Jeffrey L. Magaziner
Mark F. Walker
Dizziness
Dizziness is the ninth most common chief complaint in ambulatory settings (1). The word dizzy, however, is a very inexact term. It can refer to impending loss of consciousness, a feeling of motion or spatial disorientation, or imbalance. On the other hand, some patients use “dizziness” to refer to less specific subjective states such as fatigue or anxiety. Occasionally, patients use the word dizzy to mean sick. A correct diagnosis for a patient's complaint of dizziness is often possible on the basis of the history and physical examination. A limited number of diagnostic studies can aid the evaluation of selected patients, but these can be interpreted properly only in the light of information gained from the patient.
Categorizing a Patient's Dizziness
Evaluation of the dizzy patient starts with categorizing the exact nature of the symptoms. Categorization of symptoms can help determine what system is involved and give focus to the differential diagnosis. The major categories of dizziness are vertigo, the illusion that the patient or the environment is moving; near syncope or syncope, a sensation of impending faint or actual loss of consciousness; anddisequilibrium, a sensation of impaired balance. Finally, some patients’ symptoms simply cannot fit into a specific category and are termed nonspecific dizziness. When a patient has ill-defined dizziness that cannot be readily classified, the patient should be asked to use words more specific
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than dizziness and should be asked to describe a discrete recent episode. It is important to ask the patient to describe what they mean by dizzy, rather than asking closed-ended questions like “do you sense the room spinning” in the beginning. Table 89.1 lists typical words they may use and potential categories. If the patient's initial account is too vague, the following questions may help:
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TABLE 89.1 Categorization of Terms Used by Patients to Describe Dizziness |
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Questions about associated auditory, neurologic, or cardiac symptoms may help classify the patient's problem more specifically. Additional important information includes how many episodes of dizziness the patient has had, how long they lasted, and whether there are any specific factors that can provoke episodes.
The patient who claims to be dizzy “right now” while sitting before the physician should be checked for hypotension, first while seated and then while standing, and examined for nystagmus (see Physical Examination).
As part of the preliminary inquiry, it is important to ask the patient whether dizziness has interfered with usual activities, especially driving a motor vehicle. This information will be important in management regardless of the cause of dizziness.
Disorders of the Vestibular System
The purpose of the vestibular system is to sense movement of the head and, through the vestibulo-ocular and vestibulospinal reflexes, to maintain stable vision and posture during movement. Thus, the symptoms of vestibular dysfunction include an inappropriate sense of motion (vertigo), imbalance, and the appearance that the visual world is moving (oscillopsia).
Basic Principles of Vestibular Function
To understand disorders of the vestibular system and their symptoms and signs, it is helpful to keep in mind basic vestibular anatomy and function. The peripheral organs of the vestibular system are the labyrinths. The cochlea is the portion of the labyrinth responsible for hearing (see Chapter 110). The vestibular labyrinth consists of the three semicircular canals (horizontal or lateral, anterior or superior, and posterior) and two gravity-sensitive structures (utricle and saccule) (see Fig. 110.1). Attached to the utricle and saccule are calcium carbonate crystals termed otoconia; these are important in the pathophysiology of benign paroxysmal positional vertigo (BPPV) (seeRecurrent Vertigo). The semicircular canals sense angular rotations of the head, and the otoconia in the utricle and saccule sense linear (e.g., side-to-side) motion and the orientation of the head relative to gravity.
When the head is not moving, each vestibular nerve has an equal resting discharge rate, such that there is no net difference in the inputs from the two sides. Rotation of the head excites one labyrinth and inhibits the other, disturbing this balance. This signals the brain that the head is moving and generates the appropriate compensatory eye movement (in the direction opposite to head motion) to maintain steady gaze (vestibuloocular reflex [VOR]). For example, when the head rotates to the right, there is an increase in firing from the right horizontal canal. This causes the eyes to rotate to the left in the orbits, so that they remain fixed in space. This compensatory eye movement is called the slow phase of the VOR. If the head continues to rotate, these slow phases will be interrupted by rapid saccade-like movements in the opposite direction, termed quick phases. The combination of slow and quick phases is called nystagmus. The direction of nystagmus is usually given by the direction of its quick phases, even though it is the slow phases that reflect vestibular activity. Thus, prolonged rotation of the head to the right generates a right-beating nystagmus. This physiologic nystagmus maintains clear vision during head rotations.
Pathologic vestibular nystagmus results when one labyrinth or vestibular nerve is lesioned, removing the spontaneous discharge from that side and leaving the tonic input from the other side unopposed. The resulting imbalance creates the sensation of spinning and generates a nystagmus, in which slow phases are directed toward the side of the lesion and quick phases toward the intact side. Thus, an acute left vestibular lesion causes unopposed input from the right vestibular nerve and a right-beating nystagmus. With time, the brain readjusts central vestibular tone to
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compensate for the peripheral imbalance, sometimes leaving only minimal residual symptoms and signs.
Vertigo
Vertigo is a sense of illusory movement, either of oneself or of the surrounding environment. Patients may report feelings of spinning, tilting, or tumbling. Vertigo generally indicates an imbalance in the vestibular system. This may result either from a peripheral lesion, involving one of the labyrinths or vestibular nerves (e.g., vestibular neuritis), or from a central lesion (e.g., infarction) within the vestibular pathways of the brainstem and cerebellum. It is important to keep in mind that bilateral labyrinthine lesions, such as from aminoglycoside ototoxicity, often do not cause vertigo because the lesion is symmetric, thus creating no net imbalance. Vestibular schwannomas (acoustic neuromas) and other slowly growing tumors affecting the vestibular nerve also do not commonly produce vertigo, because the resulting vestibular imbalance is compensated centrally as it develops. The most severe vertigo occurs with an acute unilateral peripheral vestibular lesion.
Evaluation of the Undiagnosed Patient
While most patients who present with vertigo have a benign etiology for their symptoms, a subset can have a potentially life-threatening cause. For the most part, the life-threatening causes of vertigo occur in the central nervous system and are termed central vertigo. Not all causes of central vertigo, however, are life threatening (e.g., vestibular migraine). Lesions of the vestibular apparatus are most often not life-threatening. These disorders are called peripheral vertigo. Differentiation of peripheral and central vertigo is one of the primary goals in evaluating the undiagnosed patient.
History
In taking a history from a patient with vertigo, there are several questions that are particularly helpful:
Physical Examination
When examining patients with vertigo, the goals are to look for signs of vestibular hypofunction and to distinguish peripheral from central lesions. It is always important to perform a basic neurologic examination, with particular attention to the cranial nerves, cerebellar function, and walking and balance (see Chapter 86) and to do a basic office assessment of hearing (see Chapter 110). Specific tests of the vestibular system involve looking for vestibular imbalance and impairment of the VOR and testing for positional nystagmus.
As explained above, the hallmark of a static vestibular imbalance is a spontaneous nystagmus. However, it is important to remember thatperipheral vestibular nystagmus is suppressed by vision. Thus, except in the most acute stage of a peripheral lesion, nystagmus is not commonly seen during bedside examination. Techniques must be used to remove the subject's visual fixation while still allowing the examiner to view the eyes. In the vestibular clinic, this is done using specialized goggles with high magnification lenses (Frenzel lenses). An alternative method is to observe the optic disk carefully during direct ophthalmoscopy, while occluding the opposite eye with the hand. A nystagmus can be seen as alternating slow and quick movements of the optic disk. When doing this, it is important to remember that the apparent direction of nystagmus is reversed. This is because the optic disk is at the posterior pole of the eye. Thus, a right-beating movement of the optic disk is really a left-beating nystagmus. A spontaneous nystagmus that is easily seen in the light is more often a sign of central disease. Other features indicating a central lesion are a purely vertical (e.g., downbeat) nystagmus and a direction-changing (gaze-evoked) nystagmus.
Often more helpful in identifying a vestibular deficit are tests of dynamic vestibular function, that is, of the VOR. The most important of these is the head thrust test. The patient is asked to fixate a target (usually the examiner's nose) during rapid, low-amplitude, horizontal rotations of the head. If the VOR is working normally, gaze will remain stable and the patient will still be looking at the examiner at the end of the rotation. If the function of one or both labyrinths is impaired, rotation toward the affected ear(s) will fail to produce a normal excitatory stimulus, leading to a deficient VOR. The eyes will move with the head, and after the rotation, there will be a corrective rapid eye movement (saccade) to bring the eyes back to the point of original fixation. For example, in the case of a right
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vestibular lesion, when the head is turned to the left, the response will be normal and the eyes will remain stable in space. However, when the head is turned to the right, the eyes will move to the right with the head and a leftward corrective saccade will be seen. The head thrust test is the best bedside test to identify a peripheral vestibular lesion.
Another useful test of the VOR is dynamic visual acuity (2). This is based on the fact that a normal compensatory VOR is required to maintain clear vision when the head is moving. Thus, patients with an impaired VOR (particularly if bilateral as with bilateral vestibular injury) will have reduced visual acuity during head movement. To test dynamic acuity, first determine the patient's baseline visual acuity, using an eye chart or near vision card with appropriate correction (including reading glasses, if the near card is used). This is compared with the best acuity when the head is rotated back and forth (by the examiner) at a frequency of about once per second. A loss of more than one line of acuity is abnormal.
Patients with recurrent episodes of vertigo should undergo Dix-Hallpike positional testing to look for evidence of BPPV. This is discussed below in the section on BPPV and Figure 89.1.
Formal Vestibular Testing
Several ancillary tests are helpful in the evaluation of patients who are referred for problematic vestibular disorders. Formal audiometry is used to identify evidence of hearing loss, particularly asymmetric (see Chapter 110). Electronystagmography consists of a battery of tests of eye movements and vestibular function. The electronystagmography typically includes a recording in the dark to look for spontaneous nystagmus, recordings of saccades and smooth pursuit, recordings of positional nystagmus, Dix-Hallpike testing, and caloric testing. Caloric testing measures the nystagmus generated when one of the external ear canals is irrigated with warm or cold water (or air). Warm water provides an excitatory stimulus to the horizontal canal of the irrigated ear, and cold water provides an inhibitory stimulus. A comparison of responses to irrigation of each ear is used to determine if there is a relative reduction of vestibular function on one side.
Rotatory chair testing uses the natural vestibular stimulus (head rotation) to test the functions of the labyrinths and VOR pathways. The patient is seated in a chair that is rotated in the dark, either at constant velocity or sinusoidally. Unlike caloric testing, rotational testing does not stimulate each labyrinth independently: Rotation in each direction affects both sides, exciting one and inhibiting the other simultaneously. Thus, it is more difficult to identify and localize a unilateral lesion using rotational testing. However, rotational testing is of particular benefit in identifying bilateral vestibular loss.
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TABLE 89.2 Causes of Vertigo According to Temporal Pattern |
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Disorders Causing Vertigo
Table 89.2 lists common causes of vertigo and they are also discussed in this section. Causes are categorized according to the temporal pattern that emerges when the patient gives the history: acute-onset prolonged vertigo, or recurrent vertigo.
Acute Prolonged (Hours to Days) Vertigo
A single episode of prolonged (hours to days) vertigo may be because of either a peripheral or a central lesion. The primary questions to be answered are whether the lesion is in the vestibular periphery or in the brain and whether it is a stroke. It is important to remember that a peripheral lesion can be a stroke.
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The symptoms of an acute unilateral vestibular lesion are severe vertigo (from the sudden imbalance of tonic vestibular input), nausea, and vomiting. Some patients will also have a loss of hearing in the affected ear, if the cochlea or auditory nerve is affected. Patients prefer to lie still with the eyes closed, because any head movement makes the symptoms worse. They will have difficulty walking, and on Romberg testing they may fall toward the affected side.
Vestibular neuritis is a common cause of acute unilateral vestibulopathy. When hearing loss is present, the term labyrinthitis is often used, although the exact localization is not always certain. The hearing loss is sensorineural, not conductive (see Chapter 110). Vestibular neuritis is generally thought to result from a viral infection of the labyrinth or vestibular nerve or a postinfectious inflammatory process. Bacterial labyrinthitis is rarer but may be a complication of mastoiditis or bacterial meningitis.
The acute severe symptoms of vestibular neuritis usually subside over the first several days with gradual continued improvement over the next several weeks to months, as the brain compensates for the peripheral lesion. If compensation is incomplete, there may be a lingering (usually mild) imbalance that never fully recovers. Once the acute stage has passed, examination findings may be minimal, with no spontaneous nystagmus in the light. The most consistent finding is a head thrust sign when the head is rotated toward the affected side (seePhysical Examination). A reduced caloric response confirms the unilateral pathology.
A labyrinthine infarct may be difficult to distinguish clinically from labyrinthitis. Thus, older individuals, particularly those with vascular risk factors, should be evaluated for cerebrovascular disease (CVD) affecting the posterior circulation (see Chapter 91). The main concern is that a patient with vertebrobasilar disease could go on to have a second, and potentially more life-threatening, infarct in the brainstem or cerebellum. Other important diagnoses to consider are otosyphilis, vasculitis, and autoimmune inner ear disease, either isolated or as part of a systemic autoimmune process. Thus, patients should have serologic testing for syphilis (rapid plasma reagent [RPR]/fluorescent treponemal antibody [FTA]; see Chapter 37), sedimentation rate, and specific tests for connective tissue disease or vasculitis, when suspected.
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TABLE 89.3 Drugs for Symptomatic Treatment of Vertigo |
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Symptoms that should raise suspicion of a central (brainstem or cerebellar) lesion include double vision, facial or limb numbness or weakness, slurred speech, and limb incoordination. A direction changing (gaze-evoked) or vertical (e.g., downbeat) nystagmus indicates central disease, as generally do other cranial nerve or cerebellar signs. Infarction in the territory of the anterior inferior cerebellar artery may produce a combination of both central and peripheral signs (3). A cerebellar or brainstem stroke is a medical emergency.
Some patients with peripheral disease will have ipsilateral facial weakness when there is a combined lesion of cranial nerves VII and VIII. In these cases, the facial weakness should have a peripheral pattern (the forehead is not spared). Ramsey-Hunt syndrome is a reactivation of herpes zoster virus that produces facial paresis, hearing loss, vertigo, and ear pain, with vesicular lesions in the external auditory canal. Early treatment with acyclovir is important.
Although many individuals improve spontaneously from vestibular neuritis, if the patient is seen within the first 3 days after onset, a course of oral steroids may further facilitate recovery (4). Otherwise, treatment of acute peripheral vertigo is largely aimed at explaining the cause and likely course to the patient and ameliorating the symptoms. Vestibular suppressants include antihistamines (e.g., promethazine, meclizine) and benzodiazepines (e.g., diazepam, lorazepam, or clonazepam). Table 89.3 summarizes practical information about these drugs. These should be used only in the acute stage (the first several days), when vertigo is severe, because they may impede the process of central vestibular compensation. Antiemetics may be helpful when nausea and vomiting are present. Ondansetron may have fewer side effects than antidopaminergic agents (e.g., prochlorperazine, chlorpromazine, metoclopramide). Patients should be encouraged to resume activity when possible, because this may facilitate the compensation process. For patients with troublesome persistent symptoms, formal vestibular rehabilitation therapy may also help recovery.
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TABLE 89.4 Characteristic Features of Benign Paroxysmal Positional Vertigo |
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Recurrent Vertigo
Recurrent attacks of vertigo can be distinguished by several features, including their duration, provoking factors, and associated symptoms. There are many underlying etiologies (Table 89.2); some common causes include BPPV, migraine, and TIAs.
Benign Paroxysmal Positional Vertigo
BPPV is a common cause of episodic vertigo. It consists of brief attacks of vertigo, provoked by changes in head position relative to gravity.Table 89.4 lists the typical features of BPPV.
BPPV results from the accumulation of otoconial debris in one of the semicircular canals. Otoconia are particles consisting of calcium carbonate crystals that are normally adherent to the membrane of the utricle (see Basic Principles of Vestibular Function). If these particles are dispersed, either spontaneously or by trauma or inner ear injury, they may coalesce into a small clot and become free floating in the endolymph fluid. This clot of particles may fall into one of the semicircular canals, most commonly the posterior canal, because of its orientation. Then, when the head moves, this clot may move within the canal, causing pressure changes in the endolymph and deflecting the cupula. This leads to excitation of the canal, as if the head were rotating.
BPPV is diagnosed by the Dix-Hallpike positioning maneuver, illustrated in Figure 89.1. The head is first turned 45 degrees to one side. This will place the posterior canal on that side in the plane of rotation. Then, the subject is brought quickly from a sitting to a head-hanging position. A patient with BPPV will describe vertigo when the affected ear is stimulated by bringing the patient to the lying position with the head turned to that side. While supporting the head, the examiner watches the eyes for any nystagmus to indicate excitation of the posterior canal. The expected nystagmus has both vertical and torsional (rotatory) components: The eyes beat upward and the upper poles of the eyes beat toward the affected (down) ear (Fig. 89.2). There is usually a latency of several seconds from the initial positioning
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until the vertigo and nystagmus begin, and the duration is less than 1 minute (commonly about 15 to 30 seconds). It is important to keep in mind that not all positional vertigo and nystagmus is because of BPPV. For example, patients with cerebellar disease or craniocervical junction abnormalities (e.g., Chiari malformation) may have positional nystagmus. In these cases, the nystagmus is usually sustained rather than transient.
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FIGURE 89.1. Dix-Hallpike maneuver for testing a patient for positional vertigo and nystagmus. |
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FIGURE 89.2. Pathognomonic nystagmus of benign paroxysmal positional vertigo. The pathognomonic nystagmus consists of quick phases directed upward (with respect to the head) and torsionally toward the abnormal ear. In this example, the torsional element is counterclockwise toward the abnormal right ear. |
Treatment of BPPV consists of the canalith repositioning (Epley) procedure shown in Figure 89.3, which begins with the Dix-Hallpike maneuver, with the head turned to the affected ear (5). The purpose of the maneuver is to relocate the free-floating particles to the utricle. The four-step maneuver is repeated until no nystagmus is observed. This approach to treating BPPV is effective after one session in most patients (6). Contraindications to the Epley maneuver are severe disease of the neck and high-grade carotid artery stenosis. In refractory or recurrent cases, patients can be taught to perform a modification of the maneuver at home, in which the head rests on the bed but with pillows under the shoulders to simulate a head-hanging position (7). Brandt-Daroff physical therapy exercises may also be helpful (8). Making the diagnosis of BPPV quickly and accurately is important, because of the effectiveness of treatment and to avoid an unnecessary and expensive diagnostic workup for other causes (e.g., TIAs). Because BPPV may be a complication of labyrinthine injury, it may coexist with other inner ear diseases (9). Vestibular suppressant drugs (Table 89.3) may reduce the intensity of a patient's symptoms, but they do not reduce the frequency of attacks.
Vestibular Migraine
Migraine is another common cause of recurrent dizziness (10). Patients with migraine may have a variety of symptoms that include both discrete attacks of vertigo and prolonged episodes of disequilibrium and motion sensitivity. Migrainous vertigo typically lasts minutes to hours. It may occur as an aura, preceding headache, or it may be present simultaneously with headache. In many cases, headache and vertigo occur independently, and occasional patients thought to have vestibular migraine only rarely have headache. Thus, the absence of headache does not rule out migraine as a cause of dizziness, although it should raise suspicion for other causes. Only a small fraction of patients with migrainous vertigo meet criteria for basilar migraine; in these patients, vertigo occurs as part of the aura, and there must be at least one other posterior circulation symptom.
The treatment of vestibular migraine is similar to that of migraine headaches. Patients with rare episodes can be given antiemetics and vestibular suppressants (Table 89.4) to be taken at the time of an attack. Patients with chronic refractory migraine are more likely to have comorbid
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psychiatric disease, including affective and anxiety disorders (see Nonspecific Dizziness) (11). These are very important to recognize and must also be addressed in the treatment plan. Chapter 87 provides a detailed account of migraine management.
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FIGURE 89.3. Bedside maneuver for the treatment of a patient with benign paroxysmal positional vertigo affecting the right ear (Epley maneuver). The presumed position of the debris within the labyrinth during the maneuver is shown in each panel. The maneuver is a four-step procedure. First, a Dix-Hallpike test is performed with the patient's head rotated 45 degrees toward the right ear and the neck slightly extended with the chin pointed slightly upward. This position results in the patient's head hanging to the right (A). Once the vertigo and nystagmus provoked by the Dix-Hallpike test cease, the patient's head is rotated about the rostral-caudal body axis until the left ear is down (B). Then the head and body are further rotated until the head is face down (C). The vertex of the head is kept tilted downward throughout the rotation. The maneuver usually provokes brief vertigo. The patient should be kept in the final face-down position for about 10 to 16 seconds. With the head kept turned toward the left shoulder, the patient is brought into the seated position(D). Once the patient is upright, the head is titled so that the chin is pointed slightly downward. (From Furman JM, Cass SP. Benign paroxysmal positional vertigo. N Engl J Med 1999;341:1590, with permission .) |
Ménière Disease (Endolymphatic Hydrops)
The classic presentation of Ménière disease (see also Chapter 110) is recurrent attacks of vertigo, nausea, and vomiting; a transient decrease in hearing in the affected ear; ear pain, pressure, and/or fullness; and tinnitus, usually low pitched and described as “roaring” or “rushing.” Less commonly, patients may also have drop attacks, in which they feel suddenly thrown to the ground. These are called otolithic crises of Tumarkin. The pathophysiology of Ménière disease is thought to be increased endolymph pressure within the labyrinth (hence the name, endolymphatic hydrops).
The differential diagnosis of Ménière disease includes a variety of inflammatory and infectious causes, such as otosyphilis, Lyme disease, connective tissue diseases, and autoimmune inner ear disease. Thus, all patients suspected of having Ménière disease should have serologic testing for these disorders. Sometimes it is also difficult to distinguish Ménière disease from vestibular migraine, especially if auditory symptoms are less prominent. The two diagnoses may also coexist in the same patient (12).
If possible, patients suspected of having Ménière disease should have an audiogram at the time of an attack. The classic finding is a predominantly low-frequency hearing loss in the affected ear that may improve when the attack resolves. The finding of a fluctuating low-frequency hearing loss on serial audiograms is helpful in making the diagnosis.
Treatment of Ménière disease includes sodium restriction (1 g/day) and diuretics (e.g., acetazolamide, hydrochlorthiazide/triamterene). In cases refractory to diuretics, intratympanic steroid or gentamicin injections may be helpful. The goal of gentamicin therapy is to ablate vestibular function partially to eliminate attacks of vertigo with minimal effects on balance. Surgical ablation (labyrinthectomy or vestibular nerve section) is reserved only for the most severe cases, after all other treatments have failed.
Transient Ischemic Attacks
Vertigo may be a symptom of TIAs involving the posterior circulation. Vertigo because of TIAs usually lasts for minutes. Repeated episodes of vertigo on an ischemic basis are unusual in the absence of other posterior circulation symptoms, such as visual field disturbances, double vision, slurred speech, or facial or limb weakness or numbness. However, occasional patients will have isolated vertigo (13). Patients suspected of having TIAs should be evaluated as described in Chapter 91.
Perilymph Fistula
A perilymph fistula is a relatively uncommon cause of recurrent vertigo and is sometimes difficult to diagnose (14). However, it is helpful to keep in mind because it may be amenable to surgical treatment. It results from a defect in the bony labyrinth or the round or oval window, creating a communication between the inner ear and either the middle ear or the intracranial space. Causes include barotrauma, erosion by a tumor (e.g., cholesteatoma), or head trauma. Vertigo is provoked by loud noises, tragal pressure, or Valsalva, with transmission of middle ear or intracranial pressure into the labyrinth through the communicating defect. Surgical exploration and repair may be necessary. Again, this is an uncommon cause of vertigo, but if a patient presents with the above history it is prudent to refer to an otolaryngologist for further evaluation.
Bilateral Loss of Vestibular Function
Patients with bilateral loss of vestibular function have a feeling of imbalance when standing or walking. They do not have dizziness at rest, although they may have a sense of instability or oscillopsia when turning the head quickly. Because several components of the peripheral and central systems are involved in the maintenance of posture and balance, there are many causes of disequilibrium in addition to vestibular disease (see Disequilibrium). Thus, patients with disequilibrium require a thorough neurologic and vestibular examination looking for signs of parkinsonism (e.g., cogwheel rigidity, tremor), myelopathy (spasticity in the legs, increased reflexes), cerebellar disease (limb ataxia, slurred speech, cerebellar eye signs), or neuropathy (loss of vibration sense and proprioception). The diagnosis of bilateral vestibular loss may be missed if vestibular function is not explicitly tested, because there may be few other signs other than gait ataxia, a Romberg sign, and an abnormal VOR.
The chief symptoms of bilateral vestibular loss are imbalance and oscillopsia with head movement (such as when walking or riding in a car, particularly on a bumpy road). These are due to the loss of the vestibulospinal reflex and VOR, respectively. Patients do not have vertigo because the lesion is symmetric, yielding no net imbalance in the inputs from the two labyrinths. Typical findings on examination include a marked loss of dynamic visual acuity (see Physical Examination), bilateral head thrust signs, and a Romberg sign. Reduced rotatory chair responses confirm the diagnosis. The degree of disability depends both on the severity of vestibular loss and the extent of compensation. Some younger patients who are otherwise healthy may compensate well, with limited disability.
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Others, particularly those with superimposed neuropathy (causing proprioceptive loss) or poor vision, may be left with more substantial disability.
The most common identified cause of bilateral vestibular loss is ototoxic drugs, such as aminoglycosides and cisplatin (15). Gentamicin ototoxicity may occur even in the absence of “toxic” levels. If recognized early, stopping the drug may theoretically limit the damage and allow for some recovery of function. In many cases, however, the vestibular loss is not discovered until the course of treatment has been completed. Early symptoms of disequilibrium may be attributed to a general weakness arising from the patient's underlying systemic illness. Only after recovery from the acute illness, when the patient is more active, is the true balance impairment noted. For this reason, it is important to monitor vestibular function during gentamicin treatment, when possible. This can be done by measuring dynamic acuity with a near card, looking for head thrust signs, and checking for a Romberg sign, if the patient can stand. Because gentamicin is much more toxic to the vestibular organs than to the cochlea, assessing hearing is not a good way to detect ototoxicity. In fact, patients may have little or no change in hearing even with profound loss of vestibular function.
Many cases of bilateral vestibular loss are idiopathic. Other causes include hereditary vestibular loss (16), bilateral sequential vestibular neuritis, combined cerebellar and vestibular degeneration, autoimmune disease, meningitis, sarcoidosis, metabolic disease (e.g., vitamin B12deficiency), bilateral vestibular nerve tumors (e.g., schwannomas), and bilateral Ménière disease (17).
Motion Sickness
Motion sickness is a feeling of nausea and dizziness evoked by excessive or prolonged vestibular or optokinetic stimulation (18). Other symptoms include diaphoresis, yawning, light-headedness, and malaise. Susceptibility to motion sickness varies among individuals; migraineurs are particularly motion sensitive. Most individuals adapt to continued motion (e.g., cruise), although some remain persistently motion sick. Individuals with bilateral vestibular paresis are insensitive to motion.
Several medications may assist in the prevention or reduction of motion sickness, when used occasionally during exposure to a provocative stimulus. Antihistamines such as meclizine (25 to 50 mg), dimenhydrinate (50 to 100 mg), or promethazine (25 mg) may be taken orally about 1 hour before travel. The major adverse effect is sedation, most prominently with promethazine. Transdermal scopolamine is an anticholinergic agent that is effective in preventing motion sickness. The 1.5-mg patch is designed to deliver 0.5 mg of scopolamine over 3 days. It should be applied at least 4 hours before travel. Adverse effects include dry mouth and sedation. Older individuals may be more sensitive to central nervous anticholinergic effects such as confusion and hallucinations. Occasionally, withdrawal symptoms occur, particularly after prolonged use.
After prolonged exposure to motion, such as returning to land after a cruise, many individuals have a feeling of continued motion (“landsickness”) that usually resolves within 1 to 2 days. However, in some individuals these symptoms persist for months to years. This has been termed mal de debarquement syndrome (19). Typical features are a constant feeling of rocking or swaying when still. In contrast to motion sickness, these individuals feel best when moving and worse when motion stops. Mal de debarquement syndrome has been reported much more commonly in women, usually in their 40s. A history of migraine or other headaches is common.
Syncope and Near Syncope
Definitions and Pathophysiology
Syncope is “a sudden and brief loss of consciousness associated with a loss of postural tone, from which recovery is spontaneous” (20). Syncope typically lasts from seconds to minutes; longer episodes are classified as stupor or coma. Unconsciousness implies that both cerebral hemispheres have become impaired or that certain critical structures in the brainstem have failed. Generally, unilateral diseases of the cerebral hemispheres do not lead to unconsciousness (and therefore syncope) unless the brain becomes more generally affected. It is important to note that syncope is a symptom and not a disease.
There are three major pathophysiologic mechanisms of syncope (21):
Syncope must be differentiated from other disorders that may, on initial history taking, sound similar to syncope. Many types of “spells” are not syncope; a spell is “a sudden onset of a symptom or symptoms that are recurrent,
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self-limited, and stereotypic in nature” (22). Such spells are not necessarily syncope and may be caused by endocrine, cardiovascular, psychologic, pharmacologic, neurologic, or other miscellaneous disorders. Carcinoid syndrome and pheochromocytoma are classic examples of disorders in which patients describe spells that are distinct from syncope.
Presyncope, or near syncope, is the sense of imminent loss of consciousness without frank syncope. It may be a prelude to true syncope or it may be related to a spell or to unexplained dizziness.
Incidence and Mortality
In a large epidemiologic study using the Framingham cohort following 7,814 patients for 17 years, a total of 822 patients experienced syncope. The 10-year cumulative incidence was 6%. There was a sharp increase in incidence of syncope in patients over 70 years of age (23). Syncope accounts for 3% to 5% of all emergency room visits and 1% of all admissions (24); however, in the Framingham study only 56% of participants who experienced a syncopal episode sought medical attention (23).
Morbidity and mortality in patients with syncope differ according to the underlying cause of the syncopal event. Studies of patients with syncope report a 1-year mortality of 18% to 33% for patients with a cardiovascular cause of syncope, 0% to 12% for patients with a known noncardiovascular cause, and 6% for patients with an unknown cause of syncope (25). The higher mortality of patients with a cardiovascular cause of syncope appears to be because of the underlying cardiovascular disease, and not the cardiac syncope per se. Four factors, available at the time of presentation, have been shown to predict cardiac arrhythmias or death in the year after presentation with syncope: (a) age older than 45 years, (b) a history of heart failure, (c) a history of ventricular arrhythmias, and (d) an abnormal electrocardiogram. Arrhythmias or death occurred in 4.4% of patients with without any of these factors, and in 58% of patients with three or four risk factors (26).
Syncope also causes significant morbidity. Up to 35% of patients who experience a syncopal episode suffer an injury as a result. Additionally, patients who experience recurrent episodes of syncope can suffer severe functional impairment comparable to other chronic diseases (24).
Differential Diagnosis
The differential diagnosis of disorders presenting as syncope is broad. Table 89.5 lists causes, classified as hypotension, cardiac disease, metabolic conditions, intracranial conditions, or psychiatric disorders. Neurocardiogenic (or reflex-mediated) syncope is thought to be the most common cause of syncope, especially if there is no evidence of a cardiovascular cause. Neurocardiogenic syncope may account for up to 40% of all syncopal events evaluated in the ambulatory setting. The list of medications that may cause syncope continues to expand. Any patient with dizziness or syncope should have all medications, including over-the-counter (OTC) medications, reviewed in light of the patient's presenting complaint. Polypharmacy is a particularly common cause of syncope in the elderly. Depending on the diagnostic criteria used, an underlying cause will not be found for approximately 39% of patients evaluated for syncope, although more recent algorithms have reported lower percentages of unexplained syncope at 14% to 17% (27,28,29).
In a classic prospective evaluation of 204 patients presenting with syncope, 25% had the cause diagnosed on the basis of the history and physical examination. In this study population, in which approximately 50% of patients eventually received a diagnosis, the importance of the history and physical examination was well illustrated. Table 89.6 lists the diagnostic studies (including history and physical) that demonstrated the cause in patients for whom a cause was identified. This study was done before the widespread use of tilt-table testing (see Tilt-Table Testing); recent studies suggest that tilt-table testing will demonstrate neurocardiogenic syncope in one half to two thirds of patients with undiagnosed syncope (20).
Syncope from Hypotension or Circulatory Failure
Because of autoregulation, cerebral blood flow is protected over a wide range of systemic blood pressure. In normal people, a critical decrease in central nervous system (CNS) blood flow (producing near syncope or syncope) does not occur until the mean blood pressure is below 50 mm Hg. Under a number of circumstances (e.g., sympatholytic drug treatment, CVD), however, the minimal tolerated blood pressure may not be this low. Thus, symptomatic failure of the systemic circulation may occur over a wide range of blood pressures.
Neurocardiogenic (Reflex-Mediated, Vasovagal, Vasodepressor, or the Simple Faint) Syncope
Neurocardiogenic syncope has long been known to afflict young people; it is apt to occur in the setting of anxiety, fatigue, or pain and especially during venipuncture or other painful procedures. Additionally, the act of urinating (micturition syncope) and coughing (tussive syncope) can induce symptoms indistinguishable from neurocardiogenic syncope, though some believe that the underlying pathophysiology may be slightly different. Neurocardiogenic syncope is not just a disease of the young but can occur in older patients in identical settings. Episodes are believed
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to be triggered when venous pooling or catecholamine release leads to increased ventricular contractions and activation of cardiac mechanoreceptors; this causes a reflex increase in parasympathetic and decrease in sympathetic nervous system activity, resulting in symptomatic bradycardia or hypotension, termed the Bezold-Jarisch reflex. Neurocardiogenic syncope nearly always occurs while the patient is upright, but it may occur while seated; consciousness is nearly always regained promptly when the patient lies down. Typically, there is a prodromal warning period, lasting up to 5 minutes, when the patient feels dizzy or flushed, with mild nausea and occasionally palpitations or throat tightness. If the subject lies down during this stage, loss of consciousness may be avoided. An observer will note cold hands, pale skin, and tachycardia just before the patient loses consciousness. A prodrome may be absent in up to 30% of patients (particularly in the elderly), so its absence does not exclude the diagnosis of neurocardiogenic syncope. Additionally, sudden loss of consciousness does not exclude the diagnosis of neurocardiogenic syncope in any patient. After the faint, a flush replaces the pallor. If the patient is unable to lie flat, recovery may be prolonged; an occasional death has been noted if the person is held upright during the spell. Confusion can persist for up to 10 minutes particularly in elderly patients, and bradycardia may persist for up to 30 minutes after neurocardiogenic syncope. During this time the patient should remain lying down. The examination is otherwise normal unless there has been trauma or aspiration.
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TABLE 89.5 Differential Diagnosis of Syncope/Near Syncope |
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Neurocardiogenic syncope is often selected as a diagnosis of exclusion because the history and physical examination are often nondiagnostic. As noted above (see Differential Diagnosis), standardized tilt-table testing can be used to confirm susceptibility to neurocardiogenic
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syncope in patients for whom this information is needed to make a clinical decision.
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TABLE 89.6 Diagnostic Studies that Demonstrated the Cause of Syncope in 107 of 204 Patients in Whom Exhaustive Study Established a Cause |
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In the treatment of neurocardiogenic syncope, education plays an important role. Merely lying down when a prodrome develops may abort a syncopal event. There is recent evidence that crossing one's arms or legs tightly during the prodrome of an event can reduce the likelihood of syncope as well (30). Increasing salt intake may also prevent recurrence. A high-salt diet with liberal fluid intake is commonly suggested, occasionally with the addition of compression stockings. Pharmacologic agents, including disopyramide, theophylline, angiotension-converting enzyme (ACE) inhibitors, fludrocortisone, a-agonists, β-blockers, and selective serotonin reuptake inhibitors (SSRIs), have all been used to treat neurocardiogenic syncope. The best studied class of drugs is β-blockers (atenolol 50 mg daily or metoprolol 50 mg twice a day) (31,32). Despite concerns about worsening bradycardia with the addition of β-blockers, these drugs have been well tolerated when used to treat patients with neurocardiogenic syncope. In one study, β-blocker treatment prevented recurrent syncope in 90% of patients for 2 years or longer (33). However, there is also data that shows no benefit from β-blockers. Part of the difficulty in studying drug effects in neurocardiogenic syncope is that there is a very high placebo response rate in this condition (33). Paroxetine (20 mg daily) is also well tolerated in patients with vasodepressor syncope and, in one small controlled study, decreased the recurrence of syncope over 25 months of treatment as compared with those receiving placebo by two-thirds (34). For patients with vasodepressor syncope and significant bradycardia, cardiac pacing showed promise in a preliminary study, however several subsequent studies did not show benefit (35, 36, 37,38, 39). The role of cardiac pacing in neurocardiogenic syncope remains controversial, but it can be considered in patients when their syncope appears to be due predominantly to a cardioinhibitory response and in whom other noninvasive therapies have failed. Even if pacing does not prevent syncopal episodes, it may delay the time from onset of prodromal symptoms to the actual syncope and therefore may provide more time to take evasive action (40).
Carotid Sinus Hypersensitivity
Hypersensitivity of the carotid sinus is common in older men with coronary artery disease (CAD) or hypertension and may be exacerbated by tight collars, cumbersome necklaces, head turning, shaving, or large neck masses; however, this is an uncommon cause of syncope. Syncope may result when stimulation of the baroreceptors in the carotid sinus leads to an increase in vagal activity with resulting bradycardia or may lead to sympathetic relaxation with resulting hypotension. If carotid sinus syncope is suspected, one should consider performing a carotid massage (see Carotid Massage). Patients diagnosed as having carotid sinus syncope should be referred to a cardiologist for consideration of pharmacologic treatment or pacemaker insertion, if the symptoms are recurrent or severe.
Orthostatic Hypotension
There are many causes of orthostatic hypotension that can contribute to syncope. Medications are the most common cause, although autonomic impairment, volume depletion, venous pooling, as well as changes with aging or bedrest can be causes.
Medications
The most common cause of this problem is antihypertensive drug use; most syncope caused by these drugs is preventable if the drugs are prescribed cautiously and the standing blood pressure, after exercise, is monitored routinely. Other drugs may also produce orthostatic hypotension (Table 89.5). The management of drug-induced orthostasis requires discontinuation or reduced dosage of the drug.
Autonomic Impairment
Syncope/near syncope caused by autonomic impairment is always associated with orthostatic hypotension. To document this problem, blood pressure must be taken while the patient is supine and again while standing. In some patients, exercise while standing (e.g., walking for a few minutes) may be required for a significant orthostatic drop (20 mm Hg systolic) to occur.
Orthostatic hypotension can also be caused by autonomic neuropathy. In patients suspected of having this problem, the integrity of the autonomic nervous system can be assessed by noting the size and reaction of the
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pupils, the distribution of sweating, and asking about symptoms of gastrointestinal dysmotility. Sympathetic failure commonly occurs late in diabetic peripheral neuropathy (see Chapter 79) and may be the presenting feature of amyloidosis or the neuropathy associated with various neoplasms.
Multiple system atrophy (sometimes known as Shy-Drager syndrome), which occurs in late life, is caused by failure of central autonomic neurons and causes orthostatic hypotension, parkinsonism, cerebellar ataxia, and other autonomic symptoms in varying combinations. Sympathectomy, particularly when done bilaterally or in the lumbar segments, may be followed immediately by orthostatic hypotension and syncope, although usually venous tone recovers several weeks after the operation. Tabes dorsalis and more commonly diabetic pseudotabes may present with lightning pains and autonomic failure. Chapter 92 summarizes the management of orthostasis caused by autonomic neuropathy, which is symptomatic.
Decreased Intravascular Volume
Decreased intravascular volume caused by hemorrhage or volume loss (e.g., from gastroenteritis, heat exposure, or diuretics) is recognized by the combination of orthostatic hypotension and an associated basis for the volume deficit. Volume expansion, either by increased salt and water ingestion or by intravenous fluids, is the initial treatment.
Venous Pooling
Venous pooling prevents return of blood to the heart, lowering cardiac output, at times sufficiently to produce near syncope or syncope. Symptoms may occur after prolonged standing in one position, particularly after exercise, as in recruits standing at attention. Severe dependent varicose veins or the compression of pelvic veins by a fetus or a large abdominal mass may produce symptoms through a similar mechanism. Syncope 15 to 30 minutes after exercise has been attributed to dilation of the splanchnic circulation before blood flow to the skeletal muscles has completely returned to normal. Management of these conditions involves chiefly avoidance of the precipitating factors. Supportive elastic stockings may be helpful for patients with marked pooling in varicose veins (see Chapter 95).
Orthostatic Syncope/Near Syncope after Bed Rest
This problem is caused by the combined effects of venous pooling, relative hypovolemia, and probably to some degree lowered sensitivity of the baroreceptor system. It is very common at all ages but is especially common among the elderly and should be anticipated in any person who has been at bed rest for more than a few days; moreover, it may persist for 1 or 2 weeks or longer after mobilization begins. Orthostatic symptoms may be minimized or prevented by having the patient gradually stand only after several minutes of sitting on the bed with the legs dependent. Figure 89.4 illustrates practical exercises that may help convalescing or deconditioned patients in overcoming postural weakness and hypotension. These patients should be encouraged to be out of bed for at least 2 hours a day, including morning, afternoon, and evening.
Orthostasis of Aging
Transient orthostatic dizziness and hypotension occur in many healthy older people. A significant fall in systolic blood pressure also is common in elderly patients immediately after eating, even in a seated position, which may make them especially susceptible to syncope when standing up after a meal. The physiologic basis for orthostatic symptoms in the elderly is often multifactorial and may be related not only to postural hypotension but also cerebral ischemia, vestibular dysfunction, visual impairment, and abnormal proprioception. The orthostasis of aging is important because it increases the risk associated with drugs that may cause orthostatic hypotension. Clearly, older patients should have their standing blood pressure checked whenever they complain of even mild orthostatic symptoms, and they should be monitored similarly whenever a drug in one of the groups listed in Table 89.5 is prescribed. Those who are troubled by orthostatic symptoms should be advised to follow the steps recommended above for patients rising after bed rest. Dizziness in the elderly is commonly multifactorial and should prompt consideration of a combination of cardiovascular, neurologic, sensory, pharmacologic, and psychologic causes (41). Mineralocorticoid agents can be used to assist in volume expansion, but patients must be monitored for volume overload, hypokalemia, and peripheral edema. Unfortunately, elderly patients are often unable to tolerate mineralocorticoid agents over a sustained period of time (42).
Other Forms of Syncope Related to Systemic Circulation
Pulmonary embolism may cause sudden loss of consciousness in up to 10% of cases. The diagnosis of pulmonary embolism is suggested by the presence of dyspnea, hypotension, tachycardia, or acute cor pulmonale by electrocardiogram (ECG) or physical examination (see Chapter 57).
Vertebrobasilar insufficiency, due to decreased blood flow to the posterior circulation of the brain, can lead to the sudden onset of loss of postural tone, termed “drop attacks,” although loss of consciousness is not necessarily seen. These attacks may also be associated with the abrupt onset of visual loss, diplopia, and dysarthria. Besides the typical history, the diagnosis should be suspected in patients with multiple risk factors for vascular disease.
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FIGURE 89.4. Exercise for weakness and orthostatic hypotension after prolonged bed rest. Patient must be out of bed 2 hours a day, morning, afternoon, and evening. Exercises are done three times a day. (Courtesy of Karen Ryder, Registered Occupational Therapist.) |
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Syncope from Cardiac Abnormalities
Rhythm Disturbances
Arrhythmias should always be considered in patients with syncope or near syncope that are older, have known heart disease, describe palpitations, or have syncope while seated or recumbent. Suspicion should also be raised in patients taking medications that may cause arrhythmias, including antiarrhythmics themselves (Table 89.5). Premonitory symptoms such as palpitations, grayouts, sweating, nausea, and fear may be recalled, but the presence or absence of these symptoms is not sufficient to confirm or refute the diagnosis of an arrhythmia. Most patients with cerebral symptoms of arrhythmias have normal resting ECGs. In general, at least 24 hours of ECG monitoring should be performed to identify potentially important arrhythmias in patients with syncope that is not explained by
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the initial history, physical examination, and 12-lead ECG (see above) and some should have electrophysiology (EP) testing (see Diagnostic Tests).
Outflow Obstruction
An obstruction to ventricular outflow caused by aortic stenosis may lead to syncope. It nearly always follows exertion and is often associated with chest pain. Unconsciousness may be prolonged and may be followed by neurologic abnormalities. Similarly, up to 30% of patients with hypertrophic cardiomyopathy experience syncope by outlet obstruction after exercise or by an arrhythmia (43). Chapter 65 describes the diagnostic approach to patients thought to have outflow obstruction. A left-atrial myxoma (rare) may cause syncope by obstruction of blood flow when a patient leans over or undergoes exertion. Cyanotic congenital heart disease also leads to syncope after exercise or, rarely, during an airplane flight. Hypoxia and increased blood viscosity are contributing factors.
Myocardial Infarction
Acute myocardial infarction (MI) may present with syncope, which may result from an arrhythmia, low cardiac output, or severe pain. However, overall, MI is a rare cause of syncope (44). Embolization from a mural thrombus should be considered when syncope occurs during recovery from MI.
Exercise-Induced Syncope
While exercise can be a trigger of neurocardiogenic syncope, syncope that is brought on with exercise suggests cardiac or vascular causes particularly in older patients. Aortic stenosis and hypertrophic cardiomyopathy may limit cardiac output in response to increased demand (e.g., exercise) leading to syncope. Ischemia-induced arrhythmias may also be unmasked by exercise. An echocardiogram followed by exercise tolerance testing is the appropriate evaluation of patients with exercise-induced syncope (45).
An uncommon cause of exercise-induced ischemia is subclavian steal. If the subclavian artery is occluded proximal to the origin of the vertebral artery, increased oxygen demand by the distal subclavian artery territory may result in retrograde blood flow (“steal”) from the vertebral artery to the subclavian artery. Exercise involving the arm is the typical activity that unmasks subclavian steal. Much more common on the left than on the right, subclavian steal should be associated with a decreased blood pressure on the affected side.
Syncope from Metabolic Abnormalities
The initial history and physical examination should seek to identify any symptoms or signs of metabolic derangement, especially because some derangements may lead to lasting damage.
Hypoglycemia
Loss of consciousness may occur in hypoglycemic adults, although rarely in older patients, when the blood glucose level is below 40 mg/100 mL. Hunger, palpitations, sweating, and anxiety nearly always occur 5 to 15 minutes before the patient loses consciousness. Because the brain can survive for only about 10 minutes with a blood glucose of 20 mg/100 mL or less, the prophylactic administration of glucose is warranted in anyone who remains unconscious long enough for the physician to prepare the solution. Convulsions and incontinence commonly accompany hypoglycemic coma. Chapter 79 describes the evaluation and management of hypoglycemia caused by exogenous insulin. Reactive hypoglycemia and fasting hypoglycemia (which may be caused by insulinoma) may produce near syncope but only rarely unconsciousness. Chapter 81 describes these problems.
Hypocapnia (Hyperventilation)
Hypocapnia caused by hyperventilation leads to syncope, near syncope, or ill-defined dizziness by decreasing cerebral blood flow through vasoconstriction of small arterioles throughout the brain. A PCO2 of 25 mm Hg is sufficient to lower cerebral blood flow to levels at which symptoms may occur; such a value may be produced in some people by a few very deep breaths. Athletes preparing to race, musicians playing wind instruments, or anyone who is fearful or anxious may develop transient symptoms in this way. Tetany or carpopedal spasm may or may not precede the cerebral symptoms. Recovery is prompt if ventilation is slowed. Chapter 22 describes the diagnosis and management of hyperventilation related to anxiety, the most common cause of this problem.
Hypoxemia
Hypoxemia caused by any primary cause may predispose to syncope/near syncope. Severe anemia (see Chapter 55) may sufficiently deprive the brain of oxygen to lead to syncope after exercise; it may also predispose to syncope from any other cause. Asphyxiation caused by obstruction of the upper airway should be considered in small children, patients with poor dentition, or patients with masses in the neck. Short-term exposure to moderate or high altitude, even in healthy young adults, may lead to syncope, possibly mediated by a decrease in arterial oxygen saturation.
Seizures are common in patients with acute hypoxemia, and neurologic sequelae are the rule after unconsciousness lasting more than 1 or 2 minutes. The management
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of hypoxemic syncope depends entirely on prompt and accurate diagnosis to prevent recurrence or worsening of the hypoxemia.
Drug Overdose
Overdose of some drugs may cause syncope/near syncope due to orthostatic hypotension. These drugs include sedatives, which may produce venous pooling (particularly chloral hydrate, paraldehyde, and ethanol and less often benzodiazepines and barbiturates), and all the drugs listed as potential causes of autonomic impairment in Table 89.5. However, overdose of most drugs is more likely to cause stupor or coma from their sedating effects than to cause syncope or near syncope from orthostatic hypotension.
Syncope from Intracranial Abnormalities
Seizure
Seizure as a cause of syncope is a diagnosis that is thought to be made easily from historical details. However, as noted above, brief clonic movements are seen in some patients who have syncope unrelated to seizure. In the prospective evaluation of patients presenting with syncope mentioned above, 50% of patients underwent electroencephalographic (EEG) testing, and this confirmed an underlying seizure disorder in only 1.5% (20). It has been demonstrated that the best discriminating finding distinguishing seizure from syncope was orientation immediately after the event, as reported by an eyewitness. A seizure was found to be five times more likely if the patient was reported to be disoriented after the event. In the absence of an eyewitness, the age of the patient was the most useful discriminator; a seizure was three times more likely if the patient was younger than 45 years. Incontinence and trauma were not discriminative findings (46). Chapter 88 describes the diagnosis and management of seizure disorders.
Subarachnoid Hemorrhage
A brief period of unconsciousness at the beginning of subarachnoid hemorrhage is very common. This diagnosis is strongly suggested when the constellation of severe headache, confusion, and neck stiffness follows shortly after a syncopal episode. Any patient who is confused and develops headache during initial evaluation should be admitted for observation and evaluation, even if meningismus has not yet developed.
Cerebral Embolism or Thrombosis
Cerebral embolism or thrombosis may cause brief (TIA) or prolonged (cerebrovascular accident) unconsciousness if the basilar artery is affected; however, more commonly, disease of the posterior circulation leads to loss of postural tone without loss of consciousness. Very rarely, a carotid occlusion may cause unconsciousness initially, even if the remaining vessels are patent. A carotid occlusion likewise may cause loss of consciousness if the contralateral carotid is already occluded. In this instance, the period of unconsciousness is usually prolonged and seizures may occur; neurologic symptoms and signs are nearly always present. Chapter 91 describes the diagnosis and management of CVD.
Migraine
Migraine (see Chapter 87) may produce syncope or near syncope by spasm of the basilar artery or of the posterior cerebral arteries. Syncope that occurs with migraine is more often caused by hyperventilation or a neurocardiogenic mechanism rather than by a central abnormality.
Increased Intracranial Pressure
Increased intracranial pressure, whether caused by a brain tumor, trauma, or an obstruction to the ventricular system, may result in syncope when a Valsalva maneuver is performed such as during straining at defecation or bending over. The hallmarks are pre-existing symptoms, papilledema, and neurologic signs.
General Approach to the Patient (47)
Most patients who come to a physician after an episode of syncope or near syncope do so after their symptoms have resolved. The history should be obtained both from the patient and from anyone who observed the episode. The inquiry should focus on the events immediately before and after the attack, associated problems that may have been present for days to weeks before the episode, and evidence of trauma, neurologic deficit, or aspiration complicating the current episode of syncope. The objectives of these initial steps are to reach a working diagnosis or decide what further evaluation and management is needed for the patient. However, the most important focus during the evaluation of the patient who presents with syncope is to determine if the patient has evidence of intrinsic heart disease (20). As discussed above, the presence of preexisting heart disease significantly increases the risk for a cardiogenic etiology for syncope, which carries a far worse prognosis than a noncardiogenic cause.
Appropriate management may range from reassurance (e.g., the patient with neurocardiogenic syncope), to volume expansion (e.g., the patient with a diarrheal illness), to hospital admission for observation, prompt diagnostic testing, and necessary treatment (e.g., the patient with a
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history suggesting life-threatening arrhythmias or the patient with a major fracture complicating syncope). Details regarding the critical features of many of the causes of syncope listed in Table 89.5 are discussed in the following section.
History
Current Episode
The patient should always be questioned about his or her situation and body position immediately before the attack. Many patients with a cardiac etiology for syncope have no prodromal symptoms. On the contrary, neurocardiogenic syncope is often preceded by autonomic symptoms (e.g., nausea, pallor, and diaphoresis). If there was psychologic stress (e.g., an argument or fear about a medical procedure), one should consider neurocardiogenic syncope. If exercise preceded the attack, both neurocardiogenic syncope and a number of primary cardiopulmonary abnormalities are possible (including aortic stenosis, hypertrophic cardiomyopathy, arrhythmia, and pulmonary hypertension). (See discussion above of exercise-induced syncope.) If syncope was associated with micturition, coughing, or defecation, the episode may have been caused by an associated Valsalva-induced decrease in venous return as an initiating mechanism for neurocardiogenic syncope.
Syncope from most causes does not occur unless the patient is in the upright position. If the attack occurred when the patient first stood up, orthostatic hypotension should be considered.
Syncope that occurs when the patient is seated or recumbent suggests hypoglycemia, carotid sinus hypersensitivity, cardiac arrhythmia, hyperventilation, seizure, or a psychiatric disorder.
The patient also should be asked whether consciousness was lost completely and whether a fall or any injury occurred. Although patients with many different causes of syncope may recall feelings of dizziness, heaviness of the limbs, or dimming of vision before loss of consciousness, other associated symptoms may suggest a diagnosis. Nausea is characteristic of neurocardiogenic syncope but may also occur with bradyarrhythmias, myocardial ischemia, and loss of intravascular volume. Palpitations may suggest an arrhythmia, whereas chest pain and diaphoresis suggest myocardial ischemia. Headache and characteristic visual changes suggest a migraine. Incontinence and tonic–clonic movements of the extremities suggest a seizure; a seizure may be the primary problem or may be secondary to another event, such as cerebral ischemia or cardiac arrhythmia (see Seizure).
Observations made by others who witnessed the period of unconsciousness. Particular attention should be paid to the duration of the spell, whether a convulsion occurred, the sequence of events, and how the patient seemed during the period of recovery. Generally, recovery of consciousness is swift when the cause is from decreased cerebral blood flow. If recovery of clear consciousness takes more than 5 minutes, one should suspect a seizure, hypoglycemia, or stroke.
History preceding the current episode should be sought. Information about the patient during the hours, days, or weeks preceding syncope/near syncope is often helpful in the differential diagnosis. In particular, one should determine the frequency of any previous episodes of syncope or near syncope, as the frequency of episodes influences decisions regarding the urgency of obtaining diagnostic studies. Frequent episodes without injury, especially if the syncope typically is preceded by nonspecific prodromal symptoms, should raise suspicion of a psychiatric disorder. A history of dizziness in addition to syncope is a marker for a greater prevalence of psychiatric disorders, although cardiac arrhythmias may have a similar presentation. Other circumstances surrounding previous episodes of dizziness or syncope may help develop a working diagnosis for the current episode of syncope. For example, a patient may report that previous episodes of dizziness or near syncope occurred after taking a new antihypertensive or psychotropic medication. A patient convalescing from recent illness may relate the symptoms to being up and around after bed rest.
A patient with known organic heart disease, especially a patient with depressed left ventricular function or a history of ischemic heart disease, is at high risk of syncope caused by an arrhythmia. Although uncommon, a family history of cardiomyopathy or arrhythmia (such as prolonged QT syndrome) should be sought while taking the history from the patient.
Physical Examination
General Examination
The physical examination should include a search for abnormalities that may confirm a diagnosis suggested in the history or may reveal an unexpected cause. As patients with organic heart disease may have life-threatening causes of syncope, the cardiovascular examination is particularly important in all patients who present for the evaluation of a syncopal event. The heart rate and blood pressure should be measured after the patient has been recumbent for a few minutes and again after standing for 1 to 2 minutes. Very different blood pressures in the two arms would raise the possibility of aortic dissection or subclavian steal. The strength and upstroke of the carotid pulses should be appraised, and any bruits should be noted. The pulse should be palpated for 1 to 2 minutes to look for irregularities. The heart should be examined for murmurs (particularly the murmurs of aortic stenosis and hypertrophic cardiomyopathy), clicks, or gallops. Abdominal examination may reveal a large bladder or signs of a visceral
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catastrophe. If orthostatic hypotension has been found, a rectal examination should be performed to check the stool for occult or gross blood.
Carotid Massage
For patients with episodes suggestive of carotid sinus hypersensitivity (see Carotid Sinus Hypersensitivity) or older patients with recurrent syncope and a nondiagnostic evaluation, carotid massage can be performed. However, it should be performed only if there are no carotid bruits and when there is intravenous access and electrocardiographic and blood pressure monitoring, with atropine at hand. Additionally, it should not be performed in patients with a history of TIA or stroke unless recent imaging has shown no carotid disease (48). When performed, carotid massage involves application of digital pressure over each carotid sinus separately, for up to 5 seconds. A resulting carotid asystole of more than 3 seconds or a systolic blood pressure drop of more than 50 mm Hg is considered abnormal.
Neurologic Examination
A brief examination of the major components of the nervous system (see Chapter 86) may reveal evidence of pre-existing neurologic disease or of an acute insult. One should note the patient's orientation, speech, memory (for general information and the episode itself), and judgment. The fundi may reveal microemboli (see Chapter 91, Fig. 91.1) or subhyaloid hemorrhages (a sign of subarachnoid hemorrhage). Involvement of the midbrain, pons, or medulla is suggested by nystagmus, ophthalmoplegia, and other abnormalities of the cranial nerves. Weakness, sensory abnormalities, and pathologic reflexes may indicate a lesion elsewhere in the CNS. Any neurologic abnormalities should raise the suspicion of CVD, intracranial mass, subarachnoid hemorrhage, seizure, or CNS infection. If trauma has occurred in the recent past or if a fall was sustained during the syncopal episode, subdural or epidural hemorrhage should be considered. A nonfocal neurologic examination makes an intracranial cause of syncope unlikely, whereas a focal neurologic examination should prompt imaging of the CNS.
Significance of Seizures and Neurologic Deficits
Seizure activity may occur after syncope with a variety of causes, including neurocardiogenic syncope, cardiac arrhythmias, hyperventilation, orthostatic hypotension, or venous pooling. This is not surprising because unconsciousness signifies a major disruption in normal brain function. A single tonic convulsion is the most common type of postsyncopal seizure; less often a focal seizure may occur. In these instances, the patient's evaluation should include routine tests for a seizure focus (see Chapter 88). However, it should be emphasized that the presence of seizure-like activity in association with a syncopal event does not diagnose a primary neurologic cause for syncope. It makes it more likely and should prompt further neurologic evaluation, but other etiologies for syncope need to be considered.
Minor neurologic signs, such as slight focal weakness, reflex asymmetries, or pathologic reflexes, may be found after syncope from any cause, particularly if the patient is examined immediately after recovering consciousness. Such findings rarely persist for more than a few minutes. If such signs persist, are more profound, or occur in a constellation that suggests a particular anatomic lesion, they warrant further pursuit. However, one should not be surprised if a source is not found because minor neurologic signs are not uncommon after general ischemic or metabolic insults to the brain.
Diagnostic Tests
The history and physical examination lead to a diagnosis in 25% of patients with syncope (47). For these patients, no additional diagnostic tests are necessary. For the remaining patients, however, several diagnostic tests should be considered.
Electrocardiogram
An ECG, with a rhythm strip, is indicated in all patients with syncope if the cause is not obvious from the history and physical examination. Although the ECG shows some abnormality in a large proportion of patients with syncope, it confirms a diagnosis in a much smaller number (Table 89.6). Specific diagnostic workups may be prompted by certain ECG abnormalities. For instance, sinus bradycardia in the absence of a β-blocker should prompt concern for sick sinus syndrome or sinus arrest. Sinus tachycardia may be present in patients with volume depletion, congestive heart failure, or pulmonary embolus. Left ventricular hypertrophy may be caused by aortic stenosis or hypertrophic cardiomyopathy, and a prolonged QT interval increases susceptibility to ventricular tachycardia. Left bundle branch block could be caused by cardiomyopathies or MI, and bifascicular block is associated with increased risk for complete heart block (see details in Chapter 64). The noninvasive nature of the test and its low cost, with the potential to uncover a possibly life-threatening disorder, make the ECG a cornerstone of the evaluation of nearly all patients with syncope (47).
Electrocardiographic Monitoring
The Holter monitor is one of the most commonly used diagnostic tests in patients with syncope, but the correlation of symptoms and arrhythmia in patients with syncope can be as low as 4% (49). In a prospective study of 140 patients with unexplained syncope, serious diagnostic arrhythmias found with Holter monitoring occurred exclusively in patients with a positive cardiac history and
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an abnormal electrocardiogram (50), suggesting that the initial evaluation described above can be used in making decisions about Holter monitoring.
There are other methods to monitor patients for arrhythmias for longer periods such as a loop recorder (event monitor), which saves several minutes of rhythm retroactively when activated by a patient while symptoms are experienced. Surprisingly, loop monitors are generally less expensive than Holter monitoring. In a comparison of Holter monitoring and loop recorders in patients with syncope, the diagnostic yield for symptom-rhythm correlations was 56% for loop recorders versus 22% for Holter monitors (51). Unfortunately, while event recorders have many appealing qualities, one major limitation is the dependency on the patient to trigger the device. In one study, 23% of patients who experienced syncope failed to trigger the device at the time of symptoms despite being trained how to use the device (51). This type of testing may be useful in patients in whom arrhythmia is believed to be likely, who have a negative Holter monitor, and who have mild enough symptoms so that they can activate the recorder. Loop recorders may be of particular use in patients without organic heart disease who have frequent episodes of syncope (20).
A relatively new modality is an implantable subcutaneous recorder that can be left in place for more than a year. Some experts recommend using these devices in patients with cardiac disease who have recurrent unexplained syncope or falls with a completely negative evaluation (52). It is reported that a diagnosis is made in up to 55% of patients with implantable recorders versus 19% with traditional external recorders with a distinct advantage in detecting bradyarrhythmias (53). Given the invasive nature of this diagnostic technique, however, its role in the evaluation of syncope is yet to be determined.
Arrhythmias detected during electrocardiographic monitoring but not accompanied by symptoms are difficult to interpret. Although some believe that these arrhythmias, even if unaccompanied by symptoms, may provide a working diagnosis, others disagree. Some arrhythmias, such as sinus arrest and nonsustained ventricular tachycardia, can be seen in normal people. Therefore, the results must be interpreted with caution, with consideration paid to the severity of the detected arrhythmia and the presence of any underlying heart disease. The exception may be nonsustained ventricular tachycardia in a patient with a history of MI or depressed left ventricular function, since this has been shown to increase the risk for sudden death.
Electrophysiologic Testing
EP studies are considered the final step in the evaluation when arrhythmia is strongly suspected and noninvasive testing is nondiagnostic (e.g., in patients with organic heart disease and unexplained syncope). Indications for EP testing in patients with syncope include (52):
EP testing is most likely to produce abnormal findings in patients with underlying heart disease. In a study of 111 patients with unexplained syncope referred for EP testing, 50% of those with underlying heart disease had positive findings on EP testing, whereas 16% of those without underlying heart disease had positive findings (54). Because other studies have failed to identify clinical predictors that correlate with positive findings on EP studies (55) and because EP findings may lead to treatment that decreases episodes of syncope, there are no clear-cut guidelines for excluding EP testing for patients with unexplained syncope, although the European Society of Cardiology guidelines suggest that EP testing is generally not indicated in persons with no heart disease, no palpitations, and normal ECGs (52).
The most common abnormal finding in patients undergoing EP testing is ventricular tachycardia, followed by conduction disturbances and supraventricular tachycardia, with the percentage of patients with abnormal findings depending on the population studied. As with Holter monitoring, certain abnormalities detected, especially conduction abnormalities and even certain tachyarrhythmias, have questionable clinical significance. It should be noted that EP testing has a lower diagnostic yield in identifying bradyarrhythmias compared to tachyarrhythmias.
Echocardiogram
Transthoracic echocardiography is utilized in up to 60% of patients admitted to hospital for syncope. However, in a recent study, echocardiography proved useful only if the patient had a history of cardiac disease, an abnormal cardiac physical examination, or an abnormal ECG; the echocardiogram showed a significantly reduced ejection fraction in 27% of these patients. However, in patients without cardiac disease and a normal ECG, echocardiography added no useful information (56).
Tilt-Table Testing
In the past 20 years, tilt-table testing has played an increasingly important role in the diagnosis and management of syncope. The most significant impact of tilt-table testing has been in patients without organic heart disease who have unexplained syncope. However, patients with organic heart disease and a negative evaluation for syncope (including EP testing) may also be evaluated with tilt-table testing (57). Tilt-table testing has dramatically reduced the proportion of patients with unexplained syncope.
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The tilt-table test is a provocative test used to document susceptibility to neurocardiogenic syncope (see Patient Experience). In neurocardiogenic syncope that can be demonstrated by tilt-table testing, blood pooling in the lower extremities leads to central hypovolemia, which ultimately is associated with bradycardia in some individuals (the exact mechanism is a matter of debate). Resultant hypotension leads to decreased CNS perfusion, which leads to syncope. The degree to which bradycardia by the cardioinhibitory response versus hypotension by the vasodepressor response causes syncope varies between individuals and can help predict the efficacy of treatment.
Patient Experience
The tilt-table test is performed by securing a patient to the tilt table in the supine position. The patient is kept in the supine position for 15 to 30 minutes (58) before they are tilted, and then the patient is tilted to a 60- to 80-degree angle within 10 to 15 seconds. (Many patients find this experience unpleasant, because it replicates the syncopal event. It is therefore important to discuss the test with the patient beforehand.) The patient is maintained at the tilted angle for up to 60 minutes, during which time blood pressure and heart rate are monitored. The mean time to syncope in patients with a positive test is 25 minutes (59).
A tilt-table test is deemed positive if syncope or presyncope with hypotension develops. If no event occurs, provocation with either isoproterenol or nitroglycerine may be tried, increasing sensitivity but losing specificity. Even without resorting to provocative testing, establishing susceptibility to neurocardiogenic syncope does not guarantee this as the cause of the patient's event.
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TABLE 89.7 Summary of Principal Indications for Tilt-Table Testing for Evaluation of Syncope |
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Although tilt-table testing is most commonly used to establish susceptibility to neurocardiogenic syncope, other abnormal cardiovascular responses may be uncovered with the test. In the neurocardiogenic response, both heart rate and blood pressure decline. However, in some patients, blood pressure may drop without significant changes in heart rate (termed the dysautonomic response). In others, heart rate may increase while blood pressure drops, termed the postural orthostatic tachycardia syndrome (60).
The most recent guidelines for the use of tilt table testing in patients with syncope were published by the European Society of Cardiology in 2001, and updated in 2004 (Table 89.7) (52). This consensus document, along with other studies on the evaluation of the patient with syncope, can be summarized as five indications for tilt-table testing:
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Tilt table testing can be useful not only for suggesting a diagnosis of neurocardiogenic syncope, but may also allow an opportunity for patient education and reassurance. Patients can learn what their premonitory symptoms are so they can better learn when to take evasive action at the onset of symptoms. Additionally, it is often reassuring for patients to have their symptoms observed by a physician. However, it needs to be emphasized that a positive tilt-table test only suggests a diagnosis of neurocardiogenic syncope but does not prove the diagnosis. Patients with risk factors for cardiac syncope still require evaluation for that even if they have a positive tilt-table test (58).
Guidelines for Admission to a Hospital
Patients should be considered for admission to a hospital for initial evaluation and treatment if there is a high risk of injury from a recurrent event or a high risk of a life-threatening arrhythmia. Assessment of the risk of injury should be based on the degree of injury sustained in the current episode, the frequency of episodes, and the fragility of the patient. Assessment of the risk of an arrhythmia should be based on the status of any underlying heart disease and the presence of any current or previous ECG abnormalities. Unfortunately, there are no studies that specifically look at this issue, but in general if a patient has a good history for neurocardiogenic syncope (or other low-risk etiologies of syncope) and have no evidence of heart disease and a normal ECG, they can be evaluated as an outpatient (20).
Selected Conditions that May Mimic Syncope
Hysterical Faint
Fainting caused by conversion disorder or other forms of somatization occurs in a manner to avoid injury, an important distinguishing feature from true syncope. The patient crumples to the ground with a limp body and shallow respirations. Recovery is usually immediate. Often, the faint may be embellished with movements that resemble seizures, but more often voluntary movements are the rule. Hyperventilation or coaxing may reproduce the spell. Chapter 21 provides additional detail regarding the evaluation and management of such patients. It should be emphasized that in the past up to 30% of patients with syncope were labeled as being psychiatric in origin. However, the improvement in diagnostic evaluation (in particular tilt-table testing) has dramatically reduced this as a diagnostic category.
Drop Attack
Older patients, especially men, may report sudden and unprovoked falls to the ground. Consciousness is not lost, and the patients can usually remember the entire episode. The history of maintenance of consciousness distinguishes drop attacks from syncope. Ischemia of the lower brainstem is one possible cause of drop attacks, and occasionally patients report other concurrent symptoms that suggest vertebrobasilar ischemia. Management is identical to that of TIAs occurring in the posterior circulation (see Chapter 91).
Cataplexy
Cataplexy is a special kind of drop attack, not caused by ischemia, that occurs as part of the syndrome of narcolepsy. The patient falls suddenly to the ground because of a loss of extensor muscle tone but without loss of consciousness. These spells are usually provoked by a sudden startle, a joke, laughing, or sneezing. Sleep paralysis (paralysis of the limbs for a minute or 2 upon awakening) and peculiar visual hallucinations on awakening or before falling asleep may also accompany narcolepsy. (See Chapter 7 for additional details.)
Disequilibrium of Miscellaneous Origins
Some patients with persistent dizziness do not have manifestations that make it possible to classify their problem as vertigo or near syncope. Many of these patients have disequilibrium, or a sense of imbalance, that may be caused by multiple sensory deficits (e.g., partial hearing, visual, proprioceptive impairment, or vestibular impairment); lower extremity weakness (e.g., from an old stroke or from disuse after a period of bed rest); pain in a weight-bearing joint (e.g., degenerative arthritis of the hips, knees, or ankles), cerebellar ataxia (seeChapter 86); recently initiated drugs (especially anxiolytics, hypnotics, or neuroleptics); or the onset of a progressive CNS disease (e.g., parkinsonism, normal pressure hydrocephalus, or subcortical small-vessel ischemic disease) (61). These problems often occur in older patients, debilitated patients (particularly chronic alcoholics), or patients with long-standing diabetes mellitus, hypertension, and other vascular risk factors. Cervical myelopathy, either metabolic (e.g., vitamin B12 deficiency), infectious (e.g., neurosyphilis), or because of cervical stenosis, should also be considered. In some patients, CVD or autonomic neuropathy may cause periodic vertigo and near syncope to be superimposed on their day-to-day problem with imbalance.
The evaluation of patients describing imbalance consists chiefly of obtaining a history of the duration, progression, and day-to-day characteristics of the problem,
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focusing on the limitations imposed on their usual activities and on any falls or near accidents that may have occurred. Often, patients with disequilibrium will describe the dizziness as originating in their feet rather than their head (62). Patients with disequilibrium may also report their symptoms are worse in the dark when they lose visual cues that may help them compensate for some of their deficits. In the physical examination, it is important to determine which of the many problems listed above may be contributing to the patient's symptoms focusing on the patient's ophthalmologic examination, sensory examination of the feet, and musculoskeletal examination. When disequilibrium is suspected, it is crucial to observe the patient's gait.
Depending on the individual patient, management by the generalist may include referring the patient for correction of any impairment in hearing or vision (see Chapters 107 and 110), consulting a neurologist if unexplained progressive symptoms are found (e.g., cerebellar ataxia in an otherwise healthy person), consulting a physical therapist if weakness or the need for selecting a cane or walker is apparent, and discontinuing drugs that may be contributing to the patient's symptoms and avoiding drugs that may worsen symptoms (Tables 89.2 and89.5).
Nonspecific Dizziness
A subset of patients who present to primary care physicians will be categorized as having nonspecific dizziness. Up to 15% of dizzy patients in some series fall into this category (1). These patients can be the most challenging of all dizzy patients. Often, patients with nonspecific dizziness are simply incapable of explaining their symptoms beyond general terms of “I just feel dizzy.” Invariably, their physical examination is normal. Most patients with nonspecific dizziness are young. Commonly, they have concomitant psychiatric disease including depression, anxiety disorders, and somatization. The role of having the patient hyperventilate to reproduce symptoms is controversial. Some authors advocate this approach. However, as discussed above, hypocarbia can induce dizziness through near syncope in many normal patients. Therefore, the specificity of this technique is highly questionable (63).
The therapeutic approach to patients with nonspecific dizziness is similar to that of patients with somatization disorder (63). Patients require reassurance that their symptoms do not represent life-threatening pathology, but also require recognition of the impact their symptoms have on their life. In a recent study, patients with nonspecific dizziness were shown to benefit from treatment with SSRIs (64).
Chronic Dizziness: General Measures hELPFUL in Management
Patients with chronic dizziness, vertigo, syncope, or disequilibrium have a far better prognosis if their home environments are safe and others in their households are aware of risks that should be avoided and devices that may be helpful. A number of general measures to recommend include using night-lights, tacking down loose carpeting and floorboards, installing special railings in the bathroom, selecting proper footwear, and learning to assume an upright posture gradually. These measures can be accomplished most effectively if the physician or a visiting nurse evaluates the patient's home. If vertigo is a contributing factor to chronic dizziness, vestibular rehabilitation can be helpful regardless of the underlying cause (65). In some patients with unsteady gait, a cane or a walker may be helpful; a physical therapist can be very helpful in selecting the best assistive device.
Specific References*
For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.
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