Evaluation of dizziness can be a complex and challenging task for clinicians. The differential diagnosis is broad, and the literature offers no evidence-based clinical practice guidelines. Optimal care requires the identification and treatment of the condition or combination of conditions causing dizziness when possible. If treatable conditions cannot be found, then the objective becomes maximum symptomatic improvement of dizziness. Based on these objectives and on the available evidence, a stepwise approach is recommended for the evaluation of chronic dizziness, proceeding from careful history and physical examination to screening laboratory tests. A targeted battery of more elaborate and expensive tests is indicated only when routine evaluation suggests a specific disease entity and the results of these tests are likely to influence the management. For the majority of older persons in whom a routine evaluation does not suggest a single discrete cause, the clinician should try to focus on identifying various factors (Table 50-1) that might be contributing to dizziness, some of which are likely to be modifiable. When etiology is multifactorial, identifying and treating one or more contributing factors may improve, if not eliminate the dizziness.
TABLE 50-1POSSIBLE CONTRIBUTORS TO CHRONIC DIZZINESS ||Download (.pdf) TABLE 50-1 POSSIBLE CONTRIBUTORS TO CHRONIC DIZZINESS
|CONTRIBUTOR ||HISTORY ||EXAMINATION ||POSSIBLE CAUSES ||POTENTIAL INTERVENTIONS |
|Vision ||Use of bifocals or trifocals ||Abnormalities in near/distant acuity; contrast sensitivity; depth perception ||Cataract; glaucoma; macular degeneration; perceptual difficulties with glasses ||Appropriate refraction; consider avoiding bifocals or trifocals when walking; drugs for glaucoma; surgery; good lighting without glare |
|Hearing ||Deafness in one or both ears; difficulty hearing in social situations ||Abnormal findings with Rinne test, Weber test, Whisper test, or audiometry ||Presbycusis; otosclerosis ||Hearing aid; surgery (for otosclerosis); hearing rehabilitation; listening devices |
|Vestibulocochlear system ||True vertigo, worse in dark or with specific head positions; tinnitus; history of aminoglycosides, furosemide, aspirin use; ear surgery; ear or mastoid infections ||Nystagmus (horizontal or rotary nystagmus suggests a peripheral vestibular disorder; vertical nystagmus suggests a central disorder); decreased neck range of motion; decreased hearing; abnormal Hallpike maneuver; abnormal vestibular testing ||Drug toxicity; previous infections, tumor (eg, acoustic neuroma); previous surgery; vascular (eg, brainstem infarct); benign positional vertigo; Ménière disease ||Avoid toxic drugs and long-term vestibular suppressants; remove earwax; vestibular rehabilitation; surgery |
|Peripheral nerves ||Worse in dark or on uneven surfaces or inclines ||Decreased neck range of motion; signs of radiculopathy or myelopathy; clumsiness with fine motor tasks; mild spastic gait; increased tone ||Spondylosis; degenerative or inflammatory arthritis ||Treatment of underlying disease; cervical or balance exercises; appropriate assistive device; consider surgery in selected cases |
|Cerebral hypoperfusion ||Presyncope; near fainting ||Postural hypotension; signs of underlying disease ||See causes for syncope in Chapter 51; cardiovascular and pulmonary diseases; anemia ||Treatment of underlying disease |
|Postprandial hypotension ||Symptoms within 1 h of eating ||Hypotension after meals ||Postprandial hypotension ||Small meals; avoid exertion after meals; avoid hypotensive drugs near meals; have caffeine with meals |
|Postural hypotension ||Near fainting—worse when getting up, walking, exercising; complaints consistent with predisposing diseases; may be asymptomatic; history of predisposing drugs ||Blood pressure and heart rate; signs of predisposing diseases ||Drugs, volume/salt depletion; deconditioning; Parkinson syndrome; diabetes; autonomic dysfunction ||Treatment of salt and water repletion; reconditioning exercises; ankle pumps or hand clenching; slow rising; elevate head of bed; graduated stockings; lowest effective dosage of essential contributing drugs |
|Cardiac dysfunction ||Variable, depending on specific etiology ||Cardiac auscultation, ECG, echocardiography ||Cardiac arrhythmias, valvular lesions, myocardial ischemia, myxoma, hypertrophic cardiomyopathy ||Variable, depending on specific etiology |
|Brain stem ||Any sensation (eg, vertigo, near fainting, wooziness); transient neurologic symptoms (eg, slurred speech, visual change, one-sided weakness); symptoms on looking up ||Findings may be transient or fixed; ataxia ||Transient ischemic attack; brain stem infarct; vertebrobasilar insufficiency ||Low-dose aspirin; assistive device if ataxic |
|Metabolic diseases ||Symptoms of underlying disease ||Signs of underlying disease ||Any metabolic disease, (eg, thyroid disorders, diabetes) ||Treatment of underlying disease |
|Vestibulocochlear symptoms (see above) ||See above under vestibulocochlear system ||See above under vestibulocochlear system ||See above under vestibulocochlear system |
| Current ||Confusion; fatigue; weakness; dizziness often vague, may be constant ||May have postural hypotension || |
Specific: nitrates, β-blockers, antidepressants, antipsychotics, anticholinergics; vestibular depressants, benzodiazepines, others
General: total number and dose of all drugs
|Eliminate, substitute, or reduce specific offending drugs if possible; reduce all other drugs to lowest effective dose possible; remember over-the-counter drugs |
|Depression, anxiety ||Constant dizziness; multiple somatic complaints; poor concentration; positive results on anxiety or depression screening; vegetative complaints (sleep, appetite) ||See Chapter 71 ||Depression, anxiety ||Thorough consideration of risks and benefits of antidepressant drug; counseling |
Patients should be asked to describe the feelings of dizziness in their own words, supplemented by directed questions. Older patients often describe a vague sensation, such as “whirling,” or “giddiness,” or a combination of sensations. Before physicians ask leading questions, patients should be encouraged to describe symptoms in their own words. In one retrospective chart review study of 310 older patients, charts documenting patients’ dizziness symptoms in their own words were more likely to have a clinical diagnosis, compared to charts without such documentation. Narrowing the differential diagnosis can often occur following a careful history. Determining whether the attacks are episodic or continuous may help in identifying a specific disease. For example, patients with Ménière disease or BPPV will usually have episodic dizziness, the latter precipitated by specific movements, while psychogenic dizziness is usually continuous. Frequency and duration of dizziness also should be determined. Episodic dizziness lasting less than 1 minute suggests BPPV, episodes lasting 5 to 120 minutes suggest TIA or migraine, while episodes longer than 120 minutes suggest Ménière disease or recurrent vestibulopathy. One should also ask about any precipitating factors of dizziness, such as missing a meal, drinking alcohol, taking a medication, standing from a lying position, rolling over in bed, changing the position of the head or neck (such as looking up or from side to side), bending forward to pick something up, micturition, or defecation. Any relationship between the onset of dizziness and meals should be sought, because postprandial hypotension is common, especially in frail older persons. The patient should also be asked about any symptoms associated with dizziness. For example, patients with Ménière disease often will complain of tinnitus, fullness in ear, and fluctuating hearing loss. Patients with vertebrobasilar involvement may complain of double vision, dysarthria, or sudden blackouts. Patients with cervical arthritis may also complain of associated neck pain on movement. The clinician should also ask about comorbid conditions, such as anemia, cardiac diseases, or diabetes which may contribute to dizziness. One should look for symptoms suggestive of depression or anxiety disorders; use of screening instruments can be helpful. Finally, all medications, including over-the-counter, should be reviewed as potential contributors to dizziness.
The clinician should do a focused physical examination (see Table 50-1), keeping in mind the complex pathophysiology and broad differential diagnosis of dizziness. The examiner should look for spontaneous nystagmus on cranial nerve testing. The nystagmus is vertical in central lesions and horizontal or rotatory in peripheral lesions. The nystagmus of central lesions is not suppressed by visual fixation; in peripheral lesions, nystagmus can be suppressed by visual fixation. One should also test for near and distant vision. The ear examination should include both a hearing test (Whisper test or audioscope) and an otoscopic examination to rule out cerumen impaction or structural abnormalities. Blood pressure and heart rate should be assessed upright after at least 5 minutes of lying quietly to rule out orthostatic hypotension. One should examine the neck for local tenderness and restriction in the range of movement, which can result from cervical arthritis. One should also consider that the patient might voluntarily restrict the range of neck movement in order to minimize dizziness secondary to vestibular dysfunction; such patients may respond well to vestibular rehabilitation.
A neurologic examination should include cranial nerves, the motor and sensory systems, and gait and balance. In the cranial nerve examination, one should look for diplopia, dysarthria, or facial paresthesia to rule out vertebrobasilar involvement. An absence of corneal reflex suggests acoustic neuroma, especially if accompanied by unilateral hearing loss, tinnitus, and cerebellar signs. The presence of cogwheel rigidity and bradykinesia is suggestive of parkinsonism. Although most of the abnormalities detected in the balance examination are not specific, the presence of a positive Romberg sign with the eyes closed is suggestive of an abnormality of proprioception and/or the vestibular system. A wide-based stance, a worsening of the gait with the eyes closed, and an improvement in gait with minimal handheld assistance of the examiner, in combination, suggest a proprioceptive deficit.
In addition to the history and physical examination, clinicians can also perform certain provocative tests at the bedside or in the office which may help in detecting abnormalities of the vestibular system.
These tests include the Dix-Hallpike maneuver, head thrust, postheadshake, and stepping tests. The Dix-Hallpike test establishes the diagnosis of BPPV (Figure 50-1). In this test, the patient is asked to sit on an examination table with the head rotated 45 degrees to one side. The patient is then asked to fix his/her vision upon the examiner’s forehead. The examiner, while holding the patient’s head firmly in the same position, moves the patient from a seated to a supine position with the head hanging below the edge of the table. If the ipsilateral ear is affected then this maneuver will result in vertigo and nystagmus. If present, the direction, latency, and duration of nystagmus, and duration of vertigo should be noted. The diagnostic criteria for BPPV are (1) vertigo accompanied by a rotatory nystagmus; (2) a latency of 1 to 5 seconds between the completion of the maneuver and the onset of vertigo and nystagmus; (3) paroxysmal nature of the vertigo and nystagmus (lasting for 10–20 seconds); and (4) fatigability, that is, a decrease in the intensity of the vertigo and nystagmus with repeated testing. In a US emergency department study, the authors reported that Dix-Hallpike test is underused to rule out BPPV in patients presenting with complain of dizziness.
Dix-Hallpike test. (From Furman JM, Cass SP. Benign paroxysmal positional vertigo. N Engl J Med. 1999;341:1590. Copyright © 1999 Massachusetts Medical Society. All rights reserved.)
The head thrust and postheadshake tests can help in determining if the vestibuloocular reflex (VOR) is intact. The VOR helps maintain visual stability during head movement. It functions according to the information relayed by the vestibular nucleus to the sixth cranial nerve nucleus in the pons, as well as to the third and fourth cranial nerve nuclei in the midbrain through the median longitudinal fasciculus. The head thrust test requires the patient to fix vision on the examiner’s nose, while the head is quickly turned approximately 10 degrees to the left or right. If the VOR is intact, the eyes will stay fixed to the target. But in patients with a vestibular defect, the eyes move with the head away from the target before a corrective saccade back to it. For instance, head thrusts to the left in patients with left-sided vestibular lesions will cause a slipping away of the pupils from the target, followed by a corrective movement; head thrusts to the right will produce a normal visual response.
Using Frenzel lenses to eliminate fixation of vision, the postheadshake test calls for the head to be rotated for approximately 10 seconds, either passively by the examiner or actively by the patient at a frequency of approximately 2 Hz in the horizontal plane, after which the examiner checks for nystagmus. If there is a unilateral peripheral vestibular lesion, a horizontal nystagmus will result; the fast phase will usually beat away from the side of the lesion. With central lesions, the nystagmus may be vertical.
Unterberger originally introduced the stepping test, later modified by Fukuda. A positive stepping test suggests a lesion in the vestibular or vestibulospinal system. In this test, the patient stands at the center of a circle that is divided into sections, with lines intersecting at 30-degree angles. Blindfolded, the patient is asked to stretch out both arms at 90 degrees to the body and then to flex and raise high one knee and then the other, and to continue stepping in place at a normal walking speed for a total of 50 or 100 steps. The blindfolded patient marches and the examiner watches for deviation from the straight line. If there is a unilateral vestibular lesion or acoustic neuroma, a gradual rotation of the body (more than 30 degrees) toward the affected side will occur.
These tests are more useful in detecting unilateral than bilateral vestibular dysfunction. Upon finding any abnormalities, one can proceed with specialized vestibular function, tests such as ENG and the rotational chair test, described under “Laboratory Tests.” Clinicians must be aware that compensatory mechanisms may mask a vestibular deficit when these tests are used in patients with long-standing vestibular loss. There are no data addressing the specificity or sensitivity of these tests in older persons.
There is no standardized approach for laboratory testing for patients with chronic dizziness. However, a modest baseline battery of tests should be done in all older persons with chronic dizziness to rule out common modifiable contributors to dizziness. Thus, a hematocrit, basic metabolic panel, thyroid function tests, and vitamin B12 levels should be done in all patients to rule out anemia, diabetes, azotemia, hypothyroidism, and vitamin B12 deficiency.
Further testing should be tailored to the situation. Audiometry should be done in patients with a history of fluctuating or gradual hearing loss. An audiogram will reveal sensorineural loss in both Ménière disease and acoustic neuroma; the hearing loss will be greater in lower frequencies in Ménière disease and in higher frequencies in acoustic neuroma, often unilaterally. Presbycusis usually results in bilateral high-frequency hearing loss. An electrocardiogram is indicated if there is a suspicion of myocardial infarction or cardiac arrhythmia. Holter or event monitoring or tilt table testing is indicated only in selected patients with unexplained syncope (see Chapter 51).
In patients with a suspicion of cervical osteoarthritis, imaging of the cervical spine can be considered, but the frequency of false positives is great. Neuroimaging is needed when a stroke or cerebellopontine tumor is suspected. Magnetic resonance imaging (MRI) is preferred over computed tomography scans because of its greater sensitivity, particularly for lesions in the brain stem. Routine MRI is unlikely to reveal specific causes of dizziness. In one study of MRI in patients with dizziness, there were no significant differences in structural abnormalities found in the brain or neck in patients with and without dizziness. Doppler studies or a magnetic resonance angiogram (MRA) may be needed to detect vertebrobasilar insufficiency.
Abnormalities of the peripheral vestibular system can be evaluated by performing special tests, such as ENG including caloric testing, a rotational chair test, and computerized posturography. These tests can help confirm history and physical examination data. However, abnormalities are common in older persons without dizziness, so a positive test is often neither specific nor diagnostic.
In ENG, movements of the eyes (nystagmus) are recorded in the form of tracings with the help of electrodes placed around the eyes. These electrodes record changes in scalp potential produced by the corneal-retinal potential in response to visual and vestibular stimuli, which can be either spontaneous or provoked by caloric stimuli of warm and cold water in the external ear canal. In caloric testing, each ear is stimulated first with warm (111°F [44°C]) and then with cold water (86°F [30°C]), each instilled over 30 seconds. When vestibular function is normal, the temperature change will result in nystagmus, but there will be decreased or no response in an ear on the side of peripheral vestibular disorder. The caloric test assesses the symmetry of vestibular function, and is useful in detecting unilateral vestibular lesions. However, patients with bilateral vestibular loss or patients in whom caloric testing cannot be performed should undergo rotational chair testing.
A rotational chair test, in addition to quantifying the extent of lesions in patients with bilateral peripheral vestibular loss, also helps reveal the degree of peripheral or central vestibular dysfunction. In this test, the patient is seated on a chair in a dark room, and eye movements are recorded when the chair is rotated at different frequencies.
Computerized posturography evaluates the ability of the patient to maintain balance in response to individual or combinations of visual, vestibular, or proprioceptive stimuli while standing on a platform that can be perturbed in three dimensions. This test may be helpful in providing additional confirmatory data when there is a suspicion of peripheral vestibular pathology, but ENG and rotational chair testing are equivocal. In addition, computerized posturography may be the only positive test in the case of central vestibular and extravestibular CNS pathology. Posturography also may be helpful in determining which patients with dizziness are likely to benefit from vestibular rehabilitation.