Richard Jackson, MD
Jiang S, Yan Y, Yang T, Zhu Q, Wang C, Bai X, Hao Z, Zhang S, Yang Q, Fan Z, et al. Plaque Distribution Correlates With Morphology of Lenticulostriate Arteries in Single Subcortical Infarctions. Stroke. 2020;51:2801–2809.
My father, also a neurologist, used to say that if he learned one new topic at a conference, it was worth going. I love reading articles that open my eyes to a new topic or change the way I view a previous topic. I have been interested in vessel wall imaging (VWI) and its applications since I learned about eccentric and concentric plaques being higher or lower risk for ischemic stroke. This article by Jiang et al. expands on the previous work by Yoon et al. in assessing the location of MCA wall plaque location and its relation to single subcortical infarcts (SSI) as proximal or distal to lenticulostriate perforators and located superiorly or inferiorly. Jian et al. used VWI to visualize the plaque location, perforator origin and branches, and length of perforator in relation to risk for SSI and have expanded on the knowledge of an old C. Miller-Fisher concept of branch atheromatous disease (BAD) which I have really only previously thought of as a consequence of diabetes.
The group prospectively enrolled 40 patients between July 2017 and December 2019 with SSI and no MRA evidence of large vessel disease excluding patients with other possible etiologies or prior infarcts. 3-T MRI was used, and two neuroradiologists evaluated the images.
The pictures are interesting to anyone who, like myself, uses pattern recognition on MRI as a method for helping diagnose etiology. There are pictures in cross section showing different areas of plaques and coronal images of the brain showing lenticulostriate length and branching patterns.
The group found that the proximal and superior wall plaques on the symptomatic MCA side occurred more frequently than asymptomatic and control vessels but no differences in the plaque characteristics. The inference from the data was that location of plaques and not the plaque burden could be important in the pathology of SSI, and that this could serve as a biomarker for treatment evaluation and secondary prevention in the future.
The obvious limitation for my practice in the United States is that this study was not performed on a patient population that I treat, but it’s safe to say that most of us see SSI and that further progress on elucidating etiologies and sub-types of ischemic cerebrovascular disease can only be helpful in the future.