Neurogenic syncope (syncopal conditions)

Syncope (syncope) - an attack of short-term loss of consciousness and violation of postural tone with a disorder of cardiovascular and respiratory activity.

At present, there is a tendency to treat syncope in the frame of paroxysmal disorders of consciousness. In this regard, it is preferable to use the term "syncope", which implies a broader understanding of the possible mechanisms of the pathogenesis of this condition than only the concept of anoxic and hypoxic, which are associated with acute cerebral circulatory insufficiency in the pathogenesis of these conditions designated as syncopes. One should also take into account the presence of such a concept as "collapse", which denotes a vascular-regulatory disorder manifested by a paroxysmal fall, but loss of consciousness is not necessary at the same time.

Usually the syncope in most cases is preceded by dizziness, darkening in the eyes, ringing in the ears, a feeling of "imminent fall and loss of consciousness." In cases where these symptoms appear, and loss of consciousness does not develop, it is a question of pre-syncopal conditions, or lipotymia.

There are numerous classifications of syncopal states, which is due to the lack of a generally recognized concept of their pathogenesis. Even the division of these states into two classes - neurogenic and somatogenic syncopations - seems inaccurate and very conditional, especially in situations where there are no distinct changes in the nervous or somatic sphere.

Symptoms of syncope (syncopal conditions), despite the presence of a number of differences, are to some extent stereotyped. Syncope is considered as a process developed in time, therefore in most cases it is possible to single out manifestations that precede the actual fainting state and the period following it. Similar manifestations of N. Gastaut (1956) designated as parasyncopal. O. Corfariu (1971), O. Corfariu, L. Popoviciu (1972) - both pre- and post-prefabricated. NK Bogolepov et al. (1968) identified three periods: a pre-syncopal condition (pre-obstruction, or lipotymia); actually syncope, or fainting, and the post-syncopal period. Within each period there is a different degree of severity and severity. The pre -syncopal manifestations preceding the loss of consciousness last usually from a few seconds to 1-2 minutes (usually from 4-20 seconds to 1, 1.5 minutes) and are manifested by a feeling of discomfort, faintness, cold sweat, blurred vision, "fog" before eyes, dizziness, noise in the ears, nausea, pallor, a sense of imminent fall and loss of consciousness. A part of the patients have a feeling of anxiety, fear, a feeling of lack of air, a heartbeat, a lump in the throat, numbness of the lips, tongue, fingers. However, these symptoms may be absent.

Loss of consciousness usually lasts 6-60 seconds. Most often there is pallor and a decrease in muscle tone, immobility, the eyes are closed, the mydriasis is established with a decrease in the pupillary response to light. Usually there are no pathological reflexes, a weak, irregular, labile pulse, a decrease in blood pressure, and shallow breathing. With deep syncope, several clonic or tonic-clonic jerks are possible, involuntary urination and rarely defecation.

Post-syncopal period - usually lasts a few seconds, and the patient quickly wakes up, rightly orienting himself in space and time. Usually the patient is anxious, frightened by the incident, pale, adynamic; marked tachycardia, rapid breathing, severe general weakness and fatigue.

The analysis of syncopal (and parasyncopal) condition is of great importance for the diagnosis. It should be emphasized that in some cases, the key is not only the analysis of the immediate presyncopal state, but also the psycho-vegetative and behavioral background (hours, even days) on which the syncope has developed. This allows us to establish an important fact - can this syncope be considered as a paroxysmal manifestation of psychovegetative syndrome.

Despite a certain conventionality, which we mentioned above, all variants of syncopal states can be divided into two classes: neurogenic and somatogenic. We will consider that class of syncopal states that is not associated with outlined somatic (usually cardiological) diseases, but is caused by neurogenic disorders and, in particular, dysfunction of vegetative regulation.

[1], [2], [3], [4]

Vasodepressor syncope

Vasodepressor syncope (simple, vasovagal, vasomotor syncope) occurs most often as a result of various (usually stressful) effects and is associated with a sharp decrease in total peripheral resistance, mainly dilatation of the peripheral vessels of the muscles.

Simple vasodepressor syncope is the most frequent variant of short-term loss of consciousness and, according to various researchers, is from 28 to 93.1% among patients with syncopal conditions.

Symptoms of vasodepressor syncope (syncope)

Loss of consciousness usually does not occur immediately: as a rule, it is preceded by a distinct pre-syncopal period. Among the provoking factors and conditions for the appearance of syncopal conditions, afferent reactions of stress type are most often noted: fright, anxiety, fear associated with unpleasant news, accidents, the type of blood or fainting in others, preparation, waiting and taking blood, dental procedures and other medical manipulations. Often syncope occurs when there is pain (strong or minor) during these manipulations or with pains of visceral origin (gastrointestinal, pectoral, hepatic and renal colic, etc.). In some cases, direct provoking factors may be absent.

As the conditions conducive to the onset of syncope, the most common is the orthostatic factor (long standing in the transport, in the queue, etc.);

Stay in a stuffy room causes the patient as a compensatory reaction hyperventilation, which is an additional strong provoking factor. Increased fatigue, lack of sleep, hot weather, alcohol consumption, fever - these and other factors form the conditions for the realization of fainting.

During a syncope the patient is usually immobile, the skin is pale or gray-earthy in color, cold, covered with sweat. Bradycardia, extrasystole are revealed. Systolic blood pressure drops to 55 mm Hg. Art. In the EEG study, slow delta and delta bands of high amplitude are detected. The horizontal position of the patient leads to a rapid increase in blood pressure, in rare cases, hypotension can last several minutes or (on an exceptional basis) even hours. A prolonged loss of consciousness (more than 15-20 seconds) can lead to tonic and (or) clonic convulsions, involuntary urination and defecation.

Post-syncopal condition can be of different duration and severity, accompanied by asthenic and vegetative manifestations. In some cases, rising of the patient leads to a repeated fainting with all the symptoms described above.

The examination of patients reveals a number of changes in the mental and vegetative spheres: various variants of emotional disturbances (increased irritability, phobic manifestations, decreased mood, hysterical stigma, etc.), vegetative lability and a tendency to arterial hypotension.

When diagnosing vasodepressor syncope, it is necessary to take into account the presence of provoking factors, the conditions for the onset of syncope, the period of presyncopal manifestations, lowering of arterial pressure and bradycardia during loss of consciousness, skin condition in the post-syncopal period (warm and moist). An important role in diagnosis is played by the presence of psycho-vegetative syndrome in the patient, absence of epileptic (clinical and paraclinic) signs, exclusion of cardiac and other somatic pathology.

The pathogenesis of vasodepressor syncopal conditions is still unclear. Numerous factors identified by researchers in the study of syncope (hereditary predisposition, perinatal pathology, the presence of vegetative disorders, propensity to parasympathetic reactions, residual neurological disorders, etc.). Can not explain each individual cause of the loss of consciousness.

GL Engel (1947, 1962), based on an analysis of the biological meaning of a number of physiological reactions based on the works of Ch. Darwin and W. Cannon, hypothesized that vasodepressor syncope is a pathological reaction that occurs as a result of experiencing anxiety or fear in conditions where activity (motion) is inhibited or impossible. Blockade reactions "struggle or flight" leads to the fact that the excess activity of the circulatory system, tuned to muscle activity, is not compensated for the work of the muscles. The "mood" of peripheral vessels for intensive blood circulation (vasodilation), the absence of the involvement of a "venous pump" associated with muscular activity, lead to a decrease in the volume of blood flowing to the heart and the emergence of a reflex bradycardia. Thus, vasodepressor reflex (falling of arterial pressure), combined with peripheral vasoplegia is included.

Of course, as the author notes, this hypothesis is not able to explain all aspects of the pathogenesis of vasodepressor syncope. The work of recent years indicates a major role in their pathogenesis of impaired brain activation homeostasis. Specific cerebral mechanisms of disturbance of cardiovascular and respiratory system regulation associated with an inadequate supra-segmental program for regulating the pattern of autonomic functions are identified. In the spectrum of autonomic disorders, not only cardiovascular, but also respiratory dysfunction, including hyperventilation manifestations, is of great importance for pathogenesis and symptomogenesis.

Orthostatic syncopation

Orthostatic syncopal condition is a short-term loss of consciousness that occurs when a patient moves from a horizontal position to a vertical position or under the influence of a prolonged stay in an upright position. As a rule, syncope is associated with the presence of orthostatic hypotension.

Under normal conditions, a person's transition from a horizontal position to a vertical position is accompanied by a slight and short-term (a few seconds) decrease in blood pressure followed by a rapid increase in blood pressure.

The diagnosis of orthostatic syncope is based on an analysis of the clinical picture (the connection of syncope with an orthostatic factor, an instant loss of consciousness without pronounced parasyncopal conditions); the presence of low blood pressure at a normal heart rate (no bradycardia, as is usually the case with vasodepressor syncope, and lack of compensatory tachycardia, which is usually observed in healthy). An important help in diagnosis is the positive test of Schellong - a sharp fall in blood pressure when getting out of a horizontal position with no compensatory tachycardia. An important proof of the presence of orthostatic hypotension is the absence of an increase in the concentration of aldosterone and catecholamines in the blood and excretion of them with urine on rising. An important test is a sample with a 30-minute standing, which determines a gradual decrease in blood pressure. Other special studies are also needed to establish signs of peripheral vegetative innervation insufficiency.

For the purposes of differential diagnosis, a comparative analysis of orthostatic syncope with vasodepressor syncope should be performed. For the first, a close, rigid connection with orthostatic situations and the absence of other variants of provocation, characteristic for vasodepressor syncope, are important. Vaso-depressor syncope is characterized by an abundance of psycho-vegetative manifestations in pre- and post-syncopal periods, slower than with orthostatic fainting, loss and return of consciousness. Of great importance are the presence of bradycardia during vasodepressor syncope and the absence of both brady- and tachycardia in the fall of arterial pressure in patients with orthostatic syncope.

Hyperventilation syncope (syncope)

Syncopal states are one of the clinical manifestations of hyperventilation syndrome. Hyperventilation mechanisms can simultaneously play a significant role in the pathogenesis of syncope of various nature, since excessive breathing leads to numerous and polysystemic changes in the body.

The peculiarity of hyperventilation fainting lies in the fact that most often the phenomenon of hyperventilation in patients can be combined with hypoglycemia and pain manifestations. In patients prone to abnormal vasomotor reactions, in patients with postural hypotension, the hyperventilation test can cause a pre-fainting or even fainting condition, especially if the patient is in a standing position. The introduction of such insulin to a sample of 5 units of insulin significantly sensitizes the sample, and a violation of consciousness occurs more quickly. In this case, there is a certain relationship between the level of impaired consciousness and simultaneous changes in the EEG, as evidenced by slow rhythms of the 5- and G-band.

Two variants of hyperventilation syncopal states with various specific pathogenetic mechanisms should be distinguished:

• hypocapnic, or acapnic, variant of hyperventilation syncope;
• vasodepressor type of hyperventilation syncope. Identified variants in pure form are rare, more often in a clinical picture this or that variant prevails.

Hypokapnichesky (akapnichesky) a variant of a hyperventilation syncope

Hypokapnichesky (akapnichesky) variant of hyperventilation fainting is determined by its leading mechanism - the brain's reaction to the reduction of the partial voltage of carbon dioxide in the circulating blood, which along with respiratory alkalosis and Bohr effect (displacement of the curve of dissociation of oxyhemoglobin to the left, causing an increase in tropicity of oxygen to hemoglobin and difficulty of its cleavage for transition to brain tissue) leads to reflex spasm of cerebral vessels and hypoxia of brain tissue.

Clinical features consist in the presence of a long pre-patch condition. It should be noted that persistent hyperventilation in these situations can be either the expression of a vegetative crisis unfolding in a patient (panic attack) with a bright hyperventilation component (hyperventilation crisis) or a hysterical fit with increased breathing that lead to secondary shifts indicated above by the mechanism of complicated conversion. Pre-mental state, thus, can be quite long (minutes, tens of minutes), accompanied by vegetative crises with the corresponding mental, vegetative and hyperventilation manifestations (fear, anxiety, palpitation, cardialgia, lack of air, paresthesia, tetany, polyuria, etc.).

An important feature of the hypocapic variant of hyperventilation syncope is the absence of sudden loss of consciousness. As a rule, at first there are signs of an altered state of consciousness: a sense of unreality, the strangeness of the environment, a feeling of lightness in the head, a narrowing of consciousness. The aggravation of these phenomena ultimately leads to a narrowing, a reduction in consciousness, and a fall in the patient. In this case, the phenomenon of flickering of consciousness is noted - the alternation of periods of return and loss of consciousness. The subsequent inquiry reveals the presence in the field of consciousness of the patient of various, sometimes quite bright images. In a number of cases, patients indicate the absence of complete loss of consciousness and the preservation of the perception of certain phenomena of the external world (for example, reversed speech) when it is impossible to respond to them. The duration of loss of consciousness can also be much greater than with simple fainting. Sometimes it reaches 10-20 or even 30 minutes. In essence, this is the continuation of the development of hyperventilation paroxysm in prone position.

Such a duration of the phenomenon of the disturbance of consciousness with the phenomena of the flickering consciousness can also indicate the existence of a peculiar psychophysiological organization in the person with a tendency to conversion (hysterical) reactions.

When viewed from these patients, various types of breathing disorders can occur-increased respiration (hyperventilation) or long periods of respiratory arrest (apnea).

Appearance of patients during the violation of consciousness in such situations is usually little changed, hemodynamic indicators are also not significantly affected. Perhaps the concept of "fainting" in relation to these patients is not entirely adequate, most likely it is a kind of "trance" altered state of consciousness as a result of the effects of persistent hyperventilation in combination with certain features of the psychophysiological pattern. However, the imperative violation of consciousness, the fall of patients and, most importantly, the close connection of these disorders with the phenomenon of hyperventilation, as well as with other, including vasodepressor, reactions in these patients require consideration of the discussed disorders of consciousness in this section. To this we should add that the physiological consequences of hyperventilation due to their globality can reveal and include in the pathological process other, in particular cardiac, hidden pathological changes, such as the appearance of severe arrhythmias - the result of moving the pacemaker to the atrioventricular node and even in ventricle with the development of atrioventricular nodular or idioventricular rhythm.

These physiological consequences of hyperventilation should, apparently, be correlated with another - the second variant of syncopal manifestations in hyperventilation.

Vaso-depressor variant of hyperventilation syncope

The vasodepressor variant of hyperventilation syncope is associated with the inclusion of a syncope in the pathogenesis of a different mechanism-a sharp drop in the resistance of peripheral vessels with a generalized enlargement without a compensatory increase in heart rate. The role of hyperventilation in the mechanisms of redistribution of blood in the body is well known. So, under normal conditions, hyperventilation causes a redistribution of blood in the brain-muscle system, namely, a reduction in the cerebral blood flow and an increase in muscle blood flow. Excessive, inadequate inclusion of this mechanism is the pathophysiological basis of vaso-depressor syncope in patients with hyperventilation disorders.

The clinical picture of this variant of syncope is the presence of two important components, causing some differences from a simple, non-hyperventilation variant of vasodressor syncope. First, it is a more "rich" parasyncopal clinical picture, expressed in the fact that psycho-vegetative manifestations are significantly represented both in pre- and post-syncopal periods. Most often these are affective vegetative, including hyperventilation, manifestations. In addition, in a number of cases, carpopedal tetanic convulsions occur, which can be mistakenly regarded as having epileptic genesis.

As already mentioned, vasodepressor syncope is in essence a stage in the development of the reduced (and in some cases expanded) vegetative, or more precisely, hyperventilation paroxysm. Loss of consciousness for patients and others is a more significant event, therefore, in the anamnesis of the event of the presynopal period, patients are often omitted. Another important component in the clinical expression of hyperventilation vasodressor syncope is its frequent (as a rule, natural) combination with manifestations of acapnic (hypocapnic) type of consciousness disorder. Presence of elements of the altered state of consciousness in the presyncopal period and phenomena of flickering of consciousness in the period of loss of consciousness forms in a number of cases an unusual clinical pattern that causes doctors a feeling of perplexity. Thus, in patients who fainted on vasodepressor, a type habitual for doctors, during the faint itself there was a certain fluctuation-fibrillation of consciousness. As a rule, doctors have an erroneous idea of the presence in these patients of the leading hysterical mechanisms in the genesis of syncope.

An important clinical sign of this variant of syncope is repeated syncope when trying to get up in patients who are in a horizontal position in the post-syncopal period.

Another feature of vasodepressor hyperventilation syncope is the presence of a greater range of provoking factors than in patients with ordinary simple syncope. Especially important for such patients are situations where the system of breathing is objectively and subjectively involved: heat, the presence of sharp odors, stuffy, enclosed spaces that cause phobic fears in patients with the appearance of respiratory sensations and subsequent hyperventilation, etc.

The diagnosis is based on careful phenomenological analysis and finding in the structure of the parasyncopal and syncopal periods the signs indicating the presence of pronounced affective, vegetative, hyperventilation and tetanic phenomena, as well as altered states of consciousness, the presence of the phenomenon of flickering of consciousness.

It is necessary to apply criteria for the diagnosis of hyperventilation syndrome.

Differential diagnosis is carried out with epilepsy, hysteria. The pronounced psychovegetative manifestations, the presence of tetanic convulsions, the long period of impairment of consciousness (which is sometimes regarded as post-stabbing stunning) - all this in some cases leads to an erroneous diagnosis of epilepsy, in particular temporal epilepsy.

In these situations, the diagnosis of hyperventilation syncopal conditions is helped by a longer (minutes, tens of minutes, sometimes hours) than with epilepsy (seconds), a pre-syncopal period. The absence of other clinical and EEG changes characteristic of epilepsy, the lack of improvement in the appointment of anticonvulsant drugs and the presence of a significant effect in giving psychotropic medications and (or) carrying out respiratory correction make it possible to exclude the epileptic nature of suffering. In addition, a positive diagnosis of hyperventilation syndrome is essential.

Sinocarotid syncope (fainting)

Sinocarotid syncopes (hypersensitivity syndrome, carotid sinus hypersensitivity) are syncopal states, in the pathogenesis of which the high sensitivity of the sinocarotid sinus plays a leading role, leading to disturbances in the regulation of the rhythm of the heart, the tone of peripheral or cerebral vessels.

In 30% of healthy people, under pressure on the carotid sinus, various vascular reactions occur; even more often such reactions occur in patients with essential hypertension (75%) and in patients who have arterial hypertension combined with atherosclerosis (80%). In this case, syncopal states are observed only in 3% of patients of this contingent. The most common fainting associated with carotid sinus hypersensitivity occurs after 30 years, especially in elderly and senile men.

A characteristic feature of these syncope is their association with irritation of the carotid sinus. Most often this happens when the head moves, the head tilts backwards (in the hairdresser during shaving, when looking at the stars, tracking a flying airplane, viewing fireworks, etc.). It is also important to wear tight, hard collars or tight tying a tie, the presence of tumor-like formations on the neck, compressing the sinocarotid area. Fainting can also occur while eating.

The presynopal period in some patients may be practically absent; sometimes also slightly expressed and the state after syncope.

In some cases, patients have a short-term but distinctly expressed pre-syncopal condition, manifested by severe fear, shortness of breath, a feeling of constriction of the throat and chest. Part of the patients after the syncopal condition experience a sense of unhappiness, asthenia and depression are expressed. The duration of loss of consciousness can be different, most often it fluctuates within 10-60 s, in some patients cramps are possible.

Within the framework of this syndrome, it is common to distinguish three types of syncopal conditions: vagal type (bradycardia or asystole), vasodepressor type (decrease, blood pressure drop at normal heart rate) and cerebral type, when unconsciousness associated with irritation of the carotid sinus is not accompanied by a violation of the rhythm of the heart, or a drop in blood pressure.

The cerebral (central) variant of carotid syncopal conditions can be accompanied, in addition to the disorders of consciousness, also by speech disorders, episodes of involuntary lacrimation, pronounced sensations of severe weakness, loss of muscle tone manifested in the parasyncopal period. The mechanism of loss of consciousness in these cases is connected, apparently, with the increased sensitivity of not only the sinocarotid sinus, but also the boulevard centers, which, incidentally, is typical for all varieties of hypersensitivity of the carotid sinus.

Important is the fact that, in addition to losing consciousness, with the syndrome of carotid sinus hypersensitivity, other symptoms can be observed that facilitate correct diagnosis. Thus, attacks of severe weakness and even loss of postural tonus by cataplexy type without disorders of consciousness are described.

For the diagnosis of sino-carotid syncope, it is of fundamental importance to carry out a sample with pressure on the area of the carotid sinus. A pseudo-positive test can be in case a patient with an atherosclerotic lesion of the carotid arteries squeezes leads to a clotting of the carotid artery and cerebral ischemia. In order to avoid this frequent enough mistake, it is absolutely necessary to initially perform an auscultation of both carotid arteries. Then, in the prone position, press on the carotid sinus (or massage it) alternately. The criteria for diagnosing carotid sinus syndrome on the basis of the sample are as follows:

1. occurrence of a period of asystole more than 3 seconds (cardioinhibitory variant);
2. decrease in systolic blood pressure by more than 50 mm Hg. Art. Or more than 30 mm Hg. Art. With the simultaneous occurrence of syncope (vasodepressor version).

Prevention of cardioinhibitory reaction is achieved by the introduction of atropine, and vasodepressor - adrenaline.

When conducting differential diagnosis, it is necessary to distinguish the vasodepressor variant of the synocarotid syncope and the simple vasodepressor syncope. Later age, male sex, less pronounced pre-syncopal phenomena (and sometimes their absence), the presence of a disease that causes an increased sensitivity of the sinocarotid sinus (atherosclerosis of carotid, coronary vessels, the presence of various formations on the neck), and finally, the close connection of the onset of syncope with the situation irritation of the sinocarotid sinus (head movement, etc.), as well as a positive test with pressure on the carotid sinus - all these factors allow differentiating the vasodepressor variant of the sinocarotid sin copa from a simple vasodepressor syncope.

In conclusion, it should be noted that hypersensitivity of the carotid type is not always directly related to any specific organic pathology, but may depend on the functional state of the brain and the body. In the latter case, the increased sensitivity of the carotid sinus can be included in the pathogenesis of other types of fainting conditions of a neurogenic (including psychogenic) nature.

Cough syncope (fainting)

Cough syncope (syncope) - syncope associated with a cough; arise usually against the background of an attack of a pronounced cough with diseases of the respiratory system (chronic bronchitis, laryngitis, whooping cough, bronchial asthma, emphysema), cardiopulmonary pathological conditions, as well as in people without these diseases.

Pathogenesis of coughing fainting. As a result of a sharp increase in intrathoracic and intra-abdominal pressure, blood flow to the heart decreases, the minute volume of the heart decreases, and conditions for disrupting compensation of cerebral circulation arise. Other pathogenetic mechanisms are supposed: stimulation of the receptor system of the vagus nerve of the carotid sinus, baroreceptors and other vessels, which can lead to a change in the activity of the reticular formation, vasodepressor and cardioinhibitory reactions. A polygraph study of night sleep in patients with cough syncope revealed the identity of disturbances in the sleep pattern to those disorders that occur in the Pickwick syndrome caused by dysfunction of the central stem formations responsible for the regulation of respiration and forming part of the reticular formation of the brainstem. The role of delayed breathing, the presence of hyperventilation mechanisms, and the violation of venous circulation are also discussed. For a long time, it was believed that cough syncope was a variant of epilepsy, and they were therefore labeled "Bettoplexia". Cough was regarded either as a phenomenon provoking an epileptic fit, or as a kind of epileptic aura. In recent years, it has become apparent that cough fainting is not epileptic in nature.

It is believed that the mechanisms of development of cough syncope are identical and fainting, which occur with an increase in intrathoracic pressure, but in other situations. These are syncopal states with laughter, sneezing, vomiting, urination and defecation, accompanied by straining, lifting the gravity, playing the wind instruments, i.e. In all cases, when the stress is made when the larynx is closed (straining). Cough syncope, as it was already noted, occurs against the backdrop of an attack of coughing most often in patients with bronchopulmonary and cardiac diseases, with the cough usually strong, loud, with a series of successive expiratory shocks. Most authors identify and describe certain constitutional and personal characteristics of patients. This is how a generalized portrait looks: this is usually men older than 35-40 years, heavy smokers with heavy body weight, broad-chested, loving to eat and drink and drink, sthenic, business, laughing loudly and loudly and heavily coughing.

The pre -syncopal period is practically absent: in some cases, there can be no clear post-syncope manifestations. Loss of consciousness does not depend on the body posture. During cough, preceding syncope, there is cyanosis of the face, swelling of the veins of the neck. During fainting, which is most often short-term (2-10 s, although it can last up to 2-3 min), convulsive twitching is possible. Skin, as a rule, gray-cyanotic color; abundant sweating of the patient is noted.

A characteristic feature of these patients is the fact that syncope can not, as a rule, be reproduced or provoked by the trial of Valsalva, which, as is known, models in a certain sense the pathogenetic mechanisms of syncope. It is sometimes possible to cause hemodynamic disturbances or even fainting by applying a sample of pressure on the carotid sinus, which allows some authors to regard cough syncope as a kind of variant of the carotid sinus hypersensitivity syndrome.

Diagnosis usually presents no difficulties. It should be remembered that in situations where there are pronounced pulmonary diseases and a severe cough, patients may not complain of fainting, especially if they are short-lived and rare. In these cases, active inquiry is important. The connection between syncope and cough, peculiarities of the constitution of the patient's personality, the severity of parasyncopal phenomena, and the gray-cyanotic complexion during loss of consciousness are of decisive diagnostic significance.

Differential diagnosis requires a situation where a cough can be a nonspecific provoking agent of syncope in patients with orthostatic hypotension and in the presence of occlusive cerebrovascular diseases. In these cases, the clinical picture of the disease is different than with cough syncope: cough is not the only and leading factor that provokes the onset of syncope, but is only one of such factors.

[5], [6], [7]

Syncope (syncope) states when swallowing

Reflex syncopal conditions associated with increased vagal nerve activity and (or) increased sensitivity of cerebral mechanisms and cardiovascular system to vagal influences include syncope caused by ingestion of food.

The pathogenesis of such syncopes is attributed to the majority of authors with the stimulation of sensitive afferent fibers of the vagus nerve system, which lead to the activation of the vasovagal reflex, ie, an efferent discharge is carried out along the motor fibers of the vagus nerve and causes a cardiac arrest. There is also an idea of a more complex pathogenetic organization of these mechanisms in situations of fainting with swallowing, namely, the formation of an interorganic multineuronal pathological reflex against the background of dysfunction of the midline structures of the brain.

The class of vasovagal syncope is quite large: they are observed in diseases of the esophagus, larynx, mediastinum, with distension of the internal organs, irritation of the pleura or peritoneum; can occur when performing such diagnostic manipulations as esophagogastroscopy, bronchoscopy, intubation. The occurrence of syncopal conditions associated with swallowing and in practically healthy individuals is described. Syncopal conditions during swallowing are most often found in patients with esophageal diverticula, cardiospasm, esophagus stenosis, hiatal hernia, achalasia cardia. In patients with glossopharyngeal neuralgia, swallowing can cause pain paroxysm with subsequent syncope. A similar situation will be considered separately in the appropriate section.

Symptoms resemble manifestations of vasodepressor (simple) syncope; the difference is that there is a clear connection with eating and swallowing, and with the fact that in special studies (or when provoked) blood pressure does not decrease and there is a period of asystole (cardiac arrest).

Two variants of syncope associated with the act of swallowing should be distinguished: the first variant is the appearance of syncope in persons with the above pathology of the gastrointestinal tract without diseases of other systems, in particular cardiovascular; the second variant, which occurs more often, is the presence of a combined pathology of the esophagus and heart. As a rule, it is a question of angina, transferred myocardial infarction. There are syncope, as a rule, against the prescription of digitalis preparations.

The diagnosis does not cause great difficulties when there is a clear connection between the act of swallowing and the onset of a syncopal condition. In this case, one patient may have other provoking factors due to the stimulation of certain zones during probing the esophagus, its extension, etc. In these cases, as a rule, similar manipulations are performed with simultaneous registration of the ECG.

A great diagnostic value is the fact of possible prevention of syncopal conditions by pre-prescribing atropine agents.

Nicturic syncopation (syncope)

Fainting with urination is a prime example of syncopal conditions with a polyfactor pathogenesis. Nicturic syncopation due to the multiplicity of factors of pathogenesis is attributed to situational faints or to a class of fainting at night. As a rule, nicturic syncope occurs after or (less often) during urination.

The pathogenesis of syncope associated with urination is not fully understood. Nevertheless, the role of a number of factors is relatively obvious: they include the activation of vagal influences and the emergence of arterial hypotension as a result of bladder emptying (a similar reaction is also characteristic of healthy bladder), the activation of baroreceptor reflexes as a result of delay in breathing and straining (especially during defecation and urination); extensor setting of the trunk, making it difficult to return venous blood to the heart. The phenomenon of getting up from bed is also important (which is essentially an orthostatic load after a long horizontal position), the predominance of hyperparasympathicotonia at night and other factors. When examining such patients, the presence of signs of hypersensitivity of the carotid sinus, the transfer of craniocerebral injuries in the past, the recent transfer of somatic diseases, asthenizing the body, often indicate the intake of alcoholic beverages on the eve of fainting are often determined. Most often, pre -syncopal manifestations are absent or slightly expressed. The same should be said for the post-syncope period, although some researchers note the presence of asthenic and anxiety disorders in patients after syncope. Most often, the duration of a loss of consciousness is small, there are rarely convulsions. In most cases, syncopation develops in men after 40 years, usually at night or early in the morning. Part of the patients, as noted, indicate the intake of alcohol on the eve. It is important to emphasize that syncopal states can be associated not only with urination, but also with defecation. Often, the onset of syncope during the implementation of these acts raises the question of whether urination and defecation are the background on which a syncope has occurred, or it is an epileptic seizure manifested by the appearance of an aura, expressed by urge to urinate.

Diagnosis is difficult only in cases where nocturnal syncope causes suspicion of their possible epileptic genesis. Careful analysis of clinical manifestations, EEG-study with provocation (light stimulation, hyperventilation, sleep deprivation) make it possible to clarify the nature of nocturnal syncopation. If diagnostic difficulties remain after the performed studies, an EEG study is shown during a night's sleep.

Syncope for neuralgia of the glossopharyngeal nerve

It should be noted two pathological mechanisms underlying this syncope: vasodepressor and cardioinhibitory. In addition to a certain connection between glossopharyngeal neuralgia and the emergence of vagotonic discharges, the hypersensitivity of the carotid sinus, which is often encountered in these patients, is also important.

Clinical picture. Most syncope occurs as a result of an attack of glossopharyngeal neuralgia, which is both a provoking factor and an expression of a peculiar presyncopal state. The pain is intense, burning, localized at the root of the tongue in the tonsil, soft palate, pharynx, sometimes radiating to the neck and angle of the lower jaw. The pain suddenly and suddenly disappears. Characteristic of the presence of trigger zones, the irritation of which provokes a painful attack. Most often, the onset of an attack is associated with chewing, swallowing, speech or yawning. Duration of a pain attack from 20-30 seconds to 2-3 minutes. He ends up with a syncope, which can proceed either without convulsive twitching, or accompanied by convulsions.

Outside painful attacks, patients tend to feel satisfactory, in rare cases, severe dull pain may persist. These syncopes are rare, mostly in people over 50 years old. Massage of the carotid sinus in a number of cases causes short-term tachycardia, asystole or vasodilation in patients and fainting without painful attacks. Trigger zone can be located in the external auditory canal or in the mucous membrane of the nasopharynx, so manipulation in these areas provokes a painful attack and fainting. Preliminary appointment of drugs atropine series prevents the appearance of syncope.

Diagnosis, as a rule, does not cause difficulties. The connection of syncope with glossopharyngeal neuralgia, the presence of signs of carotid sinus hypersensitivity are reliable diagnostic criteria. There is an opinion in the literature that syncopal states can rarely occur in trigeminal neuralgia.

Hypoglycemic syncope (syncope)

Reducing the sugar concentration below 1.65 mmol / l usually leads to impaired consciousness and the appearance of slow waves on the EEG. Hypoglycemia, as a rule, is combined with hypoxia of brain tissue, and the body's reactions in the form of hyperinsulinemia and hyper-adrenalinemia cause various vegetative manifestations.

Most often, hypoglycemic syncopal conditions are observed in patients with diabetes mellitus, congenital intolerance to fructose, in patients with benign and malignant tumors, in the presence of organic or functional hyperinsulinism, with alimentary deficiency. In patients with hypothalamic insufficiency and vegetative lability, blood glucose fluctuation can also be observed, which can lead to the indicated changes.

There are two principal types of syncopal conditions that can occur in hypoglycemia:

• true hypoglycemic syncope, in which the leading pathogenetic mechanisms are hypoglycemic, and
• vasodepressor syncope, which can occur against a background of hypoglycemia.

Apparently, in clinical practice, most often we are talking about a combination of these two types of syncopal states.

True hypoglycemic syncope (syncope)

The name "syncope", or syncope, for this group of conditions is rather conditional, as the clinical manifestations of hypoglycemia can be very diverse. Speech can go about the changed consciousness at which on the foreground sleepiness, disorientation, an amnesia or, on the contrary, a condition of psychomotor exaltation act with aggression, delirium, etc. At the same time the degree of the changed consciousness can be various. Typical are vegetative disorders: severe sweating, internal shaking, oznobopodobny hyperkinesis, weakness. A characteristic symptom is an acute sense of hunger. Against the backdrop of a disturbed consciousness, which occurs relatively unobtrusively, normal readings of the pulse and arterial pressure are ascertained, the independence of the disturbance of consciousness from the position of the body. In this case, neurologic symptoms can be observed: diplopia, hemiparesis, a gradual transition of "fainting" to a coma. In these situations, hypoglycaemia is found in the blood; the introduction of glucose causes a dramatic effect: all manifestations disappear. The duration of loss of consciousness may be different, but for the hypoglycemic state is usually more often a long duration.

Vaso-depressor variant of hypoglycemic syncope

The altered state of consciousness (drowsiness, inhibition) and pronounced vegetative manifestations (weakness, sweating, hunger, trembling) form the real conditions for the occurrence of the usual stereotypic vasodepressor syncope. It should be emphasized that an important provocative moment is the presence of the phenomenon of hyperventilation in the structure of vegetative manifestations. The combination of hyperventilation and hypoglycemia dramatically increases the likelihood of a syncopal condition.

It should also be remembered that in patients with diabetes, peripheral vegetative fibers (progressive progressive vegetative failure syndrome) can be damaged, which causes disturbance of vascular tone regulation by the type of orthostatic hypotension. As the provoking factors most often appear physical stress, fasting, the period after eating food or sugar (immediately or after 2 hours), an overdose in the treatment of insulin.

For the clinical diagnosis of hypoglycemic syncope, the analysis of the pre-syncopal condition is of great importance. An important role is played by the altered consciousness (and even behavior) in combination with characteristic vegetative disorders (severe weakness, hunger, sweating and severe tremor) without distinct hemodynamic indices in a number of cases and the relative duration of such a condition. Loss of consciousness, especially in cases of true hypoglycemic syncope, can last several minutes, with the possibility of convulsions, hemiparesis, transition to hypoglycemic coma.

Most often the consciousness returns gradually, the post-syncopal period is characterized by a pronounced asthenia, adynamia, vegetative manifestations. It is important to find out whether the patient suffers from diabetes and whether he is treated with insulin.

Syncopal states of a hysterical nature

Hysterical syncopation is much more common than it is diagnosed, their frequency is approaching the frequency of simple (vasodepressor) syncope.

The term "syncope", or "faint", and in this particular case is quite conventional, but vasodepressor phenomena can occur in such patients quite often. In this regard, there are two types of hysterical syncopal states:

• hysterical pseudosyncope (pseudo-syncope) and
• Syncopal states as a result of a complicated conversion.

In modern literature, the term "pseudo-fits" has been established. This means that the patient has paroxysmal manifestations in sensory, motor, autonomic disorders, as well as disorders of consciousness reminiscent of epileptic seizures, however, which are hysterical in nature. By analogy with the term "pseudo-fit", the term "pseudo-syncope", or "pseudo-fainting", indicates a certain identity of the phenomenon itself with the clinical picture of simple fainting.

Hysterical pseudosyncope

A hysterical pseudosyncope is a conscious or unconscious form of the patient's behavior, which is essentially a bodily, symbolic, nonverbal form of communication reflecting a deep or obvious psychological conflict of the most neurotic type and having a "facade", a "form" of syncopal syncope. It should be said that such a seemingly unusual way of psychological expression and self-expression in certain epochs was a form of expression of strong emotions accepted in society ("the princess lost her senses").

The presyncopal period can be of different duration, and sometimes absent. It is generally accepted that for hysterical fainting, at least two conditions are required: the situation (conflict, drama, etc.) and the audience. In our opinion, the most important thing is the organization of reliable information about the "fainting" of the necessary person. Therefore, syncope is possible in a "low-income" situation, in the presence of only his child or mother, etc. The most valuable for diagnosis is the analysis of the "syncope" itself. The duration of loss of consciousness can be different - seconds, minutes, hours. When it comes to watches, it's more correct to talk about "hysterical hibernation." During the disturbed consciousness (which may be incomplete, which patients often tell after leaving the "fainting"), there may be various convulsive manifestations, often extravagant, pretentious. An attempt to open the eyes of the patient sometimes meets violent resistance. As a rule, the pupils respond to the light normally, in the absence of the motor phenomena mentioned above, the skin of normal color and moisture, heart rate and blood pressure, ECG and EEG are within normal limits. The exit from the "unconscious" state, as a rule, is rapid, which resembles the way out of hypoglycemic fainting after intravenous glucose administration. The general condition of the patients is most often satisfactory, sometimes the patient's calm attitude towards the event (the syndrome of perfect indifference) is observed, which contrasts sharply with the state of people (most often close) who observed the syncope.

For the diagnosis of a hysterical pseudosyncope, it is very important to conduct a deep psychological analysis to identify the patient's psychogenesis. It is important to find out whether the patient has had similar conversions in the history (most often in the form of so-called hysterical stigmas: emotional disappearance of the voice, visual impairment, sensitivity, movements, back pain, etc.); it is necessary to establish the age, the onset of the disease (hysterical disorders most often begin in adolescence). It is important to exclude cerebral and somatic organic pathology. However, the most reliable criterion for diagnosis is the analysis of the syncope itself with the identification of the above features.

Treatment includes carrying out of psychotherapeutic actions in a combination to psychotropic agents.

Syncopal states as a result of complicated conversion

If the patient has a faint of hysteria, this does not mean that fainting is always hysterical. The likelihood of a simple (vasodepressor) syncope in a patient with hysterical disorders is apparently the same as that of another, healthy person or in a patient with autonomic dysfunction. However, hysterical mechanisms can form certain conditions, which in many ways contribute to the appearance of syncopal conditions by other mechanisms than those described above in patients with hysterical pseudosyncopies. The point is that conversion motor (demonstrative) seizures, accompanied by pronounced autonomic disorders, lead to the appearance of syncopal conditions as a result of this autonomic dysfunction. Loss of consciousness, therefore, comes secondarily and is associated with vegetative mechanisms, and not according to the program of the usual scenario of hysterical behavior. A typical variant of the "complicated" conversion is the syncopal condition due to hyperventilation.

In clinical practice, one patient may have combinations of the two types of syncope. The consideration of different mechanisms allows for more accurate clinical analysis and more adequate treatment.

Epilepsy

There are certain situations when doctors are faced with the question of differential diagnosis between epilepsy and syncopal conditions.

Such situations can be:

1. the patient experiences convulsions during convulsions (convulsive syncope);
2. in a patient with syncopal conditions in the interictal period, paroxysmal activity on the EEG is revealed;
3. a patient with epilepsy has loss of consciousness, proceeding according to the "program" of fainting.

It should be noted that convulsions during the loss of consciousness with syncopal conditions appear, as a rule, with severe and prolonged paroxysms. With syncopation, the duration of seizures is less than in epilepsy, their clarity, severity, and changes in tonic and clonic phases are less distinct.

In the EEG study in the interictal period in patients with syncopal conditions quite often there are changes of a non-specific nature, indicating a decrease in the threshold of convulsive activity. Such changes can lead to erroneous diagnosis of epilepsy. In these cases, an additional EEG study is needed after a previous night's sleep deprivation or a nighttime sleep study. When detecting specific epileptic signs (peak-wave complexes) on the daily EEG and night polygram, one can think of the patient having epilepsy (in accordance with the clinical manifestations of paroxysm). In other cases, when examining during the day or during a night's sleep in patients with syncopal conditions, various forms of abnormal activity are detected (bilateral outbursts of high-amplitude sigma and delta activity, hypersynchronous sleep spindles, acute waves, peaks), the possibility of cerebral hypoxia consequences , especially in patients with frequent and severe fainting. The view that the detection of these phenomena automatically leads to the diagnosis of epilepsy seems to be incorrect, given that the epileptic focus can participate in the pathogenesis of syncope, contributing to the violation of central vegetative regulation.

A difficult and difficult question is the situation when a patient with epilepsy has paroxysms, reminiscent of the phenomenological syncope. There are three options.

The first option is that the loss of consciousness of the patient is not accompanied by cramps. Speech in this case can go about non-convulsive forms of epileptic seizures. However, taking into account other signs (anamnesis, provoking factors, the nature of the disorders before the loss of consciousness, well-being after the return of consciousness, EEG-study) allows us to distinguish this type of seizures, rarely found in adults, from syncopal conditions.

The second option is that syncopal paroxysm is fainting in form (by phenomenological characteristics). This formulation of the question is expressed in the concept of the "syncope-like form of epilepsy", most elaborated by LG Erokhina (1987). The essence of this concept is that the syncopal conditions encountered in patients with epilepsy, despite their phenomenological proximity to simple faints (for example, the presence of such provoking factors as staying in a stuffy place, long standing, painful irritation, the ability to prevent syncope by taking a sedentary or horizontal position, drop in blood pressure during loss of consciousness, etc.) are postulated as having an epileptic genesis. For a syncope-like form of epilepsy, a number of criteria are singled out: the inconsistency of the nature of the provoking factor of the severity of the paroxysm, the emergence of a series of paroxysms without provoking factors, the possibility of losing consciousness in any position of the patient and at any time of the day, the presence of post-paroxysmal deafness, disorientation, a tendency to serial paroxysms. It is emphasized that the diagnosis of syncope-like epilepsy is possible only with dynamic observation with EEG control.

The third variant of fainting paroxysms in patients with epilepsy may be due to the fact that epilepsy forms certain conditions for the occurrence of simple (vasodepressor) fainting. It was emphasized that the epileptic focus could significantly destabilize the state of regulatory central vegetative centers in exactly the same way as other factors, namely, hyperventilation and hypoglycemia. In principle, there are no contradictions in the fact that a patient suffering from epilepsy has syncopal states according to the classical "program" of syncope, which have a "syncopal" and not "epileptic" genesis. Of course, it is also acceptable to assume that a simple syncope in a patient with epilepsy provokes a real epileptic seizure, but this requires a certain "epileptic" pre-preparedness of the brain.

In conclusion, the following should be noted. In deciding the question of the differential diagnosis between epilepsy and syncope, the initial prerequisites on which these or other physicians or researchers stand are of great importance. There may be two approaches. The first, quite frequent, is the consideration of any fainting in terms of its possible epileptic nature. Such an extended treatment of the phenomenon of epilepsy is widely represented in the environment of clinical neurologists, and this, apparently, is associated with a more developed concept of epilepsy compared with an immeasurably fewer studies dealing with the problem of syncopal states. The second approach is that the real clinical picture should be the basis for the formation of pathogenetic reasoning, and paroxysmal changes in the EEG are not the only possible explanation for pathogenetic mechanisms and the nature of the disease.

[8], [9], [10], [11], [12], [13]

Cardiogenic syncope

In contrast to neurogenic syncopation, the idea of cardiogenic syncope has received great development in recent years. This is due to the fact that the emergence of new research methods (24-hour monitoring, electrophysiological studies of the heart, etc.) made it possible to establish more accurately the role of cardiac pathology in the genesis of a number of syncope. In addition, it became apparent that a number of syncopal states of cardiogenic nature is the cause of sudden death, which has been so widely studied in recent years. Long-term prospective studies have shown that the prognosis In patients with syncopal states of cardiogenic nature is significantly worse than in patients with other variants of syncope (including fainting of unknown etiology). Mortality among patients with cardiogenic syncope within one year is 3 times higher than in patients with other types of syncope.

Loss of consciousness in cardiogenic syncope occurs as a result of a drop in cardiac output below the critical level necessary for effective blood flow in the vessels of the brain. The most common causes of a transient decrease in cardiac output are two classes of illnesses-those associated with a mechanical obstruction to blood flow and cardiac rhythm disturbances.

Mechanical obstruction to blood flow

1. Aortic stenosis leads to a sharp drop in blood pressure and the onset of syncope, especially during physical exertion, when vasodilation occurs in the muscles. Stenosis of the aortic orifice prevents an adequate increase in cardiac output. Syncopal states in this case are an absolute indication for surgical intervention, since the life span of such patients without surgery does not exceed 3 years.
2. Hypertrophic cardiomyopathy with obstruction (idiopathic hypertrophic subaortic stenosis) causes the appearance of a syncope along the same mechanisms, but obstruction is dynamic and can be caused by the use of vasodilators and diuretics. Fainting can also occur in patients with hypertrophic cardiomyopathy without obstruction: they do not occur during the load, but at the time of its termination.
3. Stenosis of the pulmonary artery with primary and secondary pulmonary hypertension leads to the appearance of syncopal conditions during exercise.
4. Congenital heart defects can cause syncope in physical exertion, which is associated with an increase in the discharge of blood from the right into the left ventricle.
5. Thromboembolism of the pulmonary artery often leads to syncopal conditions, especially with massive embolism, which causes obstruction of more than 50% of the pulmonary blood flow. Similar situations occur after fractures or surgical interventions on the lower limbs and pelvic bones, with immobilization, prolonged bed rest, with circulatory insufficiency and atrial fibrillation.
6. Atrialmix and globular thrombus in the left atrium in patients with mitral stenosis may also in a number of cases be the cause of syncopal conditions that usually occur when the position of the body changes.
7. Cardiac tamponade and an increase in intrapericardial pressure complicate the diastolic filling of the heart, while the cardiac output decreases and a syncopal condition arises.

[14]

Heart rhythm disturbance

Bradycardia. Dysfunction of the sinus node manifests a pronounced sinus bradycardia and so-called pauses - periods of absence of teeth on the ECG, during which there is an asystole. Criteria for dysfunction of the sinus node with daily monitoring of the ECG are sinus bradycardia with a minimum heart rate within a day of less than 30 per 1 minute (or less than 50 per minute in the daytime) and sinus pauses lasting more than 2 seconds.

The organic lesion of the myocardium of the atria in the area of the sinus node location is designated as syndrome of weakness of the sinus node.

Atrioventricular blockade of II and III degree may be the cause of syncopal conditions in the occurrence of asystole with a duration of 5-10 s or more with a sudden decrease in heart rate to 20 in 1 min or less. A classic example of syncopal states of arrhythmic origin are Adams-Stokes-Morganya attacks.

Data obtained in recent years have revealed that bradyarrhythmias, even in the presence of syncopal conditions, are rarely the cause of sudden death. In most cases, the cause of sudden death is ventricular tachyarrhythmias or myocardial infarction.

Tachyarrhythmias

Fainting states are observed with paroxysmal tachyarrhythmias. In supraventricular tachyarrhythmias, syncope occurs usually at a heart rate of more than 200 in 1 min, most often as a result of atrial fibrillation in patients with ventricular hyperexcitation syndrome.

Most syncope states are observed with ventricular tachyarrhythmia such as "pirouette" or "dance of dots", when waveform changes in the polarity and amplitude of the ventricular complexes are recorded on the ECG. In the interictal period, such patients have an extension of the QT interval, which in some cases can be congenital.

The most common cause of sudden death is precisely the ventricular tachycardia, which translates into ventricular fibrillation.

Thus, cardiogenic causes occupy a large place in the problem of syncopal states. The neurologist should always recognize even the minimal probability of the patient having syncopal conditions of cardiogenic nature.

The erroneous assessment of cardiogenic syncope as having a neurogenic nature can lead to tragic consequences. Therefore, a high "index of suspicion" on the possibility of a cardiogenic nature of syncopation should not leave a neurologist even in cases when the patient received a polyclinic consultation of a cardiologist and there are results of a conventional ECG study. When referring a patient to a consultation with a cardiologist, it is always necessary to clearly articulate the purpose of the consultation, identifying those "doubts", the ambiguities in the clinical picture that raise suspicions that the patient has a cardiogenic cause of syncopal conditions.

Suspicion of a patient having a cardiogenic cause of syncope can cause the following symptoms:

1. Cardiological history in the past or recently (the presence of rheumatism in the history, follow-up and preventive treatment, the presence of patients with complaints from the cardiovascular system, treatment with a cardiologist, etc.).
2. Late debut of syncopal conditions (after 40-50 years).
3. The suddenness of loss of consciousness without pre-syncopal reactions, especially when the probability of orthostatic hypotension is excluded.
4. The sensation of "interruptions" in the heart in the pre-syncopal period, which may indicate an arrhythmic genesis of syncopal conditions.
5. The connection between the onset of syncope with physical exertion, the cessation of physical activity and the change in body position.
6. Duration of episodes of loss of consciousness.
7. Cyanosis of the skin in the period of loss of consciousness and after it.

The presence of these and other indirect symptoms should cause a neurologist to suspect a possible cardiogenic character of the syncopal condition.

The elimination of the cardiogenic cause of syncopal conditions is of great practical importance due to the fact that this class of syncope is most prognostically unfavorable due to the high risk of sudden death.

Syncope in vascular lesions of the brain

Short-term loss of consciousness in elderly people are most often associated with the defeat (or compression) of vessels supplying the brain. An important feature of syncope in these cases is a significantly rare isolated syncope without concomitant neurological symptoms. The term "syncopation" in this context, again, is sufficiently conditional. Essentially, it is a transient disorder of the cerebral circulation, one of the signs of which is loss of consciousness (a syncopal form of a transient cerebral circulation disorder).

Special studies of vegetative regulation in such patients allowed us to establish that the vegetative profile in them is identical to that of the subjects; apparently, this indicates other, mostly "non-vegetative" mechanisms of pathogenesis of this class of disorders of consciousness.

The most common loss of consciousness occurs in the defeat of the main vessels - vertebral and carotid arteries.

Vascular vertebrobasilar insufficiency is the most common cause of syncope in patients with vascular diseases. Most often, the causes of lesions of vertebral arteries are atherosclerosis or processes leading to compression of the arteries (osteochondrosis), deforming spondylosis, anomalies in the development of the vertebrae, spondylolisthesis of the cervical spine. Of great importance are the anomalies of the development of the vessels of the vertebrobasilar system.

The clinical feature of the appearance of syncope is the sudden development of syncope following the movement of the head to the sides (Unterharnsteiddt syndrome) or back (syndrome of the Sistine Chapel). The pre-focal period may be absent or be very short; there is severe dizziness, pain in the neck and occiput, marked general weakness. In patients during syncope or after syncope there may be signs of trunk dysfunction, mild boulevard disorders (dysphagia, dysarthria), ptosis, diplopia, nystagmus, ataxia, and sensitive disorders. Pyramidal disorders in the form of light hemi or tetraparesis are rare. The above symptoms can be preserved in the form of microsymptoms in the interictal period, during which the signs of vestibular-stem cell dysfunction (instability, dizziness, nausea, vomiting) often prevail.

An important feature of vertebrobasilar syncope is their possible combination with so-called drop-attacks (sudden decrease of postural tone and drop of a patient without loss of consciousness). At the same time, the patient's fall is not due to dizziness or a sense of instability. The patient falls with absolutely clear consciousness.

The variability of clinical manifestations, the two-sidedness of stem symptoms, the alteration of neurological manifestations in cases of unilateral neurological signs accompanying syncope, the presence of other signs of cerebral vascular insufficiency, along with the results of paraclinical methods of investigation (ultrasound Dopplerography, radiography of the spine, angiography) - all this makes it possible to correctly diagnose.

Vascular insufficiency in the pool of carotid arteries (most often as a result of occlusion) in some cases can lead to loss of consciousness. In addition, patients have episodes of impaired consciousness, which they describe mistakenly as dizziness. Essential is the analysis of the "environment" of the mine, which is present in patients. Most often, along with the loss of consciousness in the patient, transient hemiparesis, hemi-hemesthesia, hemianopsia, epileptic seizures, headache, etc. Are observed.

The key for diagnosis is the weakening of the pulsation of the carotid artery on the opposite side of the paresis (asphygene pyramidal syndrome). When pressing the opposite (healthy) carotid artery focal symptoms increase. As a rule, lesions of carotid arteries are rarely found in isolation and are most often combined with the pathology of vertebral arteries.

It is important to note that short-term episodes of loss of consciousness can occur in hypertensive and hypotonic diseases, migraines, infectious-allergic vasculitis. G.Akimov et al. (1987) singled out similar situations and designated them as "dyscirculatory syncopal states."

Loss of consciousness in the elderly, the presence of concomitant neurological manifestations, paraclinical research data pointing to the pathology of the cerebral vascular system, the presence of signs of degenerative changes in the cervical spine, allow the neurologist to assess the nature of syncopal conditions as associated primarily with cerebrovascular mechanisms, in contrast to syncope in which the leading pathogenetic mechanisms are disorders in the links of the autonomic nervous system.