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Updated: Sep 17, 2025
Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases
Published on: December 6, 2016
Temporal changes in symptomatic intracranial arterial disease: a longitudinal high-resolution vessel wall imaging
Dong-Wan Kang1,2, Jonguk Kim1,3, Do Yeon Kim1,4,5
1Department of Neurology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
Insights
Intracranial arterial disease (ICAD) vessel narrowing changes over time after ischemic stroke. Different causes, like dissection versus atherosclerosis, show distinct temporal patterns in vessel wall changes.
Area of Science:
- Neurology
- Radiology
- Vascular Medicine
Background:
- Intracranial arterial disease (ICAD) is a significant cause of ischemic stroke.
- The temporal evolution of vessel wall changes in ICAD is not well understood.
- Understanding these dynamics is crucial for predicting stroke recurrence and guiding treatment.
Purpose of the Study:
- To investigate the temporal changes in narrowed intracranial arteries following ischemic stroke.
- To compare the temporal dynamics of vessel wall changes based on the etiology of ICAD.
Main Methods:
- Retrospective analysis of patients with ICAD-related ischemic stroke undergoing serial high-resolution vessel wall imaging (HR-VWI).
- Manual segmentation of lumen area (LA), total vessel area (TVA), and enhancing area (EA) to calculate stenosis, enhancing proportion, and enhancement ratio.
- Linear mixed models used to assess temporal changes and differences between etiologies.
Main Results:
- Over a median follow-up of 319 days, degree of stenosis and enhancing proportion showed a trend to decrease.
- Intracranial dissection led to faster reductions in stenosis and enhancing proportion compared to atherosclerosis.
- Enhancement ratio decreased over time in atherosclerosis but remained stable in dissection.
Conclusions:
- Intracranial vessel narrowing exhibits distinct temporal changes following ischemic stroke, varying by etiology.
- Atherosclerosis and dissection demonstrate unique temporal progression patterns in ICAD.
- Serial HR-VWI is valuable for monitoring disease activity and understanding the natural history of ICAD.
Introduction:
The temporal dynamics of the vessel wall in intracranial arterial disease (ICAD) may differ depending on the etiology. We investigated temporal changes in narrowed intracranial arteries after ischemic stroke using serial high-resolution vessel wall imaging (HR-VWI).
Methods:
We retrospectively recruited patients with ICAD-related ischemic stroke who underwent two or more HR-VWI scans. The lumen area (LA), total vessel area (TVA), and enhancing area (EA) of the narrowest part of the culprit lesion were manually segmented. Degree of stenosis was estimated as [1-LA/TVA] × 100(%), the enhancing proportion as EA/TVA × 100(%), and enhancement ratio as (T1GDlesion/T1GDref)/(T1lesion/T1ref). Linear mixed models were used to investigate temporal changes in these parameters and whether such changes differed by etiologies.
Results:
Of a total of 208 patients, ICAD-related stroke was caused by atherosclerosis (69%), arterial dissection (24%), vasculitis (3%), moyamoya disease (1%), and other (2%). The median follow-up was 319 [IQR, 125-409] days. HR-VWI imaging parameters, namely, degree of stenosis, enhancing proportion, and enhancement ratio showed a trend to decrease over time. Patients with intracranial dissection as a cause of intracranial narrowing showed a faster reduction in degree of stenosis and enhancing proportion vs. when such narrowing was identified as due to atherosclerosis (β [95% CI], -0.59%[-0.80% ~ -0.38%] and -0.81%[-1.23% ~ -0.39%], respectively, both p < 0.01). The enhancement ratio did not change over time in dissection, while it decreased in atherosclerosis (-0.01 [-0.02 ~ 0], p = 0.04).
Conclusion:
Intracranial vessel narrowing in patients with ischemic stroke changes over time with different stroke etiologies having their own unique temporal patterns.
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