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Lesion-induced and training-induced brain reorganization
J Liepert1, F Hamzei, C Weiller
1Department of Neurology, University Hospital Eppendorf, D-20246 Hamburg, Germany. liepert@uke.uni-hamburg.de
Restorative Neurology and Neuroscience
|October 27, 2004
Summary
Stroke lesions alter motor cortex excitability. Central somatosensory lesions decrease inhibition, while cerebellar lesions affect facilitation and increase inhibition. Constraint-induced movement therapy (CIMT) modifies excitability, particularly in the affected hemisphere.
Area of Science:
- Neuroscience
- Rehabilitation Medicine
- Neurology
Background:
- Stroke can significantly alter motor cortex excitability.
- Understanding how different brain lesions impact motor control is crucial for effective rehabilitation.
- Investigating the effects of therapies like Constraint-induced movement therapy (CIMT) on motor excitability is essential.
Purpose of the Study:
- To determine if specific ischemic brain lesions are associated with distinct patterns of motor cortex excitability changes.
- To investigate the impact of rehabilitative therapy, specifically CIMT, on motor cortex excitability in stroke patients.
Main Methods:
- Utilized transcranial magnetic stimulation (TMS) techniques to assess motor cortex excitability.
- Employed functional magnetic resonance imaging (fMRI) to evaluate brain activity changes.
- Studied stroke patients with lesions in the central somatosensory system, cerebellum, and those undergoing CIMT.
Main Results:
- Lesions in the primary somatosensory cortex or thalamus decreased intracortical inhibition.
- Cerebellar lesions led to a loss of intracortical facilitation and increased inhibition.
- CIMT resulted in altered intracortical inhibition, predominantly in the affected hemisphere, with reduced cortical activation post-therapy.
Conclusions:
- Central somatosensory pathways exert an inhibitory influence on the motor cortex.
- The cerebellum normally provides a facilitatory influence on motor cortex excitability.
- CIMT induces significant changes in intracortical excitability, primarily within the hemisphere affected by the stroke.