Lesion patterns and mechanism of cerebral infarction caused by severe atherosclerotic intracranial internal carotid artery stenosis.

BACKGROUND AND PURPOSE

The lesion patterns and mechanisms of ischemic stroke caused by extracranial internal carotid artery (EICA) stenosis are well understood. The prognosis of intracranial internal carotid artery (IICA) stenosis is very poor. However, little is known about lesion patterns and mechanisms of cerebral infarcts caused by IICA stenosis. The objective of this study was to investigate the lesion patterns and mechanisms of infarcts produced by severe IICA stenosis and compare it with that produced by severe EICA stenosis.

METHODS

We recruited 62 patients with acute cerebral infarcts who fulfilled the following criteria: 1) lesions of acute infarcts were verified by diffusion-weighted imaging (DWI) performed within 1 week of stroke onset; 2) infarct lesions were located within the territory of unilateral internal carotid artery (ICA); 3) infarcts were definitely caused by severe atherosclerosis stenosis (stenosis rate of 70%-99%) of the ipsilateral IICA or EICA, with all other potential causes of stroke being entirely excluded. According to the distributions of infarct lesions in the arterial territory of the ICA displayed on DWI, lesion patterns were classified as either 1) single infarct [perforating artery infarct (PAI), pial artery infarct (PI) or border-zone infarct (BZI)], or 2) multiple infarcts (a combination of types described above).

RESULTS

There were 29 patients with ischemic stroke caused by severe IICA stenosis, and 33 patients with stroke caused by severe EICA stenosis. Single BZI (14/29, P=0.015), and infarcts involving the border zone (19/29, P=0.021) or the internal border zone (13/29, P=0.013) were identified more often in patients with IICA stenosis compared to those with EICA stenosis. PI and/or PAI (22/32, P=0.021) were identified more often in patients with EICA stenosis.

CONCLUSIONS

Lesion patterns in patients with severe IICA stenosis were different from those with severe EICA stenosis. The hypoperfusion mechanism leading to BZI was more important for patients with severe IICA stenosis than for those with severe EICA stenosis. Embolisms leading to PI and/or PAI were more important for patients with severe EICA stenosis.