Injuries to the central nervous system. Damage to the central nervous system, causes, symptoms

Every expectant mother is afraid of the pathologies of pregnancy and childbirth and wants to prevent them.

One of these pathologies is fetal hypoxia and hypoxia during childbirth, which can lead to disruptions in the functioning of many organs and tissues, including the brain.

The consequences of such damage can last a long time, sometimes throughout life.

Causes of hypoxic damage to the central nervous system in a newborn

The central nervous system is the first to suffer from a lack of oxygen, which can be caused by various factors during pregnancy and childbirth. It can be:

During pregnancy:

Preeclampsia in late stages;

Premature placental abruption, threat of miscarriage;

Heart defects in mother and fetus;

Anemia in mother;

Lack or excess of amniotic fluid;

Maternal intoxication (drug, occupational, smoking);

Rhesus conflict between mother and fetus;

Infectious diseases of the mother;

During childbirth:

Entanglement of the umbilical cord around the fetal neck;

Weakness of labor;

Prolonged labor;

Maternal bleeding;

Birth injuries to the neck.

As you can see, most of the dangerous factors affect the health of the baby even before birth, and only a few - during childbirth.

Excess weight, chronic diseases of the mother, or her too young or too mature age (under 18 or over 35) can aggravate the course of pregnancy pathologies leading to hypoxic damage to the central nervous system in the newborn. And with any type of hypoxia, the brain is affected first.

Symptoms of Brain Damage

In the first hours and days after birth signs of disorders of the cardiovascular system come to the fore, and symptoms of hypoxic damage to the central nervous system begin to manifest themselves later.

If brain damage is caused by pregnancy pathology, the baby may be lethargic and have weakened or completely absent reflexes that a healthy newborn should have. If there is a pathology that occurs during childbirth, the baby does not immediately begin to breathe after birth, the skin has a bluish tint, and the respiratory rate is lower than normal. And in the same way, physiological reflexes will be reduced - based on these signs, oxygen starvation can be suspected.

At an older age brain hypoxia, if it was not cured on time, manifests itself as a slowdown in psycho-emotional development up to severe forms of dementia, and motor disorders. In this case, the presence of organic pathology is possible - brain cysts, hydrocephalus (especially often occurs with intrauterine infections). Severe brain hypoxia can be fatal.

Diagnosis of hypoxic damage to the central nervous system in a newborn

The first diagnostic procedure, which is carried out for all newborns immediately after birth, is to assess their condition using the Apgar scale, which takes into account vital signs such as breathing, heartbeat, skin condition, muscle tone and reflexes. A healthy child scores 9-10 points on the Apgar scale; signs of hypoxic damage to the central nervous system can significantly reduce this indicator, which should be the reason for more accurate examinations.

Doppler ultrasound allows you to assess the condition of the blood vessels of the brain and identify their congenital anomalies, which can become one of the causes of hypoxia in the fetus and newborn.

Ultrasound, CT and MRI of the brain can identify various organic pathologies of the nervous system - cysts, hydrocephalus, areas of ischemia, underdevelopment of certain parts, tumors. The difference in the operating principles of these methods allows us to see the most complete picture of brain damage.

To assess damage to the functions of the nervous system, neurography and myography are used - these are methods based on the effect of electric current on muscle and nervous tissue, and allow us to monitor how different parts of the nerves and muscles react to it. In the case of congenital hypoxic damage to the central nervous system in a newborn, this method allows us to understand how damaged the peripheral nervous system is, and how great are the child’s chances for full physical development in this case.

Additionally, a biochemical blood test and urine test are prescribed to identify biochemical disorders associated with brain hypoxia.

Treatment of hypoxia in newborns

Treatment for hypoxic brain injury depends on its cause and severity. If hypoxia occurs during childbirth and is not accompanied by organic pathology of the brain, blood vessels, heart, lungs or spine, then, depending on the degree, it can either go away on its own within a few hours (mild form, 7-8 Apgar), or require treatment in an oxygen chamber with normal or increased pressure (hyperbaric oxygenation).

Organic pathology that causes constant brain hypoxia (heart defects, respiratory system, neck injuries) is usually treated surgically. The question of the possibility of surgery and its timing depends on the condition of the child. The same applies to organic pathology of the brain (cysts, hydrocephalus), which occurs as a consequence of intrauterine fetal hypoxia. In most cases, the earlier the operation is performed, the greater the child’s chances for full development.

Prevention of hypoxic brain damage

Since the consequences of intrauterine fetal hypoxia are extremely destructive for the child’s brain in the future, a pregnant woman needs to be very careful about her health. It is necessary to minimize the impact of factors that can disrupt the normal course of pregnancy - avoid stress, eat well, exercise in moderation, give up alcohol and smoking, and attend antenatal clinics on time.

In case of severe gestosis, as well as when signs of premature placental abruption and the threat of miscarriage appear - abdominal pain, bleeding from the genital tract, a sharp decrease in blood pressure, sudden nausea and vomiting for no reason - you should immediately consult a doctor. It may be recommended to go into conservation - this recommendation should not be neglected. A set of therapeutic measures carried out in the hospital will help avoid severe fetal hypoxia and its consequences in the form of congenital brain pathologies.

Ultrasound, which is done in the last weeks of pregnancy, allows us to identify such potentially dangerous conditions as entanglement in the umbilical cord, which during childbirth can prevent the baby from taking its first breath, pelvic or lateral presentation, which is also dangerous because hypoxia of the newborn will develop during childbirth. To correct dangerous presentation, there are sets of exercises, and if they are ineffective, a caesarean section is recommended. It is also recommended for entwined umbilical cords.

Measuring the size of the fetus and the woman's pelvis allows us to determine an anatomically and clinically narrow pelvis - a discrepancy between the size of the pelvis and the size of the child's head. In this case, giving birth naturally will be very traumatic for both mother and child, or may be completely impossible. The safest method of delivery in this case is cesarean section.

During childbirth, it is imperative to monitor the intensity of contractions - if it becomes insufficient for rapid delivery, labor is induced. Prolonged stay of the fetus in the birth canal can lead to the development of cerebral hypoxia, since the placenta no longer supplies its body with oxygen, and the first breath is possible only after birth. Physical exercises to prepare for childbirth can help you avoid this condition.

Organic damage to the central nervous system (CNS) is a diagnosis that indicates that the human brain is in an unstable state and is considered defective.

As a result of such lesions, dystrophic disorders, destruction and or necrotization occur in the brain. Organic damage is divided into several stages of development. The first stage is characteristic of most ordinary people, which is considered the norm. But the second and third require medical intervention.

Residual damage to the central nervous system is the same diagnosis, which shows that the disease appeared and persisted in a person during the perinatal period. Most often this affects infants.

From this we can draw an obvious conclusion. Residual organic damage to the central nervous system is a disorder of the brain or spinal cord that occurred while the child was still in the womb (at least 154 days from the date of conception) or within a week after his birth.

Mechanism of damage

One of all the “inconsistencies” of the disease is the fact that a disorder of this type belongs to neuropathology, but its symptoms may relate to other branches of medicine.

Due to an external factor, the mother experiences disruptions in the formation of the phenotype of cells that are responsible for the full list of functions of the central nervous system. As a result, fetal development is delayed. It is this process that can become the last link on the path to central nervous system disorders.

Regarding the spinal cord (this is also part of the central nervous system), corresponding lesions can appear as a result of incorrect obstetric care or inaccurate turns of the head when delivering the child.

Causes and risk factors

The perinatal period can also be called a “fragile period”, because during this time literally any unfavorable factor can cause the development of defects in the central nervous system of the infant or fetus.

For example, medical practice has cases that show that organic damage to the central nervous system is caused by the following reasons:

In addition, the development of pathological changes can be influenced by the use of various dietary supplements or sports nutrition. Their composition can have a detrimental effect on a person with certain characteristics of the body.

Classification of CNS lesions

Perinatal damage to the central nervous system is divided into several types:

Hypoxic-ischemic. Characterized by internal or postnatal lesions of the brain. Appears as a result of chronic asphyxia. Simply put, the main cause of such damage is oxygen deficiency in the fetal body ().
Traumatic. This is a type of injury that occurs to a newborn during childbirth.
Hypoxic-traumatic. This is a combination of oxygen deficiency with injury to the spinal cord and cervical spine.
Hypoxic-hemorrhagic. Such damage is characterized by trauma during childbirth, accompanied by a failure of blood circulation in the brain with subsequent hemorrhages.

Symptoms depending on severity

In children, residual organic damage is difficult to see with the naked eye, but an experienced neurologist, already at the first examination of the baby, will be able to determine the external signs of the disease.

Often this is an involuntary trembling of the chin and arms, a restless state of the baby (lack of tension in the skeletal muscles).

And, if the damage is severe, it can manifest itself as neurological symptoms:

paralysis of any limb;
disturbance of eye movements;
reflex failures;
loss of vision.

In some cases, symptoms can only be noticed after undergoing certain diagnostic procedures. This feature is called the silent course of the disease.

General symptoms of residual organic damage to the central nervous system:

unreasonable fatigue;
irritability;
aggression;
mental instability;
changeable mood;
decreased intellectual abilities;
constant mental anxiety;
inhibition of actions;
pronounced absent-mindedness.

In addition, the patient is characterized by symptoms of mental infantilism, brain dysfunction and personality disorders. As the disease progresses, the set of symptoms can be replenished with new pathologies, which, if left untreated, can lead to disability and, in the worst case, death.

Necessary set of measures

It is no secret that diseases of this degree of danger are difficult to cure using single methods. And even more so to eliminate residual organic damage to the central nervous system and it is even more necessary to prescribe complex treatment. Even with a combination of several therapy methods, the recovery process will take quite a long time.

To select the correct complex, you must strictly consult your doctor. Typically, the prescribed therapy includes the following set of measures.

Treatment with various medications:

psychotropic drugs;
antipsychotics;

External correction (treatment with external stimulation):

massage;
physiotherapy (laser therapy, myostimulation, electrophoresis, etc.);
reflexology and acupuncture.

Neurocorrection methods

Neurocorrection is a psychological technique that is used to restore impaired and lost functions of the brain.

If there are speech defects or neuropsychic disorders, specialists involve a psychologist or speech therapist in treatment. And in case of manifestation of dementia, it is recommended to seek help from teachers of educational institutions.

In addition, the patient is registered with a neurologist. He must undergo regular examination by the doctor who is treating him. The doctor may prescribe new medications and other therapeutic measures as the need arises. Depending on the severity of the disease, the patient may require constant monitoring by family and friends.

We emphasize that treatment of residual organic damage to the central nervous system during the period of acute manifestation is carried out only in a hospital setting, and only under the supervision of a qualified specialist.

Remember! Timely treatment of organic damage to the central nervous system can stop the development of complications, reduce the consequences of the disease, eliminate symptoms and completely rehabilitate the human nervous system.

Rehabilitation is all in the hands of the mother and doctors

Rehabilitation measures for this disease, as well as for its treatment, should be prescribed by the attending physician. They are aimed at eliminating existing complications in accordance with the patient’s age.

For remaining movement disorders, physical methods are usually prescribed. First of all, it is recommended to do therapeutic exercises, the main idea of which will be aimed at “revitalizing” the affected areas. Additionally, physical therapy relieves swelling of nerve tissue and restores muscle tone.

Mental development delays are eliminated with the help of special drugs that have a nootropic effect. In addition to the pills, they also conduct classes with a speech therapist.

To reduce activity use. The dosage and the drug itself must be prescribed by the attending physician.

Should be eliminated by constant monitoring of liquor fluid. Pharmaceutical drugs are prescribed that increase and accelerate its outflow.

It is very important to eradicate the disease at the first alarm bells. This will enable the person to lead a normal life in the future.

Complications, consequences and prognosis

According to the experience of doctors, organic damage to the central nervous system in children can cause the following consequences:

In children, quite often such disorders affect adaptation to environmental conditions, manifestations of hyperactivity or, on the contrary, chronic fatigue syndrome.

Today, the diagnosis of “residual organic damage to the central nervous system” is made quite often. For this reason, doctors are trying to improve their diagnostic and treatment abilities.

The exact characteristics and features of a certain type of lesion make it possible to calculate the further development of the disease and prevent it. In the best case, suspicion of the disease can be completely removed.

All types of traumatic brain injury
Traumatic meningeal hematomas
Traumatic intracerebral hematomas
Fractures of the bones of the vault and base of the skull
Spinal cord injuries
Consequences of severe traumatic brain and spinal injuries

Traumatic brain injury - mechanical damage to the skull and intracranial formations - the brain, blood vessels, cranial nerves, meninges.

The frequency of traumatic brain injury and the severity of its consequences give the problem great social significance. Traumatic brain injury is predominantly suffered by the most active and socially and occupationally important contingent of the population - people under 50 years of age. This also determines large economic losses due to high mortality, frequent disability of victims, as well as temporary loss of ability to work.

Main causes of traumatic brain injury- road traffic accidents, falls, industrial, sports and domestic injuries.

Brain damage may result from:
1) focal damage, usually causing contusion (contusion) of the cortical parts of the brain or intracranial hematoma;
2) diffuse axonal damage involving the deep parts of the white matter.

Symptoms of Traumatic Brain Injury:

Depending on whether the injury preserves the integrity of the skin of the skull and its tightness or whether they are broken, craniocerebral injuries are divided into closed and open.

Closed traumatic brain injuries traditionally divided into concussion, contusion and compression; Conventionally, these also include a fracture of the base of the skull and cracks of the vault while the skin is intact.

TO open traumatic brain injury include fractures of the bones of the cranial vault, accompanied by injury to the adjacent soft tissues, fractures of the base of the skull, accompanied by bleeding or liquorrhea (from the nose or ear), as well as wounds of the soft tissues of the head with damage to the aponeurosis. If the dura mater is intact, an open craniocerebral injury is classified as non-penetrating, and if its integrity is violated, it is classified as penetrating.

Traumatic brain injury Based on severity, they are divided into 3 stages: light, medium and heavy. Mild traumatic brain injury includes concussion and mild brain contusions; to moderate severity - moderate brain contusions; to severe - severe brain contusions, diffuse axonal damage and compression of the brain.

Based on the nature of brain damage, they are divided into focal(arising mainly due to shock-anti-shock biomechanics of head injury), diffuse(occurring mainly due to acceleration-deceleration trauma) and its combined injuries.

Traumatic brain injury may be isolated(no extracranial injuries); combined(at the same time there are damage to the bones of the skeleton and/or internal organs), combined(various types of energy are simultaneously affected - mechanical, thermal, radiation, chemical, etc.).

According to the characteristics of the occurrence of traumatic brain injury, there may be primary(when the effect of mechanical energy is not due to any immediately preceding cerebral disturbances) and secondary(when the impact of mechanical energy is caused by an immediately preceding cerebral catastrophe that causes the patient to fall, for example during an epileptic seizure or stroke).

Traumatic brain injury can be sustained for the first time or repeatedly, i.e. be first or second, third, etc.

During a traumatic brain injury there are: acute, intermediate, long-term periods. Their temporal and syndromological characteristics are determined primarily by the clinical form of traumatic brain injury, its nature, type, age, premorbid and individual characteristics of the victim, as well as the quality of treatment.

A concussion is characterized by a triad of symptoms: loss of consciousness, nausea or vomiting, retrograde amnesia. There are no focal neurological symptoms.

Brain contusion diagnosed in cases where general cerebral symptoms are supplemented by signs of focal brain damage. The diagnostic boundaries between concussion and brain contusion and mild brain contusion are very fluid, and in such a situation the most appropriate term is “commotion-concussion syndrome” indicating the degree of its severity. A brain contusion can occur both at the site of injury and on the opposite side due to the counter-impact mechanism. The duration of loss of consciousness during a concussion is in most cases from several to tens of minutes.

Mild brain contusion. Characterized by loss of consciousness up to 1 hour after injury, complaints of headache, nausea, and vomiting. In the neurological status, rhythmic twitching of the eyes when looking to the sides (nystagmus), meningeal signs, and asymmetry of reflexes are noted. X-rays may reveal fractures of the cranial vault. There is an admixture of blood in the cerebrospinal fluid (subarachnoid hemorrhage).

Moderate brain contusion. Consciousness turns off for several hours. There is a marked loss of memory (amnesia) for the events preceding the injury, the injury itself, and the events after it. Complaints of headache, repeated vomiting. Short-term disorders of breathing, heart rate, and blood pressure are detected. There may be mental disorders. Meningeal signs are noted. Focal symptoms manifest themselves in the form of uneven pupil size, speech impairment, weakness in the limbs, etc. Craniography often reveals fractures of the vault and base of the skull. Lumbar puncture revealed significant subarachnoid hemorrhage.

Severe brain contusion. Characterized by prolonged loss of consciousness (lasting up to 1-2 weeks). Gross violations of vital functions are detected (changes in pulse rate, pressure level, frequency and rhythm of breathing, temperature). The neurological status shows signs of damage to the brain stem - floating movements of the eyeballs, swallowing disorders, changes in muscle tone, etc. Weakness in the arms and legs, up to paralysis, as well as convulsive seizures may be detected. A severe bruise is usually accompanied by fractures of the vault and base of the skull and intracranial hemorrhages.

Brain compression implies the development of a traumatic hematoma, often epidermal or subdural. Their timely diagnosis involves two unequal situations. With a simpler one, there is a “light period”: the patient who has regained consciousness after some time begins to “load” again, becoming apathetic, lethargic, and then stuporous. It is much more difficult to recognize a hematoma in a patient in a coma, when the severity of the condition can be explained, for example, by a bruise of brain tissue. The formation of traumatic intracranial hematomas as their volume increases is usually complicated by the development of a tentorial hernia - protrusion of the brain compressed by the hematoma into the foramen of the cerebellar tentorium, through which the brain stem passes. Its progressive compression at this level is manifested by damage to the oculomotor nerve (ptosis, mydriasis, strabismus) and contralateral hemiplegia.

Fracture of the base of the skull inevitably accompanied by brain contusion of varying degrees, characterized by the penetration of blood from the cranial cavity into the nasopharynx, into the periorbital tissues and under the conjunctiva, into the cavity of the middle ear (during otoscopy, a cyanotic color of the eardrum or its rupture is detected).

Bleeding from the nose and ears may be due to local trauma, so it is not a specific sign of a basal skull fracture. Equally, the “symptom of glasses” is also often the result of a purely local facial injury. It is pathognomonic, although not necessary, to leak cerebrospinal fluid from the nose (rhinorrhea) and ears (otorrhea). Confirmation of the leakage of cerebrospinal fluid from the nose is the “teapot symptom” - a clear increase in rhinorrhea when the head is tilted forward, as well as the detection of glucose and protein in the nasal discharge, according to their content in the cerebrospinal fluid. A fracture of the temporal bone pyramid may be accompanied by paralysis of the facial and cochleovestibular nerves. In some cases, facial paralysis occurs only a few days after the injury.

Along with acute hematomas, a skull injury can also be complicated by a chronically increasing accumulation of blood above the brain. Usually in such cases there is a subdural hematoma. As a rule, such patients - often elderly people with impaired memory, who also suffer from alcoholism - are admitted to the hospital already in the stage of decompensation with compression of the brain stem. A skull injury that occurred many months ago is usually not severe, and the patient is amnesic.

Treatment of Traumatic Brain Injury:

The main goal of treatment for traumatic brain injury is to minimize secondary brain damage, since primary damage cannot be treated.

Emergency care at the prehospital stage for traumatic brain injury
The outcome of a traumatic brain injury largely depends on the early assistance provided to the victim. The neurological status is assessed at this stage. Hypotension and hypoxia associated with traumatic brain injury occur in 50% of cases; hypotension accompanies systemic injuries and may be due to hemorrhagic complications and decreased vascular tone in case of damage to the brain stem; hypoxia occurs with hemopneumothorax or with obstruction of the respiratory tract (usually the upper). The causes of obstruction may be a coma and retraction of the tongue, the entry of blood and aspiration into the airways.

Therapeutic measures are aimed at eliminating hypotension and hypoxia. Any patient with traumatic brain injury should be considered as having a full stomach, as there is a risk of aspiration of gastric contents into the tracheobronchial tree. Trained personnel at the scene should perform tracheal intubation, which reduces mortality in severe traumatic brain injury, and begin intravenous fluid resuscitation. Indications for tracheal intubation: upper airway obstruction, loss of upper airway protective reflexes (GCS)< 8 баллов), неспособность пациента обеспечить дренирование дыхательных путей, необходимость механической поддержки дыхания (тахипноэ >30 per minute). Some authors highlight indications such as hypoxia (PaO2< 70 мм рт. ст.; SjО2 < 94%), гиперкапния (РаСО2 >45 mmHg Art.).

Spinal cord injury occurs in 10% of road traffic accidents. To avoid injury to the cervical spine, intubation with the head in a neutral position is recommended. Intubation is facilitated by the administration of succinylcholine (1 mg/kg) and lidocaine (1.5 mg/kg IV). During the procedure, the method of traction of the head by the mastoid processes along the vertical axis of the body (manual in line traction) is used, which prevents hyperextension and movement of the spine in the cervical region, while the Selick maneuver (pressure on the thyroid cartilage) is used to prevent aspiration and vomiting. During transportation, inhalation of 100% humidified oxygen is carried out, and, if necessary, auxiliary ventilation is provided. The victim's neck should be immobilized with a rigid collar. The victim is placed on a special board, to which they are tied with belts, which prevents the movement of the spine during transportation. The board for immobilization must be radio-opaque, which allows the necessary studies to be carried out without shifting the victim.
At the scene of the incident, correction of hypovolemic shock begins with intravenous infusion of various solutions; after catheterization of the peripheral vein, 500-1000 ml of isotonic solution, or 50-100 ml of 10% NaCl solution, or 250-500 ml of colloidal solution are injected in a stream. The use of a hypertonic NaCl solution does not cause an increase in intracranial pressure. At the prehospital stage, the volume of intravenous infusion is limited to avoid pulmonary edema, increased bleeding and increased intracranial pressure with a sharp rise in blood pressure. At the prehospital stage, mannitol is not used. According to numerous double-blind randomized studies, dexamethasone and methylprednisolone, prescribed in the early stages of traumatic brain injury in appropriate doses, do not improve clinical outcome.

Inpatient treatment of traumatic brain injury
Activities aimed at supporting breathing and circulation continue. The neurological status according to the GCS, the size and reaction of the pupils to light, sensitivity and motor function of the extremities are re-evaluated, and other systemic damage is assessed. The efforts of specialists should be aimed at prompt diagnosis and surgical removal of brain compression.

Intracranial hematomas are diagnosed in 40% of cases of traumatic brain injury. Early surgical decompression is an imperative treatment option. With significant intracranial hemorrhage detected by CT examination, delay in surgical intervention within the first four hours increases mortality to 90%. Clinical indications for surgery are the classic triad: impaired consciousness, anisocoria and hemiparesis. However, the absence of these symptoms does not exclude hematoma. A decrease in GCS score during repeated neurological examination has diagnostic significance. A high probability of having a hematoma is observed in elderly patients, alcoholics, with injuries received from a fall, fracture of the skull bones (especially in the areas where meningeal vessels and venous sinuses pass).

At this stage, one of the most important tasks is surgical reduction of intracranial pressure using decompression craniotomy. Displacement of the midline structures of the brain is a more reliable indicator for surgical intervention than the size of the hematoma. According to Ropper, midline displacement of 8 mm is associated with coma; by 6 mm – with deep stunning. The operation is indicated for displacement of the midline structures by more than 5 mm, an increase in intracranial pressure of more than 25 mm Hg. Art.; decrease in CPP by 45 mm Hg. Art. also serves as an indication for decompression craniotomy.

For the purpose of preoperative assessment of a patient with traumatic brain injury, attention should be paid to the following points:
– airway patency (cervical spine);
– breathing (ventilation and oxygenation);
– state of the cardiovascular system;
– collateral damage;
– neurological status (GCS);
– chronic diseases;
– circumstances of the injury (time of injury, duration of unconsciousness, intake of alcohol or medications on the eve of the injury).

In order to prevent hernial protrusion and strangulation of areas of the brain with increased intracranial pressure, therapy aimed at reducing intracranial pressure is carried out before providing neurosurgical assistance. Typically, to avoid increased intracranial pressure, mannitol is used at a dose of 0.25-1 g/kg body weight quickly intravenously in a drip over 15-20 minutes. The peak decrease in intracranial pressure is observed 10-20 minutes after administration of the drug. A number of studies support the effectiveness of low doses of mannitol (0.25 g/kg) under the control of intracranial pressure, especially in cases where repeated administration is required. In some hospitals, to reduce intracranial pressure in patients with traumatic brain injury, a hypertonic NaCl solution is used, which significantly reduces the production of cerebrospinal fluid (CSF). When using it, a decrease in the volume of brain tissue and the volume of blood supply to the brain is observed to a lesser extent, and the effect of reducing intracranial pressure is less long-lasting than when using mannitol. Bolus administration of concentrated 7.5% and 10% NaCl solutions (up to 6-8 ml/kg) effectively reduces intracranial pressure and causes less risk of sodium retention in the body than drip administration of large volumes (equivalent in the amount of sodium) of moderately hypertensive drugs 2-3 % solutions. A 23.4% NaCl solution has been successfully used for mannitol-refractory increases in intracranial pressure. As a rule, the administration of NaCl is combined with the simultaneous administration of furosemide (2 ml of 1% furosemide is added to 200 ml of 10% NaCl).

Anesthetic management for traumatic brain injury
Before administering anesthesia, remember the basic principles of optimal anesthesia for traumatic brain injury.
1. Ensuring optimal brain perfusion.
2. Prevention of cerebral ischemia.
3. Avoidance of drugs that increase intracranial pressure.
4. Quick awakening of the patient after surgery.

Due to the high risk of aspiration of gastric contents, crash induction (rapid seguence induction) and the Selic maneuver should be used to prevent aspiration. Crash induction includes:
– preoxygenation with 100% oxygen for 3-5 minutes (with preserved spontaneous breathing);

– induction of anesthesia – narcotic analgesic (5 mcg/kg fentanyl), intravenous anesthetic (5-6 mg/kg sodium thiopental or 2 mg/kg propofol). Doses of anesthetics depend on the depth of the disturbance of consciousness and the state of hemodynamics. The more pronounced the disorders of consciousness and hemodynamics, the lower the doses used. In patients with unstable hemodynamics, preference should be given to etomidate (0.2-0.3 mg/kg). Sodium thiopental and propofol are not indicated in patients with hypovolemia;

– precurarization with Ardoin (10% of the calculated dose) 5 minutes before the administration of a muscle relaxant with a rapid onset of action (ditilin). The increase in intracranial pressure caused by ditilin, short-term, single administration of this drug does not affect the outcome. In patients with limb paresis (not earlier than one day after a traumatic brain injury), ditilin-induced hyperkalemia may occur; in such cases, a relaxant of a non-depolarizing type should be used;

– Selic maneuver (pressure on the thyroid cartilage);

– tracheal intubation (laryngoscopy lasting less than 15 seconds). Positioning the patient on the operating table with the head end elevated by 30 degrees improves the venous outflow of blood from the brain.

The issue of ventilation support during anesthesia is very problematic. It should be said that hyperventilation has long become a routine method of treating patients with traumatic brain injury due to the fact that it causes vasoconstriction of the arterioles of the brain and pia mater. It helps reduce cerebral blood flow and volume, as well as intracranial pressure.

Known disadvantages of the method are hypoperfusion/ischemia (in pre-existing conditions of hypoperfusion) and inhibition of oxygen delivery due to a leftward shift in the oxyhemoglobin dissociation curve. When comparing patients who underwent hyperventilation with a decrease in PaCO2 to 24 mm Hg. Art., with the control group, where PaCO2 was reduced to 35 mm Hg. Art., a significant difference was revealed in favor of normoventilation, if we consider the clinical outcome 3-6 months after the injury. It has been proven that hyperventilation can have a beneficial effect in patients with increased cerebral blood flow, especially in young patients with predominant symptoms of cerebral edema with intact brainstem function. The intracerebral pressure-lowering effect of hyperventilation in patients with reduced cerebral blood flow (late phase of traumatic brain injury, acute phase in the elderly) is, if not completely absent, then very limited. Moreover, in such situations, hyperventilation may have a detrimental effect and cause further local deterioration of cerebral blood flow, which may fall below the ischemic threshold. It is usually recommended to continue mechanical ventilation in the postoperative period, since maximum brain swelling occurs 12-72 hours after injury.

The most optimal method of anesthetic support in patients with traumatic brain injury should be considered an infusion of sodium thiopental at a rate of 4-5 mg/kg/hour. This method is especially appropriate for patients with severe traumatic brain injury and coma.

In patients with mild traumatic brain injury, low doses of isoflurane or desflurane may be given to maintain anesthesia. One should only remember the need for moderate hyperventilation when using these inhalational anesthetics. Isoflurane and desflurane at a concentration of 1-1.5 MAC (minimum alveolar concentration - the alveolar concentration of an inhalational anesthetic that prevents involuntary movements of the limbs in 50% of patients in response to a standardized stimulus (for example, a skin incision) and does not cause a noticeable increase in intracranial pressure. Enflurane and desflurane, when used over a long period of time, may interfere with the reabsorption of cerebrospinal fluid.

Nitrous oxide increases cerebral blood flow and the amount of air in the cranial cavity, so its use in pure form in such operations is limited, although a number of clinics use N2O in combination with sodium thiopental infusion. This makes it possible to reduce the rate of infusion of the latter and, thus, ensure rapid awakening of the patient. When working with N2O in this category of patients, ventilation should be carried out in the mode of moderate hyperventilation (PaCO2 = 32 mm Hg) and turned off before closing the dura mater.

To maintain myoplegia, a muscle relaxant with an antidepolarizing effect is used (vecuronium is preferred, but Arduan is widely used). Opioids are administered during surgery for pain relief. It has been established that fentanyl and sufentanil can increase intracranial pressure in traumatic brain injury. Maintaining blood pressure at a sufficient level when using opioids prevents an increase in intracranial pressure.

An important point during the operation before and after it is infusion therapy, which in patients with cerebral edema is somewhat different from that accepted in general anesthesiology and intensive care, although the general principles remain the same. Infusion therapy should ensure not only hemodynamic stability, but also adequate CPP, prevent an increase in venous pressure in the cranial cavity, maintain a stable blood plasma osmolarity within 300-310 mOsm/kg H2O and prevent the development of both hyperglycemia and hypoglycemia. Brain perfusion pressure should be maintained at 80-90 mm Hg. Art.

During operations for the removal of acute epidural and subdural hematomas, especially with rapid decompression, there is a significant decrease in blood pressure, which can be aggravated by initial hypovolemia and bleeding. With systemic injuries, patients are often hypovolemic, and doctors' efforts should be aimed at normalizing the volume of blood volume. Hypovolemia may be masked by hypoxia, a sympathetic activation in response to increased intracranial pressure. To correct initial hypovolemia, an isotonic NaCl solution is transfused until blood pressure, heart rate and diuresis are normalized. The hematocrit should be maintained at a level of at least 30% to avoid cerebral ischemia. Isotonic NaCl solution is the main and in most cases the only drug for patients with pathology of the cranial cavity. At the same time, it is important to remember that hypervolemia can increase cerebral edema and contribute to increased intracranial pressure.

The anesthesiologist should strive to awaken the patient early after surgery, which allows for an early neurological examination. The presence of consciousness in the postoperative period greatly facilitates monitoring of the patient and allows for earlier detection of the development of complications. Consciousness is the best criterion for assessing the patient's condition in the early postoperative period, but early awakening of the patient should not be an end in itself. If the patient's condition allows, extubation is performed at the end of the operation. Along with stable hemodynamics, normal body temperature and adequate breathing, restoration of the patient's consciousness is a mandatory criterion for early extubation. If an increase in cerebral edema and an increase in intracranial pressure are expected and it is intended to use hyperventilation to reduce it, there should be no rush to extubate.

The outcome of a traumatic brain injury can be assessed no earlier than 6 months after the injury. According to the Traumatik Coma Data Bank, of patients admitted to hospitals with severe traumatic brain injury, 67% survive (excluding gunshot head injuries). Of this group of patients, only 7% show good recovery upon discharge from hospital. Thus, almost all patients with severe traumatic brain injury have various neurological disorders.

Prognosis for traumatic brain injury. With a concussion, the vast majority of patients make a full recovery. The outcome of brain contusion and open skull injuries depends on the severity of the brain injury. In most cases, survivors retain some residual cerebral symptoms. Timely removal of the hematoma saves patients' lives; in many such cases there are no significant residual symptoms. With severe brain damage, mortality can reach 40-50%.

This diagnosis is currently one of the most common. Organic damage to the central nervous system (CNS) in its classical content is a neurological diagnosis, i.e. is under the purview of a neurologist. But the symptoms and syndromes accompanying this diagnosis can relate to any other medical specialty.

This diagnosis means that the human brain is defective to a certain extent. But, if a mild degree (5-20%) of “organics” (organic damage to the central nervous system) is inherent in almost all people (98-99%) and does not require any special medical interventions, then the average degree (20-50%) of organics is not just a quantitatively different condition, but a qualitatively different (fundamentally more severe) type of disorder of the nervous system.

The causes of organic lesions are divided into congenital and acquired. Congenital cases include cases where during pregnancy the mother of the unborn child suffered some kind of infection (acute respiratory infection, flu, sore throat, etc.), took certain medications, alcohol, or smoked. A unified blood supply system will bring stress hormones into the fetus’s body during periods of psychological stress of the mother. In addition, sudden changes in temperature and pressure, exposure to radioactive substances and x-rays, toxic substances dissolved in water, contained in the air, in food, etc., also affect.

There are several particularly critical periods when even a slight external impact on the mother’s body can lead to the death of the fetus or cause such significant changes in the structure of the body (and, including the brain) of the future person that, firstly, no medical intervention is possible correct, and secondly, these changes can lead to the early death of a child before the age of 5 - 15 (and usually the mother reports this) or cause disability from a very early age. And in the best case, they lead to severe brain deficiency, when even at maximum stress the brain is able to work at only 20-40 percent of its potential power. Almost always, these disorders are accompanied by varying degrees of severity of disharmony of mental activity, when, with reduced mental potential, positive qualities of character are not always sharpened.

This can also be facilitated by taking certain medications, physical and emotional overload, asphyxia during childbirth (oxygen starvation of the fetus), prolonged labor, early placental abruption, uterine atony, etc. After childbirth, severe infections (with severe symptoms of intoxication, high fever, etc. .) up to 3 years can give rise to acquired organic changes in the brain. Brain injuries with or without loss of consciousness, long or short general anesthesia, drug use, alcohol abuse, long-term (several months) independent (without prescription and constant supervision of an experienced psychiatrist or psychotherapist) use of certain psychotropic drugs can lead to some reversible or irreversible changes in brain function.

Diagnosis of organic matter is quite simple. A professional psychiatrist can already determine the presence or absence of organic matter by the child’s face. And, in some cases, even the degree of its severity. Another question is that there are hundreds of types of disorders in the functioning of the brain, and in each specific case they are in a very special combination and connection with each other.

Laboratory diagnostics are based on a series of procedures that are quite harmless to the body and informative for the doctor: EEG - electroencephalogram, REG - rheoencephalogram (examination of cerebral vessels), ultrasound doppler (M-echoEG) - ultrasound diagnostics of the brain. These three examinations are similar in form to an electrocardiogram, only they are taken from a person’s head. Computed tomography, with its very impressive and expressive name, is actually capable of identifying a very small number of types of brain pathology - a tumor, a space-occupying process, an aneurysm (pathological dilation of a brain vessel), dilation of the main cisterns of the brain (with increased intracranial pressure). The most informative study is the EEG.

Let us note that practically no disorders of the central nervous system disappear on their own, and with age they not only do not decrease, but intensify both quantitatively and qualitatively. The mental development of a child directly depends on the state of the brain. If the brain has at least some impairment, then this will certainly reduce the intensity of the child’s mental development in the future (difficulty in the processes of thinking, memorization and recollection, impoverishment of imagination and fantasy). In addition, a person’s character is formed distorted, with varying degrees of severity of a certain type of psychopathization. The presence of even small but numerous changes in the child’s psychology and psyche leads to a significant decrease in the organization of his external and internal phenomena and actions. There is an impoverishment of emotions and some flattening of them, which directly and indirectly affects the child’s facial expressions and gestures.

The central nervous system regulates the functioning of all internal organs. And if it does not work fully, then the other organs, even with the most careful care for each of them separately, will not be able, in principle, to work normally if they are poorly regulated by the brain. One of the most common diseases of our time, vegetative-vascular dystonia, against the background of organic matter, acquires a more severe, peculiar and atypical course. And thus, not only does it cause more trouble, but these “troubles” themselves are more malignant in nature. The physical development of the body comes with any disturbances - there may be a violation of the figure, a decrease in muscle tone, a decrease in their resistance to physical activity of even moderate magnitude. The likelihood of increased intracranial pressure increases by 2-6 times. This can lead to frequent headaches and various kinds of unpleasant sensations in the head area, reducing the productivity of mental and physical labor by 2-4 times. The likelihood of endocrine disorders also increases, increasing by 3-4 times, which leads, with minor additional stress factors, to diabetes mellitus, bronchial asthma, imbalance of sex hormones with subsequent disruption of the sexual development of the body as a whole (an increase in the amount of male sex hormones in girls and female hormones - in boys), the risk of a brain tumor, convulsive syndrome (local or general convulsions with loss of consciousness), epilepsy (group 2 disability), cerebrovascular accident in adulthood in the presence of hypertension of even moderate severity (stroke), diencephalic syndrome increases (attacks of unreasonable fear, various pronounced unpleasant sensations in any part of the body, lasting from several minutes to several hours). Over time, hearing and vision may decrease, coordination of movements of a sports, household, aesthetic and technical nature may be impaired, complicating social and professional adaptation.

Organic treatment is a long process. It is necessary to take vascular medications twice a year for 1-2 months. Concomitant neuropsychic disorders also require their own separate and special correction, which must be carried out by a psychiatrist. To monitor the degree of effectiveness of organic treatment and the nature and magnitude of changes in the state of the brain, monitoring by the doctor himself at the appointment and EEG, REG, and ultrasound are used.

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The main diseases of the central nervous system in athletes are functional diseases, namely neuroses.

Neuroses. Neurosis is a breakdown of higher nervous activity, which is based on overstrain of the basic nervous processes - excitation and inhibition (I.P. Pavlov). The cause of such a breakdown is acute or persistent mental trauma or mental stress. These terms do not necessarily mean any kind of shock (exceptionally strong negative emotions). Thus, mental stress can arise both as a result of strong and excessively frequent emotions, caused, for example, by a series of important competitions, and as a result of monotonous training, requiring more and more internal efforts to continue.

In other words, any situation in which demands are placed on the psyche for quite a long time that exceed its reserves in relation to the strength and mobility of basic nervous processes can become an etiological factor in the development of neurosis. The simultaneous impact of several negative factors is especially unfavorable, for example, such as excessive sports activity, anxiety and mental overload during exams, family and work conflicts, etc. If mental trauma occurs against the background of repeated physical overexertion, intoxication from foci of chronic infection , malnutrition and insufficient nutrition, nicotine and alcohol abuse, then neuroses arise more often and easier. There are the following main types of neuroses: neurasthenia, which, with appropriate negative influences, develops mainly in individuals with a balanced state of both signaling systems; psychasthenia, which, under the same conditions, develops in individuals who have a predominance of the second signaling system over the first (the so-called thinking type, according to I.P. Pavlov), and hysteria, which, under the influence of unfavorable factors, develops mainly in individuals who have the first the signaling system prevails over the second (the so-called artistic type). There are also some types of neuroses that are not related to signaling systems: obsessive-compulsive neurosis, fear neurosis, etc. As already mentioned, a state of overtraining, characterized primarily by a breakdown of higher nervous activity, is also a neurosis. The specific form of neurosis is determined by the individual characteristics of the athlete’s psyche and the nature of the traumatic circumstances.

Athletes most often have to deal with neurasthenia and obsessive-compulsive neurosis.

Neurasthenia (from the Greek neuron - nerve, asthenia - exhaustion). There are two forms of neurasthenia - hypersthenic and hyposthenic.

The hypersthenic form arises primarily due to the weakness of the process of active internal inhibition caused by its overstrain. This primarily affects the patient’s reactions to the environment - impatience, lack of restraint, anger, a tendency to tears, sleep disorders (falling asleep is difficult, sleep is superficial, with frequent interruptions, which causes drowsiness and a feeling of weakness during wakefulness). Not only mental but also physical performance decreases, especially if it is associated with performing precise movements. For an athlete, this may be associated with a distortion of the technique of a complex exercise, which he previously mastered well; Difficulties in mastering new technical skills that do not correspond to the athlete’s qualifications.

In the hyposthenic form of neurasthenia, the manifestation of increased excitability is less pronounced and the clinical picture is dominated by weakness, exhaustion, and lethargy.

Obsessive-compulsive neurosis. It is characterized by various manifestations of obsession: the athlete is haunted by thoughts of inevitable failure in sports, school or work. Often there are unfounded suspicions that he has some serious illness, for example cancer (cancerophobia), etc. A feature of obsessive-compulsive states is the patient’s ambivalent attitude towards his fears: on the one hand, he understands their groundlessness, on the other hand, he cannot overcome them .

The symptoms of neuroses described above are characteristic of a developed picture of the disease, which is relatively rarely observed in athletes. In them it often manifests itself in more erased forms. However, neurosis, which is always a source of significant internal experiences and conflict situations in a sports team, should not be regarded as a mild illness.

In the prevention of neuroses in athletes, the correct dosage of physical and especially emotional stress is of great importance. Sports activities that arouse interest, enthusiasm and excitement serve as an inexhaustible source of positive emotions that protect the nervous system from overstrain. On the contrary, monotonous training relatively quickly exhausts the nervous system. A positive reaction on the part of the athlete is facilitated by a clear understanding of the specific tasks and goals facing him. However, when analyzing the causes of neurosis, one cannot limit oneself to considering only conditions related to the field of sports: the cause of neurosis manifested in the field of sports activity may be, for example, an unfavorable family or work environment.

In the treatment of neuroses, medications and physiotherapy are used. But often only one load reduction and,

the main thing is that changing its character with the inclusion of active recreation gives a good effect. In some cases, a break from training is necessary - usually for a short period of time (2-3 weeks).

To injuries of the central nervous system include damage to the brain and spinal cord.

Brain damage occurs during traumatic brain injury. It can be the result of blows to various parts of the skull, or falls on the head, as well as bruises on the head against surrounding objects.

Traumatic brain injury can be closed or open. A closed traumatic brain injury is one in which, regardless of whether the integument and soft tissues are damaged or not, the bones of the skull remain intact.

Traumatic brain injury is most common in boxing, cycling and motor sports, football, hockey, alpine skiing, but is also observed during gymnastics, acrobatics, diving, athletics, etc.

Most skull injuries are accompanied by brain injuries, which are divided into concussion, brain contusion and brain compression. They can be isolated or combined with each other.

Any of these injuries causes more or less pronounced damage to the brain matter, swelling and damage to nerve cells with disruption of their function, which manifests itself in vascular disorders (ruptures of capillaries, arteries and veins), sometimes in hemorrhage in the brain, leading to hypoxia, ischemia and necrosis its areas, in disorders of the vestibular apparatus, brain stem and cortex.

The most common symptom of a concussion is loss of consciousness. It can be very short-term - just a few seconds or last a long time - many hours and days. The longer the loss of consciousness, the more severe the degree of concussion (see below). Having regained consciousness, patients complain of heaviness in the head, dizziness, headache, nausea, and weakness. They have sluggish and slow speech.

With more severe injuries, other symptoms of concussion are also identified: severe pallor, fixed gaze, dilated pupils and lack of reaction to light, rare and shallow breathing, rare and weak pulse, sweat, vomiting and convulsions. In extremely severe cases of concussion, the victim, without regaining consciousness, may die from respiratory arrest due to damage to the medulla oblongata, in which, as is known, the respiratory center is located.

Very rarely, with concussions, mental disorders come to the fore: severe agitation, confusion, hallucinations. These disorders usually resolve completely within a few days or weeks.

After a concussion, so-called retrograde amnesia may be observed (the victim does not remember what happened to him before the injury), headaches, dizziness, and vascular disorders may remain for a long time, manifested, in particular, in persistent arterial hypertension, heart rhythm disturbances, sweating, chilliness , and in the mental sphere - in irritability, strong emotional excitability, memory deterioration.

It is customary to distinguish between mild, moderate and severe degrees of concussion, depending on the duration of loss of consciousness: with the first degree it lasts minutes, with the second - hours, and with the third - many days. The severity of other symptoms depends on the duration of loss of consciousness.

All symptoms observed during a concussion are a consequence of circulatory disorders and molecular biochemical changes in the cells of the cerebral cortex and in the diencephalic-stem centers, accompanied by inhibition in various parts of the central nervous system, and then a disruption of the relationship between the cerebral cortex and subcortical formations. Manifestations of the latter include dysfunction of the stem and subcortical formations, the symptoms of which are nystagmus (oscillatory, involuntary movements of the eyeballs), breathing disorders, difficulty swallowing, etc.

A brain contusion is a closed skull injury in which damage to the brain substance occurs. A blow to the head can cause either direct or indirect brain injury. Direct trauma means a bruise of the brain in the area of application of force, for example, a blow to the temple bruises the temporal lobe. Indirect injury is a brain contusion in an area distant from the point of impact, for example, with a blow to the lower jaw, a brain contusion in the area of the occipital bone. This is due to the fact that kinetic energy is transferred from the site of impact to the skull, cerebrospinal fluid and brain, which is displaced away from the source of the impact and strikes the inner surface of the skull bones. The resulting wave of cerebrospinal fluid in the ventricles of the brain can also damage the brain tissue in the area of their walls. Due to the displacement of the brain, vascular ruptures can also occur. Then hemorrhage, swelling of the brain and soft meninges and reflex vascular disorders occur.

A brain contusion, in addition to the symptoms characteristic of a concussion (but more pronounced), is characterized by the presence of signs of focal brain lesions in the form of paresis, paralysis, convulsions, sensitivity disorders on the side opposite to the contusion, and speech disorders. If the hemorrhage that occurs during a bruise is a consequence of damage to a large vessel, then a large hematoma is formed, which compresses certain areas of the brain, causing corresponding pathological changes in the body. The degree of brain disorders in case of brain contusion usually decreases significantly already in the first days, since they are based not only on the death of nervous tissue, but also on some of its reversible changes (tissue swelling, etc.). However, some disorders may remain forever. Such disorders are called residual.

With compression of the brain, there is a constant increase in the above symptoms. At the time of injury, there may be symptoms similar to those of a mild concussion. However, a little later, headache, nausea, vomiting, and stupor begin to increase, which lead to loss of consciousness; Paresis of the right or left side of the body occurs and increases, bradycardia, respiratory and circulatory failure appear.

A relatively favorable state in the period of time between the injury and the development of the symptoms described above is very characteristic of hematomas. Satisfactory health, which may occur after clearing consciousness, sometimes serves as a reason for weakening medical supervision of the victim. Symptoms of brain compression, which often lead to death, can appear several hours after the injury.

Traumatic brain injury in boxing requires special attention. If in other sports such an injury is a random occurrence, an accident, then in boxing the rules of the competition allow blows with a glove to the lower jaw, face, forehead and temples.

Traumatic brain injury includes knockout, knockdown and “groggy” condition (standing knockdown) due to a blow to the head (boxing).

Most often in boxing practice, a knockout occurs with a blow to the lower jaw. It causes dizziness, spatial disorientation, falling and often loss of consciousness. The cause of knockout in this case is a concussion of the brain, as well as the otoliths of the vestibular apparatus, leading to irritation of the cerebellum and, therefore, to loss of balance. A knockout with a blow to the temporal region occurs according to the mechanism of a typical concussion.

A certain traumatic effect on the brain is caused by frequent blows to the head in boxers, which do not end in a knockout, knockdown or “groggy” state. Such shocks can lead to organic changes in brain cells and the vessels that feed it.

In most cases, loss of consciousness in boxers when hit to the head is short-lived and does not cause any disturbances in the function of the nervous system subsequently. However, even with a short-term loss of consciousness, more severe brain damage cannot be completely ruled out: bruises and hematoma formation with subsequent compression of the brain. There are cases when a boxer died a few hours after a knockout from compression of the brain by a gradually increasing hematoma.

When providing first aid for traumatic brain injuries, it is necessary to place the victim in a position with the head slightly elevated and put cold on the head, and in case of respiratory and circulatory problems, use medications (cordiamin, caffeine, camphor, lobeline, etc.).

In all cases of brain damage, urgent hospitalization of victims is indicated for a period of 2 weeks to 2 months. Transportation should be as gentle as possible. Examination of the victim and prescription of treatment measures should be carried out by a neurologist or neurosurgeon. On the first day, careful monitoring of the victim is necessary (this especially applies to those who received a knockout). In case of hematomas, in case of increasing phenomena of brain compression, surgical intervention is performed.

Often, soon after a traumatic brain injury, especially a repeated one, athletes experience various post-traumatic disorders: headache, dizziness, increased fatigue, sleep disturbances, etc.

A number of years (5-10-15 or more) after a traumatic brain injury, serious pathological changes in the brain may appear. This is the so-called post-traumatic encephalopathy syndrome, which can manifest itself in various forms. This brain damage occurs especially often in experienced boxers who have received a large number of blows to the head, knockouts and knockdowns (the so-called “boxing disease”).

Encephalopathy may appear several years after stopping boxing. Its signs are various symptoms of mental disorders and organic brain damage. Mental disorders can initially be expressed in the appearance of a state of euphoria (excitement, unnatural cheerfulness) in the boxer, followed by apathy and lethargy. Next, a gradual change in character occurs: arrogance, a sense of superiority appears, then hot temper, arrogance, resentment and suspicion, and then memory impairment, decreased intelligence, even dementia. The psychiatry term for this condition is “dementio pugilistica,” which means “dementia from fistfighting.” Along with the mental disorder, various symptoms appear that indicate organic damage to the brain: movement disorders, trembling of various parts of the body, mask-like face, increased muscle tone, speech disorders, paresis, etc. In these boxers, with the help of electroencephalography and pneumoencephalography, pronounced changes are revealed that indicate for diffuse atrophy of the cerebral cortex. The reason for this, apparently, is repeated, even minor, concussions, accompanied by hemorrhages and subsequent cicatricial changes.

Resumption of sports activities after a traumatic brain injury is permitted only after complete recovery, established on the basis of a thorough medical examination performed by a neurologist.

Adult boxers (masters of sports and dischargers) after a knockout are allowed to train no earlier than a month later, older boys - no earlier than 4 months, juniors - no earlier than 6 months. Adult boxers who have suffered two knockouts can begin training no earlier than 3 months later, and those who have suffered three knockouts - no earlier than a year after the last knockout (provided there are no neurological symptoms).

To prevent knockouts in boxing, good technical training of the boxer, perfect mastery of defensive techniques, as well as clear refereeing and timely termination of the fight when one of the boxers has a clear advantage are of great importance.

To prevent brain injuries in all sports, it is necessary to keep strict records and a thorough analysis of the causes of injuries to the central nervous system, and strictly adhere to the timing of the start of training and participation in competitions. It is unacceptable to train boxers, hockey players, cyclists, motorcyclists, ski jumpers and alpine skiers without protective helmets.

Spinal cord injuries in athletes are observed in the form of concussions, bruises, compression, partial and complete ruptures of the brain substance or its membranes. The mechanisms of injury are as follows: overstretching of the spinal cord due to excessive flexion and extension of the cervical spine; compression or transection of the spinal cord due to fractures and dislocations of the cervical, thoracic or lumbar vertebrae (when hitting the head on the bottom of a pool or reservoir, when falling on the head, when performing various techniques in wrestling); damage to the vessels of the spinal cord or its membranes when the spine hits the ground or the spine, for example, with a boot or a projectile. Most often, spinal injuries occur during wrestling, gymnastics, acrobatics, weightlifting, equestrian sports, diving, skiing, football and hockey.

With a concussion of the spinal cord, there are no gross anatomical changes, there are only minor hemorrhages and tissue swelling. Characteristic symptoms are temporary conduction disturbances, slight weakness of the muscles of the limbs, mild changes in sensitivity, and dysfunction of the pelvic organs. These symptoms appear immediately after the injury, but quickly subside and disappear after 1-3 weeks.

When the spinal cord is contused, hemorrhage, swelling and softening of individual areas of the nervous tissue occur, causing severe dysfunction. Immediately after the injury, the conductivity of the spinal cord is disrupted, which persists for a long time. In the first days, a syndrome of complete disruption of spinal cord conduction is usually observed: paralysis below the level of the injury, anesthesia, retention of urination and defecation. Then complications may arise: bedsores, pneumonia, etc. Subsequently, depending on the severity of the injury, in some cases there may be a complete restoration of spinal cord function, in others pathological changes remain for life.

Compression of the spinal cord can occur due to pressure on it from bone fragments during a spinal fracture or as a result of an increase in the intrathecal hematoma when the vessels of this area rupture. In the latter case, compression progresses as the hematoma increases, which is characterized by an increase in motor and sensory disturbances below the level of injury, as well as an increase in disorders of the pelvic organs. Long-term compression of the spinal cord can lead to irreversible changes.

With closed fractures and dislocations of the spine, there may be a partial or complete rupture of the spinal cord with complete transverse conduction disorder, characterized by paralysis of both arms or both legs or all limbs. Below the site of injury, all types of sensitivity are absent (for example, the victim does not even feel the passage of urine and feces), bedsores, swelling of the lower extremities, etc. quickly develop.

First aid for spinal injuries is as follows: the victim must be carefully placed face up on any hard flat surface and transported to a medical facility. Under no circumstances should you imprison him or allow him to do this himself, as there is a danger of damage to the spinal cord.

In most cases, spinal cord injuries lead to To disability.