Combined horizontal and posterior canal benign paroxysmal positional vertigo in three patients with head trauma

We report 3 patients who complained of positional vertigo shortly after head trauma. Positional maneuvers performed in the plane of the posterior canal (PC; Dix-Hallpike maneuver) and the horizontal canal (HC; patients were rolled to either side in a supine position with the head raised 30 degrees) revealed a complex positional nystagmus that could only be interpreted as the result of combined PC and HC benign paroxysmal positional vertigo (BPPV). Two patients had a right PC BPPV and an ageotropic HC BPPV, and 1 patient had a bilateral PC BPPV and a left geotropic HC BPPV. All 3 patients were rapidly free of vertigo after the PC BPPV was cured by the Epley maneuver and the geotropic HC BPPV was cured by the Vannucchi method. The ageotropic HC BPPV resolved spontaneously. Neuroimaging (brain computed tomography and/or magnetic resonance imaging scans) findings were normal in all 3 patients. From a physiopathological viewpoint, it is easy to conceive that head trauma could throw otoconial debris into different canals of each labyrinth and be responsible for these combined forms of BPPV. Consequently, in trauma patients with vertigo, it is mandatory to perform the Dix-Hallpike maneuver, as well as supine lateral head turns, in order to diagnose PC BPPV, HC BPPV, or the association of both. Early diagnosis and treatment of BPPV may help to reduce the postconcussion syndrome.     

Benign paroxysmal positional vertigo

Benign paroxysmal positional vertigo (BPPV) is characterized by positional vertigo (brief attacks of rotatory vertigo triggered by head position changes in the direction of gravity) and is the most common peripheral cause of vertigo. There are two types of BPPV pathophysiology: canalolithiasis and cupulolithiasis. In canalolithiasis, otoconial debris is detached from the otolithic membrane and floats freely within the endolymph of the canal. In cupulolithiasis, the otoconial debris released from the otolithic membrane settles on the cupula of the semicircular canal and the specific gravity of the cupula is increased. Consensus has been reached regarding three subtypes of BPPV: posterior-canal-type BPPV (canalolithiasis), lateral-canal-type BPPV (canalolithiasis) and lateral-canal-type BPPV (cupulolithiasis). In the interview-based medical examination of BPPV, questions regarding the characteristics of vertigo, triggered movement of vertigo, duration of vertigo and cochlear symptoms during vertigo attacks are important for the diagnosis of BPPV. The Dix–Hallpike test is a positioning nystagmus test used for diagnosis of posterior-canal-type BPPV. The head roll test is a positional nystagmus test used for diagnosis of lateral-canal-type BPPV. When the Dix–Hallpike test is repeated, positional nystagmus and the feeling of vertigo typically become weaker. This phenomenon is called BPPV fatigue. The effect of BPPV fatigue typically disappears within 30 min, at which point the Dix–Hallpike test again induces clear positional nystagmus even though BPPV fatigue had previously caused the positional nystagmus to disappear. For the treatment of BPPV, sequential head movements of patients can cause the otoconial debris in the semicircular canal to move to the utricle. This series of head movements is called the canalith repositioning procedure (CRP). The appropriate type of CRP depends on the semicircular canal in which the otoconial debris is located. The CRP for posterior-canal-type BPPV is called the Epley maneuver, and the CRP for lateral-canal-type BPPV is called the Gufoni maneuver. Including a time interval between each head position in the Epley maneuver reduces the immediate effect of the maneuver. This finding can inform the development of methods for reducing the effort exerted by doctors and the discomfort experienced by patients with posterior-canal-type BPPV during the Epley maneuver.     

The subjective visual vertical in benign paroxysmal positional vertigo. A preliminary study

In Benign Paroxysmal Positional Vertigo (BPPV), the existence of otoconial debris in the cupula or canal explains most of the symptoms and signs characteristic of this common inner ear disorder. We have studied the ability of patients with BPPV to correctly determine the subjective visual vertical, as this is a good test to evaluate utricular function. Only 1 of 10 patients with BPPV displayed a clearly abnormal response, and there was no correlation between the side of the lesion and the perceived tilt. This might imply that the limited damage induced by the dislodged otoconia does not disrupt utricular function or that the saccule is the source of the problem.     

Canalolithiasis of the superior semicircular canal: an anomaly in benign paroxysmal vertigo

According to the canalolithiasis theory, benign paroxysmal vertigo (BPPV) is caused by gravity-dependent movements of otoconial debris that collects in the endolymph of the posterior semicircular canal. Other parts of the vestibular organ are rarely affected, and it is mainly the horizontal canal that is affected by this atypical form of BPPV. Canalolithiasis of the superior semicircular canal must be considered an anomaly because the superior semicircular canal is the highest point of the vestibular organ and debris normally cannot collect in this special location. Until now, BPPV of the superior canal has mainly been dealt with theoretically in the literature. The authors present three patients with canalolithiasis of the superior semicircular canal and offer direct proof of the condition using high-resolution 3D MRI.     

Canalolithiasis of the superior semicircular canal: an anomaly in benign paroxysmal vertigo

According to the canalolithiasis theory, benign paroxysmal vertigo (BPPV) is caused by gravity-dependent movements of otoconial debris that collects in the endolymph of the posterior semicircular canal. Other parts of the vestibular organ are rarely affected, and it is mainly the horizontal canal that is affected by this atypical form of BPPV. Canalolithiasis of the superior semicircular canal must be considered an anomaly because the superior semicircular canal is the highest point of the vestibular organ and debris normally cannot collect in this special location. Until now, BPPV of the superior canal has mainly been dealt with theoretically in the literature. The authors present three patients with canalolithiasis of the superior semicircular canal and offer direct proof of the condition using high-resolution 3D MRI.     

Long-term postural abnormalities in benign paroxysmal positional vertigo

Benign paroxysmal positional vertigo (BPPV) is a disorder in which patients suffer from acute rotatory vertigo due to the presence of free otoconial debris migrating into one or more semicircular canals during head movements and resulting in abnormal stimulation of the ampullary crest. A prolonged loss of equilibrium of unclear origin is also present. Static posturography is a useful tool for the study of postural control systems and their role in these abnormalities. The aim of the present study was to evaluate the frequency of body sway and long-term instability of BPPV patients by posturography frequency analysis. Twenty patients with canalithiasis of the posterior semicircular canal and 20 normal controls were subjected to static posturography. Informed consent was obtained from all subjects. Patients were tested 1 h after diagnosis, and 3 days and 12 weeks after the characteristic Epley repositioning maneuver. Patients with BPPV showed significantly increased body sway both on lateral (X) and anteroposterior (Y) planes compared to normal subjects. Corporal oscillation with a broad-frequency spectrum was observed in both closed and open eye tests. The repositioning maneuver decreased the X plane body sway, while the anteroposterior sway was unchanged. Twelve weeks after treatment, a normalization of the anteroposterior sway was observed. Results of this study suggest that the long-term postural disturbance associated with BPPV differs from the acute disequilibrium that subsides after canalith repositioning: the former is a sagittal plane/broad spectrum body sway, while the latter is primarily a frontal plane/low frequency sway. The Epley maneuver was shown to reduce frontal sway, a postural abnormality that might therefore be linked to posterior semicircular canal function. Conversely, the observed sagittal body sway was only partially relieved by the restoration of canal function, and therefore, may be more related to the chronic dizziness observed in these patients.     

What inner ear diseases cause benign paroxysmal positional vertigo?

Benign paroxysmal positional vertigo (BPPV) originating from the posterior semicircular canal (pSCC) is a common vestibular disorder that is easy to diagnose and usually easy to treat. The majority of patients with BPPV have no known inner ear disease; they have "primary" or "idiopathic" BPPV. However, a minority does have objective evidence of an inner ear disease on the same side as the BPPV and this group has "secondary" or "symptomatic" BPPV. Previous publications differ on the prevalence of secondary BPPV and about the types of inner ear diseases capable of causing it. In order to determine what proportion of patients have secondary as opposed to primary BPPV and which inner ear diseases are capable of causing secondary BPPV, we searched our database for the 10-year period from 1988 to 1997 and found a total of 2847 patients with BPPV. Of these, 81 (3%) had definite pSCC-BPPV secondary to an ipsilateral inner ear disease. Sixteen had Menière's disease, 24 had an acute unilateral peripheral vestibulopathy, 12 had a chronic unilateral peripheral vestibulopathy, 21 had chronic bilateral peripheral vestibulopathy and 8 had unilateral sensorineural hearing loss. It seems that any inner ear disease that detaches otoconia and yet does not totally destroy pSCC function can cause BPPV and that a case can be made for audiometry and caloric testing in all patients with BPPV.     

What Inner Ear Diseases Cause Benign Paroxysmal Positional Vertigo?

Benign paroxysmal positional vertigo (BPPV) originating from the posterior semicircular canal (pSCC) is a common vestibular disorder that is easy to diagnose and usually easy to treat. The majority of patients with BPPV have no known inner ear disease; they have ?primary? or ?idiopathic? BPPV. However, a minority does have objective evidence of an inner ear disease on the same side as the BPPV and this group has ?secondary? or ?symptomatic? BPPV. Previous publications differ on the prevalence of secondary BPPV and about the types of inner ear diseases capable of causing it. In order to determine what proportion of patients have secondary as opposed to primary BPPV and which inner ear diseases are capable of causing secondary BPPV, we searched our database for the 10-year period from 1988 to 1997 and found a total of 2847 patients with BPPV. Of these, 81 (3%) had definite pSCC-BPPV secondary to an ipsilateral inner ear disease. Sixteen had Menière's disease, 24 had an acute unilateral peripheral vestibulopathy, 12 had a chronic unilateral peripheral vestibulopathy, 21 had chronic bilateral peripheral vestibulopathy and 8 had unilateral sensorineural hearing loss. It seems that any inner ear disease that detaches otoconia and yet does not totally destroy pSCC function can cause BPPV and that a case can be made for audiometry and caloric testing in all patients with BPPV.     

Management of 210 patients with benign paroxysmal positional vertigo: AMC protocol and outcomes

Conclusion: Benign paroxysmal positional vertigo (BPPV) could be treated with specific maneuvers for the involved canals. Management on a daily basis gave earlier relief than weekly treatment, especially in apogeotropic BPPV. Apogeotropic and multi-canal BPPVs were related to the increased numbers of follow-ups and trauma was related to the increased recurrence. Objective: We aimed to report the short-term outcomes of our protocol for BPPV and evaluate the factors influencing the results and recurrence. Methods: In 210 BPPV patients, posterior semicircular canal (PSCC), geotropic and apogeotropic lateral canal BPPVs were treated with the Epley maneuver, barbecue maneuver, and barbecue maneuver after head-shaking. The total number of follow-ups needed to have no provoked nystagmus, success rates at 1 week and 1 month, and factors for repeated maneuvers or recurrence were identified. Results: Apogeotropic and multi-canal BPPV needed more follow-ups than PSCC BPPV. Multi-canal BPPV showed a significantly lower 1-week success rate than other types. Anterior and multi-canal BPPV showed significantly lower 1-month success rates than other types. The 1-week success rates for PSCC and geotropic and apogeotropic BPPV in patients followed up on a daily basis were higher than those in patients with weekly follow-up and the difference was significant only in apogeotropic BPPV. The overall 1-year recurrence rate was 16% and higher recurrence rate was related to trauma.     

Mechanism Underlying the Effects of Estrogen Deficiency on Otoconia

Otoconia-related vertigo and balance deficits, particularly benign paroxysmal positional vertigo (BPPV), are common. Our recent studies in humans show that, while BPPV prevalence greatly increases with age in both genders, peri-menopausal women are especially susceptible. In the present study, we show that bilateral ovariectomized (OVX) mice have significant balance behavioral deficits, and that estrogen deficiency compromises otoconia maintenance and anchoring by reducing the expression of otoconial component and anchoring proteins. There is ectopic debris formation in the ampulla under estrogen deficiency due to aberrant matrix protein expression. Furthermore, phytoestrogen is effective in rescuing the otoconia abnormalities. By comparing the expression levels of known estrogen receptor (Esr) subtypes, and by examining the otoconia phenotypes of null mice for selected receptors, we postulate that Esr2 may be critical in mediating the effects of estrogen in otoconia maintenance.     

New treatment strategy for cupulolithiasis associated with benign paroxysmal positional vertigo of the lateral canal: the head-tilt hopping exercise

This study was performed to determine whether a novel treatment was effective against cupulolithiasis associated with benign paroxysmal positional vertigo (BPPV) of the lateral semicircular canal, which is characterized by apogeotropic direction-changing nystagmus. We herein describe our head-tilt hopping (HtH) exercise, which is designed to release otoconial debris strongly adhered to the cupula. The subjects were trained to hop while tilting their heads laterally. They completed 3 to 5 exercise sessions per day over a 4-week period. Each session ended with a 20-hop trial. The HtH exercises were performed by 27 patients with intractable lateral canal BPPV who exhibited positional vertigo and persistent nystagmus beating toward the uppermost ear for more than 4 weeks, despite performing therapeutic head shaking in the horizontal plane maneuver. All the patients were subjected to the supine roll test before and immediately after the first trial as well as after 1 and 4 weeks of the program to evaluate the effect of the treatment on their apogeotropic nystagmus. Nystagmus of 9 (33.3 %) patients disappeared immediately after the first training session. After 1 and 4 weeks of the training, the number of patients that had experienced either of these improvements had increased to 15 (55.6 %) and 19 (70.4 %) subjects, respectively. These results suggest that HtH exercises aimed at releasing otoconial debris from the cupula are feasible as a new therapy for cupulolithiasis associated with intractable lateral canal BPPV. However, further studies for comparison with control are required to confirm these preliminary results.     

Model experiment of benign paroxysmal positional vertigo mechanism using the whole membranous labyrinth

Whole membranous labyrinths of bullfrogs were used in order to replicate the human vestibule. The posterior semicircular canals (PSCs) were exposed, leaving the remaining membranous labyrinth encapsulated in the otic capsule. Vibration was applied to the surface of the bony capsule using a conventional surgical drill in order to dislodge the otoconia from the utricle. The position of the preparation was controlled so that the dislodged otoconia were attached to the cupular surface. This was regarded as a cupulolithiasis model. The action potentials changed instantaneously according to the gravitational force on the cupula. When the otoconia were dislodged and held within the PSC lumen, the position of the whole preparation was changed so that the otoconia moved back and forth within the canal lumen. This is a model of canalolithiasis. The action potentials changed in combination with the otoconial movement after a latent period. Both cupulolithiasis and canalolithasis are potentially valid mechanisms of benign paroxysmal positional vertigo (BPPV). However, canalolithiasis is the most likely mechanism of BPPV, which is usually characterized by nystagmus of short duration and long latency. A vibratory stimulus was able to detach the otoconia from the utricle, suggesting that mechanical insult could be a possible etiology of BPPV.     

中青年女性BPPV发病危险因素分析

目的 探讨中青年女性良性阵发性位置性眩晕(benign paroxysmal positional vertigo,BPPV)发病的危险因素.方法 以2016年7月～2019年12月确诊的145例中青年女性BPPV患者为研究对象,其中原发性113例(原发组),继发性32例(继发组);以98例正常中青年女性为对照组;原发...     

Recurrent benign paroxysmal positional vertigo in two DFNB16 siblings: A CARE case report

IntroductionDeletions or variants of the STRC gene coding for stereocilin cause congenital bilateral mild-to-moderate sensorineural hearing loss without vestibular disorder: DFNB16. Stereocilin is a protein present in vestibular kinocilia embedded in the otoconial membrane of the utricular macula. Benign paroxysmal positional vertigo (BPPV) is a rare form of vertigo in children. The present study reports recurrent positional vertigo in two DFNB16 siblings.ObservationTwo patients, 10 and 15 years old, presented with recurrent disabling positional vertigo episodes, triggered by turning over in bed, with a falling sensation. The diagnosis of right posterior canal BPPV was confirmed on Dix-Hallpike maneuvers in one of the patients. Variations in the response of ocular vestibular-evoked myogenic potentials were observed. Probable BPPV was diagnosed in the second patient. Their other two siblings did not have hearing loss or vertigo.ConclusionThe absence of stereocilin due to homozygous deletions of the STRC gene in DFNB16 patients can cause vestibular dysfunction, including BPPV.     

Benign paroxysmal positional vertigo showing sequential translations of four types of nystagmus

Objective

We report a case of benign paroxysmal positional vertigo (BPPV) showing sequential translation of four types of nystagmus and discuss its pathophysiology.

Methods

The case was 65-year-old female. We analyzed her nystagmus three-dimensionally.

Results

At the first visit, she showed vertical-torsio nystagmus of the posterior canal type of BPPV (P-BPPV) and subsequently showed recently reported geotropic nystagmus with a long time constant. Two weeks later, she showed apogeotropic nystagmus of the horizontal canal type of BPPV (AH-BPPV) and subsequently a geotropic nystagmus with a short time constant of the horizontal canal type of BPPV (GH-BPPV).

Conclusions

Three kind of nystagmus, namely P-BPPV, AH-BPPV and GH-BPPV can be explained by the otoconial debris hypothesis of the same ear. Finally, the recently reported geotropic nystagmus with a long time constant may be explained by a reversible lesion such as the denatured cupula or utricular imbalance of the same ear.     

Life events and benign paroxysmal positional vertigo: a case-controlled study

CONCLUSIONS: Within the poorly understood mechanisms implicated in the aetiology of benign paroxysmal positional vertigo (BPPV), the results of this trial provide clinical evidence of a potential role of emotional stress connected to adverse life events as a trigger of otoconial dysfunction. High levels of anxiety, depression and somatization were recorded and considered psychogenic precursors of BPPV, thus emphasizing the role of psychological distress in precipitating peripheral vestibular disorders. Therefore, appraisal of life stress and psychological attitudes may have potential implications in the clinical assessment of this labyrinthine vertigo and its frequent relapses. OBJECTIVES: BPPV is one of the most common peripheral vestibular disorders, and although it has been the subject of several studies and debates, its aetiology still remains unknown in most cases. Because it has been shown that emotional stress is related to the onset or worsening of other inner ear dysfunctions such as Ménière's disease and sudden hearing loss, this study investigated the hypothesis that life events, mood and psychological attitudes may have a causal relationship with BPPV. PATIENTS AND METHODS: Fifty patients (40 females and 10 men; mean age 43.5+/-10.1 years, range 30-65 years) were recruited and compared with 50 healthy volunteers matched for sex, age and socio-demographic variables. Patients were selected among dizzy patients who were referred to the ENT Clinic of the University of Modena and Reggio Emilia from the emergency unit with a primary diagnosis of 'positional vertigo' and enrolled in the study only if they had a paroxysmal positional nystagmus as diagnosed by Dix-Hallpike and Semont's manoeuvres. Patients with a history of recurrent vertigo and additional otoneurological diseases were excluded. The Paykel Life Events Scale, Spielberger State-Trait Anxiety Inventory, Symptom Check List-90 Revisited and Hamilton Depression Scale were the psychometric questionnaires used to complete the audiological and vestibular examinations. RESULTS: Patients with BPPV reported significantly more life events than control subjects in the year preceding the onset of vertigo (p<0.005). Negative life events, objective negative impact and a poor degree of control were also significantly more frequent in patients compared with controls (p<0.005). There were no significant differences between groups concerning positive life events (p>0.05). Psychometric questionnaires recorded significantly higher levels of anxiety, depression and somatization in the pathological sample (p<0.005), as well as an increased obsessive-compulsive attitude (p<0.05).     

Statistical observation of vertigo and dizziness patients]

Subjects visiting the Department of Otolaryngology at Suita Municipal Hospital reporting vertigo or dizziness numbered 664 women and 343 men from April 1999 to December 2000. As a city hospital, we play an important role in the diagnosis and treatment of acute vertigo or dizziness. The frequency of diagnosis of these cases was divided almost equally into 5 groups: (1) benign paroxysmal positional vertigo (BPPV) 23%; (2) suspected BPPV, 18%; (3) peripheral vestibular disorders other than BPPV, 22%; (4) disorders other than peripheral origin, 18%; and (5) undiagnosed, 19%. Based on our results, BPPV, other peripheral vestibular disorders, and disorders of other origins should be differentiated from the first screening. BPPV was most frequent and diagnosed by typical positioning nystagmus. Many other peripheral vestibular disorders were accompanied by nystagmus. It is also important to differentiate serious illnesses such as cerebrovascular disease (7%), space-occupying lesions in the posterior fossa (1.2%), and cardio-circulatory disease (3.6%).     

Pathological localization of so-called posterior canal BPPV

OBJECTIVE: Based on the hypothesis that the origin of nystagmus is from the posterior canal (PC), the nystagmus in the head hanging and sitting position should be mirror images. To clarify the anatomical origin of positioning nystagmus in BPPV patients, we analyzed the positioning nystagmus of benign paroxysmal positioning vertigo (BPPV) patients three-dimensionally. METHODS: Twenty-six patients with BPPV participated in this study. The positioning nystagmus was recorded in complete darkness from the patient's left eye by means of an infrared CCD camera. We performed three-dimensional analysis of nystagmus using video image analysis system (VIAS). Subsequently, the rotation axis of the 3D eye movements of the positioning nystagmus was calculated. RESULTS: Among the 26 patients tested, 20 patients demonstrated the axes of nystagmus in good or relatively good alignment to the PC axis. However, in 11 of these 20 patients there was poor alignment of the axis of nystagmus in the sitting position to the PC axis. In addition, six patients showed axes of nystagmus with poor alignment to the PC in the head hanging position. Among them, two patients exhibited axes of nystagmus in good alignment with the anterior canal, in spite of diagnosis of these patients as PC BPPV by experienced examiner based on the positioning nystagmus test. CONCLUSION: These results demonstrated that only one-third of patients who were diagnosed as BPPV, could be diagnosed as true BPPV which originates from a PC pathology. Besides the possibility that the pathology may originate from the AC, it is still unclear which part of the inner ear may be the candidate site of origin of the pathology of BPPV in the other 15 patients.     

Stapedotomy and post-operative benign paroxysmal positional vertigo

In our experience some patients subjected to stapedotomy presented vestibular symptoms characterized by brief episodes of vertigo that only lasted 10 to 20 seconds, accompanied by rapid paroxysmal nystagmus similar to that found in benign paroxysmal positional vertigo (BPPV). For this study, 141 otosclerotic patients were enroled and underwent stapedotomy following the Fisch and Dillier's technique. Twelve out (8.5%) of all the patients under study complained of post-operative vertigo and the physical examination of the positional nystagmus confirmed the presence of paroxymal positional vertigo. The percentage seems particularly high and does not agree with the data reported in literature. The onset of the vestibular symptoms appeared between the 5th and 21st day after surgery. To our knowledge, this is the first prospective study existing in literature on the incidence of BPPV after surgery of the stapes. It must also be stressed that the patient should be informed beforehand during the consultation phase of the possibility of post-stapedotomy BPPV together with the other causes of post-operative vertigo.     

The incidence and distribution of cupular deposits in the pediatric vestibular labyrinth.

OBJECTIVES: Deposits of basophilic material on the cupulae of the semicircular ducts have been described in adult human temporal bones, and such deposits have been implicated in the clinical phenomenon of benign paroxysmal positional vertigo (BPPV). Although relatively rare, BPPV has been reported to occur in children. The goal of this study was to evaluate the occurrence of cupular deposits in pediatric material. STUDY DESIGN: Basic science, two-center histopathologic temporal bone study. METHODS: We examined 186 temporal bones from 121 individuals between the ages of newborn and 10 years. The average age was 14.7 months. All temporal bones were acquired at autopsy, embedded in celloidin, and sectioned for light microscopic study. The cupulae of the semicircular ducts were identified and any deposits found were graded according to their size and position on the cupula. RESULTS: A total of 276 cupulae were identified, and in 35 (12.7%) of these a basophilic deposit was found. In many cases the deposits contained recognizable otoconial crystals. Most deposits were small and they were almost equally distributed between the three semicircular ducts. However, the lateral and posterior cupulae were somewhat more involved than the superior cupula. Our data showed that cupular deposits are less frequently found in the pediatric labyrinth, compared with adults as reported in previous studies. CONCLUSIONS: The lower occurrence in children versus adults suggests that the deposits may be a phenomenon of the aging vestibular labyrinth.