ABSTRACT
Spinal cord injury can lead to varied degrees of sensory and motor dysfunction, with high incidence, high disability rate and high cost, causing a huge burden on the patient's family and society. The researches on spinal cord injury have received much attention from all sectors of society. At present, drug therapy is the main treatment for spinal cord injury, and the clinical application of non-pharmacological treatments is still controversial. In recent years, with the deepening of the research on spinal cord injury, the application of electrical stimulation in the treatment of spinal cord injury has made some progress. The author reviews the electrical stimulation, brain stimulation, magnetic stimulation of spinal cord injury, so as to provide reference for the clinical treatment of spinal cord injury.
ABSTRACT
Spinal cord injury can lead to varied degrees of sensory and motor dysfunction,with high incidence,high disability rate and high cost,causing a huge burden on the patient's family and society.The researches on spinal cord injury have received much attention from all sectors of society.At present,drug therapy is the main treatment for spinal cord injury,and the clinical application of nonpharmacological treatments is still controversial.In recent years,with the deepening of the research on spinal cord injury,the application of electrical stimulation in the treatment of spinal cord injury has made some progress.The author reviews the electrical stimulation,brain stimulation,magnetic stimulation of spinal cord injury,so as to provide reference for the clinical treatment of spinal cord injury.
ABSTRACT
OBJECTIVE: To evaluate the effects of continuous epidural electrical stimulation (ES) on the behavioral recovery, and the molecular proliferation of synapse and neural cell in rats with photothrombotic stroke. METHOD: The male Sprague-Dawley rats were pre-trained on a single pellet reaching task (SPRT), and then received the photothrombotic infarction on dominant sensorimotor cortex (SMC) and implantation of electrode over the peri-lesion SMC surface. All rats were randomly assigned to one of two groups: anodal ES on infarcted SMC (ES group) and no ES on infarcted SMC (control group). Rats received daily SPRT and neurological examinations for 14 days. After the rats had been sacrificed, brain sections were immunostained for quantification of infarct volumes and evaluation of the structural remodeling markers (MAP2, synaptophysin and GFAP). RESULTS: The functional improvement of SPRT was significantly increased in the ES group compared to control group. There were no significant group differences in the infarct volumes, neurological examinations, structural remodeling markers. But, in the ES group, MAP2 and synaptophysin in affected peri-infarct area tended to increase compared with unaffected hemisphere. In affected hemisphere of ES group, many structural remodeling markers tended to increase compared with unaffected hemisphere. Especially, the staining of synaptophysin and GFAP in peri-infarct area showed more increased uptake than unaffected hemisphere in ES group and control group, respectively (p<0.05). CONCLUSION: The ES improved greatly the behavioral motor function after SMC infarction and induced the significant synaptogenesis with the widespread neuronal proliferation in peri-infarct area. Postischemic astrogliosis was not remarkable in ES group.