Epworth Sleepiness Scale

About: Epworth Sleepiness Scale is a research topic. Over the lifetime, 4742 publications have been published within this topic receiving 155088 citations.

Assessment of Sleep and Sleepiness in Parkinson Disease SLEEP IN NEUROLOGIC DISEASE

Abstract: Measurements and Results: Reliability of the scale was high: internal consistency of the nighttime sleep and daytime sleepiness scales were 0.88 and 0.91, respectively (Cronbach α), and test-retest reliabilities were 0.94 and 0.89, respectively (intraclass correlation coefficient). Scale scores differed significantly between patients and controls (P < .001). Construct validity was assessed by correlations with scales that addressed similar constructs. Correlation between the nighttime sleep scale and the Pittsburgh Sleep Quality Index was 0.83 (P < .001), and the correlation between the daytime sleepiness scale and the Epworth Sleepiness Scale was 0.81 (P < .001). Factor analysis revealed 1 factor each for both scales, indicating that the scales measure 1 construct, which justifies the calculation of sumscores. The coefficient of variation of both the nighttime sleep and the daytime sleepiness scale was higher than that of the Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale, indicating a better ability to detect differences between individuals. Conclusions: The SCOPA-SLEEP is a reliable and valid instrument for assessing nighttime sleep and daytime sleepiness in patients with Parkinson disease.

Drug therapy for obstructive sleep apnoea in adults

Abstract: Background The treatment of choice for moderate to severe obstructive sleep apnoea (OSA) is continuous positive airways pressure (CPAP) applied via a mask during sleep. However, this is not tolerated by all individuals and its role in mild OSA is not proven. Drug therapy has been proposed as an alternative to CPAP in some patients with mild to moderate sleep apnoea and could be of value in patients intolerant of CPAP. A number of mechanisms have been proposed by which drugs could reduce the severity of OSA. These include an increase in tone in the upper airway dilator muscles, an increase in ventilatory drive, a reduction in the proportion of rapid eye movement (REM) sleep, an increase in cholinergic tone during sleep, an increase in arousal threshold, a reduction in airway resistance and a reduction in surface tension in the upper airway. Objectives To determine the efficacy of drug therapies in the specific treatment of sleep apnoea. Search methods We searched the Cochrane Airways Group Specialised Register of trials. Searches were current as of July 2012. Selection criteria Randomised, placebo controlled trials involving adult patients with confirmed OSA. We excluded trials if continuous positive airways pressure, mandibular devices or oxygen therapy were used. We excluded studies investigating treatment of associated conditions such as excessive sleepiness, hypertension, gastro-oesophageal reflux disease and obesity. Data collection and analysis We used standard methodological procedures recommended by The Cochrane Collaboration. Main results Thirty trials of 25 drugs, involving 516 participants, contributed data to the review. Drugs had several different proposed modes of action and the results were grouped accordingly in the review. Each of the studies stated that the participants had OSA but diagnostic criteria were not always explicit and it was possible that some patients with central apnoeas may have been recruited. Acetazolamide, eszopiclone, naltrexone, nasal lubricant (phosphocholinamine) and physiostigmine were administered for one to two nights only. Donepezil in patients with and without Alzheimer's disease, fluticasone in patients with allergic rhinitis, combinations of ondansetrone and fluoxetine and paroxetine were trials of one to three months duration, however most of the studies were small and had methodological limitations. The overall quality of the available evidence was low. The primary outcomes for the systematic review were the apnoea hypopnoea index (AHI) and the level of sleepiness associated with OSA, estimated by the Epworth Sleepiness Scale (ESS). AHI was reported in 25 studies and of these 10 showed statistically significant reductions in AHI. Fluticasone in patients with allergic rhinitis was well tolerated and reduced the severity of sleep apnoea compared with placebo (AHI 23.3 versus 30.3; P < 0.05) and improved subjective daytime alertness. Excessive sleepiness was reported to be altered in four studies, however the only clinically and statistically significant change in ESS of -2.9 (SD 2.9; P = 0.04) along with a small but statistically significant reduction in AHI of -9.4 (SD 17.2; P = 0.03) was seen in patients without Alzheimer's disease receiving donepezil for one month. In 23 patients with mild to moderate Alzheimer's disease donepezil led to a significant reduction in AHI (donepezil 20 (SD 15) to 9.9 (SD 11.5) versus placebo 23.2 (SD 26.4) to 22.9 (SD 28.8); P = 0.035) after three months of treatment but no reduction in sleepiness was reported. High dose combined treatment with ondansetron 24 mg and fluoxetine 10 mg showed a 40.5% decrease in AHI from the baseline at treatment day 28. Paroxetine was shown to reduce AHI compared to placebo (-6.10 events/hour; 95% CI -11.00 to -1.20) but failed to improve daytime symptoms. Promising results from the preliminary mirtazapine study failed to be reproduced in the two more recent multicentre trials and, moreover, the use of mirtazapine was associated with significant weight gain and sleepiness. Few data were presented on the long-term tolerability of any of the compounds used. Authors' conclusions There is insufficient evidence to recommend the use of drug therapy in the treatment of OSA. Small studies have reported positive effects of certain agents on short-term outcomes. Certain agents have been shown to reduce the AHI in largely unselected populations with OSA by between 24% and 45%. For donepezil and fluticasone, studies of longer duration with a larger population and better matching of groups are required to establish whether the change in AHI and impact on daytime symptoms are reproducible. Individual patients had more complete responses to particular drugs. It is possible that better matching of drugs to patients according to the dominant mechanism of their OSA will lead to better results and this also needs further study.

Health status in obstructive sleep apnea: relationship with sleep fragmentation and daytine sleepiness, and effects of continuous positive airway pressure treatment.

Abstract: Patients with obstructive sleep apnea (OSA) have impaired health status that improves with nasal continuous positive airway pressure (nCPAP). The study reported here explored the relationships between health status, its improvement with nCPAP, sleep fragmentation, and daytime sleepiness. In the study, 51 patients (46 male, five female) ranging from nonsnorers to individuals with severe OSA (median apnea/hypopnea index [AHI] 25, 90% central range: 1 to 98) had polysomnography with microarousal scoring, respiratory arousal scoring, and measurement of pulse transit time. The Short Form-36 Health Survey (SF-36) questionnaire was administered before and after 4 wk of nCPAP treatment; daytime sleepiness was also measured before starting nCPAP. Relationships between pretreatment health status and sleep fragmentation were weak, but significant associations were found between all sleep fragmentation indices and health status improvement with nCPAP (e.g., arousals according to the criteria of the American Sleep Disorders Association versus change in the physical component summary, r = 0.44, p < 0.001). Compared with general population data, the dimensions of energy and vitality and physical role limitation were abnormal before nCPAP (p < 0.05) and normalized with treatment. Sleepiness and pretreatment SF-36 values correlated significantly (Epworth Sleepiness Scale versus energy and vitality, r = -0.47, p < 0.001; modified Maintenance of Wakefulness Test versus energy and vitality, r = 0.32, p < 0.05). We conclude that the health status of patients with OSA improves with nCPAP and this improvement correlates with sleep fragmentation severity. However, the correlation is not very close, which may reflect the improvement with nCPAP of other symptoms not directly related to disease severity.

Sleep–wake disturbances 3 years after traumatic brain injury

Abstract: Background 6 months after traumatic brain injury (TBI), almost three out of four patients suffer from sleep–wake disturbances (SWD) such as post-traumatic hypersomnia (increased sleep need of ≥2 h compared with before injury), excessive daytime sleepiness (EDS), fatigue and insomnia. The long-term course of post-traumatic SWD, however, is unknown. Objectives To assess the prevalence and characteristics of post-traumatic SWD 3 years after trauma. Design Prospective longitudinal clinical study in 51 consecutive TBI patients (43 males, eight females, mean age 40±16 years). Main outcome measures EDS (as assessed by the Epworth sleepiness scale), fatigue (fatigue severity scale), post-traumatic hypersomnia (sleep length per 24 h), insomnia, depression and anxiety. Results Post-traumatic SWD were found in 34 patients (67%): post-traumatic hypersomnia in 14 (27%), EDS in six (12%), fatigue in 18 patients (35%) and insomnia in five patients (10%). SWD were not associated with severity or localisation of, or time interval since, TBI. Insomnia was linked to depressive symptoms. Conclusions This prospective study shows that 3 years after TBI, two out of three patients suffer from residual SWD, particularly fatigue and post-traumatic hypersomnia. In 45% of TBI patients, SWD appear directly related to the trauma itself.

Correlations among Epworth Sleepiness Scale scores, multiple sleep latency tests and psychological symptoms

Abstract: The aim of this study was to identify factors other than objective sleep tendency associated with scores on the Epworth Sleepiness Scale (ESS). There were 225 subjects, of whom 40% had obstructive sleep apnoea (OSA), 16% had simple snoring, and 4.9% had snoring with sleep disruption (upper airway resistance syndrome); 9.3% had narcolepsy and 7.5% had hypersomnolence without REM sleep abnormalities; 12% had chronic fatigue syndrome; 7.5% had periodic limb movement disorder and 3% had diurnal rhythm disorders. ESS, the results of overnight polysomnography and multiple sleep latency test (MSLT) and SCL-90 as a measure of psychological symptoms were recorded. The ESS score and the mean sleep latency (MSL) were correlated (Spearman rho = -0.30, P or = 10 had poor sensitivity and specificity as a predictor of MSL < 10 min or MSL < 5 min. We conclude that the MSLT and the ESS are not interchangeable. The ESS was influenced by psychological factors by which the MSL was not affected. The ESS cannot be used to demonstrate or exclude sleepiness as it is measured by MSLT.