Chapter 022. Dizziness and Vertigo (Part 5)

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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) 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 (or air) 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 velocity decrease from one side indicates hypofunction ("canal paresis"). An inability to
induce nystagmus with ice water denotes a "dead labyrinth." Some institutions have the capability of quantitatively determining various aspects of the VOR using computer-driven rotational chairs and precise oculographic recording of the eye movements. CNS disease can produce dizzy sensations of all types. Consequently, a neurologic examination is always required even if the history or provocative tests suggest a cardiac, peripheral vestibular, or psychogenic etiology. Any abnormality on the neurologic examination should prompt appropriate neurodiagnostic studies.Vertigo: Treatment Treatment of acute vertigo consists of bed rest (1–2 days maximum) and vestibular suppressant drugs such as antihistaminics (meclizine, dimenhydrinate, promethazine), tranquilizers with GABA-ergic effects (diazepam, clonazepam), phenothiazines (prochlorperazine), or glucocorticoids (Table 22-3). If the vertigo persists beyond a few days, most authorities advise ambulation in an attempt to induce central compensatory mechanisms, despite the short-term discomfort to the patient. Chronic vertigo of labyrinthine origin may be treated with a systematized vestibular rehabilitation program to facilitate central compensation. Table 22-3 Treatment of Vertigo
Agenta Doseb Antihistamines Meclizine 25– 50 mg 3 times/day Dimenhydrinate 50 mg 1–2 times/day Promethazinec 25– 50-mg suppository or IM Benzodiazepines Diazepam 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 Patch transdermal Sympathomimeticsd Ephedrine 25 mg/d
Combination preparationsd Ephedrine and 25 promethazine mg/d of each Exercise therapy Repositioning maneuverse Vestibular rehabilitationf Other Diuretics or low- salt (1 g/d) dietg
Antimigrainous drugsh Inner ear surgeryi Glucocorticoidsc 100 mg/d for 3 days, tapered by 20 mg every 3 days