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13 Dizziness andVestibular Disorders
143
ear. The sudden change in inner ear pressure due
to leakage of this uid may trigger episodes of
vertigo as well as producing some chronic damage to hair cells. Changing pressure in the external ear (such as with insufation through an
otoscope) may also precipitate attacks in both of
these conditions. This has been termed
“Hennebert’s sign”. Although this has also been
suggested as a “stula test”, this is not specic
for perilymph stula. Precipitation of attacks by
changes in pressure (airplanes, driving in mountains, and Valsalva) is more characteristic of perilymph stula (see Chap.14).
13.5 Central Causes ofVertigo
The central causes of vertigo include cerebrovascular disease (including transient ischemic
attacks), multiple sclerosis, Chiari malformation,
and any other conditions directly damaging the
caudal brain stem or the vestibulocerebellum.
13.5.1 Chiari Malformation
Chiari malformation is dened by protrusion of
the lower portion of the cerebellum through the
foramen magnum. This compresses the caudal
brain stem and vestibular areasand can cause dizziness andimbalance. It is often associated with
an occipital headache and downbeat nystagmus,
which strongly suggest an abnormality at the craniocervical junction. Coughing, sneezing, straining, or neck extension can all make these
symptoms worse.
Vertigo can be the presentation of vertebro-
basilar ischemia, and in fact, vertigo is the most
common initial isolated symptom and sign of
ischemia in the posterior circulation.
Typical vertebrobasilar patients are older and
have multiple vascular risk factors.
Vertebrobasilar insufciency typically causes
multiple cranial nerve symptoms (e.g. visual
abnormalities, diplopia or oscillopsia, dizziness,
or dysphagia) and may culminate in frank
syncope.
Typically, vertigo in vertebrobasilar TIAs is
abrupt in onset and usually lasts several minutes.
When the vertigo is accompanied by other symptoms of brainstem ischemia (e.g. visual symptoms, drop attacks, extremity numbness, or
dysarthria), one would assume that vertigo
derives from vertebrobasilar ischemia.
13.5.3 Vertebral Artery Dissection
Vertebral artery dissection is a rare but serious
condition that can result from neck trauma. This
may occlude branches that go to the vestibular
area of the brain stem or cerebellum andcausevertigo.Any new onset of vertigo after neck trauma
should evoke the diagnosis of vertebral arerty
dissection.
13.6 Disequilibrium
This is a common type of dizziness in the
elderly. This is due to disturbance of sensory or
motor control systems that are necessary to maintain the upright posture.
13.5.2 Vertebrobasilar Insuciency
Dizziness and imbalance are common problems
inelderly patients.
Although BPPV accounts for majority of
cases of vertigo in thispopulation, the presentation of an elderlypatient with vertigo, including
position-dependent vertigo, must address the
possibility of vertebrobasilar ischemia.
• Sensory disequilibrium: The vast majority of
cases of disequilibrium are due to sensory difculties. This typically occurs with gradual
decrease in sensory acuity in several systems.
Usually, there is diminished sensitivity to joint
position in the feet, along with some decreased
sensitivity of the inner ear balance organ. The
symptoms typically are exacerbated in situations where the vision is obstructed.
144
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This kind of decit usually shows dramatic
improvement when the patient touches or
holds onto a stationary object (replacing the
loss of sensitivity in feet with the sensitivity of
the hands). These patients improve with a
cane or other gait-assistive device.
• Motor disequilibrium: Patients with
Parkinson’s disease or cerebellar disease often
have disequilibrium due to motor difculties.
This limits their ability to respond to the
changing conditions of ambulation. Slowed
responses in Parkinson’s disease or incoordination and cerebellar disease may make the
patient entirely unable to walk safely. The
patient perceives this as disequilibrium.
Take-Home Messages
• Assessment of a dizzy patient starts by
obtaining a proper history and examination in order to reach a diagnosis and
offer the best management.
• Vertigo is due to imbalances of signals
to the central vestibular apparatus. It can
either be due to peripheral or central
causes. Signs and symptoms can usually
distinguish peripheral from central
causes of vertigo.
• Peripheral vertigo is due to damage of
the inner ear receptors or to the vestibulocochlear nerve.
• Central vertigo is due to damage to the
central nervous system mainly the brain
stem. It is typically milder than peripheral vertigo.
• Vestibular disorders include vestibular
neuritis, Meniere’s disease, benign paroxysmal positional vertigo, and
migraine-associated vertigo.
• Vestibular neuritis is an inner ear dis-
ease characterized by a sudden drop in
ipsilateral vestibular function and acute
onset of severe vertigo without any neurologic decits.
• Meniere’s disease (MD) is characterized
by episodic spontaneous vertigo, uctu-
H. Haidar and R. H. A. Azzam
ating hearing loss, aural pressure, and
tinnitus.
• Benign paroxysmal positional vertigo
(BPPV) is the most common peripheral
vestibular end-organ disease and characterized by a sudden, transient vertigo
accompanied by a characteristic nystagmus. 95% of BPPV cases involve the
PSC, and 5% involve the LSC.
• Migraine-associated vertigo is diagnosed based on excluding other causes,
history of migraine, and presence of
vestibular symptoms.
References
1. Davis A, Moorjani P. The epidemiology of hearing and balance disorders. In: Luxon LM, Furman
JM, Martini A, Stephens D, editors. Textbook of
audiological medicine. London: Dunitz M; 2003.
p.89–99.
2. Neuhauser H. Epidemiology of vertigo. Curr Opin
Neurol. 2007;20:40–6.
3. Sekitani T, Imate Y, Noguchi T, etal. Vestibular neuronitis: epidemiological survey by questionnaire in
Japan. Acta Otolaryngol Suppl. 1993;503:9–12.
4. Theil D, Arbusow V, Deurfuss T, et al. Prevalence
of HSV-1 LAT in human trigeminal, geniculate, and
vestibular ganglia and its implication for cranial nerve
syndromes. Brain Pathol. 2001;11(4):408–13.
5. Baloh RW, Ishiyama A, Wackym P, et al. Vestibular
neuritis: clinical–pathological correlation.
Otolaryngol Head Neck Surg. 1996;114:586–92.
6. Schuknecht HF, Kitamura K. Vestibular neuronitis.
Ann Otol Rhinol Laryngol. 1981;78:1–19.
7. Nadol JB.Vestibular neuritis. Otolaryngol Head Neck
Surg. 1995;112:162–72.
8. Arenberg IK, Balkany TJ, Goldman G, et al. The
incidence and prevalence of Meniere’s disease–a statistical analysis of limits. Otolaryngol Clin N Am.
1980;13:597.
9. Stahle J, Stahle C, Arenberg IK. Incidence of
Meniere’s disease. Arch Otolaryngol. 1978;104:99.
10. Rauch SD, Merchant SN, Thedinger BA.Menière’s
syndrome and endolymphatic hydrops: double-blind
temporal bone study. Ann Otol Rhinol Laryngol.
1989;98:873–83.
11. Merchant SN, Adams JC, Nadol JB.Pathophysiology
of Menière’ syndrome are symptoms caused by
endolymphatic hydrops? Otol Neurotol. 2005;26:
74–81.
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13 Dizziness andVestibular Disorders
145
12. Pyykkö I, Nakashima T, Yoshida T, Zou J, Naganawa
S. Meniere’s disease: a reappraisal supported by a
variable latency of symptoms and the MRI visualisation of endolymphatic hydrops. BMJ Open.
2013;3(2):e001555.
13. Lamounier P, Gobbo DA, de Souza TSA, de Oliveira
CACP, Bahmad F.Electrocochleography for Ménière’s
disease: is it reliable? Braz J Otorhinolaryngol.
2014;80:527–32.
14. Stewart W, Shechter A, Rasmussen B. Migraine
prevalence. A review of population based studies.
Neurology. 1994;44(Suppl 4):S17–23.
15. Selby G, Lance JW. Observations on 500 cases of
migraine and allied vascular headache. J Neurol
Neurosurg Psychiatry. 1960;23:23–32.
16. Niemensivu R, Pyykko I, Erna K.Vertigo and imbalance in children. Arch Otolaryngol Head Neck Surg.
2005;131:996–1000.
17. Lempert T, Neuhauser H.Migrainous vertigo. Neurol
Clin. 2005;23:715–30.
18. Ralli G, Atturo F, deFilippis C.Idiopathic benign paroxysmal vertigo in children, a migraine precursor. Int
J Pediatr Otorhinolaryngol. 2009;73:S16–8.
Perilymphatic Fistula
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AishaLarem, Ma’inAliAl Shawabkeh,
andAdhamAljariri
14
14.1 Introduction
Perilymphatic stula is an abnormal connection
between the labyrinth and structures surrounding
it [1]. It is a condition that can present with a variety of non-specic symptoms; it is considered a
diagnostic challenge. A proper history and physical examination is a key element during workup
of those patients. Treatment options vary depending on the severity and response to medical therapy and conservative measures.
14.2 Clinical Manifestations
It has a wide range of symptoms:
1. Hearing loss [2]
(a) It is the most common symptom.
A. Larem (*)
Hamad Medical Corporation, Doha, Qatar
Otology Clinical Fellow, Hamad Medical
Corporation, Doha, Qatar
e-mail: alarem@hamad.qa
M. A. Al Shawabkeh
Otology Clinical Fellow, Hamad Medical
Corporation, Doha, Qatar
e-mail:
MAIGhshoum@hamad.qa
A. Aljariri
Hamad Medical Corporation, Doha, Qatar
e-mail: AAljariri@hamad.qa
(b) It can show high frequency, low frequency,
or even a at sensorineural hearing loss.
(c) It tends to uctuate.
(d) It can sometimes present with conductive
hearing loss.
2. Vertigo [2]
(a) It is the most common reason for seeking
medical advice.
(b) It can resemble Benign paroxysmal posi-
tional vertigo (BPPV) or Meniere’s
disease.
(c) It can mimic disequilibrium in certain
occasions. For example, patients may present with disequilibrium upon exposure to
loud voices (Tullio’s phenomenon) or by
increasing Cerebrospinal uid (CSF) pressure (during lifting or blowing of the nose).
3. Tinnitus [3]
(a) Other symptoms of perilymphatic stula
usually accompany tinnitus.
14.3 Workup
• Diagnosis of the perilymphatic stula is usually tricky, but it is mainly based on history,
physical examination ndings, and exclusion
of other diagnoses.
• Some tests that can be used are as follows:
– Audiometry: it can show high frequency,
low frequency, or at sensorineural hearing
loss. A low-frequency conductive hearing
© Springer Nature Switzerland AG 2021
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_14
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147
148
A. Larem et al.
loss can be seen in superior semicircular
canal dehiscence. It is recommended to do
the test in lateral decubitus while the
affected ear is up [4, 5].
– Fistula test: the presence of nystagmus
upon applying pressure on the external
auditory canal is considered a positive stula test. Hennebert sign is the presence of
a positive stula test without any middle
ear pathology [5].
– Measuring of postural sway upon applying
pressure on the external auditory canal [5].
– Electronystagmography/videonystagmog-
raphy: It can show unilateral weakness. It
can also be used to increase the sensitivity
of a stula test [6].
– Some other methods were utilized to help
in diagnosis, like measuring Beta 2 transferrin and using uorescein to detect perilymphatic stula. However, their
utilization has been questioned and still
in doubt [7, 8].
– Exploration: it is considered unreliable for
spontaneous perilymphatic stula.
However, its reliability is increased in the
presence of a temporal bone fracture or
stapedectomy surgery in a patient’s history [3].
Table 14.1 Location and the probable etiologic causes
of perilymphatic stula
Otic capsule Oval window Round window
• Cholesteatoma
• Temporal bone
fracture
• Superior
semicircular
canal dehiscence
Fig. 14.1 Traumatic rupture of the tympanic membrane
caused by barotrauma
• Barotrauma
• Head trauma
• Stapedectomy
• Acoustic
trauma
• Barotrauma
• Mondini
dysplasia
14.4 Management
• Conservative: Bed rest, head elevation, and
avoid straining [3].
• Surgical management in case of failure to
respond to conservative therapy. It consists of
patching the otic capsule. Some surgeons
patch the oval and round window regardless of
the intraoperative ndings as the detection
rate of the perilymphatic stula is quite low.
Fat, perichondrium, fascia, and temporalis
muscle can be used for patching [3, 9].
14.5 Etiologic Causes
Look at Table14.1.
14.5.1 Barotrauma (Fig.14.1)
• Pressure changes can cause damage to the
inner ear by three mechanisms:
– Alternobaric trauma: it occurs in cases of
increased pressure or asymmetrical pressure of the middle ear. It usually occurs
more during the ascent of the divers or
ascent of the planes. Conditions that affect
the functions of the eustachian tube
(URTI, sinusitis) can increase individual’s
susceptibility to these kinds of trauma
[10].
– Atmospheric barotrauma: it occurs in cases
of the increase of the air pressure, which
can cause middle ear and inner ear damage.
It usually gives long-lasting symptoms as
compared to the alternobaric trauma [10].
14 Perilymphatic Fistula
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149
– Inner ear decompression sickness: it occurs
due to the formation of bubbles in the labyrinth or its blood supply. It happens in deep
water divers who use mixed gases like oxyhelium [3].
14.5.2 Acoustic Trauma
• Explosive blast produces sound more than
200dB, which can cause tympanic membrane
(TM) perforation and disruption of the ossicles. Inner ear injury can happen, especially if
conductive mechanisms are not disrupted [1].
14.5.3 Trauma
• It can happen in cases of head trauma or penetrating injury with or without temporal
bone fracture. However, it is rare to have a
perilymphatic stula after trauma in normal
temporal bone anatomy. Look at Fig.14.2
[10, 11].
Fig. 14.2 Axial CT scan of left temporal transverse
fracture (arrow) (Image Reprinted with permission from
Elsevier: Elsevier books, Skull base imaging, Bert De
Foer, Abdellatif Bali, Anja Bernaerts, Joost van Dinther,
Erwin Offeciers, Jan W. Casselman, Jan 1, 2018)
14.5.4 Stapedectomy
• Perilymphatic stula can happen after stapedectomy. It can be a primary or secondary one.
– Primary: if it presents at the end of the
procedure.
– Secondary: if it manifests months or years
after the procedure.
• It is more common in stapedectomy than
stapedotomy.
• It is more common in revision surgeries.
• The use of gelatin sponge to seal the stapedectomy presents the highest risk of developing
the stula [10].
14.5.5 Superior Semicircular Canal
Dehiscence
• Prevalence: It can be seen in 4–8% in highresolution CT [2].
• Pathogenesis: It is often multifactorial (congenital and acquired factors) [10].
• Symptoms: Patients can have only vestibular
symptoms, only auditory symptoms, or a combination of both [10, 12]. They often present
with hearing loss, autophony (they can hear
their voice), pulsatile tinnitus, and hearing the
movement of their eyes (due to increased bone
conduction). They can present with the Tullio
phenomenon (vertigo and imbalance after
exposure to loud voices). They might complain
of vertigo and imbalance after conditions that
increase Cerebrospinal uid (CSF) pressure.
Pure tone audiometry shows conductive hearing loss (CHL) with a larger air-bone (AB) gap
at low frequencies [10].
• Diagnosis: High-resolution CT scan.
Dehiscence can be seen in coronal view,
Stenvers view (in the plane of orthogonal), or
Poschl view (in the place of the SSC) [13]. CT
usually overestimates the size of the dehiscence. To improve the specicity, then 0.5mm
CT scan should be reformatted to the Poschl
plane [14] Fig.14.3.
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150
Fig. 14.3 Coronal CT scan of left IAM demonstrating left superior semicircular canal dehiscence, and next image
shows SCC intraoperatively
A. Larem et al.
• VEMP: it has high sensitivity and specicity (around 90%). Patients with SSC dehiscence will have a lower threshold in the
affected ear for both air and bone conduction [1].
• Treatment: if patients have mild symptoms,
then conservative measures should be taken.
Insertion of ventilation tubes can relieve
pressure symptoms. If symptoms are severe,
then surgical correction should be considered [10].
• Surgical Approaches [10].
– Middle cranial fossa craniotomy: gives a
good exposure. Disadvantages are risks of
craniotomy, more extended hospital stay,
and temporal bone retraction.
– Endoscopic middle cranial fossa: it has
less hospital stay but still has risks of
craniotomy.
– Transmastoid: avoid craniotomy risks but
do not have direct exposure to the SSC.
• Patients usually have variable auditory functions depending on the organ of Corti formation and the number of neurons.
• Now it is subtyped into three types: Type 1,
entire modiolus and interscalar septa are lacking (it has a cystic appearance), Type 2, nor-
mal base turn with a cystic apex (Mondini
type), and Type 3, where the modiolus is de-
cient (it has partial septation on the interscalar
at the periphery of the cochlea).
14.5.7 Congenital Perilymphatic
Fistula
• It is an abnormal communication between the
inner ear and the middle ear. It is associated with
micro-ssures around the round window or oval
windows and dysplasia of labyrinthine or internal auditory meatus. It is usually suspected if a
child presents with progressive or uctuating
sensorineural hearing loss (SNHL) [10, 15].
14.5.6 Mondini Malformation [2]
(Fig.14.4)
• It is the most common malformation of the
cochlea.
• The cochlea has only 1.5 turns.
• The modiolus is hypoplastic and lacking the
interscalar septum.
14.5.8 Perilymphatic Fistula
inChildren
• It can be seen in temporal bone anomalies and
children who have severe or profound sensorineural hearing loss (SNHL).It can present with
recurrent meningitis or Cerebrospinal uid
(CSF) behind the TM [10].
14 Perilymphatic Fistula
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151
Fig. 14.4 Axial HRCT of the right temporal bone show-
ing type II incomplete partition of the cochlea (Mondini
malformation) with failure of segmentation of the middle
Take-Home Messages
• Perilymphatic stula is a diagnostic
challenge.
• Different images and diagnostic modalities should be used judiciously not to
overwhelm the patient with unnecessary
tests.
• Consider conservative management
rst.
References
1. Flint P, Haughey B, Lund V, Niparko J, Robbins K,
Regan Thomas J, Lesperance M.Cummings otolaryngology. 6th ed. Philadelphia: Elsevier; 2014.
2. Watkinson JC, Clarke RW. Scott-Brown’s otorhinolaryngology and head and neck surgery. 8th ed. Boca
Raton, FL: CRC Press; 2018.
3. Snow JB, Ashley Wackym P. Ballenger’s otorhinolaryngology and head and neck surgery. 17th ed.
Connecticut: People’s Medical Publishing House;
2008.
4. Kita AE, Kim I, Ishiyama G, Ishiyama
A.Perilymphatic stula after penetrating ear trauma.
Clin Pract Cases Emerg Med. 2019;3(2):115–8.
https://doi.org/10.5811/cpcem.2019.1.37404.
5. Hazell JW, Fraser JG, Robinson PJ. Positional audiometry in the diagnosis of perilymphatic stula. Am J
Otol. 1992;13(3):263–9.
and apical turns (arrow) associated with enlarged vestibular aqueduct (VA)
6. Hornibrook J. A balance test for chronic perilymph
stula. Int J Otolaryngol. 2012;2012:163691. https://
doi.org/10.1155/2012/163691.
7. Daspit CP, Churchill D, Linthicum FH Jr. Diagnosis
of perilymph stula using ENG and impedance.
Laryngoscope. 1980;90(2):217–23.
8. Delaroche O, Bordure P, Lippert E, Sagniez
M.Perilymph detection by beta2-transferrin immunoblotting assay. Application to the diagnosis of perilymphatic stulae. Clin Chim Acta. 1996;245(1):93–104.
9. Gehrking E, Wisst F, Remmert S, Sommer
K. Intraoperative assessment of perilymphatic stulas with intrathecal administration of uorescein.
Laryngoscope. 2002;112(9):1614–8.
10. Hughes GB, Sismanis A, House JW.Is there consensus in perilymph stula management? Otolaryngol
Head Neck Surg. 1990;102:111–7.
11. Mikulec AA, McKenna MJ, Ramsey MJ, et al.
Superior semicircular canal dehiscence presenting as conductive hearing loss without vertigo. Otol
Neurotol. 2004;25:121–9.
12. Sequeira SM, Whiting BR, Shimony JS, etal. Accuracy
of computed tomography detection of superior canal
dehiscence. Otol Neurotol. 2011;32:1500–5.
13. Belden CJ, Weg N, Minor LB, Zinreich SJ.CT evaluation of bone dehiscence of the superior semicircular
canal as a cause of sound- and/or pressure-induced
vertigo. Radiology. 2003;226:337–43.
14. Zuniga MG, Janky KL, Nguyen KD, etal. Ocular versus cervical VEMPs in the diagnosis of superior semicircular canal dehiscence syndrome. Otol Neurotol.
2013;34:121–6.
15. Weber PC, Bluestone CD, Perez B. Outcome of
hearing and vertigo after surgery for congenital
perilymphatic stula in children. Am J Otolaryngol.
2003;24:138–42.
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Temporal Bone Trauma
HassaninAbdulkarim, AbdulsalamAl-Qahtani,
andAhmedElsotouhy
Key Points
In this chapter, we will learn:
• Three main conditions involved in temporal bone trauma.
• Types of temporal bone fractures and
their clinical presentation, investigations, and management plans.
• Middle ear trauma and its clinical presentation, investigations, and management plans.
• Barotrauma causes, clinical presentation,
investigations, and management plans.
15.1 Temporal Bone Fractures
15.1.1 Introduction
• Temporal bone is the strongest bone of the
body and at the same time one of the most
complex bone as it contains many important
structures, including the vestibulocochlear
H. Abdulkarim (*) · A. Al-Qahtani · A. Elsotouhy
Hamad Medical Corporation, Doha, Qatar
e-mail: habdulkarim@hamad.qa; aaa2009@qatar-med.
cornell.edu; aelsetouhy@hamad.qa
15
apparatus, carotid artery, jugular vein, and the
facial nerve. Also, it is surrounded by the brain
and other cranial nerves.
• Temporal bone as part of skull base has many
foramina and openings causing weakness
points which are involved by head trauma
leading the fracture to follow these weak
points.
• Temporal bone may involve none or all of these
structures, and also can involve other structures
like cranial nerve (6th, 9th, 10th, and 11th).
• The head is the most commonly injured part of
the body (75% of all motor vehicle accidents).
• Approximately 30% of head traumas have
skull fracture, and the ear is the most frequently sensory organ damaged.
• Temporal bone injury happens in up to 22% of
all skull fractures and is caused mainly by
motor vehicle accidents (around 30%).
• Temporal bone fracture is a common manifestation of head trauma, and 90% of temporal
bone fractures are associated with intracranial
injuries and 9% with cervical spine injury.
• Bilateral temporal bone fractures are present
in 8–29% of all fractures.
• These can be due to blunt or penetrating
trauma, and stab and gunshot wounds are the
most common penetrating wounds. Gunshot
wounds medial to the geniculate ganglion are
usually fatal because it is associated with big
vessels bleeding.
© Springer Nature Switzerland AG 2021
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_15
153
154
H. Abdulkarim et al.
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15.1.2 Types
• Ulrich was the rst to classify temporal bone
fractures into longitudinal and transverse fractures in 1926 [1].
• Ghorayeb and Yeakley studied 150 temporal
bone fractures and found the majority is actually oblique or mixed [2].
• Other classication is otic capsule involvement or sparing.
• Ishman and Friedland classied them into
petrous and non-petrous involvement, where
the petrous-involved fractures have greater
correlation with sensorineural hearing loss
(SNHL) presence [3].
• All these classications are arbitrary but useful to predict the type of injury expected.
Although temporal bone fractures are irregular and non-uniform in their pathway.
• Despite the recent classications, Ulrich’s is
the most commonly used due to its simplicity.
15.1.2.1 Longitudinal Fractures
Longitudinal fractures involve 80% of all temporal bone fractures. They are usually caused
by a lateral force over the mastoid or temporal
squama (temporal or parietal blows). The fracture line parallels the long axis of the petrous
pyramid. It starts in the pars squamosa (mastoid or external auditory canal), extends
through the posterosuperior bony external
canal, continues across the roof of the middle
ear space anterior to the labyrinth, and ends
anteromedially in the middle cranial fossa in
close proximity to the foramen lacerum and
ovale (Table15.1).
Table 15.1 Comparison of longitudinal and transverse
temporal bone fractures with their main corresponding
features
Feature
Incidence 80% 20%
Mechanism Temporal or
CSF otorrhea Common Occasional
Tympanic
membrane
perforation
Facial nerve
damage
Hearing loss Common
Hemotympanum Common Possible
Nystagmus and
vertigo
Otorrhagia Common Rare
Longitudinal
fractures
parietal trauma
Common Rare
20%
(temporary and
delayed)
(CHL)
Common (mild
and temporary)
Transverse
fractures
Frontal or
occipital trauma
50% (severe,
permanent, and
immediate)
Common
(SNHL)
Common
(severe and
prolonged)
mid transversely and ends at the foramen magnum. It may also extend through the internal
auditory canal and injure the nerves directly
(Table
15.1).
15.1.2.3 Oblique or Mixed Fractures
They are a mixture of both longitudinal and
transverse.
15.1.3 Clinical Presentation
15.1.3.1 Bleeding
Into the ear canal from skin and tympanic membrane laceration, hemotympanum (Fig. 15.1),
external auditory canal fractures.
15.1.2.2 Transverse Fractures
Transverse fractures involve 20% of all temporal
bone fractures. They are usually caused by a
frontal, parietal, and less likely occipital blow.
The fracture line runs at a right angle to the long
axis of the petrous pyramid and starts in the middle cranial fossa (close to the foramen lacerum
and spinosum). It then crosses the petrous pyra-
15.1.3.2 Hearing Loss
Conductive hearing loss (CHL) due to ossicular
chain disruption [4, 5]:
• Incudostapedial joint separation (82%)
• Incus dislocation (57%)
• Fracture of the stapes crura (30%)
• Fixation of the ossicles in the attic (25%)
• Incudomalleolar joint separation (<3%)
AL GRAWANY
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