• Symptoms of Hyperosmolar Coma
• Treatment of hyperosmolar coma

What is Hyperosmolar Coma

Hyperosmolar coma most often occurs in people over 50 years of age with mild to moderate diabetes mellitus, well compensated by diet or sulfanylureas. Hyperosmolar coma occurs 1:10 in relation to ketoacidotic coma, and mortality during its development is 40-60%.

What causes hyperosmolar coma

This pathological condition occurs during metabolic decompensation of diabetes mellitus and is characterized by an extremely high blood glucose level (55.5 mmol / l or more) in combination with hyperosmolarity (from 330 to 500 or more mosmol / l) and the absence of ketoacidosis.

Pathogenesis (what happens?) during Hyperosmolar coma

The mechanism of this pathological condition not fully explored. It is assumed that great importance in the development of high glycemia (up to 160 mmol / l) has a blockade of glucose excretion by the kidneys.

hyperglycemia combined with fluid loss due to osmotic stimulation of diuresis, inhibition of the production of antidiuretic hormone by the neurohypophysis and a decrease in water reabsorption in the distal tubules of the kidneys.

With a rapid and significant loss of fluid, the BCC decreases, blood thickens and osmolarity increases due to an increase in the concentration of not only glucose, but also other substances contained in the plasma (for example, potassium and sodium ions). Thickening and high osmolarity (more than 330 mosmol / l) lead to intracellular dehydration (including brain neurons), impaired microcirculation in the brain, and a decrease in cerebrospinal fluid pressure, which are additional factors contributing to coma and the appearance of specific neurological symptoms.

Symptoms of Hyperosmolar Coma

Clinic of hyperosmolar coma. The provoking factors are similar to the causes that cause the development of ketoacidotic coma. Coma develops gradually. The history of diabetes mellitus before the onset of coma was usually mild and well compensated by taking oral hypoglycemic drugs and diet.

In several days before the development of coma patients note increasing thirst, polyuria, weakness. The condition is constantly deteriorating, dehydration develops. There are violations of consciousness - drowsiness, lethargy, gradually turning into a coma.

Characterized by neurological and neuropsychiatric disorders: hallucinations, hemiparesis, slurred speech, convulsions, areflexia, increased muscle tone, sometimes there is a high temperature of central genesis.

Diagnosis of Hyperosmolar Coma

In the blood there is extremely high level glycemia and osmolarity, ketone bodies are not determined.

Treatment of hyperosmolar coma

Principles of emergency care in this condition, they are similar to those in the treatment of ketoacidotic coma and consist in eliminating dehydration, hypovolemia and restoring normal plasma osmolarity, and proper infusion therapy in hyperosmolar coma becomes even more important than in ketoacidosis.

Infusion therapy with hyperosmolar coma. During the first 1-2 hours intravenously, 2-3 liters of 0.45% sodium chloride solution (hypotonic solution) are quickly injected, followed by the transition to an isotonic solution infusion and continue its administration against the background of insulin therapy until the level plasma glucose does not drop to 12-14 mmol/l. After that, to prevent the development of a hypoglycemic state, they switch to an intravenous administration of a 5% glucose solution with the appointment of insulin for its utilization (4 IU of insulin per 1 g of glucose). Assessment of the adequacy of the volume of infusion therapy is carried out according to generally accepted criteria. Quite often, for the relief of dehydration in this group of patients, very large volumes of fluid are required in the amount of up to 15-20 l / 24 hours. Naturally, infusion therapy should include the correction of electrolyte levels.

Considering that at this pathology there is no ketoacidosis, and therefore no metabolic acidosis, the use of buffer solutions is not indicated.

When conducting treatment of this pathology the doctor should not be embarrassed by the initial extremely high blood glucose levels. It must always be remembered that hyperosmolar coma occurs, as a rule, in patients with mild or moderate diabetes mellitus, so they respond very well to injected insulin. Based on this, it is not recommended to use large doses of this drug, but to use the method of continuous intravenous infusion of small doses of insulin, and the initial working dose should not be increased by more than 10 U / hour (0.1 U / kg).

Which Doctors Should You See If You Have Hyperosmolar Coma

Endocrinologist

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One of the terrible and understudied complications of diabetes mellitus is hyperosmolar coma. There are still disputes about the mechanism of its origin and development.

The disease is not acute, the condition of a diabetic may worsen for two weeks before the first impairment of consciousness. Most often, coma occurs in people over 50 years of age. Doctors are not always able to immediately make a correct diagnosis in the absence of information that the patient has diabetes.

Due to late admission to the hospital, diagnostic difficulties, severe deterioration of the body, hyperosmolar coma has a high mortality rate - up to 50%.

What is a hyperosmolar coma

Hyperosmolar coma is a condition with loss of consciousness and disturbance in all systems: reflexes, cardiac activity and thermoregulation fade, urine stops being excreted. A person at this time literally balances on the border of life and death. The reason for all these disorders is the hyperosmolarity of the blood, that is, a strong increase in its density (more than 330 mosmol / l at a rate of 275-295).

This type of coma is characterized by high blood glucose, above 33.3 mmol/l, and severe dehydration. at the same time, it is absent - ketone bodies are not detected in the urine by tests, the breath of a diabetic patient does not smell of acetone.

According to the international classification, hyperosmolar coma is classified as a violation of water-salt metabolism, the ICD-10 code is E87.0.

The hyperosmolar state leads to coma quite rarely, in medical practice there is 1 case per 3300 patients per year. According to statistics, the patient's average age is 54 years, he has non-insulin-dependent type 2 diabetes, but does not control his disease, therefore he has a number of complications, including kidney failure. In a third of patients in a coma, diabetes is long-term, but was not diagnosed and, accordingly, was not treated all this time.

Compared with ketoacidotic coma, hyperosmolar coma occurs 10 times less frequently. Most often, its manifestations are stopped by diabetics themselves at an easy stage, without even noticing it - they normalize blood glucose, start drinking more, turn to a nephrologist because of problems with the kidneys.

Reasons for development

Hyperosmolar coma develops in diabetes mellitus under the influence of the following factors:

1. Severe dehydration due to extensive burns, overdose or long-term use of diuretics, poisoning and intestinal infections, which are accompanied by vomiting and diarrhea.
2. Lack of insulin due to non-compliance with the diet, frequent skipping of glucose-lowering drugs, severe infections or physical exertion, treatment with hormonal agents that inhibit the production of one's own insulin.
3. undiagnosed diabetes.
4. Long-term infection of the kidneys without proper treatment.
5. Hemodialysis, or intravenous glucose, when doctors are unaware of the patient's diabetes.

Pathogenesis

The onset of a hyperosmolar coma is always accompanied by a pronounced one. Glucose enters the blood from food and is simultaneously produced by the liver, its entry into tissues is complicated due to. Ketoacidosis does not occur, and the reason for this absence has not yet been precisely established. Some researchers believe that the hyperosmolar type of coma develops when there is enough insulin to prevent the breakdown of fats and the formation of ketone bodies, but too little to suppress the breakdown of glycogen in the liver with the formation of glucose. According to another version, the exit fatty acids from adipose tissue is suppressed due to a lack of hormones at the beginning of hyperosmolar disorders - somatropin, cortisol and glucagon.

Further pathological changes resulting in hyperosmolar coma are well known. With the progression of hyperglycemia, the volume of urine increases. If the kidneys are working normally, then when the limit of 10 mmol / l is exceeded, glucose begins to be excreted in the urine. With impaired kidney function, this process does not always occur, then sugar accumulates in the blood, and the amount of urine increases due to a violation of reabsorption in the kidneys, dehydration begins. Fluid comes out of the cells and the space between them, the volume of circulating blood decreases.

Due to dehydration of brain cells, neurological symptoms occur; increased blood clotting provokes thrombosis, leads to insufficient blood supply to organs. In response to dehydration, the production of the hormone aldosterone increases, which prevents sodium from the blood from getting into the urine, hypernatremia develops. It, in turn, provokes hemorrhages and swelling in the brain - a coma occurs.

In the absence of resuscitation measures to eliminate the hyperosmolar state, a lethal outcome is inevitable.

Signs and symptoms

The development of hyperosmolar coma takes one to two weeks. The onset of changes is associated with a deterioration in diabetes compensation, then signs of dehydration join. IN last turn there are neurological symptoms and consequences of high blood osmolarity.

Causes of symptoms	External manifestations preceding hyperosmolar coma
Diabetes decompensation	Thirst, frequent urination, dry, itchy skin, discomfort on the mucous membranes, weakness, constant fatigue.
Dehydration	Weight and pressure drop, limbs freeze, constant dryness in the mouth appears, the skin becomes pale and cool, its elasticity is lost - after squeezing into a fold with two fingers, the skin is smoothed out more slowly than usual.
Brain dysfunction	Weakness in muscle groups, up to paralysis, inhibition of reflexes or hyperreflexia, convulsions, hallucinations, seizures similar to epileptic ones. The patient stops responding to the environment, and then loses consciousness.
Failures in the work of other organs	Disorders of the stomach, arrhythmia, frequent pulse, shallow breathing. The excretion of urine decreases and then stops completely. The temperature may rise due to a violation of thermoregulation, heart attacks, strokes, thrombosis are possible.

Due to the fact that the functions of all organs are impaired in hyperosmolar coma, this condition can be masked by a heart attack or signs similar to the development of a severe infection. Complex encephalopathy may be suspected due to cerebral edema. In order to quickly make the correct diagnosis, the doctor must know about the patient's history of diabetes or identify it in time according to the analysis.

Necessary diagnostics

Diagnosis is based on symptoms, laboratory data, and the presence of diabetes. Although this condition is more common in older people with type 2 disease, hyperosmolar coma can develop in type 1 regardless of age.

Usually, a comprehensive examination of blood and urine is needed to make a diagnosis:

Analysis		Evidence suggestive of hyperosmolar disorder
blood glucose		Significantly increased - from 30 mmol / l to exorbitant numbers, sometimes up to 110.
Plasma Osmolarity		It greatly exceeds the norm due to hyperglycemia, hypernatremia, an increase in urea nitrogen from 25 to 90 mg%.
glucose in urine		It is found if there is no severe renal failure.
Ketone bodies		Not detected in serum or urine.
Plasma electrolytes	sodium	The amount is increased if severe dehydration has already developed; is normal or slightly below it in the middle stage of dehydration, when fluid leaves the tissues into the blood.
	potassium	The situation is reversed: when water leaves the cells, it is enough, then a deficiency develops - hypokalemia.
General blood analysis		Hemoglobin (Hb) and hematocrit (Ht) are often elevated, leukocytes (WBC) are more than normal in the absence of obvious signs of infection.

To find out how much the heart has suffered, and whether it is able to endure resuscitation, an ECG is done.

Emergency Algorithm

If a diabetic patient has lost consciousness or is in an inadequate condition, the first thing to do is call an ambulance. Emergency care for hyperosmolar coma can be provided only in the intensive care unit. The faster the patient is brought there, the higher his chance of survival, the less damage to the organs, and the faster he will be able to recover.

While waiting for an ambulance:

1. Lay the patient on his side.
2. Wrap it up if possible to reduce heat loss.
3. Monitor breathing and heartbeat, if necessary, start artificial respiration and chest compressions.
4. Measure blood sugar. In case of a strong excess of the norm, make an injection. You cannot administer insulin if there is no glucometer and glucose data is not available, this action can provoke the death of the patient if he has hypoglycemia.
5. If there is an opportunity and skills, put a dropper with saline. The rate of administration is a drop per second.

When a diabetic enters the intensive care unit, he is given express tests to establish a diagnosis, if necessary, he is connected to a ventilator, urine outflow is restored, and a catheter is placed in a vein for long-term administration of drugs.

The patient's condition is constantly monitored:

• glucose is measured hourly;
• every 6 hours - potassium and sodium levels;
• to prevent ketoacidosis, ketone bodies and blood acidity are controlled;
• the amount of urine excreted is counted for the entire time when droppers are installed;
• often check pulse, pressure and temperature.

The main directions of treatment are the restoration of the water-salt balance, the elimination of hyperglycemia, the treatment of concomitant diseases and disorders.

Correction of dehydration and replenishment of electrolytes

To restore fluid in the body, volumetric intravenous infusions are carried out - up to 10 liters per day, the first hour - up to 1.5 liters, then the volume of the solution administered per hour is gradually reduced to 0.3-0.5 liters.

Choose a drug depending on the sodium indicators obtained in the course of laboratory tests:

When dehydration is corrected, in addition to restoring water reserves in the cells, the volume of blood also increases, while the hyperosmolar state is eliminated and the level of sugar in the blood decreases. Rehydration is carried out with the obligatory control of glucose, since its sharp decrease can lead to a rapid drop in pressure or cerebral edema.

When urine appears, the replenishment of potassium reserves in the body begins. Usually it is potassium chloride, in the absence of renal failure - phosphate. The concentration and volume of administration is selected based on the results of frequent blood tests for potassium.

Fighting hyperglycemia

Blood glucose is corrected with the help of short-acting insulin, in minimal doses, ideally with continuous infusion. With very high hyperglycemia, an intravenous injection of the hormone is preliminarily made in an amount of up to 20 units.

With severe dehydration, insulin may not be used until the water balance is restored, glucose at this time and so rapidly decreases. If diabetes and hyperosmolar coma are complicated comorbidities You may need more insulin than usual.

The introduction of insulin at this stage of treatment does not mean that the patient will have to switch to his lifelong intake. Most often, after stabilization of the condition, type 2 diabetes can be compensated by dieting () and taking hypoglycemic agents.

Treatment of comorbid disorders

Simultaneously with the restoration of osmolarity, correction of already existing or suspected violations is carried out:

1. Hypercoagulation is eliminated and thrombosis is prevented by the introduction of heparin.
2. If renal failure worsens, hemodialysis is performed.
3. If hyperosmolar coma is provoked by infections of the kidneys or other organs, antibiotics are prescribed.
4. Glucocorticoids are used as antishock therapy.
5. At the end of treatment, vitamins and microelements are prescribed to replenish their losses.

What to expect - forecast

The prognosis of hyperosmolar coma largely depends on the time of initiation of medical care. With timely treatment, impaired consciousness can be prevented or restored in time. Due to delayed therapy, 10% of patients with this type of coma die. The cause of the remaining deaths is considered to be old age, long-term uncompensated diabetes, a “bouquet” of diseases accumulated during this time - heart and kidney failure,.

Death in hyperosmolar coma occurs most often due to hypovolemia - a decrease in blood volume. In the body, it causes insufficiency of internal organs, primarily organs with already existing pathological changes. Cerebral edema and massive thrombosis not detected in time can also end fatally.

If the therapy turned out to be timely and effective, the patient with diabetes regains consciousness, the symptoms of coma disappear, glucose and blood osmolarity normalize. Neurological pathologies when leaving a coma can last from a couple of days to several months. Sometimes full recovery of functions does not occur, paralysis, speech problems, and mental disorders may persist.

The cerebral hemispheres are the most developed functionally important structure of the central nervous system. All parts of the brain are covered by sections of the hemispheres.

Anatomically, the hemispheres (right and left) are separated by a longitudinal fissure located in the deep sections. This gap may be in contact with the corpus callosum. The cerebellum and cerebral hemispheres are separated from each other by a transverse fissure.

The structure of the hemispheres

Outside, the hemispheres are covered with a bark (a plate of gray matter). They have 3 surfaces: upper lateral, medial (middle) and lower. Surfaces are separated by edges.

The hemispheres have poles: frontal, occipital and temporal.

Furrows are located on all surfaces of the hemispheres, except for the lower one. They can be deep or shallow irregular shape and can change direction. Each hemisphere is divided into lobes by deep furrows.

There are the following types of shares:

• frontal;
• occipital;
• parietal;
• islet;
• temporal.

frontal lobe

It is located in the anterior sections of both hemispheres and is limited by the pole of the same name, lateral and central furrows.

The central sulcus (Roland's) begins on the median surface of the hemisphere, directed towards its upper edge. Then it goes downward, but does not reach the lateral groove.

Parallel to the central sulcus is the precentral sulcus. From it go up 2 frontal grooves - upper and lower, which divide the frontal lobe into gyrus.

The convolutions separate the small furrows from each other. There are 3 gyrus in the frontal lobe - superior, middle and inferior. Broca's center is located in the region of the inferior gyrus. Its value is great. He is responsible for the interpretation of the meaning of speech, the syntactic formation of sentences and the arrangement of words in them.
The frontal lobe consists of 3 parts - triangular, orbital and tegmental.

Functions of the frontal lobe:

1. thinking;
2. regulation of behavior;
3. conscious movements;
4. physical activity;
5. speech function;
6. handwriting;
7. memory center.

parietal lobe

The parietal lobe is located behind the Roland sulcus. It is limited by the occipito-parietal and lateral furrows.

This lobe contains the postcentral sulcus, which runs parallel to the central sulcus. Between them is the postcentral gyrus. Heading towards the frontal lobe and connecting with the precentral gyrus, the paracentral lobule is formed. In addition to this lobule, the parietal lobe has upper and lower lobules of the same name. The lower parietal lobule has 2 gyrus: supramarginal and angular.

Functions of the parietal lobe:

1. deep and superficial sensitivity of the whole body;
2. automatic movements provoked by constant repetitions (washing, dressing, driving a car, etc.);
3. tactile function (the ability to recognize the size, weight of an object by touch).

Occipital lobe

It is located behind the parieto-occipital sulcus. Has a small size. The occipital lobe has grooves and gyri, which can change their shape and direction. The most pronounced are the spur and transverse furrows. The occipital lobe ends with the occipital pole.

Functions of the occipital lobe:

1. visual function (perception and processing of information);
2. perception of light.

temporal lobe

The temporal lobe is separated from the frontal and parietal Sylvian groove (lateral). The edge of this lobe covers the side of the insular lobe and is called the temporal operculum. The temporal lobe has the pole of the same name and 2 gyrus of the same name - upper and lower. It also contains three short convolutions, which are located in the transverse direction - Geschl's convolutions. In the temporal lobe, the Wernicke center is located, which is responsible for giving meaning to our speech.

Temporal lobe functions:

1. perception of sensations (hearing, taste, smell);
2. sound and speech analysis;
3. memory.

insular lobe

It is located in the depths of the Sylvius furrow. It can be seen only if the tire (temporal, frontal and parietal lobes) is moved apart. It has a circular, central furrow, long and short gyrus.

The main function of the islet is taste recognition.

In the medial region of the hemispheres are the following structures:

1. furrows: corpus callosum; hippocampus; belt.
2. gyrus: parahippocampal, dentate, cingulate, lingual.

On the lower surface of the hemispheres there are olfactory bulbs, furrows and paths. In addition, there are the nasal sulcus, the hook (the end of the parahippocampal gyrus), the occipitotemporal gyrus, and the sulcus.

The olfactory bulb, tract, triangle, perforate, cingulate, parahippocampal, dentate gyrus, and hippocampus form the limbic system.

The function of the limbic system is olfactory.

The cortex of the hemispheres

Bark big brain- This is gray matter located in the peripheral regions of the hemispheres. Its surface area is about 200 thousand mm 2 . The shape, appearance and location of neurons and other structures is not the same in different parts of the cortex and is called "cytoarchitectonics". In the cortex of the hemispheres there are nuclei of cortical analyzers of all types of sensitivity: motor, skin, auditory, olfactory and visual.

Pathology of the cerebral hemispheres

With damage to the cortex of any lobe of the cerebral hemispheres, various neurological symptoms and syndromes occur.

Need to apply in a timely manner medical care to avoid serious consequences in case of disruption of the functioning of any area of ​​the brain.

The reasons for the development of such conditions are:

1. head injury;
2. oncological diseases (benign and malignant brain tumors);
3. atrophic diseases of the brain (Pick's disease,);
4. congenital disorders (insufficient development of the structures of the nervous system);
5. birth trauma of the skull;
6. hydrocephalus;
7. infectious and inflammatory processes in the membranes of the brain (meningitis, encephalitis);
8. violation of blood circulation in the vessels of the brain.

Frontal cortex disorders

With damage to the cortex of the frontal lobe, depending on the localization, the following symptoms occur:

• frontal ataxia - imbalance, unsteady gait;
• increased muscle tone in the limbs (passive movements are limited or difficult);
• paralysis of a limb/limbs on one side;
• tonic/clonic convulsions;
• seizures (tonic-clonic or epileptic);
• difficulty in speech (a person cannot pick up synonyms, case, time of action) - Broca's aphasia;
• symptoms of the frontal psyche (a person behaves foolishly, liberated, rage may appear for no reason);
• “frontal signs” (the appearance of primitive reflexes, such as in an infant - proboscis, grasping, etc.);
• loss of smell on one side.

In addition to the pronounced symptoms of the frontal psyche, the patient may behave apathetically, indifferently, and not come into contact with others. In severe cases, there may be a tendency to immoral social acts: fights, brawls, arson.

Pathological disorders in the cortex of the parietal lobe

When the cortex of the parietal lobe is damaged, there are violations of sensitivity and surrounding perception. The following symptoms are characteristic:

• violations of skin sensitivity;
• posturality (changes in position in space, passive movements that the patient feels, but this does not happen to him);
• lack of perception of parts of your body;
• inability or refusal to respond to stimuli in areas of superficial and deep sensitivity;
• loss of reading, writing, counting skills;
• inability to find familiar places;
• when examining objects with closed eyes, the patient cannot recognize a familiar thing.

Pathological disorders in the cortex of the temporal lobe

The main manifestations of damage to the temporal lobe are:

• cortical deafness (hearing loss in which there is no ear injury);
• aphasia Wernicke - loss of the ability to perceive speech, music, etc.;
• noise in ears;
• sleep-like states (the patient remembers something that he had not seen or heard before, but claims that it was with him in reality, and not in a dream);
• the occurrence of auditory hallucinations;
• short or long-term memory loss (amnesia);
• the occurrence of moments of deja vu;
• combined hallucinations (auditory + visual, auditory + olfactory);
• temporal seizures.

Pathological disorders in the cortex of the occipital lobe

Damage to the cortex of this area is accompanied by problems with the visual analyzer. The following conditions develop:

• cortical blindness (complete loss of vision without damage to the visual analyzer);
• loss of vision, in which the patient claims that he has not lost his sight;
• hemianopsia - loss of visual fields on one side;
• inability to remember an object, color or face of a person;
• changes in surrounding objects that seem small - visual illusions;
• visual hallucinations - flashes of light, zigzags, individual for each eye.

When the limbic system is affected, there is a loss of memory or confusion of memories, there is an inability to create and remember bright moments of life, low emotional lability, lack of smell, loss of the ability to analyze and make decisions, as well as to master new skills.

Brain located in the medulla of the skull. Its average weight is 1360 g. There are three large sections of the brain: the trunk, the subcortical section, and the cerebral cortex. 12 pairs of cranial nerves emerge from the base of the brain.

1 - upper section of the spinal cord; 2 - medulla oblongata, 3 - bridge, 4 - cerebellum; 5 - midbrain; 6 - quadrigemina; 7 - diencephalon; 8 - the cerebral cortex; 9 - corpus callosum, connecting the right hemisphere with the new one; 10 - optic chiasm; 11 - olfactory bulbs.

Parts of the brain and their functions

Departments of the brain		Department structures	Functions
BRAIN STEM	Hind brain	Medulla Here are the nuclei with outgoing pairs of cranial> nerves: XII - sublingual; XI - additional; X - wandering; IX - glossopharyngeal nerves	Conductor - the connection of the spinal and overlying parts of the brain. Reflex: 1) regulation of the activity of the respiratory, cardiovascular and digestive systems; 2) food reflexes of salivation, chewing, swallowing; 3) protective reflexes: sneezing, blinking, coughing, vomiting;
		Pons contains nuclei: VIII - auditory; VII - facial; VI - outlet; V - trigeminal nerves.	Conductor - contains ascending and descending nerve pathways and nerve fibers connecting the hemispheres of the cerebellum to each other and to the cerebral cortex. reflex - responsible for vestibular and cervical reflexes that regulate muscle tone, incl. mimic muscles.
		Cerebellum The hemispheres of the cerebellum are interconnected and are formed by gray and white matter.	Coordination of voluntary movements and maintaining the position of the body in space. Regulation of muscle tone and balance.
	Reticular formation- a network of nerve fibers that braid the brain stem and diencephalon. Provides interaction between the ascending and descending pathways of the brain, coordination various functions body and the regulation of excitability of all parts of the central nervous system.
	midbrain	quadrigemina With nuclei of primary visual and auditory centers. Legs of the brain With nuclei IV - oculomotor III - block nerves.	Conductor. Reflex: 1) orienting reflexes to visual and sound stimuli, which manifest themselves in the rotation of the head and torso; 2) regulation of muscle tone and body posture.
SUBCORT	forebrain	Interbrain: a) thalamus (optic tubercle) with nuclei ll -th pair of optic nerves;	Collection and evaluation of all incoming information from the senses. Isolation and transmission to the cerebral cortex of the most important information. regulation of emotional behavior.
		b) hypothalamus.	The highest subcortical center of the autonomic nervous system and all vital body functions. Ensuring the constancy of the internal environment and metabolic processes of the body. Regulation of motivated behavior and provision of protective reactions (thirst, hunger, satiety, fear, rage, pleasure and displeasure). Participation in the change of sleep and wakefulness.
		Basal ganglia (subcortical nuclei)	Role in regulation and coordination motor activity(together with the thalamus and cerebellum). Participation in the creation and memorization of programs of purposeful movements, learning and memory.
CORK OF GREAT HEMISPHERES		Ancient and old bark (olfactory and visceral brain)Contains nuclei of the 1st pair of olfactory nerves.	The ancient and old cortex, together with some subcortical structures, formslimbic system, which: 1) is responsible for innate behavioral acts and the formation of emotions; 2) provides homeostasis and control of reactions aimed at self-preservation and preservation of the species: 3 affects the regulation of vegetative functions.
		New bark	1) Carries out higher nervous activity, is responsible for complex conscious behavior and thinking. The development of morality, will, intellect, are associated with the activity of the cortex. 2) Carries out the perception, evaluation and processing of all incoming information from the senses. 3) Coordinates the activity of all body systems. 4) Provides interaction of the organism with the external environment.

The cerebral cortex

The cerebral cortex- phylogenetically the youngest formation of the brain. Due to the furrows, the total surface area of ​​the cortex of an adult is 1700-2000 cm2. In the cortex, there are from 12 to 18 billion, nerve cells, which are located in several layers. The cortex is a layer of gray matter 1.5-4 mm thick.

The figure below shows the functional areas and lobes of the cerebral cortex.

Location of gray and white matter	Lobes of the hemispheres	Hemispheric zones
The bark is gray matter white matter located under the bark, in the white matter there are accumulations of gray matter in the form of nuclei			speech centers
	Parietal	Musculoskeletal zone	Movement control, the ability to distinguish irritations
	temporal	Hearing zone	Arcs of reflexes distinguishing sound stimuli
		Taste and olfactory zones	Reflexes of discrimination of tastes and smells
	Occipital	visual area	Distinguishing visual stimuli

Sensory and motor areas of the cerebral cortex

Left hemisphere of the brain	Right hemisphere of the brain
The left hemisphere ("thinking", logical) - - is responsible for the regulation of speech activity, oral speech, writing, counting and logical thinking. Dominant in right-handers.	The right hemisphere ("artistic", emotional) - - is involved in the recognition of visual, musical images, the shape and structure of objects, in conscious orientation in space.
Cross section of the left hemisphere through sensory centers Representation of the body in the sensitive zone of the cerebral cortex. The sensitive area of ​​each hemisphere receives information from the muscles, skin and internal organs opposite side body. Rating 5.00

glial cells; it is located in some parts of the deep brain structures, the cortex of the cerebral hemispheres (as well as the cerebellum) is formed from this substance.

Each hemisphere is divided into five lobes, four of which (frontal, parietal, occipital and temporal) are adjacent to the corresponding bones of the cranial vault, and one (insular) is located in depth, in the fossa that separates the frontal and temporal lobes.

The cerebral cortex has a thickness of 1.5–4.5 mm, its area increases due to the presence of furrows; it is connected with other parts of the central nervous system, thanks to the impulses that neurons conduct.

The hemispheres make up approximately 80% of the total mass of the brain. They carry out the regulation of higher mental functions, while the brain stem is lower, which are associated with the activity of internal organs.

Three main regions are distinguished on the hemispheric surface:

• convex upper lateral, which is adjacent to the inner surface of the cranial vault;
• lower, with the anterior and middle sections located on the inner surface of the cranial base and the posterior ones in the region of the cerebellum;
• the medial is located at the longitudinal fissure of the brain.

Features of the device and activities

The cerebral cortex is divided into 4 types:

• ancient - occupies a little more than 0.5% of the entire surface of the hemispheres;
• old - 2.2%;
• new - more than 95%;
• the average is about 1.5%.

The phylogenetically ancient cerebral cortex, represented by groups of large neurons, is pushed aside by the new one to the base of the hemispheres, becoming a narrow strip. And the old one, consisting of three cell layers, shifts closer to the middle. The main region of the old cortex is the hippocampus, which is the central department of the limbic system. The middle (intermediate) crust is a formation of a transitional type, since the transformation of old structures into new ones is carried out gradually.

The human cerebral cortex, unlike that of mammals, is also responsible for the coordinated work of internal organs. Such a phenomenon, in which the role of the cortex in the implementation of all the functional activities of the body increases, is called the corticalization of functions.

One of the features of the cortex is its electrical activity, which occurs spontaneously. Nerve cells located in this section have a certain rhythmic activity, reflecting biochemical, biophysical processes. Activity has a different amplitude and frequency (alpha, beta, delta, theta rhythms), which depends on the influence of numerous factors (meditation, sleep phases, stress, the presence of convulsions, neoplasms).

Structure

The cerebral cortex is a multilayer formation: each of the layers has its own specific composition of neurocytes, a specific orientation, and the location of processes.

The systematic position of neurons in the cortex is called "cytoarchitectonics", the fibers arranged in a certain order are called "myeloarchitectonics".

The cerebral cortex consists of six cytoarchitectonic layers.

1. Surface molecular, in which there are not very many nerve cells. Their processes are located in himself, and they do not go beyond.
2. The outer granular is formed from pyramidal and stellate neurocytes. The processes leave this layer and go to the next ones.
3. Pyramidal consists of pyramidal cells. Their axons go down where they end or form association fibers, and their dendrites go up to the second layer.
4. The internal granular is formed by stellate cells and small pyramidal. The dendrites go into the first layer, the lateral processes branch out within their own layer. Axons extend into the upper layers or into the white matter.
5. Ganglionic is formed by large pyramidal cells. Here are the largest neurocytes of the cortex. The dendrites are directed to the first layer or distributed in their own. Axons leave the cortex and begin to be fibers that connect various departments and structures of the central nervous system with each other.
6. Multiform - consists of various cells. Dendrites go to the molecular layer (some only up to the fourth or fifth layers). Axons are sent to the overlying layers or exit the cortex as association fibers.

The cerebral cortex is divided into regions - the so-called horizontal organization. There are 11 of them in total, and they include 52 fields, each of which has its own serial number.

Vertical organization

There is also a vertical division - into columns of neurons. In this case, small columns are combined into macro columns, which are called a functional module. At the heart of such systems are stellate cells - their axons, as well as their horizontal connections with the lateral axons of pyramidal neurocytes. All nerve cells in the vertical columns respond to the afferent impulse in the same way and together send an efferent signal. Excitation in the horizontal direction is due to the activity of transverse fibers that follow from one column to another.

He first discovered units that unite neurons of different layers vertically in 1943. Lorente de No - with the help of histology. Subsequently, this was confirmed using methods of electrophysiology on animals by W. Mountcastle.

The development of the cortex in fetal development begins early: as early as 8 weeks, the embryo has a cortical plate. First, the lower layers differentiate, and at 6 months, the unborn child has all the fields that are present in an adult. The cytoarchitectonic features of the cortex are fully formed by the age of 7, but the bodies of neurocytes increase even up to 18. For the formation of the cortex, coordinated movement and division of precursor cells from which neurons emerge are necessary. It has been established that this process is influenced by a special gene.

Horizontal organization

It is customary to divide the areas of the cerebral cortex into:

• associative;
• sensory (sensitive);
• motor.

When studying localized areas and their functional characteristics, scientists used a variety of methods: chemical or physical irritation, partial removal of brain areas, development of conditioned reflexes, registration of brain biocurrents.

sensitive

These areas occupy approximately 20% of the cortex. The defeat of such zones leads to a violation of sensitivity (reduction of vision, hearing, smell, etc.). The area of ​​the zone directly depends on the number of nerve cells that perceive the impulse from certain receptors: the more there are, the higher the sensitivity. Allocate zones:

• somatosensory (responsible for skin, proprioceptive, autonomic sensitivity) - it is located in the parietal lobe (postcentral gyrus);
• visual, bilateral damage that leads to complete blindness - located in the occipital lobe;
• auditory (located in the temporal lobe);
• taste, located in the parietal lobe (localization - postcentral gyrus);
• olfactory, bilateral violation of which leads to loss of smell (located in the hippocampal gyrus).

Violation of the auditory zone does not lead to deafness, but other symptoms appear. For example, the impossibility of distinguishing short sounds, the meaning of everyday noises (steps, pouring water, etc.) while maintaining the difference in pitch, duration, and timbre. Amusia can also occur, which consists in the inability to recognize, reproduce melodies, and also distinguish between them. Music can also be accompanied by unpleasant sensations.

Impulses going along afferent fibers from the left side of the body are perceived by the right hemisphere, and from the right side - by the left (damage to the left hemisphere will cause a violation of sensitivity on the right side and vice versa). This is due to the fact that each postcentral gyrus is connected to the opposite part of the body.

Motor

The motor areas, the irritation of which causes the movement of the muscles, are located in the anterior central gyrus of the frontal lobe. Motor areas communicate with sensory areas.

The motor pathways in the medulla oblongata (and partially in the spinal cord) form a decussation with a transition to the opposite side. This leads to the fact that the irritation that occurs in the left hemisphere enters the right half of the body, and vice versa. Therefore, damage to the cortex of one of the hemispheres leads to a violation motor function muscles on the opposite side of the body.

The motor and sensory areas, which are located in the region of the central sulcus, are combined into one formation - the sensorimotor zone.

Neurology and neuropsychology have accumulated a lot of information about how the defeat of these areas leads not only to elementary movement disorders (paralysis, paresis, tremors), but also to disturbances in voluntary movements and actions with objects - apraxia. When they appear, movements during writing may be disturbed, disorders may occur spatial representations, appear uncontrolled patterned movements.

Associative

These zones are responsible for linking the incoming sensory information with the one that was previously received and stored in memory. In addition, they allow you to compare information that comes from different receptors. The response to the signal is formed in the associative zone and transmitted to the motor zone. Thus, each associative area is responsible for the processes of memory, learning and thinking.. Large associative zones are located next to the corresponding functional sensory zones. For example, any associative visual function is controlled by the visual association area, which is located next to the sensory visual area.

Establishing the laws of the brain, analyzing its local disorders and checking its activity is carried out by the science of neuropsychology, which is located at the intersection of neurobiology, psychology, psychiatry and informatics.

Features of localization by fields

The cerebral cortex is plastic, which affects the transition of the functions of one department, if it is disturbed, to another. This is due to the fact that the analyzers in the cortex have a nucleus, where higher activity, and the periphery, which is responsible for the processes of analysis and synthesis in a primitive form. Between the analyzer cores there are elements that belong to different analyzers. If the damage touches the nucleus, peripheral components begin to take responsibility for its activity.

Thus, the localization of functions possessed by the cerebral cortex is a relative concept, since there are no definite boundaries. However, cytoarchitectonics suggests the presence of 52 fields that communicate with each other through pathways:

• associative (this type of nerve fibers is responsible for the activity of the cortex in the region of one hemisphere);
• commissural (connect symmetrical areas of both hemispheres);
• projection (contribute to the communication of the cortex, subcortical structures with other organs).

Table 1

		Relevant fields
Motor
sensitive
visual
Olfactory
Taste
Speech motor, which includes centers:	Wernicke, which allows you to perceive oral speech
	Broca - responsible for the movement of the tongue muscles; defeat threatens with a complete loss of speech
	Perception of speech in writing

So, the structure of the cerebral cortex involves considering it in a horizontal and vertical orientation. Depending on this, vertical columns of neurons and zones located in the horizontal plane are distinguished. The main functions performed by the cortex are reduced to the implementation of behavior, regulation of thinking, consciousness. In addition, it ensures the interaction of the body with the external environment and takes part in the control of the work of internal organs.