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Vertigo A Review of Common Peripheral and Central Vestibular Disorders
Vertigo A Review of Common Peripheral and Central Vestibular Disorders
consists of salt restriction, diuretics, vasodilators, maneuvers are reported to be 91% effective.4
anti-emetics, and anti-nausea medications. Those Patients with symptoms refractory to repositioning
who fail medical treatment may consider surgical maneuvers may be candidates for singular neurecto-
therapy. Surgical treatments can be classified as my or posterior semicircular canal occlusion.
either hearing-conservative or non–hearing-conserva-
tive procedures and are appropriately chosen based VESTIBULAR NEURONITIS
on the patient’s audiometric results. For patients with Vestibular neuronitis is the second most common
serviceable hearing, endolymphatic sac decompres- peripheral cause of vestibular vertigo. Infection of the
sion, vestibular neurectomy, and intratympanic ami- vestibular nerve results in nerve degeneration and
noglycoside infusion are options. Labyrinthectomy is may present bilaterally. Infection is most often thought
reserved for patients with no serviceable hearing. to be of viral origin, usually from the herpes virus
family. It may also result from bacterial invasion (e.g.
BENIGN PAROXYSMAL POSITIONAL Borrelia). It is believed that the superior vestibular
VERTIGO nerve is more commonly involved secondary to its
Benign paroxysmal positional vertigo (BPPV) is course throughout a long and narrower bony canal,
considered the most common peripheral vestibular making it more susceptible to compressive edema.
disorder, affecting 64 of every 100,000 Americans.2 The reported incidence of an upper respiratory
Women are more often affected and symptoms infection prior to the development of vestibular
typically appear in the fourth and fifth decades of life. symptoms varies from 23% to 100%.5
In 1980, Epley proposed that free-floating densities Patients present with complaints of sudden vertigo,
(canaliths) located in the semicircular canals deflect lasting up to several days, often with vegetative
the cupula creating the sensation of vertigo.3 This is symptoms. As this process affects only the vestibular
well documented in his Canalithiasis Theory. Although portion of the vestibulocochlear apparatus, there is an
these canaliths are most commonly located in the absence of cochlear symptoms. Vertiginous com-
posterior semicircular canal, the lateral and superior plaints gradually improve over days to weeks; howev-
canal may also be involved. er, imbalance may persist for months after resolution of
Patients with BPPV complain of vertigo with acute disease. Recurrence is not uncommon and may
change in head position, rolling over, or getting out occur several times per year. Physical examination is
of bed, and the vertigo is often side specific. Vertigo limited and should consist of audiometric evaluation
occurs suddenly and lasts for less than 1 minute. and ENG. Patients may demonstrate nystagmus and
Attacks are separated by remissions; however, caloric weakness on the affected side.
patients may complain of constant light-headedness Treatment is primarily supportive with the use of
between episodes. Classic BPPV involving the pos- anti-emetics and anti-nausea medications. Vestibular
terior semicircular canal is characterized by the suppressants should be used judiciously in the first
following: geotropic nystagmus with the problem ear few days of an acute attack. Prolonged use of these
down, predominantly rotary nystagmus toward the medications can delay recovery by inhibiting central
undermost ear, latency of a few seconds, duration compensation. Furthermore, early ambulation is par-
limited to less than 20 seconds, reversal of nystag- amount in the central nervous system’s ability to
mus when the patient returns to an upright position, compensate and is therefore recommended as soon
and a decline in response with repetitive provocation. as tolerable. High-dose methylprednisone has been
Diagnosis is made primarily through history and shown to hasten recovery; however, prospective,
also by eliciting typical physical findings during the randomized, double-blinded studies have failed to
Dix-Hallpike maneuver. The Dix-Hallpike maneuver demonstrate added benefit from the use of antivirals
entails guiding a patient through a series of move- (i.e. valacyclovir).6
ments known to elicit nystagmus in a patient with
BPPV. Electro-oculography and 2D videonystag- LABYRINTHITIS
mography are of limited use secondary to the inability Labyrinthitis is an inflammatory disorder of the
of these tests to record torsional eye movement. membranous labyrinth, affecting both the vestibular
Treatment is often supportive as a large percent- and cochlear end organs. It may present unilaterally or
age of patients will have spontaneous resolution of bilaterally, and similar to vestibular neuronitis, it is
their symptoms. For those with persistent symptoms, often preceded by an upper respiratory infection. This
the first line of treatment is canalith repositioning disorder occurs when infectious microorganisms or
maneuvers. These maneuvers attempt to reposition inflammatory mediators invade the membranous
the free-floating canalith particles from the semicir- labyrinth, damaging the vestibular and auditory end
cular canals to the utricle using gravity. These organs. Potential etiologies include viral pathogens,
symptom must be present during two or more ner’s syndrome, dysphagia, hoarseness, and rarely,
episodes of vertigo.15,16 Perhaps the most problem- facial nerve paralysis.
atic dilemma is in differentiating MAD from MD. Both Lateral pontomedullary infarction secondary to
may present with episodic vertigo and possibly occlusion of the anterior inferior cerebellar artery will
hearing loss. A thorough history is imperative and result in lateral inferior pontine syndrome. This
should inquire about headaches, photophobia, pho- syndrome is characterized by symptoms similar to
nophobia, presence of aura, and any other neurolog- Wallenberg’s syndrome with notable differences.
ical symptoms that may point towards a diagnosis of Involvement of cranial nerves VII and VIII results in
migraine. ENG and rotational testing is non-specific ipsilateral facial paralysis and tinnitus and hearing
and often adds little if anything towards a diagnosis. loss, respectively. Dysphagia and hoarseness, how-
Once the diagnosis of MAD has been reached, ever, are not apparent as cranial nerves IX and X
numerous therapies are available for treatment. Initial nuclei are uninvolved with occlusion of the anterior
management should focus on avoidance of triggers inferior cerebellar artery.
through lifestyle modification. Patients should avoid Lateral superior pontine syndrome occurs when
food and drinks as well as other agents known to the superior cerebellar artery is occluded. With this
induce migraines. Stress relief is recommended and syndrome, one can expect vertigo, nystagmus, gait
both sleep and exercise are encouraged. For those disturbance, ipsilateral limb ataxia and facial pain or
who fail to find relief with lifestyle modification alone, numbness, contralateral body hemianesthesia, and
medical treatment may be necessary. Prophylactic Horner’s syndrome. Distinguishing this syndrome is
treatment varies depending on the physician, but the finding of contralateral impairment of vibration and
most often includes one or more of the following; temperature due to medial lemniscus involvement.
amytryptyline, benzodiazepines, beta-blockers, calci- A high index of suspicion must be kept with any
um channel blockers, and selective serotonin reup- patient presenting with spontaneous vertigo to avoid
take inhibitors. Acute attacks may require anti- missing the diagnosis of ischemic stroke. It is
emetics and anti-vertiginous medications, as well as essential to consider stroke in any acutely vertiginous
triptans. Those with headaches may also benefit from patient with concomitant neurological signs and
non-steroidal anti-inflammatory drugs. symptoms. Once VIS is suspected, an expeditious
work-up is necessary. This should include a thorough
VERTEBROBASILAR ISCHEMIC STROKE physical examination, imaging, and neurology con-
The blood supply to the brainstem, cerebellum, sultation for both evaluation and treatment.
and inner ear is derived from the vertebrobasilar
system. Occlusion of any of the major branches of this VERTEBROBASILAR INSUFFICIENCY
system may result in vertigo. Symptoms of vertebro- Vertebrobasilar insufficiency is synonymous with a
basilar ischemic stroke (VIS) are highly variable and transient ischemic attack (TIA) of the vertebrobasilar
depend on which of the three major circumferential system. By definition, patients experience symptoms
branches are occluded; the posterior inferior cerebel- similar to those detailed above, but the symptoms
lar artery, anterior inferior cerebellar artery, or superior resolve within 24 hours. If left untreated, the disease
cerebellar artery. Numerous processes may occlude process will eventually progress to stroke with
the vertebrobasilar system. The most common are permanent or long-lasting seqeulae. Risk factors
atherosclerosis, emboli, and vertebral artery dissec- and causes are identical to those for VIS. Forty-eight
tion. Vertebral artery dissection can result from percent of patients who suffer a VIS report a TIA in the
trauma or neck manipulation, or can occur sponta- preceding days or weeks.17 In fact, 29% of patients
neously. Less common causes include subclavian suffer from at least one episode of vertigo, a symptom
steal syndrome, hypercoagulation disorders, and of vertebrobasilar insufficiency, prior to their VIS.18
inflammatory conditions. Patients suffering a vertebrobasilar TIA are likely to
As mentioned earlier, the symptoms associated progress to stroke more quickly than those experi-
with ischemic stroke in this area are highly variable encing TIAs in the anterior territory.
and greatly dependent upon which branch of the Vertebrobasilar insufficiency is a common cause
system is occluded. Occlusion of the posterior inferior of vertigo in the elderly. Symptoms may last from
cerebellar artery will cause a lateral medullary minutes to hours, but typically average 8 minutes in
infarction and result in lateral medullary syndrome, duration. In as many as one third of patients, vertigo is
also known as Wallenberg’s syndrome. Expected the only manifestation of their disease. Although this
manifestations include vertigo, nystagmus, gait dis- disease should always be in the differential, several
turbance, ipsilateral limb ataxia and facial pain or months of recurrent vertigo unaccompanied by other
numbness, contralateral body hemianesthesia, Hor- neurological signs suggests another disorder. The
likelihood of immediate stroke is less in patients 6. Strupp M, Zingler VC, Arbusow V, et al. Methylprednisolone,
presenting with only episodic vertigo. Patients who valacyclovir, or the combination for vestibular neuritis. N Engl J Med.
also present with paresis, blindness, or altered 2004;351:354–361.
consciousness, however, should be evaluated urgent- 7. Tos M, Thomson J. Epidemiology of acoustic neuromas. J Laryngol
Otol. 1984;98:685–692.
ly for fear of impending stroke. Evaluation is similar to
8. Khrais T, Romano G, Sanna M. Nerve origin of vestibular schwannoma:
that of an ischemic stroke. Treatment includes
a prospective study. J Laryngol Otol. 2008;122:128–131.
antiplatelets, anticoagulation, possible thrombolysis 9. Rizer FM, House JW. Perilymph fistulas: the House Ear Clinic
and percutaneous transluminal angioplasty, and experience. Otolaryngol Head Neck Surg. 1991;104:239–243.
neurological consultation. 10. Black FO, Pesznecker S, Norton T, et al. Surgical management of
perilymphatic fistulas: a Portland experience. Am J Otol.
CONCLUSION 1992;13:254–262.
Dizziness is a common complaint and can 11. Seltzer S, McCabe BF. Perilymph fistula: the Iowa experience.
represent numerous disease processes. The goal of Laryngoscope. 1986;96:37–49.
this paper was to present the more common causes 12. Minor LB, Solomon D, Zinreich JS, et al. Sound- and/or pressure-
of vertigo and disequilibrium relating to pathology of induced vertigo due to bone dehiscence of the superior
semicircular canal. Arch Otolaryngol Head Neck Surg. 1998;124:
the central and peripheral vestibular system. This is
249–258.
far from an exhaustive list but hopefully serves as a 13. Carey JP, Minor LB, Nager GT. Dehiscence or thinning of bone
good review and starting point for future readings. overlying the superior semicircular canal in a temporal bone
survey. Arch Otolaryngol Head Neck Surg. 2000;126:137–147.
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