Factors affecting distal hyperintense vessel sign, a postulated marker for intracranial collateral circulation

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Conference Proceeding

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Objective: To investigate factors affecting the distal hyperintense vessel sign (DHVS) Background: DHVS on FLAIR sequence is considered to originate from the leptomeningeal collateral flow. Older studies have analyzed factors affecting collateral circulation using CT and conventional angiographies but so far, no study has investigated the association between DHVS and said factors to strengthen the hypothesis of the origin of DHVS. Design/Methods: Two-hundred charts were reviewed based on ICD-9 codes. Thirty-eight were selected based on the presence of acute ischemic stroke due to symptomatic internal carotid or middle cerebral artery disease. A neuroradiologist blindly quantified DHVS using the number of cortical-MCA regions (defined by ASPECTS) positive for DHVS (range 0-7). The patients were dichotomized into groups of <3 and ≥3 score. Demographics, coexisting risk factors, clinical measures of stroke severity (NIHSS and mRS at discharge and follow-up) and stroke volume were compared between two groups. Fischer's exact test was used for binary variables. Two-sample t-test and Wilcoxon- test was used for continuous variables. Results: Seven (18%) patients had DHVS-score ≥3. These patients were significantly younger (53.6 vs 66.5 yr, p=0.036), less likely to have hypertension (29% v 87%, p=0.004), diabetes (0% v 47%, p=0.016), and have lower measures of glucose intolerance (mean A1c 5.6 v 6.2, p=0.006). No statistically significant difference was noted with other variables. Conclusions: We note consistencies between prior studies and our study showing that younger patients without hypertension have better collaterals. We also found an association of diabetes with less DHVS whereas prior studies have yielded an inconsistent association. While a correlation between stroke severity and stroke volume could not be confirmed, low power and wide stroke-to-MRI gap (range 1-8 d) were important limitations here. Further study correcting these shortcomings is warranted. In conclusion, our findings support the origins of DHVS from collateral circulation and are affected by traditional cerebrovascular risk factors.




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