bluuebunny/crossref_metadata_2025_split huggingface dataset:
1150 Isolated Nightmares: An Unusual Presentation of Narcolepsy?
Authors: Moawad Katherine , Raizen David 
Published: April 2024

Abstract

Introduction
A nightmare involves an internally generated conscious experience of negative emotional valence. Nightmares typically occur during REM sleep, which is most prevalent during the second half of the night. A young female presented with isolated nightmares, occurring near sleep onset and raising suspicion for narcolepsy.

Report of case(s)
A 21-year-old female presented to the sleep center due to experiencing daily nightmares for five years. Nightmares were described as “super realistic”, “distressing”, and occurred minutes after sleep onset. Nightmare content varied. Some of her nightmare themes included an apocalypse, family members dying, and animals chasing her. She had a remote history of anxiety and was previously prescribed sertraline, which had been discontinued two years ago. She reported no hallucinations, cataplexy, sleep paralysis, dream enactment or excessive sleepiness. She had been using a hormonal transdermal patch for about 2 years. On physical exam, she was noted to have mild bilateral proptosis with white sclera visible above the iris on primary gaze. Polysomnography (PSG) revealed a sleep onset latency of 30.5 minutes, N1 1.5%, N2 47.5%, N3 20.9%, and REM 30.1%. REM sleep latency was short at 63.5 minutes. There were 21.6 arousals per hour. The apnea-hypopnea index was of 0.3 events per hour. The PSG was followed by a multiple sleep latency test (MSLT), which measured a mean sleep latency of 5 minutes 42 seconds during five nap opportunities. The patient experienced REM sleep in both the first and third nap, with a REM sleep latency of 4.5 minutes. The patient’s MSLT revealed pathological sleepiness, which supported a diagnosis of narcolepsy without cataplexy, although the patient reported nightmares and not sleepiness.

Conclusion
This is an atypical presentation for narcolepsy, which is characterized by REM sleep abnormalities. Further research, classifications, and diagnostic criteria for clinical REM phenomena associated with narcolepsy should be investigated. Clinicians who treat patients with narcolepsy should monitor not only the characteristic symptoms of narcolepsy, such as cataplexy or sleepiness, but also inquire about oneiric activity.

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1159 The Cyclical Daytime Sleeper: A Rare Case of a Sighted Teenager with Non-24-Hour Sleep-Wake Disorder
Authors: Nguyen Andrea , Chaung Matthew , Valenzuela Andrew 
Published: April 2024

Abstract

Introduction
Daytime fatigue in teenagers may be hand-waved as hours of screen time the night before and it can be difficult for families to accurately describe sleep habits. These factors quite often obscure an underlying sleep disorder. Here we report the rare case of a sighted teenage patient who presented with sleep disturbance and erratic bedtimes and was found to have non-24-hour sleep wake disorder (N24SWD).

Report of case(s)
16-year-old male with a past medical history of ADHD and insomnia, presented to clinic for evaluation of recurrent and inappropriate sleep time with residual hypersomnolence. Pediatrician first saw the patient for difficulty waking up for school as well as trouble falling asleep at night. Initially, it was suspected to be insomnia due to poor sleep hygiene secondary to significant electronic usage prior to bedtime. When symptoms did not improve, the patient was started on hypnotics including clonidine to help with sleep and daytime stimulant medication was adjusted to help with wakefulness. Pharmaceuticals did not help with sleep symptoms, and the patient’s hypersomnolence led to cyclical absenteeism from school and risk for expulsion. On initial presentation to the sleep clinic, patient and family had difficulty describing his erratic sleep routine. Two weeks of sleep diaries were provided to help characterize the patient’s sleep patterns. No suspicion for sleep disordered breathing, parasomnias nor restless leg syndrome were noted. Sleep diary showed a sleep pattern delaying consistently by 1-2 hours each day. Total sleep each night was 7-9 hours, with sleep onset latency of 30 minutes and no significant awakenings. This activity is classic for non-24 sleep-wake phase disorder. This patient was treated with a combination of timed tasimelteon and bright light therapy along with chronotherapy for resynchronization of the intrinsic circadian rhythm.

Conclusion
N24SWD is commonly seen in blind individuals affecting up to 50% of that population. It is very rare in sighted individuals, and may be harder to discern when confounded with conditions like ADHD or poor sleep hygiene. Having patients complete a sleep diary is a cost effective and low investment intervention that may elucidate their condition and ensure timely treatment.

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1161 From Restless to Rest – the Use of Methadone to Treat Complex RLS in Patients with Sleep Apnea: A Case Series
Authors: Bean Steven , Patel Abha 
Published: April 2024

Abstract

Introduction
Typically, patients with restless leg syndrome (RLS) respond well to standard therapies such as dopamine agonists and alpha-2-delta calcium channel ligands. However, patients with refractory RLS may require opioids for optimal disease control 1. In the setting of concomitant obstructive sleep apnea (OSA), characterized by upper airway collapse leading to recurrent episodes of upper airflow obstruction and intermittent hypoxemia, opioids can further increase respiratory depression. Consequently, many clinicians may be hesitant to prescribe opioids in such patients. The following cases highlight chronic opioid use in patients with concurrent RLS and OSA.

Report of case(s)
Case 1: A 77 year-old man with OSA on continuous positive airway pressure (CPAP) presented to sleep clinic for optimization of longstanding RLS. Initial interventions with standard therapy were ineffective. He was started on methadone with good control of his symptoms, but eventually developed central apneas. He was subsequently switched to BiPAP ST with a residual AHI of 2.6 events/hr. His RLS remained stable on methadone 10-12.5 mg night. Case 2: A 72 year-old man with a history of low back pain previously managed with opioids, presented to sleep clinic for severe OSA and RLS. His RLS symptoms were initially controlled with gabapentin and pramipexole, but he experienced augmentation after self-titrating to high doses. His RLS was optimized with methadone 10 mg. However, he could not tolerate CPAP despite multiple interventions. In order to continue methadone, he lost 60 pounds with significant improvement in his OSA on repeat testing (AHI 6.1 events/hr). He was able to maintain weight loss and continue methadone therapy. Case 3: A 77 year-old female with long standing RLS on methadone for 20 years presented to sleep clinic for follow up of RLS. Her RLS was refractory to standard therapy. Since initiation of methadone, she gained significant weight. A repeat sleep study demonstrated moderate OSA (AHI 28.3 events/hr). She did well on CPAP with excellent compliance (Residual AHI 5.8 events/hr). She remained stable on methadone 20-30 mg daily.

Conclusion
Here we demonstrate that in the right setting, patients with RLS in the setting of OSA can be safely treated with opioid medications.

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1162 Keratoconus in an Adolescent with Obstructive Sleep Apnea
Authors: Purewal Jaskaran , Jayakumar Archana , Perez Iris 
Published: April 2024

Abstract

Introduction
Obstructive sleep apnea (OSA) is common in pediatrics. Signs of OSA vary between patients commonly reflecting an obstructed upper airway with hypoventilation and hypoxemia. There is less knowledge of the ophthalmologic findings in OSA. Corneal thickness is sensitive to oxygen desaturations that occur during sleep and may contribute to the development of keratoconus. Based on the IRIS Registry, the prevalence of keratoconus in adults is 2.9% compared to 0.27% in pediatrics. We describe a pediatric patient with keratoconus, who was found to have severe OSA.

Report of case(s)
14-year-old male with history of obesity, tonsillar hypertrophy and bilateral keratoconus s/p corneal crosslinking was admitted to the hospital for corneal transplant. Post-operatively, it was difficult to wean the patient off oxygen and inpatient he required 3L oxygen due to significant nocturnal hypoxemia. With concurrent morning headaches, witnessed apneas and weight gain (BMI 52.7, &gt;99th percentile) the patient underwent an inpatient split night polysomnogram. Results revealed severe OSA (AHI 123/hr) and hypoxemia (O2 baseline 89-91%, nadir 64% O2, ODI 105.1/hr, &lt; 90% for 40% of TST) without significant hypoventilation (PETCO2 43 - 54mmHg, &gt;50mmHg for 1% TST). He was titrated to CPAP 15cm H2O with resolution of sleep apnea (AHI 0.7, SpO2 92 - 98%). Echocardiogram showed normal right ventricular size, ejection fraction and negative for signs of pulmonary hypertension. Chest x-ray was unremarkable. He was initiated on PAP therapy, and subsequently underwent adenotonsillectomy 5 months later. He continues to follow with ophthalmology and uses prednisolone eyedrops regularly.

Conclusion
Ocular presentations are a less recognized sign of OSA particularly in pediatric patients. In adults, the intermittent hypoxemia and airflow limitations could contribute to ocular pathology and severity in presentation. Keratoconus has been associated with elevated levels of matrix metalloproteinases and protease inhibitors, which may play a role in corneal thinning in individuals with OSA. Pediatric keratoconus has been described as more aggressive compared to adults leading to more rapid deterioration. The progression of ocular disease in our patient may have been a consequence of untreated OSA. Our report highlights the importance of early recognition and treatment of OSA in pediatric patients.

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1167 Chasing Centrals
Authors: Jordan Melissa , Bliton Kyle , Patterson Patricia , Aulakh Puneet 
Published: April 2024

Abstract

Introduction
Distinguishing between obstructive and central hypopneas raises a clinical challenge when evaluating sleep apnea. Currently, absence of snoring, inspiratory flow limitation, and paradoxical thoraco-abdominal excursions can aid in identifying a central hypopnea. Defining these events is imperative as it affects options for therapy. This case highlights the importance of appropriate classification of central hypopneas.

Report of case(s)
A 57 YO F with PMH of HTN presents for snoring, frequent awakenings, and suffocation disrupting sleep. Her BMI is 35.5. Epworth Sleepiness Scale is 15. She has a family history of sleep apnea. Her STOP-BANG score is 4. In conjunction with sleep disordered breathing evaluation, she was undergoing neurologic evaluation of oropharyngeal dysphagia resulting in ILD from aspiration, weakness and numbness in bilateral hands, and worsening balance. Imaging showed a Chiari 1 Malformation. She underwent PSG to evaluate SBD and split for CPAP titration due to frequent apnea and hypopnea events. Despite titration, events worsened. Upon further review of the study, it was noted the hypopnea events were majority central in nature. The diagnostic portion showed 32 central apneas, 2 obstructive apneas, 0 mixed apneas, 49 central hypopneas and 4 obstructive hypopneas. The total AHI was 44/h with a central index of 42/h and O2 nadir of 71% with O2 less than 88% for 70 minutes. She returned for ASV versus Bipap ST titration. Again, pressures were increased due to presence of hypopneas and at the termination of the study, apnea was poorly controlled. The residual AHI of 50/h on BIPAP 18/8 rate 16. Review of PSG found optimal settings to be BIPAP 15/6 rate16. AHI on these settings was 8.9/h, nadir SPO2 82%. She is currently scheduled for chiari decompression.

Conclusion
This case demonstrates that detection of central hypopneas affects ability to titrate PAP therapy and determine best treatment options. This case is further complicated by a clinical history concerning for obstructive sleep apnea.

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Javaheri S, Rapoport DM, Schwartz AR. Distinguishing central from obstructive hypopneas on a clinical polysomnogram. J Clin Sleep Med. 2023 Apr 1;19(4):823-834. doi: 10.5664/jcsm.10420. PMID: 36661093; PMCID: PMC10071374.
1169 Hypersomnia in an Adolescent Following COVID-19 Infections
Authors: Long Ariel , Hussain Shahnoor , Viorritto Erick 
Published: April 2024

Abstract

Introduction
The International COVID-19 Sleep Study found a 2 to 3-fold increase in hypersomnolence in persons reporting COVID-19 infection. Although the pathophysiology of COVID-19-associated hypersomnolence is still unclear, a para-infectious pathogenesis has been proposed, similar to cases of post-influenza narcolepsy observed following the Spanish flu epidemic of 1918.

Report of case(s)
A 16-year-old male presented to neurology clinic with complaints of fatigue, anorexia and headaches. His parents reported the sudden onset of excessive daytime sleepiness and sleep attacks in September 2022, severely impacting his daytime functioning. His reported sleep duration was appropriate for his age, and sleep hygiene was adequate. He denied cataplexy and hallucinations, but was having sleep paralysis 1-2 times weekly. He had never been vaccinated against COVID-19, and had two confirmed COVID-19 infections in January and June of 2022. His laboratory evaluation showed no other infectious causes, nor evidence of thyroid dysfunction or other endocrine abnormalities. His brain MRI was unremarkable. In April 2023, he had an overnight polysomnography followed by a multiple sleep latency test. PSG total sleep time was 7 hours and 22 minutes, and sleep efficiency was 93.1%. His sleep latency was 5.3 minutes and REM latency was 99 minutes. His AHI was 1.9 events per hour and his SpO2 nadir was 89%. The mean sleep latency on his MSLT was reduced, at 4 minutes and 36 seconds, and there were no sleep-onset REM periods. At his sleep clinic evaluation in April 2023, his Epworth Sleepiness Scale (ESS) score was 22. He was started on Adderall, which caused severe mood changes and worsening anorexia. This was switched to Modafinil, with significant improvement in subjective sleepiness, and his ESS score was 3 at follow-up.

Conclusion
Untreated hypersomnia has been associated with behavioral problems, mood disturbances, depression, and impaired neurocognitive function especially in adolescents. Hypersomnia is also associated with long-term increased risk of cardiovascular, endocrine, and metabolic disorders. According to the World Health Organization, there have been over 700 million confirmed COVID-19 cases to date. Given the health implications of hypersomnia, the relationship between COVID-19 and CNS hypersomnia and its etiology needs further investigation.

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0118 Sleep Quality Among Sexually Abused and Non-abused Females in the Female Growth and Development Study
Authors: Omisakin Olusola , Dungula Francisca , Master Lindsay , Noll Jennie , Buxton Orfeu 
Published: April 2024

Abstract

Introduction
Lower sleep quality in adulthood can be a manifestation of trauma experienced during earlier stages of development. Sleep problems are also common among adults with chronic health conditions, such as diabetes and heart disease. However, there is scarcity of evidence on potential moderating effect of chronic health conditions in the association between post-traumatic stress disorder (PTSD) and poor sleep in adulthood. We examined the relationship between PTSD symptoms (PTSS), biomarkers of diabetes type 2, and sleep health.

Methods
Participants are comprised of sexually abused (as children) and non-abused females from the Female Growth and Development Study (FGDS), a longitudinal study following participants across seven waves from childhood to adulthood (1987-2019). From Comprehensive Trauma Interviews at waves 4-6, we identified trajectories of PTSD using growth mixture modeling. At wave 7, actigraphy was conducted and blood samples were used to measure Hemoglobin A1C. We focused on participants with ≥ 3 valid days of actigraphy data (n = 100). Analysis of covariance (ANCOVA) examined the relationship between PTSS, Hemoglobin A1C (normal, prediabetes, diabetes) and sleep [duration, efficiency, and wake time after sleep onset (WASO)], controlling for sexual abuse status, age and race.

Results
Over half of the participants (51%) ever had PTSS and 16% had HbA1C at prediabetes or diabetes stages. Although ANCOVA results did not detect significant interaction effects of PTSS and diabetes on sleep, we found heterogeneity in the distributions of the sleep measures. For instance, sleep efficiency was lower among participants who had co-occurrence of PTSS and prediabetes /diabetes (M = 88.0 %, SD = 5.1) relative to those who had prediabetes /diabetes but no PTSS (M = 91.1 %, SD = 2.0). Compared with participants with prediabetes /diabetes but no PTSS (M = 39.9 min/night, SD = 12.8), those with PTSS and prediabetes had greater mean WASO (M = 50.0 min/night, SD = 21.6).

Conclusion
Participants who had both PTSS and prediabetes/diabetes experienced elevated sleep problems. Future research should investigate how chronic health conditions may affect sleep among individuals with PTSS related to childhood maltreatment.

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T32HD101390, R01AG059682, R01HD072468, R01AG04879
1185 Cheyne-Stokes Respirations and Central Sleep Apnea in the Setting of Lacunar Infarct: A Case Report
Authors: Tripathi Poulomee , Murray Robert 
Published: April 2024

Abstract

Introduction
Cheyne-Stokes respirations and central sleep apnea have been correlated to large areas of cerebral infarction and with smaller events such as transient ischemic attacks. Few studies and cases have analyzed and reported the association between Cheyne-Stokes respirations and lacunar infarct, an intermediary of the two extremes of cerebral events.

Report of case(s)
Mr. T is an 87 year old male who originally was referred to the University of Kentucky sleep medicine clinic due to symptoms of worsening daytime hypersomnia and snoring; he had never had a sleep study. His Epworth Sleepiness Scale score was 11. Patient underwent sleep study, which found severe obstructive sleep apnea with concern for Cheyne-Stokes respirations and central sleep apnea. Medications were reviewed, none of which were contributory. With patient’s history of transient ischemia attack and atrial fibrillation, work up included an echocardiogram, which showed an ejection fraction of 50-60%, CPAP titration study, which showed severe CSA, and an MRI brain, which showed evidence of old lacunar infarct. Ultimately, the patient had BIPAP S/T titration which ordered pressures of 21/13 and rate of 12. Currently patient’s pathologies are well controlled, as evidenced by his last sleep study and AHI of 1.8. He continues to have some issues with leak, for which he is trialing different masks.

Conclusion
Cheyne-Stokes respirations and central sleep apnea are present in patients with history of multiple types of cerebral events. With lacunar strokes constituting 25% of ischemic strokes, it is imperative to make the correlation between Cheyne-Stokes respirations, central sleep apnea, and lacunar infarct in patients with otherwise no clear etiology of those sleep pathologies.

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1188 Decreased Tolerance to Hypoglossal Nerve Stimulator After Cardioversion
Authors: Van Dongen Kimberly , Knapp Sarah , Chan Lawrence 
Published: April 2024

Abstract

Introduction
Hypoglossal nerve stimulator (HNS) therapy is a treatment for moderate to severe obstructive sleep apnea (OSA) in patients who cannot tolerate positive airway pressure (PAP) therapy. HNS is an implanted device that stimulates tongue protrusion at the start of inspiration [1,2,3]. OSA is associated with atrial fibrillation and increased risk of recurrence after cardioversion and catheter ablation [4]. Currently, the presence of atrial fibrillation is not a contraindication to HNS implantation. However, there are accumulating reports that HNS patients requiring external cardioversion for atrial fibrillation have resulted in device dysfunction. [5]

Report of case(s)
An eighty-two-year-old female with past medical history of obstructive sleep apnea with respiratory event index (REI) of 27.8 and atrial fibrillation/flutter who was implanted with HNS on 3/11/22. She was activated with configuration +-+ and functional threshold of 2.0 volts and able to increase her amplitude comfortably to 2.5V. Two months after activation, she underwent cardioversion for persistent atrial fibrillation and immediately found her stimulation intolerable. She reduced her amplitude to 1.8V and was able to gradually escalate to 2.7V. Her device was checked with no apparent malfunction. She received a second cardioversion with similar results, and again reduced her amplitude and slowly increased to 2.5V. Her subsequent titration study determined that 2.6V was ideal. Following an ablation 2 months later, stimulation was intolerable once more. Therapy was paused for 2 weeks; her amplitude was reduced to 1.4V and eventually returned to 2.0V. Follow up home study showed REI of 10.5 on 2.0V.

Conclusion
This case report highlights a rare occurrence of HNS intolerance after cardioversion. There has been one other report of device intolerance related to neurapraxia after cardioversion. The neuropraxia was believed to have been a direct effect of nerve injury related to electrical current traveling along the lead body to the electrode-tissue interface [6]. It is possible that the intolerance in our case is related to a similar mechanism. Clinicians should be aware of potential complications given the high incidence of atrial fibrillation in patients with OSA. This case may also serve as an example of how to re-introduce therapy in patients with HNS intolerance proceeding cardioversion.

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