ObjectiveTo assess the suitability of deep medullary vein visibility in susceptibility weighted imaging—magnetic resonance imaging studies as a method for the diagnosis and evaluation of cerebral small vessel disease progression.MethodsA total of 92 patients with CSVD were enrolled and baseline clinical and imaging data were reviewed retrospectively. Neuroimaging biomarkers of CSVD including high-grade white matter hyperintensity (HWMH), cerebral microbleed (CMB), enlarged perivascular space (PVS), and lacunar infarct (LI) were identified and CSVD burden was calculated. Cases were grouped accordingly as mild, moderate, or severe. The DMV was divided into six segments according to the regional anatomy. The total DMV score (0–18) was calculated as the sum of the six individual segmental scores, which ranged from 0 to 3, for a semi-quantitative assessment of the DMV based on segmental continuity and visibility.ResultsThe DMV score was independently associated with the presence of HWMH, PVS, and LI (P < 0.05), but not with presence and absence of CMB (P > 0.05). Correlation between the DMV score and the CSVD burden was significant (P < 0.05) [OR 95% C.I., 1.227 (1.096–1.388)].ConclusionThe DMV score was associated with the presence and severity of CSVD.

Objective: To explore the relationships of asymmetric deep medullary veins (ADMV) to asymmetric cortical veins (ACV), leptomeningeal collaterals and prognosis in patients with occlusion of a large cerebral artery.Methods: Clinical and imaging data of 56 patients with occlusion of a large cerebral artery were collected and reviewed. We assessed the time delayed between stroke onset and MR imaging (within 24 h of stroke onset), extension of cerebral infarction using the Alberta stroke program early CT score based on diffusion-weighted imaging (ASPECTs). ADMV and ACV were assessed using susceptibility-weighted imaging. The presence of ADMV (ACV) was defined as deep medullary veins (cortical veins) of the affected hemisphere that were greater in number and diameter than in the contralateral hemisphere. To evaluate leptomeningeal collaterals, the hyperintense vessel sign (HVS) was detected using T2 weighted fluid attenuated inversion recovery images. At 90 days, a modified Rankin scale score (mRS) was assessed to evaluate the clinical outcome.Results: Of 56 patients, 27 presented with ADMV. Those patients who presented with and without ADMV differed significantly in HVS and ACV (P < 0.05) but not in time delayed between stroke onset and MR imaging, age, gender, stroke risk factors, baseline NIHSS score, or modified Rankin scale score at 3 months (P > 0.05). Logistic regression analysis found that the presence of ADMV was independently related to HVS and ACV (ACV: OR 95% C.I., 1.287–4.368; HVS: OR 95% C.I., 1.132–4.887).Conclusions: The presence of ADMV on SWI was associated with prominent ACV and good leptomeningeal collateral flow but was not related to prognosis in patients with occlusion of a large cerebral artery.

Background: This study was conducted to explore the risk factors of anterior circulation intracranial aneurysm rupture based on extracranial carotid artery (ECA) tortuosity.Methods: This retrospective study, conducted from January 1, 2017, to March 1, 2021, collected and reviewed the clinical and imaging data of 308 patients with anterior circulation intracranial aneurysm [133 (43.2%) patients in the ruptured aneurysm group; 175 (56.8%) patients in the unruptured aneurysm group]. Computed tomography angiography (CTA) of the head and neck was used to determine the ECA tortuosity (normal, simple tortuosity, kink, coil) and the morphologic parameters of the aneurysms. The relationship of aneurysm rupture to ECA tortuosity and the morphologic parameters were analyzed.Results: After univariate analysis, kink, angle of flow inflow (FA), aspect ratio (AR), aneurysm length (L), the distance from the tortuosity to the aneurysm (distance), and size ratio (SR) were significantly correlated with anterior circulation intracranial aneurysm rupture (p &lt; 0.05). Spearman correlation analysis showed that ECA tortuosity was correlated with FA and SR (p &lt; 0.05). Multiple logistic analyses showed that FA [odds ratio (OR), 1.013; 95% CI, 1.002–1.025], SR (OR, 1.521; 95% CI, 1.054–2.195), and kink (OR, 1.823; 95% CI, 1.074–3.096) were independently associated with aneurysm rupture.Conclusion: Study results suggest that FA, SR, and ECA kink were independent risk factors associated with anterior circulation intracranial aneurysm rupture.

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Objective: To explore the relation between diffusion-weighted and susceptibility weighted imaging (DWI-SWI) mismatch and collateral circulation or prognosis in patients with occluded M1 segments of middle cerebral artery (MCA).Methods: We enrolled 59 patients with MCA M1-segment occlusion for a retrospective review of baseline clinical and imaging data. As markers of circulatory collaterals, prominent laterality of posterior (PLPCA) and anterior (PLACA) cerebral arteries on magnetic resonance angiography (MRA) studies and a hyperintense vessel sign (HVS) on T2 fluid-attenuated inversion recovery (FLAIR) images were collectively scored. The extent of acute cerebral infarction was then quantified on DWI, using the Alberta Stroke Program Early CT Score (DWI-ASPECTS). Hypointensity vessel sign prominence (PVS) was also evaluated by SWI and similarly scored (SWI-ASPECT) to calculate DWI-SWI mismatch [(DWI-ASPECTS) – (SWI-ASPECTS)], ranging from −10 to 10 points.Results: DWI-SWI mismatch showed significant associations with PLPCA, PLACA, HVS prominence, and collective collateral scores (all, p &lt; 0.05). National Institutes of Health Stroke Scale (NIHSS), DWI-SWI mismatch, and DWI-ASPECTS also differed significantly according to patient prognosis (good vs. poor) after MCA M1-segment occlusion (p &lt; 0.05). In binary logistic regression analyses, NIHSS and DWI-SWI mismatch emerged as independent prognostic factors (p &lt; 0.05).Conclusions: Collateral circulation may be an important aspect of DWI-SWI mismatch, which in this study correlated with prognostic outcomes of MCA M1-segment occlusion.