Health, medicine, healthy lifestyle. Stem stroke: types (ischemic, hemorrhagic), causes, symptoms, treatment, prognosis

Stem stroke is one of the localizations of acute pathology in the blood supply to the brain.

2 variants of stroke (ischemic and hemorrhagic) have different predominant localization. If hemorrhages often occur in the cortical structures of the brain, then ischemia develops in the region of the brain stem. The severity of the course of the disease is confirmed by unfavorable statistics: in 2/3 of cases, a lethal outcome is observed in the first two days.

Where is the brain stem located?

The trunk is called the lowest part of the brain, bordering on the spinal cord. Anatomically, it is located at the base of the skull. From above and on the sides it is closed by hemispheres, and the cerebellum adjoins behind. In their structure, stem cells are more similar to spinal cells. Their tasks:

• ensuring the constant functioning of the centers of regulation and support of cardiac activity, respiration, muscle tone and movements;
• the implementation of the connection of the cortical centers with the spinal cord through the passing nerve pathways (centripetal - from the cortical centers to the spinal cord, centrifugal - back).

There are 3 parts in the trunk.

The medulla oblongata is the lowest zone, is practically a continuation of the spinal cord, contains vital centers for respiration (regulate inhalation and exhalation), blood circulation (speeds up or slows down the rhythm). Disruption of work threatens a person with a stoppage of respiratory movements, a drop in blood pressure, cessation of cardiac activity and death. Here are the nuclei that control coughing, sneezing, vomiting, swallowing, blinking.

From the cells of the medulla oblongata originate such important cranial nerves as the vagus, glossopharyngeal, hypoglossal and accessory. One of the main pathways - pyramidal - goes from the motor centers of the cortex to the cells of the spinal cord, located in formations called "anterior horns".

Bridge - all connections of the cerebral cortex with the cerebellum, spinal cord, the transmission of auditory information pass through it. It contains the nuclei of the trigeminal, statoacoustic, abducens and facial nerves.

The midbrain - the neurons of this area regulate muscle tone, provide the possibility of movements, protective reflexes in response to visual or auditory factors, unconscious human reactions, for example, the simultaneous turn of the head and eyes in the direction of the included light stimulus.

What happens during a stroke?

Stem stroke in the form of hemorrhage can occur as an independent focus, then the bridge is most often affected. Such changes often end with a breakthrough of blood into the IV ventricle. If small hemorrhagic foci accompany a larger damage to the hemispheres, then they can merge and aggravate the general neurological symptoms.

Ischemic processes in the brain tissue are associated with impaired blood flow through the anterior, middle and posterior cerebral arteries or through external supply vessels (internal carotid, vertebral). The formation of an infarct zone in a stem stroke is accompanied by swelling of the brain tissue, which compresses the nerve trunks, centers, causes venous stasis and hemorrhages.

As a result, brain volume increases, intracranial pressure increases. This contributes to the displacement of various brain structures. With wedging and infringement of a part of the medulla oblongata in the large occipital foramen of the skull, the patient's condition is extremely serious, ending in death. Such consequences pose the main task in the treatment of stroke is the fight against edema, the introduction of diuretic drugs in the first hours of the disease.

Causes

The causes of a stem stroke do not differ from cerebrovascular accidents of other localization:

• atherosclerosis of the arteries;
• diabetes;
• hypertension;
• rheumatic vasculitis.

Hereditary predisposition affects the regulation of vascular tone, the disturbed structure of the walls of blood vessels, and metabolic changes in brain tissues.

Clinical manifestations

Hemorrhage in the brain stem is characterized by:

• sharp narrowing of the pupils;
• omission of the eyelid (ptosis) on the side of the focus;
• floating movements of the eyeballs;
• paralysis of the cranial nerves;
• rapid development of pneumonia with a tendency to edema;
• violation of the type of breathing (Cheyne-Stokes);
• paralysis of the limbs of the side opposite to the focus;
• high blood pressure;
• coma;
• an increase in body temperature;
• moist skin on the side of the lesion due to increased sweating.

Ptosis of the right eyelid indicates a lesion in the right half of the trunk

Ischemia of the trunk of a thrombotic or non-thrombotic nature often occurs gradually. More characteristic is the defeat of the zone of the vertebral and basilar arteries. All signs alternate periods of improvement and deterioration, but the disease progresses steadily. The patient is concerned about:

• dizziness;
• staggering when walking;
• hearing and vision loss;
• double vision;
• speech disorder (scanning phrases).

If a heart attack develops in the affected area, the following symptoms appear:

• paralysis of half of the body with impaired sensitivity;
• violation of the patient's consciousness to the degree of coma;
• change in breathing (rare with wheezing), rapid onset of pneumonia.

Alternating syndromes in the stroke clinic

Stroke of the stem region differs from impaired circulation in the cerebral cortex by the involvement of the nuclei and pathways of the motor nerves. Therefore, patients have a combination of central palsy with peripheral manifestations due to changes in the pathways of the cranial nerves.

Branches of the facial nerve are affected in alternating syndromes

Syndromes that include sets of symptoms due to ischemia in the zone of different nuclei and pathways are called alternating. They accompany stem paralysis of half of the body in different ways, always appear on the side of the lesion, indicate the level and location of the focus. Clinical manifestations were named after the doctors who first described these combinations.

Depending on the localization, they are divided into syndromes:

• lesions of the legs of the brain (peduncular);
• changes in bridge structures;
• disorders in the medulla oblongata (bulbar).

Neurologists are familiar with the description of the syndromes and use them in differential diagnosis.

Examples of alternating lesions:

• Millar-Gubler syndrome - paralysis of the facial nerve (omission of the eyelid, corner of the mouth);
• Brissot-Sicard syndrome - spastic contractions in the region of the branches of the facial nerve;
• Jackson syndrome - paralysis of the hypoglossal nerve with impaired swallowing;
• Avellis syndrome - paralysis of the soft palate and vocal cords, choking when eating, leakage of liquid food into the nose, impaired speech;
• Wallenberg-Zakharchenko syndrome - in addition to paralysis of the soft palate and vocal cords, loss of sensation on the skin of the face.

Treatment

Treatment of stem stroke is carried out from the first hours of detection. Since it is completely impossible to immediately establish the form of a stroke, all appointments relate to the stabilization of the vital functions of the brain, the removal of tissue edema.

To normalize breathing, oxygen therapy is carried out through a mask, in the absence or impaired breathing, the patient is intubated and transferred to artificial respiration with a ventilator.

Regulation of cardiac activity requires maintaining blood pressure no higher than 10% of the patient's normal level, antiarrhythmic drugs are administered, according to indications - cardiac glycosides, nitrates.

To maintain the necessary metabolism, an alkaline solution, preparations with potassium and magnesium are needed.

Normalizes coagulation and blood density reopoliglyukin.

Protection of brain cells is carried out with the help of neuroprotective drugs (Cerebrolysin, Piracetam).

To relieve swelling of the brain tissue, magnesium sulfate is administered, diuretics according to indications.

Perhaps the patient will need symptomatic drugs: muscle relaxants, painkillers, anticonvulsants, sedatives. Their introduction is determined by the specific clinic in the patient.

The use of such specific means as thrombolytic therapy is possible only with full confidence in the thrombosis of the cerebral arteries. It is effective only in the first 6 hours of clinical manifestations.

Residual strabismus after trunk stroke

What indicates a negative prognosis?

It is possible to determine in advance the consequences of a stroke in the structures of the trunk after a few days. Neurologists believe that the restoration of functions is almost impossible in severe bulbar paralysis. The patient can live for some time on machine breathing, but dies from cardiac arrest.

The presence of such symptoms indicates a deep lesion of motor functions in paralysis:

• "spread hip" - the femoral part of the paralyzed leg becomes wide and flabby due to loss of muscle tone;
• eyelid hypotension - the inability to independently open the eye on the side of the lesion;
• turned foot outward due to atony of the muscles that turn the leg.

How to predict the prognosis for the symptoms of a stroke?

Observation of the course of stem strokes has led to predictive assumptions for the recovery of patients.

The prognosis is considered unfavorable under such circumstances:

• speech disorder;
• rare breathing (it remains possible to completely stop during sleep);
• tendency to bradycardia and low blood pressure;
• altered thermoregulation (a sharp jump in body temperature up, then falling below normal).

Uncertain forecast for:

• impaired swallowing (possibly accustoming to liquid, pureed food);
• loss of movement in the limbs (recovery should be sought within a year);
• dizziness;
• uncoordinated eye movements.

In any case, the treatment of a stroke of the trunk requires a competent approach to therapy and the use of all the possibilities of rehabilitation.

I am 39 years old. In January 2015, I had a mixed-type stroke in the vertebral basin. I still have wasting strabismus. What can be done to restore vision? Thank you in advance!

My husband suffered an ischemic stroke in the brainstem (bridge on the left), a month and a half passed, but it got worse, constantly choking while eating, and even became weaker. We comply with all doctor's prescriptions. Walks with a walker with difficulty. Often the pressure jumps up to 200. I don’t know what to expect. He is 69 years old and of course type 2 diabetes.

I have a hemorrhagic stroke in the brainstem, I walk staggering, constant dizziness, I talk. The doctors said that this was the first time they had seen such a case. Will the dizziness go away and when?

On November 17, 2017, my dad had an ischemic stroke of the brain stem. Now he has been in a coma for a month after cardiac arrest. EEG shows weak brain activity. Could you tell me, please, what are the forecasts in this case?

Violation of cerebral circulation in the brain stem

A brainstem stroke is an acute disorder of blood circulation in this area, which is accompanied by a sudden onset of symptoms of a neurological deficit that persists for more than a day.

In Russia, the frequency of occurrence is 3.3 per 1000 population per year, and most of them are people over 70 years old. Mortality during the first month from the onset of the disease is 15-25%, and 70% of the victims receive disability.

Thanks to the development of medicine, in recent years there has been a trend towards a decrease in the incidence and mortality from strokes. However, there is a "rejuvenation" of this disease.

Most often, a stroke overtakes the elderly, but thanks to the development of medicine, mortality is decreasing.

To understand what symptoms will be with this lesion, you need to understand what are the anatomical features of the brain stem.

A little about the structure

The brain consists of the cerebral hemispheres and the brainstem.

The structure of the brain

The structure of the trunk includes the medulla oblongata, midbrain and diencephalon, and the bridge.

Structure of the brain stem

It performs the following functions:

1. provides reflex behavioral activity;
2. connects the higher and lower parts of the central nervous system by conduction pathways;
3. unites the structures of the brain.

It contains gray and white matter. Gray - neurons located in the form of nuclei, having certain functions. White - conductor paths. To distinguish a stroke in the brain stem from others, as well as to accurately determine the location of the focus, you need to represent the functions of its departments.

Functions of the medulla oblongata:

1. Innervation of the muscles of the tongue (the nucleus of the XII pair of cranial nerves) and some muscles of the head (the nucleus of the XI pair), larynx and oral cavity (the nucleus of the IX pair).
2. The work of the parasympathetic nervous system (vagus nerve - X pair).
3. Maintenance of vital functions (breathing, heartbeat) - the core of the reticular formation.
4. The implementation of some motor functions - extrapyramidal nuclei (olive).

Bridge functions:

1. Conduction of auditory impulses (nuclei of the VIII nerve).
2. Ensuring facial movements, as well as tear and salivation (nuclei of the VII nerve).
3. Implementation of abduction of the eye outward (nucleus of the VI pair).
4. Chewing movements are carried out by the nuclei of the fifth pair of cranial nerves.

Functions of the midbrain:

1. Other movements of the eyeball, eyelids, pupil (IV and III pairs of nerves).
2. Regulation of movement and muscle tone (nucleus of the substantia nigra).
3. Reflex response to light and sound impulses.
4. Muscular sensation of the face and neck.
5. Coordination of the joint rotation of the neck and eyes.
6. Collection of sensitive information from internal organs.

The brain stem coordinates the work of all internal organs, reflex activity, and some important motor acts. Depending on the location of the lesion, the symptoms will vary.

Etiology

By origin, a stem stroke happens:

1. ischemic is associated with a lack of blood flow due to blockage (obstruction) of the artery supplying the area;
2. hemorrhagic due to rupture of the artery and the outflow of blood from it.

Types of stem stroke

The first type is much more common than the second, it accounts for 75-80% of all cerebrovascular accidents.

Causes of ischemic stroke

Risk factors for ischemic stroke include older age, high blood pressure, increased blood cholesterol, atherosclerosis, smoking, heart disease, and diabetes mellitus.

It should be noted that the increase in blood pressure above 140/90 mm. Hg, relative to the norm, doubles the risk of stroke.

All causes of ischemic stroke can be divided into groups:

1. Atherothrombotic - ischemia occurs due to slowly increasing plaque in the vessel area. Such a stroke is preceded by symptoms of a transient cerebrovascular accident, signs of prolonged “stealing” of the brain by oxygen and nutrients: memory loss, absent-mindedness, the development of tearfulness or irascibility, and others. It often happens at night or early in the morning.
2. Embolic develops suddenly, there is a sharp and rapid blockage of the afferent artery by an embolus. It often occurs with heart diseases (atrial fibrillation, defects, artificial valves), which are characterized by the formation of blood clots in the cavities of the heart and their spread through the bloodstream. It often happens during the day, with emotional or physical overload.
3. It is possible to develop ischemia with a decrease in blood pressure, when there is insufficient blood flow to the brain. This is the hemodynamic type.
4. Lacunar is characterized by damage to small arteries located deep in the brain. It often develops during the day, against the background of high blood pressure. Since small areas are deprived of blood supply, the symptoms are erased, and its prognosis is better than that of the others.
5. Hemorheological is rare, develops due to an increase in blood viscosity.

High blood pressure is one of the causes of ischemic stroke.

The brain is such an organ where chemical processes are actively taking place, but it does not have its own reserves of nutrients. This means that any decrease in blood flow with oxygen and nutrients quickly affects its function in a negative way. Without a blood supply, a neuron can live for a maximum of five to eight minutes, after which it dies.

Normally, through 100 g of brain per minute, blood flows, with a stroke, this figure drops to 10.

After blockage of the vessel, the following is possible: in the area that it nourished, ischemia occurs, the neurons die, their function is lost. But next to it is another area (ischemic penumbra or penumbra), in which the blood supply has not reached a dangerous minimum. However, the brain cells in it also suffer from ischemia and damage by the decay products of dead neurons. They are viable, but they are also threatened with death, so it is important to start therapy as early as possible. This will reduce the affected area and preserve more brain function.

Due to the accumulation of decay products in this area, edema develops, which compresses adjacent structures, pushes them to the side, further disrupting blood flow and functioning.

Anatomy of an ischemic stroke

Causes of hemorrhagic stroke

It occurs less frequently, but its symptoms are more severe, and the prognosis is worse. Allocate:

1. With parenchymal hemorrhage, changes occur in the substance of the brain. This is possible with arterial hypertension, bleeding disorders or weakness of the vascular wall (aneurysm).
2. Subarachnoid - an outpouring of blood on the surface of the brain due to the pathology of blood vessels in the membranes. More often it is caused by an aneurysm, so it usually affects young, apparently healthy people.

A stroke of the brain stem develops with a lesion in the region of the vertebrobasilar vascular basin.

Symptoms

Stem stroke manifests itself in different ways, depending on the location of the lesion. It is characterized by the appearance of alternating (cross) symptoms, that is, the organs of the head and neck suffer on the side of the focus, and the movements of the limbs and the sensitivity of the skin of the body are on the opposite side.

Medulla

If the medulla oblongata is damaged, there will be a complete or partial impairment of the motor function of the tongue (its tip deviates towards the lesion), muscles of the soft palate, neck, vocal cords (hoarseness) on the side of the stroke, loss of facial skin sensitivity. On the opposite - violation or impossibility of movement of arms or legs, numbness of half of the body.

Stroke has a poor prognosis in the presence of bulbar palsy. It develops when there is a violation of blood circulation in the basin of the vertebral arteries, this causes bilateral damage to the IX, X, XII pairs of cranial nerves located in the medulla oblongata. At the same time, such violations as choking when swallowing, overhanging of the soft palate, impaired diction, hoarseness, small twitching of the tongue and restriction of its mobility are noted. Often it is followed by a violation of vital functions and death.

If the pathological focus is in the bridge, then on the side of the lesion there is an impossibility of movement of the mimic muscles, loss of surface sensitivity on the face, hearing loss, the gaze is directed towards the focus. On the opposite, movement disorders in the limbs and a decrease in sensitivity are revealed. Often accompanied by impaired consciousness up to coma.

Pseudobulbar palsy manifests itself in the same way as bulbar palsy, but its cause is damage to the pathways at the level of the bridge and above, so the prognosis is more favorable, since violations of vital functions usually do not follow. A distinctive feature is the absence of twitching of the tongue, pharyngeal and palatine reflexes are preserved or increased, symptoms of oral automatism are revealed.

With thrombosis of the basilar artery, a “locked-in syndrome” develops. With intact consciousness, the patient does not move any muscles, except for the eyeballs and blinking.

midbrain

Stem stroke with localization in the midbrain is manifested by the impossibility of eye movements, the absence of pupil reaction on the side of the lesion. On the opposite side, the movement of the limbs is disturbed, a tremor (involuntary trembling) of the hand appears. Perhaps the development of pseudobulbar paralysis.

A syndrome of decerebrate and decortication rigidity indicates a poor prognosis. The reason is a stem stroke in the midbrain pathways at a level above the vestibular nuclei. Decerebrate rigidity is manifested by coma in combination with an increase in the tone of all muscles, mainly extensor muscles, when the arms and legs are brought to the body, and the head is thrown back. Decortication - the upper limbs are bent, and the lower limbs are unbent.

If the lesion is localized below the vestibular nuclei, then a coma occurs with a lack of muscle tone.

Diagnostics

If a stem stroke is suspected, as well as with other lesions, if possible, magnetic resonance or computed tomography is performed. This allows you to identify the presence and location of the area of ​​impaired blood circulation. The speed of correct diagnosis directly affects the final prognosis of the disease.

Doppler ultrasound is a technique for studying blood flow in the vessels. It reveals areas of missing blood supply or hemorrhage.

An important indicator of the functional characteristics of the body are general clinical tests (general blood and urine tests), biochemical blood tests, ECG, and, if necessary, echocardiography (visual ultrasound examination of the heart).

All this information allows you to establish the diagnosis of stroke, its localization, which determines the prognosis of recovery and treatment tactics.

Treatment

If a stroke of any localization is suspected, hospitalization in the neurological department is mandatory.

Seek medical attention if you suspect a stroke

Stem stroke is treated according to the same principles as any other. Basic therapy includes maintaining the vital functions of the body: breathing, pressure, heartbeat, body temperature, as well as reducing cerebral edema.

Specific therapy is aimed at eliminating the causes of the disease. It includes, for example, thrombolysis, normalization of blood viscosity. Measures are being taken for neuroprotection and restoration of neuronal function.

The faster the symptoms of neurological deficit pass, the better the further prognosis.

Consequences

Unfortunately, stem stroke often has a poor prognosis. Dizziness, speech and swallowing disorders, muscle paralysis of various localization and functions, loss of sensitivity remain with the patient for a long time.

Rehabilitation aimed at replacing these functions is long and permanent, and the coming improvements are slow and insignificant.

However, this does not mean that rehabilitation should be abandoned. Recovery is possible only through work on impaired functions.

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Brain stem tumor: signs, treatment tactics and survival prognosis

Brain stem tumors are one of the diseases of the central nervous system, manifested by many symptoms. The medulla oblongata and middle pons are affected.

In 90% of situations, the disease has a glial origin. Glia are cells that create the necessary conditions for the full functioning of the central nervous system.

Statistics

There are 20 people with this diagnosis per 100,000 people. The disease develops in people of different ages, races, genders.

A malignant tumor has the ICD-10 code C71.7.[

Tumors of the brainstem affect the nuclear formations that conduct the pathways, but rarely cause a violation of the outflow of cerebrospinal fluid. The latter occurs only in advanced stages and during development next to the Sylvian aqueducts.

Varieties

Neoplasms affecting the trunk are divided into benign and malignant.

The first type is characterized by a slow increase. Sometimes it takes more than 15 years. Malignant lead to rapid death.

Despite the fact that tumors are localized in different areas, more often they affect the bridge.

Stem tumors are divided into:

1. Primary-stem, forming according to the intra-stem or exophytic type. They are formed only from the tumor of the table itself.
2. Secondary-stem, appearing from other brain structures. They develop from the cerebellum, the fourth ventricle, only eventually grow into the trunk.
3. Parastem formations lead to deformation of the trunk or are simply in close interaction with it.

Tumors are classified according to the characteristics of growth. If they take development from their own cells and form a shell, pushing back tissues, then we are talking about expansive growth. If the neoplasm grows into other tissues, it is called infiltrating. In a diffuse tumor of the brain stem, which occurs in 80% of cases, the boundaries of the tumor are not determined even microscopically.

Causes

The exact prerequisites for the appearance remain hidden, but experts focus on hereditary factors and receiving high doses of ionizing radiation.

In the first case, the genetic information of cells changes. This leads to the fact that they begin to have tumor properties, multiply uncontrollably and inhibit the vital activity of other cells.

A predisposition to neoplasms is in those people who have previously received treatment with radiation from ringworm of the scalp.

Today, this method is not used, but modern methods of radiation therapy also lead to the formation of malignant cells.

There are suggestions that vinyl chloride causes brain stem cancer. This gas is used in the production of plastics.

Symptoms of brain stem tumors in adults and children

There are many structures in the brain stem, so the course of the disease can be different. In children, due to the development of compensatory mechanisms of the nervous tissue, neoplasms often have a long asymptomatic course.

In the future, the symptoms depend on the location of the neoplasm and the type of tumor. In adults, it is difficult to identify focal symptoms.

In preschool children, the first alarming signs are loss of appetite, decreased mental and motor activity. Schoolchildren experience a significant decrease in academic performance, a change in behavior, and the appearance of chronic fatigue. Almost always there is a movement disorder.

As the tumor grows, the symptoms increase. Private migraines, nausea, vomiting join. Violations affect the cardiovascular and respiratory center of the trunk. This is what causes death.

Emergence of new behavioral responses is noted

If the neoplasm is malignant, convulsions, fear of light join.

Diagnosis of neoplasms

The study involves a full range of diagnostic measures. The preliminary diagnosis is established by a neurologist.

The main importance is given to:

1. Computed tomography, which makes it possible to obtain information about the composition of tissues, identify pathologies and conduct monitoring in dynamics. During the procedure, an image of sections of the brain at different levels is obtained.
2. SCT is a method that allows ultra-fast scanning of structures, therefore it is used for patients in serious condition. Allows you to fix even the smallest deviations in the structure.
3. MRI with the introduction of a contrast agent. This method reveals formations of a small size, makes it possible to determine the presence of an exophytic component. This also allows a preliminary assessment of the presence of neoplasm growth and the degree of infiltration.

Thanks to these techniques, a brain stem tumor is differentiated from multiple sclerosis, encephalitis, stroke, and hematoma.

Additionally, angiography is performed. The method is necessary to determine the specifics of the blood supply to the formation and the vessels that feed the tumor. A biopsy is done to obtain samples of the tumor. The procedure is performed by minimally invasive surgical methods using ultrasound or X-ray control.

Treatment of pathology

Only a radical integrated approach will help to improve the patient's condition, consisting of:

The first technique is aimed at removing the formation with the maximum possible preservation of healthy trunk tissues. Surgical intervention becomes possible after a craniotomy, that is, making a hole in a pre-selected place to gain access to the tumor.

Radiation therapy can also be performed in situations where surgical treatment is contraindicated. The method is not recommended for children under three years of age, as physical and intellectual retardation develops in the future. For the procedure, special installations are used that allow you to influence the tumor from different angles.

This direction is called stereotactic radiosurgery. First, a study is carried out aimed at accurately determining the location. Then irradiation is carried out on a special technique.

Chemotherapy is aimed at suppressing the growth of malignant cells. For this, drugs are used that act on the formations, causing a minimum of side effects. This method can also be used for toddlers who have not yet reached the age of three.

Most funds are administered intravenously into the bloodstream using droppers and injections. Sometimes the doctor decides to administer medication through a long tube that is connected to a large vein in the chest. Chemotherapy is carried out cyclically.

Disease prognosis

It is believed that when a brainstem tumor is removed in childhood, the prognosis is several times better than in adults.

Benign tumors can grow up to 15 years without symptoms, but most brain stem tumors are malignant.

In this case, death occurs within a few years or months from the onset of symptoms. Usually, the treatment provided only slightly prolongs life.

What is a brain stem infarction

In fact, the trunk is nothing more than a "bridge" connecting the spinal cord to the brain. It is he who is responsible for the transmission of all the "orders" of the brain throughout the body.

Stem infarction is accompanied by damage to the cerebellum, thalamic region, medulla oblongata and midbrain, and the pons.

The nuclei of the cranial nerves are also located in this area, "guiding" the contraction of the muscles of the eyes, face, as well as the muscles that help to make swallowing movements. The trunk also contains the most important centers for human life, which are responsible for the respiratory function, thermoregulation, and blood circulation.

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A cerebral infarction is a hemorrhage in the brain, followed by the formation of a hematoma that blocks the supply of oxygen to the damaged area.

As a result of the development of hypoxia, that is, a lack of oxygen, atrophy of the brain stem occurs, which leads to disruption of the work of all internal organs.

Depending on the mechanism by which the lesion develops, ischemic and hemorrhagic infarction are distinguished. Currently, the former, according to mortality statistics, ranks second. It is also called a cerebral infarction.

Ischemic infarction is an extensive damage to the brain tissue that has arisen due to a serious failure in blood circulation. Blood simply does not reach certain areas of the brain, which leads to softening, as well as tissue death in them.

The causes of brainstem infarction are varied, but the main one is atherosclerosis. It can also develop due to diabetes mellitus, and in some cases due to rheumatism and hypertension.

When a patient has a weakening of motor activity, dizziness, problems with coordination, nausea, then all this indicates the development of an ischemic infarction.

Symptoms

Hemorrhage, or the so-called infarction of the brain stem region, occurs suddenly. As a rule, this is accompanied by dizziness, slurred speech, the occurrence of autonomic disorders, such as a decrease and then an increase in body temperature, redness or pallor of the face, sweating.

There is also a tension in the pulse, an increase in blood pressure. Further, to this list of symptoms, circulatory and respiratory disorders are added. It is possible to suspect a cerebral infarction by the occurrence of rapid, rare, complicated by exhalation and inhalation of breathing.

Sometimes, against the background of a cerebral infarction, some patients develop a "locked-in person" syndrome - due to a violation of the distribution of electrical impulses from the brain throughout the body, the patient experiences paralysis of the limbs.

At the same time, there remains the intellectual ability and the ability to evaluate and understand what is happening around. Such patients can actively help during their recovery.

When a cerebral infarction occurs, 2/3 of all cases end in death in the first two days due to damage to the most basic vital functions for the body. With timely medical attention, death can be avoided. Also, a favorable outcome can occur if a stem infarction occurs in young people.

When the first signs of a heart attack, even minor ones, appear, you should immediately call an ambulance or consult a doctor.

Prognosis for dysfunction

The prognosis for a brain stem infarction is very disappointing. 30% of patients develop speech disorders. She becomes slurred, quiet and incomprehensible. However, this problem can be slightly solved by using the services of a speech therapist. In the case of the development of the “locked-in person” syndrome, such a solution to the problem is impossible, since patients can only move their eyelids.

• most often with a cerebral infarction, malfunctions in the swallowing function occur (according to statistics, about 65%);
• for patients with dysphagia, i.e. with inflammatory processes in the pharynx or mouth, the prognosis for recovery is uncertain;
• the only option is to re-teach patients to swallow grated or soft food using various techniques.

• when a trunk infarction occurs, patients experience a malfunction in the limbs, and they begin to move spontaneously;
• a positive prognosis for such a function is possible only in the first 2-3 months;
• in the future, the more time passes from the moment of the disease, the more the recovery decreases;
• sometimes the recovery process can last for a year;
• longer periods are extremely rare.

• if the respiratory section is affected during a trunk infarction, then patients are simply not able to breathe on their own;
• unfortunately, the prognosis for them is very disappointing: their life will completely depend on the artificial respiration apparatus;
• if the respiratory center is not completely damaged, then patients may experience sleep apnea;
• it is nothing more than stopping breathing during sleep for a short period;
• there may also be slow breathing during wakefulness.

• the earliest sign indicating that a heart attack has occurred in the brain is dizziness;
• as a rule, this symptom passes fairly quickly with proper treatment and recovery;
• until the final disappearance of the symptom, the timing is uncertain and depends solely on how badly the brain was affected.

• a heart attack of the trunk can also lead to a malfunction of the cardiovascular system;
• in this case, a frequent heartbeat and increased blood pressure are observed;
• with a decrease in heart rate, the prognosis for the patient, alas, is unfavorable;
• in this case, the patient is in serious condition, which can be fatal.

• also with a heart attack of the trunk, thermoregulation may be affected, indicating a serious condition of the patient;
• as a rule, there is a rise in temperature to 39 degrees or more on the first day of a heart attack;
• this condition is difficult to manage;
• if the patient's body temperature is lowered, then this indicates that soon the brain cells will die.

• quite often, with a heart attack, the visual center located in the brain stem is affected;
• therefore, the patient may experience spontaneous eye movement (either one or both);
• the ability of a person to focus his gaze on some object or image is also impaired, it becomes difficult to move his eyes up and to the sides, strabismus may develop.

Read about the consequences and rehabilitation after a macrofocal myocardial infarction in another publication.

Stem infarction needs professional and long-term treatment. In severe conditions, it may require an operating campaign.

Treatment of brain stem infarction

As mentioned above, even if a cerebral infarction is suspected, the patient must be urgently taken to the hospital. The very first task that needs to be solved is to stop the blood circulation in the brain, including the affected part of it, and also to normalize the work of the lungs and heart.

In severe conditions of cerebral infarction, surgery is performed. As a rule, it is carried out in the first hours after the onset of an attack.

Unfortunately, quite often the infarction of the trunk has such a severe form of the course that it does not allow the use of angiographic examination and even surgery. In this case, doctors carry out the necessary resuscitation measures.

Patients with stem infarction, even after surgery, need long-term treatment and rehabilitation therapy in order to reduce and eliminate possible consequences.

To prevent a recurrent attack, it is necessary to timely treat chronic diseases of the heart and blood vessels, as well as regulate atherosclerotic processes by changing the diet.

For treatment, a heart attack of the trunk, as a rule, is prescribed:

• physiotherapy;
• medications that prevent the occurrence of blood clots in the vessels;
• drugs that lead to blood thinning, and, consequently, blood clots;
• medicines to lower blood pressure;
• medicines that lower blood cholesterol levels;
• medicines to help control heart rate.

Trunk infarction belongs to diseases that are very difficult to treat. Recently, quite often one of the ways to treat this disease is the infusion of platelets into the region of the brain damaged by a heart attack.

Rehabilitation therapy can be carried out both at home and in rehabilitation centers or specialized sanatoriums.

Also, the treatment includes resuscitation, inpatient therapy and physiotherapy methods.

Read more about intramural myocardial infarction here.

You will find a description of focal infarction in this article.

During the treatment period, it is very important to nullify all physical and emotional stress on the body, as well as maintain all its important life-support functions. This approach allows you to very quickly restore blood circulation in the affected area of ​​​​the brain.

The next stage of treatment is rehabilitation therapy. You should not postpone it for a long time, as this leads to the loss of certain brain functions, which, unfortunately, will not be possible to restore later.

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brainstem syndrome includes three levels of lesions - mesencephalic, pontine and bulbar, the anatomical and physiological features of which determine the clinical manifestations of their lesions.

mesencephalic or mesencephalic level of brain stem damage characterized by a disorder of pupillary reactions, paralysis and paresis of individual muscles of the eye, a violation of friendly movements of the eyeballs upward, a violation of muscle tone, the appearance of convergent, rotatory and vertical nystagmus. With TBI, total damage to mesencephalic structures is not observed, because these injuries are not compatible with the life of the victim. Partial injuries usually occur, among which there are quadrigeminal, tegmental, peduncular syndromes and an alternating syndrome of damage to the half of the trunk.

Four hill syndrome includes upward gaze disorders, convergence disorders, pupillary reactions disorders, various forms of nystagmus (vertical, horizontal, diagonal, convergent, rotatory).

Tegmental or tegmental syndrome includes violations of the function of the oculomotor nerves, conduction disorders of sensitivity, muscle tone, coordinating disorders. With an increase in damage to the tegmental parts of the brain, decerebrate rigidity, hyperthermia, and respiratory rhythm disturbances develop.

Peduncular Syndrome includes movement disorders in the contralateral limbs (from mono- to hemiparesis).

Pontine level defeat captures the nucleusV ,VI,VII,VIII pairs of cranial nerves, i.e. a group of nerves of the cerebellopontine angle, which determines the nature of clinical manifestations. Hearing impairment, decreased sensitivity in the area of ​​the trigeminal nerve, dysfunction of the facial, abducens nerves are often combined with cerebellar symptoms.

bulbar level characterized by damage to the medulla oblongata with the appearance of dysphagia, aphonia, anarthria with impaired swallowing and articulation. They are combined with disorders of cardiac and respiratory functions, a decrease in blood pressure, the appearance of fascicular and fibrillar twitching of the muscles of the tongue. The involvement of the medulla oblongata in the process is characterized by the appearance of homolateral pyramidal insufficiency, sensitivity disorders, or the development of alternating syndromes.

It is characteristic that in TBI, stem symptoms can be not only the result of a primary traumatic lesion of these formations, but also be a consequence of secondary injuries as a result of dislocations and wedging of stem structures.

Describing the semiotics of brain damage in TBI, it is especially necessary to note the peculiarities of the manifestationsdisengagement syndromewith DAP. They are most clearly detected when patients transition from a coma to a transient or vegetative state. In the absence of any signs of the functioning of the cerebral cortex, subcortical, stem and spinal mechanisms are clearly manifested. A variety of oculomotor, pupillary, oral, bulbar, pyramidal and extrapyramidal syndromes are found. They appear spontaneously or in response to any irritation with a wide variety of positional-tonic and defensive reactions and postures, facial synkinesis.

Separately, it is necessary to dwell on the syndromes of herniation, which often develop in victims with severe traumatic brain injury. Allocate transtentorial, temporal-tentorial, cerebellar-tentorial herniation, as well as the herniation under the falciform process and the herniation of the tonsils of the cerebellum.

Tentorial herniation occurs as a result of diffuse cerebral edema or with massive central, bilateral volumetric processes (hematomas, bruises). At the same time, the brain stem shifts caudally and symptoms develop, characterized by a violation of consciousness, the development of Cheyne-Stokes breathing, constriction of the pupils and the disappearance of their reaction to light, the appearance of a decortication and even decerebrate posture of the patient.

Temporotentorial herniation occurs as a result of lateral displacement of the brain due to the mass effect in hemispheric bruises, unilateral supratentorial hematomas. In this case, a hernial herniation of the hook of the hippocampal gyrus occurs in the gap between the edge of the tentorium and the brain stem. Clinical manifestations are characterized by progressive depression of consciousness, pupil dilation and dysfunction of the oculomotor nerve on the side of the lesion, dysfunction of the midbrain, the appearance of decerebrate rigidity and hyperventilation.

Cerebellar-tentorial herniation occurs with an increase in pressure in the subtentorial space (hematomas of the cerebellum and posterior cranial fossa). The brain stem is displaced in the rostral direction, which is accompanied by an acute impairment of consciousness, the development of the quadrigeminal syndrome.

Herniation of the tonsils of the cerebellum also occurs with volumetric processes in the posterior cranial fossa, which leads to the lowering and wedging of the cerebellar tonsils into the foramen magnum with the development of the medulla oblongata syndrome and frequent respiratory failure.

Wedging under the falciform process like the temporo-tentorial herniation, it occurs during lateral volumetric processes. The cingulate gyrus hernially protrudes under the falciform process, while the blood flow through the anterior cerebral artery is disturbed, occlusion of the foramen of Monro may occur with difficulty in the outflow of cerebrospinal fluid from the lateral ventricle.

The described signs of brain damage apply to all age groups of victims, but it is also very obvious that children in this context represent a special group of victims, and the younger the patient, the greater the differences. The study of the circumstances of the injury, premorbid history, the degree and duration of impaired consciousness, speech, mental functions, and much more is often not possible in children. Preservation of some pathological reflexes in children is often just an age norm, and the formation of psychomotor retardation and pronounced astheno-vegetative or vegetative-visceral syndrome in the late post-traumatic period in children is a well-known fact and requires its own special approach to both diagnostic constructions and therapeutic tactics. in children with TBI.

Brain contusions include focal macrostructural damage to its substance resulting from shock-impact trauma. According to the unified clinical classification of traumatic brain injury adopted in Russia, focal brain contusions are divided into three degrees of severity: mild, moderate and severe.

Severity

Pathologically, mild brain contusion is characterized by clustered petechial hemorrhages, limited ruptures of small pial vessels, and areas of local edema of the brain substance.

Mild brain contusion occurs in 10-15% of patients with TBI. It is characterized by a short-term shutdown of consciousness after an injury (several seconds or minutes). Upon its recovery, complaints of headache, dizziness, nausea, etc. are typical. Retro-, con-, anterograde amnesia and vomiting, sometimes repeated, are observed. Vital functions are usually without pronounced disturbances. Moderate bradycardia or tachycardia may occur, sometimes arterial hypertension. Respiration, as well as body temperature - without significant deviations. Neurological symptoms are usually mild (clonic nystagmus, mild anisocaria, signs of pyramidal insufficiency, meningeal symptoms), regress within 2-3 weeks.

With mild brain contusion, fractures of the bones of the cranial vault and subarachnoid hemorrhage are possible. CT in half of the observations reveals a limited zone of low density in the medulla, close in terms of tomodensitometric parameters to cerebral edema (from 18 to 28 N). In this case, as pathoanatomical studies have shown, small hemorrhages are possible, for the visualization of which the resolution of CT is not enough. In the other half of the observations, mild brain contusion is not accompanied by obvious changes in the CT picture, which is associated with the limitations of the method. Cerebral edema with a mild bruise can be not only local, but also more widespread. It is manifested by a moderate volumetric effect in the form of a narrowing of the cerebrospinal fluid spaces. These changes are detected already in the first hours after the injury, usually reach a maximum on the 3rd day and disappear after 2 weeks, leaving no traces of the nest. Local edema in mild contusion may also be iso-dense, in which case the diagnosis is based on the volumetric effect as well as the results of a dynamic CT scan.

MRI (when using devices with high resolution - 1.0-1.5 Tesla) is able to give a more detailed than CT characterization of mild brain contusion.

Pathologically, a moderate contusion is characterized by small focal hemorrhages, areas of hemorrhagic impregnation of the brain tissue with small foci of softening, while the configuration of the gyrus sulci and connections with the pia maters are preserved.

Moderate brain contusion occurs in 8-10% of victims with TBI. It is characterized by loss of consciousness after injury up to several tens of minutes - several hours. Expressed retro-, con- and anterograde amnesia. The headache is often severe. There is vomiting, sometimes multiple. There are mental disorders. Transient disorders of vital functions are possible: bradycardia or tachycardia, increased blood pressure; tachypnea without disturbing the rhythm of breathing and patency of the tracheobronchial tree; subfebrile condition. Shell signs are often expressed. Stem symptoms are detected: nystagmus, dissociation of meningeal symptoms along the axis of the body, bilateral pyramidal signs, etc. Focal symptoms (determined by the location of the brain contusion) are clearly manifested: pupillary and oculomotor disorders, paresis of the extremities, disorders of sensitivity, speech, etc. These nest marks are gradually (within 3-5 weeks) smoothed out, but they can also last for a long time. With moderate brain contusion, fractures of the bones of the vault and base of the skull, as well as significant subarachnoid hemorrhage, are often observed.

CT in most cases reveals focal changes in the form of high-density inclusions that are not compactly located in the zone of low density, or a moderate homogeneous increase in density over a small area. As the data of operations and autopsies show, these CT findings correspond to small hemorrhages in the bruised area or moderate hemorrhagic impregnation of the brain tissue without its gross destruction. Dynamic CT reveals that these changes are reversed during treatment. In terms of observations in the clinic of moderate brain contusion, CT reveals foci of low density - local edema or traumatic substrate is not convincingly visualized.

Moderate brain contusions on MRI are detected as focal changes in a heterogeneous or homogeneous structure, which is determined by the characteristics of hemorrhages in the bruised area and their duration, and reflect the situation of hemorrhagic impregnation of the brain tissue without its gross destruction.

Pathologically, a severe brain contusion is characterized by areas of traumatic destruction of the brain tissue with the formation of detritus, multiple hemorrhages (liquid blood and its convolutions) with the loss of the configuration of the sulci and convolutions and rupture of connections with the pia maters.

Severe brain contusion occurs in 5-7% of patients with TBI. It is characterized by loss of consciousness after an injury lasting from several hours to several weeks. Motor excitation is often expressed. Severe threatening violations of vital functions are observed: bradycardia or tachycardia; arterial hypertension; disturbances in the frequency and rhythm of breathing, which may be accompanied by impaired patency of the upper respiratory tract. Pronounced hyperthermia. Primary stem neurological symptoms often dominate (floating movements of the eyeballs, gaze paresis, tonic multiple nystagmus, swallowing disorders, bilateral mydriasis or miosis, eye divergence along the horizontal or vertical axis, changing muscle tone, decibratory rigidity, inhibition or irritation of tendon reflexes, reflexes from the mucous membranes and skin, bilateral pathological foot reflexes, etc.), which obscures focal hemispheric symptoms in the first hours and days after the injury. Paresis of the extremities (up to paralysis), subcortical disorders of muscle tone, reflexes of oral automatism, etc. can be detected. Generalized or focal seizures are sometimes noted. Cerebral and especially focal symptoms regress slowly; gross residual phenomena are frequent, primarily from the motor and mental spheres. A severe brain contusion is very often accompanied by fractures of the vault and base of the skull, as well as massive subarachnoid hemorrhage.

With severe brain contusion, CT often reveals focal brain changes in the form of a zone of non-uniform increase in density. With local tomodensitometry, they are determined by the alternation of areas with increased - from 64 to 76 N (density of fresh blood clots) and low density - from 18 to 28 N (density of edematous and / or crushed brain tissue). As the data of the operation and autopsy show, CT reflects such a situation in the bruised area, in which the volume of brain detritus significantly exceeds the amount of blood that has poured out. In the most severe cases, the destruction of the brain substance extends in depth, reaching the subcortical nuclei and the ventricular system.

In almost half of cases of severe brain contusion, CT scan reveals significant foci of intense homogeneous increase in density ranging from 65 to 76 N. As data from operations and autopsies show, tomodensitometric signs of such contusions indicate the presence of a mixture of liquid blood and its clots in the area of ​​brain damage with detritus of the brain, the amount of which is much inferior to the amount of blood poured out. Crush foci are characterized by the severity of perifocal edema with the formation of a hypodense path to the nearest part of the lateral ventricle, through which fluid is discharged with decay products of brain tissue and blood.

Severe brain contusions are well visualized by MRI, on which they usually represent zones of heterogeneous changes in signal intensity.

Topical options for the location of bruises and crush injuries of the brain are extremely diverse, and, accordingly, the clinic is variable. Nevertheless, it is useful for a practical doctor to present their semiotics, taking into account the main places of localization.

Frontal lobe damage

Up to 40-50% of focal damage to the substance of the brain is localized in the frontal lobes. This is due, firstly, to the significance of their mass - the frontal lobes surpass all other parts of the brain in their volume, and secondly, to the special susceptibility of the frontal lobes to both shock (when a traumatic agent is applied to the frontal region), and, especially, shockproof shock ( when applying a traumatic agent to the occipital region) injury. Due to their mass and relative remoteness, especially the anterior sections (compared to the temporal lobes), from the brainstem, the frontal lobes often have the ability to “absorb” the mass effect for a long time even with their large focal lesions. This is also facilitated by the sanogenic discharge of excess fluid along with decay products through the emerging "paths" from the crush foci into the anterior horns of the lateral ventricles.

With damage to the frontal lobes, cerebral symptoms are represented by depression of consciousness within the limits of stunning, stupor or coma (depending on the severity of the injury). Often characterized by the development of intracranial hypertension with intense headache, repeated vomiting, psychomotor agitation, bradycardia, the appearance of congestion in the fundus (especially with basal lesions). With massive crush foci with severe perifocal edema, axial displacement may develop with the occurrence of secondary midbrain symptoms (paresis of upward gaze, spontaneous nystagmus, bilateral pathological signs, etc.). With damage to the frontal lobes, sleep and wakefulness disturbances with their inversion are especially frequent: excitation at night and drowsiness during the day.

For bruises of the frontal lobes of a severe degree, the severity of meningeal symptoms is characteristic with a frequent predominance, as the cerebrospinal fluid is sanitized, Kernig's symptom over stiff neck muscles.

Among the focal signs, mental disorders dominate, which manifest themselves the brighter, the less the consciousness is depressed. In most observations, there are violations of consciousness by the type of its disintegration. With the defeat of the left frontal lobe, twilight states of consciousness, psychomotor seizures, absences with amnesia for them are possible. With damage to the right frontal lobe, confabulations or confabulatory confusion occupy the main place. Frequent changes in the emotional and personal sphere. As part of the disintegration of consciousness, disorientation in one's own personality, place and time, negativism, resistance to examination, lack of criticism of one's condition, stereotypes in speech, behavior, echolalia, perseveration, bulimia, thirst, untidiness, impaired control over the functions of the pelvic organs, etc. .P.

It should be borne in mind that in the first 7-14 days after TBI, there is often a wave of depression of consciousness within the limits of stunning-stupor with episodes of confusion and psychomotor agitation. In victims with an alcohol history, on the 2-5th day after TBI, a delirious state with visual and tactile hallucinations may develop.

As the distance from the moment of injury and conditional clarification of consciousness (exit from stupor) interhemispheric and local features of mental disorders in frontal lobes are more clearly manifested.

Patients with a predominant lesion of the right frontal lobe often show signs of personality decline (criticism of their condition, apathy, a tendency to complacency and other manifestations of simplification of emotional reactions), a decrease in initiative, and memory for current events suffer. Often there are emotional disorders of varying severity. Euphoria with disinhibition, extreme irritability, unmotivated or inadequate outbursts of anger, anger (angry mania syndrome) are possible.

Patients with a lesion of the dominant (left) frontal lobe may have speech disorders according to the type of motor aphasia (efferent - with damage to the lower parts of the premotor region), dysmnesic phenomena in the absence of pronounced disorders in the perception of space and time (more typical for lesions of the right frontal lobe).

With bilateral damage to the frontal lobes, the mentioned mental disorders are added (or aggravated) by the lack of initiative, motivation for activity, gross inertia of mental processes, loss of social skills, often against the background of abulic euphoria. In some cases, pseudobulbar syndrome develops.

For fronto-basal injuries, one- or two-sided anosmia is typical in combination with euphoria or even euphoric disinhibition, especially when the right frontal lobe is affected.

With convexital localization of damage to the frontal lobes, central paresis of the facial and hypoglossal nerves, contralateral mono- or hemiparesis of the extremities, linguofaciobrachial paresis in combination with a decrease in initiative up to aspontaneity are characteristic, especially with damage to the left frontal lobe - in the psychomotor sphere and speech.

For damage to the anterior parts of the frontal lobe, dissociation is typical between the absence of paresis of the facial muscles when following instructions ("show your teeth", etc.) and a pronounced paresis of the same muscles in facial expressions (mimic paresis of the facial nerve).

With injuries that involve the extrapyramidal parts of the frontal lobes, a symptom of resistance is often encountered. When a doctor checks passive movements in the limbs or in the neck, an involuntary tension of the antagonist muscles occurs, giving the impression of a conscious resistance of the patient.

Due to the violation of the fronto-bridge-cerebellar pathways in case of focal lesions of the frontal lobe, trunk ataxia is characteristic with the inability to sit, stand and walk (astasia-abasia), while the body deviates in the direction opposite to the lesion.

With frontal bruises, epileptic seizures often occur - general (frontal lobe pole), adversive (premotor zone), focal convulsive seizures with further generalization (anterior central gyrus).

With focal lesions of the frontal lobes, grasping reflexes, a proboscis reflex, and other symptoms of oral automatism are almost always detected.

Depending on the degree of damage to the dorsolateral, prefrontal, orbitofrontal, or mediofrontal cortex and their connections with the thalamus opticus, caudate nucleus, globus pallidus, substantia nigra, and other subcortical and stem formations, the structure of frontal lobe contusion symptoms changes.

Temporal lobe damage

The temporal lobe is a very vulnerable brain formation in TBI. The temporal lobes account for up to 35-45% of all cases of focal brain damage. This is due to the particularly frequent application of a traumatic agent to the temporal region, the suffering of the temporal lobes by the mechanism of counter-impact in almost any localization of the primary application of mechanical energy to the head, anatomical conditions (thin scales of the temporal bone, the location of the bulk of the lobe in the middle cranial fossa, limited by the bone-dural protrusions , directly adjacent to the brain stem). As a result, the temporal lobes are also among the "favorite" locations of foci of bruising and crushing of the brain.

Cerebral symptoms in damage to the temporal lobes are similar to those in damage to other lobes of the brain: changes in consciousness from moderate deafness to deep coma; headache with nausea, dizziness, vomiting; congestion in the fundus; psychomotor outbursts, etc.

However, due to the anatomical proximity of the temporal lobes to the oral parts of the trunk and hypothalamus, an increase in intracranial pressure in case of their focal damage can quickly and sharply cause life-threatening brain dislocations. The "shock-absorbing" role of a significant layer of the brain substance, which softens the impact on the trunk of focal lesions of the frontal, parietal, or occipital lobes, is much less here.

Therefore, the clinical picture of damage to the temporal lobes is more than in any other localization of brain contusions, secondary stem symptoms are intertwined. Basically, we are talking about displacements of the oral part of the trunk in cases of an increase in the volume of the affected temporal lobe and penetration of the hippocampal hook into the tentorial foramen. The diencephalon and midbrain are displaced contralaterally from the pathological focus, injured on the opposite edge of the cerebellar plaque, while secondary dysgemia in the trunk and axonal damage to the conduction systems often develop.

The midbrain dislocation syndrome in case of damage to the temporal lobe manifests itself as anisocoria, vertical nystagmus, paresis of the upward gaze, bilateral pathological foot signs, homolateral paresis of the extremities, followed by gross diffuse disorders of muscle tone and threatening disorders of vital functions. Acute dislocations and deformations of the trunk are extremely dangerous for the life of the victim. With subacute or slowly growing dislocations, there are more opportunities for stopping them.

A number of vegetative and visceral disorders, similar to those of the medial-temporal, also occurs when the diencephalic structures are displaced, while disturbances in the rhythm of sleep, thermoregulation, and vascular microcirculation are also observed; hormonal convulsions may develop. Of the secondary symptoms in injuries of the temporal lobe, pons and medulla oblongata syndromes are less common and less pronounced.

Among the local signs of damage to the temporal lobes of the dominant (left) hemisphere, the phenomena of sensory aphasia attract attention - from difficulty understanding complex turns of inverted speech to a complete loss of analysis of both audible and one's own speech, which is figuratively referred to as "verbal okroshka". In intermediate degrees of sensory aphasia, literal and verbal paraphasias are observed; defects in auditory-speech memory, recognition and reproduction of phonemes similar in sound in syllables and words, alienation of the meaning of words. With the defeat of the angular gyrus, located at the junction with the parietal and occipital lobes, that is, the zone that integrates auditory, visual and sensory afferentation, alexia, agraphia, and acalculia develop. Damage to similar zones of the subdominant (right) hemisphere causes a violation of the recognition and reproduction of "first-signal" sounds - household, street, natural noises, as well as familiar melodies, intonation and emotional structure of speech, which can be checked if the general condition of the victim allows.

Damage to the posterior third of the inferior temporal gyrus causes the development of amnestic aphasia, although this symptom after TBI can also act as a cerebral symptom, especially in the elderly.

Deep contusion foci cause contralateral homonymous hemianopia: lower quadrant - with selective damage to the visual pathway that goes above the lower horn of the lateral ventricle, and upper quadrant - with damage to this path under the lower horn.

The severity of contralateral paresis of the extremities in case of damage to the temporal lobe depends on how close they are to the internal capsule.

Small spontaneous horizontal nystagmus is often observed, beating in the direction of the lesion, as well as the phenomena of temporal ataxia.

A whole range of vegetative-visceral symptoms can occur when the medial part of the temporal lobe is affected, not only with its primary damage, but also due to wedging into the tentorial foramen of the hippocampus with its hook in case of a volume increase in the temporal lobe. Irritation of the ancient cortex causes disruptions in the regulation of visceral functions, which is realized both by subjective (feeling of heaviness, discomfort, weakness, heart failure, fever, etc.) and objective symptoms (cardiac arrhythmias, angio attacks, flatulence, hyperemia or pallor covers, etc.). The background of the mental state of the victim is changing with a predominance of negative emotions, more often in the form of constrained depression. Along with this, paroxysms of fear, anxiety, melancholy, bad forebodings can be noted. The most noticeable for the patient are violations of taste and smell in the form of perverted perception and deceit.

Medial-temporal bruises, especially in the long-term period, are often manifested exclusively by epileptic seizures or their equivalents. The latter can be olfactory and gustatory hallucinations, sensory-visceral paroxysms, vestibular attacks, "previously seen" states, relatively rare classic "streams of memories" in temporal lobe epilepsy. Epileptic seizures are also possible with damage to the convexital parts of the temporal lobe; then simple or complex (with extended speech) auditory hallucinations act as equivalents or auras.

Damage to the parietal lobe

Despite the significant volume of the parietal lobe, its damage is much less common than the substances of the frontal or temporal lobes. This is due to the topography, due to which the parietal lobes usually experience only shock trauma, and the shock-proof mechanism of their damage almost completely falls out. However, for the same reason, brain contusions due to depressed fractures are frequent here.

The parietal lobe is the only one of all the lobes of the brain that does not have a basal surface. Its relative remoteness from stem formations is the reason for the slower pace and milder deployment of the midbrain dislocation syndrome, even with extensive crush foci. Craniobasal symptoms in contusions of the parietal lobes are always secondary.

The primary nested signs of damage to the parietal lobe include: contralateral disorders of pain, as well as deep sensitivity, paresthesia, lower quadrant homonymous hemianopsia, unilateral decrease or loss of the corneal reflex, paresis of the extremities with an afferent component, and impaired binaural hearing. With damage to the parietal lobe, focal sensitive epileptic paroxysms can develop.

Along with the listed local features, which are characteristic of both the left and right parietal lobes, there are also differences in the semiotics of damage to each of them in right-handed people. With left-sided injuries, amnestic aphasia, asteriognosis, digital agnosia, apraxia, disturbances in counting, verbal thinking, and sometimes disorientation in space and time can be detected. With right-sided injuries, disorders of the emotional sphere are manifested with a tendency to the predominance of a benevolent background, unawareness of one's morbid condition, motor, visual and other defects; it is possible to develop left-sided spatial agnosia, when patients ignore or poorly perceive what is happening to their left. This may be accompanied by hemisomatognosia, pseudopolymelia (instead of one left hand, they perceive several, distinguishing among them their own).

Occipital lobe injury

Due to the largest volume of the occipital lobes, as well as the shock-absorbing role of the cerebellum, focal lesions are much less common here than in other lobes of the brain. Foci of bruising and crushing predominate in impression trauma of the occipital region.

In the clinic of injuries of the occipital lobe, cerebral symptoms predominate. With unilateral damage to the medial surface of the occipital lobe, focal signs are characterized by contralateral homonymous hemianapsia, and with bilateral damage, decreased vision in both eyes with a concentric narrowing of the visual fields up to cortical blindness. With the defeat of the convexital parts of the occipital lobes, visual agnosia is observed - not recognizing objects by their visual images. Sometimes metamorphopsia occurs - a distorted perception of the shape of observed objects, which, in addition, may appear either too small (micropsia) or too large (macropsia). When the cortex of the occipital lobe is irritated, the victim may feel flashes of light, colored sparks, or more complex visual images.

Pyramidal symptoms are not typical for damage to the occipital lobe, however, due to dysfunction of the occipital-cerebellar pathway, ataxia in the contralateral limbs may occur.

With suffering from the occipital cortical center of gaze, horizontal gaze paresis develops in the opposite direction, which are usually less pronounced than with lesions of the frontal cortical center of gaze.

Damage to the subcortical nodes

Modern possibilities of intravital diagnosis of traumatic brain damage using CT and MRI, the experience of clinical neurology and neuromorphology have expanded the understanding of damage to the basal ganglia. The most typical causes of their dysfunction in TBI are the following: 1) direct damage to the basal ganglia as a result of bruising and crushing of the brain, intracerebral and intraventricular hematomas, as well as edema and dislocation, secondary ischemia; 2) dysfunction of the basal ganglia in diffuse axonal degeneration; 3) a change in the functional state of the subcortical nodes without destruction due to a violation of the receptor apparatus and systems that provide neurotransmitter regulation of motor functions; 4) formation in the subcortical nodes of excitation and determinant foci.

The functional heterogeneity of the basal ganglia causes an extraordinary variety of their clinical syndromes. They are characteristic of the acute period of severe TBI, persist for a long time after coma; always present in a vegetative state. The most typical are: 1) various variants of persistent postural tonic reactions (decortication, decerebration, embryonic posture, etc.); 2) transient tonic convulsions; 3) hyperkinesis with a tendency to stereotypical rhythmic motor acts (throw arm movements, torso turns, automatic walking, parakinesis); 4) diffuse, chaotic motor excitation.

TBI is characterized by combined manifestations of subcortical phenomena (postural tonic reactions with choreoathetosis, tremor, corkscrew-like movements of the body, typical changes in muscle tone), often with visceral autonomic and affective reactions.

In the post-coma period, limited movements, amimia, a diffuse increase in muscle tone, tremor at rest and during static stress (Parkinson-like syndromes) are more often noted. Vivid symptoms of oral automatism may also indicate the defeat of the basal ganglia.

Cerebellar damage

Cerebellar contusions dominate among injuries of the formations of the posterior cranial fossa. Focal damage to the cerebellum is usually caused by the impact mechanism of injury (the application of mechanical energy to the occipital-cervical region when falling on the back of the head or hit by a hard object), which is confirmed by frequent fractures of the occipital bone below the transverse sinus.

Cerebral symptoms (impaired consciousness, headache, bradycardia, etc.) with cerebellar injuries often have an occlusive coloration (forced head position, vomiting when changing body position in space, early development of congestive nipples of the optic nerves, etc.) due to their proximity to CSF outflow pathways from the brain.

Among the focal symptoms dominated by unilateral or bilateral muscle hypotension, coordination disorders, large tonic spontaneous nystagmus. Localization of pain in the occipital part with irradiation to other areas of the head is characteristic. Often, this or that symptomatology from the side of the brain stem and cranial nerves is simultaneously manifested. With severe damage to the cerebellum, respiratory failure, hormetonia, and other life-threatening conditions occur.

Due to the limited subtentorial space, even with a relatively small amount of damage to the cerebellum, dislocation syndromes often unfold with infringement of the medulla oblongata by the cerebellar tonsils at the level of the occipitocervical dural funnel or infringement of the midbrain at the level of the opening of the cerebellar tenon due to the upper sections of the cerebellum being displaced from below upwards.

Brain stem damage

Primary brainstem injuries are rare. With ruptures of the trunk, the victims usually die at the site of the TBI.

Limited bruises of the trunk occur with fractures of the base of the skull (impact injury). When falling on the back (the mechanism of shock injury), as well as with simultaneous angular acceleration of the brain at the time of injury, the mesencephalic part of the trunk can be damaged.

With bruises of the midbrain, the victims appear selectively or in a complex combination of syndromes: quadrigeminal, tegmental ("tire"), peduncular ("peduncle"), as well as a number of alternating syndromes of damage to the formations of one half of the midbrain.

Quadricolnis symptoms include disturbances in up and down gaze, eye separation along the vertical axis, convergence disorders, bilateral photoreaction disturbances, and vertical, diagonal, or convergent nystagmus.

Tegmental symptoms are a violation of the functions of the III and IV cranial nerves, and only a part of their nuclei is affected, which is expressed by paresis of only individual oculomotor muscles. Conductive violations of all types of sensitivity are possible. Muscle tone changes in various ways - due to the defeat of the connections of the red nucleus and the substantia nigra. At the same time, the coordination of movements is also upset, and the coordination disorders in the limbs are contralateral to the side of the tegmental pathology. Widespread damage to the formations of the midbrain tegmentum causes the development of decerebrate rigidity with a parallel impairment of consciousness, the occurrence of hyperthermia and pathological respiratory rhythms.

Peduncular syndrome is represented by contralateral movement disorders, while monoparesis is also possible, since the somatotonic representation of the pyramidal pathway is preserved in the brain legs.

With contusions of the brain of the bridge in the clinic, various variants of homolateral lesions of the abducens, facial and motor portions of the trigeminal nerves are manifested in combination with contralateral paresis of the extremities and sensory disturbances. Spontaneous nystagmus is characteristic, as well as horizontal gaze paresis. There are also pseudobulbar phenomena.

Direct damage to the medulla oblongata causes the clinical manifestation of the primary bulbar syndrome - dysfunction of the trigeminal (segmental type), glossopharyngeal, vagus, accessory and hypoglossal nerves (dysphagia, dysphonia, dysarthria, prolapse of the pharyngeal reflex, pyramidal symptoms up to tetraparesis, coordinating and sensory disorders) . Characterized by rotatory nystagmus.

Diagnostics

Recognition of damage to the substance of the lobes is based on taking into account the biomechanics of injury, identifying characteristic mental disorders, anosmia, symptoms of oral automatism, mimic paresis of the facial nerve and other signs of damage to the anterior parts of the brain against the background of intracranial hypertension. Craniography objectifies depressed fractures and damage to the bone structures of the anterior parts of the skull base. CT and MRI provide comprehensive information about the nature of the traumatic substrate, its intralobar localization, the severity of perifocal edema, signs of axial dislocation of the trunk, etc.

Diagnosis of damage to the substance of the temporal lobes is based on the analysis of the mechanism of TBI, a combination of primary focal and secondary dislocation symptoms. However, in conditions of emergency diagnosis, it is often not possible to recognize damage to the right (subdominant) temporal lobe, and the presence of cerebral and brainstem symptoms in general can direct the formulation of a topical diagnosis along the wrong path. Invaluable assistance is provided by CT and MRI; in their absence, the traumatic process helps to lateralize echoencephalography. A certain value retains x-ray of the skull.

Recognition of damage to the substance of the parietal lobe in victims accessible to contact is based on the identification of the characteristic symptoms described above, taking into account the site of application of the traumatic agent to the head. With deep stunning, not to mention stupor and even more so coma, parietal signs are essentially impossible to detect. In this situation, CT and MRI play a decisive role in topical diagnosis, and in cases of depressed fractures, craniography.

Diagnosis of focal lesions of the substance of the occipital lobe is based on taking into account the biomechanics of the injury (especially with a blow to the occipital region) and identifying contralateral homonymous hemianopia as the leading symptom. CT and MRI well visualize crushing of the occipital localization.

When recognizing focal lesions of subcortical formations, especially in victims with impaired consciousness, it is necessary to focus on a comparison of neurological and CT-MRI data. In the intermediate and long-term periods, on the basis of a thorough clinical analysis, it is usually possible not only to state the defeat of the subcortical nodes, but also often to specify which one. Hemihypesthesia of all types of sensitivity (not only pain, but also deep, tactile, temperature) in combination with hyperpathy, and even more so accompanied by hemianopsia and hemiataxy, indicates the pathology of the thalamus. Akinetic-rigid syndrome indicates a predominant lesion of the globus pallidus and substantia nigra. Hypotonic-hyperkinetic syndrome is more typical for lesions of the striatum; hemibalism develops with interest in the process of the subthalamic nucleus.

When recognizing bruises in the formations of the posterior cranial fossa, the identification of unilateral disorders of coordination in the limbs, hypotension in them, and large spontaneous nystagmus indicate damage to the homolateral hemisphere of the cerebellum. Asynergy, trunk ataxia, unsteadiness when walking, imbalance in the Romberg position with a characteristic wide spread of the legs, slow, chanted speech indicate the interest of the cerebellar vermis.

Various combinations of damage to the nuclei of the cranial nerves, motor, coordinating, sensory disorders, variants of spontaneous nystagmus, taking into account their topical representation, underlie the clinical diagnosis of brainstem injuries. CT and especially MRI clarify the localization, nature and extent of the traumatic substrate.

(Ending follows.)

Treatment

The volume, intensity and duration of pharmacotherapy and other components of conservative treatment are determined by the severity of brain contusion, the severity of its edema, intracranial hypertension, microcirculation and CSF flow disorders, as well as the presence of TBI complications, the characteristics of the premorbid state and the age of the victims. An individual approach is the basis for the treatment of a particular patient with a brain injury.

Therapeutic effects for mild and especially moderate brain contusions include the following areas: 1) improvement of cerebral blood flow; 2) improving the energy supply of the brain; 3) restoration of the function of the blood-brain barrier (BBB); 4) elimination of pathological shifts of water sectors in the cranial cavity; 5) metabolic therapy; 6) anti-inflammatory therapy.

Restoration of cerebral microcirculation is the most important factor determining the effectiveness of other therapeutic measures. The main technique here is to improve the rheological properties of blood - increasing its fluidity, reducing the aggregation ability of formed elements, which is achieved by intravenous drip infusions of rheopolyglucin, cavinton, xanthine derivatives (eufillin, theonicol) under the control of hematocrit.

Improving microcirculation is a condition for enhancing the energy supply of the brain and preventing its hypoxia. This is especially important for restoring and maintaining the function of the cellular structures that make up the BBB. Thus, a non-specific membrane-stabilizing effect is realized. In turn, the stabilization of membrane structures normalizes the volume ratios of intracellular, intercellular and intravascular water sectors, which is a factor in the correction of intracranial hypertension. Glucose is used as an energy substrate in the form of a polarizing mixture. The presence of insulin in it contributes not only to the transfer of glucose into cells, but also to its utilization according to the energetically favorable pentose cycle. The introduction of glucose contributes to the inhibition of gluconeogenesis, functionally protecting the hypothalamic-pituitary-adrenal system (reducing the release of corticosteroids) and parenchymal organs (reducing the level of nitrogenous wastes).

Tissue hypoxia in mild and moderate brain injuries develops only in cases of untimely or incomplete elimination of respiratory disorders in the early stages after TBI or with the development of pneumonia.

Eufillin, papaverine, which contribute to the accumulation of cyclic adenosine monophosphate, which stabilizes cell membranes, have a specific effect on the function of the BBB. Given the multifactorial effect of aminophylline on cerebral blood flow, cell membrane function, airway patency, that is, on those processes and structures that are especially vulnerable in acute TBI, the use of this drug for any type of brain damage is justified. Elimination of sharp fluctuations in blood pressure also helps to maintain the function of the BBB (prevention of vasogenic edema or circulatory hypoxia of the brain). Due to the fact that during a brain injury, a mechanical "breakthrough" of the BBB occurs in the area of ​​damage, and the nervous tissue is alien to the immunocompetent system, with the development of an autoimmune aggression reaction in some cases, it is advisable to include hyposensitizing drugs (diphenhydramine, pipolfen, suprastin in injections, tavegil, calcium preparations).

Timely and rational use of many of the remedies listed above for non-severe brain contusions often prevents or eliminates disturbances in the distribution of water in various intracranial sectors. If they do develop, then we are usually talking about extracellular fluid accumulation or moderate internal hydrocephalus. At the same time, traditional dehydration therapy with saluretics, and in more severe cases with osmodiuretics (mannitol, glycerin), gives a quick effect. Dehydration therapy requires control of blood plasma osmolarity (normal values ​​are 285-310 mosmol/l).

In case of massive subarachnoid hemorrhage, according to indications, hemostatic anti-enzymatic therapy is included in the treatment complex: 5% solution of aminocaproic acid, contrical, trasilol, Gordox. The last three drugs have a more powerful antihydrolase effect, and their use blocks many pathological reactions caused by the release of enzymes and other biologically active substances from the foci of brain destruction. The drugs are administered intravenously at 25-50 thousand units 2-3 times a day. Dicynon and ascorutin are also used.

If there are subarachnoid hemorrhages, head wounds and especially liquorrhea in case of brain contusions, there are indications for anti-inflammatory therapy, including preventive therapy.

The treatment and rehabilitation complex usually includes metabolic therapy - nootropics, cerebrolysin, gliatilin, as well as vasotropic drugs that improve cerebral microcirculation (cavinton, cinnarizine, sermion, etc.).

With mild to moderate brain contusions, analgesics and sedatives, hypnotics and hyposensitizing drugs are widely used. There may be indications for the appointment of anticonvulsants (phenobarbital, clonazepam, carbamazepine, depakine, etc.).

The duration of inpatient treatment is up to 10-14 days for an uncomplicated course with mild bruises, and up to 14-21 days for moderate bruises.

With severe brain bruises (crushing of its substance), intensive therapy is carried out under the control of monitoring of cerebral, focal and stem symptoms, the activity of the cardiovascular and respiratory systems, body temperature, the most important criteria for the state of homeostasis, EEG data, ultrasound, CT, etc., and at indications - and direct measurement of intracranial pressure.

1. Dehydrators: a) saluretics (lasix - 0.5-1 mg per 1 kg of body weight per day intramuscularly); b) osmotic diuretics (mannitol - intravenous drip in a single dose of 1-1.5 g per 1 kg of body weight); c) albumin, 10% solution (intravenous drip 0.2-0.3 g per 1 kg of body weight per day).

The use of corticosteroid hormones to combat cerebral edema in severe brain injuries is currently excluded from the recognized standards for the treatment of TBI, although cooperative research on this issue continues.

2. Proteolysis inhibitors: a) contrical (gordox, trasylol) - administered intravenously in drops of 300-500 ml of 0.9% sodium chloride solution at a dose of up to 100-150 thousand units per day (single dose of 20-30 thousand units) during the first 3-5 days.

3. Antioxidants: a) emoxipin 1% solution intravenously in drops of 200 ml of 0.9% sodium chloride solution at a dose of 10-15 mg per 1 kg of body weight per day for 10-12 days; b) alpha-tocopherol acetate - up to 300-400 mg per day orally for 15 days.

4. Antihypoxants - activators of the mitochondrial electron transport system: a) cytochrome C - intravenous drip at a dose of 50-80 mg per day per 200 ml of 0.9% sodium chloride solution for 10-14 days; b) riboxin up to 400 mg per day intravenously in drops of 250-500 ml of isotonic sodium chloride solution for 10 days.

5. Means that contribute to the regulation of the aggregant state of the blood: a) direct anticoagulants - heparin (intramuscularly or subcutaneously up to 20-40 thousand units per day, 3-5 days), after the abolition of which they switch to taking indirect coagulants; b) stimulants (complamin 5-6 ml of 15% solution intravenously drip (slowly) per 100-200 ml of 5% glucose solution; amben - intravenously drip per 200 ml of isotonic sodium chloride solution in a single dose of 50-100 mg); c) agents with disaggregating properties (trental intravenously by drip at a dose of 0.1-0.2 g per day for 250-500 ml of 0.9% sodium chloride solution, reopoliglyukin intravenously by drip 400-500 mg for 5-10 days, reogluman intravenously drip for 4-5 days at the rate of 10 ml per 1 kg of body weight per day; c) native plasma (100-150 ml per day).

6. Antipyretics - reopyrin, aspirin, lytic mixtures, paracetamol, analgin.

7. Vasoactive drugs - eufillin, cavinton, sermion.

8. Normalizers of neurotransmitter metabolism and stimulators of reparative processes: a) L-dopa (nakom, madopar) - orally according to the scheme, 3 g per day; b) nootropics (nootropil, piracetam) - orally at a daily dose of 2.4 g, or intramuscularly and intravenously up to 10 g per day; c) gliatilin - orally at a daily dose of 1.2 g, or intramuscularly and intravenously, 1 g each; d) cerebrolysin - 1-5 ml intramuscularly or intravenously.

9. Vitamins: vitamin B1 (based on a daily requirement equal to 2-3 mg for an adult), vitamin B6 (at a daily dose of 0.05-0.1 g intramuscularly, 20-30 days; vitamin C (0.05- 0.1 g 2-3 times a day parenterally, 15-20 days).

10. Means that reduce the immune reactivity of the body in relation to the antigens of the nervous tissue: diprazine (0.025 g 2-3 times a day), suprastin (0.02 g 2-3 times a day), diphenhydramine (0.01 g each 2-3 times a day), according to indications - immunomodulators (decaris, thymalin, T-activin, pentaglobulin, etc.).

11. Anticonvulsants: phenobarbital, depakine, carbamazepine, etc.

Those who have undergone brain contusions are subject to long-term dispensary observation and (according to indications) rehabilitation treatment. Along with the methods of physical therapy, physiotherapy and occupational therapy, metabolic (nootropil, gliatilin, piracetam, aminalon, pyriditol, etc.), vasoactive (cavinton, sermion, cinnarizine, etc.), vitamin (B1, B6, B12, C, E etc.), general tonic preparations and biogenic stimulants (aloe, vitreous body, FiBS, solcoseryl, cogitum, apilac, ginseng, semax, etc.)

In order to prevent epileptic seizures in patients at risk, prescribe drugs containing phenobarbital (pagluferal - 1, 2, 3, gluferal, etc.). Under EEG control, their long-term (within 1-2 years) single dose at night is shown. With the development of epileptic seizures, therapy is selected individually, taking into account the nature and frequency of paroxysms, their dynamics, age, premorbidity and the general condition of the patient. Use various anticonvulsants and sedatives, as well as tranquilizers. In recent years, along with barbiturates, carbamazepine and valproates (convulex, depakine), as well as lamiktal, have been increasingly used.

Basic therapy includes a combination of nootropic and vasotropic drugs. It is preferably carried out in 2-month courses at intervals of 1-2 months for 1-2 years, taking into account, of course, the dynamics of the clinical condition.

For the prevention and treatment of post-traumatic and post-operative adhesive processes, it is advisable to additionally use agents that affect tissue metabolism: amino acids (cerebrolysin, glutamic acid, etc.), biogenic stimulants (aloe, vitreous, etc.), enzymes (lidase, lecozyme, etc. ). According to indications, on an outpatient basis, various syndromes of the postoperative period are also treated - cerebral (intracranial hypertension or hypotension, cephalgic, vestibular, asthenic, hypothalamic, etc.) and focal (pyramidal, cerebellar, subcortical, aphasia, etc.). For headaches, along with traditional analgesics, tanakan is used. With dizziness, betaserk is effective. In case of mental disorders, a psychiatrist is necessarily involved in the observation and treatment of patients. In elderly and senile patients operated on for TBI, it is advisable to increase anti-sclerotic therapy.

Mild bruises are subject only to conservative treatment. With moderate brain contusions, as a rule, there are no indications for surgical treatment. Severe brain contusions or crush injuries are a substrate that can be the subject of surgical intervention. However, the concept of expanding indications for conservative treatment of severe brain contusions has also been substantiated. Often, the body's own sanogenic mechanisms, with the correct medical support, are better able than surgical aggression to cope with severe damage to the medulla. Plays a protective role sanogenic drainage of excess fluid along with decay products into the ventricular system or subarachnoid spaces; The intact substance of the brain has a "damping" effect, especially when the bruise is located at a distance from the stem structures.

The operation does not eliminate the inevitable morphological consequences of focal lesions of the brain substance, however, it often entails additional trauma to the brain, especially when the foci of crushing are radically removed. The postulate put forward to substantiate this "removal of the focus of brain contusion within healthy tissue" is deeply erroneous for brain damage, indicating an uncritical, mechanistic transfer of the general surgical principles of operating pathological processes (inflammatory, tumor and others) of soft tissues, bones, internal organs to traumatic lesions central nervous system. Different organs and the different nature of the lesion require different approaches.

To certain limits, conservative treatment contributes better to the deployment of sanogenic mechanisms and compensatory capabilities of the affected brain than surgical intervention.

Currently at the Institute of Neurosurgery. N.N. Burdenko, based on intermittent CT-MRI monitoring, along with a comprehensive clinical analysis and study of the catamnesis, the following indications for the conservative treatment of severe brain contusions were developed and tested: 1) the victim is in the phase of subcompensation or moderate clinical decompensation; 2) a state of consciousness within the limits of moderate or deep deafness, deepening for a short time to stupor is acceptable (according to the Glasgow coma scale, at least 10 points); 3) the absence of pronounced clinical signs of stem dislocation; 4) the volume of the crush lesion according to CT or MRI data is less than 30 cm3 for temporal localization and less than 50 cm3 for frontal localization, or its structure is mosaic; 5) the absence of pronounced CT or MRI signs of lateral (displacement of the median structures no more than 5-7 mm) and axial (preservation or slight deformation of the surrounding cistern) dislocation of the brain.

Indications for surgical intervention in case of crush injuries of the brain are: 1) persistent stay of the victim in the phase of gross clinical decompensation; 2) a state of consciousness within the limits of sopor or coma (according to the Glasgow coma scale below 10 points); 3) pronounced clinical signs of stem dislocation; 4) the volume of the crush focus according to CT or MRI data is more than 30 cm3 (with temporal localization) and more than 50 cm3 (with frontal localization) with a homogeneity of its structure; 5) pronounced CT or MRI signs of lateral (displacement of median structures over 7 mm) and axial (gross deformity of the surrounding cisterna) dislocation of the brain.

Of course, the presented testimony is applied taking into account the individual characteristics of the victim.

It should also be remembered that a significant proportion of victims with severe brain contusions belong to the so-called risk group. They require intensive care during clinical observation in dynamics with repeated CT or MRI and, if necessary, a timely change in treatment tactics.

Forecast and outcomes

The prognosis for mild brain injury is usually favorable (provided that the victims follow the recommended regimen and treatment).

With a moderate brain injury, it is often possible to achieve a complete restoration of labor and social activity. A number of patients develop aseptic leptomeningitis and hydrocephalus, which cause asthenia, headaches, vegetovascular dysfunction, disturbances in statics, coordination, and other neurological symptoms.

Lethal outcomes in moderate brain contusions are rare and are caused either by intractable purulent-inflammatory complications or aggravated premorbidity, especially in the elderly and old people.

With severe brain injury, the prognosis is often unfavorable. Mortality reaches 15-30%. Among the survivors, disability is significant, the leading causes of which are mental disorders, epileptic seizures, gross motor and speech disorders. With open TBI, purulent-inflammatory complications often occur (meningitis, encephalitis, ventriculitis, brain abscesses), as well as liquorrhea.

However, with adequate treatment tactics and a coma duration of less than 24 hours, the majority of victims with brain crush can achieve a good recovery.

With severe brain contusion, if there are no aggravating circumstances and complications, after 3-6 weeks there is a regression of intracranial hypertension, meningeal symptoms, and focal neurological symptoms.

If TBI caused gross mental disorders, then its significant normalization is noted only after 2-3 months.

According to the Institute of Neurosurgery. N.N. Burdenko, with foci of crushing of the frontal lobes of the brain, good recovery was achieved in 47.4% of operated and 78.3% of non-operated victims, moderate disability - in 9.6% and 6.5%, severe disability - in 2.4 % and 6.5%, respectively; 40.6% of operated and 8.7% of non-operated victims died. Similar data were obtained with bruises in other lobes of the brain. In a comparative assessment of the results of treatment, of course, it should be taken into account that surgical intervention is resorted to in a more severe contingent of victims.

Professor Leonid LIKHTERMAN, Honored Scientist of the Russian Federation, laureate of the State Prize of the Russian Federation.
Institute of Neurosurgery. N.N. Burdenko RAMS.

As a result of acute cerebral circulation, brain neuron cells are damaged. Depending on the localization of disorders, various types of stroke are diagnosed (stem, cerebellar, hemispheric).

Stem stroke is a condition in which the brain stem is damaged as a result of a hemorrhagic or ischemic attack. When the blood supply is disturbed, the axons responsible for the motor function, as well as facial expressions, die off.

Causes of a brainstem stroke

Any stroke occurs due to acute circulatory disorders. There are two types of pathological disorders, depending on the etiology:

1. - stroke in the trunk occurs due to internal bleeding. It is the most dangerous lesion, often leading to the death of the patient. Bleeding develops against the background of atherosclerosis and other vascular anomalies.
2. - violations develop gradually, as a result of chronic deterioration of blood supply. Thrombotic neoplasms, cholesterol plaques, injuries and diseases - lead to a decrease in the intensity of blood flow. The lack of oxygen and nutrients gradually affects the work of nerve cells - axons, and leads to tissue infarction.

The consequences of a stem stroke depend on the etiology of the disorders, as well as the extent of the lesion. The outcome of the attack is also affected by the timely assistance provided. An important condition for recovery is early diagnosis and, if possible, prevention of the development of a crisis state.

Symptoms of a stem stroke

The stem part is responsible for the functioning of the human muscular system. With the defeat, the basic and vital functions of the body are violated, which are responsible for the mobility of the limbs, swallowing, breathing. The trunk connects the spinal cord and the brain, is involved in thermoregulation and other important tasks of the body.

A massive stroke in the brain stem leads to death in 70-80% of cases. Therefore, the main task of medical personnel is to diagnose disorders at an early stage and conduct timely rehabilitation procedures.

Symptoms of acute circulatory disorders are:

If the first symptoms of damage to the brain stem during a stroke are recognized in a timely manner, first aid can be provided and the intensity of complications associated with an attack can be reduced.

Secondary brain stem stroke

A repeated stroke of any part of the brain manifests itself in more severe symptoms. Particularly dangerous are violations of the cerebral blood supply to the brain stem.

A stroke permanently damages axonal nerve cells, causing loss of respiratory and other important functions. With a favorable course of the disease, the lost abilities are restored due to the fact that undamaged tissues take over and restore the lost brain capabilities. Recurrent stroke in most cases ends in the death of the patient.

What threatens a stem stroke

Hemorrhagic or ischemic brain damage leads to disruption of certain brain functions. Complications after an attack depend on the location of the hemorrhage.

The consequences of a stem stroke are:

The consequence of a stem stroke with negative dynamics is the complete paralysis of the patient with a gradual failure of the internal organs and the development of a state incompatible with the patient's life.

The most dangerous period of a stroke is the first ten days after the onset of an acute lack of blood supply. At this stage, all possible rehabilitation measures should be taken to prevent the development of complications.

How is a brainstem stroke treated?

Recovery after a stroke of the brain stem takes a long time. Even with a favorable prognosis for the development of the disease, it will take years to rehabilitate and resume normal respiratory, swallowing, speech and other functions. An important part of traditional therapy is the early diagnosis of the development of coronary or hemorrhagic disease.

Diagnostic methods

It is much easier to prevent a stroke with a lesion of the trunk than to deal with the development of complications and cope with the consequences of acute circulatory disorders.

For early diagnosis of pathological disorders, several methods are used:

• Tomography - at an early stage of disorders, a stroke may not be clinically manifested and not accompanied by neurological symptoms. The only effective and informative diagnostic method is computed or magnetic resonance imaging. If necessary, conduct a contrast study.
  Tomography allows you to identify circulatory disorders of the brain, long before the development of serious hemorrhagic or ischemic problems.
• Angiography - helps to identify existing disorders in the cardiovascular system: thrombosis, atherosclerosis, etc.
• Cardiography - is necessary to establish changes in the heart rhythm, indicating changes in the intensity of blood flow.

If the brain stem is affected during a stroke, this will immediately be displayed in characteristic manifestations: impaired motor and swallowing functions. Even a cursory examination of the patient can determine the presence of insufficient blood supply by conducting a routine neurological test.

Medical therapy

Regardless of the type of stroke, the patient is prescribed a course of therapy that includes the following:

Rehabilitation after a stem stroke

The recovery time and the likelihood of complications primarily depend on the timely assistance provided to the patient, as well as the extent of the lesion. In general, the prognosis is rather unfavorable. With a second stroke, death occurs in almost 100% of cases. Limited tissue damage makes at least partial restoration of lost brain functions likely.

How long does recovery take

The recovery process takes a long time. Even with localized and small brain damage, it will not be possible to completely eliminate all the changes that have appeared. The prognosis worsens the need to connect to an artificial respiration apparatus, as well as prolonged loss of consciousness (coma).

Patients with impaired swallowing functions, as well as those who are in a coma or have breathing problems, will require an enteral feeding device, which will also complicate rehabilitation. In general, it will take about 1-2 years to normalize the basic functions of the body. Some processes will never fully recover.

Restorative physical education

As the patient recovers, he is prescribed exercise therapy and visits to additional rehabilitation procedures. The first classes are performed lying down and are aimed at restoring the motor functions of the limbs. Over time, exercise therapy is prescribed for facial expressions and restoration of speech functions.

Accelerates the recovery of the simultaneous application of the following procedures:

1. Massage or manual therapy.
2. Reflexology.
3. Acupuncture.
4. Hirudotherapy.

There is evidence of the effectiveness of the use of magnetotherapy, which has an impact on the restoration of nerve endings. This method of treatment should be used only in the period of non-exacerbation.

The main task of the resuscitator is to prevent the development of a recurrent stroke, therefore, at the first signs of a deterioration in well-being, you should immediately stop the procedure and seek advice from a neurologist.

Stroke of the brain column is a serious pathology that can cause irreversible changes and provoke the development of conditions that end in death. The prognosis of the disease is unfavorable. Recurrent stroke most often ends in the death of the patient.

Oculo-lethargic syndrome. The predominant lesion of the oral parts of the trunk (nuclei of the oculomotor nerves), the hypothalamic region and the reticular formation of the trunk.

Damage to the left nucleus of the spinal tract.

Segmentally dissociated type of sensory disturbance. Oral divisions of the nucleus of the spinal tract of the trigeminal nerve (pons varolii) on the left.

Alternating Weber syndrome. The defeat of the brain stem, mainly the base of the midbrain (legs) on the right.

alternating syndrome. The defeat of the brain stem, mainly the bridge on the right.

Alternating Miyyar-Gubler's syndrome. The defeat of the lower part of the bridge on the right.

Alternating Jackson syndrome. medulla oblongata on the right.

Pseudobulbar paralysis. Bilateral lesion of the corticobulbar tract (more pronounced on the right).

Bulbar paralysis. The predominant lesion of the tegmentum of the brain stem at the level of the location of the nuclei of the 12th, 9th, 10th cranial nerves (medulla oblongata).

4. Damage to the cerebellum

Right hemisphere of the cerebellum.

5. DEFEAT OF THE SUBCORTICAL NODES

The defeat of the left visual tubercle.

parkinsonism syndrome. Predominant lesion of the pallidar system (pallid ball, substantia nigra).

Syndrome of choreic hyperkinesis. Predominant lesion of the striatal system (shell, caudate nucleus).

6. DEFEAT OF THE HYPOTHALAMO-PITUITARY REGION

Hypothalamo-pituitary syndrome. Primary lesion of the pituitary gland.

Sympathetic-adrenal crisis. Primary lesion of the hypothalamus (diencephalic region).

Syndrome Itsenko-Cushing. The defeat of the pituitary-hypothalamic region.

7. INTERNAL CAPSULE DEFEAT

Central paralysis of the facial and hypoglossal nerves. Inner capsule on the right.

8. IMPAIRMENT OF THE LOBS, GIRLS OF THE BRAIN

Predominant lesion of the frontal lobe on the left.

Damage to the left frontal lobe.

Predominant lesion of the frontal lobe on the left (with symptoms of irritation of the second frontal gyrus).

Motor Jacksonian epilepsy. Damage to the right precentral gyrus.

Apraxia syndrome (motor, constructive). The defeat of the left parietal lobe, mainly supramarginal and angular gyrus.

Violations of the muscular-articular, tactile sensitivity, sense of localization in the left hand, disorder of the “body scheme”. Damage to the right parietal lobe, mainly the superior parietal lobule and interparietal sulcus.

Predominant lesion of the left temporal lobe.

9. Tasks-schemes

Lateral pyramidal tracts at the level of the cervical segments.

Anterior horns of the spinal cord or anterior roots at the level of segments C 5 -C 8 on the right.

Damage to the nucleus of the facial nerve on the left (bridge) and the lateral pyramidal tract at the same level (alternating paralysis)

The lesion on the right (brain peduncle, internal capsule, corona radiata, anterior central gyrus). Hemiplegia on the left.

Multiple lesions of peripheral nerves (polyneuritis).

The anterior horns of the spinal cord and the lateral pyramidal tract on the left at the level of C 5 -C 7 segments.

The anterior horns of the spinal cord or the anterior roots of the spinal nerves at the level of segments L 1 -S 1 on both sides.

The lateral pyramidal tract at the level of the D12 segment on the left or the upper section of the right precentral gyrus.

Bilateral lesion of the lateral pyramidal tracts at the level of segments D 9 -D 10 or the upper sections of the precentral gyri.

Anterior horns of the spinal cord at the level of C 5 -C 8 segments and lateral pyramidal tracts at the same level on both sides.

Internal capsule or thalamus, or corona radiata, or postcentral gyrus. The hearth is on the left.

Multiple lesions of the peripheral nerves of the extremities (polyneuritic type of sensitivity disorder).

Posterior columns of the spinal cord at the level of the D4 segment (Gaulle's bundles).

Hind horns at the level of segments C 5 -D 10 on the right.

The posterior column of the spinal cord and the lateral spinal-thalamic path on the right at the level of the D 5 -D 6 segments.

Lateral spinal-thalamic pathway and pathways of deep sensitivity (medial loop) at the level of the brain stem (bridge), sensory nuclei of the trigeminal nerve, ibid.

Lateral dorsal-thalamic path at the level of segments D 8 -D 9 on the left.

Right brachial plexus.

Spinal nerve roots at the level of segments S 3 -S 5 on both sides:

Lateral spinal thalamic pathways on both sides at the level of segments D 10 -D 11 and the posterior funiculi of the spinal cord at the same level.

Lateral pyramidal tract at the level of segment D 10 on the right, spastic paresis of the right leg, absence of middle and lower abdominal reflexes on the right.

Anterior horns of the spinal cord at the level of segments L 2 -L 4 on both sides. Peripheral paralysis of the lower extremities (mainly the muscles of the thighs).

The anterior roots of the spinal nerves at the level of segments L 4 -S 1 on both sides. Peripheral paralysis of the muscles of the legs and feet.

The anterior roots of the spinal nerves at the level of segments C 5 -C 8 on the right. Peripheral paralysis of the right hand.

Anterior horns of the spinal cord at the level of segments L 1 -L 2 on both sides. Peripheral paralysis of the thigh muscles.

Lateral pyramidal path at the level of segments L 2 -L 3 . Spastic paralysis of the lower limb.

Lateral pyramidal tract at the level of segment D 5 on the left. Spastic paresis of the left leg, absence of abdominal reflexes on the left.

Anterior horns of the spinal cord at the level of segments C 1 -C 4 on the left.

Anterior horns of the spinal cord and lateral pyramidal tracts on both sides at the level of C 5 -C 8 segments. Peripheral upper and central lower paraparesis, urinary and fecal retention.

Anterior horns of the spinal cord, lateral pyramidal path on the right at the level of segments L 1 -L 2 . Peripheral paresis of the muscles of the thighs, central paresis of the muscles of the lower leg and foot on the right.

Anterior horns of the spinal cord at the level of segments C 5 -C 8 on the left. Peripheral paralysis of the left hand.

The anterior horns of the spinal cord and the lateral pyramidal tract on the right at the level of C 5 -C 8 segments. Peripheral paresis of the right arm with fibrillations, central paresis of the right leg. Peripheral paralysis of the neck muscles, paralysis of the diaphragm.

Lateral pyramidal path on the left at the level of segment D 12 . Spastic paralysis of the lower limb while maintaining the upper and middle abdominal reflexes.

Anterior roots of spinal nerves at the level of segments S 3 -S 5 on both sides. Peripheral sphincter paralysis (urinary and fecal incontinence). There are no paresis of the limbs.

Lateral pyramidal tract at the level of C5 segment on the left. Left-sided central hemiparesis.

Lateral dorsal-thalamic path on the right at the level of D 10 . Conduction disturbance of pain and temperature sensitivity downward from the level of the inguinal fold on the left

Spinal nerves at the level of segments C 5 -C 8 on the left, anesthesia and flaccid paralysis or paresis of the left hand

Brown-Sequard syndrome: central paresis of the left leg and a violation of deep sensitivity on the left below the axillary region, conduction disturbances of superficial sensitivity on the right.

Transverse lesion of the spinal cord at the level of segment C 4 . Central tetraplegia, anesthesia of the entire surface of the body; violation of the functions of the pelvic organs. Possible paresis of the diaphragm.

Posterior roots of spinal nerves at the level of segments S 3 -S 5 on both sides. Anesthesia in the vulva and anus.

Posterior and anterior roots at the level of segments L 4 - S 1 on the left. Peripheral paresis of the left leg, violation of all types of sensitivity.

Facial nerve (central paralysis on the left).

Facial nerve (peripheral paralysis on the left).

Oculomotor nerve (ptosis of the right upper eyelid).

Oculomotor nerve (divergent strabismus, mydriasis).

Trigeminal nerve (innervation of the face and head by segments, Zelder zones).

Trigeminal nerve (peripheral innervation of the skin of the face and head).

Hypoglossal nerve (peripheral paralysis on the left).

Abducens nerve (when looking to the left, the left eyeball is not retracted outwards).

Focal (partial) motor seizure in the right leg.

Adversive seizure (turning the head and eyes to the right)

Auditory hallucination (aura).

Complex visual hallucination (aura).

Simple visual hallucination (aura).

Olfactory, gustatory hallucination (aura).

Motor aphasia (Brock's center).

The head and eyes are turned to the left (gaze paresis), agraphia.

Central paralysis of the right leg.

1. Quadrant hemianopsia (lower left quadrant dropped out).

   Left-sided hemianopsia with preservation of the central field of view.

   visual agnosia.

   Astereognosia, apraxia.

   Sensory aphasia.

   Amnestic, semantic aphasia.

   Taste, olfactory agnosia.

   Quadrant hemianopsia (right upper quadrant dropped out).