bluuebunny/crossref_metadata_2025_split huggingface dataset:
1028 Wake Time After Morning Awakening as a Predictive Factor for Seizures in Juvenile Myoclonic Epilepsy
Authors: Villalobos Rafael , Villalobos Sarah , JR Rafael Villalobos , Diaz Saulo 
Published: April 2024

Abstract

Introduction
Seizure recurrence in the early morning is well known in Juvenile Myoclonic Epilepsy, the presence of seizures happens usually after waking up and there is a clear relationship with sleep as most of the seizures happen in a time frame that involves the next 30 to 120 minutes of wake time after sleep. We wanted to analyze the time frame that is most associated with seizure recurrence as that can have serious implications for safety, not to exclude driving in the morning hours.

Methods
We investigated on a sample of 20 patients with JME and the pattern on seizure recurrence in the morning. A time frame of wake after sleep was established as follows; the first 30 minutes, 30 to 60 minutes, 60 to 90 minutes and more than 90 minutes. Seizure diaries were given to patients and the seizure recurrence was evaluated. A variable that included earlier waking time in the morning was also taken into account. A follow up of 6 months was given in a retrospective manner. All patients were seen in an outpatient epilepsy clinic.

Results
All patients were into the JME spectrum, all patients were seen at least 3 times in the follow up time, 70 percent of all cases had at least one event of seizure recurrence, 10 percent had more than 3 events. The majority of the seizures were strongly associated with a wake after sleep time of 60 to 90 minutes. The patients that had an earlier wake time that was out of the usual sleep schedule had increased chances of seizure recurrence.

Conclusion
Patient with JME have a very close relationship of seizure recurrence with the sleep-wake cycle. The seizure recurrence is strongly associated with a time frame of 90 minutes after waking up. We conclude that the chance of seizure recurrence is less after the 90 minute mark, and that can reasonably be a potential target as far as allowing to drive a motor vehicle passed that time for safety issues. Earlier than usual morning awakenings can precipitate seizures in a greater degree.

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0103 Daily Associations Between Relationship Stress and Sleep Health in Young Adults
Authors: Jakubowski Karen , Tapia Amanda , Guzman Maria , Oryshkewych Nina , Wallace Meredith , Pedersen Sarah , Hasler Brant 
Published: April 2024

Abstract

Introduction
Stress in interpersonal relationships has been related to adverse mental health outcomes, however, fewer studies have examined associations with physical health, particularly sleep. To date, most studies rely on retrospective reports of stress and sleep measured at a single timepoint, and do not examine multiple types of relationship stress. We tested whether daily stress with family, partner/spouse, and/or friends predicted shorter total sleep time (TST), lower sleep efficiency (SE), and/or later sleep midpoint via ecological momentary assessment (EMA) among young adults.

Methods
Participants were 293 young adults (21-30 y/o; 64% female; 5% Asian, 25% Black, 5% Biracial or Multiracial, 1% Other race, 64% White) reporting regular alcohol use from two studies with a shared assessment battery and up to 18-day EMA protocol. Participants reported daily sleep (TST [hours], SE, and midpoint, calculated from sleep diary reports), cannabis use (yes/no), alcohol use (total number of drinks), and stress with family, spouse/partner, and friends (coded as: 0=not at all, 1=somewhat, 2=moderately/very much). We fit generalized linear mixed effects models and estimated within-subject and between-subject associations between each stress variable and sleep outcome, respectively, adjusting for time-invariant (age, past-year household income, assigned sex) and time-variant covariates (weekend, cannabis use, alcohol use, pre- vs. post-COVID-19 pandemic).

Results
Participants completed a median of 17 EMA daily records (range: 1-18). Considering between-person effects, participants who reported feeling somewhat stressed with family [B(SE)=-.66(.32), p=0.04] or partner/spouse [B(SE)=-.63(.35), p=0.07] reported lower average TST over the EMA protocol. No associations emerged with experiencing moderately/very much stress in any relationship, nor for SE or midpoint outcomes. Results did not suggest a within-person effect of any type of daily relationship stress on sleep that night.

Conclusion
Among a well-characterized sample with up to 18 days of EMA data, reporting some stress in family and partner/spouse relationships predicted lower TST, relative to peers without stress in these relationships. Results may suggest that cumulative stress over time may be more detrimental for sleep than acute day-to-day stressors. When intervening on sleep, clinicians should also consider relationship stress, which is amenable to evidence-based interventions such as cognitive behavioral therapy.

Support (if any)
R01AA025617 (SLP), R01AA026249 (BPH/SLP), K23HL159293 (KJ)
1031 Association Between Objective Sleep Architecture and Biomarkers of Alzheimer's Disease
Authors: Chen Jiong , Cavailles Clemence , Jin Jiangli , Stankeviciute Laura , Gao Song , Peng Dantao , Leng Yue 
Published: April 2024

Abstract

Introduction
Growing evidence suggests a bi-directional association between sleep and Alzheimer’s disease (AD), with several studies showing an association between self-reported sleep disturbances and AD biomarkers. However, the association between polysomnography (PSG)-assessed sleep architecture and AD biomarkers remains unknown. We aim to investigate the associations between sleep architecture features and AD biomarkers in a clinical population with and without cognitive impairment.

Methods
We examined 128 participants [mean age of 70.9 years (±9.7), 43.8% of men] from an outpatient memory clinic, of whom 23 were healthy controls, 41 patients with mild cognitive impairment, and 64 patients with AD. Sleep architecture features were derived from PSG data and categorized by tertiles. Four AD biomarkers were measured, including tau-181, Brain-Derived Neurotrophic Factor (BDNF), and neurofilament light (NFL) obtained from blood samples, along with Aβ levels measured from amyloid positron emission tomography scans. Multivariable linear regressions models were performed to assess the associations between sleep architecture features and AD biomarkers.

Results
After adjustment for age, gender, APOE4 status, diabetes mellitus, smoking habits, and body mass index, participants in the highest REM latency tertile (i.e., with longer REM latency; &gt;192.7 minutes) were associated with increased levels of tau-181 (β= 0.25, 95% confidence interval (CI)= 0.01;0.55) and Aβ (β= 0.15, 95% CI= 0.06;0.26), and with decreased level of BDNF (β= -0.51, 95% CI= -0.70;-0.20) compared to participants in the lowest tertile (i.e., with shorter REM latency; &lt; 98.2 minutes). Moreover, being in the middle SWS percentage tertile (i.e., SWS percentage between 2.5 and 10.2) was associated with a lower level of tau-181 (β= -0.18, 95% CI= -0.34;-0.02) compared to being in the lowest tertile (i.e., shorter SWS percentage; &lt; 2.5)). We did not find any association between AD biomarkers and sleep duration, efficiency, latency, or other sleep architecture features.

Conclusion
In this cross-sectional study of a clinical population, we highlight the importance of REM latency, and to a lesser extent, SWS percentage, in relation to AD biomarkers. Future research is needed to examine the longitudinal association between sleep architecture and AD biomarkers and clarify underlying mechanisms.

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1033 Association of the Cardiopulmonary Coupling Sleep Spectrogram with Incident Parkinson’s Disease in Older Men
Authors: Milton Sasha , Sun Haoqi , Stone Katie , Yaffe Kristine , Westover M Brandon , Thomas Robert , Leng Yue 
Published: April 2024

Abstract

Introduction
The cardiopulmonary coupling (CPC) sleep spectrogram is an increasingly recognized measure of sleep quality which integrates sleep, autonomic drive, and respiration. Specifically, CPC is an estimate of the sleep state modulated synchronization and coupling between heart rate variability and respiration. Those with Parkinson’s disease (PD) have been shown to exhibit alterations in CPC and have higher rates of sleep disturbances, respiratory abnormalities, and autonomic dysfunction. However, little is known about the longitudinal association of CPC with incident PD in community-dwelling older men.

Methods
We studied 2859 men (mean [SD] age = 76.2 [5.4] years) without PD who underwent polysomnography between 2003 and 2005 and were followed until 2016 for incident self-reported PD as part of the Osteoporotic Fractures in Men (MrOS) prospective study. CPC was calculated from the electrocardiogram (ECG) during rapid eye movement (REM) sleep, N2 and N3 (N2N3) stages of non-REM sleep, and across the whole night. CPC metrics included high, low, and very low frequency coupling (HFC, LFC, and VLFC, respectively). Ratios of the 3 power bands were computed to assess deviation from or concordance with typical stage specific CPC patterns. Associations between tertiles of CPC metrics and incident PD were assessed using multivariable logistic regression.

Results
During 11 years of follow-up, 64 incident PD cases were identified. After adjustment for covariates including age, comorbidities, and apnea-hypopnea index (AHI), men in the lowest tertile of VLFC/(LFC+HFC) during REM sleep had approximately twice the risk of developing PD [OR (95% CI) = 2.22 (1.20,4.35)] relative to men in the highest tertile. Whole-night and N2N3 CPC metrics were not associated with incident PD.

Conclusion
Disruption of the typical CPC pattern during REM, representing potential altered interactions between brain (sleep electrocortical activity), cardiac (heart rate variability) and respiratory output mechanisms, was associated with an increased risk of incident PD. Our findings may reflect a prodromal alteration of interactions between sleep subsystems, though future studies are needed to understand potential mechanisms linking CPC to incident PD.

Support (if any)
Support comes from the National Institute on Aging (R21AG085495) and the Institute for Personalized Sleep Health (Beth Israel Deaconess Medical Center).
1035 Automated Analysis of REM Sleep Without Atonia in the Lewy Body Disease Spectrum
Authors: Jagielski Jack , Kelleher Makayla , Finstuen Thomas , LeClair-Visonneau Laurene , Kejal Kantarci , McCarter Stuart , Boeve Bradley , Michael Silber , Dredla Brynn , Louis Erik St 
Published: April 2024

Abstract

Introduction
Quantitative rapid eye movement (REM) sleep without atonia (RSWA) recorded during polysomnography (PSG) represents loss of normal REM sleep atonia. RSWA is the neurophysiologic signature of REM sleep behavior disorder (RBD). Visually scored RSWA is a candidate biomarker for synucleinopathies. However, visual RSWA scoring requires expert scoring, limiting widespread application. We comparatively analyzed RSWA in DLB and iRBD using the automated Ferri REM Atonia Index (RAI).

Methods
We quantitatively analyzed the RAI in 17 DLB and 20 iRBD patients, compared to 20 controls using Hypnolab Software for Sleep Analysis (SWS Soft, Colognola ai Colli, Italy). PSG data were converted to European Data Format (.EDF), and the submentalis surface electromyogram (EMG) signal was notch-filtered at 60 Hertz and rectified. Automatically calculated RAI scores were comparatively analyzed across groups (DLB, iRBD, controls) using Kruskal Wallis H tests for group comparisons, and regression analyses determined relationships between diagnosis, age, and sex. Logistic regression ROC determined optimal RAI for distinguishing iRBD from DLB. When interpreting RAI, lower values represent greater amounts of RSWA, and higher values represent more normal REM atonia.

Results
Median age was no different between DLB (72.6 years), iRBD (69.4 years), and controls (68.0 years). The DLB group consisted of 16 men and one woman, the iRBD group had 18 men and 2 women, and controls were comprised of 16 men and 4 women. Median RAI was lowest in DLB (0.32), intermediate in iRBD (0.84) and highest in controls (0.96), indicating a gradient in RSWA amounts from DLB patients (highest) to controls (lowest). Regression demonstrated diagnosis independently predicted RAI, controlling for age and sex (adjusted R2=0.64, p=0.0001). The RAI that optimally distinguished iRBD from DLB was 0.48 (specificity 85%, sensitivity 76%, AUC=0.88).

Conclusion
The RAI demonstrated a clear gradient throughout the Lewy body spectrum; highest (indicating lowest RSWA amounts) in controls, intermediate in iRBD, and lowest (indicating greatest RSWA) in DLB. The RAI is a promising, time efficient and broadly applicable candidate biomarker for DLB and iRBD. Automated quantitative RSWA could be a valuable tool for deep phenotyping throughout the Lewy body disease spectrum.

Support (if any)
This study was supported by: U01NS100620, R34AG056639, U19AG071754, and P30AG62677.
1038 C-reactive Protein as a Risk Predictive Marker for Sleep-Related Alzheimer’s Disease in Blacks
Authors: Scott Sadeaqua , Blanc Judite , Gallop Erin-Leigh , Moise Rhoda , Chung Debbie , Thompson Michelle , Oliveira Bruno , Seixas Azizi , Rundek Tatjana , Jean-Louis Girardin 
Published: April 2024

Abstract

Introduction
Sleep is regulated by the microbiota-gut-brain axis, which plays a critical role in amyloid beta (Aβ) production and clearance; two key processes in the progression of sleep-related Alzheimer’s disease (SRAD). C-reactive protein (CRP) is an inflammatory biomarker correlated with Aβ levels in SRAD. Although Blacks are disproportionately affected by SRAD, a paucity of knowledge exists regarding effective early detection and prevention of this disease in this population. This study investigated the levels of CRP in Black participants with subjective Sleep apnea (SA) to determine what indicators or thresholds may serve as a risk predictive marker for Aβ blood biomarker screening for SRAD.

Methods
Blood from a total of 104 Blacks enrolled in two NIH-funded community-based sleep studies, ESSENTIAL and MOSAIC, was collected from January 2020 until October 2023. CRP levels were accessed according to clinical standards in ranges of normal or minor elevation, moderate elevation, marked elevation, and severe elevation. Frequency distributions and analyses were performed using SPSS29.

Results
Twenty-one participants self-reported an existing SA diagnosis; of which 19% had CRP levels at 0.3 - 1.0 mg/dL, 62% at 1.0 - 10.0 mg/dL, 19% at &gt;10.0 mg/dL, and none at &gt;50.0 mg/dL. Of the 83 participants without SA, 31% had CRP levels at 0.3 - 1.0 mg/dL, 61% at 1.0 - 10.0 mg/dL, 7% at &gt;10.0 mg/dL, and 1% at &gt;50.0 mg/dL. In total, 81% of participants with subjective SA had CRP levels above minor elevation, while 69% of participants without subjective SA had levels above minor elevation, showing a 10% difference in elevated CRP levels between both groups. These results suggest that SA can lead to greater levels of inflammation among Blacks.

Conclusion
A 10% difference in elevated CRP levels of participants with and without SA diagnosis may suggest that undiagnosed participants could be at risk for SA. Identifying factors that predict blood Aβ levels such as CRP may lead to a cost-effective, SRAD specific prescreening panel to identify patients at higher risk of SRAD, and aid risk stratification in Blacks. Future research is needed to further explore this area.

Support (if any)
R01AG067523, R01HL142066, and T32HL166609-02
0104 Biological Embedding and Sleep Quality in Adulthood: Evidence from a 30-year Prospective Longitudinal Cohort Study
Authors: Omisakin Olusola , Felt John M , Noll Jennie , Buxton Orfeu 
Published: April 2024

Abstract

Introduction
Attenuation over the life course of hypothalamic-pituitary-adrenal (HPA) axis activity, such as reduced cortisol secretion, represents biological embedding of early-life stress. Biological embedding is implicated in myriad health concerns including disruptive sleep patterns. We hypothesized that attenuation of cortisol over the first half of the life-course will be negatively correlated with objectively indicated sleep quality in adulthood.

Methods
Cohort participants included females referred by child welfare agencies for having experienced intra-family childhood sexual abuse (CSA) at mean age 10.5 years. A counterfactual group of non-abused females from the same zip codes were demographically matched. The cohort was assessed at 7 timepoints across development longitudinally from 1987-2019. Resting cortisol was obtained through blood (waves 1-3) and saliva (waves 4-6). A formula approved by the US FDA was employed to convert salivary cortisol concentrations to blood-based equivalents: (serum µg/dL) = 5.177 + 15.132*(saliva µg/dL). Using a bilinear spline model – a model for tracking trajectories at different phases of development – pre-knot slopes (rates of change during childhood of cortisol, indicative of HPA attenuation and biological embedding) from waves 1 to 6 (or ages 6-32) were extracted. Wave 7 (mean age 36.1 years) included wrist actigraphy for a week. Ordinary Least Squares (OLS) regression examined whether cortisol slope from ages 6 to 32 predicted adult sleep.

Results
We found no group differences in sleep between participants exposed to CSA and demographically similar non-abused participants. Using individual slopes from T1-T6 models of cortisol levels, we observed a positive correlation between cortisol slope and sleep maintenance efficiency (r = 0.22; p &lt; 0.05); sleep duration was not significant at Time 7. OLS regression showed that each additional year of increase in cortisol slope (µg/dL) was associated with 21.4% increase (p &lt; 0.05) in mean sleep efficiency.

Conclusion
Findings suggest that sleep quality in middle adulthood was better when participants did not experience attenuation of cortisol (biological embedding of stress) earlier in the life course. Our study provides evidence of effects of biomarker-based biological embedding on sleep quality in middle adulthood among a sample of women maltreated as children and a matched control group.

Support (if any)
T32HD101390, R01AG059682, R01HD072468, R01AG04879
1041 Increased Delta-Gamma Coupling During Phasic REM Sleep in Isolated RBD
Authors: Tea-Gon Noh , Yoonkyung Lee , Young Kim Eun , Jun-Sang Sunwoo , Ki-Young Jung 
Published: April 2024

Abstract

Introduction
This study examines the phasic and tonic states of REM sleep with a focus on idiopathic rapid eye movement sleep behavior disorder (iRBD), which is characterized by REM sleep without atonia and is thought to be a precursor to alpha-synucleinopathies. By examining specific EEG dynamics associated with dreaming, specifically delta and gamma power during phasic REM sleep states and their correlation with iRBD characteristics, we aim to develop a comprehensive understanding of dream enactment.

Methods
In-depth analysis was performed using polysomnography (PSG) and 21-channel EEG data from 13 iRBD patients and 10 controls who had been drug-free for six months and had not progressed to alpha-synucleinopathy. REM sleep states were categorized into phasic and tonic states based on eye movements, and the Kullback-Leibler modulation index was used to assess phase-amplitude coupling (PAC) and calculated phase-locked amplitudes (PLA) to determine interphase coupling. Gini coefficients were calculated to identify within- and between-component imbalances, and extensive statistical analysis was performed using permutation cluster analysis, repeated measures analysis of variance, Mann-Whitney U tests, and correlation assessments to identify differences and relationships.

Results
The results showed a significant increase in delta-gamma coupling during phasic REM sleep in RBD compared to controls (FDR p &lt; 0.0001). A detailed comparison of the delta signal component, the component in which the imbalance was found (FDR p &lt; 0.0001), at different spatial locations revealed distinct patterns of delta-gamma coupling, with significant phase-amplitude coupling (PAC) observed in frontal and parietal cortex. These results showed a clear linear relationship (FDR p &lt; 0.0001), with notable correlations with the RBDQ-KR (FDR p &lt; 0.0001) and the REM atonia index (FDR p=0.0003). The average area under the ROC-AUC curve for separating the RBD group from the control group based on PAC values was 0.88.

Conclusion
The study significantly highlights the role of EEG metrics, especially the coupling of delta and gamma oscillation during REM sleep, as key indicators of dream-related enactment in iRBD. The strong correlations with clinical indices not only underscore the diagnostic value of these EEG measures but also suggest their potential to revolutionize the diagnosis and understanding of iRBD.

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1045 Sleep Disorders in Pediatric Patients with Agenesis of the Corpus Callosum
Authors: Kwon Ashley , Gu Payal , Zhang Christina , Ward Sally , Perez Iris 
Published: April 2024

Abstract

Introduction
Agenesis of the corpus callosum (ACC) is a complete or partial absence of the corpus callosum arising from disruption of brain development. There is limited information about sleep in children with ACC. We aim to describe the sleep architecture and respiratory parameters of children with ACC.

Methods
Retrospective study of 20 patients with ACC who had polysomnography (PSG) between 2000-2023. Demographic data, BMI or weight for length (percentile), associated conditions, and PSG findings were collected. Sleep quality was compared to the National Sleep Foundation’s guidelines. Poor sleep quality indicators were sleep latency &gt;45 min, sleep efficiency (SE) &lt; 75%, N1 ≥20%, N2 &gt;81%, N3 ≤5% for 14-17 years, N3 ≤10% for &lt; 14 years, REM ≤10% excluding 6-13 year-olds, or arousal index &gt;10/h. Fisher’s exact test or unpaired t-test was used to compare groups.

Results
Average age was 5.9 ± 5.4 years old, and 12/20 patients were male. 6/20 were overweight/obese. 14/20 had complete ACC, and 6/20 had partial ACC. 8/20 had seizures. 15/20 had ≥1 poor sleep quality indicator, notably decreased SE (45%) , decreased REM (53%), and increased arousals (45%). Between complete and partial ACC, there was no difference in presence of ≥1 poor sleep quality indicator (p= 0.61), SE (p=0.34), REM (p=0.28), and arousals (p=1). Sleep quality was similar between seizure and no seizure groups (p=0.60). 11/18 had obstructive sleep apnea (OSA); 5/11 also had central sleep apnea (CSA). 1/20 had CSA alone. Only 1 with OSA was overweight. Excluding patients with tracheostomies, there was no difference in OSA between those with complete and partial ACC (p=1) or those with and without seizures (p=0.16). SpO2 baseline was 95 ± 2%; SpO2 nadir was 85 ± 0.1%. 4/20 had ≥5 minutes of total sleep time (TST) with SpO2 &lt; 90%. PETCO2 maximum was 48 ± 5 mmHg; none had PETCO2 &gt;50mmHg for &gt;25% of TST.

Conclusion
Children with ACC have poor sleep quality, and many have OSA. There was no difference in sleep quality or presence of OSA between those with complete and partial ACC. Our study supports the need for screening of sleep-related disorders in patients with ACC.

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