One of the most frequent and severe consequences of traumatic brain injury is post-traumatic epilepsy, which is the main identified cause of symptomatic epilepsy at a young age. Post-traumatic epilepsy develops in 11-20% of people who have had traumatic brain injury, its frequency and severity depends on the degree of damage to the central nervous system due to traumatic brain injury, the localization of the traumatic focus, the state of premorbid background, the presence of somatic and comorbid pathology, the state of the autonomic nervous system, etc. According to general population studies, severe traumatic brain injury increases the risk of post-traumatic epilepsy development by 29 times against mild, in which this indicator increases by 1.5 times. In children under 14 years old, the proportion of post-traumatic epilepsy can be up to 14%, while in people over 65 years old, this figure is 8%. The neurophysiological polymorphism of post-traumatic epilepsy is that traumatic brain injury is characterized by a predominantly focal nature of the development of the pathological process, but recently there have been many clinical and experimental confirmations of the presence of diffuse brain damage. These morphological and functional changes coexist and interact with each other with varying degrees of predominance. The work highlights the mechanisms of brain injury, including oxidative stress, leading to disruption of the functioning of all levels of the central nervous system. In the early period after traumatic brain injury, ischemic damage to the central nervous system dominates with the development of glutamate cascade, oxidative stress, etc. As a result of all pathological reactions, disintegration of the central nervous system develops with the development of basic neuropathological syndromes. In the intermediate period, with an unfavorable course of the pathological process, irritation syndromes are formed, in particular, epileptization of the brain with the possible appearance of repeated unprovoked paroxysms, as well as impairment of most neuropsychiatric functions due to excessive neuronal discharges. The formation of post-traumatic epilepsy has a delayed period of the emergence of a focus of epiactivity based on a cascade of morphofunctional "rewiring" of cortical and other networks, disorders of the functioning of the nervous system and depends on a number of "trigger" factors, incl. on the nature, localization, degree of damage, the state of the antiepileptic system and other factors stimulating the generator of hyperextension with the possible occurrence of secondary generators. At the same time, a pathological determinant is fully formed, which "epilepsizes" the brain. Conclusion. The issues of differentiation of post-traumatic epilepsy from other epileptic seizures, the dependence of post-traumatic epilepsy development on the severity of traumatic brain injury, the main risk factors for this type of epileptogenesis, as well as disorganization and damage to the antiepileptic system are considered. The existing wide range of seizures is described, incl. focal, taking into account the localization characteristic of traumatic brain injury
Histological and functional outcomes after traumatic brain injury in mice null for the erythropoietin receptor in the central nervous system
