Snaphaan Liselore, Rijpkema Mark, van Uden Inge, Fernández Guillén, de Leeuw Frank-Erik
Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Centre for Neuroscience, Medical Centre, Radboud University Nijmegen, The Netherlands.
Brain. 2009 Jul;132(Pt 7):1882-8. doi: 10.1093/brain/awp133. Epub 2009 May 29.
Stroke is a leading cause of disability, not only because of motor limitations, but also because of the frequent occurrence of post-stroke cognitive impairment. This is illustrated by the fact that the risk of post-stroke dementia is reportedly higher than a recurrent stroke. The loss of subcortical and cortical functions in the post-stroke cognitive dysfunction spectrum is usually well explained by the size and location of the infarction. However, this does not apply for post-stroke memory dysfunction (especially episodic memory dysfunction), as there is almost never an infarction in the medial temporal lobe. Involvement of the medial temporal lobe in post-stroke memory dysfunction seems likely since this structure is essential for memory encoding and retrieval. For a proper episodic memory function, the medial temporal lobe depends on intact connections with virtually the whole brain. Disconnection from other brain areas due to the infarction could lead to a reduced medial temporal lobe function and the attendant reduced episodic memory function. We investigated medial temporal lobe functionality in 28 'first-ever' stroke patients and 22 healthy controls with the aid of functional magnetic resonance imaging. Stroke patients with a reduced episodic memory function 6-8 weeks after infarction had reduced medial temporal lobe functionality. Post-stroke reduced medial temporal lobe functionality may be responsible for the frequent observation of impaired post-stroke episodic memory function. Insight into this mechanism could be helpful in identifying which stroke patients may be at increased risk for developing post-stroke dementia and those who could benefit from early cognitive rehabilitation.
中风是导致残疾的主要原因,不仅因为运动受限,还因为中风后认知障碍频繁发生。据报道,中风后痴呆症的风险高于复发性中风这一事实就说明了这一点。中风后认知功能障碍范围内的皮质下和皮质功能丧失通常可以通过梗死灶的大小和位置得到很好的解释。然而,这并不适用于中风后的记忆功能障碍(尤其是情景记忆功能障碍),因为内侧颞叶几乎从未发生过梗死。内侧颞叶参与中风后的记忆功能障碍似乎是可能的,因为这个结构对记忆编码和检索至关重要。对于正常的情景记忆功能,内侧颞叶依赖于与几乎整个大脑的完整连接。由于梗死导致与其他脑区的连接中断可能会导致内侧颞叶功能下降以及随之而来的情景记忆功能下降。我们借助功能磁共振成像对28名“首次”中风患者和22名健康对照者的内侧颞叶功能进行了研究。梗死6 - 8周后情景记忆功能下降的中风患者内侧颞叶功能降低。中风后内侧颞叶功能降低可能是中风后情景记忆功能受损这一常见现象的原因。深入了解这一机制可能有助于确定哪些中风患者患中风后痴呆症的风险可能增加,以及哪些患者可能从早期认知康复中受益。