Posted by sdb on April 27, 2010, at 5:22:13
In reply to Something about my movements are not normal, posted by Deneb on April 23, 2010, at 3:28:00
i have here some information from harrison' internal medicine
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20
Syncope, Faintness, Dizziness, and Vertigo
Robert B. Daroff
Mark D. Carlson
SYNCOPE
Syncope is defined as transient loss of consciousness due to reduced cerebral blood flow. Syncope is associated with postural collapse and spontaneous recovery. It may occur suddenly, without warning, or may be preceded by symptoms of faintness (presyncope). These include lightheadedness, dizziness without true vertigo, a feeling of warmth, diaphoresis, nausea, and visual blurring occasionally proceeding to blindness. Presyncopal symptoms vary in duration and may increase in severity until loss of consciousness occurs or may resolve prior to loss of consciousness if the cerebral ischemia is corrected. The differentiation of syncope from seizure is an important, sometimes difficult, diagnostic problem.
Syncope may be benign when it occurs as a result of normal cardiovascular reflex effects on heart rate and vascular tone, or serious when due to a life-threatening arrhythmia. Syncope may occur as a single event or may be recurrent. Recurrent, unexplained syncope, particularly in an individual with structural heart disease, is associated with a high risk of death (40% mortality within 2 years).
PATHOPHYSIOLOGY
Syncope results from a sudden impairment of brain metabolism, usually brought about by hypotension with reduction of cerebral blood flow. Several mechanisms subserve circulatory adjustments to the upright posture. Approximately three-fourths of the systemic blood volume is contained in the venous bed, and any interference in venous return may lead to a reduction in cardiac output. Cerebral blood flow may still be maintained as long as systemic arterial vasoconstriction occurs, but when this adjustment fails, serious hypotension, with resultant cerebral underperfusion to less than half of normal, results in syncope. Normally, the pooling of blood in the lower parts of the body is prevented by (1) pressor reflexes that induce constriction of peripheral arterioles and venules, (2) reflex acceleration of the heart by means of aortic and carotid reflexes, and (3) improvement of venous return to the heart by activity of the muscles of the limbs. Tilting a normal person upright on a tilt table causes some blood to accumulate in the lower limbs and diminishes cardiac output slightly; this may be followed by a slight transitory fall in systolic blood pressure. In a patient with defective vasomotor reflexes, however, tilt table testing may produce an abrupt and sustained fall in blood pressure, precipitating a faint.
CAUSES OF SYNCOPE
Transiently decreased cerebral blood flow is usually due to one of three general mechanisms: disorders of vascular tone or blood volume, cardiovascular disorders including cardiac arrhythmias, or cerebrovascular disease (Table 20-1). Not infrequently, however, the cause of syncope is multifactorial.
TABLE 20-1 Causes of Syncope--------------------------------------------------------------------------------
I. Disorders of vascular tone or blood volume
A. Vasovagal (vasodepressor, neurocardiogenic)
Postural (orthostatic) hypotensionDrug induced (especially antihypertensive or vasodilator drugs)
Peripheral neuropathy (diabetic, alcoholic, nutritional, amyloid)
Idiopathic postural hypotension
Multisystem atrophies
Physical deconditioning
Sympathectomy
Acute dysautonomia (Guillain-Barré syndrome variant)
Decreased blood volume (adrenal insufficiency, acute blood loss, etc.)
C. Carotid sinus hypersensitivity
D. Situational
CoughMicturition
Defecation
Valsalva
Deglutition
E. Glossopharyngeal neuralgia
II. Cardiovascular disorders
A. Cardiac arrhythmias (Chaps. 213 and 214)
Bradyarrhythmias
a. Sinus bradycardia, sinoatrial block, sinus arrest, sick-sinus syndrome
Atrioventricular blockTachyarrhythmias
a. Supraventricular tachycardia with structural cardiac disease
b. Atrial fibrillation associated with the Wolff-Parkinson-White syndrome
c. Atrial flutter with 1:1 atrioventricular conduction
d. Ventricular tachycardia
B. Other cardiopulmonary etiologies
Pulmonary embolismPulmonary hypertension
Atrial myxoma
Myocardial disease (massive myocardial infarction)
Left ventricular myocardial restriction or constriction
Pericardial constriction or tamponade
Aortic outflow tract obstruction
Aortic valvular stenosis
Hypertrophic obstructive cardiomyopathy
III. Cerebrovascular disease (Chap. 349)
A. Vertebrobasilar insufficiency
B. Basilar artery migraine
IV. Other disorders that may resemble syncope
A. Metabolic
HypoxiaAnemia
Diminished carbon dioxide due to hyperventilation
Hypoglycemia
B. Psychogenic
Anxiety attacks
Hysterical fainting
C. Seizures
--------------------------------------------------------------------------------
Disorders of Vascular Tone or Blood Volume
Disorders of autonomic control of the heart and circulation share common pathophysiologic mechanisms: a cardioinhibitory component (e.g., bradycardia due to increased vagal activity), a vasodepressor component (e.g., inappropriate vasodilatation due to sympathetic withdrawal), or both.
NEUROCARDIOGENIC (VASOVAGAL AND VASODEPRESSOR) SYNCOPE
The term neurocardiogenic is generally used to encompass both vasovagal and vasodepressor syncope. Strictly speaking, vasovagal syncope is associated with both sympathetic withdrawal (vasodilatation) and increased parasympathetic activity (bradycardia), whereas vasodepressor syncope is associated with sympathetic withdrawal alone.
These forms of syncope are the common faint that may be experienced by normal persons and account for approximately half of all episodes of syncope. Neurocardiogenic syncope is frequently recurrent and commonly precipitated by a hot or crowded environment, alcohol, extreme fatigue, severe pain, hunger, prolonged standing, and emotional or stressful situations. Episodes are often preceded by a presyncopal prodrome lasting seconds to minutes, and rarely occur in the supine position. The individual is usually sitting or standing and experiences weakness, nausea, diaphoresis, lightheadedness, blurred vision, and often a forceful heart beat with tachycardia followed by cardiac slowing and decreasing blood pressure prior to loss of consciousness. The individual appears pale or ashen; in dark-skinned individuals, the pallor may only be notable in the conjunctivae and lips. Patients with a gradual onset of presyncopal symptoms have time to
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protect themselves against injury; in others, syncope occurs suddenly, without warning.
The depth and duration of unconsciousness vary. Sometimes the patient remains partly aware of the surroundings, or there may be complete unresponsiveness. The unconscious patient usually lies motionless with skeletal muscles relaxed, but a few clonic jerks of the limbs and face may occur. Sphincter control is usually maintained, in contrast to a seizure. The pulse may be feeble or apparently absent, the blood pressure low or undetectable, and breathing may be almost imperceptible. The duration of unconsciousness is rarely longer than a few minutes if the conditions that provoke the episode are reversed. Once the patient is placed in a horizontal position, the strength of the pulse improves, color begins to return to the face, breathing becomes quicker and deeper, and consciousness is restored. Some patients may experience a sense of residual weakness after regaining consciousness, and rising too soon may precipitate another faint. Unconsciousness may be prolonged if an individual remains upright, thus it is essential that individuals with vasovagal syncope assume a recumbant position as soon as possible. Although commonly benign, neurocardiogenic syncope can be associated with prolonged asystole and hypotension, resulting in injury.
The syncope often occurs in this setting of increased peripheral sympathetic activity and venous pooling. Under these conditions, vigorous myocardial contraction of a relatively empty left ventricle activates myocardial mechanoreceptors and vagal afferent nerve fibers that inhibit sympathetic activity and increase parasympathetic activity. The resultant vasodilatation and bradycardia induce hypotension and syncope. Although the reflex involving myocardial mechanoreceptors is the mechanism usually accepted as responsible for neurocardiogenic syncope, other reflexes may also be operative. Patients with transplanted (denervated) hearts have experienced cardiovascular responses identical to those present during neurocardiogenic syncope. This should not be possible if the response depends solely on the reflex mechanisms described above, unless the transplanted heart has become reinnervated. Moreover, neurocardiogenic syncope often occurs in response to stimuli (fear, emotional stress, or pain) that may not be associated with venous pooling in the lower extremities, which suggests a cortical component to the reflex. Thus, a variety of afferent and efferent responses may cause neurocardiogenic syncope.
As distinct from the peripheral mechanisms, the central nervous system (CNS) mechanisms responsible for neurocardiogenic syncope are uncertain, but a sudden surge in central serotonin levels may contribute to the sympathetic withdrawal. Endogenous opiates (endorphins) and adenosine are also putative participants in the pathogenesis.
POSTURAL (ORTHOSTATIC) HYPOTENSION
This occurs in patients who have a chronic defect in, or variable instability of, vasomotor reflexes. Systemic arterial blood pressure falls on assumption of upright posture due to loss of vasoconstriction reflexes in resistance and capacitance vessels of the lower extremities. Although the syncopal attack differs little from vasodepressor syncope, the effect of posture is critical. Sudden rising from a recumbent position or standing quietly are precipitating circumstances. Orthostatic hypotension may be the cause of syncope in up to 30% of the elderly; polypharmacy with antihypertensive or antidepressant drugs is often a contributor in these patients.
Postural syncope may occur in otherwise normal persons with defective postural reflexes. Patients with idiopathic postural hypotension may be identified by a characteristic response to upright tilt on a table. Initially, the blood pressure diminishes slightly before stabilizing at a lower level. Shortly thereafter, the compensatory reflexes fail and the arterial pressure falls precipitously. The condition is often familial.
Orthostatic hypotension, often accompanied by disturbances in sweating, impotence, and sphincter difficulties, is also a primary feature of autonomic nervous system disorders (Chap. 354). The most common causes of neurogenic orthostatic hypotension are chronic diseases of the peripheral nervous system that involve postganglionic unmyelinated fibers (e.g., diabetic, nutritional, and amyloid polyneuropathy). Much less common are the multiple system atrophies; these are CNS disorders in which orthostatic hypotension is associated with (1) parkinsonism (Shy-Drager syndrome), (2) progressive cerebellar degeneration, or (3) a more variable parkinsonian and cerebellar syndrome (striatonigral degeneration) (Chap. 351). A rare, acute postganglionic dysautonomia may represent a variant of Guillain-Barré syndrome (Chap. 365).
There are several additional causes of postural syncope: (1) After physical deconditioning (such as after prolonged illness with recumbency, especially in elderly individuals with reduced muscle tone) or after prolonged weightlessness, as in space flight; (2) after sympathectomy that has abolished vasopressor reflexes; and (3) in patients receiving antihypertensive or vasodilator drugs and those who are hypovolemic because of diuretics, excessive sweating, diarrhea, vomiting, hemorrhage, or adrenal insufficiency.
CAROTID SINUS HYPERSENSITIVITY
Syncope due to carotid sinus hypersensitivity is precipitated by pressure on the carotid sinus baroreceptors, which are located just cephalad to the bifurcation of the common carotid artery. This typically occurs in the setting of shaving, a tight collar, or turning the head to one side. Carotid sinus hypersensitivity occurs predominantly in men ≥50 years old. Activation of carotid sinus baroreceptors gives rise to impulses carried via the nerve of Hering, a branch of the glossopharyngeal nerve, to the medulla oblongata. These afferent impulses activate efferent sympathetic nerve fibers to the heart and blood vessels, cardiac vagal efferent nerve fibers, or both. In patients with carotid sinus hypersensitivity, these responses may cause sinus arrest or atrioventricular (AV) block (a cardioinhibitory response), vasodilatation (a vasodepressor response), or both (a mixed response). The mechanisms responsible for the syndrome are not clear, and validated diagnostic criteria do not exist; some authorities have questioned its very existence.
SITUATIONAL SYNCOPE
A variety of activities, including cough, deglutition, micturition, and defecation, are associated with syncope in susceptible individuals. These syndromes are caused, at least in part, by abnormal autonomic control and may involve a cardioinhibitory response, a vasodepressor response, or both. Cough, micturition, and defecation are associated with maneuvers (such as Valsalva, straining, and coughing) that may contribute to hypotension and syncope by decreasing venous return. Increased intracranial pressure secondary to the increased intrathoracic pressure may also contribute by decreasing cerebral blood flow.
Cough syncope typically occurs in men with chronic bronchitis or chronic obstructive lung disease during or after prolonged coughing fits. Micturition syncope occurs predominantly in middle-aged and older men, particularly those with prostatic hypertrophy and obstruction of the bladder neck; loss of consciousness usually occurs at night during or immediately after voiding. Deglutition syncope and defecation syncope occur in men and women. Deglutition syncope may be associated with esophageal disorders, particularly esophageal spasm. In some individuals, particular foods and carbonated or cold beverages initiate episodes by activating esophageal sensory receptors that trigger reflex sinus bradycardia or AV block. Defecation syncope is probably secondary to a Valsalva maneuver in older individuals with constipation.
GLOSSOPHARYNGEAL NEURALGIA
Syncope due to glossopharyngeal neuralgia (Chap. 355) is preceded by pain in the oropharynx, tonsillar fossa, or tongue. Loss of consciousness is usually associated with asystole rather than vasodilatation. The mechanism is thought to involve activation of afferent impulses in the glossopharyngeal nerve that terminate in the nucleus solitarius of the medulla and, via collaterals, activate the dorsal motor nucleus of the vagus nerve.
CARDIOVASCULAR DISORDERS
Cardiac syncope results from a sudden reduction in cardiac output, caused most commonly by a cardiac arrhythmia. In normal individuals, heart rates between 30 and 180 beats/min do not reduce cerebral blood flow, especially if the person is in
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the supine position. As the heart rate decreases, ventricular filling time and stroke volume increase to maintain normal cardiac output. At rates <30 beats/min, stroke volume can no longer increase to compensate adequately for the decreased heart rate. At rates greater than ~180 beats/min, ventricular filling time is inadequate to maintain adequate stroke volume. In either case, cerebral hypoperfusion and syncope may occur. Upright posture; cerebrovascular disease; anemia; loss of atrioventricular synchrony; and coronary, myocardial, or valvular disease all reduce the tolerance to alterations in rate.
Bradyarrhythmias (Chap. 213) may occur as a result of an abnormality of impulse generation (e.g., sinoatrial arrest) or impulse conduction (e.g., AV block). Either may cause syncope if the escape pacemaker rate is insufficient to maintain cardiac output. Syncope due to bradyarrhythmias may occur abruptly, without presyncopal symptoms, and recur several times daily. Patients with sick sinus syndrome may have sinus pauses (>3 s), and those with syncope due to high-degree AV block (Stokes-Adams-Morgagni syndrome) may have evidence of conduction system disease (e.g., prolonged PR interval, bundle branch block). However, the arrhythmia is often transitory, and the surface electrocardiogram or continuous electrocardiographic monitor (Holter monitor) taken later may not reveal the abnormality. The bradycardia-tachycardia syndrome is a common form of sinus node dysfunction in which syncope generally occurs as a result of marked sinus pauses, some following termination of paroxysms of atrial tachyarrhythmias. Drugs are a common cause for bradyarrhythmias, particularly in patients with underlying structural heart disease. Digoxin, β-adrenergic receptor antagonists, calcium channel blockers, and many antiarrhythmic drugs may suppress sinoatrial node impulse generation or slow AV nodal conduction.
Syncope due to a tachyarrhythmia (Chap. 214) is usually preceded by palpitation or lightheadedness but may occur abruptly with no warning symptoms. Supraventricular tachyarrhythmias are unlikely to cause syncope in individuals with structurally normal hearts but may if they occur in patients with (1) heart disease that also compromises cardiac output, (2) cerebrovascular disease, (3) a disorder of vascular tone or blood volume, or (4) a rapid ventricular rate. These tachycardias result most commonly from paroxysmal atrial flutter, atrial fibrillation, or reentry involving the AV node or accessory pathways that bypass part or all of the AV conduction system. Patients with the Wolff-Parkinson-White syndrome may experience syncope when a very rapid ventricular rate occurs due to reentry across an accessory AV connection.
In patients with structural heart disease, ventricular tachycardia is a common cause of syncope, particularly in patients with a prior myocardial infarction. Patients with aortic valvular stenosis and hypertrophic obstructive cardiomyopathy are also at risk for ventricular tachycardia. Individuals with abnormalities of ventricular repolarization (prolongation of the QT interval) are at risk to develop polymorphic ventricular tachycardia (torsades de pointes). Those with the inherited form of this syndrome often have a family history of sudden death in young individuals. Genetic markers can identify some patients with familial long-QT syndrome, but the clinical utility of these markers remains unproven. Drugs (i.e., certain antiarrhythmics and erythromycin) and electrolyte disorders (i.e., hypokalemia, hypocalcemia, hypomagnesemia) can prolong the QT interval and predispose to torsades de pointes. Antiarrhythmic medications may precipitate ventricular tachycardia, particularly in patients with structural heart disease.
In addition to arrhythmias, syncope may also occur with a variety of structural cardiovascular disorders. Episodes are usually precipitated when the cardiac output cannot increase to compensate adequately for peripheral vasodilatation. Peripheral vasodilatation may be appropriate, such as following exercise, or may occur due to inappropriate activation of left ventricular mechanoreceptor reflexes, as occurs in aortic outflow tract obstruction (aortic valvular stenosis or hypertrophic obstructive cardiomyopathy). Obstruction to forward flow is the most common reason that cardiac output cannot increase. Pericardial tamponade is a rare cause of syncope. Syncope occurs in up to 10% of patients with massive pulmonary embolism and may occur with exertion in patients with severe primary pulmonary hypertension. The cause is an inability of the right ventricle to provide appropriate cardiac output in the presence of obstruction or increased pulmonary vascular resistance. Loss of consciousness is usually accompanied by other symptoms such as chest pain and dyspnea. Atrial myxoma, a prosthetic valve thrombus, and, rarely, mitral stenosis may impair left ventricular filling, decrease cardiac output, and cause syncope.
Cerebrovascular Disease
Cerebrovascular disease alone rarely causes syncope but may lower the threshold for syncope in patients with other causes. The vertebrobasilar arteries, which supply brainstem structures responsible for maintaining consciousness, are usually involved when cerebrovascular disease causes or contributes to syncope. An exception is the rare patient with tight bilateral carotid stenosis and recurrent syncope, often precipitated by standing or walking. Most patients who experience lightheadedness or syncope due to cerebrovascular disease also have symptoms of focal neurologic ischemia, such as arm or leg weakness, diplopia, ataxia, dysarthria, or sensory disturbances. Basilar artery migraine is a rare disorder that causes syncope in adolescents.
DIFFERENTIAL DIAGNOSIS
Anxiety Attacks and the Hyperventilation Syndrome
Anxiety, such as occurs in panic attacks, is frequently interpreted as a feeling of faintness or dizziness resembling presyncope. The symptoms are not accompanied by facial pallor and are not relieved by recumbency. The diagnosis is made on the basis of the associated symptoms such as a feeling of impending doom, air hunger, palpitations, and tingling of the fingers and perioral region. Attacks can often be reproduced by hyperventilation, resulting in hypocapnia, alkalosis, increased cerebrovascular resistance, and decreased cerebral blood flow. The release of epinephrine also contributes to the symptoms.
Seizures
A seizure may be heralded by an aura, which is caused by a focal seizure discharge and hence has localizing significance (Chap. 348). The aura is usually followed by a rapid return to normal or by a loss of consciousness. Injury from falling is frequent in a seizure and rare in syncope, since only in generalized seizures are protective reflexes abolished instantaneously. Sustained tonic-clonic movements are characteristic of convulsive seizures but brief clonic, or tonic-clonic, seizure-like activity can accompany fainting episodes. The period of unconsciousness tends to be longer in seizures than in syncope. Urinary incontinence is frequent in seizures and rare in syncope. The return of consciousness is prompt in syncope, slow after a seizure. Mental confusion, headache, and drowsiness are common sequelae of seizures, whereas physical weakness with a clear sensorium characterizes the postsyncopal state. Repeated spells of unconsciousness in a young person at a rate of several per day or month are more suggestive of epilepsy than syncope. See Table 348-7 for a comparison of seizures and syncope.
Hypoglycemia
Severe hypoglycemia is usually due to a serious disease such as a tumor of the islets of Langerhans; advanced adrenal, pituitary, or hepatic disease; or to excessive administration of insulin.
Acute Hemorrhage
Hemorrhage, usually within the gastrointestinal tract, is an occasional cause of syncope. In the absence of pain and hematemesis, the cause of the weakness, faintness, or even unconsciousness may remain obscure until the passage of a black stool.
Hysterical Fainting
The attack is usually unattended by an outward display of anxiety. Lack of change in pulse and blood pressure or color of the skin and mucous membranes distinguish it from the vasodepressor faint.
P.129APPROACH TO THE PATIENT
The diagnosis of syncope is often challenging. The cause may only be apparent at the time of the event, leaving few, if any, clues when the patient is seen later by the physician. The physician should think first of those causes that constitute a therapeutic emergency. Among them are massive internal hemorrhage or myocardial infarction, which may be painless, and cardiac arrhythmias. In elderly persons, a sudden faint, without obvious cause, should arouse the suspicion of complete heart block or a tachyarrhythmia, even though all findings are negative when the patient is seen.
Figure 20-1 depicts an algorithmic approach to syncope. A careful history is the most important diagnostic tool, both to suggest the correct cause and to exclude important potential causes (Table 20-1). The nature of the events and their time course immediately prior to, during, and after an episode of syncope often provide valuable etiologic clues. Loss of consciousness in particular situations, such as during venipuncture, micturition, or with volume depletion, suggests an abnormality of vascular tone. The position of the patient at the time of the syncopal episode is important; syncope in the supine position is unlikely to be vasovagal and suggests an arrhythmia or a seizure. Syncope due to carotid sinus syndrome may occur when the individual is wearing a shirt with a tight collar, turning the head (turning to look while driving in reverse), or manipulating the neck (as in shaving). The patient's medications must be noted, including nonprescription drugs or health store supplements, with particular attention to recent changes.View Figure FIGURE 20-1 Approach to the patient with syncope.
The physical examination should include evaluation of heart rate and blood pressure in the supine, sitting, and standing positions. In patients with unexplained recurrent syncope, an attempt to reproduce an attack may assist in diagnosis. Anxiety attacks induced by hyperventilation can be reproduced readily by having the patient breathe rapidly and deeply for 2 to 3 min. Cough syncope may be reproduced by inducing the Valsalva maneuver. Carotid sinus massage should generally be avoided, even in patients with suspected carotid sinus hypersensitivity; it is a risky procedure that can cause a transient ischemic attack (TIA) or stroke in individuals with carotid atheromas.
Diagnostic Tests
The choice of diagnostic tests should be guided by the history and the physical examination. Measurements of serum electrolytes, glucose, and the hematocrit are usually indicated. Cardiac enzymes should be evaluated if myocardial ischemia is suspected. Blood and urine toxicology screens may reveal the presence of alcohol or other drugs. In patients with possible adrenocortical insufficiency, plasma aldosterone and mineralocorticoid levels should be obtained.
Although the surface electrocardiogram is unlikely to provide a definitive diagnosis, it may provide clues to the cause of syncope and should be performed in almost all patients. The presence of conduction abnormalities (PR prolongation and bundle branch block) suggests a bradyarrhythmia, whereas pathologic Q waves or prolongation of the QT interval suggests a ventricular tachyarrhythmia. Inpatients should undergo continuous electrocardiographic monitoring; outpatients should wear a Holter monitor for 24 to 48 h. Whenever possible, symptoms should be correlated with the occurrence of arrhythmias. Continuous electrocardiographic monitoring may establish the cause of syncope in as many as 15% of patients. Cardiac event monitors may be useful in patients with infrequent symptoms, particularly in patients with presyncope. The presence of a late potential on a signal-averaged electrocardiogram is associated with increased risk for ventricular tacharrhythmias in patients with a prior myocardial infarction. Low-voltage (visually inapparent) T wave alternans is also associated with development of sustained ventricular arrhythmias.
Invasive cardiac electrophysiologic testing provides diagnostic and prognostic information regarding sinus node function, AV conduction, and supraventricular and ventricular arrhythmias (Chaps. 213 and 214). Prolongation of the sinus node recovery time (>1500 ms) is a specific finding (85 to 100%) for diagnosis of sinus node dysfunction but has a low sensitivity; continuous electrocardiographic monitoring is usually more effective for diagnosing this abnormality. Prolongation of the HV interval and conduction block below the His bundle indicate that His-Purkinje disease may be responsible for syncope. Programmed stimulation for ventricular arrhythmias is most useful in patients who have experienced a myocardial infarction; the sensitivity and specificity of this technique is lower in patients with normal hearts or those with heart disease other than coronary artery disease.
Upright tilt table testing is indicated for recurrent syncope, a single syncopal episode that caused injury, or a single syncopal event in a high-risk setting (pilot, commercial vehicle driver, etc.), whether or not there is a history of preexisting heart disease or prior vasovagal episodes. In susceptible patients, upright tilt at an angle between 60 and 80° for 30 to 60 min induces a vasovagal episode. The protocol can be shortened if upright tilt is combined with administration of drugs that cause venous pooling or increase adrenergic stimulation (isoproterenol, nitroglycerin, edrophonium, or adenosine). The sensitivity and specificity of tilt table testing is difficult to ascertain because of the lack of validated criteria. Moreover, the reflexes responsible for vasovagal syncope can be elicited in most, if not all, individuals given the appropriate stimulus. The reported accuracy of the test ranges from 30 to 80%, depending on the population studied and the techniques used. Whereas the reproducibility of a negative test is 85 to 100%, the reproducibility of a positive tilt table test is only between 62 and 88%.
A variety of other tests may be useful to determine the presence of structural heart disease that may cause syncope. The echocardiogram with Doppler examination detects valvular, myocardial, and pericardial abnormalities. The echocardiogram is the gold standard for the diagnosis of hypertrophic cardiomyopathy and atrial myxoma. Cardiac cine magnetic resonance (MR) imaging provides an alternative noninvasive modality that may be useful for patients in whom diagnostic-quality echocardiographic images cannot be obtained. This test is also indicated for patients suspected of having arrhythmogenic right ventricular dysplasia or right ventricular outflow tract ventricular tachycardia. Both are associated
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with right ventricular structural abnormalities that are better visualized on MR imaging than by echocardiogram. Exercise testing may detect ischemia or exercise-induced arrhythmias. In some patients, cardiac catheterization may be necessary to diagnose the presence or severity of coronary artery disease or valvular abnormalities. Ultrafast computed tomographic scan, ventilation-perfusion scan, or pulmonary angiography is indicated in patients in whom syncope may be due to pulmonary embolus.
In possible cases of cerebrovascular syncope neuroimaging tests may be indicated, including Doppler ultrasound studies of the carotid and vertebrobasilar systems, MR imaging, MR angiography, and x-ray angiography of the cerebral vasculature (Chap. 349). Electroencephalography is indicated if seizures are suspected.
TREATMENT
The treatment of syncope is directed toward the underlying cause. This discussion will focus on disorders of autonomic control. Arrhythmias are discussed in Chaps. 213 and 214, valvular heart diseases in Chap. 219, and cerebrovascular disorders in Chap. 349.
Certain precautions should be taken regardless of the cause of syncope. At the first sign of symptoms, patients should make every effort to avoid injury should they lose consciousness. Patients with frequent episodes, or those who have experienced syncope without warning symptoms, should avoid situations in which sudden loss of consciousness might result in injury (e.g., climbing ladders, swimming alone, operating heavy machinery, driving). Patients should lower their head to the extent possible and preferably should lie down. Lowering the head by bending at the waist should be avoided because it may further compromise venous return to the heart. When appropriate, family members or other close contacts should be educated as to the problem. This will ensure appropriate therapy and may prevent delivery of inappropriate therapy (chest compressions associated with cardiopulmonary resuscitation) that may inflict trauma.
Patients who have lost consciousness should be placed in a position that maximizes cerebral blood flow, offers protection from trauma, and secures the airway. Whenever possible, the patient should be placed supine with the head turned to the side to prevent aspiration and the tongue from blocking the airway. Assessment of the pulse and direct cardiac auscultation may assist in determining if the episode is associated with a bradyarrhythmia or tachyarrhythmia. Clothing that fits tightly around the neck or waist should be loosened. Peripheral stimulation, such as by sprinkling cold water on the face, may be helpful. Patients should not be given anything by mouth or be permitted to rise until the sense of physical weakness has passed.
Patients with vasovagal syncope should be instructed to avoid situations or stimuli that have caused them to lose consciousness and to assume a recumbent position when premonitory symptoms occur. These behavioral modifications alone may be sufficient for patients with infrequent and relatively benign episodes of vasovagal syncope, particularly when loss of consciousness occurs in response to a specific stimulus. Tilt training (standing and leaning against a wall for progressively longer periods each day) has been used with limited success, particularly for those patients who have profound orthostatic intolerance. Episodes associated with intravascular volume depletion may be prevented by salt and fluid loading prior to provocative events.
Prescription drug therapy may be necessary when vasovagal syncope is resistant to these measures, when episodes occur frequently, or when syncope is associated with a significant risk for injury. β-Adrenergic receptor antagonists (metoprolol, 25 to 50 mg bid; atenolol, 25 to 50 mg qd; or nadolol, 10 to 20 mg bid; all starting doses), the most widely used agents, mitigate the increase in myocardial contractility that stimulates left ventricular mechanoreceptors and also block central serotonin receptors. Serotonin reuptake inhibitors (paroxetine, 20 to 40 mg qd; or sertraline, 25 to 50 mg qd), appear to be effective for some patients. Bupropion SR (150 mg qd), another antidepressant, has also been used with success. β-Adrenergic receptor antagonists and serotonin reuptake inhibitors are well tolerated and are often used as first-line agents for younger patients. Hydrofludrocortisone (0.1 to 0.2 mg qd), a mineralocorticoid, promotes sodium retention, volume expansion, and peripheral vasoconstriction by increasing β-receptor sensitivity to endogenous catecholamines. Hydrofludrocortisone is useful for patients with intravascular volume depletion and those who also have postural hypotension. Proamatine (2.5 to 10 mg bid or tid), an α-agonist, has been used as a first-line agent for some patients. In a recent randomized controlled trial, proamatine was more effective than placebo in preventing syncope during an upright tilt-test. However, in some patients, proamatine and hydrofludrocortisone may increase resting supine systemic blood pressure, a property that may be problematic for those with hypertension.
Disopyramide (150 mg bid), a vagolytic antiarrhythmic drug with negative inotropic properties, and another vagolytic, transdermal scopolamine, have been used to treat vasovagal syncope, as have theophylline and ephedrine. Side effects associated with these drugs have limited their use for this indication. Disopyramide is a type 1A antiarrhythmic drug and should be used with great caution, if at all, in patients who are at risk for ventricular arrhythmias. Although several clinical trials have suggested that pharmacologic therapy for vasovagal syncope is effective, long-term prospective randomized controlled trials have yet to be completed.
Permanent dual-chamber cardiac pacing is effective for patients with frequent episodes of vasovagal syncope and is indicated for those with prolonged asystole associated with vasovagal episodes. Patients in whom vasodilatation contributes to loss of consciousness may also experience symptomatic benefit from permanent pacing. Pacemakers that can be programmed to transiently pace at a high rate (90 to 100 beats/min) after a profound drop in the patient's intrinsic heart rate are most effective.
Patients with orthostatic hypotension should be instructed to rise slowly and systematically (supine to seated, seated to standing) from the bed or a chair. Movement of the legs prior to rising facilitates venous return from the lower extremities. Whenever possible, medications that aggravate the problem (vasodilators, diuretics, etc.) should be discontinued. Elevation of the head of the bed [20 to 30 cm (8 to 12 in.)] and use of compression stockings may help.
Additional therapeutic modalities include an antigravity or g suit or compression stockings to prevent lower limb blood pooling; salt loading; and a variety of pharmacologic agents including sympathomimetic amines, monamine oxidase inhibitors, beta blockers, and levodopa. →The treatment of orthostatic hypotension secondary to central or peripheral disorders of the autonomic nervous system is discussed in Chap. 354.
Glossopharyngeal neuralgia is treated with carbamazepine, which is effective for the syncope as well as for the pain. Patients with carotid sinus syndrome should be instructed to avoid clothing and situations that stimulate carotid sinus baroreceptors. They should turn their entire body, rather than just their head, when looking to the side. Those with intractable syncope due to the cardioinhibitory response to carotid sinus stimulation should undergo permanent pacemaker implantation.
Patients with syncope should be hospitalized when the episode may have resulted from a life-threatening abnormality or if recurrence with significant injury seems likely. These individuals should be admitted to a bed with continuous electrocardiographic monitoring. Patients who are known to have a normal heart and for whom the history strongly suggests vasovagal or situational syncope may be treated as outpatients if the episodes are neither frequent nor severe.
DIZZINESS AND VERTIGO
Dizziness is a common and often vexing symptom. Patients use the term to encompass a variety of sensations, including those that seem semantically appropriate (e.g., lightheadedness, faintness, spinning, giddiness) and those that are misleadingly inappropriate, such as mental confusion, blurred vision, headache, or tingling. Moreover, some
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individuals with gait disorders caused by peripheral neuropathy, myelopathy, spasticity, parkinsonism, or cerebellar ataxia complain of dizziness despite the absence of vertigo or other abnormal cephalic sensations. In this context, the term dizziness is being used to describe disturbed ambulation. There may be mild associated lightheadedness, particularly with impaired sensation from the feet or poor vision; this is known as multiple-sensory-defect dizziness and occurs in elderly individuals who complain of dizziness only when walking. Decreased position sense (secondary to neuropathy or myelopathy) and poor vision (from cataracts or retinal degeneration) create an overreliance on the aging vestibular apparatus. A less precise but sometimes comforting designation to patients is benign dysequilibrium of aging. Thus, a careful history is necessary to determine exactly what a patient who states, Doctor, I'm dizzy, is experiencing. After eliminating the misleading symptoms or gait disturbance, dizziness usually means either faintness (presyncope) or vertigo (an illusory or hallucinatory sense of movement of the body or environment, most often a feeling of spinning). Operationally, after obtaining the history, dizziness may be classified into three categories: (1) faintness, (2) vertigo, and (3) miscellaneous head sensations.
FAINTNESS
Prior to an actual faint (syncope), there are often prodromal presyncopal symptoms (faintness) reflecting ischemia to a degree insufficient to impair consciousness (see above).
VERTIGO
Vertigo is usually due to a disturbance in the vestibular system. The end organs of this system, situated in the bony labyrinths of the inner ears, consist of the three semicircular canals and the otolithic apparatus (utricle and saccule) on each side. The canals transduce angular acceleration, while the otoliths transduce linear acceleration and the static gravitational forces that provide a sense of head position in space. The neural output of the end organs is conveyed to the vestibular nuclei in the brainstem via the eighth cranial nerves. The principal projections from the vestibular nuclei are to the nuclei of cranial nerves III, IV, and VI; spinal cord; cerebral cortex; and cerebellum. The vestibuloocular reflex (VOR) serves to maintain visual stability during head movement and depends on direct projections from the vestibular nuclei to the sixth cranial nerve (abducens) nuclei in the pons and, via the medial longitudinal fasciculus, to the third (oculomotor) and fourth (trochlear) cranial nerve nuclei in the midbrain. These connections account for the nystagmus (to-and-fro oscillation of the eyes) that is an almost invariable accompaniment of vestibular dysfunction. The vestibular nerves and nuclei project to areas of the cerebellum (primarily the flocculus and nodulus) that modulate the VOR. The vestibulospinal pathways assist in the maintenance of postural stability. Projections to the cerebral cortex, via the thalamus, provide conscious awareness of head position and movement.
The vestibular system is one of three sensory systems subserving spatial orientation and posture; the other two are the visual system (retina to occipital cortex) and the somatosensory system that conveys peripheral information from skin, joint, and muscle receptors. The three stabilizing systems overlap sufficiently to compensate (partially or completely) for each other's deficiencies. Vertigo may represent either physiologic stimulation or pathologic dysfunction in any of the three systems.
Physiologic Vertigo
This occurs in normal individuals when (1) the brain is confronted with a mismatch among the three stabilizing sensory systems; (2) the vestibular system is subjected to unfamiliar head movements to which it is unadapted, such as in seasickness; (3) unusual head/neck positions, such as the extreme extension when painting a ceiling; or (4) following a spin. Intersensory mismatch explains carsickness, height vertigo, and the visual vertigo most commonly experienced during motion picture chase scenes; in the latter, the visual sensation of environmental movement is unaccompanied by concomitant vestibular and somatosensory movement cues. Space sickness, a frequent transient effect of active head movement in the weightless zero-gravity environment, is another example of physiologic vertigo.
Pathologic Vertigo
This results from lesions of the visual, somatosensory, or vestibular systems. Visual vertigo is caused by new or incorrect spectacles or by the sudden onset of an extraocular muscle paresis with diplopia; in either instance, CNS compensation rapidly counteracts the vertigo. Somatosensory vertigo, rare in isolation, is usually due to a peripheral neuropathy or myelopathy that reduces the sensory input necessary for central compensation when there is dysfunction of the vestibular or visual systems.
The most common cause of pathologic vertigo is vestibular dysfunction involving either its end organ (labyrinth), nerve, or central connections. The vertigo is frequently accompanied by nausea, jerk nystagmus, postural unsteadiness, and gait ataxia. Since vertigo increases with rapid head movements, patients tend to hold their heads still.
LABYRINTHINE DYSFUNCTION
This causes severe rotational or linear vertigo. When rotational, the hallucination of movement, whether of environment or self, is directed away from the side of the lesion. The fast phases of nystagmus beat away from the lesion side, and the tendency to fall is toward the side of the lesion, particularly in darkness or with the eyes closed.
Under normal circumstances, when the head is straight and immobile, the vestibular end organs generate a tonic resting firing frequency that is equal from the two sides. With any rotational acceleration, the anatomic positions of the semicircular canals on each side necessitate an increased firing rate from one and a commensurate decrease from the other. This change in neural activity is ultimately projected to the cerebral cortex, where it is summed with inputs from the visual and somatosensory systems to produce the appropriate conscious sense of rotational movement. After cessation of movement, the firing frequencies of the two end organs reverse; the side with the initially increased rate decreases, and the other side increases. A sense of rotation in the opposite direction is experienced; since there is no actual head movement, this hallucinatory sensation is physiologic postrotational vertigo.
Any disease state that changes the firing frequency of an end organ, producing unequal neural input to the brainstem and ultimately the cerebral cortex, causes vertigo. The symptom can be conceptualized as the cortex inappropriately interpreting the abnormal neural input as indicating actual head rotation. Transient abnormalities produce short-lived symptoms. With a fixed unilateral deficit, central compensatory mechanisms ultimately diminish the vertigo. Since compensation depends on the plasticity of connections between the vestibular nuclei and the cerebellum, patients with brainstem or cerebellar disease have diminished adaptive capacity, and symptoms may persist indefinitely. Compensation is always inadequate for severe fixed bilateral lesions despite normal cerebellar connections: these patients are permanently symptomatic.
Acute unilateral labyrinthine dysfunction is caused by infection, trauma, and ischemia. Often, no specific etiology is uncovered, and the nonspecific terms acute labyrinthitis, acute peripheral vestibulopathy, or vestibular neuritis are used to describe the event. The vertiginous attacks are brief and leave the patient with mild vertigo for several days. Infection with herpes simplex virus type 1 has been implicated. It is impossible to predict whether a patient recovering from the first bout of vertigo will have recurrent episodes.
Labyrinthine ischemia, presumably due to occlusion of the labyrinthine branch of the internal auditory artery, may be the sole manifestation of vertebrobasilar insufficiency (Chap. 349); patients with this syndrome present with the abrupt onset of severe vertigo, nausea, and vomiting, but without tinnitus or hearing loss.
Acute bilateral labyrinthine dysfunction is usually the result of toxins such as drugs or alcohol. The most common offending drugs are the aminoglycoside antibiotics that damage the hair cells of the vestibular end organs and may cause a permanent disorder of equilibrium.
Recurrent unilateral labyrinthine dysfunction, in association with
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signs and symptoms of cochlear disease (progressive hearing loss and tinnitus), is usually due to Ménière's disease (Chap. 26). When auditory manifestations are absent, the term vestibular neuronitis denotes recurrent monosymptomatic vertigo. TIAs of the posterior cerebral circulation (vertebrobasilar insufficiency) only infrequently cause recurrent vertigo without concomitant motor, sensory, visual, cranial nerve, or cerebellar signs (Chap. 349).
Positional vertigo is precipitated by a recumbent head position, either to the right or to the left. Benign paroxysmal positional (or positioning) vertigo (BPPV) of the posterior semicircular canal is particularly common. Although the condition may be due to head trauma, usually no precipitating factors are identified. It generally abates spontaneously after weeks or months. The vertigo and accompanying nystagmus have a distinct pattern of latency, fatigability, and habituation that differs from the less common central positional vertigo (Table 20-2) due to lesions in and around the fourth ventricle. Moreover, the pattern of nystagmus in posterior canal BPPV is distinctive. When supine, with the head turned to the side of the offending ear (bad ear down), the lower eye displays a large-amplitude torsional nystagmus, and the upper eye has a lesser degree of torsion combined with upbeating nystagmus. If the eyes are directed to the upper ear, the vertical nystagmus in the upper eye increases in amplitude. Mild dysequilibrium when upright may also be present.
TABLE 20-2 Benign Paroxysmal Positional Vertigo and Central Positional Vertigo--------------------------------------------------------------------------------
Features BPPV Central--------------------------------------------------------------------------------
Latencya 340 s None: immediate vertigo and nystagmus
Fatigabilityb Yes No
Habituationc Yes No
Intensity of vertigo Severe Mild
Reproducibilityd Variable Good--------------------------------------------------------------------------------
aTime between attaining head position and onset of symptoms.
bDisappearance of symptoms with maintenance of offending position.
cLessening of symptoms with repeated trials.
dLikelihood of symptom production during any examination session.
A perilymphatic fistula should be suspected when episodic vertigo is precipitated by Valsalva or exertion, particularly upon a background of a stepwise progressive sensory-neural hearing loss. The condition is usually caused by head trauma or barotrauma or occurs after middle ear surgery.
VERTIGO OF VESTIBULAR NERVE ORIGIN
This occurs with diseases that involve the nerve in the petrous bone or the cerebellopontine angle. Although less severe and less frequently paroxysmal, it has many of the characteristics of labyrinthine vertigo. The adjacent auditory division of the eighth cranial nerve is usually affected, which explains the frequent association of vertigo with unilateral tinnitus and hearing loss. The most common cause of eighth cranial nerve dysfunction is a tumor, usually a schwannoma (acoustic neuroma) or a meningioma. These tumors grow slowly and produce such a gradual reduction of labyrinthine output that central compensatory mechanisms can prevent or minimize the vertigo; auditory symptoms of hearing loss and tinnitus are the most common manifestations.
CENTRAL VERTIGO
Lesions of the brainstem or cerebellum can cause acute vertigo, but associated signs and symptoms usually permit distinction from a labyrinthine etiology (Table 20-3). Occasionally, an acute lesion of the vestibulocerebellum may present with monosymptomatic vertigo indistinguishable from a labyrinthopathy.
TABLE 20-3 Differentiation of Peripheral and Central Vertigo--------------------------------------------------------------------------------
Sign or Symptom Peripheral (Labyrinth) Central (Brainstem or Cerebellum)--------------------------------------------------------------------------------
Direction of associated nystagmus Unidirectional; fast phase opposite lesiona Bidirectional or unidirectional
Purely horizontal nystagmus without torsional component Uncommon Common
Vertical or purely torsional nystagmus Never present May be present
Visual fixation Inhibits nystagmus and vertigo No inhibition
Severity of vertigo Marked Often mild
Direction of spin Toward fast phase Variable
Direction of fall Toward slow phase Variable
Duration of symptoms Finite (minutes, days, weeks) but recurrent May be chronic
Tinnitus and/or deafness Often present Usually absent
Associated central abnormalities None Extremely common
Common causes Infection (labyrinthitis), Ménière's, neuronitis, ischemia, trauma, toxin Vascular, demyelinating, neoplasm--------------------------------------------------------------------------------
aIn Ménière's disease, the direction of the fast phase is variable.
Vertigo may be a manifestation of a migraine aura (Chap. 14), but some patients with migraine have episodes of vertigo unassociated with their headaches. Antimigrainous treatment should be considered in such patients with otherwise enigmatic vertiginous episodes.
Vestibular epilepsy, vertigo secondary to temporal lobe epileptic activity, is rare and almost always intermixed with other epileptic manifestations.
PSYCHOGENIC VERTIGO
This is usually a concomitant of panic attacks (Chap. 371) or agoraphobia (fear of large open spaces, crowds, or leaving the safety of home) and should be suspected in patients so incapacitated by their symptoms that they adopt a prolonged housebound status. Most patients with organic vertigo attempt to function despite their discomfort. Organic vertigo is accompanied by nystagmus; a psychogenic etiology is almost certain when nystagmus is absent during a vertiginous episode.
Miscellaneous Head Sensations
This designation is used, primarily for purposes of initial classification, to describe dizziness that is neither faintness nor vertigo. Cephalic ischemia or vestibular dysfunction may be of such low intensity that the usual symptomatology is not clearly identified. For example, a small decrease in blood pressure or a slight vestibular imbalance may cause sensations different from distinct faintness or vertigo but that may be identified properly during provocative testing techniques (see below). Other causes of dizziness in this category are hyperventilation syndrome, hypoglycemia, and the somatic symptoms of a clinical depression; these patients should all have normal neurologic examinations and vestibular function tests. Depressed patients often insist that the depression is secondary to the dizziness.
P.133APPROACH TO THE PATIENT
The most important diagnostic tool is a detailed history focused on the meaning of dizziness to the patient. Is it faintness (presyncope)? Is there a sensation of spinning? If either of these is affirmed and the neurologic examination is normal, appropriate investigations for the multiple causes of cephalic ischemia or vestibular dysfunction are undertaken.
When the meaning of dizziness is uncertain, provocative tests may be helpful. These office procedures simulate either cephalic ischemia or vestibular dysfunction. Cephalic ischemia is obvious if the dizziness is duplicated during maneuvers that produce orthostatic hypotension. Further provocation involves the Valsalva maneuver, which decreases cerebral blood flow and should reproduce ischemic symptoms.
Hyperventilation is the cause of dizziness in many anxious individuals; tingling of the hands and face may be absent. Forced hyperventilation for 1 min is indicated for patients with enigmatic dizziness and normal neurologic examinations.
The simplest provocative test for vestibular dysfunction is rapid rotation and abrupt cessation of movement in a swivel chair. This always induces vertigo that the patients can compare with their symptomatic dizziness. The intense induced vertigo may be unlike the spontaneous symptoms, but shortly thereafter, when the vertigo has all but subsided, a lightheadedness supervenes that may be identified as my dizziness. When this occurs, the dizzy patient, originally classified as suffering from miscellaneous head sensations, is now properly diagnosed as having mild vertigo secondary to a vestibulopathy.
Patients with symptoms of positional vertigo should be appropriately tested (Table 20-2). A final provocative and diagnostic vestibular test, requiring the use of Frenzel eyeglasses (self-illuminated goggles with convex lenses that blur out the patient's vision, but allow the examiner to see the eyes greatly magnified), is vigorous head shaking in the horizontal plane for about 10 s. If nystagmus develops after the shaking stops, even in the absence of vertigo, vestibular dysfunction is demonstrated. The maneuver can then be repeated in the vertical plane. If the provocative tests establish the dizziness as a vestibular symptom, an evaluation of vestibular vertigo is undertaken.
Evaluation of Patients with Pathologic Vestibular Vertigo
The evaluation depends on whether a central etiology is suspected (Table 20-3). If so, MR imaging of the head is mandatory. Such an examination is rarely helpful in cases of recurrent monosymptomatic vertigo with a normal neurologic examination. Typical BPPV requires no investigation after the diagnosis is made (Table 20-2).
Vestibular function tests serve to (1) demonstrate an abnormality when the distinction between organic and psychogenic is uncertain, (2) establish the side of the abnormality, and (3) distinguish between peripheral and central etiologies. The standard test is electronystagmography (calorics), where warm and cold water (or air) are applied, in a prescribed fashion, to the tympanic membranes, and the slow-phase velocities of the resultant nystagmus from the two are compared. A velocity decrease from one side indicates hypofunction (canal paresis). An inability to induce nystagmus with ice water denotes a dead labyrinth. Some institutions have the capability of quantitatively determining various aspects of the VOR using computer-driven rotational chairs and precise oculographic recording of the eye movements.
CNS disease can produce dizzy sensations of all types. Consequently, a neurologic examination is always required even if the history or provocative tests suggest a cardiac, peripheral vestibular, or psychogenic etiology. Any abnormality on the neurologic examination should prompt appropriate neurodiagnostic studies.
TREATMENT
Treatment of acute vertigo consists of bed rest (1 to 2 days maximum) and vestibular suppressant drugs such as antihistaminics (meclizine, dimenhydrinate, promethazine), tranquilizers with GABA-ergic effects (diazepam, clonazepam), phenothiazines (prochlorperazine), or glucocorticoids (Table 20-4). If the vertigo persists beyond a few days, most authorities advise ambulation in an attempt to induce central compensatory mechanisms, despite the short-term discomfort to the patient. Chronic vertigo of labyrinthine origin may be treated with a systematized vestibular rehabilitation program to facilitate central compensation.
TABLE 20-4 Treatment of Vertigo--------------------------------------------------------------------------------
Agenta Doseb--------------------------------------------------------------------------------
Antihistamines
Meclizine 2550 mg 3 times/day
Dimenhydrinate 50 mg 12 times/day
Promethazinec 2550-mg suppository or IM
Benzodiazepines
Diazepam 2.5 mg 13 times/day
Clonazepam 0.25 mg 13 times/day
Phenothiazines
Prochlorperazinec 5 mg IM or 25-mg suppository
Anticholinergicd
Scopolamine transdermal Patch
Sympathomimeticsd
Ephedrine 25 mg/d
Combination preparationsd
Ephedrine and promethazine 25 mg/d of each
Exercise therapy
Repositioning maneuverse
Vestibular rehabilitationf
Other
Diuretics or low-salt (1 g/d) dietg
Antimigrainous drugsh
Inner ear surgeryi
Glucocorticoidsc--------------------------------------------------------------------------------
aAll listed drugs are U.S. Food and Drug Administration approved, but most are not approved for the treatment of vertigo.
bUsual oral (unless otherwise stated) starting dose in adults; maintenance dose can be reached by a gradual increase.
cFor acute vertigo only.
dFor motion sickness only.
eFor benign paroxysmal positional vertigo.
fFor vertigo other than Ménière's and positional.
gFor Ménière's disease.
hFor migraine-associated vertigo (see Chap. 14 for a listing of prophylactic antimigrainous drugs).
iFor perilymphatic fistula and refractory cases of Ménière's disease.
BPPV is often self-limited but, when persistent, may respond dramatically to specific repositioning exercise programs designed to empty particulate debris from the posterior semicircular canal. One of these exercises, the Epley procedure, is graphically demonstrated, in four languages, on a website for use in both physician's offices and self-treatment (www.charite.de/ch/neuro/vertigo.html).
Prophylactic measures to prevent recurrent vertigo are variably effective. Antihistamines are commonly utilized but are of limited value. Ménière's disease may respond to a diuretic or, more effectively, to a very low salt diet (1 g/d). Recurrent episodes of migraine-associated vertigo should be treated with antimigrainous therapy (Chap. 14). There are a variety of inner ear surgical procedures for refractory Ménière's disease, but these are only rarely necessary.
Helpful websites for both physicians and vertigo patients are: www.iVertigo.net and www.tchain.com.
FURTHER READING
Kapoor WN: Current evaluation in management of syncope. Circulation 106:1606, 2002Ovid Full TextBibliographic Links
Kaufman H et al: Midodrine in neurally mediated syncope: A double-blind, randomized, crossover study. Ann Neurol 52:342, 2002Bibliographic Links
Kaufman NH, Bhattacharya K: Diagnosis and treatment of neurally mediated syncope. The Neurologist 8:175, 2002Bibliographic Links
Maisel W, Stebenson W: Syncopegetting to the heart of the matter. N Engl J Med 347:931, 2002Ovid Full TextBibliographic Links
Soteriades E et al: Incidence and prognosis of syncope. N Engl J Med 347:878, 2002Ovid Full TextBibliographic Links
P.134BIBLIOGRAPHY
Baloh RW, Honrubia V: Clinical Neurophysiology of the Vestibular System, 3d ed. New York, Oxford University, 2001
Brandt T: Management of vestibular disorders. J Neurol 247:491, 2000Bibliographic Links
Giacomini PG et al: Long-term postural abnormalities in benign paroxysmal positional vertigo. ORL J Otorhinolaryngol Relat Spec 64:237, 2002Bibliographic Links
Grubb B, Kanjwal Y: Neurocardiogenic syncope: A review of pathophysiology, diagnosis, and management, in Encyclopedia of the Neurological Sciences, MJ Aminoff, RB Daroff (eds). San Diego, Academic Press/Elsevier Science, 2003
Strupp M, Arbusow V: Acute vestibulopathy. Curr Opin Neurol 14:11, 2001Ovid Full TextBibliographic Links
Tusa RJ: Vertigo. Neurol Clin 19:23, 2001Bibliographic Links
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