Neurotransmitter changes in patients with Parkinson's disease detected by encephalofluctuograph

来源 :中国神经再生研究(英文版) | 被引量 : 0次 | 上传用户:xmy870129
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BACKGROUND: Encephalofluctuograph Technology (ET) is an advanced and non-traumatic analytical method of brain function. ET can acquire super-slow waves from electroencephalic signals. Studies have shown that these particular spectra can reflect neurochemical processes in the brain. OBJECTIVE: To verify neurotransmitter changes in the brains Parkinson's disease (PD) patients through the use of ET. DESIGN, TIME AND SETTING: A non-randomized concurrent control experiment was performed at the Department of Neurology in Southern Building, General Hospital of Chinese PLA from August to December 2007. PARTICIPANTS: Sixty-one outpatients with PD were selected from the General Hospital of Chinese PLA from August 2007 to December 2007. In addition, 48 healthy subjects were selected as normal controls. METHODS: All patients underwent assessment of the sub scale Ⅱ,Ⅲ, and V of the Unified Parkinson's Disease Rating Scale (UPDRS), in which part Ⅱ was used to inform activity of daily living, part Ⅲ reflected athletic ability, and part Ⅴ was the Hoehn & Yahr grade for symptoms evaluation. Correlation analysis was performed between dopamine levels and UPDRS assessment. Neurotransmitter changes were observed forty-eight prior to and 1.5 hours after medicating with Benserazide. The S1, S2, S4, S5,S7, and S11 spectras respectively reflect gamma-aminobutyric acid (GABA), glutamic acid (Glu), 5-hydroxytryptamine (5-HT), acetylcholine (ACh), norepinephrine, and dopamine. MAIN OUTCOME MEASURES: Neurotransmitter changes in the brains of all subjects, and correlations between dopamine concentrations and UPDRS assessment. Neurotransmitter changes in a subgroup of patients prior to and 1.5 hours after medicating with Benserazide. RESULTS: Concentrations of 5-HT, ACh, and norepinephrine were decreased in the PD group, and GABA was increased. However, there was no significant difference compared with the normal control group (P > 0.05). The level of dopamine in PD group was significantly lower than that in the control group (P < 0.01 ). Dopamine concentrations in PD patients negatively correlated with UPDRS scores and the Hoehn &Yahr grade range (r = -0.4601, -0.4301, P < 0.01 ). Dopamine levels increased significantly in PD patients 1.5 hours after medicating with Benserazide compared with before (P < 0.01). CONCLUSION: Detection by ET demonstrated that dopamine concentrations were significantly decreased in the brains of PD patients, as well as played a role in the course of pathogenesis and therapy. These results provided useful information for future non-traumatic of PD.
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