Increased anterior cingulate cortical activity in response to fearful faces: a neurophysiological biomarker that predicts rapid antidepressant response to ketamine.
Increased anterior cingulate cortical activity in response to fearful faces: a neurophysiological biomarker that predicts rapid antidepressant response to ketamine.
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DOI：
10.1016/j.biopsych.2008.08.014
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发表时间：
2009-02-15
影响因子：
10.6
通讯作者：
Manji, Husseini K.
中科院分区：
文献类型：
--
作者：
Salvadore, Giacomo;Cornwell, Brian R.;Colon-Rosario, Veronica;Coppola, Richard;Grillon, Christian;Zarate, Carlos A., Jr.;Manji, Husseini K.
关键词：
大多数患有严重抑郁障碍(MDD)的患者在试图寻找最佳的抗抑郁药物治疗时都会经历一段漫长的反复试错期；识别可以预测抗抑郁药物治疗反应的生物标志物将是巨大的好处。我们验证了治疗前扣带回(ACC)活性可能是氯胺酮快速抗抑郁药物反应的假定生物标志物的假设，这与先前调查传统抗抑郁药物效果的发现一致。我们还研究了与健康受试者观察到的正常习惯相比，快速呈现恐惧面孔的ACC活动模式。我们通过快速呈现恐惧面孔，在无药物的MDD患者(N=11)和健康对照组(N=11)中诱发ACC活性，这是一种已知激活ACC嘴区域的范式。空间滤波分析是在脑磁图(MEG)记录上进行的，它提供了必要的时间精度来估计由于刺激的快速呈现而引起的ACC活动。患者和对照组只获得了一次脑磁图记录。随后，患者接受了单次氯胺酮输注，然后在四小时后评估抑郁症状。尽管健康受试者在反复暴露后，其吻侧ACC的神经磁活性降低，但MDD患者在治疗前ACC活性显著增加。值得注意的是，这种增加与随后对氯胺酮的快速抗抑郁反应呈正相关。探索性分析显示，治疗前杏仁核活动与抑郁症状的改变呈负相关。治疗前，嘴端ACC的激活可能是一个有用的生物标志物，可以识别对氯胺酮的抗抑郁作用有良好反应的患者亚群。
Most patients with major depressive disorder (MDD) experience a period of lengthy trial-and-error when trying to find optimal antidepressant treatment; identifying biomarkers that could predict response to antidepressant treatment would be of enormous benefit. We tested the hypothesis that pre-treatment anterior cingulate (ACC) activity could be a putative biomarker of rapid antidepressant response to ketamine, in line with previous findings that investigated the effects of conventional antidepressants. We also investigated patterns of ACC activity to rapid presentation of fearful faces compared to the normal habituation observed in healthy subjects. We elicited ACC activity in drug-free patients with MDD (N=11) and healthy controls (N=11) by rapidly presenting fearful faces, a paradigm known to activate rostral regions of the ACC. Spatial-filtering analyses were performed on magnetoencephalographic (MEG) recordings, which offer the temporal precision necessary to estimate ACC activity elicited by the rapid presentation of stimuli. MEG recordings were obtained only once for both patients and controls. Patients were subsequently administered a single ketamine infusion followed by assessment of depressive symptoms four hours later. Although healthy subjects had decreased neuromagnetic activity in the rostral ACC across repeated exposures, patients with MDD showed robust increases in pretreatment ACC activity. Notably, this increase was positively correlated with subsequent rapid antidepressant response to ketamine. Exploratory analyses showed that pretreatment amygdala activity was negatively correlated with change in depressive symptoms. Pretreatment rostral ACC activation may be a useful biomarker that identifies a subgroup of patients who will respond favorably to ketamine’s antidepressant effects.
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