Dizziness and Vertigo

The term dizziness is used by pts 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. 38) and with hyperventilation or hypoglycemia. Lightheadedness can

also occur as an aura before a seizure. Chronic lightheadedness is a common

somatic complaint in patients with depression. Elderly patients with multiple

sensory deficits,such as impaired sensation in the feet and poor vision, often

complain of chronic lightheadedness and dizziness without true vertigo (multiple

sensory-deficit dizziness).

Vertigo

An illusion of movement,most commonly a sensation of spinning. Usually due

to a disturbance in the vestibular system; abnormalities in the visual or somatosensory systems may also contribute to vertigo. Frequently accompanied by

nausea,postural unsteadiness,and gait ataxia,and may be provoked or worsened

by head movement. 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 as a

presyncopal symptom.

Pathologic vertigo may be caused by a peripheral (labyrinth or eighth nerve)

or central CNS lesion. Distinguishing between these causes is the essential first

step in diagnosis (Table 39-1).

Peripheral Vertigo Usually severe,accompanied by nausea and emesis.

Tinnitus,a feeling of ear fullness,or hearing loss may occur. The pt may appear

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 away from the

side of the lesion. It is inhibited by visual fixation. The pt senses spinning motion

away from the lesion and tends to fall towards the side of the lesion. 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 Me´nie`re’s disease (recurrent vertigo accompanied by tinnitus and deafness). Positional vertigo is usually precipitated by a recumbent head position. Benign paroxysmal positional vertigo (BPPV) of the posterior semicircular canal is particularly common; the pattern of nystagmus is distinctive (Table 39-2). 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.

Central Vertigo Identified by associated abnormal brainstem or cerebellar

signs such as dysarthria,diplopia, paresthesia, weakness, limb ataxia; depending

on the cause,headache may be present. 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 may be due to demyelinating,vascular,or neoplastic disease. Vertigo

may be a manifestation of migraine or,rarely, 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 required. The initial test is usually an MRI scan of the posterior fossa,and

depending upon the results evoked potentials or vertebrobasilar angiography

may be indicated. Vestibular function tests,including electronystagmography

(calorics),can help distinguish between central and peripheral etiologies.

TREATMENT

Treatment of acute vertigo consists of bed rest and vestibular suppressant

drugs (Table 39-3). 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 repositioning exercises such as the Epley

procedure designed to empty particulate debris from the posterior semicircular

canal (www.charite.de/ch/neuro/vertigo.html). Me´nie`re’s disease may respond

to a low-salt diet (1 g/d) or to a diuretic.