Sexsomnia Research Articles

The Parasomnias and Sleep Related Movement Disorders—A Look Back at Six Decades of Scientific Studies

The objective of this article is to provide a comprehensive personal survey of all the major parasomnias with coverage of their clinical presentation, investigation, physiopathogenesis and treatment. These include the four major members of the slow-wave sleep arousal parasomnias which are enuresis nocturna (bedwetting), somnambulism (sleepwalking), sleep terrors (pavor nocturnus in children, incubus attacks in adults) and confusional arousals (sleep drunkenness). Other parasomnias covered are sleep-related aggression, hypnagogic and hypnopompic terrifying hallucinations, REM sleep terrifying dreams, nocturnal anxiety attacks, sleep paralysis, sleep talking (somniloquy), sexsomnia, REM sleep behavior disorder (RBD), nocturnal paroxysmal dystonia, sleep starts (hypnic jerks), jactatio capitis nocturna (head and total body rocking), periodic limb movement disorder (PLMs), hypnagogic foot tremor, restless leg syndrome (Ekbom syndrome), exploding head syndrome, excessive fragmentary myoclonus, nocturnal cramps, and sleep-related epileptic seizures. There is interest in the possibility of relationships between sleep/wake states and creativity.

Olanzapine-Related Somnambulism: A Systematic Review of Literature and a Case Report of Anorexia Nervosa.

Somnambulism, or sleepwalking (SW), is one of the most common forms of arousal parasomnias. It is characterized by different complex motor behaviors leading to unwanted movements in bed or walking during sleep. It can be the consequence of psychological stress, abnormal breathing during sleep, high fever, or drug adverse effects. There is evidence of an association between antipsychotic treatment, including olanzapine, and SW. We present the case of a patient experiencing treatment-resistant anorexia nervosa whose somnambulism re-exacerbated after the addition of a low dose of olanzapine, following the CARE (CAse REport) Statement and Checklist. We also conducted a systematic review of the literature on olanzapine-induced somnambulism following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. PubMed, PsychINFO, and the Cochrane Library databases were independently reviewed up to January 2021 for articles reporting olanzapine-related somnambulism cases, without language or time restriction. We describe a case of somnambulism in a patient initially admitted to our hospital for anorexia nervosa and treated with a low dose of olanzapine. This is the first case of SW induced by olanzapine in eating disorders to be reported. Up-to-date olanzapine-related somnambulism was described in 8 patients experiencing psychiatric disorders (ie, schizophrenia and bipolar disorder). To provide a reliable estimate of incidence and prevalence for olanzapine-related somnambulism, large-scale, pharmacovigilance studies are required, to allow for comparisons of overall clinical characteristics, outcomes, including time to recovery, between different treatment options. Clinician awareness should be enhanced, and attention should be given to such infrequent adverse effects associated with antipsychotics.

Kambakutaisoto Treatment for Children With Night Crying and Arousal Parasomnias Developed During Prolonged Hospitalization for Hematological and Oncological Diseases.

The lack of an established treatment standard prompted an examination of whether kambakutaisoto, an herbal formula, is effective for non-rapid eye movement (NREM)-related parasomnias and night crying (provisionally defined as an infantile form of arousal parasomnia). This study included 137 children aged median 4.1 years (range, 0.02-18.5) who were admitted for hematological and oncological diseases. Of 137, 3 children developed recurrent episodes of NREM-related parasomnias, and 3 developed night crying. The proportion of children with night-crying/parasomnia receiving invasive procedures was significantly higher than those without (100% vs. 47%, P = .013). All 6 children with night crying/parasomnia received kambakutaisoto at a dose of 0.13-0.22 g/kg per os and responded from the start of administration with a significant reduction in the number of episodes. No adverse effects were observed. Kambakutaisoto may be a safe and promising therapy for night crying and NREM-related parasomnias in children.

Parasomnias Occurring in Non-Rapid Eye Movement Sleep.

This article discusses the clinical manifestations, diagnosis and differential diagnosis, pathophysiology, and management of parasomnias occurring in non-rapid eye movement (REM) sleep. Disorders of arousal are characterized by dissociated sleep, with wake and sleep phenomena intermingling, and local sleep, in which different areas of the brain exist simultaneously in different states of wakefulness or sleep. The frequency of arousals from slow-wave sleep with delta or mixed-frequency activity has a high sensitivity but relatively low specificity for the diagnosis of arousal parasomnias. Disorders of arousal (sleepwalking, sleep terrors, and confusional arousals) are characterized by incomplete awakenings from slow-wave sleep, limited recall of imagery, and partial or complete amnesia. They occur most frequently in childhood. Management includes correction of precipitating factors, attention to safety, behavioral techniques, and medications. Sleep-related eating disorder is a variant of arousal disorders and may be associated with the use of short-acting hypnotics and restless legs syndrome. Complex nocturnal visual hallucinations can occur with visual loss, dementia with Lewy bodies, use of β-adrenergic receptor antagonists, and anxiety. Exploding head syndrome occurs at wake-sleep transition or on waking during the night, is usually benign, and requires treatment only if significant sleep disruption occurs.

Sleep Disorders in Epilepsy: Current Trends and Future Perspectives

Sleep complaints are common in people with epilepsy (PWE). We aim to highlight the updated evidence regarding comorbid sleep disorders and epilepsy and the impact of epilepsy and its treatments on sleep. Up to two thirds of PWE report sleep disturbances which may signal presence of a comorbid sleep disorder, including insomnia, arousal parasomnias, excessive daytime sleepiness, obstructive sleep apnea, or restless legs syndrome. Uncontrolled seizures contribute to poor sleep quality, while presence of epilepsy (with or without seizures) and antiepileptic drugs is associated with changes in sleep architecture. Chronic intracranial EEG monitoring with implanted devices reveals a nocturnal peak for interictal epileptiform activity. Epilepsy surgery outcomes suggest better seizure control may improve sleep architecture and quality. Screening for and treating sleep disorders may lead to improved seizure control and quality of life in PWE. Epilepsy surgery and implanted devices to treat refractory epilepsy provide new insights into the relationship between sleep and epilepsy.

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.].

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.

Distinctive features of NREM parasomnia behaviors in parkinson's disease and multiple system atrophy.

ObjectiveTo characterize parasomnia behaviors on arousal from NREM sleep in Parkinson’s Disease (PD) and Multiple System Atrophy (MSA).MethodsFrom 30 patients with PD, Dementia with Lewy Bodies/Dementia associated with PD, or MSA undergoing nocturnal video-polysomnography for presumed dream enactment behavior, we were able to select 2 PD and 2 MSA patients featuring NREM Parasomnia Behviors (NPBs). We identified episodes during which the subjects seemed to enact dreams or presumed dream-like mentation (NPB arousals) versus episodes with physiological movements (no-NPB arousals). A time-frequency analysis (Morlet Wavelet Transform) of the scalp EEG signals around each NPB and no- NPB arousal onset was performed, and the amplitudes of the spectral frequencies were compared between NPB and no-NPB arousals.Results19 NPBs were identified, 12 of which consisting of ‘elementary’ NPBs while 7 resembling confusional arousals. With quantitative EEG analysis, we found an amplitude reduction in the 5-6 Hz band 40 seconds before NPBs arousal as compared to no-NPB arousals at F4 and C4 derivations (p<0.01).ConclusionsMany PD and MSA patients feature various NREM sleep-related behaviors, with clinical and electrophysiological differences and similarities with arousal parasomnias in the general population.SignificanceThis study help bring to attention an overlooked phenomenon in neurodegenerative diseases.

Are Absence Epilepsy and Nocturnal Frontal Lobe Epilepsy System Epilepsies of the Sleep/Wake System?

System epilepsy is an emerging concept interpreting major nonlesional epilepsies as epileptic dysfunctions of physiological systems. I extend here the concept of reflex epilepsy to epilepsies linked to input dependent physiological systems. Experimental and clinical reseach data were collected to create a coherent explanation of underlying pathomechanism in AE and NFLE. We propose that AE should be interpreted as epilepsy linked to the corticothalamic burst-firing mode of NREM sleep, released by evoked vigilance level oscillations characterized by reactive slow wave response. In the genetic variation of NFLE the ascending cholinergic arousal system plays an essential role being in strong relationship with a gain mutation of the nicotinic acethylcholin receptors, rendering the arousal system hyperexcitable. I try to provide a more unitary interpretation for the variable seizure manifestation integrating them as different degree of pathological arosuals and alarm reactions. As a supporting hypothesis the similarity between arousal parasomnias and FNLE is shown, underpinned by overlaping pathomechanism and shared familiarity, but without epileptic features. Lastly we propose that both AE and NFLE are system epilepsies of the sleep-wake system representing epileptic disorders of the antagonistic sleep/arousal network. This interpretation may throw new light on the pathomechanism of AE and NFLE.

Violent somnambulism: A parasomnia of young men with stereotyped dream-like experiences

ObjectiveTo characterize a subgroup of arousal parasomnias associated with violent behavior in adults. DesignA pilot study on clinical and polysomnographic data of 13 adult patients seen in a tertiary sleep center for the suspicion of arousal parasomnia associated with violence. ResultsNine young patients (8 males 1 female) had a common pattern of abnormalities: similar ‘claustrophobic’ dream-like experiences and complex, vehement dream enactments; no REM sleep without atonia on polysomnography. We call this syndrome ‘violent somnambulism’.The rest of the patients had alcoholic delirium, partial epilepsy, possible REM sleep behavior disorder and a single sleep walking episode provoked by a sleeping pill. Conclusions and hypothesisSleep related violence needs thorough diagnostic evaluation for preventing life-threatening consequences. Violent somnambulism appears to be a distinct NREM sleep-related overlap parasomnia.

Nocturnal Frontal Lobe Epilepsy

Nocturnal frontal lobe epilepsy (NFLE) is a syndrome of heterogeneous etiology, characterized by the occurrence of sleep-related seizures with different complexity and duration. Genetic, lesional, and cryptogenetic NFLE forms have been described. NFLE is generally considered a benign clinical entity, although severe, drug-resistant forms do exist. A significant proportion of sleep-related complex motor seizures, hardly distinguishable from NFLE, originate outside the frontal lobe. Moreover, the distinction of NFLE from the non-rapid eye movement arousal parasomnias may be challenging. A correct diagnosis of NFLE should be based on a diagnostic approach that includes the anamnestic, video-polysomnographic, morphological, and genetic aspects. Studies on the relationships between genes, arousal regulatory mechanisms, and epileptogenesis, using both clinical and experimental models of NFLE might provide key insights in the interrelationship between sleep and epilepsy.

CAP Characteristics Differ in Patients With Arousal Parasomnias and Frontal and Temporal Epilepsies

Arousal parasomnias (AP) and frontal and temporal epilepsies consist of pathologic arousals originating in abnormal thalamocortical circuits, reflecting increased sleep instability and arousal oscillations--the cyclic alternating pattern (CAP). In this study, the authors aim to investigate the CAP characteristics in 27 patients with AP, 22 patients with frontal and temporal epilepsies, and age- and gender-matched 20 healthy subjects. The mean CAP sequence and cycle was significantly higher in patients than in control subjects (P < 0.003). The total CAP duration was always higher in the patients with AP than in those with frontal and temporal epilepsies, reaching statistically significant level at the first (P = 0.044), second (P = 0.024), third (P = 0.010), and sixth (P < 0.001) sleep cycles. The duration of A1 in descending branch (P = 0.062) and trough phase of sleep cycles (P = 0.038) was longer in the patients with AP. The duration of A2 subtype of CAP in ascending branch (P = 0.039) and the number (P = 0.036) and duration (P = 0.050) of A3 subtype of CAP in descending branch of sleep cycles were higher in the patients with frontal and temporal epilepsies. This difference in CAP parameters might suggest that AP are associated with milder activation in specific brain areas, showing a similar evolution with physiologic homeostatic decrease in sleep synchronization. Frontal and temporal epilepsies, however, is associated with a moderate-to-powerful activation in wider brain networks.

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.

Treatment of Dyssomnias and Parasomnias in Childhood

Dyssomnias are sleep disorders associated with complaints of insomnia or hypersomnia. The daytime sleepiness of narcolepsy is treated by a combination of planned daytime naps, regular exercise medications such as modafinil, or salts of methylphenidate, or amphetamine. Cataplexy that accompanies narcolepsy is treated with anticholinergic agents, selective serotonin reuptake inhibitors, or sodium oxybate. Children with neurodevelopmental disabilities such as autism have sleep initiation and maintenance difficulties on a multifactorial basis, with favorable response to melatonin in some patients. Childhood onset restless legs syndrome is often familial, associated with systemic iron deficiency, and responsive to iron supplementation and gabapentin. Parasomnias are episodic phenomena events which occur at the sleep -- wake transition or by intrusion on to sleep. Arousal parasomnias such as confusional arousals and sleep walking can sometimes be confused with seizures. A scheme for differentiating arousal parasomnias from nocturnal seizures is provided. Since arousal parasomnias are often triggered by sleep apnea, restless legs syndrome, or acid reflux, treatment measures directed specifically at these disorders often helps in resolution. Clonazepam provided in a low dose at bedtime can also alleviate sleep walking and confusional arousals. Obstructive sleep apnea affects about 2 percent of children. Adeno-tonsillar hypertrophy, cranio-facial anomalies, and obesity are common predisposing factors. Mild obstructive sleep apnea can be treated using a combination of nasal corticosteroids and a leukotriene antagonist. Moderate to severe obstructive sleep apnea are treated with adeno-tonsillectomy, positive airway pressure breathing devices, or weight reduction as indicated. This paper provides an overview of the topic, with an emphasis on management steps. Where possible, the level of evidence for treatment recommendations is indicated.

Nocturnal Frontal Lobe Epilepsy vs Parasomnias

The diagnosis and treatment of nocturnal events can present significant challenges to the clinician. Correct diagnosis is the first step towards appropriate treatment, but may not be straightforward. In particular, non-rapid eye movement (NREM) arousal parasomnias, such as sleepwalking, sleep terrors, and confusional arousal can present in a similar fashion to nocturnal frontal lobe epilepsy (NFLE); dramatic and often bizarre behaviors from sleep are features of both conditions, and may result in diagnostic confusion. A careful clinical history, however, often enables accurate diagnosis, and the frontal lobe epilepsy and parasomnia (FLEP) scale, a validated questionnaire for the diagnosis of nocturnal events, can add diagnostic confidence. Recording of events on video-EEG-polysomnography is required if diagnostic doubt remains although is not always achievable, particularly if events are occurring infrequently. Treatments for NFLE and parasomnias are different, but lifestyle modification and treatment of coexisting sleep disorders (such as obstructive sleep apnoea) may have a role in both. In NFLE, medical treatment with antiepileptic drugs, particularly carbamazepine and topiramate, forms the mainstay of treatment; a small proportion of individuals with treatment-resistant seizures may benefit from epilepsy surgery. For parasomnias, reassurance and the removal of priming and precipitating factors is often sufficient. A minority of individuals will, however, need medical treatment, usually with benzodiazepines or tricyclic antidepressants. Unfortunately, there are few data on which to base treatment decisions in this area, with the evidence comprising predominantly case reports and case series. Well-designed studies, including randomised control trials, are needed and may require a multicentre approach.

Physiopathogenetic Interrelationship between Nocturnal Frontal Lobe Epilepsy and NREM Arousal Parasomnias

Aims. To build up a coherent shared pathophysiology of NFLE and AP and discuss the underlying functional network. Methods. Reviewing relevant published data we point out common features in semiology of events, relations to macro- and microstructural dynamism of NREM sleep, to cholinergic arousal mechanism and genetic aspects. Results. We propose that pathological arousals accompanied by confused behavior with autonomic signs and/or hypermotor automatisms are expressions of the frontal cholinergic arousal function of different degree, during the condition of depressed cognition by frontodorsal functional loss in NREM sleep. This may happen either if the frontal cortical Ach receptors are mutated in ADNFLE (and probably also in genetically not proved nonlesional cases as well), or without epileptic disorder, in AP, assuming gain in receptor functions in both conditions. This hypothesis incorporates the previous “liberation theory” of Tassinari and the “state dissociation hypothesis” of Bassetti and Terzaghi). We propose that NFLE and IGE represent epileptic disorders of the two antagonistic twin systems in the frontal lobe. NFLE is the epileptic facilitation of the ergotropic frontal arousal system whereas absence epilepsy is the epileptic facilitation of burst-firing working mode of the spindle and delta producing frontal thalamocortical throphotropic sleep system. Significance. The proposed physiopathogenesis conceptualize epilepsies in physiologically meaningful networks.

Characteristics of REM sleep behavior disorder in childhood.

To describe our experience regarding the clinical and polysomnographic features of REM sleep behavior disorder (RBD) in childhood. This was a retrospective chart review of children and adolescents with RBD and REM sleep without atonia. Demographics, and clinical and polysomnographic information were tabulated. Our findings were compared with those in the existing literature. The 15 subjects identified (13 RBD and 2 having REM sleep without atonia) had a mean age at diagnosis of 9.5 years (range 3-17 years); 11/15 (73%) were male. Nightmares were reported in 13/15 and excessive daytime sleepiness in 6/15. Two children had caused bodily harm to bedmate siblings. Comorbidities, which were multiple in some subjects, included anxiety (8/15), attention deficit disorder (10/15), nonspecific developmental delay (6/15), Smith-Magenis syndrome (1/15), pervasive developmental disorder (1/15), narcolepsy (1/15), idiopathic hypersomnia (1/15), and Moebius Syndrome (1/15). Abnormal MRI scans were seen in 5/8 evaluated subjects. Treatments consisted of clonazepam (10/15), melatonin (2/15), and discontinuation of a tricyclic agent (1/15), with a favorable response in 11 of 13. Two of 15 patients with REM sleep without atonia did not require pharmacotherapy. RBD in children may be associated with neurodevelopmental disabilities, narcolepsy, or medication use. It seems to be modestly responsive to benzodiazepines or melatonin. The etiology is distinct from that of common childhood arousal parasomnias and RBD in adults; congenital and neurodevelopmental disorders, medication effect, and narcolepsy coexisted in some, but none had an extrapyramidal neurodegenerative disorder.

Dissociated local arousal states underlying essential clinical features of non‐rapid eye movement arousal parasomnia: an intracerebral stereo‐electroencephalographic study

Sleep has been shown to be a global phenomenon in which the presence of local processes of both activation and deactivation are finely orchestrated. Dysfunctional and independent action of the systems involved in non-rapid eye movement (NREM) sleep and wakefulness is deemed to be at the basis of arousal parasomnias. We show, in a patient with confusional arousals, persistence of sleep in the hippocampal and frontal associative cortices in contrast to the presence of awakening in the motor, cingulate, insular, amygdalar and temporopolar cortices. The clinical features of the confusional arousals in this patient are highly consistent with a dysfunctional coexistence of local cortical arousal and local cortical sleep.

Primary Sleep Disorders and Paroxysmal Nocturnal Nonepileptic Events in Adults With Epilepsy From the Perspective of Sleep Specialists

Sleep specialists are frequently referred adults with epilepsy to evaluate their sleep/wake complaints, sometimes to determine whether their paroxysmal nocturnal behaviors are epileptic or not. Many patients with epilepsy have at least one parasomnia (some more than one), and the sleep specialists are often asked to differentiate and treat these. Sleep specialists review which primary sleep disorders are more common in adults with epilepsy and how to evaluate and best treat these. The authors summarize (1) how to evaluate and differentiate parasomnias using video-polysomnography; (2) the value of sleep deprivation and loud auditory stimuli to increase the likelihood of provoking a non-rapid eye movement arousal parasomnia with a single night of video-polysomnography; and (3) how to score excessive muscle activity during rapid eye movement sleep to confirm a diagnosis of rapid eye movement sleep behavior disorder. The clinical semiology and video-polysomnography features of simple and complex sleep-related movement disorders and parasomnias are reviewed.

Increased frequency of arousal parasomnias in families with nocturnal frontal lobe epilepsy: A common mechanism?

Retrospective observations disclosed an overlap between parasomnias and nocturnal frontal lobe epilepsy (NFLE) not only in patients but also in their relatives, suggesting a possible common pathogenetic mechanism. This study aimed to verify whether relatives of patients with NFLE have a higher frequency of parasomnias, namely arousal disorders, and thereby shed light on the still unknown pathophysiologic mechanisms underlying NFLE. We undertook a case-control family study in which we recruited NFLE probands and healthy controls, matched for age, sex, education, and geographic origin. At least four relatives were included for each proband and control. Each subject underwent a standardized interview, with application of the International Classification of Sleep Disorders-Revised (ICSD-R 2001) minimal criteria to diagnose the lifetime prevalence of the main parasomnias. Four hundred fifty-eight individuals were recruited: 33 NFLE probands, 200 relatives of probands, 31 controls, and 194 control relatives. All NFLE probands but one have sporadic NFLE. The lifetime prevalence of the following parasomnias differed in proband relatives versus control relatives: arousal disorders [odds ratio (OR) 4.7, 95% confidence interval (CI) 2.0-11.6; p < 0.001] and nightmares (OR 2.6, 95% CI 1.6-4.2; p < 0.001) were more frequent among NFLE proband relatives. In the secondary analysis comparing NFLE probands to controls, arousal disorders (OR 6.3, 95% CI 1.3-31.7; p = 0.023) and bruxism (OR 5.4, 95% CI 1.3-21.7; p = 0.017) were more frequent among NFLE probands. The higher frequency of arousal disorders in NFLE families suggests an intrinsic link between parasomnias and NFLE and an abnormal (possibly cholinergic) arousal system as a common pathophysiologic mechanism.