bluuebunny/crossref_metadata_2025_split huggingface dataset:
816 A Case of obstructive Sleep Apnea in an Adolescent girl with crouzon syndrome
Authors: Tariq Musaddiq , Oscar Rodriguez 
Published: May 2021

Abstract

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

Abstract

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.
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825 Central Sleep Apnea and Sinus Bradycardia
Authors: Colvert Jared , Greenough Glen 
Published: May 2021

Abstract

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.
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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

Abstract

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 &lt;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 &lt;1 per day.
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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

Abstract

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 &lt;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

Abstract

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

Abstract

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

Abstract

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

Abstract

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

Abstract

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):