The Dizzy Patient: How You Can Help
ABSTRACT: Painstaking elucidation of a patient’s symptoms is the key component of the diagnostic workup for dizziness and vertigo. Light-headedness and imbalance that occur when the patient assumes an upright position suggests dysautonomia. Objective imbalance points to a degenerative, vascular, metabolic, or neoplastic disorder affecting the cerebellum or spinocerebellar system. Vague, imprecise sensations of light-headedness are characteristic of chronic subjective dizziness, which is a manifestation of a chronic anxiety disorder. Central vertigo is caused by disorders of the lower brainstem and cerebellum, including ischemia, demyelination, migraine and, rarely, neoplasm. Unlike vertigo of central origin, vertigo arising from dysfunction of the inner ear or eighth cranial nerve has few associated symptoms, except for auditory dysfunction. Thus, peripheral vertiginous disorders are best classified based on the duration of the episodes, as well as on the presence or absence of unilateral hearing loss.
Most primary care practitioners approach the patient who complains of dizziness with some trepidation. This is chiefly because the differential diagnosis involves multiple organ systems and a wide variety of disorders. In this article, I offer a rational, straightforward, and cost-effective approach that uses only minimal, selective diagnostic testing.
DEFINING “DIZZINESS”
Dizziness is a nonspecific complaint that can have different meanings in different patients. Thus, a careful analysis of the patient’s symptoms is the most critical component of the workup (Table 1). When they are questioned about the specific sensations that characterize their “dizziness,” patients typically describe one of the following situations.
Lightheadedness and imbalance that occur when assuming an upright posture. This common complaint of presyncope is usually attributable to cerebral hypoperfusion when patients rise from a sitting or supine position. It is typically worse in the morning after prolonged bed rest. Patients do not experience these symptoms when they assume a supine position.
These periods of cerebral hypoperfusion may result from obstruction in the carotid and vertebrobasilar circulations, typically secondary to atherosclerosis. More commonly, symptoms result from a dysautonomia, which prevents an appropriate cardiovascular response to changes in posture. Dysautonomias are most frequently associated with antihypertensive or antiarrhythmic therapy (eg, ß-blockers, calcium channel blockers, alpha-blockers, angiotensin-converting enzyme inhibitors, and amiodarone).1 Primary dysautonomias (such as Shy-Drager syndrome) are rare; they are suggestive of multi-systemic autonomic dysfunction.
Diagnosis of this form of dizziness, which is more common in the elderly, is usually straightforward. Symptoms occur only when the patient rises; typically, there is a history of cardiovascular disease and/or diabetes mellitus. Bedside examination (lying and standing blood pressure testing with a postural drop of 20 mm Hg systolic and/or 10 mm Hg diastolic) may confirm orthostatic hypotension; however, the lack of this physical finding should not rule out the diagnosis if the patient’s history is highly suggestive. Frequently, tilt table testing will elicit symptoms accompanied by a drop in blood pressure that cannot be demonstrated at the bedside. A stenotic lesion can be ruled out with transcranial Doppler echocardiography or magnetic resonance angiography of the head and neck.
Treatment of presyncope may be as simple as advising the patient to rise slowly, to squeeze his or her legs together before rising, and/or to wear support hose. Altering medi- cations or adjusting the dosages may also help. Under cer tain circumstances, pharmacotherapy may prove beneficial.2
Objective imbalance. Patients may equate an inability to maintain normal gait with dizziness, even if they are not suffering from true rotatory vetigo. This includes ataxia, which is not discussed in this article.
Vague sensation of light-headedness, subjective sensations of imbalance. These complaints, which can be characterized by their imprecision, are consistently among the most common that clinicians encounter when evaluating dizziness. Eliciting a history from these patients can be frustrating; often, they cannot describe their symptoms precisely. Rather than feeling frustrated, one can feel encouraged because the nonspecific, non-physical nature of the complaints leads to a specific diagnosis. Formerly referred to as “psychogenic dizziness,” persistent nonspecific dizziness that cannot be explained by active medical conditions is now a defined clinical entity known as chronic subjective dizziness, or CSD.3,4 Barber has noted that this diagnosis is suggested during the first 5 to 10 minutes of the office visit if the patient has no specific physical complaints.5
Diagnostic criteria for CSD include greater than 3 months of sensations such as nonvertiginous dizziness, lightheadedness, heavy-headedness or subjective imbalance present on most days, as well as greater than 3 months of chronic hypersensitivity to one’s own motion or the movement of objects in the environment.3,4 Complex visual stimuli, such as walking in grocery stores or shopping malls, or using a computer, characteristically exacerbate the symptoms. The physical examination is usually normal in these patients, except that hyperventilation typically reproduces their symptoms.
CSD most commonly represents a chronic anxiety disorder with or without associated panic and/or phobic disorders. Although the patient’s history may strongly suggest CSD, a full neurotologic history taking and physical examination must be performed, and selective tests, such as videonystagmography (VNG) and MRI, also are frequently ordered. This is done to reassure the clinician and—perhaps even more important—the patient that no organic disease is present.
Treatment of these patients incorporates typical strategies used to manage anxiety disorders. Slowly increasing doses of selective serotonin reuptake inhibitors are the mainstay of treatment, often coupled with psychotherapeutic approaches such as cognitive behavioral therapy.
VERTIGO: CENTRAL OR PERIPHERAL?
True vertigo is an illusion that the environment is moving (typically, rotating or spinning). The sensation is usually accompanied by nausea. Vertigo may be of central (brainstem or cerebellum) or peripheral (inner ear or vestibular nerve) origin. Once you have determined that the patient is suffering from vertigo, the next step is to establish whether this represents central or peripheral disease (Table 2). The history and physical examination are the most useful tools in determining the site of a suspected lesion.
Central vertigo. Disorders of the lower brainstem and cerebellum—including ischemia, demyelination, mi- graine and, rarely, neoplasm—are responsible for central vertigo.
Ischemia. The patient presenting with vertigo resulting from vertebrobasilar insufficiency, a transient ischemic attack (TIA), or a cerebral vascular accident (CVA) involving the brainstem will typically have associated symptoms that may include diplopia, dysarthria, dysphagia, drop attacks, paresthesias, and loss of motor function.
Cerebellar dysfunction may be more difficult to rule out based on history because symptoms of a cerebellar stroke can sometimes closely resemble those associated with peripheral vestibular disorders. However, on physical examination, patients with a cerebellar stroke demonstrate difficulty in rapidly alternating supination and pronation of the hands and may perform poorly on finger-to-nose testing (dysdiadochokinesia). Patients who display these signs and/or who have significant risk factors for ischemic disease, such as smoking, hypercholesterolemia, or diabetes mellitus, should undergo appropriate radiologic studies to rule out a CVA.
Multiple sclerosis. Vertigo is the initial complaint in approximately 5% of patients with multiple sclerosis and eventually is observed in up to 50% of those with this disorder.6
Migraine. The common cause of central vertigo will be discussed below.
Peripheral vertigo. Unlike vertigo of central origin, vertigo originating from dysfunction of the inner ear or eighth cranial nerve has few associated symptoms. When these symptoms are present, they are typically related to auditory dysfunction. Thus, peripheral ver tiginous disorders are best classified based on the duration of the actual vertigo attacks, as well as on the presence or absence of symptoms of unilateral auditory dysfunction. Determining the duration of actual vertigo—as distinct from constitutional symptoms connected with the event (e.g., nausea or fatigue)—is critical to establishing the diagnosis. Rarer causes of peripheral vertigo are discussed in Table 3.
Episodes that last for seconds. Patients with benign positional vertigo (BPV) experience episodes of vertigo lasting less than 1 minute that are brought on by a rapid head movement in a nonaxial plane (e.g., rolling over in bed or looking up rapidly). As soon as the patient steadies himself, the vertigo resolves.
BPV is the most common peripheral vestibular disorder. It is typically idiopathic, but it may occur because of head trauma or subsequent to a vestibular neuronitis or labyrinthitis (see below). BPV is thought to result from the accumulation of organic debris (canaliths) within one of the semicircular canals of the inner ear—typically, the posterior canal.7
The diagnosis of BPV can be made from the history; it can be confirmed by the Dix-Hallpike (or Bárány) maneuver. This consists of moving the patient from a sitting to supine position, with his head turned and hanging over the head of the bed or table so that the affected ear faces the floor. The elicitation of vertigo and nystagmus with the patient in this position confirms the diagnosis of BPV.
The prognosis for this disorder is excellent, since the natural course is spontaneous remission. However, the duration of the symptomatic period varies and may persist for months. During this time, the patient may be incapacitated because of recurrent episodes of vertigo and the fear associated with these unpredictable attacks.
A safe, simple, and effective treatment for BPV is the Epley canalith repositioning maneuver. This technique incorporates positional maneuvers performed at the bedside that cause the canaliths to fall out of the semicircular canal and into the labyrinthine vestibule, where they cause no adverse effects. This treatment eliminates vertigo in more than 90% to 95% of cases and allows the patient to resume a normal lifestyle.7 (Never theless, BPV tends to recur, and although the Epley maneuver eliminates the acute episodes, it does not prevent recurrences, which may occur months to years after the initial diagnosis.)
Episodes that last for minutes. Superior semicircular canal dehiscence, a rare peripheral vestibular disorder first described in 1998, causes vertigo that lasts for minutes.8 Patients experience vertigo and nystagmus in response to loud sounds and in response to pressure from coughing, sneezing, or straining. Other characteristic symptoms include hearing unusually loud self generated sounds such as one’s own voice (autophony), pulse, eye movements or impact of feet while walking or running. Aural fullness is another common complaint. Audiometric assessment may demonstrate a mild conductive hearing loss.
Semicircular canal dehiscence occurs due to a congenital dehiscence of the otic capsule of the superior semicircular canal. This results in the membranes of the inner ear being directly apposed to the dura of the middle fossa. Although the lesion is congenital, it typically only becomes symptomatic in adulthood, usually after some traumatic event such as a blunt head injury, acoustic trauma, or barotrauma. Conservative therapy including avoidance of stimuli is recommended for mild cases, while surgical repair of the semicircular canal can be performed for patients debilitated by their symptoms.
If vertigo lasts for minutes and is accompanied by central neurologic symptoms, vertebrobasilar insufficiency should be considered. Evaluation of the posterior fossa circulation, typically with arteriography, is warranted.
Episodes that last for hours. Both Ménière’s disease and vestibular migraines cause vertigo that lasts for hours, but they can be distinguished by the presence or absence of unilateral auditory dysfunction. Episodes of vertigo lasting for hours, fluctuating and progressive sensorineural hearing loss, and tinnitus constitute the trio of symptoms that defines Ménière’s disease. Aural fullness or pressure is commonly reported as well.
Ménière’s disease is an idiopathic disorder that typically occurs in patients aged between 30 and 60 years. It ultimately affects both ears in 45% of patients.9 No definitive theor y for the pathogenesis of this disorder exists. Although it has generally been attributed to the accumulation of fluid within the inner ear (endolymphatic hydrops), the validity of this theory has been questioned.
The history strongly suggests the diagnosis. Physical examination may reveal evidence of hearing loss on tuning-fork testing, as well as signs of peripheral vestibular loss (e.g., poor performance on tandem gait assessment with eyes closed— although in older patients, this examination is less valid). The typical disease course consists of clusters of vertiginous episodes separated by periods of remission. Hearing loss and tinnitus are usually exacerbated during the vertiginous episodes. In most patients, the disease “burns out,” and they are left with chronic moderate to severe hearing loss, tinnitus, and imbalance, particularly in the dark.
The treatment of Ménière’s disease is controversial10-12; a comprehensive discussion is beyond the scope of this article. Note that this condition has an extraordinarily high (60% to 80%) short-term response rate to nonspecific (placebo) therapies. The medical management of this disorder has focused on vestibular suppressants (e.g., diazepam or meclizine) to control vertigo and diuretics and a low-sodium diet.
Of these therapies, only vestibular suppressants have proved effective in controlling vertigo; none has been shown to improve auditory function. Nonetheless, many of these agents remain in use; their beneficial effects are likely attributable to the nonspecific therapeutic responses seen in patients who have Ménière’s disease. Long-term vestibular suppressant therapy should be discouraged because use of these agents hinders accurate diagnosis and treatment, prevents central compensation to a peripheral vestibular loss, and may predispose elderly persons to falling.
Surgical therapies include those that attempt to preserve hearing (endolymphatic shunt, gentamicin perfusion, or vestibular nerve section) and those in which hearing and vestibular function are lost (i.e., labyrinthectomy, which is performed only when the patient’s hearing is virtually nonexistent). Indications for these surgeries are controversial; discussions of the options may be found elsewhere.10,12,13
Vertigo lasting for minutes to hours without significant auditory symptoms is most commonly migrainous in origin (85% to 90% of cases).14-16 The typical presentation is recurrent episodes of true vertigo occurring in a patient with a personal or strong family history of migraine. The vertiginous episode is typically not directly associated with the headache.
There is considerable confusion concerning this disorder, which has been somewhat erroneously referred to as recurrent vestibulopathy, benign recurrent vertigo, or vestibular Ménière’s disease. At present, a considerable amount of effort is being expended to better define the pathogenesis, diagnostic criteria, and therapeutic interventions for vestibular migraines. Currently, vestibular suppressants are recommended acute vertigo. Patients experiencing frequent attacks should be treated with migraine prophylaxis.
Episodes that last for days to weeks. Vestibular neuronitis is a common and frightening disorder that often precipitates a visit to the emergency department. It is characterized by an acute onset of vertigo associated with nausea and vomiting but no symptoms of auditory or CNS dysfunction.17 The lack of associated symptoms, the absence of dysdiadochokinesia, and the fact that symptoms do not recur are key factors that help differentiate this relatively benign disorder from other neurovestibular pathologies. The vertigo slowly remits over a period of days to weeks. Vestibular suppressants are the mainstay of treatment for vestibular neuronitis; corticosteroids may reduce the duration and severity of symptoms if administered soon after the onset of the episode.
Labyrinthitis is a rare condition in which inflammation within the inner ear results in vertigo lasting for days and hearing loss. It is discussed in greater detail in Table 3.
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