Vertigo
Frank S. Celestino
Dizziness accounts for 1% to 2% of all office visits, 7% of visits by patients aged more than 80 years and 20% to 25% of all non–pain-related emergency room visits (1–3). Dizziness and vertigo are usually benign, self-limited processes not associated with excess mortality, although some individuals suffer impaired quality of life because of recurrent or persistent symptoms (4) (Chapter 2.2).
Approach
A. Classification of dizziness. Careful interviewing allows placement of patient complaints into one of four categories, each implying certain pathophysiologic mechanisms and, thus, specific differential diagnoses (2,4).
1. True vertigo. This is an hallucination of movement—a feeling that the body or environment is moving. Patients often report rotation or spinning. It often begins abruptly and, if severe, is accompanied by nausea, vomiting, and staggering gait. True vertigo most often implies a disturbance of the peripheral vestibular system (labyrinth and its connections to the brainstem) or, less commonly, of the central vestibular apparatus (brainstem or cerebellum) (2,3,5).
Peripheral causes of vertigo (in approximate order of frequency in primary care) include viral labyrinthitis or vestibular neuronitis (acute unilateral vestibulopathy), benign paroxysmal positional vertigo (BPPV), serous otitis, perilymphatic fistula, Ménière’s disease, and drugs (alcohol, aminoglycosides) (4,5). Central causes of vertigo include vertebrobasilar transient ischemic attack, cerebellar infarction or neoplasm, demyelinating disease, brainstem infarction or neoplasm, cerebellopontine angle tumors, migraine, hyperventilation, seizures, spinocerebellar degeneration, and certain systemic disorders (infections, vasculitis, syphilis) (2,4). Rarely, the cervical spine is the source of vertigo, by either osteoarthritic spur occlusion of vertebral arteries or proprioceptive overstimulation by facet joint arthropathy (2).
2. Presyncope is a sensation of impending faint (“severe lightheadedness”) implies a temporary decrement of cerebral circulation. Common causes include postural hypotension, vasovagal reactions, impaired cardiac output, and hypoglycemia (Chapter 2.12).
3. Disequilibrium is a feeling of unsteadiness of gait or imbalance in the absence of any abnormal head sensation indicating a disturbance of the motor control system. Causes include alcoholism, drugs, cervical facet joint arthropathy, multiple sclerosis, and multiple neurosensory deficits (e.g., a combination of visual impairment, vestibular hypofunction, deconditioning, peripheral neuropathy, and medications).
4. Other or atypical. Often described as a vague or mild wooziness, lightheadedness or heavy headedness, this category has a high association with psychological disturbances such as anxiety, depression, and panic (2,4).
B. Patient’s age. In young adults (<30 years) psychological causes predominate, whereas vestibular disorders do in middle age. In the elderly, cerebrovascular and cardiac disorders, combined with multiple sensory deficits, outweigh simple vestibular causes (1,5).
C. Special concerns. These include potentially life-threatening central nervous system (CNS) neoplasms, brainstem ischemia, and cardiac dysfunction manifest by focal neurologic and cardiovascular abnormalities.
History
The patient’s age, underlying comorbidities, and symptom classification category will help limit the diagnostic possibilities. Further specificity is gained by eliciting the following:
A. Temporal pattern. Are the symptoms episodic or continuous? If episodic, how long do they last? Peripheral origin vertigo is often intermittent and of sudden onset compared with the usual, more gradual onset of central vertigo. A continuous history suggests CNS pathology, drug or toxin effects, metabolic dysfunction, or psychiatric disease. BBPV episodes last less than a minute; vertebrobasilar transient ischemic attacks last minutes to an hour; Ménière’s disease persists 1 to 24 hours; and vestibular neuronitis or acute labyrinthitis continues several days.
B. Precipitating or exacerbating factors. Has there been recent head trauma (implying perilympathic fistula) or viral illness (labyrinthitis)? What is the relationship to sudden head movement or turning over in bed (BPPV), coughing or sneezing (perilymphatic fistula), postural changes (orthostasis), exercise (arrhythmias), foods (salty meals exacerbating Ménière’s), walking and turning (multiple sensory deficits), micturition or pain (vasovagal reaction), and emotional upset (hyperventilation)?
C. Associated symptoms. Marked nausea, vomiting, diaphoresis, aural fullness, and recruitment (perception of sounds being too loud) are typical of peripheral vestibular disorders. Episodic vertigo associated with tinnitus and gradual (unilateral) hearing loss involving low frequencies preferentially suggests Ménière’s disease. Asymmetric weakness, cranial nerve or cerebellar dysfunction, diplopia, or dysarthria suggests brainstem or CNS disease. Headache, scotomata, or tunnel vision points to migraine. Numbness or paresthesias may indicate neuropathy contributing to multiple sensory deficits (Chapter 4.6). A single, abrupt episode of severe vertigo with negative Dix-Hallpike (DH) testing (section III.A) that gradually subsides over days implies labyrinthitis (if hearing is affected) or vestibular neuronitis (if hearing is unaffected). Mild vertigo with prominent tinnitus, unilateral hearing loss, and loss of corneal reflex is worrisome for an acoustic neuroma.
D. Medications or toxins. Many medications can cause “dizziness,” although few (aminoglycosides, lead, mercury) cause vertigo. Assess toxin exposure by exploring job and recreational activities.
Physical examination (PE)
This will emphasize orthostatic vital signs, the eyes, ears, and neurologic and cardiovascular systems.
A. Detection of nystagmus is critical because it is the only objective sign of vertigo (5). Nystagmus can occur spontaneously or in response to changes in eye or body position. Peripheral vestibular disorders usually cause horizontal or rotatory nystagmus, whereas CNS pathology is reflected by vertical nystagmus—an ominous sign. In true vertigo caused by BPPV, DH maneuvers will often confirm the diagnosis (sensitivity 60% to 90%, specificity 90% to 95%) (2,3). The patient is moved rapidly from a sitting to a supine position with the head turned at a 30-degree angle, first to one side and then to the other. A positive DH test includes precipitation of vertigo, latency of onset by a few seconds, rotational nystagmus, resolution within a minute, and lessened symptoms and nystagmus with prolonged latency on repeated testing (i.e., fatiguability). Lack of latency and fatiguability characterize vertigo caused by serious central lesions.
B. Neurologic examination serves to detect brainstem or CNS pathology.
C. Otoscopy can detect otitis media or cholesteatoma. Nystagmus with vertigo following positive or negative pressure applied to the tympanic membrane (pneumatic otoscopy) suggests a perilymphatic fistula.
D. Other provocative tests (forced hyperventilation, vestibulo-ocular reflex testing, vigorous horizontal head shaking) are not routinely helpful.
Testing
A. Clinical laboratory tests. Most (80% to 90%) patients will need no laboratory testing (2,4,5). Audiometry is suggested if tinnitus or hearing loss is present. Blood tests are dictated by appropriate clinical indications only. Brainstem auditory-evoked responses can help elucidate multiple sclerosis. Holter monitoring is indicated if arrhythmias are suspected. Specialized testing—posturography, rotational chair testing, electronystagamography—is best ordered by a consultant.
B. Diagnostic imaging. Consider Doppler ultrasound for suspected transient ischemic attack and magnetic resonance imaging if CNS lesions are suspected.
Diagnostic assessment
A comprehensive history can categorize the patient’s problem as one of vertigo, presyncope, disequilibrium, or other (atypical). PE maneuvers (especially DH testing), detection of nystagmus, and assessment of neurologic function will further pinpoint the likely diagnosis. It is helpful to remember that true vertigo results most often from peripheral vestibular disorders, presyncope from cardiovascular dysfunction, disequilibrium from neurologic disorders, and other (atypical or vague) symptoms from psychological or psychiatric disease.
References
1. Sloane PD. Dizziness in primary care: results from the National Ambulatory Medical Care Survey. J Fam Pract 1989;29:33–38.
2. Derebery MJ. The diagnosis and treatment of dizziness. Med Clin North Am 1999;83:163–176.
3. Walker JS, Barnes SB. Dizziness—the difficult diagnosis. Emerg Med Clin North Am 1998;16:845–878.
4. Sloane PD. Evaluation and management of dizziness in the older patient. Clin Geriatr Med 1996;12:785–801.
5. Drachman DA. Clinical crossroads—a 69-year-old man with chronic dizziness. JAMA 1998;280:2111–2118. >
Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
Other Book Chapters Related to Fainting
Read excerpts from these other book chapters related to Fainting:
Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2008 Williams & Wilkins.
More About Causes of Fainting
» Next page: Coma (Field Guide to Bedside Diagnosis)
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