Organic brain damage mcb 10. Organic, including symptomatic, mental disorders (f00-f09)

This block includes a number of mental disorders grouped together on the basis of the presence of clear etiological factors, namely, the cause of these disorders was brain disease, brain injury or stroke, leading to cerebral dysfunction. Dysfunction can be primary (as in diseases, brain injuries and strokes that directly or selectively affect the brain) and secondary (as in systemic diseases or disorders when the brain is involved in the pathological process along with other organs and systems)

Dementia [dementia] (F00-F03) is a syndrome caused by damage to the brain (usually chronic or progressive) in which many higher cortical functions are impaired, including memory, thinking, orientation, understanding, counting, learning ability, speech and judgment . Consciousness is not obscured. Cognitive decline is usually accompanied, and sometimes preceded, by deterioration in control of emotions, social behavior, or motivation. This syndrome is noted in Alzheimer's disease, in cerebrovascular diseases, and in other conditions that primarily or secondarily affect the brain.

If necessary, an additional code is used to identify the underlying disease.

Alzheimer's disease is a primary degenerative brain disease of unknown etiology with characteristic neuropathological and neurochemical manifestations. The disease usually begins insidiously and slowly, but progresses steadily over several years.

Vascular dementia is the result of cerebral infarction due to cerebrovascular disease, including cerebrovascular disease in hypertension. Heart attacks are usually small, but their cumulative effect is manifested. The disease usually begins at a late age.

Includes: atherosclerotic dementia

Cases of dementia associated (or suspected to be associated) with causes other than Alzheimer's disease or cerebrovascular disease. The disease can begin at any age, but less often in old age.

Dementia, unspecified

Presenile(th):

• dementia NOS
• psychosis NOS

Primary degenerative dementia NOS

Senile:

• dementia:
  • NOS
  • depressive or paranoid type
• psychosis NOS

If necessary, indicate senile dementia with delirium or acute confusion, use an additional code.

last modified: January 2017

Organic amnestic syndrome not caused by alcohol or other psychoactive substances

A syndrome characterized by a pronounced deterioration in memory for recent and distant events, with the ability to retain immediate memories, a decrease in the ability to study new material and disorientation in time. Confabulations may be a characteristic feature, but perception and other cognitive functions, including intelligence, are usually preserved. The prognosis depends on the course of the underlying disease.

Korsakov's psychosis, or syndrome, non-alcoholic

Excluded:

• amnesia:
  • anterograde (R41.1)
  • dissociative (F44.0)
  • retrograde (R41.2)
• korsakoff's syndrome
  • alcoholic or unspecified (F10.6)
  • caused by the use of other psychoactive substances (F11-F19 with a common fourth character.6)

Ecologically non-specific organic cerebral syndrome, characterized by a simultaneous violation of consciousness and attention, perception, thinking, memory, psychomotor behavior, emotions, cyclical sleep and wakefulness. The duration of the condition varies, and the severity ranges from moderate to very severe.

Included: acute or subacute(s):

• brain syndrome
• a state of confusion (non-alcoholic etiology)
• infectious psychosis
• organic reaction
• psychoorganic syndrome

Excludes: delirium tremens, alcoholic or unspecified (

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170

The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.

With amendments and additions by WHO.

Processing and translation of changes © mkb-10.com

Organic damage to the brain and the entire central nervous system: from myths to reality

1. Place of pathology in the ICD 2. What is APCNS? 3. Types of organic lesions 4. What cannot cause APCNS? 5. Clinic 6. Diagnosis 7. Treatment 8. Consequences

The main feature of our time is an accessible information space in which everyone can contribute. Medical sites on the Internet are often created by people who have little to do with medicine. And, when it comes to specific diagnoses, for example, diabetes mellitus or thrombophlebitis, useful knowledge can be gleaned from the article.

But when, on request, search engines try to find a problem or something indefinite, then often there is not enough knowledge and confusion begins. This fully applies to such a topic as organic brain damage.

If you take a serious reference book on neurology and try to find such a diagnosis as an organic lesion of the central nervous system (that is, the brain and spinal cord), you won't find it. What is it? A transient disease or a more complex disorder leading to irreversible changes in the structure of the central nervous system in adults and children? Or is it a whole group of diseases? There are many questions, we will try to start from the position of official medicine.

Place of pathology in the ICD

Each case of any disease, both a functional disorder and a life-threatening condition, must be submitted medical statistics, and encrypted, having received the ICD code - 10 (International Classification of Diseases).

Does the ICD provide a place for the "organics" of the central nervous system? By the way, doctors often abbreviate this name to "OPTSNS".

If you look closely at the entire section of nervous diseases (G), then everything is there, including "unspecified" and "other" lesions of both the central and peripheral nervous systems, but there is no such disorder as "organic brain damage". In the section of psychiatry in the ICD, there is the concept of "organic personality disorder", it is associated with the consequences of severe diseases of the nervous system, such as diseases such as encephalitis, meningitis or stroke, which can be life-threatening.

The reason for this can be understood: it is easier for psychiatrists. The personality of a person is an integral structure, and it can have a persistent disorder of individual components, but at the same time, the personality suffers as an indivisible category, since it cannot be “divided” into its component parts.

And the central nervous system may also suffer, while the damaging factors can be firmly established, the pathogenesis of the disorder is known, the signs and there is a final separate diagnosis. Therefore, even only on the basis of the official classification of diseases, one can draw a conclusion and create a definition of what this mysterious pathology is.

Definition

Organic brain damage is a persistent violation of both the structure of the brain and its individual functions, which is manifested by various symptoms, is irreversible, based on morphological changes in the central nervous system.

This means that all brain diseases in adults and children, including young children, can be divided into two large groups:

• functional disorders. They do not have any morphological substrate. talking in simple words, this means that, despite complaints, according to all the data of the examination, MRI, lumbar puncture and other research methods, no pathological changes are detected.

Such diseases, for example, include vegetative-vascular dystonia with diencephalic crises, or migraine headaches. Despite a thorough ultrasound of both the vessels of the brain and the vessels of the head and neck, no pathology can be detected. This is due to a sharp change in vascular tone, which leads to severe, throbbing pain with nausea and vomiting, against the background of normal study results.

• organic pathology. She "leaves traces" that are found many years later. All pathophysiological mechanisms of its appearance are known: for example, acute ischemia, or perinatal damage to the central nervous system in a child of the first year of life. Leads to permanent change inflammatory process both on the membranes of the brain and in the brain itself.

Therefore, in the event that any specific disease or brain damage in the past can be “attached” to the patient’s complaints, and also if these complaints are associated with disorders in the structure of the medulla (for example, according to MRI), which are persistent, then The patient is given a diagnosis such as:

Organic brain disease of complex genesis: residual period of extensive ischemic stroke in the middle cerebral artery, severe right-sided hemiparesis, motor aphasia, consequences of a closed craniocerebral injury, post-traumatic encephalopathy, moderate cognitive impairment against the background of severe cerebral atherosclerosis.

As you can see, "there is nowhere to put samples." Usually, after such a main diagnosis, there is a list of concomitant ones: hypertension, diabetes, obesity and so on. But it is immediately clear what reasons led to the development of OPTSNS.

We gave an example of an organic lesion of the central nervous system associated with stroke and trauma, occurring against the background of atherosclerosis in an elderly person. And what diseases are generally associated with the subsequent appearance and development of organic disorders?

Types of organic lesions

In order not to bore the reader with a detailed description of diseases that “leave” a permanent mark on the patient’s life in the form of an organic brain lesion, we briefly list these causes.

You just need to remember that all the diseases listed below can be cured without a trace, without any consequences. In addition, the patient may have persistent changes in the structure of the brain, such as a cyst of the septum pellucidum in a child, or calcification of the caudate nucleus, which may be an incidental finding on an MRI done just for fun.

And what does it mean that the patient has an organic lesion? This is where the most interesting part of the story begins: purely formally, morphologically, from the point of view of pathological anatomy- Yes. But, since the patient does not complain, neurologists do not make any diagnosis for him. In addition, these changes in the brain, if they occurred quietly and asymptomatically, and one of the following diagnoses was not documented, then there seems to be no basis for APCNS.

Therefore, an organic lesion is exhibited in the presence of changes in the structure, and corresponding complaints and symptoms. Separately, the components are "not taken into account".

However, there is one disease in which there may not be striking changes on neuroimaging, and the diagnosis will still sound like ALPNS. This is a long-term (20-30 days) stay of the patient in a coma caused by metabolic rather than destructive coma. This period is quite enough for lifelong disorders caused by hypoxia, which cannot be "seen", to appear. So here is a list of the most common reasons:

In addition, such systemic diseases of the whole organism as atherosclerosis, in its cerebral form, can lead to organic damage, leading to dementia, and persistent cognitive disorders, which were previously called intellectual-mnestic.

It's interesting that true diseases central nervous system with unknown cause ( multiple sclerosis, amyotrophic lateral sclerosis, hereditary diseases in children) - despite the rough symptoms and early, aggressive onset, they are not called an organic lesion.

What cannot cause OPCNS?

Of course, all diseases that are characteristic of the peripheral nervous system cannot be the cause of organic damage to the central nervous system. Such diseases include:

• osteochondrosis with radicular symptoms (with the exception of the development of myelopathy);
• compression-ischemic neuropathies and other lesions of peripheral nerves.

Clinic

As readers have already guessed, the symptoms and signs of the above diseases are very extensive and varied. However, they can be grouped into several major syndromes:

As it has already become clear, the diagnosis of APCNS is not a sudden finding of “something in the head” against the background of complete health. This is a whole story of the treatment of a disease that may have been cured, but the consequences remained - both in terms of complaints and in terms of an objective assessment of the work of the nervous system.

AT last years neuroimaging techniques are very widely used: computed and magnetic resonance imaging, angiography with contrast, myelography. Of course, the diagnosis of cognitive impairment and the consequences of higher cortical functions involves, for example, testing for memory, attention, concentration, vocabulary, exhaustion and so on. The results are also important for making a diagnosis of APCNS.

Treatment

There is a certain paradox: OLTCs are persistent and lifelong. Timely and competent treatment of the cause, or underlying disease, can lead to the fact that an organic lesion simply does not form. On the other hand, if a massive focus of necrosis has already appeared in the brain during an extensive stroke, then this change occurs immediately and forever, since it is determined by the pathogenesis of the disease itself.

If it is not known whether there will be any consequences or not, then they are not talked about yet: therefore, as long as a person is ill, for example, with meningitis, and this underlying disease is being treated, then there is no diagnosis of APCNS, and there is nothing to treat.

Only after a year or more, while maintaining complaints, the presence of an organic lesion is exposed, and the treatment also acquires a "chronic" character. Organic consequences and changes are prone to an undulating course, with periods of exacerbations and remissions. Therefore, treatment is palliative. Sometimes they say that symptomatic treatment is carried out, since this process is lifelong. You can get used to it, but get rid of it only by transplanting a new head.

Effects

Changes in organic lesions can vary over an extremely wide range. For example, after an injury or tumor, a "frontal psyche" may occur. A person becomes slovenly, foolish, prone to flat humor. The scheme of purposeful actions is violated: for example, he can first urinate, and only then take off his pants. In other cases, such consequences as persistent headaches, decreased vision are of concern.

Disability in organic pathology is given, but this is decided not by a doctor, but by experts medical and social bureau. Currently, they are faced with a strict task - to save public funds, and everything is decided by the degree of dysfunction. Therefore, with paralysis of the hand, the chance of getting disability of group 3 is much higher than with complaints of memory loss.

In conclusion, it must be said that the presence of an organic lesion of the central nervous system is not a verdict, a stigma, and, even more so, a reason for accusation of inferiority or idiocy. An example is the well-known proverb expressing extreme extreme positions: “after meningitis, either he died or he was a fool.” In fact, there are a large number of people among us who, if they take care of their sores, will quite legitimately remember “everything”, and acquire this diagnosis. This is sometimes done, by the way, for the military registration and enlistment office, if you are reluctant to serve, but in your head, “thank God”, they found something. After that, “complaints” are urgently invented, and the desired delay has been obtained.

The problem of diagnosing an organic lesion, apparently, is not so simple and unambiguous. We can say, only one thing is known for sure: in order to avoid consequences, you need to immediately treat all diseases, and do not hesitate to consult a doctor.

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ICD 10 codes residual encephalopathy

Residual organic lesion of the CNS

Residual-organic damage to the central nervous system - the consequences of structural damage to the brain and spinal cord of the perinatal period. This period corresponds to the period from 154 days of gestation (22 weeks), when the fetal weight reaches 500 g, to the seventh day after birth. Given the modern possibilities of nursing newborns, it is believed that from now on the child remains viable even with premature birth. However, it remains vulnerable to a variety of pathological effects that can adversely affect the functioning of the nervous system.

Origin of residual-organic pathology of the CNS

Factors that adversely affect the development of the fetus and newborn include:

• chromosomal diseases (mutations and consequences of gametopathies);
• physical factors (poor ecology, radiation, lack of oxygen consumption);
• chemical factors (use of medicines, household chemicals, chronic and acute intoxication with alcohol and drugs);
• malnutrition (starvation, vitamin and mineral depletion of the diet, protein deficiency);
• diseases of a woman (acute and chronic diseases of the mother);
• pathological conditions during pregnancy (preeclampsia, damage to the child's place, anomalies of the umbilical cord);
• deviations in the course of labor (birth weakness, rapid or prolonged labor, premature detachment of the placenta).

Under the influence of these factors, tissue differentiation is disrupted, and fetopathy, intrauterine growth retardation, prematurity are formed, which can subsequently provoke an organic lesion of the central nervous system. The following perinatal pathology leads to the consequences of organic lesions of the central nervous system:

Clinical manifestations of residual CNS damage

Clinically, organic damage to the central nervous system in children manifests itself from the first days of life. Already at the first examination, a neurologist can find external signs of brain suffering - tonic disorders, tremor of the chin and arms, general anxiety, and a delay in the formation of voluntary movements. With a gross lesion of the brain, focal neurological symptoms.

Sometimes signs of brain damage are detected only during additional methods examinations (for example, neurosonography). In this case, they speak of a clinically silent course of perinatal pathology.

Important! In cases of absence clinical symptoms organic pathology of the brain damage to the nervous system, identified using methods instrumental diagnostics does not require treatment. All that is needed is dynamic observation and repeated studies.

Residual damage to the central nervous system in children is manifested by:

• cerebrosthenic syndrome (rapid exhaustion, unreasonable fatigue, mood lability, lack of adaptation to mental and physical activity, tearfulness, irritability, capriciousness);
• neurosis-like syndrome (tics, enuresis, phobias);
• encephalopathy (decrease in cognitive functions, scattered focal neurological symptoms);
• psychopathy (phenomena of affect, aggressive behavior, disinhibition, reduced criticism);
• organic-psychic infantilism (apato-abulic manifestations, suppression, list, formation of addictions);
• minimal brain dysfunction (motor hyperactivity disorder with attention deficit).

A detailed decoding of the syndromes can be obtained by watching the thematic video.

Treatment of residual CNS damage

Monitoring of patients with the consequences of an organic CNS lesion, the treatment of which implies a rather long process, should be comprehensive. Taking into account the progression of the disease and the subtype of its course, a personal selection of therapy for each patient is necessary. Comprehensive monitoring is based on the involvement of doctors, relatives and, if possible, friends, teachers, psychologists, and patients themselves in the correction process.

The main areas of treatment include:

• medical supervision of the general condition of the child;
• regular examination by a neurologist using neuropsychological techniques, testing;
• drug therapy(psychostimulants, neuroleptics, tranquilizers, sedatives, nootropics, vasoactive drugs, vitamin and mineral complexes);
• non-drug correction (massage, kinesitherapy, physiotherapy, acupuncture);
• neuropsychological rehabilitation (including correction of speech disorders);
• psychotherapeutic impact on the environment of the child;
• work with teachers in educational institutions and organization of special education.

Important! Complex treatment from the first years of a child's life will help to significantly improve the effectiveness of rehabilitation.

Residual-organic damage to the nervous system is more clearly identified as it matures. They directly correlate with the time and duration of the impact of the damaging factor on the central nervous system.

Residual effects of brain damage in the perinatal period may predispose to the development of cerebral diseases and form a model of deviant behavior. Timely and competent treatment will stop the symptoms, restore the full functioning of the nervous system and socialize the child.

Organic lesion of the central nervous system

Organic damage to the central nervous system is a pathology that consists in the death of neurons in the brain or spinal cord, necrosis of the tissues of the central nervous system or their progressive degradation, due to which the central nervous system of a person becomes defective and cannot adequately perform its functions in ensuring the functioning of the body , motor activity of the body, as well as mental activity.

An organic lesion of the central nervous system has another name - encephalopathy. It can be a congenital or acquired disease due to a negative effect on the nervous system.

Acquired can develop in people of any age due to various injuries, poisoning, alcohol or drug addiction, infectious diseases, exposure, and similar factors.

Congenital or residual - damage to the organs of the central nervous system of the child, inherited due to genetic failures, impaired fetal development in the perinatal period (the period between one hundred and fifty-fourth day of pregnancy and the seventh day of extrauterine existence), as well as due to birth trauma.

Classification

The classification of lesions depends on the cause of the development of pathology:

• Discirculatory - caused by a violation of the blood supply.
• Ischemic - dyscirculatory organic lesion, supplemented by destructive processes in specific foci.
• Toxic - cell death due to toxins (poisons).
• Radiation - radiation damage.
• Perinatal-hypoxic - due to fetal hypoxia.
• Mixed type.
• Residual - obtained due to a violation of intrauterine development or birth trauma.

Causes of acquired organic brain damage

It is not at all difficult to acquire damage to the cells of the spinal cord or brain, since they are very sensitive to any negative impact, but most often it develops for the following reasons:

• Spinal injury or traumatic brain injury.
• Toxic damage, including alcohol, drugs, drugs and psychotropic drugs.
• Vascular diseases that cause circulatory disorders, and with it hypoxia or nutritional deficiencies, or tissue injury, such as stroke.
• Infectious diseases.

It is possible to understand the reason for the development of one or another type of organic lesion, based on the name of its variety, as mentioned above, it is on the reasons that the classification of this disease is based.

How and why residual CNS damage occurs in children

Residual organic damage to the central nervous system in a child occurs due to a negative impact on the development of his nervous system, or due to hereditary genetic abnormalities or birth injuries.

The mechanisms of development of a hereditary residual organic lesion are exactly the same as in any hereditary diseases, when the distortion of hereditary information due to DNA breakdowns leads to an abnormal development of the child's nervous system or the structures that ensure its vital activity.

An intermediate process to a non-hereditary pathology looks like a failure in the formation of cells or even entire organs of the spinal cord and brain due to negative environmental influences:

• Severe illnesses suffered by the mother during pregnancy, as well as viral infections. Even the flu or a simple cold can provoke the development of a residual organic lesion of the central nervous system of the fetus.
• Lack of nutrients, minerals and vitamins.
• Toxic effects, including drugs.
• Maternal bad habits, especially smoking, alcoholism and drugs.
• Bad ecology.
• Irradiation.
• Fetal hypoxia.
• The physical immaturity of the mother, or, conversely, the advanced age of the parents.
• The use of special sports nutrition or some dietary supplements.
• Strong stress.

The mechanism of the influence of stress on premature birth or miscarriage by convulsive contraction of its walls is clear, not many people understand how mother's stress leads to the death of the fetus or disruption of its development.

With strong or systematic stress, the mother's nervous system suffers, which is responsible for all processes in her body, including the life support of the fetus. With a violation of its activity, a variety of failures and the development of vegetative syndromes can occur - violations of the functions of internal organs, due to which the balance in the body, which ensures the development and survival of the fetus, is destroyed.

Traumatic injuries of a different nature during childbirth, which can cause organic damage to the central nervous system of the child, are also very different:

• Asphyxia.
• Injury to the spine or base of the skull in case of improper removal with twisting of the child from the uterus.
• The fall of a child.
• premature birth.
• Atony of the uterus (the uterus is unable to contract normally and push the baby out).
• Head squeezing.
• Entry of amniotic fluid into the respiratory tract.

Even in the perinatal period, the child can become infected with various infections both from the mother during childbirth and hospital strains.

Symptoms

Any lesion of the central nervous system has symptoms in the form of impaired mental activity, reflexes, motor activity and impaired functioning of internal organs and sensory organs.

It is rather difficult even for a professional to immediately see the symptoms of a residual organic CNS lesion in an infant, since the movements of infants are specific, mental activity is not immediately determined, and it is possible to notice disturbances in the functioning of internal organs with the naked eye only with severe pathologies. But sometimes clinical manifestations can be seen from the first days of life:

• Violation muscle tone.
• Tremor of the limbs and head (most often tremor in newborns has benign character but can also be a symptom of neurological disease).
• Paralysis.
• reflex disorder.
• Chaotic rapid eye movements back and forth or a frozen look.
• Violation of the functions of the sense organs.
• epileptic seizures.

At an older age, somewhere from three months, the following symptoms can be noticed:

• Violation of mental activity: the child does not follow toys, shows hyperactivity or vice versa - apathy, suffers from a lack of attention, does not recognize acquaintances, etc.
• Delay in physical development, both directly growth and acquisition of skills: does not hold his head, does not crawl, does not coordinate movements, does not try to stand up.
• Rapid physical and mental fatigue.
• Emotional instability, capriciousness.
• Psychopathy (tendency to affects, aggression, disinhibition, inadequate reactions).
• Organic-psychic infantilism, expressed in the suppression of the personality, the formation of addictions and increased awareness.
• Impaired coordination.
• Memory impairment.

If the child has a suspected CNS lesion

If any symptoms of a violation of the central nervous system in a child appear, you should immediately contact a neurologist and undergo a comprehensive examination, which may include the following procedures:

• General analyzes, different kinds tomography (each type of tomography examines for its part and therefore gives different results).
• Fontanelle ultrasound.
• EEG is an electroencephalogram that allows you to determine the foci of pathological activity of the brain.
• X-ray.
• Liquor analysis.
• Neurosonography is an analysis of the conduction of neurons, which helps to detect small hemorrhages or disturbances in the functioning of peripheral nerves.

If you suspect any deviations in the health of your child, you should consult a doctor as soon as possible, since timely treatment will help to avoid a huge number of problems, and will also significantly reduce the recovery time. Do not be afraid of false suspicions and unnecessary examination, since they, unlike probable pathologies, will not harm the baby.

Sometimes the diagnosis of this pathology occurs even during fetal development at a scheduled ultrasound examination.

Methods of treatment and rehabilitation

Treatment of the disease is quite laborious and lengthy, however, with minor injuries and competent therapy, congenital residual organic damage to the central nervous system in newborns can be completely eliminated, since nerve cells Infants are able to divide for a while, and the entire nervous system of young children is very flexible.

• First of all, with this pathology, constant monitoring by a neurologist and the attentive attitude of the parents themselves are required.
• If necessary, drug therapy is carried out both to eliminate the root cause of the disease, and in the form of symptomatic treatment: removal of a convulsive symptom, nervous excitability, etc.
• At the same time, as a method of treatment or recovery, physiotherapy is carried out, which includes massage, acupuncture, zootherapy, swimming, gymnastics, reflexology or other methods designed to stimulate the nervous system, encourage it to begin recovery through the formation of new neural connections and to teach the child himself to use his body in the event of a violation of motor activity in order to minimize his inferiority to an independent life.
• At a later age, psychotherapeutic influences are applied both on the child himself and on his immediate environment in order to improve the moral situation around the child and prevent the development of mental deviations in him.
• Speech correction.
• Specialized training tailored to individual characteristics child.

Conservative treatment is carried out in a hospital and consists in taking medicines in the form of injections. These drugs reduce cerebral edema, seizure activity and improve blood circulation. Almost everyone is prescribed piracetam or drugs with a similar effect: pantogam, caviton or phenotropil.

In addition to the main drugs, symptomatic relief of the condition is carried out with the help of sedatives, painkillers, which improve digestion, stabilize the heart and reduce any other negative manifestations of the disease.

After eliminating the cause of the disease, the therapy of its consequences is carried out, designed to restore the functions of the brain, and with them the work of internal organs and motor activity. If it is impossible to completely eliminate residual manifestations, the goal of rehabilitation therapy is to teach the patient to live with his body, use his limbs and self-service as much as possible.

Many parents underestimate the benefits of physiotherapy in the treatment of neurological ailments, but they are the fundamental methods to restore lost or impaired functions.

The recovery period is extremely long, and ideally lasts a lifetime, since if the nervous system is damaged, the patient has to overcome himself every day. With due diligence and patience, by a certain age, a child with encephalopathy can become completely independent and even lead an active lifestyle, the maximum possible with the level of his defeat.

It is impossible to cure the pathology on your own, and with mistakes made due to lack of medical education, you can not only exacerbate the situation at times, but even get a fatal outcome. Collaboration with a neurologist in people with encephalopathy becomes lifelong, but the application folk methods Therapy is not prohibited.

Alternative methods of treatment of organic lesions of the central nervous system are most effective methods restorations that do not replace conservative treatment with physiotherapy, but complement it very qualitatively. Only when choosing one or another method, again, consultation with a doctor is necessary, since it is necessary to distinguish between useful and effective methods from useless and harmful is extremely difficult without deep specialized medical knowledge, as well as minimal chemical literacy.

If it is impossible to visit specialized institutions in order to take a course of exercise therapy, massage and aqua therapy, they can be easily carried out at home, having mastered simple techniques with the help of a neurologist's consultation.

Another important aspect of treatment is social rehabilitation with the psychological adaptation of the patient. You should not unnecessarily patronize a sick child, helping him in everything, because otherwise he will not be able to fully develop, and as a result, he will not be able to fight the pathology. Help is needed only in vital things or special cases. In everyday life, doing daily chores on your own will work as an additional physical therapy or exercise therapy, and will also teach the child to overcome difficulties and that patience and perseverance always lead to excellent results.

Effects

Organic damage to the central nervous system in the perinatal period or at an older age leads to the development of a large number of various neurological syndromes:

• Hypertensive-hydrocephalic - hydrocephalus, accompanied by an increase in intracranial pressure. It is determined in infants by an increase in the fontanel, its swelling or pulsation.
• Hyperexcitability syndrome - increased muscle tone, sleep disturbance, increased activity, frequent crying, high convulsive readiness or epilepsy.
• Epilepsy is a convulsive syndrome.
• Coma syndrome with opposite symptoms of hyperexcitability, when the child is lethargic, lethargic, moves little, lack of sucking, swallowing or other reflexes.
• Vegetative-visceral dysfunction of the internal organs, which can be expressed as frequent regurgitation, digestive disorders, skin manifestations and many other deviations.
• Movement disorders.
• Cerebral palsy - movement disorders complicated by other defects, including mental retardation and weakness of the senses.
• Hyperactivity is the inability to concentrate and attention deficit.
• Retardation in mental or physical development, or complex.
• Mental illness against the background of disorders of the brain.
• Psychological ailments due to the discomfort of the patient among society or physical inferiority.

• Endocrine disorders, and as a result, a decrease in immunity.

Forecast

The prognosis of an acquired organic lesion of the central nervous system is rather fuzzy, since everything depends on the level of damage. In the case of a congenital type of disease, in some cases the prognosis is more favorable, since the child’s nervous system recovers many times faster, and his body adapts to it.

After well-conducted treatment and rehabilitation, the function of the central nervous system can be either completely restored or have any residual syndrome.

The consequences of early organic damage to the central nervous system often lead to mental and physical retardation in development, and also lead to disability.

On the positive side, many parents whose children received this terrible diagnosis, with the help of intensive rehabilitation therapy, achieve magical results, refuting the most pessimistic forecasts of doctors, providing their child with a normal future.

The information on the site is provided for informational purposes only, does not claim to be reference and medical accuracy, and is not a guide to action. Do not self-medicate. Consult with your physician.

/F00 - F09/ Organic, including symptomatic, mental disorders Introduction This section includes a group of mental disorders grouped together on the basis that they share a common, clear etiology of cerebral disease, brain injury, or other injury resulting in cerebral dysfunction. This dysfunction may be primary, as in certain diseases, injuries, and strokes that affect the brain directly or preferentially; or secondary, as in systemic diseases and disorders that affect the brain as only one of many organs or body systems. Brain disorders due to alcohol or drug use, although logically should have been included in this group, are classified in section F10 to F19 based on the practical convenience of grouping all substance use disorders into one section. . Despite the breadth of the spectrum of psychopathological manifestations of the conditions included in this section, the main features of these disorders fall into two main groups. On the one hand, there are syndromes where the most characteristic and constantly present are either impairment of cognitive functions, such as memory, intelligence, and learning, or disturbances in awareness, such as disorders of consciousness and attention. On the other hand, there are syndromes where the most striking manifestation is disorders of perception (hallucinations), the content of thoughts (delusions), mood and emotions (depression, elation, anxiety) or the general personality and behavior. Cognitive or sensory dysfunctions are minimal or difficult to identify. The last group of disorders has less reason to be assigned to this section than the first, since. many of the disorders included here are symptomatically similar to conditions in other sections (F20-F29, F30-F39, F40-F49, F60-F69) and may occur without gross cerebral pathology or dysfunction. However, there is increasing evidence that many cerebral and systemic diseases are causally related to the occurrence of such syndromes and this sufficiently justifies their inclusion in this section in terms of a clinically oriented classification. In most cases, the disorders classified in this section, at least theoretically, can begin at any age except apparently early childhood. In practice, most of these disorders tend to begin in adulthood or later in life. While some of these disorders (with the current state of our knowledge) appear to be irreversible, a number of others are transient or respond well to currently available treatments. The term "organic" as used in the table of contents of this section does not mean that conditions in other sections of this classification are "inorganic" in the sense that they do not have a cerebral substrate. In the present context, the term "organic" means that the syndromes so qualified can be explained by a self-diagnosed cerebral or systemic disease or disorder. The term "symptomatic" refers to those organic mental disorders in which the central interest is secondary to the systemic extracerebral disease or disorder. It follows from the above that in most cases, recording a diagnosis of any disorder in this section will require the use of 2 codes, one for characterizing the psychopathological syndrome and one for the underlying disorder. The etiological code should be selected from other relevant chapters of the ICD-10 classification. It should be noted: In the adapted version of the ICD-10, for the registration of mental disorders listed in this heading, it is mandatory to use an additional sixth character to characterize an "organic", "symptomatic" disease (meaning mental disorders due to somatic diseases, traditionally referred to as "somatogenic disorders") that underlie the diagnosed mental disorder: F0x.xx0 - in connection with a brain injury; F0х.хх1 - due to vascular disease brain; F0х.хх2 - due to epilepsy; F0x.xx3 - in connection with a neoplasm (tumor) of the brain; F0х.хх4 - in connection with the human immunodeficiency virus (HIV infection); F0x.xx5 - due to neurosyphilis; F0x.xx6 - due to other viral and bacterial neuroinfections; F0х.хх7 - due to other diseases; F0х.хх8 - due to mixed diseases; F0x.xx9 - due to an unspecified disease. dementia This part provides a general description of dementia to outline the minimum requirements for diagnosing dementia of any type. The following are criteria by which one can determine how to diagnose a more specific type of dementia. Dementia is a syndrome caused by a brain disease, usually chronic or progressive, in which there are impairments to a number of higher cortical functions, including memory, thinking, orientation, comprehension, numeracy, learning ability, language, and judgment. Consciousness is not changed. As a rule, there are cognitive impairments, which may be preceded by disturbances in emotional control, social behavior, or motivations. This syndrome occurs in Alzheimer's disease, cerebrovascular disease, and other conditions that primarily or secondarily affect the brain. When assessing the presence or absence of dementia, particular care must be taken to avoid false positive ratings: motivational or emotional factors, especially depression, in addition to motor retardation and general physical weakness, may be more responsible for poor performance than intellectual loss. abilities. Dementia leads to a marked decrease in intellectual functioning and most often also to a disturbance in daily activities, such as: washing, dressing, eating habits, personal hygiene, self-management. physiological functions. Such a decline can largely depend on the social and cultural environment in which a person lives. Role changes, such as reduced ability to continue or seek employment, should not be used as a criterion for dementia because of the significant cross-cultural differences that exist in determining what is appropriate behavior in a given situation; often external influences affect the possibility of getting a job even within the same cultural environment. If symptoms of depression are present, but they do not meet the criteria for a depressive episode (F32.0x - F32.3x), their presence should be indicated by the fifth character (the same applies to hallucinations and delusions): F0x .x0 without additional symptoms; F0x .x1 other symptoms, mostly delusional; F0x .x2 other symptoms, mostly hallucinatory; F0x .x3 other symptoms, mostly depressive; F0x .x4 other mixed symptoms. It should be noted: The allocation of the fifth sign of additional psychotic symptoms in dementia refers to the headings F00 - F03, while in the subheadings F03.3x and F03.4x the fifth character specifies which particular psychotic disorder is observed in the patient, and in F02.8xx after the fifth character it is also necessary to use the sixth character, which will indicate the etiological nature of the observed mental disorder. Diagnostic instructions: Main diagnostic requirement are data indicating a decrease in both memory and thinking, to such an extent that it leads to a disruption of individual daily life. Memory impairment in typical cases concerns the registration, storage and reproduction of new information. Previously acquired and familiar material may also be lost, especially in the later stages of the disease. Dementia is more than dysmnesia: there are also disturbances in thinking, reasoning abilities, and a reduction in the flow of thought. The processing of incoming information is impaired, which manifests itself in increasing difficulties in responding to several stimuli at the same time, such as when participating in a conversation in which several people are engaged and when switching attention from one topic to another. If dementia is the only diagnosis, then it is necessary to state the presence of a clear consciousness. However, dual diagnosis, such as delirium in dementia, is quite common (F05.1x). The above symptoms and disorders must be present for at least 6 months for a clinical diagnosis to be conclusive. Differential diagnosis: Consider: - depressive disorder (F30 - F39), which may show many of the features early dementia, especially memory impairment, slow thinking and lack of spontaneity; - delirium (F05.-); - mild or moderate mental retardation (F70 - F71); - states of subnormal cognitive activity associated with a serious impoverishment of the social environment and limited ability learn; - iatrogenic mental disorders due to drug treatment (F06.-). Dementia may follow any of the organic mental disorders classified in this section or coexist with some of them, in particular delirium (see F05.1x). It should be noted: Rubrics F00.- (dementia in Alzheimer's disease) and F02.- (de- mentia in other diseases classified elsewhere) are marked with an asterisk ( * ). In accordance with chapter 3.1.3. Collection of instructions ("International Statistical Classification of Diseases and Related Health Problems. Tenth Revision" (vol. 2, WHO, Geneva, 1995, p. 21), the main code in this system is the code of the main disease, it is marked with a "cross" ( + ); an optional additional code related to the manifestation of the disease is marked with an asterisk ( * ). A code with an asterisk should never be used on its own, but together with a code marked with a cross. The use of a particular code (with an asterisk or a cross) in statistical reporting is regulated in the instructions approved by the Ministry of Health of Russia for compiling the relevant forms.

/F00 * / Dementia in Alzheimer's disease

(G30.- + )

Alzheimer's disease (AD) is a primary degenerative cerebral disease of unknown etiology with characteristic neuropathological and neurochemical features. The disease usually has a gradual onset and develops slowly but steadily over several years. In terms of time, it can be 2 or 3 years, but sometimes much more. The onset may be in middle age or even earlier (AD with onset in presenile age), but the incidence is higher in late age and older (AD with senile onset). In cases with the onset of the disease before 65-70 years of age, there is a possibility of a family history of similar forms of dementia, a faster pace of the course and characteristic signs of brain damage in the temporal and parietal region, including symptoms of dysphasia and dyspraxia. In cases with a later onset, there is a tendency to slower development, the disease in these cases is characterized by a more general lesion of higher cortical functions. Patients with Down syndrome are at high risk of developing AD. There are characteristic changes in the brain: a significant decrease in the population of neurons, especially in the hippocampus, innominate substance, locus coeruleus; changes in the temporo-parietal region and frontal cortex; the appearance of neurofibrillary plexuses, consisting of paired spiral filaments; neuritic (argentophilic) plaques, predominantly amyloid, showing a certain tendency to progressive development (although there are plaques without amyloid); granulovascular bodies. Neurochemical changes have also been found, which include a significant decrease in the enzyme acetylcholine transferase, acetylcholine itself and other neurotransmitters and neuromodulators. As already described, Clinical signs usually accompanied by brain damage as well. However, the progressive development of clinical and organic changes does not always proceed in parallel: there may be an undeniable presence of some symptoms with a minimal presence of others. However, the clinical features of AD are such that it is often possible to make a presumptive diagnosis based on clinical findings alone. Currently, BA is irreversible. Diagnostic guidelines For a definite diagnosis, the following features must be present: a) The presence of dementia, as described above. b) Gradual onset with slowly increasing dementia. Although it is difficult to establish the time of onset of the disease, the discovery of existing defects by others can occur suddenly. There may be some plateau in the development of the disease. c) Lack of data from clinical or special studies that could speak in favor of the fact that the mental state is due to other systemic or brain diseases leading to dementia (hypothyroidism, hypercalcemia, vitamin B-12 deficiency, nicotinamide deficiency, neurosyphilis, normal pressure hydrocephalus, subdural hematoma). d) Absence of a sudden apoplectic onset or neurological symptoms associated with brain damage, such as hemiparesis, loss of sensation, changes in visual fields, impaired coordination, occurring early in the course of the disease (however, such symptoms may later develop on the background of dementia). In some cases, signs of AD and vascular dementia may be present. In such cases, double diagnosis (and coding) must take place. If vascular dementia precedes AD, then the diagnosis of AD cannot always be established on the basis of clinical findings. Includes: - primary degenerative dementia of the Alzheimer's type At differential diagnosis it is necessary to keep in mind: - depressive disorders (F30 - F39); - delirium (F05.-); - organic amnestic syndrome (F04.-); - other primary dementias such as Pick's disease, Creutzfeldt-Jakob disease, Huntington's disease (F02.-); - secondary dementias associated with a number of somatic diseases, toxic conditions, etc. (F02.8.-); - mild, moderate and severe forms of mental retardation (F70 - F72). Dementia in AD may be associated with vascular dementia (code F00.2x should be used) when cerebrovascular episodes (multi-infarct symptoms) may overlap with clinical and medical history suggestive of AD. Such episodes can cause a sudden exacerbation of the manifestations of dementia. According to autopsy, a combination of both types of dementia is found in 10-15% of all cases of dementia.

F00.0x * Dementia in Alzheimer's disease with early onset

(G30.0 + )

Dementia in AD with an onset before the age of 65 with a relatively rapidly progressive course and with multiple severe disorders of higher cortical functions. In most cases, aphasia, agraphia, alexia, and apraxia appear in the relatively early stages of dementia. Diagnostic guidelines Bear in mind the pattern of dementia above, with onset before age 65 and rapid progression of symptoms. Family history data indicating the presence of AD patients in the family may be an additional, but not mandatory factor for establishing this diagnosis, just like information about the presence of Down's disease or lymphoidosis. Includes: - Alzheimer's disease, type 2; - primary degenerative dementia, Alzheimer's type, presenile onset; - presenile dementia of the Alzheimer's type. F00.1x * Dementia in late-onset Alzheimer's disease (G30.1 + ) Dementia in AD, where there is a clinically established time of onset of the disease after 65 years (usually at 70 years and later). There is a slow progression with memory impairment as the main feature of the disease. Diagnostic guidelines: Follow the description of dementia above, with special attention to the presence or absence of symptoms that differentiate it from early-onset dementia (F00.0). Includes: - Alzheimer's disease, type 1; - primary degenerative dementia, Alzheimer's type, senile onset; - senile dementia of the Alzheimer's type. F00.2 X * Dementia in Alzheimer's disease, atypical or mixed (G30.8 + ) This should include dementias that do not fit the description and diagnostic guidelines for F00.0 or F00.1, as well as mixed forms of AD and vascular dementia. Includes: - atypical dementia, Alzheimer's type. F00.9x * Dementia in Alzheimer's disease, unspecified (G30.9 + ) /F01/ Vascular dementia Vascular (former arteriosclerotic) dementia, including multi-infarct dementia, differs from dementia in Alzheimer's disease in terms of the onset of the disease, the clinical picture and subsequent course. In typical cases, there are transient ischemic episodes with a short-term loss of consciousness, unstable paresis, loss of vision. Dementia can also occur after a series of acute cerebrovascular episodes or, more rarely, after a single large hemorrhage. In such cases, a violation of memory and mental activity becomes apparent. Onset (of dementia) may be sudden, following a single ischemic episode, or dementia may have a more gradual onset. Dementia is usually the result of cerebral infarction due to vascular disease, including hypertensive cerebrovascular disease. Heart attacks are usually small but have a cumulative effect. Diagnostic guidelines: Diagnosis suggests the presence of dementia, as noted above. Cognitive impairment is usually uneven and memory loss, intellectual decline, and focal neurological signs may be seen. Criticism and judgment can be relatively spared. Acute onset or gradual worsening, as well as the presence of focal neurological signs and symptoms, increase the likelihood of diagnosis. Confirmation of the diagnosis can in some cases be provided by computed axial tomography or, ultimately, pathological findings. Associated symptoms include: hypertension, carotid murmur, emotional lability with transient depressive mood, tearfulness or bursts of laughter, transient episodes of clouded consciousness or delirium, which can be provoked by further heart attacks. It is believed that personality traits are relatively preserved. However, in some cases, personality changes may also be evident, with the appearance of apathy or lethargy, or a sharpening of previous personality traits such as egocentrism, paranoia, or irritability. Includes: - arteriosclerotic dementia. Differential diagnosis: It is necessary to consider: - delirium (F05.xx); - other forms of dementia, and in particular Alzheimer's disease (F00.xx); - (affective) mood disorders (F30 - F39); - mild and moderate mental retardation (F70 - F71); subdural hemorrhage, traumatic (S06.5), non-traumatic (I62.0)). Vascular dementia may coexist with Alzheimer's disease (code F00. 2x), if vascular episodes occur against the background of a clinical picture and anamnesis, indicating the presence of Alzheimer's disease.

F01.0x Vascular dementia with acute onset

It usually develops rapidly after a series of strokes or cerebrovascular thrombosis, embolism, or hemorrhage. In rare cases, a single massive hemorrhage may be the cause.

F01.1x Multi-infarct dementia

The onset is more gradual, followed by several small ischemic episodes that create an accumulation of infarcts in the cerebral parenchyma. Includes: - predominantly cortical dementia

F01.2 Subcortical vascular dementia

Includes cases characterized by a history of hypertension and ischemic destructive foci in the deep layers of the white matter of the cerebral hemispheres. The cerebral cortex is usually preserved, and this contrasts with the clinical picture of Alzheimer's disease. F01.3x Mixed cortical and subcortical vascular dementia A mixed picture of cortical and subcortical vascular dementia may be suggested based on the clinical presentation, findings of investigations (including autopsy), or both.

F01.8x Other vascular dementia

F01.9x Vascular dementia, unspecified

/F02 * / Dementia in other diseases,

classified elsewhere

Cases of dementia due or suspected to be due to causes other than Alzheimer's disease or cerebrovascular disease. The onset can occur at any age, but rarely late. Diagnostic guidelines Presence of dementia as above; the presence of features characteristic of one of the specific syndromes outlined in the following categories.

F02.0x * Dementia in Pick's disease

(G31.0 + )

The progressive course of dementia begins in middle age (usually between the ages of 50 and 60), with slowly progressive character changes and social decline, and subsequent intellectual impairment, memory loss, speech decline with apathy, euphoria, and (sometimes) extrapyramidal phenomena. The pathoanatomical picture of the disease is characterized by selective atrophy of the frontal and temporal lobes, but without the appearance of neuritic (argentophilic) plaques and neurofibrillary plexuses in excess compared to normal aging. With an early onset, there is a tendency to a more malignant course. Social and behavioral manifestations often precede overt memory impairment. Diagnostic guidelines For a definite diagnosis, the following features are necessary: ​​a) progressive dementia; b) the prevalence of frontal symptoms with euphoria, emotional blanching, rude social behavior, disinhibition and either apathy or restlessness; c) such behavior usually precedes distinct memory impairments. Frontal symptoms are more pronounced than temporal and parietal, in contrast to Alzheimer's disease. Differential diagnosis: It is necessary to keep in mind: - dementia in Alzheimer's disease (F00.xx); - vascular dementia (F01.xx); - dementia secondary to other diseases, such as neurosyphilis (F02.8x5); - dementia with normal intracranial pressure (characterized by severe psychomotor retardation, impaired gait and sphincter function (G91.2); - other neurological and metabolic disorders.

F02.1x * Dementia in Creutzfeldt-Jakob disease

(A81.0 + )

The disease is characterized by progressive dementia with extensive neurological symptoms due to specific pathological changes (subacute spongiform encephalopathy), which are presumably caused by a genetic factor. The onset is usually in middle or late age, and in typical cases in the fifth decade of life, but can occur at any age. The course is subacute and leads to death in 1-2 years. Diagnostic guidelines: Creutzfeldt-Jakob disease should be considered in all cases of dementia that progress rapidly over months or 1–2 years and are accompanied by multiple neurological symptoms. In some cases, as in the so-called amyotrophic forms, neurological signs may precede the onset of dementia. Progressive spastic paralysis of the extremities is usually noted, with concomitant extrapyramidal signs, tremor, rigidity, and characteristic movements. In other cases, there may be ataxia, loss of vision, or muscle fibrillation and atrophy of the upper motor neuron. The triad, consisting of the following signs, is considered very typical for this disease: - rapidly progressive, devastating dementia; - pyramidal and extrapyramidal disorders with myoclonus; - characteristic three-phase EEG. Differential diagnosis: Consideration should be given to: - Alzheimer's disease (F00.-) or Pick's disease (F02.0x); - Parkinson's disease (F02.3x); - postencephalitic parkinsonism (G21.3). The rapid course and early onset of motor disturbances may speak in favor of Creutzfeldt-Jakob disease.

F02.2x * Dementia in Huntington's disease

F02.3x * Dementia in Parkinson's disease

F02.8x0 * dementia

(S00.- + - S09.- + )

F02.8x2 * Dementia due to epilepsy (G40.-+)

C79.3 + , D32.- + , D33.- + , D43.- + )

F02.8x5 * Dementia due to neurosyphilis

(A50.- + -A53.- + )

F02.8x6 * Dementia due to other viral and bacterial neuroinfections (A00.- + -B99.- + ) Includes: - dementia due to acute infectious encephalitis; - dementia due to meningo-encephalitis due to lupus erythematosus.

F02.8x7 * Dementia due to other diseases

Includes: - dementia due to: - carbon monoxide poisoning (T58 +); - cerebral lipidosis (E75.- +); - hepatolenticular degeneration (Wilson's disease) (E83.0 +); - hypercalcemia (E83.5 +); - hypothyroidism, including acquired (E00.- + - E07.- +); - intoxications (T36.- + - T65.- +); - multiple sclerosis (G35 +); - deficiency nicotinic acid(pellagra) (E52+); - polyarthritis nodosa (M30.0 +); - trypanosomiasis (African B56.- + , American B57.- +); - deficiency of vitamin B 12 (E53.8 +).

F02.8х8 * dementia

F02.8х9 * dementia

/F03/ Dementia, unspecified

This category should be used when the general criteria meet the diagnosis of dementia, but it is not possible to specify their specific type (F00.0x - F02.8xx). Includes: - presenile dementia NOS; - senile dementia NOS; - presenile psychosis NOS; - senile psychosis NOS; - senile dementia of depressive or paranoid type; - primary degenerative dementia NOS. Excludes: - involutional paranoid (F22.81); - Alzheimer's disease with late onset (F00.1x *); - senile dementia with delirium or confusion (F05.1x); - old age NOS (R54).

F03.1x Presenile dementia, unspecified

F03.2 Senile dementia, unspecified

F03.3x Presenile psychosis, unspecified

F03.4 Senile psychosis, unspecified

/F04/ Organic amnestic syndrome,

not caused by alcohol or

other psychoactive substances

Syndrome of severe memory impairment for recent and distant events. While direct reproduction is preserved, the ability to assimilate new material is reduced, resulting in anterograde amnesia and disorientation in time. retrograde amnesia different intensity is also present, but its range may decrease over time if the underlying disease or pathological process tends to recover. Confabulations can be pronounced, but are not a mandatory feature. Perception and other cognitive functions, including intellectual ones, are usually preserved and create a background against which the memory disorder becomes especially obvious. The prognosis depends on the course of the underlying disease (usually affecting the hypothalamic-diencephalic system or the hippocampal region). In principle, a full recovery is possible. Diagnostic guidelines: For a reliable diagnosis, the presence of the following symptoms is necessary: ​​a) the presence of impaired memory for recent events (decrease in the ability to assimilate new material); anterograde and retrograde amnesia, reduced ability to reproduce past events in the reverse order of their occurrence; b) history or objective evidence suggestive of stroke or brain disease (especially those involving bilaterally diencephalic and midtemporal structures); c) the absence of a defect in direct reproduction (tested, for example, by memorizing numbers), impaired attention and consciousness, and global intellectual impairment. Confabulations, lack of criticism, emotional changes (apathy, lack of initiative) are an additional, but not mandatory factor in all cases for establishing a diagnosis. Differential Diagnosis: This disorder differs from other organic syndromes where memory impairment is the leading clinical picture(for example, with dementia or delirium). From dissociative amnesia (F44.0), from memory impairment in depressive disorders (F30 - F39) and from simulation, where the main complaints concern memory loss (Z76.5). Korsakov's syndrome caused by alcohol or drugs should be coded not in this section, but in the appropriate one (F1x.6x). Included: - states with extensive amnestic disorders without dementia; - Korsakov's syndrome (non-alcoholic); - Korsakov's psychosis (non-alcoholic); - pronounced amnestic syndrome; - moderate amnestic syndrome. Excludes: - mild amnesic disorders without signs of dementia (F06.7-); - amnesia NOS (R41.3) - anterograde amnesia (R41.1); - dissociative amnesia (F44.0); - retrograde amnesia (R41.2); Korsakov's syndrome, alcoholic or unspecified (F10.6) - Korsakov's syndrome caused by the use of other psychoactive substances (F11 - F19 with a common fourth character.6). F04.0 Organic amnestic syndrome due to brain injury F04.1 Organic amnestic syndrome F04.2 Organic amnestic syndrome due to epilepsy F04.3 Organic amnestic syndrome due F04.4 Organic amnesic syndrome F04.5 Organic amnestic syndrome due to neurosyphilis F04.6 Organic amnestic syndrome F04.7 Organic amnestic syndrome due to other diseases F04.8 Organic amnesic syndrome due to mixed diseases F04.9 Organic amnestic syndrome due to disease unspecified /F05/ Delirium not caused by alcohol or other psychoactive substances An etiologically non-specific syndrome characterized by a combined disorder of consciousness and attention, perception, thinking, memory, psychomotor behavior, emotions, and sleep-wake rhythm. It can occur at any age, but is more common after age 60. The delirious state is transient and fluctuating in intensity. Usually recovery occurs within 4 weeks or less. However, fluctuating delirium lasting up to 6 months is not uncommon, especially if it occurs during chronic liver disease, carcinoma, or subacute bacterial endocarditis. The distinction that is sometimes made between acute and subacute delirium is of little clinical significance and such conditions should be considered as a single syndrome of varying duration and severity (from mild to very severe). A delirious state can occur against the background of dementia, or develop into dementia. This section should not be used to refer to delirium due to the use of psychoactive substances, which are listed in F10 - F19. Delirious states due to medication should be included under this heading (such as an acute state of confusion in the elderly due to antidepressants). In this case, the drug used must also be identified by 1 ms code Class XIX, ICD-10). Diagnostic guidelines: Lungs or severe symptoms from each of the following groups: a) altered consciousness and attention (from stunning to coma; reduced ability to direct, focus, maintain and switch attention); b) global cognitive disorder (distortions of perception, illusions and hallucinations, mostly visual; disturbances in abstract thinking and understanding with or without transient delusions, but usually with some degree of incoherence; impaired direct recall and memory for recent events with relative preservation of memory for distant events ; disorientation in time, and in more severe cases in place and self); c) psychomotor disorders (hypo- or hyperactivity and unpredictability of the transition from one state to another; increase in time; increased or decreased speech flow; horror reactions); d) sleep-wake rhythm disorders (insomnia, and in severe cases - total loss of sleep or inversion of the sleep-wake rhythm: drowsiness during the day, worsening of symptoms at night; restless dreams or nightmares that, upon awakening, may continue as hallucinations); e) emotional disorders such as depression, anxiety or fears. Irritability, euphoria, apathy or bewilderment and confusion. The onset is usually rapid, the condition fluctuates during the day, and the total duration is up to 6 months. The clinical picture described above is so characteristic that a relatively reliable diagnosis of delirium can be made even if its cause is not established. In addition to anamnestic indications of cerebral or physical pathology underlying the delirium, evidence of cerebral dysfunction (eg, an abnormal EEG, usually but not always showing a slowdown in background activity) is also needed if the diagnosis is in doubt. Differential diagnosis: Delirium must be distinguished from other organic syndromes, especially dementia (F00 - F03), acute and transient psychotic disorders (F23.-) and acute schizophrenic conditions (F20.-) or mood (affective) disorders (F30 - F39), in which features of confusion may be present. Delirium caused by alcohol and other psychoactive substances should be classified in the appropriate section (F1x.4xx). Included: - acute and subacute confusional state (non-alcoholic); - acute and subacute brain syndrome; - acute and subacute psychoorganic syndrome; - acute and subacute infectious psychosis; - acute exogenous type of reaction; - acute and subacute organic reaction. Excludes: - delirium tremens, alcoholic or unspecified (F10.40 - F10.49).

/F05.0/ Delirium not associated with dementia as described

This code should be used for delirium that does not occur in the background of previous dementia. F05.00 Delirium not associated with dementia due to brain injury F05.01 Delirium without dementia due to cerebrovascular disease F05.02 Delirium other than dementia due to epilepsy F05.03 Delirium not associated with dementia in connection with a neoplasm (tumor) of the brain F05.04 Delirium not associated with dementia due F05.05 Delirium other than dementia due to neurosyphilis F05.06 Delirium not associated with dementia due F05.07 Delirium not associated with dementia due to other diseases F05.08 Delirium not associated with dementia due to mixed diseases F05.09 Delirium other than dementia due to unspecified disease /F05.1/ Delirium due to dementia This code should be used for conditions that meet the above criteria but develop during dementia (F00 - F03). It should be noted: In the presence of dementia, dual codes can be used. F05.10 Delirium due to dementia due to brain injury F05.11 Delirium due to dementia due to cerebrovascular disease F05.12 Delirium due to dementia due to epilepsy F05.13 Delirium due to dementia in connection with a neoplasm (tumor) of the brain F05.14 Delirium due to dementia due to human immunodeficiency virus (HIV) infection F05.15 Delirium due to dementia due to neurosyphilis F05.16 Delirium due to dementia in connection with other viral and bacterial neuroinfections F05.17 Delirium due to dementia due to other diseases F05.18 Delirium due to dementia due to mixed diseases F05.19 Delirium due to dementia due to unspecified disease/F05.8/ Other delirium Includes: - delirium of mixed etiology; - subacute state of confusion or delirium. It should be noted: This subheading should include cases where it is not possible to establish the presence or absence of dementia. F05.80 Other delirium due to brain injury F05.81 Other delirium due to cerebrovascular disease F05.82 Other delirium due to epilepsy F05.83 Other delirium in connection with a neoplasm (tumor) of the brain F05.84 Other delirium due to human immunodeficiency virus (HIV) infection F05.85 Other delirium related to neurosyphilis F05.86 Other delirium in connection with other viral and bacterial neuroinfections F05.87 Other delirium due to other diseases F05.88 Other delirium due to mixed diseases F05.89 Other delirium due to unspecified disease/F05.9/ Delirium, unspecified It should be noted: This subcategory includes cases that do not fully meet all the criteria for delirium described in ICD-10 (F05.-).

F05.90 Delirium unspecified

due to brain injury

F05.91 Delirium unspecified

/F06.0/ Organic hallucinosis

It is a disorder in which persistent or recurrent hallucinations, usually visual or auditory, occur when the mind is lucid and may or may not be recognized as such by the patient. A delusional interpretation of hallucinations may occur, but criticism is usually retained. Diagnostic guidelines In addition to the general criteria given in the introduction to F06, the presence of persistent or recurrent hallucinations of any kind is required; lack of clouded consciousness; lack of pronounced intellectual decline; no dominant mood disorder; absence of dominant delusional disorders. Includes: - dermatozoic delirium; - organic hallucinatory state (non-alcoholic). Excludes: - alcoholic hallucinosis (F10.52); - schizophrenia (F20.-).

F06.00 Hallucinosis due to brain injury

F06.01 Hallucinosis due to

with cerebrovascular disease

F06.02 Hallucinosis due to epilepsy

F06.03 Hallucinosis due to

with neoplasm (tumor) of the brain

F06.04 Hallucinosis due to

with human immunodeficiency virus (HIV)

F06.05 Hallucinosis due to neurosyphilis

F06.06 Hallucinosis due to

with other viral and bacterial neuroinfections

F06.07 Hallucinosis associated with other diseases

F06.08 Hallucinosis due to mixed diseases

F06.09 Hallucinosis due to disease unspecified

/F06.1/ Organic catatonic state

A disorder with reduced (stupor) or increased (arousal) psychomotor activity, accompanied by catatonic symptoms. Polar psychomotor disturbances may intermittent. It is not yet known whether the full range of catatonic disorders described in schizophrenia can also occur in organic conditions. Also, it has not yet been established whether an organic catatonic state can occur with clear consciousness, or whether it is always a manifestation of delirium followed by partial or total amnesia. Therefore, it is necessary to approach the establishment of this diagnosis with caution and to a clear delimitation of the condition from delirium. It is believed that encephalitis and poisoning carbon monoxide cause this syndrome more often than other organic causes. Diagnostic guidelines: The general criteria suggesting an organic etiology as outlined in the introduction to F06 must be met. In addition, there must be: a) either stupor (decrease or complete absence spontaneous movements, with partial or complete mutism, negativism and freezing); b) either agitation (general hypermobility with or without a tendency to aggression); c) or both states (rapidly, unexpectedly changing states of hypo- and hyperactivity). Other catatonic phenomena that increase the reliability of the diagnosis include stereotypy, waxy flexibility, and impulsive acts. Excludes: - catatonic schizophrenia (F20.2-); - dissociative stupor (F44.2); - sump NOS (R40.1). F06.10 Catatonic state due to brain injury F06.11 Catatonic state due to cerebral vascular disease F06.12 Catatonic state due to epilepsy F06.13 Catatonic state due to with neoplasm (tumor) of the brain F06.14 Catatonic state due to with human immunodeficiency virus (HIV) F06.15 Catatonic state due to neurosyphilis F06.16 Catatonic state due to with other viral and bacterial neuroinfections F06.17 Catatonic state due to other diseases F06.18 Catatonic state due to mixed diseases F06.19 Catatonic state due to unspecified disease /F06.2/ Organic delusional (schizophrenia-like) disorder A disorder in which persistent or recurrent delusions dominate the clinical picture. Delusions may be accompanied by hallucinations, but are not tied to their content. Schizophrenic-like clinical symptoms may also be present, such as fanciful delusions, hallucinations, or thought disturbances. Diagnostic guidelines: The general criteria suggesting an organic etiology as outlined in the introduction to F06 must be met. In addition, there must be delusions (persecution, jealousy, exposure, illness or death of the patient or another person). Hallucinations, thought disturbances, or isolated catatonic phenomena may be present. Consciousness and memory should not be upset. The diagnosis of organic delusional disorder should not be made in cases where the organic cause is nonspecific or supported by limited evidence, such as cerebral ventricular enlargement (visually marked on axial computed tomography) or "mild" neurological signs. Included: - paranoid or hallucinatory-paranoid organic states. Excludes: - acute and transient psychotic disorders (F23.-); - drug-related psychotic disorders (F1x.5-); - chronic delusional disorder (F22.-); - schizophrenia (F20.-). F06.20 Delusional (schizophrenia-like) disorder due to brain injury F06.21 Delusional (schizophrenia-like) disorder due to cerebrovascular disease F06.22 Delusional (schizophrenia-like) disorder due to epilepsy Includes: - schizophrenia-like psychosis in epilepsy. F06.23 Delusional (schizophrenia-like) disorder in connection with a neoplasm (tumor) of the brain F06.24 Delusional (schizophrenia-like) disorder due to human immunodeficiency virus (HIV) infection F06.25 Delusional (schizophrenia-like) disorder due to neurosyphilis F06.26 Delusional (schizophrenia-like) disorder in connection with other viral and bacterial neuroinfections F06.27 Delusional (schizophrenia-like) disorder due to other disorders F06.28 Delusional (schizophrenia-like) disorder due to mixed illness F06.29 Delusional (schizophrenia-like) disorder due to disease unspecified /F06.3/ Organic mood disorders (affective) Disorders characterized by changes in mood, usually accompanied by a change in the level of general activity. The only criterion for inclusion of such disorders in this section is that they are presumably directly related to a cerebral or physical disorder, the presence of which must be demonstrated by an independent method (for example, by adequate physical and laboratory research) or on the basis of adequate anamnestic information. Affective disturbances should follow the discovery of the putative organic factor. Such mood changes should not be regarded as an emotional response of the patient to the news of the disease or as symptoms of concomitant (affective disorders) brain disease. Post-infection depression (following influenza) is a common example and should be coded here. Persistent mild euphoria not reaching the level of hypomania (which is sometimes seen, for example, with steroid therapy or antidepressant treatment) should not be reported under this section, but under F06.8-. Diagnostic guidelines In addition to the general criteria for organic etiology set out in the introduction to F06, the condition must meet the diagnostic requirements of F30-F33. It should be noted: To specify a clinical disorder, it is necessary to use 5-digit codes in which these disorders are divided into psychotic and non-psychotic disorders, unipolar (depressive or manic) and bipolar. /F06.30/ Psychotic manic disorder of organic nature; /F06.31/ psychotic bipolar disorder of an organic nature; /F06.32/ psychotic depressive disorder of an organic nature; / F06.33 / psychotic mixed disorder of an organic nature; /F06.34/ hypomanic disorder of an organic nature; / F06.35 / non-psychotic bipolar disorder of organic nature; /F06.36/ non-psychotic depressive disorder of an organic nature; / F06.37 / non-psychotic mixed disorder of an organic nature. Excludes: - mood disorders (affective), inorganic or unspecified (F30 - F39); - right hemispheric affective disorders (F07.8x).

/F06.30/ Psychotic manic disorder

organic nature

F06.300 Psychotic manic disorder due to brain injury F06.301 Psychotic manic disorder due to cerebrovascular disease F06.302 Psychotic manic disorder due to epilepsy F06.303 Psychotic manic disorder in connection with a neoplasm (tumor) of the brain F06.304 Psychotic manic disorder due to the human immunodeficiency virus (HIV)

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170

The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.

With amendments and additions by WHO.

Processing and translation of changes © mkb-10.com

ICD 10 codes residual encephalopathy

Residual organic lesion of the CNS

Residual-organic damage to the central nervous system - the consequences of structural damage to the brain and spinal cord of the perinatal period. This period corresponds to the period from 154 days of gestation (22 weeks), when the fetal weight reaches 500 g, to the seventh day after birth. Given the modern possibilities of nursing newborns, it is believed that from now on the child remains viable even with premature birth. However, it remains vulnerable to a variety of pathological effects that can adversely affect the functioning of the nervous system.

Origin of residual-organic pathology of the CNS

Factors that adversely affect the development of the fetus and newborn include:

• chromosomal diseases (mutations and consequences of gametopathies);
• physical factors (poor ecology, radiation, lack of oxygen consumption);
• chemical factors (use of medicines, household chemicals, chronic and acute intoxication with alcohol and drugs);
• malnutrition (starvation, vitamin and mineral depletion of the diet, protein deficiency);
• diseases of a woman (acute and chronic diseases of the mother);
• pathological conditions during pregnancy (preeclampsia, damage to the child's place, anomalies of the umbilical cord);
• deviations in the course of labor (birth weakness, rapid or prolonged labor, premature detachment of the placenta).

Under the influence of these factors, tissue differentiation is disrupted, and fetopathy, intrauterine growth retardation, prematurity are formed, which can subsequently provoke an organic lesion of the central nervous system. The following perinatal pathology leads to the consequences of organic lesions of the central nervous system:

Clinical manifestations of residual CNS damage

Clinically, organic damage to the central nervous system in children manifests itself from the first days of life. Already at the first examination, a neurologist can find external signs of brain suffering - tonic disorders, tremor of the chin and arms, general anxiety, and a delay in the formation of voluntary movements. With a gross lesion of the brain, focal neurological symptoms are detected.

Sometimes signs of brain damage are detected only during additional examination methods (for example, neurosonography). In this case, they speak of a clinically silent course of perinatal pathology.

Important! In cases where there are no clinical symptoms of organic pathology of the brain, damage to the nervous system, detected using instrumental diagnostic methods, does not require treatment. All that is needed is dynamic observation and repeated studies.

Residual damage to the central nervous system in children is manifested by:

• cerebrasthenic syndrome (rapid exhaustion, unreasonable fatigue, mood lability, lack of adaptation to mental and physical stress, tearfulness, irritability, capriciousness);
• neurosis-like syndrome (tics, enuresis, phobias);
• encephalopathy (decrease in cognitive functions, scattered focal neurological symptoms);
• psychopathy (phenomena of affect, aggressive behavior, disinhibition, reduced criticism);
• organic-psychic infantilism (apato-abulic manifestations, suppression, list, formation of addictions);
• minimal brain dysfunction (motor hyperactivity disorder with attention deficit).

A detailed decoding of the syndromes can be obtained by watching the thematic video.

Treatment of residual CNS damage

Monitoring of patients with the consequences of an organic CNS lesion, the treatment of which implies a rather long process, should be comprehensive. Taking into account the progression of the disease and the subtype of its course, a personal selection of therapy for each patient is necessary. Comprehensive monitoring is based on the involvement of doctors, relatives and, if possible, friends, teachers, psychologists, and patients themselves in the correction process.

The main areas of treatment include:

• medical supervision of the general condition of the child;
• regular examination by a neurologist using neuropsychological techniques, testing;
• drug therapy (psychostimulants, neuroleptics, tranquilizers, sedatives, nootropics, vasoactive drugs, vitamin and mineral complexes);
• non-drug correction (massage, kinesitherapy, physiotherapy, acupuncture);
• neuropsychological rehabilitation (including correction of speech disorders);
• psychotherapeutic impact on the environment of the child;
• work with teachers in educational institutions and organization of special education.

Important! Comprehensive treatment from the first years of a child's life will help to significantly improve the effectiveness of rehabilitation.

Residual-organic damage to the nervous system is more clearly identified as it matures. They directly correlate with the time and duration of the impact of the damaging factor on the central nervous system.

Residual effects of brain damage in the perinatal period may predispose to the development of cerebral diseases and form a model of deviant behavior. Timely and competent treatment will stop the symptoms, restore the full functioning of the nervous system and socialize the child.

Residual organic lesion of the central nervous system in children and adults

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 the brain is dystrophic changes- 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 cause of 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

To identify residual-organic lesion of the central nervous system in children without instrumental methods surveys are quite difficult. 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 drawn to characteristics infant pathology:

• involuntary trembling 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:

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• 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.

What diagnostic procedures will confirm the diagnosis?

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

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, hypnotics, neuroleptics, 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 may develop, spasm of the respiratory muscles, malfunction of the center that controls the work of cardio-vascular system. 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.

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Residual-organic lesion of the central nervous system is a formidable and, unfortunately, a very common diagnosis. It indicates a congenital inferiority of brain tissue. But if no complaints and symptoms occur with such a violation, then treatment is not required. This is exactly the case when time can work not against, but for the patient. Many people who had such a problem in childhood or adolescence do not feel its effects in adulthood.

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MKB 10 residual organic lesion of the central nervous system

The CNS is the main regulator of the entire body. Indeed, in the cortical structures of the brain there are departments that are 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. Most often, pathologies develop in the first year of a child's life, but they 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 is known, the CNS is a 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, the 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 general condition patient. Sometimes residual-organic CNS damage occurs in adults. Most 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 site of injury. After all, each of the brain structures must perform certain functions.

Causes of residual organic brain damage in children

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

• genetic predisposition. If the parents have any psycho-emotional deviations, then the risk of developing 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 Down's disease, Shershevsky-Turner syndrome, Patau, etc. arise.
• Influence 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. Particularly dangerous for the condition of the fetus are late gestosis (pre - eclampsia).
• Violation of the 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 head trauma early age. Also, risk factors include the use of 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, but they are present in some patients. Often the cause of such episodes are injuries received in early childhood. At the same time, neuropsychiatric disorders are long-term effects. 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 for brain tumors, which are removed with the capture of adjacent 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 prolonged use of opioids, 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 during fetal development. 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, childbirth ahead of schedule gestation. 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 damage to the central nervous system

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

• Cerebrosthenic syndrome. Its manifestations are considered to be increased fatigue, poor mastering of the school curriculum, general weakness, tearfulness, mood changes.
• neurotic syndrome. It is characterized by the development of phobias, enuresis (involuntary urination at night), motor excitation (tics).
• Syndrome of hyperactivity and attention deficit. It is observed in children of primary and secondary school age.
• encephalopathy. The main manifestations are sleep disturbances, memory loss, perseverance. In severe cases, focal neurological symptoms, convulsions are observed.
• Psychopathies. Characterized by disobedience, aggressiveness. In adulthood - mood lability, hysterical reactions, antisocial behavior.

Most often, cerebral hypoxia leads to scattered symptoms, when the listed syndromes are combined with each other, they are not very pronounced. The predominance of focal symptoms is rare.

Clinical picture with CNS damage

Most often, the symptoms of residual organic damage to the central nervous system appear some time after exposure to an adverse factor. With perinatal fetal hypoxia, violations can be noticeable already in the first month of life. Depending on the degree of damage, the following symptoms may be observed:

• Slight damage to the nervous tissue: tearfulness, bad dream, memory loss. At school age, a child may experience attention deficit hyperactivity disorder, a tendency to hysterical states, phobias.
• Damage to the central nervous system of moderate severity has such manifestations as constant crying, refusal of the breast, convulsive syndrome, enuresis.
• In severe cases, focal neurological symptoms are observed. It includes muscle weakness, paresis and paralysis of the limbs, delayed physical and mental development, generalized convulsions, etc.

Residual organic lesion of the central nervous system: ICD-10 code

Like all pathologies, disorders of neuropsychic development have a certain code in the international classification of diseases. It is worth understanding the vastness of the concept of "residual-organic lesion of the central nervous system." The code (ICD-10) for this pathology is G96.9. This code means the diagnosis "lesion of the central nervous system, unspecified." In more specific cases, the ICD-10 code is changed to a specific nosology.

Residual organic lesion of the central nervous system: treatment of pathology

Treatment of residual-organic lesions is aimed at strengthening the nervous system, the rehabilitation of a person in society. It is important to understand that the patient's relatives must be patient. With the right approach, treatment can significantly improve the prognosis of the disease. As drug therapy apply nootropic, sedative drugs, antipsychotics, tranquilizers and psychostimulants. To improve cerebral circulation, solutions "Piracetam", "Curantil", "Cerebrolysin" are prescribed. Physiotherapeutic treatment, massage, bioacoustic correction of the brain are also shown.

What are the consequences of residual organic damage?

The consequences of residual-organic damage to the central nervous system 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 with residual-organic lesion

Treatment should be started as soon as an appropriate diagnosis of "residual-organic lesion of the CNS" is established. 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, please contact medical care. It is also worth refraining from taking medications, bad habits.

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Benign intracranial hypertension. Residual-organic state of the CNS

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)

Version: Archive - Clinical protocols Ministry of Health of the Republic of Kazakhstan (Order No. 239)

general information

Short description

Idiopathic (benign) intracranial hypertension is characterized by increased intracranial pressure in the absence of evidence of mass formation or hydrocephalus. Typical symptoms are headache and disc swelling optic nerves. Occasionally, the fundus is not changed. In most cases, the etiology remains unknown. Focal neurological symptoms absent, except in rare cases. Increased CSF pressure, confirmed by lumbar puncture, congestive optic discs, with normal or slightly enlarged ventricles, detected by CT or MRI of the head, and normal CSF composition.

The residual-organic state of the brain is a large group of nervous and mental disorders of various etiology, structure and severity, which are the result of previously transferred organic brain damage at different stages of ontogenesis (including intrauterine). Due to the special reactivity and vulnerability of the nervous system during its formation, intensive differentiation and myelination, the causes of these disorders are not only trauma, inflammatory diseases of the brain, but also somatic, endocrine teratogenic factors of the prenatal period, malnutrition, hypovitaminosis, allergies, etc. .d.

The general main sign of residual organic damage to the nervous system is the absence of progression, the progression of the course with mild injuries due to the phenomena of reparation, compensation, and positive evolutionary dynamics characteristic of the child's body. Non-severe residual-organic damage to the nervous system smoothes out with age and passes into a state of asymptomatic residual-organic insufficiency or becomes a factor in the development of a number of diseases (epilepsy, psychopathy, etc.). However, residual organic damage to the nervous system can also be decompensated under the influence of additional hazards (trauma, intoxication, helminthic invasions, overwork, overheating) in critical age periods, revealing the failure of certain systems (speech, endocrine).

Protocol "Benign intracranial hypertension. Residual organic state of the CNS"

Classification

Classification of etiological factors of idiopathic intracranial hypertension

Endocrine and metabolic disorders:

Obesity and menstrual dysfunction;

Pregnancy and the postpartum period (without sinus thrombosis);

Overdose of female sex hormones;

Adrenal steroid withdrawal syndrome;

Intracranial thrombosis of the venous sinuses with:

Consequences of a head injury;

Pregnancy and in the postpartum period;

Use of oral contraceptives;

Primary (idiopathic) sinus thrombosis.

Hematological disorders and connective tissue diseases:

Systemic lupus erythematosus.

Tumors of the spinal cord;

Meningism in systemic bacterial or viral infections.

Syndrome of an empty Turkish saddle.

Rapid growth in early childhood.

The classification of residual organic damage to the nervous system is based on the predominant pathological factor (dysontogenetic or encephalopathic) and the underlying syndrome.

Predominantly dysontogenetic forms

1. Syndromes of impaired development of individual brain systems: speech (delayed speech development, underdevelopment of speech like alalia), psychomotor (delayed development of general and fine motor skills), spatial representations, "school skills" (dyslexia, dysgraphia, dyscalculia), primary (dysontogenetic ) enuresis.

2. Syndromes of mental and psychophysical infantilism (simple and complex).

3. Syndrome of "organic autism".

4. Syndrome of residual oligophrenia (with a uniform defect structure).

Mostly encephalopathic forms:

1. Cerebrosthenic syndromes.

2. Neurosis-like (non-procedural) syndromes: depressive-dysthymic, neurosis-like fears, senestopathic-hypochondriac, hysteriform, systemic motor and somatovegetative disorders (neurosis-like stuttering and stumbling, tics, secondary neurosis-like enuresis, neurosis-like disorders of sleep, appetite, etc.).

3. Psycho-like syndromes: increased affective excitability, mental instability, impulsive-epileptoid.

4. Diencephalic (hypothalamic) syndromes: cerebro-endocrine syndromes (violation of the pace of puberty, Itsenko-Cushing, adiposogenital dystrophy, cerebral dwarfism, etc.), vegetative-vascular, violation of thermoregulation, neuro-trophic disorders, neuromuscular.

5. Hydrocephalus syndrome (congenital and acquired).

6. Epileptiform syndromes (convulsive and non-convulsive).

7. Syndromes of residual organic dementia.

8. Periodic psychosis in adolescents.

Forms of mixed (encephalopathic-dysontogenetic) pathogenesis:

1. Cerebral palsy.

2. Atypical residual oligophrenia.

3. Hyperdynamic syndrome.

Diagnostics

Complaints and anamnesis: complaints of frequent headaches, which are localized more often in the forehead and neck, less often in the temporal and parietal regions, are accompanied by nausea, sometimes vomiting, which brings relief; dizziness, weakness, fatigue, irritability, disturbed, restless sleep. Meteorological dependence, emotional lability, decreased memory, attention.

Physical examination: a study of the psycho-emotional sphere, neurological status, autonomic nervous system reveals functional disorders of the nervous system, emotional lability, cerebroasthenia phenomena, and sometimes organic damage to the central nervous system.

Laboratory studies: KLA, OAM, biochemical blood test.

1. Radiography - according to indications for the detection of pathology of the bones of the skull.

2. EEG - electroencephalography, a method of recording brain biocurrents, a study of background EEG, with hyperventilation and photostimulation. Changes in the electrical activity of the brain in patients with residual organic lesions of the nervous system are nonspecific. Usually they manifest themselves as a violation of the regularity of the main rhythm, unevenness of its frequency and amplitude, violation of zonal differences, the presence of slow waves.

3. USDG of vessels brain - for clarification vascular pathology of the brain, in which basin the catastrophe occurred - in the vertebrobasilar basin or in the basin of the carotid arteries, and which ones.

4. Neurosonography - according to indications to confirm intracranial hypertension.

5. CT scan of the brain reveals the majority of supratentorial and part of infratentorial lesions that can cause papilledema. It is especially important to assess the condition of the cerebral sinuses. The size of the ventricles of the brain is reduced or normal. Ventricular enlargement indicates hydrocephalus and thus excludes the diagnosis of idiopathic intracranial hypertension.

6. MRI is particularly useful in diagnosing sinus venous obstruction, which can be confused with idiopathic intracranial hypertension.

If the above methods did not reveal pathology and there are no focal neurological symptoms, then, despite the swelling of the optic nerves, lumbar puncture is safe. The diagnosis of idiopathic intracranial hypertension is confirmed if the CSF pressure is elevated (usually DOMM H2O) but its composition is normal. Any changes in CSF (cellular composition, protein or glucose content) serve as indications for additional examination.

If CT or MRI reveals changes, extreme caution is required during LP.

Indications for specialist consultations: ophthalmologist, speech therapist, neurosurgeon, orthopedist, psychologist, ENT, audiologist.

Minimum examinations when referring to a hospital:

1. General analysis blood.

2. General analysis of urine.

3. Feces on the eggs of the worm.

The main diagnostic measures:

1. Complete blood count.

2. General analysis of urine.

3. CT or MRI of the brain.

List of additional diagnostic measures:

Organic lesion of the central nervous system

Organic damage to the central nervous system is a pathology that consists in the death of neurons in the brain or spinal cord, necrosis of the tissues of the central nervous system or their progressive degradation, due to which the central nervous system of a person becomes defective and cannot adequately perform its functions in ensuring the functioning of the body , motor activity of the body, as well as mental activity.

An organic lesion of the central nervous system has another name - encephalopathy. It can be a congenital or acquired disease due to a negative effect on the nervous system.

Acquired can develop in people of any age due to various injuries, poisoning, alcohol or drug addiction, infectious diseases, exposure, and similar factors.

Congenital or residual - damage to the organs of the central nervous system of the child, inherited due to genetic failures, impaired fetal development in the perinatal period (the period between one hundred and fifty-fourth day of pregnancy and the seventh day of extrauterine existence), as well as due to birth trauma.

Classification

The classification of lesions depends on the cause of the development of pathology:

• Discirculatory - caused by a violation of the blood supply.
• Ischemic - dyscirculatory organic lesion, supplemented by destructive processes in specific foci.
• Toxic - cell death due to toxins (poisons).
• Radiation - radiation damage.
• Perinatal-hypoxic - due to fetal hypoxia.
• Mixed type.
• Residual - obtained due to a violation of intrauterine development or birth trauma.

Causes of acquired organic brain damage

It is not at all difficult to acquire damage to the cells of the spinal cord or brain, since they are very sensitive to any negative impact, but most often it develops for the following reasons:

• Spinal injury or traumatic brain injury.
• Toxic damage, including alcohol, drugs, drugs and psychotropic drugs.
• Vascular diseases that cause circulatory disorders, and with it hypoxia or nutritional deficiencies, or tissue injury, such as stroke.
• Infectious diseases.

It is possible to understand the reason for the development of one or another type of organic lesion, based on the name of its variety, as mentioned above, it is on the reasons that the classification of this disease is based.

How and why residual CNS damage occurs in children

Residual organic damage to the central nervous system in a child occurs due to a negative impact on the development of his nervous system, or due to hereditary genetic abnormalities or birth injuries.

The mechanisms of development of a hereditary residual organic lesion are exactly the same as in any hereditary diseases, when the distortion of hereditary information due to DNA breakdowns leads to an abnormal development of the child's nervous system or the structures that ensure its vital activity.

An intermediate process to a non-hereditary pathology looks like a failure in the formation of cells or even entire organs of the spinal cord and brain due to negative environmental influences:

• Severe illnesses suffered by the mother during pregnancy, as well as viral infections. Even the flu or a simple cold can provoke the development of a residual organic lesion of the central nervous system of the fetus.
• Lack of nutrients, minerals and vitamins.
• Toxic effects, including drugs.
• Maternal bad habits, especially smoking, alcoholism and drugs.
• Bad ecology.
• Irradiation.
• Fetal hypoxia.
• The physical immaturity of the mother, or, conversely, the advanced age of the parents.
• The use of special sports nutrition or some dietary supplements.
• Strong stress.

The mechanism of the influence of stress on premature birth or miscarriage by convulsive contraction of its walls is clear, not many people understand how mother's stress leads to the death of the fetus or disruption of its development.

With strong or systematic stress, the mother's nervous system suffers, which is responsible for all processes in her body, including the life support of the fetus. With a violation of its activity, a variety of failures and the development of vegetative syndromes can occur - violations of the functions of internal organs, due to which the balance in the body, which ensures the development and survival of the fetus, is destroyed.

Traumatic injuries of a different nature during childbirth, which can cause organic damage to the central nervous system of the child, are also very different:

• Asphyxia.
• Injury to the spine or base of the skull in case of improper removal with twisting of the child from the uterus.
• The fall of a child.
• premature birth.
• Atony of the uterus (the uterus is unable to contract normally and push the baby out).
• Head squeezing.
• Entry of amniotic fluid into the respiratory tract.

Even in the perinatal period, the child can become infected with various infections both from the mother during childbirth and hospital strains.

Symptoms

Any lesion of the central nervous system has symptoms in the form of impaired mental activity, reflexes, motor activity and impaired functioning of internal organs and sensory organs.

It is rather difficult even for a professional to immediately see the symptoms of a residual organic CNS lesion in an infant, since the movements of infants are specific, mental activity is not immediately determined, and it is possible to notice disturbances in the functioning of internal organs with the naked eye only with severe pathologies. But sometimes clinical manifestations can be seen from the first days of life:

• Violation of muscle tone.
• Tremor of the limbs and head (most often, tremor in newborns is benign in nature, but can also be a symptom of neurological diseases).
• Paralysis.
• reflex disorder.
• Chaotic rapid eye movements back and forth or a frozen look.
• Violation of the functions of the sense organs.
• epileptic seizures.

At an older age, somewhere from three months, the following symptoms can be noticed:

• Violation of mental activity: the child does not follow toys, shows hyperactivity or vice versa - apathy, suffers from a lack of attention, does not recognize acquaintances, etc.
• Delay in physical development, both directly growth and acquisition of skills: does not hold his head, does not crawl, does not coordinate movements, does not try to stand up.
• Rapid physical and mental fatigue.
• Emotional instability, capriciousness.
• Psychopathy (tendency to affects, aggression, disinhibition, inadequate reactions).
• Organic-psychic infantilism, expressed in the suppression of the personality, the formation of addictions and increased awareness.
• Impaired coordination.
• Memory impairment.

If the child has a suspected CNS lesion

If any symptoms of a violation of the central nervous system in a child appear, you should immediately contact a neurologist and undergo a comprehensive examination, which may include the following procedures:

• General analyzes, various types of tomography (each type of tomography examines from its own side and therefore gives different results).
• Fontanelle ultrasound.
• EEG is an electroencephalogram that allows you to determine the foci of pathological activity of the brain.
• X-ray.
• Liquor analysis.
• Neurosonography is an analysis of the conduction of neurons, which helps to detect small hemorrhages or disturbances in the functioning of peripheral nerves.

If you suspect any deviations in the health of your child, you should consult a doctor as soon as possible, since timely treatment will help to avoid a huge number of problems, and will also significantly reduce the recovery time. Do not be afraid of false suspicions and unnecessary examination, since they, unlike probable pathologies, will not harm the baby.

Sometimes the diagnosis of this pathology occurs even during fetal development at a scheduled ultrasound examination.

Methods of treatment and rehabilitation

The treatment of the disease is quite laborious and lengthy, however, with minor injuries and competent therapy, the congenital residual organic lesion of the central nervous system in newborns can be completely eliminated, since the nerve cells of infants are able to divide for some time, and the entire nervous system of young children is very flexible.

• First of all, with this pathology, constant monitoring by a neurologist and the attentive attitude of the parents themselves are required.
• If necessary, drug therapy is carried out both to eliminate the root cause of the disease, and in the form of symptomatic treatment: removal of a convulsive symptom, nervous excitability, etc.
• At the same time, as a method of treatment or recovery, physiotherapy is carried out, which includes massage, acupuncture, zootherapy, swimming, gymnastics, reflexology or other methods designed to stimulate the nervous system, encourage it to begin recovery by forming new neural connections and teach the child himself to use his body in case of violation of motor activity, in order to minimize its inferiority to independent life.
• At a later age, psychotherapeutic influences are applied both on the child himself and on his immediate environment in order to improve the moral situation around the child and prevent the development of mental deviations in him.
• Speech correction.
• Specialized education tailored to the individual needs of the child.

Conservative treatment is carried out in a hospital and consists in taking medications in the form of injections. These drugs reduce cerebral edema, seizure activity and improve blood circulation. Almost everyone is prescribed piracetam or drugs with a similar effect: pantogam, caviton or phenotropil.

In addition to the main drugs, symptomatic relief of the condition is carried out with the help of sedatives, painkillers, which improve digestion, stabilize the heart and reduce any other negative manifestations of the disease.

After eliminating the cause of the disease, the therapy of its consequences is carried out, designed to restore the functions of the brain, and with them the work of internal organs and motor activity. If it is impossible to completely eliminate residual manifestations, the goal of rehabilitation therapy is to teach the patient to live with his body, use his limbs and self-service as much as possible.

Many parents underestimate the benefits of physiotherapy in the treatment of neurological ailments, but they are the fundamental methods to restore lost or impaired functions.

The recovery period is extremely long, and ideally lasts a lifetime, since if the nervous system is damaged, the patient has to overcome himself every day. With due diligence and patience, by a certain age, a child with encephalopathy can become completely independent and even lead an active lifestyle, the maximum possible with the level of his defeat.

It is impossible to cure the pathology on your own, and with mistakes made due to a lack of medical education, you can not only exacerbate the situation at times, but even get a fatal outcome. Cooperation with a neurologist in people with encephalopathy becomes lifelong, but no one forbids the use of alternative methods of therapy.

Alternative methods of treatment of organic lesions of the central nervous system are the most effective methods of recovery that do not replace conservative treatment with physiotherapy, but complement it very qualitatively. Only when choosing one or another method, again, consultation with a doctor is necessary, since it is extremely difficult to distinguish useful and effective methods from useless and harmful without deep specialized medical knowledge, as well as minimal chemical literacy.

If it is impossible to visit specialized institutions in order to take a course of exercise therapy, massage and aqua therapy, they can be easily carried out at home, having mastered simple techniques with the help of a neurologist's consultation.

An equally important aspect of treatment is social rehabilitation with psychological adaptation of the patient. You should not unnecessarily patronize a sick child, helping him in everything, because otherwise he will not be able to fully develop, and as a result, he will not be able to fight the pathology. Help is needed only in vital things or special cases. In everyday life, doing daily chores on your own will work as an additional physical therapy or exercise therapy, and will also teach the child to overcome difficulties and that patience and perseverance always lead to excellent results.

Effects

Organic damage to the central nervous system in the perinatal period or at an older age leads to the development of a large number of various neurological syndromes:

• Hypertensive-hydrocephalic - hydrocephalus, accompanied by an increase in intracranial pressure. It is determined in infants by an increase in the fontanel, its swelling or pulsation.
• Hyperexcitability syndrome - increased muscle tone, sleep disturbance, increased activity, frequent crying, high convulsive readiness or epilepsy.
• Epilepsy is a convulsive syndrome.
• Coma syndrome with opposite symptoms of hyperexcitability, when the child is lethargic, lethargic, moves little, lack of sucking, swallowing or other reflexes.
• Vegetative-visceral dysfunction of the internal organs, which can be expressed as frequent regurgitation, digestive disorders, skin manifestations, and many other abnormalities.
• Movement disorders.
• Cerebral palsy - movement disorders complicated by other defects, including mental retardation and weakness of the senses.
• Hyperactivity is the inability to concentrate and attention deficit.
• Retardation in mental or physical development, or complex.
• Mental illness against the background of disorders of the brain.
• Psychological ailments due to the discomfort of the patient among society or physical inferiority.

• Endocrine disorders, and as a result, a decrease in immunity.

Forecast

The prognosis of an acquired organic lesion of the central nervous system is rather fuzzy, since everything depends on the level of damage. In the case of a congenital type of disease, in some cases the prognosis is more favorable, since the child’s nervous system recovers many times faster, and his body adapts to it.

After well-conducted treatment and rehabilitation, the function of the central nervous system can be either completely restored or have any residual syndrome.

The consequences of early organic damage to the central nervous system often lead to mental and physical retardation in development, and also lead to disability.

On the positive side, many parents whose children received this terrible diagnosis, with the help of intensive rehabilitation therapy, achieve magical results, refuting the most pessimistic forecasts of doctors, providing their child with a normal future.

The information on the site is provided for informational purposes only, does not claim to be reference and medical accuracy, and is not a guide to action. Do not self-medicate. Consult with your physician.