Recent small subcortical infarcts (RSSIs) can occur in different brain regions. Distinct etiologies might be involved for RSSIs in different locations and could further affect RSSI cavitation and functional outcomes. In this study, we aim to analyze the baseline clinical and imaging characteristics associated with the occurrence and cavitation of RSSIs in different locations. We retrospectively include patients who presented with RSSIs from a database for cerebral small vessel disease. Detailed information, including demographic, clinical, laboratory, and radiological data, were collected. We identify baseline RSSIs on diffusion-weighted images and divide them into brainstem, subcortical white matter, and basal ganglia region groups. Cavitation is evaluated on follow-up T2 fluid-attenuated inversion recovery (FLAIR) images. Statistical analysis is performed to determine factors associated with the occurrence and cavitation of RSSIs in different locations. We find that patients with brainstem RSSIs have a higher proportion of diabetes (64.1%) compared to patients with subcortical white matter (27.3%, P < 0.001) and basal ganglia region RSSIs (35.2%, P = 0.006) and have higher levels of HbA1c (7.20%) compared to patients with subcortical white matter (6.10%, P = 0.001) and basal ganglia region RSSIs (6.20%, P = 0.003). In addition, patients with brainstem RSSIs have higher NIHSS scores than patients with subcortical white matter RSSIs (2 vs 0, P = 0.001). Patients with subcortical white matter RSSIs have higher a white matter hyperintensity (WMH) burden compared to patients with basal ganglia region RSSIs (21.64 cm3 vs 11.10 cm3, P = 0.004). Follow-up analysis demonstrates that basal ganglia region RSSIs are less likely to cavitate than subcortical white matter RSSIs (61.4% vs 83.6%, P = 0.010), and contacting with WMH is associated with the cavitation of subcortical white matter RSSIs (OR: 101.760, P = 0.003). Our study demonstrates that RSSIs in different locations are associated with different clinical and imaging characteristics. Furthermore, cavitation of RSSIs might be affected by local lesion features and the surrounding environment rather than general demographic and clinical factors.
We assess microstructural alterations in superficial white matter (SWM) in cerebral small vessel disease (CSVD) and evaluate their contributions to the decline in processing speed, which is the main dysfunction in CSVD. We identify that the significant decline in processing speed may relate to the involvement of WMH in the SWM under high burden of disease. The increased extracellular free water may be the main SWM microstructural change under low burden of disease. These observations suggest that the SWM may serve as a potential target for monitoring pathophysiological processes in CSVD. This study extends the current understanding of CSVD-related dysfunction.
Understanding the pathophysiology of white matter hyperintensity (WMH) is necessary to reduce its harmfulness. Dilated perivascular space (PVS) had been found related to WMH. In the present study, we aimed to examine the topological connections between WMH and PVS, and to investigate whether increased interstitial fluid mediates the correlation between PVS and WMH volumes. One hundred and thirty-six healthy elder subjects were retrospectively included from a prospectively collected community cohort. Sub-millimeter T2 weighted and FLAIR images were acquired for assessing the association between PVS and WMH. Diffusion tensor imaging and free-water (FW) analytical methods were used to quantify white matter free water content, and to explore whether it mediates the PVS-WMH association. We found that most (89%) of the deep WMH lesions were spatially connected with PVS, exhibiting several interesting topological types. PVS and WMH volumes were also significantly correlated (r = 0.222, p < 0.001). FW mediated this association in the whole sample (β = 0.069, p = 0.037) and in subjects with relatively high WMH load (β = 0.118, p = 0.006). These findings suggest a tight association between PVS dilation and WMH formation, which might be linked by the impaired glymphatic drainage function and accumulated local interstitial fluid.
Objectives: We hypothesized that the presence of delayed contrast filling sign (DCFS), which possibly reflected contrast penetration into the thrombus, was associated with stroke etiology with different clot component. We then aimed to evaluate its predictive value for stroke subtype in acute ischemic stroke (AIS) patients with M1 segment of MCA (MCA-M1) occlusion. Methods: We retrospectively included MCA-M1 occlusion patirnts who underwent CTP within 8 hours post-stroke onset. DCFS was defined as the presence of contrast diffusion through the thrombi after the arterial peak phase on 4D-CTA derived from CTP. We measured the straight distance from the origin site of MCA-M1 to the proximal occlusion site on the arterial peak phase (distance peak ), and the maximum distance among every continuous phase after the arterial peak phase (distance maximum ). We calculated the distance of DCFS as distance maximum -distance peak and investigated its value for predicting the stroke subtype. Results: Among 144 included patients, 80 were in cardiogenic embolism (CE) group, 31 in large artery atherosclerosis (LAA) group, and 33 in undetermined etiology (UE) group. The median distance of DCFS was 1.3mm, 0.4mm and 0.6mm in CE, LAA and UE groups, respectively. CE group had a longer distance of DCFS than LAA group ( p =0.001). The optimal cut-off value of distance of DCFS for predicting CE was 1.5mm. The sensitivity, specificity, positive predictive value and negative predictive value of a distance of DCFS>1.5mm for predicting CE were 55.0%, 87.1%, 90.0% and 38.0%. Moreover, a distance of DCFS>2.0mm had a specificity of 100% for predicting CE. Figure A-E shows a patient with DCFS>1.5mm, and Figure F-J shows a patient with DCFS<1.5mm. Conclusion: Long distance of DCFS was associated with cardiogenic embolism, which could provide clues of stroke etiology and help the pattern selection of reperfusion therapy in future.
Cognitive processing speed is crucial for human cognition and declines with aging. White matter hyperintensity (WMH), a common sign of WM vascular damage in the elderly, is closely related to slower psychomotor processing speed. In this study, we investigated the association between WMH and psychomotor speed changes through a comprehensive assessment of brain structural and functional features. Multi-modal MRIs were acquired from 60 elderly adults. Psychomotor processing speeds were assessed using the Trail Making Test Part A (TMT-A). Linear regression analyses were performed to assess the associations between TMT-A and brain features, including WMH volumes in five cerebral regions, diffusivity parameters in the major WM tracts, regional gray matter volume, and brain activities across the whole brain. Hierarchical regression analysis was used to demonstrate the contribution of each index to slower psychomotor processing speed. Linear regression analysis demonstrated that WMH volume in the occipital lobe and fractional anisotropy of the forceps major, an occipital association tract, were associated with TMT-A. Besides, resting-state brain activities in the visual cortex connected to the forceps major were associated with TMT-A. Hierarchical regression showed fractional anisotropy of the forceps major and regional brain activities were significant predictors of TMT-A. The occurrence of WMH, combined with the disruption of passing-through fiber integrity and altered functional activities in areas connected by this fiber, are associated with a decline of psychomotor processing speed. While the causal relationship of this WMH-Tract-Function-Behavior link requires further investigation, this study enhances our understanding of these complex mechanisms.
Objectives: With the trend of an aging population, an increasing prevalence of late-life depression has been identified. Several studies demonstrated that iron deposition was significantly related to the severity of symptoms in patients with depression. However, whether brain iron deposits influence depressive symptoms is so far unclear in the community of older adults. We measured iron deposition in deep intracranial nucleus by quantitative susceptibility mapping (QSM) and aimed to explore the relationship between iron deposition and depressive symptoms. Methods: We reviewed the data of a community population from CIRCLE study, which is a single-center prospective observational study that enrolled individuals above 40 years old with cerebral small vessel disease (SVD), while free of known dementia or stroke. We evaluated regional iron deposits on QSM, measured the volume of white matter hyperintensities (WMHs) on T2 fluid-attenuated inversion recovery, and assessed depressive symptoms by Hamilton depression scale (HDRS). We defined depressive symptom as HDRS > 7. Results: A total of 185 participants were enrolled. Participants in depressive symptom group had higher QSM value in thalamus than control group (18.79 ± 14.94 vs 13.29 ± 7.64, p = 0.003). The QSM value in the thalamus was an independent factor for the presence of depressive symptoms (OR = 1.055; 95% CI: 1.011-1.100; p = 0.013). The regional QSM values in other areas were not associated with HDRS score (all p > 0.05). No significant correlations were observed between WMHs volume and HDRS score (p > 0.05), or regional QSM values and WMHs volume (all p > 0.05). Conclusions: Our study demonstrated that iron deposits in the thalamus were related to the depressive symptoms in older adults.
Aim White matter hyperintensities (WMH) and lacunes were important features of cerebral small vessel disease (CSVD), which contributes to 25% of ischemic strokes and 45% of dementias. Currently, the underlying mechanisms of WMH and lacunes are not clear, and the role of hemodynamic changes is not fully investigated. In this study, we aimed to measure the cerebral blood flow (CBF) and arterial transit in CSVD patients and to investigate their association with WMH and lacunes. Methods We retrospectively analyzed the prospectively collected database of CSVD patients. Ninety-two CSVD patients with complete imaging data were included. We used arterial spin labeling (ASL) with post-labeling delay time (PLD) of 1,525 ms and 2,025 ms to measure CBF respectively, and the difference between CBF PLD1.5 and CBF PLD2.0 was recorded as δCBF. We performed regression analysis to understand the contribution of CBF, δCBF to CSVD imaging markers. Results We found that CBF derived from both PLDs was associated with WMH volume and the presence of lacune. CBF PLD1.5 was significantly lower than CBF PLD2.0 in CSVD patients, and δCBF was correlated with WMH volume but not the presence of lacune. Furthermore, CBF PLD2.0 and δCBF were both associated with WMH in multiple regression analyses, suggesting an independent effect of delayed arterial transit. On an exploratory basis, we also investigated the relationship between venous disruption on δCBF, and we found that δCBF correlated with deep medullary veins score. Conclusion Both CBF and arterial transit were associated with WMH. ASL with multiple PLDs could provide additional hemodynamic information to CSVD-related studies.
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