In patients with drug-resistant focal epilepsy requiring surgery, hippocampal sclerosis was the most common histopathological diagnosis among adults, and focal cortical dysplasia was the most common diagnosis among children. Tumors were the second most common lesion in both groups. (Funded by the European Union and others.).

Meningiomas are mostly benign tumours originating from the arachnoid cap cells, represent 13-26% of all intracranial tumours. They are more common in older age and in females. Deletion in NF2 gene and exposure to ionizing radiation are established risk factors, while the role of sex hormones is yet not clarified. Five-year survival for typical meningiomas exceeds 80%, but is poorer (5-year survival <60%) in malignant and atypical meningiomas. Papillary and haemangiopericytic morphology, large tumour size, high mitotic index, absence of progesterone receptors, deletions and loss of heterozygosity are poor prognostic factors. Complete surgical excision is the standard treatment. Radiotherapy is currently used in the clinical practice in atypical, malignant or recurrent meningioma at a total dose of 45-60Gy. However, the role of adjuvant irradiation is still controversial and has to be compared in a randomised prospective setting with a policy of watchful waiting. Radiosurgery has gained more and more importance in the management of meningiomas, especially in meningiomas that cannot be completely resected as for many skull base meningiomas. Medical therapy for patients with recurrent, progressive and symptomatic disease after repeated surgery, radiosurgery and radiotherapy is investigational. Hormonal therapy with progesterone antagonists has shown modest results, while chemotherapy with hydroxyurea appears moderately active.

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Ongoing challenges in diagnosing focal cortical dysplasia (FCD) mandate continuous research and consensus agreement to improve disease definition and classification. An International League Against Epilepsy (ILAE) Task Force (TF) reviewed the FCD classification of 2011 to identify existing gaps and provide a timely update. The following methodology was applied to achieve this goal: a survey of published literature indexed with ((Focal Cortical Dysplasia) AND (epilepsy)) between 01/01/2012 and 06/30/2021 (n = 1349) in PubMed identified the knowledge gained since 2012 and new developments in the field. An online survey consulted the ILAE community about the current use of the FCD classification scheme with 367 people answering. The TF performed an iterative clinicopathological and genetic agreement study to objectively measure the diagnostic gap in blood/brain samples from 22 patients suspicious for FCD and submitted to epilepsy surgery. The literature confirmed new molecular-genetic characterizations involving the mechanistic Target Of Rapamycin (mTOR) pathway in FCD type II (FCDII), and SLC35A2 in mild malformations of cortical development (mMCDs) with oligodendroglial hyperplasia (MOGHE). The electro-clinicalimaging phenotypes and surgical outcomes were better defined and validated for FCDII. Little new information was acquired on clinical, histopathological, or genetic characteristics of FCD type I (FCDI) and FCD type III (FCDIII). The survey identified mMCDs, FCDI, and genetic characterization as fields for improvement in an updated classification. Our iterative clinico-pathological and genetic agreement study confirmed the importance of immunohistochemical staining, neuroimaging, and genetic tests to improve the diagnostic yield. The TF proposes to include mMCDs, MOGHE, and "no definite FCD on histopathology" as new categories in the updated FCD classification. The histopathological classification can be further augmented by advanced neuroimaging and genetic studies to comprehensively diagnose FCD subtypes; these different levels should then be integrated into a multi-layered diagnostic scheme. This update may help to foster multidisciplinary efforts toward a better understanding of FCD and the development of novel targeted treatment options.

No data exist on angiogenic patterns and their prognostic impact in human glioblastoma. Such data are relevant for translation of antiangiogenic therapies into clinical applications. Using immunohistochemistry for CD34, we assessed vascular patterns in 114 primary glioblastomas. Vascular patterns comprised unevenly distributed glomeruloid/ garland-like/clustered bizarre vascular formations and evenly distributed delicate capillary-like microvessels ("classic" vascular pattern). The combination of low content of bizarre vascular formations and prominent classic vascular pattern (n = 29) was an independent factor for longer survival (p = 0.006, Cox regression), as well as postoperative high Karnofsky performance status (p = 0.005). In patients with a prominent classic vascular pattern, there was no difference of MIB1 labeling index whereas microvessel density and apoptotic index (TUNEL) were significantly higher as compared to all other patients (p<0.05). In addition, diffuse expression of hypoxia-inducible factor (HIF)-1␣ and strong expression of vascular endothelial growth factor were more common (p<0.05, Chi-square test). FISH revealed loss of chromosomes 1p and 19q only in 1/7 long-time survivors with classic pattern. We conclude that vascular patterns in primary glioblastoma influence clinical outcome and associate with variable expression of angiogenic proteins. Our findings denote for the first time distinct angiogenic sub-types of human glioblastoma which may prove relevant for anti-angiogenic therapy approaches.