modern representations aboutan aetiology and a pathogenesis perinatalnoj encephalopathies

The main feature of a pathology of children's age at the present stage is growth of prevalence of chronic somatic and psychological illnesses. One of the leading reasons of occurrence of pathological deviations at children at early age is trouble in perinatalnom the period of their development [13, 35, 36, 145].

Perinatalnye the damages of a brain quite often accompanied by occurrence of a diencephalic pathology, can be the reason of development not only destructively - dystrophic processes in leading departments TSNS, but also variety gumoralno - somato - the endocrine disturbances leading to functional and morphological shifts in many systems. In this connection perinatalnaja the pathology of nervous system is one of key and actual problems not only neurologies, but also pediatrics.

perinatalnoe a lesion of nervous system or peyorinatalnaja the encephalopathy is understood as the term a pathological condition

Nervous system of a foetus or: the newborn; arisen in the pre-natal period, in the period of sorts or early postnatalnom the period [15-18, 81, BUT].

The term «perinatalnaja an encephalopathy» has been borrowed from the western literature in the middle. 70th years also it was used as generalising interdisciplinary concept; covering all various deviations in the psychological status of children of the first 1,5 — 2th years of a life [36].

Frequency perinatalnyh lesions of nervous system in the different countries and regions fluctuates in limits from 1,8 % to 80 % among all children of the first year of a life. Such variability of data is bound to various standards of diagnostics perinatalnoj encephalopathies, with various representations about an aetiology, a pathogenesis and disease clinic [18; 36, 110, 113, 143,213].

Перинатальные¹ Encephalopathies can be, are caused

gipoksicheskimi; traumatic, toxic, infectious; metabolic and genetic factors [18, 22, 35, 36; 59, 86, 110].

Contributing factors. Developments. perinatalnoj gipoksicheskoj encephalopathies can be various diseases, mothers, gestozy pregnancy, abortion threats, immunologic deviations in system "mother-placenta-fruit", traumatic, toxic, radiative, metabolic, stressful influences,

The professional and household harmfulnesses including a drug intake during pregnancy, smoking.upotreblenie alcohol [81].

According to ShChepljaginoj L.A. [171] it is possible to allocate following preconditions of disturbance of development of the healthy child: complications of a current of pregnancy and placental insufficiency; chronic illnesses at mother; deficiency of fiber, vitamins, essential mikronutrientov (iron, iodine, zinc) in a food of the pregnant woman; pollution

Environment radionuclides and xenobiotics; geochemical trouble of territories (deficiency of iodine in biosphere, excess of iron, fluorine, etc.); mediko-social trouble (the low social status of a family); social deprivatsija, a hypodynamia; the stresses bound to extreme situations both inadequate mental and exercise stresses of the woman during pregnancy.

In Lilina E.T.'s works [86, 87] the hypothesis about the secondary nature of proof consequences perinatalnyh encephalopathies at the newborns who were born with low mass of a body is put forward. It is shown, that in group of children who were born with mass of a body less of 2000 grammes, rasping lesions TSNS are taped by five years in 1,15 % of cases, while at children with mass of a body more than 2000 grammes — in 0,19 %. The author also surveys premature birth, as the essential factor of a birth of the child with rasping disturbances of nervous system (from 18 to 33 %), and multifetal pregnancy as the factor contributing to development perinatalnyh of lesions TSNS (the pathology of nervous system is registered in 6-7 times more often, than at normal pregnancy). In respect of a problem «twins — the rasping lesion of nervous system» is discussed a role feto-fetalnogo a transfusion syndrome. Feto-fetalnyj the transfusion syndrome conducts to shunting of blood from one foetus to another, as a result one foetus becomes the donor, another - the recipient. At the first the anaemia, an arrest of development, at the second - an erythremia, a hydramnion develops.

Palchik A.B. [ON] especially allocates an anaemia of the pregnant woman, lasting more than 2 weeks and digestive tube disease in an exacerbation stage, as one of leading contributing factors in development perinatalnoj gipoksicheskoj encephalopathies.

Recently there are reports on a possible role nejrosensibilizatsii in a pathogenesis perinatalnogo lesions TSNS [145] that can testify to direct involving of immune system in

_? Development of the given pathology. However, the starting factor leading

To changes in immune system, quite often bind to a hypoxia [127,

⁽128].

Conducting etiopatogeneticheskim the occurrence and development factor perinatalnogo lesions TSNS throughout many years

ch the hypoxia [17, 18, 36, 109, 110, 144, 163, 164, 200 is considered; 213, 215, 242].

Among set of theories »a pathogenesis gipoksicheskoj encephalopathies

Now leaders are two interconnected hypotheses: the theory of "a metabolic crisis» in which basis the hypoxia lays,

> The leader, behind itself disturbance of metabolic processes in an organism and

{

Brain damage by toxic metabolic products and «tserebroyovaskuljarnaja the theory» which substantive provision is pathological influence of deficiency kisloroda'na blood supply of a brain [18,113].

< Патофизиологические механизмы влияния гипоксии на развитие перинатальнойэнцефалопатии выглядят следующим образом. Недостаток

[Oxygen causes damage gemato-entsefalicheskogo a barrier,

Leading to disturbance of a metabolism of a glucose, lipids and nucleic

* Acids. As a result in brain tissues there is an accumulation of lactic acid,

Partial pressure СО2 raises, rate of the cerebral decreases

⁴ blood flows, occur disturbance calcium and laktatnogo an exchange.

As the immediate factors damaging a brain are considered: an acidosis (promoting lactic acid accumulation), f accumulation of amino acids (g-aminobutirovaja, a glutamate, aspartate,

_t ethanolamine, fosfoetanolamin, a taurine) and free radicals.

End of this cascade of reactions is permeability disturbance

< нейронов, что приводит к нарушению ауторегуляции мозгового кровотока.

‘ last decade the leading part in a pathogenesis perinatalnyh

• ' lesions TSNS many domestic and foreign researchers

Define process of an apoptosis which is immediately bound to a hypoxia promoting an expression of some factors, inducing an apoptosis [22, 24, 81, 114, 190, 200, 213, 233, 234, 235]. By them it has been put forward, so-called, glutamatnaja the theory of damage of neurones at the gipoksicheski-ischemic encephalopathy which short consists in  destruction of neurones at the expense of damaging action of a glutamate.

About 85 % of synapses of neurones of a cortex and gipokampa make basic exciting receptors TSNS — glutamatnye (mainly NMDA-receptors). Toxic influence glutamatnyh receptors immediately raises complex Са2 + and starts two interconnected processes - a necrosis and an apoptosis. At a necrosis the  destruction of a neurone occurs owing to an edema and a swelling, a vacuolation and lizisa intracellular structures. At an apoptosis - the programmed  destruction of a cell, the  destruction of a neurone is stretched in time and carried out under the control of genes of an apoptosis. The primary site of damage is not limited in space, and at the expense of secondary changes in a brain, in perinatalnom the period it can be enlarged in sizes, affecting as nervous cells and their communications, and a microglia and brain vessels [14-18, 199, 233, 238].

Besides, it is necessary to notice, that gravity and a symptomatology gipoksicheskogo damages depends immediately and from gestatsionnogo age of the newborn [143, 193, 197, 201]. It is caused by that on different terms gestatsii degrees of myelination of nervous fibers are various, sinaptogeneza and susceptibilities to • various nejrotransmitteram (including, and to a glutamate).

Despite damaging mechanisms of a hypoxia and  destruction of nervous cells, the nervous system of the child possesses ability to neogenesis. It speaks occurrence of the kompensatorno-adaptive mechanisms referred on replacement functional and

Structural defect of a nervous tissue. Nervous cells, podvergshiesja to hypoxia influence are capable to carry out the functions and their functionality it is possible to improve by adequate therapeutic actions.

Many researchers assert, that in reply to damage or  destruction of neurones, in a brain new interneural communications are established, there is a migration of "healthy" nervous cells in the damaged sites of nervous system, protective mechanisms for the account nejrotroficheskih the factors allocated in extracellular space after  destruction of a neurone [18 join; 19, 219].

Barashnev J.I. [14, 15, 16, 17, 18] conditionally allocates four phases of development of the pathological process started by a hypoxia at children of the first year of a life. The first phase — the acute period of illness, in till 1 month, arising at an immediate infarct of the brain started by a hypoxia/ischemia and characterised swelling of neurones, lizisom intracellular structures in cells of a cortex, a cerebellum, gipokampa. Within the first 72 hours of a life the secondary changes consisting in synchronisation of process, activation of bioelectric activity of the damaged cells join the primary and transfer of a "suicidal" signal on the intact neurones [18, 31, 133, 189, 227, 247].

The second stage of a gipoksicheski-ischemic encephalopathy occurs on 2-3rd month of a life and is characterised by "false normalisation» when the general condition improves, expression of neurologic disorders decreases, however to the extremity of 2-3rd month of a life this phase passes in the following phase.

The third phase - a phase of spastic disturbances proceeds with 3rd till 6th month of a life of the child, and for it the accurate picture of spastic paresises and paralyses is characteristic. Patomorfologicheski the third phase

Gipoksicheski-ischemic encephalopathy it is shown by a progressing degeneration of the nervous cells, arising ' at the expense of ruptures mezhsinapticheskoj transfers to the first phase.

The fourth stage — a stage of end of pathological process begins with 7-9th month of a life. Vetoj stages damage has already played the role, and; it is realised or »in recover, or in proof consequences. perinatalnogo brain lesions. Thus; most; effective regenerative treatment can be reached in the first-second; a fazah.gipoksicheski-ischemic encephalopathy.

With positions of regenerative medicine, as criteria of the lowered, reserve possibilities of an organism following functional disturbances can be allocated: hyperactivation, stress - of initiating mechanisms and first of all simpatoadreialovoj the systems, the lowered potential stress — limiting systems (the antioxidatic system, inhibiting enzymes and media even - mechanisms, systems prostoglandinov, immunity, etc.); presence stress - damaging effects (the raised destruction of cellular membranes, an ischemia and a hypoxia of tissues; disturbances in system of a hemostasis and; immunodefitsitnye the conditions, lowered, tolerance to carbohydrates, endocrine disorders and others), and also signs of a neurotization of the person, disturbance of the psychophysiological status. disinhronoz biological rhythms of functional parametres, disturbance of the reflex answer and bioenergoinformatsionnye disorders; the lowered shipping of functional loading assays [142].

As in the first years of a life of the child plastic and regeneratornye properties of cells and tissues are high; optimum preconditions for fuller correction of functional deviations and prevention of formation of some psychosomatic diseases and rasping psychoneurological disturbances are framed.

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