In the inner ear, water homeostasis is of crucial importance to maintain the function of hearing and equilibrium. The morphological characteristics of Ménière's disease, endolymphatic hydrops, reflect the malregulation of water homeostasis in the inner ear. The water channels composed of aquaporin (AQP) proteins are well known to play a very important role in water homeostasis in the body. At least 8 types of AQPs are also reported to be expressed in the inner ear. It is notiable that the AQP-2 water channel, mediated by vasopressin (VP), is localized in the inner ear. In the present paper, it is reviewed how water homeostasis is mediated by the AQP system in the inner ear, and how this AQP system, especially the VP-AQP2 system, is linked to the formation of endolymphatic hydrops.
Vestibular neurons in the internal auditory canal are composed of afferent and efferent fibers. Vestibular primary afferent neurons have their cell somata, so-called Scarpa's ganglion cells, localized in the canal. Vestibular afferents receive afferent signals from vestibular hair cells and transmit them to vestibular nuclei and vestibulocerebellum. Vestibular afferents also receive efferent signals via axo-dendritic synapses between calyxes and vestibular efferent fibers. According to the afferent and efferent information, vestibular afferents have crucial bipolar effects both on distal and proximal synapses. In this review article, I would like to discuss the roles of vestibular neurons, including both afferents and efferents, in terms of neurotransmitters and neuromodulators.
It is well known that antiepileptic drugs can cause dizziness or vertigo. Although the diagnosis of intoxication is relatively straight forward in simple cases, it is not easy in complex cases with other diseases. We report on a 63-year-old woman who had cen-tral disequilibrium due to taking antiepileptic drugs (carbamazepin and/or sodium valproate), with peripheral vertigo and hearing loss due to Meniere disease. She presented with unsteadiness. She took sodium valproate and/or carbamazepin to suppress epileptic seizure. On examination, she had down beating nystagmus at the lateral and downward gaze, saccadic pursuit, disturbed optokinetic nystagmus, and disturbances of visual suppression. Additionally, she had absence of caloric responses on the right and right sensorineural hearing loss. Her brain MRI was unremarkable. On the basis of these findings, she was diagnosed with central disequilibrium probably due to the intoxication of carbamazepin and/or sodium valproate with right inner ear disorders. After the reduction of antiepileptic drugs her signs and symptoms of central disequilibrium disappeared. This case suggested that knowledge of drug history is crucial in the neuro-otology clinic.
This study examined the relationship between changes in an individual's condition and sway pattern changes using four body sway factors: unit time sway, frontback sway, left-right sway and the high frequency band power. Each subject's sway pattern was determined according to the procedure reported in our previous study. Because respective factors were divided into 7 domains which consist of 4 main (A, B1, B2 and C) and 3 boundary (ab, bb and bc) domains, factor scores for each individual were ranked in any of the above domains and their sway pattern, based on the 4 sway factors, was decided. Measurement of the center of foot pressure (CFP) and examination of the conscious condition were conducted on 10 subjects for 100 days. The CFP was twice each day measured for 1 min, with a 1 min rest between measurements. The measurement device was an Anima's stabilometer G5500. The data sampling frequency was 20 Hz. We identified the sway pattern when each subject felt comfortable that they were performing their standard pattern. It was clarified that the standard pattern differs for each individual; subjects have respective unique patterns, and the sway patterns under normal conditions are mostly similar to the standard pattern. Meanwhile, sway patterns under abnormal conditions were considered to differ from the standard pattern. When a person feels in an abnormal condition or experiences somewhat of a change in the inner body, this may be reflected in their sway pattern. In addition, it was suggested that even under abnormal conditions, sway patterns under cold and myalgia conditions differ. The evaluation method of sway pattern proposed in our previous study can simply evaluate an individual's conscious body change or abnormal con-dition, and may be useful in health care.
Two patients presenting supranuclear gaze palsy with thalamomesencephalic vascular lesions were reported on. One developed bilateral exotropia in the primary position. CT and MRI scans revealed bilateral thalamic infarction caused by occlusion of the paramedian thalamic arteries. He was unable to adduct both eyes in the lateral gaze, although adduction palsy could be overcome by covering the contralateral eye. The vertical gaze was remarkably restricted. The other patient showed right thalamic hemorrhage with vertical gaze limitation and weakness of abduction in the left eye. The limitation of abduction, how-ever, could be overcome by covering the right eye and through caloric stimulation. It is postulated that the present cases of supranuclear horizontal gaze palsy were due to the interruption of cortico-bulber pathways to the paramedian pontine reticular formation (PPRF), or output from the PPRF to control horizontal gaze passing near the thalamic lesion extending to the rostral part of the mesencephalon.
We report on a case with periodic nystagmus on lateral gaze during vertigo attack. The case is a 19-year-old woman who had repeated vertigo attacks in the early stage of the disease. During remission, she had continuous nystagmus on lateral gaze with a large amplitude. During vertigo attack, she had periodic nystagmus with a small amplitude on lateral gaze with null periods of 8s. At onset, her tentative diagnosis was spinocerebellar degeneration such as dentatorubral-pallidoluysian atrophy because of brain stem tegmentum and cerebellar vermis atrophy identified on MRI, but brainstem encephalitis and cerebellitis couldn't be excluded. Periodic nystagmus during vertigo attack may be induced by the depression of higher neural control which was indicated by lesions in the cerebellar vermis shown on MRI.