Speaker
Zev Rymer, Ph.D.
Date
Location
SEC 204
Abstract
Muscular weakness in hemispheric stroke is a major clinical problem, often giving rise to severe motor impairment in contralesional limbs, and to continuing disability.
One widely accepted factor causing such weakness is the stroke-related interruption of corticospinal connections innervating relevant spinal motor networks. But that is not the only potential source of motor impairment. There are also disruptions in motor unit recruitment profiles and in motor unit firing rates mediated by spinal cord circuits, and there is also a progressive change in skeletal muscle structure and function.
The emergence of new motor unit recording techniques, single motor unit discrimination methods, and in the electrical and mechanical analyses of muscle properties, is helping us to probe these complex issues.
It appears that disruptions in motor unit regulation, together with changes in muscle architecture and mechanical properties, all make major contributions to clinical muscle weakness. These disruptions in muscle structure and in neural control will be reviewed, and their relative contributions to voluntary weakness will be analyzed and discussed.
One widely accepted factor causing such weakness is the stroke-related interruption of corticospinal connections innervating relevant spinal motor networks. But that is not the only potential source of motor impairment. There are also disruptions in motor unit recruitment profiles and in motor unit firing rates mediated by spinal cord circuits, and there is also a progressive change in skeletal muscle structure and function.
The emergence of new motor unit recording techniques, single motor unit discrimination methods, and in the electrical and mechanical analyses of muscle properties, is helping us to probe these complex issues.
It appears that disruptions in motor unit regulation, together with changes in muscle architecture and mechanical properties, all make major contributions to clinical muscle weakness. These disruptions in muscle structure and in neural control will be reviewed, and their relative contributions to voluntary weakness will be analyzed and discussed.