Evaluation of the patient with vertigo

INTRODUCTION — Vertigo is a symptom of illusory movement. Almost everyone has experienced vertigo as the transient spinning dizziness immediately after turning around rapidly several times. Vertigo can also be a sense of swaying or tilting. Some perceive self-motion whereas others perceive motion of the environment.

Vertigo is a symptom, not a physical sign or a diagnosis. It arises because of asymmetry in the vestibular system due to damage to or dysfunction of the labyrinth, vestibular nerve, or central vestibular structures in the brainstem or cerebellum.

Vertigo is a troubling problem for many clinicians because it is symptomatic of a large range of diagnoses from benign to immediately life threatening (table 1). However, in most cases, the clinical history, especially the tempo of the symptoms (table 2), with examination findings that distinguish between central and peripheral etiologies (table 3) identify those patients that require urgent diagnostic evaluation.

Vertigo is only one type of dizziness. Other symptoms that patients may identify as dizziness include presyncopal faintness, disequilibrium, and nonspecific or ill-defined light-headedness. The initial approach to the patient who complains of dizziness is to localize the cause of the symptom into one of these broad categories. This is described separately. (See "Approach to the patient with dizziness".)

This topic will discuss the clinical approach to a patient with vertigo. The pathophysiology, etiology, and treatment of vertigo are discussed separately. (See "Causes of vertigo" and "Treatment of vertigo".)

CLINICAL FEATURES

Vertigo — Vertigo is the predominant symptom of vestibular dysfunction. Patients often experience vertigo as an illusion of motion; some interpret this as self-motion, others as motion of the environment. The most common motion illusion is a spinning sensation. A spinning sensation is not required; vertigo can also be a sense of swaying or tilting. Also, not all patients are able to describe their vertigo in such concrete terms. Vague dizziness, imbalance, or disorientation may eventually prove to be due to a vestibular problem [1]. On the other hand, some patients with presyncope sometimes interpret the woozy, faint feeling as a spinning sensation. Thus, a symptom of vertigo is not particularly sensitive or specific for a vestibular problem. More specific is dizziness that is aggravated by head motion. Since the vestibular system is designed to detect head accelerations, vestibular deficits are most apparent when its function is required. (See 'Aggravating and provoking factors' below.)

Severe vertigo may occur with both acute central and peripheral lesions. However, when symptoms are less pronounced, particularly when there is pronounced nystagmus out of proportion to the severity of vertigo, this strongly suggests a central rather than a peripheral lesion.

Nausea and vomiting — Nausea and vomiting are typical with acute vertigo, unless it is mild or very brief, as with benign paroxysmal positional vertigo (BPPV). Vomiting can be severe, causing dehydration and electrolyte imbalance. Severe nausea and vomiting are more common with peripheral than with central lesions but can occur with both [2].

Postural and gait instability — Postural stability can be affected in patients with vertigo. The vestibular nuclei send signals to the vestibulospinal tract, which in turn stimulates antigravity muscles that maintain posture.

The effects of unilateral lesions of the vestibular apparatus upon postural stability are variable. In general, vertigo of central origin impairs gait and posture to a greater degree than does vertigo of peripheral origin, probably because central etiologies likely also impair other pathways involved in balance and posture [1,2]. Patients with vertigo of peripheral origin are usually able to walk, but may be very reluctant to move.

Other symptoms of vestibular dysfunction — Patients with vestibular injury may not complain of vertigo. In fact, vertigo is unusual in chronic vestibular injury or acute, bilaterally symmetric vestibular injury. Other symptoms of vestibular injury may include:

Tilt illusion — Patients feel that they and their environment are tilted with respect to gravity, even to the point of being upside down. This usually reflects damage to otolithic organs (utricle and saccule) or their central connections. Otolith dysfunction may also cause lateropulsion or the tendency to fall to the side of the lesion.

Drop attacks — Patients with drop attacks of vestibular origin often have a sensation of being pushed or pulled to the ground [3,4]. Unlike presyncope and seizures, there is no faintness or loss of consciousness with drop attacks unless the fall causes a head injury as well.

Drop attacks are often attributed to a sudden loss of tone mediated by vestibulospinal reflexes but can have other causes. (See "Seizures and epilepsy in older adults: Etiology, clinical presentation, and diagnosis", section on 'Sudden unexplained falls/drop attacks'.)

Drop attacks are an unusual feature of Meniere disease. Sometimes called Tumarkin's otolithic crisis, this symptom is usually seen only in advanced cases. Superior canal dehiscence and aminoglycoside toxicity are also associated with this presentation [5,6].

Spatial disorientation — A fleeting spatial disorientation with rapid head turns often remains after the patient has recovered from an acute attack of vertigo. The most astute patients will observe that this is more pronounced with head turns to the side of the lesion. This, rather than vertigo, may be how patients with bilateral vestibular failure present.

Oscillopsia — Oscillopsia, a visual illusion of to-and-fro environmental motion and blurred vision whenever the head is in motion, is a manifestation of an impaired vestibuloocular reflex (VOR). Affected patients notice that everything jiggles when they are walking or driving on rough pavement; they often have to stop and stand still to read signs.

Impaired balance without vertigo — Impaired balance without vertigo is a common manifestation of acute simultaneous bilateral vestibular loss such as that occurring with aminoglycoside antibiotic toxicity. Vertigo does not occur because there is no marked vestibular asymmetry. Most patients with bilateral vestibular loss have oscillopsia during passive head movement, as when walking or riding in a car over rough terrain [7]. Imbalance is most marked in the dark when visual cues to position in space are not available.

Aminoglycoside toxicity is the most common identified etiology of bilateral vestibulopathy, followed by Meniere disease and meningitis [8]. Bilateral vestibular failure is also a key feature of cerebellar ataxia, neuropathy and vestibular areflexia syndrome (CANVAS) [9]. Most cases, however, are cryptogenic in origin. Impaired balance without vertigo is also characteristic of acute midline cerebellar lesions or thiamine deficiency. (See "Wernicke encephalopathy" and "Overview of cerebellar ataxia in adults", section on 'Autosomal recessive ataxias'.)

EVALUATION

History — The history should allow the clinician to distinguish vertigo from other types of dizziness and to make a hypothesis about the site and type of lesion. It is customary to organize causes of vertigo into peripheral and central disorders (table 1). These have distinctive clinical features, but with some overlap. The clinical features of the most common disorders are summarized in the table (table 2).

Time course — Vertigo is never a permanent, continuous symptom. Even when the vestibular lesion is permanent, the central nervous system adapts to the defect so that vertigo subsides over days or weeks. Constant vertigo lasting months is not vestibular (though constant imbalance can be). However, some patients describe constant dizziness but actually mean that they have a constant susceptibility to frequent episodic dizziness.

Vertigo can occur as single or recurrent episodes and may last seconds, hours, or days. This time course of symptoms provides one of the best clues to the underlying pathophysiology of vertigo (table 2).

●Recurrent vertigo lasting under one minute is usually benign paroxysmal positional vertigo (BPPV) [10].

●A single episode of vertigo lasting several minutes to hours may be due to migraine or to transient ischemia of the labyrinth or brainstem [11].

●The recurrent episodes of vertigo associated with Meniere disease or vestibular migraine also typically last hours but can be briefer [12,13].

●More prolonged, severe episodes of vertigo that occur with vestibular neuritis can last for days [14,15]. This is also characteristic for vertigo originating from multiple sclerosis or infarction of the brainstem or cerebellum.

Aggravating and provoking factors — All vertigo is made worse by moving the head. Many patients in the midst of a vertiginous attack may be extremely reluctant to move. If head motion does not worsen the symptoms, the patient is less likely to be experiencing vertigo. This feature does not distinguish among the various causes of vertigo [16].

Certain kinds of movements may increase suspicion of damage to the otoliths, the organs that detect linear accelerations to the head. These include imbalance provoked by stop-and-go movements of elevators or cars in traffic, as well as standing on a boat or floating dock.

Attacks of BPPV are often provoked by specific head movements or postures (eg, rolling over in bed, extending the neck).

Vertigo aggravated by coughing, sneezing, exertion, or loud noises (Tullio phenomenon) should raise suspicion of either a perilymphatic fistula, in which there is an abnormal connection between the middle ear and the perilymphatic space of the inner ear, or a superior semicircular canal dehiscence, in which there is a defect in the roof of the superior semicircular canal. Both conditions allow pressure to be transmitted from the cerebrospinal fluid (CSF) space to the inner ear [17,18]. (See "Causes of vertigo".)

Head trauma is an important historical feature and can produce vertigo by a variety of mechanisms [19] (see "Sequelae of mild traumatic brain injury", section on 'Posttraumatic vertigo and dizziness'). Barotrauma, middle ear surgery, and straining with weight-lifting and bowel movements have been reported to produce a perilymphatic fistula.

When dizziness is provoked by static visual stimuli, such as patterned carpets or walls, or moving stimuli, such as sports or action movies on large screens, scrolling on the computer, or crowds at malls, this points to persistent postural perceptual dizziness (also known as visual vertigo, visuo-vestibular mismatch) [20].

Recent hyperextension injury to the neck, usually with persistent neck pain, suggests the possibility of vertebral artery dissection with brainstem or labyrinthine ischemia.

Recent viral symptoms may suggest acute vestibular neuritis, which is believed to be produced by viral or postviral inflammation of the eighth cranial nerve. However, a history of recent viral illness is both nonspecific and insensitive; less than one-half of patients with vestibular neuritis will report this [14,21,22].

Associated symptoms — A number of associated symptoms may help to distinguish the etiology of vertigo:

●Acute vertigo due to a vertebrobasilar stroke is almost always accompanied by other evidence of brainstem ischemia such as diplopia, dysarthria, dysphagia, weakness, or numbness [1]. However, infarction of the cerebellum may present as vertigo with no other symptoms. Focal neck pain may suggest vertebral artery dissection.

●Vertigo in patients with multiple sclerosis may also be preceded by or associated with other neurologic dysfunction, depending on the locus of demyelination.

●Deafness and tinnitus suggest a peripheral lesion of the inner ear. A sensation of aural fullness typically accompanies attacks of Meniere disease [13]. (See "Meniere disease: Evaluation, diagnosis, and management".)

●Headache, photophobia, and phonophobia suggest migrainous vertigo. Many patients with migrainous vertigo will also experience visual aura in at least some of their attacks.

●Shortness of breath, palpitations, and sweating may suggest a panic attack but can occur with vertigo too. Vertigo is often so terrifying that such symptoms are not uncommon with vestibular disease [23].

Prior medical history

●A prior history of migraine suggests that this may be the etiology of vertigo.

●The presence of stroke risk factors such as hypertension, diabetes mellitus, smoking, and a history of vascular disease support a diagnosis of vertebrobasilar ischemia [1]. Patients with an episode of vertigo and one or more risk factors for stroke have a substantial risk of subsequent stroke: an 8 percent two-year risk with one or two risk factors and 14 percent two-year risk with three or more risk factors [24].

●Past head trauma is a common antecedent to BPPV and persistent postural perceptual dizziness.

●Certain medications are associated with vestibular (eg, cisplatin, aminoglycosides) or cerebellar (eg, phenytoin) toxicity.

Examination — The physical examination should confirm vestibular dysfunction and distinguish central from peripheral causes of vertigo. Features most helpful in distinguishing central and peripheral vertigo are shown in the table (table 3).

Nystagmus — Nystagmus is a rhythmic oscillation of the eyes. There are many types of nystagmus. Some types of nystagmus can be localized to a specific pathology in the vestibular system.

An important role of the vestibular system is to maintain gaze during head movement through the vestibuloocular reflex (VOR). Acute unilateral vestibular lesions lead to a pathologic asymmetry in vestibular activity. This results in a slow drift of the eyes away from the target in one direction, followed by a fast corrective movement in the reverse direction. The eyes appear to "beat" in the direction of the fast phase. This nystagmus, which is often labeled "spontaneous jerk nystagmus," continues until the asymmetry of vestibular activity is restored to normal or until the central nervous system adapts to the vestibular lesion. (See "Overview of nystagmus".)

In a patient with acute vertigo, nystagmus is usually visible with the patient looking straight ahead. If the lesion is peripheral, the fast phase is away from the affected side. Usually, nystagmus increases in frequency and amplitude with gaze toward the side of the fast phase, eg, leftward gaze increases left-beating nystagmus, if present (Alexander law).

Other features of nystagmus have localizing value for central versus peripheral vertigo (table 3):

●Type of nystagmus. A mixed horizontal-torsional jerk nystagmus results if a peripheral lesion affects all three semicircular canals or the vestibular nerve on one side. The horizontal fast phases beat toward the normal ear, as do the upper poles of the eyes for the torsional fast phases. The jerk nystagmus from peripheral disease occasionally appears purely horizontal, but it is never purely torsional or vertical. (Also, pendular nystagmus is never due to peripheral vestibular disease.) The jerk nystagmus with central lesions may have any trajectory.

●Visual fixation tends to suppress nystagmus that is due to a peripheral lesion, but it does not usually suppress nystagmus from a central lesion [25]. This can be tested with Frenzel lenses, which are large magnifiers that blur vision and prevent visual fixation. A peripheral lesion is likely if nystagmus increases when Frenzel lenses are in place.

Another way to test the effect of fixation is by covering and uncovering one eye during fundoscopy of the other. One group of investigators has proposed that examination with a penlight (substituting for the ophthalmoscope) may also allow examination for nystagmus with and without fixation [26]. A peripheral disorder is likely if nystagmus increases on covering the fixating eye. It should be kept in mind that, in the ophthalmoscopic examination, the direction of nystagmus appears reversed because the optic nerve head is behind the center of eye rotation [27].

●Testing nystagmus in different gaze positions can provide other localizing clues. In peripheral lesions, the predominant direction of nystagmus remains the same in all directions of gaze. Nystagmus that reverses direction (ie, right-beating in right gaze then left-beating in left gaze) suggests gaze-evoked nystagmus, which is due to an abnormality of central circuits (figure 1) [25]. However, the absence of this feature does not rule out a central cause of vertigo. Nystagmus that reverses direction with convergence also suggests a central lesion.

Balance and gait — The ability to stand or walk unsupported and the direction of falling may provide useful clues to the origin of vertigo, although it may be difficult to persuade a patient with severe vertigo to attempt to walk.

Unilateral peripheral disorders generally cause patients to lean or fall toward the side of the lesion. Patients may be uncomfortable and reluctant to move because of their vertigo, but they can still walk. Romberg testing will cause the patients to fall or tilt to one side.

Patients with an acute cerebellar stroke are often unable to walk without falling. The direction of tilting or falling with Romberg testing may vary.

The sensitivity of balance testing may be increased by other maneuvers such as eye-closing, standing on foam, and performing head movements [28].

Other neurologic signs — A careful neurologic examination should be performed since the presence of additional neurologic abnormalities strongly suggests the presence of a central lesion. A search should be made for cranial nerve abnormalities, motor or sensory changes, dysmetria, or abnormal reflexes. (See "The detailed neurologic examination in adults".)

In particular, the abnormal facial sensation, ptosis, anisocoria, and diplopia of a lateral medullary infarction may be overlooked by both patients and clinicians when the vertigo is profound. (See "Causes of vertigo", section on 'Wallenberg syndrome' and "Posterior circulation cerebrovascular syndromes".)

However, the absence of other neurologic signs does not exclude a central process. In particular, a midline or inferior cerebellar infarction may produce no neurologic signs other than nystagmus and gait instability on examination.

Office hearing tests — Bedside tests of hearing and an examination of the tympanic membrane can be useful in distinguishing the etiology of vertigo. The otoscopic examination provides evidence of acute or chronic otitis media.

The examiner can easily test hearing by several methods. One is to softly whisper into each ear and then ask the patient to repeat what was whispered. Another is to hold the examiner's hands next to the patient's ears but out of the patient's eyesight. The examiner then rubs the fingers together on one side, with a sham rubbing movement on the opposite side, and asks the patient to report when the finger scratching sound is heard and from which ear it is heard. Another method is to vibrate a 512 Hz tuning fork, placing it close to one ear and then the other in rapid succession so that the patient can compare the loudness.

The Weber and Rinne tests are used to distinguish conductive and sensorineural hearing loss (table 4):

●In the Weber test, a vibrating tuning fork is placed on the forehead in the midline. With normal hearing, the sound is heard equally in both ears. With sensorineural hearing loss, the sound localizes to the normal ear. With conductive hearing loss, the sound localizes to the affected ear (figure 2 and table 4).

●The Rinne test looks for conductive hearing loss. The tuning fork is placed on the mastoid bone behind the ear of the affected side in order to test bone conduction of sound. The vibrating tuning fork is then placed approximately 2.5 cm from the ear to test air conduction. Normally, air conduction of sound is better than bone conduction, and the sound is heard louder next to the ear than when placed on the mastoid. With conductive hearing loss, the tuning fork is heard less well or not at all when the tuning fork is adjacent to the ear. With sensorineural hearing loss, both air and bone conduction may be quantitatively decreased, but air conduction remains better than bone conduction (figure 2 and table 4).

Unilateral sensorineural hearing loss suggests a peripheral lesion; audiometry is required for confirmation. If no obvious cause of unilateral sensorineural hearing loss (eg, Meniere disease) has been identified by history, a magnetic resonance imaging (MRI) or computed tomography (CT) scan of the posterior fossa and internal auditory canal is necessary. (See "Evaluation of hearing loss in adults".)

While associated hearing loss strongly points to a peripheral origin of vertigo, the absence of hearing loss has less localizing value.

Dix-Hallpike maneuver — Positional maneuvers are designed to produce vertigo and elicit nystagmus in patients with a history of positional dizziness. These maneuvers are most useful in patients who do not have symptoms or nystagmus at rest and whose vertigo is episodic. The Dix-Hallpike maneuver tests for canalithiasis of the posterior semicircular canal, which is the most common cause of BPPV [10]. Other maneuvers are used to provoke the nystagmus of less common variants of BPPV (anterior canal, horizontal canal). These are discussed separately. (See "Benign paroxysmal positional vertigo", section on 'Response to provoking maneuvers'.)

With the patient sitting, the neck is extended and turned to one side. The patient is then placed supine rapidly, so that the head hangs over the edge of the bed. The patient is kept in this position until 30 seconds have passed if no nystagmus occurs. The patient is then returned to upright, observed for another 30 seconds for nystagmus, and the maneuver is repeated with the head turned to the other side (figure 3). A video demonstrating this maneuver can be viewed from the American Academy of Neurology (video 1).

The Dix-Hallpike maneuver will usually provoke paroxysmal vertigo and nystagmus if posterior canal dysfunction is present in the lower ear. The nystagmus and vertigo usually appear after a latency of a few seconds and last less than 30 seconds. It has a typical trajectory, beating upward and torsionally, with the upper poles of the eyes beating toward the ground. After the patient sits up, the nystagmus will recur but in the opposite direction. The maneuver should be repeated to the same side; with each repetition the intensity and duration of nystagmus will diminish, confirming the fatigable nature of the phenomenon. However, repetition of the maneuver can interfere with the ability to immediately perform a therapeutic particle repositioning maneuver; repetition may be deferred when this is being considered. (See "Benign paroxysmal positional vertigo", section on 'Particle repositioning maneuvers'.)

The latency, transience, and fatigability, coupled with the typical mixed upward vertical and torsional direction, are important features in diagnosing BPPV due to posterior canalithiasis (table 5) [14]. Deviation from these features may occur with rarer types of peripheral positional vertigo, such as those due to anterior or horizontal canalithiasis, but should also raise suspicion of a central lesion. The sensitivity of the Dix-Hallpike maneuver in patients with posterior canal BPPV is said to be as high as 88 percent [29]. (See "Benign paroxysmal positional vertigo".)

Head impulse test — The head impulse test (or head thrust test) is performed by instructing the patient to keep his or her eyes on a distant target while wearing his or her usual prescription eyeglasses. The head is then turned quickly and unpredictably by the examiner, approximately 15°; the starting position should be approximately 10° from straight ahead.

The normal response is that the eyes remain on the target (figure 4). The abnormal response is that the eyes are dragged off of the target by the head turn (in one direction), followed by a saccade back to the target after the head turn; this response indicates a deficient VOR on the side of the head turn, implying a peripheral vestibular lesion (inner ear or vestibular nerve) on that side [15,30]. Use of video nystagmography (VNG) can aid in the interpretation and accuracy of this test [31].

For distinguishing vestibular dysfunction from nonvestibular dizziness, the head impulse test is reported to have a higher specificity (82 to 100 percent) than sensitivity (34 to 39 percent) [32-34]. However, the use of caloric testing as the gold standard in these studies may not be appropriate and may underestimate sensitivity [35]. In one report, flexing the head forward 30° during the test increased sensitivity to as high as 71 to 84 percent [36]. In one small case series, head impulse tests were abnormal in all 14 patients with aminoglycoside vestibulotoxicity [37].

An abnormal head impulse test is reported to be a useful test to distinguish between central and peripheral vertigo, particularly in the setting of acute prolonged vertigo, when the examiner is trying to differentiate between vestibular neuritis and cerebellar infarction (figure 1) [15,30,31]. The head impulse test is normal in most patients with isolated cerebellar lesions (31 of 34 in one series) [38]. It is important to note that a peripheral injury may result from infarction to the inner ear or eighth cranial nerve, though [25]. (See "Vestibular neuritis and labyrinthitis", section on 'Clinical manifestations'.)

Other vestibular signs — Other signs of vestibular dysfunction can be elicited on examination. The clinical and diagnostic utility of most of these signs is not known, as they have not been systematically studied against a gold standard.

These tests are often categorized as to those indicating static vestibular imbalance (spontaneous nystagmus, skew deviation, ocular tilt reaction (OTR), and tilt of the subjective visual vertical [SVV]) and those indicating dynamic vestibular imbalance. The latter implies functional impairment of the VOR, which acts to keep the line of sight steady during head movements. This can be detected clinically in four ways: head impulse test, head-shaking visual acuity, post-head-shaking nystagmus, and caloric tests.

●Skew deviation – A skew deviation is a vertical misalignment of the two eyes resulting from a supranuclear (relative to the ocular motor nuclei) pathology, usually located in the brainstem (figure 1) [25]. This may also be caused by a vestibular lesion because of imbalance in otolithic-ocular reflexes.

The vertical separation can be tested by placing a red lens over one eye, shining a white point-light at the patient, and asking him or her to note the relative position of the red spot to the white spot. The light should be moved to see how the separation changes with lateral and vertical gaze. Alternative methods to detect and characterize strabismus include the cover-uncover test or Maddox rod.

Skew deviation is often "comitant," meaning that gaze direction has little effect upon the distance between the images. When it is incomitant, it needs to be differentiated from other problems such as IV nerve palsies. (See "Overview of diplopia".)

●HINTS examination – An examination that includes the head impulse test (ie, head thrust test), evaluation for direction-changing (ie, gaze-evoked) nystagmus, and a test of skew has been called the HINTS examination (figure 1). The presence of any one of three clinical signs (a normal head impulse test, direction-changing nystagmus, or a skew deviation) suggests central rather than peripheral vertigo in patients with an acute sustained vestibular syndrome [39-43]. This is discussed in more detail separately. (See "Vestibular neuritis and labyrinthitis", section on 'Clinical manifestations' and "Posterior circulation cerebrovascular syndromes".)

●Ocular tilt reaction – The OTR is a triad of skew deviation, torsional tilt of the eyes with the upper poles tilted toward the eye that is lower, and head tilt toward the eye that is lower. This typically results from a central lesion affecting otolithic pathways.

●Tilt of the subjective visual vertical – Tilt of the SVV is a sensitive sign of acute static vestibular imbalance [44] attributed to dysfunction of the utricular component of the otoliths. SVV tilt can be measured at the bedside using a simple device made from a bucket with a straight line drawn on the bottom (picture 1) [45].

Skew deviation, OTR, and tilt of the SVV can occur with acute peripheral vestibular (otolithic) lesions or with acute central lesions involving the cerebellum or brainstem vestibular pathways [46-48]. Lesions of the peripheral vestibular system or medulla cause a skew deviation with the ipsilateral eye lower and extorted (ipsiversive), along with an ipsiversive tilt of SVV [49]. Lesions of the midbrain cause the opposite (contraversive). Cerebellar lesions, which involve the dentate nucleus, also cause contraversive OTR, while those that spare the dentate nucleus can cause an ipsiversive OTR [47,50]. Patients with these manifestations may complain of vertical diplopia but may also experience a tilt illusion of their vision [27].

●Head-shaking visual acuity – Head-shaking visual acuity is tested by having the patient look at an eye chart in the distance wearing his or her customary distance vision eyeglasses. Customary eyeglasses are important since the VOR is calibrated for a given rotational magnification that varies with different strengths of glasses. The patient reads the eye chart while his or her head is shaken continuously over a small range at approximately 2 Hz. Then, the patient reads the chart again while his or her head is still. Head-shaking acuity that is more than four lines worse than the head-still acuity indicates a poor VOR.

●Head-shaking nystagmus – Head-shaking nystagmus is elicited by the patient shaking the head from side to side for 15 to 40 seconds with eyes closed or Frenzel lenses in place. The shaking causes vigorous stimulation of the horizontal semicircular canals of both sides; head velocity data are stored in the cerebellum, decaying slowly after the head stops moving. When the shaking stops, the patient then opens his or her eyes and attempts to look straight ahead. If both sides were equally activated, the decay of velocity information will be balanced, and the eyes will be still. If there is unilateral labyrinthine damage, the asymmetric neural output will generate a nystagmus that beats away from the damaged side. This test will be normal in patients with bilateral symmetric disease, unlike rapid head thrusts or caloric responses. The test is abnormal in patients with unilateral central vestibular lesions.

Using caloric testing as the gold standard, head-shaking nystagmus has a sensitivity of 46 percent and a specificity of 75 percent for the detection of unilateral peripheral or central vestibular lesions [51,52]. In two series of patients with vestibular neuritis, head-shaking nystagmus was present in 95 to 100 percent [53,54].

Head-shaking nystagmus may also differentiate central and peripheral lesions, although this is less predictable than other signs. While the induced nystagmus is contralateral to the lesion in peripheral vestibulopathy, nystagmus produced by head shaking in patients with medullary lesions is usually ipsilateral to the lesion, even in cases in which the spontaneous nystagmus is contralateral [55]. When head-shaking produces a vertical nystagmus, this is called "perverted nystagmus" and increases the likelihood of a central lesion [56].

●Caloric testing – Caloric testing is performed by infusing warm or cold water into the external ear canal. Otoscopy should be performed first to ensure that cerumen is not obstructing the flow of water to the tympanic membrane and to verify that there is no tympanic membrane perforation. The head of the patient should be tilted at 30° up from supine for optimal stimulation of the horizontal semicircular canals.

When warm water at 44°C is infused into an ear canal, the normal response is nystagmus with the fast component toward the infused ear. The opposite response occurs when cool water at 30°C is infused; the normal response is nystagmus with the fast component away from the cold water-infused ear.

Lack of a response to warm or cold water on one side suggests disease on that side, usually in peripheral lesions. Central vestibular disorders may also cause caloric hyposensitivity, especially if they involve the vestibular root entry in the medulla. This test can cause significant distress, including nausea and vomiting in awake patients; it is rarely performed in the office evaluation of vertigo but may be useful in the vestibular laboratory (see 'Electronystagmography and video nystagmography' below). Caloric testing is also used in the evaluation of coma. (See "Stupor and coma in adults".)

●Others – Hyperventilation can elicit nystagmus in several central and peripheral vestibular pathologies, and may be a particularly sensitive test in patients with cerebellopontine tumors. In one study, ipsilesional hyperventilation-induced nystagmus was found in 84 percent of patients with cerebellopontine tumors compared with 34 percent in other vestibular diseases [57].

Diagnostic tests — Tests that may be useful in patients with vertigo include brain imaging, electronystagmography (ENG) and VNG, vestibular evoked myogenic potentials (VEMPs), audiometry, and brainstem auditory evoked potentials (BAEPs). The indications for this more specialized testing (as well as indications for specialist referral) are not precise. The relatively low prevalence of serious disorders should be balanced against their prognostic and treatment implications when deciding whether to order these tests [29].

Brain imaging — MRI of the brain is indicated in selected patients when the history and examination suggest either a central cause of vertigo or a vestibular schwannoma (acoustic neuroma) (table 3). CT scans are significantly less sensitive for the diagnosis of cerebellar infarction and for pathologies affecting the brainstem or vestibular nerve [58]. (See "Causes of vertigo".)

In a patient with acute sustained vertigo, it is often difficult to distinguish between a vascular event involving the cerebellum and vestibular neuritis (figure 1) [59]. While the latter has a benign course, the former can be acutely life threatening. A younger patient with acute sustained vertigo, with no other neurologic signs or symptoms, and with nystagmus and an examination that is consistent with a peripheral origin (suppression with visual fixation, falling in opposite direction to the fast phase of nystagmus, horizontal/torsional nystagmus, abnormal head impulse testing) does not need immediate imaging if there is improvement within 48 hours [14]. However, neuroimaging is indicated if the examination is not entirely consistent with a peripheral lesion, if there are prominent risk factors for stroke, if there are neurologic signs or symptoms, if the patient cannot walk, or if there is a new headache accompanying the vertigo [14,24,59].

The procedure of choice is MRI and magnetic resonance angiography (MRA). MRI can detect infarction in the posterior fossa on the first day, but has improved sensitivity when performed later or sequentially. MRA has a specificity and sensitivity exceeding 95 percent in detecting stenosis or occlusion of the posterior circulation [60].

CT scanning with thin cuts through the cerebellum is an alternative when MRI scanning is not available or in patients with metallic implants. The scan is usually normal in the first hours after an infarct and is overall a less sensitive test than MRI for early infarcts and small mass lesions. However, intraparenchymal hemorrhage will usually be evident immediately. A brain CT scan should therefore be performed if the clinical picture is compatible with cerebellar hemorrhage and the MRI scan is not immediately available. In one emergency department-based study, the diagnostic yield of head CT was low compared with MRI (2 versus 16 percent) [61].

Electronystagmography and video nystagmography — ENG uses electrodes to record eye movements. VNG uses video cameras to record eye movements. These techniques record and quantify both spontaneous and induced nystagmus. Most balance disorder centers and many specialists use ENG or VNG to assess vestibular function and ocular motility.

Using a battery of tests such as ocular motor screening, positional testing, head impulse testing [31], caloric testing, and rotational testing with ENG or VNG can help to discriminate between central and peripheral etiologies. Caloric testing in the vestibular laboratory has a reasonable sensitivity for vestibular disorders, but it does not accurately discriminate between central and peripheral vestibulopathies [62].

In general, vestibular laboratory testing is indicated when a patient's symptoms do not respond to simple remedies such as meclizine or betahistine, persist for more than one to two weeks, or are incapacitating and thus require further diagnostic information.

Vestibular evoked myogenic potentials — VEMPs are a new means of assessing otolith function [63]:

●For cervical VEMPs (cVEMPs), which assess saccular function, a loud sound is delivered to one ear while muscular activity is recorded in the ipsilateral sternocleidomastoid muscle.

●Ocular VEMPs primarily assess utricular function and record extraocular muscle potentials during head vibration [64].

As an example, cVEMPs are especially useful for detecting superior semicircular canal dehiscence syndrome, which will manifest as a cVEMP with a reduced threshold [65].

Audiometry — Audiometry is more sensitive than office testing to detect hearing loss and can quantify the loss at high and low frequencies. The audiometric battery also establishes if recruitment is present and tests for word recognition.

Audiometry has some limited use in the diagnosis of patients with vertigo. While conditions such as Meniere disease and vestibular schwannoma are said to have characteristic patterns, the audiometric battery is not truly diagnostic of a specific disorder independent of other factors [66]. Nevertheless, the audiogram is sensitive enough to detect unilateral hearing loss in almost all cases of vestibular schwannoma, and may be a useful screening test for this condition [67,68] (see "Vestibular schwannoma (acoustic neuroma)"). Also, a finding of low-frequency sensorineural hearing loss helps confirm the diagnosis of Meniere disease.

Brainstem auditory evoked potentials — BAEPs have a 90 to 95 percent sensitivity for detecting acoustic neuromas (see "Vestibular schwannoma (acoustic neuroma)"). Any type of sensorineural hearing loss will disrupt the pattern of sound passing from the cochlea to the brainstem; abnormal results are therefore nonspecific [67-69]. BAEPs are no longer routinely used in the evaluation of patients with vertigo or suspected vestibular schwannoma.

DIAGNOSTIC APPROACH — As a first step, it is important to confirm that the patient's problem is vertigo rather than a different form of dizziness. The features that distinguish vertigo from other forms of dizziness are discussed separately. (See "Approach to the patient with dizziness", section on 'General approach' and "Approach to the patient with dizziness", section on 'Vertigo'.)

There are many causes of vertigo. It is customary to organize causes of vertigo into peripheral and central disorders, using features of nystagmus, and the presence or absence of postural instability, hearing loss or tinnitus, and other neurologic signs (table 3). While the resulting differential diagnosis (table 1) remains broad, some conditions are more common than others and these are typically considered first, based upon the clinical features, as summarized in the table. (table 2)

Another practical approach to diagnosis often starts with the time course of symptoms, in part because patients are more reliable at describing the duration rather than the quality of their symptoms.

●Acute onset, sustained vertigo – Common diagnoses in this setting include vestibular neuritis, demyelinating disease, and a stroke in the brainstem or cerebellum. Clinicians use the presence of cerebrovascular risk factors and associated neurologic deficits to determine the relative probability of a cerebrovascular etiology [70]. The HINTS examination, in particular the head impulse test, can also be particularly useful in this setting to distinguish a peripheral cause of vertigo (eg, vestibular neuritis) from a central, cerebrovascular cause (figure 1). In a young patient without cerebrovascular risk factors in whom a normal head impulse test suggests a localization within the central nervous system, multiple sclerosis might be more likely. However, the utility of the head impulse test or the HINTS examination has not been specifically studied in this setting. (See 'Head impulse test' above and 'Other vestibular signs' above.)

An MRI focusing on the brainstem should be performed when a central nervous system etiology is suspected. This is discussed in detail separately. (See "Vestibular neuritis and labyrinthitis", section on 'Differential diagnosis' and "Posterior circulation cerebrovascular syndromes".)

●Episodic vertigo – Likely diagnoses in patients with episodic vertigo depend on the duration of events as well as the presence of associated features:

•Very brief episodes of isolated vertigo that are precipitated by predictable movements or positions of the head are often caused by benign paroxysmal peripheral vertigo (BPPV). The Dix-Hallpike maneuver can help confirm this diagnosis. (See 'Dix-Hallpike maneuver' above and "Benign paroxysmal positional vertigo".)

•The diagnosis of episodes with a longer duration (minutes to hours) may be further distinguished by the presence or absence of associated clinical features. As examples, associated headache suggests vestibular migraine; unilateral hearing loss, tinnitus, and ear fullness suggest Meniere disease; and other brainstem neurologic deficits suggest vertebrobasilar transient ischemia. The diagnoses of these conditions are discussed separately. (See "Vestibular migraine" and "Meniere disease: Evaluation, diagnosis, and management" and "Posterior circulation cerebrovascular syndromes" and "Causes of vertigo", section on 'Brainstem ischemia'.)

A more inclusive description of the causes of vertigo along with characteristic clinical features and diagnosis are discussed separately. (See "Causes of vertigo".)

Vertigo in the setting of recent head trauma is discussed separately. (See "Sequelae of mild traumatic brain injury", section on 'Posttraumatic vertigo and dizziness'.)

MANAGEMENT — Treatments for vertigo are reviewed in detail separately. (See "Treatment of vertigo".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Vertigo (a type of dizziness) (The Basics)")

●Beyond the Basics topics (see "Patient education: Vertigo (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Causes – Vertigo is a symptom of illusory movement, most commonly of spinning of oneself or of the environment.

Vertigo can be caused by disorders of the peripheral vestibular system, including the vestibular labyrinth and the vestibular portion of the eighth cranial nerve, or by lesions within the central nervous system, usually the brainstem or cerebellum (table 1). Underlying conditions can be benign and self-limiting, or severe and life threatening. (See "Causes of vertigo".)

●Historical features – Historical features, particularly the nature and time course of the symptoms, can help confirm the presence of vertigo and identify a likely etiology (table 2). (See 'History' above and 'Diagnostic approach' above.)

•Recurrent vertigo lasting under one minute is usually benign paroxysmal positional vertigo (BPPV).

•A single episode of vertigo lasting several minutes to hours may be due to migraine or to transient ischemia of the labyrinth or brainstem.

•The recurrent episodes of vertigo associated with Meniere disease or recurrent vestibulopathy also typically last hours but can be briefer.

•Acute onset of vertigo that is sustained can occur with vestibular neuritis, demyelinating disease (multiple sclerosis), or a brainstem or cerebellar stroke.

●Nystagmus – Nystagmus represents the physical manifestation of a patient's complaint of vertigo. The presence of nystagmus helps confirm that the patient's complaint is vertigo, rather than an alternative form of dizziness. Its absence does not rule out vertigo. (See "Approach to the patient with dizziness", section on 'Nystagmus'.)

Features of the nystagmus, including its direction (horizontal, torsional, vertical), its tendency to suppress with visual fixation, and whether or not its direction alters with gaze position, can suggest a central versus peripheral localization (table 3 and figure 1). (See 'Nystagmus' above.)

●Other neurologic symptoms and signs – Numbness, weakness, pronounced gait impairment, diplopia, and dysarthria point toward a central etiology of vertigo. However, their absence does not rule out a central etiology (table 3). (See 'Postural and gait instability' above and 'Other neurologic signs' above.)

●Audiologic symptoms and signs – The presence of abnormal hearing, tinnitus, or ear pain points toward a peripheral etiology of vertigo. However, their absence does not rule out a peripheral etiology. (See 'Office hearing tests' above.)

●Vestibular examination – For patients with acute-onset sustained vertigo, an examination that includes the head impulse test, evaluation for direction-changing nystagmus, and a test of skew (the HINTS examination) can be useful in distinguishing peripheral from central vertigo (figure 1). (See 'Other vestibular signs' above and "Vestibular neuritis and labyrinthitis", section on 'Clinical manifestations' and "Posterior circulation cerebrovascular syndromes".)

The Dix-Hallpike maneuver is most useful to confirm the diagnosis of BPPV in patients with episodic vertigo (figure 3 and table 5). (See 'Dix-Hallpike maneuver' above.)

●Neuroimaging – MRI and magnetic resonance angiography (MRA) are indicated for patients with suspected central causes of vertigo including those with other signs or symptoms of brainstem dysfunction (figure 1).

In acute sustained vertigo, MRI or CT should be performed urgently to rule out a vascular event in the cerebellum or brainstem in patients who are older, have vascular risk factors, have headache, and whose examination is not completely typical of a peripheral vestibulopathy (figure 1). (See 'Brain imaging' above.)

●Audiometry – Audiometry is useful to confirm a diagnosis of Meniere disease and to evaluate hearing loss in other causes of peripheral vertigo. (See 'Audiometry' above.)