Le Berre Anne-Pascale, Sullivan Edith V
Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Road, Stanford, CA, 94305-5723, USA.
Neuropsychol Rev. 2016 Dec;26(4):420-431. doi: 10.1007/s11065-016-9323-3. Epub 2016 Jul 22.
In addiction, notably Alcohol Use Disorder (AUD), patients often have a tendency to fail to acknowledge the reality of the disease and to minimize the physical, psychological, and social difficulties attendant to chronic alcohol consumption. This lack of awareness can reduce the chances of initiating and maintaining sobriety. Presented here is a model focusing on compromised awareness in individuals with AUD of mild to moderate cognitive deficits, in particular, for episodic memory impairment-the ability to learn new information, such as recent personal experiences. Early in abstinence, alcoholics can be unaware of their memory deficits and overestimate their mnemonic capacities, which can be investigated with metamemory paradigms. Relevant neuropsychological and neuroimaging results considered suggest that the alcoholics' impairment of awareness of their attenuated memory function can be a clinical manifestation explained mechanistically by neurobiological factors, including compromise of brain systems that result in a mild form of mnemonic anosognosia. Specifically, unawareness of memory impairment in AUD may result from a lack of personal knowledge updating attributable to damage in brain regions or connections supporting conscious recollection in episodic memory. Likely candidates are posterior parietal and medial frontal regions known to be integral part of the Default Mode Network (DMN) and the insula leading to an impaired switching mechanism between the DMN and the Central-Executive Control (i.e., Lateral Prefronto-Parietal) Network. The cognitive concepts and neural substrates noted for addictive disorders may also be relevant for problems in self-identification of functional impairment resulting from injury following war-related blast, sport-related concussion, and insidiously occurring dementia.
成瘾,尤其是酒精使用障碍(AUD)患者,往往倾向于不承认疾病的现实,并将长期饮酒带来的身体、心理和社会困难最小化。这种意识的缺乏会降低开始并保持清醒的几率。本文提出了一个模型,该模型关注轻度至中度认知缺陷的AUD患者的意识受损情况,特别是情景记忆损害——学习新信息(如近期个人经历)的能力。在戒酒初期,酗酒者可能没有意识到自己的记忆缺陷,高估自己的记忆能力,这可以通过元记忆范式进行研究。所考虑的相关神经心理学和神经影像学结果表明,酗酒者对其减弱的记忆功能的意识受损可能是一种临床表型,可由神经生物学因素进行机制性解释,包括脑系统受损导致轻度形式的记忆失认症。具体而言,AUD患者对记忆损害的无意识可能是由于支持情景记忆中意识回忆的脑区或连接受损导致个人知识更新不足所致。可能的候选脑区是后顶叶和内侧额叶区域,已知它们是默认模式网络(DMN)的组成部分,以及岛叶,这会导致DMN与中央执行控制(即外侧额顶叶)网络之间的切换机制受损。成瘾性障碍中提到的认知概念和神经基质也可能与战争相关爆炸、运动相关脑震荡和隐匿性痴呆导致的损伤后功能损害的自我识别问题有关。