Atherosclerosis Might Be Responsible for Branch Artery Disease: Evidence From White Matter Hyperintensity Burden in Acute Isolated Pontine Infarction

Abstract

Objective: To investigate an MRI-based etiological classification for acute isolated pontine infarcts and to assess differences in vascular risk factors, clinical characteristics and WMH burden among the etiological subtypes.Methods: All participants from SMART cohort with DWI-proven acute isolated pontine infarcts (AIPI) were included and categorized into 3 groups: large-artery-occlusive disease (LAOD), basilar artery branch disease (BAD), and small vessel disease (SVD), according to basilar artery atherosclerosis severity and lesion extent of the transverse axial plane. The vascular risk factors and 6-month functional outcome was analyzed among 3 groups.Results: Of the 1129 patients enrolled, 175 had AIPI. BAD was the most frequent subtype of AIPI (46.3%), followed by SVD (36.0%) and LAOD (17.7%). Neurological impairment on admission was more severe in the LAOD group, followed by BAD. The BAD group had greater frequencies of female sex, hypertension, diabetes mellitus compared to the SVD group (P < 0.05). NIHSS on admission were significantly higher in the BAD group as compared with the SVD group (P < 0.001), but no difference was found between BAD and LAOD group. Poor outcome (mRS≥3) was found in only 13.7% of patients at 6-month post-stroke and there was no difference among 3 groups. WMH severity was significant higher in the SVD group compared to the BAD group for the deep subcortical region; however, there was no difference for the periventricualr region. There was no significant difference in either DWMH or PVWMH severity between the BAD and LAOD groups.Conclusion: BAD is the most frequent etiology of AIPI followed by SVD and LAOD. WMH burden, vascular risk factors and clinical characteristics in BAD group were more similar to the LAOD group, rather than to the SVD group, suggesting the atherothrombotic nature of BAD.

Consecutive Slides on Axial View Is More Effective Than Transversal Diameter to Differentiate Mechanisms of Single Subcortical Infarctions in the Lenticulostriate Artery Territory

“…Previous studies of subtentorial SSIs mainly focused on pontine infarction and supratentorial SSIs on lenticulostriate artery territory (3). As for pontine infarctions, unilateral lesions extending to the ventral pontine surface were usually considered as atherosclerotic mechanisms (16–18). However, as for SSIs in the lenticulostriate artery territory, approaches to differentiate mechanisms still remain controversial.…”

Lacunar stroke: mechanisms and therapeutic implications

“…This has been described particularly in patients with pontine lacunar stroke in the setting of branch atheromatous disease of the basilar artery. 19 Other atherosclerotic mechanisms that have been described include embolism from a proximal intracranial or extracranial artery 20 as well as aortic arch disease. 21 These associations, however, do not prove a causal relationship with lacunar stroke because atherosclerosis and lacunar stroke share common risk factors.…”

Efficacy and Safety of Intravenous Thrombolysis on Acute Branch Atheromatous Disease: A Retrospective Case–Control Study

“…Figure 1 shows the flowchart of selection of eligible study subjects. Moreover, as illustrated in Figure 2, BAD-related infarctions were previously defined as follows (6,(11)(12)(13)(14)(15): (1) infarcts with a diameter ≥15 mm that involves ≥3 axial slices on DWI in the blood-supply region of lenticulostriate artery, or lesions extending to the ventral pontine surface in the blood-supply region of paramedian pontine artery; (2) neither evidence of large arterial stenosis (>50%) or occlusion, nor evidence of cardiogenic embolism.…”

“…subcortical infarction larger than lacunar stoke and lack of severe stenosis (≥50%) of the parent artery that supplies the regions of deep perforators, mainly the lenticulostriate arteries and pontine paramedian arteries (22). In recent years, the majority of clinical studies have followed the diagnostic criteria (12)(13)(14)(15); however, these criteria neither reflect infarcts in the territories of other perforating arteries, nor explain the coexistence of BAD and large artery atherosclerosis. In spite of these shortcomings, no better alternative can be found based on the routine imaging techniques.…”