Obstructive sleep apnea syndrome

Introduction to obstructive sleep apnea syndrome Obstructive sleep apnea hypopnea syndrome (OSAHS) is an unexplained sleep-disordered disease with clinical manifestations of nighttime sleep snoring with apnea and daytime sleepiness. Repeated episodes of nocturnal hypoxia and hypercapnia caused by apnea can lead to complications such as hypertension, coronary heart disease, diabetes and cerebrovascular disease, and traffic accidents, and even sudden death at night. Therefore OSAHS is a potentially lethal sleep breathing disorder. basic knowledge The proportion of sickness: 0.4%-0.6% Susceptible people: no specific population Mode of infection: non-infectious Complications: chronic rhinitis, nasal septum deviation, hypertension, impotence

Causes of obstructive sleep apnea syndrome

Blockage or stenosis of the upper airway (30%):

The cause of obstructive sleep apnea is mainly caused by obstruction or stenosis of the upper respiratory tract during sleep. Therefore, stenosis or obstruction of any part from the anterior nares to the upper trachea may cause apnea. The following diseases are common:

(1) Nasal disease: Nasal stenosis or obstruction caused by various causes, such as acute and chronic rhinitis, sinusitis, anterior and posterior nostril atresia, nasal septum deviation, hematoma, abscess, nasal adhesion, nasal polyps, nasal cavity, nasal passage Sinus tumors and other space-occupying lesions, anterior and posterior nostril tamponade.

(2) Nasopharyngeal diseases: common adenoid hypertrophy, nasopharyngeal tumor, nasopharyngeal atresia, nasopharynx filling, skull base tumor.

(3) Oropharynx diseases: such as tonsil hypertrophy, soft palate, drooping, hypertrophy, excessive sag, hypertrophy, hypertrophy of the pharyngeal side, scarring of the oropharyngeal cavity, tumors in the parapharyngeal space, abscesses, etc.

(4) hypopharyngeal diseases: such as tongue lymphoid tissue hyperplasia, tongue root tumor, giant epiglottic cyst, abscess, epiglottic tumor, abscess of the posterior pharyngeal wall or side wall, tumor and so on.

(5) Stomatological diseases: such as hypertrophy of the tongue or giant tongue, tongue, tongue root, tumor at the base of the mouth, submandibular abscess, congenital small mandibular or mandibular retraction.

(6) Other diseases: pathological obesity, acromegaly, hypothyroidism, huge neck tumors, etc.

Central sleep apnea (25%):

Periodical hypopnea is observed in the elderly or infants during sleep. It can be regarded as the central cause. Normal adults can also see central sleep apnea and pathological central sleep breathing in the fast moving eye sleep phase or in the plateau. Suspension can be seen in a variety of conditions:

(1) Neurological, motor system lesions, such as anterior spinal cord cutting, vascular embolization or degeneration caused by bilateral posterior spinal cord lesions.

(2) Abnormal function of autonomic nerves, such as familial autonomic abnormalities, insulin-related diabetes, Shy-Drager syndrome, encephalitis.

(3) Muscle diseases, such as diaphragmatic muscles, myotonic dystrophy, etc.

(4) abnormalities of the cerebrospinal cord, such as Ondine's Curse syndrome (the failure of respiratory autonomic control on normal respiratory stimuli), occipital macropore developmental malformation, poliomyelitis, lateral medullary syndrome.

(5) Patients with narcolepsy and some obstructive sleep apnea syndrome after tracheotomy or pharyngeal vaginoplasty.

Pathophysiological changes (20%):

The pathogenesis is complex and involves multidisciplinary issues such as internal medicine (breathing, cardiovascular, endocrine, etc.), pediatrics, neurology, psychiatry, oral, maxillofacial surgery, otolaryngology and head and neck surgery, etc., which are still not very clear. Further research is needed.

(1) Central sleep apnea: the mechanism of occurrence is not very clear, the following factors may be involved in the onset.

1 When the awakening is transferred to sleep, the respiratory center has various respiratory stimuli (such as resistance to hypercapnia, hypoxemia, alveolar, mechanical receptors and respiratory movements of the chest wall and upper airway). The reactivity is reduced, especially in the fast-moving eye sleep period.

2 The central nervous system is unstable to respiratory feedback control caused by hypoxemia and other pathological conditions.

(2) Obstructive sleep apnea: Some people think that the obstructive part of obstructive sleep apnea is only in the pharynx. It turns out that this statement is incomplete. Clinically, many pharyngeal cavities are not narrow, or have been successfully done. In patients with pharyngeal surgery, severe sleep-disordered breathing can still occur. These patients often find different degrees of abnormalities in the nasal cavity, nasopharynx or hypopharynx during examination, and the corresponding treatments have solved or alleviated these parts. Blocking, apnea can be significantly relieved or even completely disappeared.

Therefore, when discussing the pathogenesis of obstructive sleep apnea, we should not only discuss the problems of the oropharynx, but should be discussed separately according to the different parts of the obstruction.

1Arrhythmia caused by nasal and nasopharynx diseases: When the nasal cavity or nasopharynx is blocked, the body will compensate by opening the mouth, that is, through the contraction of the mouth muscle, which is achieved in the awake state. No problem, but after going to sleep, the tension of the mouth muscles will gradually decrease until it is completely relaxed. The passage through which the body is ventilated will become smaller and smaller until it is completely closed. Since the physiological nasal breathing cannot be performed, airflow occurs. The interruption, over time, the aggravation of hypoxia and a series of pathophysiological changes in the body, the patient's sleep from deep to shallow and restore the contraction of the mouth muscle, so the airflow channel recovers, the breathing also recovers, the nasal obstruction In this case, even if the oropharynx and hypopharynx are completely normal, the patient may experience sleep apnea.

2 apnea caused by oropharyngeal disease: except for the bronchospasm of the oropharynx, most of them are soft tissue, such as soft palate, palate, pharyngeal side, tonsil, etc. Therefore, the oropharynx is a vulnerable Factors affecting the shape and size of the changing cavity, from the anatomical factors, the soft palate hypertrophy, the position is too low, the drooping hypertrophy, too thick and too long, tonsil hypertrophy, pharyngeal lateral hypertrophy and peripancreatic space fat The hyperplasia can cause the actual space of the pharyngeal cavity to become smaller. Physiologically, the muscle relaxation caused by various reasons is called the decrease of muscle tension, especially the enlargement of the muscle tension of the pharyngeal cavity, and the inhalation. The increase of negative pressure in the pharyngeal cavity can cause the inward collapse of the soft tissue around the pharyngeal cavity, so that the pharyngeal cavity is further narrowed or even completely blocked. The oropharynx muscle belongs to medium fatigue muscle, the muscle fiber is less and the oxidized muscle fiber component is high. Fatigue and muscle relaxation are also one of the factors that cause the pharyngeal cavity to collapse when inhaling. In addition, the soft palate that relaxes when lying on the back, and the collapse caused by gravity can also aggravate the narrowing of the pharyngeal cavity.

3 apnea caused by lower pharyngeal disease: hypopharyngeal space-occupying lesions, scarring of the tongue, hypertrophy of the tongue or hypertrophy of the tonsil tonsils, and excessive accumulation of fat in the throat of obese patients (Homer, 1989) can lead to the hypopharyngeal cavity Anatomical stenosis, increased pressure in the hypopharynx caused by insufflation caused by stenosis of the oropharynx and above, and the fall of the tongue in the supine position further makes the hypopharyngeal cavity smaller or even completely blocked. In addition, the lowering of the genioglossus, the hyoid and lingual muscles is also one of the important reasons. The congenital small mandible shortens the anterior-posterior distance from the posterior pharyngeal wall to the anterior border of the mandible, thus making the base of the tongue to the posterior pharynx. The distance between the walls is also shortened accordingly.

When the supine position is subjected to gravity, the tongue falls and the soft palate, and the sagging of the tongue can explain why snoring and breathing disorders tend to increase in the supine position.

The role of nerves, body fluids, and endocrine factors in sleep-disordered breathing: The movement of the upper respiratory tract is controlled by two different independent and independent nervous systems. The autonomic nerves originate from the pons and the medulla, and the voluntary nerves originate from the cerebral cortex and the cortex. The nerve impulse action is used to expand the muscles of the ankle and upper airway, causing the inspiratory movement of the diaphragm to contract and keep the upper airway open. If the two are not coordinated, or if the upper airway negative pressure cannot be effectively adjusted, then There may be a blockage of the upper airway.

Exhaustion, excessive drinking, taking sleeping pills or sedatives can aggravate sleep apnea, which may be related to inhibiting the excitability of the above nerves.

The mechanism of how the upper airway is closed during apnea and how it is opened later is not very clear. Some people think that it is mainly due to the arousal reaction caused by hypoxia (PO2) stimulation of carotid body receptors. Patients with bilateral carotid body resection. The time of apnea is longer than that of normal people. Some people think that it is the result of interaction between hypoxemia and hypercapnia.

Because obstructive sleep apnea syndrome is more common in men, postmenopausal women, obesity, acromegaly, hypothyroidism or testicular injection of patients, it is speculated that the occurrence of this disease may be related to endocrine disorders.

2. Pathophysiological changes in sleep apnea

(1) Impact on the nervous system: There is increasing evidence that snoring and SAS are associated with cerebrovascular diseases, especially with cerebral infarction. Multivariate logistic regression analysis was performed on 177 patients with cerebral infarction, suggesting snoring And SAS are independent risk factors for cerebral infarction (Palomaki H, 1989).

Repeated episodes of hypoxemia during sleep in SAS patients can lead to cerebral hypoxia. Increased systemic blood pressure can lead to cerebral arteriosclerosis and increased intracranial pressure. Increased erythrocytosis can cause increased blood viscosity. All of the above factors can cause stroke in patients. Increased risk, other factors closely related to snoring and SAS such as hypertension, coronary heart disease, age, obesity, smoking, alcohol abuse, etc., are also known or potential risk factors for stroke.

SAS and epilepsy can affect each other and make the disease worse. The hypoxemia caused by apnea, sleep fragments and chronic sleep deprivation in SAS patients can lead to a decrease in the threshold of paralysis in patients with epilepsy, while anticonvulsants and anticonvulsants can Aggravating existing SAS or having the potential to cause SAS (Ezpeleta, 1998).

OSAS may also be associated with neurasthenia because many clinical manifestations of neurasthenia overlap with the clinical manifestations of OSAS. You Guoxiong et al. (1998) conducted a special study to suggest that OSAS may cause "neurasthenia" or make existing nerves Debilitating symptoms worsen.

OSAS can lead to memory loss and cognitive dysfunction, sleep structural disorder and hypoxemia are considered to be the main causes of the above manifestations. Domestic Peng Bin et al. through auditory evoked event-related potential (P3) and clinical memory scale examination in OSAS patients It was found that the patient's P3 latency and memory quotient were significantly different from the normal control group, further confirming the above viewpoint.

In addition, some people believe that OSAS may be associated with depression, anxiety, paranoia and other mental symptoms and adult dementia.

(2) Impact on the cardiovascular system: SAS has the most obvious influence on the cardiovascular system. In recent years, many scholars believe that SAS is an independent risk factor for hypertension and coronary heart disease, which can lead to heart failure, arrhythmia, angina, and myocardium. Infarction and sudden death at night.

According to statistics, the incidence of hypertension in SAS patients is 48% to 96%, and the incidence of SAS in patients with hypertension is 20% to 40%. The mechanism of SAS-induced hypertension may be repeated apnea, sleep arousal and Hypoxemia stimulates sympathetic excitation, increased secretion of catecholamines, peripheral vasoconstriction, elevated arterial blood pressure, and the heart is one of the organs with the highest oxygen consumption in the human body. The most harmful to hypoxia is hypoxia. Endothelial cells are damaged, lipids are easily deposited under the inner membrane; increased red blood cells increase blood viscosity, slow blood flow, platelets tend to accumulate on the damaged endometrial surface to form thrombus, causing coronary artery stenosis or obstruction, easily causing angina , myocardial infarction, various arrhythmias and even sudden death.

(3) Effects on the respiratory system: apnea and hypopnea can cause hypoxemia and hypercapnia, severe cases can cause respiratory acidosis and acute respiratory failure, hypoxemia causes pulmonary vasoconstriction, causing pulmonary artery High blood pressure, long-term pulmonary hypertension can develop into right heart hypertrophy and right heart failure.

(4) The impact on the genitourinary system: the kidney function of the patient can be damaged at night, such as the reduction of creatinine clearance, renal tubular recovery dysfunction, renal dysfunction, etc., manifested as nocturia, enuresis, etc. Proteinuria occurs, characterized by glomerular, reversible, and proteinuria can be reduced or eliminated with the correction of OSAS.

The effects on the reproductive system were characterized by decreased sexual function and even impotence. Schivavi et al. studied the sexual behavior frequency, erection duration and other indicators of 70 male patients aged 45-75 years, and the results were significantly different from the control group.

(5) Effects on the endocrine system: Palomaki et al found that the glucose tolerance of OSAS patients with AHI10 was lower than that of the control group. OSAS can cause disorders of glucose metabolism, impaired glucose tolerance, and increased non-insulin-dependent diabetes mellitus. The mechanism may be related to hypoxia-induced insulin resistance and increased secretion of catecholamines.

Hypoxemia causes pituitary, hypothalamic dysfunction, and thyrotropin secretion is reduced, so OSAS may cause hypothyroidism, and hypothyroidism may cause or aggravate OSAS.

Obstructive sleep apnea syndrome prevention

For patients with snoring or varying degrees of nasal cavity, nasopharyngeal or hypopharyngeal abnormalities, early diagnosis, early treatment, and corresponding treatment should be used to solve or reduce the blockage of these parts, which can prevent apnea, or obviously relieve or even completely Eliminate obstructive sleep apnea symptoms.

Complications of obstructive sleep apnea syndrome Complications chronic rhinitis nasal septum deviation hypertensive impotence

Guilleminaut et al reported 50 patients with obstructive sleep apnea syndrome, the clinical manifestations of snoring 100%; excessive daytime sleepiness 78%, abnormal body flip during sleep 100%, sleep disturbance 23%, memory loss 78%, adult bedwetting 30%, headache in the morning 36%, personality changes such as anxiety, depression, etc. 48%, hypertension 52%, impotence 42%.

Halperin et al reported that more than 90% of patients with obstructive sleep apnea had ear, nose and throat abnormalities, 46% had obesity neck short 23% had mandibular deformity or chronic rhinitis, and 18% had nasal septum deviation.

Obstructive sleep apnea syndrome symptoms Common symptoms fatigue nightmare snoring sleep awakening reaction airway trapping snoring polyuria lack of deep sleep hair loss sleep disorders insomnia

1. Snoring patients with sleep-disordered breathing have different degrees of snoring, Guilleminaut reported 50 cases, snoring 100%, but patients often do not know that they sleep snoring, mostly informed by the same room sleepers, there are patients When I suddenly wake up in the snoring, I can occasionally hear my own snoring, the snoring is uneven, and there is a pause. After a few seconds or even a few minutes, it suddenly bursts out, and the sound is extremely loud, up to 85 decibels.

2. Apnea in normal people may also occur in central apnea during sleep, but less than 10 times in 7h sleep, usually only in the REM period, mostly in obesity or snoring, pathological apnea refers to a pause The time lasts for more than 10s, and the number of pauses for 7h is more than 30 times.

Those with milder disease do not occur at the beginning of sleep. As the sleep deepens, the snoring increases, accompanied by apnea. In severe cases, apnea occurs when you fall asleep. Suspension mainly occurs during inhalation, and the snoring is interrupted. Air cessation, obstructive sleep apnea patients still have breathing action at this time, accompanied by increased frequency, shallower chest or abdominal breathing movement and mandibular stretching movement, but no airflow through the nose and mouth, After this condition lasts for a few ten seconds to a few minutes, with a deep inhalation, the patient has several rapid breathing exercises to compensate for the oxygen debt owed during the apnea, which will occur after a period of time. The next apnea.

The length of the interval between two pauses is related to the severity of the patient's condition. The interval between the patients will be longer, and the interval between the patients will be shorter. The number of pauses in the cases monitored by Li Danian in China will be 7h. Up to 572 times, AHI=74.05, more than once per minute, the longest apnea time was 233.5s (Huang Xizhen reported 216s), the pause time was 248min, accounting for 59% of sleep time 7h.

Some patients with apnea with irregular limb twitching, especially for the lower limbs, called restless legs syndrome, severe patient expression pain, facial cyanosis, and some accompanied by sweating, foaming at the mouth and body movement, even falling to Under the bed, there is a coma, a small number of patients with nightmares, and can suddenly wake up, terrified, called sleep terror, which is more common in children.

Patients with central sleep apnea are often associated with some systemic neurological and muscular diseases. Therefore, in addition to apnea during sleep, there are clinical manifestations of the disease, such as polio, myotonia, and lateral medulla. Syndrome, low brainstem lesions, diabetic neuritis, etc.

3. Polyuria or enuresis and polyuria refers to an increase in the number of urination at night. It has been reported that a severe OSAS patient has a urinary frequency of 4 to 6 times before treatment, and the number of urination after surgery is significantly reduced, only 0 to 1 time. This may be related to nighttime hypoxia and increased uric acid excretion caused by anaerobic metabolism in OSAS patients. Nighttime bedwetting is more common in children with OSAS, but adult bedwetting is not uncommon. Stanford University Sleep Lab reports 62 OSAS patients. Among them, 12 children and 3 adults had night bedwetting.

4. Daytime sleepiness and prolonged sleep time have different degrees of daytime sleepiness, especially when you are quiet or do monotonous repetitive work, such as sitting, riding, reading, watching TV, etc., serious standing, walking, eating and even When cycling, it is possible to fall asleep. Among the 50 cases reported by Guilleminaut et al, 39 cases of excessive daytime sleepiness accounted for 78%. Due to the deterioration of sleep quality, the body tries to compensate by increasing sleep time. Therefore, the patient's sleep time is often the same. When the normal person of the age is prolonged and the quality of sleep is improved (such as after surgery or during CPAP treatment), the patient's sleep time can be significantly shortened.

5. Dizziness, fatigue, morning headache, cognitive decline due to nighttime sleep structure disorder in OSAS patients, increased proportion of shallow sleep and decreased proportion of deep sleep, and nighttime hypoxia, the physical and energy of patients after sleep Not getting a good recovery, often complained of morning headaches, dizziness, general weakness, and a decline in cognitive function.

Cognitive impairment is manifested in changes in memory, judgment, attention, concentration, abstract reasoning and alertness. Findley et al performed comprehensive cognitive function tests on 26 OSAS patients, including intelligence, attention, concentration, alertness, Hand-eye coordination ability, rapid and complex problem solving ability, real-time and short-term memory, etc. Through eight psychological tests, it was found that the cognitive function of patients was fully affected, with attention, concentration, complex problem solving ability and short-term memory damage most obvious. The alarminess of OSAS patients is reduced, which increases the incidence of motor vehicle accidents. It is reported that 10% of traffic accidents in the United States are related to sleep diseases, OSAS patients are difficult to maintain alertness and attention, reaction time and concentration ability are reduced, and Findley and other applications The simulator was used to measure the alertness of OSAS patients and normal controls. It was found that the number of OSAS patients who were out of orbit and the number of knockdown obstacles were dozens of times that of the normal control group, the reaction time and braking time were significantly slow, and all OSAS The patient has at least one sleep during driving, and the impairment of cognitive function in OSAS patients, Severity of the patient-related diseases, sleep disorders and hypoxemia structure is considered to be the main cause of cognitive dysfunction.

Normal sleep structure disorder can cause cognitive decline; while the frequency of nighttime arousal in OSAS patients, the length and duration of sleep in stage III and IV, and the duration of REM can affect the cognitive function of patients.

Hypoxemia affects the biochemical and hemodynamic aspects of the central nervous system. At high altitudes, hypoxemia impairs cognitive function in humans. Findlety et al. have shown that patients with hypoxemia have no OSAS. The cognitive impairment of OSAS patients with hypoxemia is more obvious. The degree of cognitive impairment is significantly correlated with the oxygen saturation at night and the oxygen partial pressure during the day.

6. Personality changes and mental symptoms manifested as temperament, depression, anxiety, etc., may be related to long-term nocturnal hypoxia and sleep structural disorders in patients, depression is the most common psychiatric symptoms of OSAS, Mosko et al found in 233 OSAS patients, 67% of patients had depressive symptoms 5 years before the visit, while 26% were recent depressive symptoms. Depressive symptoms were more pronounced in patients with OSAS and narcolepsy and restless legs syndrome. The more severe the condition of OSAS patients, the more obvious the depressive symptoms. Many OSAS patients have hallucinations, especially before going to sleep, or patients are more likely to appear in the fight against dozing. Some patients also have simple paranoid psychosis. Mad psychosis, etc., behavioral abnormalities are not uncommon, such as sleepy hands and feet, sometimes sleepwalking phenomenon, when working during the day, often occur in the absence of seizures, and even suspected of psychomotor seizures, in essence, naps Attacks, sudden suspicions, embarrassing and other unreasonable behaviors are often considered mental illnesses.

As a companion symptom, OSAS is often associated with the improvement of the disease. Mosko et al observed 22 patients with OSAS. After surgery, symptoms such as depression, anxiety and fatigue were significantly improved. After CPAP treatment, OSAS The symptoms of depression, anxiety, panic attacks, and fatigue were significantly improved.

7. Hypertension OSAS patients have a higher incidence of hypertension, reported as 25% to 96%, and in hypertensive patients, about 30% with OSAS, therefore, Kaplan in 1986 secondary hypertension The etiology of OSAS and OSAS on blood pressure often has the following characteristics: The peak of general hypertension is often in the afternoon or evening after a day of fatigue, after a rest of the night, the next morning is generally low, and related to OSAS High blood pressure is not the case, due to lack of oxygen overnight, carbon dioxide retention and changes in sleep structure, the morning blood pressure is higher than in the afternoon or evening, and the response to antihypertensive drugs is relatively poor.

8. Most of the patients were obese, the neck was short, but it also occurred in the elongated body. Many patients looked older than the actual age, and some showed dark complexion, cyanosis, apathetic or lower extremity edema. Children can be characterized by dull expression, unresponsiveness, and delayed development.

Otolaryngology examination can often find different degrees of upper anatomical abnormalities or stenosis, such as nasal septum deviation, nasal cavity occupying, adenoid hypertrophy, soft palate, drooping, hypertrophy, large sag, hypertrophy of tongue, tonsil tonsil hyperplasia and small Mandibular, facial deformity, etc.

Examination of obstructive sleep apnea syndrome

1. Use the EEG multi-lead tracing device to monitor the nighttime sleep process.

2. Polysomnography can clearly identify the above three different types of sleep apnea, the central type of respiratory dysfunction disappears, no respiratory activity in the chest and abdomen, no airflow through the airway, central respiratory impulses in the obstructive type Exist, there is chest, abdominal breathing activity exists, but the airway has no airflow, the mixed type first appears airway obstruction, the airflow stops, and then the respiratory action stops.

Sleep apnea syndrome In patients with excessive sleep during the day, multiple sleep nap test (MSLT) can be found that the sleep latency is shortened within 10 min, usually within 5 min.

3. Blood gas analysis.

Based on the medical history and key neurological examinations, other necessary optional auxiliary examination items include:

4. CT and MRI examinations.

5. Blood routine, blood electrolytes, blood sugar, urea nitrogen.

6. ECG, abdominal B ultrasound, chest penetration.

Diagnosis and diagnosis of obstructive sleep apnea syndrome

Diagnostic criteria

1. Qualitative, quantitative diagnosis of PSG (polysomnography) 7h monitoring results are the current recognized standard for OSAS. PSG is a continuous, simultaneous recording of patients' EEG, myoelectricity, eye movement, nose and mouth airflow during nighttime sleep. , snoring, chest and abdomen respiratory motility, arterial oxygen saturation, ECG, leg movement and body position and other indicators, and then through computer automatic or manual manual data analysis, the patient's night sleep, breathing and other conditions analysis report If 7h apnea times 30 times, or sleep apnea times + hypopnea times reach or exceed 35 times, that is, the number of apneas per hour + the number of hypopneas is equal to or greater than 5 times (AHI 5), you can diagnose SAS, the severity of the disease depends on the number of pauses, as well as the duration of the pause and the degree of decline in oxygen saturation.

2. Etiology diagnosis The etiology diagnosis of obstructive sleep apnea is mainly to find or judge the location and cause of stenosis or obstruction of the airway, the pressure in the esophagus under sleep, the endoscopy of the upper airway and the Muller's test, CT or MRI's upper airway imaging scan and X-ray cranial lateral slice analysis are important methods for judging the obstruction site, but these methods have their own advantages and disadvantages, and can be selected or applied according to the situation.

Pure central sleep apnea is relatively rare, and its etiology is mainly related to the examination of related nerves, muscles, body fluids and endocrine, to determine or eliminate diseases that can cause sleep-disordered breathing.

Differential diagnosis

1. PMS (periodic movement during sleep) The daytime sleepiness caused by this disease may be more obvious than SAS. In the standard polysomnography (with tibialis anterior muscle), the tibialis anterior muscle has periodic outbreak activity, lasting O. 5 to 5 s, with an interval of 15 to 60 s.

2. Narcolepsy is a rare sleep disorder characterized by lethargy and stumbling. It is a sudden onset of fainting and is difficult to suppress. From ten to hundreds of times a day, tripping refers to sudden body muscle relaxation. Loss of voluntary exercise, but not accompanied by loss of consciousness, recovery after a few minutes, sleep paralysis and pre-sleeping hallucinations are also important symptoms of narcolepsy.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.