Shift from Unilateral to Bilateral Sensory-Motor Connectivity in Chronic Hemiparetic Stroke

点击翻译按钮获取中文摘要

Abstract. The emergence of abnormal movement synergies following a stroke presents a major limitation to the recovery of independent function by constraining voluntary movements to stereotypical muscle coactivation patterns. The resulting expression of the flexion synergy limits arm/hand function, like reaching and hand opening; and has also been reported to be linked to hyperactive stretch reflexes or spasticity. Previous studies found that flexion synergy and spasticity are associated with the recruitment of contralesional descending cortico- bulbospinal pathways. However, how the somatosensory system adapts to this change in the use of motor pathways and the role of adaptive sensory feedback to the abnormal motor control of the paretic arm remain largely unknown. The ascending sensory pathways that convey somatosensation from the paretic arm project contralaterally to the primary sensory cortex in the lesioned hemisphere. Our preliminary data, however, suggests that, in individuals that express the flexion synergy and spasticity, this sensory information is subsequently transferred to the contralesional hemisphere, a process that may support the manifestation of the abnormal movement patterns in hemiparetic stroke. The overall goal of the proposed research is to examine the pathophysiology of this maladaptive hemispheric somatosensory “shift” and its relationship to the upper limb motor impairments following a hemiparetic stroke. The results will lead to a greater understanding of abnormal limb synergies and spasticity by closing the sensorimotor loop, which should provide a novel means by which to therapeutically prevent and mitigate the emergence and expression of upper limb motor impairments, following a stroke. The proposed research aims to test the following key hypotheses in our specific aims: Following a unilateral motor stroke, a hemispheric shift in somatosensory processing provides sensory feedback to support the maladaptive hemispheric shift in the motor system. This hemispheric sensory shift not only influences volitional movement control which contributes to the expression of the flexion synergy (Aim 1), but also the transcortical loop of the stretch reflex that is related to the hyperactive stretch reflexes (or spasticity) and the increased onset delay of the long-latency stretch reflex (Aim 2). Furthermore, the hemispheric sensory shift, as a result of neuroplasticity in an injured brain, can occur in the absence of motor output; and this sensory shift can indicate the extent of motor deficits (Aim 3). By testing these hypotheses, the proposed research will improve our understanding of the role of sensory feedback in post-stroke motor impairments. This should allow for the determination of motor deficits from a new sensory perspective for more impaired individuals or acute/subacute patients who have difficulty performing motor tasks. Furthermore, the knowledge gained in this study will facilitate the future development of targeted, hypothesis-driven therapeutical interventions that aim at reducing maladaptive cross-hemispheric sensory-motor connectivity during recovery thus, promoting motor function without inducing abnormal synergy and spasticity impairments.