2017年 · 第50卷第08期

sleep perception refers to an individual's self-evaluation of sleep state, mainly including the subjective description of sleep quantity and quality. This subjective evaluation has become the primary basis for the diagnosis and efficacy evaluation of sleep disorders. By comparing and analyzing the subjective sleep parameters of insomnia patients with the objective sleep parameters detected by polysomnography (PSG), the researchers found that there were significant differences between subjective and objective sleep parameters of some insomnia patients, mainly because patients underestimated their actual sleep time and sleep quality. The 1997 revised International Classification of sleep Disorders (ICSD-R) classified this condition as a clinical type of endogenous sleep disorder, named "sleep state misperception", also known as "pseudoinsomnia", "paradoxical insomnia" or "subjective insomnia", and considered it to be less than 5% of all insomnia patients in clinical practice^[1,2,3]。 It has gradually been found that this kind of sleep perception disturbance occurs in patients with insomnia caused by various causes, and there is a large sample study^[4]The results show that up to 50% of insomnia patients have sleep perception disorders, so whether "sleep state perception disorders" can be an independent clinical diagnostic classification entity has always been controversial^[5]There is also a lack of clinical quantitative diagnostic criteria with clear operability. International Classification of Sleep Disorders, Third Edition (ICSD-3), 2014^[6]The diagnostic classification of "sleep state perception disorder" as a subtype of insomnia has been abandoned. In recent years' clinical work, the author gradually found that sleep perception disorder has become an important interference factor for clinicians to correctly evaluate the diagnosis and efficacy of insomnia. Therefore, it is necessary to understand the formation of sleep perception and analyze its related influencing factors, which is helpful for the correct diagnosis, differentiation and efficacy evaluation of insomnia.

rapid-eye-movement sleep behavior disorder (RBD) is a sleep disorder characterized by dreams and physical activity during REM sleep. Violent behavior during attack can cause injury to oneself and your bedmate and disrupt sleep^[1]。 RBD usually occurs in people over 50 years of age, but onset at 15 years of age has also been reported^[2]。 The incidence rate is 0.4% ~0.5% in the general population^[3,4]The incidence rate of people over 70 years old is 7% ~8%^[5]。 According to the epidemiological survey in Hong Kong, China, the prevalence of RBD in people over 70 years old is 0.38%^[6]； A large-scale community survey based on the RBD scale found that the prevalence of suspicious RBD in mainland China ranged from 4% to 5%^[7]。 RBD was significantly higher in males than in females, ranging from 2:1 to 5:1, and the onset and diagnosis age in females may be later than in males^[8]。 Previously, RBD was considered to be an independent sleep disorder, but more and more clinical follow-up studies have shown that it is closely related to Parkinson's disease, multiple system atrophy, Lewy body dementia and other neurodegenerative diseases^[9]。 At present, it is believed that RBD is important for early warning of neurodegenerative diseases.

Ischemic stroke has high morbidity, disability and mortality, which brings heavy economic burden to society and family, and becomes the main reason affecting the health of middle-aged and elderly people^[1,2,3]。 In 2013, a random sample survey of more than 480,000 adults over the age of 20 in 31 provinces and municipalities in China, including urban and rural areas, showed that the incidence of stroke was 345.1 per 100,000, and the mortality rate of stroke was 159.2 per 100,000^[1]。 In the prevention and treatment of ischemic stroke, we should pay attention not only to the risk factors such as hypertension, diabetes, dyslipidemia, obesity, smoking, but also to the evaluation and treatment of head and neck atherosclerosis.

Patients with increased sleep and sleep-related movement disorders are not uncommon, but multiple sleep disorders in the same patient are relatively rare. sleep related rhythmic movement disorder (SRMD) is characterized by episodic, stereotypical and repetitive characteristics, and is easily confused with epilepsy and other episodic disorders. We report a case of misdiagnosed frontal lobe epilepsy, a less common sleep disorder with adult SRMD and narcolepsy as the core symptoms.

Rapid eye movement (REM) sleep behavior disorder (RBD) is the disappearance of muscle flaccidity (RWA) during REM sleep, accompanied by nightmares and intense speech or complex involuntary movements of limbs associated with dreams. According to the etiological classification, it can be divided into two categories. One is idiopathic RBD (iRBD), which means that the patient does not have other definite neurological diseases; Another type is secondary RBD (or symptomatic RBD), which refers to patients who are concomitantly associated with other neurological diseases such as narcolepsy, neurodegenerative diseases, and the like. However, some prospective studies in recent years suggest that iRBD can be used as an early clinical marker of neurodegenerative diseases, especially synucleinopathy^[1,2,3,4,5]It provides a great degree of help for the early diagnosis of neurodegenerative diseases and has great significance.

Sleep disorders are a kind of disorders related to physiological-psychological factors, body quality, environmental conditions, neuropsychiatric diseases, adverse drug reactions and other factors, and appear by affecting sleep-related structures and functions in the brain, which are abnormal sleep quality, sleep and wake rhythm alternating disorder. More and more evidence shows that neuronal autoantibodies are directly related to various sleep disorders, which has become a research hotspot in the field of neuroimmunology. We review the latest research progress of neuronal autoantibodies and sleep disorders, aiming to strengthen clinicians' awareness and attention, so as to facilitate early diagnosis and timely treatment of diseases.

Narcolepsy is a common primary central hypersomnia disease, with uncontrolled daytime sleep and cataplexy as the core clinical symptoms, and the incidence rate is different between different races and regions. The incidence rate is (3-16) /10 000 in the United States and 1/600 in Japan^[1]； Epidemiological survey in Hong Kong, China shows that the incidence of this disease is 1/3 000^[2]； It is estimated that the incidence rate in mainland China is more than 4/10 000^[3,4]。 Affected by the influenza virus epidemic in the winter of 2009, the number of new cases of narcolepsy reported in North and East China in 2010 was about three times that in previous years^[5,6]Some Nordic countries reported a significant 6-to 9-fold increase in narcolepsy incidence in 2010^[7]According to the analysis, the reason for the increase in incidence in 2010 may be closely related to influenza A (H1N1) infection and vaccination with AS03 adjuvant in winter 2009^[5,7]。 According to whether it is accompanied by a decrease in hypocretin/orexin (Hcrt/orexin) content in cerebrospinal fluid, narcolepsy can be divided into type 1 and type 2, of which type 1 accounts for about 85%^[4,8,9]。 The vast majority of narcolepsy type 1 is clinically accompanied by cataplexy, also known as cataplexy^[8]。 Frequent daytime sleep and cataplexy interfered with patients' interpersonal communication and significantly affected their social function^[3,4,8]。 Because the core symptoms of this disease persist for life, it is of great significance to study the mechanism of cataplexy to improve the daytime learning and life of patients and restore social function^[3,4,5,6]。 In addition, the elucidation of the mechanism of cataplexy is also crucial for improving our understanding of brain motor control networks and regulation. We present a complete review of the mechanisms of narcolepsy cataplexy from the central nervous system (CNS) to the periphery.

Stroke has become a major disabling and fatal disease worldwide, with approximately 795,000 new or recurrent strokes in the United States every year^[1]。 Acute large vessel occlusion is a class of malignant diseases that disable and kill nearly 80% of patients, similar to ST-segment elevation myocardial infarction in heart disease. With the advancement of interventional technology, the use of new generation of thrombus aspiration or resection devices can achieve rapid recanalization of blood vessels. A series of multicenter randomized controlled studies in recent years (MR CLEAN, ESCAPE, SWIFT PRIME, EXTEND-IA, REVASCAT)^[2,3,4]Endovascular therapy has been demonstrated to have obvious superiority over intravenous thrombolysis alone in acute ischemic stroke caused by large vessel occlusion, which can improve the likelihood of a favorable prognosis in stroke patients. These trials are similar to previous related studies on myocardial infarction. Through the construction of chest pain centers and the rapid implementation of emergency percutaneous coronary intervention (PCI), the survival rate of patients with myocardial infarction has been significantly improved. However, although the treatment technology of stroke is changing with each passing day, the time delay caused by the defects of the treatment system is still the main influencing factor that hinders patients to obtain a good prognosis. Therefore, it is urgent to improve the stroke treatment process.

primary central nervous system lymphoma (PCNSL) is an extranodal non-Hodgkin's lymphoma primarily in the central nervous system (CNS), involving the eye, brain, spinal cord, meninges or cranial nerves, accounting for about 1% to 5% of primary intracranial tumors, 4% to 6% of extranodal lymphomas, and 1% of all lymphomas^[1,2]。 The disease is rare in clinic, its clinical manifestations lack specificity, and it is easy to be misdiagnosed. Especially for patients with intracranial space-occupying lesions and onset of cognitive impairment or binocular vision loss, it is easy to be misdiagnosed as CNS tumefactive demyelinating lesions (TDLs). Some biopsies (referred to as biopsy) are given hormone therapy in advance, resulting in atypical pathological changes, thus delaying diagnosis and treatment; Some require multiple biopsies to confirm the diagnosis. Ma Aimei et al.^[3]One case of PCNSL was reported after 3 biopsies at an interval of 3 years. We reviewed the clinical progress of PCNSL at home and abroad in recent years to improve the understanding of this disease.