Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular disorder. Although it is easily cured with physical therapy such as a canal repositioning procedure (CRP), intractable BPPV patients show relapses or poor response to physical therapy. Anatomic variations, stenoses in the membranous labyrinth of the semi-circular canal (SCC), or multiple clots of particles in the SCC, and the short-arm type BPPV are related to intractable BPPV. Other backgrounds related to intractability in BPPV have been reported including osteoporosis, head trauma, position during bed rest, Ménière's disease, and sudden sensorineural hearing loss. Appropriate management of intractable BPPV requires the correct diagnosis. The background of BPPV hold the key to the diagnosis of intractable BPPV. Differential diagnosis of the common cause between long-arm type BPPV and short-arm type BPPV becomes very important, with particular attention required to check the duration and characteristics of positional nystagmus. The positional nystagmus during CRP allows speculations on the movement of debris and the appropriate treatment strategy. Physical therapy for intractable BPPV may be based on release of the otoconial debris, and transfer and fixation of the debris to the utricle.
The horizontal semicircular canal (HSCC) type of benign paroxysmal positional vertigo (BPPV) (H-BPPV) is caused by either canalolithiasis or cupulolithiasis and affects the horizontal semicircular canal. When the patient with HSCC canalolithiasis performs a lateral head turn toward the affected ear, free-floating debris will create an ampullopetal endolymph flow. As a result, a geotropic nystagmus (fast phase toward the ground) will be present (GH-BPPV). When the patient turns away from the affected side, free-floating debris will create an ampullofugal flow. When the patient with HSCC cupulolithiasis performs a lateral head turn toward the affected ear, the cupula undergoes an ampullofugal deflection causing apogeotropic nystagmus. A head turn to the opposite side creates an ampullopetal deflection. The natural history of H-BPPV is good and several positioning techniques to treat H-BPPV have been developed, but a few patients with refractory H-BPPV exist. In this review, I explain how to diagnose H-BPPV, how to diagnose the affected side in H-BPPV, and how to treat H-BPPV with canalith repositioning maneuvers. I show two types of GH-BPPV. One type shows transient positioning geotropic nystagmus, and the other type shows continuous positional geotropic nystagmus. Finally, I explain how to deal with refractory H-BPPV and the surgical treatment of H-BPPV.
Purpose This study was performed to examine what duration the feeling of being shaken can persist after the end of an earthquake by subjecting 12 volunteers to an artificial earthquake using an earthquake simulator vehicle. Methods The time from cessation of shaking in the earthquake simulator vehicle to the point at which the subject felt that the shake had ceased was measured. Experiment 1: The seismic intensity was set at lower 6 to 2 on the Japanese seismic scale. Experiment 2: The seismic stimulation time of 1 minute and 3 minutes were compared. Experiment 3: Seismic stimulation was compared between rolling and pitching. Experiment 4: The experiment was carried out with the subject's body position changed. Experiment 5: Seismic stimulation was delivered intermittently rather than continuously. Experiment 6: Seismic stimulation was delivered upon each of the following two different explanations: “The earthquake will cease in 1or 3 minutes”. “We don't know how long the earthquake will last. The seismic intensity may also change”. However, the actual stimulation delivered was at seismic intensities of upper 5 for 1 minute and 2 for 1 minute. Results Experiment 1 to 5: The duration from the end of the evoked quake until cessation of the post-quake feeling of ground shaking was within 3 seconds on average in all instances. Experiment 6: There was a significant prolongation of the mean time after an intensity 2 shake as well as that after an intensity of upper 5 when the test was conducted with the prior explanation:“We don't know how long the earthquake will last. The seismic intensity may also change” (P<0.05). Discussion This finding indicated that the feeling of the ground shaking after an earthquake is likely to be affected by psychosomatic or psychological factors.
The Usher syndrome (USH) is a group of recessively inherited disorders characterized by deafness and vision loss. The standard Usher syndrome classification recognizes three clinical types. Usher syndrome type 1 (USH1) is the most severe form of USH. It appears to have profound non-syndromic hearing loss and vestibular dysfunction in childhood and retinitis pigmentosa develops in later years. Five causative genes have been identified: MYO7A, USH1C, CDH23, PCDH15, and USH1G. We previously reported that the basis for the classification of USH is ambiguous. It was particularly unclear whether the diagnosis regarding the vestibular dysfunction of USH1 was based on a vestibular examination or a complaint of dizziness. In this study, we considered cases in which USH1 gene mutations were identified. Of five USH1 patients, only two patients (50%) complained of dizziness. However, all patients had no response to the caloric test. In addition, two patients demonstrated delayed onset of walking (18 months and 24 months). In conclusion, we think the assessment of USH1 vestibular function should be based on a vestibular examination. Moreover, a delay in motor development is one clinical indication of the congenital absence of vestibular function.
An inner ear disorder is one of the main causes of vertigo. Though it has not been proven, many of the inner ear disorders are probably induced by ischemia or virus infection. It is not easy to evaluate the circulation of the vestibule because of its anatomical location. The objectives of the current study were to establish a vestibular ischemia model using the bullfrog, and to investigate changes in the vestibular apparatus in the ischemic condition. Bullfrogs (Rana catesbeiana) were used. Under anesthesia with ether, the unilateral temporal bone was opened from the oral cavity by drilling to expose the vestibular nerve. The vestibular artery on the nerve was cut (vestibular ischemia model). In some cases, the vestibular artery was not cut (sham surgery). The intact temporal bones served as controls. Two to 7 days later, the semicircular canals were removed. The cupulae were stained with India ink and investigated in frog Ringer solution. The ampullae were fixed, cut into 4μm slices and stained with hematoxylin-eosin. Neuroepithelia of the ampullae were investigated under the light microscope. In the vestibular ischemia model, 30-50% of cupulae in each semicircular canal were damaged to various degrees. In the sham surgery and control groups, no cupula was damaged. The neuroepithelia of the ampulla were damaged in 50-80% of the vestibular ischemia model and 1 sham surgery, and were intact in controls. Cupulae were damaged easily when the damage to the neuroepithelia was extensive. Vestibular ischemia can damage both the neuroepithelia and cupulae.
Morphological changes in the cupula could be confirmed not only after injecting the ototoxic agent into the inner ear, but also after mechanical rupturing of the membranous labyrinth. This study aimed to investigate the differences in cupula changes in each semicircular canal after rupturing the membranous labyrinth. For mechanical rupturing, a fine needle was inserted into the center of the saccule of the bull frog under anesthesia. The degrees of cupula change were observed under a stereoscopic microscope as of 1 or 2 weeks after rupturing. The ampullary nerve compound action potentials (CAPs) in response to mechanical endolymphatic flow were recorded to assess the sensory cell activity. Severe changes were observed in 24.2% of the posterior semicircular canals (PC), 34.8% of the anterior semicircular canal (AC), and 58.4% in the lateral semicircular canal (LC). The changes in the cupulae in all canals developed with time. Especially in the LC at 2 weeks after rupturing, cupulae showed severe morphological shrinkages, and also the deformities of the cupula other than the shrinkage were found in 25.0%. The CAP results were not different among each canal. It has been suggested that an inflammatory change, and/or mixture of endolymph and perilymph in the inner ear caused the morphological changes of cupula, particularly in the LC. Multiple cupula changes in one inner ear were observed in some subjects. One of the reasons why the LC is more susceptible than the AC or PC is that the LC is located closer to the rupturing site. Another possibility is the LC is smaller than the others, thus making it more difficult to maintain its homeostasis. These findings make us reconsider about the etiology and examination of dizziness.
While canalolithiasis is a well known pathophysiology of posterior canal benign paroxysmal positional vertigo (pc-BPPV), there have been a few recent reports of pathophysiological pathways distinct from canalolithiasis (pc-BPPV-ca), including cupulolithiasis (pc-BPPV-cu) and canalolithiasis of the short-arm type (pc-BPPV short-arm-ca). The present study included 39 patients with persistent vertical-torsional nystagmus triggered by the Head positional test, the Head positioning test and the Dix-Hallpike maneuver, suggesting pc-BPPV-cu or pc-BPPV short-arm-ca. The observed positional nystagmus was weakened, and the findings of nystagmus in each head position and the pattern of positional nystagmus were not helpful in discriminating pc-BPPV-cu versus pc-BPPV short-arm-ca. It is known that the right ear is more commonly involved in pc-BPPV-ca, however the left ear was affected significantly more often than the right ear in 39 patients. If detached otoconias from the utricle enter the long-arm of pc-BPPV, the right ear tends to be affected more than the left ear. It is speculated that detached otoconias from the utricle enter the short-arm of pc-BPPV, inducing pc-BPPV short-arm-ca or pc-BPPV short-arm-cu. When a 3D model of the human temporal bone is considered in the supine position, the direction of the pc-short-arm is perpendicular to the direction of gravity whereas in the sitting position, the direction of the pc-short-arm is in line with the direction of gravity. In order for the otoconias to return from the pc-short-arm into the utricle, it appears to be important to place the head in a position 180 degrees opposite to the sitting position.
The purposes of this study was to elucidate the clinical characteristics of patients suffering from migraine-associated vertigo (MAV) including results of cervical vestibular evoked myogenic potential (cVEMP) and ocular VEMP (oVEMP). Thirty patients diagnosed as having MAV based on the diagnostic criteria by Sakata et al. were enrolled. We performed a retrospective chart review. These patients underwent medical history taking and examinations including cVEMP, oVEMP and a caloric test. All examinations were performed during a symptom-free interval. Twenty one patients (70%) experienced rotatory vertigo, 5 patients (17%) had floating dizziness and 4 patients (13%) had both. Twenty six patients (87%) reported tinnitus and/or aural fullness unilaterally or bilaterally. Their vertigo or dizziness lasted under 60 minutes in 10 patients (34%), 1 hour to 24 hours in 14 patients (46%), and over one day in 5 patients (17%). Canal paresis in the caloric test was observed in 5 patients (17%). Concerning cVEMP, 4 of the 30 patients (13%) showed absent cVEMPs bilaterally, 2 patients (7%) showed absent cVEMPs reflexes unilaterally, and one (3%) demonstrated decreased cVEMP amplitudes unilaterally. Only one patient showed prolonged cVEMP latencies. Concerning oVEMP, 6 of the 30 patients (20%) had absent oVEMP reflexes bilaterally, 2 (7%) had absent oVEMP reflexes unilaterally, and one (3%) had decreased oVEMP amplitudes unilaterally. In 2 patients prolonged oVEMP latencies were observed. No significant correlation was observed among cVEMP, oVEMP and the caloric test. This study showed abnormal vestibular reflexes could be shown by oVEMP as well as the caloric test and cVEMP. It was suggested that a portion of those patients with MAV have abnormal otolith-ocular reflexes.