Non-rapid Eye Movement Parasomnias Research Articles

L-Tryptophan As Treatment for Pediatric Non-Rapid Eye Movement Parasomnia.

Parasomnias are common in childhood but there is no established treatment for parasomnias. The aim of this study was to (1) report on the outcome of using L-tryptophan to manage parasomnias in children and (2) examine sleep architecture and subjective psychological/sleep symptoms in children with parasomnia. A retrospective analysis was conducted of charts of children (3-18 years old) who underwent polysomnographic testing and were diagnosed with primary parasomnia. Study patients were either prescribed L-tryptophan (daily dose range: 500-4500 mg, mean dose of 2400 mg) to manage their parasomnias or administered no treatment whereby parents/guardians declined treatment. Questionnaires assessing sleep and psychosocial symptoms were administered at the initial clinical consultation and a follow-up parasomnia outcome questionnaire was administered over the phone to parents/guardians. One hundred and sixty-five children (106 boys, 59 girls) received a sleep diagnosis of primary parasomnia. A significantly (p < 0.001) higher proportion (84%) of children taking L-tryptophan experienced improvements in their parasomnia symptoms compared with those (47%) who chose not to use L-tryptophan. Polysomnography revealed that children with parasomnias had an altered sleep architecture based on age-related normative values. Children with a diagnosis of parasomnia were also subjectively more fatigued and endorsed more depressive symptoms. This study finds that parasomnias in children are not benign and that treatment with L-tryptophan provides a favorable outcome. Children diagnosed with parasomnia had altered sleep architecture, were more fatigued, and endorsed depressive symptoms. This study supports the need to diagnose and treat parasomnias in children.

Non-Rapid Eye Movement Sleep Parasomnias and Migraine: A Role of Orexinergic Projections.

Sleep and migraine share a common pathophysiological substrate, although the underlying mechanisms are unknown. The serotonergic and orexinergic systems are both involved in the regulation of sleep/wake cycle, and numerous studies show that both are involved in the migraine etiopathogenesis. These two systems are anatomically and functionally interconnected. Our hypothesis is that in migraine a dysfunction of orexinergic projections on the median raphe (MR) nuclei, interfering with serotonergic regulation, may cause Non-Rapid Eye Movement parasomnias, such as somnambulism. Acting on the serotonergic neurons of the raphe nuclei, the dysfunction of orexinergic neurons would lead to a higher release of serotonin. The activation of serotonergic receptors located on the walls of large cerebral vessels would lead to abnormal vasodilatation and consequently increase transmural pressure. This process could activate the trigeminal nerve terminals that innervate vascular walls. As a consequence, there is activation of sensory nerve endings at the level of hard vessels in the meninges, with release of pro-inflammatory peptides (e.g., substance P and CGRP). Within this hypothetical frame, the released serotonin could also interact with trigeminovascular afferents to activate and/or facilitate the release of the neuropeptide at the level of the trigeminal ganglion. The dysregulation of the physiological negative feedback of serotonin on the orexinergic neurons, in turn, would contribute to an alteration of the whole system, altering the sleep-wake cycle. Serotonergic neurons of the MR nuclei receive an excitatory input from hypothalamic orexin/hypocretin neurons and reciprocally inhibit orexin/hypocretin neurons through the serotonin 1A receptor (or 5-HT1A receptor). Considering this complex system, if there is an alteration it may facilitate the pathophysiological mechanisms involved in the migraine, while it may produce at the same time an alteration of the sleep-wake rhythm, causing sleep disorders such as sleepwalking. Understanding the complex mechanisms underlying migraine and sleep disorders and how these mechanisms can interact with each other, it would be crucial to pave the way for new therapeutic strategies.

Diagnostic criteria for disorders of arousal: A video-polysomnographic assessment.

To assess video-polysomnographic (vPSG) criteria and their cutoff values for the diagnosis of disorders of arousal (DOAs; sleepwalking, sleep terror). One hundred sixty adult patients with DOAs and 50 sex- and age-matched healthy participants underwent a clinical evaluation and vPSG assessment to quantify slow wave sleep (SWS) interruptions (SWS fragmentation index, slow/mixed and fast arousal ratios, and indexes per hour) and the associated behaviors. First, a case-control analysis was performed in 100 patients and the 50 controls to define the optimal cutoff values using receiver operating characteristic curves. Their sensitivity was then assessed in the other 60 patients with DOAs. The SWS fragmentation index and the mixed, slow, and slow/mixed arousal indexes and ratios were higher in patients with DOAs than controls. The highest area under the curve (AUC) values were obtained for the SWS fragmentation and slow/mixed arousal indexes (AUC = 0.88 and 0.90, respectively). The SWS fragmentation index cutoff value of 6.8/h reached a sensitivity of 79% and a specificity of 82%. The slow/mixed arousal index had a sensitivity of 94% for the 2.5/h cutoff, and 100% specificity for 6/h. Both parameters showed good interrater agreement, and their sensitivities were confirmed in the second group of patients. Combining electroencephalographic parameters and video-based behavioral analyses increased the correct classification rate up to 91.3%. Frequent slow/mixed arousals in SWS and complex behaviors during vPSG are strongly associated with DOAs, and could be promising biomarkers for the diagnosis of non-rapid eye movement parasomnias. Ann Neurol 2018;83:341-351.

Non-Rapid Eye Movement Arousal Parasomnias in Children.

Parasomnia is a common pediatric sleep disorder that can cause parents or caregivers distress when experienced by their children. Based on the International Classification of Sleep Disorders, parasomnias can be divided into two subgroups: non-rapid eye movement (NREM) parasomnias and rapid eye movement (REM) parasomnias. REM sleep parasomnias include nightmares, REM behavior disorder, and sleep paralysis, whereas NREM sleep parasomnias include disorders of arousal such as confusional arousals, sleepwalking, sleep talking, night terrors, and sleep-related eating disorder. This review focuses on the epidemiology, clinical presentation, diagnosis, and treatment of the most common form of parasomnias-NREM arousal parasomnias. Additionally, this review aims to help clinicians distinguish NREM parasomnias from nocturnal frontal lobe seizures, as this distinction is important to avoid diagnostic delays and inappropriate medication exposure. [Pediatr Ann. 2017;46(9):e327-e331.].

Gray matter abnormalities of the dorsal posterior cingulate in sleep walking

ObjectiveThis study aimed to determine whether voxel-based analysis of T1 weighted magnetic resonance imaging (MRI) and diffusion tensor imaging is able to detect alterations of gray and white matter morphometry as well as measures of mean diffusivity and fractional anisotropy in patients with non-rapid eye movement parasomnia. Methods3 Tesla MRI was performed in 14 drug-free, polysomnography-confirmed adult patients with non-rapid eye movement parasomnia (age: 29 ± 4.2 years; disease duration 19.2 ± 7.7 years) and 14 healthy subjects, matched for age and gender. Statistical parametric mapping was applied to objectively identify focal changes of MRI parameters throughout the entire brain volume. ResultsStatistical parametric mapping localized significant decreases of gray matter volume in the left dorsal posterior cingulate cortex (BA23) and posterior midcingulate cortex (BA24) in patients with non-rapid eye movement parasomnias compared to the control group (p < 0.001, corrected for multiple comparisons). No significant differences of mean diffusivity and fractional anisotropy measures were found between the non-rapid eye movement parasomnia group and the healthy control group. ConclusionsRecently, the simultaneous co-existence of arousal or wakefulness originating from the motor and cingulate cortices and persistent sleep in associative cortical regions was suggested as a functional framework of somnambulism. Gray matter volume decline in the dorsal posterior and posterior midcingulate cortex reported in this study might represent the neuroanatomical substrate for this condition.

Is there a common motor dysregulation in sleepwalking and REM sleep behaviour disorder?

This study sought to determine if there is any overlap between the two major non-rapid eye movement and rapid eye movement parasomnias, i.e. sleepwalking/sleep terrors and rapid eye movement sleep behaviour disorder. We assessed adult patients with sleepwalking/sleep terrors using rapid eye movement sleep behaviour disorder screening questionnaires and determined if they had enhanced muscle tone during rapid eye movement sleep. Conversely, we assessed rapid eye movement sleep behaviour disorder patients using the Paris Arousal Disorders Severity Scale and determined if they had more N3 awakenings. The 251 participants included 64 patients with rapid eye movement sleep behaviour disorder (29 with idiopathic rapid eye movement sleep behaviour disorder and 35 with rapid eye movement sleep behaviour disorder associated with Parkinson's disease), 62 patients with sleepwalking/sleep terrors, 66 old healthy controls (age-matched with the rapid eye movement sleep behaviour disorder group) and 59 young healthy controls (age-matched with the sleepwalking/sleep terrors group). They completed the rapid eye movement sleep behaviour disorder screening questionnaire, rapid eye movement sleep behaviour disorder single question and Paris Arousal Disorders Severity Scale. In addition, all the participants underwent a video-polysomnography. The sleepwalking/sleep terrors patients scored positive on rapid eye movement sleep behaviour disorder scales and had a higher percentage of 'any' phasic rapid eye movement sleep without atonia when compared with controls; however, these patients did not have higher tonic rapid eye movement sleep without atonia or complex behaviours during rapid eye movement sleep. Patients with rapid eye movement sleep behaviour disorder had moderately elevated scores on the Paris Arousal Disorders Severity Scale but did not exhibit more N3 arousals (suggestive of non-rapid eye movement parasomnia) than the control group. These results indicate that dream-enacting behaviours (assessed by rapid eye movement sleep behaviour disorder screening questionnaires) are commonly reported by sleepwalking/sleep terrors patients, thus decreasing the questionnaire's specificity. Furthermore, sleepwalking/sleep terrors patients have excessive twitching during rapid eye movement sleep, which may result either from a higher dreaming activity in rapid eye movement sleep or from a more generalised non-rapid eye movement/rapid eye movement motor dyscontrol during sleep.

Somnambulism: Emergency Department Admissions Due to Sleepwalking-Related Trauma.

IntroductionSomnambulism is a state of dissociated consciousness, in which the affected person is partially asleep and partially awake. There is pervasive public opinion that sleepwalkers are protected from hurting themselves. There have been few scientific reports of trauma associated with somnambulism and no published investigations on the epidemiology or trauma patterns associated with somnambulism.MethodsWe included all emergency department (ED) admissions to University Hospital Inselspital, Berne, Switzerland, from January 1, 2000, until August 11, 2015, when the patient had suffered a trauma associated with somnambulism. Demographic data (age, gender, nationality) and medical data (mechanism of injury, final diagnosis, hospital admission, mortality and medication on admission) were included.ResultsOf 620,000 screened ED admissions, 11 were associated with trauma and sleepwalking. Two patients (18.2%) had a history of known non-rapid eye movement parasomnias. The leading cause of admission was falls. Four patients required hospital admission for orthopedic injuries needing further diagnostic testing and treatment (36.4%). These included two patients with multiple injuries (18.2%). None of the admitted patients died.ConclusionAlthough sleepwalking seems benign in the majority of cases and most of the few injured patients did not require hospitalization, major injuries are possible. When patients present with falls of unknown origin, the possibility should be evaluated that they were caused by somnambulism.

Behavioral Treatments for Non-Rapid Eye Movement Parasomnias in Children

Non-rapid eye movement (NREM) parasomnias are common in childhood and include a range of clinical presentations including confusional arousals, sleepwalking, sleep terrors, and sleep-related eating disorder. While parasomnia episodes can be dramatic and elicit concern from parents, parasomnias are predominantly benign and self-limited. A comprehensive clinical evaluation is necessary for appropriate diagnosis and ruling out underlying medical disorders. For youth with parasomnia episodes that are infrequent or limited in severity, standard treatment recommendations, including safety measures and minimizing triggering factors, are highlighted. Scheduled awakening is an evidence-based behavioral treatment that can be effective at decreasing or resolving frequent and severe NREM parasomnias but may be burdensome for parents to implement.

Progress in elucidating the pathophysiological basis of nonrapid eye movement parasomnias: not yet informing therapeutic strategies.

Nonrapid eye movement (NREM) or arousal parasomnias are prevalent conditions in children and young adults, apparently provoked by any medical, physical, mental, or pharmacologic/toxic agent disturbing normal biorhythm and causing sleep fragmentation or abundant amount of slow wave sleep. The nadir and the ascending slope of the first sleep cycle of night sleep are the typical periods when NREM parasomnias, especially sleepwalking may occur on sleep-microstructural level; microarousals are the typical moments allowing NREM parasomnias. While sleep-disturbing factors have a clear precipitating effect, a genetic predisposition appears necessary in most cases. A candidate gene for sleepwalking has been identified on chromosome 20q12-q13.12 in one sleepwalking family. NREM parasomnias have a genetic and clinical link with nocturnal-frontal lobe epilepsies; possibly through an abnormality of the acetylcholine-related sleep-control system. The association of NREM parasomnias with the human leukocyte antigen system might be the sign of an autoimmune background to be further clarified. In the treatment of arousal parasomnias, the main tools are adequate sleep hygiene and the management of underlying conditions. Their pharmacotherapy has remained unresolved; the best options are clonazepam and some of the antidepressants, while a psychotherapy approach is also justified.

The utility of polysomnography for the diagnosis of NREM parasomnias: an observational study over 4 years of clinical practice.

Polysomnography (PSG) is considered the gold standard for diagnosis of non-rapid eye movement (NREM) parasomnias, however its diagnostic yield has been rarely reported. We aimed to assess the diagnostic value of polysomnography in different categories of patients with suspected NREM parasomnia and define variables that can affect the outcome. 124 adults referred for polysomnography for suspected NREM parasomnia were retrospectively identified and divided into clinical categories based on their history. Each polysomnography was analysed for features of NREM parasomnia or different sleep disorders and for presence of potential precipitants. The impact on the outcome of number of recording nights and concomitant consumption of benzodiazepines and antidepressants was assessed. Overall, PSG confirmed NREM parasomnias in 60.5 % patients and showed a different sleep disorder in another 16 %. Precipitants were found in 21 % of the 124 patients. However, PSG showed limited value when the NREM parasomnia was clinically uncomplicated, since it rarely revealed a different diagnosis or unsuspected precipitants (5 % respectively), but became essential for people with unusual features in the history where different or overlapping diagnoses (18 %) or unsuspected precipitants (24 %) were commonly identified. Taking benzodiazepines or antidepressants during the PSG reduced the diagnostic yield. PSG has a high diagnostic yield in patients with suspected NREM parasomnia, and can reveal a different diagnosis or precipitants in over 40 % of people with complicated or atypical presentation or those with a history of epilepsy. We suggest that PSG should be performed for one night in the first instance, with leg electrodes and respiratory measurements and after benzodiazepine and antidepressant withdrawal.

Alcohol and Non-Rapid Eye Movement Parasomnias: Where Is the Evidence?

Alcohol and Non-Rapid Eye Movement Parasomnias: Where Is the Evidence?

Dreaming and enacting dreams in nonrapid eye movement and rapid eye movement parasomnia: a step toward a unifying view within distinct patterns?

Dreaming and enacting dreams in nonrapid eye movement and rapid eye movement parasomnia: a step toward a unifying view within distinct patterns?

NREM Parasomnias: An important comorbidity in epilepsy patients of pediatric age

Objectives: We here aimed to investigate our pediatric group of patients to reveal the comorbidity of epilepsy and non-rapid eye movement (NREM) parasomnias and their clinical and polysomnographic characteristics. Methods: We retrospectively investigated all patients at the age of 18 or younger internalized within the last two years patients for a full night polysomnographic evaluation in our Sleep and Wake Disorders Unit. The diagnosis of epilepsy was made on the basis of clinical findings and electroencephalography findings; and the diagnosis of NREM parasomnia was made according to the International Classification of Sleep Disorders. Results: A total of 29 male (67.4%) and 14 female (32.6%) patients were investigated. Nineteen (44.2%) out of 43 patients were diagnosed as epilepsy. Nine (47.4%) of the patients with epilepsy also had delta-alpha paroxysms (DAP) and partial wakefulness during sleep – which are the characteristics polysomnographic features of NREM parasomnias. Conclusion: We observed a high comorbidity of epilepsy and NREM parasomnia in pediatric group of patients investigated in our sleep center. The arousal parasomnias are increasingly being reported to be more common in patients with epilepsy, probably due to shared common physiopathological mechanism characterized by pathological arousals originating in abnormal thalamo-cortical circuits produced by the central pattern generators.

Polysomnographic recording of a child with paroxysmal hypnogenic dyskinesia and NREM parasomnia

Paroxysmal dyskinesias are rare movement disorders characterized by involuntary episodicmovements including any combination of dystonia, ballism, chorea, or athetosis. Paroxysmal kinesigenic dyskinesias (PKD) and nonkinesigenic dyskinesias (PNKD) are the most common types. Though, paroxysmal hypnogenic dyskinesia (PHD) characterized by events occurring during non-rapid eye movement (NREM) sleep is rarely encountered [1].

Parasomnias: an updated review.

Parasomnias are abnormal behaviors emanating from or associated with sleep. Sleepwalking and related disorders result from an incomplete dissociation of wakefulness from nonrapid eye movement (NREM) sleep. Conditions that provoke repeated cortical arousals, 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 an arousal from sleep. SRED is often associated with the use of sedative-hypnotic medications; in particular, the widely prescribed benzodiazepine receptor agonists. Recently, compelling evidence suggests that nocturnal eating may in some cases be a nonmotor manifestation of Restless Legs Syndrome (RLS). rapid eye movement (REM) Sleep Behavior Disorder (RBD) is characterized by a loss of REM paralysis leading to potentially injurious dream enactment. The loss of atonia in RBD often predates the development of Parkinson's disease and other disorders of synuclein pathology. Parasomnia behaviors are related to an activation (in NREM parasomnias) or a disinhibition (in RBD) of central pattern generators (CPGs). Initial management should focus on decreasing the potential for sleep-related injury followed by treating comorbid sleep disorders. Clonazepam and melatonin appear to be effective therapies in RBD, whereas paroxetine has been reported effective in some cases of sleep terrors. At this point, pharmacotherapy for other parasomnias is less certain, and further investigations are necessary.

Epilepsy and sleep

There is a complex relationship between epilepsy, sleep and sleep disorders. Recent studies have provided new insights into the links between the disorders that may facilitate differential diagnosis and treatment but may also improve our understanding of underlying pathophysiological mechanisms. Sleep and sleep deprivation have long been recognized to influence interictal epileptiform discharges and seizures. More recent studies have shown that primary sleep disorders such as obstructive sleep apnoea may worsen epilepsy and treatment of these sleep disorders can lead to improved seizure control. Seizures may interfere with night-time sleep structure and cause excessive day-time somnolence (EDS). Antiepileptic drugs may also cause EDS or influence sleep. Despite more frequent use of video-electroencephalographic telemetry and polysomnography, the differential diagnostic challenges between nonrapid eye movement parasomnia and nocturnal frontal lobe epilepsy remain. There is also ongoing debate regarding the possibility of a common pathogenic background for parasomnias and nocturnal seizures that is summarized in the review. Accurate identification and diagnosis of sleep disorders as well as epilepsy is clinically important to ensure optimal treatment of both epilepsy and sleep disorders. Further studies of these nocturnal events may advance our understanding of underlying pathological mechanisms and the complex relationship between sleep and epilepsy.

Epilepsy and Sleep Disorders

There is a close association between sleep and epilepsy. In some epilepsy syndromes, seizures occur predominantly (or even exclusively) during sleep or on awakening. Excessive daytime sleepiness is common in patients with epilepsy and may be due not only to medication but also to nocturnal seizures or concomitant sleep disorders. Sleep disorders such as obstructive sleep apnoea can worsen epilepsy, with improvement of seizure control following appropriate treatment of the sleep disorder. Conversely, epilepsy and antiepileptic medication can worsen sleep disorders. Nocturnal epileptic seizures may be difficult to differentiate from parasomnias, in particular non-rapid eye movement parasomnias such as night terrors, sleepwalking and confusional arousals, on history alone since there are semiological similarities between the two disorders. Schemes have been developed to facilitate differential diagnosis, although this remains a challenge even using the gold standard, video-electroencephalography telemetry.

Epilepsy and Sleep Disorders

There is a close association between sleep and epilepsy. In some epilepsy syndromes, seizures occur predominantly (or even exclusively) during sleep or on awakening. Excessive daytime sleepiness is common in patients with epilepsy and may be due not only to medication but also to nocturnal seizures or concomitant sleep disorders. Sleep disorders such as obstructive sleep apnea can worsen epilepsy, with improvement of seizure control following appropriate treatment of the sleep disorder. Conversely, epilepsy and antiepileptic medication can worsen sleep disorders. Nocturnal epileptic seizures may be difficult to differentiate from parasomnias, in particular non-rapid eye movement parasomnias such as night terrors, sleepwalking and confusional arousals, on history alone since there are semiologic similarities between the two disorders. Schemes have been developed to facilitate differential diagnosis, although this remains a challenge even using the gold standard, video-electroencephalography telemetry.

Nocturnal Frontal Lobe Epilepsy - An Update on Differential Diagnosis with Non-rapid Eye Movement Parasomnia

Nocturnal Frontal Lobe Epilepsy - An Update on Differential Diagnosis with Non-rapid Eye Movement Parasomnia

Hypersynchronous Delta Waves and Somnambulism: Brain Topography and Effect of Sleep Deprivation

Hypersynchronous delta activity (HSD) is usually described as several continuous high-voltage delta waves (> or = 150 microV) in the sleep electroencephalogram of somnambulistic patients. However, studies have yielded varied and contradictory results. The goal of the present study was to evaluate HSD over different electroencephalographic derivations during the non-rapid eye movement (NREM) sleep of somnambulistic patients and controls during normal sleep and following 38 hours of sleep deprivation, as well as prior to sleepwalking episodes. N/A. Sleep disorders clinic. Ten adult sleepwalkers and 10 sex- and age-matched control subjects were investigated polysomnographically during a baseline night and following 38 hours of sleep deprivation. N/A. During normal sleep, sleepwalkers had a significantly higher ratio of HSD over the time spent in stage 2, 3 and 4 on frontal and central derivations when compared with controls. Sleep deprivation resulted in a significant increase in the ratio of the time in HSD over the time in stage 4 on the frontal lead in both groups and on the central lead in controls. There was no evidence for a temporal accumulation of HSD prior to the episodes. HSD shows a clear frontocentral gradient across all subjects during both baseline and recovery sleep and has relatively low specificity for the diagnosis of NREM parasomnias. Increases in HSD after sleep deprivation may reflect an enhancement of the homeostatic process underlying sleep regulation.