Perry E K, Perry R H
MRC Neurochemical Pathology Unit, Newcastle General Hospital, Newcastle upon Tyne, United Kingdom.
Brain Cogn. 1995 Aug;28(3):240-58. doi: 10.1006/brcg.1995.1255.
Newly proposed criteria for Lewy body dementia include alterations in consciousness. Lewy body dementia is also associated with a disturbance in cholinergic transmission; neocortical cholinergic deficits in this disorder are more extensive than in Alzheimer's disease and are correlated with symptoms commonly associated with delirium, such as visual hallucinations. The traditional view that derangements of the basal forebrain cholinergic system in Alzheimer's disease relate specifically to memory impairment is assessed in terms of a more general role for cortical acetylcholine in consciousness. This extends the concept that cortical acetylcholine enhances neuronal signal to noise ratio. It is suggested that muscarinic receptor activation in the cortex is involved in confining the contents of the discrete self-reported conscious "stream." In the absence of cortical acetylcholine, currently irrelevant intrinsic and sensory information, which is constantly processed in parallel at the subconscious level, enters conscious awareness. This is consistent with the ability of anti-muscarinic drugs administered medically, recreationally, or ritualistically to induce visual hallucinations and other perceptual disturbances. The hypothesis is explored through comparisons between muscarinic and nicotinic receptor psychopharmacology and between the pathology of the basal forebrain as opposed to pedunculopontine cholinergic systems in different diseases of the human brain affecting consciousness and cognition. The paradoxical effects of muscarinic receptor blockade to induce hallucinations and of REM sleep-associated cholinergic activation of the thalamus to induce dreaming may be related to the differential distribution and activity of muscarinic receptor subtypes or to the differing responses of intrinsic GABA neurons in cortex and thalamus.
新提出的路易体痴呆标准包括意识改变。路易体痴呆还与胆碱能传递障碍有关；该疾病中的新皮质胆碱能缺陷比阿尔茨海默病更广泛，且与通常与谵妄相关的症状相关，如视幻觉。根据皮质乙酰胆碱在意识中的更普遍作用，对阿尔茨海默病中基底前脑胆碱能系统紊乱与记忆障碍具体相关的传统观点进行了评估。这扩展了皮质乙酰胆碱增强神经元信噪比的概念。有人提出，皮质中的毒蕈碱受体激活参与限制离散的自我报告的有意识“流”的内容。在缺乏皮质乙酰胆碱的情况下，目前在潜意识水平并行处理的不相关的内在和感觉信息进入意识觉知。这与医学、娱乐或仪式性使用抗毒蕈碱药物诱导视幻觉和其他感知障碍的能力一致。通过比较毒蕈碱和烟碱受体的精神药理学，以及比较基底前脑与脚桥被盖胆碱能系统在影响意识和认知的不同人脑疾病中的病理情况，对该假说进行了探讨。毒蕈碱受体阻断诱导幻觉的矛盾效应以及快速眼动睡眠相关的丘脑胆碱能激活诱导做梦的效应，可能与毒蕈碱受体亚型的不同分布和活性有关，或者与皮质和丘脑中内在GABA神经元的不同反应有关。
