The Effect Of Transcranial Magnetic Stimulation On Neurological Function, Brain Plastic Substance And Structure In Cerebral Infarction Rats

PartⅠObjective: To investigate the effect and its underlying mechanism oflong-term transcranial magnetic stimulation (TMS) on the recovery ofneurological function.Methods: A TMS group and a sham TMS group composed of 6 rats eachwere administered with 2 sessions of TMS (200 pulses) and sham TMS daily,respectively, in 3 weeks from the 2nd day after the rats were performed theright middle cerebral artery occlusion for 120 min followed by reperfusion(MCAO/R). The recovery of neurological function were detected 1d,3d,7d, 14d and 21d after MCA0/R, meanwhile the potentials of motor evokedpotential (MEP) in left limb were detected before MCA0/R and 7d,21 d afterMCA0/R.Results: At the 7th and 14th day after treatment, neurological deficit scores ofTMS group showed a significant decrease compared with that of the shamTMS group (P＜0.05). After operations the latencies of MEP increased and theamplitudes of MEP decreased,and gradually decreased and increased on 7thday after treatment in two groups, and there was no significantdifference(P＞0.05). The latencies of MEP in TMS group decreased faster andthe amplitudes of MEP in this group also increased faster on 21th day aftertreatment. Compared with the postinjury level, the latencies of MEP inforward limbs and hind limbs respectively decreased 0.49ms and 0.67ms in TMS group and decreased 0.35 ms and 0.44ms in sham TMS group, theamplitudes of MEP in forward limbs and hind limbs respectively increased5.82mv and 8.82mv in TMS group and increased 5.52mv and 5.53mv in shamTMS group. There was also no significant difference between twogroups(P＞0.05). But compared with the preinjury level, the latencies of MEPwere little shorter in TMS group and longer in sham TMS group,theamplitudes of MEP were higher in TMS and sham TMS group except lowerin hindlimb of sham TMS group.Conclusions: The long-term TMS had some effects of promoting therecovery of neurological function, the level of MEP of paralytic limb canprovide information for neurological function.PartⅡObjective: To investigate the effect and its underlying mechanism oflong-term transcranial magnetic stimulation (TMS) on the brain plasticsubstance and brain structure in rats with cerebral infarction.Methods: A TMS group and a sham TMS group composed of 32 rats eachwere administered with 2 sessions of TMS (200 pulses) and sham TMS daily,respectively, in 3 weeks from the 2nd day after the rats were performed theright middle cerebral artery occlusion for 120 min followed by reperfusion(MCAO/R). The expressions of SY38 and NFP-200 positive cells weredetected 1d 3d, 7d, 14d and 21d after MCA0/R. Ultrastructures of bloodvessells, neurocytes, synapsis in the ischemic penumbra cortex area wereassessed morphologically by transmission electron microscope. Results: The expressions of SY38,NFP-200 down regulated remarkably in theboundary zone of the infarcts in sham TMS group and TMS group on 1st dayafter MCAO, reached their lowest level on 3rd day, and slightly increased on7th day. Compared with normal group,SY38,NFP-200 immunoreactivitiesincreased on 14th day and 21st day after MCAO/R in the boundary zone ofthe infarcts in TMS group(P＜0.05). The expressions of SY38,NFP-200 wereremarkably higher in TMS group than sham TMS group on 14th day and 21stday respectively(P＜0.05). Transmission electron microscope showed that theextent of ischemic and engorgement in chondrosome were slighter,ultrastructures arounded blood vessells were integrity in the TMS group.Compared with the sham TMS group,the synaptic curvatures andpost—synaptic densities(PSD)were increased, and the widthes of synapticclefts were narrower in the TMS group. Conclusions: The long-term TMScould upregulate the experssions of SY38 and NFP-200, lessen theimpairments of blood vessells and nervous tissue, change synapticultrastructures and increase synaptic plasticity and function in the ischemicpenumbra cortex areas in rats with cerebral infarction.TMS may haveprotective effect on the cerebral infarction rats.