bluuebunny/crossref_metadata_2025 huggingface dataset:
789 Obstructive Sleep Apnea (OSA) and Vestibular Dysfunction in Patients with Traumatic Brain Injury (TBI)
Authors: Skop Karen , Bajor Laura , Swank Chad , Sevigny Mitch , Tallavajhula Sudha , Nakase-Richardson Risa , Miles Shannon
Published: May 2021

Introduction

Recent work has highlighted prevalent OSA after TBI. Vestibular dysfunction is also common and associated with adverse outcomes particularly in military personnel. Vestibular dysfunction has been identified in patients with moderate to severe OSA, yet the relationship remains unexplored in those with TBI. This study examined the relationship of vestibular dysfunction with OSA in a large cohort of Veterans and Military Service Members (V/SM) with documented TBI.

Methods

Data are secondary analyses from a five-center prospective observational cohort study of V/SM admitted for inpatient rehabilitation for TBI and enrolled in the VA TBI Model Systems. Participants completing study measures from 2015 to March of 2020 were included in analyses. Study measures includes the Centers for Disease and Control’s National Health and Nutrition Education Survey (NHANES, OSA item embedded) epidemiologic survey and Neurobehavioral Symptom Inventory (NSI). T-tests and chi-square tests compared patients with OSA to those without OSA on the vestibular subscale on the NSI.

Results

The sample was mostly male (93%), a mean of 38 years of age, and predominantly with mild (52%) or severe (41%) TBI. OSA was reported in 30.6% on the NHANES. Vestibular symptoms were more common among those with OSA (24%) compared to those without (12%) with a significant difference on the NSI Vestibular Total Score (3.84 vs 2.88 respectively; p<0.001). Similar results were seen across all three NSI vestibular items (dizziness, balance difficulties, poor coordination).

Conclusion

Participants with TBI and comorbid OSA are more likely to endorse the presence and greater severity of vestibular symptoms compared to those without OSA. Future research is needed to improve understanding of the inter-relationship of OSA and vestibular dysfunction to inform clinical management.

Support (if any)

VA TBIMS & TBICoE (HT0014-19-C-0004), NIDILRR, North Texas TBI Model System (Grant #90DPTB0013), TIRR TBIMS (Grant #90DPTB0016)
793 Obstructive Sleep Apnea and Hypoventilation in Patients with Muscular Dystrophies: Analysis of 42 Polysomnogram Studies
Authors: Halani Pallav , Ahn Mihye , Vaughn Bradley , Ewing Travis , Fan Zheng
Published: May 2021

Introduction

Patients with muscular dystrophies (dystrophinopathy, congenital muscular dystrophy and limb-girdle muscular dystrophy) are at greater risk of obstructive sleep apnea (OSA). However, few studies have examined if they are also at risk for hypoventilation and its relationship with OSA. We hypothesize that these two conditions occur independently of each other as an impaired ventilator drive and diaphragm weakness.

Methods

Retrospective review of diagnostic polysomnograms (PSG) in a tertiary care facility over 15 years was conducted. The polysomnography included either end tidal CO2 or transcutaneous CO2 measurements. Descriptive data analysis was performed on results described. We computed Pearson correlation coefficients to examine the relationships between PSG indices and other parameters. Pearson’s Chi-squared test with Yates’ continuity correction is used to test if hypoventilation is independent from OSA.

Results

42 PSG studies in patients with muscular dystrophies were included after excluding 2 studies due to insufficient sleep duration. The average age at the time of study was 14.2 yrs with 41 being male and average BMI of 24.1. 64% of the group met the definition for OSA with average AHI 8.0. 36% of the group met the criteria for hypoventilation, and 33% patients with hypoventilation did not have OSA. Chi squared analysis (p=1.0) shows that hypoventilation is independent of OSA.

Conclusion

Sleep disordered breathing is common in patients with muscular dystrophy. This study supports that OSA and CO2 retention may be independent processes.

Support (if any):
797 Obstructive Sleep Apnea is a Risk Factor for Sudden Unexplained Death in Epilepsy (SUDEP)
Authors: Soontornpun Atiwat , Andrews Noah , Bena James , Grigg-Damberger Madeleine , Foldvary-Schaefer Nancy
Published: May 2021

Introduction

Epilepsy is associated with a substantial risk of morbidity and mortality, including sudden unexplained death in epilepsy (SUDEP). Prior data demonstrated a possible association between obstructive sleep apnea (OSA) based on nocturnal oximetry oxyhemoglobin saturation index (ODI) and risk of SUDEP. We aimed to evaluate the relationship between PSG-defined OSA and SUDEP risk using the revised SUDEP Risk Inventory (rSUDEP-7).

Methods

We identified adults with epilepsy who underwent PSG between January 2004 and December 2016 at Cleveland Clinic. OSA was defined as an apnea-hypopnea index (AHI) ≥5 and moderate-to-severe OSA as an AHI ≥ 15. SUDEP risk was determined by the rSUDEP-7. The higher the rSUDEP-7 score, the greater the risk for SUDEP. Associations between rSUDEP-7 score and OSA groups (AHI>15 vs. <15) used Wilcoxon rank sum tests, and multivariable linear models adjusting for age, sex, BMI, and smoking status. Spearman correlations measured relationships between rSUDEP-7 score with AHI and ODI.

Results

214 patients were identified; 134 (62.6%) had OSA, moderate-to-severe in 75 (35%). Those with AHI≥15 were older and more likely to have: pharmacoresistant epilepsy, nocturnal seizures, higher BMI, and longer epilepsy duration (all p<0.05). Median rSUDEP-7 score was 1(0,3), and > 35% had rSUDEP-7 score of > 3. Patients with moderate-to-severe OSA had higher rSUDEP-7 than those with AHI<15 (p=0.001). Higher AHI and ODI positively correlated with rSUDEP-7 (p=0.002 and p=0.016) while SpO2 nadir negatively correlated with rSUDEP-7 (p=0.007). After adjustment, those with AHI≥15 had mean rSUDEP-7 score 1.14 points (95%CI 0.55–1.72, p<0.001) higher than those with AHI<15.

Conclusion

Epilepsy patients with moderate-to-severe OSA, have higher risk of SUDEP based on the rSUDEP-7. Our findings provide further support for routine screening of OSA in epilepsy populations.

Support (if any):
798 Diffusion tensor imaging as a potential biomarker of sleep dysfunction in warfighters with chronic, severe, traumatic brain injury
Authors: Kent Werner J , Gerstenslager Brian , Yeh Ping-Hong , Srikanchana Rujirutana , Kenney Kimbra , Ollinger John
Published: May 2021

Introduction

Traumatic brain injury (TBI) plagues service members in times of war and training. Diagnosis and management of TBI remain challenging, with many suffering from sleep disorders. We hypothesized that TBI-related damage to the hypothalamus, a master regulator of breathing and sleep, could be related to post-TBI obstructive sleep apnea (OSA) and serve as a pathophysiological biomarker for a subpopulation of OSA patients.

Methods

This was a retrospective study of warfighters with TBI from the National Intrepid Center of Excellence (NICoE). Subjects were identified by severe TBI on neuroimaging and compared against a control group without TBI. All subjects underwent screening polysomnography (PSG). MRI was acquired via 3T scanner. The hypothalamus was automatically segmented using a diffeomorphic algorithm. DTI scalar values were analyzed with scalar t-tests between subjects and controls. Generalized linear modeling with DTI scalar values was used to predict AHI in subjects.

Results

6 subjects and 61 controls were identified. There was significant sleep dysfunction amongst TBI subjects (mean apnea-hypopnea index (AHI) 5.1+/-6.6 events/hour; mild OSA incidence 33.3%; Pittsburgh Sleep Quality Index (PSQI) mean 13.3+/-2.6). Radial diffusivity (RD), axial diffusivity (AD) and mean diffusivity (MD) were significantly higher among subjects (control RD 9.64x10^-10+/-7.54x10^-11 m^2/s, subject RD 1.13x10^-9+/-1.20x10^-10m^2/s, p = 0.023; control AD 1.32x10^-9+/-7.64x10^-11m^2/s, subject AD 1.50x10^-9+/-1.43x10^-10m^2/s, p = 0.029; control MD 1.08x10^-9+/-7.43x10^-11m^2/s, subject MD 1.25x10^-9+/-1.34x10^-10m^2/s, p = 0.025). There were no differences in age or body-mass index. Generalized linear modeling with diffusivity measures as predictors of AHI in subjects was not significant.

Conclusion

Using a diffeomorphic algorithm to define the hypothalamus reveals significantly elevated scalar DTI measures in chronic, severe TBI compared to controls. DTI differences in the hypothalamus are a novel finding and possibly underlie part of the pathophysiology of TBI. Although this may have potential to serve as a biomarker in severe TBI patients with sleep disorders, these initial data do not support a relationship between DTI and AHI, despite high incidence of OSA and subjective sleep dysfunction. Future studies with more subjects may better elucidate the changes in hypothalamic DTI after TBI for clinical outcomes analysis.

Support (if any)

This work was supported by grant 130132 from USAMRMC.
800 Similarities of Sleep Macrostructure in Cognitively Normal Elderly and Patients with Traumatic Brain Injury
Authors: Williams Ellita , Mullins Anna , Bubu Omonigho , Kam Korey , Parekh Ankit , Blanc Judite , Donley Tiffany , Briggs Anthony , Rogers April , Seixas Azizi , Rapoport David , Ayappa Indu , Jean-Louis Giardin , Dams-O’Conner Kristen , Varga Andrew
Published: May 2021

Introduction

The stability of sleep architecture and breathing across nights can depend on factors relating to the integrity of the nervous system. Traumatic brain injury (TBI) represents a sudden-onset dysfunction of the nervous system while normal aging is associated with more gradual changes to the nervous system. While normal aging and history of TBI are both associated with sleep complaints, less is known about the stability of sleep physiology variables in these populations. Therefore, the aims of our study are to determine which sleep variables have greater night-to-night stability in separate populations of individuals with TBI and in cognitively normal older individuals.

Methods

All volunteers completed 2 consecutive in-laboratory nocturnal polysomnograms (NPSG). The TBI sample (N=35) comprised 71% women and 26% men (average age of 47.3 years). The cognitively normal older sample (N=78) included 74% women and 25% men (average age of 66.4 years). Descriptive statistics and intra-class correlations (ICCs) were calculated for sleep macrostructure variables (total sleep time (TST), sleep efficiency (SE), arousal index (ArI), rapid eye movement (REM), non-REM 1 & 2 (N1, N2), slow-wave sleep (SWS)), and sleep apnea including stage-specific apneas (i.e., AHI4%, AHI3A).

Results

Among volunteers with TBI, ICCs for sleep architecture variables were: TST (0.68), SE (0.65), ArI (0.92), %SWS (0.77), %REM (0.50), %N1 (0.83), %N2 (0.62). ICC’s for sleep apnea variables were: AHI4% (0.86), AHI3A (0.86), REM AHI4% (0.63), REM AHI3A (0.65). Among cognitively normal older volunteers, ICCs for sleep architecture variables were: TST (0.26), SE (0.29), ArI (0.80), %SWS (0.68), %REM (0.39), %N1 (0.66), %N2 (0.49). ICC’s for sleep apnea variables were: AHI4% (0.91), AHI3A (0.92), REM AHI4% (0.85), REM AHI3A (0.83). All ICCs were statistically significant in both groups, except for %N1 among cognitively normal older volunteers.

Conclusion

In both populations, ICC’s for arousal index were greater than for TST or SE. Likewise, ICC’s were higher in %SWS and %N1 than for %N2 or %REM. Breathing variables were more stable than architecture variables. REM-specific breathing variables showed comparatively less consistency, possibly the product of lower ICC’s for %REM sleep versus other sleep stages.

Support (if any)

5T32HL129953-04, R01AG056682, R01AG066870, R21AG059179, 1RF1NS115268-01, K24HL109156, P30AG059303, P30AG066512, AASM 231-BS-20, R25HL105444
809 Innovative electronic sleep mitigation tool for medical trainees
Authors: Tran Danielle , Nelson Kaz , Irfan Muna
Published: May 2021

Introduction

The ACGME (Accreditation Council for Graduate Medical Education) has been advocating for training of medical learners in sleep and fatigue mitigation, in attempt to enhance their wellbeing. While some educational programs include a one-time sleep didactic, prone to being overlooked, there is need for an educational resource which can be accessible to the learners throughout their training span. The trainees’ needs and readiness to learn may vary from time to time, therefore, continued access to educational resources can be very beneficial.

Methods

An electronic tool was created on Coggle, comprising of educational resources and content on the basic tenets of sleep quality, regulation, effects of deprivation and strategies to mitigate these effects. Links to free resources made available by AASM, such as “Choose Sleep,” were also included. The sleep resources were then incorporated in the overall continuum of Graduate Medical Education (GME) resources available to trainees, and was advertised in newsletters, incorporated in orientations (n=324) and wellness sessions (n=254). The GME Institutional Quality of Life data was obtained in 2018–2019 and in 2020 to ascertain baseline and post-intervention measures of wellness, workload and burn-out in trainees.

Results

Data collected in 2020, after introduction of Coggle, demonstrated: 1) A 4% increase of residents (n=1041) would rate their workload as “just right.” 2) A 9% increase of residents (n=1040) said their personal health and wellbeing was “very good” and “good.” 3) A 12% decrease of residents (n=1040) said they felt burned out at work. 4) A 5% decrease of residents (n=1037) said they felt they had become more calloused towards people since they first started training.

Conclusion

The analysis of learners’ feedback demonstrated that access to sleep training resources on a continuous, on-demand basis improved trainees’ personal health and wellbeing. The positive impact was sustained despite unprecedented stress caused by the COVID-19 pandemic. Future steps include: 1) Moving the electronic tool to a more advanced platform with analytical capabilities. 2) Obtaining longitudinal data to assess the impact of the electronic tool on medical trainees’ sleep parameters. 3) Sharing the electronic tool with other organizations to improve wellbeing of all medical trainees and health professionals.

Support (if any):
810 How much does it really cost? Barriers, Bottlenecks and Billing in Sleep Diagnostics
Authors: Jambulingam Nikita , Stretch Robert , Butz David , Zeidler Michelle
Published: May 2021

Introduction

Utilization rates of home sleep apnea tests (HSATs) versus in-lab polysomnograms (PSGs) vary greatly among healthcare institutions. HSATs can provide expanded testing capacity and offload operational bottlenecks in sleep labs, however, the financial benefit of this is not well quantified. Comparison of testing utilization and profitability between institutions can provide greater insight into decisions regarding sleep lab operations and expansion.

Methods

We analyzed profitability of HSATs and PSGs in 2018–2019 at two separate institutions with vastly different operational constraints and healthcare delivery models: Greater Los Angeles VA Healthcare System (GLA-VAHS) and University of California Los Angeles Health System (UCLA-HS). Both institutions own and operate independent sleep labs and offer HSATs for the diagnosis of sleep apnea. Profitability was calculated using contribution margin (CM) which factors out high fixed costs of healthcare infrastructure. CM was calculated by subtracting variable direct costs from revenue.

Results

The non-diagnostic HSAT rate was higher at GLA-VAHS compared to UCLA-HS (30.5% versus 13.1%). At both GLA-VAHS and UCLA-HS, HSATs were more profitable than PSGs on a per-unit basis (CM 47% for HSATs and 29% for PSGs at GLA-VAHS vs. 78% and 66% at UCLA-HS, respectively). Comparing the two institutions, PSGs were 14.8 times more profitable and HSATs were two times more profitable at UCLA-HS versus GLA-VAHS. When analyzed on a per-day basis, HSATs were more profitable at GLA-VAHS but PSGs were more profitable at UCLA-HS.

Conclusion

Reimbursement rates significantly impact institutional decisions to expand utilization of HSATs versus PSGs. Due to higher per-unit reimbursement rates, non-governmental and larger academic institutions may opt to aggressively expand sleep lab capacity. However, risks and benefits of such a strategy should be taken into account in light of changing market patterns and declining reimbursement rates for PSGs. Despite the seemingly higher profitability at the current time, future market volatility in PSG profitability may cause delayed amortization of costs for PSGs at large academic and private institutions compared to the relatively lower cost of expanding HSAT capacity. It may be beneficial for all types of institutions, regardless of current reimbursement rates, to expand HSAT capacity concomitantly with sleep lab expansion to mitigate financial risk.

Support (if any):
816 A Case of obstructive Sleep Apnea in an Adolescent girl with crouzon syndrome
Authors: Tariq Musaddiq , Oscar Rodriguez
Published: May 2021

Introduction

Crouzon syndrome is an autosomal dominant type of craniosynostosis, first reported by French neurologist Octave Crouzon in 1912. Craniosynostosis refers to the premature closure of cranial sutures. The orofacial manifestations of this syndrome includes maxillary hypoplasia, external nasal deformity and prognathism, which can all contribute to breathing difficulties. The prevalence of Obstructive Sleep Apnea (OSA) is above 60%. The severity of obstruction can be life threatening prompting early surgical intervention ranging from tracheostomy to mid facial distraction like LeFort III osteotomy. Report of case(s): An 18-year-old girl with Crouzon syndrome, who was referred for snoring. She had a significant past surgical history of craniotomy and ventricular-peritoneal shunt at the age of 2 years, tracheostomy dependency until the age of 5 years after undergoing a LeFort III osteotomy, and adeno-tonsillectomy at 6 years. She had never had a polysomnography (PSG) before. Her in-lab PSG showed moderate to severe OSA with an Apnea-Hypopnea Index (AHI) of 28.5/hr. She had no central apneas. Obstructive events were not controlled with Continuous Positive Airway Pressure (CPAP), but did respond to Bi-level therapy. Plastic Surgery favored a repeat LeFort III osteotomy and cranioplasty instead. A post-surgical PSG showed resolution of OSA with an AHI of 2.8/hr.

Conclusion

This case reminds us that patients with craniofacial abnormalities are at higher risk for OSA and are more difficult to treat. Our patient had significant sleep apnea despite prior surgical interventions. Patients with Crouzon syndrome should be studied for OSA, and re-assessed over time. Her repeat surgery had a positive outcome, and avoided PAP therapy. Therefore, Plastic Surgery should always be part of the therapeutic discussion.

Support (if any)

1. Samuel N, Arvind B, Sameep K and Eugene M (2014) Revisiting Crouzon syndrome: reviewing the background and management of a multifaceted disease. 2. J Sirotnak 1, L Brodsky, M Pizzuto (1995) Airway obstruction in the Crouzon syndrome: case report and review of the literature. 3. Mitsukawa N, Satoh K, Hayashi T, Furukawa Y, Uemura T (2004) A reflectable case of obstructive sleep apnea in an infant with Crouzon syndrome.
817 A Case of Parasomnia Overlap Disorder in a Patient on Lithium
Authors: Bachuss Amanda
Published: May 2021

Introduction

The literature contains few case reports of parasomnia overlap disorder. There are also few case reports of lithium inducing sleep walking behaviors. Here we seek to present a case of a patient with multiple parasomnias, is taking a number of psychotropic medications for bipolar I disorder, and is on PAP for OSA.

Report of case(s)

The patient is a 43 year old male with a history of occasional mild sleep walking since childhood that remitted approximately 10 years prior to the onset of treatment, but returned when he traveled out of area for a family gathering approximately one year prior to presentation in the sleep clinic. He reported not only the return of sleepwalking, on a nightly basis, as well as more severe symptoms (including enuresis and violence/aggression). He also reported several episodes of dream enactment, as well as a history of sleep paralysis and vivid hypnogogic hallucinations, both of which had been improved in the last year. He denied any history of cataplexy. He did complain of symptoms of significant RLS symptoms. He was partially compliant with CPAP for obstructive sleep apnea, though the sleep behaviors continued regardless of CPAP usage. His psychiatrist had started him on clonazepam (titrated to 2mg/night) prior to his intake in the sleep clinic, but with minimal benefit. His other medications included propranolol 40mg BID, lithium 900mg/1200mg, oxcarbazepine 600mg bid, lamictal 225mg bid, lurasidone 80mg qday, and benztropine 2mg bid. Attended polysomnography demonstrated five episodes of sleep behaviors, as well as loss of atonia during REM, and severe obstructive sleep apnea (AHI of 61.2).

Conclusion

The patients various parasomnias could be due to the side effects of his psychotropic medications, represent a genetic or structural defect that is causing the various parasomnias, or be due to or worsened by his undertreated obstructive sleep apneas. His workup and treatment is still ongoing, but he has continued on clonazepam 2mg but taken 2 hours earlier, and has started a new APAP. Because of the severity of his bipolar disorder (including severe suicidal ideation), he is not a candidate to tapering the lithium or to taking serotonergic antidepressants.

Support (if any):
825 Central Sleep Apnea and Sinus Bradycardia
Authors: Colvert Jared , Greenough Glen
Published: May 2021

Introduction

Central sleep apnea (CSA) is characterized by a lack of respiratory drive during sleep resulting in repetitive periods of apneas. There are multiple manifestations of CSA as defined by the ICSD3. CSA with Cheyne-Stokes Breathing (CSB) is characterized by a series of crescendo-decrescendo pattern of ventilation followed by central apnea and is often associated with heart failure. Bradyarrythmias have been associated with obstructive sleep apnea (OSA), but an association with central sleep apnea is less clear.

Report of case(s)

A 76 y/o male with no significant past medical history but with multiple instances of sinus bradycardia on previous EKGs, was referred to sleep medicine for evaluation of snoring, witnessed apneas, and daytime sleepiness. He had no history of CVA, CHF, atrial fibrillation, renal disease, or opioid use. PSG was completed for suspected OSA, and revealed moderate CSA (AHI 10.9 using hypopnea type 1B criteria, CAI 6.1). Central apneas at the latter portion of the study were consistent with a CSA-CSB. Awake heart rate at time of study was 44 bpm. During sleep, his heart rate ranged from 39–89 with a mean of 57 bpm. Due to this unexpected central apnea finding, cardiac evaluation was recommended and echocardiogram revealed a LVEF of 51%, a dilated left atrium, normal left ventricle chamber size, no wall motion abnormalities, and an inability to assess left sided filling pressures. EKG was consistent with sinus bradycardia without AV blocks. Holter monitor revealed sinus rhythm with moderate burden of ectopy. He underwent CPAP titration which revealed an effective CPAP pressure to control obstructive events, but central apneas persisted without CSB pattern.

Conclusion

In this patient, CSA/CSA-CSB was found in the absence of known risk factors for CSA. Although potentially an early sign of HFpEF related to his longstanding sinus bradycardia, this case raises the question as to whether sinus bradycardia in isolation could decrease cardiac output enough to destabilize ventilation and promote this finding of CSA/CSA-CSB.

Support (if any):
829 Chronic sleep deprivation in a 75-year-old female leading to micro-sleeps with atonia causing increased falls
Authors: Remmers Neeley , Anderson Michael , Nelson John
Published: May 2021

Introduction

Each year, 3 million older people are treated in emergency departments for fall-related injuries. These falls can lead to serious injuries and expensive health care costs. Some have looked into the relationship between chronic sleep disturbances and falls linking chronic sleep deprivation or excessive sleep to falling. Here, we present a unique case of chronic sleep deprivation causing sleep attacks or micro-sleeps with atonia causing falls.

Report of case(s)

We present a 75-year-old F with a history of increased daily falls up to 4x per day that began 3 years ago. She denies any triggering events, auras, frequent tripping, loss of balance or weakness. Reportedly, she will be walking along then suddenly falls. She is aware that she is falling yet feels as though she cannot prevent/stop the fall or break her fall. No one has witnessed her fall, but is frequently found lying on the floor. She has never sustained a serious injury as a result of her falls. She has an 8 year history of restless legs syndrome treated with ropinirole and a 10 year history of obstructive sleep apnea (OSA) treated with CPAP. Her general bedtime is 2200 and wake-time is 0400 with an average 3–4 hrs of quality sleep per night for many years. She endorses severe daytime hypersomnolence and chronic hypoxemia on 3L home oxygen. We hypothesized her falls were secondary to sleep attacks or micro-sleeps where she enters REM sleep and develops atonia. Nocturnal sleep study followed by MSLT showed severe OSA with severe, persistent daytime sleeping with REM sleep and atonia. She had a mean sleep latency of 2 minutes with 1 sleep-onset REM period. We started NIPPV with supplemental oxygen treatment, and within 4 months her daytime hypersomnolence resolved, exercise intolerance improved, saturations improved to 89–90% on room air, and has <1 fall per day.

Conclusion

Here, we presented a unique case of a 75 yo F with recurrent falls secondary to chronic sleep deprivation causing micro-sleeps involving REM sleep and atonia. She was treated with NIPPV which improved her oxygenation and reduced her number of falls to <1 per day.

Support (if any):
833 Evolution of sleep disordered breathing types in heart failure
Authors: Anne Pratibha , Koothirezhi Rupa , Okorie Ugorji , Tam Ho Minh , Monceaux Brittany , Liendo Cesar , Asghar Sheila , Chernyshev Oleg
Published: May 2021

Introduction

Central sleep apnea is commonly seen in patients with heart failure. Here we present a case demonstrating shifting of predominant apneic events from central to obstructive type after placement of left ventricular assist device (LVAD) in end stage heart failure patient.

Report of case(s)

Case Presentation: 66 year-old African American male has past medical history of chronic congestive heart failure diabetes, hypertension, paroxysmal atrial fibrillation, anemia, hypothyroidism, chronic kidney disease and sleep apnea. Prior to his LVAD placement, his left ventricular ejection fraction (EF) was <10%. Patient was diagnosed with central sleep apnea with AHI of 58 (with 92% of apneic events being central events), oxygen nadir of 74%. Subsequently, patient had LVAD placed for symptomatic heart failure and repeat polysomnogram repeated at six month demonstrated an improved AHI of 45.8 with predominantly obstructive and mixed apneic events, with only 12.5% being central events.

Conclusion

This case report highlights not only the improvement of the sleep apnea in CHF treated with LVAD but also shows the shift of apneic events from predominantly central to obstructive type post LVAD.

Support (if any)

1. Henein MY, Westaby S, Poole-Wilson PA, Cowie MR, Simonds AK. Resolution of central sleep apnoea following implantation of a left ventricular assist device. Int J Cardiol. 2010 Feb 4;138(3):317–9. PMID: 18752859. 2. Köhnlein T, Welte T, Tan LB, Elliott MW. Central sleep apnoea syndrome in patients with chronic heart disease: a critical review of the current literature. Thorax. 2002 Jun;57(6):547–54. PMID: 12037232 3. Monda C, Scala O, Paolillo S, Savarese G, Cecere M, D’Amore C, Parente A, Musella F, Mosca S, Filardi PP. Apnee notturne e scompenso cardiaco: fisiopatologia, diagnosi e terapia [Sleep apnea and heart failure: pathophysiology, diagnosis and therapy]. G Ital Cardiol (Rome). 2010 Nov;11(11):815–22. Italian. PMID: 21348318.
834 Help Me Stop Eating Please…
Authors: Arslan Ahmad , El Ali Mazen , Atwood Charles
Published: May 2021

Introduction

Sleep related eating disorder (SRED) is an uncommon NREM parasomnia, predominantly seen in females in their 20s and 30s and is commonly associated with sleep walking, daytime eating disorders (anorexia and bulimia) and use of certain sedative-hypnotics. Here, we describe a case of unique therapeutic dilemma in a middle-aged female, in whom SRED affected the use of continuous positive airway pressure device (CPAP) for her obstructive sleep apnea (OSA) which lead to worsening sleep quality and daytime functionality.

Report of case(s)

42-year-old female with history of migraines and OSA, came to the clinic with 6-month history of SRED which started after the demise of her husband and was associated with significant weight gain and injuries. During typical episode, she would take CPAP mask off, walk down the stairs and eat in the kitchen area and then fall asleep in the living area. She denied predilection for particular food, food allergies, consumption of inedible materials or use of offending drugs. Upon further inquiry, she reported recent unsuccessful attempts at smoking cessation, frequent nighttime smoking, significant body image issues and discontinuation of topiramate use for her migraines recently. Telemedicine visit limited the physical examination but included increase in BMI from 32 to 35 kg/m2. Compliance report, sleep diary and surveillance videos were consistent with the history with compliance report showing 17% of nights with optimal usage and 59% of nights with any usage. Beside locking the food, safety measures and napping, we recommended her to use clonazepam 1.5 mg. Unfortunately, she continued to have episodes. She was then started on Topiramate 50 mg which was gradually increased to 100 mg with reduction in her episodes and increase in her compliance to 60%.

Conclusion

In sleep medicine, treatment of OSA usually precede the treatment of comorbid conditions. However, SRED with comorbid OSA, requires a reverse strategy where improvement in compliance and coexisting daytime symptoms requires the treatment of SRED first. Moreover, detailed history to investigate the potential precipitating factors, co-existing medical and sleep conditions can help with choice of therapy e.g. patients with depression and SRED can benefit from Selective Serotonin Reuptake Inhibitors rather than other choices.

Support (if any):
835 Ictal Central Apneic Events Detected on Polysomnogram: An Educational Case Report
Authors: Shenoy Shanti , Chen Hai , Karroum Elias
Published: May 2021

Introduction

Ictal central apneas (ICA) are frequently observed in focal epilepsy, mostly with temporal lobe seizures, and have been considered as potential biomarkers of sudden unexpected death in epilepsy (SUDEP), particularly when they are prolonged and associated with significant hypoxemia. We present an interesting educational case report of occurrence of such ictal apneic events as recorded during a nocturnal diagnostic polysomnogram (PSG).

Report of case(s)

A 39-year-old woman with history of left focal epilepsy, hypertension, and headaches was referred to the sleep clinic for loud snoring, witnessed apneic events, and excessive daytime sleepiness. She subsequently underwent a diagnostic (PSG) that demonstrated severe obstructive sleep apnea (apnea-hypopnea index of 63.1) associated with significant hypoxemia (nadir SpO2 of 58%). In addition, the patient had one ictal discharge detected on the PSG’s limited electroencephalogram that occurred in N2 sleep and lasted for almost three minutes with a focal onset and progression in the left hemisphere. The ictal discharge was briefly preceded by central apneic events that continued to occur during and shortly after the termination of the ictal discharge. These ICA events were associated with severe oxygen desaturations down to an SpO2 of 62%. The only time during the PSG recording that the patient had central apneic events was around the ictal event. There were no behavior changes on the video during the seizure, but the ictal discharge was associated with a sustained increase in the mentalis muscles activity and a brief tachycardia. The patient’s neurologist was alerted about the above findings on PSG. The patient was taking a lower dose then prescribed of her anti-epileptic medication (topiramate) that was adjusted, and the patient was counseled on the risks associated with the above findings and positive airway pressure therapy was recommended for her severe sleep apnea.

Conclusion

The above case report illustrates the importance of polysomnography (specifically the recording of respiratory variables rarely performed in epilepsy monitoring units) in the evaluation of patients with epilepsy given that central apneic events (ICA and post-convulsive central apneas) potentially underlie SUDEP, the most common cause of mortality in refractory epilepsy patients and usually occurring during sleep.

Support (if any)

None
841 PAP Therapy Data Provides Clues To Comorbid Sleep Disorders
Authors: Bartley Bethany , Cai Alice , Epstein Lawrence
Published: May 2021

Introduction

Obstructive sleep apnea (OSA) is a common condition and positive airway pressure (PAP) therapy is the treatment of choice. Treatment guidelines recommend monitoring objective PAP usage data to track treatment efficacy. A typical report includes the percentage of days/month and cumulative hours/day a PAP device was used. In addition, PAP therapy timing can be graphically viewed with use plotted by time/day. This latter presentation reveals patterns of usage that can identify comorbid sleep disorders.

Report of case(s)

Case 1: A 65-year-old male with OSA presented with sleep inertia despite compliance with PAP therapy. Therapy timing data revealed a delayed circadian phase, with bedtime of 4 am and wake time of 1 pm. Circadian phase advancement therapy was added. Case 2: An 86-year-old male with OSA presented with daytime sleepiness after years of excellent PAP usage. Two years earlier, he was diagnosed with Parkinson’s disease and developed increasing afternoon sleepiness. Compliance data showed a mild reduction in PAP usage. However, therapy timing data revealed an irregular sleep-wake rhythm disorder with sleep scattered around the clock, consistent with neurodegenerative disease. Case 3: A 70 year-old-female with PTSD and OSA presented with persistent tiredness and difficulty initiating and maintaining sleep despite good compliance with PAP therapy. Her timing data showed irregular sleep times with long gaps in usage suggestive of sleep maintenance insomnia. After starting a behavioral treatment regimen her pattern regularized and awakenings reduced, seen by consistent PAP use. Case 4: An 80-year-old female with OSA complained of early morning awakenings despite PAP use with good compliance. Review of PAP therapy timing revealed a pattern suggestive of advanced sleep-wake phase disorder. Circadian phase delay therapy was started.

Conclusion

Patients with OSA on PAP therapy may have comorbid sleep disorders impacting sleep quality. PAP therapy data can provide information on sleep-wake behavior similar to actigraphy to help diagnose these conditions and track treatment response.

Support (if any)

None
842 PAP Therapy in a Pandemic: Management of Severe Mixed Apnea Predominant OSA & CSA during the COVID-19 Pandemic
Authors: Okorie Ugorji , Koothirezhi Rupa , Anne Pratibha , Chernyshev Oleg , Liendo Cesar , Monceaux Brittany
Published: May 2021

Introduction

Introduction/Background: A new protocol and standard of care was created amidst the COVID-19 Pandemic that began in 2020. Traditional split night studies fell out of favor and were replaced by solely diagnostic studies with placement on Auto-PAP therapy if treatment of sleep disordered breathing was required. Some patients, however, required a more tailored approach if diagnostic polysomnogram (PSG) was particularly concerning. Our case report describes the treatment of a patient with severe Mixed Apnea Predominant Obstructive Sleep Apnea (OSA) with accompanying Central Sleep Apnea (CSA) using COVID-19 Precautions.

Report of case(s)

Case Description: A 48 year old AAM patient with a PMH of HTN, pre-diabetes, GERD, obesity and tobacco abuse initially presented to Sleep Medicine in late January 2020 with complaints of snoring, witnessed apneas, waking up gasping, excessive daytime sleepiness, fatigue, and non-restorative sleep for many years with ESS 24 and FSS 48 on initial evaluation. Diagnostic PSG showed AHI 76.9 with O2 desaturation to 59% and demonstrated the presence of severe Mixed Apnea predominant OSA and CSA with worsening during REM sleep. Because of the severity, he underwent a PAP titration in August 2020 using the AASM COVID-19 sleep study precautions which included use of a negative pressure room. Optimal control of snoring, apneic respiratory events and oxygen desaturations was achieved at 14 cm H2O in the supine body position during REM sleep. Follow up with Sleep Medicine in October and December 2020 showed objective compliance over a 30 day period not completely at goal due to issues with mask desensitization and sleep hygiene, however the patient subjectively reported that he noticed great improvement in snoring, excessive daytime sleepiness and fatigue.

Conclusion: Discussion/Conclusion

With a diagnosis of Severe Mixed Apnea Predominant OSA as well as CSA noted during the study, the differential diagnosis included CHF, Chiari malformation, opioid abuse and idiopathic CSA as the cause. Despite a dangerous pandemic, appropriate therapy for certain patients must still be attained. Special protocols developed during the COVID-19 Pandemic allowed for our patient to receive adequate treatment, while ensuring the safety of all involved.

Support (if any)

References COVID 19: FAQs for Sleep Clinicians. AASM official website. https://aasm.org/covid-19-resources/covid-19-faq/
843 Paradoxical Waking Hypoxemia that Improves with Sleep
Authors: Cho Jessica , Dai David , Fung Constance
Published: May 2021

Introduction

We present a case of paradoxically worsened hypoxia during wake phase of polysomnography while undergoing a CPAP titration study. Nighttime hypoxemia is a common feature in obstructive sleep apnea, due to obstructive events that manifest while sleeping. Excluding OSA, there remains an extensive differential for disease processes that cause hypoxemia while asleep; however, none of these processes can explain waking hypoxemia that improves upon sleeping.

Report of case(s)

A 70 year old male with severe OSA diagnosed by home sleep test (REI 46.5, nadir O2=76%) underwent polysomnography with PAP titration and demonstrated several hours of interrupted sleep without hypoxia and minimal obstructive events on CPAP 9–13 cmH2O. During the study, while awake at CPAP of 14 cmH2O, he developed hypoxia to mid-high 80s and supplemental oxygen bleed in was added starting at 3L and increased to 5L during a prolonged period of wakefulness. On CPAP 15 cmmH2O with 5L bleed-in, the patient fell asleep and oxygen saturation again increased to low 90s. He underwent an extensive workup for other cardiopulmonary causes of hypoxemia, with pulmonary function testing showing moderate obstructive ventilatory defect and mild DLCO impairment. An echocardiogram with saline contrast bubble study was relatively unremarkable, without evidence of right to left shunting. He underwent a chest CTA which was negative for pulmonary embolism, though it did reveal an enlarged pulmonary artery consistent with pulmonary hypertension. His chronic hypoxemia was treated with 2L supplemental oxygen during the day and bleed-in with CPAP at night.

Conclusion

Though nocturnal hypoxemia is common with OSA, polysomnography with paradoxical hypoxemia during wake phase has not been reported. Notably, the patient was without prolonged hypoxia during his sleep phase while on CPAP treatment with minimal apneic/hypopneic events. Pulmonary hypertension can also present as nocturnal hypoxemia, but it should worsen with sleep, rather than improve. There are case reports of right to left shunting worsened by PAP, though his hypoxemia persisted despite PAP. His paradoxical worsening hypoxemia with wakefulness is still unexplained.

Support (if any):
844 Pediatric Vagus Nerve Stimulator-Induced Obstructive Sleep Apnea
Authors: Nouraddin Nouraddin , Amos Louella
Published: May 2021

Introduction

Vagus nerve stimulation (VNS) is an adjunct treatment for seizures refractory to medications. VNS in children with epilepsy can reduce seizures by up to 90%. VNS settings include stimulation on-time, off-time, frequency and output current. Complications of VNS include sleep-disordered breathing due to laryngopharyngeal dysfunction, which can also cause voice alteration, hoarseness, and cough. Both obstructive apneas (more common) and central apneas can be seen in those patients who have VNS-induced sleep-disordered breathing.

Report of case(s)

A 14-year-old male with Lennox-Gastaut syndrome treated with multiple antiepileptic drugs and VNS was admitted to the PICU with worsening seizures. He developed acute respiratory failure due to status epilepticus, requiring intubation. After extubation, he was observed to have repetitive respiratory obstruction at regular intervals, occurring throughout the day and night, and associated with mild oxygen desaturations. Polysomnography showed cyclical obstructive respiratory events lasting 30 seconds followed by approximately 2-minute intervals of regular breathing. Interrogation of his VNS device revealed the following settings: output current of 1.75 mA, 30 seconds on, and 1.8 minutes off. CPAP therapy improved his oxygen saturations, but he continued to clinically exhibit the repetitive obstructive apneas even on positive pressure. However, after his VNS device settings were decreased, repeat polysomnography showed resolution of his obstructive breathing.

Conclusion

This case report demonstrates pediatric VNS-induced obstructive sleep apnea. Activation of the vagus nerve can cause laryngopharyngeal dysfunction, including laryngospasm and vocal cord dysfunction, with subsequent upper airway obstruction, causing obstructive apneas or hypopneas. Treatment options for pediatric VNS-induced OSA include CPAP, decreasing the VNS settings and adenotonsillectomy.

Support (if any):
845 Progressive external ophthalmoplegia in sleep apnea presenting as floppy eyelid syndrome
Authors: Anne Pratibha , Koothirezhi Rupa , Okorie Ugorji , Tam Ho Minh , Monceaux Brittany , Liendo Cesar , Asghar Sheila , Chernyshev Oleg
Published: May 2021

Introduction

Floppy eye lid syndrome (FES) is known to be associated with Obstructive sleep apnea (OSA) and chronic progressive external ophthalmoplegia (CPEO) is a rare genetic disorder with mitochondrial myopathy that may present with isolated eye lid ptosis in the initial stages. In a patient with loud snoring and obesity, treating obstructive sleep apnea may improve Floppy eyelid syndrome.

Report of case(s)

52-year-old African – American male with past medical history of Hypertension, obesity, glaucoma, CPEO status bilateral blepharoplasty with failed surgical treatment. Patient was referred to Sleep medicine team to rule out Obstructive Sleep Apnea aa a cause of possible underlying FES and residual ptosis. On exam, patient was noted to have bilateral brow and eyelid ptosis and mild ataxic gait. MRI brain with and without contrast was unremarkable. Deltoid muscle biopsy was suggestive of possible congenital myopathy and mild denervation atrophy. Polysomnogram showed severe OSA with AHI of 74.1 per hour and patient was initiated on Auto CPAP at a pressure setting of 7–20 cm H2O. CPAP treatment improved snoring, OSA and subjective symptoms of excessive day time sleepiness but did not improve the residual ptosis.

Conclusion

Treatment of severe OSA in a patient previously diagnosed with CPEO and failed surgical treatment with bilateral blepharoplasty, did not alter the course of residual ptosis/ floppy eyelids even though his other sleep apnea symptoms have improved.

Support (if any)

1. McNab AA. Floppy eyelid syndrome and obstructive sleep apnea. Ophthalmic Plast Reconstr Surg. 1997 Jun;13(2):98–114. doi: 10.1097/00002341-199706000-00005. PMID: 9185193.
849 REM Behavioral Disorder as a Predictor of Lewy body Dementia- A Case Report
Authors: Koothirezhi Rupa , Anne Pratibha , Ho Minh Tam , Monceaux Brittany , Liendo Cesar , Chernyshev Oleg , Kilaikode Sasikumar , Okorie Ugorji
Published: May 2021

Introduction

Dementia with Lewy bodies (DLB) is one of the most common types of degenerative dementia after Alzheimer’s dementia. The core clinical features for diagnosis includes cognitive fluctuations, visual hallucinations, rapid eye movement (REM) sleep behavior disorder (RBD), and parkinsonism. Other symptoms include daytime drowsiness, longer daytime naps, prolonged staring spells, and episodes of disorganized speech. REM behavioral disorder (RBD) is commonly associated with DLB, occurring in 85 percent of individuals, often early in the course of the disease. It can precede the clinical diagnosis of DLB by up to 20 years.

Report of case(s)

A seventy-six-year-old female with a history of well controlled obstructive sleep apnea was diagnosed with REM behavioral disorder in 2012. She had presented with episodes of screaming, attempt to ambulate during sleep, resulting in injury. Her polysomnogram revealed evidence of REM without atonia and a screaming episode during REM. Her RBD symptoms were controlled with clonazepam and melatonin with less frequency of the RBD episodes. The patient gradually started noticing memory issues and by January 2020 she was diagnosed with dementia and was initiated on Aricept. Within 7 months of diagnosis of dementia, she started reporting vivid hallucinations that were not threatening or violent compared to her violent content of RBD. Physical exam revealed impaired cognitive function and mild intermittent resting tremor of the right hand. The neurological exam was normal including normal tone, strength, and gait. She also reported repeated falls and fractures. The diagnosis of Lewy body dementia was made based on the presence of 2 core clinical features.

Conclusion

The current management of these conditions is mainly symptomatic. In the evolution of neurodegenerative disorder, RBD precedes other conditions like LBD, parkinsonism, etc. Research suggests that alpha-synuclein neurodegeneration is the common pathology behind these conditions. The understanding that RBD presents at the beginning of the evolution, provides us with a unique opportunity for preemptive treatment to prevent further degeneration in turn preventing the debilitation consequence like dementia, parkinsonism, neuroleptic sensitivity, and dysautonomia. Further research is needed for developing these early interventional strategies.

Support (if any)

NOne