In the past years significant advances have been made in our understanding of the functional significance of free radicals in the inner ear. This localization of free radical production sites has now been established by immunohistochemistry and the fluorescent indicator of NO and ROS. Increasing evidence suggests that excessive free radical production may play an essential role in vestibular disorders. Based on the mechanisms of inner ear disorders, new pharmacological strategies for preventing and/or treating vestibular disorders have been also suggested.
It is well-known that the inner ear hair cells are easily damaged by ototoxic stresses (e.g. aminoglycosides, ischemia). Hair cell death often results in permanent hearing loss and vestibular dysfunction. To treat the inner ear diseases with loss of hair cells, we should understand the signaling pathway of sensory hair cell death and protection. In this article, I would like to discuss some recent findings about inner ear hair cell death and protection. There are many reports that hair cell death is induced in the form of apoptosis. The key molecules are caspases and c -Jun N2 terminal kinase (JNK) in the signaling pathway of hair cell death. The inhibition of these molecules can protect the hair cells against ototoxic chemicals. The heat shock response is a fundamental mechanism of cells to cope with adverse environments, and is regulated mainly at the level of transcription by heat shock transcription factor (HSF1) in mammals. The activations of caspases and JNK are inhibited by heat shock proteins, and result in the survival of cells. Therefore, we performed experiments to analyze the role of the heat shock response in the inner ear. Our results showed that the heat shock response protected the inner era against intense noise, and that the heat shock response was regulated by HSF1. The heat shock response is the one of the potential candidates for the protection of the inner ear. But more in vivo experiments will be required for the clinical treatment of inner ear diseases.
Previous experiments have established that visual stimulation in the roll plane causes people to feel roll vection. However, few experiments have been aimed at characterizing the relationship between changes in the subjective visual vertical (SVV) and the generation of vection. In this experiment we investigate the relationship between SVV, a quasi-subjective parameter, and vection, the visually induced perception of selfmotion. We observed three different patterns of change in SVV. Even with fixed visual stimuli, in many cases SVV changed continuously. These results suggest that conflicts among different sensory inputs produce dynamic changes in the priority of these sensory inputs. The longer vection is perceived, the more predominant the visual sensory input becomes.
The purpose of this study was to determine factors associated with recurrence of Benign Paroxysmal Positional Vertigo (BPPV). We studied 122 patients with BPPV. Recurrence was observed in 46 patients. We examined patient age, smoking habit and alcohol consumption, canal paresis (CP) on caloric test, complications, type of BPPV, positional nystagmus observed after recovery and duration of BPPV. Complications or CP was recognized with higher frequency in patients with recurrence than in those without recurrence. Complications such as hypertension or hyperlipemia were significantly associated with recurrence of BPPV. Duration of BPPV was significantly longer in patients with recurrence. There were no differences in age, smoking habit and alcohol consumption, type of BPPV and positional nystagmus after recovery between patients with recurrence and those without recurrence. It appeared that patients with recurrence of BPPV might have pathophysiological changes causing detached otoconia.
The origin of vertigo is difficult to identify since a similar symptom occurs in either central or peripheral impairment. An initial evaluation of the patient's clinical history, as well as his clinical manifestations are important for correct diagnosis. Final diagnosis typically depends on conventional imaging techniques, such as CT and MRI. Here, we describe a patients whose functional examination was quite helpful to identify the lesion. The patient was case a 44-year-old man with cavernous hemangio-ma in the brainstem presenting acute hearing loss with vertigo. Initially he was diagnosed as having peripheral vertigo by neurological examinations together with CT images. Later a rare cavernous hemangioma was identified by head MRI. In the process of diagnosis, the result of auditory brainstem response (ABR) strongly suggested brainstem impairment. This case reveals that conventional imaging procedures, such as CT, are inadequate for diagnosis, whereas functional exams, such as the auditory brain stem response (ABR), are quite helpful for clinical evaluation. ABR can work as a screening examination for patients with vertigo to rule out brainstem lesion even in patients with normal hearing.
The authors presented a case of a 46-year old male with a complaint of unilateral progressive sensorineural hearing loss and dizziness, diagnosed with fourth ventricle ependymoma. A Large unilateral acoustic neuroma compressing the cerebellum and brainstem was suspected at first, however results of detailed equilibrium tests including eye tracking test, optokinetic pattern test, caloric test and visual suppression test indicated bilateral lesions of the cerebellum and brainstem. MR images depicted a tumor mass from the fourth ventricle invading the bilateral cerebellum and brainstem, and the postoperative histological examination demonstrated typical findings of ependymoma. The possibility of a fourth ventricle ependymoma mimicking acoustic neuroma should be considered when we encounter cases with not only unilateral progressive sensorineural hearing loss and dizziness but also abnormal equilibrium test findings indicating bilateral cerebellum and brainstem lesions.
We saw a sixty-year-old male patient who had had sudden deafness in the right ear 10 years after he received endolymphatic sac surgery in the left ear affected with Meniere's disease at another hospital. The right hearing could not recov-ered to the left ear level, although steroid-administration therapy at another hospital and subsequent defibrinogenation therapy with Batroxobin at our hospital were systemically performed. He eventually had to use his left post-operative ear with Meniere's disease in his daily life, although he had always made use of his right ear before the onset of sudden deafness. It is possible that the contralateral better hearing ear in the unilateral Meniere's patients' future might be affected with sudden deafness as in this case and/or bilateral endolymphatic hydrops. However, we cannot make a prognosis of the contralateral in-ner ear function in patients with unilateral Meniere's disease by any examination in advance. We at first should perform functional improvement surgery such as endolymphatic sac surgery and intratympanic steroid therapy for intractable unilateral Meniere's disease, and then vestibular ablation surgery like vestibular neurectomy and intratympanic gentamicin therapy can be performed.
This study analyzed Mann's posture maintenance using motion capture technology. Subjects participating in this study were healthy people between 20-29 years old (group H, n=12) and patients with unilateral vestibular disorders (group P, n=26). Small reflective markers were placed on the right and left side of the head and shoul-ders. Postural analysis was performed with a video motion analyzer. Two cameras were positioned 4 m behind the subject. The 3-dimensional position of the marker was detected by computer. All subjects were instructed to stand with the right foot in front of the left foot for 30 seconds with eyes closed. We measured the deviation angle in the roll plane (D-angle) of the head and shoulder using the marker positions. Thereafter, the coefficient of correlation between the pair of angles was calculated. Next, we calculated and compared the degree by measurement of the D-angle's wave area, which was high-pass filtered with 0.12 Hz. Group H showed various coefficients of correlation in the D-angles in the task, indicating that the strategy for postural control differed among individuals. Group P showed rigidity between the head and shoulder along the D-angle in the task, as esti-mated by the high coefficient of correlation. In group P, the area of the D-angle for both head and shoulder was larger than that of group H. Patients with large D-angle tend toward a larger D-angle at the shoulder than that at the head. On the contrary in patients with a small D-angle and in group H, there were some cases showing a larger D-angle at the head than that at the shoulder. In this study, we compared the difference in deviation during Mann's posture maintenance between healthy people and patients with unilateral vestibular disorders.
In this retrospective study, the authors asked whether the presence of cerebral lesions (lacunar infarcts and/or white matter lesions) on magnetic resonance images (MRI) affected vestibulo-ocular reflex (VOR) gain, fixation-suppressed VOR (fVOR) gain, and visual suppression rate (VSR) in 46 elderly patients with disequilibrium symptoms treated at Department of Otolaryngology, Matsue City Hospital between January 2004 and December 2004. The VOR and fVOR were examined with manually-rotated sinu-soidal stimuli using an infrared camera system. VOR gain in the dark did not differ significantly, irrespective of the MRI findings. On the other hand, fVOR gain in patients with cerebral lesions was significantly higher than that in patients without cerebral lesions, resulting in significantly lower VSR in the former patients. Impairment of visual suppression of VOR due to brain lesions outside the cerebellum or pons may not be uncommon in the elderly.
Whole membranous labyrinths of the bull frogs were used in order to replicate the human vestibule.The posterior semicircular canals (PSC) were exposed leaving the remaining membranous labyrinth encapsulated in the otic capsule. The membranous labyrinth was cut by 0.5 mm at the crus commune to create a tiny opening. The cupula was visualized by gently injecting India ink of the opening. The motion of the cupula was analyzed during compression of the canal wall by a needle. The motion appeared to be that of a "diaphragma" when the compression was weak. The motion appeared to be that of a "swing door" with the base of the cupula hinged on the crista when the compression was strong. A small piece of otoconia removed from the sacculus of the other ear was introduced through this opening into the canal lumen. The position of the preparation was controlled so that the otoconia were attached onto the cupular surface. This was regarded as a cupulolithiasis model. We performed the same experiments on the cupulolithiasis models and results were almost same, except that the motion of the cupula of cupulolithiasis models was shorter than those of the normal models. It was inferred that the motion of the cupula of cupulolithiasis models was suppressed by the weight of the otoconia. It was observed that the india ink traversed the cupula during the compression and even the otoconia traversed the cupula. Therefore, it was inferred that the adhesion of the cupula and the ampula wall is not strong, thus protecting the cupula from detaching from the crista.