I. Definition: Syncope is a sudden and brief loss of consciousness accompanied by a decrease or loss of muscle tone, which lasts for a few seconds to a few minutes and recovers on its own, and is essentially a temporary decrease in cerebral blood flow. Syncope can be caused by cardiovascular diseases, neurological diseases and metabolic diseases, but many patients cannot find the cause according to their clinical history, physical examination and auxiliary examination, so it has long been called “unexplained syncope”. With the development of medical technology, it has been found that vasovagal syncope (VS) is the most common cause of unexplained syncope in pediatrics, and according to incomplete statistics, about 80% of syncope belongs to this category. Vaso-vagal syncope refers to the reflex of various stimuli mediated by the vagus nerve, resulting in dilation and bradycardia of small blood vessels in the internal organs and muscles, sudden dilation of peripheral vessels, and reduction of venous blood flow back to the heart, resulting in reflex action of the heart to speed up and strengthen contraction, and in some cases, over-stimulation of the vagus and parasympathetic nerves, which in turn causes sudden slowing of the heartbeat and dilation of peripheral vessels, resulting in lower blood pressure and Vagal syncope is very common and often recurs, especially when under considerable emotional stress, extreme fatigue, pain, panic, or in a crowded, hot room. Since blood vessels in the body are not innervated by the vagus nerve except for the heart, some scholars have recently suggested that the term “neurocardiogenic syncope” may be more appropriate. The main clinical manifestation is recurrent syncope. Although Lewis has proposed the diagnosis of vasovagal syncope for nearly 70 years, its etiology and pathogenesis have not yet been fully elucidated. Most scholars now believe that the basic pathophysiological mechanism is that the compensatory reflexes of the autonomic nervous system of the child are inhibited, and the compensatory cardiovascular response to prolonged upright posture cannot be maintained. In normal individuals, when upright, the blood collects in the lower parts of the limbs due to gravity, the blood in the head and chest is reduced, and venous return is reduced, causing the ventricular filling and pressure receptors located in the ventricles to be unloaded and the afferent impulses to the brainstem center to be reduced, reflexively causing increased sympathetic excitability and reduced parasympathetic activity. This is usually manifested by an increased heart rate, a slight decrease in systolic blood pressure and an increase in diastolic blood pressure. In contrast, children with vasovagal syncope are unable to maintain a compensatory cardiovascular response to prolonged upright posture. It has been reported that patients with vasovagal syncope have a sustained increase in circulating blood catecholamine levels and cardiac adrenergic nerve tone, leading to a hypercontracted state of relative ventricular emptying, which in turn overstimulates mechanoreceptors (unmyelinated C nerve fibers) in the inferior posterior wall of the left ventricle, causing a sudden increase in vagal impulses to the brainstem, inducing reflex bradycardia and peripheral vasodilation in contrast to normal subjects, leading to severe hypotension and cardiovascular dilation. This leads to severe hypotension and bradycardia, causing cerebral underperfusion, cerebral hypoxia and syncope. In addition, it has been found that neuroendocrine regulation is also involved in the pathogenesis of vasovagal syncope, including the renin-angiotensin-aldosterone system, catecholamines, 5-hydroxytryptamine, endorphins and nitric oxide, but the exact mechanism is not clear. Clinical manifestations: vasovagal syncope is most common in school-age children, more in girls than in boys, and usually manifests as sudden syncope when rising from a standing or sitting position. If you can be alert to this aura and lie down in time, it can be relieved or disappear. When the systolic blood pressure drops to 10.7Kpa (80mmHg), loss of consciousness may occur for a few seconds or minutes, and a few patients may have urinary incontinence, weakness, dizziness and other discomfort after waking up. The symptoms last 1-2 days and disappear. During the seizure, physical examination may show signs such as decreased blood pressure, slow heartbeat and dilated pupils. There are often no positive signs during the interictal period. Some studies have found that vasovagal syncope can induce tonic clonic-like movements (convulsive syncope), which can be misdiagnosed as epilepsy. High temperature, poor ventilation, exertion and various chronic diseases can induce this disease. The diagnosis of neurally mediated vasovagal syncope has long been indirect, time-consuming, and expensive, and often without definitive results. The head-up tilt test (HUT) is a new test developed in recent years and plays a decisive role in the diagnosis of vasovagal syncope. The positive reaction is the occurrence of syncope with a significant decrease in blood pressure or heart rate after the child is tilted from the prone to the standing position during the test. The mechanism of the upright tilt test for the diagnosis of vasovagal syncope is not fully understood. In normal subjects, in the upright tilt position, due to the decrease in the amount of return blood, the ventricular filling is insufficient, the effective beat volume is reduced, the inhibitory impulses from the arterial sinus and aortic arch pressure receptors to the vasomotor center are weakened, and the sympathetic tone is increased, causing the heart rate to accelerate and maintaining the blood pressure at a normal level. In children with vasovagal syncope, such autonomic compensatory reflexes are inhibited and normal heart rate and blood pressure cannot be maintained. Combined with the reduced ventricular volume in the upright tilt position, sympathetic tone increases, especially when accompanied by the positive inotropic effect of isoproterenol, causing a marked increase in contraction of the underfilled ventricles, at which point the receptors in the posterior wall of the left ventricle are stimulated, activating vagal afferent fibers and impulses to the At this point, stimulation of receptors in the posterior wall of the left ventricle activates vagal afferent fibers and impulses are transmitted to the center, causing inhibition of the vasoconstrictor center and excitation of the diastolic center, resulting in bradycardia and/or decreased blood pressure, which reduces cerebral blood flow and causes syncope. It has been suggested that bradycardia induced by inhibitory reflexes is due to vagal mediation, whereas hypotension induced by resistance vasodilation and volume vasoconstriction is the result of sympathetic inhibition. In addition, Fish suggested that the mechanism of HUT-induced syncope is due to activation of the Bezold-Jarisch reflex. V. Diagnosis and differential diagnosis: For children with recurrent syncopal episodes, it is not difficult to diagnose after detailed history taking, understanding the symptoms and signs during the episodes, and then through necessary auxiliary examinations such as electrocardiogram, electroencephalogram, biochemical examination and upright tilt test, but it should be differentiated from the following diseases: cardiogenic syncope This disease is caused by a sudden decrease in cardiac blood displacement or suspension of blood displacement caused by cardiac disorders, resulting in cerebral ischemia. It is caused by a sudden decrease in cardiac output or a pause in blood flow caused by a cardiac disorder, resulting in cerebral ischemia. It is usually seen in severe aortic or pulmonary stenosis, atrial mucus aneurysm, acute myocardial infarction, severe arrhythmias, and Q-T interval prolongation syndrome. It is easily identified by careful history taking, physical examination, and electrocardiographic changes. Hypoglycemia This disease often has a history of hunger or use of hypoglycemic drugs, mainly manifested as weakness, sweating, hunger, and then syncope and confusion, syncope attack slowly, the attack of blood pressure and heart rate are mostly unchanged, there may be no impairment of consciousness, the blood glucose is lowered, and the symptoms are quickly relieved by glucose injection. Epilepsy In children with vasovagal syncope that manifests as convulsive syncope, attention should be paid to differentiate it from epilepsy, which is not difficult to identify by doing EEG and upright tilt test. Upright adjustment disorder The children with this disease may show symptoms such as dizziness, dizziness, chest tightness and discomfort when they stand upright from the prone position instantly or for a little longer time, and in serious cases, they may have nausea, vomiting and even fainting, and they can wake up quickly and return to normal without treatment. It can be differentiated by upright test, upright tilt test, etc. Hysterical syncope The attack is preceded by obvious psychiatric factors and is preceded by a crowd. During the attack, the mind is clear, there is breath-holding or hyperventilation, the limbs struggle and move about, the eyes are tightly closed, and the face is flushed. The pulse and blood pressure are normal, there are no pathological neurological signs, the seizure lasts from several minutes to several hours, the mood is unstable after the seizure, if there is fainting, it also proceeds slowly, there is no injury, there is often a history of similar seizures, and it is easy to differentiate vasovagal syncope. In addition, the disease should be distinguished from hyperventilation syndrome. Treatment There is still a lack of special treatment and drugs for vasovagal syncope. Prophylactic treatment is needed for a portion of the population at risk who have no prodromal symptoms and who often have sudden syncopal falls, especially those who have repeated trauma or are frequently exposed to injury-prone environments. The goal of treatment is to reduce the frequency of severe syncopal events and to reduce trauma. Treatment of vasovagal syncope has a variety of approaches and is individualized. Education and lifestyle improvement Vasovagal syncope is often triggered by certain factors, and some may only occur in specific situations. Therefore, it is important to educate patients and their families to avoid these triggers as much as possible and to discontinue medications that can cause postural hypotension as much as possible. Once the precursor symptoms of syncope occur, the patient should lie flat immediately to avoid trauma as well as to prevent syncope. One study reported that in patients with recurrent vasovagal syncope, flexion and extension of the arms and legs during prodromal symptoms can help prevent syncope, which may be related to the skeletal muscle pump action to increase venous blood return. Increasing fluid and sodium intake may also help prevent syncope from occurring. younoszai and El-Sayed et al. found that patients with vasovagal syncope consuming at least 2L of fluid and 120mmol of sodium (about 7g of salt) per day can elevate blood pressure, increase blood volume, and reduce the frequency of syncope. Some clinicians also recommend standing training, similar to “desensitization” therapy. Patients are asked to stand against a wall for 10-30 min each day to gradually adapt to the effects of this postural volume change. However, this treatment method is still very controversial and long-term compliance is poor. Chinese herbal medicine may have good results and is being studied.