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Management of Peripheral Dizziness

Vestibular neuronitis
Vestibular neuronitis is the most common cause of acute vertigo, with an incidence of 170 cases per
100,000 people. It is believed to result from reactivation of herpes simplex virus infection that affects the
vestibular ganglion and vestibular nerves.[10] A prodromal upper respiratory tract illness may or may not be
present. Vertigo is without auditory or other central nervous system (CNS) symptoms and lasts for several
days. Patients are usually ill and cannot perform home or work activities. They are commonly rated
symptomatically.
A brief course of antiemetic and vestibular suppressants is usually needed in the acute phase but should
be withdrawn as soon as possible to facilitate the process of central vestibular compensation.
[10]
Corticosteroids may improve long-term outcomes. Early vestibular rehabilitation is important. [10] Antiviral
medications have not proved helpful, possibly because a large spectrum of viruses can cause vestibular
neuronitis. The pharmacological treatment of choice for acute vestibular neuritis is oral steroids beginning
as soon as possible with gradual tapering of the dose. One third of patients have chronic vestibular
symptoms and develop benign paroxysmal positioning vertigo (BPPV).

Benign paroxysmal positioning vertigo


BPPV is the second most common cause of vertigo. The typical symptom is brief episodic vertigo upon
changing head or body position. Patients may have a residual sensation of disequilibrium between
episodes. BPPV is commonly either idiopathic or posttraumatic. Other causes of vertigo, such as
vestibular neuronitis, Mnire disease, and delayed endolymphatic hydrops, are also associated with
BPPV.
The mechanism of BPPV can involve canalithiasis (otoconia floating in the endolymph) or cupulolithiasis
(otoconia adherent to cupula). The most commonly affected canal is the posterior canal (90% of cases);
the horizontal canal may also be affected, but to a lesser extent.
The American Academy of Neurology has published a practice parameter for the treatment of BPPV.
[11]
The most effective treatment is canalith repositioning from the affected canal back to the vestibule
where it is absorbed using the most common maneuvers: Epley, Semont, Lempert, and Hamid (for
horizontal canal cupulolithiasis). Medications can be helpful for short-term reduction of symptoms but
have not been shown to be effective in the long-term treatment of BPPV.
It is important to note that most cases of BPPV can be treated in the office once the history and
examination confirm the diagnosis. Prolonged sessions of physical therapy are not necessary and not
cost effective. Some of these patients may also require medications, which should be given under
physician supervision, to treat severe nausea and vomiting that can result from CRP treatments.
The most common complication of the Semont or Epley maneuver is conversion of the posterior
canalhorizontal canal BPPV, which is treated with the Lempert or Hamid maneuvers. A less common
complication is undue cervical strain, which is especially likely with the Semont maneuver or with neck
hyperextension during the Epley maneuver.

Mnire disease
Mnire disease is a disorder of the inner ear with typical symptoms of episodic vertigo, tinnitus, and
hearing loss. Untreated, severe hearing loss and unilateral vestibular paresis are inevitable. Bilateral
involvement occurs in about 25% of patients. The etiology is idiopathic in most cases and can also be
hereditary, autoimmune, infectious, or allergic. The common pathophysiology is disordered fluid
homeostasis in the inner ear, with endolymphatic hydrops representing a histologic footprint rather than
an etiology.
Most patients respond to conservative therapy with salt restriction and diuretics. Corticosteroids, given
orally or intratympanically, can be used to stabilize active disease and to recover speech discrimination,
especially when used in early stages of the disease. Intratympanic gentamicin (chemical labyrinthectomy)

is a minimally invasive procedure that has emerged as an effective method for treating the disabling
vertigo of Mnire disease when hearing loss and speech discrimination have progressed to severe
levels. Gentamicin is also very effective in treating Tumarkin attacks of Mnire disease.
The role of surgical therapy for Mnire disease (eg, shunting the endolymphatic sac) is controversial.
The literature demonstrates wide variation in the effectiveness, or lack thereof, of surgery.

Autoimmune inner-ear disease


Patients with autoimmune inner-ear disease typically present with rapidly progressive, bilateral hearing
loss, with or without vertigo. Initial onset may be unilateral. However, the rapid progression, bilateral
involvement, and response to steroids distinguish this disorder from Mnire disease. Autoimmune innerear disease can occur with or without other autoimmune disease or laboratory evidence of a systemic
inflammatory disorder. Specific laboratory markers for inner-ear antigenicity have low sensitivity and thus
are of little clinical utility.
Oral and intratympanic corticosteroids are effective in controlling this disease. Patients with recurrent
symptoms that are steroid responsive may benefit from methotrexate or other steroid-sparing
medications. These patients should be treated by a rheumatologist.

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