Background: The intracranial lipomas are rare congenital malformations accounting for approximately 0.1–1.3% of all intracranial tumors, of which Sylvian fissure lipomas account for <5%. These lesions are frequently associated with dysgenesis of neuronal brain tissues and vascular malformations and in the majority are asymptomatic. Intracranial lipomas on magnetic resonance imaging (MRI) may mimic late subacute hemorrhage due to similar radiological features. Due to the tight adhesion of the lipoma to the surrounding nerve structures and vessels, complete removal is difficult and does not guarantee the disappearance of symptoms. Case Description: We present the case of a 42-year-old woman with chronic headaches and short-term memory impairment who was admitted to the emergency room after an out-of-hospital brain MRI with suspected ruptured right middle cerebral artery (MCA) aneurysm and late subacute intracranial hemorrhage. In the hospital, after clinical evaluation, emergency computed tomography (CT) angiography was performed, which revealed an unruptured fusiform aneurysm located in the right MCA trifurcation surrounded by an extremely hypodense lesion corresponding to fat in the right Sylvian fissure. No features of intracranial hemorrhage were present. The diagnosis of intracranial lipoma was finally confirmed after the MRI of the brain with a fat suppression sequence. Surgical treatment was not attempted, and the patient was treated conservatively with a satisfactory general outcome. Conclusion: A Sylvian fissure lipoma may be associated with a fusiform aneurysm in the MCA trifurcation. By modifying the standard MRI protocol and performing a CT scan, an intracranial lipoma can be detected and a late subacute intracranial hemorrhage can be excluded.

Objectives: In this study, we explore the molecular basis of the literature-reported inverse association between brain neoplasms and neurodegenerative disorders, including Parkinson’s disease (PD). As miRNAs are post-transcriptional regulators, we selected them as candidates underlying opposite processes of neurodegeneration and glioma development. Methods: We used bioinformatic analyses for disease-gene extraction, miRNA target prediction, enrichment analyses, and miRNA ranking. We identified 953 shared genes between PD and glioblastoma (GBM) in DisGeNET, then prioritized miRNAs predicted to regulate the largest number of shared targets. Next, we collected peripheral blood from patients with PD (n = 12), patients with gliomas (the most advanced—grade IV, n = 10 and grade III n = 3) and controls undergoing spinal surgery for disk pathology (n = 10). Blood samples were obtained pre-operatively in controls and glioma patients. Tumor and peritumoral tissues were obtained from glioma patients, whereas tissue sampling is not feasible in PD. Brain tissues and plasma were analyzed using RT-qPCR (miRNA) and ELISA (p53). Results: We observed increased levels of miR-16-5p (p < 0.05) and p53 protein (p < 0.05) in tumor tissues compared with peritumoral tissue. Additionally, miR-16-5p and miR-32-5p plasma levels were elevated in glioma patients compared with both PD patients (p < 0.01 and p < 0.001, respectively) and controls (p < 0.01 and p < 0.001, respectively). Plasma levels in PD did not differ from controls. Conclusions: Although these analyses highlight miR-16-5p and miR-32-5p as candidate biomarkers associated with glioma related pathways, the results did not provide evidence for the expected opposite regulation between PD and glioma. Future studies with a larger cohort of patients using high-throughput methods are needed to validate these findings and to elucidate the mechanisms driving neurodegeneration or excessive proliferation.