Dizziness in Primary Care Patients ELIZABETH A. WARNER, MD, PAUL M. WALLACH, MD, HAROLD M. ADELMAN, MD, KAREN SAHLIN-HUGHES, MD IN THE PRIMARY CARE PRACTICE of medicine, patients often c o m p l a i n of dizziness, one of the most c o m p l e x and frustrating s y m p t o m s for the physician to evaluate. "Dizziness" describes an uncomfortable, disturbed state of spatial awareness. Multiple systems maintain the p r o p e r p e r c e p t i o n of the relationship b e t w e e n the person and the environment, including the vestibular, visual, and p r o p r i o c e p t i v e systems; disorders in any of these areas can lead to the s y m p t o m of dizziness. 1 There are n u m e r o u s causes of dizziness, ranging from benign problems, such as i m p a c t e d cerumen, to devastating events, such as brain-stem infarctions. In this r e v i e w article, w e describe the f r e q u e n c y of dizziness as a c o m p l a i n t and the main categories of dizziness in the p r i m a r y care setting. A systematic a p p r o a c h to dizziness can greatly ease the task of evaluating a patient w h o has this p r o b l e m .

FREQUENCY Dizziness is e n c o u n t e r e d with varying f r e q u e n c y d e p e n d i n g on the type of practice. In a 1985 nationwide p r i m a r y care survey, dizziness a c c o u n t e d for 1% of all chief complaints b y patients over 25 years of age. The p e r c e n t a g e increased with age, to a f r e q u e n c y of 3.7% for patients over 85 years old. Only 1.5% of the patients w h o had dizziness w e r e admitted to the hospital, 4.4% w e r e referred to a specialist, and 89% w e r e given a prescription (most c o m m o n l y meclizine). The diagnoses of the patients admitted included a variety of c o m m o n medical problems: influenza, acute gastritis, adverse drug reaction, syncope, coronary insuflficiency, arrhythmia, cerebrovascular disease, and diabetic ketoacidosis. 2 At an a m b u l a t o r y internal m e d i c i n e clinic, Kroenke and Mangelsdorff c o n d u c t e d a retrospective review of 14 symptoms. Dizziness rated as the third most c o m m o n complaint, w i t h a three-year incidence of 5.5 %.3 A cause for the dizziness was d o c u m e n t e d for only 20% of these patients. When patients at the same clinic w e r e asked p r o s p e c t i v e l y to note w h i c h c o m m o n s y m p t o m s r e p r e s e n t e d " m a j o r health p r o b l e m s , " 17% listed dizziness. 4 Since the classic study of Drachman and Hart in

Received from the University of South Florida College of Medicine, Division of General Internal Medicine, Department of Internal Medicine, 12901 Bruce B. Downs Boulevard, Box 19, Tampa, Florida 33612. Address correspondence and reprint requests to Dr. Warner.

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1972, the s y m p t o m c o m p l e x of dizziness has b e e n divided into four categories: vertigo, p r e s y n c o p e , disequilibrium, and lightheadedness. 5 Vertigo represents a definite rotational sensation. The feeling that one m a y faint w i t h o u t actually losing consciousness describes presyncope. Disequilibrium refers to a p r o b l e m w i t h balance, usually associated with an unsteady gait. Lightheadedness is a vague sensation, not characterized b y any of the other three categories, often imprecisely described by the patient. The f r e q u e n c y of each category of dizziness relates to the clinical setting. In a study of a n e u r o l o g y clinic specializing in dizziness, a diagnosis was made for 91% of the 104 patients, s The evaluation included an extensive battery of tests in addition to a history and physical examination: n e u r o - o p h t h a l m o l o g i c examination, neuro-otologic studies (including electronystagmography and caloric testing), psychological tests, and laboratory studies. Peripheral vestibular disorders c o m p r i s e d the most c o m m o n category of dizziness, accounting for 38% of the diagnosis. Next in f r e q u e n c y was hyperventilation, a type of lightheadedness, diagnosed in 23% of the patients. Other m o r e well-defined psychiatric disorders, such as anxiety and depression, a c c o u n t e d for 9% of the diagnoses. W h e n added together, hyperventilation and these psychiatric disorders a c c o u n t e d for nearly a third of the total diagnoses. Disequilibrium, caused by m u l t i p l e sensory deficits, was responsible for 13% of the diagnoses. Cerebrovascular disease was the cause for only 5% of the patients. In e m e r g e n c y rooms, peripheral vestibular disorders w e r e also f o u n d to be the most c o m m o n diagnosis.6, 7 Next in f r e q u e n c y w e r e cardiovascular diseases 7 or infections, 6 usually viral. No diagnosis was m a d e for 10% to 37% of the e m e r g e n c y r o o m patients. In the geriatric population, disequilibrium and presync o p e due to orthostatic hypotension are m o r e frequent causes of dizziness. 8

VERTIGO Vertigo, the sensation of abnormal m o t i o n either of the surroundings or of the body, may result from a disc r e p a n c y in the brain's e x p e c t a t i o n of position sense and the incorrect cues it receives from the vestibular system. 9 The vestibular system provides an awareness of the body's position in space. ~oThe p e r i p h e r a l vestibular system consists of the semicircular canals and the vestibule in the inner ear, w h i c h sense m o v e m e n t and

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changes in static head position. 11 Axons from these receptors form the vestibular nerve, joining the cochlear nerve to b e c o m e the eighth cranial nerve, which ultimately synapses in the vestibular nuclei in the brain stem. Afferent nerves from the semicircular canals and vestibule of each labyrinth fire a tonic discharge into the vestibular nuclei. An unbalanced or asymmetric vestibular discharge leads to the sensation of abnormal movement or vertigo. 10.12 In addition to peripheral vestibular disturbances, dysfunctions in the vestibular nuclei of the brain stem and their connections account for central causes of vertigo. With prolonged abnormal vestibular input, the central nervous system can adapt and suppress the sensation of vertigo. Central causes of vertigo can be differentiated from peripheral causes. Approximately 85% of patients with vertigo have a peripheral vestibular disorder, while 15% have a central disorder. 13 Certain clinical characteristics help determine the origin of the vertigo (Table 1). Peripheral disorders that cause vertigo may have associated hearing loss and tinnitus, without other neurologic deficits. Central lesions are not associated with hearing loss, but may be accompanied by other neurologic signs, reflecting brain-stem involvement. The onsets of these two types of vertigo are also usually different. Except for vascular events, the symptoms of central lesions develop more insidiously and are longer-lasting and more continuous. The symptoms of peripheral lesions often develop acutely and are intermittent and shorter-lasting. Paradoxically, the peripheral lesions tend to cause more severe vertigo, with associated nausea and vomiting, whereas the central lesions usually cause less severe symptoms. Patients w h o have vertigo often describe their difficulty as spinning, whirling, or swaying, or state that the " r o o m is moving," but loss of consciousness is not a c o m p o n e n t of vertigo.9

Nystagmus Vertigo is generally accompanied by nystagmus, a rhythmic eye movement, the characteristics of which may help localize the origin of the vertigo. Nystagmus may be the only objective finding in the assessment of the vertiginous patient and should be present w h e n there is true vertigo. 14 The direction of jerk nystagmus, w h i c h is found in vestibular disease, is denoted by the direction of the fast component. Spontaneous nystagmus is seen with diseases of the vestibular system, due to disturbances of o c u l a r - v e s t i b u l a r signals. Positional nystagmus refers to the nystagmus induced by specific rapid head movements. The nystagmus associated with central lesions is different from that seen with peripheral disease. Peripheral lesions cause only horizontal or rotatory nystagmus, while central lesions may cause any type of nystagmus, including vertical. The nystagmus of pe-

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TABLE 1 Characteristics of Central versus PeripheralVertigo Central Duration Intensity Nausea/vomiting Neurologicsymptoms Hearing loss Affected by headposition

Long Moderate Mild Common Rare Not usually

Peripheral Brief Severe Moderate to severe Rare May be present Frequently

ripheral lesions is suppressed by visual fixation; the failure of nystagmus to be suppressed by visual fixation is a sign of central lesions.Central lesions may p r o d u c e nystagmus without vertigo; in peripheral lesions, nystagmus is always accompanied by vertigo. 15

Peripheral Causes of Vertigo There are three main peripheral vestibular disorders causing vertigo: benign positional vertigo (BPV), vestibular neuronitis/labyrinthitis, and M~ni~re's disease. Benign positional vertigo is the most c o m m o n single cause of vertigo, occurring twice as frequently as any other vestibular disorder. 5 It is associated with a typical history: the patient has intense but brief episodes of vertigo that are associated with changes of head position, usually w h e n lying down. The neurologic examination is normal, e x c e p t for positional nystagmus. Benign positional vertigo may o c c u r after trauma or a viral infection or may be idiopathic. In a retrospective study, the average age of the patients diagnosed as having BPV was 51 years, and the incidence increased in f r e q u e n c y with advancing age. 16 Approximately 15% of the patients with BPV had sustained previous trauma, but the majority of the cases were idiopathic. The physical examination is essential in reproducing the symptoms using the Nylen-B:ir~ny (or Dix-Hallpike) 17 maneuver, in which the patient's head is rotated to one side and then the patient is gradually lowered to 30 ° b e l o w the horizontal position. When the affected ear is in the downward position, an attack is triggered. There is a characteristic latency of a few seconds before the nystagmus and vertigo are demonstrated. The vertigo is transient, generally fading within 30 seconds. The nystagmus is usually rotatory and changes direction when the patient sits up. In addition, repeated maneuvers extinguish the ability to reproduce the symptoms. When these typical signs and symptoms are present, the diagnosis of BPV is confirmed. The definite cause of BPV is unknown, but the prevailing theory implicates sediment falling on the cupula of the posterior semicircular canal, la The vertigo usually resolves within three to six months, but may recur later. Vestibular neuronitis presents with sudden severe

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vertigo, lasting u p to ten days. Nausea and v o m i t i n g are c o m m o n , but there is no hearing loss or other neurologic sign. Residual unsteadiness may persist for several w e e k s after an attack. Spontaneous nystagmus is present toward the affected ear, and sophisticated vestibular testing demonstrates decreased function in the affected side. 19 The exact location of the d e r a n g e m e n t is unknown. Acute labyrinthitis (often used interchangeably w i t h vestibular neuronitis) may represent a separate entity. Typically labyrinthitis follows a viral u p p e r respiratory infection and is associated w i t h decreased hearing. ~9 The distinction b e t w e e n these two syndromes is often vague, and s o m e authors suggest using the term " a c u t e or recurrent v e s t i b u l o p a t h y " to describe these two disorders. M~ni~re's disease, an abnormal a c c u m u l a t i o n of e n d o l y m p h a t i c fluid in the inner ear, is characterized by episodic vertigo, tinnitus, fullness in the ear, and progressive sensorineural hearing loss. The vertigo increases in intensity over a f e w minutes and lasts for several hours. Usually the disease is unilateral, but occasionally there is bilateral involvement. The vertigo is characteristically severe, d e v e l o p i n g rapidly, and lasting for several hours. Motion sickness is characterized b y dizziness pallor, diaphoresis, abdominal distress, increased salivation, and vomiting p r o v o k e d by motion. 2° It is a physiologic response to intense vestibular stimuli or conflicting visual and vestibular inputs. The s y m p t o m s are worse w h e n the e n v i r o n m e n t appears to m o v e w i t h the subject, because there is a discrepancy b e t w e e n visual and vestibular inputs. For e x a m p l e , riding in a closed cabin in a boat generates vestibular signals indicating m o v e m e n t . However, because the person and boat m o v e together, the e n v i r o n m e n t appears stationary, so the visual p e r c e p t i o n conflicts w i t h the vestibular signals. This disparity can be r e d u c e d b y standing on deck, looking at the horizon, w h e r e the sensation of movem e n t is m a t c h e d with visual cues showing the movem e n t of the boat. A p p r o x i m a t e l y one-third of the p o p u lation is highly susceptible, although the only individuals not affected are those with nonfunctioning vestibular systems. O t h e r disorders of the ear can occasionally be associated with vertigo, including i m p a c t e d c e r u m e n or foreign bodies in the external auditory canal, 2~ otitis media, cholesteatoma, otosclerosis, mastoiditis, local ear trauma, 13 and p e r i l y m p h a t i c fistula. O t o t o x i c drugs, such as aminoglycosides (streptomycin and gentamicin being the m o s t vestibular-toxic), l o o p diuretics, aspirin, quinine, caffeine, alcohol, 22 phenytoin, and cisplatin have b e e n associated w i t h vertigo.

Central Causes of Vertigo Diseases affecting the brain stem and c e r e b e l l u m m a y cause vertigo, although they are less c o m m o n than

peripheral vestibular disorders as causes of vertigo. In addition, vertigo is usually not the dominant manifestation of these disorders. ~ The circulation to the vestibular nuclei is derived from the vertebrobasilar circulation. W h e n brain-stem ischemia is the cause of vertigo, it is usually associated w i t h other brain-stem signs, such as diplopia, ataxia, dysarthria, or facial weakness. Vertebrobasilar insufficiency can cause transient ischemic attacks of the posterior circulation, with episodic vertigo, visual loss, dysarthria, ataxia, or d r o p attacks. The diagnosis of vertebrobasilar insufficiency is m a d e too often in the assessment of elderly p e o p l e w h o have isolated vertigo 23 and should be reserved for those patients w h o have vertigo associated w i t h other signs of brain-stem disease. Infarction of the lateral medulla, or W a l l e n b e r g ' s syndrome, occurs with occlusion of the vertebral or posterior inferior cerebellar artery, p r o d u c i n g a characteristic clinical picture w i t h vertigo, ataxia, diplopia, dysphagia, H o m e r ' s syndrome, ipsilateral facial n u m b ness, and contralateral decreased pain and t e m p e r a t u r e sense. Cerebellar infarction m a y also present with severe vertigo; however, it is distinguished b y the presence of cerebellar signs and the absence of other brainstem signs. Multiple sclerosis can present with vertigo 7% to 1 0% of the time, and u p to one-third of patients w h o have multiple sclerosis e x p e r i e n c e vertigo s o m e t i m e during the course of the disease. The neurologic examination may reveal other brain-stem signs, such as internuclear o p h t h a l m o p l e g i a , as well as signs of diffuse central nervous system involvement. 24 Tumors in the brain stem m a y also be associated with vertigo. Acoustic neuromas, w h i c h are benign tumors of the eighth nerve, are the most c o m m o n cerebellopontine-angle tumor. The p r o m i n e n t s y m p t o m s are hearing loss and tinnitus. Vertigo associated w i t h acoustic neuromas is usually m i l d or m a y even be absent; the slow growth rate of the t u m o r allows for central compensation. Other than eighth-nerve dysfunction, the earliest neurologic sign in these patients is loss of corneal reflex. 2s Vertigo can be associated w i t h basilar artery migraine, characteristically a t h r o b b i n g occipital headache, often associated with other posterior circulation signs. 26 Subclavian steal, due to atherosclerosis in the proximal subclavian artery, can induce a syndrome with vertigo as the b l o o d flow is diverted from the vertebral artery, usually during periods of arm exercise. A discrepancy in b l o o d pressure b e t w e e n the two arms and a bruit over the subclavian artery heighten the suspicion of subclavian steal. Vertigo m a y also be a c o m p o n e n t of t e m p o r a l - l o b e seizures, w h i c h may have other sensory or visual hallucinations in the aura.

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Jannetta et al.27 have described a sudden and severe form of vertigo, w h i c h does not i m p r o v e with time or vestibular suppressant medication, called disabling positional vertigo. It is due to vascular c o m p r e s s i o n on the eighth nerve, near its entry into the brain stem. Microvascular d e c o m p r e s s i o n has b e e n found to relieve the symptoms.27, 28

PRESYNCOPE Dizziness associated with the feeling of an impending faint is t e r m e d p r e s y n c o p e . Presyncope differs from syncope in that actual loss of consciousness does not occur; however, the two are caused by the same mechanism, a transient reduction in cerebral b l o o d flow. The relative f r e q u e n c y w i t h w h i c h p r e s y n c o p e causes dizziness varies from 4% in the Drachman study in a neurology clinic s to 21% of patients presenting to the emerg e n c y r o o m with complaints of dizziness. 7 Syncope and p r e s y n c o p e can be due to inadequate cardiac return, ineffective cardiac output, orthostatic hypotension, and noncardiac causes. There are several excellent recent reviews of syncope. 29-31 Decreased right ventricular filling may cause sync o p e or p r e s y n c o p e because of c o n c o m i t a n t r e d u c e d cardiac output. The vasovagal reflex, w h i c h can be prov o k e d by stressful, painful, or other noxious stimuli, leads to peripheral vasodilatation with a d r o p in heart rate and cardiac output. 32 Vagal reactions, w h i c h are the most c o m m o n explanation for syncope and presync o p e in the y o u n g adult, are often a c c o m p a n i e d by a p r o d r o m e of diaphoresis, pallor, nausea, or abdominal distress. Visceral stimuli for vasovagal reactions inc l u d e cough, micturition, or defecation. Orthostatic hypotension, defined as a d r o p in systolic b l o o d pressure of 20 m m Hg or m o r e within three minutes of assuming an upright posture, may cause sync o p e or presyncope. To be considered the cause of the patient's dizziness, the drop in b l o o d pressure should be associated with lightheadedness. When the normal individual stands up, a p p r o x i m a t e l y 5 00 mL of b l o o d is p o o l e d in the lower extremities, leading to decreased venous return, decreased cardiac output, and a fall in b l o o d pressure. Arterial baroreceptors c o m p e n s a t e by sympathetic stimulation, p r o d u c i n g an increase in heart rate and vasoconstriction.33, 34 In the normal individual w h o stands up, there is only a transient fall in systolic b l o o d pressure of 5 - 15 m m Hg with an associated rise in diastolic b l o o d pressure. 3~ Patients with orthostatic hypotension have a greater and more sustained fall in systolic b l o o d pressure w i t h o u t a rise in diastolic b l o o d pressure. Baroreceptor sensitivity has b e e n s h o w n to decrease w i t h aging, 3s one explanation for the increased f r e q u e n c y of orthostatic hypotension in the elderly. Caird et al. have demonstrated that 24% of the elderly have a drop of at least 20 m m Hg in systolic b l o o d pressure u p o n standing. 36

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Many diverse clinical entities can lead to orthostatic hypotension. Decreased intravascular v o l u m e from hemorrhage, dehydration, diarrhea, vomiting, or excessive diuresis 31 causes orthostasis. It can also result from n e u r o p a t h y secondary to disorders such as diabetes, amyloidosis, and vitamin deficiency. The use of drugs also is a frequent cause of orthostatic hypotension, most c o m m o n l y antihypertensives, nitrates, tranquilizers, phenothiazines, and antidepressants. 34 Prolonged bedrest, because of its association with diminished b a r o r e c e p t o r sensitivity, 3s may also cause orthostasis. Surgical s y m p a t h e c t o m y and p r i m a r y auton o m i c insufficiency are other less c o m m o n causes of orthostatic hypotension. Inadequate cardiac o u t p u t from either p o o r contractility, obstruction to flow, or cardiac arrhythmias may cause p r e s y n c o p e or faintness. These episodes may be of sudden onset w i t h o u t the s y m p t o m s seen in vasovagal reactions. When s y m p t o m s do p r e c e d e these episodes, they may include chest pain, shortness of breath, or palpitations. This type of dizziness is often associated with serious underlying cardiac disease. Structural heart disease, by interfering with cardiac output, can cause p r e s y n c o p e w h e n cerebral perfusion is reduced. Mechanical obstruction of the left ventricular outflow tract, in particular from aortic stenosis or h y p e r t r o p h i c cardiomyopathy, typically causes exertional dizziness or syncope. O t h e r causes of p o o r cardiac o u t p u t include diffuse ischemia, cardiomyopathy, aortic dissection, valvular disease, atrial myxomas, acute myocardial infarction, constrictive pericarditis, and cardiac tamponade.3~ Arrhythmias are a significant cause of dizziness and presyncope, often unrelated to exertion or postural changes. Bradycardias p r o d u c i n g heart rates of less than 40 beats per m i n u t e can cause symptoms, as can tachyarrhythmias p r o d u c i n g heart rates of m o r e than 160. 37 Typically, high-degree atrioventricular b l o c k causes sudden drop in cardiac output, leading to dizziness or syncope. Ventricular tachycardias may decrease cardiac o u t p u t enough to c o m p r o m i s e cerebral perfusion, often in the setting of decreased left ventricular function. Atrial tachycardias can cause faintness w h e n associated with a rapid ventricular rate. In studies of patients w h o had dizziness or syncope, supraventricular tachyarrthythmias w e r e found to be the most comm o n arrhythmia. 38'39 Because m a n y p e o p l e have a s y m p t o m a t i c arrhythmias, caution must be taken in considering an arrhythmia to be the cause of a patient's complaint, especially w h e n no s y m p t o m is elicited by a m b u l a t o r y electrocardiographic monitoring. 4°' 41 Carotid sinus hypersensitivity is an infrequent cause of p r e s y n c o p e or syncope. Baroreceptors in the carotid sinus normally sense increased intracarotid pressure, triggering a reflex that reduces heart rate and systemic b l o o d pressure. With the hypersensitivity syndrome, there is an exaggerated decline in either pulse

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or b l o o d pressure. 4z The most c o m m o n form of carotid sinus hypersensitivity is an exaggerated cardioinhibitory response, defined b y a period o f asystole longer than three seconds. The vasodepressor response, w h i c h is less frequent, is defined b y a b l o o d pressure d r o p of 5 0 m m Hg w i t h carotid massage, or a d r o p of 30 m m Hg w i t h associated symptoms, w i t h o u t a simultaneous decline in pulse, a3 This f o r m of p r e s y n c o p e usually occurs with brief s y m p t o m s during standing up, and is associated w i t h n e c k manipulation, such as shaving or fastening a necktie. Metabolic causes of p r e s y n c o p e or lightheadedhess are less c o m m o n than the cardiac factors that have b e e n previously described. H y p o g l y c e m i a and hypoxemia can cause s y m p t o m s related to dizziness. True hyp o g l y c e m i a is rare in the nondiabetic population; it can b e seen as a c o m p l i c a t i o n of insulin and oral hypoglyc e m i c therapies.

DISEQUILIBRIUM Equilibrium, or maintenance of balance, requires the integration of sensory input and m o t o r output. Coordinated function of the visual, vestibular, cerebellar, and p r o p r i o c e p t i v e systems, including righting reflexes, is necessary for equilibrium. 44 Different pathophysiologic m e c h a n i s m s in any o n e o f these systems can be responsible for disequilibrium, a variant o f dizziness that is not true vertigo or faintness. With aging, there is a decline in sensory input into the central nervous system, c o m p r o m i s i n g the ability to maintain balance. 44 Postural reflexes are r e d u c e d severely in 44% of the elderly and m o d e r a t e l y in 24%. 45 The p r o p r i o c e p tive system declines w i t h age as well: 5 7% of the elderly patient s in one study had a loss of vibratory sensation in the ankle and 14% had no position sense in the big toe. 46 In addition, vestibular function undergoes degenerative changes with age, subjecting the elderly to rely m o r e on visual cues for balance. 47 The hallmark of disequilibrium is unsteadiness, m o s t p r o m i n e n t w i t h ambulation. Typically patients with disequilibrium do not feel dizzy w h e n sitting or lying down. s Disequilibrium is not associated with nystagmus. The diagnosis of a specific pathologic cause for disequilibrium may be difficult. In one study of 740 patients o v e r age 65 evaluated clinically for disequilibrium, a specific cause was f o u n d for 21%.4s The authors labeled the r e m a i n d e r p r i m a r y disequilibrium of aging, presbyastasis. With sophisticated vestibular and balance testing, 7 5% of 63 patients in another study c o u l d b e given a specific diagnosis. 44 Perhaps the most c o m m o n cause of disequilibrium in the elderly is the syndrome of multiple sensory deftcits. s Peripheral neuropathies, vestibular abnormalities, visual impairment, and o r t h o p e d i c p r o b l e m s (including muscle weakness, osteoarthritis, and cervical spondylosis) are the causes of the m u l t i p l e sensory de-

fects syndrome. Difficulty maintaining balance on ambulation results. Altered visual input can also result in dizziness or disequilibrium. Extraocular muscle paralysis, a n e w refraction, recent cataract surgery, and correction of astigmatism can lead to dizziness. The dizziness is usually short-lived, due to adaptation b y the central nervous system. 2° Vertigo is generally not seen w i t h visual causes of dizziness. With failing vision and declining vestibular input, s o m e elderly patients are especially p r o n e to gait disturbances, particularly at night or in unfamiliar surroundings. O t h e r important causes of disequilibrium are cerebellar disease, frontal-lobe apraxia, and parkinsonism. O f the medications that can cause disequilibrium, most p r o m i n e n t are the anticonvulsants, the psychotropics, including lithium and haloperidol, and the benzodiazepines. In the young, dise q u i l i b r i u m is most often the result o f drug use or vestibular disease, or is psychogenic. °

LIGHTHEADEDNESS Dizziness is frequently a s y m p t o m of an underlying psychological disorder. In this setting, the c o m p l a i n t of dizziness is often e x t r e m e l y vague and difficult to define. The patient w i t h dizziness of functional origin is m o r e likely to describe an internal spinning within the head, rather than the sensation of the external environm e n t ' s spinning, as described by those w h o have vertigo. 5° Psychiatric disorders associated w i t h dizziness include stress reactions, anxiety, depression, 51 and panic disorder. In one study, 18% of patients w i t h panic disorder w h o w e r e referred to a psychiatrist initially presented w i t h dizziness or vertigo. 52 The dizziness associated with an anxiety disorder is c o m m o n l y associated with hyperventilation. In a referral-based n e u r o l o g y clinic, 32% of the patients had psychiatric disorders or hyperventilation as the cause of their dizziness, second in f r e q u e n c y only to peripheral vestibular disorders. 5 In a "dizziness unit," staffed b y otolaryngologists, " p s y c h o g e n i c dizziness" r e p r e s e n t e d the most c o m m o n diagnosis, occurring in 21% of the patients. The c o m b i n a t i o n of a normal neuro-otologic examination, associated psychiatric symptoms, an a p p r o p r i a t e history, and reproduction of s y m p t o m s by hyperventilation established the diagnosis, s3 In a s u b s e q u e n t study, psychiatric assessments of the patients w h o had psychogenic dizziness found that 94% of the patients had anxiety disorders 54 and 76% had diagnoses in the p a n i c - a g o r a p h o b i a grouping. Dizziness was found to be the most frequent sympt o m in patients w h o had hyperventilation syndrome. 5s The s y m p t o m s are attributed to the h y p o c a p n e a , w h i c h causes cerebral vasoconstriction. Most of the time the patient does not recognize an abnormal pattern of breathing, and often it is not apparent to the examiner.

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Shortness of breath, headaches, palpitations, weakness, chest pain, and paresthesias are often found with hyperventilation, s6 With deliberate hyperventilation, the typical s y m p t o m s can be r e p r o d u c e d . In addition, s y m p t o m s related to hyperventilation can be relieved by controlled slow breathing. Various degrees of vestibular dysfunction have b e e n found in patients with primary psychiatric disorders. W h e n e x a m i n e d b y sophisticated vestibular testing, over 60% of patients with a panic disorder had nystagmus or an abnormal electronystagmogram. 57, 5a

ELDERLY PATIENTS Dizziness in the elderly is a c o m m o n and potentially serious p r o b l e m , with unsteadiness predisposing this p o p u l a t i o n to the risk of falls and serious fractures. Falls represent a p p r o x i m a t e l y two-thirds of all accidental deaths in the elderly, and only half of the paTABLE 2

Causesof Dizziness Type of Dizziness Vertigo-- a rotational sensation; a spinningor whirling

Differential Diagnosis Peripheralcauses Benign positional vertigo Vestibular neuronitis/labyrinthitis M~ni~re's disease Motion sickness Drug use Local ear dysfunction Central causes Brain stem ischemia Cerebellarischemia Acoustic neuromas Multiple sclerosis Basilar artery migraine Temporal lobe seizure Posterior fossa tumor

Presyncope--the perceptionof an impendingfaint

Arrhythmias Vasovagalreflex Orthostatic hypotension Aortic stenosis, hypertrophic cardiomyopathy Low cardiac output states Carotid sinus hypersensitivity Anemia Hypoglycemia Hypoxemia

Disequilibrium--the loss of balanceon ambulation

Syndrome of multiple sensory deficits Altered visual input Primary disequilibrium of aging (presbyastasis) Cerebellardisease Frontal lobe apraxia Parkinsonism Drug use

Llghtheadedness-- a vague sensation, giddiness

Anxiety Depression Panic disorders Hyperventilation

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TABLE 3

DizzinessSimulation Tests Type of Dizziness Vertigo Presyncope Disequilibrium Lightheadedness

Provoking Test Nylen-Baranytest Orthostatic blood pressuremeasurement Romberg test, tandem gait Hyperventilation

tients admitted to a hospital after a fall are alive a year later. 59 In one study, multiple sensory deficits and orthostatic hypotension played a greater role in the primary care evaluation of dizziness in the elderly, ~ whereas in a study of a neuro-otology referral clinic, peripheral vestibular disorders and cerebrovascular disorders a c c o u n t e d for 65% of the diagnoses. 6° In the elderly patient, vertigo caused by peripheral vestibular disorders may be prolonged, as diminished central nervous system adaptation leads to i n c o m p l e t e central compensation. In a study of individuals over the age of 60 living in the c o m m u n i t y , 18% had dizziness within the preceding year severe enough to interfere w i t h their usual daily activities. 61 The p r e s e n c e of dizziness was associated with self-perceived nervousness, depression, cardiovascular disease, prior neurologic disease, and p o o r self-assessment of health status. No correlation was found b e t w e e n the p r e s e n c e of dizziness and the one-year institutionalization or death rate.61

CLINICAL EVALUATION OF THE DIZZY PATIENT The diagnostic a p p r o a c h to the dizzy patient begins with categorizing the form of dizziness the patient is e x p e r i e n c i n g (Table 2). The history is the most valuable part of the assessment of a dizzy patient, w h i l e the physical examination adds useful information to the evaluation. The history and physical examination alone may provide the diagnosis for over 80% of patients. 6 Sophisticated laboratory studies and imaging modalities usually add little that is not s u s p e c t e d after a careful history and physical examination. The initial distinction should differentiate vertigo, a spinning or moving sensation, from a nonvertiginous sensation, such as giddiness, unsteadiness, faintness, or lack of concentration. Often the patient provides a vague description that must be clarified. A history of m e d i c a t i o n use may identify a drug-related side effect, w h i c h may be one of the most easily manageable forms of dizziness. 62 The history should guide the physical examination .63 After focusing on the characteristics of the dizziness, certain simulation tests may p r o v e to be quite helpful in r e p r o d u c i n g the patient's symptoms. 5 These simulation tests are simple and often sufficient to make the diagnosis w h e n they replicate the symptoms. For each of the types of dizziness, there are specific maneuvers that are helpful (Table 3).

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Warner eta/., DIZZINESSIN PRIMARYCARE PATIENTS

In the evaluation of vertigo, certain features o f the history are helpful. The patient should be asked about prior episodes of vertigo, the onset and duration of the episodes, any provoking factors, w h e t h e r the dizziness is related to head position, w h e t h e r it is associated with nausea and vomiting, and w h e t h e r there is associated hearing loss or tinnitus. Essential in the evaluation o f vertigo is the differentiation of central causes from peripheral causes. This is necessary to identify serious problems that are associated with central causes of vertigo, such as brain-stem or cerebellar infarctions, tumors, or demyelinating diseases. This distinction of central versus peripheral causes is required to provide a prognosis and a treatment plan. A history o f dysphagia, diplopia, dysarthria, or hemiparesis suggests brainstem disease. A history of ataxia may suggest cerebellar disease. A careful neurologic examination should be performed to identify any abnormal neurologic signs or symptoms. If the examination is negative, the disorder is most likely to be peripheral. Examination of the ear may detect impacted cerumen, evidence of middle-ear disease, or signs of hearing loss. A history of hearing loss or tinnitus localizes the p r o b l e m to the ear or the eighth nerve. In the absence of neurologic abnormalities, hearing loss, or an abnormal ear examination, the most likely causes are BPV and vestibular neuronitis. In the assessment of a patient w h o has vertigo, perhaps the most helpful test done at the bedside is the Nylen-Bhr~ny (or Dix-Hallpike) maneuver, described earlier, w h i c h can establish the diagnosis of BPV. When the neurologic examination shows abnormal cranial nerve or cerebellar findings, neuroimaging studies should be undertaken. Magnetic resonance imaging is more sensitive than c o m p u t e d tomography in diagnosing acoustic neuroma or other posterior fossa or brain-stem lesions. In the absence of a clear-cut diagnosis for the vertigo, caloric testing, audiologic evaluation, and electronystagmography may aid in diagnosis. The clinical approach to the patient with presync o p e involves an assessment of cardiovascular function, including careful examination of pulse and blood pressure. Orthostatic hypotension is detected by examining the blood pressure in the supine position, preferably after resting for 15 minutes, then at one-minute intervals for five minutes while the patient stands. The pulse and presence of symptoms should also be rec o r d e d after the patient stands up. Three types of responses are noted with orthostatic hypotension. 64 When the pulse rises concomitantly with a drop in blood pressure, this implies a normal compensatory response to a physiologic stress such as v o l u m e depletion, deconditioning, or vasodilation. If the heart rate does not rise, then a defect in the autonomic nervous system is inferred. A drop in the pulse coinciding with a fall in blood pressure is seen with a vasovagal response. The history and physical examination can identify

patients with p o o r cardiac output, and occasionally echocardiography and chest radiography may be confirmatory. Evaluation of patients suspected of having cardiac arrhythmias should include electrocardiography and prolonged cardiac monitoring. A study by Bass et al. found that two 24-hour Holter monitors w e r e n e e d e d to uncover significant arrhythmias in 25% o f their patients w h o had syncope. A third 24-hour monitor revealed arrhythmias in only another 4% of patients.65 In a study of 32 dizzy patients, using Holter monitors to correlate symptoms of dizziness with arrhythmias, Ringqvist et al. found that only 13% of patients had their typical symptoms associated with arrhythmias. Perhaps more importantly, they found that half of their patients had typical symptoms of dizziness with no arrhythmia, thereby suggesting that the symptoms were not related to underlying rhythm disturbances. 66 Because disequilibrium represents unsteadiness with ambulation, gait testing and station testing are essential. Static balance can be tested with the Romberg test, in which the patient stands with the legs together and then closes the eyes. An abnormal Romberg test suggests proprioceptive impairment or vestibular dysfunction. The gait may be tested by asking the patient to rise from a chair, without using the arms, walk 10 feet, then turn around. If a patient demonstrates difficulty with gait, offering a hand may lesson the sensation o f dizziness. In addition, evaluation of muscle strength, coordination, reflexes, and p r o p r i o c e p t i o n should be conducted. When a peripheral n e u r o p a t h y is suspected, one should consider diabetes, alcohol abuse, and vitamin B12 deficiency as possible etiologic factors. The posture may be inspected; typically patients with postural instability stand bent over, with their knees and hips flexed. A gentle tap on the chest (the nudge test) while standing behind the patient can give an indication of the patient's likelihood of falling backwards. 67 Testing visual fields and acuity may uncover visual impairment. The last category of dizziness, lightheadedness, often becomes a diagnosis of exclusion. One should perform a psychiatric history to identify possible anxiety, depression, recent stress, or panic attacks. Deliberate hyperventilation may often r e p r o d u c e recognizable symptoms.

LABORATORY TESTING The use of laboratory testing in the diagnosis of the dizzy patient should be selective. In a study o f 125 patients evaluated in the e m e r g e n c y r o o m for dizziness, routine testing of electrolytes had a low yield. 7 Two patients were found to have severe hypokalemia, one of w h i c h was associated with a serious ventricular arrhythmia. Hypoglycemia was not found, some patients were hyperglycemic, and diabetes may have contrib-

461

JOURNALOF GENERAL[NTERNALMEDICINE, Volume 7 (.July/August). 1992 TABLE 4

Drugs Used to Treat Patients Who Have Vertigo

Dosage

Side Effect

Advantage

Antihistamines Meclizine(Antivert) Dimenhydrinate (Dramamine) Promethazine (Phenergan)

2 5 - 5 0 mg po q6h 50 mg po q6h 2 5 - 5 0 mg po q6h

Anticholinergic Scopolamine (Transderm ScOp)

0.5 mg transdermally q3d

Blurred vision, dry mouth

Useful for motion sickness

10 mg po q6h or 25-mg suppository PR q 12h

Extrapyramidal effects

Antiemetic effect

2 - 10 mg po, IM, or IV q6h

Drowsiness

Anxiolytic

Phenothiazine Prochlorperazine (Compazine) Benzodiazepine Diazepam (Valium)

All have anticholinergic effects

uted to their symptoms. The complete blood c o u n t detected a significant anemia only in those w h o had histories of anemia or physical examinations suggestive of gastrointestinal bleeding.

MANAGEMENT OF DIZZINESS Effective treatment of patients w h o have symptoms of dizziness requires establishing the cause. The course and management of centrally caused vertigo d e p e n d on the underlying disease process. Several classes of drugs have been used to treat vertigo patients (Table 4). Anticholinergic agents, such as scopolamine and atropine, decrease the spontaneous firing of the vestibular nuclei and thereby decrease the response to vestibular stimulation. Scopolamine is the most effective agent for motion sickness. 68 The mode of action of antihistamines, including meclizine and promethazine, is less clear, but may be due to central actions. 69 Meclizine has been shown to r e d u c e symptoms for both patients with central and those with peripheral causes of vertigo. 7° Benzodiazepines inhibit resting activity of the vestibular nuclei and may diminish activity in the reticular-activating system. 69 There is some controversy about the appropriate use of these medications, mainly because the primary response to abnormal vestibular input is to adapt with central nervous system compensation. By diminishing vestibular imbalance, compensation may not be as effective. 7~ When peripheral vertigo is related to labyrinthine dysfunction, the use of drugs acting as vestibular suppressants may r e d u c e the symptoms, but probably does not alter the natural history of the disease. In general, pharmacologic treatment for BPV is not helpful, but specific head-moving exercises may lessen the severity and duration of the vertigo. These habituation exercises deliberately repeat the head maneuvers that elicit the symptoms of vertigo. 72, 73 Vestibular neuronitis should be managed with bedrest and, possibly, vestibular-suppressant medications, such as meclizine. Diuretics and salt restriction may be used to reduce the f r e q u e n c y of

Sedation

attacks in M~ni~re's disease. An acute attack can be managed with vestibular suppressants and bed rest. For refractory cases of M~ni~re's disease with disabling vertigo, ablative surgery (i.e., sectioning of the vestibular nerve or labyrinthectomy) may relieve symptoms, although usually sacrificing hearing in the involved side. Diseases of the external or middle ear should be managed appropriately. For example, impacted c e r u m e n should be removed or otitis media should be managed with antibiotics. Complicated ear dysfunction may necessitate referral to an otolaryngologist. Treatment for presyncope involves identifying the precipitating factor. With vasovagal attacks, the inciting factor should be avoided. Correcting the cause for orthostatic hypotension may involve one of three approaches: 1) a specific response, i.e., eliminating the responsible drug or correcting the underlying disorder; 2) nonspecific support measures, such as wearing elastic stockings or avoiding prolonged standing; and 3) pharmacologic treatment, with agents such as fludrocortisone to promote volume expansion. 35 Emphasis can be placed on improving cardiac o u t p u t in patients with congestive heart failure. Attention should be directed at potentially reversible causes such as aortic stenosis. If an arrhythmia is identified, antiarrhythmics or cardiac pacing may be indicated. The treatment of disequilibrium is also determined by the cause. Occasionally an isolated treatable problem such as the neuropathy of pernicious anemia is found. More likely, a patient may have multiple sensory deficits that are not readily corrected. Eyeglasses, a cane or a walker, physical therapy, and patient education may help the patient ambulate easier. An assessment of the individual's environmental risks may help prevent falls by eliminating hazards in the home. 59 When dizziness is related to psychological disorders, supportive psychotherapy or medication (anxiolytics or antidepressants) may be helpful. If hyperventilation is a significant c o m p o n e n t of the symptom complex, deliberate slow breathing can relieve symptoms.

Warner etal., DIZZINESSiN PRIMARYCARE PATIENTS

46~.

CONCLUSION In summary, the evaluation of the complaint of dizziness relies on defining the characteristics of the dizziness. Four main categories exist: vertigo, presyncope, disequilibrium, and lightheadedness. A careful history and physical examination can be tailored to best approach each type of dizziness.Making a specific diagnosis can guide treatment for this complex and distressing symptom. The authors thank Susan Warner for critical review of the paper.

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examination in panic disorder and agoraphobia with panic attacks: a pilot study. AmJ Psychiatry. 1985; 142:715-20. Rubenstetn LZ, Robbins AS, Schulman BL, RosadoJ, Osterweil D, Josephson KR. Falls and instability in the elderly. J Am Geriatr Soc. 1988;36:266-78. Sloane PD, Baloh RW. Persistent dizziness in geriatric patients. J Am Geriatr Soc. 1989;37:1031-8. Sloane PD, Blazer D, George LK. Dizziness in a community elderly population. J Am Geriatr Soc. 1989;37:101-8. Wennmo K, Wennmo C. Drug-related dizziness. Acta Otolaryngol. 1988;(suppl 455): 11-3. Towler HM. Dizziness and vertigo. Br MedJ. 1984 ;288:1739-43. Thulesius O. Pathophysiological classification and diagnosis of orthostatic hypotension. Cardiology. 1976;61(suppl 1): 180-90. Bass EB, Curtis EI, Arena VC, et al. The duration of Holter monitoring in patients with syncope. Is 24 hours enough? Arch Intern Med. 1990;150:1073-8.

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66. Ringqvist I, Jonason T, Nilsson G, Khan AR. Diagnostic value of longterm ambulatory ECG in patients with syncope, dizziness or palpitations. Clin Physiol. 1989;9:47-55. 67. Caranasos GJ, Israel R. Gait disorders in the elderly. Hosp Pract. 1991;26:67-71, 75, 79-82, 91-94. 68. Wood CD. Antimotion sickness and antiemetic drugs. Drugs. 1979;17:471-9. 69. OlssonJE, AtkinsJS. Vestibular disorders. Otolaryngol Clin North Am. 1987;20:83-111. 70. Cohen B, deJongJM. Meclizine and placebo in treating vertigo of vestibular origin. Arch Neurol. 1972;27:129-35. 71. Zee DS. Perspectives on the pharmacotherapy of vertigo. Arch Otolaryngol. 1985; 111:609-12. 72. Norre ME, Beckers A. Benign paroxysmal positional vertigo in the elderly. Treatment by habituation exercises. J Am Geriatr Soc. 1988;36:425-9. 73. Brandt T, Daroff RB. Physical therapy for benign paroxysmal positional vertigo. Arch Otolaryngol. 1980; 106:484-5.

AMERICAN CANCER SOCIETY Cancer Control Career Development Award f o r Primary Care Physicians The American Cancer Society is pleased to a n n o u n c e the 1993 Cancer Control Career D e v e l o p m e n t Award for Primary Care Physicians (CCCDA). This award is i n t e n d e d to d e v e l o p a c a d e m i c leaders in primary care specialties emphasizing cancer control. T h r o u g h the CCCDA, the Society seeks to s u p p o r t individuals in supervised programs that w i l l d e v e l o p the candidate's clinical and teaching expertise and his or her capacity to perform i n d e p e n d e n t clinical research in cancer control. It is anticipated that physicians trained u n d e r these awards will i m p r o v e cancer control through i n v o l v e m e n t in primary care practice, education, and research activities related to c a n c e r control. A candidate for a first-year CCCDA may not have an a c a d e m i c rank above that of assistant professor and must not be t e n u r e d or be the section head (or e q u i v a l e n t ) in his or her discipline. These awards are i n t e n d e d to support the early developm e n t of a c a d e m i c careers w h i c h place emphasis on cancer control; physicians w i t h well-established careers and substantial research funding s h o u l d not apply. In addition, candidates for these awards must be citizens or p e r m a n e n t residents of the United States. This is a two-year award. The stipend for the award is $ 2 5 , 0 0 0 for the first year and $ 3 0 , 0 0 0 for the second. The application deadline is August 15, 1992, for awards to begin July 1, 1993. Brochures and applications are currently available. To r e q u e s t further information or application materials, please contact: Virginia Krawiec, MPA Professional Education Department American Cancer Society, Inc. 1599 Clifton Road, NE Atlanta, GA 3 0 3 2 9 - 4 2 5 1 404-329-5734

Dizziness in primary care patients.

Dizziness in Primary Care Patients ELIZABETH A. WARNER, MD, PAUL M. WALLACH, MD, HAROLD M. ADELMAN, MD, KAREN SAHLIN-HUGHES, MD IN THE PRIMARY CARE PR...
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