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  • Title: Topographic location of acute pontine infarction is associated with the development of progressive motor deficits.
    Author: Oh S, Bang OY, Chung CS, Lee KH, Chang WH, Kim GM.
    Journal: Stroke; 2012 Mar; 43(3):708-13. PubMed ID: 22343639.
    Abstract:
    BACKGROUND AND PURPOSE: Motor weakness progression is relatively common in acute pontine infarction and frequently associated with increased functional disability. We designed this study to identify the predictors of progression of motor weakness in patients with pontine infarction during the acute phase. METHODS: We identified consecutive patients with acute ischemic stroke in the pons. Patients were defined as having progressive motor deficits (PMD) if their motor National Institutes of Health Stroke Scale scores increased by ≥1 unit between the maximal and initial neurological deficits. To define the predictors of PMD in patients with a pontine infarct, clinical, laboratory, diffusion-weighted imaging lesion location, and magnetic resonance angiographic variables were investigated. RESULTS: A total of 190 patients (male:female=112:78, 66.4±10.6) were identified, and 49 (25.8%) patients were diagnosed with progressive motor deficits. Logistic multiple regression analysis identified lesion involvement of the lower pons (odds ratio, 3.768; 95% confidence interval, 1.696-8.371) as an independent risk factor contributing to motor progression. Although 34 patients (17.9%) had significant basilar artery stenosis, there was no relationship between PMD in pontine infarct patients and the presence of basilar artery stenosis. Additionally, female and previous hypertension were associated with PMD (odds ratio, 2.651, 95% confidence interval, 1.211-5.802; odds ratio, 3.051, 95% confidence interval, 1.087-9.673). CONCLUSIONS: Our results suggest that lower pons lesions may contribute to progressive motor deficits in patients with isolated acute pontine infarction. Infarct topography is therefore a potential prognostic factor of PMD, because the location of the infarct can affect the extent of ischemic degeneration of the corticospinal tract.
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