Introduction

The problem of dizziness can be one of the most exasperating in the practice of medicine. Physicians all know that sinking feeling elicited by the pa tient who sits down and, when one asks “What can I do for you?”, says, “I’m dizzy.” The goal of this article is to offer urgent care practitioners a reasoned approach to dizziness that will lead expeditiously to diagnosis and effective therapy.

Principles of Diagnosis

The first principle in evaluating a dizzy patient is to take an open-ended history.

This is a good rule in taking any medical history, but it is particularly applicable in this instance. When the patient says to you, “I am dizzy,” sit back in your chair, slowly spin around, perhaps stare aimless ly out the window, and reply, “What do you mean, dizzy?” Then wait for the response.

This may take what seems to be a long time; nonetheless, don’t probe further by asking “Does the room spin?” “Do your legs get weak?” “Do you feel as if you might stagger?” “Are you light headed?” because the answer to all these questions will nearly always be “yes.” If you are fortunate enough to be the first physician to examine a patient complaining of dizziness, always take the un directed approach and wait for the response. There are several possible responses.

Syncope or Near-Syncope
“I feel as if I might faint,” or “I feel giddy or light-headed.” Some patients do faint or report that they have done so while others have never actually fainted (nearsyncope).

Pathophysiologically, both syndromes suggest any of several cardiovascular disorders that produce a generalized decrease in cerebral blood flow. There is no qualitative difference between syncope and near-syncope with respect to the differential diagnosis. This topic was discussed in detail in the October 2006 issue of JUCM, and will not be explored further here.

Circulatory syndromes that should be considered include orthostatic hypotension, which may have a number of causes, many of them iatrogenic (e.g., antihypertensive agents and/or vasodilators).

Cardiac arrhythmias are a very infrequent cause of syncope and near-syncope; however, dizziness during or just following exercise should raise the specter of a cardiac problem, such an arrhythmia or left ventricular outflow obstruction (e.g. aortic stenosis or asymmetric septal hypertrophy). If the history suggests arrhythmic episodes, Holter monitoring and even long-term loop monitoring of the cardiac rhythm may be required.

Hypersensitive carotid sinus is relatively uncommon.

Neurocardiogenic syncope and near-syncope, otherwise known as vasovagal syncope, may be called a swoon or faint by patients. Neurocardiogenic syncope is probably due to overactivity of the baroreceptor reflex, such that brief periods of hypertension result in disproportionate bradycardia and hypotension resulting in decreased cerebral blood flow and consequent loss of consciousness. Any failure of the autonomic reflex necessary to maintain cerebral blood flow in the upright posture can cause dizziness related to near-syncope. High ambient temperature, emotional excitement, and natural vasodilators such as alcohol all may disable the systemic vasoconstriction, mediated by sympathetic alpha receptors, that allows for preservation of cerebral blood flow with orthostatic stress.

Disequilibrium
“My balance is off and I feel as if I might fall.” This version of dizziness generally reflects one of two major categories of neurologic disease, apart from disorders of the vestibular system.

Cerebellar ataxia is due either to a primary disease of the cerebellum (e.g., cerebellar degeneration, tumor in or near the cerebellum, cerebellar infarct) or disorders of the tracts leading to (cerebellopetal) or from (cerebellofugal) the cerebellum. Neurologic ex amination will ordinarily unveil such pathology by revealing axial (e.g., wide-based gait; falling to one side) or appendicular ataxia (e.g. side-to-side tremor on goal-directed action).

Multiple sensory deficits syndrome is due to several abnormalities in the various sensory proprioceptive systems. When a number of these systems fail, the central nervous system receives conflicting proprioceptive input, with consequent dizziness.

The typical patient is rather elderly, perhaps with some visual disorder due to cataracts, some auditory disorder due to presbyacusis, some myelopathy, perhaps related to cervical spondylosis or cobalamin deficiency, and peripheral neuropathy due to diabetes and/or chronic use of alcohol.

Typically, such a patient complains of dizziness at night—for instance, when the lights are out or dim and he or she has to go to the bathroom. On occasion, the patient may fall, particularly in environments in which there are no reliable visual cues (e.g., the shower).

The treatment of this extremely common syndrome is common sense (as many of the sensory abnormalities that can be corrected should be). Cataracts and hearing disorders can be treated, and the progression of some peripheral neuropathies prevented, by abstinence from alcohol. One might also advise the patient to keep the lights on at night, which would help the visual system com pensate for other sensory abnormalities. Such patients should not be treated with drugs that might sedate them, as antivertigo medica tions would do. Mistaking this syndrome for vertigo would, in fact, make matters worse.

Anxiety and/or Depression
There are patients who when asked, “What do you mean, dizzy?” respond, usually after a pause, “Dizzy.” If the physician per sists with “Do you mean you might faint?” or “Do you mean that you might fall?” or “Do you mean that the room spins?” the pa tient repeats, “No, I mean I’m dizzy.”

This disorder can only be called true dizziness, and it generally arises from various psychological disorders, most commonly anxiety (with or without hyperventilation) and/or depression.

Affective disorders can often be recognized because of the ef fect that the patient has on the examiner’s mood. If one feel depressed or anxious oneself after spending time with a patient, it may well be because the patient is depressed or anxious. It is extremely important to recognize instances in which dizziness represents a metaphor for anxiety or depression; treatment for vertigo is likely to exacer bate these disorders, whereas treatment for depression and anxiety might dramatical ly relieve the dizziness.

Vertigo
The fourth and last category of disorder found in patients who complain of dizziness is true vertigo (an illusion or hallucination of motion). Some patients insist that they themselves are moving, while others— such as the one presented above—have the sense that the environ ment is moving. In either case, these patients transmit the message that they feel as if they are tilting, rocking, falling, spinning, or moving in some fashion.

Vertigo indicates a disturbance in the vestibular system, which is responsible for keeping the central nervous system informed of the head’s position in space, its relation to the pull of gravity, and its acceleration in various planes. The important clinical question is whether the vertigo is due to a disorder in the peripheral nervous system (the end organ or the peripheral nerve) or in the central nervous system (the brainstem or its projections to parts of the cerebral cortex, par - ticularly the temporal lobe). Each lesion has its own differential diagnosis and treatment.

Evaluation of Vertigo

The first step is to perform a complete history and physical examina tion, as well as a neurological exami - nation with particular at tention to the VIII cranial nerve.

The VIII cranial nerve is, in fact, two separate cranial nerves: the vesti bular and cochlear. These two nerves have closely juxtaposed end organs, run closely together in the in ternal auditory meatus, and have two completely different pathways in the central nervous system. Because of the close proximity of these two nerves and their end organs, it is common for disease of one to affect the other. Therefore, the physician should examine both aspects of the VIII cranial nerve whenever there is a com plaint of vertigo. (Symptoms that may reflect a true dizziness emergency are listed in Table 1.)

Cochlear VIII Nerve Function
Pure Tone Hearing Loss
Examination of the cochlear system involves three steps, whether the patient complains of hearing loss or not.

The first is to test for pure tone hearing loss. This can be done in the office by assessing the sensitivity of the patient’s hearing or comparing the patient’s hearing with one’s own, using a ticking watch or the sound of fingers rubbing together.

Sensory Neural vs. Conductive Hearing Loss
If there is a hearing loss, the next step is to determine whether it is a sensory neural hearing loss (i.e., a neuro- logic problem) or a conductive hearing loss (i.e., a disorder in the middle ear interfering with the functions of the ossicles). These determinations are made by using the Weber test and the Rinne test.

The Weber test is performed by placing a vibrating tuning fork at the midline of the skull and asking the patient on which side the sound can be heard. If there is a definite lateralization to one side, one can determine whether there is sensory neural or conductive hearing loss.

For example, if the Weber lateralizes to the left, this may be interpreted as either a leftsided conductive hearing loss or rightsided sensory neural hearing loss. Combining this information with the knowledge of which ear has the hearing loss, one can determine whether that loss is sensory neural on the right or conductive on the left.

The Rinne test is easy to apply in an office setting. Bone and air conduction are compared by placing the tuning fork first over the mastoid bone and then in front of the ear, asking the patient which is louder.

Under normal cir cumstances, air conduction is better because the ossicles in the mid dle ear amplify and transmit the impulse through the mid dle ear to the inner ear. If the ossicles are not functioning because of otosclerosis, cholesteatoma, or fluid in the middle ear, air conduction may suffer, which leads to a situation in which air and bone conduction are equal or bone conduction is the better of the two. If, however, there is sensory neural hearing loss, air conduction remains better than bone conduction.

Cochlear vs. Retrocochlear Hearing Loss
The third step in the hearing examination, needed only if there is a sensory neural loss, is perhaps the most important of the dif ferential procedures but, paradoxically, the one least well known to many physicians. The issue is whether the senso ry neural deficit is due to end organ disease (cochlear) or to disease of the nerve or the central nervous system (retrocochlear).

Speech discrimination testing can be done in the office to differentiate a cochlear sensory neural hearing loss from retrocochlear sensory neural hearing loss. There are a number of ways to make this distinction, but many require the services of an audiologist: The physician whispers words in the affected ear (e.g., hot dog, ice cream) loud enough for the patient to hear. At the same time, a sound is made in the other ear so that the patient cannot hear the words using the unaffected ear. Putting a finger in the patient’s other ear and moving it around will serve the purpose. This is done on both sides several times, having the patient repeat the words each time, and comparing the two ears. One can also use the telephone for this purpose, testing each ear separately for words delivered through the handset.

In people with cochleartype sensory neural hearing loss, such as occurs in Ménière disease, speech discrimination is not perfect, but it is relatively preserved.

On the other hand, in patients with retrocochlear hearing loss, such as accompanies a vestibular Schwan - noma, there is a disproportionate loss of speech discrimination. Thus, a patient with a cochlear hearing loss should be able to understand 70% or more of the words heard, whereas a patient with a retrocochlear hearing loss might understand only two out of ten words.

If there is any question of a retrocochlear hearing loss, one may order an audiogram or go directly to an MRI to image the VIII cranial nerve.

Vestibular VIII Nerve Function
Testing for Nystagmus
The vestibular aspect of the VIII cranial nerve may be examined by testing for nystagmus. First, ask the patient to sit on the end of the examining table and to look about 45° to the right and to the left. (Asking the patient to look beyond 45° is not useful, since when asked to look too far in either direction, about 10% of the normal population show some degree of gaze-evoked endpoint nystagmus.) If nystagmus develops when the gaze is directed to 45°, note the direction of the fast phase, the direction of the slow phase, and in what position of the eyes they occur.

Next, the patient should be put through a series of positions called the Dix- Hallpike maneuver (Figure 1).

All vertigo is positional to some extent, but there are specific pathogenetic and prognostic implications if vertigo is exclusively positional. Once position testing has been done, the physician knows in which direction the world seems to be spinning and in which direc tion the patient seems to be falling when the vertigo develops. The directions of the fast and slow phases of the nystagmus have been recorded. The next step is the interpretation of these data.

Peripheral or Central Nervous System?
A basic understanding of the neuroanatomy and neurophysiology of the vestibular system is necessary for effectively interpreting findings from the neurological exam. (See Figure 2.)

Vestibuloocular Reflex
The end organ of the vestibular nerve is located in the semicircular ducts, utricle, and saccule. The lateral, or horizontal, semicircular duct is oriented in the inner ear so that it tilts at about 30° above the horizontal plane (Figure 3). When the head is held in the usual carrying position, this duct is approximately parallel to the ground. Thus, turning the head right and left would be expressed almost entirely in a vector within the plane of the lateral semicircular duct.

The series of events that make up the active phase of the vestibulo-ocular reflex is as follows: When the head turns to the left, a series of impulses (beginning with stimula tion of the hair cells in the left lateral semicircular duct) that leads to contraction of the right lateral rectus muscle (right eye abductor) is initiated.

This sequence, taken no further, would of course lead to a situation in which the eyes are pointed in two different directions, which would produce diplopia, an unacceptable situation for the nervous system. Therefore, a corresponding series of impulses must also reach the left medial rectus muscle in order for the left eye adduc tor to contract, as well.

In a comatose patient with an intact brainstem but with cortical signals in abeyance, the vestibulo-ocular reflex can be elicited by turning the patient’s head, which produces the oculocephalic reflex, or the socalled doll’s eyes. In an awake patient, the reflex may be demonstrated by having the patient fix his or her gaze on a distant object or by infusing the ears with warm or cold water (the caloric reflex). Although the caloric reflex should be a routine part of the evaluation of a comatose patient, it is a procedure perhaps best left to the otologist or neurologist in an awake patient.

Cerebral Cortex
In the hypothetical situation just described, the eyes have deviated to the right. This information is transmitted to the cerebral cortex by more than one mechanism. The movement of images on the retina sends information to the occipital cortex through the usual visual pathways. However, it is presumed that information regarding the movement of the eyes may reach the cerebral cortex even in the absence of visual stimuli, as proprioceptive organs in the orbit probably convey information to the parietal cortex.

The cerebral cortex, however, finds itself in a dilemma. In effect, it asks itself, “Have I, in fact, turned the eyes to the right?” The left fron tal eye fields could, of course, turn the eyes under normal circumstances to produce a voluntary saccade (rapid conjugate eye movement) to the right.

However, in this instance the left frontal eye fields have not fired. It is possible that the right parietaloccipital region could have turned the eyes to the right by producing a conjugate pursuit or tracking eye movement, but in this case these areas have not fired either. Thus, the cerebral cortex has received conflicting information.

On the one hand, it seems that the eyes have turned to the right. On the other hand, it seems as if the eyes have not been moved to the right. What conclusion can the cerebral cortex draw? It concludes not that the eyes have moved to the right but that the world has moved to the left.

This erroneous conclusion is based on conflicting information. Thus, the resultant sensation of vertigo is usually a misperception of a stimulus (illusion). Vertigo may also occur as the result of a perception without a stimulus (hallucination). Migrainous vertigo and epileptic vertigo would be examples of hallucinatory vertigo.

Frontal Lobe
The frontal lobe makes a correction for the abnormal eye movement that was generated by the disabled vestibular dysfunction. The corrective phase of the vestibuloocular reflex arises from the frontal eye fields and results in rapid turning of the eyes back to the left.

In the circumstance postulated, the stimulus has arisen from the left vestibular system and caused a slow conjugate eye movement to the right, followed by intermittent rapid conjugate correction back to the left. It is associated with a vertigo in which the patient has a feeling that the world is spinning to the left while he or she is being pulled to the right.

The patient’s feeling of being pulled may become worse when the eyes are closed, because closing the eyes removes another pro prioceptive system that would help to compensate. Romberg’s sign ( i.e., a patient’s balance is seen to become worse with the eyes closed), may be seen in any abnormality producing a proprioceptive disorder, including peripheral neuropathy and disease of the spinal cord, as well as disease of the vestibular system.

The Two Phases of Nystagmus

As we have seen, the vestibular imbalance nystagmus consists of two components. The first (active) phase originates in the brainstem or vestibular system, is caused by different vestibular input from the ears, and is associated with slow eye movement. The second (corrective) phase is initiated by the frontal eye fields in the cerebral cortex and is associated with fast eye movement. Both phases act through the final common pathway of the ocular motor system of the brainstem.

Under normal circumstances (Figure 3A), the entire vestibular system functions bilaterally with all of its central connections. There is no vertigo or nystagmus with ordinary accelerations of the head.

The pathologic situation illustrated in Figure 3B depicts a “lesion” in the right ear, functional or anatomic. In this situation, an imbalance develops between the two sets of vestibular apparatus in the ears. With disruption of the vestibular impulses from the right ear, it is as if the left side has been stimulated or the head has been turned with acceleration to the left.

What symptomatology does such a lesion produce? The eyes are driven conjugately toward the side of the lesion. This move ment is interrupted by intermittent rapid corrective movement away from the side of the lesion. The patient has a sensation of vertigo, with the world spinning away from the lesion (or toward the fast phase) and a feeling of falling toward the side of the lesion (or toward the slow phase).

Criteria for Locating the Lesion
There are four criteria for a peripheral type of vertigo and nystagmus (see Table 2). If there are 1) fast-phase nystagmus away from the lesion, 2) slow-phase nystagmus toward the lesion, 3) environment spinning away from the lesion, and 4) Romberg’s sign toward the lesion, one can say with confidence that there is a lesion of the peripheral nervous system, probably in either the end organ or the peripheral nerve. If any of these four rules fails to hold, one can assume by exclusion that the lesion is in the central nervous system.

Central nervous system lesions can cause bilateral nystagmus in the same position of the head, vertical nystagmus of any kind, and any conditions in which the directions of the fast and slow phases, the Romberg’s sign, and the spinning of the environment do not strictly fit the four criteria specified. Those criteria specify only the anatomic localization without implying anything about the severity or seriousness of the underlying disease. Peripheral diseases can be selflimiting (e.g., vestibular neuronitis) or very serious (e.g., vestibular schwannoma). Central diseases can range from the trivial complications of many drugs (e.g. benzodiazepines) to vertebrobasilar insufficiency.

Synthesizing the Data
Thus by testing the auditory system and the vestibular system, one can divide all cases of vertigo into three categories: 1) peripheral (by vestibular criteria) cochlear disease (by auditory criteria and signs); 2) peripheral (by vestibular criteria) retrocochlear disease with hearing loss (by auditory criteria); and 3) central disease.

With this in mind, we can now consider the major diseases in each category.

Peripheral Cochlear Lesions
Labyrinthitis is thought to be a result of viral infection of the endolymph and perilymph, affecting both the vestibular and cochlear components of the system. The usual history is viral illness followed by acute onset of severe spinning vertigo and sensory neural deafness with tinnitus. Examination shows a classic peripheral pic ture by vestibular criteria and a classic cochlear picture by auditory criteria. De spite its severe onset, labyrinthitis is a benign illness that resolves completely in three to six weeks. Patients regain normal hearing and vestibular function.

Vestibular neuritis, or acute vestibulopathy, is thought to be pathogenetically identical to labyrinthitis but without any hearing symptomatology. If the patient has vertigo unaccompanied by a hearing abnormality, it is strictly speaking impossible to be sure whether the disease is cochlear or retrocochlear. However, its natural history is also benign, and it resolves completely in three to six weeks, which makes a retrocochlear illness very unlikely.

Cochlear neuritis is the syndrome of acute pure deafness without vestibular symptoms or signs. It is thought to be analogous to vestibular neuritis.

Ménière’s disease is caused by a cryptogenic hydrops of the endolymph such that there is intermittent swelling of the semicir cular ducts, with damage to the hair cells.

Typically, an attack of Ménière’s disease is characterized by a dull ache in the region of the mastoid process or around the ear associated with severe tinnitus, a cochlear kind of sensory neural hearing loss, and a classic peripheral type of vestibular syndrome with severe spinning ver tigo. It is identical in almost every respect to an acute attack of labyrinthitis. However, it does not resolve completely in three to six weeks, and patients are left with residual hearing loss. Several months or years later, a similar attack may occur, leaving the pa tient with even more severe hearing loss. Tinnitus, a nonspecific sign of auditory system disorder, is a major problem for these pa tients, who can be terribly disabled for weeks at a time by the ver tigo that accompanies acute attacks.

Many therapies have been tried, including shunting of the perilym phatic system and diuretics, but none are curative. About 15% of these patients have bilateral disease in subsequent years. Management of such patients is complex and often best entrusted to an otolaryngologist or otoneurologist, as deliberate toxic (e.g., intraaural aminoglycoside antibiotics infusion) destruction or surgical severing of the vestibular nerve may be required.

Benign positional vertigo, or Bárány’s vertigo, usually occurs in older patients and is characterized by the sudden onset of a peripheral vestibular syndrome with no auditory aspect. It is pres ent only in certain positions, which are specific to the individual.

Typically, the patient reports that a few moments after attaining a certain position, perhaps in bed at night, severe vertigo occurs in which the world spins in one direction while the patient has a sensation of falling in the other direction.

If he or she does not move, the vertigo stops, which implies that it is transient in type. If the patient sits up, the vertigo recurs, but this time in reverse. If the patient repeats the posture several times, the tendency toward ver tigo and nystagmus will fade.

All the symptoms can be reproduced using the Dix- Hallpike maneuver, during which the patients will experience vertigo with the affected ear down and an associated nystagmus that is rotatory in the dependent eye and vertical in the opposite eye. Benign positional vertigo has a benign natural history, which improves gradually over a six-month period and ends with complete recovery.

Etiology of Benign Positional Vertigo
Canalolithiasis is one of two causes to explain benign positional vertigo.

The theory of canalolithiasis maintains that bits of calcium break off from the otolithic apparatus in the ear, perhaps as a consequence of aging or minor head trauma. If these bits of calcium are floating in the posterior vertical canal’s endolymph, they will fall with gravity, which initiates an impulse arise from the dependent ear. Since the calcium tends to fall into the most dependent of the three semicircular ducts, the canalolithiasis tends to affect the posterior vertical semicircular duct, resulting in the characteristic vertigo and nystagmus pattern only when the affected ear is down.

Canalolithiasis of the horizontal canal is relatively rare and of the anterior vertical canal unknown, probably simply due to the proximity of posterior and, to a lesser extent, the horizontal canal to the utricle from whence the otolithic debris arise.

Perilymphatic fistula is a rarer cause of positional vertigo.

Normally, the middle ear and inner ear are separated by the oval and round win dows, which are completely sealed. If for some reason (e.g., head trauma) a crack develops in the oval or round window, some of the perilymph may leak from the inner ear into the middle ear. Such patients may have intermittent episodes of conductive hearing loss superimposed on a sensory neural hearing loss. This pathology is established by an audiogram.

Superior canal dehiscence is another fistula in which the leak comes from the superior vertical canal. This unusual syndrome causes the characteristic sign of vertigo and nystagmus being exacerbated by sound (Tullio phenomenon).

The presence of a fistula may be detected by placing the otoscope in the ear and closing the glass window, which produces an air-tight space. Air is then pumped into the external ear using the balloon attachment to the otoscope. This air distorts the tym panic membrane, which briefly increases the pressure in the mid dle ear. Under normal circumstances, a mild sensation in the ear is produced, but no vertigo. If, however, there is a pathologic connection between the middle ear and the inner ear, increased pressure in the middle ear will be transmitted to the perilymphatic space in the inner ear, which produces an abnormal stimulus and causes vertigo and nystagmus.

Peripheral Retrocochlear Syndromes

Vestibular Schwannoma
A second category of disease is a pe ripheral type of vertigo, characterized by retrocochlear hearing loss (i.e., patients are found to have poor speech discrimination). Such patients should have an image of the inner ear, preferable an MRI. If an MRI cannot be obtained (e.g., due to the presence of a pacemaker), a CT scan with thin cuts through the inner ear is also very useful.

It is important to recognize the presence of a tumor while it is still contained within the internal auditory meatus and thus easily surgical ly resectable. Vestibular schwannomas (often incorrectly called acoustic neuromas) are histologically benign tumors, but they can become quite dangerous by position. If a vestibular schwan noma is allowed to grow into the brainstem, treatment requires a posterior fossa craniotomy, with significant morbidity and even some mortality. Any patient with a history of progressive hearing loss should at some time during the evaluation have a careful auditory examination, and if any retrocochlear characteristics are found, a brain image with careful views of the internal auditory meatus should be obtained.

If you are treating a dizzy patient with peripheral cochlear findings of hearing loss and there has been no improvement in three to six weeks, referral and/or imaging may be indicated.

Central Lesions
The last category of vertigo is central disease (i.e., patients with vestibular symptomatology that does not meet the criteria for peripheral disease). This group includes patients who exhibit vertical nystagmus or bilateral nystagmus when their head is in an identical position.

Drugs
All drugs that act by intoxicating the reticular activating system in the core of the brainstem—including all anticonvulsants, all sedatives, and some sleeping pills— will by their nature produce nystagmus in two different directions in the same position of the head. When the patient looks to the right, the nystagmus beats to the right. When the patient looks to the left, it beats to the left. Overdosage can produce vertigo. Most sedatives (e.g., benzodiazepines) cause this type of nystagmus.

The fact that the lesion is central does not necessarily mean that it is serious. In fact, the appearance of this form of nystagmus may prove that a given drug (e.g. phenytoin) is in the therapeutic range. Such patients should be asked specifically about their use of drugs, including alcohol; before any invasive studies are performed, it is useful to order blood and urine toxic screening.

Demyelinating Illness
Demyelinating illnesses, such as multiple sclerosis, can and often do produce vertigo, presumably because there are lesions somewhere in the vestibular system in the brainstem. Although such vertigo usually has characteristics that indicate a central lesion, occasionally it can resemble peripheral vertigo and be misdiagnosed as vestibular neuritis. If the same patient returns a year later with optic neuritis, it would be clear in retrospect that the first disorder was due to multiple sclerosis. However, nothing has been lost in the interim, because multiple sclerosis of this mild degree would not be treated.

Vascular Disease Affecting the Brainstem
In approaching vascular disease affecting the brainstem, it should be remembered that the most common manifestation of vertebrobasilar insufficiency is vertigo, but vertigo is almost never the only manifestation.

Such patients can also be expected to complain of double vision, weakness of the limbs, sensory loss, dysarthria, and dysphagia. It might be possible for disease of the small branch of the vertebral artery to produce vertigo as its only symptom, but in such instances there is no specific or emergency therapy anyway. This presentation may also be seen in the same type of patient who presents with multiple sensory deficit syndrome. Referral may be indicated.

Disorders of the Temporal Lobe
Temporal lobe seizures aris ing from trauma, tumors, or prior strokes can, as one of their manifestations, produce vertigo. Vertigo is rarely the only symptom of a temporal lobe seizure, however, and such a diagnostic consideration requires neurologic consultation.

Migraine

Migraine is strongly associated with vertigo. About 10% of patients with vertigo will, ultimately, be found to have migrainous vertigo. The reverse association is even more common. The majority of migraineurs have a history of motion sickness, which is physiological vertigo, and some patients have vertigo as the only aura of migraine. Episodes of vertigo lasting about 20 minutes, with or without associated headache, should raise this possibility. Often, a therapeutic trial with anti-migraine medication is required to make this diagnosis.

Treatment of Vertigo

Antiserotonin and Antihistamine-type
There are three categories of drugs for treating true vertigo: anticholinergic and antihistamine-type drugs, and the phenothiazine agent promethazine.

Anticholinergic and antihistaminetype drugs include dimenhydrinate, diphenhydramine, meclizine, and cyclizine. All of these drugs are effective if the dosage is adequate—about 50 mg every six hours (see Table 3). They can produce major sedation at higher doses or in susceptible patients such as the elderly or those on multiple medications, but this is often of no concern. In patients for whom drowsiness is a serious problem, modafinil or methylphenidate may be used in concert with the anticholinergic drug.

Promethazine is the only phenothiazine that works against the nausea associated with vestibular imbalance and vertigo. Other phenothiazines, useful for chemical nausea, are of no help what soever in this setting. Promethazine may be effective primarily because it is an anticholinergic, not because it is a phenothiazine. It is useful also because it can be given together with the anticholinergic drugs and may be administered by a non-oral (e.g., rectal) route. A combination of pro - methazine and antihistamine is particularly effective for acute vertigo.

Beladonna Alkaloids
A belladonna alkaloid, usually scopolamine, is used only for severe recurrent vertigo (e.g., in difficult cases of Ménière’s disease) because it is a dangerous drug with many cardiovascular and psychiatric side effects.

Transdermally absorbed scopolamine, although helpful for motion sickness, is of inadequate dosage for use in treating most acute vestibular syndromes. Many otoneurologists use benzodiazepines in addition to the anticholinergic drugs. These may have a specific antivertigo effect or may be acting on the almost universal associated anxiety in severely vertiginous patients.

Non-vertiginous types of dizziness are treated depending on the specific diagnosis. In near syncope, the treatment may be as simple as discontinuing the precipitating drugs or may require a more specific therapy of the autonomic insufficiency (e.g., midodrine, an alpha adrenergic agonist) or a simple maneuver, such as leg crossing with thigh clenching, which simply squeezes blood out of the extremities to restore cerebral blood flow.

In patients with disequilibrium, one would treat the underlying disorder, such as neuropathy, myelopathy, or Parkinsonism.

For anxiety, confident reassurance alone may be adequate with or without concomitant use of anxiolytic drugs.

Summary

To evaluate dizziness, one must first decide whether it can be categorized as near-syncope, disequilibrium, illdefined light-headedness, or vertigo. If it is vertigo, vestibular and auditory testing will allow one to place the patient into one of three categories: peripheral cochlear disease, peripheral retrocochlear disease with hearing loss, or central disease. When this distinction is made, one can create a reasonable differential diagnosis and arrive at the likely diagnosis. Some of these disorders (e.g., vestibular schwannoma) require specific evaluation and treatment, whereas others have a benign natural history and require only symptomatic relief for the duration. Symptomatic therapy of vertigo is straightforward and makes use of the three categories of drugs discussed.

Selected Reading