Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5609_Библиотеки_им_академика_М_И_Перельмана

TBI can be described as the disruption of the brain’s physiological and regular activ­ities as a result of an external mechanical impact (Khellaf et al, 2019). TBI is one of the leading causes of disability and death, globally (Najem et al, 2018). Pathogenesis of TBI consists of two phases: primary injury and subsequent secondary injury. A direct mechanical impact to the head causes primary injuries such as cortical con­tusions, axonal shearing hematomas at epidural or subdural regions and microvas­cular injuries (Najem et al, 2018). An initial blow results in a delayed, long-lasting secondary injury that lasts for hours to months to years. Mechanisms involved in secondary injuries include excitotoxicity, mitochondrial dysfunction, neuroinam­mation, oxidative stress, axon deterioration, and consequently neuronal death (Ng and Lee, 2019). TBI also causes cerebral oedema as a result of the obstruction of the outow. This in turn results in rise in a intracranial pressure (ICP), which ulti­mately leads to herniation, a primary cause of death. To prevent the swollen brain from being compressed, a section of the cranium is removed in the decompressive craniectomy (DC) (Bor-Seng-Shu et al, 2013). However, literature reported that DC lowers mortality, but it also leads to brain damage (Cole et al, 2011; Lad et al, 2019) and turns fatalities into survivors with signicant disabilities (Honeybul, 2017). Our results show that pre-treatment with eugenol in rats ameliorated TBI-induced func­tional disabilities (motor coordination, locomotor activity, and short-term memory). Additionally, eugenol pre-treatment reduced trauma-induced enhanced neuronal cell death, lipid peroxidation, oedema, and impaired BBB integrity (Barot and Sa xena , 2021).