Therapies for depression in Parkinson's disease

Abstract

Background: Depression is one of the most common neuropsychiatric disturbances in Parkinson's disease. 40% of observed variation in quality of life is due to depression. However, there is little hard evidence of the efficacy and safety of antidepressant therapies in Parkinson's disease. Objectives: To assess the efficacy and safety of antidepressant therapies in idiopathic Parkinson's disease. Safety refers to both the direct side-effects of the therapy and also the therapy's interactions with the symptoms of Parkinson's disease and with the antiparkinsonian medications. Search methods: Relevant clinical trials were identified by electronic searches the Cochrane Controlled Trials Register (the Cochrane Library Issue 3, 2001), MEDLINE(1996-2001), EMBASE (1974-2001), PsychLit (1800's-2001), CINAHL (1982-2001) databases. The reference list of all trial reports and reviews were examined. Queries were sent out to all manufacturers and distributors of antidepressants within the UK requesting information on any relevant clinical trials. Selection criteria: Randomised controlled trials (RCT) examining licensed oral antidepressants, electroconvulsive therapy (ECT) or behavioural therapy in the treatment of depression in idiopathic Parkinson's disease. Data collection and analysis: Data was extracted and assessed independently by three of the authors. Disagreements were resolved by discussion. Main results: Three randomised controlled trials were found examining oral antidepressant medications in Parkinson's disease in a total of 106 patients. No eligible trials of ECT or behavioural therapy were found. In the first arm of the crossover trial by Andersen 1980 (n=22) patients in the nortriptyline group showed a larger improvement than placebo group in median depression score in a self-made 31-item depression rating scale after 16 weeks of treatment but statistical significance was not calculated. A parallel group trial by Wermuth 1998 (n=37) did not show any statistically significant difference between the citalopram and placebo groups in the Hamilton Depression Scale after 52 weeks of treatment. The third study by Rabey 1996 (n=47) was a randomised open-label trial to compare fluvoxamine versus amitriptyline. Similar numbers of patients in amitriptyline and fluvoxamine groups (60% vs 55%) had a 50% reduction of Hamilton score after 16 months of treatment. However, further assessment of this trial was not possible because only summary results were available from an abstract and attempts to contact the authors failed. Visual hallucinations or confusion had been reported in patients with fluvoxamine and amitriptyline. Otherwise, no other major side effects were found in the other two trials. Authors' conclusions: Insufficient data on the effectiveness and safety of any antidepressants therapies in Parkinson's disease are available on which to make recommendations for their use. Further large scale randomised controlled trials are urgently required in this area.