Temporoinsular Extraventricular Neurocytoma Initially Diagnosed as Glioblastoma in a 57-Year-Old Woman: A Case Report and Literature Review.

Adult neurogenesis represents possibly one of the most intriguing forms of neuroplasticity in the postnatal mammalian brain and, in this sense, it has attracted the close attention of researchers around the world over the past few decades. The pioneering studies of Altman and Das, who initially showed the generation of new neurons in the adult mammalian brain by using a 3H-thymidine method, date back to the 1960s, but at that time they were generally left without proper attention [,,]. True progress in this field started again in the 1990s with the identification of numerous molecular markers typical of immature neurons and the development of immunohistochemical methods to detect them. In combination with synthetic nucleotide labeling (primarily 5-bromo-2′-deoxyuridine), this gave researchers a range of powerful instruments for detailed investigation of adult neurogenesis. To date, the total number of publications on the topic of adult neurogenesis exceeds 14,000. Attempts have also been made to understand the significance of this form of plasticity and the role of young cells in the functioning of the adult brain under normal and pathological conditions. The first straightforward assumptions regarding the reparative function of newly born neurons were rejected [] shortly after the strict spatial localization and quantitative limitations of this process became clear. Along with this, experimental findings gradually accumulated, indicating changes in the rate of adult neurogenesis. Acute and chronic stress, social isolation, aging, exposure to corticosteroids, and neuroinflammation were accompanied by decreased generation of new neurons. Increased neurogenesis was observed after exposure to enriched-environment conditions and physical exercise during pregnancy in females [,,]. Some pathological situations were also found to be accompanied by enhanced neurogenesis: seizures of different origin [], ischemic stroke [] or brain injury []. Based on the accumulated experimental material, several intriguing biomedical hypotheses have been put forward linking changes in the normal course of hippocampal neurogenesis and the development of various neurological and psychiatric pathologies. For example, the discovery of increased formation and atypical maturation of new cells after severe seizures formed the basis for the hypothesis of the involvement of neurogenesis in the development of epilepsy []. Indeed, after seizures, resting progenitor cells of neurons are usually involved in the cell cycle, after which their descendants can migrate to the polymorphic layer of the dentate gyrus instead of the granular one, as well as give off atypical apical dendrites and demonstrate increased branching of regrowing axons (so-called “sprouting of mossy fibers”). The collaterals of these axons can be directed into the dentate gyrus instead of the CA3 field, thus creating opportunities for local circulation of excitation. Similar structural changes have also been observed in human epileptic tissues, obtained either post-mortem or following amygdalohippocampectomy for pharmacoresistant temporal lobe epilepsy. This parallelism strongly supports the hypothesis that young neurons, generated during seizure-induced neurogenesis, actively participate in forming the epileptogenic focus. An additional argument in favor of such involvement was also the fact that young neurons tend to be more excitable for stimulation. Another interesting hypothesis was the possible role of neurogenesis in the development of depression []. By that time, it was known that chronic stress and increased glucocorticoid level, which play a role in the development of depressive disorders, may reduce the proliferation and survival of newly born cells in the hippocampus []; subsequently confirmed by []. On the other hand, treatment with antidepressant drugs has been found to enhance cell proliferation in the hippocampus in laboratory animals [,,]. The effect of antidepressant drugs usually takes several weeks to completely develop, corresponding to the time required for neuronal differentiation of newly born cells and their functional integration into the hippocampal neuronal circuits. In addition, experimental conditions such as electroconvulsive shock, physical activity, and environmental enrichment, on the one hand, lead to an increase in adult neurogenesis, and on the other to a decrease in depressive-like symptoms in experiments [,]. Based on these consistent data, it was hypothesized that development of depressive-like symptoms may involve decreased hippocampal neurogenesis, and the therapeutic effect of antidepressant drugs is associated with their ability to restore its normal level [].