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The idea behind semicircular canal occlusion is based on the fact that the vertigo is caused by movement of particles within one of the semicircular canals.A A Crushing the canal would obviously immobilize these particles and thus stop the vertigo. Sometimes a course of vestibular rehabilitation is useful in compensating for the lack of the abolished semicircular canal.
If one looks at the number of patients that are seen in dizzy clinics, The peak age for BPPV is roughly 60 (see below). If you decide to wait it out, certain modifications in your daily activities may be necessary to cope with your dizziness. Both treatments are very effective, with roughly an 80% cure rate, ( Herdman et al, 1993; Helminski et al, 2010).
The office maneuvers for BPPV, perhaps provided on 2 or 3 occasions, are effective in 85-95% of patients with BPPV.
Occasional patients travel to a facility where a device is available to position the head and body to make the maneuvers more effective. We offer a home treatment DVD that illustrates the best maneuver - -the home Epley maneuver (also called the CRP or canalith repositioning procedure). The frequency of surgical treatment has been dropping rapidly in favor of other treatments (Leveque et al, 2007). Surgical treatment of BPPV is not easy -- your local ear doctor will probably have had no experience at all with this operation.
BPPV variant, accounting for about 3-12 percent of cases (Korres et al, 2002; Hornibrook 2004). We think it is best to select someone who treats BPPV at least on a weekly basis, or if this is not possible, someone who has attended a course on vestibular rehabilitation AND who has the equipment in their office to visualize BPPV (i.e. If a physical therapist gives you Brandt-Daroff maneuvers to do, or puts their main emphasis on treatment of neck mobility -- they are probably not very knowledgable about BPPV. We offer a home treatment DVD that illustrates the home CRP, Brandt-Daroff and Log-roll exercises.
Treatment of BPPV is based on identification of which side and which canal is involved and is achieved with the Epley Maneuver, also known as canal repositioning maneuver. Call us at 612-339-2836 or toll-free at 866-316-0769 to refer your patient for an appointment, or submit an online referral.
How to cite this article Bittar RSM, Mezzalira R, Furtado PL, Venosa AR, Sampaio ALL, Oliveira CACP. Benign Paroxysmal Positional Vertigo (BPPV) is one of the most prevalent clinical disorders in common Neurotology practice and accounts for approximately 17% of complaints of vertigo1. Given the noteworthy prevalence of BPPV, its health care and societal impacts are tremendous8. Positional vertigo is defined as a spinning sensation produced by changes in head position relative to gravity. Significant improvements in the diagnosis and treatment of patients with BPPV may lead to significant health care quality improvements as well as medical and societal cost savings. The purpose of this paper is to review the available methods for diagnosis and treatment of BPPV intended for clinicians who are likely to diagnose and manage patients with BPPV, and applies to any setting in which BPPV would be identified, monitored, or managed.
Of the two variants of BPPV, canalithiasis is the most common, and the posterior semicircular canal is the most affected because of its anatomical position (85-95% of cases of BPPV)8.
Recently, Gacek21 proposed a neural theory for BPPV, in which there was degeneration of the saccular ganglion secondary to a latent viral reactivation. Identifying the affected canal includes observation of the position that triggers the dizziness and the resulting type of nystagmus. When the patient gets in the position that triggers the dizziness, eye movement is observed resulting from the contraction of muscles related to the affected canal (slow component), followed by subsequent rapid correction in the opposite direction (fast component). In the vertical canals, there are excitatory connections to the ipsilateral superior oblique and contralateral inferior rectus to the posterior canal; ipsilateral superior rectus and contralateral inferior oblique to the superior canal, so that the arising movements are always rotational, but the nystagmus is vertical upward in the posterior canal and vertically downward in the superior canal23. The characterization of the nystagmus, allows the identification of the canal involved as well as the mechanism involved, and it is essential to choose the repositioning procedure. The Dix-Hallpike maneuver is considered the gold standard tool for the diagnosis of BPPV of posterior canal8. The Dix-Hallpike maneuver is performed by the clinician moving the patient through a set of specified head-positioning maneuvers to elicit the expected characteristic nystagmus of posterior canal BPPV (Figure 1). The maneuver begins with the patient in the upright seated position with the examiner standing at the patient's side.
After resolution of the subjective vertigo and the nystagmus, if present, the patient may be slowly returned to the upright position. The particles present inside the semicircular canal undergo the effects of gravity and are shifted downward, and after a short latency, the liberating force created on the ampullar crista triggers the vertigo and nystagmus (Figure 2). In the case of the superior semicircular canal, a torsional downbeating nystagmus is exhibited. If the patient has a history compatible with BPPV and the Dix-Hallpike test is negative, the clinician should perform a supine roll test to assess for lateral semicircular canal BPPV8.
Lateral canal BPPV (also called horizontal canal BPPV) is the second most common type of BPPV. In many instances, the presenting symptoms of lateral canal BPPV are indistinguishable from posterior canal BPPV.
Due to an adaptation of the central nervous system8,26 or to the reversion of the direction of movement of the debris by the gravitational action26, it is not unusual that nystagmus spontaneously changes the direction without the head turning to the opposite side8,26. Additional exams are essential to clarify the trigger and associated features of BPPV1,15, 23,35. Imaging is not useful in the routine diagnosis of BPPV because there are no radiological findings characteristic of or diagnostic for BPPV8.
Electronystmography has limited utility in the vertical canal BPPV diagnosis, since the torsional component of nystagmus cannot be registered by conventional techniques. Audiometry is not required for diagnosing BPPV, however it may offer additional information in cases where the clinical diagnosis of vertigo is unclear8. The treatment of BPPV is based on the performance of liberatory maneuvers or canalith repositioning procedures, with the aim of returning the displaced particles to their original location: utricular macula. A standard protocol, that is described in Table 3, is used in our service, considering the better results for each maneuver indicated for each BPPV variant. Some patients manifest severe symptoms with dizziness, nausea, sweating and vomiting while undergoing diagnostic or therapeutic maneuvers. The Epley maneuver39 is the most frequently performed repositioning maneuver of the vertical canal.
According to the clinical practice guideline8, based on the review of the literature, it was not possible to determine the optimal number of cycles for the repositioning maneuvers. The maneuver described by Semont41 is indicated for the treatment of posterior canal cupulolithiasis.
Lempert42 described a maneuver (Barbecue Maneuver or Roll Maneuver) which is the most commonly employed maneuver for the treatment of lateral canal BPPV. Forced prolonged position is another treatment maneuver, described by Vannuchi44, for the treatment of lateral canal BPPV.
The Brandt-Daroff exercises were developed for home self-administration, as an additional therapy for patients who have been symptomatic, even after Epley or Semont maneuver40.
Many patients complain of imbalance during and between vertigo attacks, as observed by Celebisoy45.
The otolithic dysfunction induced by unequal loads of the macular beds has been considered as the underlying mechanism46.
The repositioning maneuvers are associated to mild and self-limited adverse effects in about 12 percent of the treated patients8. During the course of repositioning maneuvers of vertical canals, the displaced particles could migrate into the lateral canal, in 6 to 7 % of the cases8. During the repositioning maneuvers, some patients develop severe, persistent vertigo, nausea, vomiting and nystagmus, which has the same features observed in the diagnostic maneuvers. The treatment consists of performance of the reverse maneuver, to aim to eliminate the blockade. By virtue of possible complications during the repositioning procedures, it is not a proper conduct to guide the patient self-treatment at home, without a physician. After repositioning procedures, it is important to keep the patient in sitting position, for 10 minutes, to avoid falls51. Epley39, in his original paper, described the application of a bone conduction vibrator associated to repositioning maneuver, in order to release some adhered particles in the ampullar crista. The effectiveness of repositioning and liberatory maneuvers varies from 70% to 100%14,15,23,48.
It is important to be careful when performing diagnostic, repositioning and liberatory maneuvers in obese patients, with limited cervical range of motion or with unstable heart failure or carotid stenois8,25,58. Some authors believe in natural course of BPPV toward spontaneous relief48,59,60,61,62, which is possible in up to 89% of the patients in the first month, with subsequent recurrence in up to 33%, in three years37,38.
Thirty to 50 % of the patients have vestibular system dysfunction associated with initially treated BPPV, which can be demonstrated by caloric testing abnormalities.
Benign Paroxysmal Positional Vertigo (BPPV) is a condition where vertigo (a sensation of spinning) is brought on by changing the position of the head (e.g. This illustration shows the location of the sediment in the semicircular canals after a repositioning maneuver has been performed. Treatment is canal specific and is determined by the results of the Dix-Hallpike and Roll Tests.
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This is due to a combination of the age-risk of BPPV combined with the larger number of persons in the population at certain ages. The head injury need not be that direct - -even whiplash injuries have a substantial incidence of BPPV (Dispenza et al, 2011). Patients with certain types of central vertigo caused by cerebellar injuries can have similar symptoms. This is a little used treatment maneuver, called the "Gans maneuver by it's inventor (R.
The median response in treated patients was 81%, compared to 37.% in placebo or untreated subjects. For this reason, in persons who have continued dizziness, a follow-up visit is scheduled and another nystagmus test with video-Frenzel goggles is done.
This is in spite of reports that it often takes a few visits to treat BPPV (Hughes et al, 2016). Just imagine -- what if insurance companies tried to save money by limiting the number of EKG's that can be done in a person with a heart attack ? While daily use of exercises would seem sensible, we did not find it to prevent recurrence (Helminski et al, 2005; Helminski and Hain, 2008). The risk of the surgery to hearing derives from inadvertent breaking into the endolymphatic compartment while attempting to open the bony labyrinth with a drill. It is especially common to have supine downbeating nystagmus after a successful Epley maneuver (Cambi et al, 2012). This is one way to a local treating health care provider interested in treating this condition. Benign paroxysmal positional vertigo associated with Meniere's disease: epidemiological, pathophysiologic, clinical, and therapeutic aspects. Combined horizontal and posterior canal benign paroxysmal positional vertigo in three patients with head trauma. Benign paroxysmal positional nystagmus in hospitalized subjects receiving ototoxic medications. Subjective visual vertical during eccentric rotation in patients with benign paroxysmal positional Vertigo.
Natural course of the remission of vertigo in patients with benign paroxysmal positional vertigo. Success of posterior semicircular canal occlusion and application of the dizziness handicap inventory. Management of 210 patients with benign paroxysmal positional vertigo: AMC protocol and outcomes.
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractBenign paroxysmal positional vertigo (BPPV), the most common cause of dizziness, occurs in all age groups.
This vestibular syndrome is characterized by transient attacks of vertigo, caused by change in head position, and associated with paroxysmal characteristic nystagmus. It represents the most important peripheral vestibular impairment along the lifespan1,2,3, although the age at onset is commonly between the fifth and seventh decades of life4. It is estimated that it costs approximately US$2000 to arrive at the diagnosis of BPPV, and that 86 percent of patients suffer some interrupted daily activities and lost days at work because of BPPV8.
Benign paroxysmal positional vertigo is defined as a disorder in the inner ear, characterized by repeated episodes of positional vertigo8, with typical paroxysmal nystagmus. Despite its significant prevalence, and quality of-life and economic impacts, considerable practice variations exist in the management of BPPV across disciplines8. Such improvements may be achievable with the reduction of the inappropriate use of vestibular suppressant medications, decreasing the inappropriate use of unnecessary tests such as radiographic imaging, and by increasing the use of appropriate cost effective therapeutic repositioning maneuvers. Displaced particles from utricule otoliths float around in the endolymph (canalithiasis)11 or adheren to the cupulae (cupulolithiasis)12 and may change the density relation of the cupulae-endolymph system.
The ampulla of the posterior semicircular canal is located in the lower region of the vestibule, both in the supine and standing position. Such reinfection could result in the loss of its antagonistic effect on the posterior semicircular canal.
The classic complaint is vertigo in episodes, triggered by changes in the body position or head movements, lasting seconds and ceasing spontaneously. Each of the semicircular canals is directly connected to a pair of extrinsic muscles in the eye, having an excitatory and inhibitory influence, which determines the movement of the eyeball in the same plane as the canal24 (Table 1). This biphasic movement, called nystagmus, is a standard direction that is known as being the same as the fast component.
In Table 2, we can observe the main features of involvement of different semicircular canals. Before beginning the maneuver, the clinician should counsel the patient regarding the upcoming movements and warn that they may provoke a sudden onset of intense subjective vertigo, possibly with nausea, which will subside within 60 seconds. During the return to the upright position, a reversal of the nystagmus may be observed and should be allowed to resolve8. Mechanism of displacement of the debris from the dome of the canal at rest and under the action of gravity (g), indicated by the arrow. The direction of the torsional component of the positioning nystagmus indicates which ear is the origin of nystagmus.
Because this type of BPPV has received considerably less attention in the literature, clinicians may be relatively unaware of its existence and the appropriate diagnostic maneuvers for lateral canal BPPV8.
The supine roll test is performed by initially positioning the patient supine with the head in neutral position, followed by quickly rotating the head 90 degrees to one side with the clinician observing the patient's eyes for nystagmus. In canalithiasis, the movement of the head toward the affected ear promotes the displacement of free particles in the direction of the ampulla, triggering a horizontal nystagmus whose fast component will be toward the tested ear, so geotropic (towards the ground). The mechanisms that initiate geotropic and apogeotropic eye movements can be seen in Figure 3. We can observe the mechanism of displacement of the ampullar crista that is responsible for the origin of geotropic nystagmus in canalithiasis(a), or for apogeotropic nystagmus in cupulolithiasis (b). De la Meilleure et al.26 reported the inversion of the horizontal nystagmus, in electronystagmography, in 75% of patients with BPPV of the lateral canal, always on the affected side.
Further radiographic imaging may play a role in diagnosis if the clinical presentation is felt to be atypical, if the diagnostic maneuvers are unusual, or if additional symptoms aside from those attributable to BPPV are present, suggesting an accompanying modifying central nervous system or otological disorders8. On the other hand in horizontal semicircular canal BPPV diagnosis, the nystagmus is present in the positional testing23. These are non-invasive procedures that have been found to be long term effective for BPPV2,14. In these cases, vestibular suppressant medications are recommended as adjuncts not only to relieve the vertigo after maneuver but also to control the clinical symptoms until the procedure can be repeated4.
The patient is placed in the upright position with the head turned 45 degrees to left when the left ear is affected.
If the posterior canal is affected, the patient is seated in the upright position; then the patient's head is turned 45 degrees toward the unaffected side, and then is rapidly moved to the side-lying position.
Demonstration of Lempert Maneuver sequence - treatment of lateral semicircular canal BPPV (right ear in black).
This maneuver involves rolling the patient 360 degrees in a series of steps to effect particle repositioning8. The strategy consists of maintaining the forced lateral decubitus, with affected ear in the undermost position for 12 hours23,25.
Some authors indicate them one week before the therapeutic maneuver, aiming to improve the patient's tolerability14. This observation lead to the investigation of postural balance in patients with lateral and posterior semicircular canal BPPV. Other possibilities are the persistency of small amounts of residual debris in the canal, paresis of the ampullar receptors or the vestibular re-adaptation after peripheral disorder45.
This phenomenon could result from a jamming of the otolithic debris (named jam) when migrating from a wider to narrower segment, such as from the ampulla to the canal or at the bifurcation of the commom crus50. The use of a cervical collar, positional avoidance, or other restrictions are not necessary52,53,54. However, studies found no benefit in the BPPV treatment, since it does not modify the results of repositioning or liberatory maneuvers2,55,56,57.
The successful treatment is based on the identification of the affected semicircular canal, the distinction between cupulolithiasis and canalithiasis, the right choice of the most indicated maneuver2. The spontaneous resolution is faster in the lateral semicircular canal BPPV than in posterior canal because the former spatial and anatomic orientation facilitates the return of the particles to their original place63,64. Therefore, even if symptoms are typical of BPPV, the diagnostic maneuver has been positive, the repositioning maneuver has been successful, it is important that complete neurotological evaluation is obtained to rule out other vestibular disorders.
For the therapeutic maneuvers, correct diagnosis of the BPPV variant and affected semicircular canal is necessary. Central etiologies must be investigated when atypical nystagmus is found and therapeutic maneuvers are unsucessfully. Bhattacharayya N, Baugh RF, Orvidas L, Barrs D, Bronston LJ, Cass S, Chalian AA, Desmond AL, Earll JM, Fife TD, Fuller DC, Judge JO, Mann NR, Rosenfeld RM, Schuring LT, Steiner RWP, Whitney SL, Haidari J. Sanjay Prasad MD FACS is a board certified physician and surgeon with over twenty years of sub-specialty experience in Otology, Neurotology, advanced head and neck oncologic surgery, and cranial base surgery. Above the age of 60, 3.4% of the population has BPPV every year (Neuhauser and Lempert, 2009).
Patients with migraine associated vertigo can also sometimes show eye movements resembling bilateral BPPV.
In our opinion, position 'C' has utility as it gives patients a chance to regroup between position 'B' and 'D'. A metanalysis published in 2010 indicated that there is very good evidence that the Epley maneuver (CRP) is effective (Helminski et al, 2010). Gacek is the only surgeon who has published any results with this procedure post 1993 (Leveque et al, 2007).
This should not be of any concern as long as it is unaccompanied by upbeating nystagmus on sitting. Because BPPV is so common, most major cities will have at least one person who fits these minimal criteria. It presents with vertigo on head movement, but in older patients presentation may be typical and thus accounting for a low recognition rate in the primary care setting. The symptoms result from movement of the free floating otoconia particles in the endolymph or their attachment to the cupulae of the semicircular canal.
These variations relate to both diagnostic strategies for BPPV and rates of utilization of various treatment options available for BPPV within and across the various medical specialties and disciplines involved in its management.
In this context, BPPV should be mentioned not only because of the high prevalence, but also because of the relative simplicity of the diagnosis and cost effectiveness of the treatment9. The semicircular canals change their gravitational orientation plane while the patients move their head.
The fragments in suspension inside the labirinth tend to be deposited in this region, by the action of gravity1,13,14,15. Typically, the vertigo arises in the lateral position of one or both sides, in hyperextension of the head, when standing up or lying down.
Because the patient is going to be placed in the supine position relatively quickly with the head position slightly below the body, the patient should be oriented so that, in the supine position, the head can "hang" with support off the posterior edge of the examination table by about 20 degrees.
The examiner rotates the patient's head 45 degrees to the left and, with manual support, maintains the 45-degree head turn to the left during the next part of the maneuver8. The Dix-Hallpike maneuver should then be repeated for the right side, with the right ear arriving at the dependent position.
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. Patients with a history compatible with BPPV (ie, repeated episodes of vertigo produced by changes in head position relative to gravity) who do not meet diagnostic criteria for posterior canal BPPV should be investigated for lateral canal BPPV. After the nystagmus subsides (or if no nystagmus is elicited), the head is then returned to the straight face-up supine position.
When the head is rotated to the healthy side, the particles displace and lead to a current moving in the opposite direction from the ampulla (also generating geotropic nystagmus), and the stimulation is less intense than that observed on the affected side. Lee and colleagues27 described the spontaneous reversal of nystagmus bilaterally, and the primary phase of nystagmus was shorter and with greater velocity of the slow-phase. Other possible causes are ovarian hormonal dysfunction, hyperlipidemia, hypoglycemia or hyperglycemia, hyperinsulinemia, migraine, cervical trauma, otological surgery, sedentary and prolonged bed rest2,15,32,33,34. Successful treatment depends mainly on the choice of the most appropriate maneuver for the case. The patient is rapidly laid back in a supine head-hanging position, which is maintained for a period of 1 to 2 minutes. The patient is in supine position; the patient's head is turned 90 degrees slowly toward the unaffected side.
The Brandt-Daroff exercises (Figure 8) are positioning exercises that, theoretically, promote habituation4.

The treatment of each affected semicircular canal will be performed, in protocols according to the observed ocular movements and the correct identification of each affected semicircular canal. Patients with posterior BPPV had impaired static balance ability when visual and proprioceptive inputs were inadequate as described by Celebisoy45, Di Girolamo46. The conversion to lateral canal BPPV (so called canal switch) and Canalith Jam are unusual conditions, however when present must be promptly diagnosed and treated47. In the Epley Maneuver, it happens when the head of the patient is turned to facedown position (Figure 5 - position c and d). If the patient develops important symptoms, vestibular suppressant medications may be considered to help in a later repositioning. Therefore, it is possible to propose to the patient to wait the spontaneous resolution, in cases where the maneuver can't be indicated. Benign paroxysmal positional vertigo: 10 year experience in treating 592 patients with canalith repositioning procedure.
Neuro-otological features of benign paroxysmal vertigo and benign paroxysmal positioning vertigo in children: a follow-up study.
Free-floating endolymph particles: a new operative finding during posterior semicircular canal occlusion.
Effectiveness of treatment techniques in 923 cases of benign paroxysmal positional vertigo. Benign paroxysmal positional vertigo due to a simultaneous involvement of both horizontal and posterior semicircular canals. Monitoring of caloric response and outcome in patients with benign paroxysmal positional vertigo. Diagnostic, pathophysiologic, and therapeutic aspects of benign paroxysmal positional vertigo. Reversal of initial positioning nystagmus in benign paroxysmal positional vertigo involving the horizontal canal. Eletronytagmographic (ENG) findings in paroxysmal positional vertigo (PPV) as a sign of vestibular dysfunction. Canalith repositioning for benign paroxysmal positional vertigo: a randomized controlled trial. The canalith repositioning procedure for treatment of benign paroxysmal positional vertigo. A positional maneuver for treatment of horizontal-canal benign paroxysmal positional vertigo. Balance in posterior and horizontal canal type benign paroxysmal positional vertigo before and after repositioning maneuvers.
Treatment efficacy of benign paroxysmal positional vertigo (BVVP) with canalith repositioning maneuver and Semont liberatory maneuver in 376 patients. Treatment of benign paroxysmal ositional vertigo: necessity of postmaneuver patient restrictions. Vibration with the canalith repositioning maneuver: a prospective randomized study to determine efficacy. The canalith repositioning procedure with and without mastoid oscillation for the treatment of benign paroxysmal positional vertigo.
Natural history of benign paroxysmal positional vertigo and efficacy of Epley and Lempert maneuvers. Treatment of anterior canal benign paroxysmal positional vertigo by a prolonged forced position procedure.
Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review. He is chief surgeon and founder of the private practice, Metropolitan NeuroEar Group, located in the metropolitan Washington D.C.
With BPPV, one needs to see the results of the last treatment, and be sure that things haven't changed. Of course, someone who treats BPPV and similar conditions as their main work activity is best. The diagnosis is essentially clinical and should be confirmed by performing diagnostic maneuvers. Delays in the diagnosis and treatment of BPPV have both cost and quality-of-life implications for both patients and their caregivers8. The debris dislocates and promotes anomalous activation of the ampullar crista and may interfere with the neuronal output index that normally would be expected for that head and canal position. The lateral semicircular canal may be involved in 5 to 15% of patients8 and the anterior canal is rarely involved8; but there is still the possibility of simultaneous involvement of two canals18,19,20. The examiner should ensure that he can support the patient's head and guide the patient through the maneuver safely and securely, without the examiner losing support or balance himself8.
Next, the examiner fairly quickly moves the patient (who is instructed to keep the eyes open) from the seated to the supine left-ear down position and then extends the patient's neck slightly (approximately 20 degrees below the horizontal plane) so that the patient's chin is pointed slightly upward, with the head hanging off the edge of the examining table and supported by the examiner. Again, the examiner should inquire about subjective vertigo and identify objective nystagmus, when present.
After any additional elicited nystagmus has subsided, the head is then quickly turned 90 degrees to the opposite side, and the eyes are once again observed for nystagmus. Thus, the resulting eye movement is always stronger when the affected ear is placed downward23. The arrows indicate the direction of displacement of the cupulae by gravity with the lateralization movement of the head. It has been proposed by Korres22 that the unilateral vestibular hypofunction is more common in cases secondary to head trauma or viral infection. Next, the head is turned 90 degrees, to the right (usually necessitating the patient's body to move from supine position to the lateral decubitus position). The jam generates a constant counter-attraction force in the cupulae, as result from negative pressure. Possible explanations include some comorbidities and patient limitations during the maneuvers (for example: limited cervical range of motion or vascular failure)14. Avoid bending down to pick up things, and extending the head, such as to get something out of a cabinet. Similarly, it would be ridiculous to prevent a cardiologist from checking an EKG on a patient who had sustained a heart attack, but was not in chest pain. BPPV is associated with displacement of fragments of utricular otoconia into the semicircular canals, most commonly the posterior semicircular canal.
Treatment is based on the identification of the affected semicircular canal and performance of liberatory maneuvers or repositioning of free floating particles of otoliths.
Some other symptoms could be associated and often persist after the interruption of the episode, such as nausea, imbalance, or postural instability1,15. The examiner observes the patient's eyes for the latency, duration, and direction of the nystagmus. Two potential nystagmus findings may occur with this maneuver, reflecting two types of lateral canal8. In cupulolithiasis, the fragments are adhered to the cupulae of the affected semicircular canal, which make them heavier than the endolymph. Some authors prefer to wait for the natural course towards a spontaneous relief, considering BPPV a self-limited condition. The patient is rapidly moved to the opposite side-lying position without pausing in the sitting position and without changing the head position relative to the shoulder. Then, the head is turned to the facedown position and the body is moved to the ventral decubitus.
The jam pressure induces cupulae displacement and consequent depolarization (vertical canals) or hyperpolarization (lateral canals).
Be careful when at the dentist's office, the beauty parlor when lying back having ones hair washed, when participating in sports activities and when you are lying flat on your back. Otoconia are composed of otoconin and otolin forming the organic matrix on which calcium carbonate mineralizes.
Besides the clinical history, the diagnosis of BPPV takes into account the type, direction and duration of nystagmus provoked by maneuvers that provide clues for identifying the affected canal and the pathophysiological mechanism involved (whether canalithiasis or cupulolithiasis). Again, the provoked nystagmus in posterior canal BPPV is classically described as a mixed torsional and vertical movement with the upper pole of the eye beating toward the dependent ear. When the head is rotated to one side, the action of gravity on the ampullar crista moves the debris into the opposite direction and it is possible to observe the nystagmus that is in the opposite direction from the tested ear (apogeotropic type)24,25. Gradually the patient resumes the upright sitting position8.If the superior semicircular canal is affected, the movement is performed in the direction opposite to the procedure for posterior semicircular canal4,15,23,40.
Later the patient's head is turned 90 degrees, and the body is placed on lateral decubitus.
Then the patient is asked to rest the chin on the shoulder and sit up slowly, completing the maneuver8 (Figure 4).
Figure 6 demonstrates the Semont Maneuver for treatment of right-sided posterior semicircular canal cupulolithiasis.
Presentation varied because otoconia fragments can be displaced into any of the semicircular canals on either (or both) side and may be free floating (canalolithiasis) or attached to the cupula (cupulolithiasis). The head must stay in that position for some moments, before it returns to the normal position1,4,23,40. Each step is maintained for 15 seconds - for slow migration of the particles, in response to gravity. Most cases of BPPV are idiopathic, but head trauma, otologic disorders, and systemic disease appear to be contributory in a subset. To complete the maneuver, the patient is brought into the upright sitting position with head bowed down at 30 degrees23,43,44.
A strong association with osteoporosis suggests that idiopathic BPPV may have diagnostic and management implications beyond that of a purely otologic condition.1.
Epidemiology and ImpactDizziness arising from vertigo is a common morbidity that adversely affects balance and quality of life. They also found that, compared to nonvestibular dizziness, vestibular vertigo was more frequently followed by medical consultation, sick leave, interruption of daily activities, and avoidance of leaving the house.Population studies such as the above consistently show that benign paroxysmal positional vertigo (BPPV) is the most common cause of dizziness [2]. While presentation with complaints consistent with BPPV is very common, the prevalence of undiagnosed BPPV is also high. In a prospective study in a community-based hospital located in a small Midwestern US city, 198 young adults (99 men and 99 women), aged 18–34 years, who were not being treated for dizziness or balance problems, were recruited [5]. Besides obtaining history and completing questionnaires, subjects underwent vestibular positional assessment for BPPV with infrared camera-equipped goggles recorded on digital media.
Similar to the rate observed in the young adults, consecutive examinations of 100 older patients in an urban geriatric clinic revealed a 9% rate of undiagnosed BPPV [6]. These statistics are very reproducible, for example, 11% of a large population of 75-year-olds manifested BPPV symptoms [7]. Patients with BPPV are 5 times more likely to have relatives with BPPV compared to other dizzy patients suggesting a familial tendency [8].Subjectively, the primary complaint at presentation is dizziness triggered by movement, such as looking up or on head turn. The intense sensation of vertigo triggered typically is short; however, patients feel off balance even when avoiding sudden head movements. As such, BPPV has adverse psychosocial consequences including reduced health-related quality of life [9], severe subjective impairment, and avoidance behavior in 70% of sufferers [10]. Patients with BPPV are more likely to have depression and reduced activities of daily living scores and sustained a fall in the previous 3 months [6].
Older patients (older than 70 years of age) with BPPV take longer to seek help and may present with complaints of unsteadiness or imbalance without vertigo sensation [12].
This was also found in a group of older patients referred to a Falls and Syncope Unit for evaluation who were eventually diagnosed with BPPV [13]. The reason for referral for evaluation of falls and syncope in this group of older, undiagnosed BPPV patients may be their less obvious and less characteristic presentation [13].The economic burden of vertigo was evaluated using, in the 4,294 patients, multinational REVERT database which includes data from 618 centers [14]. Therefore, in addition to the negative impact on the patient from a humanistic perspective, vertigo, including BPPV, has considerable impact on work productivity and healthcare resource use. Episodes of BPPV are mostly short with a median duration of 2 weeks, possibly accounting for why only 8% of all participants with BPPV received effective therapy [2]. In more than half of the patients, BPPV is a recurrent disease with a recurrence risk of approximately 15% per year [2].
The failure to correctly diagnose BPPV likely accounts for the poor referral patterns and low proportion of patients who receive appropriate symptom relief from the available treatments.2. The peripheral vestibular system consists of five distinct elements on each side: three semicircular canals and two otolithic organs, the saccule and the utricle (Figure 1). There are excellent reviews of peripheral vestibular anatomy and function available elsewhere [18, 19]. Structural relationship of the semicircular canals relative to one another and the utricle is demonstrated.The inner ear membranous structures and epithelium are encased in the otic capsule which is one of the densest bones in the body.
The otic capsule, located in the petrous portion of the temporal bone, unlike other bones in the body, has very little turnover, in part because of factors such as osteopontin in inner ear fluids that suppress bone remodeling [20]. The bony canal houses a membranous duct with the space in between being filled by perilymph.
Secretion of endolymph is localized to the stria vascularis in the cochlea and the dark cells in the vestibule. The ampulla of the semicircular canal secrete a potassium-rich, positively polarized fluid, the secretion of which is dependent on basolateral Na+, K(+)-ATPase, and Na-K-Cl cotransporter [21]. The crista ampullaris includes sensory transducers (the hair cells) and the supporting structures, as well as a gelatinous fibrillar matrix, referred to as the cupula, in which stereocilia of the hair cells are embedded. With rotation of the head, the endolymph filling the membranous ducts is displaced resulting in pushing or pulling of the cupula thus deflecting the stereocilia.
Depending on the direction of the deflection and the ear in question (toward or away from the kinocilium), the hair cells can be stimulated or suppressed.
The resulting signal is carried to the brain by the vestibular branch of the cranial nerve VIII which consists of bipolar afferents whose peripheral endings include large calyxes for faithful sensorineural synaptic transmission from the hair cells.The three canals lie nearly perpendicular to each other and can code three planes (roll, pitch, and yaw) along the -, -, and -axes [22]. Pitch plane corresponds to laying down, sitting up from supine position, or looking up- or downward, while movement along the roll plane corresponds to rotating the head toward the right or left in supine position [23]. Movement along the yaw plane is rotating head to the left or right in the sitting position. Therefore, the semicircular canals are best suited for detecting angular acceleration during rotational head movements. The kinocilium faces the utricle in the horizontal semicircular canal and faces away from the utricle for the posterior and superior semicircular canals. Deflection toward the kinocilium (utricopedal) results in excitation and away from the kinocilium (utricofugal) produces inhibition. The kinocilia of the crista ampullaris in the posterior and superior (anterior or vertical) semicircular ducts are oriented to depolarize the hair cells when endolymph moves in the utricofugal direction. Head turn to one direction in a given plane results in movement of the endolymph in the opposite direction. Each semicircular canal works in concert with the corresponding canal located on the other side of the head. Because of their orientation, which is orthogonal to one another, the utricle is more sensitive to linear acceleration and head movements in the horizontal plane, whereas the saccule is more sensitive to linear acceleration and head movements in the vertical plane. The saccule is in continuity with the cochlea through ductus reunions, thus has some low-frequency sound sensitivity.
The utricle is more proximate to the semicircular canals which are in continuity with the vestibule, but appears to have some sound sensitivity as well [24]. The sensory epithelium projects hair cells into an otoconial membrane (a viscous gel layer) on which the otoconia rest. The crystals get displaced during linear acceleration, which in turn deflects the ciliary bundles of the hair cells and thus alters the vestibular signal sent to the brain. Because of their mass, they permit sensitivity to gravitational forces.Saccular function can be measured using vestibular evoked myogenic potentials (VEMP) [26, 27]. VEMP can help identify lesions along the pathway that connects the saccule via the inferior vestibular nerve and the descending vestibulospinal pathways to primarily the ipsilateral sternocleidomastoid muscle. The stimulus is a series of tone bursts and the evoked potentials are averaged to generate a waveform. Subjectively, dizziness with sensation of falling is typically associated with saccular dysfunction and VEMP abnormalities [28]. A variant of the cervical VEMP is a myogenic response that has been evoked around the eye (ocular VEMP) [29, 30]. In ocular VEMP, tone bursts delivered to one ear evoke myogenic potentials in the contralateral inferior oblique muscles with information being conveyed through afferent fibers travelling in the superior vestibular nerve. However, in one study, abnormal function of the utricle was implied by abnormal ocular VEMPs recorded in BPPV patients [28].3. Formation and Structure of OtoconiaWang and colleagues were able to identify the principal organic component of the otoconia and partially sequenced and cloned the major protein component of murine otoconia, otoconin 90 [31].
Because of its similarity to secretory phospholipase A2 (sPLA2), this gene was referred to as PLA2-like (PLA2L) and enabled the identification of human otoconin 90. The rigid structure of sPLA2 is conveyed by six or seven disulfide bonds and is conserved in the otoconia and is essential for optimal interaction of the molecule with the mineral phase [32].
The molecular weight of otoconin 90 ranges between 90 and 100 kD, about half of which is accounted for by posttranslational modifications, consisting predominantly of sulfated glycosaminoglycans. Using a hyaluronidase-gold labeling technique, the localization of glucuronic acid-containing glycosaminoglycans in the gerbil utricle was examined by Tachibana and Morioka [33]. They observed that otoconia and the gelatinous layer of the otoconial membrane were strongly labeled by hyaluronidase-gold and secretory granules in supporting cells suggesting that the organic matrix of otoconia is secreted from these cells. The hyaluronidase labeling is lost as otoconia degenerate and are absorbed into dark cells.Another protein, otolin, was described as the principal scaffold protein which was initially characterized in the zebra fish [34, 35].
Zhao and colleagues used gene targeting and protein analysis techniques to demonstrate that otoconin 90 is essential for formation of the organic matrix of otoconia by specifically recruiting other matrix components, which include otolin [38]. They demonstrated that this matrix controlled otoconia growth and morphology by embedding the crystallites during seeding and growth. During otoconia development, the organic matrix forms prior to calcium carbonate (CaCO3) deposition and provides optimal calcification efficiency.
Yang and colleagues showed that matrix components are recruited to form the crystal matrix and sequester Ca(2+) for spatial specific formation of otoconia [36]. In wild type mice otoconin 90 leads to an enrichment of Ca(2+) in the luminal matrices of the utricle and saccule, whereas absence of otoconin 90 in the null mice leads to significantly reduced matrix-Ca(2+). Both otoconin 90 and otolin were noted to increase the propensity of extracellular matrix to calcify in cell culture, but together they had a synergistic effect on calcification.Andrade and colleagues used immunogold TEM to localize matrix proteins in mice [39]. First, they demonstrated a high density of otoconin 90 in the inner core of otoconia, where they are arranged in oval patterns implying that otoconin 90 is attached to a scaffold consisting of the hexagonal fibrillar meshwork, characteristic of otolin. Second, the level of mineralization was much higher in the outer cortex where mineralized fiber bundles are arranged parallel to the surface.
Based on this finding and observation from decalcification experiments, they concluded that otolin matrix fibrils serve as scaffold to guide mineralization mediated by otoconin 90. Third, they showed that individual crystallites assemble into iso-oriented columns and that the columns are arranged in parallel lamellae which convert into mineralized blocks for hierarchical assembly into the complex otoconial mosaic. Fourth, they demonstrated that in young mice the fibrils interconnecting otoconia consisted of the short chain collagen otolin. Fifth, they also observed that in old mice the superficial layer of mouse otoconia demineralized thus producing weakening or loss of anchoring of the organic fibrils interconnecting otoconia.Using energy dispersive X-ray microanalysis and powder X-ray diffraction, otoconia have been described as calcite-based nanocomposites consisting of a relatively uniform outer shape with a cylindrical bulbous body (belly) and three rhombohedral, terminal planes at both ends which are part of its branches [40]. Degenerative changes can range from mild structural alteration such as fissures and surface roughening of the less dense belly area to fractures and disintegration leading to loss of otoconia [40]. The final component of the disintegrating otoconia that leads to fragment formation occurs in the belly [40].
With age, the superficial layer of mouse otoconia becomes demineralized resulting in weakening or loss of anchoring of the fibrils interconnecting otoconia [39]. Consequently, otoconia can detach from each other and be released into the endolymphatic space by minor mechanical disturbances.
The mechanisms leading to degeneration and eventual fragmentation of otoconia remain unknown.Other mechanisms that could contribute to otoconia fragmentation include a change in endolymph such as change in pH, specifically acidic range, or calcium concentration. For example, EDTA exposure causes an anisotropic solubility of human otoconia, affecting the belly region [41]. Aminoglycosides such as gentamicin can also induce morphological changes in the structure of otoconia leading to eventual fragmentation and dissolution [41].In summary, these results demonstrate that otoconia are composed of organic and inorganic components. The combination of these two components attracts and facilitates mineralization of calcium carbonate around the inorganic matrix to form calcite crystals. The structure of otoconia and the fibrils that hold them together is affected by the aging process and other disease processes, thus creating conditions under which otoconia can fragment and separate from the otoconial membrane.4. Mechanisms of DiseaseBPPV is believed to arise from displacement of particulate matter, likely fragments of otoconia from the utricle, into the semicircular canals. This idea was initially put forth by Schuknecht [42, 43] based on intricate insight in vestibular structure and function and histopathologic observations of basophilic staining masses of granular or homogeneous material found attached to the cupula of the posterior semicircular canal on the affected side. Although the mechanisms leading to BPPV symptoms were a matter of long-standing debate [45], today, there is little doubt about the role of particulate matter. The involvement of particulate matter within the posterior semicircular canal has been established intraoperatively in patients with BPPV [46, 47].
Welling and colleagues prospectively examined the posterior semicircular canal of patients with and without a clinical history of BPPV for the presence of particulate matter.
No particles were observed intraoperatively in any of the 73 patients undergoing labyrinthine surgery (vestibular schwannoma excision or labyrinthectomy) without a history of BPPV [48]. Particulate matter was observed in only 8 of 26 patients with intractable BPPV at the time of the posterior semicircular canal occlusion procedure.
Similarly, Beyea and colleagues reported 20% incidence of free floating particles in the posterior semicircular canal of patients undergoing transmastoid posterior canal plugging for intractable BPPV [49].
However, particulate matter has also been reported in non-BPPV patients who underwent posterior canal fenestration carried out in patients undergoing acoustic tumor removal via a translabyrinthine approach [50].
Posterior semicircular canal ampullary nerve action potentials instantaneously changed according to the direction of the gravity produced by otoconia. When the otoconia were dropped into the canal to mimic the condition of moving otoconia in the canal, the action potentials changed together with the otoconial flow after a latent period.
Using a similar approach Otsuka and colleagues used a whole membranous labyrinth of bullfrogs to replicate the human vestibule [52].
They exposed the posterior semicircular canals but left the remaining membranous labyrinth encapsulated in the otic capsule.

They demonstrated that a vibratory stimulus (a surgical drill applied to the surface of the bony capsule) was able to detach the otoconia from the utricle, consistent with the view that mechanical insult could be a possible etiology of BPPV.
They adjusted the position of the preparation so that the dislodged otoconia were attached to the cupular surface to model cupulolithiasis.
Alternatively, when the otoconia were dislodged and held within the posterior semicircular canal lumen and the position of the whole preparation was changed so that the otoconia moved back and forth within the canal lumen, canalolithiasis was modeled.
In the cupulolithiasis model, the vestibular nerve action potentials changed instantaneously according to the gravitational force on the cupula.
In the canalolithiasis model, the action potentials changed in combination with the otoconial movement after a latent period. This experimental preparation has been used to model canalolithiasis and cupulolithiasis and recorded ampullary nerve discharges in the bullfrog [53]. In the canalolithiasis model, the acceleration of the otoconia was greater for the quick positional change. In the cupulolithiasis model, the discharges were sustained and their magnitude did not differ between the quick and slow positional changes. The canalolithiasis model influenced the magnitude of discharge of the posterior semicircular canal depending on the speed of the positional change.Rajguru and Rabbitt induced canalolithiasis in an animal model (oyster toadfish, Opsanus tau) by introducing heavy glass microbeads into the lumen of the lateral semicircular canal [54]. Bead movement under the action of gravity and canal afferent nerve discharge near the ampulla were recorded extracellularly in vivo. When the head was oriented nose-down, beads moved toward the nose and the lateral canal afferent discharge rate increased. Afferents that normally encoded angular velocity during oscillatory head rotations responded with tonic increases in the discharge rate during gravity-dependent bead movement.
Other afferents, such as the units that rapidly adapt to a step increase in angular head velocity, responded with an initial increase in discharge rate followed by a period of adaptation.
Afferent responses occurred in the complete absence of head movement and quantified the pathological inputs to the brain that arise from canalolithiasis.Others have adopted a mathematical modeling approach to BPPV. Squires and colleagues utilized known hydrodynamic calculations and make reasonable geometric and physical approximations to derive an expression for the transcupular pressure exerted by a settling solid particle in canalolithiasis [55]. This group also utilized their model to estimate dynamic cupular and endolymph displacements elicited during horizontal canal BPPV provocative diagnostic maneuvers and canalith repositioning procedures [56]. Results explained why the onset latency of ocular nystagmus evoked by the Dix-Hallpike provocative maneuver for posterior canal BPPV are typically longer than the latencies evoked by analogous tests for horizontal canal BPPV.Obrist and colleagues used an in vitro model to test the canalolithiasis hypothesis [57].
They carefully scaled the physical and geometrical parameters to study the mechanics of BPPV on an enlarged model of a single semicircular canal with laser vibrometry and video particle tracking. They demonstrated that normal endolymph can dissolve otoconia very rapidly (in about 20 hours).
However, a critical mass appears to be needed to evoke clinical symptoms, as mere presence of fragments within the semicircular canal is not always sufficient to induce a change in vestibular nerve activity.
Experimental models effectively simulate canalolithiasis and cupulolithiasis providing empirical evidence in support of prevalent hypothesis on pathophysiology of BPPV. Concentration of calcium in the endolymph plays an important role in the rate of resorption of otoconia and may influence the duration of a BPPV episode.5.
Diagnosis of Cupulolithiasis and Canalolithiasis and Identifying the Affected CanalHistorical recognition of BPPV and use of provocative positioning techniques in its diagnosis had been a point of discussion. They also credited Dix and Hallpike [59] as being the first to clearly describe both the currently used provocative positioning technique and the essential clinical manifestations of BPPV elicited by that technique. The Dix-Hallpike maneuver is now a standard component of the evaluation of the dizzy patient. When performing this procedure, the examiner stands to one side of the patient and rotates the patient’s head 45 degrees to that side to align the ipsilateral posterior semicircular canal with the sagittal plane of the body. Next, the examiner moves the patient, whose eyes are open, from the seated to the supine test-ear-down position and then extends the patient’s neck slightly so that the chin is pointed slightly upward. The latency, duration, and direction of nystagmus, if present, and the latency and duration of vertigo, if present, are noted. Each position should be maintained at least 30–45 seconds or until nystagmus resolves. If positive, rotary nystagmus toward the test ear is commonly observed, which is induced by the movement of free-floating debris within the affected canal (away from the cupula, inducing deflection of the cupula away from the vestibule). If no nystagmus is observed, or if observed once it resolves, the patient is seated upright and once again eyes are monitored for nystagmus which is once again documented as above. More recently, head shaking during the exam has been proposed to increase the diagnostic yield of the Dix-Hallpike exam [60].
Specifically, patients suspected of having posterior canal BPPV, but with negative Dix-Hallpike, are recommended to undergo head shaking Dix-Hallpike. The side-lying test which also stimulates the posterior semicircular canal may be more suitable for older patients because the head and neck are fully supported by the examination table [7]. Hall and colleagues brought clarity to understanding the mechanisms underlying posterior canal BPPV by emphasizing the importance of fatigability of symptoms [62]. Hall and colleagues noted that, under the influence of gravity, a density differential between the endolymph and the cupula will cause displacement of the cupula when changes in head position occur. They explained that BPPV can be divided into two types based on the presence or absence of fatigability. Specifically, nonfatigable nystagmus was the result of particles being fixed on the cupula (cupulolithiasis), whereas fatigable nystagmus was due to free floating particles within the body of posterior semicircular canal. This latter condition was subsequently referred to as canalolithiasis [63].Theoretically, if particulate matter can be located in the long arm of the semicircular canals or attached to the cupula, distally, it could also be present in the short arm or attached to the cupula, proximally. Indeed a histopathologic study reported that canaliths have been found to be located in the short arm of the semicircular canals (proximate to the utricle) [64].
Clinical correlate of this entity has yet to be defined.Posterior canal BPPV is the most common. In contrast, the superior semicircular canal is the highest point of the labyrinth, thus it is rarely involved in BPPV. To settle particles into the superior canal, very marked hyperextension of the head is required [65].Several authors have characterized horizontal BPPV [66, 67]. Horizontal BPPV is triggered when the head of the supine patient is turned from side to side and is characterized by a bidirectional horizontal nystagmus.
As with posterior BPPV there are also two subtypes of horizontal BPPV depending on the location of the otoconia fragments. In canalolithiasis, fragments of otoconia move freely in the horizontal semicircular canal inducing stimulatory utriculopetal endolymph flow, whereas in cupulolithiasisotoconia are attached to the cupula or are trapped in the proximal segment of the canal near to the cupula. In canalolithiasis, vertigo is triggered by circular acceleration in the plane of the horizontal semicircular canal while, in cupulolithiasis, vertigo is triggered when the head changes position, but not by circular acceleration.
In canalolithiasis, nystagmus is geotropic (toward the undermost ear) and more intense after rotation of the head toward the affected side.
In cupulolithiasis, the nystagmus during cupulolithiasis of the horizontal semicircular canal is apogeotropic (away from the undermost ear) and more intense after rotation of the head toward the unaffected ear. It is recommended that, for patients presenting with symptoms of BPPV, if the Dix-Hallpike test is negative, a supine roll test be performed to assess for lateral canal BPPV [68].Clinically identifying the affected side in horizontal canal BPPV can be challenging.
As noted above, horizontal BPPV-related nystagmus can be geotropic or apogeotropic, but the direction of the nystagmus relative to the ground is the same in both positions of the supine head roll test.
Ewald’s three laws were generated after experiments in pigeons whose semicircular canals were stimulated using pneumatic devices [69]. They state that a stimulation of the semicircular canal causes a movement of the eyes in the plane of the stimulated canal. In the horizontal semicircular canals, an ampullopetal endolymph movement causes a greater stimulation than an ampullofugal one. The directional asymmetry implies that, in persons who have lost inner ear function on one side, the remaining side should produce higher velocity nystagmus when the head is being rotated towards the remaining intact ear (ampullopetal), but less when the head is being rotated towards the side of vestibular loss. Aron and Bance provided validation of Ewald’s second law in a rare case combining horizontal canal BPPV with a dead ear on the contralateral side, therefore arising from a known side [70]. They presented the case of an 87-year-old male with history of invasive left ear cholesteatoma which had fistulized into the horizontal canal. Ten years later, the patient presented with chronic dysequilibrium aggravated by head movements. Dix-Hallpike test was negative, but a supine head roll test demonstrated bilateral apogeotropic, horizontal nystagmus, which was more pronounced with the head turned to the left.
It beats toward the healthy side when the lateral canal BPPV is geotropic and toward the affected side when it is apogeotropic and when absent [71, 72]; it is sometimes possible to evoke it with a mild shaking of the head [71]. In a prospective study, for diagnostic purposes, subjects were divided into two groups: standard head roll test versus the bow and lean test. The latter group had better remission rates for both canalolithiasis and cupulolithiasis of the lateral canal.Initial presenting history can be an important aid in identification of the involved canal.
There is a relationship between the position that initially provoked vertigo and the affected semicircular canal in patients with BPPV. History taking regarding the side of provoking position at the onset of vertigo helps predict the side affected by BPPV in both posterior canal BPPV and geotropic horizontal canal BPPV [23]. Although the type of BPPV cannot be predicted by the initial position provoking vertigo, the side of the BPPV is strongly correlated to the head-turning side in the supine position that initially provide vertigo in this group of patients.When apogeotropic horizontal canal BPPV is suspected, further detailed examinations using additional localization methods, including supine head roll test and pitch-plane test, are typically needed. The waking-up position was the most common situation that initially provoked vertigo in all subtypes of BPPV, including geotropic and apogeotropic horizontal canal BPPV [23].Until recently diagnosing of superior (anterior) semicircular canal BPPV was controversial. Because of its anatomical location, the superior semicircular canal is rarely affected in BPPV. In a retrospective study where over a 1-year period 4,320 patients consulting for otoneurological disease were investigated by otological, videonystagmography, and neurological examination, BPPV was diagnosed in 1,430 patients (33%) [65]. In the 20 patients with superior semicircular canal BPPV, the Dix-Hallpike test induced apogeotropic horizontal torsional nystagmus beating towards the uppermost ear in the lateral supine position with reversal on standing.
That is nystagmus beating towards the uppermost ear on the Dix-Hallpike test is consistent with BPPV involving the superior semicircular canal of the uppermost ear. The author suggests that the torsional component of nystagmus and not just the vertical component must be taken into account to facilitate the diagnosis.Multiple canals can be involved at presentation, not uncommonly after head trauma [74].
Involvement of multiple canals can give rise to atypical presentation and challenging management with repositioning maneuvers [74, 75]. It has been argued that the most significant factor in diagnosis of the type of BPPV is observation of the characteristics of the provoked nystagmus during the diagnostic positional maneuvers, although the combination of posterior-anterior canal involvement remains particularly challenging [76].Special considerations are warranted in the geriatric population, because geriatric patients with BPPV usually report dizziness or imbalance and do not always describe a rotatory crisis. Batuecas-Caletrio and colleagues have argued that the Dix-Hallpike and supine roll tests should be performed in older patients with dizziness, despite the fact that they do not complain of spinning sensation with positional changes [12].Finally, a number of studies have reported that the right ear is predominantly affected [10, 12, 16]. It has been suggested that prolonged lying may facilitate the deposition of otoconia on the cupula or contribute to their loosening from the utricle (see below) and that this mechanism might also explain why the laterality of BPPV often corresponds to the preferred side of lying during sleep [77].6. Brandt and Daroff used a physical therapy approach involving repeated maneuvers to loosen and disperse the degenerated otolithic material from the cupula [78]. These efforts were followed by liberatory maneuver of Semont [79] and subsequently canalith repositioning procedure of Eply (Figure 2) [80, 81].
Given that the dominant view at that time was that BPPV arose from the involvement of the posterior semicircular canal, these repositioning procedures were mainly directed at providing relief of posterior canal BPPV. However, several varieties of BPPV can be experienced depending on the semicircular canal involved, whether or not cupula is involved, single or multiple canal involvement, and sidedness of the affected structures.
The patient is laid down with the head rotated to the left and neck is extended (3rd from top). Next, the head is turned 90° to the right (4th from top) followed by rolling the body to the right such that patient is lying on the right shoulder looking toward the floor (2nd from bottom). Finally, the patient is returned to the seated position with head remaining rotated to the right (bottom). Each position is held for at least 30–60 seconds or until nystagmus or vertigo has resolved. Adapted from Mitka [151].To assess the effectiveness of the Epley maneuver in treatment of posterior semicircular canal BPPV, Hilton and Pinder, in a Cochrane review, compared Epley maneuver versus placebo Epley maneuver versus untreated controls [82].
Fifteen randomized trials were identified but twelve studies were excluded because of a high risk of bias, leaving three trials in the review.
Trials were mainly excluded because of inadequate concealment during randomization, or failure to blind outcome assessors. The studies included in the review addressed the efficacy of the Epley maneuver against a sham maneuver or control group. They concluded that the Epley maneuver is a safe effective treatment for posterior canal BPPV. They both offer thorough reviews of the available evidence and validate the effectiveness of the Epley maneuver in management of posterior semicircular canal BPPV.A more recent Cochrane review compared a modification of Epley maneuver to the standard Epley maneuver [84]. Such restrictions could include using a neck brace, head movement restrictions (avoiding bending the head up and down or bending over), and instructions to sleeping upright. The review concluded that there was a statistically significant advantage of post-Epley postural restrictions. The Gufoni maneuver is another technique that has been reported as effective in treating horizontal canal BPPV.
In somersaults, acceleration in the forward-facing direction may induce an intracanalicular force strong enough to detach otoconia debris from the cupula and the ongoing rolling may move loose otoconia debris back into the utricle [91].
Yamanaka and colleagues described the head-tilt hopping exercise in treatment of cupulolithiasis associated with BPPV of the horizontal semicircular canal, which is characterized by apogeotropic direction-changing nystagmus [92]. This treatment is designed to release otoconial debris adherent to the cupula as the patients hopped while tilting their heads laterally.
Fourteen percent of patients had recurrences, with this group of patients having characteristics of being older or having history of head trauma or vestibular neuropathy. However, in another report, therapeutic maneuvers were found to be more effective in resolving posterior canal or horizontal canal BPPV than superior canal BPPV [16]. Minor adverse events of canalith repositioning include severe nausea and vertigo during the procedure and instability or light-headedness for approximately 48 hours after the procedure [89]. The most common complication is canal switching, where otoliths from one semicircular canal are unintentionally displaced into another.
Canal switching has been reported in 6% of the patients with posterior canal BPPV [95]. Canal switching appears to more likely during Epley than Semont maneuver because of the higher number of maneuver steps during which the head is in the dependent position [96].
Posterior ampullary (singular) nerve transaction was the first proposed surgical treatment for intractable posterior canal BPPV [99]. Gacek was motivated by Schuknecht’s observations of otoconial mass embedded in the cupula of the posterior canal crista (see above) which is innervated by the posterior ampullary branch of the inferior vestibular nerve (Figure 3).
Singular nerve innervates the ampulla of the posterior semicircular canal.Posterior semicircular canal occlusion (canal plugging) was first described by Parnes and McClure [47]. Plugging is performed with bone dust mixed with fibrinogen sealant (bone pate) which is gently packed into a fenestration drilled into the posterior semicircular canal. In one series, all but one of 44 patients who underwent this procedure were relieved of BPPV on follow-up between 6 months and 12 years [101]. This treatment produces temporary postoperative imbalance and motion sensitivity for several weeks, but spares hearing.7.
Severe systemic disease included patients with carcinoma who were receiving treatment with radiotherapy or chemotherapy, recent myocardial infarction, leukemias treated with chemotherapy, sarcoidosis, and active ulcerative colitis.Head trauma is a long recognized cause of BPPV [102]. Maxillofacial (orthognathic) surgery has been reported to result in BPPV which can be bilateral and incapacitating occurrence which resolves slowly [105, 106].
In comparing management of posttraumatic BPPV with idiopathic vertigo, it appears that typically more positioning maneuvers are needed to achieve relief in the former [108, 109].Physical activity can also influence occurrence of BPPV independent of any specific trauma.
Physical activity such as swimming [110] and mountain biking [111] have also been reported to trigger BPPV.
On the other hand, prolonged bed rest has been recognized for a long time as a provoking factor for BPPV. It was suggested that prolonged lying may facilitate the deposition of otoconia on the cupula or contribute to their loosening from the utricle [112]. The above mechanism might also explain why the laterality of BPPV often corresponds to the preferred side of lying during sleep [77].
Consequently, it has been hypothesized that mild to moderate physical activity might relocate the particles from the canal, thus preventing the accumulation of an adequate number of otoconia necessary for forming an agglomerate [113]. Authors quantified physical activity during leisure, household, and occupational activities over a 7-day period in a group of 63 BPPV and 63 age- and gender-matched subjects.
Physical activity was significantly lower in patients with idiopathic BPPV than in controls regardless of gender and occupational activity. Most of the individuals at this age are retired, which explains why leisure and household activities may become more important. While geriatric patients did not differ from controls in occupational activity, they demonstrated less daily leisure and household activity than controls. For example, radiation therapy for treatment of nasopharyngeal carcinoma has been reported to induce BPPV [114].
Other unusual causes include occlusion of the anterior vestibular artery causing a sudden vertigo crisis (Lindsay-Hemenway syndrome) that includes otolith disease [115].Given that BPPV affects a substantial proportion of the population and that there remain significant limitations in our ability to fully control its symptoms and recurrences, over the past decade effort has been directed at identification of medical factors that may predispose a patient to development of idiopathic BPPV.
In a case-control histopathologic human temporal bone study, temporal bones from patients with type 1 diabetes mellitus and normal temporal bones from age-matched individuals were histopathologically examined [117].
It was found that the prevalence of cupular and free-floating deposits in the lateral and posterior semicircular canals was significantly higher in type 1 diabetes mellitus patients compared with normal temporal bones. Another systemic link was described recently where the lipid profiles and serum uric acid levels were found to be higher in patients with BPPV than in controls [118]. Curiously, serum uric acid levels decreased one month after the BPPV attack; however, the mechanisms behind these observations have not yet been elucidated.
Other conditions that have been associated with BPPV include chronic thyroiditis [119], hypertension, hyperlipidemia, and stroke [2].To find a statistical link between common comorbidities affecting the elderly population (hypertension, diabetes, osteoarthrosis, osteoporosis, and depression) and recurrent episodes of BPPV data from over 1,000 BPPV patients in 11 centers across 7 countries were examined [120]. They also reported that patients with low BMD measured by DEXA had increased recurrence rate and required an increased number of canalith repositioning maneuvers. Jeong and colleagues evaluated BMD of 209 Korean men and women with idiopathic BPPV and compared them to control subjects without history of vertigo. The prevalence of osteopenia and osteoporosis was higher in both women and men with BPPV than in controls [123].
Finally, Korean patients with BPPV show a higher prevalence of vitamin D deficiency [126] and a recent pilot study showed that in 4 Austrian patients with BPPV recurrence, vitamin D levels were lower than those without recurrence and recurrences were relieved with vitamin D supplementation [127].Although these studies have investigated the association between BPPV and low bone mineral density, the cooccurrence of two morbidities is not by itself supportive of causation.
Furthermore, a limitation of asserting an association based on DEXA scan findings is that any physiological alterations in bone turnover take about one year to be detectable by DEXA scan [129]. Since osteoporosis is a slowly changing disease process there is an obvious incongruence between DEXA scan findings and BPPV episodes, which tend to present abruptly and typically are self-limited (days to weeks in duration). An alternative approach is to examine biochemical markers of bone turnover, whose levels change rapidly (within 1–3 months) and are more temporally relevant to the natural history of BPPV.
Parham and colleagues used these markers to demonstrate that idiopathic BPPV patients tend to have higher levels of biochemical markers of bone turnover and that these levels are influenced by vitamin D level [130].8. Differential DiagnosisAlthough BPPV is one of the most common causes of vertigo, it is not the only disorder associated with recurrent vertigo. Meniere’s disease, migraines, vertebrobasilar insufficiency, and panic disorder are also characterized by recurrent episodes. Caution in diagnosis BPPV is warranted as other conditions can present with BPPV-like symptoms. For example, central vestibular disorders can give rise to positional nystagmus, which can be mistaken for BPPV.
In inner ear pathologies which may cause vestibulopathies, such as perilymph fistulas, nystagmus may be enhanced by Dix-Hallpike testing.
Furthermore, as spontaneous nystagmus associated with a perilymph fistula improves, nystagmus toward the affected ear in the downward position may misdirect the examiner from the initial pathological trigger of the symptoms. Other vestibulopathies that cause horizontal nystagmus may also be enhanced by Dix-Hallpike testing. Welgampola and colleagues cite another example where spontaneous horizontal nystagmus from acute peripheral vestibulopathies may be enhanced by Dix-Hallpike testing [132]. Specifically, spontaneous nystagmus from a right-sided vestibular neuritis will be left beating in the left lateral and right lateral positions. In contrast, nystagmus from left horizontal canal BPPV will be vigorously left beating in the left lateral position and will beat less vigorously to the right in the right lateral position. Low-velocity sustained horizontal, vertical, or torsional nystagmus can be found in patients with clinically definite vestibular migraine [133]. One study reported that migraines were 3 times more likely in BPPV patients than in general population and a family history of migraine is present in nearly 60% of BPPV patients [135]. In Meniere’s disease, it has been suggested that hydropic distension or rupture damages the otolithic apparatus, leading to the release of otoconia debris which migrate to the semicircular canals where they may result in BPPV [138]. Balatsouras and colleagues reported that the BPPV associated with Meniere’s disease differs from idiopathic BPPV in regard to several epidemiological and clinical features, may follow a different course, and responds less effectively to treatment [139]. They further noted that Meniere’s associated BPPV most commonly involved the lateral canal.
Others suggest that this condition may be related to chronic canalolithiasis within the short arm of a posterior canal [145]. An alternate explanation was put forward when Johkura and colleagues noted that nystagmus may be present but may be too subtle to detect without additional instrumentation [146]. They investigated 200 geriatric patients with dizziness with an infrared camera and video-oculography and found a faint positional apogeotropic horizontal nystagmus, compatible with horizontal semicircular canal BPPV in nearly 50% of the patients. Gans has offered a fourth explanation based on a change in the calcium metabolism and the consequent nonabsorption of free otoliths [147], which would increase their quantity in the semicircular canals and enable the triggering of vertigo upon head movement. Alvarenga and colleagues suggest that the affected labyrinth can be identified based on which side induced nausea or vertigo on positioning testing [144].Regardless of etiology, BPPV arising from other inner ear diseases [140, 148] and subjective BPPV [149] can be treated using the same approach as to typical BPPV, although success rate may be slightly lower.
Finally, intracranial tumors can cause positional vertigo which should be differentiated from BPPV based on history and neurotological examination findings [150]. The differentiating features include symptoms duration >35 days, sensorineural hearing loss, nonfatiguability positional nystagmus, variable duration and latency of nystagmus on positional changes, nonresponsiveness to canalith repositioning, and possible rollover phenomenon.

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20.02.2015, author: admin
Category: Bv Remedies 2016

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