Neurogenic syncope (syncope)

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

Currently, there is a tendency to consider fainting as a paroxysmal disorder of consciousness. In this regard, it is preferable to use the term "syncope", which implies a broader understanding of the possible mechanisms of pathogenesis of this condition than only the concept of anoxic and hypoxic, which are associated with acute cerebral circulatory failure in the pathogenesis of these conditions, designated as fainting. It is also necessary to take into account the existence of such a concept as "collapse", which denotes a vascular-regulatory disorder, manifested by a paroxysmal fall, but loss of consciousness is not necessary.

Usually, syncopal states are preceded in most cases by dizziness, darkening of the eyes, ringing in the ears, and a feeling of "inevitable fall and loss of consciousness." In cases where the above symptoms appear, and loss of consciousness does not develop, we are talking about presyncopal states, or lipothymia.

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

Symptoms of fainting (syncopal states), despite the presence of a number of differences, are to a certain extent quite stereotypical. Syncope is considered as a process developed in time, therefore in most cases it is possible to distinguish manifestations preceding the actual fainting state and the period following it. H. Gastaut (1956) designated such manifestations as parasyncopal. O. Corfariu (1971), O. Corfariu, L. Popoviciu (1972) - as pre- and post-attack. N. K. Bogolepov et al. (1968) distinguished three periods: presyncopal state (pre-syncope, or lipothymia); actual syncope, or fainting, and the postsyncopal period. Within each period, a different degree of expression and severity is distinguished. Presyncopal manifestations preceding loss of consciousness usually last from several seconds to 1-2 minutes (most often from 4-20 seconds to 1-1.5 minutes) and are manifested by a feeling of discomfort, nausea, cold sweat, blurred vision, "fog" before the eyes, dizziness, tinnitus, nausea, pallor, a feeling of imminent fall and loss of consciousness. Some patients experience a feeling of anxiety, fear, a feeling of shortness of breath, palpitations, a lump in the throat, numbness of the lips, tongue, fingers. However, these symptoms may be absent.

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

Postsyncopal period - usually lasts a few seconds, and the patient quickly comes to his senses, orienting himself in space and time quite correctly. Usually the patient is anxious, frightened by what happened, pale, adynamic; tachycardia, rapid breathing, pronounced general weakness and fatigue are noted.

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

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

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Vasodepressor syncope

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

Simple vasodepressor syncope is the most common type of short-term loss of consciousness and, according to various researchers, accounts for 28 to 93.1% of patients with syncopal states.

Symptoms of vasodepressor syncope (fainting)

Loss of consciousness usually does not occur instantly: as a rule, it is preceded by a distinct presyncopal period. Among the provoking factors and conditions for the occurrence of syncopal states, the most common are afferent reactions of the stress type: fright, anxiety, fear associated with unpleasant news, accidents, the sight of blood or fainting in others, preparation, expectation and performance of blood sampling, dental procedures and other medical manipulations. Syncopes often occur when pain (severe or minor) occurs during the above-mentioned manipulations or with pain of visceral origin (gastrointestinal, chest, liver and renal colic, etc.). In some cases, direct provoking factors may be absent.

The most common conditions that contribute to the onset of fainting are the orthostatic factor (standing for a long time in transport, in a queue, etc.);

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

During fainting, the patient is usually motionless, the skin is pale or gray-earthy, cold, covered in sweat. Bradycardia and extrasystole are detected. Systolic blood pressure drops to 55 mm Hg. EEG examination reveals slow delta and delta-range waves of high amplitude. The horizontal position of the patient leads to a rapid increase in blood pressure, in rare cases hypotension can last for several minutes or (as an exception) even hours. Prolonged loss of consciousness (more than 15-20 sec) can lead to tonic and (or) clonic seizures, involuntary urination and defecation.

Postsyncopal state may vary in duration and severity, accompanied by asthenic and vegetative manifestations. In some cases, the patient's getting up leads to repeated fainting with all the symptoms described above.

Examination of patients allows us to detect a number of changes in their mental and vegetative spheres: various types of emotional disorders (increased irritability, phobic manifestations, low mood, hysterical stigmas, etc.), vegetative lability and a tendency toward arterial hypotension.

When diagnosing vasodepressor syncopes, it is necessary to take into account the presence of provoking factors, conditions for the occurrence of fainting, the period of presyncopal manifestations, a decrease in blood pressure and bradycardia during loss of consciousness, the condition of the skin in the postsyncopal period (warm and moist). An important role in diagnostics is played by the presence of manifestations of psychovegetative syndrome in the patient, the absence of epileptic (clinical and paraclinical) signs, the exclusion of cardiac and other somatic pathology.

The pathogenesis of vasodepressor syncopal states is still unclear. Numerous factors identified by researchers when studying syncopes (hereditary predisposition, perinatal pathology, the presence of vegetative disorders, a tendency to parasympathetic reactions, residual neurological disorders, etc.) cannot explain each separately the cause of loss of consciousness.

G. L. Engel (1947, 1962), based on the analysis of the biological meaning of a number of physiological reactions based on the works of Ch. Darwin and W. Cannon, put forward a hypothesis that vasodepressor syncope is a pathological reaction that occurs as a result of experiencing anxiety or fear in conditions when activity (movement) is inhibited or impossible. Blockade of the "fight or flight" reactions leads to the fact that the excess activity of the circulatory system, tuned to muscle activity, is not compensated by muscle work. The "tuning" of the peripheral vessels to intensive blood circulation (vasodilation), the lack of inclusion of the "venous pump" associated with muscle activity lead to a decrease in the volume of blood flowing to the heart, and the occurrence of reflex bradycardia. Thus, the vasodepressor reflex (drop in arterial pressure) is included, combined with peripheral vasoplegia.

Of course, as the author notes, this hypothesis is not able to explain all aspects of the pathogenesis of vasodepressor syncope. Recent studies indicate a major role in their pathogenesis of impaired cerebral activation homeostasis. Specific cerebral mechanisms of impaired regulation of the cardiovascular and respiratory systems associated with an inadequate suprasegmental program for regulating the pattern of vegetative functions are identified. In the spectrum of vegetative disorders, not only cardiovascular but also respiratory dysfunction, including hyperventilation manifestations, are of great importance for pathogenesis and symptomatogenesis.

Orthostatic syncope

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

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

Orthostatic syncope is diagnosed based on the clinical picture (connection of fainting with an orthostatic factor, instantaneous loss of consciousness without pronounced parasyncopal states); the presence of low blood pressure with a normal heart rate (absence of bradycardia, as usually occurs with vasodepressor syncope, and the absence of compensatory tachycardia, which is usually observed in healthy people). An important aid in diagnosis is a positive Schelong test - a sharp drop in blood pressure when standing up from a horizontal position with the absence of compensatory tachycardia. Important evidence of the presence of orthostatic hypotension is the absence of an increase in the concentration of aldosterone and catecholamines in the blood and their excretion with urine when standing up. An important test is a 30-minute standing test, which determines a gradual decrease in blood pressure. Other special studies are also needed to establish signs of peripheral autonomic innervation deficiency.

For the purposes of differential diagnosis, it is necessary to conduct a comparative analysis of orthostatic syncope with vasodepressor syncope. For the former, a close, rigid connection with orthostatic situations and the absence of other provocation options characteristic of vasodepressor syncope are important. Vasodepressor syncope is characterized by an abundance of psychovegetative manifestations in the pre- and post-syncopal periods, slower than in orthostatic syncope, loss and return of consciousness. Of significant importance are the presence of bradycardia during vasodepressor syncope and the absence of both brady- and tachycardia during a drop in blood pressure in patients with orthostatic syncope.

Hyperventilation syncope (fainting)

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

The peculiarity of hyperventilation syncope is that most often the phenomenon of hyperventilation in patients can be combined with hypoglycemia and pain manifestations. In patients prone to pathological vasomotor reactions, in persons with postural hypotension, the hyperventilation test can cause a pre-syncope or even a fainting state, especially if the patient is in a standing position. The introduction of 5 U of insulin to such patients before the test significantly sensitizes the test, and the impairment of consciousness occurs faster. At the same time, there is a certain connection between the level of impairment of consciousness and simultaneous changes in the EEG, as evidenced by the slow rhythms of the 5- and G-range.

It is necessary to distinguish two variants of hyperventilation syncopal states with different specific pathogenetic mechanisms:

• hypocapnic, or acapnic, variant of hyperventilation syncope;
• vasodepressor type of hyperventilation syncope. The identified variants in pure form are rare, more often one or another variant predominates in the clinical picture.

Hypocapnic (acapnic) variant of hyperventilation syncope

The hypocapnic (acapnic) variant of hyperventilation syncope is determined by its leading mechanism - the brain's reaction to a decrease in the partial pressure of carbon dioxide in the circulating blood, which, along with respiratory alkalosis and the Bohr effect (shift of the oxyhemoglobin dissociation curve to the left, causing an increase in the tropism of oxygen to hemoglobin and difficulty in its splitting off for passage into brain tissue) leads to a reflex spasm of the cerebral vessels and hypoxia of brain tissue.

Clinical features include the presence of a prolonged pre-syncope state. It should be noted that persistent hyperventilation in these situations may be an expression of either an unfolding vegetative crisis in the patient (panic attack) with a pronounced hyperventilation component (hyperventilation crisis), or a hysterical attack with increased breathing, which lead to the secondary above-mentioned shifts in the mechanism of complicated conversion. The pre-syncope state, therefore, can be quite long (minutes, tens of minutes), accompanied in vegetative crises by the corresponding mental, vegetative and hyperventilation manifestations (fear, anxiety, palpitations, cardialgia, shortness of breath, paresthesia, tetany, polyuria, etc.).

An important feature of the hypocapnic variant of hyperventilation syncope is the absence of sudden loss of consciousness. As a rule, signs of an altered state of consciousness appear at first: a feeling of unreality, strangeness of the surroundings, a feeling of lightness in the head, narrowing of consciousness. Aggravation of these phenomena ultimately leads to narrowing, reduction of consciousness and a fall of the patient. In this case, the phenomenon of flickering of consciousness is noted - alternation of periods of return and loss of consciousness. Subsequent questioning reveals the presence of various, sometimes quite vivid images in the patient's field of consciousness. In some cases, patients indicate the absence of a complete loss of consciousness and the preservation of the perception of some phenomena of the external world (for example, addressed speech) with the inability to respond to them. The duration of loss of consciousness can also be significantly longer than with simple fainting. Sometimes it reaches 10-20 or even 30 minutes. In essence, this is a continuation of the development of hyperventilation paroxysm in the supine position.

Such a duration of the phenomenon of impaired consciousness with the phenomena of flickering consciousness may also indicate the presence of a unique psychophysiological organization in an individual with a tendency to conversion (hysterical) reactions.

On examination, these patients may exhibit various types of respiratory distress - increased breathing (hyperventilation) or prolonged periods of respiratory arrest (apnea).

The appearance of patients during a disturbance of consciousness in such situations is usually little changed, and hemodynamic parameters are also not significantly disturbed. Perhaps the concept of "fainting" in relation to these patients is not entirely adequate; most likely, we are talking about a kind of "trance" altered state of consciousness as a result of the consequences of persistent hyperventilation in combination with some features of the psychophysiological pattern. However, the imperative disturbance of consciousness, the fall of patients and, most importantly, the close connection of the said disturbances with the phenomenon of hyperventilation, as well as with other, including vasodepressor, reactions in these same patients, require consideration of the discussed disorders of consciousness in this section. It should be added to this that the physiological consequences of hyperventilation, due to their global nature, can reveal and include in the pathological process other, in particular cardiac, hidden pathological changes, such as, for example, the appearance of severe arrhythmias - the result of the movement of the pacemaker into the atrioventricular node and even into the ventricle with the development of atrioventricular nodal or idioventricular rhythm.

The indicated physiological consequences of hyperventilation should apparently be correlated with another, second variant of syncopal manifestations during hyperventilation.

Vasodepressor variant of hyperventilation syncope

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

The clinical picture of this type of fainting condition consists of two important components, which determine some differences from the simple, non-hyperventilation type of vasodepressor syncope. Firstly, it is a more "rich" parasyncopal clinical picture, which is expressed in the fact that psychovegetative manifestations are significantly represented both in the pre- and post-syncopal period. Most often, these are affective vegetative manifestations, including hyperventilation. In addition, in some cases, carpopedal tetanic seizures occur, which can be mistakenly assessed as having an epileptic genesis.

As has already been said, vasodepressor syncope is essentially, in a certain sense, a stage in the development of reduced (and in some cases, expanded) vegetative, or more precisely, hyperventilation paroxysm. Loss of consciousness is a more significant event for patients and those around them, therefore, in the anamnesis, the events of the pre-syncopal period are often omitted by patients. Another important component in the clinical expression of hyperventilation vasodepressor syncope is its frequent (usually natural) combination with manifestations of the acapnic (hypocapnic) type of disorder of consciousness. The presence of elements of an altered state of consciousness in the pre-syncopal period and the phenomena of flickering of consciousness during the period of loss of consciousness in a number of cases forms an unusual clinical picture, causing a feeling of bewilderment in doctors. Thus, in patients who fainted according to the vasodepressor type, which is familiar to doctors, a certain fluctuation was observed during the fainting itself - flickering of consciousness. As a rule, doctors have the erroneous idea that these patients have leading hysterical mechanisms in the genesis of fainting states.

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

Another feature of vasodepressor hyperventilation syncopes is the presence of a wider range of provoking factors than in patients with ordinary simple fainting. Situations where the respiratory system is objectively and subjectively involved are especially significant for such patients: heat, the presence of strong odors, stuffy, closed rooms that cause phobic fears in patients with the appearance of respiratory sensations and subsequent hyperventilation, etc.

The diagnosis is made taking into account a thorough phenomenological analysis and the presence in the structure of parasyncopal and syncopal periods of 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 the diagnostic criteria for hyperventilation syndrome.

Differential diagnostics are carried out with epilepsy and hysteria. Expressed psychovegetative manifestations, the presence of tetanic seizures, a long period of impaired consciousness (which is sometimes regarded as post-seizure stunning) - all this in some cases leads to an erroneous diagnosis of epilepsy, in particular temporal epilepsy.

In these situations, a longer (minutes, tens of minutes, sometimes hours) presyncopal period than in epilepsy (seconds) helps diagnose hyperventilation syncopal states. The absence of other clinical and EEG changes characteristic of epilepsy, the absence of improvement when prescribing anticonvulsants and the presence of a significant effect when giving psychotropic drugs and (or) performing breathing correction allow us to exclude the epileptic nature of the suffering. In addition, a positive diagnosis of hyperventilation syndrome is essential.

Carotid syncope (fainting)

Carotid sinus syncope (hypersensitivity syndrome, hypersensitivity of the carotid sinus) is a fainting condition in the pathogenesis of which the leading role is played by increased sensitivity of the carotid sinus, leading to disturbances in the regulation of the heart rhythm, tone of peripheral or cerebral vessels.

In 30% of healthy people, various vascular reactions occur when pressure is applied to the carotid sinus; such reactions are even more common in patients with hypertension (75%) and in patients with arterial hypertension combined with atherosclerosis (80%). At the same time, syncopal states are observed in only 3% of patients in this group. Fainting associated with hypersensitivity of the carotid sinus most often occurs after 30 years of age, especially in elderly and senile men.

A characteristic feature of the above fainting spells is their connection with irritation of the carotid sinus. Most often, this occurs when moving the head, tilting the head back (at the barber's during shaving, looking at the stars, watching a flying airplane, looking at fireworks, etc.). Wearing tight, rigid collars or tightly tying a tie, the presence of tumor-like formations on the neck that compress the carotid sinus region are also important. Fainting can also occur during eating.

The presyncopal period may be practically absent in some patients; sometimes the condition after syncope is also poorly expressed.

In some cases, patients have a short-term but clearly expressed presyncopal state, manifested by severe fear, shortness of breath, a feeling of constriction in the throat and chest. In some patients, after the syncopal state, a feeling of unhappiness is observed, asthenia and depression are expressed. The duration of loss of consciousness may vary, most often it fluctuates within 10-60 seconds, in some patients convulsions are possible.

Within the framework of this syndrome, it is customary to distinguish three types of syncopal states: vagal type (bradycardia or asystole), vasodepressor type (decrease, fall in blood pressure with a normal heart rate) and cerebral type, when loss of consciousness associated with irritation of the carotid sinus is not accompanied by either a disturbance in heart rhythm or a drop in blood pressure.

The cerebral (central) variant of carotid syncopal states may be accompanied, in addition to disorders of consciousness, 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 apparently associated with increased sensitivity of not only the carotid sinus, but also the boulevard centers, which, incidentally, is characteristic of all variants of carotid sinus hypersensitivity.

It is important to note that, in addition to loss of consciousness, other symptoms may be observed in carotid sinus hypersensitivity syndrome, which facilitate correct diagnosis. Thus, attacks of severe weakness and even loss of postural tone by the type of cataplexy without disorders of consciousness have been described.

For diagnostics of carotid syncope, it is of fundamental importance to conduct a test with pressure on the carotid sinus area. A pseudo-positive test may be the case if in a patient with atherosclerotic lesions of the carotid arteries, compression leads essentially to compression of the carotid artery and cerebral ischemia. To avoid this fairly common error, it is imperative to first auscultate both carotid arteries. Then, in the supine position, pressure is applied to the carotid sinus (or its massage is performed) in turn. The following should be considered the criteria for diagnosing carotid sinus syndrome based on the test:

1. occurrence of a period of asystole longer than 3 s (cardioinhibitory variant);
2. a decrease in systolic blood pressure by more than 50 mm Hg or more than 30 mm Hg with the simultaneous occurrence of fainting (vasodepressor variant).

Prevention of the cardioinhibitory reaction is achieved by administering atropine, and the vasodepressor reaction is prevented by administering adrenaline.

When conducting differential diagnostics, it is necessary to distinguish between the vasodepressor variant of carotid sinus syncope and simple vasodepressor syncope. Older age, male gender, less pronounced presyncopal phenomena (and sometimes their absence), the presence of a disease causing increased sensitivity of the carotid sinus (atherosclerosis of the carotid and coronary vessels, the presence of various formations on the neck), and, finally, a close connection between the occurrence of syncope and the situation of irritation of the carotid sinus (head movements, etc.), as well as a positive test with pressure on the carotid sinus - all these factors allow differentiating the vasodepressor variant of carotid sinus syncope from simple vasodepressor syncope.

In conclusion, it should be noted that carotid hypersensitivity 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, increased sensitivity of the carotid sinus may be involved in the pathogenesis of other types of syncope of neurogenic (including psychogenic) origin.

Cough syncope (fainting)

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

Pathogenesis of cough syncope. As a result of a sharp increase in intrathoracic and intra-abdominal pressure, blood flow to the heart decreases, cardiac output falls, and conditions arise for the breakdown of cerebral circulation compensation. Other pathogenetic mechanisms are also suggested: 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. Polygraphic study of night sleep in patients with cough syncope revealed the identity of sleep pattern disorders to those observed in Pickwickian syndrome caused by dysfunction of the central brainstem formations responsible for breathing regulation and being part of the reticular formation of the brainstem. The role of breath holding, the presence of hyperventilation mechanisms, and venous circulation disorders are also discussed. For a long time, cough syncope was considered a variant of epilepsy, and was therefore called "bettolepsy". Cough was regarded either as a phenomenon that provoked an epileptic seizure or as a peculiar form of epileptic aura. In recent years, it has become clear that cough syncope is not epileptic in nature.

It is believed that the mechanisms of cough syncope development are identical to fainting, which occurs with increased intrathoracic pressure, but in other situations. These are syncopal states during laughter, sneezing, vomiting, urination and defecation, accompanied by straining, when lifting weights, playing wind instruments, i.e. in all cases when straining occurs with a closed larynx (straining). Cough syncope, as already noted, occurs against the background of a coughing attack most often in patients with bronchopulmonary and cardiac diseases, while the cough is usually strong, loud, with a series of expiratory shocks following one after another. Most authors identify and describe certain constitutional and personality characteristics of patients. Here is what the general portrait looks like: these are, as a rule, men over 35-40 years old, heavy smokers, overweight, broad-chested, loving to eat and drink well and a lot, sthenic, businesslike, laughing loudly and coughing loudly and heavily.

The presyncopal period is practically absent: in some cases, there may be no distinct postsyncopal manifestations. Loss of consciousness does not depend on the body position. During coughing preceding syncope, cyanosis of the face and swelling of the veins of the neck are observed. During fainting, which is most often short-lived (2-10 sec, although it can last up to 2-3 min), convulsive twitching is possible. The skin is usually gray-blue; profuse sweating of the patient is noted.

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

Diagnosis is usually straightforward. It should be remembered that in situations where there are severe pulmonary diseases and a strong cough, patients may not complain of fainting, especially if they are short-lived and rare. In these cases, active questioning is of great importance. The connection between syncope and cough, the constitutional features of the patient's personality, the severity of parasyncopal phenomena, and the gray-cyanotic complexion during loss of consciousness are of decisive diagnostic importance.

Differential diagnostics is required when cough can be a non-specific provoking agent of fainting 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 in cough syncopes: cough is not the only and leading factor provoking the occurrence of fainting, but is only one of such factors.

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Syncope (fainting) states when swallowing

Reflex syncopal states associated with increased activity of the vagus nerve and/or increased sensitivity of cerebral mechanisms and the cardiovascular system to vagal influences also include syncopes that occur during swallowing food.

Most authors associate the pathogenesis of such syncopes with irritation of the sensory afferent fibers of the vagus nerve system, which trigger the vasovagal reflex, i.e. an efferent discharge occurs, conducted along the motor fibers of the vagus nerve and causing cardiac arrest. There is also a concept of a more complex pathogenetic organization of these mechanisms in situations of fainting during swallowing, namely, the formation of an interorgan multineuronal pathological reflex against the background of dysfunction of the midline structures of the brain.

The class of vasovagal syncopes is quite large: they are observed in diseases of the esophagus, larynx, mediastinum, with stretching of internal organs, irritation of the pleura or peritoneum; they can occur during diagnostic manipulations such as esophagogastroscopy, bronchoscopy, intubation. The occurrence of syncopal states associated with swallowing has been described in practically healthy individuals. Syncopal states during swallowing are most often found in patients with diverticula of the esophagus, cardiospasm, stenosis of the esophagus, hernia of the esophageal opening, achalasia of the cardia. In patients with glossopharyngeal neuralgia, the act of swallowing can cause a painful paroxysm followed by syncope. We will consider such a situation separately in the corresponding section.

The symptoms resemble those of vasodepressor (simple) syncope; the difference is that there is a clear connection with food intake and the act of swallowing, as well as with the fact that during special studies (or provocation) the arterial pressure does not decrease and there is a period of asystole (cardiac arrest).

It is necessary to distinguish two variants of syncope associated with the act of swallowing: the first variant is the occurrence of fainting in persons with the above-mentioned pathology of the gastrointestinal tract without diseases of other systems, in particular the cardiovascular system; the second variant, which is more common, is the presence of a combined pathology of the esophagus and heart. As a rule, we are talking about angina pectoris, a previous myocardial infarction. Syncope usually occurs against the background of the prescription of digitalis preparations.

The diagnosis does not cause much difficulty when there is a clear connection between the act of swallowing and the occurrence of syncope. In this case, one patient may also have other provoking factors caused by irritation of certain zones during probing of the esophagus, its stretching, etc. In these cases, as a rule, such manipulations are carried out with simultaneous recording of the ECG.

The fact that syncopal conditions can be prevented by pre-administering atropine-type drugs is of great diagnostic significance.

Nocturic syncope (fainting)

Fainting states during urination are a striking example of syncopal states with multifactorial pathogenesis. Nocturic syncopes, due to the multiple factors of pathogenesis, are classified as situational syncopes or as a class of syncopes during nocturnal rising. As a rule, nocturic syncopes occur after or (less often) during urination.

The pathogenesis of fainting associated with urination has not been fully studied. However, the role of a number of factors is relatively obvious: these include activation of vagal influences and the occurrence of arterial hypotension as a result of emptying the bladder (a similar reaction is also characteristic of healthy people), activation of baroreceptor reflexes as a result of holding the breath and straining (especially during defecation and urination), and an extension position of the trunk, which complicates the return of venous blood to the heart. The phenomenon of getting out of bed (which is essentially an orthostatic load after a long horizontal position), the prevalence of hyperparasympathicotonia at night, and other factors are also important. When examining such patients, the presence of signs of carotid sinus hypersensitivity, a history of craniocerebral trauma, recent somatic diseases that asthenize the body are often determined, and drinking alcoholic beverages on the eve of fainting is often noted. Most often, presyncopal manifestations are absent or expressed insignificantly. The same should be said about the postsyncopal period, although some researchers note the presence of asthenic and anxiety disorders in patients after syncope. Most often, the duration of loss of consciousness is short, convulsions are rare. In most cases, syncope develops in men after 40 years, usually at night or early in the morning. Some patients, as noted, indicate alcohol consumption the day before. It is important to emphasize that syncopal states can be associated not only with urination, but also with defecation. Often, the occurrence of fainting during the implementation of these acts raises the question of whether urination and defecation are the background against which fainting occurred, or we are talking about an epileptic seizure, manifested by the occurrence of an aura, expressed by the urge to urinate.

The diagnosis is difficult only in cases where nocturnal syncopes raise suspicion of their possible epileptic genesis. Careful analysis of clinical manifestations, EEG examination with provocation (light stimulation, hyperventilation, sleep deprivation) allow to clarify the nature of nocturic syncopes. If diagnostic difficulties remain after the conducted studies, EEG examination during night sleep is indicated.

Syncopal conditions in neuralgia of the glossopharyngeal nerve

It is necessary to distinguish two pathological mechanisms underlying this syncope: vasodepressor and cardioinhibitory. In addition to a certain connection between glossopharyngeal neuralgia and the occurrence of vagotonic discharges, the hypersensitivity of the carotid sinus, which is often found in these patients, is also of great importance.

Clinical picture. Most often, fainting 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 area of the tonsil, soft palate, pharynx, sometimes radiating to the neck and angle of the lower jaw. The pain occurs suddenly and disappears just as suddenly. The presence of trigger zones is characteristic, the irritation of which provokes a pain attack. Most often, the onset of an attack is associated with chewing, swallowing, speech or yawning. The duration of a pain attack is from 20-30 seconds to 2-3 minutes. It ends with syncope, which can occur either without convulsive twitching or be accompanied by convulsions.

Outside of pain attacks, patients usually feel satisfactory, in rare cases severe dull pain may persist. The above syncopes are quite rare, mainly in people over 50 years of age. Carotid sinus massage in some cases causes short-term tachycardia, asystole or vasodilation and fainting without pain attacks in patients. The trigger zone may also be located in the external auditory canal or in the mucous membrane of the nasopharynx, so manipulations in these areas provoke a pain attack and fainting. Preliminary administration of atropine drugs prevents the occurrence of syncope.

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

Hypoglycemic syncope (fainting)

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

Most often, hypoglycemic syncopal states are observed in patients with diabetes mellitus, with congenital fructose intolerance, in patients with benign and malignant tumors, in the presence of organic or functional hyperinsulinism, and in alimentary insufficiency. In patients with hypothalamic insufficiency and autonomic lability, fluctuations in blood sugar levels may also be observed, which may lead to the above changes.

It is necessary to distinguish two fundamental types of syncopal conditions that can occur with hypoglycemia:

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

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

True hypoglycemic syncope (fainting)

The name "syncope" or fainting is rather arbitrary for this group of conditions, since clinical manifestations of hypoglycemia can be quite diverse. We may be talking about altered consciousness, in which drowsiness, disorientation, amnesia or, conversely, a state of psychomotor agitation with aggression, delirium, etc. come to the fore. The degree of altered consciousness may vary. Vegetative disorders are characteristic: severe sweating, internal tremors, chill-like hyperkinesis, weakness. A characteristic symptom is an acute feeling of hunger. Against the background of impaired consciousness, which occurs relatively slowly, normal pulse and blood pressure readings are noted, and the impairment of consciousness is independent of body position. Neurological symptoms may be observed: diplopia, hemiparesis, gradual transition of "fainting" to a comatose state. In these situations, hypoglycemia is detected in the blood; the introduction of glucose causes a dramatic effect: all manifestations disappear. The duration of loss of consciousness may vary, but a hypoglycemic state is most often characterized by a longer duration.

Vasodepressor variant of hypoglycemic syncope

An altered state of consciousness (drowsiness, lethargy) and pronounced vegetative manifestations (weakness, sweating, hunger, trembling) form the real conditions for the occurrence of a common stereotypical vasodepressor syncope. It should be emphasized that an important provoking moment is the presence of the hyperventilation phenomenon in the structure of vegetative manifestations. The combination of hyperventilation and hypoglycemia sharply increases the likelihood of syncope.

It is also necessary to remember that patients suffering from diabetes may have damage to peripheral vegetative fibers (progressive vegetative failure syndrome), which causes a violation of the regulation of vascular tone by the type of orthostatic hypotension. The most common provoking factors are physical stress, fasting, the period after eating or sugar (immediately or after 2 hours), overdose during insulin treatment.

For clinical diagnostics of hypoglycemic syncope, the analysis of the presyncope state is of great importance. An important role is played by altered consciousness (and even behavior) in combination with characteristic vegetative disorders (sharp weakness, feeling of hunger, sweating and pronounced tremor) without clear changes in hemodynamic parameters in some cases and the relative duration of such a state. Loss of consciousness, especially in cases of true hypoglycemic syncope, can last for several minutes, with possible convulsions, hemiparesis, transition to hypoglycemic coma.

Most often, consciousness returns gradually, the post-syncopal period is characterized by 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 hysterical nature

Hysterical syncopes occur much more frequently than they are diagnosed, their frequency approaching the frequency of simple (vasodepressor) fainting.

The term "syncope" or "fainting" is quite arbitrary in this case, but vasodepressor phenomena can be quite common in such patients. In this regard, two types of hysterical syncopal states should be distinguished:

• hysterical pseudosyncope (pseudofainting) and
• syncopal states as a result of complicated conversion.

In modern literature, the term "pseudo-seizures" has become established. This means that the patient has paroxysmal manifestations, expressed in sensory, motor, vegetative disorders, as well as disorders of consciousness, resembling epileptic seizures in their phenomenology, but having, however, a hysterical nature. By analogy with the term "pseudo-seizures", the term "pseudosyncope" or "pseudo-fainting" indicates a certain identity of the phenomenon itself with the clinical picture of simple fainting.

Hysterical pseudosyncope

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

The presyncopal period may vary in duration, and sometimes be absent. It is generally accepted that hysterical fainting requires at least two conditions: a situation (conflict, dramatic, etc.) and spectators. In our opinion, the most important thing is to organize reliable information about the "fainting" to the required person. Therefore, syncope is possible in a "sparsely populated" situation, in the presence of only one's child or mother, etc. The most valuable for diagnostics is the analysis of the "syncope" itself. The duration of loss of consciousness may vary - seconds, minutes, hours. When talking about hours, it is more correct to talk about "hysterical hibernation". During impaired consciousness (which may be incomplete, which patients often report after coming out of "fainting"), various convulsive manifestations may occur, often of an extravagant, fanciful nature. An attempt to open the patient's eyes sometimes meets with violent resistance. As a rule, the pupils react normally to light, in the absence of the motor phenomena mentioned above, the skin is of normal color and moisture, the heart rate and blood pressure, ECG and EEG are within normal limits. The exit from the "unconscious" state is usually fast, which resembles the exit from hypoglycemic syncope after intravenous administration of glucose. The general condition of patients is most often satisfactory, sometimes a calm attitude of the patient to what happened is observed (syndrome of beautiful indifference), which sharply contrasts with the state of people (usually relatives) who observed syncope.

For the diagnosis of hysterical pseudosyncope, it is of great importance to conduct a deep psychological analysis to identify the patient's psychogenesis. It is important to find out whether the patient has had similar or other conversion manifestations in his/her anamnesis (most often in the form of so-called hysterical stigmas: emotive loss of voice, impaired vision, sensitivity, movement, back pain, etc.); it is necessary to establish the age and 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 diagnostic criterion is the analysis of the syncope itself with the identification of the above features.

Treatment includes psychotherapeutic measures in combination with psychotropic drugs.

Syncopal states as a result of complicated conversion

If a hysterical patient faints, this does not mean that the fainting is always hysterical. The probability of a simple (vasodepressor) fainting in a patient with hysterical disorders is probably the same as in another, healthy person or in a patient with vegetative dysfunction. However, hysterical mechanisms can form certain conditions that largely contribute to the occurrence of syncopal states by mechanisms other than those described above in patients with hysterical pseudosyncopes. The point is that conversion motor (demonstrative) seizures, accompanied by pronounced vegetative disorders, lead to the occurrence of syncopal states as a result of the said vegetative dysfunction. Loss of consciousness occurs, therefore, secondarily and is associated with vegetative mechanisms, and not according to the program of the usual scenario of hysterical behavior. A typical variant of “complicated” conversion is syncope due to hyperventilation.

In clinical practice, one patient may experience combinations of the two types of syncope. Taking into account the various mechanisms allows for a 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 states.

Such situations may include:

1. the patient experiences convulsions (convulsive syncope) during loss of consciousness;
2. in a patient with syncopal states, paroxysmal activity is detected on the EEG during the interictal period;
3. A patient with epilepsy experiences loss of consciousness, which occurs according to the fainting “program”.

It should be noted that convulsions during loss of consciousness in syncopal states usually occur during severe and prolonged paroxysms. During syncopes, the duration of convulsions is shorter than in epilepsy, their clarity, severity, and change of tonic and clonic phases are less distinct.

During EEG examination in the interictal period in patients with syncope, nonspecific changes indicating a decrease in the seizure threshold are quite common. Such changes may lead to an erroneous diagnosis of epilepsy. In these cases, additional EEG examination after preliminary nocturnal sleep deprivation or a nocturnal polygraphic sleep study is necessary. If specific epileptic signs (peak-wave complexes) are detected in the daytime EEG and nighttime polygram, one may suspect the presence of epilepsy in the patient (subject to the clinical manifestations of the paroxysm). In other cases, when various forms of abnormal activity (bilateral bursts of high-amplitude sigma and delta activity, hypersynchronous sleep spindles, sharp waves, peaks) are detected in patients with syncope during the daytime or during nighttime sleep, the possibility of consequences of cerebral hypoxia should be discussed, especially in patients with frequent and severe fainting. The opinion that the detection of these phenomena automatically leads to a diagnosis of epilepsy seems incorrect, given that the epileptic focus can participate in the pathogenesis of fainting, contributing to the disruption of central autonomic regulation.

A complex and difficult issue is the situation when an epileptic patient experiences paroxysms that resemble fainting states in their phenomenology. Three options are possible here.

The first option is that the patient's loss of consciousness is not accompanied by convulsions. In this case, we may be talking about non-convulsive forms of epileptic seizures. However, taking into account other signs (anamnesis, provoking factors, the nature of disorders before loss of consciousness, well-being after regaining consciousness, EEG examination) allows us to differentiate this type of seizure, which is rare in adults, from syncopal states.

The second option is that the syncopal paroxysm is fainting in form (according to phenomenological characteristics). This formulation of the question is expressed in the concept of the "fainting-like form of epilepsy", developed in most detail by L. G. Erokhina (1987). The essence of this concept is that syncopal states occurring in patients with epilepsy, despite their phenomenological closeness to simple fainting (for example, the presence of such provoking factors as being in a stuffy room, prolonged standing, painful stimuli, the ability to prevent syncope by taking a sitting or horizontal position, a drop in blood pressure during loss of consciousness, etc.), are postulated as having an epileptic genesis. A number of criteria are distinguished for the fainting-like form of epilepsy: inconsistency of the nature of the provoking factor with the severity of the paroxysm that has arisen, occurrence of a number of paroxysms without provoking factors, possibility of loss of consciousness in any position of the patient and at any time of the day, presence of post-paroxysmal stupor, disorientation, tendency to serial occurrence of paroxysms. It is emphasized that the diagnosis of fainting-like epilepsy is possible only with dynamic observation with EEG control.

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

In conclusion, the following should be noted. In solving the problem of differential diagnosis between epilepsy and fainting, the initial assumptions of certain doctors or researchers are of great importance. There can be two approaches. The first, quite common, is to consider any fainting from the point of view of its possible epileptic nature. Such an expanded interpretation of the phenomenon of epilepsy is widely represented among clinical neurologists, and this is apparently due to the greater development of the concept of epilepsy compared to the immeasurably smaller number of studies concerning the problem of syncopal states. The second approach is that the real clinical picture should underlie the formation of pathogenetic reasoning, and paroxysmal changes in the EEG are not the only possible explanation of the pathogenetic mechanisms and nature of the disease.

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

Cardiogenic syncope

In contrast to neurogenic syncope, the concept of cardiogenic syncope has been greatly developed in recent years. This is due to the fact that the emergence of new research methods (daily monitoring, electrophysiological studies of the heart, etc.) has made it possible to more accurately establish the role of cardiac pathology in the genesis of a number of syncopes. In addition, it has become obvious that a number of syncopal states of cardiogenic origin are 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 origin is significantly worse than in patients with other types of syncope (including syncope 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 required for effective blood flow in the cerebral vessels. The most common causes of transient decrease in cardiac output are two classes of diseases - those associated with mechanical obstruction of blood flow and heart rhythm disorders.

Mechanical obstruction of blood flow

1. Aortic stenosis leads to a sharp drop in blood pressure and fainting, especially during physical exertion, when vasodilation occurs in the muscles. Stenosis of the aortic orifice prevents an adequate increase in cardiac output. Syncope in this case is an absolute indication for surgical intervention, since the life expectancy of such patients without surgery does not exceed 3 years.
2. Hypertrophic cardiomyopathy with obstruction (idiopathic hypertrophic subaortic stenosis) causes syncope by the same mechanisms, but the obstruction is dynamic and can be caused by taking vasodilators and diuretics. Fainting can also be observed in patients with hypertrophic cardiomyopathy without obstruction: it occurs not during exercise, but at the moment of its termination.
3. Pulmonary artery stenosis in primary and secondary pulmonary hypertension leads to the development of syncope during physical exertion.
4. Congenital heart defects can be the cause of fainting during physical exertion, which is associated with an increase in the discharge of blood from the right to the left ventricle.
5. Pulmonary embolism often leads to syncope, especially in the case of massive embolism, which causes obstruction of more than 50% of the pulmonary blood flow. Such situations occur after fractures or surgical interventions on the lower extremities and pelvic bones, with immobilization, prolonged bed rest, in the presence of circulatory failure and atrial fibrillation.
6. Atrial myxoma and spherical thrombus in the left atrium in patients with mitral stenosis can also in some cases be the cause of syncopal conditions, which usually occur when changing body position.
7. Cardiac tamponade and increased intrapericardial pressure impede diastolic filling of the heart, thereby decreasing cardiac output and causing syncope.

[ 14 ]

Heart rhythm disturbance

Bradycardia. Dysfunction of the sinus node is manifested by pronounced sinus bradycardia and so-called pauses - periods of absence of teeth on the ECG, during which asystole is observed. The criteria for dysfunction of the sinus node during daily ECG monitoring are sinus bradycardia with a minimum heart rate during the day of less than 30 per 1 min (or less than 50 per 1 min during the day) and sinus pauses lasting more than 2 s.

Organic damage to the atrial myocardium in the area of the sinus node is referred to as sick sinus syndrome.

Atrioventricular block of the second and third degree can be the cause of syncopal states when asystole lasts 5-10 seconds or more with a sudden decrease in heart rate to 20 per 1 min or less. A classic example of syncopal states of arrhythmic genesis are Adams-Stokes-Morgagni attacks.

Recent data have shown that bradyarrhythmias, even in the presence of syncope, are rarely the cause of sudden death. In most cases, sudden death is caused by ventricular tachyarrhythmias or myocardial infarction.

Tachyarrhythmia

Fainting states are observed with paroxysmal tachyarrhythmias. With supraventricular tachyarrhythmias, syncope usually occurs at a heart rate of more than 200 beats per minute, most often as a result of atrial fibrillation in patients with ventricular overexcitation syndrome.

Most often, syncopal states are observed with ventricular tachyarrhythmia of the "pirouette" or "dancing dots" type, when wave-like changes in the polarity and amplitude of ventricular complexes are recorded on the ECG. In the interictal period, such patients experience an extension of the QT interval, which in some cases may be congenital.

The most common cause of sudden death is ventricular tachycardia, which turns into ventricular fibrillation.

Thus, cardiogenic causes occupy a large place in the problem of syncopal states. A neurologist should always recognize even the minimal probability of the presence of syncopal states of cardiogenic origin in a patient.

Mistaken assessment of cardiogenic syncope as having a neurogenic nature can lead to tragic consequences. Therefore, a high "suspicion index" for the possibility of a cardiogenic nature of syncope should not leave a neurologist even in cases where the patient has received an outpatient consultation with a cardiologist and there are results of a routine ECG examination. When referring a patient to a cardiologist for consultation, it is always necessary to clearly formulate the purpose of the consultation, indicating those "doubts" and ambiguities in the clinical picture that raise suspicions about the presence of a cardiogenic cause of syncope in the patient.

The following signs may raise suspicion that the patient has a cardiogenic cause of syncope:

1. Past or recent cardiac history (history of rheumatism, follow-up observation and preventive treatment, presence of cardiovascular complaints in patients, treatment by a cardiologist, etc.).
2. Late onset of syncopal states (after 40-50 years).
3. Sudden loss of consciousness without presyncopal reactions, especially when the possibility of orthostatic hypotension has been excluded.
4. A feeling of “interruptions” in the heart in the pre-syncopal period, which may indicate an arrhythmic genesis of syncopal conditions.
5. The relationship between the occurrence of fainting and physical activity, cessation of physical activity and changes in body position.
6. Duration of episodes of loss of consciousness.
7. Cyanosis of the skin during and after loss of consciousness.

The presence of these and other indirect symptoms should make the neurologist suspect a possible cardiogenic nature of the syncopal condition.

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

Syncopal states in vascular lesions of the brain

Short-term loss of consciousness in elderly people is most often associated with damage (or compression) of the vessels supplying the brain. An important feature of fainting in these cases is the significantly rare isolated syncope without accompanying neurological symptoms. The term "syncope" in this context is again quite conditional. In essence, we are talking about a transient cerebrovascular accident, one of the signs of which is loss of consciousness (a fainting-like form of transient cerebrovascular accident).

Special studies of vegetative regulation in such patients have made it possible to establish that their vegetative profile is identical to that of the subjects being examined; apparently, this indicates other, predominantly “non-vegetative” mechanisms of pathogenesis of this class of disorders of consciousness.

Most often, loss of consciousness occurs when the main vessels - the vertebral and carotid arteries - are damaged.

Vascular vertebrobasilar insufficiency is the most common cause of syncope in patients with vascular diseases. Most often, the causes of damage to the 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. Anomalies in the development of the vessels of the vertebrobasilar system are of great importance.

The clinical feature of syncope is the sudden development of a fainting state following a head movement to the sides (Unterharnstein syndrome) or backwards (Sistine Chapel syndrome). The presyncopal period may be absent or very short; severe dizziness, pain in the neck and back of the head, and severe general weakness occur. During or after syncope, patients may exhibit signs of brainstem dysfunction, mild boulevard disorders (dysphagia, dysarthria), ptosis, diplopia, nystagmus, ataxia, and sensory disorders. Pyramidal disorders in the form of mild hemi- or tetraparesis are rare. The above signs may persist in the form of microsymptoms during the interictal period, during which signs of vestibular-brainstem dysfunction (instability, dizziness, nausea, vomiting) often predominate.

An important feature of vertebrobasilar syncopes is their possible combination with so-called drop attacks (a sudden decrease in postural tone and a fall of the patient without loss of consciousness). In this case, the patient's fall is not caused by dizziness or a feeling of instability. The patient falls with absolutely clear consciousness.

Variability of clinical manifestations, bilaterality of brainstem symptoms, alteration of neurological manifestations in cases of unilateral neurological signs accompanying syncope, the presence of other signs of cerebrovascular insufficiency along with the results of paraclinical research methods (ultrasound Doppler, X-ray of the spine, angiography) - all this allows us to make the correct diagnosis.

Vascular insufficiency in the carotid artery basin (most often as a result of occlusion) can in some cases lead to loss of consciousness. In addition, patients experience episodes of impaired consciousness, which they mistakenly describe as dizziness. Analysis of the mental "environment" that patients have is essential. Most often, along with loss of consciousness, the patient experiences transient hemiparesis, hemihypesthesia, hemianopsia, epileptic seizures, headache, etc.

The key to diagnosis is weakening of the carotid artery pulsation on the side opposite to the paresis (asphygopyramidal syndrome). When pressing the opposite (healthy) carotid artery, focal symptoms increase. As a rule, damage to the carotid arteries rarely occurs in isolation and is most often combined with pathology of the vertebral arteries.

It is important to note that short-term episodes of loss of consciousness may occur in hypertension and hypotension, migraine, infectious-allergic vasculitis. G.A. Akimov et al. (1987) identified such situations and designated them as "dyscirculatory syncopal states".

Loss of consciousness in the elderly, the presence of concomitant neurological manifestations, paraclinical examination data indicating pathology of the vascular system of the brain, the presence of signs of degenerative changes in the cervical spine allow the neurologist to assess the nature of syncopal states as associated primarily with cerebrovascular mechanisms, in contrast to syncopes, in which the leading pathogenetic mechanisms are disturbances in the links of the autonomic nervous system.