Abstract
Introduction: The presence of white matter hyperintensities (WMH) is associated with stroke, dementia, depression and other medical problems. The presence of WMHs is an independent risk factor for stroke and is associated with worse outcomes after stroke. WMH is frequently seen on neuroimaging in above patients. Hypothesis: The pathophysiology behind the development of WMHs is poorly understood. It has been postulated that there is a link between the presence of carotid artery stenosis (CAS) and WMHs. The presence of carotid atherosclerotic disease could indicate the presence of atheromatous disease in smaller distal vessels leading to chronic small vessel disease and appearance of WMHs. Others have suggested chronic cerebral hypoperfusion resulting from CAS as the underlying mechanism behind the appearance of WMHs. Methods: We reviewed data for 99 stroke patients. We used CT angiogram to grade the degree of CAS. We developed a score of 0 to 3 based on the degree of stenosis. A score of 0 meant no stenosis while a score of 3 meant severe stenosis with > 70% stenosis. A score of 1 for mild stenosis (<50%) and score of two for moderate stenosis (50-69%). Score for right and left side were calculated and added, total range 0 to 6. Using the scoring system, we had 25 patients with no stenosis, 38 with mild, 11 with moderate and 25 with severe stenosis. Patients were matched according to age, NIHSS, CV risk factors. The degree of WMH was scored using Fazekas scoring system (0-3) using T2 FLAIR MRI. Results: Patients with any degree of CAS are 8.5 times more likely to have WMHs than patients without CAS (p>0.001). 74% of patients with CAS have WMHs compared to only 24% of patients without CAS. There is a significant correlation between increased CAS severity and increase WMHs (higher Fazekas score) (r=.324, p=.001). 39% of patients with CAS moderate to severe WMHs (Fazekas 2 or 3) compared to only 16% of patients without CAS. Conclusion: In our patient sample, there seems to be a strong correlation between the presence of carotid artery stenosis and white matter hyperintensities.
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