The advent of modern neuroimaging in the late 1970s and 1980s greatly expanded our understanding of causes of dizziness and vertigo. Prior to this time, stroke was considered an exceedingly rare cause of vertigo (Fisher, 1967). Though it remains a controversial topic even today, infarctions within the cerebellum and brainstem have been identified on imaging studies in patients with isolated vertigo. Imaging studies continue to lead to new discoveries of causes of vertigo, as demonstrated by the recently described disorder of superior canal dehiscence (SCD). But the most common causes of vertigo—Meniere disease, BPPV, and vestibular neuritis—still have no identifiable imaging characteristics.

Over the last 25 years, our understanding of the mechanisms for the common neuro-otological disorders has been greatly enhanced. BPPV can now be readily identified and cured at the bedside with a simple positional maneuver, and variants have also been described (Aw et al., 2005; Fife et al., 2008). The head-thrust test can be used at the bedside to identify a vestibular nerve lesion, and because of this it has particular utility in helping distinguish vestibular neuritis from a posterior fossa stroke (Halmagyi and Curthoys, 1988; Kattah et al., 2009; Newman-Toker et al., 2008; Nuti et al., 2005). Controversies regarding Meniere disease have been clarified, and medical and surgical treatments have improved (Minor et al., 2004). It is now clear that patients with recurrent episodes of vertigo without hearing loss, a condition once called vestibular Meniere disease, do not actually have Meniere disease.

Migraine is now recognized as an important cause of dizziness, even in patients without simultaneous headaches. In fact, benign recurrent vertigo (patients with recurrent episodes of vertigo without accompanying auditory symptoms or other neurological features) is usually a migraine equivalent (Oh et al., 2001b). The disorder of SCD was only recently described and provides important insight into the physiology of the vestibular system (Minor, 2005). A more detailed description of the rotational vertebral artery syndrome has led to appreciation of the high metabolic demands of the inner ear and its susceptibility to ischemia (Choi et al., 2005). Genetic research has identified ion channel dysfunction in disorders such as episodic ataxia and familial hemiplegic migraine, and patients with these disorders also commonly report vertigo (Jen et al., 2004a). It is hoped that identifying specific genes causing vertigo syndromes will lead to a better understanding of the mechanisms and also create the opportunity to develop specific treatments in the future.

Epidemiology of Vertigo, Dizziness, and Hearing Loss

A recent population-based telephone survey in Germany showed nearly 30% of the population had experienced moderate to severe dizziness (Neuhauser et al., 2005). Though most subjects reported nonspecific forms of dizziness, nearly a quarter had true vertigo. Dizziness is more common among females and older people and has important healthcare utilization implications; up to 80% of patients with dizziness seek medical care at some point. In the United States, the National Centers for Health Statistics report 7.5 million annual ambulatory visits to physician offices, hospital outpatient departments, and emergency departments (EDs) for dizziness, making it one of the most common principal complaints (Burt and Schappert, 2004).

Hearing loss affects approximately 16% of adults (age >18 years) in the United States (Lethbridge-Cejku et al., 2006). Men are more commonly affected than women, and the prevalence of hearing loss increases dramatically with age, so that by age 75, nearly 50% of the population reports hearing loss. Hearing loss is an important cause of disability. The most common type of hearing loss is sensorineural, and both idiopathic presbycusis and noise-induced forms are common etiologies. Bothersome tinnitus is less frequent in the U.S. population, with about 3% reporting it, although this increases to about 9% for subjects older than 65 (Adams et al., 1999). The most common type of tinnitus is a high-pitched ringing in both ears.

Normal Anatomy and Physiology

The inner ear is composed of a fluid-filled sac enclosed by a bony capsule with an anterior cochlear part, central chamber (vestibule), and a posterior vestibular part (Fig. 37.1). Endolymph fills up the fluid-filled sac and is separated by a membrane from the perilymph. These fluids primarily differ in their composition of potassium and sodium, with the endolymph resembling intracellular fluid with a high potassium and low sodium content, and perilymph resembling extracellular fluids with a low potassium and high sodium content. Perilymph communicates with the cerebrospinal fluid (CSF) through the cochlear aqueduct.

Fig. 37.1 Anatomy of the inner ear. CSF, Cerebrospinal fluid.

(From Baloh, R.W., 1998. Dizziness, Hearing Loss, and Tinnitus. F.A. Davis Company, Philadelphia, Figure 6, p. 16.)

The cochlea senses sound waves after they travel through the external auditory canal and are amplified by the tympanic membrane and ossicles of the middle ear (Baloh and Kerber, 2011). The stapes, the last of three ossicles in the middle ear, contacts the oval window, which directs the forces associated with sound waves along the basilar membrane of the cochlea. These forces stimulate the hair cells, which in turn generate neural signals in the auditory nerve. The auditory nerve enters the lateral brainstem at the pontomedullary junction and synapses in the cochlear nucleus. The trapezoid body is the major decussation of the auditory pathway, but many fibers do not cross to the contralateral side. Signals then travel to the superior olivary complex. Some projections travel from the superior olivary complex to the inferior colliculus through the lateral lemnisci, and others terminate in one of the nuclei of the lateral lemniscus. Next, fibers travel to the ipsilateral medial geniculate body, and then auditory radiations pass through the posterior limb of the internal capsule to reach the auditory cortex of the temporal lobe.

The peripheral vestibular system is composed of three semicircular canals, the utricle and saccule, and the vestibular component of the eighth cranial nerve (Baloh and Kerber, 2011). Each semicircular canal has a sensory epithelium called the crista; the sensory epithelium of the utricle and saccule is called the macule. The semicircular canals sense angular movements, and the utricle and saccule sense linear movements. Two of the semicircular canals (anterior and posterior) are oriented in the vertical plane nearly orthogonal to each other; the third canal is oriented in the horizontal plane (horizontal canal). The crista of each canal is primarily activated by movement occurring in the plane of that canal. When the hair cells of these organs are stimulated, the signal is transferred to the vestibular nuclei via the vestibular portion of cranial nerve VIII. Signals originating from the horizontal semicircular canal then pass via the medial longitudinal fasciculus along the floor of the fourth ventricle to the abducens nuclei in the middle brainstem and the ocular motor complex in the rostral brainstem. The anterior (also referred to as the superior) and posterior canal impulses pass from the vestibular nuclei to the ocular motor nucleus and trochlear nucleus triggering eye movements roughly in the plane of each canal. A key feature is that once vestibular signals leave the vestibular nuclei they divide into vertical, horizontal, and torsional components. As a result, a lesion of central vestibular pathways can cause a pure vertical, pure torsional, or pure horizontal nystagmus.

The primary vestibular afferent nerve fibers maintain a constant baseline firing rate of action potentials. When the baseline rate from each ear is symmetrical (or an asymmetry has been centrally compensated), the eyes remain stationary. With an uncompensated asymmetry in the firing rate, either resulting from increased or decreased activity on one side, slow ocular deviation results. By turning the head to the right, the baseline firing rate of the horizontal canal is physiologically altered, causing an increased firing rate on the right side and a decreased firing rate on the left side (Fig. 37.2). The result is a slow deviation of the eyes to the left. In an alert subject, this slow deviation is regularly interrupted by quick movements in the opposite direction (nystagmus) so the eyes do not become pinned to one side. In a comatose patient, only the slow component is seen because the brain cannot generate the corrective fast components.

Fig. 37.2 Primary afferent nerve activity associated with rotation-induced physiological nystagmus and spontaneous nystagmus resulting from a lesion of one labyrinth. Thin straight arrows indicate the direction of slow components; thick straight arrows indicate the direction of fast components; curved arrows show the direction of endolymph flow in the horizontal semicircular canals. AC, Anterior canal; HC, horizontal canal; PC, posterior canal.

(From Baloh, R.W., 1998. Dizziness, Hearing Loss, and Tinnitus. F.A. Davis Company, Philadelphia, Figure 16, p. 36.)

The plane in which the eyes deviate as a result of vestibular stimulation depends on the combination of canals that are stimulated (Table 37.1). If only the posterior semicircular canal on one side is stimulated (as occurs with BPPV), a vertical-torsional deviation of the eyes can be observed, which is followed by a fast corrective response generated by the conscious brain in the opposite direction. However, if the horizontal canal is the source of stimulation (as occurs with the horizontal canal variant of BPPV), a horizontal deviation with a slight torsional component (because this canal is slightly off the horizontal plane) results. If the vestibular nerve is lesioned (vestibular neuritis) or stimulated (vestibular paroxysmia), a horizontal greater than torsional nystagmus is seen that is the vector sum of all three canals—the two vertical canals on one side cancel each other out.

Table 37.1 Physiological Properties and Clinical Features of the Components of the Peripheral Vestibular System

Over time, an asymmetry in the baseline firing rates either resolves (the stimulation has been removed), or the central nervous system (CNS) compensates for it. This explains why an entire unilateral peripheral vestibular system can be surgically destroyed and patients only experience vertigo for several days to weeks. It also explains why patients with slow-growing tumors affecting the vestibular nerve, such as an acoustic neuroma, generally do not experience vertigo or nystagmus.

History of Present Illness

The history and physical examination provide the most important information when evaluating patients complaining of dizziness (Colledge et al., 1996; Lawson et al., 1999). Often, patients have difficulty describing the exact symptom experienced, so the onus is on the clinician to elicit pertinent information. The first step is to define the symptom. No clinician should ever be satisfied to record the complaint simply as “dizziness.” For patients unable to provide a more detailed description of the symptom, the physician can ask the patient to place their symptom into one of the following categories: movement of the environment (vertigo), lightheadedness, or strictly imbalance without an abnormal head sensation. Because patient descriptions about dizziness can be unreliable and inconsistent (Newman-Toker et al., 2007), other details about the symptom become equally important. The physician should also ask the following questions: Is the symptom constant or episodic, are there accompanying symptoms, how did it begin (gradual, sudden, etc.), and were there aggravating or alleviating factors? If episodic, what was the duration and frequency of attacks, and were there triggers? Table 37.2 displays the key distinguishing features of common causes of dizziness. One key point is that any type of dizziness may worsen with position changes, but some disorders such as BPPV only occur after position change.

Table 37.2 Distinguishing Among Common Peripheral and Central Vertigo Syndromes

Physical Examination

General Medical Examination

A brief general medical examination is important. Identifying orthostatic blood pressure can be diagnostic in the correct clinical setting, so blood pressure should be checked for this pattern in any patient with orthostatic symptoms. Orthostatic hypotension is probably the most common general medical cause of dizziness among patients referred to neurologists. Identifying an irregular heart rhythm may also be pertinent. Other general examination measures to consider in individual patients include a visual assessment (adequate vision is important for balance) and a musculoskeletal inspection (significant arthritis can impair gait).

General Neurological Examination

The general neurological examination is very important in patients complaining of dizziness, because dizziness can be the earliest symptom of a neurodegenerative disorder (de Lau et al., 2006) and can also be an important symptom of stroke, tumor, demyelination, or other pathologies of the nervous system.

The cranial nerves should be thoroughly assessed in patients complaining of dizziness. The most important part of the examination lies in evaluating ocular motor function (described in more detail in the neurotology exam section). One should ensure that the patient has full ocular ductions. A posterior fossa mass can impair facial sensation and the corneal reflex on one side. Assessing facial strength and symmetry is important because of the close anatomical relationship between the seventh and eighth cranial nerves. The lower cranial nerves should also be closely inspected by observing palatal elevation, tongue protrusion, and trapezius and sternocleidomastoid strength.

The general motor examination determines strength in each muscle group and also assesses bulk and tone. Increased tone or cogwheel rigidity could be the main finding in a patient with an early neurodegenerative disorder. The peripheral sensory examination is important because a peripheral neuropathy can cause a nonspecific dizziness or imbalance. Temperature, pain, vibration, and proprioception should be assessed. Reflexes should be tested for their presence and symmetry. One must take into consideration the normal decrease in vibratory sensation and absence of ankle jerks that can occur in elderly patients. Coordination is an important part of the neurological examination in patients with dizziness because disorders characterized by ataxia can present with the principal symptom of dizziness. Observing the patient’s ability to perform the finger-nose-finger test, the heel-knee-shin test, and rapid alternating movements adequately assesses extremity coordination.

Neuro-otological Examination

The neuro-otological examination is a specialty examination expanding upon certain aspects of the general neurological examination and also includes an audio-vestibular assessment.

Ocular Motor

The first step in assessing ocular motor function is to search for spontaneous involuntary movements of the eyes. The examiner asks the patient to look straight ahead while observing for nystagmus or saccadic intrusions. Nystagmus is characterized by a slow- and fast-phase component and is classified as either spontaneous, gaze-evoked, or positional. The direction of nystagmus is conventionally described by the direction of the fast phase, which is the direction it appears to be “beating” toward. Recording whether the nystagmus is vertical, horizontal, torsional, or a mixture of these provides important localizing information. Spontaneous nystagmus can have either a peripheral or central pattern. Although central lesions can mimic a “peripheral” pattern of nystagmus (Lee and Cho, 2004; Newman-Toker et al., 2008), some very unusual and unlikely circumstances are required for peripheral lesions to cause “central” patterns of nystagmus. A peripheral pattern of spontaneous nystagmus is unidirectional, that is, the eyes beat only to one side (Video 37.1). Peripheral spontaneous nystagmus never changes direction. It is usually a horizontal greater than torsional pattern because of the physiology of the asymmetry in firing rates within the peripheral vestibular system whereby the vertical canals cancel each other out. The prominent horizontal component results from the unopposed horizontal canal. Other characteristics of peripheral spontaneous nystagmus are suppression with visual fixation, increase in velocity with gaze in the direction of the fast phase, and decrease with gaze in the direction opposite of the fast phase. Some patients are able to suppress this nystagmus so well at the bedside, or have partially recovered from the initiating event, that spontaneous nystagmus may only appear by removing visual fixation. Several simple bedside techniques can be used to remove the patient’s ability to fixate. Frenzel glasses are designed to remove visual fixation by using +30 diopter lenses. An ophthalmoscope can be used to block fixation. While the fundus of one eye is being viewed, the patient is asked to cover the other eye. Probably the simplest technique involves holding a blank sheet of paper close to the patient’s face (so as to block visual fixation) and observing for spontaneous nystagmus from the side.

Video 37.1

Acute peripheral vestibular nystagmus. Spontaneous left-beating nystagmus is demonstrated. With gaze to the left, the left-beating nystagmus increases in velocity, whereas with gaze to the right, it stops.

Saccadic intrusions are spontaneous, unwanted saccadic movements of the eyes, without the rhythmic fast and slow phases characteristic of nystagmus. Saccades are fast movements of the eyes normally under voluntary control and used to shift gaze from one object to another. Square-wave jerks and saccadic oscillations are the most common types of saccadic intrusions. Square-wave jerks refer to small-amplitude, involuntary saccades that take the eyes off a target, followed after a normal intersaccadic delay (around 200 ms) by a corrective saccade to bring the eyes back to the target. Square-wave jerks can be seen in neurological disorders such as cerebellar ataxia, Huntington disease (HD), or progressive supranuclear palsy (PSP), but they also occur in normal individuals. If the square-wave jerks are persistent or of large amplitude (macro–square wave jerks), pathology is more likely.

Saccadic oscillations refer to back-to-back saccadic movements without the intersaccadic interval characteristic of square-wave jerks, so their appearance is that of an oscillation. When a burst occurs only in the horizontal plane, the term ocular flutter is used (Video 37.2). When vertical and/or torsional components are present, the term opsoclonus (or so-called dancing eyes) is used. The eyes make constant random conjugate saccades of unequal amplitude in all directions. Ocular flutter and opsoclonus are pathological findings typically seen in several different types of CNS diseases involving brainstem-cerebellar pathways. Paraneoplastic disorders should be considered in patients presenting with ocular flutter or opsoclonus.

Video 37.2

Ocular flutter. Spontaneous back-and-forth saccades without an intersaccadic delay are seen.

Gaze Testing

The patient should be asked to look to the left, right, up, and down; the examiner looks for gaze-evoked nystagmus in each position (Video 37.3). A few beats of unsustained nystagmus with gaze greater than 30 degrees is called end-gaze nystagmus and variably occurs in normal subjects. Gaze-evoked downbeating nystagmus (Video 37.4), vertical nystagmus that increases on lateral gaze, localizes to the craniocervical junction and midline cerebellum. Gaze testing may also trigger saccadic oscillations.

Video 37.3

Gaze-evoked nystagmus and impaired smooth pursuit. Gaze to either side initiates a horizontal nystagmus in the direction of gaze. Additionally, impaired or “saccadic” pursuit is demonstrated as the patient attempts to track an object back and forth.

Video 37.4

Gaze-evoked downbeating nystagmus. Downbeating nystagmus occurs with gaze to either side.

Smooth Pursuit

Smooth pursuit refers to the voluntary movement of the eyes used to track a target moving at a low velocity. It functions to keep the moving object on the fovea to maximize vision. Though characteristically a very smooth movement at low frequency and velocity testing, smooth pursuit inevitably breaks down when tested at high frequencies and velocities. Though smooth pursuit often becomes impaired with advanced age, a recent study found no significant decline in smooth pursuit in a group of healthy elderly individuals (>75 years) tested yearly for at least 9 years (Kerber et al., 2006). Patients with impaired smooth pursuit require frequent small saccades to keep up with the target, thus the term saccadic pursuit is used to describe this finding (see Video 37.3). Abnormalities of smooth pursuit occur as the result of disorders throughout the CNS and with tranquilizing medicines, alcohol, inadequate concentration or vision, and fatigue. Patients with diffuse cortical disease, basal ganglia disease, or diffuse cerebellar disease consistently have bilaterally impaired smooth pursuit. Patients with early or mild cerebellar degenerative disorders may have markedly impaired smooth pursuit with mild or minimal truncal ataxia as the only findings.

Saccades

Saccades are fast eye movements (velocity of this eye movement can be as high as 600 degrees per second) used to quickly bring an object onto the fovea. Saccades are generated by the burst neurons of the pons (horizontal movements) and midbrain (vertical movements). Lesions or degeneration of these regions leads to slowing of saccades, which can also occur with lesions of the ocular motor neurons or extraocular muscles. Severe slowing can be readily appreciated at the bedside by instructing the patient to look back and forth from one object to another. The examiner observes both the velocity of the saccade and the accuracy. Overshooting saccades (missing the target and then needing to correct) indicates a lesion of the cerebellum (Video 37.5). Undershooting saccades are less specific and often occur in normal subjects.

Video 37.5

Hypermetric saccades. Eyes overshoot the target during saccade testing. A corrective saccade is then necessary to bring the eyes back on target.

Optokinetic Nystagmus and Fixation Suppression of the Vestibulo-ocular Reflex

Optokinetic nystagmus (OKN) and fixation suppression of the vestibulo-ocular reflex (VOR suppression) can also be tested at the bedside. OKN is a combination of fast (saccadic) and slow (smooth pursuit) movements of eyes and can be observed in normal individuals when, for example, watching a moving train. OKN is maximally stimulated with both foveal and parafoveal stimulation, so the proper laboratory technique for measuring OKN uses a full-field stimulus by having the patient sit stationary while a large rotating pattern moves around them. This test can be approximated at the bedside by moving a striped cloth in front of the patient, though this technique only stimulates the fovea. Patients with disorders causing severe slowing of saccades will not be able to generate OKN, so their eyes will become pinned to one side. VOR suppression can be tested at the bedside using a swivel chair. The patient sits in the chair and extends his or her arm in the “thumbs-up” position out in front. The patient is instructed to focus on the thumb and to allow the extended arm to move with the body so the visual target of the thumb remains directly in front of the patient. The chair is then rotated from side to side. The patient’s eyes should remain locked on the thumb, demonstrating the ability to suppress the VOR stimulated by rotation of the chair. Nystagmus will be observed during the rotation movements in patients with impairment of VOR suppression, which is analogous to impairment of smooth pursuit. Both OKN and VOR suppression can also be helpful when examining patients having difficulty following the instructions for smooth pursuit or saccade testing.

Vestibular Nerve Examination

Often omitted as part of the cranial nerve examination in general neurology texts, important localizing information can be obtained about the functioning of the vestibular nerve at the bedside. A unilateral or bilateral vestibulopathy can be identified using the head-thrust test (Halmagyi et al., 2008) (Fig. 37.3 and Video 37.6). To perform the head-thrust test, the physician stands directly in front of the patient, who is seated on the exam table. The patient’s head is held in the examiner’s hands, and the patient is instructed to focus on the examiner’s nose. The head is then quickly moved about 5 to 10 degrees to one side. In patients with normal vestibular function, the VOR results in movement of the eyes in the direction opposite the head movement. Therefore the patient’s eyes remain on the examiner’s nose after the sudden movement. The test is repeated in the opposite direction. If the examiner observes a corrective saccade bringing the patient’s eyes back to the examiner’s nose after the head thrust, impairment of the VOR in the direction of the head movement is identified. Rotating the head slowly back and forth (the doll’s eye test) also induces compensatory eye movements, but both the visual and vestibular systems are activated by this low-velocity test, so a patient with complete vestibular function loss and normal visual pursuit will have normal-appearing compensatory eye movements on the doll’s eye test. This slow rotation of the head, however, is helpful in a comatose patient who is not able to generate voluntary visual tracking eye movements. Slowly rotating the head can also be a helpful test in patients with impairment of the smooth-pursuit system, because smooth movements of the eyes during slow rotation of the head indicates an intact VOR, whereas continued saccadic movements during slow rotation indicates an accompanying deficit of the VOR (Migliaccio et al., 2004).

Fig. 37.3 Head-Thrust Test. The head thrust test is a test of vestibular function that can be easily done during the bedside examination. This maneuver tests the vestibulo-ocular reflex (VOR). The patient sits in front of the examiner and the examiner holds the patient’s head steady in the midline. The patient is instructed to maintain gaze on the nose of the examiner. The examiner then quickly turns the patient’s head about 10-15 degrees to one side and observes the ability of the patient to keep the eyes locked on the examiner’s nose. If the patient’s eyes stay locked on the examiner’s nose (i.e., no corrective saccade) (A), then the peripheral vestibular system is assumed to be intact. If, however, the patient’s eyes move with the head (B) and then the patient makes a voluntary eye movement back to the examiner’s nose (i.e., corrective saccade), then this indicates a lesion of the peripheral vestibular system and not the central nervous system (CNS). Thus, when a patient presents with the acute vestibular syndrome, the test result shown in A would suggest a CNS lesion (because the VOR is intact), whereas the test result in B suggests a peripheral vestibular lesion on the right side (because the VOR is not intact).

(From: Edlow JA, Newman-Toker DE, Savitz SI, 2008. Lancet Neurology 7, 951-964.)

Video 37.6

Head-thrust test. The patient’s eyes stay on the camera with head thrusts to the left, but a corrective saccade is seen after head thrusts to the right. Thus the horizontal vestibule-ocular reflex is reduced on the right side.

Positional Testing

Positional testing can help identify peripheral or central causes of vertigo. The most common positional vertigo, BPPV, is caused by free-floating calcium carbonate debris, usually in the posterior semicircular canal, occasionally in the horizontal canal, or rarely in the anterior canal. The characteristic burst of upbeat torsional nystagmus is triggered in patients with BPPV by a rapid change from an erect sitting position to supine head-hanging left or head-hanging right (the Dix-Hallpike test) (Video 37.7). When present, the nystagmus is usually only triggered in one of these positions. A burst of nystagmus in the opposite direction (downbeat torsional) occurs when the patient resumes the sitting position. A repositioning maneuver can be used to liberate the clot of debris from the posterior canal. We use the modified Epley maneuver (Fig. 37.4 and Video 37.8), which is more than 80% effective in treating patients with posterior canal BPPV, compared to 10% effectiveness of a sham procedure (Fife et al., 2008). The key feature of this maneuver is the roll across in the plane of the posterior canal so that the clot rotates around the posterior canal and out into the utricle. Once the clot enters the utricle, it may reattach to the membrane, dissolve, or may even remain free-floating in the utricle, but the debris no longer disrupts semicircular canal function. Recurrences are common, however.

Fig. 37.4 Treatment maneuver for benign paroxysmal positional vertigo affecting the right ear. Procedure can be reversed for treating the left ear. Drawing of labyrinth in the center shows position of the debris as it moves around the posterior semicircular canal (PSC) and into the utricle (UT). A, Patient is seated upright with head facing examiner, who is standing on the right. B, Patient is then rapidly moved to head-hanging right position (Dix-Hallpike test). This position is maintained until nystagmus ceases. Examiner moves to the head of the table, repositioning hands as shown. C, Patient’s head is rotated quickly to the left, with right ear upward. This position is maintained for 30 seconds. D, Patient rolls onto the left side while examiner rapidly rotates the head leftward until the nose is directed toward the floor. This position is then held for 30 seconds. E, Patient is then rapidly lifted into the sitting position, now facing left. The entire sequence should be repeated until no nystagmus can be elicited. Following the maneuver, the patient is instructed to avoid head-hanging positions to prevent the debris from reentering the posterior canal.

(From Baloh, R.W., 1998. Dizziness, Hearing Loss, and Tinnitus. F.A. Davis Company, Philadelphia, Figure 69, p. 166.)

Video 37.7

Benign paroxysmal positional vertigo. A burst of upbeat torsional nystagmus is demonstrated after the patient is placed into the right head-hanging position (Dix-Hallpike position). The nystagmus resolves over 20 seconds.

Video 37.8

Epley maneuver. From the sitting position, the patient is first placed into the right head-hanging position (Dix-Hallpike position) and then is guided through the particle repositioning maneuver (Epley maneuver) to cure benign paroxysmal positional vertigo stemming from the right posterior semicircular canal.

If the debris is in the horizontal canal, direction-changing horizontal nystagmus is seen. Patients are tested for the horizontal canal variant of BPPV by turning the head to each side while lying in the supine position. The nystagmus can be either paroxysmal geotropic (beating toward the ground) or persistent apogeotropic nystagmus (beating away from the ground). In the case of geotropic nystagmus, the debris is in the posterior segment (or “long arm”) of the horizontal canal, whereas the debris is in the anterior segment (or “short arm”) when apogeotropic nystagmus is triggered. When geotropic nystagmus is triggered, the side with the stronger nystagmus is the involved side. However, when apogeotropic nystagmus is observed, the involved side is generally opposite the side of the stronger nystagmus. With the geotropic variant, the debris can be removed from the canal by rolling the patient (barbecue fashion) toward the normal side. Other repositioning maneuvers for horizontal canal BPPV include the Gufoni maneuver and the “forced prolonged position” (Fife et al., 2008; Vannucchi et al., 1997). In cases of the apogeotropic variant, performing the barbeque maneuver toward the affected side can convert the nystagmus to geotropic because it moves the particles from the short arm of the canal to the long arm. Once the nystagmus is converted to geotropic, the typical treatments for the geotropic variant are used.

Positional testing can also trigger central types of nystagmus (usually persistent downbeating), which may be the most prominent examination finding in patients with disorders like Chiari malformation or cerebellar ataxia (Kattah and Gujrati, 2005; Kerber et al., 2005a). Central positional nystagmus can mimic the nystagmus of horizontal canal BPPV. Positional nystagmus may also be prominent in patients with migraine-associated dizziness (von Brevern et al., 2005).

Finger rubs at different intensities and distances from the ear are a rapid, reliable, and valid screening test for hearing loss in the frequency range of speech (Torres-Russotto et al., 2009). If a patient can hear a faint finger rub stimulus at a distance of 70 cm (approximately one arm’s length) from one ear, then a hearing loss on that side—defined by a gold-standard audiogram threshold of greater than 25 dB at 1000, 2000, and 4000 Hz—is highly unlikely. On the other hand, if a patient cannot hear a strong finger rub stimulus at 70 cm, a hearing loss on that side is highly likely. The whisper test can also be used to assess hearing at the bedside (Bagai et al., 2006). For this test, the examiner stands behind the patient to prevent lip reading and occludes and masks the non–test ear, using a finger to rub and close the external auditory canal. The examiner then whispers a set of three to six random numbers and letters. Overall, the patient is considered to have passed the screening test if they repeat at least 50% of the letters and numbers correctly. The Weber and Rinne tests are commonly used bedside tuning fork tests. To perform these, a tuning fork (256 Hz or 512 Hz) is gently struck on a hard rubber pad, the elbow, or the knee about two-thirds of the way along the tine. To conduct the Weber test, the base of the vibrating fork is placed on the vertex (top or crown of the head), bridge of the nose, upper incisors, or forehead. The patient is asked if the sound is heard and whether it is heard in the middle of the head or in both ears equally, toward the left, or toward the right. In a patient with normal hearing, the tone is heard centrally. In asymmetrical or a unilateral hearing impairment, the tone lateralizes to one side. Lateralization indicates an element of conductive impairment in the ear in which the sound localizes, a sensorineural impairment in the contralateral ear, or both. The Rinne test compares the patient’s hearing by air conduction with that by bone conduction. The fork is first held against the mastoid process until the sound fades. It is then placed 1 inch from the ear. Normal subjects can hear the fork about twice as long by air as by bone conduction. If bone is greater than air conduction, a conductive hearing loss is suggested.