BACKGROUND AND PURPOSE: The severity of functional deficits after a cortical infarction often does not correlate with lesion size. The stroke may affect pathways connecting to distant brain regions and therefore may also alter the function of remote parts of the cortex. Remote changes in electric activity, blood flow, and metabolism are called diaschisis. In the present study we addressed the question of whether in brain areas contralateral to a photochemically induced cortical infarction alteration of excitability can be observed as an indication of the effects of diaschisis. METHODS: We induced focal lesions in the sensory area at the border of the motor and occipital cortices by injecting the photosensitizing dye rose bengal and illuminating the skull stereotaxically. Seven days after induction of photothrombosis, electrophysiological recordings were obtained with standard methods from 400-microns-thick neocortical coronal slices. As an indication of inhibition we used a paired-pulse stimulus protocol and calculated a ratio of the amplitudes of the second versus the first excitatory postsynaptic potential. RESULTS: In lesioned animals we found a significant increase of the ratio over a wide zone of the neocortex, both ipsilateral and contralateral, compared with unlesioned animals. CONCLUSIONS: 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.
BACKGROUND AND PURPOSE: The severity of functional deficits after a cortical infarction often does not correlate with lesion size. The stroke may affect pathways connecting to distant brain regions and therefore may also alter the function of remote parts of the cortex. Remote changes in electric activity, blood flow, and metabolism are called diaschisis. In the present study we addressed the question of whether in brain areas contralateral to a photochemically induced cortical infarction alteration of excitability can be observed as an indication of the effects of diaschisis. METHODS: We induced focal lesions in the sensory area at the border of the motor and occipital cortices by injecting the photosensitizing dye rose bengal and illuminating the skull stereotaxically. Seven days after induction of photothrombosis, electrophysiological recordings were obtained with standard methods from 400-microns-thick neocortical coronal slices. As an indication of inhibition we used a paired-pulse stimulus protocol and calculated a ratio of the amplitudes of the second versus the first excitatory postsynaptic potential. RESULTS: In lesioned animals we found a significant increase of the ratio over a wide zone of the neocortex, both ipsilateral and contralateral, compared with unlesioned animals. CONCLUSIONS: 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.