Onset Insomnia Research Articles

0862 A unique case of severe sleep onset and maintenance insomnia following COVID-19 vaccination

IntroductionThe COVID-19 vaccines have documented transient side effects, including injection site soreness, redness, headache, fatigue, and fever. In addition, there have been few reported long-term side effects, including Guillain-Barre, pericarditis, and cerebral venous sinus thrombosis. We present a rare case of severe insomnia as a long-term side effect following COVID-19 vaccination. Report of Cases: A 59-year-old female with a past medical history of well-controlled hypothyroidism and migraine presented to the sleep center with four months of insomnia. She had a history of COVID infection in November 2020 with only mild symptoms of sore throat and fatigue. The patient finished her two-shot series of the Moderna COVID-19 vaccine in April 2021. Immediately following the vaccination, the patient had severe trouble falling and staying asleep. Her insomnia was resistant to multiple medications including zolpidem Immediate-release(IR), Controlled-release(CR) formulas, zaleplon, eszopiclone, trazodone, melatonin, clonazepam, suvorexant, and lemborexant. However, magnetic resonance imaging (MRI) brain imaging only showed nonspecific white matter disease. She had no mood disorders or psychosocial stressors, and the patient had excellent sleep hygiene measures. However, insomnia caused severe impairment of her daily life activities to a point where she was almost seeking inpatient admission for her insomnia. During the COVID-19 pandemic, the effects on sleep have been significant, particularly insomnia. Prescriptions for sleep medications have increased. Many have attributed the rise of insomnia to pandemic-related stress, disturbance of circadian rhythm from home confinement, and worsening mental health.ConclusionTo our knowledge, there have not been documented side effects of insomnia on the COVID-19 vaccines, with some studies suggesting sleep deprivation reducing their effectiveness. As vaccination efforts continue worldwide, awareness of side effects from vaccines is paramount for clinicians facing the challenges in patient care.This case demonstrates that chronic insomnia can be a side effect of the COVID-19 vaccines. Therefore, further surveillance of patients and side effects from COVID-19 vaccination is warranted as insomnia can have significant clinical and psychosocial consequences.Support (If Any)

0813 Post-Pinealectomy Insomnia and Melatonin Therapy

Abstract Introduction Melatonin is a hormone produced in the pineal gland that has an important role in sleep; immune, neurologic, psychiatric, metabolic, and endocrinologic function; cardiac-autonomic regulation and even cancer risk. We present a case of insomnia, somnambulism, dream enactment, and periodic limb movements of sleep (PLMS) after a pinealectomy. Report of Cases: A 40-year-old woman with a history of a complete pinealectomy due to a pineal cyst presented to the sleep medicine clinic. Shortly after the pinealectomy, she developed sleep onset and maintenance insomnia. Two years later she developed somnambulism, and four years later she developed dream enactment and PLMS. She reported no prior treatments for her sleep issues, including no history of melatonin use. On average, her total sleep time (TST) was 2-8 hours/night with awakenings every 2 hours. Sleep latency was 10-45 minutes. Polysomnograghy demonstrated an apnea-hypopnea index of 0.6/hr, PLM index of 68.1/hr, normal REM atonia, and no complex behaviors. The patient started 1mg immediate release (IR) melatonin, which did not help her insomnia, but parasomnias resolved. She had improvement in her PLMS with iron supplementation and melatonin. The melatonin dose was increased to 3mg IR which helped increase her TST to 4-8 hours. She was switched to 3mg extended release (ER) melatonin, and then increased to 4mg ER. She obtained the most benefit for her insomnia with 1mg IR plus 4mg ER with sleep latency reduced to 5-10 minutes and TST improved up to 7.5 hours with rare awakenings. Conclusion Pinealectomy in humans is rarely reported. Most data about the consequences of pinealectomy and pathophysiology of melatonin come from animal research. Melatonin level after pinealectomy is often undetectable or severely diminished. Current limited literature on patients with pinealectomy consists of case reports about patients who experienced insomnia, non-24-hour sleep-wake rhythm disorder [SSM1] and mood disorders. Melatonin doses ranging from 0.5mg to 14mg IR and up to 5mg ER have been trialed with most patients having symptomatic improvement with doses above 3mg. We found that a combination of 1mg immediate and 4mg extended release melatonin was the most beneficial for our patient. Support (If Any)

0840 Be Wary Of Adjustment Disorder with Anxiety In Patient With Insomnia And Discomfort With Positive Pressure Airway Therapy

Abstract Introduction Insomnia is a common complaint. When it occurs in the context of treatment with continuous positive airway pressure (CPAP), it can complicate treatment and lead to dissatisfaction with CPAP therapy. Adjustment disorder with anxiety (ADWA) is a condition that develops following an identifiable stressor and can be associated with insomnia. We describe a case of ADWA causing disrupted sleep and dissatisfaction with CPAP therapy. Report of Cases: The patient is an 80-year-old man with history of severe obstructive sleep apnea (OSA) and chronic obstructive lung disease, under stable management with CPAP. During a routine follow up visit, he reported the recent onset of frequent, and often prolonged, nocturnal awakenings associated with daytime sleepiness and fatigue. Insomnia was associated with discomfort with breathing, especially during exhalation, while using CPAP. His machine report indicated a significant decrement in compliance. Upon questioning, he reported that a few of his family members had died unexpectedly, following which he began to experience significant anxiety. His wife noted that he had become moody and irritable. On examination, the patient was visibly anxious; his speech was accelerated and animated, and he displayed psychomotor activation. Affect also displayed despondency. The patient was diagnosed with ADWA leading to insomnia and discomfort with CPAP use. He was prescribed buspirone 10 mg twice daily. On two week follow up patient reported no improvement in symptoms and was switched to escitalopram 10 mg daily. Following approximately three weeks, his clinical evaluation revealed significant improvement in mood; anxiety had dissipated, and sleep was more continuous with infrequent and brief awakenings. Daytime alertness had been restored. Of interest was the temporary return of anxiety and insomnia symptoms following the brief discontinuation of escitalopram because of hospitalization. Conclusion ADWA can occur in the setting of recent stressors and can result in sudden onset of insomnia, compromise CPAP adherence and decrease subjective benefit from PAP therapy. This case highlights the importance of questioning patients for the possibility of recent stressors and traumatic events when they develop difficulties with PAP use. These may indicate the presence of ADWA, whose management can restore CPAP compliance and improve sleep quality and daytime functioning. Support (If Any)

0821 Narcolepsy after West Nile Virus Meningoencephalitis infection

Abstract Introduction Narcolepsy is a sleep disorder characterized by hypersomnia and inappropriate intrusion of REM sleep into wakefulness. Etiology is heterogeneous, and is broadly classified into Narcolepsy Type 1 and Type 2. There is growing evidence that the pathogenesis in many cases have a post-infectious autoimmune basis. We present the case of a patient seen in our sleep clinic who was eventually diagnosed with Narcolepsy type 2 following West Nile Virus (WNV) Meningoencephalitis. Report of Cases: · The patient is a 44 year old Hispanic woman who had no prior sleep difficulties before 2013, when she was diagnosed with WNV meningitis. Lumbar puncture results from the time of infection are not available, as this evaluation occurred in the Dominican Republic. Subsequent lumbar punctures have shown the presence of anti-WNV IgG antibodies in her CSF. MRI and MRA brain were unremarkable. · She also has a history of migraine, fibromyalgia, depression, and adrenal insufficiency. · She presented with sleep complaints, including sleep onset insomnia, symptoms of sleep disordered breathing, and excessive daytime sleepiness. · She underwent home sleep apnea test in 12/2020 which revealed mild obstructive sleep apnea. Overall AHI was 7.9/hour without significant hypoxemia. She was subsequently started on CPAP therapy with good adherence, but she continued to have significant daytime sleepiness, notably with an Epworth Sleepiness Scale score of 21/24. · She subsequently underwent overnight polysomnogram and multiple sleep latency test in our sleep laboratory. · Overnight PSG confirmed mild obstructive sleep apnea (AHI 12.0) along with short REM latency (10.5 minutes). Next day MSLT showed mean sleep latency of 2.3 minutes, for 5 attended naps, with 2 SOREMPs, which was diagnostic of Narcolepsy type 2. Conclusion This case demonstrates the onset of narcolepsy after WNV meningoencephalitis. Support (If Any)

Lemborexant, an orexin receptor antagonist sedative-hypnotic: Is it useful for insomnia in psychiatric disorders?

Lemborexant, an orexin receptor antagonist similar to suvorexant, has been approved for the treatment of sleep onset and/or maintenance insomnia. Lemborexant is reviewed and compare to suvorexant from a psychiatric perspective. Rapidly absorbed (peak 1-3h), lemborexant has a half-life of 17-19h (suvorexant half-life 12h). It is metabolized by CYP3A4/5, with no significant effects of age, sex or weight. Trials for insomnia indicate sustained efficacy beyond 6months. Lemborexant has not been trialled in major psychiatric disorders. Commenced at 5mg, lemborexant can then be increased to 10mg, taken at least 7h before planned awakening. Adverse effects are higher at 10mg: somnolence occurs in about 10% while headache and nightmares affect 2-5%, approximately similar to 40mg suvorexant (recommended suvorexant dose 20mg). Sleep paralysis, hypnagogic/hypnopompic hallucinations, and cataplexy-like symptoms, complex sleep behaviours and emergence of depression/suicidal ideation can occur. Neither tolerance to sedation nor withdrawal effects on discontinuation have been observed. Whether the differences between lemborexant and suvorexant are clinically relevant is unclear. Like suvorexant, lemborexant appears to be effective in longer-term use for insomnia, but until efficacy and safety are adequately investigated in major mental disorders, clinicians need to monitor patient experience closely.

Sleep phase and pre-sleep arousal predicted co-developmental trajectories of pain and insomnia within adolescence

The onset of both chronic pain and insomnia is high during adolescence. Although a bidirectional relationship between pain and insomnia has support, how pain and sleep co-develop throughout adolescence remains unknown. Sleep–wake patterns, pre-sleep behavior and pre-sleep arousal may influence the co-development of pain and insomnia. Four waves of longitudinal self-report data were used (Nbaseline = 2767, Agebaseline M = 13.65 years, SD = 0.65). Multidimensional growth mixture modeling was used to identify four subgroups of adolescents with different concurrent trajectories of pain and insomnia. The trajectories followed each other across time in all classes: one class of consistently low pain and insomnia (68.7%), one class with persistent high symptoms (4.9%), as well as one class of increasing (13.9%), and one of decreasing (12.5%), trajectories. Later sleep–wake patterns and more pre-sleep cognitive-emotional arousal predicted both increasing and decreasing trajectories of concurrent pain and insomnia. The current study showed that developmental trajectories of pain and insomnia follow each other within adolescents and across adolescence. Both sleep-phase focused interventions as well as psychological interventions that focus on pre-sleep cognitive-emotional arousal may prove beneficial for adolescents with comorbid pain and insomnia.

New-onset psychosis in an elderly patient: Thiamine to the rescue

<h3>Introduction</h3> Alcohol-related neurocognitive disorders result from chronic and excessive alcohol consumption in combination with liver dysfunction and/or dietary deffiencies. Long-term alcohol abuse can affect higher and lower-order functions of neurocognition including but not limited to global deficits in visuospatial abilities, impulsivity, executive functions, working and episodic memory. According to the DSM-5, these disorders are divided in mild and major, forms with further division of the latter into amnestic-confabulatory and non-amnestic form. We present here a patient with new-onset psychosis that after careful evaluation of etiological causes was attributed to alcohol consumption with subsequent fullfilment for diagnostic criteria of Wernicke-Korsakoff. These disorders may be increasing worldwide, particularly in the elderly population. Interventions such as treatment of amnestic features as well as comorbidites, medication and engagement with psychosocial support systems has been associated with better outcomes. <h3>Methods</h3> We describe the case of a Latinx 74-year-old male with no past psychiatric history and a past medical history of hypertension and DM2 admitted to geriatric unit after exhibiting agitated behavior and paranoia. Collateral information obtained from family revealed that patient had recent on-set of insomnia, paranoia, visual hallucinations, confabulation and impulsivity that started 2 to 3 months before admission to our unit. It was also disclosed that patient had a history of nicotine and a chronic alcohol use which led to peptic ulcer disease and subsequent alcohol abstinence. A thorough medical work up revealed microcytic anemia and hyperglycemia with otherwise unremarkable hepatic function, TSH, Vitamin B12, folic acid and STD panel. MRI was remarkable for scattered hyperdensities suggestive of chronic small vascular ischemia. <h3>Results</h3> During first encounter, patient had bizarre behavior (holding a napkin between his lips to avoid air contamination), was seen talking to himself and exhibited paranoid ideation towards team. He was started on oral thiamine 100mg, medications for comorbidities and risperidone 0.5mg twice daily which he refused on multiple occasions requiring Olanzapine 2.5mg intramuscullarly. On day three, patient reported paranoid ideation towards family; he felt threatened, therefore he admitted he hid a machete under his bed at home before admission. On multiple ocassions patient was seen writing incomprehensible notes with nonsensical themes. The patient refused formal cognitive screening (MOCA) initially, yet he was oriented to sourroundings. On further evaluation, patient continued paranoid, isolated and refusing medication as he believed team was trying to poison him. Further collateral information from family revealed that patient exhibited neurocognitive symptoms at least 1 year before presentantion as well as increased alcohol consumption one month before admission into our unit. On day nine, thiamine was switched to intramuscular formulation as a 100mg twice a day dosing. By day twelve, patient was more cooperative and calm, exhibiting less psychosis and disorganization. He was able to perform a MOCA, with deficits in encoding and information retrieval and MMSE of 19/30. By day 15, patient was less delusional, socializing and with improved insight into his condition. We postulate that resolution of psychosis was achieved after intramuscular thiamine was initiated. <h3>Conclusions</h3> This presentation highlight a case of new-onset psychosis in an elderly patient with multiple comorbidities and imaging suggestive of vascular dementia. Management included a multifaceted approach with antipsychotic and thiamine treatment that after careful evaluation was attributed to alcohol induced amnestic disorder. Psychiatrists should understand the symptoms that could be associated to chronic ethanol use in the elderly population as well as treatment strategies to target symptoms. <h3>This research was funded by</h3> None

Approches thérapeutiques des troubles du sommeil et des rythmes chez l’enfant avec TSA

Sleep disturbances are extremely common (40–86%) in children and adolescents, especially those with autism spectrum disorders (ASD) and are often among the first symptoms identified by parents at a very early stage of their child's development. These abnormalities are among the main parental concerns when having a child with ASD and have a significant impact on the quality of life of patients, their parents, and more broadly their siblings. Sleep disorders are essentially abnormalities of the sleep-wake rhythm – primarily sleep onset insomnia or nocturnal awakenings (with difficulty falling back to sleep). These disturbances can be accompanied by other sleep disorders, requiring notably a systematic elimination of the presence of a sleep apnea or restless legs syndrome – to ensure a personalized and efficient therapeutic approach. Physiologically, the determinants of these sleep disorders are poorly understood, even though several studies point to a significant decrease in melatonin synthesis in people with ASD. Melatonin is a hormone that facilitates falling asleep and maintaining sleep and is also involved in the endogenous synchronization of internal biological clocks. However, the causal factors of this decrease in melatonin synthesis are largely unknown, involving to a small extent the genes involved in melatonin synthesis pathway. The treatment of sleep disorders is relatively systematic: after eliminating other specific sleep disorders associated with the complaint of insomnia, as well as other possible associated comorbidities (such as seizures), a global and graduated therapeutic approach must be put in place. This treatment will be non-pharmacological as a first line, then pharmacological as a second line. A number of non-pharmacological treatment strategies for sleep disorders in typically developing children and adolescents, as well as those with ASD, have been shown to be effective. This treatment requires a combination of: 1) parental education to promote sleep development; 2) setting up bedtime rituals adapted to the child's age and particularities; 3) specific behavioral strategies including bedtime fading, gradual extinction and positive reinforcement of adapted behaviors. It is very essential that the parents are accompanied throughout this therapy. Sleep hygiene and behavioral care must also take into consideration the important role of the zeitgebers of sleep-wake rhythms, i.e. the external environmental factors involved in the synchronization of the biological clocks: regular exposure to light at adapted times, regular meal and wake-up times, social activities and times for going to school. The evidence for the effectiveness of behavioral interventions in the treatment of behavioral insomnia in the typical developmental child is strong, since 94% of children show clinically significant improvements in nighttime sleepiness and waking. By contrast, only about 25% of children with ASD are improved by an approach combining sleep hygiene and behavioral therapy. Melatonin has a special and prominent place in the drug management of sleep disorders associated with ASD. Several clinical trials have shown that melatonin is effective in treating sleep disorders in patients with ASD. This work led to the European Medicines Agency (EMA) granting marketing authorization in September 2018 for a sustained-release paediatric melatonin molecule (Slenyto®). This synthetic molecule is a prolonged release melatonin (PRM) which mimics the physiological pharmacokinetic and secretory characteristics of endogenous melatonin, having a very short blood half-life and prolonged secretion for several hours during the night. A recent study evaluated the efficacy and safety of pediatric PRM (mini-tablets) in 125 children, aged 2 to 17.5 years with mainly ASD. After 15 days on placebo, the children were randomized into two parallel groups, PRM or placebo in a double-blind design for 13 weeks. At endpoint, total sleep time was increased by an average of 57.5 minutes on PRM and only 9.14 minutes on placebo (P=0.034). This difference between the two groups was already significant after three weeks of treatment (P=0.006). Sleep latency was also improved in the PRM group (−39.6 minutes) compared to placebo (−12.51 minutes) (P=0.01). Consolidated sleep duration (uninterrupted by awakenings) was improved by 77.9 minutes for the PRM group and only 25.4 minutes for the placebo group (P<0.001). PRM was well tolerated, the most frequent side effects being headache and daytime drowsiness at the same level with PRM or placebo. In addition, the acceptability by the children for swallowing the mini-tablets was excellent (100% compliance). The efficacy and tolerability of PRM was maintained over the medium and long term in the open phase, over a total study duration of 2 years.

The risk of insomnia after surgical operation: A longitudinal, population-based, case-crossover study.

The acute onset of insomnia following surgical operations has long been neglected, and long-term outcomes are not clear. Our aims were (1) to evaluate the risk of postoperative insomnia, (2) to identify which surgeries are related, and (3) to follow patients with postoperative insomnia for the development of major mental and physical disorders. We conducted a case-crossover study comprising 9898 participants with new-onset insomnia from the Taiwan National Health Insurance Research Database between 1997 and 2011. We determined the odds of having surgery in the case period (30 days) before the onset of insomnia by logistic regression analysis. Types of surgery that postoperative insomniacs had undergone were compared with age-/gender-/timing-matched controls. Longitudinal follow-up of postoperative and non-postoperative insomniacs was performed. The odds ratio of surgical exposure vs. nonexposure within 30 days was 12.05 (p < 0.001) before new-onset insomnia. Surgery of musculoskeletal and nervous systems predisposed to insomnia. The duration of hypnotic drug use (0.83 years) was shorter and with a nearly 2-fold faster remission rate in postoperative than in non-postoperative insomniacs (1.45 years). Approximately 25% of each insomnia group developed persistent sleep disturbance. Surgery is associated with subsequent insomnia, which has a shorter duration and a faster remission than non-postoperative insomnia. Our data provide a reference for postoperative care, and warrant future studies.

Validation of the Thyrotoxicosis-associated Insomnia Model Induced by Thyroxine through Sympathetic Stimulation: Face, Construct and Predictive Perspectives.

Insomnia has become a common central nervous system disease. At present, the pathogenesis of insomnia is not clear. Animal models can help us understand the pathogenesis of the disease and can be used in transformational medicine. Therefore, it is very necessary to establish an appropriate model of insomnia. Clinical data show that insomnia patients with high levels of thyroxine and often accompanied by cardiovascular problems, a common mechanism underlying all of these physiological disruptions is the sympathetic nervous system. Combined with the characteristics of chronic onset of clinical insomnia, an insomnia model induced by long-term intraperitoneal injection of thyroid hormone has been created in our laboratory. In this paper, the insomnia-like state of the model was evaluated based on three validity criteria. Face validity has been demonstrated in metabolism, the Morris water maze, electrocardiogram (ECG) and electroencephalogram (EEG). Structure validity has been proved by the results of targeted metabolomics. After treatment with diazepam, a commonly used clinical anti-insomnia drug, the above physiological and pathological disorders were reversed. The results of comprehensive analysis show that the established thyrotoxicosis-associated insomnia model meets the validity requirement to establish an appropriate animal model of insomnia. The model presented in this article might help to study pathogenetic mechanisms of clinical insomnia, as well as to test promising methods of insomnia treatment.

The Association Between Self-Reported Screen Time, Social Media Addiction, and Sleep Among Norwegian University Students.

The aim of this study was to assess the relationship between daily screen time and sleep, evening screen time and sleep, and between social media addiction and sleep in a student population. This cross-sectional study is based on data from a national survey of all college and university students in Norway (the SHoT2018 study; n = 49,051). The sleep outcomes were sleep duration, sleep onset latency, sleep efficiency, and insomnia operationalized according to formal DSM-5 criteria. The results show a strong negative association between time spent on screen-based devices and sleep quality and quantity, and where screen use in bed had more consistent negative associations with sleep. Furthermore, there were higher rates of insomnia among those with higher levels of addiction, and curvilinear relationships with sleep duration, sleep onset latency, and sleep efficiency. Those with higher levels of addiction also had more evening screen time. The findings suggest that screen use plays an important role in students' sleep quantity and quality, where evening screen time has a stronger relationship with sleep compared to total daily screen time. The results also suggest a role of social media addiction, and addictive social media use may be a target for intervention in order to reduce evening screen time.

P.088 Dysautonomia and Diabetes: A Prodrome to Fatal Familial Insomnia (FFI)

Background: Fatal Familial Insomnia (FFI) is an autosomal dominant multisystem prion disease, with sleep disorders often being the first presentation. Although autonomic dysfunctions are key features, the frequency and timing vary between reports, and may accompany early insomnia. Moreover, endocrine changes are reported, but diabetes rarely is - with unclear timing of onset in relation to the insomnia. Methods: N/A Results: Here we present a 46-year-old previously healthy male, who within 22 months prior to the onset of sleep disturbances, developed hypertension and diabetes. Then within 3-4 months after onset of sleep disturbances development tachycardia and diaphoresis. His sleep continued to deteriorate, and later developed bulbar impairment, ataxia, diplopia, sleep apnea and cognitive decline. He passed away 20 months from onset of insomnia. Polysomnography showed status dissociates and central apnea. He had positive genetic testing, PRNP c.532G&gt;A (p.Asp178Asn) and PRNP c.385A&gt;G (pMet129Val), a pathological confirmation, and a positive family history Conclusions: Here diabetes and hypertension significantly preceded sleep disturbances, and tachycardia and diaphoresis developed shortly after. This illustrates that dysautonomia and endocrine dysfunction may be unrecognized prodromes in some cases of FFI, and could be an early marker of clinical disease onset and therapeutic interventions, especially in genetically confirmed asymptotic patients.

Early objective adherence to hypoglossal nerve stimulation therapy.

To assess early adherence to therapy with hypoglossal nerve stimulation therapy. This is a prospective study of consecutive patients with moderate to severe obstructive sleep apnea who underwent implantation of hypoglossal nerve stimulation therapy within a single academic practice and attended a follow-up appointment after greater than 30 days of therapy use. Objective adherence data were extracted from an objective monitoring database and compared to patient characteristics. The study population was 79 participants who were 29.1% female with a mean age of 58.7 ± 12.8 years old, body mass index of 28.9 ± 3.4 kg/m2, and baseline apnea-hypopnea index of 33.8 ± 17.6 events/h. In the first 7 days after device activation, average use was 7.8 h/night, with 91.9% of nights with greater than 4 hours of therapy use and an average of 0.2 pauses in therapy per night. These figures remained stable after 30 days of use: 7.7 h/night, 91.0% of nights longer than 4 hours, and 0.3 pauses per night. Objective evidence of difficulty with acclimatization was associated with age less than 60 years (odds ratio 2.8, 95% confidence interval 1.1-7.1, P = .03) and a history of prior upper airway surgery (3.9, 1.2-11.9, P = .015). Insomnia was present in 31 patients and was not associated with objective evidence of difficulty tolerating therapy. Early adherence to hypoglossal nerve stimulation is excellent (92.4% >4 hours on >70% of nights), suggesting that the acclimatization period is straightforward in most. Younger age and a history of prior upper airway surgery appear to be associated with an increased risk of difficulty with acclimatization. Huyett P. Early objective adherence to hypoglossal nerve stimulation therapy. J Clin Sleep Med. 2022;18(2):631-636.

Treatment of insomnia - effect of trazodone and hypnotics on sleep.

Sedative antidepressants are commonly used drugs in the treatment of insomnia. However, some recommendations claim that only hypnotics have been proven effective in the treatment of sleep initiation and maintenance disorders. The aim of this article is to compare the effect of hypnotics and trazodone on sleep, and to analyse the evidence for the use of trazodone in the treatment of insomnia. Three studies investigated the effects of trazodone on sleep in primary insomnia, 5 studies on insomnia in the course of affective disorders and 6 studies on insomnia in other indications (PTSD, Alzheimer's disease, alcohol and opiate dependence, somatoform disorder, and insomnia during pregnancy). In the treatment of insomnia, trazodone is less effective than hypnotics in the treatment of sleep onset insomnia (i.e., disorders of falling asleep). For this indication it needs to be administered earlier than hypnotics, at least 1 hour before bedtime. It is, however, very effective in the treatment of sleep-maintenance insomnia, especially in patients with comorbid mental disorders or patients treated with activating antidepressants. Hypnotics and trazodone have the opposite effect on deep sleep. Trazodone increases the duration of deep sleep, which is associated with better sleep quality as assessed by patients. In contrast, hypnotics decrease slow-wave activityin sleep EEG, which is the biomarker of deep sleep. The main mechanism through which trazodone promotes sleep is its antagonistic effect on 5-HT2 serotonin receptors, while hypnotics are agonists of gamma-aminobutyric acid GABAA receptors, and other sedative antidepressants block H1 histamine receptors. This is associated with a low risk of weight gain, which is rare with trazodone treatment.

Insomnia episodes, new-onset pharmacological treatments, and other sleep disturbances during the COVID-19 pandemic: a nationwide cross-sectional study in Brazilian health care professionals.

To evaluate the impact of the coronavirus disease 2019 (COVID-19) pandemic on insomnia and other sleep disturbances in health care professionals. A survey was distributed using social media and organizational emails to Brazilian active health care professionals during the COVID-19 outbreak. We explored potential associated factors including age, sex, occupation, workplace, work hours, income, previous infection with COVID-19, recent/current contact with COVID-19 patients, regional number of incident deaths, anxiety, and burnout. We evaluated new-onset/previous insomnia worsening episodes (primary outcome), new pharmacological treatments, sleep quality, duration, nightmares, and snoring (secondary outcomes). A total of 4,384 health professionals from all regions of the country were included in the analysis (44 ± 12 years, 76% females, 53.8% physicians). Overall, 55.7% were assisting patients with COVID-19, and 9.2% had a previous COVID-19 infection. The primary outcome occurred in 32.9% of respondents in parallel to 13% new pharmacological treatments for insomnia. The sleep quality worsened for 61.4%, while 43.5% and 22.8% reported ≥ 1-hour sleep duration reduction and worsening or new-onset nightmares, respectively. Multivariate analyses showed that age (odds ratio [OR]: 1.008; 95% confidence interval [CI] 1.001-1.015), females (OR: 1.590; 95% CI 1.335-1.900), weight change (decrease: OR: 1.772; 95% CI 1.453-2.161; increase: OR: 1.468; 95% CI 1.249-1.728), prevalent anxiety (OR: 3.414; 95% CI 2.954-3.948), new-onset burnout (OR: 1.761; 95% CI 1.489-2.083), family income reduction > 30% (OR: 1.288; 95% CI 1.069-1.553), and assisting patients with COVID-19 (OR: 1.275; 95% CI 1.081-1.506) were independently associated with new-onset or worsening of previous insomnia episodes. We observed a huge burden of insomnia episodes and other sleep disturbances in health care professionals during the COVID-19 pandemic. Drager LF, Pachito DV, Moreno CRC, etal. Insomnia episodes, new-onset pharmacological treatments, and other sleep disturbances during the COVID-19 pandemic: a nationwide cross-sectional study in Brazilian health care professionals. J Clin Sleep Med. 2022;18(2):373-382.

Characteristics of Calls to a COVID-19 Mental Health Hotline in the First Wave of the Pandemic in New York.

This report describes the development, implementation and outcomes of a "COVID-19 Anxiety Hotline," designed to address the community's mental health crisis provoked by the coronavirus pandemic. The service was specifically designed using survey data regarding the effects of the COVID-19 pandemic on its staff and community members. Callers had around-the-clock direct access to mental healthcare providers at no cost. Quantitative analysis showed that nearly three out of four callers experienced new onset anxiety and insomnia driven by fear of exposure, and had difficulty accessing mental health care. In addition to immediate support, referral to tele-mental health care was provided to 86% of callers. Qualitative analysis indicates the effectiveness of immediate support and appropriate referrals using a tele-health platform. Our report indicates that the service was utilized by the general population, by health care workers, and rapidly provided referrals to individuals with limited access to mental health care during the pandemic.

Characterization of sleep in six patients with pantothenate kinase-associated neurodegeneration

BackgroundPantothenate kinase-associated neurodegeneration (PKAN) is a rare neurologic disorder included in the group of neurodegeneration with brain iron accumulation diseases (NBIA). Information regarding sleep in patients with PKAN is limited. ObjectivesTo describe the clinical and polysomnographic characteristics of sleep in six patients with genetically confirmed PKAN. MethodsThe evaluation included a clinical interview, sleep questionnaires -Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI) and Hospital Anxiety and Depression Scale (HADS)- and a video-polysomnography (VPSG). In addition to standard sleep measures we manually quantified sleep spindle density in stage N2 and rapid eye movements in REM sleep comparing the results with matched controls. Quantification of EMG activity in REM sleep was performed following standard criteria. ResultsAll the patients reported at least one sleep complaint, most commonly sleep fragmentation (4/6) and sleep onset insomnia (3/6). ESS and PSQI were abnormal in 3/6 and 4/6, respectively. VPSG showed in 4/6 decreased ocular movements during REM sleep, an increase in sleep spindles in 3/6 (all of them with deep brain pallidal stimulation), an absence of slow wave sleep in 2 and undifferentiated NREM sleep and delayed sleep phase in one. Three patients had an abnormal sleep apnea/hypopnea index, and 2 periodic limb movements of sleep. REM sleep muscular atonia was preserved in all. ConclusionsSleep disorders are common in patients with PKAN. Although our sample is small and heterogeneous, with different symptomatic treatments possibly influencing the results, it suggests that evaluation of sleep should be considered in their management.

Sleep microstructure in attention deficit hyperactivity disorder according to the underlying sleep phenotypes.

The analysis of sleep microstructure in attention deficit hyperactivity disorder (ADHD) revealed an under-representation of the EEG slow component during NREM sleep. Previous studies either excluded or did not characterize objectively sleep disorders, which notoriously affect sleep architecture. The present study aimed to investigate the cyclic alternating pattern in a real clinical sample of children with ADHD, in whom sleep disorders could be considered. Twenty-seven consecutively enrolled drug-naïve children (mean age, 10.53 years; nine females) and 23 controls (mean age, 10.22years; 11 females) underwent a full sleep investigation, including attended video-polysomnography. Visual cyclic alternating pattern analysis was performed in a blinded way. Children with ADHD had one or more sleep disorders (a narcolepsy-like phenotype was found in two cases, sleep onset insomnia in three cases, arousal disorder in one case, movement disorder phenotype in six cases and obstructive sleep apnea in 11 cases, and six children had sleep-related epileptiform discharges). Children with ADHD and normal controls showed a similar microstructure with a cyclic alternating pattern rate of about 50%. Children with obstructive sleep apnea had a significantly higher cyclic alternating pattern rate during stage N3. Despite not reaching statistical differences, a lower cyclic alternating pattern rate and A1 index were found in children without epileptic abnormalities/obstructive sleep apnea. Our analysis might allow differentiation of the "primary form" of ADHD associated with a decrease of NREM instability from those forms associated with sleep apnea and epileptic activity.

National Survey on the importance of sleep in the quality of academic life and mental health of college students in Portugal.

The academic years are a period of vulnerability when considering sleep problems and mental health. Growing evidence suggests poor sleep patterns are related to impaired academic life and lower psychological well-being. The aim of this study was to explore the importance of sleep habits and report the associations of sleep problems with quality of academic life and different dimensions of mental health (e.g. worries, anxiety, self-regulation and resilience) in a large sample of college students. The HBSC/JUnP data base comprises a representative sample of 2991 college students (n=2203; 73.7% women), aged from 18 to 35 years old (22.43±3.83). Participants socio-demographic characteristics included sex and age. Besides, participants were inquired about sleep duration, characteristics of their sleep habits, questions about quality academic life, namely feeling bored in university, pressure from academic work and academic performance perception and mental health, namely worries, anxiety, self-regulation and resilience. Results showed most young people report an average value for sleep habits (M=4.41; SD=1.46) and that they sleep an average of 7 hours a night. More than half of the young people report either being affected by difficulty falling asleep, showing signs of sleep onset insomnia (67.7%). The conducted analyses indicated that the difficulty falling asleep (having insomnia) was associated with poor/reasonable academic performance perception, higher levels of concerns and anxiety, and lower levels of self-regulation and resilience, thus jeopardizing the mental health of college students. In turn, that characteristics of sleep was also associated with poor sleep habits. In conclusion, this study showed that poor sleep habits were associated with a worse level of academic performance perception and low levels of mental health among college students in Portugal. Universities offer enormous potential as settings to promote sleep-health programs since they can reach many young people who are future-oriented and willing to learn. There is then the need for academic researchers, teaching staff and health professionals working for college students health, to develop and test a wide array of sleep-promoting interventions (e.g., education classes, online programs, adjustment of class time), thus preventing negative secondary outcomes.

818 A Ghost from the Past: Unmasked Insomnia Affecting Hypoglossal Nerve Stimulation Therapy Adherence

Abstract Introduction Hypoglossal nerve stimulation (HNS) is an efficacious option for treating moderate to severe obstructive sleep apnea (OSA). However, there is sparse evidence regarding tolerance and adherence to HNS therapy in patients with a diagnosis of insomnia. Report of case(s) A 57-year-old man with well-controlled depression presented for evaluation for HNS therapy. He had been diagnosed with moderate OSA with an apnea-hypopnea index of 22/hour, intolerant of continuous positive airway pressure and mandibular advancement device. He underwent uvulopalatopharyngoplasty without significant improvement. At the time of initial evaluation, he denied history of insomnia and prior sleep aid use. He subsequently underwent successful HNS device implantation and activation. One week after HNS initiation, the patient reported new symptoms of significant difficulty with sleep onset and inability to fall back asleep, which was worse than his untreated OSA symptoms. Device interrogation did not reveal any hardware problems. Adjustments to start delay, pause time and device configuration with awake endoscopy did not improve tolerance. Subsequently, the patient disclosed a remote history of insomnia, which was treated with multiple hypnotics in addition to cognitive-behavioral therapy for insomnia (CBTi) and had resolved. He was diagnosed with recurrent chronic insomnia, for which eszopiclone was initiated without significant improvement. He eventually agreed to CBTi, with partial improvement in device tolerance and improvement in insomnia symptoms. Conclusion This case highlights that HNS therapy adherence can be affected by prior history of, or a current diagnosis of insomnia. Our patient had a predisposition for insomnia that was well controlled prior to HNS therapy initiation. The onset of recurrent insomnia with HNS activation suggests that HNS was a precipitating factor for his now chronic insomnia. Although there is insufficient evidence to suggest whether history of insomnia should affect the decision to initiate HNS therapy, this case illustrates the importance of screening for insomnia at pre-implant evaluation. Our center is now routinely screening for a history of insomnia to identify patients who may benefit from treatment prior to HNS implantation. Larger studies are needed to explore a possible relationship between insomnia and HNS adherence. Support (if any):