Clinical and neuroradiological features of internal watershed infarction and the occlusive diseases of carotid artery system

Background: To describe the clinical and neuroradiological features of internal watershed (IWS) infarction and to analyze the relationship between IWS infarction and occlusive diseases of carotid artery system. Methods: We identified 27 IWS infarction patients with diffusion-weighted magnetic resonance imaging by commonly used templates within 10 days after the onset. Patients with potential cardiac sources of embolism were excluded. Occlusive diseases of carotid arteries were assessed by magnetic resonance angiography or digital subtraction angiography. Baseline characteristics, clinical course, prognosis, neuroradiological features and symptomatic arteries were analyzed. Results: Two patterns were identified: 14 patients had confluent IWS (C-IWS) infarction, and 13 patients had partial IWS (P-IWS) infarction. Twelve patients in C-IWS group and 10 patients in P-IWS group had severe stenosis (> 70%) or occlusion in either the internal carotid artery (ICA) or middle cerebral artery (MCA). Occlusive diseases of ICA and non-lacunar syndrome were more prevalent in C-IWS group, while occlusive diseases of MCA and lacunar syndrome were more prevalent in P-IWS group. Concomitant small cortical lesions ipsilateral to IWS infarcts were more common in C-IWS group than in P-IWS group, and were significantly associated with ICA diseases. Clinical deterioration during the first seven days after admission and poor outcome assessed by the Modified Rankin Score 3 months after stroke were more prevalent in C-IWS group than in P-IWS group. Conclusions: There is a relatively definite relationship between IWS infarction and occlusive diseases of carotid arteries. The distribution of symptomatic arteries (ICA or MCA) in C-IWS group is significantly different from that in P-IWS group. Both hypoperfusion and microembolism are probable mechanisms. There may be some differences in their roles in pathogenesis of C-IWS and P-IWS infarction. Microembolism may contribute C-IWS infarction in addition to hypoperfusion, which is the major pathogenesis of P-IWS infarction.