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双相情感障碍中的神经心理功能障碍:批判性观点。

Neuropsychological dysfunction in bipolar affective disorder: a critical opinion.

作者信息

Savitz Jonathan, Solms Mark, Ramesar Rajkumar

机构信息

MRC/UCT Human Genetics Research Unit, University of Cape Town, Cape Town, South Africa.

出版信息

Bipolar Disord. 2005 Jun;7(3):216-35. doi: 10.1111/j.1399-5618.2005.00203.x.

DOI:10.1111/j.1399-5618.2005.00203.x
PMID:15898960
Abstract

Data from the imaging literature have led to suggestions that permanent structural brain changes may be associated with bipolar disorder. Individuals diagnosed with bipolar disorder display deficits on a range of neuropsychological tasks in both the acute and euthymic phases of illness, and correlations between experienced number of affective episodes and task performance are commonly reported. These findings have renewed interest in the neuropsychological profile of individuals with bipolar disorder, with deficits of attention, learning and memory, and executive function, asserted to be present. This paper critically reviews five different potential causes of neurocognitive dysfunction in bipolar disorder: (i) iatrogenic, (ii) acute functional changes associated with depression or mania, (iii) permanent structural lesions of a neurodegenerative origin, (iv) permanent structural lesions that are neurodevelopmental in origin, and (v) permanent functional changes that are most likely genetic in origin. Although the potential cognitive effects of residual symptomatology and long-term medication use cannot be entirely excluded, we conclude that functional changes associated with genetically driven population variation in critical neural networks underpin both the neurocognitive and affective symptoms of bipolar disorder. The philosophical implications of this conclusion for neuropsychology are briefly discussed.

摘要

影像学文献的数据表明,永久性大脑结构变化可能与双相情感障碍有关。被诊断为双相情感障碍的个体在疾病的急性期和缓解期在一系列神经心理学任务中均表现出缺陷,并且经常报告情感发作次数与任务表现之间的相关性。这些发现重新引发了对双相情感障碍患者神经心理学特征的兴趣,据称该疾病存在注意力、学习和记忆以及执行功能方面的缺陷。本文批判性地综述了双相情感障碍中神经认知功能障碍的五种不同潜在原因:(i)医源性的,(ii)与抑郁或躁狂相关的急性功能变化,(iii)神经退行性起源的永久性结构损伤,(iv)神经发育起源的永久性结构损伤,以及(v)最可能由遗传引起的永久性功能变化。尽管不能完全排除残留症状和长期药物使用对认知的潜在影响,但我们得出结论,关键神经网络中由基因驱动的群体变异所关联的功能变化是双相情感障碍神经认知和情感症状的基础。本文简要讨论了这一结论对神经心理学的哲学意义。

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