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Abstract
Parasomnias are defined as “disorders characterized by abnormal behavioral, experiential, or physiological events occurring in association with sleep, specific sleep stages, or sleep–wake transitions” in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). The clinical presentation and polysomnographic characteristics, associated factors, pathophysiology, prevalence, and treatment options of the NREM sleep parasomnias (somnambulism and sleep terrors), REM sleep parasomnias (nightmare disorder, recurrent isolated sleep paralysis, and REM sleep behavior disorder), and other parasomnias (sleep enuresis, sleep-related bruxism, sleep-related rhythmic movement disorder, somniloquy, and sleep-related groaning) are reviewed in this chapter. Some of these phenomena remind us that wakefulness and sleep states are not as mutually exclusive as one might believe.
Rapid eye movement (REM) sleep behaviour disorder (RBD) is a parasomnia that is characterized by loss of muscle atonia during REM sleep (known as REM sleep without atonia, or RSWA) and abnormal behaviours occurring during REM sleep, often as dream enactments that can cause injury. RBD is categorized as either idiopathic RBD or symptomatic (also known as secondary) RBD; the latter is associated with antidepressant use or with neurological diseases, especially α-synucleinopathies (such as Parkinson disease, dementia with Lewy bodies and multiple system atrophy) but also narcolepsy type 1. A clinical history of dream enactment or complex motor behaviours together with the presence of muscle activity during REM sleep confirmed by video polysomnography are mandatory for a definite RBD diagnosis. Management involves clonazepam and/or melatonin and counselling and aims to suppress unpleasant dreams and behaviours and improve bedpartner quality of life. RSWA and RBD are now recognized as manifestations of an α-synucleinopathy; most older adults with idiopathic RBD will eventually develop an overt neurodegenerative syndrome. In the future, studies will likely evaluate neuroprotective therapies in patients with idiopathic RBD to prevent or delay α-synucleinopathy-related motor and cognitive decline.
Purpose of Review
This manuscript briefly discusses the differential diagnosis and classification of nocturnal movements, as well as their etiology, significance, and available treatment options.
Recent Findings
The sympathetic hyperactivity accompanying nocturnal movements such as periodic limb movements of sleep and sleep bruxism is being increasingly recognized. Patterns of propagation of intensified hypnic jerks have been identified. Predisposing genetic factors for both non-rapid eye movement (NREM) and rapid eye movement (REM) parasomnias have been described. A new classification scheme for NREM movements and a new instrument to distinguish between NREM parasomnias and sleep-related hypermotor epilepsy (SHE, formerly known as “nocturnal frontal lobe epilepsy”) are being evaluated.
Summary
Clinicians should be able to evaluate simple and complex nocturnal movements, distinguish between physiological and pathological nocturnal movements on clinical and polysomnographic grounds, and identify nocturnal seizures or those nocturnal movements that may suggest an underlying neurological process.
Sleep terrors are characterized by marked CNS arousal and typically occur during stage 3-4 sleep within the first NREM cycle. Studies of the EEG during sleep terrors suggest that delta power and synchrony in the EEG may be important physiological markers of sleep terror presence and intensity. An EEG mapping study was undertaken with a single participant who experienced three sleep terror episodes in the laboratory. A one-minute section of EEG was sampled immediately prior to the onset of each of the three sleep terrors. Similar EEG sections were taken from 10 healthy sex- and age-matched controls. The sleep tenors and control (normative) data were then compared topographically with z-scores (z-mapping). The z-maps indicated that all three sleep terrors contained more total and delta power in central and frontal areas than the control EEG sections. Moreover, relative delta power in these areas for the three sleep terrors was proportional to the subjective intensity of the episode. Although this pre-arousal EEG pattern may be related to ongoing slow-wave sleep mentation that may sometimes trigger sleep terror episodes, its functional significance remains an open question. The results demonstrate the utility of EEG mapping for the quantification of brain activation during sleep terror attacks and suggest that discrete activity profiles are identifiable for different types of dreaming-related arousal.
We performed a nationwide epidemiological study to evaluate the prevalence and characteristics of nocturnal enuresis (NE) in Korean adolescents and adults. A questionnaire was sent via e-mail to 51,073 people aged 16-40 yr by stratified sampling according to age, sex, and region among a 200,000 internet survey panel pool. The questionnaire included following information; presence or absence of NE, frequency of NE, possible risk factors for NE, self-esteem scale score and depression score results, and measures for the treatment of NE. Among the 2,117 responders, 54 (2.6%) had NE (≥1 enuretic episode within 6 months). Of 54 bedwetters, 9.3% wet ≥1 night per week and 20.5% wet ≥1 per month. The prevalence rates remained relatively stable with no apparent trend of reduction with age. The presence of sleep disturbance, family history, urgency, or urge incontinence increased the probability of NE episode significantly. The self-esteem score was lower (P=0.053) and the depression scale score was higher (P=0.003) in bedwetters compared with non-bedwetters. Overall 2.6% of Korean aged 16-40 yr have NE. The higher rate of urgency and urge incontinence in adolescent and adult enuretics suggests that bladder function has an important role in adolescent and adult NE.
Background:
Enuresis (bedwetting) is a socially stigmatising and stressful condition which affects around 15% to 20% of five-year olds and up to 2% of young adults. Although there is a high rate of spontaneous remission, the social, emotional and psychological costs to the children can be great. Drugs (including desmopressin, tricyclics and other drugs) have often been tried to treat nocturnal enuresis.
Objectives:
To assess the effects of drugs other than desmopressin and tricyclics on nocturnal enuresis in children and to compare them with other interventions.
Search methods:
We searched the Cochrane Incontinence Group Specialised Register of trials (searched 15 December 2011), which includes searches of MEDLINE and CENTRAL, to identify published and unpublished randomised and quasi-randomised trials. The reference lists of relevant articles were also searched.
Selection criteria:
All randomised trials of drugs (excluding desmopressin or tricyclics) for treating nocturnal enuresis in children up to the age of 16 years were included in the review. Trials were eligible for inclusion if children were randomised to receive drugs compared with placebo, other drugs or behavioral interventions for nocturnal enuresis. Studies which included children with daytime urinary incontinence or children with organic conditions were also included in this review if the focus of the study was on nocturnal enuresis. Trials focused solely on daytime wetting and trials of adults with nocturnal enuresis were excluded.
Data collection and analysis:
Two review authors independently assessed the quality of the eligible trials and extracted data. Differences between review authors were settled by discussion with a third review author.
Main results:
A total of 40 randomised or quasi-randomised controlled trials (10 new in this update) met the inclusion criteria, with a total of 1780 out of 2440 children who enrolled receiving an active drug other than desmopressin or a tricyclic. In all, 31 different drugs or classes of drugs were tested. The trials were generally small or of poor methodological quality. There was an overall paucity of data regarding outcomes after treatment was withdrawn.For drugs versus placebo, when compared to placebo indomethacin (risk ratio [RR] 0.36, 95% CI 0.16 to 0.79), diazepam (RR 0.22, 95% CI 0.11 to 0.46), mestorelone (RR 0.32, 95% CI 0.17 to 0.62) and atomoxetine (RR 0.81, 95% CI 0.70 to 0.94) appeared to reduce the number of children failing to have 14 consecutive dry nights. Although indomethacin and diclofenac were better than placebo during treatment, they were not as effective as desmopressin and there was a higher chance of adverse effects. None of the medications were effective in reducing relapse rates, although this was only reported in five placebo controlled trials.For drugs versus drugs, combination therapy with imipramine and oxybutynin was more effective than imipramine monotherapy (RR 0.68, 95% CI 0.50 to 0.94) and also had significantly lower relapse rates than imipramine monotherapy (RR 0.35, 95% CI 0.16 to 0.77). There was an overall paucity of data regarding outcomes after treatment was withdrawn.For drugs versus behavioural therapy, bedwetting alarms were found to be better than amphetamine (RR 2.2, 95% CI 1.12 to 4.29), oxybutynin (RR 3.25, 95% CI 1.77 to 5.98), and oxybutynin plus holding exercises (RR 3.3, 95% CI 1.84 to 6.18) in reducing the number of children failing to achieve 14 consecutive dry nights.Adverse effects of drugs were seen in 19 trials while 17 trials did not adequately report the occurrence of side effects.
Authors' conclusions:
There was not enough evidence to judge whether or not the included drugs cured bedwetting when used alone. There was limited evidence to suggest that desmopressin, imipramine and enuresis alarms therapy were better than the included drugs to which they were compared. In other reviews, desmopressin, tricyclics and alarm interventions have been shown to be effective during treatment. There was also evidence to suggest that combination therapy with anticholinergic therapy increased the efficacy of other established therapies such as imipramine, desmopressin and enuresis alarms by reducing the relapse rates, by about 20%, although it was not possible to identify the characteristics of children who would benefit from combination therapy. Future studies should evaluate the role of combination therapy against established treatments in rigorous and adequately powered trials.
To examine the prevalence and clinical characteristics of REM sleep behavior disorder (RBD) and subclinical RBD in the Korean elderly population.
A community-based Korean Longitudinal Study on Cognitive Aging and Dementia and time-synchronized video-polysomnography (vPSG) in a laboratory.
Sleep laboratory in a university hospital.
348 individuals aged 60 years or older.
N/A.
Among 696 subjects who were invited to participate in a vPSG study, 348 completed the vPSG. RBD was diagnosed when subjects showed REM sleep without atonia (RSWA) in the vPSG, and had history of complex and vigorous behaviors during sleep or abnormal REM sleep behaviors in the vPSG. Subjects with RSWA but no abnormal REM sleep behaviors were diagnosed with subclinical RBD. Seven subjects (5 male, 2 female) had RBD, three of whom (1 male, 2 female) had Parkinson disease. Two subjects reported history of sleep-related injury. The crude prevalence of RBD and idiopathic RBD was 2.01% (95% confidence interval [CI] = 0.54% to 3.49%) and 1.15% (95% CI = 0.03% to 2.27%). An age and sex-adjusted prevalence estimate of RBD and idiopathic RBD in the Korean elderly was 2.01% and 1.34%. Eighteen subjects were diagnosed with subclinical RBD, and the prevalence of subclinical RBD was estimated to be 4.95%.
RBD and subclinical RBD are not rare in the elderly in the community with abnormal REM sleep behaviors of RBD being mild to injurious and violent. The clinical significance and long-term progression of subclinical RBD needs to be further explored, given the prevalence and its possible relation to RBD.
Kang SH; Yoon IY; Lee SD; Han JW; Kim TH; Kim KW. REM sleep behavior disorder in the Korean elderly population: prevalence and clinical characteristics. SLEEP 2013;36(8):1147-1152.
Objective: The aim of the present work was to systematically review the literature and identify all peer-reviewed papers dealing with etiological and risk factors associated with bruxism. Data sources: Data extraction was carried out according to the standard Cochrane systematic review methodology. The following databases were searched for randomized clinical trials (RCT), controlled clinical trials (CCT) or cohort studies: Cochrane Library, Medline, and Embase from 1980 to 2011. Unpublished literature was searched electronically using ClinicalTrials.gov. Data selection: The primary outcome was bruxism etiology. Studies should have a standardized method to assess bruxism. Data extraction: Screening of eligible studies, assessment of the methodological quality and data extraction were conducted independently and in duplicate. Two reviewers inspected the references using the same search strategy and then applied the same inclusion criteria to the selected studies. They used criteria for methodological quality that was previously described in the Cochrane Handbook. Among the 1247 related articles that were critically assessed, one randomized clinical trial, one controlled clinical trial and seven longitudinal studies were included in the critical appraisal. Of these studies, five were selected, but reported different outcomes. Data synthesis: There is convincing evidence that (sleep-related) bruxism can be induced by esophageal acidification and also that it has an important relationship with smoking in a dose-dependent manner. Disturbances in the central dopaminergic system are also implicated in the etiology of bruxism.
Rapid eye movement sleep behavior disorder (RBD) is a parasomnia characterized by the occurrence of intense movements during rapid eye movement (REM) sleep, also named paradoxical sleep. The neuronal dysfunctions at the origin of the loss of atonia in RBD patients are not known. One possibility is that RBD is due to the degeneration of neurons inducing the muscle atonia of REM sleep. Therefore, in our paper we review data on the populations of neurons responsible for the atonia of REM sleep before discussing their potential role in RBD. We first review evidence that motoneurons are tonically hyperpolarized by gamma-aminobutyric acid (GABA) and glycine and phasically excited by glutamate during REM sleep. Then, we review data indicating that the atonia of REM sleep is induced by glycinergic/GABAergic REM-on premotoneurons contained within the raphe magnus and the ventral and alpha gigantocellular reticular nuclei localized in the ventral medullary reticular formation. These neurons are excited during REM sleep by a direct projection from glutamatergic REM-on neurons localized in the pontine sublaterodorsal tegmental nucleus (SLD). From these results, we discuss the possibility that RBD is due to a specific degeneration of descending REM-on glutamatergic neurons localized in the caudal SLD or that of the REM-on GABA/glycinergic premotoneurons localized in the ventral medullary reticular formation. We then propose that movements of RBD are induced by descending projections of cortical motor neurons before discussing possible modes of action of clonazepam and melatonin.
To validate a questionnaire focused on REM sleep behavior disorder (RBD) in a community-based sample.
RBD is a parasomnia manifested by recurrent dream enactment behavior during REM sleep. While confirmation of RBD requires the presence of REM sleep without atonia on polysomnography (PSG), a screening measure for RBD validated in older adults would be desirable for clinical and research purposes.
We had previously developed the Mayo Sleep Questionnaire (MSQ) to screen for the presence of RBD and other sleep disorders. We assessed the validity of the MSQ by comparing the responses of subjects' bed partners with the findings on PSG. All subjects recruited from 10/04 to 12/08 in the Mayo Clinic Study of Aging-a population-based study of aging in Olmsted County, Minnesota-who had also undergone a previous PSG were the focus of this analysis.
The study sample included 128 subjects (104 male; median age 77 years [range 67-90]), with the following clinical diagnoses at baseline assessment: normal (n = 95), mild cognitive impairment (n = 30), and mild Alzheimer disease (n = 3). Nine (5%) subjects had RBD based on history and PSG evidence of REM sleep without atonia. The core question on recurrent dream enactment behavior yielded sensitivity (SN) of 100% and specificity (SP) of 95% for the diagnosis of RBD. The profile of responses on four additional subquestions on RBD improved specificity.
These data suggest that the MSQ has adequate SN and SP for the diagnosis of RBD among elderly subjects in a community-based sample.
Boeve BF; Molano JR; Ferman TJ; Lin Siong-Chi; Bieniek K; Tippmann-Peikert M; Boot B; St. Louis EK; Knopman DS; Petersen RC; Silber MH. Validation of the Mayo Sleep Questionnaire to screen for REM sleep behavior disorder in a community-based sample. J Clin Sleep Med 2013;9(5):475-480.
Primary nocturnal enuresis (PNE) is a common problem in developmental age with an estimated overall prevalence ranging from 1.6% to 15%, and possible persistence during adolescence. There is a growing interest in the sleep habits of children affected by PNE, which is derived from the contradictory data present in clinical literature. The aim of the present study was to evaluate the presence of sleep disturbances in a population of children affected by PNE, and to identify whether PNE could be considered as a risk factor for sleep disturbances among children.
A total of 190 PNE children (97 males, 93 females) aged 7-15 years, (mean 9.64 ± 1.35 years), and 766 typically developing children matched for age (P = 0.131) and gender (P = 0.963) were enrolled. To evaluate the presence of sleep habits and disturbances, all of the subjects' mothers filled out the Sleep Disturbances Scale for Children (SDSC), a questionnaire consisting of six subscales: Disorders in Initiating and Maintaining Sleep (DIMS), Sleep Breathing Disorders (SBD), Disorders of Arousal (DA), Sleep-Wake Transition Disorders (SWTD), Disorders of Excessive Somnolence (DOES), and Nocturnal Hyperhidrosis (SHY). The results were divided into "pathological" and "normal" scores using a cut-off value (pathological score = at least three episodes per week), according to the validation criteria of the test. Then, the Chi-square test was used to calculate the statistical difference and a univariate logistic regression analysis was applied to determine the role of PNE as a risk factor for the development of each category of sleep disorders and to calculate the odds ratio (OR).
PNE children show a higher prevalence of all sleep disturbances (41.03% DIMS; 85.12% SBD; 63.29% DA; 67.53% SWTD; 31.28% DOES; 37.92% SHY; 25.33% SDSC total score), and according to OR results (SDSC total score OR = 8.293, 95% confidence interval [CI] = 5.079-13.540; DIMS OR = 7.639, 95% CI = 5.192-11.238; SBD OR = 35.633, 95% CI = 22.717-55.893; DA OR = 13.734, 95% CI = 9.476-19.906; SWTD OR = 14.238, 95% CI = 9.829-20.625; DOES OR = 5.602, 95% CI = 3.721-8.432; SHY OR = 6.808, 95% CI = 4.608-10.059), PNE could be considered as a risk factor for the development of sleep disorders.
Among PNE children, sleep could be strongly altered, thus helping to affirm the hypothesis that PNE tends to alter sleep architecture, or it could itself be the consequence of an abnormal sleep structure. The findings also point to the existence of a potential increase in the risk of developing sleep disorders in the presence of PNE.
The parasomnias are classified as disorders of arousal, partial arousal, and sleep stage transition. Many of these parasomnias manifest dramatic symptoms causing an activation of central nervous system. Most parasomnias appear early in childhood. Some parasomnias, for example REM sleep behavior disorders (RBD) and sleep-related penile problems are seen in adult and aged people (Figure 1). Usually, these patients have predisposing factors including neurologic disorders and aging (Figure 2). Despite these explosive features, most of children with these parasomnias show spontaneous remission at the time of puberty.
Arousal parasomnias (night terrors, sleepwalking, and confusional arousals) have seldom been investigated in the adult general population. Clinical studies of parasomnias, however, show that these disorders may be indicators of underlying mental disorders and may have serious consequences.
A representative sample of the United Kingdom population (N = 4972) was interviewed by telephone with the Sleep-EVAL system.
Night terrors were reported by 2.2% (95% CI = 1.8% to 2.6%) of the sample, sleepwalking by 2.0% (1.6% to 2.4%), and confusional arousals by 4.2% (3.6% to 4.8%). The rate of these 3 parasomnias decreased significantly with age, but no gender difference was observed. Multivariate models identified the following independent factors as associated with confusional arousals (odds ratio [OR]): age of 15-24 years (OR = 4.1), shift work (OR = 2.1), hypnagogic hallucinations (OR = 3.3), deep sleep (OR = 1.6), daytime sleepiness (OR = 1.9), sleep talking (OR = 1.7), daily smoking (OR = 1.7), adjustment disorder (OR = 3.1), and bipolar disorder (OR = 13.0). Factors associated with night terrors were subjective sense of choking or blocked breathing at night (OR = 5.1), obstructive sleep apnea syndrome (OR = 4.1), alcohol consumption at bedtime (OR = 3.9), violent or injury-causing behaviors during sleep (OR = 3.2), hypnagogic hallucinations (OR = 2.2), and nightmares at least 1 night per month (OR = 4.0). Factors associated with sleepwalking were age of 15-24 years (OR = 5.2), subjective sense of choking or blocked breathing at night (OR = 5.1), sleep talking (OR = 5.0), and a road accident in the past year (OR = 3.9) after controlling for possible effects of sleep deprivation, life stress, and mental and sleep disorders.
Arousal parasomnias, especially night terrors and confusional arousals, are often the expression of a mental disorder. Other life or medical conditions, such as shift work or excessive need of sleep for confusional arousals and stressful events for sleepwalking, may also trigger parasomnias. Prevalence rates are based on self-reported data and, consequently, are likely underestimated.
IN ORDER to explore the proposed relationship between nightmare occurrence and schizotypy, 30 frequent-nightmare subjects (at least one occurrence per week) and 30 low-nightmare controls, all of whom were female college students, were compared on several converging measures of schizotypal signs and behaviors. Consistent with previous research, frequent nightmare subjects demonstrated greater deviance on psychometric scales of schizotypy, and reported significantly greater schizotypal symptomatology on a structured clinical interview, than controls did. In addition, nightmare subjects produced similar electrodermal habituation patterns to auditory orienting stimuli as those that have been documented in schizophrenia-spectrum disorders. The results suggest that nightmare experience may be a useful conjoint behavioral indicator for the early detection of schizophrenia-spectrum psychopathology.
Background: Although the relative incidence of violent behavior during sleep (VBS) is presumed to be low, no epidemiologic data exist to evaluate the prevalence of the phenomenon or to begin to understand its precursors or subtypes. This study examined the frequency of violent or injurious behavior during sleep and associated psychiatric risk factors.
Method: A representative United Kingdom sample of 2078 men and 2894 women between the ages of 15 to 100 years (representing 79.6% of those contacted) participated in a telephone interview directed by the Sleep-EVAL expert system specially designed for conducting such diagnostic telephone surveys.
Results: Two percent (N=106) of respondents reported currently experiencing VBS. The VBS group experienced more night terrors and daytime sleepiness than the non-VBS group. Sleep talking, bruxism, and hypnic jerks were more frequent within the VBS than the other group, as were hypnagogic hallucinations (especially the experience of being attacked), the incidence of smoking, and caffeine and bedtime alcohol intake. The VBS group also reported current features of anxiety and mood disorders significantly more frequently and reported being hospitalized more often during the previous 12 months than the non-VBS group. Subjects with mood or anxiety disorders that co-occurred with other nocturnal symptoms had a higher risk of reporting VBS than all other subjects.
Conclusion: We have identified a number of sleep, mental disorder, and other general health factors that characterize those experiencing episodes of VBS. These findings suggest that specific factors, perhaps reflecting an interaction of lifestyle and hereditary contributions, may be responsible for the observed variability in this rare but potentially serious condition.
The prevalence of night terrors and nightmares was studied in a school sample of 900 children of both sexes (age range 6-12 years) representative of all socioeconomic levels. Of the 487 children for whom valid questionnaires were returned, 6% had night terrors, whereas 22% had nightmares. Across the successive age groups both disorders showed a general decline; in each disorder, the prevalence for the 6-8 year old group was moderately higher than that for the 9-12 year old group. These findings provide evidence in support of the maturation/developmental nature of these two sleep disorders.
• Fifty adults with either a present or past complaint of somnambulism were evaluated to determine the development and clinical course of their disorder as well as their personality patterns. Generally, when sleepwalking was outgrown, its onset was before age 10 years and its termination before age 15 years. Current sleepwalkers, compared with past sleepwalkers, started sleepwalking at a later age, had a higher frequency of events, and had episodes earlier in the night. Their episodes were also characterized by more intense clinical manifestations. Furthermore, current sleepwalkers demonstrated high levels of psychopathology, whereas past sleepwalkers had essentially normal psychological patterns. Specifically, the current sleepwalkers showed active, outwardly directed behavioral patterns, suggestive of difficulties in handling aggression. The clinical application of these findings is discussed and practical recommendations are given for the evaluation and management of sleepwalking.
Childhood nocturnal enuresis has traditionally been regarded as a multifaceted problem with a variety of treatment interventions. This paper proposes a model based on the notion that nocturnal enuresis arises through the ill functioning of one or more of the following three systems - a lack of vasopressin release during sleep; bladder instability; and/or an inability to arouse from sleep to bladder sensations. Clinical signs of each system are outlined and the appropriate treatment intervention for each is discussed. It is argued that addressing nocturnal enuresis in this way will enhance overall treatment effectiveness.
Two cases of severe night terrors with sleepwalking in adults are described. In one of these, an episode resulted in three deaths; in the other, there was serious concern of death and bodily harm. Both men were employed, married, and functioning well without serious psychopathology. Neither could be given a definite DSM-III diagnosis, though both had some features of compulsive personality disorder. Both improved considerably with treatment.
Disturbed dreaming has been identified as a common primary or secondary symptom in several medical conditions, in addition to idiopathic nightmares and sleep–wake transition disorders. In these medical conditions, dream disturbances vary along a continuum of dream experience intensity. At the lower extreme of this continuum, dream recall ceases entirely (global cessation of dreaming) or is unusually impoverished in quantity or content (dream impoverishment). Impoverishment affects patients with alexithymia, posttraumatic stress disorder (PTSD), and some brain syndromes. At the higher extreme, dreaming is uncharacteristically excessive, vivid, and emo-tional (excessive dreaming). Excessive dreaming occurs in patients with epic dreaming, some brain lesions, and with-drawal from some medications. Dreaming may become so intense that it is confused with reality (dream–reality confu-sion), as is the case with the existential dreams of bereave-ment, with postpartum infant peril dreams, with intensive care unit delirium dreams, with dreams resulting from limbic lobe damage, and with psychotic dream-related aggression. Intense dreaming may also become rigidly stereotyped in structure (dream stereotypy). Conditions such as rapid eye movement (REM) sleep behavior disorder (RBD) with or with-out parkinsonism, epilepsy, PTSD reexperiencing dreams, migraine dreams, and prodromal cardiac dreams are affected by dream stereotypy. In many cases, dream disturbances appear to be aberrations of otherwise normal dream qualities, such as intensification, reality-mimesis, or recurrence. Often, sleep fragmentation is implicated in the disturbance, but causal relationships are not yet clear. Although it is primarily REM sleep that is involved, some disturbances are also seen in disorders affecting non-REM sleep. Effective treatments are available for many common disturbances, and other treat-ments are under development. In addition to the common dream disturbances of idiopathic nightmares and sleep–wake transition disorders (see Chapter 77), disturbed dreaming has been identified as a common primary or secondary symptom in several other medical con-ditions (Table 78–1). These disturbances can be organized conveniently along a continuum of varying vividness or intensity of the dream experience. At the lower extreme of this continuum, dream recall ceases entirely or is unusually impoverished in quantity or content. At the higher extreme, it is uncharacteristically excessive, vivid, and emotional, frequently confused with reality or rigidly stereotyped in structure.
Sleepwalking (SW) often has been associated with psychopathology, but the nature and magnitude of this relation remains unclear. The aim of our study was to investigate the presence of psychopathology in a large cohort of sleepwalkers and to determine if levels of psychopathology showed differential relations to specific characteristics of the disorder, including clinical history.
One-hundred and five sleepwalkers (39 men, 66 women; mean age, 32.4±9.5years) referred to our sleep disorders clinic for chronic SW underwent a comprehensive clinical investigation that included an overnight polysomnography (PSG) assessment in 90% of cases. All participants also completed a series of questionnaires, including the Beck Depression Inventory, Second Revision (BDI-II), the Beck Anxiety Inventory (BAI), and the Symptom Checklist 90-Revised (SCL-90-R).
The proportion of sleepwalkers who scored above the minimal clinical threshold on the BDI-II, BAI, and SCL-90-R was 27%, 40%, and 28%, respectively. Only 15% of sleepwalkers showed moderate to severe symptoms on the BDI-II and 19% on the BAI. Taken as a whole, these profiles are similar to those observed in the general adult population. The presence of psychopathology in sleepwalkers was associated with a negative family history for SW, a higher frequency of nightmares, and with potentially injurious behaviors enacted during somnambulistic episodes.
A majority of adult sleepwalkers consulting for the disorder do not report clinically significant levels of depression or anxiety. Overall, sleepwalkers with and without psychopathology appear more similar than dissimilar.
College students were administered an abbreviated form of the Imaginal Processes Inventory along with scales of sleep disturbance, positive mood, and dream recall. Results confirmed the earlier report by Starker and Hasenfeld that sleep disturbances were significantly associated with dysphoric patterns of daydreaming, and not associated with a positive daydreaming pattern. Correlational, factor-analytic and multiple linear regression analyses revealed sex differences possibly related to differential sensitivity to inner experience.
The present study prospectively investigated the relationship between nightmare prevalence, nightmare distress, and waking imaginative involvement. One hundred and sixteen individuals completed self-report indices of fantasy proneness, psychological absorption, and daydreaming as well as a sleep and dreaming questionnaire and a nightmare distress measure. Participants then kept a dreaming and nightmare log for 21 consecutive nights. As predicted, both nightmare prevalence and nightmare distress were associated with higher levels of fantasy proneness, psychological absorption, and a guilty-dysphoric daydreaming style but not with positively-toned daydreams or a highly distractible daydreaming style. Further, these results were not due to higher levels of overall dream recall. Last, these effects were additive as high scores on either fantasy proneness or absorption added significantly higher incremental validity to the prediction of nightmare prevalence and distress than just from the dysphoric daydreaming measure alone. The results are discussed within the context of emerging etiological theories of nightmare production.
Purpose:
The aim of this systematic review was to evaluate the efficacy of any biofeedback treatment on sleep bruxism.
Methods:
We searched the Cochrane Central Register of Controlled Trials, MEDLINE, Embase, ISI Web of Science, System for Information on Grey Literature in Europe, Chinese Biomedical Literature Database, and PsycINFO up to October 2012 for randomized controlled trials and controlled clinical trials involving biofeedback treatment for sleep bruxism. Reference lists of relevant studies were hand searched. Quality assessment and data extraction were performed by two reviewers independently.
Results:
Seven eligible studies involving 240 participants were finally included. Three of them had moderate risk of bias, and four had high risk of bias. In an electromyographic-measured sleep bruxism episode, meta-analysis showed no significant difference between contingent electrical stimulation and blank control (95% confidence interval = -12.33, 3.38, P = 0.26). Moreover, five studies reported electromyographic activity index. Due to the diversity of biofeedback modalities (auditory, electrical, and visual stimulus) and controls (splint, occlusal adjustment, etc.), these data were unable to be pooled, so only qualitative description was provided.
Conclusions:
In the current stage, there is no powerful evidence to support the use of biofeedback technology on sleep bruxism treatment. Contingent electrical stimulation which is defined as a kind of biofeedback modality shows no effect on reducing sleep bruxism episode compared with the no-treatment group. Although many studies support the efficacy of biofeedback treatment, more large sample-sized randomized controlled trials which adopt uniform outcome index are necessitated to verify its application.
The goal of the current study was to estimate the prevalence of sleep bruxism (SB) in the general population using a representative sample of 1,042 individuals who answered questionnaires and underwent polysomnography (PSG) examinations. After PSG, the individuals were classified into 3 groups: absence of SB, low-frequency SB, and high-frequency SB. The results indicated that the prevalence of SB, indicated by questionnaires and confirmed by PSG, was 5.5%. With PSG used exclusively as the criterion for diagnosis, the prevalence was 7.4% regardless of SB self-reported complaints. With questionnaires alone, the prevalence was 12.5%. Of the 5.5% (n = 56) with confirmed SB, 26 were classified as low-frequency SB, and 30 as high-frequency. The episodes of SB were more frequent in stage 2 sleep, and the phasic bruxism events were more frequent than tonic or mixed events in all sleep stages in individuals with SB. A positive association was observed between SB and insomnia, higher degree of schooling, and a normal/overweight body mass index (BMI). These findings demonstrate the prevalence of SB in a population sampled by PSG, the gold standard methodology in the investigation of sleep disorders, combined with validated questionnaires (ClinicalTrials.gov, NCT00596713).
The aim of the present investigation was to perform a systematic review of the literature dealing with the issue of sleep bruxism prevalence in children at the general population level. Quality assessment of the reviewed papers was performed to identify flaws in the external and internal validity. Cut-off criteria for an acceptable external validity were established to select studies for the discussion of prevalence data. A total of 22 publications were included in the review, most of which had methodological problems limiting their external validity. Prevalence data extraction was performed only on eight papers that were consistent as for the sampling strategy and showed only minor external validity problems, but they had some common internal validity flaws related with the definition of sleep bruxism measures. All the selected papers based sleep bruxism diagnosis on proxy reports by the parents, and no epidemiological data were available from studies adopting other diagnostic strategies (e.g. polysomnography or electromyography). The reported prevalence was highly variable between the studies (3·5-40·6%), with a commonly described decrease with age and no gender differences. A very high variability in sleep bruxism prevalence in children was found, due to the different age groups under investigation and the different frequencies of self-reported sleep bruxism. This prevented from supporting any reliable estimates of the prevalence of sleep bruxism in children.
Objective:
To compare the frequency of proxy-reported REM sleep behavior disorder (RBD) among relatives of patients with polysomnogram-diagnosed idiopathic RBD (iRBD) in comparison to controls using a large multicenter clinic-based cohort.
Methods:
A total of 316 patients with polysomnography-confirmed iRBD were recruited from 12 RBD study group centers, along with 316 controls matched on sex and age group. All subjects completed a self-administered questionnaire that collected proxy-reported information on family history of tremor, gait trouble, balance trouble, Parkinson disease, memory loss, and Alzheimer disease. The questionnaire also included a single question that asked about possible symptoms of RBD among first-degree relatives (siblings, parents, and children).
Results:
A positive family history of dream enactment was reported in 13.8% of iRBD cases compared to 4.8% of controls (odds ratio [OR] = 3.9, 95% confidence interval [CI] 2.0-7.7). ORs were increased for both siblings (OR = 6.1, 95% CI 2.1-18.1) and parents (OR = 3.2, 95% CI 1.4-7.8). We found no significant difference in sex, current age (65.3 ± 10.2 vs 66.9 ± 10.2 years), or age at self-reported RBD onset (55.2 ± 11.7 vs 56.6 ± 15.1 years) in possible familial vs sporadic iRBD. No differences were found in family history of tremor, walking and balance troubles, Parkinson disease, memory loss, or Alzheimer disease.
Conclusion:
We found increased odds of proxy-reported family history of presumed RBD among individuals with confirmed iRBD. This suggests the possibility of a genetic contribution to RBD.
Objective
Sleep bruxism (SB) and periodic limb movements during sleep (PLMS) may have a common underlying neurophysiologic mechanism, especially in relation to the occurrence of sleep-related electroencephalographic (EEG) arousals. To test this hypothesis, three research questions were assessed. First, it was assessed whether PLMS events occur more frequently in SB patients than in individuals without SB. Second, the question was put forward whether the combined presence of SB and PLMS events is more common than that of isolated SB or PLMS events in a group of SB patients. Third, as to further unravel the possible role of EEG arousals in the underlying neurophysiologic mechanism of SB and PLMS, it was assessed in a group of SB patients whether combined SB/PLMS events with associated EEG arousals are more common than those without associated EEG arousals. Positive answers to these questions could suggest a common neurophysiological basis for both movement disorders.
Materials and methods
Seventeen SB patients and 11 healthy controls were polysomnographically studied. SB, PLMS, and EEG arousals were scored. An association was noted when the occurrence was within a 3-s association zone.
Results
The PLMS index was higher in SB patients than in healthy controls (P < 0.001). Within the group of SB patients, the combined SB/PLMS index was higher than the isolated SB index (P < 0.001) and the isolated PLMS index (P = 0.018). Similarly, the combined SB/PLMS index with EEG arousal was higher than the combined SB/PLMS index without EEG arousal in SB patients (P < 0.001).
Conclusion
The results of this study indicate that SB, PLMS, and EEG arousals commonly concur during sleep in a time-linked manner.
Clinical relevance
SB and PLMS probably have a common underlying neurophysiological mechanism.
Objective:
The main objective of our study was to clarify the prevalence of disorders of arousal (confusional arousals, sleepwalking, sleep terrors) and sleep-related bruxism (teeth grinding) and their associated factors among Japanese adolescents.
Methods:
Our study was designed as a cross-sectional sampling survey. The targets were students attending junior and senior high schools throughout Japan. The questionnaire asked for personal data and information on lifestyle, depressive state, and sleep status including the frequency of experiencing disorders of arousal and sleep-related bruxism.
Results:
A total of 99,416 adolescents responded. The overall response rate was 63.7%, and 98,411 questionnaires were subjected to analysis. The prevalence of disorders of arousal was 7.1% (95% confidence interval [CI], 6.9-7.3%) among boys and 7.7% (95% CI, 7.5-7.9%) among girls. The prevalence of sleep-related bruxism was 2.3% (95% CI, 2.2-2.4%) among boys and 3.0% (95% CI, 2.8-3.2%) among girls. The factors associated with disorders of arousal were the grade in school, smoking habit, alcohol consumption, naptime (min), breakfast habit, participation in club activities, sleep duration, difficulty initiating sleep, nocturnal awakening, early morning awakening, subjective sleep assessment, snoring, decrease in positive feelings, and depression (all p<.001). The factors associated with sleep-related bruxism were gender, smoking habit, nocturnal awakening, snoring, early morning awakening, decrease in positive feelings, and depressive feelings (all p<.001).
Conclusions:
If disorders of arousal or sleep-related bruxism are observed in an adolescent, his or her smoking habit, alcohol consumption, sleep status, and depressive state should be considered.
Background:
We postulated that idiopathic rapid-eye-movement (REM) sleep behaviour disorder (IRBD) represents the prodromal phase of a Lewy body disorder and that, with sufficient follow-up, most cases would eventually be diagnosed with a clinical defined Lewy body disorder, such as Parkinson's disease (PD) or dementia with Lewy bodies (DLB).
Methods:
Patients from an IRBD cohort recruited between 1991 and 2003, and previously assessed in 2005, were followed up during an additional period of 7 years. In this original cohort, we sought to identify the nature and frequency of emerging defined neurodegenerative syndromes diagnosed by standard clinical criteria. We estimated rates of survival free from defined neurodegenerative disease by means of the Kaplan-Meier method. We further characterised individuals who remained diagnosed as having only IRBD, through dopamine transporter (DAT) imaging, transcranial sonography (TCS), and olfactory testing. We did a neuropathological assessment in three patients who died during follow-up and who had the antemortem diagnosis of PD or DLB.
Findings:
Of the 44 participants from the original cohort, 36 (82%) had developed a defined neurodegenerative syndrome by the 2012 assessment (16 patients were diagnosed with PD, 14 with DLB, one with multiple system atrophy, and five with mild cognitive impairment). The rates of neurological-disease-free survival from time of IRBD diagnosis were 65·2% (95% CI 50·9 to 79·5) at 5 years, 26·6% (12·7 to 40·5) at 10 years, and 7·5% (-1·9 to 16·9) at 14 years. Of the four remaining neurological-disease-free individuals who underwent neuroimaging and olfactory tests, all four had decreased striatal DAT uptake, one had substantia nigra hyperechogenicity on TCS, and two had impaired olfaction. In three patients, the antemortem diagnoses of PD and DLB were confirmed by neuropathological examination showing widespread Lewy bodies in the brain, and α-synuclein aggregates in the peripheral autonomic nervous system in one case. In these three patients, neuronal loss and Lewy pathology (α-synuclein-containing Lewy bodies and Lewy neurites) were found in the brainstem nuclei that regulate REM sleep atonia.
Interpretation:
Most IRBD individuals from our cohort developed a Lewy body disorder with time. Patients who remained disease-free at follow-up showed markers of increased short-term risk for developing PD and DLB in IRBD, such as decreased striatal DAT binding. Our findings indicate that in most patients diagnosed with IRBD this parasomnia represents the prodromal phase of a Lewy body disorder. IRBD is a candidate for the study of early events and progression of this prodromal phase, and to test disease-modifying strategies to slow or stop the neurodegenerative process.
Funding:
None.
This is a randomised placebo-controlled clinical trial investigating the efficacy of hydroxyzine for treating parent-reported sleep bruxism in children. Participants of this trial were 30 patients randomly allocated to one of the two groups in a ratio of 1:2. One group received hydroxyzine and the other group received placebo. The outcome measures were Visual Analogue Scale test and Clinical Global Severity scale. Assessments occurred at baseline and at the end of week 4. The side effects of drugs were assessed using a checklist. The number of children in the hydroxyzine and placebo groups was 21 and 9, respectively. The mean age of children in the hydroxyzine and placebo groups was 8·4(s.d. = 3·3) and 6·5(s.d. = 1·5) years, respectively. Hydroxyzine more than placebo decreased bruxism score (3·8 versus 2·2). No serious adverse effect was reported. Current evidence support that hydroxyzine is effective and well tolerated for treating bruxism in children.
To analyze the night-to-night variability of REM sleep electromyographic (EMG) features of REM sleep behavior disorder (RBD) by using the automatic quantitative method known as atonia index (AI), and to evaluate the improvement in sensitivity and specificity of AI for the diagnosis of RBD when a second recording night is available.
Sleep research center.
N/A.
A group of 17 idiopathic RBD patients was recruited for whom 2 all-night polysomnographic (PSG) recordings were available. Thirty normal controls were also recruited and subgrouped into Young (< 45 years of age) or Aged (> 45 years). Chin EMG analysis was run on all recordings; night-to-night variability of both AI and number of chin EMG activations/h during REM sleep was additionally quantified as the absolute difference between the 2 nights standardized as the percentage of their mean.
Night-to-night variability of AI was higher in RBD patients (19.7%) than in the 2 groups of controls (Young 1.8% and Aged 2.8%). The values of variability of chin EMG activations were much higher than those of AI, especially in the Aged controls. Sensitivity of AI ≤ 0.9 for RBD was always higher than 82% and reached 88.9% for the combined-night analysis; specificity was also high, with a value of 92.3% for the combined-value analysis.
The night-to-night variability of AI seems to be very low in normal controls and remains under 20% in RBD patients; that of the number of EMG activations is higher. However, even a single PSG recording provides high values of sensitivity and specificity when a threshold value of AI ≤ 0.9 is used to define abnormal chin EMG levels during REM sleep that increase only moderately when a second night recording is available.
Ferri R; Marelli S; Cosentino FII; Rundo F; Ferini-Strambi L; Zucconi M. Night-to-night variability of automatic quantitative parameters of the chin EMG amplitude (atonia index) in REM sleep behavior disorder. J Clin Sleep Med 2013;9(3):253-258.
Objective:
We aim to analyze in detail the characteristics of nonrapid eye movement (NREM) sleep in drug-free patients with idiopathic rapid eye movement sleep behavior disorder (iRBD). We compare drug-free iRBD patients to both normal controls and drug-free patients with narcolepsy/RBD and evaluate the changes following the long-term use of bedtime clonazepam.
Participants and methods:
Forty-six participants were recruited: 15 with iRBD (13 men, 2 women; mean age, 65.8±4.39years), 13 with narcolepsy/RBD (10 men, 3 women; mean age, 63.0±6.73years), and 18 normal controls (10 men, 8 women; mean age 69.4±7.72years). Sleep was video polysomnographically recorded and the RBD severity scale (RBDSS) was obtained. Chin electromyography (EMG) amplitude was quantitatively assessed and the atonia index was computed. Additionally, NREM sleep instability was evaluated using an automatic quantitative analysis. Participants with iRBD were re-evaluated after 2.75±1.62years of regular therapy with 0.5 to 1-mg clonazepam at bedtime.
Results:
Slow transient electroencephalography (EEG) events were increased in iRBD and decreased in narcolepsy/RBD, while fast transient events decreased in iRBD and increased in narcolepsy/RBD. During rapid eye movement (REM) sleep the atonia index was reduced in both iRBD and narcolepsy/RBD groups and during NREM sleep atonia index was increased in iRBD participants, remaining low in narcolepsy/RBD participants. After long-term therapy with clonazepam, wakefulness after sleep onset was decreased together with an increase in both slow-wave sleep (SWS) and sleep stage 2, in which the latter reached statistical significance; sleep stages 1 and 2 instability significantly decreased and the duration of EEG transients also slightly but significantly decreased. Finally, chin tone was not modified by clonazepam.
Conclusions:
Our study confirms that clonazepam modifies some aspects of NREM sleep in iRBD participants with a decrease in its instability. Moreover, we also show that a complex modification of sleep chin atonia exists in these participants, which also involves NREM sleep; for iRBD more complex neuropathologic models encompassing REM sleep and NREM sleep mechanisms are needed.
Objective:
To determine the pathologic substrates in patients with rapid eye movement (REM) sleep behavior disorder (RBD) with or without a coexisting neurologic disorder.
Methods:
The clinical and neuropathologic findings were analyzed on all autopsied cases from one of the collaborating sites in North America and Europe, were evaluated from January 1990 to March 2012, and were diagnosed with polysomnogram (PSG)-proven or probable RBD with or without a coexisting neurologic disorder. The clinical and neuropathologic diagnoses were based on published criteria.
Results:
172 cases were identified, of whom 143 (83%) were men. The mean±SD age of onset in years for the core features were as follows - RBD, 62±14 (range, 20-93), cognitive impairment (n=147); 69±10 (range, 22-90), parkinsonism (n=151); 68±9 (range, 20-92), and autonomic dysfunction (n=42); 62±12 (range, 23-81). Death age was 75±9 years (range, 24-96). Eighty-two (48%) had RBD confirmed by PSG, 64 (37%) had a classic history of recurrent dream enactment behavior, and 26 (15%) screened positive for RBD by questionnaire. RBD preceded the onset of cognitive impairment, parkinsonism, or autonomic dysfunction in 87 (51%) patients by 10±12 (range, 1-61) years. The primary clinical diagnoses among those with a coexisting neurologic disorder were dementia with Lewy bodies (n=97), Parkinson's disease with or without mild cognitive impairment or dementia (n=32), multiple system atrophy (MSA) (n=19), Alzheimer's disease (AD)(n=9) and other various disorders including secondary narcolepsy (n=2) and neurodegeneration with brain iron accumulation-type 1 (NBAI-1) (n=1). The neuropathologic diagnoses were Lewy body disease (LBD)(n=77, including 1 case with a duplication in the gene encoding α-synuclein), combined LBD and AD (n=59), MSA (n=19), AD (n=6), progressive supranulear palsy (PSP) (n=2), other mixed neurodegenerative pathologies (n=6), NBIA-1/LBD/tauopathy (n=1), and hypothalamic structural lesions (n=2). Among the neurodegenerative disorders associated with RBD (n=170), 160 (94%) were synucleinopathies. The RBD-synucleinopathy association was particularly high when RBD preceded the onset of other neurodegenerative syndrome features.
Conclusions:
In this large series of PSG-confirmed and probable RBD cases that underwent autopsy, the strong association of RBD with the synucleinopathies was further substantiated and a wider spectrum of disorders which can underlie RBD now are more apparent.