case 4
82 Case 5
84 Elements Specific to Amniotic Fluid Cellular Content
85 Mastoid Pneumatization
86 Comment
86 General Comments
86 Histological Considerations regarding Amniotic Fluid Cellular Content-Associated Pathology
87 Mastoid Pneumatization
88 Clinical Considerations
89 References

VI Contents
 Part 3

91 Microsurgical Approaches to Inflammatory Ear Disease

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

103 Subject Index

Contents VII
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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 fun-
damentally improved upon.
The knowledge of human anatomy and pathology,
obtained at autopsies and complemented by light-micro-
scopic 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 in-
creased the knowledge of the anatomy based solely on the
naked eye. The magnified view, nevertheless, has not ren-
dered 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 mag-
nification, still contains many valuable observations. Es-
pecially 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 dissa-
tisfied with the articles discussing the anatomy of the epi-
tympanum and was convinced that some of the described
features did not reflect the facts. The contemporary au-
thoritative 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 Ham-
mar’s study of the fetal development of epitympanic folds
did I feel close to understanding the epitympanic com-
partments and their origin. This was followed by going
personally back to the dissection laboratory and begin-
ning 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 mi-
crodissection by having the continuing cooperation with
Clarinda Northrop of the Temporal Bone Foundation in
Boston who permitted me to use their magnificent collec-
tion 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 Otola-
ryngology 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 semi-
nars of anatomy, pathology and surgery of the ear. It
appeared that the initial level of knowledge of the resi-
dents 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 ap-
peared 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 photo-
graphs 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 understand-
ing 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 microdissec-
tion approaches we have advocated, to become familiar
with the structures forming the epitympanic compart-
ments. We are convinced that afterwards work in the
operation theater becomes even more interesting, when
structures discovered and understood as a result of mi-
crodissection 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 func-
tional 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 cel-
lular content into the different compartments of the mid-
dle 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 cen-
tury, and both Aschoff and Wittmaack produced volumi-
nous 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 Cor-
tese.
The Ear Research Foundation, Helsinki, the Depart-
ment 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
Part 1
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Anatomy and Pathology of the

Epitympanum

1
 Part 1
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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 por-
tion superior to the main tympanic cavity. In his concise
chapter entitled ‘Mittelohr und Labyrinth’ in Karl von
Bardeleben’s Handbuch der Anatomie des Menschen, Sie-
benmann [1] still referred to this superior segment as ‘adi-
tus (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 supe-
rior region, and that it was Bezold who described its ana-
tomic 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 Ger-
man language but one should continue to use the estab-
lished 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 con-
nection 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 inferi-
or 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 supe-
riorly 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 protym-
panic 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, to-
wards the eustachian tube, showed a downwards sloping
form while the posterior portion remained horizontal.
The lateral limit of the epitympanum was formed superi-
orly 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 histo-
pathological studies in the 1990s we also became familiar
with the considerable knowledge available in the old writ-
ings. 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 signifi-
cantly 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 sig-
nificant 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 Ger-
man) 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 de-
picted 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 tym-
panic membrane. A further mistake was that Arnold con-
sidered the folds not constant and left them out of several
figures which showed the medial side of the tympanic
4 Color Atlas of the Anatomy and Pathology of the Epitympanum
membrane. The conviction of von Tröltsch that especially
the posterior pouch was a duplicate of the tympanic mem-
brane 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 de-
scription 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 irregular-
ly 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 tis-
sue.
The medial border of the anterior pouch, on the other
hand, was no longer considered [2] as a duplicate tym-
panic membrane. The pouch formed between the tym-
panic 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 mem-
brane. 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 crit-
ical remarks that von Tröltsch made on the work of oth-
ers, 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 Prus-
sak’s space, essentially holds true today. Although Prussak
accepted the concept of von Tröltsch [2] that the mem-
brane forming the posterior pouch represented a dupli-
cate 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 tym-
panum, 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 fol-
lows: (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 clini-
cal 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 tym-
panic 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 mal-
leus 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. Helm-
holtz agreed that the superior pouch was in open connec-
tion 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]. Further-
more, Helmholtz gave the name ‘posterior malleal liga-
ment’ 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 supe-
rior pouch but also to the anterior pouch and in two tem-
poral bones there was a connection superiorly, to a space
1 Anatomy and Pathology of the Epitympanum
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 coch-
leariformis; 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, insert-
ing 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 differ-
ent 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 anteri-
or 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 mal-
leus’ 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 orga-
nization 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,
5
Fig. 2. Original sketch by Politzer [9] from
1870, showing Prussak’s space in a child. k =
Processus brevis of the malleus; s = Shrap-
nell’s membrane from which a curved mem-
brane 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 = anteri-
or tympanic spine; f = inconstant folds later-
al 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 Politz-
er [10] from 1908. h = Head of the malleus;
te = annulus tendinosus; b = processus bre-
vis; u = umbo; t = chorda tympani; s = Shrap-
nell’s membrane; e = external (lateral) mal-
leal ligament; ae = external attic; P = Prus-
sak’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.
Fig. 4. Another sketch by Politzer [10] also
from 1908 was based on his collection of
temporal bones. ls = Superior malleal liga-
ment; le = lateral malleal ligament; s = pars
flaccida; o = Prussak’s space; t = tensor tym-
pani tendon; r = network of spaces between
the malleus head and the lateral attic bone.
This sketch is accurate. Note that the net-
work of spaces inside Prussak’s space is no
longer present in figure 3 and here. In the lat-
eral malleal space it has been reduced to one
tissue strand, apparently a postinflammato-
ry change.

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 Prus-
sak’s original description.
In 1897 Siebenmann [1] summarized the main epitym-
panic compartments and presented two alternative pic-
tures 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 epitympa-
num, the tensor fold, even if it was drawn in both sketches
as a vertical fold between the tensor tendon and the trans-
verse crest. He thus also had a clear representation of the

6 Color Atlas of the Anatomy and Pathology of the Epitympanum

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 Trommel-
felltaschen), and of the upper and lower lat-
eral attics (oberer and unterer Hammer-Am-
boss-Schuppenraum). The tensor fold (hori-
zontal arrow) between the anterior epitym-
panum 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 meso-
tympanum. 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 aris-
ing 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 devel-
opment of the various soft tissue structures in the epitym-
panum, from a 3-mm embryo to the term fetus, was done
in 1902 by Hammar [5] in Uppsala. He sectioned the tem-
poral 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 concentra-
tion are necessary to read it, and being written in the Ger-
man 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 em-
bryonic connective tissue, except for a slit running from
1 Anatomy and Pathology of the Epitympanum
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 epi-
tympanic subcompartments formed. In this context we
will not follow these processes in detail but first limit our-
selves 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 chor-
da tympani nerve, which can be passed on both sides, the
sac divides into two, one portion continuing over the lat-
eral, 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 posi-
tion-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 meet-
ing connective tissue sides merge, and the epithelium pre-
vails on both sides. Large duplicate folds are likely to per-
sist even if they sometimes show membrane defects.
Small duplicate folds, however, may remain slender and
7
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 discuss-
ing 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 di-
vides 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 ante-
rior 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, re-
placing 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 epithe-
lium 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.
8 Color Atlas of the Anatomy and Pathology of the Epitympanum
Consequently, its posterior portion, consisting of the lat-
eral 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 poste-
rior ligamental portion is always present and has a con-
stant 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 anteri-
orly. 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 tym-
panum the nerve is part of the major structure, the anteri-
or malleal ligamental fold, and receives its mucosa from
the advancing anterior air sac. In the posterior tympa-
num, specifically in the lower lateral attic, the advancing
medial air sac provides the nerve with its fold which pos-
teriorly 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 pos-
terior 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 disap-
peared before birth because the superior and medial air
sacs ended, after the merge, with atrophy. Of the continu-
ing 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 obtura-
tor 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 isth-
mus was distinct, both becoming narrow at this site and
expanding again more superiorly. Discussing the 330-
mm-long fetus Hammar stressed that of the various epi-
tympanic main compartments it was only the medial attic
which via the tympanic isthmus is in direct communica-
tion with the tympanic cavity. Even if during the earlier
stages the fold of the long process of incus and the stape-
dial 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 supe-
rior 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 path-
way.
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 epi-
tympanic compartments. Second, the separate narrow
route from the lateral mesotympanum formed the aera-
tion and drainage pathway via the posterior pouch to the
small space of Prussak. Hammar [5] even stressed, com-
menting 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 be-
came united with another aeration route, fully indepen-
dent of the tympanic isthmus.
The basic data on Prussak’s space, so accurately de-
scribed by Prussak himself, became largely forgotten dur-
ing the latter part of the 20th century and the contempora-
ry detailed anatomic knowledge has not remained at the
level set by the pioneers. Responsible for this was a publi-
1 Anatomy and Pathology of the Epitympanum
cation by Proctor [13] in 1964 in which beautiful art
work drawings beguiled the reader for decades into be-
lieving 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 Proc-
tor did not seem to understand that the lateral incudo-
malleal 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 later-
al malleal space, consisting of the lateral malleal ligamen-
tal fold, is the intact roof of Prussak’s space. Even if the
posterior pouch was accurately placed between the poste-
rior 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 unfor-
tunately also adopted from Proctor by Schuknecht and
Guluya [15], who suggested that Prussak’s space is anteri-
orly 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 aerat-
ing 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 erro-
neous statements in Proctor’s text regarding the major
epitympanic compartments, but restrict ourselves here to
stressing another major one regarding the tympanic isth-
mus. Proctor suggested that the isthmus should be ana-
tomically divided into two portions, the ‘isthmus tympani
anticus’ and ‘the isthmus tympani posticus’. The anterior
9
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 isth-
mus 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 mesotympa-
num is almost completely separated from the attic by the
ossicular chain and mucosal folds’. This erroneous ar-
rangement has been quoted over and over again in many
later studies.
If this nearly complete separation of the posterior por-
tion 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 open-
ing, 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 lenti-
cular 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 tem-
poral 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 Insti-
tute 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 Uni-
versity 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 abso-
lutely 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
10 Color Atlas of the Anatomy and Pathology of the Epitympanum
and white or color photography, or both, using the operation micro-
scope.
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 ap-
proach 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 thin-
ning 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, documenta-
tion 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 pro-
ceed 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 struc-
tures 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 teg-
mental 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 tym-
panic 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 mem-
brane 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 observa-
tion 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 anteri-
or 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 clin-
ical 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 han-
dle laterally, when the anterior malleal ligament remained attached
partially to both, the head is removed with microforceps and refa-
shioned to be placed on the long process of the incus as a riding colu-
mella [24]. This gives good practise for teaching purposes in simulat-
ing 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 adhe-
sive 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 togeth-
er 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 mar-
gin opens the anterior epitympanum and discloses the anterior por-
tion of the head of the malleus superior to the anterior malleal liga-
ment. 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 microdissec-
tions. 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 con-
fidence.
The majority of the material for serial sections derives from the
collection of the Temporal Bone Foundation, Boston, Mass. consist-
ing 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 hema-
toxylin-eosin, alternately by van Gieson’s, and a few specimens with
Masson’s trichrome. All sections were studied by microscopy and
1 Anatomy and Pathology of the Epitympanum
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. Horizon-
tal 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 adopt-
ed 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 point-
ing 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 histo-
logical 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 addi-
tion 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 dia-
phragm, its roof, the lateral malleal ligamental fold, being
the dividing structure. Chatellier and Lemoine linked
their anatomic study to clinically important aspects en-
countered 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 tempo-
ral 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 ante-
rior 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-
11

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 liga-
ment; 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 epi-
tympanum, the larger compartment, houses both the me-
dial 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 tym-
panic isthmus to be one single entity calling it the ‘anteri-
or tympanic isthmus’, we gave the name ‘posterior tym-
panic isthmus’ to a pathway behind the tip of the incus.
Later we dropped the word ‘anterior’ from the main aera-
tion pathway to the attic and called it, as the 19th century
authors did, the tympanic isthmus. The posterior tym-
panic isthmus behind the incus tip proved to be so incon-
stant and small that we will refer to it now as an inconsis-
tent auxiliary aeration pathway via the incudal fossa. Fig-
ure 6 shows the modified sketch of the epitympanic dia-
phragm 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 seri-
al sections (for example fig. 33, 44 and 46).
12 Color Atlas of the Anatomy and Pathology of the Epitympanum
Normal Anatomy of Prussak’s Space (with the Lateral
Malleal Space)
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, adi-
tus 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 compart-
ments and seriously impairs the middle ear function. In
the discussion of the anatomy of Prussak’s space, how-
ever, 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 micro-
dissection, 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 mal-
leus, a view opens to the lateral malleal space. The space
is limited medially by the malleus head and neck and lat-
erally by the lateral attic bony wall. Anteriorly its bound-
aries are formed by the inconstant anterior malleal sus-
pensory ligament and inferior to it, by the anterior mal-
leal 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 liga-
mental fold. As the latter fold also becomes broader infe-
riorly, the lateral malleal space becomes bowl-shaped
near its floor, which is formed by the lateral malleal liga-
mental 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 incudo-
malleal fold (vertical arrow) forms the superior portion of the posteri-
or limit. The anterior portion of the floor is thick, the posterior por-
tion is thin and contains a weak spot (curved arrow) limited by sepa-
rate, whitish ligamental bundles. I = Incus.
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 descend-
ing towards the floor, becomes often thicker and undulat-
ing 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 Prus-
sak’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 transpar-
ent whitish structures through the covering epithelium.
The floor often shows a weak area posteriorly (fig. 7) and
1 Anatomy and Pathology of the Epitympanum
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 mal-
leal 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 (obli-
que arrow) forms the larger portion of the floor which posteriorly has
a membrane defect (horizontal arrow). The inner blade of the posteri-
or pouch (open arrow) is inferiorly united with the chorda tympani
nerve (C). M = Malleus; I = incus; B = lateral attic bone; T = tensor
tendon.
in about 6% of our total material a membrane defect con-
nected the lateral malleal space to Prussak’s space (fig. 8,
9). The lateral malleal ligamental fold, the roof of Prus-
sak’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 alrea-
dy 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 horizon-
tal 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 por-
tion 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
13
Fig. 9. Series G, adult case 11, left ear, superior view. A central mem-
brane 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 mem-
brane 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 path-
way 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-
14 Color Atlas of the Anatomy and Pathology of the Epitympanum
Fig. 10. Series A, adult case 13, right ear, superior view. A large por-
tion 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 superi-
or portion of the aeration pathway (open arrow) leads to the posterior
pouch, formed medially by the posterior malleal ligamental fold (ver-
tical 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 tym-
panic 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 ante-
rior 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 path-
way. 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 secre-
tion 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 posteri-
or 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 mal-
leus (M) and medial to the tympanic membrane (TM). The mem-
brane 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 mem-
brane 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 lat-
eral malleal space well above its floor, the anterior wall
consisting of the upper portion of the anterior malleal liga-
mental 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
Fig. 14. Series A, adult case 7, left ear. Lateral anterior approach. The
wall remains thin or may, as in the ear shown, end before
tympanic membrane (TM) has been detached from the anterior sul-
reaching the posterior malleal ligamental fold (fig. 15b). cus and turned posteriorly together with Shrapnell’s membrane.
Thus in this case the lower lateral attic and the lateral mal- Prussak’s space (horizontal arrow) appears superior to the short pro-
leal space became united. Further sections showed the cess of the malleus (M) and extends superiorly past the rim of the
weaker bundles of the lateral malleal ligament, adjacent to lateral attic bone (B). This lateral anterior approach provides a view
of the low portion of the tensor fold (curved arrow).
the strong anterior malleal ligament, to spread from the
malleus neck to the opposite lateral attic wall, thus form-
ing the resistant anterior half of the floor. When the dome
of Prussak’s space made its appearance the lateral malleal parts of Prussak’s space are situated above the bony rim of
ligamental bundles were still present anteriorly (fig. 15c). the attic bone where the membrane has its insertion. At
Shrapnell’s Membrane. We limit ourselves in this con- times it is large, covering a sizeable Prussak’s space under
nection only to the observation that Shrapnell’s mem- the bony rim. Both these situations were well illustrated
brane (fig. 15d) is also subject to a considerable variation also by Politzer [10] in 1908 (fig. 3, 4). Even normally the
in size and in structure. It may be very small when most covering epidermis may show distinct changes, the papil-

1 Anatomy and Pathology of the Epitympanum 15

Fig. 15. Adult patient, otosclerosis, right ear. Sections across the later-
al 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 later-
al 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
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 dupli-
cate fold when the anterior air sac, advancing posteriorly,
meets the expanding projection of either the medial or
superior air sac, advancing anteriorly and forming Prus-
sak’s space. The membrane fastens laterally to the tym-
panic membrane and medially regularly to the anterior
portions of the malleus neck, or anterior to it, to the tensor
16 Color Atlas of the Anatomy and Pathology of the Epitympanum
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. Magni-
fication !28 (a–c), !12 (d).
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 ante-
rior 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].

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 (ar-
row) 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 defin-
ing the aeration and drainage pathways satisfactorily. Ini-
tially we [16] thought that the posterior pouch is the high-
ly 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 struc-
ture was present in all examined ears. However, it func-
tioned 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 tym-
panic 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. Prus-
sak’s space (fig. 17a) moves first posterior to the malleus,
becoming the superior portion of the posterior pouch
1 Anatomy and Pathology of the Epitympanum
(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 tympa-
num [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 poste-
rior 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 meso-
tympanum. 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 men-
tion of the number of cases he had studied, but they prob-
ably were not very many as he referred to his initial 1856
congress report as the only data of the pouch in the text-
17
Fig. 17. Series P, a child aged 4 years, left ear. Sections across Prus-
sak’s space (P) and posterior pouch (PP). a Prussak’s space at the
level of the superior portion of Shrapnell’s membrane (SM). The pos-
terior 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-
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 microdis-
section and by serial sections leave no place for specula-
tion. The two pathways, one via the posterior pouch and
another directly to the lower lateral attic and mesotym-
panum, 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-
18 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 aera-
tion pathway was 1.4 mm. Hematoxylin-eosin stain. Magnification
!20.
tween the ‘lateral incudal and lateral malleolar folds’
advocated by Proctor [13, 14] has not been documented
and is not realistic.
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 aera-
tion 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 poste-
rior to the malleus (M) where it measures 0.8 ! 1.1 mm and is inferi-
orly open to the lower lateral attic (L) and mesotympanum. The chor-
da (C) is connected to the posterior malleal ligamental fold (oblique
arrow) . b A section 0.3 mm inferior to a. The pathway is also medial-
ly open to the mesotympanum (vertical arrow), the chorda remains
ice of the posterior pouch, and thus the route is open via
these regular aeration pathways to Prussak’s space. Simi-
larly, 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, inflammato-
ry 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
1 Anatomy and Pathology of the Epitympanum
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.
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 infec-
tion 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 ante-
rior pouch or the lateral malleal space.
19
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 mal-
leal 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. 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.
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
20 Color Atlas of the Anatomy and Pathology of the Epitympanum
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. 22. Series G, adult case 16, left ear, superior view after removal
of the incus. Prussak’s space (horizontal arrow) is filled with secre-
tion 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.
overpressure can change the position of the three strong
position-fixed malleal ligamental folds forming its bor-
ders. What can be observed frequently is a marked retrac-
tion of the lateral incudomalleal fold drawing its inferiorly
directed anterior portion even below the level of the floor
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 with-
out ligamental fibers (oblique arrow) and inserts to the spine (S) and
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 granula-
tion tissue the lateral malleal space shows similar involve-
ment.
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-
1 Anatomy and Pathology of the Epitympanum
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 be-
tween the tympanic membrane and the annular bone. The chorda
enters its bony canal. The height of the pouch was 2.4 mm. This regu-
lar aeration pathway was filled throughout with secretion and a few
clusters of round cells. Hematoxylin-eosin stain. Magnification
!20.
sak’s space has occurred, Shrapnell’s membrane being
united with the neck of the malleus, this can be ascer-
tained 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 find-
ing 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 mesotym-
panum attracts both amniotic fluid cellular content
21
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 (verti-
cal 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
(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-
22 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 sep-
arate 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.
way via the posterior pouch can be seen in figure 23. Prus-
sak’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 secre-
tion, 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 later-
al 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 gen-
erous pathway for drainage of secretions (fig. 18), exten-
sive inflammatory processes in the lower lateral attic may
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) mea-
sures 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 ante-
rior pouch, secretion drains into it through a large pathway. A verti-
cal arrow points to a superiorly blind extension of the lower lateral
also spread to Prussak’s space. In this type of a process
Prussak’s space can be invaded by granulation tissue aris-
ing from the lower lateral attic and advancing to Prussak’s
space (fig. 24a, b). The more inferiorly situating blind pos-
terior pouch was relatively free of pathology even if there
was much inflammatory tissue around the chorda tym-
pani 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
1 Anatomy and Pathology of the Epitympanum
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.
(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 devel-
oped and the ligamental fibers spread to the posterior tym-
panic 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 tym-
panic 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 aera-
tion route as the regular aeration pathway went normally
23
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) con-
nects the two spaces and measures 0.8 ! 1 mm. Sections both superi-
or 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 poste-
rior 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 = anteri-
or 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 capil-
laries. 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 sepa-
rated from Prussak’s space by a thick connective tissue layer infil-
trated 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.

24 Color Atlas of the Anatomy and Pathology of the Epitympanum

 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 granula-
tion 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 meso-
tympanum. 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 devel-
op 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). Res-
toration of an air filled Prussak’s space is no longer possi-
ble [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 choles-
teatoma. Another possibility is the filling of Prussak’s
space with abundant granulation tissue which finally,
after maturing, fills the entire space allowing even consid-
erable 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 con-
nective tissue.

1 Anatomy and Pathology of the Epitympanum 25

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 anteri-
or membrane (horizontal arrow) is thin, the anterior pouch (AP) con-
tains 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 fol-
lowed by retraction of the posterior portion of the pars
tensa and of Shrapnell’s membrane, and by gradual reten-
tion of keratin and bone resorption at the posterior retrac-
tion edge. The disease progresses relentlessly but the
26 Color Atlas of the Anatomy and Pathology of the Epitympanum
arrow) is thick, the anterior membrane of Prussak’s space thin (hori-
zontal 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 (ver-
tical arrow), filled with cholesterol crystals. The epidermis of Shrap-
nell’s membrane (oblique arrow) is very thin, without papillae and
adherent to the malleus. There is hemorrhage between the artifac-
tually separated tympanic membrane (TM) and the posterior malleal
ligament (L). C = Chorda tympani nerve; T = tensor tendon. Mas-
son’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 poste-
rior 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 aera-
tion 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 bor-
derline between the two is formed by the head of the mal-
leus which blocks much of the direct communication but
1 Anatomy and Pathology of the Epitympanum
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 epi-
dermis (curved arrow) is displaced laterally at sectioning. The anteri-
or 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.
27
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 tym-
panic 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.
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.
Posterior Epitympanum
A substantial proportion of the volume of the posterior
epitympanum is taken up by the body and the short pro-
cess 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 nar-
rower 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
28 Color Atlas of the Anatomy and Pathology of the Epitympanum
Fig. 34. Same ear as in figure 33, anterosuperior view. The downgo-
ing 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.
air space without any limiting borders. Above the superi-
or surface of the ossicles the upper lateral attic, together
with the medial attic, forms the superior attic, which nor-
mally 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 com-
municates with the mesotympanum via the large tym-
panic isthmus.
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 in-
depth 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 meso-
tympanum without any obstruction. Structures and sub-
compartments which are usually present are discussed
individually below.
Lateral Incudomalleal Fold. This thin fold starts poste-
riorly 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 incudomal-
leal fold (horizontal arrow) allowing for slightly different sloping of
the anterior and posterior halves of the fold. Another ligamental bun-
dle starting from the malleus (oblique arrow) appears at the down-
ward turn of the fold towards the lateral malleal space (L). The tym-
panic isthmus (TI) is fully open. M = Malleus; I = incus; A = anterior
malleal ligamental fold.
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 ten-
don; TF = tensor fold.

posterior edge of the malleus head (fig. 33). Here it regu-

larly turns downwards to become united with the posteri-
or malleal ligamental fold, forming with it the posterior
border of the lateral malleal space (fig. 34), closing com-
pletely 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 direct-
ly 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 ante-
riorly, without turning down, along the malleus head and
forms a thin roof for the lateral malleal space (fig. 37). It
Fig. 37. Series A, adult case 14, left ear, superior view. The lateral
still remains the same thin duplicate fold and should not
incudomalleal fold (horizontal arrow) is thin and there is a curved
be confused with the lateral malleal ligamental fold that tissue strand (oblique arrow) in its anterior portion. Anterior to it a
more inferiorly forms the floor of the lateral malleal space. thin lateral malleal fold (curved arrow) covers the lateral malleal
The aeration of the lateral malleal space in such cases space. M = Malleus; I = incus; A = anterior malleal ligament.
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 nar-
rower or broader strip, crossing from the malleus head to ligamental fold and thus leave the lower lateral attic to
the lateral attic wall, forming a partial roof for the lateral communicate freely with both the upper lateral attic and
malleal space. the lateral malleal space (fig. 15, 38). In such cases a rare
The anterior portion of the fold is subject to large vari- view to the lower lateral attic under the lateral incudomal-
ations. The fold may end short of the posterior malleal leal fold may be obtained from the anterior direction [18].

1 Anatomy and Pathology of the Epitympanum 29

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 poste-
rior 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 com-
munication to the lateral malleal space.
Membrane defects appear in the lateral incudomalleal
fold in around 15% (fig. 38, 39); therefore, in such cases
30 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 liga-
mental 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 lat-
erally 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 appar-
ent, 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, there-
fore, 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 incu-
dal fossa to the mesotympanum. Suctioning rapidly evacuated water
from the tympanum.
Fig. 42. Series G, adult case 18, right ear, superior view. A large open-
ing 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 incu-
domalleal fold.

romedial direction [18] in microdissection but serial sec-

tions 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 epi-
tympanum, 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
Fig. 43. Series G, adult case 52, left ear, superoposterior view. The
and incudal sagittal and frontal folds included in the superior malleal ligament (vertical arrow) connects the head of the
sketches of Proctor [13, 14], and reproduced by Wullstein malleus (M) to the attic roof. There is no trailing fold, a general find-
and Wullstein [11], are pure fantasy in normal ears. Only ing. The space between the malleus and attic bone is narrow and
inflammatory webs often cross the superior attic air space there is one narrow tissue strand across the space (horizontal arrow).
The oblique arrow points to the medial portion of the transverse
in a haphazard manner.
crest.
Tympanic Isthmus. This regular large aeration path-
way 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 superoposterior- anterior epitympanum. In adults, the breadth of the me-
ly (fig. 33–36). Medially it is limited by the attic bone and dial attic at the middle of the short process of the incus is
laterally by the body and short process of the incus and the around 1.3 mm, the narrowest width at the level of the
head of the malleus. The space limited by these structures body of the incus may be less than 1 mm. The anteroinfer-
is the medial attic, which inferior to the incus body ior portion of the tympanic isthmus between the tensor
becomes the mesotympanum. The anterior portion of the tendon and the inferior surface of the malleus head is larg-
tympanic isthmus, superior to the level of the tensor tym- er, around 3 mm (fig. 34). The distance from the tensor
pani tendon, is in large open communication with the tendon to the anterior edge of the posterior incudal liga-

1 Anatomy and Pathology of the Epitympanum 31

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 later-
al mesotympanum. M = Malleus; I = incus; T = composite tissue
insertion ring for the tensor fold. Masson’s trichrome stain. Magnifi-
cation !7.
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 pro-
viding insertion points for inflammatory folds which may
seriously restrict the passage to the isthmus itself, the isth-
mus 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 posterior-
ly 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 mal-
leal 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
32 Color Atlas of the Anatomy and Pathology of the Epitympanum
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.
have unquestionably been seen in serial sections. They
usually start from the incus, do not always reach the oppo-
site 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]. Nev-
ertheless, 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.
Normal Anatomy by Serial Sections
In the absence of inflammatory changes, microdissec-
tion can instantly provide an idea of the compartments
compared to serial sections (fig. 44), necessitating exami-
nation of a large number of slides. The lateral incudomal-
leal 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 final-
ized, 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 epitympan-
um 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 pos-
terior 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 pos-
terior incudal fold closes the auxiliary aeration pathway via the incu-
orly towards the posterior malleal ligamental fold
(fig. 15a) is well visible at thin cross sections. The majori-
ty 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 rela-
tively spacious area underneath the incus tip, bordered by
the air cells, while the larger posterior incudal aeration
pathway route appears behind the tip.
1 Anatomy and Pathology of the Epitympanum
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 poste-
rior malleal ligamental fold (between horizontal arrows), is distinct.
The floor of the lateral malleal space is intact (curved arrow). T =
tensor tendon.
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 tym-
panic 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-
33
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 attach-
ments 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.
34 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 epitym-
panum, 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 multi-
layered inflammatory network (curved arrows) closes the major por-
tion 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 epitym-
panum 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 isth-
mus (fig. 49, 50).Without surgical interference such cases
lead to a prestage of an adhesive otitis media, with recur-
rent 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 imma-
ture or mature connective scar tissue (fig. 51) or as a con-
tinuous 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, medio-
posterior view. The tympanic isthmus posterior to the stapes (S) and
medial to the incus (I) is blocked by a multilocular inflammatory tis-
sue 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. Gran-
ulation 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). Simi-
lar 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 Re-
moval of the incus left a cast in the mesotym-
panic granulation tissue. The horizontal ar-
row 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 microdissec-
tion 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 oblitera-
tion of the middle ear spaces.

1 Anatomy and Pathology of the Epitympanum 35

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 ar-
rows). Hematoxylin-eosin stain. Magnifica-
tion !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 muci-
nous together with its cellular content, and the appearance
of the epitympanic mucosa make it possible to draw con-
clusions 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 obli-
terated by connective tissue and some by cholesterol crys-
tals. Round cells containing secretion also appear in the
major air compartments (fig. 55b), the amount depending
upon the available open drainage pathways. The tym-
panic isthmus may become partially blocked by inflam-
matory webs or by polypoid tissue at times covered by
advancing squamous epithelium from the mesotympa-
num (fig. 55c). These changes become also well apparent
around the incudal fossa where the ligamental fold epithe-
36 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 suffer-
ing from secretory otitis media even if the main pneuma-
tization process remains halted.
Extensive development of granulation tissue in the
posterior epitympanum occurs, even during the era of
antibiotics and disappearance of florid mastoid infec-
tions, since the process of organization involves the non-
removed masses of mucoid secretion filling the attic. This
may be seen in association with an undiagnosed AFCC-
linked 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 edema-
tous. 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-
it was closed by the vertically rising tensor fold, the inser-
tion of which was into the transverse crest in the attic teg-
men (fig. 5). The writers of that period defined the space
anterior to the fold as a ‘pneumatic cell’ which was partial-
ly 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 spe-
cifically pointed out that it is part of the mesotympanum,
not the epitympanum. His description differs from our
1 Anatomy and Pathology of the Epitympanum
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 lat-
eral 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 cap-
illaries 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 (ver-
tical arrow) go directly lateral and medial from the incus. Masson’s
trichrome stain. Magnification !25 (a, d), !7 (b, c).
concepts [19, 20] of the anterior epitympanum concern-
ing 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
37
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
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.
Normal Anatomy by Microdissection
The medial attic continued in all dissected bones unob-
structed, superior to the tensor tendon and medial to the
head of the malleus, and became the anterior epitympa-
num. 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 com-
partments, 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 lat-
eral portion of the anterior epitympanum is as a rule dis-
38 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 exten-
sion of the anterior attic appears when normal large air cells have
been opened towards the supratubal recess tegmen (oblique arrows).
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 forma-
tion 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 struc-
ture have been misunderstood by most of the contempo-
rary writers even if Siebenmann already in 1897 pub-
lished 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 inde-
pendent 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 general-
ly 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-
Fig. 57. Series P, case 11, a child aged 2 years, left ear, superoposter-
ior view. The anterior attic has an extension in the superior direction
(between horizontal arrows). The tensor fold is very thin and con-
tains a membrane defect (oblique arrow). M = Malleus; TI = tym-
panic isthmus; A = anterior malleal ligamental fold; T = tensor ten-
don.
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 Su-

peroposterior 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 ar-
rows 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 eus-
tachian 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 ante-
rior epitympanum and the space in front of it is the supra-
tubal 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 contem-
porary 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 ob-
struction’ 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-

1 Anatomy and Pathology of the Epitympanum 39

Fig. 60. Series G, adult case 15, left ear, superoposterior view. The
tensor fold (TF) contains large thin areas with a few stronger connec-
tive tissue strands across the fold. The thin fold from the malleus (M)
to the tensor fold (oblique arrow) was present in 40% of microdissec-
tions. The chorda tympani nerve (C) is always positioned at the later-
al 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.
ly prevents communication between the supratubal re-
cess, part of the mesotympanum, and the anterior epitym-
panum (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 speci-
mens, 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 vary-
ing further course. If the insertion is to the transverse
crest, then the direction is nearly vertical, when the inser-
tion 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 an-
terior epitympanic-supratubal tegmen. The fold appears
generally thicker close to its borders and may have cross-
ing strands, while the central portion is thin like a pseu-
domembrane (fig. 60). Nevertheless it is a tough structure
40 Color Atlas of the Anatomy and Pathology of the Epitympanum
Fig. 61. Series G, adult case 2, right ear, superoposterior view. A
small portion of the tensor fold is present, attached to the tensor ten-
don (T), while the major portion shows a membrane defect (horizon-
tal arrow). M = Malleus; TI = anterior portion of the tympanic isth-
mus. A membrane defect of this size provides a large and effective
auxiliary aeration and drainage pathway from the anterior epitym-
panum to the supratubal recess (R) and eustachian tube.
that does not break even if subjected to vigorous move-
ment 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, dem-
onstrate 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 inferi-
or-superior direction in the tegmental bone.
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 (obli-
que 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. Hematoxylin-
eosin stain. Magnification !21.

Fig. 65. A broad composite tissue insertion ring removed during

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-
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.

1 Anatomy and Pathology of the Epitympanum 41


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 (horizon-
tal 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 multi-
layered 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).
42 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 sepa-
rated 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 pro-
vided 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 superi-
orly 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 liga-
mental 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 ten-
don is around 3 mm, but shows much individual varia-
tion, 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 tis-
sue [18]. In active chronic inflammation granulation tis-
sue either obscured the details of the space (fig. 68) or
Fig. 67. Adult patient, otosclerosis, left ear. The posterior portion of Fig. 68. Series A, adult case 12, left ear, supe-
the anterior attic (AA) is narrow between the malleus (M) and the roposterior view. Thick mucosa and granula-
transverse crest (horizontal arrow), while its major anterior portion is tion tissue mask the details of the anterior
situated between the crest and the anterior attic bony wall (B). The attic. Vertical arrow points to the area of the
spaces merged fully in a section 1 mm more inferior. The walls of the tensor fold covered by granulation tissue and
well-pneumatized anterior attic as well as the crest itself show an webs, horizontal arrow to the place of the
unusual amount of bony ridges and tags. Hematoxylin-eosin stain. tensor tendon. There is similar tissue on top
Magnification !12. of the lateral malleal space (oblique arrow).
M = Malleus.

Fig. 69. Series A, adult case 15, left ear, supe-

rior view. a The anterior attic is full of
immature granulation tissue and no details
can be discerned. b Same region after remov-
al 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 ante-
rior 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 pro-
gress 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 ac-
tive inflammation and development of granulation tissue
in the anterior epitympanum are shown in Part 2 dealing
with the AFCC-associated pathology.

1 Anatomy and Pathology of the Epitympanum 43

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. 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.
44 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 lat-
eral 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 sus-
pensory ligament. Masson’s trichrome stain. Magnification !12.
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.
Fig. 74. Series A, adult case 13, right ear,
anterior approach, oblique view from the
protympanum to mesotympanum. The mal-
leus handle (M) and the tympanic mem-
brane (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 tym-
panic isthmus.
Fig. 75. Series P, case 11, a child aged 2
years, left ear, anterior approach. Direct
view onto the ossicles in the mesotympan-
um. M = Malleus handle; T = tensor tendon;
I = long process of the incus; S = stapes. Ver-
tical arrow points to hypotympanum, hori-
zontal arrow to the low lateral portion of the
supratubal recess.
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 = pro-
montory; T = tensor tendon. Oblique arrow
points to the area of the anterior membrane
of Prussak’s space.

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 smal-
lest 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 mesotym-
panum, outside the borders of the epitympanum.
In the conventional superior microdissection removal
of the tensor fold made a reasonable evaluation of a nor-
mal 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 tis-
sues, fixed to the anterior surface of the fold. We, there-
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 ante-
rior sulcus of the tympanic membrane. Usually a good
deal of enlargement must be done with a drill to give ade-
quate 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).

1 Anatomy and Pathology of the Epitympanum 45

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 me-
sotympanum. The anterior membrane of
Prussak’s space (horizontal arrow) in the an-
terior pouch and the low portion of the
supratubal recess (oblique arrow), superior
to the tensor tendon (T), are in full commu-
nication with the mesotympanum. The ante-
rior 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 an-
terior membrane of Prussak’s space (be-
tween vertical arrows) showing its typical
oval form, the horizontal diameter being lon-
ger than the vertical. The anterior malleal
ligamental fold (A), housing the chorda tym-
pani 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 ten-
don.
Fig. 79. Series S, adult case 4, left ear, anteri-
or approach. An oblique view more medially
makes a large part of a shallow supratubal
recess visible. The central portion of the ten-
sor 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 ante-
rior membrane of Prussak’s space. M = Mal-
leus handle; TM = tympanic membrane; A =
anterior malleal ligamental fold; C = chorda
tympani nerve.

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 supra-
tubal recess (fig. 77). The anterior membrane of Prussak’s
space, its anterior wall, appears as a truly delicate dupli-
cate 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 cross-
ing thicker strands. The fold margins generally appeared
thicker and could contain whitish strands resembling
fibers seen in the thin portions of the lateral malleal liga-
mental 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 path-
way 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,

46 Color Atlas of the Anatomy and Pathology of the Epitympanum

Fig. 80. Series S, adult case 10, right ear,
anterior approach. Direct view medially into
a broad and high supratubal recess, the ante-
rior membrane of Prussak’s space is no lon-
ger 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 por-
tion of the tympanic isthmus, posterior to
the tensor tendon (T). CP = Cochleariform
process.
Fig. 81. Series A, adult case 14, left ear, ante-
rior approach. Total absence of both the ten-
sor 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.
Fig. 82. Same ear as in figure 81, superior
approach. Neither the tensor tendon nor the
tensor fold is present and the anterior epi-
tympanum communicates directly with the
supratubal recess (R). The lateral incudo-
malleal fold (horizontal arrow) and the later-
al 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.

steadily descends with a convex slope to join the tubal teg-

men. 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 exten-
sive pneumatization, air cells also extended to the supra-
tubal 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
Fig. 83. Series A, adult case 13, right ear,
the dome of the space, varied between 1 and 5 mm. The
anterior approach. A membrane defect (be-
dome as a rule extended only to a slightly higher level than tween horizontal arrows) appears in the up-
the tensor fold insertion ring, with the exception of 2 ears per portion of the tensor fold. The oblique
with the fold insertion into a long transverse crest when arrow points to the more posterior trans-
the upward extension was 2–2.5 mm. The width from the verse crest. The curved arrow points to the
anterior portion of the tympanic isthmus,
tensor tendon to the eustachian tube tegmen varied from
the regular pathway of aeration of the epi-
1.5 to 4 mm. At the midpoint the tensor fold width mea- tympanum. T = Tensor tendon.
sured around 2.5–3 mm. The length of the tensor tendon

1 Anatomy and Pathology of the Epitympanum 47

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 lamel-
la (B) of the muscle canal. M = Malleus; ET = eustachian tube; E =
external ear canal. Masson’s trichrome stain. Magnification !12.
measured from the malleus handle to the medial leg of the
transverse crest varied between 2.5 and 3.5 mm.
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 sec-
tions. 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 mem-
brane, 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 orif-
ice mediosuperiorly reveals the entire normal gross ap-
pearance of the supratubal recess.
48 Color Atlas of the Anatomy and Pathology of the Epitympanum
Fig. 85. Series A, adult case 21, left ear, ante-
rior approach. The view of the mesotympan-
um 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 = tym-
panic membrane.
Pathology as Seen in Microdissection
The anterior approach also allows a good view of the
pathological changes in the anterior portion of the tym-
panic 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 ten-
don, 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 tis-
sue insertion ring, the head of the malleus and epitympan-
um. Pathological changes in different compartments be-
come obvious and can be studied in detail.
Pathological changes in the supratubal recess itself
were clearly less frequent than those seen in the epitym-
panum. 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
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 inflam-
matory fold (horizontal arrow) blocks com-
pletely the anterior portion of the tympanic
isthmus between the incudostapedial articu-
lation (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 to-
wards the posterior portion of the tympanic
isthmus. I = Long process of the incus; S =
stapes; PP = pyramidal process.
Fig. 88. Series A, adult case 15, left ear, ante-
rior approach. The entire tegmental roof is
removed. A thick inflammatory web (hori-
zontal 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) or covering the entire membrane by dense scar

tissue (fig. 90). The membrane could be indrawn into obli-
terative 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 forma-
tion 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 tis-
sue webs at times appeared at the level of the tubal tegmen
(fig. 91), resembling the inflammatory web in Sieben-
mann’s drawing [1] (fig. 5). Thick soft granulomatous tis-
sue or extensive, more mature tissue webs could fill the
entire space (fig. 92). In the early stages they could easily Fig. 89. Series A, adult case 21, left ear, ante-
rior approach. Mature, thin postinflammato-
be peeled off from the surface of the tensor fold, in later
ry webs (oblique arrow) crossing the thick-
stages of organization this process was very tedious. At the ened anterior face of the anterior membrane
end, however, the thin intact tensor fold could generally be of Prussak’s space (vertical arrow) M = Mal-
dissected free, testifying to the spread not through the leus handle; TM = tympanic membrane; A =
membrane but around the tensor tendon (fig. 93). Biop- anterior malleal ligamental fold.
sies 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 eus-
tachian tube remained singularly unaffected.

1 Anatomy and Pathology of the Epitympanum 49

Fig. 90. Series A, adult case 11, lef ear, ante-
rior approach. An oblique view shows a
thick, mature scar tissue (horizontal arrow),
which obscures the entire anterior mem-
brane of Prussak’s space. M = Handle of the
malleus; I = long process of the incus.
Fig. 91. Series A, adult case 12, right ear,
anterior approach. The malleus handle (M),
the tympanic membrane (TM) and the en-
trance to the eustachian tube (vertical arrow)
are normal. The supratubal recess contains a
mass of fibrotic scar tissue (between horizon-
tal 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 ten-
don (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. 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 fi-
brotic 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 epitym-
panum (curved arrow). M = Head of the mal-
leus; TC = transverse crest.
Fig. 94. Case A89-13, right ear of a neonate, Temporal Bone Founda-
tion. 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 mal-
leal ligamental fold. In more inferior sections the two spaces merged.
Hematoxylin-eosin stain. Magnification !12.

50 Color Atlas of the Anatomy and Pathology of the Epitympanum

Fig. 95. Case A89-295, right ear of an infant aged 15 months, Tempo-
ral 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 por-
tal (vertical arrow). The highest point of the anterior pouch (horizon-
tal 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 secre-
tion 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.
1 Anatomy and Pathology of the Epitympanum
Fig. 96. Case A92-168, right ear of an infant aged 8 months, Tempo-
ral Bone Foundation. The anterior attic (AA) is filled with thick cellu-
lar 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 show-
ing large, mature granulation tissue masses in the supratu-
bal 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 mem-
brane defect in the tensor fold, secretion was seen to pass
from the anterior attic through the defect into the supratu-
bal recess, from where the drainage continued to the eus-
tachian tube (fig. 96, 97).
This pathology is more extensively discussed in Part 2
of this atlas, dealing specifically with AFCC and chronic
inflammation.
51
 References
1 Siebenmann F: Mittelohr and Labyrinth; in
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5, Abt. 2, pp 244–287.
2 von Tröltsch A: Lehrbuch der Ohrenheilkunde
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3 Prussak A: Zur Anatomie des menschlichen
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4 Helmholtz H: Die Mechanik der Gehörknö-
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5 Hammar JA: Studien über die Entwicklung des
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gane. 1. Allgemeine Morphologie der Schlund-
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telohrraumes und des äusseren Gehörganges.
Arch Mikrosk Anat 1902;59:471–628.
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7 Wittmaack K: Die entzündlichen Erkran-
kungsprozesse des Gehörorgans; in Henke F,
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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 Sur-
gery. Stuttgart, Thieme, 1995.
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13 Proctor B: The development of the middle ear
spaces and their surgical significance. J Laryn-
gol Otol 1964;78:631–648.
14 Proctor B: Surgical Anatomy of Ear and Tem-
poral 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 epitym-
panic 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
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21 Palva T, Ramsay H: Mucosal pathology of the
attic; in Tos M, Thomsen J, Balle V (eds): Otitis
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22 Aimi K: The clinical significance of epitym-
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23 Aimi K: The tympanic isthmus: Its anatomy
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88:1067–1081.
24 Palva T, Ramsay H: Chronic inflammatory ear
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25 Palva T: Surgical treatment of adhesive tym-
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26 Palva T, Ramsay H: Myringoplasty and tympa-
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27 Northrop C, Piza J, Eavey R: Histological ob-
servations 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 Oto-
rhinolaryngol 2001;57:55–65.
30 Chatellier HP, Lemoine J: Le diaphragme in-
terattico-tympanique du nouveau-né. Ann
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534–566.
31 Palva T, Northrop C, Ramsay H: Spread of
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nate middle ear. Int J Pediatr Otorhinolaryngol
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32 Palva T, Northrop C, Ramsay H: Effect of
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33 Palva T, Johnsson L-G, Ramsay H: Attic aera-
tion 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–
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38 Tono T, Schachern P, Morizono T, et al: Devel-
opmental anatomy of the supratubal recess in
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39 Palva T, Northrop C, Ramsay H: Supratubal
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Part 2
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Pathology Related to Amniotic Fluid

Cellular Content and Superimposed
Infection

53
 Part 2
OOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOO
Pathology Related to Amniotic Fluid
Cellular Content and Superimposed
Infection
Introduction and Short Review of the Literature
on Amniotic Fluid Cellular Content
Towards the end of the 19th century the scientific liter-
ature contained numerous publications on the ‘otitis me-
dia 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 sapro-
phytic 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 de-
cided to concentrate on studying the cellular composition
of the middle ear secretion by microscopy and on evaluat-
ing 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 essen-
tial 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 secre-
tion 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 inflam-
matory 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 neonato-
rum’ thus was a typical reaction against this foreign mate-
rial.
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, increas-
ing 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
55
and it was universally accepted that the filling of the neo-
natal 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 com-
partments. 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 organiza-
tion. The open space lost to granulation tissue could be
partly regained by its maturation and subsequent shrink-
age.
However, Wittmaack observed that there was a varia-
tion 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 oth-
er. If the child suffered, for example, from periods of vom-
iting, 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 viru-
lent 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 investi-
gators. 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 nor-
mal 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
56 Color Atlas of the Anatomy and Pathology of the Epitympanum
Aschoff [1], namely that the results do not correlate with
the findings of pathology. Nevertheless, even if she specu-
lated that the pathological process could be due to a for-
eign 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 investiga-
tions.
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 pulmo-
nary airways.
While the second group with AFCC in the middle ears
conforms well with the findings of Aschoff [1] and Witt-
maack [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 Pseudo-
monas. They thus can be set apart from the group of pure
infant otitis media but represent ears of generalized infec-
tion 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 re-
mainder a wide range of changes were observed, from
glandular metaplasia, retained squamous debris, squa-
mous 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 chil-
dren aged from 10 min to 70 days, 39 of 43 bones of neo-
nates 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 ob-
served, the most involved types showing large, complete-
ly epithelialized masses of granulation tissue still contain-
ing 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 inflamma-
tory 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 devel-
opment of cholesteatoma from the inoculated squamous
cells.
The importance of the amount of AFCC contamina-
tion was further evaluated by comparing the temporal
bones of 9 patients born through meconium-contami-
nated 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 eval-
uated. 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 inflamma-
tory foreign body reaction.
Of this same group, Eavey [11] published a compre-
hensive report of the abnormalities in a neonate ear. Oto-
scopic observations in 44 neonates of 1–24 days of age
showed that nearly all (97.7%) of the tympanic mem-
branes 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 tem-
poral 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 confir-
mation of the presence of AFCC in the middle ears. Final-
ly, 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 for-
mation and mucosal thickening which increased in 14
days and showed also some osteogenesis. These altera-
tions increased further in severity and cholesterol granu-
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
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 pos-
sibly 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 pres-
ence 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 exten-
sive treatise, we will nevertheless review the relevant liter-
ature at this stage because AFCC has been shown to play
an important role in arrested pneumatization [2, 3]. Nu-
merous 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 ob-
served 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
57
by Eckert-Möbius [13] who gave a short version of Witt-
maack’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 me-
senchyme. The basic process involved invasion of the vas-
cular 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 contin-
ued until the age of 3 years. Towards the end of the first
year the histological picture started to show a major con-
tinuous change in the form of a more rapid bone resorp-
tion 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 tis-
sue 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 sur-
rounding the tubal orifice. At the end of the second period
the mastoid bone showed a mixed picture of pneumatiza-
tion 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
58 Color Atlas of the Anatomy and Pathology of the Epitympanum
concerned, these changes did not essentially change the
picture seen at the end of the fifth year of life.
Pathological pneumatization was divided by Witt-
maack [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 gen-
erally 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 fas-
tened 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 con-
nective 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 associ-
ated 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 in-
vagination 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 secre-
tion which together with the granulation tissue was partic-
ularly 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 develop-
ment 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 nor-
mal by their irregular form and by the thicker than normal
bony septa. Some of the air cells were filled with connec-
tive 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 sub-
epithelial 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 mate-
rial. Further growth of bone and its preformation contin-
ues guided by hereditary factors, leading to the develop-
ment of bone spaces filled with connective tissue. Simul-
taneously with this process the mesenchyme becomes
thinner, and at the end of 1 year all bone surfaces are nor-
mally 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
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
process occurs when there is a physiological equality of
pressure between the enlarging lumen and the living tis-
sues. Neonate otitis media with underpressure and associ-
ated 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 his-
tology 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 in-
fluence during the first 3 years of life. This notion was chal-
lenged in 1940 especially by Diamant [16] and later ampli-
fied 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 environ-
mental 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 admit-
ted 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 plani-
meter from an X-ray film taken in a modified lateral pro-
jection. The data showed that in the studied groups the
areal figures became progressively smaller with increasing
severity of middle ear disease. After a statistical assess-
ment 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 environmen-
tal factors were was not clarified, even if the presence of
amniotic fluid in the ear during the fetal period was con-
sidered 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 ar-
rested pneumatization with chronic otitis media.
59
 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 consti-
tution’ is not pathognomonic to otitis media in infancy
alone but may occur at any age under the same condi-
tions, 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 pneumatiza-
tion. He did not accept the conclusions drawn by the
Swedish investigators [16–18] and took pains to reexam-
ine 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 conclu-
sion, 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 mar-
red by the speculation on the dominant role of the mucous
membrane, the hyperplastic mucosa arising from the pre-
natal foreign body inflammation and the hypoplastic mu-
cosa resulting from fibrosis following exudative postnatal
infections. Tumarkin felt that this complicated histologi-
cal 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 inade-
quate and thought that the aseptic type of inflammation
was due to the middle ear process in children we now call
secretory otitis media.
60 Color Atlas of the Anatomy and Pathology of the Epitympanum
Tumarkin’s own data derived from planimetric mea-
surements similar to those used by Diamant [16] of the
size of the mastoid pneumatization in groups of working-
class children from Liverpool slums with frequent infec-
tions in contrast to middle-class children with much bet-
ter living standards, with a smaller number of infections
and better access to medical care. The results were clear-
cut, the working-class group showing poorer pneumatiza-
tion 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 hypocellu-
lar mastoids, affected by persistent chronic inflammation,
gradually sclerosed and became ultimately acellular.
These results are the same as the histological ones present-
ed by Wittmaack [2, 3] with the difference that Witt-
maack stressed the type of mucous membrane determin-
ing 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 pneu-
matization. Because of these differences to Wittmaack’s
thesis Tumarkin considered himself a neo-Wittmaack-
ian.
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 deposi-
tion of bone leading to a reconstruction of the normal pat-
tern, 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 pneumati-
zation 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 fora-
men pneumaticum which can be blocked either tempo-
rarily 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 pneu-
matization of the humerus. After occlusion of the fora-
men 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 foa-
my and laden with fat. The subepithelial tissue initially
showed marked congestion of blood vessels, followed by
tissue edema with protein-rich fluid collection. Mesen-
chymal proliferation formed polyps accompanied by an
outgrowth of blood vessels. After 6–8 weeks the mesen-
chymal cells showed intracellular deposits of lipoid mate-
rial, 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 epi-
thelium 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 fol-
lows long-standing middle ear infections [2, 3, 19–25],
even if Wittmaack’s original idea of the mucous mem-
brane dependence as such is outdated. A lack of aeration
alone, without infection, can convert an already pneuma-
tized system into an obliterated state with new bone for-
mation and sclerosis [26, 27]. It can be said that the gener-
al process of arrested pneumatization is well known, but
detailed data of the normal speed and extent of undis-
turbed 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 num-
bers of serially sectioned temporal bones from neonates
and young children.
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
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 pulmo-
nary 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 consid-
erably 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 epi-
tympanic bony roof showed a common air space extend-
ing 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 tym-
panum 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
61
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 mod-
erate 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 pre-
formed 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. 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.
62 Color Atlas of the Anatomy and Pathology of the Epitympanum
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).
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 nor-
mally. 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. 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.
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
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 = chor-
da tympani nerve. Magnification !25.
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 supratu-
bal 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.
63
Fig. 105. Case 2 (A89-13), section 361, right ear. Prussak’s space (P)
contains a small amount of AFCC, the anterior membrane (horizon-
tal arrow) is thin, some AFCC is present in the anterior pouch (obli-
que 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. Mag-
nification !25.
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 mesotympan-
um (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. Magnifica-
tion !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 con-
tained only small amounts of amniotic fluid with occa-
64 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 ante-
rior 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 later-
al 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).
Medial Attic and Tympanic Isthmus
In case 1 the amniotic fluid filling the space contained
a few AFCC clusters which adhered to the epithelial sur-
faces. In case 2 both ears contained massive amounts of
floating AFCC clusters (fig. 108–110), contacting espe-
cially 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 (hori-
zontal arrow) appears in the medial attic. AFCC-containing fluid also
appears in the mastoid antrum (MA), lower lateral attic (LL), anteri-
or attic (AA) and in the supratubal recess (R). The tensor fold (obli-
que arrow) is thin. E = Ear canal; I = incus; M = malleus. Magnifica-
tion !8.
Fig. 110. Case 2, left ear, section 371. A magnified view of the con-
tinuing 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 multinu-
cleated cells. Magnification !200.
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 form-
ing 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
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
Fig. 109. Case 2, section 336, left ear. A polypoid remnant of the
vertical medial ossicular fold contains many capillaries and is infil-
trated 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. 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 (obli-
que arrow) contains scant fluid. E = Ear canal; F = facial nerve; M =
malleus. Magnification !12.
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 devel-
opment of portals for organization.
65
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.
Eustachian Tube
In all temporal bones the lateral portion of the protym-
panum and the bony eustachian tube contained moderate
numbers of amniotic cells and fluid, not attaching to the
walls.
Mastoid Pneumatization
The mastoid antrum was well formed in all 8 speci-
mens, 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 occa-
sional short trabeculae projecting to the antral lumen and
was lined by mucosa which contained some embryologi-
cal mesenchyme. The squamous bone, the smaller antero-
lateral 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 em-
bryonal mesenchyme, generally rich in capillaries, be-
tween them (fig. 98). The marrow spaces close to the per-
iosteum contained no hemopoietic tissue, only connective
tissue and a few capillaries. The bone preformation con-
tinued from the attic roof until the fossa incudis. In sever-
al specimens there was a marked lateral formation of air
cells with spaces lined by epithelium, the subepithelial tis-
sue still containing thick mesenchyme. Many such air
66 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 (horizon-
tal arrow). Magnification !200.
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 mar-
row bone.
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 anteri-
or 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 supra-
tubal 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 incudosta-
pedial 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 definite-
ly propels much of the freely floating meso- and hypotym-
panic 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, supra-
tubal recess, Prussak’s space, hypotympanum and the
mastoid would later result in local soft tissue thickening
and postinflammatory folds, but would not create func-
tional 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 granula-
tion tissue and lead to a partial or even a full block of the
tympanic isthmus. Organization of cell clusters in the pos-
terior 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 com-
parable 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 dehy-
dration [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 tis-
sue. In the left ear the findings were close to those seen on
the right side.
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
Fig. 114. Case 1 (A86-055), right ear, section 170, general view. A
granulation tissue mass with pseudocysts in the mastoid antrum (ver-
tical 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 squa-
mous bone has some air cells still containing mesenchyme (horizon-
tal 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 con-
tained an epithelialized granulation tissue sheet measur-
ing 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 mal-
leal space and both lateral attics. The mucosa was edema-
tous 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 con-
tinued 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.
67
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 con-
tact 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 epithe-
lium-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. 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.
68 Color Atlas of the Anatomy and Pathology of the Epitympanum
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. 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 secre-
tion with round cells. M = Malleus; I = incus. Magnification !12.
Fig. 119. Case 3 (A88-022), left ear, section 230. Thick mucus, con-
taining 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.
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 con-
tracting 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
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
Fig. 120. Case 3, right ear, section 181. The tensor fold (horizontal
arrow) is edematous and the dome of the supratubal recess (R) con-
tains mucoid secretion with a few cells. Prussak’s space (P) is partial-
ly obliterated by organizing secretion. The lower lateral attic (LL)
shows secretion containing round cells and a cross section of a granu-
lation 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. Magnifica-
tion !12.
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 lat-
ter 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).
69
Fig. 121. Case 2, right ear, section 166. Prussak’s space has been
passed and a superior portion of the posterior pouch appears (hori-
zontal 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.
Fig. 122. Case 3, right ear, section 130. Secretion containing a moder-
ate 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.

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 low-
er lateral attic, partially filled with a meshwork of granula-
tion 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 Prus-
sak’s space drained through a large pathway to the mucus-
filled 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 acel-
lular secretion. Posterior to the neck of the malleus there Fig. 123. Case 1, right ear, section 250. Prussak’s space (P) opens
directly to the lower lateral attic (LL) which contains both secretion
was a normal-sized aeration pathway via the posterior
with round cells and epithelialized granulation tissue (oblique ar-
pouch which contained mucoid secretion with round cells rows). The anterior pouch (AP) and the supratubal recess (R) are free
and giant cells (fig. 126). of pathology, the lowest portion of the anterior malleal ligamental
Case 3. In the left ear Prussak’s space was shallow, only fold (vertical arrow) still separates the two spaces. The posterior
0.3 mm in height. The posterior pouch contained thick pouch, the dome of which appears (curved arrow), is separate from
and inferior to Prussak’s space. Its walls are covered by thick mucus
secretion with round cells and also polyp formations
with a moderate number of round cells; further inferiorly it was free
(fig. 127). The pouch opened to the upper lateral meso- of pathology for its whole length of 1.4 mm. The horizontal arrow
tympanum where mucus and a thick polypous mucosa points to the anterior membrane of Prussak’s space. M = Malleus; I =
surrounded the chorda tympani nerve and the incus long long process of incus; C = chorda tympani nerve. Magnification
process. In the right ear the lumen of the 1-mm-high !12.

70 Color Atlas of the Anatomy and Pathology of the Epitympanum

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 ten-
don (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. 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 liga-
ment appears. S = Posterior tympanic spine; M = malleus. Magnifica-
tion !12.
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
Fig. 125. Same ear as in figure 124, section 259. The separate posteri-
or 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 con-
tains both epithelialized granulation tissue (oblique arrow) and thick
mucoid secretion. M = Malleus; S = posterior tympanic spine. Magni-
fication !40.
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. Magnifi-
cation !12.
71
Fig. 128. Case 3, right ear, section 211. Aeration pathway to Prus-
sak’s space posterior to the neck of the malleus (M) shows round cell
infiltrated mucus and a granulation tissue polyp (curved arrow). Sim-
ilar polyp formation and secretion appears in the lower lateral attic
(oblique arrow). The tensor fold adjoining the tendon (T) is edema-
tous and infiltrated by round cells, similarly to the mucosa surround-
ing the malleus. The anterior mesotympanum shows cell free secre-
tion (vertical arrow). I = Incus; C = chorda tympani nerve; S = poste-
rior tympanic spine. Magnification !25.
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 foot-
plate (S). Magnification !40.
72 Color Atlas of the Anatomy and Pathology of the Epitympanum
Fig. 129. Case 3, right ear, section 270. The end portion of the poste-
rior 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 organ-
izing 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).
Tympanic Isthmus and Posterior Tympanum
Case 1. In the right ear the tympanic isthmus was prac-
tically 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 to-
wards 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 orga-
nized 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 orga-
nized 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 infil-
tration. Several tissue bridges appear and organization of the remain-
ing secretion is in progress. A large polypoid granulation tissue sheet
(vertical arrow) extends towards the facial recess. Magnification
!25.
was free. The stapes was surrounded by heavily infiltrated
thick, polypous mucosa. In the right ear the whole posteri-
or tympanum and facial recess presented polypous muco-
sa 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).
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 mem-
brane 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 win-
dow 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.
Eustachian Tube
In case 1 both eustachian tubes had normal mucosa
and practically no secretion. In case 2 the eustachian tube
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
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 hypo-
tympanum is edematous and polypous (oblique arrow), contains
pseudocysts and shows marked round cell infiltration. Magnification
!40.
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 eusta-
chian tube.
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 granula-
tion tissue, exceptionally also in the free space, in all com-
partments 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.
Mastoid Pneumatization
The petrous bone in 4 specimens showed similar char-
acteristics 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
73
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 infil-
tration by round cells of varying sizes and numerous pseudocysts
(vertical arrows) 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 perios-
teum contained marrow bone without hemopoietic tissue.
Towards the antral cavity there was the preformed trabe-
cular arrangement and distinct air cells had formed be-
tween the bone ridges medially, lined with a thick, mesen-
chyme-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.
Comment
The hospital records of these 3 children contained nei-
ther 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 infil-
trates 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 ascer-
tained 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
74 Color Atlas of the Anatomy and Pathology of the Epitympanum
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. Verti-
cal arrow points to numerous pseudocysts in the granulation tissue.
Magnification !200.
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 begin-
ning 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 asso-
ciated factors which could have contributed to an inflam-
matory 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 associ-
ated 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
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 path-
ways. This in time will lead to epithelial damage and
mucus organization which may cause partial or total obli-
teration of Prussak’s space and its aeration pathways. Fur-
ther changes will be the indrawing of Shrapnell’s mem-
brane 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 tympanosto-
my 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 mas-
toid disease may remain as a source for repeated recur-
rences and necessitates more energetic methods of active
treatment [31]. There is a great need for studies of tempo-
ral bones of older infants and young children for evalua-
tion 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 con-
traction may cause permanent indrawing of the posterior
portion of the pars tensa. This in turn causes further nar-
rowing of the already affected tympanic isthmus and leads
to an irreversible attic aeration defect. Posterior retrac-
tion is a serious sign suggesting a need to create additional
aeration pathways for safeguarding the attic ventilation.
The process of organization destroys foreign sub-
stances 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-
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
mation of granulation tissue in the present ears had anni-
hilated 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 mid-
dle 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 des-
quamative 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 syn-
drome who after 3 months of age had respiratory symp-
toms, 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 extu-
bation failed and at the age of 4 months a tracheotomy
was performed but she continued to need assisted ventila-
tion. The principal cause of death was bronchopneumo-
nia and cultures of the lung tissues grew Haemophilus
influenzae.
Case 4 was 15 months of age and had congenital agene-
sia 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 admis-
sion to hospital. The blood cultures grew E. coli and coa-
gulase-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 postopera-
tively had a cardiac arrest, was resuscitated but died 14
days later with signs of ischemia, hepatic necrosis and
75
Fig. 135. Case 1 (A80-126), right ear, section level 00K. Superior epi-
tympanum contains a 6-mm-long epithelialized granulation tissue
mass (vertical arrow) with wide bridges (horizontal arrow) to the lat-
eral 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. Organiza-
tion portals to secretion appear (oblique arrow). M = Malleus;
I = incus; A = antrum; U = upper lateral attic. Magnification !9.
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.
Case 1
Right Temporal Bone
The superior epitympanum contained epithelium-cov-
ered 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 compart-
ments. 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 mem-
brane defect. The upper portion of the supratubal recess
76 Color Atlas of the Anatomy and Pathology of the Epitympanum
Fig. 136. Case 1, right ear, section level 161. Tensor fold defect (verti-
cal arrow) allows secretion to pass from the anterior epitympanum
(A) to the supratubal recess (R). Prussak’s space (P) contains secre-
tion 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 granula-
tion 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.
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 pos-
terior 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 ap-
peared in the superior attic as an epithelialized block of
granulation tissue, and as thinner strands in the tympanic
isthmus and in the posterior tympanum.
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 inva-
sion 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 pass-
ing 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 ante-
rior 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 nonpneu-
matized red bone marrow. The vertical arrow points to the dome of
Prussak’s space. M = Malleus; I = incus. Magnification !6.
Fig. 138. Case 1, left ear, section level 221. An organization process of
longer standing around the stapes. Pseudocystic epithelialized fibrot-
ic 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.

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 organiza-
tion portals to cell-rich secretion indicated recent changes.
Long-standing changes appeared around the stapes as epi-
thelialized granulation tissue with pseudocysts. 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
Case 2 many bridges to the attic mucosa. Its edges are more pseudocystic,
Right Temporal Bone the central portion more fibrotic. The cortex of the squamous bone is
The superior epitympanum was filled with an epithe- thin and the preformed air cells are filled with secretion (vertical
lialized granulation tissue mass connected with numerous arrow) or connective tissue (horizontal arrow). The antral mucosa
has direct contact with the bone marrow of the petrous bone (open
tissue bridges to the inflamed attic mucosa (fig. 139). At
arrow), with some bone resorption. The anterior attic (A) contains
the superior level of the short process of the incus the mass fluid with dispersed round cells and one cluster. Many organization
still occupied half of the medial attic but more inferiorly it portals (oblique arrow) indicate ongoing organization. I = Incus.
became thinner and filled only portions of the posterior Magnification !4.

2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection 77


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. Pseudo-
cystic 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 trabecu-
lae show marked resorption. M = Malleus. Magnification !4.
portion of the isthmus (fig. 140). The antral mass per-
sisted 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 granula-
tion tissue with numerous bridges to mucosa. The promon-
tory 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 ab-
sent, and only a deformed stapes was present. The foot-
plate 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 ar-
row) has normal mucosa towards the anteri-
or pouch (AP) while the surface towards
Prussak’s space is edematous. New portals of
organization are developing from the edem-
atous mucosa (vertical arrows). M = Malleus.
The blind superior end of the posterior
pouch appeared 1 mm inferior to this level.
Magnification !36.

78 Color Atlas of the Anatomy and Pathology of the Epitympanum

Fig. 142. Case 2, left ear with Goldenhar’s syndrome, general view. Fig. 143. Case 2, left ear, section 386. A clus-
The middle ear forms one common space from the eustachian tube ter of squamous epithelial cells and round
(E) to the mastoid antrum (A), part of which is filled with fetal mesen- cells in the round window niche posterior to
chyme. The ossicles are missing. All spaces are filled partly with the membrane. Organization portals have
mucoid secretion (vertical arrow), partly with dense clusters of round not yet formed. Solitary squamous cells sur-
cells (horizontal arrow). The mucosa is polypous, infiltrated by round rounded by macrophages show signs of dis-
cells which at some places form distinct follicles. Squamous cells integration. Magnification !90.
appear solitary and in small clusters in the secretion. Magnification
!5.

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 cavi-
ty 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 tis-
sue and as free clusters.
Fig. 144. Case 3 (A92-168), right ear, section level 123, general view.
Desiccated mucoid secretion in an early phase of organization with
Case 3
degenerate cells, macrophages, a few multinucleated cells and granu-
Right Temporal Bone lation tissue polyps (vertical arrow) fills all spaces from the anterior
A thick desiccated mucinous secretion undergoing or- attic (A) via the tympanic isthmus (T) to the mastoid antrum (MA).
ganization filled the superior attic and the antrum Mucosa in the isthmus shows moderate round cell infiltration. The
(fig. 144). It contained areas with degenerated cells, mac- petromastoid bone contains red bone marrow with a dense layer of
sclerotic bone parallel to the mucosa, making only minute contacts
rophages, multinucleated cells and polymorphonuclear
(oblique arrow) between the two possible. The cortex of the squa-
leukocytes and relatively few fibrocytes. Inside the muci- mous bone is thin, many trabeculae are resorbed, and much of the
nous mass there were nonepithelialized cross sections of loose mesenchyme is retained. M = Malleus; I = incus. Magnification
granulation tissue and short stretches of epithelium ap- !4.
peared on the surface. The mass in the attic continued

2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection 79

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) con-
tains organizing secretion and granulation tissue. Medially the dense
plate of bone still separates the antral mucosa from the red bone mar-
row, 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 = exter-
nal 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 degen-
erating cells. The vertical arrow points to a cross section of a granula-
tion tissue polyp. M = Malleus. Magnification !25.
80 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 granula-
tion tissue and is walled by a similar type of bone as shown in figure
145. M = Malleus; S = stapes footplate; F = facial nerve. Magnifica-
tion !4.
through the tympanic isthmus (fig. 145) as far as the hypo-
tympanum (fig. 146). The subepithelial tissue showed a
moderate round cell infiltration, some areas had em-
bryonic 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 eusta-
chian 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 mesotympan-
um (fig. 147). Remaining embryonic tissue together with
mucosal pseudocysts resulted in a thick mucosa and a nar-
row lower lateral attic. The anterior portion of the tym-
panic 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 hemo-
poietic bone marrow, is walled off from the antrum (A) by a dense
bone lamella with minute contacts (oblique arrow) to the mesen-
chyme. The preformed squamous bone shows prominent trabeculae,
their interspaces are still filled with embryonal mesenchyme. M =
Malleus. Magnification !5.
In summary, changes due to ongoing infection in-
cluded degenerating cells and all classes of inflammatory
cells in desiccated secretion undergoing organization,
with immature granulation tissue and a polypous, in-
flamed mucosa. Long-standing changes appeared as a
pseudocystic network of epithelialized granulation tissue
in the tympanic isthmus and in the 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 con-
tained 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 con-
tained partly embryonic tissue and partly old inflammato-
ry pseudocysts, causing a thickening of the whole mucosal
layer. The upper and lower lateral attics were connected
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
Fig. 149. Case 3, left ear, section 196. The intact tensor fold (horizon-
tal 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 squa-
mous bone shows insignificant air cell preformation. M = Malleus;
I = incus. Magnification !4.
with a narrow passage showing polypoid changes. The
tympanic isthmus was full of a network of epithelium-
covered pseudocystic granulation tissue (fig. 149).
The intact tensor fold separated the supratubal recess
from the anterior attic and showed sections of inflamma-
tory 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 cell-
rich secretion in the attic and in the tympanic sinus and
round window niche. Extensive long-standing changes
appeared as pseudocystic, epithelium-covered granula-
tion tissue network which filled the superior and lateral
attics, mastoid antrum, tympanic isthmus and posterior
tympanum.
81
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 granula-
tion 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 polymor-
phonuclear 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 dis-
tinct 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 secre-
tion 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 compart-
ments 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 postinflamma-
tory 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
82 Color Atlas of the Anatomy and Pathology of the Epitympanum
Fig. 151. Case 4 (A89-295), right ear, section 191, general view.
Secretion containing clusters of round cells and signs of early organi-
zation 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 posteri-
or portion of the petromastoid bone is pneumatized while the medial
portion still contains red bone marrow. Some air cells contain secre-
tion and thick mucosa. M = Malleus; I = incus; E = ear canal. Magni-
fication !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 macro-
phages. Prussak’s space was empty, scant secretion ap-
peared in the oval window niche, in the sinus tympani
and in the round window niche. Also on this side the mas-
toid 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 tym-
panum 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 secre-
tion 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 secre-
tion in a meshwork of inflamed inflammato-
ry webs (a magnified view is shown in fig.
73). In the mastoid antrum (MA) many epi-
thelialized thin postinflammatory connec-
tive tissue strands appear, one (vertical ar-
row) starting from the anterior portion of the
tympanic isthmus (T). The lower lateral attic
(L) contains scant secretion and small epi-
thelial mucosal polyps in the incudal (I) mu-
cosa. 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 secre-
tion fills the supratubal recess (R), the tym-
panic isthmus (T) and a large part of the
antrum (A). There is a good pneumatization
around the antrum. The squamous bone lat-
erally shows only the dense cortex (vertical
arrow) and also much of the petromastoid
bone is pneumatized, the remaining hemo-
poietic bone marrow being thin (oblique ar-
row). M = Malleus, I = incus. Magnification
!4.

Fig. 154. Case 5, right ear, section 381. Epi-

thelialized fibrotic tissue strands (oblique ar-
rows) with a few pseudocysts and bridges to
the mucosa appear in the round window
niche. Fresh changes appear as new organi-
zation portals (vertical arrow) into the round
cells in the secretion. One portal starts from
the locally thickened round window mem-
brane (horizontal arrow). Magnification
!25.

2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection 83


Fig. 155. Case 5, left ear, section 162, general view. Secretion con-
taining 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 similar-
ly 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 tym-
pani was full of round cells and mucus. The round win-
dow niche showed the ongoing organization process of the
mucoid secretion. The mastoid process was well pneuma-
tized 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 phago-
cytes. Magnification !12 (a), !250 (b).

84 Color Atlas of the Anatomy and Pathology of the Epitympanum

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 exten-
sive 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 squa- Fig. 157. Case 3, right ear, section 123. A magnified view of a granu-
lation tissue polyp marked with a vertical arrow in the mastoid
mous bone in cases 2 and 3 showed distinct pneumatiza-
antrum in figure 144. A disintegrating squamous epithelial cell (verti-
tion with filling of the air cells with secretion or connec- cal arrow) is surrounded by macrophages and giant phagocytes. The
tive tissue, resulting in a slight lateral enlargement of the cell remnant is so thin that the round cells shimmer through it. Mag-
antrum (fig. 139, 140, 144, 145). On the other hand, in nification !250.
cases 4 and 5 with minor signs of old or recent inflamma-
tion, pneumatization was much more advanced. In case 4,
15 months of age, the entire squamous bone and the later-

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).

2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection 85

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 cell-
free secretion filled practically all compartments. In addi-
tion 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 disap-
pear. 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 histolog-
ical 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 mid-
dle 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 histological-
ly 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 histologi-
cally, 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
86 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 gravi-
ty becomes then ineffective, aided by many horizontally
placed attic structures, and the cell clusters no longer
descend to the hypotympanum and eustachian tube orif-
ice. 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, multi-
nucleated cells and giant cells, at times with polymorpho-
nuclear leukocytes, indicates a relatively recent and an
ongoing process. In many compartments there were only a
few organization portals, as the mucosal damage was min-
imized by the intensive use of antibiotics during the ter-
minal 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 substan-
tial 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 con-
taining, 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 be-
coming the dominating cells. This process starts peripher-
ally 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 proba-
bly 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 possi-
ble (fig. 116). When a thick, desiccated secretion filled all
compartments including the supratubal recess, the trans-
port via any of the drainage pathways seemed unsuccess-
ful (fig. 144–146).
Collection of AFCC in the posterior pouch and the low-
er 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 orga-
nization 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 old-
er 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 muco-
sa enveloping the stapes (fig. 129, 131) to marked obliter-
ating 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).
2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection
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 granula-
tion 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 irri-
tants, reaches its end stage during a period of this length.
Wittmaack [2, 3], Döderlein [33] and Ojala [34] alrea-
dy presented comprehensive histological analyses of ears
as discussed above. These processes apply to cases devel-
oping initially from AFCC contamination as well as to
those following recurrent bacterial infections filling the
middle ear compartments with fibrin and cellular secre-
tion. 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 speci-
mens in the Temporal Bone Foundation. The data pre-
sented 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 pos-
teromedial 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
87
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 trabecu-
lae projected from it to the antral cavity and the superior
epitympanum, their interspaces still containing embryo-
nal 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 neona-
tal state. Because of inflammation, pneumatization of
these preformed spaces continued slowly, and some of the
developed air cells contained mucoid secretion with in-
flammatory cells. In others the medial trabeculae showed
absorption and remodelling, the embryonal mesenchyme
regressed and the epithelium advanced to the cells. Later-
al 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 gen-
erally unchanged but exceptionally showed a beginning
pneumatization (fig. 139, 140). These data are in agree-
ment with the histological evidence presented by Witt-
maack [2, 3] and Rüedi [14, 15] on the first phase of mas-
toid 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. Sim-
ilarly, 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
88 Color Atlas of the Anatomy and Pathology of the Epitympanum
a good portion of the petromastoid bone in the four tem-
poral bones. Our data concur with the notion of Witt-
maack [2, 3], Rüedi [14, 15], Tumarkin [20–22] and
Friedmann [23, 24] that normally all mastoids pneuma-
tize 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 Tem-
poral 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 pul-
monary damage (case 3). We have suggested earlier [28,
29] that if a child is subjected to bronchoscopy and pul-
monary lavage because of an AFCC aspiration, myringo-
tomy 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 simultaneous-
ly with pulmonary aspiration.
Difficulties arise in cases comparable to cases 1 and 2
in the oldest group, with extensive pathology without pul-
monary aspiration. The departments taking care of new-
borns and infants should establish a database of children
born through meconium-stained amniotic fluid and fol-
low 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 sug-
gests that there is no need to worry about a slight contami-
nation 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 pro-
cess.
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 heal-
ing 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 patholo-
gy has become dormant, old signs of serious disease hav-
ing 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 recur-
ring 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 re-
move 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 mu-
cosa? This issue will be discussed in Part 3 of this atlas.

References
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4 Benner M: Congenital infection of the lungs,
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10 Piza J, Gonzales M, Northrop C, Eavey RD:
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11 Eavey R: Abnormalities of the neonatal ear:
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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
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lems? 3rd Extraordinary Symposium on Re-
cent Advances in Otitis Media, Copenhagen,
June 1–5, 1997. The Hague, Kugler, 1999, pp
321–325.
13 Eckert-Möbius A: Die pathologisch-anato-
mische Untersuchungstechnik und die normal-
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O (eds): Handbuch der speziellen patholo-
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14 Rüedi L: Die Mittelohrraumentwicklung vom
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15 Rüedi L: Mittelohrraumentwicklung und Mit-
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17 Dahlberg G, Diamant M: Inheritance of pneu-
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18 Diamant M: Chronic otitis. A critical analysis.
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20 Tumarkin A: On the nature and vicissitudes of
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21 Tumarkin A: On the nature and vicissitudes of
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2 Pathology Related to Amniotic Fluid Cellular Content and Superimposed Infection 89

22 Tumarkin A: On the nature and vicissitudes of
the accessory air spaces of the middle ear. V.
More arguments. VI. Conclusions. J Laryngol
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23 Friedmann I: The comparative pathology of
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24 Friedmann I: The pathology of otitis media
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25 Palva T, Friedmann I, Palva A: Mastoiditis in
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27 Beaumont G: The effects of exclusion of air
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28 Palva T, Northrop C, Ramsay H: Spread of
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29 Palva T, Northrop C, Ramsay H: Effect of
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30 Palva T, Johnson L-G, Ramsay H: Attic aera-
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31 Palva T, Ramsay H: Chronic inflammatory ear
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ry 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
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Part 3
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Microsurgical Approaches to
Inflammatory Ear Disease

91
 Part 3
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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 in-
creases 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 ventila-
tion 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 histo-
logical evidence of this is only sporadic. Our first histolog-
ically 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 obli-
terated and Shrapnell’s membrane retracted and fixed to
the neck of the malleus. Nevertheless, there was no indica-
tion that the squamous epithelium was to start a choles-
teatomatous 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 epi-
tympanic 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 secre-
tion and beginning organization to full obliteration, in one
93
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 sec-
tions, 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. How-
ever, even this additional direct attic aeration route and
the use of a ventilation tube did not prevent the destruc-
tion of the epithelium in Prussak’s space and its gradual
fibrotic obliteration.
These documented observations, arrived at by com-
bining data obtained by microdissection with those ob-
tained by studying serial sections of diseased temporal
bones, made us search for new microsurgical approaches
with a better guarantee of improving aeration and drain-
age 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 patholo-
gy, 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 basi-
cally similar approach that he called ‘anterior tympanoto-
my’. While we worked with limited disease through the
94 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 drill-
ing 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 struc-
ture between the two compartments. From the two pre-
ceding parts of this atlas it is clear that the dividing struc-
ture 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 pos-
terior 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 mem-
brane 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 pre-
vent 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 mal-
leus. 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 in-
flammatory 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 inferi-
orly 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 quick-
ly afterwards.
While the canal skin, the pars tensa portion and Shrap-
nell’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, possi-
bly without a mucous membrane and a large pathway con-
nects 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 epi-
thelium-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 proce-
dure.
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 manipula-
tive 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.
3 Microsurgical Approaches to Inflammatory Ear Disease
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 retrac-
tion 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 compart-
ments had been aerated and the problem seems to be lim-
ited 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 remov-
al 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
95
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 ossi-
cles, 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 mov-
ing 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
96 Color Atlas of the Anatomy and Pathology of the Epitympanum
Fig. 161. Same ear as in figure 160. The malleus neck has been cut
(vertical arrow) with a malleus head nipper, allocating the tensor ten-
don 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 liga-
ment, 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 ten-
don and the tensor fold instantly visible (fig. 162). With-
out 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 mandato-
ry 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 posi-
tion 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.
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 re-
moved 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.
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
3 Microsurgical Approaches to Inflammatory Ear Disease
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 isth-
mus has inflammatory webs both anteriorly and posteriorly (horizon-
tal arrows). Note that the malleus head (M) has kept its position
despite the cutting of its neck. I = Incus.
removal. We were initially perplexed by the term ‘attic
plate’ used by their group [9, 12] which was said to sepa-
rate the anterior epitympanum from the supratubal re-
cess. Since the days of Siebenmann [13] and Hammar
[14], more than a hundred years ago, it has been recog-
nized that the separation is done by the tensor fold. We
then understood that in the lateral approach the trans-
verse 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 hori-
zontal serial sections, the transverse crest is seen to play
no role except at times it divides the anterior epitympa-
num superiorly into two sections (fig. 67, 114).
We use the frontolateral atticotomy in generalized cho-
lesterol 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 com-
bining the air spaces of the upper and lower lateral attics
(fig. 39).
97
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.
Fig. 167. Same ear as in figure 166, surgery
completed and the tensor fold removed, ex-
posing the supratubal recess (R). Chorda
tympani nerve (horizontal arrow) is seen ad-
jacent to the neck of the malleus (M). I =
Incus.

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 ante-
romedial 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 por-
tion of the crest is drilled away.
Extensive Attic and Mesotympanic Disease in Chronic
Otitis media
In recurring inflammatory ear disease, both the epi-
tympanum as well as the mesotympanum may present
with an extensive amount of granulation tissue. In addi-
tion to the blockade of both the tympanic isthmus and the
aeration pathway to Prussak’s space, granulomatous obli-
terating tissue and polyps may envelope the incus so that
preservation of an intact ossicular chain becomes too ris-
ky (fig. 52, 53). In addition to the above-described proce-
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 epithe-
lial 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 mini-
mum. 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 com-
partment 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

98 Color Atlas of the Anatomy and Pathology of the Epitympanum

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 pro-
cess of the incus (I), shimmering through the tympanic membrane.
M = Malleus handle.
the basal lamina, into adjacent granulation tissue in Prus-
sak’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 epi-
thelium in the inner lining of the cystic formation, con-
nective tissue covering the outside. However, any granu-
lation tissue adjacent to the connective tissue may contain
papillae from the squamous epithelium, regardless of the
type 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
3 Microsurgical Approaches to Inflammatory Ear Disease
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 meso-
tympanum 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.
touch either the fold insertion ring or mucosa of the supra-
tubal recess, which are well outside the area of cholestea-
toma.
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 connec-
tion 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 pro-
cess 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 mem-
brane perforation (fig. 168) and complicated during the
terminal stage of septicemia with extensive mastoid gran-
ulomatous infection. When we started with the anterior
microdissection we found that there had been a disrup-
tion of the cholesteatoma sac and the keratin mass had
spread anteriorly as far as the bony eustachian tube
(fig. 169).
99
Fig. 170. Surgical case, adult, right ear, endaural approach. Choles-
teatoma 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 cavi-
ty. M = Malleus, A = anterior malleal ligamental fold.
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 por-
tion 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 adi-
tus 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 sur-
face. 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.
100 Color Atlas of the Anatomy and Pathology of the Epitympanum
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 ero-
sion (oblique arrow). I = Incus long process.
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 ten-
don 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 ossi-
culoplasty 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 articula-
tion.
 Final Remarks Finally, the lateral route via the regular posterior tym-
panotomy completes the picture of the anatomic arrange-
We have suggested earlier [8] that the supervised ment of the structures which will confront the trainee sur-
microdissection training, including the lateral and anteri- geon in the operation theater. Moving aside Shrapnell’s
or approaches, be incorporated into the temporal bone membrane allows one to view the roof of Prussak’s space
surgery teaching programs for acquiring the necessary and the anterior membrane which is anteroinferior to the
anatomic knowledge. Surgical competence can only be neck of the malleus. Cutting the head of the malleus as
achieved through personal work, combined with preced- indicated above gives a greater sense of dexterity and safe-
ing seminars with documented figures of microdissections ty in doing the same procedures in one’s daily work, in the
and of serial sections of temporal bones. Documented evi- creation of additional attic aeration pathways or in pre-
dence is the only valid reference when seeking to under- paring adequate access for the removal of anterior glomus
stand anatomy, and sketches must always be accompa- tumors. When the ear surgeon knows the detailed anato-
nied by photographs of the anatomic structures on which my of the middle ear inside out it gives him great confi-
they are based. dence in planning and executing successfully any type of
The trainees will profit immediately from traditional surgery for inflammatory middle ear disease.
superior microdissection, when done personally once they
have obtained sufficient theoretical knowledge of the
structures to be encountered. He or she can instantly rec-
ognize 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 imme-
diately 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 fol-
lowing the lateral incudomalleal fold anteriorly one can
see how it descends towards the posterior malleal liga-
mental fold and how the lateral malleal space forms
between the three malleal ligamental folds.
After further removal of the tegmen, the anterior epi-
tympanum 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 mem-
brane 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 supra-
tubal 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.

3 Microsurgical Approaches to Inflammatory Ear Disease 101

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recurring otitis media. Tympanostomy tubes
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8 Palva T, Ramsay H: Chronic inflammatory ear
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ry attic aeration pathways by microdissection.
Am J Otol 1999;20:145–151.
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Tympanotomy. Tokyo, Springer, 1997, pp 1–
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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,
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11 Palva T: Glomus tympanicum tumors. Remov-
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 OOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOO

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 Cochleariform process 38, 47, 96 – obturator 8
Aeration pathway 9, 14, 17–19, 21–27, 30, Cog 38 – posterior incudal 30
31, 40, 46, 66, 70, 75, 80, 93, 94, 99 Cornelius 4 – stapedial 8, 32
Aimi 10, 40 Cutting of malleus neck 96 – tensor 6–8, 11, 37, 38, 39, 40, 42, 43,
Air sac 46, 47, 62, 66, 69, 94
– – anterior 7, 8, 16 Dahlberg 59 – trailing medial surface of malleus to
– – medial 7, 8, 16, 31 Diamant 59, 60 tensor fold 42
– – posterior 7 Döderlein 87 – trailing superior malleal ligament 8, 41
– – superior 7, 16 Drainage pathway → Aeration pathway Foreign body 18, 56, 57, 60
Amniotic fluid 59, 61 Duplicate folds 7 Fossa incudis 30, 66
– – cellular content 21, 61–66, 93 Friedmann 60, 88
Animal model of pneumatization 60, 61 Eavey 57 Frontolateral atticotomy 97
Annular bone 4, 8 Eckert-Möbius 58
Anterior attic → Epitympanum Endaural incision 94 Giant cells 69, 70, 73, 84, 86
– membrane of Prussak’s space 13, 16, Epidermal papillae 26 Glomus tumor 95
19, 46, 95 Epitympanic diaphragm 11, 12 Goldenhar’s syndrome 75, 79
– pouch 4, 23, 27, 46, 48, 95 – folds → Folds Granulation tissue 21, 23, 25, 34–36, 42,
– tympanic isthmus 12 – ligaments → Ligaments 43, 56–58, 67, 69, 70, 72–74, 81,
Arnold 4 – sinus 38, 39 85–87, 98
Aschoff 55, 56, 59 Epitympanum Guluya 9
Attic → Epitympanum – anterior 11, 27, 28, 31, 36–44, 58, 61,
– bone 5, 15, 30, 31 94, 97 Hammar 4, 5, 7–9, 13, 14, 32, 40, 45, 97
– roof 8, 28, 30, 31 – medial 9, 11, 12, 28, 31–33, 38, 42, 64 Hammer-Amboss-Schuppenraum 7
Atticotomy 97 – posterior 12, 27, 28–36, 42, 101 Helmholtz 4, 5, 13
Auxiliary aeration pathway 12, 30 – superior 8, 28, 31, 61, 62, 76, 77, 81, 88 Henle 5
Eustachian tube 7, 40, 48, 59, 66, 73, 93, Hypotympanum 35, 56, 61
von Bardeleben 3 94
Beaumont 60, 61, 88 Eysell 3 Incudal fossa 30, 66
Benner 56 Incudostapedial articulation 32, 35, 66
Bezold 3 Fetal development 7 Inferior tympanic artery 4, 12
Buch 56 Fibrosis 60 Interatticotympanic diaphragm 11
Folds (variable, position-changing)
Chatellier 11 – chordal 8 Jörgensen 56
Cholesteatoma 26, 27, 37, 57, 94, 95, 98–100 – cruris longi incudis 8
Cholesterol crystals 27, 36, 43, 55, 93 – incus intercrural 32 Kuppelraum 3
– granuloma 57, 61, 86, 97 – interossicular 47
Chorda tympani nerve 4, 5, 8, 12, 17, 42, – lateral incudomalleal 8, 11, 12, 15, 20, Labyrinth capsule 3
72, 95 28, 30, 32, 62 Labyrinthine bone 58
Chordal fold 8 – medial ossicular 32 Lanugo hair 57, 75, 86

103
Lateral attics 8, 12, 62, 69 – – infant 56–58, 60 Sheehy 38
– attic bone 5, 12 – – infectious 55 Shrapnell 5
– incudomalleal fold → Folds – – neonatorum 32, 55, 59 Shrapnell’s membrane 3–5, 14–16, 18, 19,
– malleal space 5, 6, 8, 9, 12, 13, 15, 16, – – recurrent 87–89, 93 21, 24–27, 75, 93, 94
18–21, 27–29, 38, 64, 66, 69 – – secretory 5, 6, 11, 27, 34, 36, 60, 93 Siebenmann 3, 6, 7, 9, 37, 38, 40, 42, 49,
Lemoine 11 – – sterile 32 50, 97
Ligaments (ligamental folds, position-fixed) Otosclerosis 43 Sinus tympani → Tympanic sinus
– anterior malleal 4, 5, 8, 12, 15, 42, 46, 48 Spina capitis mallei 5
– anterior malleal suspensory 12 Paukenhöhle 3 Squamous bone 3, 61, 66, 74, 85–88
– lateral malleal 5, 9, 12, 13, 15 Periosteal bone 88 – epithelial cells 55, 75, 79, 85
– posterior incudal 8, 10, 28, 30, 31, 36 Petrotympanic fissure 12, 42 Stapedial fold → Folds
– posterior malleal 5, 12, 13, 29 Petrous bone 3, 66, 73, 85–88 Stapedius tendon 5
– superior malleal 28, 38 Plica cruris longi incudis 8 Superior attic → Epitympanum
Lower lateral attic 8, 13, 15, 17, 21, 22, – transversa 3, 7 – pouch 4, 9
28–30, 29, 63, 66, 74, 95 Pneumatic cell 7 Supratubal recess 3, 6–8, 27, 39, 40, 42, 43,
Pneumatization 36, 38, 47, 57–61, 66, 73, 45–51, 62, 63, 66, 69, 94
McLellan 56 85–88
Malleal ligaments 4, 5 Politzer 5, 6, 14, 15, 17, 22 Tensor fold → Folds
– spine 5 Portal for organization 26, 62, 68 – tendon 3, 6, 10, 16, 31, 36, 38, 40, 47, 48
Margo tympanicus 5 Position-changing folds 7 Tos 6
Mastoid antrum 3, 12, 59, 61, 62 Position-fixed folds 7 Transverse crest 3, 6, 38, 39, 94
Mastoidectomy 97 Postauricular incision 94, 95 von Tröltsch 3, 5, 12, 18
Mastoiditis 60 Posterior attic → Epitympanum Trommelfelltasche 7
Meconium 55, 57, 61 – pouch 4, 9, 17, 18, 21, 23, 25, 95 Tubal orifice 5
Medial attic → Epitympanum – tympanic isthmus 12, 30 – tegmen 38
– ossicular fold → Folds – tympanotomy 21 Tumarkin 60, 88
Mesotympanum 4, 17, 18, 21, 26, 28, 40, – tympanum 12, 27, 30, 59, 61, 72, 74 Tympanic cavity 3, 9, 49, 58, 64, 79
45, 56, 98 Potter 57 – glomus tumor → Glomus tumor
Microsurgery 94–97 Proctor 9, 12, 13, 16, 18, 31, 32, 38, 46 – isthmus 9, 10, 12, 28, 31–33, 34–36, 40,
Morimitsu 94, 97 Protympanic recess 12 48, 64, 67, 72, 93, 94
Mucosal fibrosis 58 Prussak 4, 5, 9, 17, 22 – membrane 4, 5, 17, 23, 57
– hyperplasia 58, 59 Prussak’s space 5, 6, 9, 11–27, 46, 49, 63, – sinus 65, 67, 73
– polyps 56, 69, 73 64, 66–70, 72, 93–95, 98 – spine
Multinucleated cells 64, 79, 81, 82, 86 Pseudocystic granulation 67, 78–81, 84 – – anterior 5, 12, 38
Pyramidal process 10, 31 – – posterior 5, 17, 23
Northrop 57 Tympanostomy tube 27, 34, 75, 89, 93
Notch of Rivinus 3, 94, 95 Recessus epitympanicus 3 Tympanotomy
Retraction pocket 25, 27, 75, 93–95 – anterior 11, 94
Obturator fold → Folds Riding columella 95 – posterior 11, 94, 95
Ojala 60, 87 Round window membrane 65, 73, 84
Organization 74, 80–83, 87 – – niche 73, 79 Upper lateral attic 8, 12, 13, 28, 38, 62
Otitis media Rüedi 59, 60, 68
– – acute 5, 19, 59 Wildberg 4
– – adhesive 34, 89, 93 de Sa 56 Wittmaack 4, 26, 55–61, 87, 88
– – chronic 26, 37, 40, 48, 59, 60, 93, 98 Schuknecht 9 Wullstein 6, 31
– – hyperplastic 58 Schwartze 3

104 Subject Index