The impact of early and late damage to the human amygdala on 'theory of mind' reasoning
The impact of early and late damage to the human amygdala on 'theory of mind' reasoning
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DOI：
10.1093/brain/awh168
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发表时间：
2004-07-01
期刊：
影响因子：
14.5
通讯作者：
David, AS
中科院分区：
文献类型：
--
作者：
Shaw, P;Lawrence, EJ;David, AS
人们对将精神状态归因于他人的能力的神经基础越来越感兴趣;这种能力被称为“心理理论”（ToM）。我们研究了在不同发育阶段出现的杏仁核损伤对社会认知这一关键方面的影响。对先天性或儿童早期杏仁核损伤的受试者（“早期损伤”，n = 15）、成年后获得性杏仁核损伤的受试者（"晚期损伤“，n = 11）以及匹配的临床对照组（n = 14）和健康对照组（n = 38）进行ToM、执行和一般神经心理功能测试。杏仁核早期受损的受试者，特别是如果损伤与儿童癫痫发作有关，在更高级的ToM推理测试中，如检测不得体或讽刺的评论或解释非文字话语，相对于所有其他组都受到损害。这些缺陷适用于左侧或右侧早期杏仁核损伤的受试者，包括对他人信仰和情绪状态的理解。相比之下，受试者谁收购损害杏仁核在成年期（通常作为前颞叶切除术的一部分）没有受损的心理理论推理相对于临床和健康对照组，支持的立场，杏仁核是不是神经回路的一部分，介导的“在线”性能的心理理论推理。与声称心理理论是一种独立的认知能力的理论相一致，我们发现，在执行功能，记忆和一般智力功能的措施共同变化后，结果的模式。我们讨论的结果，在最近的理论联系在一起的早期发展的侮辱杏仁核的心理理论障碍，这被认为是一个核心的神经认知缺陷，如自闭症。我们的结论是杏仁核可能在支持心理理论推理正常发展的神经系统中发挥重要作用。
There is a burgeoning interest in the neural basis of the ability to attribute mental states to others; a capacity referred to as 'theory of mind' (ToM). We examined the effects of lesions of the amygdala which arise at different stages of development on this key aspect of social cognition. Tests of ToM, executive and general neuropsychological function were given to subjects with lesions of the amygdala arising congenitally or in early childhood ('early damage', n = 15), subjects who acquired damage to the amygdala in adulthood ('late damage' n = 11) and matched clinical (n = 14) and healthy comparison groups (n = 38). Subjects with early damage to the amygdala, particularly if the lesion was associated with childhood onset of seizures, were impaired relative to all other groups on more advanced tests of ToM reasoning, such as detecting tactless or ironic comments or interpreting non-literal utterances. These deficits held for subjects with either left or right early amygdala damage and encompassed the understanding of both the beliefs and emotional states of others. In contrast, subjects who acquired damage to the amygdala in adulthood (usually as part of an anterior temporal lobectomy) were not impaired in ToM reasoning relative to both clinical and healthy controls, supporting the position that the amygdala is not part of the neural circuitry mediating the 'on-line' performance of ToM reasoning. In line with theories which claim that ToM is an independent faculty of cognition, we found that the pattern of results held after co-varying for measures of executive function, memory and general intellectual functioning. We discuss the results in the light of recent theories which link early developmental insults to the amygdala with the ToM impairments which are thought to be a core neurocognitive deficit found in disorders such as autism. We conclude that the amygdala may play an important role in the neural systems supporting the normal development of ToM reasoning.