Etiology of isolated pontine infarctions: a study based on high-resolution MRI and brain small vessel disease scores.

BACKGROUND

In this retrospective study, we investigated the main pathogenesis of the two types of isolated pontine infarction: paramedian pontine infarcts (PPIs) and small deep pontine infarcts (SDPIs).

METHODS

Acute ischemic stroke patients, comprising 117 PPI patients and 40 SDPI patients, were enrolled. High-resolution magnetic resonance imaging (HR-MRI) and routine MRI sequences were performed for each patient, and clinical data were collected. The following brain small vessel disease (SVD) features of the MRI scans were each rated (0 or 1) separately: asymptomatic lacunar infarcts, white matter lesions (WMLs), deep and infratentorial cerebral microbleeds (CMBs), and enlarged perivascular spaces in the basal ganglia. The ratings were also summed in an ordinal "SVD score" (range: 0-4). The difference in the SVD score between the PPI and SDPI groups was determined. The presence and location of basilar artery (BA) atherosclerotic plaques (based on HR-MRI) in the two groups was evaluated.

RESULTS

There was a significant difference in the total SVD score and three of the four independent SVD features (asymptomatic lacunar infarcts, WMLs, and deep and infratentorial CMBs) between the two groups. The prevalence of BA plaques relevant to the infarcts in the PPI group was significantly higher than that in the SDPI group, whereas the prevalence of plaques irrelevant to the infarcts was similar between the two groups. The degree of BA stenosis was slightly higher in the PPI group than in the SDPI group. Diabetes mellitus was much more prevalent in the PPI group. The National Institute of Health Stroke Scale score was higher in the PPI group, which is in accordance with the larger infarct size in the PPI group.

CONCLUSION

BA atherosclerosis may be the major cause of PPI, while SVD may be the main mechanism underlying SDPI. HR-MRI combined with the total SVD score should be helpful to explore the pathogenesis underlying isolated pontine infarctions, especially in cases involving low-grade BA stenosis.