Our results suggest that a neocortical infarction leads to hyperexcitability not only in its direct vicinity but also in the contralateral hemisphere. Such hyperexcitability may contribute to increased activation of contralateral brain areas and to functional reorganization after stroke.

The effect of an ischaemic focal cortical lesion on the excitability of surrounding and remote brain areas was investigated. Infarcts were produced photothrombotically in rat frontal cortex and brain excitability was assessed by a extracellular paired-pulse stimulation in coronal slices 7 days later. The cortical lesions caused a reduction of inhibition. The extent and grade of these electrophysiological effects depended on the depth of the lesion: in animals with a lesion affecting the deeper cortical layers a pronounced transcortical diaschisis was found, whereas animals with a shallow lesion showed only a slight ipsilateral affliction. The study shows that focal lesions in the motor cortex cause widespread disinhibition, probably resulting from deafferentation, and these may have a significant impact on recovery of function.

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