Effects of Cognitive Behavioral Therapy for Insomnia on Sleep, Symptoms, Stress, and Autonomic Function Among Patients With Heart Failure.

Background: Insomnia is common among patients with stable heart failure (HF) and associated with inflammation and altered autonomic function. Purpose: The purposes of this study were to examine the effects of cognitive behavioral therapy for insomnia (CBT-I) on the Hypothalamic Pituitary (HPA) Axis, autonomic function, inflammation, and circadian rhythmicity and the associations between these biomarkers and insomnia, sleep characteristics, symptoms, functional performance, and sleep-related cognitions. Methods: We conducted a subanalysis of a pilot randomized controlled trial (RCT, NCT02827799) whose primary aim was to test the effects of CBT-I on insomnia. We randomized 51 patients with stable Class II-IV HF to CBT-I (n = 30) or attention control (n = 21). Participants completed wrist actigraphy and self-reported insomnia severity, sleep characteristics, sleep-related cognitions, daytime symptoms, and functional performance. We measured day and nighttime urinary free cortisol, melatonin sulfate, epinephrine, and norepinephrine at baseline, and two weeks after CBT-I and computed general linear models and partial correlations. Results: CBT-I had no effects on the biomarkers, but there were statistically significant negative cross-sectional correlations between the ratio of day and night urinary free cortisol and sleep disturbance, anxiety, fatigue, depression, and negative sleep cognitions. Increases in the ratio between day and night cortisol were associated with statistically significant improvements in fatigue, depression, sleep duration, and sleep-related cognitions. Conclusions: Biomarkers of stress and autonomic function are associated with sleep, sleep-related symptoms, and cognitions among people with chronic HF. Future studies are needed to identify potential causal relationships and the impact of sleep interventions.

Effects of Cognitive Behavioral Therapy for Insomnia on Sleep-Related Cognitions Among Patients With Stable Heart Failure.

OBJECTIVE/BACKGROUND: Cognitive behavioral therapy for insomnia (CBT-I) improves insomnia and fatigue among chronic heart failure (HF) patients, but the extent to which sleep-related cognitions explain CBT-I outcomes in these patients is unknown. We examined the effects of CBT-I on sleep-related cognitions, associations between changes in sleep-related cognitions and changes in sleep and symptoms after CBT-I, and the extent to which cognitions mediated the effects of CBT-I. PARTICIPANTS: Stable New York Heart Association Class II-III HF patients (total n = 51; n = 26 or 51.0% women; M age = 59.1 ± 15.1 years). METHODS: HF patients were randomized in groups to group CBT-I (n = 30) or attention control (HF self-management education, n = 21) and completed actigraphy, the Insomnia Severity Index, Pittsburgh Sleep Quality Index, Dysfunctional Beliefs and Attitudes about Sleep (DBAS) and Sleep Disturbance Questionnaires (SDQ), and self-reported fatigue, depression, anxiety, and sleepiness (baseline, immediately after treatment, six months). We used mixed-effects modeling, mediation analysis with a bootstrapping approach, and Pearson correlations. RESULTS: There was a statistically significant group × mult time effect on DBAS. DBAS mediated the effects of CBT-I on insomnia severity and partially mediated CBT-I effects on fatigue. Improvements in dysfunctional cognitions were associated with improved sleep quality, insomnia severity, sleep latency and decreased fatigue, depression, and anxiety, with sustained effects at six months. CONCLUSIONS: Improvement in dysfunctional sleep-related cognitions is an important mechanism for CBT-I effects among HF patients who are especially vulnerable to poor sleep and high symptom burden.

Mechanisms of reduced sleepiness symptoms in heart failure and obstructive sleep apnea.

Patients with both heart failure and obstructive sleep apnea often have poor, repeatedly disrupted sleep, and yet they frequently do not complain of excessive daytime sleepiness. Understanding this lack of perceived sleepiness is crucial for the case identification and treatment of obstructive sleep apnea in the heart failure population at high risk of this disease, especially given the association between untreated obstructive sleep apnea and mortality among patients with heart failure. In this review, we present epidemiologic evidence concerning the lack of sleepiness symptoms in heart failure and obstructive sleep apnea, explore possible mechanistic explanations for this relationship, assess the benefits of treatment in this population, discuss implications for clinical practice and explore directions for future research.

Lung Function of Children at Three Sites of Varying Ambient Air Pollution Levels in Uganda: A Cross Sectional Comparative Study.

Air pollution is a major cause of sub-optimal lung function and lung diseases in childhood and adulthood. In this study we compared the lung function (measured by spirometry) of 537 Ugandan children, mean age 11.1 years in sites with high (Kampala and Jinja) and low (Buwenge) ambient air pollution levels, based on the concentrations of particulate matter smaller than 2.5 micrometres in diameter (PM2.5). Factors associated with lung function were explored in a multiple linear regression model. PM2.5 level in Kampala, Jinja and Buwenge were 177.5 µg/m³, 96.3 µg/m³ and 31.4 µg/m³ respectively (p = 0.0000). Respectively mean forced vital capacity as % of predicted (FVC%), forced expiratory volume in one second as % of predicted (FEV1%) and forced expiratory flow 25⁻75% as % of predicted (FEF25⁻75%) of children in high ambient air pollution sites (Kampala and Jinja) vs. those in the low ambient air pollution site (Buwenge subcounty) were: FVC% (101.4%, vs. 104.0%, p = 0.043), FEV1% (93.9% vs. 98.0, p = 0.001) and FEF25⁻75% (87.8 vs. 94.0, p = 0.002). The proportions of children whose %predicted parameters were less than 80% predicted (abnormal) were higher among children living in high ambient air pollution than those living in lower low ambient air pollutions areas with the exception of FVC%; high vs. low: FEV1 < 80%, %predicted (12.0% vs. 5.3%, p = 0.021) and FEF25⁻75 < 80%, %predicted (37.7% vs. 29.3%, p = 0.052) Factors associated with lung function were (coefficient, p-value): FVC% urban residence (-3.87, p = 0.004), current cough (-2.65, p = 0.048), underweight (-6.62, p = 0.000), and overweight (11.15, p = 0.000); FEV1% underweight (-6.54, p = 0.000) and FEF25⁻75% urban residence (-8.67, p = 0.030) and exposure to biomass smoke (-7.48, p = 0.027). Children in study sites with high ambient air pollution had lower lung function than those in sites with low ambient air pollution. Urban residence, underweight, exposure to biomass smoke and cough were associated with lower lung function.

Practical approach to detection and management of acute kidney injury in critically ill patient.

BACKGROUND: Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with high morbidity and mortality. This paper provides a critical review of the etiologies of AKI and a systematic approach toward its diagnosis and management with emphasis on fluid volume assessment and the use of urine biochemical profile and microscopy in identifying the nature and the site of kidney injury. MATERIALS AND METHODS: The search of PubMed and selection of papers had employed observational designs or randomized control trials relevant to AKI. RESULTS: AKI is defined by the rate of rise of serum creatinine and a decline in urine output. The pathophysiology is diverse and requires a careful and systematic assessment of predisposing factors and localization of site of injury. The majority of AKIs are due to prerenal causes such as fluid volume deficit, sepsis, or renal as in acute tubular injury. The use of central venous and arterial blood pressure monitoring and inferior vena cava echocardiography complemented by urine analysis and microscopy allows assessment of fluid volume status and AKI etiology. CONCLUSIONS: Timely intervention by avoidance of fluid volume deficit and nephrotoxic agents and blood pressure support can reduce the incidence of AKI in critically ill patients.

Chitinase-3-like protein-1 (YKL-40) as a marker of endothelial dysfunction in obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is a highly prevalent disorder affecting 15-24% of adults and triples the risk for hypertension independent of other risk factors. The exact mechanisms of endothelial dysfunction and variable susceptibility to hypertension in OSA are not entirely clear. No biomarker to date has been found to be associated with hypertension in OSA. Chitinase-3-like protein-1(YKL-40) is a circulating moiety with roles in injury, repair and angiogenesis that is dysregulated in atherosclerosis and correlates with increased cardiovascular morbidity and mortality. We sought to determine the role of YKL-40, as a biomarker, for endothelial dysfunction and hypertension in OSA. METHODS: All subjects underwent polysomnography for suspected sleep-disordered breathing. Endothelial-dependent vasodilatory capacity was assessed using flow-mediated vasodilation (FMD). YKL-40 was measured in plasma using ELISA methodology. RESULTS: We studied 95 subjects in four groups according to OSA and hypertension status. FMD was markedly impaired in hypertensive OSA (8.0% ± 0.5 vasodilation) compared to normotensive OSA (13.5% ± 0.5, P <0.0001) and non-OSA with hypertension (10.5% ± 0.8, P <0.01) and without hypertension (16.1% ± 1.0, P <0.0001). YKL-40 was significantly elevated only in hypertensive OSA compared to other three groups and had a negative correlation with FMD (r=-0.37, P = 0.0008). Receiver operating characteristic (ROC) curve analysis for YKL-40 in predicting endothelial dysfunction had a sensitivity of 71% and a specificity of 64% with AUC = 0.68, 0.57 to 0.80, P = 0.004. CONCLUSIONS: Elevated circulating levels of YKL-40 are observed in only hypertensive OSA and have a significant negative correlation with endothelial function. This specificity suggests YKL-40 could be a potential biomarker for endothelial dysfunction in OSA.

The emerging role of microRNAs in hypoxia-induced pulmonary hypertension.

PURPOSE: The aim of this review is to discuss hypoxia-induced pulmonary hypertension (PH) and the role of microRNAs (miRNAs). BACKGROUND: Acute global hypoxia causes pulmonary vasoconstriction and increased pulmonary arterial blood pressure. Chronic exposure to sustained or intermittent hypoxia as in high altitude residents, chronic obstructive lung disease and sleep-disordered breathing can lead to pulmonary hypertension (PH) and right ventricular dysfunction. The development of PH is a poor prognostic sign in these patients that affects both quality of life and mortality. The mechanism of PH due to hypoxia has not been fully established. However, its pathophenotype is similar to idiopathic pulmonary arterial hypertension in the form of vascular cell proliferation and aberrant vascular remodeling. MicroRNAs (miRNAs) are small non-coding RNA molecules that negatively regulate gene expression, therefore potentially regulating a host of cellular signaling pathways. Several miRNAs have been identified to be involved in hypoxia models of PH in animals, in patients with PH, congestive heart failure and myocardial infarction. RESULTS: MiRNAs have been mechanistically linked to the control of a wide range of cellular responses-hypoxia, TGF-ß signaling and inflammatory pathways-known to influence normal developmental physiology as well as regulating pulmonary arterial smooth muscle cell and endothelial cell phenotypes and their influence on pulmonary remodeling in the setting of hypoxia and pulmonary arterial hypertension (PAH). The blood levels of these miRNAs correlate with disease severity and prognosis. CONCLUSIONS: Research on the role of these potential biomarkers will provide insight into the pathogenesis of PH and right heart failure and opportunities in therapeutics.

Modafinil and sleep architecture in an inpatient-outpatient treatment study of cocaine dependence.

OBJECTIVE: To determine whether the increase in slow-wave sleep associated with modafinil treatment in chronic cocaine users mediates improved clinical outcomes. METHOD: 57 cocaine dependent participants were randomized to receive modafinil 400mg or placebo daily during a period of inpatient treatment followed by six weeks of outpatient treatment. Participants underwent polysomnographic sleep recording during inpatient treatment prior to and after starting modafinil. Outpatient treatment consisted of weekly cognitive behavioral therapy. Contingency management was used to promote participation in treatment and research demands, including thrice weekly visits during the outpatient phase for urine toxicology screens and other assessments. The primary clinical outcome was the percent of urine toxicology screens that were negative for cocaine. RESULTS: Modafinil treatment was associated with a higher mean percentage (52% vs. 26%) of cocaine-free urine screens (p=0.02) and an increase in N3 sleep time (p=0.002). The change in N3 sleep time mediated the higher rate of cocaine-free urine screens. Modafinil treatment was also associated with more consecutive days abstinent during outpatient treatment, greater survival of abstinence, higher daily rates of abstinence, and less sleep degradation typically associated with abstinence from chronic cocaine use. CONCLUSIONS: Morning-dosed modafinil improves slow-wave sleep in abstinent cocaine users in the inpatient setting, and this effect is a statistical mediator of improved clinical outcomes associated with continued modafinil treatment. The high rates of abstinence achieved in this trial suggest that promoting healthy sleep physiology in an inpatient setting may be important in the effective treatment of cocaine dependence.

The State of Ambient Air Quality in Two Ugandan Cities: A Pilot Cross-Sectional Spatial Assessment.

Air pollution is one of the leading global public health risks but its magnitude in many developing countries' cities is not known. We aimed to measure the concentration of particulate matter with aerodynamic diameter <2.5 µm (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3) pollutants in two Ugandan cities (Kampala and Jinja). PM2.5, O3, temperature and humidity were measured with real-time monitors, while NO2 and SO2 were measured with diffusion tubes. We found that the mean concentrations of the air pollutants PM2.5, NO2, SO2 and O3 were 132.1 µg/m3, 24.9 µg/m3, 3.7 µg/m3 and 11.4 µg/m3, respectively. The mean PM2.5 concentration is 5.3 times the World Health Organization (WHO) cut-off limits while the NO2, SO2 and O3 concentrations are below WHO cut-off limits. PM2.5 levels were higher in Kampala than in Jinja (138.6 µg/m3 vs. 99.3 µg/m3) and at industrial than residential sites (152.6 µg/m3 vs. 120.5 µg/m3) but residential sites with unpaved roads also had high PM2.5 concentrations (152.6 µg/m3). In conclusion, air pollutant concentrations in Kampala and Jinja in Uganda are dangerously high. Long-term studies are needed to characterize air pollution levels during all seasons, to assess related public health impacts, and explore mitigation approaches.

Time Spent in Lateral Sleep Position and Asymmetry in Glaucoma.

PURPOSE: To explore sleep position in asymmetric primary open-angle glaucoma (POAG) with a focus on low pressure glaucoma (LPG). METHODS: Sleep laboratory videos of 54 POAG patients were examined for lateral sleep. Then, 29 LPG patients (intraocular pressure [IOP] < 22 mm Hg) with an intereye visual field index (VFI) asymmetry of more than 5% continuously recorded their sleep position at home for 2 nights by using a portable device. Correlations were sought between sleep position, visual field (VF), and retinal nerve fiber layer (RNFL) symmetry as well as ocular biometric data and positional IOP changes. Finally, an expanded data set of 178 POAG patients (63 LPG and 115 high pressure glaucoma [HPG; IOP ≥ 22 mm Hg]) was used to correlate VF and the RNFL symmetry to the self-assessed sleep position collected in a survey. RESULTS: In the video analysis, patients spent 19% ± 2% (mean ± SEM) more time sleeping on one side than on the other. Right-sided sleep was preferred. Right-sided sleep was 1.6 times more common in continuously recorded home data and correlated to an asymmetric VF that was worse in the left eye (b = -0.422, P = 0.002). Pulse amplitude of left eyes was lower in the right decubitus position (P = 0.02). In the expanded survey, 73% of LPG and 58% of HPG patients slept asymmetrically. Right-sided sleepers had a worse RNFL symmetry score. CONCLUSIONS: Asymmetric sleep behavior is common. Right-sided sleep was preferred and correlated with a lower VFI on the left.

Pulmonary hypertension in obstructive sleep apnea: is it clinically significant? A critical analysis of the association and pathophysiology.

The development of pulmonary hypertension is a poor prognostic sign in patients with obstructive sleep apnea (OSA) and affects both mortality and quality of life. Although pulmonary hypertension in OSA is traditionally viewed as a result of apneas and intermittent hypoxia during sleep, recent studies indicate that neither of these factors correlates very well with pulmonary artery pressure. Human data show that pulmonary hypertension in the setting of OSA is, in large part, due to left heart dysfunction with either preserved or diminished ejection fraction. Longstanding increased left heart filling pressures eventually lead to pulmonary venous hypertension. The combination of hypoxic pulmonary vasoconstriction and pulmonary venous hypertension with abnormal production of mediators will result in vascular cell proliferation and aberrant vascular remodeling leading to pulmonary hypertension. These changes are in many ways similar to those seen in other forms of pulmonary hypertension and suggest shared mechanisms. The majority of patients with OSA do not receive a diagnosis and are undertreated. Appreciating the high prevalence and understanding the mechanisms of pulmonary hypertension in OSA would lead to better recognition and management of the condition.

Feasibility and Efficacy of a Self-Management Intervention for Insomnia in Stable Heart Failure.

BACKGROUND: Chronic insomnia is common among patients with heart failure (HF) and may contribute to fatigue and poor function. However, to date there have been no randomized controlled trials focused on treatment of insomnia or daytime symptoms in this population. OBJECTIVES: The purpose of this study was to examine the preliminary efficacy, feasibility, and acceptability of a self-management intervention (cognitive behavioral therapy [CBT-I]) for insomnia among patients with stable HF. METHODS: We conducted a pilot randomized controlled trial (RCT) in which patients with stable Class I-III HF (n = 25/52.1% women; mean age = 59 ± 14.8 years) were randomized in groups to CBT-I (n = 29) or an attention control condition (HF self-management with sleep hygiene; n = 19). Participants completed 2 weeks of wrist actigraphy, the insomnia severity index, and measures of fatigue, depression, sleepiness, and functional performance at baseline and follow-up. We computed the size of the effects on the dependent variables and used MANOVA to evaluate the effects of CBT-I on insomnia and fatigue. RESULTS: CBT-I was feasible and acceptable and had a statistically significant effect on insomnia and fatigue, while controlling for the effects of comorbidity and age. CONCLUSIONS: CBT-I has short-term efficacy as a treatment for chronic insomnia among patients with stable HF. Future studies are needed to address its sustained effects.

Obstructive sleep apnea: a new preventive and therapeutic target for stroke: a new kid on the block.

Stroke is the second leading cause of death worldwide and a major cause of mental and physical impairment. Numerous studies have identified risk factors for stroke, including hypertension, atrial fibrillation, diabetes, and smoking. However, even after considering these well-recognized risk factors, there is substantial variation in stroke rates and stroke-related outcomes. There is emerging evidence that obstructive sleep apnea increases the risk of stroke independently of traditional risk factors. Obstructive sleep apnea is present in the majority of patients with stroke and contributes to persistent neurologic impairment. Early recognition and treatment of obstructive sleep apnea during the post-stroke period lead to better neurologic outcome. Healthcare providers should be aware of the strong association of obstructive sleep apnea as a risk factor for stroke and its effect on neurologic recovery. The presence of hypertension and diabetes-the 2 most common comorbid conditions in obstructive sleep apnea-should prompt diagnostic workup for and treatment of obstructive sleep apnea as a way of primary and secondary prevention of stroke.

Assessment of preload and fluid responsiveness in intensive care unit. How good are we?

Early recognition and treatment of acute circulatory failure and tissue hypoperfusion are paramount for improving the odds of survival in critically ill patients. Fluid volume resuscitation is the mainstay intervention in redistributive and hypovolemic shock. Correct identification of a patient who would benefit from fluid administration allows optimization of hemodynamics and avoids ineffective or even deleterious volume expansion that may result in worsening of gas exchange and pulmonary edema in fluid unresponsive patients, in whom inotropic and/or vasopressor support should preferentially be used. The use of dynamic changes in central venous pressure, pulse pressure, and echocardiography for assessment of inferior vena cava diameter variations during respiration allows prediction of fluid volume responsiveness in hemodynamically unstable patients. The use of these bedside approaches and passive leg raising maneuver, which is a reversible and quick fluid volume challenge, allows timely formulation of treatment strategy in patients with shock.

Common High Altitudes Illnesses a Primer for Healthcare Provider.

Exposure to high altitude imposes significant strain on cardiopulmonary system and the brain. As a consequence, sojourners to high altitude frequently experience sleep disturbances, often reporting restless and sleepless nights. At altitudes above 3,000 meters (9,800 ft) almost all healthy subjects develop periodic breathing especially during NREM sleep. Sleep architecture gradually improves with increased NREM and REM sleep despite persistence of periodic breathing. The primary reason for periodic breathing at high altitude is a hypoxic-induced increase in chemoreceptor sensitivity to changes in PaCO2 - both above and below eupnea, leading to periods of apnea and hyperpnea. Acetazolamide improves sleep by reducing the periodic breathing through development of metabolic acidosis and induced hyperventilation decreasing the plant gain and widening the PCO2 reserve. This widening of the PCO2 reserve impedes development of central apneas during sleep. Benzodiazepines and GABA receptor antagonist such as zolpidem improve sleep without affecting breathing pattern or cognitive functions.

Obstructive sleep apnea and hypertension: a critical review.

Obstructive sleep apnea (OSA) is a prevalent sleep disorder which is characterized by recurrent upper closure with oxygen desaturation and sleep disruption. OSA increases the risk of vascular disorders in the form of stroke, myocardial infarction, congestive heart failure, and hypertension. The mechanisms underlying the vascular disorders are several and include intermittent hypoxia with release of cytokines, angiogenic inhibitors, free radicals, and adhesion molecules. During apneas, arterial blood pressure gradually rises and surges abruptly after the termination of apnea. Two thirds of patients with OSA will ultimately have diurnal hypertension. This review discusses the literature supporting the significant role of OSA in hypertension and the effect of OSA treatment on blood pressure.

Sleep in asthma.

Many patients with asthma experience worsening of symptoms at night. Understanding the mechanism of nocturnal asthma and the factors that exacerbate asthma during sleep would lead to better management of the condition.

Increased plasma YKL-40/chitinase-3-like-protein-1 is associated with endothelial dysfunction in obstructive sleep apnea.

PURPOSE: Obstructive sleep apnea (OSA) is a common disorder affecting 15-24% of the adults and is associated with increased risk of hypertension and atherosclerosis. The exact mechanisms underlying hypertension in OSA are not entirely clear. YKL-40/Chitinase-3-like protein-1 is a circulating moiety with roles in injury, repair and angiogenesis that is dysregulated in atherosclerosis and a number of other diseases. We sought to determine the role of YKL-40 in endothelial dysfunction and hypertension in OSA. METHODS: We studies 23 normotensive OSA (N-OSA) and 14 hypertensive OSA (H-OSA) without diabetes and apparent cardiovascular disease. Endothelial-dependent nitric oxide-mediated vasodilatory capacity was assessed by flow-mediated vasodilation (FMD). YKL-40, vascular endothelial growth factor (VEGF) and the soluble form of VEGF receptor-1 or sFlt-1 were measured in plasma using ELISA methodology. RESULTS: N-OSA subjects aged 49.1 ± 2.3 years and H-OSA aged 51.3 ± 1.9 years with BMI 36.1 ± 1.6 and 37.6 ± 1.9 kg/m(2), respectively. The apnea-hypopnea index (AHI) was 41 ± 5 events/hr in N-OSA and 46 ± 6 in H-OSA with comparable degree of oxygen desaturations during sleep. FMD was markedly impaired in H-OSA (8.3% ± 0.8) compared to N-OSA (13.2% ± 0.6, P<0.0001). Plasma YKL-40 was significantly elevated in H-OSA (55.2 ± 7.9 ng/ml vs. 35.6 ± 4.2 ng/ml in N-OSA, P = 0.02) and had an inverse relationship with FMD (r = -0.52, P = 0.013). There was a significant positive correlation between sFlt-1/VEGF, a measure of decreased VEGF availability, and YKL-40 (r = 0.42, P = 0.04). CONCLUSION: The levels of plasma YKL-40 were elevated in H-OSA group and inversely correlated with the endothelial-dependent vasodilatory capacity whereas there was a positive correlation between sFlt-1/VEGF and YKL-40. These findings suggest that YKL-40 is dysregulated, in part, due to perturbation of VEGF signaling, and may contribute to endothelial dysfunction and hypertension in OSA.

The impact of gender on timeliness of narcolepsy diagnosis.

STUDY OBJECTIVES: To examine the impact of gender in narcoleptic patients on timeliness of diagnosis, symptomology, and health and lifestyle impairment. METHODS: This is a cross-sectional study of 109 consecutive patients (68 women) with newly diagnosed narcolepsy with and without cataplexy, from a University sleep disorders center. Consecutive patients were administered an 8-page questionnaire at the time of their diagnosis regarding sleep habits, medications, and medical conditions, lifestyle impairments, as well as details regarding narcolepsy-related symptoms. RESULTS: Men and women presented with remarkably similar narcolepsy related symptoms, yet women were more likely to be delayed in diagnosis; 85% of men were likely to be diagnosed by 16 years after symptom onset, compared to 28 years in women. More women were likely to remain undiagnosed at any given time point after symptom onset (hazard ratio for diagnosis of men compared to women 1.53; 95% CI 1.01-2.32; p = 0.04). Men and women reported similar degree of subjective sleepiness as measured by the Epworth Sleepiness Scale (mean 16.2 ± 4.5; p = 0.18), though women demonstrated significantly more severe objective sleepiness on multiple sleep latency testing (MSLT) (mean sleep latency in women = 5.4 min (± 4.1), in men 7.4 min (± 3.5); p = 0.03). Despite being more objectively sleepy, women were less likely to report lifestyle impairments in the areas of personal relationships (71% men, 44% women, p = 0.01) and physical activity (36% men, 16% women, p = 0.02), but were also more likely to self-medicate with caffeine (63.4% men, 82.4% women; p = 0.03). CONCLUSIONS: Narcolepsy impacts men and women's health and lifestyle differently, and may cause delays diagnosis for women.

Diagnosis and management of sleep disorders in posttraumatic stress disorder:a review of the literature.

OBJECTIVE: International and societal conflicts and natural disasters can leave physical and mental scars in people who are directly affected by these traumatic experiences. Posttraumatic stress disorder (PTSD) is the clinical manifestation of these experiences in the form of re-experiencing the trauma, avoidance of trauma-related stimuli, and persistent symptoms of hyperarousal. There is growing evidence that sleep disruption that occurs following trauma exposure may in fact contribute to the pathophysiology of PTSD and poor clinical outcomes. The purpose of this review is to highlight the importance of recognition and management of sleep disorders in patients with PTSD. DATA SOURCES: English-language, adult research studies published between 1985 and April 2014 were identified via the PubMed database. The search terms used were PTSD AND sleep disorders. STUDY SELECTION: The search identified 792 original and review articles. Of these, 53 articles that discussed or researched sleep disorders in PTSD were selected. Fourteen randomized controlled trials of therapy for PTSD are included in this review. RESULTS: Impaired sleep is a common complaint mainly in the form of nightmares and insomnia among people with PTSD. Sleep apnea and periodic limb movement disorder are particularly prevalent in patients with PTSD and, yet, remain unrecognized. Although selective serotonin reuptake inhibitors are effective in improving PTSD global symptoms, they have a variable and modest effect on sleep disorder symptoms. Cognitive-behavioral treatment targeted to sleep and/or the use of the centrally acting selective α1 antagonist prazosin have been more successful in treating insomnia and nightmares in PTSD than other classes of medications. In view of the high occurrence of sleep apnea and periodic leg movement disorder, a thorough sleep evaluation and treatment are warranted. CONCLUSIONS: Patients with PTSD have a high prevalence of sleep disorders and should be queried for insomnia, nightmares, periodic limb movement disorder, and sleep-disordered breathing.