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  • Title: Spectrum of superficial posterior cerebral artery territory infarcts.
    Author: Kumral E, Bayulkem G, Ataç C, Alper Y.
    Journal: Eur J Neurol; 2004 Apr; 11(4):237-46. PubMed ID: 15061825.
    Abstract:
    Posterior cerebral artery (PCA) territory infarction is not uncommon. Published series were concentrated either on isolated deep PCA territory infarcts or on incomplete calcarine artery territory infarcts. Although, correlations between clinical symptoms, causes of stroke and outcome at 6-months in patients with superficial PCA territory stroke are less well known. We sought prospectively stroke causes, infarct topography, and clinical findings of 137 patients with superficial PCA territory infarcts with or without mesencephalic/thalamic involvement, representing 11% of patients with posterior circulation ischemic stroke in our Stroke Registry. We analyzed patients by subdividing into three subgroups; (1). cortical infarct (CI) group; (2). cortical and deep infarcts (CDI) (thalamic and/or mesencephalic involvement) group; (3). bilateral infarcts (BI) group. We studied the outcomes of patients at 6-month regarding clinical findings, risk factors and vascular mechanisms by means of comprehensive vascular and cardiac studies. Seventy-one patients (52%) had cortical (CI) PCA infarct, 52 patients (38%) had CDI, and 14 patients (10%) had bilateral PCA infarct (BI). In the CDI group, unilateral thalamus was involved in 38 patients (73%) and unilateral mesencephalic involvement was present in 27% of patients. The presumed causes of infarction were intrinsic PCA disease in 33 patients (26%), proximal large-artery disease (PLAD) in 33 (24%), cardioembolism in 23 (17%), co-existence of PLAD and cardioembolism in 7 (5%), vertebral or basilar artery dissection in 8 (6%), and coagulopathy in 2. The death rate was 7% in our series and stroke recurrence was 16% during 6-month follow-up period. Features of the stroke that was associated with significant increased risk of poor outcome included, consciousness disturbances at stroke onset (RR, 66.6; 95% CI, 8.6-515.5), mesencephalic and/or thalamic involvement (RR, 3.79; 95% CI, 1.49-9.65), PLAD (RR, 2.71; 95% CI, 1.09-6.73), and basilar artery disease (RR, 5.94; 95% CI, 1.73-20.47). The infarct mechanisms in three different types of superficial PCA territory stroke were quite similar, but cardioembolism was found more frequent in those with cortical PCA territory infarction. Although, the cause of stroke could not reliably dictate the infarct topography and clinical features. Visual field defect was the main clinical symptom in all groups, but sensorial, motor and neuropsychological deficits occurred mostly in those with CDI. Outcome is good in general, although patients having PLAD and basilar artery disease had more risk of stroke recurrence and poor outcome rather than those with intrinsic PCA disease.
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