Search

Background and purpose: Migraine and sleep disorders share a bidirectional relationship, but little is known about the specific association between migraine and rapid eye movement (REM) sleep behaviour disorder (RBD). The aim was to assess the prevalence of RBD and associated clinical characteristics in adults with migraine. Methods: This analysis is part of a cross‐sectional survey study conducted at the Headache Centre of the Charité—Universitätsmedizin Berlin between August 2020 and March 2023. At the end of their regular medical consultation, patients with migraine filled out (1) the validated RBD Screening Questionnaire (RBDSQ), (2) a questionnaire on REM sleep intrusions and (3) the Depression, Anxiety and Stress Scale 21. The primary endpoint was the percentage of patients with a positive RBD screening. A multivariate analysis was performed to identify characteristics independently associated with features of RBD. Results: A total of 751 patients (44.1 ± 13.2 years; 87.4% female) with complete RBDSQ were included in this analysis, of which 443 (58.9%) screened positive for RBD. In multivariate analysis, a positive screening for RBD was associated with younger age (odds ratio [OR] 0.9, 95% confidence interval [CI] 0.8–0.9 per 10‐year increase; p = 0.005) and with features suggestive of REM sleep intrusions (OR 4.3, 95% CI 1.8–10.4; p = 0.001). Migraine aura remained in the model without reaching statistical significance (OR 1.3, 95% CI 0.9–1.8; p = 0.079). Discussion: Symptoms of RBD are frequent in adults with migraine. Further studies including polysomnography are required to confirm this association, and to explore potential common pathophysiological mechanisms. [ABSTRACT FROM AUTHOR]

Research criteria for the diagnosis of prodromal dementia with Lewy bodies (DLB) include three clinical subtypes: mild cognitive impairment with Lewy bodies (MCI‐LB), delirium‐onset prodromal DLB, and psychiatric‐onset prodromal DLB. Late‐onset psychiatric manifestations are at a higher risk of developing dementia, but its relation to prodromal DLB remains unclear. In addition to the risk of severe antipsychotic hypersensitivity reactions, accurate discrimination from non‐DLB cases is important due to the potential differences in management and prognosis. This article aims to review a rapidly evolving psychiatric topic and outline clinical pictures of psychiatric‐onset prodromal DLB, including the proposed biomarker findings of MCI‐LB: polysomnography‐confirmed rapid eye movement sleep behaviour disorder, cardiac [123I]metaiodobenzylguanidine scintigraphy, and striatal dopamine transporter imaging. We first reviewed clinical pictures of patients with autopsy‐confirmed DLB. Regarding clinical reports, we focused on the patients who predominantly presented with psychiatric manifestations and subsequently developed DLB. Thereafter, we reviewed clinical studies regarding the diagnostic applications of the proposed biomarkers to patients with late‐onset psychiatric disorders. Clinical presentations were mainly late‐onset depression and psychosis; however, other clinical manifestations were also reported. Psychotropic medications before a DLB diagnosis may cause extrapyramidal signs, and potentially influences the proposed biomarker findings. These risks complicate clinical manifestation interpretation during the management of psychiatric symptoms. Longitudinal follow‐up studies with standardised evaluations until conversion to DLB are needed to investigate the temporal trajectories of core features and proposed biomarker findings. In patients with late‐onset psychiatric disorders, identification of patients with psychiatric‐onset prodromal DLB provides the opportunity to better understanding the distinct prognostic subgroup that is at great risk of incident dementia. Advances in the establishment of direct biomarkers for the detection of pathological α‐synuclein may encourage reorganising the phenotypic variability of prodromal DLB. [ABSTRACT FROM AUTHOR]

Summary: REM sleep behaviour disorder (RBD) is common in narcolepsy type 1 (NT1). Abnormalities in the reward system have been observed in NT1, possibly related to impaired orexin projections towards the mesolimbic reward system, but also in RBD when associated with Parkinson's disease. Our study aimed to explore the psychobehavioural profile of NT1 patients with and without RBD compared with healthy controls (HC). Forty patients with NT1 were compared with 20 sex‐ and age‐matched HC. All patients with NT1 underwent a video‐polysomnography including a measure of REM sleep without atonia (RSWA). The following neuropsychobehavioural variables were assessed: apathy, impulsivity, depression, cognition, subjective and objective attention, sensation‐seeking, and behavioural addictions. The patient population included 22 patients with NT1‐RBD and 18 patients with NT1‐noRBD. Compared with the healthy controls, patients with NT1 had higher scores of apathy, impulsivity, and depression; a lower score on global cognition, and poorer self‐perceived attention. No differences were found between patients with NT1 with and without RBD in all neuropsychological variables, except for impaired objective attention in patients with NT1‐RBD. In patients with NT1, a positive correlation was observed between RSWA and both apathy and impulsivity subscale. Moreover, in patients with NT1‐RBD, RSWA was positively correlated with depression. Patients with NT1 showed higher depression, apathy, and impulsivity compared with controls. These measures correlate with the severity of RSWA, suggesting a transdiagnostic association between RBD and abnormalities of the reward system at least for patients with NT1. [ABSTRACT FROM AUTHOR]

Introduction: Rapid eye movement (REM) sleep behaviour disorder (RBD) is a parasomnia characterised by the loss of REM sleep muscle atonia and the enactment of dreams. Acute RBD associated with alcohol withdrawal syndrome is known, but the studies are limited, particularly on its neurobiological underpinnings and management alongside the withdrawal state. This work attempts to address this using a case study and relevant literature review. Case Presentation: A 40‐year‐old male with alcohol dependence (for 20 years) reported new‐onset terrifying nightmares and violent behaviours in his sleep precipitated by alcohol withdrawal states for the last 18 months. The polysomnographic finding of REM‐without‐atonia supported the diagnosis of RBD. He was treated with chlordiazepoxide 100 mg/day (gradually tapered and stopped) and thiamine supplements. Post‐discharge, he remained abstinent and symptom‐free during the three months of follow‐up. Discussion: RBD related to alcohol withdrawal syndrome has been previously described in a few anecdotal reports. Sudden withdrawal from central nervous system suppressants like alcohol is hypothesised to cause a homeostatic imbalance in gamma‐aminobutyric acid (GABA) pathways and 'REM rebound', resulting in the clinical and polysomnographic picture of RBD. Benzodiazepines have been found to be useful in both RBD and alcohol withdrawal. Conclusions: Alcohol withdrawal syndrome may present with acute RBD, which can be treated with a short course of benzodiazepine. However, further studies are needed to explore the long‐term course of RBD in these patients. [ABSTRACT FROM AUTHOR]

Summary: Rapid eye movement (REM) sleep behaviour disorder is a REM sleep parasomnia characterised by the loss of the physiological muscle atonia during REM sleep, resulting in dream enactment behaviours that may cause injuries to patients or their bed partners. The nocturnal motor episodes seem to respond to the dream contents, which are often vivid and violent. These behavioural and oneiric features make the REM sleep behaviour disorder a potential model to study dreams. This review aims to unify the literature about dream recall in REM sleep behaviour disorder as a privileged approach to study dreams, systematically reviewing studies that applied retrospective and prospective experimental designs to provide a comprehensive overview of qualitative and quantitative aspects of dream recall in this REM sleep parasomnia. The present work highlights that the study of dreaming in REM sleep behaviour disorder is useful to understand unique aspects of this pathology and to explore neurobiological, electrophysiological, and cognitive mechanisms of REM sleep and dreaming. [ABSTRACT FROM AUTHOR]

Our objectives were to assess the prevalence of REM sleep behaviour disorder in patients with Essential Tremor, using video‐polysomnography and to compare REM sleep behaviour disorder features in essential tremor with those of patients with alpha‐synucleinopathies. Forty‐nine patients with essential tremor were screened with the REM Sleep Behaviour Disorder Screening Questionnaire. Patients scoring positive and those with spontaneous complaints of REM sleep behaviour disorder (n = 6) underwent video‐polysomnography. The clinical features of essential tremor were compared between patients with and without REM sleep behaviour disorder. Video‐polysomnography data were compared between patients who had essential tremor and Parkinson's disease with REM sleep behaviour disorder and those with idiopathic REM sleep behaviour disorder. Fourteen patients (23.5%) screened positive for REM sleep behaviour disorder, confirmed by video‐polysomnography in five (11.6%). All patients with essential tremor and REM sleep behaviour disorder had rest tremor, compared with 13 (34.2%) in the group with essential tremor but without REM sleep behaviour disorder (p =.009). In video‐polysomnography, patients with essential tremor and REM sleep behaviour disorder were similar to patients with Parkinson's disease with REM sleep behaviour disorder and presented worse sleep dysfunction and lower severity of REM sleep behaviour disorder compared to those with idiopathic REM sleep behaviour disorder. We found a high prevalence of REM sleep behaviour disorder in patients with essential tremor, associated with a predominance of rest tremor. Polysomnography data from patients with essential tremor and REM sleep behaviour disorder were similar to those in patients with Parkinson's disease. This suggests a relation between this subgroup of patients with essential tremor and the alpha‐synucleinopathies. [ABSTRACT FROM AUTHOR]

Background and purpose: Isolated rapid eye movement (REM) sleep behavior disorder (iRBD) is characterized by abnormal behaviours during REM sleep. Several studies showed that iRBD is a prodromal stage of synucleinopathies. Therefore, identifying iRBD in the general population is of utmost importance. In this study, we explore whether the assessment of rest–activity rhythm features can distinguish patients with iRBD from patients with disorders characterized by other pathological motor activity during sleep and healthy controls. Methods: Nineteen patients with video‐polysomnographic diagnosis of iRBD, 39 patients with other disorders with motor activity during sleep [19 with restless leg syndrome (RLS) and 20 with untreated sleep apnea syndrome (SAS)] and 16 healthy controls underwent 2‐week actigraphy and video‐polysomnography, and completed REM sleep behavior disorder screening questionnaires. Non‐parametric analyses were applied to assess the rest–activity rhythm features. Results: Patients with iRBD showed lower sleep efficiency, increased estimated wake after sleep onset and increased frequency of prolonged activity bouts compared to those with RLS and controls, while no difference emerged compared with SAS patients. Moreover, patients with iRBD presented increased occurrence of estimated nap in comparison to those with RLS, those with SAS and controls. The I < O, a 24‐h measure that expresses the relationship between nocturnal and diurnal motor activity intensity, distinguished patients with iRBD from those with RLS, those with SAS and controls, with an area under the curve greater than that of REM sleep behavior disorder screening questionnaires. An I < O of 98.32 shows the best balance between sensitivity (63.2%) and specificity (89.1%). Discussion: The I < O index distinguished iRBD patients from those with other pathological motor activity during sleep and controls, confirming its use as an objective measure suitable to screen large at‐risk populations. [ABSTRACT FROM AUTHOR]

Background and purpose: Visualization of phosphorylated α‐synuclein at serine 129 (p‐syn) in skin nerves is a promising test for the in vivo diagnosis of synucleinopathies. Here the aim was to establish the intra‐ and inter‐laboratory reproducibility of measurement of intraneural p‐syn immunoreactivity in two laboratories with major expertise (Würzburg and Bologna). Methods: In total, 43 patients affected by Parkinson's disease (PD 21 patients), dementia with Lewy bodies (DLB 1), rapid eye movement sleep behaviour disorder (RBD 11), multiple system atrophy (MSA‐P 4) and small fibre neuropathy (SFN 6) were enrolled. Skin biopsy was performed at the C7 paravertebral spine region and distal skin sites (thigh or leg). The analysis was standardized in both laboratories and carried out blinded on a single skin section double stained with antibodies to p‐syn and the pan‐axonal marker protein gene product 9.5. Fifty skin sections were randomly selected for the analysis: 25 from C7 and 25 from distal sites. Differently classified sections were re‐evaluated to understand the reasons for the discrepancy. Results: The intra‐laboratory analysis showed an excellent reproducibility both in Würzburg (concordance of classification 100% of sections; K = 1; P < 0.001) and Bologna (96% of sections; K = 0.92; P < 0.001). Inter‐laboratory analysis showed reproducibility in 45 sections (90%; K = 0.8; P < 0.001) and a different classification in five sections, which was mainly due to fragmented skin samples or weak fluorescent signals. Conclusions: Analysis of p‐syn showed excellent inter‐ and intra‐laboratory reproducibility supporting the reliability of this technique. The few ascertained discordances were important to further improve the standardization of this technique. [ABSTRACT FROM AUTHOR]

In the article, the authors discuss their study of outpatients at the Shiga Medical Centre in Japan to examine the prevalence of core clinical features and other neuropsychiatric symptoms in dementia with Lewy bodies (DLB). Among the features and symptoms are parkinsonism, hallucinations, and recurrent sleep talking. Also cited are the supportive features of DLB like depression and anxiety.

Background and purpose Rapid eye movement sleep behaviour disorder ( RBD) is related to striatal dopamine depletion. This study was performed to confirm whether clinically probable RBD (cp RBD) in patients with Parkinson's disease ( PD) is associated with a specific pattern of striatal dopamine depletion. Methods A prospective survey was conducted using the RBD Screening Questionnaire ( RBDSQ) in 122 patients with PD who had undergone dopamine transporter ( DAT) positron emission tomography scan. Results Patients with cp RBD (RBDSQ ≥ 7) exhibited greater motor deficits, predominantly in the less-affected side and axial symptoms, and were prescribed higher levodopa-equivalent doses at follow-up than those without cp RBD (RBDSQ ≤ 4), despite their similar disease and treatment durations. Compared to patients without cp RBD, those with cp RBD showed lower DAT activities in the putamen, particularly in the less-affected side in all putaminal subregions, and a tendency to be lower in the ventral striatum. In addition, greater motor deficits in patients with cp RBD than in those without cp RBD remained significant after controlling for DAT binding in the putamen and other confounding variables. Conclusions These results demonstrated that the presence of RBD in patients with PD is associated with different patterns of both motor deficit distribution and striatal DAT depletion, suggesting that the presence of RBD represents a distinct PD subtype with a malignant motor parkinsonism. [ABSTRACT FROM AUTHOR]

Background and purpose There is an urgent need for early predictive markers for the course of disease in prodromal α-synucleinopathies such as idiopathic rapid eye movement ( REM) sleep behaviour disorder. Autonomic cardiac/vascular dysfunction is a prominent feature in advanced α-synucleinopathies, but its diagnostic value as an early neurodegenerative marker remains unclear. The latter may be complicated since synuclein-mediated neurodegeneration may involve central and peripheral components of the autonomic nervous system. Methods The diagnostic value of autonomic symptoms and central and peripheral autonomic markers of blood pressure and heart rate regulation were prospectively evaluated in 20 subjects with idiopathic REM sleep behaviour disorder and 20 age-matched healthy controls. Results Although subjects with REM sleep behaviour disorder showed no clinical autonomic symptoms, blood pressure ( P ≤ 0.035) and heart rate response ( P ≤ 0.065) were slightly diminished during orthostatic challenge. Autonomic dysregulation was distinctively reflected in lower resting heart rate (all components, P ≤ 0.05) and blood pressure variability (low frequency component, P ≤ 0.024) indicating peripheral cardiac/vascular denervation. In contrast, baroreflex sensitivity and central cardiac autonomic outflow (sympathovagal balance) were well preserved indicating intact central autonomic regulation. Heart rate variability [very low frequency component, receiver operating characteristic ( ROC) area under the curve ( AUC) 0.80, P ≤ 0.001] and blood pressure variability (low frequency component ROC AUC 0.73, P ≤ 0.01) but not baroreflex sensitivity and sympathovagal balance showed an excellent diagnostic accuracy in identifying subjects with REM sleep behaviour disorder and healthy controls. Conclusions Cardiac/vascular dysfunction in prodromal α-synucleinopathy arises from peripheral rather than from central autonomic degeneration. Autonomic indices encoded in heart rate and blood pressure variability are precise functional markers of early synuclein-mediated neurodegeneration. [ABSTRACT FROM AUTHOR]

A case study is presented of a 68-year-old woman who used to see human faces on the ceiling as she lay at night before falling asleep. She was suspected of having rapid eye movement sleep behavior disorder and dementia with Lewy bodies; mini-mental state examination score showed 29/30; audio and video monitoring showed overnight polysomnography. She is still being diagnosed of pareidolic illusions of a patient with suspected late-onset, sleep-related epilepsy.

Dementia with Lewy bodies ( DLB) is defined pathologically as neurodegeneration associated with Lewy bodies ( LB). LB-related symptoms, including olfactory dysfunction, dysautonomia, and mood and sleep disorders, are increasingly recognized as clinical signs that enable the early detection of DLB, because these symptoms often antedate dementia by years or even decades. It remains unknown if the clinical history of LB-related symptoms is sufficient for the prodromal state of DLB to be suspected in memory clinics. We retrospectively investigated the clinical courses, including olfactory dysfunction, dysautonomia, depression, and rapid eye movement sleep behaviour disorder, of 90 patients with probable DLB. The timing of LB-related symptoms that preceded or followed relative to the onset of memory loss was calculated. LB-related symptoms were present in 79 of 90 patients (87.8%) with probable DLB before or at the time of memory loss onset. These symptoms preceded the onset of memory loss between 1.2 and 9.3 years. We also report on four non-demented patients with a clinical history of LB-related symptoms in our memory clinic. All four patients showed reduced cardiac [123 I]-metaiodobenzylguanidine levels. Moreover, [18 F]fluoro-D-glucose positron emission tomography scans revealed glucose hypometabolism in the occipital cortex in two patients. One patient converted to probable DLB with the development of parkinsonism 2 years after major depression was diagnosed. Based on a clinical history of LB-related symptoms, we propose a conceptual framework to identify these symptomatic but non-demented individuals that led us to suspect the underlying pathophysiology of Lewy body disease. Further prospective study is warranted to determine the clinical significance of LB-related symptoms in non-demented patients. [ABSTRACT FROM AUTHOR]

Rapid eye movement (REM) sleep behaviour disorder (RBD) has been suggested to predict the development of neurodegenerative disorders. Patients with RBD are acting out dream behaviour associated with loss of normal muscle atonia of REM sleep. The aim of the present study was to confirm that exogenous melatonin improves RBD. Eight consecutively recruited males (mean age 54 years) with a polysomnographically (PSG) confirmed diagnosis of RBD were included in a two-part, randomized, double-blind, placebo-controlled cross-over study. Patients received placebo and 3 mg of melatonin daily in a cross-over design, administered between 22:00 h and 23:00 h over a period of 4 weeks. PSG recordings were performed in all patients at baseline, at the end of Part I of the trial and at the end of Part II of the trial. Compared to baseline, melatonin significantly reduced the number of 30-s REM sleep epochs without muscle atonia (39% versus 27%; P = 0.012), and led to a significant improvement in clinical global impression (CGI: 6.1 versus 4.6; P = 0.024). Interestingly, the number of REM sleep epochs without muscle atonia remained lower in patients who took placebo during Part II after having received melatonin in Part I (-16% compared to baseline; P = 0.043). In contrast, patients who took placebo during Part I showed improvements in REM sleep muscle atonia only during Part II (i.e. during melatonin treatment). The data suggest that melatonin might be a second useful agent besides clonazepam in the treatment of RBD. [ABSTRACT FROM AUTHOR]

The aim of this review is to provide data on sleep disturbances in three categories of neurodegenerative disorders: synucleinopathies, tauopathies, and other diseases (this heterogeneous group includes also spinocerebellar degeneration and amyotrophic lateral sclerosis). Analysing and knowing sleep disorders in neurodegenerative diseases may offer important insights into the pathomechanism of some of these diseases and calls attention to the still insufficiently known 'sleep neurology'. The identification of sleep disorders in some neurodegenerative conditions may make their diagnosis easier and earlier; for example, rapid eye movements sleep behaviour disorder may precede any other clinical manifestation of synucleinopathies by more than 10 years. [ABSTRACT FROM AUTHOR]

Objective Two common and characteristic sleep disturbances have been described in dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD); excessive daytime sleepiness and REM sleep behaviour disorder (RBD). This study is an analysis of a secondary outcome measure of a larger study already reported, aimed to determine whether memantine has an effect on the sleep disturbances in DLB and PDD patients. Methods Patients with DLB or PDD were included in a placebo-controlled, randomised controlled study of memantine (20 mg per day) for 24 weeks. The Stavanger Sleep Questionnaire and the Epworth Sleepiness Scale were used to evaluate the effect on sleep disturbances. Results Forty two patients started treatment; 20 with memantine and 22 with placebo. The primary analysis was the comparison of change between the two groups during a 24-week period, using the modified ITT population (last observation carried forward). At 24 weeks, patients treated with memantine were less physically active during sleep while patients in the placebo group worsened. Mean difference between the groups (0.5 [0.05-0.90]) was significant (p = 0.006). No significant change was observed in severity of excessive daytime sleepiness. Conclusions Memantine decreases probable REM sleep behaviour disorder in patients with DLB and PDD. Both diagnostic groups contributed equally to the outcome. Copyright © 2010 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Wakefulness, rapid eye movement (REM) and non-REM sleep are not always mutually exclusive conditions, as commonly assumed. In some cases, the declaration of any state may be incomplete and states can fluctuate rapidly, resulting in peculiar behavioural syndromes such as narcolepsy, REM sleep behaviour disorder and status dissociatus. We briefly introduce this topic and discuss three suggestive clinical cases. [ABSTRACT FROM AUTHOR]

Background and purpose Rapid eye movement (REM) sleep behaviour disorder (RBD) is frequently present in patients with Parkinson's disease (PD) and may have prognostic implications. There are few longitudinal studies of RBD in patients with PD. Our aim was to investigate whether RBD was a persistent feature in a follow-up study of 107 patients with PD. Methods After a mean follow-up time of 3 years, 96 patients were available for reassessment. Probable RBD (pRBD) was diagnosed by the REM sleep behaviour disorder screening questionnaire. Results At follow-up, pRBD was found in 49% of the patients, versus 38% at baseline. The pRBD status remained unchanged in three-quarters of the patients, whilst 17% had new pRBD symptoms. Disease duration was longer in the pRBD group, 9.4 vs. 7.6 years ( P = 0.02). Conclusions Probable RBD is a persistent feature in PD and probably increases over time. [ABSTRACT FROM AUTHOR]

REM sleep behaviour disorder is a recently described parasomnia characterized by a history of excessive motor activities during sleep and is associated with pathological absence of muscle atonia during REM sleep. There is very limited literature on the condition. Two out of 349 elderly patients referred to a psychogeriatric unit were identified to have REM sleep behaviour disorder. These two patients are presented to illustrate the clinical features of the condition. Both of them showed a good response to clonazepam treatment. © 1997 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Background: Rapid eye movement (REM) sleep behaviour disorder (RBD) is a common sleep disorder that can be associated with a number of neurodegenerative conditions as well as with narcolepsy. Current diagnostic criteria require overnight polysomnography, and there are no other biomarkers available. The control of REM sleep is complex with a putative on/off switch within the brainstem activated, amongst other things, by hypocretinergic pathways from the lateral hypothalamus. Methods: Cerebrospinal fluid hypocretin levels were measured in five patients with idiopathic RBD. Results: Hypocretin levels were between 254 and 450 pg/ml and therefore within the normal range of >100 pg/ml. Conclusion: Hypocretin levels in patients with idiopathic RBD are normal. [ABSTRACT FROM AUTHOR]

Summary We estimated the interobserver reliability (IR) of the diagnosis of rapid eye movement (REM) Sleep Behaviour Disorder (RBD) among trained neurologists, with the application of International Classification of Sleep Disorders Revised (ICSD-R), by means of videotaped interviews of people with motor sleep behaviour disorders of different nature. IR of clinical judgement for the diagnosis of RBD was ‘‘substantial’’ (Kappa 0.65); nevertheless, some criteria (‘limb or body movement associated with dream mentation’, criterion B, and ‘sleep behaviours (that) disrupt sleep continuity’, criterion C3) showed a ‘moderate’ IR, resulting from the intrinsic limitations of the patient report and terminological ambiguity. Further clarification of terminology of the ICSD-R criteria would be useful to improve the reliability. [ABSTRACT FROM AUTHOR]