Harrison’s Manual of Medicine



Pathologic Vertigo

Patients use the term dizziness to describe a variety of head sensations or gait unsteadiness. With a careful history, symptoms can be placed into more specific neurologic categories, of which faintness and vertigo are the most important.
FAINTNESS   Faintness is usually described as light-headedness followed by visual blurring and postural swaying. It is a symptom of insufficient blood, oxygen, or, rarely, glucose supply to the brain. It can occur prior to a syncopal event of any etiology (Chap. 8) and with hyperventilation or hypoglycemia. Lightheadedness can also occur as an aura before a seizure. Chronic light-headedness is a common somatic complaint in patients with depression.
VERTIGO   Vertigo is an illusion of movement, most commonly a sensation of spinning. It is usually due to a disturbance in the vestibular system; abnormalities in the visual or somatosensory systems may also contribute to vertigo. Physiologic vertigo results from unfamiliar head movement (seasickness) or a mismatch between visual-proprioceptive-vestibular system inputs (height vertigo, visual vertigo). True vertigo almost never occurs in the presyncopal state.
Pathologic Vertigo
Frequently accompanied by nausea, postural unsteadiness, and gait ataxia, vertigo is provoked or worsened by head movement. May be caused by a peripheral (labyrinth or eighth nerve) or central CNS lesion. Distinguishing between peripheral and central causes is the essential first step in diagnosis (Table 9-1).

Table 9-1 Differentiation of Peripheral and Central Vertigo

PERIPHERAL VERTIGO   Usually severe, accompanied by nausea and emesis. Tinnitus, a feeling of ear fullness, or hearing loss may occur. The pt may be pale and diaphoretic. A characteristic jerk nystagmus is almost always present. The nystagmus does not change direction with a change in direction of gaze, it is horizontal with a torsional component and has its fast phase to side of normal ear. It is inhibited by visual fixation. The pt senses spinning motion in direction of slow phase and falls or mispoints to that side. No other neurologic abnormalities are present.
Acute unilateral labyrinthine dysfunction may be caused by infection, trauma, or ischemia. Often no specific etiology is uncovered, and the nonspecific term acute labyrinthitis (or vestibular neuronitis) is used to describe the event. The attacks are brief and leave the patient for some days with a mild positional vertigo; recurrent episodes may occur. Acute bilateral labyrinthine dysfunction is usually due to drugs (aminoglycoside antibiotics) or alcohol. Recurrent labyrinthine dysfunction with signs of cochlear disease is usually due to Ménière’s disease (recurrent vertigo accompanied by tinnitus and deafness). Positional vertigo is usually precipitated by a recumbant head position. Benign paroxysmal positional vertigo (BPPV) of the posterior semicircular canal is particularly common; the pattern of nystagmus is distinctive (Table 9-2). BPPV may follow trauma but is usually idiopathic; it generally abates spontaneously after weeks or months. Schwannomas of the eighth cranial nerve (acoustic neuroma) usually present as auditory symptoms of hearing loss and tinnitus, sometimes accompanied by facial weakness and sensory loss due to involvement of cranial nerves VII and V. Psychogenic vertigo should be suspected in pts with chronic incapacitating vertigo who also have agoraphobia, a normal neurologic exam, and no nystagmus.

Table 9-2 Benign Paroxysmal Positional Vertigo (BPPV) and Central Positional Vertigo

CENTRAL VERTIGO   Identified by associated abnormal brainstem or cerebellar signs such as dysarthria, diplopia, paresthesia, headache, weakness, limb ataxia. The nystagmus can take almost any form, i.e., vertical or multidirectional, but is often purely horizontal without a torsional component. Central nystagmus is not inhibited by fixation. Central vertigo may be chronic, mild, and is often unaccompanied by tinnitus or hearing loss. It is usually a sign of brainstem dysfunction and may be due to demyelinating, vascular, or neoplastic disease. Rarely, it occurs as a manifestation of temporal lobe epilepsy.

Approach to the Patient

The “dizzy” patient usually requires provocative tests to reproduce the symptoms. Valsalva maneuver, hyperventilation, or postural changes may reproduce faintness. Rapid rotation in a swivel chair is a simple provocative test to reproduce vertigo. Benign positional vertigo is identified by positioning the turned head of a recumbent patient in extension over the edge of the bed to elicit vertigo and the characteristic nystagmus. If a vestibular nerve or central cause for the vertigo is suspected (e.g., signs of peripheral vertigo are absent or other neurologic abnormalities are present), then prompt evaluation for central pathology is indicated, including an MRI scan of the posterior fossa and possibly electronystagmography, evoked potential tests, or vertebrobasilar angiography.

Treatment of acute vertigo consists of bed rest and vestibular suppressant drugs (Table 9-3). If the vertigo persists more than a few days, most authorities advise ambulation in an attempt to induce central compensatory mechanisms. BPPV may respond to specific repositioning exercises such as the Epley procedure (www.charite.de/ch/neuro/vertigo.html). Ménière’s disease may respond to a low-salt diet (1 g/d) or to a diuretic.

Table 9-3 Treatment of Vertigo


For a more detailed discussion, see Daroff RB, Carlson MD: Faintness, Syncope, Dizziness, and Vertigo, Chap. 21, p. 111, in HPIM-15.


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