bluuebunny/crossref_metadata_2025_split huggingface dataset:
1214 Higher Bedroom Temperature Associated With Poorer Sleep: Data From Over 3.75 Million Nights
Authors: Raj A , Ruder M , Rus H M , Gahan L , O’Mullane B , Danoff-Burg S , Raymann R 
Published: May 2020

Abstract

Introduction
Bedroom temperature can influence nocturnal thermoregulation and sleep. To date, limited, small experimental studies have shown that bedroom temperatures outside the recommended range of 65 and 70°F can negatively impact sleep. However, this association has not been studied in a large-scale data set. Using over 3.75 million nights of objectively measured data, we analyzed the associations between habitual bedroom temperatures and sleep.

Methods
Over 3.75 million nights of sleep and bedroom temperature data were collected using S+ by ResMed technology from 34,096 Individuals (57% male, 20-90 years, mean age 48.7 +/-14.5 years, all US residents). Multilevel regression analyses were used to analyze associations between bedroom temperature and sleep. A stricter alpha level of 0.001 was used to account for the large number of observations in the dataset.

Results
Bedroom temperature was above 70°F for 69% of nights, with the average temperature ranging between 68.8 and 76.2°F. For each 1°F increase in bedroom temperature between 60-85°F, sleep efficiency decreased by 0.06%. Likewise, higher bedroom temperatures were linked to shorter Total Sleep Time duration (-0.45 mins/°F), longer Sleep Onset Latency (+0.04 mins/°F), and longer Wake After Sleep Onset (+0.11 mins/°F), all ps&lt;0.001.

Conclusion
Analyzing data from over 3.75 million nights, we found that many people sleep in a bedroom warmer than the optimal temperature. Further, higher bedroom temperatures - even within the recommended range for optimal sleep - are associated with poorer sleep and higher wakefulness. Bedroom thermostats and cooling options should be considered to achieve optimal sleeping temperature conditions.

Support
N/A
1223 Central sleep apnea and Chiari 1 malformation in a pediatric patient with Klippel-Feil sequence
Authors: Martirosyan Zara , Malhotra Sonal 
Published: May 2020

Abstract

Introduction
Klippel- Feil Sequence (KFS) is a rare congenital condition that classically presents with a triad of congenital cervical spine fusion, reduced cervical spine flexion and low posterior hairline. KFS has been associated with several comorbidities including congenital heart defects, hearing loss, renal dysfunction, Chiari malformation and sleep disordered breathing (SDB). The co-occurrence of SDB and chiari malformation type 1 (CM1) has been reported in multiple individuals. However, the pathological basis of the connection between CM1 and SDB in the setting of KFS is not clearly understood.

Report of Case
Here we present a pediatric case report of a patient with KFS, SDB, drooling and dysphagia. The drooling and dysphagia prompted an MRI that revealed CM1. Baseline polysomnogram (PSG) showed mild central sleep apnea with apnea-hypopnea index (AHI) 6.06 comprised of central apnea index 4.81 and obstructive apnea index 1.28. Posterior fossa decompression of this patient, following neurology recommendations, resolved majority of the symptoms, namely the drooling, nocturnal cough, dysphagia and sleep disturbances. However unexpectedly repeat polysomnogram eight weeks after posterior fossa decompression revealed worsening central sleep apnea despite the patient being clinically asymptomatic.

Conclusion
Taken together this case highlights the point that while it is critical to recognize the association of SDB in the setting of KFS, decompression alone may not be sufficient to completely alleviate SDB and/or certain neurological symptoms such as nocturnal coughing. Our observations are consistent with the hypothesis that SDB in a setting of KFS is multifactorial and pathophysiology is not clearly understood.
1237 Positional central sleep apnea in a child: not always obstructive
Authors: Powell Weston , Chen Maida 
Published: May 2020

Abstract

Introduction
Spinal cord compression at the craniocervical junction can cause central sleep apnea (CSA) in children, due to mechanical disruption of respiratory control centers. Polysomnography (PSG) pre/post surgical decompression is indicated to evaluate treatment response.

Report of Case
A 5-year-old with Wolf-Hirschhorn syndrome, developmental delay, partial agenesis of the corpus callosum, hypotonia, incomplete segmentation of C1 with subluxation leading to stenosis, cleft palate, and obstructive sleep apnea (OSA) presented for post-surgical PSG. Prior PSGs revealed oAHI 55/hr and 7/hr, cAHI 3/hr and 2/hr at 1 and 10 months of age, respectively. At 46 months, patient underwent suboccipital decompression at C1 for severe craniocervical stenosis. Post-operative PSG revealed emergence of CSA with cAHI 8/hr and stability of OSA with an oAHI 8/hr. Positional analysis revealed worsening in lateral position (lateral cAHI 10.6/hr, supine cAHI 4.6/hr). Central events were up to 33 seconds long with nadir desaturation of 76% in lateral position compared to 20 seconds and nadir 88% in supine position. Head CT and MRI showed incomplete ossification of the C1 vertebra with subluxation of the left lateral mass leading to absence of CSF flow at the craniocervical junction. Repeat decompression and fixation is planned by neurosurgery; in the interim supine sleep was recommended and family declined BiPAP.

Conclusion
In our case, CSA worsened with left lateral positioning and improved with supine positioning. Lateral positioning likely increased subluxation of the left lateral mass seen on CT/MRI, and eased subluxation in supine sleep causing position-dependent dynamic impingement of the respiratory control centers at the level of subluxation. The absence of findings prior to decompression may reflect increased instability after decompression or increased stenosis with growth. Our case highlights the importance of positional analysis for central as well as the more conventional obstructive sleep apnea to understand pathogenesis and guide therapy.
1249 Reverse platypnoea-orthodeoxia syndrome: A rare cause of hypoxemia during in lab polysomnography
Authors: Sessums Mary T , Guzman Maria P , Dredla Brynn K 
Published: May 2020

Abstract

Introduction
Sleep related hypoxemia carries a broad differential diagnosis. Right-to-left shunting is a known cause of hypoxemia that is not correctable with supplemental oxygen. A patent foramen ovale (PFO) is an intra-cardiac shunt that results in hypoxemia and in rare instances can lead to platypnea-orthodeoxia syndrome (POS). POS is characterized by dyspnea and hypoxemia in the upright position, which improves when supine. We present a case of nocturnal hypoxemia and PFO with a unique clinical presentation consistent with reverse POS discovered on PSG.

Report of Case
57-year-old male with Class I obesity and a remote diagnosis of mild sleep-disordered breathing not treated with CPAP was referred to Sleep Medicine for excessive daytime sleepiness, snoring, and witnessed apneas. Polysomnography revealed basal oxygen saturation of ~88% during sleep. There was no evidence of apnea or hypopnea. Hypoxemia was not correctable with supplemental oxygen, suggestive of shunt physiology. Oxygen saturation was normal during upright exercise. Pulmonary hypertension was ruled out. Transesophageal echocardiogram revealed PFO with right-to-left shunt. Overall presentation was consistent with reverse POS secondary to PFO, which will be treated with percutaneous trans-catheter closure.

Conclusion
This is a rare case of reverse POS secondary to PFO, with shunt physiology initially suspected during Sleep Medicine evaluation based on PSG. Reverse POS is characterized by dyspnea and hypoxemia while supine, as opposed to upright as in classic POS. The precise pathophysiology of reverse POS is unclear. This case emphasizes the need to consider reverse POS in patients with supine hypoxemia refractory to oxygen therapy. Such findings on PSG should prompt further workup for causes of right-to-left shunt. This diagnosis should not be overlooked, as the underlying abnormality is often correctable. In this patient, we expect hypoxemia to resolve with percutaneous trans-catheter closure of PFO.
1259 Periodic Neck Myoclonus During Sleep (PNMS) is Associated with Upper Airway Resistant Syndrome, but Resolves with CPAP
Authors: Alfi Majed A , Avidan Alon Y 
Published: May 2020

Abstract

Introduction
Periodic neck myoclonus during Sleep (PNMS) is a movement disorder of sleep characterized by sudden myoclonic flexion or version of the head that manifest during REM and NREM sleep. While its finding has been attributed to a normal physiologic phenomenon, to the best of our knowledge, our case represents the first report of with PNMS attributed to sleep disordered breathing with resolution using CPAP

Report of Case
A 22 y/o male with no significant clinical history was referred for evaluation of snoring and excessive sleepiness. Nocturnal polysomnogram coupled with expanded EMG montage demonstrates evidence of upper airway resistance syndrome (UARS), characterized by frequents respiratory effort-related arousals (RERAS), primarily during REM sleep associated with arousals. The majority of these events resulted in sudden myoclonic movements of the neck and head that were associated with arousals and sleep fragmentation. PNMS manifested in the PSG as a flexion myoclonic motor artifact lasting 200-800 ms during REM sleep with an associated EEG arousal. The overall Respiratory Disturbance Index (RDI) was12/hr. The subsequent application of CPAP at a setting of 5-6 cm resolved these movements supporting this origin as a phenomenon of sleep-state instability.

Conclusion
While previous investigators have explained PNMS as an incidental finding or one common in patients with RBD, our case highlights a potential new mechanism for their appearance. This case helps shed more light on the origin of PNMS as a secondary phenomenon related to sleep state instability due to sleep disordered breathing given the temporal association with RERAS and dramatic resolution with CPAP therapy.
1262 Case Series on the Use of Volume Assured Pressure Support (VAPS) in Patients with Interstitial Lung Disease and Progressive Hypercapnia
Authors: LeMaster William , Jun Dale , De Cruz Sharon , Zeidler Michelle , Saggar Rajan 
Published: May 2020

Abstract

Introduction
Many patients with interstitial lung disease (ILD) experience progressive respiratory failure. While various therapies are implemented for acute hypercapnic respiratory failure during inpatient ILD flares, there is little data regarding the management of chronic hypercapnia in ILD with nocturnal Volume Assured Pressure Support (VAPS). We present three patients who were prescribed nocturnal VAPS for their progressive hypercapnia as a bridge to lung transplantation.

Report of Case
Patient 1 is a 45-year-old woman with rheumatoid arthritis related ILD and progressive hypercapnia. Despite optimal therapy, her ILD resulted in an admission for hypercapnic and hypoxemic respiratory failure requiring treatment with BPAP, then transition to nocturnal VAPS on discharge. Dyspnea and pCO2 improved as an outpatient (Fig. 1). Patient 2 is a 70-year-old female with history of scleroderma associated ILD with severe PH and hypercapnia. Initiation of VAPS improved her pCO2 levels although she was readmitted after a few months of treatment for an ILD flare. Patient 3 is a 60-year-old patient with connective tissue disease related ILD who was admitted for respiratory failure due to pneumonia and was transitioned to BPAP for hypercapnic respiratory failure. Due to insurance issues she has been unable to obtain a home VAPS and her pCO2 remains elevated. A plot of each patient’s pCO2 over time is in Figure 1.

Conclusion
In patients with severe lung disease, the normal decrease in tidal volumes that occurs with sleep can result in CO2 retention. Non-invasive ventilation (NIV) is well-studied in both stable obstructive lung disease and exacerbations but there is little data examining the utility of NIV to treat the chronic hypercapnia of ILD. In this case series, nocturnal VAPS stabilized or reduced PCO2 in patients with ILD and hypercapnia. Additional studies are needed to assess long term effects of VAPS in these patients.
1266 Primary Central apnea and loss of muscle atonia during REM
Authors: Hernandez M Elizabeth C , Velamuri Kanta 
Published: May 2020

Abstract

Introduction
Central sleep apnea (CSA) syndrome is defined when five or more central apneas and/or hypopneas are present per hour of sleep, more than 50% of all respiratory events. CSA usually occur during NREM stage and rarely during REM. CSA is important to recognize because of complications ranging from frequent nighttime awakenings,sleepiness to adverse cardiovascular outcomes. We present a 40 year old female patient with rare CSA during REM sleep and dream enactment.

Report of Case
40yo African American female with history of loud snoring, witnessed sleep apnea, and daytime fatigue. She reported nightmares, sleep talking, and acting out her dreams without injury. Epworth sleepiness score was 5 /24. Her past medical history is significant for depression and anxiety. She has no history of head trauma, no neurologic or cardiovascular disorders. Her medications include fluoxetine and,quetiapine. She denied substance use, narcotic use, or alcohol use.
Her level 1 sleep study showed predominantly REM-associated central sleep apneas which is rare. She also was observed to have loss of REM sleep muscle atonia suggestive of REM Behavior disorder.
Her sleep architecture was atypical with decreased N3 sleep stage. REM sleep duration was adequate. She was noted to have loss of REM muscle atonia based on AASM guidelins elevated chin EMG, excessive transient muscle activity, and witnessed movement during REM stage via video monitoring.
During the study, she had an apnea/hypopnea index (AHI) of 13.1 per hour of sleep, Central apneas were predominantly noted during REM stage, 10 per hour, comprised of 50% of her respiratory events. The minimum SpO2 value with CSA was 94%. She had normal sinus rhythm.
Her sleep was fragmented. A total arousals were 28.4/hour,and 7.9/hour were respiratory arousals, and the rest were spontaneous arousals.
An echocardiogram showed normal left ventricular ejection fraction of 55 to 60 %. Her room air arterial blood gas was normal with PaC02 of 37 mmHg. MRI of the brain/brainstem was ordered given her atypical REM sleep. She had no acute intracranial abnormalities. There is a non specific finding of a low lying cerebellar tonsils without evidence of Chiari I malformation.

Conclusion
Our patient has rare idiopathic central apnea in REM stage and is third case reported. She also has loss of muscle atonia during REM with dream enactment which is also rare in her age group. Injury precaution advised.
0132 Sex Differences in Evening Food Intake and Associated Weight Gain During Insufficient Sleep
Authors: Withrow D , Depner C M , Boland E M , Birks B R , Melanson E L , Higgins J , Eckel R H , Perreault L , Bergman B C , Wright K P 
Published: May 2020

Abstract

Introduction
Timing of food intake has emerged as a novel risk factor for weight gain and obesity. Higher evening food intake, especially during insufficient sleep, is associated with weight gain. We aimed to explore initial changes in evening food intake and the respiratory quotient (RQ) during insufficient sleep and subsequent weight gain. We also explored sex differences.

Methods
28 healthy adults (14F) aged 26.3±4.5y completed a 14–16 daylong laboratory protocol. In their home environment participants maintained one week of ~9h/night sleep schedules and consumed energy balanced diets for 3 days prior to completing the laboratory protocol. The laboratory protocol consisted of 3 baseline days of 9h/night scheduled sleep with energy balanced diets followed by 10 days of 5h/night scheduled sleep with ad-libitum food intake, with (n=14) and without (n=14) weekend recovery sleep. RQ was assessed on days 3 and 5 in a whole room calorimeter. Evening (dinner and after-dinner snacks) energy intake and body weight were assessed daily.

Results
A significant sex by condition effect was observed for evening food intake such that men and women were similar at baseline, but men ate more than women during insufficient sleep, when controlling for body mass (p&lt;0.05). A significant sex by condition effect was also observed for RQ with women showing similar RQ during baseline and insufficient sleep and men showing a higher RQ during insufficient sleep versus baseline (p&lt;0.05). Linear regression with food intake and RQ as predictors of weight gain showed that increased evening food intake, but not RQ, on the second day of sleep restriction was associated with weight gain in men, but not women, at the end of the study eight days later (p&lt;0.05).

Conclusion
Findings suggest that rapid changes in evening food intake during insufficient sleep contributes to subsequent weight gain during sustained insufficient sleep, especially in men.

Support
NIH HL109706, DK111161, TR001082, DK048520, Sleep Research Society Foundation grant 011-JP-16 and Office of Naval Research MURI (N00014-15-1-2809).
0133 NLRP3 Inflammasomes Modulate Brain Vasohemodynamic Responses to Sleep Loss
Authors: Zielinski M R , Atochin D N , Desrosiers G 
Published: May 2020

Abstract

Introduction
Increased cerebral blood flow (CBF) is positively associated with non-rapid eye movement (NREM) sleep electroencephalogram (EEG) delta power, also known as slow-wave activity (SWA). The pro-inflammatory somnogenic cytokine interleukin-1 beta (IL-1β) can induce vasodilation and increase CBF. Nucleotide leucine-rich protein complex-3 (NLRP3) inflammasomes, which activate IL-1β, are increased in the cortex after sleep deprivation and increase SWA. We aimed to determine the relationship of NLRP3 inflammasomes on sleep loss-induced alterations in vasohemodynamics and SWA.

Methods
NLRP3 knock-out (KO) and wild-type (WT) mice underwent ad libitum sleep, 6 hours of sleep deprivation, or were given 10 ng of IL-1β or the vehicle intracerebroventricularly. SWA and CBF, blood velocity, and blood volume were determined concurrently during sleep/wake states using polysomnography and laser doppler flowmetry. Regional brain changes in CBF were determined using transponders, spectrophotometry, and fluorescent microspheres.

Results
SWA and CBF were significantly increased during the first 6 hours after sleep deprivation in WT but not NLRP3 KO mice. SWA and CBF significantly increased in the first 6 hours after IL-1β in both NLRP3 KO and WT mice. Additionally, alterations in cerebral blood velocity and volume demonstrated state specific changes that varied significantly during the transitions between states. SWA and CBF were significantly positively correlated during both ad libitum sleep and sleep after sleep deprivation in WT mice, although this relationship was not observed in NLRP3 KO mice. We also found significant phase-amplitude frequency coupling between SWA and CBF. Cortical changes CBF were significantly enhanced after sleep deprivation and IL-1β administration in WT mice, although were attenuated in the hypothalamus. NLRP3 KO mice showed these same regional effects in CBF after IL-1β but not sleep deprivation.

Conclusion
Our findings indicate that NLRP3 inflammasomes are involved in neurovascular coupling involving SWA.

Support
Department of Veterans Affairs IBX002823A (MRZ)
0147 Dynamic Alterations in Functional Connectivity Between Sleep- and Wake-Promoting Regions of the Human Brain at the Sleep Onset Period
Authors: Ishii T , Koike T , Nakagawa E , Sumiya M , Sadato N 
Published: May 2020

Abstract

Introduction
The sleep onset period, involving so-called stage N1 sleep largely, is characterized by a reduction in the amount of alpha activity compared to wakefulness. Various kinds of physiological and psychological changes are also apparent, such as slow eye movements, changes in muscle tonus, and the hypnagogic dream-like mentation. These phenomena are thought to be the reflection of dynamic alterations in the brain during the transition period, however, details of these changes have still been uncovered.

Methods
We aimed to investigate a dynamic shift in the brain connectivity at sleep onset using the method of EEG-fMRI simultaneous recording. Twenty-three healthy subjects participated. EEG/fMRI were recorded simultaneously during an hour’s nap in a 3T-MRI scanner and real-time monitoring of EEG was performed. To record the transition period between multiple times, an experimenter inside a scanner room touched a subject’s foot for inducing arousal when a shift to NREM sleep stage 1 was observed. EEG data were scored according to the AASM criteria. Based on sleep stages defined by polysomnographic findings, we investigated alterations in functional connectivity of sleep- and wake- promoting regions within the hypothalamus and other areas including the thalamus.

Results
Posterior alpha power showed significant positive correlation with BOLD signals in the anterior and medial dorsal thalamus. Connectivity between the thalamus and cortical regions reduced sharply in the descent to sleep stage. Meanwhile, BOLD signals of the sleep- and wake- promoting regions within the hypothalamus fluctuated with certain temporal lags from fluctuations of alpha rhythm at sleep onset.

Conclusion
Present findings provide preliminary evidence of dynamics of wake- and sleep- promoting regions in the human brain in vivo. Our data also support the hypothesis that reduced thalamocortical connectivity which limits the capacity to integrate information is associated with the transition of consciousness at sleep onset.

Support
None