Shift from unilateral to bilateral sensory-motor connectivity in chronic hemiparetic stroke

The emergence of abnormal movement synergies following a stroke presents a major limitation to the recovery of independent function by enslaving voluntary movements to stereotypical muscle coactivation patterns. 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 have found that abnormal movement synergies and spasticity are associated with the recruitment of contralesional descending cortico-bulbospinal pathways. However, how sensory systems might adapt 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 with abnormal movement synergies and spasticity, this sensory information is subsequently transferred to the contralesional hemisphere, a process that may support 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 post-stroke motor disorders. The results will lead to a novel understanding of post-stroke movement control by closing the sensorimotor loop, and thereby should provide a novel means by which to therapeutically manipulate the emergence and expression of upper limb motor impairments. 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 that contributes to the expression of flexion synergy (Aim 1), but also the transcortical loop of the stretch reflex that is related to the hyperactive stretch reflexes (or spasticity) and increased delays in 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 that 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. It should also provide a foundation to develop additional hypothesis-driven therapeutic rehabilitation strategies from a novel sensory or sensory-motor perspective to reduce post-stroke motor impairments.