Abstract: BACKGROUND: Obstructive sleep apnea (OSA) involves intermittent hypoxia and sleep fragmentation and is associated with adverse outcomes. Remote ischemic conditioning (RIC), a noninvasive intervention with vascular protective effects, modulates mechanisms shared by OSA and ischemic injury, including oxidative stress, inflammation, endothelial dysfunction, and autonomic imbalance. Its efficacy in OSA populations remains insufficiently studied. METHODS: This post hoc analysis of the RIC-PS trial included stroke patients with OSA (Apnea-Hypopnea Index ≥ 5). We compared pre-to-post changes between the original RIC and sham-RIC groups. Outcomes covered sleep (Pittsburgh Sleep Quality Index [PSQI], Insomnia Severity Index [ISI]), wearable parameters, HRV, psychology (Self-rating Anxiety Scale [SAS]/Self-rating Depression Scale [SDS]), and ICF-based function. Effect sizes (Cohen’s d ), Spearman correlations, and subgroup analyses (within RIC group) were performed to compare the effects of RIC versus sham on multidimensional recovery. RESULTS: Among 60 screened participants, 45 met OSA criteria (mean age 69 years; 25 male and 20 female). RIC ( n = 24) versus sham ( n = 21) showed significant medium-to-large effects on ISI ( d = 0.807), SAS ( d = 0.834), SDS ( d = 0.870), and ICF-based functional scale ( d = 1.111). Subjective sleep quality (PSQI) favored RIC ( d = 0.547, nonsignificant). Objective sleep parameters showed small, inconsistent effects. Improvements in sleep quality (PSQI) were positively correlated with reductions in anxiety (SAS, r = 0.518) and depression (SDS, r = 0.482). Greater benefits were observed in ischemic stroke (ISI improvement: r = −0.453) and subacute patients (sleep efficiency: r = −0.511), with trends toward stronger effects in those with ≥ 2 comorbidities. CONCLUSIONS: RIC may serve as a promising adjunctive therapy for improving sleep-related, psychological, and functional outcomes in stroke patients with OSA. The observed inter-domain associations and subgroup variability suggest integrated therapeutic effects and highlight the potential value of patient stratification in poststroke rehabilitation. However, given the modest sample size and the exploratory, post hoc nature of this analysis, these findings should be interpreted with caution. Larger prospective studies are warranted. TRIAL REGISTRATION: www.chictr.org.cn (identifier: ChiCTR2600128371).
Abstract: BACKGROUND: Cervical artery dissection is a major cause of ischemic stroke in young adults, but its etiology often remains unclear in the absence of connective-tissue disease. Variation in styloid process (SP) anatomy and its proximity to the internal carotid artery (ICA) may contribute mechanically to arterial injury, but its role in ICA dissection is not well defined. METHODS: We conducted a retrospective, single-center observational study using a continuously maintained computed tomography angiography registry. Patients with spontaneous ICA dissection were identified and matched 1:2 by age and sex to control subjects without cervical vascular abnormalities. Quantitative computed tomography measurements of the stylohyoid complex morphology and stylocarotid distance were obtained using oblique multiplanar reconstructions. RESULTS: The analysis included 44 measurements from patients with ICA dissection and 88 matched control measurements. Among patients with ICA dissection, the distance between the stylohyoid complex and the ICA on the affected side was smaller than on the contralateral side (median: 3.3 mm [interquartile range (IQR): 2.08–5.15] vs. 4.7 mm [IQR: 3.08–7.05]; P < 0.01). A shorter stylocarotid distance was independently associated with ICA dissection (odds ratio: 0.71; 95% confidence interval: 0.58–0.84; P < 0.001), whereas no associations were observed for SP length, thickness, or ligamentous ossification. CONCLUSION: Close spatial proximity between the stylohyoid complex and the ICA represents an anatomical susceptibility factor for ICA dissection. Recognizing this relationship may improve individualized risk stratification and inform tailored imaging follow-up, while underscoring the need for prospective studies to clarify its implications for long-term management.
Abstract: BACKGROUND: Remote ischemic conditioning (RIC) is a simple, low-cost, and safe intervention. Clinical evidence regarding its effects on sleep disturbances and related psychological symptoms during the poststroke rehabilitation phase remains limited. This pilot study evaluated the feasibility and clinical effects of RIC in this population. METHODS: In this multicenter, randomized, double-blind, sham-controlled pilot trial, patients undergoing poststroke rehabilitation with comorbid sleep disturbances were randomized to receive either RIC or a sham intervention for 2 weeks. As a pilot trial, no single primary outcome was prospectively designated; all endpoints were considered exploratory and were intended to generate preliminary effect estimates to inform future confirmatory studies. Objective sleep parameters were obtained using a portable monitoring system, and subjective sleep and psychological outcomes were evaluated using validated questionnaires. Between-group comparisons were performed on change from baseline values, and safety was monitored throughout the study. RESULTS: Sixty patients completed the study (30 RIC, 30 sham-RIC). Compared with the Sham group, the RIC group exhibited a greater reduction in nocturnal awakenings ( P < 0.001) and mean hypopnea duration ( P = 0.041). Reductions in Insomnia Severity Index, Zung Self-Rating Anxiety Scale, and Zung Self-Rating Depression Scale scores were also greater in the RIC group (all P < 0.05), No between-group differences were observed in total Pittsburgh Sleep Quality Index scores, sleep architecture parameters, or heart rate variability indices. No serious RIC-related adverse events occurred. CONCLUSIONS: A 2-week RIC intervention was safe and well-tolerated and was associated with improvements in sleep continuity and mood-related symptoms in stroke patients undergoing rehabilitation, without short-term changes in overall sleep architecture. Given the exploratory pilot design and the limited sample, these findings should be interpreted as preliminary signal estimates that support feasibility and justify evaluation in larger adequately-powered randomized trials. TRIAL REGISTRATION: www.chictr.org.cn (identifier: ChiCTR2600128371).
Mild traumatic brain injury (mTBI) constitutes a pervasive yet often overlooked public health challenge with far-reaching implications for individual well-being and healthcare systems globally. This review synthesizes contemporary evidence on diagnosis, management, and emerging treatment paradigms for mTBI using a structured, comprehensive literature search strategy. Through comprehensive literature analysis spanning multiple databases-PubMed, Cochrane Library, EMBASE, and Web of Science-from January 2018 to January 2025. A total of 183 studies met inclusion criteria, comprising 42 systematic reviews and meta-analyses, 58 randomized controlled trials, and 83 observational studies. We have identified transformative advances in biomarker research, neuroimaging techniques, and targeted interventions while uncovering persistent challenges in standardizing diagnostic and treatment protocols. Recent randomized controlled trials and meta-analyses reveal promising outcomes for early intervention strategies, cognitive rehabilitation approaches, and novel pharmacological treatments. However, methodological limitations-including heterogeneous mTBI definitions, inconsistent outcome measures, and insufficient long-term follow-up-underscore the need for large-scale trials using standardized definitions and common data elements. Future research must prioritize personalized treatment approaches, integration of cutting-edge technology in assessment and monitoring, and addressing the troubling disparities in access to specialized care for mTBI patients-particularly among vulnerable populations.
Abstract: The triglyceride–glucose (TyG) index, recognized as a novel surrogate marker for insulin resistance (IR), has been established by multiple studies to be significantly associated with ischemic stroke. Current evidence indicates that the TyG index is closely correlated with the risk of ischemic stroke onset, disease progression (clinical deterioration), clinical prognosis, recurrence, and mortality. This suggests its potential utility as a biomarker reflecting different stages of ischemic stroke (e.g., acute, recovery, and chronic phases) and prognostic outcomes (e.g., functional recovery, recurrence, and mortality). However, there remains a lack of systematic reviews comprehensively examining the correlation between the TyG index and the various stages of ischemic stroke and their prognostic outcomes, along with an exploration of the underlying mechanisms. This review aims to systematically elucidate the background and evidence establishing the TyG index as a surrogate marker for IR, explore the potential mechanisms by which it contributes to the pathogenesis and progression of ischemic stroke from the core pathophysiological perspective of IR, while concurrently critically evaluating the existing research evidence on the association between the TyG index and the different stages of ischemic stroke as well as prognostic outcomes, and highlighting current research limitations. By synthesizing current knowledge, this review expects to provide a theoretical foundation for utilizing the TyG index to identify high-risk populations for ischemic stroke at an early stage and predict the risk of adverse prognostic outcomes (including disease progression and mortality), thereby exploring its potential clinical applications and early-warning value.
Abstract: Semaglutide, a glucagon-like peptide-1 receptor agonist, has attracted increasing scientific interest for its potential relevance to neurological and psychiatric conditions beyond its established indications for type 2 diabetes and obesity. Emerging evidence from preclinical models, observational human studies, and early-phase clinical investigations suggests that semaglutide engages central nervous system pathways implicated in neurodegeneration, reward processing, and behavioral regulation. Proposed mechanisms include modulation of neuroinflammatory signaling, oxidative stress, protein aggregation, autophagy, mitochondrial function, and dopaminergic neurotransmission. This narrative review synthesizes current evidence examining semaglutide’s associations with neurological and psychiatric outcomes, including Alzheimer’s disease, Parkinson’s disease, substance use disorders, and disordered eating behaviors. Large-scale epidemiological studies report consistent associations between semaglutide exposure and reduced incidence or recurrence of several substance use and eating disorders, while preclinical models demonstrate biologically plausible effects on disease-relevant pathways. However, available human data are predominantly observational, and randomized controlled trials establishing clinical efficacy for off-label neuropsychiatric indications are limited or ongoing. Evidence regarding mood and anxiety outcomes is mixed, with randomized trial data in selected populations suggesting psychiatric safety comparable to placebo, contrasted by signals of potential risk in real-world and pharmacovigilance datasets. These findings highlight the importance of careful patient selection, monitoring, and further investigation. Ongoing clinical trials and mechanistic studies will be critical to clarifying semaglutide’s central effects, defining appropriate clinical contexts, and determining whether observed associations translate into meaningful therapeutic benefit.
Abstract: There are close interactions between acute ischemic stroke (AIS) and heart diseases, including heart-to-brain interactions (cardioembolic strokes), brain-to-heart interactions (cardiac complications after AIS), and brain-and-heart interactions (coexisting coronary artery disease in AIS). The heart problems not only add complexity to the etiological diagnosis but also account for a significant proportionate mortality in AIS patients. Cardiac coronary computed tomography angiography (CCTA) is becoming a promising and convenient technique allowing for evaluating both coronary atherosclerosis and cardiac structures or function. This review discussed the emerging clinical applications of CCTA in AIS patients, contributing to comprehensive management for optimizing the treatment of AIS and related heart diseases. Summarily, CCTA has been validated as a trustworthy alternative imaging technique to transesophageal echocardiography for detecting cardioaortic embolism sources for patients with AIS, and incorporating CCTA into the stroke CT imaging protocol during the hyperacute stage for AIS patients eligible for reperfusion therapy seems practical. In addition, as AIS patients had higher cardiovascular risk, the use of CCTA to evaluate coronary stenosis, plaque burden, and high-risk plaque may benefit the treatment and prognosis of some AIS patients, particularly those with any cervicocephalic artery stenosis ≥ 50% and multiple vascular risk factors. CCTA might help achieve a more all-encompassing cardiovascular evaluation for AIS patients with possible cardiac complications. As there were limited reports and literature about the relevant issues, there is a need for targeted studies to assess if CCTA could lead to a more accurate reclassification of the causes of cardiac complications after AIS.
Abstract: Ischemic stroke not only causes localized cerebral injury but also triggers systemic disturbances across multiple organs, most prominently within the gastrointestinal tract. Emerging evidence underscores the gut–brain axis (GBA) as a key determinant of stroke pathogenesis, recovery, and prognosis. Acupuncture—a core modality of traditional Chinese medicine—has demonstrated reproducible clinical efficacy in stroke rehabilitation; however, its mechanistic basis within the GBA framework remains incompletely defined. This narrative review synthesizes findings from preclinical and clinical studies retrieved from PubMed and Web of Science up to October 2025. This review integrates current experimental and clinical findings to elucidate how acupuncture mitigates ischemic stroke through multilevel modulation of the GBA. Specifically, acupuncture (1) rectifies gut dysbiosis by restraining pathogenic taxa and enriching commensal microbiota, thereby reinforcing intestinal barrier integrity through upregulation of tight junction proteins (ZO-1, occludin); (2) rebalances neuroendocrine activity by inhibiting hypothalamic–pituitary–adrenal axis hyperactivation while enhancing vagus-mediated cholinergic anti-inflammatory signaling; (3) reprograms gut-derived metabolic profiles by increasing neuroprotective short-chain fatty acids and reducing neurotoxic trimethylamine N-oxide; and (4) restores immune homeostasis by modulating peripheral–central immune crosstalk and promoting neurorepair. Collectively, these insights establish acupuncture as a system-level regulator capable of restoring GBA homeostasis after stroke, providing a mechanistic framework for precision-targeted and translational interventions. The synthesized framework not only elucidates acupuncture’s system-level mechanisms but also highlights its potential as a precision neuromodulatory therapy, guiding future translational research in integrative stroke care.
Abstract: How can we avoid secondary brain injury due to failed , delayed , or physiologically unfavorable ventilator liberation in neurosurgical patients outside of the operating room ? This question has exposed us to a dilemma between prolonged mechanical ventilation (MV)/weaning and the potential development of secondary neurological insults. In turn, one of the main dilemmas in neurocritical care units (NCCUs) is whether the neurological status of this vulnerable population might worsen as a result of prolonged MV. Accordingly, failed extubation attempts constitute one of the main risk factors that can significantly increase mortality and hospital length of stay. Given this: Should We Do Individualized Management during Extubation in Neurocritically Ill Patients? To address this question, a hypothesis-generating framework that led to the development of a Clinical Algorithm to Protect neurocritically ill patients under Mechanical Ventilation through Acute Brain Injury during extubation (CAPREVI), which synthesizes conceptually key neurological, hemodynamic, and respiratory parameters to mitigate secondary neurological insults during ventilator weaning and shorten MV duration. In addition, following the Scale for the Assessment of Narrative Review Articles (SANRA) checklist, we conducted a literature review of prospective studies (2000–2026) about weaning in neurocritically ill patients.
Abstract: Stroke remains a major global contributor to mortality and long-term disability, imposing substantial burdens on both individuals and societal systems. Current therapeutic interventions remain limited despite extensive scientific exploration. Small extracellular vesicles termed exosomes have emerged as a focal point in cerebrovascular research, owing to their distinctive biological properties including blood–brain barrier permeability, minimal immunogenic responses, and intercellular signaling capabilities. This comprehensive analysis synthesizes contemporary understanding of exosomal roles in stroke pathophysiology, encompassing diagnostic biomarker potential, therapeutic applications, and mechanistic insights. Through systematic database interrogation and critical evaluation of multidisciplinary studies, we identify the exosome-mediated transport of protein complexes, regulatory microRNAs, long noncoding RNAs, and circular RNAs as critical modulators of inflammatory cascades, vascular remodeling, neural regeneration, and programmed cell death pathways. Diagnostic applications demonstrate that exosomal signatures may enable stroke subtype discrimination and prognostic stratification. Therapeutically, preclinical evidence highlights neuroprotective outcomes from mesenchymal, neural progenitor, and astrocyte-derived exosome administration. Translational challenges persist regarding isolation protocol standardization, targeted delivery optimization, and comprehensive safety profiling. While exosomal technologies hold transformative potential for stroke management, realization requires coordinated multidisciplinary investigation to overcome existing technical and biological barriers.
Abstract: Extracorporeal membrane oxygenation (ECMO) is increasingly used to support patients with severe cardiac or respiratory failure. Neurological complications occur across ECMO configurations and represent a major contributor to mortality and long-term disability. Major neurological complications include ischemic and hemorrhagic stroke, hypoxic ischemic brain injury, seizures, delirium, spinal cord and peripheral nervous system injury, and brain death. The mechanisms underlying neurological injury during ECMO are multifactorial and are influenced by ECMO configuration, reflecting differences in cerebral perfusion, gas exchange, anticoagulation exposure, and precannulation physiologic insults. This review synthesizes neurological complications associated with ECMO, neurological monitoring, and outcomes.
INTRODUCTION: There is an ongoing controversy on the predictive value of the disperse variables involved in cerebral aneurysm rupture. A better understanding of how such variables interact with each other is needed. OBJECTIVES: The initial aim of the study was to propose how exactly, into a hemodynamic model, such morphologic variables might work together to optimize such predictive rupture value. METHODS: We hypothesized, based on previous research, that the aneurysm rupture phenomenon might be related to hemodynamic interference. Hence, we selected the Helmholtz's resonator equation because its resemblance to aneurysm morphology and that it may also be used on elastic walls. We collected the morphologic data (transverse area of the neck diameter, the length of the neck, the aneurysm height, length, and width radius) from the unique large enough published series (n = 425) for ruptured (n = 140) and no ruptured (n = 285) aneurysms that included all the required variables by the equation on the same sample. Given that the Helmholtz's equation also requires as an input variable the speed of the pulse wave (PW), we collected these data from the published series that provides this information by age. This proposed arrangement provided the cerebral aneurysm resonance frequency (the hemodynamic vibratory frequency range, in Hertz, where aneurysms might adsorb most of the oscillating PW energy) for ruptured and no ruptured aneurysms (RAs) by age. Hence, at this point, the working hypothesis was to figure out the predictive value for rupture when the aneurysm resonant frequency (maximal vibratory energy absorption) in Hertz equals the PW frequency range of maximal vibratory energy transmission of 225-275 Hz. RESULTS: What we found is that the mean of the resonance frequency values of the RA series almost entirely matches into the PW frequency range of 225-275 Hz (alpha < 0.016, beta = 0.4, and power = 0.6). Interestingly, the mean of the resonance frequency values for the no RA series barely intersects such PW frequency range (alpha < 0.024, beta = 0.4, and power 0.6). In synthesis, we propose a novel multivariate hemodynamic vibratory interference phenomenon for aneurysm rupture that is activated when the PW frequency matches the resonant frequency of a cerebral aneurysm. The results turned out to have a 99.04% of negative predictive value. DISCUSSION: We hope that a better understanding of this phenomenon might preclude superior treatment strategies. This manuscript aims to provide additional predictive value to better detect patients on a crash course with aneurysm rupture. The required input parameters may be swiftly acquired during an individualized assessment. With this model, PW frequency and hemodynamic interference seem to emerge as novel arterial-damaging factors. CONCLUSION: The Specifity of 97.54%, reflects the ability of the model to correctly identify individuals with lower risk of cerebral aneurysm rupture.
INTRODUCTION: Moyamoya disease (MMD) is a cerebrovascular disorder wherein progressive occlusion of the intracranial arteries leads to cerebral ischemia. This study aimed to compare the influence of anesthesia techniques, namely, inhalational anesthesia (INHA) and total intravenous anesthesia (TIVA), on intraoperative cerebral oxygenation and outcomes following combined direct and indirect revascularization for MMD. MATERIALS AND METHODS: This retrospective observational study was conducted at a tertiary care center, where we analyzed data from 73 patients who underwent combined revascularization for MMD between December 2007 and November 2023. Patients with incomplete records or deviations from standard anesthesia protocols were excluded. Collected data included demographics, clinical presentation, anesthetic and surgical details, intraoperative parameters (hemodynamics, jugular oximetry, cerebral oxygenation, and blood gases), and postoperative outcomes (neurological deficits, complications, and modified Rankin scale [mRS] scores). Statistical analyses compared TIVA (n = 25) and INHA (n = 22) groups using appropriate tests for continuous and categorical variables. RESULTS: The patient demographic and clinical parameters, such as age, gender, preoperative neurological status, and surgical parameters, were similar between groups. The TIVA group demonstrated low arteriovenous oxygen difference with high jugular venous oxygen saturation along with significantly lower cerebral metabolic rate of oxygen, cerebral oxygen extraction, and lactate-oxygen index compared to the INHA group (P < 0.05). No differences were observed with regard to postoperative neurological events or mRS scores at discharge and 3 months (P > 0.005). CONCLUSION: TIVA may enhance cerebral oxygenation and metabolic parameters during MMD revascularization, likely due to propofol's neuroprotective effects. However, these benefits did not translate into significant improvements in postoperative neurological outcomes or hospital stay.
OBJECTIVE:The objective of this study was to explore the selection of confirmation test techniques when there are flaws in the clinical brain death determination (BDD).METHODS:Three comparison analyses were conducted using three confirmation tests according to the Chinese criteria for BDD. First, based on the clinical results of brain death (BD), patients were divided into a BD group and a non-BD group. Second, according to the clinical results of BD, patients were divided into a BD group without flaws (BD1 group) and with flaws (BD2 group). Third, the BD1 group and BD2 group were divided according to different brain injury sites.RESULTS:The first comparison revealed that the area under the receiver operating characteristic curve (AUC) of transcranial Doppler (TCD) combined with electroencephalography (EEG)/short-latency somatosensory evoked potential (SLSEP) was 0.997/0.995, with a false-positive rate of 0, which was better than independent TCD. The second comparison revealed that the AUC of TCD combined with EEG/SLSEP in the BD1 and BD2 groups increased to 0.990-1.000, with a false-positive rate reduced to 0, which was better than independent TCD. The third comparison revealed that for different brain injury sites in the BD1 group, the AUC of TCD combined with EEG/SLSEP was 1.000, with a false-positive rate of 0, which was better than independent TCD. For different brain injury sites in the BD2 group, the AUC of TCD combined with EEG/SLSEP was 0.985-1.000, with a false-positive rate of 0, which was better than that of independent TCD.CONCLUSION:If there are flaws in clinical BDD, the use of TCD combined with EEG/SLSEP can improve the accuracy of BDD.
BACKGROUND: Obstructive sleep apnea (OSA) frequently coexists with headaches, with the relationship between the two disorders not fully elucidated. The Vivos Complete Airway Repositioning and/or Expansion (CARE) Systems are the Food and Drug Administration-approved removable oral appliances for maxillary expansion, mandibular advancement, and treatment of OSA. OBJECTIVE: This study aimed to assess the impact of Vivos CARE Systems on headache burden in nonclassified headache types in patients with OSA. METHODS: This retrospective pre- and posttreatment study used anonymized data from 114 patients with OSA who used one of two Vivos devices (the daytime-nighttime appliance and the mandibular repositioning nighttime appliance). RESULTS: Posttreatment, the mean Headache Impact Test-6 (HIT-6) score significantly reduced from 55.6 (44.5-62) to 43.9 (36.0-48.5) (P < 0.001), indicating a decreased headache impact from substantial to little or none. About 61% of patients showed an improvement in their categorical HIT-6 score, and the percentage of patients in the population whose headache impact was substantial or severe decreased from 49.1% to 12.7%. The average time difference between the headache impact questionnaires was 477 days, with a median of 378 days. Fifty-five patients completed before and after sleep studies without the appliances in place to evaluate OSA severity. There was no improvement in OSA severity, although the study was not powered to evaluate the change in OSA severity. The average time difference between the sleep studies was 652 days, with a median of 443 days. CONCLUSIONS: These results suggest the potential efficacy of maxillary expansion and mandibular advancement devices in reducing headache impact as measured by the HIT-6 score. The minimal reduction in AHI in the previous study and no reduction in AHI in the present study could imply a different underlying mechanism, possibly associated with device-induced structural changes. However, the limitations, including the lack of data on specific headache disorders and reliance on HIT-6 as a composite headache metric, warrant further investigation, ideally based on randomized controlled trials, to clarify the specific anatomical traits influencing this outcome.
BACKGROUND: Circulating microparticles (MPs) may trigger a hypercoagulable state, leading to thrombosis. Cerebral venous thrombosis (CVT) is a rare but serious thrombotic disease. Yet, the correlation between circulating MPs and CVT remains unclear. Therefore, this study aimed to clarify the relationship between circulating MPs and CVT. MATERIALS AND METHODS: A total of 110 patients newly diagnosed with CVT and 89 healthy controls were enrolled. MPs derived from endothelial cell (CD144+), tissue factor (TF+), monocyte cell (CD14+), and platelet (CD41a+) were isolated from platelet-poor plasma prepared by centrifugation and determined using flow cytometry. To analyze disease severity and prognosis, CVT patients were stratified into subgroups based on their Glasgow Coma Scale score at admission or their Modified Rankin Scale score at the 3-month follow-up. RESULTS: Plasma levels of CD144+, TF+, CD14+, and CD41a+ MPs were significantly higher in CVT patients than in healthy controls (all P < 0.05). Furthermore, the circulating TF+ MP levels showed significant positive correlations with both CVT severity (r = 0.401, P = 0.003) and prognosis (r = 0.316, P = 0.012). Logistic regression analysis revealed that higher TF+ MP levels were an independent predictor for severity (P = 0.005) at admission and poor prognosis (P = 0.027) at 3 months of CVT. Moreover, the area under the curve was 0.824 and 0.843 in severity and prognosis of CVT, respectively, as shown by the receiver operating characteristic curve. CONCLUSIONS: Compared with healthy controls, circulating MP amounts were higher in CVT patients. The TF+ MP levels may be effectively utilized as a biomarker of CVT severity and clinical prognosis.
OBJECTIVE: The objective of the study was to describe and characterize the cross-sectional association between cerebral microbleeds (CMBs) and white matter hyperintensities (WMH) in patients with primary hypertension. MATERIALS AND METHODS: Hospitalized patients with primary hypertension were enrolled. Brain magnetic resonance imaging was scanned for the qualitative and semi-quantitative evaluations of CMBs and WMH. Univariate and multivariate analyses were conducted to investigate the correlation between CMBs and WMH. Subgroup analyses were performed in patients with CMBs, based on the severities and distributions of CMBs. RESULTS: This prospective study recruited 400 patients, and CMBs and WMH were detected in 86 (21.5%) and 250 (62.5%) patients, respectively. Moderate (a Fazekas score of 3-4) (odds ratio [OR] = 2.650 [1.367-5.139], P = 0.004) and severe (a Fazekas score of 5-6) WMH (OR = 6.793 [3.253-14.185], P < 0.001) were both independent risk factors for CMBs presence. Subgroup analysis showed that the patients detected with moderate-severe CMBs (a CMBs number of > 5) exhibited a higher Fazekas score, compared with those with mild CMBs (a CMBs number of 1-5) (5 vs. 2, P = 0.006). The number of CMBs was positively correlated with the Fazekas score of WMH (r = 0.465, P < 0.001) in the 65 (16.3%) patients exhibiting both CMBs and WMH. In addition, those with CMBs in both lobar and deep/infratentorial regions exhibited a higher Fazekas score than those with CMBs only in lobes or only in deep/infratentorial regions (5 vs. 2, P = 0.003). CONCLUSIONS: Both moderate and severe WMH are independent risk factors for CMBs in patients with primary hypertension. More severe CMBs are associated with more severe WMH.
