ABSTRACT
@#Constraint induced movement therapy (CIMT) is considered to be effective in restoring the impaired limb motor function in patients after stroke. CIMT enhanced neurogenesis in sub-ventricular zone and promoted the proliferation and long-term survival of the newborn neurons in the ischemic penumbra region. CIMT also enhanced the midline-crossing phenomenon, which means the midline crossing of the contralesional corticospinal tract originated nerve fibers to the denervated side in the cervical spinal cord. CIMT down-regulated the expression of Neurite outgrowth inhibitor-A (Nogo-A) as well as regulated other molecules to promote the growth of nerve fibers. In addition, CIMT ajusted the expression of brain- derived neurotrophic factor and Rho kinsase. Nevertheless, whether the structural plasticity caused by CIMT really participated in limb function remains unknown. And many studies on molecular mechanisms lack the evidence of necessary promotion and inhibition of the related molecule.
ABSTRACT
Constraint induced movement therapy (CIMT) is considered to be effective in restoring the impaired limb motor function in patients after stroke. CIMT enhanced neurogenesis in sub-ventricular zone and promoted the proliferation and long-term survival of the new-born neurons in the ischemic penumbra region. CIMT also enhanced the midline-crossing phenomenon, which means the midline crossing of the contralesional corticospinal tract originated nerve fibers to the denervated side in the cervical spinal cord. CIMT down-regulated the expression of Neurite outgrowth inhibitor-A (Nogo-A) as well as regulated other molecules to promote the growth of nerve fibers. In addi-tion, CIMT ajusted the expression of brain-derived neurotrophic factor and Rho kinsase. Nevertheless, whether the structural plasticity caused by CIMT really participated in limb function remains unknown. And many studies on molecular mechanisms lack the evidence of necessary promotion and inhibition of the related molecule.