Mechanisms of working memory dysfunction after mild and moderate TBI: Evidence from functional MRI and neurogenetics
Mechanisms of working memory dysfunction after mild and moderate TBI: Evidence from functional MRI and neurogenetics
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DOI：
10.1089/neu.2006.23.1450
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发表时间：
2006-10-01
影响因子：
4.2
通讯作者：
Saykin, Andrew J.
中科院分区：
文献类型：
--
作者：
McAllister, Thomas W.;Flashman, Laura A.;Saykin, Andrew J.
认知主诉是轻中度创伤性脑损伤(TBI)后痛苦和残疾的常见来源。虽然在几个认知领域存在缺陷，但这些抱怨和缺陷的许多方面表明，工作记忆(WM)问题起着重要作用。对健康人的功能成像研究概述了WM的神经底物，并表明WM回路中的重要区域与TBI中常见的易受损伤的区域重叠。功能磁共振成像(FMRI)在轻度和中度脑外伤患者中的应用表明，他们在WM的激活和分配方面可能存在问题，多条证据表明，中枢儿茶酚胺能敏感性的细微变化可能是这些问题的基础。我们回顾了来自功能磁共振成像和神经遗传学研究的证据，这些证据支持儿茶酚胺能失调在轻中度脑损伤后西医主诉和缺陷的病因中所起的作用。
Cognitive complaints are a frequent source of distress and disability after mild and moderate traumatic brain injury (TBI). While there are deficits in several cognitive domains, many aspects of these complaints and deficits suggest that problems in working memory (WM) play an important role. Functional imaging studies in healthy individuals have outlined the neural substrate of WM and have shown that regions important in WM circuitry overlap with regions commonly vulnerable to damage in TBI. Use of functional MRI (fMRI) in individuals with mild and moderate TBI suggests that they can have problems in the activation and allocation of WM, and several lines of evidence suggest that subtle alterations in central catecholaminergic sensitivity may underlie these problems. We review the evidence from fMRI and neurogenetic studies that support the role of catecholaminergic dysregulation in the etiology of WM complaints and deficits after mild and moderate TBI.