| Project/Area Number |
61570389
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Saga Medical School |
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Principal Investigator |
SHIBASAKI Hiroshi Department of Internal Medicine, Saga Medical School, 医学部, 助教授 (30037444)
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| Co-Investigator(Kenkyū-buntansha) |
NESHIGE Ryuji Department of Internal Mecicine, Saga Medical School, 医学部, 助手 (60172756)
KAKIGI Ryusuke Department of Internal Medicine, Saga Medical School, 医学部, 助手 (10145196)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1987: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1986: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Central motor control / Movement-related cortical potentials / Pre-movement slow negativity / Effect of aging / Parkinson's disease / Cerebellar ataxia / Cerebellar efferent system / 硬膜下電極 / 運動準備電位 / 小脳失調症,ラムゼーハント症侯群 |
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| Research Abstract |
Cortical potentials associated with self-paced voluntary middle finger extension were recorded from scalp electrodes in 10 healthy young and 10 healthy old subjects, 10 patients with with Parkinson's disease and 4 patients with cerebellar ataxia. Recording was also made from subdural electrodes in 7 patients with intractable epilepsy during the pre-operative investigation. The computer-assisted method for detecting the precise onset of EMG discharge that we have previously developed was employed. In addition to the two previously known negative slopes (Bereitschaftspotential; BP and negative slope; NS') before the movement onset, we identified a new slope (intermediate slope; IS) between the two. Based on the scalp distribution of each potential shift, BP,IS and NS'were postulated to be generated mainly in the supplementary motor cortex, premotor cortex and primary motor cortex, respectively. In old subjects, NS' was maximum at the midline whereas it was steeper over the contralateral
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central region in young subjects. Those negative slopes were normal in patients with Parkinson's disease; the scalp distribution of NS' was not different from that in healthy old subjects. The cortical slow negativity was absent in patients with dyssynergia cerebellaris myoclonica (Ramsay Hunt syndrome) whereas it was normal in patients with cortical cerebellar degeneration, suggesting a strong influence of the cerebellar efferent system on the motor cortices. BP was restricted to the subdural electrodes placed over the bilateral sensorimotor areas and the supplementary motor area, and NS' was localized to the contralateral sensorimotor area. We have also studied the physiological mechanism underlying stimulus-sensitive or reflex myoclonus. The study of scalp topography of cortical somatosensory evoked potentials (SEP) suggested that the giant SEP commonly observed in those patients with cortical reflex myoclonus resulted from a pathological enhancement of certain cortical components of the normal SEP. In patients with reflex myoclonus sensitive to flash stimulation, the reflex pathway was shown to involve cerebral cortex; mainly the frontal cortex but probably the occipital cortex as well. Less
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