Assessment of the severity of the condition of patients in the provision of emergency therapeutic and surgical medical care at the prehospital stage.

Vestibular syndrome — absent; systemic dizziness; nausea, vomiting; nystagmus (horizontal, vertical, rotatory, large-small-sweeping), ataxia, decreased muscle tone.

IX (n. glossopharyngeus), X (n. vagus). Swallowing — preserved, a dysphagia. Phonation is preserved, a dysphonia. Articulation is preserved, but dysarthria.

Bulbar syndrome — paresis of the soft palate (right, left), decreased pharyngeal reflex (right, left). Pseudobulbar syndrome — paresis of the soft palate on both sides (yes, no), increased pharyngeal reflexes (yes, no), oral automatism reflexes (dis- tance-oral, palmomental, naso-labial, proboscis), forced laughter or crying. Taste disturbance on the back 1/3 of the tongue (right, left). Dry mouth (yes, no).

XI (n. accessorius). Strength of the trapezius muscle, strength of the digging muscle (unchanged, reduced, right, left).

XII (n. hypoglossus). Tongue in the midline, tongue deviation to the right, left; hypotrophy of the tongue, fibrillation (yes, no).

Propulsion system.

The range of active movements in the limbs is full, limited (Barre test upper and lower; test with counter-hold, pronation phenomenon, Bogolepov’s symptom of rotated foot).

Hemiparesis, monoparesis, tetraparesis, paraparesis with a decrease in muscle strength to points in the arm and points in the leg (right, left).

Muscle tone — unchanged, increased: spastic, plastic; reduced (in which muscle groups).

Tendon reflexes — unchanged, decreased, increased (from the biceps tendon S5–6, triceps S7–8, knee L2–4, Achilles tendon S1–2) on the right, on the left.

Clonus — chin, hand, gluteal muscles, patella, foot, (right, left).

Periosteal reflexes — carpo-radial S5–8 (unchanged, decreased, increased, right, left).

Superficial reflexes — abdominal, cremasteric, plantar (not changed, reduced). Pathological reflexes — extensor (Babinsky, Oppenheim, Gordon, Schaeffer,

etc.), flexion (Jacobson — Lask, Rossolimo, Bekhterev I and II, Zhukovsky, etc.). Protective reflexes — shortening, lengthening (the level from which the reflex

is triggered).

Pathological synkinesis — global, coordination, imitation. Fasciculations, fibrillations (in which muscle groups). Hypothorophy, hypertrophy (in which muscle groups). Tremor (at rest, during movement, frequency).

Hyperkinesis — chorea, athetosis, tremor, myoclonus, tics (simple/complex; motor, vocal), dystonia (blepharospasm, oromandibular, laryngeal, spastic torticollis, writer's cramp, foot dystonia, torsion dystonia).

31

Coordination system.

Static ataxia — Romberg’s position, Babinsky synergy test.

Dynamic ataxia — finger-nose, calcaneal, index test, Stewart — Holmes symptom, Schilder test, diadochokinesis test, dysmetria test (negative, positive).

Scanned speech. Nystagmus. Microor megalography. Gait — not changed, ataxic, stepping, stamping, “star test”.

Sensitivity system.

Types of sensitivity:

−superficial sensitivity: pain, temperature, tactile;

−deep sensitivity: joint-muscular feeling, vibration, kinesthetic, feeling of pressure and weight;

−complex types of sensitivity: discriminative sensitivity, localization sense, two-dimensional spatial sense.

Nature of sensitivity disorders:

1) anesthesia — complete loss of one or another type of sensitivity; 2) hepaesthesia — reduction of one or another type of sensitivity; 3) hyperesthesia — an increase in one or another type of sensitivity; 4) hyperpathy — perversion of sensitivity with unpleasant pain;

5) dysesthesia — perversion of sensitivity (cold seems hot; touch feels like

pain);

6) paresthesia — a feeling of coldness, numbness, tingling, crawling “goose bumps” that occurs without disturbance of external irritations;

7) pains — aching, dull, stabbing, throbbing, cutting, etc.

Types of distribution of sensitivity disorders:

−neural — indicate the nerve;

−polyneuritic — “socks” and/or “gloves”;

−segmental (root) — indicate the segment, the presence of pain, tension symptoms;

−segmental dissociated — indicate the segment;

−conductive spinal — mono, hemi, para, tetra type; level of damage by segment;

−conductive cerebral — mono, hemi type, tetra type.

Aphasia's higher mental functions:

1)efferent motor (Broca) — complete absence of expressive speech/embolism/ perseveration;

2)afferent motor — violation of the pronunciation of closely articulated sounds (table — elephant — moan);

32

3)sensory (Wernicke) — violation of expressive speech and impressive speech (literal and verbal paraphasias “word salad”);

4)optical-mnestic — disruption of connections between the visual image of an object and its name;

5)acoustic-mnestic — decreased auditory-speech memory, inability to remember a series of 3–5–10 words, impoverished speech;

6)semantic — impaired understanding of complex logical and grammatical constructions of temporal and comparative relations;

7)dynamic — there is no detailed speech, no elementary phrases;

8)total; sensorimotor.

Apraxia:

–kinetic — “fist-edge-palm” test;

–kinesthetic — “transferred poses” test.

Agnosia: visual (object, facial, letter), auditory, olfactory, gustatory. Amnesia: impaired short-term memory, impaired long-term memory.

Vegetative system.

Dermographism — red, white, diffuse, sublime.

Bernard — Horner symptom (sympathetic denervation of the eye) — narrowing of the palpebral fissure, miosis, hypohidrosis of 1/2 of the face (right, left).

Clinostatic test — heart rate, blood pressure while standing; heart rate, blood pressure while lying down.

Orthostatic test — heart rate, blood pressure lying down, heart rate, blood pressure standing,

Plan for a neurological examination of a patient in a comatose state. Primary actions when managing a patient with a coma: assessment of the state of vital functions (function of external respiration and cardiovascular system), elimination of hypoxia (restoration of the patency of the upper respiratory tract, placement of an airway or tracheal intubation, oxygen inhalation or artificial ventilation), normalization of hemodynamics. Then the naked patient is examined (consistently covering the head, eyes, ears, nose and throat, as well as the lungs, heart, abdomen, limbs and skin; including thermometry):

1.Assess the degree of respiratory impairment (normal, tachypnea, bradypnea, respiration: Grocca, Cheyne — Stokes, Biot, Kussmaul), blood pressure + heart rate

(Cushing’s phenomenon).

2.Meningeal symptoms, with an assessment of indirect signs of paresis (see above): stiffness of the neck muscles is not examined if there is a suspicion that the patient has an injury to the cervical spine.

3.Pupil diameter and their reactivity, ciliospinal reflex.

33

4.Position of the eyeballs (squint: convergent, divergent, including vertically, horizontally), adversion (or paresis) of gaze.

5.Corneal reflex.

6.Movement of the eyeballs: oculocephalic reflex, nystagmus (spontaneous);

7.Posture (decortiation, decerebration), other position of the limbs.

8.Movement of limbs: spontaneous, stimulated.

9.Babinsky reflex (cutaneous (abdominal, plantar) and tendon-periosteal re-

flexes).

10.presence or absence of myoclonus.

Eye movements in a comatose patient. In a comatose state, gaze fixation is absent, so any tracking movements and, in most cases, also saccades and nystagmus are absent. Deviation of the eyeballs to the side indicates a pathological focus in the ipsilateral hemisphere or in the contralateral parts of the pons. Only during epileptic seizures can transient nystagmus and tonic rotation of the eyes in the direction opposite to the focus be observed. Slow floating eye movements during shallow coma indicate the preservation of the functions of the brainstem. Other spontaneous eye movements, such as bobbing or ping-pong, are always a sign of brain damage

Ocular bobbing (from the English bobbing — blow or squat) is a quick abduction of the eyeballs down, accompanied by a longer return to the starting position. Reflex eye movements are not caused in this condition.

Bobbing usually indicates severe damage to the pons. Reverse bobbing (or ocular dipping — from the English dipping — immersion) is an illogical movement in the opposite direction.

Ping-pong (periodic alternating deviation of gaze in the horizontal plane) — the eyeballs change direction of movement every few seconds, which indicates diffuse bilateral damage to the cortex.

Eye movement study. The only way to assess oculomotor functions in a patient in a coma is to study the vestibulo-ocular and oculocephalic (oculocephalic) reflexes. Based on the study of these two reflexes, we can draw a conclusion about the state of the midbrain, pons, and medulla oblongata. Before examining the oculocephalic reflex, you need to make sure that there is no trauma with a fracture or subluxation of the cervical vertebrae.

Oculocephalic reflex (OCR). The head of a patient in a coma, lying on his back, is covered with both hands and rotated to the sides (in the horizontal plane), while using the thumbs to lift the eyelids to observe eye movements.

The normal response is that the eyeballs initially turn slightly passively along with the head, but then move in the opposite direction (positive ORP = doll eye phenomenon).

34

The pathological reaction is the loss of the oculocephalic reflex: the eyeballs remain motionless relative to the orbit and passively follow the turn of the head (negative OCR). Then the patient's head is tilted forward and returned to its original position (moving in the sagittal plane). When the function of the brain stem is preserved, the eyeballs in this case also move in the direction opposite to the direction of head movement (the phenomenon of a doll's eyes). When the midbrain is damaged, the OCR study causes normal eye movements in the horizontal plane, while they cannot be caused in the vertical plane; sometimes only downward eye movements are possible. When the pons is affected, the ORC turns out to be negative or pathological in both planes.

Violation of the concordance of eye movements during OCR indicates internuclear ophthalmoplegia or damage to subnuclear structures, for example, the abducens nerve.

Impaired consciousness is a manifestation of dysfunction of the hemispheres, the upper parts of the brain stem, or both areas at the same time. Metabolic or infectious diseases can have a depressing effect on hemispheric and brainstem function through abnormal levels of blood components or direct toxic effects. Impaired consciousness can also be observed when there is a violation of cerebral circulation or when there is a change in the bioelectrical activity of the brain (epilepsy). Inadequate cerebral blood flow and chemical imbalances in the blood can also cause abnormal electrical activity in the brain. Concussion and psychological disorders cause impairment of consciousness without visible structural changes in the brain.

Impairments of consciousness can be short-term or profound. Brief loss of consciousness occurs with syncope. With seizures, loss of consciousness may last longer, and with a concussion it can last up to 24 hours. Long-term impairment of consciousness is observed with intracranial pathology or metabolic disorders.

Acute and subacute disturbances of consciousness:

1.Stunning is characterized by decreased levels of wakefulness and is usually accompanied by drowsiness.

2.Obnubilation (“clouding of consciousness”) — a mild degree of deafness, slowed reactions and a “foggy” perception of reality.

3.Moderate stun — partial disorientation, moderate drowsiness, execution of all commands.

4.Deep stupor — disorientation, deep drowsiness, execution of only simple commands.

5.Sopor — severe depression of consciousness and pathological sleep, the patient does not follow instructions, it is possible to receive a reaction of opening the eyes with strong stimulation (to pain or sound). With stupor, deep depression of con-

35

sciousness occurs, during which verbal communication with the patient is impossible. Coordinated defensive reactions are preserved — opening the eyes to painful, sound and other irritations. The patient is drowsy and lies with his eyes closed. It is possible to remove it from a state of drowsiness with the help of various stimulations.

6. Stupor is a concept in English literature similar to sopor. In addition, the term is used in psychiatry to denote a state of immobility with mutism and weakened reactions to irritations (including pain).

7. Doubtfulness action editredlink — a mild disturbance of consciousness in which the patient often falls asleep and is inhibited, but adequate reactions can be caused by short-term external stimuli.

Coma is characterized by lack of response and inability to awaken:

a)coma I: consciousness is lost, the patient does not open his eyes, in response to painful stimuli he responds with uncoordinated defensive movements without localizing the pain;

b)coma II, deep: consciousness is lost, there is no reaction to pain, there are no spontaneous movements;

c)coma III, extreme: loss of consciousness, bilateral mydriasis, areflexia, muscle atony, catastrophic state of vital functions.

Chronic disturbances of consciousness:

1. Akinetic mutism: the patient is clearly conscious, lies motionless with open eyes, does not speak or answer questions. All motor functions are suppressed (except for movements fixing the eyeballs).

2. Apallic syndrome (waking coma) — a condition in which consciousness remains intact, the patient’s eyes are open, he rotates them in the sockets, but does not fix his gaze, speech and emotional reactions are absent, verbal commands are not perceived by the patient and contact with him is impossible, but the patient doesn't lie still.

3. “Locked-in person” syndrome (isolation syndrome): reflects the patient’s condition in which consciousness is preserved, but contact with it is impossible due to bilateral paralysis of all parts of the body, with the exception of eye movements, with which the patient encodes his response. Various diseases can lead to this condition, which results from bilateral damage to the corticospinal tract between the midbrain and the pons or from massive damage to the lower motor neurons (anterior horns of the spinal cord). This condition is also sometimes called “pseudocoma”.

4. A vegetative state is defined as the inability to engage in spontaneous mental activity due to extensive damage or dysfunction of the cerebral hemispheres, with preservation of the diencephalic region and brain stem, preserving autonomic and motor reflexes, as well as the sleep-wake cycle.

36

5. Brain death is a state of complete loss of consciousness and all brain functions.

Syndromes of confusion in psychiatry.

Confusion of consciousness, disorders of reflection of surrounding reality:

–amentive syndrome;

–aura of consciousness;

–delirious syndrome;

–oneiric syndrome;

–twilight stupefaction.

The most common causes of impaired consciousness.

The effect of lateral displacement of the midline structures of the brain on the level of loss of consciousness:

1)0–3 mm — full consciousness (alert);

2)3–4 mm — drowsy;

3)6–8.5 mm — stuporous;

4)8–13 mm — coma (comatose).

Pathological conditions leading to displacement of the midline structures of the brain and impairment of consciousness:

–supratentorial volumetric processes;

–epidural hematoma;

–subdural hematoma;

–cerebral infarction or intracerebral hemorrhage;

–a brain tumor;

–brain abscess;

–subtentorial damage;

–brainstem infarction;

–brain stem tumor;

–hemorrhage in the brain stem;

–hemorrhage into the cerebellum;

–brain stem injury;

–diffuse and metabolic brain disorders;

–trauma (concussion, brain injury or bruises);

–anoxia or ischemia (syncope, cardiac arrhythmia, pulmonary infarction, shock, pulmonary failure, carbon monoxide poisoning, vascular collagen disease);

–epilepsy;

–condition after an epileptic seizure;

–infections (meningitis, encephalitis);

–subarachnoid bleeding;

37

–exogenous toxins (alcohol, barbiturates, glutethimide, morphine, heroin, methyl alcohol, hypothermia);

–endogenous toxins and metabolic disorders (uremia, hepatic coma, diabetic acidosis, hypoglycemia, hyponatremia);

–psychomotor status epilepticus.

Brain death. The possibility of carrying out artificial ventilation of the lungs to maintain the activity of the lungs and heart for a long time is largely based on the diagnosis of human death with the determination of the complete absence of brain activity and brain stem structures. To make a diagnosis of brain death, the doctor must base it on knowledge of the structural or metabolic causes of brain death, while excluding the possibility of the influence of anesthetic or paralyzing drugs, especially those taken by the patient independently. In this case, you should pay attention to reliable signs of clinical death and biological death.

Signs of clinical death include coma, apnea, absence of pulse in the main arteries. This triad concerns the early period of death (when several minutes have passed since asystole), and does not apply to those cases where there are already clear signs of biological death. The shorter the period between the declaration of clinical death and the start of resuscitation measures, the greater the patient’s chances of life, therefore diagnosis and treatment are carried out in parallel.

Coma is diagnosed based on lack of consciousness and pupillary reflex.

Apnea is recorded visually by the absence of respiratory movements of the

chest.

Absence of pulses in the great vessels may occur with asystole, ventricular fibrillation, or electromechanical dissociation.

Additional signs of clinical death are:

–wide pupils;

–areflexia (no corneal reflex and pupillary reaction to light);

–paleness, cyanosis of the skin.

Biological death (true death) is the irreversible cessation of physiological processes in cells and tissues. Over time, medicine’s ability to resuscitate clinically dead patients changes. Therefore, the signs of biological death are clarified at each stage of the development of medicine.

Early signs of biological death include the appearance of Beloglazov's symptom (cat's eye): with lateral compression of the eyeball, the pupil transforms into a vertical fusiform slit, similar to a cat's pupil (10–15 minutes).

Late signs of biological death include:

–drying of the skin and mucous membranes;

–cooling (decrease in body temperature after death);

38

–cadaveric spots in sloping areas;

–rigor mortis;

–autolysis (decomposition).

2.6.EXAMINATION OF THE STATE OF THE SENSES —

VISION, TASTE, HEARING

Vision examination. There are two types of visual perception — central and peripheral. Central vision is provided by the central part of the retina, where the nerve cells, cones, which are responsible for clarity of vision and color perception, are located. Peripheral vision is responsible for the nerve cells of the retina, the rods, which allow a person to better navigate in space and see in low light.

To separate peripheral vision from central vision, you should find some object in the room and fix your gaze on it. However, in addition to this object, some other objects that are nearby also come into view. These objects are not seen clearly because the gaze is fixed on another object. Peripheral vision is necessary for perceiving objects not located in the field of central vision. The boundaries of peripheral vision are normally considered to be a field of 120°.

When some areas of the retina weaken, the field of vision narrows, and in some cases, peripheral vision may disappear altogether. This pathology is called tunnel vision.

Causes of peripheral vision impairment may include:

1.Glaucoma. This disease appears due to increased intraocular pressure, leading to deterioration of the visual field. At the initial stage, peripheral vision narrows, and as the disease progresses, it is completely impaired, then central vision deteriorates, and as a result, complete blindness.

2.Damage to the retina, in which the nerve cells of the eye are damaged, resulting in a narrowing of the peripheral field of vision. For example, detachment, dystrophy, dissection, retinal degeneration.

3.Poor vascular circulation of the optic nerve, as well as various types of eye

tumors.

4.Impaired cerebral circulation, increased cerebrospinal fluid (intracerebral fluid), stroke, traumatic brain injury.

Intracranial pressure affects the condition of the fundus of the eye, the nerve cells of the retina are affected, and peripheral vision suffers from this.

Study of taste sensations. The sense of taste is one of the five basic human senses. On the one hand, determining the taste of food is necessary to increase appe-

39

tite and reflexively trigger the work of the glands of the gastrointestinal tract, which promotes normal digestion; on the other hand, the sense of taste helps to distinguish inedible or spoiled food products, protecting against poisoning. Taste is perceived through taste buds. Most of them are located on the surface of the tongue in structures called taste buds. We feel salty, sweet, bitter, sour tastes. Impulses from the taste buds are transmitted along nerve fibers to the cells of the subcortical centers and the cerebral cortex, where a particular sense of taste is formed. The system of taste receptors, nerves and areas of the brain in which information received from the receptors is processed is called a taste analyzer.

Types of taste disorders.

The first type is an exacerbation of the sense of taste (hypergeusia), which is characterized by the occurrence of a taste sensation of high intensity, disproportionate to the usual level.

The second type is a decrease in the severity of taste (hypogeusia). This condition is characterized by the appearance of a taste sensation of low intensity, up to a complete absence of taste, the so-called ageusia.

The third type is a perversion of taste, or dysgeusia. In this case, for example, irritation of the receptors that are normally responsible for the development of the sense of sweetness leads to another feeling — spicy, bitter, salty.

Quite often, the cause of taste disturbance lies in a change in the mucous membrane of the mouth and tongue, which leads to direct damage to the taste buds or the inability to deliver the chemical to them. Most often, changes in the mucous membrane are caused by infectious processes and the consequences of a deficiency in the body of certain nutrients.

For taste buds to function normally, chemical irritants must be dissolved in saliva. This is associated with taste disorders due to disruption of secretion production by the salivary glands. The sense of taste is closely related to the sense of smell (smell). That is why in acute and chronic rhinitis (inflammation of the mucous membrane of the nasal cavity) there is a disturbance in the perception of taste. Taste sensations change or even disappear completely when the nerves and centers of the brain related to the taste analyzer are damaged. It is worth saying that changes in taste perception can be observed in mental disorders.

Pregnant women complain of taste disturbances, which is associated with a specific restructuring of metabolism during this period. Smoking also causes dullness of taste. Changes in taste sensations are recorded after taking certain medications, as well as when consuming certain foods that have an extremely intense taste (for example, lemon).

40