Asymmetry of v4 segments of vertebrates. Hypoplasia of the intracranial v4 segment of the right vertebral artery: mr signs, consequences

Post date: 07.08.2011 16:16

shift

My mother did an MRI: MRA of the arteries of the brain + venous sinuses.
Here is what showed

On a series of MR angiograms performed in the TOF mode in the axial projection, followed by processing using the MIP algorithm and three-dimensional reconstruction in the coronal and axial planes, the internal carotid, basilar, and intracranial segments of the vertebral arteries and their branches are visualized. A variant of the development of the circle of Willis in the form of a lack of blood flow in the left posterior communicating artery. The median artery of the corpus callosum is visualized, equal in diameter to the anterior cerebral arteries.
There is a moderate narrowing of the lumen of the intracranial segment of the right vertebral artery, throughout its length in the study area.
The pronounced asymmetry of the lateral ventricles (D>S) is determined.

Internal and external jugular veins and their branches, sinuses (superior longitudinal, straight, sigmoid and transverse sinuses).
There is a pronounced asymmetry of blood flow in the transverse and sigmoid sinuses (D>S). The rest of the sinuses are unremarkable.
No additional venous network was identified.

Conclusion: MR picture of the variant of the development of the circle of Willis. Moderate narrowing of the lumen of the intracranial segment of the right vertebral artery. Asymmetry of blood flow in the transverse and sigmoid sinuses (D>S). Lateroventriculoasymmetry.

Decipher please what is here and if so, how to treat. she is very worried, because. can not understand anything.

Post date: 07.08.2011 20:43

Papkina E.F.

shift, your mother's MRI angio mode reveals a violation of blood flow in the region of the right vertebral artery and uneven blood flow through the sinuses, where venous blood flows. This is most likely a developmental variant, that is, it has been like this since birth. age-related changes An anomaly of vascular development that has not previously manifested itself in any way can manifest itself as headaches, dizziness, memory loss, impaired coordination. You need to consult a neurologist in order to conduct adequate treatment and eliminate neurological symptoms. The prognosis is favorable, since in most cases the surrounding vessels take over the functions narrowed, altered vessel.

Post date: 08.08.2011 19:40

Guest

Commenting on an MRI without a clinic is not grateful. I think you were sent for research by a doctor? so you need to ask him if he found what he was looking for.

Post date: 05.10.2011 19:48

Guest

consultations of this kind can be given by an MRI doctor (for this he was specially trained!))) And the treatment is prescribed by the attending physician who referred.
A full examination is necessary - this is also an MRI of the brain (the cause of lateroventriculoasymmetry) and cervical of the spine (a decrease in blood flow through one of the vertebral arteries may not be congenital, but acquired as a result of osteochondrosis!)

Post date: 25.06.2012 12:28

Guest

My son has a draft board, they did an MRI (complaints of headaches, pain in right temple, B in the conclusion they wrote: MRA picture of the variant of the development of the circle of Willis in the form of a decrease in blood flow in both posterior communicating arteries, Please explain what kind of circle of Willis is, and how dangerous it is for health, what about the army?

Post date: 27.06.2012 19:17

Papkina E.F.

In practice, very often there are variants of the development of the so-called circle of Willis (this system of arterial supply to the base of the brain). For life, these changes are not dangerous. The issue of conscription is decided individually after examination by a neurologist.

Post date: 24.04.2013 22:46

Olga

The woman underwent an MRI, the conclusion: MRI picture of a moderately pronounced external replacement hydrocephalus. A variant of the development of the circle of Willis. Decreased blood flow in the intracranial segment of the right VA. HELP DESCRIPT.

Post date: 14.11.2013 23:50

Angela

The daughters on the MRI gave a conclusion ... please explain how serious it is and whether it is treated. She has a baby of 9 months, we are very worried. Conclusion: MR picture of AVM in the pool of the left MCA and PCA. The circle of Willis is closed. Decreased blood flow in the A1 segment of the left ACA (hypoplasia). Reduced blood flow in the intracranial segment of the right VA (hypoplasia).

Post date: 30.11.2013 17:40

Galina

I had an MRI today. I have pain in my neck when turning my head.. the noise in the left one is already.. terrible, about 10 years old.. the right eye does not obey.. double vision when looking straight.. I tilt my head to the left.. double vision disappears ... therefore adjusting for over 10 years..tilting my head to the left.Here is the result-
Series of MR tomograms (T2 TSE sag + cor + tra, T1 SE sag) lordosis is straightened. The height of the C4-C7 intervertebral discs is reduced. surfaces of the vertebral bodies, covering the old protrusions of the discs, smooth the anterior contour of the dural sac. the brain is structural, the signal from it (by T1 and T2) is not changed. The shape and size of the vertebral bodies are normal, without signs of bone marrow edema. The cranio-vertebral region is without features. manual therapy? And what else? Thank you.

Post date: 16.12.2013 19:46

Catherine

What is the asymmetry of the transverse and sigmoid sinuses D>S, a moderately pronounced expansion of the collateral veins in the PCF on the left, and what does it threaten?

Post date: 04.02.2014 13:31

Ramilla

Good afternoon Please tell me! I did an MRI, but I don’t understand everything. A variant of the development of the circle of Willis in the form of a lack of blood flow in both posterior communicating arteries (open). In the white matter of the left frontal and parietal lobe subcortically, single foci are determined, sizes up to 4 mm, hyperintense according to T2 WI, probably of vascular origin. The subarachnoid space is locally expanded in the fronto-parietal regions. The right vertebral artery is of small diameter. Is it very dangerous! I am worried about severe headaches, but not constantly, as well as pressure up to 150 to 100, all these symptoms appeared during pregnancy, after it seems to have passed, but now it worries me again. I am 24 years old, gave birth 3 months ago. I would like to know what this means and what a diagnosis! Thank you in advance!

Post date: 11.06.2014 12:45

Guest

MRI: MR signs of reduced blood flow in the A1 segments of both ACAs, M3 M4 segments of both MCAs in the distal segments of both ACAs, V5 segment of the PCA, most likely due to atherosclerotic changes. What does this mean and what therapy is needed. What are the recommendations?

Post date: 15.06.2014 18:00

Irishka

Please tell me if it is worth doing an MRI on the machine open type, like this http://radio-med.ru/makers/mrt/open-mri-10/hitachi-airis-ii-0.3t
Or still find a clinic with the usual one?
And what about mobile MRI scanners who thinks?

Post date: 21.08.2014 19:19

natalia *d*

help me figure it out! MRA-signs of lack of blood flow in the right vertebral artery, pathological tortuosity of internal carotid arteries, development option venous system with a decrease in blood flow along the transverse sinus on the left. Thank you.

Post date: 25.08.2014 14:17

Christina

Hello! Please consult the results of MRI of the cerebral vessels. I went for examinations due to frequent headaches from an early age, now I am 23. Here is the conclusion: there is a variant of the development of the circle of Willis (aplasia A1 ACA on the right, aplasia of the posterior communicating artery on the right and hypoplasia on the left ).MRI signs of lack of blood flow in the intracranial segment of the right vertebral artery (aplasia).Please tell me how serious it is and what treatment to choose? Thank you in advance for your advice

Syndrome of the vertebral artery cervical osteochondrosis- this is one of the most insidious and serious ailments that can affect different people. Cervical spine stenosis affects both old and young patients. It is caused by disturbances in the supply of blood to brain cells due to lesions in one or both arteries, through which blood components enter the cerebral hemispheres.

Causes of the vertebral artery syndrome

This phenomenon occurs in several cases:

1. Under the influence of various adverse factors in humans, there is a clamping of the main vessels that supply the brain cells with blood. Usually the narrowing occurs on one of the arteries, less often on both.
2. Nutrients and oxygen stop getting into right places in the required quantity.
3. Show themselves various signs diseases: dizzy, dark in the eyes.
4. At untimely treatment an ischemic stroke may develop.
5. A risk factor may be atherosclerosis or hypoplasia of the spinal artery.

Blood enters the brain mainly through the carotid arteries (up to 70%), and the rest of the nutrient liquid goes 2 lateral vessels. When the main channels of the blood flow are affected, lesions occur that are usually incompatible with life, and if there are problems in the other 2 arteries, a person may feel worse, then vision problems will begin, damage hearing aid which can lead to disability.

Sometimes the disease is caused by asymmetry of blood flow along blood vessels spine - it is not treated, but can go into other diseases. Another risk factor is instability in the cervical region, which leads to disc prolapse. spinal column. This can also happen after an injury (both ordinary and birth), with seated life.

The appearance of the syndrome may big influence render osteochondrosis or a pathology known as tortuosity of the arteries on the spine.

Symptoms of the disease

It is quite difficult to immediately identify signs of vertebral vein syndrome, when a person is diagnosed with stenosis of the spinal canal in the cervical region. This is because the manifestations of this disease strongly resemble osteochondrosis or diseases that usually cannot be associated with problems in the spine. Therefore, if at least one symptom of those listed below is detected, the patient must be urgently taken for examination to a medical facility.

The symptom that most often manifests itself in this disease is headaches. They can manifest themselves in the form of seizures that roll over the patient with some frequency, or as permanent pain. The main area of ​​distribution of such pains is the back of the head, but they can move to the temporal lobes and to the frontal part.

Over time, such pain intensifies and manifests itself when tilting or turning the head. Then the pain moves to the skin under the hair. It appears when you touch the hair with your hands. This action may cause a burning sensation. The vertebrae of the neck begin to make a crunch when turning the head.

All of the above troubles are complemented by the following symptoms:

1. The patient's blood pressure rises.
2. There is noise and ringing in the ears.
3. The person may be nauseated.
4. Pain begins in the region of the heart muscle.
5. The patient gets tired quickly.
6. With frequent dizziness, the patient may faint or lose consciousness.
7. Spinal stenosis causes sharp pain in the cervical region.
8. Arise various violations in the eyes and pain in the ears. Usually they are unilateral.

With a long course of the disease, it can cause an increase in pressure inside the skull and vegetative dystonia. The patient's fingers are numb. A person develops irritability, mood swings, causeless fear.

Diagnosis of arterial syndrome in cervical osteochondrosis

Examination of the patient begins with an external examination. At the same time, doctors give Special attention factors such as: pain on skin in a patient, muscle tension in the occipital region, pain on the vertebrae of the neck when pressed.

Diagnosis is carried out using Doppler ultrasound. Using this equipment, you can examine all the vessels that feed the brain with blood, determine their condition at the time of the test and identify various violations and deviations.

Another way to diagnose the disease is the use of x-ray equipment. If a person becomes worse during the examination, then to clarify the reasons, the patient is sent for magnetic resonance imaging to check areas of the brain. According to the results of such a study, the patient can be urgently hospitalized.

Errors in the diagnosis of the disease (they are possible, since the disease coincides with other diseases in terms of symptoms) can lead to irreparable consequences. Therefore, when making a primary diagnosis, it is advisable to repeat the examination in order to identify signs of the disease that were missed during the first diagnosis.

What methods are used to treat the disease

If the cause of the disease is established accurately and this is a pinching of the arteries, then doctors prescribe a course of therapy that should help to completely heal the person. Treatment should be carried out under the strict supervision of the attending physician, even when the patient is at home.

Self-medication in this case is strictly prohibited, as it can lead to irreversible consequences up to and including death.

The treatment process must be complex. Below is a list existing ways the fight against the syndrome. Doctors can use either all of these methods, or choose the most appropriate for a particular case. The disease is cured in the following ways:

1. Assign a course of vascular therapy.
2. The patient is prescribed therapeutic exercises.
3. The patient is discharged medications to improve blood flow.
4. To get rid of fainting, it is recommended to use special stabilizing medications. They are also needed to relieve dizziness, vomiting, nausea and eliminate problems with the vestibular apparatus.
5. Sometimes acupuncture and acupuncture are used.
6. The patient is prescribed a massage, which must be performed by a licensed specialist.
7. In some cases, manual therapy may be used.
8. It is possible to use reflexology.
9. IN medical therapy include autogravity methods of curing the disease.

Non-drug therapies can also be used, which are prescribed only by the attending physician. This is done depending on the severity of the disease, its stage and the main causes that led to the appearance of the syndrome. The main thing is complex use various methods for the most effective fight with illness.

If the patient has a congenital pathology of the asymmetry of the arteries of the spine, then doctors will only cure the secondary syndrome, and the main cause is incurable. This can lead to a relapse of the disease if the person does not follow the recommendations of the attending physician.

According to the WHO definition (1970), vertebrobasilar insufficiency is “a reversible impairment of brain function caused by a decrease in blood supply to the area fed by the vertebral and basilar arteries”

Both vertebral and basilar arteries form vertebrobalilar system (VBS), which has a number of features.

It supplies blood to various and functionally heterogeneous formations: posterior sections hemispheres brain (occipital lobe and mediobasal parts of the temporal lobe), optic tubercle, most of the hypothalamic region, cerebral peduncles with quadrigemina, pons varolii, medulla, mesh formation of the trunk - reticular formation (RF), upper divisions spinal cord.

The same departments often have several sources of blood supply, which determines the presence of zones of adjacent blood circulation, more vulnerable in case of circulatory failure.

Trunk blood supply to intracranial departments of the vertebral arteries and their branches, the main artery and its branches. The zone of adjacent blood supply is the reticular formation.
Cerebellum receives blood supply from three pairs of cerebellar arteries: superior and anterior inferior(branches of the main artery) and posterior inferior cerebellar arteries (terminal branch of the vertebral artery).
especially significant area adjacent blood supply- area of ​​the worm.
Posterior regions of the cerebral hemispheres receive blood supply from front, middle(branches of the internal carotid artery) and anterior cerebral artery(terminal branch of the main artery).
The most important area of ​​adjacent blood supply: posterior third of interparietal sulcus(the junction zone of the branches of all three cerebral arteries); wedge and precuneus, posterior corpus callosum and temporal lobe pole(zone of junction of PMA and ZMA); superior occipital, inferior and middle temporal and fusiform gyrus(ZMA and SMA junction zone).

Merging of the vertebral arteries into the main unique feature all arterial system , because the basilar artery represents an already prepared path collateral circulation without spending time on its formation. This has a positive meaning - the rapid inclusion of collateral circulation leads to the restoration of blood flow in the vertebral artery when it is compressed and negative, because. creates conditions for the development of the syndrome "subclavian steal", i.e. with blockage of the proximal subclavian artery before the vertebral leaves it, blood is redistributed to the arm, sometimes to the detriment of the VBS, which can hard work hand lead to the development of transient ischemia in the WBS.

IN normal conditions blood flows from the vertebral arteries continue their movement in the main artery, maintaining the same blood flow volumes and not mixing with each other. Between these flows, zones of "mobile" (dynamic) equilibrium are created. Occlusion or stenosis of one of the vertebral arteries disrupts it, mixing of flows occurs, displacement of the zones of "mobile" balance and blood flow from the other vertebral artery through the main artery. This can lead to the development of thrombosis even without pronounced atherosclerosis - "stagnant" thrombi at the points of "mobile" balance.

Small penetrating arteries depart from the large arteries (basilar, posterior cerebral) at a right angle, have a straight course and the absence of lateral branches.
Blood circulation in the VBS (according to angiography) is two times slower than in the carotid system. Cerebral blood flow in the cerebral hemispheres (system of the internal carotid artery) is 55-60 ml per 100 g of brain tissue per 1 minute, and in the cerebellum - 33. This enhances the influence of the hemodynamic factor in the development of reversible cerebral ischemia in the IBS. Transient ischemic attacks in IBS are much more common, accounting for 70% of all TIAs. Collateral circulation, improving or restoring cerebral perfusion, develops and is created during arterial stenosis or occlusion based on existing anastomoses. Of the intracranial anastomoses, the circle of Willis is extremely important. Decreased blood flow in the IBS leads to retrograde blood flow through the posterior communicating arteries, sometimes to the detriment of the carotid system - "internal steal". The extracranial retromastoid anastomosis provides two additional sources of blood supply to the IBP. Large branches extending from the vertebral artery at the level of the atlas anastomose with the branches of the occipital artery from the system of the external carotid artery and the ascending and deep cervical arteries from the subclavian artery system. Anastomoses between cerebellar arteries: back bottom ( final branch vertebral artery) and the superior and anterior inferior cerebellar arteries (branches of the basilar artery). good development anastomosis ensures sufficient functioning of the collaterals and, in the event of a decrease in blood flow in the VBS, prevents the development of neurological disorders.

In 70% of cases, the left vertebral artery is 1.5-2 times wider than the right , which predetermines its importance as the main source of blood supply posterior divisions brain. The asymmetry of the caliber of the vertebral arteries creates the possibility of thrombus formation in the basilar artery.
The uniqueness of the course of the vertebral artery: at the level of the CVI–CII cervical vertebrae, it goes in its own bone canal, then, exiting it, goes around the CI, describing an arch convex outwardly around it, then rises up and, piercing the hard meninges enters the cranial cavity through the foramen magnum.

Anomalies in vascular development are common in VBS. 20% in patients with IBS pathology, anomalies in the development of the vertebral arteries are detected. According to Powers et al (1963) hypoplasia occurs in 5-10% cases, aplasia 3% , lateral displacement of the mouth of the vertebral artery - in 3-4% , origin of the vertebral artery from the posterior surface of the subclavian artery - 2% , entry of the vertebral artery into spinal canal at the level of CV, CIV, sometimes CIII - in 10,5% cases, there are other anomalies: the discharge of the vertebral artery from the aortic arch, from the subclavian artery in the form of two roots, etc.
A decrease in blood supply with insufficient compensation by collateral circulation leads to the development of ischemia of the brain tissue fed from the IBS.

ischemia pathogenesis.

Through research recent years it has been shown that cerebral ischemia, or circulatory hypoxia of the brain, is a dynamic process and implies the potential reversibility of functional and morphological changes in the brain tissue, not being identical to the concept " cerebral infarction”, reflecting the formation of an irreversible morphological defect - structural destruction and the disappearance of neuronal function. The stages of hemodynamic and metabolic changes occurring in the brain tissue at various stages of its circulatory insufficiency were revealed. A scheme of successive stages is proposed "ischemic cascade" on the basis of their causal relationships (Gusev E.I. and co-authors, 1997,1999):

> decline cerebral blood flow;
> glutamate "excitotoxicity";
> intracellular accumulation of calcium ions;
> activation of intracellular enzymes;
> increased synthesis of nitric oxide NO and development of oxidative stress;
>expression of early response genes;
> “remote” consequences of ischemia (reaction local inflammation, microvascular disorders, damage to the blood-brain barrier;
> apoptosis.

For normal flow metabolism brain tissue requires constant cerebral blood flow to ensure adequate supply to the brain nutrients: proteins, lipids, carbohydrates (glucose) and oxygen. Stable maintenance of cerebral blood flow at the level of 50-55 ml / 100 g of brain tissue in 1 min. at the level of the hemispheres and 33 ml/100 g of brain tissue in 1 min. at the level of the cerebellum, it is supported by autoregulation of cerebral blood flow, which is carried out reflexively at the level of large vessels due to the adrenergic and cholinergic receptors of their walls with the help of the regulatory mechanism of the carotid sinus and chemical regulation in the vessels of the microvasculature (with an excess supply of O2, i.e. hypocapnia, the tone of the precapillary arterioles increases; with insufficient supply of O2 to the brain, hypercapnia, the tone decreases; in conditions of an increase in the amount of carbon dioxide, the sensitivity of microvessels to it increases). The rheological properties of blood are important (viscosity, aggregation ability shaped elements blood, etc.) and the value of perfusion pressure, which is defined as the difference between the average blood pressure and the average intracranial pressure. Critical Level cerebral perfusion pressure - 40 mm Hg, below this level, cerebral circulation decreases and then stops.
In acute circulatory failure I of a certain area of ​​the brain, the latter is able to temporarily compensate for local ischemia through the mechanisms of autoregulation and increased collateral blood flow. However, a further decrease in cerebral blood flow leads to disruption of autoregulation and the development of metabolic disorders. It has been established that the processes of O2 and glucose consumption by the brain run in parallel. Glucose is the only supplier of energy necessary for the normal course of metabolic processes, because. most of them are energy-dependent: synthesis of proteins, many neurotransmitters, binding of a neurotransmitter to a receptor, impulse transmission, exchange of ions through plasma membrane etc. The first reaction to brain hypoxia occurs in the form of inhibition of protein synthesis. Protein and RNA synthesis proceeds more actively in the cerebral cortex and cerebellum. The metabolism of glucose usually proceeds with a predominance of the aerobic pathway, which gives large quantity macroergic compounds (36 ATP molecules from 1 glucose molecule). Increasing hypoxia leads to the predominance of anaerobic glycolysis, which is more unfavorable energetically (2 ATP molecules from 1 glucose molecule). Due to energy deficiency in mitochondria, oxidative phosphorylation is inhibited, and lactic acid accumulates in the cell. At the same time, the content of carbon dioxide in the brain tissue increases and PH shifts to the acid side. There is lactic acidosis. As a result, in the focus of ischemia there is a decrease in cerebral blood flow, while in its environment there is an increase in blood flow to the detriment of the ischemic zone - the phenomenon of "luxurious perfusion" (according to Lassen). The growing energy deficit under these conditions leads to further disruption of energy-dependent processes. The transition to anaerobic glycolysis leads to an increase in the alpha-ketoglutaric acid not used in the Krebs cycle into the amino acid glutamate, which also has the properties of an excitatory mediator (Swanson et al., 1994). In addition, increasing lactic acidosis blocks the reuptake of glutamate. Thus, the excitatory neurotransmitter accumulates in the intercellular space, which leads to the development of "glutamate excitotoxicity", i.e. excitation of cells by glutamate. Lactic acidosis combined with increasing hypoxia causes a disorder electrolyte balance nerve and glial cells: the release of K + ions from the cell into the extracellular space and the movement of Na + and Ca ++ ions into the cell, which suppresses the excitability of neurons and reduces their ability to conduct nerve impulses.
Exciting amino acids(glutamate, aspartate) act on neuronal receptors for N-methyl - D-aspartate (NMDA - receptors) that control calcium channels. Their overexcitation leads to a "shock" opening of ionic calcium channels and additional excess influx of Ca++ ions from the intercellular space into neurons and its accumulation in them.
Norepinephrine, whose release during hypoxia initially increases sharply, activates the adenylatskylase system, which stimulates the formation of AMP, which causes an increase in energy deficit and leads to an increase in Ca ++ ions in nerve cells.
Excessive intracellular accumulation of Ca++ ions leads to the activation of intracellular enzymes: lipase, protease, endonuclease, phospholipase and the prevalence of catabolic processes in the nerve cell. Under the influence of phospholipases, phospholipid complexes are decomposed in the membranes of mitochondria (phospholipase A2), intracellular organelles (lysosomes) and in the outer membrane. Their breakdown enhances lipid peroxidation (LPO). The end products of lipid peroxidation are: malondialdehyde, unsaturated fatty acid(especially arachidonic) and free radicals O2. End products of decay arachidonic acid: thromboxane A2, etc., hydroperoxides, leukotrienes. Thromboxane A2 and others cause spasm cerebral vessels, enhance platelet aggregation and coagulation shifts in hemostasis. Leukotrienes have vasoactive properties. Microvascular disorders lead to an increase in ischemia in the ischemic area. The free radical O2 is a molecule or atom that has an unpaired electron in the outer orbit, which determines its aggressiveness to convert cell membrane molecules into free radicals, i.e. provide a self-sustaining avalanche reaction. The activation of lipid peroxidation processes is also facilitated by the rapid depletion of the antioxidant system, the enzymes of which inhibit the formation of peroxides and free radicals and ensure their destruction. In addition, in the ischemic focus, the content of substances decreases: alpha-tocopherol, ascorbic acid, reduced glutamate, which bind LPO end products. The accumulation of hydroperoxides leads to the formation of hydroxy acids and the development of oxidative stress.
Microglial cells activated by increasing hypoxia synthesize potentially neurotoxic factors: proinflammatory cytokines (interleukins 1,6,8), tumor necrosis factors, ligands for the glutamate NMDA receptor complex, proteases, superoxide anion, etc. Excitation of NMDA receptors leads to the activation of the NO- synthetase involved in the formation of nitric oxide from arginine. The complex of nitric oxide with superoxide anion helps to reduce the production of neutrophins. Neutrophins are regulatory proteins nervous tissue synthesized in its cells (neurons and glia), acting locally - at the site of release and inducing branching of dendrites and growth of axons. These include: nerve growth factor, cerebral growth factor, neutrophin-3, etc. Anti-inflammatory factors (interleukins 4,10) and neutrophins prevent the damaging effect on the ultrastructure of nerve and glial cells of neurotoxic factors - the end products of lipid peroxidation. Destruction of the phospholipid complex nerve cells leads to the production of antibodies to them. The release of anti-inflammatory and vasoactive substances from ischemic brain tissue leads to the penetration of neurospecific proteins into the blood, which leads to the development of an autoimmune reaction and the production of antibodies to nervous tissue.
Under conditions of increasing energy deficiency, further inhibition of the synthesis of RNA, proteins, phospholipids, and neurotransmitters occurs. Inhibition of the synthesis of neurotransmitters disrupts the connections between neurons and deepens metabolic disorders in them. A decrease in protein synthesis in the ischemic focus leads to the expression of cell death genes and triggers a genetically programmed cell death mechanism - apoptosis, in which the cell breaks up into parts in the form of apoptotic bodies, which are separated in membrane vesicles that are absorbed by neighboring cells and/or macrophages. IN pathological process glial cells are involved faster and to a greater extent, brain neurons are involved more slowly and less significantly (Pulsinelli, 1995). At this stage of ischemia, metabolic disorders are reversible.
The volume of blood flow is 10-15 ml per 100 g of brain tissue in 1 min. is a critical threshold beyond which irreversible changes– necrosis (Hossman, 1994), which is accompanied by the release of cell contents into the intercellular space and the development of an inflammatory reaction.
Acute deficiency cerebral circulation in the WBS is considered as transient disorder cerebral circulation or transient ischemic attack (TIA) in VBS. It is characterized acute onset focal neurological symptoms usually without cerebral symptoms(less often against the background of their weak severity) due to short-term local ischemia of the brain. Focal neurological symptoms last from several minutes (usually 5-20 minutes) to several hours (less often up to 24) and ends full recovery impaired functions within 24 hours. Chronic cerebrovascular insufficiency in VBS is considered in discirculatory encephalopathy. However, the ischemic process of brain tissue in dyscirculatory encephalopathy is irreversible and is accompanied by the development of necrosis (i.e., infarcts in the white matter and basal ganglia, less often in the visual tubercle, bridge) and an inflammatory reaction (spongiosis, proliferation of astrocytes, myelin breakdown with partial collapse of the axial cylinders), occurring mainly perivascular. At the same time, CT and MRI reveal infarctions in the white matter and subcortical nodes and signs intracranial hypertension: expansion of the ventricles of the brain (to a greater extent the anterior, less often the posterior horns of the lateral ventricles with the phenomenon of "leukoareosis" around them due to a decrease in density white matter) or atrophy of the cortex with the expansion of the subarachnoid spaces of the cerebral hemispheres. For the same reason, chronic cerebrovascular insufficiency in the arteries of the IBS cannot be considered as a small ischemic stroke, i.e. lacunar infarction. This makes it possible to isolate TIA and CNMC in SBS in special form vascular pathology brain - vertebrobasilar insufficiency (VBI). The ischemic process in VBI is reversible and CT and MRI, as a rule, do not reveal morphological changes.

In the mechanism of origin of VBN more significant are the atherothrombotic factor and hemodynamic, "subclavian steal", less significant: embolic factor, angiospasm and changes rheological properties blood (hyperlipidemia, hyperfibrinemia, polycythemia, etc.).
To the development of VBN (according to the degree of significance) are: occlusive and stenosing lesions of the arteries of the VBS (especially stenosis of the vertebral arteries and primary thrombosis);
1) deformation of the vertebral arteries;
2) extravasal compression of the extracranial parts of the vertebral arteries.

Occlusions more often develop according to the type of thrombosis, less often embolism. The main cause of occlusion is atherosclerosis. Atherosclerotic plaques in atherosclerosis are more often localized in the orifices of the vertebral arteries, in the area of ​​the bifurcation of the basilar artery, and in the orifices of their branches. Decaying, atherosclerotic plaques cause thrombosis. Thrombus detached from atherosclerotic plaque, clogs the distal branches of these arteries. The second most important is arterial hypertension. It plays a dual role: firstly, it promotes the formation and development of atherosclerotic plaques in the mouths of small penetrating arteries and their embolism (which is facilitated by the characteristics of these arteries) and, secondly, it causes pathological tortuosity of these vessels, changing vascular wall. Parietal thrombi are less important in vasculitis: nonspecific aortoarthritis (or pulseless disease or Takayasu's disease) and secondary manifestations in tuberculosis, SLE, syphilis, AIDS, etc. Rarely, emboli in vertebral arteries can get from atheromatous plaques or vegetations on heart valves in diseases hearts, even less often from veins lower extremities And internal organs at congenital pathology heart (non-closure of the foramen ovale).

With a sharp tilting of the head back the vertebral artery may be strangulated by the posterior margin of the foramen magnum. With a lateral displacement of the mouth of the vertebral artery, turning the head can lead to compression of the vertebral artery, often together with the subclavian artery.
The vertebral artery can be elongated and have a "C" and "S" shaped course, go in the form of a loop or have kinks and tortuosity. Pathology can be congenital and acquired (with hypertension, age-related changes).
Cervical osteochondrosis can cause compression of the vertebral artery due to the penetration of lateral and posterolateral osteophytes of the uncovertebral joints into its canal, as well as spasmodic scalenus muscle (scalenus syndrome) in the department before it enters the bone canal. Paired intervertebral joints that form back wall canals of the vertebral artery are introduced into the canal with subluxations according to Kovacs (slipping in front of the vertebral body) due to inferiority of the muscular and ligamentous-articular apparatus or trauma to the cervical spine, due to arthrosis with deforming spondyloarthrosis, rheumatoid arthritis, Bechterew's disease. Especially often, the vertebral artery is subjected to compression with anomalies of the craniovertebral junction. This is the Kimmerle anomaly; an abnormal bone canal instead of a wide and shallow groove of the vertebral artery on the dorsal side of the lateral mass of the atlas; atlas assimilation (CI), i.e. fusion with the base occipital bone; asymmetry or high location of the odontoid process of the epistrophy (CII), basilar impression, i.e. funnel-shaped depression of the hypoplastic margins of the foramen magnum, atlanto-occipital joints and distal parts of the Blumenbach clivus into the cranial cavity and the latter often combined with an anomaly of the CI and CII vertebrae; Arnold-Chiari anomaly, i.e. descent of the tonsils of the cerebellum through the foramen magnum into the upper sections of the spinal canal. Prolonged compression of the vertebral arteries contributes to the formation and growth of atherosclerotic plaques.

Clinical picture

The clinical picture is determined the place and degree of damage to the arteries of the vertebrobasilar basin, general condition hemodynamics, blood pressure level, the state of collateral circulation and is manifested by transient focal neurological disorders several (at least two) different departments brain, fed by VBS. Particularly significant are dizziness, ataxia and visual disturbances (according to Hutschinson, 1968). An attack of dizziness is often the first symptom of VBI, often accompanied by nausea and vomiting. The cause of dizziness is: ischemia of the labyrinth, vestibular nerve and / or trunk. In the first two cases, dizziness is systemic: according to the type of object rotation with the appearance of horizontal or rotational nystagmus, often accompanied by hearing loss; in the second - non-systemic, aggravated by turning the head with small-scale horizontal nystagmus, accompanied by dysphonia and dysarthria. With ischemia of the occipital cortex, visual disturbances occur: simple photopsies (flashing of sparkles, stars, etc.), visual hallucinations, visual field defects in the form of homonymous hemianopsia, more often in the upper quadrant type. Transient ischemia of the mesencephalic part of the brain stem is manifested by oculomotor disorders in the form of diplopia, paresis oculomotor muscles, short-term gaze paresis (vertical or horizontal) with paresis of convergence, slight strabismus, ptosis of the eyelids. Ischemia in the area of ​​ascending RF systems can cause loss of consciousness. It is usually accompanied by stem symptoms: double vision, dizziness, nystagmus, dysarthria, facial numbness, ataxia, or hemianopsia. transient ischemia lower olive and RF can cause an attack of sudden falling due to bilateral weakness in the legs and immobility. An attack of a sudden drop in postural tone without loss of consciousness is called a drop attack. With VBN, after an attack, the patient cannot immediately rise, although he was not injured. Transient ischemia of the mediobasal regions temporal lobes accompanied by the development of global amnesia - a short-term loss random access memory. Patients during this period are not quite adequate, they lose their plan of behavior, they vaguely state their thoughts. After a few hours, they show transient amnesia for a certain period of time. Transient ischemia of the cerebellum causes ataxia, more often standing and walking. Often there is paresis of facial muscles peripheral type(of the entire half of the face). Sensitivity disorders: paresthesia, hyper- and hypoesthesia more often around the mouth, less often on both halves of the face or body, in the limbs in any combination, including all four. Movement disorders are manifested in the form of increased tendon reflexes, weakness, awkwardness of movements in the limbs in any combination. During various attacks, the side of motor and sensory disturbances changes. An inverted type of transient paresis is noted - muscle weakness, mainly in the proximal parts of the arm and / or leg, a more persistent nature of changes in tendon reflexes. Unlike strokes, VBS is not characterized by alternating trunk symptoms. The permanent form is also characterized by headaches in the occipital region, which sometimes appear in the paroxysmal form.

Currently in the diagnosis of VBI the leading place is occupied by ultrasound research methods. Doppler ultrasonography (USDG) is based on the Doppler effect: when a sound source moves relative to the receiver, the frequency of the sound perceived by it differs from the frequency of the sound source by an amount directly proportional to the speed of the relative (linear) movement. Ultra sound signal from moving blood (erythrocytes) is perceived by the apparatus, which registers LSC (linear velocity of erythrocytes). For analysis ultrasound results the asymmetry coefficient of the LCS is derived. It is defined as the ratio of the difference in LBF in both vertebral arteries to the smaller LBF in one of them and is expressed as a percentage. Normally, it does not exceed 20%. The method allows to detect stenosis with a degree of more than 50%. Duplex scanning allows you to get an image of the vascular bed with the characteristics of blood flow in it. In this case, the ultrasonic signal sent in the direction of the investigated vessel is reflected from the moving erythrocytes. The difference between the frequency of the sent and reflected ultrasound waves is the linear velocity of the blood flow. By sequentially scanning the area above the vessels with a sensor attached to the sensory arm, data are obtained on the spatial location of the sensor, synchronous with the Doppler signal, which are subjected to computer analysis and, based on them, a map of the studied vascular zone is drawn - a Doppler ultrasonogram. It can be either in gray tones or in color if the device has a color Doppler coding program.
Fine spectrogram cerebral vessels has the form of a pulse half-wave lying above the isoline, with a systolic peak and diastolic incisura. A change in blood flow leads to a change in the Doppler spectra. With stenosis of the artery, the speed of movement in the stenotic area increases in proportion to the degree of stenosis, and at the exit from it, an expansion of the range of velocities and a partially reverse movement of blood are noted. Accordingly, on the spectrogram, this looks like a sharp increase in the amplitude of the systolic peak, an expansion of the range of velocities, with a stenosis of 75% or more, the appearance of spectral components below the isoline. A complete ultrasound examination includes recording of spectrograms of the main main vessels head: common (OSA), external (NSA), internal (ICA) carotid arteries, right and left vertebral arteries (VA), branches of the ophthalmic (GA) and facial artery. The performance of functional compression tests makes it possible to judge the safety of the circle of Willis. The sample is considered positive (i.e., the anastomosis is functioning) if there is an increase (or registration) of blood flow. Ultrasound examination allows you to explore the extracranial parts of the carotid and vertebral arteries and identify their occlusive lesions and deformation of the vertebral arteries.
Transcranial dopplerography (TCD or TKDG) is based on the use of lower frequency ultrasound waves that can penetrate the thin part of the skull bones. The method allows studying the blood flow in the anterior, middle and posterior cerebral and basilar arteries and assessing intracranial hemodynamics in occlusive lesions of the extracranial arteries, identifying angiospasm in SAH, occlusive lesions of the intracranial arteries, arterial aneurysms, arteriovenous malformations, disorders of the venous circulation of the brain. TKD combined with functional tests(compression, orthostatic, with nitroglycerin, with CO2, etc.) allow assessing the state of cerebral hemodynamics and vascular reserves of the brain. Ultrasound and TKD study with duplex scanning(and especially enhanced by color duplex coding) make it possible to isolate the vascular wall from the bloodstream, which makes it possible to study the intima-media complex, the nature of an atherosclerotic plaque, and resolve the issue of its embologenicity (homogeneous with low density and heterogeneous with a predominance of structures of low ultrasound density). TKD monitoring by fixing sensors on the head in a special helmet makes it possible to detect microemboli in the vessels of the brain, and both the analysis of spectrograms and the sound signal from emboli (“chirping”, “whistling”, “pop” or constant sound) matter.

Thus, the diagnosis of VBN should include an ultrasound study to detect damage to extracranial vessels and be supplemented by TCD to study the state of the vascular reserves of the brain. Ultrasound and TCD allow for an objective assessment of the treatment of VBI.

Bibliography
1. Vilensky B.S. Stroke. - St. Petersburg, 1990.
2. Differential Diagnosis nervous diseases./ Ed. G.A. Akimova and M.M. The same guide for doctors. - St. Petersburg: Hippocrates, 2001.
3. Neurological journal №3,2001. IN AND. Skvortsova. Ischemic stroke: pathogenesis of ischemia, therapeutic approaches.
4. Neurology./ Ed. M. Samuels. Per. from English. - M.: Practice, 1997.
5. Nervous diseases./ Ed. M.N. Puzin. Tutorial for students of the system of postgraduate education - M.: Medicine, 2002.
6. Troshin V.D. Vascular diseases nervous system. Early diagnosis, treatment, prevention. Guide for doctors. - N. Novgorod, 1992.
7. Troshin V.M., Kravtsov Yu.I. Diseases of the nervous system in children. Guide for doctors and students, v.2 - N. Novgorod: Sarpi, 1993.
8. Shtulman D.R., Levin O.S. Neurology. Reference book of a practical doctor - M.: MED press-inform, 2002.
9. Yakovlev N.A. Vertebrobasilar insufficiency. Syndrome of the vertebrobasilar arterial system - Moscow, 2001.
10. Yakhno N.N., Shtulman D.R. Diseases of the nervous system. Guide for doctors, v.1 - M.: Medicine, 2001.