RESUMEN
STUDY OBJECTIVES: This cross-sectional study aimed to characterize sleep patterns, the quality and duration of sleep, and estimate the prevalence of common sleep disorders and posttraumatic stress disorder (PTSD) in a hospital-based Veterans Affairs MOVE! (Managing Overweight Veterans Everywhere) clinic. METHODS: Participants completed five instruments: the Pittsburgh Sleep Quality Index (PSQI), Smith's Measure of Morningness/Eveningness, Restless Legs Syndrome Rating Scale, the STOP Questionnaire, and the Posttraumatic Stress Disorder (PTSD) Checklist - Civilian Version (PCL-C). RESULTS: Enrolled Veterans (n = 96) were mostly male (78%), African American (49%), mean age 58 (standard deviation [SD] 10.6) years, and mean body mass index (BMI) 38.4 kg/m(2) (SD 8.4). By PSQI, 89% rated sleep quality as "poor" (mean = 11.1, SD = 5.1), consistent with severely impaired sleep. Most were at high risk for sleep disorders including restless leg syndrome (53%), obstructive sleep apnea (66%), and circadian sleep disorders (72%). Forty-seven percent endorsed clinically significant symptoms of PTSD. Hypotheses-generating regression models suggest sleep latency (minutes before falling asleep) was associated with BMI (p = 0.018). Bedtime, getting up time, hours of sleep, waking up in the middle of the night or early morning, having to get up to use the bathroom, inability to breathe comfortably, cough or snore loudly, feeling too cold or too hot, having bad dreams, pain, and frequency of having trouble sleeping, were not significantly associated with BMI. CONCLUSIONS: Our cross-sectional study suggests that sleep difficulties are common among Veterans referred to a weight loss program at a Veterans Affairs Hospital. Controlled studies are needed to investigate whether the results are generalizable and whether obesity among veterans is a risk factor for sleep disorders and PTSD. COMMENTARY: A commentary on this article appears in this issue on page 943.
Asunto(s)
Obesidad/complicaciones , Obesidad/terapia , Pacientes Ambulatorios/estadística & datos numéricos , Trastornos del Sueño-Vigilia/complicaciones , Trastornos por Estrés Postraumático/complicaciones , Veteranos/estadística & datos numéricos , Programas de Reducción de Peso/métodos , Estudios Transversales , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estados Unidos , United States Department of Veterans Affairs , Población UrbanaRESUMEN
BACKGROUND & AIMS: In patients with cirrhosis, sleep disturbances are assumed to result from hepatic encephalopathy (HE). The effects of obstructive sleep apnea (OSA) on cognition, sleep parameters, or driving in patients with cirrhosis are unclear. METHODS: We performed a cross-sectional and prospective study of 118 subjects. Subjects were assigned to 1 of 4 groups: those with OSA and cirrhosis (without hepatic encephalopathy or ascites, n = 34), those with cirrhosis only (n = 30), those with OSA only (n = 29), and those without OSA or cirrhosis (controls, n = 25). None of the OSA patients were receiving continuous positive airway pressure (CPAP) therapy. Subjects underwent cognitive testing (paper-pencil tests for psychomotor speed and attention, as well as executive function tests), sleep assessment (daytime sleepiness and night-time sleep quality), and a monotonous driving simulation (worsening lane deviations over time indicated poor performance). We also tested patients with OSA, with cirrhosis (n = 10) and without cirrhosis (n = 7), before and after CPAP therapy. RESULTS: Daytime sleepiness and sleep quality were worse in subjects in the OSA groups (with or without cirrhosis) than subjects with cirrhosis alone or controls. Of subjects with only OSA, 36% had impaired psychomotor speed and attention, compared with more than 60% of subjects in both cirrhosis groups. In contrast, executive function was uniformly worse in subjects with OSA, with or without cirrhosis, than groups without OSA. Simulator performance (lane deviations) worsened over time in both OSA groups. CPAP therapy significantly increased executive function and sleep quality, and reduced simulator lane deviations and sleepiness, in OSA subjects with and without cirrhosis. After CPAP therapy, performance on the paper-pencil test improved significantly only in subjects with OSA without cirrhosis. CONCLUSIONS: OSA should be considered in evaluating sleep impairment in patients with cirrhosis. In patients with cirrhosis and OSA, psychomotor speed and attention issues likely are related to cirrhosis, whereas executive function and simulator performance are affected by OSA. CPAP therapy improves executive function and simulator performance in patients with OSA, regardless of cirrhosis.
Asunto(s)
Conducción de Automóvil , Cognición , Cirrosis Hepática/complicaciones , Apnea Obstructiva del Sueño/complicaciones , Trastornos del Sueño-Vigilia , Adulto , Anciano , Presión de las Vías Aéreas Positiva Contínua , Estudios Transversales , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Apnea Obstructiva del Sueño/terapiaRESUMEN
STUDY OBJECTIVES: Sleep disturbances in cirrhosis are assumed to be due to hepatic encephalopathy (HE). The interaction between cirrhosis, prior HE, and obstructive sleep apnea (OSA) has not been evaluated. We aimed to evaluate the additional effect of cirrhosis with and without prior HE on the sleep architecture and perceived sleep disturbances of OSA patients. METHODS: A case-control review of OSA patients who underwent polysomnography (PSG) in a liver-transplant center was performed. OSA patients with cirrhosis (with/without prior HE) were age-matched 1:1 with OSA patients without cirrhosis. Sleep quality, daytime sleepiness, sleep quality, and sleep architecture was compared between groups. RESULTS: Forty-nine OSA cirrhotic patients (age 57.4 ± 8.3 years, model for end-stage liver disease (MELD) 8.3 ± 5.4, 51% HCV, 20% prior HE) were age-matched 1:1 to OSA patients without cirrhosis. Apnea-hypopnea index, arousal index, sleep efficiency, daytime sleepiness, and effect of sleepiness on daily activities were similar between OSA patients with/ without cirrhosis. Sleep architecture, including %slow wave sleep (SWS), was also not different between the groups. MELD was positively correlated with time in early (N1) stage (r = 0.4, p = 0.03). All prior HE patients (n = 10) had a shift of the architecture towards early, non-restorative sleep (higher % [N2] stage [66 vs 52%, p = 0.005], lower % SWS [0 vs 29%, p = 0.02], lower REM latency [95 vs 151 minutes, p = 0.04]) compared to the rest. Alcoholic etiology was associated with higher latency to N1/N2 sleep, but no other effect on sleep architecture was seen. CONCLUSIONS: OSA can contribute to sleep disturbance in cirrhosis and should be considered in the differential of sleep disturbances in cirrhosis. Prior HE may synergize with OSA in worsening the sleep architecture.