白质瓶颈损伤导致左半球卒中后语言障碍
Damage to white matter bottlenecks contributes to language impairments after left hemispheric stroke
摘要：
左后颞叶下方的白质损伤导致多种语言功能的缺陷。后颞叶白质可能对应于一个瓶颈，在那里背侧和腹侧语言通路容易受到同时损害。损伤的第二个假定的白质瓶颈在左深前额叶白质涉及与腹侧语言通路和丘脑-皮层的预测预测最近被提出作为中风后的语义缺陷的来源。然而，损伤的影响，先验确定的白质瓶颈语言功能还没有直接调查。在这里，我们首先使用白质图谱来识别先前描述的后颞叶和深前额白质中的白质瓶颈。然后，我们评估了43例慢性失语症患者的类别流畅性，图片命名和听觉语义决策措施的影响，每个区域的损害。后颞瓶颈的损害预测赤字的所有语言措施，而前瓶颈的损害只预测赤字类别流畅性。重要的是，对瓶颈区域的损伤的影响并不归因于损伤体积、穿过瓶颈的神经束上的损伤负荷或对附近皮质语言区的损伤。多变量病变症状映射和纤维跟踪分析证实了这些发现。总之，我们的研究结果提供了强有力的支持的建议，空间特异性白质损伤影响白质瓶颈，特别是在后颞叶，有助于慢性语言障碍后左半球中风。我们的研究结果表明，该区域的损伤可能会通过同时破坏背侧和腹侧语言处理流来同时破坏信号传导。
英文摘要：
Damage to the white matter underlying the left posterior temporal lobe leads to deficits in multiple language functions. The posterior temporal white matter may correspond to a bottleneck where both dorsal and ventral language pathways are vulnerable to simultaneous damage. Damage to a second putative white matter bottleneck in the left deep prefrontal white matter involving projections associated with ventral language pathways and thalamo-cortical projections has recently been proposed as a source of semantic deficits after stroke. However, the effects of damage to a priori identified white matter bottlenecks on language function have not been directly investigated. Here, we first used white matter atlases to identify the previously described white matter bottlenecks in the posterior temporal and deep prefrontal white matter. We then assessed the effects of damage to each region on measures of category fluency, picture naming, and auditory semantic decision-making in 43 patients with chronic aphasia. Damage to the posterior temporal bottleneck predicted deficits on all language measures, while damage to the anterior bottleneck only predicted deficits in category fluency. Importantly, the effects of damage to the bottleneck regions were not attributable to lesion volume, lesion loads on the tracts traversing the bottlenecks, or damage to nearby cortical language areas. Multivariate lesion-symptom mapping and fiber tracking analyses corroborated these findings. Together, our results provide strong support for the proposal that spatially specific white matter damage affecting white matter bottlenecks, particularly in the posterior temporal lobe, contribute to chronic language deficits after left hemispheric stroke. Our results suggest that damage to this area is likely to simultaneously disrupt signaling via the simultaneous disruption of dorsal and ventral language processing streams.
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