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Chronic behavioral disorders of human REM sleep: a new category of parasomnia. 1986 [classical article]
... In particular, two poorly explored dimensions of dream contents, namely their voluntary control and behavioral enactment, promise important insights into the neural basis and the cognitive processes of dreaming. Indeed, previously agreed contents may be inserted by lucid dreamers into the ongoing dream experience in REM sleep [159,160,165], and dream contents may be enacted during episodes of REM sleep behavior disorder (RBD) in patients with this para- somnia [166,167]. The finding that there is a greater level of reactivation of the cerebral regions involved in learning a new task in trained subjects than in controls during REM sleep [112] and SWS [168] suggests that such cerebral reactivation should also be accompanied by that of the task-related information. ...
... A close correspondence between one or more PSG markers and specific contents of dream reports can also be established by observing video-PSG recordings of patients with RBD disorder. Indeed, external raters blindly analyzing video-PSG and dream re- ports [181] can establish reliably whether dream contents, such as movements and vocalizations enacted during RBD episodes, correspond to those reported after awakening [166]. This means that some observed motor behaviors can be considered markers of the concomitant elaboration of specific REM dream contents, which thus become predictable before reporting. ...
... Poslednjih decenija je više otkrića " potreslo " svet spavanja. Opisano je nekoliko bolesti ( " Ishrana vezana za spavanje " u okviru NREM parasomnija; " Poremećaj ponašanja u REM spavanju " kao REM parasomnija) [10, 11] čija je patofiziologija u velikom stepenu shvaćena . Proizveden je i usavršen aparat (pozitivni kontinuirani vazdušni pritisak) koji gotovo u potpunosti sprečava prestanke disanja (apnoea ad somnum) u spavanju. ...
... Sledeći korak je načinio Carlos Schenck 1986. godine koji je kod ljudi opisao bolest koju je nazvao Poremećaj ponašanja u REM spavanju (REM sleep behavior disorder, RBD) [10] u kojoj, obično stariji ljudi, odigraju svoje snove. Najčešće se dešava da sanjaju da ih napadaju životinje ili ljudi tako da im je život u opasnosti. ...
Engrami, vol. 36, januar-jun 2014, br. 1-2
Although the process of sleep is probably as old as the whole living world and although it occupies one third of our lives, and although it is a vital form of behavior whose purpose we do not fully understand - still, the first steps enabling us to enter some of the secrets of the process of sleep were made only in the past century. The first human electroencephalogram (EEG) was performed by the German neurologist Hans Berger in 1908. in Jenna. He published his discovery some twenty years later, in 1929. Formally the first school-textbook on sleep, with the title „Sleep and Wakefulness“, was published in Chicago (USA) in 1939. by professor Nathaniel Kleitmann. The dual nature of sleep was described by Eugen Aserinsky and Nathaniel Kleitmann in 1953. In Serbia, the first textbook on sleep with the title “Wakefulness, sleep and dreaming” was written by the Academician professor Veselinka Šušić in 1977. The last decades of the 20th century “shook” the world of sleep with new discoveries. Several diseases were described (i.e., Sleep related eating disorder as NREM sleep, and REM sleep behavior disorder as REM sleep parasomnia) whose pathophysiology was comprehended. A CPAP apparatus was produced and perfected for the treatment of sleep apnea. The last decades of the past century with the discoveries of neurotransmitters hypocretin/orexin brought about the knowledge on the nature of narcolepsy whose therapy was significantly improved. The pathophysiology of NREM parasomnias (sleep walking or somnambulism and sleep terrors, confusional awakenings and nightmares, sleep related eating or sex) as well as some of the REM parasomnias (REM sleep behavior disorder) were explained in a novel manner. These fundamental discoveries threw new views on the nature of the process of sleep. They enabled us to better perceive the nature of the sleep process its physiology and pathology, and to better comprehend the processes called “the dissociation of sleep stages”.
Key words: sleep, NREM and REM parasomnia, narcolepsy
... Soon after the disorder was recognized by Schenck and colleagues , a relationship between RBD and the development of neurodegenerative disease, particularly PD and dementia with Lewy bodies, has become apparent [93]. Several studies have since confirmed increased risk of developing a neurodegenerative disease over several years [94, 83,959697. ...
... However, no large randomized controlled trials have been performed in RBD. Clonazepam, a longacting benzodiazepine, is the most commonly used medication for RBD, since it was shown to improve RBD symptoms [93]. A low dose of clonazepam (up to 1 mg) is effective in the majority of patients [106]. ...
Sleep disturbances are common in neurodegenerative disease and impair quality of life. People with Alzheimer’s disease (AD) develop daytime hypersomnia and nighttime insomnia. These symptoms likely result from circadian rhythm disruption due to reduced zeitgeber input, suprachiasmatic nucleus dysfunction, and melatonin alterations. In Parkinson’s disease (PD), various sleep disorders, such as insomnia, hypersomnia, and REM sleep behavior disorder (RBD) are often seen. These problems are related to neurodegeneration of brain structures influencing sleep and wake states, circadian rhythm dysfunction, and motor and non-motor symptoms. RBD can precede PD motor symptoms by several years, and it represents a window of opportunity to treat the disease process when a disease-modifying therapy for PD becomes available in the future. Effective treatments for sleep disturbances in AD and PD are limited. Deeper understanding of sleep and circadian dysfunction is necessary to develop treatments that improve quality of life and potentially alter the degenerative course.
... Several prognostic factors including postural instability, predominance of type and body side of motor features at disease onset impact the evolution of motor and non-motor symptoms in Parkinson's disease (PD)1234. In the first description of REM sleep behavior disorder (RBD) by Schenck et al. in 1986, a close link to neurodegenerative disorders was already reported [5]. RBD consists of two features: loss of atonia during REM sleep, so called REM sleep without atonia (RWA) and acting out of dreams, most often of violent content [6]. ...
... Several prognostic factors including postural instability, predominance of type and body side of motor features at disease onset impact the evolution of motor and non-motor symptoms in Parkinson's disease (PD)1234. In the first description of REM sleep behavior disorder (RBD) by Schenck et al. in 1986, a close link to neurodegenerative disorders was already reported [5]. RBD consists of two features: loss of atonia during REM sleep, so called REM sleep without atonia (RWA) and acting out of dreams, most often of violent content [6]. ...
Estimation of progression in Parkinson's disease (PD) is useful to guide clinical decisions and to enable patients to plan and manage their life with PD. Rapid eye movement (REM) sleep behavior disorder (RBD) and REM sleep without atonia (RWA) are recognized as early harbingers of neurodegeneration and may precede motor symptoms by years. However, their impact on motor progression remains elusive.
We retrospectively analyzed polysomnographic and clinical data of 59 PD patients, grouping them into patients with RBD (n = 15), RWA (n = 22) and those with normal muscle atonia (n = 22). We compared the three groups with regard to motor progression, defined as changes in Unified Parkinson's Disease Rating Scale (UPDRS) III values per year, and selected PD specific characteristics.
Motor disability at first visit and time interval between first and last visits were similar between groups. We observed a significantly faster motor progression in PD patients with RBD and RWA than in those with preserved REM sleep atonia.
Our findings suggest that impaired muscle atonia during REM sleep might represent a marker of faster motor progression in PD.
... First described in 1986 [1], rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by repeated episodes of dream enactment behavior and REM sleep without atonia (RWA), evident during polysomnographic recording and manifested as increased phasic or tonic muscle activity on electromyogram channels [2]. RBD may be idiopathic or symptomatic and both forms are strongly associated with neurodegerative diseases; finally, RBD can be iatrogenic [3, 4]. ...
... The time lag between the occurrence of RBD and synucleinopathy can span from one to many years or decades [6]. RBD was observed in narcoleptic patients even before its first recognition as a clinical entity by Schenck et al. [1] and was called " ambiguous sleep " [7] because of its " low phasic atonia with an extreme abundance of twitches and muscular discharges. " The prevalence of RBD in narcolepsy with cataplexy (NC) is high, being clinically evident in 45– 61% of patients and polysomnographically detectable in 36– 43% of them [8, 9]. ...
A patient is reported in whom signs and symptoms of REM sleep behavior disorder (RBD) and narcolepsy have been associated for almost two decades with a late development of parkinsonism and rheumatoid arthritis. A 78-year-old male patient in whom RBD was first diagnosed was followed-up by clinical examination, video-polysomnography, multiple sleep latency test, cerebral magnetic resonance imaging, and dopamine transporter imaging by single-photon emission computerized tomography. The patient was found to present for almost two decades, in addition to RBD, also narcolepsy. Moreover, a late development of parkinsonism and the occurrence of rheumatoid arthritis were detected and clinically and instrumentally characterized. Patients predisposed to RBD and later parkinsonism might be susceptible to a variety of triggers that, in our patient, might have been represented by a possible latent autoimmune process leading to the development of narcolepsy with cataplexy and rheumatoid arthritis, later.
... Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by a history of recurrent nocturnal dream enactment behavior and loss of skeletal muscle atonia and increased phasic muscle activity during REM sleep: REM sleep without atonia (RSWA). RBD was first described in animals by Jouvet in 1965 1 and in humans by Schenck et al in 1986 and Sforza et al in 1988. 2–4 RBD is a complex, multidimensional parasomnia that is frequently linked with other sleep disorders (eg, untreated sleep apnea, narcolepsy with cataplexy of hypocretin-deficient type), a wide range of neurodegenerative disorders, and the pharmacotherapy of psychiatric and medical disorders (eg, antidepressants, beta-blockers). ...
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by a history of recurrent nocturnal dream enactment behavior and loss of skeletal muscle atonia and increased phasic muscle activity during REM sleep: REM sleep without atonia. RBD and associated comorbidities have recently been identified as one of the most specific and potentially sensitive risk factors for later development of any of the alpha-synucleinopathies: Parkinson's disease, dementia with Lewy bodies, and other atypical parkinsonian syndromes. Several other sleep-related abnormalities have recently been identified in patients with RBD/Parkinson's disease who experience abnormalities in sleep electroencephalographic frequencies, sleep-wake transitions, wake and sleep stability, occurrence and morphology of sleep spindles, and electrooculography measures. These findings suggest a gradual involvement of the brainstem and other structures, which is in line with the gradual involvement known in these disorders. We propose that these findings may help identify biomarkers of individuals at high risk of subsequent conversion to parkinsonism.
... PD displays a broad spectrum of symptoms and a discussion of all PD related disorders would be beyond the scope of this review article. However, some of the more common symptoms observed in people suffering with PD include (1) Cognition issues, related to impaired judgment and loss of memory particularly during latter age [7]; (2) Sleep disorders manifested by changes in normal sleeping schedule and time [8]; (3) Psychiatric problems such as depression anxiety and stress which add to the motor symptoms. Importantly, stress may cause imbalance of neurotransmitters that can worsen muscular movements related to other activities such as writing, speaking, blinking etc. [9]. ...
A gradual loss of dopamine-producing nerve cells gives rise to a common neurodegenerative Parkinson’s disease (PD). This disease causes a neurotransmitter imbalance in the brain and initiates a cascade of complications in the rest of the body that appears as distressing symptoms which include gait problems, tremor, gastrointestinal (GI) disorders and cognitive decline. To aid dopamine deficiency, treatment in PD patients includes oral medications, in addition to other methods such as deep brain stimulation and surgical lesioning. Scientists are extensively studying molecular and signaling mechanisms, particularly those involving phenotypic transcription factors and their co-regulatory proteins that are associated with neuronal stem cell (SC) fate determination, maintenance and disease state, and their role in the pathogenesis of PD. Advancement in scientific research and “personalized medicine” to augment current therapeutic intervention and minimize the side effects of chemotherapy may lead to the development of more effective therapeutic strategies in the near future. This review focuses on PD and associated GI complications and summarizes the current therapeutic modalities that include stem cell studies and combinatorial drug treatment.
... Although RBD is often associated with other neurological disorders, the majority of cases are diagnosed as " idiopathic " ; however, many of these cases are actually associated with a progressive neurodegenerative process that culminates, late in life, with the onset of Parkinson disease (PD) and other a-synucleinopathies[4e7]. By the time RBD was officially classified as a human disorder in 1986[8], a similar phenomenond " REM sleep without atonia " dhad already been studied extensively in cats with brainstem lesions[9]. These lesioned animals exhibited many signs of REM sleep as they also engaged in various rudimentary and complex behaviorsdfrom alternating leg movements to standing and walking, to orienting toward, searching for, and attacking invisible prey. ...
... In adults 18 years of age or older, the lifetime prevalence of sleepwalking has been estimated at 29.2 % [100], and it has been recently estimated, based upon interview and attended polysomnography with simultaneous video monitoring, that the prevalence of RBD in a Korean elderly population is 2.01 % and subclinical RBD is 4.95 % [101]. There has been very little animal research in this area, although pontine tegmental brain-stem lesion studies in cats result in " dream enacting " behavior suggestive of the more recently described RBD in humans [102, 103]. Not surprisingly, there does not appear to be a naturally occurring model of parasomnias in the animal world. ...
Phylogenetic studies have established that sleep is present in virtually all living organisms, but behavior and electrophysiology in nonmammalian organisms are different from that of mammals. Recently, significant genetic, molecular, and neurochemical insights into human sleep and its disorders have occurred as the result of utilizing model organisms which have well-known genomes with homologous relationships to the human genome. Sleep in other, less well-known mammalian and nonmammalian organisms has also provided insight into human sleep disorders. However, despite these advances in knowledge, the function of sleep still remains an incompletely understood biological process.
... Rapid Eye Movement (REM) sleep Behaviour Disorder (RBD) is a REM sleep parasomnia first described by Schenck and collaborators in 1986 [1]. It is characterized by loss of the muscle atonia that typically occurs during REM sleep, therefore allowing patients to act out their dreams [2]. ...
... Rapid eye movement (REM) sleep behaviour disorder (RBD) is a parasomnia characterized by intermittent or complete loss of REM sleep atonia resulting in motor activity during REM sleep and, often, injury (Schenck et al., 1986). The disorder is a predictor of cognitive impairments, such as difficulties in executive functions, decision-making (Delazer et al., 2012; Massicotte-Marquez et al., 2008; Sasai et al., 2012) and non-declarative memory (Fantini et al., 2011; Terzaghi et al., 2008). ...
To investigate differences in sleep spindle properties and scalp topography between patients with rapid eye movement sleep behaviour disorder (RBD) and healthy controls, whole-night polysomnograms of 35 patients diagnosed with RBD and 35 healthy control subjects matched for age and sex were compared. Recordings included a 19-lead 10-20 electroencephalogram montage and standard electromyogram, electrooculogram, electrocardiogram and respiratory leads. Sleep spindles were automatically detected using a standard algorithm, and their characteristics (amplitude, duration, density, frequency and frequency slope) compared between groups. Topological analyses of group-discriminative features were conducted. Sleep spindles occurred at a significantly (e.g. t34 = -4.49; P = 0.00008 for C3) lower density (spindles∙min(-1) ) for RBD (mean ± SD: 1.61 ± 0.56 for C3) than for control (2.19 ± 0.61 for C3) participants. However, when distinguishing slow and fast spindles using thresholds individually adapted to the electroencephalogram spectrum of each participant, densities smaller (31-96%) for fast but larger (20-120%) for slow spindles were observed in RBD in all derivations. Maximal differences were in more posterior regions for slow spindles, but over the entire scalp for fast spindles. Results suggest that the density of sleep spindles is altered in patients with RBD and should therefore be investigated as a potential marker of future neurodegeneration in these patients.
© 2015 European Sleep Research Society.
... In healthy subjects, rapid eye movement (REM) sleep is characterized by rapid eye movements combined with suppression of skeletal muscle tension (atonia). However, atonia is absent in patients with REM sleep behavior disorder (RBD)123 , a condition called REM sleep without atonia (RWA) [4]. Because of the lack of atonia, RBD patients physically act out their dreams during REM sleep, which can result in injury to themselves or others. ...
Atonia during rapid eye movement (REM) sleep is absent in patients with REM sleep behavior disorder (RBD), a phenomenon called REM sleep without atonia (RWA). RBD patients have symptoms in common with neurodegenerative diseases, and data from follow-up studies on idiopathic RBD patient indicate that RBD predicts development of neurodegenerative diseases, particularly Parkinson's disease (PD). Therefore, early diagnosis of RWA can help identify and possibly prevent neurodegenerative diseases. Currently, RWA assessment by visual analysis of polysomnogram (PSG) is only moderately reliable and extremely time-consuming, making it difficult to obtain objective, quantifiable results. We developed an algorithm to automatically quantify tonic and phasic electromyographic (EMG) activities of the musculus mentalis during REM sleep using the scoring manual proposed by the American Academy of Sleep Medicine. Hilbert transform and average rectification were used to calculate the amplitudes of phasic and tonic muscular activities, respectively. Parameter values in the algorithm were optimized by cross-referencing the classification result obtained from the algorithm with the result from epoch-by-epoch visual inspection by a neurologist. A total of 2315 REM epochs from 24 PD patients were analyzed. We calculated the optimal parameter set, at which the sum of sensitivity and specificity was the highest, as well as the area under the receiver operating characteristic (ROC) curve (AUC). Verification tests showed good detection accuracy (phasic: sensitivity = 88%, specificity = 82%, AUC = 0.92; tonic: sensitivity = 88%, specificity = 85%, AUC = 0.93). Thus, this automated RWA detection algorithm is potentially useful for rapid and accurate diagnosis of RBD.
... Interestingly, impairment of this inhibitory mechanism leads to oniric behaviors— known as " Rem Behavioral Disorders " —that appears to be dream enactment given they seem to match subsequent report of the dreaming flow (Leclair-Visonneau, Oudiette, Gaymard, Leu-Semenescu, & Arnulf 2010; Valli et al., 2012). Still RBD can't in itself index consciousness, given that, far from proving intelligent and adaptive, it is dangerously dissociated from external input (Schenck, Bundlie, Ettinger, & Mahowald, 1986; see also Revonsuo, 2006). In short, though the received view is not undermined by the ordinary lack of associated behavior, ...
Owing to the fact that frontal regions of the brain are severely deactivated during sleep, there is a seeming inconsistency between the prominent Global Neuronal Workspace Theory of consciousness and the received view that dreams are vivid experiences occurring while sleeping. Indeed, based on the canonical criterion of reportability, Global Neuronal Workspace theorists claim that frontal activation of the brain is a necessary condition for conscious experience. Does it mean the received view is scientifically questionable? We argue the opposite way considering dreaming as a conscious experience that strikingly satisfies the current use of the canonical criterion though occurring under constraint of delayed reports. Further, this compelling condition of delayed report depends on a constitutional dissociation between experiencing and the cognitive mechanisms preparing report that proves very insightful. In line with recent findings from research on waking perception, this dissociation hints that Global Neuronal Workspace Theory is biased. Eventually, we discuss a recent claim according to which dreaming could "settle the debate opposing cognitive and noncognitive theories of consciousness.".
... Lesions affecting these neurons result in a peculiar parasomnia named REM sleep behavior disorder (RBD). RBD was first described in 1986 [31] in patients who were acting out their dreams. The behavior included moving their limbs, sleep talking, shouting, and screaming. ...
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia frequently affecting patients with synucleinopathies, but its exact prevalence in multiple system atrophy (MSA) is unclear. Whether questionnaires alone are sufficient to diagnose RBD is also unknown.
We performed a cross-sectional study of patients with probable MSA from six academic centers in the US and Europe. RBD was ascertained clinically and with polysomnography; we also performed a meta-analysis according to PRISMA guidelines for studies published before September 2014 that reported the prevalence of RBD in MSA. A random-effects model was constructed using weighted prevalence proportions. Only articles in English were included. Studies were classified into those that ascertained the presence of RBD in MSA clinically and with polysomnography. Case reports or case series (≤5 patients) were not included.
Forty-two patients completed questionnaires and underwent polysomnography. Of those, 32 (76.1 %) had clinically suspected RBD and 34 (81 %) had polysomnography-confirmed RBD. Two patients reported no symptoms of RBD but had polysomnography-confirmed RBD. The primary search strategy yielded 374 articles of which 12 met the inclusion criteria. The summary prevalence of clinically suspected RBD was 73 % (95 % CI, 62-84 %) in a combined sample of 324 MSA patients. The summary prevalence of polysomnography-confirmed RBD was 88 % (95 % CI, 79-94 %) in a combined sample of 217 MSA patients.
Polysomnography-confirmed RBD is present in up to 88 % of patients with MSA. RBD was present in some patients that reported no symptoms. More than half of MSA patients report symptoms of RBD before the onset of motor deficits.
... Idiopathic RBD and PD-Related Diseases RBD was first described by Schenck in 1986 [42] and is characterized by a loss of normal muscle atonia during REM sleep and dream-enacting behavior. The clinical manifestation includes vocalizations, such as talking and shouting, and violent , aggressive complex behavior during REM sleep in association with vivid, unpleasant, and violent dreams that can cause sleep-related injury to the patient or bed partner [43]. ...
Sleep disturbances are a common non-motor feature in patients with Parkinson's disease (PD). Early diagnosis and appropriate management are imperative for enhancing patient quality of life. Sleep disturbances can be caused by multiple factors in addition to age-related changes in sleep, such as nocturnal motor symptoms (rigidity, resting tremor, akinesia, tardive dyskinesia, and the "wearing off" phenomenon), non-motor symptoms (pain, hallucination, and psychosis), nocturia, and medication. Disease-related pathology involving the brainstem and changes in the neurotransmitter systems (norepinephrine, serotonin, and acetylcholine) responsible for regulating sleep structure and the sleep/wake cycle play a role in emerging excessive daytime sleepiness and sleep disturbances. Additionally, screening for sleep apnea syndrome, rapid eye movement sleep behavior disorder, and restless legs syndrome is clinically important. Questionnaire-based assessment utilizing the PD Sleep Scale-2 is useful for screening PD-related nocturnal symptoms. In this review, we focus on the current understanding and management of sleep disturbances in PD.
... Rapid eye movement (REM) sleep behavior disorder (RBD) is clinically characterized by the intermittent loss of physiological skeletal muscle atonia during REM sleep with the appearance of elaborate motor activity associated with dream mentation [1]. Apart from the characteristic clinical picture, polysomnography (PSG) demonstrating REM sleep without atonia is required for establishing a definite diagnosis of RBD [2]. ...
... In their seminal description of four patients with RBD in 1986, Schenck et al. mentioned a patient with Guillain- Barré syndrome. 23 Despite Guillain-Barré syndrome affects mostly the peripheral nervous system, signs of central nervous dysfunction such as sleepiness, hallucinations , abnormal antidiuretic hormone secretion and abnormally low CSF levels of hypocretin are noted. ...
Rapid eye movement (REM) sleep behavior disorder (RBD) and hypnagogic hallucinations are salient symptoms of abnormal and dissociated REM sleep that are frequently associated in serious neurological diseases. RBD is a strong, independent risk factor for hallucinations in narcolepsy (odds ratio: 4.3) and in Parkinson's disease (odds ratio: 2.7). In Parkinson's disease, RBD also predicts incident hallucinations and psychosis in prospective cohorts. Status dissociatus (a mixture of hallucinations, RBD, and dissociated sleep–wake states) is observed in patients with Guillain-Barré when hallucinating, but also in Lewy bodies dementia, delirium tremens, fatal familial insomnia, and Morvan's chorea. This co-occurrence of RBD and visual hallucinations suggests a common, extensive lesion within REM sleep executive systems.
... This loss of muscle atonia is typically described by patients as ''acting out'' their dreams. A high percentage of idiopathic RBD patients eventually develop neurodegenerative disease [5] , and RBD has been recognized as a strong predictor of the development of synucleinopathies, including PD [6,7]. RBD has been reported to affect up to 58% of PD patients [8], yet few studies have systematically assessed the relationship between RBD and NMS in PD. ...
... Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by loss of the normal atonia of REM sleep, such that patients appear to act out dream content [1]. In the past few years, some research showed that patients with idiopathic RBD (iRBD) are at very high risk of developing a neurodegenerative synucleinopathy, such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), or multiple system atrophy (MSA)234. ...
Patients with idiopathic REM sleep behavior disorder (iRBD) are at very high risk of developing neurodegenerative synucleinopathies, which are disorders with prominent autonomic dysfunction. Several studies have documented autonomic dysfunction in iRBD, but large-scale assessment of autonomic symptoms has never been systematically performed. Patients with polysomnography-confirmed iRBD (318 cases) and controls (137 healthy volunteers and 181 sleep center controls with sleep diagnoses other than RBD) were recruited from 13 neurological centers in 10 countries from 2008 to 2011. A validated scale to study the disorders of the autonomic nervous system in Parkinson's disease (PD) patients, the SCOPA-AUT, was administered to all the patients and controls. The SCOPA-AUT consists of 25 items assessing the following domains: gastrointestinal, urinary, cardiovascular, thermoregulatory, pupillomotor, and sexual dysfunction. Our results show that compared to control subjects with a similar overall age and sex distribution, patients with iRBD experience significantly more problems with gastrointestinal, urinary, and cardiovascular functioning. The most prominent differences in severity of autonomic symptoms between our iRBD patients and controls emerged in the gastrointestinal domain. Interestingly, it has been reported that an altered gastrointestinal motility can predate the motor phase of PD. The cardiovascular domain SCOPA-AUT score in our study in iRBD patients was intermediate with respect to the scores reported in PD patients by other authors. Our findings underline the importance of collecting data on autonomic symptoms in iRBD. These data may be used in prospective studies for evaluating the risk of developing neurodegenerative disorders.
... Mirror behaviors, such as empathizing with another's emotions or imitating their actions or speech, are more frequent among individuals who act out fictive behaviors in their dreams than they are among individuals who do not (Nielsen & Kuiken, 2013). Dream-enacting behaviors are frequently the culmination of highly disturbing dreams, including the typical nightmares of college students (Nielsen, Svob, & Kuiken, 2009), the unpleasant 'baby-in-peril' dreams of postpartum mothers (Nielsen & Paquette, 2007), and the violence-filled nightmares of patients with REM sleep behavior disorder (RBD) (Schenck, Bundlie, Ettinger, & Mahowald, 1986; Schenck, Lee, Bornemann, & Mahowald, 2009 ). However, it is unknown whether a propensity for mirroring others' emotions and behaviors while awake is associated specifically with self-reported nightmare frequency. ...
... REM-sleep behavior disorder (RBD) is a REM sleep parasomnia characterized by violent behavior during sleep, related to loss of REM sleep muscular atonia and enactment of vivid dreams [1]. RBD can occur in isolation, but is most frequent in patients with neurodegenerative disorders, particularly those associated with Lewy body deposition, like Multiple System Atrophy, Lewy-body dementia and Parkinson's disease (PD) [2]. ...
Longitudinal assessment of a Parkinson's disease (PD) cohort, to investigate the evolution or REM sleep behavior symptoms (RBD) over time and to test the relation between RBD at onset and motor dysfunction progression.
An early stage PD cohort (n = 61) was assessed at two time points, separated by a two years interval. Diagnostic criteria for RBD were: violent behavior during sleep and body movements or vocalization indicative of dream enacting and at least six affirmative answers in the REM sleep behavior disorder screening questionnaire. Motor function assessment was performed with the Unified Parkinson's Disease Scale part II and III (total and partial scores for tremor, bradykinesia, rigidity, gait/postural instability and dysarthria).
25 Patients had RBD at baseline, vs. 35 at follow-up. Three RBD changed to non-RBD at follow-up, while 10 non-RBD patients developed RBD at follow-up (annual incidence of 12.5%). RBD and non-RBD patients did not differ significantly at baseline or follow-up. The presence of RBD at baseline was significantly related to an increase in UPDRS total and bradykinesia scores over time.
RBD symptoms can vary over time and have a tendency to increase during the early stages of disease. The presence of RBD symptoms could be a risk factor for motor function deterioration and particularly for bradykinesia worsening.
... Dream-enacting behaviors (DEBs), or acting out of the fictive movements, speech or emotions of a dream, are prevalent among normal college students (Nielsen, Svob, & Kuiken, 2009). Although most young adults experience them occasionally, frequent and intense DEBs are symptomatic of REM sleep behavior disorder (RBD) (Schenck, Bundlie, Ettinger, & Mahowald, 1986), sleep walking and sleep terrors (), and other nocturnal anomalies (Ohayon & Schenck, 2010) such as sleep-related eating disorders (Brion et al., 2012) and obstructive sleep apnea (Iranzo & Santamaria, 2005). One hypothesis is that DEBs occur during dreams that are of sufficient perceptual, dramatic, and emotional intensity to over-ride the neuromuscular inhibition of REM sleep. ...
... It is a dissociated state in which EEG is similar to deep sleep (slow frequency and high amplitude waves) and motor activity is similar to waking [82]. In ''REMS behavior disorder'' subjects do not present typical REMS muscle atonia and perform motor activity associated with dream imagery [83]. It was recently shown that this disturbance is associated with Parkinson disease and other motor disorders [84] . ...
Several lines of evidence converge to the idea that rapid eye movement sleep (REMS) is a good model to foster our understanding of psychosis. Both REMS and psychosis course with internally generated perceptions and lack of rational judgment, which is attributed to a hyperlimbic activity along with hypofrontality. Interestingly, some individuals can become aware of dreaming during REMS, a particular experience known as lucid dreaming (LD), whose neurobiological basis is still controversial. Since the frontal lobe plays a role in self-consciousness, working memory and attention, here we hypothesize that LD is associated with increased frontal activity during REMS. A possible way to test this hypothesis is to check whether transcranial magnetic or electric stimulation of the frontal region during REMS triggers LD. We further suggest that psychosis and LD are opposite phenomena: LD as a physiological awakening while dreaming due to frontal activity, and psychosis as a pathological intrusion of dream features during wake state due to hypofrontality. We further suggest that LD research may have three main clinical implications. First, LD could be important to the study of consciousness, including its pathologies and other altered states. Second, LD could be used as a therapy for recurrent nightmares, a common symptom of depression and post-traumatic stress disorder. Finally, LD may allow for motor imagery during dreaming with possible improvement of physical rehabilitation. In all, we believe that LD research may clarify multiple aspects of brain functioning in its physiological, altered and pathological states.
... Dream enactment in rapid eye movement behavior disorder REM behavior disorder is another sleep disorder in which there is a failure to maintain REM sleep. These patients not only have abrupt arousals from REM with vivid recall of a fearful dream, they also act it out [51]. Swinging at imaginary intruders they punch holes in the bedroom walls, upset lamps, hurt themselves, and damage property. ...
This article reviews the major psychologic functions occurring during sleep and the evidence that patients who present with disorders of sleep have specific psychologic dysfunctions related to the type and degree of their sleep disturbance. The study of sleep disorders provides insights into this regular nocturnal updating of the self program, and of the specific psychologic effects of interrupted sleep or abnormalities in the timing of the cycles. The application of these findings to understanding and treating these patients is discussed.
... In separate experiments, it has been shown that the optogenetic activation of locus coeruleus neurons rapidly awoke mice that were asleep [12]. The prodrome of PD and dementia with Lewy bodies, which is characterised by neuropathological changes that precede parkinsonism and dementia, includes rapid eye movement (REM) sleep behaviour disorder, a parasomnia with dream-enacting behaviour, and loss of REM sleep atonia [13,14]. Lewy pathology is abundant in the lower brainstem, with only minimal damage in the substantia nigra [15 ]. ...
The major neurodegenerative diseases are characterised by a disabling loss of the daily pattern of sleep and wakefulness, which may be reflective of a compromise to the underlying circadian clock that times the sleep cycle. At a molecular level, the canonical property of neurodegenerative diseases is aberrant aggregation of otherwise soluble neuronal proteins. They can thus be viewed as disturbances of proteostasis, raising the question whether the two features - altered daily rhythms and molecular aggregation - are related. Recent discoveries have highlighted the fundamental contribution of circadian clocks to the correct ordering of daily cellular metabolic cycles, imposing on peripheral organs such as the liver a strict programme that alternates between anabolic and catabolic states. The discovery that circadian mechanisms are active in local brain regions suggests that they may impinge upon physiological and pathological elements that influence pro-neurodegenerative aggregation. This review explores how introducing the dimension of circadian time and the circadian clock might refine the analysis of aberrant aggregation, thus expanding our perspective on the cell biology common to neurodegenerative diseases.
... ? Evidence from one population-based or cohort study ± No evidence from population-based or cohort studies, but respective non-motor symptom is frequently seen in early PD (Erro et al. 2013; Khoo et al. 2013; Barone et al. 2009) RBD rapid eye movement sleep behavior disorder, PLMS periodic limb movements during sleep, RLS restless legs syndrome Need to redefine Parkinson's disease REM sleep behavior disorder RBD is a parasomnia clinically characterized by dreamenacting behaviors related to loss of physiological atonia during REM sleep (Schenck et al. 1986). The prevalence of ''idiopathic'' RBD in the population is not well defined and a commonly cited figure of 0.4 % may well be an underestimate (Gagnon et al. 2006). ...
Parkinson's disease (PD) is classically defined by its cardinal motor features and current clinical diagnostic criteria require the presence of bradykinesia and at least one additional motor symptom out of tremor, rigidity or postural instability. However, converging evidence from clinical, neuropathological, imaging and genetic research suggests initiation of PD-specific pathology prior to appearance of classical motor signs. This is of particular relevance in relation to the development of disease-modifying or neuroprotective therapies which would require intervention at the earliest stages of disease. A key challenge in PD research, therefore, is to better characterize markers for the 'preclinical' stages of the illness. Development of PD criteria by combining such markers allowing for an early diagnosis and intervention could pave the way for the design and implementation of future disease modification trials.
Sleep disorders are frequently diagnosed in Parkinson’s disease and manifested in the prodromal and advanced stages of the disease. These conditions, which in some cases affect more than 50% of Parkinson’s disease (PD) patients, include hypersomnia, often manifested as excessive daytime sleepiness, insomnia, characterized by delayed initiation and fragmentation of sleep at night, and disruption of rapid eye movement (REM) sleep, resulting in loss of atonia and dream enactment. Standard dopamine replacement therapies for the treatment of motor symptoms are generally inadequate to combat sleep abnormalities, which seriously affect the quality of life of PD patients. Rodent models still represent a major tool for the study of many aspects of PD. They have been primarily designed to eliminate midbrain dopamine neurons and elicit motor impairment, which are the traditional pathological features of PD. However, rodent models are increasingly employed to investigate non-motor symptoms, which are often caused by degenerative processes affecting multiple monoaminergic and peptidergic structures. This review describes how neurotoxic and genetic manipulations of rats and mice have been utilized to reproduce some of the major sleep disturbances associated with PD and to what extent these abnormalities can be linked to nondopaminergic dysfunction, affecting for instance noradrenaline, serotonin, and orexin transmission. Strengths and limitations are discussed, as well as the consistency of results obtained so far, and the need for models that better reproduce the multisystemic neurodegenerative nature of PD, thereby allowing to replicate the complex etiology of sleep-related disorders.
Sleep disorders are prevalent in Parkinson disease (PD), a disease with well recognized motor dysfunction. Sleep related problems received little attention until the last three decades. Sleep disorders seen in PD patients include insomnia, excessive sleepiness, restless legs syndrome, REM sleep behavior disorder. Some of these can have significant impact and lower the quality of life in these patients. An understanding of sleep issues in PD can help identify them early and result in optimal management.
Multiple system atrophy (MSA) is a neurodegenerative movement disorder characterized by parkinsonian symptoms and cerebellar symptoms. Sleep disturbances also play a crucial role in MSA. One of the most convincing animal models in MSA research is the PLP α-SYN model, but to date no studies on sleep disturbances in this mouse model, frequently found in MSA patients are available. We identified spectral shifts within the EEG of the model, strikingly resembling results of clinical studies. We also characterized muscle activity during REM sleep, which is one of the key symptoms in REM sleep behavioral disorder. Spectral shifts and REM sleep-linked muscle activity were age dependent, supporting Face Validity of the PLP α-SYN model. We also strongly suggest our findings to be critically evaluated for Predictive Validity in future studies. Currently, research on MSA lacks potential compounds attenuating or curing MSA. Future drugs must prove its potential in animal models, for this our study provides potential biomarkers.
Background:
Muscle activity during rapid eye movement sleep is markedly increased in people with rapid eye movement sleep behavior disorder and people with Parkinson's disease (PD) who have freezing of gait. This study examined whether individuals with rapid eye movement sleep behavior disorder who do not have a diagnosis of PD show abnormalities in gait initiation that resemble the impairments observed in PD and whether there is a relationship between these deficits and the level of rapid eye movement sleep without atonia.
Methods:
Gait initiation and polysomnography studies were conducted in 4 groups of 10 participants: rapid eye movement sleep behavior disorder, PD with and without freezing of gait, and controls.
Results:
Significant reductions were seen in the posterior shift of the center of pressure during the propulsive phase of gait initiation in the groups with rapid eye movement sleep behavior disorder and PD with freezing of gait when compared with controls and PD nonfreezers. These reductions negatively correlated with the amount of rapid eye movement sleep without atonia. The duration of the initial dorsiflexor muscle burst during gait initiation was significantly reduced in both PD groups and the rapid eye movement sleep behavior disorder cohort.
Conclusions:
These results provide evidence that people with rapid eye movement sleep behavior disorder, prior to a diagnosis of a degenerative neurologic disorder, show alterations in the coupling of posture and gait similar to those seen in PD. The correlation between increased rapid eye movement sleep without atonia and deficits in forward propulsion during the push-off phase of gait initiation suggests that abnormities in the regulation of muscle tone during rapid eye movement sleep may be related to the pathogenesis of freezing of gait. © 2016 International Parkinson and Movement Disorder Society.
Objective:
REM sleep behavior disorder (RBD) is associated with psychiatric symptoms, such as anxiety and alexithymia. However, only a few studies on the relationship between depression and RBD have been published. In this study, we investigated the occurrence of depression and associated factors in patients with RBD.
Methods:
In total 94 patients (mean age: 61.9±12.7 years, male: 70.2%) diagnosed as RBD were examined using detailed clinical histories, the Beck Depression Inventory (BDI), the Epworth Sleepiness Scale (ESS), and nocturnal polysomnography (PSG).
Results:
The mean BDI score of all patients was 12.4±10.3 and 44.7% of RBD patients showed depressed mood (BDI >11 points). Depressed RBD patients were less able to recall enacted dreams than were non-depressed patients (61.9% vs. 86.5%, p=0.008). Logistic regression analysis showed that failure to recall enacted dreams was significantly associated with depression, after controlling for confounding variables including the respiratory disturbance index and a history of psychiatric disorders (odds ratio=0.323, p=0.041).
Conclusion:
In this study, 44.7% of RBD patients were found to suffer from depressed mood. And, depression was found to be associated with reduced ability to recall enacted dreams. We suggest that routine evaluation of depression be performed in RBD patients, particularly when failure to recall enacted dreams is evident. We speculate that such failure may be associated with emotional dysregulation or neurodegeneration.
Objective: To describe the clinical phenotype of idiopathic rapid eye movement (REM) sleep behavior disorder (IRBD) at presentation in a sleep center. Methods: Clinical history review of 203 consecutive patients with IRBD identified between 1990 and 2014. IRBD was diagnosed by clinical history plus video-polysomnographic demonstration of REM sleep with increased electromyographic activity linked to abnormal behaviors. Results: Patients were 80% men with median age at IRBD diagnosis of 68 y (range, 50-85 y). In addition to the already known clinical picture of IRBD, other important features were apparent: 44% of the patients were not aware of their dream-enactment behaviors and 70% reported good sleep quality. In most of these cases bed partners were essential to convince patients to seek medical help. In 11% IRBD was elicited only after specific questioning when patients consulted for other reasons. Seven percent did not recall unpleasant dreams. Leaving the bed occurred occasionally in 24% of subjects in whom dementia with Lewy bodies often developed eventually. For the correct diagnosis of IRBD, video-polysomnography had to be repeated in 16% because of insufficient REM sleep or electromyographic artifacts from coexistent apneas. Some subjects with comorbid obstructive sleep apnea reported partial improvement of RBD symptoms following continuous positive airway pressure therapy. Lack of therapy with clonazepam resulted in an increased risk of sleep related injuries. Synucleinopathy was frequently diagnosed, even in patients with mild severity or uncommon IRBD presentations (e.g., patients who reported sleeping well, onset triggered by a life event, nocturnal ambulation) indicating that the development of a neurodegenerative disease is independent of the clinical presentation of IRBD. Conclusions: We report the largest IRBD cohort observed in a single center to date and highlight frequent features that were not reported or not sufficiently emphasized in previous publications. Physicians should be aware of the full clinical expression of IRBD, a sleep disturbance that represents a neurodegenerative disease. Commentary: A commentary on this article appears in this issue on page 7.
Background: Increasing evidence provides a clear association between rapid eye movement sleep behavior disorders (RBD) and Parkinson's disease (PD), but the clinical features that determine the co-morbidity of RBD and PD are not yet fully understood.
DLB is a progressive multisystem neurodegenerative disorder with widespread alpha-synuclein (αSyn) deposits in the central and peripheral nervous system as well as within the autonomic nervous system. In addition to dementia, its distinctive clinical features are visual hallucinations, parkinsonism, cognitive fluctuations, dysautonomia, sleep disorders, and neuroleptic sensitivity. The disease has an insidious onset and progresses to death with variable disease duration of on average 6.4 years. “Dementia with Lewy bodies” (DLB) is the clinical syndrome and “Lewy body disease” (LBD) refers to the pathological disease. The neuropathological hallmark of LBD is the presence of αSyn-positive neuronal inclusions in the form of Lewy bodies and Lewy neuritis. Neurochemically, DLB is associated with alterations in several neurotransmitter systems, the main changes occurring in the cholinergic, dopaminergic, and serotoninergic systems.
Currently no disease-modifying therapy is available, and management is therefore focused on symptomatic relief, but the combination of extrapyramidal symptoms, neuropsychiatric symptoms, and neuroleptic sensitivity makes the pharmacological treatment of DLB challenging. The mainstay of treatment includes levodopa for the parkinsonism and cholinesterase inhibitors for the cognitive deficits. Non-pharmacological, behavioral strategies aimed at modifying stressors in the environment should be employed whenever possible.
Parkinson's disease (PD) is currently clinically defined by a set of cardinal motor features centred on the presence of bradykinesia and at least one additional motor symptom out of tremor, rigidity or postural instability. However, converging evidence from clinical, neuropathological, and imaging research suggests initiation of PD-specific pathology prior to appearance of these classical motor signs. This latent phase of neurodegeneration in PD is of particular relevance in relation to the development of disease-modifying or neuroprotective therapies which would require intervention at the earliest stages of disease. A key challenge in PD research, therefore, is to identify and validate markers for the preclinical and prodromal stages of the illness. Currently, several nonmotor symptoms have been associated with an increased risk to develop PD in otherwise healthy individuals and ongoing research is aimed at validating a variety of candidate PD biomarkers based on imaging, genetic, proteomic, or metabolomic signatures, supplemented by work on tissue markers accessible to minimally invasive biopsies. The definition of diagnostic criteria for prodromal PD will have to include combinations of markers which could define target populations and influence outcomes of future disease modification trials.
Introduction Dementia with Lewy bodies (DLB) is clinical syndrome characterized by progressive dementia, parkinsonism and neuropsychiatric symptoms (McKeith et al.,2004a). Pathologically, DLB is a synuclein disorder with widespread Lewy body pathology in the brainstem and cerebral cortex. Research has suggested that in individuals over 75 years, DLB is the second most common type of neurodegenerative dementia after Alzheimer's disease (AD). Although prevalent, our understanding of this complex disorder is in its relative infancy. The accurate diagnosis of DLB can be difficult owing to its frequent co-occurrence with AD and perceived similarity to other motor disorders such as Parkinson's disease (PD). However, the identification of individuals with DLB is extremely important because of the potential for life-threatening reactions to neuroleptic medications, and more encouraging, their ability to benefit greatly from treatment with anticholinesterase (AChEI) therapies. Epidemiology Epidemiological estimates have suggested that after AD, DLB is the second most common dementia in individuals over 75, with a prevalence rate of approximately 22% (Rahkonen et al., 2003). Similarly, estimates of prevalence based on pathological data have suggested that DLB may represent between 15–35% of all dementia cases (Zaccai et al., 2005), while population-based studies have estimated that DLB accounts for 5% of the population (Rahkonen et al., 2003). In a pathologically confirmed sample, Williams et al. (2006) found that DLB was associated with increased mortality rates compared with AD (hazard ratio = 1.88), with a median survival of 78 years in DLB and 85 years in AD.
Are rapid eye movements (REMs) in sleep associated with visual-like activity, as during wakefulness? Here we examine single-unit activities (n ¼ 2,057) and intracranial electroencephalography across the human medial temporal lobe (MTL) and neocortex during sleep and wakefulness, and during visual stimulation with fixation. During sleep and wakefulness, REM onsets are associated with distinct intracranial potentials, reminiscent of ponto-geniculate-occipital waves. Individual neurons, especially in the MTL, exhibit reduced firing rates before REMs as well as transient increases in firing rate immediately after, similar to activity patterns observed upon image presentation during fixation without eye movements. Moreover, the selectivity of individual units is correlated with their response latency, such that units activated after a small number of images or REMs exhibit delayed increases in firing rates. Finally, the phase of theta oscillations is similarly reset following REMs in sleep and wakefulness, and after controlled visual stimulation. Our results suggest that REMs during sleep rearrange discrete epochs of visual-like processing as during wakefulness.
Pontine tegmental lesions can eliminate the atonia of rapid eye movement sleep (REM) and allow animals to exhibit overt behavior at the same time that other electrophysiological signs of REM are intact. We produced electrolytic lesions in the reticularis pontis oralis (RPO) and reticularis pontis caudalis (RPC) in rats and observed them for behavior during REM without atonia (REM-A) and for alterations in sleep and waking compared to normal rats. Relatively small unilateral lesions were sufficient to remove the atonia of REM, whereas larger, bilateral lesions were required to release overt behavior during REM-A. Lesions in both RPO and RPC were capable of releasing elaborate behaviors, including full locomotion, during REM-A. The results are discussed with respect to their importance for understanding the neural activity of REM and with respect to REM-A being a model for REM Behavior Disorder (RBD) in humans.
Abstract Prevalence studies suggest that Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are the most common dementing illnesses in the elderly. The aim of this narrative review was to provide data on sleep-related behaviors in AD and DLB. This paper contains arguments, with a clinical approach, on both circadian rhythm changes and dissociated states of wakefulness and sleep in these two conditions.
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of muscle atonia during paradoxical (REM) sleep (PS). The neuronal dysfunctions responsible for RBD are not known. In the present review, we propose an updated integrated model of the mechanisms responsible for PS and explore different hypotheses explaining RBD. We propose that RBD appears based on a specific degeneration of PS-on glutamatergic neurons localized in the caudal pontine sublaterodorsal tegmental nucleus or the glycinergic/GABAergic premotoneurons localized in the medullary ventral gigantocellular reticular nucleus.
Objectives: This study was performed to review the research trends in treatment for REM sleep behavior disorder (RBD) in Traditional Chinese Medicine (TCM) and Kampo in Japan. Methods: We searched articles in CNKI (China National Knowledge Infrastructure) under the key words, "RBD", and Chinese words related with it in Traditional Chinese Medicine, Traditional Chinese Medicinal Herbs and Combination of Traditional Chinese Medicine With Western Medicine' field, and also in CiNii (Citation Information by NII); we also searched articles in Kampo Square in Japan under the key words, "RBD" and Japanese words related with it. We found 10 papers, and then selected 6 of them except the non-clinical and unrelated studies. We then analyzed their way of diagnosis, treatments, study type and etc.. Results: 6 studies were divided into 4 case reports, one control study, and one literature review study. All of the studies reported that Herbal medicine for RBD was effective as much as Western medicine like clonazepam and paroxetine. However, the quality and the quantity of these clinical studies were not enough. Conclusions: It seems that the researches for RBD have gradually been performed in TCM and Kampo. We hope that our study can activate/push forward clinical research for this disorder in Korean traditional medicine.
Using the rapid eye movement (REM) sleep behavior disorder severity scale (RBDSS) as a reliable clinical tool we further assessed the phenomenology of REM sleep behavior disorder (RBD) in 56 Parkinson's disease patients with RBD. The scale uses phenomenological categories based on the localization of movements in the distal or proximal extremities and/or involving the trunc and on the presence or absence of vocalizations. Inter-rater reliability has been published previously. In the current study we looked into the distribution of motor and vocal phenomena. We identified a small percentage of patients with only vocalizations (4/56), and 8/56 patients with and 10/56 patients without vocalizations and small nonviolent movements of the distal extremities or facial jerks. Ten patients showed more forceful movements of the proximal extremities, 11 patients with movements involving the proximal extremities had additional vocalizations, 5 patients were recorded with axial involvement, and 12 patients with axial movements and vocalizations. These findings underline the clinical variety of RBD manifestation in Parkinson's disease patients without a certain pattern. However, both extreme variants, the mild one and the violent one, are rare. The RBDSS facilitates the risk estimate for harmful behaviors and may be recommended for comparative studies on RBD and its pharmacotherapy.
Study objectives:
Idiopathic REM sleep behavior disorder (iRBD) is characterized by atypical REM sleep motor activity, vivid dreams and nightmares, and dream-enacting behaviors that can result in injuries to the patient and bed partner. It is also a known predictor of Parkinson disease (PD). Alexithymia has been associated with disturbances in sleep and dreaming (e.g., nightmares) and is a non-motor symptom of PD. We assessed alexithymia and disturbed dreaming in iRBD patients with the aim of determining if these two factors are elevated and interrelated among this population.
Design:
Questionnaire study of clinically diagnosed patients.
Setting:
Clinical sleep disorders center.
Patients or participants:
Thirty-two iRBD patients and 30 healthy age- and sex-matched control participants.
Measurements and results:
Participants completed the 20-item Toronto Alexithymia Scale (TAS-20), the Dream Questionnaire, and the Beck Depression Inventory. iRBD patients obtained higher TAS-20 total scores (62.16 ± 13.90) than did controls (52.84 ± 7.62; F 1,59 = 10.44, P < 0.01), even when controlling for depressive symptoms, and more frequently attained the suggested cutoff for alexithymia than did controls (P < 0.01). iRBD patients obtained higher scores on the Difficulty Identifying Feelings alexithymia subscale. For both iRBD and control groups, the Difficulty Indentifying Feelings subscale correlated positively with the Nightmare Distress scale of the Dream Questionnaire.
Conclusions:
Elevated alexithymia scores among idiopathic rapid eye movement sleep behavior disorder patients, and especially a difficulty in identifying feelings, parallels evidence of dysautonomia in this population. The higher incidence of distressing nightmares and the association of nightmares with alexithymia further extend similar findings for both clinical and non-clinical samples and suggest that an affect regulation disturbance may be common to the two sets of symptoms.
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia manifested by vivid,often frightening dreams associated with simple or complex motor behavior during REM sleep. Patients appear to “act out their dreams”, in which the exhibited behaviors mirror the content of the dreams, and the dream content often involves a chasing or attacking theme. The polysomnographic features of RBD include increased electromyographic tone ± dream enactment behavior during REM sleep. In this review, the terminology, clinical and polysomnographic features, epidemiologic features, diagnostic criteria, differential diagnosis, and management strategies are discussed. Recent data on the suspected pathophysiologic mechanisms of RBD are also reviewed. Several issues relating to evolving concepts, controversies, and future directions are then reviewed, with an emphasis on idiopathic RBD representing an early feature of a neurodegenerative disease and particularly an evolving synucleinopathy.
The recently described intranigral rotenone model of Parkinson's disease (PD) in rodents provides an interesting model for studying mechanisms of toxin-induced dopaminergic neuronal injury. The relevance of this model remains unexplored with regard to sleep disorders that occur in PD. On this basis, the construction of a PD model depicting several behavioral and neurochemical alterations related to sleep would be helpful in understanding the association between PD and sleep regulation. We performed bilateral intranigral injections of rotenone (12 μg) on day 0 and the open-field test initially on day 20 after rotenone. Acquisition phase of the object-recognition test, executed also during day 20, was followed by an exact period of 24 hr of rapid eye movement (REM) sleep deprivation (REMSD; day 21). In the subsequent day (22), the rats were re-exposed to the open-field test and to the object-recognition test (choice phase). After the last session of behavioral tests, the rat brains were immediately dissected, and their striata were collected for neurochemical purposes. We observed that a brief exposure to REMSD was able to impair drastically the object-recognition test, similarly to a nigrostriatal lesion promoted by intranigral rotenone. However, the combination of REMSD and rotenone surprisingly did not inflict memory impairment, concomitant with a moderate compensatory mechanism mediated by striatal dopamine release. In addition, we demonstrated the existence of changes in serotonin and noradrenaline neurotransmissions within the striatum mostly as a function of REMSD and REMSD plus rotenone, respectively. © 2013 Wiley Periodicals, Inc.
REM sleep behaviour disorders (RBD) are vigorous, complex movements corresponding to enacted dreams. They may disturb sleep, and injure the patients or their bed partner. RBD are frequently associated with neurodegenerative diseases, especially synucleopathies. They can precede parkinsonism or dementia for 5 to 10 years, co occur, or follow parkinsonism and dementia for few years.The presymptomatic RBD are frequently associated with EEG slowing, reduced olfaction, mild visuo-spatial cognitive impairment, and decreased dopamine transport in functional brain imaging. In Parkinson's disease, 15 to 59 % patients speak, laugh, shout, kick, punch or fight invisible enemies during REM sleep. In contrast to sleepwalkers, patients with RBD rarely stand up or walk, but can fall out their bed. Sleep monitoring indicates an imperfect abolition of muscle tone during REM sleep in these patients. RBD are probably caused by non-dopaminergic pontine lesions in the REM sleep atonia system. This condition may also expose patients with Parkinson's disease to a higher risk of daytime and night-time hallucinations. Interestingly, several spouses reported that they observed a sharp contrast between the slow, limited movements, and poorly intelligible, low voice of their affected spouse when awake, and the fast, vigorous movements with loud voice that the very same patient exhibited during enacted dreams. We recently demonstrated,in a large study combining the interview of 100 couples and the sleep and video monitoring of 50 patients, that parkinsonism indeed disappears during RBD. The mechanism of this improvement is now explored.
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.
Loss of sleep can result from multiple medical and psychiatric conditions as well as from primary sleep disorders. Large epidemiological studies indicate that obstructive sleep apnea a higher risk of stroke and cardiovascular disease. Insomnia, as well as sleep restriction may increase worsen cardiac disease. Metabolic consequences of poor sleep include higher risk of diabetes and obesity. Parasomnias may be seen in association with various conditions, for example of REM behavior disorder is frequently associated with Parkinson's disease. Tables with specific research studies and their main findings are provided for detail.
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