Explore the vast range of titles available.

Abstract Introduction Isolated sleep paralysis (ISP) occurs when rapid eye movement (REM)-based atonia intrudes into wakefulness, outside the context of narcolepsy, substance abuse, mental disorder or other medical conditions. No “gold standard” assessment and diagnostic instrument currently exists. Report of Case A 63-year old female with hypersomnia and positive airway pressure (PAP)-controlled obstructive sleep apnea was referred for recurrent episodes of paralysis during sleep-wake transitions, lasting 15-20 seconds, occurring every 2-3 years since the age of 15, and associated with fear and anxiety. Episodes were more frequent in the last 2 years after significant sleep deprivation and starting a weight loss supplement, BIO-X4, which contains green tea and probiotics. No cataplexy, or history of traumatic brain injury and stroke were identified. Epworth Sleepiness Scale score was 14 on armodafinil. Reported sleep amounts were regularly scheduled 6-7-hour periods, with no suggestion of circadian dysfunction. In 2016, polysomnogram showed Apnea-Hypopnea index of 2.6/hour, Respiratory Disturbance Index of 13.8/hour with oxygen nadir of 92% in the setting of hypersomnia. Continuous PAP of 11 cmH20 was initiated after a successful titration with controlled residual AHI during follow-ups. Multiple Sleep Latency Test during the same time revealed mean sleep latency of 5.5 minutes and no sleep-onset REM with 5 naps. Brain imaging and electroencephalogram were both normal as well as drug panel, blood counts, metabolic profile and thyroid function. Decreased episodes and severity of recurrent ISP were reported after discontinuation of the supplement. Apart from anxiety related to the episodes, the patient denied any interference with daytime function. Conclusion Isolated sleep paralysis is an important sleep disorder that requires proper evaluation to rule out competing diagnoses and consideration of therapeutic interventions. Likely associated with a lack of understanding and available literature, the prevalence in the general population is likely higher than what is currently perceived.

Abstract Non-24-hour sleep-wake rhythm disorder is characterized by inability to maintain stable entrainment to a 24h sleep-wake pattern. Non-24-hour sleep-wake rhythm disorder occurs more in blind individuals and is uncommon in sighted individuals. Here we report a 57-y-old male with obstructive sleep apnea adequately controlled with CPAP therapy, who presented with a chief complaint of \"sleep cycling\" over the past year including intermittent insomnia. His usual bedtime was 21:00, but he noticed that his bedtime kept getting delayed every day to the extent that he had to \"reset\" his bedtime every two weeks. As his adherence to CPAP therapy was very good in that he used CPAP therapy whenever he slept, a sample of his sleep pattern was able to be obtained from his PAP download data (Figure 1). He reported that he was unemployed and rarely left the room he rented in a house, and that he kept his window blinds closed at all times. He denied signs/symptoms suggestive of untreated or under-treated obstructive sleep apnea, restless leg syndrome, depression, or anxiety. His other medical history and medications are noncontributory. His history and documented progressively delayed bedtime out of phase with 24-hour light-dark cycle as demonstrated on his PAP download pointed to a diagnosis of non-24-hour sleep-wake rhythm disorder. Our patient's non-24-hour sleep-wake rhythm disorder was most likely associated with his reclusive lifestyle with resultant lack of exposure to natural light and other zeitgebers. The regression line derived from his PAP download showed a daily bedtime delay of approximately 40 minutes (tau = 24.7 hr). To our knowledge, this is the first case of non-24-hour sleep-wake rhythm disorder that was diagnosed through PAP download. Given the prevalence of obstructive sleep apnea, PAP download can be utilized to facilitate the diagnose of circadian rhythm disorders in patients with good PAP adherence.

Obstructive sleep apnea (OSA) is a common sleep disorder affecting approximately 16% of adults (24% of men and 9% of women), and, if untreated, it can cause significant complications (Young, 2009). This study evaluates 56 adult patients with Down syndrome and analyzed retrospective data to determine the: (1) prevalence of OSA, (2) severity of OSA, and (3) association between body mass index (BMI) and OSA. Of those participants that had polysomnography (PSG) testing available, 82.1% were diagnosed with OSA, divided by severity into mild (45.7%), moderate (15.2%), and severe (39.1%) levels. Because of the high prevalence of OSA among our study population, we recommend that all adults with DS be screened for OSA with PSG.

Objective: We sought to ascertain the validity of two screening scales for obstructive sleep apnea (OSA) in pregnancy and to establish the prevalence of OSA in pregnancy. Study Design: In this prospective observational study, two screening scales were administered. Screen positive subjects were referred for diagnostic polysomnography (PSG); if admitted for antepartum care, screen positive subjects underwent a modified study with a type 3 device (T3D). Result: A total of 1509 subjects underwent OSA screening; 58 completed diagnostic testing. Neither measure was a reliable diagnostic tool for OSA as determined by T3D or PSG (detection rates of 10.3% and 18.0%, respectively). Among screen positive subjects undergoing PSG or T3D testing, 15.5% ultimately met ‘gold standard’ OSA diagnostic criteria for an estimated point prevalence of 4.9%. Conclusion: In this prospective trial, screening positive on the Berlin questionnaire or Epworth sleepiness scale was poorly predictive of OSA among gravidae and was associated with a high false referral rate.

Background The coexistence of COPD and asthma is widely recognized but has not been well described. This study characterizes clinical features, spirometry, and chest CT scans of smoking subjects with both COPD and asthma. Methods We performed a cross-sectional study comparing subjects with COPD and asthma to subjects with COPD alone in the COPDGene Study. Results 119 (13%) of 915 subjects with COPD reported a history of physician-diagnosed asthma. These subjects were younger (61.3 vs 64.7 years old, p = 0.0001) with lower lifetime smoking intensity (43.7 vs 55.1 pack years, p = 0.0001). More African-Americans reported a history of asthma (33.6% vs 15.6%, p < 0.0001). Subjects with COPD and asthma demonstrated worse disease-related quality of life, were more likely to have had a severe COPD exacerbation in the past year, and were more likely to experience frequent exacerbations (OR 3.55 [2.19, 5.75], p < 0.0001). Subjects with COPD and asthma demonstrated greater gas-trapping on chest CT. There were no differences in spirometry or CT measurements of emphysema or airway wall thickness. Conclusion Subjects with COPD and asthma represent a relevant clinical population, with worse health-related quality of life. They experience more frequent and severe respiratory exacerbations despite younger age and reduced lifetime smoking history. Trial registration ClinicalTrials.gov: NCT00608764

BackgroundThe value of quantitative CT (QCT) to identify chronic obstructive pulmonary disease (COPD) phenotypes is increasingly appreciated. The authors hypothesised that QCT-defined emphysema and airway abnormalities relate to St George's Respiratory Questionnaire (SGRQ) and Body-Mass Index, Airflow Obstruction, Dyspnea and Exercise Capacity Index (BODE).Methods1200 COPDGene subjects meeting Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria for COPD with QCT analysis were included. Total lung emphysema was measured using the density mask technique with a −950 Hounsfield unit threshold. An automated programme measured mean wall thickness (WT), wall area percentage (WA%) and 10 mm lumenal perimeter (pi10) in six segmental bronchi. Separate multivariate analyses examined the relative influence of airway measures and emphysema on SGRQ and BODE.ResultsIn separate models predicting SGRQ score, a 1 unit SD increase in each airway measure predicted higher SGRQ scores (for WT, 1.90 points higher, p=0.002; for WA%, 1.52 points higher, p=0.02; for pi10, 2.83 points higher p<0.001). The comparable increase in SGRQ for a 1 unit SD increase in emphysema percentage in these models was relatively weaker, significant only in the pi10 model (for emphysema percentage, 1.45 points higher, p=0.01). In separate models predicting BODE, a 1 unit SD increase in each airway measure predicted higher BODE scores (for WT, 1.07-fold increase, p<0.001; for WA%, 1.20-fold increase, p<0.001; for pi10, 1.16-fold increase, p<0.001). In these models, emphysema more strongly influenced BODE (range 1.24–1.26-fold increase, p<0.001).ConclusionEmphysema and airway disease both relate to clinically important parameters. The relative influence of airway disease is greater for SGRQ; the relative influence of emphysema is greater for BODE.

Background Chronic bronchitis (CB) has been related to poor outcomes in Chronic Obstructive Pulmonary Disease (COPD). From a clinical standpoint, we have shown that subjects with CB in a group with moderate to severe airflow obstruction were younger, more likely to be current smokers, male, Caucasian, had worse health related quality of life, more dyspnea, and increased exacerbation history compared to those without CB. We sought to further refine our clinical characterization of chronic bronchitics in a larger cohort and analyze the CT correlates of CB in COPD subjects. We hypothesized that COPD patients with CB would have thicker airways and a greater history of smoking, acute bronchitis, allergic rhinitis, and occupational exposures compared to those without CB. Methods We divided 2703 GOLD 1–4 subjects in the Genetic Epidemiology of COPD (COPDGene®) Study into two groups based on symptoms: chronic bronchitis (CB+, n = 663, 24.5%) and no chronic bronchitis (CB-, n = 2040, 75.5%). Subjects underwent extensive clinical characterization, and quantitative CT analysis to calculate mean wall area percent (WA%) of 6 segmental airways was performed using VIDA PW2 ( http://www.vidadiagnostics.com ). Square roots of the wall areas of bronchi with internal perimeters 10 mm and 15 mm (Pi10 and Pi15, respectively), % emphysema, %gas trapping, were calculated using 3D Slicer ( http://www.slicer.org ). Results There were no differences in % emphysema (11.4 ± 12.0 vs. 12.0 ± 12.6%, p = 0.347) or % gas trapping (35.3 ± 21.2 vs. 36.3 ± 20.6%, p = 0.272) between groups. Mean segmental WA% (63.0 ± 3.2 vs. 62.0 ± 3.1%, p < 0.0001), Pi10 (3.72 ± 0.15 vs. 3.69 ± 0.14 mm, p < 0.0001), and Pi15 (5.24 ± 0.22 vs. 5.17 ± 0.20, p < 0.0001) were greater in the CB + group. Greater percentages of gastroesophageal reflux, allergic rhinitis, histories of asthma and acute bronchitis, exposures to dusts and occupational exposures, and current smokers were seen in the CB + group. In multivariate binomial logistic regression, male gender, Caucasian race, a lower FEV 1 %, allergic rhinitis, history of acute bronchitis, current smoking, and increased airway wall thickness increased odds for having CB. Conclusions Histories of asthma, allergic rhinitis, acute bronchitis, current smoking, a lower FEV 1 %, Caucasian race, male gender, and increased airway wall thickness are associated with CB. These data provide clinical and radiologic correlations to the clinical phenotype of CB.

Chronic bronchitis is, by definition, a chronic condition, but the development and remission of this condition in cigarette smokers with or without chronic obstructive pulmonary disease (COPD) are poorly understood. Also, it is unclear how the persistence or new development of chronic bronchitis affects symptoms and outcomes.RATIONALEChronic bronchitis is, by definition, a chronic condition, but the development and remission of this condition in cigarette smokers with or without chronic obstructive pulmonary disease (COPD) are poorly understood. Also, it is unclear how the persistence or new development of chronic bronchitis affects symptoms and outcomes.To ascertain the relationship between smoking status and the presence or absence of chronic bronchitis and the subsequent effects on symptoms and outcomes.OBJECTIVESTo ascertain the relationship between smoking status and the presence or absence of chronic bronchitis and the subsequent effects on symptoms and outcomes.We analyzed 1,775 current or ex-smokers with GOLD (Global Initiative for Chronic Obstructive Lung Disease) stage 0-IV COPD in phase 2 of the Genetic Epidemiology of COPD (COPDGene) Study, which included subjects after 5 years of follow-up from phase 1. We asked subjects at enrollment and at 5 years of follow-up about symptoms consistent with chronic bronchitis. We divided subjects into four groups: persistent chronic bronchitis- (negative at phase 1/negative at phase 2), resolved chronic bronchitis (positive/negative), new chronic bronchitis (negative/positive), and persistent chronic bronchitis+ (positive/positive). We analyzed respiratory symptoms, health-related quality of life, lung function, exacerbation frequency, and 6-minute walk distance.METHODSWe analyzed 1,775 current or ex-smokers with GOLD (Global Initiative for Chronic Obstructive Lung Disease) stage 0-IV COPD in phase 2 of the Genetic Epidemiology of COPD (COPDGene) Study, which included subjects after 5 years of follow-up from phase 1. We asked subjects at enrollment and at 5 years of follow-up about symptoms consistent with chronic bronchitis. We divided subjects into four groups: persistent chronic bronchitis- (negative at phase 1/negative at phase 2), resolved chronic bronchitis (positive/negative), new chronic bronchitis (negative/positive), and persistent chronic bronchitis+ (positive/positive). We analyzed respiratory symptoms, health-related quality of life, lung function, exacerbation frequency, and 6-minute walk distance.Compared with the persistent chronic bronchitis- group, members of the persistent chronic bronchitis+ group were more likely to have continued smoking (53.4%). Subjects with new chronic bronchitis were more likely to have resumed (6.6%) or continued smoking (45.6%), whereas subjects with resolved chronic bronchitis were more likely to have quit smoking (23.5%). Compared with the persistent chronic bronchitis- group, the other groups had a shorter 6-minute walk distance, worse lung function, greater exacerbation frequency, and worse respiratory symptoms. Modified Medical Research Council dyspnea and St. George's Respiratory Questionnaire scores worsened between phase 1 and phase 2 in subjects with new chronic bronchitis but improved in the resolved chronic bronchitis group. On multinomial logistic regression, quitting smoking conferred an odds ratio (OR) of 4.289 (95% confidence interval [CI], 2.689-6.842) for resolved chronic bronchitis, whereas resuming smoking had an OR of 4.585 (95% CI, 2.008-10.471) for new chronic bronchitis. Persistent smoking had an OR of 2.621 (95% CI, 1.677-4.096) and 5.767 (95% CI, 3.702-8.983) for subjects with new chronic bronchitis and subjects with persistent chronic bronchitis, respectively.MEASUREMENTS AND MAIN RESULTSCompared with the persistent chronic bronchitis- group, members of the persistent chronic bronchitis+ group were more likely to have continued smoking (53.4%). Subjects with new chronic bronchitis were more likely to have resumed (6.6%) or continued smoking (45.6%), whereas subjects with resolved chronic bronchitis were more likely to have quit smoking (23.5%). Compared with the persistent chronic bronchitis- group, the other groups had a shorter 6-minute walk distance, worse lung function, greater exacerbation frequency, and worse respiratory symptoms. Modified Medical Research Council dyspnea and St. George's Respiratory Questionnaire scores worsened between phase 1 and phase 2 in subjects with new chronic bronchitis but improved in the resolved chronic bronchitis group. On multinomial logistic regression, quitting smoking conferred an odds ratio (OR) of 4.289 (95% confidence interval [CI], 2.689-6.842) for resolved chronic bronchitis, whereas resuming smoking had an OR of 4.585 (95% CI, 2.008-10.471) for new chronic bronchitis. Persistent smoking had an OR of 2.621 (95% CI, 1.677-4.096) and 5.767 (95% CI, 3.702-8.983) for subjects with new chronic bronchitis and subjects with persistent chronic bronchitis, respectively.Persistent and newly developed chronic bronchitis are associated with continued or resumed smoking, greater respiratory symptoms, worse health-related quality of life, worse lung function, and greater exacerbation frequency. These findings stress the importance of repeatedly assessing chronic cough and sputum production in smokers to identify those at risk for poor outcomes.CONCLUSIONSPersistent and newly developed chronic bronchitis are associated with continued or resumed smoking, greater respiratory symptoms, worse health-related quality of life, worse lung function, and greater exacerbation frequency. These findings stress the importance of repeatedly assessing chronic cough and sputum production in smokers to identify those at risk for poor outcomes.

Activity-related breathlessness, measured using the modified Medical Research Council (mMRC) breathlessness scale, is about twice as common among women as among men in the population for unclear reasons (1, 3). All models were adjusted for age, level of chronic airflow limitation (FEVj/FVC), body mass index, pack-years of smoking, current smoking, and physician-diagnosed asthma, COPD, chronic bronchitis, emphysema, congestive heart failure, ischemic heart disease, and diabetes mellitus. Relative and absolute lung volumes provide complementary information on the lung volume impairment and remaining ventilatory reserve and should be evaluated in both research and clinical care. ? M.E. was supported by unrestricted grants from the Swedish Society of Medicine, the Swedish Respiratory Society, the Swedish Heart-Lung Foundation, the Scientific Committee of Blekinge County Council, the Wera and Emil Cornell Foundation, and the Swedish Society for Medical Research.

Chronic obstructive pulmonary disease (COPD) is a complex disease with strong environmental and genetic influences and sexually dimorphic features. Although genetic risk factors for COPD have been identified, much of the heritability remains unexplained. Sex-based genetic association studies may uncover additional COPD genetic risk factors. We studied current and former smokers from COPD case–control cohorts (COPDGene non-Hispanic whites and African Americans, Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-Points, and Genetics of Chronic Obstructive Lung Disease). COPD was defined as post-bronchodilator forced expiratory volume in 1 second/forced vital capacity less than 0.70 and forced expiratory volume in 1 second percent predicted less than 80. Testing was performed across all cohorts and combined in a meta-analysis adjusted for age, pack-years, and genetic ancestry. We first performed genome-wide single-nucleotide polymorphism (SNP)-by-sex interaction testing on the outcome of COPD affection status. We performed sex-stratified association testing for SNPs with interaction P less than 10−6. We examined over 8 million SNPs in four populations, including 6,260 subjects with COPD (40.6% female) and 5,269 smoking control subjects (47.3% female). The SNP rs9615358 in the cadherin gene CELSR1 approached genome-wide significance for an interaction with sex (P = 1.24 × 10−7). In the sex-stratified meta-analysis, this SNP was associated with COPD among females (odds ratio, 1.37 [95% confidence interval, 1.25–1.49]; P = 3.32 × 10−7) but not males (odds ratio, 0.90 [95% confidence interval, 0.79–1.01]; P = 0.06). CELSR1 is involved in fetal lung development. In a human fetal lung tissue dataset, we observed greater CELSR1 expression in female compared with male samples. This SNP-by-sex genome-wide association analysis identified the fetal lung development gene, CELSR1, as a potential sex-specific risk factor for COPD. Identifying sex-specific genetic risk factors may reveal new insights into sexually dimorphic features of COPD.