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153
Spontaneous Perilymphatic Fistulae
A spontaneous perilymphatic stula is one that occurs without an obvious external
inuence. This includes the absence of any antecedent external events such as diving, ying or head trauma. Using this rigid denition, the medical literature documents only a very small percentage of patients developing a spontaneous
perilymphatic stula [25].
Symptoms of “spontaneous” PLF are similar to those of poststapedectomy
PLF—vertigo and hearing loss with Valsalva-type maneuvers (bending, straining,
coughing, etc.).
In an attempt to explain the concept of spontaneous PLFs, Goodhill [26] proposed the following theory: An implosive (originating from Valsalva force-induced
increased pressure in the middle ear) which then resulted in either the oval and or
round window rupturing which then resulted in a PLF.He also postulated that an
increased cerebrospinal uid (CSF) pressure could result in an explosive force
resulting in a PLF.
There are some reports in which individuals were found to have PLF symptoms
with no history of trauma or an antecedent event. The precise numbers of these
“spontaneous” or “idiopathic” cases of PLF are hard to truly ascertain. Although
many patients were termed to be suffering from PLF and were characterized as
“spontaneous,” it is probably more accurate to refer to them as “idiopathic.” This is
because the term “spontaneous” can have a small but signicant difference in its
categorization. Occasionally some of these “spontaneous” patients will cite a signicant event which they will link to the onset of the suspected PLF, including
something as trivial as sneezing, straining, nose blowing, laughing, or even bending
over. This loose denition has thus spawned controversy over what constitutes an
idiopathic PLF.
One possible cause of idiopathic PLF may be from congenital malformations
and microssure formation. Microssures can occasionally develop in multiple
areas in the temporal bone. Microssures that develop between the round window
niche and the posterior canal ampulla and around the oval window have been
described [5]. These microssures are postulated to act as a possible cause of PLFs.
Microssures can also present as a variant of normal ndings on radiological imaging [27] On occasion, defective temporal bone remodeling can contribute to the
development of PLF [19]. Similarly, perilymph can leak through the ssula ante
fenestram as well [9]. In normal human development, the ssula ante fenestram is a
bony cleft present in all individuals that remodels and lls with cartilage and mesenchymal tissue in embryological development. Should this remodeling get altered
in any way this could possibly result in a patent cleft through which perilymph
can leak.
An additional postulated cause of idiopathic perilymphatic stula is elevations in
intracranial pressure [26]. The theory holds that increased CSF pressure is transmitted to the labyrinthine uids, which in turn leads to a leakage at the oval and/or
round window.
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One challenge in diagnosing PLF without an obvious contributing event is that
the audiovestibular symptoms of a PLF overlap with many other clinical conditions,
including third mobile window syndromes (superior or posterior canal dehiscence),
vestibular migraine, endolymphatic hydrops, Meniere’s disease, Eustachian tube
dysfunction, and persistent postural-perceptual dizziness. Thus, clinicians should
maintain high index of suspicion for a PLF when individuals with nonspecic
audiovestibular symptoms do not respond to conventional medical treatments or
vestibular rehabilitation. This is particularly true when there is a history of onset of
symptoms after trauma or an antecedent inciting event.
When patients present with vague auditory or vestibular complaints provided by
movement, a full battery of audiologic and vestibular testing is warranted to rule out
other potential causes of symptoms. These include
1. Audiometry in PLF it would demonstrate a sensorineural hearing loss
2. Cervical vestibular-evoked myogenic potential (cVEMP)
3. Electrocochleography
4. The stula test, during videonystagmography
These methods have varying sensitivity. They are helpful in localizing the
affected side or in distinguishing nystagmus invoked by noise or pressure changes.
The stula sign is a clinical nding that has traditionally been used; a positive
stula sign is dened as nystagmus when negative pressure is applied to the external
auditory canal using Siegel’s speculum.
These basic tests though they lack specicity must be performed as base line
tests in the documentation of patients suspected to be suffering from PLFs.
C. de Souza et al.
Radiological Imaging
High-resolution computed tomography (CT) and magnetic resonance imaging
(MRI) have played a signicant role in the detection of PLFs. One of the earliest
described radiological signs of a PLF is a pneumolabyrinth. Small bubbles of air can
be hard to visualize on a standard CT scan. Patients suspected to be suffering from
PLFs should undergo high-resolution CT imaging with reformations in the coronal
and sagittal planes. Fluid in the round and oval window is a reliable sign of a PLF.A
study by Venkatasamy et al. [28] found that high-resolution CT scanning of the
temporal bone has a sensitivity for detection of PLFs of over 80% when compared
to intraoperative visualization of the suspected perilymph leak. They reported that
when CT scanning and MRI were used in patients suspected to be suffering from
PLFs the specicity was reported to be close 100% of cases. Some authors have
found that axial and coronal CISS (constructive interference in steady state) also
called FIESTA (fast imaging employing steady-state acquisition) or MPR (magnetic resonance perfusion) sequence to be the most useful sequences in the detection of PLFs. MRI was found to be very helpful and accurate in identifying
congenital abnormalities that contribute to PLF formation. MRI was also found to
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signicantly reduce the need for CT imaging in children. While avoiding CT scanning in children will eliminate concerns with regard to radiation, MRI imaging in
children will often require a general anesthetic. False-negative cases may be due to
scarring or intermittent or slow leakage of uid, whereas false-positive cases were
likely caused by normal hypodensities seen in the cochlea motion artifacts, or
inammation. Furthermore it should be remembered that PLFs can be intermittent
in nature, increasing the amount of false-negative cases. CT and MRI imaging have
increased value in acute posttraumatic or postoperative patients with large PLFs. CT
scanning is very helpful in ruling out other causes of third window syndrome such
as superior or posterior canal dehiscence, enlarged vestibular or cochlear aqueduct,
and carotid or facial nerve-cochlea stula, all of which have similar presentations to
that of PLFs.
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Biomarkers
The use of biomarkers for the detection of perilymph uid has greatly increased the
accuracy of the detection of PLF by its high sensitivity. Beta-2 transferrin is actively
used around the world for the diagnosis of CSF leakage, and has recently been proposed as a marker for perilymph. Cochlin tomoprotein (CTP) was introduced by
Ikezono etal. in 2009 [29], and has been recently approved in 2020in Japan as an
ELISA test for perilymph detection, though is not widely available for use. Beta-2
transferrin is a protein found in higher concentration in CSF, vitreous humor, and
perilymph. While many consider it a promising biomarker for perilymph, some
researchers have raised concerns regarding sample contamination with blood, blood
plasma, CSF, and beta-1 transferrin. Unlike beta-2 transferrin, CTP is a protein
found in perilymph. Its presence in CSF is negligible. Western blot and ELISA testing of uid and lavages from the middle ear for CTP shows promise as a reliable
diagnostic tool for PLFs. Currently, the test is limited by the presence of CTP in
blood. This could possibly represent a route for sample contamination. Lavage techniques and centrifugation should dilute or remove any blood in the collected in the
sample so as not to affect the nal result of the CTP analysis.
Conclusions
1. Perilymphatic stulae can present in diverse ways.
2. PLFs predominant symptoms are (a) uctuating hearing loss, (b) tinnitus, (c)
Vertigo, and (d) aural fullness.
3. Idiopathic PLFs are the most difcult to prove.
4. Radiological imaging using CT scans of the temporal bone and MRI has proved
to be very valuable in the diagnosis of PLFs.
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5. Biomarkers such as Beta-2 transferrin and cochlin tomoprotein (CTP) are prom-
ising in conrming the presence of a PLF.
6. Surgery is the treatment modality of choice when treating a conrmed PLF that
does not immediately respond to conservative measures.
C. de Souza et al.
Vertebral Artery Dissection
Christopherde Souza, AishanPatil, Rosemariede Souza, VimalSomeshwar
and ManishSrivastav
Introduction
Vertebral artery dissection (VAD) is an unusual and rare cause of Cerebrovascular
accident (CVA)/stroke. However, in patients younger than 45years of age, the incidence of VAD has been found to be higher. Signs and symptoms of VAD are not
pathognomonic which makes diagnosis difcult. While spontaneous dissections are
known to occur, incidental, minor trauma is usually responsible for precipitating
this potentially dangerous condition.
Neck manipulation through chiropractic manipulation [30], bending of the neck,
or blunt trauma causes the dissection. Spontaneous dissection is also known to
occur but is far less common. The dissection of the artery may ultimately lead to a
stroke which often can be delayed for days following the acute dissection.
Most of VAD are intracranial. Several reports nd that vertebral artery dissection
may be responsible for around 20% of ischemic strokes in the young.
Etiology
Patients often report minor, trivial precipitating events before the onset of symptoms. Coughing, vomiting, chiropractic procedures are frequently reported by
patients before symptoms manifest themselves. Blunt trauma to the neck is also
reported to be an initiating event in VAD [31]. Patients with connective tissue disorders like Ehlers–Danlos syndrome is the most common connective tissue disorder
that can likely cause vertebral artery dissection. Twenty percent to 40% of patients
with serious cervical cord injury or spine fractures will demonstrate VAD [32].
Other risk factors [33, 34] for vertebral artery dissection include:
• Forceful nose blowing
• Extension of neck for prolonged periods of time
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• Wrestling
• Hypertension
• Fibromuscular dysplasia
• Oral contraceptives
• Vasculitis. Matrix metalloproteinase (MMP-9) [35] is thought to be one of the
factors MMP 9 is a gelatinase involved in inammation in several vascular dis-
eases. Its role in VAD is unclear at this time although serum MMP 9 has been
found to be grossly elevated in the acute phase of VAD.
• Hypercholesterolemia and obesity
• Migraine
• Hypertension
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Epidemiology
Vertebral artery dissection is thought to be the likely cause of approximately 2% of
all ischemic strokes. However, in young patients, the incidence is higher and
10%–25% of the population is affected by this condition. The combined incidence
of both vertebral artery and carotid artery dissections is estimated to be 2.6 per
100,000 [36]. Carotid artery dissections are more three to ve times more common
than vertebral artery dissections [37].
Pathophysiology
Dissections are caused by the penetration of blood into the arterial wall through the
site of injury which is the intima of the arterial wall. Blood enters the media from
the site of intimal injury, The dissection then extends cranially in the same direction
as the bloodstream. The intramural hematoma causes compression and compromise
of the lumen of the artery. This in turn causes enlargement of the external diameter
of the artery. If the dissection extends toward the adventitia, then a pseudoaneurysm
(dissecting aneurysm) will likely be the result. The resulting dissecting aneurysm
could likely become a source for distal thromboembolism.
Vertebral Artery Anatomy
Segment 1 starts at the rst branch of the subclavian artery until the region of the
foramina of C5–C6.
Segment 2 runs within the transverse foramina from C5/C6 until C2.
Segment 3 is the tortuous segment that begins at the transverse foramina of C2 and
then loops around C1 and then passes between the atlas and the occiput. This
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segment of the artery is encased with nerves, muscles, and the atlanto-occipital
membrane.
Segment 4 is the intracranial segment; it pierces the dura at the foramen magnum
runs until the junction of the medulla and pons where it merges with the basi-
lar artery.
The majority of spontaneous dissections occur in segment 3, which at times
extends to involve segment 4.
The arterial anatomy consists of three layers
(a) the intima (innermost),
(b) the media (middle), and
(c) the adventitia (outermost layer).
Dissection occurs when the structural integrity of the arterial wall is compromised. Intimal tears lead to arterial blood separating (dissecting) the layers of the
arterial wall. The blood within the arterial wall results in a hematoma with clot
formation. The resulting compromise in arterial blood ow results in stroke.
Vertebral artery dissection can be either extracranial or intracranial. Extracranial
dissections frequently occur at the distal extracranial segment near the atlas and
axis. Intracranial dissections are frequently associated with subarachnoid hemorrhage and thus are associated with a much worse prognosis. Neurological sequelae
of both extracranial and intracranial dissections result in cerebral ischemia caused
by thromboembolism, hypoperfusion, or a combination of both [38].
C. de Souza et al.
History andPhysical Examination
History
Patients typically present with an acute and severe unilateral neck pain and/or a
headache. A history of trivial neck trauma preceding the pain will often be present.
The pain is located in the occipital-cervical area of the neck.
Neurological symptoms are often delayed in onset. However, 70% of patients
will have some type of neurological decit which may present late in the course of
the disease.
Lateral medullary syndromes (Wallenberg Syndrome) and cerebellar infarctions
are often the most common sites for VAD related strokes. Wallenberg Syndrome is
dened by sensory decits affecting the trunk and extremities on the opposite side
of the infarction and sensory decits affecting the face and cranial nerves on the
same side as the infarction. The major neurological symptoms that occur following
VAD are, dizziness, ataxia, dysphagia (cranial nerves 9 and 10 are involved), disequilibrium, unilateral hearing loss, dysarthria and diplopia.
Extracranial dissections often have a bruit present on palpation and are heard
very clearly on auscultation. The bruit has even been reported on the contralateral
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side due to increased collateral blood ow that occurs secondarily. The distinguishing factor that separates patients suffering from cerebellar infarctions secondary to
atherosclerotic disease is the age of the patient and the presence of pain. When the
dissection is located intracranially, a subarachnoid hemorrhage is present 50% of
the time [39]. This subset of patients have severe neurological symptoms and an
accompanying poorer prognosis than those with extracranial dissections.
Physical Exam
The following are present in VAD
• Nystagmus and vertigo
• Truncal ataxia
• Ipsilateral loss of taste (hypogeusia) and numbness
• Horner’s syndrome
• Impaired proprioception and ne touch
• Contralateral impairment in thermal and pain sensation in the extremities
• Tongue deviation to the side of the lesion
• Internuclear ophthalmoplegia
• Ipsilateral loss of taste (nucleus and tractus solitarius)
• Hiccups
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Radiological Imaging
MRI and CT angiography (Figs. 8.1, 8.2 and 8.3a, b) are the best modalities to
evaluate VAD and remain the gold standard [40].
CT scanning and CT angiography are commonly used rst line imaging modalities. CT scan can demonstrate posterior fossa ischemia along with subarachnoid
hemorrhage. It can also identify the site where the occluded vertebral artery or
mural thrombus occurs. CT Angiography are far superior to plain CT scans because
of the information it yields and should be performed. CT Angiography will identify
the irregularity of the vascular lumen or thickening of the arterial wall [41]. Vascular
Duplex scanning demonstrates abnormal ow in 95% of patients.
MRI is useful in detecting an intimal ap and luminal thrombosis. Hyperintensity
of the vessel wall may be visualized on T1-weighted images and are considered
pathognomonic of VAD.
A cerebral angiogram may be required if the MRI and CT scan have failed to
reveal any pathology.
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C. de Souza et al.
a
b
c d
Fig. 8.1 Forty-eight-year-old female with recurrent posterior circulation strokes with V4 dissecting aneurysm. (a) Acute right cerebellar infarct. (b) MRI contrast angiogram Recon images showing outpouching at right V4. (c) DSA, right VA showing dissecting aneurysm at V4 level. (d) 4D
angiogram showing right VA dissecting aneurysm
Multisection CT Angiography Findings inVertebral Artery
Dissection (Figs.8.1, 8.2, and8.3)
Multisection CT angiography has been found to be a very sensitive and accurate
technique for the diagnosis of vertebral artery dissection. The reported sensitivity
was 100% and specicity was 98%. The reported ndings are increased external
diameter of the affected blood vessel and crescent-shaped mural thickening in
patients suffering from vertebral artery dissection. It should be noted that these criteria should be applied with caution because both signs can be found in nondissected vertebral arteries as well. Multisection computed tomographic (CT)
angiography provides very high-resolution and excellent high-contrast images of
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Fig. 8.2 Twenty-nineyear-old male developed
sudden neck pain while
dancing with friends, and
MRI showed patchy right
posterior cerebellar
infarcts. Right VA DSA
demonstrates, nonow
limiting short segment
dissection of V2 segment
(arrow)
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the arterial lumen and wall. Two-dimensional (2D) and 3D visualization increase its
value in helping diagnose the site and extent of dissection and vascular compromise.
MR imaging too demonstrated excellent sensitivity and specicity of 84% and
99%, respectively, compared with conventional angiography in diagnosis of internal
carotid dissection. The criteria were an increase in the external diameter of the
artery and narrowing of the lumen. It should be noted that ow void narrowing is a
much less useful indicator of dissection because it can be seen in many other
conditions.
Transcranial Doppler has been also been found to be a very useful tool in VAD
[42]. Sonographic curves, microembolic signals (MES), and breath holding index
(BHI) were found to be very useful parameters in predicting ischemic events.
Routine blood work with specic reference to the patient’s coagulation prole
should be obtained.
Should radiological imaging reveal the absence of hemorrhage, anticoagulation
can be then initiated.
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C. de Souza et al.
a
Fig. 8.3 Forty-year-old female with acute left cerebellar infarcts. (a) Left V4 dissection with
underline thrombus. (b) Poststenting angiogram shows improved ow across stent and into the
distal circulation
b
Management
Outcomes
Stenotic-type and almost completely occlusive dissections often and frequently heal
with minor residual wall abnormalities. Occlusions are likely to recanalize early.
However, the outer diameter of the dissected vessel will remain much smaller when
compared to that of the normal contralateral vessel. Dissecting aneurysms behave in
a similar fashion. However, improvement and recovery are not as remarkable as
those which occur in a dissection.
Treatment of patients suffering from a craniocervical artery dissection is controversial at this time because controlled studies are lacking. Administration of anticoagulants is the most frequent therapy to prevent thrombosis and embolism in
extracranial dissections [43]. In intracranial artery dissections, the risks that accompany administration of anticoagulants may be high because of the possible risk of
subarachnoid hemorrhage. Anticoagulant therapy is clearly contraindicated in cases
of intracranial dissecting aneurysms with subarachnoid hemorrhage. Endovascular
or surgical interventional procedures are considered [44, 45] for patients who still
remain symptomatic due to thromboembolic events and in situations of dissecting
aneurysm.
Should recurrences occur they often occur within the rst 4–6weeks following
the onset of symptoms. After the rst month following dissection, the risk of
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