Vertigo is a disorienting form of dizziness in which there is often an illusion of rotating movement. It can be caused by any disruption of the otolith organs, semicircular canals, inner ear and deep paravertebral stretch receptors of the neck, as well as various centers in the brain stem, cerebellum, thalamus and cortex, and the connections between them. Baloh reviews the causes and presentations of some common types of vertigo.

Associated nausea is generally more pronounced when the cause of vertigo is peripheral. Conversely, imbalance tends to be more severe in cases of vertigo of central origin. The best guide to the site of origin of vertigo is given by the associated clinical picture. Lesions of the labyrinth or eighth nerve are associated with ear pain, tinnitus, hearing loss and other auditory symptoms. More central lesions produce neurologic signs and symptoms determined by the site and size of the lesion. In vertigo of peripheral origin, nystagmus generally resolves on fixation within 24 to 48 hours, whereas nystagmus associated with central vertigo does not.

Common causes of prolonged spontaneous vertigo include otomastoiditis, vestibular neuritis, labyrinthine concussion, lateral medullary infarction and cerebellar infarction. Urgent magnetic resonance imaging should be considered if vertigo is of sudden onset or is accompanied by severe headache, direction-changing nystagmus or neurologic signs, or if the patient has risk factors for stroke or is unable to stand or walk.

Recurrent attacks of vertigo result from sudden, temporary and usually reversible impairment of one labyrinth or its central connections. If the attacks last for hours, the cause is likely to be an abnormality of the inner ear. Common causes of recurrent attacks of vertigo include Ménière's syndrome, autoimmune disease of the inner ear, perilymph fistula, migraine and vertebrobasilar insufficiency.

A careful history focusing on activities occurring immediately before the onset of symptoms distinguishes positional vertigo from spontaneous or recurrent attacks. Positional vertigo has been attributed to lesions of the semicircular canals, particularly their enclosed otoliths, and their central connections. Besides the relationship to movement or position, patients with positional vertigo may report a sensation of motion sickness that persists for hours.

The three strategies for management of vertigo are symptomatic, specific (or cause-directed) and rehabilitative. Symptoms of vertigo, nausea and vomiting can be suppressed with short courses of meclizine, dimenhydrinate, promethazine or diazepam. Stronger anti-emetics such as prochlorperazine or metoclopramide may be added if required. Sedation is a serious side effect of these agents.

Examples of specific therapies include salt restriction and diuretics for management of Ménière's disease, prophylactic therapy for migraine using beta-blocking drugs, and aspirin or anticoagulant therapy for verte-brobasilar insufficiency. Benign paroxysmal positional vertigo may respond to maneuvers designed to reposition calcium deposits in the semicircular canals. Vestibular rehabilitation consists of exercises to assist patients in compensating for permanent vestibular damage. Although these exercises initially induce dizziness, they should be started as soon as possible and performed at least twice daily.