Shigeyo Nagase

Deafness-induced plasticity in the mature central auditory system.

Studies in rats and guinea pigs indicate that local changes in inhibitory transmitters may underlie deafness-induced plastic changes in electrophysiological responsiveness of cells of the mature central auditory system. Following 21 days of bilateral deafness there is an increase in evoked Fos-immunoreactive neurones in the central nucleus of the inferior colliculus (CIC) to contralateral cochlear electrical stimulation, compared with normal or 1-day deafened animals. Deafness is also associated with a dramatic reduction in the population of CIC neurones that respond with suppression of activity to electrical stimulation. Moreover, in vivo microdialysis reveals a marked decrease in γ-aminobutyric acid (GABA) release from the CIC cells in deafened animals. The results may have general implications for the mediation of central nervous system plasticity induced by deafferentation of sensory input.

Changes in cochlear electrical stimulation induced Fos expression in the rat inferior colliculus following deafness.

Fos immunoreactive (IR) staining was used to examine changes in excitatory neuronal activity in the rat inferior colliculus (IC) between normal hearing and 21 day deaf rats evoked by basal or apical monopolar cochlear electrical stimulation. The location of evoked Fos IR neurons was consistent with expected tonotopic areas. The number of Fos IR cells increased as stimulation intensity increased in both normal and 21 day deaf animals. Stimulation at 1. 5x threshold evoked fewer Fos IR cells in 21 day deafened animals compared to normal hearing animals. At 5x and above, however, significantly increased numbers of Fos IR neurons (in a larger grouping) were evoked in 21 day deafened animals compared to normal hearing animals. Another group of animals had 7 days of deafness followed by 14 days of chronic basal cochlear electrical stimulation. In this group basal monopolar stimulation at 5x evoked not only a greater number of Fos IR neurons, compared to normal hearing animals, but the location of their grouping was slightly shifted to a more dorso-lateral region in the contralateral IC, compared to the normal hearing and 21 day deaf groups. These observations indicate that both deafness and chronic electrical stimulation may alter central auditory processing.

Changes in the Central Auditory System with Deafness and Return of Activity via a Cochlear Prosthesis

It is well established that sensory deprivation during development results in lasting changes in the central nervous system (CNS) (Wiesel and Hubel. 1963). This is certainly the case for the auditory system where in developing animals, sound deprivation and/or cochlear ablation are especially potent means of producing significant neuronal atrophy and reorganization in central structures (Rubel et al., 1984). The loss of afferent input often occurs in the adult auditory system and there is increasing evidence that the mature central auditory system (CAS) also displays substantial changes in structure and function following deafferentation (Gerken, 1979; Rajan et al., 1993, 1996, Willott et al., 1994). However, despite the high incidence of inner ear pathology and a growing utilization of the cochlear prosthesis in deaf adults, little is known about the effects of cochlear damage on the mature CAS, the mechanisms underlying CNS physiological changes produce by deafness, or how deafness induced changes may affect processing with subsequent reactivation of the CAS via a cochlear prosthesis. Elucidating how the CAS responds to such deafferentation is fundamental to our understanding the mechanisms of plasticity and homeostasis of the brain throughout an organisms lifetime.

The inferior collicular potential in acoustic and electrical stimulation of the cochlea: an experimental study of guinea pig.

We made experiments of the inferior collicular potentials in acoustic and electrical stimulation for the purpose of studying fundamental issues for cochlear implantation. Guinea pigs with normal Preyers reflex were used for this study. The results were as follows: (1) in acoustic stimulation relatively wide and large waveforms were gained but in electrical stimulation sharp and narrow ones were gained, (2) in acoustic stimulation the input-output curve of latency and amplitude was biphasic but in electrical stimulation it was monophasic. For this reason, in acoustic stimulation by click, when the intensity is low (under 80 dB SPL) stimulus site would be comparatively low frequency fibers. When the intensity is high (over 80 dB SPL) the stimulus site would shift to high frequency fibers. Therefore, many more neighboring fibers start responding. This results in biphasic input-output curves of latecy and amplitude. By electrical stimulation, however, it would be possible to stimulate only a restricted area among the bipolar electrode. Therefore, as the intensity increases, the response amplitude increases and becomes saturated at a constant level. This results in monophasic input-output curves of latency and amplitude.

Primary Position Upbeat Nystagmus; A Report of Three Cases.

Primary position upbeat nystagmus (PPUN) is an extremely rare disease, and there is no general agreement about its etiology. Most investigators believe, however, that it is associated with disorders in areas extending from the brain stem to the cerebellum. We studied the etiology of and lesions responsible for this disease from the results of various tests and examinations conducted in 3 patients who had different clinical courses. Finding 1: Horizontal and vertical eye movements showed dissociation in Case 2, suggesting that different nerve tracts are involved in these movements. Finding 2: All 3 patients showed evidence of disorders in the brain stem and cerebellum, suggesting that the conduction route between the brain stem and the cerebellum was impaired.

Low frequency perceptive hearing loss in a patient with a brainstem tumor.

This paper reports a case of brainstem tumor with low frequency perceptive hearing loss. A 10-year-old girl had complained of headache, vomiting, dizziness and tinnitus of the right ear for 2 months and was admitted to Tokyo Medical College Hospital. Clinical examinations revealed a glioma in the lower brainstem which caused hydrocephalus, perceptive deafness with low frequency hearing loss, abnormal ABR consisting of only waves I-III, gaze nystagmus in all directions and abnormal patterns in both eyetracking and optokinetic nystagmus tests. MRI showed a tumor, probably a glioma, in the lower brainstem.She was treated with a V-P shunt operation to decrease cerebrospinal pressure followed by irradiation to lessen the tumor size. She showed noticeable improvement, and her hearing recovered to within the normal range with ABRs of I-IV waves.Low frequency perceptive hearing loss due to brainstem lesions is discussed with reference to our own 48 patients plus 14 described in the literature. Approximately one fourth of patients with hearing impairment due to a brain stem lesion have low frequency hearing loss. Ventro-lateral lesions of the pons and the medulla oblongata may be responsible for this type of deafness.