Residual-organic lesion of the central nervous system. Development of the central nervous system and signs of pathology

If a doctor talks about neuralgia and even VVD, then an ordinary person has at least a rough idea of what it is about. But the diagnosis of “residual organic lesion of the central nervous system”, as a rule, confuses everyone (except physicians). It is clear that this is "something in the head." But what? How dangerous and whether it can be treated - this topic requires a serious approach.

What is hidden behind the complex term?

Before revealing such a medical concept as a residual organic lesion of the central nervous system, it is necessary to understand what is generally understood as an organic disorder. This means that dystrophic changes occur in the brain - cells are destroyed and die, that is, this organ is in an unstable state. The word "residual" indicates that the pathology appeared in a person during the perinatal period (when he was still in the womb) - from 154 days of gestation (in other words, at 22 weeks), when the fetus weighed 500 g, and 7 days after emergence into the world. The disease consists in the fact that the work of the central nervous system organs is disrupted. Thus, a person acquires this pathology as an infant, and it can manifest itself both immediately after birth and in adulthood. The reason for its development in adults is trauma, intoxication (including alcohol, drugs), inflammatory diseases (encephalitis, meningitis).

Why does the brain or spinal cord suffer (it also belongs to the central nervous system)? If we talk about the second, then the reason may be incorrect obstetric care - for example, inaccurate turns of the head when removing the baby. Residual organic brain damage develops due to genetic disorders that are inherited, maternal diseases, abnormal childbirth, stress, malnutrition and behavior of a pregnant woman (in particular, taking dietary supplements, medications that adversely affect the formation of organs of the nervous system), asphyxia during time of childbirth, infectious diseases of a nursing woman and other adverse factors.

Not like everyone else! External signs of a dangerous inheritance

It is quite difficult to detect residual organic CNS damage in children without instrumental methods of examination. Parents may not notice anything unusual in the physical condition and behavior of the baby. But an experienced neurologist is likely to notice alarming symptoms. His attention will be attracted by such characteristic signs of pathology in an infant:

involuntary trembling of the upper limbs and chin;
unmotivated anxiety;
lack of muscle tension (which is typical for newborns);
lagging behind the accepted terms of formation of arbitrary movements.

With gross brain damage, the picture of the disease looks like this:

paralysis of any of the limbs;
blindness;
violation of pupil movements, strabismus;
reflex failure.

In an older child and an adult, pathology can manifest itself with the following symptoms:

fatigue, unstable mood, inability to adapt to physical and mental stress, increased irritability, capriciousness;
tic, fears, nocturnal enuresis;
mental anxiety, distraction;
poor memory, lag in intellectual and speech development, low learning ability, impaired perception;
aggression, agitation, tantrums and, lack of self-criticism;
inability to make independent decisions, suppression, dependence;
motor hyperactivity;
diffuse headache (especially in the morning);
progressive loss of vision;
sometimes vomiting without nausea;
convulsions.

Important! At the first, even minor, signs of organic brain damage, it is recommended to immediately contact a highly qualified specialist, since a timely diagnosis significantly reduces the risk of developing dangerous and irreversible consequences.

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What diagnostic procedures will confirm the diagnosis?

Today, the following methods are used to diagnose this pathology:

MRI of the brain;
electroencephalography;
raoencephalography.

The patient must be examined by several specialists: a neurologist, a psychiatrist, a defectologist, a speech therapist.

Can the brain be healed?

It must be understood that the term "unspecified residual organic lesion of the central nervous system" (ICB code 10 - G96.9) means several pathologies. Therefore, the choice of therapeutic methods of exposure depends on the prevalence, location, degree of necrosis of the nervous tissue and the patient's condition. The medicinal component of treatment usually includes sedatives, nootropics, tranquilizers, sleeping pills, antipsychotics, psychostimulants, drugs that improve cerebral circulation, vitamin complexes. Good results are given by physiotherapy, acupuncture, bioacoustic correction of GM, massage sessions. A child with such a diagnosis needs psychotherapeutic intervention, neuropsychological rehabilitation, and the help of a speech therapist.

Although it is believed that organic lesions of the nervous system are persistent and lifelong, with mild disorders and an integrated approach to therapy, it is still possible to achieve a complete recovery. In severe lesions, brain edema, spasm of the respiratory muscles, and a malfunction of the center that controls the work of the cardiovascular system are possible. Therefore, constant medical monitoring of the patient's condition is indicated. The consequence of this pathology can be epilepsy, mental retardation. In the worst case, when the scale of damage is too great, it can lead to the death of the newborn or fetus.

The central nervous system is the main regulator of the entire body. Indeed, in the cortical structures of the brain there are departments responsible for the functioning of each system. Thanks to the central nervous system, the normal functioning of all internal organs, the regulation of hormone secretion, and psycho-emotional balance are ensured. Under the influence of adverse factors, organic damage to the structure of the brain occurs. Often, pathologies develop in the first year of a child's life, but can also be diagnosed in the adult population. Despite the fact that the central nervous system is directly connected with organs due to nerve processes (axons), damage to the cortex is dangerous due to the development of severe consequences even in the normal state of all functional systems. The treatment of brain diseases should be started as early as possible, in most cases it is carried out for a long time - for several months or years.

Description of residual-organic lesion of the CNS

As you know, the central nervous system is a well-coordinated system in which each of the links performs an important function. As a result, damage to even a small part of the brain can lead to disruption in the functioning of the body. In recent years, damage to the nervous tissue has been increasingly observed in pediatric patients. To a greater extent, this applies only to born babies. In such situations, a diagnosis of "residual organic lesion of the central nervous system in children" is made. What is it and can this disease be treated? The answers to these questions worry every parent. It should be borne in mind that such a diagnosis is a collective concept, which may include many different pathologies. The selection of therapeutic measures and their effectiveness depend on the extent of damage and the general condition of the patient. Sometimes residual-organic CNS damage occurs in adults. Often, pathology occurs as a result of trauma, inflammatory diseases, intoxication. The concept of "residual-organic lesion of the central nervous system" implies any residual effects after damage to the nervous structures. The prognosis, as well as the consequences of such a pathology, depend on how severely the brain function is impaired. In addition, great importance is attached to the topical diagnosis and identification of the injury site. After all, each of the brain structures must perform certain functions.

Causes of residual organic brain damage in children

Residual organic lesion of the central nervous system in children is diagnosed quite often. Causes of nervous disorders can occur both after the birth of a child and during pregnancy. In some cases, damage to the central nervous system occurs due to complications of childbirth. The main mechanisms for the development of residual organic damage are trauma and hypoxia. There are many factors that provoke a violation of the nervous system in a child. Among them:

genetic predisposition. If the parents have any psycho-emotional deviations, then the risk of developing them in the baby increases. Examples are pathologies such as schizophrenia, neurosis, epilepsy.
Chromosomal abnormalities. The reason for their occurrence is unknown. Incorrect DNA construction is associated with adverse environmental factors, stress. Due to chromosomal disorders, pathologies such as Shershevsky-Turner syndrome, Patau, etc. occur.
The impact of physical and chemical factors on the fetus. This refers to the unfavorable environmental situation, ionizing radiation, the use of narcotic drugs and medicines.
Infectious and inflammatory diseases during the laying of the nervous tissue of the embryo.
Toxicosis of pregnancy. Especially dangerous for the condition of the fetus are late gestosis (pre- and eclampsia).
Violation of placental circulation, iron deficiency anemia. These conditions lead to fetal ischemia.
Complicated childbirth (weakness of uterine contractions, narrow pelvis, placental abruption).

Residual organic lesions of the central nervous system in children can develop not only in the perinatal period, but also after it. The most common cause is a head injury at an early age. Also, risk factors include taking drugs with a teratogenic effect and narcotic substances during breastfeeding.

Occurrence of residual organic brain damage in adults

In adulthood, signs of residual organic damage are less common, however, they are present in some patients. Often the cause of such episodes are traumas received in early childhood. At the same time, neuropsychic deviations are long-term consequences. Residual organic brain damage occurs for the following reasons:

post-traumatic illness. Regardless of when CNS damage occurs, residual (residual) symptoms remain. Often these include headache, convulsive syndrome, mental disorders.
Condition after surgery. This is especially true of brain tumors, which are removed with the capture of nearby nervous tissue.
Taking drugs. Depending on the type of substance, the symptoms of residual organic damage may vary. Most often, serious violations are observed with long-term use of opiates, cannabinoids, synthetic drugs.
Chronic alcoholism.

In some cases, residual organic damage to the central nervous system is observed after suffering inflammatory diseases. These include meningitis, various types of encephalitis (bacterial, tick-borne, post-vaccination).

The mechanism of development of CNS lesions

Residual damage to the central nervous system is always caused by adverse factors that preceded earlier. In most cases, the basis of the pathogenesis of such symptoms is cerebral ischemia. In children, it develops even during the period. Due to insufficient blood supply to the placenta, the fetus receives little oxygen. As a result, the full development of the nervous tissue is disrupted, fetopathy occurs. Significant ischemia leads to intrauterine growth retardation, the birth of a child before the gestational age. Symptoms of cerebral hypoxia can appear already in the first days and months of life. Residual-organic damage to the central nervous system in adults often develops due to traumatic and infectious causes. Sometimes the pathogenesis of nervous disorders is associated with metabolic (hormonal) disorders.

Syndromes with residual-organic lesions of the central nervous system

In neurology and psychiatry, several main syndromes are distinguished, which can occur both independently (against the background of a brain disease) and regarded as a residual CNS lesion. In some cases, there is a combination of them. The following signs of residual organic damage are distinguished:

What are the consequences of residual organic damage?

The consequences of residual-organic CNS damage depend on the degree of the disease and the approach to treatment. With mild disorders, full recovery can be achieved. Severe damage to the central nervous system is dangerous for the development of conditions such as cerebral edema, spasm of the respiratory muscles, and damage to the cardiovascular center. To avoid such complications, constant monitoring of the patient is necessary.

Disability in residual-organic lesions

Treatment should be started as soon as the appropriate diagnosis is established - "residual-organic lesion of the central nervous system." Disability in this disease is not always assigned. With severe violations and the lack of effectiveness of treatment, a more accurate diagnosis is established. Most often it is "post-traumatic brain disease", "epilepsy", etc. Depending on the severity of the condition, 2 or 3 disability groups are assigned.

Prevention of residual-organic damage to the central nervous system

To avoid residual organic damage to the central nervous system, it is necessary to be observed by a doctor during pregnancy. In case of any deviations, medical attention should be sought. It is also worth refraining from taking medicines, bad habits.

7.2. Clinical variants of residual-organic insufficiency of the CNS

Here is a brief description of some of the options.

1) cerebrosthenic syndromes. Described by many authors. Residual cerebrasthenic syndromes are basically similar to asthenic conditions of another origin. Asthenic syndrome is not a static phenomenon, it, like other psychopathological syndromes, goes through certain stages in its development.

At the first stage, irritability, impressionability, emotional tension, inability to relax and wait, haste in behavior to the point of fussiness and, outwardly, increased activity, the productivity of which is reduced due to the inability to act calmly, systematically and prudently, - "fatigue that does not seek rest" (Tiganov A.S., 2012). it hypersthenic variant of asthenic syndrome or asthenohyperdynamic syndrome in children (Sukhareva G.E., 1955; and others), it is characterized by a weakening of the processes of inhibition of nervous activity. Asthenohyperdynamic syndrome is more often a consequence of early organic lesions of the brain.

The second stage of development of asthenic syndrome is characterized by irritable weakness- approximately parity combination of increased excitability with rapid exhaustion, fatigue. At this stage, the weakening of the processes of inhibition is complemented by a rapid depletion of the processes of excitation.

In the third stage of the development of asthenic syndrome, lethargy, apathy, drowsiness predominate, a significant decrease in activity up to inactivity - astheno-adynamic option asthenic syndrome or asthenodynamic syndrome in children (Sukhareva G.E., 1955; Vishnevsky A.A., 1960; and others). In children, it is described mainly in the late period of severe neuro- and general infections with secondary brain damage.

Subjectively, patients with cerebral palsy experience heaviness in the head, inability to concentrate, a persistent feeling of fatigue, overwork, or even impotence, which grows under the influence of habitual physical, intellectual, and emotional stress. Ordinary rest, unlike physiological fatigue, does not help patients.

In children, points out V.V. Kovalev (1979), irritable weakness comes to light more often. At the same time, asthenic syndrome with residual organic insufficiency of the central nervous system, i.e., the cerebrasthenic syndrome itself, has a number of clinical features. Thus, the phenomena of asthenia in schoolchildren are especially enhanced during mental stress, while memory indicators are significantly reduced, resembling erased amnestic aphasia in the form of transient forgetting of individual words.

In post-traumatic cerebral palsy, affective disturbances are more pronounced, emotional explosiveness is observed, and sensory hyperesthesia is more common. In post-infectious cerebral palsy, among affective disorders, dysthymic phenomena predominate: tearfulness, capriciousness, discontent, sometimes anger, and in cases of early neuroinfection, violations of the body scheme occur more often.

After perinatal and early postnatal organic processes, violations of higher cortical functions may persist: elements of agnosia (difficulties in distinguishing figures and backgrounds), apraxia, disturbances in spatial orientation, phonemic hearing, which can cause a belated development of school skills (Mnukhin S.S., 1968) .

As a rule, more or less pronounced disorders of autonomic regulation, as well as scattered neurological microsymptoms, are found in the structure of the cerebrasthenic syndrome. In cases of organic damage in the early stages of intrauterine development, anomalies in the structure of the skull, face, fingers, internal organs, expansion of the ventricles of the brain, etc. are often detected. Many patients experience headaches that worsen in the afternoon, vestibular disorders (dizziness, nausea, feeling of when driving), signs of intracranial hypertension (paroxysmal headaches, etc.) are revealed.

According to a follow-up study (in particular, V.A. Kollegov, 1974), cerebrosthenic syndrome in children and adolescents in most cases has a regressive dynamics with the disappearance of post-pubertal asthenic symptoms, headaches, smoothing of neurological microsymptoms and fairly good social adaptation.

However, states of decompensation may occur, usually this occurs during periods of age-related crises under the influence of training overloads, somatic diseases, infections, repeated head injuries, and psychotraumatic situations. The main manifestations of decompensation are increased asthenic symptoms, vegetative dystonia, especially vasovegetative disorders (including headaches), as well as the appearance of signs of intracranial hypertension.

2) Violations sexual development in children and teenagers. In patients with disorders of sexual development, residual organic neurological psychiatric pathology is often detected, but there are also procedural forms of nervous and endocrine pathology, tumors, as well as congenital and hereditary disorders of the hypothalamic-pituitary system, adrenal glands, thyroid gland, gonads.

1. premature sexual development (PPR). PPR is a condition characterized in girls by the appearance of thelarche (growth of the mammary glands) before 8 years of age, in boys by an increase in testicular volume (volume of more than 4 ml or length of more than 2.4 cm) before 9 years. The appearance of these signs in girls 8–10 years old, and in boys 9–12 years old is considered as early sexual development which most often does not require any medical intervention. There are the following forms of PPR (Boyko Yu.N., 2011):

true PPR when the hypothalamic-pituitary system is activated, which leads to an increase in the secretion of gonadotropins (luteinizing and follicle-stimulating hormones), which stimulate the synthesis of sex hormones;
false PPR due to autonomous (not dependent on gonadotropins) excessive secretion of sex hormones by the gonads, adrenal glands, tissue tumors that produce androgens, estrogens or gonadotropins, or excessive intake of sex hormones into the child's body from the outside;
partial or incomplete PPR characterized by the presence of isolated thelarche or isolated adrenarche without the presence of any other clinical signs of PPR;
diseases and syndromes accompanied by PPR.

1.1. True PPR. It is due to the premature onset of impulse secretion of GnRH and is usually only isosexual (corresponds to the genetic and gonadal sex), always only complete (there is a consistent development of all secondary sexual characteristics) and always complete (menarche occurs in girls, virilization and stimulation of spermatogenesis in boys).

True PPR can be idiopathic (more common in girls), when there are no obvious reasons for early activation of the hypothalamic-pituitary system, and organic (more common in boys), when various diseases of the central nervous system lead to stimulation of impulse secretion of GnRH.

The main causes of organic PPS: brain tumors (chiasmatic glioma, hypothalamic hamartoma, astrocytoma, craniopharyngioma), non-tumor brain damage (congenital brain anomalies, neurological pathology, increased intracranial pressure, hydrocephalus, neuroinfections, TBI, surgery, head irradiation, especially in girls, chemotherapy). In addition, late treatment of virilizing forms of congenital adrenal hyperplasia due to disinhibition of the secretion of GnRH and gonadotropins, as well as, which rarely happens, long-term untreated primary hypothyroidism, in which a high level of thyroliberin stimulates not only the synthesis of prolactin, but also impulse secretion of GnRH.

True PPR is characterized by the sequential development of all stages of puberty, but only by the premature, simultaneous appearance of secondary effects of androgen action (acne, change in behavior, mood, body odor). Menarche, which normally occurs no earlier than 2 years after the first signs of puberty appear, can appear much earlier (after 0.5–1 year) in girls with true PPR. The development of secondary sexual characteristics is necessarily accompanied by an acceleration in growth rates (more than 6 cm per year) and bone age (which is ahead of chronological age). The latter progresses rapidly and leads to premature closure of the epiphyseal growth zones, which ultimately leads to short stature.

1.2. False PPR. It is caused by hyperproduction of androgens or estrogens in the ovaries, testicles, adrenal glands and other organs or hyperproduction of chorionic gonadotropin (CG) by CG-secreting tumors, as well as by the intake of exogenous estrogens or gonadotropins (false iatrogenic PPR). False PPR can be both isosexual and heterosexual (in girls - according to the male type, in boys - according to the female). False PPR is usually incomplete, i.e., menarche and spermatogenesis do not occur (excluding McCune syndrome and familial testotoxicosis syndrome).

The most common causes of the development of false PPR: in girls - estrogen-secreting ovarian tumors (granulomatous tumor, luteoma), ovarian cysts, estrogen-secreting tumors of the adrenal glands or liver, exogenous intake of gonadotropins or sex steroids; in boys - virilizing forms of congenital adrenal hyperplasia (CAH), androgen-secreting tumors of the adrenal glands or liver, Itsenko-Cushing's syndrome, androgen-secreting testicular tumors, CG-secreting tumors (including often in the brain).

Heterosexual false PPR in girls can be with virilizing forms of CAH, androgen-secreting tumors of the ovaries, adrenal glands or liver, Itsenko-Cushing's syndrome; in boys - in the case of tumors that secrete estrogens.

The clinical picture of the isosexual form of false PPR is the same as in true PPR, although the sequence of development of secondary sexual characteristics may be somewhat different. Girls may have uterine bleeding. In the heterosexual form, there is hypertrophy of the tissues that are affected by the excess hormone, and atrophy of those structures that normally secrete this hormone at puberty. Girls have adrenarche, hirsutism, acne, clitoral hypertrophy, low voice, male physique, boys have gynecomastia and female-type pubic hair. In both forms of false PPR, growth acceleration and a significant progression of bone age are always present.

1.3. Partial or incomplete PPR:

premature isolated thelarche. It is more common in girls aged 6-24 months, as well as in 4-7 years. The reason is a high level of gonadotropic hormones, especially follicle-stimulating hormone in the blood plasma, which is normal for children under 2 years of age, as well as periodic estrogen surges or increased sensitivity of the mammary glands to estrogens. It is manifested only by an increase in the mammary glands on one or two sides and most often regresses without treatment. If there is also an acceleration of bone age, this is assessed as an intermediate form of PPR, requiring more careful monitoring with control of bone age and hormonal status;
premature isolated adrenarche associated with an early increase in the secretion of testosterone precursors by the adrenal glands, which stimulate pubic and axillary hair growth. It can be triggered by non-progressive intracranial lesions that cause hyperproduction of ACTH (meningitis, especially tuberculosis), or be a symptom of a late form of CAH, tumors of the gonads and adrenal glands.

1.4. Diseases and syndromes, accompanying PPR:

syndrome Poppy-Kyuna-Albright. This is a congenital disease, more common in girls. It occurs at an early embryonic age as a result of a mutation of the gene responsible for the synthesis of G-protein, through which the signal is transmitted from the hormone-LH and FSH receptor complex to the germ cell membrane (LH - luteinizing hormone, FSH - follicle-stimulating hormone). As a result of the synthesis of abnormal G-protein, hypersecretion of sex hormones occurs in the absence of control from the hypothalamic-pituitary system. Other tropic hormones (TSH, ACTH, STH), osteoblasts, melanin, gastrin, etc. interact with receptors through the G-protein. one side of the body or face and in the upper half of the trunk, bone dysplasia and cysts in the tubular bones. There may be other endocrine disorders (thyrotoxicosis, hypercortisolism, gigantism). Often there are ovarian cysts, lesions of the liver, thymus, gastrointestinal polyps, cardiac pathology;
syndrome family testotoxicosis. An inherited disease, transmitted in an autosomal dominant manner with incomplete penetrance, occurs only in males. Caused by a point mutation in the LH and CG receptor gene located on Leydig cells. As a result of constant stimulation, Leydig cell hyperplasia and hypersecretion of testosterone uncontrolled by LH occur. Signs of PPG appear in boys at the age of 3–5 years, while androgen-mediated effects (acne, pungent sweat, deepening of the voice) can occur as early as 2 years of age. Spermatogenesis is activated early. Fertility in adulthood is often not impaired;
syndrome Russell-Silvera. Congenital disease, mode of inheritance unknown. The cause of development is an excess of gonadotropic hormones. Main features: intrauterine developmental delay, short stature, multiple dysembryogenesis stigmas (small triangular "bird" face, narrow lips with lowered corners, moderately blue sclera, thin and brittle hair on the head), impaired skeletal formation in early childhood (asymmetry), shortening and curvature of the 5th finger, congenital dislocation of the hip, café-au-lait spots on the skin, renal anomalies and PPR from 5–6 years of age in 30% of children;
primary hypothyroidism. It occurs, presumably, because due to the constant hyposecretion of thyroid-stimulating hormone in long-term untreated primary hypothyroidism, chronic stimulation of gonadotropic hormones and the development of PPR with an increase in the mammary glands and occasionally galactorrhea occur. There may be ovarian cysts.

In the treatment of true PPR, analogues of gonadoliberin or gonadotropin-releasing hormone (analogues of gonadoliberin are 50–100 times more active than the natural hormone) are used to suppress the impulse secretion of gonadotropic hormones. Long-acting drugs are prescribed, in particular diphereline (3.75 mg or 2 ml once a month i / m). As a result of therapy, the secretion of sex hormones decreases, growth slows down and sexual development stops.

Isolated premature thelarche and adrenarche do not require medical treatment. In the treatment of hormonally active tumors, surgical intervention is required; in case of primary hypothyroidism, thyroid hormone replacement therapy (to suppress TSH hypersecretion) is required. CAH is treated with corticosteroid replacement therapy. Therapy for McCune-Albright syndromes and familial testotoxicosis has not been developed.

2. Delayed sexual development (ZPR). It is characterized by the absence of growth of the mammary glands in girls at the age of 14 years and older, in boys - the absence of growth in the size of the testicles at the age of 15 years and older. The appearance of the first signs of sexual development in girls aged 13 to 14 years, and in boys - from 14 to 15 years is considered as later sexual development and does not require medical intervention. If sexual development began in a timely manner, but menstruation does not occur within 5 years, they speak of isolated delayed menarche. If we are talking about a true delay in sexual development, this does not at all mean the presence of a pathological process.

In 95% of children with mental retardation, there is a constitutional delay in puberty, in the remaining 5% of cases, mental retardation is due to severe chronic diseases rather than primary endocrine pathology. They differ: a) a simple delay in puberty; b) primary (hypergonadotropic) hypogonadism; c) secondary (hypogonadotropic) hypogonadism.

2.1. Simple delay puberty (PZP). It occurs most often (95%), especially in boys. Reasons for development:

heredity and / or constitution (cause of the bulk of cases of PZP);
untreated endocrine pathology (hypothyroidism or isolated growth hormone deficiency that appeared at the age of normal puberty);
severe chronic or systemic diseases (cardiopathy, nephropathy, blood diseases, liver diseases, chronic infections, psychogenic anorexia);
physical overload (especially in girls);
chronic emotional or physical stress;
malnutrition.

Clinically, PZP is characterized by the absence of signs of sexual development, growth retardation (starting at 11-12 years old, sometimes earlier) and delayed bone age.

One of the most reliable signs of PZP (its non-pathological form) is the complete correspondence of the child's bone age to the chronological age, which corresponds to his real height. Another equally reliable clinical criterion is the degree of maturation of the external genital organs, i.e. the size of the testicles, which in the case of PZP (2.2–2.3 cm in length) borders on normal sizes characterizing the onset of sexual development.

The test with chorionic gonadotropin (CG) is very informative diagnostically. It is based on the stimulation of Leydig cells in the testicles that produce testosterone. Normally, after the introduction of hCG, there is an increase in the level of testosterone in the blood serum by 5–10 times.

Most often, no treatment is required for PPD. Sometimes, in order to avoid undesirable psychological consequences, substitution therapy with small doses of sex steroids is prescribed.

2.2. Primary (hypergonadotropic) hypogonadism. It develops due to a defect at the level of the gonads.

1) Congenital primary hypogonadism (HSV) occurs in the following diseases:

intrauterine gonadal dysgenesis, can be combined with Shereshevsky-Turner syndrome (karyotype 45, XO), Klinefelter syndrome (karyotype 47, XXY);
congenital syndromes not associated with chromosomal abnormalities (20 syndromes associated with hypergonadotropic hypogonadism, such as Noonan's syndrome, etc.);
congenital anorchism (lack of testicles). A rare pathology (1 in 20,000 newborns), accounts for only 3-5% of all cases of cryptorchidism. It develops due to atrophy of the gonads in the later stages of intrauterine development, after the end of the process of sexual differentiation. The cause of anorchism is presumably trauma (torsion) of the testicles or vascular disorders. The child at birth has a male phenotype. If testicular agenesis occurs due to impaired testosterone synthesis at 9-11 weeks of gestation, the phenotype of the child at birth will be female;
true gonadal dysgenesis (female phenotype, karyotype 46, XX or 46, XY, the presence of a defective sex chromosome, as a result of which the gonads are presented in the form of rudimentary strands);
genetic disorders in the production of enzymes involved in the synthesis of sex hormones;
insensitivity to androgens due to genetic disorders of the receptor apparatus, when the gonads function normally, but the peripheral tissues do not perceive them: testicular feminization syndrome, female or male phenotype, but with hypospadias (congenital underdevelopment of the urethra, in which its external opening opens on the lower surface of the penis, on the scrotum or in the perineum) and micropenia (small penis).

2) Acquired primary hypogonadism (PPG). Causes of development: radio or chemotherapy, trauma to the gonads, surgery on the gonads, autoimmune diseases, infection of the gonads, untreated cryptorchidism in boys. Antitumor agents, especially alkylating agents and methylhydrazines, damage Leydig cells and spermatogenic cells. In prepubertal age, damage is minimal, since these cells are in a dormant state and are less sensitive to the cytotoxic effect of anticancer drugs.

In postpubertal age, these drugs can cause irreversible changes in the spermatogenic epithelium. Often, primary hypogonadism develops as a result of past viral infections (mumps virus, Coxsackie B and ECHO viruses). Gonadal function is impaired after high doses of cyclophosphamide and whole-body irradiation in preparation for bone marrow transplantation. There are such variants of PPG:

BCP without hyperandrogenization. More often it is caused by an autoimmune process in the ovaries. It is characterized by a delay in sexual development (in the case of complete testicular failure) or, with an incomplete defect, a slowdown in puberty when primary or secondary amenorrhea occurs;
PPG with hyperandrogenization. May be due to polycystic ovary syndrome (PCOS) or the presence of multiple follicular ovarian cysts. It is characterized by the presence of spontaneous puberty in girls, but is accompanied by a violation of the menstrual cycle;
multiple follicles ovaries. They can develop in girls at any age. Most often, signs of premature sexual development are not observed, cysts can spontaneously resolve.

The clinical presentation of PPG depends on the etiology of the disorder. Secondary sexual characteristics are completely absent or pubic hair is present due to the timely normal maturation of the adrenal glands, however, as a rule, it is not enough. With PCOS, acne, hirsutism, obesity, hyperinsulinism, alopecia, absence of clitoromegaly, and a history of premature pubarche are detected.

Treatment by an endocrinologist. In PCOS, hormone replacement therapy is prescribed with moderate doses of estrogens orally along with progestogens.

2.3. Secondary (hypogonadotropic) hypogonadism (VG). It develops due to a defect in the synthesis of hormones at the hypothalamic-pituitary level (FSH, LH - low). May be congenital or acquired. Causes of congenital VH:

Kallman's syndrome (isolated gonadotropin deficiency and anosmia) (see hereditary diseases);
Lynch syndrome (isolated gonadotropin deficiency, anosmia and ichthyosis);
Johnson syndrome (isolated gonadotropin deficiency, anosmia, alopecia);
Pasqualini syndrome or low LH syndrome, fertile eunuch syndrome (see hereditary diseases);
deficiency of gonadotropic hormones (FSH, LH) as part of multiple pituitary insufficiency (hypopituitarism and panhypopituitarism);
Prader-Willi syndrome (see hereditary diseases).

The most common cause of acquired VH are tumors of the hypothalamic-pituitary region (craniopharyngioma, dysgerminoma, suprasellar astrocytoma, chiasmatic glioma). VH can also be post-radiation, post-surgical, post-infectious (meningitis, encephalitis) and due to hyperprolactinemia (more often prolactinoma).

Hyperprolactinemia always leads to hypogonadism. Clinically, it is manifested in adolescent girls by amenorrhea, in boys by gynecomastia. Treatment consists of lifelong sex steroid replacement therapy, starting before age 13 in boys and before age 11 in girls.

cryptorchidism characterized by the absence of palpable testicles in the scrotum in the presence of a normal male phenotype. It occurs in 2-4% of full-term and 21% of premature boys. Normally, fetal testicular descent occurs between 7 and 9 months of gestation due to an increase in the level of placental chorionic gonadotropin (CG).

The causes of cryptorchidism are different:

deficiency of gonadotropins or testosterone in the fetus or newborn, or insufficient intake of hCG from the placenta into the blood;
testicular dysgenesis, including chromosomal abnormalities;
inflammatory processes during intrauterine development (orchitis and peritonitis of the fetus), as a result of which the testicles and spermatic cord grow together, and this prevents the testicles from descending;
autoimmune damage to gonadotropic pituitary cells;
anatomical features of the structure of the internal genital tract (narrowness of the inguinal canal, underdevelopment of the vaginal process of the peritoneum and scrotum, etc.);
cryptorchidism can be combined with congenital malformations and syndromes;
in premature babies, the testicles can descend into the scrotum during the 1st year of life, which happens in more than 99% of cases.

Treatment of cryptorchidism begins as early as possible, from 9 months of age. It begins with drug therapy with human chorionic gonadotropin. Treatment is effective in 50% for bilateral cryptorchidism and 15% for unilateral cryptorchidism. With ineffective medical treatment, surgical intervention is indicated.

Microsinging characterized by a small penis that is less than 2 cm at birth or less than 4 cm at prepubertal age. Causes of micropenia:

secondary hypogonadism (isolated or combined with other pituitary deficiencies, especially growth hormone deficiency);
primary hypogonadism (chromosomal and non-chromosomal diseases, syndromes);
incomplete form of androgen resistance (isolated micropenia or in combination with violations of sexual differentiation, manifested by indefinite genitalia);
congenital anomalies of the central nervous system (defects in the median structures of the brain and skull, septo-optic dysplasia, hypoplasia or aplasia of the pituitary gland);
idiopathic micropenia (the cause of its development has not been established).

In the treatment of micropenia, intramuscular injections of prolonged testosterone derivatives are prescribed. With partial resistance to androgens, the effectiveness of therapy is negligible. If there is no effect at all in early childhood, the problem of gender reassessment arises.

Features of sexual development, possible sexual anomalies in patients with premature sexual development and delayed sexual development are known only in general terms. Premature sexual development is usually accompanied by early onset of sexual desire, hypersexuality, early onset of sexual activity, and a high likelihood of developing sexual perversions. The delay in sexual development is most often associated with the late appearance and weakening of sexual desire up to asexuality.

V.V. Kovalev (1979) points out that among the residual-organic psychopathic disorders, a special place is occupied by psychopathic states with an accelerated rate of puberty, studied in the clinic headed by him by K.S. Lebedinsky (1969). The main manifestations of these states are increased affective excitability and a sharp increase in drives. In adolescent boys, the component of affective excitability with explosiveness and aggressiveness predominates. In a state of passion, patients can pounce with a knife, throw an object that accidentally falls under the arm at someone. Sometimes, at the height of affect, a narrowing of consciousness occurs, which makes the behavior of adolescents especially dangerous. There is an increased conflict, constant readiness to participate in quarrels and fights. Possible dysphoria with tense-malicious affect. Girls are less likely to be aggressive. Their affective outbursts have an hysteroid color, are distinguished by the grotesque, theatrical nature of their behavior (shouts, wringing of hands, gestures of despair, demonstrative suicidal attempts, etc.). Against the background of a narrowed consciousness, affective-motor seizures may occur.

In the manifestations of psychopathic states with an accelerated rate of puberty in adolescent girls, an increased sexual desire comes to the fore, sometimes acquiring an irresistible character. In this regard, all the behavior and interests of such patients are aimed at the realization of sexual desire. Girls abuse cosmetics, are constantly looking for acquaintances with men, young men, teenagers, some of them, starting from the age of 12-13, have an intense sex life, having sex with casual acquaintances, often become victims of pedophiles, people with other sexual perversions, venereal pathology .

Especially often, teenage girls with accelerated sexual development are involved in antisocial companies, they begin to joke dirty and scold, smoke, drink alcohol and drugs, and commit offenses. They are easily drawn into brothels, where they also experience sexual perversions. Their behavior is distinguished by swagger, arrogance, nakedness, lack of moral delays, cynicism. They prefer to dress in a special way: loudly caricatured, with an exaggerated representation of secondary sexual characteristics, thereby attracting the attention of a specific audience.

Some teenage girls have a tendency to make up sexual content. Most often there are slanders from classmates, teachers, acquaintances, relatives that they are subjected to sexual persecution, rape, that they are pregnant. Slanders can be so skillful, vivid and convincing that even miscarriages of justice happen, not to mention the difficult situations in which the victims of slanders find themselves. Sexual fantasies are sometimes stated in diaries, as well as in letters, often containing various threats, obscene expressions, etc., which teenage girls write to themselves, changing their handwriting, on behalf of imaginary admirers. Such letters can become a source of conflict in the school, and sometimes give rise to a criminal investigation.

Some girls with precocious puberty leave home, run away from boarding schools, wander. Usually only a few of them retain the ability to critically assess their condition and behavior and accept medical help. The prognosis in such cases may be favorable.

3) neurosis-like syndromes. They are disorders of the neurotic level of response caused by residual-organic lesions of the central nervous system and characterized by features of symptoms and dynamics that are not characteristic of neuroses (Kovalev V.V., 1979). The concept of neurosis turned out to be among the discredited for various reasons and is now used rather in a conditional sense. The same seems to be happening with the concept of "neurosis-like syndromes."

Until recently, descriptions of various neurosis-like disorders were given in Russian child psychiatry, such as neurosis-like fears (flowing like panic attacks), senestopathic-hypochondriac neurosis-like states, hysteriform disorders (Novlyanskaya K.A., 1961; Aleshko V.S., 1970 ; Kovalev V.V., 1971; and others). It was emphasized that systemic or monosymptomatic neurosis-like conditions are especially common in children and adolescents: tics, stuttering, enuresis, sleep disturbances, appetite disorders (Kovalev V.V., 1971, 1972, 1976; Buyanov M.I., Drapkin B.Z. , 1973; Gridnev S.A., 1974; and others).

It was noted that neurosis-like disorders, in comparison with neurotic ones, are more resistant, prone to protracted treatment, resistance to therapeutic measures, a weak reaction of the personality to a defect, as well as the presence of mild or moderate psycho-organic symptoms and residual neurological micro-symptoms. Pronounced psycho-organic symptoms limit the possibilities of a neurotic response, and neurosis-like symptoms in such cases are relegated to the background.

4) psychopathic syndromes. The general basis of psychopathic states associated with the consequences of early and postnatal organic brain lesions in children and adolescents, as V.V. Kovalev (1979), is a variant of the psycho-organic syndrome with a defect in the emotional-volitional properties of the personality. The latter, according to G.E. Sukhareva (1959), manifests itself in a more or less pronounced insufficiency of the highest personality traits (lack of intellectual interests, pride, a differentiated emotional attitude towards others, weakness of moral attitudes, etc.), a violation of instinctive life (disinhibition and sadistic perversion of the self-preservation instinct, increased appetite) , insufficient focus and impulsiveness of mental processes and behavior, and in young children, in addition, motor disinhibition and weakening of active attention.

Against this background, some personality traits may dominate, which makes it possible to identify certain syndromes of residual-organic psychopathic conditions. So, M.I. Lapides and A.V. Vishnevskaya (1963) distinguish 5 such syndromes: 1) organic infantilism; 2) mental instability syndrome; 3) syndrome of increased affective excitability; 4) impulsive-epileptoid syndrome; 5) a syndrome of disturbance of inclinations. Most often, according to the authors, there is a syndrome of mental instability and a syndrome of increased affective excitability.

According to G.E. Sukhareva (1974), one should speak of only 2 types of residual psychopathic states.

The first type is brakeless. It is characterized by underdevelopment of volitional activity, weakness of volitional delays, the predominance of the motive for obtaining pleasure in behavior, instability of attachments, lack of self-love, a weak reaction to punishment and censure, lack of purposefulness of mental processes, especially thinking, and, in addition, the predominance of the euphoric background of mood, carelessness , frivolity and disinhibition.

The second type is explosive. He is characterized by increased affective excitability, explosiveness of affect and at the same time stuck, prolonged nature of negative emotions. Also characteristic are the disinhibition of primitive drives (increased sexuality, voracity, a tendency to vagrancy, alertness and distrust towards adults, a tendency to dysphoria), as well as inertia of thinking.

G.E. Sukhareva draws attention to some somatic features of the two described types. In children belonging to the non-braking type, there are signs of physical infantilism. Children of the explosive type are distinguished by a dysplastic physique (they are stocky, with shortened legs, a relatively large head, an asymmetrical face, and wide, short-fingered hands).

The rough nature of behavioral disorders usually entails pronounced social maladjustment and often the inability of children to stay in preschool child care institutions and attend school (Kovalev V.V., 1979). It is advisable to transfer such children to individual education at home or to educate and educate in specialized institutions (specialized preschool sanatoriums for children with organic lesions of the central nervous system, schools at some psychiatric hospitals, etc., if any). In any case, inclusive education of such patients in a public school, as well as children with mental retardation and some other disabilities, is inappropriate.

Despite this, the long-term prognosis of residual-organic psychopathic conditions in a significant part of cases can be relatively favorable: psychopathic personality changes are partially or completely smoothed out, while acceptable social adaptation is achieved in 50% of patients (Parkhomenko A.A., 1938; Kolesova V.I. A., 1974; and others).

All living things cannot exist without taking into account the signals of the external environment. Perceives them, processes and provides interaction with the surrounding nature of the nervous system. It also coordinates the work of all systems within the body.

neurological disease

The central nervous system plays an important role in regulating human behavior. Diseases of the central nervous system today affect people of all ages.

Damage to the central nervous system is a neurological disease. Patients with disorders of the central nervous system are under the supervision of a neurologist, although diseases of any other organs may be concomitant.

Violations of the nervous system are closely intertwined with a pronounced disharmony of mental activity, which provokes changes in the positive qualities of a person's character. Damage to the central nervous system can affect the functioning of the brain and spinal cord, leading to neurological and psychiatric disorders.

Causes of CNS damage

The central nervous system can be affected as a result of the use of certain drugs, physical or emotional overload, difficult and difficult childbirth.

Damage to the central nervous system can be caused by drug use and the abuse of alcoholic beverages, which leads to a decrease in the potential of important brain centers.

CNS diseases are caused by trauma, infections, autoimmune diseases, structural defects, tumors, and stroke.

Types of CNS damage

One of the varieties of diseases of the central nervous system are neurodegenerative diseases, which are characterized by progressive dysfunction and cell death in certain areas of the nervous system. These include Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease, amyotrophic lateral sclerosis (ALS). Alzheimer's disease causes memory loss, personality changes, dementia, and eventually death. Parkinson's disease causes tremors, rigidity, and impaired movement control as a result of loss of dopamine. The most characteristic symptoms of Huntington's disease are random and uncontrolled movements.

A potential threat to the central nervous system is presented by retroviral infections, which illustrate the molecular interaction between some viral pathogens and pathological reactions resulting from this interaction.

Viral infections of the nervous system are increasing from year to year, which confirms the significant increase in global epidemics in recent years.

Disorders in the work of the central nervous system in some cases occur during fetal development or during childbirth.

With damage to the central nervous system, an imbalance occurs in all human organs, the work of which is regulated by the central nervous system.

Failure of the central nervous system in any case will lead to damage or disruption of the activity of other organs.

Organic damage to the CNS

Inadequate brain activity means that an organic lesion of the nervous system has occurred, which can be congenital or acquired. Most people develop mild lesions that do not require treatment. The presence of a moderate and severe degree of this disease requires medical intervention, as there is a violation of the central nervous system.

Signs of an organic lesion of the central nervous system are increased excitability, rapid distractibility, daytime urinary incontinence, and sleep disturbance. In some cases, the work of the organs of hearing and vision worsens, and coordination of movements is also disturbed. The human immune system suffers.

Viral infections that occur in a woman who is carrying a child, the use of various medications, smoking or drinking alcohol during pregnancy affect the functioning of the central nervous system and lead to its disruption.

Organic damage to the nervous system can be observed in both children and adults.

The central nervous system is precisely the mechanism that helps a person grow and navigate in this world. But sometimes this mechanism fails, "breaks". It is especially scary if this happens in the first minutes and days of the child's independent life or even before he is born. About why the child is affected by the central nervous system and how to help the baby, we will tell in this article.

What it is

The central nervous system is a close "bundle" of the two most important links - the brain and spinal cord. The main function that nature assigned to the central nervous system is to provide reflexes, both simple (swallowing, sucking, breathing) and complex ones. CNS, or rather, its middle and lower sections, regulate the activity of all organs and systems, provides communication between them. The highest department is the cerebral cortex. It is responsible for self-awareness and self-awareness, for the connection of a person with the world, with the reality surrounding the child.

Violations, and consequently, damage to the central nervous system, can begin even during the development of the fetus in the mother's womb, and can occur under the influence of certain factors immediately or some time after birth.

Which part of the central nervous system is affected will determine which body functions will be impaired, and the degree of damage will determine the degree of consequences.

The reasons

In children with CNS disorders, about half of all cases are intrauterine lesions, doctors call this perinatal CNS pathologies. At the same time, more than 70% of them are premature babies, which appeared earlier than the prescribed obstetric period. In this case, the main root cause lies in the immaturity of all organs and systems, including the nervous one, it is not ready for autonomous work.

Approximately 9-10% of toddlers born with lesions of the central nervous system were born on time with normal weight. The state of the nervous system, experts believe, in this case is affected by negative intrauterine factors, such as prolonged hypoxia experienced by the baby in the womb during gestation, birth trauma, as well as the state of acute oxygen starvation during difficult delivery, metabolic disorders of the child, which began even before birth, infectious diseases transferred by the expectant mother, complications of pregnancy. All lesions caused by the above factors during pregnancy or immediately after childbirth are also called residual organic:

Fetal hypoxia. Most often, babies whose mothers abuse alcohol, drugs, smoke or work in hazardous industries suffer from a lack of oxygen in the blood during pregnancy. The number of abortions that preceded these births is also of great importance, since the changes that occur in the tissues of the uterus after an abortion contribute to the disruption of uterine blood flow during a subsequent pregnancy.

traumatic causes. Birth injuries can be associated with both incorrectly chosen delivery tactics and medical errors during the birth process. Injuries also include actions that lead to a violation of the central nervous system of the child after childbirth, in the first hours after birth.
Fetal metabolic disorders. Such processes usually begin in the first - the beginning of the second trimester. They are directly related to the disruption of the functioning of the organs and systems of the baby's body under the influence of poisons, toxins, and some medications.
Maternal infections. Especially dangerous are diseases that are caused by viruses (measles, rubella, chickenpox, cytomegalovirus infection and a number of other ailments) if the disease occurs in the first trimester of pregnancy.

pathology of pregnancy. The state of the central nervous system of the child is affected by a wide variety of features of the gestation period - polyhydramnios and oligohydramnios, pregnancy with twins or triplets, placental abruption and other reasons.
Severe genetic diseases. Usually, pathologies such as Down and Evards syndromes, trisomy, and a number of others are accompanied by significant organic changes in the central nervous system.

At the current level of development of medicine, CNS pathologies become obvious to neonatologists already in the first hours after the birth of a baby. Less often - in the first weeks.

Sometimes, especially with organic lesions of mixed genesis, the true cause cannot be established, especially if it is related to the perinatal period.

Classification and symptoms

The list of possible symptoms depends on the causes, extent and extent of lesions of the brain or spinal cord, or combined lesions. Also, the outcome is affected by the time of negative impact - how long the child was exposed to factors that affected the activity and functionality of the central nervous system. It is important to quickly determine the period of the disease - acute, early recovery, late recovery or the period of residual effects.

All pathologies of the central nervous system have three degrees of severity:

Light. This degree is manifested by a slight increase or decrease in the tone of the baby's muscles, convergent strabismus may be observed.

Average. With such lesions, muscle tone is always reduced, reflexes are completely or partially absent. This condition is replaced by hypertonicity, convulsions. There are characteristic oculomotor disorders.
Heavy. Not only motor function and muscle tone suffer, but also internal organs. If the central nervous system is severely depressed, convulsions of varying intensity may begin. Problems with cardiac and renal activity can be very pronounced, as well as the development of respiratory failure. The intestines may be paralyzed. The adrenal glands do not produce the right hormones in the right amount.

According to the etiology of the cause that caused problems with the activity of the brain or spinal cord, pathologies are divided (however, very conditionally) into:

Hypoxic (ischemic, intracranial hemorrhages, combined).
Traumatic (birth trauma of the skull, birth spinal lesions, birth pathologies of peripheral nerves).
Dysmetabolic (nuclear jaundice, excess in the blood and tissues of the child of the level of calcium, magnesium, potassium).
Infectious (consequences of maternal infections, hydrocephalus, intracranial hypertension).

Clinical manifestations of different types of lesions also differ significantly from each other:

ischemic lesions. The most "harmless" disease is cerebral ischemia of the 1st degree. With it, the child demonstrates CNS disorders only in the first 7 days after birth. The reason most often lies in fetal hypoxia. The baby at this time can observe relatively mild signs of arousal or depression of the central nervous system.
The second degree of this disease is put in the event that if violations and even convulsions last more than a week after birth. We can talk about the third degree if the child has constantly increased intracranial pressure, frequent and severe convulsions are observed, and there are other autonomic disorders.

Usually this degree of cerebral ischemia tends to progress, the child's condition worsens, the baby may fall into a coma.

Hypoxic cerebral hemorrhages. If, as a result of oxygen starvation, a child has a hemorrhage into the ventricles of the brain, then at the first degree there may be no symptoms and signs at all. But already the second and third degrees of such a hemorrhage lead to severe brain damage - a convulsive syndrome, the development of shock. The child may go into a coma. If blood enters the subarachnoid cavity, then the child will be diagnosed with overexcitation of the central nervous system. There is a high probability of developing dropsy of the brain in an acute form.

Bleeding into the ground substance of the brain is not always noticeable at all. Much depends on which part of the brain is affected.

Traumatic lesions, birth trauma. If during childbirth, doctors had to use forceps on the baby's head and something went wrong, if acute hypoxia occurred, then most often this is followed by a cerebral hemorrhage. With a birth injury, the child experiences convulsions to a more or less pronounced degree, the pupil on one side (the one where the hemorrhage occurred) increases in size. The main sign of traumatic damage to the central nervous system is an increase in pressure inside the child's skull. Acute hydrocephalus may develop. The neurologist testifies that in this case the central nervous system is more often excited than suppressed. Not only the brain, but also the spinal cord can be injured. This is most often manifested by sprains and tears, hemorrhage. In children, breathing is disturbed, hypotension of all muscles, spinal shock is observed.
Dysmetabolic lesions. With such pathologies, in the overwhelming majority of cases, the child has increased blood pressure, convulsive seizures are observed, and consciousness is quite pronouncedly depressed. The cause can be established by blood tests that show either a critical calcium deficiency, or a lack of sodium, or another imbalance of other substances.

Periods

The prognosis and course of the disease depends on the period in which the baby is. There are three main periods of development of pathology:

Spicy. Violations have just begun and have not yet had time to cause serious consequences. This is usually the first month of an independent life of a child, the neonatal period. At this time, a baby with CNS lesions usually sleeps poorly and restlessly, cries often and for no apparent reason, he is excitable, can shudder without an irritant even in his sleep. Muscle tone is increased or decreased. If the degree of damage is higher than the first, then reflexes may weaken, in particular, the baby will begin to suck and swallow worse and weaker. During this period, the baby may begin to develop hydrocephalus, this will be manifested by a noticeable growth of the head and strange eye movements.

Restorative. It may be early or late. If the baby is at the age of 2-4 months, then they talk about early recovery, if he is already from 5 to 12 months, then about late. Sometimes parents notice disturbances in the work of the central nervous system in their crumbs for the first time in the early period. At 2 months, such little ones almost do not express emotions, they are not interested in bright hanging toys. In the late period, the child noticeably lags behind in his development, does not sit, does not coo, his cry is quiet and usually very monotonous, emotionally uncolored.
Effects. This period begins after the child is one year old. At this age, the doctor is able to most accurately assess the consequences of a CNS disorder in this particular case. Symptoms may disappear, however, the disease does not disappear anywhere. Most often, doctors give such children a year such verdicts as hyperactivity syndrome, developmental delay (speech, physical, mental).

The most severe diagnoses that can indicate the consequences of CNS pathologies are hydrocephalus, cerebral palsy, epilepsy.

Treatment

It is possible to talk about treatment when CNS lesions are diagnosed with maximum accuracy. Unfortunately, in modern medical practice there is a problem of overdiagnosis, in other words, every baby whose chin trembled during a month of examination, who does not eat well and sleeps restlessly, can easily be diagnosed with cerebral ischemia. If the neurologist claims that your baby has CNS lesions, you should definitely insist on a comprehensive diagnosis, which will include ultrasound of the brain (through the fontanel), computed tomography, and in special cases, an x-ray of the skull or spine.

Every diagnosis that is somehow related to CNS lesions must be diagnostically confirmed. If signs of a CNS disorder were noticed in the maternity hospital, then the timely assistance provided by neonatologists helps to minimize the severity of possible consequences. It just sounds scary - CNS damage. In fact, most of these pathologies are reversible and subject to correction if detected in time.

For treatment, drugs are usually used that improve blood flow and blood supply to the brain - a large group of nootropic drugs, vitamin therapy, anticonvulsants.

The exact list of drugs can only be called by a doctor, since this list depends on the causes, degree, period and depth of the lesion. Drug treatment for newborns and infants is usually provided in a hospital setting. After the relief of symptoms, the main stage of therapy begins, aimed at restoring the correct functioning of the central nervous system. This stage usually takes place at home, and the parents bear a great responsibility for complying with numerous medical recommendations.

Children with functional and organic disorders of the central nervous system need:

therapeutic massage, including hydromassage (procedures take place in water);
electrophoresis, exposure to magnetic fields;
Vojta therapy (a set of exercises that allow you to destroy reflex incorrect connections and create new ones - correct ones, thereby correcting movement disorders);
Physiotherapy for the development and stimulation of the development of the senses (music therapy, light therapy, color therapy).

Such exposures are allowed for children from 1 month old and should be supervised by specialists.

A little later, parents will be able to master the techniques of therapeutic massage on their own, but it is better to go to a professional for several sessions, although this is quite an expensive pleasure.

Consequences and predictions

Forecasts for the future for a child with lesions of the central nervous system can be quite favorable, provided that he is provided with prompt and timely medical care in the acute or early recovery period. This statement is true only for mild and moderate CNS lesions. In this case, the main prognosis includes a full recovery and restoration of all functions, a slight developmental delay, the subsequent development of hyperactivity or attention deficit disorder.

In severe forms, the forecasts are not so optimistic. The child may remain disabled, and deaths at an early age are not excluded. Most often, lesions of the central nervous system of this kind lead to the development of hydrocephalus, to cerebral palsy, to epileptic seizures. As a rule, some internal organs also suffer, the child has parallel chronic diseases of the kidneys, respiratory and cardiovascular systems, marbled skin.

Prevention

Prevention of pathologies from the central nervous system in a child is the task of the expectant mother. At risk - women who do not leave bad habits while carrying a baby - smoke, drink alcohol or drugs.

All pregnant women must be registered with an obstetrician-gynecologist in a antenatal clinic. During pregnancy, they will be asked to undergo so-called screening three times, which reveals the risks of having a child with genetic disorders from this particular pregnancy. Many gross pathologies of the fetal central nervous system become noticeable even during pregnancy, some problems can be corrected with drugs, for example, uteroplacental blood flow disorders, fetal hypoxia, the threat of miscarriage due to a small detachment.

A pregnant woman needs to monitor her diet, take vitamin complexes for expectant mothers, not self-medicate, and be wary of various medications that have to be taken during the period of bearing a child.

This will help to avoid metabolic disorders in the baby. You should be especially careful when choosing a maternity home (the birth certificate, which all pregnant women receive, allows you to make any choice). After all, the actions of personnel during the birth of a child play a large role in the possible risks of traumatic lesions of the central nervous system in a baby.

After the birth of a healthy baby, it is very important to visit the pediatrician regularly, protect the baby from injuries of the skull and spine, and do age-appropriate vaccinations that will protect the little one from dangerous infectious diseases, which at an early age can also lead to the development of pathologies of the central nervous system.

In the next video, you will learn about the signs of a nervous system disorder in a newborn that you can determine for yourself.