Posted by: Thixia | June 25, 2008

Dizziness, Vertigo, and Imbalance Section 5 of 8



Acute dizziness and vertigo is usually managed with vestibular suppressants, antiviral medication, and antiemetic medications.  Steroids can be used in selected patients.  Vestibular suppressants should be used for a few days at most because they delay the brain’s natural compensatory mechanism for peripheral vertigo. 

Peripheral dizziness

Vestibular neuronitis

Vestibular neuronitis is a common cause of acute vertigo with an incidence of 170 cases per 100,000 people.  It is believed to be of viral etiology.  A prodromal upper respiratory tract illness may or may not be present.  Vertigo without auditory symptoms develops and last for several days.

Vestibular compensation proceeds in the usual fashion, with the most severe vertigo resolving in 1 week.  The predilection for the superior division of the vestibular nerve leaves the function of the posterior canal intact in most cases.  This effect predisposes to posterior canal benign paroxysmal positioning vertigo as a sequela.

A brief course of an antiemetic and vestibular suppressants is usually needed in the acute phase.  Corticosteroids may improve long-term outcomes.  Early vestibular rehabilitation is important.  Antiviral medications have not proven helpful, possibly because a large spectrum of viruses can cause vestibular neuronitis.  One third of patients have chronic vestibular symptoms.

Benign paroxysmal positioning vertigo

BPPV is a common cause of vertigo.  The typical symptom is brief vertigo on changing position.  Patients may have a residual sensation of disequilibrium between episodes.  One half have a symptomatic etiology, such as vestibular neuronitis, Ménière disease, delayed endolymphatic hydrops, sudden sensorineural hearing-loss syndrome, head trauma, or migraine.  The remaining patients are usually idiopathic.

Treatment involves dispersing otolithic debris in the semicircular canals (Brandt-Daroff exercises) or repositioning the particles to the utricle (Epley, Semont, Lempert, and Hamid maneuvers, among others).  Medications are not effective in the treatment of BPPV.

BPPV treatment should be administered if the patient has the typical history and benign paroxysmal positioning nystagmus (BPPN) on examination.  Treatments based on only the history or those applied to atypical nystagmus are not effective and can lead to unwarranted complications.

The most common complication of the Semont or the Epley maneuver is the conversion of the posterior canal-horizontal canal BBPV, which is treated with the Lempert or Hamid maneuvers.  Less common is undue cervical strain, especially with the Semont maneuver or with neck hyperextension during the Epley maneuver.

Ménière disease

Ménière disease entails the triad of episodic vertigo, tinnitus, and hearing loss.  Untreated, severe hearing loss and unilateral vestibular paresis are inevitable.  Bilateral involvement occurs in one third of patients.  The mechanism can be hereditary, autoimmune, infectious, or idiopathic.  The common pathophysiology is disordered fluid homeostasis in the inner ear, with endolymphatic hydrops representing a histologic footprint rather than an etiology.

More than 80% of patients respond to conservative therapy with salt restriction and diuretics.  Corticosteroids, given orally or intratympanically, can be used to stabilize active disease.  Intratympanic gentamicin can be used to reduce vestibular symptoms, but it should be used only in an ear with no serviceable hearing.  The role of surgical therapy, such as 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 and vestibular hypofunction.  The initial onset may be unilateral.  However, the rapid progression and early bilateral involvement distinguishes this disorder from Ménière syndrome.  This disease can occur without clinical or laboratory evidence of a systemic inflammatory disorder.  Specific laboratory markers for inner-ear antigenicity are of little clinical utility because of their low sensitivity.  Corticosteroids are effective.  Patients with recurrent symptoms may benefit from methotrexate.

Central dizziness


Migraine is a common disorder, affecting 10% of men and 30% of women.  About 25% of migraineurs have dizziness.  All forms of dizziness can occur with migraine: vertigo, positional dizziness, disequilibrium, motion intolerance, and visual motion sensitivity.  Dizziness can occur as an aura or as part of a headache.  However, one third of patients consistently have dizziness in the interval between headaches.

The treatment of migraine related dizziness is the same as the treatment of migraine.  Headache hygiene and trigger factors should be reviewed.  Prophylactic medications are prescribed, if indicated.  Abortive medications, such as triptans, are effective for migraine related dizziness, whether accompanied by headache or not.

Cerebrovascular disease

Stroke is the third most common cause of death and the most common cause of disability in adults.  The vertebrobasilar circulation supplies the brainstem, cerebellum, and the inner-ear auditory and vestibular structures.  Infarction of the cerebellar midline can cause acute vertigo without auditory or other neurologic features (eg, isolated vertigo).  This potentially life-threatening occurrence must be differentiated from vestibular neuronitis.  About one half of patients have other features of bulbar or long tract involvement, which make the diagnosis of stroke clear.

Evaluation of the patient with stroke is directed at identifying correctable vascular risk factors (hypertension, diabetes, hyperlipidemia, smoking) and at determining the mechanism of stroke (small vessel, large vessel, cardioembolic, dissection, hypercoagulability, vasculitis).  Secondary prophylactic therapy and rehabilitation are individualized.  Both hearing loss and vertigo can occur in the setting of stroke due to either central and/or peripheral injury.

Multiple sclerosis

Multiple sclerosis is a disorder of recurrent, inflammatory CNS demyelination due to underlying autoimmune disorder.  The onset is usually at 20-40 years of age.  Episodes begin over hours to a few days and last weeks to months.  Typical symptoms include optic neuritis, ocular motor dysfunction, trigeminal neuralgia, sensorimotor deficits, myelopathy, ataxia, and bladder dysfunction.  Vertigo, at times mimicking vestibular neuronitis, is a presenting symptom in less than 10% of patients.  Dizziness or vertigo occurs at some point in the course in a third of patients.  Few patients present with hearing loss due to brainstem involvement.

The diagnosis of multiple sclerosis requires the presence of dissemination in time and space, ie, different neurologic symptoms at different times.  Careful history taking, examination, and serial follow-up combined with MRI and spinal-fluid analysis helps in establishing the diagnosis.  The diagnosis should not be based on MRI abnormalities alone.  Disease-modifying therapy is available, but it is only modestly effective.  The search for improved treatment is ongoing.

Masses and malformations of the posterior fossa

Vestibular schwannoma (acoustic neuroma) is an uncommon lesion with an incidence of 1.1 per 100,000.  It typically manifests with slowly progressive, unilateral hearing loss, and tinnitus.  Dizziness is not a common symptom, as the vestibular system can compensate for such gradual unilateral hypofunction.  Dizziness can occur as the tumor expands in the cerebellopontine angle and effaces the brainstem and cerebellum.  Arachnoid cysts can also occur in the posterior fossa and result in subtle and non-specific dizziness and auditory symptoms.

Chiari malformation occurs in a few adults.  It is congenital, but often does not become symptomatic until the age of 20-40 years.  Occipital headache precipitated by Valsalva maneuvers, coughing, exertion, or changing position is common.  Dizziness may occur with the same precipitants.

Once suspected, the diagnosis can be confirmed with MRI.  Surgery should be considered for patients with more-than-mild symptoms.


The most common fall is a simple fall in which the patient trips and has no ominous underlying peripheral or central disorder.  Hazards in the environment (eg, rugs, electrical wires, poor lighting), polypharmacy, and orthopedic factors often contribute to fall.

Because of the substantial risk of injury and the resultant decline in independence and/or quality of life after a fall, a well-directed evaluation is indicated.  Balance is not a single physiologic function.  The sensory inputs are vision, vestibular, and proprioceptive.  While a person is walking, the CNS must instantaneously integrate this information and execute appropriate motor plan and output.  This function must be supported by an adequate musculoskeletal system.  All of these factors change with age.  Any further disease related decline in any of these systems further impairs balance.  Bilateral vestibular failure is a contributor in one fourth of elderly patients with disequilibrium.  Untreated BPPV can be a risk factor for falling.

Orthostatic hypotension due to aging or to medications is also a common contributor.  Vestibular rehabilitation is an important consideration is all patients with acute or chronic vestibular dysfunction.  Patients with gait and balance problems should undergo physical therapy and a home-safety evaluation.

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