Abstract：
Treatment-resistant depression (TRD) is defined as patients diagnosed with depression having a history of failure with different antidepressants with an adequate dosage and treatment duration. The NMDA receptor antagonist ketamine rapidly reduces depressive symptoms in TRD. We examined neural correlates of treatment response to ketamine in TRD through a systematic review of brain magnetic resonance imaging (MRI) studies. A comprehensive search in PubMed was performed using \"ketamine AND depression AND magnetic resonance.\" The time span for the database queries was \"Start date: 2018/01/01; End date: 2024/05/31.\" Total 41 original articles comprising 1,396 TRD and 587 healthy controls (HC) were included. Diagnosis of depression was made using the Structured Clinical Interview for DSM Disorders (SCID), the Mini-International Neuropsychiatric Interview (MINI), and/or the clinical assessment by psychiatrists. Patients with affective psychotic disorders were excluded. Most studies applied ketamine [0.5mg/kg racemic ketamine and/or 0.25mg/kg S-ketamine] diluted in 60cc of normal saline via intravenous infusion over 40 min one time, four times, or six times spaced 2-3 days apart over 2 weeks. Clinical outcome was defined as either remission, response, and/or percentage changes of depressive symptoms. Brain MRI of the T2*-weighted imaging (resting-state or task performance), arterial spin labeling, diffusion weighted imaging, and T1-weighted imaging were acquired at baseline and mainly 1-3days after the ketamine administration. Only the study results replicated by ≥ 2 studies and were included in the default-mode, salience, fronto-parietal, subcortical, and limbic networks were regarded as meaningful. Putative brain-based markers of treatment response to ketamine in TRD were found in the structural/functional features of limbic (subgenual ACC, hippocampus, cingulum bundle-hippocampal portion; anhedonia/suicidal ideation), salience (dorsal ACC, insula, cingulum bundle-cingulate gyrus portion; thought rumination/suicidal ideation), fronto-parietal (dorsolateral prefrontal cortex, superior longitudinal fasciculus; anhedonia/suicidal ideation), default-mode (posterior cingulate cortex; thought rumination), and subcortical (striatum; anhedonia/thought rumination) networks. Brain features of limbic, salience, and fronto-parietal networks could be useful in predicting the TRD with better response to ketamine in relief of anhedonia, thought rumination, and suicidal ideation.
摘要：
难治性抑郁症（TRD）定义为被诊断患有抑郁症的患者，有使用不同剂量和治疗持续时间的抗抑郁药的失败史。NMDA受体拮抗剂氯胺酮迅速减轻TRD中的抑郁症状。我们通过对脑磁共振成像（MRI）研究的系统回顾，检查了TRD中氯胺酮治疗反应的神经相关性。使用“氯胺酮和抑郁症和磁共振”在PubMed中进行了全面搜索。\"数据库查询的时间跨度为\"开始日期：2018/01/01;结束日期：2024/05/31。“总共包括41篇原创文章，包括1396篇TRD和587例健康对照（HC）。抑郁症的诊断是使用DSM疾病的结构化临床访谈（SCID），迷你国际神经精神病学访谈（MINI），和/或精神科医生的临床评估。情感性精神障碍患者被排除在外。大多数研究应用氯胺酮[0.5mg/kg外消旋氯胺酮和/或0.25mg/kgS-氯胺酮]稀释在60cc生理盐水中，一次静脉输注40分钟，四次,或在2周内间隔2-3天六次。临床结果定义为缓解，回应,和/或抑郁症状的百分比变化。T2*加权成像的脑MRI（静息状态或任务表现），动脉自旋标记，弥散加权成像,和T1加权成像在基线和主要在氯胺酮给药后1-3天获得。只有≥2项研究复制的研究结果被纳入默认模式，显著性,额顶叶,皮质下,边缘网络被认为是有意义的。在边缘的结构/功能特征中发现了TRD中对氯胺酮的治疗反应的基于大脑的标志物（亚遗传ACC，海马体,扣带束-海马部分；快感缺失/自杀意念），显著性(背侧ACC，脑岛,扣带束回部分；思考/自杀意念），额顶叶（背外侧前额叶皮质，上纵束；快感缺失/自杀意念)，默认模式(后扣带回皮质；思维沉思)，和皮层下（纹状体；快感缺失/思考）网络。大脑边缘的特征，显著性,和额顶叶网络可用于预测TRD，对氯胺酮有更好的反应，以缓解快感缺乏症，沉思，和自杀意念。
