Treatment chronic bppv youtube,home remedies for chronic sore throat medicine,how to relieve ear pain from a sore throat treatment - 2016 Feature

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Finding An Effective TreatmentFive Years Post StrokeA 70 year-old male with a five-year history of left medullary stroke was referred to the balance center by his family practitioner because of increased complaints of difficulty walking and further restriction of his daily life activities.
Wearing hearing aids has been such a positive experience for Marie Redfern, she wants to encourage others with hearing loss to try them, too.
Your experience can provide helpful information to someone looking for a great hearing care provider, reward a clinic for taking good care of their patients and create a sense of community where you live. It’s the beginning of another year and, hopefully, hearing health is one of your priorities. Your auditory system is complex and should be trusted to someone who has education in and experience with hearing health. Once you have a list of three to five potential hearing healthcare professionals, spend a few minutes researching their qualifications.
Will I see the hearing healthcare professional or an assistant during my hearing evaluation? If your medical insurance does not cover testing and treatment, ask what types of payment plans are available. Good qualifications and experience are important, but so is working with someone who genuinely likes what they do and takes a personal interest in your care. Now that you’ve done the research, make a decision and schedule an appointment for a hearing evaluation with the professional or hearing clinic that seems to meet your needs. Allow for enough time to find the office and arrive 15-30 minutes before your appointment so you can fill out any paperwork that’s required.
Make a list of any concerns you’ve been having with your hearing, such as ringing in the ears or problems hearing normal conversation. If you live long enough, the odds for developing some degree of hearing loss are definitely in your favor.
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The prevalence of vertigo and dizziness in people aged more than 60 years reaches 30%, and due to aging of world population, the number of patients is rapidly increasing. The terms dizziness and vertigo cover a variety of symptoms regarding disorders of spatial orientation and motion perception, such as the illusion of rotatory motion (classical rotatory vertigo) or the feeling of unsteadiness, which can affect objectively the ability to achieve a stable gaze, posture, and gait (1).
Although the majority of these patients present benign balance disorders, (7–9), in the elderly, common causes of vertigo may manifest differently, with a more confusing constellation of symptoms, as patients tend to report less rotatory vertigo and more non-specific dizziness and instability than younger patients presenting with the same condition (9).
On the other hand, a small number of patients harbor a serious and potentially life-threatening cause, mainly associated with stroke, and this risk of more serious diagnoses increases with age (12, 13). Age-related degeneration of different neural structures affects balance, including the vestibular receptors, central vestibular neurons, cerebellum, and visual and proprioceptive pathways. Similarly, elderly patients with chronic pathological asymmetric vestibular evoked myogenic potentials (VEMPs) or deviated subjective visual vertical (SVV) tests, do not report dizziness or vertigo as significant symptoms, which may relate to central compensation occurring from the beginning of this slow onset of vestibular function (18, 19, 26, 27). In summary, in order to maintain balance, the brain uses all available sensorial cues from vestibular, visual, and proprioceptive inputs, which in turn are integrated by the central nervous system to execute adequate motor responses. Reaching a complete, meaningful, and treatment-oriented diagnosis in elderly dizzy patients remains an important challenge for even the most experienced clinician.
A systematic assessment of balance should be achieved in this type of patient, for which recent technological developments are of great assistance.
Besides HIT, the SVV bucket test and modified Romberg and Fukuda tests represent low complexity alternatives for the same assessment, and may be used to develop simple, low cost, and quick screening procedures (20, 42). A particular scenario exists in acute onset of severe dizziness or vertigo; an acute vestibular syndrome, where ruling out stroke is critical, particularly in the elderly. The majority of diseases that cause dizziness in any age group become more prevalent in older individuals. As with younger patients, disease-specific therapies should be provided, such as repositioning maneuvers for BPPV and rehabilitation exercises for vestibular hypofunction.
Current knowledge advises the initiation of vestibular rehabilitation (VR) as soon as possible after an acute vestibular syndrome (29, 30). Chronic dizziness derived from previously acquired vestibular loss (vestibular neuritis, bilateral vestibulopathy among others) has good results with VR, particularly in terms of independence and quality of life, although it may need longer and more intensive therapy (28, 59). Importantly, spontaneous compensation strategies differ among patients (half of the population tend to rely on visual cues, while the other half rely on postural information), supporting the need for customized rehabilitation programs (30). Initiatives using Internet resources and mobile devices to support adherence and the realization of rehabilitation exercises at home have been developed (60, 62).
Dizziness in the elderly remains a difficult subject, given the underlying factor of vestibular impairment due to aging in the form of presbystasis.
Current vestibular testing allows a complete characterization of balance function and its deficits, and is becoming useful as a guide to planning treatment, where a cause-specific pathology is present, or presbystasis is the sole issue. Future challenges on the subject include the further determination of vestibular impairment profiles and their specific VR alternatives, in order to achieve the shortest and most efficient therapy possible. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
This blog discusses Ear, nose and throat problems in simple language for common person to understand. Bilateral Sloughed vocal cords in a case of non hodgekin lymphoma patient on chemotherapy and diabetic. These are the two pictures of before and after giving steroids in a case of Contact granuloma of the vocal cord. Whitish spicules due to hyperkeratinized areas of epithelium are sometimes extensive over tonsils and lingual tonsils. 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. If you already have a hearing healthcare professional and are happy with the service they provide, you’re well on your way to better hearing.
Although there are several different types of hearing healthcare professionals, each with their own educational requirements, all are required to be licensed by the state in which they practice.
If you know someone who is personally satisfied with the care they are receiving from a hearing healthcare professional, you might like them, too. Do a quick Internet search to find their website, where clinics typically list biographies and credentials of their professionals as well as their philosophy on hearing health. Some medications are ototoxic and, if you are having difficulty with your hearing, may be contributing to the problem. The practitioner will most likely ask you if you have any concerns, so it’s best to write them down ahead of time. Fortunately, research by the National Council on Aging on those with hearing loss and their significant others revealed that hearing loss treatment (such as hearing aids) significantly improved quality of life, including communication with friends and family, family relationships, physical health, social participation and even earning power. Back in Business Physiotherapy pays for all aspects of this website and does not endorse any paid advertising on this site. Because of rapid advances in the medical sciences, the author recommends that there should be independent verification of diagnoses and exercise prescription. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button.
This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. The presence of dizziness in the elderly is a strong predictor of falls, which is the leading cause of accidental death in people older than 65 years. Altogether they represent a common and serious issue in the elderly, where its prevalence reaches 30% beyond 60 years of age (1, 2), while rising to 50% beyond 85 years (1). Moreover, the presence of abnormal balance tests increases the risk of hip and wrist fractures (4).
Underlying this phenomenon is the progressive multimodal impairment of balance, including the loss of vestibular and proprioceptive functions, and the impairment of central integration of these and other sensory inputs associated with aging, which may also be called as presbystasis, presbyequilibrium, or multisensory dizziness (4, 7, 10).
Altogether, vertigo, dizziness, and balance disorders in the elderly constitute a major public health issue, which needs adequate management by trained physicians.
The number of hair cells in the vestibular organs and the number of fibers in the superior and inferior vestibular nerves decrease with age (14–16). The sole presence of VOR asymmetry (which may present in elderly patients without history of an acute vestibular syndrome, and rarely in the form of bilateral vestibulopathy) is a significant predictor of falling (4, 22). In this manner, age-related balance deterioration does not appear to behave as a unique standardized phenomenon, but the opposite, it seems to be extremely variable from patient to patient (17, 18, 20, 27).
The impairment of each of the three semicircular canals can be examined by means of vHIT (37) procuring a reliable, objective, and quantitative value for VOR. SVV by means of bucket test may even provide sensible assessment of utricular components beyond VEMP contributions (27).
The HINTS assessment protocol (head impulse test, nystagmus directionality, and test of skew) can be performed at the bedside, with high sensitivity and specificity to diagnose stroke in an acute vestibular syndrome (43).
This can be explained by the cumulative probability of exposure or by age-related changes that make the elderly more susceptible to these pathologies (47). Vestibular suppressants should be tapered quickly due to their inhibitory effect on central compensation (57). VR works as a catalyzer and enhancer of central compensation on the basis of three principles: adaptation (rearrangement of VOR networking), substitution (strengthening of non-vestibular components of balance), and habituation (increase of sensory thresholds). Moreover, VR is indicated in presbystasis, whereas the objective is to reduce symptoms or decrease the risk of falling (29, 30, 60).
Other balance-improving treatments being currently explored include biofeedback devices worn all day, which give tactile or acoustic cues when the center of gravity is being lost, allowing the patient to react accordingly (63). The diagnostic and therapeutic approach must be multi-systemic and oriented to the visual, proprioceptive, and vestibular systems.
Under this last condition, VR should be considered in the elderly where no other plausible balance disorder is suspected, in order to treat a probably symptomatic presbystasis. Batuecas-Caletrio A, Trinidad-Ruiz G, Zschaeck C, Del Pozo De Dios JC, De Toro Gil L, Martin-Sanchez V, et al. Most of the time they are asymptomatic but with their mass effect they can cause stuffy nose.
Download Case StudyReturn to Work DeterminationAcuity & Steadiness During Active Movement A 47 year-old construction worker complains of a six month history of intermittent dizziness and mild unsteadiness accompanied by visual blurring. 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.
Ask specific questions about their office staff (are they friendly, efficient?) and the professional’s quality of care (do they explain things well? She may know someone in the community who has a good reputation or to whom she has successfully referred patients in the past. Is the staff courteous or do they seem to be in a hurry? How long did you have to wait on hold? Finding the right hearing healthcare professional to take care of your hearing health is the first step in ensuring you’ll be hearing your best for as long as possible. David also has good insight into sports injuries having played Rugby Union for 30 years, competed in Athletics for 14 years, and has provided Physiotherapy coverage to teams and events. Back in Business Physiotherapy does have an affiliate program with Lunar pages who host this website. Balance disorders in the elderly constitute a major public health problem, and require an adequate diagnosis and management by trained physicians. Injuries related to falls lead to mobility restriction and loss of independence, and increase the fear of falling, which also predicts subsequent falls (2). In addition, the skeletal muscle strength and mass are reduced with aging, increasing the risk of fall-related injuries in elderly patients (11).
This mini review presents recent advances in the diagnosis and management of dizziness in elderly patients.
From a functional perspective, age-related deficits appear to be larger on semicircular canals, followed by saccular function, while the utriculus remains less affected (17–19). In addition, compensation phenomena after vestibular loss are weakened in elderly patients, for example, impairment after vestibular neuritis is harsher on the elderly (23). Therefore, it is still controversial whether presbystasis by itself should be always considered pathological or not.
Moreover, minor new or acute impairments can affect disproportionately their capacity to cope difficult equilibrium scenarios, as every sensory modality may already be partially deteriorated. It has been reported that more than half of elderly patients with balance disorders are vague, inconsistent, or contradictory in describing their symptoms (31). Ocular and cervical VEMPs give equally reliable information over utricular and saccular function independently (38). Head-shaking nystagmus and dynamic visual acuity testing among others constitute bedside, fast, inexpensive, and easy to interpret vestibular tests for VOR (4, 7, 18).
This three-step bedside oculomotor examination has shown better sensitivity than early magnetic resonance imaging (MRI). With a simple diagnosis–treatment scheme (even in the absence of rotatory symptoms), testing should be performed routinely (8). An accurate anamnesis and physical examination will determine further vestibular, neurological, or cardiovascular tests. Although steroids have been proven to diminish functional loss over time, they may not contribute to acute symptomatic relief (58). In addition, if there are deficits in lower extremity muscle strength, specific therapies directed to locomotor dysfunctions should be indicated (61). In severe cases of bilateral VOR loss and inadequate compensation strategies, the role of vestibular implants (devices similar in their concept to cochlear implants) is beginning to be explored, and interventions have already been made in the first patients with satisfying functional outcomes (64). BPPV and stroke (particularly in acute syndromes) should always be considered, given the frequency of the first and the severity of the latter. Here, resolution of symptomatology would confirm the assumed working hypothesis of presbystasis, while lack of progress would lead to further exploration of less common causes. The threshold between what may be considered non-significant vestibular abnormalities and those correlating with a higher risk of falling should be better explored.
Disorders of balance and vestibular function in US adults: data from the national health and nutrition examination survey, 2001-2004. Burden of disability attributable to vertigo and dizziness in the aged: results from the KORA-Age study. Deviated nasal septum can be associated with this compromising other side of the nose as well.
He is a self-referral, concerned about his ability to perform his job safely, particularly in elevated locations.
Depending upon your particular health circumstances, your physician may have specific reasons for referring you to a specific hearing health professional over another.
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In the elderly, common causes of vertigo may manifest differently, as patients tend to report less rotatory vertigo and more non-specific dizziness and instability than younger patients, making diagnosis more complex. In addition, falls are the leading cause of accidental death in persons older than 65 years (5), while dizziness is one of the strongest contributors to the disability burden after age 65 (6). A steady asymmetrical decrease in the ability of sensing angular rotation with age has been reported, as assessed by video head impulse testing (vHIT) of the vestibulo-ocular reflex (VOR) (4, 19, 20). Besides, there is not a single symptom that can predict with specificity the underlying causes of dizziness, and most of the times, elderly patients have more than one cause of dizziness (32, 33). The non-vestibular proprioceptive and visual sensory components of balance and their central integration in overall equilibrium performance can be thoroughly assessed by dynamic computed posturography (39). Testing for postural hypotension, joint position sense, and gait disorders can also contribute to assess non-vestibular components in a bedside low-cost manner, contributing to designing an integral but component-specific treatment. MRI can give a false negative result in vertebrobasilar stroke (44), and is not always readily available (45). Consequently, to seek a precise diagnosis, it seems to be mandatory to obtain a good clinical history and perform thorough neuro-otologic bedside examination, including postural testing, while the majority of patients may benefit from vestibular tests, and stroke assessment protocols for an acute balance disorder. Steroids side effects should be carefully considered before administration, particularly on this age group. Proper balance characterizations may help in designing more specific and efficient interventions. This will inevitably lead to the establishment of a reasonable battery of (hopefully, bedside, low-cost, easy to interpret) examinations designed to rule out unacceptable risk for falling, in the fashion of the HINTS protocol for stroke. BPPV is associated with displacement of fragments of utricular otoconia into the semicircular canals, most commonly the posterior semicircular canal. David can also assist those people requiring casts or post-op rehabilitation due to his past experience in Fracture Clinics and Orthopaedic departments. Links to other sites are based on the relevance of that sites information to the principles of this websites desire to enhance the standards of Physiotherapy.
This fact is associated with a loss of dynamic visual acuity due to the inability to compensate fast head rotations with corrective eye movements, thus assuring a steady image over the retina (21). For instance, the medial vestibular nucleus, important in vestibular compensation due to its commissural fibers, shows lower neuron density in healthy older adults (24). While asymmetric, severe, and multimodal balance impairments due to aging are likely to cause symptomatology per se, the magnification and distortion of the symptom spectrum of specific pathologies by presbystasis is perhaps more common. Moreover, caloric test responses depend on several factors that could be affected by age, such as ear canal volume, temporal bone thickness, and blood supply to the temporal bone (34).
Altogether these tests provide an objective assessment of every component and subsystem of balance, allowing specific profiling of patients (40, 41). A full description of the management of acute vertigo in the elderly is beyond the scope of this mini review, further readings can be obtained elsewhere (13, 46). In dubious cases, treatment attempts should be preferred, given diminished symptomatology and the safety and simplicity of reposition maneuvers (56).
After that, and depending on the available resources, office or laboratory tests help to estimate the risk of falling and define the balance profile to guide the management of these patients. For instance, a patient lacking postural stability will require postural- and gait-focused therapy.
Concha bullosa may obstruct the drainage of maxillary sinus giving rise to maxillary sinusitis as well.
Otoconia are composed of otoconin and otolin forming the organic matrix on which calcium carbonate mineralizes.
Unless I am the author of the content of a linked site, these links are not based on reciprocal agreements. Diagnostic and therapeutic approaches oriented to the specific impaired system, including visual, proprioceptive, and vestibular pathways, are proposed. However, while on the acute phase of vestibular loss, this may cause intense rotatory vertigo (due to a sudden vestibular asymmetry), on elderly patients the slow onset of these chronic impairments would not manifest with vertigo.


All these factors should be taken into account in the diagnosis and management of elderly patients.
Several studies have found that caloric responses tend to increase in middle age with a peak between 50 and 70 years, and then decline modestly thereafter (35, 36). Care should be taken in focusing therapy on ongoing symptoms rather than solely on testing abnormalities, as certain patients could require other treatments prior to benefit from VR, such as in the case of vestibular migraine, or visually induced dizziness, among others.
No banner adds or pop-ups should appear on your browser as a result of browsing this website. Instead, they complain about movement intolerance, instability, and insecure gait, particularly when sudden turns are needed, as there is an incapability of processing these movements properly. Vibration and touch thresholds, the ability to detect position and direction of joint movements, and muscle strength also deteriorate with age (2).
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).
However, if you leave this website to a related one, Back in Business Physiotherapy cannot accept responsibility for neither changes in their contents nor their advertising or privacy policies. This may also explain the observed lack of rotatory vertigo in elderly patients with benign paroxysmal positional vertigo (BPPV) (8). Visual accommodation, depth perception, and the ability to suppress nystagmus by visual fixation is diminished due to aging of the oculomotor system with increased saccade latency, and reduced eye tracking velocity (2). Download Case StudySimplifying Treatment DilemmasImpairments Drive Specialized Treatment Plan Patients A and B are elderly individuals referred from family practice presenting with mild dizziness, increasing imbalance and decreased activity levels over the last several months. Most cases of BPPV are idiopathic, but head trauma, otologic disorders, and systemic disease appear to be contributory in a subset. Patient A reports multiple ‘near fall’ events, whereas Patient B reports a single fall without injury. Both have known diabetic neuropathy that has been evaluated and confirmed by their neurologists. 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. Management to date has included multiple episodes of rehabilitation care, medical management with injections, and corrective shoe orthotics—all with limited relief.
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].
He complains of positional vertigo, confirmed on clinical examination as BPPV or canalithiasis of the right posterior semicircular canal. 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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