Chapter 022. Dizziness and Vertigo (Part 5)

Evaluation of Patients with Pathologic Vestibular Vertigo The evaluation depends on whether a central etiology is suspected (Table 22-2). If so, MRI of the head is mandatory. Such an examination is rarely helpful in cases of recurrent monosymptomatic vertigo with a normal neurologic examination. Typical BPPV requires no investigation after the diagnosis is made (Table 22-1).Vestibular function tests serve to (1) demonstrate an abnormality when the distinction between organic and psychogenic is uncertain, (2) establish the side of the abnormality, and (3) distinguish between peripheral and central etiologies. The standard test is electronystagmography (calorics), where warm and cold water...
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Chapter 022. Dizziness and Vertigo (Part 5) Chapter 022. Dizziness and Vertigo (Part 5) Evaluation of Patients with Pathologic Vestibular Vertigo The evaluation depends on whether a central etiology is suspected (Table22-2). If so, MRI of the head is mandatory. Such an examination is rarely helpfulin cases of recurrent monosymptomatic vertigo with a normal neurologicexamination. Typical BPPV requires no investigation after the diagnosis is made(Table 22-1). Vestibular function tests serve to (1) demonstrate an abnormality when thedistinction between organic and psychogenic is uncertain, (2) establish the side ofthe abnormality, and (3) distinguish between peripheral and central etiologies. Thestandard test is electronystagmography (calorics), where warm and cold water (orair) are applied, in a prescribed fashion, to the tympanic membranes, and the slow-phase velocities of the resultant nystagmus from the two are compared. A velocitydecrease from one side indicates hypofunction (canal paresis). An inability toinduce nystagmus with ice water denotes a dead labyrinth. Some institutionshave the capability of quantitatively determining various aspects of the VOR usingcomputer-driven rotational chairs and precise oculographic recording of the eyemovements. CNS disease can produce dizzy sensations of all types. Consequently, aneurologic examination is always required even if the history or provocative testssuggest a cardiac, peripheral vestibular, or psychogenic etiology. Any abnormalityon the neurologic examination should prompt appropriate neurodiagnosticstudies.Vertigo: Treatment Treatment of acute vertigo consists of bed rest (1–2 days maximum) andvestibular suppressant drugs such as antihistaminics (meclizine, dimenhydrinate,promethazine), tranquilizers with GABA-ergic effects (diazepam, clonazepam),phenothiazines (prochlorperazine), or glucocorticoids (Table 22-3). If the vertigopersists beyond a few days, most authorities advise ambulation in an attempt toinduce central compensatory mechanisms, despite the short-term discomfort to thepatient. Chronic vertigo of labyrinthine origin may be treated with a systematizedvestibular rehabilitation program to facilitate central compensation. Table 22-3 Treatment of VertigoAgenta DosebAntihistaminesMeclizine 25– 50 mg 3 times/dayDimenhydrinate 50 mg 1–2 times/dayPromethazinec 25– 50-mg suppository or IMBenzodiazepinesDiazepam 2.5 mg 1–3 times/day Clonazepam 0.25 mg 1–3 times/day Phenothiazines Prochlorperazinec 5 mg IM or 25 mg suppository Anticholinergicd Scopolamine Patchtransdermal Sympathomimeticsd Ephedrine 25 mg/d Combinationpreparationsd Ephedrine and 25promethazine mg/d of each Exercise therapy Repositioningmaneuverse Vestibularrehabilitationf Other Diuretics or low-salt (1 g/d) dietg Antimigrainousdrugsh Inner ear surgeryi Glucocorticoidsc 100 mg/d for 3 days, tapered by 20 mg every 3 days