Continuum, August 2006, Volume 12, Issue 4

A challenge for the clinical neurologist is to decide which of the myriad patients with symptoms of dizziness, lightheadedness, or imbalance have a genuine vestibular disorder, be it peripheral or central. The clinical examination is often the key. A series of systematically applied, physiologically based maneuvers, designed to probe static and dynamic function of the vestibulo-ocular reflexes and the individual labyrinthine sensors, will almost always reveal the evidence of a vestibular system anomaly, which either clarifies the diagnosis or points to a need for a further evaluation.This chapter will describe these maneuvers and indicate their diagnostic usefulness. They include dynamic visual acuity, occlusive ophthalmoscopy, head impulse (rotational vestibulo-ocular reflex) and head heave (translational vestibulo-ocular reflex) testing, mastoid vibration-induced nystagmus (equivalent of a hot-water caloric stimulus in a patient with unilateral vestibular loss), hyperventilation-induced nystagmus (abnormal in fistula, craniocervical junction anomalies, compressive and demyelinating lesions, and cerebellar degenerations), Valsalva-induced nystagmus (abnormal in fistula and craniocervical junction anomalies), head-shaking-induced nystagmus (vertical nystagmus after horizontal head shaking points to a central disorder), positional nystagmus (lateral canal, posterior canal, central) and sound-induced nystagmus (superior canal dehiscence). When combined with a careful examination of eye alignment, gaze holding, saccade accuracy and speed, and smooth pursuit, a central or peripheral localization is usually possible.(C) 2006 American Academy of Neurology

Patients with an acute unilateral peripheral vestibular loss present with severe vertigo, nausea, and vomiting. The diagnosis rests on finding spontaneous nystagmus (horizontal/torsional, unidirectional), gait imbalance (falling toward the side of lesion) and a positive head thrust sign (corrective saccades after head thrusts toward the lesion side). When no associated auditory or neurological symptoms and signs are present, the disorder usually results from viral or postviral inflammation of the vestibular nerve (vestibular neuritis). Recent studies suggest that early treatment with high-dose steroids improves the outcome with vestibular neuritis, but the risk/benefit of such treatment has not been adequately assessed. Most patients return to normal even if there is permanent unilateral peripheral vestibular loss. Patients with bilateral symmetrical peripheral vestibular loss do not have vertigo or spontaneous nystagmus but rather complain of imbalance and oscillopsia. They have a positive head thrust sign in both directions and have decreased visual acuity with head shaking. Most causes of bilateral peripheral vestibular loss are associated with bilateral hearing loss, although some ototoxic drugs, such as gentamicin, are remarkably selective for vestibular damage. Treatment is directed at prevention when possible and vestibular rehabilitation to help the patient compensate for the vestibular loss.(C) 2006 American Academy of Neurology

This chapter reviews the causes and treatments for positionally evoked vertigo. Benign paroxysmal positional vertigo (BPPV) is the most common cause of this so the clinical features, pathophysiology, and treatment techniques for this condition are discussed. This chapter also outlines ways to recognize and treat some of the less common variants of BPPV, including treatment complications and posttreatment care. The final section of the chapter focuses on central nervous system causes of positional vertigo.GLOSSARY:* Benign paroxysmal positional vertigo (BPPV): An inner ear vertigo syndrome caused by calcium carbonate material, presumably dislodged from the utricle, in a semicircular canal, which inappropriately stimulates the ampulla of one of the semicircular ducts by the effect of gravity during certain changes in head position. If not otherwise specified, BPPV refers to the posterior canal type of BPPV. Benign positional vertigo is used synonymously with BPPV.* Benign paroxysmal vertigo of childhood: Like benign recurrent vertigo, a condition consisting of spontaneous attacks of vertigo in children typically 4 to 10 years of age. It is generally considered to be an acephalgic manifestation of migraine. It is unrelated to benign paroxysmal positional vertigo.* Benign recurrent vertigo: A condition unrelated to benign positional vertigo that causes recurrent spontaneous episodes of vertigo that are not positional. Most cases are attributable to migraine-associated vertigo.* Canalith repositioning maneuver: Maneuver described by Epley.* Canalithiasis (or canalolithiasis): Calcium carbonate material free floating or loose in the semicircular duct (canal).* Cupula: Vestibular sense organ of the semicircular canals that consists of a gelatinous structure overlying specialized hair cells. The nerve impulses generated relate to the degree and direction of deflection of the cupula caused by fluid (endolymph) movement in the semicircular canal. Each canal has its own cupula. The bulge in which the cupula resides is referred to as the ampulla.* Cupulolithiasis: Calcium carbonate material adherent to the cupula.* Dix-Hallpike maneuver: A specific maneuver that elicits paroxysmal positional nystagmus and vertigo in benign positional vertigo of the posterior semicircular canal.* Epley maneuver(s): Maneuver described by Epley, now sometimes given his name.* Liberatory maneuver: Maneuver described by Semont.* Mastoid oscillation: Direct application of vibration stimulus to the mastoid process done with the intention to "loosen up" and enhance movement of canalith material during canalith repositioning maneuvers.* Modified Epley maneuver: Any of the various alterations on the original maneuver described by Epley in 1992.* Nylen-Barany maneuver: Often used to refer to the Dix-Hallpike maneuver, although the original description entailed moving the head in differing positions to elicit nystagmus.* Otoconia: Calcium carbonate (calcite crystals) ranging from 5 [mu]m to 25 [mu]m in diameter, which is part of the otolithic membrane of the maculae.* Particle repositioning maneuver: Another name for the canalith repositioning maneuver.* Roll test: Supine head turning to elicit horizontal canal benign paroxysmal positional nystagmus.* Semicircular canal: One of three (anterior or superior, posterior or inferior, and lateral or horizontal) bony channels within the labyrinth of the temporal bone. The membranous labyrinth inside this canal is the semicircular duct.* Utricle: Along with the saccule, a portion of the membranous labyrinth that generates and utilizes otoconia to detect gravity and translational motion. The utricle and saccule are often referred to as the otolith organs of the inner ear.(C) 2006 American Academy of Neurology

Hearing loss and tinnitus are common symptoms among the general population, and both increase in frequency and severity with age. The initial evaluation determines the site of the lesion: conductive hearing loss from the middle ear, or sensorineural hearing loss from the inner ear. Unilateral hearing loss is of most concern because of the possibility of a mass lesion. Most forms of hearing loss can be helped with amplification (hearing aid), surgical correction, or cochlear implantation in the case of profound hearing loss.(C) 2006 American Academy of Neurology

This review discusses the pharmacological treatment of dizziness, focusing particularly on the vertigo subtype of dizziness. Classes of medications useful in the treatment of vertigo include anticholinergics, antihistamines, benzodiazepines, calcium channel blockers, and dopamine blockers. These medications often have multiple actions. They may modify the intensity of symptoms (eg, vestibular suppressants) or they may affect the underlying disease process (eg, calcium channel blockers in the case of vestibular migraine). Most of these agents, particularly those that are sedating, also have a potential to modulate the rate of compensation for damage. This consideration has become more relevant in recent years, as vestibular rehabilitation physical therapy is now often recommended in an attempt to improve compensation. Accordingly, therapy of vertigo is optimized when the prescriber has detailed knowledge of the pharmacology of medications being administered as well as the precise actions being sought.(C) 2006 American Academy of Neurology