Radiologists play a key role in brain tumor diagnosis and management and must stay abreast of developments in the field to advance patient care and communicate with other health care providers. In 2016, the World Health Organization (WHO) released an update to its brain tumor classification system that included numerous significant changes. Several previously recognized brain tumor diagnoses, such as oligoastrocytoma, primitive neuroectodermal tumor, and gliomatosis cerebri, were redefined or eliminated altogether. Conversely, multiple new entities were recognized, including diffuse leptomeningeal glioneuronal tumor and multinodular and vacuolating tumor of the cerebrum. The glioma category has been significantly reorganized, with several infiltrating gliomas in children and adults now defined by genetic features for the first time. These changes were driven by increased understanding of important genetic factors that directly impact tumorigenesis and influence patient care. The increased emphasis on genetic factors in brain tumor diagnosis has important implications for radiology, as we now have tools that allow us to evaluate some of these alterations directly, such as the identification of 2-hydroxyglutarate within infiltrating gliomas harboring mutations in the genes for the isocitrate dehydrogenases. For other tumors, such as medulloblastoma, imaging can demonstrate characteristic patterns that correlate with particular disease subtypes. The purpose of this article is to review the changes to the WHO brain tumor classification system that are most pertinent to radiologists. RSNA, 2017.

Although autoimmune epilepsy (AE) is a relatively new concept in the radiology literature, evidence for immunological mechanisms in epilepsy has increased in the last several years. 1-9 AE was originally described in the context of more generalized autoimmune encephalopathy, predominately as a paraneoplastic phenomenon targeting the limbic system. Certain tumors expressing neuronal proteins were found to provoke a cell-mediated neurological disorder as a byproduct of an attack on cancer cells. The classically described paraneoplastic limbic encephalitis (LE) reflects involvement of limbic structures including the anteromedial temporal lobe, hippocampus and amygdala and is clinically characterized by the subacute onset of temporal lobe seizures, anterograde memory impairment and psychiatric symptoms. Similar to other paraneoplastic syndromes, neurologic symptoms can present well before a cancer is detectable. Antibodies traditionally considered paraneoplastic include anti-Hu (ANNA-1) and anti CRMP-5 antibodies, usually found in conjunction with small cell lung carcinoma (SCLC), and anti-N-methyl-Daspartate (NMDA) receptor antibodies which are often associated with ovarian teratoma.

Using simple successive tasks we assessed the influence of Alzheimer's disease on the processing of different odours. Fifteen patients with Alzheimer's disease, 15 old control subjects and 15 young control subjects were tested. The experiment included two sessions. Initially 12 odorants were presented, one odorant every minute. For each odour the subjects were asked to rate intensity, pleasantness, familiarity and edibility using linear rating scales. The odorants were then presented a second time and the subjects were asked to identify them. The results show that the intensity scores were lower in old control subjects and Alzheimer patients than in the young control subjects and that familiarity and identification scores were lower in Alzheimer patients than in old control and young control subjects. When we compared the five olfactory tasks the impairment of performance in Alzheimer patients was relatively higher for identification than familiarity, itself higher than the intensity judgement. No difference was observed between the three groups of subjects for pleasantness and edibility judgements.

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Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for dopaminergic neurons. Since dopaminergic neurons degenerate in Parkinson's disease, this factor is a potential therapeutical tool that may save dopaminergic neurons during the pathological process. Moreover, a reduced GDNF expression may be involved in the pathophysiology of the disease. In this study, we tested whether altered GDNF production may participate in the mechanism of cell death in this disease. GDNF gene expression was analyzed by in situ hybridization using riboprobes corresponding to a sequence of the exon 2 human GDNF gene. Experiments were performed on tissue sections of the mesencephalon and the striatum from 8 patients with Parkinson's disease and 6 control subjects matched for age at death and for post mortem delay. No labelling was observed in either group of patients. This absence of detectable expression could not be attributed to methodological problems as a positive staining was observed using the same probes for sections of astroglioma biopsies from human adults and for sections of a newborn infant brain obtained at post-mortem. These data suggest that GDNF is probably expressed at a very low level in the adult human brain and its involvement in the pathophysiology of Parkinson's disease remains to be demonstrated. GDNF may represent a powerful new therapeutic agent for Parkinson's disease, however.