King's College London Institute of Psychiatry, DeCrespigny Park, London SE5 8AF, UK.
Neuroimage. 2010 Oct 15;53(1):58-64. doi: 10.1016/j.neuroimage.2010.05.069. Epub 2010 Jun 8.
Neuroimaging studies have demonstrated abnormalities in patients with bipolar disorder, including overactivity in anterior limbic structures in response to fearful or happy facial expressions. We investigated whether such anomalies might constitute heritable deviations underlying bipolar disorder, by virtue of being detectable in unaffected relatives carrying genetic liability for illness. Twenty patients with bipolar I disorder, twenty of their unaffected 1st degree relatives and twenty healthy volunteers participated in functional magnetic resonance imaging experiments of facial emotion processing. In one of these experiments, the participants watched faces expressing fear of varying intensities (moderate and high), intermixed with the non-emotional faces, and in another experiment - faces expressing moderate or high degrees of happiness intermixed with non-emotional faces. Repeated measures 2x3x3 ANOVA with emotion (fear and happy), intensity (neutral, moderate, and high) as within-subjects variables and group (patients, relatives, and controls) as between-subjects variable produced two clusters of differential activation, located in medial prefrontal cortex and left putamen. Activity in medial prefrontal cortex was greater in patients and in relatives compared with healthy volunteers in response to both fearful and happy faces. Activity in left putamen in response to moderate fear was greater in patients and in relatives compared with controls. Patients (but not relatives) showed also a greater activation in response to high intensity happy faces, compared with controls. Region of Interest analysis of amygdala activation showed increased activity in left amygdala in both patients and relatives groups in response to intensively happy faces. Exaggerated medial prefrontal cortical and subcortical (putamen and amygdala) responses to emotional signals may represent heritable neurobiological abnormalities underlying bipolar disorder.
神经影像学研究表明，双相情感障碍患者存在异常，包括在前边缘结构对恐惧或快乐面部表情的过度活跃。我们通过研究无病症的一级亲属是否携带疾病遗传易感性，来探讨这些异常是否可能构成双相情感障碍的遗传偏差。二十名双相 I 型障碍患者、二十名无病症的一级亲属和二十名健康志愿者参与了面部情绪处理的功能性磁共振成像实验。在其中一个实验中，参与者观看了表达不同强度恐惧的面孔（中度和高度），与非情绪面孔混合，而在另一个实验中——观看表达中度或高度快乐的面孔与非情绪面孔混合。带有情绪（恐惧和快乐）、强度（中性、中度和高度）作为内源性变量，以及组（患者、亲属和对照组）作为外源性变量的重复测量 2x3x3 ANOVA 产生了两个差异激活簇，位于内侧前额叶皮层和左侧壳核。与健康志愿者相比，患者和亲属在面对恐惧和快乐面孔时，内侧前额叶皮层的活动增加。在对中度恐惧的反应中，左侧壳核的活动在患者和亲属中比对照组更高。与对照组相比，患者（而非亲属）在面对高强度快乐面孔时也表现出更大的激活。杏仁核激活的感兴趣区域分析显示，在患者和亲属组中，左杏仁核在面对强烈快乐的面孔时活动增加。对情绪信号的内侧前额叶皮质和皮质下（壳核和杏仁核）反应过度可能代表双相情感障碍潜在的遗传神经生物学异常。
