VERTIGO AND DIZZINESS

Complaints of dizziness and light-headedness are among the most common in emergency medicine, and their evaluation can test the problem-solving ability of the physician. Dizziness itself may not be life-threatening, but it is usually bothersome and potentially disabling. The primary challenge to the emergency physician is establishing what a given patient means by dizziness, which is an ambiguous, nonmedical, subjective term that derives from the old English word dysig, meaning foolish or stupid. It may be used to articulate a sensation of weakness, unsteadiness, giddiness, malaise, instability, swimming in the head, faintness or near faintness, or a disturbance of mentation. A variety of disorders affecting the central nervous system, ears, cardiovascular system, eyes, and psyche may all produce dizziness, and thus a systematic approach is imperative.

Vertigo is used to refer to an illusion of motion where no motion exists and derives from the Latin vertere, meaning to turn. Either the patient or the environment seems to be moving. Movement is classically described as spinning or whirling, but may also be described as rocking, staggering, or swaying, or as a sensation of impulsion, where the person feels as though he or she is being pulled to one side or to the ground as if by a magnet. The distinction between a feeling that the patient is moving versus a feeling that the environment is moving (subjective versus objective vertigo) is not useful. Oscillopsia, a visual illusion that objects in the environment are moving, may occur.

Syncope means a transient loss of consciousness, with rapid return to normal, on the basis of diminished cerebral blood flow, oxygen, or glucose. Near syncope is an impending loss of consciousness, or a gray-out feeling.

Disequilibrium refers to a feeling of imbalance or unsteadiness while walking. When the subjective complaint of dizziness is not well defined and cannot be classified as vertigo or near syncope, the term ill-defined dizziness is often used.

Spatial orientation is determined by the interaction between the visual, labyrinthine, and proprioceptive systems and the integration of impulses by the central nervous system. Dysfunction in either the pathways that integrate those systems or the sensors themselves may be the cause of disordered sensations of spatial orientation, position, and motion.

The visual system, consisting of the eyes, the optic pathways, and the visual cortex create for the person a visual-spatial orientation. The labyrinthine system consists of the otoliths, which primarily produce an orientation to gravity, and the semicircular canals, which produce an orientation to movement or the tilt of the head. The semicircular canals are filled with fluid and lined by hair cells. Movement of the fluid causes movement of the hair cells, which results in a change in afferent vestibular nerve impulses. There is a balanced vestibular neuronal input to the brain stem from both vestibular nerves. Alteration of input from one is perceived as motion. The proprioceptors in the joints and muscles of limbs and neck relate movement and the tilt of the head to that of the body and also sense body position when lying, walking, or sitting.

The integrative structures involved in mediating the sensory input from the receptor systems are the cerebellum, the brain stem (primarily the vestibular nuclei and the medial longitudinal fasciculus), the basal ganglia (red nuclei), and the cerebral cortex (superior temporal gyrus and parietal lobes). Dizziness can occur as a result of dysfunction in one or all of the receptor systems or the mediating structures.

The pathophysiologic mechanisms that can affect these structures include all of the processes which affect the nervous system in general, including vascular, metabolic-nutritional, toxic, neuronal, and psychogenic.

Age-related changes that can contribute to dizziness or vertigo include diminished labyrinthine hair cells, diminished labyrinthine nerve fibers, diminished visual, auditory, and proprioceptive sensations, and diminished integrative abilities.

Nystagmus due to injury to the vestibular system is a to-and-fro movement of the eyes that has a slow component (due to vestibular-ocular reflex) and a fast component. It is named for the fast component. Excitation of one semicircular canal produces eye movement away from that canal (vestibular-ocular reflex). The cortex exerts a quick corrective movement in the opposite direction, resulting in nystagmus. Ocular fixation tends to suppress nystagmus of peripheral vestibular origin. The normally balanced input from the semicircular canals of both ears results in no net eye movement. Most peripheral (vestibular) disorders result in inhibition of one more semicircular canals, and thus nystagmus beating with the quick phase away from the affected ear. Patients with peripheral vertigo feel that the environment is spinning in the direction of the fast component, or that their bodies are spinning in the direction of the slow component. Vestibular nystagmus occurs in the plane of the affected semicircular canal and may be either horizontal or torsional-vertical. Strictly vertical nystagmus is rarely the result of vestibular involvement and usually points to a brain stem origin. It is normal to have a few beats of nystagmus on extreme lateral gaze.

The major characteristics of central and peripheral vertigo are given in Table -1. The etiologies of vertigo are classically separated into peripheral vertigo, which is caused by disease processes affecting structures peripheral to the brain stem (eighth nerve, vestibular apparatus), and central vertigo, which is caused by processes affecting structures central to the brain stem (cerebellum).

Associated symptoms leading away from a vestibular disturbance include headache, loss of consciousness and neurologic symptons including seizures.

The vast majority of patients with vertigo seen in emergency practice have peripheral vertigo. Peripheral vertigo is characterized by an intense vertiginous or whirling feeling, often accompanied by profound associated symptoms such as nausea, vomiting, sweating, pallor, diarrhea, and alteration of blood pressure and pulse. Impulsion is very strongly suggestive of peripheral vertigo. These symptoms may be of abrupt onset. Peripheral vertigo may be dramatically influenced by position change, greatly worsened by movement or by the assumption of certain positions of the head, and is extremely distressing to the patient. The symptoms of patients with peripheral vertigo resemble those of classic motion sickness.

Vestibular neuronitis is characterized by peripheral vertigo without hearing loss. If tests of cochlear function are done, they show no abnormality. Patients may complain of fullness in the ear or tinnitus. Positional nystagmus occurs in one-third of cases. Caloric vestibular testing is usually abnormal on one side. This illness is of suspected viral origin and may occur in epidemics. It may be a mild viral encephalitis affecting the brain stem or a neuronitis affecting the vestibular nerve. The exact site of the lesion is not known. Patients typically complain of acute onset and severe symptoms and may have had an upper respiratory infection in the preceeding two to three weeks. The vertigo is worsened by any movement of the head. It may last for days, and residual symptoms may persist for weeks. Most cases of casually diagnosed labyrinthitis probably fall into this category.

Labyrinthitis is characterized by peripheral vertigo associated with hearing loss. While the etiology of many cases of labyrinthitis is a presumed viral infection, there is no proof of this. Occasional cases occur in association with mumps and measles. Bacterial labyrinthitis is an extremely rare condition usually associated with long-standing otitis media with fistula, meningitis, mastoid disease, dermoid tumor, or postsurgical infection. Bacterial labyrinthitis is potentially devastating and requires appropriate antibiotic therapy.

If there is a perilympathic leak from a fistula at the round or oval window, pneumatic changes in the middle ear may be transmitted to the labyrinthine apparatus and cause subjective vertigo. This may occur as a result of trauma. Patients with perilymphatic fistula complain of intermittent or positional vertigo exacerbated by straining, sneezing, and coughing, which may also cause such a fistula. Fluctuating hearing loss occurs. Hennebert's sign, which is subjective vertigo and nystagmus induced by pneumatic otoscopy, is diagnostic.

Menière's disease is a condition characterized by recurrent attacks of severe vertigo, vomiting, and prostration, and usually associated with progressive deafness and tinnitus. It tends to run a recurrent and protracted course over time associated with less severe attacks of vertigo and progressively more severe deafness. It occurs in middle age, and in men and women equally. While little is known about the underlying etiology, there is a gross dilatation of the endolymphatic system of the internal ear.

The typical history in Menière's disease is that of a patient over the age of 50 with slowly progressive tinnitus and deafness in one or rarely both ears over months to years who suddenly develops severe vertigo. It may occur so suddenly that the patient falls. More commonly, it worsens over several minutes. There is an intense sensation of rotation, more commonly of the surroundings than of the patient. nausea and vomiting are common and may be severe. The pulse may be rapid or slow, and the blood pressure raised or lowered. Occasionally patients may develop diarrhea. There may be profound diaphoresis. Preexisting deafness and tinnitus, usually unilateral, may become intensified. The attack may last from half an hour to many hours with gradual offset. The patient is frequently unable to stand or walk and may be unsteady and staggering on attempted ambulation. Between attacks, deafness, usually unilateral, is found. The attacks often occur at regular intervals separated by weeks to years. The severity of the attacks tends to diminish and finally cease as deafness increases. A similar picture may be produced by tertiary syphilis. Tumors at the cerebellopontine angle, such as acoustic schwannoma, may produce progressive unilateral hearing loss and vertigo and simulate Meniere's disease.

A variety of drugs affect the inner ear. Most affect both vestibular and cochlear mechanisms, but the degree to which they affect them is variable. Aspirin in toxic doses affects predominantly cochlear function and produces tinnitus and hearing loss, but little vertigo. Aminoglycosides may produce vestibular neuroepithelial damage before any cochlear damage is evident. Anticonvulsants such as phenytoin may produce exclusively vestibular symptoms. Drugs which affect the inner ear are listed in Table -2.

Benign positional vertigo is a syndrome in which patients have repeated attacks of vertigo precipitated by changes in posture, typically a sudden turning of the head as in rolling over in bed. There is no acute hearing loss or tinnitus. It is a very common cause of vertigo, and the most common cause in the elderly. The attacks usually last a few seconds to minutes, and usually subside within a few weeks. Nylen-Barany (Hallpike) testing is diagnostic, and distinguishes between peripheral and central vertigo (Table -3). Some patients with positional vertigo may not have nystagmus elicited on exam. Benign positional vertigo is also known as Barany's vertigo, and is thought to result from calcium carbonate crystals which have detached from the otoconia of the utricle and fallen against the cupula of the posterior semicircular canal.

Eighth-nerve lesions, such as acoustic schwannomas or meningiomas, may affect the eighth nerve and produce vertigo. Typically, this gradual-onset vertigo is preceded by hearing loss, and there may be other symptoms to suggest involvement of the cerebellopontine (CP) angle, such as a constant unsteadiness or ataxia and a chronically progressive course. Patients typically complain more of unsteadiness than vertigo. Patients with unilateral sensorineural hearing loss, including those who seem to have Meniere's disease, should be evaluated for cerebellopontine angle tumor.

Many patients with tumors at the CP angle, such as meningiomas and dermoids, exhibit chronic deafness and disequilibrium, and occasionally vertigo. They may demonstrate ipsilateral impairment of the corneal reflex, facial weakness, and cerebellar signs on the involved side.

The delicate labyrinthine membranes are susceptible to accelerational forces, and head trauma may result in unilateral contusion or concussion to the labyrinth. After cerebral concussion, up to 20 percent of people develop vertigo. Acute posttraumatic vertigo caused by labyrinthine concussion begins immediately after head injury and results in continuous vertigo, nausea, and vomiting. Symptoms usually improve over the first few days, with gradual resolution over a few weeks. Posttraumatic positional vertigo may develop days to weeks after injury, and may replace the constant vertigo of acute posttraumatic vertigo. Symptoms are precipitated by changes in head position, as with benign positional vertigo. Symptoms tend to resolve over months, and most are gone by 2 years post injury.

A condition of severe brief attacks of vertigo in children, usually under the age of 3 years, benign paroxysmal vertigo of childhood, is generally self-limited, resolving spontaneously within months to a few years. It is felt to be labyrinthine in origin and of unknown etiology. Because vertigo may represent the aura of a seizure, EEG might be considered in very selected cases of childhood vertigo.

Central vertigo is characterized symptomatically by a much less dramatic vertiginous feeling than peripheral vertigo and is not exacerbated by motion or by assuming specific positions. Typically, central vertigo is not an intense feeling, and has little or no associated nausea, vomiting, pallor, or diaphoresis. The onset is gradual. The nystagmus characteristic of central vertigo may be present in the absence of the subjective sensation of vertigo. Central vertigo is produced by conditions that affect the cerebellum and brain stem. All conditions that affect the brain stem and cause vertigo typically have other brain stem signs associated with them, such as dysphagia, dysarthria, ataxia, diplopia, facial numbness, bilateral limb weakness, or bilateral visual blurring. Oscillopsia may occur.

Conditions producing central vertigo affect the brain stem and cerebellum. Hearing is characteristically unimpaired, and tinnitus is rare. Cerebellar infarction and hemorrhage may result in central vertigo. The typical history of cerebellar hemorrhage is acute vertigo and ataxia, with or without nausea and vomiting, and with or without acute headache. Less typically there may be conjugate eye deviation to the side opposite the hemorrhage, or a sixth-nerve palsy. The patient with cerebellar hemorrhage may not be able to sit without support, although casual neurologic testing done only in the supine position or a supported position may not be abnormal. Cerebellar infarction may present in a similar fashion. Vertigo from cerebellar disease may be described as recurrent front-to-back or side-to-side movement, which may be evoked by position change.

Conditions affecting the brain stem can produce vertigo as part of their clinical symptomatology, particularly lateral medullary infarction (Wallenberg's syndrome), which consists of vertigo; ipsilateral paralysis of the soft palate, pharynx, and larynx with dysphagia and dysphonia; ipsilateral facial numbness with loss of corneal reflex; ipsilateral Horner's syndrome; and ipsilateral cerebellar asynergia and hypotonia. Sixth-, seventh-, and eighth-nerve lesions have been reported with vertigo, nausea and vomiting, nystagmus, and hiccups. There is contralateral loss of pain and temperature on the limbs and trunk.

Transient ischemic attacks affecting the brain stem may produce similar short-lasting symptoms and positional nystagmus, but by definition must include more than simply vertigo. Other structures in the brain stem must be affected in order to render the diagnosis.

Neoplasms of the fourth ventricle, typically ependymomas in young patients and metastases in elderly patients, can likewise affect the brain stem.

Multiple sclerosis, with its myriad manifestations, may produce isolated lesions in the brain stem, producing vertigo and other brain stem findings. Marked nystagmus with little no vertigo should suggest a brain stem origin.

Physiologic vertigo, as in motion sickness, results from mismatched vestibular, visual, and somatosensory input. Similar mismatch may occur when the visual sensation of motion, as in watching a movie of an automobile chase, is not accompanied by matching vestibular input.

Vertigo may occur on a psychogenic basis, typically as a long-standing vertiginous feeling unaffected by motion and position and without associated nausea or vomiting. As a prodrome to seizure, a cortical focus may produce transient vertigo prior to the seizure. This is very rare. Rare ocular causes of vertigo include watching a rapidly moving series of objects, such as the car or train from a stationary position or telephone poles from a moving car, inducing a sensation of vertigo and motion sickness. Recent ophthalmoplegia may cause brief vertigo. Serous labyrinthitis due to otitis media may produce vertigo.

The blood supply to the inner ear is not supported by a collateral circulation, and is tenuous. However, direct evidence for reduced blood flow to the inner ear as a cause of vertigo is lacking. While it is postulated that vertigo may occur as a result of imbalanced proprioceptive input due to cervical muscle lesions, its clinical occurrence is doubtful. Basilar migraine may cause throbbing occipital headache, visual hallucinations, vertigo, tinnitus, dysarthria, and drop attacks. Patients with herpetic vesicles of the auditory canal and fascial palsy (Ramsay Hunt syndrome) may have deafness and vertigo.

Disequilibrium syndrome consists of an ill-defined dizziness as a result of multiple sensory abnormalities. There is a chronic mismatch of input from the body systems providing spatial orientation. The patient, typically elderly, may have diminished vision, diminished hearing, and diminished proprioceptive, cerebellar, or peripheral neurologic function. The disequilibrium may be exaggerated or precipitated by sudden worsening in one or more of these sensory modalities, and typically worsens at night when diminished ambient lighting reduces visual input. Unfamiliar situations and surroundings may exacerbate the symptoms. Sedative medications can exaggerate or precipitate the problem. Typically these patients have multiple etiologies for near syncope as well; at times it is difficult to establish a precise diagnosis.

Patients with ill-defined light-headedness frequently cannot characterize their symptomatology in any way that is useful for the physician. They may have concomitant complaints of generalized fatigue or aching and nonfocal weakness. It is very difficult to ascribe a specific etiology to these subjective complaints.

Some patients with dizziness or light-headedness may suffer from a primary hyperventilation syndrome. Reproduction of their symptoms with directed hyperventilation aids in the diagnosis. Primary hyperventilation must be distinguished from hyperventilation secondary to a variety of medical disorders or insufficient oxygenation.

Anxiety itself may produce dizziness characterized by disequilibrium. Many times the dizziness has been present for very long periods of time, there is no clear relationship to any exacerbating or precipitating factors, and the history and physical and neurologic examinations do not reveal any recognizable pattern. It is sometimes difficult to isolate other possible causes of dizziness when the patient presents with a host of symptoms seemingly precipitated by anxiety.

Patients with near syncope may complain of dizziness. On detailed questioning, it can usually be elicited that patients have a feeling that they would pass out if the symptomatology became worse. The causes of syncope and near syncope are essentially identical and only differ in magnitude. Near syncope may be produced by orthostatic, autonomic, reflex, and cardiac mechanisms, or by hypoglycemia. Possible orthostatic causes include volume depletion, poor conditioning, venous insufficiency, peripheral neuropathy including that produced by diabetes mellitus, and the effects of antihypertensive, vasodilating, and anti-Parkinson drugs. Preganglionic autonomic dysfunction, such as that presenting with Shy-Drager syndrome, may produce a near syncopal feeling. Reflex causes include a hyperactive carotid sinus, micturition, cough, and swallow syncope. Vasovagal syncope is actually less common in elderly patients and may be associated with multiple causes for stress or prolonged bed rest. Cardiac mechanisms for syncope include mechanical causes, such as valvular disease or subaortic stenosis, and arrhythmias.

Despite thorough history, physical, and neurological exam, extensive neurological and cardiac testing and specialty follow-up, many patients will not have a cause for their dizziness found.

In intensive studies of patients with persistent dizziness, only about one-half have a single cause.

Most causes of vertigo are benign, but potentially disabling. Some forms of dizziness may represent life-threatening emergencies, e.g., arrhythmia. Since the primary problem in the diagnosis of a patient with dizziness is establishing a precise definition of the patient's symptomatology, the history is of paramount importance. There is nowhere that the classic neurologic approach to the patient (defining the nature of the disturbance first and its localization second) is more important.

Even though the symptoms may be very difficult for the patient to describe, it is important not to ask leading questions or to suggest to the patient what the symptoms might mean because patients may incorporate the words used by the examiner into the description of their symptoms, whether they fit or not. In general, patients must be given time to elaborate exactly what the subjective feeling of dizziness means to them. At some point it must be established whether or not they have a vertiginous feeling. Whether the feeling is that of syncope should be determined, as well as the relationship to movement, head position, and particular postures.

The temporal profile at onset, such as the rate of development of symptoms and the duration of symptoms, should be elicited. The time of day of any worsening of symptoms should be elicited. All associated symptoms, such as nausea, vomiting, blurriness or double vision, tinnitus, focal or generalized weakness, numbness, visual loss, palpitations, and loss of consciousness should be noted. Past medical facts of most importance are the use of medications, both prescribed and over the counter, any history of trauma, and a history of similar episodes.

The physical examination should focus on several areas. Bedside tests of hearing and physical examination of the ears should be done. Eye movements, with particular emphasis on nystagmus, both direction and fatigue, should be evaluated. The details of cranial nerve testing are important, particularly eighth-nerve function; the cranial nerves most closely associated with the eighth nerve, specifically fifth-nerve function, including corneal reflex; seventh-nerve function; and ninth- and tenth-nerve function (gag reflex, swallowing). Of particular importance on the motor examination is testing of coordination, such as finger-to-nose testing or rapid alternating movements. Gait testing and an evaluation of the patient's ability to sit without support, as a test for truncal ataxia, may be necessary. Orthostatic vital signs are not reliable unless there are marked changes and reproduce identically the clinical symptomatology. The range of pulse and blood pressure changes in normal patients is wide and encompasses many recommended parameters for the diagnosis of orthostasis.

Perhaps the best bedside test of hearing is that of the soft whispered voice. One masks the ear not being tested with light pressure on the external canal or by rubbing the fingers in front of it and whispers names or letters in the unmasked ear that the patient must repeat. If there is a decrease in hearing, then Webber's and Rinne's test may be done to help distinguish between conductive and neurosensory loss.

Of particular importance in the evaluation of the potentially vertiginous patient is the Nylen-Barany maneuver outlined in Table 194-3. The type and duration of nystagmus are noted. In addition to the findings noted in the table, peripheral vertigo is more likely than central vertigo to be associated with nausea and vomiting and relatively severe symptoms (Table -1).

Other tests can be done as indicated by the initial history and physical examination. Drachman's dizziness stimulation battery is given in Table -4.

Of particular importance on the cardiac exam is to note the rate and rhythm of the heart and to evaluate for evidence of valvular heart disease.

History and physical examination alone may provide the diagnosis in the vast majority of patients.

Laboratory testing is selected based on the history and physical examination. Glucose testing in particular may be a productive test in patients with disequilibrium syndrome. Diabetes is one major cause of diminished peripheral neurologic function. In patients with typical peripheral vertigo and little else to suggest other medical problems, laboratory testing is not needed. In patients with presyncopal feeling, cardiac rhythm monitoring may be in order. Depending upon the physical examination, other testing to detect cardiac etiology may be indicated, such as echocardiography, ambulatory cardiac rhythm monitoring, etc. In the evaluation of long-term hearing loss with vestibular dysfunction, serologic testing for syphilis is commonly done.

When cerebellar hemorrhage or infarction is suspected, CT scanning should be considered. If tumor at the CP angle is a possibility, CT scanning may be done, although MRI is more sensitive. Patients with suspected central vertigo will require an imaging study and neurologic consultation. Most patients with peripheral vertigo and no suspicion of eighth-nerve lesion or CP angle tumor do not require an urgent imaging study.

The principle of most importance in emergency department management is to firmly establish the nature of the patient's dizziness. Virtually all of the medications that are useful for peripheral vertigo will result in worsening symptoms of patients with disequilibrium syndromes or ill-defined light-headedness.

There are multiple medications used in the emergency department and outpatient management of peripheral vertigo. Antihistamines have been known to be effective for the treatment of peripheral vertigo for 40 years. Not all antihistamines are useful, and their peripheral potency as antihistamines does not correlate with suppression of vertigo. The most useful ones have anticholinergic properties. Antihistamines may act both centrally, at the brain stem level, and peripherally, within the labyrinthine apparatus. Anticholinergics such as atropine and scopolamine are also quite effective. The efferent nerves of the vestibular sensory cells are cholinergic, and thus affected by anticholinergics. The central effects of anticholinergics may also mediate their action. Diazepam acts centrally on the lateral vestibular nucleus and is useful in acute peripheral vertigo. More recently the calcium channel blocker flunarizine has been found useful in the management of vertigo. Other commonly used antiemetics, such as prochlorperazine and chlorpromazine, are of little use in relieving patients with vertigo. Hydroxyzine and promethazine, however, with their antihistaminic activity, are. Effective agents for the management of peripheral vertigo are listed in Table -5.

Most patients need reassurance that the symptoms, while overpowering, are self-limiting, are not a reflection of serious pathology, and are not a serious threat to their health. An explanation that symptoms are caused by an imbalanced input from the two ears, and that the nervous system will accommodate to it, is helpful. The component of management that usually requires little explanation for the vertiginous patient is that of either bed rest or resting in a position of comfort and a slowing of all movements so as to not precipitate the vertiginous feeling. Visual fixation on a nearby object may inhibit vertigo of peripheral origin and is preferable to lying with closed eyes.

The efficacy of the many regimens used in the chronic treatment of Menière's disease (low salt diet, ammonium chloride, diuretics, glycerol) has not been proved. Acute management is the same as for other forms of peripheral vertigo. Surgical destruction of the labyrinth or endolymphatic shunt can be done in the long-term management of Menière's disease.

Benign positional vertigo (Barany's) is treated with the same medications as other peripheral disorders, but is seldom very responsive. Some advocate repeated head movement to provoke attacks, fatiguing the response and or dispersion of the otolithic fragments.

In cases of disequilibrium syndrome, if no specific causes are found, one might consider withdrawal of any sedative or hypnotic medications. If the problem appears to be one of multiple sensory deficit syndrome, consideration of changes in ambient light, especially later in the day, and changing some factors in the surroundings may be indicated.

Emergency department management of patients with near syncope is similar to that for those with syncope.

For ill-defined light-headedness, when it is impossible to place the patient in a better-defined category of dizziness and when preliminary emergency department testing does not indicate any specific pathology, it is best to avoid medications used for vertigo.

The evaluation of the dizzy patient is a challenge to the skills of the physician. An initial open-ended history is important to define the clinical symptomatology precisely, without suggesting a particular entity. Precision in history taking will be rewarded by narrowing the field of potential insults causing symptoms. A thorough neurologic examination, with particular emphasis upon nystagmus, must be done. If vertigo is indeed the problem, one must separate peripheral (benign) causes from more ominous central causes. Recognition that symptoms may be quite disabling yet reflect benign processes may be reassuring to the patient. Careful selection of medications for vertigo can only be done when the syndrome is precisely defined and should be avoided unless the diagnosis of peripheral vertigo is established.

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Peripheral origin
Intense spinning, swaying or impulsion
Nausea, vomiting, possibly diarrhea
Diaphoresis
Aggravated by change of position, movement
Possible tinnitus, hearing loss
Acute onset
Fatiguable, unidirectional nystagmus
Nystagmus inhibited by ocular fixation
Central origin
Ill-defined, less intense vertigo
Not positionally related, concomitant brain stem or cerebellar signs and
symptoms (diplopia, dysphagia, facial numbness or weakness, ataxia,
hemiparesis)
Nystagmus not inhibited by ocular fixation
Nonfatiguable, multidirectional nystagmus

Antibiotics           Cytotoxic agents
Aminoglycosides             Vinblastine
Erythromycin     Cisplatin
Minocycline      Nitrogen mustard
Diuretics              Anticonvulsants
Ethacrinic acid   Phenytoin
Furosemide        Barbiturates
Bumetanide        Carbamazepine
Nonsteroidal anti-inflamma-            Ethosuccimide
   tory agents        Others
Salicylates          Quinine
Ibuprofen            Chloroquine
Naproxen            Propylene glycol
Indomethacin     Ethanol
               Methanol
               Mercury

Test:   Patient is in sitting position on stretcher. Clinician supports head
        and has patient rapidly assume supine position, first with head straight, then
        with head turned 45 degrees left, then 45 degrees right.
Findings with peripheral vertigo:
        Vertigo and nystagmus produced, latency 2–20 s
        Duration less than 1 min
        Unidirectional nystagmus
        Nystagmus and vertigo fatigue with repeated testing
        Even straight head position may elicit vertigo (Barany's)
Findings with central vertigo
        Latency of nystagmus, none
        Nystagmus nonfatiguing, multidirectional
        Duration greater than 1 min