Sopor. Coma

Clear consciousness during wakefulness is one of the indicators normal functioning brain. Various pathological conditions can lead to a decrease in the depth of consciousness up to its shutdown. It is very important that in this case consciousness does not change qualitatively, but is only depressed. One of these quantitative disorders of consciousness is stupor. The appearance of such a disorder requires establishing its exact cause and eliminating factors that negatively affect brain function.

Stupor is a sign of dysfunction of the cerebral cortex and the predominance of the inhibitory influence of the reticular formation. It can occur due to various damage to nervous tissue, severe hypoxia of the brain, or the action of a number of substances that can be produced in the body itself or come from outside.

Basic conditions that may be accompanied by stupor:

• ONMK ( acute disorder cerebral circulation) in the form or, especially if they involve the upper parts of the brain stem;
• heavy hypertensive crisis;
• leading to damage to nervous tissue and/or hematomas of various locations;
• pronounced deviations in glucose and/or food levels carbohydrate metabolism for diabetes mellitus;
• hypothyroidism;
• space-occupying formations (most often) causing swelling and swelling of the brain or displacement of its structures;
• severe metabolic disorders in liver and kidney failure;
• subarachnoid hemorrhage due to aneurysm rupture;
• brain damage as a result of the action of carbon monoxide or certain substances (methyl and ethyl alcohols, barbiturates, opioids and any drugs in high toxic dosages);
• infectious and inflammatory diseases of the central nervous system, leading to the development of meningoencephalitis;
• sepsis;
• pronounced disturbances of electrolyte and water metabolism;
• severe heart failure (for example, after myocardial infarction, with severe impairment heart rate etc.);
• heatstroke or hypothermia.

The clinical picture of stupor does not depend on its cause; the symptoms of the underlying disease are supplemented by signs of depression of consciousness.

Signs of a soporous state

A person in stupor looks asleep; only strong stimuli cause a reaction. At a sharp sound, his eyes open, but no purposeful searching movements occur. After pressing on the nail bed, the limb is withdrawn. And an injection, a pat on the cheek or another painful effect causes a person in stupor to have a fairly bright, but short-term negative reaction. Sometimes the patient fights back and scolds.

When viewed, it attracts attention general decline muscle tone, suppression deep reflexes. Pyramid signs are often found due to decreased influence central motor neurons. The reaction of the pupils to light is sluggish, the corneal reflex and swallowing are preserved.

Along with this, focal neurological symptoms may be detected, indicating local damage to certain structures and areas in the brain. If stupor is caused by intracranial hemorrhage or meningoencephalitis, neck stiffness and other meningeal symptoms. Convulsive seizures and muscle twitching in the form of myoclonus, untargeted, may also appear.

Sometimes a hyperkinetic version of stupor occurs, when a person mutters incoherently, wriggles around, makes individual unfocused movements, and productive contact with him is impossible. This condition resembles delirium delirium, which refers to qualitative disorders of consciousness.

Examinations for stupor

The doctor conducts an objective examination, determines the depth of the disturbance of consciousness and identifies possible reasons this condition.

In case of disturbances of consciousness, it is necessary to determine the level of its depression, differentiating stupor from coma and stunning. Basic examinations are aimed at identifying the cause of brain dysfunction and any accompanying metabolic changes.

The doctor needs to obtain as much information as possible about what preceded the depression of consciousness. For this purpose we are studying medical documentation, a survey of accompanying persons and relatives is conducted. The patient’s clothing and personal belongings are also inspected, which sometimes makes it possible to detect packaging of drugs used, individual cards with information about existing diseases.
If stupor is detected, it is necessary to quickly conduct a series of screening tests:

• examination of the patient’s body to identify injuries, rashes, hemorrhages, injection marks, and detect the smell of alcohol;
• level measurement blood pressure;
• measuring body temperature;
• determination of blood glucose levels;
• ECG and auscultation (listening) of the heart.

At the same time, tests are taken to determine the blood picture, basic biochemical parameters and electrolyte levels. If poisoning is suspected, blood is taken for toxicological testing and urine is taken to screen for major drugs. In some cases, the neurologist decides to emergency implementation and MRI (CT) of the brain.

Principles of treating stupor

Stupor is not an independent disease, but evidence of a dysfunction of the brain. Therefore, treatment should be aimed at eliminating the cause of depression of consciousness, and it should begin as soon as possible.

In the development of stupor, ischemia and edema of brain tissue play an important role, which can occur with the most different states. Early treatment will help prevent the brain from herniating into the natural openings of the skull and preserve the viability of neurons. Particularly vulnerable nerve cells in the so-called penumbra zone (or ischemic penumbra) - the area directly adjacent to the source of damage in the brain. With inadequate therapy, symptoms will increase due to the death of neurons in this area. In this case, stupor can turn into a coma, and neurological disorders will be persistent and pronounced.

When treating stupor, the main actions are aimed at eliminating swelling of the nervous tissue and maintaining adequate blood supply to the brain. They also correct the level of glucose in the blood and replenish the deficiency of microelements, eliminate heart rhythm disturbances and begin treatment of renal and liver failure. For infections it is prescribed antibacterial agents, and the presence of hemorrhages requires measures to stop the bleeding.

The prognosis for stupor depends on its cause, the depth and nature of the damage to the nervous tissue and the volume of treatment measures taken. The earlier the etiology is identified and severe disorders are corrected, the higher the chance of quickly restoring clear consciousness and regressing the symptoms of the underlying disease.

Usual clinical stupor manifests itself in the depressed psychological state of the patient, weak reaction of the pupils to light and dulling of pain.

The soporous state can transform into a coma, which is extreme suppression of all body functions. It is completely switched off at the reflex level. To prevent this condition, you should know what causes stupor.

What is the difference between stupor and coma

The main difference between stupor and coma is that the first state is a lack of contact with the outside world, accompanied by But a person can be taken out of it at least for a short time. This can be achieved by vigorous shaking, tingling, in a loud voice. Coma is an unconscious state that can be compared to very deep sleep or anesthesia, from which awakening is impossible. A person in a comatose state does not even respond to pain.

Cause of stupor

The most common causes of stupor include:

• complications caused by cerebral hemorrhage;
• the presence of benign or malignant neoplasms in the brain;
• chronic diseases;
• toxic damage to the body;
• viruses and infections;
• thrombophlebitis;
• atherosclerosis;
• overdose of drugs, especially tranquilizers;
• wrong lifestyle;
• disruption of metabolic processes in the body;
• severe hypertensive crisis;
• head injury;
• pronounced deviations in glucose levels in diabetes mellitus;
• reduced function thyroid gland(hypothyroidism);
• metabolic disorders due to nephritis;
• aneurysm rupture;
• body poisoning carbon monoxide, barbiturates, opioids;
• meningitis;
• meningoencephalitis;
• cardiac ischemia;
• blood poisoning (sepsis);
• violation electrolyte balance in organism;
• heatstroke.

Symptoms of the disease

If a healthy central nervous system constantly responds to changing conditions environment, then in a state of stupor, brain activity is inhibited. The body seems to be in a long sleep. The stuporous state can transform into a coma.

The brain cannot make any decisions. Wakefulness and sleep can abruptly replace each other.

Many people are interested in: “How long does the stuporous state last?” Blackout periods can last from a few seconds to months. It all depends on the reason that caused the process.

With stupor, the patient may feel some fog and confusion in understanding everything that is happening around. He may experience disorientation in space. The patient may confuse dates and names, may not remember events that happened yesterday, but at the same time clear pictures of the distant past emerge in his memory.

Strong irritants can cause a reaction in a person. A sharp sound causes the eyelids to open, but the patient purposefully does not look for anything. Impact on the nail bed provokes withdrawal of the limb. An injection or a pat on the cheek can cause a short-term negative reaction in the patient.

On examination, a decrease in muscle tone and inhibition of deep reflexes are noted. A pyramidal syndrome caused by suppression of central neurons is often detected. The reaction of the pupils to light is sluggish, corneal and persists.

In parallel with all these symptoms, neurological signs focal in nature, indicating local damage to certain areas in the cerebral cortex.

If the soporous state is provoked by a stroke or meningoencephalitis, then stiffness of the neck muscles and other meningeal symptoms will be detected. Uncontrollable muscle twitching may also occur.

In some cases, doctors are faced with a hyperkinetic version of stupor, in which a person says something incoherently, turns around, and makes purposeful movements. Establishing productive contact with the patient is impossible. similar to delirium, which is classified as qualitative violations consciousness.

The stuporous state after a stroke can be characterized by a high degree of agitation or complete indifference to everything around.

Stupor during stroke

A stroke is a very dangerous disease, which causes unpredictable complications. Stupor is one of them. Translated from Latin, the word “stupor” means “sleep”, “numbness”, “lethargy”, “memory loss”. In medicine, this condition is usually called subcoma, since it is a step towards the development of coma and is in many ways similar to this serious condition.

The soporous state during a stroke is expressed in the dulling of all human reactions. The activity of consciousness is in an extremely depressed state.

Stroke is caused by pathological processes in blood vessels that provoke acute dysfunction of the brain. The effects last for more than a day. A stroke can lead to rapid death.

Stupor does not always, but quite often accompanies a stroke. It is observed in approximately one fifth of cases of all cerebral necrosis. The manifestation of this condition can be observed not only during the acute period of the disease, but also during its rehabilitation. The process is directly dependent on the area and degree of brain damage.

Such a complication cannot be ignored under any circumstances, since most often it quickly turns into a coma.

Clinical picture of stupor during stroke

The soporous state during stroke, the prognosis of which depends on the extent of cerebral necrosis, manifests itself in the patient’s drowsiness and lethargy. In parallel with this, defensive reactions to stimuli such as pain persist sharp sound and light. The patient does not react to the environment around him, cannot answer questions, and is unable to complete any task. Muscle tension in the limbs it is decreased, tendon reflexes are dulled, coordination of movements is lost.

Stupor in epilepsy

Stopper always accompanies Epilepsy in medicine is called a state of increased convulsive readiness. In such patients, the appearance of seizures is provoked by a certain situation, which healthy people they don't react that way. Many researchers believe that the disease is hereditary.

Typically, an epileptic seizure is preceded by a sharp change in the patient’s emotional background. 2-3 days before a seizure, a person becomes agitated, tense and anxious. Some patients withdraw into themselves, others show aggression towards others. Shortly before the attack, an aura appears that is difficult to describe in words. It is characterized by a variety of tactile sensations: taste in the mouth, vague sounds and smells. We can say that the aura marks an epileptic seizure.

A focus of excitation appears in the cerebral cortex of a person. It covers more and more nerve cells. The end result is a seizure. Usually the duration of the phase is 30 seconds, less often one minute. The patient's muscles are under severe tension. The head is thrown back. The patient screams and breathing stops.

The convulsive stage lasts up to 5 minutes. With it, all the patient’s muscles involuntarily contract. After the seizure ends, the muscles relax again. The patient's consciousness turns off. The stuporous state in epilepsy lasts 15-30 minutes. After recovering from stupor, the patient falls into deep sleep.

Stupor due to dehydration

A complication such as stupor can also accompany dehydration. In medicine, water deficiency is usually called exicosis. In this condition, there is a low content of electrolytes and water, which is provoked by repeated persistent vomiting and severe stomach upset.

In addition, fluid loss can be caused by pathological processes in the kidneys and lungs. Typically, exicosis develops gradually within 2-3 days from the onset of the provoking disease.

Dehydration is characterized by the patient's lethargy, loss of appetite, and refusal to drink. Ingestion of liquid causes profuse vomiting. There is a decrease in muscle tone, the patient’s body temperature, as well as blood pressure, drops sharply. Oliguria or anuria is noted.

A stuporous state from dehydration can progress to a coma.

Prognosis for stupor

What is the outcome of the disease? A stuporous condition, the prognosis of which depends on the provoking cause, must undergo timely treatment. The degree of damage to the nervous tissue and the volume of therapy play a major role.

The sooner measures were taken to correct the disorder, the higher the patient’s chance of restoring clear consciousness and regressing the symptoms of the underlying disease.

Diagnostics

Stupor caused by a stroke can be fatal. At the first mild manifestations of complications, it is necessary to carry out timely diagnosis.

Priority measures include:

• blood pressure measurement;
• checking heart rate and breathing;
• checking the reaction of the pupils to light and determining the degree of their mobility;
• measuring body temperature; if it is high, one can judge the presence of infection in the patient’s blood;
• examination of the skin for injuries, vascular lesions or allergic manifestations.

Necessary examinations

The examination, which must be carried out in mandatory, is electroencephalography. She gives medical workers an idea of ​​the degree of damage to brain cells.

If the presence of stupor is confirmed, hospitalization is usually indicated. In the hospital, the patient will be able to provide support for the functions necessary for life and conduct more detailed diagnostics.

After electroencephalography, a spectral blood test is performed to identify high rate sugar and other provocateurs of the pathological condition. If intoxication is suspected, a blood test is also done and urine is examined for the presence of narcotic substances in organism. In some cases, a neurologist prescribes a lumbar puncture and magnetic resonance therapy of the brain.

Principles of treating stupor

A stuporous state, the consequences of which can be very severe, is not an independent phenomenon. It indicates a malfunction of the brain. Therefore, the goal of treatment should be to eliminate the underlying factor. In this case, therapy should be started as quickly as possible.

The trigger for stupor is often ischemia and swelling of the brain tissue. Early treatment prevents the brain from wedging into the natural openings of the skull and helps preserve the functionality of neurons.

Nerve cells in the penumbra (ischemic penumbra) are especially vulnerable. This is the area that is adjacent to the affected lesion in the brain. Incorrect treatment provokes an increase in symptoms due to the death of neurons in this area. In this case, the soporous state may turn into a coma, and neurological disorders will become more pronounced.

When treating stupor, the main actions are aimed at combating swelling of the nervous tissue and maintaining adequate blood circulation in the brain. The level of glucose in the blood is also corrected, the lack of microelements is compensated, and the causes of disturbances in the functioning of the heart, kidneys and liver are eliminated.

In case of infection, the use of antibiotics is indicated, and in the presence of hemorrhages, they resort to stopping the bleeding.

For stupor, all medications are administered intravenously into the body. At the same time, the most an effective drug is glucose 40% and thiamine, as well as the use of these drugs with naloxone.

Further therapy for stupor depends on the degree of damage to the body and is prescribed by a doctor on an individual basis.

Stupor is a deep depression of a person’s consciousness, resulting in drowsiness. At this state the patient’s voluntary activity is suppressed, but his reflex activity is preserved.

In particular, the sluggish reaction of the pupils of the eyes to light and a defensive reaction to pain remain. With further depression of a person's consciousness, coma develops. So, stupor is intermediate state between stunned consciousness and coma. Coma is a state of severe depression of the nervous system. In this case, the person loses consciousness, his reflex activity disappears, and dysregulation of basic vital functions appears.

Causes

Stupor and coma can be caused by many serious illnesses, conditions and injuries, such as: tumor-like brain diseases, traumatic brain injuries, vascular and toxic brain lesions, etc. Short term loss consciousness may occur after minor head injuries, due to decreased blood circulation to the brain or as a result of seizures. Poor blood circulation in the brain is often observed during fainting or stroke.

Serious head injuries, certain serious illnesses, toxic effects of drugs or an overdose of sedatives can lead to prolonged loss of consciousness. Metabolic disorders that affect the content of sugar, salts and some other substances in the blood can also negatively affect brain function.

Symptoms

Normally, brain activity in humans is constantly changing. Thus, the brain activity of a awake person is significantly different from the activity of a sleeping person. Also, brain activity in these conditions is different from brain activity, for example, during a difficult exam or during emergency situations requiring a quick solution. Such differences in brain activity between different activities are normal. Moreover, such states can move from one to another quite quickly.

With an altered level of consciousness, the brain is no longer able to switch to different modes their work in accordance with current circumstances. The area that is dedicated to regulating activity is located deep in the brain stem. This area actively stimulates the brain, thereby determining the level of consciousness and wakefulness. To determine the condition, the entire set of information received from the ears, eyes, skin and other sensory organs. Using this information, the brain changes its activity level accordingly.

If the activating system in the brain stem is damaged or its communication with certain other parts of the brain is disrupted, then sensory perceptions in the brain are no longer able to sufficiently influence the level of wakefulness and the level of brain activation. This leads to a disorder of consciousness. This can even lead to loss of consciousness.

Periods of disturbance of consciousness can be either long-term or short-term. Moreover, consciousness can change from a slight clouding of the patient’s mind to his complete non-contact.

With confusion, the patient may well remain active. At the same time, he is disoriented. This condition is often characterized by the patient being unable to differentiate between events that happened in the past and events that are happening now. In addition, the patient is agitated and often cannot correctly understand the speech of the people around him. The state of inhibition in this case is the appearance of reduced brain activity. In some cases, patients experience a condition called somnolence. This state is a state that resembles long and deep sleep. Often, in order to bring a person out of this state, you have to shout loudly and push him away.

Stupor represents a deep lack of contact, a loss of human consciousness and a condition from which a sick person can only be brought out for a short period of time. This requires repeated vigorous shaking, loud calls, or needle pricks. In this case, the person does not react to the environment, cannot answer questions posed, and does not complete any tasks. The swallowing function is preserved.

The next state, after soporosis, is coma. Coma is an unconscious state that is somewhat similar to the state of general anesthesia or per condition deep sleep. The patient cannot be brought out of this state by trying to awaken him. In addition, a patient who is in the stages of a deep coma usually does not have any response, including pain. In this condition, it is difficult to predict the patient's likelihood of recovery. The likelihood of recovery largely depends on the cause of the coma. If the cause of the coma was a head injury, then full recovery is possible if the loss of consciousness lasts no more than three months. If the cause of the coma is cardiac arrest or cessation of breathing, the duration of the coma is more than a month, then recovery occurs quite rarely.

In some cases, after a brain injury, due to a severe illness that damages the brain or due to lack of oxygen, the patient usually goes into a vegetative state. It should be noted that in this case the patient can fall asleep, wake up, swallow and breathe normally. In addition, the patient may have a motor reaction to all loud noises. However, permanently or temporarily, he loses the ability to engage in normal conscious behavior and thinking. Patients in vegetative state able to perform some reflex movements, such as twitching, tension in the legs and arms.

In some cases, the patient may experience the so-called “locked-in person” syndrome. This syndrome is a rare condition in which the affected person is conscious and can think relatively normally. However, as a result of severe paralysis, the patient is able to communicate with people only by opening or closing his eyes. This is the only way he can answer questions addressed to him. This condition usually occurs with severe peripheral paralysis. The same condition can occur with some types of stroke.

The most severe form of the condition is brain death. In this condition, the brain irreversibly loses all basic vital functions, including loss of consciousness and the ability to breathe normally. If the patient is not provided with artificial ventilation and the necessary medications, death will quickly occur. In general, a person is legally considered dead if his brain loses all its basic functions, even if he still has a pulse.

It is customary to declare brain death when, twelve hours after the elimination of all treatable disorders of a person’s condition, the patient’s brain still does not respond to external stimuli. In this case, the person does not react to light and cannot breathe on his own.

If there is doubt about the state of brain activity, then electroencephalography is performed, which shows the presence or absence of brain functionality. Electroencephalography records the electrical activity of the brain. Even after brain death, some functions may remain spinal cord. In this case, a person may exhibit some reflexes.

Diagnostics

Coma and stuporous state are emergency pathologies that require the use of resuscitation measures. This is due to the fact that the severity of the psychoorganic syndrome, which subsequently does not develop, depends on the duration of loss of consciousness. Main in clinical picture Any coma is considered to be a shutdown of consciousness, in which a person loses the possibility of normal perception not only of the environment, but also of himself.

Upon arrival at the scene, emergency doctors diagnose the soporous condition. In particular, they must make sure how clear the patient's airways are. In addition, they should check your breathing pulse and blood pressure. Special attention It is worth paying attention to body temperature. If a patient has a high temperature, this may be one of the signs of an infectious disease. If the body temperature, on the contrary, is low, this may mean that the patient has been exposed to cold for a long time.

Also during the diagnosis, a skin examination is carried out. This is necessary in order to identify possible traces of infections, injuries or allergic reactions. In addition, the head is examined for bruises and wounds. In any case, a complete neurological examination is necessary. This can reveal signs of brain damage.

An eye examination is equally important. It allows you to get important information about the state of the central nervous system. At the same time, the position and mobility of the eyeballs are checked, the size of the pupils, the reaction to light are checked, the appearance of the retina and the patient’s ability to follow all moving objects are checked. Different pupil sizes may be a sign of compression of the brain.

Treatment

In case in soporotic state the main reactions are passive in nature, then with the development of coma the patient, as a rule, stops responding to all external stimuli. In particular, a person in such a state does not respond to patting, changing the position of individual parts of the body, injections, turning the head, and especially to any approach to the patient. It is worth noting that in coma, unlike stupor, there is no reaction of the pupils to light.

Patients who are in a coma, the cause of which is not clear, are always tested for glycemia. If it is known for certain that the patient is suffering diabetes mellitus, and it is difficult to identify the hyperglycemic or hypoglycemic origin of the coma, it is recommended to perform intravenous administration glucose. This is necessary to carry out differential diagnosis, and for the purpose of providing emergency care with hypoglycemic coma. If the patient has a low blood glucose level, then such injections improve the symptoms of the lesions. In addition, it allows the two conditions to be distinguished. In case of coma due to high content glucose, the administration of glucose has virtually no effect on the patient’s condition. If it is impossible to measure the amount of glucose in the blood, then experimentally you need to introduce high concentration glucose.

If a rapid change in consciousness occurs, the person should be provided with immediate health care. However, not always in short time manages to install correct diagnosis, necessary for the correct treatment of brain disorders. Until the test results are received, the person is sent to intensive care, where his pulse, body temperature, blood pressure and blood levels will be constantly monitored. required quantity oxygen.

After being transported to intensive care, the person is immediately given oxygen and an intravenous system is set up, which will allow the necessary medication to be administered in a timely manner. Glucose is administered intravenously until the results of blood sugar tests are obtained. If there is a suspicion that disorders of consciousness were caused by narcotic drugs, then before the results of urine and blood tests are received, the patient is given the antidote naloxone.

If you suspect that a disorder of consciousness has led to toxic substance, the patient's stomach is washed. This will also prevent further absorption of the toxic substance.

To support normal pulse and normal blood pressure, blood transfusion and intravenous administration are used necessary medications and liquids.

If it is not possible to clarify the diagnosis and urgent hospitalization, the main drugs for patients in a coma are thiamine, 40% glucose solution and naloxone. The combination of these drugs is in most cases considered the most effective and safe.

In the deepest stages of coma, the brain has damage that prevents the body from normally providing vital functions. IN similar cases the device is used artificial ventilation lungs, allowing to facilitate the work of the lungs.

Stupor and coma are disturbances of consciousness due to dysfunction of both hemispheres of the brain or the ascending activating reticular system. Stupor is a state of unresponsiveness from which the patient can only be brought out by a short time intense repeated stimulation. Coma is a state of unresponsiveness from which the patient cannot be brought out by stimulation. The causes can be local organic and functional cerebral (often metabolic). Diagnosis is made based on clinical findings; to determine the cause are needed laboratory research and neuroimaging. Treatment is immediate stabilization of the condition and targeted action on the cause. For prolonged stupor or coma, supportive care includes passive movements in range of motion in all joints, enteral nutrition and prevention of bedsores. The prognosis depends on the cause.

For a state of wakefulness it is necessary full-time job hemispheres of the brain and the mechanisms of the ascending reticular activating system (ARS) - a wide network of nuclear connections in the upper part of the pons, midbrain and posterior sections interstitial brain.

Infarction or hemorrhage in the upper brain stem

The pathogenesis of stupor and coma often includes hypoxia and cerebral ischemia. Mental disorders (for example, mutism) can mimic disorders of consciousness, but they are usually differentiated from true stupor or coma by physical and neurological examination.

Herniation syndromes. After infancy, the skull is rigid, so that intracranial space-occupying lesions or cerebral edema lead to increased intracranial pressure, which is fraught with protrusion of brain tissue through the natural openings of the skull bones or dura mater.

In transtentorial herniation (involving the uncus parahippocampal gyrus), the temporal lobe protrudes beyond the edge of the tentorium (the tent-like structure on which the temporal lobe normally rests). The hook - the medial edge of the protrusive lobe - presses on the diencephalon and top part trunk, provoking ischemia and infarction of the tissues that make up the VARS. Herniation of both temporal lobes (central herniation) is usually associated with bilateral mass lesions or diffuse edema and causes symmetrical compression of the midbrain and brainstem.

Herniation of the cerebellar tonsils is associated with infra- or supratentorial (less commonly) space-occupying formations. The cerebellar tonsils, when wedged into the foramen magnum, compress the brain stem and block the flow of cerebrospinal fluid, causing acute hydrocephalus. Intrusions both under the tentorium and into the foramen magnum threaten the patient’s life.

With lateral dislocation, the cingulate gyrus is wedged under the falx cerebri.

Symptoms of coma and stupor

Repeated painful stimulation cannot awaken comatose patients, and patients in stupor are brought to consciousness only for a short time. Against the background of coma, stimulation causes only primitive reflex movements (for example, decerebrate and decortication postures).

Diagnosis of coma and stupor

Diagnosis and stabilization of the condition should be carried out simultaneously. First of all, it is necessary to ensure permeability respiratory tract, normalize respiratory and circulatory function. In case of rare respiratory movements or low O2 saturation (according to the criteria of pulse oximetry or arterial blood gas composition), intubation is indicated. Correction of hypotension is necessary. The glucose content in peripheral blood is determined. If glucose levels are low, 100 mg of thiamine (to prevent the development of Wernicke encephalopathy) and 50 ml of 50% glucose are administered intramuscularly. If an opiate overdose is suspected, 2 mg of naloxone is administered intravenously. If there is evidence of injury, the neck is stabilized with a rigid orthopedic collar until a fracture can be radiographically ruled out.

The medial part is wedged through the cerebellar tentorium temporal lobe. The usual cause is an ipsilateral mass lesion. First of all, the ipsilateral nerve of the third pair is compressed (unilateral dilatation and fixation of the pupil, paresis of the extraocular muscles), the posterior cerebral artery (homonymous hemianopsia) and the contralateral cerebral peduncle (ipsilateral hemiparesis). Then a picture of compression of the midbrain and brainstem develops, manifested by impaired consciousness, pathological breathing, fixation of the pupils in a central position, loss of oculocephalic and oculo-vestibular reflexes (the eyes do not move when turning the head and caloric test), development of symmetrical paresis with decerebrate rigidity or flaccid paralysis, the Cushing reflex appears ( arterial hypertension, especially systolic and bradycardia). Displacement of both temporal lobes (central herniation) is usually associated with a bilateral space-occupying lesion and leads to symmetrical compression of the midbrain and brainstem with the symptoms already described.

Herniation of the cerebellar tonsils is a consequence of infra- or supratentorial (less commonly) space-occupying formations. Wedged into the foramen magnum, the cerebellar tonsils compress the brain stem and block the flow of cerebrospinal fluid with the development of acute hydrocephalus. Symptoms include: lethargy, drowsiness, headache, vomiting, meningism, unfriendly eye movements, sudden stop of breathing and heart function.

Anamnesis. Medical identification bracelets and the contents of a purse or wallet may contain useful information (eg, documents, medications). Relatives, emergency medical personnel, and police should be interviewed about the circumstances of the incident (for example, seizures, headache, vomiting, head injury, medication or drug use), and find out the environment in which the patient was found; packaging of food, alcohol, medicines, narcotic and toxic substances should be inspected and preserved for chemical analysis and as possible physical evidence. Relatives should be asked about the patient's recent infections, mental problems and a history of diseases. It is advisable to look at medical documents.

Objective examination. The medical examination must be focused and effective. Signs of traumatic brain injury include paraorbital hematomas (“raccoon eyes,” synonymous with “spectacles symptom”), bruising behind the ears (Battle’s sign), hematotympanum, mobility upper jaw, naso-and/or otoliquorhea. Bruises of the soft tissues of the head and small bullet entry holes are often unnoticeable. The fundus should be examined for papilledema, hemorrhage, and exudate. With passive flexion of the neck (if no injury is proven!), stiffness may be detected, indicating subarachnoid hemorrhage or meningitis. Until a fracture has been ruled out (based on history, physical examination, and x-ray), the cervical spine should be immobilized.

Fever or petechial rash suggests CNS infection. Needle marks raise the possibility of drug overdose (eg, opioids or insulin). A bitten tongue indicates convulsive attack. A specific smell may indicate alcohol intoxication.

Neurological examination. A neurological examination determines whether the brain stem is damaged or not and where in the central nervous system the lesion is located. State of consciousness, pupils, eye movements, breathing and physical activity help determine the level of central nervous system dysfunction.

Attempts are made to awaken the patient, first with verbal commands, then with mild stimulation, and finally with painful stimuli (for example, pressure on the eyebrow, nail bed, or sternum). According to the Glasgow Coma Scale, responses to a stimulus are assessed by a number of points. Eye opening, grimacing, and purposeful withdrawal of limbs in response to a painful stimulus indicate relatively mild degree disturbances of consciousness. Asymmetric motor activity in response to painful irritation indicates focality of damage to the cerebral hemispheres.

When stupor progresses to coma, painful stimuli only cause the formation of stereotypical reflex postures. Decorticate posture (flexion and adduction of the arms, extension of the legs) indicates damage to the cerebral hemispheres, including the corticospinal tract, while the brain stem is preserved. Decerebrate rigidity (neck, back, limbs extended, jaw clenched) suggests impairment upper sections brain stem. Flaccid paralysis without any movement is a manifestation severe defeat throughout the entire nervous axis, this is the worst case of motor impairment. Asterixis (fluttering tremor) and multifocal myoclonus accompany metabolic disorders, for example uremia, liver failure, hypoxia and drug intoxication. With mutism, there is no motor response, but muscle tone and reflexes are preserved.

With tentorial herniation, displacement of the temporal lobe primarily compresses the ipsilateral nerve of the third pair (unilateral dilatation and fixation of the pupil, paresis of the extraocular muscles); rear cerebral artery(homonymous hemianopsia) and the opposite cerebral peduncle (ipsilateral hemiparesis). Then a picture of compression of the midbrain and brainstem develops, manifested by impaired consciousness, pathological breathing, fixation of the pupils in a central position, loss of the oculocephalic and oculovestibular reflexes (the eyes do not move when turning the head and caloric test), the development of bilateral paresis with decerebrate rigidity or flaccid paralysis, appears Cushing's reflex (arterial hypertension, especially systolic, and bradycardia). Symptoms of compression of the midbrain also appear with central herniation.

When the cerebellar tonsils are herniated, the symptoms include lethargy, headache, vomiting, meningismus, unrelated eye movements, sudden stop of breathing and cardiac activity.

Ophthalmological examination provides information about the functioning of the brain stem. The examination includes pupillary reflexes, analysis of eye movements, ophthalmoscopy (for papilledema and hemorrhages), and assessment of other neuro-ophthalmic signs. Fixed pupils are an early manifestation of organic damage, and in metabolic coma, pupillary reflexes remain intact for a long time.

If there are no eye movements, the oculocephalic reflex is checked using the “doll's eye” technique: observing eye movements as the patient's head passively turns from side to side. Normally, in a conscious person, eye movements follow head movements. In case of injury, this technique cannot be performed until a fracture has been ruled out. cervical spine spine. If consciousness is depressed and the brain stem is not damaged, then when turning the head, the gaze seems fixed on the ceiling. When the brain stem is damaged, the eyes move along with the head, as if they are fixed in the sockets.

In the absence of the oculocephalic reflex, the oculovestibular reflex is examined (cold caloric study). After integrity confirmation eardrum it is irrigated for 30 s through the external auditory canal ice water in an amount of 10-40 ml, using a syringe and a soft catheter. In response, in a conscious patient (for example, in a psychogenic coma), eyeballs deviate towards the ear where the water was injected, and the nystagmus beats in the opposite direction. In a coma, while the functions of the trunk are preserved, both eyes also deviate towards the irritation, but without nystagmus. At organic damage trunk or deep metabolic coma there is no reaction or it is unfriendly.

Breathing pattern. Dysfunction of both hemispheres or diencephalon is manifested by periodic cyclic breathing (Cheyne-Stokes or Biot); dysfunction of the midbrain or upper pons is accompanied by central neurogenic hyperventilation with a respiratory rate of more than 40 per minute. Bridge lesions or medulla oblongata usually lead to long-term take deep breaths(apneustic breathing), often turning into respiratory arrest.

Research. They begin with pulse oximetry, peripheral blood glucose testing, and cardiac monitoring. They take clinical analysis blood with determination leukocyte formula and platelets, tests for biochemistry, electrolytes, coagulability and urea nitrogen. The gas composition of arterial blood is determined and, if the diagnosis remains unclear, the levels of carboxyhemoglobin, sulfhemoglobin and methemoglobin are checked.

Blood and urine smears should be Gram stained, cultures taken, standard toxicology screening performed, and alcohol levels determined. Often more than one drug is taken at the same time, so if drug poisoning is suspected, several are usually determined at once (for example, salicylates, paracetamol, tricyclic antidepressants). It is necessary to take a 12-lead ECG.

When the cause is unclear, urgent CT scan of the brain without contrast is indicated to rule out mass lesions, hemorrhage, edema, and hydrocephalus. If questions remain, contrast is added, after which a CT or MRI can reveal a subdural hematoma in the isodense phase, multiple metastases, sagittal sinus thrombosis, herpetic encephalitis and other possible causes not detected by a conventional CT scan. A chest x-ray is also indicated.

If you suspect infection A lumbar puncture is performed to assess CSF pressure. In the CSF, cell types and their numbers, protein, glucose are determined, cultures are done, Gram stain is performed, and special tests are performed according to indications (for example, for cryptococcal antigen, VDRL for syphilis, PCR to detect the virus herpes simplex). In patients unconscious before performing lumbar puncture CT is required to exclude a space-occupying intracranial formation or occlusive hydrocephalus, since in such cases a sharp decline cerebrospinal fluid pressure during lumbar puncture is fraught with the risk of herniation with a fatal outcome.

If the diagnosis remains unclear, an EEG may help: in rare cases sharp waves or peak-slow wave complexes indicate that the patient is in epistatus, although outwardly there are no convulsions. But in most cases, in coma, the EEG shows nonspecific slow low-amplitude waves, common for metabolic encephalopathy.

Prognosis and treatment of coma and stupor

The prognosis for stupor or coma depends on the cause, duration and degree of depression of consciousness. A Glasgow Coma Scale score of 3–5 after trauma indicates fatal brain damage, especially if the pupils are fixed or there are no oculovestibular reflexes. If, 3 days after cardiac arrest, pupillary reactions and motor responses to painful stimuli do not appear, the patient has virtually no chance of a favorable prognosis in neurological terms. When coma is associated with an overdose of barbiturates or reversible disorder exchange, even in cases where all stem reflexes have disappeared and there are no motor reactions, the possibility full recovery is saved.

In parallel with the diagnostic process, it is necessary to urgently stabilize the condition and maintain vital functions. In most cases of stupor and coma, hospitalization in the intensive care unit is required to provide mechanical ventilation and monitor the neurological status. Specific treatment depends on the cause of the condition.

In case of herniation, intravenous administration of 25-100 grams of mannitol, endotracheal intubation and mechanical ventilation are indicated, providing PC0 2 in arterial blood of 25-30 mm Hg. For herniation associated with a brain tumor, glucocorticoids are necessary (eg, dexamethasone 16 mg intravenously, then 4 mg orally or intravenously every 6 hours). Surgical decompression of mass lesions should be performed as soon as possible.

Patients in stupor and coma require careful and long-term care. The use of stimulant drugs and opiates should be avoided. Feeding begins with taking measures against possible aspiration (for example, raising the head of the bed); If necessary, a jejunostomy is applied. To prevent bedsores, it is necessary to pay attention from the very beginning of the disease to the integrity of the skin in places high blood pressure on the skin. To prevent drying of the conjunctiva, medications are used local action. To prevent contractures of the limbs, passive movements are performed within the limits of the joints.