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The auditory brainstem implant (ABI) represents a new modality for the treatment of patients deafened as a result of complete excision of a bilateral VIIIth nerve tumor. However, little work has been done on the effect of the ABI on the mammalian auditory pathway. The aim of this study was to demonstrate the effect of the ABI using Fos-like immunoreactivity.A bipolar electrode was implanted in the dorsal cochlear nucleus of bilaterally deafened Sprague-Dawley rats, and electrical stimulation was presented at an intensity four times that of threshold.Fos-like immunoreactivity was induced in the neurons of various auditory brainstem nuclei and observed in the low-to-middle frequency area. In the ipsilateral dorsal cochlear nucleus, ipsilateral posterior ventral cochlear nucleus and bilateral inferior colliculus, Fos-like immunoreactive neurons were observed as a distinct banding pattern.This study showed that Fos-like immunoreactivity was observed in the restricted area of the primary brainstem auditory pathway with the appropriate tonotopicity. These results indicate that the ABI can provide auditory information suitable for speech recognition.

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 Preyer's 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.

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 gamma-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.

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.

Methamphetamine activates catecholaminergic neurons and releases noradrenalin from their nerve endings in the central nervous system. Many reports have described the distribution of methamphetamine in the central nervous system after systemic administration. However, there have been only a few studies on the effect of this drug on peripheral organs, and known dealing with the inner ear.The authors used immunohistochemical methods to investigate the effect of methamphetamine on the pheripheral auditory system. Methamphetamine was administered to guinea pigs via intraperitoneal injection. The distribution of methamphetamine in the cochlea was studied by light microscopy following its immunohistochemical staining, and the methamphetamine concentration in the serum was also measured.1. Histochemical examination revealed that methamphetamine was present in the hair cells of the organ of Corti, spiral ligament and spiral ganglion cells 30 minutes after administration.2. The drug concentration in the serum rose rapidly, and then dropped in a logarithmic way with time until it became nearly horinzontal after 6 hours.The results suggest that methamphetamine penetrated the blood-labyrinth barrier (BLB) and then reached the organ of Corti, although some methamphetamine took a route to the inner ear via the cerebrospinal fluid. The pharmacological effect of methamphetamine on the cochlea was excitation of the sensory cells, the afferent nerve fibers connecting to them, and the spiral ganglion cells.

モルモット1匹あたり10mg/kgのメタンフェタミンを腹腔内注射し, 同剤が聴覚系に及ぼす影響をプライエル反射域値測定器やABRを用いて測定した。 この結果, プライエル反射域値は薬剤投与後30分, 60分で有意に低下した。 一方, ABRについては, 薬剤投与後ABRのI, II, IV波潜時は240分まで, III波潜時は180分までに有意に短縮し, 波間潜時についてもほぼ同様の傾向を示した。 しかし, 振幅や域値については, 薬剤投与前後で変化がみられなかった。 以上より, メタンフェタミンは聴覚伝導路全搬において, 潜時を短縮させる作用をもつことが判明した。

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.

The influence of neonatal deafness on cochlear electrically evoked Fos expression in the auditory brainstem was examined. Newborn rats were deafened by systemic injection of kanamycin, 1 mg/g daily for 12 days. At 4, 5, 6 or 8 weeks of age, these animals received cochlear electrical stimulation with a basal monopolar electrode for 90 minutes. Age-matched untreated control animals received similar stimulation. Experimental and control animals were assessed for spiral ganglion cell densities and Fos immunoreactive staining in the central nucleus of the inferior colliculus. Spiral ganglion cell assessments showed significant decreases in spiral ganglion cell densities in deafened rats compared to age-matched controls, at 5 weeks of age in lower turns and 6 and 8 weeks in all turns. Cochlear electrical stimulation induced Fos immunoreactive staining in the nucleus of auditory brain stem neurons in treatment and control groups. A significantly greater number of Fos immunoreactive neurons was found in the contralateral central nucleus of inferior colliculus in 5, 6 and 8 week old deafened animals compared to age-matched controls. The increases were larger with a longer duration of deafness. These results suggest that there are changes in auditory processing as a consequence of neonatal 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 1.5× threshold evoked fewer Fos IR cells in 21 day deafened animals compared to normal hearing animals. At 5× 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 5× 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.

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.

Four series of experiments were performed to evaluate the effects of methamphetamine on the auditory system of guinea pigs. Methamphetamine was administered to guinea pigs via intraperitoneal injection, and the time course of latencies of waves I, II, III, and IV, interpeak latencies of waves I-III, III-IV, and I-IV of the ABR, and the near-field potential of the inferior colliculus and cochlear nerve were measured. These physiological data were analyzed in comparison with the distribution of methamphetamine in the inferior colliculus and cochlea following its immunohistochemical staining, as well as the serum methamphetamine concentration. The following results were obtained; 1. The wave latencies and interpeak latencies of ABR decreased up to 120 minutes after the administration. 2. In the cochlear nerve recording, the amplitude of the response increased and the latency decreased up to 90 minutes after the administration. These changes in responses were, however more prominent in the inferior colliculus recording. 3. Immunohistochemical examination revealed that methamphetamine was present in the hair cells of the organ of Corti, spiral ligament, spiral ganglion cells and the inferior colliculus 30 minutes after the administration. 4. The serum concentration of methamphetamine rapidly reached its maximal level, and then dropped gradually, logarithmically, having become almost horizontal at a low level 6 hours later. These results suggest that methamphetamine does exert an effect on the peripheral auditory system, as well as on the central nervous system, which is generally regarded as the effector organ. It is assumed that the pharmacological effect of methamphetamine on the cochlea involves excitation of sensory cells, afferent nerve fibers and spiral ganglion cells.