Alizadeh Narges Shams, Maroufi Azad, Jamshidi Mehnoosh, Hassanzadeh Kambiz, Gharibi Fardin, Ghaderi Ebrahim
*Department of Psychiatry, Social Determinants of Health Research Center; †Department of Psychiatry, ‡Department of Physiology and Pharmacology, §Health Management Deputy of Research, and ∥Social Determinants of Health Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Clin Neuropharmacol. 2015 Nov-Dec;38(6):236-40. doi: 10.1097/WNF.0000000000000109.
Various strategies such as adding cholinesterase inhibitors are used to reduce cognitive impairments during electroconvulsive therapy. In this study, we aimed to assess the effectiveness and safety of memantine as an N-methyl-D-aspartate receptor antagonist in the prevention of cognitive deficits due to ECT.
Thirty-eight adult patients with various mental disorders were randomized to memantine (10 mg/day initially and 20 mg/day at the end of the first week) or placebo during the ECT period. Mini Mental Status Examination, Digit Span Subtest, and backward memory span of Wechsler Adult Intelligence Scale were used to assess the cognitive functions 24 hours before and after ECT. Subjective ratings of side effects were obtained in the first, second, and fourth week of the treatment.
The mean Mini Mental Status Examination score relatively increased in the intervention group showing a significant improvement with memantine (P < 0.001). The direct digit span had decreased in the control group, whereas no significant change was observed in the intervention group (P < 0.001). Backward memory span test showed a decrease in the control group after the ECT sessions, whereas a relative increase was observed in the intervention group (P = 0.001). The most frequently reported side effects in the intervention group did not differ significantly from the control group.
This initial study showed that cognitive performance was enhanced in patients receiving memantine during ECT, indicating the possible role of the glutamatergic system in creating ECT-induced deficits. Larger long-term studies are necessary for understanding the role of the glutamatergic system in these disorders.
采用多种策略（如添加胆碱酯酶抑制剂）来减少电休克治疗期间的认知障碍。在本研究中，我们旨在评估美金刚作为N-甲基-D-天冬氨酸受体拮抗剂在预防电休克治疗所致认知缺陷方面的有效性和安全性。
38例患有各种精神障碍的成年患者在接受电休克治疗期间被随机分为美金刚组（初始剂量为10毫克/天，第一周结束时为20毫克/天）或安慰剂组。在电休克治疗前后24小时，使用简易精神状态检查表、数字广度分测验和韦氏成人智力量表的逆向记忆广度来评估认知功能。在治疗的第一、第二和第四周获得副作用的主观评分。
干预组的简易精神状态检查表平均得分相对增加，表明美金刚有显著改善（P < 0.001）。对照组的直接数字广度下降，而干预组未观察到显著变化（P < 0.001）。逆向记忆广度测试显示，电休克治疗后对照组下降，而干预组相对增加（P = 0.001）。干预组最常报告的副作用与对照组无显著差异。
这项初步研究表明，在接受电休克治疗期间服用美金刚的患者认知表现得到增强，表明谷氨酸能系统在产生电休克治疗所致缺陷中可能发挥作用。需要进行更大规模的长期研究来了解谷氨酸能系统在这些疾病中的作用。
