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Stroke results in irreversible brain damage, with the type and severity of symptoms dependent upon the location and the amount of injured brain tissue. The most common neurological impairment caused by stroke is partial weakness, called paresis, reflecting a reduced ability to voluntarily activate spinal motoneurons. In conjunction with the general reduced ability to voluntarily activate spinal motoneurons, there is often a reduced ability to selectively activate the spinal motoneuron pools, i.e. turning on some neurons while not turning on others. Together, these mechanisms result in altered movement control of many muscles, especially the contralesional hand and arm muscles used for grasping. Because of the altered muscle control, a variety of kinematic and kinetic alterations are observed during grasping in people with paresis post stroke. Impairments in grasping are related to the inability to use the hand for functional activities during daily life. In rare instances, stroke affects the posterior parietal lobe, resulting in distinct grasping deficits that are substantially different from grasping deficits seen after corticospinal system damage. Future studies investigating grasping post stroke could include the examination of both kinematic and kinetic aspects of grasping in the same subject samples, the examination of different types of grasping (e.g. palmar, precision), and the examination of different time points post stroke.
General information about stroke
Stroke is an acute neurological event that is caused by an alteration in blood flow to the brain.
This chapter explains how areas of the cerebral cortex and their descending pathways contribute to voluntary motor control in humans in the context of how these areas provide compensatory control for each other in the damaged brain. It reviews evidence that supports the current, more complex view of primary motor cortical (M1). The chapter discusses how the current view indicates that M1 is a flexible control system with an inherent capacity for plastic reorganization after brain injury. The non-primary motor cortical areas (NPMAs) are well-suited to provide compensatory control of voluntary movement after damage to M1. Motor control signals from M1 and the NPMAs travel to the spinal cord via several descending tracts. The corticospinal tract is the most direct pathway from the cerebral cortex to the spinal motoneurons. Finally, the chapter shows how spared territories and tracts might affect the capacity for functional recovery of movement.
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