Chapter 14. The Dizzy Patient The Dizzy Patient: Introduction

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CHAPTER 14. THE DIZZY PATIENT THE DIZZY PATIENT: INTRODUCTION

The principal problem in any patient complaining of "dizziness" is defining the problem. Dizziness is not a medical term and must be clarified (through careful history taking) and categorized into one of four general groups: vertigo, disequilibrium, presyncope, and nonspecified lightheadedness. The key for the clinician is to identify potentially lifethreatening conditions, specifically distinguishing a central nervous system process from a peripheral one.
CLASSIFICATION Vertigo
Vertigo is the feeling or sensation of movement. This may be described by the patient as swaying, spinning, whirling, leaning, or tilting. In general, when there is a definite illusion of movement, the problem lies somewhere along the peripheral or central nervous system pathways related to the vestibular apparatus.
Presyncope
Presyncopal episodes are often described by patients as dizziness. Unlike the vertiginous patient, however, these patients will describe an impending loss of consciousness. They feel as if they are about to faint and may describe the sensation as lightheadedness or "graying out" (see Chapter 13).
Disequilibrium
Equilibrium depends on a constant stream of sensory information from the vestibular, proprioceptive, and visual systems. This information is integrated by cerebellar centers and influenced by the extrapyramidal pathways to produce confident and rhythmic motion by the patient. Patients with various problems in any of these systems, such as the decreased proprioception as seen in diabetic patients with peripheral neuropathy or decreased vision, may experience disequilibrium. Most such patients have comorbidities with minor defects in multiple systems, which in combination produce a sense of imbalance, without a sensation of motion, however.
Nonspecified Lightheadedness
The most difficult patients are those who do not fall into any of the three groups mentioned above. These patients generally have extremely vague histories and are unable to pin down any specific symptoms. This group includes patients with hyperventilation syndromes, anxiety neuroses, and other psychiatric disorders. Diagnosing this group represents a considerable challenge to both the patience and the skill of the physician. The focus of this chapter is to provide a framework for approaching the patient with a chief complaint of dizziness, primarily in order to distinguish central from peripheral etiologies. Hypoperfusion states causing presyncope, neuropathies causing disequilibrium, and systemic processes causing generalized weakness are presented in other chapters, although they are important conditions that should be considered when approaching these patients.
EPIDEMIOLOGY
Dizziness is a common component of many acute medical conditions. The incidence increases with age and is one of the most common chief complaints in patients over 75 years of age.1 Dizziness accounts for up to 5% of emergency department (ED) visits and contributes to the ED presenting complaint in up to 24% of patients.2 True vertigo accounts for approximately half of patients complaining of dizziness, 17% to 42% of who ultimately receive a diagnosis of benign paroxysmal positional vertigo (BPPV).3 Of those patients with vertigo, vertebrobasilar insufficiency and posterior circulation stroke are the most concerning diagnoses to be considered and pose the greatest risk management concern for the practicing emergency physician.4 Even in the absence of posterior circulation disease, dizziness from all causes is associated with disability and injury, especially from falls in the elderly.
PATHOPHYSIOLOGY OF VERTIGO
Vertigo results from dysfunction in the vestibular system from either its peripheral or central components. The peripheral vestibular apparatus includes the labyrinth located in the petrous portion of the temporal bone and the vestibular portion of the eighth cranial nerve, which courses through the cerebellopontine angle connecting the labyrinth to the brainstem. The labyrinth is composed of three semicircular canals, which register head rotation, and the otoliths (utricle and saccule), which sense head position relative to gravity. The central vestibular apparatus consists of vestibular nuclei at the pontomedullary junction in the brainstem; these nuclei are intimately connected to the nuclei controlling eye movement and the cerebellum. Position is registered centrally based on balanced input from the paired labyrinths.
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Vertigo occurs when input from two labyrinths is unequal; the resulting unbalanced input creates the sensation of movement. In general, acute processes result in vertigo. Chronic processes, such as degenerative disease or expanding tumors, usually result in disequilibrium but not actual vertigo since the brain has time to accommodate to the deficit.
DIFFERENTIAL DIAGNOSIS Central Vestibular Causes

Although less common than peripheral causes, central causes of vertigo are the most concerning (Table 14-1). Disorders include vertebrobasilar insufficiency, brainstem and cerebellum infarct, and hemorrhage; basilar artery migraine, cerebellopontine angle (CPA) tumors, and degenerative diseases are other considerations.
Table 14-1 Differential Diagnosis of Dizziness Peripheral vestibular causes Benign paroxysmal positional vertigo Vestibular neuritis Vestibular neuronitis Labyrinthitis Mnire's disease Perilymphatic fistulas Central neurologic causes Transient ischemic attack/stroke Vertebrobasilar ischemia Cerebellopontine angle mass Basilar artery migraine Multiple sclerosis Multisensory deficit syndrome/disequilibrium syndrome Cardiopulmonary causes Arrhythmias Postural hypotension Hypovolemia (anemia) Myocardial ischemia Structural cardiac or valvular disease Hypoxia Vasovagal episode (also neurologic) Other Drug effects Thyroid disorder Hyperventilation Anxiety/panic disorder
Table 14-2 summarizes findings that help to distinguish central from peripheral vertigo. In general, when compared with peripheral vertigo, the symptoms of central vertigo are less acute, more persistent, and associated with neurologic deficits. Symptoms associated with brainstem ischemia include diplopia, ataxia, dysarthria, or facial weakness. However, many exceptions exist, and clinicians must always have a high index of suspicion, especially in those patients with cardiovascular risk factors. Of note, even patients with no cardiovascular risk factors may develop central vertigo, e.g., from vertebral artery dissection or from cardiac emboli. Slowly growing lesions such as acoustic neuromas do not generally produce symptoms because compensatory mechanisms have time to evolve. Indeed, it is these compensatory mechanisms that facilitate recovery from acute insults. CPA tumors and posterior fossa masses may produce vertigo, or if their principal involvement is the cerebellum, they may produce only a feeling of unsteadiness. Such disequilibrium is usually unrelenting and progressive and may move to involve multiple cranial nerves and long tract signs.
Table 14-2 Peripheral Vertigo versus Central Vertigo Central Peripheral
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Intensity Tinnitis CN findings Nystagmus Visual fixation Horizontorotary Vertical Latency Fatigue
Mild Rare Frequent
Severe Common None
No inhibition Rare Common None None
Inhibits Common Never 340 s Yes
Benign Paroxysmal Positional Vertigo

Benign paroxysmal positional vertigo is the most common cause of peripheral vertigo and most common cause of recurrent vertigo with a lifetime prevalence of 2.4%.5 This syndrome is characterized by a rapid onset of vertigo, associated with a change of head position, which lasts less than 30 to 60 seconds (Table 14-3). Often, patients will complain of the acute onset of symptoms after rolling over in bed, gazing upward, or bending forward. Findings include a horizontal/rotary nystagmus with associated nausea and/or vomiting. Characteristically, symptoms abate when the patient lies still with the eyes closed. The pathogenesis of this condition is thought to be due to the accumulation of freefloating calcium carbonate particulate debris that forms a plug in the posterior semicircular canal, which accounts for approximately 80% of cases of BPPV.6 When the affected canal is down, as when the patient is in a recumbent position, the calcium carbonate plug acts as a plunger and stimulates the labyrinth. The latency reflects the time required for the plug to move in the canal and stimulate the system; fatigue reflects the process of the plug breaking apart. A history of prior head trauma has been linked to the onset of BPPV, presumably due to dislodged endolymphatic debris.
Table 14-3 Characteristic Findings in Benign Paroxysmal Positional Vertigo Episodic periods of vertigo lasting less than 1 minute Provoked by head movement Nystagmus that has delayed onset and short duration Fatigability of nystagmus on repeat testing Reversal of nystagmus on returning to an upright position Surpression of nystagmus with visual fixation
Mnire's Disease
Mnire's disease is a peripheral nervous system disorder resulting from an increase in endolymph volume (endolymphatic hydrops). Distention of the endolymphatic system results in vertigo, and the increased pressure on hair cells results in an associated hearing loss. The duration of the vertigo and nausea/vomiting in Mnire's disease tends to be hours rather than seconds, as in BPPV. Onset is most frequently in the fifth decade of life. It also differs from BPPV in that it is associated with a sensation of "fullness" in the affected ear with a fluctuating sensorineural hearing loss and tinnitus. Disequilibrium may also be present.
Vestibular Neuritis and Neuronitis

Vestibular neuritis results when the vestibular nerve becomes infected and results in an imbalance of input from the labyrinths causing vertigo. Vestibular neuronitis implies damage to the sensory neurons of vestibular ganglion; the two terms, neuritis and neuronitis, are often used for the same clinical syndrome reflecting difficulty localizing the site of the lesion since they often occur on a continuum. Neuronitis may evolve and involve damage to the brainstem vestibular nucleus and consequently result in hearing loss. Vestibular neuritis and neuronitis cause a constellation of symptoms that includes acute-onset vertigo, nausea, vomiting, and disequilibrium. It is thought to be viral in etiology, generally occurring in otherwise healthy individuals. As mentioned above, hearing remains unimpaired when only the vestibular apparatus is involved, i.e., all audiologic testing is normal, versus impaired hearing that accompanies a neuronitis. No brainstem findings or other cranial nerve abnormalities are found. The time course of symptoms tends to be over a period of days, with symptoms usually peaking during the first day and then gradually improving over the next few days. As may be seen with all the peripheral causes of vertigo, the patients appear acutely and severely ill.
Labyrinthitis
Labyrinthitis may be differentiated from vestibular neuritis in that there is both nystagmus and vertigo along with hearing loss. Viral labyrinthitis has been reported in association with multiple-viral illness and is generally short-lived and of little consequence. Bacterial labyrinthitis, however, can occur in patients with middle ear disease with fistulas, or mastoid disease, or in association with meningitis. Viral labyrinthitis is generally painless; when pain is present, a bacterial
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etiology should be suspected. These patients represent a medical emergency and require prompt diagnosis and treatment.
Posttraumatic Vestibular Syndromes

Perilymphatic fistulas between the middle and inner ear may result after trauma, after a forceful Valsalva maneuver, or after acute external pressure changes as in scuba diving. Replication of the patient's symptoms on Valsalva maneuver or pneumatic otoscopy, combined with a suggestive history, is diagnostic. Acute traumatic tympanic membrane rupture can also lead to immediate onset of vertigo, nausea, and/or vomiting associated with hearing loss. A similar constellation of symptoms can be seen in patients with fractures through the petrous portion of the temporal bone.
Disequilibrium Syndromes (Multisensory Deficits Syndromes)

A generalized feeling of unsteadiness in the nonvertiginous elderly patient usually represents a multisensory deficits syndrome. These patients frequently relate that their problem is worse in the evening when they are fatigued and their visual inputs are diminished. Such patients frequently do well in familiar surroundings where only minimal information is necessary for them to make decisions but do poorly in unfamiliar situations. Multisensory deficits can be tremendously exaggerated by medications including those used to treat vertigo.
Other Causes
Other causes of dizziness include drug toxicity, hypoglycemia, anemia, hypothyroidism, and multiple sclerosis; psychiatric causes include anxiety and hyperventilation, although these diagnoses are ones of exclusion and rarely definitively made by emergency physicians. All tranquilizers, antiepileptic drugs, and antipsychotic drugs may, through multiple mechanisms, cause a combination of disequilibrium, near-syncope, and mild forms of vertigo that the patient may be unable to separate on a historical basis (Table 14-4). Ototoxic drugs that cause a sense of unsteadiness and hearing loss rarely actually cause vertigo since the deficits are bilateral.
Table 14-4 Drugs Associated with Dizziness Anticonvulsants Alcohols Aminoglycosides Other antibiotics Heavy metals Cinchona alkaloids Salicylates Minor tranquilizers Major tranquilizers Diuretics -Blockers -Blockers Centrally acting antihypertensives
Migraine-related vertigo accounts for up to 14% of vertigo cases in adults.7 Making the diagnosis for migrainous vertigo involves first ruling out other causes of vertigo and criteria include episodes of vertigo, migraine according to International Headache Society criteria, and at least two of the following symptoms during the events: headache, photophobia, phonophobia, visual, or other aura.
EVALUATION
Patients presenting with a complaint of dizziness require a complete set of vital signs and an assessment at triage for cardiovascular risk factors. Oxygenation and cardiovascular stability should be assessed; if fluid intake has been compromised, dehydration needs to be addressed. Patients with vertigo are at risk of vomiting, and thus appropriate precautions should be taken. Vertigo/dizziness may be a symptom of stroke; since many triage screens do not take posterior circulation deficits into consideration special care must be taken in select patients upon initial presentation to the emergency department.
History
The key to diagnosis of the dizzy patient lies in careful history taking, allowing the patient to describe the symptoms. The correct etiology of dizziness can be made by history alone in over half of patients seen8 (Table 14-5). If patients report that they have a sense of motion or spinning, follow-up questions regarding relationship of symptoms to position and movement are important. The time course for various causes of vertigo may also be helpful: BPPV usually has an abrupt onset, vertebral basilar insufficiency may develop over minutes or have a stuttering course, Mnire's syndrome has
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vertigo that may last for hours, and vestibular neuronitis and labyrinthitis have persistent symptoms for days. Patients with near-syncope as the underlying mechanism of their dizziness will frequently have an increase of symptoms with autonomic stress. Information about the relationship to orthostatic change as well as swallowing, coughing, and urinating may be helpful. Patients with disequilibrium have particular difficulty when one of their sensory modalities is reduced. In particular, older patients with decreasing vision find that in the evening when rooms are inadequately lighted, they have considerably more difficulty in walking. Also, patients with multisensory deficits have greater difficulty as the day progresses and fatigue affects their system. A seemingly endless list of drugs may cause not only vertigo but also generalized weakness and/or autonomic changes that may be interpreted by the patient as dizziness. Many of the medications that affect blood pressure, electrolytes, or central or peripheral nervous system structures may be the cause of the patient's symptoms. A history of both prescription drugs and over-the-counter medications used should be elicited.
Table 14-5 Historical Features Important to Characterize in a Patient with a Chief Complaint of Dizziness/Vertigo Sensation of motion, whirling, spinning, tilting, leaning Relation to change of position, sharp turns, specific positions Rate of onset and duration of symptoms Relation to autonomic nervous system stress Time of day Drugs and medications: prescription and nonprescription Associated symptoms: nausea, vomiting, blurred vision, loss of vision, motor weakness, hearing loss, tinnitus, headache, difficulty speaking or swallowing, incoordination Other medical problems (thyroid disease, diabetes, hypertension, stroke)
There are several caveats that need to be highlighted in the history of patients with dizziness/vertigo. Head motion or position that triggers the symptom suggests a peripheral etiology. However, this is true only if the events are brief and episodic; it is not true if the event is a single event that lasts hours to days and yet is exacerbated by position. Cardiac events and TIAs that cause vertigo are generally spontaneous and not position related; strokes may produce persistent dizziness or vertigo that is made worse with changes in position or turning of the head.4
Physical Examination
The physical and neurologic examination should be performed systematically with a focus on the vital signs, cardiovascular system, cranial nerves, posterior column, and sensory functions. The head examination should assess for evidence of trauma. Examine the tympanic membranes and external auditory canals for the presence of infection or tympanic membrane rupture. Impacted cerumen or foreign body should not cause vertigo but may give a sense of disequilibrium. Clinical findings of otitis media raise concerns for a labyrinthitis. The eye examination includes checking for the presence of nystagmus.3 Peripheral vestibular nystagmus is typically horizontal rotatory with a slow and fast component. The fast component points away from the affected side. It typically extinguishes with repeated testing or ocular fixation.4 In peripheral disease the nystagmus is in a constant direction regardless of direction of gaze, although the intensity of the nystagmus may vary. The nystagmus increases in intensity with gaze in the direction of the fast phase. Visual fixation will reduce the intensity of nystagmus in peripheral disorders. Central disorders can produce nystagmus that changes direction with gaze (gaze-evoked nystagmus), although nystagmus can be present in only one direction of gaze. Vertical nystagmus that is spontaneous and nonfatigable represents a central pathology until proven otherwise. Visual fixation does not affect the degree of nystagmus produced by central disorders. A cardiovascular examination should be done particularly in patients at risk for cardiovascular disease. The carotid arteries should be assessed for bruits. Bruits suggest carotid stenosis, which may suggest cerebrovascular insufficiency as a cause of the patient's symptoms. A systolic murmur suggests aortic stenosis, which may explain near-syncope or syncope also associated with exertion.
Neurologic Examination
The neurologic examination in the patient with dizziness/vertigo focuses on cranial nerves III, IV, VI, VII, VIII, and IX, and on cerebellar function. Failure to ambulate patients and to assess for ataxia has been identified as a common pitfall in the failure to diagnose stroke in patients presenting with dizziness/vertigo.9 Patients presenting to the emergency department with a complaint of dizziness, vertigo, or imbalance who have a normal neurologic examination have less than 1% chance of having an underlying stroke as the etiology of their presentation.9 Cranial nerve VIII deficits may help elucidate the etiology of vertigo. The best general test of cranial nerve VIII is the use of soft whispered speech. The test is performed by having the examiner whisper letters and numbers in one ear while masking sound in the opposite ear. Masking can be accomplished by simply rubbing the fingers or hair in front of the opposite ear. Soft-whispered speech, whispered-speech, loud-whispered speech, spoken-speech, loud-spoken speech, and finally no response are the levels generally employed for the whispered-speech test.
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The Weber test and Rinne test (see Chapter 3) are used to differentiate conduction from neurosensory disorders. Cerebellar function is assessed using finger-to-nose, finger-to-finger, and rapid alternating movement tests. Ambulation is a key component of the evaluation, although care must be taken to ensure the patient does not fall. Patients with peripheral vertigo are typically able to walk without assistance, whereas patients with an acute cerebellar infarction or hemorrhage are generally unable to ambulate unassisted. Romberg testing is used to distinguish somatosensory deficits from cerebellar processes (see Chapter 3, on the Neurologic Examination).
Diagnostic Maneuvers
The Dix-Hallpike maneuver (Fig. 14-1) (sometimes referred to as the NylenBrny maneuver) is a provocative test designed to precipitate BPPV originating from the posterior semicircular canal (the majority of cases of BPPV) and thus to help distinguish BPPV from central vertigo. It will not be helpful in diagnosing other types of peripheral vertigo. Before doing the test, the clinician should warn the patient that the maneuver may precipitate the vertigo and associated vomiting. The maneuver begins with the patient in the upright position with the head turned 45 degrees to the right; the patient is then quickly moved from the sitting position to a supine position with the head hanging off the edge of the stretcher with the neck extended and the chin pointing slightly upward. The maneuver is then repeated from the sitting position with the head turned 45 degrees to the left. When positive, the patient will, after a brief (up to 60 seconds) latency period, complain of a sensation of rotational vertigo, accompanied by nystagmus. The nystagmus tends to be horizontal or rotatory, with the superior aspect of the eye bearing toward the dependent ear. The sensitivity of the maneuver for BPPV is approximately 80% with a negative predictive value of 52%; therefore, a negative test does not rule out the diagnosis of BPPV.3 Repetition of the maneuver leads to a reduction in the intensity of vestibular symptoms, and thus it is also used in therapeutic management. A video of the maneuver can be found at www.neurology.org/cgi/content/full/70/22/2067.
Figure 14-1
Dix-Hallpike test. (A) For testing the right posterior semicircular canal, the patient sits on the examination table and turns his or her head to the right 45 degrees. This places the posterior semicircular canal in the sagittal plane. The examiner stands facing the patient on the patient's right side or behind the patient. (B) The patient is then moved by the examiner from the seated to the supine position with the head slightly hanging over the edge of the table. The right ear is down and the chin is pointing slightly up. The eyes are observed for the characteristic nystagmus. (Reprinted with permission from Lalwani AK. Current Diagnosis & Treatment in OtolaryngologyHead & Neck
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Surgery. 2nd ed. New York: The McGraw-Hill Companies Inc; 2008.)
Diagnostic Testing
No one panel of tests is indicated for all patients with a complaint of dizziness; instead, testing is tailored to clinical suspicion with a low testing threshold for anemia, hypoglycemia, and pregnancy. Likewise, a single 12-lead ECG is rarely definitive but is indicated along with continuous rhythm monitoring when dysrhythmias are in the differential diagnosis. Neuroimaging is not recommended in clear cases of BPPV.3 It is indicated in patients with signs of a central process, focal neurologic deficits, headache, or risk factors for cerebrovascular disease for which no other explanation of the symptoms can be found. A noncontrast head computed tomography (CT) scan is a reasonable screening test for patients with suspected central lesions causing vertigo, but it has limitations that preclude it from being definitive. Magnetic resonance (MR) brain imaging and angiography are preferred except for detecting acute hemorrhage. MR imaging is more likely to detect subtle brainstem or inferior cerebellar infarction, whereas CT or MR angiography is indicated to assess for vertebrobasilar occlusive disease. Decision making for advanced neuroimaging must take into consideration the patient's presentation, risk factors, and availability for follow-up care. Special mention needs to be made regarding the patient with sudden onset of headache, severe vertigo, vomiting, and cerebellar incoordination. Such patients should be considered as having an acute cerebellar hemorrhage and are best treated as if they have a life-threatening emergency. An emergent noncontrast head CT is indicated. Along with vertigo, patients with acute cerebellar hemorrhage often present with unilateral ataxia, small pupils, vomiting, and diaphoresis. Paralysis of conjugate lateral gaze or sixth nerve palsies may also be seen.
Specialized Neurologic Testing

Audiometry is used in evaluating dizzy patients with unilateral hearing loss. It is helpful in diagnosing Mnire's disease and acoustic neuromas. It is not recommended in the diagnostic evaluation of BPPV.3 Vestibular function testing involves a battery of tests designed to record nystagmus in response to labyrinthine stimulation or voluntary eye movements. It may be helpful in cases of atypical nystagmus, and vestibular dysfunction of unclear etiology; it is not recommended in patients with BPPV.3
EMERGENCY DEPARTMENT MANAGEMENT

Management of vertigo depends on the underlying etiology. Rest, reassurance, antiemetics, and fluids provide the framework for supportive care of these patients. Treatment of acute posterior circulation stroke is time dependent and may include thrombolysis (see Chapter 5).
Therapeutic Maneuvers
The canalith repositioning maneuver (CRP), often called the Epley maneuver (Fig. 14-2), is a noninvasive bedside intervention designed to reposition particulate debris from the posterior semicircular canal to the utricle3,6 (Table 14-6). Once the particulate matter is repositioned, abnormal vestibular input is eliminated. The CRP is reported to have a 40% to 95% success rate in patients with posterior canal BPPV, with a reported odds ratio of 5.1 in favor of conversion of a negative Dix-Hallpike test.3 A video of the maneuver can be found at www.neurology.org/cgi/content/full/70/22/2067. Originally, patients were instructed to restrict postmaneuver activities, to wear a soft collar, and to remain in an upright position for up to 48 hours; these steps are not supported by the literature and no longer recommended.6
Figure 14-2
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Epley maneuver. The patient is taken through four moves, starting in the sitting position with the head turned at a 45 degree angle toward the affected side. (1) The patient is placed into the Dix-Hallpike position (supine with the affected ear down) until the vertigo and nystagmus subside. (3) The patient's head is then turned to the opposite side, causing the affected ear to be up and the unaffected ear to be down. (4) The whole body and head are then turned away from the affected side to a lateral decubitus position, with the head in a face-down position. (5) The last step is to bring the patient back to a sitting position with the head turned toward the unaffected shoulder. (Reprinted with permission from Lalwani AK. Current Diagnosis & Treatment in OtolaryngologyHead & Neck Surgery. 2nd ed. New York: The McGraw-Hill Companies Inc; 2008.) Table 14-6 Canalith Repositioning Maneuver (Epley Maneuver) for Treating Benign Paroxysmal Positional Vertigo 1. Begin with the patient in a sitting position with the head turned 45 degrees toward the side that was positive in the DixHallpike test: calcium carbonate debris settles in the bottom of the posterior canal. 2. Rapidly lay patient down with the head hanging 30 degrees off the edge of the gurney for 30 s. 3. Rotate head clockwise to opposite side so that the other ear is toward the floor for 30 s. 4. Rotate the head so that the face is toward the floor (this will require the patient's body to move from the supine position to the left lateral decubitus position) for 30 s: in this position the debris should enter the common crus of the posterior and anterior semicircular canals. 5. Sit the patient up.
Vestibular rehabilitation exercises are used to promote habituation, adaptation to vertigo. These exercises can consist of repetitive side-to-side head movements performed while lying down, or may involve use of the CRP. Both have been shown to decrease the intensity of vertiginous episodes in BPPV and to facilitate recovery. These exercises can be provided as part of the discharge instructions.3
Vestibular Suppressants
Four categories of medications have been used in the management of vertigo: antihistamines, anticholinergics, phenothiazines, and benzodiazepines. The biggest advantage in these agents is most likely their antiemetic effect. There is no evidence that any medication is effective in treating BPPV and the CRP is the intervention of choice.6 Antihistamines and anticholinergics may work through inhibiting muscarinic acetylcholine receptors. Meclizine is probably the most commonly used antihistamine although dimenhydrinate and diphenhydramine are alternatives. The benzodiazepines may work through inhibiting GABA receptors. In patients with prominent nausea or vomiting, the phenothiazine antiemetics such as promethazine or prochlorperazine may be effective. It is key to emphasize that all the
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medications mentioned may cause drowsiness and indeed may exacerbate symptoms in patients with disequilibrium syndromes, presyncope, or vertigo/dizziness of undefined etiology. Long-term use of these medications may also impair vestibular compensation.
DISPOSITION
Patients with suspected posterior circulation disease require hospitalization or consultation with a neurologist. Admission may be necessary for patients with severe symptoms accompanied by disequilibrium despite therapy (particularly the elderly at risk for falling). Patients discharged home should be advised not to drive and to minimize situations in which falling could cause harm. The canalith repositioning procedure is recommended in the literature as the treatment of choice for BPPV. Vestibular suppressant medications are of questionable value and potentially dangerous in patients with disequilibrium, presyncope, and undifferentiated dizziness. Patients with BPPV should be instructed on the importance of vestibular rehabilitation exercises and the possibility of recurrent symptoms.
SUMMARY
Successful ED management of a patient with an acute complaint of dizziness is built on a careful history and physical examination. The history focuses on symptom description and time course. The physical examination investigates abnormal vital signs, the presence of nystagmus (horizontal or vertical, fatiguing or nonfatigable), hearing loss, evidence of head trauma, or neurologic deficits. For patients with peripheral vestibular symptoms, the Dix-Hallpike maneuver may be confirmatory. Patients with peripheral vertigo do not need extensive diagnostic testing but instead require supportive care that includes hydration and the canolith repositioning procedure. Patients who have acute neurologic deficits should have emergent neuroimaging with appropriate neurology or neurosurgical consultation.
REFERENCES
1. Tinetti ME, Williams CS, Gill TM. Dizziness among older adults: a possible geriatric syndrome. Ann Intern Med. 2000;132:337344.[PMID: 10691583] [Full Text] 2. Newman-Toker D, Cannon L, Stofferahn M, et al. Imprecision in patient reports of dizziness symptom quality: a crosssectional study conducted in an acute care setting. Mayo Clin Proc. 2007;82:13291340.[PMID: 17976352] [Full Text] 3. Bhattacharyya N, Baugh R, Orvidas L, et al. Clinical practice guideline: benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg. 2008;139:S47S81. 4. Stanton V, Hsieh Y, Camargo C, et al. Overreliance on symptom quality in diagnosing dizziness: results of a multicenter survey of emergency physicians. Mayo Clin Proc. 2007;82:13191328.[PMID: 17976351] [Full Text] 5. van Brevern M, Radtke A, Lezius F, et al. Epidemiology of benign paroxysmal positional vertigo: a population based study. J Neurol Neurosurg Psychiatry. 2007;78:710715. 6. Fife T, Iverson T, Lempert J, et al. Practice parameter: therapies for benign paroxysmal positional vertigo. Neurology. 2008;70:20672074.[PMID: 18505980] [Full Text] 7. Reploeg M, Goebel J. Migraine associated dizziness: patient characteristics and management options. Otol Neurotol. 2002;12:364371. 8. Hoffman RM, Einstadter D, Kroenke K. Evaluating dizziness. Am J Med. 1999;107:468478.[PMID: 10569302] [Full Text] 9. Kerber K, Brown D, Lisabeth L, et al. Stroke among patients with dizziness, vertigo, and imbalance in the emergency department: a population based study. Stroke. 2006;37:24822487.
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