Xiang Yawen, Rodrigues Mark A, Lerpiniere Christine, Moullaali Tom J, Loan James J M, Wilkinson Tim, Humphreys Catherine A, Smith Colin, Al-Shahi Salman Rustam, Samarasekera Neshika
Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh EH16 4SB, UK.
Department of Neuroradiology, NHS Lothian, Edinburgh EH16 4SA, UK.
Brain Commun. 2024 Aug 22;6(5):fcae275. doi: 10.1093/braincomms/fcae275. eCollection 2024.
Little is known about whether clinical, radiological or neuropathological features are associated with cognitive impairment before intracerebral haemorrhage. We conducted a community-based cohort study of 125 adults with intracerebral haemorrhage (lobar = 71, non-lobar = 54) with consent to brain autopsy. We compared small vessel disease biomarkers on diagnostic CT head and neuropathological findings including neurofibrillary tangles and amyloid plaques in adults without cognitive impairment versus cognitive impairment without dementia versus dementia before intracerebral haemorrhage, stratified by lobar and non-lobar intracerebral haemorrhage. In non-lobar intracerebral haemorrhage, severe cortical atrophy was less common in those without cognitive impairment (8/36, 22%) and cognitive impairment without dementia (0/9, 0%) versus dementia (5/9, 56%); = 0.008. Irrespective of intracerebral haemorrhage location, adults without cognitive impairment had milder neurofibrillary tangle pathology measured by median Braak stage (lobar intracerebral haemorrhage: no cognitive impairment 2 [interquartile range, 2-3] versus cognitive impairment without dementia 4 [2-6] versus dementia 5.5 [4-6]; = 0.004; non-lobar intracerebral haemorrhage: no cognitive impairment 2 [1-2] versus cognitive impairment without dementia 2 [1-2] versus dementia 5 [3-6]; < 0.001). Irrespective of intracerebral haemorrhage location, adults without cognitive impairment had milder amyloid plaque pathology measured by median Thal stage (lobar intracerebral haemorrhage: no cognitive impairment 2 [1-2] versus cognitive impairment without dementia 2 [2-3] versus dementia 2.5 [2-3.5]; = 0.033; non-lobar intracerebral haemorrhage: no cognitive impairment 1 [0-1] versus cognitive impairment without dementia 0 [0-2] versus dementia 3 [2-3]; = 0.002). Our findings suggest that irrespective of intracerebral haemorrhage location, adults with cognitive impairment before an intracerebral haemorrhage have more Alzheimer's disease neuropathologic change.
关于脑出血前的临床、影像学或神经病理学特征是否与认知障碍相关,目前所知甚少。我们开展了一项基于社区的队列研究,纳入了125名同意进行脑尸检的脑出血成人患者(叶性脑出血71例,非叶性脑出血54例)。我们比较了诊断性头颅CT上的小血管疾病生物标志物以及神经病理学发现,包括无认知障碍、无痴呆的认知障碍以及脑出血前痴呆的成人患者中的神经原纤维缠结和淀粉样斑块,按叶性和非叶性脑出血进行分层。在非叶性脑出血中,无认知障碍者(8/36,22%)和无痴呆的认知障碍者(0/9,0%)中严重皮质萎缩的发生率低于痴呆患者(5/9,56%);P = 0.008。无论脑出血位置如何,无认知障碍的成人患者通过Braak分期中位数测量的神经原纤维缠结病理学较轻(叶性脑出血:无认知障碍2[四分位间距,2 - 3],无痴呆的认知障碍4[2 - 6],痴呆5.5[4 - 6];P = 0.004;非叶性脑出血:无认知障碍2[1 - 2],无痴呆的认知障碍2[1 - 2],痴呆5[3 - 6];P < 0.001)。无论脑出血位置如何,无认知障碍的成人患者通过Thal分期中位数测量的淀粉样斑块病理学较轻(叶性脑出血:无认知障碍2[1 - 2],无痴呆的认知障碍2[2 - 3],痴呆2.5[2 - 3.5];P = 0.033;非叶性脑出血:无认知障碍1[0 - 1],无痴呆的认知障碍0[0 - 2],痴呆3[2 - 3];P = 0.002)。我们的研究结果表明,无论脑出血位置如何,脑出血前有认知障碍的成人患者有更多阿尔茨海默病神经病理学改变。