Abstract

The human brain is capable of spontaneous recovery after stroke; this process can be accelerated and enhanced, provided that the appropriate treatments are undertaken in adequate amounts and at the right time. Ipsilateral motor cortex can modulate the plasticity of contralateral motor areas damaged by stroke.1 The paradigm for motor control therefore has shifted from strict cerebral localization to interactive functioning of cortical areas in both hemispheres, modulated by the changing balance of transcallosal inhibition. Following a stroke, ipsilesional interhemispheric transcallosal inhibition decreases, resulting in 1) the unveiling or recruitment of structurally preexisting but functionally silent ipsilateral motor pathways from the unaffected hemisphere; and 2) unopposed inhibition of surviving motor pathways in the affected hemisphere.2 The recruitment of ipsilateral motor pathways from the unaffected hemisphere at the expense of inhibition of motor pathways in the affected hemisphere does not always herald a good recovery. Ipsilateral motor pathways have additional synapses, low fiber density, and little output to upper limb muscles; a poor motor outcome is more often seen in stroke patients who recover by ipsilateral pathways compared with those recovering through perilesional motor …

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