Dizziness

Author: Robert Frank, MD, Clinical Instructor, Mercy Hospital of Pittsburgh.

Peer Reviewers: Steven M. Winograd, MD, FACEP, Attending Physician, Emergency Department, Adena Regional Medical Center, Chillicothe, OH; and Andrew D. Perron, MD, FACEP, FACSM, Residency Program Director, Maine Medical Center, Falmouth, ME.

Introduction

Few chief complaints cause more apprehension and dread for emergency physicians (EPs) than dizziness. It is a common condition seen in the emergency department (ED), is understood poorly, and has potentially malignant etiologies. Dizziness cannot be measured. It can mean different things to different patients and is often difficult to precisely characterize. Unfortunately, it is the ability to obtain a precise history and perform an exacting examination that allows a diagnosis to be made and appropriate treatment instituted. This article examines some of the different causes of dizziness, how they can be differentiated via history and physical examination, and their appropriate treatments and dispositions.

Epidemiology

Dizziness is a sensation of abnormal orientation in space.1 It is the third most common outpatient complaint.2 It accounted for about 1.5 million ED visits in 2001.3 Patients with benign paroxysmal positional vertigo (BPPV) on average are seen by four physicians at a cost of more than $2000 per work-up.4 Twenty percent of patients older than 60 years have experienced dizziness significant enough to affect their daily activities.5,6 Drachman and Hart described four subtypes that still remain the basis for dizziness definition and classification today: vertigo, presyncopal lightheadedness, disequilibrium, and “other” dizziness.7 A meta-analysis by Kroenke and colleagues found that the most common etiologies for dizziness were peripheral vestibulopathies (44%), psychiatric disorders (16%), central vestibulopathies (11%), other causes (26%), and unknown causes (13%).8 Causes of disequilibrium are rarely the primary cause of dizziness, though they are common contributory factors. Serious causes of dizziness include cerebrovascular disease (6%), arrhythmia (1.5%), and brain tumors (<1%). While a significant proportion of dizziness will resolve within a two-week time frame, dizziness that remains longer generally has a multifactorial etiology.8

Pathophysiology

The pathophysiology of dizziness is specific to the condition that accounts for the underlying cause. The maintenance of balance is a complex interaction whereby the central nervous system coordinates and integrates sensory input from vestibular, visual, and proprioceptive systems. Vestibular input is transmitted via the 8th cranial nerve. The labyrinth (inner ear) includes three semicircular canals that are perpendicular to each other and are oriented in three planes of space. Rotational acceleration causes endolymph within the semicircular canals to deform hair cells attached to the cupula generating signals that allow perception of movement and position.9 This input helps form the impression of orientation of head and body and the perception of motion.

Sensory input that helps maintain balance is symmetric from the bilateral vestibular systems. If this input becomes asymmetric it causes vertigo.10 In BPPV, canalithiasis is thought to be the most common mechanism and describes free-floating otoconia (i.e., calcium carbonate crystals) in a semicircular canal. These otoconia are displaced from the otolithic membrane in the utricle.9 The right posterior semicircular canal is most commonly affected because it is the most gravity dependent portion of the vestibular labyrinth.9,11 Head movements then cause the otoconia to move, which in turn causes a plunger effect on endolymph in the canal. This leads to hair cell stimulation, and the cupula is displaced.10,12 The central nervous system (CNS) interprets these signals as angular acceleration of the head when none exists, producing vertigo and nystagmus.10,13 Cupulolithiasis, where otoconia are adherent to the cupula of a semicircular canal, also can occur but is less common.9 The cupula with the attached otoconia is thought to become heavy relative to the endolymph and deflects hair cells with position change causing vertigo and nystagmus.13 Vertigo found in other conditions (e.g., migraine and stroke) is thought to be due to ischemia to labyrinth. 14 Tumors can cause vertigo through deformation of the labyrinth or vestibular structures. In Meniere’s disease, vertigo is thought to occur from end organ deformation due to endolymphatic hydrops.15 Presyncopal lightheadedness is caused by transient global hypoperfusion to the brain, which usually is due to cardiovascular-mediated abnormalities. Common causes include arrhythmias, orthostatic hypotension, autonomic dysfunction, cerebrovascular atherosclerotic disease, anemia, and dehydration.10,16 Disequilibrium is thought to cause dizziness through a loss of visual, vestibular, and/or somatosensory input needed to maintain balance.17

History

The history obtained in the evaluation of a dizzy patient is the most important aspect of the EP’s workup. In up to 76% of cases of dizziness, a diagnosis may be made from history alone.18,19 History was most sensitive in diagnosing vertigo (87%), presyncope (74%), psychiatric disorders (55%), and least sensitive in disequilibrium (33%).19 Unfortunatel,y it has been found that up to 40% of some patients’ complaints are too indistinct to fit into a single category18 Regardless, a meticulous history that attempts to precisely define symptoms and elicits inciting and modifying factors is paramount. It is important to have the patient describe exactly what he experiences when he complains of dizziness without biasing his answer. This often can be accomplished by asking the patient to describe his symptoms without using the word “dizzy.” Even then it can be very difficult for the patient to put the symptoms into a meaningful description. Determining the exact sense of imbalance is important. A sense that the patient or his environment is moving (i.e., usually spinning) suggests vertigo. Presyncopal lightheadedness is described as a sense of impending faint and is due to transient diffuse cerebral hypoperfusion as may occur with orthostatic hypotension.

Disequilibrium is a loss of balance without head sensation often due to neuromuscular problems. The “Other” category of dizziness, frequently attributed to psychiatric illness, often is accompanied by other somatic complaints and/or signs of underlying psychiatric involvement.20,21 Rapidity of onset and severity of symptoms are important to elicit. Generally, rapid severe symptoms suggest peripheral vertigo, though this also may occur with cerebellar bleeding/infarction. Mild symptoms with gradual onset are more suggestive of a central process (e.g. tumor). Associated symptoms are important to ascertain; benign conditions usually are not associated with such complaints as headache, altered mental status, focal weakness/numbness, speech difficulty, neck pain, or vision disturbance. Symptoms such as nausea/vomiting, diaphoresis, and pallor are not uncommon with vertigo.22 Noting the duration of symptoms is also essential; an episodic nature is often suggestive of a benign peripheral process, whereas continuous symptoms are more likely due to a more malignant central one. Modifying or inciting factors are important to identify. Symptoms that are brought on by head movement suggest a vestibular process.23 Medication history also is critical; prescribed medication toxicity has been found to cause dizziness in up to 10% of cases.20 Past medical history is also important to obtain. Patients with benign vertigo may have had previous similar episodes. Knowing other medical conditions may give clues as to the etiology of a current episode (i.e., similar lightheadedness in a patient with a history of cardiac arrhythmia). Unfortunately, while these historical features often are useful and generally hold true, they are not foolproof in determining benign etiologies from more serious ones. The practitioner’s clinical suspicion should be considered. Additionally, history from family members also is helpful to add to and corroborate the information obtained from the patient.

Physical Examination

In addition to a thorough history, a methodical physical examination is vital. Physical examination has been found helpful in confirming the diagnosis made by the patient’s history but rarely changed it.19 Potentially useful examination maneuvers include Dix- Hallpike testing, determination of orthostatic vital signs, gaze testing for nystagmus, and gait testing. It is difficult to limit the examination to certain body systems; there may be multiple systems that are potentially causative or at least involved in the patient’s dizziness. Orthostatic vital signs may be important to check because they can indicate volume depletion as a factor. Specifics of the head examination include checking the ears for cerumen impaction and otitis media, which have been reported to cause vertigo. Tympanic membrane perforation or nystagmus elicited by pneumatic otoscopy may indicate perilymphatic fistula. 24 Cholesteatoma may be suggested by noting a white pearl-like mass behind the tympanic membrane. Detection of vertigo with impaired hearing to whispered voice may indicate sensorineural hearing loss from tumor with compression of the ipsilateral 8th nerve.1 The eye examination is vital to differentiate central from peripheral processes. Peripheral vertigo may have either horizontal or rotatory nystagmus, which abates with visual fixation. With horizontal nystagmus, the slow component of eye movement is toward the affected ear with rapid movement back to the midline. Central vertigo can be horizontal or rotatory, but does not fatigue with visual fixation. Vertical, direction-changing or dyscongugate nystagmus, or nystagmus that is not suppressed with visual fixation is always abnormal and indicates a central process.1 A few beats of horizontal nystagmus on extremes of lateral gaze is normal. One study found that about 10% of patients with BPPV will not have clinically detectable nystagmus.25 A fundoscopic examination looking for papilledema may be important in assessing indirect signs of increased intracranial pressure as with an intracranial mass. Pupillary function and extraocular movement examination is also crucial. Third or sixth nerve palsy may indicate brainstem pathology or multiple sclerosis. 22 Visual acuity and visual field testing helps to determine if there is a sensory input deficit contributing to the patient’s dizziness. More thorough cranial nerve examination is indicated based upon clinical findings. Testing for gait, dysmetria, and dysdiadochokinesia, and pronator drift should be performed for cerebellar dysfunction. Gait examination that shows a tendency to fall to the side of the lesion while walking is typical of peripheral vestibulopathy. Falling away from the lesion is usually from a central cause. 26 Cerebellar abnormalities suggest infarction or bleeding and are not found with peripheral vestibulopathies. Romberg testing should be done, but it actually tests proprioception rather than the cerebellum. Auscultation of bruits along the carotid artery may suggest atherosclerotic disease as the etiology of dizziness. Hyperventilation, if present, is nearly always associated with a psychiatric cause, usually an anxiety disorder.2

Another helpful test in differentiating peripheral from central vertigo is the Dix-Hallpike maneuver. This often erroneously is referred to as the Barany or Nylen-Barany test. This is the classic test for BPPV due to canalithiasis in the posterior semicircular canal, which is the most commonly affected canal.27 The maneuver begins with the patient seated in the upright position (Figure 1). The examiner supports the patient’s head and turns it 45 degrees to one side. The patient then quickly assumes the supine position with the head hyperextended approximately 45 degrees over the edge of the bed. The patient should keep his eyes open even if he feels dizzy and should look straight ahead. The procedure then is repeated with the head turned 45 degrees in the opposite direction.28 The ear in the downward position when nystagmus and vertigo are elicited is the affected ear.13 Nystagmus from a peripheral vestibulopathy is either horizontal or rotatory, has latency of onset of several seconds, extinguishes with fixation, and lasts fewer than 30 seconds.23,29 The nystagmus also may reverse direction when the patient assumes the sitting position.13 Nystagmus that has immediate onset, is vertical, or does not fatigue is suggestive of a central disorder. In a meta-analysis by Hoffman, the Dix-Hallpike maneuver was positive in 50-88% of those patients with BPPV.29-32 If initial testing in patients with symptoms suggesting BPPV fails to elicit nystagmus, lying supine and repeating the test will confirm the diagnosis up to 20% of the time. If symptoms of BPPV are present and Dix-Hallpike testing is negative, a side-lying variation of the Dix-Hallpike should be performed to test for horizontal canal BPPV, which occurs less than 1% of the time.33 Dix-Hallpike testing may have limited utility in obese patients and those without normal range of motion in the neck, trunk, and hips. An alternative side-lying technique has been described that was shown to have equivalent findings to the traditional technique.34

Laboratory Testing

Laboratory testing adds little to the evaluation of dizziness. In a meta-analysis by Hoffman, lab abnormalities that explained the dizziness were found in only 3 of 4538 patients.29 A study by Stewart and colleagues found blood laboratory studies to have low utility and were determined not to be cost effective in the routine work-up of vertigo.35 Hemoglobin and hematocrit levels determination may be indicated if anemia is suspected. Chemistry studies to evaluate for pre-renal azotemia or adrenal insufficiency also may be indicated if these conditions are suspected. Blood glucose level determination also may be helpful occasionally. Other laboratory studies are not routinely indicated.2 Routine use of electrocardiogram (ECG), blood testing, and magnetic resonance imaging (MRI) is not recommended due to the frequency of abnormalities seen in symptom-free controls.36

Cardiovascular Testing

Electrocardiograms rarely are helpful in the evaluation of the dizzy patient. Two studies found no electrocardiogram changes that were diagnostic in dizzy patients.37,38 An ED series reported significant electrocardiogram findings in six of 125 patients, five of whom had a known history of arrhythmia.39 Ambulatory electrocardiographic monitoring was normal in 70% of dizzy patients, half of whom had symptoms. Paroxysmal atrial fibrillation was the most common abnormality found, but no patients had symptoms during episodes of the arrhythmia.36 Noninvasive carotid studies found hemodynamically significant lesions in 21 of 101 patients referred with dizziness but were normal in the seven patients with complaints of isolated vertigo.40

Imaging

Routine imaging of the dizzy patient is not required. Computerized tomography (CT) scans frequently are not helpful; they are not the ideal study to evaluate for intracranial mass lesions, and cannot diagnose multiple sclerosis. Additionally, CT is not ideal for imaging the posterior fossa (e.g., cerebellum, pons, medulla), which is often the area of the brain with abnormalities causing central vertigo. In the evaluation of vertigo/dizziness thought to be due to a central process, MRI is usually the imaging modality of choice.41 When MRI is used as a general screening tool for undifferentiated vertigo, it is not cost effective. If applied more selectively in patients with symptoms that suggest a central cause, the cost effectiveness likely increases.35

The Subtypes of Dizziness

Vertigo. Vertigo is a subtype of dizziness with patients describing the illusion that they (subjective vertigo) or their environment (objective vertigo) is spinning.13 Although there are a large number of causes, an immediate concern for the EP is to distinguish between relatively benign peripheral causes and potentially life-threatening central causes (Figure 2). Central versus peripheral causes will be discussed further.

Figure 2.
Differentiating Peripheral Versus Central Vertigo

Peripheral Vertigo. BPPV. First described by Barany in 1921, BPPV is characterized by brief, self-limited (paroxysmal) episodes of vertigo provoked by typical position changes.42 It is most common between the 5th-7th decades. There is a female predominance 1.6:1.13 The most common cause of BPPV is primary or idiopathic and accounts for 50-70% of cases. The most common secondary cause is trauma accounting for up to 17% of cases.9 Symptoms include sudden onset of vertigo, nystagmus, nausea, and a tendency to fall to the side of the lesion without cochlear or other neurologic symptoms.26 Symptoms are usually acute onset, short in duration (i.e., lasting < 30 seconds), severe, and brought on by certain head positions and movements. Common movements include rolling over in bed, looking up, and bending forward.28 Although usually a benign condition, patients are at risk for falls and other traumatic injuries (i.e., motor vehicle crash while driving). History, eye findings, and response to the Dix-Hallpike maneuver are usually all that is needed to make the diagnosis. Nystagmus usually has a latency of several seconds, is horizontal or rotatory, and fatigues with visual fixation. Vertigo does tend to recur with rates of about 10-15% per year.43

Canalith Repositioning Procedures

The recommended treatment for BPPV is a canalith repositioning procedure (CRP). There are several CRPs described in the literature; the most studied and used in the United States was first described by Epley in 1992.9,44 It is a series of position changes that attempts to restore the free-floating otoliths in the posterior semicircular canal to their proper place in the utricle. The maneuvers are effective, safe, inexpensive, and have few side effects or relative contraindications. The Vestibular Disorders Association recommends the Epley maneuver as firstline treatment for BPPV.42 The Epley maneuver is performed as follows (Figure 3):

1. The patient starts in the sitting position. 2. Then, he assumes the supine position with head extended over the edge of a table (stretcher) at a 45-degree angle with the head turned toward the affected side. 3. Once the vertigo and nystagmus have ceased, the head is then turned opposite the affected labyrinth 45 degrees from the midline. 4. The patient’s body then is turned in that direction assuming the lateral decubitus position with the head slightly angled and looking at the floor. 5. The patient then is returned to the sitting position. 6. The chin is tilted down to touch the chest.28

This maneuver may need to be performed more than once. Another CRP, the Semont maneuver, involves having the patient assume a side-lying position with the affected ear down for four minutes, then quickly turning over so that the other ear is down for four minutes, then returning to the sitting position.45,46

A meta-analysis that includes a Cochrane review found that those patients treated with CRP were more likely to demonstrate symptom resolution at the time of first follow-up, though there were few methodologically sound studies from which to extract these data.12 Multiple studies have shown that the Epley maneuver provides both objective (i.e, positive Dix-Hallpike maneuver to negative maneuver) and subjective improvement in treating BPPV. 45,47-52 It has also been shown that generalists and EPs have been able to effectively use the Epley maneuver in the treatment of BPPV.53,31 In many patients, BPPV will resolve spontaneously; at one month as many as 23% of patients still will be symptomatic.54 Tirelli found that if patients have symptoms of BPPV, but nystagmus cannot be elicited with Dix-Hallpike testing, CRPs still were 60% effective in relieving symptoms.25 Steenerson found equivalent efficacy with Epley and Semont techniques in resolving BPPV with 94% and 98% success rates, respectively.44 The Epley maneuver required fewer treatment sessions than Semont (2.98 vs. 4.34, respectively) and had fewer recurrences at six months (12% Epley vs. 21.8% Semont).44,12 Success rates of relieving BPPV with single treatment sessions for the Epley maneuver are reported from 44-88%.45,48,55-58 The only factor shown to be associated with need for multiple treatments was BPPV not located in a single posterior semicircular canal.58 The Epley maneuver also is thought to be easier to perform in older patients.45,48 Some advocate having the patient remain upright for one or two days after CRP, sleep upright, and avoid bending over, though studies have not shown post-CRP position instructions to make a difference.13,59,60 CRP maneuvers can be taught to patients who can do them at home, either for continued treatment of their BPPV that is not resolved completely in the ED or for recurrences. In this case, the Epley maneuver was shown to be more effective in relieving BPPV than the Semont maneuver.61 There is no evidence to show that these maneuvers affect later recurrences of BPPV.62

Vestibular sedatives, benzodiazepines, and antihistamines (e,g., meclizine) are thought to improve symptoms through blocking cholinergic transmission in the vestibular nuclei. Although some physicians recommend them, there are little data to support their efficacy, and they should be considered only as adjunctive therapy to those with BPPV with severe symptoms (primarily nausea).63 CRP maneuvers are considered definitive firstline treatment.13,61 Because it has antiemetic properties, meclizine may be an effective adjunct to CRP treatment of BPPV.64 Also, these medications may impair vestibular compensation and habituation and cause sedation with increased fall risk.65 Treatment of associated nausea may require use of antiemetics. Medications (e.g., promethazine and metoclopromide) are useful for their effects on nausea and due to anticholinergic and antidopaminergic properties, which may help reduce vertigo symptoms.10 Patients with BPPV usually are treated as outpatients, provided they have adequate support, do not have intractable vomiting, and their vertigo is not so severe as to put them at risk for falls. They should be encouraged not to drive or perform any other similarly dangerous activity until their symptoms have resolved completely. Outpatient otolaryngology or neurology referral is indicated.

Meniere’s Disease

The classic triad of tinnitus, fluctuating hearing loss, and vertigo characterizes this condition. Attacks can be severe with vomiting and aural pressure/fullness. Unilateral sensorineural hearing loss suggests Meniere’s disease. Usually with spontaneous recovery in hours to days, the disease becomes progressively more frequent and severe. Hearing abnormalities may not resolve between episodes. Meniere’s disease is caused by excessive production or reduced resorption of endolymph.24 An autoimmune mechanism also may be involved. The mechanism of vertigo in Meniere’s disease is not understood well but does not appear to be due to cupulolithiasis or canalithiasis.26 Treatment is generally effective and includes salt restriction, smoking cessation, caffeine avoidance, and diuretics to reduce endolymphatic fluid. A histamine derivative, betahistine, also has been shown to be effective by reducing asymmetrical vestibular function and increasing vestibular blood flow.10,65 Vestibular suppressants (e.g., meclizine) and central suppressants (e.g., valium) may be effective in reducing symptoms but not correcting the underlying pathophysiology.24,64 As with BPPV, patients with Meniere’s disease usually can be treated as outpatients with otolaryngology or neurology follow-up.

Vestibular Neuronitis (Acute Labyrinthitis)

The terms labyrinthitis and vestibular neuronitis are used interchangeably by some physicians. Others differentiate vestibular neuronitis as affecting only the vestibular fibers of the 8th nerve and not causing hearing loss. Labyrintitis affects both the vestibular and cochlear portions of the 8th nerve and usually is associated with hearing loss.64 Here, they both will be referred to as vestibular neuronitis because the pathophysiology and treatment are the same. Most commonly thought to be caused by viral infections (without much support) that affect the vestibular nuclei, symptoms usually follow an upper respiratory infection within two weeks.24,66 Other viruses (e.g., measles, mumps and rubella) also have been implicated. Otic herpes zoster that also affects CN VII and VIII is known as Ramsay Hunt syndrome.24 Bacterial infections such as otitis media also are thought to cause vestibular neuronitis.10 This condition is characterized by single or recurrent sudden episodes of vertigo that are severe for several days then subside during the course of a few weeks. Frequently it is associated with nausea, vomiting, and hearing loss. Also, the patient with vestibular neuronitis will have a positive (i.e., abnormal) head impulse (head thrust) test. In a patient with right-sided vestibular neuronitis, if the head is turned rapidly 15 degrees to the right, the patient is unable to maintain visual fixation on a distant object and must make voluntary rapid eye movements (saccades) back to the target, indicating loss of the vestibulooccular reflex. If this reflex is preserved, vestibular neuronitis is not present and symptoms likely are due to a cerebellar infarction.66,67Treatment centers on bed rest and pharmacologic suppression of symptoms with vestibular sedatives and antiemetics. 24,65 Medication usage should be withdrawn after a few days, if possible, and activity encouraged facilitating central compensation.64 Viral testing is not indicated because causation of a vestibular syndrome cannot be proven.67 Prednisone is helpful in the first ten days of treatment and may accelerate the process of central compensation.65,68 Treatment with antivirals is indicated only for Ramsay Hunt syndrome.68 Patients with vestibular neuronitis usually can be treated as outpatients with otolaryngology or neurology referral.

Traumatic Vertigo

Mild traumatic brain injury is the second most common neurologic disorder. The mechanism by which vertigo is caused is unclear but may be due to labyrinthine concussion with massive dislodging of otoconia.69 This conditon can occur with blunt or whiplash-type trauma. Vertigo or nonspecific dizziness may be part of a postconcussive syndrome. Temporal bone fracture also must be ruled out, especially if there is hearing loss. Perilymphatic fistulas may occur after trauma and cause vertigo.70 The mechanism is thought to be due to disruption of the lining membranes of the labyrinth at the oval or round windows.15 Perilymphatic fistula may result from trauma such as straining with weight lifting, barotraumas from diving and flying, or forceful coughing or nose blowing.65 An opening in either the round or oval window allows pressure changes to be transmitted to the vestibular apparatus. Diagnosis is made by inducing vertigo with pneumatic otoscopy. This condition usually heals spontaneously. Noncontrast CT scans generally are indicated at the time of traumatic injury to rule out intracranial bleeding or skull fracture.10 Bed rest and avoiding head positions and other activities (e.g., sneezing, cough, straining) that elicit symptoms are helpful.65 Surgery to repair the fistula occasionally is required.71 Otolaryngology or neurology referral for follow-up examination and treatment is indicated

Other Causes of Peripheral Vertigo

Cerumen impaction and external auditory canal foreign bodies can cause vertigo. Usually, symptoms will resolve with removal of the offending material.10

Central Causes of Vertigo

Central vertigo is caused by dysfunction of the vestibular portion of the 8th nerve, vestibular nuclei in the brainstem, and their central connections.72 It is uncommon in ED settings, accounting for less than 5% of vertigo cases.64

Cerebrovascular Disorders. Cerebrovascular disorders account for the largest proportion of causes of central vertigo. Vertigo rarely accompanies strokes/transient ischemic attacks of the anterior circulation, which supplies the bilateral cerebral hemispheres, internal carotids, and middle and anterior cerebral arteries. Vertigo is present in more than 75% of strokes/transient ischemic attacks involving the posterior circulation, which supplies the brainstem, cerebellum, and peripheral vestibular apparatus, basilar, vertebral, anterior and posterior inferior cerebellar arteries.73 Posterior circulation etiologies for vertigo also are accompanied by other neurologic symptoms, usually dysarthria, numbness, diplopia, or hemiparesis.

These findings, though, may be very subtle and not even obvious to the patient.10,73 A crossed defect (e.g., sensory/motor defect on one side of the face and the opposite side of the body) is characteristic of a brainstem lesion. Transient blindness, diplopia, or hemianopia may occur with occipital lobe ischemia. Ataxia, imbalance, and disequilibrium may occur with cerebellar ischemia.72 Isolated, transient vertigo can occasionally occur.68 This condition may occur with vertebral artery atherosclerosis, where certain head positions (i.e., turning to the side) may occlude the vessel and impair brainstem blood flow inducing transient ischemia. This condition is referred to as vertebrobasilar insufficiency (VBI). VBI usually is associated with other neurologic signs or symptoms that resolve. Cerebellar infarction is the primary serious condition to rule out in the patient with suspected vestibular neuronitis.66 This is especially important because about one third of cerebellar infarctions will develop life-threatening posterior fossa edema requiring neurosurgical decompression. Also, the cause of cerebellar infarction is usually from a cardioembolic source and requires anticoagulation.74 Examination findings that indicate cerebellar infarction include vertical or dysconjugate nystagmus that is not suppressed with visual fixation and the inability to stand without support.66,72 Additionally, the patient has a normal head impulse (head thrust) test result differentiating this condition from vestibular neuronitis (See section on vestibular neuronitis.). Dissection of the vertebral or basilar arteries most commonly is associated with vertigo and head or neck pain. Vertigo associated with head or neck pain is a dissection until proven otherwise.75 Dissections have been well described after relatively minor trauma (e.g., motor vehicle crashes and chiropractic manipulation). MRI usually is required to radiographically diagnose posterior circulation cerebrovascular accidents. MR angiogram is the imaging modality of choice for suspected dissection and other posterior circulation abnormalities. Treatment of VBI usually requires antiplatelet agents and neurology consultation.65 Treatment of dissection involves neurology/neurosurgical consultation and heparinization.

Migraine. Vertigo occurs in up to 33% and nonspecific dizziness occurs in up to 72% of patients with migraine.14 Vertigo may be part of the aura before headache, a migraine equivalent, or may be unrelated to headache.66 It is thought to be due to vascular damage to the labyrinth.76 It can be spontaneous or positional.77 Usually migraine- associated vertigo repeatedly is accompanied by migraine symptoms (e.g., photophobia).78 Basilar artery migraine has symptoms similar to vertebrobasilar insufficiency (VBI) as described below.10 Other causes of vertigo also must be ruled out. Vertigo in patients with migraines often can be treated with medicines used to treat migraines (e.g., ergots and triptans).66 Tricyclic antidepressants and beta blockers also have been found to be effective.14 Vestibular suppressants and referral for neurology follow-up and vestibular rehabilitation therapy is indicated.

Tumor. Cerebellopontine angle tumors (usually acoustic neuromas) rarely present with isolated vertigo. Headache often is present. Decreased hearing or tinnitus usually is present from compression of the cochlear portion of the 8th nerve. Disequilibrium usually is more commonly present than vertigo.71,72 Posterior fossa tumors may present with symptoms of central vertigo and also have oscillopsia (i.e., a visual illusion of objects bouncing or jiggling).72 Diagnosis is confirmed with MRI, and neurosurgical consultation is required.

Cerebellar Hemorrhage. Cerebellar hemorrhage usually presents with acute ataxia, ipsilateral gaze palsy, and ipsilateral cranial nerve VII palsy. The vertigo that accompanies this condition is usually of a sense of front-to-back or side-to-side motion rather than spinning.10 Other accompanying symptoms include dizziness, repeated vomiting, dysmetrias, dysarthria, and inability to stand or walk. Rarely is this condition associated with hemiparesis or hemiplegia. Cerebellar edema may cause herniation of the tonsils into the foramen magnum with brainstem compression. Rapid recognition and neurosurgical decompression is often life-saving.10,71,79

Multiple Sclerosis. This condition is caused by CNS demyelinization. Patients present with vertigo that is quite variable in severity and duration, ataxia, severe nystagmus, and often other ocular symptoms such as neuritis. Diagnosis is confirmed by MRI. Neurology referral is required.10

Wallenberg Lateral Medullary Syndrome. This syndrome is caused by an infarction of the lateral medulla from occlusion of the intracranial vertebral artery and also the posterior inferior cerebellar artery. Symptoms begin acutely with vertigo, ataxia, nausea, and nystagmus. There is loss of ipsilateral facial pain and temperature sensation. Additionally, Horner’s syndrome and paresis of pharyngeal and laryngeal muscles resulting in dysphagia and dysphonia are present. Loss of pain and temperature sensation also occurs on the contralateral side of the body. MRI and urgent neurology referral are indicated.10,79

Systemic Causes of Vertigo. Drugs are commonly found to cause vertigo. These include anticonvulsants, hypnotics, antihypertensives, furosemide, analgesics, tranquilizers, and aminoglycoside antibiotics.72 Symptoms usually will abate with discontinuing the offending drug, though aminoglycosides can result in permanent effects.71 Acute and chronic alcohol use may also cause vertigo. Endocrine disorders (e.g., hypothyroidism and diabetes mellitus) though more likely to cause disequilibrium, also can cause vertigo.72

Psychiatric Dizziness

Dizziness is a common complaint with certain psychiatric disorders and is the second most common symptom reported by patients with panic disorder.80 It is often difficult to determine the cause of psychiatric dizziness because it is hard to know if the underlying psychiatric disorder is causing the dizziness or if the dizziness (usually vertigo) is causing the psychiatric symptoms. Often these spells, if psychogenic, can be reproduced by having the patient hyperventilate.71,80 Frequently, psychiatric vertigo is associated with situational or environmental fears similar to agoraphobia.80 Other features of patients with psychogenic dizziness include moment- to-moment fluctuations in symptoms; excessive slowness or hesitation; exaggerated sway with Romberg testing (often distractible); extreme caution with restricted steps (e.g., walking on ice); or sudden buckling of the knees usually without falling.68 It has been proposed that psychiatric dizziness “should occur exclusively in combination with other symptoms as part of a recognized psychiatric symptom cluster, and this symptom cluster is not itself related to vestibular dysfunction.”80 Treatment for the underlying psychiatric disorder often improves the dizziness. Because this condition is usually related to anxiety and panic disorders, benzodiazepines are the mainstay of treatment.64

Disequilibrium

This can be a very difficult complaint to assess and treat. There are usually multiple factors involved, some of which are amenable to treatment, and some are not. Frequently, it is seen in the elderly population with multiple age-related issues contributing to the disequilibrium. Patients often complain of ill-defined dizziness and gait unsteadiness.36 It often is associated with age-related decreases in vision and hearing, neuropathy, impaired proprioceptive input, and central compensatory mechanisms. Frequently, there is muscle mass decrease, decreased range of motion, and increased reflex time involved.68 Cervical spondylosis may be associated with dizziness related to disturbance in postural control.81 Frequently, there is some degree of postural instability. Anxiety is commonly a contributing factor but less likely in elderly patients to be the primary cause.36,37 Many medications prescribed can contribute to these symptoms (e.g., beta blockers, diuretics, sedatives). Central vascular and cardiovascular causes —especially carotid sinus hypersensitivity— are common.36,82 Parkinson’s disease must be ruled out. Thorough history and physical examination is required, but a diagnosis can be made in most cases.82 Falls are a major risk for those patients with disequilibrium and occur four times as often as in controls.17 Treatment is based upon the specific etiology that is found. Referrals for balance training and vestibular rehabilitation may be helpful.36

Presyncope

Presyncope was found as the cause in up to 16% of patients presenting with dizziness to EDs.39 It is an impending feeling that one is about to pass out and is due to transient cerebral hypoperfusion. Occasionally, this is the prodrome to an actual syncopal event. Syncope often may be avoided if the patient assumes the supine position or the underlying etiology resolves (e.g., paroxysmal arrhythmia). The causes of presyncope are the same as for the causes of syncope. The most common broad categories of presyncope include neurocardiogenic (e.g., vasovagal), postural (e.g., orthostatic) hypotension, and cardiac causes (e.g., arrhythmias and valvular disease).10 Frequently, etiologies for this symptom are not found. Neurocardiogenic causes account for about 50% of cases and may be precipitated by fear, pain, or emotional stress. There is an inappropriate vasodilation with relative bradycardia that leads to hypotension, lightheadedness, tunnel vision, diaphoresis, and diffuse weakness. It usually can be averted by assuming the supine position and elevating the legs.83 Postural hypotension is defined variably. In general, there is a drop (> 20 Torr) in systolic blood pressure and a drop (> 10 Torr) in diastolic blood pressure within 3 minutes of standing. Reproduction of symptoms of lightheadedness is also important.16 Many conditions can cause that including dehydration, anemia, medications (e.g., diuretics, beta blockers), and autonomic dysfunction (e.g., diabetes mellitus, Parkinson’s disease). Frequently, there are multiple factors contributing to the individual patient’s condition. Treatment of this condition requires finding a specific etiology and possible referral for tilt table testing.10

Conclusion

Dizziness can be a very challenging complaint for the EP to evaluate. In general it is due to benign, self-limited conditions. Unfortunately, there can be significant morbidity and disability even with these benign conditions. Frequently, the cause of dizziness can be a serious and life-threatening condition that requires prompt recognition and treatment for a favorable outcome. It is essential that the EP understand the pathophysiology of the different causes of dizziness. It is also imperative that the EP be able to take an accurate history and perform a thorough physical examination; these are the investigative tools that will allow the condition to be appropriately diagnosed and treated. (See Dizziness flowchart.)

References

1. Harwood-Nuss A et al, eds. The Clinical Practice of Emergency Medicine. 3rd ed. Philadelphia:Lippincott, Williams and Wilkins, 2001.

2. Kroenke K, Mangelsdorff D. Common symptoms in ambulatory care: incidence, evaluation, therapy and outcome. Am J Med 1989;86:262-6.

3. McCaig LF, Burt CW. National Hospital Ambulatory Medical Data from Vital and Health Statistics; no 335, Hyattsville, MD National Center for Health Statistics, 2003.

4. Li JC, Li CJ, Epley J, et al. Cost-effective management of benign positional vertigo using canalith repositioning. Otolaryngol Head Neck Surg 2000;122:334-9.

5. Sloane PD, Blazer D, George LK. Dizziness in a community elderly population. J Am Geriatr Soc 1989;37:101-8.

6. Boult C, Murphy J, Sloane P, et al. The relation of dizziness to functional decline. J Am Geriatr Soc 1991;39:858-61.

7. Drachman DA, Hart CW. An approach to the dizzy patient. Neurology 1972; 22:322- 334.

8. Kroenke K, Hoffman FM, Einstadter D. How common are various causes of dizziness? A critical review. South Med J 2000;92: 160-167.

9. Parnes LS, Agrawal SK, Atlas J. Diagnosis and management of benign paroxysmal positional vertigo (BPPV). Can Med Assoc Journal 2003;169:681-93.

10. Tintinalli JE, Kellen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw-Hill, 2004.

11. von Brevern M, Seelig T, Neuhauser H,et al. Benign paroxysmal positional vertigo predominantly affects the right labyrinth. J Neurol Neurosurg Psychiatry 2004;75:1487-1488.

12. Woodworth BA, Gillespie MB, Lambert PR. The canalith repositioning procedure for benign positional vertigo: a meta-analysis. Laryngoscope 2004;114:1143-1146.

13. Koelliker P, Summers RL, Hawkins B. Benign paroxysmal positional vertigo: Diagnosis and treatment in the emergency department- a review of the literature and discussion of canalith-repositioning maneuvers. Ann Emerg Med 2001;37:392-398.

14. Reploeg M, Goebel J. Migraine-associated dizziness: patient characteristics and management options. Otol Neurotol 2002;23:364-71.

15. Baloh RW. Vertigo. Lancet 1998;352:1841-1846.

16. Hermosillo AG, Marquez MF, Jauregui-Renaud K, et al. Orthostatic hypotension, 2001. Cardiol Rev 2001;9:339-47

17. Kerber KA, Enrietto JA, Jacobson KM, et al. Disequilibrium in older people: a prospective study. Neurology 1998;51:574-580.

18. Sloane PD, Baloh RW. Persistent dizziness in geriatric patients. J Am Geriatr Soc 1989;37:1031-1038.

19. Kroenke K, Lucas CA, Rosenberg ML, et al. Causes of persistent dizziness. A prospective study of 100 patients in ambulatory care. Ann Intern Med 1992;117:898-904.

20. Sloane PD, Coeytaux RR, Beck RS, et al. Dizziness: state of the science. Ann Intern Med 2001;134:823-32.

21. Sloane PD, Hartman M, Mitchell CM. Psychological factors associated with chronic dizziness in patients aged 60 and older. J Am Geriatr Soc 1994;42:847-852.

22. Marx JA et al, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis: Mosby, 2002.

23. Eggers SDZ, Zee DS. Evaluating the dizzy patient: bedside examination and laboratory assessment of the vestibular system. Seminars in Neurology 2003; 23:47-57.

24. Rubin AM, Zafar SS. The assessment and management of the dizzy patient. Otolaryngol Clin N Am 2002;35:255-273.

25. Tirelli G, D’Orlando E, Giacomarra V, et al. Benign positional vertigo without detectable nystagmus. Laryngoscope 2001;111:1053-1056.

26. Magnusson M, Karlberg M. Peripheral vestibular disorders with acute onset of vertigo. Curr Opin Neurol 2002;15:5-10.

27. Dix MR, Hallpike CS. The pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Proceedings of the Royal Society of Medicine 1952;45:341-354.

28. Furman JF, Cass SP. Primary care: benign paroxysmal positional vertigo. N Engl J Med 1999; 341:1590-1596.

29. Hoffman RM, Einstadter D, Kroenke K. Evaluating dizziness. Am J Med 1999;107:468-478.

30. 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;66:596-601.

31. Bloom J, Katsarkas A. Paroxysmal positional vertigo in the elderly. J Otolaryngol 1989;18:96-98.

32. Katsarkas A, Kirkham TH. Paroxysmal positional vertigo- a study of 255 cases. J Otolaryngol 1978;7:320-330.

33. Viiree E, Purcell I, Baloh RW. The Dix-Hallpike test and the canalith repositioning maneuver. Laryngoscope 2005;115:184-187.

34. Cohen HS. Side-lying as an alternative to the Dix-Hallpike test of the posterior canal. Otol Neurotol 2004;25:130-134.

35. Stewart JG, Chen AY, Wyatt JR, et al. Cost-effectiveness of the diagnostic evaluation of vertigo. Laryngoscope 1999;109:600-605.

36. Colledge NR, Barr-Hamilton RM, Lewis SJ, et al. Evaluation of investigations to diagnose the cause of dizziness in elderly people: a community based controlled study. BMJ 1996;313:788-792

37. Kroenke K, Lucas CA, Rosenberg ML, et al. Causes of persistent dizziness: a prospective study of 100 patients in ambulatory care. Ann Int Med 1992;117:898-904.

38. Madlon-Kay DJ. Evaluation and outcome of the dizzy patient. J Fam Pract 1985;21:109-113

39. Herr RD, Zun L, Matthews JJ. A directed approach to the dizzy patient. Ann Emerg Med 1989;18:664-672.

40. Weinberger J, Biscarra V, Weisberg MK. Hemodynamics of the carotid-artery circulation in the elderly “dizzy” patient. J Am Geriatr Soc 1981;29:402-406.

41. Delaney KA. Bedside diagnosis of vertigo: value of the history and neurological examination. Acad Emerg Med 2003;10:1388-1395.

42. Strickland C, Russell R, Hoekzema G. What is the best way to manage benign paroxysmal positional vertigo? J Fam Pract 2003; 52: 971-973.

43. Sakaida M, Takeuchi K, Ishinaga H, et al. Long-term outcome of benign paroxysmal positional vertigo. Neurology 2003;60:1532-1534.

44. Steenerson RL, Cronin GW, Marbach PM. Effectiveness of treatment techniques in 923 cases of benign paroxysmal positional vertigo. Laryngoscope 2005;115:226- 231.

45. Herdman SJ, Tusa RJ, Zee DS. Single treatment approaches to benign paroxysmal positional vertigo. Arch Otolaryngol Head Neck Surg 1993;119: 450-453.

46. 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;75 :695-700.

47. Epley JM. The canalith repositioning procedure: for treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 1992;107:399-404.

48. Parnes LS, Price-Jones RG. Particle repositioning maneuver for benign paroxysmal positional vertigo. Ann Otol Rhinol Laryngol 1993;102:325-331.

49. Lynn S, Pool A, Rose D, et al. Randomized trial of the canalolith repositioning procedure. Otolaryngol Head Neck Surg 1995; 113:712-720.

50. Wolf M, Hertanu T, Novikov I, et al. Epley’s manoeuvre for benign paroxysmal positional vertigo: a prospective study. Clin Otolaryngol 1996;24:43-46.

51. Asawavichianginda S, Isipradit P, Snidvoras K, et al. Canalolith repositioning for benign paroxysmal positional vertigo: a randomized controlled trial. Ear Nose Throat J 2000;79:732-737.

52. Cohen HS, Jerabek J. Efficacy of treatment for posterior canal benign paroxysmal positional vertigo. Laryngoscope 1999; 109:584-590.

53. Chang AK, Schoeman G, Hill MA. A randomized clinical trial to assess the efficacy of the Epley maneuver in the treatment of acute benign positional vertigo. Acad Emerg Med 2004;11:918-924.

54. Baloh RW, Honrubia V, Jacobson K. Benign positional vertigo: clinical and oculographic features in 240 cases. Neurology 1987; 37:371-378.

55. Blakely BW. A randomized, controlled assessment of the canalolith repositioning maneuver. Otolaryngol Head Neck Surg 1994;3:55-7.

56. Weider DJ, Ryder CJ, Stram JR. Benign paroxysmal positional vertigo: analysis of 44 cases treated by the canalolith repositioning procedure of Epley. Am J Otol 1994;15:321-326.

57. Welling DB, Barnes DE. Particle repositioning maneuver for benign paroxysmal positional vertigo. Laryngoscope 1996;104:946-949.

58. Macias JD, Lambert KM, Massingale S, et al. Variables affecting treatment in benign paroxysmal positional vertigo. Laryngoscope 2000;110:1921-1924.

59. Nuti D, Nati C, Passali D. Treatment of benign paroxysmal positional vertigo: no need for postmaneuver restrictions. Otolaryngol Head Neck Surg 200;122:440-444.

60. Massoud EA, Ireland DJ. Post-treatment instructions in the nonsurgical management of benign paroxysmal positional vertigo. J Otolaryngol 1996;25:121-125.

61. Radtke A, von Brevern M, Tiel-Wilck K, et al. Self-treatment of benign paroxysmal positional vertigo: Semont maneuver vs. Epley procedure. Neurology 2004;63:150-152.

62. Hilton M, Pinder D. The Epley (canalolith repositioning) manoeuvre for benign paroxysmal positional vertigo. The Cochrane Database of Systematic Reviews 2005;1.

63. McClure JA, Willett JM. Lorazepam and diazepam in the treatment of benign paroxysmal vertigo. J Otolaryngol 1980;9:472-477.

64. Hain T, Uddin M. Pharmacological treatment of vertigo. CNS Drugs 2003;17:85-100.

65. Dieterich M. Dizziness. Neurology 2004;10:154-64.

66. Halmagyi GM, Cremer PD. Assessment and treatment of dizziness. J Neurol Neurosurg Psychiatry 2000;68:129-134.

67. Baloh RW. Vestibular neuritis. N Engl J Med 2003;348:1027-1032.

68. Tusa RJ. Dizziness. Med Clin N Am 2003;87:609-6041.

69. Guyot JP, Liard P, Thielen K, et al. Isolated vestibular areflexia after blunt head trauma. Ann Otol Rhinol Laryngol 2001;110:562-564.

70. Marzo SJ, Leonetti JP, Raffin MJ, et al. Diagnosis and management of post- traumatic vertigo. Laryngoscope 2004;114:1720-1723.

71. Rowland LP, ed. Merritt’s Neurology. 10th ed. Philadelphia: Lippincott, Williams and Wilkins, 2000.

72. Bradley WG et al, eds. Neurology in Clinical Practice: Principles of Diagnosis and Management. 3rd ed. Boston: Butterworth Heinemann, 2000.

73. McGee SR. Dizzy patients: Diagnosis and treatment. West J Med 1995;162:37-42.

74. Amarenco P. The spectrum of cerebellar infarction. Neurology 1991;41: 973-979.

75. Saeed AB, Shuaib A, Al-Sulaiti G, et al. Vertebral artery dissection: warning symptoms, clinical features and prognosis in 26 patients. Can J Neurol Sci 2000;27:292-296.

76. Lee H, Lopez I, Ishiyama A, et al. Can migraine damage the inner ear? Arch Neurol 2000;57:1631-1634.

77. Neuhauser H, Leopold M, von Brevern M, et al. The interrelations of migraine, vertigo and migrainous vertigo. Neurology 2001; 56:436-441.

78. von Brevern M, Radtke A, Clarke AH, et al. Migrainous vertigo presenting as episodic positional vertigo. Neurology 2004:62:469-472.

79. Toole JF et al. Cerebrovascular Disorders. Philadelphia: Lippincott, Williams and Wilkins, 1999.

80. Furman JM, Jacob RG. Psychiatric dizziness. Neurology 48; 1161-1166.

81. Karlberg M, Johansen R, Magnusson M, et al. Dizziness of suspected cervical origin distinguished by posturographic assessment of human postural dynamics. J Vestib Res 1996;6:37-42.

82. Lawson J, Fitzgerald J, Birchall J, et al. Diagnosis of geriatric patients with severe dizziness. J Am Geriatr Soc 1999;47:12-17.

83. Fauci AS et al, eds. Harrison’s Principles of Internal Medicine. 14th ed. New York: McGraw Hill, 1998.