Abstract:
BACKGROUND:Pontine infarcts can be classified into four regions based on the vascular anatomy: anteromedial, anterolateral, lateral and posterior. The purpose of this study was to determine if different etiological mechanisms are responsible for these four types of pontine infarcts. METHODS:We studied consecutive patients within 7 days of symptom onset who had isolated pontine infarcts on diffusion-weighted imaging. The factors associated with infarct topography were determined by multivariate logistic regression analysis. RESULTS:A total of 205 patients were enrolled (78 women; mean age, 72 ± 11 years). The distribution of the infarcts was anteromedial in 73%, anterolateral in 14%, lateral in 3% and posterior in 10%. In multivariate logistic regression analysis, major cardioembolic sources (odds ratio (OR), 4.17; 95% confidence interval (CI), 1.21-14.1) and previous ischemic stroke (OR, 2.92; 95% CI, 1.09-7.89) were positively associated with lateral or posterior infarcts compared with anteromedial infarcts. In contrast, advanced age (OR, 0.55; 95% Cl, 0.35-0.81 per 10-year increase), diabetes mellitus (OR, 0.31; 95% CI, 0.11-0.80) and basilar artery disease (OR, 0.27; 95% CI, 0.08-0.75) were negatively associated with lateral or posterior pontine infarcts. CONCLUSIONS:Baseline characteristics were significantly different among patients with isolated pontine infarcts in different topographic locations. Our results suggest that cardioembolism is relatively common in lateral or posterior pontine infarcts, whereas basilar artery atherosclerosis is more common in anteromedial infarcts.
journal_name
J Neurol Scijournal_title
Journal of the neurological sciencesauthors
Kobayashi J,Ohara T,Minematsu K,Nagatsuka K,Toyoda Kdoi
10.1016/j.jns.2014.01.039subject
Has Abstractpub_date
2014-04-15 00:00:00pages
113-7issue
1-2eissn
0022-510Xissn
1878-5883pii
S0022-510X(14)00063-Xjournal_volume
339pub_type
杂志文章abstract::3G11, a sialylated carbohydrate epitope on the disialoganglioside molecule, is expressed predominantly on the surface of mouse CD4(+) T cells. Our previous studies suggested that lack of the 3G11 molecule could be a new cell surface marker for regulatory CD4(+) T cells. In the present study, we explore the relationshi...
journal_title:Journal of the neurological sciences
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journal_title:Journal of the neurological sciences
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pub_type: 杂志文章,收录出版
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journal_title:Journal of the neurological sciences
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