Objective:To observe the clinical effect of electroacupuncture(EA)for stroke with obstructive sleep apnea syndrome(OSAS).Methods:Thirty cases in conformity with the diagnostic criteria were selected and treated by EA....Objective:To observe the clinical effect of electroacupuncture(EA)for stroke with obstructive sleep apnea syndrome(OSAS).Methods:Thirty cases in conformity with the diagnostic criteria were selected and treated by EA.Before treatment and four weeks after treatment,nocturnal polysomnography,Epworth sleeping scale(ESS),National Institutes of Health stroke scale(NIHSS)were assessed.Two years after treatment,ESS was assessed and the relevant symptoms were examined.Results:Twenty-one cases completed the observation and 9 cases dropped out.In the 21 cases after treatment,apnea hyponea index(AHI)decreased obviously(P<0.05),and the lowest oxyhemoglobin saturation(SaO2)increased obviously in sleep(P<0.05)and ESS score decreased obviously(P<0.05).NIHSS score didn’t improve obviously(P>0.05).In the follow-up examination two years later,16 cases completed the observation and 5 cases dropped out.In the 16 cases,ESS score didn’t obviously improve in comparison of those before treatment and four weeks after treatment(both P>0.05).Conclusion:EA therapy for stroke with OSAS can reduce AHI,and enhance the lowest SaO2in sleep and improve the clinical symptoms of the patients.In the follow-up examinations two years after treatment,the long-term effect was not obvious.展开更多
Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8...Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8 and age-matched homologous normal aging mice（SAMR1） were adopted in this study. EA stimulation at Baihui（GV 20） and Yintang（EX-HN 3） was performed every other day for 12 weeks, 4 weeks as a course. Morris water maze test and Nissl-stained with cresyl violet were used for cognitive impairments evaluation and brain morphometric analysis. Amyloid-β（Aβ） expression in hippocampus and parietal cortex was detected by immunohistochemistry, and apoptosis was observed by TUNEL staining. Results： After 3 courses of EA preventive treatment, the escape latencies of 8-month-old SAMP8 mice in EA group were significantly shortened than those of un-pretreated SAMP8 mice. Compared with SAMR1 mice, extensive neuronal changes were visualized in the CA1 area of hippocampus in SAMP8 mice, while these pathological changes and attenuate cell loss in hippocampal CA1 area of SAMP8 mice markedly reduced after EA preventive treatment. Furthermore, Aβ expression in hippocampus and parietal cortex of SAMP8 mice decreased significantly after EA treatment, and neuronal apoptosis decreased as well. Conclusion： EA preventive treatment at GV 20 and EX-HN 3 might improve cognitive deficits and neuropathological changes in SAMP8 mice, which might be, at least in part, due to the effects of reducing brain neuronal damage, decreasing neuronal apoptosis and inhibiting Aβ-containing aggregates.展开更多
文摘Objective:To observe the clinical effect of electroacupuncture(EA)for stroke with obstructive sleep apnea syndrome(OSAS).Methods:Thirty cases in conformity with the diagnostic criteria were selected and treated by EA.Before treatment and four weeks after treatment,nocturnal polysomnography,Epworth sleeping scale(ESS),National Institutes of Health stroke scale(NIHSS)were assessed.Two years after treatment,ESS was assessed and the relevant symptoms were examined.Results:Twenty-one cases completed the observation and 9 cases dropped out.In the 21 cases after treatment,apnea hyponea index(AHI)decreased obviously(P<0.05),and the lowest oxyhemoglobin saturation(SaO2)increased obviously in sleep(P<0.05)and ESS score decreased obviously(P<0.05).NIHSS score didn’t improve obviously(P>0.05).In the follow-up examination two years later,16 cases completed the observation and 5 cases dropped out.In the 16 cases,ESS score didn’t obviously improve in comparison of those before treatment and four weeks after treatment(both P>0.05).Conclusion:EA therapy for stroke with OSAS can reduce AHI,and enhance the lowest SaO2in sleep and improve the clinical symptoms of the patients.In the follow-up examinations two years after treatment,the long-term effect was not obvious.
基金Supported by the National Natureal Science Foundation of China(No.30701121)
文摘Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8 and age-matched homologous normal aging mice（SAMR1） were adopted in this study. EA stimulation at Baihui（GV 20） and Yintang（EX-HN 3） was performed every other day for 12 weeks, 4 weeks as a course. Morris water maze test and Nissl-stained with cresyl violet were used for cognitive impairments evaluation and brain morphometric analysis. Amyloid-β（Aβ） expression in hippocampus and parietal cortex was detected by immunohistochemistry, and apoptosis was observed by TUNEL staining. Results： After 3 courses of EA preventive treatment, the escape latencies of 8-month-old SAMP8 mice in EA group were significantly shortened than those of un-pretreated SAMP8 mice. Compared with SAMR1 mice, extensive neuronal changes were visualized in the CA1 area of hippocampus in SAMP8 mice, while these pathological changes and attenuate cell loss in hippocampal CA1 area of SAMP8 mice markedly reduced after EA preventive treatment. Furthermore, Aβ expression in hippocampus and parietal cortex of SAMP8 mice decreased significantly after EA treatment, and neuronal apoptosis decreased as well. Conclusion： EA preventive treatment at GV 20 and EX-HN 3 might improve cognitive deficits and neuropathological changes in SAMP8 mice, which might be, at least in part, due to the effects of reducing brain neuronal damage, decreasing neuronal apoptosis and inhibiting Aβ-containing aggregates.
