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 adaptive sensory shift likely not only
supports the adaptive contralesional control of volitional movement that is associated with the expression of the
flexion synergy (Aim 1), but also affects 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 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, facilitating motor
recovery in more impaired individuals.
