Ischemic stroke in the left cm basin. Ischemic stroke in the VBB what is it. Similar works to - Ischemic stroke in the right MCA. Acute period. Atherothrombotic type. Central left-sided hemiparesis and hemihypesthesia. Central steam

The article discusses variants of speech disorders and variants of changes in the brain substance during a stroke in the basin of the left middle cerebral artery (MCA), Special attention devoted to aphasia and the variants of ischemic, usually cerebral infarction that cause it. The effectiveness of a set of classes to improve speech is analyzed.
Target research: to study the relationship between the volume of brain damage during a stroke in the left MCA and the degree of speech impairment.
Material and methods: The study included 356 people with suspected acute cerebrovascular accident (ACVA), who were examined by a neurologist and assessed for neurological deficit. Subsequently, if the patients’ condition allowed, they underwent speech therapy examination, in most cases, the day after admission to the hospital. All patients upon admission and most patients over time underwent a CT scan of the brain to confirm/exclude focal brain lesions and to clarify the extent of the lesion and the location of the pathological area.
results: according to the results of a CT scan of the brain, in 32 (25.8%) people out of 124, typical ischemic changes in the LMCA basin were revealed, of which in 7 - during a dynamic study, i.e., upon admission, the changes were not yet obvious (initial stage of stroke ). The main comparison groups were 3 groups of patients: with dysarthria (20 people), motor aphasia (13 people) and sensorimotor aphasia (23 people). The comparison criteria were the volume and nature of the lesion, the state of consciousness, and the timing of speech recovery.
conclusions: sensorimotor aphasia during ischemic cerebral infarction can occur both with damage to a large area around the Sylvian fissure of the dominant hemisphere, and with local damage in the area of one of the speech cortical centers or the white matter zone between them. Aphasic syndrome is more common with the cryptogenic variant of ischemic stroke; the sensorimotor variant of aphasia often occurs with repeated strokes. Taking into account the less pronounced dynamics of speech recovery in the group of patients with sensorimotor aphasia, it is important for these patients to continue speech therapy classes after discharge in order to achieve significant/complete recovery.

Keywords: stroke, left middle cerebral artery, aphasia, cerebral infarction, Broca's center, Wernicke's center, computed tomography, dysarthria.

For quotation: Kutkin D.V., Babanina E.A., Shevtsov Yu.A. Stroke in the basin of the left middle cerebral artery: correlation of speech disorders with a variant of cerebral infarction // RMJ. Medical Review. 2016. No. 26. S. 1747-1751

Left middle cerebral artery stroke: the correlation between speech disorders and cerebral infarction
Kut"kin D.V., Babanina E.A., Shevtsov Yu.A.

City Clinical Hospital No. 5, Barnaul

Background. The paper discusses speech disorders and variants of brain injury after left middle cerebral artery (MCA) stroke. Aphasia and underlying types of ischemic stroke are of special interest. The efficacy of speech therapy exercises is analyzed.
Aim. To study the correlation between brain injury severity after left MCA stroke and speech disorder degree.
Patients and methods. The study enrolled 356 patients with probable acute stroke who were examined by neurologist to assess the severity of neurological deficiency. If the condition was satisfactory, the patient was examined by speech therapist. At admission and dynamically, the patients underwent brain CT to verify or to exclude focal brain injury and to specify lesion size and localization.
Results. Brain CT revealed typical ischemic lesions in the left MCA perfusion area in 32 of 124 patients (25.8%). In 7 patients, these lesions were not obvious (early stroke). Three study groups were compared: patients with dysarthria (n = 20), motor aphasia (n = 13), or sensorimotor aphasia (n = 23). Comparison criteria were lesion size and localization, consciousness, and speech recovery time.
Conclusions. Sensorimotor aphasia after ischemic strokes may result from large lesions around Sylvian fissure as well as from local lesions of cortical speech center(s) or white matter between them. Aphasia is more common in cryptogenic ischemic strokes while sensorimotor aphasia is more common in recurrent strokes. Considering delayed speech recovery in sensorimotor aphasia group, these patients should proceed with the speech therapy after the discharge to achieve significant improvement or full speech recovery.

Key words: stroke, left middle cerebral artery, aphasia, cerebral infarction, Broca’s area, Wernicke’s area, computed tomography, dysarthria.

For citation: Kut"kin D.V., Babanina E.A., Shevtsov Yu.A. Left middle cerebral artery stroke: the correlation between speech disorders and cerebral infarction // RMJ. 2016. No. 26. P. 1747–1751.

The article discusses variants of speech disorders and variants of changes in the brain substance during a stroke in the basin of the left middle cerebral artery

Introduction

The clinical picture of left hemisphere strokes is characterized by speech disorders, among which the most significant is aphasia. Aphasia, which manifests itself acutely, indicates a circulatory disorder in the middle cerebral artery (MCA).
Speech processes, as a rule, show a significant degree of lateralization and in most people depend on the leading (dominant) hemisphere. It must be taken into account that in determining the dominant hemisphere responsible for speech, the approach that associates dominance only with right-handedness or left-handedness is simplified. The profile of the distribution of functions between the hemispheres is usually diverse, which is reflected in the degree of speech disorders and the possibilities of speech restoration. Many people exhibit only partial and unequal hemispheric dominance for different functions. While speech function in right-handers (≥90%) and most left-handers (>50%) is predominantly left-hemisphere dependent, there are three exceptions to this rule:
1. In less than 50% of left-handers, speech function is associated with the right hemisphere.
2. Anomic (amnestic) aphasia can occur with metabolic disorders and volumetric processes in the brain.
3. Aphasia may be associated with damage to the left thalamus.
The so-called crossed aphasia (aphasia caused by a cerebral lesion ipsilateral to the dominant hand) is currently attributed only to right-handers.
The area of the cortex responsible for speech function is located around the Sylvian and Rollandian fissures (SMA basin). Speech production is determined by four zones of this area, closely interconnected and located sequentially along the posteroanterior axis: Wernicke's area (posterior part of the superior temporal gyrus), angular gyrus, arcuate fasciculus (AF) and Broca's area (posterior part of the inferior frontal gyrus) (Fig. 12) .

The DP is a subcortical white matter fiber that connects Broca's area and Wernicke's area. There is evidence that in the left hemisphere DP occurs in 100% of cases, while in the right hemisphere - only in 55%. A number of researchers believe that there are several pathways involved in ensuring speech function. Other authors have received reliable confirmation only of the role of DP.
The pathogenesis of dysarthric speech disorders is determined by focal brain lesions of different locations. Complex forms of dysarthria are often observed.
Purpose of the study: to study the relationship between the volume of brain damage in stroke in the left MCA and the degree of speech impairment.

Material and methods

Over a 4-month period, 356 people were admitted to the emergency room of the City Hospital No. 5 with suspected stroke. All patients were examined by a neurologist in the hospital emergency room, the neurological deficit was assessed, and the presence/absence of speech disorders was reflected. Subsequently, if the patients’ condition allowed, they underwent speech therapy examination, in most cases, the day after admission to the hospital.
In 124 cases (every third patient) a preliminary diagnosis was made: stroke in the territory of the left middle cerebral artery (MCCA). This localization is most relevant when studying aphasia in patients with stroke.
All patients upon admission and most patients over time underwent a CT scan of the brain (Bright Speed 16 tomograph) to confirm/exclude focal brain lesions and clarify the extent of the lesion and the location of the pathological area.
According to the results of CT scan of the brain, 32 (25.8%) people out of 124 revealed typical ischemic changes in the LMCA basin, of which 7 were examined dynamically, i.e., upon admission, the changes were not yet obvious (initial stage of stroke). In 5 (4.0%) cases, hemorrhages were detected: left-sided medial hematomas and 1 case of subarachnoid hemorrhage (SAH). In 5 (4.0%) cases out of 124, infarctions of other localization (not in the LSMA basin) were detected (Table 1).

In 22 (17.7%) cases, according to CT scans of the brain, no infarction was detected in the area of interest, but the patients were hospitalized in the primary neurological department for patients with stroke, because they had significant neurological symptoms: atrophy of the brain substance , vascular focal changes, vascular leukoaraiosis, post-infarction cysts. This group also includes patients whose symptoms were caused by a transient ischemic attack.
In 60 (48.4%) cases, patients were not hospitalized. In most cases, stroke was not confirmed (there were no corresponding changes in CT data or in the neurological status). The number of patients not hospitalized in the acute stroke department also included patients with various types of atrophy of the brain substance in combination with significant neurological symptoms who refused the proposed hospitalization. A few patients were transferred to other hospitals because they were diagnosed with traumatic changes in the skull, brain, and tumors. Some patients were transferred to the on-duty neurology department of another hospital, for example, with a diagnosis of osteochondrosis.
64 patients hospitalized in the acute stroke department with stroke had speech impairments (Table 2). The detailed nature of speech disorders was determined by a speech therapist. In 20 (31.2%) cases, patients were diagnosed with dysarthria and absence of aphasia. In 2 cases, dysarthria was accompanied by dysphonia and dysphagia. Aphasia was detected in 44 (68.8%) people, of which in 7 cases it regressed by the time of consultation with a speech therapist the next day (in 2 cases, ischemic infarctions were detected with regression of aphasia). 3 people from the group with sensorimotor aphasia had severe dysarthria, 9 people had dysphagia. In 4 people from the group with motor aphasia, symptoms of dysarthria were also noted, in 1 case - severe dysarthria.

Two left-handed patients, who were initially suspected of having a stroke in the left MCA, were diagnosed with a stroke in the right MCA based on the results of a CT scan of the brain. In one case there was aphasia, which regressed within 24 hours, in another case dysarthria was noted.
In patients with dysarthria without aphasia, 4 types of dysarthria were identified: extrapyramidal (3 cases), afferent cortical (1 case), bulbar (1 case), pseudobulbar (8 cases), in other cases it was difficult to clearly determine the type of dysarthria, the manifestations were mild ( Table 3).
In groups of patients with dysarthria and regression of aphasia within 24 hours, there is a slight predominance of men.

Aphasia is observed with lesions of the cerebral cortex. In one case, the cause of aphasia was damage to the subcortical structures of the left hemisphere (medial intracerebral hematoma in the thalamus (Fig. 3). Speech disorders in such cases do not correspond to any of the main types of aphasia. Damage to the subcortical structures can be suspected in cases where amnestic aphasia is combined with dysarthria or aphasia - with hemiparesis. This patient had a right-sided hemiparesis of 4 points.

According to the TOAST classification of ischemic strokes in hospitalized patients with speech disorders, the following types of strokes were identified: in the group of patients with sensorimotor aphasia, the cryptogenic variant was the most common (47.6% of cases), in 2nd place was cardioembolic (28.6%), on 3rd – atherothrombotic (23.8%), the highest frequency of recurrent strokes was noted. In the group of patients with motor aphasia, the cryptogenic variant was also the most common, but in a smaller percentage of cases (41.7%), the atherothrombotic variant was in 2nd place (25.0%), and the cardioembolic variant was in 3rd place (16.7 %). In the group with dysarthria, the lacunar variant was most common (38.9% of cases), followed by cardioembolic and cryptogenic variants in 2nd place (22.2% of cases each).
In the group of patients with sensorimotor aphasia (23 people), in 39.1% (9 people) of cases in patients with sensorimotor aphasia, a large infarction was detected in the LCMA basin of the dominant hemisphere (Fig. 4–6). In 47.8% (11 people) of cases, a small infarction was detected (Fig. 7).

In 1 (4.3%) case, SAH was diagnosed due to rupture of the anterior communicating artery aneurysm, which was combined with intraventricular hemorrhage. In 2 (8.7%) cases, CT upon admission and over time did not reveal a reliable “fresh” area of infarction and post-infarction changes; the patients had significant atrophy of the brain substance, pronounced vascular leukoaraiosis, the clinical diagnosis in both cases was: “Repeated ischemic stroke in the LSMA basin."
The main comparison groups were 3 groups of patients: with dysarthria (20 people), motor aphasia (13 people) and sensorimotor aphasia (23 people). The comparison criteria were the volume and nature of the lesion, the state of consciousness, and the timing of speech recovery.
Table 4 shows in parentheses cases where the localization of pathological changes corresponds to functional anatomical zones (for sensorimotor aphasia - a large area around the Sylvian fissure; for motor aphasia - Broca's center; for dysarthria - local changes at the level of the midbrain, subcortical structures, cortex).

3 medial hematomas were identified on the left, 2 of which were thalamic (one was accompanied by motor aphasia, the other by dysarthria), 1 was thalamic with extension to the internal capsule (accompanied by dysarthria). In one case, in the group of patients with dysarthria, no pathological changes were detected; dysarthria regressed in less than 24 hours (Table 5).

There were no cases of stupor or coma.
It is often not possible to achieve a significant improvement in speech in patients with sensorimotor aphasia in a hospital (Table 6). Therefore, the speech therapist gives recommendations to each patient to continue classes at home.

results

Typical “fresh” ischemic changes, accompanied by aphasia, were identified in 30 people according to the results of CT scan of the brain. Half of them were diagnosed with sensorimotor aphasia, and in turn, only half of them had lesions that covered a large area around the Sylvian fissure. The localization of lesions did not always clearly correspond to the localization of cortical speech centers. In all 3 cases of medial hematomas, good results in speech restoration were noted (1 case of motor aphasia and 2 cases of dysarthria), and its significant improvement.
These data are confirmed in studies of aphasic syndrome conducted in the second half of the twentieth century, according to which patients who have survived a hemorrhagic stroke have the opportunity to restore speech and can count on a favorable prognosis. In dynamics, the degree of speech impairment, as a rule, decreased with complex treatment, including with the preservation of hemodynamically significant stenosis of the internal carotid artery (according to duplex ultrasound scanning), but in the absence of stroke recurrence or severe hemorrhagic transformation.

conclusions

1. Sensorimotor aphasia during ischemic cerebral infarction can occur both with damage to a large area around the Sylvian fissure of the dominant hemisphere, and with local damage in the area of one of the speech cortical centers or the area of white matter between them.
2. In patients with sensorimotor aphasia caused by stroke, stunned consciousness was noted more often than in other groups, despite the fact that the size of the confirmed infarction was not large in more than half of the cases.
3. The actual boundaries of speech centers appear to vary individually, so the accuracy of the expected anatomical lesion does not always match the degree of functional impairment (aphasia).
4. Full correspondence between the volume of the detected cerebral infarction and the volume of speech disorders was noted in the group of patients with sensorimotor aphasia, when the infarction was large.
5. Aphasic syndrome is more common with the cryptogenic variant of ischemic stroke; the sensorimotor variant of aphasia often occurs with repeated strokes.
6. Taking into account the less pronounced dynamics of speech recovery in the group of patients with sensorimotor aphasia, these patients should continue speech therapy classes after discharge in order to achieve significant/complete recovery.

Literature

1. Weiner G., Levitt L. Neurology. M., 1998. 256 p. .
2. Luria A.R. Higher cortical functions of humans and their disturbances in local brain lesions. M., 1962. 431 p. .
3. Sergienko E.A., Dozortseva A.V. Functional asymmetry of the brain // Functional interhemispheric asymmetry: Reader. M., 2004. pp. 219–257. .
4. Mikhailenko A.A., Litvinenko I.V., Anoshina E.A. and others. Crossed aphasia // Bulletin of the Russian Military Medical Academy. 2015. No. 4(52). pp. 228–235.
5. Glasser M.F., Rilling J.K. DTI tractography of the human brain's language pathways // Cerebral Cortex. 2008. Vol. 18(11). P. 2471–2482, doi: 10.1093/cercor/bhn011.
6. Saur D., Kreher B.W., Schnell S. et al. Ventral and dorsal pathways for language // PNAS USA. 2008. Vol. 105. P. 18035–18040.
7. Potapov A.A., Goryainov S.A., Zhukov V.Yu. and others. Long associative pathways of the white matter of the brain: a modern view from the position of neuroscience // Problems of neurosurgery. 2014. No. 78(5). pp. 66–77.
8. Marcina C., Zhu L.L., Norton A. et al. The degree of damage of the left arcuate beam is a predictor of the development of speech disorders // Stroke. 2011. Vol. 3. P. 193–199.
9. Vinarskaya E.N. Dysarthria. M., 2006. 141 p. .
10. Tonkonogiy I.M. Stroke and aphasia. L., 1968. 268 p. .
11. Stolyarova L.G. Aphasia in cerebral stroke. M., 1973. 218 p. .

PACIFIC STATE MEDICAL UNIVERSITY

Department of Psychiatry and Neurology

Head Department: Doctor of Medical Sciences, Professor Ulyanov I.G.

Teacher: Doctor of Medical Sciences, Professor Gulyaeva S. E.

DISEASE HISTORY

Clinical diagnosis

Related: Stage III hypertension

Completed by: student 402 gr. l/f

Barabash A.S.

Vladivostok

PASSPORT PART

Age: 48 years old

Nationality Russian

marital status: Not maried

Profession: driver

Location:

Date of admission to the clinic: 03/29/2015

COMPLAINTS

Weakness in the left hand and its numbness, as well as speech impairment.

ANAMNESlS MORBI:

On the evening of March 29, I began to feel numbness in my left arm, it became weak. Then he called a friend and noted that he could not express himself clearly, his speech was impaired. Then he called an ambulance team, which took him to the hospital of the Regional Clinical Hospital No. 1. The emergency doctor stated that the blood pressure was 260/120 mm. rt. st

ANAMNESIS VITAE:

Denies viral hepatitis, tuberculosis, sexually transmitted diseases and AIDS. There were no injuries, surgeries or head injuries. There is no allergic history. Increased blood pressure from age 35. Material and living conditions at various periods of life are satisfactory. Family history: the patient’s mother had hypertension and obesity. Bad habits: does not smoke. Denies alcohol abuse and drug use. There are no occupational hazards.

STATUS PRAESENS:

The condition is of moderate severity. Consciousness is clear. Body temperature is normal (36.6). He understands spoken speech. Has stage 4 obesity. Height 173 cm, weight 199 kg.

Skin, visible mucous membranes Pink colour, normal humidity; subcutaneous fat tissue is overdeveloped.

The occipital, cervical, parotid, anterior cervical, submandibular, supraclavicular, subclavian, axillary, inguinal and popliteal lymph nodes are not palpable.

Mild swelling is detected in the ankle joint. The degree of muscle development and their tone are normal. There is no trembling or tremor of individual muscles. Deformation of the bones and changes in the terminal phalanges of the fingers and toes are not detected. The configuration of the joints is normal, skin color and local temperatures in the joint area are also normal. There is no curvature of the spine.

Respiratory organs: The chest is hypersthenic. Type of breathing - mixed, respiratory rate - 21 per minute, breathing through the nose is free; silent, rhythmic, moderate depth. On palpation, the chest is painless, the right and left halves evenly participate in the act of breathing. The lower limit of the lungs is within normal limits. Percussion - clear pulmonary sound. Auscultation - vesicular breathing, no wheezing.

CVS organs:

Limits of relative dullness of the heart:

Left: in the 5th intercostal space on the midclavicular line

Right: in the 4th intercostal space 1 cm outward from the right edge of the sternum

Upper: on the 3rd rib, along the left parasternal line.

The heart configuration is normal. The width of the vascular bundle in the second intercostal space is 7 cm. Auscultation: heart sounds are clear, pure, rhythmic, accent of the second tone at the point of auscultation of the aortic valve. HR-95. Noises and pathological rhythms are not heard. No splitting or splitting of tones was detected. There is no pericardial friction rub. A/D 140/90 mm. rt. Art.

Digestive organs: The tongue is moist and clean. The mucous membrane of the inner surface of the lips, cheeks, and palate is pink and clean. The tonsils are not enlarged. Stomach correct form, normal size, soft and painless on palpation. Evenly participates in the act of breathing. There is no visible peristalsis of the stomach and intestines. The pancreas is painless on palpation, liver dimensions according to Kurlov:

)10cm

)9cm

)8 cm

The lower edge of the liver is at the level of the costal arch, rounded, soft, painless; the gallbladder is not palpable. The Shchetkin-Blumberg phenomenon is negative.

Organs of the genitourinary system: Upon examination, the lumbar region is not changed, the kidneys are not palpable; the tingling symptom is negative. The kidneys and bladder are not palpable. There are no dysuric disorders. Primary and secondary sexual characteristics are formed according to gender and age. There are no growth disturbances.

The thyroid gland is not visible and not palpable.

NEUROLOGICAL STATUS

Consciousness is clear. The patient is oriented in time, place and space. Dysarthria, with increased speech activity.

Meningeal symptoms: Kernig's symptoms are negative, upper, middle and lower Brudzinski's symptoms are negative. There is no stiffness of the neck muscles. Bechterew's syndrome and Gordon's syndrome are absent.

Cranial nerves.

I pair - olfactory nerves.

Smells are distinguished and differentiated from both nostrils.

II pair - optic nerve.

No decrease in visual acuity is noted. Color discrimination is not impaired. There is no loss of visual fields. The fundus was not examined.

ΙΙΙ, ΙV, VI pairs - oculomotor, trochlear, abducens nerves.

The palpebral fissures are symmetrical. The movements of the eyeballs are not limited in volume. The pupils are identical, of a regular round shape. The reaction of the pupils to light is direct and friendly. The reaction to convergence is well expressed. The pair is the trigeminal nerve.

Palpation of the trigeminal points is painless. Movement of the lower jaw is not limited. The tone of the masticatory and temporal muscles is the same. Corneal and conjunctival reflexes are alive, identical on both sides. II pair - facial nerve. The face at rest is asymmetrical, there is a drooping of the left corner of the mouth. The patient may close his eyes and frown, wrinkle his forehead, and bare his teeth (symmetrically). There is no lacrimation or dryness of the eyes. The pair is the vestibulocochlear nerve.

The hearing is not impaired, he understands whispered speech from 6 meters. Nystagmus is not observed., X pairs - glossopharyngeal and vagus nerves.

Swallowing and phonation were preserved. The soft palate is mobile. Palatine and pharyngeal reflexes are alive on both sides. The pair is an accessory nerve.

There are no muscle atrophies or deformities of the sternocleidomastoid muscle. Head turns are preserved.

XII pair - hypoglossal nerve.

Speech is not clear, the tongue deviates to the left. There are no atrophies or fibrillary twitches.

Motor sphere

When examining the muscles of the limbs and trunk, muscle atrophy is not determined, fibrillary and fascicular twitching is not detected. Movements of the upper limbs are possible in full:

· in the shoulder joint, movements are performed in the frontal plane - abduction up to 90 degrees and around the long axis of the shoulder - rotation inward and outward 20 degrees. In the sagittal plane - flexion up to 130, extension up to 35 degrees. The arm extended forward to a horizontal position can be retracted back to an angle of 120 degrees and brought towards the opposite arm (towards the midline of the body) to an angle of 30 degrees.

· At the elbow joint, the forearm is flexed to an angle of 140 degrees.

· In the wrist joint, movements are made towards the palmar surface - palmar flexion of the hand up to 50 degrees, towards the rear - dorsiflexion (or dorsal extension) up to 50 degrees, deviation of the hand to the radial side (abduction) - 15 degrees and ulnar (adduction) - 35 degrees . Prosupination movements of the hand (turning inward and outward) together with the forearm are performed within 80 degrees in either direction.

No gear, jackknife, or plastic hypertonicity phenomena were detected. Strength in the muscles of the shoulder, forearm, hand and fingers of the right hand is 5 points, of the left hand - 4 points. Movements of the lower extremities are possible in full:

· In the hip joint, flexion-extension movements are performed from the sagittal plane: flexion up to 120 degrees, extension up to 10 degrees. In the frontal plane, abduction up to 30 degrees and adduction up to 30 degrees are performed. Rotational movements are determined in the position of full extension of the hip or when it is flexed at the hip joint at an angle of 90 degrees.

· The range of these movements occurs within 45 degrees in one direction (internal rotation) and the other (external rotation). Further movements in the hip joint are possible, but they are performed with the pelvis.

· In the ankle joint: plantar flexion up to 45 degrees, dorsiflexion (extension) up to 25 degrees. Adduction and abduction of the forefoot within 30 degrees, carried out through movement in small joints.

The strength of the muscles of the left thigh, lower leg and foot is 4 points, the right thigh, lower leg and foot is 5 points. The pace of movement is sufficient.

Bare's test: upper and lower are positive on the left.

Reflex sphere

Deep reflexes from hands:

flexion-elbow (C 5-C6) - yes, alive, stronger on the left

wrist (C 5-C8) - present, alive, stronger on the left

extensor elbow - yes, alive, stronger on the left

upper (D 7-D8) - yes, lowered on the left

middle (D9 - D10) - yes, reduced on the left

lower (D11-D12) - yes, lowered on the left

Deep reflexes from the legs:

knee (L 3- L4) - yes, alive, stronger on the left

Achilles (L5 - S1) - yes, alive, stronger on the left

Pathological reflexes of oral automatism are absent.

Pathological foot reflexes:

Babinski's sign(with line irritation of the sole, reflex extension of the fingers) negative

Rossolimo's symptom(reflex flexion of fingers II - V as a result of a short blow to their tips with a hammer) negative

Bekhterev-Mendel's sign(flexion of the II - V fingers when tapping with a hammer on the anterior outer surface of the dorsum of the foot) negative

Zhukovsky's symptom(plantar flexion of fingers II - V when tapping with a hammer on the sole under the fingers) negative.

Oppenheim's sign(as a result of pressing the pad of the thumb along the anterior surface of the tibia from top to bottom, a reflex extension of the thumb is observed) negative.

Gordon's sign(as a result of hand compression of the mass of the calf muscle, a reflex extension of the thumb is observed) negative.

Poussep's sign(abduction of the fifth finger with line irritation of the outer edge of the foot), negative.

Coordination area

Gait is not impaired.

Static tests:

Romberg position - the patient is stable.

Dynamic tests:

Finger-nose test: performs correctly.

Heel-knee test: performed correctly

Sensitive Sphere

Hypoesthesia in left limbs.

Functions of the pelvic organs

The function is not affected.

Higher cortical functions

Cognitive functions preserved

DATA OF ADDITIONAL RESEARCH METHODS

1.General urine analysis:

red blood cells +++ 250

bilirubin-

urea+ 16

protein ++ 1g

density 1.025

leukocytes + 25

2.Urinalysis according to Nechiporenko: leukocytes - 18,000, erythrocytes - 82,000.

3.No helminth eggs were found.

Blood glucose 10.1 mmol/l
Blood chemistry:

Albumin 46.8 g/l

Total protein 81g/l

Cholesterol 6.8 mmol/l

Triglycerides 1.44 mmol/l

Urea 6.8 mmol/l

Total bilirubin 10.3 µmol/l

Direct bilirubin 3.4 µmol/l

SASS: PTT-19.1 sec, fibrinogen 2.8 g/l, APTT-31.2 sec, INR-1.54, RFMK-
EMF is negative.
Antibodies to the HIV virus - not detected
ECG: Sinus rhythm 106, blockade of the anterior-left branch of the left bundle of His. Diffuse changes in the myocardium of the left ventricle.
Ultrasound of the abdominal organs and kidneys: pathological ECHO signs of steatohepatosis, pancreatic lipomatosis.
Ultrasound of brachiocephalic vessels:

In PSMA there is increased peripheral resistance. CPP on the right SMA is 80 mm. rt. Art., left SMA-106 mm. rt. Art. AD-198/119 mm. rt. Art.

SYNDROME DIAGNOSIS

1. Central paresis of the VII and XII pairs of the cranial nerve on the left:

· Drooping of the left corner of the mouth

· Dysarthria

· Tongue deviation to the left

Central left hemiparesis

· Strength in the muscles of the shoulder, forearm, hand and fingers of the left hand - 4 points. The strength of the muscles of the left thigh, lower leg and foot is 4 points.

· Deep reflexes from the hands are preserved S>D

· Abdominal: upper, middle, lower - reduced S>D

· Deep reflexes from the legs, knees, Achilles - preserved S>D

Sensory impairment in the form of hypoesthesia in the left extremities.

Movement disorders in the form of central left-sided hemiparesis indicate damage to the pyramidal tract, which begins in the right hemisphere in the neurons of the anterior central gyrus, then it goes to the internal capsule (anterior two-thirds of the posterior thigh), then it passes through the middle part of the cerebral peduncles, descending through the base of the pons and in the lower part of the medulla oblongata passes to the opposite side and approaches the anterior horns.

Central paresis of the VII and XII pairs of the cranial nerves indicates a unilateral lesion of the corticonuclear pathway passing in the knee of the internal capsule, in the middle part of the cerebral peduncles. The path crosses when approaching the cores.

Sensory disorders in the form of left-sided hemihypesthesia.

Pathways of superficial sensitivity (pain, temperature and partially tactile). The first neurons for all types of sensitivity lie in the spinal ganglia. The fibers from them, through the dorsal roots, enter the dorsal horns of the spinal cord of the same side, where the second neuron is located, then the fibers pass through the anterior commissure to the opposite side, obliquely rising 2-3 segments higher, and as part of the anterior sections of the lateral cords of the spinal cord they are directed upward , ending in the lower part of the external nucleus of the visual thalamus. This pathway is called the lateral spinothalamic tract.

The third neuron starts from the cells of the ventral lateral nucleus of the thalamus optica, forming the thalamocortical pathway. Through the posterior third of the posterior leg of the internal capsule and then as part of the corona radiata, it is directed to the projection sensitive zone - the posterior central gyrus, to the cortex of the superior parietal region.

Pathways of deep sensitivity (muscular-articular sense, vibration, and also partially tactile). Entering the spinal cord through the dorsal roots, the central fibers of the spinal ganglion cells (1 neuron) do not enter the dorsal horns, but are directed to the dorsal cords, in which they are located on the side of the same name. Fibers coming from the underlying sections (lower limbs) are located more medially, forming a thin bundle, or Gaulle's bundle (fasciculus gracilis). Fibers carrying irritations from the proprioceptors of the upper extremities occupy the outer part of the posterior funiculi, forming a wedge-shaped bundle, or Burdach's bundle (fasciculus cuneatum). Since fibers from the upper limbs pass through the sphenoid fasciculus, this path is mainly formed at the level of the cervical and upper thoracic segments of the spinal cord.

As part of thin and wedge-shaped bundles, the fibers reach the medulla oblongata, ending in the nuclei of the posterior cords (nucl. fasciculi gracilis et fasciculi cuneati), where the second neurons of the deep sensitivity pathways begin, forming the bulbothalamic tract.

The pathways of deep sensitivity cross at the level of the medulla oblongata, forming a medial loop (lemniscus medialis), to which, at the level of the anterior sections of the pons, fibers of the spinothalamic tract and fibers coming from the sensory nuclei of the cranial nerves join. As a result, conductors of all types of sensitivity coming from the opposite half of the body are concentrated in the medial loop. Conductors of deep sensitivity enter the ventral lateral nucleus of the thalamus opticus, where the third neuron begins. From the visual thalamus, as part of the thalamocortical pathway of deep sensitivity, through the posterior section of the posterior limb of the internal capsule they come to the posterior central gyrus of the cerebral cortex, the superior parietal lobule and partly to some other sections.

ETIOLOGICAL DIAGNOSIS

Central paresis of the VII and XII pairs of the cranial nerve, motor disorders in the form of central left-sided hemiparesis, sensory disorders in the form of left-sided hemianaesthesia indicate a unilateral location of the focus in the right hemisphere. In combination with elevated cholesterol levels (6.8 mmol/l), arterial hypertension and metabolic syndrome, neurological syndromes may indicate a heart attack in the right middle cerebral artery, due to the formation of blood clots at the site of an atherosclerotic plaque.

CLINICAL DIAGNOSIS

Basic: Ischemic stroke in the basin of the right MCA on March 29, 2015. Acute period. Atherothrombotic type. Central left-sided hemiparesis and hemihypesthesia. Central paresis of the VII and XII pairs of the cranial nerves on the left.

Concomitant: Stage III hypertension.

RATIONALE FOR CLINICAL DIAGNOSIS

Clinical diagnosis was made based on:

Complaint: Weakness in the left hand and its numbness, as well as speech impairment. PRAESENS: 4th degree obesity.

Neurological status: central paresis of the VII and XII pairs of the cranial nerve on the left, motor disorders in the form of central left-sided hemiparesis, sensory disorders in the form of left-sided hemianaesthesia. Absence of meningeal symptoms and headache.

Additional research methods: cholesterol 6.8 mmol/l, blood sugar 10.1 mmol/l, ultrasound of brachiocephalic vessels: Increased peripheral resistance is noted in PSMA. CPP on the right SMA is 80 mm. rt. Art., left SMA-106 mm. rt. Art. AD-198/119 mm. rt. Art.

The leading clinical syndromes in this patient are central paresis of the VII pair of cranial nerves, motor disorders in the form of central left-sided hemiparesis, sensory disorders in the form of left-sided hemianaesthesia.

Thus, taking into account all of the above factors, syndromes and the slow onset of the disease, it can be argued that the patient has an ischemic stroke in the right MCA, of the atherothrombotic type.

DIFFERENTIAL DIAGNOSIS

neurological diagnosis stroke treatment

Due to various treatment tactics for cerebral hemorrhage and cerebral infarction, the differential diagnosis of these diseases is great importance. Classic signs hemorrhagic stroke are the sudden, apoplectiform development of the disease, loss of consciousness and the immediate onset of neurological symptoms (usually paralysis). Cerebral infarction is characterized by a period of precursors, gradual dysfunction, and preservation of consciousness at the onset of the disease. However, the disease does not always follow this classic pattern. In some cases, hemorrhage is not initially accompanied by loss of consciousness and neurological symptoms increase over time. Even more often there is an atypical course of ischemic stroke, which can begin extremely acutely, with immediate loss of other brain functions. Therefore, to diagnose the type of stroke, it is also necessary to take into account other signs. Cerebral hemorrhage is characterized by a history of arterial hypertension with hypertensive crises. Ischemic stroke is preceded by heart disease, often accompanied by cardiac arrhythmias; there may be a history of myocardial infarction. The onset of the disease with hemorrhage can be sudden, during vigorous activity, during emotional or physical stress. Cerebral infarction often begins during sleep or during rest. Cerebral, meningeal and autonomic symptoms are more pronounced in hemorrhagic stroke. The addition of focal symptoms, signs indicating displacement and compression of the brain stem (oculomotor disorders, disturbances in muscle tone, breathing, cardiac activity) also more often indicates a cerebral hemorrhage. High blood pressure, satisfactory heart activity, and a tense, often slow pulse are characteristic of a hemorrhagic stroke. Ischemic stroke usually occurs with normal or low blood pressure, heart sounds are muffled, the pulse is insufficiently filled, arrhythmia is often observed, and there are frequent cases of impaired peripheral circulation in the extremities.

Also, differential diagnosis is carried out with other diseases manifested by the rapid development of neurological disorders. X-ray CT or MRI of the head can exclude many diseases (tumor, intracerebral hemorrhage, and others), which are sometimes clinically indistinguishable from a stroke and account for almost 5% of cases of sudden onset of symptoms of focal brain damage.

Dysmetabolic encephalopathies due to hypoglycemia, hyperglycemia, hypoxia, uremia, hyponatremia or other disorders usually manifest as impaired consciousness with minimal focal neurological symptoms (hyperreflexia, tone changes, Babinski's sign), but are sometimes accompanied by severe focal disorders (hemiparesis, aphasia) resembling a stroke. In their diagnosis, anamnestic data and the results of biochemical studies are of great importance, revealing corresponding abnormalities in the blood plasma and the absence of changes on CT or MRI of the head characteristic of a stroke. Alcoholic or, less commonly, nutritional Wernicke-Korsakoff encephalopathy may resemble a stroke in cases of rapid development of diplopia, ataxia, and confusion. The diagnosis of encephalopathy is confirmed by anamnestic data on alcohol abuse or nutritional disorders with thiamine deficiency, the presence in many cases of Korsakoff amnestic syndrome and polyneuropathy, changes in MRI of the head in the area of the Sylvian aqueduct and medial nuclei of the thalamus, regression of symptoms during treatment with thiamine.

Traumatic brain injury can resemble and be combined with a stroke. In cases of amnesia for trauma and no external signs of head injury, traumatic intracranial hemorrhage or brain contusion is often regarded as a stroke. In such cases, clarification of the medical history and the results of CT or MRI of the head (if they are not available, radiography of the skull, echoencephaloscopy and lumbar puncture reveal the traumatic genesis of the disease.

In patients with epilepsy, seizures sometimes lead to disturbances of consciousness and post-seizure neurological disorders, such as hemiparesis (Tod's palsy), which can be mistakenly regarded as an ischemic stroke. In these cases, it is of great importance to clarify the anamnestic data on previous seizures and the results of an EEG, CT or MRI of the head. Patients who have suffered a stroke may develop epileptic seizures that occur after a stroke, accompanied by worsening neurological deficits, which can be regarded as a recurrent stroke. In such cases, only repeated CT or MRI of the head, showing the absence of new changes in the brain substance, can rule out a stroke.

Patients with migraine may rarely develop migraine stroke, which usually manifests as homonymous hemionopsia. More often, patients with migraine develop “ordinary” strokes, and sometimes an attack of migraine pain occurs immediately before or after the development of a stroke, but upon examination a “normal”, for example, atherothrombotic stroke is revealed. One of the rare forms of migraine - basilar migraine - is manifested by blurred vision, dizziness, ataxia, bilateral paresthesia in the limbs, mouth and tongue, which resembles an ischemic stroke in the vertebrobasilar system. At at a young age patients, the absence of risk factors for stroke and the presence of previous migraine attacks, the diagnosis of stroke is unlikely, but an MRI of the head is necessary to exclude it.

TREATMENT PLAN

Mode - ward

Diet - No. 9

Basic principles of therapy:

) Normalization of blood pressure (hypo- or hypertensive drugs, depending on the initial blood pressure). The patient needs to reduce blood pressure: beta blockers (atenolol), ACE inhibitors (captopril, enalapril), Ca channel blockers (amlodipine). Enalapril 5 - 10 mg, orally or sublingually, 1.25 mg, IV slowly over 5 minutes;

) Correction of water-electrolyte balance and acid-base status;

) Prevention of pneumonia (breathing exercises (deep breathing) and early activation of the patient);

Special treatment for ischemic stroke includes: restoring blood flow in the affected area and maintaining normal brain function. To restore blood flow in the affected area: antiplatelet agents (acetylsalicylic acid, pentoxifylline) - acetylsalicylic acid from 80 to 325 mg/day; anticoagulants - sodium heparin under the skin of the abdomen, 5000 units every 4-6 hours for 7-14 days under the control of blood clotting time; vasoactive agents (cavinton, vinpocetine, nimodipine) - nimodipine 4-10 mg intravenously through an infusion pump slowly (at a rate of 1-2 mg/h) under blood pressure control 2 times a day for 7-10 days, angioprotectors - ascorutin 200 mg /day

For normal brain function: vitamin E, glycine, ascorbic acid, piracetam.

Piracetam 4-12 g/day. intravenous drip for 10-15 days. Glicini up to 1 g per day under the tongue.

Tab.Aspirini ¼ for the night.

Physiotherapy: phototherapy, laser therapy.

FORECAST

The greatest severity of the condition in patients with ischemic stroke is observed in the first 10 days of the disease, then a period of improvement is noted when the patient’s severity of symptoms begins to decrease. However, the pace of recovery may vary. With good and rapid development of collateral circulation, it is possible to restore function on the first day of a stroke, but more often after a few days. Mortality reaches 20-25%. In the case of this patient, the prognosis is favorable.

LITERATURE

1. Geltser, B.I.. Propaedeutics of internal diseases. General clinical research and semiotics: Lectures for students and beginning doctors / B.N. Geltser, E. F. Semisotova.-Vladivostok: Dalnauka, 2001. -420 s.

Gusev G.S. neurology and neurosurgery / E.I. Gusev, G.S. Burd, A.N. Konovalov.- St. Petersburg: Medicine, 2000.-347 p.

Computer program “Cito! Analyzes"

Kulganov, Yu.V. Case history diagram / Yu.V. Kulganov, G.I. Bykova.-Vladivostok, 1996 -35 p.

Mikhailenko A.A. Topical diagnostics in neurology/ A.A. Mikhailenko.-SPb.: Hippocrates, 2000.-264 p.

Fedotov, P.I. Atlas of photo illustrations for physical methods clinical trial internal organs normal and pathological human / P.I. Fedotov, N.A. Korosteleva.-Vladivostok: Far Eastern Book Publishing House, 1976 -261 p.

Kharkevich, D.A. Pharmacology: textbook / D.A. Kharkevich.-M.: GEOTAR-Media, 2006 - 736 p.

Similar works to - Ischemic stroke in the right MCA. Acute period. Atherothrombotic type. Central left-sided hemiparesis and hemihypesthesia. Central paresis of VII and XII pairs of cranial nerves on the left

Weakness in the right hand

Marked limitation of active movements

Contact with the patient is difficult due to aphasic disorders and anisognosia.

There are no complaints from other bodies or systems.

05/05/11 - for the first time, blood pressure (BP) increased to 160/100 mm. rt. Art., blood pressure was not previously controlled. I didn't ask for help.

05/10/2011 - against the background of a hypertensive crisis (180/110), an ischemic stroke developed in the basin of the left middle cerebral artery with deep right-sided hemiparesis to the point of plegia in the arm, elements of sensory-motor aphasia. She was hospitalized by the ambulance team to a district hospital.

20.g. - MRI showed signs of acute ischemic stroke in the LSMA basin, obstructive hydrocephalus with a block at the level of the cerebral aqueduct, which was a consequence of a previous heart attack in the LSMA basin.

05/21/2011 - examined by a neurosurgeon - does not require neurosurgical correction.

August 2011 – was treated at the City Hospital. She was discharged with some improvement.

01/14/20112 - for treatment and additional examination, she was sent to the Central Clinical Hospital of Uzbekistan.

Acute rheumatic fever at age 10 (June 1993)

Viral hepatitis, tuberculosis, sexually transmitted diseases – denies

Infections suffered in childhood - denies

Other past illnesses: bronchitis, pneumonia (2010)

Hereditary diseases have not been established

Allergy history is not burdened

No blood transfusions were performed.

Medicinal history is not burdensome.

General condition – moderate severity

The skin is clean and of normal color.

The heart sounds are rhythmic, the accent of the second tone is on the aorta. Blood pressure 135/80 mm. rt. Art. Heart rate 78/min

Auscultation of vesicular breathing in the lungs, no wheezing

Palpation of the abdomen is soft and painless. Liver at the edge of the costal arch

Physiological effects – without any peculiarities

No peripheral edema

Controls stool and urination

The effleurage symptom is negative on both sides.

Meningeal symptom complex is negative

Palpebral fissures and pupils D=S, convergent strabismus due to the left eye. Full movement of the eyeballs. The reaction of the pupils to light is of average vivacity. Installation nystagmus

Central paresis of facial muscles on the right

The tongue is slightly deviated to the left. The pharyngeal reflex is preserved. Elements of sensory aphasia

Muscle tone in the right extremities is increased according to the spastic type. There is a moderate increase in muscle tone of the spastic type in the left extremities. Muscle strength in the right extremities was reduced to 0-1 points in the arm, 1-2 points in the leg. Movements in the limbs are possible due to the proximal parts

Tendon and periosteal reflexes from the hands D>S, high, with an expanded zone of evocation; from the feet D>S, high, polykinetic. Pathological foot and hand phenomena on both sides

No convincing sensitivity disorders were identified

Emotionally labile. Dysphoria. Elements of anosognosia

Diagnosis on admission

Condition after an ischemic stroke in the LSMA pool with severe right-sided hemiparesis in the arm to the point of plegia, elements of sensory-motor aphasia, liquor-hypertensive syndrome.

Combined rheumatic mitral disease with predominant insufficiency.

Examination plan and results

Magnetic resonance imaging of the brain

Occlusive hydrocephalus was a consequence of an infarction in the basin of the left middle cerebral artery, as a consequence of prolonged ischemia - the formation of an adhesive process with a block at the level of the cerebral aqueduct.

Sclerotic changes in the walls of the aorta, the leaflets of the aortic and mitral valves. Prolapse of the anterior and posterior leaflets of the mitral valve, stage II. with regurgitation grade I-II. on the valve (formation of mitral insufficiency against the background of rheumatic changes in the mitral valve leaflets). Dilatation of the ascending aorta. Mild hypertrophy of the posterior wall of the left ventricle. An additional chord in the lumen of the left ventricle, hemodynamically not significant.

The rhythm is sinus. Correct. Horizontal position of the electrical axis. Signs of right atrial hypertrophy. Reduced repolarization processes in the apical-anterolateral region.

Doppler ultrasound of the carotid arteries

No hemodynamically significant disturbances in blood flow were detected in all segments of the carotid system on both sides.

Ultrasound examination of the abdominal organs

Diffuse changes in the parenchyma of the liver and pancreas without their enlargement. Cholesterosis of the gallbladder walls. Microurolithiasis. Nephroptosis on the right – stage I. Focal neoplasm of the right adrenal gland.

Focal and infiltrative changes in the lungs were not detected. Roots are structural. Not enlarged. The sinuses are free. The diaphragm is clearly defined. The heart is of normal shape and size. The aorta is not changed.

General blood analysis

Reactive thrombocytosis, leukocytosis, increased ESR

General urine analysis

Transient proteinuria caused by damage to the basement membrane.

Blood lipid spectrum

Hypercholesterolemia. Dyslipidemia: Type II-B

Blood chemistry

Hyperglycemia caused by ischemia in the area of projection of the left

middle cerebral artery.

Blood clotting indicators

Within the physiological norm.

Middle cerebral artery lesion

Dyslipidemia type II-B

Heart failure II B, FC III

Damage to the mitral valve with a predominance of stage I insufficiency

Ischemic stroke in the basin of the left middle cerebral artery (05/10/11). Late recovery period. Arterial hypertension degree III, stage III. Heart failure stage II, FC III. Atherosclerosis. Dyslipidemia type II-B. Reactive thrombocytosis.

Post-rheumatic mitral disease with a predominance of stage I insufficiency. Neoplasm in the adrenal gland.

Normalization of lifestyle, rehabilitation measures

Motor rehabilitation (full or partial restoration): range of motion, strength and dexterity in paretic limbs, balance function in ataxia, self-care skills

Speech rehabilitation: classes with a speech therapist-aphasiologist and neuropsychologist, exercises to restore writing, reading and counting, which are usually impaired in aphasia (and preserved in dysarthria), using “homework” for the second half of the day

Psychological and social readaptation: creating a healthy climate in the family, developing an optimistic and at the same time realistic outlook on life, participating in cultural events within the social circle

Taking antidepressants: selective serotonin reuptake inhibitors.

Training in rehabilitation centers for stroke patients

Cardiomagnyl 75 mg/day

Instantaneous mortality in ischemic stroke is 20%

70% of patients remain with persistent defects in motor and sensory areas

In the absence of therapy, the relapse rate is 10% per year

Antiplatelet drugs reduce the risk of recurrent stroke by 20%

Statins and antihypertensive therapy (primarily ACE inhibitors!) reduce the risk of relapse by 35%

50% of patients retain the ability to self-care

Up to 80% of patients regain the ability to walk

Almost 50% of patients who have suffered an ischemic stroke die from myocardial infarction

Rehabilitation therapy (physical education, classes with a speech therapist, occupational therapy) is effective in 90% of rehabilitation cases

Favorable for life

For work – unfavorable, disability.

Ischemic stroke is a weather-related disease, the risk of which increases sharply in unfavorable weather.

Timokhin A.V., Zaritskaya N.A., Ph.D. Lebedinets D.V., associate professor Lysenko N.V., prof. Yabluchansky N. I.

Kharkov National University named after. V.N. Karazin

Acute cerebrovascular accident in the left MCA of ischemic type. Right-sided hemiparesis. Stage III hypertension, risk IV. Obesity II degree

Ischemic stroke - a complication of hypertension and atherosclerosis - is caused by diseases of the heart valve apparatus, myocardial infarction, congenital anomalies of cerebral vessels, hemorrhagic syndromes and arteritis. Symptomatic therapy.

Send your good work in the knowledge base is simple. Use the form below

Students, graduate students, young scientists who use the knowledge base in their studies and work will be very grateful to you.

Altai State Medical University

Head Department: Professor Schumacher G.I.

Teacher: assistant Gorbunova N.I.

Curator: student 408 gr. Tashtamyshev V.N.

Clinical history

Patient: ______________________

Barnaul-2008

FULL NAME. _________________________

Age: 49 years old. (born November 19, 1958)

Location: ________________________________________

Family status: Married. Husband _________________________

Place of work: ___________________________________________

Date of admission to the hospital: 03/13/2008

Date of supervision from 03/17/08. to 03/20/08.

Clinical diagnosis: Acute cerebrovascular accident in the left MCA of ischemic type. Right-sided hemiparesis and hemihypoanesthesia. Motor aphasia. Stage III hypertension, risk IV. Obesity II degree.

COMPLAINTS

- Difficulty speaking, during excitement, cannot pronounce words clearly and clearly.

For headaches in the temporal and parieto-occipital regions, aggravated in evening time, and also after sleep. The pain is acute and occurs in the left temporal region with subsequent transition to the occipital and the opposite temporal region.

For periodic dizziness, tinnitus, nausea, vomiting,

To reduce superficial sensitivity in the right half of the body.

Glushkova Elena Gavrilovna, born on November 11, 1958 in the Zalesovsky district of the Altai Territory in the village of Cheryomushkino. She grew and developed normally, mentally and physical development did not lag behind her peers. Graduated from 10th grade of secondary school. In 1976, she trained as a machine operator, where she worked for 3 years. From 1979 to 2003 she worked as a merchandiser. In 2003, she became the director of a rural cultural center, where she works to this day.

Epidemic history: tuberculosis, viral hepatitis, sexually transmitted diseases denies. She was not in contact with infectious patients.

Bad habits: No

Allergy history: No.

Operations: caesarean section in 1990.

Blood transfusion in 1982 during childbirth.

The general condition of the patient is moderate. Consciousness is clear, position in bed is active. The skin is warm, moist, turgor is preserved. The oral mucosa and conjunctiva are pink. Peripheral lymph nodes are not enlarged. Supra-subclavian, ulnar, axillary, and inguinal lymph nodes are not palpable. The patient's behavior is normal, answers questions adequately, and makes contact easily. The physique is correct, the constitution is normosthenic, high nutrition. There is no edema or subcutaneous emphysema. Height 144cm, weight 72kg. There are no scars or defects in the head area. Type of hair growth female type. Hair is dark. No asymmetry of the chest or changes in the shape of the joints were detected. Full range of mobility in the cervical, thoracic and lumbar regions. Movements in the joints are preserved. Muscular system: on the left half of the body - muscles are toned, there are no atrophies, pain on palpation. On the right: hypotonia, hyposthesia. The thyroid gland is not enlarged, painless, and not fused with the surrounding tissues.

Nasal breathing is free. The chest is of regular shape; both halves are symmetrical and participate equally in the act of breathing. Breathing is vesicular, no wheezing. RR=16/min. Palpation: the chest is painless, resistance is good, vocal tremor is carried out with equal force. With comparative percussion, a clear pulmonary sound is heard at all points. With topographic percussion: the height of the apexes of the lungs is 4.5 cm on the right and left, the width of the Krenig fields on the left and right is 5 cm. The boundaries of the lungs are within normal limits.

Auscultation: at the junction of the manubrium of the sternum with the body, on the thyroid cartilage, on the spinous processes of 1-3 cervical vertebrae, bronchial breathing is clearly audible, and at standard points of comparative and topographic auscultation - vesicular breathing. No pathologies were identified. There are no wheezes, noises or crepitations.

On palpation no seals along the veins, no pain was detected. The pulse in both arms is 65 beats per minute, coincides with the rhythm of heart contractions, the rhythm is correct, normal filling, synchronous in both arms, there is no pulse deficit. The arterioles of the nail phalanges do not pulsate. Blood pressure in both arms is 150/100 mm. rt. pillar During auscultation, sounds 1 and 2 are muffled at all points of auscultation, the accent of the second tone is above the aorta in the second m/r on the right. No pathologies of the valvular apparatus of the heart were found. Noises are also not audible. During auscultation of the abdominal aorta, no stenotic murmur is heard. The pulse is large, full, symmetrical, rhythmic, not tense.

The apical impulse is in the 6th m/r, 1-1.5 cm outward from the midclavicular line.

Percussion revealed an enlarged left ventricle and relative and absolute dullness of the heart.

When examining the oral cavity, the tongue is moist, pink, without cracks or ulcerations, not covered with plaque, and the papillae are not hypertrophied.

No dentures. The oral mucosa is without features. The pharynx is not hyperemic, the tonsils are not enlarged. The act of swallowing is not impaired. The abdomen is of the correct shape, symmetrical, not swollen, actively participates in the act of breathing, there are no visible pulsations, no visible peristalsis of the stomach and intestines. There is no bulge in the right hypochondrium.

Palpation. The temperature is the same in superficially symmetrical areas, the skin is moist. Subcutaneous fat is well expressed. The abdomen is soft, there are no discrepancies of the rectus abdominis muscles, hernial orifices, or protrusions. There is a scar after caesarean section. The Shchetkin-Blumberg symptom is negative. With deep palpation according to Obraztsov-Strazhesko, the sigmoid colon in the left iliac region is palpated in the form of a smooth, painless cord. The cecum could not be palpated. Other parts of the large intestine and stomach are not palpable. The pancreas and spleen are not identified. The lower edge of the liver is located along the edge of the costal arch, the contour is smooth, soft-elastic consistency, painless. The dimensions of the liver according to Kurlov are 9 / 8 / 7 cm. No free fluid was detected in the abdominal cavity using percussion and the fluctuation method. On auscultation there is a sound of intestinal peristalsis. The stool is regular, well formed, without pathological impurities, and of normal color.

When examining the lumbar region, no swelling or edema was detected. The kidneys and bladder are not palpable. Urination is not difficult, painless, once a day. Pasternatsky's symptom is negative on both sides.

The patient's consciousness is clear. Obsessions, no affects, no peculiarities of behavior. Fully oriented in space and time, speech is correct, slightly inhibited. Reacts adequately to external stimuli. There is a disturbance in sleep and wakefulness. There are no meningeal symptoms.

I pair - n.olfactorius The sense of smell is not impaired, there are no olfactory hallucinations.

II pair - n. opticus: vis 1.0/1.0, field of view

Ischemic stroke in the territory of the right middle cerebral artery

Ischemic stroke in the territory of the right middle cerebral artery has different case statistics, but it is worth noting that this kind of stroke can be the root cause of various symptoms. Not all patients can recognize many of the symptoms of this disease. Since, for example, acute gross motor deficits that arise, which are signs of strokes, may not appear or not be clearly expressed.

What are the features of the symptoms of this disease?

In the presence of an ischemic stroke in the territory of the right middle cerebral artery, it is possible to identify symptoms of lesions of the midbrain and cerebral hemisphere, depending on the location and conditions of collateral blood supply in the clinical pictures. Quite often you can find a combination of damage to the thalamus and the cerebral hemisphere or isolated infarctions of the thalamus. It should be noted that in most cases, the symptoms of the disease in patients can be combined. The most common symptoms include visual damage, neuropsychological damage, and hemiparesis.

What are the features of diagnosing ischemic stroke in the territory of the right middle cerebral artery?

It is worth noting that often computed tomography does not allow identifying any ischemic changes in the brain parenchyma for a certain moment after the onset of strokes, precisely the time that is very important as the beginning of the treatment of this type of disease.

Thanks to the use of magnetic resonance imaging, it becomes possible to more accurately determine the presence and nature of any ischemic changes in the main brain during strokes. After obtaining data from magnetic resonance imaging, it becomes possible to identify early ischemic changes. Today it has become possible to combine different modes, which makes it possible to determine more severe, subacute and congenital ischemic changes in the brain parenchyma.

What is the procedure for treating ischemic stroke in the territory of the right middle cerebral artery?

To begin with, it is worth noting that the healing process is quite long and requires patience on the part of patients. At the very beginning of the healing process, you should normalize your lifestyle and attend rehabilitation events. The motor rehabilitation process includes strength and dexterity in each limb, self-care skills, all of which can be fully or partially rehabilitated. The speech rehabilitation process includes every session with specialists, in particular with speech therapists and neuropsychologists, every exercise necessary to restore common reading or counting disorders. As for the psychological and social healing processes, a healthy climate should be created in families, participation in any cultural event within social circles.

Quite often, specialists in this field of activity prescribe their patients to use various kinds antidepressants, which are selected individually for each patient. Great attention should be paid to this, because using your own assumptions about taking antidepressants can only lead to various complications and side effects that can provoke undesirable consequences. That is why only the attending physician can prescribe the period of taking the drugs and the immediate dosage. The use of antiaggregates can reduce the risk of stroke recurrence, and in cases of no therapy, the disease may also return.

Clinical observations of a neurosurgeon, doctor of the highest category, candidate of medical sciences Evgeniy Evgenievich Zavalishin

This clinical example shows how dangerous the malignant course of ischemic stroke can look, the frequency of which reaches 25% of all ischemic strokes. This disease occurs as a result of the closure of the lumen of the vessel and the lack of blood supply in a large area of the brain.

Ischemic stroke in the right MCA, malignant course.

The presented operation is not a panacea, it is quite debatable, but in many cases (and in this case) a necessary operation. The purpose of this operation is to respond to a brain problem in time and create additional space for a swollen brain.

The brain is the most important integrative center, which concentrates all the control functions of the body, but reacts to any problems one-sidedly - with swelling, which is shown in these photographs.

Computed tomography 1 day from the onset of the disease

(lines indicate ischemic zones, arrows indicate extended thrombus in the vessel)

Intraoperative picture

(edematous brain, smoothed grooves, pale pink color)

Computed tomography after surgery

(a formed ischemic zone, the edematous substance of the brain does not infringe on the intact brain tissue, the arrows indicate the formed ischemic zone)

I do not undertake to discuss the ethical side of the issue of these photographs, but I want to convey to people the need for early prevention of stroke, a healthy and active lifestyle, healthy food and comprehensive preventive medical examinations.

Ischemic strokes in the middle cerebral artery basin

Most strokes occur in the middle cerebral artery. Homonymous hemianopsia is characteristic, indicating damage to the optic radiance. The eyeballs are turned towards the affected hemisphere11; on the opposite side there is weakness of the facial muscles of the lower half of the face and spastic hemiparesis (the arms suffer more than the legs). Muscle tone in paralyzed limbs may initially be reduced, but after a few days or weeks spasticity develops. Sometimes sensory and motor disturbances are limited to the contralateral arm and half of the face, while the leg and torso are almost unaffected. If the dominant hemisphere is damaged, motor and sensory aphasia is possible. When the parietal lobe of the non-dominant hemisphere is damaged, complex sensitivity disorders and perceptual disorders occur. Damage to the right hemisphere is often accompanied by confusion, and the left hemisphere is often accompanied by depression in the later stages of the disease.

Cerebral edema can cause narrowing and occlusion of one or both posterior cerebral arteries; the consequence of this is hemianopsia or cortical blindness.

When the cervical part of the internal carotid artery is occluded, blood enters the anterior cerebral artery through the anterior communicating artery from the opposite side, thereby preventing stroke in the frontal lobe and the medial surface of the hemisphere. Blood enters the posterior cerebral artery from the vertebrobasilar system. Therefore, when the internal carotid artery is occluded, a stroke usually develops in the territory of the middle cerebral artery, and not in the entire internal carotid artery.

Stenosis of the internal carotid artery can be suspected by weakening of the pulse in it. However, the result of palpation, like the result of auscultation (see above), must be interpreted with caution - what seems to the doctor to be a normal pulsation of the internal carotid artery, may in fact be a pulsation of the external one. Comparison of the pulse on the right and left carotid arteries helps in diagnosis: a significant weakening of the pulse on one side suggests occlusion of the common carotid artery of the same name. Occlusion of the internal carotid artery may be indicated by increased pulsation of the facial and superficial temporal arteries of the same side, since they are branches of the external carotid artery, into which all the blood from the common carotid artery begins to flow. However, this symptom is difficult to assess. A murmur in the orbital area may indicate stenosis of the internal carotid artery.

“Ischemic strokes in the middle cerebral artery basin” - an article from the Nervous Diseases section

Ischemic stroke

Ischemic stroke (cerebral infarction) is a clinical syndrome manifested by acute disruption of local brain functions, lasting more than a day, or leading to death during this period. Ischemic stroke may be caused by insufficient blood supply to a certain area of the brain due to decreased cerebral blood flow, thrombosis or embolism associated with vascular, cardiac or blood diseases.

Classification

There are different classifications of ischemic strokes, depending on the etiopathogenetic and clinical aspects, the localization of the infarction zone.

According to the rate of formation of neurological deficit and its duration

transient cerebrovascular accident (TCI) is a clinical syndrome represented by focal neurological and/or cerebral disorders, developing suddenly due to an acute disturbance of cerebral circulation.

According to the severity of the patients' condition

minor stroke - neurological symptoms are mild, regress within 3 weeks of the disease
ischemic stroke of moderate severity - without clinical signs of cerebral edema, without disturbance of consciousness, with a predominance of focal neurological symptoms in the clinic
severe stroke - with severe cerebral disorders, depression of consciousness, signs of cerebral edema, vegetative-trophic disorders, severe focal deficiency, often dislocation symptoms

On pathogenesis (Research Institute of Neurology of the Russian Academy of Medical Sciences, 2000)

atherothrombotic stroke (including arterio-arterial embolism)
cardioembolic stroke
hemodynamic stroke
lacunar stroke
stroke by type of hemorheological microocclusion

By location of cerebral infarction

In accordance with the topical characteristics of focal neurological symptoms, according to the affected arterial system: internal carotid artery; main artery and its distal branches; middle, anterior and posterior cerebral arteries.

Etiology and pathogenesis

The following are identified as local etiotropic factors of stroke:

atherosclerosis of the main and intracerebral arteries. Soft, loose atheromatous plaques become a source of embolism, while dense ones narrow the lumen of the arteries, limiting blood flow. A 60% reduction in cerebral blood flow is critical for the development of stroke.
thrombus formation. The main stages of thrombus formation: damage to the endothelium of the vascular wall, slowdown and turbulence of blood flow at the site of stenosis, increased aggregation of blood elements, fibrin coagulation and decreased local fibrinolysis.
Cardiac pathology is the cause of 30 to 60% of strokes. This pathology includes damage to the heart valves, left ventricular hypertrophy, blood clots in the heart cavity, arrhythmias, and myocardial ischemia.
degenerative and deforming changes in the cervical spine (osteochondrosis of the spine, deforming spondylosis, anomalies of the craniocerebral region), leading to compression of the vertebral arteries with the development of strokes in the vertebrobasilar region.
rare vascular pathology: Takayasu's disease, Moyamoya disease, infectious arteritis.

The systemic factors contributing to the development of ischemic stroke are:

disturbance of central hemodynamics:
- cardiac hypodynamic syndrome - manifested by impaired circulation, heart rhythm, decreased minute blood volume and stroke volume, which leads to a decrease in blood flow in the arterial system of the brain, disruption of the mechanisms of autoregulation of cerebral circulation and the formation of thrombotic stroke or the development of cerebral ischemia such as cerebrovascular insufficiency ( hemodynamic stroke).
- arterial hypertension - intensifies hemodynamics and leads to the development of arterio-arterial, cardiogenic embolisms, or the formation of small (lacunar, microcirculatory) strokes.
- arrhythmias are a factor in the development of arterio-arterial and cardiogenic embolisms. In combination with severe arterial hypertension, the risk of embolism is highest.
Other systemic factors include coagulopathies, erythrocytosis and polycythemia.

Depending on the etiopathogenetic factors, ischemic stroke is divided into atherothrombotic, cardioembolic, hemodynamic, lacunar and hemorheological microocclusion type stroke.

Atherothrombotic stroke (34%) usually occurs against the background of atherosclerosis of cerebral arteries of large or medium caliber. Atherosclerotic plaque narrows the lumen of the vessel and promotes thrombus formation. Possible arterio-arterial embolism. This type of stroke develops in stages, with an increase in symptoms over several hours or days, and often debuts during sleep. Often, atherothrombotic stroke is preceded by transient ischemic attacks. The size of the focus of ischemic damage varies.
Cardioembolic stroke (22%) occurs when a cerebral artery is completely or partially blocked by an embolus. The most common causes of stroke are cardiogenic embolism due to valvular heart disease, recurrent rheumatic and bacterial endocarditis, and other heart lesions that are accompanied by the formation of parietal thrombi in its cavities. Often, embolic stroke develops as a result of paroxysm of atrial fibrillation. The onset of cardioembolic stroke is usually sudden, while the patient is awake. At the onset of the disease, the neurological deficit is most pronounced. More often, a stroke is localized in the area of the blood supply of the middle cerebral artery, the size of the focus of ischemic damage is medium or large, and a hemorrhagic component is characteristic. There may be a history of thromboembolism in other organs.
Hemodynamic stroke (15%) is caused by hemodynamic factors - a decrease in blood pressure (physiological, for example during sleep; orthostatic, iatrogenic arterial hypotension, hypovolemia) or a drop in cardiac output (due to myocardial ischemia, severe bradycardia, etc.). The onset of a hemodynamic stroke can be sudden or gradual, while the patient is at rest or active. The sizes of infarctions vary; localization is usually in the area of adjacent blood supply (cortical, periventricular, etc.). Hemodynamic strokes occur against the background of pathology of extra- and/or intracranial arteries (atherosclerosis, septal artery stenosis, abnormalities of the cerebral vascular system).
Lacunar stroke (20%) is caused by damage to small perforating arteries. As a rule, it occurs against a background of high blood pressure, gradually, over several hours. Lacunar strokes are localized in the subcortical structures (subcortical nuclei, internal capsule, white matter of the semioval center, base of the bridge), the size of the lesions does not exceed 1.5 cm. There are no general cerebral and meningeal symptoms, there are characteristic focal symptoms (purely motor or purely sensory lacunar syndrome, atactic hemiparesis, dysarthria or monoparesis).
Stroke of the hemorheological microocclusion type (9%) occurs in the absence of any vascular or hematological disease of established etiology. The cause of stroke is pronounced hemorheological changes, disturbances in the hemostasis and fibrinolysis systems. Characterized by scant neurological symptoms in combination with significant hemorheological disorders.

The process of cerebral ischemia is dynamic and, as a rule, potentially reversible. The degree of ischemic damage depends on the depth and duration of the decrease in cerebral blood flow. When the level of cerebral blood flow is below 55 ml per 100 g of substance per minute, a primary reaction is noted, which is characterized by inhibition of protein synthesis in neurons - the “marginal zone of ischemia”. When cerebral blood flow is below 35 ml per 100 g/min. anaerobic glycolysis is activated. This zone of dynamic changes in metabolism, the so-called “ischemic penumbra” or “penumbra” (eng. penumbra). Along with the existing functional changes in brain structures, there are no morphological changes in the penumbra. The penumbra exists for 3-6 hours from the onset of the first clinical manifestations of cerebral ischemia. This period is the “therapeutic window” during which it is possible to limit the prevalence of infarction; During this period of time, therapeutic measures are most promising. Cell death in the penumbra area leads to expansion of the infarct area. The final formation of the infarction zone is completed after 48 - 56 hours. In the area of decreased cerebral blood flow below 20 ml per 100 g/min. a central zone of infarction is formed (the “core” of ischemia), which is formed in 6 - 8 minutes. In this zone, disturbances in energy metabolism are irreversible, with the development of necrosis of brain tissue. Cerebral ischemia leads to a series of interrelated pathobiochemical changes, called the “pathobiochemical cascade” or “ischemic cascade” (Gusev E.I. et al., 1997). According to Skvortsova V.I. (2000), its stages are:

decreased cerebral blood flow.
glutamate excitotoxicity (exciting mediators glutamate and aspartate have a cytotoxic effect).
intracellular accumulation of calcium.
activation of intracellular enzymes.
increased NO synthesis and development of oxidative stress.
expression of early response genes.
long-term consequences of ischemia (local inflammation reaction, microvascular disorders, damage to the blood-brain barrier).
apoptosis is genetically programmed cell death.

Ischemic processes in brain tissue are accompanied by cerebral edema. Cerebral edema develops a few minutes after the development of local ischemia; its severity directly depends on the size of the cerebral infarction. The triggering point for the development of edema is the penetration of water into the cells from the intercellular space due to a violation of the permeability of cell membranes. After this, extracellular (vasogenic) edema is added to the intracellular edema, which is caused by a violation of the blood-brain barrier with the accumulation of under-oxidized products formed during the process of anaerobic glycolysis in the damaged area. Intracellular and vasogenic edema lead to an increase in brain volume and intracranial hypertension, which causes dislocation syndrome (“superior” herniation - herniation of the basal parts of the temporal lobe into the notch of the cerebellar tentorium with entrapment of the midbrain, and "lower" herniation - herniation into the foramen magnum of the cerebellar tonsils with compression of the lower parts of the medulla oblongata - the most common cause of death in patients).

Clinical picture

The clinical picture of ischemic stroke consists of general cerebral and focal neurological symptoms.

General cerebral symptoms

General cerebral symptoms are characteristic of moderate and severe strokes. Characterized by disturbances of consciousness - stupor, drowsiness or agitation, short-term loss of consciousness is possible. A typical headache, which may be accompanied by nausea or vomiting, dizziness, pain in the eyeballs, aggravated by eye movement. Convulsive phenomena are observed less frequently. Possible vegetative symptoms: feeling of heat, sweating, palpitations, dry mouth.

Focal neurological symptoms

Against the background of general cerebral symptoms of stroke, focal symptoms of brain damage appear. The clinical picture is determined by which part of the brain is affected due to damage to the blood vessel supplying it.

Stroke in the basin of the left middle cerebral artery: the relationship between speech disorders and a variant of cerebral infarction

About the article

The article discusses variants of speech disorders and variants of changes in the brain substance during a stroke in the basin of the left middle cerebral artery (MCA), special attention is paid to aphasia and the variants of ischemic, usually cerebral infarction, that cause it. The effectiveness of a set of classes to improve speech is analyzed.

research: to study the relationship between the volume of brain damage during a stroke in the left MCA and the degree of speech impairment.

Material and methods: the study included 356 people with suspected acute cerebrovascular accident (ACVA), who were examined by a neurologist and assessed for neurological deficit. Subsequently, if the patients’ condition allowed, they underwent speech therapy examination, in most cases, the day after admission to the hospital. All patients upon admission and most patients over time underwent a CT scan of the brain to confirm/exclude focal brain lesions and to clarify the extent of the lesion and the location of the pathological area.

Results: according to the results of a CT scan of the brain, 32 (25.8%) people out of 124 revealed typical ischemic changes in the LMCA basin, of which 7 were diagnosed during a dynamic study, i.e., upon admission, the changes were not yet obvious (initial stage stroke). The main comparison groups were 3 groups of patients: with dysarthria (20 people), motor aphasia (13 people) and sensorimotor aphasia (23 people). The comparison criteria were the volume and nature of the lesion, the state of consciousness, and the timing of speech recovery.

Conclusions: sensorimotor aphasia in ischemic cerebral infarction can occur both with damage to a large area around the Sylvian fissure of the dominant hemisphere, and with local damage in the area of one of the speech cortical centers or the white matter zone between them. Aphasic syndrome is more common with the cryptogenic variant of ischemic stroke; the sensorimotor variant of aphasia often occurs with repeated strokes. Taking into account the less pronounced dynamics of speech recovery in the group of patients with sensorimotor aphasia, it is important for these patients to continue speech therapy classes after discharge in order to achieve significant/complete recovery.

Key words: stroke, left middle cerebral artery, aphasia, cerebral infarction, Broca's center, Wernicke's center, computed tomography, dysarthria.

For citation: Kutkin D.V., Babanina E.A., Shevtsov Yu.A. Stroke in the basin of the left middle cerebral artery: correlation of speech disorders with a variant of cerebral infarction // RMJ. 2016. No. 26. WITH.

Left middle cerebral artery stroke: the correlation between speech disorders and cerebral infarction Kut’kin D.V., Babanina E.A., Shevtsov Yu.A. City Clinical Hospital No. 5, Barnaul

Background. The paper discusses speech disorders and variants of brain injury after left middle cerebral artery (MCA) stroke. Aphasia and underlying types of ischemic stroke are of special interest. The efficacy of speech therapy exercises is analyzed.

Aim. To study the correlation between brain injury severity after left MCA stroke and speech disorder degree.

Patients and methods. The study enrolled 356 patients with probable acute stroke who were examined by neurologist to assess the severity of neurological deficiency. If the condition was satisfactory, the patient was examined by speech therapist. At admission and dynamically, the patients underwent brain CT to verify or to exclude focal brain injury and to specify lesion size and localization.

Results. Brain CT revealed typical ischemic lesions in the left MCA perfusion area in 32 of 124 patients (25.8%). In 7 patients, these lesions were not obvious (early stroke). Three study groups were compared: patients with dysarthria (n = 20), motor aphasia (n = 13), or sensorimotor aphasia (n = 23). Comparison criteria were lesion size and localization, consciousness, and speech recovery time.

Conclusions. Sensorimotor aphasia after ischemic strokes may result from large lesions around Sylvian fissure as well as from local lesions of cortical speech center(s) or white matter between them. Aphasia is more common in cryptogenic ischemic strokes while sensorimotor aphasia is more common in recurrent strokes. Considering delayed speech recovery in sensorimotor aphasia group, these patients should proceed with the speech therapy after the discharge to achieve significant improvement or full speech recovery.

Key words: stroke, left middle cerebral artery, aphasia, cerebral infarction, Broca’s area, Wernicke’s area, computed tomography, dysarthria.

For citation: Kut’kin D.V., Babanina E.A., Shevtsov Yu.A. Left middle cerebral artery stroke: the correlation between speech disorders and cerebral infarction // RMJ. 2016. No. 26. P. 1747–1751.

The article discusses variants of speech disorders and variants of changes in the brain substance during a stroke in the basin of the left middle cerebral artery

Introduction

Speech processes, as a rule, show a significant degree of lateralization and in most people depend on the leading (dominant) hemisphere. It must be taken into account that in determining the dominant hemisphere responsible for speech, the approach that associates dominance only with right-handedness or left-handedness is simplified. The profile of the distribution of functions between the hemispheres is usually diverse, which is reflected in the degree of speech disorders and the possibilities of speech restoration. Many people exhibit only partial and unequal hemispheric dominance for different functions. While speech function in right-handers (≥90%) and most left-handers (>50%) is predominantly left-hemisphere dependent, there are three exceptions to this rule:

1. In less than 50% of left-handers, speech function is associated with the right hemisphere.

2. Anomic (amnestic) aphasia can occur with metabolic disorders and volumetric processes in the brain.

3. Aphasia may be associated with damage to the left thalamus.

The so-called crossed aphasia (aphasia caused by a cerebral lesion ipsilateral to the dominant hand) is currently attributed only to right-handers.

The area of the cortex responsible for speech function is located around the Sylvian and Rollandian fissures (SMA basin). Speech production is determined by four zones of this area, closely interconnected and located sequentially along the posteroanterior axis: Wernicke's area (posterior part of the superior temporal gyrus), angular gyrus, arcuate fasciculus (AF) and Broca's area (posterior part of the inferior frontal gyrus) (Fig. 12) .

The pathogenesis of dysarthric speech disorders is determined by focal brain lesions of different locations. Complex forms of dysarthria are often observed.

Purpose of the study: to study the relationship between the volume of brain damage during stroke in the left MCA and the degree of speech impairment.

Material and methods

In 124 cases (every third patient) a preliminary diagnosis was made: stroke in the territory of the left middle cerebral artery (MCCA). This localization is most relevant when studying aphasia in patients with stroke.

All patients upon admission and most patients over time underwent a CT scan of the brain (Bright Speed 16 tomograph) to confirm/exclude focal brain lesions and clarify the extent of the lesion and the location of the pathological area.

According to the results of CT scan of the brain, 32 (25.8%) people out of 124 revealed typical ischemic changes in the LMCA basin, of which 7 were examined dynamically, i.e., upon admission, the changes were not yet obvious (initial stage of stroke). In 5 (4.0%) cases, hemorrhages were detected: left-sided medial hematomas and 1 case of subarachnoid hemorrhage (SAH). In 5 (4.0%) cases out of 124, infarctions of other localization (not in the LSMA basin) were detected (Table 1).

In 60 (48.4%) cases, patients were not hospitalized. In most cases, stroke was not confirmed (there were no corresponding changes in CT data or in the neurological status). The number of patients not hospitalized in the acute stroke department also included patients with various types of atrophy of the brain substance in combination with significant neurological symptoms who refused the proposed hospitalization. A few patients were transferred to other hospitals because they were diagnosed with traumatic changes in the skull, brain, and tumors. Some patients were transferred to the on-duty neurology department of another hospital, for example, with a diagnosis of osteochondrosis.

64 patients hospitalized in the acute stroke department with stroke had speech impairments (Table 2). The detailed nature of speech disorders was determined by a speech therapist. In 20 (31.2%) cases, patients were diagnosed with dysarthria and absence of aphasia. In 2 cases, dysarthria was accompanied by dysphonia and dysphagia. Aphasia was detected in 44 (68.8%) people, of which in 7 cases it regressed by the time of consultation with a speech therapist the next day (in 2 cases, ischemic infarctions were detected with regression of aphasia). 3 people from the group with sensorimotor aphasia had severe dysarthria, 9 people had dysphagia. In 4 people from the group with motor aphasia, symptoms of dysarthria were also noted, in 1 case - severe dysarthria.

In patients with dysarthria without aphasia, 4 types of dysarthria were identified: extrapyramidal (3 cases), afferent cortical (1 case), bulbar (1 case), pseudobulbar (8 cases), in other cases it was difficult to clearly determine the type of dysarthria, the manifestations were mild ( Table 3).

In groups of patients with dysarthria and regression of aphasia within 24 hours, there is a slight predominance of men.

In the group of patients with sensorimotor aphasia (23 people), in 39.1% (9 people) of cases in patients with sensorimotor aphasia, a large infarction was detected in the LCMA basin of the dominant hemisphere (Fig. 4–6). In 47.8% (11 people) of cases, a small infarction was detected (Fig. 7).

The main comparison groups were 3 groups of patients: with dysarthria (20 people), motor aphasia (13 people) and sensorimotor aphasia (23 people). The comparison criteria were the volume and nature of the lesion, the state of consciousness, and the timing of speech recovery.

Table 4 shows in parentheses cases where the localization of pathological changes corresponds to functional anatomical zones (for sensorimotor aphasia - a large area around the Sylvian fissure; for motor aphasia - Broca's center; for dysarthria - local changes at the level of the midbrain, subcortical structures, cortex).

It is often not possible to achieve a significant improvement in speech in patients with sensorimotor aphasia in a hospital (Table 6). Therefore, the speech therapist gives recommendations to each patient to continue classes at home.

results

These data are confirmed in studies of aphasic syndrome conducted in the second half of the twentieth century, according to which patients who have survived a hemorrhagic stroke have the opportunity to restore speech and can count on a favorable prognosis. In dynamics, the degree of speech impairment, as a rule, decreased with complex treatment, including with the preservation of hemodynamically significant stenosis of the internal carotid artery (according to duplex ultrasound scanning), but in the absence of stroke recurrence or severe hemorrhagic transformation.

conclusions

2. In patients with sensorimotor aphasia caused by stroke, stunned consciousness was noted more often than in other groups, despite the fact that the size of the confirmed infarction was not large in more than half of the cases.

3. The actual boundaries of speech centers appear to vary individually, so the accuracy of the expected anatomical lesion does not always match the degree of functional impairment (aphasia).

4. Full correspondence between the volume of the detected cerebral infarction and the volume of speech disorders was noted in the group of patients with sensorimotor aphasia, when the infarction was large.

5. Aphasic syndrome is more common with the cryptogenic variant of ischemic stroke; the sensorimotor variant of aphasia often occurs with repeated strokes.

6. Taking into account the less pronounced dynamics of speech recovery in the group of patients with sensorimotor aphasia, these patients should continue speech therapy classes after discharge in order to achieve significant/complete recovery.

Ischemic stroke in the posterior cerebral arteries

article in PDF format

Etiology. The most common cause of isolated infarctions in the PCA territory is embolic occlusion of the PCA and its branches, which occurs in 80% of cases (cardiogenic > arterio-arterial embolism from the vertebral and basilar [syn.: main] arteries > cryptogenic embolism). In 10% of cases, thrombosis in situ is detected in the PCA. Vasoconstriction associated with migraine and coagulopathy are the causes of cerebral infarction in 10% of cases. If isolated infarctions in the PCA territory in most cases are of a cardioembolic nature, then involvement of the brainstem and/or cerebellum in combination with an infarction in the PCA territory is most often associated with atherosclerotic lesions of the vessels of the vertebrobasilar region (VBB). A very rare cause of infarction in this region can also be arterial dissection affecting the PCA. Regardless of the cause of the infarction, it usually only partially involves the PCA area.

materials from the article “Ischemic stroke in the posterior cerebral artery basin: problems of diagnosis and treatment” by I.A. Khasanov (doctor of the neurological department for patients with acute cerebrovascular accidents), E.I. Bogdanov; Republican Clinical Hospital of the Ministry of Health of the Republic of Tatarstan, Kazan; Kazan State Medical University (2013) [read] or [read];

Please note: TRANSIENT NEUROLOGICAL ATTACK

The diagnosis of stroke is frightening and is associated with complete disability or death of a person. This is a truly serious condition, which is a clinical syndrome of vascular lesions of various sizes. Ischemic stroke is an infarction (death) of brain cells due to disruption of its blood supply and lack of oxygen and nutrition. The death of brain tissue, in turn, leads to a decrease or loss of some functions.

Types of strokes and their differences

There are two types of stroke: hemorrhagic and ischemic. The hemorrhagic form occurs more often in men in young and middle age. The basis of pathogenesis is the rupture of a vessel and the leakage of blood into the brain tissue. Ischemic stroke (IS) or acute cerebrovascular accident (ACVA) develops due to blockage of a vessel by a thrombus, atherosclerotic plaque or embolus. It is the outcome of cardiovascular diseases and mainly affects older people.

The etiology and symptoms of the two types of stroke are different, although the risk factors for them are almost the same. Hemorrhagic occurs due to:

abnormalities in the structure of blood vessels;
aneurysms;
injuries;
tumors in the brain;
general blood poisoning:
high pressure.

The ischemic form manifests itself against the background of chronic diseases:

diabetes mellitus;
atherosclerosis;
arrhythmias;
taking hormonal contraceptive pills.

In both cases, provoking and aggravating factors are a sedentary lifestyle, bad habits(smoking, drinking), obesity, physical and emotional stress. A hemorrhagic catastrophe of the brain always occurs at the peak of a hypertensive crisis. Ischemic stroke is accompanied by normal or low blood pressure.

Research has found that women are more likely to have a stroke at a young age and in old age than men. But from 30 to 80 years of age, men are at greater risk. We are talking about population groups that have not previously suffered from heart and brain pathologies. Also, some scientists claim a high family predisposition to ischemic stroke.

Classification of ischemic stroke

In neurology, AI is classified into types depending on its pathogenesis. This may be non-thrombotic occlusion of deep small vessels of the cortex, blocking of the lumen of a cerebral artery by an embolus of cardiac or arterial origin, arterial thrombosis leading to significant impairment of cerebral circulation. The following types of pathologies are distinguished:

Type of stroke

What's happening

Atherothrombotic	Formation of cholesterol plaques in large and medium-sized arteries, gradually blocking blood flow
Cardioembolic	Embolism by a blood clot in one of the vessels of the middle artery of the brain, large areas of brain tissue are affected, the process begins abruptly
Lacunar	The lumen of small arteries is blocked, causing focal ischemia (the size of one lesion is no more than 1.5 cm), gradually affecting the brain stem
Rheological	Associated with disturbances in blood composition and hemostasis
Hemodynamic	Associated with fluctuations in blood pressure or changes in cardiac output

Stroke can be primary or secondary. Primary means that stroke occurred for the first time in the patient. The acute stage lasts 28 days (previously it was believed that it lasts 21 days). If another stroke occurs before the expiration of this period, it is considered as a second attack of the primary one. A stroke that occurs again after 4 weeks is called secondary. There are periods of ischemic stroke: the acute phase lasts 3 days from the onset of pathology, acute - 4 weeks, early recovery - six months, late rehabilitation period- about 2 years.

The reversibility of neurological changes depends on the duration and degree of reduction in blood flow. Classification by damage:

transient ischemic attack has stroke symptoms that disappear within 24 hours;
minor stroke - prolonged ischemic attack, the patient is completely rehabilitated within 3 weeks;
progressive - a stepwise increase in focal and cerebral manifestations, complete restoration of functions does not occur;
completed - a completed cerebral infarction with gradually regressing symptoms.

Clinical picture of ischemic stroke

Despite the fact that both forms of stroke have a common name, they have different pathogenesis, clinical manifestations, prognosis and consequences.

The hemorrhagic stroke clinic is developing rapidly. The attack begins with general cerebral and focal symptoms - severe sudden headache, nausea and vomiting, then comes photophobia, paralysis of the right or left half of the body, pain when trying to rotate the eyeballs, impaired consciousness up to coma. In 10% of patients, a stroke begins as epileptic seizure. Breathing becomes hoarse, the pupil of the eye on the affected side dilates, and on the opposite side the corner of the eyelid and mouth droops. If blood spreads over a large area, heart function and breathing are disrupted.

Unlike hemorrhagic, ischemic stroke is characterized by focal symptoms. There may be no general cerebral symptoms, such as vomiting and nausea, or severe headache. The clinical picture of ischemic stroke depends on the location and size of the lesion. Cerebral vessels are divided into pools that supply blood to different parts of the brain. When the cerebral hemispheres (carotid basin) are affected, the stroke clinical picture manifests itself differently, depending on which hemisphere is affected. Right hemisphere damage causes:

loss of pain sensitivity on the left side of the body - it can disappear throughout the body, but more often the border runs along the line between the tip of the nose and the navel:
paresis of the limbs in the direction opposite to the lesion;
speech disorder;
loss of language memory;
lethargy and depression, caution, slowness.

The consequences of damage to the right hemisphere are expressed in facial asymmetry - an upturned left corner of the mouth, a smoothed right nasolabial fold. A person does not remember recent events, but retains the memory of past ones. His concentration is impaired.

Symptoms of left hemisphere stroke:

immobilization of the right side of the body;
disorientation in space;
fussiness, impulsive behavior;
motor memory deficit.

The consequences of a cerebral infarction in the left hemisphere are mental abnormalities. The person does not recognize his loved ones and does not recognize himself as sick.

In both cases, the patient may lose consciousness, breathing becomes irregular, with long breaks between inhalation and exhalation. Some patients experience oscillatory movement of the eyeballs (nystagmus). Another manifestation of a stroke in the hemispheres is speech impairment. A person may not understand what is being said to him (sensory aphasia), and this frightens him. At the same time, the patient himself can speak quite confidently, but his speech will be absolutely incoherent in meaning (verbal hash). In some cases, patients are unable to pronounce words and realize that their speech is impaired. Sometimes they cannot speak at all (mutism).

Poor circulation in the brain stem (vertebrobasilar region) leads to the following disorders:

systemic dizziness - it seems to a person that surrounding objects are spinning around him, his head is spinning regardless of the position in which he is - standing, sitting, lying down;
loss of coordination - imprecise, sweeping movements;
unsteadiness of gait - a person feels unsteady and sways while standing;
visual impairment - limitation of movement of the eyeballs or its complete absence, fixation of gaze in one direction (towards the lesion), partial or complete loss of vision;
difficulty swallowing.

Manifestations that are possible with any location of cerebral infarction are cognitive impairment. They consist of disorientation in time and surroundings; the patient cannot count, read and write (confuses letters and syllables).

Of all cases of ischemic strokes, 80% occur in the carotid region. Moreover, their consequences and prognosis are better than those of strokes in the vertebrobasilar region.

Rate of development of symptoms in ischemic stroke

Acute cerebrovascular accident caused by thrombosis develops gradually (within 1–2 days), adding more and more pronounced neurological symptoms. The deterioration of the condition occurs as a “flickering” type, either decreasing or intensifying again. External manifestations are slight cyanosis of the lips and nasolabial triangle, normal or low blood pressure, a slightly rapid, weakly filled pulse.

In the case of embolism, symptoms increase rapidly within a few minutes. A short-term loss of consciousness occurs, in addition to focal manifestations, tension of the neck muscles is observed, a condition similar to an epileptic attack.

Fat embolism (blockage of an artery with a piece of fatty tissue), like thrombosis, gives a gradual development of symptoms (from several hours to a day). Before reaching the brain, the fat embolus passes through the pulmonary vessels and causes shortness of breath, cough and hemoptysis.

What family members should know

Relatives should be alert to changes in the patient's behavior. It becomes difficult for him to perform usual activities, such as brushing his teeth. He began to have poor spatial orientation and forget basic things. In this case, you need to call a general practitioner at home. He will give practical recommendations and will refer you for examinations for differential diagnosis with other diseases with similar symptoms. Consultation with an ophthalmologist and neurologist is also necessary.

Condition requiring an ambulance call: nausea, vomiting, dizziness, severe headache, speech impairment. The patient's further condition and treatment prognosis depend on the speed with which he is hospitalized - about 50% of the lesion develops in the first hour and a half. The next 6 hours are important - this time accounts for up to 80% of ischemia. It is important to provide assistance to the patient within the first two hours in order to minimize the lesion as much as possible.

Complications of ischemic stroke

Due to prolonged bed rest, the patient develops bedsores, infectious pneumonia and inflammation of the urinary tract and kidneys. Immobility leads to deep vein thrombosis of the lower extremities, and the detachment of a blood clot leads to pulmonary embolism.

As a result of the death of parts of the brain, motor, intellectual and mental disorders in the form of depression and mood swings can persist for life. A fifth of patients who have had a stroke subsequently suffer from epilepsy. Such complications are especially typical in cases where first medical aid was not provided in a timely manner.

Causes of death

Most often, death occurs in the first week of the disease. Death occurs when the brain edema or when the infarction is localized in the brain stem with damage to the centers responsible for breathing and cardiac activity. Another reason is the complication of ischemic stroke with secondary cerebral hemorrhage or repeated infarction with the formation of foci in the brain stem.

In general, stroke occurs due to an episode of ischemia (80-85% of patients), hemorrhage (15-20% of patients).

A number of risk factors for stroke are listed below:

Old age
Family history
High blood pressure
Cardiac ischemia
Diabetes
Smoking cigarettes
Heart diseases
Obesity
Physical inactivity
Alcoholism

The onset and duration of vertebral stroke symptoms depends, to a large extent, on etiology. Patients with basilar artery thrombosis typically have a waxing and waning pattern of symptoms; as many as 50% of patients experience transient ischemic attacks (TIAs) in the days to weeks before the onset of occlusion.

In contrast, emboli are sudden, without a prodromal stage, with an acute and dramatic presentation.

Common symptoms associated with vertebrobasilar stroke

Dizziness
Nausea and vomiting
Headache
Decreased level of consciousness
Abnormal oculomotor signs (eg, nystagmus, diplopia, pupillary changes)
Ipsilateral weakness of muscles innervated by cranial nerves: dysarthria, dysphagia, dysphonia, weakness of facial and tongue muscles.
Loss of sensation in the face and scalp
Ataxia
Contralateral hemiparesis, tetraparesis
Loss of pain and temperature sensitivity
urinary incontinence
loss of visual fields
neuropathic pain
hyperhidrosis in the face and limbs

Features of symptoms of stroke in the VBB with embolic variant

rapid onset - from the appearance of the first symptoms to their maximum development in no more than 5 minutes
motor disorders: weakness, clumsiness of movements or paralysis of the limbs of any combination, up to tetraplegia;
Sensory disorders: loss of sensation OR paresthesia of the limbs in any combination or spreading to both sides of the face or mouth;
homonymous hemianopsia, or cortical blindness;
movement coordination disorders, imbalance, instability;
systemic and non-systemic dizziness in combination with double vision, swallowing disorders and dysarthria.

Symptoms that can also be observed in patients

Horner's syndrome
nystagmus (especially vertical)
rarely hearing impairment.

Dizziness, ataxia and visual disturbances form a characteristic feature of this

pathology triad indicating ischemia of the brain stem, cerebellum and occipital lobes of the brain.

Sometimes a typical syndrome of vascular lesions in the VBD can be combined with a violation of higher brain functions, for example, with aphasia, agnosia, and acute disorientation.

Alternating syndromes with clearly localized foci within the VBD, for example, Weber, Millard-Gubler, Wallenberg-Zakharchenko syndromes, are rarely found in their pure form.

A special form of acute cerebrovascular accident

in the VBB is an “archer” stroke associated with mechanical compression of the vertebral artery at the level of C1-C2 with extreme rotation of the head to the side

Currently, the mechanism of such a stroke is explained by the tension of the artery at the C1-C2 level when turning the head, accompanied by a tear in the intima of the vessel, especially in patients with pathological changes in the arteries. In the case of compression of the dominant VA, there is no sufficient compensation for blood flow in the VBB. due to hypoplasia of the opposite vertebral artery or its stenosis, as well as incompetence of the posterior communicating arteries is a factor contributing to the development of archer stroke. One of the predisposing factors for this pathology is the presence in patients of Kimmerli's anomaly - an additional bone arch-semi-ring, which can compress the vertebral arteries above the arch of the first cervical vertebra.

ACVA in the VBB is an emergency condition requiring hospitalization in a specialized vascular neurological department; treatment of ischemic stroke in the VBB occurs in a hospital setting in a number of cases in the neurointensive care unit.

Rehabilitation after stroke in the vertebrobasilar region

Rehabilitation after stroke plays a critical role in restoring brain function. Doctors and nurses play a critical role in rehabilitation.

nurses are often the first to suggest initiating therapy services because they have the most involvement with the patient. Before starting a discussion of specific disciplines of therapy, addressing nursing issues in the care of patients with vertebrobasilar stroke.

may vary depending on symptoms and the severity of brain damage. Initial intervention includes nursing, maintaining skin integrity, regulating bowel function, and Bladder, maintaining nutrition, and ensuring patient safety from injury.

Other important questions in consultation with the attending physician, include restoration of self-service swallowing function. In some patients, the severity of the neurological deficit makes it impossible to stand, however, patients should be mobilized including active participation in physical rehabilitation (physical therapy) and occupational therapy.

Positioning in bed and chair ensures patient comfort and prevents complications from bedsores. If the upper limb is flaccid or paretic, proper posture is critical to preventing shoulder subluxation and shoulder pain.

Nursing staff should train family members in caring for a person who has had a stroke. The patient's family members may not be familiar with stroke and its consequences. Education aims to make the patient and family members aware of the importance of continued rehabilitation and prevention of recurrent episodes, appropriate precautions, and continuation of therapy after discharge home.

Some patients have fluctuating signs and symptoms, which are often related to position. Because of this possibility, precautions are necessary with activities that can be taken until symptoms have stabilized.

The physical therapist is responsible for improving gross motor skills such as walking, body balance, and the ability to move and change positions within the confines of a bed or wheelchair.

The physical therapy doctor also develops an exercise program and instructs the patient with the goal of overall strengthening and increasing movement. Education of the patient's family members in the use of lower limb prosthetics may be necessary to ensure functional mobility. Vestibular gymnastics is also shown.

Search:

Healthy food blog philosophy

It is clear that you are always very busy. However, by reading a blog about healthy food, you will understand how easier it is to eat properly and eat well in order to maintain and increase your health. We live in contradictory times, on the one hand we are faced with a large selection of products (more than ever), on the other hand with the complexity of choice: who to believe? what food is not harmful? On diet-and-treatment.rf you will find accurate and objective information about healthy eating. The blog gives you simple answers to important questions about food and healthy eating.

Our dietary dishes section is rich in recipes for delicious dietary dishes with affordable ingredients and simple preparation. Healthy food articles provide accurate information about food and its health benefits that you can rely on. Other sections of the site will tell you about diets for various diseases, will offer a menu and simple recipes for diabetes, hepatitis, gout.

Why can diet-and-treatment.rf be trusted?

Everything written about is based on scientific data and also written by experts. Articles on nutrition, weight loss and therapeutic diets contain unbiased, objective information. The healthy food blog is not sponsored by any commercial entity or organization.

Features of ischemic stroke in the vertebrobasilar region

Disorders of the blood supply to the brain (stroke) remain the most pressing problem in the world medical practice of neurologists.

According to medical statistics, up to 80% of all cases of identified strokes were of ischemic origin.

Of these, up to 30% account for the localization of a negative focus in the vertebrobasilar vascular system, but

the probability of death is much higher than with other localizations of the lesion.

Experts have also reliably established that up to 70% of the formation of a cerebral catastrophe was preceded by transient ischemic attacks. In the absence of adequate treatment, an ischemic stroke with severe consequences would subsequently occur.

Characteristics of the vertebrobasilar system

It is this vascular structure that accounts for up to 30% of the total intracranial blood flow.

This is possible due to the features of its structure:

paramedian arteries branching directly from the main arterial trunks;
circumflex arteries designed to supply blood to the lateral territories of the brain;
the largest arteries located in the extracranial and intracranial parts of the brain.

It is precisely this abundance of vessels and arteries with different lumen diameters, varied structures and anastomotic potential that determines the widest clinical picture of dyscirculations.

Along with the formation of clinical manifestations typical of transient ischemic attacks, a specialist may also identify atypical forms of ischemic stroke, which significantly complicates the diagnosis.

Reasons for development

Experts today talk about the following most significant causes of ischemic stroke:

Atherosclerotic lesion of intracranial vessels;
Features of the structure of the vascular bed of a congenital nature;
Formation of microangiopathies against the background of hypertensive pathology, diabetes and other diseases;
Severe compression of the arteries by pathologically altered cervical structures of the spine;
Extravasal compression formed as a result of hypertrophied scalene muscle or hyperplastic transverse processes of the cervical segments of the spine;
Traumatization;
Damages to the vascular wall due to inflammatory phenomena - various arteritis;
Changes in rheological blood parameters.

It is customary to distinguish the following types of stroke in the vertebrobasilar region:
in the basilar artery itself;
in the area of the posterior cerebral artery;
right-sided ischemic lesion;
left-sided variant of cerebral catastrophe.

For the identified reason, the violation may be:

Symptoms

Most victims, upon careful questioning, can recall that the stroke was preceded by symptoms of transient ischemic attacks: previously uncharacteristic dizziness, instability when walking, painful sensations in the head of a local nature, memory impairment.

If a person does not contact a specialist in a timely manner or in the absence of treatment, the symptoms of a stroke intensify many times over. Their severity is largely determined by the localization of the negative focus, the extent of damage to brain structures, the initial state of human health, and the adequacy of the collateral blood supply.

The patient’s illusory perception of his own and external movements due to severe dizziness;
Inability to maintain an upright position – static ataxia;
Pain sensations of varying severity in the occipital region of the head, sometimes radiating to the neck and eye sockets;
Some visual disturbances;
The possibility of forming drop attacks - a person suddenly feels the maximum severity of weakness in the lower extremities and falls;
Significant memory impairment.

If you have one symptom or a combination of them, it is recommended to immediately consult a neurologist and the necessary list of diagnostic procedures. Ignoring a transient ischemic attack that precedes a cerebral catastrophe can subsequently lead to very serious complications.

Diagnostics

In addition to carefully collecting anamnesis and conducting a diagnostic study, the specialist will make a diagnosis. Mandatory diagnostic procedures:

Dopplerography;
duplex scanning;
angiography;
CT or MRI of the brain;
contrast panangography;
radiography;
various blood tests.

Only the completeness of the data allows for an adequate differential diagnosis of stroke in the vertebrobasilar region.

Treatment

A stroke requires mandatory transportation of the victim to a neurological hospital for comprehensive treatment.

Thrombolytic therapy - modern drugs are introduced into the bloodstream to promote the fastest possible dissolution of the embolus that has blocked the lumen of the intracranial vessel. The decision-making falls on the specialist, who takes into account the variety of indications and contraindications for the procedure.
To lower blood pressure parameters in the event of a hypertensive crisis, antihypertensive medications are administered to a person.
Neuroprotectors are designed to maximally improve blood circulation in the brain and speed up their recovery.
To restore an adequate heart rhythm, antiarrhythmic drugs are prescribed.

In the absence of positive dynamics from conservative therapy for stroke, the neurosurgeon makes a decision to carry out surgical intervention– removal of thrombotic mass directly from the area of the damaged vessel.

Prevention

As you know, it is easier to prevent a disease than to treat its complications later. That is why the main efforts of specialists are aimed at promoting preventive measures to prevent strokes:

diet correction;
daily intake of recommended antihypertensive and antiarrhythmic drugs, anticoagulants;
constant monitoring of pressure parameters;
taking modern statins;
annual conduct of a full range of diagnostic procedures for individuals at risk for stroke;
in case of detection of blockage of an intracranial vessel by atherosclerotic or thrombotic masses, appropriate surgical treatment tactics are used.

The prognosis for stroke in the vertebrobasilar region in the case of adequate treatment measures is very favorable.

Leave your opinion

How long do people live after a stroke?

Garlic for cleaning blood vessels and blood circulation

Rehabilitation center for stroke and trauma in Sestroretsk hospital No. 40

What to do after having a stroke

Major stroke: consequences, chances of survival, recovery

Drugs to improve blood circulation in the brain and memory

How to increase your brain's thinking ability

Reader about how to choose a doctor after a stroke.

Why does the desire to recover disappear after a stroke?

Questions for the doctor: mechanism of spasticity, myostimulators, ointments

The extreme importance of prompt hospitalization and rehabilitation of a person after a stroke

Neurologist: excess weight increases blood pressure; snoring slows down recovery

Proper nutrition after a stroke - how should a person be fed?

Nutrition that will help restore brain function after a stroke

Ischemic cerebral stroke

Ischemic cerebral stroke is an acute disruption of the blood supply to the brain resulting from interruption or obstruction of blood supply. The disease is accompanied by damage to brain tissue and disruption of its functioning. Acute ischemic circulatory disorders of the brain account for 80% of all strokes.

Stroke poses a serious threat to able-bodied and elderly people, leading to prolonged hospitalization, severe disability, large financial costs for the state, and deterioration in the quality of life of the affected people and their family members.

Stroke - the disease of the century

Every year, stroke affects about 6 million people in the world, about 4 million of them die, half remain disabled. The number of patients in Russia is at least 450 thousand people per year. The worst thing is that the incidence rate is increasing and the age of sick people is getting younger.

There are 5 types of ischemic stroke depending on the mechanism of its origin, that is, pathogenesis:

Thrombotic. The cause (or etiology) is atherosclerosis of the large and medium arteries of the brain. Pathogenesis: an atherosclerotic plaque narrows the lumen of the vessel, then, after exposure to certain factors, a complication of atherosclerosis occurs: the plaque ulcerates, platelets begin to settle on it, forming a blood clot that blocks the internal space of the vessel. The pathogenesis of thrombotic stroke explains the slow, gradual increase in neurological symptoms; sometimes the disease can develop within 2–3 hours in several acute episodes.

Thrombotic stroke usually develops against the background of atherosclerosis

Embolic. Etiology – blockage of a vessel with a blood clot coming from internal organs. Pathogenesis: a blood clot forms in other organs, then it breaks off and enters the brain vessel with the bloodstream. Therefore, the course of ischemia is acute and rapid, and the lesion is of impressive size. The most common source of blood clots is the heart; cardioembolic stroke develops with myocardial infarction, cardiac arrhythmias, artificial valves, endocarditis; less often, the source of blood clots is atherosclerotic plaques in large main vessels.

A common cause of cerebral vessel obstruction is cardiogenic embolus.

Hemodynamic. The pathogenesis is based on a violation of blood flow through the vessels. The etiology is low blood pressure, this phenomenon can be observed with a slow heart rate, ischemia of the heart muscle, during sleep, and prolonged stay in an upright position. The onset of symptoms can be both rapid and slow, the disease occurs both at rest and during wakefulness.
Lacunar (the size of the lesion does not exceed 1.5 cm). Etiology – damage to small arteries due to hypertension, diabetes mellitus. The pathogenesis is simple - after a cerebral infarction, small cavities-lacunae appear in its depth, the vascular wall thickens, or the lumen of the artery is blocked due to compression. This explains the peculiarity of the course - only focal symptoms develop, there are no signs of cerebral disorders. Lacunar stroke is most often recorded in the cerebellum, the white matter of the brain.

Lacunar stroke is usually a consequence of arterial hypertension

Rheological. Etiology is a blood clotting disorder not associated with any diseases of the blood or vascular system. Pathogenesis – the blood becomes thick and viscous, this condition prevents it from entering the smallest vessels of the brain. During the course of the disease, neurological disorders, as well as problems associated with blood clotting disorders, come to the fore.

The most common reasons Ischemic stroke is thrombosis and embolism.

Types of stroke according to the rate of increase in neurological symptoms

Depending on the speed of formation and duration of persistence of symptoms, 4 types are distinguished:

Microstroke or transient ischemic attack, transient cerebral ischemia. The disease is characterized by mild severity, all symptoms disappear without a trace within 1 day.
Minor stroke. All symptoms persist for more than 24 hours but less than 21 days.
Progressive ischemic stroke. It is distinguished by the gradual development of the main neurological symptoms - over several hours or days, sometimes up to a week. After this, the health of the sick person is either gradually restored, or neurological abnormalities persist.
Completed stroke. Symptoms persist for more than 3 weeks. Usually a cerebral infarction develops, after which severe physical and mental health problems sometimes persist. With a major stroke, the prognosis is poor.

Clinic

Movement disorders of varying severity. Cerebellar dysfunction: lack of coordination, decreased muscle tone.
Impaired pronunciation of one’s own and the perception of someone else’s speech.
Visual impairment.
Sensory disorders.
Dizziness, headache.
Violation of the processes of memorization, perception, cognition. The severity depends on the size of the lesion.

The clinic depends on the cause of the disease, the size and location of the lesion. It is worth distinguishing between lacunar infarction, lesions of the carotid, anterior, middle, posterior and villous cerebral arteries; special attention is paid to ischemia of the vertebrobasilar region.

Ischemic stroke of the vertebrobasilar region (VBB)

The vertebral arteries merge at the base of the brain into the basilar artery

Two vertebral arteries, merging, form one basilar, that is, the main one. With vascular insufficiency of these arteries, two important parts of the brain are affected at once - the brainstem and the cerebellum. The cerebellum is responsible for coordination, balance and tone of the extensor muscles. Dysfunction of the cerebellum can be called “cerebellar syndrome”. The brainstem contains 12 cranial nerve nuclei, which are responsible for swallowing, eye movement, chewing, and balance. After a stroke in the brain stem, these functions may be impaired to varying degrees. In ischemic strokes, focal dysfunction of the cerebellum in combination with symptoms of brain stem damage predominate.

Symptoms of acute vascular insufficiency of the vertebral arteries: as a result of damage to the cerebellum, an imbalance and coordination of movements occurs; if the cerebellum is damaged, muscle tone decreases; as a result of damage to the cerebellum, there is a violation of the coordination of muscle movements. When the trunk is damaged, oculomotor disorders, paralysis of the facial nerve, paresis of the limbs (alternating syndrome), chaotic movement of the eyeballs, combined with nausea, vomiting and dizziness, appear, and the person has difficulty hearing. The trunk also regulates chewing and swallowing reflexes.

With simultaneous damage to the basilar or both vertebral arteries, the course of the disease worsens, paralysis of both arms and legs, and coma are observed.

The course of TIA with damage to the intracranial part of the vertebral artery and the posterior cerebellar artery is not severe; it is manifested by nystagmus, dizziness with vomiting and nausea, impaired facial sensitivity, changes in the perception of pain and temperature.

Diagnostics

Treatment tactics are determined by the type of stroke

To select a treatment regimen, it is very important to establish the form of the acute vascular disorder, because medical tactics for hemorrhage and ischemia have serious differences.

Diagnosis of ischemic cerebrovascular accidents begins with a medical examination, taking into account the main symptoms of the disease and existing risk factors. The doctor listens to the heart and lungs, measures the pressure in both arms and compares the readings. To clarify neurological disorders and determine the severity, it is necessary to undergo an examination by a neurologist.

To make an emergency diagnosis and find out the cause of the disease, ultrasonography vascular bed of the brain, electroencephalogram; angiography allows you to more accurately see changes in the vascular system of the brain - contrast is injected into the vessels and an X-ray is taken; often it is necessary to do an MRI and CT scan of the brain. In addition, the diagnosis of ischemic stroke should include a finger and vein blood test, a clotting test, general analysis urine.

Prevention

Prevention of ischemic cerebrovascular accidents is aimed at eliminating risk factors and treating concomitant diseases. Primary prevention is aimed at preventing the first attack in life, secondary prevention is aimed at preventing stroke recurrence.

The International Health Organization has established a list of preventive measures:

Quitting cigarettes. After quitting active and passive smoking, the risk of developing a stroke decreases significantly, even in older people who have smoked their entire adult life.
Quitting alcohol. It is not recommended to drink alcohol even in moderation, because each person has his own individual concept of moderation. It is necessary to completely give up alcohol for people who have already suffered an acute disorder of cerebral blood supply in their lives.
Physical activity. Regular physical exercise at least 4 times a week will have a positive effect on the weight, condition of the cardiovascular system, and the fat composition of the blood of a sick person.
Diet. The diet consists of moderate consumption of fats, it is recommended to replace animal fats with vegetable fats, eat less simple carbohydrates, eat more fiber, pectins, vegetables, fruits and fish.
Reducing excess body weight. Weight loss should be achieved by reducing the caloric content of food, establishing a 5-6 daily diet, and increasing physical activity.
Normalizing blood pressure is the most effective prevention of ischemic stroke. With healthy blood pressure, the risk of developing a primary and recurrent stroke is reduced, and heart function is normalized.
It is necessary to adjust blood sugar levels in case of diabetes.
It is necessary to restore the functioning of the heart.
Women are advised to avoid contraceptives containing a large number of estrogens.
Drug prevention. Secondary prevention of ischemic stroke must necessarily contain antiplatelet and anticoagulant drugs - Aspirin, Clopidogrel, Dipiradamol, Warfarin.

Medication measures for secondary prevention

By following the listed preventive measures for a long time, you can reduce the risk of developing any diseases of the cardiovascular system.

75% of strokes are primary, which means that by following preventive measures, the overall incidence of stroke can be reduced.

Forecast

The chances of a favorable outcome are different for each person and are determined by the size and location of the lesion. Patients die after developing cerebral edema, displacement of internal brain structures. 75–85% of patients have a chance of survival by the end of the first year, 50% after 5 years, and only 25% after 10 years. Mortality is higher in thrombotic and cardioembolic strokes, and is very low in the lacunar type. Low survival rate in elderly people, hypertensive patients, smokers and alcohol drinkers, people after a heart attack, and arrhythmia. Chances of good recovery decrease rapidly if neurological symptoms persist for more than 30 days.

In 70% of surviving people, disability persists for a month, after which the person returns to normal life, 15–30% of patients after a stroke remain permanently disabled, and the same number of people have every chance of developing a recurrent stroke.

Patients who have suffered a microstroke or minor stroke have a chance to go to work early. People with major strokes may return to their previous place of work after a long recovery period or may not return at all. Some of them can return to their previous place, but to an easier job.

With timely assistance, properly selected treatment and rehabilitation, it is possible to improve the patient’s quality of life and restore ability to work.

Stroke is not a hereditary, chromosomal and inevitable disease. For the most part, stroke is the result of chronic human laziness, overeating, smoking, alcoholism and irresponsibility to doctor’s prescriptions. Enjoy life - run in the morning, go to the gym, eat natural light foods, spend more time with your children and grandchildren, spend the holidays with delicious non-alcoholic cocktails and you will not have to get acquainted with the causes and statistics of stroke.

Tatyana on Prognosis after a stroke: how long will life be?
Musaev on Duration of treatment for meningitis
Yakov Solomonovich on Consequences of stroke for life and health

Copying site materials is prohibited! Reprinting of information is permitted only if an active indexed link to our website is provided.

Stroke in the vertebrobasilar area

Vertebrobasilar insufficiency: clinical picture and diagnosis

Acute (ACVE) and chronic cerebrovascular accidents remain one of the pressing problems of modern medicine. According to various authors, up to 20% of stroke patients become deeply disabled, up to 60% have a pronounced disability and require long-term and costly rehabilitation, and only less than 25% of patients return to their usual work activities.

Among survivors, 40-50% have a recurrent stroke within the next 5 years.

It has been established that up to 80% of all strokes are ischemic in nature. And although only 30% of strokes occur in the vertebrobasilar region. the mortality rate from them is 3 times higher than from strokes in the carotid system. More than 70% of all transient ischemic attacks occur in the vertebrobasilar region. Every third patient with a transient ischemic attack subsequently develops an ischemic stroke.

The prevalence of brachiocephalic artery pathology is 41.4 cases per person. Of these, 30-38% are pathologies of the subclavian and vertebral arteries.

Widespread distribution, constant increase in incidence, high mortality in patients of working age, high percentage of disability among patients place the problem of cerebrovascular ischemia in the group of socially significant ones.

The vertebrobasilar system accounts for about 30% of all cerebral blood flow. It supplies blood to various formations: the posterior parts of the cerebral hemispheres of the brain (occipital, parietal lobes and mediobasal parts of the temporal lobe), the optic thalamus, most of the hypothalamic region, the cerebral peduncles with the quadrigeminal, the pons, the medulla oblongata, the reticular formation, the cervical spinal cord.

From an anatomical and functional point of view, 4 segments are divided along the course of the subclavian artery: V 1 - from the subclavian artery to the transverse segment C VI. V 2 - from vertebra C VI to vertebra C II. V 3 - from vertebra C II to the dura mater in the region of the lateral foramen magnum, V 4 - to the point of confluence of both vertebral arteries into the main one (see figure).

Vertebrobasilar insufficiency is a condition that develops due to insufficient blood supply to the area of the brain supplied by the vertebral and basilar arteries and causes temporary and permanent symptoms. In ICD-10, vertebrobasilar insufficiency is classified as “Vertebrobasilar arterial system syndrome” (section “Vascular diseases” nervous system"); and also categorized in the section “Cerebrovascular diseases”. In the domestic classification, vertebrobasilar insufficiency is considered within the framework of dyscirculatory encephalopathy (cerebrovascular pathology, the morphological substrate of which is multiple focal and (or) diffuse lesions of the brain), “vertebral artery syndrome”. Others synonyms are "irritation syndrome of the sympathetic plexus of the subclavian artery", "posterior cervical sympathetic syndrome", "Barré-Lieu syndrome". In foreign literature, along with the term "vertebrobasilar insufficiency" (vertebrobasilar insufficiency), the term "circulatory insufficiency in the posterior cranial fossa" is becoming increasingly widespread "(posterior circulation ischemia).

Various etiological factors lead to the development of vertebrobasilar insufficiency. They can be conditionally divided into 2 groups: proper vascular and extravascular.

Table. Etiological factors of vertebrobasilar insufficiency and their frequency of occurrence

Stroke with localization of lesions in the vertebrobasilar region

Both acute, in their form, violations of the usefulness of cerebral circulation, and, in fact, its chronic forms today remain one of the most pressing, pressing problems of modern world medicine. According to estimates by various authors, about 18, 20% of all patients who once survived a stroke turn out to be deeply disabled, about 55, 60% of such patients retain pronounced limitations in their ability to work or require constant exercise for quite a long and often very expensive rehabilitation.

Moreover, only about 20 or 25% of all patients who have suffered a state of stroke pathology, in one form or another (an ischemic or hemorrhagic cerebral stroke in the anamnesis) are able to return to their previously usual work activity after discharge from the hospital. These statistics are shown more clearly in the diagram below:

At the same time, doctors have found that almost 80% of all emerging stroke pathologies are ischemic in nature or the nature of their occurrence. And, although no more than about 30% of stroke conditions turn out to be localized in the so-called vertebrobasilar area, the development of a fatal outcome after such is almost three times higher than from the more common stroke pathologists with localization of the lesion of brain tissue in the carotid area.

In addition, more than 70% of all transient ischemic attacks (or other transient disturbances of cerebral blood flow) that precede the state of a full-fledged stroke lesion occur precisely in the vertebrobasilar region mentioned above. Moreover, every third such patient who has suffered a transient ischemic attack with a similar localization of the problem will subsequently develop a very severe ischemic stroke.

What is our vertebrobasilar system?

It is necessary to understand that the so-called vertebrobasilar system usually accounts for about 30% of the total cerebral blood flow. It is the vertebrobasilar system that is responsible for the blood supply to a wide variety of brain organ formations, such as:

The posterior sections belonging to the cerebral hemispheres (these are the occipital and parietal lobes and the so-called medio-basal sections of the temporal lobes).
Visual thalamus.
Most of the vital hypothalamic region.
The so-called cerebral peduncles with its quadrigeminal region.
Medulla oblongata.
Pons.
Or the cervical region of our spinal cord.

In addition, in the system of the described vertebrobasilar system, doctors distinguish three groups of different arteries. This is about:

The smallest arteries, or the so-called paramedian arteries, arise directly from the main trunks of both the vertebral and basilar arteries, from the anterior spinal artery. This also includes deep perforating arteries, which originate from the larger posterior cerebral artery.
The short type of circumflex (or circular) arteries, which are designed to wash the lateral territories related to the brain stem with arterial blood, as well as the long type of circumflex arteries.
The largest or largest arteries (which include the vertebral and basilar arteries), located in the extracranial and intracranial parts of the brain.

Actually, the presence in a standard vertebrobasilar basin of such a number of arteries with different calibers, with different structures, with different anastomotic potential and with different areas of blood supply, usually determines the localization of a particular focus of a stroke lesion, its specific manifestations, as well as the clinical course of the pathology.

However, possible individual characteristics The location of such arteries and diversity in pathogenetic mechanisms quite often determine differences in the neurological clinic during the development of such pathology as acute ischemic stroke localized in the vertebrobasilar zone.

This means that, along with the development of neurological syndromes typical for stroke pathology, doctors can often note not only the standard clinical picture with the development of pathology in the vertebrobasilar zone, which is described by clinical guidelines, but rather the atypical course of such stroke pathology. Which, in turn, often significantly complicates diagnosis, determining the nature of a specific stroke pathology and the subsequent selection of adequate therapy for it.

Why does this type of brain stroke occur?

The condition of primary vertebrobasilar insufficiency, often preceding the stroke pathology of the same name, can develop due to varying degrees of severity of insufficient blood supply to areas of brain tissue fed by vertebral or basilar arteries. In other words, a wide variety of etiological factors can lead to the development of such a pathology, which are conventionally divided into two groups:

This is a group of vascular factors.
And a group of extravascular factors.

The first group of factors that often become the causes of the development of such stroke pathology usually include: atherosclerosis, stenosis or occlusion of the subclavian arteries, their developmental anomalies (say, pathological tortuosity, the same anomalies of the entrance to the bone feces, numerous hypoplasias, etc. The reasons for the occurrence of this pathologies of an extravascular nature are usually attributed to: embolism of various etiologies in the vertebrobasilar zone or extravasal compression of the subclavian artery itself.

In rare cases, a brain stroke of this type can be caused by fibromuscular dysplasia, damage to the subclavian artery after neck injuries or after non-professional manipulation during manual therapy.

Symptoms

Most authors write about the polysymptomatic manifestations of stroke pathology with a similar localization of the focus of damage to brain tissue, the severity or severity of which, as a rule, is determined by the specific location and extent of arterial damage, the general situation of hemodynamics, the actual level of blood pressure, the state of the so-called collateral circulation and etc. The disease can manifest itself as persistent focal neurological disorders and some general cerebral symptoms. Among these symptoms:

International Neurological Journal 3(3) 2005

Return to number

Infarctions in the vertebrobasilar region: clinical picture and diagnosis

Authors: S.M.Vinichuk, I.S.Vinichuk, National Medical University, Kyiv; T.A. Yalynskaya, Clinical Hospital “Feofania”, Kyiv

print version

The work carried out a clinical neuroimaging analysis in 79 patients with a clinical picture of ischemic infarction in the vertebrobasilar region (VBB). The features of the neurological clinic of lacunar and non-lacunar posterior circular infarctions are described. To verify them, we used the magnetic resonance imaging (MRI) technique. The diffusion-weighted magnetic resonance imaging (DWMRI) technique turned out to be more informative for the diagnosis of acute lacunar and non-lacunar infarctions in the brain stem.

Occlusive lesions of arteries in the vertebral-basilar basin (VBB) lead to the development of posterior circulation infarcts with localization in various parts of the brain stem, thalamus, occipital lobes and cerebellum. The frequency of their development ranks second (20%) after infarction in the middle cerebral artery (MCA) (Kamchatov P.R. 2004) and is 10-14% in the structure of all ischemic strokes (Vinichuk S.M. 1999; Evtushenko S. K. 2004; Toi H. et al, 2003). According to other authors, in Europeans, pathology of intracranial arteries in the VBB is more common than in the carotid region (Worlow C.P. et al. 1998).

The posterior vertebrobasilar system is evolutionarily more ancient than the anterior carotid system. It develops completely separately from the carotid system and is formed by arteries that have different structural and functional characteristics: vertebral and main arteries and their branches.

In the vertebral-basilar system, three groups of arteries are distinguished (Worlow C.P. et al. 1998) (Fig. 1):

Small arteries, the so-called paramedian ones, arising directly from the trunks of the vertebral and basilar arteries, from the anterior spinal arteries, as well as deep perforating arteries originating from the posterior cerebral artery (PCA);

Short circumflex (or circular) arteries, respectively, supplying blood to the lateral territories of the brain stem, the tegmental area, as well as long circumflex arteries - posterior inferior cerebellar artery (PICA), anterior inferior cerebellar artery (PICA), superior cerebellar artery (SCA), PCA with its branches and anterior villous artery;

Large or large arteries (vertebral and main) in the extra- and intracranial sections.

The presence in the posterior vertebrobasilar basin of arteries of different calibers with differences in their structure, anastomotic potential and with different areas of blood supply of small, deep perforating arteries, short and long circumflex arteries, as well as large arteries in most cases determine the localization of the lesion, its size and clinical course of posterior circular infarctions. At the same time, individual differences in the location of the arteries and the diversity of pathogenetic mechanisms very often determine the individual characteristics of the neurological clinic in acute ischemic strokes in the VBD. Therefore, along with the presence of typical neurological syndromes, doctors often note not the clinical picture of vertebrobasilar stroke, which is described in clinical guidelines, but its atypical course, which makes it difficult to determine the nature of the stroke and choose adequate therapy. In such a clinical situation, only brain imaging methods can help.

Materials and research methods

A comprehensive clinical and neuroimaging examination was carried out on 79 patients (48 men and 31 women) aged from 37 to 89 years (on average 65.2±1.24 years). The study included all patients admitted with a clinical picture of acute ischemic stroke to the VBH. Patients were admitted within 6-72 hours from the onset of the first symptoms of the disease. The main cause of ischemic cerebrovascular accidents (ICDs) was arterial hypertension in combination with vascular atherosclerosis (74.7%), in another 22.8% of those examined it was combined with diabetes mellitus; in 25.3% of patients, the main etiological factor of the disease was atherosclerosis. Patient information was recorded in standard protocols, which included demographics, risk factors, clinical symptoms, laboratory and neuroimaging results, outcome, etc.

The degree of impairment of neurological functions was assessed during patient hospitalization, during treatment and at the end of therapy using the NIHSS scale (National Institutes of Health Stroke Scale, USA). At the same time, the scale of B. Hoffenberth et al (1990) was used, which suggests a more adequate assessment of clinical parameters in acute cerebrovascular accidents in the VBD. To assess the degree of recovery of neurological functions, the modified Rankin scale was used (G.Sulter et al. 1999). Subtypes of ischemic strokes were classified according to the National Institute of Neurological Disorders and Stroke Study Group scale (Special Report from the National Institute of Neurological Disorders and Stroke (1990) Classification of cerebrovascular diseases III. Stroke 21:; TOAST criteria (Trial of ORGin) were also taken into account Acute Stroke Treatment - a study of low molecular weight heparin ORG in the treatment of acute stroke (A.J.Grau et al. 2001).The definition of lacunar syndromes was based on data from clinical studies by C.M. Fisher (1965; 1982) and neuroimaging methods.

Standard laboratory tests were carried out: examination of the levels of glucose, urea, creatinine, hematocrit, fibrinogen, acid-base balance, electrolytes, lipids, and indicators of blood coagulating properties.

All patients underwent ultrasound Dopplerography of the great vessels of the head in the extracranial region (USDG) and transcranial Dopplerography (TCD), in some cases - duplex scanning; a 12-electrode ECG was performed, blood pressure (BP) was monitored; volumetric MV was determined in the internal carotid artery (ICA) and vertebral artery (VA).

Spiral computed tomography (SCT) of the brain was performed in all cases immediately upon admission of patients to the hospital. It made it possible to determine the type of stroke: ischemia or hemorrhage. However, the use of SCT did not always make it possible to detect brainstem infarction during the acute period of the disease. In such cases, routine magnetic resonance imaging (MRI) was used, since magnetic resonance images of the posterior cranial fossa are more informative than SCT. MRI of the brain was performed on a Magnetom Symphony device (Siemens) with a magnetic field strength of 1.5 Tesla and on a Flexart device (Toshiba) with a magnetic field strength of 0.5 Tesla. A standard scanning protocol was used, including obtaining TIRM (Turbo Inversion Recovery Magnifucle) and T 2 -weighted images (T 2 -BI) in the axial plane, T 1 -weighted images (T 1 -BI) in the sagittal and coronal planes. However, in the presence of several pathological foci, using MRI techniques it was difficult to determine the extent of their age and to verify the source of the infarction in the medulla oblongata, especially in the acute period. In such cases, a more sensitive neuroimaging technique was used - diffusion-weighted magnetic resonance imaging (DW MRI).

Diffusion-weighted imaging (DWI) can identify the site of acute cerebral ischemia within a few hours of stroke, as evidenced by a decrease in the measured diffusion coefficient (MDI) of water and an increase in the MR signal on DWI. Limitation of water diffusion occurs due to energy deficiency (loss of tissue ATP, weakening of the sodium-potassium pump function) and the ensuing cytotoxic edema of ischemic brain tissue (Neumann-Haefelin T at al. 1999). Therefore, it is believed that DWI is particularly sensitive in identifying a focus of ischemia with a reduced ATP content and a high risk of irreversible neuronal damage (von Kummer R. 2002). Brain tissue after acute focal ischemia with a high MR signal on DWI and a low ICD corresponds to an infarct focus.

Another modern sensitive technique for brain neuroimaging is perfusion-weighted (PV) MRI, which is used in clinical practice, provides information about the hemodynamic state of brain tissue and can detect perfusion disorders both in the ischemic core and in the surrounding collateral areas. Therefore, during the first hours after the onset of stroke, areas of perfusion disorders on a perfusion-weighted image (PWI) are usually more extensive than on DWI. It is believed that this zone of diffusion-perfusion mismatch (DWI/PVI) reflects the ischemic penumbra, i.e. “tissue at risk” for functional impairment (Neumann-Haefelin T at al. 1999).

We performed DW MRI in the axial plane when examining 26 patients (32.9%): 12 patients were examined within 24 hours after the onset of infarction, including 1 within 7 hours, 2 before 12 hours from the onset of the disease. The remaining patients underwent DWI on days 2-3 and in the dynamics of the disease: 4 patients were examined 3 times, 2 times - 14.1 times - 8.

Magnetic resonance angiography, which allows visualization of large extra- and intracranial arteries, was performed in 17 patients (30.4%) with nonlacunar ischemic infarction.

The purpose of our study is to evaluate the value of clinical and neuroimaging methods in the diagnosis of lacunar and non-lacunar posterior circular infarctions.

Results and its discussion

Clinical neuroimaging examination of 79 patients (48 men and 31 women, aged 60 to 70 years) with a clinical picture of ischemic stroke in the VBB allowed us to identify the following clinical forms of acute ischemic disorders of cerebral circulation: transient ischemic attacks (TIA) (n=17) , lacunar TIA (n=6), lacunar infarction (n=19), non-lacunar infarction in the VSB (n=37). In patients with TIA and lacunar TIA, the neurological deficit regressed within the first 24 hours from the onset of the disease, although in patients with lacunar TIA small foci of lacunar infarction were detected on MRI. We analyzed them separately. Therefore, the main study group consisted of 56 patients.

Taking into account the causes and mechanisms of development of acute ischemic infarction, the following subtypes of ischemic infarction were identified: lacunar infarction (n=19), atherothrombotic (n=21), cardioembolic (n=12) infarction and infarction of unknown cause (n=4).

The frequency of localization of detected ischemic infarction in the VSB, verified by neuroimaging methods, was different (Fig. 2). As can be seen from the data presented, most often foci of infarction were detected in the area of the pons (32.1%), thalamus (23.2%), less often - in the area of the cerebral peduncles (5.4%). In many of the subjects (39.4%), posterior circular infarctions were caused by multifocal lesions: the medulla oblongata and cerebellar hemispheres (19.6%); various parts of the brain stem and cerebellar hemisphere, occipital lobe of the brain; cerebellar hemispheres and thalamus; occipital lobes of the brain.

Although on the basis of clinical data it was impossible to accurately determine the arterial localization of the lesion, neuroimaging methods made it possible to conduct a clinical description of the infarction in the VBB, taking into account the vascular territory of the blood supply and, using TOAST criteria, to classify all posterior circular ischemic infarctions into lacunar and non-lacunar.

Classification of ischemic infarctions in the VBD according to etiological and pathogenetic characteristics:

Lacunar infarctions due to damage to small perforating arteries, caused by microangiopathies against the background of arterial hypertension and diabetes mellitus, provided there are no sources of cardioembolism and stenosis of large vertebrobasilar arteries (n=19);

Non-lacunar infarctions due to damage to the short and/or long circumflex branches of the vertebral and basilar arteries in the presence of sources of cardioembolism and the absence of stenosis of the large vertebrobasilar arteries (n=30);

Non-lacunar infarctions due to occlusive lesions of large arteries (vertebral and main), in the extra- or intracranial sections, i.e. caused by macroangiopathies (n=7).

As can be seen from the data presented, damage to small branches was the cause of lacunar infarctions in 33.9% of cases; damage to the short or long circumflex branches of the vertebral or basilar arteries was the most common (53.6%) cause of nonlacunar infarction; occlusion of large arteries also led to the occurrence of nonlacunar infarction and was detected in 12.5% of subjects. The localization of the lesion on MRI and DW MRI of the brain relatively often correlated with the neurological clinic.

I. Lacunar infarctions in the VBB

The clinical characteristics and outcome of 19 patients with lacunar infarctions (LI) in the VBB, verified by neuroimaging methods, are given in Table. 1. The lesions of LI usually had a round outline, about 0.5-1.5 cm in diameter. If the LI diameter was more than 1 cm during the first study, it often increased with repeated MRI.

Lacunar infarctions occurred as a result of damage to a separate paramedian branch of the VA, OA, or one perforating thalamogenic artery, a branch of the PCA, against the background of arterial hypertension, which was often combined with hyperlipidemia, and in 6 patients with diabetes mellitus. The onset of the disease was acute, sometimes accompanied by dizziness, nausea, and vomiting. The background neurological deficit on the NIHSS scale corresponded to 4.14±0.12 points, on the B. Hoffenberth scale - 5.37±0.12 points, i.e. corresponded to mild neurological dysfunction.

More often (n=9) a purely motor infarction (PMI) was detected, caused by damage to the motor pathways in the area of the base of the bridge, which are supplied with blood by small paramedian arteries arising from the main artery. It was accompanied by paresis of the facial muscles and arms, or the entire arm and leg suffered on one side. Complete motor syndrome was detected in 3 patients, partial - in 6 (face, arm or leg), they were not accompanied by objective symptoms of sensory disorders, obvious dysfunctions of the brain stem: loss of visual fields, hearing loss or deafness, tinnitus, diplopia, cerebellar ataxia and severe nystagmus. For illustration, we present an MRI of the patient (Fig. 3), performed 27 hours from the onset of the disease, T 2 TIRM - weighted tomogram in the axial projection, which revealed a lacunar infarction in the right parts of the pons. The diagnosis of LI is confirmed by DW MRI findings and the diffusion map (Fig. 4). ChDI was clinically determined.

Lacunar infarctions in the thalamus in 5 patients caused the development of pure sensory syndrome (PSS), the cause of which was damage to the lateral parts of the thalamus due to occlusion of the thalamogenic artery (Fig. 5, 6). Hemisensory syndrome was complete in 2 patients and incomplete in 3. Complete hemisensory syndrome was manifested by a decrease in superficial and/or deep sensitivity or numbness of the skin according to the hemitype in the absence of homonymous hemianopsia, aphasia, agnosia and apraxia. In incomplete hemisensory syndrome, sensory disorders were recorded not on the entire half of the body, but on the face, arm or leg. In 2 patients, cheiro-oral syndrome was detected, when sensory disturbances occurred in the area of the corner of the mouth and palm homolaterally; One patient had cheiro-oral-pedal syndrome; it was manifested by hypalgesia of pain sensitivity in the area of the corner of the mouth, palms and feet on one side without motor disorders.

In 2 patients, lacunar infarction of the thalamus was accompanied by the spread of ischemia towards the internal capsule, which caused the development of sensorimotor stroke (SMI) (Fig. 7, 8). Neurological symptoms were caused by the presence of a lacuna in the lateral nucleus of the thalamus, but there was an effect on the adjacent tissue of the internal capsule. The neurological status revealed disturbances in sensitivity and movements, but disturbances in sensitivity preceded disturbances in motor skills.

2 patients were diagnosed with “atactic hemiparesis”. Gaps were revealed at the base of the bridge. The neurological clinical picture was manifested by hemiataxia, moderate weakness of the leg, and mild paresis of the arm. Dysarthria-clumsy hand syndrome (dysarthria-clumsy - hand syndrome) was detected in one patient; it was caused by the localization of the lacuna in the basal parts of the pons and was accompanied by dysarthria and severe dysmetry of the arms and legs.

Lacunar infarctions in the VBB were characterized by a good prognosis, restoration of neurological functions occurred on average on the 10.2±0.4 day of treatment: in 12 patients there was complete recovery, in 7 minor neurological microsymptoms (dysesthesia, pain) remained, which did not affect the performance of their tasks. previous responsibilities and daily life activities (1 point on the Rankin scale).

II. Nonlacunar infarctions in the VBB

Clinical characteristics of patients with non-lacunar infarction in the VBB of various etiologies are given in Table. 2. As evidenced by the data presented, the most common neurological symptoms in patients with acute ischemic infarction due to damage to the short or long circumflex branches of the vertebral (VA) or basilar (BA) arteries were: systemic dizziness, headache, hearing impairment with noise in the same ear , motor and cerebellar disorders, sensory disorders in Zelder areas and/or mono- or hemitype. The clinical and neurological profile of posterior circular infarctions due to damage to large arteries (vertebral and main) in all patients was manifested by a defect in the visual field, movement disorders, disturbances in statics and coordination of movements, pontine gaze paresis, and less often - dizziness, hearing impairment.

Analysis of the background neurological deficit in patients with non-lacunar infarctions due to damage to the short or long circumflex arteries of the VA or OA indicates that the impairment of neurological functions according to the NIHSS scale corresponded to moderate severity (11.2 ± 0.27 points), and according to the B. Hoffenberth scale - severe disorders (23.6±0.11 points). Thus, the scale of V. Hoffenberth et al (1990) compared with the NIHSS scale when assessing acute vertebrobasilar stroke more adequately reflected impaired neurological functions and the severity of the patients’ condition. At the same time, in case of infarctions in the VSB due to damage to large arteries and the development of a gross neurological defect, the scales used unidirectionally reflected the volume of neurological deficit, probably because extensive ischemic infarctions predominated in patients.

The initial blood pressure level in patients with occlusion of the large arteries of the spinal vein was significantly lower than in patients with lesions of the short or long circumflex branches of the vertebral or basilar artery. In some patients with occlusion of large arteries, which caused the development of large-focal brainstem infarction, arterial hypotension was recorded upon admission. On the other hand, arterial hypertension in the first day after a stroke in patients with damage to the short or long circumflex branches of the VA and OA could be a manifestation of a compensatory cerebrovascular reaction (Cushing's phenomenon), which occurred in response to ischemia of the brainstem formations. Noteworthy was the lability of blood pressure during the day, with its increase in the morning hours after sleep.

The clinical picture of nonlacunar infarctions caused by damage to the short and/or long circumflex branches of the vertebral and basilar arteries in the presence of sources of cardioembolism and the absence of stenosis of the large vertebrobasilar arteries was heterogeneous with a different clinical course. All other things being equal, the development of focal changes in the posterior parts of the brain depended on the level of the lesion, the arterial bed and the size of the infarct.

Blockage of the posterior inferior cerebellar artery was manifested by alternating Wallenberg-Zakharchenko syndrome. IN classic version it was manifested by systemic dizziness, nausea, vomiting, dysphagia, dysarthria, dysphonia, impaired sensitivity on the face of a segmental dissociated type in the Zelder zones, Berner-Horner syndrome, cerebellar ataxia on the side of the lesion and movement disorders, hypoesthesia of pain and temperature sensitivity on the trunk and limbs from the opposite side. The same neurological disorders were characterized by blockage of the intracranial part of the VA at the level of the origin of the posterior inferior cerebellar artery and paramedian arteries.

Variants of Wallenberg-Zakharchenko syndrome were often observed, which occurred with occlusive lesions of the paramedian arteries of the VA, medial or lateral branches of the PICA and were clinically manifested by systemic dizziness, nystagmus, and cerebellar ataxia. MRI of the brain revealed infarcts in the medial or lateral parts of the medulla oblongata and lower parts of the cerebellar hemispheres.

In the case of cardioembolic occlusion of the paramedian or short circumflex branches of the basilar artery, nonlacunar infarctions occurred in the pontine region (Fig. 9, 10). Their neurological clinical picture was polymorphic and depended on the level of damage to the arterial bed and the location of the infarction. Blockage of the paramedian arteries of the bridge was manifested by alternating Foville syndrome - peripheral paresis of the facial muscles and external rectus muscle of the eye on the side of the lesion with contralateral hemiparesis or Millard-Hubler syndrome: peripheral paresis of the facial muscles on the side of the lesion and hemiparesis on the opposite side.

When the branches of the main artery supplying the midbrain were blocked, paresis of the muscles innervated by the oculomotor nerve occurred on the side of the lesion and hemiplegia on the opposite side (Weber syndrome) or hemiataxia and athetoid hyperkinesis in the contralateral limbs (Benedict syndrome) or intentional hemitremor, hemiataxia with muscle hypotonia (Claude's syndrome). With a heart attack in the quadrigeminal artery basin, upward gaze paralysis and convergence insufficiency (Parinaud's syndrome) occurred, which was combined with nystagmus.

Bilateral infarctions in the region of the paramedian and short circumflex arteries of the OA were characterized by the development of tetraparesis, pseudobulbar syndrome and cerebellar disorders.

Cerebellar infarction occurred acutely as a result of cardiac or arterio-arterial embolism of the anterior inferior cerebellar artery or superior cerebellar artery and was accompanied by general cerebral symptoms and impaired consciousness. Blockage of the PICA led to the development of an infarct focus in the area of the inferior surface of the cerebellar hemispheres and the pons. The main symptoms were dizziness, tinnitus, nausea, vomiting and on the side of the lesion, paresis of the facial muscles of the peripheral type, cerebellar ataxia, Berner-Horner syndrome. With occlusion of the SMA, the focus of the infarction formed in the middle part of the cerebellar hemispheres and was accompanied by dizziness, nausea, and cerebellar ataxia on the side of the focus (Fig. 11). Cerebellar ischemic strokes also occurred when the vertebral or basilar arteries were blocked.

Blockage of the internal auditory (labyrinthine) artery, which in most cases originates from the anterior inferior cerebellar artery (can also arise from the main artery) and is the terminal one, occurred in isolation and was manifested by systemic dizziness, unilateral deafness without signs of damage to the brain stem or cerebellum.

Blockage of the PCA or its branches (calcar and parieto-occipital artery) was usually accompanied by contralateral homonymous hemianopia, visual agnosia with preservation of macular vision. In the case of left-sided localization of the infarction, amnestic or semantic aphasia and alexia occurred. Damage to the branches of the PCA, which supply blood to the cortex of the parietal lobe at the border with the occipital lobe, was manifested by cortical syndromes: disorientation in place and time, visual-spatial disturbances. Large-focal infarctions of the occipital lobe of the brain were accompanied by hemorrhagic transformation of the infarction (Fig. 12).

Thalamic infarctions occurred as a result of damage to the thalamo-subthalamic (thalamoperforating, paramedian branches) and thalamogenicular arteries, which are branches of the posterior cerebral artery. Their occlusion was accompanied by depression of consciousness, paresis of upward gaze, neuropsychological disorders, memory impairment (anterograde or retrograde amnesia), and contralateral hemihypesthesia. More severe disorders (depression of consciousness, paresis of upward gaze, amnesia, thalamic dementia, akinetic mutism syndrome) occurred with bilateral thalamic infarction, which developed as a result of atheromatous or embolic occlusion of the common pedicle of the thalamo-subthalamic artery, the paramedian branches of which supply blood to the posteromedial parts of the thalami (Fig. 13). Occlusion of the thalamo-genicular artery caused the development of an infarction of the ventrolateral region of the thalamus and was accompanied by Dejerine-Roussy syndrome: on the side opposite the lesion, transient hemiparesis, hemianesthesia, choreoathetosis, ataxia, hemialgia and paresthesia were detected.

Blockage of the posterior villous arteries, which are branches of the PCA, led to the development of an infarction in the region of the posterior parts of the thalamus (cushion), geniculate bodies and was manifested by contralateral hemianopia, and sometimes mental impairment.

Occlusion of the vertebral artery (VA) occurred at both extracranial and intracranial levels. With occlusion of the extracranial part of the VA, short-term loss of consciousness, systemic dizziness, visual impairment, oculomotor and vestibular disorders, disturbances in statics and coordination of movements were noted, paresis of the limbs, and sensory disturbances were also detected. Often there were attacks of sudden falling - drop attacks with impaired muscle tone, autonomic disorders, breathing disorders, and cardiac activity. MRI of the brain revealed infarct foci in the lateral parts of the medulla oblongata and the lower parts of the cerebellar hemispheres (Fig. 14, 15).

Occlusion of the intracranial part of the VA was manifested by alternating Wallenberg-Zakharchenko syndrome, which in the classical version was also detected when the PICA was blocked.

Blockage of the basilar artery was accompanied by damage to the pons, midbrain, cerebellum, and was characterized by loss of consciousness, oculomotor disorders caused by pathology of the III, IV, VI pairs of cranial nerves, the development of trismus, tetraplegia, impaired muscle tone: short-term decerebrate rigidity, hormetonic convulsions, which were followed by muscle hypo - and atony. Acute embolic occlusion of the arterial artery in the area of the bifurcation led to ischemia of the ristral parts of the brainstem and bilateral ischemic infarction in the blood supply of the posterior cerebral arteries (Fig. 16, 17). Such a heart attack was manifested by cortical blindness, oculomotor disorders, hyperthermia, hallucinations, amnesia, sleep disorders, and in most cases resulted in death.

Thus, posterior circular ischemic infarctions are different etiologically, heterogeneous in clinical course and with different outcomes.

The results of our study indicate that the MRI technique is sensitive in detecting acute ischemic posterocircular strokes. However, it did not always allow visualization of acute lacunar infarction or ischemic foci in the brain stem, especially in the medulla oblongata. To identify them, the diffusion-weighted MRI technique was more informative.

The sensitivity of DWI in detecting acute brainstem infarction up to 24 hours after the onset of stroke was 67%; the infarct focus was not detected during this time in 33% of patients, i.e. One third of those examined with clinical symptoms of brainstem infarction had false negative results. Repeated examinations of patients after 24 hours using DW MRI of the brain revealed the infarcted area.

The insufficient information content of the DWI technique in determining acute infarction when localized in the brain stem can be explained by two factors. Firstly, the presence of small ischemic foci, since the perforating arteries vascularize very small areas of the brain stem. Secondly, neurons of the brain stem are more resistant to ischemia than neurons of the evolutionarily younger cerebral hemispheres. This could be one of the reasons for their higher tolerance to ischemia and the later development of cytotoxic edema of brain stem tissue (Toi H. et al. 2003).

List of literature / References

1. Vinichuk S.M. Sudina's illness of the nervous system. - Kiev: Nauk. thought. - 1999. - 250 p.

2. Worlow Ch.P. Dennis M.S. van Geyn J. Khankiy G.Zh. Sandercock P.A.G. Bamford J.M. Wardlau J. Stroke: A practical guide for the management of patients (Translated from English). - Polytechnic, St. Petersburg, 1998. - 629 p.

3. Evtushenko S.K. V.A. Simonyan, M.F. Ivanova. Optimization of treatment tactics in patients with heterogeneous ischemic brain damage // Bulletin of emergency rehabilitation medicine. - 2001. - T.1, No. 1. - P. 40-43.

4. Kamchatov P.R. Vertebro-basilar insufficiency // Breast cancer. - 2004. - No. 12(10). - WITH..

5. Grau A.J. Weimar C. Buggle F. et al. Risk factors, outcome, and treatment in subtypes of ischemic stroke // Stroke. - 2001. - Vol. 32. - P..

6. Fisher C.M. Lacunes: small, deep cerebral infarcts // Neurology. - 1965. - Vol. 15. - P..

7. Fisher C.M. Lacunar strokes and infarcts: a review // Neurology. - 1982. - Vol. 32. - P..

8. Von Kummer R. From stroke imaging to treatment. In Stroke: clinical aspects and imaging (teaching courses of the ENS). - 2002. - P. 5-24.

9. Neumann-Haefelin T. Wittsack H.J. Wenserski F. Sieler M. Seitz R.J. Modder V. Freund H.J. Diffusion - and perfusion - weighted MRI. The DWI/PWI mismatch region in acute stroke. // Stroke. - 1999. - Vol. 30, No. 8. - P..

10. Sulter G. Steen C. Dekeyser J. Use of the Barthel Index and Modified Rankin Scale in acute stroke trials //Stroke. - 1999. - Vol. 30. - P..

11. Toi H. Uno M. Harada M. Yoneda K. et al. Diagnosis of acute brain-stem infarcts using diffusion - weighed MRI. // Neurology. - 2003. - Vol. 46, No. 6. - P..

Ischemic stroke in the left cm basin. Ischemic stroke in the VBB what is it. Similar works to - Ischemic stroke in the right MCA. Acute period. Atherothrombotic type. Central left-sided hemiparesis and hemihypesthesia. Central steam

Introduction

Material and methods

results

conclusions

Similar works to - Ischemic stroke in the right MCA. Acute period. Atherothrombotic type. Central left-sided hemiparesis and hemihypesthesia. Central paresis of VII and XII pairs of cranial nerves on the left

Acute cerebrovascular accident in the left MCA of ischemic type. Right-sided hemiparesis. Stage III hypertension, risk IV. Obesity II degree

Ischemic stroke - a complication of hypertension and atherosclerosis - is caused by diseases of the heart valve apparatus, myocardial infarction, congenital anomalies of cerebral vessels, hemorrhagic syndromes and arteritis. Symptomatic therapy.

Send your good work in the knowledge base is simple. Use the form below

Clinical history

Patient: ______________________

Barnaul-2008

FULL NAME. _________________________

Age: 49 years old. (born November 19, 1958)

Location: ________________________________________

Family status: Married. Husband _________________________

Place of work: ___________________________________________

Date of admission to the hospital: 03/13/2008

Date of supervision from 03/17/08. to 03/20/08.

Clinical diagnosis: Acute cerebrovascular accident in the left MCA of ischemic type. Right-sided hemiparesis and hemihypoanesthesia. Motor aphasia. Stage III hypertension, risk IV. Obesity II degree.

COMPLAINTS

- Difficulty speaking, during excitement, cannot pronounce words clearly and clearly.

Ischemic stroke in the territory of the right middle cerebral artery

What are the features of the symptoms of this disease?

What are the features of diagnosing ischemic stroke in the territory of the right middle cerebral artery?

What is the procedure for treating ischemic stroke in the territory of the right middle cerebral artery?

Clinical observations of a neurosurgeon, doctor of the highest category, candidate of medical sciences Evgeniy Evgenievich Zavalishin

Ischemic stroke in the right MCA, malignant course.

Computed tomography 1 day from the onset of the disease

Intraoperative picture

Computed tomography after surgery

Ischemic strokes in the middle cerebral artery basin

Ischemic stroke

Classification

According to the rate of formation of neurological deficit and its duration

According to the severity of the patients' condition

On pathogenesis (Research Institute of Neurology of the Russian Academy of Medical Sciences, 2000)

By location of cerebral infarction

Etiology and pathogenesis

Clinical picture

General cerebral symptoms

Focal neurological symptoms

Stroke in the basin of the left middle cerebral artery: the relationship between speech disorders and a variant of cerebral infarction

About the article

Introduction

Material and methods

results

conclusions

Ischemic stroke in the posterior cerebral arteries

Types of strokes and their differences

Classification of ischemic stroke

Clinical picture of ischemic stroke

Rate of development of symptoms in ischemic stroke

What family members should know

Complications of ischemic stroke

Causes of death

Common symptoms associated with vertebrobasilar stroke

Features of symptoms of stroke in the VBB with embolic variant

Symptoms that can also be observed in patients

Rehabilitation after stroke in the vertebrobasilar region

Search:

Categories

Healthy food blog philosophy

Why can diet-and-treatment.rf be trusted?

Features of ischemic stroke in the vertebrobasilar region

Characteristics of the vertebrobasilar system

Reasons for development

Symptoms

Diagnostics

Treatment

Prevention

Leave your opinion

Ischemic cerebral stroke

Types of stroke according to the rate of increase in neurological symptoms

Clinic

Ischemic stroke of the vertebrobasilar region (VBB)

Diagnostics

Prevention

Forecast

Stroke in the vertebrobasilar area