OUP user menu

CORTICAL HYPOPERFUSION AS A POSSIBLE CAUSE OF ‘SUBCORTICAL APHASIA’

T. SKYHØJ OLSEN, P. BRUHN, R. G. E. ÖBERG
DOI: http://dx.doi.org/10.1093/brain/109.3.393 393-410 First published online: 1 June 1986

Summary

The 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 acccute 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 mildly to severely aphasic in the acute stat. Recovery was always excellent. Five patients recovered completely, while 3 showed only discrete (clinically undetectable) aphasia after six months. The rCBF demostrated 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 fuctional 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 penumbbral 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 expansions of collaterals, giving rise to enhancement of flow in the hypoperfused cortical penumbra.