Scalp arteriovenous malformations (AVMs) are abnormal vascular lesions that can be treated safely and effectively, with surgical or endovascular approaches. Because of their complex vascularity, the detailed preoperative evaluation must be carefully performed. Here, we present a case of scalp AVM that required two operations as a result of a misdiagnosis because of inadequate preoperative assessment.

Objective : Intracranial aneurysm (IA) is a cerebrovascular disease in which the cerebral arteries become pathologically weakened. The molecular mechanisms behind the pathogenesis of IAs are poorly understood. MicroRNAs (miRNAs) are highly stable in body fluids and the expression signatures of specific circulating miRNAs may be associated with high rupture risk, severity, and clinical outcome of subarachnoid hemorrhage (SAH).Methods : The presented study aimed to detect miRNA-based biomarkers and evaluating the usability of blood for a non-invasive approach. Blood samples from 24 patients with unruptured IA (group 1), blood and cerebrospinal fluid (CSF) samples collected on day 5 after aneurysmal SAH (aSAH) from 24 patients with ruptured IA (group 2), and both the blood and CSF samples from 24 individuals without any positive IA history (control group) were subjected to quantitative real time polymerase chain reaction for evaluating the expression profiles of eight miRNAs.Results : miR-29a, miR-200a-3p, miR-451a, miR-1297, and miR-502-5p in blood and miR-29a, miR-200a-3p, miR-451a, miR-126, miR- 146a-5p, and miR-27b-3p in CSF were found to be differentially expressed in ruptured patients compared to controls. In both biofluids of ruptured cases, the differences in the expression profiles of miR-29a, miR-200a-3p, and miR-451a compared to controls were striking. The upregulation of miR-126, miR-200a-3p, miR-451a, and miR-502-5p in the ruptured group compared to unruptured patients suggesting that these miRNAs may be informative in predicting the risk of an aneurysmal rupture.Conclusion : miR-29a, miR-200a-3p, and miR-451 were significantly altered in patients with aSAH compared to controls in both biofluids. These findings suggest that these miRNAs could be candidate non-invasive biomarkers for aSAH.

Background/Objectives: Aneurysmal subarachnoid hemorrhage (aSAH) is frequently complicated by cerebral vasospasm, a major contributor to delayed cerebral ischemia and poor neurological outcomes. Early prediction remains challenging, and there is a critical need for reliable biomarkers. MicroRNAs (miRNAs) in cerebrospinal fluid (CSF) have emerged as promising indicators of acute neuropathological changes. This study aimed to evaluate CSF miRNA expression profiles in patients with aSAH to identify early predictors of vasospasm and improve clinical risk stratification. Methods: We conducted a prospective observational study involving 48 patients (40 patients with aSAH (20 who developed vasospasm, 20 who did not) and 8 healthy controls). A panel of 20 candidate miRNAs was analyzed in CSF samples collected on days 1 and 5 post−hemorrhage using quantitative real−time PCR. Expression differences between groups were assessed, and receiver operating characteristic (ROC) curves were used to evaluate diagnostic performance. Results: Several miRNAs were differentially expressed in patients who developed vasospasm. On day 1, miR−221−3p and miR−183−5p were significantly upregulated (p = 0.014, p = 0.009), while miR−126, miR−29a, and miR−27b−3p were downregulated (p = 0.006, 0.021, 0.028) compared with controls. MiR−126 remained suppressed on day 5 (p = 0.002). These early changes showed high predictive accuracy (e.g., day 1 AUC for miR−221−3p ≈ 0.98, 95% CI 0.83–1.00). Compared with non−vasospasm patients, miR−221−3p was lower (0.12−fold), while miR−9−3p and miR−183−5p were higher (13.4−fold and 2.7−fold, respectively; all p < 0.01). MiR−24 and miR−21−5p correlated with more severe grades and poorer outcomes (p < 0.05). Conclusions: Specific CSF miRNAs—particularly miR−221−3p, miR−9−3p, and miR−183−5p—may serve as early biomarkers for vasospasm, warranting further validation in larger cohorts.

Ischemia-reperfusion injury activates both apoptotic and necroptotic pathways, contributing to neuronal damage. This study aimed to investigate the effects of pannexin-1 inhibition by probenecid on these pathways in a rat model of transient focal cerebral ischemia-reperfusion. Additionally, the synergistic neuroprotective potential of co-administering probenecid and the pan-caspase inhibitor Z-VAD-fmk was evaluated. Transient focal ischemia was induced by clamping the right common carotid artery for 2 hours, followed by 24 hours of reperfusion. Male Wistar rats were divided into six groups, receiving either probenecid, Z-VAD-fmk, both, or vehicle. Gene and protein levels of apoptotic (caspase-3, caspase-8) and necroptotic (RIPK1, RIPK3, MLKL) markers were assessed by qRT-PCR, ELISA, and immunohistochemistry. TTC staining was used for infarct visualization, H&E for tissue morphology, and TUNEL assay for DNA fragmentation. TNF-α levels were measured to evaluate inflammation. Probenecid reduced necroptotic and apoptotic markers and suppressed TNF-α levels. Notably, Z-VAD-fmk reduced apoptosis but paradoxically increased necroptotic signaling, highlighting a cell death switch between these pathways. Simultaneous treatment significantly attenuated both pathways, reduced infarct size, and preserved tissue architecture. TNF-α levels were most effectively reduced by the combination therapy. Simultaneous inhibition of pannexin-1 and caspase activity provides superior neuroprotection in cerebral ischemia-reperfusion injury. This dual-targeting strategy effectively limits cell death and inflammation. Importantly, these findings may help explain the limited success of prior anti-apoptotic monotherapies in stroke and emphasize the necessity of targeting both apoptosis and necroptosis to achieve meaningful neuroprotection.

< /B > Spinal cord injuries negatively affect the individuals and the life quality of their families due to neurological deficits caused by trauma. The prevalence of spinal cord injury is 15-45/1 million in the world. Caffeic acid phenethyl ester (CAPE) is the most active component of propolis and has neuroprotective, anti-oxidant and anti-apoptotic effects. Our aim was to determine the effects of CAPE on the prevention of secondary injury and to compare with methylprednisolone. Forty rats were divided into 4 groups. The control group did not undergo surgery (Group I), only trauma group (Group II), trauma+CAPE treatment group (Group III), and trauma+methylprednisolone treatment group (Group IV). Histopathological assessment was performed with two staining methods as hematoxylin-eosin (HE) and terminal deoxynucleotidyl Transferase Biotin - dUTP Nick End Labeling (TUNEL). The groups were statistically compared. The apoptotic cells decreased in treatment groups compared with the trauma. CAPE has more anti-apoptotic effect than methylprednisolone. The histological difference between the Group II, and Groups III and IV was statistically significant. CAPE has a positive effect on spinal cord injuries by preventing apoptosis.

Background/Objectives: Aneurysmal subarachnoid hemorrhage (aSAH) is frequently complicated by cerebral vasospasm, a major contributor to delayed cerebral ischemia and poor neurological outcomes. Early prediction remains challenging, and there is a critical need for reliable biomarkers. MicroRNAs (miRNAs) in cerebrospinal fluid (CSF) have emerged as promising indicators of acute neuropathological changes. This study aimed to evaluate CSF miRNA expression profiles in patients with aSAH to identify early predictors of vasospasm and improve clinical risk stratification. Methods: We conducted a prospective observational study involving 48 patients with aSAH (20 who developed vasospasm, 20 who did not) and eight healthy controls. A panel of 20 candidate miRNAs was analyzed in CSF samples collected on days 1 and 5 post-hemorrhage using quantitative real-time PCR. Expression differences between groups were assessed, and receiver operating characteristic (ROC) curves were used to evaluate diagnostic performance. Results: Several miRNAs were differentially expressed in patients who developed vasospasm. On day 1, miR-221-3p and miR-183-5p were significantly upregulated (p = 0.014, p = 0.009), while miR-126, miR-29a, and miR-27b-3p were downregulated (p = 0.006, 0.021, 0.028) compared to controls. MiR-126 remained suppressed on day 5 (p = 0.002). These early changes showed high predictive accuracy (e.g., day-1 AUC for miR-221-3p ≈ 0.98, 95% CI 0.83–1.00). Compared to non-vasospasm patients, miR-221-3p was lower (0.12-fold), while miR-9-3p and miR-183-5p were higher (13.4-fold and 2.7-fold; all p < 0.01). MiR-24 and miR-21-5p correlated with more severe grades and poorer outcomes (p < 0.05). Conclusions: Specific CSF miRNAs—particularly miR-221-3p, miR-9-3p, and miR-183-5p—may serve as early biomarkers for vasospasm, warranting further validation in larger cohorts.