Malignant glioma is one of the most intractable malignant neoplasms. Standard treatment consists of surgery, radiotherapy, and chemotherapy, although substantial therapeutic effects cannot be expected. In particular, the blood-brain barrier (BBB) protects the central nervous system, reducing the effectiveness of chemotherapy. Temozolomide is the standard treatment, but it only prolongs the median survival time by about two months compared to surgery and radiation. Molecular-targeted therapies, which have revolutionized the treatment of many cancer types, have all failed to treat malignant gliomas, and the focus is now on the spatial and temporal diversity of tumors. In addition, the problem of drug penetration across the BBB has been refocused. Precision medicine is also attracting great expectations, but panel testing can only be done once. Even if an expert panel recommends a treatment, there is a problem in that most treatments have to rely on investigational therapies. It is also known that even if there is a draggable genetic abnormality in tumors, drugs targeting those abnormalities are often ineffective against brain tumors. Therefore, it is necessary that all novel therapeutic approaches, such as virus therapy, neutron capture therapy, and drug delivery techniques like convection-enhanced delivery, be employed to improve treatment outcomes in malignant glioma.

  The WHO 5th edition requires molecular information, such as IDH, 1p/19q, and CDKN2A/B, for diagnosing and grading low-grade gliomas. The diagnosis will provide a more favorable survival outcome. However, the available evidence of treatments is derived from previous clinical trials planned before the molecular diagnosis era. Clinicians should consider the therapeutic strategy with each therapy's known benefits and risks.

  The incidence of primary central nervous system lymphoma (PCNSL) has grown recently, and neurosurgeons in Japan frequently have the opportunity to treat it. PCNSL causes cognitive impairment and has several atypical imaging findings, making it challenging to diagnose. In cases where biopsy is challenging, certain biomarkers in cerebrospinal fluid and deoxyribonucleic acid and ribonucleic acid assays via liquid biopsy have recently been reported to be significant. Rituximab, methotrexate (MTX), procarbazine, and vincristine are increasing accepted as routine therapies in Japan, and MTX-based multidrug chemotherapy is recommended as induction therapy. High-dose cytarabine is employed for subsequent consolidation therapy. High-dose whole-brain radiation therapy should be avoided as much as possible during initial therapy due to neurotoxicity, such as cognitive impairment. MTX re-challenge is effective at recurrence ; however, the time until recurrence should be considered. Recently developed Bruton's tyrosine kinase inhibitors have attracted attention and show high response rates. However, there are issues with persistence and adverse events ; therefore, further research is required its use.

  Diagnosis and treatment approaches for central nervous system germ cell tumors (GCTs) have been evolving over decades ; however, they remain globally heterogeneous. There are major differences in how tumor markers and histopathological findings are weighed in Japan and Europe/North America at the time of diagnosis. It remains debatable whether non-germinomatous GCTs (NGGCTs) could be diagnosed solely based on elevated tumor markers without a biopsy, partly because of the suboptimal specificity of tumor markers of tumor tissues for future research. The historical three-class system in Japan (germinoma, intermediate prognosis group, and poor prognosis group) contrasts with the two-class system in Europe/North America (germinoma and NGGCTs). The difference stems from the debate over whether NGGCTs mixed with teratoma should be treated as intensively as other malignant NGGCTs. Hopefully, thorough analyses of previous clinical trials conducted across continents would result in clinical questions that would best guide the design of clinical trials. Additionally, the Intracranial GCT Genome Analysis Consortium of Japan (2012) has yielded multi-omics analyses on the pathogenesis, investigating the unique biological characteristics of GCTs. It is essential to conduct translational research based on biological investigation to develop novel treatments by unveiling crucial elements in the pathogenesis.

  The aim of this study was to evaluate relationships between cognitive impairment, return to work and treatment modality in patients with ruptured anterior communicating artery aneurysms.

  This study included 44 patients who underwent coiling (4 patients), clipping through the interhemispheric approach (IH, 12 patients) or through the pterional approach (PT, 28 patients). A neuropsychological assessment was conducted and outcomes were evaluated.

  The rate for good outcome with mRS 0-2 was 77.3%, and 50% returned to work. Memory and attention deficits were present in 88.6% and 97.7% of the patients, respectively, with 52.3% and 27.3% of them having severe deficits. Injury to the basal forebrain resulted in significantly more severe cognitive impairment and a poorer outcome. Injury to the rectal and orbital gyri was present in 65.9% of patients (45.5% surgical) and to the head of the caudate nucleus in 25 patients (all surgical), but did not affect cognitive impairment or outcome. The severity of cognitive impairment and outcome was least with coil embolization followed by IH, and PT, in that order, but there were no significant differences.

  Injury to the basal forebrain resulted in significantly more severe cognitive impairment and a poorer outcome.

  A 69-year-old woman was followed up for 3 years for a meningioma on the left convexity region. She developed a sudden-onset headache, and the next morning she had difficulty moving and was taken to the emergency department of our hospital. Computed tomography (CT) scans showed a left acute subdural hematoma, but magnetic resonance imaging, contrast-enhanced CT, and cerebral angiography did not reveal any source of bleeding other than the existing meningioma. A craniotomy was performed simultaneously to remove the hematoma and the meningioma. Intraoperatively, a red mass contiguous with a cerebral cortical artery was removed from the vicinity of the meningioma. The pathological diagnosis was capillary hemangioma with a fresh hemorrhage in the interstitium, which was thought to be the cause of the acute subdural hematoma. Here, we report a very rare case of an intracranial capillary hemangioma that lacked contrast enhancement, arose from an artery, and presented as an acute subdural hematoma.