AUTHOR INFORMATION

Section 1 of 11

Authored by Andrew K Chang, MD, Assistant Professor, Department of Emergency Medicine, Albert Einstein College of Medicine, Montefiore Medical Center

Coauthored by Martin A Samuels, MD, Chief, Department of Neurology, Brigham and Women's Hospital

Andrew K Chang, MD, is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Edited by Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; J Stephen Huff, MD, Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health System; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School

Author's Email:	Andrew K Chang, MD
Editor's Email:	Edward Bessman, MD

eMedicine Journal, July 12 2006, VOLUME 7, Number 7

INTRODUCTION

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Background: Dizziness is a common complaint of patients presenting to the emergency department. The 4 main categories of dizziness that patients describe include vertigo, near-syncope, dysequilibrium, and psychophysiologic dizziness. Of these 4 categories, vertigo is the most common (40-50%). Of the various causes of vertigo, benign positional vertigo (BPV) is the most common cause. Approximately 25-40% of patients who present with the chief complaint of dizziness have BPV.

Although this article focuses on BPV, the authors give a brief description of the 3 other categories of dizziness. The average person may describe more than one type of dizziness.

Near-syncope is due to reduced blood flow to the entire brain. Because our head is above our heart and we have the habit of frequently standing up from either a sitting or lying position, our CNS has evolved a complicated neural reflex that allows us to preserve blood flow to the brain in the standing position. However, many things can interfere with this reflex. Common causes include orthostatic hypotension (anemia, volume depletion, antihypertensive medications), cardiac disease (cardiomyopathy, dysrhythmias, aortic stenosis), vasovagal episodes (or neurocardiogenic syncope), and hyperventilation (decreases pCO₂, which constricts blood vessels in the brain).

Dysequilibrium is essentially a gait disorder, most often caused by cervical spondylosis. Other causes include extrapyramidal disease and cerebellar disease.

Psychophysiologic dizziness is the least understood and is thought to be due to altered central integration of sensory signals arising from normal end organs. Some patients are overfocused on the normal physiological sensations, while others (such as those with panic syndrome) may have a neurochemical imbalance. Patients with psychophysiologic dizziness typically have mild symptoms and may have difficulty describing their dizziness in terms other than the word "dizzy.” Some describe an out-of-body type of experience. Unlike BPV, occurrences are not episodic.

Vertigo is an illusion of motion (an illusion is a misperception of a real stimulus) and represents a disorder of the vestibular proprioceptive system.

BPV was first described by Adler in 1897 and then by Bárány in 1922; however, Dix and Hallpike did not coin the term benign paroxysmal positional vertigo until 1952. This terminology defined the characteristics of the vertigo and introduced the classic provocative test that is still used today. Using positional testing, BPV can readily be diagnosed in the emergency department. BPV is one of the few neurologic entities the emergency physician can cure at the patient's bedside by performing a series of simple and safe head-hanging maneuvers.

Pathophysiology: BPV is caused by calcium carbonate particles called otoliths (or otoconia) that are inappropriately displaced into the semicircular canals of the vestibular labyrinth of the inner ear. These otoliths are normally attached to hair cells on a membrane inside the utricle and saccule. Because they are denser than the surrounding endolymph, changes in head movement vertically causes the otoliths to tilt the hair cells. This is how our brain knows which way is up or down (without looking).

The utricle is connected to the semicircular canals. The otoliths may become displaced from the utricle by aging, head trauma, or labyrinthine disease. When this occurs, the otoliths have the potential to enter the semicircular canals. When they do, they almost always enter the posterior semicircular canal because this is the most dependent (inferior) of the 3 canals.

According to the canalolithiasis theory (the most widely accepted theory of the pathophysiology of BPV), the otoliths are free-floating within the canal. Changing head position causes the otoliths to move through the canal. Endolymph is dragged along with the movement of the otoliths, and this stimulates the hair cells of the cupula of the affected semicircular canal, causing vertigo. When the otoliths stop moving, the endolymph also stops moving and the hair cells return to their baseline position, thus terminating the vertigo and nystagmus. Reversing the head maneuver causes the particles to move in the opposite direction, producing nystagmus in the same axis but reversed in direction of rotation. The patient may describe that the room is now spinning in the opposite direction. When repeating the head maneuvers, the otoliths become dispersed and are progressively less effective in producing the vertigo and nystagmus (hence, the concept of fatigability).

Frequency:

• In the US: The incidence of BPV is 64 cases per 100,000 population per year (conservative estimate).

• Internationally: One study in Japan found an incidence of 11 cases per 100,000 population per year, but patients were counted only if examined by a subspecialist or at a referral center.

Mortality/Morbidity: The B of BPV stands for benign and designates that the cause of the vertigo is peripheral to the brain stem and, hence, likely to be benign. However, realizing that BPV can be chronic and severely incapacitating is important.

Sex: Women are affected twice as often as men.

Age: BPV, in general, is a disease of elderly persons, although onset can occur at any age. Several large studies show an average age of onset in the mid 50s. Vertigo in young patients is more likely to be caused by labyrinthitis (associated with hearing loss) or vestibular neuronitis (normal hearing).

CLINICAL

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History: When asked about their dizziness, patients with benign positional vertigo (BPV) characteristically describe that the room or world is spinning. However, other descriptions, such as rocking, tilting, somersaulting, and the like, are also possible. All that matters is that an illusion of motion is caused by a misperception of a stimulus (the otoliths). Diagnosis of BPV is based on a characteristic history and a positive Hallpike test.

• Episodic vertigo may occur with the following head movements:

• Rolling over in bed

• Lying down

• Sitting up

• Leaning forward

• Turning the head in a horizontal plane

• Symptoms of BPV are usually worse in the morning (the otoliths are more likely to clump together as the patient sleeps and exert a greater effect when the patient gets up in the morning) and mitigate as the day progresses (the otoliths become more dispersed with head movement).

• Nausea is typically present (vomiting is less common).

• A history of head trauma may be present, especially in young patients with BPV. The head trauma may dislodge the otoliths off their membrane within the utricle, allowing them the opportunity to enter the semicircular canals.

• Eliciting that the individual episodes of vertigo in BPV last for seconds at a time is important. Patients may describe that they are having continuous vertigo, when in reality, they are having repeated episodes (with each episode lasting less than a minute). Patients with vestibular neuritis and labyrinthitis have continuous vertigo, often for hours to days.

• This author asks the patient if the room is spinning during the interview (while the patient's head is still and prior to any manipulative tests). If the patient states that he or she is currently symptomatic, then it is highly unlikely that the patient has BPV because the vertigo in BPV lasts for seconds at a time and occurs only after head movement.

Physical: In addition to the patient's history, a diagnosis of BPV is indicated by a positive Hallpike test (rotatory nystagmus and reproduction of symptoms). In this test, the patient is placed in the head-hanging position. After a short delay of a few seconds, nystagmus and reproduction of the vertigo occurs and typically resolves within 30-60 seconds. The neurologic examination is otherwise unremarkable.

• Nystagmus (an involuntary rhythmic oscillation of the eyes) is described in terms of the fast-phase component.

• Classic nystagmus occurs when the patient's head is dependent and turned to the affected side.

• The most common nystagmus seen is torsional or rotatory. In the head-hanging position, the fast phase should beat toward the forehead (upbeat) and in the same direction as the affected side (ipsilateral). Although some describe the fast phase in terms of being clockwise or counterclockwise, most experts avoid this terminology because it can be unclear if the clock is being viewed from the patient's or physician's perspective.

• Nystagmus usually occurs within 10 seconds after positioning but may present as late as 40 seconds. Hence, if the history is classic, observe the patient for at least 40 seconds while he or she is in the head-hanging position during the Hallpike test.

• Duration varies from a few seconds to a minute and parallels the sensation of vertigo.

• Response fatigues if the patient is repeatedly placed into the provoking position (due to dispersion of the otoliths).

• Note: If the patient has a classic history of BPV (after a short delay, the room spins, but then revolves in 20-30 seconds, and then the rooms spins in the opposite direction when he or she sits back up) but no nystagmus is seen during the Hallpike test, most experts would agree to go ahead and treat the patient with the modified Epley maneuver (see Treatment).

• Nystagmus may be blocked by fixation suppression. Most emergency physicians do not have access to Frenzel lenses or infrared nystagmography that specialists use to prevent fixation suppression.

• One study showed that treating such patients with the Epley maneuver is still effective (despite the lack of nystagmus). Again, these patients must have a classic history.

• Perform the Hallpike test as follows (Caution: For patients with cervical spondylosis, it may not be advisable to extend the neck. However, because having the head dependent is important, the same effect can be achieved if the gurney is placed in the Trendelenburg position for such patients).

• First, warn the patient that symptoms of vertigo will likely be reproduced but that they will resolve after a few seconds.

• Seat the patient close enough to the end of the gurney so that when he or she lies supine, the head can extend backward an additional 30-45°.

• Instruct the patient to keep his or her eyes open no matter how bad he or she feels. This is important because you want to observe the direction of the nystagmus.

• To test the left posterior canal, follow these steps:
  • Turn the patient's head 45° to the left. This position orients the head such that the left posterior semicircular canal is going to be in the plane of the head movement (next step). This will result in the greatest chance of the otoliths moving if they are indeed in the posterior semicircular canal.

  • With your hands on either side of the patient's head, lay the patient down until the head is dependent (hanging over the edge of the gurney). Note that this step does not need to be performed rapidly.

  • Check for reproduction of symptoms and nystagmus (This author often uses his thumb to help hold the eyelid open). In most cases, the fast phase of the nystagmus should be upbeat (toward the forehead) and ipsilateral (in this example, toward the patient's left).

  • Return the patient to the upright position. Nystagmus may be observed in the opposite direction, and the patient may describe that the world is spinning in the opposite direction.

• To test the right posterior canal, repeat the Hallpike test with the head turned 45° to the right side. In general, if the patient has BPV, only one side should test positive during the Hallpike test. Although having bilateral posterior semicircular canal BPV is possible, it is highly unlikely and should suggest horizontal canal involvement, vestibular neuritis/labyrinthitis, or a central cause.

• Note that almost all patients experience mild dizziness when being brought up from the head-hanging position to the sitting position. It is important not to confuse this dizziness (which is more near-syncope in character) with true vertigo.

• Side-lying test: This is an alternative test used to diagnose BPV if the patient cannot perform the Hallpike test. The patient sits with his or her legs over one side of the gurney. To test the left posterior semicircular canal, turn the patient's head 90° to the opposite side (in this case, the right side). Then lay the patient on his left side. By turning the patient's head to the right, the left posterior semicircular canal is aligned in the same plane as the sideways movement. As in the Hallpike test, this will allow the greatest chance for otoliths to move if they are indeed located in the posterior semicircular canal.

• The neurologic examination findings should be otherwise normal; if not, strongly consider alternative diagnoses.

Causes: Several disorders affecting the peripheral vestibular system may precede the onset of BPV.

• Idiopathic (50-60%)

• Infection (viral neuronitis)

• Head trauma, especially in younger patients

• Degeneration of the peripheral end organ

• Surgical damage to the labyrinth

DIFFERENTIALS

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Headache, Migraine
Labyrinthitis
Meniere Disease
Multiple Sclerosis
Stroke, Hemorrhagic
Stroke, Ischemic
Systemic Lupus Erythematosus
Vestibular Neuronitis

Other Problems to be Considered:

Acoustic schwannoma
Chronic otomastoiditis
Congenital malformation (inner ear)
Medications (alcohol, phenytoin, diuretics, salicylates, quinidine, quinine, barbiturates, antibiotics)
Otosclerosis
Ototoxicity
Polyarteritis nodosa
Posttraumatic injuries
Posterior fossa neurosurgery
Postsurgery (general)
Postsurgery (ear)
Vertebrobasilar insufficiency

WORKUP

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Lab Studies:

• No pathognomonic laboratory test for benign positional vertigo (BPV) exists. Laboratory tests may be performed to rule out other pathology.

Imaging Studies:

• Currently, no imaging study can demonstrate the presence of otoliths.

• Head CT scanning or MRI is indicated if the diagnosis is in doubt.

Other Tests:

• Although most patients with BPV have posterior semicircular canal involvement, some patients have horizontal canal involvement. This canal should be suspected if the patient has bilateral symptoms during the Hallpike test. Use the Roll test to formally diagnose horizontal canal BPV, and use the bar-b-que treatment to treat horizontal canal BPV.

• Roll test: Have the patient lie in the supine position on the gurney. Unlike the Hallpike test, the head does not need to hang over the edge of the gurney.

• Turn the patient's head 90° to one side. The patient should experience a reproduction of symptoms and the presence of horizontal nystagmus. The fast phase should beat toward the earth (geotropic).

• Now, turn the patient's head 180° (or 90° to the opposite side). The patient should again experience a reproduction of symptoms and the presence of horizontal nystagmus. The fast phase again beats toward the earth (note that it has changed direction). This is known as direction-changing nystagmus (nystagmus that changes direction based on turning the head) and is different from gaze-evoked nystagmus (which is nystagmus that changes direction depending on where the patient is looking, as in Dilantin toxicity).

• Note that both sides will have nystagmus and a reproduction of symptoms, but one side will be much more symptomatic (and demonstrate stronger nystagmus) than the other side. This is considered the involved side.

• A positive Roll test should be treated with the bar-b-que treatment (see Treatment).

• Head-thrust test

• When the Epley maneuver does not work, it is usually because it is being applied to patients with vestibular neuritis and labyrinthitis.

• The head-thrust test is used to diagnose vestibular neuritis and labyrinthitis.

• In this test, the patient is told to look at the examiner's nose. The examiner places both his or her hands on the patient's head and rapidly turns it approximately 10-15° to one side. If the vestibular apparatus is functioning properly, the patient will be able to maintain his or her focus on the examiner's nose. If the vestibular apparatus is not working properly, the patient's eyes will deviate to the side and then quickly jerk back to view the examiner's nose. This jerking eye movement is called a saccade and indicates a positive head-thrust test.

Procedures:

• The Hallpike test, along with the patient's history, confirms the diagnosis of BPV. See Physical for details of this procedure.

• The modified Epley maneuver is used to treat posterior canal BPV (see Treatment as well as Image 15 for a video demonstration).

TREATMENT

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Emergency Department Care: If the history and physical examination are typical, no further evaluation is necessary, and the emergency physician may proceed with the modified Epley maneuver described below (see Image 15 for a video demonstration). If the history and physical examination findings are atypical, consider other causes of positional vertigo, which may occur with tumor or infarcts in the posterior fossa.

Contraindications to performing the Epley maneuver include ongoing CNS disease (ie, stroke or transient ischemic attack [TIA]), unstable heart disease, severe neck disease (eg, rheumatoid arthritis) or history of cervical spine fracture or surgery, carotid bruit on examination indicating carotid stenosis, or body habitus preventing performance of the maneuver.

• The goal of the Epley maneuver is to move the otoliths out of the posterior semicircular canal and back into the utricle where they belong.

• The success rate of the Epley maneuver is very high (approximately 85-90%). When it fails, it is the author's experience that it is being incorrectly applied to patients with vestibular neuritis or labyrinthitis.

• Epley maneuver, general guidelines

• The head must be in the dependent (head-hanging) position for this to work. If the patient does not tolerate this position, put the gurney in the Trendelenburg position to simulate this head-hanging position.

• Maintain each position until the symptoms and nystagmus have disappeared or for at least 30 seconds.

• If the patient cannot tolerate the maneuver because of vomiting or severity of the vertigo, premedicate with a vestibular sedative, such as 25 mg IV promethazine (Phenergan).

• Epley maneuver steps

• Have the patient sit upright on the gurney with the head turned 45° to the affected side (this was predetermined using the Hallpike test). Make sure the patient is sitting far enough back in the gurney so that the head will hang over the edge of the gurney when the patient is laid back. Make sure the guardrail on the opposite side has been lowered (the patient will eventually sit up so his or her legs overhang the edge of the gurney).

• Place your hands on either side of the patient's head and guide the patient down with the head dependent (as in the Hallpike test).

• Rotate the head 90° to the opposite side with the patient’s face upward and be sure to maintain the head-dependent position (head is hanging over the edge of the gurney).

• Ask the patient to roll onto his or her side while holding the head in this position and then rotate the head so that it is facing downward (tell the patient to look to the ground).

• Raise the patient to a sitting position while maintaining head rotation (This author finds that sitting the patient up so that he or she is sitting with his legs hanging over the edge of the gurney is easier. This is why the side guardrails need to be lowered before the procedure is started).

• Simultaneously rotate the head to a central position and move it 45° forward.

• The Semont maneuver (liberatory maneuver)

• This maneuver is primarily used in Europe. Although it can be used to treat classic posterior canal BPV, in the United States, it is usually reserved to treat the cupulolithiasis form of BPV (where the otoliths are not free-floating but instead are attached to the cupula of the posterior semicircular canal). Because of its somewhat violent nature (and the fact that most patients with BPV are elderly), the author does not advocate its use but includes it to be complete.

• As in the side-lying test, the patient sits on the edge of the gurney with the head turned opposite to the involved side. The patient is brought rapidly down onto his or her side (this serves to dislodge the otoliths off the cupula). The patient is then rapidly brought to the other side, maintaining the head in the same position (so the patient's face will be facing the gurney). The patient is then brought to the original sitting position. See Image 16 for a video demonstration.

Consultations: Neurologic consultation is indicated for cases of positional vertigo and nystagmus that do not satisfy criteria for BPV. For example, downbeat nystagmus usually indicates a central cause. Although downbeat nystagmus can also indicate anterior canal involvement (which is benign), this is extremely rare.

MEDICATION

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Medical treatment is generally ineffective but may be used to lessen the symptoms. The natural history of BPV is to resolve with time as the otoliths eventually dissolve while in the semicircular canals.

The use of vestibular suppressants is based on the sensory conflict theory, in which sensory input is compared from different systems, and if a conflict exists, then nausea and vomiting result. Over time, habituation occurs. Several main neurotransmitters mediate these functions: GABA, acetylcholine, and histamine/serotonin.

Drug Category: Antihistaminic antiemetics -- The antihistaminic antiemetics block the emetic response. For patients with severe vertigo or vomiting, intravenous promethazine (Phenergan) is the drug of choice; prochlorperazine (Compazine) is not very useful in this context. Meclizine is given orally and does not work fast enough to be effective acutely. Most antiemetics have anticholinergic activity as well.

Drug Name	Promethazine (Phenergan, Anergan, Prorex) -- Antidopaminergic agent used to treat emesis. Blocks postsynaptic mesolimbic dopaminergic receptors in the brain and reduces stimuli to brainstem reticular system. Also has cross reactivity with the cholinergic receptors.
Adult Dose	25 mg IV/IM/PR q6h
Pediatric Dose	<2 years: Contraindicated <12 years: Not established >12 years: 12.5 mg IV/IM/PR q6h
Contraindications	Documented hypersensitivity; comatose state or depressed CNS; children younger than 2 y (incidences of death due to respiratory depression)
Interactions	May have additive effects when used concurrently with other CNS depressants or anticonvulsants; coadministration with epinephrine may cause hypotension
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in cardiovascular disease, impaired liver function, seizures, sleep apnea, and asthma

Drug Name	Meclizine (Antivert, Antrizine, Dramamine) -- Decreases excitability of middle ear labyrinth and blocks conduction in middle ear vestibular-cerebellar pathways. These effects are associated with relief of nausea and vomiting.
Adult Dose	25-50 mg PO q12-24h; not to exceed 100 mg/d
Pediatric Dose	<12 years: Not established >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	May increase toxicity of CNS depressants, neuroleptics, and anticholinergics
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Caution in angle-closure glaucoma, prostatic hypertrophy, pyloric or duodenal obstruction, and bladder neck obstruction

Drug Category: Benzodiazepines -- These agents block the GABA receptors and serve as the "brakes" to the system. Although they can be used acutely in the ED, they are not recommended for long-term use because they interfere with the process of vestibular rehabilitation.

Drug Name	Lorazepam (Ativan) -- Sedative hypnotic in benzodiazepine class that has short time to onset and relatively long half-life. Depresses all levels of CNS, including limbic and reticular formation, probably through increased action of GABA, a major inhibitory neurotransmitter.
Adult Dose	1-10 mg/d PO/IM/IV divided bid/tid
Pediatric Dose	0.05 mg/kg/dose PO/IM/IV q4-8h
Contraindications	Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma
Interactions	Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAO inhibitors
Pregnancy	D - Unsafe in pregnancy
Precautions	Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Drug Category: Anticholinergics -- These agents block the conflict signal sites.

Drug Name	Scopolamine (Isopto, Scopace Tablet) -- Blocks action of acetylcholine at parasympathetic sites in the smooth muscle, secretory glands, and CNS. Antagonizes histamine and serotonin action. Transdermal scopolamine may be most effective agent for motion sickness. Use in the treatment of BPV is limited by slow onset of action.
Adult Dose	0.5 mg topical patch
Pediatric Dose	<12 years: Not recommended >12 years: Administer as in adults
Contraindications	Documented hypersensitivity; primary glaucoma (including initial stages); pyloric obstruction; toxic megacolon; hepatic disease; paralytic ileus; severe ulcerative colitis; renal disease; obstructive uropathy; myasthenia gravis
Interactions	Antipsychotic effectiveness of phenothiazines may be decreased by coadministration with scopolamine; anticholinergic adverse effects may be increased by concurrent therapy and phenothiazine dosages should be adjusted as necessary; coadministration with tricyclic antidepressants may increase anticholinergic adverse effects (eg, dry mouth, constipation, urinary retention) because of additive effect (tricyclic antidepressants with less anticholinergic activity may be beneficial)
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in elderly patients because of increased prevalence of glaucoma; large doses may suppress intestinal motility and precipitate or aggravate toxic megacolon; anticholinergics may aggravate hiatal hernia associated with reflux esophagitis; patients with prostatism can have dysuria and may require catheterization; use cautiously in patients with asthma or allergies; a reduction in bronchial secretions can lead to inspissation and formation of bronchial plugs

Drug Name	Dimenhydrinate (Dimetabs, Dramamine) -- Mixture of 1:1 salt consisting of 8-chlorotheophylline and diphenhydramine. Believed to be useful, particularly in treatment of vertigo. Diminishes vestibular stimulation and depresses labyrinthine function through central anticholinergic effects. However, prolonged treatment may decrease rate of recovery of vestibular injuries.
Adult Dose	25-50 mg PO/IV/IM/PR q6h
Pediatric Dose	2-6 years: 12.5-25 mg PO q6-8h, not to exceed 75 mg/d; alternatively, 1.25 mg/kg or 37.5 mg/m2 IM qid, not to exceed 300 mg/d 6-12 years: 25-50 mg PO q6-8h, not to exceed 150 mg/d; alternatively, 1.25 mg/kg or 37.5 mg/m2 IM qid, not to exceed 300 mg/d >12 years: Administer as in adults
Contraindications	Documented hypersensitivity; do not administer to neonates; IV products may contain benzyl alcohol, which has been associated with fatal "gasping syndrome" in premature infants and low birth weight infants
Interactions	Alcohol or other CNS depressants may have additive effect on dimenhydrinate; caution when administering concurrently with antibiotics that may cause ototoxicity; may mask ototoxic symptoms caused by certain antibiotics and irreversible damage may result
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Do not treat severe emesis with antiemetic drugs alone; may contain either sulfites or tartrazine, which may cause allergic-type reactions in susceptible persons; may impede diagnosis of conditions, such as brain tumors, intestinal obstruction, and appendicitis; may obscure signs of toxicity from overdosage of other drugs

Drug Category: Sympathomimetic -- These agents are useful in reversing soporific effects of vestibular sedatives.

Drug Name	Methylphenidate (Ritalin) -- Piperidine derivative most commonly prescribed; efficacy has been demonstrated in randomized, double-blind, dose-response, and placebo-controlled trials. Stimulates cerebral cortex and subcortical structures.
Adult Dose	10 mg PO bid/tid up to 60 mg/d
Pediatric Dose	50 mg PO qd
Contraindications	Documented hypersensitivity; glaucoma; Tourette syndrome; motor tics; patients with agitation, tension, and anxiety
Interactions	Reduces effects of guanethidine and bretylium; toxicity of phenytoin, tricyclic antidepressants, warfarin, primidone, and phenobarbital may increase when administered concurrently with methylphenidate; MAO inhibitors increase toxicity of methylphenidate
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in dementia, seizures, and hypertension

FOLLOW-UP

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Further Inpatient Care:

• Patients with persistent vomiting or intractable vertigo may require admission for hydration and vestibular suppressant medication.

• Surgical elimination of posterior canal function is restricted to rare cases of long-standing refractory BPV.

Further Outpatient Care:

• Head exercise therapy (positional exercises of Brandt and Daroff) that promotes central accommodation may be helpful for BPV, although most patients have difficulty tolerating these maneuvers. The patient can perform the following therapy:

• Sit on the edge of the bed near the middle, with legs hanging down.

• Turn the head 45° to the right side. Quickly lie down on the left side, with the head still turned, and touch the bed with a portion of the head behind the ear.

• Maintain this position and every subsequent position for about 30 seconds.

• Sit up again.

• Quickly lie down to the right side after turning head 45° toward the left side.

• Sit up again.

• Do 6-10 repetitions, 3 times per day.

• If the patient becomes confused about the direction to turn his head, tell him his or her nose should always point toward the ceiling

In/Out Patient Meds:

• Meclizine is the most common outpatient medication. This medication is indicated for vertigo but should not be given for other categories of dizziness (near-syncope, dysequilibrium, or lightheadedness).

Deterrence/Prevention:

• Avoid provocative movements and limit activities.

Complications:

• No complications (eg, neck injury, vertebral dissection) other than vomiting have been reported from the use of the Epley maneuver.

Prognosis:

• BPV tends to resolve spontaneously after several weeks or months. An Italian researcher removed the otoliths from an animal, placed them in a Petri dish full of endolymph, and noted that the otoliths dissolved in approximately 100 hours.

• Some patients experience recurrences months or years later.

• Variants range from a single, short-lived episode to decades of vertigo with only short remissions.

Patient Education:

• For excellent patient education resources, visit eMedicine’s Brain and Nervous System Center. Also, see eMedicine’s patient education article Benign Positional Vertigo.

TEST QUESTIONS

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CME Question 1: Which of the following is the most common cause of benign positional vertigo (BPV)?

A: Infection
B: Idiopathic
C: Head trauma
D: Degeneration of the peripheral end organ
E: Surgical damage to the labyrinth

The correct answer is B: The cause of benign positional vertigo is unknown in more than 50% of cases. Other causes include infection (viral neuronitis); head trauma, especially in younger patients; degeneration of the peripheral end organ; and surgical damage to the labyrinth.

CME Question 2: What is the treatment of choice for benign positional vertigo (BPV)?

A: Antivert (Meclizine)
B: Dix-Hallpike test
C: Modified Epley maneuver
D: Subspecialty referral
E: No treatment necessary

The correct answer is C: The modified Epley maneuver is the treatment of choice for BPV. BPV is one of the few neurologic entities that the emergency physician can cure at the patient`s bedside by performing a series of simple and safe head-hanging maneuvers.

Pearl Question 1 (T/F): Nystagmus in benign positional vertigo (BPV) is characterized by no latency of onset.

The correct answer is False: Nystagmus in BPV is usually rotatory and characterized by latent onset (up to 40 seconds).

Pearl Question 2 (T/F): The Dix-Hallpike test is a specific test that can help diagnose benign positional vertigo (BPV).

The correct answer is True: In addition to the patient`s history, a diagnosis of BPV is indicated by reproduction of symptoms and nystagmus (an involuntary rhythmic oscillation of the eyes) during the Hallpike test. Neurologic examination results are otherwise normal.

Pearl Question 3 (T/F): The Epley maneuver is the treatment for benign positional vertigo.

The correct answer is True: The Epley maneuver is the treatment of choice and should be performed in the emergency department. Contraindications to performing the Epley maneuver include ongoing CNS disease (ie, stroke or transient ischemic attack [TIA]), unstable heart disease, severe neck disease (eg, rheumatoid arthritis) or history of cervical spine fracture or surgery, carotid bruit on examination indicating carotid stenosis, or body habitus preventing performance of the maneuver.

Pearl Question 4 (T/F): The cupulolithiasis theory is the most likely cause of benign positional vertigo (BPV).

The correct answer is False: The canalolithiasis theory is the more accepted theory regarding the pathophysiology of BPV. In this theory, the otoliths are free-floating in the semicircular canals. In the cupulolithiasis theory, the otoliths are also in the posterior semicircular canal, but they are attached to the cupula and are not free-floating.

PICTURES

Section 10 of 11

Caption: Picture 1. Anatomy of the semicircular canals.
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Caption: Picture 2. Epley maneuver. Move the patient back in the gurney such that when he lies down, his head will hang over the edge of the gurney. Emphasize to the patient to keep his eyes open during each position so that nystagmus can be observed. Lower the guardrails of the gurney on the opposite side from which the patient's head is turned.
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Caption: Picture 3. Epley maneuver. Turn the patient's head 45° to the side that had the most prominent symptoms during the Hallpike test. In this example, the patient's head is turned 45° to the left. With both hands holding the patient's head, gently lay the patient down in the supine position with the head hanging over the edge of the bed. Note: Each maneuver does not need to be performed rapidly. The Epley maneuver is positional, not positioning.
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Caption: Picture 4. Epley maneuver. The patient's head should be at 45° and hanging off the edge of the bed. Observe the patient's eyes and look for torsional nystagmus. Keep the patient in this position for at least 30 seconds or until the nystagmus or symptoms resolve.
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Caption: Picture 5. Epley maneuver. Because the patient's head will be turned 90° in the other direction, the physician needs to move to the head of the gurney and regrip the patient's head so that the fingers are pointing toward the patient's feet.
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Caption: Picture 6. Epley maneuver. Turn the patient's head 90° in the opposite direction (in this case, the patient's head is now facing to the right). Again, observe for nystagmus and hold this position for at least 30 seconds or until nystagmus or symptoms resolve.
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Caption: Picture 7. Epley maneuver. Close-up view of step shown in Image 6.
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Caption: Picture 8. Epley maneuver. Ask the patient to turn onto his shoulder.
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Caption: Picture 9. Epley maneuver. Guide the patient's head down so that he is looking at the ground. Again, wait for at least 30 seconds.
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Caption: Picture 10. Epley maneuver. Close-up of view shown in Image 9.
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Caption: Picture 11. Epley maneuver. The patient's head needs to be regripped again. Then, the patient needs to sit up with the legs hanging over the side of the gurney (which is why the guardrails need to be lowered before the start of the procedure).
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Caption: Picture 12. Epley maneuver. The patient is now sitting upright.
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Caption: Picture 13. Epley maneuver. Move the patient's head slightly forward. This completes the Epley maneuver. The maneuver may be performed multiple times.
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Caption: Picture 14. Hallpike test. In this example, the right posterior semicircular canal is being tested. Note that the head extends over the edge of the gurney. The thumb can be used to help keep the eyelids open since noting the direction of the nystagmus is important.
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Caption: Picture 15. Epley maneuver. In this example, the left posterior semicircular canal is being treated. In this clip, the maneuvers are performed quickly. In a real patient, each position should be held for at least 30 seconds or until resolution of the nystagmus and vertigo.
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Caption: Picture 16. Semont maneuver. Generally reserved for the cupulolithiasis form of benign positional vertigo, in which the otoliths are attached to the cupula of the semicircular canal. This maneuver has to be performed rapidly to be effective, and it is not recommended in elderly persons. In this example, the right posterior semicircular canal is being treated.
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Caption: Picture 17. Bar-b-que maneuver. This maneuver is used to treat horizontal canal benign positional vertigo. In this example, the right horizontal canal is being treated. Each position should be held at least 20-30 seconds.
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BIBLIOGRAPHY

Section 11 of 11

• Baloh RW: Dizziness and vertigo. In: Samuels MA, Feske S, eds. Office Practice of Neurology. London: Churchill Livingstone; 1996:83-91.
• Brandt T, Daroff RB: Physical therapy for benign paroxysmal positional vertigo. Arch Otolaryngol 1980 Aug; 106(8): 484-5[Medline].
• Chang AK, Schoeman G, Hill M: A randomized clinical trial to assess the efficacy of the Epley maneuver in the treatment of acute benign positional vertigo. Acad Emerg Med 2004 Sep; 11(9): 918-24[Medline].
• Epley JM: Particle repositioning for benign paroxysmal positional vertigo. Otolaryngol Clin North Am 1996 Apr; 29(2): 323-31[Medline].
• Froehling DA, Silverstein MD, Mohr DN, et al: Benign positional vertigo: incidence and prognosis in a population-based study in Olmsted County, Minnesota. Mayo Clin Proc 1991 Jun; 66(6): 596-601[Medline].
• Froehling DA, Bowen JM, Mohr DN, et al: The canalith repositioning procedure for the treatment of benign paroxysmal positional vertigo: a randomized controlled trial. Mayo Clin Proc 2000 Jul; 75(7): 695-700[Medline].
• Furman JM, Cass SP: Benign paroxysmal positional vertigo. N Engl J Med 1999 Nov 18; 341(21): 1590-6[Medline].
• Lempert T, Gresty MA, Bronstein AM: Benign positional vertigo: recognition and treatment. BMJ 1995 Aug 19; 311(7003): 489-91[Medline].
• Marill KA, Walsh MJ, Nelson BK: Intravenous Lorazepam versus dimenhydrinate for treatment of vertigo in the emergency department: a randomized clinical trial. Ann Emerg Med 2000 Oct; 36(4): 310-9[Medline].
• Massoud EA, Ireland DJ: Post-treatment instructions in the nonsurgical management of benign paroxysmal positional vertigo. J Otolaryngol 1996 Apr; 25(2): 121-5[Medline].
• Troost BT, Patton JM: Exercise therapy for positional vertigo. Neurology 1992 Aug; 42(8): 1441-4[Medline].

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