Bearden C E, Hoffman K M, Cannon T D
Department of Psychiatry, University of Pennsylvania, Philadelphia, USA.
Bipolar Disord. 2001 Jun;3(3):106-50; discussion 151-3. doi: 10.1034/j.1399-5618.2001.030302.x.
Bearden CE, Hoffman KM, Cannon TD. The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review. Bipolar Disord 2001: 3: 106 150. C Munksgaard, 2001
To present a comprehensive review of the existing neuropsychological and neuroimaging literature on bipolar affective disorder. This review critically evaluates two common conceptions regarding the neuropsychology of bipolar disorder: 1) that, in contrast to schizophrenia, bipolar affective disorder is not associated with general cognitive impairment independent of illness episodes, and 2) relative right hemisphere (RH) dysfunction is implicated in bipolar illness patients, supported by reports of relatively greater impairment in visuospatial functioning, lateralization abnormalities, and mania secondary to RH lesions.
The major computerized databases (Medline and PSYCInfo) were consulted in order to conduct a comprehensive, integrated review of the literature on the neuropsychology and neuroanatomy of bipolar disorder. Articles meeting specified criteria were included in this review.
In a critical evaluation of the above notions, this paper determines that: 1) while there is little evidence for selective RH dysfunction, significant cognitive impairment may be present in bipolar illness, particularly in a subgroup of chronic, elderly or multiple-episode patients, suggesting a possible toxic disease process, and 2) the underlying functional correlate of these cognitive deficits may be white matter lesions ('signal hyperintensities') in the frontal lobes and basal ganglia, regions critical for executive function, attention, speeded information processing, learning and memory, and affect regulation. While this hypothesized neural correlate of cognitive impairment in bipolar disorder is speculative, preliminary functional neuroimaging evidence supports the notion of frontal and subcortical hypometabolism in bipolar illness.
The etiology of the structural brain abnormalities commonly seen in bipolar illness, and their corresponding functional deficits, remains unknown. It is possible that neurodevelopmental anomalies may play a role, and it remains to be determined whether there is also some pathophysiological progression that occurs with repeated illness episodes. More research is needed on first-episode patients, relatives of bipolar probands, and within prospective longitudinal paradigms in order to isolate disease-specific impairments and genetic markers of neurocognitive function in bipolar disorder.
比尔登CE、霍夫曼KM、坎农TD。双相情感障碍的神经心理学与神经解剖学：一项批判性综述。《双相情感障碍》2001年；3：106 - 150。芒克斯gaard出版社，2001年
对现有的关于双相情感障碍的神经心理学和神经影像学文献进行全面综述。本综述批判性地评估了关于双相情感障碍神经心理学的两种常见观念：1）与精神分裂症不同，双相情感障碍与不依赖疾病发作的一般性认知损害无关；2）双相情感障碍患者存在相对右半球（RH）功能障碍，这一观点得到了关于视觉空间功能相对更严重损害、偏侧化异常以及RH损伤继发躁狂的报道的支持。
查阅主要的计算机化数据库（Medline和PSYCInfo），以便对双相情感障碍的神经心理学和神经解剖学文献进行全面、综合的综述。符合特定标准的文章被纳入本综述。
在对上述观念的批判性评估中，本文确定：1）虽然几乎没有证据支持选择性RH功能障碍，但双相情感障碍患者可能存在显著的认知损害，尤其是在慢性、老年或多次发作的患者亚组中，这提示可能存在毒性疾病过程；2）这些认知缺陷的潜在功能相关因素可能是额叶和基底神经节中的白质病变（“信号高增强”），这些区域对执行功能、注意力、快速信息处理、学习和记忆以及情感调节至关重要。虽然这种双相情感障碍认知损害的假设神经关联具有推测性，但初步的功能神经影像学证据支持双相情感障碍患者额叶和皮质下代谢减低的观点。
双相情感障碍中常见的脑结构异常及其相应的功能缺陷的病因仍然未知。神经发育异常可能起作用，反复疾病发作时是否也存在某种病理生理进展仍有待确定。需要对首发患者、双相情感障碍先证者的亲属进行更多研究，并在前瞻性纵向范式内进行研究，以分离双相情感障碍中特定疾病的损害和神经认知功能的遗传标记。
