Cummings J L
Department of Neurology, University of California, School of Medicine, Los Angeles.
Am J Psychiatry. 1992 Apr;149(4):443-54. doi: 10.1176/ajp.149.4.443.
The purpose of this review is to provide an update of the research regarding depression in Parkinson's disease and to synthesize the information into a neurobiological model relating the structural and biochemical changes in this disorder to the behavioral manifestations.
The author used a computer-based search of the literature, augmented by extensive bibliography-guided article reviews, to find information on depression and Parkinson's disease.
Depression occurs in approximately 40% of patients with Parkinson's disease; depression in Parkinson's disease is distinguished from other depressive disorders by greater anxiety and less self-punitive ideation. Lower CSF levels of 5-hydroxyindoleacetic acid, a past history of depression, and greater functional disability are associated with a greater risk of depression in Parkinson's disease. Female gender, early age at onset of Parkinson's disease, and greater left brain involvement may also be risk factors. Approximately half of depressed patients with Parkinson's disease meet criteria for major depressive episodes; half have dysthymia. Depression is more common in Parkinson's disease with prominent bradykinesia and gait instability than in tremor-dominant syndromes. Depressed patients with Parkinson's disease have greater frontal lobe dysfunction and greater involvement of dopaminergic and noradrenergic systems than nondepressed patients with the disease. Mood changes in Parkinson's disease respond to treatment with conventional tricyclic antidepressants or ECT.
Neurobiological investigations suggest that depression in Parkinson's disease may be mediated by dysfunction in mesocortical/prefrontal reward, motivational, and stress-response systems. Neuropsychological, metabolic, clinical, pharmacological, and anatomical studies support the involvement of frontal dopaminergic projections in patients with Parkinson's disease and depression.
本综述旨在更新有关帕金森病抑郁的研究,并将这些信息综合成一个神经生物学模型,将该疾病的结构和生化变化与行为表现联系起来。
作者通过计算机检索文献,并辅以广泛的参考文献引导的文章综述,以查找有关抑郁和帕金森病的信息。
约40%的帕金森病患者会出现抑郁;帕金森病所致抑郁与其他抑郁障碍的区别在于焦虑更严重,自罚观念更少。脑脊液中5-羟吲哚乙酸水平较低、有抑郁病史以及功能残疾程度较高与帕金森病患者发生抑郁的风险较高相关。女性、帕金森病发病年龄较早以及左脑受累程度较高也可能是风险因素。约一半的帕金森病抑郁患者符合重度抑郁发作的标准;另一半患有心境恶劣障碍。与以震颤为主的综合征相比,帕金森病伴明显运动迟缓及步态不稳时抑郁更为常见。与未患该病的非抑郁患者相比,帕金森病抑郁患者的额叶功能障碍更严重,多巴胺能和去甲肾上腺素能系统受累更明显。帕金森病的情绪变化对传统三环类抗抑郁药或电休克治疗有反应。
神经生物学研究表明,帕金森病抑郁可能由中皮质/前额叶奖赏、动机和应激反应系统功能障碍介导。神经心理学、代谢、临床、药理学和解剖学研究支持额叶多巴胺能投射参与帕金森病伴抑郁患者的发病过程。