ABSTRACT
The nature and degree of objective sleep impairments in insomnia disorder remain unclear. This issue is complicated further by potential changes in sleep architecture on the first compared with subsequent nights in the laboratory. Evidence regarding differential first-night effects in people with insomnia disorder and controls is mixed. Here, we aimed to further characterize insomnia- and night-related differences in sleep architecture. A comprehensive set of 26 sleep variables was derived from two consecutive nights of polysomnography in 61 age-matched patients with insomnia and 61 good sleeper controls. People with insomnia expressed consistently poorer sleep than controls on several variables during both nights. While poorer sleep during the first night was observed in both groups, there were qualitative differences regarding the specific sleep variables expressing a first-night effect. Short sleep (total sleep time < 6 hr) was more likely during the first night and in insomnia, although approximately 40% of patients with insomnia presenting with short sleep on night 1 no longer met this criterion on night 2, which is important given the notion of short-sleeping insomnia as a robust subtype.
Subject(s)
Sleep Initiation and Maintenance Disorders , Sleep Wake Disorders , Humans , Sleep Initiation and Maintenance Disorders/complications , Sleep , Polysomnography , LaboratoriesABSTRACT
Sleep bruxism (SB) has been associated with biological and psychosocial factors. The assessment of SB includes self-report, clinical evaluation, and polysomnography. This study aimed to investigate the associations of self-reported SB with other sleep disorders and demographic, psychological, and lifestyle factors in the adult general population, and to investigate whether self-reported SB and polysomnographically (PSG) confirmed SB provide similar outcomes in terms of their associated factors. We recruited 915 adults from the general population in Sao Paulo, Brazil. All participants underwent a one-night PSG recording and answered questions about sex, age, BMI, insomnia, OSA risk, anxiety, depression, average caffeine consumption, smoking frequency, and alcohol consumption frequency. We investigated the link between SB and the other variables in univariate, multivariate, and network models, and we repeated each model once with self-reported SB and once with PSG-confirmed SB. Self-reported SB was only significantly associated with sex (p = 0.042), anxiety (p = 0.002), and depression (p = 0.03) in the univariate analysis, and was associated with insomnia in the univariate (p < 0.001) and multivariate (ß = 1.054, 95%CI 1.018-1.092, p = 0.003) analyses. Network analysis showed that self-reported SB had a direct positive edge to insomnia, while PSG-confirmed SB was not significantly associated with any of the other variables. Thus, sleep bruxism was positively associated with insomnia only when self-reported, while PSG-confirmed SB was not associated with any of the included factors.
Subject(s)
Sleep Bruxism , Sleep Initiation and Maintenance Disorders , Adult , Humans , Sleep Initiation and Maintenance Disorders/epidemiology , Sleep Initiation and Maintenance Disorders/complications , Sleep Bruxism/epidemiology , Brazil/epidemiology , Polysomnography , Self Report , SleepABSTRACT
Sleep bruxism (SB) is a repetitive jaw-muscle activity characterised by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible. Sleep bruxism has been linked with insomnia symptoms. Moreover, it has been suggested that there is a positive association between distress and the occurrence of sleep bruxism. However, the occurrence of sleep bruxism and its association with distress have not been studied in patients with insomnia. Therefore, we hypothesised that: (1) the occurrence of sleep bruxism is higher in patients with insomnia than in healthy controls; and (2) the occurrence of sleep bruxism in insomnia patients with moderate to high distress (IMHD) is higher than that in insomnia patients with slight distress (ISD). A total of 44 controls (34 females, 10 males, mean ± SD age = 46.8 ± 14.4 years) and 42 participants with insomnia (35 females, 7 males, mean ± SD age = 51.3 ± 12.1 years) were enrolled in this study. Among 42 participants with insomnia, 20 participants were subtyped as IMHD, 17 participants as ISD. Another five participants were not subtyped due to insufficient information. Group differences in rhythmic masticatory muscle activity (RMMA), a biomarker of sleep bruxism, were evaluated with Mann-Whitney U tests. The medians and interquartile ranges of the RMMA indices were 0.8|1.8|3.3 in controls, 1.1|1.6|2.3 in IMHD and 1.2|1.9|2.9 in ISD. There was no significant difference in the RMMA index, neither between participants with insomnia and controls (P = 0.514) nor between IMHD versus ISD (P = 0.270). The occurrence of RMMA indicators of possible sleep bruxism is not significantly different between individuals with insomnia and controls, nor between IMHD versus ISD.
Subject(s)
Sleep Bruxism , Sleep Initiation and Maintenance Disorders , Male , Female , Humans , Adult , Middle Aged , Sleep Bruxism/complications , Sleep Bruxism/diagnosis , Sleep Initiation and Maintenance Disorders/complications , Polysomnography , Masticatory Muscles/physiology , Masseter Muscle , Electromyography , Sleep/physiologyABSTRACT
OBJECTIVE: To investigate the association of the severity of temporomandibular disorders (TMD) pain and dysfunction with the frequency of self-reported awake bruxism (AB), sleep bruxism (SB), and stress in an adult TMD-patient population. MATERIALS AND METHODS: This cross-sectional study included 237 TMD patients based on the Diagnostic Criteria for TMD. Age, sex, frequency of self-reported AB and SB, and stress were included as independent variables. TMD pain and TMD dysfunction were included as dependent variables in regression analyses. Univariate and multivariable linear regression analyses were used to predict TMD pain and TMD dysfunction in two separate models. Finally, network analysis was performed to investigate the associations between all variables. RESULTS: In the univariate analyses, TMD pain was significantly associated with self-reported AB-frequent (unstandardized coefficient (B) = 3.196, 95%CI 1.198-5.195, p = 0.002). TMD dysfunction was significantly associated with AB-frequent (B = 2.208, 95%CI 0.177-4.238, p = 0.033) and SB-sometimes (B = 1.698, 95%CI 0.001-3.394, p = 0.050). In the multivariable analyses, TMD pain was significantly associated with TMD dysfunction (B = 0.370, p < 0.001), stress (B=0.102, p < 0.001). TMD dysfunction was significantly associated with TMD pain (B = 0.410, p < 0.001) only. Network analysis showed that TMD pain is a bridge factor between AB, stress, and TMD dysfunction. CONCLUSIONS: TMD pain is directly associated with AB, stress, and TMD dysfunction, while TMD dysfunction is only associated with TMD pain. CLINICAL RELEVANCE: Reducing pain may improve pain-related dysfunction, and the management of AB and stress may improve TMD pain and dysfunction, and vice versa.
Subject(s)
Bruxism , Sleep Bruxism , Temporomandibular Joint Disorders , Adult , Humans , Sleep Bruxism/complications , Bruxism/complications , Bruxism/diagnosis , Self Report , Wakefulness , Cross-Sectional Studies , Facial PainABSTRACT
Insomnia disorder comprises symptoms during night and day that strongly affect quality of life and wellbeing. Prolonged sleep latency, difficulties to maintain sleep and early morning wakening characterize sleep complaints, whereas fatigue, reduced attention, impaired cognitive functioning, irritability, anxiety and low mood are key daytime impairments. Insomnia disorder is well acknowledged in all relevant diagnostic systems: Diagnostic and Statistical Manual of the American Psychiatric Association, 5th revision, International Classification of Sleep Disorders, 3rd version, and International Classification of Diseases, 11th revision. Insomnia disorder as a chronic condition is frequent (up to 10% of the adult population, with a preponderance of females), and signifies an important and independent risk factor for physical and, especially, mental health. Insomnia disorder diagnosis primarily rests on self-report. Objective measures like actigraphy or polysomnography are not (yet) part of the routine diagnostic canon, but play an important role in research. Disease concepts of insomnia range from cognitive-behavioural models to (epi-) genetics and psychoneurobiological approaches. The latter is derived from knowledge about basic sleep-wake regulation and encompass theories like rapid eye movement sleep instability/restless rapid eye movement sleep. Cognitive-behavioural models of insomnia led to the conceptualization of cognitive-behavioural therapy for insomnia, which is now considered as first-line treatment for insomnia worldwide. Future research strategies will include the combination of experimental paradigms with neuroimaging and may benefit from more attention to dysfunctional overnight alleviation of distress in insomnia. With respect to therapy, cognitive-behavioural therapy for insomnia merits widespread implementation, and digital cognitive-behavioural therapy may assist delivery along treatment guidelines. However, given the still considerable proportion of patients responding insufficiently to cognitive-behavioural therapy for insomnia, fundamental studies are highly necessary to better understand the brain and behavioural mechanisms underlying insomnia. Mediators and moderators of treatment response/non-response and the associated development of tailored and novel interventions also require investigation. Recent studies suggest that treatment of insomnia may prove to add significantly as a preventive strategy to combat the global burden of mental disorders.
Subject(s)
Cognitive Behavioral Therapy , Sleep Initiation and Maintenance Disorders , Adult , Cognitive Behavioral Therapy/methods , Female , Humans , Polysomnography , Quality of Life , Sleep , Sleep Initiation and Maintenance Disorders/diagnosis , Sleep Initiation and Maintenance Disorders/therapy , Treatment OutcomeABSTRACT
INTRODUCTION: The global disease burden of major depressive disorder urgently requires prevention in high-risk individuals, such as recently discovered insomnia subtypes. Previous studies targeting insomnia with fully automated eHealth interventions to prevent depression are inconclusive: dropout was high and likely biased, and depressive symptoms in untreated participants on average improved rather than worsened. OBJECTIVE: This randomized controlled trial aimed to efficiently prevent the worsening of depressive symptoms by selecting insomnia subtypes at high risk of depression for internet-based circadian rhythm support (CRS), cognitive behavioral therapy for insomnia (CBT-I), or their combination (CBT-I+CRS), with online therapist guidance to promote adherence. METHODS: Participants with an insomnia disorder subtype conveying an increased risk of depression (n = 132) were randomized to no treatment (NT), CRS, CBT-I, or CBT-I+CRS. The Inventory of Depressive Symptomatology - Self Report (IDS-SR) was self-administered at baseline and at four follow-ups spanning 1 year. RESULTS: Without treatment, depressive symptoms indeed worsened (d = 0.28, p = 0.041) in high-risk insomnia, but not in a reference group with low-risk insomnia. Therapist-guided CBT-I and CBT-I+CRS reduced IDS-SR ratings across all follow-up assessments (respectively, d = -0.80, p = 0.001; d = -0.95, p < 0.001). Only CBT-I+CRS reduced the 1-year incidence of clinically meaningful worsening (p = 0.002). Dropout during therapist-guided interventions was very low (8%) compared to previous automated interventions (57-62%). CONCLUSIONS: The findings tentatively suggest that the efficiency of population-wide preventive strategies could benefit from the possibility to select insomnia subtypes at high risk of developing depression for therapist-guided digital CBT-I+CRS. This treatment may provide effective long-term prevention of worsening of depressive symptoms. TRIAL REGISTRATION: the Netherlands Trial Register (NL7359).
Subject(s)
Depressive Disorder, Major , Sleep Initiation and Maintenance Disorders , Circadian Rhythm , Cognition , Depression/prevention & control , Depressive Disorder, Major/prevention & control , Humans , Internet , Sleep Initiation and Maintenance Disorders/complications , Sleep Initiation and Maintenance Disorders/prevention & control , Treatment OutcomeABSTRACT
PURPOSE: Psychosocial health problems, such as social isolation, loneliness, depression and anxiety, have gained attention during the COVID-19 pandemic and are commonly co-occurring. We investigated the network of psychosocial health constructs during the COVID-19 pandemic. METHODS: This study included 4553 participants (mean age: 68.6 ± 11.2 years, 56% women) from the prospective Rotterdam Study, who filled out a questionnaire between April and July 2020, the time of the first COVID-19 wave in the Netherlands. Psychosocial health constructs included were depressive symptoms (Center for Epidemiological Studies Depression scale), anxiety symptoms (Hospital Anxiety and Depression scale), loneliness (University of California, Los Angeles loneliness scale), social connectedness (five items) and pandemic-related worry (five items). We estimated mixed graphical models to assess the network of items of these constructs and whether age and sex affected the network structure. RESULTS: Within the network of psychosocial constructs, a higher depressive symptoms score was particularly associated with items of loneliness and social connectedness, whereas overall anxiety was particularly associated with items of pandemic-related worry. Between people from different sex and age, the network structure significantly altered. CONCLUSION: This study demonstrates that within the same network of psychosocial health constructs, depressive symptom score is particularly associated with loneliness and social connectedness, whereas anxiety symptom score is associated with pandemic-related worry during the first COVID-19 lockdown. Our results support that psychosocial constructs should be considered in conjunction with one another in prevention and treatment efforts in clinical care, and that these efforts need to be tailored to specific demographic groups.
Subject(s)
COVID-19 , Middle Aged , Female , Humans , Aged , Male , Pandemics/prevention & control , Prospective Studies , Communicable Disease Control , Loneliness/psychology , Anxiety/epidemiology , Anxiety/psychology , Depression/epidemiology , Depression/psychologyABSTRACT
Pediatric attention deficit/hyperactivity disorder (ADHD) is a heterogeneous condition. In particular, children with ADHD display varying profiles of dispositional traits, as assessed through temperament and personality questionnaires. Previous data-driven community detection analyses based on temperament dimensions identified an irritable profile of patients with ADHD, uniquely characterized by elevated emotional dysregulation symptoms. Belonging to this profile increased the risk of developing comorbid disorders. Here, we investigated whether we could replicate this profile in a sample of 178 children with ADHD, using community detection based on personality dimensions. Stability of the identified profiles, of individual classifications, and clinical prediction were longitudinally assessed over a 1-year interval. Three personality profiles were detected: The first two profiles had high levels of neuroticism, with the first displaying higher ADHD severity and lower openness to experience (profile 1; N = 38), and the second lower agreeableness (profile 2; N = 73). The third profile displayed scores closer to the normative range on all five factors (profile 3; N = 67). The identified profiles did only partially replicate the temperament-based profiles previously reported, as higher levels of neuroticism were found in two of the three detected profiles. Nonetheless, despite changes in individual classifications, the profiles themselves were highly stable over time and of clinical predictive value. Whereas children belonging to profiles 1 and 2 benefited from starting medication, children in profile 3 did not. Hence, belonging to an emotionally dysregulated profile at baseline predicted the effect of medication at follow-up over and above initial ADHD symptom severity. This finding suggests that personality profiles could play a role in predicting treatment response in ADHD.
Subject(s)
Attention Deficit Disorder with Hyperactivity/psychology , Personality Inventory/standards , Predictive Value of Tests , Adolescent , Child , Female , Humans , Male , Surveys and QuestionnairesABSTRACT
People with Insomnia Disorder tend to underestimate their sleep compared with polysomnography or actigraphy, a phenomenon known as paradoxical insomnia or sleep-state misperception. Previous studies suggested that night-to-night variability could be an important feature differentiating subtypes of misperception. This study aimed for a data-driven definition of misperception subtypes revealed by multiple sleep features including night-to-night variability. We assessed features describing the mean and dispersion of misperception and objective and subjective sleep duration from 7-night diary and actigraphy recordings of 181 people with Insomnia Disorder and 55 people without sleep complaints. A minimally collinear subset of features was submitted to latent class analysis for data-driven subtyping. Analysis revealed three subtypes, best discriminated by three of five selected features: an individual's shortest reported subjective sleep duration; and the mean and standard deviation of misperception. These features were on average 5.4, -0.0 and 0.5 hr in one subtype accommodating the majority of good sleepers; 4.1, -1.4 and 1.0 hr in a second subtype representing the majority of people with Insomnia Disorder; and 1.7, -2.2 and 1.5 hr in a third subtype representing a quarter of people with Insomnia Disorder and hardly any good sleepers. Subtypes did not differ on an individual's objective sleep duration mean (6.9, 7.2 and 6.9 hr) and standard deviation (0.8, 0.8 and 0.9 hr). Data-driven analysis of naturalistic sleep revealed three subtypes that markedly differed in misperception features. Future studies may include misperception subtype to investigate whether it contributes to the unexplained considerable individual variability in treatment response.
Subject(s)
Actigraphy/methods , Polysomnography/methods , Sleep Initiation and Maintenance Disorders/diagnosis , Adult , Aged , Female , Humans , Male , Middle Aged , Young AdultABSTRACT
BACKGROUND: Major depressive disorder is among the most burdening and costly chronic health hazards. Since its prognosis is poor and treatment effectiveness is moderate at best, prevention would be the strategy of first choice. Insomnia may be the best modifiable risk factor. Insomnia is highly prevalent (4-10%) and meta-analysis estimates ±13% of people with insomnia to develop depression within a year. Among people with insomnia, recent work identified three subtypes with a particularly high lifetime risk of depression. The current randomized controlled trial (RCT) evaluates the effects of internet-guided Cognitive Behavioral Therapy for Insomnia (CBT-I), Chronobiological Therapy (CT), and their combination on insomnia and the development of depressive symptoms. METHODS: We aim to include 120 participants with Insomnia Disorder (ID) of one of the three subtypes that are more prone to develop depression. In a two by two factorial repeated measures design, participants will be randomized to CBT-I, CT, CBT-I + CT or treatment as usual, and followed up for one year. The primary outcome is the change, relative to baseline, of the severity of depressive symptoms integrated over four follow-ups spanning one year. Secondary outcome measures include a diagnosis of major depressive disorder, insomnia severity, sleep diaries, actigraphy, cost-effectiveness, and brain structure and function. DISCUSSION: Pre-selection of three high-risk insomnia subtypes allows for a sensitive assessment of the possibility to prevent the development and worsening of depressive symptoms through interventions targeting insomnia. TRIAL REGISTRATION: Netherlands Trial Register (NL7359). Registered on 19 October 2018.
Subject(s)
Cognitive Behavioral Therapy , Sleep Initiation and Maintenance Disorders , Cognition , Depression , Humans , Internet , Netherlands , Sleep Initiation and Maintenance Disorders/complications , Sleep Initiation and Maintenance Disorders/therapy , Treatment OutcomeABSTRACT
Personalized networks of psychological symptoms aim to advance therapy by identifying treatment targets for specific patients. Statistical relations in such networks can be estimated from intensive longitudinal data, but their causal interpretation is limited by strong statistical assumptions. An alternative is to create networks from patient perceptions, which comes with other limitations such as retrospective bias. We introduce the Longitudinal Perceived Causal Problem Networks (L-PECAN) approach to address both these concerns. 20 participants screening positive for depression completed 4 weeks day of brief daily assessments of perceived symptom interactions. Quality criteria of this new method are introduced, answering questions such as "Which symptoms should be included in networks?", "How many datapoints need to be collected to achieve stable networks?", and "Does the network change over time?". Accordingly, about 40% of respondents achieved stable networks and only few respondents exhibited network structure that changed during the assessment period. The method was time-efficient (on average 7.4 min per day), and well received. Overall, L-PECAN addresses several of the prevailing issues found in statistical networks and therefore provides a clinically meaningful method for personalization.
Subject(s)
Depression , Humans , Depression/diagnosis , Data Collection , Symptom AssessmentABSTRACT
BACKGROUND: Insomnia disorder is the most common sleep disorder. A better understanding of insomnia-related deviations in the brain could inspire better treatment. Insufficiently recognized heterogeneity within the insomnia population could obscure detection of involved brain circuits. In the current study, we investigated whether structural brain connectivity deviations differed between recently discovered and validated insomnia subtypes. METHODS: Structural and diffusion-weighted 3T magnetic resonance imaging data from 4 independent studies were harmonized. The sample consisted of 73 control participants without sleep complaints and 204 participants with insomnia who were grouped into 5 insomnia subtypes based on their fingerprint of mood and personality traits assessed with the Insomnia Type Questionnaire. Linear regression correcting for age and sex was used to evaluate group differences in structural connectivity strength, indicated by fractional anisotropy, streamline volume density, and mean diffusivity and evaluated within 3 different atlases. RESULTS: Insomnia subtypes showed differentiating profiles of deviating structural connectivity that were concentrated in different functional networks. Permutation testing against randomly drawn heterogeneous subsamples indicated significant specificity of deviation profiles in 4 of the 5 subtypes: highly distressed, moderately distressed reward sensitive, slightly distressed low reactive, and slightly distressed high reactive. Connectivity deviation profile significance ranged from p = .001 to p = .049 for different resolutions of brain parcellation and connectivity weight. CONCLUSIONS: Our results provide an initial indication that different insomnia subtypes exhibit distinct profiles of deviations in structural brain connectivity. Subtyping insomnia may be essential for a better understanding of brain mechanisms that contribute to insomnia vulnerability.
ABSTRACT
BACKGROUND: Depressive symptoms are highly prevalent, present in heterogeneous symptom patterns, and share diverse neurobiological underpinnings. Understanding the links between psychopathological symptoms and biological factors is critical in elucidating its etiology and persistence. We aimed to evaluate the utility of using symptom-brain network models to parse the heterogeneity of depressive complaints in a large adolescent sample. METHODS: We used data from the third wave of the IMAGEN study, a multi-center panel cohort study involving 1317 adolescents (52.49 % female, mean ± SD age = 18.5 ± 0.7). Two network models were estimated: one including an overall depressive symptom severity sum score based on the Adolescent Depression Rating Scale (ADRS), and one incorporating individual ADRS item scores. Both networks included measures of cortical thickness in several regions (insula, cingulate, mOFC, fusiform gyrus) and hippocampal volume derived from neuroimaging. RESULTS: The network based on individual item scores revealed associations between cortical thickness measures and specific depressive complaints, obscured when using an aggregate depression severity score. Notably, the insula's cortical thickness showed negative associations with cognitive dysfunction (partial cor. = -0.15); the cingulate's cortical thickness showed negative associations with feelings of worthlessness (partial cor. = -0.10), and mOFC was negatively associated with anhedonia (partial cor. = -0.05). LIMITATIONS: This cross-sectional study relied on the self-reported assessment of depression complaints and used a non-clinical sample with predominantly healthy participants (19 % with depression or sub-threshold depression). CONCLUSIONS: This study showcases the utility of network models in parsing heterogeneity in depressive complaints, linking individual complaints to specific neural substrates. We outline the next steps to integrate neurobiological and cognitive markers to unravel MDD's phenotypic heterogeneity.
Subject(s)
Depression , Magnetic Resonance Imaging , Humans , Female , Male , Adolescent , Depression/physiopathology , Depression/psychology , Brain/diagnostic imaging , Brain/physiopathology , Cohort Studies , Hippocampus/diagnostic imaging , Hippocampus/pathology , Hippocampus/physiopathology , Cerebral Cortex/diagnostic imaging , Cerebral Cortex/physiopathology , Cerebral Cortex/pathology , Psychiatric Status Rating Scales , Young Adult , Gyrus Cinguli/diagnostic imaging , Gyrus Cinguli/physiopathologyABSTRACT
Statistical network models describing multivariate dependency structures in psychological data have gained increasing popularity. Such comparably novel statistical techniques require specific guidelines to make them accessible to the research community. So far, researchers have provided tutorials guiding the estimation of networks and their accuracy. However, there is currently little guidance in determining what parts of the analyses and results should be documented in a scientific report. A lack of such reporting standards may foster researcher degrees of freedom and could provide fertile ground for questionable reporting practices. Here, we introduce reporting standards for network analyses in cross-sectional data, along with a tutorial and two examples. The presented guidelines are aimed at researchers as well as the broader scientific community, such as reviewers and journal editors evaluating scientific work. We conclude by discussing how the network literature specifically can benefit from such guidelines for reporting and transparency. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
Subject(s)
Research Design , Research Report , Humans , Cross-Sectional Studies , Models, StatisticalABSTRACT
Background: There is an urgent need to better understand and prevent relapse in major depressive disorder (MDD). We explored the differential impact of various MDD relapse prevention strategies (pharmacological and/or psychological) on affect fluctuations and individual affect networks in a randomised setting, and their predictive value for relapse. Methods: We did a secondary analysis using experience sampling methodology (ESM) data from individuals with remitted recurrent depression that was collected alongside a randomised controlled trial that ran in the Netherlands, comparing: (I) tapering antidepressants while receiving preventive cognitive therapy (PCT), (II) combining antidepressants with PCT, or (III) continuing antidepressants without PCT, for the prevention of depressive relapse, as well as ESM data from 11 healthy controls. Participants had multiple past depressive episodes, but were remitted for at least 8 weeks and on antidepressants for at least six months. Exclusion criteria were: current (hypo)mania, current alcohol or drug abuse, anxiety disorder that required treatment, psychological treatment more than twice per month, a diagnosis of organic brain damage, or a history of bipolar disorder or psychosis. Fluctuations (within-person variance, root mean square of successive differences, autocorrelation) in negative and positive affect were calculated. Changes in individual affect networks during treatment were modelled using time-varying vector autoregression, both with and without applying regularisation. We explored whether affect fluctuations or changes in affect networks over time differed between treatment conditions or relapse outcomes, and predicted relapse during 2-year follow-up. This ESM study was registered at ISRCTN registry, ISRCTN15472145. Findings: Between Jan 1, 2014, and Jan 31, 2015, 72 study participants were recruited, 42 of whom were included in the analyses. We found no indication that affect fluctuations differed between treatment groups, nor that they predicted relapse. We observed large individual differences in affect network structure across participants (irrespective of treatment or relapse status) and in healthy controls. We found no indication of group-level differences in how much networks changed over time, nor that changes in networks over time predicted time to relapse (regularised models: hazard ratios [HR] 1063, 95% CI <0.0001->10 000, p = 0.65; non-regularised models: HR 2.54, 95% CI 0.23-28.7, p = 0.45) or occurrence of relapse (regularised models: odds ratios [OR] 22.84, 95% CI <0.0001->10 000, p = 0.90; non-regularised models: OR 7.57, 95% CI 0.07-3709.54, p = 0.44) during complete follow-up. Interpretation: Our findings should be interpreted with caution, given the exploratory nature of this study and wide confidence intervals. While group-level differences in affect dynamics cannot be ruled out due to low statistical power, visual inspection of individual affect networks also revealed no meaningful patterns in relation to MDD relapse. More studies are needed to assess whether affect dynamics as informed by ESM may predict relapse or guide personalisation of MDD relapse prevention in daily practice. Funding: The Netherlands Organisation for Health Research and Development, Dutch Research Council, University of Amsterdam.
ABSTRACT
Background: Depressive symptoms are highly prevalent, present in heterogeneous symptom patterns, and share diverse neurobiological underpinnings. Understanding the links between psychopathological symptoms and biological factors is critical in elucidating its etiology and persistence. We aimed to evaluate the utility of using symptom-brain networks to parse the heterogeneity of depressive symptomatology in a large adolescent sample. Methods: We used data from the third wave of the IMAGEN study, a multi-center panel cohort study involving 1,317 adolescents (52.49% female, mean±SD age=18.5±0.72). Two network models were estimated: one including an overall depressive symptom severity sum score based on the Adolescent Depression Rating Scale (ADRS), and one incorporating individual ADRS symptom/item scores. Both networks included measures of cortical thickness in several regions (insula, cingulate, mOFC, fusiform gyrus) and hippocampal volume derived from neuroimaging. Results: The network based on individual symptom scores revealed associations between cortical thickness measures and specific symptoms, obscured when using an aggregate depression severity score. Notably, the insula's cortical thickness showed negative associations with cognitive dysfunction (partial cor.=-0.15); the cingulate's cortical thickness showed negative associations with feelings of worthlessness (partial cor. = -0.10), and mOFC was negatively associated with anhedonia (partial cor. = -0.05). Limitations: This cross-sectional study included participants who were relatively healthy and relied on the self-reported assessment of depression symptoms. Conclusions: This study showcases the utility of network models in parsing heterogeneity in depressive symptoms, linking individual symptoms to specific neural substrates. We outline the next steps to integrate neurobiological and cognitive markers to unravel MDD's phenotypic heterogeneity.
ABSTRACT
OBJECTIVES: To investigate the association between self-reported sleep bruxism and insomnia and their potential risk factors (eg, depression and anxiety), and to construct a network model with all these factors. METHODS: We recruited 2251 participants from the Netherlands Sleep Registry. All participants completed questionnaires on self-reported sleep bruxism, insomnia, depression, anxiety, smoking frequency, and alcohol and caffeine consumption. The associations between self-reported sleep bruxism and other variables were analyzed by univariate analysis, multivariate logistic regression, and network analysis. RESULTS: Although univariate analysis showed that there was a positive association between sleep bruxism and insomnia (P < 0.001), this association disappeared in the multivariate logistic regression model (P = 0.258). However, multivariate logistic regression did show an association between self-reported sleep bruxism and anxiety (OR = 1.087, 95% CI 1.041-1.134). The network model showed that there was no direct link between self-reported sleep bruxism and insomnia. However, there was an indirect link between self-reported sleep bruxism and insomnia via anxiety. CONCLUSIONS: Although self-reported sleep bruxism has no direct association with insomnia, anxiety is a bridging factor between these variables.
Subject(s)
Bruxism , Sleep Bruxism , Sleep Initiation and Maintenance Disorders , Demography , Humans , Netherlands/epidemiology , Registries , Self Report , Sleep , Sleep Bruxism/complications , Sleep Bruxism/epidemiology , Sleep Initiation and Maintenance Disorders/complications , Sleep Initiation and Maintenance Disorders/epidemiology , Surveys and QuestionnairesABSTRACT
Human social behavior plays a crucial role in how pathogens like SARS-CoV-2 or fake news spread in a population. Social interactions determine the contact network among individuals, while spreading, requiring individual-to-individual transmission, takes place on top of the network. Studying the topological aspects of a contact network, therefore, not only has the potential of leading to valuable insights into how the behavior of individuals impacts spreading phenomena, but it may also open up possibilities for devising effective behavioral interventions. Because of the temporal nature of interactions-since the topology of the network, containing who is in contact with whom, when, for how long, and in which precise sequence, varies (rapidly) in time-analyzing them requires developing network methods and metrics that respect temporal variability, in contrast to those developed for static (i.e., time-invariant) networks. Here, by means of event mapping, we propose a method to quantify how quickly agents mingle by transforming temporal network data of agent contacts. We define a novel measure called contact sequence centrality, which quantifies the impact of an individual on the contact sequences, reflecting the individual's behavioral potential for spreading. Comparing contact sequence centrality across agents allows for ranking the impact of agents and identifying potential 'behavioral super-spreaders'. The method is applied to social interaction data collected at an art fair in Amsterdam. We relate the measure to the existing network metrics, both temporal and static, and find that (mostly at longer time scales) traditional metrics lose their resemblance to contact sequence centrality. Our work highlights the importance of accounting for the sequential nature of contacts when analyzing social interactions.