Maladaptive plasticity for motor recovery after stroke: mechanisms and approaches

Abstract

Many studies in human and animal models have shown that neural plasticity compensates for the loss of motor function after stroke. However, neural plasticity concerning compensatory movement, activated ipsilateral motor projections and competitive interaction after stroke contributes to maladaptive plasticity, which negatively affects motor recovery. Compensatory movement on the less-affected side helps to perform self-sustaining activity but also creates an inappropriate movement pattern and ultimately limits the normal motor pattern. The activated ipsilateral motor projections after stroke are unable to sufficiently support the disruption of the corticospinal motor projections and induce the abnormal movement linked to poor motor ability. The competitive interaction between both hemispheres induces abnormal interhemispheric inhibition that weakens motor function in stroke patients. Moreover, widespread disinhibition increases the risk of competitive interaction between the hand and the proximal arm, which results in an incomplete motor recovery. To minimize this maladaptive plasticity, rehabilitation programs should be selected according to the motor impairment of stroke patients. Noninvasive brain stimulation might also be useful for correcting maladaptive plasticity after stroke. Here, we review the underlying mechanisms of maladaptive plasticity after stroke and propose rehabilitation approaches for appropriate cortical reorganization.

Figure 1

Maladaptive plasticity induced by disinhibition of motor-related areas in stroke patients. (a) Localized disinhibition in the ipsilesional primary motor cortex (M1). Localized disinhibition in the ipsilesional M1 promotes motor recovery by facilitating neural plasticity without competitive interaction between hand and proximal arm. (b) Widespread disinhibition in the ipsilesional M1 and premotor cortex (PMC). The disinhibition in the ipsilesional PMC causes uneven excitability distribution in the proximal arm and proximal-dominant competitive interaction in the ipsilesional M1 and PMC. As a result, this widespread disinhibition induces maladaptive plasticity that poorly controls the paretic hand in stroke patients.

Figure 2

Mechanism of motor function change after noninvasive brain stimulation (NIBS) in stroke patients. (a) Inhibitory NIBS over the unaffected hemisphere. Inhibitory NIBS decreases excitability of the contralesional motor cortex (M1) and increases excitability of the ipsilesional M1 by reducing interhemispheric inhibition from the unaffected to the affected hemisphere. Facilitation of the ipsilesional M1 improves motor function of the paretic hand in stroke patients. However, the antiphase bimanual movement deteriorates owing to the reduction of interhemispheric inhibition, which controls bimanual movement. (b) Bilateral NIBS. Excitatory NIBS along with inhibitory NIBS also decreases excitability of the contralesional M1, increases excitability of the ipsilesional M1, and improves motor function of the paretic hand in stroke patients. Bilateral NIBS lessens the reduction of interhemispheric inhibition induced by inhibitory NIBS and prevents deterioration of antiphase bimanual movement. Modified from Takeuchi et al. [88].