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Fig. 6.6 The right ear. Regular buffer function of the mastoid. Sagittal
section at the level of the tympanic membrane. Pink: middle ear; red:
mastoid antrum; brown: mastoid
Fig. 6.7 The right ear. Sagittal section at the level of the tympanic
membrane. Worse buffer function of a small mastoid that leads to wider
pressure variations in the tympanic cavity, with a consequent retraction
of the tympanic membrane (arrows) and a reduction of volume in the
middle ear (arrows)
the fact that the mastoid plays an important buffering role in
regulating the pressure of the middle ear [20].
As previously stated, the pressure balance is the result of
the interaction between gas exchange in the mastoid air cells’
mucosa, directly related to the degree of mastoid pneumatization, and a functioning Eustachian tube. Since these two
mechanisms are interdependent, an isthmus blockage, even
with a working Eustachian tube, could prevent mastoid cells’
ventilation, leading to sclerotization of the mastoid itself.
Görür etal. [21] classied the degree of radiological mastoid
pneumatization shown in computed tomography (CT) scans
as follows:
• Type 1 (normal pneumatization): The aerated mastoid
cells reach the mastoid tip and the zygomatic, perisig-
moid, and periantral regions and the aditus ad antrum is
open.
A. Rubini et al.
• Type 2 (hypopneumatization): The aerated mastoid cells
are found only in the antral and periantral regions and the
aditus ad antrum is open.
• Type 3 (sclerotic): Mastoid pneumatization is absent and
the aditus ad antrum is blocked.
Marchioni etal. ran CT scans on a group of subjects with
an impairment of the middle ear aeration pathways. The vast
majority of this group (18 out of 22) presented a hypopneumatized or scleroid mastoid. The degree of mastoid pneumatization was worse in the pathological ear, when compared to
the contralateral one [22].
Blockage oftheVentilation Pathways
A primarily acquired cholesteatoma is morphologically
characterized by epithelial cell proliferation. Unfortunately,
despite a large number of studies, our understanding of the
mechanisms underlying the pathogenesis of cholesteatoma is
still limited. In the past, Bezold and Young suggested that the
etiology of attic cholesteatoma could be attributed to an
Eustachian tube dysfunction, resulting in an increased negative pressure in the tympanic cavity [19, 23]. On the other
hand, Palva etal. observed how an attic retraction pocket
could occur even in the case of a regular Eustachian tube
function. Therefore, there must be other factors that affect
the pathogenesis of attic cholesteatoma. The group led by
Palva studied children with a blockage of the isthmus, who
had undergone a tympanostomy tube placement, and they
observed the persistence of inammatory materials and cholesterol granuloma in the superior attic, despite the tympanostomy tube. They believed that an epitympanic diaphragm
obstruction might be the origin of an attical cholesteatoma,
stemming from an attical retraction. In contrast, children
with an incomplete or absent tensor fold showed good ventilation of the anterior attic [24].
The theory that the obstruction of the aeration route
between the mesotympanum and the attic is a contributing
factor in the pathogenesis of attic retraction and cholesteatoma was severely challenged years ago by Yamasoba [25]
and Kobayashi [26]. Yamasoba pointed out that it is possible
for a cholesteatoma to stem from an attic retraction pocket
despite the aeration of the mesotympanum in the middle ear.
However, the importance of tensor fold removal during the
surgical treatment of middle ear attic cholesteatoma remains
of paramount importance, to restore the ventilation route
from the protympanum to the anterior epitympanum, thus
preventing the development of an attic cholesteatoma.
In microscopic ear surgery, since it is difcult to visualize
the tensor fold due to its anterior position, some authors
proposed different surgical approaches to microscopically
6 Understanding theAeration Avenues oftheMiddle Ear withtheAid oftheEndoscope
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65
visualize that fold. Morimitsu etal. [27] proposed an “anterior tympanotomy;” they removed the bone from the lateral
attic to the zygoma, allowing for a possible drilling in front
of the malleus head to remove the tensor fold. Palva etal.
[28] suggested a tensor fold excision to create a large, new
attic aeration pathway during cholesteatoma surgery through
an endaural atticotomy extending to the supratubal recess.
With the introduction of an endoscope during middle ear
surgery, it has become possible to study the anatomical variations and the ventilation pathways in pathological patients,
owing to the magnication of critical areas such as the tensor
fold and tympanic isthmus [16]. The exclusive transcanal
endoscopic approach allows for a wide exposure of the anterior epitympanic compartment, especially the tensor fold and
its inclination and its complete or incomplete structure, also
granting the possibility of tensor fold removal with an angled
instrument, thus restoring the ventilation of the upper unit.
The endoscopic approach to the tensor fold and to the
anterior epitympanic compartment mainly depends on the
dimensions of the anterior epitympanic space [29]. In most
cases, it is wide, and the inferior endoscopic approach to the
tensor fold area provides a good exposure to the inferior edge
of the tensor fold, allowing for its removal and restoring
direct ventilation from the protympanic space to the anterior
epitympanic space.
In subjects with an extremely narrow anterior epitympanic space, associated with a vertical orientation of the tensor fold, it is only possible to explore the fold component
close to the cochleariform process. In this case, a removal of
the incus and the head of the malleus is necessary to obtain a
good visualization of the superior edge of the tensor fold.
Selective Epitympanic Dysventilation
Syndrome
state is an obstruction of the isthmus associated with a complete tensor fold, determining a selective dysventilation of
the upper unit [30]. Several factors may obstruct the tympanic isthmus or von Tröltsch’s pouch, such as mucosal fold
variations, inammatory webs, a retracted tympanic membrane, a pathological attic mucosa, and a cholesteatoma. In
the two abovementioned conditions, a limited disease in the
respective areas, possibly associated with an attical retraction, might occur [14]. As a conrmation of this, a tympanic
isthmus obstruction is a consistent nding in patients with a
limited attic cholesteatoma (Fig.6.8).
A selective epitympanic dysventilation syndrome thus
appears with four simultaneous distinctive features: an attic
retraction pocket or cholesteatoma, a type A tympanogram
or a regular tubal function test, a complete epitympanic diaphragm, and an isthmus blockage. In patients with this syndrome, while the epitympanum is poorly ventilated, with a
subsequent decreased pressure that also extends to the mastoid, the mesotympanum is well-aerated, receiving air
directly from a functioning Eustachian tube. In clinical practice, it is not uncommon to nd an isolated retraction pocket
of the pars accida and/or a cholesteatoma in this region,
with a normal pars tensa and mesotympanum. Conversely,
when the Eustachian tube function is impaired, the middle
ear mucosa is usually widely involved in the inammation
process, and the tympanic membrane is completely retracted.
So, in patients with a selective epitympanic dysventilation, it is usually possible to intraoperatively appreciate an
open Eustachian tube, a good protympanic and mesotympanic mucosa, and a partial or complete isthmus blockage
that could alone explain it, thus strengthening the preoperative evaluation of a working Eustachian tube [14, 31]. From
this, we can understand the importance of a surgical approach
that can completely visualize the epitympanic diaphragm
and surgically restore the ventilation pathways.
As stated above, a physiological middle ear pressure seems
to be connected to a functioning Eustachian tube and to the
transmucosal gas exchange through the mastoid mucosa,
which is directly related to the degree of pneumatization. An
inammatory middle ear chronic disease may thus be due to
an Eustachian tube dysfunction and subsequent poor tympanic ventilation, which is often associated with the hypopneumatization or sclerotization of the mastoid cells [15,
16]. Conversely, in subjects with an excellent Eustachian
tube function, two different conditions could give rise to an
epitympanic selective dysventilation. The rst condition is
an obstruction of the posterior pouch of von Tröltsch, which
closes the gap between the tympanic membrane and the posterior malleal ligamental fold, creating a selective dysventilation of the lower unit (Prussak space) [24]. The second
Selective Dysventilation
oftheMesotympanum
Pars tensa cholesteatoma is a primarily acquired (retraction
pocket) cholesteatoma that has a different pathogenesis from
that of the attic, and it is associated with a negative middle ear
pressure, due to a chronic Eustachian tube dysfunction.
However, a ventilation dysfunction in the mesotympanum
could also be attributed to brous or mucous webs between
the medial wall of the tympanic cavity and the tympanic
membrane that can exclude the tubal orice and can create
selective dysventilation areas in the anterior or posterior
mesotympanum. This often leads to selective mesotympanic
retraction pockets rather than the whole mesotympanum [32].
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Fig. 6.8 The right ear.
Lateral-to-medial view with a
slight anterior rotation.
Selective epitympanic
dysventilation syndrome:
blockage of the tympanic
isthmus with a complete
tensor fold. The arrow
indicates the ventilation of the
mesotympanum, through the
Eustachian tube. The
epitympanum is not properly
ventilated due to the tympanic
isthmus blockage. Prussak
space is regularly aerated
through von Tröltsch’s pouch.
****: blockage of the
tympanic isthmus. PLIN,
lateral and medial posterior
incudal ligaments; IMLF,
lateral incudomalleal fold; IN,
incus; MA, malleus; MLF,
lateral malleal fold; PRS,
Prussak space; TF, tensor
fold; ET, Eustachian tube
A. Rubini et al.
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M. Endoscopic anatomy of the tensor fold and anterior attic.
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14. Marchioni D, Alicandri-Ciufelli M, Molteni G, Artioli FL,
Genovese E, Presutti L. Selective epitympanic dysventilation
syndrome. Laryngoscope. 2010;120(5):1028–33. https://doi.
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15. Aimi K. The tympanic isthmus: its anatomy and clinical signicance. Laryngoscope. 1978;88(7 Pt 1):1067–81. https://doi.
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16. Marchioni D, Mattioli F, Alicandri-Ciufelli M, Presutti
L.Endoscopic approach to tensor fold in patients with attic cholesteatoma. Acta Otolaryngol. 2009;129(9):946–54. https://doi.
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17. Sadé J, Ar A. Middle ear and auditory tube: middle ear clearance, gas exchange, and pressure regulation. Otolaryngol Head
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F, Presutti L. Endoscopic evaluation of middle ear ventilation
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25. Yamasoba T, Kikuchi S. Is an isthmus block a prerequisite for
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Regulated Balance ofPressure
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Variations intheTemporal Pneumatic
Spaces
BernardArs andDominiqueEstève
7
Brief Basic andMorpho-Functional Quotes
From a quantitative point of view, gaseous spaces of the middle ear cleft embody the largest part of the pneumatic spaces
of the temporal bone. It consists of interconnected gas cells
lined with the same respiratory mucosa.
The middle ear cleft consists of both the mastoid gas cell
system and the tympanic cavity. The latter includes the tympanum and four annexes: the epi- and hypo-tympanum and
the retro- and pro-tympanum that corresponds to the bony
Eustachian tube. The brocartilaginous Eustachian tube is
part of contiguous organs, including the nose, palate, and rhinopharynx, and is connected to the middle ear cleft. It is not
a simple tube but is rather a complex organ consisting of a
dynamic conduit with an innervated and vascularized
mucosa, cartilage, surrounding soft tissue, peritubal muscles
(i.e., the tensor and elevator veli palatini, salpingopharyngeus, and tensor tympani), and the superior bony support,
namely, the sphenoid sulcus.
The middle ear cleft, in the tympanic cavity, is constricted
in its superior third by the inter-attico-tympanic diaphragm,
a bony membranous barrier perforated by two small permanent openings: the anterior tympanic isthmus, which is
located between the tensor tympani tendon and the stapes,
and the posterior tympanic isthmus, which is located between
the double posterior ligament of the incus and the bony posterior tympanic wall.
This barrier divides the middle ear cleft into two separate
compartments: an anteroinferior one and a posterosuperior
one [1, 2]. The anteroinferior compartment of the middle ear
cleft, located under the diaphragm, includes the pro-, meso-,
and hypo-tympanum and is mainly covered by secretory or
non-secretory ciliated cells performing mucociliary clearance. It consists of a exible chamber due to the presence of
the eardrum. Because of the brocartilaginous Eustachian
tube, it consists of an gas pocket with intermittent gas transfers. It communicates with the posterosuperior compartment
by both the anterior and posterior tympanic isthmi.
The posterosuperior compartment of the middle ear cleft,
located above the diaphragm, includes the epi- and retrotympanum, aditus ad antrum, antrum, and the mastoid gas
cell system. It is mainly covered by a richly vascularized
cuboidal epithelium primarily devoted to gas exchanges. It
consists of a rigid chamber and an open gas pocket that communicates with the anteroinferior compartment via both
openings. The middle ear cleft is essentially a non- collapsible
gas pocket with poor gas exchanges, through which sound
wave energy is transported to the inner ear.
The gas must be contained in a three-dimensional container with volume V. The pressure of the gas P is created by
the molecules of the gas striking the walls of the container. It
is dened as force per unit area. The physical characteristics
of the gas are linked together by the ideal gas law: PV=nRT,
where n is the mass expressed in molecule grams, R is the
universal gas constant, and T is the absolute temperature.
The middle ear cleft is subjected to physiological variations
in volume and pressure. It has the capacity to maintain
steady-state volume and pressure; this is achieved by different regulatory mechanisms, which neutralize or minimize
pressure and volume variations. This is performed by adjusting either the quantity of gas, its diffusion, and/or the volume
of the middle ear cleft.
Gas Exchanges
B. Ars (*)
University of Namur, Brussels, Belgium
Temporal Bone Foundation, Brussels, Belgium; http://www.
arsbernard.com
D. Estève
Chemin de Sainte-Roustagne, Manosque, France
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. V. Goycoolea et al. (eds.), Textbook of Otitis Media, https://doi.org/10.1007/978-3-031-40949-3_7
Morphological Structures
The gas content of the middle ear cleft is constituted and
maintained due to gas exchanges between the middle ear
cleft and the neighboring structures, including the environ-
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B. Ars and D. Estève
ment across the tympanic membrane, the inner ear via the
round-window membrane, the blood compartment via the
mucosa, and the rhinopharynx through the brocartilaginous
Eustachian tube [3, 4].
What Happens intheMucosa?
The gases present in the middle ear cleft are identical to
those found in the blood and in the atmosphere: oxygen (O2),
carbon dioxide (CO2), nitrogen (N2), argon (Ar), and water
vapor (H2O). Their relative amounts may be expressed as
their partial pressure P (x). Nitrogen is neither produced nor
consumed in the middle ear cleft. P(O2) in the middle ear
cleft is slightly lower, and P(CO2) is slightly higher than in
venous blood. This means that there is modest O2 consumption and CO2 production in the middle ear cleft. Oxygen and
nitrogen are absorbed from the middle ear cleft through the
mucosa into the blood compartment. CO2 and water vapor
diffuse from the blood compartment, through the mucosa,
into the middle ear cleft.
The steady exchange of gas through the mucosa depends
on the functional properties of the cells of the mucosa, the
specic diffusion rate of the gas, which is a constant value,
characteristic of a particular gas, and the behavior of the vascular system [5, 6]. The primary purpose of the mucosa is to
facilitate gas exchanges between the middle ear cleft and the
blood compartment through a constitutive tissular barrier.
Middle ear cleft gas exchange is an ongoing process that
continually generates a net absorption of gases, resulting in
an increasingly negative pressure between tubal dilations.
There is a gradient of partial pressures of gases between the
middle ear cleft gases and the venous capillary soluble gases
that drives the net ow of gas toward the circulation over
time. CO2 has the highest diffusion coefcient and is most
rapidly exchanged with the net exchange passing from the
venous blood to the middle ear cleft. The next fasted diffusion is that of O2, passing from the middle ear cleft into the
blood. N2, the predominant partial pressure in both air and
blood and the source of the largest gradient, diffuses much
more slowly into the circulation. It is the slow absorption of
N2 that causes the increasing relative vacuum between ambient air and the middle ear cleft over time.
In the Eustachian tube, the proximal third of the tubal tent
is a bony funnel-shaped extension of the middle ear cleft, the
“protympanum,” which narrows down at the isthmus. The
distal third of the tubal length is the pharyngeal portion,
which is made up of a cartilaginous skeleton to which is
attached a complex arrangement of peritubal muscles, capable of a wide range of dynamic movements [7].
This cartilaginous portion is normally closed in the resting position due to apposition of the mucosal walls. Closure
occurs over a variable length (a 5–10-mm segment), just a
few millimeters distal to the bony isthmus where the cartilaginous skeleton becomes exible. This portion that inter-
mittently dilates to the open position is termed the “functional
valve” because it serves such a purpose.
Contraction of the elevator veli palatini muscle raises the
soft palate and rotates the medial cartilaginous lamina medially. Contraction of the tensor veli palatini muscle tenses the
anterolateral membranous wall and pulls it laterally to dilate
the tubal valve to the open position. Intermittent brief tubal
dilation is most likely the principal mechanism of equalizing
the middle ear cleft pressure with the ambient atmosphere.
Involuntary dilatation of the brocartilaginous Eustachian
tube occurs throughout the day, typically during swallowing
or yawning, but it does not accompany every swallow or
yawn.
Tubal dilation occurs in normal subjects approximately
1.4 times per minute during daytime with an average duration of opening of 0.4s. During sleep, the frequency of tubal
opening is substantially reduced. Sequential muscular contractions initiate rotational movements of the cartilaginous
framework and create tension within the anterolateral wall,
causing the effacement of its resting bulge. This effacement
is the primary action that opens the lumen to the middle ear
cleft.
Tubal dilation begins with the action of the elevator veli
palatini muscle to medially rotate the cartilaginous skeleton,
primarily its mobile distal half of the medial cartilaginous
lamina. Tensor veli palatini muscle contraction follows,
causing the resting convexity of the anterolateral wall to
become effaced or even concave as the nal step to transiently open the lumen.
Intermittent brief dilation of the tube is the principal
mechanism for equalizing the middle ear cleft pressure with
the ambient atmosphere, regulating the nitrogen balance.
Tubal dilation is likely facilitated by the presence of surface
tension-lowering substances that are found in its mucus.
Surfactants are produced within the tubal mucosa and probably help reduce the surface tension of the lumen, which
reduces the work required to dilate the tube.
1. The in situ adaptation and local control systems of gas
exchanges in the middle ear cleft mainly consist of the
compliance of the tympanic membrane lamina propria,
the brocartilaginous Eustachian tube function, and the
behavior of the vascular system of the middle ear cleft
mucosa, especially that of the mastoid.
(a) The compliance of the tympanic membrane lamina
propria [8] is used in the case of sudden pressure
changes (altitude, diving, ight, explosion, etc.). This
is largely due to the viscoelastic properties of the
lamina propria and the exibility of the incudomallear joint, which acts as a static pressure receptor for
the tympanic membrane, ensuring three- dimensional
movement into the malleus. Distortion of the eardrum causes a volume change of the semirigid mid-
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dle ear cleft and can therefore partially compensate
for fast pressure changes. The tympanic membrane’s
lamina propria is not only an active pressure buffer
but also a passive pressure victim.
(b) The brocartilaginous Eustachian tube does not
function as a ventilation hole, which keeps pressure
inside the middle ear cleft equal to the outside pressure. Only at large pressure differences, above 2kPa,
will the brocartilaginous Eustachian tube open
spontaneously [9]. Changes in position seem to affect
the function of the brocartilaginous Eustachian
tube. The mean volume of gas passing through the
tube in the upright position is reduced by a third
when the body raised at 20° with respect to the horizontal position. It is reduced by two-thirds in the
horizontal position. This is the result of an increase in
the venous tissular pressure around the brocartilaginous Eustachian tube.
(c) The vascular system, in combination with the mas-
toid gas cell system, plays an important regulatory
role in the physiological balance of pressure variations in the middle ear cleft. Variations in the middle
ear cleft blood ow, associated with variations in the
permeability of the vessels, allow ample adaptation
to normal gas pressure uctuations [10–13].
The normal extensive variations observed in the middle
ear cleft pressure over a 24-h period, which appear regularly,
are related to the vascular adaptations required by body position and sleep.
The mastoid gas cell system constitutes the most important volume of the middle ear cleft, and, therefore, it represents the largest part of the area of the middle ear cleft
mucosa, accessible to the vascular network, further increased
by a large number of mucosal folds. The extent of mastoid
gas exchanges is important for regulating middle ear cleft
pressure variations for two reasons.
First, the physical and anatomical properties of mastoid
volume affect compliance: the larger the volume, the more
compliant the system.
Second, the mucosal surface area affects mucosal gas
exchanges: the larger the surface area, the more efcient the
middle ear cleft gas exchanges.
The mastoid carries out the function of a passive pressure
buffer as a gas reservoir for pressure variation regulations,
obtained by its volume. However, it also carries out an active
pressure buffer function. Cros demonstrated retroauricular
microchannels connecting the outer cortical bone surface
directly to the underlying mastoid gas cells. Gaheide showed
the presence of a separate vascular supply for the mucosa
lining the mastoid gas cell system, in these microchannels. If
a certain number of such channels run in parallel, as some of
the pictures of the authors seem to demonstrate, there must
exist a mechanism of counter-current exchange that maintains the two compartments with a stable difference of composition. We may conclude that the mastoid also carries out
an active buffer function.
The size of the mastoid gas cell system varies to a large
extent between individuals. Irrespective of the cause, genetically determined growth, or environmental factors, there is
unanimous agreement that a small mastoid gas cell system
has a pathophysiological association. The smaller the system, the faster the deviation from normal pressures. However,
nature is a matter of balance. It is not a single question of
determining the volume of the mastoid in order to predict its
clinical potential.
In normal conditions, with a healthy mucosa, a small mastoid in an adult is normal in so far as it constitutes the complete outcome of normal and standard development, i.e., the
individual simply has the morphological particularity of
being “small.” A small mastoid in an adult is normal, in that it
is sufcient for the physiological balance of pressure variations in the middle ear cleft. However, this small mastoid is
not more likely to particularly develop a pathology. However,
when the mucosa undergoes an inammatory process, a small
mastoid in an adult, e.g., resulting from a disturbed or failed
development, is certainly at a disadvantage when it is exposed
to excessive pressure variations. This mastoid is “too small”
compared to the rest of the middle ear cleft. If the expansion
reservoir is too small, then it cannot adequately play its role.
In normal conditions, with a healthy mucosa, a “normal,”
small, negative pressure is present in the middle ear cleft
compared to the outside air, created by exchanges of gas
between the cleft and the blood compartment. Gas exchanges
through the mucosa of the middle ear cleft are driven by the
gradient of partial pressure of gases between the cleft and the
capillaries of the submucosal connective tissue.
Given the capacity of gas diffusion in the middle ear cleft,
partial pressures of these gases aim at balancing both sides of
the mucosal barrier of the middle ear cleft.
The progressive diffusion of gases is capable of modifying the gas composition in the middle ear cleft and in the
circulating blood. The gas, which penetrates into the middle
ear cleft from the rhinopharynx, is not outside air. Its composition is rather close to that of exhaled gas.
Quantitatively, the main gas entering the middle ear cleft
is nitrogen. N2 diffuses much more slowly in the blood than
do other gases (35 times more slowly than CO2 and 1.8 times
less than O2). Considering this nitrogen in steady state, there
is a difference in partial pressure between the middle ear
cleft and the blood ow around the middle ear cleft. This
steady state corresponds more or less to the total amount of
pressure difference (54–56mmHg) between the middle ear
cleft and blood. In the steady state, oxygen, carbon dioxide,
and water vapor have nearly the same partial pressures in the
middle ear cleft as in the blood compartment.
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B. Ars and D. Estève
Consequently, an increase in blood ow in the middle ear
cleft has little effect on gas exchanges, except perhaps during
the night, when CO2 increases and O2 is reduced in the blood
ow. On the other hand, N2 always maintains a higher partial
pressure in the middle ear cleft as compared with the blood.
Therefore, there is a clear and continuous elimination of N2
from the middle ear cleft in the direction of the blood compartment. This leads to a slight negative pressure in the middle ear cleft.
The innervation of the mucosa of the middle ear cleft
originates from the autonomic nervous system, which sends
and receives information from both the sympathetic and
parasympathetic networks at the same time. Adrenergic
nerve endings have been detected, most of them in the vicinity of vessels. They probably control their muscle tonus. The
peptidergic system would also play a role. It has been established that the presence of peptide mediators such as P substance, vasoactive intestinal peptide (VIP), or calcitonin
gene-related peptide (CGRP) lead to vasodilatation and an
increase in vascular permeability.
In the middle ear cleft, chemosensors located in the glomic tissue of the mucosa respond to variations in the gas
composition and send impulses to reexes of gas transfer
from the rhinopharynx toward the middle ear cleft. In normal
conditions, under the control of the isobaric system, the
elimination of nitrogen from the middle ear cleft to the blood
compartment is regularly compensated for by the gas contribution originating from the rhinopharynx. Inammatory processes increase both the number and diameter of the blood
vessels, thus increasing blood supply to the mucosa. The
middle ear cleft is 210 times more perfused than ventilated
under normal conditions and is 251 times more perfused than
ventilated under inammatory conditions. The result of this
increased blood perfusion is a larger diffusion of nitrogen
from the middle ear cleft toward the blood. This explains the
apparent contradiction between the increase in thickness and
the barrier of the mucosa and the increase in gas elimination
in inammatory conditions. The negative pressure of the
“normally” slightly balanced middle ear cleft thus increases.
Higher nitrogen absorption would normally be sufciently compensated through the brocartilaginous
Eustachian tube but could now generate pathological negative pressure in the middle ear cleft compared with the atmospheric pressure. This conditions carries a “gas decit,” and
therefore a negative pressure, which could constitute a
mutual physical–pathological support to the development of
chronic otitis media.
The Neural Regulating System: TheIsobaric
System oftheMiddle Ear Cleft
The principle of the isobaric system of the middle ear cleft is
based not only on the presence of pressure-sensitive mecha-
noreceptors, i.e., barosensors, which are able to collect the
middle ear cleft pressure, but also on the atmospheric pressure in the upper airway.
Barosensors Located intheMiddle Ear Cleft
Gussen’s report [14] indicate that the human tympanic cavity
and antrum contained Pacinian corpuscles. Lim etal. [15]
located these sensors in the mucosa, most commonly in the
epitympanum and the epitympanic recess. Nagai and Tono
[16] identied encapsulated nerve endings in the subepidermal connective tissue and the lamina propria of the second
quadrant of the pars tensa of the tympanic membrane. The
structure of the corpuscles was round or oval with diameters
that were about 40μm and contained a number of axon terminals with the mitochondria, Schwann cell processes, and
amorphous materials in the intercellular space. These features appear to be at work in transmitting mechanical forces
(stretching of the tympanic membrane) and are comparable
to the function of mechanoreceptors that could detect middle
ear cleft pressure [17]. Based on the studies by Nagai etal.
[18], showing that the tubal function changed following topical anesthesia of the eardrum, Estève [19] pointed out that
opening of the tube occurs when a pressure imbalance occurs
between the two sides of the tympanic membrane.
After anesthesia of the drum, many subjects felt some dull
sensation on external ear pressures or stated that they could
not detect the gas coming into the tympanic cavity during the
Valsalva maneuver. Out of 20 subjects, 13 ears needed more
than 2 swallows and 4 ears failed to equalize middle ear cleft
pressure in spite of repeated swallows.
The mechanoreceptors, located in the middle ear cleft,
might possibly play an effective role in tubal function where
the mechanoreceptors on the drum seem to have a minor
effect.
With different elasticity and histological structures from
the rest of the membrane, the pars accida has been suggested as a highly sensitive and fast reacting part of the tympanic membrane, providing pressure balance with the middle
ear cleft in the range of natural levels of atmospheric pressure uctuations. The pars accida could act as a barosensor,
initiating the physiological reactions in the body in the
course of adaptation to atmospheric pressure uctuations.
Barosensors Located intheRhinopharynx
In a study of the human rhinopharyngeal innervation,
Kanagasuntheram etal. [20] reported a predominance of free
nerve endings and a few organized non-encapsulated endings, with the latter only in the subepithelial tissue. From
patients undergoing adenoidectomy or biopsy examination
of the postnasal space for the exclusion of neoplasia, Guindi
[21] identied free nerve endings in the rhinopharynx and
encapsulated receptors in the subepithelial tissue of the pharyngeal recess. In the histological study by Salburgo etal.
[17], Rufni corpuscles were accurately identied in the
7 Regulated Balance ofPressure Variations intheTemporal Pneumatic Spaces
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73
rhinopharynx, with a higher concentration in the pharyngeal
recess and the posterior rhinopharyngeal wall.
The “Neuronal Reex Arc” oftheIsobaric System
oftheMiddle Ear Cleft (Fig.7.1)
Owing, above all, to the stretch receptors of the pars accida,
sensitive to extremely weak horizontal changes in Patm
(atmospheric pressure) (>0.1mbar), and owing to the Rufni
corpuscles of the pharyngeal recess, sensitive to vertical
changes in Patm (>10mbar), the neurosensory reex loop
implements gas exchanges essentially at the level of the mastoid and of the opening of the brocartilaginous Eustachian
tube, depending on the intensity of the initial stimulus. There
is a true specialization of the sensors as well as of the
effectors.
In this isobaric system, the brocartilaginous Eustachian
tube and the mastoid are capable of active counter-regulation
of the middle ear cleft pressure variations and function in a
complementary way where the tube is related to the intermittent regulation of higher pressures (it is a security valve) and
where the mastoid is related to the continuous regulation of
smaller pressures, especially of climatic origin. In the isobaric system of the middle ear cleft, the key point is the “neuronal reex arc,” based on a mechanism that is highly
sensitive to a pressure gradient between the middle ear cleft
and the ambient environment, on the one hand, and on an
effector process of pressure balancing, on the other hand—a
neural feedback control similar to the respiratory control and
related to similar central centers in the nucleus of the solitary
tract of the brainstem [22–24].
The afferent plexus of the “neuronal reex arc” are the
mechanoreceptors, barosensors, located in the epitympanum
and antrum, the pars accida, and those located in the pharyngeal recess and the posterior rhino pharyngeal wall. The
efferent plexus of the “neuronal reex arc” are the tubal muscles, resulting in tube opening, and the blood vessels of the
mastoid mucosa, regulating middle ear cleft gas exchanges.
In normal conditions, i.e., in a healthy mucosa, when a
pressure gradient between the middle ear cleft and the ambient environment is detected, two distinct and combined patterns contribute to maintain near-ambient pressures in the
middle ear cleft, namely, the tubal opening with steep intermittent changes in pressure against 0Pa and mastoid-related
changes in pressure, which are gradual and appear in both
negative and positive directions and which could transverse
0Pa into opposite pressures. These gradual pressure changes
by gas exchanges are related to the perfusion of the mastoid
mucosa (Table7.1).
The “neuronal reex arc” of the isobaric system of the
middle ear cleft can be reeducated, an extremely important
property in the clinical management of gas and pressure disorders in the middle ear cleft [25, 26].
Fig. 7.1 Schematic representation of the middle ear cleft isobaric system
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B. Ars and D. Estève
Table 7.1 Schematic characterization of the middle ear cleft isobaric
system effectors
Gas exchanges Isobaric function
System type Sensory reex loop then neuro-muscular and
neuro-vascular with common barostatic
integrating center
Starting point
Baroreceptor
sensitivity (innate
character)
Center Inferior salivary nucleus
Level of intervention Immediate Tubal opening:
Type of response
after implementation
Effects on middle
Ear/blood gas
concentration
Circumstances of
implementation
Acknowledgment We thank Professor Jean Lebacq for thoroughly
reviewing this chapter.
Pars accida of the
tympanic membrane
(TM)
Stretch receptors
∆P>0.1mbar and low
pressure rise slope
Slow Fast
Maintained balance Imbalance
Works permanently Only if there is
Tubal ridge area
Rufni corpuscles
∆P≥10mbar and
high pressure rise
slope
early, late, or
absent (areexia)
middle ear cleft
barotrauma risk
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