Vertebral artery syndrome (VAS) is a complex of symptoms resulting from disruption of blood flow in the vertebral (or vertebral) arteries. In recent decades, this pathology has become quite widespread, which is probably due to the increase in the number of office workers and people leading a sedentary lifestyle who spend a lot of time at the computer. If previously the diagnosis of SPA was made mainly to elderly people, today the disease is diagnosed even in twenty-year-old patients. Since any disease is easier to prevent than to treat, it is important for everyone to know for what reasons vertebral artery syndrome occurs, what symptoms are manifested and how this pathology is diagnosed. We will talk about this, as well as the principles of SPA treatment, in our article.

Fundamentals of Anatomy and Physiology

Blood enters the brain through four large arteries: the left and right common carotid and the left and right vertebral. It is worth noting that 70-85% of the blood passes through the carotid arteries, so disruption of blood flow in them often leads to acute cerebrovascular accidents, that is, ischemic strokes.

The vertebral arteries supply the brain with only 15-30% of blood. Violation of blood flow in them, as a rule, does not cause acute, life-threatening problems - chronic disorders occur, which, however, significantly reduce the patient’s quality of life and even lead to disability.

The vertebral artery is a paired formation originating from the subclavian artery, which in turn arises on the left - from the aorta, and on the right - from the brachiocephalic trunk. The vertebral artery goes upward and slightly backward, passing behind the common carotid artery, enters the opening of the transverse process of the sixth cervical vertebra, rises vertically through similar openings of all overlying vertebrae, through the foramen magnum enters the cranial cavity and follows to the brain, supplying blood to the posterior parts of the brain : cerebellum, hypothalamus, corpus callosum, midbrain, partially temporal, parietal, occipital lobes, as well as the dura mater of the posterior cranial fossa. Before entering the cranial cavity, branches depart from the vertebral artery, carrying blood to the spinal cord and its membranes. Consequently, when blood flow in the vertebral artery is disrupted, symptoms arise that indicate hypoxia (oxygen starvation) of the areas of the brain that it supplies.

Causes and mechanisms of development of vertebral artery syndrome

Along its length, the vertebral artery comes into contact with both the hard structures of the spinal column and the soft tissues surrounding it. Pathological changes that occur in these tissues are the prerequisites for the development of SPA. In addition, the cause may be congenital characteristics and acquired diseases of the arteries themselves.

So, there are 3 groups of causative factors of vertebral artery syndrome:

1. Congenital structural features of the artery: pathological tortuosity, course anomalies, kinks.
2. Diseases that result in a decrease in the lumen of the artery: atherosclerosis, all kinds of arteritis (inflammation of the artery walls), thrombosis and embolism.
3. Compression of the artery from the outside: osteochondrosis of the cervical spine, abnormalities of bone structure, trauma, scoliosis (these are vertebrogenic, that is, associated with the spine, causes), as well as tumors of the neck tissue, their scar changes, spasm of the neck muscles (these are non-vertebrogenic causes).

Often, SPA occurs under the influence of several causative factors.

It is worth noting that RAS develops more often on the left, which is explained by the anatomical features of the left vertebral artery: it arises from the aortic arch, which often has atherosclerotic changes. The second leading cause, along with atherosclerosis, is degenerative diseases, that is, osteochondrosis. The bone canal in which the artery passes is quite narrow, and at the same time mobile. If there are osteophytes in the area of ​​the transverse vertebrae, they compress the vessel, disrupting blood flow to the brain.

In the presence of one or more of the above reasons, factors predisposing to the deterioration of the patient’s well-being and the appearance of complaints are sudden turns or tilts of the head.

Symptoms of vertebral artery syndrome

Patients with vertebral artery syndrome often experience dizziness and headaches.

The pathological process in SPA goes through 2 stages: functional disorders, or dystonic, and organic (ischemic).

Stage of functional impairment (dystonic)

The main symptom at this stage is headache: constant, aggravated by head movements or prolonged forced positions, burning, aching or throbbing in nature, covering the back of the head, temples and moving forward to the forehead.

Also at the dystonic stage, patients complain of dizziness of varying intensity: from a feeling of slight instability to a feeling of rapid rotation, tilting, and falling of one’s own body. In addition to dizziness, patients are often bothered by tinnitus and hearing impairment.

Various visual disturbances may also occur: sand, sparks, flashes, darkening of the eyes, and when examining the fundus, a decrease in the tone of its blood vessels.

If at the dystonic stage the causative factor is not eliminated for a long time, the disease progresses and the next, ischemic stage occurs.

Ischemic or organic stage

At this stage, the patient is diagnosed with transient disorders of cerebral circulation: transient ischemic attacks. They are sudden attacks of severe dizziness, impaired coordination of movements, nausea and vomiting, and speech disorders. As mentioned above, these symptoms are often provoked by a sharp turn or tilt of the head. If, with such symptoms, the patient takes a horizontal position, there is a high probability of their regression (disappearance). After an attack, the patient feels tired, weak, ringing in the ears, sparks or flashes before the eyes, and a headache.

Clinical variants of vertebral artery syndrome

These are:

• drop attacks (the patient suddenly falls, his head is thrown back, he cannot move or stand up during the attack; consciousness is not impaired; within a few minutes, motor function is restored; this condition occurs due to insufficient blood supply to the cerebellum and caudal parts of the brain stem);


• syncopal vertebral syndrome, or Unterharnsteidt syndrome (with a sharp turn or tilt of the head, as well as in the case of a prolonged stay in a forced position, the patient loses consciousness for a short time; the cause of this condition is ischemia of the region of the reticular formation of the brain);
• posterior cervical sympathetic syndrome, or Bare-Lieu syndrome (its main symptom is constant intense headaches of the “removing the helmet” type - localized in the occipital region and spreading to the anterior parts of the head; pain intensifies after sleeping on an uncomfortable pillow, when turning or tilting head; the nature of the pain is pulsating or shooting; may be accompanied by other symptoms characteristic of SPA);
• vestibulo-atactic syndrome (the main symptoms in this case are dizziness, a feeling of instability, imbalance, darkening of the eyes, nausea, vomiting, as well as disorders of the cardiovascular system (shortness of breath, pain in the heart and others);
• basilar migraine (the attack is preceded by visual disturbances in both eyes, dizziness, unsteadiness of gait, tinnitus and blurred speech, after which intense headache occurs in the back of the head, vomiting, and then the patient loses consciousness);


• ophthalmic syndrome (complaints from the organ of vision come to the fore: pain, a feeling of sand in the eyes, lacrimation, redness of the conjunctiva; the patient sees flashes and sparks before the eyes; visual acuity decreases, which is especially noticeable when there is strain on the eyes; fields partially or completely fall out vision);
• cochleo-vestibular syndrome (the patient complains of decreased hearing acuity (perception of whispered speech is especially difficult), tinnitus, a feeling of swaying, body instability or rotation of objects around the patient; the nature of the complaints changes - they directly depend on the position of the patient’s body);
• syndrome of autonomic disorders (the patient is concerned about the following symptoms: chills or a feeling of heat, sweating, constantly wet cold palms and feet, stabbing pain in the heart, headaches, and so on; often this syndrome does not occur on its own, but is combined with one or more others );
• transient ischemic attacks, or TIA (the patient notes periodically occurring transient sensory or motor disturbances, disturbances in the organ of vision and/or speech, unsteadiness and dizziness, nausea, vomiting, double vision, difficulty swallowing).

Diagnosis of vertebral artery syndrome

Based on the patient’s complaints, the doctor will determine the presence of one or more of the above syndromes and, depending on this, will prescribe additional research methods:

• X-ray of the cervical spine;
• magnetic resonance or computed tomography of the cervical spine;
• duplex scanning of the vertebral arteries;
• vertebral Dopplerography with functional loads (flexion/extension/rotation of the head).

If the diagnosis of SPA is confirmed during further examination, the specialist will prescribe appropriate treatment.

Treatment of vertebral artery syndrome

The effectiveness of treatment for this condition directly depends on the timeliness of its diagnosis: the earlier the diagnosis is made, the less thorny the path to recovery will be. Complex spa treatment should be carried out simultaneously in three directions:

• therapy for pathology of the cervical spine;
• restoration of the lumen of the vertebral artery;
• additional treatment methods.

First of all, the patient will be prescribed anti-inflammatory and decongestant drugs, namely non-steroidal anti-inflammatory drugs (meloxicam, nimesulide, celecoxib), angioprotectors (diosmin) and venotonics (troxerutin).

In order to improve blood flow through the vertebral artery, agapurine, vinpocetine, cinnarizine, nicergoline, instenon and other similar drugs are used.

To improve the metabolism (metabolism) of neurons, use citicoline, gliatilin, cerebrolysin, actovegin, mexidol and piracetam.

To improve metabolism not only in nerves, but also in other organs and tissues (vessels, muscles), the patient takes mildronate, trimetazidine or thiotriazoline.

In order to relax the spasmodic striated muscles, mydocalm or toldel will be used, vascular smooth muscles - drotaverine, better known to patients as No-shpa.

For migraine attacks, antimigraine drugs, such as sumatriptan, are used.

To improve the nutrition of nerve cells - B vitamins (Milgamma, Neurobion, Neurovitan and others).

To eliminate mechanical factors compressing the vertebral artery, the patient may be prescribed physical treatment (manual therapy, post-isometric muscle relaxation) or surgical intervention.

During the recovery period, neck massage, physical therapy, acupuncture, and sanatorium-resort treatment are widely used.

Prevention of vertebral artery syndrome

The main preventive measures in this case are an active lifestyle and healthy sleep on comfortable bedding (it is highly desirable that they be classified as orthopedic). If your work involves keeping your head and neck in one position for a long time (for example, working at a computer or activities associated with continuous writing), it is strongly recommended to take breaks from it, during which you perform gymnastics for the cervical spine. If the complaints mentioned above appear, you should not wait for their progression: the right decision would be to consult a doctor as soon as possible. Don't get sick!

Source: doctor-neurologist.ru

There are several ways to alleviate the condition of a patient with hypoplasia of the right vertebral artery:

1. Traditional drug treatment. It involves the use of medications that have a positive effect on blood composition, improve blood circulation in the cerebral vessels and accelerate metabolism. Medicines will not lead to a complete cure, but will help prevent critical deterioration of the condition. As a rule, the drugs prescribed are acetylsalicylic acid, Thiocytes, Ceraxon, Trental, Cinnarizine, Actovegin, Cerebrolysin, Vinpocetine, etc.
2. Surgical intervention. It is resorted to only in extreme cases, after unsuccessful attempts to improve cerebral circulation using conservative therapy. The operation is quite complex - it is an endovascular intervention and is performed by neurosurgeons.

Treatment of the disease does not lead to positive dynamics in all cases. However, in the absence of therapy, the prognosis looks much worse.

Medicines

Drug name	Directions for use and doses	Side effects	Special instructions
Cinnarizine	Prescribe 1 tablet three times a day.	Reactions such as drowsiness, dyspepsia, and allergies are possible.	Cinnarizine is best taken after meals to minimize irritation to the digestive tract.
Actovegin	Prescribe 1-2 tablets orally three times a day before meals.	Sweating, increased body temperature, and allergies may occur.	In severe cases, parenteral administration of the drug is used.
Cerebrolysin	Administered intramuscularly or intravenously, after dilution in sodium chloride solution or 5% glucose solution. Dosages are individual.	Rarely, with rapid administration, dizziness, headache, and tachycardia are observed.	The drug is not used to treat patients with allergic diathesis and renal failure.
	Prescribe 2-4 tablets up to three times a day, or intravenously in the form of a solution - according to indications.	Possible redness of the face, headache, irritability.	Trental is used with caution for stomach ulcers, heart failure, and also in the postoperative period.
Vinpocetine	Prescribe 1-2 tablets three times a day, for a long time.	Symptoms such as dizziness, nausea, redness of the upper body, tachycardia are possible.	In severe cases, Vinpocetine is administered intravenously.

Vitamins

To prevent complications, treatment must be supplemented with vitamins that are included in food products or in the form of pharmaceutical preparations. The following vitamins are considered the most suitable for hypoplasia:

• Retinol (A) – improves metabolism, prevents vascular damage by atherosclerosis. Contained in fish oil, dairy products, carrots, pumpkin, bell pepper.
• Ascorbic acid (C) – prevents the formation of cholesterol plaques, strengthens the heart and vascular walls. Contained in berries, fruits, citruses.
• Rutin (P) – makes the vascular wall strong. Contained in citrus fruits, berries, rose hips.
• Tocopherol (E) is an antioxidant, improves fat metabolism and prevents intoxication. Contained in vegetable oils, eggs, nuts.
• Pyridoxine (B 6) – removes excess cholesterol, stabilizes metabolic processes. Contained in fish, dairy products, brown rice, beans.

• Vitrum cardio;
• Doppel Hertz cardio system-3;
• Vitalarix Cardio;
• Cardio forte;
• Centrum cardio.

Physiotherapeutic treatment

For hypoplasia of the right vertebral artery, physiotherapy is not the primary therapeutic method. However, its use helps alleviate the patient’s condition and eliminate certain unpleasant signs of the disease.

The following physiotherapeutic effects are allowed:

• Exercise therapy – includes a set of exercises to restore blood circulation, walking.
• Mud therapy – normalizes the activity of the nervous and cardiovascular systems.
• Hydrotherapy, mineral waters, contrast shower.
• Fresh baths with warm water relax and calm the nervous system.
• Dry carbon dioxide bath - helps to dilate blood vessels and lower blood pressure.

Electric sleep, pine baths and other procedures improve well-being. The standard course of physiotherapy lasts 10 days.

Traditional treatment

Treatment with folk remedies, unfortunately, cannot completely cure the disease. But with the help of such recipes, you can improve the patient’s condition and prevent the development of exacerbations and complications. It is better if folk remedies are used against the background of traditional treatment prescribed by a doctor.

• Pour six full tablespoons of dried hawthorn berries and motherwort herbs into a thermos. Pour 1500 ml of boiling water and leave overnight. In the morning, filter the infusion and consume 100 ml up to 4 times a day.
• Squeeze the juice from ten lemons. We peel five heads of garlic and pass the cloves through a press. Mix all the ingredients with a liter of honey, place in a jar, cover with a lid and put in the refrigerator for one week. After seven days, the medicine can be consumed: 4 tsp. half an hour before dinner, gradually dissolving the mass in the mouth.
• We definitely include dried apricots in our diet: it is recommended to eat 100-150 g every day. This will improve the condition of the heart and blood vessels.
• Prepare a decoction of bean leaves in a ratio of 1:10. We drink it 100 ml three times a day 30 minutes before meals. The decoction improves heart function, relieves edema, prevents atherosclerosis, and normalizes blood pressure.
• We use natural honey 1 tbsp. l. three times a day. Honey can be diluted in warm water or poured over fruits.

Herbal treatment

• Such a well-known plant as dandelion perfectly stabilizes blood cholesterol levels. For example, dandelion rhizome powder is taken one third of a teaspoon three times a day, about half an hour before meals.

Fresh leaves are added to salads and soups: in addition to atherosclerotic effects, the leaves have antianemic and joint-protective activity.

• To prevent complications with hypoplasia, it is recommended to prepare tea from St. John's wort (20 g), fireweed (50 g), motherwort (15 g), and birch leaves (15 g). One tablespoon of the mixture is infused in 300 ml of boiling water for twenty minutes. Used instead of tea throughout the day.
• Elecampane tincture helps: 30 g of rhizome is poured with 300 ml of vodka and kept in the dark for 40 days. For treatment, take 35 drops of tincture in 100 ml of water 20 minutes before meals.

Homeopathy

Along with medications, homeopathic remedies, prescribed by a doctor in the appropriate field, are also successful. Homeopathy affects the body according to the principle of “treating like with like.” There are a number of drugs that have a positive effect on the vertebral arteries and blood vessels of the brain.

• Cholesterinum – lowers cholesterol levels, improves the condition of blood vessels in atherosclerosis.
• Gold iodine is effective against atherosclerosis of cerebral vessels.
• Conium - helps with stroke and post-stroke conditions.
• Crategus – improves cerebral circulation.

In case of circulatory insufficiency, complex homeopathic preparations can be used:

• Traumeel in the form of tablets and ointments;
• Goal T - in the form of tablets and ointments;
• Discus compositum in the form of intramuscular injections.

The dosage of drugs is selected individually. There are practically no side effects: only occasionally does an allergic reaction to a particular drug occur - in isolated cases.

Surgical treatment

The essence of the operation for hypoplasia of the right vertebral artery is the restoration of normal blood flow in it, which at the same time serves as the prevention of severe and life-threatening consequences.

Previously, to improve the patient's condition, surgical extra-intracranial anastomosis was performed. But such an operation was subsequently recognized as ineffective and lost its relevance.

In order to qualitatively restore blood flow, the following surgical methods are currently used:

1. Stenting is the insertion of a special “insert” into a narrowed area of ​​a vessel to prevent further narrowing. Stents can be a mini-structure like a frame, which is often additionally impregnated with medicinal solutions to prevent thrombosis and the formation of scarring in the vessel.
2. Angioplasty is the restoration of the artery to its original shape. During the operation, a mechanical force is applied to the narrowed area (usually balloon dilatation of the vessel), which allows the previous lumen diameter to be restored.
3. A reconstructive operation is the removal of a narrowed section of a vessel with its further prosthetics. A part of the patient’s own vein, which is taken from other areas, is usually used as a prosthesis. Such an operation is performed only in the most severe cases.

Often, stenting and angioplasty are performed in combination with each other.

After surgery, patients are prescribed blood-thinning therapy and special exercises to normalize general circulation. Moderate physical activity after surgery can prevent the formation of blood clots. However, the loads should be moderate: intense exercise and heavy lifting are contraindicated during this period.

Source: ilive.com.ua

What reasons need to be dealt with?

A feature of the anatomy of the vertebral arteries is their varying degrees of risk during the process of compression (narrowing). Before ascending to the cervical spine, the left artery arises directly from the aorta, and the right artery arises directly from the subclavian artery. Therefore, the left side is more susceptible to stenosis of atherosclerotic origin. In addition, an anomaly in the structure of the first rib (additional cervical rib) often develops here.

One of the main influencing factors is a change in the bone structure of the canal formed by the transverse processes of the thoracic and cervical vertebrae. The patency of the canal is impaired when:

• degenerative-dystrophic changes associated with cervical osteochondrosis;
• intervertebral hernia;
• proliferation of osteophytes in spondylosis;
• inflammation of facet (joints between vertebrae) joints;
• vertebral injuries.

These causes are classified as vertebrogenic, associated with the spine. But there are also non-vertebral factors that should be taken into account in treatment. These include:

• atherosclerosis of one or both vertebral arteries;
• abnormal narrowing or tortuosity (congenital hypoplasia);
• increased influence of sympathetic innervation, causing spastic contractions of the vessel walls with a temporary decrease in blood flow.

How does ICD-10 differentiate syndromes by cause?

In ICD-10, compression of the vertebral artery is taken into account along with the anterior spinal artery and is included in 2 classes of diseases:

• diseases of the musculoskeletal system with code M47.0;
• lesions of the nervous system with code G99.2.

Accurate diagnosis, taking into account the development of anastomoses and anastomoses with other cervical arteries, allows you to choose treatment that is as close as possible to the source of the disease.

Main directions of treatment

Before treating vertebral artery syndrome, the patient must undergo a comprehensive examination to diagnose the type of vascular compression. The doctor receives essential information after:

• Ultrasound of head and neck vessels;
• magnetic resonance imaging;
• angiography of vertebral and other cerebral vessels.

The methods allow you to accurately determine the degree of narrowing of the arteries. If normally the diameter should be from 3.6 to 3.9 mm, then with pathology its sharp decrease is detected. Localization of the narrow area is important for the likely surgical approach.

Main treatment options:

• long-term use of medications that improve blood flow;
• course physiotherapy;
• using the possibilities of physical therapy and a special set of exercises;
• surgical intervention according to indications.

Drug therapy

In the treatment of vertebral artery syndrome, a complex of drugs is used that affect the patency of the artery and extravasal pathology.

The most important medications are non-steroidal anti-inflammatory drugs. They cause anti-inflammatory, analgesic effects by inhibiting the migration of neutrophils to the site of inflammation, in addition, they reduce the ability of platelets to stick together and form blood clots. From the entire group, drugs are selected that are least toxic to the patient’s stomach and intestines. These include:

• Nimesulide,
• Meloxicam,
• Celecoxib,
• Aceclofenac (Aertal).

Airtal is a new drug in this series, its toxicity is 2 times less than Diclofenac.

Muscle relaxants - centrally acting drugs are used, they relieve increased tone, muscle cramps, and reduce pain. Applicable:

• Tolperisone,
• Baclofen,
• Mydocalm.

Of these drugs, Mydocalm has the greatest analgesic effect. By reducing muscle spasm, it simultaneously activates blood circulation.

For acute symptoms, drugs are prescribed intramuscularly.

Vasodilators or vasoactive drugs such as Cavinton, Trental, Instenon can improve microcirculation in ischemic neurons of the brain. They act at the level of metabolic activation and provide energy to cells by accumulating ATP. At the same time, vascular tone and the ability of the brain to regulate its own blood circulation are restored.

Medicines to activate metabolism in brain cells:

• Glycine,
• Piracetam,
• Actovegin,
• Cerebrolysin,
• Semax.

They eliminate tissue hypoxia and have antioxidant properties. Treatment courses are carried out for 3 months twice a year. If necessary, synthetic antioxidants are prescribed: vitamins A, E, C, drugs Ionol, Phenosan.

Symptomatic remedies - according to indications, sedatives and antidepressants are used. For dizziness, Betaserc is prescribed. It is not recommended for long-term use.

Physiotherapeutic methods

In the acute phase of the disease, physiotherapy helps block pain impulses along sympathetic nerve fibers. For this we use:

• diadynamic current for 5 minutes;
• ultrasound in pulsed mode;
• phonophoresis with solutions of Analgin, Anestezin;
• electrophoresis with ganglion blockers;
• d'Arsonval's currents on the head.

In the subacute stage, you can use electrophoresis with iodine, Novocaine, Euphyllin, Papaverine.

Reliable physiotherapeutic methods include: acupuncture, galvanization of the collar area. An individual mode of pulsed currents and ultrasound is also selected.

Manual therapy and massage can only be entrusted to a trained specialist.

Surgical treatment

Surgery is prescribed for patients with ineffective conservative treatment and identified narrowing of the lumen of the vertebral artery to 2 mm or more.

In specialized departments of vertebrology and neurosurgery, surgical interventions are currently performed using endoscopic techniques. In this case, the skin incision is up to 2 cm, eliminating the risk of damage to vital organs. The technique comes down to two options:

• excision of the site of narrowing and plasticity of the vessel;
• insertion of a balloon with a stent;
• in cases of detection of a tumor or hernia, the operation should eliminate the compressive effect on the arteries as much as possible.

The effectiveness of the surgical method is up to 90%. In patients, symptoms of insufficient blood supply to the brain completely disappear.

If the narrowing of the vertebral artery is associated with osteochondrosis, then neurologists recommend wearing a Shants collar for 2.5 hours a day.

Only a semi-rigid mattress or a shield is suitable for sleeping. You should purchase a pillow at an orthopedic supply store or make your own low, hard, flat cushion. It should prevent bending in the cervical spine.

To relieve pain, you can use wool scarves, rubbing with bee and snake venom.

A home remedy - a roller massager - is convenient to use while sitting in front of the TV.

As an antioxidant therapy, patients are recommended to include fresh berries, fruit juices, prunes, sea buckthorn, cranberries, currants, chokeberries, nuts, and beans in their diet.

Therapeutic gymnastics

The areas of the hands have a reflex effect on the vessels of the neck. Therefore, the following light exercises are recommended:

• clenching your fingers into a fist and sharply spreading them out;
• circular movements in both directions in the wrist joint;
• finger massage.

To relieve heaviness and “pinching” in the neck area, any flexion and rotation movements of the arms are suitable:

• lifting and lowering;
• "mill";
• training biceps with light weight;
• “shrug” of the shoulders with lifting and lowering up and down.

While lying in bed, you can try to tense your muscles and rest the back of your head and heels on the surface of the bed. Or do this exercise while standing against a wall. While sitting, you can slowly tilt your head to the sides, back and forth.

If any symptoms of vertebral artery syndrome appear, you should undergo an examination. If it is possible to obtain good results from the use of medications, then the person lives and forgets about previously suffered ischemic manifestations.

Source: icvtormet.ru

Definition. Cerebral hyperperfusion syndrome (CHS or hyperperfusion syndrome) is a complication of revascularization interventions on the carotid arteries, manifested in the carotid region on the ipsilateral side by a significant increase in cerebral cerebral blood flow (CMB) with the development of persistent clinical and morphological signs of cerebral damage associated with impaired vascular autoregulation.

A significant increase in CMB is defined as an increase of 2 times or more compared to the initial level (usually hyperperfusion is defined as an increase in CMB by 100% or more relative to the preoperative value). However, clinical signs of SCPH may also be present in patients with a moderate increase in CMB, that is, 30 - 50% higher than the initial one (in many patients with developed intracerebral hemorrhage, an intraoperative study with 133Xe and a magnetic resonance study with contrast revealed an increase in CMB only by 20 - 44%).

Revascularization interventions on the carotid arteries that can lead to the development of SCGP are: carotid endarterectomy (CAE), stenting of the carotid (CA) and subclavian arteries, endovascular embolectomy, blood vessel replacement (which involves the cerebral circulation), angioplasty of the carotid and vertebral arteries, extra -intracranial shunting.

Due to the lack of uniform, clearly formulated diagnostic criteria for SCGP and due to different understanding by researchers of the boundary between the presence of signs of hyperperfusion (reperfusion) and the formation of SCGP, data on the prevalence of SCGP varies significantly: according to different authors, from 0.4 to 14% of cases of surgical interventions on carotid arteries.

Pathogenesis. The most important pathophysiological factor of SCGP is considered to be a violation of the autoregulation of cerebral hemodynamics due to long-term ischemia against the background of severe stenosis of the carotid arteries. In conditions of initially impaired autoregulation, a significant increase in arterial inflow, which occurred against the background of dilatation of the microvascular bed, is no longer accompanied by an adequate response necessary for the regulation of cerebral blood flow—spasm at the level of arterioles. As a result, a zone of hyperemia is formed, which is the pathophysiological basis of hyperperfusion syndrome (CHPS).

The first peak of the increase in CMB occurs during surgery, immediately after restoration of blood flow through the internal carotid artery. This phase is short-lived and, as a rule, by the end of the operation there is a slight decrease in the CMB. It should be noted that this stabilization occurs under conditions of anesthetic protection and accompanying hemodynamic monitoring. The second peak of the increase in CMB develops in the postoperative period from the first day and lasts up to two weeks. In patients with cerebral hyperperfusion, CMB usually reaches its maximum 3 to 4 days after surgery and decreases to its original state on the 7th day. However, the period of stabilization of autoregulation may take 6 weeks.

Arterial hypertension (AH) plays an important role in the development of SCGP. It undoubtedly increases cerebral blood flow and disrupts the autoregulatory mechanism, leading to hyperperfusion. The role of hypertension as a trigger for the development of hemorrhage has not been proven, but is present in almost all “symptomatic” patients in the postoperative period. Preoperative hypertension is the single most important determinant of the development of postoperative hypertension (including due to baroreceptor dysfunction). The presence of hypertension in the postoperative period is considered by many authors as the main factor in the development of severe, including lethal, forms of SCGP. Blood pressure instability is observed in 2/3 of patients during the first 24 hours after CE surgery. Postoperative hypertension (defined as systolic blood pressure >200 mmHg or diastolic blood pressure >100 mmHg) is reported in approximately 19–35% of patients following CE surgery.

Urgent CEA, that is, a short period of time between ischemic symptoms and endarterectomy, has also been identified as a potential risk factor for SCGP. Some scientists believe that a significant risk factor for the development of SCGP is severe bilateral damage to the carotid arteries, both alone and in combination with hypertension and a history of adverse vascular events (transient ischemic attacks). It has been suggested that age over 72 years is a predictor of SCGP. Of great interest are the data of Russian authors on the relationship between venous blood flow and the development of cerebral hyperperfusion. It is suggested that in patients with an initially existing difficulty in venous outflow, venous congestion, arteriovenous relationships are disrupted and their imbalance develops, which leads to impaired perfusion of the organ, including the brain.

Clinic. The time period for the development of clinical manifestations of SCGP (see below) in most cases ranges from 1 to 8 days (mostly within 5 days), but symptoms can develop as early as the 1st day after revascularization. Delayed development of SCGP is considered quite rare - more than 1 week after the intervention. There is evidence of the development of SCGP 3 weeks after SSA (and even a month later). Therefore, some researchers extend the period of postoperative observation of patients to 30 days. A rare clinical case of repeated occurrence of HPS in a patient after restentation is described, and the second episode of HPS was significantly more severe, ending in bleeding into the basal ganglia and death.

In the classical sense, from a clinical point of view, SCGP is understood as the development of a symptom complex, including a triad of clinical (neurological) manifestations: headache, often unilateral, with nausea and vomiting (signs of intracerebral hypertension and cerebral edema), convulsive syndrome, as well as focal neurological symptoms (in the absence of cerebral ischemia or the development of cerebral circulatory disorders of the hemorrhagic type). These manifestations in most patients are accompanied by the development of systemic hypertension.

Three subtypes of cephalgia have been described after both CEA and SSA. Most often, in the first days after surgery, diffuse minor limited pain of a benign nature is noted, which soon goes away on its own. The second subtype is unilateral cluster-like pain, occurring with a frequency of 1 - 2 times a day in the form of attacks lasting 2 - 3 hours; usually goes away within 2 weeks. The third subtype of headache (typical of SCGP and caused by pronounced congestion of the cerebral vessels on the side of the operation) is characterized by high intensity, pulsation, localization on the side ipsilateral to the intervention, a feeling of pressure and pain in the corresponding eyeball (these signs determine the migraine-like nature of the headache), and also the lack of effect from conventional analgesic therapy. Headache is often the first symptom of hyperperfusion and is regarded by many authors as the initial sign of SCGP. The occurrence of headache is associated with arterial congestion on the affected side, and in the presence of only this symptom, SCGP is quite easily relieved.

The occurrence of a convulsive syndrome, initially local, followed by generalization, is a more serious clinical manifestation of SCGP. Epileptiform seizures most often develop within 24 hours after the intervention. Some authors associate this fact with a possible pathogenetic mechanism for the formation of electrical activity in the brain as a result of disruption of the blood-brain barrier and extravasation of albumin. This mechanism is still being studied. Some authors consider the development of generalized seizures to be a predictor of severe forms of SCGP (i.e., the development of severe neurological complications) and recommend intensive therapy for such patients. Changes in the electroencephalogram in the form of focal symptoms have diagnostic value, but do not always appear and do not appear immediately. Moreover, after relief of the convulsive syndrome, there is a tendency to decrease the bioelectrical activity of the brain. Many authors insist on the importance of dynamic EEG in such patients.

Local neurological deficits (usually cortical) resulting from SCGP may manifest in a variety of ways. More often this is weakness, motor disturbances in the limbs - hemiplegia (but usually weakness develops in the upper limbs, depending on the side of the lesion). Aphasia and hemianopsia develop less frequently. A case of SCGP with clinical manifestations in the form of neurological deficit (hemianopia, confusion) as a result of hemorrhage in the vertebrobasilar region (against the background of hypertension) after stenting of the subclavian artery is also described. Such variants of GPS are extremely rare.

Another early clinical sign of hyperperfusion is cognitive impairment, which may be associated with reversible swelling of brain tissue and may be a sign of SCGP in the absence of morphological changes in the brain. The incidence of cognitive impairment is quite high and reaches 45% in patients with asymptomatic hyperperfusion. However, structural changes are not always detected on MRI. It follows that cognitive impairment may indicate the development of hyperperfusion in the early stages. In some cases, the manifestation of SCGP can be mental disorders - psychoses, usually occurring along with headaches and cognitive impairment.

A rarer and one of the most severe clinical manifestations of SCGP is subarachnoid hemorrhage. Even less common in the literature is a description of cases of isolated subarachnoid hemorrhage in patients after revascularization interventions. Clinically, it manifests itself as a neurological deficit in the form of hemiplegia or hemiparesis, depression of sensory functions. Despite the low incidence of this complication, neuroimaging after CEA or SSA is recommended for its timely diagnosis. The incidence of the most serious clinical manifestation of SCGP - intracerebral hemorrhage after CEAE is 0.3 - 1.2%. It is characterized by the occurrence of general cerebral symptoms (impaired consciousness, depression of vital functions, decerebrate rigidity, etc.), and the progression of focal symptoms. With the development of cerebral edema and hemorrhage in the stem structures, death occurs. In some cases, hemorrhagic stroke ends in recovery. A predictor of death as a result of intracerebral hemorrhage is old age (over 75 years).

It is interesting that initially a fairly high incidence of strokes after CEA and SSA was associated exclusively with ischemic disorders and embolism. It was only in the late 1990s and early 2000s that it was established that a significant proportion of postoperative strokes are hemorrhagic in nature and occur as a result of hyperperfusion. In this case, the clinical picture is not clearly defined, which predetermines the importance of instrumental monitoring of SCGP.

Diagnostics. To date, there are no uniform standards for diagnosing and determining the risks of hyperperfusion. Transcranial Doppler sonography (TCD), single-photon emission computed tomography (SPECT), as well as perfusion modes of computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET) are most often used to diagnose SCGP. The easiest way to diagnose hyperperfusion in terms of efficiency, ease of use and economic feasibility is TCD, which determines the linear velocity of blood flow in the cerebral vessels. In addition, the TCD method is also applicable for predicting hyperperfusion. However, the results of such studies are quite contradictory. In recent years, information has begun to appear in the literature on the use of angiography to assess changes in intracerebral blood flow in patients during and after revascularization interventions on the carotid arteries. It is likely that angiographic determination of changes in blood flow after CE and SSA may be appropriate to identify the risk of hemorrhagic complications. Some authors argue that the use of cerebral angiography allows for more accurate detection of local hyperperfusion after revascularization compared with SPECT.

When discussing issues of timely assessment of the risk of developing SCGP, most authors agree that preoperative determination of vascular disorders, regardless of the technique used, is the optimal and even the only proven way to predict and prevent its severe forms. And yet, despite numerous attempts by researchers to predict and prevent the development of SCGP based on the identified initial vascular disorders, a clear identification of a high-risk group is still not possible. We can speak with confidence only about factors that increase risk to one degree or another, and about methods of compensating them. In general, this issue requires further study.

Prevention. In order to prevent SCHP, many researchers emphasize the role of maintaining optimal blood pressure in the pre-, intra- and postoperative periods (according to a number of researchers, at a level of 140/90 mm Hg, and in patients with risk factors for SCHP at a level of less than 120/80 mmHg). Other methods for preventing SCGP have been proposed. One such method is the use of an intraoperative small-diameter intraluminal shunt in patients with critical bilateral stenoses or contralateral occlusion of the internal carotid artery. Another way to prevent hyperperfusion in severe stenosis of the carotid arteries is the so-called “stepped” angioplasty, which consists of gradually, in several stages, increasing the lumen of the stenotic artery.

Treatment. The treatment of SCGP is based on therapeutic measures (including the use of antihypertensive, decongestant and anticonvulsant drugs) aimed at relieving clinical symptoms and preventing their progression. To relieve cephalgic syndrome, only opioid analgesics are recommended. [!] If hyperperfusion is detected, it is necessary to strictly control blood pressure. Further reduction of blood pressure should be carried out even in normotensive patients with hyperperfusion, since in some cases hypertension may be delayed. The prognosis for SCGP depends on the timeliness of diagnosis and the initiation of adequate therapy. With early detection and full treatment, in most situations, complete recovery is observed; in advanced cases, there is a high risk of death and (or) permanent disability.

Read more about SCGP in the following sources:

article “Cerebral hyperperfusion syndrome in patients with stenotic and occlusive lesions of the internal carotid arteries after surgical treatment. Literature review” A.V. Kokshin, A.M. Nemirovsky, V.I. Danilov; Children's Republican Clinical Hospital of the Ministry of Health of the Republic of Tatarstan, Kazan; Kazan State Medical University, Kazan; Interregional Clinical Diagnostic Center of the Ministry of Health of the Republic of Tatarstan, Kazan (magazine “Neurological Bulletin” No. 4, 2018) [read];

article “Cerebral hyperperfusion syndrome” by T.V. Strelkova, A.G. Hayroyan; FSBI Scientific Center for Cardiovascular Surgery named after. A.N. Bakulev" (director - academician of the Russian Academy of Sciences and Russian Academy of Medical Sciences L.A. Bockeria) Ministry of Health of Russia, Moscow (journal "Clinical Physiology of Circulation" No. 3, 2015) [read] or [read];

article “Surgical treatment of patients with bilateral lesions of the carotid arteries” Yu.V. Belov, R.N. Komarov, P.A. Karavaykin; First Moscow State Medical University named after. THEM. Sechenov, Moscow (magazine “Cardiology and Cardiovascular Surgery” No. 5, 2014) [read]

A) Terminology:

1. Abbreviations:
Cerebral hyperperfusion syndrome (CHPS)

2. Synonyms:
Hyperperfusion after carotid endarterectomy
Rich Perfusion

3. Definition:
A rare (1-3%) disorder, most often developing as a complication of revascularization of the cerebral arteries:
o Moderate CBF, often developing after carotid endarterectomy (CEA), and usually asymptomatic
o FHMS is defined as >100% increase in rCBF compared to preoperative values
Significant increase in ipsilateral cerebral blood flow (CBF) above normal metabolic demands:
o Usually develops after a carotid artery revascularization procedure
o May develop in association with other conditions (eg, status epilepticus, MELAS syndrome)

b) Visualization:

1. :
Best diagnostic criterion
o Ipsilateral swelling of the gyri, blurring of the sulci in patients after carotid endarterectomy
o CBF, CBV on perfusion MRI (pMRI), perfusion CT (pCT)
Dimensions:
o Variable
Morphology:
o Corresponds to the area of ​​blood supply to the vessels

2. Imaging Guidelines:
The best imaging tool about MRI with DWI, PWI
about SPECT
Study Protocol Tips:
o Add a T2* sequence (GRE or SWI) to the study to look for hemorrhage

3. CT scan for cerebral hyperperfusion syndrome (CHPS):
Non-contrast CT:
o Edema of the gyri
o Blurred crustal relief
o ± hypodensity (can be observed in the absence of changes in tissue density)
< 1 % случаев
CT with contrast:
o Increased contrast intensity of blood vessels
o In severe cases, contrast extravasation may be detected (rare)

(a) A 56-year-old man with >70% stenosis of the proximal cervical left ICA underwent carotid endarterectomy. Several hours after surgery, the patient experienced acute confusion and right-sided muscle weakness. Initial perfusion image: there is a noticeable increase in blood flow through the vessels of the left hemisphere.
(b) CT perfusion study performed in the same patient: the picture is relatively normal, but CBF values ​​in the left hemisphere region are increased compared to those on the right (ROIs designated 2a and 2b).

4. MRI for cerebral hyperperfusion syndrome (CHPS):
T1-VI:
o Cortical edema
o ± mild hypointensity
o Blurred furrows
T2-VI:
o Edema of the gyri, hyperintense signal
FLAIR:
o Hyperintense signal from the cortex
o Hyperintense inclusions in the subarachnoid spaces on post-contrast FLAIR are observed when the integrity of the BBB is violated
Т2* GRE:
o Obvious hemorrhage develops in< 1 % случаев
o Areas of “fading” in the GRE or SWI image
DVI:
o Changes are usually absent if the edema is vasogenic and not cytotoxic in nature
o In 25% of patients, on postoperative DWI, compared with preoperative ones, small foci of diffusion restriction are observed
PVI:
o Increased CBV, CBF
o Increase MTT:
- Deviation in both directions for three seconds is a predictor of FHMS
Post-contrast T1-weighted images:
o Pathological changes may be absent
o It is possible to detect a slight increase in the degree of contrast of cerebral vessels
o Contrasting brain parenchyma in severe cases
MR angiography:
o When detecting ↓ signal intensity from the MCA in patients during the preoperative period, it is possible to identify the risk of developing VHS

5. Other research methods:
SPECT:
o N-isopropyl-p-l-123-iododamphetamine or l-123-yomazenil SPECT study:
- Detection of hyperperfusion in the ipsilateral cerebral hemisphere after surgery
- Can be detected even in asymptomatic patients
- Possible correlation with neural damage in the long term, which is not detected on CT, MRI
- Possible connection with the development of crossed cerebellar diaschisis

V) Differential diagnosis:

1. Acute cerebral ischemia-infarction:
Prolongation of time to peak/average circulation time (no shortening)
As a rule, there is a restriction of diffusion on DWI (this often does not happen with BHMS)

2. Status epilepticus:
Metabolic hyperperfusion in affected brain tissue
A history of seizures is helpful in making the diagnosis, but information about them may not be obtained

3. Acute hypertensive encephalopathy, SES:
Autoregulation failure → hyperperfusion → endothelial damage/vasogenic edema
Characteristic development of changes in the area of ​​posterior circulation
Markedly elevated blood pressure (many causes):
o Eclampsia, preeclampsia
o Chemotherapy
o Kidney failure
o Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura
o Taking drugs (especially cocaine)

4. MELAS syndrome:
Acute defect in oxidative phosphorylation
Stroke-like episodes associated with the development of vasogenic edema, hyperperfusion, and neuronal damage
Hyperintense signal from the cortex, cortical contrast
Perform MR spectroscopy of the unaffected area, note the lactate peak

5. Hypercapnia:
Carbon dioxide is a powerful CBF stimulant
Vasodilator effect on cerebral vessels

G) Pathology. General characteristics of cerebral hyperperfusion syndrome (CHPS):
Etiology:
o Cognitive impairment after CEA/stenting may occur due to:
- Embolization of cerebral arteries during dissection, stenting
- Global cerebral hypoperfusion during carotid artery clamping
- Cerebral hyperperfusion syndrome
o FHH probably develops due to inadequate autoregulation, changes in cerebral hemodynamics:
- “A sharp jump in perfusion pressure”:
Chronic ischemia → autoregulation disorder
Loss of normal ability to vasoconstrict
“Resisting” vessels become chronically dilated
Rapid restoration of normal perfusion due to revascularization → hyperperfusion in previously non-perfused brain tissue

(a) After restoration of normal blood flow in the previously occluded MCA, the patient’s condition worsened in the form of increased right-sided muscle weakness and the appearance of a throbbing headache. MR perfusion, axial slice: increased (red-shaded area), rather than decreased, CBF in the left temporal and parietal lobes.
(b) MR perfusion, axial section: in the same patient, an increase in the volume of cerebral blood flow is detected.
(a) Cerebral hyperperfusion in status epilepticus developed in a 52-year-old woman with muscle weakness on the left side of the body after a prolonged seizure, shown on post-contrast fat-suppressed T1-weighted image. Note the higher contrast enhancement intensity of the vascular structures in the sulcal region of the right temporal lobe compared to that in the left hemisphere.
(b) Perfusion MRI: in the same patient, an increase in CBF in the region of the right temporal lobe is detected, corresponding to an increase in the intensity of contrast of the vascular structures detected on post-contrast T1-weighted images.

d) Clinical picture:

1. Manifestations of cerebral hyperperfusion syndrome (CHPS):
Classic triad: unilateral headache, neurological deficit and seizures
Other signs/symptoms:
o Variable cognitive impairment o Facial pain, eye pain

2. Demography:
Age:
o In postendarterectomy BHMS, the patient is usually elderly
o For other etiologies (eg, seizures, MELAS syndrome), the age can be any
Epidemiology:
o 3% of patients after carotid endarterectomy develop mild FHMS
o Covariation of clinical risk factors:
- Age
- Arterial hypertension (especially postoperative)
- Diabetes
- Bilateral lesions
- Degree of ICA stenosis:
High > low degree
- Presence of occlusion or high degree of stenosis of the contralateral carotid artery
- Duration of clamping
- Reduced carotid reserve
- Poor collateral blood flow
- Decreased cerebral vascular reactivity in response to acetalozamide

3. Course and prognosis:
Neurological emergency:
o In the absence of timely/adequate treatment, death or severe disability may occur
In the absence of intracranial hemorrhage:
o Changes are usually reversible
o There is no significant destruction of brain tissue
o Possible outcome of persistent mild cognitive impairment
1% of patients with FHH develop intracranial hemorrhage:
o Poor prognosis

V. Shishkova, Candidate of Medical Sciences
Center for Speech Pathology and Neurorehabilitation, Moscow

In women with menopausal syndrome that has developed against the background of manifestations of chronic cerebral ischemia, the use of phytoestrogens appears to be a safe alternative to traditional hormone replacement therapy. The use of Inoclim in women with cerebrovascular disease was evaluated in an open, prospective, placebo-controlled study.
Key words: climacteric syndrome, phytoestrogens, Inoclim, chronic cerebral ischemia.

PHYTOESTROGENS IN EARLY MANIFESTATIONS OF MENOPAUSAL SYNDROME IN WOMEN WITH CHRONIC BRAIN ISCHEMIA

V. Shishkova, Candidate of Medical Sciences
Center for Speech Pathology and Neurorehabilitation, Moscow

The use of phytoestrogens in women with menopausal syndrome developing in the presence of manifestations of chronic brain ischemia is a safe alternative to traditional hormone replacement therapy. The administration of Inoclim in women with cerebrovascular disease was assessed in an open-label placebo-controlled study.
Key words: menopausal syndrome, phytoestrogens, Inoclim, chronic brain ischemia.

According to the World Health Organization (WHO), the trend towards an increase in the number of people in the older age group will continue in the 21st century. It is expected that by 2015, about 46% of all women will be over 45 years of age. This explains the great interest in studying the changes occurring in a woman’s body during this period.

The duration of the active period of a woman’s life, regardless of her age and menopausal status, largely depends on lifestyle, nutrition, the presence and severity of concomitant somatic diseases, psychological well-being, as well as socio-economic living conditions. The highest average active life expectancy is observed among women in Japan (74.5 years) and the lowest in African countries (about 30 years); in Russia this figure currently exceeds 60 years.

Menopause is a natural transition to the non-reproductive period in a woman’s life, however, the somatic and psychological problems accumulated by this time, expressed in hormonal and metabolic changes, lead to the development of menopausal syndrome of varying severity in 48% of women.

Thus, by the time of menopause, most women, unfortunately, have concomitant somatic diseases that affect the psychological and intellectual spheres of health, as well as worsen the course of the menopause. The most common pathology is type 2 diabetes mellitus (T2DM), obesity, arterial hypertension (AH), coronary heart disease, atherosclerosis, atrial fibrillation and chronic cerebral ischemia (CHI), which also serve as a springboard for the development of ischemic stroke of the brain.

One of the first places among the causes of morbidity, mortality and disability throughout the world is occupied by vascular diseases of the brain, and, according to the results of epidemiological studies, their frequency is constantly increasing. The annual mortality rate from strokes in Russia is one of the highest in the world.

Morbidity and mortality rates from stroke among people of working age in Russia have increased over the past 10 years by more than 30%. Early 30-day mortality after stroke is 34.6%, and about 50% of patients die within 1 year. Stroke is the leading cause of disability in the population; 1/3 of patients who have suffered it require outside assistance, another 20% cannot walk independently, and only every 5th person can return to work. A stroke imposes special obligations on the patient’s family members, significantly reducing their work potential, and places a heavy socio-economic burden on society as a whole.

Menopausal syndrome acts as a risk factor for the development of cerebrovascular pathology, while the presence of long-term CCI, a precursor of stroke, significantly worsens the course of the menopausal period. For a practicing obstetrician-gynecologist, the meaning of many neurological terms is hidden under a layer of years that have passed since studying at the department of neurology during the institute years. However, the high prevalence of pathology of the central nervous system (CNS) in women in the peri- and postmenopausal periods and the obvious comorbidity of pathologies dictate, on the one hand, the need to fill the knowledge gap in this area of ​​medicine, and on the other hand, to learn how to effectively and safely correct menopausal disorders against the background diseases of the central nervous system, in particular such as CCI.

CHEM AND ITS CAUSES

CCI is a slowly progressive state of gradual decrease or change in normal brain activity, resulting from diffuse and (or) small-focal damage to brain tissue in conditions of long-term insufficiency of cerebral blood supply, regardless of age.

Doctors of different specialties who encounter such patients in their practice and deal with this problem often use different terms (not always CCI), implying this particular pathology. The term most often used is “dyscirculatory encephalopathy” or simply “encephalopathy” (despite the absence of such a term in the International Classification of Diseases, 10th revision - ICD-10), less often “chronic cerebral circulatory failure”, “slowly progressive cerebral circulatory failure”, “ ischemic brain disease”, “cerebrovascular insufficiency”, “cerebrovascular disease”, etc. .

As a rule, CCI does not reflect an isolated lesion of only the cerebral vessels. There are many other causes and diseases that lead to pathology of cerebral circulation. The development of CCI is promoted by a number of conditions that are commonly called risk factors. The latter are divided into correctable (they can be influenced by medication or other treatment) and non-correctable, i.e. unchangeable.

Uncorrectable risk factors include: old age, gender and hereditary predisposition. It is known, for example, that a stroke or CCI in parents increases the likelihood of developing vascular diseases in children. These factors cannot be influenced, but they help to identify in advance those at increased risk of developing cerebrovascular pathology and help prevent them from developing the disease early.

The main and main correctable factors in the development of CCI, and subsequently stroke, are atherosclerosis and hypertension. Diabetes, obesity, smoking, alcohol, insufficient physical activity, irrational and unbalanced nutrition are the reasons leading to additional progression of atherosclerosis in the vessels of the brain and deterioration of the patient’s condition. Identification of additional factors that significantly aggravate the course of CCI is necessary to develop the correct treatment tactics, taking into account all the causes and manifestations of the disease.

Currently, as a rule, clinically detected CCI is of mixed etiology, i.e. 1 patient has many factors – both correctable and non-correctable.

So, for the main reasons, atherosclerotic, hypertensive and mixed CCI are distinguished, although other, rarer causes are also possible (rheumatism, vasculitis of other etiologies, blood diseases, etc.).

MECHANISM OF CHEMICAL DEVELOPMENT

The universal mechanism for the development of CCI at any age is acute or chronic brain hypoperfusion, i.e. prolonged lack of supply by the brain of basic vital substances - oxygen and glucose, delivered by the bloodstream.

HOW DOES BRAIN HYPOPERFUSION DEVELOP?

A high level of blood flow is required for adequate brain function. The brain, which weighs only 2–2.5% of the total body weight, consumes up to 15–20% of the blood circulating in the body. The main indicator of the completeness of the blood supply to the brain is the level of blood flow per 100 g of brain matter per minute. The average cerebral blood flow (CBF) is approximately 50 ml/100 g/min, but there are significant differences in the blood supply to individual brain structures. For example, in gray matter, MK is 3–4 times higher than in white matter; There is also a relative physiological acceleration of blood flow in the frontal regions of the brain (the so-called frontal lobes). With age, the value of blood flow MK decreases, and the acceleration of blood flow in the anterior parts of the brain also disappears, which plays a certain triggering role in the development and increase of CCI.

Under resting conditions, the brain's oxygen consumption is 4 ml per 100 g/min, which corresponds to approximately 20% of the total oxygen entering the body. Glucose consumption is 30 µmol per 100 g/min - this is also the maximum requirement for the body as a whole.

Under conditions of intense work or stress (for example, while reading this article), the brain's needs for oxygen and glucose increase significantly compared to those at rest. Critical values ​​of cerebral blood flow have been established: when it decreases to 50%, reversible disorders of brain function are observed; with a persistent decrease in blood flow, MB also depends on perfusion pressure (PP) in the main arteries of the head (MAG) and the resistance of cerebral vessels. PP is the difference between arterial pressure (BP), which ensures the movement of blood, and venous pressure, which carries out its outflow. Normally, due to the mechanism of self-regulation, MB remains stable, despite fluctuations in systemic blood pressure from 60 to 160 mm Hg. Art. With the development of cerebral vascular damage, MBF is more dependent on the state of systemic hemodynamics, i.e. from changes and “jumps” in blood pressure, especially those not controlled by taking antihypertensive drugs.

DEVELOPMENT OF CHEM IN PATIENTS WITH AH

With long-term hypertension, there is a shift in the upper limit of systolic blood pressure, in which MBF still remains stable and self-regulation does not occur for quite a long time. Adequate brain perfusion is maintained by an increase in vascular resistance, which in turn leads to an increase in the load on the heart. It is assumed that an adequate level of sUA is possible until pronounced changes in small intracerebral vessels occur with the formation of a lacunar state (small cerebral infarction), characteristic of hypertension. Consequently, there is a certain amount of time (no one has measured how much) when timely treatment of hypertension can prevent the formation of irreversible changes in the vessels and brain or reduce their severity.

However, hypertensive crises that occur even in young women against the background of regularly taking antihypertensive therapy are always a breakdown of self-regulation with the development of acute hypertensive vascular damage, which each time aggravates the symptoms of CCI and makes the risk of developing the first stroke very high.

Thus, normal regulation of MB in conditions of developing pathology is possible (to certain limits) due to changes in cerebral vascular resistance, which, in turn, greatly affects the state of cardiac activity. The connections between brain and heart dysfunction are two-way. A decrease in cardiac output and impaired contractile function of the heart (for example, in conditions of heart failure) cause deterioration of MBF, contributing to the formation or worsening of the manifestations of CCI. On the other hand, hypoxia and cerebral ischemia lead to disruption of the central mechanisms of blood circulation regulation, which aggravates the course of cardiac pathology. Consequently, MK can suffer not only when the MAG is damaged, but also when there are disturbances in systemic hemodynamics, which in turn is determined by the state of the heart and all extracranial vessels.

In hypertension, it is primarily the perforating (intracerebral) arteries that supply the deep parts of the brain that are affected. With predominant damage to small-caliber arteries, a small local lesion (lacunar, “silent” stroke), diffuse damage to brain tissue (leukoaraiosis) or a combination of both develops. Gradually, the development of leukoaraiosis and (or) an increase in the number of lacunar strokes begin to dominate in the white matter, as a result of which the first clinical manifestations of a decrease in normal brain function arise - fatigue, memory loss, poor sleep, mood changes.

DEVELOPMENT OF CHEMISTRY IN ATHEROSCLEROSIS OF CEREBRAL VESSELS

A certain sequence of development of atherosclerotic vascular lesions in the human body is known: first, the process is localized in the aorta (the most important and largest human vessel leaving the heart), then in the coronary vessels of the heart (which supply blood to the heart itself), then or simultaneously with the coronary vessels - in the vessels brain and later - in the limbs.

With progressive systemic atherosclerosis, changes initially develop mainly in the main arteries and arteries of the surface of the brain. Atherosclerotic lesions of cerebral vessels are, as a rule, multiple, localized simultaneously in the external and internal parts of the carotid and vertebral arteries, as well as in the arteries that form the circle of Willis and its branches. As atherosclerosis progresses, the lumen of the artery gradually decreases or becomes completely blocked, and the brain stops receiving the oxygen and glucose it needs. Changes in large arteries lead to the formation of extensive territorial or “watershed” strokes of the brain (based on the localization of the trunk of a large artery that supplies blood to a large area of ​​the brain).

The atherosclerotic process in the vessels of the brain is characterized not only by local changes in the form of plaques, but also by hemodynamic restructuring of the arteries in the area localized before the narrowing of the vessel. The structure of the plaques is of great importance. So-called unstable plaques lead to the development of arterio-arterial thrombosis with pieces of this plaque and the occurrence of acute MV disorders, most often in the form of a transient ischemic attack. Hemorrhage into such a plaque is accompanied by a rapid increase in its volume with an increase in the degree of narrowing of the vessel and aggravation of signs of chronic insufficiency of MK - CIM.

Numerous studies have shown that hemodynamically significant stenosis (i.e., narrowing of the vessel, leading to a significant drop in the intensity of MV) develops when the lumen of the MAG is narrowed by 70–75%. But MV depends not only on the severity of stenosis, but also on the state of collateral circulation (i.e., the development and preservation of level 2 vessels - those that perforate the brain and supply blood to the deep parts of the brain), as well as on the ability of cerebral vessels to change their diameter (due to their inherent elasticity, which is lost during atherosclerosis).

These hemodynamic reserves of the brain allow asymptomatic stenoses to exist (i.e., without clinical manifestations of the disease with already developing damage to blood vessels and the brain). However, even with hemodynamically insignificant stenosis, chronic MV insufficiency and, as a consequence, CCI will inevitably develop.

With atherosclerotic lesions of the MAG, cerebral blood flow becomes very dependent on systemic hemodynamic processes (hypertension or hypotension). Such patients are especially sensitive to arterial hypotension (low blood pressure), which can lead to a drop in PP and an increase in ischemic disorders in the brain.

DEVELOPMENT OF CHEM IN PATIENTS WITH DM

In recent decades, diabetes has become epidemic in the population: by 2030, according to WHO experts, the number of patients with this pathology in the world is expected to increase to 552 million people, with >90% of them suffering from T2DM. According to data presented at the congress of the International Diabetes Federation, in Russia in 2011 the number of patients with diabetes reached 12.5 million, which is almost 10% of the country's population.

The high prevalence of diabetes is associated with high morbidity, disability and mortality. The main cause of mortality in patients with T2DM is vascular complications, including the prevailing cerebrovascular ones - acute cerebrovascular accidents (stroke) and CCI. Diabetes is the most important risk factor for the development of ischemic strokes and transient ischemic disorders in the brain, even at a young age in men and women. The relative risk of stroke increases with the development of diabetes by 1.8–6 times. The MRFIT study showed that the risk of death from stroke among patients with diabetes was 2.8 times higher than in patients without diabetes, death from ischemic stroke was 3.8 times higher, from subarachnoid hemorrhage was 1.1 times higher, and from intracerebral hemorrhage – 1.5 times.

Diabetes is a risk factor for the development of cerebrovascular accidents, regardless of the presence of other risk factors (increased blood pressure and cholesterol levels). The majority of patients with diabetes (72–75%) have an ischemic stroke, which is higher than among the general population). It was also noted that patients with diabetes have a worse recovery process after a stroke. CCI plays a major role in the development of stroke in diabetes. A significant role in the development of CCI in diabetes is played by the pathology of the MAG: the carotid and vertebral arteries, which in diabetes are quickly affected by atherosclerosis. It has been proven that diabetes and hyperglycemia without diabetes (prediabetes - impaired fasting glycemia and glucose tolerance) are independent risk factors for the development of systemic atherosclerosis with damage to vessels of various locations, including the brain.

In addition, DM is characterized by systemic damage to the microvasculature (microangiopathy), which is accompanied by the development of microcirculation disorders in the target organ, including the brain. Microangiopathy of cerebral vessels aggravates the metabolic disorders that develop with CCI and increases the risk of developing dementia, while there is a significant increase in the risk of Alzheimer's disease.

An additional problem in diabetes is compensation of blood sugar levels, which is associated with the risk of severe hypoglycemia (a decrease in blood glucose to a level below normal). It is known that the hypoglycemia index increases with a duration of diabetes >6 years, while in patients severe hypoglycemia is associated with a high risk of dementia, and its additional risk in the group of those examined without hypoglycemic episodes and with the presence of them was 2.39% per year. Numerous publications indicate that in diabetes, much earlier than in isolated hypertension or atherosclerosis, there is a decrease in the speed of psychomotor reactions, dysfunction of the frontal lobe, memory impairment, complex motor disorders, decreased attention and other clinical manifestations of CCI.

Thus, the severity of brain damage in diabetes is determined by the degree and duration of the decrease in sUA (due to atherosclerosis and (or) hypertension) and metabolic disorders in the brain.

Clinical manifestations of cerebrovascular pathology in diabetes are very diverse. Leukoaraiosis, which characterizes hypertensive and post-hypoglycemic brain lesions, can be asymptomatic or manifest as a combination of cognitive disorders progressing to dementia syndrome and various neurological disorders.

MANIFESTATIONS OF CHEMO IN PATIENTS

Clinical manifestations of CCI are not always detected by computed tomography (CT) and magnetic resonance imaging (MRI). Therefore, the diagnostic significance of neuroimaging methods cannot be overestimated. To make a correct diagnosis for a patient, the doctor needs an objective analysis of the clinical picture and instrumental examination data.

As the severity of the clinical picture increases, pathological changes in the vascular system of the brain intensify. The clinical picture of CCI in its progressive development is divided into 3 stages according to the severity of symptoms: initial manifestations, subcompensation and decompensation.

In stage I of the disease, patients may complain of headache and a feeling of heaviness in the head, general weakness, dizziness, noise and (or) ringing in the head or ears, deterioration of memory and attention, decreased mental performance, and sleep disturbances. As a rule, these symptoms occur during a period of significant emotional and mental stress, requiring a significant increase in MC. If 2 or more of these symptoms are often repeated or exist for a long time (at least the last 3 months) and there are no signs of another serious disease of the nervous system, a presumptive diagnosis of CCI is made.

At this stage, as a rule, the formation of distinct neurological syndromes has not yet occurred, and with adequate therapy, it is possible to reduce the severity or eliminate both individual symptoms and the disease as a whole. The advantage of identifying the disease at this stage is the patient’s almost complete recovery, since the processes in the brain tissue are still completely reversible.

At stage II of CCI, patients more often complain of more severe memory impairment, loss of ability to work, severe dizziness, instability when walking, and less often of manifestations of an asthenic symptom complex (general weakness, fatigue). At the same time, focal neurological symptoms become more distinct: revival of reflexes of oral automatism, central insufficiency of the facial and hypoglossal nerves, oculomotor disorders, pyramidal insufficiency. At this stage, a diagnosis of mild cognitive impairment is possible. Treatment is determined by the severity of existing symptoms of CCI progression.

In stage III of CCI, objective neurological disorders associated with serious brain damage, up to the development of psychoorganic syndrome and dementia, are more clearly identified. Paroxysmal conditions are more often observed: falls, fainting. In the stage of decompensation, cerebral circulation disorders are possible in the form of “small strokes” or transient MB disturbances (with reversible ischemic manifestations), the duration of focal disorders in which ranges from 24 hours to 2 weeks. Another manifestation of decompensation may be a progressive “complete stroke” and residual effects after it.

In CCI, there is a clear correlation between the severity of neurological symptoms and the age of the patients. Along with the progression of neurological symptoms, as the pathological process develops in the neurons of the brain, cognitive disorders increase. This applies not only to memory and intelligence, which are impaired in stage III to the level of dementia, but also to such functions as praxis and gnosis. Initial, essentially subclinical disorders of these functions are observed already in stage I, even in the middle age of the patient, then they intensify, change, and become distinct; Stages II and especially III of the disease are characterized by pronounced impairments of higher brain functions, which sharply reduces the quality of life and social adaptation of patients.

SELECTION OF OPTIMAL THERAPY FOR PATIENTS WITH CHEMISTRY

Treatment of a patient with CCI should be aimed at preventing further progression of the disease and include mandatory correction of hypertension, hyperlipidemia, control of blood sugar levels, treatment of all concomitant somatic diseases, and cerebroprotective therapy. Non-medicinal means also play a certain role: increasing physical activity, limiting the intake of table salt and alcohol, quitting smoking, and increasing the content of vegetables in the diet.

The frequency of detection of stages I and II of CCI in women in the peri- and postmenopausal period determines the need to use in gynecological practice drugs that are safe from the point of view of the risk of strokes and deterioration of cerebral circulation to relieve early vasomotor symptoms of menopausal syndrome, which worsen the course of CCI itself.

CLIMACTERIC PERIOD IN PATIENTS WITH CNS DISEASES AND THE PROBLEM OF CHOOSING THERAPY

It has been established that in menopausal women, the prevalence of cerebral vascular diseases - CCI of an atherosclerotic, hypertensive or mixed nature is about 43%. The severe course of the climacteric syndrome itself additionally leads to the early formation of late and severe forms of cerebrovascular pathology. Treatment of menopausal symptoms in the presence of cerebrovascular pathology - slowly and imperceptibly progressing CCI - is a complex problem.

An effective method for correcting the vegetative manifestations of menopausal syndrome is the prescription of hormone replacement therapy, however, in conditions of a woman already having cardiovascular disease or subclinical vascular atherosclerosis or CCI, this will be an absolute contraindication.

We conducted a comparative analysis of the course of premenopause and early postmenopause in women with CCI and without signs of cerebral vascular damage, and also assessed the effectiveness and safety of using the drug Inoclim (Laboratory Innotec International, France) in patients with CCI.

The prospective study included 2 groups of pre- and postmenopausal women: 1st (main) group (n=88) women aged 44 to 58 years (average age 51.39±3.50 years) with established CCI (in accordance with ICD-10); The 2nd (control) group (n=85) consisted of women without clinical signs of CCI (average age 52.4±3.30 years).

Exclusion criteria for this study were: duration of postmenopause >5 years; a history of surgical interventions on the pelvic organs with removal of the ovaries; oncological diseases at the time of the study and in the anamnesis; use of hormone replacement therapy (HRT) and other methods of treating menopausal syndrome at the time of the study and in history; use of combined oral contraception during the period of inclusion in the study and during the 10 years preceding this period, previous stroke, lack of independent movement.

All women were surveyed using a specially designed card, which included blocks of medical and social history, the presence of somatic and gynecological diseases, and a contraceptive history; The climacteric syndrome was assessed using the Kupperman menopausal index scale modified by E.V. Uvarova (1982), which is based on the definition of neurovegetative, metabolic-endocrine and psycho-emotional symptom complexes. Clinical and laboratory examination included assessment of somatic and neurological status; standard gynecological examination with a cytogram of the endo-exocervix and determination of the degree of purity of the vaginal secretion; transvaginal sonography of the pelvic organs. All women had their body mass index (BMI) assessed (WHO criteria, 1999); performed a breast examination and mammography; electrocardiography; according to indications - ultrasound of the thyroid gland; laboratory tests (blood glucose, coagulogram, lipid profile - total cholesterol, triglycerides, low and high density lipoproteins); neuroimaging methods (MRI and CT of the brain, ultrasound of cerebral vessels).

The average age at the onset of natural menopause was almost the same: in group 1 – 49.55±1.90 years, in group 2 – 49.13±1.48 (p>0.05). It was found that in women with CCI, the first manifestations of climacteric syndrome (neurovegetative) more often occurred in premenopause - in 52 (59%) and with the onset of menopause - in 31 (35%), and 1-2 years after menopause - only in 5 (6%), while in the 2nd group - in the premenopausal period - in 25 (29%), with the onset of menopause - in 8 (9%) and during early postmenopause - in 52 (61 %) (p The severity of clinical manifestations of climacteric syndrome was assessed using the International Menopausal Index (IMI); neurovegetative, metabolic-endocrine and psycho-emotional disorders were analyzed, assessing the number of points in each group of symptoms, as well as the frequency distribution of severity levels. The severity of neurovegetative and psycho-emotional manifestations (MMI indicators) was significantly higher in women with cerebral ischemia (see table).

Table.
Changes in MMI in those examined under the influence of treatment with Inoclim, points

Note.* - p

Thus, at the 1st stage of the study, it was found that in the presence of CCI in women, the first symptoms of menopausal syndrome usually appear in the premenopausal period and immediately with the onset of menopause (in contrast to women without CCI, in whom these manifestations occurred mainly during early postmenopausal). The clinical course of the syndrome was complicated by changes in the psycho-emotional background. The majority of women in group 1 showed asthenic disorders, more pronounced than in the control group. A high frequency of extragenital somatic pathology in women with CCI has been established - hypertension, dyslipidemia, hypertriglyceridemia, ischemic heart disease, etc., which are significant independent risk factors for the occurrence and progression of CCI.

At the 2nd stage of the study, the effectiveness and safety of using Inoclim (Laboratory Innotec International, France) was studied to relieve the main early symptoms of menopause in patients with CCI and without CNS pathology.

The basis of Inoklim is a standardized soybean extract with a high content of 2 important phytoestrogens - genistin and daidzein, recommended for use in menopausal syndrome. By now, most is known about the phytoestrogens contained in soy. These are, first of all, the isoflavones genistein and daidzein. Soy, soy products and dietary supplements based on soybeans have found wide use for the treatment of menopausal syndrome due to their high content of phytoestrogens, which have a unique selective effect on estrogen β-receptors, in contrast to endogenous estrogens and estrogens in composition of HRT, which affect both types of receptors (b and c) almost equally. According to a number of studies, soy isoflavones are not only more effective in eliminating hot flashes in menopausal women than placebo, but the effectiveness of soy isoflavones is comparable to that of using drugs for HRT. In addition to influencing the neurovegetative symptoms of menopause, soy isoflavones reduce the level of total cholesterol in the blood serum, help reduce the content of low and very low density lipoproteins and increase the level of high density lipoproteins, i.e. have an antiatherosclerotic effect. According to some data, soy isoflavones demonstrate an antithrombotic effect. In addition, it has been established that gynestein, which is one of the main soy isoflavones, has antioxidant activity and is able to inhibit the growth of tumor cells due to antiproliferative and antiangiogenic activity and has protective properties against breast cancer.

All patients of groups 1 and 2 were prescribed Inoclim 1 capsule (40 mg of soy isoflavones) 2 times a day for 3 months. During the observation period, there were no dropouts from the study, as well as cases of intolerance or refusal to use Inoclim. No side effects or allergic reactions have been reported. According to repeated transvaginal sonography of the pelvic organs in women, there was no effect of Inoclim on an increase in endometrial thickness. The effectiveness of therapy was assessed after 3 months according to the dynamics of the severity of the main components of the menopausal syndrome according to the Kupperman menopausal index scale as modified by E.V. Uvarova (see table).

As can be seen from the presented results, therapy with Inoclim at the studied dose in patients with manifestations of the atherosclerotic process in the central nervous system and a precursor of stroke - CCI, turned out to be very effective. There was a significant improvement in indicators in the block of neurovegetative and psychoemotional disorders, which influenced the severity of the manifestations of menopausal syndrome in this category of women, since in most patients the severity of disorders changed from severe to moderate and mild.

In the group of patients without CCI, neurovegetative and psychoemotional indicators also significantly improved, and the severity of menopausal disorders decreased during 3 months of therapy with Inoclim.

Thus, it should be emphasized that in the presence of CCI in women, the first neurovegetative and psycho-emotional symptoms of menopausal syndrome usually appear earlier than in women without CNS pathology, are detected already in the premenopausal period and immediately with the onset of menopause and are accompanied by more severe disorders. Consequently, in women with CCI who are at high risk of developing early severe manifestations of menopausal syndrome, on the one hand, and who have absolute contraindications to the prescription of traditional HRT, on the other, the use of phytoestrogens may be the only pathogenetic option for the treatment and prevention of menopausal disorders. The drug Inoclim at a dose of 2 capsules (80 mg of soy isoflavones) per day for 3 months demonstrated high efficacy and safety in patients with CCI, as well as in patients without central nervous system disorders.

Literature

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Syncope occurs for the following reasons.

Hypoperfusion of the brain:

• increased sensitivity of the autonomic nervous system to psycho-emotional stress (excitement, fear, panic attack, hysterical neurosis, etc.), as a result of which peripheral vascular resistance decreases and blood rushes down, forming an oxygen deficiency in the brain tissues;
• a decrease in cardiac output, which causes hemodynamic disturbances and, as a consequence, oxygen starvation and a lack of nutrients (organic damage to the myocardium, arrhythmias, stenosis of the aortic heart valve, etc.);
• orthostatic syncope - pathologically low blood pressure (hypotension) in a standing position (when the vessels of the lower extremities do not have time to adapt and narrow, thereby provoking the outflow of blood from the head, and consequently, cerebral hypoxia);
• atherosclerosis of large vessels (atherosclerotic plaques narrow the lumen of blood vessels, reducing hemodynamics and cardiac output);
• thrombosis (occurs as a result of occlusion, especially in the postoperative period);
• anaphylactic (allergic reaction to drugs) and infectious-toxic shock.

Metabolic disorders (hypoglycemia, hypoxia, anemia, etc.);

Disturbances in the transmission of impulses along the axons of the brain or the occurrence of pathological discharges in its neurons (epilepsy, ischemic and hemorrhagic strokes, etc.).

Loss of consciousness is also possible if you receive a head injury, such as a concussion.

As a rule, before an attack of syncope, the patient feels dizziness, nausea, weakness, sweating, and blurred vision.

As noted above, loss of consciousness is not an independent disease. It acts as a concomitant symptom of an ongoing pathological process in the body, the most dangerous of which for the patient’s life is cardiac dysfunction.

Additionally, syncope can occur while driving a vehicle or walking down stairs, which can result in serious injury or death to the patient. Therefore, it is very important to identify the cause that led to such an attack and begin appropriate treatment.

To diagnose the causes of the disease, the doctor collects the patient’s medical history and conducts a visual examination.

If metabolic disorders are suspected, they are referred for laboratory blood tests.

To exclude abnormalities in the functioning of the brain, MRI and duplex scanning of the head are recommended.

State Institution “Institute of Emergency and Reconstructive Surgery named after V.K. Gusak" NAMS of Ukraine, Donetsk

Intracranial pressure (IP) is the pressure in the cranial cavity (in the venous sinuses of the brain, cerebral ventricles, epidural and subarachnoid spaces), which is caused by the dynamic balance of volumetric cerebral blood flow, volumes of cerebrospinal fluid and brain tissue. Normal VD is a necessary condition for ensuring adequate blood supply to the brain, its metabolism and functional activity. VD is provided by complex mechanisms for regulating cerebral perfusion pressure, cerebral vascular tone, volumetric cerebral blood flow, the rate of production and resorption of cerebrospinal fluid, the permeability of the blood-brain barrier, colloid-osmotic homeostasis inside and outside the brain fluid and some other factors.

An important component of increasing VD is the venous component. An increase in VD is accompanied by compression of the bridging veins and expansion of the convexital subarachnoid spaces. The role of the basal veins in the outflow of blood from the brain increases significantly, which leads to an acceleration of blood flow in the deep veins of the brain, in particular in the veins of Rosenthal. An increase in VD, in turn, causes an increase in the pressure gradient at the interface between venous blood and cerebrospinal fluid with a probable slowdown in cerebrospinal fluid resorption. Aresorptive liquor hypertension develops, the diagnostic sign of which is echoscopic dilatation of the third ventricle of the brain.

Pharmacological correction of the tone of the venous wall with diosmin with hesperidin (DG) improves the outflow of venous blood from the cranial cavity and helps normalize cerebrospinal fluid pressure. The results of the study indicate the possibility of intervening in the mechanism of aresorptive liquor hypertension by improving venous outflow from the cranial cavity using venotonic drugs. V.V. Kupriyanov (1975) and M.I. Kholodenko (1963) established abundant innervation of the deep veins of the brain and the presence of a muscular layer in the veins of Rosenthal and the vein of Galen. Therefore, the use of venotonic is justified for influencing the neuromuscular apparatus of the deep veins of the brain, which can probably regulate the outflow of venous blood.

Cerebral hyperperfusion syndrome (CHS) is a combination of increased blood pressure with a clinical triad of symptoms (relating to the corresponding side of the body): migraine-like headache, seizures and transient neurological deficit in the absence of cerebral ischemia after successful carotid endarterectomy (CE). Much more often, “minor hyperperfusion syndrome” occurs, occurring in the form of a headache of varying intensity (unilateral cluster-like, occurring with a frequency of 1-2 times a day in the form of attacks lasting 2-3 hours, or unilateral throbbing pain of significant intensity).

In the available literature, we did not find any mention of venous regulation to prevent cerebral hyperperfusion syndrome in CE. As is known, an imbalance of cerebral venous circulation reduces the hemodynamic reserve of cerebral circulation, contributing to the development of chronic cerebral ischemia and the formation of structural pathology.

Purpose of the work

Study of the venous and liquor components of intracranial pressure in patients with benign intracranial hypertension syndrome during carotid endarterectomy, evaluation of a method for correcting intracranial pressure by pharmacological improvement of venous outflow for the prevention of cerebral hyperperfusion syndrome.

Materials and methods

Based on clinically and instrumentally confirmed syndrome of benign intracranial hypertension (ADHD), the study included 60 patients who were treated in the vascular department of the Institute of Emergency and Reconstructive Surgery named after. V.K. Gusak NAMS of Ukraine", aged from 40 to 65 (average age - 55 years).

All patients underwent a comprehensive clinical, instrumental and laboratory examination, as well as an orthopedic and neurological examination. Venous outflow from the cranial cavity was studied using sonography (sensors: linear with a frequency of 7 MHz for the extracranial region and vector with a frequency of 2.5 MHz for intracranial research). Two-dimensional and Doppler modes were used, which made it possible to assess morphological changes in the vessels and functional parameters of blood flow. The criterion for impaired venous outflow was hemodynamic parameters in the deep veins of the brain, in particular, in the veins of Rosenthal.

Cerebral hyperperfusion syndrome was manifested by: hemodynamic instability with severe hypertension in the postoperative period, cephalalgia resistant to therapy, the development of euphoria and inadequacy, psychosis and aggression, and epileptic seizures. Obvious clinical signs of SCGP were also observed in various combinations and with varying degrees of severity.

Pharmacological correction of venous tone in patients with signs of increased VD was carried out with bioflavonoids with venotonic and angioprotective activity - the combined drug DG "Normoven" (Kiev Vitamin Plant) at a dose of 500 mg 2 times a day with an interval of 12 hours for 14 days. This regimen of taking the drug ensured its stable concentration in the blood.

The patients were divided into two groups. The control group consisted of 30 patients operated on in the department of emergency and reconstructive vascular surgery, who did not take venotonic drugs in the preoperative period. Main group (30 patients) for 1 month. Before surgery, they received DH (provided for the study by the manufacturer) 1 tablet 2 times a day. The distribution of patients by gender and age was homogeneous in both groups. The degree of damage and previous neurological symptoms were approximately the same.

Considering that one of the most common symptoms of hyperperfusion in the postoperative period is headache, which remains the main memory of patients about the postoperative period, in order to objectify the data and assess the intensity of pain, we used a visual analogue scale (VAS). The intensity of headache was determined by the patients themselves using a 10-point system (weak pain - from 1 to 3 points, moderate - from 4 to 6 points, severe - from 7 to 10 points). We also used the Leda Questionnaire (LDQ), which reflects the dependence of patients on analgesics used to relieve headaches before therapy and one month after it. A short questionnaire (HIT-6) was used to assess the patient's general condition and quality of life: the higher the score, the greater the impact of headache on quality of life.

Statistical processing of the material was carried out using calculation formulas and methods of mathematical statistics. The arithmetic mean of the indicators (M), their standard deviation (σ), and standard error of the mean (m) were calculated. To assess the significance of differences, the t-test for two dependent samples was used. Differences were considered significant when t>2 (probability of error - p<0,05). Связь между показателями определяли при помощи коэффициента линейной корреляции Пирсона (r). Силу связи оценивали по величине коэффициента корреляции: сильная - при r - 0,7–0,99, средняя - при r - 0,3–0,69, слабая - при r - 0,01–0,29.

Results and discussion

According to the data obtained, an increase in VD with ultrasound signs of liquor-venous hypertension was accompanied by vegetative-vascular disorders in 36% of cases, cephalgic or vestibulocerebellar syndrome - in 23%. IN

In less than 5% of cases, increased VD was manifested by a progressive decrease in visual acuity, sensory hearing loss, attention deficit syndrome, hyperactivity, visual disturbances in the form of fog before the eyes, lethargy, and lack of initiative. At the same time, according to ultrasound, an increase in the maximum blood flow velocity in the basal veins of the brain (Rosenthal, Galen and straight sinus), as well as pseudopulsations in these vessels, which were assessed by the time-averaged mean maximum velocity, was recorded. TAMx). The increase in TAMx was accompanied by a pronounced or strong pulsation of the M-echo. Weak pulsation was regarded as normal.

Analysis of the data obtained indicated the presence of signs of increased VD due to the liquor and venous components. The interdependence of these processes was traced: a reliable direct strong relationship was established between the systolic velocity of venous blood flow (Vps) and the width of the M-echo (r=0.77; p<0,05), между диастолической скоростью венозного кровотока (Ved) и TAMx (r=0,76; р<0,01), а также прямая связь средней силы между Vps и TAMx (r=0,65; р<0,05). Наличие таких связей указывает на устойчивую взаимозависимость повышения ВД и ускорения кровотока в глубоких венах мозга.

The use of the drug "Normoven" contributed to a significant (p<0,01) снижению скорости венозного кровотока по венам Розенталя, что свидетельствовало об улучшении венозного оттока из полости черепа и снижении ВД (табл. 1).

Stabilization of venous blood flow in the brain correlated with statistically significant (r=0.77, p<0,05) уменьшением размеров III желудочка мозга. Нормализация ликворно-венозных показателей сопровождалась положительной динамикой состояния больных с регрессом большинства описанных клинических признаков.

In all patients, in the pre- and postoperative period, blood flow indicators in the venous bed of the “return vessels” receiving blood from the brain region (in particular, in the internal jugular vein) were examined. No significant differences were obtained (p = 0.05), however, there was a tendency for blood flow in the internal jugular vein to slow down, starting from the first hour after surgery, as SCGP developed.

The blood flow velocity during the development of SCGP in the internal jugular vein decreased by 14% in the main group and by 18% in the control group, although the differences in these values ​​with the control values ​​did not reach a statistically significant level (p>0.05). Venous blood flow in the ophthalmic veins in a horizontal position of patients with cerebral ischemia significantly increased by 11.9% (p<0,05) уже на начальных стадиях СЦГП, тогда как в глубоких венах мозга он существенно отличался от нормы (замедление) лишь при выраженных стадиях СЦГП (соответственно на 19,1 и 29,6%).

According to ultrasound examination, the patients had a vascular (venous) factor in the form of an increase in the maximum speed of blood flow in the basal veins of the brain (Rosenthal, Galen and straight sinus). There was pronounced pseudopulsation in these vessels, assessed by TAMx. The increase in TAMx was accompanied by a pronounced or strong pulsation of the M-echo. Stabilization of cerebral venous blood flow correlated with statistically significant (r=0.77, p<0,05) уменьшением размера III желудочка мозга.

A rapid normalization of venous-cerebrospinal fluid parameters was observed in the group of patients who, in addition to standard drug therapy, received DH, which was accompanied by positive dynamics in the condition of patients with regression of most of the mentioned clinical signs. A positive effect of DG on venous hemodynamics was noted in the form of normalization of blood flow through the basal vein of Rosenthal and in the straight sinus, the transition of retrograde blood flow to antegrade through the vein of Galen. During treatment, the number of patients with a distinct pulsation of the cerebral portion of the retinal vein increased (Table 2).

During the operation, retrograde pressure (RP) in the internal carotid artery was assessed, measured by the direct method. It averaged (51.1±17.9) mmHg. Art. Cerebral perfusion pressure (CPP) was determined using the formula: CPP=RAP - VP (jugular vein). It averaged (39.9±18.0) mmHg. Art. The critical indicator is 1/2 of system blood pressure. Consequently, the lower the VD, the higher the probability of performing the operation without the use of an internal shunt, which significantly simplifies the operation, reduces its duration and the risk of postoperative complications.

Positive dynamics were noted according to transcranial Dopplerography (TCD): linear systolic velocity in the carotid and vertebral arteries increased, hemodynamic asymmetries leveled out, and the pulsation index normalized.

Patients note a clinical effect in the postoperative period in the form of a reduction in headaches when taking DG for at least 7 days before surgery, although the best results were observed when taking the drug for a month before surgery (Table 3).

Conclusions

Improving venous outflow from the brain is an important hemodynamic reserve for improving the results of carotid endarterectomy.

The use of the drug "Normoven" helps to improve venous outflow from the cranial cavity by reducing the venous and liquor components in patients with benign intracranial hypertension syndrome when performing carotid endarterectomy.

It is advisable to include venotonics in the treatment of patients with cerebral hyperperfusion syndrome.

Unter Kodertum

The difference in volumetric abnormalities between PVI and DWI corresponds to the “ischemic penumbra.” With vertebral artery syndrome, hypoxia of part of the brain develops - vertebrobasilar insufficiency, which causes dizziness. A special case is dizziness with normal pressure, because then it is not clear where the pathological symptom came from and how to deal with it. Dizziness can also appear with a sharp decrease in blood pressure, even to normal levels in hypertensive patients.

To implement autoregulation of cerebral circulation, it is necessary to maintain certain values ​​of blood pressure (BP) in the main arteries of the head. Adequate brain perfusion is maintained by increasing vascular resistance, which in turn leads to an increase in the load on the heart. In addition to repeated acute disorders, the presence of chronic ischemia in the areas of terminal circulation is also assumed.

These hemodynamic reserves of the brain allow “asymptomatic” stenoses to exist without complaints or clinical manifestations. The structure of the plaques is also of great importance: the so-called. unstable plaques lead to the development of arterio-arterial embolisms and acute cerebrovascular accidents - often of a transient type.

Violations of memory, praxis and gnosis can be identified, as a rule, only when special tests are carried out. Professional and social adaptation of patients decreases. They often serve as the most important diagnostic criterion for CNM and are a sensitive marker for assessing the dynamics of the disease.

Dizziness with normal, high and low blood pressure

In this regard, the use of drugs that combine several mechanisms of action is justified. It contains an ergot derivative (dihydroergocryptine) and caffeine. Next, the asymmetry coefficient (AC) is assessed. This is a very important indicator by which it is possible to determine the difference in blood supply both within the studied pool and between the hemispheres.

Such an indicator, in particular, is the maximum speed of the rapid filling period (Vb), determined using a differential rheogram. In this case, the following conclusions are used: if MB is within normal limits, then it is noted that venous outflow is not obstructed. Thus, with a decrease in APR in all leads, they indicate cerebral hypoperfusion syndrome, which is most often caused by systolic myocardial dysfunction (insufficient pumping function).

We propose to evaluate the reactivity of cerebral vessels during the NG test as satisfactory and unsatisfactory, as well as its nature: “adequate” and “inadequate”. Vascular reactivity is regarded as “satisfactory” if there is a decrease in the tone of the arteries of distribution and resistance (in terms of speed indicators!). Postoperative period after carotid endarterectomy: Postoperative hypertension is observed in 20% of patients after CE, hypotension in approximately 10% of cases.

Transcranial Doppler ultrasound for monitoring MCAFV has a role in reducing the risk of hyperperfusion. If left untreated, such patients are at risk of developing cerebral edema, intracranial or subarachnoid hemorrhage, and death. Monitoring should include upper airway control, frequent blood pressure measurements, and neurological examination. All patients are screened for symptoms and asked to report any signs of hematoma enlargement.

It usually has a thromboembolic cause and is not fatal. Temporary bypass of the intervention site may reduce the risk of cerebral ischemia and injury from surgical arterial clamping, although the usefulness of this intervention remains controversial.

Study of pathomorphological and immunohistochemical brain damage in patients who died from severe forms of preeclampsia and eclampsia. Today, throughout the world, transplantation is a generally accepted method of treating irreversible diffuse and focal liver diseases. The main indications for performing this operation are cirrhosis of various etiologies, primary cholestatic diseases, inborn errors of metabolism and some types of tumors.

The review presents the point of view of many authors on the problem of cerebral hyperperfusion during operations on the structures of the brachiocephalic trunk, and substantiates its relevance.

In experiments on 43 cats, cardiac output, cerebral blood flow and the dynamics of neurovegetative indices were studied in the early post-resuscitation period. It has been established that the period of hyperperfusion is combined with a decrease in the values ​​of the Kerdo and Algover indices and an increase in the Robinson index. During the development of hypoperfusion syndrome, the values ​​of the Kerdo and Algover indices increase and the Robinson index is restored.

A close, direct connection has been established between the post-resuscitation dynamics of cerebral blood flow and cardiac output and its redistribution. One of the pressing problems of nephrology is improving the quality of life and overall survival of patients with chronic renal failure (CRF), the prevalence of which is steadily increasing in the world. Materials and methods: 20 patients with atherosclerotic lesions of the brachiocephalic arteries were examined and operated on.

One of these phenomena in the brain is the phenomenon of cerebral post-ischemic hyperperfusion (reactive hyperemia). Perinatal hypoxia can cause various changes in the organs and tissues of the fetus and newborn, including the myocardium. In the genesis of myocardial damage, diselectrolyte changes, hypoglycemia, and tissue acidosis, accompanied by oxygen deficiency and hypo- or hyperperfusion of the heart, play an important role.

The severity of the body's condition during acute massive blood loss is determined by circulatory disorders leading to tissue hyperperfusion, the development of hypoxia and metabolic disorders.

Duplex scanning of head and neck vessels

Among the mechanisms of progression of chronic kidney diseases, along with immunological ones, non-immune ones are widely discussed, including changes in intrarenal hemodynamics. This condition is as dangerous as it is unpleasant. Most often, dizziness occurs with fluctuations in blood pressure. If the pressure rises sharply, and accordingly, vasoconstriction occurs sharply, then cerebral ischemia and dizziness develop.

If this occurs, surgical clips (if present) must be immediately removed to decompress the neck, and the patient must be taken to the operating room. Dizziness is one of the most common complaints of patients when visiting a doctor, and this problem is observed in both older people and young patients. These are very difficult pathologies to treat, and in most cases require special surgical otolaryngological care.

Hyperperfusion and hypoperfusion of the brain

Cerebral hyperperfusion

A rare but dangerous complication is cerebral hyperperfusion. It occurs when, as a result of anatomical variations in the origin or accidental cannulation of the common carotid artery, a significant portion of the blood coming from the arterial cannula is sent directly to the brain.

The most serious consequence of this complication is a sharp increase in cerebral blood flow with the development of intracranial hypertension, edema and rupture of brain capillaries. In this case, the development of unilateral otorrhea, rhinorrhea, facial edema, petechiae, and conjunctival edema is possible.

If cerebral hyperperfusion is not detected in time and active therapy for intracranial hypertension is not started, then this complication can lead to death of the patient (Orkin F.K., 1985).

Cerebral hypoperfusion

A decrease in perfusion pressure to a level below the autoregulation threshold (about 50 mmHg) is associated with low cerebral blood flow. Hypoperfusion plays an important role not only in the development of fatal diffuse encephalopathy, which is based predominantly on necrotic processes in the brain, but also in the formation of various reduced forms of encephalopathy.

Clinically, it manifests itself from the development of mild postoperative disorders in the central and peripheral nervous systems in the form of behavioral changes, intellectual dysfunction, epileptic seizures, ophthalmological and other disorders, to global cerebral damage with a persistent vegetative state, neocortical brain death, total cerebral and brainstem death (Show P.J., 1993).

The definition of "acute ischemia" has been revised.

Previously, acute ischemia was considered only as a deterioration in the delivery of arterial blood to an organ while maintaining venous outflow from the organ.

Currently (Bilenko M.V., 1989), acute ischemia is understood as a sharp deterioration (incomplete ischemia) or complete cessation (complete, total ischemia) of all three main functions of local circulation:

1. delivery of oxygen to tissue,
2. delivery of oxidation substrates to tissue,
3. removal of tissue metabolic products from tissue.

Only a violation of all processes causes a severe symptom complex, leading to severe damage to the morphofunctional elements of the organ, the extreme degree of which is their death.

The state of cerebral hypoperfusion may also be associated with embolic processes.

Example. Patient U., 40 years old, was operated on for rheumatic disease (restenosis) of the mitral valve and a parietal thrombus in the left atrium. With technical difficulties, mitral valve replacement with a disc prosthesis and removal of a thrombus from the left atrium were performed. The operation lasted 6 hours (duration of ECC - 313 minutes, aortic cross-clamping - 122 minutes). After the operation, the patient is on mechanical ventilation. In the postoperative period, in addition to pronounced signs of total heart failure (BP - 70 - 90/40 - 60 mm Hg, tachycardia up to 140 per minute, ventricular extrasystoles), signs of post-ischemic encephalopathy developed (coma, periodic tonic-clonic convulsions) and oliguria. 4 hours after the operation, acute myocardial infarction of the posterolateral wall of the left ventricle of the heart was detected. 25 hours after the end of the operation, despite vasopressor and pacemaker therapy, hypotension occurred - up to 30/0 mmHg. Art. followed by cardiac arrest. Resuscitation measures with 5-fold defibrillation were not successful.

At autopsy: the brain weighs 1400 g, the gyri are flattened, the grooves are smoothed, at the base of the cerebellum there is a groove from a herniation into the foramen magnum. The cut brain tissue is moist. In the right hemisphere, in the area of ​​the subcortical nuclei, there is a cyst measuring 1 x 0.5 x 0.2 cm with serous contents. Bilateral hydrothorax (on the left - 450 ml, on the right - 400 ml) and ascites (400 ml), severe hypertrophy of all parts of the heart (heart weight 480 g, thickness of the myocardium of the wall of the left ventricle - 1.8 cm, right - 0.5 cm, ventricular index - 0.32), dilatation of the heart cavities and signs of diffuse myocardial cardiosclerosis. In the posterolateral wall of the left ventricle there is an acute extensive (4 x 2 x 2 cm) myocardial infarction with a hemorrhagic rim (about 1 day old). Histologically confirmed the presence of severe edema of the brain stem, venous and capillary congestion, ischemic (even necrotic) damage to neurons in the cerebral cortex. Physicochemically - pronounced hyperhydration of the myocardium of all parts of the heart, skeletal muscles, lungs, liver, thalamus and medulla oblongata. In the genesis of myocardial infarction in this patient, in addition to atherosclerotic lesions of the coronary arteries, long periods of surgical intervention as a whole and its individual stages were important.

Recommendations and opinions published on the site are for reference or popular information and are provided to a wide range of readers for discussion. The information provided does not replace qualified medical care based on medical history and diagnostic results. Be sure to consult your doctor.

Cerebral hyperperfusion syndrome

Neurology (6479)

Artem Nikolaev

Question: “Hello, I am constantly bothered by dizziness, darkening of the eyes, convulsions and numbness of the limbs.”

Answer: “Have you been examined in any way?”

Question: “This diagnosis was made on the basis of REG this summer”

Answer: “REG is a research method that is long outdated and extremely uninformative. It is impossible to give any conclusions based on it. A face-to-face consultation with a competent neurologist is recommended in order to prescribe an adequate examination.”

Question: “I signed up for an MRI of the brain and blood vessels in a week, but in general the condition is very similar to hypotension, the pressure was 110/60 yesterday and was very bad with weakness and failure and dizziness.”

Question: “Neurologists diagnose me with VSD and neurosis, the temperature often stays at 37-37.1, it was I who flew over the sea with a parachute in the summer, after that I’ll move on. the day all these nightmares began to this day, the tests are all normal"

Answer: “Do an MRI - maybe something will become clearer.”

Question: “Hello, MRI showed a decrease in blood flow in the sigmoid and transverse sinuses on the left. decreased blood flow through the left jugular vein. variant of the development of the circle of Willis - the circle is closed, there is a decrease in the signal from the blood flow in both posterior communicating arteries"

Answer: “Please rewrite the full text of the MRI, or better yet, scan the report and attach the file to the question.”

A special case is dizziness with normal pressure, because then it is not clear where the pathological symptom came from and how to deal with it. Dizziness can also appear with a sharp decrease in blood pressure, even to normal levels in hypertensive patients.

To implement autoregulation of cerebral circulation, it is necessary to maintain certain values ​​of blood pressure (BP) in the main arteries of the head. Adequate brain perfusion is maintained by increasing vascular resistance, which in turn leads to an increase in the load on the heart. In addition to repeated acute disorders, the presence of chronic ischemia in the areas of terminal circulation is also assumed.

These hemodynamic reserves of the brain allow “asymptomatic” stenoses to exist without complaints or clinical manifestations. The structure of the plaques is also of great importance: the so-called. unstable plaques lead to the development of arterio-arterial embolisms and acute cerebrovascular accidents - often of a transient type.

Violations of memory, praxis and gnosis can be identified, as a rule, only when special tests are carried out. Professional and social adaptation of patients decreases. They often serve as the most important diagnostic criterion for CNM and are a sensitive marker for assessing the dynamics of the disease.

Dizziness with normal, high and low blood pressure

In this regard, the use of drugs that combine several mechanisms of action is justified. It contains an ergot derivative (dihydroergocryptine) and caffeine. Next, the asymmetry coefficient (AC) is assessed. This is a very important indicator by which it is possible to determine the difference in blood supply both within the studied pool and between the hemispheres.

Such an indicator, in particular, is the maximum speed of the rapid filling period (Vb), determined using a differential rheogram. In this case, the following conclusions are used: if MB is within normal limits, then it is noted that venous outflow is not obstructed. Thus, with a decrease in APR in all leads, they indicate cerebral hypoperfusion syndrome, which is most often caused by systolic myocardial dysfunction (insufficient pumping function).

We propose to evaluate the reactivity of cerebral vessels during the NG test as satisfactory and unsatisfactory, as well as its nature: “adequate” and “inadequate”. Vascular reactivity is regarded as “satisfactory” if there is a decrease in the tone of the arteries of distribution and resistance (in terms of speed indicators!). Postoperative period after carotid endarterectomy: Postoperative hypertension is observed in 20% of patients after CE, hypotension in approximately 10% of cases.

Transcranial Doppler ultrasound for monitoring MCAFV has a role in reducing the risk of hyperperfusion. If left untreated, such patients are at risk of developing cerebral edema, intracranial or subarachnoid hemorrhage, and death. Monitoring should include upper airway control, frequent blood pressure measurements, and neurological examination. All patients are screened for symptoms and asked to report any signs of hematoma enlargement.

It usually has a thromboembolic cause and is not fatal. Temporary bypass of the intervention site may reduce the risk of cerebral ischemia and injury from surgical arterial clamping, although the usefulness of this intervention remains controversial.

Study of pathomorphological and immunohistochemical brain damage in patients who died from severe forms of preeclampsia and eclampsia. Today, throughout the world, transplantation is a generally accepted method of treating irreversible diffuse and focal liver diseases. The main indications for performing this operation are cirrhosis of various etiologies, primary cholestatic diseases, inborn errors of metabolism and some types of tumors.

The review presents the point of view of many authors on the problem of cerebral hyperperfusion during operations on the structures of the brachiocephalic trunk, and substantiates its relevance.

In experiments on 43 cats, cardiac output, cerebral blood flow and the dynamics of neurovegetative indices were studied in the early post-resuscitation period. It has been established that the period of hyperperfusion is combined with a decrease in the values ​​of the Kerdo and Algover indices and an increase in the Robinson index. During the development of hypoperfusion syndrome, the values ​​of the Kerdo and Algover indices increase and the Robinson index is restored.

A close, direct connection has been established between the post-resuscitation dynamics of cerebral blood flow and cardiac output and its redistribution. One of the pressing problems of nephrology is improving the quality of life and overall survival of patients with chronic renal failure (CRF), the prevalence of which is steadily increasing in the world. Materials and methods: 20 patients with atherosclerotic lesions of the brachiocephalic arteries were examined and operated on.

One of these phenomena in the brain is the phenomenon of cerebral post-ischemic hyperperfusion (reactive hyperemia). Perinatal hypoxia can cause various changes in the organs and tissues of the fetus and newborn, including the myocardium. In the genesis of myocardial damage, diselectrolyte changes, hypoglycemia, and tissue acidosis, accompanied by oxygen deficiency and hypo- or hyperperfusion of the heart, play an important role.

The severity of the body's condition during acute massive blood loss is determined by circulatory disorders leading to tissue hyperperfusion, the development of hypoxia and metabolic disorders.

Duplex scanning of head and neck vessels

Among the mechanisms of progression of chronic kidney diseases, along with immunological ones, non-immune ones are widely discussed, including changes in intrarenal hemodynamics. This condition is as dangerous as it is unpleasant. Most often, dizziness occurs with fluctuations in blood pressure. If the pressure rises sharply, and accordingly, vasoconstriction occurs sharply, then cerebral ischemia and dizziness develop.

If this occurs, surgical clips (if present) must be immediately removed to decompress the neck, and the patient must be taken to the operating room. Dizziness is one of the most common complaints of patients when visiting a doctor, and this problem is observed in both older people and young patients. These are very difficult pathologies to treat, and in most cases require special surgical otolaryngological care.

Hypoperfusion

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Hyperperfusion and hypoperfusion of the brain

Cerebral hyperperfusion

A rare but dangerous complication is cerebral hyperperfusion. It occurs when, as a result of anatomical variations in the origin or accidental cannulation of the common carotid artery, a significant portion of the blood coming from the arterial cannula is sent directly to the brain.

The most serious consequence of this complication is a sharp increase in cerebral blood flow with the development of intracranial hypertension, edema and rupture of brain capillaries. In this case, the development of unilateral otorrhea, rhinorrhea, facial edema, petechiae, and conjunctival edema is possible.

If cerebral hyperperfusion is not detected in time and active therapy for intracranial hypertension is not started, then this complication can lead to death of the patient (Orkin F.K., 1985).

Cerebral hypoperfusion

A decrease in perfusion pressure to a level below the autoregulation threshold (about 50 mmHg) is associated with low cerebral blood flow. Hypoperfusion plays an important role not only in the development of fatal diffuse encephalopathy, which is based predominantly on necrotic processes in the brain, but also in the formation of various reduced forms of encephalopathy.

Clinically, it manifests itself from the development of mild postoperative disorders in the central and peripheral nervous systems in the form of behavioral changes, intellectual dysfunction, epileptic seizures, ophthalmological and other disorders, to global cerebral damage with a persistent vegetative state, neocortical brain death, total cerebral and brainstem death (Show P.J., 1993).

The definition of "acute ischemia" has been revised.

Previously, acute ischemia was considered only as a deterioration in the delivery of arterial blood to an organ while maintaining venous outflow from the organ.

Currently (Bilenko M.V., 1989), acute ischemia is understood as a sharp deterioration (incomplete ischemia) or complete cessation (complete, total ischemia) of all three main functions of local circulation:

1. delivery of oxygen to tissue,
2. delivery of oxidation substrates to tissue,
3. removal of tissue metabolic products from tissue.

Only a violation of all processes causes a severe symptom complex, leading to severe damage to the morphofunctional elements of the organ, the extreme degree of which is their death.

The state of cerebral hypoperfusion may also be associated with embolic processes.

Example. Patient U., 40 years old, was operated on for rheumatic disease (restenosis) of the mitral valve and a parietal thrombus in the left atrium. With technical difficulties, mitral valve replacement with a disc prosthesis and removal of a thrombus from the left atrium were performed. The operation lasted 6 hours (duration of ECC - 313 minutes, aortic cross-clamping - 122 minutes). After the operation, the patient is on mechanical ventilation. In the postoperative period, in addition to pronounced signs of total heart failure (BP - 70 - 90/40 - 60 mm Hg, tachycardia up to 140 per minute, ventricular extrasystoles), signs of post-ischemic encephalopathy developed (coma, periodic tonic-clonic convulsions) and oliguria. 4 hours after the operation, acute myocardial infarction of the posterolateral wall of the left ventricle of the heart was detected. 25 hours after the end of the operation, despite vasopressor and pacemaker therapy, hypotension occurred - up to 30/0 mmHg. Art. followed by cardiac arrest. Resuscitation measures with 5-fold defibrillation were not successful.

At autopsy: the brain weighs 1400 g, the gyri are flattened, the grooves are smoothed, at the base of the cerebellum there is a groove from a herniation into the foramen magnum. The cut brain tissue is moist. In the right hemisphere, in the area of ​​the subcortical nuclei, there is a cyst measuring 1 x 0.5 x 0.2 cm with serous contents. Bilateral hydrothorax (on the left - 450 ml, on the right - 400 ml) and ascites (400 ml), severe hypertrophy of all parts of the heart (heart weight 480 g, thickness of the myocardium of the wall of the left ventricle - 1.8 cm, right - 0.5 cm, ventricular index - 0.32), dilatation of the heart cavities and signs of diffuse myocardial cardiosclerosis. In the posterolateral wall of the left ventricle there is an acute extensive (4 x 2 x 2 cm) myocardial infarction with a hemorrhagic rim (about 1 day old). Histologically confirmed the presence of severe edema of the brain stem, venous and capillary congestion, ischemic (even necrotic) damage to neurons in the cerebral cortex. Physicochemically - pronounced hyperhydration of the myocardium of all parts of the heart, skeletal muscles, lungs, liver, thalamus and medulla oblongata. In the genesis of myocardial infarction in this patient, in addition to atherosclerotic lesions of the coronary arteries, long periods of surgical intervention as a whole and its individual stages were important.

What is hypoperfusion of both hands?

Tone (Greek τόνος - tension) is a state of prolonged persistent excitation of nerve centers and muscle tissue, not accompanied by fatigue.

Tone is determined by the natural properties of the muscles and the influence of the nervous system. Thanks to tone, the maintenance of a certain posture and position of the body in space, pressure in the cavity of the digestive organs, bladder, uterus, as well as blood pressure are ensured.

Hypo - [Greek hypo – below, below, under] A prefix indicating a decrease against the norm, for example. , hypotension, hypoperfusion, hypotonicity.

Hyperfusion is

Interhemispheric fissure - dash. (I can’t understand why there is a dash, there must be some meaning?)

front horn - right - 3.3, left - 4.0

posterior horn - spr-11.2, sl-12.1

lateral horn - spr-dash, sl-dash.

Choroid plexus: sp-7.3, sl-8.1.

Monroe hole: spr-2.0, sl-2.1.

Third ventricle - 3.9.

Large tank - 5.9.

The structures of the brain are differentiated and symmetrical. The interhemispheric fissure and the cerebrospinal fluid space are not expanded.

The liquor pathways are passable.

Choroid plexuses: clear, even contours.

The pulsation of cerebral vessels was not visually changed.

In the studied fragments of brain structures there were no echo signs of damage or pathological inclusions.

PMA: Vps - 99.46 cm/s, RI - 0.63

V.Galena: V average. - 16.24 cm/s.

Conclusion: cerebral hyperfusion.

What can you say from the results of the study? Is the diagnosis correct? If yes, what is it?

Cavinton (1/4 once a day for a month) and magnesium B6 (1/4 2 times a day, for 3 weeks) were prescribed. Is the treatment prescribed correctly and is it necessary? The doctor did not give a clear answer as to what this diagnosis means.

Hyperfusion is

Ischemic damage to the brain parenchyma develops as a result of a persistent circulatory disorder, usually as a result of occlusion of arterial vessels supplying blood to the brain, or (less often) as a result of a violation of venous outflow, leading to stagnation of blood in the cerebral vessels in combination with a secondary disruption of the delivery of oxygen and nutrients substances to brain tissue.

The central nervous system has an extremely high energy requirement, which is satisfied only by the continuous delivery of metabolic substances to the brain tissue. Normally, the brain receives energy as a result of only one process - aerobic glycolysis. He is not able to accumulate energy that would allow him to survive a possible cessation of nutrition. A few seconds after the neurons stop receiving enough glucose and oxygen, their vital activity stops.

The amount of energy required to maintain the viability of brain cells (maintaining brain structure) varies significantly from the amount that the brain requires to function normally. The minimum level of blood flow required to preserve the structure of the brain is 5-8 ml/100 g/min (in the 1st hour of ischemia). For comparison, the minimum level of blood flow required to maintain function is 20 ml/100 g/min. It follows that functional failure may well develop without the death of brain tissue (infarction).

In the case of rapid restoration of blood flow, as occurs after thrombolysis - spontaneous or as a result of treatment - the brain tissue is not damaged, and its function is gradually restored to its previous level, that is, the neurological deficit completely regresses. A similar sequence of events can be observed in a transient ischemic attack (TIA), which from a clinical point of view appears as a transient neurological deficit lasting no more than 24 hours. In 80% of cases, the duration of TIA does not exceed 30 minutes. Clinical manifestations depend on which artery basin the circulatory disturbance occurred in.

Often transient ischemic attacks occur in the middle cerebral artery. The clinical picture is dominated by transient paresthesia and sensory disorders on the opposite side, as well as transient weakness in the limbs of the opposite side. Seizures of this kind are sometimes difficult to distinguish from focal epileptic seizures. Ischemia in the vertebrobasilar system is, accordingly, accompanied by transient symptoms of brainstem damage, including dizziness.

In some cases, subsidence of neurological disorders caused by ischemia is possible even if they persist for longer than 24 hours. In such cases, they do not talk about TIA, but about a stroke with a reversible neurological deficit (minor stroke).

Long-term hypoperfusion beyond the functional capacity of neurons leads to cell death. Ischemic stroke is an irreversible condition. Cell death, combined with the destruction of the blood-brain barrier, causes an influx of water into the area of ​​​​the affected brain tissue (the site of the infarction), which causes cerebral edema to develop. Swelling in the infarction area increases within several hours after the onset of ischemia, after a few days it reaches a maximum, and then gradually decreases.

When a large infarction is combined with extensive edema, clinical signs of life-threatening intracranial hypertension appear: headache, vomiting and impaired consciousness, which require timely detection and effective treatment. Depending on the age of the patient and the volume of the brain, the critical size of the infarct that causes the appearance of these clinical symptoms varies significantly. In young people with normal brain volume, the risk of their development increases when only one area of ​​the middle cerebral artery is involved. In elderly people with an atrophied brain, on the contrary, a life-threatening situation can arise only if a heart attack develops in the basin of two or more cerebral vessels.

Often, when such a threat arises, the patient’s life can be saved only by timely drug treatment aimed at reducing intracranial pressure, or by surgical intervention (hemicraniectomy), during which a large fragment of bone is resected from the cranial vault in order to reduce the compression of the swollen brain.

The brain tissue that has died after a heart attack is subsequently liquefied and resorbed, so that what is left in its place is a cyst filled with CSF and probably containing a small number of blood vessels and strands of connective tissue, which is combined with reactive gliotic changes (astrogliosis) in the surrounding brain parenchyma. A scar in the full sense of the word (with proliferation of connective tissue) is not formed.

The importance of collateral circulation. The dynamics of development and extent of edema in the brain parenchyma depend not only on the patency of the blood vessels that normally supply blood to the area of ​​the brain at risk of infarction, but also on the development of collateral blood flow in it. In general, cerebral arteries are terminal arteries in terms of their function because collateral vessels normally cannot provide sufficient blood flow to preserve brain tissue distal to the site of acute arterial occlusion. However, with a very slow and gradual narrowing of the lumen of the affected artery, the possibilities of collateral blood flow significantly expand.

Chronic moderate tissue hypoxia sometimes seems to “train” collateral vessels, as a result of which even a fairly long cessation of blood flow in the basin of a large arterial trunk can be replenished by collaterals that completely cover the energy needs of the brain tissue. In this case, the focus of the infarction and the number of dead neurons are significantly less than in the case of sudden occlusion of the same artery, if its lumen was not initially narrowed.

The source of collateral circulation can be the circle of Willis or superficial leptomeningeal anastomoses of the cerebral arteries. It has been noted that at the periphery of the infarction, collateral circulation is better developed than in its center. Ischemic brain tissue at the periphery of the infarction is called the infarction penumbra (ischemic penumbra zone), because the risk of cell death (infarction) in this zone remains high, but due to collateral blood flow, irreversible cell damage does not occur for the time being. Salvage of cells within this zone is the main goal of all therapeutic measures in the acute period of stroke, including thrombolytic therapy.

Loss of consciousness

Loss of consciousness (fainting) is not a separate nosological form. This is a symptom that is expressed in short-term transient attacks of impaired consciousness and its spontaneous recovery.

Syncope occurs for the following reasons.

Hypoperfusion of the brain:

• increased sensitivity of the autonomic nervous system to psycho-emotional stress (excitement, fear, panic attack, hysterical neurosis, etc.), as a result of which peripheral vascular resistance decreases and blood rushes down, forming an oxygen deficiency in the brain tissues;
• a decrease in cardiac output, which causes hemodynamic disturbances and, as a consequence, oxygen starvation and a lack of nutrients (organic damage to the myocardium, arrhythmias, stenosis of the aortic heart valve, etc.);
• orthostatic syncope - pathologically low blood pressure (hypotension) in a standing position (when the vessels of the lower extremities do not have time to adapt and narrow, thereby provoking the outflow of blood from the head, and consequently, cerebral hypoxia);
• atherosclerosis of large vessels (atherosclerotic plaques narrow the lumen of blood vessels, reducing hemodynamics and cardiac output);
• thrombosis (occurs as a result of occlusion, especially in the postoperative period);
• anaphylactic (allergic reaction to drugs) and infectious-toxic shock.

Metabolic disorders (hypoglycemia, hypoxia, anemia, etc.);

Disturbances in the transmission of impulses along the axons of the brain or the occurrence of pathological discharges in its neurons (epilepsy, ischemic and hemorrhagic strokes, etc.).

Loss of consciousness is also possible if you receive a head injury, such as a concussion.

As a rule, before an attack of syncope, the patient feels dizziness, nausea, weakness, sweating, and blurred vision.

As noted above, loss of consciousness is not an independent disease. It acts as a concomitant symptom of an ongoing pathological process in the body, the most dangerous of which for the patient’s life is cardiac dysfunction.

Additionally, syncope can occur while driving a vehicle or walking down stairs, which can result in serious injury or death to the patient. Therefore, it is very important to identify the cause that led to such an attack and begin appropriate treatment.

To diagnose the causes of the disease, the doctor collects the patient’s medical history and conducts a visual examination.

If metabolic disorders are suspected, they are referred for laboratory blood tests.

To exclude abnormalities in the functioning of the brain, MRI and duplex scanning of the head are recommended.

Chronic cerebrovascular accidents

"PHARMATEKA"; Current reviews; No. 15; 2010; pp. 46-50.

Department of Pathology of the Autonomic Nervous System, Research Center of the First Moscow State Medical University named after. THEM. Sechenov, Moscow

Chronic cerebrovascular accidents (CVA) are a progressive form of cerebrovascular pathology with the gradual development of a complex of neurological and neuropsychological disorders. The main reasons leading to chronic cerebral hypoperfusion include arterial hypertension, atherosclerotic vascular damage, and heart disease accompanied by chronic heart failure. In the complex treatment of patients with CNM, drugs are used that have complex antioxidant, angioprotective, neuroprotective and neurotrophic effects. One of these drugs is Vasobral (dihydroergocriptine + caffeine) - an effective and safe treatment for CNM.

Key words: cerebrovascular pathology, chronic cerebral ischemia, Vasobral

Chronic cerebrovascular disease (CCVD) is a progressive form of cerebrovascular pathology with gradual development of neurological and neuropsychological disorders. The main causes leading to chronic hypoperfusion of the brain are hypertension, atherosclerosis, and heart disease accompanied by chronic heart failure. In the complex treatment of patients with CCVD, drugs with comprehensive antioxidant, angioprotective, neuroprotective and neurotrophic action are usually used. One these drugs is Vazobral (dihydroergocryptine + coffein), effective and safe preparation for treatment of CCVD.

Key words: cerebrovascular pathology, chronic cerebral ischemia, Vasobral

Chronic cerebrovascular accidents (CVA) are a progressive form of cerebrovascular pathology, characterized by multifocal or diffuse ischemic brain damage with the gradual development of a complex of neurological and neuropsychological disorders. This is one of the most common forms of cerebrovascular pathology, usually occurring against the background of general cardiovascular diseases.

There are many extracerebral causes leading to pathology of cerebral circulation. First of all, these are diseases accompanied by a disorder of systemic hemodynamics, leading to a chronic decrease in adequate blood supply - chronic cerebral hypoperfusion. The main reasons leading to chronic cerebral hypoperfusion include arterial hypertension (AH), atherosclerotic vascular damage, and heart disease accompanied by chronic heart failure. Other causes include diabetes mellitus, vasculitis in systemic connective tissue diseases, other diseases accompanied by vascular damage, blood diseases leading to changes in its rheology (erythremia, macroglobulinemia, cryoglobulinemia, etc.).

Pathomorphological changes in CNM

A high level of perfusion is required for adequate brain function. The brain, whose mass is 2.0-2.5% of body weight, consumes 15-20% of the blood circulating in the body. The main indicator of brain perfusion is the level of blood flow per 100 g of brain matter per minute. The average value of hemispheric cerebral blood flow (CBF) is approximately 50 ml/100 g/min, but there are significant differences in the blood supply to individual brain structures. The magnitude of MK in gray matter is 3-4 times higher than in white matter. At the same time, in the anterior parts of the hemispheres, blood flow is higher than in other areas of the brain. With age, the value of MB decreases, and frontal hyperperfusion also disappears, which is explained by diffuse atherosclerotic changes in cerebral vessels. It is known that with CNM, the subcortical white matter and frontal structures are more affected, which may be explained by the indicated characteristics of the blood supply to the brain. Initial manifestations of insufficiency of cerebral blood supply to the brain occur if the blood flow to the brain is less than 30-45 ml/100 g/min. The advanced stage is observed when the blood supply to the brain decreases to a level of 20-35 ml/100 g/min. The threshold of regional blood flow within 19 ml/100 g/min (functional threshold of blood supply to the brain), at which the functions of the corresponding areas of the brain are impaired, is considered critical. The process of death of nerve cells occurs when regional arterial cerebral blood flow is reduced to 8-10 ml/100 g/min (infarction threshold of cerebral blood supply).

In conditions of chronic brain hypoperfusion, which is the main pathogenetic link of CNM, compensation mechanisms are depleted, the energy supply of the brain becomes insufficient, as a result, functional disorders first develop, and then irreversible morphological damage. In chronic cerebral hypoperfusion, a slowdown in cerebral blood flow, a decrease in the oxygen and glucose content in the blood, a shift in glucose metabolism towards anaerobic glycolysis, lactic acidosis, hyper-osmolarity, capillary stasis, a tendency to thrombus formation, depolarization of cells and cell membranes, activation of microglia, which begins to produce neurotoxins, which, along with other pathophysiological processes, leads to cell death.

Damage to small penetrating cerebral arteries (cerebral microangiopathy), on which the blood supply to the deep parts of the brain depends, in patients with CNM is accompanied by various morphological changes in the brain, such as:

diffuse damage to the white matter of the brain (leukoencephalopathy);

multiple lacunar infarctions in the deep parts of the brain;

microinfarctions;

microhemorrhages;

atrophy of the cerebral cortex and hippocampus.

To implement autoregulation of cerebral circulation, it is necessary to maintain certain values ​​of blood pressure (BP) in the main arteries of the head. On average, systolic blood pressure (SBP) in the main arteries of the head should range from 60 to 150 mm Hg. Art. With long-term hypertension, these limits shift slightly upward, so autoregulation does not become impaired for a long time and MB remains at a normal level. Adequate brain perfusion is maintained by increasing vascular resistance, which in turn leads to an increase in the load on the heart. Chronic uncontrolled hypertension leads to secondary changes in the vascular wall - lipohyalinosis, which is observed mainly in the vessels of the microvasculature. The resulting arteriolosclerosis leads to changes in the physiological reactivity of blood vessels. Under these conditions, a decrease in blood pressure as a result of the addition of heart failure with a decrease in cardiac output or as a result of excessive antihypertensive therapy, or as a result of physiological circadian changes in blood pressure leads to the occurrence of hypoperfusion in the areas of the terminal circulation. Acute ischemic episodes in the basin of deep penetrating arteries lead to the occurrence of small-diameter lacunar infarcts in the deep parts of the brain. If the course of hypertension is unfavorable, repeated acute episodes lead to the emergence of the so-called. lacunar state, which is one of the variants of multi-infarct vascular dementia.

In addition to repeated acute disorders, the presence of chronic ischemia in the areas of terminal circulation is also assumed. A marker of the latter is a rarefaction of the periventricular or subcortical white matter (leukoaraiosis), which pathomorphologically represents a zone of demyelination, gliosis and expansion of the perivascular spaces. In some cases of an unfavorable course of hypertension, subacute development of diffuse damage to the white matter of the brain with a clinical picture of rapidly progressing dementia and other manifestations of disconnection is possible, which is sometimes referred to in the literature as “Binswanger’s disease.”

Another significant factor in the development of CNM is atherosclerotic damage to cerebral vessels, which is usually multiple, localized in the extra- and intracranial parts of the carotid and vertebral arteries, as well as in the arteries of the circle of Willis and their branches, forming stenoses. Stenoses are divided into hemodynamically significant and insignificant. If a decrease in perfusion pressure occurs distal to the atherosclerotic process, this indicates a critical or hemodynamically significant narrowing of the vessel.

It has been shown that hemodynamically significant stenoses develop when the vessel lumen narrows by %. But cerebral blood flow depends not only on the severity of stenosis, but also on the mechanisms that prevent the development of ischemia: the state of collateral circulation, the ability of cerebral vessels to dilate. These hemodynamic reserves of the brain allow “asymptomatic” stenoses to exist without complaints or clinical manifestations. However, the obligatory development of chronic cerebral hypoperfusion during stenosis leads to CNM, which is detected by magnetic resonance imaging (MRI). MRI visualizes periventricular leukoaraiosis (reflecting ischemia of the white matter of the brain), internal and external hydrocephalus (caused by atrophy of brain tissue); Cysts may be detected (as a consequence of cerebral infarctions, including clinically “silent” ones). It is believed that CNMC is present in 80% of patients with stenotic lesions of the main arteries of the head. Atherosclerotic changes in cerebral vessels are characterized not only by local changes in the form of plaques, but also by hemodynamic restructuring of the arteries in the area distal to atherosclerotic stenoses and occlusions. All this leads to the fact that “asymptomatic” stenoses become clinically significant.

The structure of the plaques is also of great importance: the so-called. unstable plaques lead to the development of arterio-arterial embolisms and acute cerebrovascular accidents - often of a transient type. When hemorrhaging into such a plaque, its volume quickly increases with an increase in the degree of stenosis and worsening of the signs of CNM. In the presence of such plaques, blocking the lumen of the vessel up to 70% will be hemodynamically significant.

In the presence of damage to the main arteries of the head, cerebral blood flow becomes very dependent on systemic hemodynamic processes. Such patients are especially sensitive to arterial hypotension, which can occur when moving to a vertical position (orthostatic hypotension), with cardiac arrhythmias leading to a short-term decrease in cardiac output.

Clinical manifestations of CNM

The main clinical manifestations of CNM are disturbances in the emotional sphere, balance and gait disorders, pseudobulbar disorders, impairment of memory and learning ability, neurogenic urination disorders, which gradually lead to maladjustment of patients.

During CNM, three stages can be distinguished:

At stage I, the clinic is dominated by subjective disorders in the form of general weakness and fatigue, emotional lability, sleep disturbances, decreased memory and attention, and headaches. Neurological symptoms do not form distinct neurological syndromes, but are represented by anisoreflexia, discoordination, and symptoms of oral automatism. Violations of memory, praxis and gnosis can be identified, as a rule, only when special tests are carried out.

At stage II, there are more subjective complaints, and neurological symptoms can already be divided into distinct syndromes (pyramidal, discoordination, amyostatic, dysmnestic), with one neurological syndrome usually dominating. Professional and social adaptation of patients decreases.

At stage III, neurological symptoms increase, a distinct pseudobulbar syndrome appears, and sometimes paroxysmal conditions (including epileptic seizures); Severe cognitive impairment leads to disruption of social and everyday adaptation and complete loss of working capacity. Ultimately, CNMK contributes to the formation of vascular dementia.

Cognitive impairment is a key manifestation of CNM, which largely determines the severity of the patient’s condition. They often serve as the most important diagnostic criterion for CNM and are a sensitive marker for assessing the dynamics of the disease. It is worth noting that the location and extent of vascular changes detected by MRI or computed tomography are only partially correlated with the presence, type and severity of neuropsychological findings. In case of CNMC, there is a more pronounced correlation between the severity of cognitive impairment and the degree of brain atrophy. Correcting cognitive impairment is often critical to improving the quality of life of the patient and his relatives.

Methods for diagnosing cognitive impairment

To assess the overall severity of cognitive defect, the Mini-Mental State Examination scale is most widely used. However, this method is not an ideal screening tool, since its results are significantly influenced by the patient's premorbid level and type of dementia (the scale is less sensitive to frontal cortex dysfunction and therefore better detects the early stages of Alzheimer's disease than the early stages of vascular dementia). In addition, its implementation requires more than 10-12 minutes, which the doctor does not always have at an outpatient appointment.

Clock drawing test: subjects are asked to draw a clock with its hands pointing to a specific time. Normally, the subject draws a circle, places the numbers from 1 to 12 inside it in the correct order at equal intervals, draws 2 hands (the hour hand is shorter, the minute hand is longer), starting in the center and showing the specified time. Any deviation from correct test performance is a sign of fairly severe cognitive dysfunction.

Speech activity test: subjects are asked to name as many names of plants or animals as possible in a minute (semantically mediated associations) and words starting with a certain letter, for example “l” (phonetically mediated associations). Normally, most elderly people with secondary and higher education name from 15 to 22 plants and from 12 to 16 words starting with “l” per minute. Naming fewer than 12 semantically mediated associations and fewer than 10 phonetically mediated associations usually indicates significant cognitive dysfunction.

Visual memory test: patients are asked to remember 10-12 images of simple, easily recognizable objects presented on one sheet; Subsequently, the following are assessed: 1) immediate reproduction, 2) delayed reproduction after interference (a verbal association test can be used as an interfering effect), 3) recognition (the patient is asked to recognize previously presented objects among other images). Failure to remember more than half of previously presented images may be considered a sign of severe cognitive dysfunction.

Main directions in the treatment of CNM

The main directions in the treatment of CNM stem from the etiopathogenetic mechanisms that led to this process. The main goal is to restore or improve brain perfusion, which is directly related to the treatment of the underlying disease: hypertension, atherosclerosis, heart disease with the elimination of heart failure.

Taking into account the diversity of pathogenetic mechanisms underlying CNM, preference should be given to agents that have complex antioxidant, angioprotective, neuroprotective and neurotrophic effects. In this regard, the use of drugs that combine several mechanisms of action is justified. Among such drugs, I would like to mention Vasobral, a combined drug that has both nootropic and vasoactive effects. It contains an ergot derivative (dihydroergocryptine) and caffeine. Dihydroergocriptine blocks α1 and α2 adrenergic receptors of vascular smooth muscle cells, platelets, and erythrocytes, and has a stimulating effect on dopaminergic and serotonergic receptors of the central nervous system.

When using the drug, the aggregation of platelets and erythrocytes decreases, the permeability of the vascular wall decreases, blood supply and metabolic processes in the brain improve, and the resistance of brain tissue to hypoxia increases. The presence of caffeine in Vasobral determines the stimulating effect on the central nervous system, mainly on the cerebral cortex, respiratory and vasomotor centers, and increases mental and physical performance. Studies have shown that Vasobral has a vegetative stabilizing effect, which manifests itself in increased pulse blood filling, normalization of vascular tone and venous outflow, which is due to the positive effect of the drug on the sympathetic nervous system while reducing the activity of the parasympathetic system. A course of treatment with Vasobral leads to a decrease or disappearance of symptoms such as dizziness, headache, palpitations, and numbness of the extremities. Positive dynamics of the neuropsychological status of the patient with CNM are noted: increased attention span; improving orientation in time and space, memory for current events, intelligence; increased mood, decreased emotional lability. The use of Vasobral helps reduce fatigue, lethargy, and weakness; there is a feeling of cheerfulness.

The drug is prescribed in a dose of 2-4 ml (1-2 pipettes) or 1/2-1 tablet 2 times a day for 2-3 months. The drug is taken with a small amount of water. Side effects occur rarely and are mild. It should be noted that due to the presence of liquid and tablet forms, double dosing and good tolerability, Vasobral is convenient for long-term use, which is extremely important in the treatment of chronic diseases.

Non-drug ways to correct the manifestations of CNM should include:

proper organization of work and rest, avoidance of night shifts and long business trips;

moderate physical activity, therapeutic exercises, measured walking;

diet therapy: limiting the total calorie content of food and salt consumption (up to 2-4 g per day), animal fats, smoked meats; introduction of fresh vegetables and fruits, fermented milk and fish products into the diet;

climatic treatment at local resorts, in low altitudes and at sea resorts; balneotherapy, which has a positive effect on central hemodynamics, contractile function of the heart, and the state of the autonomic nervous system; the means of choice are radon, carbon dioxide, sulfide, iodine-bromine baths.

In general, an integrated approach to the treatment of CNM and repeated pathogenetically based course treatment can contribute to better adaptation of the patient in society and prolong the period of his active life.

Kotova Olga Vladimirovna - researcher at the Department of Pathology of the Autonomic Nervous System of the Research Center of the First Moscow State Medical University named after. THEM. Sechenov.

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Cerebral circulation disorders. Postoperative complications

Embolism in the vessels of the brain (when isolating the carotid or vertebral arteries, introducing an internal shunt, non-compliance with the sequence of starting blood flow upon completion of the reconstruction stage);

Thrombosis of the reconstructed artery as a result of its inadequate disobliteration or narrowing of its lumen. Less commonly, thrombosis is caused by disorders of the blood coagulation system with a tendency to hypercoagulation.

Brain perfusion study

Brain perfusion is a state of blood flow, in other words, an indicator of the blood supply to an organ. When perfusion decreases, unpleasant symptoms are observed: tinnitus, floaters, darkening of the eyes, weakness. At the same time, increased perfusion in brain tumors is a poor prognostic sign, since the tumor grows faster in this case. Studying this indicator using CT and MRI is a way to diagnose many pathologies of the central nervous system.

Retrograde perfusion is not a diagnostic procedure, but a protective measure aimed at preventing hypoxia of the central nervous system during hypothermic cardiac arrest. Retrograde perfusion is used during surgery on the aorta.

Perfusion assessment

Magnetic resonance or computed tomography with perfusion assessment is a method of studying the brain to determine the capacity of blood vessels and the intensity of blood flow.

The central nervous system is generously supplied with a network of blood vessels for adequate nutrition and respiration of cells. Impaired cerebral perfusion can lead to the following symptoms:

Everything about angiography of cerebral vessels: how the procedure is performed, preparation for the examination.

This can occur due to atherosclerotic processes, vasculitis, and problems with the cardiovascular system. Reduced perfusion increases the risk of developing parkinsonism, vascular dementia, ischemic stroke, and cell death from oxygen starvation.

In case of tumor diseases, their blood supply is examined using a tomograph. The level of perfusion affects the further growth of the tumor. Malignant tumors differ from benign tumors in the speed of blood flow and type of vascularization.

Indications for perfusion studies

Perfusion computed tomography or magnetic resonance imaging is one of the methods for diagnosing brain pathologies. It is prescribed by neurologists and neurosurgeons for the following purposes:

1. Assessment of tumor blood flow, monitoring the effectiveness of chemotherapy and radiotherapy.
2. Diagnosis of perfusion disorders after strokes and thrombosis.
3. To prepare for brain surgery to find out where the blood vessels go.
4. Determining the causes of migraines, epilepsy, fainting.
5. Detection of an aneurysm - arterial dissection.

CT brain perfusion is performed using a tomograph that emits X-rays. MRI is based on the action of electromagnetic waves. The reflected signals are caught by scanners, and the computer displays them on the monitor. Photos can be saved to external media.

To study the condition of the blood vessels, a contrast agent is injected into the cubital vein. A catheter is installed and connected to an automatic infusion device - an infusion pump. First, the tissue is scanned without contrast. Next, an examination is carried out after the injection of 40 ml of contrast agent. Infusion rate – 4 ml/s. The tomograph takes images every second.

Interpretation of perfusion scanning

A perfusion scan of the brain reveals the following indicators:

1. CBV is the volume of cerebral blood flow, which reflects the amount of blood per mass of brain tissue. Normally, for every 100 g of gray and white matter there should be at least 2.5 ml of blood. If a perfusion study determines a smaller volume, then this indicates ischemic processes.
2. CBF – volumetric blood flow velocity. This is the volume of contrast agent that passes through 100 g of brain tissue in a certain amount of time. With thrombosis and embolism of various origins, this indicator decreases.
3. MTT – average contrast circulation time. The norm is 4–4.5 seconds. Closure of the lumen of blood vessels leads to its significant increase.

To calculate the results, special computer software is used.

CT and MRI perfusion studies allow simultaneous assessment of both the condition of blood vessels and the intensity of blood flow, as well as the pathology of brain tissue.

Important! Doppler ultrasound also detects vascular disorders, but poorly sees the parenchyma itself - the white and gray matter, neurons and their fibers. Angiography, like PCT, shows ischemia and thrombosis, but does not visualize soft tissue well.

Benefits of the study

Computer, magnetic resonance perfusion tomography is an informative study for detecting narrowings or hernial protrusions of blood vessels and determining the speed of blood flow.

There are several differences between MRI and CT perfusion examination. Computed tomography uses harmful x-ray radiation, which is contraindicated during pregnancy and lactation. CT scans are faster than MRI scans, but the time is evened out with contrast.

Important! Pregnancy, lactation, allergy to iodine are contraindications to the use of contrast agents, which can be potentially dangerous to the child.

Advantages of PCT and perfusion MRI:

1. Affordable price: about 3000–4000 rub.
2. Clear cross-sectional image.
3. The results can be saved to storage media.

Restrictions

For pregnant women, examination is performed only if there is a threat to the life of the baby or its mother due to brain pathology. When breastfeeding, please note that the removal of the contrast agent from the body takes some time. Therefore, the child can be fed only two days after the examination.

Carrying out the procedure

Before the CT and MRI perfusion procedure, it is necessary to remove all jewelry and metal objects. Clothing should not restrict movement, since the procedure lasts about half an hour. If you have a pacemaker or implants, you should inform your doctor about this before prescribing the procedure.

It is important to learn about NSH of the brain of newborns: what can be detected using neurosonography.

Note: what is a brain echogram and for what diseases is the procedure indicated?

What parents need to know about EEG of the brain in children: features of the study, indications.

Conclusion

Perfusion testing is an accurate and relatively safe method for studying both brain structures and blood vessels. Three indicators give an idea of ​​​​the blood circulation of the entire head and individual areas.