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Insomnia is common, affecting approximately 10% of the population. In addition to night-time sleep difficulties, insomnia disorder requires the presence of concomitant daytime impacts, making it a 24-hour problem. It is not surprising, therefore, that insomnia disorder is associated with significant impacts to quality of life and economic costs. Many patients with insomnia also have comorbid physical and/or mental health disorders, and sometimes also other sleep disorders. This chapter reviews the key features, prevalence, and consequences of insomnia disorder, and provides background information to aid clinicians as they begin to think about formulating treatment approaches.
Sleep and epilepsy have bidirectional relationships, and various endocrine interactions. Besides the commonly observed increase in seizure frequency in association with sleep loss or with sleep disorders, such as sleep apnea, seizures themselves may lead to sleep fragmentation. Furthermore, nocturnal seizures may be associated with more severe and longer lasting respiratory consequences, as well as higher risk of sudden death. It is common for sleep to change during pregnancy in relation to endocrine changes and these changes may in turn affect seizure frequency. Overall, estrogens may have excitatory effects and may increase the consolidation of wakefulness and decrease REM sleep duration. Progesterone tends to have a sedative effect and the decrease in level may lead to more complaints of insomnia pre-menstrual and after menopause. Common sleep disorders are discussed. Obstructive sleep apnea becomes much more common after menopause, and sometimes may be seen in the third trimester of pregnancy as a result of weight gain. Restless legs syndrome is more common in pregnancy. Overall, insomnia is more common in women. Consideration should be given to comorbid primary sleep disorders whenever symptoms of insomnia or hypersomnolence are reported by patients with epilepsy.
Sleep-related complaints are quite common in the long-term care setting. It is estimated that 40-70% of older adults have some type of chronic sleep-related complaint. Up to 50% of these go undiagnosed. Older adults are known to have increased wakefulness at night, increased number of sleep arousals, and increased sleep latency. Older adults are known to have decreased total sleep time, slow wave sleep, REM sleep, and sleep efficiency. Some common sleep-wake cycle disturbances seen in older adults include primary insomnia, delayed sleep phase syndrome, advanced sleep phase syndrome, irregular sleep-wake rhythm, non-24-hour sleep-wake disorder, sleep state misperception, hypersomnia, and narcolepsy. Good nonpharmacologic principles beneficial to sleep quality are often safer and more effective than pharmacologic therapies. These include good sleep hygeine practices, sleep restriction, increased physical activity, limiting daytime naps, and daytime bright light exposure.
Difficulty falling asleep and/or maintaining sleep are common complaints in patients visiting medical clinics. Insomnia can occur alone or in combination with other medical or psychiatric disorders. Diagnosis and management of insomnia at times are perplexing. This updated study review aimed at a clinical algorithm for diagnosis and treatment of insomnia in adults. We developed an easy-to-apply algorithm to diagnose and manage insomnia that can be used by general practitioners and non-sleep specialists. To this end, our team reviewed the previous studies to determine the prevalence, evaluation, and treatment of insomnia. We used the results to develop a clinical algorithm for diagnosing and managing insomnia.
Insomnia occurs in a short (less than 3 months duration) or chronic form (≥3 months duration). Insomnia management includes both pharmacological and non-pharmacological interventions. There is ample research evidence for the impact of a variety of non-pharmacological treatments, but both types of treatments can be used for each patient. If there are any contradictions in the diagnosis process, therapists should use objective instruments, such as polysomnography, but they should not be in a hurry to use these instruments.
Edited by
David Kingdon, University of Southampton,Paul Rowlands, Derbyshire Healthcare NHS foundation Trust,George Stein, Emeritus of the Princess Royal University Hospital
Sleep is one of the great mysteries of human experience. It is a behaviour that is highly preserved throughout the animal kingdom, and it constitutes a third of our existence. It begins before birth and is with us throughout life. For a newborn baby, it is their predominant behaviour and continues to occupy a large proportion of our lives as we age. It has long been suspected that it is essential for good mental and physical health, and in the last century, there has been growing scientific evidence to confirm this suspicion. Yet, we know very little about the functions of sleep and are only just beginning to understand the mechanisms that control it. In the past, it was commonly assumed that sleep had ’a function’, but the more we have come to understand, the clearer it has become that sleep performs multiple functions. Precisely what those functions are is still uncertain, and they may change across the lifespan or possibly even vary across different species. We know that sleep is essential for life and total sleep deprivation for long enough is fatal, and the fact that we spend a third of our lives in this vulnerable state underlines how important sleep must be.
We aim to assess the relationship between validated smoking cessation pharmacotherapies and electronic cigarettes (e-cigarettes) and insomnia and parasomnia using a systematic review and a network meta-analysis. A systematic search was performed until August 2022 in the following databases: PUBMED, COCHRANE, CLINICALTRIAL. Randomized controlled studies against placebo or validated therapeutic smoking cessation methods and e-cigarettes in adult smokers without unstable or psychiatric comorbidity were included. The primary outcome was the presence of “insomnia” and “parasomnia.” A total of 1261 studies were selected. Thirty-seven studies were included in the quantitative analysis (34 for insomnia and 23 for parasomnia). The reported interventions were varenicline (23 studies), nicotine replacement therapy (NRT, 10 studies), bupropion (15 studies). No studies on e-cigarettes were included. Bayesian analyses found that insomnia and parasomnia are more frequent with smoking cessation therapies than placebo except for bupropion. Insomnia was less frequent with nicotine substitutes but more frequent with bupropion than the over pharmacotherapies. Parasomnia are less frequent with bupropion but more frequent with varenicline than the over pharmacotherapies. Validated smoking cessation pharmacotherapies can induce sleep disturbances with different degrees of frequency. Our network meta-analysis shows a more favorable profile of nicotine substitutes for insomnia and bupropion for parasomnia. It seems essential to systematize the assessment of sleep disturbances in the initiation of smoking cessation treatment. This could help professionals to personalize the choice of treatment according to sleep parameters of each patient. Considering co-addictions, broadening the populations studied and standardizing the measurement are additional avenues for future research.
Edited by
Andrea Fiorillo, University of Campania “L. Vanvitelli”, Naples,Peter Falkai, Ludwig-Maximilians-Universität München,Philip Gorwood, Sainte-Anne Hospital, Paris
Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder that persists into adulthood. We provide an overview of prevalence, diagnosis, and treatment. Future directions highlight key areas of progress. ADHD is not always an early childhood onset disorder; it may emerge as an impairing condition during the adolescent years. Transition from child to adult services is poor and greater efforts are needed to ensure effective treatment during this critical stage. There are sex differences in the expression of ADHD. Related to this, the diagnosis of ADHD is often missed in girls but is increasingly recognized in adult life. The impact of emotional instability as a core feature of ADHD on mental health is widely recognized. It is still the case that ADHD is often misdiagnosed for other common mental health conditions, and greater awareness of ADHD is needed among health care professionals. Prominent comorbidities include substance use and sleep problems. Finally, we consider the cognitive and neural processes that explain persistence of ADHD. The balance of default mode to task positive network activity may lead to core symptoms such as spontaneous mind wandering, and the role of saliency on task performance.
To investigate the informative value of nightmares on neurobehavioral functioning in individuals with mild traumatic brain injury (mTBI) beyond general sleep disturbance.
Participants and Methods:
A sample of 146 adults with mTBI (mean age = 45.1±16.0), recruited from a specialized concussion treatment center, underwent an assessment of neurobehavioral functioning using the Behavioral Assessment Screening Tool (BAST), self-reported habitual sleep disturbance and quality (via the Pittsburgh Sleep Quality Index; PSQI), and reported nightmare frequency in the past two weeks.
Results:
Nightmare frequency was the strongest predictor of negative affect (ß = .362, p <.001), anxiety (ß = .332, p <.001), and impulsivity (ß = .270, p <.001) after controlling for sex and age. Sleep disturbance accounted for the greatest variance in depression (ß = .493, p <.001), burden from concussion (ß = .477, p <.001), and fatigue (ß = .449, p <.001) after controlling for sex and age.
Conclusions:
Nightmares independently associate with neurobehavioral symptoms and likely have differential etiology from reported sleep disturbance. Nightmare frequency was more strongly related to positive neurobehavioral symptoms (i.e., added factors that impact functioning, e.g., anxiety), while general sleep disturbance was associated with negative neurobehavioral symptoms (i.e., factors taken away that impact functioning, e.g., lack of energy). Our findings suggest that neuropsychological evaluations of individuals with mTBI should assess for sleep disturbance and nightmare frequency as risk factors for neurobehavioral barriers to functioning.
Laterality of motor symptom onset in Parkinson’s disease (PD) is well-known and under-appreciated. It is still unclear though if this laterality might have an influence on other symptoms. Specifically, REM sleep behavior disorder has been shown to be a factor that has a high probability to be lined to PD. In this study we analyzed the longitudinal effect of REM symptomatology on brain lateralization in PD.
Participants and Methods:
We used the baseline and 3-year visit data of 116 participants (67 without REM (PD-non-REM), 49 with REM (PD-REM)) aged 37-81 years from the Parkinson’s Progression Markers Initiative (PPMI) dataset. Statistical 3T MRI data (cortical thicknesses, areas, foldings of cortical Desikan atlas and volumes of subcortical regions) were obtained via FreeSurfer 7.1.1. Lateralization was computed using the formula: (left-right)/(lef +right). Mixed ANOVAs were performed on each region of interest.
Results:
Our findings showed an increased right asymmetry of the paracentral lobule area and of the pars orbitalis area and volume in PD-REM. There was a reduced right asymmetry of the parietal inferior volume at baseline in PD-REM, whereas REM symptomatology had a stable effect at the 3 years visit. At baseline, there was an increased left asymmetry of the thickness of the caudal anterior cingulate, pars orbitalis and pars triangularis regions in PD-REM. After 3 years, there was an increased right asymmetry in those regions. The precentral, frontal superior and transversal temporal gyri showed inverse results: an increased right asymmetry of the thickness at baseline and an increased left asymmetry after 3 years. Finally, REM symptomatology is associated with more significant increases of the left asymmetry of the frontal superior gyrus volume and of the right asymmetry of the supramarginal gyrus volume after 3 years than at baseline.
Conclusions:
These results provide evidence of the modulating effect of the disease progression on the relationship between REM symptoms and brain lateralization in PD.
Stress is well known to increase the severity of somatization and insomnia. A recent major stressor that could have influenced the severity of these presentations was world-wide COVID-19 Pandemic. Somatization is the physical expression of stress and emotional distress that can manifest itself throughout various corporal domains and can be a comorbidity to insomnia. Headaches represent some of the most common complaints associated with brain injuries and neurological disorders but are common in somaticized disorders as well. In large survey study we examined whether exercise was associated with severity of somatization and headaches. We hypothesized that both healthy individuals and those with insomnia who exercised during the pandemic would report less severe somatic symptoms and headaches than those who did not.
Participants and Methods:
A large survey was sent out to 4,073 individuals to measure their experience in numerous domains during the COVID-19 pandemic. This survey included a short symptom questionnaire used to measure somatization and the Insomnia Scale Index to measure insomnia. These questionnaires were administered along with a “yes or no” question on whether the participants exercised regularly in that period. A univariate ANOVA was performed to analyze the data to determine if exercise during the pandemic was beneficial in the reduction of somatic symptoms and headache severity. Furthermore, these tests were run to determine if the effect was greater on those with insomnia.
Results:
The effect of insomnia and exercise on total somatic symptoms were significant at F(1, 3445)=650.5, p<0.001 and F(1, 3445)=26.1, p<0.001, respectively. For reported headache severity, there was a significant effect of exercise F(1, 4073)=14.5, p<0.001 and insomnia F(1, 4073)=160.5, p<0.001; therefore, those who exercised reported less severe headaches and those who suffered from insomnia reported more severe somatic symptoms. This meant that those who exercised reported less severe somatization and headaches than those who didn’t and those with insomnia reported more severe somatization and headaches than healthy individuals. However, the interaction between exercise and insomnia on overall somatization severity was not significant at F(1, 3445)=3.4, p=0.066 nor for reported headache severity F(1, 4073)=0.81, p=0.370. Despite there not being a significant interaction, the benefit of exercise was slightly greater on healthy individuals than those with insomnia.
Conclusions:
Those with insomnia reported more severe headaches and overall somatic symptoms than non-insomniacs regardless of whether they exercised or not. Exercise did make a difference on the reported severity of headaches and somatization in both groups; however, the benefit of exercise on headaches and somatization was greater in individuals who do not suffer from insomnia. Thus, exercise was noted to be beneficial to those in the general population and those suffering from insomnia as it can potentially reduce the severity of somatization and headaches. Of course, this research was cross sectional and correlational, so the directionality of the effects cannot be inferred. For future research, it would be instrumental to use experimental methods to help determine the duration and type of exercise that may optimize its potential benefits on headaches and somatic symptoms.
Resiliency has been shown to attenuate and even protect against cognitive impairment from mental and physical stressors. Recently, it has been demonstrated that individuals who score high in psychological resilience tend to have less impairment following a mTBI.The COVID-19 pandemic proved to be an uncertain time for many. Periods of isolation, unemployment, and of course, sickness, meant more time at home. The partial or complete breakdown of an individual’s day-to-day routine paired with the stress of the pandemic has reinforced the need for psychological resilience. This analysis investigates the relationship between self-reported routine adherence and an individual’s corresponding psychological resilience. We hypothesize that individuals who maintained a structured daily routine during the pandemic will have higher levels of psychological resilience, enabling them to better handle periods of extreme stress.
Participants and Methods:
8963 English-speaking adults (18-92 years old; 59.5% female) from across the U.S. completed an online, monthly cross-sectional (∼1000 participants per month), battery of questions that included the Connor-Davidson Resilience Scale (CD-RISC), and a self-reported sleep and routine rating(s) between June 2020 and April 2021. We measured the level of an individual’s routine by adding the self-reported survey scores of waking at the same time and maintaining a routine throughout the day. Both questions were scored 0-4 (Likert-style) for a score range of 0 to 8; higher scores indicated a higher adherence to a daily structure. Weeknight sleep (Sun-Thurs) was a self-reported average of the hours of sleep obtained over the past 4 weeks. A two-way ANCOVA was used to analyze the effects that routine had on subsequent psychological resilience scores while controlling for average sleep duration.
Results:
A significant main effect routine on psychological resilience was found F(8,8953) =227, p=<.00001 after controlling for average reported weeknight sleep. An independent t-test was performed to determine the differences between those who fall above and below the average score (M= 5.1) for routine adherence. Individuals who were above average in adherence (M=71.1, SD=15.5) had significantly higher CD-RISC scores than individuals who did not (M=59.2, SD=16.7); t(9166)=35.1, p <0.001.
Conclusions:
Individuals who maintained a more structured day throughout the pandemic were more likely to score higher on psychological resilience assessments than those who did not. Chronic stress is known to contribute to the development and exacerbation of many common psychiatric conditions like anxiety and depression. These results suggest that having a regular routine may have positive effects on an individual’s ability to bounce back from stressful cognitive and psychological events. This relationship should be further investigated in clinical populations as a potential intervention or adjunctive treatment for common neuropsychiatric conditions.
Obstructive sleep apnea (OSA) has been associated with cognitive deficits as evidenced by neuropsychological testing in the domains of attention/working memory, verbal memory, processing speed, and executive function. OSA is often comorbid with hypertension and has been considered a risk factor for hypertension (Kareem et al., 2018; Tietjens et al., 2019). Both hypertension and OSA have been shown to be independent predictors of memory (Kinoshita et al., 2012). OSA and posttraumatic stress disorder (PTSD) are also frequently co-occurring, especially among veterans. In a group of veterans with a history of PTSD, we seek to explore the effects of sleep apnea and hypertension on cognitive functioning, particularly auditory learning/memory.
Participants and Methods:
One hundred and three male and female participants with comorbid OSA and PTSD symptomology were screened as part of a larger VA Palo Alto Health Care System study. Participants (age: x=56.3, a=13.8, 24-81 years; education: x=14.6, a=2.3, 8-20 years; 9.6% female, 89.6% male) completed a neuropsychological battery, including the CVLT-II and WMS-IV Logical Memory. Presence or absence of hypertension was dichotomously coded and AHI severity was categorically coded. An auditory learning/memory composite variable was created using the z-score transformation method (Dodge et al., 2020). Variables and covariates were entered into a hierarchical regression.
Results:
The initial regression model revealed hypertension and OSA severity to be independent predictors of performance on auditory learning/memory (hypertension: ß= -0.71, p<0.01; OSA: ß= -0.42, p<0.01), where presence of hypertension or increased severity of OSA resulted in worse performance on the auditory learning/memory composite.
Conclusions:
Results suggest that hypertension and OSA may independently and negatively affect performance on measures of auditory learning/memory in veterans with PTSD symptomology and OSA. Such findings underscore the importance of assessing and treating both hypertension and OSA among veterans with PTSD to improve not only physical health, but also cognitive health. Further research demonstrating similar findings is recommended along with studies investigating whether or not the treatment of hypertension and OSA can improve auditory learning/memory.
Chronic insomnia is a highly prevalent disorder affecting approximately one-in-three Americans. Insomnia is associated with increased cognitive and brain arousal. Compared to healthy individuals, those with insomnia tend to show greater activation/connectivity within the default mode network (DMN) of the brain, consistent with the hyperarousal theory. We investigated whether it would be possible to suppress activation of the DMN to improve sleep using a type of repetitive transcranial magnetic stimulation (rTMS) known as continuous theta burst stimulation (cTBS).
Participants and Methods:
Participants (n=9, 6 female; age=25.4, SD=5.9 years) meeting criteria for insomnia/sleep disorder on standardized scales completed a counterbalanced sham-controlled crossover design in which they served as their own controls on two separate nights of laboratory monitored sleep on separate weeks. Each session included two resting state functional magnetic resonance imaging (fMRI) sessions separated by a brief rTMS session. Stimulation involved a 40 second cTBS stimulation train applied over an easily accessible cortical surface node of the DMN located at the left inferior parietal lobe. After scanning/stimulation, the participant was escorted to an isolated sleep laboratory bedroom, fitted with polysomnography (PSG) electrodes, and allowed an 8-hour sleep opportunity from 2300 to 0700. PSG was monitored continuously and scored for standard outcomes, including total sleep time (TST), percentage of time various sleep stages, and number of arousals.
Results:
Consistent with our hypothesis, a single session of active cTBS produced a significant reduction of functional connectivity (p < .05, FDR corrected) within the DMN. In contrast, the sham condition produced no changes in functional connectivity from pre- to post-treatment. Furthermore, after controlling for age, we also found that the active treatment was associated with meaningful trends toward greater overnight improvements in sleep compared to the sham condition. First, the active cTBS condition was associated with significantly greater TST compared to sham (F(1,7)=14.19, p=.007, partial eta-squared=.67). Overall, individuals obtained 26.5 minutes more sleep on the nights that they received the active cTBS compared to the sham condition. Moreover, the active cTBS condition was associated with a significant increase in the percentage of time in rapid eye movement (REM%) sleep compared to the sham condition (F(1,7)=7.05, p=.033, partial eta-squared=.50), which was significant after controlling for age. Overall, active treatment was associated with an increase of 6.76% more of total sleep time in REM compared to sham treatment. Finally, active cTBS was associated with fewer arousals from sleep (t(8) = -1.84, p = .051, d = .61), with an average of 15.1 fewer arousals throughout the night than sham.
Conclusions:
Overall, these findings suggest that this simple and brief cTBS approach can alter DMN brain functioning in the expected direction and was associated with trends toward improved objectively measured sleep, including increased TST and REM% and fewer arousals during the night following stimulation. These findings emerged after only a single 40-second treatment, and it remains to be seen whether multiple treatments over several days or weeks can sustain or even improve upon these outcomes.
REM sleep behavior disorder (RBD) is a parasomnia characterized by vivid dreams and motor behavior such that people appear to “act out their dreams.” These are sudden and often violent bodily movements such as punching or kicking, or vocalizations such as laughing or shouting. RBD is mostly associated with the older adult male population. However, recent studies show that RBD and REM sleep without atonia (RSWA) also occur in other populations, including women, children, and adolescents. Given the prodromal period before an individual can develop the classic symptoms of RBD and that RBD is not just limited to older adult males, it is important to study subclinical features of RBD. RBD is a parasomnia and poor sleep is well known to affect cognitive domains. Additionally, RBD is separately shown to negatively affect cognition in older adults. Given these connections, the association between RBD symptoms and cognition among young adults warrants further study. The purpose of this study was to evaluate the association between RBD symptoms and cognitive domains, specifically attention, processing speed, executive function, and working memory.
Participants and Methods:
University students from the Bronx, NY (N=50, mean age = 19.8, female = 78.4%) completed the REM Sleep Behavior Disorder Screening Questionnaire (RBDSQ). Estimated intellectual ability was assessed using the Wechsler Test of Adult Reading (WTAR). Cognitive assessment included the Delis-Kaplan Executive Function System (D-KEFS) Color-Word Interference Test (attention and executive function) and the Cogstate battery (Groton Maze Learning Test (executive function), Chase Test (processing speed), Identification Test (attention), One Back Test (attention), and Two Back Test (working memory)). Psychosocial assessment included the Perceived Stress Scale (PSS), Beck Depression Inventory-II (BDI-II), and Beck Anxiety Inventory (BAI).
Results:
A series of general linear models were used to determine the relationship between RBD symptoms and cognition. Race/ethnicity, depressive symptoms, and estimated intellectual ability were included as covariates. Using a cutoff score of five (range: 0-13) on the RBDSQ, the ANCOVAs determined that there was no association between RBD symptoms and the cognitive domains of attention, processing speed, executive function, and working memory. However, there was a trend for attention as measured by the Identification task (F(1,41) = 3.85, p = 0.057). Interestingly, Pearson’s chi-square test revealed that the relationship between depressive symptoms and RBD symptoms was significant (x2 = 6.87, p = 0.009). Those who had high RBD symptoms were more likely to have high depressive symptoms.
Conclusions:
Our analyses indicated that in healthy young adults, RBD symptoms are not associated with the cognitive domains of attention, processing speed, executive function, or working memory. However, there may be a trend for attention, which warrants further research with a larger sample size. Of interest, young adults with RBD symptoms were more likely to have clinically significant depressive symptoms. Given that RBD in older adults is associated with incident dementia with Lewy body and Parkinson’s disease, which are associated with cognitive decline and depression, further work is necessary to explore the mechanisms of this connection as well as the development of clinical disorders.
Insomnia affects 30-45% of the world population, is related to mortality (i.e., auto accidents and job-related accidents), and is related to mood and affect disorders such as anxiety and depression. Better understanding of insomnia via increased research will decrease the burden on insomnia. The neurocognitive model of sleep proposes that conditioned somatic and cognitive hyperarousal develop in response to repeated pairings of sleep-related stimuli with insomnia-related wakefulness. The purpose of this study was to examine the neurocognitive model of sleep using a novel laboratory paradigm, the Sleep Approach Avoidance Task (SAAT). It was hypothesized that individuals who report symptoms of insomnia will display a bias for negative sleep-related images from the SAAT, which is presumably a reflection of cognitive, behavioral and physiological processes associated with hyperarousal. It was also hypothesized that participants who report poor sleep would provide different subjective ratings for negative images (i.e., stronger valence and arousal) than individuals who reported better sleep.
Participants and Methods:
An initial sample of 66 healthy college-aged participants completed the Insomnia Severity Index (ISI), the Pittsburgh Sleep Quality Index (PSQI) the Dysfunctional Attitudes and Beliefs about Sleep (DBAS) scale and the Epworth Sleepiness Scale (ESS). Participants also completed the SAAT. The SAAT was developed to assess sleep-related bias in adults. The SAAT is a visual, joystick controlled reaction time task that measures implicit bias for positive and negative sleep-related images. At the end of the task the participants are also asked to rate each image along three dimensions included valence, arousal and dominance.
Results:
There was a positive correlation between the SAAT and the ISI [r(61) = .30, p = .01], indicating that symptoms of insomnia are related to negative approach-related bias for sleep-related images. No other correlations were observed between the SAAT and self-report sleep measures. With regard to rating of images, higher dominance ratings for negative images were correlated with the SAAT [r(62) = .24, p = .03], which indicates that the approach bias for negative images is associated with “being in control.” Multiple linear regression was used to test if ISI scores and dominance ratings for negative images significantly predicted SAAT bias scores. The overall regression was statistically significant [r2 = .13, F(2, 58) = 4.15, p = .02]. ISI scores significantly predicted SAAT scores (ß = .27, p = .04), whereas dominance ratings for negative images did not significantly predict SAAT scores (ß = .20, p = .11). Exploratory correlational analyses were also completed for ratings of images and other sleep self-report measures. Valence ratings for positive sleep-related images were positively correlated with the ESS [r(64) = .36, p = .01], whereas valence ratings for negative sleep-related images were negatively correlated with the ESS [r(64) = -.24, p = .03].
Conclusions:
Hypotheses were partially supported with the ISI being the only self-report measure associated with negative bias for sleep-related images. While ratings of dominance are associated with bias for negative sleep-related images, these ratings do not provide unique variance. These findings indicate a cognitive processing bias for sleep-related stimuli among young adult poor sleepers. Limitations, implications for assessment and intervention are discussed.
Previous research indicates that women tend to struggle with insomnia at higher rates both prior to and during the global COVID-19 pandemic; however, not much research has investigated the extent to which insomnia correlates with comorbid problems, including aggression, depression, anxiety, PTSD severity, and alcohol use between the sexes. On a neurobiological level, insomnia could be associated with those mood disorders due to the effects of sleep disturbance on serotonergic and GABA neurotransmission, and males might experience such associations at a lower frequency due to their increased rates of serotonin synthesis. Consequently, we hypothesized that women would demonstrate higher prevalence of the aforementioned comorbidities during COVID than males due to higher rates of insomnia reported in women during COVID.
Participants and Methods:
We surveyed a total of 13,313 adults, with 5,598 females (Mage=36.4, SD=11.9) and 7,654 males (Mage=37.81, SD=12.7) using Amazon Mechanical Turk between April 2020 and April 2021. Insomnia was measured using the Insomnia Severity Index (ISI), while levels of depression, anxiety, PTSD severity, and alcohol use, and aggression were assessed through Patient Stress Questionnaires (PSQs) and the Buss Perry Aggression Questionnaire (BPAQ).
Results:
As expected, there were significant positive correlations between ISI and BPAQ (r(13306)=0.364, p<0.0001), PSQ Depression (r(13300)=0.694, p<0.0001), PSQ Anxiety (r(13211)=0.627, p<0.0001), PSQ PTSD (r(13305)=0.444, p<0.0001), and PSQ Alcohol (r(12915)=0.218, p<0.001). The strength of these associations was significantly higher in males than females in almost all categories: aggression (z=4.27, p<0.0001), depression (z=2.41, p=0.016), anxiety (z=3.16, p=0.0016), and alcohol use (z=5.89, p<0.0001) - not significant for PTSD severity (z=1.48, p=0.14).
Conclusions:
We found that insomnia was more strongly correlated with comorbid emotional and behavioral problems among males than females. This stands in contrast to our initial hypothesis, as the findings suggest that men who suffer from greater insomnia are more likely to experience those four comorbidities than females. This suggests that sex may play a role in the association between sleep disturbances and other clinical presentations relevant to neuropsychology. Further work will be necessary to identify the neurobiological mechanisms that drive the sex differences in these associations. While the present findings cannot determine the causal direction of the association, it will be crucial to determine the directionality of these associations and the mechanisms that lead to differences in expression between the sexes.
Obstructive sleep apnea (OSA) may be a modifiable risk factor for late-life cognitive impairment. We previously demonstrated that non-Hispanic Black older adults are less likely to be diagnosed with OSA despite having equal or greater health risk for OSA compared to non-Hispanic White older adults, and this disparity in diagnosis was strongest among individuals with lower education. Here, we aimed to determine 1) whether there are racial differences in continuous positive airway pressure (CPAP) treatment, 2) how CPAP treatment may influence OSA-cognition associations, and 3) whether CPAP differentially influences OSA-cognition associations across racial groups.
Participants and Methods:
Cross-sectional data were obtained from 424 socioeconomically diverse community-dwelling adults ages 55-83 (63.4±3.2 years, 41.7% male, 53.5% Black) from the Michigan Cognitive Aging Project. Physician-diagnosed OSA and current CPAP use were self-reported. Global cognition was operationalized as a composite of five factor scores derived from a comprehensive neuropsychological battery. Racial group differences were investigated with chi-square and Fisher’s exact tests with statistical significance set at the .05 level. Associations between OSA and cognition (adjusted for age, gender, race, and years of education) were investigated with linear regressions. Subsequent models isolated effects of uncontrolled OSA by excluding individuals using CPAP. Racial differences in OSA-cognition associations were investigated with race-stratified models.
Results:
Fewer Black participants (9.2%) reported diagnosed OSA compared to White participants (12.3%; x2 (1, N=424) =5.314, p=.021, cp=.112). In the whole sample, 47.3% of participants with diagnosed OSA reported CPAP use, and this proportion did not differ across race (x2 [1, N=86] =.048, p=.826). In the whole sample, OSA diagnosis was only associated with cognition when CPAP users were excluded (excluding CPAP users: ß=-.085, SE=.037, p=.024; including CPAP users: ß=-.067, SE=.036, p=.062). In race-stratified models, diagnosed OSA was only associated with cognition among Black participants, and this association was stronger when CPAP users were excluded (excluding CPAP users: ß=-.142, SE=.060, p=.018; including CPAP users: ß=-.126, SE=.058, p=.030). Diagnosed OSA was not associated with cognition among White participants, irrespective of whether CPAP users were included (excluding CPAP users: ß=-.084,SE=.068, p=.215; including CPAP users: ß=-.056, SE=.064, p=.378).
Conclusions:
Our findings support CPAP treatment as a potential intervention to mitigate late-life cognitive impairment among those with OSA. Despite being less likely to receive a diagnosis of OSA, Black older adults were equally likely to engage in CPAP treatment as White older adults when diagnosed. The detrimental impact of OSA on cognition may be more salient among Black older adults, which may reflect racial disparities in cardiovascular risk and/or resources that promote cognitive reserve. However, CPAP appears to be an effective treatment to reduce OSA-related cognitive impairment for Black older adults, highlighting the critical importance of diagnosis and treatment in this group. Intervention efforts that abate racial inequalities in access to quality healthcare in order to facilitate acquisition of a formal OSA diagnosis and CPAP treatment may help to reduce preventable cognitive health disparities among older adults.
This review summarizes evidence on the modulation of functional responses mediated by activation of the MT1 and/or MT2 melatonin receptors by endogenous or exogenous melatonin. Selective MT1 inverse agonists, discovered by docking ultra large compound libraries to the MT1 crystal structure, decelerated the rate of re-entrainment of activity rhythms to a new dark onset. Surprisingly, these inverse agonists advanced circadian phase when given at subjective dusk mimicking melatonin through actions at MT1 receptors. The efficacy of environmental carbamates with structural similarity to melatonin interact with melatonin receptors and in turn advance circadian clock phase, as with melatonin. In summary, melatonin receptors are targets for drugs modulating circadian rhythms to yield therapeutic effects (i.e., synchronization), as well as for environmental chemicals that may induce harmful effects on human health due to actions on melatonin and on/off target receptors (e.g., serotonin) involved in signaling circadian time at inappropriate times of day.
Since 2018, the International Task Force on Benzodiazepines (ITFB), a group of academic psychiatrists and academic psychologists, has advocated that clinical guidelines should change to promote benzodiazepines from second- to first-line treatment for anxiety disorders, accept their use as maintenance treatment for anxiety conditions (in particular, panic disorder) and increase their use in gastrointestinal disorders. There is merit in much of what the ITFB argues, but in this article I analyse four major claims it has made in opinion editorials that I believe are not fully supported by the available evidence.