From the Cognitive Neuroscience (C.C.S., E.I.S.A., N.N.K., M.K.R., G.R.F., P.H.W.), Institute of Neuroscience and Medicine (INM-3), Forschungszentrum Jülich, Germany; and Department of Neurology (E.I.S.A., K.B., N.N.K., M.K.R., N.S., G.R.F., P.H.W.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.
Neurology. 2023 Sep 12;101(11):e1137-e1144. doi: 10.1212/WNL.0000000000207598. Epub 2023 Jul 18.
Apraxia is commonly attributed to left hemisphere (LH) lesions of the cortical fronto-temporo-parietal praxis networks or white matter lesions causing disconnections between cortical nodes. By contrast, the contribution of lesions to the subcortical gray matter, that is, basal ganglia or thalamus, to apraxic deficits remains controversial. Here, we investigate whether damage to these subcortical gray matter structures (i.e., caudate nucleus, putamen, globus pallidus, and thalamus) or the adjacent white matter tracts was associated with apraxic deficits.
We identified patients with distinct subcortical lesions with and without apraxia from a large retrospective sample of subacute LH ischemic stroke patients (n = 194). To test which subcortical structures (caudate nucleus, putamen, globus pallidus, thalamus, and adjacent white matter tracts), when lesioned, contributed to apraxic deficits, we statistically compared the proportion of lesioned voxels within subcortical gray and white matter structures between the apraxic and nonapraxic patients.
Of the 194 stroke patients screened, 39 (median age = 65 years, range 30-82 years; median time poststroke at the apraxia assessment = 7 days, range 1-44 days) had lesions confined to subcortical regions (gray and white matter). Eleven patients showed apraxic deficits when imitating gestures or pantomiming object use. Region-wise statistical lesion comparison (controlled for lesion size) revealed a more significant proportion of damage ('lesion load') in the caudate nucleus in apraxic stroke patients (mean difference = 6.9%, 95% CI 0.4-13.3, = 0.038, = 0.11). By contrast, apraxic patients had lower lesion load in the globus pallidus (mean difference = 9.9%, 95% CI 0.1-19.8, = 0.048, = 0.10), whereas the lesion load in other subcortical structures (putamen, thalamus, and adjacent white matter tracts) did not differ significantly between the apraxic and nonapraxic patients.
These findings provide new insights into the subcortical anatomy of apraxia after LH stroke, suggesting a specific contribution of caudate nucleus lesions to apraxic deficits.
失用症通常归因于左半球（LH）皮质额颞顶叶运动网络的病变或白质病变导致皮质节点之间的连接中断。相比之下，皮质下灰质（基底节或丘脑）对失用症缺陷的病变的贡献仍存在争议。在这里，我们研究了这些皮质下灰质结构（即尾状核、壳核、苍白球和丘脑）或相邻的白质束的损伤是否与失用症缺陷有关。
我们从大量亚急性 LH 缺血性中风患者的回顾性样本中（n = 194）确定了有和没有失用症的具有明显皮质下病变的患者。为了测试哪些皮质下结构（尾状核、壳核、苍白球、丘脑和相邻的白质束）在病变时会导致失用症缺陷，我们对失用症和非失用症患者的皮质下灰质和白质结构内的病变体素比例进行了统计学比较。
在筛选出的 194 名中风患者中，有 39 名（中位数年龄 = 65 岁，范围 30-82 岁；失用症评估时的中位卒中后时间 = 7 天，范围 1-44 天）病变局限于皮质下区域（灰质和白质）。11 名患者在模仿手势或用哑剧模仿物体使用时表现出失用症缺陷。基于区域的统计学病变比较（控制病变大小）显示，失用症中风患者的尾状核损伤比例（“病变负荷”）更高（平均差异 = 6.9%，95%CI 0.4-13.3， = 0.038， = 0.11）。相比之下，失用症患者的苍白球病变负荷较低（平均差异 = 9.9%，95%CI 0.1-19.8， = 0.048， = 0.10），而其他皮质下结构（壳核、丘脑和相邻的白质束）的病变负荷在失用症和非失用症患者之间没有显著差异。
这些发现为 LH 中风后失用症的皮质下解剖结构提供了新的见解，表明尾状核病变对失用症缺陷有特定的贡献。
