Treatment response in late-onset depression: relationship to neuropsychological, neuroradiological and vascular risk factors
Treatment response in late-onset depression: relationship to neuropsychological, neuroradiological and vascular risk factors
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DOI：
10.1017/s0033291703008870
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发表时间：
2004-01-01
影响因子：
6.9
通讯作者：
Burns, A
中科院分区：
文献类型：
--
作者：
Baldwin, R;Jeffries, S;Burns, A
背景晚发性抑郁症与白色物质损害和神经心理缺陷有关，在一些研究中，这些与抑郁症的不良结局有关。一些白色病变可能起源于血管。本研究探讨了抗抑郁药单药治疗的反应或无反应与神经心理功能、脑结构测量和血管因素的关系。这是一项病例对照研究。将50例迟发性重性抑郁症患者（29例抗抑郁药单药治疗有效，21例无效）与35例非抑郁对照组进行比较。测量包括血管危险因素评估、神经心理测试和磁共振成像（MRI）扫描。在评估时调整抑郁情绪和药物治疗后，与对照组相比，两个患者组在涉及立即或延迟回忆的言语学习任务上有更大的障碍。对抗抑郁药单药治疗无反应的患者在涉及视觉空间能力、语言、单词识别和执行功能测试的测试中的表现明显低于对照组，而对照组受试者和反应者之间没有差异。在两项执行功能测试（语言流畅性和Stroop测试）中，无应答者的得分明显低于应答者。与对照组相比，除了无应答者的脑室周围高信号评分较高外，萎缩或白色病变的MRI测量值无显著组间差异。两组间血管疾病的测量结果无差异。这些结果支持了新出现的证据，即迟发性抑郁症对治疗的抵抗可能与执行功能受损有关。可能涉及微妙的脑血管机制。
Background. Late-onset depressive disorder is associated with white matter lesions and neuropsychological deficits that in some studies are linked to a poorer outcome for depression. Some white matter lesions may be vascular in origin. This study investigated the relationship between response or non-response to antidepressant monotherapy and neuro-psychological function, structural brain measures and vascular factors.Method. This was a case-control study. Fifty patients with late-onset major depressive disorder (29 who were responders to antidepressant monotherapy and 21 who were not) were compared with 35 non-depressed control subjects. Measures included assessment of vascular risk factors, neuro-psychological testing and a magnetic resonance imaging (MRI) scan.Results. After adjustment for depressed mood and medication at evaluation, both patient groups had significantly more impairment compared to control subjects on verbal learning tasks involving immediate or delayed recall. Patients who did not respond to antidepressant monotherapy had significantly poorer performance than controls on tests involving visuospatial ability, language, word recognition and tests of executive function, whereas there were no differences between control subjects and responders. On two tests of executive function (verbal fluency and the Stroop test) non-responders scored significantly worse than responders. There were no significant group differences on MRI measures of atrophy or of white matter lesions apart from a higher periventricular hyper-intensity score in non-responders compared to controls. There were no group differences on measures of vascular disease.Conclusion. The results lend support to the emerging evidence that resistance to treatment in late-onset depression may be associated with impaired executive function. Subtle cerebrovascular mechanisms may be involved.