Current Neurovascular Research - Volume 19, Issue 5, 2022

Background: Retinal artery occlusion (RAO) is an emergency condition in both neurology and ophthalmology departments. However, RAO's management and visual outcome in different initial departments remain unclear. Therefore, we aimed to investigate the impact of the initial department on the management and prognosis of RAO. Methods: Consecutive cases of RAO between January 2011 and December 2021 were retrospectively analyzed. The neurology and ophthalmology departments compared the baseline characteristics, relevant evaluation, and treatment. The primary outcome was the visual recovery rate. The secondary outcomes were newly diagnosed cardiovascular factors, concurrent stroke and new-onset cardiovascular events. Results: A total of 74 RAO patients were included. The median age was 54 years, and 67.6% were male. 42 (56.8%) patients were admitted to the neurology department and 32 (43.2%) to the ophthalmology department. The visual recovery rate was higher in the neurology department than in the ophthalmology department, although the difference did not reach statistical significance (27.8 vs. 12.5%, p = 0.120). Risk factor evaluation and secondary prevention were taken more frequently in the neurology department (p < 0.001). Cardiovascular risk factors and concurrent stroke were all discovered in the neurology department. However, the incidence of new-onset cardiovascular events was similar between the two departments. Conclusion: The study demonstrated that the visual prognosis of RAO was devastating regardless of the neurology and ophthalmology department. Given the admission delay, inadequate management, and high risk of cardiovascular risk factors and stroke, stroke centers should be recommended as initial admission departments for RAO patients.

Background: Depressive symptoms are one of the main clinical features of the cerebral small-vessel disease (CSVD). However, the pathogenesis of depressive symptoms of CSVD has not been fully studied, and a lack of effective diagnostic methodseffective diagnostic methods exists. Recently, the emerging body of evidence regarding exosomes has rendered them potentially key players in the neuropsychiatric disease theragnostic. This study’s aim was to investigate serumexosome proteomic expression in CSVD patients with depressive symptoms and to screen and analyze potential biomarkers for clinical diagnosis. Methods: Serum samples were collected from 36 CSVD patients, including 18 cerebral small-vessel disease (CSVD+D) patients with depressive clinical manifestations and 18 cerebral small-vessel disease patients that did not present depression-related clinical manifestations (CSVD-D). This investigation employed tandem mass tag (TMT) combined with mass spectrometry for sample detection and quantitative analysis of proteins. The differential proteins with significant dysregulated expression levels in patient plasma exosomes were screened and analyzed through bioinformatics techniques. Results: This investigation focused on a global collection of 659 quantifiable proteins. Compared to the CSVD-D group, 7 up-regulated and 30 down-regulated proteins were identified in the CSVD+D group (P < 0.05). Gene ontology (GO) enrichment analyses revealed proteomic expression profile dysregulations within serum exosomes in patients with depression, such as desmosomes and keratins, rendering them as potential biomarkers. Kyoto encyclopedia of genes and genomes (KEGG) database investigations revealed the differentially expressed proteins to be highly aggregated within the estrogen signaling pathway. Conclusion: This investigation pioneered TMT proteomic evaluation of serum exosomes within CSVD patients suffering from depression and reveals the shifts in proteomic expression profiles by serum exosomes within such patients. This study identified several important molecular / signal pathway abnormalities related to depression. These results provide a possible means to further clarify the pathogenesis of depressive symptoms of cerebrovascular disease and its diagnosis and treatment in the future.

Introduction: Diindolylmethane (DIM), a major acid condensation product of Indole-3- carbinol, is known to inhibit platelet aggregation and thrombosis. The drugs with antiplatelet and antithrombotic activities are used to treat ischemic stroke. Objective: The present study investigated the role of DIM on platelet aggregation inhibitory properties in middle cerebral artery occluded (MCAO) rats. Methods: DIM (12.5, 25, and 50 mg/kg) was orally administered to MCAO rats for 3 days. Platelet aggregation, platelet cyclic adenosine monophosphate (cAMP), reactive oxygen species (ROS), hydrogen peroxide (H2O2), and serum cyclooxygenase (COX-1), thromboxane B2 (TXB2), and prostaglandin E2 (PGE2), and inflammatory markers were estimated. Further brain structural and functional recovery was evaluated by measuring cerebral blood flow, neurological deficits, brain infarction, blood-brain barrier (BBB) leakage, brain water content, and histological abnormalities. Results: DIM significantly ameliorated adenosine diphosphate (ADP), collagen, thrombin, and arachidonic acid-induced platelet aggregation by inhibiting COX-1, TXB2, and PGE2 and elevating cAMP. Further, DIM also alleviated platelet-mediated oxidative stress (ROS and H2O2) and reduced the serum inflammatory markers, tumor necrosis factor-α (TNF-α) and interleukin -6 (IL-6), and increased anti-inflammatory cytokine, IL-10, in MCAO rats. Conclusion: DIM treatment confers neuroprotection in MCAO rats by inhibition of platelet aggregation, platelet-mediated oxidative stress, and inflammation. Correspondingly, DIM improved cerebral blood flow and reduced neurological deficits, brain infarction, BBB leakage, brain water content, and histopathological abnormalities indicating the preservation of brain structural integrity. Thus, the present study provided preclinical evidence of DIM neuroprotection against ischemic stroke.

Objective: Treatment of deep-seated cerebral arteriovenous malformations (AVMs) remains challenging for neurosurgeons or neuroradiologists. This study aims to review the experiences of one center in using multimodality treatment for deep-seated AVMs. Methods: The AVM database of Xuanwu Hospital, Capital Medical University was searched, and 96 patients who were diagnosed with a deep-seated cerebral AVM between 2010 and 2020 were identified. The following information was collected and analyzed: patients’ clinical features, treatment modality used, posttreatment complications, AVM obliteration rate, rebleeding rate, and functional outcome during follow-up. The patients’ posttreatment modified Rankin scale (mRS) scores were split into two groups: good outcome (mRS score ≤ 2) and poor outcome (mRS score ≥ 3). Univariate and multivariate logistic regression analyses were applied to test the predictors of clinical outcomes and AVM obliteration. Results: Eighty-eight out of 96 patients (91.7%) presented with initial hemorrhaging. The pretreatment mRS score was ≤ 2 in 80 patients (88.3%) patients and ≥ 3 in 16 patients (16.7%). Limb weakness was present in 42 patients (43.8%). In this sample, 210 hemorrhages occurred during 2056 person-years before diagnosis, yielding an annual hemorrhage rate of 10.2% per person-year. Angiographic obliteration was achieved in 29 patients (30.2%). At the last follow-up, 80 patients (83.3%) had good clinical outcomes, whereas 16 (16.7%) had a deterioration in their clinical presentation following treatment. Multivariate analyses indicated that pretreatment limb weaknesses and a high Spetzler–Martin grade predicted poor clinical outcomes (P = 0.003 and 0.008, respectively). Fewer feeding arteries were a predictor for AVM obliteration (P = 0.034). Conclusion: Good outcomes can be achieved through multimodal treatment of deep-seated AVMs. A single supplying artery is a predictor of AVM obliteration. Pretreatment limb weaknesses and high Spetzler-Martin grades predict poor clinical outcomes.

Background: A certain number of patients with single subcortical small infarction (SSSI) in the lenticulostriate artery (LSA) territory present with early neurological deterioration (END). Objective: We sought to identify a more specific predicting imaging marker for END in lenticulostriate SSSI patients. Methods: We screened patients in a prospective hospital-based registry of stroke in the first Affiliated Hospital of Zhengzhou University from January 2015 to December 2020. Lesion locations were defined as posterior type when more than half of the lesion was located in the posterior part of the corona radiata divided by the midline, which was drawn between the tangents of the anterior and posterior horns of the lateral ventricle and was adjacent to the lateral ventricle at the same time. END was defined as an increase of ≥2 points in total National Institutes of Health Stroke Scale score or ≥1 point. A multivariate logistic analysis was used to assess the imaging predictors for END. Results: 418 patients were enrolled in the final data analysis. Among them, 206 (49. 3) cases were rated as the posterior type and7117. 0cases had to END. A multivariate logistic analysis showed that only the posterior type (adjusted odds ratio, 2. 126; 95% confidence interval, 1. 250–3. 614; P = 0. 005) was independently associated with the risk of END. Conclusion: The posterior type of lesion location represented an imaging marker predicting END in lenticulostriate SSSI patients.

Objective: The objective of this study is to investigate the relationship between mean platelet volume (MPV)/platelet count (PC) ratio and post-thrombolytic early neurological deterioration (END) in patients with mild and moderate stroke. Methods: Mild and moderate stroke patients treated with intravenous thrombolysis (IVT) at the Affiliated Changsha Central Hospital of the University of South China between January 2016 and March 2022 were prospectively and consecutively enrolled. END was defined as an increase in the total National Institutes of Health Stroke Scale (NIHSS) score of ≥4 points or an increase in the motor items of ≥1 point within 24 hours after IVT treatment. Logistic regression and restricted cubic spline models were used to estimate the relationship between the MPV/PC ratio and postthrombolytic END. Results: Among the 406 patients recruited, 64 (15.8%) patients developed END. Patients in the first quintile of MPV/PC ratio (adjusted OR = 0.27, 95% CI = 0.11-0.66, p = 0.004) and the fifth quintile (adjusted OR = 0.26, 95% CI = 0.10-0.69, p = 0.007) had a significantly lower risk of END compared with those in the third quintile. Restricted cubic spline analysis revealed an inverted U-shaped relationship between the MPV/PC ratio and END (p for nonlinearity = 0.016). MPV/PC ratio cut-off value associated with the highest END risk was 51.0. An MPV/PC ratio ≤ 51.0 was shown to be positively associated with END (adjusted OR = 1.07, 95% CI = 1.02-1.14, p = 0.012), while an MPV/PC ratio >51.0 was negatively associated with END (adjusted OR = 0.94, 95% CI = 0.88-1.00, p = 0.040). A significant interaction existed between the MPV/PC ratio and age in the low MPV/PC ratio group (p = 0.012). MPV/PC ratio was positively associated with END only in patients ≥ 60 years, whereas this association was insignificant in patients < 60 years. Conclusion: An inverted U-shaped relationship between the MPV/PC ratio on admission and postthrombolytic END was identified in patients with mild and moderate stroke, with a threshold MPV/PC ratio of 51.0. The MPV/PC ratio closer to the threshold was associated with a higher risk of post-thrombolytic END.

Background: Cognitive impairment after acute intracerebral hemorrhage (ICH) is common. While the evidence of early cognitive impairment at the acute stage after ICH is limited. We determined the frequency and risk factors of early cognitive impairment at the acute stage and investigated its association with delayed cognitive impairment after ICH. Methods: A total of 208 patients with acute ICH were enrolled from January 2017 to February 2019. Cognitive function was assessed during the acute stage and at follow-up using Montreal Cognitive Assessment (MoCA) score. Significant cognitive impairment was defined as having a MoCA score <20 at the acute stage (within 1 week after hospital admission) or during follow-up. Results: The mean observation period was 20 (IQC 17-23) months, and follow-up cognitive function data were collected from 185 patients. 89 (42.8%) and 86 (46.5%) patients had an acute stage and delayed significant cognitive impairment, respectively. Older age, large baseline hematoma volume, more severe ICH, and low level of education were significantly associated with significant cognitive impairment at the acute stage (all P ≤ 0.009). In the multivariable logistic regression model, the low MoCA score (odds ratio [OR] 0.59; 95% confidence interval [CI] 0.48-0.71; P0.001) at the acute stage was independently associated with delayed significant cognitive impairment after ICH. Conclusion: Near half of the patients had significant cognitive impairment at the acute stage after ICH. Cognitive impairment is more frequent in the elderly, those with large baseline hematoma volume, and more severe initial neurological deficit. Having a lower MoCA score during the acute phase was independently associated with an increased risk of delayed cognitive impairment.