Olsen T S, Bruhn P, Oberg R G
Brain. 1986 Jun;109 ( Pt 3):393-410. doi: 10.1093/brain/109.3.393.
This study was designed to investigate whether aphasia in stroke patients with subcortical lesions ('subcortical aphasia') was due to the subcortical lesion itself or to dysfunction of cortical language zones. A consecutive series of 25 right-handed stroke patients with left hemisphere lesions verified by CT scanning were examined for aphasia in the acute stage, and two weeks, three months and six months after the insult. Cerebral angiography, CT scan and regional cerebral blood flow (rCBF) measurements with the 133Xe intracarotid method were performed in the acute stage. The CT scan was repeated six months later. Seven patients had lesions which involved cortical structures. All of these were severely aphasic in the acute stage and six months later. The rCBF studies showed severe reduction of flow in the infarcts; the perfusion was incompatible with tissue viability. Eighteen patients had subcortical lesions. Eight of these were midly to severely aphasic in the acute state. Recovery was always excellent. Five patients recovered completely, while 3 showed only discrete (clinically undetectable) aphasia after six months. The rCBF demonstrated low-flow areas in the cortex overlying the deep lesions, with a blood flow which was sufficient for tissue viability, but insufficient for normal tissue function (an 'ischaemic penumbra'). The blood flow was pressure dependent (showing impaired autoregulation) in these low flow areas. Ten patients with subcortical lesions were not aphasic. Their CBF was normal. The subcortical lesions were permanent on CT scan while aphasia was transient in these patients as recovery was seen within three months. It was therefore unlikely that the subcortical lesions as such were the cause of aphasia. The present findings indicate that aphasia in patients with subcortical lesions may be due to hypoperfusion and functional loss in cortical language zones. The cortical low-flow areas were invariably confined to occluded vascular territories. These territories were kept viable by collateral circulation characterized by penumbral flow and impaired autoregulation. The patients showed excellent recovery from aphasia. We suggest that the recovery of language is caused by spontaneous arterial recanalization or expansion of collaterals, giving rise to enhancement of flow in the hypoperfused cortical penumbra.
本研究旨在调查皮质下病变的中风患者（“皮质下失语症”）的失语是否归因于皮质下病变本身，还是归因于皮质语言区功能障碍。对连续25例经CT扫描证实为左半球病变的右利手中风患者在急性期、发病后两周、三个月和六个月进行失语症检查。急性期进行了脑血管造影、CT扫描以及用133Xe颈动脉注射法测量局部脑血流量（rCBF）。六个月后重复进行CT扫描。7例患者的病变累及皮质结构。所有这些患者在急性期和六个月后均为严重失语。rCBF研究显示梗死区血流量严重减少；灌注与组织存活不相容。18例患者有皮质下病变。其中8例在急性期为轻度至重度失语。恢复情况始终良好。5例患者完全恢复，而3例在六个月后仅表现为轻微（临床无法检测到）失语。rCBF显示深部病变上方皮质有低血流区，其血流量足以维持组织存活，但不足以维持正常组织功能（“缺血半暗带”）。这些低血流区的血流依赖于压力（显示自动调节受损）。10例有皮质下病变的患者无失语。他们的脑血流量正常。CT扫描显示皮质下病变是永久性的，而这些患者的失语是短暂的，因为在三个月内可见恢复。因此，皮质下病变本身不太可能是失语的原因。目前的研究结果表明，皮质下病变患者的失语可能归因于皮质语言区灌注不足和功能丧失。皮质低血流区总是局限于闭塞血管区域。这些区域通过以半暗带血流和自动调节受损为特征的侧支循环得以存活。患者失语恢复良好。我们认为语言恢复是由动脉自发再通或侧支扩张引起的，从而导致灌注不足的皮质半暗带血流增加。
