Motor System Plasticity in Stroke Models

Abstract

Background and Purpose The natural response to disability in one limb is to learn new ways of using the other limb. This compensatory behavioral strategy after stroke has long been thought to contribute to persistent dysfunction in the paretic limb by encouraging its disuse. Our recent findings suggest that it goes beyond the encouragement of disuse to disrupt neural substrates of paretic limb functional improvements. Methods We overview recent findings from rodent models of chronic upper extremity impairments in which precise control and manipulation of forelimb experiences were used to understand bilateral and interhemispheric contributions to motor functional outcome. Results Skill learning with the less-affected (nonparetic) forelimb promotes neural plasticity in the contralesional motor cortex that subserves its function. At the same time, it exacerbates dysfunction and limits the efficacy of rehabilitative training in the paretic limb. The maladaptive effects of skill learning with the nonparetic forelimb are dependent on callosal connections and contralesional motor cortex, and linked with reduced neural activation of peri-infarct motor cortex during rehabilitative training. Conclusions These findings suggest that learning to rely on the nonparetic body side has the capacity to disrupt functionality in a region of the injured hemisphere that contributes to outcome of the paretic limb. Whether this effect generalizes across injury loci and functional modalities remains to be tested.

Recovery after brain injury: mechanisms and principles

“…As in other studies, the neuronal activation in the peri-infarct cortex was reduced (Jones et al, 2013). Motor cortex infarcts resulted in the somatosensory map to emerge in the undamaged motor cortex near the lesion.…”

Motor compensation and its effects on neural reorganization after stroke

“…This was revealed in studies that modelled the effects of learning to compensate with the non-paretic forelimb by training this limb daily in skilled reaching tasks, beginning between 4 days to 3 weeks after subtotal M1 infarcts 11,116 (FIG. 3).…”

“…Another reason to attend to compensation is that it is both a mechanism for improved function and a contributor to persisting impairment after CNS injury 8,10,11 . There is currently much interest in the potential to optimize functional outcome after CNS damage by capitalizing on early endogenous mechanisms of neural repair and remodelling after stroke, which are sensitive to behavioural manipulation and could facilitate the efficacy of motor rehabilitation 12–15 .…”

Early constraint-induced movement therapy promotes functional recovery and neuronal plasticity in a subcortical hemorrhage model rat

“…Because neurite outgrowth is accompanied by the formation of new synapses [1,45,46], we can infer that early CIMT also led to the creation of new synapses. However, we must also consider the possibility that early CIMT can down-regulate inhibitory factors such as the Nogo-A receptor or RhoA/Rho-associated kinase [27].…”