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Comorbid Depression Is Associated with a Negative Treatment Response in Idiopathic REM Sleep Behavior Disorder

Authors
Sunwoo, JS | Kim, YJ | Byun, JI | Kim, TJ  | Jun, JS | Lee, ST | Jung, KH | Park, KI | Chu, K | Kim, M | Lee, SK | Kim, HJ | Schenck, CH | Jung, KY
Citation
Journal of clinical neurology (Seoul, Korea), 16(2). : 261-269, 2020
Journal Title
Journal of clinical neurology (Seoul, Korea)
ISSN
1738-65862005-5013
Abstract
BACKGROUND AND PURPOSE: The first-line medications for the symptomatic treatment of rapid eye movement sleep behavior disorder (RBD) are clonazepam and melatonin taken at bedtime. We aimed to identify the association between depression and treatment response in patients with idiopathic RBD (iRBD). METHODS: We reviewed the medical records of 123 consecutive patients (76 males; age, 66.0+/-7.7 years; and symptom duration, 4.1+/-4.0 years) with iRBD who were treated with clonazepam and/or melatonin. Clonazepam and melatonin were initially administered at 0.25-0.50 and 2 mg/day, respectively, at bedtime, and the doses were subsequently titrated according to the response of individual patients. Treatment response was defined according to the presence or absence of any improvement in dream-enacting behaviors or unpleasant dreams after treatment. RESULTS: Forty (32.5%) patients were treated with clonazepam, 56 (45.5%) with melatonin, and 27 (22.0%) with combination therapy. The doses of clonazepam and melatonin at followup were 0.5+/-0.3 and 2.3+/-0.7 mg, respectively. Ninety-six (78.0%) patients reported improvement in their RBD symptoms during a mean follow-up period of 17.7 months. After adjusting for potential confounders, depression was significantly associated with a negative treatment response (odds ratio=3.76, 95% confidence interval=1.15-12.32, p=0.029). CONCLUSIONS: We found that comorbid depression is significantly associated with a negative response to clonazepam and/or melatonin in patients with iRBD. Further research with larger numbers of patients is needed to verify our observations and to determine the clinical implications of comorbid depression in the pathophysiology of iRBD.
Keywords

DOI
10.3988/jcn.2020.16.2.261
PMID
32319243
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
Ajou Authors
김, 태준
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