Schaapsmeerders Pauline, van Uden Inge W M, Tuladhar Anil M, Maaijwee Noortje A M, van Dijk Ewoud J, Rutten-Jacobs Loes C A, Arntz Renate M, Schoonderwaldt Hennie C, Dorresteijn Lucille D A, de Leeuw Frank-Erik, Kessels Roy P C
Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Centre for Neuroscience, Radboud University Medical Centre, Nijmegen, The Netherlands.
Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom.
Hum Brain Mapp. 2015 Jul;36(7):2432-42. doi: 10.1002/hbm.22782. Epub 2015 Mar 10.
Memory impairment after stroke in young adults is poorly understood. In elderly stroke survivors memory impairments and the concomitant loss of hippocampal volume are usually explained by coexisting neurodegenerative disease (e.g., amyloid pathology) in interaction with stroke. However, neurodegenerative disease, such as amyloid pathology, is generally absent at young age. Accumulating evidence suggests that infarction itself may cause secondary neurodegeneration in remote areas. Therefore, we investigated the relation between long-term memory performance and hippocampal volume in young patients with first-ever ischemic stroke. We studied all consecutive first-ever ischemic stroke patients, aged 18-50 years, admitted to our academic hospital center between 1980 and 2010. Episodic memory of 173 patients was assessed using the Rey Auditory Verbal Learning Test and the Rey Complex Figure and compared with 87 stroke-free controls. Hippocampal volume was determined using FSL-FIRST, with manual correction. On average 10 years after stroke, patients had smaller ipsilateral hippocampal volumes compared with controls after left-hemispheric stroke (5.4%) and right-hemispheric stroke (7.7%), with most apparent memory dysfunctioning after left-hemispheric stroke. A larger hemispheric stroke was associated with a smaller ipsilateral hippocampal volume (b=-0.003, P<0.0001). Longer follow-up duration was associated with smaller ipsilateral hippocampal volume after left-hemispheric stroke (b=-0.028 ml, P=0.002) and right-hemispheric stroke (b=-0.015 ml, P=0.03). Our results suggest that infarction is associated with remote injury to the hippocampus, which may lower or expedite the threshold for cognitive impairment or even dementia later in life.
年轻人中风后的记忆障碍目前还知之甚少。在老年中风幸存者中，记忆障碍和海马体体积的相应减少通常被解释为与中风相互作用的同时存在的神经退行性疾病（如淀粉样蛋白病变）所致。然而，在年轻时一般不存在神经退行性疾病，如淀粉样蛋白病变。越来越多的证据表明，梗死本身可能会导致远隔部位的继发性神经变性。因此，我们研究了首次发生缺血性中风的年轻患者的长期记忆表现与海马体体积之间的关系。我们研究了1980年至2010年间入住我们学术医院中心的所有连续的首次发生缺血性中风的18至50岁患者。使用雷伊听觉词语学习测验和雷伊复杂图形对173例患者的情景记忆进行评估，并与87名无中风的对照组进行比较。使用FSL-FIRST并通过手动校正来确定海马体体积。中风后平均10年，与对照组相比，左半球中风患者（5.4%）和右半球中风患者（7.7%）同侧海马体体积较小，左半球中风后记忆功能障碍最为明显。较大的半球性中风与同侧海马体体积较小相关（b=-0.003，P<0.0001）。更长的随访时间与左半球中风（b=-0.028 ml，P=0.002）和右半球中风（b=-0.015 ml，P=0.03）后同侧海马体体积较小相关。我们的结果表明，梗死与海马体的远隔损伤有关，这可能会降低或加快认知障碍甚至晚年痴呆的阈值。
