Organic brain damage: causes, symptoms, treatment. Speech restoration centers Reading strengthens neural connections

Any form of encephalopathy requires severe treatment and a responsible approach of doctors and patients to their own condition. Encephalopathy, unspecified, is a special type of diagnosis that is made when there is insufficient information to 100% confirm the exact form of the pathology.

ICD-10 defines unspecified encephalopathy as G93. Synonym: acquired unspecified encephalopathy.

The diagnosis has specific features:

  • put when it is not possible to clarify with additional research;
  • Pediatricians often find symptoms unspecified encephalopathy in newborns;
  • in 80% of cases the diagnosis is not confirmed after 2-3 years;
  • men get sick more often than women by 21%;
  • The accuracy of the diagnosis is higher if it is made at 5 or 65 years of age (peak disease identification).

An unspecified form of the disease requires additional examinations and is not confirmed in all cases. Most often, true encephalopathy is found in middle-aged and elderly people.

Classification of forms

When making a diagnosis, the signs of the disease are taken into account. At the first stage, unspecified encephalopathy is confirmed less frequently, since pathologies are not detected during examinations, while cerebral changes are already present.

The second degree of severity allows for a faster diagnosis, as patients exhibit mild and moderate symptoms diseases. At the third stage, severe neuralgic disorders are noticeable and the diagnosis is confirmed even without additional examinations.

The specificity of unspecified encephalopathy is such that depending on the type of disease (intoxication, infectious), the type of stages also changes. At acute course infectious pathology, the first degree almost immediately passes into the second or third.

Causes of the disease

Any encephalopathy - unspecified or confirmed - can be either congenital or acquired. Congenital pathology is associated with several factors. The first is prenatal, it is characterized by fetal injuries and other negative factors affecting the embryo. The second is perinatal, caused by childbirth, as well as adverse effects after birth.

Most often, these forms of encephalopathy develop as a result of:

  • trauma to the skull received during the passage of the fetus through the birth canal;
  • metabolic diseases inherited from parents;
  • developmental abnormalities nervous system and brain;
  • alcoholism, drug addiction, infectious diseases of the mother during pregnancy.

There is a more precise classification of encephalopathies, the types of which may occur in an unspecified form. This form, known as metabolic, is divided into several subtypes. They may be associated with other disorders, for example, vascular: cholesterol plaques narrow the lumen and cause metabolic disorders.

Medical researchers believe that main reason any encephalopathy is cerebral hypoxia.

Diagnosis of the disease is multi-stage, complex process, time consuming. You cannot rely on the results of one analysis, since any type of encephalopathy may hide other disorders. And pathology can never arise as an independent disease.

Development mechanism

For a more precise understanding of what unspecified encephalopathy is, you need to consider the mechanism of development:

  • Happening. It is caused by vascular spasms and other disturbances in the functioning of organs and the circulatory system.
  • Metabolic disorder. Cells don't get enough nutrients, atrophy and degeneration begin.
  • Proliferation of lesions. Demyelinated lesions, dying tissue, form in the white matter of the brain.
  • arise. At first they become small and isolated, then they grow.
  • Swelling and congestion . The formation of these signs leads to the death of large areas of the brain.

Gradually, a person loses cognitive functions, and the nervous system suffers. Advanced encephalopathy cannot be treated; dead areas of the brain are not restored.

The brain reacts very quickly to any changes, since this organ contains minimum stock oxygen. As soon as it is no longer enough, pathological processes immediately develop.

Symptoms of pathology

Encephalopathy occurs slowly, and at least 3-6 months must pass from the onset of the disease to achieve the first symptoms. However acute types are characterized by an accelerated course. At an early stage, regardless of the type of disease, certain signs are detected:

  • difficulties in performing mental activities that previously did not cause problems;
  • problems with step-by-step activities;
  • memory loss;
  • severe sleep disturbances that lead to daytime drowsiness and nighttime insomnia, the patient experiences nightmares;
  • severe fatigue even when doing familiar things that used to be enjoyable;
  • extraneous noise in the ears, dizziness, headaches that constantly bother the patient;
  • after stress, the patient feels an incredible loss of strength and emptiness;
  • the character becomes hot-tempered, the mood often changes, irritability and tearfulness appear;
  • the patient suffers from visual and hearing impairment.

On initial stages illness, the patient remains in normal health, and changes begin mainly when weather conditions change. Symptoms are influenced by stress, anxiety and mental overload.

Dysfunctions of the nervous system develop slowly, beginning with a lack of coordination and mild seizures. Constantly getting worse mental state: apathy develops, the range of interests narrows, memory, speech, and attention suffer. Dementia is the final stage of encephalopathy.

Each type of encephalopathy, which may initially have been unspecified, develops its own symptoms.

Vascular form

Develops in older people due to problems with blood vessels, less common in adults 30-50 years old. The vessels of the neck, head, and upper half of the body suffer. At stage 2, it manifests itself with pronounced neurological symptoms: shuffling, instability, tremors, urination problems, disorientation.

Appears in at different ages due to injuries, accompanied severe nausea and headaches, as well as severe fatigue. Medicines only provide temporary relief. Attacks of falling, convulsions, asthenia, as well as problems with mental activity are possible.

Hypertensive form

Appears during a hypertensive crisis or from constant exposure high pressure. Characterized by unclear speech, muscle weakness, and marked slowness in movement. Patients may experience headaches and deteriorating swallowing functions.

Venous form

The predominant symptoms are those affecting memory and intelligence, as well as thought processes. In the hot season, chills may occur with venous encephalopathy. The patient is bothered by a cough and heaviness in the head. Facial puffiness and pallor may appear.

Toxic form

Unspecified encephalopathy of the toxic type is characterized by convulsions, a feeling of stupor, problems with breathing and circulation. Nausea, weakness and pressure changes, combined with difficulty controlling urination or bowel movements, can be chronic.

Severe poisoning in almost all cases is accompanied by loss of consciousness, hallucinations, and delirium. At neglected form The disease often results in death.

Alcohol form

Included in the group of intoxication encephalopathy, accompanied by delirium tremens (delusions and hallucinations). If the disease is chronic, then after a few months constant use Alcohol causes tremors, weakness, anxiety, depression and personality collapse.

Leukoencephalopathy

A form of illness that causes nausea severe pain in the head, a person suffers from hallucinations, phobias and obsessive fears. All brain functions are inhibited.

Occurs with attacks of confused consciousness. The person becomes slow and has difficulty with processes such as speaking and performing everyday activities. Over time, drowsiness and hallucinations develop, and the patient falls into a coma.

Acute encephalopathy

Rarely occurs in an unspecified form. Severe and extensive brain damage appears, which means its rapid death after a stroke or edema. Symptoms of the acute form overlap with other diseases and do not allow an accurate diagnosis to be made without additional research.

The diagnosis of unspecified encephalopathy is most often made in infants under 6 months of age. However, it can only be confirmed after tests.

In a child, the disease occurs in 3 degrees:

Lightweight. Crying, excitability and constant anxiety appear. Sleep deteriorates, stress levels increase, appetite decreases, and vomiting attacks become more frequent. Muscle tone changes significantly, sometimes strabismus develops.

Average. The functioning of the nervous system worsens: blood pressure rises, convulsions and hydrocephalus appear. The child’s skin becomes marbled, the eyes become slightly closed, as in “setting sun” syndrome. The child almost always presses his arms and legs to his body. Constant crying and insomnia develop.

Heavy. There is a complete suppression of brain functions, consciousness is impaired. The baby falls into a coma. In most cases, death occurs.

Childhood encephalopathy often leads to complications. In adults they also develop in 80% of cases.

Forecast

If a person has survived encephalopathy, and therapy was provided on time, then the risk of complications is minimal. Here are the most common consequences of the disease: paralysis and paresis, convulsions, strabismus, metabolic disorders, overweight, —epilepsy—.

In severe forms, movement problems almost always develop, epilepsy occurs, mental disorders. The patient is given .

The worst consequences are toxic; they are almost never unspecified. Treatment of the disease is complicated by the fact that the symptoms of all its forms are almost the same, and even modern diagnostic methods do not allow us to accurately determine the cause of the pathology.

Unspecified encephalopathy is not a disease, but a diagnosis that precedes a detailed study of the patient to make a more accurate verdict. In order to notice the disease in time and prevent its development, you need to undergo a full medical examination at the first signs and get an opinion from several doctors.

There are many well-known brain diseases that probably everyone has heard of. For example, multiple sclerosis, stroke or encephalitis, but such a concept as organic brain damage often leads to a stupor. This term is not spelled out in the international classification of diseases, but many diagnoses associated with brain damage begin with these words. What is it, what are the symptoms of the pathology and its causes?

Organic brain damage is not a separate disease, but an irreversible process in the brain tissue that began due to the development of one of the diseases of this organ. In fact, organic changes in the brain structure are the result of damage, infection or inflammatory process in the brain.

What are the reasons?

Organic lesions can be congenital or acquired, and the cause of their occurrence depends on this. In the case of innate “organics” of the brain, the reasons for this process may be the following factors:

  • premature placental abruption;
  • infectious diseases of pregnant women;
  • taking alcohol, drugs or smoking by the expectant mother;
  • fetal hypoxia;
  • difficult birth, possible injuries fetal head during them;
  • uterine atony;
  • taking illegal medications during pregnancy;
  • genetic damage, etc.

Acquired organic changes in the brain can occur for a number of other reasons, including:

  • traumatic brain injuries (bruise or concussion, skull fracture, etc.);
  • vascular pathologies: atherosclerosis, strokes, encephalopathy;
  • persistent circulatory disorders in the brain;
  • infectious pathologies: meningitis, encephalitis, abscess;
  • intoxication narcotic substances or alcohol;
  • Parkinson's disease, Alzheimer's disease;
  • brain tumors;
  • damage to the nervous system by the herpes virus;
  • vasculitis, etc.

The severity of the pathology

The peculiarity of organic lesions is that their appearance is not accompanied by bright severe symptoms. The clinical picture increases gradually, so many patients may not even be aware that they have a similar problem.

So, if we talk about perinatal period, when a child’s organics are congenital, its symptoms may occur in preschool age or even at school. Most often, the disease is accompanied by a general developmental delay, including speech, memory and perception.

Organic brain damage is conventionally divided into three degrees, depending on the severity and globality of the pathological process. There are three degrees:

  • the first one, she mild degree. In this case, no more than 20% of the brain tissue is affected. As a rule, such changes do not have much effect on everyday life and may remain undetected;
  • second degree - average. Brain destruction reaches from 20 to 50%, in in this case expressed neurological symptoms and treatment of the patient is required;
  • third degree - severe. Damage reaches 70%, the destruction process becomes uncontrollable. The clinical picture of psycho-neurological disorders is clearly expressed, drug treatment is aimed at maintaining human life, but is not able to stop this process.

Clinical picture

Since organic lesions are consequences of individual pathologies of the brain and central nervous system, the clinical picture can be widely varied. It is difficult to say exactly how the disease will manifest itself in a particular case, but we can distinguish the main groups of symptoms, for example:

  • focal lesions. This group includes all musculoskeletal disorders, for example, paresis or paralysis of the limbs, vegetative-trophic disorders, atrophy of the visual or facial nerve, which is accompanied by strabismus, loss of vision or distortion of the face;
  • cerebral symptoms. Most often it forms as a consequence of previous infectious diseases brain, tumor or cyst growth. These symptoms include: severe headaches, vomiting not associated with food intake, fainting, dizziness, high inside cranial pressure, development of hydrocephalus, the latter mainly in children;
  • mental disorders. Reduced intelligence, even dementia, memory loss, partial or complete amnesia.

If we consider the symptoms separately for each disease, they will be different and the rate of increase in such symptoms will also be different. For example, in the case of a stroke, when blood circulation in the brain is disrupted due to a rupture or blockage of a vessel, the symptoms of the lesion appear immediately and after the consequences of the stroke are eliminated, organic changes still remain. Often this is a violation of diction, paralysis of the limbs on one side, memory impairment, etc.

Diagnostics

Most popular in recent years Diagnostic methods are studies using neuroimaging. For example, MRI or agnography with contrast. These instrumental methods I help to examine in detail the state of brain structures. MRI allows you to see the presence of:

  • aneurysm;
  • tumors;
  • cysts;
  • determine the extent of the damage, for example, after hemorrhage.

Thanks to agnography with contrast, the condition of the blood vessels can be assessed. See places where the walls of blood vessels are narrowed or blocked, as well as places where there are ruptures, etc.

Besides instrumental studies conduct additional tests to determine cognitive impairments, such as memory impairment, concentration, speech, etc.

Treatment

Treatment for brain disorders has never been simple. This is a whole complex of various measures aimed at inhibiting the processes of destruction and suppressing the symptoms that arise. It is not the organic brain damage itself that is treated, but the pathology that preceded it. In many cases, if treatment is started in time, it is entirely possible to avoid organic damage. Of course, in some cases they are inevitable even with timely treatment, for example, with a major stroke they will be observed in any case pathological changes. They can be expressed both in disturbances of speech, memory or attention, and in motor activity, often in unilateral paralysis.

In this case, treatment is necessary in any case. Since only correctly selected drug treatment, as well as physiotherapeutic procedures, will help partially make the patient’s life easier and reduce the risk of relapse.

Since organic disorders are irreversible, it is unfortunately not possible to get rid of them completely; treatment in this case is palliative and lifelong.

Regarding the drugs necessary for treatment, they are prescribed individually, depending on the disease suffered and its consequences. Self-treatment in this case is strictly contraindicated and can lead to a deterioration in the patient’s well-being.

Organic brain damage, once started, cannot be stopped. It's slowly progressive pathological process, leading to degenerative changes in the structure of the brain. The main goal of therapy is to slow down this process as much as possible and reduce clinical manifestations that prevent a person from living a full life. Organic changes in the brain require lifelong systematic therapy.

Reading strengthens neural connections:

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Antonov P.V., Ph.D. honey. sciences,
Head of the Pathology Department
children's infectious diseases hospital No. 5 named after N.F. Filatova,
Saint Petersburg.

The diagnosis of organic brain damage (OBD) in children is very common occurrence V pediatric practice. It is easier to diagnose a child with severe neurological pathology than to understand the nature of the disease. However, experience shows that a carefully collected anamnesis, data from objective examination methods, as well as the results of an assessment of laboratory and instrumental studies allow both the pediatrician and the pathologist (in the event of the patient’s death) to clarify a lot in the diagnosis.

OPM is a broad concept for which there is no established definition. It is a consequence of pre- and perinatal pathology with the exception of genetic diseases and birth defects development. Acquired infectious and non-communicable diseases, in particular, traumatic brain injury, neuroinfections (meningoencephalitis), hypoxic conditions, the assessment of which is not the purpose of this article.

Practical experience shows that the diagnosis of APM is overused. On the one hand, this is explained by the insufficient level of methodological capabilities, on the other hand, by the abundance of diseases that lead to APM, and on the third, by the reluctance of some clinicians involved in the treatment of intercurrent diseases in such children to delve into neurological pathology.

Since WMD is not included in International Classification Diseases X revision (ICD X), for its encryption they use the faceless formulations “encephalopathy, unspecified” G93.4 or “brain lesion, unspecified” G93.9. The ICD also includes asphyxia (in relation to the perinatal period), P20-21, birth trauma, P10-11, and various intracranial hemorrhages, P52, and nosological units are not provided to indicate the consequences of these conditions.

Let us list the main, most common diseases in the practice of pediatricians, which can be formulated in terms of ICD X as independent diagnoses:

  • congenital malformations of the brain, Q00-07,
  • thesaurismosis with damage to the central nervous system, E70-83,
  • intrauterine infections (toxoplasmosis, cytomegaly, tuberculosis, and others), A50, P35, P37, P39,
  • children's cerebral palsy (CP), G80,
  • hydrocephalus, G91.
The main factors in making a diagnosis are: the mother’s medical history, the course of pregnancy and childbirth, the condition of the placenta, the results of laboratory research, dynamics clinical symptoms in a child, the topic of brain damage and, in the event of the child’s death, the morphological picture of changes not only in the brain, but also internal organs. This information helps to carry out differential diagnosis with others neurological diseases and determine the leading and secondary etiological factors diseases.

Most significant reasons APM in children are the following:

  1. Asphyxia. To ascertain it, a thorough history taking from the mother is necessary (decompensated heart defects, severe, chronic lung diseases, pregnant women), as well as the course of labor, objective clinical data.
  2. Intracranial birth injury. The main thing to pay attention to is the discrepancy between the size of the fetus and birth canal, a long anhydrous period, a protracted or rapid progress of the birth act.
  3. Intracranial hemorrhages intra- and postnatal, primarily cerebral, intraventricular, subarachnoid. Such hemorrhages, as a rule, are associated with birth trauma or asphyxia during childbirth, but they directly lead to APM.
  4. Intrauterine infections affecting the central nervous system. In this regard, infectious (acute and chronic) diseases of the mother both before and during pregnancy are important, despite the fact that there is often no direct relationship between the severity of the disease of the pregnant woman and the fetus; prenatal fetus, prematurity, chronic placental. The range of pathogens is very wide: protozoa, fungi, bacteria, mycoplasma, ureaplasma, chlamydia and, finally, numerous viruses (simple a viruses, respiratory viruses, enteroviruses, rubella virus, human immunodeficiency virus and others). Some of them can penetrate the central nervous system antenatally, some intranatally and postnatally.
  5. Hemolytic disease of newborns, accompanied by “kernicterus”.
  6. Toxic effects on the fetus during pregnancy.
  7. Mixed etiology, which is most often observed because pathological conditions, characteristic of the perinatal period, are usually closely interrelated.
Let us briefly present the clinical data that can be detected during APM, noting that given the diversity of the clinic, it is still possible to identify individual syndromes:
  1. Cerebral palsy syndromes: spastic diplegia, double hemiplegia, hyperkinetic form, atonic-astatic form, hemiplegia.
  2. Convulsive syndrome. With asphyxia in newborns, tonic and tonic-clonic convulsions are most often observed. With intracranial hemorrhage they are focal in nature. Their duration is usually short. They occur immediately (1-3 minutes) or shortly after birth. After an acute period of asphyxia, convulsions may stop and resume at the age of 1.5 - 2 months due to the onset of morphological changes in the brain. In traumatic brain injury, seizures are often partial in nature: face, limb, or hemitype; also more often, convulsions appear after a few hours or even 2-3 days due to an increase in hemorrhagic syndrome; further after a light interval from 2 months to several years convulsive syndrome may appear again. At kernicterus tonic convulsions with transition to opisthotonus. With intrauterine infectious lesions of the brain, seizures can occur different character and occur, as a rule, after a light interval of several days after birth.
  3. Mental retardation varying degrees(lag in psychomotor development), speech disorders and disorders of simple and/or complex sensitivity may arise in connection with all of the above etiological factors.
  4. Secondary - a decrease in the size of the skull begins after the birth of a child; the skull can be symmetrical or asymmetrical.
  5. Occlusal.
  6. Minimal syndrome cerebral dysfunction- may begin in children infancy, and the most striking manifestations are observed in schoolchildren; fundamentally characterized by moderately expressed motor, speech and autonomic disorders.
The pathological picture (in case of death of a child) also makes it possible to carry out differential diagnosis in such situations and often clarify the nature of the suffering. In case of severe asphyxia in the perinatal period, as a rule, the so-called hypoxic-ischemic asphyxia occurs. It has several options.
  1. With prolonged, gradually developing hypoxia, generalized and cortical necrosis occurs with damage to the cortex cerebral hemispheres brain and cerebellum. The cells of the 3rd, 5th and 6th layers of the cortex and Purkinje cells are the most vulnerable; necrosis of the brainstem nuclei often develops. Clinically - mental retardation, cerebral,.
  2. Periventricular leukomalacia - multiple small foci of necrosis in the periventricular white matter. Clinically - spastic diplegia.
  3. Damage to the border arterial zone - the parietal-occipital region - often results in hemorrhagic infarction. The clinic correlates with the affected area.
  4. Defeat zones arterial blood supply manifests itself as necrosis in areas of vascularization of the main cerebral arteries. False porencephaly develops; with multiple necrotic cavities, the term multicystic encephalomalacia is used.
The consequences of the described processes are false cysts of the corresponding localizations, as well as foci of gliosis and glial scars. Moreover, asphyxia is characterized by multiple cysts.

Traumatic brain birth injury is manifested primarily by hemorrhages of various locations in the central nervous system. The outcome of hemorrhages in the brain is resorption with the formation of cysts, in the wall of which siderophages can be found,

Encephalopathy is a non-inflammatory diffuse brain injury that results in death nerve cells under the influence various factors: cessation of blood flow, lack of oxygen, disease.

The disease is diagnosed by the location and severity of the lesion, its location in the white or gray matter, degree of blood flow disturbance.

In cases where the cause cannot be established, they speak of unspecified (idiopathic) encephalopathy.

The most common is vascular encephalopathy.

Encephalopathy can be congenital or acquired. The first is divided into prenatal (when a damaging factor acts on the fetus before it is born) and perinatal (the cause of the baby’s illness lies in last weeks before or after birth) and may be caused by:

  • abnormal brain development;
  • metabolic diseases caused by genetics;
  • damaging effects during pregnancy;
  • birth trauma of the skull.

A type of congenital encephalopathy is mitochondrial - the result of pathology of the cellular organelles of mitochondria.

Acquired occurs when various injuries and is divided into several types.

Table. Classification of acquired encephalopathy

Type of disease Cause
post-traumaticdystrophic, cicatricial, atrophic changes nerve tissue due to traumatic brain injury
toxicsystematic ingestion of toxins: alcohol, heavy metals, solvents, bacterial waste products, hypovitaminosis
radialionizing radiation for radiation sickness
metabolicmetabolic disorders in diseases of internal organs - liver, pancreas, kidneys
vascularpoor blood supply to the brain due to hypertension, atherosclerosis, impaired venous outflow, vascular diseases brain, etc.
hypoglycemica strong decrease in blood glucose levels, the main nutrient component of the brain, which leads to the destruction of cellular proteins and fats

This is far from full list encephalopathies.

Thus, as a result of traumatic exposure in the womb, infection or other reasons, older children are diagnosed with residual encephalopathy. A special case of vascular encephalopathy is venous (dyscirculatory), in which venous blood stagnates in the brain due to a violation of its outflow.

Metabolic encephalopathy is divided into several separate diseases:

  • bilirubin encephalopathy develops against the background of jaundice and poisons the body with the liver pigment bilirubin;
  • Wernicke encephalopathy is a consequence of vitamin B deficiency;
  • small focal progressive leukoencephalopathy appears after an infection due to weakened immunity;
  • atherosclerotic is caused by oxygen starvation of blood vessels due to the deposition of cholesterol plaques on them.

Scientists tend to consider the cause of any encephalopathy to be brain hypoxia ( oxygen starvation). This occurs due to deterioration in blood flow to the organ, excessive venous filling, edema, hemorrhage, and the action of external and internal toxic substances.

Hypoxic (anoxic) encephalopathy occurs when there is a low supply of nutrients to neurons (for example, due to low pressure) and is classified as a separate disease.

Metabolic encephalopathy – special case toxic: with it, toxins are not eliminated and enter the blood.

Symptoms

Clinical manifestations of the disease are varied and depend on the type, severity, treatment used, and age.

On early stages there is sleep disturbance, daytime sleepiness, lethargy, tearfulness, absent-mindedness, fatigue, lack of interest and initiative, decreased memory (usually for recent events), mental abilities, verbosity.

Possible pain, noise or ringing in the head, mood changes, decreased vision and hearing, irritability, and loss of coordination.

These symptoms progress, and in advanced cases appear neurological syndromes: parkinsonism (trembling of the limbs combined with slow movements) and falsebulbar palsy (impaired speech, chewing and swallowing).

Possible violation mental functions(depression, death wish, phobias). Trauma is characterized by cranial pressure compressing the brain.

Senile dementia is caused by leukoencephalopathy of vascular origin - a disease in which the interaction between neurons is disrupted due to the destruction of their membranes due to poor nutrition brain

Epidemiology

The disease is more often diagnosed in middle-aged and elderly people. It occurs at any time of the year, individual species encephalopathies (toxic, infectious) are observed during the cold season.

Infectious encephalopathy occurs under the influence of various pathogens (rubella, tetanus, HIV, mad cow disease). In the latter case, the disease is most severe and is called spongiform encephalopathy.

Diagnostics

To establish the form of the disease, the doctor carefully analyzes the medical history: whether the patient has had concussions, intoxication, any pathologies (atherosclerosis, hypertension, liver, kidney, pancreas, lung diseases), genetic or acquired metabolic disorders, whether he has been exposed to radiation.

Diagnostics includes the following procedures:

  • biochemical urine analysis;
  • biochemical blood test;
  • biochemical analysis of cerebral fluid;
  • nuclear magnetic tomography;
  • echography in newborns and children.

Encephalopathy in pregnant women is not a pathology. The condition is associated with hormonal changes.

Treatment

The fight against the disease is aimed at eliminating the symptoms and causes that gave impetus to the development of encephalopathy. Medicinal and conservative methods are used for therapy.

In the acute form, doctors reduce cranial pressure, eliminate convulsions, and use methods that support life processes: artificial ventilation, hemodialysis, and the administration of nutrients through a dropper bypassing the stomach.

Then the patient is prescribed medications that he takes for 1-3 months:

  • lipotropic drugs - normalize the metabolism of fats and cholesterol (Lipostabil, dietary supplements with carnitine, methionine, choline, lecithin);
  • angioprotectors - prescribed for heart disease, normalize the walls of blood vessels, improve movement and outflow venous blood(Detralex, Troxerutin, Indovazin, Cavinton);
  • medications against blood clots (Aspirin, Ginkgo Biloba, Cardiomagnyl);
  • neuroprotectors – nourish nervous tissue (Piracetam, B vitamins);
  • sedatives and tranquilizers - reduce rapid nerve impulses in affected neurons (Sibazon);
  • amino acids, vitamins;
  • performance stimulants.

For speedy rehabilitation, the patient is prescribed physiotherapeutic procedures, gymnastics, acupuncture, massage, walks, and a certain daily and rest regimen.

Epileptic encephalopathy, which occurs in young children with an EEG pattern characteristic of epilepsy, stands apart. This only indicates a predisposition to epilepsy, which does not exclude its development in the future. The cause is a violation of brain formation.

Prognosis and complications

Characteristic of any encephalopathy headache, nausea, vomiting, dizziness.

In the case of severe damage or swelling of the brain, a serious violation of microcirculation, encephalopathy develops acutely, severe headache appears, especially in the back of the head, dizziness, restlessness, anxiety, blurred vision, staggering, and possible numbness of the ends of the fingers, nose, lips, tongue. Subsequently, anxiety replaces lethargy and clouding of consciousness.

In the acute form of hepatic, pancreatic and renal encephalopathy, disturbances of consciousness and convulsive seizures are common.

For encephalopathy caused by pneumonia (including exacerbation chronic form), heart attack, pulmonary embolism, eye movements not controlled by consciousness, decreased muscle strength, and mental disorders are observed.

Among the typical complications of all encephalopathies are:

  • convulsions;
  • paralysis;
  • to whom.
If you follow the doctor's recommendations, the prognosis is favorable.

Advanced cases of the disease threaten:

  • epilepsy;
  • paralysis, movement disorders;
  • loss of brain functions, intelligence, memory;
  • emotional instability, mood swings, depression;
  • disability.

It is most difficult and has worst consequences toxic encephalopathy.

Due to the fact that one type of disease contains many special cases that are classified as a separate type, the symptoms of different encephalopathies are similar and it is often impossible to establish the cause of the disease. Tricky enemy is fraught with life-threatening complications and requires constant monitoring by a specialist and long-term rehabilitation.

Video on the topic

Organic brain damage


The diagnosis of organic brain damage (OBD) in children is a very common occurrence in pediatric practice. It is easier to diagnose a child with severe neurological pathology than to understand the nature of the disease. However, experience shows that a carefully collected anamnesis, data from objective examination methods, as well as the results of an assessment of laboratory and instrumental studies make it possible to clarify quite a lot in the diagnosis for both the pediatrician and the pathologist (in the event of the patient’s death).

OPM is a broad concept for which there is no established definition. It is a consequence of pre- and perinatal pathology, with the exception of genetic diseases and congenital malformations. Acquired infectious and non-infectious diseases, in particular, traumatic brain injury, neuroinfections (meningoencephalitis), and hypoxic conditions, the assessment of which is not the purpose of this article, can lead to such manifestations of APM. Practical experience shows that the diagnosis of APM is overused. On the one hand, this is explained by the insufficient level of methodological capabilities, on the other hand, by the abundance of diseases that lead to APM, and on the third, by the reluctance of some clinicians involved in the treatment of intercurrent diseases in such children to delve into neurological pathology.

Since WMD is not included in the International Classification of Diseases, X Revision (ICD X), the faceless formulations “encephalopathy, unspecified” G93.4 or “brain lesion, unspecified” G93.9 are used to encrypt it. The ICD also contains asphyxia (in relation to the perinatal period), P20-21, birth trauma, P10-11, and various intracranial hemorrhages, P52, and nosological units are not provided to indicate the consequences of these conditions. Let us list the main, most common diseases in the practice of pediatricians, which can be formulated in terms of ICD X as independent diagnoses:

  • congenital malformations of the brain, Q00-07,
  • thesaurismosis with damage to the central nervous system, E70-83,
  • intrauterine infections (toxoplasmosis, cytomegaly, tuberculosis, syphilis and others), A50, P35, P37, P39,
  • children's cerebral palsy(cerebral palsy), G80,
  • hydrocephalus, G91.

The main factors in making a diagnosis are: the mother’s medical history, the course of pregnancy and childbirth, the condition of the placenta, the results of laboratory tests, the dynamics of the child’s clinical symptoms, the topic of brain damage and, in the event of the child’s death, the morphological picture of changes not only in the brain, but also in the internal organs. This information helps to make a differential diagnosis with other neurological diseases and determine the leading and secondary etiological factors of the disease.

The most significant causes of APM in children are the following:

  1. Asphyxia. To ascertain it, a thorough history taking from the mother is necessary (decompensated heart defects, hypertension, severe anemia, chronic diseases lungs, diabetes mellitus, toxicosis of pregnant women), as well as the course of labor, objective clinical data.
  2. Intracranial birth injury. The main thing you need to pay attention to is the discrepancy between the size of the fetus and the birth canal, a long anhydrous period, a protracted or rapid progress of the birth act.
  3. Intracranial hemorrhages intra- and postnatal, primarily cerebral, intraventricular, subarachnoid. Such hemorrhages, as a rule, are associated with birth trauma or asphyxia during childbirth, but they directly lead to APM.
  4. Intrauterine infections affecting the central nervous system. In this regard, infectious (acute and chronic) diseases of the mother are important both before and during pregnancy, despite the fact that there is often no direct relationship between the severity of the disease of the pregnant woman and the fetus; prenatal fetal hypotrophy, prematurity, chronic placental insufficiency. The range of pathogens is very wide: protozoa, fungi, bacteria, mycoplasma, ureaplasma, chlamydia and, finally, numerous viruses (viruses herpes simplex, respiratory viruses, enteroviruses, rubella virus, human immunodeficiency virus and others). Some of them can penetrate the central nervous system antenatally, some intranatally and postnatally.
  5. Hemolytic disease of newborns, accompanied by “kernicterus”.
  6. Toxic effects on the fetus during pregnancy.
  7. Mixed etiology, which is observed most often, since the pathological conditions characteristic of the perinatal period are usually closely interrelated. Let us briefly present the clinical data that can be detected during APM, noting that with the diversity of the clinic, it is still possible to distinguish individual syndromes:
    1. Cerebral palsy syndromes: spastic diplegia, double hemiplegia, hyperkinetic form, atonic-astatic form, hemiplegia.
    2. Convulsive syndrome. With asphyxia in newborns, tonic and tonic-clonic convulsions are most often observed. With intracranial hemorrhage they are focal in nature. Their duration is usually short. They occur immediately (1-3 minutes) or shortly after birth. After an acute period of asphyxia, convulsions may stop and resume at the age of 1.5 - 2 months due to morphological changes in the brain. In traumatic brain injury, seizures are often partial in nature: face, limb, or hemitype; Also, more often, convulsions appear after a few hours or even 2-3 days due to the increase in hemorrhagic syndrome; then, after a light interval of 2 months to several years, the convulsive syndrome may appear again. With kernicterus, tonic convulsions transition to opisthotonus. With intrauterine infectious lesions of the brain, seizures can be of a different nature and usually occur after a light interval of several days after birth.
    3. Oligophrenia of varying degrees (lag in psychomotor development), speech disorders and disorders of simple and/or complex sensitivity can arise in connection with all of these etiological factors.
    4. Secondary microcephaly - a decrease in the size of the skull begins after the birth of a child; the skull can be symmetrical or asymmetrical.
    5. Occlusive hydrocephalus.
    6. Minimal cerebral dysfunction syndrome - can begin in infants, and the most striking manifestations are observed in schoolchildren; fundamentally characterized by moderately expressed motor, speech and autonomic disorders.

The pathological picture (in the case of the death of a child) also makes it possible to carry out differential diagnosis in such situations and often clarify the nature of the suffering. With severe asphyxia in the perinatal period, as a rule, so-called hypoxic-ischemic encephalopathy occurs. It has several options.

    1. With prolonged, gradually developing hypoxia, generalized and cortical necrosis occurs with damage to the cerebral cortex and cerebellum. The cells of the 3rd, 5th and 6th layers of the cortex and Purkinje cells are the most vulnerable; necrosis of the brain stem nuclei often develops. Clinically - mental retardation, cerebral palsy, epilepsy.
    2. Periventricular leukomalacia - multiple small foci of necrosis in the periventricular white matter. Clinically - spastic diplegia.
    3. Damage to the border arterial zone results in ischemia of the parietal-occipital region, and hemorrhagic infarction often develops. The clinic correlates with the affected area.
    4. Damage to areas of arterial blood supply is manifested by necrosis in areas of vascularization of the main cerebral arteries. False porencephaly develops; with multiple necrotic cavities, the term multicystic encephalomalacia is used.

The consequences of the described processes are false cysts of the corresponding localizations, as well as foci of gliosis and glial scars. Moreover, asphyxia is characterized by multiple cysts. Traumatic birth injury is manifested primarily by hemorrhages of various locations in the central nervous system. The outcome of hemorrhages in the brain is resorption with the formation of cysts, in the wall of which siderophages and hemosiderin can be found.

With the consequences of kernicterus, degeneration and necrosis of neurons occurs, as well as focal gliosis in the subthalamic nuclei, cornu ammonis, globus pallidus, inferior olive, dentate nucleus of the cerebellum. Often the described changes in the non-infectious etiology of APM are accompanied by secondary changes. These include:

  • secondary microcephaly, which differs from congenital by a relatively uniform decrease in the size of the skull;
  • occlusive hydrocephalus due to proliferation of glial elements, blockage by organized blood clots, inflammatory detritus;
  • secondary microgyria due to the collapse of nervous tissue after necrotic changes, it is usually expressed unevenly and asymmetrically.
  • histologically, foci of neuron loss, disturbance of the architecture of the cortex, bodies of dead neurons.

In the absence of an infectious factor, these changes, except for hydrocephalus, do not progress after formation. I would like to once again emphasize that the described processes can be combined in different combinations and do not always correspond to the severity of asphyxia or birth trauma.

From a practical point of view, OPM brings together large number diseases and syndromes that have their own etiology and require special therapeutic approaches. The diagnosis of APM is not nosological and should be made only in cases where it is not possible to determine its nature using available methods.