Syncope due to glossopharyngeal neuralgia or other visceral diseases

Introduction Syncope caused by glossopharyngeal neuralgia or other visceral diseases: this type of syncope is rare. Transient syncope occurs in glossopharyngeal neuralgia, biliary colic, renal stenosis, bronchial or digestive tract endoscopy. Associated with severe pain and hyperreflexive responses to visceral receptors. The most basic cause of syncope is the lack of temporary cerebral blood supply, so understanding some of the problems related to cerebral blood flow is beneficial for further understanding of syncope. Adult brain weighs about 1500 grams, accounting for 2% to 2.5% of body weight. The blood flow in the brain accounts for 15% of the systemic blood flow, and the brain oxygen consumption accounts for 20% of the total oxygen consumption of the whole body, and children up to 40%. Normal adult blood flow per 100g brain tissue is 40 ~ 50ml per minute, if reduced to 31.5ml, cerebral ischemia symptoms will occur.

Cause

(1) Causes of the disease

The classification of the cause of syncope is not uniform. The syncope is generally divided into different types depending on the disease. Including: 1 vasomotor dysfunction syncope; 2 cardiogenic syncope; 3 brain-derived syncope; 4 drug-induced syncope; 5 metabolic syncope; 6 physical factors caused by syncope;

Some scholars simply summarize: cardiogenic syncope, non-cardiac syncope and unexplained syncope.

Domestically, according to the cause, syncope can be divided into 4 categories: 1 hypotensive syncope; 2 cardiogenic syncope; 3 cerebral vasospasm; 4 multifactorial and other types of syncope.

It is also believed in the country that brain-derived syncope actually refers to cerebrovascular sickness syncope, and can be classified into the same type as other vascular diseases such as hypertension and arteritis. Therefore, the authors believe that syncope can be divided into the following four categories: 1 vasomotor dyssyncope; 2 cardiogenic syncope; 3 vascular disease syncope; 4 others, including metabolic syncope, drug-induced syncope. The specific contents are as follows: 1 vasomotor dyssyncope: vasopressive syncope, orthostatic hypotension, carotid sinus syndrome, reflex syncope, hyperreactivity of receptors, syncope epilepsy, swallowing syncope, etc. 2 cardiogenic syncope: sick sinus syndrome, atrioventricular block, paroxysmal supraventricular tachycardia, pre-excitation syndrome, ventricular tachycardia, long QT syndrome, arrhythmogenic right Dysplasia, aortic stenosis, cardiac myxoma, primary cardiomyopathy, secondary cardiomyopathy, coronary heart disease, mitral valve prolapse syndrome, viral myocarditis, infective endocarditis, pericardial disease, Heart valvular thrombosis, pacemaker syndrome, congenital heart disease, etc. 3 vascular disease syncope: hypertension, arteritis, aortic dissection, primary pulmonary hypertension, cerebral arteriosclerosis, transient ischemic attack, subclavian artery steal syndrome. 4 other: A. Metabolic syncope: hypoglycemia, hyperventilation syndrome, hyponatremia, and other symptoms. B. Drug-induced syncope: quinidine syncope, doxorubicin syncope, prazosin first dose syndrome. C. Others: upper gastrointestinal bleeding, hiatal hernia, pulmonary embolism, pregnancy-induced hypertension syndrome, cervical heart syndrome, thermal syncope, exercise syncope, etc.

(two) pathogenesis

The most basic cause of syncope is the lack of temporary cerebral blood supply, so understanding some of the problems related to cerebral blood flow is beneficial for further understanding of syncope.

Adult brain weighs about 1500 grams, accounting for 2% to 2.5% of body weight. The blood flow in the brain accounts for 15% of the systemic blood flow, and the brain oxygen consumption accounts for 20% of the total oxygen consumption of the whole body, and children up to 40%. Normal adult blood flow per 100g brain tissue is 40 ~ 50ml per minute, if reduced to 31.5ml, cerebral ischemia symptoms will occur. Therefore, it is necessary to ensure normal cerebral blood flow. The amount of blood that must flow through the brain within 24 hours of normal people is about 1700L, and the oxygen consumption is about 72L. Cerebral blood flow is closely related to effective perfusion pressure and cerebral vascular resistance, and is also related to intracranial pressure, blood viscosity, and blood vessel diameter.

The cerebral blood flow varies with age and the state of the body. For example, cerebral blood flow increases when thinking, high fever, and anxiety, and cerebral blood flow decreases when body temperature decreases. However, this cerebral blood flow fluctuation range is limited. The automatic regulation of cerebral blood flow is a guarantee for obtaining essential blood flow when the brain tissue is in normal activity. Under normal circumstances, due to the automatic regulation of cerebral blood vessels, changes in systemic blood pressure do not affect cerebral blood flow, when the blood pressure rises, the cerebral vascular resistance increases, when the blood pressure drops, the cerebral vascular resistance decreases, the cerebral blood flow remains constant, and the cerebral blood vessels The auto-regulation function works within a large range of blood pressure fluctuations. When the mean arterial blood pressure is lower than 8 to 10.8 kPa (60 to 80 mmHg), the protective cerebral blood flow autoregulation function is lost. Some people have blocked the -adrenergic receptors in the experiment and lowered the lower blood pressure limit to 4.7 kPa. Therefore, it is considered that the automatic regulation of cerebral blood flow is achieved by innervation. However, there are other factors that can affect cerebral blood flow, such as carbon dioxide and oxygen concentration in arterial blood, blood viscosity, and blood vessel diameter. If the cerebral blood flow stops for 6 to 7 minutes and the blood partial oxygen pressure is lower than 2.7 kPa, the brain cells may not be subjected to normal oxygen metabolism, so serious brain dysfunction may occur.

Regarding the pathophysiology of syncope, it is believed that cerebral ischemia first affects the cerebral cortex and basal ganglia, which are highly sensitive to hypoxic conditions, followed by the hypothalamus and midbrain, while the medullary pons reticular structure has an abnormal state of hypoxia. Great tolerance. According to this, it is believed that in the first stage of syncope episodes, slow waves appear in the EEG, indicating hypoxic damage in the hypothalamic-cortex level of the brain, which can be clinically manifested as loss of consciousness, decreased muscle tone, and falls. When the cerebral hypoxia continues to exist and endangers the pons and the medullary life center, a safe feedback mechanism to stop cerebral hypoxia plays a role in promoting cardiac reflex and vascular reflex reflex, producing a normal rhythm and maintaining an effective circulation of blood vessels. Tension, the syncope is terminated.

an examination

Related inspection

Basic embryonic protein cerebrospinal fluid glucose and serum glucose ratio

Free triiodothyronine (FT3) --

T3 is a hormone synthesized and secreted by thyroid follicular cells. FT3 accounts for about 0.3% of T3. It can enter the tissue cells through the cell membrane and exert physiological effects. Its concentration is consistent with the concentration of triiodothyronine in the tissue, and it is also consistent with the metabolic state of the body. It also has diagnostic value for non-thyroid diseases. Clinically, the RIA method is commonly used.

Plasma thyroid stimulating hormone releasing hormone (TRH) --

Plasma thyroid stimulating hormone releasing hormone (TRH) is an indicator of hypothalamic function.

Triiodothyronine inhibition test--

After taking exogenous T3 in normal people, the T3 concentration in the blood is increased. Negative feedback can inhibit the secretion of TSH in the anterior pituitary, and the 131I rate of thyroid is significantly reduced. Diffuse goiter with hyperthyroidism, due to the presence of long acting thyroid stimulator (LATS) and long-acting thyroid stimulant protectants in the blood, can stimulate the thyroid to cause an increase in 131I rate, and is not affected T3 inhibition. The thyroid absorbing 131 iodine function test sometimes overlaps with the values of normal people and hyperthyroidism, which affects the diagnosis of the disease.

Triiodothyronine inhibition test method: for differential diagnosis of patients with high iodine intake rate. The method was as follows: 60-100 g of sodium triiodothyronine was orally administered on the 1st, and it was taken in 3 times for 6 days, and the radioactive isotope iodine iodine test was repeated.

Dexamethasone inhibition test--

Normal people take oral dexamethasone 3 mg daily (ie, small dose method), take 4 times, and take 2 to 3 days.

Adrenocorticotropic hormone (ACTH) --

Corticotropin is a micro-peptide hormone secreted by the pituitary gland and is a major regulator of adrenal cortex activity.

Serum insulin (SI) --

Insulin can lower blood sugar, and when blood glucose or amino acid concentration is high, it can promote insulin secretion.

Serum aldosterone (ALD, ALS) --

The action of aldosterone is to promote the reabsorption of sodium by the renal distal convoluted tubule epithelial cells and promote the excretion of potassium. The secretion of aldosterone has a diurnal secretion pattern similar to cortisol, which is lower in the morning than in the night. The standing position is increased compared with the lying position, and the plasma concentration is also changed accordingly.

Serum cortisol (FC) --

Cortisol is produced and secreted by the adrenal cortex and belongs to the corpus callosum glucocorticoids. Its secretion is controlled by the anterior pituitary adrenocorticotropic hormone. The determination of serum cortisol directly reflects the secretory function of the adrenal cortex.

Follicle Stimulating Hormone (FSH) --

Follicle stimulating hormone and luteinizing hormone collectively called gonadotropin have the effect of promoting follicular maturation and promoting estrogen secretion together with luteinizing hormone.

Thyroid stimulating hormone (TSH) --

Thyroid stimulating hormone is a hormone secreted by the pituitary gland to promote the growth and function of the thyroid gland. It has the function of promoting the proliferation of thyroid follicular epithelial cells and the synthesis and release of thyroid hormone.

Prolactin (PRL) --

Prolactin mainly promotes the growth and development of the breast and the formation of milk, and inhibits the secretion of gonadotropins.

Alkaline phosphatase (ALP, AKP) --

Alkaline phosphatase is a phosphomonoesterase widely distributed in human tissues and body fluids, in bone, liver, breast, intestinal mucosa, kidney, and placenta.

Differential diagnosis

Differential diagnosis of syncope caused by glossopharyngeal neuralgia or other visceral diseases:

A. Vasopressor syncope: Also known as vasovagal syncope or simple syncope, it is the most common type in clinical practice. Both men and women of any age can develop symptoms. 20% to 25% of young people suffer from this disease, and more common in younger women. There are obvious causes of the disease, such as pain, fear, seeing bleeding, receiving injections or minor operations, sultry weather, crowded places, hunger, fatigue and so on. Most of the onset occurs when standing, occasionally when sitting, and the lying position will never occur.

The clinical manifestations were typical of 3 phases. The systolic blood pressure decreased to 7.98 kPa (60 mmHg) or below when syncope, and the pulse slowed to 40-50 times/min. Most patients have only occasional seizures, a small number of patients have a family history, and blood pressure is in the normal range or normal low level.

B. micturition syncope: The patient is almost all male, the middle-aged patient is the most, fainting occurs during standing urination or just after urinating, often at night, morning or nap when getting up and urinating, more prodromal symptoms Suddenly syncope, the symptoms of recovery are milder. After drinking, cold weather and fatigue are possible causes. In addition to the reflex arc dysfunction mainly due to the regulation of blood pressure and heart rate, it also increases the intrathoracic pressure with the breath holding during urination. The waking up after a long time makes the blood supply to the brain insufficient, and the nighttime vagal nerve tension is high, and the blood pressure is low. Some people attribute it to multifactorial syncope. Defecation syncope is rare and its mechanism is similar to urinary syncope.

C. tussive syncope: loss of consciousness immediately after severe cough, low muscle tone, short-lived. A small number of patients felt dizzy and dazzled, and their complexion changed from bruising to pale and sweating. Most of the patients were obese men after middle age, who often smoked and had bronchitis and emphysema. Children who developed pertussis or asthma also developed symptoms. Most after repeated coughing, occasionally fainted after a single cough, call, sneezing, yawning or laughing. Cough increases the intrathoracic pressure, causing venous return obstruction and cardiovascular reflex factors to play a role in the disease.

D. swallowing syncope: seen in patients with pharynx, larynx, esophagus, mediastinal disease and/or atrioventricular block, sick sinus syndrome, bradycardia, myocardial infarction, swallowing cold, hard Short-term syncope after acid, spicy food or gas-producing beverages, no obvious discomfort before and after the attack, and has nothing to do with body position. The pathogenesis and mechanical stimulation of the upper digestive tract, abnormal afferent impulses trigger cardiovascular reflex inhibition, and cardiac conduction system is sensitive to vagal excitation abnormalities.

E. Syncope caused by glossopharyngeal neuralgia or other visceral diseases: this type of syncope is rare. Transient syncope occurs in glossopharyngeal neuralgia, biliary colic, renal stenosis, bronchial or digestive tract endoscopy. Associated with severe pain and hyperreflexive responses to visceral receptors.

F. Carotid sinus syncope: also known as hypersensitive carotid sinus. It is a common cause of syncope in men over middle age. Patients often have carotid atherosclerosis, or carotid body tumor, inflammation of the carotid sinus, or compression of adjacent tumors or enlarged lymph nodes, mediastinal tumors, etc., in case of excessive neck, bow, head, or collar High and tight, and thus ill.

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