such intrapolygraphic estimates of sleep fragmentation may provide accurate markers for probability indexing of sleep propensity. In the present study, however, sleep pressure scores did not differentiate between obese and nonobese subjects with respect to their biological and physiological responses to such sleep disruption. Simi- larly, although we cannot comment with certainty on whether obese children at risk for OSA would display different electroencephalographic response characteris- tics during the respiratory cycle, compared with nono- bese subjects, we posit that this electroencephalography- TABLE 1 Demographic and Polysomnographic Characteristics of 50
(16 - 85 years) and dialysed since >6 months in three dialysis centres. For each patient, we as- sessed insomnia according to international definition, obstructivesleepapnea syndrome (OSAS) with the Berlin questionnaire, restless leg syndrome (RLS) using abridged version of Cambridge- Hopkins RLS questionnaire, and excessivedaytimesleepiness (EDS) with Epworth sleepiness scale. Logistic multivariate regression was used to identify factors associated with different SD. Results: Overall prevalence of SD was 88% comprising: insomnia (64.3%), OSAS (49.1%), RLS (24.1%) and EDS (20.5%). Forty-two patients presented at least two disorders. No difference was noticed in prevalence of SD between genders (p = 0.14). Level of blood pressure were not different across patients with and without SD. Insomnia correlated with anemia, inflammation and EDS. OSAS was associated with age ≥50 years, EDS and neck circumference ≥25 cm. RLS correlated with anemia and EDS. Other parameters such as gender, dialysis vintage, KT/V, obesity, diabetes status and hypoalbuminemia were not associated with the different SD. The majority of patients had not been diagnosed before the survey and none of them was under treatment. Conclusions: Our findings are
The behavioral manifestations of daytime sleepi- ness in young children, such as hyperactivity, clearly overlap with problematic behaviors that do not re- sult from sleep deprivation/disruption. The results of a cross-sectional study, such as this one, do not allow us to draw direct conclusions about the nature of the relationship between sleep disturbance and daytimesleepiness-associated behavior. Alternative explanations for the finding of increased externaliz- ing behavior problems in the BSD groups include the possibility that children with oppositional or aggres- sive behavior during the day are also likely to man- ifest similar behavior at bedtime. Other factors, such as an overall negative parental perception of both their child’s bedtime and daytime behavior, may be operative. It would be important in future studies to correlate more objective sleepiness measures, such as the Multiple Sleep Latency Test, 39 and multiple ob-
Most data regarding sleep disorders in psychiatric patients are usually collected from the general (outpatient) psychiatric population; among those with severe mental illness (hospitalized), little is known about the prevalence of sleep disorders. Individuals with severe mental illness are a high-risk group for poor health in general, with reduced access to preventative medical care for multiple reasons, including stigma and low socioeconomic status. Sleep-related complaints in this high-risk population are frequently dismissed as normal or as unavoidable con- sequences of psychotropic medications, lifestyle, or the mental illness itself. Identifying and treating sleep dis- orders in hospitalized psychiatric patients may improve outcomes, overall health, and quality of life in a vulnerable population.
The aim of a change in diet or surgical intervention in patients with obesity is addressed to improve both health and quality of life through sufficient weight loss in order to reduce or even eliminate comorbidities and promote psychological wellbeing . Bariatric surgery is often the only effective treatment cure in severe obesity, which remains largely refractory to diet and pharmacologic treatment . We hypothesize that in severely obese patients significant weight loss induced by bariatric surgery would provide an effective improvement in pulmonary function and sleep quality. Study endpoints were (i) to assess the effect of bariatric surgery on sleep parameters, mainly the apnea-hypopnea index as measured by standard overnight polysomnography (PSG) and (ii) symptoms of daytimesleepiness and risk of OSA.
Mean daytimesleep latencies were 23.7 ⫾ 3.0 min- utes in C, 23.7 ⫾ 3.1 minutes in PS, and 20.0 ⫾ 7.1 minutes in OSA patients (P ⬍ .01 analysis of variance vs PS or C). The evolution of sleep latencies through- out the day is shown in Fig 1 for the 3 groups, and illustrates the early afternoon increase in sleep pro- pensity in all study groups. Only 7 children with OSA (13%) had mean sleep latencies ⬍ 10 minutes. Of note, only 4 parents indicated daytimesleepiness in the questionnaire (7.5%), and of these, only 1 had MSLT ⬍ 10 minutes. Sleep latencies were more likely to be shorter in OSA patients with more severe apnea index (Fig 2; r: ⫺ 075; P ⬍ .0001), with higher arousal index (r: ⫺ 0.69, P ⬍ .001), with higher percent of total sleep time spent with SaO 2 below 90% (r: ⫺ 0.70; P ⬍
OSA or increased risk for OSA, nor excessivedaytime sleepi- ness. Patients with OSA showed a prolonged reaction time of perception to visual stimulus, of solving simple arithmetic opera- tions, and psychomotor limbs coordination, in comparison to controls. When age was accounted for, sleepiness did not con- tribute to the psychomotor outcome in OSA patients. The novelty of the current study is the evaluation of patients with an instru- ment assessing reaction time, including an assessment of execu- tive function and processing speed, abilities that have been indicated as important in carrying out complex behaviors asso- ciated with safe driving. In addition, the study provided data on impaired stability in reaction time during the process of testing among male OSA patients compared to controls.
Our patient was referred to a pediatric pulmonologist at age two years 10 months for a screening polysomno- graph (PSG) sleep study prior to initiation of growth hormone (GH) therapy. An initial screening overnight oximetry study was carried out before the PSG due to concerns that she might not tolerate the monitoring equipment. The screening oximetry was normal; no significant desaturations to suggest obstructivesleepapnea were found. At the follow-up with the sleep specialist, our patient’s mother reported episodes sug- gestive of narcolepsy. Dating back to early infancy, epi- sodes were reported of our patient falling forward for a few seconds at a time with her eyes rolling back in her head. During these events, she was unresponsive, but appeared to be conscious. The events occurred three to four times per week and were provoked by laughter. The episodes typically occurred after waking from a nap in the mornings, and resolved spontaneously. She was not sleepy afterwards. The episodes were deter- mined not to be seizures; no other associated motor activity, eye deviation or stereotypy consistent with a description of a seizure was present. Daytime hyper- somnia was also noted with sleep duration of greater than 12 hours per night in addition to a two- to three- hour daytime nap.
be poor. Adequate compliance with CPAP was defined roughly as using the device for at least 4 hours 5 nights a week [3,4], the recommended standards for CPAP com- pliance to reduce the incidence of cardiovascular diseases [1,4]. On the other hand, any standard management, es- pecially for the long-term management to improve ex- cessive daytimesleepiness (EDS) determined by daytime performance and cognition does not exist. Recent meta- analyses demonstrated that CPAP elicited only small improvements in subjective sleepiness in mild to moder- ate OSAS, and the effects on objective sleepiness are of limited clinical significance . Another meta-analysis showed that CPAP therapy does not improve general QOL scores associated with EDS, but does improve physical domains and vitality .
impairment of studied cognitive function, quality of life, mood disturbance as depressed or anxious mood, and more affection of SDQ and ESS in patients with OSA than control group. These results could be attributed to multiple mechanisms, thought to contribute to sleepiness in patients with OSA. These include sleep fragmentation , hypoxia , partial chronic sleep deprivation from sleep time lost due to arousals , cytokine dysregulation , and interactions with individual adaptations . Other studies had proposed the hypothesis that both daytime somnolence and hypoxemia may contribute to cognitive dysfunction in OSA patients. In particular, the impairment of executive functions, motor and visuo-constructive abilities (such as language, fluency, drawing) may be related to severity of hypoxemia. Also, attention and memory deficits may be due to excessivedaytime somnolence associated with sleep fragmentation [27-29]. Other studies suggested the importance of REM sleep for memory consolidation [30,31], particularly for those individuals with insomnia .
The authors acknowledge some limitations of this study. The reliance on the self-reported questionnaire in data collection made our data more subjective. The number of women enrolled in our sample was higher than men; this is due to the high proportion of women in our faculty. Also, in order to reduce the duration of the interview and maintain a high response rate, we did not include questions regarding socioeconomic dimension of students and the existence of specific sleep disorder as obstructivesleepapnea or periodic limb movement in our survey. Larger multicenter and lon- gitudinal studies are needed to examine the causes of sleep disorders and to implement preventive measures to enhance the university students’ academic performance.
In conclusion, different factors affect healthy sleep. The current study showed that Iranian pre- schoolers have short sleep duration and that they are late sleepers. The late bedtime may result in problems. Not putting children to bed until some hours after they are tired may make them less resistant to sleeping. However, a delayed bedtime may have implications for bed sharing, daytime behaviour, daytimesleepiness and morning wake- up times. The high percentage of sleep problems in children highlights the importance of paying attention to sleep in primary care practice.
High-fat-diet rodent model is widely used to study hu- man obesity. It’s a model that mimics human obesity and its-related disturbances. Two months High-fat-diet lead to an overt obesity in rats characterized by body weight gain, along with an increase of lung weight. Ex- cessive ingestion of lipids, through a relatively long period, induced dyslipidemia into plasma as assessed by high cholesterol and LDL-C and high LDL-C/HDL-C ra- tio and into lung by high triglyceride level and high lipid content. HFD provokes lipotoxicity without affecting insulinemia nor glycemia and decreases adiponectine- mia. Our data rather indicated the lipotoxic but not glu- cotoxic effect of this specific HFD. Lipid deposition in lung induced oxidative stress through the increase of free radical levels as evidenced by hydrogen peroxide elevation, lipid peroxidation augmentation, and the de- crease of antioxidant enzymes activities such as SOD, CAT and POD. Similar HFD-induced oxidative stress was described by many previous studies. However, high- fat diet-induced oxidative stress mechanism is not well elucidated. Several reports proposed that obesity- induced oxidative stress is provoked by exacerbated nu- trient oxidation, such as beta-oxidation, as it has been reported after glucose uptake . We do think that high-fat diet-induced oxidative stress may by induced from excessive mitochondria functioning which can cause mitochondria damages and by decreasing peroxi- some proliferator-activated receptor γ (PPAR- γ) due to fatty acid accumulation . PPAR- γ downregulation decrease carnitine palmitoyl transferase-1 expression and fatty acid-oxidation. High-fat diet also affected Table 5 Effect of high-fat diet (HFD) and grape seed extract on body weight, lung Index and lipid content. (December 2016)
Each sleep factor showed a rather characteristic risk profile that was consistent with the intended construct for that factor. For example, a decreased odds ratio for females and an increased odds ratio for increased neck size were found only for the sleepapnea factor, consistent with known risks for polysomnography validated sleepapnea. The non-restorative factor was normed based on CFS and fibromyalgia patients with the alpha EEG sleep disorder and subjects with CFS were 28 times more likely to have abnormalities in this factor compared to non-fatigued subjects. Interestingly, CFS subjects currently failing to meet CFS criteria because of a reduction in symptoms or fatigue (CSF-R) also had significantly reduced odds for scoring abnormal in this factor. These observations are
Obstructivesleepapnea (OSA), is the most prevalent form of sleep disordered breathing both in adults and children [1-3] and has been associated with significant neurocognitive, metabolic, and cardiovascular morbid- ities [4-8]. OSA is characterized by episodes of total and/or partial collapse of the upper airway alternating with normal breathing during sleep, leading to chronic intermittent hypoxia and hypercapnia, sleep fragmenta- tion and increased swings in intrathoracic pressures. This condition may affect 1– 3% of healthy school-aged children . There is accumulating evidence that OSA is strongly linked to cardiovascular morbidity independent of obesity [9-11]. The presence of altered endothelial function is currently viewed as an early risk marker of cardiovascular disease, and is a relatively common oc- currence in both adult and pediatric patients with OSA [12-14], and can precede the onset of hypertension . However, not every child with OSA will develop ED, suggesting that genetic factors may play a role.
We showed that the disease duration and severity, impairments of cognitive or frontal function, as well as sleep quality that was evaluated by PSG, were not asso- ciated with EDS, while we identified a dose-dependent effect of antiparkinson drugs on EDS. Although this finding was not consistent with the SLEEMSA study, which showed a lack of correlation between the amount of dopaminergic treatment and EDS , it suggests still another possibility that antiparkinson drugs may cause EDS, as is the case with PD . However, because 84% of the patients in the present study had MSA-C, we were able to recruit only 11 patients who had been treated with antiparkinson drugs. In addition, it remains the possibility that there may be confounding factors that are correlated with EDS and LED, such as the disease severity and duration. Further studies should be per- formed in order to further investigate the effects of antiparkinson drugs on sleepiness in MSA patients.
Narcolepsy is a chronic neurological disorder specifying the abnormal sleep manifestations which mainly impact the quality of life of narcolepsy patients. The exact cause is unclear but found significant evidences that orexin/hypocretin deficiency causes narcolepsy which regulates sleep. Treatment focuses on symptomatic relief throughout medication, education, and behavioral therapy. Stimulants are the first line treatment for the excessivedaytimesleepiness. Modafinil, sodium oxybate, amphetamine, methylphenidate, and selegiline are effectual treatments for somnolence associated with narcolepsy. Tricyclic antidepressants and SSRIs are one of the best treatments for cataplexy, sleep paralysis, and hypnagogic hallucinations. Benzodiazepines are the best regimen for disturbed nocturnal sleep.
PSQI test results were analyzed with regard to clinical and demographic characteristics of those suffering from epilepsy: gender, age, profession, BMI, illness duration, number of medicines taken, type of seizures, frequency of seizures, time which elapsed since last seizure, provocative factor of seizure attacks, and occurrence of adverse effects of AEDs. Furthermore, the existence of a relationship between PSQI test result and particular sleep-related factors or particular sleep conditions was examined. However, the examination of a relationship between certain independent variables and the final PSQI test result did not prove the existence of a statistically relevant influence (in all cases P.0.05).
in screening for the diagnoses of iron deﬁciency, lead toxicity, or thalassemia in children with Down syndrome. Serum ferritin concen- tration is a sensitive parameter for assessment of iron stores in healthy subjects but is an acute-phase reac- tant and may be increased in the presence of chronic inﬂammation or infection and should be evaluated together with C-reactive protein (CRP) concentration. An elevated CRP level is an indication that a nor- mal ferritin level may be falsely ele- vated and is not a reliable indication of normal iron status. Serum ferri- tin and CRP or reticulocyte hemoglo- bin (CHr) concentrations should be obtained at annual visits for pa- tients who are at increased risk of
Table 4 demonstrates the direction and magnitude of association of the studied explanatory variables which are non-overlapping domains with EDS using a logistic regression model. This model is not adjusted for interaction and confounding variables. Here, SHI scores and weekly sleep and work hours are taken on a continuous scale, along with other important continuous and categorical variables. The observed results are consistent with the earlier measures of linearity and crude odds ratios. It is evident that variables such as SHI score, night shifts in past month, number of nocturnal awakenings, being in a clinical department, mixed sleep pattern, and non-refreshing sleep in past week have a positive relationship.