Emotion Recognition in Individuals at Clinical High-Risk for Schizophrenia
Emotion Recognition in Individuals at Clinical High-Risk for Schizophrenia
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DOI：
10.1093/schbul/sbr015
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发表时间：
2012-09-01
影响因子：
6.6
通讯作者：
McGorry, Patrick D.
中科院分区：
文献类型：
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作者：
Amminger, G. Paul;Schaefer, Miriam R.;McGorry, Patrick D.
在感知情感材料的问题，特别是在识别负刺激的缺陷，已被证明在精神分裂症，包括在第一次发作的样本。然而，它在很大程度上是未知的，如果情绪识别障碍存在于阈下精神病症状的人。在这里，我们研究了识别面部表达的情绪和情感韵律的能力，在79个人在精神病的超高风险，30个临床稳定的个人首次发作的精神分裂症评估为门诊病人在疾病的早期恢复阶段，和30个未受影响的健康对照组。我们比较了（1）面部和声音模态的恐惧-悲伤综合指数评分，（2）各模态特定情绪的汇总评分，以及（3）每种感觉模态的特定情绪评分。研究结果支持赤字识别的恐惧和悲伤的两种方式的临床组（超高风险和首次发作组）相比，健康对照组。此外，计划的对比表明，与健康的对照组相比，两个临床组有一个显着的赤字的恐惧和悲伤的面孔识别和愤怒的声音识别。在精神病完全表现出来之前，精神分裂症临床高危人群的情绪识别可能会出现特定的障碍。结果表明，特徴缺陷和参与杏仁核的病理超高危状态。
Problems in the perception of emotional material, in particular deficits in the recognition of negative stimuli, have been demonstrated in schizophrenia including in first-episode samples. However, it is largely unknown if emotion recognition impairment is present in people with subthreshold psychotic symptoms. Here, we examined the capacity to recognize facially expressed emotion and affective prosody in 79 individuals at ultra high-risk for psychosis, 30 clinically stable individuals with first-episode schizophrenia assessed as outpatients during the early recovery phase of illness, and 30 unaffected healthy control subjects. We compared (1) scores for a combined fear-sadness aggregate index across face and voice modalities, (2) summary scores of specific emotions across modalities, and (3) scores for specific emotions for each sensory modality. Findings supported deficits in recognition of fear and sadness across both modalities for the clinical groups (the ultra high-risk and first-episode group) as compared with the healthy controls. Furthermore, planned contrasts indicated that compared with the healthy control subjects, both clinical groups had a significant deficit for fear and sadness recognition in faces and for anger recognition in voices. Specific impairments in emotion recognition may be apparent in people at clinical high-risk for schizophrenia before the full expression of psychotic illness. The results suggest a trait deficit and an involvement of the amygdala in the pathology of ultra high-risk states.