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(Stroke. 1997;28:1357-1360.)
© 1997 American Heart Association, Inc.
Articles |
From the Departments of Neurology (V.I.H.K., J.S., L.M.B.) and Radiology (B.V.), Academic Medical Center, University of Amsterdam (Netherlands).
Correspondence to Vincent I.H. Kwa, MD, Department of Neurology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, PO Box 22700, 1100 DE Amsterdam, Netherlands. E-mail i.h.kwa{at}amc.uva.nl
Background and Purpose Pontine hyperintense lesions (PHL) on T2-weighted MRI have been recognized recently. Histopathological findings resemble periventricular leukoaraiosis, and a vascular etiology has been suggested. We studied the frequency and the associated factors of PHL in patients with symptomatic atherosclerosis.
Methods Two independent observers assessed brain MRIs in a prospective cohort of patients with symptomatic atherosclerosis. Only patients in whom both observers scored PHL on T2- and proton densityweighted images, but not on T1-weighted images, were considered to have the lesion.
Results We studied 229 patients: 31% presenting with ischemic stroke, 31% with myocardial infarction, and 38% with peripheral artery disease. Both observers scored PHL in 23% of all patients. Patients with PHL were significantly older and had more lacunar infarcts and periventricular leukoaraiosis than patients without PHL. There were more women, more hypercholesterolemic and diabetic patients, and more cortical infarcts on MRI (P=NS). After logistic regression the presence of leukoaraiosis (odds ratio, 2.4; 95% confidence interval, 1.6 to 3.4) and lacunar infarcts (odds ratio, 2.2, 95% confidence interval, 1.5 to 3.1) remained independently associated with PHL. PHL was more common in patients with ischemic strokes (39%) than in patients with myocardial infarctions (11%) or peripheral artery disease (19%) (P<.001).
Conclusions We found that PHL on T2- and proton densityweighted MR images are often found in patients with symptomatic atherosclerosis. The association with periventricular leukoaraiosis and lacunar infarcts suggests that PHL is a variant of leukoaraiosis, with possibly the same pathophysiology. The clinical symptoms and consequences of PHL, however, are not yet clear.
Key Words: atherosclerosis ischemia leukoaraiosis magnetic resonance imaging pons
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