Evaluation of Dizziness
Amy A. Pruitt
Dizziness can be one of the more frustrating complaints to assess; the task is often made difficult by a vague history and a large number of possible causes, ranging from psychiatric disease and cardiovascular disorders to peripheral and central defects within the nervous system. However, with a bit of patience and careful attention to the history and physical examination findings, the primary physician can conduct a sophisticated clinical evaluation, one that will help to exclude potentially dangerous conditions, direct further workup and treatment, and, at times, provide immediate relief for those patients who have less worrisome conditions such as benign positional vertigo (BPV).
The term “dizziness” encompasses a host of symptoms that include lightheadedness, vertigo, near passing out, unsteadiness, wooziness, floating, internal sensation of movement, motion intolerance, unsteadiness, and other nonspecific descriptors of imbalance. Etiologies range from cardiovascular causes to central and peripheral neurologic conditions and psychophysiologic states. Some produce momentary symptoms (episodic, transient dizziness), and others acutely trigger more continuous dizziness, which persists for more than 24 hours (sometimes referred to as the acute vestibular syndrome). Key goals of the initial assessment (which can be performed effectively in the primary care office setting) include differentiation of cardiovascular causes from neurologic sources and central from peripheral vestibular pathology.
The patient complaining of “dizziness” may have a malfunction of virtually any organ system, including vestibular dysfunction, cardiovascular insufficiency, psychiatric illness, metabolic
derangement, multiple sensory deficits, cerebellar disease, or a combination of problems.
derangement, multiple sensory deficits, cerebellar disease, or a combination of problems.
Vestibular Disease
Patients with vestibular disease often experience true vertigo, which is defined as a head sensation of abnormal movement or (and the distinction does not matter) abnormal movement of the environment. Descriptive terms include not only “spinning” but also “weaving,” “seasickness,” “ground rising and falling,” “rocking,” “things moving,” and “merry-go-round” sensation. Nausea, vomiting, and diaphoresis accompany severe cases. Tinnitus and hearing loss indicate associated injury to the auditory component of the eighth cranial nerve. Nystagmus is frequently found on examination (see later discussion) or can be induced.
The vestibular problem may be central or peripheral; peripheral lesions include those that are cochlear or retrocochlear. Central lesions differ from peripheral ones in that they typically present with vertigo in association with other brainstem deficits; in peripheral disease, vertigo occurs in isolation except for accompanying tinnitus or hearing loss.
Peripheral Lesions
Peripheral etiologies are characterized by absence of brainstem symptoms and signs and include benign positional vertigo, acute vestibular neuronitis, Ménière disease, and acoustic neuroma.
Benign Positional Vertigo (BPV).
In this common problem of the elderly, vertigo is experienced only in specific positions. Onset is sudden, usually within a few seconds after the triggering position has been assumed. Symptoms cease after several minutes if the patient does not move, but they resume with further change in position. In many patients, the condition resolves within 6 months; recovery is usually complete. Head trauma sometimes results in this type of temporary vertigo. The mechanism is stimulation of the labyrinth by free-floating particulate matter in the posterior semicircular canal. A less common but more persistent cause of positional vertigo is believed to be vascular compression of the vestibular nerve.
Ménière Disease.
Ménière disease ensues from idiopathic endolymphatic hydrops, with damage to the hair cells caused by swelling of the semicircular ducts. Patients report tinnitus, pressure in the ear, and hearing loss in conjunction with vertigo. Episodes are paroxysmal, last minutes to hours, and then decrease in frequency after multiple attacks, only to recur in several months or years. Hearing loss and tinnitus usually accompany the episodes of vertigo, and the hearing loss, although initially reversible, eventually becomes permanent.
Acute Labyrinthitis (Vestibular Neuritis).
Acute vestibular neuritis develops as a consequence of probable viral infection involving the cochlea and labyrinth. The patient reports a viral upper respiratory syndrome followed by onset of vertigo, tinnitus, and hearing loss. Symptoms resolve entirely by 3 to 6 weeks, with no residual deficits. Some patients may have no hearing loss. Many have incomplete recovery, with residual impaired balance during walking and head movement.
Ototoxins.
Ototoxins can injure the peripheral vestibular apparatus, although hearing impairment usually predominates. Streptomycin and gentamicin are among the toxins that are most injurious to the vestibular portion of the eighth cranial nerve.
Acoustic Neuroma.
Acoustic neuroma (benign schwannoma of the eighth cranial nerve), the most worrisome of the peripheral lesions, is retrocochlear in location. It is distinguished from the others in that it causes the retrocochlear type of hearing loss (see later discussion) and can produce serious brainstem compression if untreated. Symptoms start almost imperceptibly, with mild hearing loss, tinnitus, and vague dizziness, and may resemble those of other forms of peripheral vestibular disease. However, the clinical course is progressive, and the hearing loss is asymmetric, which differentiates it from that associated with other peripheral lesions. In advanced stages of the condition, there may be cranial nerve deficits from tumor extending to the cerebellopontine angle and compressing exiting roots of cranial nerves.
Central Lesions
Central lesions, as already noted, are accompanied in most instances by other brainstem symptoms. In addition, the vertigo and any accompanying nystagmus can be bidirectional or vertical, signs that do not occur in peripheral vestibular disease.
Multiple Sclerosis.
Multiple sclerosis associated with focal demyelination in the vestibular pathways of the brainstem is an important central cause of vertigo. Because of the often transient nature of attacks (days to weeks) and the subtlety of accompanying symptoms (slight facial numbness or huskiness of voice), multiple sclerosis may at first be mistaken for one of the self-limited peripheral causes of vertigo. Only with repeated episodes might the diagnosis become evident. The population afflicted with multiple sclerosis in general is younger than the patients (median age of 54 years) with canalithiasis as a cause of BPV. In the aftermath of an acute attack, a central type of positional nystagmus may persist after the vertigo resolves. The vertigo has no characteristic features; attacks can be sudden, transient, recurrent, or persistent. Diagnosis depends on magnetic resonance imaging (MRI) evidence of discrete central nervous system lesions and a course of recurrent dysfunction and intervals of remission.
Vertebrobasilar Insufficiency.
Vertebrobasilar insufficiency usually produces vertigo in conjunction with diplopia, sensory loss, dysarthria, dysphagia, hemiparesis, and other brainstem deficits. Self-limited episodes are manifestations of transient ischemic attacks (TIAs). In rare instances and almost exclusively in diabetics, transient vertigo may be the initial and sole complaint of impending infarction in the territory of the anterior inferior cerebellar artery supplying the inner ear; vertigo and/or unilateral hearing loss may be reported. Most other vertebrobasilar TIAs do not cause isolated vertigo as the sole symptom; rather, they present initially or subsequently with vertigo plus other brainstem symptoms. A subtler, progressive form of dizziness, usually without true vertigo, can be seen when multiple lacunar infarctions are present, particularly if the pons is involved. The MRI appearance of this so-called ischemic pontine rarefaction can be quite dramatic.
Migraine-Associated Vertigo.
True vertigo is reported by up to 25% of migraine sufferers. This is an atypical form of migraine with aura. The dizziness often antedates the headache phase of the syndrome and can persist in a less vivid form after the migraine headache is over. Persons with basilar migraine may report vertigo, ataxia, dysarthria, tinnitus, and visual disturbances. At times, there may be no relation to headache, making etiology more difficult to establish, but it may be suggested by a personal or family history of migraine or motion sickness.
Drugs.
Drugs that suppress the reticular activating system of the brainstem (e.g., sedatives, anticonvulsants) can cause vertigo of a central nature, especially when taken in excess. Therapeutic doses of many drugs (e.g., phenytoin, carbamazepine) produce nystagmus.
Cardiovascular Disease
Cardiac and vascular insufficiency leading to inadequate cerebral perfusion can result in dizziness, which patients tend to describe
as lightheadedness or a sense of faintness (see Chapter 24). This form of dizziness is seen in patients with fixed or limited cardiac output, serious cardiac dysrhythmias, diminished vascular tone, or severe intravascular volume depletion. Symptoms typically worsen on standing and improve on lying down; postural changes in blood pressure and pulse are characteristic.
as lightheadedness or a sense of faintness (see Chapter 24). This form of dizziness is seen in patients with fixed or limited cardiac output, serious cardiac dysrhythmias, diminished vascular tone, or severe intravascular volume depletion. Symptoms typically worsen on standing and improve on lying down; postural changes in blood pressure and pulse are characteristic.
Multiple Sensory Deficits, Cerebellar Disease, and Other Causes of Disequilibrium
These neurologic problems produce sensations of impaired balance and disequilibrium. In this form of dizziness, patients report the sensation to be in the feet rather than in the head. Like light-headedness, it may come on with standing; like true vertigo, it can be aggravated by walking or turning.
Multiple Sensory Deficits
Patients with multiple sensory deficits are usually elderly and have diabetes or other conditions that impair eyesight, sense of position, and motor function. Symptoms typically worsen in the dark (because of elimination of visual positional data) and improve with the use of a cane or holding onto a railing.
Cerebellar Disease
Cerebellar disease may present as disequilibrium or gait difficulty and be reported by the patient as “dizziness.” The physical examination is notable for marked gait ataxia and may be accompanied by other cerebellar signs. Acute onset of ataxia typically occurs in the context of alcohol intoxication, medication excess, toxin exposure, stroke, CNS infection, or exacerbations of multiple sclerosis (see Table 166-1). A less acute presentation is characteristic of cerebellar degenerative disease (with its gradual, progressive course) and of paraneoplastic syndromes associated with a host of cancers (see Table 166-2) and the appearance of autoantibodies that cross-react with cerebellar antigens. Onset of symptoms in the paraneoplastic syndrome often predates the clinical presentation of the cancer, and the ataxia may occur during cancer remission.
Psychiatric Illness
Patients with psychiatric difficulties complain of ill-defined dizziness (“I just feel dizzy”), constant “lightheadedness,” or a “foggy” feeling. Depression, anxiety states, and psychosis, in addition to the medications used to treat such conditions, are common precipitants. The precise mechanism of the light-headedness is unknown, but it is thought to be related to a confusional state induced by these illnesses or by the medications used to treat them. In the case of a panic attack leading to hyperventilation (see Chapter 226), the ensuing metabolic alkalosis usually causes paresthesias and light-headedness, although sometimes vertigo is reported. Staab’s article in the bibliography provides a lucid discussion of the overlap of anxiety disorders, migraines, and presyncopal states that lead to the complaint of chronic dizziness.
Metabolic Disturbances
Alterations in central nervous system metabolic homeostasis can cause dizziness resembling that associated with inadequate cerebral perfusion. The patient describes light-headedness or feeling faint. Precipitants of acute symptoms include hypoglycemia, hypoxia, hypocarbia, hypercarbia, and drugs.
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