Syndrome of lesions of the brain stem at different levels. Focal contusions of the brain. Extrastem alternating syndromes

As a consequence of the unique anatomical structure of the brainstem, unilateral lesions often cause overlapping (alternating) syndromes, in which ipsilateral dysfunction of one or more cranial nerves is accompanied by hemiplegia and/or hemihypesthesia on the opposite side. Accurate topical diagnosis of brainstem lesions is based, on the one hand, on signs of dysfunction of long pathways (for example, corticospinal and spinothalamic pathways), which allow localization of the lesion in the longitudinal (sagittal) plane, and on the other hand, on signs of cranial nerve dysfunction, which allows you to localize the lesion in the transverse (axial) plane. The localization of brainstem lesions can be simplified by summing up the neurological symptoms observed in the patient and answering the following questions: Is the lesion unilateral or bilateral? What is the level of failure? If the lesion is unilateral, is it medial or lateral?

KEY FACTS: KEY FUNCTIONS OF THE CRANIAL NERVE

Provide motor functions and general чувствительность!}
Provide special types of sensitivity:, hearing, Smell, -i; cf. The ability of a person and women to distinguish between smells in-in, located in the external environment, with the help of specialized organs; used for finding and selecting food, tracking prey, chemocommunication, etc. human sense of smell. The ability of a person to perceive and distinguish odors with the help of special sensitive cells located in the nasal cavity, from which information is transmitted to the brain.
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Provides parasympathetic innervation internal organs

8. List the main subjective and objective symptoms of trunk lesions.

Subjective symptoms

doubling
Disorders of coordination
Walking disorders
Facial numbness
Hoarseness of voice
Swallowing and speech disorders Objective symptoms

Objective symptoms

Multiple cranial nerve dysfunction
Loss of the ability to move one muscle or system of muscles due to damage to their nervous regulation.
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nystagmus
Sympathetic dysfunction (Horner's syndrome)
Hearing loss
Deviation or atrophy of the tongue
Paresis, [re] -a; m. Weakening of voluntary movements, accompanied by a decrease in muscle strength due to impaired innervation; for example, when the facial nerve is damaged, paresis of the muscles of the face innervated by it occurs.
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Ipsilateral hemiparesis and ataxia
Oppression of consciousness and Coma, -s; and. A life-threatening condition caused by dysfunction of the brain stem; characterized by a complete loss of human consciousness, the disappearance of muscle reflexes, impaired blood circulation, respiration and metabolism in-in; deep K. is accompanied by the absence of even primitive responses (for example, to pain) and refers to terminal states
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9. How to localize an isolated cranial nerve dysfunction?

Isolated dysfunction of the cranial nerve, especially VI and VII, most often occurs due to peripheral rather than stem damage.

10. What is the difference between the manifestations of intraaxial and extraaxial lesions?

A lesion that primarily affects the substance of the brainstem is called intraaxial, or intramedullary. It usually manifests itself with symptoms of damage to the long conductors and the cranial nerve, which occur simultaneously. A lesion outside the medulla oblongata is called extraaxial.

At first, compression and dysfunction of individual cranial nerves develop, later, as the formation grows, neighboring structures of the trunk can be affected, which leads to the appearance of signs of damage to long conductors.

11. What diseases can cause damage to the brain stem?

Intraaxial lesions:

tumors
ischemia/infarction
vascular malformation
demyelinating disease
inflammatory focus Extraaxial lesions:
acoustic neuroma
menngioma
chordoma
aneurysms
epidermoid
arachnoid cyst

12. What neuroimaging study is the method of choice for lesions of the trunk?

Magnetic resonance imaging (MRI) is the method of choice for suspected lesion of the trunk. MRI is a highly sensitive, non-invasive method for obtaining images of the posterior cranial fossa that are devoid of artefacts associated with the bones of the base of the skull. Contrast enhancement with gadolinium may be useful for assessing the integrity of the blood-brain barrier. MR angiography can help in the study of the main arteries of the vertebrobasilar system in brainstem infarction.

Oculo-lethargic syndrome. The predominant lesion of the oral sections 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 sensory disturbance. Oral divisions of the nucleus of the spinal tract of the trigeminal nerve (pons varolii) on the left.

Alternating Weber syndrome. Damage to the brain stem, mainly the base of the midbrain (peduncles) on the right.

alternating syndrome. The defeat of the brain stem, mainly the bridge on the right.

Alternating Miyyar-Gubler's syndrome. The defeat of the lower part of the bridge on the right.

Alternating Jackson syndrome. medulla oblongata on the right.

Pseudobulbar paralysis. Bilateral lesion of the corticobulbar tract (more pronounced on the right).

Bulbar paralysis. The predominant lesion of the tegmentum of the brain stem at the level of the location of the nuclei of the 12th, 9th, 10th cranial nerves (medulla oblongata).

4. Damage to the cerebellum

Right hemisphere of the cerebellum.

5. DEFEAT OF THE SUBCORTICAL NODES

The defeat of the left visual tubercle.

parkinsonism syndrome. Predominant lesion of the pallidar system (pallid ball, substantia nigra).

Syndrome of choreic hyperkinesis. Predominant lesion of the striatal system (shell, caudate nucleus).

6. DEFEAT OF THE HYPOTHALAMO-PITUITARY REGION

Hypothalamo-pituitary syndrome. Primary lesion of the pituitary gland.

Sympathetic-adrenal crisis. Primary lesion of the hypothalamus (diencephalic region).

Syndrome Itsenko-Cushing. The defeat of the pituitary-hypothalamic region.

7. INTERNAL CAPSULE DEFEAT

Central paralysis of the facial and hypoglossal nerves. Inner capsule on the right.

8. IMPAIRMENT OF THE LOBS, GIRLS OF THE BRAIN

Predominant lesion of the frontal lobe on the left.

Damage to the left frontal lobe.

Predominant lesion of the frontal lobe on the left (with symptoms of irritation of the second frontal gyrus).

Motor Jacksonian epilepsy. Damage to the right precentral gyrus.

Apraxia syndrome (motor, constructive). The defeat of the left parietal lobe, mainly supramarginal and angular gyrus.

Violations of the muscular-articular, tactile sensitivity, sense of localization in the left hand, disorder of the “body scheme”. Damage to the right parietal lobe, mainly the superior parietal lobule and interparietal sulcus.

Predominant lesion of the left temporal lobe.

9. Tasks-schemes

Lateral pyramidal tracts at the level of the cervical segments.

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 (bridge) and the lateral pyramidal tract at the same level (alternating paralysis)

The lesion on the right (brain 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 C 5 -C 7 segments.

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.

The lateral pyramidal tract at the level of the D12 segment on the left or the upper section of the right precentral gyrus.

Bilateral lesion of the lateral pyramidal tracts at the level of segments D 9 -D 10 or the upper sections of the precentral gyri.

Anterior horns of the spinal cord at the level of C 5 -C 8 segments and lateral pyramidal tracts at the same level on both sides.

Internal capsule or thalamus, or corona radiata, or postcentral gyrus. The hearth is on the left.

Multiple lesions of the peripheral nerves of the extremities (polyneuritic type of sensitivity disorder).

Posterior columns of the spinal cord at the level of the D4 segment (Gaulle's bundles).

Hind horns at the level of segments C 5 -D 10 on the right.

The posterior column of the spinal cord and the lateral spinal-thalamic path on the right at the level of the D 5 -D 6 segments.

Lateral spinal-thalamic pathway and pathways of deep sensitivity (medial loop) at the level of the brain stem (bridge), sensory nuclei of the trigeminal nerve, ibid.

Lateral dorsal-thalamic path 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 spinal thalamic pathways on both sides at the level of segments D 10 -D 11 and the posterior funiculi 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 the muscles of the thighs).

The 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.

The anterior roots of the spinal nerves at the level of segments C 5 -C 8 on the right. Peripheral paralysis of the right hand.

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 C 5 -C 8 segments. Peripheral upper and central lower paraparesis, urinary and fecal retention.

Anterior horns of the spinal cord, lateral pyramidal path on the right at the level of segments L 1 -L 2 . Peripheral paresis of the muscles of the thighs, central paresis of the muscles of the lower leg and foot on the right.

Anterior horns of the spinal cord at the level of segments C 5 -C 8 on the left. Peripheral paralysis of the left hand.

The anterior horns of the spinal cord and the lateral pyramidal tract on the right at the level of C 5 -C 8 segments. 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 path 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 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 C5 segment on the left. Left-sided central hemiparesis.

Lateral dorsal-thalamic path on the right at the level of 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 hand

Brown-Sequard syndrome: central paresis of the left leg and a violation 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 C 4 . Central tetraplegia, anesthesia of the entire surface of the body; violation of the functions of the pelvic organs. Possible paresis of the diaphragm.

Posterior roots of spinal nerves at the level of segments S 3 -S 5 on both sides. Anesthesia in the vulva and anus.

Posterior and anterior roots at the level of segments L 4 - S 1 on the left. Peripheral paresis of the left leg, violation of all types of sensitivity.

Facial nerve (central paralysis 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 paralysis on the left).

Abducens nerve (when looking to the left, the left eyeball is not retracted outwards).

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 (Brock's center).

The head and eyes are turned to the left (gaze paresis), agraphia.

Central paralysis of the right leg.

Quadrant hemianopsia (lower left quadrant dropped out).
Left-sided hemianopsia with preservation of the central field of view.
visual agnosia.
Astereognosia, apraxia.
Sensory aphasia.
Amnestic, semantic aphasia.
Taste, olfactory agnosia.
Quadrant hemianopsia (right upper quadrant dropped out).

Stem stroke is one of the most severe forms of brain damage against the background of acute blood flow disorders. This is no coincidence, because it is in the trunk that the main life-support nerve centers are concentrated.

Among patients with stroke of the brain stem, elderly people predominate, having appropriate prerequisites for impaired blood flow - hypertension, atherosclerosis, pathology of blood clotting, heart, predisposing to thromboembolism.

The brain stem is the most important area that serves as a link between the central nervous system, spinal cord and internal organs. It controls the work of the heart, the respiratory system, maintaining body temperature, motor activity, regulates muscle tone, autonomic reactions, balance, sexual function, participates in the work of the organs of vision and hearing, provides chewing, swallowing, contains fibers of taste buds. It is difficult to name a function of our body that would do without the participation of the brain stem.

structure of the brain stem

The stem structures are the oldest and include the pons, medulla oblongata and midbrain, sometimes they are also referred to. In this part of the brain, the nuclei of the cranial nerves are located, and the conductive motor and sensory nerve pathways pass. This department is located under the hemispheres, access to it is extremely difficult, and with swelling of the trunk, its displacement and compression quickly occur, which are fatal for the patient.

Causes and types of stem strokes

The causes of stem stroke do not differ from those in other localizations of blood flow disorders in the central nervous system:

, which causes irreversible changes in the arteries and arterioles of the brain, the walls of the vessels become brittle and sooner or later they may rupture with hemorrhage;
, observed in the vast majority of older people, leads to the appearance in the arteries that feed the brain, the result is plaque rupture, thrombosis, blockage of the vessel and necrosis of the medulla;
and - cause strokes in young patients without or in combination with comorbidities.

To a large extent, other metabolic disorders, rheumatism, heart valve defects, blood clotting disorders, including when taking blood-thinning drugs, usually prescribed for cardiological patients, also contribute to the development of a stroke of the trunk.

Depending on the type of damage, stroke of the brain stem is ischemic and hemorrhagic. In the first case, a focus of necrosis (heart attack) is formed, in the second case, blood flows into the brain tissue when a blood vessel ruptures. Ischemic stroke is more favorable, and with hemorrhagic edema and intracranial hypertension rapidly increase, therefore, mortality is much higher in the case of hematomas.

Video: basic about the types of stroke - ischemic and hemorrhagic

Manifestations of damage to the brain stem

Stem stroke is accompanied by damage to the conduction tracts, the nuclei of the cranial nerves, therefore, it is accompanied by rich symptoms and severe disorders of the internal organs. ailments manifest themselves acutely, starting with intense pain in the occipital region, impaired consciousness, paralysis, dizziness, tachycardia or bradycardia, and sharp fluctuations in body temperature.

Cerebral symptoms associated with an increase in intracranial pressure, it includes nausea and vomiting, headache, impaired consciousness up to a coma. Then join symptoms of damage to the nuclei of the cranial nerves, focal neurological symptoms.

Ischemic stem stroke is manifested by a variety of alternating syndromes and signs of involvement of the nuclei of the cranial nerves of the side where the necrosis occurred. In this case, you may observe:

Paresis and paralysis of muscles from the affected part of the trunk;
Deviation of the tongue in the direction of the lesion;
Paralysis of the part of the body opposite to the focus with the preservation of the work of the facial muscles;
Nystagmus, imbalance;
Paralysis of the soft palate with difficulty breathing, swallowing;
Omission of the eyelid on the side of the stroke;
Paralysis of the facial muscles on the side of the lesion and hemiplegia of the opposite half of the body.

This is only a small part of the syndromes that accompany a stem heart attack. With a small focus (up to one and a half centimeters), isolated violations of sensitivity, movements, central paralysis with pathology of balance, disruption of the hand (dysarthria), an isolated violation of the muscles of the face and tongue with a speech disorder are possible.

With hemorrhagic stem stroke, symptoms increase rapidly, in addition to motor and sensory disorders, intracranial hypertension is clearly manifested, consciousness is disturbed, and the likelihood of coma is high.

Signs of hemorrhage in the trunk can be:

Hemiplegia and hemiparesis - paralysis of the muscles of the body;
Visual disturbances, gaze paresis;
Speech disorder;
Decrease or lack of sensitivity on the opposite side;
Oppression of consciousness, coma;
Nausea, dizziness;
Increase in body temperature;
Violation of breathing, heart rhythm.

A stroke usually occurs suddenly and can be witnessed by loved ones, colleagues or passers-by on the street.. If a relative suffers from hypertension or atherosclerosis, then a number of symptoms should alert loved ones. So, sudden difficulty and incoherence of speech, weakness, headache, impossibility of movement, sweating, jumps in body temperature, palpitations should be the reason for an immediate call for an ambulance. A person's life may depend on how quickly others orient themselves, and if the patient gets to the hospital in the first few hours, the chances of saving a life will be much greater.

Sometimes small foci of necrosis in the brain stem, especially those associated with, proceed without abrupt change states. Weakness gradually increases, dizziness appears, gait becomes uncertain, the patient has double vision, hearing and vision decrease, food intake is difficult due to choking. These symptoms also cannot be ignored.

Stem stroke is considered the most severe pathology, and therefore its consequences are very serious. If during the acute period it is possible to save life and stabilize the patient's condition, bring him out of a coma, normalize pressure and respiration, then significant obstacles arise at the stage of rehabilitation.

After a stem stroke, paresis and paralysis are usually irreversible, the patient cannot walk or even sit, speech and swallowing are disturbed. Difficulties arise with food intake, and the patient needs either parenteral nutrition or a special diet with liquid and pureed food.

Contact with a patient who has had a stem stroke is difficult due to speech impairment, while the intellect and awareness of what is happening can be preserved. If there is a chance to at least partially restore speech, then a specialist aphasiologist who knows the techniques and special exercises will come to the rescue.

After a heart attack or a hematoma in the brainstem, patients remain disabled, requiring constant participation and assistance in eating, carrying out hygiene procedures. The burden of care falls on the shoulders of relatives, who must be aware of the rules for feeding and handling the seriously ill.

Complications of stem stroke are not uncommon and can cause death. most common cause death is considered to be swelling of the brain stem with its infringement under the dura mater of the brain or in the occipital foramen, uncorrectable disorders of the heart and breathing are possible,.

In a later period, urinary tract infections, pneumonia, thrombosis of the veins of the legs, bedsores occur, which is facilitated not only by a neurological deficit, but also by the forced recumbency of the patient. Sepsis, myocardial infarction, bleeding in the stomach or intestines are not excluded. Patients with milder forms of stem stroke who attempt to move around are at high risk of falls and fractures, which can also be fatal.

Relatives of patients with stroke of the brain stem already in the acute period want to know what are the chances of a cure. Unfortunately, in a number of cases, doctors cannot reassure them at least somehow, since with this localization of the lesion, we are talking about saving lives in the first place, and if it is possible to stabilize the condition, then the vast majority of patients remain severely disabled.

The inability to correct blood pressure, high body temperature that does not go astray, coma are unfavorable prognostic signs, in which there is a high probability of death during the first days and weeks after the onset of the disease.

Treatment of stem stroke

Stem stroke is a severe, life-threatening condition that requires immediate therapeutic measures; the prognosis of the disease largely depends on how quickly treatment is started. All patients, without exception, must be admitted to specialized departments, although in some regions this figure is appallingly low - about 30% of patients get to the hospital on time.

The optimal time to start treatment is the first 3-6 hours from the onset of the disease, while even in large cities with high availability medical care Often, treatment is started after 10 hours or more. is carried out to single patients, and round-the-clock CT and MRI is more a fantasy than a reality. As a result, forecast indicators continue to be disappointing.

A patient with a stem stroke should spend the first week in the intensive care unit under the constant supervision of specialists. When the most acute period is over, a transfer to the early rehabilitation ward is possible.

The nature of therapy has features in the ischemic or hemorrhagic type of lesion, but there are some general patterns and approaches. Basic treatment aimed at maintaining blood pressure, body temperature, lung and heart function, blood constants.

To keep your lungs working you need:

Sanitation of the upper respiratory tract, tracheal intubation, artificial lung ventilation;
Oxygen therapy at low saturation.

The need for tracheal intubation in stem stroke is associated with a violation of swallowing and cough reflex, which creates the preconditions for the contents of the stomach to enter the lungs (aspiration). Blood oxygen is controlled by, and its oxygen saturation (saturation) should not be lower than 95%.

If the brain stem is damaged, there is a high risk of disorders from the side of cardio-vascular system so you need:

Blood pressure control - ;
ECG monitoring.

Even for those patients who did not suffer arterial hypertension, antihypertensive drugs are shown in order to prevent recurrent stroke. In addition, when the pressure exceeds 180 mm Hg. Art., the risk of aggravation of brain disorders increases by almost half, and a poor prognosis - by a quarter, which is why it is so important to constantly monitor pressure.

If the pressure was high before brain damage, then maintaining it at a level of 180/100 mm Hg is considered optimal. Art., for people with initial normal pressure - 160/90 mm Hg. Art. Such relatively high numbers are due to the fact that when the pressure drops to normal, the degree of blood supply to the brain also decreases, which can aggravate Negative consequences ischemia.

Used to correct blood pressure labetalol, captopril, enalapril, dibazol, clonidine, sodium nitroprusside. In the acute period, these drugs are administered intravenously under pressure control, later oral administration is possible.

Some patients, on the contrary, suffer from hypotension, which is very detrimental to the affected part of the brain, because hypoxia and neuronal damage increase. To correct this condition, infusion therapy is carried out with solutions ( reopoliglyukin, sodium chloride, albumin) and use vasopressors ( norepinephrine, dopamine, mezaton).

Mandatory is the control of biochemical blood constants. So, with a decrease in sugar levels, glucose is introduced, with an increase of more than 10 mmol / l - insulin. In the intensive care unit, sodium levels, blood osmolarity are constantly measured, and the amount of urine excreted is taken into account. Infusion therapy is indicated with a decrease in the volume of circulating blood, but at the same time, a slight excess of diuresis over the amount of infused solutions is allowed as a measure to prevent cerebral edema.

Almost all patients with stem strokes have an elevated body temperature, because the center of thermoregulation is located in the affected part of the brain. The temperature should be reduced starting from 37.5 degrees, for which they use paracetamol, ibuprofen, naproxen. A good effect is also obtained when injected into a vein. magnesium sulfate.

The most important step in the treatment of brainstem stroke is the prevention and control of cerebral edema, which can lead to displacement of the median structures and wedging them into the foramen magnum, under the cerebellum tenon, and this complication is accompanied by high mortality. To combat cerebral edema, apply:

Osmotic - glycerin, mannitol;
The introduction of a solution of albumin;
Hyperventilation during mechanical ventilation;
Muscle relaxants and sedatives (pancuronium, diazepam, propofol);
If the measures listed above do not bring results, a barbiturate coma, cerebral hypothermia is indicated.

In very severe cases, when it is not possible to stabilize, muscle relaxants, sedatives are used simultaneously, and artificial ventilation of the lungs is established. If this does not help, a surgical intervention is performed - a hemicraniotomy aimed at decompressing the brain. Sometimes the ventricles of the brain are drained - with hydrocephalus with an increase in pressure in the cranial cavity.

Symptomatic therapy includes:

Anticonvulsants (diazepam, valproic acid);
Cerucal, motilium with severe nausea, vomiting;
Sedatives - Relanium, haloperidol, magnesia, fentanyl.

specific therapy for ischemic stroke is to carry out thrombolysis, the introduction and to restore blood flow in a thrombosed vessel. Intravenous thrombolysis should be carried out in the first three hours after the blockage of the vessel, using alteplase.

Antiplatelet therapy consists in the appointment of aspirin, in some cases, the use of anticoagulants (heparin, fraxiparin, warfarin) is indicated. Reopoliglyukin can be used to reduce blood viscosity.

All of the listed methods of specific therapy have strict indications and contraindications, so the appropriateness of their use in a particular patient is decided individually.

Needed to restore damaged brain structures. For this, glycine, piracetam, encephabol, cerebrolysin, emoxipin and others are used.

Specific treatment hemorrhagic strokes consists in the use of neuroprotectors (mildronate, emoxipin, semax, nimodipine, actovegin, piracetam). Surgical removal of the hematoma is difficult due to its deep location, while stereotactic and endoscopic interventions have advantages, minimizing surgical trauma.

The prognosis for a brain stem stroke is very serious, the mortality rate for heart attacks reaches 25%, with hemorrhages, more than half of the patients die by the end of the first month. Among the causes of death, the main place belongs to cerebral edema with displacement of the stem structures and their infringement in the occipital foramen, under the dura mater. If it is possible to save life and stabilize the patient's condition, then after a stem stroke, he will most likely remain disabled due to damage to vital structures, nerve centers and pathways.

The brain stem includes

1. midbrain- located between the diencephalon and the bridge and includes

a. Roof of the midbrain and handles of the superior and inferior colliculi- the formation of two pairs of mounds located on the roof plate and dividing by a transverse groove into upper and lower. The pineal gland lies between the superior colliculi, and the anterior surface of the cerebellum extends above the inferior ones. In the thickness of the mounds lies an accumulation of gray matter, in the cells of which several systems of pathways end and arise. Part of the fibers of the optic tract terminates in the cells of the superior colliculus, the fibers from which go to the tire of the legs of the brain to the paired accessory nuclei of the oculomotor nerve. The fibers of the auditory pathway approach the inferior colliculus.

From the cells of the gray matter of the roof of the midbrain, the tectospinal tract begins, which is a conductor of impulses to the cells of the anterior horns of the spinal cord of the cervical segments, which innervate the muscles of the neck and upper shoulder girdle, which provide head turns. Fibers of the visual and auditory pathways approach the nuclei of the roof of the midbrain, and there are connections with the striatum. The operculospinal tract coordinates reflex orienting movements in response to unexpected visual or auditory stimuli. Each hillock in the lateral direction passes into a white roller, forming the handles of the upper and lower hillocks. The handle of the superior colliculus, passing between the pillow of the thalamus and the medial geniculate body, approaches the external geniculate body, and the handle of the inferior colliculus goes to the medial geniculate body.

Defeat syndrome: cerebellar ataxia, damage to the oculomotor nerve (gaze paresis up, down, divergent strabismus, mydriasis, etc.), hearing disorder (one or two-sided deafness), choreoathetoid hyperkinesis.

B. Legs of the brain- located on the lower surface of the brain, they distinguish between the base of the brain stem and the tire. Between the base and the tire is a pigment-rich black substance. Above the tire lies a plate of the roof, from which the upper cerebellar peduncle and the lower one go to the cerebellum. The nuclei of the oculomotor, trochlear nerves and the red nucleus are located in the tegmentum of the brain stem. The pyramidal, fronto-pontine, and temporal-pontine pathways pass through the base of the brain stem. Pyramidal occupies the middle 2/3 of the base. The frontal-bridge path passes medially to the pyramidal one, and the temporal-bridge path passes laterally.

in. Posterior perforated substance

The cavity of the midbrain is the aqueduct of the brain, which connects the cavities of the III and IV ventricles.

2. hindbrain:

a. Bridge- located on the slope of the base of the skull, it distinguishes between the anterior and posterior parts. The anterior surface of the bridge faces the base of the skull, the upper one takes part in the formation of the anterior sections of the bottom of the rhomboid fossa. Along the midline of the anterior surface of the bridge, there is a longitudinally running basilar sulcus, in which the basilar artery lies. On both sides of the basilar sulcus, pyramidal elevations protrude, in the thickness of which pyramidal pathways pass. In the lateral part of the bridge are the right and left middle cerebellar peduncles, which connect the bridge to the cerebellum. The trigeminal nerve enters the anterior surface of the bridge, at the point of origin of the right and left cerebellar peduncles. Closer to the posterior edge of the pons, in the cerebellopontine angle, the facial nerve exits and the vestibulocochlear nerve enters, and between them there is a thin stem of the intermediate nerve.

In the thickness of the anterior part of the bridge there are more nerve fibers than in the back. The latter contains more clusters of nerve cells. In front of the bridge, there are superficial and deep fibers that make up the system of transverse fibers of the bridge, which, crossing along the midline, pass through the cerebellar peduncles to the bridge, connecting them to each other. Between the transverse bundles are longitudinal bundles belonging to the system of pyramidal pathways. In the thickness of the anterior part of the bridge lie the own nuclei of the bridge, in the cells of which the fibers of the cortical-bridge pathways end and the fibers of the cerebellopontine pathway leading to the cortex of the opposite hemisphere of the cerebellum originate.

b. Medulla- the front surface is located on the slope of the skull, occupying its lower section to the foramen magnum. The upper border between the bridge and the medulla oblongata is the transverse groove, the lower border corresponds to the exit point of the superior radicular thread of the 1st cervical nerve or the lower level of the pyramidal decussation. On the anterior surface of the medulla oblongata passes the anterior median fissure, which is a continuation of the fissure of the same name in the spinal cord. On each side of the anterior median fissure is a cone-shaped roller - the pyramid of the medulla oblongata. The fibers of the pyramids by means of 4-5 bundles in the caudal section partially cross each other, forming a cross of the pyramids. After crossing, these fibers go in the lateral funiculi of the spinal cord in the form of a lateral cortical-spinal tract. The remaining, smaller, part of the bundles, without entering the decussation, passes in the anterior cords of the spinal cord, making up the anterior cortical-spinal tract. Outside of the pyramid of the medulla oblongata is an elevation - the olive, which separates the anterior lateral groove from the pyramid. From the depths of the latter, 6-10 roots of the hypoglossal nerve come out. The posterior surface of the medulla oblongata takes part in the formation of the posterior sections of the bottom of the rhomboid fossa. The posterior median sulcus runs along the middle of the posterior surface of the medulla oblongata, and outward from it is the posterior lateral sulcus, which limit the thin and wedge-shaped bundles, which are a continuation of the posterior cord of the spinal cord. The thin bundle passes at the top into a thickening - the tubercle of the thin nucleus, and the wedge-shaped bundle - into the tubercle of the sphenoid nucleus. The thickenings contain thin and wedge-shaped nuclei. In the cells of these nuclei, the fibers of the thin and wedge-shaped bundles of the posterior cords of the spinal cord terminate. From the depths of the posterior lateral sulcus, 4-5 roots of the glossopharyngeal, 12-16 of the vagus and 3-6 cranial roots of the accessory nerve emerge on the surface of the medulla oblongata. At the upper end of the posterior lateral sulcus, the fibers of the thin and wedge-shaped bundles form a semicircular thickening - the rope body (lower cerebellar peduncle). The right and left lower cerebellar peduncles limit the rhomboid fossa. Each lower cerebellar peduncle contains fibers of the pathways.

3. IVventricle. It communicates above through the cerebral aqueduct with the cavity of the III ventricle, below with the central canal of the spinal cord, through the median aperture of the IV ventricle and two lateral ones with the cerebellar cistern and with the subarachnoid space of the brain and spinal cord. Anteriorly, the IV ventricle is surrounded by the pons and medulla oblongata, and posteriorly and laterally by the cerebellum. The roof of the IV ventricle is formed by the superior and inferior medullary sails. The bottom of the IV ventricle forms a rhomboid fossa. A median sulcus runs along the length of the fossa, which divides the rhomboid fossa into two identical triangles (right and left). The top of each of them is directed to the lateral pocket. A short diagonal passes between both lateral pockets and divides the rhomboid fossa into two triangles of unequal size (upper and lower). In the posterior part of the upper triangle there is a facial tubercle formed by the inner knee of the facial nerve. In the lateral corner of the rhomboid fossa is the auditory tubercle, in which the cochlear nuclei of the vestibulocochlear nerve lie. From the auditory tubercle in the transverse direction, the cerebral strips of the IV ventricle pass. In the region of the rhomboid fossa, the nuclei of the cranial nerves lie symmetrically. The motor nuclei lie more medially in relation to the sensory nuclei. Between them are the vegetative nuclei and the reticular formation. In the caudal part of the rhomboid fossa is the triangle of the hypoglossal nerve. Medially and slightly below it there is a small dark brown the site (triangle of the vagus nerve), where the nuclei of the glossopharyngeal and vagus nerves lie. In the same section of the rhomboid fossa in the reticular formation, the respiratory, vasomotor and vomiting centers are located.

4. cerebellum- Department nervous system involved in automatic coordination of movements, regulation of balance, accuracy and proportionality ("correctness") of movements and muscle tone. In addition, it is one of the highest centers of the autonomic (autonomous) nervous system. It is located in the posterior cranial fossa above the medulla oblongata and the bridge, under the cerebellar tenon. Two hemispheres and located between them middle part- worm. The cerebellar vermis provides static (standing), and the hemispheres - dynamic (movements in the limbs, walking) coordination. Somatotopically, in the cerebellar vermis, the muscles of the trunk are represented, and in the hemispheres, the muscles of the limbs. The surface of the cerebellum is covered with a layer of gray matter that makes up its cortex, which is covered with narrow convolutions and grooves that divide the cerebellum into a number of lobes. The white matter of the cerebellum is composed of various kinds of nerve fibers, ascending and descending, which form three pairs of cerebellar peduncles: lower, middle and upper. The inferior cerebellar peduncles connect the cerebellum to the medulla oblongata. In their composition, the posterior spinal-cerebellar path goes to the cerebellum. The axons of the cells of the posterior horn enter the posterior part of the lateral funiculus of their side, rise to the medulla oblongata, and reach the cortex of the vermis along the inferior cerebellar peduncle. Nerve fibers from the nuclei of the vestibular root also pass here, which end in the core of the tent. As part of the lower cerebellar peduncles, from the nucleus of the tent to the lateral vestibular nucleus, and from it to the anterior horns of the spinal cord goes the vestibulo-spinal path. The middle cerebellar peduncles connect the cerebellum to the pons. They contain nerve fibers from the nuclei of the bridge to the cortex of the opposite hemisphere of the cerebellum. The superior cerebellar peduncles connect it to the midbrain at the level of the roof of the midbrain. They include nerve fibers both to the cerebellum and from the dentate nucleus to the roof of the midbrain. These fibers, after crossing, end in the red nuclei, from where the red nuclear-spinal path begins. Thus, in the lower and middle cerebellar peduncles, mainly the afferent pathways of the cerebellum pass, and in the upper ones, the efferent pathways.

The cerebellum has four paired nuclei located in the thickness of its cerebral body. Three of them - serrated, corky and spherical - are located in the white matter of the hemispheres, and the fourth - the core of the tent - in the white matter of the worm.

Alternating syndromes occur with a unilateral lesion of the brain stem, consist in damage to the cranial nerves on the side of the focus with the simultaneous appearance of paresis (paralysis), sensitivity disorders (according to the conduction type) or coordination on the opposite side.

A) with damage to the legs of the brain:

1. Weber's alternating palsy - peripheral paralysis of the oculomotor nerve on the side of the lesion and spastic hemiplegia on the opposite

2. Benedict's alternating palsy - peripheral paralysis of the oculomotor nerve on the side of the lesion, hemiataxia and intentional tremor on the opposite

3. Claude's alternating syndrome - peripheral paralysis of the oculomotor nerve on the side of the lesion, extrapyramidal hyperkinesis and cerebellar symptoms on the opposite

B) with the defeat of the bridge:

1. Fauville's alternating paralysis - peripheral paralysis of the facial and abducens nerves (or gaze paresis to the side) on the side of the lesion and spastic hemiplegia on the opposite

2. Alternating palsy Miyard - Gubler - peripheral paralysis

Facial nerve on the side of the lesion and spastic hemiplegia on the opposite

3. alternating Brissot-Sicara syndrome - spasm of the facial muscles (irritation of the nucleus of the facial nerve) on the side of the lesion and hemiplegia on the opposite

4. Raymond-Sestan alternating paralysis - gaze paralysis towards the focus, ataxia, choreoathetoid hyperkinesis on the side of the lesion, and on the opposite side - hemiplegia and sensitivity disorders.

C) with damage to the medulla oblongata:

1. Avellis syndrome - peripheral paralysis of the glossopharyngeal, vagus and hypoglossal nerves on the side of the lesion and spastic hemiplegia on the opposite

2. Jackson syndrome - peripheral paralysis of the hypoglossal nerve on the side of the lesion and spastic hemiplegia on the opposite

3. Schmidt's syndrome - peripheral paralysis of the hyoid, accessory, vagus, glossopharyngeal nerves on the affected side and spastic hemiplegia on the opposite

4. Wallenberg-Zakharchenko syndrome occurs when the posterior inferior cerebellar artery is blocked and is characterized by a combined lesion of the IX, X nerves, the nucleus of the descending root of the V pair, the vestibular nuclei, the sympathetic tract, the inferior cerebellar peduncle, the spinocerebellar and spinothalamic pathways.

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brainstem syndrome includes three levels of lesions - mesencephalic, pontine and bulbar, the anatomical and physiological features of which determine the clinical manifestations of their lesions.

mesencephalic or mesencephalic level of brain stem damage characterized by a disorder of pupillary reactions, paralysis and paresis of individual muscles of the eye, a violation of friendly movements of the eyeballs upward, a violation of muscle tone, the appearance of convergent, rotatory and vertical nystagmus. With TBI, total damage to mesencephalic structures is not observed, because these injuries are not compatible with the life of the victim. Partial injuries usually occur, among which there are quadrigeminal, tegmental, peduncular syndromes and an alternating syndrome of damage to the half of the trunk.

Four hill syndrome includes upward gaze disorders, convergence disorders, pupillary reactions disorders, various forms of nystagmus (vertical, horizontal, diagonal, convergent, rotatory).

Tegmental or tegmental syndrome includes violations of the function of the oculomotor nerves, conduction disorders of sensitivity, muscle tone, coordinating disorders. With an increase in 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 defeat captures the nucleusV ,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 area of the trigeminal nerve, dysfunction of the facial, 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 impaired swallowing and articulation. They are combined with disorders of cardiac and respiratory functions, a decrease in blood pressure, the appearance of fascicular and fibrillar twitching of the muscles of the tongue. The 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, stem symptoms can be not only the result of a primary traumatic lesion of these formations, but also be a consequence of secondary injuries as a result of dislocations and wedging of stem structures.

Describing the semiotics of brain damage in TBI, it is especially necessary to note the peculiarities of the manifestationsdisengagement syndromewith DAP. They are most clearly detected when patients transition from a coma to a transient or vegetative state. In the absence of any signs of the functioning of the cerebral cortex, subcortical, stem 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 the syndromes of herniation, which often develop in victims with severe traumatic brain injury. Allocate transtentorial, temporal-tentorial, cerebellar-tentorial herniation, as well as the herniation under the falciform process and the herniation of the tonsils of the cerebellum.

Tentorial herniation occurs as a result of diffuse cerebral edema or with massive central, bilateral volumetric processes (hematomas, bruises). At the same time, the brain stem shifts caudally and symptoms develop, characterized by a violation of consciousness, the development of Cheyne-Stokes breathing, constriction of the pupils and the disappearance of their reaction to light, the appearance of a 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 bruises, unilateral supratentorial hematomas. In this case, a hernial herniation of the hook of the hippocampal gyrus occurs in 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 side of the lesion, dysfunction of the midbrain, the appearance of decerebrate rigidity and hyperventilation.

Cerebellar-tentorial herniation occurs with an increase in pressure in the subtentorial space (hematomas of the cerebellum and posterior cranial fossa). The brain stem is displaced in the rostral direction, which is accompanied by an acute impairment of consciousness, the development of the quadrigeminal syndrome.

Herniation of the tonsils of the cerebellum also occurs with volumetric processes in the posterior cranial fossa, which leads to the lowering and wedging of the cerebellar tonsils into the foramen magnum with the development of the medulla oblongata syndrome and frequent respiratory failure.

Wedging under the falciform process like the temporo-tentorial herniation, it occurs during lateral volumetric processes. The cingulate gyrus hernially protrudes under the falciform process, while the blood flow through the anterior cerebral artery is disturbed, occlusion of the foramen of Monro 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 younger age patient, the greater the difference. The study of the circumstances of the injury, premorbid history, the degree and duration of impaired consciousness, speech, mental functions, and much more is often not possible in children. Preservation of some pathological reflexes in children is often just an age norm, and the formation of psychomotor retardation 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 constructions and therapeutic tactics. in children with TBI.