Main mechanisms of post-traumatic brain’s epileptization (Literature review)

Abstract

The problem of traumatic brain injury, its consequences in the long term is relevant for neurologists and doctors of related specialties involved in the treatment, diagnosis and rehabilitation of such a contingent of patients. There are about a dozen syndromes; yaks are most common after an injury. However, one of the most frequent and formidable consequences of traumatic brain damage is post-traumatic epilepsy, which is the main identified cause of symptomatic epilepsy at a young age. The work highlights the “trigger” mechanisms of traumatic brain injury, in particular, oxidative stress, which is an essential component both in the early and long-term periods of CNS damage and leads to the disintegration of all its levels, contributes to the development of basic neuropathological syndromes and primarily post-traumatic epilepsy. The problems of interpreting terminology are considered, when the diagnosis is based only on the fact of the presence of a brain injury, differentiation of this kind of symptomatic convulsive syndrome from other epileptic seizures, the dependence of development on the severity of a head injury (severe injury gives an increased risk of seizures 29 times higher than mild), staging and major risk factors for this type of epileptogenesis, as well as disorganization and damage to the antiepileptic system. A spectrum of convulsive seizures is described, in particular partial, taking into account the localization characteristic of a traumatic brain injury with the predominance of its lesion forms. It is necessary to take into account the occurrence of delayed brain damage, in particular disorders of the immune system, the correlation of the course of post-traumatic epilepsy with the degree of development of hydrocephalus, hypoperfusion of brain areas, glial barrier insufficiency, will contribute to the formation of convulsive activity. It is necessary to take into account the family history. Keywords: post-traumatic epilepsy, epileptogenesis, risk factors