Parkinsonian daytime sleep-wake classification using deep brain stimulation lead recordings.

Excessive daytime sleepiness is a recognized non-motor symptom that adversely impacts the quality of life of people with Parkinson's disease (PD), yet effective treatment options remain limited. Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective treatment for PD motor signs. Reliable daytime sleep-wake classification using local field potentials (LFPs) recorded from DBS leads implanted in STN can inform the development of closed-loop DBS approaches for prompt detection and disruption of sleep-related neural oscillations. We performed STN DBS lead recordings in three nonhuman primates rendered parkinsonian by administrating neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Reference sleep-wake states were determined on a second-by-second basis by video monitoring of eyes (eyes-open, wake and eyes-closed, sleep). The spectral power in delta (1-4 Hz), theta (4-8 Hz), low-beta (8-20 Hz), high-beta (20-35 Hz), gamma (35-90 Hz), and high-frequency (200-400 Hz) bands were extracted from each wake and sleep epochs for training (70% data) and testing (30% data) a support vector machines classifier for each subject independently. The spectral features yielded reasonable daytime sleep-wake classification (sensitivity: 90.68 ± 1.28; specificity: 88.16 ± 1.08; accuracy: 89.42 ± 0.68; positive predictive value; 88.70 ± 0.89, n = 3). Our findings support the plausibility of monitoring daytime sleep-wake states using DBS lead recordings. These results could have future clinical implications in informing the development of closed-loop DBS approaches for automatic detection and disruption of sleep-related neural oscillations in people with PD to promote wakefulness.

Exploration of dimensionality and psychometric properties of the Pittsburgh Sleep Quality Index in cases with temporomandibular disorders.

BACKGROUND: This study assessed the dimensional structure of sleep quality with the Pittsburgh Sleep Quality Index (PSQI) and investigated its psychometric properties in cases with temporomandibular disorders (TMD). METHODS: A convenience sample of 609 TMD cases (age: 37.1 ± 13.1 yrs, 18-67 yrs, 85% female) of the multi-center Validation Project meeting Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) and with sufficient PSQI data were included in this study. To investigate PSQI scores' dimensionality, exploratory factor analysis was used. Factors were identified using the Scree plot. To investigate internal consistency, Cronbach's alpha was calculated. Analyses were separately performed for TMD cases with (N = 496) and TMD cases withouta pain-related diagnosis (N = 113). RESULTS: The mean PSQI score for all TMD cases was 7.1 ± 4.0 units, range: 0-19. The exploratory factor analysis identified one factor for cases with at least one pain-related TMD diagnosis as well as one factor for cases with a pain-free TMD diagnosis that explained 41% of the variance in cases with pain-related TMD and 37% in cases with pain-free TMD. Internal consistency for PSQI scores was alpha of 0.75 in cases with pain-related TMD, alpha of 0.66 in cases with pain-free TMD and alpha = 0.75 for all TMD cases. CONCLUSIONS: Sleep quality in TMD patients is a unidimensional construct and can therefore be represented by one summary score; a finding that is in line with previous reports in TMD patients.

Slow-wave sleep dysfunction in mild parkinsonism is associated with excessive beta and reduced delta oscillations in motor cortex.

Increasing evidence suggests slow-wave sleep (SWS) dysfunction in Parkinson's disease (PD) is associated with faster disease progression, cognitive impairment, and excessive daytime sleepiness. Beta oscillations (8-35 Hz) in the basal ganglia thalamocortical (BGTC) network are thought to play a role in the development of cardinal motor signs of PD. The role cortical beta oscillations play in SWS dysfunction in the early stage of parkinsonism is not understood, however. To address this question, we used a within-subject design in a nonhuman primate (NHP) model of PD to record local field potentials from the primary motor cortex (MC) during sleep across normal and mild parkinsonian states. The MC is a critical node in the BGTC network, exhibits pathological oscillations with depletion in dopamine tone, and displays high amplitude slow oscillations during SWS. The MC is therefore an appropriate recording site to understand the neurophysiology of SWS dysfunction in parkinsonism. We observed a reduction in SWS quantity (p = 0.027) in the parkinsonian state compared to normal. The cortical delta (0.5-3 Hz) power was reduced (p = 0.038) whereas beta (8-35 Hz) power was elevated (p = 0.001) during SWS in the parkinsonian state compared to normal. Furthermore, SWS quantity positively correlated with delta power (r = 0.43, p = 0.037) and negatively correlated with beta power (r = -0.65, p < 0.001). Our findings support excessive beta oscillations as a mechanism for SWS dysfunction in mild parkinsonism and could inform the development of neuromodulation therapies for enhancing SWS in people with PD.

Validation of the RBD Symptom Severity Scale in the North American Prodromal Synucleinopathy Consortium.

BACKGROUND AND OBJECTIVES: REM sleep behavior disorder (RBD) is a parasomnia characterized by dream enactment. The International RBD Study Group developed the RBD Symptom Severity Scale (RBDSSS) to assess symptom severity for clinical or research use. We assessed the psychometric and clinimetric properties of the RBDSSS in participants enrolled in the North American Prodromal Synucleinopathy (NAPS) Consortium for RBD. METHODS: NAPS participants, who have polysomnogram-confirmed RBD, and their bedpartners completed the RBDSSS (participant and bedpartner versions). The RBDSSS contains 8 questions to assess the frequency and severity/impact of (1) dream content, (2) vocalizations, (3) movements, and (4) injuries associated with RBD. Total scores for participant (maximum score = 54) and bedpartner (maximum score = 38) questionnaires were derived by multiplying frequency and severity scores for each question. The Clinical Global Impression Scale of Severity (CGI-S) and RBD symptom frequency were assessed by a physician during a semistructured clinical interview with participants and, if available, bedpartners. Descriptive analyses, correlations between overall scores, and subitems were assessed, and item response analysis was performed to determine the scale's validity. RESULTS: Among 261 study participants, the median (interquartile range) score for the RBDSSS-PT (participant) was 10 (4-18) and that for the RBDSSS-BP (bedpartner) was 8 (4-15). The median CGI-S was 3 (3-4), indicating moderate severity. RBDSSS-BP scores were significantly lower in women with RBD (6 vs 9, p = 0.02), while there were no sex differences in RBDSSS-PT scores (8 vs 10.5, p = 0.615). Positive correlations were found between RBDSSS-PT vs RBDSSS-BP (Spearman rs = 0.561), RBDSSS-PT vs CGI-S (rs = 0.556), and RBDSSS-BP vs CGI-S (rs = 0.491, all p < 0.0001). Item response analysis showed a high discriminatory value (range 1.40-2.12) for the RBDSSS-PT and RBDSSS-BP (1.29-3.47). DISCUSSION: We describe the RBDSSS with adequate psychometric and clinimetric properties to quantify RBD symptom severity and good concordance between participant and bedpartner questionnaires and between RBDSSS scores and clinician-assessed global severity.

Comorbid neurotrauma increases neurodegenerative-relevant cognitive, motor, and autonomic dysfunction in patients with rapid eye movement sleep behavior disorder: a substudy of the North American Prodromal Synucleinopathy Consortium.

STUDY OBJECTIVES: Rapid eye movement sleep behavior disorder (RBD) is strongly associated with phenoconversion to an overt synucleinopathy, e.g. Parkinson's disease (PD), Lewy body dementia, and related disorders. Comorbid traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD)-henceforth "neurotrauma" (NT)-increase the odds of RBD by ~2.5-fold and are associated with an increased rate of service-connected PD in Veterans. Thus, RBD and NT are both independently associated with PD; however, it is unclear how NT influences neurological function in patients with RBD. METHODS: Participants ≥18 years with overnight polysomnogram-confirmed RBD were enrolled between 8/2018 to 4/2021 through the North American Prodromal Synucleinopathy Consortium. Standardized assessments for RBD, TBI, and PTSD history, as well as cognitive, motor, sensory, and autonomic function, were completed. This cross-sectional analysis compared cases (n = 24; RBD + NT) to controls (n = 96; RBD), matched for age (~60 years), sex (15% female), and years of education (~15 years). RESULTS: RBD + NT reported earlier RBD symptom onset (37.5 ±â€…11.9 vs. 52.2 ±â€…15.1 years of age) and a more severe RBD phenotype. Similarly, RBD + NT reported more severe anxiety and depression, greater frequency of hypertension, and significantly worse cognitive, motor, and autonomic function compared to RBD. No differences in olfaction or color vision were observed. CONCLUSIONS: This cross-sectional, matched case:control study shows individuals with RBD + NT have significantly worse neurological measures related to common features of an overt synucleinopathy. Confirmatory longitudinal studies are ongoing; however, these results suggest RBD + NT may be associated with more advanced neurological symptoms related to an evolving neurodegenerative process.

Excessive cortical beta oscillations are associated with slow-wave sleep dysfunction in mild parkinsonism.

Increasing evidence associates slow-wave sleep (SWS) dysfunction with neurodegeneration. Using a within-subject design in the nonhuman primate model of Parkinson's disease (PD), we found that reduced SWS quantity in mild parkinsonism was accompanied by elevated beta and reduced delta power during SWS in the motor cortex. Our findings support excessive beta oscillations as a mechanism for SWS dysfunction and will inform development of neuromodulation therapies for enhancing SWS in PD.

Baseline characteristics of the North American prodromal Synucleinopathy cohort.

OBJECTIVE: Rapid eye movement (REM) sleep behavior disorder (RBD) is widely considered a prodromal synucleinopathy, as most with RBD develop overt synucleinopathy within ~10 years. Accordingly, RBD offers an opportunity to test potential treatments at the earliest stages of synucleinopathy. The North American Prodromal Synucleinopathy (NAPS) Consortium has created a multisite RBD participant, primarily clinic-based cohort to better understand characteristics at diagnosis, and in future work, identify predictors of phenoconversion, develop synucleinopathy biomarkers, and enable early stage clinical trial enrollment. METHODS: Participants ≥18 years of age with overnight polysomnogram-confirmed RBD without Parkinson's disease, dementia, multiple system atrophy, or narcolepsy were enrolled from nine sites across North America (8/2018 to 4/2021). Data collection included family/personal history of RBD and standardized assessments of cognitive, motor, sensory, and autonomic function. RESULTS: Outcomes are primarily reported based on sex (361 total: n = 295 male, n = 66 female), and secondarily based on history of antidepressant use (n = 200 with, n = 154 without; with correction for sex differences) and based on extent of synucleinopathy burden (n = 56 defined as isolated RBD, n = 305 defined as RBD+ [i.e., exhibiting ≥1 abnormality]). Overall, these participants commonly demonstrated abnormalities in global cognition (MoCA; 38%), motor function (alternate tap test; 48%), sensory (BSIT; 57%), autonomic function (orthostatic hypotension, 38.8%), and anxiety/depression (BAI and PHQ-9; 39.3% and 31%, respectively). INTERPRETATION: These RBD participants, assessed with extensive history, demographic, cognitive, motor, sensory, and autonomic function demonstrated a lack of sex differences and high frequency of concomitant neurological abnormalities. These participants will be valuable for future longitudinal study and neuroprotective clinical trials.

Pediatric sleep and pain: etiologies, consequences, and clinical considerations.

STUDY OBJECTIVES: To examine current evidence of the relationship between sleep and pain from the neonatal period through adolescence. This review serves as a critical review of the literature and of the needs for future research on pediatric sleep and pain. METHODS: The PubMed online database was queried from January 1, 1960, to March 1, 2020, producing 149 articles applicable to pain and sleep in the pediatric population. Of those, 97 articles were cited in this review with the key articles including over 3800 participants. RESULTS: The pediatric literature supports the relationship between poor sleep (both sleep efficiency and nighttime awakenings) and subsequent risk for pain, especially among children with chronic disease. The reverse effect of pain on sleep is not yet well delineated. The key moderating factors explored in the literature are pharmacologic and nonpharmacologic therapies, psychologic health, and the etiology of pain. There is evidence that both altered sleep and pain early in life impact neurodevelopment, as seen by changes in sleep structure in clinical studies and alterations in brain development in animal models. CONCLUSIONS: The complicated relationship between sleep and pain is critically important during pediatric development when alterations to a normal sleep structure can have a lifelong impact. It is becoming clear that sleep deprivation and poor sleep quality exacerbate pain. Further research is needed into the complex alterations of sleep in chronic pain conditions as well as treatments to improve sleep in pediatric care. CITATION: Morris EE, Howell MJ, Pickup E, Iber C, Wang SG. Pediatric sleep and pain: etiologies, consequences, and clinical considerations. J Clin Sleep Med. 2022;18(9):2281-2289.

Basal ganglia engagement during REM sleep movements in Parkinson's disease.

To elucidate the role of the basal ganglia during REM sleep movements in Parkinson's disease (PD) we recorded pallidal neural activity from four PD patients. Unlike desynchronization commonly observed during wakeful movements, beta oscillations (13-35 Hz) synchronized during REM sleep movements; furthermore, high-frequency oscillations (150-350 Hz) synchronized during movement irrespective of sleep-wake states. Our results demonstrate differential engagement of the basal ganglia during REM sleep and awake movements.

NonREM Disorders of Arousal and Related Parasomnias: an Updated Review.

Parasomnias are abnormal behaviors and/or experiences emanating from or associated with sleep typically manifesting as motor movements of varying semiology. We discuss mainly nonrapid eye movement sleep and related parasomnias in this article. Sleepwalking (SW), sleep terrors (ST), confusional arousals, and related disorders result from an incomplete dissociation of wakefulness from nonrapid eye movement (NREM) sleep. Conditions that provoke repeated cortical arousals, and/or promote sleep inertia, lead to NREM parasomnias by impairing normal arousal mechanisms. Changes in the cyclic alternating pattern, a biomarker of arousal instability in NREM sleep, are noted in sleepwalking disorders. Sleep-related eating disorder (SRED) is characterized by a disruption of the nocturnal fast with episodes of feeding after arousal from sleep. SRED is often associated with the use of sedative-hypnotic medications, in particular the widely prescribed benzodiazepine receptor agonists. Compelling evidence suggests that nocturnal eating may in some cases be another nonmotor manifestation of Restless Legs Syndrome (RLS). Initial management should focus upon decreasing the potential for sleep-related injury followed by treating comorbid sleep disorders and eliminating incriminating drugs. Sexsomnia is a subtype of disorders of arousal, where sexual behavior emerges from partial arousal from nonREM sleep. Overlap parasomnia disorders consist of abnormal sleep-related behavior both in nonREM and REM sleep. Status dissociatus is referred to as a breakdown of the sleep architecture where an admixture of various sleep state markers is seen without any specific demarcation. Benzodiazepine therapy can be effective in controlling SW, ST, and sexsomnia, but not SRED. Paroxetine has been reported to provide benefit in some cases of ST. Topiramate, pramipexole, and sertraline can be effective in SRED. Pharmacotherapy for other parasomnias continues to be less certain, necessitating further investigation. NREM parasomnias may resolve spontaneously but require a review of priming and predisposing factors.

Motor Dysfunction in REM Sleep Behavior Disorder: A Rehabilitation Framework for Prodromal Synucleinopathy.

Parkinson disease (PD) and other related diseases with α-synuclein pathology are associated with a long prodromal or preclinical stage of disease. Predictive models based on diagnosis of idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) make it possible to identify people in the prodromal stage of synucleinopathy who have a high probability of future disease and provide an opportunity to implement neuroprotective therapies. However, rehabilitation providers may be unaware of iRBD and the motor abnormalities that indicate early motor system dysfunction related to α-synuclein pathology. Furthermore, there is no existing rehabilitation framework to guide early interventions for people with iRBD. The purpose of this work is to (1) review extrapyramidal signs of motor system dysfunction in people with iRBD and (2) propose a framework for early protective or preventive therapies in prodromal synucleinopathy using iRBD as a predictive marker. Longitudinal and cross-sectional studies indicate that the earliest emerging motor deficits in iRBD are bradykinesia, deficits performing activities of daily living, and abnormalities in speech, gait, and posture. These deficits may emerge up to 12 years before a diagnosis of synucleinopathy. The proposed rehabilitation framework for iRBD includes early exercise-based interventions of aerobic exercise, progressive resistance training, and multimodal exercise with rehabilitation consultations to address exercise prescription, progression, and monitoring. This rehabilitation framework may be used to implement neuroprotective, multidisciplinary, and proactive clinical care in people with a high likelihood of conversion to PD, dementia with Lewy bodies, or multiple systems atrophy.

REM Sleep Without Atonia and Gait Impairment in People with Mild-to-Moderate Parkinson's Disease.

BACKGROUND: Subtle gait deficits can be seen in people with idiopathic rapid eye movement (REM) sleep behavior disorder (RBD), a prodromal stage of Parkinson's disease (PD) and related alpha-synucleinopathies. It is unknown if the presence and level of REM sleep without atonia (RSWA, the electromyographic hallmark of RBD) is related to the severity of gait disturbances in people with PD. OBJECTIVE: We hypothesized that gait disturbances in people with mild-to-moderate PD would be greater in participants with RSWA compared to those without RSWA and matched controls, and that gait impairment would correlate with measures of RSWA. METHODS: Spatiotemporal characteristics of gait were obtained from 41 people with PD and 21 age-matched controls. Overnight sleep studies were used to quantify muscle activity during REM sleep and group participants with PD into those with RSWA (PD-RSWA+, n = 22) and normal REM sleep muscle tone (PD-RSWA-, n = 19). Gait characteristics were compared between groups and correlated to RSWA. RESULTS: The PD-RSWA+ group demonstrated significantly reduced gait speed and step lengths and increased stance and double support times compared to controls, and decreased speed and cadence and increased stride velocity variability compared to PD-RSWA- group. Larger RSWA scores were correlated with worse gait impairment in the PD group. CONCLUSION: The presence and level of muscle tone during REM sleep is associated with the severity of gait disturbances in PD. Pathophysiological processes contributing to disordered gait may occur earlier and/or progress more rapidly in people with PD and RBD.

Effect of Levetiracetam on Cognition in Patients With Alzheimer Disease With and Without Epileptiform Activity: A Randomized Clinical Trial.

Importance: Network hyperexcitability may contribute to cognitive dysfunction in patients with Alzheimer disease (AD). Objective: To determine the ability of the antiseizure drug levetiracetam to improve cognition in persons with AD. Design, Setting, and Participants: The Levetiracetam for Alzheimer's Disease-Associated Network Hyperexcitability (LEV-AD) study was a phase 2a randomized double-blinded placebo-controlled crossover clinical trial of 34 adults with AD that was conducted at the University of California, San Francisco, and the University of Minnesota, Twin Cities, between October 16, 2014, and July 21, 2020. Participants were adults 80 years and younger who had a Mini-Mental State Examination score of 18 points or higher and/or a Clinical Dementia Rating score of less than 2 points. Screening included overnight video electroencephalography and a 1-hour resting magnetoencephalography examination. Interventions: Group A received placebo twice daily for 4 weeks followed by a 4-week washout period, then oral levetiracetam, 125 mg, twice daily for 4 weeks. Group B received treatment using the reverse sequence. Main Outcomes and Measures: The primary outcome was the ability of levetiracetam treatment to improve executive function (measured by the National Institutes of Health Executive Abilities: Measures and Instruments for Neurobehavioral Evaluation and Research [NIH-EXAMINER] composite score). Secondary outcomes were cognition (measured by the Stroop Color and Word Test [Stroop] interference naming subscale and the Alzheimer's Disease Assessment Scale-Cognitive Subscale) and disability. Exploratory outcomes included performance on a virtual route learning test and scores on cognitive and functional tests among participants with epileptiform activity. Results: Of 54 adults assessed for eligibility, 11 did not meet study criteria, and 9 declined to participate. A total of 34 adults (21 women [61.8%]; mean [SD] age, 62.3 [7.7] years) with AD were enrolled and randomized (17 participants to group A and 17 participants to group B). Thirteen participants (38.2%) were categorized as having epileptiform activity. In total, 28 participants (82.4%) completed the study, 10 of whom (35.7%) had epileptiform activity. Overall, treatment with levetiracetam did not change NIH-EXAMINER composite scores (mean difference vs placebo, 0.07 points; 95% CI, -0.18 to 0.32 points; P = .55) or secondary measures. However, among participants with epileptiform activity, levetiracetam treatment improved performance on the Stroop interference naming subscale (net improvement vs placebo, 7.4 points; 95% CI, 0.2-14.7 points; P = .046) and the virtual route learning test (t = 2.36; Cohen f2 = 0.11; P = .02). There were no treatment discontinuations because of adverse events. Conclusions and Relevance: In this randomized clinical trial, levetiracetam was well tolerated and, although it did not improve the primary outcome, in prespecified analysis, levetiracetam improved performance on spatial memory and executive function tasks in patients with AD and epileptiform activity. These exploratory findings warrant further assessment of antiseizure approaches in AD. Trial Registration: ClinicalTrials.gov Identifier: NCT02002819.

Proposed diagnostic criteria for night eating syndrome.

OBJECTIVE: To propose criteria for diagnosis of the night eating syndrome (NES). METHOD: An international research meeting was held in April 2008, and consensus criteria for NES diagnosis were determined. RESULTS: The core criterion is an abnormally increased food intake in the evening and nighttime, manifested by (1) consumption of at least 25% of intake after the evening meal, and/or (2) nocturnal awakenings with ingestions at least twice per week. Awareness of the eating episodes is required, as is distress or impairment in functioning. Three of five modifiers must also be endorsed. These criteria must be met for a minimum duration of 3 months. DISCUSSION: These criteria help standardize the definition of NES. Additional aspects of the nosology of NES yet to be fully elaborated include its relationship to other eating and sleep disorders. Assessment and analytic tools are needed to assess these new criteria more accurately.

Rapid Eye Movement Sleep Behavior Disorder and Other Rapid Eye Movement Parasomnias.

PURPOSE OF REVIEW: The discovery of rapid eye movement (REM) sleep and, in particular, REM sleep behavior disorder (RBD) have brought elusive nightmarish experiences to scientific scrutiny. This article summarizes a century of sleep research to examine the maladies of dreaming, their pathophysiologic significance, and management. RECENT FINDINGS: Under healthy physiologic conditions, REM sleep is characterized by vivid mentation combined with skeletal muscle paralysis. The loss of REM sleep atonia in RBD results in vivid, potentially injurious dream enactment to patients and bed partners. RBD is common, affecting at least 1% of the population and is primarily caused by α-synuclein pathology of REM sleep-related brainstem neurons. The majority of patients with RBD ultimately develop a neurodegenerative syndrome such as Parkinson disease, dementia with Lewy bodies, or multiple system atrophy. Among patients with Parkinson disease, RBD predicts an aggressive disease course with rapid cognitive, motor, and autonomic decline. RBD is diagnosed by the presence of dream enactment episodes (either recorded or clinically recalled) and physiologic evidence of REM sleep without atonia demonstrated on polysomnography. Bedroom safety is of paramount importance in the management of RBD while pharmacokinetic options include melatonin or clonazepam. SUMMARY: The injurious dream enactment of RBD is common and treatable. It is a syndrome of α-synuclein pathology with most patients ultimately developing Parkinson disease, dementia with Lewy bodies, or a related disorder.

REM sleep without atonia is associated with increased rigidity in patients with mild to moderate Parkinson's disease.

OBJECTIVE: Increased muscle activity during rapid eye movement (REM) sleep (i.e. REM sleep without atonia) is common in people with Parkinson's disease (PD). This study tested the hypotheses that people with PD and REM sleep without atonia (RSWA) would present with more severe and symmetric rigidity compared to individuals with PD without RSWA and age-matched controls. METHODS: Sixty-one individuals participated in this study (41 PD, 20 controls). An overnight sleep study was used to classify participants with PD as having either elevated (PD-RSWA+) or normal muscle activity (PD-RSWA-) during REM sleep. Quantitative measures of rigidity were obtained using a robotic manipulandum that passively pronated and supinated the forearm. RESULTS: Quantitative measures of forearm rigidity were significantly higher in the PD-RSWA+ group compared to the control group. Rigidity was significantly more asymmetric between limbs in the PD-RSWA- group compared with controls, while there was no significant difference in symmetry between the control and PD-RSWA+ groups. CONCLUSION: In people with mild to moderate PD, RSWA is associated with an increased and more symmetric presentation of upper limb rigidity. SIGNIFICANCE: Dysfunction of brainstem systems that control muscle tone during REM sleep may contribute to increased rigidity during wakefulness in people with PD.

A review of nighttime eating disorders.

Nighttime eating is categorized as either night eating syndrome (NES) or sleep-related eating disorder (SRED). These conditions represent an interruption in the overnight fast that characterizes human sleep. A critical review of the literature on NES and SRED will suggest that they are situated at opposite poles of a disordered eating spectrum. NES could be considered an abnormality in the circadian rhythm of meal timing with a normal circadian timing of sleep onset. Conversely, the feeding behavior in SRED is characterized by recurrent episodes of eating after an arousal from nighttime sleep with or without amnesia. Both conditions are often relentless and chronic. Multiple definitions of night eating have limited our ability to determine the exact prevalence of NES. Studies have suggested that central nervous system (CNS) serotonin modulation may lead to an effective treatment of NES. SRED is frequently associated with other sleep disorders, in particular parasomnias. Early studies have shown that the anti-seizure medication topiramate may be an effective treatment for SRED.

Corrigendum: Multi-modal Brain MRI in Subjects with PD and iRBD.

[This corrects the article on p. 709 in vol. 11, PMID: 29311789.].

Non-Rapid Eye Movement Sleep and Overlap Parasomnias.

PURPOSE OF REVIEW: This article reviews the spectrum of non-rapid eye movement (non-REM) sleep parasomnias, including sleepwalking, confusional arousals, and sleep terrors, which represent the range of phenotypic disorders of arousal from non-REM sleep that occurs in children and adults. RECENT FINDINGS: The International Classification of Sleep Disorders, Third Edition (ICSD-3) classifies parasomnias according to the sleep stage they emerge from: REM, non-REM, or other. Demographics, clinical features, and diagnosis of non-REM parasomnias are reviewed in this article, and an up-to-date synopsis of guidelines for management strategies to assist in the treatment of these sleep disorders is provided. SUMMARY: The non-REM parasomnias are most common in children and adolescents but may persist into adulthood. They can be distinguishable from REM parasomnias and nocturnal epilepsies, and, importantly, may lead to injury. Additionally, other parasomnias in this spectrum include sleep-related eating disorder and sexsomnia. Overlap parasomnia disorder includes one or more manifestations of a non-REM parasomnia seen in combination with REM sleep behavior disorder, representing an apparent erosion of the normally distinct stages of non-REM and REM sleep. A similar yet much more extreme dissociation of states underlies agrypnia excitata and status dissociatus, which represent rare, severe dissociations between non-REM, REM, and wake states resulting clinically in oneiric behaviors and severe derangement of normal polysomnographic wake and sleep stage characteristics. Management of non-REM and overlap parasomnias and state dissociation disorders include ensuring bedroom safety and prescription of clonazepam or hypnosis, in select cases, although in children and adolescents with noninjurious behaviors, non-REM parasomnias are often age-limited developmental disorders, which may ultimately remit by adulthood, and, in these cases, counseling and education alone may suffice. Timely and accurate recognition of the non-REM and overlap parasomnias is crucial to limiting potential patient injury.

Test-Retest Reliability of Two Consecutive Mean Sleep Latency Tests in Patients with Hypersomnia.

Reliability of mean sleep latency testing (MSLT) over consecutive days in patients with hypersomnia is unknown. We reviewed MSLTs of patients with hypersomnia without cataplexy who underwent our two consecutive MSLT protocol (N=29). Average MSLs were 10.9 and 10.9 minutes for days 1 and 2, respectively. Agreement for pathological hypersomnia (defined as MSL≤8 minutes) between MSLT days showed k=0.85 for all (N=29) and k=0.76 for those without sleep apnea (N=20). In patients with subjective complaints of hypersomnia, a single MSLT is sufficient (vs. addition of 2nd day MSLT) in the setting of carefully implemented protocol controlling for potential confounding variables.