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Absence of cortical reorganization following an internal capsule stroke in rodents

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Abstract Stroke is a leading cause of disability, causing chronic motor impairments in many survivors. Although recovery is correlated with cortical reorganization, the impact of lesion location on post-stroke reorganization is uncertain. We compared movement-related neural activity following experimental infarcts to the motor cortex (M1) or internal capsule in rats. Neural activity was recorded from motor and somatosensory regions during a skilled pellet retrieval task longitudinally during the course of recovery. Cortical lesions resulted in early behavioral recovery accompanied by widespread reductions in neural activity across ipsilesional regions, indicative of large-scale reorganization. In contrast, internal capsule lesions produced delayed recovery with no evidence of long-term ipsilesional cortical reorganization. These findings challenge the relevance of cortical reorganization for recovery from subcortical lesions and indicate that post-stroke recovery mechanisms are lesion-specific and that models targeting subcortical white matter are essential for maximizing translational relevance.
Title: Absence of cortical reorganization following an internal capsule stroke in rodents
Description:
Abstract Stroke is a leading cause of disability, causing chronic motor impairments in many survivors.
Although recovery is correlated with cortical reorganization, the impact of lesion location on post-stroke reorganization is uncertain.
We compared movement-related neural activity following experimental infarcts to the motor cortex (M1) or internal capsule in rats.
Neural activity was recorded from motor and somatosensory regions during a skilled pellet retrieval task longitudinally during the course of recovery.
Cortical lesions resulted in early behavioral recovery accompanied by widespread reductions in neural activity across ipsilesional regions, indicative of large-scale reorganization.
In contrast, internal capsule lesions produced delayed recovery with no evidence of long-term ipsilesional cortical reorganization.
These findings challenge the relevance of cortical reorganization for recovery from subcortical lesions and indicate that post-stroke recovery mechanisms are lesion-specific and that models targeting subcortical white matter are essential for maximizing translational relevance.

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