Unité de neuropsychologie, département de neurologie, université de Toulouse, CHU de Toulouse, place du Docteur-Baylac, TSA 40031, 31059 Toulouse cedex 9, France; Inserm, université de Toulouse, Toulouse NeuroImaging Centre, place du Docteur-Baylac, 31024 Toulouse cedex 3, France.
Unité de neuropsychologie, département de neurologie, université de Toulouse, CHU de Toulouse, place du Docteur-Baylac, TSA 40031, 31059 Toulouse cedex 9, France; Inserm, université de Toulouse, Toulouse NeuroImaging Centre, place du Docteur-Baylac, 31024 Toulouse cedex 3, France.
Rev Neurol (Paris). 2017 Nov;173(9):562-565. doi: 10.1016/j.neurol.2017.09.006. Epub 2017 Oct 6.
Cerebral amyloid angiopathy is diagnosed in stroke units after lobar intracerebral hemorrhage. CAA can also be diagnosed in memory clinics when patients are referred for cognitive impairment assessment, and may be a reason for admission to emergency or neurology departments because of rapidly progressive cognitive or neurological decline, or a transient focal neurological episode. CAA may even be observed in older community-dwelling individuals. Neuropsychological impairment in CAA has been described over the past 20 years. The symptoms most commonly reported are perceptual speed, episodic memory, semantic memory, attention and executive function, and global cognitive impairments. Psychiatric symptoms, such as personality changes, behavioral disturbances and depression, have been more recently described. CAA is also a risk factor for the development of dementia, and its relationship with Alzheimer's disease has been demonstrated in post-mortem studies. Yet, despite the increase in literature on CAA-related cognitive and psychiatric symptoms, the specific characteristics of symptoms in CAA are difficult to assess because of the substantial prevalence of comorbidities such as small vessel disease due to high blood pressure, Lewy body disease and, of course, AD, all of which act as important confounding factors. Also, within the entity of CAA itself, the additive and perhaps synergistic effects of each lesion on cognition remain to be assessed. In the present paper, the focus is on the latest evidence of neuropsychological impairment observed in CAA patients, and the emergence of a possible specific neuropsychological profile due to CAA is also discussed.
脑淀粉样血管病(Cerebral amyloid angiopathy,CAA)在发生大脑半球脑内出血后于卒中单元被诊断。当患者因认知障碍评估而被转至记忆诊所时,也可诊断为 CAA,可能因认知或神经功能迅速下降、短暂性局灶性神经功能障碍发作而被收入急诊或神经科病房。甚至在年龄较大的社区居住者中也可观察到 CAA。过去 20 年来,CAA 患者的神经心理学损害已被描述。最常报告的症状是知觉速度、情景记忆、语义记忆、注意力和执行功能以及整体认知障碍。最近还描述了精神病症状,如人格改变、行为障碍和抑郁。CAA 也是痴呆发生的一个危险因素,其与阿尔茨海默病的关系已在尸检研究中得到证实。然而,尽管与 CAA 相关的认知和精神症状的文献不断增加,但由于高血压引起的小血管疾病、路易体病以及 AD 等合并症的高患病率,难以评估 CAA 症状的具体特征,这些合并症都是重要的混杂因素。此外,在 CAA 本身的实体中,每个病变对认知的附加和可能的协同作用仍有待评估。在本文中,重点是 CAA 患者观察到的最新神经心理学损害证据,以及由于 CAA 而出现的可能特定的神经心理学特征也将被讨论。