In mammals, the circadian system controls various physiological processes to maintain metabolism, behavior, and immune function during a daily 24 h cycle. Although driven by a cell-autonomous core clock in the hypothalamus, rhythmic activities are entrained to external cues, such as environmental lighting conditions. Exposure to artificial light at night (ALAN) can cause circadian disruption and thus is linked to an increased occurrence of civilization diseases in modern society. Moreover, alterations of circadian rhythms and dysregulation of immune responses, including inflammasome activation, are common attributes of neurodegenerative diseases, including Alzheimer’, Parkinson’s, and Huntington’s disease. Although there is evidence that the inflammasome in the hippocampus is activated by stress, the direct effect of circadian disruption on inflammasome activation remains poorly understood. In the present study, we aimed to analyze whether exposure to constant light (LL) affects inflammasome activation in the mouse hippocampus. In addition to decreased circadian power and reduced locomotor activity, we found cleaved caspase 1 significantly elevated in the hippocampus of mice exposed to LL. However, we did not find hallmarks of inflammasome priming or cleavage of pro-interleukins. These findings suggest that acute circadian disruption leads to an assembled “ready to start” inflammasome, which may turn the brain more vulnerable to additional aversive stimuli.

The neuroinflammatory response to aneurysmal subarachnoid hemorrhage (SAH) might have a crucial impact on the burden of disease. We aimed to analyze the behavior of interleukin-6 (IL-6) in cerebrospinal fluid (CSF) during SAH and its relation to complications and outcomes. We included consecutive SAH patients with regular CSF IL-6 measurements treated between January 2005 and June 2016 (n = 420). IL-6 levels were recorded every 72 hours (from day 1-3 [d1-3] until day 19-21 [d19-21]). Study endpoints were delayed cerebral infarction (DC-infarction), in-hospital mortality, and unfavorable outcome at 6 months after SAH (modified Rankin scale >3). There was an initial increase of IL-6 on d4-6 (median: 3121 vs. 1467 pg/mL on d1-3), with a gradual decrease over the remaining time. The IL-6 value on d1-3 showed associations with in-hospital mortality and unfavorable outcomes, whereas IL-6 on d4-6 was related to the risk of DC-infarction and in-hospital mortality. According to receiver operating characteristic curves, clinically relevant cutoffs were defined for IL-6 on d1-3 (>2000 pg/mL) and d4-6 (>2500 pg/mL). In multivariate analysis, IL-6 >2000 pg/mL on d1-3 was independently associated with in-hospital mortality (adjusted odds ratio [aOR = 2.67; P = 0.009) and unfavorable outcome (aOR=2.30; P = 0.006). In turn, IL-6 >2500 pg/mL on d4-6 was independently associated with in-hospital mortality (aOR = 2.28; P = 0.017) and DC-infarction (aOR = 1.64; P = 0.044). SAH individuals with angiographic vasospasm showed marked elevation of IL-6 from d1-3 to d4-6 compared to their counterparts without vasospasm (+1770.5 vs. -21 pg/mL; P = 0.02). Our data confirm the substantial impact of neuroinflammation on SAH. CSF IL-6 values measured during the first week after SAH occurrence present the most valuable outcome predictors.

Objective: Central neurocytomas (CNs), classified as CNS (central nervous system) grade 2 tumors, are exceptionally rare tumors, accounting for approximately 0.1–0.5% of all intracranial neoplasms, and are typically characterized by a benign clinical course and frequent association with hydrocephalus. This study aims to present a comprehensive analysis of surgical and adjuvant therapies for CN. Methods: The study comprised all patients who underwent microsurgical tumor removal in our center over the past decade (2013–2023). Clinical manifestations, surgical and adjuvant therapy approaches, MRI and histological findings, clinical outcomes, and recurrence-free survival were evaluated. Results: A total of eleven patients (six men, mean age of 28.0 years; five women, mean age of 53.6 years) underwent surgical treatment. Intraventricular tumors were the most common (72.7%, n = 8). The predominant presenting symptoms were headache and visual disturbances. All tumors exhibited contrast enhancement on MRI. Hydrocephalus was present in five patients. The Ki67 proliferation index ranged from 2% to 10%, with nine patients exhibiting Ki67 > 3%. The median recurrence-free survival was 38.0 months (IQR: 25.0–53.0). The most severe postoperative complications included aphasia, hemiparesis, and memory impairment, resulting in a postoperative Karnofsky Performance Status (KPS) below 70% in five patients. Follow-up assessments showed significant symptomatic improvement in all affected patients. Conclusions: Gross total resection is the recommended first-line therapy with favorable neurological outcomes and for atypical CN as well. Adjuvant radiotherapy should be reserved for tumor progression and recurrence. The role of adjuvant chemotherapy remains unclear, but it may be an option for CN with a high proliferation index.

Objective: A rupture of the intracranial aneurysm is frequently complicated, with an increase of intracranial pressure (ICP) requiring conservative and/or surgical treatment. We analyzed the risk factors related to the duration of pathologic ICP increase and the relationship between ICP burden and the outcome of subarachnoid hemorrhage (SAH). Methods: Consecutive cases with aneurysmal SAH treated at our institution between 01/2003 and 06/2016 were eligible for this study. Different admission variables were evaluated to predict the duration of ICP increase >20 mmHg in univariate and multivariate analyses. The association of the ICP course with SAH outcome parameters (risk of cerebral infarction, in-hospital mortality, and unfavorable outcome at 6 months defined as modified Rankin scale >3) was adjusted for major outcome-relevant confounders. Results: Of 820 SAH patients, 378 individuals (46.1%) developed at least one ICP increase requiring conservative and/or surgical management after aneurysm treatment (mean duration: 1.76 days, range: 1 - 14 days). In the multivariable linear regression analysis, patients’ age (unstandardized coefficient [UC]=-0.02, p <0.0001), World Federation of Neurosurgical Societies (WFNS) grade 4-5 at admission (UC=0.71, p <0.004), regular medication with the angiotensinconverting enzyme (ACE) inhibitors (UC=-0.61, p =0.01), and presence of intracerebral hemorrhage (UC=0.59, p =0.002) were associated with the duration of ICP increase. In turn, patients with longer ICP elevations were at higher risk for cerebral infarction (adjusted odds ratio [aOR]=1.32 per-day-increase, p <0.0001), in-hospital mortality (aOR=1.30, p <0.0001) and unfavorable outcome (aOR=1.43, p <0.0001). SAH patients who underwent primary decompressive craniectomy (DC) showed shorter periods of ICP increase than patients with a secondary decompression (mean: 2.8 vs 4.9 days, p <0.0001). Conclusion: The duration of ICP increase after aneurysm rupture is a strong outcome predictor and is related to younger age and higher initial severity of SAH. Further analysis of the factors impacting the course of ICP after SAH is essential for the optimization of ICP management and outcome improvement.

Background/Objectives: Cerebral infarction significantly worsens outcomes after aneurysmal subarachnoid hemorrhage (SAH). This retrospective study analyzed early predictors of infarct-free survival and the impact of infarct timing on clinical outcomes. Methods: We reviewed 988 consecutive SAH patients treated from 2003 to 2016, all with follow-up CT scans. Baseline clinical and SAH characteristics were recorded to identify predictors of infarct-free survival and assess the relationship between infarct timing and outcomes. Results: Cerebral infarctions occurred in 475 patients (48.1%) at a median of 3.4 days post-SAH; 70.9% happened within the first week. Earlier infarctions were associated with higher in-hospital mortality (odds ratio [OR] = 0.91 per day increase, p < 0.0001) and poor 6-month outcomes (modified Rankin Scale > 3; OR = 0.96 per day increase, p = 0.012), especially within 48 h. Independent predictors of infarct-free survival included poor initial condition (WFNS ≥ 4, adjusted hazard ratio [aHR] = 1.82, p < 0.0001), intraventricular hemorrhage (aHR = 1.25, p = 0.041), aneurysm rebleeding (aHR = 1.76, p < 0.0001), acute hydrocephalus (aHR = 1.38, p = 0.020), and daily aspirin intake (aHR = 0.68, p = 0.002). The number of baseline risk factors (0–5) strongly influenced both infarction likelihood and timing (p < 0.0001). Conclusions: Cerebral infarctions predominantly occur within the first week after SAH, with earlier infarctions having a more severe impact on outcomes. Initial risk factor-adapted SAH management may improve functional outcomes.

Objective: Delayed cerebral ischemia (DCI) is one of the most severe complications following aneurysmal subarachnoid hemorrhage (SAH) and can significantly worsen clinical outcomes. This study aimed to analyze the association between patients’ home medications and the risk of cerebral infarction and poor functional outcomes after SAH. Methods: This retrospective analysis included 995 patients with aneurysmal SAH treated at our clinic between January 2003 and June 2016. Various demographic and clinical baseline characteristics were examined, with a particular focus on regular use of home medications. The study endpoints were the occurrence of early (within 72 h post-SAH) and DCI-related infarcts (> 72 h) in follow-up computed tomography scans, as well as the functional disability at six months, defined as a modified Rankin Scale > 2. Results: There was no association between the occurrence of early infarcts and patients’ regular medications. In contrast, individuals with calcium channel blockers (CCB) use ( n = 93) showed a higher rate of DCI (32.6% vs 19.3%, p = 0.005) and 6-months functional disability (57.8% vs 46.8%, p = 0.048). In multivariable analysis, CCB use was independently associated with the risk of DCI (adjusted odds ratio [aOR] = 4.05; p < 0.0001) and functional disability after six months (aOR = 2.73; p = 0.036). Conclusions: Regular CCB use was independently associated with an increased risk of DCI and functional disability at six months. These findings warrant cautious interpretation and further validation in prospective studies.