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Brainstem syndrome includes three levels of damage - mesencephalic, pontine and bulbar, the anatomical and physiological features of which determine the clinical manifestations of their damage.
Mesencephalic or midbrain level of brain stem damage characterized by a disorder of pupillary reactions, paralysis and paresis of individual muscles of the eye, a violation of the conjugate upward movements of the eyeballs, a violation of muscle tone, and the appearance of converging, rotatory and vertical nystagmus. In case of TBI, total damage to mesencephalic structures is not observed, because these injuries are incompatible with the life of the victim. Typically, partial damage occurs, among which quadrigeminal, tegmental, peduncular syndromes and alternating syndrome involving half of the trunk are distinguished.
Quadrigeminal syndrome includes disturbances in upward gaze, disturbances in convergence, disturbances in pupillary reactions, various forms of nystagmus (vertical, horizontal, diagonal, converging, rotatory).
Tegmental or tegmental syndrome includes dysfunction of the oculomotor nerves, conduction disturbances of sensitivity, muscle tone, and coordination disorders. With increasing damage to the tegmental parts of the brain, decerebrate rigidity, hyperthermia, and respiratory rhythm disturbances develop.
Peduncular syndrome includes movement disorders in the contralateral limbs (from mono- to hemiparesis).
Pontine level lesions capture nucleiV,VI,VII,VIII pairs of cranial nerves, i.e. a group of nerves of the cerebellopontine angle, which determines the nature of clinical manifestations. Hearing impairment, decreased sensitivity in the trigeminal nerve area, dysfunction of the facial and abducens nerves are often combined with cerebellar symptoms.
Bulbar level characterized by damage to the medulla oblongata with the appearance of dysphagia, aphonia, anarthria with swallowing and articulation disorders. They are combined with disturbances in cardiac and respiratory functions, decreased blood pressure, and the appearance of fascicular and fibrillar twitching of the tongue muscles. Involvement of the medulla oblongata in the process is characterized by the appearance of homolateral pyramidal insufficiency, sensitivity disorders, or the development of alternating syndromes.
It is characteristic that in TBI, brain stem symptoms can be not only the result of primary traumatic damage to these formations, but also be a consequence of secondary damage as a result of dislocations and herniation of stem structures.
When describing the semiotics of brain damage in TBI, it is especially necessary to note the uniqueness of the manifestations"disconnection" syndromeat DAP. They are most clearly detected during the transition of patients from coma to a transient or vegetative state. In the absence of any signs of functioning of the cerebral cortex, subcortical, brainstem and spinal mechanisms are clearly manifested. A variety of oculomotor, pupillary, oral, bulbar, pyramidal and extrapyramidal syndromes are found. They appear spontaneously or in response to any irritation with a wide variety of positional-tonic and defensive reactions and postures, facial synkinesis.
Separately, it is necessary to dwell on herniation syndromes, which often develop in victims with severe traumatic brain injury. There are transtentorial, temporotentorial, cerebellar-tentorial herniation, as well as herniation under the falciform process and herniation of the cerebellar tonsils.
Tentorial herniation occurs as a result of diffuse cerebral edema or with massive central, bilateral space-occupying processes (hematomas, bruises). In this case, the brain stem shifts caudally and symptoms develop, characterized by impaired consciousness, the development of Cheyne-Stokes type breathing, constriction of the pupils and the disappearance of their reaction to light, the appearance of decortication and even decerebrate posture of the patient.
Temporotentorial herniation occurs as a result of lateral displacement of the brain due to the mass effect in hemispheric contusions, unilateral supratentorial hematomas. In this case, a herniated herniation of the hook of the hippocampal gyrus occurs into the gap between the edge of the tentorium and the brain stem. Clinical manifestations are characterized by progressive depression of consciousness, pupil dilation and dysfunction of the oculomotor nerve on the affected side, dysfunction of the midbrain, the appearance of decerebrate rigidity and hyperventilation.
Cerebellar-tentorial herniation occurs when pressure in the subtentorial space increases (hematoma of the cerebellum and posterior cranial fossa). The brain stem shifts in the rostral direction, which is accompanied by an acute disturbance of consciousness and the development of quadrigeminal syndrome.
Herniation of the cerebellar tonsils also occurs with space-occupying processes in the posterior cranial fossa, which leads to lowering and herniation of the cerebellar tonsils into the foramen magnum with the development of medulla oblongata syndrome and frequent breathing disorders.
Herniation under the falciform process just like temporotentorial herniation occurs during lateral space-occupying processes. The cingulate gyrus hernially protrudes under the falx process, and the blood flow through the anterior cerebral artery is disrupted; occlusion of the foramen of Monroe may occur with difficulty in the outflow of cerebrospinal fluid from the lateral ventricle.
The described signs of brain damage apply to all age groups of victims, but it is also very obvious that children in this context represent a special group of victims and the younger the patient’s age, the greater the differences. Studying the circumstances of the injury, premorbid history, the degree and duration of impairment of consciousness, speech, mental functions and much more is often not possible in children. The preservation of some pathological reflexes in children is often just an age-related norm, and the formation of psychomotor lag and pronounced astheno-vegetative or vegetative-visceral syndrome in the late post-traumatic period in children is a well-known fact and requires its own special approach to both diagnostic constructs and treatment tactics in children with TBI.
Brainstem syndromes include symptoms of damage to the midbrain, pons, medulla oblongata,
Midbrain syndromes. Symptoms associated with damage to the oculomotor nerve(external, internal, total ophthalmoplegia), trochlear nerve (convergent strabismus, double vision when looking down). Quadrigeminal syndrome: increased righting reflexes, paresis of upward or downward gaze, vertical nystagmus, incoordination of movements of the eyeballs, ophthalmoplegia, horizontal nystagmus, Nothnagel syndrome (impaired balance, hearing, paralysis of the oculomotor muscles, choreic hyperkinesis), paresis and paralysis of the limbs, cerebellar disorders, decerebrate rigidity , associated with damage to the mesencephalic centers regulating muscle tone below the red nucleus.
Red core syndrome: intentional hemitremor, hemihyperkinesis, Claude's syndrome (inferior red nucleus syndrome) - damage to the gosomotor nerve on the side of the lesion, on the opposite side there is intentional hemitremor, hemiataxia. Foix syndrome (superior red nucleus syndrome) - intentional hemitremor, hemihyperkinesis.
Substantia nigra syndrome characterized by plastic muscle hypertension and the development of akinetic-rigid syndrome.
Tegmental syndrome: homolateral ataxia, Horner's syndrome, tremor, myoclonus, contralateral hemihypesthesia, violation of the quadrigeminal reflexes - rapid indicative movements in response to unexpected visual and auditory stimuli (start reflexes).
Pontine brain syndromes include symptoms associated with damage to the nuclei of the V, VI, VII and VIII nerves, the medial lemniscus, the pyramidal tract, the posterior longitudinal fasciculus, paralysis of the muscles innervated by the facial and abducens nerves, paresis or paralysis of gaze (pontine center of gaze, posterior longitudinal fasciculus), sensitivity disorders on the face, hearing loss, vestibular disorders, vegetative-trophic disorders - hyperthermia, sphincter disorders, sweating disorders, convulsions, hormetonia.
When the lesion is localized in areas of the cerebellopontine angle symptoms are observed from the VII, VIII, less often VI and V nerves, cerebellar disorders; on the opposite side - spastic hemiplegia.
Medulla oblongata syndrome includes symptoms of damage to the nuclei of the IX, X, XI and XII nerves, inferior olive, spinothalamic tract, Gaulle, Burdach nuclei, pyramidal and descending extrapyramidal tracts, descending sympathetic fibers to the ciliospinal center, Flexig and Govers tracts.
Hemiparesis, tetraparesis or paralysis of the limbs may be observed; if the lesion is localized in the area of the pyramidal chiasm, alternating hemiplegia (paralysis of the arm on the affected side, paralysis of the legs on the opposite side); sensitivity disorder: hemianesthesia, alternating hemianesthesia; when the lesion is localized in the lateral parts of the spinal cord - dissociated loss of superficial sensitivity on the opposite half of the body, when the lesion is localized in the medial parts of the medulla oblongata - dissociated disorders of deep sensitivity on one or both sides. Impairments in coordination, movements on the side of the lesion, and Bernard-Horner syndrome are also detected. Damage to the caudal part of the medulla oblongata is accompanied by respiratory failure (respiratory paralysis, disturbance of rhythm and frequency of breathing), and cardiovascular activity. Bulbar and pseudobulbar syndrome.
Methodology for studying the coordination system:
Are used tests to determine static ataxia, dynamic ataxia, dysmetria, asynergy, research muscle tone.
For determining static ataxia used Romberg test: legs together, arms at your sides, head straight, eyes closed - stability is assessed. Extend your arms in front of you at shoulder level, close your eyes. The pose becomes more complicated - the heel of one leg is brought to the toe of the other. Stability is assessed in Romberg pose.
Gait assessment tests are used:
Normal gait.
Walk in one line, bringing your heels to your toes.
Possibility of flanking gait.
Samples to determine dynamic ataxia: hands in front of you, close your eyes, reach for the tip of your nose with your index finger. A hit, a missed hit, and the presence of inversion tremor are assessed. Likewise index test: touch the tip of the hammer with one and the other hand.
Try on asynergy. Adiadochokinesis assessed: hands in front of you, a rotational movement is made with the hands, such as rotating and screwing in light bulbs. The speed and symmetry of movements is assessed.
Try on dysmetria: hands in front of you, palms up and down, then a little faster. Next try on dysmetria– sample Schilder: hands in front of you, the right hand rises up, and then lowers to the level of the left hand. Then with the other hand.
When the cerebellar system is damaged in a person, it is examined nystagmus. When the cerebellum is damaged, horizontal nystagmus.
The state of speech is assessed (say the 333rd Cavalry Division). If the cerebellum is damaged, speech will not be smooth, intermittent, or scanned.
Examined in the supine position samples on dynamic ataxia in the legs: you need to raise your right leg and place your right heel on the knee of your left leg, then move down the leg. The presence of misses and slips is assessed. Same thing with the other leg.
Try on asynergy – asynergic Babinski phenomenon. Lying down, the patient crosses his arms and sits down: when the cerebellum is affected, the legs are raised, not the upper body.
Try to the absence of a reverse shock. When the cerebellum is damaged, the patient hits himself in the chest with his fist (see video).
Researched muscle tone by palpation muscles and passive movements in small and then large joints. With damage to the cerebellum there is muscular hypotension.
3.Task:
1. Leading syndrome - generalized minor seizures such as absences
2. Topical diagnosis - the pathological focus is localized in the medio-basal regions of the frontal
3. Clinical diagnosis: Epileptic disease.
4. Treatment: anticonvulsant therapy (Depakine, Topomax, lamotrigine).
5. Prof: rational work and rest regime, exclusion of alcohol, normal sleep, regular use of anticonvulsants.
1. Severe traumatic brain injury. Clinic, diagnosis, treatment, clinical manifestations of the consequences of TBI.
Severe TBI is accompanied by prolonged loss of consciousness, coma of varying degrees, the presence of brainstem disorders => gross impairment of vital functions.
severe - severe brain contusion, diffuse axonal damage and acute compression of the brain.
For severe contusion on CT zones of heterogeneous increase in density are determined (alternating areas of increased and decreased density). Perifocal cerebral edema is severe. A hypodense track is formed in the area of the nearest section of the lateral ventricle. Through it, fluid with breakdown products of blood and brain tissue is discharged.
For diffuse axonal brain damage is typically a long-term coma after a traumatic brain injury, as well as pronounced brain stem symptoms. Coma is accompanied by symmetrical or asymmetrical decerebration or decortication, both spontaneous and easily provoked by irritations (for example, painful ones). Changes in muscle tone are very variable (hormetonia or diffuse hypotension). A typical manifestation is pyramidal-extrapyramidal paresis of the limbs, including asymmetric tetraparesis. In addition to gross disturbances in the rhythm and frequency of breathing, autonomic disorders also appear: increased body temperature and blood pressure, hyperhidrosis, etc. A characteristic feature of the clinical course of diffuse axonal brain damage is the transformation of the patient’s condition from a prolonged coma to a transient vegetative state. The onset of this state is indicated by spontaneous opening of the eyes (with no signs of tracking or fixation of gaze).
CT picture Diffuse axonal brain damage is characterized by an increase in brain volume, as a result of which the lateral and third ventricles, subarachnoid convexital spaces, as well as the cisterns of the base of the brain are under compression. The presence of small focal hemorrhages in the white matter of the cerebral hemispheres, corpus callosum, subcortical and brain stem structures is often detected.
Oculolethargic syndrome. Predominant damage to the oral parts of the trunk (nuclei of the oculomotor nerves), the hypothalamic region and the reticular formation of the trunk.
Damage to the left nucleus of the spinal tract.
Segmentally dissociated type of sensitivity disorder.
Oral parts of the nucleus of the spinal tract of the trigeminal nerve (pons) on the left.
Alternating Weber syndrome. Damage to the brain stem, mainly the base of the midbrain (peduncle) on the right.
Alternating syndrome. Damage to the brain stem, mainly the pons on the right.
Alternating Millard-Gubler syndrome. Damage to the lower part of the bridge on the right.
Alternating Jackson syndrome. Medulla oblongata on the right.
Pseudobulbar palsy. Bilateral damage to the corticobulbar tract (more pronounced on the right).
Bulbar palsy. Predominant damage to the tegmentum of the brain stem at the level of the nuclei of the 12th, 9th, 10th cranial nerves (medulla oblongata).
4. Damage to the cerebellum
Right hemisphere of the cerebellum.
5. DAMAGE TO THE SUBCORTICAL NODES
Parkinsonism syndrome. Predominant damage to the pallidal system (globus pallidus, substantia nigra).
Choric hyperkinesis syndrome. Predominant damage to the striatal system (putamen, caudate nucleus).
6. DAMAGE TO THE HYPOTHALAMIC-PITITUITARY AREA
Hypothalamic-pituitary syndrome. Predominant damage to the pituitary gland.
Sympathetic-adrenal crisis. Predominant damage to the hypothalamus (diencephalic region).
Itsenko-Cushing syndrome. Damage to the pituitary-hypothalamic region.
7. DAMAGE TO THE INTERNAL CAPSULE
Central palsy of the facial and hypoglossal nerves.
Internal capsule on the right.
8. DAMAGE TO THE LOBE, GYRIUS OF THE BRAIN
Predominant damage to the frontal lobe on the left.
Lesion of the left frontal lobe.
Predominant damage to the frontal lobe on the left (with symptoms of irritation of the second frontal gyrus).
Motor Jacksonian epilepsy. Lesion of the right precentral gyrus.
Apraxia syndrome (motor, constructive).
Damage to the left parietal lobe, mainly the supramarginal and angular gyri.
Disorders of muscle-joint, tactile sensitivity, sense of localization in the left hand, disorder of the “body diagram”. Damage to the right parietal lobe, mainly the superior parietal lobule and interparietal sulcus.
Quadrant hemianopsia (lost lower left quadrant).
Left-sided hemianopsia with preservation of the central visual field.
Visual agnosia.
Astereognosia, apraxia.
Sensory aphasia.
Amnestic, semantic aphasia.
Gustatory, olfactory agnosia.
Quadrant hemianopsia (the right upper quadrant has fallen out).
Predominant damage to the left temporal lobe.
9. Task-schemes
Lateral pyramidal tracts at the level of the cervical segments.
The anterior horns of the spinal cord or anterior roots at the level of segments C 5 -C 8 on the right.
Damage to the nucleus of the facial nerve on the left (pons) and the lateral pyramidal tract at the same level (alternating paralysis)
The lesion is on the right (cerebral peduncle, internal capsule, corona radiata, anterior central gyrus). Hemiplegia on the left.
Multiple lesions of peripheral nerves (polyneuritis).
The anterior horns of the spinal cord and the lateral pyramidal tract on the left at the level of segments C5-C7.
The anterior horns of the spinal cord or the anterior roots of the spinal nerves at the level of segments L 1 -S 1 on both sides.
Lateral pyramidal tract at the level of segment D 12 on the left or the upper part of the right precentral gyrus.
Bilateral damage to the lateral pyramidal tracts at the level of segments D 9 - D 10 or the upper parts of the precentral gyri.
Multiple lesions of the peripheral nerves of the extremities (polyneuritic type of sensitivity disorder).
Posterior columns of the spinal cord at the level of segment D 4 (Gaull's bundles).
Posterior horns at the level of segments C 5 - D 10 on the right.
The posterior column of the spinal cord and the lateral spinothalamic tract on the right at the level of segments D 5 - D 6.
Lateral spinothalamic tract and deep sensory pathways (medial lemniscus) at the level of the brain stem (pons), sensory nuclei of the trigeminal nerve, ibid.
Lateral spinothalamic tract at the level of segments D 8 - D 9 on the left.
Right brachial plexus.
Spinal nerve roots at the level of segments S 3 -S 5 on both sides:
Lateral spinothalamic tracts on both sides at the level of segments D 10 - D 11 and the posterior cords of the spinal cord at the same level.
Lateral pyramidal tract at the level of segment D 10 on the right, spastic paresis of the right leg, absence of middle and lower abdominal reflexes on the right.
Anterior horns of the spinal cord at the level of segments L 2 -L 4 on both sides. Peripheral paralysis of the lower extremities (mainly thigh muscles).
Anterior roots of the spinal nerves at the level of segments L 4 -S 1 on both sides. Peripheral paralysis of the muscles of the legs and feet.
Anterior roots of the spinal nerves at the level of segments C 5 -C 8 on the right. Peripheral paralysis of the right arm.
Anterior horns of the spinal cord at the level of segments L 1 -L 2 on both sides. Peripheral paralysis of the thigh muscles.
Lateral pyramidal path at the level of segments L 2 -L 3.
Spastic paralysis of the lower limb.
Lateral pyramidal tract at the level of segment D 5 on the left. Spastic paresis of the left leg, absence of abdominal reflexes on the left.
Anterior horns of the spinal cord at the level of segments C 1 - C 4 on the left.
Anterior horns of the spinal cord and lateral pyramidal tracts on both sides at the level of segments C5-C8.
Peripheral upper and central lower paraparesis, urinary and fecal retention.
The anterior horns of the spinal cord and the lateral pyramidal tract on the right at the level of segments C5-C8. Peripheral paresis of the right arm with fibrillations, central paresis of the right leg. Peripheral paralysis of the neck muscles, paralysis of the diaphragm.
Lateral pyramidal tract on the left at the level of segment D 12. Spastic paralysis of the lower limb while maintaining the upper and middle abdominal reflexes.
Anterior roots of the spinal nerves at the level of segments S 3 -S 5 on both sides. Peripheral sphincter paralysis (urinary and fecal incontinence).
There are no paresis of the limbs.
Lateral pyramidal tract at the level of segment C 5 on the left. Left-sided central hemiparesis.
Lateral spinothalamic tract on the right at level D 10. Conduction disturbance of pain and temperature sensitivity downward from the level of the inguinal fold on the left
Spinal nerves at the level of segments C 5 -C 8 on the left, anesthesia and flaccid paralysis or paresis of the left arm
Brown-Séquard syndrome: central paresis of the left leg and disturbance of deep sensitivity on the left below the axillary region, conduction disturbances of superficial sensitivity on the right.
Transverse lesion of the spinal cord at the level of segment C4. Central tetraplegia, anesthesia of the entire surface of the body; dysfunction of the pelvic organs.
Possible paresis of the diaphragm. - The posterior roots of the spinal nerves at the level of segments S 3 -S 5 on both sides. Anesthesia in the area of the external genitalia and anus.
Posterior and anterior roots at the level of segments L 4
S 1 on the left. Peripheral paresis of the left leg, disturbance of all types of sensitivity.
Facial nerve (central palsy on the left).
Facial nerve (peripheral paralysis on the left).
Oculomotor nerve (ptosis of the right upper eyelid).
Oculomotor nerve (divergent strabismus, mydriasis).
Trigeminal nerve (innervation of the face and head by segments, Zelder zones).
Trigeminal nerve (peripheral innervation of the skin of the face and head).
Hypoglossal nerve (peripheral palsy on the left).
Abducens nerve (when looking to the left, the left eyeball is not diverted outward).
Focal (partial) motor seizure in the right leg.
Adversive seizure (turning the head and eyes to the right)
Auditory hallucination (aura).
Complex visual hallucination (aura).
Simple visual hallucination (aura).
Olfactory, gustatory hallucination (aura).
Motor aphasia (Broca's center).
As a result of acute cerebral circulation, brain neuron cells are damaged. Depending on the location of the disorders, various types of stroke are diagnosed (brain, cerebellar, hemispheric).
Brainstem stroke is a condition in which the brainstem is damaged as a result of a hemorrhagic or ischemic attack. When the blood supply is disrupted, the axons responsible for motor function and facial expressions die.
Causes of brain stem stroke
Any stroke occurs due to acute disruption of blood supply. There are two types of pathological disorders, depending on the etiology:- – a stroke in the trunk area occurs due to internal bleeding. It is the most dangerous lesion, often leading to the death of the patient. Bleeding develops against the background of atherosclerosis and other vascular abnormalities.
- – disorders develop gradually, as a result of chronic deterioration of blood supply. Thrombotic neoplasms, cholesterol plaques, injuries and diseases lead to a decrease in the intensity of blood flow. The lack of oxygen and nutrients gradually affects the functioning of nerve cells - axons, and leads to tissue infarction.
Symptoms of brainstem stroke
The stem part is responsible for the functioning of the human muscular system. When affected, the basic and vital functions of the body, responsible for the mobility of the limbs, swallowing, and breathing, are disrupted. The trunk connects the spinal cord and brain, participates in thermoregulation and other important tasks of the body.A large stroke in the brainstem leads to death in 70-80% of cases. Therefore, the main task of medical personnel is to diagnose disorders at an early stage and carry out timely rehabilitation procedures.
Symptoms of acute circulatory disorders are: 
If you promptly recognize the first symptoms of brain stem damage during a stroke, you can provide first aid and reduce the intensity of complications associated with the attack.
Secondary brainstem stroke
Repeated stroke of any part of the brain manifests itself in more severe symptoms. Particularly dangerous are disorders of the cerebral blood supply to the brain stem.A stroke causes irreversible damage to nerve cells' axons, causing loss of breathing and other important functions. With a favorable course of the disease, lost abilities are restored due to the fact that intact tissues take over and restore the lost capabilities of the brain. A recurrent stroke in most cases ends in the death of the patient.
What are the dangers of a brainstem stroke?
Hemorrhagic or ischemic brain damage leads to disruption of certain brain functions. Complications after an attack depend on the location of the hemorrhage.The consequences of a brainstem stroke are: 
The consequence of a brainstem stroke with negative dynamics is complete paralysis of the patient with gradual failure of the internal organs and the development of a condition incompatible with the patient’s life.
The most dangerous period of a stroke is the first ten days after the onset of an acute lack of blood supply. At this stage, all possible rehabilitation measures should be taken to prevent the development of complications.
How is a brainstem stroke treated?
Recovery from a brainstem stroke takes a long time. Even with a favorable prognosis for the development of the disease, it will take years for rehabilitation and restoration of normal respiratory, swallowing, speech and other functions. An important part of traditional therapy is the early diagnosis of the development of ischemic or hemorrhagic disease.Diagnostic methods
It is much easier to prevent a stroke with damage to the trunk than to combat the development of complications and cope with the consequences of an acute circulatory disorder.
Several methods are used for early diagnosis of pathological disorders:
- Tomography - at an early stage of disorders, a stroke may not manifest clinically and not be accompanied by neurological symptoms. The only effective and informative diagnostic method is computed tomography or magnetic resonance imaging. If necessary, a contrast study is performed.
Tomography allows you to detect cerebral circulatory disorders long before the development of serious hemorrhagic or ischemic problems. - Angiography – helps to identify existing disorders in the cardiovascular system: thrombosis, atherosclerosis, etc.
- Cardiography is necessary to identify changes in heart rhythm indicating changes in the intensity of blood flow.
Drug therapy
Regardless of the type of stroke, the patient is prescribed a course of therapy that includes the following:
Rehabilitation after brainstem stroke
Recovery time and the likelihood of complications primarily depend on the timely assistance provided to the patient, as well as the extent of the lesion. In general, the prognosis is quite unfavorable. With a recurrent stroke, death occurs in almost 100% of cases. Limited tissue damage makes at least partial restoration of lost brain function likely.How long does recovery take?
The recovery process takes a long time. Even with localized and minor brain damage, it will not be possible to completely eliminate all the changes that have appeared. The prognosis is worsened by the need to be connected to an artificial respiration apparatus, as well as prolonged loss of consciousness (coma). Patients with impaired swallowing function, those who are in a coma or have breathing problems will need an enteral feeding device, which will also complicate rehabilitation. In general, it will take about 1-2 years to normalize the basic functions of the body. Some processes will never be fully restored.
Rehabilitation physical education
As the patient recovers, he is prescribed exercise therapy and additional rehabilitation procedures. The first classes are performed lying down and are aimed at restoring motor functions of the limbs. Over time, exercise therapy is prescribed to improve facial expressions and restore speech functions.The simultaneous use of the following procedures speeds up recovery:
- Massage or manual therapy.
- Reflexology.
- Acupuncture.
- Hirudotherapy.
The main task of the resuscitator is to prevent the development of a recurrent stroke, therefore, at the first signs of deterioration in health, you should immediately stop the procedure and seek advice from a neurologist.
Stroke of the cerebral column is a serious pathology that can cause irreversible changes and provoke the development of conditions that end in death. The prognosis of the disease is unfavorable. A recurrent stroke most often ends in the death of the patient.