APPROACH TO THE PATIENT Dizziness or Vertigo
The term dizziness is used by pts to describe a variety of head sensations or gait unsteadiness. With a careful history, distinguishing between faintness (presyncope; Chap. 56) and vertigo (an illusory or hallucinatory sense of movement of the body or the environment, most often a feeling of spinning) is usually possible.
When the meaning of dizziness is uncertain, provocative tests to reproduce the symptoms may be helpful. Valsalva maneuver, hyper-ventilation, or postural changes leading to orthostasis may reproduce faintness. Rapid rotation in a swivel chair is a simple provocative test to reproduce vertigo.
Benign positional vertigo is identified by the Dix-Hallpike maneuver to elicit vertigo and the characteristic nystagmus; the pt begins in a sitting position with head turned 45 degrees; holding the back of the head, examiner gently lowers pt to supine position with head extended backward 20 degrees and observes for nystagmus; after 30 s the pt is raised to sitting position and after 1 min rest the maneuver is repeated on other side.
If a 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. Distinguishing between central and peripheral etiologies can be accomplished with vestibular function tests, including videonystagmography and simple bedside exams including the head impulse test(rapid, small amplitude head rotations while pt instructed to fixate on the examiner’s face; if peripheral, a catch-up saccade is seen at the end of the rotation) and dynamic visual acuity (measure acuity at rest and with head rotated back and forth by examiner; a drop in acuity of more than one line on a near card or Snellen chart indicates vestibular dysfunction).
FAINTNESS
Faintness is usually described as light-headedness followed by visual blurring and postural swaying along with a feeling of warmth, diaphoresis, and nausea. 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. 56) and with hyperventilation or hypoglycemia. Lightheadedness can rarely occur during an aura before a seizure. Chronic lightheadedness is a common somatic complaint with depression.
VERTIGO
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; 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 during motion picture chase scenes). 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 57-1) as central lesions require urgent imaging, usually with MRI.
TABLE 57-1 FEATURES 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. A characteristic jerk nystagmus is almost always present. The nystagmus does not change direction with a change in direction of gaze; it is usually 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 have difficulty walking, with falls towards the side of the lesion, particularly in the darkness or with eyes closed. No other neurologic abnormalities are present.
Acute prolonged vertigo may be caused by infection, trauma, or ischemia. Often no specific etiology is found, and the nonspecific term acute labyrinthitis (or vestibular neuritis) is used to describe the event. Acute bilateral labyrinthine dysfunction is usually due to drugs (aminoglycoside antibiotics), alcohol, or a neurodegenerative disorder. Recurrent labyrinthine dysfunction with signs and symptoms of cochlear disease is usually due to Ménière’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. BPPV may follow trauma but is usually idiopathic; it generally abates spontaneously after weeks or months. Vestibular schwannomas of the eighth cranial nerve (acoustic neuroma) usually present as 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, panic attacks, a normal neurologic exam, and no nystagmus.
Central Vertigo
Identified by associated brainstem or cerebellar signs such as dysarthria, diplopia, dysphagia, hiccups, other cranial nerve abnormalities, weakness, or 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 and changes direction with different directions of gaze. Central nystagmus is not inhibited by fixation. Central vertigo may be chronic, mild, and is usually not accompanied by tinnitus or hearing loss. It may be due to vascular, demyelinating, or neoplastic disease. Vertigo may be a manifestation of migraine or, rarely, of temporal lobe epilepsy.
TREATMENT Vertigo
• Treatment of acute vertigo consists of vestibular suppressant drugs for short-term relief (Table 57-2). They may hinder central compensation, prolonging the duration of symptoms, and therefore should be used sparingly.
TABLE 57-2 TREATMENT OF VERTIGO
• Vestibular rehabilitation promotes central adaptation processes and may habituate motion sensitivity and other symptoms of psychosomatic dizziness.
• BPPV may respond dramatically to repositioning exercises such as the Epley procedure designed to empty particulate debris from the posterior semicircular canal (www.youtube.com/watch?v=pa6t-Bpg494).
• For vestibular neuritis, antiviral medications are of no proven benefit unless herpes zoster oticus is present. Some data suggest that glucocorticoids improve the likelihood of recovery in vestibular neuritis.
• Ménière’s disease may respond to a low-salt diet (1 g/d) or to a diuretic. Otolaryngology referral is recommended.
• Recurrent episodes of migraine-associated vertigo should be treated with antimigraine therapy (Chap. 55).
For a more detailed discussion, see Walker MF, Daroff RB: Dizziness, and Vertigo, Chap. 21, p. 178, in HPIM-18.