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Yoichi Katayama

Researcher at Nihon University

Publications -  447
Citations -  17664

Yoichi Katayama is an academic researcher from Nihon University. The author has contributed to research in topics: Deep brain stimulation & Stimulation. The author has an hindex of 59, co-authored 446 publications receiving 16839 citations. Previous affiliations of Yoichi Katayama include VCU Medical Center & University of California, Los Angeles.

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Journal ArticleDOI

Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury.

TL;DR: The data suggest that concussive brain injury causes a massive K+ flux which is likely to be related to an indiscriminate release of excitatory amino acids occurring immediately after brain injury.
Book ChapterDOI

Chronic Motor Cortex Stimulation for the Treatment of Central Pain

TL;DR: The effect of stimulation on pain and capability of producing muscle twitch disappeared simultaneously in these cases and the effect reappeared after the revisions, indicating that appropriate stimulation of the motor cortex is definitely necessary for obtaining satisfactory pain control in these patients.
Journal ArticleDOI

Dynamic changes in local cerebral glucose utilization following cerebral concussion in rats: evidence of a hyper- and subsequent hypometabolic state

TL;DR: Results indicate that, although not mechanically damaged from the insult, cells exposed to concussive injury dramatically alter their metabolic functioning, and this period of post-concussive metabolic dysfunction may delineate a period of time, following injury, during which cells are functionally compromised.
Journal ArticleDOI

Chronic motor cortex stimulation in patients with thalamic pain

TL;DR: While stimulation of the first- to third-order sensory neurons at the level of the thalamic relay nucleus or below cannot bring about good pain inhibition in patients withThalamic pain, activation of hypothetical fourth- order sensory neurons through precentral stimulation may be able to inhibit deafferented nociceptive neurons within the cortex.