Vertigo Presentations in the Emergency Department

Transcription

1 Vertigo Presentations in the Emergency Department Kevin A. Kerber, M.D. 1 ABSTRACT Vertigo is among the most common reasons that patients present to the emergency department. Even though the cause is typically a benign disorder, management decisions can be challenging because some sinister causes such as stroke can mimic benign peripheral vestibular disorders. Fortunately, common benign peripheral vestibular disorders all have characteristic features enabling a bedside diagnosis. Thus the most effective way to rule-out a central disorder is to rule-in a specific peripheral vestibular disorder. In this article, the author emphasizes the key elements of the bedside examination and describes a method for managing vertigo patients in the emergency department. KEYWORDS: Vertigo, vestibular disorders, stroke, emergency department You are called about a 50-year-old patient with vertigo in the emergency department and your spirits sink. Despite years of neurology training and clinical practice, vertigo consultations continue to trigger angst. You realize that many vertigo patients can be cured with simple maneuvers, but you also recall a vertigo patient who had a cerebellar stroke. You do not want to be the one who recommends symptomatic care, only to find out later that the patient suffered a stroke. The patient already had a negative computerized tomography (CT) scan, but as a neurologist you are well aware of the limitations of CT scans for identifying central disorders particularly acute stroke. So, magnetic resonance imaging (MRI) is the test of choice. But, a MRI scan is not readily available in most emergency situations and the test can substantially increase the cost and time of the evaluation. You are not alone in your concerns. The identification of central or serious vertigo was voted as the top priority for clinical decision rule development in adults, 1 demonstrating widespread uncertainty involved in decisions related to vertigo presentations. The good news, however, is that vertigo evaluations can be straightforward and even rewarding with the use of an organized approach and by incorporating a few additional components into your bedside examination. The most important diagnostic tools are all part of the bedside clinical examination: the neurologic exam (with particular emphasis on an assessment of nystagmus), the Dix Hallpike test, and the head thrust test. Considering these components in the context of the type of vertigo presentation namely acute severe vertigo, recurrent spontaneous vertigo attacks, or recurrent positional vertigo allows physicians to sort through emergency vertigo presentations and make informed decisions about which patients are likely to benefit from known effective treatments without the need for further testing, and also which patients may benefit from diagnostic testing for a sinister cause of vertigo, such as stroke. BEDSIDE CLINICAL EVALUATION Determine the Type of Vertigo Presentation The first objective of the evaluation is to categorize the presentation into one of the following types of vertigo Department of Neurology, University of Michigan Health System, Ann Arbor, Michigan. Address for correspondence and reprint requests: Kevin A. Kerber, M.D., Assistant Professor, Department of Neurology, University of Michigan Health System, 1500 E. Medical Center Drive, Ann Arbor, MI ( kakerber@umich.edu). Neurotology; Guest Editor, Robert W. Baloh, M.D. Semin Neurol 2009;29: Copyright # 2009 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) DOI /s ISSN

2 VERTIGO PRESENTATIONS IN THE EMERGENCY DEPARTMENT/KERBER 483 presentations: acute severe vertigo, recurrent spontaneous vertigo attacks, or recurrent positionally triggered vertigo attacks. The type of presentation is determined based on the details of the history of present illness. These categories help to organize the formulation of the differential diagnosis. Acute severe vertigo is the sudden onset of what is generally a debilitating symptom. Recurrent spontaneous vertigo attacks are reported by patients who have had at least several attacks that come on without any apparent inciting event. Recurrent positionally triggered vertigo attacks consist of vertigo triggered by certain head movements. Utilize Bedside Examination Components In some vertigo presentations, the lesion can be localized with a general examination. When this is not possible, then the key examination components are the following: an assessment of nystagmus, positional testing when applicable, and the head thrust test when applicable. Nystagmus is a term used to describe alternating slow and fast movements of eyes. These alternating movements create the appearance that the eyes are beating in the direction of the fast movement. Pathologic nystagmus occurs as the result of an acute imbalance of the vestibular system due to a lesion (or aberrant stimulation) of peripheral or central structures. Most physicians notice when nystagmus is present, but it is the pattern of nystagmus not the mere presence that is important for discriminating a peripheral (and typically benign) lesion from a central (and potentially lifethreatening) etiology. The localizing value of the patternofnystagmusisalsodependentonthetypeof presentation. Some general rules about the localizing value of nystagmus apply (Table 1). In patients with acute severe vertigo, a unidirectional spontaneous horizontal nystagmus is highly suggestive of a lesion of the vestibular nerve. The lesioned side is the side opposite the direction of the fast phase of nystagmus. Unidirectional spontaneous nystagmus implies that the nystagmus is present in primary gaze and that the nystagmus never changes direction. For example, if nystagmus beats to the left side, then it should never transition to beating to the right side. The left beating nystagmus does increase in velocity when the patient looks to the left side and also decrease (or stop) when the patient looks to the right side, but it will not transition to a right beating nystagmus if the lesion is on the vestibular nerve. A central lesion is presumed in acute severe vertigo presentations whenever a pattern other than unidirectional spontaneous horizontal nystagmus is observed. The most common central patterns of nystagmus in acute severe vertigo presentations are direction changing gaze-evoked nystagmus (i.e., patient looks to the right and nystagmus beats to the right; then, patient looks to the left and nystagmus beats to the left) and spontaneous vertical (typically down-beating) nystagmus. In positionally triggered vertigo presentations, the general rules for patterns of nystagmus are different. In positionally triggered vertigo attacks caused by benign paroxysmal positional vertigo (BPPV), the nystagmus can change direction with changes in head position, and a principally vertical nystagmus is the characteristic pattern of the most common BPPV variant (i.e., posterior canal BPPV). In posterior canal BPPV, the Dix Hallpike test (Fig. 1) triggers a burst of upbeating and torsional nystagmus, which lasts less than 1 minute. If the patient then sits back up from the Dix Hallpike position, then a burst of downbeating and torsional nystagmus is triggered. The reason for the reversal upon sitting up is that the particles move in the opposite direction compared with the Dix Hallpike position. However, if persistent downbeating nystagmus is Table 1 Patterns of Nystagmus Associated with the Type of Vertigo Presentation Peripheral Vestibular Patterns Central Vestibular Patterns Acute severe vertigo Unidirectional, horizontal spontaneous y Direction-changing, gaze-evoked ô Spontaneous vertical or pure torsional Recurrent spontaneous vertigo attacks* Unidirectional, horizontal spontaneous y Direction-changing, gaze-evoked Spontaneous vertical or pure torsional Recurrent positionally Dix Hallpike test: Burst of upbeat torsional z Downbeating persistent triggered attacks Supine positional test: Horizontal nystagmus with direction of nystagmus changing with head movement to opposite side Pure-torsional *May not have nystagmus if evaluation takes place in-between attacks. y Pattern can less commonly be caused by central lesions, increasing the importance of assessing risk for a central lesion and the results of the head thrust test. z Upon sitting up from Dix Hallpike test, a burst of downbeating torsional nystagmus will often be triggered. Thus, a direction-changing positionally evoked nystagmus. In rare circumstances, pattern can be caused by a central lesion. ô Example of direction-changing gaze-evoked nystagmus: left-beating nystagmus with gaze to the left; then, right-beating nystagmus with gaze to the right.

3 484 SEMINARS IN NEUROLOGY/VOLUME 29, NUMBER Figure 1 The Dix Hallpike test for the diagnosis of posterior canal benign paroxysmal positional vertigo affecting the right ear, and the Epley maneuver for the treatment of posterior canal benign paroxysmal positional vertigo affecting the right ear. The procedure can be reversed for treating the left ear. The drawing of the labyrinth in the center shows the position of the debris as it moves around the posterior semicircular canal (PSC) and into the utricle. The patient is seated upright, with head facing the examiner, who is standing on the right. (A) The patient is then rapidly moved to head-hanging right position (Dix Hallpike test). This position is maintained until the nystagmus ceases. (B) The examiner moves to the head of the table, repositioning hands as shown. (C) The head is rotated quickly to the left with right ear upward. This position is maintained for 30 seconds. (D) The patient rolls onto the left side while the examiner rapidly rotates the head leftward until the nose is directed toward the floor. This position is then held for 30 seconds. (E) The patient is rapidly lifted into the sitting position, now facing left. The entire sequence should be repeated until no nystagmus can be elicited. Following the maneuver, the patient is instructed to avoid head-hanging positions to prevent the debris from reentering the posterior canal. (From Rakel RE. Episodic vertigo. Conn s Current Therapy 1995;46(1):839. Reprinted with permission from Elsevier.) triggered by the Dix Hallpike test, then a central lesion is presumed. Positional testing is an important component of the bedside examination when the type of presentation is recurrent positional vertigo. The main positional test is the Dix Hallpike test (Fig. 1). 2,3 If the Dix Hallpike test does not trigger the nystagmus of BPPV, then supine positional testing can be used to test for the less common horizontal canal variant of BPPV. The head thrust test is an important bedside examination component when the type of vertigo presentation is acute severe vertigo (Fig. 2). The head thrust test allows a direct assessment of the vestibuloocular reflex (VOR) and an abnormal result is highly suggestive of a lesion of the vestibular nerve. 4,5 This test is different from the doll s eye test because the doll s eye test uses slow rotation of the head to either side, whereas the head thrust test uses quick movements which isolate the vestibular system function. The corresponding eye movements of the doll s eye test can be generated by either the vestibular system or the smooth pursuit system in a conscious patient. But only the vestibular system

4 VERTIGO PRESENTATIONS IN THE EMERGENCY DEPARTMENT/KERBER 485 Figure 2 The head thrust test. The head thrust test is a test of vestibular function that can be easily done during the bedside examination. This maneuver tests the vestibuloocular reflex (VOR). The patient sits in front of the examiner and the examiner holds the patient s head steady in the midline. The patient is instructed to maintain gaze on the nose of the examiner. The examiner then quickly turns the patient s head 10 to 15 degrees to one side and observes the ability of the patient to keep the eyes locked on the examiner s nose. If the patient s eyes stay locked on the examiner s nose (i.e., no corrective saccade) (A), then the peripheral vestibular system is assumed to be intact. Thus in a patient with acute dizziness, this finding suggests a central nervous system localization. If, however, the patient s eyes move with the head (B) and then the patient makes a voluntary eye movement back to the examiner s nose (i.e., corrective saccade), then this indicates a lesion of the peripheral vestibular system and not the central nervous system. Thus, when a patient presents with the acute vestibular syndrome, the test result shown in (A) would suggest a central nervous system lesion, whereas the test result in (B) would suggest a peripheral vestibular lesion (thus, vestibular neuritis). (From Edlow JA, Newman-Toker DE, Savitz SI. Diagnosis and initial management of cerebellar infarction. Lancet Neurology 2008;7(10): Reprinted with permission from Elsevier.)

5 486 SEMINARS IN NEUROLOGY/VOLUME 29, NUMBER generates the reflex movement of the eyes after the quick movement of the head thrust test. To test the VOR using the head thrust test, the examiner stands in front of the patient and grasps the patient s head with both hands. The patient is instructed to focus on the examiner s nose and then the examiner initiates a quick 10- to 15-degree movement of the patient s head to one side. When there is a lesion of the VOR on one side, a corrective eye movement (i.e., a corrective saccade) back to the examiner s nose is seen after the head is moved toward the affected side. In contrast and serving as an internal control, the eyes will stay on target (i.e., the examiner s nose) after the head thrust test toward the normal side because the VOR is intact on that side. These features can be appreciated even when spontaneous nystagmus is present. The reason for the corrective saccade with a peripheral vestibular lesion is rooted in the physiology of the vestibular system. 6 When the head is moved quickly in one direction, the reflex (i.e., the VOR) that moves the eyes toward the opposite direction is generated by the side the head moved toward. Thus, a patient with vestibular neuritis of the right side will present with a left-beating unidirectional nystagmus, and the head thrust test will be positive with movement toward the right side. FORMULATION OF THE DIFFERENTIAL DIAGNOSIS Acute Severe Vertigo Vestibular neuritis is the most common cause of acute severe vertigo. 7 It is caused by a viral lesion of the eighth cranial nerve. Vertigo is accompanied by severe nausea, vomiting, and imbalance. Patients will often describe the need to hold onto objects when walking or may even need to crawl. Typically hearing is not affected, but if severe vertigo is accompanied by hearing loss then the most common cause is labyrinthitis also of a presumed viral etiology. The hallmark examination signs of vestibular neuritis are a spontaneous unidirectional horizontal nystagmus and a positive head thrust test to the side opposite the fast beating component of the nystagmus. Patients with vestibular neuritis are typically debilitated for the first day. Then, the natural history of the disorder is a gradual recovery over weeks to months. Vestibular physical therapy programs can help to speed the recovery. 8 In addition, the use of a burst and taper of oral corticosteroids can improve the recovery of the affected vestibular system as measured by the laboratory caloric response. 9 In any patient who presents with acute severe vertigo, stroke diagnosis should be considered. Stroke is an obvious concern when the patient reports other focal neurologic symptoms or has other focal neurologic signs. Up to 50% of stroke patients report dizziness symptoms of some type. 10 Although the likelihood of stroke diagnosis drops substantially when the patient presents with isolated vertigo (i.e., no symptoms other than vertigo, nausea, and imbalance), 11 case reports now demonstrate just how closely stroke can mimic vestibular neuritis This information may, in part, account for the dramatic increase in use of neuroimaging in patients with emergency department presentations of dizziness. 15 Lacking is a formal validated tool to assess the probability of stroke in acute severe vertigo presentations. However, recently published research does help to assess bedside risk of stroke in acute vertigo presentations. From epidemiologic study designs, the risk of stroke etiology among patients presenting to the emergency department with dizziness symptoms is 3%. 11 If the dizziness is an isolated symptom, then the risk of stroke etiology drops to less than 1%. However, the population of this study was patients with any dizziness symptom presentation, not just the acute severe vertigo presentation. This distinction is important because the probability of stroke is highest for acute severe vertigo presentations compared with the other types of presentations. One series that looked at acute vertigo presentations found a 25% (6 out of 24 patients) rate of stroke diagnosis. 16 Another series found that 25 out of 33 patients (76%) with acute severe vertigo presentations had stroke etiology, although a higher rate of stroke was selected for because at least one stroke risk factor was required for inclusion, and a recent viral infection was an exclusion criterion. 13 Even in these series, which show very concerning rates of stroke among acute severe vertigo presentations, the rate of stroke etiology dropped substantially among patients with isolated dizziness, unidirectional spontaneous horizontal nystagmus, and a corresponding positive head thrust test. Despite this, we still need large studies of the patients with acute severe vertigo so that validated and clinically meaningful probabilities can inform decisions. Recurrent Spontaneous Vertigo Attacks Ménière s disease is the prototypical disorder characterized by recurrent vertigo attacks. Overall, the prevalence of Ménière s disease in the general population is low. 17 In addition, Ménière s disease patients are probably less likely to present to the emergency department during acute attacks compared with those with acute severe vertigo. The reason may be that Ménière s disease attacks are typically limited to a few hours, and patients learn over time that the attacks resolve with rest. To make the diagnosis of Ménière s disease requires the presence of a unilateral hearing loss, which is typically a fluctuating symptom early in the course, but then becomes a fixed and progressive feature. Other auditory symptoms are also common, including unilateral tinnitus (typically a low roaring sound rather than a high pitched sound) or

6 VERTIGO PRESENTATIONS IN THE EMERGENCY DEPARTMENT/KERBER 487 bothersome pressure in one ear. The examination in patients with Ménière s disease can be variable in the acute setting because nystagmus can be caused by either stimulation or inhibition of the affected side. However, a central pattern of nystagmus (e.g., spontaneous downbeating nystagmus or bidirectional gaze-evoked nystagmus) would be a reason for a workup for a central disorder. Patients with Ménière s disease do not typically have a positive head thrust test. Transient ischemic attacks should be considered when the vertigo attacks are accompanied by other neurologic signs or symptoms, are new in onset, or have a crescendo-like presentation. Many patients eventually suffering a posterior circulation stroke report transient vertigo episodes preceding the stroke. 18 As with stroke in general, auditory symptoms can accompany the vertigo symptoms if the anterior inferior cerebellar artery is involved. Recurrent Positionally Triggered Vertigo Benign paroxysmal positional vertigo is the most common cause of positionally triggered vertigo and, in fact, is also believed to be the most common cause of vertigo in general. 19 Benign paroxysmal positional vertigo can be cured at the bedside with a simple repositioning maneuver. 20 Thus, the ability to identify and treat BPPV is a major step not only for improving patient outcomes, but also for reducing unnecessary tests. The key feature of the history is that the episodes are triggered by head movements, not simply worsened by head movements. It is important to know that dizziness of any cause can worsen after certain position changes. But for patients with BPPV, the vertigo attacks are triggered by position changes. The patient with constant vertigo who reports that the symptom is better in a certain position and worse with movement should be classified as having acute severe vertigo rather than recurrent positionally triggered vertigo. The history of the patient with BPPV is vertigo triggered by head tilts, rolling over in bed, or getting in/out of bed. The vertigo attacks last less than one minute, followed by a return to normal. Some patients will report attacks only in the morning or evening when getting in or out of bed, but others will report attacks throughout the day. Benign paroxysmal positional vertigo is caused by calcium carbonate deposits, which are free floating in a semicircular canal, typically the posterior canal. The deposits break from the otolith membrane for reasons that are not clear. This can occur as the result of head trauma, but typically occurs spontaneously. When the particles enter the posterior canal they can become trapped. After certain head turns, the fluid in the canal moves, which does not cause symptoms, but if particles are present then a strong aberrant stimulation of the nerve endings can occur. This stimulation triggers a burst of nystagmus. Because the particles settle quickly after the movement, the symptoms and nystagmus last for only a brief period of time (<1 minute). The particles can less commonly enter the horizontal canal and rarely enter the anterior canal. The pattern of nystagmus is different depending on which canal is affected. 21 When the particles are in the posterior canal, a burst of upbeat and torsional nystagmus is seen after the patient is placed in the Dix Hallpike position with the head turned toward the affected side (Fig. 1). 3 The nystagmus typically lasts only 20 to 30 seconds. When the particles are in the horizontal canal, the history of presentation will be the same, but the Dix Hallpike test will not trigger a burst of upbeat torsional nystagmus. Instead, the nystagmus of the horizontal canal variant of BPPV is best triggered using supine positional testing. For supine positional testing, the patient lies flat on his back and then the head is turned to either side. The nystagmus triggered will be in the horizontal plane, but can beat either in the direction of the head turn or in the opposite direction, depending on where in the canal the particles are located. In addition, when the head is then turned to the opposite side, a nystagmus in the opposite direction will be triggered thus a direction changing positionally triggered nystagmus. Central disorders can cause positional vertigo attacks, but it is rare that the attacks mimic the characteristics of attacks in BPPV. A downbeating positional nystagmus is the most common pattern of nystagmus indicating a central localization typically a midline cerebellar lesion from a Chiari malformation or a cerebellar degenerative disorder. In these disorders, the central pattern of positional nystagmus may even be the most prominent finding. Downbeating positional nystagmus can be caused by the anterior canal variant of BPPV, but this variant is rare. Multiple sclerosis can also cause various types of positional nystagmus as can any other lesion involving central vestibular pathways in the brainstem or cerebellum. Importantly, central lesions do not cause the characteristic nystagmus pattern of posterior canal BPPV. However, central lesions particularly lesions around the fourth ventricle can cause a pattern of nystagmus identical to the pattern caused by horizontal canal BPPV. 22 Thus, a central lesion should be considered when a patient with the horizontal canal BPPV pattern of nystagmus has atypical features or is refractory to repositioning. OTHER DIZZINESS SYMPTOMS AND PRESENTATIONS Dizziness symptoms are often difficult for patients to describe. 23 As such, vestibular disorders should be considered even when patients do not describe true vertigo if the other clinical characteristics fit with a vestibular disorder. In the emergency department

7 488 SEMINARS IN NEUROLOGY/VOLUME 29, NUMBER setting, the symptom of imbalance is associated with higher odds of stroke diagnosis compared with the symptom of dizziness ; whereas vertigo is not associated with higher odds of stroke diagnosis compared with dizziness. 11 In stroke patients with prominent imbalance, the lesion is typically in the midline cerebellum; often the imbalance is severe enough that a one-person assist is required for ambulating, if ambulation is possible at all. 12 Because the lesions are typically in the midline cerebellum, appendicular ataxia may be lacking. Some patients with dizziness in the emergency room will present with a chronic constant dizziness presentation rather than one of the three common presentation types described previously. If the neurologic exam is normal in the patient with chronic dizziness, then the chance of a structural neurologic disorder is very low. Migraine is the great mimicker of all causes of dizziness. 24 Symptoms in migraine can present as an acute severe attack, positional episodes, recurrent spontaneous attacks, or chronic constant symptoms. An accompanying headache occurs in less than 50% of the presentations, although a personal history of migraine headaches or a strong family history of migraine is common, and often considered a requirement for the diagnosis. 25,26 Other migrainous features are also common and include hypersensitivities, positive visual phenomena, and prominent nausea. Unfortunately, the diagnosis of migraine remains a diagnosis of exclusion. Thus, if the symptom is new in onset and does not fit the features of a specific peripheral vestibular disorder, then serious central causes should be considered. However, if the symptoms have been present for at least a few months and the neurologic exam is nonfocal, then the chance of uncovering a causative structural lesion of the central nervous system is very low. Panic disorder and anxiety disorder often have dizziness or even vertigo as a symptom. Common accompaniments of these psychiatric disorders are a sense of doom or fear, heart palpitations, shortness of breath, and nonfocal numbness and tingling. Similar to migraine vertigo, these diagnoses are also diagnoses of exclusion. General medical disorders can cause various types of dizziness presentations. Vertigo is not typically the symptom reported unless the vestibular system is involved by the process. Orthostatic hypotension is probably the most common general medical cause of dizziness. Medication side effects or metabolic derangements should also be a considered in the differential diagnosis. MANAGEMENT OF EMERGENCY VERTIGO PRESENTATIONS The goal in the emergency department is to stabilize symptoms and identify treatable disorders or monitor those patients at risk for worsening. After categorizing the presentation type and examining the patient, the next step is to determine if the presentation fits with a common peripheral vestibular disorder (i.e., vestibular neuritis, BPPV, or Ménière s disease). Thus, an optimal way to rule-out a central disorder is to rule-in a peripheral vestibular disorder. This is the reason it is important for neurologists to recognize these common disorders. Simply determining the cause to be a peripheral disorder probably leaves too much room for error. BPPV is not only readily identifiable at the time of the clinical presentation, but the most common type (i.e., posterior canal BPPV) can be effectively treated with the Epley maneuver. 2,3,27 If the features are atypical for BPPV or the patient does not respond to repositioning maneuvers, then central disorders can be considered. If the patient presents with acute severe vertigo, then the history and the examination are the key elements. The patient with isolated vertigo has a very low probability of stroke, 11 but this may still be a concerning probability. The probability of stroke drops further when isolated vertigo is accompanied by a unidirectional horizontal spontaneous nystagmus. 12,13 And, the probability of stroke drops even further when the patient has isolated vertigo, unidirectional horizontal spontaneous nystagmus, and a corresponding positive head thrust test. 12,13 If a patient presents with recurrent spontaneous episodes of vertigo, the chance of transient ischemic attack (TIA) as the cause is low if the symptom lasts for hours, the attacks date back more than a couple months, and prominent unilateral auditory features are reported. On the other hand, if the attacks are new in onset, brief in duration (minutes rather than hours), and not accompanied by prominent unilateral auditory features, then TIA should be a strong consideration. Symptoms can be managed with either oral or intravenous medications. Few randomized controlled trials have been conducted on the symptomatic treatment of acute dizziness. In one recent study of 74 patients with acute dizziness, the average effect of 50 mg of intravenous dimenhydrinate was superior to that of 2 mg of intravenous lorazepam. 28 Antinausea medications can be considered when nausea and vomiting are prominent symptoms. Corticosteroids do not likely improve acute dizziness symptoms. But in patients with vestibular neuritis, a randomized placebo-controlled trial of oral corticosteroids and valacyclovir (2 2 factorial design) found that on average, patients treated with corticosteroids had a superior improvement in vestibular recovery as measured by the surrogate outcome of caloric response at 12 months compared with placebo. 9 Valacyclovir did not demonstrate a beneficial effect. It is not known if corticosteroids improve functional outcome because functional outcome was not assessed in this trial and many patients with a chronic caloric asymmetry are asymptomatic. Vestibular physical

8 VERTIGO PRESENTATIONS IN THE EMERGENCY DEPARTMENT/KERBER 489 therapy is recommended for patients with acute vestibular neuritis. 8 IMAGING STUDIES IN EMERGENCY VERTIGO PRESENTATIONS The use of neuroimaging studies in emergency department presentations of dizziness has risen dramatically. In a population of vertigo-dizziness emergency department presentations, 25% of patients received a CT scan in 2004 compared with less than 10% of patients in In some subgroups, the percentage receiving a CT scan was nearly 40%. 15 Nevertheless, the sensitivity of CT scans for identifying stroke in the acute setting is a dismal 26%, 29 meaning that a negative test does not change the probability of stroke diagnosis in a meaningful way. Magnetic resonance imaging is a much more sensitive test, but is not generally available in the acute setting, takes more time, and has much greater expense. In addition, the sensitivity of MRI is lowest (thus can miss a stroke) when the test is performed within 24 hours of the onset and when the lesion is in the brainstem or cerebellum. 13,29,30 A validated clinical decision rule to determine which patients are likely to benefit from neuroimaging could go a long way in optimizing patient outcomes and healthcare utilization. But such a rule would need to be supported by policy to have an impact. In the absence of such a rule, clinical judgment must be used when evaluating individual patients. The vertigo patients at highest risk for stroke etiology are those with other focal neurologic symptoms or signs (including central patterns of nystagmus), stroke risk factors, acute severe vertigo or imbalance type of presentation, and acute severe vertigo patients having a negative head thrust test ,16 SUMMARY The evaluation of emergency department vertigo patients is facilitated by a strategy to categorize the type of presentation and utilize bedside examination tools. The optimal way to rule-out a central disorder is to rule-in a specific peripheral vestibular disorder (i.e., vestibular neuritis, BPPV, or Ménière s disease). When the key clinical features fit with a specific peripheral vestibular disorder, then the likelihood of a serious central disorder is extremely low. CT scans are not a valid discriminator of central versus peripheral vertigo presentations in the emergency department. 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