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Motor cortex activation in hemiparetic stroke patients
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Little is known about the function of surviving motor cortex after hemiparetic stroke. Though the corticospinal tract may be damaged, function may persist via intact intracortical connections. We probed motor cortex function using paradigms unrelated to genesis of paretic limb movement. Seven patients with chronic post-stroke hemiparesis, including total hand plegia, were studied with functional MRI (fMRI). Brain activation was achieved by alternating between rest and one of several stimuli. For the plegic hand, stimuli were passive index finger movement, or viewing active movements; for the non-plegic hand, active or passive index finger movement. Brain activation maps (p<.001) were generated, after which anatomical landmarks were used to identify regions of interest within non-infarcted tissue. Tasks were rehearsed before fMRI, during which surface EMG leads were placed on 5 muscles in each arm. Patients were median 5 months post-stroke, median age 66 years. Median NIH stroke scale score was 9; Rankin, 3; and arm motor Fugl-Meyer score, 18 (normal=66); Motor Activity Log confirmed no plegic hand use. Studies with excess head movement were excluded, including all plegic hand tasks for 1 patient. Plegic hand tasks (10 studies across 6 patients) activated the stroke hemisphere in all patients, including primary motor cortex (5 patients), primary sensory cortex (5 patients), premotor cortex (4 patients), and supplementary motor area (3 patients). Non-stroke hemisphere was also activated, particularly primary motor cortex (5 patients). In a few instances, EMG disclosed paretic arm muscle activity, but this had no relationship to fMRI activation. Non-plegic hand tasks (9 studies across 7 patients) activated the stroke hemisphere ipsilaterally, including supplementary motor area in all 7 patients, and primary motor cortex in 6 patients. In patients with post-stroke hemiparesis, passive stimulation activates surviving motor cortex regions within the stroke-affected hemisphere. After corticospinal tract damage, motor cortex can still be activated during tasks unrelated to paretic limb movement. The results may suggest therapeutic avenues for improving motor function after stroke.
Ovid Technologies (Wolters Kluwer Health)
Title: Motor cortex activation in hemiparetic stroke patients
Description:
100
Little is known about the function of surviving motor cortex after hemiparetic stroke.
Though the corticospinal tract may be damaged, function may persist via intact intracortical connections.
We probed motor cortex function using paradigms unrelated to genesis of paretic limb movement.
Seven patients with chronic post-stroke hemiparesis, including total hand plegia, were studied with functional MRI (fMRI).
Brain activation was achieved by alternating between rest and one of several stimuli.
For the plegic hand, stimuli were passive index finger movement, or viewing active movements; for the non-plegic hand, active or passive index finger movement.
Brain activation maps (p<.
001) were generated, after which anatomical landmarks were used to identify regions of interest within non-infarcted tissue.
Tasks were rehearsed before fMRI, during which surface EMG leads were placed on 5 muscles in each arm.
Patients were median 5 months post-stroke, median age 66 years.
Median NIH stroke scale score was 9; Rankin, 3; and arm motor Fugl-Meyer score, 18 (normal=66); Motor Activity Log confirmed no plegic hand use.
Studies with excess head movement were excluded, including all plegic hand tasks for 1 patient.
Plegic hand tasks (10 studies across 6 patients) activated the stroke hemisphere in all patients, including primary motor cortex (5 patients), primary sensory cortex (5 patients), premotor cortex (4 patients), and supplementary motor area (3 patients).
Non-stroke hemisphere was also activated, particularly primary motor cortex (5 patients).
In a few instances, EMG disclosed paretic arm muscle activity, but this had no relationship to fMRI activation.
Non-plegic hand tasks (9 studies across 7 patients) activated the stroke hemisphere ipsilaterally, including supplementary motor area in all 7 patients, and primary motor cortex in 6 patients.
In patients with post-stroke hemiparesis, passive stimulation activates surviving motor cortex regions within the stroke-affected hemisphere.
After corticospinal tract damage, motor cortex can still be activated during tasks unrelated to paretic limb movement.
The results may suggest therapeutic avenues for improving motor function after stroke.
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