Benign positional vertigo (BPV), also called benign positioning vertigo and benign paroxysmal positional vertigo, is a common inner ear disorder resulting from abnormal stimulation of the semicircular canals (usually the posterior). The direction of the provocative movement and the appearance of the induced eye movements (nystagmus) identify the involved canal(s). The abnormal stimulation is due to the presence of detached otoconia (canaliths) moving in the canal endolymph under the influence of gravity. In order for positional vertigo to occur, two events must happen: (1) otoconia must be dislodged from the utricular macule, and (2) the head must be held in a critical position that allows the otoconia to enter a semicircular canal. BPV is not a disease; rather, it is a syndrome that can have multiple causes of the detached otoconia.
The basic features of BPV and the associated paroxysmal positional nystagmus were first described in a single patient by Bárány in 1921,1 but it was not until 1952 that Dix and Hallpike described the provocative positioning maneuver and clearly defined the clinical syndrome.2 Bárány speculated that the paroxysmal positional nystagmus was caused by a lesion of the otolith organs, as it was induced by a change in head position relative to gravity. Dix and Hallpike came to a similar conclusion after reviewing the clinical features of 100 patients with BPV and identifying unilateral degeneration of the utricular macule at necropsy in a typical case.
In 1961, Schuknecht reviewed the temporal bone specimens from three patients who had been reported to have BPV and was struck by the remarkable similarity of the pathologic changes.3 Each had a selective degeneration of the superior part of the labyrinth, including the superior branch of the vestibular nerve, the utricle, and the crista of the horizontal and anterior semicircular canals. He concluded that in each case the damage to the labyrinth resulted from occlusion of the anterior vestibular artery, the branch of the internal auditory artery that supplies these organs. Schuknecht felt that the paroxysmal positional nystagmus that occurred in these cases must have originated from the posterior semicircular canal since it was the only peripheral sensory organ capable of generating nystagmus that was still functioning. He did not feel that the intact saccular macule was capable of generating nystagmus.
With this hypothesis in mind, Schuknecht attempted to produce paroxysmal positional nystagmus in four cats by cutting off the blood supply in the left anterior vestibular artery.3 Each animal developed the expected acute vestibular syndrome with horizontal nystagmus and imbalance in the immediate postoperative period. These symptoms gradually subsided over several days. One of the animals, however, developed typical benign paroxysmal positional nystagmus 3 months after the operation, which persisted until termination of the experiments at 7 months. Schuknecht theorized that loose otoconia from the degenerating utricular macule came in contact with the cupula of the posterior semicircular canal, causing it to move in the plane of the canal after position changes.
In 1969, Schuknecht found basophilic deposits on the cupulae of the posterior semicircular canals in two patients who manifested isolated BPV without any other ear symptoms prior to death from unrelated disease (Fig. 10–1).4 The deposits were present on the side that was undermost when the paroxysmal positional nystagmus was induced. These findings supported his earlier hypothesis and, even though he observed particles in the canal in addition to those attached to the cupula, he coined the term cupulolithiasis.
The cupulolithiasis theory of Schuknecht gained general acceptance, but there were features of the characteristic paroxysmal positional nystagmus that were not adequately explained—the transient duration and the fatigability with repeated positioning. If the particles are adherent to the cupula, transient duration and fatigability would not be expected. In his initial report,3 Schuknecht suggested that the otoconial debris might dislodge from the cupula and float away, allowing the cupula to return to its normal position, and that the particles might become dispersed within the endolymph with repeated positionings. However, when his subsequent postmortem studies showed that the otolithic debris was firmly attached to the cupula of the posterior semicircular canal, he felt that these possibilities were less likely.4
In the late 1970s, McClure began to experiment with mechanical models of the inner ear to see if these problems could be resolved. His simple model consisted of a water bottle representing the utricular chamber and two attached rounded tubes representing the posterior and anterior semicircular canals. He placed mercury in the canals to represent the otoconial debris and noted that repeated positional changes from sitting to head-hanging position caused the mercury to enter the utricle. He recognized that freely floating debris in the posterior semicircular canal could readily explain both the paroxysmal nature of the nystagmus and the fatigability. In 1979, along with Hall and Ruby5, McClure published his model and suggested that benign paroxysmal positional nystagmus could be divided into two types: type A, a nonfatigable form caused by debris adherent to the cupula (i.e., cupulolithiasis), and type B, a more common fatigable form caused by free-floating particles in the endolymph, canalithiasis. This work served as the theoretical basis for the subsequent use of positional exercises and positional maneuvers to treat BPV.
Epley did not distinguish between cupulolithiasis and canalithiasis but rather suggested that debris was both attached to the cupula and free floating in the canal in most cases of BPV.6 He recognized that debris moving within the narrow semicircular canal would be much more effective in deviating the cupula than an equal amount of debris floating within the ampulla next to the cupula. He saw the analogy of the bolus of particles acting as a piston moving within the narrow confines of the semicircular canal, which, according to Pascal’s formula, would lead to a magnified force acting on the cupula. Epley argued that if this bolus of debris could move so easily with position change, it should be possible to move it around and out of the posterior semicircular canal and into the utricle with appropriate positional changes. In a case series report in 1992, he reported that a simple particle repositioning maneuver cured most patients with BPV.7 Later, randomized placebo-controlled (sham positional maneuvers) trials confirmed the treatment effect of what has become known as the Epley maneuver.8
At about the same time of Epley’s original reports, Parnes and McClure described a surgical procedure for blocking the posterior semicircular canal with a bony plug that was highly effective in curing intractable cases of BPV.9 During the process of exposing the membranous labyrinth of the posterior semicircular canal for the plugging operation, Parnes and McClure observed a chalky white substance within the endolymph of the posterior semicircular canal. Their observation supported the canalithiasis model proposed by Hall et al.5 and was consistent with the success of Epley’s particle repositioning maneuver.
Causes of Benign Positional Vertigo
The first event that must happen for BPV to occur is that otoconia must be free floating in the utricule. However, in most cases, there is no easily explainable reason for why the otoconia are released. The attacks of positionally triggered vertigo are not typically preceded by a specific event. However, the prevalence of the disorder dramatically increases with increasing age so that release of the otoconia could be an effect of the aging process. Osteopenia and osteoporosis are also more common in patients with idiopathic BPV than in controls, suggesting that abnormal calcium metabolism is an important etiological factor.10–12 Both osteopenia and BPV are more common in women and older people. In osteopenic rats, otoconia have decreased density and increased size compared to controls so the otoconia may be more easily dislodged.13 Furthermore, degeneration of otoconia is seen in older rats regardless of osteopenia.14
Another important association with BPV is migraine. Migraine is more common in patients with idiopathic BPV than in controls particularly in patients under the age of 50.15,16 The reason for this association is not clear, but it is possible that migranous vasospasm could lead to dislodged otoconia.
Head trauma is the most common identifiable cause for dislodging otoconia. The most common cause of head trauma is motor vehicle accidents followed by common falls.17 BPV after head trauma tends to be more severe and more protracted than BPV from other causes. Infection and ischemia of the inner ear are the next most common causes for free-floating otoconia. In animal models, brief periods of ischemia result in prominent release of otoconia from the utricular macule (see Anatomy of Otolith Organs, Chapter 2). Nearly half of patients with vestibular neuritis have BPV as a sequela (see Chapter 9). Vigorous exercise such as aerobics, mountain biking, and swimming are associated with recurrent BPV.18–20 Presumably repeated abrupt accelerations can dislodge otoconia. Surgeries involving drilling of the temporal bone such as with cochlear implants can dislodge otoconia and predespose to BPV.21
The second event that must happen for BPV to occur is the otoconial debris must enter a semicircular canal. Free-floating otoconia in the utricle are not believed to cause symptoms. It is only when the otoconia enter a semicircular canal that symptoms occur. Because of its position in the head the posterior semicircular canal is most vulnerable. Loose otoconia in the utricle will fall into the posterior semicircular canal and become trapped if the head is held backward below the horizontal plane for a few minutes. This explains why BPV often first occurs after situations such as going to a hairdresser, a dentist, or fixing a leaky kitchen sink. People with certain occupations, such as auto mechanics and plumbers, are particularly prone to developing recurrent BPV. It is not too farfetched to assume that otoconial debris is floating freely within the endolymph in nearly everyone, particularly older people.22 It is just a matter of whether the head is held in the critical position long enough for the particles to drop into the posterior semicircular canal. Benign positional vertigo commonly occurs after surgical procedures regardless of the nature or location of the surgery. Initially this was thought to result from some metabolic changes associated with the trauma of surgery or from the anesthesia, but more likely the BPV is secondary to prolonged positioning with the head back in people who already have free-floating debris in the vestibule. Positioning for dental and radiological procedures is another common precipitating factor for BPV.23,24 Interestingly BPV occurs more commonly on the right side compared to the left, possibly because people tend to sleep more on the right side than the left.25,26
Posterior Canal Variant of Benign Positional Vertigo
By far the most common variety of BPV is that associated with debris in the posterior semicircular canal (PC-BPV).27 Patients develop brief episodes of vertigo and nystagmus (usually lasting <30 sec) with position change: typically when turning over in bed, getting in and out of bed, bending over and straightening up, or extending the neck to look up.28 (See Video 6–12 and Video 6–13) Importantly, the vertigo of BPV is triggered by certain position changes. Any patient with vertigo will report worsening of the vertigo in certain positions, but patients with BPV will report that the vertigo is triggered by the position change. “Top shelf vertigo,” in which a patient experiences an episode of vertigo while reaching for something on a high shelf, is nearly always due to PC-BPV. Since the most common provocative movements for inducing PC-BPV occur in bed or when getting in and out of bed, patients report that the vertigo is severe in the morning and tends to disappear once they are up. The common report of having attacks mostly in the morning may also be because the particles have had a chance to accumulate in one part of the canal while the patient is lying still sleeping. Turning the head from side to side while erect does not induce nystagmus because this movement does not stimulate the posterior semicircular canal. Often after a flurry of episodes, patients complain of more prolonged nonspecific dizziness (a motion-sick sensation) that may last hours or even persist throughout the day. Vertigo can awaken the patient; presumably, positional vertigo occurs when they turn over while sleeping, and some patients experience severe nausea and vomiting, which can be even more bothersome than the vertigo.
As the name implies, BPV is a benign disorder meaning that it is not progressive and in most cases will eventually remit spontaneously.29 However, spontaneous remission can take months or longer, and there are some patients who report having symptoms for many years and are only cured after a canalith repositioning maneuver. In a longitudinal cohort study of patients who presented to an Otolaryngology clinic, the mean time to symptom resolution was 39 days with a wide standard deviation of 47 days.29 In a population-based telephone survey study, patients with BPV reported a mean symptom duration of 2 weeks (range 0.5 days to 104 weeks), with about one-third reporting symptoms more than 1 month.30,31 The duration of symptoms in control groups of randomized trials was generally more than 1 month for about 80% of the patients.32 The “benign” label also cannot be mistaken to mean that the symptoms are trivial. Patients with BPV have an increased incidence of falls, depression, and impairment of daily activities.33–35 During periods of symptomatic BPV, 24% of patients reported giving up driving a car and 18% avoided leaving their home.31 Also reflecting the burden of BPV on patients, in the population-based study nearly 80% of BPV patients reported a visit to a medical doctor.31 More than half of patients with PC-BPV have at least one recurrence after a remission.15,27,31 In some patients, bouts of PC-BPV are intermixed with variable periods of remission over many years.
In their initial description of the syndrome in 1952, Dix and Hallpike found evidence of ear disease in approximately two-thirds of their 100 patients with BPV.2 When the ear disease was unilateral, the nystagmus was usually induced when the abnormal ear was undermost. Subsequent reports confirmed the benign nature of the disorder but suggested that most cases were unassociated with identifiable lesions.28,36,37 Despite its common occurrence, there have been relatively few reports of large series of patients with BPV.
We reviewed the clinical features of 240 cases of BPV, each with a typical clinical history and the stereotyped paroxysmal positional nystagmus.28 The mean age of onset was 54 years (range 11 to 84 years). The two largest diagnostic categories were posttraumatic and postviral (Table 10–1). Patients with the former had the onset of BPV within 3 days of well-documented head trauma. Patients in the viral group reported a prior episode of acute vertigo gradually resolving over 1 to 2 weeks. In 25 of 37 postviral patients, there was an associated sudden hearing loss that improved as vertigo subsided, although most patients were left with a residual unilateral sensorineural hearing loss. The associated hearing loss suggests that the viral process targeted the labyrinth (i.e., “labyrinthitis”) rather than the more common target, the vestibular nerve (i.e., “vestibular neuritis”). Episodes of BPV can begin as soon as 1 week and long as 8 years after the acute viral syndrome. Most patients reported a cold or flu-like illness within 2 weeks of the acute vertiginous episode. Eleven patients reported typical symptoms of vertebrobasilar insufficiency (in addition to vertigo) prior to the onset of BPV. In these cases, the BPV could have resulted from ischemic damage to the labyrinth. It is important to recognize that these episodes of positional vertigo in such patients do not indicate recurrent vascular ischemia.
Table 10–1 Diagnoses in 240 Patients with Benign Paroxysmal Positional Vertigo28
Basilar vertebral insufficiency
Females outnumbered males by a ratio of 1.6:1, combining all diagnostic categories. This ratio was approximately 2:1 if only the idiopathic and miscellaneous groups were considered. Other investigators have reported an even higher female-to-male preponderance with idiopathic BPV.37 The age of onset peaked in the sixth decade in the idiopathic group, in the fourth and fifth decades in the postviral group, and was evenly distributed over the second to sixth decades in the posttraumatic group.
As noted earlier, the most likely explanation for PC-BPV is canalithiasis involving the posterior semicircular canal.7,38,39 With the patient sitting upright, a clot of calcium carbonate crystals forms at the most dependent portion of the posterior canal (Fig. 10–2A). Movement of the head back and to the side in the plane of that posterior canal (such as with the standard positioning test) causes the clot to move in an ampullofugal direction, producing ampullofugal displacement of the cupula due to the “plunger” effect of the clot moving within the narrow canal (Fig. 10–2B). Fatigability with repeated positioning is explained by dispersion of particles from the clot, making the plunger less effective. Reactivation of the positional vertigo after prolonged bed rest is also explained as the particles reform into a clot. The induced vertigo and nystagmus are brief in duration because once the clot reaches its lowest position in the canal with respect to the earth’s surface, the cupula returns to its primary position with its usual time constant determined primarily by cupular elasticity. The typical latency of about 5 seconds before onset of nystagmus is explained by the delay in setting the clot into motion. It also explains why slow positioning does not induce vertigo or nystagmus, as the clot would move slowly along the undermost wall of the canal without producing a plunger effect.
Probably the most convincing argument for the canalithiasis theory is the dramatic response of PC-BPV to positional maneuvers designed to move the clot around the posterior semicircular canal into the utricle.7,27 By rotating the subject about the plane of the posterior canal, the clot moves from a position next to the cupula, as shown in Figure 10–2A, into the utricle as shown in Figure 10–2E. It is of particular note that when the patient is moved from the initial head-hanging position (which induced the nystagmus) to the opposite head-hanging position (with the abnormal ear up), an identical burst of positioning nystagmus often occurs, in both cases with the upper pole of the eye beating toward the abnormal ear. This phenomenon is readily explained by following the movement of the clot around the posterior semicircular canal, which in each case produces ampullofugal displacement of the posterior canal cupula. If the debris were attached to the cupula as suggested by the cupulolithiasis theory, one would expect the nystagmus to change direction in the opposite head-hanging position.
The diagnosis of PC-BPV rests on finding the characteristic paroxysmal positional nystagmus in a patient with a typical history of positional vertigo. The nystagmus is induced by rapidly moving the patient from the sitting to head-hanging position as originally described by Dix and Hallpike (see Fig. 6–6 in Chapter 6). It is important to prepare the patient in advance by explaining that the goal is to induce positional vertigo and that the patient must cooperate by keeping the eyes open and avoid blinking as much as possible. The typical nystagmus has torsional and vertical components. The eyes beat upward (toward the forehead) with the upper poles beating toward the ground (thus an upbeat-torsional nystagmus is seen).40,41 The vertical component is larger in the contralateral eye and the torsional component is larger in the ipsilateral eye, consistent with the known excitatory connections from the posterior semicircular canal to the eye muscles (see Fig. 3–8c in Chapter 3). A reverse nystagmus (downbeat and torsional) of lesser magnitude usually occurs if the patient is brought directly back up from the head-hanging position to the sitting position, a finding which is also highly supportive of free-floating particles in the canal because sitting up reverses the movement of the particles in the canal, thus triggering nystagmus in the reverse direction. The nystagmus triggered in the head-hanging position fatigues (decreases with repeated positioning) in more than 90% of patients, but there are occasional patients with otherwise typical BPV and nystagmus who do not show fatigue with repeated positioning. There is usually a latency from the time the head-hanging position is achieved to the onset of positioning nystagmus but, as with fatigability, it is not an absolute feature. The presence of positioning nystagmus correlates with the clinical symptoms. Unless the patient is tested during a period when he or she is having acute episodes of vertigo, the positioning nystagmus may not be observed. Patients with BPV may have negative positional testing if the particles are dispersed within the canal rather than coalescent as a clot.
With the development of particle repositioning maneuvers designed to remove debris from the posterior semicircular canal, treating the patients with these maneuvers also serves to confirm the diagnosis.27 Once the typical positioning nystagmus is induced, we proceed with a positional maneuver to cure the condition (see later discussion). If the positioning nystagmus and symptoms are gone after completing the maneuver, the diagnosis was correct.
Since BPV can generally be diagnosed and cured at the time of the office visit, ancillary testing is rarely indicated. Laboratory tests are generally not helpful for the diagnosis of BPV. Patients with recurrent BPV might be screened for osteopenia, although it is unproven whether correcting osteopenia decreases the likelihood of recurrent BPV. ENG and VNG are not helpful since there is usually a minimal horizontal component to record and the prominent torsional component cannot easily be recorded. VNG allows one to actually view the nystagmus so that the torsional component can be appreciated, but the pattern of nystagmus is readily identifiable at the bedside without the need for VNG. The characteristic nystagmus is easily observed visually even if the patient attempts to fixate (i.e., there is no need for Frenzel lenses or infrared video recordings). MRI of the brain is not indicated, but high resolution MRI of the inner ear might be informative for visualizing the otoconia debris and canal structure in very rare atypical or refractory cases.42,43
Once BPV is diagnosed, a simple explanation of the nature of the disorder and its favorable prognosis can help relieve the patient’s anxiety. Because of the dramatic nature of the episodes of vertigo, many patients believe that they have a life-threatening disorder such as a tumor or stroke, and they need to be reassured that they have a benign inner ear disorder. It is important to be aware, however, that although it is a benign disorder, recurrences are common. Episodes of positional vertigo typically occur in flurries and about half of the patients will have at least one exacerbation after an initial remission.31 The likelihood of a recurrence should be explained to patients so they are not unduly frightened if it occurs.
We typically perform a particle repositioning maneuver designed to liberate the clot from the posterior semicircular canal immediately after the diagnosis is confirmed with the Dix-Hallpike positioning test. We use a modified Epley maneuver, shown in Fig. 10–3. (See Video 10–1) The Semont maneuver (Fig. 10–4) may be equally effective, although there have been fewer controlled studies using this maneuver.32 The key feature of the particle repositioning maneuvers is to move the patient in the plane of the posterior semicircular canal to allow the clot of debris to rotate around the canal and enter the utricle.
The Epley maneuver is among the most efficacious interventions in all of clinical medicine. The maneuver has been tested in numerous randomized placebo (i.e., sham procedures) controlled trials. Trial quality has been rigorously scrutinized independently by the Cochrane Collaboration,8 the American Academy of Neurology Quality Standards Subcommittee,32 a multidisciplinary guideline development panel chosen by the American Academy of Otolaryngology–Head and Neck Surgery Foundation,44 and other independent groups.45,46 The summary results of all the valid randomized controlled trials indicate that the Epley maneuver has a large effect size in treating patients with BPV. In these studies, 61%–80% of patients treated with the maneuver had resolution of BPV compared with only 10%–20% of patients in the control groups with outcomes measured from 1 day to 1 month. These effect sizes translate into a “number needed to treat” (NNT) of 1.43 to 2.44. The NNT is a statistical measure that indicates the number of patients that had to have treatment to achieve the beneficial outcome in one patient. Thus, approximately two patients with BPV require treatment with the Epley maneuver to eliminate the symptoms in one patient; this is among the largest effect sizes achievable in clinical medicine, and it is particularly impressive considering that the outcome used was elimination of symptoms (i.e., cure of symptoms) as opposed to only an improvement in symptoms.
Despite the large effect size of the Epley maneuver for BPV, the maneuver appears to be substantially underutilized in routine practice. Of patients with BPV who presented to a physician, only 27% reported undergoing diagnostic positional testing (i.e., the Dix-Hallpike test) and only 10% underwent a particle repositioning maneuver of any type.31
It is doubtful that physicians are just instructing patients to avoid provocative positions and await spontaneous resolution because about 75% of patients with BPV who present to a physician end up having at least one diagnostic test ordered, including imaging studies, vestibular tests, an audiogram, and blood tests.31,47
Although most patients are cured after a single particle repositioning maneuver, the cure rate is improved by repeating the procedure until no vertigo or nystagmus occurs in any position. Occasionally a patient will develop severe nausea and have to be rescheduled and premedicated with a vestibular suppressant drug. Although not routinely recommended, occasionally, vibration applied to the mastoid region is useful if, rather than a burst of nystagmus with position change, the patient develops a slow, persistent nystagmus, suggesting that the otolithic debris is stuck to the wall of the semicircular canal or to the cupula and not freely moving. A sign that the modified Epley maneuver is going to be successful is the production of a second identical burst of positional nystagmus when the patient is moved from the initial head-hanging position across to the opposite head-hanging position.48 This indicates that the particles are moving along in the canal in the correct direction toward the utricle. If, on the other hand, a burst of nystagmus in the reverse direction occurs when moving from one head-hanging position to the other, the particles are most likely moving in the wrong direction back toward the cupula, a sign that the particle repositioning maneuver will be unsuccessful. When this occurs, the patient most likely elevated the head while rolling over from the head-hanging position to the other side because this can cause the particles to move back in the opposite direction because of gravity. It is critical that the head stay down during this phase of the positioning maneuver. When returning to the sitting position at the end of the particle repositioning maneuver, patients may have a brief but severe burst of vertigo (falling sensation) as late as 30 min after assuming the position.49 This delayed vertigo in the sitting position presumably occurs as the bolus of otolithic debris drops out of the common crus of the posterior and anterior semicircular canals into the utricle. Rarely, patients will develop a persistent vertigo and nystagmus after returning to the sitting position. This phenomenon might result from a jamming of the otolithic debris (a canalith jam) when migrating from a wider to narrower segment, such as from the ampulla to the canal or at the bifurcation of the common crus to the posterior and anterior canals.7 Repeating the particle repositioning with vibration applied to the skull (i.e., mastoid region of affected side) will usually break up the “canalith jam” and cure the BPV.
What happens to the particles once they enter the utricle? When the otoconia are separated from the gelatinous layer of the otolith membrane, they can dissolve in the endolymph fluid, be taken up into the membrane by the process of phagocytosis, or simply remain free floating within the endolymph. The calcium concentration of the endolymph seems to be critical for determining whether the otolithic debris will dissolve.50 Otolith debris may not be cleared in patients who have recurrent attacks of BPV. As noted earlier, osteopenia and osteoporosis are more common in patients with recurrent BPV than in patients with de novo BPV.12
After performing a particle repositioning maneuver, we recommend that patients avoid all extreme head-back positions such as those mentioned earlier. Other restrictions, such as having the patient sleep propped up for a few nights or wearing a cervical neck collar, do not improve the outcome.51Antivertiginous medications such as meclizine or promethazine have relatively little use in the management of patients with BPV because the acute attacks are not suppressed by these drugs; moreover, the particle repositioning maneuver is much more effective in controlling the condition. For the very rare patient with prolonged refractory BPV, one might still consider a surgical procedure such as the singular neurectomy or the canal plugging procedure.9,52,53 The main complication of these procedures is a sensorineural hearing loss, which may occur in as many as 10% of patients.
Patients who have multiple recurrences of BPV can be taught to perform the particle repositioning maneuver on their own.55,56 We regularly give our patients a diagram for performing the maneuver on a bed at home (e.g., Figs. 10–3 and 10–4). One study compared the efficacy of self-treatment with a modified Epley maneuver and a modified Semont maneuver and found that the response rate was significantly greater with the modified Epley maneuver.56 Although minor complications such as those described earlier can occur, none of them is serious and most are cured by simply repeating the maneuver. Patients can pre-sedate themselves and often they feel more comfortable performing the maneuver on their own in the controlled environment of their bedroom. Vibration applied to the mastoid is rarely required,57 but a simple neck massage vibrator can be used if one is available. Of course, one key point that cannot be ignored is that the particle repositioning maneuver (i.e., Epley maneuver or Semont maneuver) only works for treating PC-BPV. It is of no use for treating other causes of vertigo.
Other Variants of Benign Positional Vertigo
As noted earlier, the most common type of BPV occurs when otoconial debris are within the posterior semicircular canal, probably because this is the canal in which it is most easily trapped. However, the otoconia can enter either one of the other canals and patients do present clinically with BPV from these canals. After posterior canal BPV, the next most common variant is horizontal canal BPV. Anterior canal BPV is much less common. The clinician must also add a bit more caution when making the diagnosis of either the horizontal or anterior canal variants of BPV because the patterns of nystagmus seen with these variants can be similar to patterns of positional nystagmus caused by lesions in the central nervous system.58,59 This is different than the clinical scenario with posterior canal BPV because the characteristic pattern of nystagmus in posterior canal BPV (i.e., a burst of upbeat, torsional nystagmus lasting <30 seconds, and then having the nystagmus convert to downbeat torsional nystagmus if the patient is brought directly back up to the sitting position) is not a pattern expected or ever reported to be caused by a central lesion. For the PC-BPV variant, further adding to the confidence in the bedside diagnosis is the fact it is readily cured at the bedside. On the other hand, horizontal canal BPV can at times be difficult to make an immediate impact at the bedside.
The horizontal and anterior canal variants have clinical syndromes that resolve on average more quickly than the posterior canal variant,29 likely because the debris in these canals more readily falls back out based on the anatomy. Although, in rare cases the otolithic debris in these variants can become attached to the cupula, producing true cupulolithiasis.
It is also possible for otoconia to enter multiple canals at once, particularly after head trauma,60 which leads to more challenging approach to repositioning.
Lastly, these other variants of BPV can be produced after performing the particle repositioning maneuver for the typical posterior canal variant. For example, as the debris is moved from the posterior semicircular canal, it can enter the anterior canal from the common crus or it can enter the horizontal canal after it falls into the utricle (Fig. 10–5).
Horizontal Canal Benign Positional Vertigo
The clinical history of horizontal canal BPV is similar to that of the posterior canal variant, although there are important differences.61–63 With both syndromes, positional vertigo commonly occurs in bed, particularly when patients turn over from one side to the other. Patients with PC-BPV, however, develop vertigo when getting in and out of bed and when bending down and straightening up or extending the head backward to look up. In contrast, patients with horizontal canal BPV develop vertigo primarily when turning over in bed or when turning the head to the side when lying back in an easy chair. Occasionally, patients with horizontal canal BPV experience episodes of vertigo when turning the head to the side while sitting or walking. Remissions and exacerbations commonly occur with both types of BPV, but exacerbations are typically shorter in duration with the horizontal canal variant than with the posterior canal variant,29,64 though recurrences may be more common in the horizontal canal variant.54 With horizontal canal BPV, patients can develop two patterns of positionally triggered nystagmus (i.e., “geotropic” or “apogeotropic”) depending on whether the canaliths are in the anterior segment or the posterior segment of the horizontal canal.
When the canaliths are in the posterior segment (or “long arm”) of the horizontal canal, patients will develop a paroxysmal, horizontal direction–changing nystagmus that beats toward the ground (so-called geotropic nystagmus) when the head is turned to the side while they are lying supine (the nystagmus will also be triggered by a body roll to the side). Thus, when the head is turned to the left side, a left-beating nystagmus is triggered. Then, when the head is turned toward the right side, a right-beating nystagmus is triggered. The nystagmus lasts about a minute. Though it occurs with the head to either side, it is nearly always stronger on one side (the abnormal side). The debris enters the canal side of the horizontal semicircular canal when the patient lies supine. When the head is rapidly turned to the abnormal side, the mass is accelerated downward in the canal. The deceleration that occurs once the lateral position is reached would normally rapidly return the cupula to the center position and there would be no post-positioning nystagmus. Because of the continued effect of gravity on the freely floating clot, however, it continues to move downward in the canal toward the ampulla until it reaches the bottom of the canal in that lateral position. Movement of the clot within the canal results in an ampullopetal deviation of the cupula and a burst of nystagmus beating toward the ground. When the clot stops moving, the cupula returns to the primary position, with the normal time constant. The longer duration of horizontal canal variant BPV compared to the posterior canal variant is explained by the longer time constant of the horizontal vestibulo-ocular reflex (VOR) than that of the vertical VOR.65 Once the free-floating clot moves to the bottom of the canal in the lateral position, returning to the supine position results in a movement of the clot back to its original position and a burst of nystagmus in the opposite direction. Furthermore, rotation of the head to the opposite side causes the clot to move in the opposite direction and produces ampullofugal displacement of the cupula and geotropic nystagmus.
Unlike PC-BPV, the horizontal canal variant has only minimal latency and no fatigability. With PC-BPV, latency is explained by a delay in movement of the calcium carbonate clot and fatigability by dispersion of the calcium carbonate particles with repeated positioning. There may be a viscous plug or gel in the horizontal canal, rather than a clot of calcium carbonate crystals, which could explain the lack of fatigability.61
The second pattern of nystagmus that occurs with otoconia in the horizontal canal is the “apogeotropic” (i.e., away from the ground) pattern that is caused by otoconia in the anterior segment of the canal.66 This again can result from otoconia adherent to the cupula (cupulolithiasis) or free floating in the anterior segment of the canal (canalithitiasis). When patients have otoconia in these regions of the horizontal canal, a head turn to the left side while lying supine triggers a right-beating (thus away from the ground, “apogeotropic”) nystagmus. Turning the head to the right side will trigger a left-beating nystagmus. The dynamics of the buildup and decay of nystagmus depends on whether the debris is free floating or attached to the cupula and the dynamics of the horizontal VOR. When the debris is attached to the cupula, the stimulus is constant acceleration, which causes a gradual buildup of slow-phase velocity determined by the dominant time constant, defined as the time it requires for the response to reach 63% of maximum. An average time constant of the horizontal VOR in normal subjects is in the range of 12–20 sec. The gradual decay in slow-phase velocity after reaching a peak response can be explained on the basis of central VOR adaptation.
Treatment of Horizontal Bpv
Unlike treatment for the posterior canal variant, there are no high-level randomized controlled trials of positional treatments for the horizontal canal variant.32 However, there are several different positional treatments that suggest efficacy in cohort and case series designs. In general, it is easier to treat HC-BPV when the otoconia are in the posterior segment (rendering geotropic positional nystagmus) because the particles are closer to the exit of the canal to the utricle and because they are less likely to be adherent to the cupula. In fact, when the patient is identified as having apogeotropic nystagmus, the first goal in repositioning is generally to move the otoconia from the anterior segment to the posterior segment, thus converting the apogeotropic nystagmus to a geotropic nystagmus.
For patients with geotropic pattern of nystagmus, one commonly used maneuver is the “barbeque” maneuver (Fig. 10–6). With the “barbeque” maneuver, the patient is rotated in the plane of the horizontal canal.67–69 The patient starts in the supine position and is rolled 90 degrees to the normal side (the side with lesser nystagmus), then in 90-degree steps to prone, to the abnormal side, and back to the supine. Another maneuver gaining acceptance is the Gufoni maneuver. With the Gufoni maneuver70 the patient is rapidly moved from the sitting position (feet forward) to a head lateral position (normal ear down). The head is held in this position for about 2 minutes until the geotropic nystagmus disappears. The head is then quickly turned to the side, nose down toward the ground. After 2 minutes the patient returns to the starting position. (See Video 10–2) Finally, the “forced prolonged position” is another option. With the “forced prolonged position” the patient is instructed to sleep overnight with the normal ear down,71 which allows the otoconia to naturally fall out of the affected canal. The forced prolonged position is typically selected if the other maneuvers are not effective or if the patient is not tolerating the other maneuvers.
When the pattern of nystagmus is apogeotropic, performing the barbeque maneuver toward the affected side can convert the nystagmus to geotropic.72 The Gufoni maneuvers can also do this.73 Once the nystagmus is converted, the typical treatments for geotropic can be used. More than half of patients with apogeotropic BPV were cured by having them lie on the side of weakest nystagmus for 2 nights.74 Barbaque rotation and the Gufoni maneuver (toward the side with weaker nystagmus) can also get the debris to move from the anterior to posterior arm and out of the horizontal canal.72,73
Anterior Canal Benign Positional Vertigo
Rarely patients with a typical history of BPV, particularly after head trauma, exhibit a torsional downbeat nystagmus rather than the usual torsional upbeat nystagmus on the standard Dix-Hallpike positional test.28,75,76 The positioning nystagmus otherwise has all of the typical features of posterior canal BPV—the most important of these features is the brief duration, since persistent downbeat nystagmus is a central nervous system sign. With the standard Dix-Hallpike test, turning the head to the right and lowering the patient into the head-hanging right position activates the right posterior semicircular canal and the left anterior semicircular canal. Since the ampullae are on the opposite ends of these two vertical canals, this positional change results in ampullofugal movement (excitation) of endolymph in the posterior semicircular canal and ampullopetal movement (inhibition) of the endolymph in the contralateral anterior canal. Thus, if there were debris in the anterior canal of the contralateral ear, it would be driven back toward the cupula rather than away from the cupula, as occurs in the posterior semicircular canal. Once the final position is reached, however, debris within the canal would move downward away from the cupula of the anterior canal since the ampullary segments of both anterior canals point downward in the head-hanging positions. The direction of the torsional component of the positioning nystagmus indicates which ear is the origin of the nystagmus.76,77 If the upper pole of the eye beats away from the ground toward the uppermost ear, then it originates from the anterior canal of the uppermost ear. If it beats toward the ground, then it originates from the anterior canal of the undermost ear. The standard particle repositioning maneuver used for treating PC-BPV on the same side is also successful for treating the anterior canal variant of BPV.76
Mimics of Benign Positional Vertigo
BPV is by far the most common cause of brief recurrent attacks of positional vertigo. But it is important to know that any patient with constant or prolonged vertigo will report worsening of the symptom with certain position changes. For example, if a patient has vestibular neuritis and presents with severe and constant vertigo, the patient will typically report feeling much better lying still and much worse with any movement. This history is frequently misinterpreted as a positional vertigo syndrome.
It is also important to know that positionally triggered nystagmus can be a central nervous system finding. The most common pattern of a central positional nystagmus is a persistent downbeating nystagmus, which can be misinterpreted as nystagmus from anterior canal BPV.58 The next most common central pattern of positional nystagmus is a horizontal direction changing nystagmus, which can be identical to the patterns of nystagmus seen with horizontal canal BPV.59 Thus, when managing a patient with findings suggestive of either anterior or horizontal canal BPV but when the patient is not able to be effectively treated over a reasonable time frame or if there are any important inconsistencies, then a central lesion should be considered. The most common central lesions that mimic anterior and horizontal canal BPV are Chiari malformations, tumors or other structural lesions involving the cerebellum or peri-forth ventricular regions, or neurodegenerative disorders involving the cerebellum (i.e., spinocerebellar ataxia syndromes).
Fortunately, the pattern of nystagmus seen with PC-BPV is not a pattern at all typical of a central lesion. To our knowledge there has been no convincing report of a central lesion causing all the characteristic features of PC-BPV (i.e., a burst of upbeat torsional nystagmus in the head-hanging position with the duration of nystagmus being less than 30 seconds). Any reports that suggest this occurrence are much more likely to be an example of a common disorder (i.e., PC-BPV) co-occurring with a rare central lesion.
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