Leptin has been recognized as a potential tumor growth promoter in various cancers including cranial tumor pathologies such as pituitary adenomas, meningiomas and gliomas. Despite recent advances in adjunctive therapy and the established surgical resection, chemo- and radiotherapy regimen, glioblastoma multiforme remains a particular diagnostic and therapeutic challenge among the intracranial tumor pathologies, with a poor long-term prognosis. Systemic inflammation and immune-metabolic signaling through diverse pathways are thought to impact the genesis and recurrence of brain tumors, and glioblastoma multiforme in particular. Among the various circulating mediators, leptin has gained especial diagnostic and therapeutic interest, although the precise relationship between leptin and glioblastoma biology remains largely unknown. In this narrative review (MEDLINE/OVID, SCOPUS, PubMed and manual searches of the bibliographies of known primary and review articles), we discuss the current literature using the following search terms: leptin, glioblastoma multiforme, carcinogenesis, immunometabolism, biomarkers, metformin, antidiabetic medication and metabolic disorders. An increasing body of experimental evidence implicates a relationship between the development and maintenance of gliomas (and brain tumors in general) with a dysregulated central and peripheral immune-metabolic network mediated by circulating adipokines, chemokines and cellular components, and in particular the leptin adipokine. In this review, we summarize the current evidence of the role of leptin in glioblastoma pathophysiology. In addition, we describe the status of alternative diagnostic tools and adjunctive therapeutics targeting leptin, leptin-receptors, antidiabetic drugs and associated pathways. Further experimental and clinical trials are needed to elucidate the mechanism of action and the value of immune-metabolism molecular phenotyping (central and peripheral) in order to develop novel adjunctive diagnostics and therapeutics for newly diagnosed and recurrent glioblastoma patients.

Objective: Metabolomics has growing importance in the research of inflammatory processes. Chronic subdural hematoma (cSDH) is considered to be, at least in part, of inflammatory nature, but no metabolic analyses yet exist. Therefore, a mass spectrometry untargeted metabolic analysis was performed on hematoma samples from patients with cSDH. Methods: A prospective analytical cross-sectional study on the efficacy of subperiosteal drains in cSDH was performed. Newly diagnosed patients had the option of granting permission for the collection of a hematoma sample upon its removal. The samples were analyzed using liquid chromatography–mass spectrometry to obtain different types of metabolites from diverse biochemical classes. The statistical analysis included data cleaning, imputation, and log transformation, followed by PCA, PLS-DA, HCA, and ANOVA. The postoperative course of the disease was followed for 3 months. The metabolite concentrations in the hematoma fluid were compared based on whether a recurrence of the disease was recorded within this time frame. Results: Fifty-nine samples from patients who were operated on because of a cSDH were gathered. Among those, 8 samples were eliminated because of missing metabolites, and only 51 samples were analyzed further. Additionally, 39 samples were from patients who showed no recurrence over the course of a 3-month follow-up, and 12 samples were from a group with later recurrence. We recorded a noticeable drop (35%) in the concentration of acylcarnitines in the ”recurrence group“, where 10 of the 22 tested metabolites showed a significant reduction (p < 0.05). Furthermore, a noticeable reduction in different Acyl-CoA-dehydrogenases was detected (VLCAD-deficiency p < 0.05, MCAD-deficiency p = 0.07). No further changes were detected between both populations. Conclusions: The current study presents a new approach to the research of cSDH. The measurements presented us with new data, which, to date, are without any reference values. Therefore, it is difficult to interpret the information, and our conclusions should be considered to be only speculative. The results do, however, point in the direction of impaired fatty acid oxidation for cases with later recurrence. As fatty acid oxidation plays an important role in inflammatory energy metabolism, the results suggest that inflammatory processes could be aggravated in cases with recurrence. Because our findings are neither proven through further analyses nor offer an obvious therapy option, their implications would not change everyday practice in the management of cSDH. They do, however, present a further possibility of research that might, in the future, be relevant to the therapy.

Background Chronic subdural hematomas (cSDHs) are most frequently treated by evacuation via a burr-hole craniostomy procedure. Subperiosteal drains have been introduced as alternatives to subdural ones, but only a few prospective studies have explored their efficacy. Thus, a prospective randomized trial was designed to assess their use. Methods The study enrolled patients with newly diagnosed surgically amenable cSDH. These patients were randomized into two groups. The first group underwent cSDH evacuation via a single burr hole craniostomy procedure, followed by placement of a subperiosteal drain; the second group underwent the identical procedure without drain placement. Patient demographics, drain volumes, duration of drainage, cSDH recurrence, and postoperative outcomes were recorded. Results Eighty-eight patients presenting with cSDH (12 with bilateral cSDHs) from a total of 100 surgical cases were enrolled. Nine patients (1 bilateral) were lost to follow-up. Of all remaining 90 procedures, 37 were carried out with drain placement and the remaining 53 without drain placement. There were five recurrent cases (13.5%) in the drain placement group and 17 (32.1%) in the group without drain placement. This resulted in a statistical significance (odds ratio [OR]: 0.33; p < 0.05) favoring the use of a drain. Conclusion Subperiosteal drain placement can be used safely and effectively to treat cSDH in conjunction with a burr-hole craniostomy procedure, significantly reducing the rate of recurrence without any additional disadvantages.

Background/Objectives: Several imaging scores have been developed for subarachnoid hemorrhage (SAH), but their prognostic performance for long-term functional outcome and post-hospital complications remains insufficiently characterized. We evaluated whether five admission imaging scores (modified Fisher, Claassen, Hijdra, Graeb, IVH) independently predict 12-month functional outcome and major secondary endpoints. Methods: We performed a retrospective cohort study of 479 consecutive patients with atraumatic SAH recorded in a prospectively maintained institutional registry. Admission CT/MRI was scored by two board-certified neuroradiologists blinded to clinical outcomes. The primary endpoint was unfavorable functional outcome at 12 months (modified Rankin scale [mRS] 4–6). Secondary endpoints included 12-month mortality, delayed cerebral ischemia (DCI), post-hemorrhagic epilepsy, shunt-dependent hydrocephalus, return to work, and patient-reported health. Receiver operating characteristic (ROC) analyses and multivariable logistic regression adjusted for established predictors were conducted. Results: All imaging scores were significantly associated with the primary endpoint and demonstrated adequate discrimination (area under the curve [AUC] ~0.70–0.74), with the Graeb and IVH scores performing highest for long-term functional outcome, mortality, and shunt dependence. Associations with DCI and epilepsy were modest. In multivariable analyses, all imaging scores remained independently associated with mRS 4–6. Subgroup analyses showed stronger prognostic performance in good-grade SAH, aneurysmal SAH, and cases with concomitant intraventricular hemorrhage. Conclusions: Admission imaging burden independently predicts 12-month functional outcome, mortality, and shunt dependence after SAH. Incorporating IVH-oriented measures alongside established clinical grading may improve individualized risk stratification, particularly in good-grade and aneurysmal SAH.