Ischemic stroke in the basin of the posterior cerebral arteries. Ischemic stroke in the right MCA basin. Acute period. Atherothrombotic type. Central left-sided hemiparesis and hemihypesthesia. Central paresis of VII and XII pairs of FMN on the left Ischemic stroke

Acute (ACVA) and chronic disorders of cerebral circulation remain one of the urgent 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 need long and costly rehabilitation, and only less than 25% of patients return to their usual work activities.

Among the survivors, 40-50% have a second 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 basin. mortality from them is 3 times higher than from strokes in the carotid pool. More than 70% of all transient ischemic attacks occur in the vertebrobasilar basin. Every third patient with a transient ischemic attack subsequently develops an ischemic stroke.

The prevalence of pathology of brachiocephalic arteries is 41.4 cases per 1,000 population. Of these, 30-38% is the pathology of the subclavian and vertebral arteries.

Wide spread, constant increase in morbidity, high mortality in patients of working age, a high percentage of disability among patients put the problem of cerebrovascular ischemia in the socially significant group.

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 (occipital, parietal lobes and mediobasal parts of the temporal lobe), the optic tubercle, most of the hypothalamic region, the legs of the brain with a quadruple, the pons varoli, the medulla oblongata, the reticular formation, the cervical spinal cord.

From the anatomical and functional point of view, 4 segments are divided along 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 the vertebra C II to the dura mater in the area of ​​the lateral occipital foramen, V 4 - to the fusion of both vertebral arteries into the main one (see Fig.).

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

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

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

Stroke with lesion localization in the vertebrobasilar basin

As acute, in its form, violations of the usefulness of cerebral circulation, so, in fact, its chronic forms today remain one of the most pressing, burning problems of world modern medicine. According to the estimates of 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 disabilities or need constant exercise for a rather long and often very costly rehabilitation.

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

At the same time, doctors 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 are localized in the so-called vertebrobasilar basin, the development of a fatal outcome after such events is almost three times higher than from the more common stroke pathologists with the localization of the focus of brain tissue damage in the carotid basin.

In addition, more than 70% of all emerging transient ischemic attacks (or other transient disorders of cerebral blood flow) preceding the state of full-fledged stroke damage occur precisely in the above-mentioned vertebrobasilar basin. At the same time, every third such patient who has undergone a transient ischemic attack with a similar localization of the problem subsequently develops a very difficult ischemic stroke.

What is our vertebrobasilar system?

It should be understood that the share of the so-called physicians, the 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 of a wide variety of cerebral organ formations, such as:

• The posterior parts of the cerebral hemispheres (these are the occipital and parietal lobes and the so-called medio-basal parts of the temporal lobes).
• The visual hillock.
• Most of the vital hypothalamic area.
• The so-called legs of the brain with its quadruple.
• Oblong part of the brain.
• Pons.
• Or the cervical region of our spinal cord.

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

• The smallest arteries, or about the so-called paramedial arteries, extending directly from the main trunks of both the vertebral and main arteries, from the anterior spinal artery. This also includes deeply perforating arteries that originate from the larger posterior cerebral artery.
• The short type of circumflex (or circular) arteries, which are designed to wash the lateral areas 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 main arteries) located in the extracranial and intracranial cerebral regions.

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

Nevertheless, the possible individual features of the location of such arteries, the diversity in the pathogenetic mechanisms, quite often, predetermine the differences in the neurological clinic in the development of such pathologies as acute ischemic stroke with localization in the vertebrobasilar zone.

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

Why does this type of brainstroke occur?

The state of primary vertebrobasilar insufficiency, often preceding the same-name stroke pathology, has the ability to develop due to varying degrees of severity of insufficient blood supply to the regions of brain tissue fed by the vertebrates or the main 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.

It is customary to refer to the first group of factors that often become the reasons for the development of such a stroke pathology: atherosclerosis, stenosis or occlusion of the subclavian arteries, their developmental anomalies (say, pathological tortuosity, the same anomalies of the entrance to the bone cocoa, numerous hypoplasias, etc.). pathologies of an extravascular nature are usually referred to: embolism of different etiology in the vertebrobasilar zone or extravasal compression of the subclavian artery itself.

In rare cases, fibromuscular dysplasia, damage to the subclavian artery after neck injuries or after non-professional manipulations during manual therapy can lead to a brainstroke of this type.

Symptoms

Most authors write about the polysymptomatic manifestations of stroke pathology with a similar localization of the lesion of brain tissue, the severity or severity of which, as a rule, is determined by the specific location and extent of arterial lesions, the general position of hemodynamics, the real 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. These symptoms include:

International Neurological Journal 3 (3) 2005

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Heart attacks in the vertebrobasilar basin: clinical picture and diagnosis

Authors: S. M. Vinichuk, I. S. Vinichuk, National Medical University, Kiev; T.A. Yalynska, Clinical Hospital "Feofania", Kiev

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Abstract / Abstract

In this work, a clinical neuroimaging analysis was carried out in 79 patients with a clinical picture of ischemic infarction in the vertebrobasilar basin (VBB). The features of the neurological clinic of lacunar and non-acunar posterior circulatory infarctions are described. To verify them, we used the method of magnetic resonance imaging (MRI). The technique of diffusion-weighted magnetic resonance imaging (DW MRI) turned out to be more informative for the diagnosis of acute lacunar and nonacunar infarctions in the brainstem.

Occlusive lesion of the arteries in the vertebrobasilar basin (VBB) leads 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 takes second place (20%) after a heart attack in the basin of 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, the pathology of intracranial arteries in the VBD occurs more often than in the carotid basin (Vorlow Ch.P. et al. 1998).

The posterior vertebrobasilar system is evolutionarily more ancient than the anterior - carotid. 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 system of the vertebrobasilar basin, there are three groups of arteries (Vorlow Ch.P. et al. 1998) (Fig. 1):

- small arteries, the so-called paramedian, extending directly from the trunks of the vertebral and main arteries, from the anterior spinal arteries, as well as deep perforating arteries originating from the posterior cerebral artery (PCA);

- short enveloping (or circular) arteries, respectively supplying the lateral areas of the brain stem, the tegmental area, as well as long enveloping arteries - the posterior inferior cerebellar artery (PICA), the anterior inferior cerebellar artery (PNMA), the superior cerebellar artery (VMA), PCA with its branches and the 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 caliber with differences in their structure, anastomotic potential and with different zones 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 circulatory infarction. At the same time, individual differences in the location of arteries, a variety of pathogenetic mechanisms very often determine the individual characteristics of the neurological clinic in acute ischemic strokes in 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 the choice of adequate therapy. In such a clinical situation, only brain imaging techniques can help.

Materials and research methods

A comprehensive clinical and neuroimaging examination was carried out in 79 patients (48 men and 31 women) aged 37 to 89 years (on average 65.2 ± 1.24 years). The study included all those admitted with a clinical picture of acute ischemic stroke to the VBB. Patients were admitted within 6-72 hours after the onset of the first symptoms of the disease. The main cause of ischemic cerebral circulation disorders (CMC) was arterial hypertension in combination with vascular atherosclerosis (74.7%), in another 22.8% of the 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 demographic indicators, risk factors, clinical symptoms, laboratory and neuroimaging studies, outcome, etc.

The degree of impairment of neurological functions was assessed during hospitalization of patients, during treatment, and at the end of therapy using the NIHSS scale (National Institutes of Health Stroke Scale, USA). At the same time, we used the scale of B. Hoffenberth et al. (1990), which suggests a more adequate assessment of clinical parameters in acute CCD in VBD. To assess the degree of recovery of neurological functions, a modified Rankin scale was used (G. Sulter et al. 1999). Ischemic stroke subtypes were classified according to the Special Report from the National Institute of Neurological Disorders and Stroke (1990) Classification of cerebrovascular diseases III. Stroke 21: 637-676; the TOAST criteria ( Trial of ORG 10172 in Acute Stroke Treatment - a study of low molecular weight heparin ORG 10172 in the treatment of acute stroke) (AJGrau et al. 2001). The definition of lacunar syndromes was based on data from clinical studies by K. Miller Fisher (CM Fisher, 1965; 1982) and methods neuroimaging.

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

All patients underwent ultrasound Doppler ultrasound of the great vessels of the head in the extracranial section (USDG) and transcranial Doppler (TCD), in some cases, duplex scanning; 12-electrode ECG was performed, blood pressure (BP) was monitored; the volumetric MC was determined by the internal carotid (ICA) and vertebral arteries (PA).

Spiral computed tomography (SCT) of the brain was performed in all cases immediately upon admission to the hospital. It allowed to determine the type of stroke: ischemia or hemorrhage. At the same time, the use of SCT did not always allow detecting a brain stem infarction in the acute period of the disease. In such cases, the technique of routine magnetic resonance imaging (MRI) was used, since magnetic resonance images of the posterior fossa are more informative than SCT. MRI of the brain was performed using a Magnetom Symphony (Siemens) apparatus with a magnetic field strength of 1.5 T and a Flexart apparatus (Toshiba) with a magnetic field strength of 0.5 T. A standard scanning protocol was used, including 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 coronary planes. However, in the presence of several pathological foci using the MRI technique, it was difficult to determine the degree of their prescription, to verify the foci of 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).

With the help of diffusion-weighted images (DWI), it is possible to determine the area of ​​acute cerebral ischemia within a few hours after the development of a stroke, which is manifested by a decrease in the measured diffusion coefficient (CDI) of water and an increase in the MR signal on DWI. Restriction of water diffusion occurs due to insufficient energy (loss of tissue ATP, weakening of the sodium-potassium pump function) and the onset of cytotoxic edema of ischemic brain tissue (Neumann-Haefelin T at al. 1999). Therefore, it is believed that DWI is especially sensitive in identifying an ischemic focus with a reduced ATP content and a high risk of irreversible damage to neurons (von Kummer R. 2002). The brain tissue after acute focal ischemia with a high MR signal on DWI and a low ICD corresponds to the infarction focus.

Another modern sensitive technique for brain imaging, perfusion-weighted (PV) MRI, which is used in clinical practice, provides information on the hemodynamic state of brain tissue and can reveal perfusion disorders both in the ischemic nucleus zone and in the surrounding collateral areas. Therefore, during the first hours after the onset of a stroke, the areas of perfusion disorders on the perfusion-weighted image (PVI) 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” of 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 development of a heart attack, including 1 - within 7 hours, 2 - up to 12 hours from the onset of the disease. The rest of the 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 visualizing large extra- and intracranial arteries, was performed in 17 patients (30.4%) with non-acunar ischemic infarction.

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

Results and its discussion

Clinical and neuroimaging examination of 79 patients (48 men and 31 women, aged 60 to 70 years) with a clinical picture of ischemic stroke in VBB made it possible to identify such clinical forms of acute ischemic cerebrovascular accidents: transient ischemic attacks (TIA) (n = 17) , lacunar TIA (n = 6), lacunar infarction (n = 19), non-acunar infarction in VBP (n = 37). In patients with TIA and lacunar TIA, 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 the development of acute IUD, the following subtypes of ischemic infarctions were identified: lacunar infarction (n = 19), atherothrombotic (n = 21), cardioembolic (n = 12) infarctions and infarction of unknown cause (n = 4).

The frequency of localization of the detected ischemic infarction in VBD, verified by neuroimaging, was different (Fig. 2). As can be seen from the data presented, most often infarction foci were detected in the area of ​​the bridge (32.1%), thalamus (23.2%), less often in the area of ​​the cerebral pedicles (5.4%). In many surveyed (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 an infarction in VBB, taking into account the vascular territory of the blood supply and, according to the TOAST criteria, classify all posterior-circular ischemic infarctions into lacunar and non-acunar ones.

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

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

- non-acunar infarctions due to lesions of short and / or long enveloping branches of the vertebral and basilar arteries in the presence of sources of cardioembolism and the absence of stenosis of large vertebrobasilar arteries (n = 30);

- non-acunar infarctions due to occlusive lesions of large arteries (vertebral and main), in the extra- or intracranial regions, i.e. due to macroangiopathies (n = 7).

As can be seen from the above data, the defeat of small branches was the cause of lacunar infarctions in 33.9% of cases; the defeat of the short or long enveloping branches of the vertebral or basilar arteries was the most frequent (53.6%) cause of the development of non-acunar infarction; occlusion of large arteries also led to the occurrence of non-acunar infarction and was detected in 12.5% ​​of the subjects. The localization of the lesion on MRI and DW MRI of the brain was relatively often correlated with the neurological clinic.

I. Lacunar infarctions in VBB

Clinical characteristics and outcomes of 19 patients with lacunar infarction (LI) in VBD, verified by neuroimaging methods, are shown in Table. 1. LI lesions usually had rounded outlines, about 0.5-1.5 cm in diameter. If during the first study the LI diameter was more than 1 cm, it more often increased with repeated MRI.

Lacunar infarctions occurred as a result of damage to a separate paramedian branch of the PA, OA, or one perforating thalamogenicular artery - a branch of 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. responded to mild neurological dysfunctions.

More often (n = 9) purely motor infarction (PDI) 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 extending from the main artery. It was accompanied by paresis of the facial muscles and arms, or the arm and leg were completely affected 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 sensitivity disorders, obvious disorders of the brain stem function: loss of visual fields, hearing loss or deafness, tinnitus, diplopia, cerebellar ataxia and gross nystagmus. For illustration, we present the patient's MRI (Fig. 3), performed 27 hours after 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 data and a diffusion map (Fig. 4). PDI was clinically determined.

Lacunar infarctions in the thalamus in 5 patients caused the development of a purely sensory syndrome (HR), which was caused by damage to the lateral thalamus due to occlusion of the thalamogenicular 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; in one patient the cheiro-oral-pedal syndrome was determined; 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 thalamic infarction was accompanied by the spread of ischemia towards the inner capsule, which led to the development of sensorimotor stroke (SM) (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 inner capsule. In neurological status, sensory and movement impairments were determined, but sensory impairments preceded motor impairments.

Two patients were diagnosed with "atactic hemiparesis". Gaps were found at the base of the bridge. The neurological clinic was manifested by hemiataxia, moderate leg weakness, and mild arm paresis. The syndrome of dysarthria and clumsy hands (dysarthria-clumsy - hand syndrom) was detected in one patient, was due to the localization of the lacuna in the basal parts of the pons and was accompanied by dysarthria and severe dysmetry of the arm and leg.

Lacunar infarctions in VBB were characterized by a good prognosis, restoration of neurological functions occurred on average on 10.2 ± 0.4 days of treatment: 12 patients had complete recovery, 7 had insignificant neurological microsymptoms (dysesthesia, pain), which did not affect the performance of their previous duties and daily life activity (1 point on the Rankin scale).

II. Non-lacunar infarction in VBB

The clinical characteristics of patients with non-acunar infarction in VBD of various etiologies are given in table. 2. As evidenced by the above data, the most common neurological symptoms in patients with acute ischemic infarction due to damage to short or long circumflex branches of the vertebral (PA) or main (OA) arteries were: systemic dizziness, headache, hearing impairment with noise in the same ear , motor and cerebellar disorders, sensory disturbances in Zelder's zones and / or according to mono- or hemitype. The clinical and neurological profile of posterior circulatory infarctions due to damage to large arteries (vertebral and main) in all patients was manifested by a defect in the visual field, movement disorders, impaired statics and coordination of movements, palsy gaze, less often - dizziness, hearing impairment.

Analysis of the background neurological deficit in patients with non-acunar infarctions due to lesions of short or long circumflex arteries of PA or OA indicates that impairments 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 B. Hoffenberth et al. (1990) compared with the NIHSS scale in assessing acute vertebrobasilar stroke more adequately reflected the impairment of neurological functions, the severity of the patient's condition. At the same time, in case of heart attacks in VBP 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 the patients were dominated by extensive ischemic infarctions.

The baseline blood pressure level in patients with occlusion of large arteries of VBP was significantly lower than in patients with lesions of 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 on the first day after a stroke in patients with lesions of the short or long circumferential branches of PA and OA could be a manifestation of a compensatory cerebrovascular reaction (Cushing's phenomenon), which arose in response to ischemia of brain stem formations. Attention was drawn to the lability of blood pressure during the day, with an increase in the morning hours after sleep.

The clinical picture of non-acunar infarctions caused by lesions of 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 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 heart attack.

Blockage of the posterior inferior cerebellar artery was manifested by the alternating Wallenberg-Zakharchenko syndrome. In the classical version, it manifested itself as systemic dizziness, nausea, vomiting, dysphagia, dysarthria, dysphonia, impaired sensitivity on the face according to the segmental dissociated type in the Zelder zones, Berner-Horner syndrome, cerebellar ataxia on the side of the focus and movement disorders, hypesthesia of pain and temperature sensitivity trunk and limbs from the opposite side. The same neurological disorders were characteristic of the blockage of the intracranial section of the PA at the level of the posterior inferior cerebellar artery and paramedian arteries branching from it.

Variants of the Wallenberg-Zakharchenko syndrome were often observed, which arose with occlusive lesions of the paramedian arteries of the PA, medial or lateral branches of PICA and were clinically manifested by systemic dizziness, nystagmus, and cerebellar ataxia. On MRI of the brain, they revealed foci of infarction in the medial or lateral regions of the medulla oblongata and the lower regions of the cerebellar hemispheres.

In the case of cardioembolic occlusion of the paramedian or short circumflex branches of the basilar artery, non-acunar infarctions occurred in the pons (Fig. 9, 10). Their neurological clinic was polymorphic and depended on the level of arterial lesions and the localization of the heart attack. Blockage of the paramedian arteries of the pons was manifested by alternating Fauville syndromes - peripheral paresis of the facial muscles and the external rectus muscle of the eye on the side of the focus with contralateral hemiparesis or Miyara-Gubler: peripheral paresis of the facial muscles on the side of the focus and hemiparesis on the opposite side.

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

Bilateral infarctions in the pool of paramedian and short circumflex arteries of 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 cerebral symptoms and impaired consciousness. Blockage of PNMA led to the development of a heart attack in the region of the lower surface of the cerebellar hemispheres and 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, and Berner-Horner syndrome. In the case of occlusion of the IAV, the infarction focus was 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 have also occurred when the vertebral or basilar arteries are blocked.

Blockage of the internal auditory (labyrinth) artery, which in most cases originates from the anterior inferior cerebellar artery (can also extend from the main artery) and is terminal, arose in isolation and manifested itself as systemic dizziness, unilateral deafness without signs of damage to the brain stem or cerebellum.

Blockage of the PCA or its branches (spur and parieto-occipital artery) was usually accompanied by contralateral homonymous hemianopsia, visual agnosia, with preserved macular vision. In the case of left-sided localization of the heart attack, amnestic or semantic aphasia and alexia occurred. The defeat of the branches of the PCA, which supply blood to the cortex of the parietal lobe on the border with the occipital, manifested itself as 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 gaze upward, neuropsychological disorders, memory impairment (anterograde or retrograde amnesia), contralateral hemihypesthesia. More severe disorders (depression of consciousness, paresis of gaze upward, amnesia, thalamic dementia, akinetic mutism syndrome) occurred in bilateral thalamic infarction, which developed as a result of atheromatous or embolic occlusion of the common leg of the thalamo-subthalamic artery, the paramedian branches of which supply the thalamic artery with blood supply to the posterior medial arteries. thirteen). Occlusion of the thalamo-genicular artery caused the development of infarction in the ventrolateral region of the thalamus and was accompanied by Dejerine-Russi syndrome: transient hemiparesis, hemianesthesia, choreoathetosis, ataxia, hemialgia and paresthesia were detected on the side opposite to the lesion focus.

Blockage of the posterior villous arteries, which are branches of the PCA, led to the development of a heart attack in the posterior thalamus (cushion), geniculate bodies and was manifested by contralateral hemianopsia, sometimes by impaired mental activity.

Vertebral artery (VA) occlusion occurred at both the extracranial and intracranial levels. With occlusion of the extracranial part of the PA, short-term loss of consciousness, systemic dizziness, visual impairments, oculomotor and vestibular disorders, impaired statics and coordination of movements were noted, paresis of the extremities, and impaired sensitivity were also detected. Often there were attacks of sudden falls - drop attacks with impaired muscle tone, autonomic disorders, respiratory disorders, cardiac activity. MRI of the brain revealed infarction foci of the lateral regions of the medulla oblongata and the lower regions of the cerebellar hemispheres (Fig. 14, 15).

The occlusion of the intracranial part of the PA was manifested by the Wallenberg-Zakharchenko alternating syndrome, which in the classical version was also detected with blockage of the PICA.

Blockage of the main artery was accompanied by damage to the pons, midbrain, cerebellum, characterized by loss of consciousness, oculomotor disorders caused by the pathology of pairs III, IV, VI of cranial nerves, the development of trismus, tetraplegia, impaired muscle tone: short-term decerebrational rigidity, hormone-tonic muscle cramps, which were replaced - and atony. Acute embolic occlusion of OA in the area of ​​the fork 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, was fatal.

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

The results of our study show that the MRI technique is sensitive for the detection of acute ischemic posterior circulatory strokes. At the same time, it did not always allow visualizing an 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 in the period up to 24 hours after the onset of stroke was 67%, the infarction focus during this time was not detected in 33% of patients, i.e. a third of those examined with clinical symptoms of a brain stem infarction had false negative results. Repeated examination of patients after 24 hours using DW MRI of the brain revealed an infarction zone.

The lack of information content of the DWI technique in determining acute infarction when localized in the brain stem can be explained by two factors. First, the presence of small ischemic foci, since perforating arteries vascularize very small areas of the brainstem. Second, neurons in the brain stem are more resistant to ischemia than neurons in 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 the brain stem tissue (Toi H. et al. 2003).

References / References

1. Vinichuk S.M. Sudden illness of the nervous system. - Kiev: Science. dumka. - 1999 .-- 250 p.

2. Vorlow Ch.P. Dennis M.S. van Gein J. Hanky ​​G. Zh. Sandercock P.A.G. Bamford J.M. Vordlau J. Stroke: A Practical Guide for Patient Management (Translated from English). - Polytechnic, St. Petersburg, 1998 .-- 629 p.

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

4. Kamchatov P.R. Vertebrobasilar insufficiency // BC. - 2004. - No. 12 (10). - S. 614-616.

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. 2559-2566.

6. Fisher C.M. Lacunes: small, deep cerebral infarcts // Neurology. - 1965. - Vol. 15. - P. 774-784.

7. Fisher C.M. Lacunar strokes and infarcts: a review // Neurology. - 1982. - Vol. 32. - P. 871-876.

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 MRІ. The DWI / PWI mismatch region in acute stroke. // Stroke. - 1999. - Vol. 30, no.8. - P. 1591-1597.

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. 1538-1541.

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. 352-356.

Weakness in the right hand

Severe limitation of active movements

Contact with the patient is difficult due to aphatic disorders, anisognosia.

There are no complaints from other bodies and systems.

05/05/11 - the first increase in blood pressure (BP) up to 160/100 mm. rt. Art., previously blood pressure was not controlled. She did not 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 up to plegia in the hand, elements of sensory-motor aphasia. Was hospitalized by the ambulance team in the regional hospital.

20.g. - on MRI, 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.

May 21, 2011 - examined by a neurosurgeon - does not need neurosurgical correction.

August 2011 - was treated at the City Hospital. Discharged with some improvement.

01/14/20112 - sent to the Central Clinical Hospital of the UZ for treatment and additional examination.

Acute rheumatic fever at age 10 (June 1993)

Viral hepatitis, tuberculosis, sexually transmitted diseases - denies

Childhood infections - denies

Other past illnesses: bronchitis, pneumonia (2010)

Hereditary diseases not established

Allergic history is not burdened

No hemotransfusions were performed.

Medical history - not burdened.

General condition - moderate severity

The skin is clean, normal color

Rhythmic heart sounds, accent of II tone on the aorta. HELL 135/80 mm. rt. Art. Heart rate 78 / min

Vesicular breathing is auscultatory in the lungs, no wheezing

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

Physiological functions - no peculiarities

No peripheral edema

Stool and urination is controlled

The tapping symptom is negative on both sides.

Meningeal symptom complex negative

Eye slits and pupils D = S, converging strabismus due to the left eye. The movement of the eyeballs in full. Pupil reaction to light of medium vividness. 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 limbs is increased in a spastic manner. There is a moderate increase in muscle tone in the spastic type and in the left extremities. Muscle strength in the right limbs is reduced to 0-1 points in the arm, 1-2 points in the leg. Movements in the limbs are possible due to the proximal sections

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

No convincing sensory disturbances have been identified

Emotionally labile. Dysphoria. Elements of anosognosia

Diagnosis on admission

Condition after an ischemic stroke in the LSMA pool with gross right-sided hemiparesis in the hand up to plegia, elements of sensory-motor aphasia, cerebrospinal fluid-hypertensive syndrome.

Combined rheumatic mitral disease with a predominance of insufficiency.

Examination plan and results

Magnetic resonance imaging of the brain

Occlusive hydrocephalus was a consequence of a heart attack 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 aqueduct of the brain.

Sclerotic changes in the walls of the aorta, cusps of the aortic and mitral valves. Prolapse of the anterior and posterior cusps of the mitral valve II stage. with regurgitation of I-II st. on the valve (the formation of mitral insufficiency against the background of rheumatic altered mitral valve leaflets). Dilation of the ascending aorta. Weakly expressed hypertrophy of the posterior wall of the left ventricle. Additional notochord in the lumen of the left ventricle, hemodynamically insignificant.

The rhythm is sinus. Right. The horizontal position of the electrical axis. Signs of right atrial hypertrophy. Decrease in repolarization processes in the apical anterolateral region.

Doppler ultrasonography of the carotid arteries

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

Ultrasound examination of the abdominal organs

Diffuse changes in the parenchyma of the liver and pancreas without their increase. Cholesterosis of the walls of the gallbladder. Microurolithiasis. Right nephroptosis - I st. Focal neoplasms of the right adrenal gland.

Focal and infiltrative changes in the lungs were not identified. The roots are structural. Not enlarged. The sinuses are free. The diaphragm is clearly defined. Heart of regular shape and size. The aorta is not changed.

General blood analysis

Reactive thrombocytosis, leukocytosis, increased ESR

General urine analysis

Transient proteinuria due to damage to the basement membrane.

Lipid spectrum of blood

Hypercholesterolemia. Dyslipidemia: Type II-B

Blood chemistry

Hyperglycemia due to ischemia in the projection area of ​​the left

middle cerebral artery.

Blood clotting indicators

Within the physiological norm.

Lesion of the middle cerebral artery

Dyslipidemia type II-B

Heart failure II B, FC III

The defeat of the mitral valve with a predominance of insufficiency of stage I

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

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

Normalization of lifestyle, rehabilitation measures

Motor rehabilitation (full or partial recovery): 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 that are usually impaired in aphasia (and preserved in dysarthria), reading and counting, using "homework" for the afternoon

Psychological and social rehabilitation: 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

Cardiomagnet 75 mg / day

Instant mortality in ischemic stroke is 20%

In 70% of patients, persistent defects of the motor and sensory spheres remain

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

Antiplatelet drugs reduce the risk of recurrent stroke by 20%

Statins and a / hypertensive 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 recover the ability to walk

Almost 50% of patients with ischemic stroke die from myocardial infarction

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

For life - favorable

For work - unfavorable, disability.

Ischemic stroke from meteorological diseases, the risk of which increases sharply in unfavorable weather.

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

Kharkiv National University V.N. Karazin

Acute cerebrovascular accident in the basin of the left MCA by ischemic type. Right-sided hemiparesis. GB III Art, risk IV. Obesity II degree

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

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Altai State Medical University

Head Department: Professor Schumacher G.I.

Teacher: assistant Gorbunova N.I.

Curator: student 408 gr. Tashtamyshev V.N.

Clinical history of the disease

Patient: ______________________

Barnaul-2008

FULL NAME. _________________________

Age: 49 (19.11.1958 year of birth)

Place of residence: ________________________________________

Family status: Married. Husband _________________________

Place of work: ___________________________________________

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

The date of supervision is from 17.03.08. until 03.20.08.

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

COMPLAINTS

- For difficulty in speaking, during excitement, he cannot pronounce words clearly and clearly.

Headaches in the temporal and parieto-occipital regions, aggravated in the evening, as well as after sleep. The pains are acute, and arise in the left temporal region, followed by the transition to the occipital and to the opposite temporal region.

Periodic dizziness, tinnitus, nausea, retching,

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

Glushkova Elena Gavrilovna, was born on November 11, 1958 in the Zalesovsky district of the Altai Territory in the village of Cheryomushkino. She grew and developed normally, she did not lag behind her peers in mental and physical development. She graduated from the 10th grade of secondary school. In 1976 she studied as a machine operator, where she worked for 3 years. From 1979 to 2003 she worked as a commodity expert. In 2003 she became the director of the rural house of culture, where she still works.

Epidemic history Denies tuberculosis, viral hepatitis, venereal diseases. I have not been in contact with infectious patients.

Bad habits: No

Allergic history: No.

Operations: cesarean section in 1990.

Blood transfusion in 1982 during childbirth.

The general condition of the patient is of moderate severity. Consciousness is clear, the position in bed is active. The skin is warm, moist, the turgor is preserved. The mucous membrane of the mouth, the conjunctiva is pink. Peripheral lymph nodes are not enlarged. The supraclavicular, ulnar, axillary, inguinal lymph nodes are not palpable. The patient's behavior is normal, he answers questions adequately, easily comes into contact. The physique is correct, the constitution is normosthenic, increased nutrition. No edema or subcutaneous emphysema. Height 144cm, weight 72kg. The presence of scars, defects in the head area is not observed. Type of hair growth for the female type. The hair is dark. Asymmetry of the chest, changes in the shape of the joints were not revealed. Full mobility in the cervical, thoracic and lumbar spine. The movements in the joints are preserved. Muscular system: on the left side of the body - muscles are in good shape, no atrophy pain on palpation. On the right: hypotonia, hypoesthesia. The thyroid gland is not enlarged, painless, and is not welded to the surrounding tissues.

Nasal breathing is free. The ribcage is of the correct shape; both halves are symmetrical, equally involved in the act of breathing. Vesicular breathing, no wheezing. RR = 16 / min. Palpation: the chest is painless, the resistance is good, the voice tremor is carried out with equal strength. With comparative percussion, a clear lung sound is heard at all points. With topographic percussion: the height of standing of the tops of the lungs is 4.5 cm on the right and left, the width of Krenig's fields on the left and on the right is 5 cm. The boundaries of the lungs are within normal limits.

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

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

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

Percussion revealed an increase in the left ventricle, relative and absolute dullness of the heart.

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

No dentures. The oral mucosa was unremarkable. The pharynx is not hyperemic, the tonsils are not enlarged. The act of swallowing is not disturbed. The abdomen is of the correct shape, symmetrical, not swollen, actively participates in the act of breathing, there are no visible pulsations, there is no visible peristalsis of the stomach and intestines. There is no bulging in the right hypochondrium.

Palpation... The temperature is the same on superficially symmetrical areas, the skin is moist. Subcutaneous fat is well expressed. The abdomen was soft, divergence of the rectus abdominis muscles, hernial orifices, no protrusions were found. There is a scar after a cesarean section. Symptom Shchetkin - Blumberg negative. With deep palpation according to Obraztsov - Strazhesko palpates the sigmoid colon in the left iliac region 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 undetectable. The lower edge of the liver is located along the edge of the costal arch, the contour is smooth, soft-elastic consistency, painless. The size of the liver according to Kurlov is 9/8/7 cm. Free fluid in the abdominal cavity using percussion and the method of fluctuation was not revealed. On auscultation - the noise of intestinal motility. The stool is regular, shaped, free of pathological impurities, normal color.

On examination of the lumbar region, no swelling or edema was found. 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. There are no obsessions, affects, behaviors. Fully oriented in space and time, speech is correct, slightly inhibited. Reacts to external stimuli adequately. There is a disturbance in sleep and wakefulness. There are no meningeal symptoms.

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

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

Ischemic stroke in the basin of the right middle cerebral artery

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

What are the features of the symptoms of this disease?

In the presence of ischemic stroke in the basin of the right middle cerebral artery, it is possible to reveal the symptoms of lesions of the midbrain and cerebral hemisphere, depending on the location and conditions of collateral blood supply in the clinical picture. Quite often, you can find a combination of damage to the thalamus and the cerebral hemisphere, or isolated thalamic infarctions. 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 the diagnosis of ischemic stroke in the basin of the right middle cerebral artery?

It is worth noting that often computed tomography does not allow detecting any ischemic modification in the parenchyma of the brain for a certain moment from the onset of strokes, exactly that time, which is very important as the beginning of the cure for this kind of diseases.

Thanks to the use of magnetic resonance imaging, it becomes possible to more accurately determine the presence and nature of any ischemic change in the main brain during strokes. After receiving the data after the performed magnetic resonance imaging, it becomes possible to detect early ischemic modification. Today, it has become possible to combine various modes, which makes it possible to determine a sharper, subacute and congenital ischemic change in the brain parenchyma.

What is the procedure for the treatment of ischemic stroke in the basin 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 the patients. At the very beginning of the healing process, you should normalize the way of life, attend rehabilitation events. The motor process of rehabilitation includes strength and dexterity in each limb, self-service skills, all of which can be fully or partially rehabilitated. The speech rehabilitation process includes each session with specialists, in particular with speech therapists and neuropsychologists, each exercise necessary to restore ordinary reading or counting disorders. As for the psychological and social healing processes, it is necessary to create a healthy climate 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 of antidepressants, which are selected individually for each patient. Much attention should be paid to this, because using your own assumptions about taking antidepressants can only lead to the appearance of 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 recurrence of a stroke, and in the absence of therapy, the disease can also return.

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

This clinical example shows how menacing the malignant course of ischemic stroke can look, the frequency of which reaches 25% of all ischemic strokes. This disease arises 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 substance.

Ischemic stroke in the right MCA basin, malignant course.

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

The brain is the most important integrative center, which has concentrated on itself all the control functions of the body, but reacts one-sidedly to any problems - edema, which is shown in these photographs.

Computed tomography 1 day from the onset of the disease

(lines indicate zones of ischemia, arrows indicate an extended thrombus in the vessel)

Intraoperative picture

(edematous brain, smoothed furrows, pale pink color)

Computed tomography after surgery

(the 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 photos, but I want to convey to people about the need for early prevention of stroke, a correct and active lifestyle, healthy food and full preventive medical examinations.

Ischemic strokes in the basin of the middle cerebral artery

Most strokes develop in the middle cerebral artery. Homonymous hemianopsia is characteristic, indicating damage to visual radiance. The eyeballs are directed towards the affected hemisphere11; on the opposite side, there is a weakness of the facial muscles of the lower half of the face and spastic hemiparesis (the hands suffer more than the legs). Muscle tone in paralyzed limbs may initially decrease, but spasticity develops after a few days or weeks. Sometimes sensory and movement disorders are limited to the contralateral arm and half of the face, and the leg and trunk are almost not affected. If the dominant hemisphere is damaged, motor and sensory aphasia is possible. With the defeat of the parietal lobe of the non-dominant hemisphere, complex disorders of sensitivity and perception disorders occur. The defeat of the right hemisphere is often accompanied by confusion, and the left hemisphere - depression in the later stages of the disease.

Cerebral edema can cause narrowing and occlusion of one or both of the 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 a stroke in the frontal lobe and the medial surface of the hemisphere. Blood in the posterior cerebral artery comes from the vertebrobasilar system. Therefore, with occlusion of the internal carotid artery, stroke usually develops in the basin of the middle cerebral artery, and not the entire internal carotid artery.

Internal carotid artery stenosis can be suspected by a weakening of the pulse on it. However, the result of palpation, as well as the result of auscultation (see above), must be interpreted with caution - what seems to the doctor as a normal pulsation of the internal carotid artery may in fact be an external pulsation. In diagnosis, a comparison of the pulse on the right and left carotid arteries helps: a significant weakening of the pulse on one side suggests occlusion of the common carotid artery of the same name. The 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 blood from the common carotid artery begins to flow. However, it is difficult to assess this symptom. Vascular murmur in the orbit area may indicate stenosis of the internal carotid artery.

"Ischemic strokes in the basin of the middle cerebral artery" - an article from the section Nervous diseases

Ischemic stroke

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

Classification

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

By the rate of formation of neurological deficit and its duration

• transient disorders of cerebral circulation (PNMC) is a clinical syndrome presented by focal neurological and / or cerebral disorders, which develops suddenly due to an acute violation of cerebral circulation.

According to the severity of the patient's condition

• minor stroke - neurological symptoms are not significantly expressed, regresses 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, gross focal deficit, often dislocation symptoms

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

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

By localization of cerebral infarction

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

Etiology and pathogenesis

The following are distinguished as local etiotropic factors of stroke:

• atherosclerosis of the main and intracerebral arteries. Soft, loose atheromatous plaques become a source of embolism, dense ones narrow the lumen of the arteries, restricting blood flow. A 60% decrease 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, slowing and turbulence of blood flow at the site of stenosis, increased aggregation of blood elements, coagulation of fibrin and a decrease in 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, 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 vertebral-basilar basin.
• rare vascular pathology: Takayasu's disease, Moyamoya, infectious arteritis.

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

1. violation of central hemodynamics:
   • cardiac hypodynamic syndrome - manifested by impaired blood circulation, heart rhythm, a decrease in the minute volume of blood and stroke volume of blood, 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 by the type of cerebrovascular insufficiency ( hemodynamic stroke).
   • arterial hypertension - intensifies hemodynamics and leads to the development of arterio-arterial, cardiogenic embolism, 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.
2. Other systemic factors include coagulopathy, erythrocytosis and polycetemia.

Depending on the etiopathogenetic factors, ischemic stroke is subdivided into atherothrombotic, cardioembolic, hemodynamic, lacunar and stroke according to the type of hemorheological microocclusion.

• Atherothrombotic stroke (34%) usually occurs against the background of atherosclerosis of the cerebral arteries of large or medium caliber. Atherosclerotic plaque narrows the lumen of the vessel and promotes thrombus formation. Arterio-arterial embolism is possible. This type of stroke develops stepwise, with an increase in symptoms over several hours or days, often debuting in a dream. Often, atherothrombotic stroke is preceded by transient ischemic attacks. The size of the ischemic lesion focus 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 in valvular heart disease, recurrent rheumatic and bacterial endocarditis, in other heart lesions, which are accompanied by the formation of parietal thrombi in its cavities. Often an embolic stroke develops as a result of a 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 ​​blood supply to the middle cerebral artery, the size of the focus of ischemic damage is medium or large, and a hemorrhagic component is characteristic. A history of possible thromboembolism of 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 hemodynamic stroke can be sudden or stepwise, at rest or in the active state of the patient. The sizes of heart attacks are different, 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 stenosis of the arteries, abnormalities of the vascular system of the brain).
• Lacunar stroke (20%) is caused by damage to small perforating arteries. As a rule, it occurs against the 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 semi-oval center, base of the pons), the size of the foci does not exceed 1.5 cm.General cerebral and meningeal symptoms are absent, there are characteristic focal symptoms (purely motor or purely sensitive lacunar syndrome, atactic hemiparesis, dysarthria or monoparesis).
• A stroke of the type of hemorheological microocclusion (9%) occurs against the background of the absence of any vascular or hematological disease of the established etiology. Stroke is caused by pronounced hemorheological changes, disturbances in the system of hemostasis and fibrinolysis. Scanty neurological symptoms in combination with significant hemorheological disorders are characteristic.

The cerebral ischemia process 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". With cerebral blood flow 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 the structures of the brain, there are no morphological changes in the penumbra. Penumbra exists for 3-6 hours from the onset of the first clinical manifestations of cerebral ischemia. This period is a "therapeutic window" during which it is possible to limit the prevalence of heart attack; during this period of time, therapeutic measures are most promising. Cell death in the area of ​​the penumbra leads to the expansion of the infarction area. The final formation of the infarction zone is completed in 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 "nucleus" of ischemia), which is formed in 6 - 8 minutes. In this zone, energy metabolism disorders are irreversible, with the development of brain tissue necrosis. Cerebral ischemia leads to a series of interrelated pathobiochemical changes called "pathobiochemical cascade" or "ischemic cascade" (Gusev EI et al., 1997). According to V.I. Skvortsova (2000), its stages are:

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

Ischemic processes in the 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 starting point for the development of edema is the penetration of water from the intercellular space into the cells due to a violation of the permeability of cell membranes. After that, extracellular (vasogenic) edema joins the intracellular edema, which is caused by a violation of the blood-brain barrier with the accumulation of under-oxidized products in the damaged area, which are formed during anaerobic glycolysis. Intracellular and vasogenic edema leads to an increase in brain volume and intracranial hypertension, which causes dislocation syndrome ("upper" insertion - insertion of the basal parts of the temporal lobe into the notch of the cerebellar sign with entrapment of the midbrain, and "lower" insertion - insertion 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 cerebral and focal neurological symptoms.

General cerebral symptoms

General cerebral symptoms are characteristic of moderate and severe strokes. Disturbances of consciousness are characteristic - stunnedness, drowsiness or agitation, a short-term loss of consciousness is possible. Headache is typical, which may be accompanied by nausea or vomiting, dizziness, pain in the eyeballs, aggravated by eye movement. Convulsive phenomena are less common. Vegetative symptoms are possible: feeling of heat, sweating, palpitations, dry mouth.

Focal neurological symptoms

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

Stroke in the basin of the left middle cerebral artery: the ratio of speech disorders with a variant of cerebral infarction

About article

The article examines the variants of speech disorders and variants of changes in the brain substance in stroke in the left middle cerebral artery (MCA) basin, special attention is paid to aphasia and the variants of ischemic, as a rule, cerebral infarction that caused it. The effectiveness of a set of classes to improve speech has been analyzed.

Research: to study the ratio of the volume of brain damage in stroke in the left MCA basin 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 the neurological deficit was assessed. Later, if the condition of the patients allowed, they underwent speech therapy, in most cases - the next day after admission to the hospital. All patients on admission and the majority of patients underwent a CT scan of the brain in dynamics in order to confirm / exclude focal brain lesions and clarify the extent of the lesion and localization of the pathological area.

Results: according to the results of CT of the brain, 32 (25.8%) out of 124 people showed typical ischemic changes in the LSMA basin, of which 7 - during the study in dynamics, 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 restoration.

Conclusions: sensorimotor aphasia in ischemic cerebral infarction can occur both when a large area around the Sylvian groove of the dominant hemisphere is affected, and when a local lesion occurs in the area of ​​one of the speech cortical centers or the area of ​​white matter between them. Aphasic syndrome is more common in cryptogenic ischemic stroke, sensorimotor aphasia often occurs in recurrent strokes. Taking into account the less pronounced dynamics of speech restoration 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: the ratio of speech disorders with a variant of cerebral infarction // RMZh. 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 a 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 group 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 substance of the brain during stroke in the basin of the left middle cerebral artery.

Introduction

Speech processes, as a rule, exhibit a significant degree of lateralization and in most people depend on the leading (dominant) hemisphere. It should be borne in mind that in defining the dominant hemisphere responsible for speech, the approach linking 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 ability to restore speech. Many people exhibit only partial and unequal dominance of the hemisphere in relation to different functions. While speech function in right-handers (≥90%) and most left-handers (> 50%) is associated primarily with the left hemisphere, there are three exceptions to this rule:

1. Less than 50% of left-handers have speech function associated with the right hemisphere.

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

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

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

The area of ​​the cortex responsible for the function of speech is located around the Sylvian and Rolland furrows (MCA basin). The speech production is determined by four zones of this area, closely related to each other and located sequentially along the anterior anterior axis: Wernicke's zone (posterior part of the superior temporal gyrus), angular gyrus, arcuate bundle (DP) and Broca's zone (posterior part of the inferior frontal gyrus) (Fig. 12) .

DP is a subcortical fibers of white matter connecting 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 - only 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 caused by focal lesions of the brain, different in localization. Complex forms of dysarthria are often observed.

Purpose of the study: to study the ratio of the volume of brain damage in stroke in the left MCA basin and the degree of speech impairment.

Material and methods

In 124 cases (every third patient), a preliminary diagnosis was made: stroke in the basin of the left middle cerebral artery (LSMA). This localization is most relevant in the study of aphasia in patients with stroke.

All patients on admission and the majority of patients underwent a CT scan of the brain (Bright Speed ​​16 tomograph) in dynamics in order to confirm / exclude focal brain lesions and clarify the extent of the lesion and localization of the pathological area.

According to the results of CT scan of the brain, 32 (25.8%) of 124 people showed typical ischemic changes in the LSMA pool, of which 7 during the study in dynamics, that is, at admission, the changes were not yet obvious (the initial stage of stroke). In 5 (4.0%) cases, hemorrhages were revealed: 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, ACVA was not confirmed (there are no corresponding changes in CT and neurological status). The number of those who were not hospitalized in the ACVA 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, since they were diagnosed with traumatic changes in the skull, brain, neoplasms. Some of the patients were transferred to the neurology emergency department of another hospital, for example, with a diagnosis of osteochondrosis.

64 patients admitted to the stroke department with stroke had speech impairments (Table 2). The detailed nature of speech disorders is determined by a speech therapist. In 20 (31.2%) cases, the patients had dysarthria and the absence of aphasia. In 2 cases, dysarthria was accompanied by dysphonia and dysphagia. Aphasia was revealed in 44 (68.8%) people, of whom in 7 cases it regressed by the time of consultation with a speech therapist the next day (in 2 cases, with regression of aphasia, ischemic heart attacks were detected). In 3 people from the group with the sensorimotor variant of aphasia, severe dysarthria was noted, in 9 people - 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, patients with sensorimotor aphasia had a large infarction in the LSMA basin of the dominant hemisphere (Fig. 4-6). In 47.8% (11 people) of cases, 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 restoration.

In table 4, in parentheses, cases of correspondence of the localization of pathological changes to the functional and anatomical zones are indicated (with sensorimotor aphasia - a vast area around the Sylvian groove; with motor aphasia - with Broca's center; with dysarthria - with local changes at the level of the midbrain, subcortical structures, and cortex).

It is often not possible to achieve a significant improvement in speech in patients with sensorimotor aphasia in the 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 the aphasic syndrome conducted in the second half of the twentieth century, according to which patients who have survived a hemorrhagic stroke have opportunities to restore speech, and a favorable prognosis can be expected. In dynamics, the degree of speech impairment, as a rule, decreased against the background of complex treatment, including while maintaining hemodynamically significant stenosis of the internal carotid artery (according to ultrasound duplex scanning), but in the absence of recurrent stroke or severe hemorrhagic transformation.

conclusions

2. In patients with sensorimotor aphasia caused by stroke, more often than in other groups, deafened consciousness was noted, 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 the speech centers individually, most likely, vary, therefore, the accuracy of the alleged anatomical lesion is not always found to coincide with the degree of functional impairment (aphasia).

4. Full correspondence of the volume of the revealed cerebral infarction to 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 in cryptogenic ischemic stroke, sensorimotor aphasia often occurs in recurrent strokes.

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

Ischemic stroke in the pool of the posterior cerebral arteries

article in PDF format

Etiology. The most common cause of isolated infarctions in the PCA basin is embolic occlusion of PCA and its branches, which occurs in 80% of cases (cardiogenic> arterio-arterial embolism from vertebral and basilar [syn: main] arteries> cryptogenic embolism). Thrombosis in situ is detected in PCA in 10% of cases. Vasoconstriction associated with migraine and coagulopathy are the causes of cerebral infarction in 10% of cases. If isolated infarctions in the PCA basin in most cases have a cardioembolic nature, then the involvement of the brain stem and / or cerebellum in combination with a heart attack in the PCA basin is most often associated with atherosclerotic vascular lesions of the vertebrobasilar basin (VBB). Arterial dissection involving PCA can be a very rare cause of a heart attack in this area. Regardless of the cause of the heart attack, it usually only partially captures the PCA pool.

the materials of the article "Ischemic stroke in the basin of the posterior cerebral arteries: problems of diagnosis, treatment" by I.А. Khasanov (physician 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: TRANSITION NEUROLOGICAL ATTACK

PACIFIC STATE MEDICAL UNIVERSITY

Department of Psychiatry and Neurology

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

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

DISEASE HISTORY

Clinical diagnosis

Concomitant: Hypertension III degree

Completed: student 402 gr. l / f

Barabash A.S.

Vladivostok

PASSPORT SECTION

Age: 48 years old

Nationality Russian

marital status: Not maried

Profession: driver

Place of residence:

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

COMPLAINTS

For weakness in the left hand and its numbness, as well as for speech impairment.

ANAMNESlS MORBI:

In the evening of March 29, I began to feel numbness in my left hand, it became weak. Then he called a friend and noted that he could not clearly express himself, his speech was broken. Then he called the ambulance team, which took him to the hospital of the KGBUZ VKB No. 1. The ambulance 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, operations or TBI. Allergic history is not burdened. Increase in blood pressure from 35 years. Material and living conditions at different periods of life are satisfactory. Hereditary history: the patient's mother had hypertension, obesity. Bad habits: does not smoke. He denies alcohol abuse and drug use. There are no occupational hazards.

STATUS PRAESENS:

A condition of moderate severity. Consciousness is clear. Body temperature is normal (36.6). He understands the addressed speech. Has grade 4 obesity. Height 173 cm, weight 199 kg.

Skin, visible mucous membranes of pink color, normal moisture; subcutaneous fat is overdeveloped.

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

Mild edema is defined in the ankle joint. Muscle development and tone are normal. Tremors and tremors of individual muscles are absent. Deformation of the bones and changes in the terminal phalanges of the fingers and feet are not detected. The configuration of the joints is normal, the color of the skin and local temperatures in the area of ​​the joints are also normal. There is no spinal curvature.

Respiratory organs: The chest is hypersthenic. Breathing type - mixed, breathing 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 border of the lungs is within normal limits. Percussion - clear pulmonary sound. Auscultatory - vesicular breathing, no wheezing.

Bodies of the CCC:

The boundaries of the relative dullness of the heart:

Left: in the 5th intercostal space on the mid-clavicular line

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

Upper: on the 3rd rib, on the left peri-sternal line.

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

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

)10cm

)9cm

)8 cm

The lower edge of the liver 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: On examination, the lumbar region is not changed, the kidneys are not palpable; the tapping symptom is negative. Kidneys, 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 disorders.

The thyroid gland is not visible, not palpable.

NEUROLOGICAL STATUS

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

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

Cranial nerves.

I pair - olfactory nerves.

Odors distinguish and differentiate from both nostrils.

II pair - the optic nerve.

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

ΙΙΙ, ΙV, VI pairs - oculomotor, block, abducent nerves.

The eye slits are symmetrical. The movements of the eyeballs are not limited in volume. The pupils are the same, of the correct rounded shape. The reaction of the pupils to light is direct, friendly. The reaction to convergence is well expressed. Para - trigeminal nerve.

Palpation of the trigeminal points is painless. The movements of the lower jaw are not limited. The tone of the masticatory, temporal muscles is the same. Corneal, conjunctival reflexes are vivid, identical on both sides. II pair - facial nerve. The face at rest is asymmetric, there is a ptosis of the left corner of the mouth. The patient may close his eyes and frown, wrinkle his forehead, bared his teeth (symmetrically). Lachrymation or dryness of the eyes is not observed pair - the vestibular cochlear nerve.

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

Swallowing and phonation are preserved. The soft palate is mobile. Palatine and pharyngeal reflexes live on both sides. Pair - accessory nerve.

There are no muscular atrophies and deformities of the sternocleidomastoid muscle. Head turns are saved.

XII pair - the hypoglossal nerve.

Speech is not clear, the tongue deviates to the left. There are no atrophies and fibrillar twitchings.

Motor sphere

When examining the muscles of the limbs and trunk, muscle atrophy is not detected, fibrillar and fascicular twitching was not detected. The 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 - inward and outward rotation of 20 degrees. In the sagittal plane - flexion up to 130 degrees, extension up to 35 degrees. The arm extended forward to a horizontal position can be pulled back to an angle of 120 degrees and brought to the side of the opposite arm (towards the midline of the body) to an angle of 30 degrees.

· In the elbow joint, the flexion of the forearm is performed up to an angle of 140 degrees.

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

The phenomena of a cogwheel, a folding knife, and plastic hypertonicity were not found. Strength in the muscles of the shoulder, forearm, hand and fingers of the right hand 5 points, the left hand 4 points. Lower limb movements are possible in full:

· Flexion-extension movements are performed in the hip joint 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 flexing it in the hip joint at an angle of 90 degrees.

· The range of these movements is within 45 degrees in one (internal rotation) and the other (external rotation) sides. 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 by movement in the small joints.

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

Baret test: upper and lower positive on the left.

Reflex sphere

Deep reflexes from the hands:

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

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

extensor ulnar - is, alive, stronger on the left

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

medium (D9 - D10) - yes, lowered 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:

Babinsky's symptom(reflex extension of the fingers in case of streak irritation of the sole) negative

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

Ankylosing spondylitis-Mendel's symptom(flexion of the II - V fingers when tapping with a hammer on the antero-outer surface of the back of the foot) negative

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

Oppenheim's symptom(as a result of holding the thumb pad with pressure on the front surface of the tibia from top to bottom, reflex extension of the thumb is observed) negative.

Gordon's symptom(as a result of squeezing the mass of the gastrocnemius muscle with the hand, reflex extension of the thumb is observed) negative.

Pussep's symptom(abduction of the V toe with dashed stimulation of the outer edge of the foot), negative.

Coordinating sphere

The gait is not disturbed.

Static samples:

Romberg's pose - the patient is stable.

Dynamic probes:

Finger-nose test: performs correctly.

Calcaneal knee test: performs correctly

Sensitive sphere

Hypesthesia in the left extremities.

Functions of the pelvic organs

The function is not broken.

Higher cortical functions

Cognitive functions preserved

DATA OF ADDITIONAL RESEARCH METHODS

1.General urine analysis:

erythrocytes +++ 250

bilirubin-

urea + 16

protein ++ 1g

density 1.025

leukocytes + 25

2.Urine analysis according to Nechiporenko: leukocytes-18000, erythrocytes 82000.

3.No helminth eggs were found.

1. Blood glucose 10.1 mmol / l
2. Blood chemistry:

Albumin 46.8 g / l

Total protein 81g / l

Cholesterol 6.8 mmol / L

Triglycerides 1.44mmol / l

Urea 6.8 mmol / l

Total bilirubin 10.3 μmol / L

Direct bilirubin 3.4 μmol / L

1. SASS: PTV-19.1 sec, fibrinogen 2.8 g / l, APTT-31.2 sec, INR-1.54, RFMK-
2. EMF - negative.
3. Antibodies to HIV virus - not detected
4. ECG: Sinus rhythm 106, blockade of the anterior-left branch of the left leg p. His. Diffuse changes in the left ventricular myocardium.
5. Ultrasound of the abdominal cavity and kidneys: pathological echoes - signs of steatohepatosis, pancreatic lipomatosis.
6. Ultrasound of brachiocephalic vessels:

In PSMA, there is an increased peripheral resistance. CPD on the right SMA-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 FMN on the left:

· Descent of the left corner of the mouth

· Dysarthria

· Tongue deviation to the left

Central left-sided hemiparesis

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

· Deep reflexes from hands saved S> D

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

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

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

Movement disorders in the form of central left-sided hemiparesis indicates a lesion of the pyramidal pathway, which begins in the right hemisphere in the neurons of the anterior central gyrus, then it goes into the inner capsule (anterior two-thirds of the hind thigh), then it passes in the middle part of the legs of the brain, descends through the base of the bridge 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 FMN indicates a unilateral lesion of the cortico-nuclear pathway passing in the knee of the inner capsule, in the middle part of the cerebral peduncles. The path crosses when approaching the nuclei.

Sensory disorders in the form of left-sided hemihypesthesia.

Pathways of superficial sensitivity (pain, temperature and partly tactile). The first neurons for all types of sensitivity lie in the spinal ganglia. Fibers from them through the posterior roots enter the posterior 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 go up , ending in the lower part of the outer nucleus of the optic hillock. This pathway is called the lateral spino-thalamic pathway.

The third neuron starts from the cells of the ventralateral nucleus of the optic tubercle, forming the thalamocortical pathway. Through the posterior third of the posterior leg of the internal capsule and then as part of the radiant crown, it is sent to the projection sensitive zone - the posterior central gyrus, to the cortex of the superior parietal region.

Paths of deep sensitivity (muscular-articular feeling, vibrational, and also partly tactile). Getting through the posterior roots into the spinal cord, the central fibers of the cells of the spinal ganglion (1 neuron) do not enter the posterior horns, but go to the posterior cords, in which they are located on the side of the same name. The fibers coming from the underlying sections (lower limbs) are located more medially, forming a thin bundle, or Gaul's bundle (fasciculus gracilis). Fibers carrying irritations from the proprioceptors of the upper extremities occupy the outer part of the posterior cords, forming a wedge-shaped bundle, or Burdakh's bundle (fasciculus cuneatum). Since fibers from the upper extremities pass in the wedge-shaped bundle, 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, 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 pathway.

The paths of deep sensitivity cross at the level of the medulla oblongata, forming a medial loop (lemniscus medialis), to which fibers of the spinothalamic pathway and fibers coming from the sensory nuclei of the cranial nerves join at the level of the anterior sections of the bridge. As a result, conductors of all types of sensitivity, coming from the opposite half of the body, are concentrated in the medial loop. The conductors of deep sensitivity enter the ventralateral nucleus of the optic tubercle, where the third neuron begins. From the optic hillock as part of the thalamocortical pathway of deep sensitivity, through the posterior part of the posterior leg of the inner capsule, they come to the posterior central gyrus of the cerebral cortex, the superior parietal lobe and partly to some other parts.

ETIOLOGICAL DIAGNOSIS

Central paresis of the VII and XII pairs of FMN, movement disorders in the form of central left-sided hemiparesis, sensory disorders in the form of left-sided hemianesthesia indicate a one-sided location of the focus in the right hemisphere. Together with high cholesterol levels (6.8 mmol / L), arterial hypertension and metabolic syndrome, neurological syndromes may indicate a heart attack in the basin of the right middle cerebral artery, due to the formation of blood clots at the site of an atherosclerotic plaque.

CLINICAL DIAGNOSIS

Main: Ischemic stroke in the basin of the right MCA from 03/29/2015. Acute period. Atherothrombotic type. Central left-sided hemiparesis and hemihypesthesia. Central paresis of the VII and XII pairs of FMN on the left.

Concomitant: Hypertension III degree.

JUSTIFICATION OF CLINICAL DIAGNOSIS

The clinical diagnosis was made on the basis of:

Complaints: weakness in the left hand and its numbness, as well as impaired speech. PRAESENS: obesity grade 4.

Neurological status: central paresis of the VII and XII pairs of FMN on the left, movement disorders in the form of central left-sided hemiparesis, sensory disorders in the form of left-sided hemianesthesia. Absence of meningeal symptoms and headache.

Additional research methods: cholesterol 6.8 mmol / l, blood sugar 10.1 mmol / l, ultrasound of the brachiocephalic vessels: There is an increased peripheral resistance in PSMA. CPD on the right SMA-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, movement disorders in the form of central left-sided hemiparesis, sensory disorders in the form of left-sided hemianesthesia.

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

DIFFERENTIAL DIAGNOSIS

neurological diagnosis stroke treatment

In connection with different therapeutic tactics for cerebral hemorrhage and cerebral infarction, the differential diagnosis of these diseases is of great importance. The classic signs of a hemorrhagic stroke are the sudden, apoplectiform development of the disease, loss of consciousness, and the instant onset of neurological symptoms (usually paralysis). A cerebral infarction is characterized by a period of precursors, a gradual dysfunction, and the 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 the instant loss of other cerebral functions. Therefore, to diagnose the type of stroke, it is necessary to take into account also other signs. A 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, and may have a history of myocardial infarction. The onset of the disease with hemorrhage is sudden, during vigorous activity, with emotional or physical stress. Cerebral infarction often begins during sleep or while resting. General cerebral, meningeal and autonomic symptoms are more pronounced in hemorrhagic stroke. Attachment to them of focal symptoms, signs indicating displacement and compression of the brain stem (oculomotor disorders, disorders of muscle tone, respiration, heart activity), also more often indicates a cerebral hemorrhage. High blood pressure, satisfactory heart function, tense, often slow pulse are characteristic of hemorrhagic stroke. Ischemic stroke usually occurs with normal or low blood pressure, heart sounds are muffled, the pulse is insufficiently filled, arrhythmia is often noted, and peripheral circulation in the extremities is not uncommon.

Also, the 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, etc.), 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 encephalopathy due to hypoglycemia, hyperglycemia, hypoxia, uremia, hyponatremia, or other disorders are usually manifested by impaired consciousness with minimal focal neurological symptoms (hyperreflexia, changes in tone, Babinsky's symptom), but sometimes accompanied by severe focal disorders (hemiparesis, aphasia), reminiscent of In their diagnosis, anamnestic data and the results of biochemical studies are of great importance, revealing the corresponding abnormalities in the blood plasma, the absence of changes on CT or MRI of the head, characteristic of a stroke. Alcoholic or, less commonly, alimentary 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 Korsakov 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 a stroke and be combined with it. In cases of amnesia for trauma and the absence of external signs of head injury, traumatic intracranial hemorrhage or brain contusion is often regarded as a stroke. In such cases, the specification of the anamnesis and the results of CT or MRI of the head (if they are unavailable - X-ray of the skull, echoencephaloscopy and lumbar puncture reveal the traumatic genesis of the disease.

In people with epilepsy, seizures sometimes lead to impaired consciousness and post-seizure neurological disorders, such as hemiparesis (Tod's palsy), which can be mistakenly regarded as ischemic stroke. In these cases, it is of great importance to find out anamnestic data about previous seizures and the results of EEG, CT or MRI of the head. Stroke patients may develop post-stroke epileptic seizures, accompanied by a deepening neurological deficit, 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 brain matter, can rule out stroke.

In patients with migraine, in rare cases, migraine stroke may develop, which is usually manifested by homonymous hemionopsy. More often, patients with migraine develop "ordinary" strokes, and sometimes immediately before the development of a stroke or after an attack of migraine pain occurs, but the examination reveals a "normal" stroke, for example, an atherothrombotic stroke. One of the rare forms of migraine - basilar migraine - is manifested by visual impairment, dizziness, ataxia, bilateral paresthesias in the extremities, in the mouth and tongue, which resembles an ischemic stroke in the vertebrobasilar system. At a young age of 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 lower blood pressure: beta-blockers (atenolol), ACE inhibitors (captopril, enalapril), Ca channel blockers (amlodipine). Enalapril 5-10 mg, by mouth or sublingually, 1.25 mg, IV slowly over 5 minutes;

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

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

Special treatment for ischemic stroke includes: restoring blood flow to 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 drip through an infusomat slowly (at a rate of 1-2 mg / h) under the control of blood pressure 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 at night.

Physiotherapy: light therapy, 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 there is a period of improvement, when the patient's symptoms begin to decrease. At the same time, the rate of recovery can be different. With a good and rapid development of collateral circulation, it is possible to restore function on the very 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, BI .. Propedeutics of internal diseases. General clinical research and semiotics: Lectures for students and novice doctors / B.N. Geltser, E F. Semisotova.-Vladivostok: Dalnauka, 2001. -420 p.

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

Computer program “Cito! Analyzes "

Kulganov, Yu.V. Scheme of the case history / Yu.V. Kulganov, G.I. Bykova.-Vladivostok, 1996 -35 p.

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

Fedotov, P.I. Atlas of photo illustrations to physical methods of clinical research of human internal organs in health and disease / P.I. Fedotov, N.A. Korosteleva.-Vladivostok .: Far East book publishing house, 1976 -261 p.

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

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

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

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

Stroke is a disease of the century

Stroke affects about 6 million people in the world every year, about 4 million of them die, half of them remain disabled. The number of patients in Russia is at least 450 thousand people per year. Worst of all, the incidence is increasing and the age of sick people is getting younger.

Types

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 thrombus, which blocks the inner space of the vessel. The pathogenesis of thrombotic stroke explains a 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 by a thrombus coming from internal organs. Pathogenesis: a thrombus forms in other organs, after which it breaks off and enters the cerebral vessel with the blood flow. Therefore, the course of ischemia is acute, rapid, the lesion focus is impressive in size. The most common source of blood clots is the heart, cardioembolic stroke develops with myocardial infarction, cardiac arrhythmias, artificial valves, endocarditis; less often, atherosclerotic plaques in large major vessels are the source of blood clots.

A common cause of cerebral obstruction is a cardiogenic embolus.

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

Lacunar stroke, as a rule, is a consequence of arterial hypertension

• Rheological. Etiology is a blood clotting disorder that is not associated with any diseases of the blood and 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 come to the fore, as well as problems associated with blood clotting disorders.

The most common causes of ischemic stroke are thrombosis and embolism.

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

Depending on the rate of formation and the duration of the 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.
• Small stroke. All symptoms persist for more than 24 hours but less than 21 days.
• Progressive ischemic stroke. Differs in the gradual development of the main neurological symptoms - over several hours or days, sometimes up to a week. After that, the health of the sick person is either gradually restored, or neurological abnormalities persist.
• Completed stroke. Symptoms persist for more than 3 weeks. A cerebral infarction usually develops, after which severe physical and mental health problems sometimes persist. With extensive stroke, the prognosis is poor.

Clinic

The main symptoms are:

• Movement disorders of varying severity. Disorders of the cerebellum: lack of coordination, decreased muscle tone.
• Violation of the pronunciation of one's own and the perception of someone else's speech.
• Visual impairment.
• Sensitive 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 vertebro-basilar basin.

Ischemic stroke of the vertebrobasilar basin (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 suffer at once - the trunk and the cerebellum. The cerebellum is responsible for the coordination, balance and tone of the extensor muscles. The dysfunction of the cerebellum can be called "cerebellar syndrome". The brain stem contains 12 cranial nerve nuclei, which are responsible for swallowing, eye movement, chewing, and balance. After a stroke in the brain stem, these functions can be impaired to varying degrees. In ischemic strokes, focal dysfunctions 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, imbalance and coordination of movements occur, with damage to the cerebellum, muscle tone decreases, as a result of damage to the cerebellum, there is a violation of the coordination of muscle movements. If the trunk is damaged, oculomotor disorders, facial nerve palsy, paresis of the extremities (alternating syndrome), chaotic movement of the eyeballs, combined with nausea, vomiting and dizziness, appear, a person has poor hearing. The trunk also regulates the reflexes of chewing and swallowing.

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

The course of TIA with damage to the intracranial part of the vertebral artery and the posterior cerebellar artery is not severe, 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 an acute vascular disorder, because medical tactics for hemorrhages and ischemia have serious differences.

Diagnosis of cerebrovascular accident by ischemic type begins with a medical examination, the main symptoms of the disease and the existing risk factors are taken into account. The doctor listens to the heart, lungs, measures the pressure on both hands and compares the indicators. To clarify neurological disorders, to determine the severity, it is imperative to undergo a neurological examination.

For an urgent diagnosis and clarification of the cause of the disease, an ultrasound examination of the vascular bed of the brain, an electroencephalogram is carried out, 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 MRI and CT of the brain. In addition, the diagnosis of ischemic stroke should include a finger and vein blood test, a coagulation test, and a general urine test.

Prophylaxis

Prevention of ischemic cerebral circulation disorders is aimed at eliminating risk factors and treating concomitant diseases. Primary prevention is aimed at preventing the first seizure in life, secondary prevention of recurrent stroke.

Prevention of ONMK

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

• Refusal from cigarettes. After quitting active and passive smoking, the risk of stroke is reduced significantly even in older people who have smoked their entire adult life.
• Avoiding alcohol. It is not recommended to drink alcohol even in moderation, because each person has his own individual concept of moderation. It is completely necessary to give up alcohol for people who have already suffered an acute disturbance of cerebral blood supply in their lives.
• Physical activity. Regular physical activity at least 4 times a week will have a positive effect on weight, the state of the cardiovascular system, and the fatty composition of a sick person's blood.
• Diet. The diet consists in moderate consumption of fats, it is recommended to replace animal fats with vegetable fats, eat fewer simple carbohydrates, eat more fiber, pectins, vegetables, fruits and fish.
• Reducing excess body weight. Weight loss should be achieved by reducing the calorie content of food, establishing 5-6 meals a day, increasing physical activity.
• Normalization of blood pressure is the most effective prevention of ischemic stroke. With a healthy blood pressure, the risk of developing a primary and repeated stroke is reduced, and the work of the heart is normalized.
• It is necessary to adjust the blood sugar level in diabetes mellitus.
• It is necessary to restore the work of the heart.
• Women are advised to stop using contraceptives that contain large amounts of estrogen.
• Drug prophylaxis. Secondary prevention of ischemic stroke must necessarily contain antiplatelet and anticoagulant drugs - Aspirin, Clopidogrel, Dipiradamol, Warfarin.

Secondary prevention medication

Observing 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 observing preventive measures, it is possible to reduce the overall incidence of stroke.

Forecast

The chances of a favorable outcome for each person are different and are determined by the size and location of the lesion. Patients die after the development of cerebral edema, displacement of the internal structures of the brain. The chances of surviving are 75–85% of patients 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 very low in lacunar type. Low survival rate in elderly people, hypertensive patients, smokers and drinkers of alcohol, people after a heart attack, with arrhythmias. The chances of a good recovery decrease rapidly if neurologic symptoms persist for more than 30 days.

In 70% of the surviving people, disability persists for a month, after which the person returns to his usual life, 15-30% of patients after a stroke remain stable disabled, the same number of people have every chance of developing a second stroke.

Patients who have had a microstroke or a minor stroke have a chance to leave for work early. People with extensive strokes may or may not return to their previous jobs after a long recovery period. Some of them can return to their original place, but for an easier job.

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

Stroke is not a hereditary, chromosomal and inevitable disease. For the most part, a 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 food, devote more time to your children and grandchildren, spend the holidays with delicious non-alcoholic cocktails and you will not have to learn about the causes and statistics of stroke.

Relevance... Ischemic strokes in the basin of the posterior cerebral arteries (PCA) constitute, according to various sources, from 5 to 10 to 25% of all ischemic strokes. They can cause a number of clinical symptoms, which are not always timely and adequately recognized by the patients themselves, their relatives and doctors, because the acutely arisen gross motor deficit, which is usually associated with a stroke, in this case may not be expressed or completely absent. At the same time, a delay in timely diagnosis or an incorrect diagnosis call into question the possibility of providing the patient with adequate therapy (first of all), which in turn cannot but affect the outcome of the disease.

Etiology... The most common cause of isolated infarctions in the PCA basin is embolic occlusion of PCA and its branches, which occurs in 80% of cases (cardiogenic> arterio-arterial embolism from vertebral and basilar [syn: main] arteries> cryptogenic embolism). Thrombosis in situ is detected in PCA in 10% of cases. Vasoconstriction associated with migraine and coagulopathy are the causes of cerebral infarction in 10% of cases. If isolated infarctions in the PCA basin in most cases have a cardioembolic nature, then the involvement of the brain stem and / or cerebellum in combination with a heart attack in the PCA basin is most often associated with atherosclerotic vascular lesions of the vertebrobasilar basin (VBB). Arterial dissection involving PCA can be a very rare cause of a heart attack in this area. Regardless of the cause of the heart attack, it usually only partially captures the PCA pool.

Anatomy... Paired PCA, which are formed by the bifurcation of the basilar artery (OA) and are its terminal branches, serve as the main sources of blood supply to the upper midbrain, thalamus, and posterior inferior parts of the cerebral hemispheres, including the occipital lobes, mediobasal temporal lobes, and lower medial parietal regions.

In the early stages of human development, the posterior cerebral artery is a branch of the internal carotid artery (ICA) and is supplied with blood from the carotid system, while the posterior communicating artery (PCA) plays the role of its proximal segment. Subsequently, blood into the posterior cerebral arteries begins to flow from the OA, and the PCA, being a branch of the internal carotid artery, becomes the most significant anastomosis between the carotid and vertebrobasilar regions (PCA flows into the PCA about 10 mm distal to the place of bifurcation of the basilar artery). According to various sources, from 17 to 30% of adults have a fetal (embryonic) type of PCA structure, in which the ICA remains the main source of PCA blood supply throughout life. The fetal type of PCA structure in most cases is observed unilaterally, with the opposite PCA usually starting from an asymmetrically located, curved OA. In cases where both posterior cerebral arteries are branches of the internal carotid arteries, as a rule, well-developed large posterior communicating arteries are observed, and the upper segment of the OA is shorter than usual (the OA ends with two superior cerebellar arteries extending from it). In about 8% of cases, both PCA originate from the same ICA.

Each ZMA can be conditionally divided into 3 parts:

■ pre-communication part (P1-segment [according to Fisher]) - a portion of the PCA proximal to the place where the PCA flows into it; from this segment, the paramedian mesencephalic, posterior thalamoperforating and medial posterior choroidal arteries depart, which are involved mainly in the blood supply to the ventrolateral nuclei of the thalamus and the medial geniculate body (the left and right posterior thalamoperforating arteries can branch off from the common Persheron artery, usually called an artery of the stratum with unilateral hypoplasia of the P1 segment and fetal structure of the PCA);

■ postcommunication part (P2-segment) - a portion of the PCA located distal to the place where the PCA flows into the PCA; from this segment are peduncular perforators, thalamogeniculatory and lateral posterior choroidal arteries that supply blood to the lateral geniculate body, dorsomedial nuclei and cushion of the thalamus, part of the midbrain and lateral wall of the lateral ventricle;

■ the terminal (cortical) part (P3 and P4-segments), giving branches to the corresponding areas of the cerebral cortex; The main cortical branches of the PCA are the anterior and posterior temporal, parietal-temporal, and spur arteries (the boundaries of the watershed of the basins of the middle and posterior cerebral arteries fluctuate considerably; usually the Sylvian groove serves as the boundary of the PCA basin, but sometimes the middle cerebral artery also supplies blood to the outer parts of the occipital lobe up to the occipital poles; in this case, PCA always supplies blood to the areas of the cerebral cortex in the region of the groove, and the visual radiance in some cases receives blood from the middle cerebral artery, respectively, homonymous hemianopsia does not always imply a heart attack in the PCA pool).

Symptoms of defeat ... With ischemic strokes in the PCA basin, depending on the localization of the vessel occlusion, as well as on the state of collateral blood supply, the clinical picture may reveal symptoms of damage to the midbrain, thalamus and cerebral hemispheres. In general, up to 2/3 of all heart attacks in the PCA basin are cortical, the thalamus are involved only in 20 - 30% of cases, and the midbrain in less than 10% of cases. Accordingly, the most frequent variant of ischemic stroke in the PCA basin is an isolated infarction of the cerebral hemispheres, primarily of the occipital lobes, less common lesions of the thalamus and cerebral hemispheres, in a small percentage of cases - isolated thalamic infarction and, finally, a combination of lesions of the midbrain, thalamus and / or hemisphere is the rarest option.

Apex OA syndrome... Sometimes there is a bilateral lesion of the brain regions supplied with blood from the PCA. This occurs primarily in top of the basilar syndrome, which is an embolic occlusion of the distal basilar artery and is characterized by depression of consciousness, visual impairment, oculomotor and behavioral disorders, often without motor dysfunction.

According to a number of authors, the most characteristic signs of heart attacks in the PCA basin are: visual disturbances> homonymous hemianopsia> central paresis of the facial nerve> headache, mainly in the occipital region> sensory disturbances> aphatic disturbances> hemiparesis> neglect (ignoring [unilateral spatial ignoring, in mainly with the defeat of the right hemisphere]). Patients usually have a combination of symptoms.

Visual impairment... Homonymous hemianopsia occurs on the contralateral side with heart attacks in the areas of blood supply to the hemispheric branches of the PCA due to damage to the striatal cortex, visual radiance, or the lateral geniculate body. In the absence of involvement of the occipital pole, macular vision remains intact. The visual field defect can be limited to only one quadrant. Upper quadrant hemianopsia occurs with an infarction of the striatal cortex below the groove or the lower part of the visual radiance in the temporo-occipital region. The lower quadrant hemianopsia is a consequence of the defeat of the striate cortex above the furrow or the upper part of the visual radiance in the parieto-occipital region. Sulcus occlusion can also be associated with pain in the ipsilateral eye. Visual impairment can be more complex, especially with bilateral occipital lobes, including visual hallucinations, visual and color agnosia, prosopagnosia (agnosia for familiar faces), blindness denial syndrome (Anton's syndrome), visual attention deficit and optic-motor agnosia ( Balint's syndrome). Often, visual impairments are accompanied by afferent disorders in the form of paresthesias, disorders of deep, pain and temperature sensitivity. The latter indicate the involvement of the thalamus, parietal lobe, or brainstem (due to occlusion of the proximal VBD).

Neuropsychological disorders associated with heart attacks in PCA vary considerably and are present in more than 30% of cases. A stroke in the pool of the corpus callosum of the left PCA in right-handers, affecting the occipital lobe and the corpus callosum, is manifested by alexia without agraphia, sometimes by color, subject, or photographic anomie. Right hemispheric infarctions in the PCA basin often cause contralateral heminiglect. With extensive heart attacks involving the medial parts of the left temporal lobe or bilateral mesotemporal infarctions, amnesia develops. Agitated delirium can also develop with mono- or bilateral mesotemporal infarction. Extensive infarctions in the basin of the left posterior temporal artery may clinically present with anomia and / or sensory aphasia. Thalamic infarctions in the blood supply zones of the penetrating branches of the PCA can cause aphasia (if the left pillow is interested), akinetic mutism, global amnesia and Dejerine-Russi syndrome (disorders of all types of sensitivity, gross dysesthesias and / or thalamic pain and vasomotor disorders in the contralateral half of the body, combined with usually transient hemiparesis, choreoathetosis and / or ballism). Also, heart attacks in the PCA basin can be associated with dyscalculia, spatial and temporal disorientation.

Bilateral thalamic infarctions are often associated with deep coma. Thus, occlusion of the Percheron artery causes the development of bilateral infarctions in the intralaminar nuclei of the thalamus, which leads to severe impairment of consciousness.

Hemiparesis with heart attacks in the basin, PCA occurs in only 1/5 of patients, is more often mild and transient and is usually associated with the involvement of the cerebral pedicles in the pathological process. Cases of heart attacks in the PCA basin are described, when hemiparesis was detected in patients without involvement of the cerebral peduncles. These patients had lesions of the distal PCA, primarily the involvement of the thalamo-geniculatory, lateral and medial posterior choroidal arteries. It is assumed that hemiparesis in infarction in the pool of the posterior choroidal arteries may be associated with damage to the cortico-bulbar and cortico-spinal tracts, even in the absence of visible damage to the internal capsule or midbrain according to neuroimaging data. There are opinions that the development of hemiparesis is associated with compression of the inner capsule by the edematous tissue of the thalamus.

In about 1/5 of patients, infarctions in the PCA pool mimic those in the carotid pool, especially with a combined lesion of the superficial and deep branches of PCA, which is observed in about 1/3 of cases. Differential diagnosis can be difficult due to the presence of aphatic disorders, neglect, sensory deficit, as well as usually mild and transient hemiparesis resulting from the involvement of the pyramidal tracts. In addition, memory impairments and other acute neuropsychological impairments can significantly complicate the examination of such patients. Some infectious diseases (primarily toxoplasmosis), neoplastic lesions, both primary and metastatic, and thalamic infarctions caused by deep cerebral vein thrombosis should be distinguished among other conditions that often clinically mimic heart attacks in the ZMA basin. Often, neuroimaging methods play a decisive role in making a diagnosis..

Neuroimaging ... Computed tomography (CT) usually does not detect ischemic changes in the brain parenchyma during the first few hours after the onset of a stroke, the time most important for starting therapy, and sometimes even later in the course of the disease. Imaging of the posterior parts of the brain is especially difficult due to artifacts caused by the bones of the skull. However, with strokes in the basin of the PCA, as with strokes in the basin of the middle cerebral artery, in some cases, CT can show a hyperintense signal from the PCA itself, which is the earliest sign of a stroke in its basin and is detected in 70% of cases within the first 90 minutes from onset of the disease and in 15% of cases within 12 to 24 hours. This symptom appears due to the visualization of a calcified embolus or atherothrombosis in situ.

Magnetic resonance imaging (MRI) allows you to more accurately determine the presence and nature of ischemic changes in the brain in stroke. Diffusion-weighted imaging (DWI) can detect early ischemic changes, often within an hour of symptom onset, and more accurately determine the location and extent of lesions than CT. The combined use of DWI, ADC and FLAIR modes allows to differentiate acute, subacute and chronic ischemic changes in the brain parenchyma, as well as to distinguish cytotoxic cerebral edema observed in ischemic stroke from vasogenic edema in posterior reversible leukoencephalopathy syndrome and hypertensive encephalopathy.

In the non-invasive diagnosis of steno-occlusive lesions of large extra- and intracranial arteries, CT angiography (CTA) plays a significant role. This technique makes it possible to reveal the degree of stenosis, the morphology of the plaque, as well as the presence of arterial dissection in both the lesions of the VBD vessels and the carotid basins. In addition, the anatomical features of collaterals and variants of PCA circulation are assessed. Additional information on vascular anatomy can be obtained using contrast-enhanced MR angiography, which, in combination with CTA, allows you to operate on data that previously could only be obtained with classical angiography. In addition, these methods are important in assessing the effectiveness of thrombolytic therapy in the case of arterial recanalization (currently