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Study ObjectivesIncreased incidence of narcolepsy was reported in children during the 2009 H1N1 pandemic following Pandemrix, a H1N1 flu vaccine. A link with A(H1N1) pdm09 infections remains controversial. Using nationwide surveillance data from China (1990 to 2017), the epidemiology of narcolepsy was analyzed.MethodsIndividual records of narcolepsy patients were collected from 15 of 42 hospitals across China known to diagnose cases. Incidence was estimated assuming the representativeness of these hospitals. Age-specific incidence, epidemiological and clinical characteristics of patients were evaluated before, during, and after the 2009 H1N1 pandemic. Sensitivity analyses were conducted by including NT1 cases only and excluding the effect of the 2009 H1N1 vaccination.ResultsAverage annual incidence was 0.79 per 100 000 person-years (PY) from 1990 to 2017 and 1.08 per 100 000 PY from 2003 to 2017. Incidence increased 4.17 (95% CI 4.12, 4.22) and 1.42 (95% CI 1.41, 1.44) fold during and after the 2009 H1N1 pandemic when compared to baseline. These results were robust in sensitivity analyses. Patients with the onset of narcolepsy during the pandemic period were younger (notably in 5–9-year-old strata), and the age shift toward younger children reversed to baseline following the pandemic.ConclusionsIncreased incidence of narcolepsy was observed during the 2009 H1N1 pandemic period. This is likely to be associated with the circulation of the wild type A(H1N1)pdm09 virus. This observation should be considered for future influenza pandemic preparedness plans.

Introduction Previous studies assessed different components of telemedicine instead of the whole telemedicine management pathway for OSA. The current study aimed to demonstrate that telemedicine management was not clinically inferior to in-person care in China based on the change in Functional Outcomes of Sleep Questionnaire (FOSQ) score following three months of an auto-adjusted positive airway pressure (APAP) treatment. Methods Adults suspected of OSA were randomized to telemedicine (n=178) or in-person (n=178) management. Participants with AHI ≥ 15 events/hour diagnosed by a home sleep apnea test (HSAT) were treated with an APAP with a wireless modem. The participants were followed up by call at week 1 and visit at month 1 and month 3. Results We measured the change in FOSQ score as the primary outcome, with an a priori noninferiority delta of -1, and the mean daily hours of objectively measured APAP adherence, with an a priori noninferiority delta of -45min/day. Of the 356 subjects enrolled, 313 (87.9%) were diagnosed with OSA, and 261 (73.3%) underwent PAP setup. The mean functional outcome score following 3 months improved 1.73 points (95%CI: 1.31, 2.14) in the telemedicine group and 2.05 points (95% CI: 1.64, 2.46) in the in-person group. The lower bound of the one-sided 95% noninferiority confidence interval was -0.812. Mean daily APAP adherence at 3 months was 243.3 minutes/night (95% CI: 223.1, 263.5) in the telemedicine arm and 241.6 minutes/night (95% CI: 221.3, 261.8) in the in-person arm. The lower bound of the one-sided 95% noninferiority confidence interval was -22.2 minutes/night. Compared to in-person management, the telemedicine pathway had lower patients cost and similar health care cost. Conclusion Functional outcome and treatment adherence in patients managed by a comprehensive telemedicine approach is not clinically inferior to that in patients receiving in-person care. Support (if any) ResMed Australia funded the APAP machines. The study was supported by the National Key R&D Program of China (Z161100002616012). Liyue Xu is supported by a grant from the National Natural Science Foundation of China (NSFC 82100104).

Study Objectives Excessive daytime sleepiness (EDS) is a frequent cause for consultation and a defining symptom of narcolepsy and idiopathic hypersomnia (IH). The associated mechanisms remain unclear. Lipocalin-type prostaglandin D synthase (LPGDS) is a plausible sleep-inducing candidate. This study is to compare cerebral spinal fluid (CSF) and serum LPGDS levels in patients group with hypersomnia of central origin, including those with narcolepsy type 1 (NT1) and type 2 (NT2) and IH, to those in healthy controls (Con). Methods Serum LPGDS, CSF LPGDS, and CSF hypocretin-1(Hcrt-1) levels were measured by ELISA in 122 narcolepsy patients (106 NT1 and 16 NT2), 27 IH, and 51Con. Results LPGDS levels in CSF (p = 0.02) and serum (p < 0.001) were 22%–25% lower in control subjects than in patients with EDS complaints, including NT1, NT2, and IH. In contrast to significant differences in CSF Hcrt-1 levels, CSF L-PGDS levels and serum L-PGDS were comparable among NT1, NT2, and IH (p > 0.05), except for slightly lower serum LPGDS in IH than in NT1 (p = 0.01). Serum L-PGDS correlated modestly and negatively to sleep latency on MSLT (r = −0.227, p = 0.007) in hypersomnia subjects. Conclusions As a somnogen-producing enzyme, CSF/serum LPGDS may serve as a new biomarker for EDS of central origin and imply a common pathogenetic association, but would complement rather than replaces orexin markers.

Introduction Patients with nocturnal oximetry shows SpO2 during sleep of ≤ 90% in children for ≥ 5 minutes and sleep related hypoventilation is not documented could be diagnosed as sleep related hypoxemia (ICSD-3). However, known physiological causes should be indicated. Report of Case A 5-year-old Chinese boy was referred to sleep lab for daytime sleepiness for three months. Type I narcolepsy was confirmed. Nocturnal PSG indicated a continuous low SpO2 baseline around 82%, with a nocturnal mean SpO2 of 83%, but no respiratory events. Voluntary hyperventilation made SpO2 increase from 83% to 95%, and hypoventilation syndrome was considered. PtcCO2 during PSG maintained 40mmHg, and no sleep related elevation observed. BPAP treatment had no effect on both SpO2. No dyspnea was complained. When he was 12 years old, follow-up PSG and MSLT indicated narcolepsy remained. During the past 7 years, no comorbidities occurred. Hb 104 g/L, RBC 3.53 × 1012/L, Hct 31%. ABG showed SaO2 of 97%, PaO2 98mmHg and PaCO2 40mmHg. Inconsistency between SpO2 and SaO2 reminds the existence of abnormal hemoglobin. A positive isopropanol precipitation test and further hemoglobin electrophoresis showed abnormal Hb and HbA were 37.6% (normal 0%) and 58.4% (normal 94.3–98.5%), respectively, but HPLC did not identify. Spectrophotometric analysis indicated that the absorption spectra were significantly different at 450nm~540nm and 600nm~1000nm. Hemoglobin structure analysis found the abnormal site. Gene sequencing identified a novel HBB: c.212 C>A mutation, resulting in amino acid 71 to change from alanine(Ala) to aspartic(Asp) acid as a de novo mutation. A diagnosis of Hemoglobin Seattle [β71:Ala→Asp；HBB:c.212C>A] was confirmed. Conclusion Pediatric sleep medicine has a rapid development. Before a diagnosis of sleep related hypoxemia is made, in rare situation, abnormal hemoglobin should be considered.

Introduction Narcolepsy type 1 (NT1) is considered to be an autoimmune disease, and streptococcal infection may be an environmental trigger. However, previous studies from Asian narcolepsy patients did not reveal elevated anti-streptolysin O [ASO]. The aim is to investigate whether large sample Chinese patients with NT1 have an increase in antistreptococcal antibody titers. Methods A total of 214 narcolepsy patients and 360 healthy controls were recruited. All patients were DQB1*0602 positive with clear-cut cataplexy or had low CSF hypocretin-1. Participants were tested for ASO and anti DNAse B [ADB]. These patients were divided into five groups according to disease duration, including 29 patients less than 3 months; 25 from 3 months to 1 year; 40 from 1 to 3 years; 61 from 3 to 10 years and 59 patients over 10 years. Comparison was also made between children and adults with age matched controls, respectively. Results There were no significant differences between patients and healthy controls in regard to both ASO ≥ 200 IU (19.2% vs. 16.9%, p = 0.50) and ADB≥480IU (9.8% vs. 10.3%, p = 0.86). For children narcolepsy patients, ASO positive rates(19.8% vs. 18%, p = 0.68) and ADB positive rates(10.4% vs. 12%, p = 0.72) had no differences compared to age matched controls. And no difference was observed in adult narcolepsy patients either, with ASO positive rates (18.5% vs. 13.8%, p = 0.39) and ADB positive rates (9.3% vs. 5.3%, p = 0.42) compared to age matched controls, respectively. ASO (ADB) positive rates had no significant differences among different disease duration groups(p= 0.55, 0.9). Conclusion It is indicated that positive rates of ASO and ADB were not significantly different between Chinese patients with NT1 and healthy controls, including recent onset cases and children. Support The study was supported by the National Natural Science Foundation of China (No. 81420108002 and NO. 81570083)

Introduction Catathrenia/nocturnal groaning, is a rare sleep disorder characterized by repeated groaning in a protracted expiration preceded by a deep inspiration. The classification was moved from ICSD-2 as parasomnia to sleep-disordered breathing(SDB) in ICSD-3. The pathogenesis of catathrenia is unknown. Methods To investigate catathrenia’s response to continuous positive airway pressure (CPAP) treatment, and its relationship with SDB. We analyzed patients diagnosed at the Sleep Center of Peking University People’s Hospital from 2009 to 2016. All patients were confirmed with nocturnal groaning by polysomnography(PSG), and recording of the sounds. The patients were recommended for treatment of CPAP. Results A total of 49 patients were recruited into this study, including 31 female and 18 male, age ranging from 16 to 64 years. The average onset age was 19.81 ± 8.65 years old, the average BMI was 21.76 ± 2.62 kg/m², the average groaning index (GI) was 11.58 ± 13.32 times per hour, and the average apnea hypopnea index (AHI) was 3.59 ± 8.83 times per hour. The GI in REM and NREM sleep were 39.31 ± 44.39 and 6.74 ± 8.5 times per hour respectively (p Conclusion Catathrenia occurs mainly in REM sleep, and treatment with CPAP is effective, although cannot be completely eliminated. Suggest that catathrenia might be a sleep breathing disorder Support There is no support of this study

Introduction Narcolepsy is a chronic sleep disorder that can affects significantly patient functioning, involving social, work, and affective life. At present, many drugs have been developed to treat narcolepsy efficiently. But there is no Chinese version of Narcolepsy Severity Scale (NSS) available yet, for that the aim of this study is to translate the NSS into Chinese and evaluate reliability and validity of the NSS in adult patients with narcolepsy type 1 (NT1). Methods NSS was translated according to the standard procedures of double-back translation and cross-cultural adaptation steps. The NSS was administered to 62 adult patients (42 males, 20 females; mean age 34 years; range 19 to 67 years) with NT1 from April 2019 to December 2019. The validity of the scale was assessed by the exploratory factor analysis, discriminant validity and convergent validity. The reliability was assessed by the Cronbach’s α coefficient and test-retest reliability. Results Three common factors were extracted and 15 items explained 57.4% of the total variance. Cronbach’s α coefficient for total scale was 0.767 and Cronbach’s α for three dimensions ranged from 0.729 to 0.787. Scores were significant difference between treated and untreated group in dependent samples (p=0.036), but no differences in the independent samples (p>0.05). The NSS had good correlations with Epworth Sleepiness Scale (r=0.302, p=0.017) and Insomnia Severity Index (r=0.526, p=0.000). The NSS showed good test-retest reliability (r=0.72, p=0.029). Conclusion The Chinese version of NSS was proved to be valid and reliable and can be used to evaluate the severity and consequences of symptoms in Chinese adult patients with NT1. Support

Introduction To determine the presence of respiratory impairment in community-living subjects with a history of poliomyelitis. Methods In a study conducted from July 2013-January 2014, we used a national database to recruit individuals (212 males, 86 females) from north and south provinces in China with a known prior poliomyelitis infection >25 years previously. 298 subjects (96.8%) completed overnight oximetry to collect the number/hr of drops in oxygen saturation >4% (ODI4) and Epworth Sleepiness Scale (ESS); many completed a metabolic and lipid panel, arterial blood gas analysis, chest x-ray (CXR), spirometry and maximal voluntary ventilation (MVV). Some completed risk profiling for OSA. Results Age was 47.8 ± 6.7 years (M±SD) and, when known, the age of infection was 2.3 ± 1.8 yrs. As defined by ODI4 ≥ 5/hr, the frequency of sleep-disordered breathing (SDB) was 37.2%; 9% (n = 27) had an ODI4 ≥15/hr. Those with vs. those without SDB differed by male gender (81% vs 65%, p = 0.004) and BMI (25.9 vs 23.0kg/m2, p < 0.001). ESS was within the normal range, but was higher in those with 6.8 ± 5.0 vs. without 5.2 ± 4.0 (p < 0.01) SDB. Spirometry and MVV revealed no differences among groups. Scoliosis on the CXR was present 26.1% of those with and 14.4% of those without SDB. ODI4 correlated weakly with body mass index (r = 0.40). Glucose levels or hyperglycemia were not different. A triglyceride level > 1.7 mmol/L was present in 47.2% of those with and 21.3% of those without SDB (p < 0.001). Conclusion Mild (28%) and to a smaller extent moderate-severe (9%) SDB is present many years after surviving poliomyelitis in infancy. In most, sleepiness is low but scoliosis is often present, and associations to hyperlipidemia and obesity are not reflected in fasting glucose levels. Support no

Introduction To evaluate the utility of the ring pulse oximeter for screening of OSA in adults. Methods 87 adults were monitored by a ring pulse oximeter and PSG simultaneously during a nocturnal in-lab sleep testing. 3% oxygen desaturation index (ODI3); Mean oxygen saturation(MSpO2), Saturation impair time below 90% (SIT90) derived from an automated algorithm of the ring pulse oximeter. Meanwhile, the parameters of PSG were scored manually according to the AASM Manual. Correlation and receiver operator characteristic curve analysis were used to measure the accuracy of ring pulse oximeter and its diagnostic value for moderate to severe OSA (AHI≥15). Results Among the 87 participants, 18 cases were AHI0.05], Further analysis indicated that two parameters from the oximeter correlated well with that derived from PSG (r=0.889, 0.567, respectively, both p Conclusion The pilot study indicated that ring pulse oximeter can detect oxygen desaturation events accurately, therefore to be used as a screening tool for moderate to severe OSA. Support The study was supported by the National Natural Science Foundation of China (No. 81420108002 and NO. 81570083).

Introduction To evaluate resting state functional connectivity and topological properties of brain network in narcolepsy compared with healthy controls. Methods Resting state fMRI was performed in 26 adult narcolepsy patients and 30 matched healthy controls. MRI data was first analyzed by group independent component analysis, then a graph theoretical method was applied to evaluate topological properties within whole brain. Small-world network parameters and nodal topological properties were measured. Altered topological properties in brain areas between groups were selected as ROI-seeds, then functional connectivity among these ROI-seeds were compared between groups. Partial correlation analysis was performed to evaluate the relationship between sleepiness severity and functional connectivity or topological properties in the narcolepsy. Results 21 independent components out of 48 components were obtained. Compared with healthy controls, narcolepsy exhibited a significant decreased functional connectivity within the executive and salience network, while increased functional connectivity in bilateral frontal lobe within executive network can be detected in narcolepsy. There were no differences in small-world network properties between narcolepsy and healthy controls. The altered brain areas in nodal topological properties were mainly located in inferior frontal cortex, basal ganglia, anterior cingulate, sensory cortex, supplementary motor cortex and visual cortex between groups. In the partial correlation analysis, nodal topological properties in putamen, anterior cingulate and sensory cortex as well as functional connectivity between these brain regions were correlated with the severity of sleepiness (sleep latency, REM sleep latency and ESS) among narcolepsy. Conclusion Altered connectivity within executive network and salience network were found in narcolepsy. Functional connection changes between left frontal cortex and left caudate nucleus may be one of the parameters describing the severity of narcolepsy. Nodal topological properties alterations in left putamen and left posterior cingulate, changes in functional connectivity between left supplementary motor area and right occipital as well as changes in functional connectivity between left anterior cingulate gyrus and bilateral postcentral gyrus can be considered to be a specific indicator for evaluating the severity of narcolepsy. Support National Natural Science Foundation of China (81700088)National Program on Key Basic Research Project of China (973 Program, 2015CB856405)

Study Objectives: To identify rare allelic variants and HLA alleles in narcolepsy patients with hypocretin (orexin, HCRT) deficiency but lacking DQB1*06:02. Settings: China (Peking University People's Hospital), Czech Republic (Charles University), Denmark (Golstrup Hospital), Italy (University of Bologna), Korea (Catholic University), and USA (Stanford University). Design: CSF hypocretin-1, DQB1*06:02, clinical and polysomnographic data were collected in narcolepsy patients (552 with and 144 without cataplexy) from 6 sites. Numbers of cases with and without DQB1*06:02 and low CSF hypocretin-1 were compiled. HLA class I (A, B, C), class II (DRBs, DQA1, DQB1, DPA1, and DPB1), and whole exome sequencing were conducted in 9 DQB1*06:02 negative cases with low CSF hypocretin-1. Sanger sequencing of selected exons in DNMT1, HCRT, and MOG was performed to exclude mutations in known narcolepsy-associated genes. Measurements and Results: Classic narcolepsy markers DQB1*06:02 and low CSF hypocretin-1 were found in 87.4% of cases with cataplexy, and in 20.0% without cataplexy. Nine cases (all with cataplexy) were DQB1*06:02 negative with low CSF hypocretin-1, constituting 1.7% [0.8%-3.4%] of all cases with cataplexy and 1.8% [0.8%-3.4%] of cases with low CSF hypocretin independent of cataplexy across sites. Five HLA negative subjects had severe cataplexy, often occurring without clear triggers. Subjects had diverse ethnic backgrounds and HLA alleles at all loci, suggesting no single secondary HLA association. The rare subtype DPB1*0901, and homologous DPB1*10:01 subtype, were present in 5 subjects, suggesting a secondary association with HLA-DP. Preprohypocretin sequencing revealed no mutations beyond one previously reported in a very early onset case. No new MOG or DNMT1 mutations were found, nor were suspicious or private variants in novel genes identified through exome sequencing. Conclusions: Hypocretin, MOG, or DNMT1 mutations are exceptional findings in DQB1*06:02 negative cases with hypocretin deficiency. A secondary HLA-DP association may be present in these cases. These represent particularly difficult diagnostic challenges.

Introduction We investigate how characteristics of sleep-wake dynamics in humans are modified by narcolepsy, a clinical condition that is supposed to destabilize sleep-wake regulation. Subjects with and without cataplexy are considered separately. Differences in sleep scoring habits as a possible confounder have been examined. Aims and methods Four groups of subjects are considered: narcolepsy patients from China with (n = 88) and without (n = 15) cataplexy, healthy controls from China (n = 110) and from Europe (n = 187, 2 nights each). After sleep-stage scoring and calculation of sleep characteristic parameters, the distributions of wake-episode durations and sleep-episode durations are determined for each group and fitted by power laws (exponent α) and by exponentials (decay time τ). Results We find that wake duration distributions are consistent with power laws for healthy subjects (China: α = 0.88, Europe: α = 1.02). Wake durations in all groups of narcolepsy patients, however, follow the exponential law (τ = 6.2-8.1 min). All sleep duration distributions are best fitted by exponentials on long time scales (τ = 34-82 min). Conclusions We conclude that narcolepsy mainly alters the control of wake-episode durations but not sleep-episode durations, irrespective of cataplexy. Observed distributions of shortest wake and sleep durations suggest that differences in scoring habits regarding the scoring of short-term sleep stages may notably influence the fitting parameters but do not affect the main conclusion.

STUDY OBJECTIVES Obesity is a common feature of narcolepsy. In addition, an increased occurrence of non-insulin dependent diabetes has been reported. So far, it is not known whether glucose metabolism in narcolepsy is disturbed due to, or independently of obesity. DESIGN Case-control study. SETTING Sleep medicine clinic at a research institute. PATIENTS We studied 17 patients with narcolepsy/cataplexy compared to 17 healthy controls matched for age, sex, and body mass index (BMI). INTERVENTIONS A 75-g oral glucose tolerance test was performed. MEASUREMENTS Glucose tolerance was determined by computing plasma glucose curve following oral glucose challenge for 240 minutes; insulin sensitivity and insulin secretion by homeostasis model assessment and minimal model analysis. RESULTS Standard outcome measures and indices of the oral glucose tolerance test did not differ between the patient group and the group of control subjects. CONCLUSIONS In this study, no clinically relevant pathologic findings in the glucose metabolism of narcoleptic patients compared to weight matched controls were found. Thus, narcolepsy is unlikely to be a risk factor per se for impaired glucose tolerance or diabetes.

STUDY OBJECTIVES Kleine-Levin syndrome (KLS) is a rare disorder of relapsing sleepiness. The hypothesis was that the syndrome is related to a change in the vigilance peptide orexin A. METHODS From 2002 to 2013, 57 patients with relapsing hypersomnolence were clinically assessed in a referral academic center in Beijing, China, and 44 (28 males and 16 females; mean age 18.3 ± 8.9 y (mean ± standard deviation, range 9-57 y) were determined to have clinical and behavioral criteria consistent with KLS. Cerebrospinal fluid orexin A levels and diurnal blood pressure were measured in relapse versus remission in a subgroup of patients. RESULTS Presenting symptoms included relapsing or remitting excessive sleepiness-associated parallel complaints of cognitive changes (82%), eating disorders (84%); depression (45%); irritability (36%); hypersexuality (18%); and compulsions (11%). Episodes were 8.2 ± 3.3 days in duration. In relapse, diurnal values for blood pressure and heart rate were lower (P < 0.001). In a subgroup (n = 34), cerebrospinal fluid orexin A levels were ∼31% lower in a relapse versus remission (215.7 ± 81.5 versus 319.2 ± 95.92 pg/ml, P < 0.001); in three patients a pattern of lower levels during subsequent relapses was documented. CONCLUSIONS There are lower orexin A levels in the symptomatic phase than in remission and a fall and rise in blood pressure and heart rate, suggesting a role for orexin dysregulation in KLS pathophysiology.

Study objectives The purpose is to report the results of an effort to diagnose children with narcolepsy in a pediatric referral clinic. Design Between September 1998 and December 1999, a program was implemented to emphasize recognition of childhood narcolepsy. Patients underwent brain computed tomography (CT) scan and magnetic resonance imaging (MRI) testing. All children received a MSLT test following a routine night's sleep, and serological HLA typing for HLA DR2. Three who reported occasional snoring also underwent nocturnal PSG prior to the MSLT. Setting N/A. Patients or participants N/A. Interventions N/A. Measurements and results 29 (21 male, 8 female) children were identified with sleepiness and cataplexy. There was no evidence for brain functional or structural disease or for drug use. Sleep paralysis was elicited in 41%; hypnagogic hallucinations, in 59%. Psychosocial problems including emotional irritability and social isolation were present in 93% of the patients. Mean sleep latency on MSLT was 2.0+/-1.3 minutes; sleep-onset rapid eye movement (SOREM) occurred during 2/5 naps in 28 of 29 patients and 3/5 in 26/29 patients. The average number and latency of SOREM episodes were 4.2+/-0.9 episodes and 4.0+/-1.7 minutes, respectively. In those with snoring, a nocturnal PSG did not disclose sleep apneas/hypopneas. All patients but one were HLA DR2 positive. The estimated clinic incidence was 0.04%. Conclusions A program for recognition in a referral neurology clinic combined with an availability of the MSLT and HLA testing resulted in the new identification in North China of a number of children with narcolepsy syndromes.

OBJECTIVE To retrospectively describe childhood presentations of primary hypersomnia with an emphasis on narcolepsy-cataplexy in a Chinese population. METHODS A total of 417 children (< 18 years old) successively presenting with complaints of hypersomnia without anatomic cause or sleep apnea risk were evaluated using the Stanford Sleep Inventory, human leukocyte antigen (HLA) DQB1*0602 typing, and MSLT recordings. CSF hypocretin-1 was measured in 47 cases to document hypocretin deficiency. A subgroup ("narcolepsy/hypocretin deficiency") with likely hypocretin deficiency (low hypocretin-1 or HLA positive with clear-cut cataplexy) was further examined for presentations prior to, around, or after puberty. RESULTS Narcolepsy with (n = 361) or without (n = 17) cataplexy presented at an earlier age and with increased male predominance when compared to idiopathic hypersomnia (n = 39, P < 0.01). Nearly 70% of those with narcolepsy/hypocretin deficiency (n = 271) had disease onset before age 10 y, and 15% had onset before age 6, an unusually young age distribution. Onset was prior to puberty in 78% of cases. Clinical features were similar in presentations across puberty groups except for sleep paralysis, which increased in frequency with age/puberty. Mean sleep latency (MSL) decreased and the number of sleep onset REM periods (SOREMPs) increased with age/puberty, but MSLT diagnosis criteria (MSL ≤ 8 min, ≥ 2 SOREMPs) were similarly positive across groups. Familial clustering was present in only 1.7% of probands. CONCLUSION In children presenting with a complaint of primary hypersomnia to a sleep clinic in China, 86% (361/417) meet criteria for narcolepsy with cataplexy. Puberty did not affect positivity on the MSLT as a diagnostic feature. Sleep paralysis was the only symptom that increased with increasing age. In addition, narcolepsy with cataplexy in our clinic population appeared to begin at a younger age than usually reported in other studies.