Patients with presyncope may describe their dizziness as “lightheadedness” or “feeling like I’m going to faint.” This sensation may be
associated with generalized weakness, visual blurring or blackout, diaphoresis, pallor, shortness of breath, or palpitations. Presyncope is typically episodic and is caused by a transient reduction in global cerebral perfusion. Therefore, presyncope is usually a primary cardiovascular problem rather than a neurologic one.

Patients who have vertigo experience a false sensation of movement. Most commonly, they report that their environment is spinning around them; however, sensations of tilting, swaying, and being impelled forward, backward, or to either side are also vertiginous. Nausea, vomiting, and some degree of imbalance are common, as are autonomic signs such as diaphoresis, pallor, and tachycardia. Classically, patients with vertigo are thought to have a disorder of either the peripheral or central vestibular system, with peripheral vestibular disorders comprising approximately 90% of cases. Cerebellar lesions, however, may also cause vertigo and may mimic a peripheral vestibular problem.

Disequilibrium is a more complex category than the previous two. Whereas patients with presyncope and vertigo tend to have episodic symptoms or attacks, patients with disequilibrium typically have more continuous symptoms. Patients with disequilibrium are dizzy primarily when standing or walking and tend to improve when seated or supine. Disequilibrium may be difficult for patients to describe. Complains of “bad balance,” “poor equilibrium,” or “I’m just dizzy” are common. Disequilibrium is the result of dysfunction at one or more points in the complex system required for balance and ambulation.

Hyperventilation is a common cause of presyncope typically seen in anxious, pressured individuals. Patients with high-grade hyperventilation tend to have acute episodes of dizziness precipitated by stressful situations or panic attacks. They often are aware of breathing rapidly or feeling short of breath and may complain of visual blurring, paresthesias of the lips or fingers, and generalized weakness. Patients with lowgrade hyperventilation have a more protracted and insidious form of dizziness in which symptoms tend to wax and wane over longer periods. Visual blurring, paresthesias, and generalized weakness are usually absent. Patients are almost never aware that they are overbreathing, and they may not feel short of breath.

Artificial hyperventilation can be useful in the evaluation of patients with dizziness. Hyperventilation results in a drop in arterial PCO₂ with subsequent cerebral arterial vasoconstriction and global reduction in cerebral blood flow. Hyperventilation can be induced by holding a tissue 12 inches in front of the patient’s mouth and having the patient blow the tissue with rapid and deep breaths for up to 3 minutes. The tissue must be displaced significantly with each exhalation to ensure hyperventilation. If this procedure exactly reproduces the patient’s dizziness, hyperventilation syndrome is suggested.

Both high-grade and low-grade hyperventilators tend to be very sensitive to even short periods of induced hyperventilation. Reassurance regarding the etiology and benign nature of their symptom complex is the most important aspect of treatment for these patients. The highgrade hyperventilator may be helped by placement of a paper or plastic bag over the mouth during the attacks. Supportive psychotherapy or counseling may be helpful in some patients. Anxiolytic medication may be appropriate in selected patients.

Orthostatic hypotension is another common cause of presyncope, particularly in the elderly. The symptoms almost always occur when the patient is standing and are frequently maximal just after the patient rises from the sitting or supine position. Gravity decreases venous return to the heart, resulting in a decline in left heart filling. The autonomic nervous system normally is able to adjust peripheral resistance, cardiac rate, and contractility so that cardiac output and blood pressure are maintained, but if patients are hypovolemic from fluid loss or diuretic therapy, if they have been pharmacologically vasodilated, or if their compensatory autonomic responses are blunted by medication or disease, cardiac output and blood pressure may fall sufficiently to produce presyncopal symptoms. In these patients, a significant drop in blood pressure usually can be demonstrated at the bedside and this procedure often will reproduce the patient’s symptom complex.

To evaluate a patient for orthostatic hypotension, blood pressure should always be checked as the patient goes directly from the supine to the standing position. A drop of greater than 20/10 mm Hg 3 minutes after standing is considered abnormal. It is important to note that asymptomatic but demonstrable orthostatic blood pressure changes are common in the elderly. If the patient’s history does not suggest orthostatic hypotension and orthostatic testing does not reproduce the symptoms, then the observed drop in blood pressure may not be the cause of the dizziness.

Diuretics and other antihypertensive medications are common causes of orthostasis. Other causes of this syndrome include autonomic neuropathy, primary orthostatic hypotension, and multiple system atrophy, also known as Shy-Drager syndrome.

Symptomatic orthostatic hypotension from antihypertensive medications should be treated by medication adjustments. Neurologic causes of chronic orthostatic hypotension have several possible treatments. Raising the head of the patient’s bed by 10 to 15 degrees or recommending elastic stockings may be helpful. If these maneuvers do not provide adequate symptomatic relief, then sodium chloride tablets can be added judiciously if they are not contraindicated by hypertension, congestive heart failure, hepatic disease, or renal failure. The mineralocorticoid fludrocortisone acetate can be used in difficult cases, but blood pressure and serum electrolytes must be monitored closely. The alpha agonist midodrine also can be used in selected patients.

Vasovagal presyncope is probably more correctly called neurocardiogenic presyncope. The patient’s history is usually diagnostic. Vasovagal dizziness may occur in a hot crowded room or in the setting of sudden pain or strong emotion. The patient is almost always standing and may have premonitory symptoms of yawning, diaphoresis, and pallor. In vasovagal syncope, reductions in blood pressure and cerebral blood flow are caused by sudden, reflux dilation of the resistance arterioles. This syndrome usually occurs in young, otherwise healthy adults but can occur in the elderly. Heat favors vasodilation and could produce symptomatic hypotension in an elderly patient with otherwise compensated mild orthostatic hypotension. The only treatments for this syndrome are reassurance and avoidance of the precipitating circumstances.

Cardiac presyncope usually is caused by an arrhythmia that produces a sudden decrease in cardiac output and a subsequent decrease in cerebral perfusion. Common offending arrhythmias include sick sinus syndrome, paroxysmal supraventricular tachycardia, atrial fibrillation-flutter, complete heart block, and ventricular tachycardia. This diagnosis should be strongly considered in any patient whose presyncope occurs in the sitting or supine position. Workup includes an electrocardiogram and Holter monitoring, although it sometimes requires repeated or prolonged monitoring to document the arrhythmia.

Exercise-related presyncope may be caused by aortic stenosis or idiopathic hypertrophic subaortic stenosis. An echocardiogram is used for the diagnosis of these conditions. Paroxysmal episodes of lightheadedness and dizziness may sometimes be a manifestation of coronary ischemia, which should be considered in any patient with unexplained episodes of presyncope and the appropriate risk factors.

Carotid sinus hypersensitivity is primarily a disorder of the elderly in which the carotid sinus in the neck becomes abnormally sensitive to pressure and produces episodes of bradycardia and reduced cardiac output. Classically, this syndrome was described in men who wore tight collars. Such a history, however, will not be present in most patients with this disease. It should be suspected in middle-aged or elderly patients with ongoing bouts of presyncope or syncope. The diagnosis is made by carotid massage under strictly controlled conditions (i.e., the presence of a crash cart and personnel skilled in cardiopulmonary resuscitation). The treatment is placement of a permanent pacemaker.

Although this metabolic derangement does not cause a reduction in cerebral blood flow, its symptom complex is similar to that seen in presyncope. Thus, it should be considered in evaluating patients with episodic dizziness.

Most patients with symptomatic hypoglycemia are insulin-dependent diabetics who either did not consume an adequate caloric load for their insulin dose or took an excessive dose of insulin. Oral hypoglycemic agents are occasionally unpredictable in their action and can produce symptoms of hypoglycemia. Early diabetics who are not yet on therapy can have reactive hypoglycemia from surges of insulin. This typically occurs 2 to 5 hours after eating and is more often manifested by diaphoresis and palpitations than lightheadedness or other neurologic symptoms. The diagnosis is made by documenting serum hypoglycemia while the patient is symptomatic. In general, a serum glucose less than 50 mg/dL is necessary to produce neurologic symptoms. Rarely, insulin-secreting tumors may present with repeated episodes of hypoglycemia.

Because peripheral causes of vertigo are typically benign while central causes of vertigo are usually more serious, emphasis has traditionally been placed on determining whether vertigo is of central or peripheral origin. The presence of associated signs and symptoms may be helpful in making this distinction (Table 20.1), but the
clinician should keep in mind that in rare cases peripheral vertigo may be caused by stroke or TIA and that some causes of central vertigo are benign.

Hearing Loss and Tinnitus Peripheral vestibular lesions are frequently associated with hearing loss and tinnitus. These occur in diseases affecting the cochlea, the middle ear, and the acoustic portion of the eighth cranial nerve. Processes that disrupt the vestibular portion of the eighth nerve in the cerebellopontine angle or in the internal auditory canal usually also affect the acoustic portion. Likewise, labyrinthine processes also may affect the cochlea or middle ear.