Venous circle of the brain. Blood supply to the human brain

The delivery of oxygen to the brain through the blood is one of the most important processes in the body. Thanks to it, nerve cells receive the necessary energy for their functioning. It is not surprising that this system is quite complex and extensive. So, let's consider the blood supply to the brain, the diagram of which will be discussed in the article below.

Structure (briefly)

If we briefly consider the blood supply to the brain, it is carried out with the participation of the carotid arteries, as well as the vertebral arteries. The former provide about 65% of all blood, and the latter - the remaining 35%. But in general, the blood supply scheme is much broader. It also includes the following structures:

vertebrobasilar system;
special circle of Willis;
carotid basin.

In total, about 50 ml of blood per 100 g of brain tissue enters the brain per minute. It is important that the volumes and speed of blood flow are constant.

Blood supply to the brain: diagram of the main vessels

So, as already mentioned, 4 arteries supply blood to the brain. It is then distributed to other vessels. Let's look at them in more detail.

Internal carotid arteries

These are branches of the large carotid arteries, which are located on the side of the neck. They can be easily felt as they pulsate quite well. In the area of the larynx, the carotid arteries diverge into external and internal branches. The latter passes through the cranial cavity and carries oxygen to different areas of the blood supply to the brain. As for the external arteries, they are needed to supply oxygen to the skin and muscles of the face, as well as the neck.

Vertebral arteries

They begin with the subclavian arteries and pass through various parts of the cervical vertebrae, then entering the cranial cavity through an opening in the back of the head.

These vessels are characterized by high pressure and significant blood flow speed. Therefore, they have characteristic curves in the area where they meet the skull to reduce both pressure and speed. Further, all these arteries connect in the cranial cavity and form the arterial circle of Willis. It is necessary in order to compensate for the disturbance in any part of the blood flow and prevent oxygen starvation of the brain.

Cerebral arteries

The branches of the internal carotid artery are divided into the middle and anterior branches. They go further into the cerebral hemispheres and nourish their outer and inner surfaces, including the deep parts of the brain.

The vertebral arteries, in turn, form other branches - the posterior cerebral arteries. They are responsible for feeding the occipital areas of the brain, the cerebellum, and the trunk.

Subsequently, all these arteries branch into many thin arteries that penetrate into the brain tissue. They may vary in diameter and length. The following arteries are distinguished:

short (used to feed the bark;
long (for white matter).

There are other sections in the cerebral blood flow system. Thus, the BBB, a mechanism for controlling transport between capillaries and nervous tissue cells, plays an important role. The blood-brain barrier prevents foreign substances, toxins, bacteria, iodine, salt, etc. from entering the brain.

Venous drainage

The removal of carbon dioxide from the brain is carried out through a system of cerebral and superficial veins, which then flow into venous formations - sinuses. The superficial cerebral veins (inferior and superior) transport blood from the cortical part of the cerebral hemispheres, as well as from the subcortical white matter.

Veins, which are located deep in the brain, collect blood from the ventricles of the brain and subcortical nuclei, capsule. Later they unite into the common cerebral vein.

Collected in the sinuses, the blood flows into the vertebral and internal jugular veins. In addition, diploic and emissary cranial veins participate in the blood outflow system.

It should be noted that the cerebral veins do not have valves, but many anastomoses are present. The venous system of the brain is distinguished by the fact that it allows for ideal blood flow in a confined space of the skull.

There are only 21 venous sinuses (5 unpaired and 8 pairs). The walls of these vascular formations are formed from processes of solid MO. If you cut through the sinuses, they form a characteristic triangular lumen.

So, the circulatory system of the brain is a complex structure with many different elements, which have no analogues in other human organs. All these elements are needed to quickly and in the right quantity deliver oxygen to the brain and remove waste products from it.

CEREBRAL CIRCULATION- blood circulation through the cerebral vascular system. The blood supply to the brain is more intense than to any other organs: approx. 15% of the blood entering the systemic circulation during cardiac output flows through the blood vessels of the brain (its weight is only 2% of the body weight of an adult). Extremely high cerebral blood flow ensures the greatest intensity of metabolic processes in brain tissue. This blood supply to the brain is also maintained during sleep. The intensity of metabolism in the brain is also evidenced by the fact that 20% of the oxygen absorbed from the environment is consumed by the brain and used for oxidative processes occurring in it.

PHYSIOLOGY

The circulatory system of the brain provides perfect regulation of the blood supply to its tissue elements, as well as compensation for disturbances in cerebral blood flow. The human brain (see) is supplied with blood simultaneously by four main arteries - paired internal carotid and vertebral arteries, which are interconnected by wide anastomoses in the area of the arterial (Willisian) circle of the cerebrum (color. Fig. 4). Under normal conditions, the blood does not mix here, flowing ipsilaterally from each internal carotid artery (see) into the cerebral hemispheres, and from vertebrates - mainly into the parts of the brain located in the posterior cranial fossa.

Cerebral arteries are not elastic, but muscular type vessels with abundant adrenergic and cholinergic innervation, therefore, changing their lumen within a wide range, they can participate in regulating blood supply to the brain.

Paired anterior, middle and posterior cerebral arteries, extending from the arterial circle, branching and anastomosing among themselves, form a complex system of arteries of the pia mater (pial arteries), which has a number of features: branching of these arteries (down to the smallest, diameter 50 microns or less ) are located on the surface of the brain and regulate blood supply to extremely small areas; each artery lies in a relatively wide canal of the subarachnoid space (see Meninges), and therefore its diameter can vary within wide limits; the arteries of the pia mater lie on top of the anastomosing veins. From the smallest arteries of the pia mater radial arteries branch off in the thickness of the brain; they do not have free space around the walls and, according to experimental data, are the least active in terms of changes in diameter when regulating the muscle. There are no interarterial anastomoses in the thickness of the brain.

The capillary network in the thickness of the brain is continuous. Its density is greater, the more intense the metabolism in the tissues, so it is much thicker in gray matter than in white matter. In each part of the brain, the capillary network is characterized by specific architecture.

Venous blood flows from the capillaries of the brain into the widely anastomosing venous system of both the pia mater (pial veins) and the great cerebral vein (vein of Galen). Unlike other parts of the body, the venous system of the brain does not perform a capacitive function.

For more details on the anatomy and histology of the blood vessels of the brain, see Brain.

Regulation of cerebral circulation is carried out by a perfect physiological system. The effectors of regulation are the main, intracerebral arteries and arteries of the pia mater, which are characterized by specific functions. features.

Four types of regulation of M. to. are shown in the diagram.

When the level of total blood pressure changes within certain limits, the intensity of cerebral blood flow remains constant. Regulation of constant blood flow in the brain during fluctuations in total blood pressure is carried out due to changes in resistance in the arteries of the brain (cerebrovascular resistance), which narrow when total blood pressure increases and expand when it decreases. Initially, it was assumed that vascular shifts were caused by the reactions of the smooth muscles of the arteries to varying degrees of stretching of their walls by intravascular pressure. This type of regulation is called autoregulation or self-regulation. The level of increased or decreased blood pressure, at which cerebral blood flow ceases to be constant, is called the upper or lower limit of autoregulation of cerebral blood flow, respectively. Experimental and wedge studies have shown that autoregulation of cerebral blood flow is in close relationship with neurogenic influences, which can shift the upper and lower boundaries of its autoregulation. The effectors of this type of regulation in the arterial system of the brain are the main arteries and arteries of the pia mater, active reactions of which maintain constant blood flow in the brain when the total blood pressure changes.

Regulation of M. to. with a change in the gas composition of the blood is that cerebral blood flow increases with an increase in the CO 2 content and with a decrease in the O 2 content in arterial blood and decreases when their ratio is inverse. The influence of blood gases on the tone of the arteries of the brain, according to a number of authors, can be carried out humorally: with hypercapnia (see) and hypoxia (see), the concentration of H + in the brain tissue increases, the ratio between HCO 3 - and CO 2 changes, which together with other biochemicals, shifts in the extracellular fluid directly affect the metabolism of smooth muscles, causing dilatation) of the arteries. The neurogenic mechanism also plays an important role in the action of these gases on the vessels of the brain, in which chemoreceptors of the carotid sinus and, apparently, other cerebral vessels participate.

Elimination of excess blood volume in the vessels of the brain is necessary, since the brain is located in a hermetically sealed skull and its excessive blood supply leads to increased intracranial pressure (see) and to compression of the brain. Excessive blood volume can occur when there is difficulty in the outflow of blood from the veins of the brain and when there is excessive blood flow due to dilation of the arteries of the pia mater, for example, during asphyxia (see) and post-ischemic hyperemia (see Hyperemia). There is evidence that the effectors of regulation in this case are the main arteries of the brain, which narrow reflexively due to irritation of the baroreceptors of the cerebral veins or arteries of the pia mater and limit blood flow to the brain.

Regulation of adequate blood supply to brain tissue ensures correspondence between the intensity of blood flow in the microcirculation system (see) and the intensity of metabolism in brain tissue. This regulation occurs when there is a change in the intensity of metabolism in the brain tissue, for example, a sharp increase in its activity, and when there is a primary change in blood flow into the brain tissue. Regulation is carried out locally, and its effector is the small arteries of the pia mater, which control blood flow in negligibly small areas of the brain; the role of smaller arteries and arterioles in the thickness of the brain has not been established. Control of the lumen of effector arteries when regulating cerebral blood flow, according to most authors, is carried out humorally, i.e., under the direct action of metabolic factors accumulating in brain tissue (hydrogen ions, potassium, adenosine). Some experimental data indicate a neurogenic mechanism (local) of vasodilation in the brain.

Types of regulation of cerebral circulation. Regulation of cerebral blood flow when the level of total blood pressure changes (III) and when there is excessive blood supply to the cerebral vessels (IV) is carried out by the main arteries of the brain. When the content of oxygen and carbon dioxide in the blood changes (II) and when the adequacy of the blood supply to brain tissue is impaired (I) Small arteries of the pia mater are included in the regulation.

METHODS FOR STUDYING CEREBRAL BLOOD FLOW

The Kathy-Schmidt method allows you to determine blood flow in the entire human brain by measuring the rate of saturation (saturation) of brain tissue with an inert gas (usually after inhaling small amounts of nitrous oxide). Saturation of brain tissue is determined by determining the gas concentration in venous blood samples taken from the jugular vein bulb. This method (quantitative) allows one to determine the average blood flow of the whole brain only discretely. It was found that the intensity of cerebral blood flow in a healthy person is approximately 50 ml of blood per 100 g of brain tissue per minute.

The clinic uses a direct method to obtain quantitative data on cerebral blood flow in small areas of the brain using the clearance (clearance rate) of radioactive xenon (133 Xe) or hydrogen gas. The principle of the method is that the brain tissue is saturated with easily diffusible gases (133 Xe solution is usually injected into the internal carotid artery, and hydrogen is inhaled). Using appropriate detectors (for 133Xe they are installed above the surface of the intact skull; for hydrogen, platinum or gold electrodes are inserted into any area of the brain) the rate at which brain tissue is cleared of gas is determined, which is proportional to the intensity of blood flow.

Direct (but not quantitative) methods include the method of determining changes in blood volume in superficially located vessels of the brain using radionuclides, which mark blood plasma proteins; in this case, radionuclides do not diffuse through the walls of the capillaries into the tissue. Blood albumins labeled with radioactive iodine have become especially widespread.

The reason for the decrease in the intensity of cerebral blood flow is a decrease in the arteriovenous pressure difference due to a decrease in total blood pressure or an increase in total venous pressure (see), with the main role played by arterial hypotension (see Arterial hypotension). Total blood pressure may drop sharply, and total venous pressure increases less frequently and less significantly. A decrease in the intensity of cerebral blood flow may also be due to an increase in resistance in the vessels of the brain, which may depend on reasons such as atherosclerosis (see), thrombosis (see) or vasospasm (see) of certain arteries of the brain. A decrease in the intensity of cerebral blood flow may depend on the intravascular aggregation of blood cells (see Red blood cell aggregation). Arterial hypotension, weakening blood flow throughout the brain, causes the greatest decrease in its intensity in the so-called. areas of adjacent blood supply, where intravascular pressure drops the most. When certain arteries of the brain are narrowed or occluded, pronounced changes in blood flow are observed in the center of the basins of the corresponding arteries. Of great importance are secondary patol, changes in the vascular system of the brain, for example, changes in the reactivity of the cerebral arteries during ischemia (constrictor reactions in response to vasodilator effects), unrestored blood flow in the brain tissue after ischemia or spasm of the arteries in the area of blood extravasation, in particular subarachnoid hemorrhages. An increase in venous pressure in the brain, which plays a less significant role in weakening the intensity of cerebral blood flow, may have independent significance when it is caused, in addition to an increase in general venous pressure, by local causes that lead to difficulty in the outflow of venous blood from the skull (thrombosis or tumor). In this case, phenomena of venous stagnation of blood in the brain occur, which lead to an increase in blood supply to the brain, which contributes to an increase in intracranial pressure (see Hypertensive syndrome) and the development of cerebral edema (see Edema and swelling of the brain).

Patol, increased intensity of cerebral blood flow may depend on an increase in total blood pressure (see Arterial hypertension) and may be due to primary dilatation (patol, vasodilation) of the arteries; then it occurs only in those areas of the brain where the arteries are dilated. Patol, an increase in the intensity of cerebral blood flow can lead to an increase in intravascular pressure. If the walls of the vessels are pathologically changed (see Arteriosclerosis) or there are arterial aneurysms, then a sudden and sharp increase in total blood pressure (see Crises) can lead to hemorrhage. Patol, an increase in the intensity of cerebral blood flow may be accompanied by a regulatory reaction of the arteries - their constriction, and with a sharp increase in total blood pressure it can be very significant. If the functional state of the smooth muscles of the arteries is changed in such a way that the contraction process is enhanced, and the relaxation process, on the contrary, is reduced, then in response to an increase in total blood pressure, vasoconstriction occurs patol, such as vasospasm (see). These phenomena are most pronounced with a short-term increase in total blood pressure. When the blood-brain barrier is disrupted and there is a tendency to cerebral edema, an increase in pressure in the capillaries causes a sharp increase in the filtration of water from the blood into the brain tissue, where it is retained, resulting in the development of cerebral edema. An increase in the intensity of cerebral blood flow is especially dangerous under the influence of additional factors (traumatic brain injury, severe hypoxia) that contribute to the development of edema.

Compensatory mechanisms are an obligatory component of the symptom complex, which characterizes every violation of M. k. In this case, compensation is carried out by the same regulatory mechanisms, which function under normal conditions, but they are more intense.

When total blood pressure increases or decreases, compensation is carried out by changing the resistance in the vascular system of the brain, with the main role played by the large cerebral arteries (internal carotid and vertebral arteries). If they do not provide compensation, then microcirculation ceases to be adequate and the arteries of the pia mater are involved in regulation. With a rapid increase in total blood pressure, these compensation mechanisms may not work immediately, and then the intensity of cerebral blood flow sharply increases with all possible consequences. In some cases, compensatory mechanisms can work very well and even with chronic hypertension, when general blood pressure is sharply increased (280-300 mm Hg) for a significant time; the intensity of cerebral blood flow remains normal and neurol, disturbances do not occur.

When total blood pressure decreases, compensatory mechanisms can also maintain the normal intensity of cerebral blood flow, and depending on the degree of perfection of their work, the limits of compensation may vary from person to person. With perfect compensation, normal intensity of cerebral blood flow is observed when total blood pressure decreases even to 30 mm Hg. Art., while usually the lower limit of autoregulation of cerebral blood flow is considered to be blood pressure not lower than 55-60 mm Hg. Art.

When resistance increases in certain arteries of the brain (during embolism, thrombosis, vasospasm), compensation is carried out due to collateral blood flow. In this case, compensation is provided by the following factors:

1. The presence of arterial vessels through which collateral blood flow can occur. The arterial system of the brain contains a large number of collateral pathways in the form of wide anastomoses of the arterial circle, as well as numerous interarterial macro- and microanastomoses in the system of arteries of the pia mater. However, the structure of the arterial system is individual, and developmental anomalies are not uncommon, especially in the area of the arterial (circle of Willis) area. Small arteries located deep in the brain tissue do not have arterial-type anastomoses, and although the capillary network throughout the brain is continuous, it cannot provide collateral blood flow to neighboring tissue areas if the blood flow into them from the arteries is disrupted.

2. An increase in the pressure drop in the collateral arterial pathways when there are obstacles to blood flow in one or another cerebral artery (hemodynamic factor).

3. Active expansion of collateral arteries and small arterial branches to the periphery from the site of closure of the artery lumen. This vasodilation is, apparently, a manifestation of the regulation of adequate blood supply to brain tissue: as soon as a deficiency of blood flow into the tissue occurs, a physiological mechanism begins to work, causing dilatation) of those arterial branches that lead to this microcirculatory system. As a result, the resistance to blood flow in the collateral pathways is reduced, which promotes blood flow to the area with reduced blood supply.

The effectiveness of collateral blood flow to the area of reduced blood supply varies from person to person. The mechanisms that ensure collateral blood flow, depending on specific conditions, may be disrupted (as well as other mechanisms of regulation and compensation). Thus, the ability of collateral arteries to expand during sclerotic processes in their walls decreases, which prevents collateral blood flow to the area of impaired blood supply.

Compensation mechanisms are characterized by duality, i.e. compensation for some disorders causes other circulatory disorders. For example, when blood flow in brain tissue that has experienced a deficiency of blood supply is restored, post-ischemic hyperemia may occur, in which the intensity of microcirculation can be significantly higher than the level necessary to ensure metabolic processes in the tissue, i.e., excessive blood perfusion occurs, promoting, in particular, the development of post-ischemic cerebral edema.

On adequate and pharmacological effects, a perverted reactivity of the arteries of the brain can be observed. Thus, the basis of the “intracerebral steal” syndrome is the normal vasodilator reaction of healthy vessels surrounding the focus of ischemia of brain tissue, and the absence of such in the affected arteries in the focus of ischemia, as a result of which blood is redistributed from the focus of ischemia to healthy vessels, and ischemia is aggravated.

PATHOLOGICAL ANATOMY OF CEREBRAL CIRCULATION DISORDERS

Morphol. signs of disturbance of M. to. are revealed in the form of focal and diffuse changes, the severity and localization of which are different and largely depend on the underlying disease and the immediate mechanisms of development of circulatory disorders. There are three main forms of violation

M. to.: hemorrhages (hemorrhagic stroke), cerebral infarctions (ischemic stroke) and multiple different types of small focal changes in the brain substance (vascular encephalopathy).

Wedge, manifestations of occlusive lesions of the extracranial part of the internal carotid artery in the initial period occur more often in the form of transient disorders of M. K. Nevrol, the symptoms are varied. In approximately 1/3 of cases, there is an alternating optic-pyramidal syndrome - blindness or decreased vision, sometimes with atrophy of the optic nerve on the side of the affected artery (due to discirculation in the ophthalmic artery), and pyramidal disorders on the side opposite to the lesion. Sometimes these symptoms occur simultaneously, sometimes dissociated. The most common signs of occlusion of the internal carotid artery are signs of discirculation in the middle cerebral artery basin: paresis of the limbs of the side opposite to the lesion, usually of the cortical type with a more pronounced defect of the arm. With infarctions in the left internal carotid artery, aphasia often develops, usually motor. Sensory disturbances and hemianopsia may occur. Occasionally, epileptiform seizures are observed.

In heart attacks caused by intracranial thrombosis of the internal carotid artery, which occurs with disconnection of the arterial circle, along with hemiplegia and hemihypesthesia, pronounced cerebral symptoms are observed: headache, vomiting, impaired consciousness, psychomotor agitation; secondary stem syndrome appears.

The syndrome of occlusive lesions of the internal carotid artery, in addition to the intermittent course of the disease and the indicated neurol manifestations, is characterized by a weakening or disappearance of the pulsation of the affected carotid artery, often the presence of a vascular noise above it and a decrease in retinal pressure on the same side. Compression of the unaffected carotid artery causes dizziness, sometimes fainting, and convulsions in healthy limbs.

An occlusive lesion of the extracranial section of the vertebral artery is characterized by “spotty” lesions of various parts of the spinobasilar system: vestibular disorders (dizziness, nystagmus), disorders of statics and coordination of movements, visual and oculomotor disturbances, dysarthria often occur; motor and sensory disorders are less frequently detected. Some patients experience attacks of sudden falling due to loss of postural tone, adynamia, and hypersomnia. Quite often there are memory disorders for current events such as Korsakov's syndrome (see).

When the intracranial part of the vertebral artery is blocked, persistent alternating syndromes of damage to the medulla oblongata are combined with transient symptoms of ischemia of the oral parts of the brain stem, occipital and temporal lobes. In approximately 75% of cases, Wallenberg-Zakharchenko, Babinsky-Nageotte syndromes and other syndromes of unilateral damage to the lower parts of the brain stem develop. With bilateral thrombosis of the vertebral artery, severe swallowing and phonation disorders occur, breathing and cardiac activity are impaired.

Acute blockage of the basilar artery is accompanied by symptoms of predominant damage to the pons with a disorder of consciousness up to coma, rapid development of lesions of the cranial nerves (III, IV, V, VI, VII pairs), pseudobulbar syndrome, paralysis of the limbs with the presence of bilateral patols. reflexes. Autonomic-visceral crises, hyperthermia, and disturbance of vital functions are observed.

Diagnosis of cerebrovascular disorders

The basis for the diagnosis of the initial manifestation of M.'s inferiority is: the presence of two or more subjective signs, often repeated; absence during normal neurol examination of symptoms of organic damage to c. n. With. and detection of signs of general vascular disease (atherosclerosis, hypertension, vasculitis, vascular dystonia, etc.), which is especially important, since the patient’s subjective complaints are not pathognomonic for the initial manifestations of vascular inferiority of the brain and can also be observed in other conditions (neurasthenia , asthenic syndromes of various origins). In order to establish a general vascular disease in a patient, it is necessary to conduct a comprehensive wedge and examination.

The basis for the diagnosis of an acute disorder of M. to. is the sudden appearance of symptoms of organic brain damage against the background of a general vascular disease with significant dynamics of cerebral and local symptoms. If these symptoms disappear in less than 24 hours. a transient disorder of M. is diagnosed; in the presence of more persistent symptoms, a cerebral stroke is diagnosed. In determining the nature of a stroke, it is not the individual signs, but their combination that is of key importance. There are no pathognomonic signs for one type of stroke or another. For the diagnosis of hemorrhagic stroke, high blood pressure and a history of cerebral hypertensive crises, sudden onset of the disease, rapid progressive deterioration of the condition, significant severity of not only focal but also general cerebral symptoms, distinct autonomic disorders, early onset of symptoms caused by displacement and compression of the brain stem, are important. rapidly occurring changes in the blood (leukocytosis, neutrophilia with a shift to the left in the leukocyte formula, an increase in the Krebs index to 6 or higher), the presence of blood in the cerebrospinal fluid.

Cerebral infarction is evidenced by the development of a stroke during sleep or against the background of weakened cardiovascular activity, the absence of arterial hypertension, the presence of cardiosclerosis, a history of myocardial infarction, the relative stability of vital functions, the preservation of consciousness with massive neurol, symptoms, the absence or mild severity of secondary stem syndrome, relatively slow development of the disease, no changes in the blood in the first day after the stroke.

Echoencephalography data (see) help in diagnosis - the shift of the M-echo towards the contralateral hemisphere is more likely to speak in favor of intracerebral hemorrhage. X-ray, examination of cerebral vessels after administration of contrast agents (see Vertebral angiography, Carotid angiography) for intrahemispheric hematomas reveals an avascular zone and displacement of the arterial trunks; In case of cerebral infarction, an occlusive process is often detected in the main or intracerebral vessels; dislocation of the arterial trunks is uncharacteristic. Computed tomography of the head provides valuable information when diagnosing a stroke (see Computer tomography).

Basic principles of therapy for cerebrovascular accidents

With initial manifestations of M.'s inferiority, therapy should be aimed at treating the underlying vascular disease, normalizing the work and rest regime, and using agents that improve the metabolism of brain tissue and hemodynamics.

In case of acute violations of M. to., urgent measures are required, since it is not always clear whether the violation of M. to. will be transient or persistent, therefore, in any case, complete mental and physical rest is necessary. A cerebral vascular attack should be stopped at the earliest stages of its development. Treatment of transient disorders of M. to. (vascular cerebral crises) should primarily involve the normalization of blood pressure, cardiac activity and cerebral hemodynamics with the inclusion, if necessary, of antihypoxic, decongestant and various symptomatic drugs, including sedatives, in some cases they are used anticoagulants and antiplatelet agents. Treatment for cerebral hemorrhage is aimed at stopping bleeding and preventing its resumption, combating cerebral edema and impairment of vital functions. When treating a heart attack

brain carry out measures aimed at improving blood supply to the brain: normalizing cardiac activity and blood pressure, increasing blood flow to the brain by dilating regional cerebral vessels, reducing vascular spasm and improving microcirculation, as well as normalizing physical-chemical. properties of blood, in particular to restore balance in the blood coagulation system to prevent thromboembolism and to dissolve already formed blood clots.

Bibliography: Akimov G. A. Transient disorders of cerebral circulation, L., 1974, bibliogr.; Antonov I.P. and Gitkina L.S. Vertebro-basilar strokes, Minsk, 1977; B e to about in D. B. and Mikhailov S. S. Atlas of arteries and veins of the human brain, M., 1979, bibliogr.; Bogolepov N.K. Comatose states, p. 92, M., 1962; about n e, Cerebral crises and stroke, M., 1971; Gannushkina I.V. Collateral circulation in the brain, M., 1973; K Dosovsky B. N. Blood circulation in the brain, M., 1951, bibliogr.; K o l t o-vera. N.idr. Pathological anatomy of cerebral circulation disorders, M., 1975; Mints A. Ya. Atherosclerosis of cerebral vessels, Kyiv, 1970; Moskalenko Yu.E. and others. Intracranial hemodynamics, Biophysical aspects, L., 1975; Mchedlishvili G. I. Function of vascular mechanisms of the brain, L., 1968; o n, Spasm of the cerebral arteries, Tbilisi, 1977; Vascular diseases of the nervous system, ed. E. V. Schmidt, p. 632, M., 1975; Sh m and d t E. V. Stenosis and thrombosis of the carotid arteries and cerebrovascular accidents, M., 1963; Schmidt E. V., Lunev D. K. and Vereshchagin N. V. Vascular diseases of the brain and spinal cord, M., 1976; Cerebral circulation and stroke, ed. by K. J. Ztilch, B. u. a., 1971; Fisher S. M. The arterial lesions underlying lacunes, Acta neuropath. (Berl.), v. 12, p. 1, 1969; Handbook of clinical neurology, ed. by P. J. Vinken a. G. W. Bruyn, v. 11 -12, Amsterdam, 1975; Jorgensen L. a. Torvik A. Ischemic cerebrovascular diseases in an autopsy series, J. Neurol. Sci., v. 9, p. 285, 1969; Olesen J. Cerebral blood flow, Copenhagen, 1974; P u r v e s M. J. The physiology of the cerebral circulation, Cambridge, 1972.

D. K. Lunev; A. N. Koltover, R. P. Tchaikovskaya (pat. an.), G. I. Mchedlishvili (physics., path. physics.).

The blood supply to the brain is carried out by two arterial systems - the internal carotid and vertebral arteries.

The internal carotid artery on the left arises directly from the aorta, on the right - from the subclavian artery. It penetrates into the cranial cavity through a special canal and enters there on both sides of the sella turcica and the optic chiasm. Here a branch immediately departs from it - the anterior cerebral artery. Both anterior cerebral arteries are connected to each other by the anterior communicating artery. The direct continuation of the internal carotid artery is the middle cerebral artery.

The vertebral artery arises from the subclavian artery, passes through the canal of the transverse processes of the cervical vertebrae, enters the skull through the foramen magnum and is located at the base of the medulla oblongata. At the border of the medulla oblongata and the pons, both vertebral arteries are connected into one common trunk - the basilar artery. The basilar artery divides into two posterior cerebral arteries. Each posterior cerebral artery is connected to the middle cerebral artery by means of the posterior communicating artery. Thus, at the base of the brain, a closed arterial circle is obtained, called the Wellisian arterial circle (Fig. 33): the basilar artery, the posterior cerebral arteries (anastomosing with the middle cerebral artery), the anterior cerebral arteries (anastomosing with each other).

From each vertebral artery, two branches depart and go down to the spinal cord, which merge into one anterior spinal artery. Thus, on the basis of the medulla oblongata, a second arterial circle is formed - the Zakharchenko circle.

Thus, the structure of the circulatory system of the brain ensures uniform distribution of blood flow over the entire surface of the brain and compensation of cerebral circulation in case of its disturbance. Due to a certain ratio of blood pressure in the circle of Wellisian, blood does not flow from one internal carotid artery to another. In case of blockage of one carotid artery, blood circulation to the brain is restored due to the other carotid artery.

The anterior cerebral artery supplies the cortex and subcortical white matter of the inner surface of the frontal and parietal lobes, the lower surface of the frontal lobe lying on the orbit, the narrow rim of the anterior and upper parts of the outer surface of the frontal and parietal lobes (the upper parts of the anterior and posterior central gyri), the olfactory tract, the anterior 4/5 of the corpus callosum, part of the caudate and lentiform nuclei, anterior thigh of the internal capsule (Fig. 33, b).

Impaired cerebral circulation in the anterior cerebral artery basin leads to damage to these areas of the brain, resulting in disturbances of movement and sensitivity in the opposite extremities (more pronounced in the leg than in the arm). Peculiar mental changes also occur due to damage to the frontal lobe of the brain.

The middle cerebral artery supplies the cortex and subcortical white matter of most of the outer surface of the frontal and parietal lobes (except for the upper third of the anterior and posterior central gyri), the middle part of the occipital lobe, and most of the temporal lobe. The middle cerebral artery also supplies blood to the knee and the anterior 2/3 of the internal capsule, part of the caudate, lenticular nuclei and the optic thalamus. Impaired cerebral circulation in the middle cerebral artery basin leads to motor and sensory disorders in the opposite limbs, as well as to disturbances in speech and gnostic-praxic functions (if the lesion is localized in the dominant hemisphere). Speech disorders are of the nature of aphasia - motor, sensory or total.

A - arteries at the base of the brain: 1 - anterior communicating; 2 - forebrain; 3 - internal carotid; 4 - middle cerebral; 5 - rear connecting; 6 - posterior brain; 7 - main; 8 - vertebral; 9 - anterior spinal; II - zones of blood supply to the brain: I - superolateral surface; II - inner surface; 1 - anterior cerebral artery; 2 - middle cerebral artery; 3 - posterior cerebral artery

The posterior cerebral artery supplies blood to the cortex and subcortical white matter of the occipital lobe (with the exception of its middle part on the convex surface of the hemisphere), the posterior part of the parietal lobe, the lower and posterior parts of the temporal lobe, the posterior parts of the visual thalamus, the hypothalamus, the corpus callosum, the caudate nucleus, and also the quadrigeminal peduncle and cerebral peduncles (Fig. 33, b). Disturbances of cerebral circulation in the posterior cerebral artery basin lead to disturbances in visual perception, dysfunction of the cerebellum, thalamus opticus, and subcortical nuclei.

The brainstem and cerebellum are supplied with blood by the posterior cerebral, vertebral and basilar arteries.

The blood supply to the spinal cord is carried out by the anterior and two posterior spinal arteries, which anastomose with each other and create segmental arterial rings.

The spinal arteries receive blood from the vertebral arteries. Circulatory disorders in the system of arteries of the spinal cord lead to loss of functions of the corresponding segments.

The outflow of blood from the brain occurs through a system of superficial and deep cerebral veins, which flow into the venous sinuses of the dura mater. From the venous sinuses, blood flows through the internal jugular veins and ultimately enters the superior vena cava.

From the spinal cord, venous blood collects into two large internal veins and into the external veins.

Unpaired vessel, formed at the connection of the two anterior spinal arteries, is directed down along the anterior fissure of the spinal cord and is called the anterior spinal artery.

Right and left front spinal arteries, together with the vertebral arteries and the proximal part of the OA on the ventral surface of the medulla oblongata, form an arterial circle (diamond-shaped), which is called the bulbar arterial ring (Zakharchenko circle).

From basilar arteries At the level of the bridge, several paired branches arise. The largest of these are the anterior inferior cerebellar artery (can also arise from the terminal vertebral artery), which goes to the inferior surface of the cerebellum, and the superior cerebellar artery, which arises from the OA at the anterior edge of the pons, goes laterally and posteriorly to the upper parts of the cerebellum.
Between these big ones branches The arteries of the labyrinth (to the inner ear), several pairs of arteries of the pons and the arteries of the midbrain also depart.

This circle was first described by Sir Thomas Willis in 1664 and was named - Circle of Willis. Thus, the anterior, middle cerebral arteries, anterior communicating artery, posterior cerebral arteries, distal basilar artery and posterior communicating arteries take part in the formation of a typical circle of Willis. According to various authors, the typical structure of the Circle of Willis (“classic version”) occurs in 20-50% of cases. The anterior and posterior cerebral arteries are usually divided into two segments.

Precommunicative segment of the anterior cerebral artery(before the separation of the RCA) is designated as segment A1, and its post-communication segment is designated as segment A2. The precommunicating segment of the posterior cerebral artery (before the entry of the PCA) is called the P1 segment, and its postcommunicating segment is called the P2 segment. The middle cerebral artery is divided into segments: before division into medial and lateral branches - segment M1, after division - segment M2.

Extracranial collaterals are a connecting link between the branches of the internal carotid, external carotid and subclavian arteries located outside the skull. Thus, the external carotid artery anastomoses with the subclavian artery through branches of the superior and inferior thyroid arteries. This anastomosis connects the carotid and subclavian artery systems of both sides. In addition, the external carotid artery anastomoses with the subclavian artery through the occipital artery (a branch of the ECA) and the muscular branches of the vertebral artery.

Branches of the subclavian artery(deep cervical and ascending cervical artery) anastomose with the vertebral artery. The external carotid artery (facial, maxillary and superficial temporal arteries) anastomoses with the internal carotid artery (ophthalmic artery) using a system called the ophthalmic anastomosis and located in the area of the internal canthus. It is this anastomosis that is second in importance after the circle of Willis and is activated in case of its functional failure.

Educational video of vascular anatomy of the Circle of Willis

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Carried out by two arterial systems: internal sleep And vertebral arteries.

The internal carotid artery on the left arises directly from the aorta, on the right - from the subclavian artery.

It penetrates into the cranial cavity through a special canal and enters there on both sides of the sella turcica and the optic chiasm.

Here a branch immediately branches off from it - anterior cerebral artery. Both anterior cerebral arteries are connected to each other by the anterior communicating artery. The direct continuation of the internal carotid artery is the middle cerebral artery.

The vertebral artery arises from the subclavian artery, passes through the canal of the transverse processes of the cervical vertebrae, enters the skull through the foramen magnum and is located at the base. At the border of the medulla oblongata and both vertebral arteries are connected into one common trunk - main artery. The basilar artery divides into two posterior cerebral arteries. Each posterior cerebral artery is connected to the middle cerebral artery by means of the posterior communicating artery. Thus, at the base of the brain, a closed arterial circle is obtained, called the Wellisian arterial circle: the basilar artery, the posterior cerebral arteries (anastomosing with the middle cerebral artery), the anterior cerebral arteries (anastomosing with each other).

From each vertebral artery, two branches depart and go down to the spinal cord, which merge into one anterior spinal artery. Thus, on the basis of the medulla oblongata, the second arterial circle- Zakharchenko circle.

The anterior rosacea artery supplies the cortex and subcortical white matter of the inner surface and, the lower surface of the frontal lobe lying on the orbit, the narrow rim of the anterior and upper parts of the outer surface of the frontal and parietal lobes (the upper parts of the anterior and posterior central gyri), the olfactory tract, the anterior 4/5 corpus callosum, part of the caudate and lentiform nuclei, anterior femur of the internal capsule.

The middle cerebral artery supplies the cortex and subcortical white matter of most of the outer surface of the frontal and parietal lobes (with the exception of the upper third of the anterior and posterior central gyri), the middle part and most of the temporal lobe. The middle cerebral artery also supplies blood to the knee and anterior 2/3, part of the caudate, lenticular nuclei and. Impaired cerebral circulation in the middle cerebral artery basin leads to motor and sensory disorders in the opposite extremities, as well as to disorders of speech and gnosticopraxic functions (if the lesion is localized in the dominant hemisphere). are of the nature of aphasia - motor, sensory or total.

The posterior cerebral artery supplies blood to the cortex and subcortical white matter of the occipital lobe (with the exception of its middle part on the convex surface of the hemisphere), the posterior part of the parietal lobe, the lower and posterior parts of the temporal lobe, the posterior parts thalamus, hypothalamus, corpus callosum, caudate nucleus, as well as. Disturbances of cerebral circulation in the posterior cerebral artery basin lead to disturbances in visual perception, dysfunction of the cerebellum, thalamus opticus, and subcortical nuclei.

The brainstem and cerebellum are supplied with blood by the posterior cerebral, vertebral and basilar arteries.

The blood supply to the spinal cord is carried out by the anterior and two posterior spinal arteries, which anastomose with each other and create segmental arterial rings.

The spinal arteries receive blood from the vertebral arteries. Circulatory disorders in the system of arteries of the spinal cord lead to loss of functions of the corresponding segments.
The outflow of blood from the brain occurs through a system of superficial and deep cerebral veins, which flow into the venous sinuses of the dura mater. From the venous sinuses, blood flows through the internal jugular veins and ultimately enters the superior vena cava.

From the spinal cord, venous blood collects into two large internal veins and into the external veins.