Biomedical subjects
Publications and source records attributed to H Shibasaki.
Currently available evoked potential techniques can be applied in various combinations not just for supplementing diagnosis, classification and follow-up of myoclonus but also for investigating physiological mechanisms of various kinds of myoclonus.
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Slow negative potential preceding voluntary self-paced middle finger extension, as recorded from scalp electrodes by backward averaging technique, was absent in two patients with dyssynergia cerebellaris myoclonica (Ramsay Hunt syndrome); but present in two patients with cerebellar cortical degeneration. As the main pathological lesion in Ramsay Hunt syndrome is in the dentate nucleus and its efferent pathway, the present results are in conformity with the experimental finding that the premotor and motor cortices receive strong inputs from the cerebellar efferent system.
To demonstrate genetic susceptibility to Creutzfeldt-Jakob disease (CJD), 10 Japanese patients with pathologically proved CJD and 6 patients with clinically definite CJD were tissue typed for 48 class I and 14 class II human leukocyte antigen (HLA) specificities. The patients were scattered throughout Japan and there were no consanguineous relationships. Among 62 HLA specificities, HLA-DRw53 and DQw3 were found in all pathologically proved CJD cases. When the frequencies of the HLA antigens in the 16 CJD cases were compared to those of normal Japanese, a highly significant (p less than 0.005) increase was found for HLA-DQw3 in the CJD group. The present findings provide evidence for genetic control of susceptibility to CJD in humans.
We have recorded movement-related cortical potentials (MRCPs) to voluntary middle finger extension from 10 young and 10 old subjects free of neurological disease using the method of detecting EMG onset associated with each movement described by Barrett et al. (1985). The slow potential shifts preceding movement were measured by fitting a linear regression line to the wave forms to obtain a measure of their slope. Three separate potential shifts were identified. The first had a scalp distribution and onset latency similar to the Bereitschaftspotential (BP) first reported by Kornhuber and Deecke (1964, 1965). The potential shift immediately preceding movement corresponded with the NS' of Shibasaki et al. (1980). We identified, for the first time, a third shift intervening between BP and NS' and named it the intermediate shift (IS). The onset of BP occurred about 1.6 sec before EMG onset and was followed by IS which began about 875 msec before movement. The onset of NS' occurred 300 msec before EMG onset and terminated about 90 msec before this event. The slope of BP preceding right finger movement was steeper than that preceding left hand movement in all our right-handed subjects. The distribution of BP was symmetric about the midline. The IS potential shift had a slope which was steeper on the average preceding left finger movement than right. The distribution of IS was symmetric about the midline preceding left finger movement but had a contralateral tendency preceding right hand movement. NS' had a maximum slope at contralateral electrodes over the hand motor area and parietal areas. It was suggested that the BP potential shift originates in the supplementary motor area on the medial surface of the cerebral cortex. The differing distribution of the IS shift for the two hands suggests that this potential may be generated bilaterally preceding left finger movement but from the contralateral hemisphere only preceding movement of the right finger. The most likely origin of this potential was thought to be superior premotor cortex. NS' was considered to originate in primary motor cortex with possible contributions from other cortical areas associated with movement.
We have recorded movement-related cortical potentials (MRCPs) preceding voluntary finger extension from 10 subjects with Parkinson's disease and compared the results with those obtained from groups of young and old subjects described in the previous paper in this volume (Barrett et al. 1986). Three separate potential shifts preceding voluntary movement were identified in the wave forms of all subjects. There were no differences between the healthy aged subjects and those with Parkinson's disease in terms of the onset latencies or gradients of these potential shifts. The potential shift associated with the final phase of preparation (NS') was significantly less widespread over central scalp for the older subjects compared with the young. Equivalent results for a 35-year-old subject with Parkinson's disease were indistinguishable from those obtained from the young subjects suggesting that this restriction in the distribution of NS' is related to normal ageing rather than the disease process of parkinsonism. There were no differences within the group of parkinsonian subjects with respect to potential shifts associated with differing degrees of movement disability between the two hands. Our results contradict previous reports of abnormal MRCPs in Parkinson's disease (Deecke et al. 1977; Deecke and Kornhuber 1978; Shibasaki et al. 1978). We attribute this primarily to an improved method of recording MRCP which compensates for time jitter between EMG onset and the production of a trigger pulse for averaging (Barrett et al. 1985).
We have used a simple method to detect autoantibodies that react with extracellularly exposed antigenic determinants of acetylcholine receptor (AChR) of cultured rat muscle. Immunoglobulins from 30 patients with myasthenia gravis contained antibodies to detergent-solubilized AChR and bound to extracellularly exposed AChR. The antibody titer with solubilized rat AChR did not correlate with clinical severity, but ability of antibody to bind to extracellularly exposed AChR did correlate well and was also closely related to the acceleration of AChR degradation.
We report a case of chronic recurrent polymyositis associated with increasing antibody titers of coxsackievirus A9 in serum during clinical exacerbations. Muscle biopsy specimens showed pathologic changes consistent with chronic myositis, including perivascular mononuclear cell infiltration and hyalinization of muscle fibers with cytoplasmic vacuolations. The specific fluorescence was observed in the muscle fibers stained with antiserum for coxsackievirus A9. These findings indicate that this viral subtype as the etiologic agent in this case and virus plays a pathogenic role in some cases of chronic polymyositis.
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Fifty-five consecutive cases of myoclonus owing to various etiologies were studied by conventional EEG-EMG polygraphic recordings and/or jerk-locked or back averaging. The technique of back-averaging was shown to be useful not only for detecting EEG correlates of myoclonus that are not recognizable on the routine polygraph but also for investigating the temporal and topographic relationship between the EEG activities and myoclonus. Thirteen of 17 cases of PME and related disorders, in whom back-averaging and SEP were studied, were shown to have both a myoclonus-related cortical spike over the contralateral central area, preceding the myoclonus of an upper extremity by 6 to 22 msec, and a giant SEP accompanied by an enhanced C reflex. In these cases of "cortical reflex myoclonus," the myoclonus-related spike was similar to the P25-N33 components of the giant SEP in its wave form, scalp topography, temporal relationship to myoclonus or to C reflex, succeeding cortical excitability, and drug effect. All of this suggests participation of common physiological mechanisms in those two activities. In two cases of PME, in which myoclonus involved bilateral proximal muscles synchronously, the myoclonus-related spike was maximal near the vertex, and there was no giant SEP. The significance of this subgroup remains undetermined. In six cases of the PME group, back-averaging was inapplicable because of rare occurrence of myoclonus, but they showed a typical giant SEP accompanied by an enhanced C reflex. In CJD, back-averaging demonstrated a sharp wave or PSD over the contralateral hemisphere, preceding the myoclonus by 50 to 85 msec. This form of myoclonus seems to be subcortical in origin. In essential myoclonus and oculopalatal-somatic myoclonus, there was neither myoclonus-related cortical spike nor giant SEP. Electrical stimulation of the peripheral nerve at variable intervals after the myoclonus onset (jerk-locked-SEP paradigm) was shown to be useful for investigating the influence of myoclonus on cortical excitability.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
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The recording of movement-related cortical potentials (MRCP) relies on the use of EMG activity or some other index of movement as a trigger for averaging. EMG activity can vary considerably from one movement to the next, particularly in patients with movement disorders. This results in an MRCP formed from individual sweeps which are averaged with respect to differing periods during the EMG activity. We describe a computer-assisted method for identifying EMG onset associated with each movement made by the subject. The method allows the experimenter to reject trials associated with artefacts or with spurious trigger pulses produced by resting EMG activity. It is also possible to average the MRCP into categories associated with differing EMG characteristics such as EMG duration, peak EMG amplitude and the duration from EMG onset to peak. Using this method we have been able to record reliable MRCP from patients with movement disorders in whom this would otherwise have been technically impossible.