scholarly journals Sex differences in slow-wave electroencephalographic activity (SWA) in adolescent depression

2012 ◽  
Vol 4 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Jorge Lopez ◽  
Robert Hoffmann ◽  
Graham Emslie ◽  
Roseanne Armitage
Keyword(s):  
Sex Differences ◽  
Slow Wave ◽  
Sleep Disturbances ◽  
Adolescent Depression ◽  
Nrem Sleep ◽  
Healthy Controls ◽  
Adult Males ◽  
Major Depressive ◽  
Sleep Period ◽  
Electroencephalographic Activity

Sleep disturbances, present in more than 90% of major depressive disorder (MDD) patients, are moderated by sex in adult MDD. In particular, slow-wave electroencephalographic activity (SWA; 0.5-4 Hz) accumulation is low and dissipation impaired. This SWA abnormality in depressed adult males does not change with age, suggesting that SWA abnormality appears at early ages. The present study evaluated sex differences in SWA in adolescents with MDD compared to healthy controls. We evaluated regularized sleep-wake schedules at home for 5-7 days, followed by two consecutive nights of sleep EEG recording. The study included 104 participants, 52 symptomatic and depressed subjects (MDD: 20 males and 32 females) and 52 healthy controls (HC: 20 males and 32 females), aged 13-18 years. SWA power and dissipation, and duration and latencies to each Non-Rapid Eye Movement (NREM) sleep period were calculated for each group. Results showed that SWA accumulation in the first NREM period was lower and its dissipation across the night more irregular in MDD males compared to HC males (P<0.009). By contrast, SWA was equivalent in MDD and HC females. In conclusion, as reported in adult MDD, the accumulation and dissipation of SWA was abnormal in depressed adolescents, but only in males. SWA abnormalities in adolescent MDD may relate to different depressive symptoms in females and males. These results underscore the need to develop sex-specific therapies to enhance and restore SWA in depressed adolescents.

069 Chronic pain in Veterans with TBI is associated with decreased EEG slow wave coherence during NREM sleep

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A28-A29
Author(s):  
Nadir Balba ◽  
Christina Reynolds ◽  
Mo Modarres ◽  
Alisha McBride ◽  
Selda Yildiz ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Slow Wave ◽  
Sleep Disturbances ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Poor Sleep ◽  
Signal Processing Algorithm ◽  
History Of ◽  
Underlying Mechanisms ◽  
The Relationship

Abstract Introduction Chronic pain and sleep disturbances are intricately linked to one another, especially in individuals with a history of traumatic brain injury (TBI) who are at greater risk for both symptoms. Although prior studies have analyzed differences in sleep electroencephalogram (EEG) in these clinical populations, the association between sleep EEG slow wave coherence and pain complaints is not fully examined or known. Our novel slow wave coherence approach may provide new insights into the relationship between TBI, chronic pain, and sleep Methods Ninety-six veterans were recruited and enrolled under a VA IRB-approved protocol. Participants completed a semi-structured clinical interview to determine their history of TBI, Symptom Impact Questionnaire Revised (SIQR), a measure of chronic pain complaints, and underwent an attended overnight in-lab polysomnogram (PSG). We developed a novel computational signal processing algorithm to identify and quantify EEG slow waves within 100 ms bins across the 6 standard PSG EEG channels. When a slow wave was simultaneously observed in 4 or more of the 6 leads, slow wave coherence was inferred, and a percentage of slow wave coherence across each of the sleep stages was then calculated for each subject. Results In our sample, 65 participants (67.7%) endorsed experiencing chronic pain lasting 3 months or longer, and 54 had a history of TBI (56.3%). Participants endorsing chronic pain had a significantly lowered percent of EEG slow wave coherence during NREM sleep than subjects without chronic pain (p = 0.01). NREM EEG slow wave coherence did not correlate with SIQR scores in subjects without TBI (r = -0.03, p = 0.90), but was significantly negatively correlated in subjects with TBI (r = -0.32, p = 0.02). Conclusion EEG slow wave coherence during NREM sleep is correlated with chronic pain complaints in Veterans with a history of TBI, and could be indicative of neuronal dysfunction during sleep. Further research on slow wave coherence is warranted to understand the underlying mechanisms for the association between chronic pain and poor sleep following TBI. Support (if any) D01 W81XWH-17-1-0423

scholarly journals Schizophrenia-associated variation at ZNF804A correlates with altered experience-dependent dynamics of sleep slow-waves and spindles in healthy young adults

2020 ◽  
Author(s):  
Ullrich Bartsch ◽  
Laura J Corbin ◽  
Charlotte Hellmich ◽  
Michelle Taylor ◽  
Kayleigh E Easey ◽  
...  
Keyword(s):  
Slow Wave ◽  
Memory Consolidation ◽  
Neural Circuit ◽  
Activity Patterns ◽  
Nrem Sleep ◽  
Slow Waves ◽  
Network Activity ◽  
Healthy Population ◽  
Adult Males ◽  
Performance Improvements

ABSTRACTBackgroundThe rs1344706 polymorphism in ZNF804A is robustly associated with schizophrenia (SZ), yet brain and behavioral phenotypes related to this variant have not been extensively characterized. In turn, SZ is associated with abnormal non-rapid eye movement (NREM) sleep neurophysiology. To examine whether rs1344706 is associated with intermediate neurophysiological traits in the absence of disease, we assessed the relationship between genotype, sleep neurophysiology, and sleep-dependent memory consolidation in healthy participants.MethodsWe recruited healthy adult males, with no history of psychiatric disorder, from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort. Participants were homozygous for either the SZ-associated ‘A’ allele (N=25) or the alternative ‘C’ allele (N=22) at rs1344706. Actigraphy, polysomnography (PSG) and a motor sequencing task (MST) were used to characterize daily activity patterns, sleep neurophysiology and sleep-dependent memory consolidation.ResultsAverage MST learning and sleep-dependent performance improvements were similar across genotype groups, but with increased variability in the AA group. CC participants showed increased slow-wave and spindle amplitudes, plus augmented coupling of slow-wave activity across recording electrodes after learning. Slow-waves and spindles in those with the AA genotype were insensitive to learning, whilst slow-wave coherence decreased following MST training.ConclusionWe describe evidence that rs1344706 polymorphism in ZNF804A is associated with changes in experience- and sleep-dependent, local and distributed neural network activity that supports offline information processing during sleep in a healthy population. These findings highlight the utility of sleep neurophysiology in mapping the impacts of SZ-associated variants on neural circuit oscillations and function.

scholarly journals Sleep slow-wave oscillations trigger seizures in a genetic epilepsy model of Dravet syndrome

2022 ◽  
Author(s):  
Mackenzie A. Catron ◽  
Rachel K. Howe ◽  
Gai-Linn K. Besing ◽  
Emily K. St. John ◽  
Cobie Victoria Potesta ◽  
...  
Keyword(s):  
Slow Wave ◽  
Epileptic Seizures ◽  
Nrem Sleep ◽  
Dravet Syndrome ◽  
Brain State ◽  
Synaptic Potentiation ◽  
Sleep Period ◽  
State Dependent ◽  
Slow Wave Oscillations

Sleep is the brain state when cortical activity decreases and memory consolidates. However, in human epileptic patients, including genetic epileptic seizures such as Dravet syndrome, sleep is the preferential period when epileptic spike-wave discharges (SWDs) appear, with more severe epileptic symptoms in female patients than male patients, which influencing patient sleep quality and memory. Currently, seizure onset mechanisms during sleep period still remain unknown. Our previous work has shown that the sleep-like state-dependent synaptic potentiation mechanism can trigger epileptic SWDs (Zhang et al., 2021). In this study, using one heterozygous (het) knock-in (KI) transgenic mice (GABAA receptor γ2 subunit Gabrg2Q390X mutation) and an optogenetic method, we hypothesized that slow-wave oscillations (SWOs) themselves in vivo could trigger epileptic seizures. We found that epileptic SWDs in het Gabrg2+/Q390X KI mice exhibited preferential incidence during NREM sleep period, accompanied by motor immobility/ facial myoclonus/vibrissal twitching, with more frequent incidence in female het KI mice than male het KI mice. Optogenetic induced SWOs in vivo significantly increased epileptic seizure incidence in het Gabrg2+/Q390X KI mice with increased duration of NREM sleep or quiet-wakeful states. Furthermore, suppression of SWO-related homeostatic synaptic potentiation by 4-(diethylamino)-benzaldehyde (DEAB) injection (i.p.) greatly decreased seizure incidence in het KI mice, suggesting that SWOs did trigger seizure activity in het KI mice. In addition, EEG delta-frequency (0.1-4 Hz) power spectral density during NREM sleep was significantly larger in female het Gabrg2+/Q390X KI mice than male het Gabrg2+/Q390X KI mice, which likely contributes to the gender difference in seizure incidence during NREM sleep/quiet-wake as that in human patients.

Slow-wave activity in NREM sleep: sex and age effects in depressed outpatients and healthy controls

2000 ◽  
Vol 95 (3) ◽  
pp. 201-213 ◽  
Author(s):  
Roseanne Armitage ◽  
Robert Hoffmann ◽  
Madhukar Trivedi ◽  
A.John Rush
Keyword(s):  
Slow Wave ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Age Effects ◽  
Slow Wave Activity ◽  
Healthy Controls ◽  
Sleep Sex

129 Greater NREM Sleep Rebound in Response to Experimental Sleep Disturbance Associated with Higher Inflammatory Resolution in Humans

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A52-A53
Author(s):  
Larissa Engert ◽  
Marc Dubourdeau ◽  
Rammy Dang ◽  
Janet Mullington ◽  
Monika Haack
Keyword(s):  
Sleep Disturbance ◽  
Slow Wave ◽  
Rem Sleep ◽  
Sleep Disturbances ◽  
Slow Wave Sleep ◽  
Sleep Onset ◽  
Nrem Sleep ◽  
Low Grade ◽  
German Research Foundation ◽  
Recovery Sleep

Abstract Introduction Sleep disturbances deteriorate immune function by not only affecting pro-inflammatory pathways, but also inflammatory resolution pathways, which actively terminate inflammation. It is assumed that slow wave sleep (SWS) amount and slow wave activity (SWA) convey the immune-supportive functions of sleep. We investigated whether changes in SWS induced by experimental sleep disturbance followed by recovery sleep predict changes in inflammatory resolution mediators. Methods The randomized controlled within-subjects trial (N=24, 20-42 years, 12 women) consisted of two 19-day in-hospital protocols (experimental sleep disturbance/control). After three nights of baseline sleep (8h/night), participants in the experimental sleep disturbance condition were exposed to three cycles of three nights of disturbed sleep (delayed sleep-onset, hourly sleep disruption, advanced sleep-offset) followed by one night of 8h-recovery sleep. The protocol ended with three nights of recovery sleep. In the control condition, participants had uninterrupted sleep (8h/night). Sleep (PSG) and resolvin lipid mediators in plasma (1100h, LC-MS/MS) were assessed at baseline, during the last cycle of sleep disturbance, and during/after the first and third night of final recovery sleep. Data were analyzed using generalized linear mixed models and Pearson/Spearman correlations. Results As expected, SWS amount decreased during experimental sleep disturbance and increased during the first recovery sleep night (p&lt;.001). Similarly, resolvin (Rv) D2 and RvD3 decreased during sleep disturbance and RvD2 increased with subsequent recovery sleep (p&lt;.001). The SWS response did not correlate with the resolvin response to sleep disturbance or to recovery sleep. However, the NREM sleep response correlated with the resolvin response during the third recovery sleep night, i.e., a greater NREM response was associated with a greater RvD2 and RvD3 response (r=.68, p=.002; r=.58, p=.012). In contrast, a greater REM sleep response was associated with a lower resolvin response (r=−.63, p=.005; r=−.66, p=.003). Conclusion These data suggest that during recovery from sleep disturbance, NREM rather than REM sleep promotes inflammatory resolution, thereby acting as the sleep state that protects against low-grade systemic inflammation, which has been frequently observed as a consequence of sleep disturbances. Analysis whether SWA is related to inflammatory resolution is in progress. Support (if any) NIH/NINDS R01-NS091177; NIH/NCRR UL1-RR02758, M01-RR01032; German Research Foundation (DFG) EN1291/1-1.

scholarly journals Characterization of Potential Protein Biomarkers for Major Depressive Disorder Using Matrix-Assisted Laser Desorption Ionization/Time-of-Flight Mass Spectrometry

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4457
Author(s):  
Chieh-Hsin Lin ◽  
Hung Su ◽  
Chung-Chieh Hung ◽  
Hsien-Yuan Lane ◽  
Jentaie Shiea
Keyword(s):  
Mass Spectrometry ◽  
Time Of Flight ◽  
Laser Desorption ◽  
Healthy Controls ◽  
Laser Desorption Ionization ◽  
Major Depressive ◽  
Ionization Time ◽  
Maldi Tof ◽  
Matrix Assisted Laser ◽  
Matrix Assisted Laser Desorption

Matrix-assisted laser desorption ionization/time-of-flight (MALDI-TOF) mass spectrometry is a sensitive analytical tool for characterizing various biomolecules in biofluids. In this study, MALDI-TOF was used to characterize potential plasma biomarkers for distinguishing patients with major depressive disorder (MDD) from patients with schizophrenia and healthy controls. To avoid interference from albumin—the predominant protein in plasma—the plasma samples were pretreated using acid hydrolysis. The results obtained by MALDI-TOF were also validated by electrospray ionization-quadrupole time-of-flight (ESI-QTOF) mass spectrometry. The analytical results were further treated with principal component analysis (PCA), hierarchical clustering analysis (HCA), and receiver operating characteristic (ROC) curve analysis. The statistical analyses showed that MDD patients could be distinguished from schizophrenia patients and healthy controls by the lack of apolipoprotein C1 (Apo C1), which, in fact, was detected in healthy controls and schizophrenia patients. This protein is suggested to be a potential plasma biomarker for distinguishing MDD patients from healthy controls and schizophrenia patients. Since sample preparation for MALDI-TOF is very simple, high-throughput plasma apolipoprotein analysis for clinical purposes is feasible.

scholarly journals Sex Difference in Self-Reported Sexual Functioning Among Frail Older Adults

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 313-313
Author(s):  
Brianne Olivieri-Mui ◽  
Sandra Shi ◽  
Ellen McCarthy ◽  
Dae Kim
Keyword(s):  
Older Adults ◽  
Logistic Regression ◽  
Sex Differences ◽  
Sexual Function ◽  
Older Adult ◽  
Sexual Functioning ◽  
Social Life ◽  
Well Being ◽  
Adult Males ◽  
Males And Females

Abstract Frailty may differentially impact how older adult males and females perceive sexual functioning, an important part of well-being. We assessed the level of frailty (robust, pre-frail, frail) for anyone with data on 11 sexual functioning questions asked in wave 2 of the National Social Life, Health, and Aging Project, 2010-2011 (n=2060). Questions covered five domains: overall sexual function (OSF), sexual function anxiety (SFA), changes in sexual function (CSF), erectile/vaginal dysfunction (EVD), and masturbation. Logistic regression identified sex differences in frailty and reporting worse sexual functioning. Linear regression predicted the number of domains reported as worse. Among males (n=1057), pre-frailty meant higher odds of reporting SFA (OR 1.8 95%CI 1.2-6.6), CSF (OR 1.7 95%CI 1.1-2.7), and EVD (OR 1.5 95%CI 1.0-2.2). Among females (n=1003), there was no difference in reporting by frailty. Females were more likely to report worse OSF (Robust: OR 7.4, 95%CI 4.8-11.4; Pre-frail: OR 6.2, 95%CI 3.9-9.9; Frail: OR 3.4 95%CI 1.7-6.6), but less likely to report SFA (Robust OR .3, 95%CI .2-.5; Pre-frail OR .2, 95%CI .1-.3; Frail OR .2 95%CI .1-.3). Pre-frail and frail females reported fewer domains as worse (Pre-frail coefficient -0.21 SE 0.09, Frail -0.43 SE 0.14). As frailty worsened, males reported more domains as worse (Pre-frail 0.24 SE 0.07, Frail 0.29 SE 0.08). Self-reported sexual functioning differs by sex at all levels of frailty, and reporting by males, but not females, changes with frailty. Providers should be aware that sexual functioning is of importance to both sexes despite varying degrees of frailty.

scholarly journals AB0562 SLEEP HYGIENE: COULD IT BE A CONFOUNDING FACTOR FOR SLEEP QUALITY IN SYSTEMIC SCLEROSIS?

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1578.2-1578
Author(s):  
N. Gokcen ◽  
A. Komac ◽  
F. Tuncer ◽  
A. Yazici ◽  
A. Cefle
Keyword(s):  
Systemic Sclerosis ◽  
Sleep Quality ◽  
Disease Activity ◽  
Beck Depression Inventory ◽  
Sleep Disturbances ◽  
Activity Index ◽  
Univariate Analysis ◽  
Sleep Hygiene ◽  
Healthy Controls ◽  
Clinical Variables

Background:Sleep disturbances have been described in Systemic Sclerosis (SSc). Confounding factors related to sleep quality are also investigated. Although sleep hygiene plays an important role in sleep quality, as far as we know, there are not enough data to show the effect of sleep hygiene on sleep quality of SSc.Objectives:To investigate sleep hygiene, its impact on sleep quality, and its association with demographic-clinical factors in patients with SSc, rheumatoid arthritis (RA), and healthy controls.Methods:The study was designed as cross-sectional. Forty-nine patients with SSc who fulfilled the 2013 ACR/EULAR classification criteria for SSc, 66 patients with RA who fulfilled 1987 revised classification criteria, and 30 healthy controls were included in the study. All participants were female. Demographic and clinical variables were documented. Disease activity index of both SSc and RA was calculated. SSc patients were assessed by questionnaires including Short Form 36 (SF-36), The Health Assessment Questionnaire Disability Index (HAQ-DI), Beck Anxiety and Beck Depression Inventory, Pittsburg Sleep Quality Index (PSQI), Sleep Hygiene Index (SHI). Additionally, RA patients and healthy controls were estimated by HAQ-DI, Beck Anxiety and Beck Depression Inventory, PSQI, and SHI. Logistic regression analysis was used to determine the predictors of sleep quality.Results:Preliminary results of the study were given. The baseline demographics were similar among groups. When comparing groups according to HAQ-DI, Beck Anxiety and Beck Depression Inventory, PSQI, and SHI, we found higher scores in SSc and RA rather than healthy controls (p<0.001, p=0.001, p=0.001, p<0.001, p=0.003; respectively). While depression and sleep hygiene were determined as the risk factors of sleep quality in SSc in univariate analysis, depression (OR=1.380, 95%CI: 1.065−1.784, p=0.015) and sleep hygiene (OR=1.201, 95%CI: 1.003−1.439, p=0.046) were also found in multivariate logistic model. In RA patients, while health status, depression, and anxiety were found as risk factors according to the univariate analysis, depression (OR=1.120, 95%CI: 1.006−1.245, p=0.038) was the only factor according to multivariate logistic model (Table).Conclusion:Although depression is a well-known clinical variable impacting on sleep quality, sleep hygiene should also be kept in mind as a confounding factor.References:[1]Milette K, Hudson M, Körner A, et al. Sleep disturbances in systemic sclerosis: evidence for the role of gastrointestinal symptoms, pain and pruritus. Rheumatology (Oxford). 2013 Sep;52(9):1715-20.[2]Sariyildiz MA, Batmaz I, Budulgan M, et al. Sleep quality in patients with systemic sclerosis: relationship between the clinical variables, depressive symptoms, functional status, and the quality of life. Rheumatol Int. 2013 Aug;33(8):1973-9.TableUnivariate logistic regression analysis of clinical variables to assess predictors of sleep qualitySystemic sclerosisRheumatoid arthritisOR (95% CI)pOR (95% CI)pHAQ-DI1.019 (0.882−1.177)0.8011.089 (1.011−1.173)0.025BDI score1.293 (1.082−1.547)0.0051.129 (1.036−1.230)0.006BAI score1.080 (0.997−1.169)0.0591.122 (1.038−1.214)0.004SHI1.200 (1.060−1.357)0.0041.048 (0.965−1.137)0.264Disease activitya0.707 (0.439−1.138)0.1531.446 (0.839−2.492)0.185aDisease activity was calculated by Valentini disease activity index for SSc and DAS28-CRP for RA.Disclosure of Interests:None declared

scholarly journals Leakage of astrocyte-derived extracellular vesicles in stress-induced exhaustion disorder: a cross-sectional study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Johanna Wallensten ◽  
Anna Nager ◽  
Marie Åsberg ◽  
Kristian Borg ◽  
Aniella Beser ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Cd40 Ligand ◽  
Cross Sectional Study ◽  
Healthy Controls ◽  
Sectional Study ◽  
Major Depressive ◽  
Cross Sectional ◽  
Ligand Expression ◽  
Minor Traumatic Brain Injury ◽  
Exhaustion Disorder

AbstractPatients with stress-induced exhaustion disorder (SED) demonstrate cognitive dysfunction similar to patients with minor traumatic brain injury (TBI). We have previously detected elevated concentrations of astrocyte-derived extracellular vesicles (EVs) in patients with TBI. As such, we hypothesized that astrocyte-derived EVs could be higher in patients with SED than in patients with major depressive disorder (MDD) and healthy controls. Patients with SED (n = 31), MDD (n = 31), and healthy matched controls (n = 61) were included. Astrocyte-derived EVs (previously known as microparticles) were measured in plasma with flow cytometry and labeled against glial fibrillary acidic protein (GFAP) and aquaporin 4 (AQP4). In addition, platelet EVs and their CD40 ligand expression were measured. Patients with SED had significantly higher concentrations of AQP4 and GFAP-positive EVs and EVs co-expressing AQP4/GFAP than patients with MDD and healthy controls. Patients with MDD had significantly higher concentrations of GFAP-positive EVs and EVs co-expressing AQP4/GFAP than healthy controls. Platelet EVs did not differ between groups. CD40 ligand expression was significantly higher in patients with SED and MDD than in controls. In conclusion, the present study suggests that patients with SED, and to some extent, patients with MDD, have increased leakage of astrocyte-derived EVs through the blood–brain barrier.

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