Assessing the clinical effect of residual cortical disconnection after ischemic strokes.
Assessing the clinical effect of residual cortical disconnection after ischemic strokes.
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DOI：
10.1161/strokeaha.113.004137
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发表时间：
2014-04
期刊：
影响因子：
8.3
通讯作者：
Fridriksson J
中科院分区：
文献类型：
--
作者：
Bonilha L;Rorden C;Fridriksson J
评估慢性卒中后语言障碍（失语症）和缺血性脑损伤之间关系的研究通常依赖于测量磁共振成像（MRI）上观察到的脑坏死程度。尽管如此，临床观察表明，患者可能表现出比基于病变位置和大小的预期更严重的缺陷。这种现象通常被解释为皮层断开的结果。为了了解断开连接是否会导致临床症状，我们评估了中风后慢性失语症患者的语言障碍与结构性脑连接（连接体）之间的关系。39名慢性失语症患者接受了语言评估和MRI扫描。依靠MRI数据，我们从T1加权和扩散张量成像（DTI）重建单个连接体。确定性纤维束描记术被用来评估每对可能的皮质布罗德曼区（BA）之间的连接。多元线性回归分析，以评估语言性能和皮质坏死和皮质分离之间的关系。我们观察到BA 45的结构断开（被坏死组织保留）与命名性能独立相关，控制BA 45坏死的程度（F=4.62，p<0.01;坏死：β=0.43; p=0.03;断开β=1.21; p<0.001）。我们认为，皮质分离，作为衡量的结构连接体，是一个独立的预测命名障碍的慢性失语症患者。仅通过目视检查皮质坏死，可能无法充分认识缺血性卒中后临床相关脑损伤的程度。
Studies assessing the relationship between chronic post-stroke language impairment (aphasia), and ischemic brain damage usually rely on measuring the extent of brain necrosis observed on magnetic resonance image (MRI). Nonetheless, clinical observation suggests that patients can exhibit deficits that are more severe than what would be expected based on lesion location and size. This phenomenon is commonly explained as being the result of cortical disconnection. To understand if disconnection contributes to clinical symptoms, we assessed the relationship between language impairments and structural brain connectivity (the connectome) in patients with chronic aphasia after a stroke Thirty-nine patients with chronic aphasia underwent language assessment and MRI scanning. Relying on MRI data, we reconstructed the individual connectome from T1 weighted and diffusion tensor imaging (DTI). Deterministic fiber tractography was employed to assess connectivity between each possible pair of cortical Brodmann areas (BA). Multiple linear regression analyses were performed to evaluate the relationship between language performance and cortical necrosis and cortical disconnection. We observed that structural disconnection of BA 45 (spared by the necrotic tissue) was independently associated with naming performance, controlling for the extent of BA 45 necrosis (F=4.62, p<0.01; necrosis: β=0.43; p=0.03; disconnection β=1.21; p<0.001). We suggest that cortical disconnection, as measured by the structural connectome, is an independent predictor of naming impairment in patients with chronic aphasia. The full extent of clinically relevant brain damage after an ischemic stroke may be underappreciated by visual inspection of cortical necrosis alone.