By depth disturbances of consciousness The following states can be distinguished.
Stunned- disturbance of consciousness, characterized by the following signs: preservation of limited verbal contact, increased threshold for perception of external stimuli, decreased own activity. With deep stupor, drowsiness, disorientation, and execution of only simple commands occur. Stupefaction can be combined with hallucinations, delusions and symptoms of adrenergic activation (mydriasis, tachycardia, tremor, increased blood pressure, etc.), which amounts to clinical picture delirium. The most common causes of the latter are alcohol withdrawal, high body temperature, intoxication with psychostimulants - sydnofen, etc., including antidepressants with psychostimulant properties (melipramine, etc.) or sedatives(benzodiazepines, barbiturates, etc.).
Sopor- switching off consciousness, characterized by the preservation of coordinated defensive reactions, opening the eyes in response to painful, sound and other stimuli, episodic short-term minimal verbal contact - the patient, at the request of the doctor, opens his eyes, raises his hand, etc. The rest of the time the commands are not carried out. Reflexes are preserved.
Coma- complete shutdown of consciousness - divided into three degrees.
First degree coma(coma I, moderate coma): coordinated reactions to external stimuli are absent, uncoordinated reactions of the defensive type are preserved (for example, motor restlessness in response to painful stimulation, bending of the leg in response to a foot prick, etc.). The eyes do not open to painful stimuli. Pupillary reactions to light and corneal (corneal) reflexes are preserved. Swallowing is difficult. The cough reflex is relatively preserved. Deep reflexes are usually induced.
Second degree coma(coma II, deep coma) is characterized by the absence of any reactions to any external irritations, a decrease in muscle tone or hormetonia (a periodic short-term increase in muscle tone in all limbs or limbs of one side, leading to their tension). All reflexes (pupillary, corneal, deep, etc.) are sharply reduced or absent. Spontaneous breathing is preserved, although impaired (wave-like shortness of breath, tachypnea, Cheyne-Stokes breathing, etc.), as well as activity cardiovascular system(tachycardia, decreased blood pressure, etc.).
Third degree coma(coma III, extreme coma) is characterized by mydriasis, total areflexia, muscle hypotension, disturbance of vital functions (blood pressure is either critical or not determined; respiratory distress up to apnea).
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 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; laboratory tests and neuroimaging are needed to determine the cause. Treatment is immediate stabilization of the condition and targeted action on the cause. For prolonged stupor or coma, supportive care includes passive range of motion in all joints, enteral nutrition, and prevention of bedsores. The prognosis depends on the cause.
A state of wakefulness requires full functioning of the cerebral hemispheres and the mechanisms of the ascending activating reticular system (ARS) - a wide network of nuclear connections in the upper part of the pons, midbrain and posterior parts of the interstitial brain.
R40 Doubt, stupor and coma
Various organic and functional disorders in the functioning of the central nervous system lead to stupor or coma. Depression of consciousness occurs due to dysfunction of the VARS or both hemispheres of the brain; Damage to one hemisphere of the brain leads to the development of severe neurological deficits, but not coma. As the lesion worsens, stupor turns into coma, and coma turns into brain death. Other forms of impaired consciousness include delirium (usually characterized by agitation rather than lethargy), fainting and seizures; in the last two cases, the loss of consciousness is short-term.
Organic lesions lead to the development of stupor or coma through direct mechanical destruction of the VARS or indirectly through the mass effect (compression, displacement) and/or edema. A unilateral massive focal lesion of the hemisphere (for example, cerebral infarction in the territory of the left middle cerebral artery) does not interfere with consciousness unless the opposite hemisphere is already compromised or swollen. Infarctions of the upper part of the trunk, in accordance with the volume of the lesion, give varying degrees stupor or coma.
Common causes of stupor and coma
The pathogenesis of stupor and coma often includes hypoxia and cerebral ischemia. Mental disorders(eg, mutism) can mimic disturbances 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 mass formations or cerebral edema lead to increased intracranial pressure, which can cause brain tissue to protrude 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.
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 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. When rare breathing movements or low O2 saturation (according to pulse oximetry or gas composition criteria arterial blood) 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 of the temporal lobe is wedged through the cerebellar tentorium. The usual reason- ipsilateral space-occupying 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, purse or wallet contents may contain useful information(e.g. 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, psychiatric problems, and history of illness. It is advisable to look at medical documents.
Objective examination. Medical examination must be targeted and effective. Signs of traumatic brain injury include paraorbital hematomas (“raccoon eyes,” synonymous with “glasses symptom”), bruising behind the ears (Battle’s sign), hematotympanum, mobility of the upper jaw, naso- and/or otoliquorrhea. Bruises of the soft tissues of the head and small bullet entry holes are often unnoticeable. The fundus should be examined for disc swelling optic nerves, hemorrhages 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 a seizure. 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 motor 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 stimulation indicates focal damage to the cerebral hemispheres.
When stupor passes into 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 upper brainstem involvement. Flaccid paralysis without any movement is a manifestation of severe damage along the entire nerve axis, this worst case scenario motility disorders. Asterixis (fluttering tremor) and multifocal myoclonus accompany metabolic disorders, such as 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); the posterior cerebral artery (homonymous hemianopsia) and the opposite cerebral peduncle (ipsilateral hemiparesis). Then a picture of compression of the midbrain and trunk 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. Immobility of pupils - early manifestation 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, but 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 confirming the integrity of the eardrum, it is irrigated for 30 s through the external ear 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 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. Lesions of the pons or medulla oblongata usually lead to prolonged deep breaths (apneustic breathing), often leading to respiratory arrest.
Research. They begin with pulse oximetry, peripheral blood glucose testing, and cardiac monitoring. They take clinical analysis blood with determination of the 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 CT or MRI can reveal a subdural hematoma in the isodense phase, multiple metastases, thrombosis of the sagittal sinus, herpetic encephalitis and others possible reasons undetected by conventional CT scans. A chest x-ray is also indicated.
If an infectious disease is suspected, a lumbar puncture is performed to assess CSF pressure. In the CSF, cell types and their numbers, protein, glucose are determined, culture is done, Gram stain is performed, according to indications special tests(for example, for cryptococcal antigen, VDRL for syphilis, PCR to detect the virus herpes simplex). In unconscious patients, a CT scan is required before performing a lumbar puncture to exclude a space-occupying intracranial formation or occlusive hydrocephalus, since in such cases a sharp decrease in cerebrospinal fluid pressure during lumbar puncture is fraught with the risk of herniation with a fatal outcome.
If the diagnosis remains unclear, an EEG can help: in rare cases, sharp waves or peak-slow wave complexes indicate that the patient is in epistatus, although outwardly there are no seizures. But in most cases, in coma, the EEG shows nonspecific slow low-amplitude waves, common for metabolic encephalopathy.
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 for volumetric formations must be completed 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.
Hepatic coma is the most serious condition, diagnosed with hepatic encephalopathy(PE). PE refers to the entire spectrum neuropsychiatric disorders, developing with hepatic cell failure or portosystemic blood shunting.
There are many different diseases that lead to impaired consciousness. Before touching on the causes of disorders of consciousness, we should briefly dwell on the brain structures responsible for the state of clear consciousness.
A person is characterized by alternating periods of clear consciousness (wakefulness) and sleep. There is also an intermediate state - dormancy. The ascending reticular formation located in the upper parts of the brain stem (mainly in the midbrain) is responsible for controlling the cyclic sleep-wake rhythm - the formation of the brain that connects the cerebral hemispheres with the long brain.
Based on the depth of the disturbance of consciousness, coma, stupor and stupor are distinguished.
Coma- this is an extreme degree of impairment of consciousness:
Sopor(in foreign literature the term stupor is more often used) - a milder degree of impairment of consciousness compared to coma. For stupor:
Stun- a state of incomplete wakefulness, which is characterized by loss or disruption of varying degrees of severity of the coherence of thoughts and actions due to a gross disorder of attention, drowsiness.
Stunning should be distinguished from delirium (most common cause which is), in which stunning is combined with psychomotor agitation, delusions, hallucinations, activation of the sympathetic nervous system(increased blood pressure, sweating, trembling, tachycardia).
In coma and deep stupor, in addition to impaired consciousness, other symptoms are observed:
Disruption of the normal breathing rhythm; in severe cases, breathing becomes chaotic; Respiratory depression may even occur.
Impaired reaction of the pupils to light.
Disturbed eye movements (observed when lifting the eyelids): or floating movements, fixation of gaze.
A variety of pathological activities may be observed: epileptic seizures, muscle twitching (myoclonus), parakinesis ( involuntary movements, reminiscent of arbitrary character - according to the popular expression: “before death, it is robbed”).
There may be a sharp increase in muscle tone or, conversely, a decrease (“atonic coma”).
Opening your eyes
Spontaneous - 4
Opening for speech - 3
Opening to pain - 2
Missing - 1
Motor response
Follows verbal command - 6
Localizes pain - 5
Withdrawals a limb with flexion in response to pain - 4
Pathological flexion of all limbs from pain (decorticate rigidity) - 3
Pathological extension of all limbs from pain (decerebrate rigidity) - 2
No movement - 1
Preservation of verbal responses
Oriented and talking - 5
Confused speech - 4
Says incomprehensible words - 3
Inarticulate sounds - 2
No speech - 1
The total score is the sum of the scores of the three groups. 15 points - clear consciousness, 14-13 - mild stun, 12-11 - severe stun, 10-8 - stupor, 7-6 moderate coma, 5-4 - deep coma, 3 - death of the pulp, extreme coma.
It is important to establish not only the degree of impairment of consciousness, but also its cause. In addition to the medical history, which may remain unknown either in the absence of the patient’s relatives or due to their ignorance, additional research helps clarify the diagnosis.
Blood and urine tests - general analysis, analysis for the content of glucose in the blood, urine, the content of electrolytes, creatinine, calcium, phosphates in the blood, biochemical indicators of liver function, blood osmolality.
Screening of toxic substances (carried out in specialized toxicology laboratories).
Electrocardiography (ECG).
Chest X-ray
X-ray of the skull (if TBI is suspected)
CT and MRI of the brain, revealing the presence of stroke, consequences of TBI (brain contusion, subdural hematoma, epidural hematoma, confusion of brain structures), encephalitis.
Lumbar puncture followed by examination of the cerebrospinal fluid if meningitis or subarachnoid hemorrhage is suspected.
Electroencephalography (EEG), which makes it possible to distinguish coma from mental “reactivity (with hysteria, catatonia).
Impaired consciousness (coma, stupor) can be caused by various causes: neurological, metabolic (diabetes mellitus, hypothyroidism, adrenal insufficiency, uremia, hyponatremia, liver failure), poisoning, hypoxia (asphyxia, severe heart failure), sunstroke and heat stroke.
Neurological causes of impaired consciousness:
Diabetic coma
Hypoglycemic and diabetic (ketoacidotic) comas occur with diabetes mellitus. The first one occupies 3rd place, and the second coma takes 5th place in the structure of coma. Hypoglycemic coma most often occurs in type 1 diabetes on insulin therapy (and in those patients with type 2 diabetes receiving insulin) with fasting blood glucose at a level of 3 mmol/l.
Provoking factors:
Taking medications can also cause a hypoglycemic state. These include: adrenergic blockers, sulfonamides, salicylates, anabolic hormones, tetracycline, lithium carbonate, monoamine oxidase inhibitors, calcium-containing drugs.
Symptoms develop quickly (usually within minutes, less often within hours). The first symptoms include profuse sweating, pale skin, a feeling of extreme hunger, trembling hands, weakness, and sometimes dizziness. They appear quite quickly inappropriate behavior, psychomotor agitation (sometimes with aggression), impaired coordination of movements, further confusion, development of coma, sometimes convulsions.
At the first signs of hypoglycemia, the patient should eat a lump of sugar (a tablespoon of granulated sugar) or candy and drink a cup of very sweet tea. Comatose states are treated with intravenous jet injection 60 ml of 40% glucose no more than 10 ml per minute. Then 5% glucose is administered intravenously (up to 1.5 liters per day) under blood glucose monitoring.
Diabetic (most often ketoacidotic) coma when taking insufficient doses of glucose-lowering drugs or skipping insulin due to unauthorized withdrawal of medications and non-compliance with the diet. Provoking factors may include physical activity, alcohol abuse, taking certain medications (steroids, oral contraceptives, calcitonin, saluretics, adrenoblockers, diphenin, lithium carbonate, diacarb). Diabetic hyperglycemic coma develops more slowly than hypoglycemic coma.
With moderate ketoacidosis, asthenia and thirst increase; dyspepsia, weight loss, and the smell of acetone in the exhaled air. Subsequently, a precomatous state occurs, characterized by stunning, an increase in dyspeptic symptoms (anorexia, vomiting, abdominal pain), shortness of breath, decreased muscle tone and eye turgor, and dry skin. On examination - tongue with brown coating, decreased pressure, temperature, absence of tendon reflexes.
Data helps diagnostics laboratory research: hyperglycemia and glycosuria, increased ketone bodies blood, acidosis.
In the precoma stage, the glucose level reaches 28 mmol/l, in the coma stage - 30 mmol/l or more.
Necessary emergency measures for diabetic coma include the elimination of dehydration (dehydration), hypovolemia (reduction in circulating blood volume) and the prevention of possible hemorrhagic complications and the normalization of glucose and blood levels.
Intensive infusion therapy is carried out - saline solution 1 l/hour (up to 5-7 l) under the control of blood pressure, pulse rate, diuresis. If necessary, oxygen therapy and warming are carried out. To prevent thrombosis, 500 units of heparin (preferably low molecular weight heparin) is administered intravenously. Insulin therapy is carried out with blood glucose control.
Coma due to sunstroke
Often they are faced with a comatose state that arose in earlier healthy people as a result of sun (or heat) stroke. Sunstroke can occur during heavy physical work under the scorching sun with your head uncovered, or during prolonged sunbathing on the beach. A risk factor is excessive alcohol intake. Symptoms can occur not only directly during exposure to the sun, but also several hours after exposure. In relatively mild cases (without loss of consciousness) and in a precomatous state, redness of the facial skin, increased sweating, increased body temperature (in severe cases up to 41 ° C), tachycardia, and shortness of breath occur. Subsequently, tachycardia gives way to bradycardia, breathing becomes arrhythmic, convulsions, delirium and impaired consciousness may occur.
Immediate measures for sunstroke include:
Development heatstroke associated with general overheating of the body, which appears when staying in a hot and humid room, during intense work in stuffy conditions, during long hikes (military, tourist) in the heat.
Apaleic syndrome
What differs from coma is such a special state of impaired consciousness as apalic syndrome (synonyms: vegetative state, chronic persistent vegetative state, “waking” coma). The apalic state is a total disorder of the function of the cerebral cortex with preserved functioning of the brainstem (including the midbrain), which is characterized by:
Some patients may then have a partial (and in the case of apallic syndrome of traumatic origin, sometimes quite good) restoration of consciousness. During the transitional stage, gaze fixation and monitoring of others, primitive emotional reactions and purposeful movements occur.
Isolation syndrome
“Isolation” syndrome (synonyms: “locked up” syndrome) is sometimes perceived by the patient’s relatives as a gross violation of consciousness and intellect. This syndrome occurs with extensive infarctions of the base of the brain stem. It is characterized by:
Impaired consciousness in the form of coma and stupor should be differentiated from some mental conditions, externally reminiscent of a coma: with conversion (hysterical) and catatonic (in schizophrenia) stupor. At psychogenic disorder consciousness there are no involuntary slow movements of the eyeballs, the eyes are often open, there are no changes in muscle tone and changes in the EEG.
A general practitioner who finds a patient in a coma must:
The following types of consciousness are distinguished: clear, darkened, stupor, stupor, coma, delirium, hallucinations.
In therapeutic clinics, patients often experience clear consciousness. The patient is completely oriented in the environment and clearly answers questions.
Darkened (unclear) consciousness manifests itself in the patient’s indifferent, indifferent attitude towards his condition; He answers questions correctly, but late.
At stupor (stunning) the patient is poorly oriented in his surroundings, sluggishly, slowly answers questions, sometimes not to the point, and immediately begins to doze off, fall asleep: falls into a state of numbness.
Sopor- deep confusion of consciousness (dullness). In this case, the patient is in a state of “hibernation”. Only a loud shout, painful effects (injections, pinches, etc.) can bring him out of this state, but for a very short time; soon he “falls asleep” again.
Coma (deep hibernation)- complete loss of consciousness. The patient does not respond to shouting, painful stimulation or inhibition. In coma there are no reflexes. Coma indicates significant severity of the disease. It develops, for example, in severe diabetes mellitus, in renal and liver failure, in alcohol poisoning, etc.
In diabetes mellitus, in the case of metabolic disorders, mainly carbohydrates and fats, due to a lack of insulin in the body, a hyperglycemic (diabetic) coma occurs. It develops slowly. It is usually preceded by malaise, loss of appetite, headache, nausea, and vomiting. Further, muscle tone decreases, dry skin develops, their turgor decreases, the face becomes pink, the eyeballs become soft, tendon reflexes partially or completely disappear, it is noted noisy breathing(Kussmaul breathing), a characteristic smell of acetone (fruity) is felt in the exhaled air, the pulse slows down, and blood pressure drops.
With adrenal insufficiency, as well as with an overdose of insulin and for a number of other reasons, a hypoglycemic coma occurs as a result of a sharp decrease in blood sugar levels. It starts quickly. Sometimes it is preceded by a feeling of hunger, weakness, and sweating. Skin with this disease they become pale, moist, there is muscle rigidity, body tremors, convulsive twitching, and the pupils dilate.
Due to severe diffuse liver damage as a result of complete failure of its function, hepatic coma develops. In this case, severe weakness and drowsiness appear, alternating with periods of excitement. The skin becomes jaundiced and scratches are noted, “ spider veins", hemorrhages. Muscle twitching is also observed, and a sweetish (liver) odor is felt from the mouth. Breathing is noisy (Kussmaul), pupils are motionless, dilated, blood pressure is reduced, urine is dark yellow, feces are discolored.
In patients with chronic kidney disease, accompanied by severe functional insufficiency, uremic coma occurs. Its initial signs are general weakness, headaches, nausea, vomiting (especially in the morning, before meals), general anxiety, and insomnia. Then comes loss of consciousness. The skin becomes pale yellowish, dry, with traces of scratching and hemorrhages. The mucous membranes of the oral cavity also become pale and dry, breathing is like Cheyne-Stokes, less often - Kussmaul, muscle tone increases, an ammonia smell is felt from the mouth (smell of urine).
Patients with alcoholic coma are characterized by a cyanotic face, dilated pupils, hyperemic sclera of the eyes, superficial, hoarse breathing, smell of alcohol on the breath, Cheyne-Stokes type breathing, low rapid pulse, low blood pressure.
In the case of an anemic coma, there is a “dead” pallor, clammy sweat, muffled heart sounds, threadlike pulse, decreased blood pressure blood.
In some diseases (especially infectious diseases with severe intoxication), poisoning with alcohol, sleeping pills and other drugs, patients experience excitation of the central nervous system, i.e., a state opposite to those described above. Such patients are restless and agitated.
In addition, there may be a disturbance in consciousness leading to delirium. Rave- this is an objectively false, absolutely uncorrectable judgment. With violent delirium, patients are extremely excited, jump out of bed, run somewhere, and experience hallucinations.
Hallucinations There are auditory, visual, tactile (the feeling of worms, insects, microbes crawling over the body, etc.).
During auditory hallucinations the patient talks to himself or to an imaginary interlocutor.
With visual hallucinations, patients see something that is not really there, for example, mice that rush at them, devils, etc. This often happens with alcoholism.
Quiet delirium is also characterized by unrealistic ideas, hallucinations, only patients behave outwardly calmly, often in a state of stupor or stupor, muttering something, uttering incomprehensible and incoherent phrases.
Clear consciousness during wakefulness is one of the indicators of normal brain functioning. 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 with a variety of injuries nerve 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:
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.
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.
Upon examination, attention is drawn to a general decrease in muscle tone and suppression of deep reflexes. Pyramidal signs are often found due to a decrease in the influence of 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, indicating local damage to certain structures and areas in the brain. If the stupor is caused by intracranial hemorrhage or meningoencephalitis, a stiff neck and other meningeal symptoms will be found. 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.
The doctor conducts an objective examination, determines the depth of the disturbance of consciousness and identifies possible causes of 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. To do this, medical documentation is studied and accompanying persons and relatives are interviewed. The patient’s clothing and personal belongings are also examined, which sometimes makes it possible to detect packaging of medications used, and individual cards with information about existing diseases.
If stupor is detected, it is necessary to quickly conduct a series of screening tests:
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 a toxicological study and urine to screen for major narcotic substances. In some cases, the neurologist decides to urgently perform an MRI (CT) of the brain.
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.
Ischemia and swelling of brain tissue, which can occur under a variety of conditions, play an important role in the development of stupor. Early treatment will help prevent the brain from herniating into the natural openings of the skull and preserve the viability of neurons. Nerve cells are especially vulnerable in the so-called penumbra zone (or ischemic penumbra) - the area immediately 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 conductive therapeutic measures. 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.
