Showing papers on "Sleep disorder published in 2009"

Quantifying the risk of neurodegenerative disease in idiopathic REM sleep behavior disorder

Abstract: Objective Idiopathic REM sleep behavior disorder (RBD) is a potential preclinical marker for the development of neurodegenerative diseases, particularly Parkinson disease (PD) and Lewy body dementia. However, the long-term risk of developing neurodegeneration in patients with idiopathic RBD has not been established. Obtaining an accurate picture of this risk is essential for counseling patients and for development of potential neuroprotective therapies. Methods We conducted a follow-up study of all patients seen at the sleep disorders laboratory at the Hopital du Sacre Coeur with a diagnosis of idiopathic RBD. Diagnoses of parkinsonism and dementia were defined according to standard criteria. Survival curves were constructed to estimate the 5-, 10-, and 12-year risk of developing neurodegenerative disease. Results Of 113 patients, 93 (82%) met inclusion criteria. The mean age of participants was 65.4 years and 75 patients (80.4%) were men. Over the follow-up period, 26/93 patients developed a neurodegenerative disorder. A total of 14 patients developed PD, 7 developed Lewy body dementia, 4 developed dementia that met clinical criteria for AD, and 1 developed multiple system atrophy. The estimated 5-year risk of neurodegenerative disease was 17.7%, the 10-year risk was 40.6%, and the 12-year risk was 52.4%. Conclusions Although we have found a slightly lower risk than other reports, the risk of developing neurodegenerative disease in idiopathic REM sleep behavior disorder is substantial, with the majority of patients developing Parkinson disease and Lewy body dementia.

Cognitive behavioral therapy, singly and combined with medication, for persistent insomnia: a randomized controlled trial.

Abstract: Context Cognitive behavioral therapy (CBT) and hypnotic medications are efficacious for short-term treatment of insomnia, but few patients achieve complete remission with any single treatment. It is unclear whether combined or maintenance therapies would enhance outcome. Objectives To evaluate the added value of medication over CBT alone for acute treatment of insomnia and the effects of maintenance therapies on long-term outcome. Design, Setting, and Patients Prospective, randomized controlled trial involving 2-stage therapy for 160 adults with persistent insomnia treated at a university hospital sleep center in Canada between January 2002 and April 2005. Interventions Participants received CBT alone or CBT plus 10 mg/d (taken at bedtime) of zolpidem for an initial 6-week therapy, followed by extended 6-month therapy. Patients initially treated with CBT attended monthly maintenance CBT for 6 months or received no additional treatment and those initially treated with combined therapy (CBT plus 10 mg/d of zolpidem) continued with CBT plus intermittent use of zolpidem or CBT only. Main Outcome Measures Sleep onset latency, time awake after sleep onset, total sleep time, and sleep efficiency derived from daily diaries (primary outcomes); treatment response and remission rates derived from the Insomnia Severity Index (secondary outcomes). Results Cognitive behavioral therapy used singly or in combination with zolpidem produced significant improvements in sleep latency, time awake after sleep onset, and sleep efficiency during initial therapy (all P Conclusion In patients with persistent insomnia, the addition of medication to CBT produced added benefits during acute therapy, but long-term outcome was optimized when medication is discontinued during maintenance CBT. Trial Registration clinicaltrials.gov Identifier: NCT00042146

Insomnia with objective short sleep duration is associated with a high risk for hypertension.

Abstract: INSOMNIA IS, BY FAR, THE MOST COMMONLY ENCOUNTERED SLEEP DISORDER IN MEDICAL PRACTICE. HOWEVER, RELATIVELY LITTLE IS KNOWN about the mechanisms, causes, clinical course, and consequences of this highly prevalent chronic condition.1,2 Many studies have established that insomnia is highly comorbid with psychiatric disorders and is a risk factor for the development of depression, anxiety, and suicide.1,2 However, in contrast to the other most common sleep disorder, sleep disordered breathing (SDB), chronic insomnia has not been linked with significant medical morbidity, e.g., cardiovascular disorders. Few studies that have examined the association of chronic insomnia with hypertension have reported modest and inconsistent effects of little or no clinical significance.3–6 In fact, Kripke et al. found a reduced mortality rate for those individuals complaining of sleep difficulties after 6 years of follow-up.7 Most, but not all, studies have reported that insomnia is associated with an overall hypersecretion of ACTH and cortisol, suggesting an activation of the hypothalamic-pituitary-adrenal (HPA) axis in these patients.8–11 Given the well-established association of hypercortisolemia with significant medical morbidity, e.g., hypertension, metabolic syndrome, osteoporosis,12 the paucity of data linking insomnia with these medical disorders is a paradox. In our studies, we observed and reported that the activation of the HPA axis in insomnia was strongly and positively correlated with objective indices of sleep disturbance.8,9 Specifically, hypercortisolemia was found primarily in insomniacs who demonstrated short sleep duration in the sleep laboratory but not in those whose objective sleep duration was similar to that of normal sleepers. Similarly, earlier studies have shown higher autonomic activation, including heart rate, 24-h metabolic rate, and impaired heart rate variability, in insomniacs selected based on objective polysomnographic criteria.13–16 Based on these observations, we speculate that objective short sleep duration may be an index of the biological severity of the disorder and that insomniacs with short sleep duration are at high risk for adverse medical outcomes. To test this hypothesis, we examined the joint effect of the complaints of chronic insomnia and poor sleep (a milder form of insomnia), and objective sleep duration on the prevalent hypertension in a large cross-sectional population-based sample from central Pennsylvania. We hypothesized that chronic insomnia is associated with a significant risk of hypertension, and that the comorbidity of insomnia and hypertension is enhanced by objective short sleep duration.

Insomnia With Objective Short Sleep Duration Is Associated With Type 2 Diabetes: A population-based study

Abstract: Objective: We examined the joint effects of insomnia and objective short sleep duration, the combination of which is associated with higher morbidity, on diabetes risk. Research Design and Methods: 1,741 men and women randomly selected from Central Pennsylvania were studied in the sleep laboratory. Insomnia was defined by a complaint of insomnia with duration of ≥ 1 year while poor sleep was defined as a complaint of difficulty falling asleep, staying asleep, or early final awakening. Polysomnographic sleep duration was classified into three categories: ≥ 6 hours of sleep (top 50% of the sample); 5-6 hours (approximately third quartile of the sample); and ≤ 5 hours (approximately the bottom quartile of the sample). Diabetes was defined either based on a fasting blood glucose > 126 mg/dl or using medication. In the logistic regression model we simultaneously adjusted for age, race, sex, body mass index, smoking, alcohol use, depression, sleep disordered breathing (SDB), and periodic limb movement. Results: Chronic insomnia but not poor sleep was associated with a higher risk for diabetes. Compared to the normal sleeping and ≥ 6 hour sleep duration group, the highest risk of diabetes was in individuals with insomnia and ≤ 5 hour sleep duration group [OR (95% CI) 2.95 (1.2 – 7.0)], and in insomniacs who slept 5-6 hours [OR (95% CI) 2.07 (0.68 – 6.4)]. Conclusions: Insomnia with short sleep duration is associated with increased odds of diabetes. Objective sleep duration may predict cardiometabolic morbidity of chronic insomnia, whose medical impact has been underestimated.

The Natural History of Insomnia : A Population-Based 3-Year Longitudinal Study

Abstract: Background Despite its high prevalence, little information is available about the natural history of insomnia. The extent to which episodes of insomnia will persist or remit over time is difficult to predict. We examined the natural history of insomnia and describe the most common trajectories over 3 years. Methods Three hundred eighty-eight adults (mean [SD] age, 44.8 [13.9] years; 61% women) were selected from a larger population-based sample on the basis of the presence of insomnia at baseline. They completed standardized sleep/insomnia questionnaires at 3 annual follow-up assessments. For each follow-up assessment, participants were classified into 1 of 3 groups (individuals with an insomnia syndrome, individuals with insomnia symptoms, and individuals with good sleep) on the basis of algorithms using standard diagnostic criteria for insomnia. Rates of persistent insomnia, remission, and relapse were computed for each group. Results Of the study sample, 74% reported insomnia for at least 1 year (2 consecutive assessments) and 46% reported insomnia persisting over the entire 3-year study. The course of insomnia was more likely to be persistent in those with more severe insomnia at baseline (ie, insomnia syndrome) and in women and older adults. Remission rate was 54%; however, 27% of those with remission of insomnia eventually experienced relapse. Individuals with subsyndromal insomnia at baseline were 3 times more likely to remit than worsen to syndrome status, although persistence was the most frequent course in that group as well. Conclusion These findings indicate that insomnia is often a persistent condition, in particular when it reaches the diagnostic threshold for an insomnia disorder.

Incidence and risk factors of insomnia in a population-based sample.

Abstract: INSOMNIA IS AMONG THE MOST PREVALENT HEALTH COMPLAINTS. APPROXIMATELY 9% OF THE GENERAL POPULATION REGULARLY SUFFER FROM INSOMNIA, and about 30% do so occasionally.1–3 Incidence rates reported in longitudinal studies vary extensively (from 3% to 20%), depending on the population studied, the time interval (e.g., 1 year versus 10 years), and the definition of insomnia used (i.e., insomnia syndrome versus symptoms). For instance, it is estimated that over a period of one year, approximately 6% of the general population develop an insomnia syndrome,4 and approximately 20% develop insomnia symptoms, with the latter figures being based on samples of older adults5 and individuals with chronic health problems.6 Furthermore, new onset of insomnia is generally more frequent among women and individuals with medical conditions, psychiatric disorders, and a perceived stressful life.4,7–9 Based on a tripartite conceptual framework widely used to explain the development of insomnia,10–12 3 types of factors are involved at different times during the course of insomnia. First, everyone is, to some degree, predisposed to develop insomnia. Second, a precipitating event is usually associated with the onset of insomnia. Third, insomnia is perpetuated over time by psychological and behavioral factors, even after precipitating factors have been controlled or eliminated. The most commonly hypothesized predisposing factors include demographic factors (e.g., aging, female gender, living alone),1,3,13 familial/hereditary conditions (a personal or family history of insomnia),14–16 psychological factors (e.g., anxiety, depression, personality traits),4,17–19 and physiological and lifestyle factors (e.g., arousability and smoking).20,21 Precipitating factors include stressful life events (e.g., divorce),9,22 as well as psychological and health-related factors (e.g., pain, mental health problems).10,23 Finally, maintaining factors include maladaptive sleep habits (e.g., excessive amounts of time spent in bed, napping, chronic medication use) and dysfunctional cognitions about sleep loss and its impact on life (e.g., worry over sleep loss).10 Most studies investigating insomnia risk factors have been either retrospective or cross-sectional, precluding unequivocal inference about the relationship between these factors and the development of insomnia. The extent to which depression and anxiety trigger insomnia or represent consequences of insomnia remains ambiguous. The few longitudinal studies of insomnia have provided informative data about incidence and risk factors, although most of those studies have focused predominantly on selected samples such as young adults,7,28 elderly adults,8,24,25 or patients attending medical practices.6,26,27 Only one longitudinal study evaluating the relation between sleep problem symptoms (i.e., insomnia and hypersomnia) and psychiatric disorders sampled the population at large.4 Few studies have used standard diagnostic criteria to define insomnia. Moreover, previous studies have used various time frames and most have not adequately operationalized their measure of incidence. For instance, most studies have not differentiated between incident cases of first episode of insomnia (no prior history of insomnia) and cases of recurrence (with past history of insomnia). Furthermore, the majority of studies included only individuals experiencing insomnia at the time of the second assessment in their incidence estimates5,6,8,29 rather than all cases emerging during the interval between baseline and follow-up assessment.7 Since insomnia may prove transient or episodic, incidence rates may have been underestimated in previous studies. The National Institutes of Health30 called for additional longitudinal studies using well-operationalized and stringent diagnostic criteria to estimate insomnia incidence and identify risk factors within the general population. The objectives of this study were to estimate the incidence of insomnia symptoms and syndrome and to identify associated risk factors in a cohort of good sleepers sampled from the general population and followed over a one-year period.

Efficacy of an Internet-based behavioral intervention for adults with insomnia.

Abstract: Context Insomnia is a major health problem with significant psychological, health, and economic consequences. However, availability of one of the most effective insomnia treatments, cognitive behavioral therapy, is significantly limited. The Internet may be a key conduit for delivering this intervention. Objective To evaluate the efficacy of a structured behavioral Internet intervention for adults with insomnia. Design, setting, and participants Forty-five adults were randomly assigned to an Internet intervention (n = 22) or wait-list control group (n = 23). Forty-four eligible participants (mean [SD] age, 44.86 [11.03] years; 34 women) who had a history of sleep difficulties longer than 10 years on average (mean [SD], 10.59 [8.89] years) were included in the analyses. Intervention The Internet intervention is based on well-established face-to-face cognitive behavioral therapy incorporating the primary components of sleep restriction, stimulus control, sleep hygiene, cognitive restructuring, and relapse prevention. Main outcome measures The Insomnia Severity Index and daily sleep diary data were used to determine changes in insomnia severity and the main sleep variables, including wake after sleep onset and sleep efficiency. Results Intention-to-treat analyses showed that scores on the Insomnia Severity Index significantly improved from 15.73 (95% confidence interval [CI], 14.07 to 17.39) to 6.59 (95% CI, 4.73 to 8.45) for the Internet group but did not change for the control group (16.27 [95% CI, 14.61 to 17.94] to 15.50 [95% CI, 13.64 to 17.36]) (F(1,42) = 29.64; P Conclusions Participants who received the Internet intervention for insomnia significantly improved their sleep, whereas the control group did not have a significant change. The Internet appears to have considerable potential in delivering a structured behavioral program for insomnia. Trial registration clinicaltrials.gov Identifier: NCT00328250.

Evidence‐Based Recommendations for the Assessment and Management of Sleep Disorders in Older Persons

Abstract: Sleep-related disorders are most prevalent in the older adult population. A high prevalence of medical and psychosocial comorbidities and the frequent use of multiple medications, rather than aging per se, are major reasons for this. A major concern, often underappreciated and underaddressed by clinicians, is the strong bidirectional relationship between sleep disorders and serious medical problems in older adults. Hypertension, depression, cardiovascular disease, and cerebrovascular disease are examples of diseases that are more likely to develop in individuals with sleep disorders. Conversely, individuals with any of these diseases are at a higher risk of developing sleep disorders. The goals of this article are to help guide clinicians in their general understanding of sleep problems in older persons, examine specific sleep disorders that occur in older persons, and suggest evidence- and expert-based recommendations for the assessment and treatment of sleep disorders in older persons. No such recommendations are available to help clinicians in their daily patient care practices. The four sections in the beginning of the article are titled, Background and Significance, General Review of Sleep, Recommendations Development, and General Approach to Detecting Sleep Disorders in an Ambulatory Setting. These are followed by overviews of specific sleep disorders: Insomnia, Sleep Apnea, Restless Legs Syndrome, Circadian Rhythm Sleep Disorders, Parasomnias, Hypersomnias, and Sleep Disorders in Long-Term Care Settings. Evidence- and expert-based recommendations, developed by a group of sleep and clinical experts, are presented after each sleep disorder.

The genetic and molecular regulation of sleep: from fruit flies to humans.

Abstract: It has been known for a long time that genetic factors affect sleep quantity and quality. Genetic screens have identified several mutations that affect sleep across species, pointing to an evolutionary conserved regulation of sleep. Moreover, it has also been recognized that sleep affects gene expression. These findings have given valuable insights into the molecular underpinnings of sleep regulation and function that might lead the way to more efficient treatments for sleep disorders.

Elevated anti-streptococcal antibodies in patients with recent narcolepsy onset

Abstract: NARCOLEPSY-CATAPLEXY IS A LIFELONG, DISABLING NEUROLOGICAL DISORDER, AFFECTING 1 IN 2000. CHARACTERISTIC SYMPTOMS INCLUDE EXCESSIVE daytime sleepiness and episodes of sudden loss of muscle tone, triggered by strong emotions (cataplexy). Onset is typically during adolescence, and predisposition involves both genetic and non-genetic factors, as suggested by the low monozygotic concordance but increased familial predisposition.1 The disorder is unique because of its extremely tight association with HLA-DQB1*0602 and hypocretin cell loss, suggesting autoimmune destruction; only 5 patients in the world have been described with low CSF hypocretin-1, a marker of hypocretin cell destruction, and DQB1*0602 negativity.2 Recently, using a Genome Wide Association, we found association with polymorphisms in the T-cell receptor α (TCR) loci.3 TCR is the major receptor of HLA-peptide presentation, and plays a critical role in mediating immune responses in normal (e.g., infectious) or abnormal (e.g., autoimmune) responses. Whereas much progress has been made toward understanding genetic predisposition in narcolepsy, little is known regarding environmental triggers. Retrospective questionnaire studies have found increased stress and decreased sleep amounts prior to narcolepsy onset.4 Case reports, describing a few unusual cases, have found sudden onset of narcolepsy 3 days after head trauma5 or various other unusual triggers (bee sting, etc). In all these cases, however, findings may be coincidental and are likely confounded by bias recall. More recently, a well-designed population based study of narcolepsy has been initiated and found increased smoking exposure in patients with narcolepsy as a risk factor6; the authors suggested the effect to be secondary to increased upper respiratory tract infections in secondary smoking. This, together with the report more than 20 years ago of increased ASO and ADB titers in a small number of narcoleptic patients regardless of disease duration,7,8 a finding that was later refuted,9 led us to reexamine the topic of infectious trigger in narcolepsy. It has been our clinical experience that narcolepsy is increasingly recognized close to onset, whereas 10-20 years ago, the disorder was diagnosed more than 10 years after onset (median time).10 We reasoned that a possible infectious trigger would not be detectable long after onset of narcolepsy, thus explaining variable results obtained in these first studies. Indeed, we also ourselves attempted to duplicate these anti-streptococcal findings in long standing narcolepsy cases, but could not find any differences with controls (Scott Fromhertz, unpublished results). We hypothesized that if streptococcal infections were indeed a trigger for narcolepsy onset, it would be best detected in newly identified patients, many of which had recent onset.

Somatic diseases and sleep complaints. An epidemiological study of 3,201 Swedish men.

Abstract: The prevalence of sleep complaints and somatic diseases was estimated in a random sample of 4064 Swedish men aged 30-69 years. Great difficulty initiating sleep (DIS) was experienced by 6.9% and moderate problems in DIS by 14.3%. Complaints of major difficulty maintaining sleep (DMS) were reported by 7.5% of the men and of moderate DMS by 14.9%. DMS was more frequent with increasing age. Excessive daytime sleepiness (EDS) was reported by 5.7%. Altogether 879 men were attending regular medical examinations for somatic diseases. Among the 299 hypertensive men, major complaints of DMS (13.5%), DIS (8.4%) and EDS (8.8%) were more common, but the 167 men treated with beta-blockers rather showed a proportionally somewhat lower prevalence of sleep complaints. Men with obstructive pulmonary disease (n = 113) had a higher prevalence of DMS (18.8%) and EDS (12.4%). Diabetic men (n = 74) complained also more often of DMS (21.9%), DIS (21.1%) and EDS (12.2%). Men with rheumatic disease (n = 176) and obesity (n = 221) also had increased prevalence of sleep complaints.

Cognitive Behavioral Therapy for Insomnia Improves Sleep and Decreases Pain in Older Adults with Co-Morbid Insomnia and Osteoarthritis

Abstract: Osteoarthritis is a common cause of pain and disability among older adults, affecting 20 million Americans. The prevalence of osteoarthritis is rapidly increasing with the accelerating growth of the older portion of the US population.1 Osteoarthritis is characterized by joint degeneration, pain, and dysfunction, with 80% of patients with osteoarthritis experiencing limitations of movement.1 Osteoarthritis demonstrates a broad spectrum of symptom severity, ranging from intermittent aching and joint stiffness to loss of motion and severe chronic pain.2 Severity and disability tend to increase with age, although severity can fluctuate markedly over short periods of time. Sleep quality is a major concern among persons with osteoarthritis, with 60% of people with osteoarthritis reporting pain during the night.3 In fact, pain secondary to arthritis is the most common factor predicting sleep disturbance in the population at large.4 It is well established that pain interferes with sleep5 and, more recently, that disturbed sleep lowers the pain threshold.6–8 Whether sleep disturbance precedes or follows pain onset is unclear, but reciprocal effects are likely.5 Patients with osteoarthritis who report having pain and stiffness in the morning have more sleep-related muscle spasms and objectively assessed sleep disturbance.9 Even after treatment with anti-inflammatory medications, patients with osteoarthritis show significantly greater objective sleep disturbance, as compared with age-matched control subjects.10 Chronic sleep disturbance, so common among older patients with osteoarthritis, is itself associated with impaired daytime function, daytime sleepiness and fatigue, reduced quality of life, and increased health care utilization.11–12 Given the likely reciprocal effects between pain and sleep disturbance, teasing apart unique causal pathways is difficult. Chronic pain initiates and exacerbates sleep disturbance; disturbed sleep in turn maintains and exacerbates chronic pain and related dysfunction.5,13–14 Sleep disruption, fragmentation, or restriction produces hyperalgesia6–8 and can interfere with analgesic treatments involving opioidergic and serotonergic mechanisms of action.13 The basis for this reciprocal relationship may be the modulation of pain during sleep and waking by reciprocally active neurons in the raphe magnus of the brainstem, providing a potential neural substrate for the reciprocal relationship of chronic pain and sleep disruption.14 Given this reciprocal relationship between sleep and pain, a question with major clinical implications is whether an intervention that improves sleep, per se, in individuals with disturbed sleep and a co-morbid pain state, such as osteoarthritis, might reduce pain as well. A recent randomized controlled trial of cognitive behavioral therapy for insomnia (CBT-I) versus an attention control in a group of older adults with co-morbid illnesses—osteoarthritis, coronary artery disease, or chronic obstructive pulmonary disease—reported clinically significant improvements in sleep quality.15 Although CBT-I has been shown to achieve high levels of efficacy when treating insomnia in otherwise healthy populations,16 prior to the study of Rybarczyk et al.,15 CBT-I was not tested in a well-controlled study of individuals with insomnia and co-morbid chronic medical illnesses. Until recently, the assumption has been that such insomnias usually had medical causes and that the best approach to correcting the insomnia was to treat the medical condition.17 Rybarczyk and colleagues' CBT-I treatment protocol did not specifically address pain management. However, the study investigated the hypothesis that improvements in sleep would result in improvements in daytime functioning, so a broad array of measures were included in their analyses. The CBT-I–treated group showed no reductions in pain report on the McGill Pain Questionnaire (MPQ) across the 3 co-morbid medical illnesses, or for the osteoarthritis group alone, relative to an attention-control group.15 However, Rybarczyk and colleagues analyzed neither a second available pain measure (ie, SF-36 pain subscale) nor the within-group effects. Given the possibility that the attention-control group might have received some pain benefits, examining within-group effects is an important analytic consideration. To better explore the potential impact of improved sleep on osteoarthritis pain, we reanalyzed the Rybarczyk et al. data, using within-group analyses to examine both available measures of pain, as well as previously unavailable 1-year follow-up sleep and pain data, for osteoarthritis participants only. We also examined effects among participants who crossed over from the control group to the CBT-I treatment.

Clinical review: The impact of noise on patients' sleep and the effectiveness of noise reduction strategies in intensive care units.

Abstract: Excessive noise is becoming a significant problem for intensive care units (ICUs). This paper first reviews the impact of noise on patients' sleep in ICUs. Five previous studies have demonstrated such impacts, whereas six other studies have shown other factors to be more important. Staff conversation and alarms are generally regarded as the most disturbing noises for patients' sleep in ICUs. Most research in this area has focused purely on noise level, but work has been very limited on the relationships between sleep quality and other acoustic parameters, including spectrum and reverberation time. Sound-absorbing treatment is a relatively effective noise reduction strategy, whereas sound masking appears to be the most effective technique for improving sleep. For future research, there should be close collaboration between medical researchers and acousticians.

Long Working Hours and Sleep Disturbances: The Whitehall II Prospective Cohort Study

Abstract: STUDY OBJECTIVE: To examine whether exposure to long working hours predicts various forms of sleep disturbance; short sleep, difficulty falling asleep, frequent waking, early waking and waking without feeling refreshed. DESIGN: Prospective study with 2 measurements of working hours (phase 3, 1991-1994 and phase 5, 1997-1999) and 2 measurements of subjective sleep disturbances (phase 5 and phase 7, 2002-2004). SETTING: The Whitehall II study of British civil servants. PARTICIPANTS: Full time workers free of sleep disturbances at phase 5 and employed at phases 5 and 7 (n = 937-1594) or at phases 3, 5, and 7 (n = 886-1510). MEASUREMENTS AND RESULTS: Working more than 55 hours a week, compared with working 35-40 hours a week, was related to incident sleep disturbances; demographics-adjusted odds ratio (95% CI) 1.98 (1.05, 3.76) for shortened sleeping hours, 3.68 (1.58, 8.58) for difficulty falling asleep; and 1.98 (1.04, 3.77) for waking without feeling refreshed. Repeat exposure to long working hours was associated with odds ratio 3.24 (1.45, 7.27) for shortened sleep, 6.66 (2.64, 16.83) for difficulty falling asleep, and 2.23 (1.16, 4.31) for early morning awakenings. Some associations were attenuated after adjustment for other risk factors. To a great extent, similar results were obtained using working hours as a continuous variable. Imputation of missing values supported the findings on shortened sleep and difficulty in falling asleep. CONCLUSION: Working long hours appears to be a risk factor for the development of shortened sleeping hours and difficulty falling asleep.

Markers of neurodegeneration in idiopathic rapid eye movement sleep behaviour disorder and Parkinson's disease

Abstract: Idiopathic rapid eye movement sleep behaviour disorder is an important risk factor in the development of Parkinson's disease. Numerous potential predictive markers of Parkinson's disease may present before motor symptoms emerge, but testing of these markers in rapid eye movement sleep behaviour disorder has been performed only in small studies. There has been no comparison of markers between patients with idiopathic rapid eye movement sleep behaviour disorder and Parkinson's disease, and between men and women. We evaluated an array of potential Parkinson's disease predictive markers in 159 patients; including 68 with idiopathic rapid eye movement sleep behaviour disorder, 36 controls, 34 Parkinson's patients with rapid eye movement sleep behaviour disorder and 21 Parkinson's patients without rapid eye movement sleep behaviour disorder. Compared with controls, patients with idiopathic rapid eye movement sleep behaviour disorder demonstrated substantial olfactory loss (P < 0.001). Olfaction was more impaired in Parkinson's disease than idiopathic rapid eye movement sleep behaviour disorder and did not differ between Parkinson's patients with, or without, rapid eye movement sleep behaviour disorder. Numerous measures of motor function including the Unified Parkinson Disease Rating Scale alternate tap, Purdue Peg Board and Timed 'Up and Go' were impaired in idiopathic rapid eye movement sleep behaviour disorder compared with controls (P < 0.01). All of these motor measures were worse with Parkinson's disease than with idiopathic rapid eye movement sleep behaviour disorder, regardless of rapid eye movement sleep behaviour disorder status. Autonomic symptoms and systolic blood pressure drop were impaired in patients with idiopathic rapid eye movement sleep behaviour disorder compared with controls (P = 0.003). Orthostatic abnormalities in Parkinson's disease were found in the group with rapid eye movement sleep behaviour disorder (P < 0.001). However, Parkinson's patients without rapid eye movement sleep behaviour disorder were not different than controls and had less impairment than those with idiopathic rapid eye movement sleep behaviour disorder (P = 0.004) and Parkinson's patients with rapid eye movement sleep behaviour disorder (P < 0.001). Colour vision was impaired in idiopathic rapid eye movement sleep behaviour disorder compared with controls (P < 0.001). However, only Parkinson's patients with rapid eye movement sleep behaviour disorder had abnormalities significantly different than controls (P < 0.001), and there were significant differences between Parkinson's patients with or without rapid eye movement sleep behaviour disorder (P < 0.04). Idiopathic rapid eye movement sleep behaviour disorder patients had slightly increased harm avoidance scores on personality testing (P = 0.04). Other than slightly better performances among women in the Purdue Peg Board, there was no difference in any measure between men and women, suggesting similar pathogenic processes underlying rapid eye movement sleep behaviour disorder. Patients with idiopathic rapid eye movement sleep behaviour disorder demonstrate abnormalities in numerous potential markers of neurodegenerative disease--these markers are heterogeneous, generally correlate with each other and occur equally in men and women. Although these abnormalities are usually intermediate between control values and Parkinson's patients, autonomic dysfunction and colour vision appear to be more linked to rapid eye movement sleep behaviour disorder status than Parkinson's disease, suggesting a unique pathophysiology of these abnormalities.

Cognitive behavioral therapy for patients with primary insomnia or insomnia associated predominantly with mixed psychiatric disorders: a randomized clinical trial.

Abstract: CHRONIC INSOMNIA IS A SERIOUS FORM OF SLEEP DISTURBANCE ASSOCIATED WITH REDUCED QUALITY OF LIFE, INCREASED RISKS FOR SERIOUS PSYCHIATRIC illness, and enhanced healthcare utilization among millions worldwide.1–3 Insomnia may present either as a primary sleep disorder or as a disorder comorbid with another sleep, medical, or psychiatric disorder or a combination thereof. Both primary insomnia (PI) and comorbid insomnia (CMI) are relatively common maladies, but CMI is more prevalent than PI in both clinical venues4,5 and the general population at large.6 Moreover, CMI may be more persistent and have even more serious consequences than PI. Recent data,7 for example, show that insomnia sufferers with comorbid gastrointestinal problems, chronic pain, hypertension, or problems with breathing or urination report more chronic insomnia than do those without such conditions. Furthermore, when insomnia occurs comorbid with a psychiatric illness such as major depression, it complicates disease management and often remains as a residual symptom that enhances risk for both suicide and relapse.8,9 In view of these considerations, patients who present with insomnia and particularly those with CMI warrant early and effective treatment. Pharmacotherapy with benzodiazepine receptor agonists or sedating antidepressants currently remains the most common treatment offered to patients with insomnia.10 However, cognitive behavioral therapy (CBT), designed to address sleep-disruptive beliefs and habits, has become an increasingly well-regarded insomnia treatment.10 Results of meta-analyses (e.g., Smith, et al.11) and head-to-head comparisons12 suggest CBT produces short-term sleep improvements that compare favorably to those achieved with various forms of pharmacotherapy. Furthermore, sleep improvements following CBT appear to endure long after treatment is completed,13 and limited data suggest that patients prefer CBT over treatment with sleep medications.14 Given such observations, CBT has become a popular alternative for insomnia management. Most evidence supporting the efficacy of CBT comes from studies conducted with patients with PI, although there is some limited evidence supporting use of this treatment with CMI as well. Some uncontrolled case series or clinic-based studies have suggested the efficacy of CBT among patients with CMI and mixed psychiatric and medical conditions.15 Other case series or quasi-experimental studies have suggested CBT may be efficacious for treating insomnia in such specific patient groups as those with chronic pain,16 cancer,17 posttraumatic stress disorder,18 and clinical depression19 and those with mixed serious mental disorders.20 In addition, a number of small to moderately sized, single-site, randomized clinical trials have suggested that CBT is efficacious for patients with insomnia and comorbid chronic peripheral pain syndromes,21 treated breast cancer,22 fibromyalgia23, mixed medical disorders,24 mixed psychiatric and medical disorders,25 and alcoholism.26 Despite these findings, it is yet to be determined whether patients with PI or CMI show similar improvement from an equal and standard dose of CBT intervention. The current study tested the relative efficacy of CBT against a sleep hygiene control treatment (SH) in patients with PI and in a group of patients with CMI composed predominantly of individuals with mixed comorbid psychiatric disorders. The study hypotheses predicted that CBT would produce significantly greater short- and longer-term improvements in insomnia symptoms than would sleep hygiene in the sample as a whole. The data obtained were also examined to assess the relative efficacy of CBT in the PI and CMI groups considered separately.

Sleep disorders and their association with laboratory pain sensitivity in temporomandibular joint disorder.

Abstract: TEMPOROMANDIBULAR JOINT DISORDER (TMD) HAS BEEN DESCRIBED AS A PROTOTYPIC IDIOPATHIC PAIN SYNDROME CHARACTERIZED BY POORLY understood, episodic, masticatory muscle and/or joint pain. TMD affects an estimated 12% of the population.1 As in other idiopathic pain disorders such as fibromyalgia and irritable bowel syndrome, patients often present with overlapping signs and symptoms including psychological distress, neuroendocrine abnormalities, and chronic insomnia.2,3 Recent theoretical perspectives have proposed that these “central sensitivity syndromes” share a common central nervous system substrate characterized by heightened processing of noxious input, which contributes to overlapping daytime sequelae among these disorders.4 Several cross-sectional studies have demonstrated that compared to controls, TMD patients exhibit enhanced responsivity to a variety of painful stimuli measured both at facial and extracranial anatomic sites.5–7 Pain sensitivity at “unaffected” (i.e., non-jaw) sites suggests the involvement of central pain processing mechanisms, beyond peripheral contributions. Recent longitudinal work has reported that enhanced laboratory pain sensitivity in pain free individuals is linked to genetic polymorphisms that predict the development of new onset TMD.8 This suggests that central processes associated with pain amplification may be critical to understanding the etiopathophysiology of TMD. Clinical factors that contribute to pain amplification in TMD, however, are poorly understood. Our group has focused on the possibility that sleep disturbance is one such factor that may directly contribute to central sensitization and pain amplification.9 We recently reported, for example, that sleep onset insomnia symptoms predict the development of chronic pain following serious burn injury.10 While it is often assumed that insomnia or sleep loss occurring in the context of chronic pain occurs secondarily to the sleep interrupting effects of pain, we and others have demonstrated that insomnias associated with chronic pain are often phenotypically similar to primary insomnia.11 Shared features include high levels of pre-sleep cognitive rumination and evidence of maladaptive coping strategies that may exist prior to the development of pain and/or independently contribute to insomnia symptoms. It is unknown, however, whether primary insomnia is associated with alterations in laboratory pain sensitivity when it occurs either as a sole condition or as part of a chronic pain disorder such as TMD. Only a handful of investigations have systematically sought to evaluate the sleep quality of TMD patients. These studies have consistently found that the majority ( > 50%) of TMD patients report poor sleep quality, and that subjective ratings of poor sleep are associated with increased clinical pain severity and psychological distress.12–14 Fundamental descriptive data using polysomnography and standard research diagnostic interviews to quantify the range of sleep disorders in TMD and determine their possible associations with laboratory measures of pain sensitivity are lacking. The extant literature has largely focused on possible relationships between sleep bruxism and TMD.15,16 Sleep bruxism, however, has not been found to be associated with either poor sleep quality or polysomnographic measures of sleep continuity or architecture disturbances.17–19 The objective of this study was to address two critical gaps in the literature: (1) characterize the spectrum of sleep disorders in a well-described sample of myofascial TMD patients, using polysomnography and state-of-the art structured diagnostic interviews; and (2) evaluate possible associations between observed sleep disorder indices and laboratory measures of pain threshold. We hypothesized that rates of primary insomnia would be substantive in TMD and that primary insomnia would be associated with reductions in pain threshold at both masseter and extracranial sites.

Sleep-related breathing and sleep-wake disturbances in ischemic stroke

Abstract: Background: Sleep-related breathing disturbances (SDB) and sleep-wake disturbances (SWD) are often neglected in stroke patients. Recent studies suggest that they are frequent and have an impact on stroke outcome. Methods: We review current knowledge about frequency, clinical presentation, and consequences of poststroke SDB and SWD, and discuss treatment options. Results: SDB, presenting with obstructive, central, or mixed apneas, is present in 50%–70% of stroke patients. We recommend screening for SDB in all stroke patients by respirography. Continuous positive airway pressure (CPAP) is the treatment of choice for obstructive SDB, which reverses the vascular risk of the patients. In the absence of controlled trials, CPAP treatment should be reserved for patients with severe obstructive SDB, daytime symptoms (e.g., sleepiness), or high cardiovascular risk profile. Oxygen and adaptive servoventilation may be used for central SDB. SWD including insomnia, disturbances of wakefulness (hypersomnia, excessive daytime sleepiness, fatigue), sleep-related movement disorders (restless legs syndrome, periodic limb movements during sleep), and parasomnias (REM sleep behavior disorder) are found in 10%–50% of patients. SWD are associated with cognitive disturbances and may compromise neurologic recovery. Hypnotics and sedative antidepressants may aggravate SDB and neurologic recovery and should be used with caution. For disturbances of wakefulness, dopaminergic drugs, modafinil, or activating antidepressants may be considered. Poststroke sleep-related movement disorders can be treated with dopaminergic drugs; REM sleep behavior disorder with clonazepam. Conclusions: Sleep-related breathing disturbances and sleep-wake disturbances are frequent conditions that affect stroke outcome. In view of existing treatment options, these conditions deserve the neurologist9s awareness.

Localized loss of hypocretin (orexin) cells in narcolepsy without cataplexy

Abstract: STANDARD NOSOLOGY CLASSIFIES PATIENTS WHO HAVE SHORT SLEEP LATENCY AND ≥ 2 SLEEP ONSET REM SLEEP PERIODS ON THE MULTIPLE SLEEP LATENCY test as narcoleptic1 Under this definition, more than a quarter of those classified as narcoleptic do not have cataplexy2,3 The intensity of cataplexy in patients classified as having narcolepsy with cataplexy varies greatly: it is the most debilitating symptom in a few patients, causing total loss of muscle tone and consequent collapse several times a day; it occurs rarely and causes only transient weakness of the facial musculature in others4 Narcolepsy with cataplexy has been shown to be characterized by a loss of the hypocretin (orexin) peptide and of the cells generating this peptide5–8 All human narcoleptic brains we have examined have some surviving hypocretin cells with approximately normal morphology9 Unfortunately, collection of the brains of human narcoleptics has been largely limited to patients with cataplexy We now present data from an analysis of the complete hypothalamus of one patient with narcolepsy without cataplexy (patient 1), data from a second narcolepsy without cataplexy patient from which we received only anterior hypothalamic tissue (patient 2), 5 narcolepsy with cataplexy patients, and 6 normal individuals

Does cognitive-behavioral therapy for PTSD improve perceived health and sleep impairment?

Abstract: There is a paucity of empirical study about the effects of evidence-based psychotherapy for posttraumatic stress disorder (PTSD) on concurrent health concerns including sleep impairment. This study compares the differential effects of cognitive processing therapy (CPT) and prolonged exposure (PE) on health-related concerns and sleep impairment within a PTSD sample of female, adult rape survivors (N = 108). Results showed that participants in both treatments reported lower health-related concerns over treatment and follow-up, but there were relatively more improvements in the CPT condition. Examination of sleep quality indicated significant improvement in both CPT and PE across treatment and follow-up and no significant differences between treatments. These results are discussed with regard to the different mechanisms thought to underlie the treatments and future innovations in PTSD treatment.

Defining the sleep phenotype in children with autism.

Abstract: Sleep concerns are common in children with autism spectrum disorders (ASD). We identified objective sleep measures that differentiated ASD children with and without parental sleep concerns, and related parental concerns and objective measures to aspects of daytime behavior. ASD poor sleepers differed from ASD good sleepers on actigraphic (sleep latency, sleep efficiency, fragmentation) and polysomnographic (sleep latency) measures, and were reported to have more inattention, hyperactivity, and restricted/repetitive behaviors. Fragmentation was correlated with more restricted/repetitive behaviors. This work provides the foundation for focused studies of pathophysiology and targeted interventions to improve sleep in this population.