Search

Sleep-related dissociative disorder (SRDD) is a female-predominant psychiatric parasomnia that was first identified as a condition that mimics sleepwalking in 1989, and was included in the International Classification of Sleep Disorders, 2nd edition, in 2005, with a subsequent expanding literature of case series and case reports. The objective hallmark of SRDD, found in about half of the reported cases, is sustained electroencephalogram (EEG) wakefulness during dissociative episodes emerging during wake-sleep transitions or after awakenings from light non-rapid eye movement (NREM) sleep or rapid eye movement (REM) sleep. Herein are reported two additional cases of SRDD in two female patients aged 53 and 40 years with prominent histories of multimodal abuse (typical of SRDD), with childhood emotional and food deprivation abuse in Case 1, and childhood emotional, sexual, and physical abuse in Case 2. Both patients were affected by “sleep phobia” and had recurrent nocturnal eating episodes. Major findings from the cumulative literature on SRDD are reinforced by these cases, with additional findings being described, particularly nocturnal eating behaviors and priming/triggering factors.

Rationale: Sleep disturbances (insomnia and nightmare symptoms) are the most sensitive and persistent symptoms of pediatric post-traumatic stress disorder (PTSD). Untreated, these sleep disturbances (SD) associated with PTSD are predictive of PTSD persistence and increased psychiatric complications. The aim of this study was to evaluate sleep and circadian rhythms in children with PTSD under both laboratory and ecological conditions in comparison with a control population and to test for the first time the hypothesis that SD and circadian rhythms are positively correlated with PTSD severity and its comorbidities. Method: This prospective pilot study evaluated PTSD, SD (insomnia, nightmares), and sleep-wake rhythms in 11 children with PTSD (aged 3–18), compared with the age and sex-matched control groups. Assessment of PTSD and subjective and objective measures of sleep and sleep-wake rhythms (questionnaires, 24-h in-laboratory video-polysomnography, 15-day at-home actigraphy recording) were performed between 1 and 6 months after the traumatic event. Results: Children with PTSD had higher sleep fragmentation (increased wake-after-sleep onset, increased number of sleep stage changes) compared to controls, with a change in sleep microarchitecture (micro-arousal index at 14.8 versus 8.2, p = 0.039). Sleep fragmentation parameters correlated with PTSD symptomatology, insomnia, and post-traumatic nightmare severity. The within-group comparison revealed a better sleep architecture in the controlled (sleep laboratory) than in the ecological condition (at home) (total sleep time 586 versus 464 min, p = 0.018). Conclusions: Sleep and rhythm disturbances are strongly associated with PTSD in children. The assessment of SD in children with PTSD should be carried out systematically and preferentially under ecological conditions, and management of SD should integrate the environment (environmental design, psycho-education for the children and their parents) more fully into therapy focused on sleep and trauma. [ABSTRACT FROM AUTHOR]

The pathogenesis of rapid eye movement (REM) sleep behavior disorder (RBD) is unclear. According to the cortical hypothesis, severe RBD episode (RBDE) occurs when spinal motoneurons are less inhibited and cortical and limbic systems are more active. We made this study to prove the hypothesis for the development of RBDE using video-polysomnography (VPSG). VPSG records of 35 patients with RBD were analyzed. According to severity, RBDEs were classified into three motor events (MEs): ME 1; small movements or jerks, ME 2; proximal movements including violent behavior, and ME 3; axial movements including bed falls. For each ME, we measured the number of MEs preceded or not preceded by both REM sleep without atonia (RWA) and REMs during the 10-s-period immediately before ME onset. In severe RBDE (ME 3), the number of MEs preceded by both RWA and REMs was significantly higher than that of MEs not preceded by both (0.8 vs. 0.2, P = 0.033). This was not the case for mild RBDE (ME 1) and moderate RBDE (ME 2). Our results suggest that both RWA and REMs are associated with the development of severe RBDE. [ABSTRACT FROM AUTHOR]

Sleep-related rhythmic movement disorder (SRRMD) occurs in both infants and children. This disorder rarely occurs or persists in adolescence or adulthood. Rhythmic movement during sleep in children is often asymptomatic and considered a benign condition. It is classified as SRRMD when movement significantly disrupts sleep, results in daytime functional impairment, or causes self-inflicted body injury. Several studies have demonstrated that SRRMD occurs in all sleep stages. Few studies have investigated rhythmic movement disorder (RMD) in children. SRRMD is a clinical diagnosis supported by home video recordings. When the clinical history is insufficient to provide a definitive diagnosis of SRRMD, and other sleep-related conditions or seizure disorders are suspected, video-polysomnography is indicated. There are currently no clinical guidelines for treating SRRMD. [ABSTRACT FROM AUTHOR]

Sleep-related rhythmic movement disorder (SRRMD) occurs in both infants and children. This disorder rarely occurs or persists in adolescence or adulthood. Rhythmic movement during sleep in children is often asymptomatic and considered a benign condition. It is classified as SRRMD when movement significantly disrupts sleep, results in daytime functional impairment, or causes self-inflicted body injury. Several studies have demonstrated that SRRMD occurs in all sleep stages. Few studies have investigated rhythmic movement disorder (RMD) in children. SRRMD is a clinical diagnosis supported by home video recordings. When the clinical history is insufficient to provide a definitive diagnosis of SRRMD, and other sleep-related conditions or seizure disorders are suspected, video-polysomnography is indicated. There are currently no clinical guidelines for treating SRRMD.

Gengyao Hu,1,2,* Na Yuan,1,* Yuanhang Pan,1,* Bi Wang,1 Xiaoli Wang,1 Zezhi Wang,1 Ze Chen,1 Yonghong Liu1 1Department of Neurology, Xijing Hospital, Fourth Military Medical University (Air Force Medical University), Xi’an, 710032, People’s Republic of China; 2Department of Neurology, Xi’an People’s Hospital (Xi’an Fourth Hospital), Xi’an, 710061, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yonghong LiuDepartment of Neurology, Xijing Hospital, Fourth Military Medical University (Air Force Medical University), Xi’an, People’s Republic of ChinaTel +86 13991236602Email liuyhong@fmmu.edu.cnStudy Objectives: To evaluate clinical and electrophysiological features of sleep-related head jerk (SRHJ) and electromyographic activity of superficial neck muscles during head jerk.Methods: Totally, 850 cases with video-polysomnography recording were collected, among which 50 presented with SRHJ. In these 50 patients, 15 underwent electromyography (EMG) check on bilateral sternocleidomastoid (SCM) and trapezius muscles as well as chin, while 35 had only chin EMG check. Further, the sensitivity and specificity of the both EMGs were calculated and compared.Results: Six among the 50 SRHJ patients had a primary complaint of involuntary head jerks associated with impaired sleep. Approximately 76.1% of head jerks occurred during REM sleep with the median head jerk index of 5.9/h, 64.5% of which were associated with electroencephalogram arousals and 66.4% with body movements. One patient showed SRHJ predominantly in NREM sleep but also in wakefulness. Surface EMG of SCM/trapezius muscles showed a sensitivity of 92% and a specificity of 97.8%, whereas chin EMG had a sensitivity of 14.5% and a specificity of 98.8%.Conclusion: SRHJ was associated with electroencephalogram arousals and might interfere with sleep. Surface EMG of SCM/trapezius muscles exhibited a good accuracy in the revelation of SRHJ.Keywords: sleep-related head jerk, neck myoclonus, movement disorder, video-polysomnography, electromyography

Abstract Disorders of Arousal (DOA) are mental and motor behaviors arising from NREM sleep. They comprise a spectrum of manifestations of increasing intensity from confusional arousals to sleep terrors to sleepwalking. Although DOA in childhood are usually harmless, in adulthood they are often associated with injurious or violent behaviors to the patient or others. Driving motor vehicles, suspected suicide, and even homicide or attempted homicide have been described during sleepwalking in adults. Furthermore, adult DOA need to be differentiated from other sleep disorders such as Sleep-related Hypermotor Epilepsy or REM Sleep Behavior Disorder. Although many aspects of DOA have been clarified in the last two decades there is still a lack of objective and quantitative diagnostic criteria for DOA. Recent advances in EEG analysis and in the semiological characterization of DOA motor patterns have provided a better definition of DOA diagnosis. Our article focuses on the DOA diagnostic process describing accurately the newest DOA clinical, EEG and video-polysomnographic tools in order to aid clinicians in DOA assessment.

Background: Rapid eye movement (REM) sleep behavior disorder (RBD) is associated with neurodegenerative diseases; however, few longitudinal studies assess the individual evolution of RBD and REM sleep without atonia (RWA) in Parkinson's disease (PD). Objectives: We aimed to evaluate RBD and RWA changes over time as well as potentially influential factors. Methods: RBD and RWA were analyzed using video‐supported polysomnography (vPSG) in initially de novo PD patients at baseline and every 2 years for a total of 6 years. The influence of time, age, sex, levodopa equivalent daily dose (LEDD), unified Parkinson's disease rating scale (UPDRS) sum scores, benzodiazepine intake, Mini‐Mental State Examination (MMSE) total scores, and dyskinesia on RWA were investigated using mixed‐effect models to account for intra‐individual correlations. Results: After 6 years, vPSG data were available from 98 of the initial 159 de novo PD patients. RBD prevalence increased from 25% at baseline to 52%. Of the 31 PD patients with RBD and valid vPSGs at all time‐points, RWA increased from an average of 19% at baseline to 41% at 6‐year follow‐up modeled to grow by 29.7% every 2 years (P < 0.001). Time was an independent factor (P < 0.001) for RWA increase. Age was an independent factor influencing RWA increase (P = 0.04). Sex, LEDD, UPDRS sum scores, benzodiazepines, MMSE total scores, and dyskinesia did not have any significant influence. Conclusions: RBD and RWA increased significantly over time in PD; time and age were independent factors in a prospective cohort. RBD and RWA can be considered PD progression markers. [ABSTRACT FROM AUTHOR]

Objective: Sleep‐related hypermotor epilepsy (SHE) is a focal epilepsy characterized by seizures occurring mostly during sleep, ranging from brief seizures with paroxysmal arousals (SPAs) to hyperkinetic seizures and ambulatory behaviors. SPAs are brief and stereotypic seizures representing the beginning of a major seizure. Distinguishing SPAs from disorders of arousal (DOAs) and their briefest episodes called simple arousal movements (SAMs) is difficult. We performed a characterization of SPAs and SAMs to identify video‐polysomnographic (VPSG) features that can contribute to the diagnosis of SHE or DOA. Methods: Fifteen SHE, 30 DOA adult patients, and 15 healthy subjects underwent full‐night VPSG. Two neurologist experts in sleep disorders and epilepsy classified all the sleep‐related movements and episodes recorded. For each SPAs and SAMs, sleep stage at onset, duration, limb involvement, progression, and semiology have been identified. Results: A total of 121 SPAs were recorded, emerging mostly during stage 1‐2 non–rapid eye movement (NREM) sleep (median duration: 5 seconds). At the beginning, the SPAs motor pattern was hyperkinetic in 78 cases (64%), involving more than three non‐contiguous or all body parts. The standard was a constant progression of movements during SPAs without any motor arrests. In DOA patients a total of 140 SAMs were recorded (median duration: 12 seconds) mostly emerging during stage 3 NREM sleep. In SAMs, we did not observe any tonic/dystonic or hypermotor patterns or stereotypy; motor arrest was present over the course of about half of the episodes. In comparison with both DOA and healthy subjects, SHE patients showed a higher number of sleep‐related movements per night and a reduction of sleep efficiency. Significance: SPAs and SAMs present different semiological and clinical features. Their recognition could be useful to drive the diagnosis when major episodes are not recorded during VPSG in patients with a clear clinical history of SHE or DOA. [ABSTRACT FROM AUTHOR]

Background: The brain stem is found to be impaired in multiple system atrophy-cerebellar types (MSA-C). Rapid eye movement (REM) sleep behavior disorder (RBD) is reported as a marker of progressive brain stem dysfunction. Few systematic studies about the sleep disturbances in MSA-C patients combined with or without RBD were reported. This study aimed to explore the polysomnographic (PSG) features of sleep disturbances between MSA-C patients with and without RBD. Methods: Totally, 46 MSA-C patients (23 with RBD, and 23 without RBD) were enrolled in this study. All patients underwent a structured interview for their demographic data, history of sleep pattern, and movement disorders; and then, overnight video-PSG was performed in each patient. All the records were evaluated by specialists at the Sleep Medicine Clinic for RBD and the Movement Disorder Clinic for MSA-C. The Student's t-test, Mann-Whitney U-test for continuous variables, and the Chi-square test for categorical variables were used in this study. Results: MSA-C patients with RBD had younger visiting age (52.6 ± 7.4 vs. 56.7 ± 6.0 years, P = 0.046) and shorter duration of the disease (12.0 [12.0, 24.0] vs. 24.0 [14.0, 36.0] months, P = 0.009) than MSA-C patients without RBD. MSA-C with RBD had shorter REM sleep latency (111.7 ± 48.2 vs. 157.0 ± 68.8 min, P = 0.042), higher percentage of REM sleep (14.9% ±4.0% vs. 10.0% ± 3.2%, P = 0.019), and lower Stage I (9.5% ±7.2% vs. 15.9% ±8.0%, P = 0.027) than MSA-C without RBD. Moreover, MSA-C patients with RBD had more decreased sleep efficiency (52.4% ±12.6% vs. 65.8% ±15.9%, P = 0.029) than that without RBD. Conclusions: In addition to the RBD, MSA-C patients with RBD had other more severe sleep disturbances than those without RBD. The sleep disorders of MSA patients might be associated with the progress of the disease.

Objective: To present findings on a series of cases of sporadic nocturnal frontal lobe epilepsy (NFLE), a form of NFLE that is infrequently reported, in contrast to familial (autosomal dominant) NFLE. Both forms of NFLE need to be distinguished from parasomnias, nocturnal temporal lobe epilepsy, and other nocturnal disorders. Methods: Eight consecutive cases of sporadic NFLE were evaluated at a sleep clinic in Taiwan. All patients had clinical evaluations, daytime waking and sleeping EEGs, brain MRIs, and overnight video-polysomnography (vPSG) with seizure montage. Results: Gender was equal (four males, four females); mean age was 18.4 yrs (range, 7–41 yrs). Age of NFLE onset was by puberty. Premorbid history was negative for any neurologic, medical or psychiatric disorder. NFLE subtypes: nocturnal paroxysmal dystonia, n=6; paroxysmal arousals, n=2. MRI brain scan abnormalities with clinical correlates were found in one patient. Daytime awake EEGs were negative for ictal/interictal activity in all patients, but two patients had daytime sleep EEGs with interictal epileptiform EEG activity. During vPSG studies, three of eight patients with NFLE seizure events had concurrent epileptiform EEG activity, and two patients had interictal epileptiform EEG activity during their vPSG studies. No case had a spontaneous remission. Anticonvulsant therapy was highly effective in all eight cases (>75% reduction in seizure frequency). Discussion: These cases confirm that sporadic NFLE closely resembles familial NFLE, and comprises a set of distinct clinical manifestations, with variable intensity, and variable scalp EEG epileptiform abnormalities across sleep and wakefulness, which have previously been identified in Caucasian patients from Europe and North America.

Nocturnal frontal lobe epilepsy (NFLE) is a focal epilepsy with seizures arising mainly during sleep and characterized by complex, often bizarre, motor behavior or sustained dystonic posturing. First described in 1981, it was initially considered a motor disorder of sleep and was named nocturnal paroxysmal dystonia (NPD). The unusual seizure semiology, onset during sleep, and often uninformative scalp EEG and brain MRI make it difficult to distinguish NPD attacks from other non-epileptic nocturnal paroxysmal events, namely parasomnias. The long-debated epileptic origin of the condition was finally demonstrated in 1990 and the term NFLE introduced. Even though many aspects of parasomnias and NFLE have been clarified in the last two decades, the differential diagnosis remains a challenge for clinicians. To address controversial issues and define the diagnostic criteria for NFLE, a Consensus Conference was held in Bologna, Italy in 2014. Major points of agreement emerged on: (i) the relationship of the seizures with sleep and not with the circadian pattern of seizure occurrence; (ii) the possible extrafrontal origin of hypermotor seizures, without substantial differences in seizure semiology. In the wake of the Consensus, the syndrome was renamed Sleep-Related Hypermotor Epilepsy (SHE). [ABSTRACT FROM AUTHOR]

Background and aims: Rapid eye movement (REM) sleep behavior disorder (RBD) is commonly associated with neurodegenerative disorders characterized by α-synuclein deposition, including Parkinson's disease, multiple system atrophy, and Lewy body dementia. However, this tendency in tauopathy-mediated diseases is rare and only sporadically reported. We systematically illustrate the occurrence of RBD and sleep features among a cohort of patients with Alzheimer's disease (AD), a non-synucleinopathy. Methods: We recruited 105 clinically probable AD patients. Fifteen clinically probable AD patients with suspected RBD underwent a video-polysomnography (vPSG) examination. Results: Five patients with probable AD exhibited RBD. One of the patients performed repeated touching of the head and the face with his hands and flailed his arms. Three patients exhibited hand twisting, exploring, prominent limb kicking, and jerking. The fifth patient exhibited all of the characteristics of RBD (he recalled a dream about fighting animals), and his wife was awakened by his screaming. Of these five patients, one patient took the acetylcholinesterase inhibitor drug donepezil. The patients with AD + RBD demonstrated increases in both tonic and phasic electromyography activity during REM sleep, but sleep architecture did not differ between the AD + RBD and AD-alone groups. Conclusion: RBD can occur in patients with AD. The occurrence of RBD does not change the sleep architecture of AD patients. [ABSTRACT FROM AUTHOR]

Although parasomnias should be considered benign conditions without a deleterious impact on sleep quality and quantity, especially in children, it is important to recognize and properly diagnose these phenomena. Moreover, parasomnias may be misdiagnosed as epileptic seizures, in particular seizures with a predominant complex motor behavior as seizures occurring in nocturnal frontal lobe epilepsy (NFLE), leading to unnecessary and expensive investigations and prolonged and unsuccessful treatment. In this article we describe the clinical and neurophysiologic features of the most common parasomnias, giving the most reliable elements of differential diagnosis between parasomnias and epileptic nocturnal seizures, namely the typical seizures occurring in NFLE. The diagnostic value of history-taking, video-polysomnography, home video recording, and diagnostic scales is discussed. Next we describe the intriguing aspect of the frequent coexistence, in the same family and even in the same patients, of epileptic and parasomniac attacks, giving a common neurophysiologic interpretation. Finally some brief indications to the treatment of parasomnias are suggested. [ABSTRACT FROM AUTHOR]

Study Objectives: To update the literature on the diagnostic category of sleep-related dissociative disorders (SRDDs), involving psychogenic dissociation, since the time of their inclusion in the parasomnias section of the International Classification of Sleep Disorders, second edition, in 2005; to summarize the most salient clinical and video-polysomnographic (vPSG) findings and typical clinical profile from all reported cases; and to provide the rationale for the re-inclusion of the group of SRDDs in future editions of the International Classification of Sleep Disorders., Methods: A systematic computerized literature search was conducted searching for SRDDs, nocturnal dissociative disorders, and nocturnal dissociation., Results: Nine additional cases were identified, with sufficient clinical history and vPSG findings to justify the diagnosis of SRDDs, supplementing the 11 cases cited in the International Classification of Sleep Disorders, second edition, for a total of 20 cases. Twenty-six other cases with vPSG testing were found, with 18 cases reported in abstracts and 8 cases reported in a publication with compelling histories of SRDDs and 2 consecutive vPSG studies, but without the vPSG findings explicitly reported for any case. In more than half of all reported cases, there was objective diagnostic confirmation for SRDDs consisting of the hallmark finding of abnormal nocturnal behaviors arising from sustained electroencephalography wakefulness, or during wake-sleep transitions, without epileptiform activity. These nocturnal behaviors often replicated daytime psychogenic dissociative behaviors. A history of trauma (physical, sexual, emotional) was an almost universal finding, along with major psychopathology. All patients, except for one, had prominent histories of daytime dissociative disorders. Many of the patients were referred on account of a presumed parasomnia., Conclusions: Cases of SRDDs continue to be reported, often as a "parasomnia mimic," with psychogenic dissociation being clearly distinguished from physiologic sleep-wake dissociation as found in primary sleep disorders such as narcolepsy, rapid eye movement sleep behavior disorder, etc. Eleven reasons are provided for why the category of SRDDs should be re-included in future editions of the International Classification of Sleep Disorders, and in the parasomnias section., (© 2021 American Academy of Sleep Medicine.)

Study Objectives: This case-control study aimed to identify and validate behavioral markers supporting the diagnosis of disorders of arousal (DOA) with video polysomnography., Methods: All behaviors associated with 1,335 episodes of N3 interruptions were compared in 52 adult patients with DOA versus 52 participants without DOA (healthy control patients and patients with insomnia, hypersomnia, or sleep apnea syndrome)., Results: Patients with DOA had more frequent (5.1 ± 2.4 versus 3.4 ± 1.9 interruptions/N3 time) and longer (35.8 ± 33 versus 23.1 ± 21.4 sec) arousals and awakenings from N3 than control patients. In the DOA group, the onset of behaviors was more abrupt, and behaviors including eye opening (69% versus 16%), head raising (41% versus 9%), visually exploring the environment (27% versus 1%), expression of fear/surprise (21% versus zero), speaking (18% versus 0.3%), trunk raising (13% versus 0.3%), and interacting with the environment (13% versus 0.5%), were (unlike quiet, comfort behaviors) more frequent than in control patients. A cutoff of two or more N3 interruptions containing eye opening yielded a sensitivity of 94.2% and a specificity of 76.9% for a DOA diagnosis. This accuracy was confirmed in a second set of data (second night of monitoring). Behaviors including an expression of fear/surprise (67.3%), sitting (32.7%), screaming, and standing up were specific to patients with DOA., Conclusions: A simple, behavioral video marker of behavioral reactions during N3 interruption (ie, opening the eyes at least two times in the same night) was sensitive, specific, and reproducible for discriminating patients with DOA from sleep laboratory control patients., Clinical Trial Registration: This study is a surrogate study of NCT02648568 and NCT03074578 on ClinicalTrials.gov., (© 2020 American Academy of Sleep Medicine.)

Study Objectives: REM sleep behavior disorder (RBD) is a common manifestation of Parkinson disease (PD). In this study, we assessed the effects of rotigotine transdermal patch on RBD features in patients with PD., Methods: In this prospective open-label study, eleven PD patients with untreated RBD were administered rotigotine patches for up to seven months to ameliorate their parkinsonism. The severities of their RBD symptoms before and after rotigotine therapy were evaluated through patient and bed partner interviews, a validated evaluation scale (REM sleep behavior disorder questionnaire-Hong Kong, RBDQ-HK), and blinded assessments based on video-polysomnographic (VPSG) measure., Results: Rotigotine improved parkinsonism and subjective sleep quality in PD patients with RBD. The RBDQ-HK total score, especially the Factor 2 score, was decreased, which demonstrated that the subjective severity of RBD symptoms was improved after rotigotine treatment, especially the frequency and severity of abnormal RBD-related motor behaviors. The VPSG analyses showed that the total sleep time (TST) and stage 1% were increased and that the PLMS index was decreased. However, no differences in the RBD-related sleep measures were observed., Conclusions: The improved RBD symptoms and VPSG measures of PD patients in this study (TST, stage 1%, and PLMS index) suggest that, in PD, rotigotine may partially improve RBD-related symptoms. Rotigotine should be considered to be an optional drug for the treatment of RBD symptoms in PD., (© 2016 American Academy of Sleep Medicine)

Study Objectives: Despite the high prevalence and clinical relevance of NREM parasomnias, data on supportive genetic markers are scarce, and mainly refer to sleepwalking only., Methods: We retrospectively analyzed clinical, polysomnographic, and HLA findings of 74 adults (37 men) with NREM parasomnia gathered from four neurological sleep centers. Parasomniac events were classified according to ICSD-2 criteria. HLA DQB1 genotyping was compared to regional-matched reference allele-frequencies., Results: Fifty-six patients had more than 2 different parasomnia type: 11 sleepwalking, 4 sleep terrors, 3 confusional arousals only. Parasomniac events were documented during video-polysomnography (V-PSG) in 70% (49/70) of subjects (71.4% confusional arousals, 8.2% sleep terrors, 4.1% sleepwalking, 16.3% ≥ 2 NREM parasomnia types). Violent behavior during V-PSG occurred in 8.5% (6/71). NREM parasomnia onset was reported after the age of 30 years in 6.8% (5/74). The HLA DQB1*05:01 allele was present in 41% (29/71) compared to 24.2% in the regional-matched reference allele group (p < 0.05). This haplotype prevalence did not differ within the NREM parasomnia type. Epworth Sleepiness Score was 10 or higher in 28.6%., Conclusions: This is a large polysomnography-based case series of patients with NREM parasomnia. In patients with suspected sleepwalking or sleep terrors, polysomnography is highly useful in detecting arousals from NREM sleep as a marker of NREM parasomnia. We confirmed previous findings by demonstrating a high prevalence of the HLA DQB1*05:01 genotype for different types of NREM parasomnias. Our findings therefore support a common genetic background, and corroborate the importance of video-polysomnography in the work-up of parasomnia., (© 2016 American Academy of Sleep Medicine.)

The first case of video-polysomnography (vPSG) documented sleep masturbation in a male is reported, and the second reported case of shift work induced sexsomnia. A 20 y.o. soldier with childhood sleepwalking (SW) developed sleep masturbation and SW triggered by military shift work. vPSG documented two episodes of sleep masturbation from N2 sleep in the fourth sleep cycle and from N3 sleep during the fifth sleep cycle. There was no sleep-disordered breathing nor periodic limb movements. vPSG thus confirmed confusional arousals from NREM sleep as the cause of the masturbation. Bedtime clonazepam therapy controlled the SW but not the masturbation.

Study Objectives: To describe three cases of sleep related, idiopathic rhythmic movement disorder (RMD) with atypical headbanging, consisting of head punching and head slapping., Methods: Three consecutive patients (2 males [11 and 13 years old) and one female [22 years old]) presented with atypical headbanging of 6 years, 7 years, and 17 years duration. In 2 cases, typical rhythmic headbanging (with use of the head) shifted after 3-4 years to atypical headbanging, with frontal head punching that was quasi-rhythmic. In one case, atypical headbanging (head-slapping) was the initial and only RMD. There was no injury from the headbanging. Prenatal, perinatal, developmental, behavioral-psychological, medical-neurological, and family histories were negative. Clinical evaluations and nocturnal video-polysomnography with seizure montage were performed on all patients., Results: Atypical headbanging was documented in all 3 cases; episodes always emerged late in the sleep cycle: from N2 sleep in 11 episodes, from REM sleep in 4 episodes, and from N1 sleep in 1 episode. Epileptiform activity was not detected. Clonazepam therapy was substantially effective in 1 case but not effective in 2 cases., Conclusions: These 3 cases of idiopathic atypical headbanging expand the literature on this RMD variant, as to our knowledge only one previously documented case has been reported.