Rapid Eye Movement Atonia Research Articles

Biomarkers of neurodegeneration in isolated and antidepressant-related rapid eye movement sleep behavior disorder.

This study compared the features of isolated rapid eye movement (REM) sleep behavior disorder (iRBD) and antidepressant-related REM sleep behaviour disorder (RBD) with the aim of highlighting markers that might distinguish the two entities. The observational cohort study included RBD patients with and without antidepressant use (antiD+ and antiD- patients, respectively), without cognitive impairment and parkinsonism. Clinical features of RBD, subtle motor and non-motor symptoms of parkinsonism, sleep architecture, REM atonia index, dopamine transporter-single photon emission computed tomography (DAT-SPECT) and skin biopsies for the intraneuronal alpha-synuclein (α-syn), were evaluated in the baseline work-up. Thirty-nine patients, 10 antiD+ and 29 antiD-, were included. AntiD+ patients (more frequently female) reported more psychiatric symptoms, less violent dream enactment, and less frequent hyposmia. Dermal α-syn was detected in 93.1% of antiD- versus 30% of antiD+ patients (p = 0.00024). No differences appeared in other motor and non-motor symptoms, Movement Disorder Society-Unified Parkinson's Disease Rating Scale part III score, DAT-SPECT, or polysomnographic features. Patients with antidepressant-related RBD have clinical and neuropathological features suggesting a lower risk of evolution than those with iRBD.

Automated Analysis of REM Sleep without Atonia in the Lewy Body Disease Spectrum

AbstractBackgroundQuantitative rapid eye movement (REM) sleep without atonia (RSWA) recorded during polysomnography (PSG) represents loss of normal REM sleep atonia. RSWA is the neurophysiologic signature of REM sleep behavior disorder (RBD). Visually scored RSWA is a candidate biomarker for synucleinopathies. However, visual RSWA scoring requires expert scoring, limiting widespread application. We comparatively analyzed RSWA in DLB and iRBD using the automated Ferri REM Atonia Index (RAI).MethodWe quantitatively analyzed the RAI in 12 DLB and 20 iRBD patients, compared to 20 controls using Hypnolab Software for Sleep Analysis (SWS Soft, Inc, Colognola ai Colli, Italy). PSG data were converted to European Data Format (.EDF), and the submentalis surface electromyogram (EMG) signal was notch‐filtered at 60 Hertz and rectified. Automatically calculated RAI scores were comparatively analyzed across groups (DLB, iRBD, controls) using Kruskal Wallis H tests for group comparisons, and regression analyses determined relationships between diagnosis, age, and sex. Logistic regression ROC determined optimal RAI for distinguishing iRBD from DLB. When interpreting RAI, lower values represent greater amounts of RSWA, and higher values represent more normal REM atonia.ResultMean age was older in DLB than in iRBD or controls (72.6 vs. 68.7 vs. 66.5 years). All 12 DLB participants were men, the iRBD group had 18 men and 2 women, and controls were comprised of 16 men and 4 women. Mean RAI was lowest in DLB (0.46), intermediate in iRBD (0.71) and highest in controls (0.96), indicating a gradient in RSWA amounts from DLB patients (highest) to controls (lowest) (Figure). Regression demonstrated diagnosis independently predicted RAI, controlling for age and sex (adjusted R2 = 0.49, p = 0.0001). The RAI that optimally distinguished iRBD from DLB was 0.46 (specificity 85%, sensitivity 58%, AUC = 0.75).ConclusionThe RAI demonstrated a clear gradient throughout the Lewy body spectrum; highest (indicating lowest RSWA amounts) in controls, intermediate in iRBD, and lowest (indicating greatest RSWA) in DLB. The RAI is a promising, time efficient and broadly applicable candidate biomarker for DLB and iRBD. Automated quantitative RSWA could be a valuable tool for deep phenotyping throughout the Lewy body disease spectrum.

Contemporary diagnostic visual and automated polysomnographic REM sleep without atonia thresholds in isolated REM sleep behavior disorder.

Accurate diagnosis of isolated rapid eye movement (REM) sleep behavior disorder (iRBD) is crucial due to its injury potential and neurological prognosis. We aimed to analyze visual and automated REM sleep without atonia (RSWA) diagnostic thresholds applicable in varying clinical presentations in a contemporary cohort of patients with iRBD using submentalis (SM) and individual bilateral flexor digitorum superficialis (FDS) and anterior tibialis electromyography limb recordings during polysomnography. We analyzed RSWA in 20 patients with iRBD and 20 age-, REM-, apnea-hypopnea index-matched controls between 2017 and 2022 for phasic burst durations, density of phasic, tonic, and "any" muscle activity (number of 3-second mini-epochs containing phasic or tonic muscle activity divided by the total number of REM sleep 3-second mini-epochs), and automated Ferri REM atonia index (RAI). Group RSWA metrics were comparatively analyzed. Receiver operating characteristic curves determined optimized area under the curve (AUC) and maximized specificity and sensitivity diagnostic iRBD RSWA thresholds. All mean RSWA metrics were higher in patients with iRBD than in controls (P < .05), except for selected anterior tibialis measures. Optimized, maximal specificity AUC diagnostic cutoffs for coprimary outcomes were: SM "any" 6.5%, 14.0% (AUC = 92.5%) and combined SM+FDS "any" 15.1%, 27.4% (AUC = 95.8%), while SM burst durations were 0.72, and 0.72 seconds (AUC 90.2%) and FDS RAI = 0.930, 0.888 (AUC 92.8%). This study provides evidence for current quantitative RSWA diagnostic thresholds in chin and individual 4 limb muscles applicable in different iRBD clinical settings and confirms the key value of SM or SM+FDS to assure accurate iRBD diagnosis. Evolving iRBD recognition underscores the necessity of continuous assessment with future large, prospective, well-harmonized, multicenter polysomnographic analyses. Leclair-Visonneau L, Feemster JC, Bibi N, etal. Contemporary diagnostic visual and automated polysomnographic REM sleep without atonia thresholds in isolated REM sleep behavior disorder. J Clin Sleep Med. 2024;20(2):279-291.

Motor neuron involvement threatens survival in spinocerebellar ataxia type 1.

Motor neuron involvement threatens survival in spinocerebellar ataxia type 1.

0557 Diagnostic Visual and Automated Polysomnagraphic REM Sleep Without Atonia Thresholds in Isolated REM Sleep Behavior Disorder 2.0

Abstract Introduction Accurate, early diagnosis of isolated rapid eye movement (REM) sleep behavior disorder (iRBD) is crucial given its injury potential and neurological prognosis. We aimed to analyze visual and automated REM sleep without atonia (RSWA) diagnostic thresholds in a current cohort of iRBD patients using submentalis (SM) and individual four limb electromyography (EMG) recordings, including bilateral flexor digitorum superificialis (FDS) and anterior tibialis (AT) during polysomnography. Methods We analyzed RSWA in 20 iRBD patients and 20 age-sex-AHI matched controls who underwent polysomnography between 2017-2021 for phasic burst durations, phasic, tonic, and "any" muscle activity, and automated REM atonia index (RAI). Group RSWA metrics were analyzed with non-parametric comparisons, logistic regression, and receiver operating characteristic (ROC) curves to determine optimal diagnostic cutoff thresholds for iRBD. Correlation explored associative relationships between RSWA metrics, and principal components analysis (PCA) defined determinants of RSWA metric variance. Results All mean RSWA metrics were higher in iRBD patients than controls (p&amp;lt;0.05), except for left and bilateral AT phasic density and duration. RSWA(phasic%, AUC; "any"%, AUC) cutoffs were: SM (6.5%, AUC=90.2; 6.5%, AUC=92.5); L FDS (7.3%, AUC=95.8; 7.3%, AUC=95.8%); R FDS (5.4%, AUC=93.5; 5.8%, AUC=93.2%); Bilateral FDS (10.7%, AUC=96; 15.3%, AUC=95.8); L AT (6.7%, AUC=74.5; 6.7%, AUC=74.8%); R AT (4.7%, AUC=76.8; 4.7%, AUC=76.8%); Bilateral AT (7.5%, AUC=77.5; 7.5%, AUC=77.5%), combined SM/FDS (15.0%, AUC=95.5; 15.1%; AUC=95.8), combined SM/AT (16.5%, AUC=85.8; 21.0%; AUC=88.8),tonic (0.5%; AUC=85.9), and RAI (0.90; AUC=91.4). Phasic burst duration cutoffs were: SM=0.7s (AUC=90.2), L FDS=0.5 s (AUC=83.2), R FDS=0.6 (AUC=85.2), L AT=0.3 s (AUC=65.0) and R AT=0.4 s (AUC=77.0). PCA demonstrated that FDS and combined SM/FDS and SM/AT RSWA metrics best explained RSWA variance and differentiated controls from RBD, while SM and AT alone were less explanatory. Conclusion This study provides evidence for quantitative RSWA diagnostic thresholds applicable in current iRBD populations, and confirms the key importance of FDS to assure accurate iRBD diagnosis. Interestingly, these RSWA diagnostic thresholds are lower than previously determined thresholds, suggesting secular trends toward earlier iRBD detection and heterogeneous disease duration relative to polysomnography acquisition, underscoring the necessity of future large scale prospective, multicenter polysomnographic analyses to determine definitive iRBD diagnostic RSWA thresholds. Support (If Any)

Automatic analysis of muscular activity in the flexor digitorum superficialis muscles: a fast screening method for rapid eye movement sleep without atonia.

To identify a fast and reliable method for rapid eye movement (REM) sleep without atonia (RWA) quantification. We analyzed 36 video-polysomnographies (v-PSGs) of isolated REM sleep behavior disorder (iRBD) patients and 35 controls' v-PSGs. Patients diagnosed with RBD had: i) RWA, quantified with a reference method, i.e. automatic and artifact-corrected 3-s Sleep Innsbruck Barcelona (SINBAR) index in REM sleep periods (RSPs, i.e. manually selected portions of REM sleep); and ii) v-PSG-documented RBD behaviors. We quantified RWA with other (semi)-automated methods requiring less human intervention than the reference one: the indices proposed by the SINBAR group (the 3-s and 30-s phasic flexor digitorum superficialis (FDS), phasic/"any"/tonic mentalis), and the REM atonia, short and long muscle activity indices (in mentalis/submentalis/FDS muscles). They were calculated in whole REM sleep (i.e. REM sleep scored following international guidelines), in RSPs, with and without manual artifact correction. Area under curves (AUC) discriminating iRBD from controls were computed. Using published cut-offs, the indices' sensitivity and specificity for iRBD identification were calculated. Apnea-hypopnea index in REM sleep (AHIREM) was considered in the analyses. RWA indices from FDS muscles alone had the highest AUCs and all of them had 100% sensitivity. Without manual RSP selection and artifact correction, the "30-s phasic FDS" and the "FDS long muscle activity" had the highest specificity (85%) with AHIREM < 15/h. RWA indices were less reliable when AHIREM≥15/h. If AHIREM<15/h, FDS muscular activity in whole REM sleep and without artifact correction is fast and reliable to rule out RWA.

Chromatic Pupillometry in Isolated Rapid Eye Movement Sleep Behavior Disorder.

BackgroundMelanopsin retinal ganglion cell (mRGC)‐mediated pupillary light reflex (PLR) abnormalities have been documented in several neurodegenerative disorders including Parkinson's disease. Overall, isolated rapid eye movement (REM) sleep behavior disorder (iRBD) represents the strongest prodromal risk factor for impending α‐synucleinopathies.ObjectivesTo quantitatively compare PLR and mRGC‐mediated contribution to PLR in 16 iRBD patients and 16 healthy controls.MethodsiRBD and controls underwent extensive neuro‐ophthalmological evaluation and chromatic pupillometry. In iRBD, PLR metrics were correlated with clinical variables and with additional biomarkers including REM atonia index (RAI), DaTscan, and presence of phosphorylated‐α‐synuclein (p‐α‐syn) deposition in skin biopsy.ResultsWe documented higher baseline pupil diameter and decreased rod‐transient PLR amplitude in iRBD patients compared to controls. PLR rod‐contribution correlated with RAI. Moreover, only iRBD patients with evidence of p‐α‐syn deposition at skin biopsy showed reduced PLR amplitude compared to controls.ConclusionThe observed PLR abnormalities in iRBD might be considered as potential biomarkers for the risk stratification of phenoconversion of the disease. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society

Quantitative REM Sleep without Atonia in Parkinson's Disease and Essential Tremor.

Rapid eye movement (REM) sleep behavior disorder (RBD) occurs occasionally in essential tremor (ET), but polysomnographic REM sleep without atonia (RSWA) analyses have been sparse. To characterize the amount and distribution of polysomnographic RSWA, the electrophysiologic substrate of RBD, in patients with Parkinson's disease (PD) and ET. We analyzed quantitative RSWA in 73 patients: PD (23), ET (23), and age-sex-matched controls (27). None had dream-enactment behavior history or received antidepressants. Phasic, tonic, "any," and phasic-burst duration RSWA measures were calculated in the submentalis (SM) and anterior tibialis (AT) muscles. The automated REM atonia index (RAI) was also determined. Statistical analysis was performed by Kruskal-Wallis rank-sum and Mann-Whitney tests. SM phasic RSWA was significantly greater for PD than ET patients and controls (12.5% ± 12.8% vs. 4.9% ± 6.7%, 3.9% ± 2.6%), as was SM "any" (13.54% ± 14.30% vs. 5.2% ± 7.6%, 4.2% ± 2.6%). RAI was significantly lower in PD than in ET and controls (0.78 ± 0.23 vs. 0.92 ± 0.09 vs. 0.90 ± 0.17, P ≤ 0.005), but no different between ET and controls. AT phasic and "any" RSWA was similar between the 3 groups. ET and control RSWA was similar in all measures. Two ET patients (8.7%) had SM RSWA similar to PD patients. Elevated SM RSWA distinguished PD from ET in patients without dream-enactment symptoms and occurs frequently in PD patients, and in isolated tremor suggests underlying synucleinopathy. Prospective studies will further validate these findings.

Sleep Disturbances in Patients with Disorders of the Nerve and Muscle Diseases

Recognize sleep disorders associated with neuromuscular diseases. Neuromuscular diseases can be associated with various sleep disorders. Diaphragmatic weakness, bulbar dysfunction, pharyngeal neuropathy, and central neurodegeneration cause sleep-disordered breathing. Spinal cord hyperexcitability, loss of inhibitory descending pathways, and neuropathy promote restless legs syndrome. Reduced cerebrospinal fluid (CSF) hypocretin, central dysfunction of sleep regulation, and degeneration of GABAergic intracortical circuits may contribute to central hypersomnia. Dysfunction of the nigrostriatal dopaminergic system, associated with neurodegenerative diseases and certain neuromuscular disorders, may be a common pathophysiologic mechanism responsible for the loss of rapid eye movement (REM) sleep muscle atonia and REM sleep behavior disorder (RBD). Different neuromuscular disorder may be more susceptible to specific sleep disturbances. A low threshold needs to be maintained for the diagnosis and treatment of sleep disorders in neuromuscular diseases, due to their high prevalence, lack of symptom specificity, and presence even in minimally symptomatic patients. However, loss of REM atonia may be protective against sleep-disordered breathing. There are reasonable pathophysiologic mechanisms such as respiratory muscle weakness, upper airway obstruction, and central dysfunction that explain the link between sleep disorders and neuromuscular diseases

A comparative study of methods for automatic detection of rapid eye movement abnormal muscular activity in narcolepsy

ObjectiveTo evaluate rapid eye movement (REM) muscular activity in narcolepsy by applying five algorithms to electromyogram (EMG) recordings, and to investigate its value for narcolepsy diagnosis. Patients/methodsA modified version of phasic EMG metric (mPEM), muscle activity index (MAI), REM atonia index (RAI), supra-threshold REM EMG activity metric (STREAM), and Frandsen method (FR) were calculated from polysomnography recordings of 20 healthy controls, 18 clinic controls (subjects suspected with narcolepsy but finally diagnosed without any sleep abnormality), 16 narcolepsy type one without REM sleep behavior disorder (RBD), nine narcolepsy type one with RBD, and 18 narcolepsy type two. Diagnostic value of metrics in differentiating between groups was quantified by area under the receiver operating characteristic curve (AUC). Correlations among the metrics and cerebrospinal fluid hypocretin-1 (CSF-hcrt-1) values were calculated using linear models. ResultsAll metrics excluding STREAM found significantly higher muscular activity in narcolepsy one cases versus controls (p < 0.05). Moreover, RAI showed high sensitivity in the detection of RBD. The mPEM achieved the highest AUC in differentiating healthy controls from narcoleptic subjects. The RAI best differentiated between narcolepsy 1 and 2. Lower CSF-hcrt-1 values correlated with high muscular activity quantified by mPEM, sMAI, lMAI, PEM and FR (p < 0.05). ConclusionsThis automatic analysis showed higher number of muscle activations in narcolepsy 1 compared to controls. This finding might play a supportive role in diagnosing narcolepsy and in discriminating narcolepsy subtypes. Moreover, the negative correlation between CSF-hcrt-1 level and REM muscular activity supported a role for hypocretin in the control of motor tone during REM sleep.

Comparison Between Automatic and Visual Scorings of REM Sleep Without Atonia for the Diagnosis of REM Sleep Behavior Disorder in Parkinson Disease

To compare three different methods, two visual and one automatic, for the quantification of rapid eye movement (REM) sleep without atonia (RSWA) in the diagnosis of REM sleep behavior disorder (RBD) in Parkinson's disease (PD) patients. Sixty-two consecutive patients with idiopathic PD underwent video-polysomnographic recording and showed more than 5 minutes of REM sleep. The electromyogram during REM sleep was analyzed by means of two visual methods (Montréal and SINBAR) and one automatic analysis (REM Atonia Index or RAI). RBD was diagnosed according to standard criteria and a series of diagnostic accuracy measures were calculated for each method, as well as the agreement between them. RBD was diagnosed in 59.7% of patients. The accuracy (85.5%), receiver operating characteristic (ROC) area (0.833) and Cohen's K coefficient (0.688) obtained with RAI were similar to those of the visual parameters. Visual tonic parameters, alone or in combination with phasic activity, showed high values of accuracy (93.5-95.2%), ROC area (0.92-0.94), and Cohen's K (0.862-0.933). Similarly, the agreement between the two visual methods was very high, and the agreement between each visual methods and RAI was substantial. Visual phasic measures alone performed worse than all the other measures. The diagnostic accuracy of RSWA obtained with both visual and automatic methods was high and there was a general agreement between methods. RAI may be used as the first line method to detect RSWA in the diagnosis of RBD in PD, together with the visual inspection of video-recorded behaviors, while the visual analysis of RSWA might be used in doubtful cases.

Isolated rapid eye movement sleep without atonia in amyotrophic lateral sclerosis

ObjectiveThe aim of this study was to quantitatively analyze, with the most recent and advanced tools, the presence of periodic leg movements during sleep (PLMS) and/or rapid eye movement (REM) sleep without atonia (RSWA), in a group of patients with amyotrophic lateral sclerosis (ALS), and to assess their eventual correlation with the clinical severity of the disease. MethodsTwenty-nine ALS patients were enrolled (mean age 63.6 years) along with 28 age-matched “normal” controls (mean age 63.8 years). Functional impairment due to ALS was evaluated using the ALS-Functional Rating Scale-Revised (ALS-FRS) and the ALS severity scale (ALSSS). Full video polysomnographic night recordings were obtained, and PLMS were analyzed by considering their number/hour of sleep and periodicity index, the distribution of intermovement intervals, and the distribution during the night. The characteristics of the chin electromyogram (EMG) amplitude during REM sleep were analyzed by means of the automatic atonia index and the number of chin EMG activations (movements). ResultsThe ALS patients showed longer sleep latency than the controls, together with an increase in number of stage shifts, increased sleep stage 1, and decreased sleep stage 2. None of the leg PLMS parameters were different between the ALS patients and controls. The REM atonia index was significantly decreased in the ALS patients, and the number of chin movements/hour tended to increase. Both REM atonia index and number of chin movements/hour correlated significantly with the ALS-FRS; REM atonia was higher and chin movements were less in ALS patients with more preserved function (higher scores on the ALS-FRS). ConclusionAbnormal REM sleep atonia seemed to be a genuine effect of ALS pathology per se and correlated with the clinical severity of the disease. It is unclear if this might constitute the basis of a possible risk for the development of REM sleep behavior disorder or represent a form of isolated RSWA in ALS.

Diagnostic REM sleep muscle activity thresholds in patients with idiopathic REM sleep behavior disorder with and without obstructive sleep apnea

ObjectivesWe aimed to determine whether visual and automated rapid eye movement (REM) sleep without atonia (RSWA) methods could accurately diagnose patients with idiopathic REM sleep behavior disorder (iRBD) and comorbid obstructive sleep apnea (OSA). MethodsIn iRBD patients (n = 15) and matched controls (n = 30) with and without OSA, we visually analyzed RSWA phasic burst durations, phasic, tonic, and “any” muscle activity by 3-s mini-epochs, phasic activity by 30-s (AASM rules) epochs, and automated REM atonia index (RAI). Group RSWA metrics were analyzed with regression models. Receiver operating characteristic (ROC) curves were used to determine the best diagnostic cutoff thresholds for REM sleep behavior disorder (RBD). Both split-night and full-night polysomnographic studies were analyzed. ResultsAll mean RSWA phasic burst durations and muscle activities were higher in iRBD patients than in controls (p < 0.01). Muscle activity (phasic, “any”) cutoffs for 3-s mini-epoch scorings were as follows: submentalis (SM) (15.8%, 19.5%), anterior tibialis (AT) (29.7%, 29.7%), and combined SM/AT (39.5%, 39.5%). The tonic muscle activity cutoff was 0.70% and RAI (SM) cutoff 0.86. The phasic muscle burst duration cutoffs were 0.66 s for SM and 0.71 s for AT. Combining phasic burst durations with RSWA muscle activity improved the sensitivity and specificity of iRBD diagnosis. ConclusionsThis study provides evidence for quantitative RSWA diagnostic thresholds applicable in iRBD patients with OSA. Our findings in this study were very similar to those seen in patients with Parkinson’s disease–REM sleep behavior disorder (PD–RBD), consistent with a common mechanism and presumed underlying etiology of synucleinopathy in both groups.

Rapid Eye Movement Sleep Behavior Disorder: Overview and Current Perspective

Rapid eye movement (REM) stage of sleep in normal circumstances is composed of vivid dream mentation associated with physiological skeletal muscle paralysis and thus, quiescence of motor activity. REM sleep behavior disorder (RBD) is a parasomnia characterized by disinhibition of motor control facilitating dream enactment behaviors. These nocturnal motoric behaviors due to lack of REM atonia range from benign limb movements to complex aggressive actions but are often manifested by violent, aggressive flailing, punching and kicking with vocalizations enacting action-filled hostile dreams. Polysomnographic evidence of increased electromyographic tone during REM with or without capturing clinical dream enactment together with careful history helps diagnose RBD. It is considered a prodromal feature of neurodegenerative alpha-synucleinopathies with high rate of eventual phenoconversion. The mainstay of treatment is to first ensure physical safety. When medications are necessary, options include either low-dose clonazepam, high-dose melatonin or both. Yearly surveillance with detailed neurological evaluation is vital for early detection and eventual management of neurodegenerative disorder.

Duality of sleep mechanisms – A background of present-day clinical and neurophysiological knowledge

Rapid Eye Movement (REM) sleep discovery initiated a new area of scientific as well as clinical research in sleep medicine. Non-REM (NREM) and REM sleep have been studied from the neurophysiological, neuroanatomical and neurotransmitter points of view. The development of improved imaging techniques including electroencephalography (EEG), polysomnography (PSG), positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) along with the power of advanced computational techniques help to improve our knowledge. While NREM sleep is characterized by slow oscillations and connected with decreased global and regional cerebral blood flow, REM sleep is characterized by high frequency, low amplitude activity and correlates with increased cerebral blood flow. Recent research suggests NREM sleep correlation with synaptic plasticity in the brain (particularly in childhood). Sleep macro- and microstructure (cyclic alternating patterns, CAP) revealed new connections with clinical implications (epilepsy, parasomnia). Besides rapid eye movements, changes in circulation and respiration, muscle atonia is a fundamental characteristic of REM sleep. Lack of REM atonia causes REM behavior disorder – a clinical entity preceding many neurodegeneratice diseases. In contrast, narcolepsy is associated with excessive and unwanted REM atonia – cataplexy, hypnagogic hallucinations or sleep paralysis. Neurophysiological knowledge then helps us to understand the background of different sleep disorders.

Management of REM sleep behavior disorder: An evidence based review.

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by dream enactment behavior resulting from a loss of REM skeletal muscle atonia. The neurobiology of REM sleep and the characteristic features of REM atonia have an important basis for understanding the aggravating etiologies the proposed pharmacological interventions in its management. This review outlines the evidence for behavioral and therapeutic measures along with evidence-based guidelines for their implementation, impact on falls, and effect on polysomnography (PSG) while highlighting the non-motor, autonomic, and cognitive impact of this entity. PubMed databases were reviewed upto May 2013 in peer-reviewed scientific literature regarding the pathophysiology and management of RBD in adults. The literature was graded according to the Oxford centre of evidence-based Medicine Levels. An early intervention that helps prevent consequences such as falls and provides a base for intervention with neuroprotective mechanisms and allocates a unique platform that RBD portrays with its high risk of disease conversion with a sufficiently long latency. RBD provides a unique platform with its high risk of disease conversion with a sufficiently long latency, providing an opportunity for early intervention both to prevent consequences such as falls and provide a base for intervention with neuroprotective mechanisms.

Quantification of REM Sleep without Atonia in Korean REM Sleep Behavior Disorder Patients: Comparison of Manual and Computer-Assisted Scoring Methods

Address for correspondence Won Chul Shin, MD, PhD Department of Neurology, Kyung Hee University Hospital at Gangdong, Kyung Hee University School of Medicine, 892 Dongnam-ro, Gangdong-gu, Seoul 134-727, Korea Tel: +82-2-440-6166 Fax: +82-2-440-7262 E-mail: shinwc@khu.ac.kr Objectives: The polysomnographic hallmark of rapid eye movement (REM) sleep behavior disorder (RBD) is loss of muscle atonia during REM sleep; REM sleep without atonia (RSWA). However, the International Classification of Sleep Disorders (ICSD) criteria did not suggest optimized diagnostic value of RSWA and how to score muscle activity during REM sleep. Many previous studies have been tried to figure out the objective quantitative cut-off values of RSWA. We investigated RSWA in Korean RBD patients compared with normal control, to quantify the cut-off value in diagnosis of RBD, using both manual and computer-assisted scoring methods (REM atonia index, RAI). Methods: We retrospectively analyzed polysomnography and clinical data of 40 patients, 10 age-matched controls by ICSD-3 criteria. The quantitative analysis of chin electromyography density during REM sleep was done by both manual and computerized method. The RSWA and RAI were compared within two groups. Results: In computerized method, the mean RAI of RBD patient was 0.66±0.20, and 0.93±0.38 in control group (p<0.001). Also, in manual method, RSWA were also significantly increased within RBD patient compared with normal controls (tonic activity: 9.1±10.3 vs. 0.1±0.2, phasic activity: 7.5±6.4 vs. 1.6±1.2, p<0.002). Conclusions: We quantify the characteristics of RSWA in Korean RBD patients and suggest that we may diagnose RBD who present RSWA with 4.1% or more increase in total REM sleep duration and RAI more than 0.84. J Korean Sleep Res Soc 2014;11(2):50-56

4.: Exploring the neural circuitry of rapid eye movement sleep behaviour disorder in Parkinson’s disease using functional MRI

Rapid eye movement (REM) sleep behaviour disorder (RBD) is observed in over half of all Parkinson’s disease (PD) patients. The development of this symptom has also been associated with cognitive dysfunction, freezing of gait and visual hallucinations. These associations raise the possibility of common neural underpinnings. This study aims to explore impairments in neural circuitry of RBD, identified electrophysiologically within a cohort of patients with PD. Patients with and without RBD will be compared utilizing resting state functional MRI. Thirty one patients with PD underwent neurological, sleep assessment and resting state functional MRI. The REM atonia index was derived for all participants as an objective measure of REM sleep without atonia and patients with a REM atonia index less than 0.9 were deemed positive for RBD. RBD positive and negative patients were compared between regions of interests (ROI), using correlations between the blood-oxygen-level dependent time course in 50 Brodmann areas, along with 4 mm bilateral ROI centered on the putamen, the caudate and the ventral striatum. Patients identified to be RBD positive showed a significant decrease in the connectivity between the left putamen and the dorsolateral prefrontal cortex bilaterally. Connectivity between the left putamen and the right frontal eye fields was reduced. Similarly there was reduced connectivity between the right caudate and the right frontal eye fields. Patients with RBD and PD in this study displayed impaired connectivity within frontostriatal networks subserving cognition and cognitive control. The cortical regions that were “disconnected” in the RBD positive patients have also been implicated in the pathophysiology of freezing of gait and visual hallucinations, suggesting that commonalities between these disorders may reflect the breakdown of effective communication within neural networks underlying cognitive control. Identifying a similar pattern of connectivity using resting state MRI could be used to predict PD in at risk populations and if identified in PD cohorts, could predict attributes associated with significant comorbidity and burden to the community.

Rapid eye movement atonia is not rapid eye movement sleep behavior disorder

Rapid eye movement atonia is not rapid eye movement sleep behavior disorder

Investigating rapid eye movement sleep without atonia in Parkinson's disease using the rapid eye movement sleep behavior disorder screening questionnaire

Rapid eye movement (REM) sleep behavior disorder (RBD) is frequently observed in patients with Parkinson's disease (PD). Accurate diagnosis is essential for managing this condition. Furthermore, the emergence of idiopathic RBD in later life can represent a premotor feature, heralding the development of PD. Reliable, accurate methods for identifying RBD may offer a window for early intervention. This study sought to identify whether the RBD screening questionnaire (RBDSQ) and three questionnaires focused on dream enactment were able to correctly identify patients with REM without atonia (RWA), the neurophysiological hallmark of RBD. Forty-six patients with PD underwent neurological and sleep assessment in addition to completing the RBDSQ, the RBD single question (RBD1Q), and the Mayo Sleep Questionnaire (MSQ). The REM atonia index was derived for all participants as an objective measure of RWA. Patients identified to be RBD positive on the RBDSQ did not show increased RWA on polysomnography (80% sensitivity and 55% specificity). However, patients positive for RBD on questionnaires specific to dream enactment correctly identified higher degrees of RWA and improved the diagnostic accuracy of these questionnaires. This study suggests that the RBDSQ does not accurately identify RWA, essential for diagnosing RBD in PD. Furthermore, the results suggest that self-report measures of RBD need to focus questions on dream enactment behavior to better identify RWA and RBD. Further studies are needed to develop accurate determination and quantification of RWA in RBD to improve management of patients with PD in the future.