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CAUSES AND PATHOGENESIS OF PERINATAL BRAIN LESIONS
Ergasheva Maftun Ozodovna
Ergashev Sukhrob Saidovich
Samarkand State Medical University
https://doi.org/10.5281/zenodo.13892960
Abstract:
Fetal hypoxia is a non–specific manifestation of various
complications of pregnancy and childbirth, primarily toxicosis of pregnant
women. The degree and severity of toxicosis, its connection with the extragenital
pathology of a woman (especially with diseases of the cardiovascular system)
determine the duration and severity of fetal hypoxia, whose central nervous
system is most sensitive to oxygen deficiency.
Key words:
perinatal lesion, central nervous system
The aim of the study
was to identify the clinical features of the course of
perinatal CNS lesions and criteria for predicting the results of treatment of these
disorders.
Introduction.
Among the causes of perinatal brain lesions, intrauterine
and intranatal fetal hypoxia occupies a leading place, the second most important
place belongs to the factor of mechanical traumatization of the child during
childbirth – as a rule, in combination with one or another severity preceding
intrauterine hypoxia. Also, the structure of etiopathogenetic factors of perinatal
pathology includes infectious (including viral) and toxic-metabolic variants of
damage to the nervous system. Thus, among the factors contributing to perinatal
CNS damage, the following are distinguished:
1. Fetal intrauterine hypoxia.
2. Intranatal fetal hypoxia.
3. Mechanical injury during childbirth.
4. Infectious (viral) factors.
5. Toxic factors.
6. Hereditary factors.
7. A combination of these factors.
Antenatal hypoxia leads to a slowdown in the growth of brain capillaries,
increases their permeability. The permeability of cell membranes and metabolic
acidosis increase, and cerebral ischemia with intracellular acidosis develops.
Antenatal hypoxia is often combined with intranatal asphyxia. The frequency of
primary asphyxia is 5%. Hypoxia and asphyxia are accompanied by a complex of
compensatory and adaptive reactions, the most important of which is an
increase in anaerobic glycolysis. The effect of hypoxia leads to a complex of
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microcirculatory and metabolic disorders, which at the tissue level cause two
main damages: hemorrhagic infarction and the development of ischemia
followed by leukomalacia of the brain substance. Hemorrhagic (especially) and
ischemic damage to the brain substance is facilitated by some manipulations in
the first 48-72 hours of a child's life: the introduction of hyperosmolar solutions,
artificial lung ventilation (ventilator) and associated hypoperfusion of the brain
against the background of a drop in carbon dioxide voltage, insufficient
correction of circulating blood volume, etc. Hemorrhagic infarction and ischemia
most often develop in fetuses and newborns in the area of the periventricular
plexuses – subependimally in combination with damage to the brain substance.
Hemorrhage can also occur in the lateral ventricles of the brain and in the
subarachnoid space. In addition to the described changes, the morphological
substrate of hypoxia, as a rule, is the fullness of the brain, its general or local
edema. In the pathogenesis of hypoxic-traumatic and hypoxic-ischemic
encephalopathies, causes and effects change places, intertwine in complex
"vicious circles". Violation of hemodynamics (macro- and microcirculation)
leads to multivariate metabolic shifts (violation of the acid-base state and
electrolyte balance, destabilization of cell membranes, hypoxemia and tissue
hypoxia), and these shifts, in turn, exacerbate microcirculation disorders[9]. In
premature infants, the damaging effect of intrauterine hypoxia is potentiated by
immaturity, maladaptation in the intranatal period. The immaturity factor
predisposes to mechanical traumatization of the child, especially with abnormal
exposures, pelvic presentations, and some obstetric aids. Traumatization of the
cervical and thoracic spinal cord is possible when protecting the perineum and
even during cesarean section with a so-called cosmetic incision (insufficient for
gentle removal of the baby's head). Chronic intrauterine intoxication can have
both a non-specific damaging effect (hypoxia) and cause clearly defined
metabolic disorders and, accordingly, specific clinical syndromes – fetal alcohol
syndrome, nicotine syndrome, narcotic withdrawal syndrome. In recent years,
the subtle mechanisms of the pathogenesis of hypoxic-ischemic brain lesions
have been deciphered.
The importance of intrauterine infections in the formation of pediatric cerebral
pathology was first pointed out by 3. Freud (Freud S., 1897).
Сonclusions:
Currently, the leading role of intrauterine infections in the
development of 1111HC and cerebral palsy has been convincingly proven.
Particular importance is attached to intrauterine viral lesions: congenital
rubella, herpetic infection, inclusive cytomegaly and toxoplasmosis, as well as
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diseases caused by various bacterial agents and protozoa. It is believed that
intrauterine infection in 50% of cases causes the death of neurons, and also
causes damage to the periventricular region of the brain with the subsequent
development of necrosis of the white matter.
References:
1. Zakharova Olesya Vladimirovna Neuroprotective therapy of hypoxic-ischemic
encephalopathy in newborns: a systematic review of the literature. //
Neonatology: News. Opinions. Training, (2023). 11 (2 (40)), 74-86.
2. Koehler R.K., Yang Z.-J., Lee J.K., Martin L.J. Perinatal hypoxic-ischemic brain
damage in large animal models: relation to human neonatal encephalopathy. //
Journal of Cerebral blood flow and Metabolism. 2018;38(12):2092-2111.
doi:10.1177/0271678X18797328
3. Kornet M.S., Kuznetsevich M., Scheffler A., Forker H., Hamilton E., Newman
T.B., Wu Yu.V. Perinatal hypoxic-ischemic encephalopathy: prevalence over time
in a modern cohort of newborns in the USA. // Pediatric Neurology, (2023). 149,
145-150.
4. Lee B.R., Klass H.S. Cognitive consequences of neonatal hypoxic-ischemic
encephalopathy in late childhood and adolescence. // Clinical and Experimental
Pediatrics, 2021;64 (12), pp. 608-18.
5. Munzant A, Srivastava K, Recasens M and Jimenez-Llort L. Severe perinatal
hypoxic-ischemic brain injury causes long-term sensorimotor deficits, anxiety-
like behavior, and cognitive impairment in C57BL/6 mice, depending on gender,
age, and tasks, but can be corrected with neonatal treatment. // Front.
Behaviour. Neurology. 2019, №13, 7.
