Neurocardiogenic syncope is a group of clinical syndromes associated with the pathological reflex effect of the autonomic nervous system on the regulation of vascular tone and heart rhythm. Characterized by short-term loss of consciousness caused by acute arterial hypotension and /or slowing of the pulse, occur with parasyncopal symptoms, accompanied by an increased risk of physical injury. The neurogenic nature of syncope is confirmed by tilt test, ECG monitoring, supplemented by video EEG registration. Complex treatment includes non-drug methods, pharmacotherapy, implantation of a pacemaker.
ICD 10
R55 G90.0
General information
Neurocardiogenic (reflex, neurogenic) syncope is the most common type of syncope among children and adults. According to the results of various studies, it accounts for 22-66% of cases. Reflex fainting is more typical for adolescents and young people – the first episode of pathology usually occurs at the age of 10 to 20 years. In the future, more than half of them experience a recurrent event. Throughout their lives, women suffer from syncopal conditions twice as often as men.
Causes
Syncopal condition develops due to a sudden decrease in cerebral blood flow caused by a reflex decrease in peripheral vascular tone and/or cardiac output. Neurocardiogenic syncope occurs under the influence of various external triggers against the background of a special predisposition associated with a violation of cerebral vasopressor mechanisms. The following factors play a role in the etiology of syncope:
- Vasovagal. Syncope is most often caused by strong psychoemotional stress, which negatively affects the autonomous regulation of vascular tone. Reflex syncope of the vasovagal type is also found in people experiencing prolonged orthostatic stress (standing or sitting position).
- Situational. Neurogenic syncope can be provoked by various circumstances that stimulate the activity of the vagus nerve. Patients indicate a connection with straining with coughing, defecation, lifting weights. This reaction is a response to swallowing, sneezing, urination. The influence of physical activity, visceral and neuralgic pain, and food intake was noted.
- Irritation of the carotid sinus. Manipulations caused by pressure on the area of the carotid sinus can provoke fainting. A reflex response in the form of stimulation of the parasympathetic system is observed in men when wearing narrow collars, ties, while shaving. Syncopal state is provoked by carotid artery massage, head rotation or compression by a tumor.
Neurogenic syncope is not associated with organic pathology, it is often caused by a combination of reflex and physical factors. Sometimes they develop under unclear circumstances – even after a thorough examination, it is not possible to identify the provoking factor in almost 50% of patients. In such cases, the diagnosis is confirmed with the exclusion of other causes of loss of consciousness.
Pathogenesis
The mechanisms of neurocardiogenic syncope have not been sufficiently studied. Syncope is the result of an abnormal vegetative response to various stimuli, which is accompanied by activation of the vagus nerve, provokes reflex changes in heart rate and vascular tone. Stimulation of the vasodepressor region of the brain stem can occur by activating mechanoreceptors of the heart, intestines, genitourinary system, cardiopulmonary baroreceptors, sensitive fibers of cranial nerves, cerebral cortex.
The sequence of events ending in fainting is initiated by the deposition of blood in the veins. Mild irritation of the aortic and carotid baroreceptors provokes an increase in cardiac output. Increased contractility of the left ventricle activates cardiac mechanoreceptors that send signals to the brain stem. As a result, there is an unjustified suppression of sympathetic stimulation with an increase in vagal influence, which is manifested by hypotension, bradycardia and loss of consciousness. This mechanism is known as the Bezold-Yarish reflex.
The development of neurocardiogenic syncope is considered by some researchers from the standpoint of psychosomatics. According to this concept, the systematic impact of any factors that violate the cortical regulation of physiological functions can provoke the occurrence of psychovegetative syndrome. Such reactions can have a significant impact on the formation of paroxysmal states, especially in childhood.
Classification
Neurocardiogenic syncope unites a rather heterogeneous group of functional disorders characterized by episodic vasodilation and/or bradycardia with short-term loss of consciousness. In practical neurology, a classification of reflex syncope has been adopted, according to which several variants of pathology are distinguished:
- Vasovagal. They are the most common form of neurogenic syncope. Reflex vasomotor reactions occur against the background of increased excitability of the vagus nerve. There are emotional (stressful), orthostatic.
- Situational. Such syncopations are associated with a stereotypical situation – cough (bettolepsia), nocturic, post-loading, postprandial, etc. They are caused by local hypersensitivity of the vagus nerve in different zones, pathological reflex reactions to pain and other stimuli.
- Sinocarotidae. Occur due to increased sensitivity of the carotid sinus and mechanical irritation of this area. They occur in several variants – vagal, vasodepressor, cerebral.
- Atypical. They develop under the influence of uncertain factors, in the absence of obvious triggers or with atypical manifestations. They can be combined with other syncopal states. This group also includes fainting associated with low levels of adenosine in the blood.
Neurocardiogenic syncope symptoms
There is a clear stage in the development of syncope. For a pre-fainting state lasting no more than 1-2 minutes, weakness, dizziness, nausea are characteristic. Patients note tinnitus, visual disturbances (“flies”, “fog” in front of the eyes), discomfort in the epigastrium. Many people pay attention to the feeling of anxiety, lack of air, the inevitability of falling. Numbness of the fingers, tongue and lips, palpitations, increased sweating may occur. In a horizontal position, the phenomena of lipothymia are quickly stopped.
After the increasing phenomena of the presyncopal period, fainting itself occurs directly. Against the background of a decrease in blood pressure and bradycardia, there is a loss of consciousness or its short–term loss – from a few seconds to 1 minute. The skin turns pale, muscle tone decreases, the photoreaction of dilated pupils decreases. Pulse becomes weak, irregular, breathing becomes shallow. Deep syncope is accompanied by muscle twitching, involuntary urination.
In the post-fainting state, consciousness is quickly restored, the patient does not lose his temporal-spatial orientation. The whole body feels warm, the skin turns red, remains moist. Bradycardia is replaced by tachycardia, breathing is somewhat rapid. The patient is alarmed by what has happened, notes short-term weakness, nausea, dizziness. These symptoms can persist from a couple of minutes to several hours after the resolution of the syncopal episode.
Bouts of bettolepsy, one of the variants of situational neurocardiogenic fainting, occur with a strong cough caused by chronic bronchopulmonary diseases. Similar paroxysms may appear when sneezing, laughing, lifting heavy objects. At the peak of the cough reflex, there is an increase in pressure in the chest cavity, large veins and inside the skull, which leads to a violation of cerebral blood flow. Against this background, sudden weakness and short-term loss of consciousness develop.
A special case of neurocardiogenic syncope is caused by neuralgia of the lingopharyngeal nerve. Fainting is always preceded by severe paroxysmal pains of typical localization: in the lower jaw, tongue root, throat and larynx. Irradiation in the ear can be observed with concomitant damage to the tympanic nerve. There were no sensory or motor disorders in the affected area. In many people, a syncopal attack is provoked by swallowing.
Complications
The most likely complication of neurocardiogenic fainting is injuries associated with a fall. Life-threatening traumatization is especially typical for people whose profession is associated with working at height or moving mechanisms. Fainting in drivers, drivers of electric trains, pilots can pose a danger not only to the patients themselves, but also to others. A number of patients have malignant syncope with periods of asystole, in which the risk of ventricular tachyarrhythmia due to ischemia or bradycardia increases.
Diagnostics
An assessment of anamnestic information and a thorough physical examination provide important clues to find out the causes of fainting, helping to conduct basic testing. But for half of the patients with reflex syncope, they are not indicative, which necessitates additional studies. The neurovegetative nature of syncope is established through diagnostic measures:
- Passive positional test (tilt test). It is the method of choice in the diagnosis of neurogenic syncope. With the help of a special inclined table, after a 15-minute stay in the supine position, the patient is quickly transferred to the vertical (at an angle of 60-80 °) with the registration of ECG, blood pressure and pulse indicators. The test is considered positive with the development of syncope, a decrease in pressure by 30 mm Hg, the appearance of bradycardia. The sensitivity of the sample can be increased by the introduction of low doses of drug stressors (isoproterenol, nitroglycerin).
- ECG monitoring. Cardioinhibitory mechanisms of syncope are confirmed by daily ECG monitoring. The test can be performed in several ways: with skin electrodes (Holter), implantable recorders, remote telemetry. The study is especially useful in cases of suspected tachyarrhythmia, in the case of previously operated congenital heart defects in children.
- Video EEG registration. Synchronous recording of the patient’s video image and brain biopotentials during the tilt test increases the reliability of observation of neurogenic syncope. The method helps to determine the clinical signs of lipothymia and syncope, their relationship with hemodynamic parameters, to exclude neurological causes of syncope.
When the syncopal state is associated with physical exertion, an appropriate provocative test, echocardiography is performed. In unclear cases, a number of biomarkers can be examined – levels of troponin, natriuretic peptide, adenosine. It is necessary to differentiate neurogenic syncope with cardiac and cerebrovascular syncope, psychogenic pseudo-syncope.
Treatment
Conservative therapy
Reflex syncope requires complex treatment, since individual methods are less effective. The aim of therapy is to reduce the frequency of syncopal states, to prevent injuries from falling, which is carried out due to the effect on the mechanisms of development of neurocardiogenic fainting. The main methods of correction are considered to be:
- Patient training. It is important to provide information about the causes of fainting, the need to avoid provoking circumstances, and training in coping with mental stress. In the event of precursor symptoms, patients are recommended to take a horizontal position to prevent syncope.
- Diet. Increasing fluid and salt intake can prevent further syncopal episodes. A decrease in the frequency of neurocardiogenic fainting in adolescents is reported against the background of an increased drinking regime (2-3 liters per day). The increase in orthostatic tolerance also increases with the liberalization of salt consumption.
- Physical methods. To interrupt syncopal episodes with recurrent neurogenic syncope, isometric exercises involving limb muscles and elastic compression are used. The effect is due to the activation of the musculoskeletal pump and an increase in venous return. Vegetative stability is increased by respiratory gymnastics.
- Medicines. Pathogenetic therapy of neurogenic syncope is performed with vasoconstrictors (midadrin), selective serotonin reuptake inhibitors (paroxetine), mineralocorticosteroids (fludrocortisone). Anticonvulsants and cholinolytics are used to treat situational fainting. Nootropics, vasoactive agents, vitamins are indicated as undifferentiated therapy.
Surgical treatment
To prevent relapses of neurogenic syncope developing by the cardiodepressor mechanism, implantation of a permanent pacemaker is used as a minor surgical intervention. The method is used when conservative therapy is ineffective, usually in people over 40 years of age with frequent fainting without prodromal symptoms, when the risk of concomitant injury is high. Two-chamber electrical stimulation is the most acceptable, but in situations where a drop in blood pressure precedes bradycardia, the method does not give the expected result.
Experimental treatment
Ablation of cardiac ganglia is considered as a potential treatment option for recurrent reflex syncope with a predominantly cardioinhibiting component. It can become an alternative to electrocardiostimulation, as it does not require permanent implantation of the device. But the method requires further randomized trials to determine the overall benefit, patient selection criteria, long-term risk profiles and relapses.
Prognosis and prevention
Most neurogenic syncope is benign in nature, short periods of unconsciousness usually do not cause long-term harm to health. But frequent relapses and physical injuries negatively affect the ability to work, social activity, thereby worsening the quality of life of patients. The potential harm can be reduced by complex therapy, although some syncopal episodes can self-simulate. Primary prevention involves the elimination of predisposing factors, increasing psychovegetative stability.
