MORPHO-HISTOLOGICAL CHARACTERISTICS OF CHANGES AFTER BRAIN INJURIES (LITERATURE REVIEW)

Аннотация

INTRODUCTION in people under the age of 35. In economically Brain injuries make up 30-40% of all injuries and developed countries, the increase in motor cause disability in 25-30% of cases. [15]. More than vehicles and the automation of work processes are 90% of those who died were found to be caused by leading to an increase in the incidence of traumatic ischemic damage of the brain during histological brain injuries. For example, in the United States, examination(19). The cause of death remains there are 180 to 250 cases per 100,000 people, and unexplained in one-third of 70-72% of brain injury in Europe, up to 235 cases, of which 1.6 million are deaths after traumatic brain injury [20]. Clinical hospitalized, of whom 66,000 die. According to the observations and computer tomographic World Health Organization, traumatic brain examinations revealed that 3-25% of patients injuries are predominantly chronic diseases, the develop acute cerebral blood circulation disorders, consequences of which are irreversible, require that is, secondary cerebral stroke [20,25,26]. long-term rehabilitation, and ultimately result in In the Russian Federation, the number of deaths disability. [18] due to injuries ofbrain in second place, accounting Complete general criteria for the correct for 15.8%, and this indicator is a ratio of 6:9 among assessment of the severity and consequences of the working-age population [15]. brain damage in patients after head injuries have Traumatic brain injuries are one of the leading not been developed [15]. causes of death and the leading cause of disability https://www.theamericanjournals.com/index.php/tajmspr 35 THE USA JOURNALS THE AMERICAN JOURNAL OF MEDICAL SCIENCES AND PHARMACEUTICAL RESEARCH (ISSN – 2689-1026) VOLUME 06 ISSUE11 The most common cause of dislocation syndromes and neuronal cell damage, are characteristic in head injuries is injuries accompanied by pathological conditions observed after traumatic intracranial hemorrhage. The cause of these brain injury [19]. pathological processes in head injuries is a In traumatic brain injury, signs of secondary condition such as damage to the brain stem. As we intracranial and extracranial brain injury must know, we study primary and secondary forms of develop for primary brain damage. Intracranial brain stem injuries separately. Primary changes changes include changes such as brain hematoma include contusions, compression and rupture of compression, impaired hemo- and the stem, diffuse axonal injuries, and hemorrhage microcirculation, cerebral edema, intracranial into the stem. Secondary changes include damage infection, and hydrocephalus. Extracranial changes to the structure of the stem, compression of the include signs such as hypoxemia, arterial brain with a hematoma, swelling and congestion of hypotension, anemia, impaired blood-brain the brain, pathological changes in blood circulation barrier permeability, and impaired neurohumoral and cerebrospinal fluid circulation. The control. occurrence and development of the above changes The system that undergoes the main pathogenetic result in clinical manifestations associated with changes in the acute period of traumatic brain dislocation syndrome [4]. After head injuries, injury is the dysfunction of the central nervous intracerebral hypertension, systemic hypotension, system [1,3,9,13]. Pathological conditions such as cerebral edema, brain compression with focal contusions, hematomas, dislocations, and brain hematomas, and the development of pathologies in contusions cause dysfunction of the central small blood vessels (vasospasm) cause ischemic nervous system [4,16]. processes in the brain. Clinical and pathogenetic changes in injuries are In traumatic brain injuries, the primary manifested depending on the location of the lesion pathological changes in the brain are necrosis and and the nature of the central nervous system dystrophy. Histological examination reveals damage [5,28]. Depending on the time of the lesion, rupture of axons of the corpus callosum, brain the lesion is divided into manifestations of stem, cerebellar peduncle, internal capsules, resistance to changes, and depending on the rupture of blood vessels in sections, and the changes in the surrounding tissue, inflammation, appearance of hemorrhagic infarction foci in edema and secondary hemorrhage. Focal changes numerous subcortical formations, less often in the cause various pathological changes depending on peduncle [17]. their location. General cerebral symptoms develop In the late stages, post-traumatic necrosis may from varying degrees of change in consciousness develop. Histological examination reveals to a state of unconsciousness. The development of circulatory disorders (white and red infarction cerebral edema begins with a period of “colorful foci, edematous effusions, perivascular interval” and progresses to profound impairment encephalolysis), inflammatory processes of consciousness [19]. (purulent and h