Russell Mitesh Cerejo, MD
 

Ryoo S, Lee MJ, Cha J, Jeon P, and Bang OH. Differential Vascular Pathophysiologic Types of Intracranial Atherosclerotic Stroke: A High-Resolution Wall Magnetic Resonance Imaging Study. Stroke. 2015

In the study titled “Differential Vascular Pathophysiologic Types of Intracranial Atherosclerotic Stroke: A High-Resolution Wall MRI Study” the authors hypothesize that intracranial stenosis due to atherosclerosis (ICAD) may have subtypes of braches occlusive disease (BOD) and non- BOD which may differ in arterial remodeling and plaque characteristics using high resolution MRI.


Patients with ICAD (n=80) were divided into two cohorts, patient with BOD (defined as patient with deep infarctions within the striatocapsular area) and non-BOD group (with infarcts beyond the striatocapsular area such as cortical infarctions, regardless of any subcortical deep infarcts). They included patients with MCA and basilar artery involvement. They had 45% patients in the BOD subgroup. Vascular risk factors and laboratory results were similar between BOD and non-BOD patients. Using high resolution MRI, patients in the BOD group had milder stenosis than patients in the non-BOD group (stenosis degree: 40.7 ± 27.4% vs. 74.5 ± 19.9%, respectively; p<0.001). Most patients with BOD (78.1%) did not show positive remodeling, whereas more than half of patients in the non-BOD group (52.8%) showed positive remodeling (p=0.004). Although all symptomatic vessels in the non-BOD group showed enhancement, a substantial proportion of symptomatic vessels in the BOD group (25.0%) were non-enhancing (p=0.003). Both BOD and non-BOD groups showed similar enhancement patterns; most of them were eccentric (BOD: 92.6% and non-BOD: 90.7%). However, the enhancement location was different. Enhancement was more frequently distributed at the superior half of the MCA or the posterior half of the basilar artery in the BOD group, where the perforators arose, compared to the non-BOD group. As the number of ICAD stenoses increased, the degree of stenosis also increased in the BOD group, although the enhancement area did not increase. In contrast, the enhancement area got larger as the number of stenoses increased in the non-BOD group. The degree of stenosis did not correlate with increasing number of stenosis in the non-BOD group.

Intracranial stenosis has been a prominent risk factor for stroke and this study suggest that there may be different subtypes with different pathophysiology. The study has some interesting findings that patient in the non-BOD group had more positive remodeling and also the BOD group area of remodeling / enhancement was more towards the perforators’ ostia. As suggested by the study, this understanding of wall remodeling will definitely help guide treatment strategies in these patients.