Kuhn W, Müller T, Gerlach M, Sofic E, Fuchs G, Heye N, Prautsch R, Przuntek H
Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Federal Republic of Germany.
J Neural Transm (Vienna). 1996;103(12):1441-5. doi: 10.1007/BF01271258.
Etiology of depression in Parkinson's disease (PD) is associated with serotonergic dysfunction. Previous studies, supporting this hypothesis, were performed on patients treated with antiparkinsonian drugs. To eliminate the influence of parkinsonian drug therapy and to elucidate significance of different biochemical pathways in PD associated with depression we determined levels of biogenic amines in cerebrospinal fluid (CSF) of 26 untreated "de novo" Parkinsonian patients.
Patients were scored with the Hamilton depression scale (HD) and subdivided into groups with HD score > or = 18 and HD score < 18. Diagnosis of depression was made according to DSM III R. Both groups were matched for age and motor disability.
In both groups no significant differences appeared between CSF levels of dopamine, noradrenaline, 3,4-dihydroxyphenylacetic acid, homovanillic acid, 3-methoxy-4-hydroxyphenylglycol and 5-hydroxyindole acetic acid, determined by high-performance liquid chromatography.
In contrast to previous studies on treated Parkinsonian patients no sign of altered serotonin metabolism especially in context with severity of depression in early stages of PD was found. Due to our results, we suggest, that biochemical markers of depression in CSF of PD may be influenced by antiparkinsonian therapy and that depression in PD may respond to serotonin reuptake inhibitors mainly in later stages of PD.
帕金森病(PD)中抑郁症的病因与血清素功能障碍有关。此前支持这一假说的研究是在接受抗帕金森病药物治疗的患者身上进行的。为了消除帕金森病药物治疗的影响,并阐明与PD相关的抑郁症中不同生化途径的意义,我们测定了26例未经治疗的“初发”帕金森病患者脑脊液(CSF)中生物胺的水平。
患者用汉密尔顿抑郁量表(HD)评分,并分为HD评分≥18分和HD评分<18分的组。根据《精神疾病诊断与统计手册》第三版修订版(DSM III R)进行抑郁症诊断。两组在年龄和运动障碍方面进行了匹配。
通过高效液相色谱法测定,两组脑脊液中多巴胺、去甲肾上腺素、3,4-二羟基苯乙酸、高香草酸、3-甲氧基-4-羟基苯乙二醇和5-羟吲哚乙酸的水平均无显著差异。
与之前对接受治疗的帕金森病患者的研究不同,未发现血清素代谢改变的迹象,尤其是在PD早期抑郁症严重程度方面。基于我们的研究结果,我们认为,PD患者脑脊液中抑郁症的生化标志物可能受抗帕金森病治疗的影响,并且PD患者的抑郁症可能主要在PD后期对血清素再摄取抑制剂有反应。