Vicarious Function of Remote Cortex following Stroke: Recent Evidence from Human and Animal Studies

Abstract

Following a lesion, the adult central nervous system undergoes dramatic structural and physiological reorganization in diverse subcortical and cortical areas. Our knowledge of the events that parallel recovery within the tissue surrounding the lesion and other distant cortical areas has evolved greatly in the past few years. Particularly, recent efforts have increased our understanding of the potential implication of premotor areas in recovery from lesions disturbing the primary motor cortex (M1) and its corticospinal outputs. Because these areas share extensive connections with M1 and have direct access to the spinal cord through corticospinal projections, they are particularly well positioned to take over the role of M1 in a vicarious manner and thus compensate for the neuronal loss resulting from M1 lesions. The impressive postlesional reorganization known to occur in many areas of the CNS including the premotor cortex traditionally has been assumed to play a beneficial role in recovery. However, recent experiments suggest that in some cases, reorganization of distant cortical areas correlates with poor recovery, raising the concept of maladaptive vicarious process. This concept might be particularly critical in the development of new treatment approaches favoring postlesion plasticity and even more so for interventions targeting specific area(s). Here, the author reviews human and animal studies that show the plastic potential of the adult CNS after stroke, highlighting the vicarious role of the premotor cortex in the recovery of motor control.

Stroke Induces Long-Lasting Deficits in the Temporal Fidelity of Sensory Processing in the Somatosensory Cortex

“…[13][14][15] In parallel with the reorganization of periinfarct cortex, brain regions more distant but functionally related to the site that was damaged, also show changes in activation patterns. [16][17][18][19][20] Collectively, these findings suggest that sensory deficits and their spontaneous recovery correlate with new patterns of functional brain activation in the damaged and undamaged hemisphere. Unfortunately though, the majority of previous imaging studies did not or could not adequately assess cortical responsiveness on millisecond timescale.…”

Can endocrine disruptors influence neuroplasticity in the aging brain?

“…Carmichael's (2006) review of post-stroke functional recovery treats the possible mechanisms by which new growth might occur. He chooses, as one example, axonal sprouting in nonhuman primates subjected to stroke Dancause, 2006) that connects premotor cortex to primary sensory cortex, far from the site of injury. One of the signals he cites as a means of recruiting migrating neuroblasts to the area of injury is the cytokine erythropoietin (EPO).…”

Correspondence between Altered Functional and Structural Connectivity in the Contralesional Sensorimotor Cortex after Unilateral Stroke in Rats: A Combined Resting-State Functional MRI and Manganese-Enhanced MRI Study

“…The poststroke increase in neuroanatomical and functional connectivity in the contralesional cortex may be brought about by remodeling of neuronal elements, i.e., axonal sprouting, synaptogenesis, and dendritic growth, which has been detected in various animal stroke models (reviewed in Nudo, 1999;Dancause, 2006). Similarly, in chronic human stroke patients, elevated activation responses to sensory stimulation of the unaffected hand have been found in an area of the contralesional somatosensory cortex with increased cortical thickness (Schaechter et al, 2006).…”

“…Task-or stimulus-induced functional imaging studies in stroke patients and animal models have provided evidence for shifts of activation patterns in ipsilesional and contralesional sensorimotor cortices in relation to sensorimotor recovery (Calautti and Baron, 2003;Dijkhuizen et al, 2003), which may be based on unmasking or strengthening of existing pathways and/or by formation of new connections (Nudo, 1999;Dancause, 2006). Resting-state functional magnetic resonance imaging (MRI) (rs-fMRI), which assesses the temporal correlation of spontaneous lowfrequency blood oxygenation level-dependent (BOLD) signals between brain areas as a measure of functional connectivity (Biswal et al, 1995), has recently showed that patients and rats with a unilateral infarction exhibit initial loss and subsequent restitution of interhemispheric functional connectivity, in parallel to changes in functional status (He et al, 2007;van Meer et al, 2010).…”