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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4507_Библиотеки_им_академика_М_И_Перельмана.pdf
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history of otitis media is common. Labyrinth involvement causing vertigo and facial
nerve involvement causing facial paresis are rare symptoms. In facial paresis, the
diagnosis of congenital cholesteatoma should not be sufcient, and causes such as
carcinoma and neuroma should be investigated. The lower incidence of intracranial
complications in congenital cholesteatoma in developed countries is associated with
a relatively higher incidence of facial nerve damage and ossicular destruction and
common malformations but with better postoperative hearing outcomes. Propst
etal. found that children with cholesteatoma also have vestibular anatomical anomalies. The most common of these anomalies are a dilated endolymphatic sac, a wide
vestibular aqueduct, and a dysplastic vestibule [38, 39].
Histologically, congenital cholesteatoma is indistinguishable from middle ear
cholesteatoma. Both have a cystic structure formed by desquamated at epithelium
with keratin lamellae in the center. If a child has conductive hearing loss and the
tympanic membrane is normal, a congenital cholesteatoma may be present in addition to congenital anomalies. This child should be evaluated with imaging studies.
High-resolution computed tomography (CT) or MRI is essential. CT is the imaging
modality of choice. CT can show not only the location of the cholesteatoma but also
its size. A congenital cholesteatoma will appear as a smooth and round mass that is
less dense and whose density cannot be altered by contrast. The inability to change
its density is important because it allows differentiation from other neuroma, glomus, tumor, sarcoma, and meningioma. In contrast to patients with chronic otitis,
mastoid cells and cell growth are normal. Because of the possibility of increasing
density, MRI is helpful in the differential diagnosis between congenital cholesteatomas and neuromas, meningiomas, adenomas, and schwannomas. On the T1
sequence, a congenital cholesteatoma is hypointense relative to the brain but sometimes has the same intensity. On T2 sequence the intensity is high as in BOS.There
is no gadolinium enhancement. Diffusion-weighted imaging can differentiate cholesteatoma from other cystic lesions.
19.7.2 Acquired Cholesteatoma
Acquired cholesteatomas are classied as primary and secondary. While primary
acquired cholesteatomas express the cholesteatomas that develop due to accumulation of keratinous debris in the retraction pouch, secondary acquired cholesteatomas
refer to the cholesteatomas that develop in the presence of perforation of the tympanic membrane. Cholesteatoma should be considered in the presence of deep
retraction pockets, a possible white mass behind the tympanic membrane or granular or polypoid structures, and persistent otorrhea. No single mechanism has been
dened to explain the development of acquired cholesteatoma. The following theories have been proposed for the development of acquired cholesteatoma [40, 41].
19.7.2.1 Epithelial Metaplasia oftheMiddle Ear Mucosa
It has been argued that the middle ear mucosa transforms into a cholesteatoma
matrix by metaplastic transformation. This theory claimed that as a result of chronic
19 Cholesteatoma
389
and recurrent otitis, the middle ear mucosa is transformed into a desquamated and
keratinized squamous epithelium. It was von Troltsch who stated in 1864 that under
the inuence of pressure and infection, the middle ear mucosa changes into cholesteatoma [42]. Wendt argued that nonkeratinized epithelium of the middle ear can
undergo metaplastic transformation to keratinized epithelium [43]. Sade reviewed
this theory and provided some evidence. Several elements have been shown to facilitate the development of epithelial metaplasia. It has also been shown that vitamin
A deciency and variations in oxygen and carbon monoxide in the environment
facilitate the development of metaplasia. However, while these studies have shown
that the middle ear mucosa undergoes metaplastic changes, they have not shown
that this leads to the development of cholesteatoma. Thus, only the development of
nonkeratinized squamous epithelium has been shown, not the development of keratin production [44–46].
19.7.2.2 Epithelial Migration Theory
It is dened as the growth of at epithelium from a defect adjacent to the tympanic
membrane into the middle ear. These defects are usually marginal perforations and
attic perforations adjacent to the annulus. This situation has been used to explain
secondary acquired cholesteatomas. They occur as a result of migration of the external ear canal skin or multilayered at epithelium in the outermost layer of the membrane into the middle ear. Habermann in 1888 and Bezold in 1890 proposed the
theory of epithelial migration, claiming that squamous epithelium migrates into the
middle ear cavity through perforation of the tympanic membrane [47, 48]. In 1901,
Politzer demonstrated that the epithelium of the external auditory canal could grow
into the middle ear as a result of perforation of the tympanic membrane [49]. This
development can occur as a result of perforation of the tympanic membrane due to
infection, explosion, foreign body or iatrogenic reasons. Since the epithelium of the
tympanic membrane and the epithelium of the cholesteatoma have similar properties, it is assumed that the sides of the perforation will also migrate.
19.7.2.3 Basal Cell Hyperplasia Theory
Proponents of this theory suggest that the subepithelium of the Prossack’s cavity is
invaded by keratinized pseudopods that develop in the basal cell layer of the pars
accida epithelium. An inammatory reaction, possibly due to inadequate ventilation, leads to a rupture of the basal membrane and an epithelial cordon that begins
to proliferate inward. The result is invasive papillary growth of keratinocytes in the
stratum basale. As a result of damage to the basal germinative layer associated with
infection, basal cells send papillary protrusions into the subepithelial cells, and a
cholesteatoma may develop even in the absence of perforation [50, 51].
19.7.2.4 Epithelial Invagination that Develops inRetraction Pockets
In this theory, it has been suggested that retraction pockets develop in the tympanic membrane as a result of ventilation problems in the middle ear, and keratin that accumulates in these pockets leads to the development of cholesteatomas.
Although many studies have been conducted on the pathology of
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cholesteatomas, there is no consensus on how the epidermis reaches the middle
ear. The tympanic membrane plays an important role in the pathogenesis of
cholesteatoma. While the pars flaccida, which makes up the upper 1/3 of the
tympanic membrane, is two-layered, the pars tensa, which makes up the lower
1/3 of the tympanic membrane, is three- layered. Retractions usually occur in
the pars flaccida. The annulus, where the tympanic membrane attaches,
becomes thinner in the posterosuperior part of the external auditory canal and
disappears toward the posterior tympanic bone. Therefore, this region is prone
to the development of retraction pockets. In the medial part of the pars tensa,
there are collagens arranged in a circular structure. This collagen structure
degrades with inflammation, setting the stage for the development of retraction
pockets. Although these precipitating factors can lead to the development of a
retraction pocket, the primary factor is the disruption of ventilation in the middle ear. While Eustachian tube dysfunction is the main factor in middle ear
ventilation, it is not the only factor responsible for the development of a retraction pocket. Blood vessels in the mastoid cells and middle ear mucosa and gas
exchange between the cavities in these regions are the other factors responsible
for regulating middle ear pressure. Causes such as recurrent infections that lead
to decomposition in structures that provide ventilation disrupt middle ear ventilation and cause the development of retraction pockets that trigger the development of cholesteatoma.
Retraction pockets behave differently at different stages. The depth of the retraction pocket, its relationship to middle ear structures, its ability to self-clean, and the
presence of keratinous debris within the pocket are important features in the development of cholesteatoma. To demonstrate how patients should be treated and followed in the event of retraction pocket development, these pockets have been staged
by Mirko Tos and Jacop Sade [52, 53]. These are;
Tos Staging
Stage 1: Retraction pocket is supercial and does not contact middle ear structures.
Ossicular chain is intact.
Stage 2: The bottom of the retraction pocket is visible through the otoscope. It is in
contact with the malleus or long arm of the incus. In cases where the pocket can-
not clean itself, erosion of the ossicular chain may occur.
Stage 3: The retraction pouch adheres to middle ear structures. Scutum erosion is
present.
Stage 4: The retraction pouch is deep and cannot be moved by simple aspiration.
Tympanic anulus bone damage is present.
Sade Staging
Stage 1: Simple retraction of the tympanic membrane
Stage 2: Retraction attached to the incudostapedial joint
Stage 3: Retraction not adhering to the promontorium
Stage 4: Retraction adhering to the promontorium and accumulating keratin (adhe-
sive otitis media)
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391
19.7.2.5 Cholesteatoma Development fromaRetraction Pocket
The upper 1/3 of the middle ear cavity is separated from the other 2/3 by a membranous barrier with some grooves. The air in the middle ear passes through the anterior and posterior isthmuses of this barrier to the epitympanum and ventilates it. If
these two isthmuses are blocked, the pars accida collapses toward the epitympanum. If either is blocked, the upper part of the posterior pars tensa collapses toward
the retrotympanum. For cholesteatomas to develop in these collapse areas, keratinocytes in the stratum basale at the bottom of the collapse zone should grow toward
the middle ear mucosa. Epithelial debris in this retraction begins to destroy the
ossicular chain and adjacent tissues. When the epithelium accumulates in the retraction pockets and cannot clean itself, the process of cholesteatoma development
begins. After the accumulation of keratinous debris, two developments occur. The
rst is the disruption of the self-cleaning process of the at epithelium toward the
center, and the second is the development of Langerhans cells, which are not normally observed in the tympanic membrane. Langerhans cells are known to be the
phagocytic cells of the skin. These cells are thought to be involved in the proliferative activity of cholesteatoma.
Most retraction pockets in the attic region do not lead to cholesteatoma because
the at epithelial migration is not disturbed and they are self-cleaning. In rare cases,
when the self-cleaning mechanism is disrupted with the onset of keratinized epithelial proliferation, keratinous debris accumulating in the pocket may trigger the cholesteatoma development process.
19.7.3 Unclassified Cholesteatomas
A third classication of cholesteatomas, for lesions whose origin cannot be precisely determined, is called unclassied cholesteatomas. In some large and open
cases, it may not be possible to classify the lesions as congenital or acquired cholesteatomas; therefore, they are classied as unclassied cholesteatomas. Other classications, such as posttraumatic and postoperative iatrogenic cholesteatomas, have
also been made.
19.7.4 Petrous Bone Cholesteatomas
Petrous bone cholesteatomas are rare [54]. While they are usually congenital, cholesteatomas located in the mastoid bone may extend to the petrous bone [55]. They can be
difcult to diagnose and treat. In the seventh week of fetal life, ectodermal and endodermal structures are juxtaposed without mesenchymal boundaries between them. At
this time, there is no boundary tissue between the internal and external auditory meatus.
As the epithelium of the external auditory meatus is deposited around the internal auditory meatus, petrous cholesteatomas begin to form. These cholesteatomas cause no
symptoms until they grow and erode the bone. They can damage the internal carotid
and internal acoustic canals in their vicinity. The incidence of facial paralysis due to
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petrous cholesteatoma has been reported to range from 34.6% to 100% [56, 57].
Petrous apex cholesteatomas present with very vague symptoms. Parietal and occipital
headaches may occur as a result of recession of the dura in the immediate vicinity. If
the Eustachian tube is involved, serous otitis may develop. Cholesteatoma of the
petrous bone, which may grow to large sizes, may compress the foramen ovale and
cause paresthesias of the mandibular nerve. In addition, pressure on the carotid artery
may cause confusion, dizziness, and rarely hemiparesis. Posterior diffusion may cause
jugular foramen syndrome. Anteromedial diffusion can lead to the development of cavernous sinus pressure and third, fourth, and fth cranial nerve symptoms. The treatment method is to remove the lesion completely. However, because the petrosal bone
is difcult to access due to its location, marsupialization may be sufcient in some
cases. Approaches such as suboccipital transetmoidal-transsphenoidal approach, middle cranial fossa approach, transplatal-transclival approach, and translabyrinthinetranscochlear approach have been dened to access the petrosal bone [58].
M. Tan et al.
19.8 Practical Classification
Although classical pathogenetic theories are adopted, due to the need for a practical
classication in terms of surgery, cholesteatomas are topographically classied by
Tos as attic, sinus, and pars tensa cholesteatomas, which gained general acceptance
as this classication was useful in understanding the pathogenesis. In this classication, sinus tympany cholesteatomas of the pars tensa segment of the tympanic membrane are posterior retractions. Pars tensa retractions are anterior, inferior, and
posterior pathologies of the tympanic cavity.
19.8.1 Attic Cholesteatomas
These are the types of cholesteatomas that develop from epitympanum, which originates from the retraction of the tympanic membrane associated with the pars accia
and extends to the aditus ad antrum. It may progress to the mastoid and middle ear.
The theory of retraction basal cell metaplasia has been implicated in many mechanisms responsible for the pathology of cholesteatoma. Cholesteatomas do not
always develop from the retraction sac. When it loses its ability to clean itself, debris
begins to accumulate in the sac.
As keratin accumulates, the bottom of the retraction sac opens and the cholesteatoma at this stage deepens toward the middle ear cavities. Thus, resorption of the
adjacent ossicles and scutum begins in attic cholesteatoma [59, 60].
19.8.2 Sinus Cholesteatomas
Sinus cholesteatoma originates from the posterosuperior segment of the pars
tensa of the tympanic membrane. There are vital structures and pockets in close
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393
proximity that are extremely difcult to clean. Sinus cholesteatomas grow and
spread along the tympanic membrane to the facial nerve and medial to the body
of the incus, one of the middle ear ossicles. The anterior part of the tympanic
cavity and the anterior attic are not involved, but they may spread to the posterior
attic and the antrum [61, 62]. Cholesteatomas have been explained by Tos by
retraction and proliferation mechanisms under the classical developmental theories. Acute perforation and accumulation of keratinized epithelium inside and
development of cholesteatoma could not be demonstrated by migration theory.
Metaplasia theory could not explain or prove the development of cholesteatoma.
However, clinical evidence was found with the retraction and proliferation theory. In this theory, there is an unexplained situation in the transformation from
retraction pocket to destructive cholesteatoma. In a study conducted, attic retraction was found to be common in children with tubal dysfunction and recurrent
otitis media [63]. The rst stage is the retraction pocket stage. In this stage, the
retraction pocket cleans itself and there is no accumulation of keratin in it. The
next stage is the two-stage stage of cone formation and cone fusion. These two
stages are proliferation stages. When the migration of the squamous epithelium
from the basal layer to the epithelial layer is normal, keratin does not accumulate
in the retraction pouch and it cleans itself. When this cleansing is disrupted and
proliferation begins in the keratinized epithelium, accumulation in the pouch
begins. It is not clear what triggers this proliferation. Infections of the external
ear canal and cerumen-induced debris accumulation may play a role. Changes in
the middle ear may also interfere with the self-cleaning ability of the retraction
pocket. Middle ear infections and negative middle ear pressure due to Eustachian
tube dysfunction can also trigger this situation. When this cleaning is disrupted,
a cholesteatoma begins to form, and cholesteatoma growth and bone resorption,
which are the nal stages, begin.
The importance of sinus tympany in cholesteatoma surgery is that it is difcult
to clean. Endoscopic control can be performed during surgery. If the surgery is performed with a microscope, prevention by external auditory meatus can be encountered [64].
19.8.3 Pars Tensa Cholesteatomas
The strength of the pars tensa segment of the tympanic membrane is greater than
that of the pars accida. A cholesteatoma resulting from retraction of the pars
tensa grows anteriorly and posteriorly in the middle ear cavity to the entrance of
the Eustachian tube and hypotympanum. It extends into the anterior and posterior attic and medial to the malleus fold. Clinically, pars tensa-related cholesteatomas are not very common [65]. In cases where middle ear ventilation is
impaired and the Eustachian tube does not function, a negative pressure is created. This negative pressure leads to atelectatic changes and retraction of the
membrane. And if the retraction pocket cannot clean itself, a cholesteatoma
develops [66].
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M. Tan et al.
19.9 Clinical Presentations
A cholesteatoma may remain occult for years without clinical symptoms or aggressive progression. It may grow slowly in the temporal bone and lead to life- threatening
intracranial and extracranial complications [67–71]. Patients diagnosed with cholesteatoma may present with a variety of complaints. The diagnosis of cholesteatoma is not difcult for an experienced otolaryngologist. In particular, the use of
endoscopy in the outpatient setting has made the diagnosis easy. These patients may
present with a variety of clinical complaints. The most common complaints are
otorrhea and hearing loss. Patients presenting with these complaints are usually
easy to diagnose. If the patient has developed a complication, the patient may be
referred to another clinic such as pediatrics or neurology. In some cases, the diagnosis of such an important condition may be made incidentally [72].
Ear discharge is one of the most common complaints. Ear discharge is the most
common complaint of patients with chronic otitis media and reduces quality of life.
The discharge is usually malodorous and purulent. It sometimes disappears and
reappears. One of the most important features of this discharge is that it smells bad
due to the high fatty acid content. Purulent odor is caused by bacteria and is eliminated with local therapy. However, the odor associated with bone resorption does
not disappear with treatment and has a thick consistency and yellowish color. Blood
is not present in the discharge of patients, but in the presence of blood, malignancy
should be considered. On otoscopic examination, debris can be seen in the external
auditory canal. They are white and stratied.
19.9.1 Cholesteatoma Microbiology
The middle ear ora of cholesteatoma cases is different from that of simple chronic
otitis media. Gram-negative bacilli are generally dominant in this ora. In addition,
the presence of anaerobic bacteria in the ora has been demonstrated. Microbacteria
may also accompany this picture. Some studies have shown that no bacteria are
produced in 40% of ears with cholesteatoma [73]. Cholesteatoma sets the stage for
infection. In the absence of effective antibiotics, serious complications such as acute
mastoiditis, brain abscess, meningitis, and septic cavernous sinus thrombosis may
occur. Pseudomonas aeruginosa, Staphylococcus aureus, and various Proteus spe-
cies are common aerobic bacteria. Anaerobic bacteria include Bacteroides and
Peptococcus/Peptostreptococcus [74, 75].
Another clinical complaint of patients is hearing loss. The degree of hearing loss may
vary depending on the location of the cholesteatoma. Otoscopic examination, audiological ndings, and radiographic evaluation can be used to determine the extent to which
the cholesteatoma affects hearing. The presence of an air-bone gap greater than 45dB
may indicate a disruption of the integrity of the ossicular chain. Cholesteatoma tissue
also causes ossicular chain lysis by expressing lytic enzymes and mediators. With
respect to this lysis, the long arm of the incus is the most sensitive part of the ossicular
chain because it is the least sanguineous area. The second most common area of erosion
19 Cholesteatoma
is the stapes superstructure [76]. Under the inuence of the cholesteatoma mass, the
ossicles act as a chain and lead to a normal hearing result in the patient. Therefore, an
otoscopic examination of the patient is important. As the cholesteatoma begins to
destroy the inner ear, sensorineural hearing loss and vertigo may occur.
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19.9.2 Dizziness inCholesteatomas
When dizziness and vertigo occur in an ear suspected of having a cholesteatoma, a
labyrinthine stula is the rst thing that comes to mind. The stula test helps in the
diagnosis. In addition, cholesteatoma labyrinth, dizziness, and vertigo may occur
due to the effect of irritation.
19.9.3 Facial Paralysis inCholesteatomas
Cholesteatoma can lead to loss of facial nerve function due to both mechanical and
enzymatic effects. In addition, iatrogenic injury may occur during surgery in cases
of cholesteatoma progressing with granulation tissue. Knowledge of the anatomic
course of the facial nerve and good differentiation from granulation tissue can prevent these iatrogenic injuries. Facial paralysis may be a presenting symptom at the
time of initial presentation. If the cholesteatoma has completely invaded the facial
nerve and cannot be excised, an open surgical technique can be used and the patient
followed closely in the postoperative period. In cholesteatoma-related facial paralysis, facial nerve function has a poor prognosis. In general, facial paralysis occurs as
a result of invasion of the cholesteatoma into the area between the fallopian canal
and the nerve. In addition, inammatory changes that often occur in the vicinity of
the cholesteatoma may lead to the development of cholesteatoma-related facial
palsy. One study showed that early surgical intervention positively inuenced the
prognosis of cholesteatoma-related facial paralysis [77]. Fever, headache, and otalgia are atypical symptoms associated with cholesteatoma. If intracranial and extracranial complications have not developed, these symptoms will not be seen, and if
these symptoms are seen, prompt intervention is necessary. Delayed surgical intervention may result in fatal complications. These symptoms are particularly important in children. If otorrhea persists for more than two weeks and is refractory to
treatment, cholesteatoma should be considered. Hearing loss in a previously operated patient may be a warning sign [78, 79]. Together with a higher socio- cultural
status, it is possible to identify patients at an early stage.
19.9.4 Complications inCholesteatomas
Cholesteatomas can cause erosion of the middle ear bones and lead to intratemporal and intracranial complications. While cholesteatomas in the mastoid
bone are at risk for intracranial complications, erosion of the fallopian canal,
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can lead to facial paralysis. Especially in cholesteatoma, it is possible to see
Fallopian canal dehiscence (FCD) due to chronic otitis media (COM). The
prevalence of FCD was reported as 11.29% [80]. Total sensorineural hearing
loss and dizziness may result from labyrinth bone erosion [81]. Petrositis may
develop as a result of cholesteatoma of the petrous apex. The comorbidity of
cholesteatoma and infection may lead to mastoid erosion and subperiosteal
abscess, and the patient may present with a posterior mastoid rash and discharge. The presence of meningeal irritation symptoms such as severe headache in a chronic otitis patient with intermittent otorrhea suggests cholesteatoma,
and similar symptoms in patients diagnosed with cholesteatoma should suggest
intracranial complications. Most of these symptoms have become less common
in recent years due to easy access to an otolaryngologist.
19.10 Diagnosis
Early diagnosis of cholesteatoma is important to prevent potential complications.
These complications can range from very mild to life-threatening. Surgery to protect hearing is possible in patients diagnosed early, especially in the case of congenital cholesteatoma. Clinical suspicion should be followed by otoscopic,
endoscopic, and microscopic evaluation. Subsequent imaging and audiologic testing facilitate diagnosis.
19.10.1 Otoscopic andEndoscopic Examination
In the past, only otoscopy was performed. Now, all patients presenting to most outpatient clinics can be evaluated with endoscopy. An otoscopic examination should
be performed rst. The otoscope should have adequate illumination and the speculum of the otoscope facing the ear should be suitable for the external auditory canal.
For effective examination, the external auditory canal should be clean and free of
cerumen. After cleaning the external auditory canal, all quadrants of the membrane
should be examined. In particular, the posterosuperior segment should be examined
carefully. Any infection in the external ear canal should be treated to avoid misdiagnosis. Later, microscopic examination can be performed, but the widespread use of
endoscopy in recent years has made endoscopic examination more practical. Easy
installation and use have contributed to this popularity. In particular, it has made it
easy to examine the retraction pouch. It makes it easy to see keratin accumulation in
the pouch.
A patient presenting with an ear problem should be evaluated in both ears and a
complete otolaryngologic evaluation should be performed. It should be remembered
that comorbid eustachian dysfunction is common in pediatric patients. A patient
with a problem in one ear may have a problem in the other ear. Findings should be
documented. Endoscopic documentation of a retraction pocket will facilitate patient
follow-up.
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397
19.10.2 Computed Tomography
After otoscopic and endoscopic examination, CT is the rst examination to be
requested when cholesteatoma is suspected. It is of great importance in determining the extent of the disease and the surgical limits of the operation to be performed. Along with the use of high-resolution CT, otologists have begun to use it
in diagnosis. In preoperative planning, the tomography should be carefully analyzed. It helps the surgeon determine whether the disease has resulted in potential
bone destruction and damage to vital structures. The course of the facial nerve
should be examined. It should be checked if there is an opening on it. The structures of the middle ear should be examined to see if the jugular bulb is high or not.
Check for resorption and tegmen defects in the semicircular canals. Whether a
sclerotic and well- ventilated mastoid will be encountered during surgery and
whether there is an anteriorly located sigmoid sinus or inferiorly located dura can
be determined by tomography. High-resolution CT also has limitations. It is difcult to differentiate cholesteatoma from granulation, brosis, and chronic inammation [82, 83].
Tomography is inadequate to assess the status of membranous structures, e.g.
labyrinthine structures, and the degree of involvement of intracranial structures. It is
not possible to differentiate cholesteatoma from brosis that develops in the evaluation and follow-up of operated patients [84–86].
19.10.3 Magnetic Resonance Imaging
MRI is now widely used in the preoperative and follow-up phases. The absence of
radiation is a major advantage of this imaging technique. It should be used especially for recurrent imaging and follow-up in children with congenital cholesteatoma. The classic technique is postgadolinium MRI (DP-MRI). With DP-MRI, it is
difcult to differentiate granulation tissue from brosis or hemorrhage [87, 88].
There have been some advances in MRI algorithms. In this context, diffusionweighted imaging (DW-MRI) has begun to be used. Studies support DW-MRI as a
reliable diagnostic tool for unoperated and recurrent/residual cholesteatoma, and
second-look surgery has been found to be an appropriate choice [89]. The sensitivity and specicity of DW-MRI in the diagnosis of cholesteatoma were found to be
greater than 94% [90]. When comparing the two modalities, echoplanar (EPI)
DW-MRI and non-echoplanar (non-EPI) DW-MRI, non-EPI was found to be technically superior [91, 92]. Non-EPI can give good results in the presence of signicant difculties such as poor spatial resolution and radiologic artifacts secondary to
the air–bone interface of the skull base [89]. A signicant difference between these
two techniques is related to the size of the cholesteatoma. Non-EPI MRI can detect
up to 2mm, while EPI MRI can detect up to 5mm [93, 94]. The combined use of
high-resolution CT and MRI is important for diagnosis and follow-up. The use of
non-EPI DW MRI in postoperative follow-up reduces the frequency of second-look
surgery [95, 96].