Abstract

Following large strokes that encompass the cerebral cortex, it has been suggested that the corticospinal tract originating from the non-ischaemic hemisphere reorganises its pattern of terminal arborisation within the spinal cord to compensate for loss of function. However many strokes in humans predominantly affect subcortical structures with minimal involvement of the cerebral cortex. The aim of the present study was to determine whether remodelling of corticospinal terminals arising from the non-ischaemic hemisphere was associated with spontaneous recovery in rats with subcortical infarcts. Rats were subjected to transient middle cerebral artery occlusion or sham surgery and 28 days later, when animals exhibited functional recovery, cholera toxin b subunit was injected into the contralesional, intact forelimb motor cortex in order to anterogradely label terminals within cervical spinal cord segments. Infarcts were limited to subcortical structures and resulted in partial loss of corticospinal tract axons from the ischaemic hemisphere. Quantitative analysis revealed there was no significant difference in the numbers of terminals on the contralesional side of the spinal grey matter between ischaemic and sham rats. The results indicate that significant remodelling of the corticospinal tract from the non-ischaemic hemisphere is not associated with functional recovery in animals with subcortical infarcts.

Highlights

  • Stroke is the leading cause of neurological disability in the adult population and while spontaneous recovery of neurological function can occur in some patients, improvement is often limited and many live with significant and permanent disability

  • The rats subjected to middle cerebral artery occlusion (MCAO) included in this this study exhibited subcortical infarcts and this was associated with loss of approximately 35% of corticospinal tract (CST) axons originating from the ischaemic hemisphere

  • Animals with MCAO recovered over time such that sensorimotor function had recovered to baseline levels at the time when spinal cord tissue was examined

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Summary

Introduction

Stroke is the leading cause of neurological disability in the adult population and while spontaneous recovery of neurological function can occur in some patients, improvement is often limited and many live with significant and permanent disability. Following permanent middle cerebral artery occlusion [6,7], destruction of the primary motor cortex [8] or unilateral pyramidotomy [9], corticospinal tract (CST) axons originating from the contralesional hemisphere have been reported to sprout into the denervated spinal grey matter. Blocking the neurite growth inhibitor Nogo-A after experimental stroke increases sprouting and improves performance in motor tasks [10] while knockdown of plasminogen reduces sprouting and impairs performance in motor tasks [11]

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