Cardiac Autonomic Dysfunction Is Associated with Severity of REM Sleep without Atonia in Isolated REM Sleep Behavior Disorder.
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SUBMITTER: You S
PROVIDER: S-EPMC8621819 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Values for normative REM sleep without atonia (RSWA) remain unclear. Older age and male sex are associated with greater RSWA, and isolated elevated RSWA has been reported. We aimed to describe normative RSWA and characterize isolated RSWA frequency in adults without REM sleep behavior disorder (RBD). We visually quantified phasic, "any," and tonic RSWA in the submentalis (SM) and anterior tibialis (AT) muscles, and the automated Ferri REM Atonia Index during polysomnography in adults without RBD aged 21-88. We calculated RSWA percentiles across age and sex deciles and compared RSWA in older (≥ 65) versus younger (<65) men and women. Isolated RSWA (exceeding diagnostic RBD cutoffs, or >95th percentile) frequency was also determined. Overall, 95th percentile RSWA percentages were SM phasic, any, tonic = 8.6%, 9.1%, 0.99%; AT phasic and "any" = 17.0%; combined SM/AT phasic, "any" = 22.3%, 25.5%; and RAI = 0.85. Most phasic RSWA burst durations were ≤1.0 s (85th percentiles: SM = 1.07, AT = 0.86 seconds). Older men had significantly higher AT RSWA than older women and younger patients (all p < 0.04). Twenty-nine (25%, 18 men) had RSWA exceeding the cohort 95th percentile, while 17 (14%, 12 men) fulfilled diagnostic cutoffs for phasic or automated RBD RSWA thresholds. RSWA levels are highest in older men, mirroring the demographic characteristics of RBD, suggesting that older men frequently have altered REM sleep atonia control. These data establish normative adult RSWA values and thresholds for determination of isolated RSWA elevation, potentially aiding RBD diagnosis and discussions concerning incidental RSWA in clinical sleep medicine practice.
| S-EPMC6783903 | biostudies-literature
Project description:Despite decades of research, there is a persistent debate regarding the localization of GABA/glycine neurons responsible for hyperpolarizing somatic motoneurons during paradoxical (or REM) sleep (PS), resulting in the loss of muscle tone during this sleep state. Combining complementary neuroanatomical approaches in rats, we first show that these inhibitory neurons are localized within the ventromedial medulla (vmM) rather than within the spinal cord. We then demonstrate their functional role in PS expression through local injections of adeno-associated virus carrying specific short-hairpin RNA in order to chronically impair inhibitory neurotransmission from vmM. After such selective genetic inactivation, rats display PS without atonia associated with abnormal and violent motor activity, concomitant with a small reduction of daily PS quantity. These symptoms closely mimic human REM sleep behavior disorder (RBD), a prodromal parasomnia of synucleinopathies. Our findings demonstrate the crucial role of GABA/glycine inhibitory vmM neurons in muscle atonia during PS and highlight a candidate brain region that can be susceptible to ?-synuclein-dependent degeneration in RBD patients.
| S-EPMC5799338 | biostudies-literature
Project description:Study objectivesREM sleep behavior disorder (RBD) is associated with antidepressant treatment, especially in younger patients; but quantitative REM sleep without atonia (RSWA) analyses of psychiatric RBD patients remain limited. We analyzed RSWA in adults receiving antidepressants, with and without RBD.DesignWe comparatively analyzed visual, manual, and automated RSWA between RBD and control groups. RSWA metrics were compared between groups, and regression was used to explore associations with clinical variables.SettingTertiary-care sleep center.ParticipantsParticipants included traditional RBD without antidepressant treatment (n = 30, 15 Parkinson disease [PD-RBD] and 15 idiopathic); psychiatric RBD receiving antidepressants (n = 30); and adults without RBD, including antidepressant-treated psychiatric (n = 30), untreated psychiatric (n = 15), and OSA (n = 60) controls.InterventionsN/A.Measurements and resultsRSWA was highest in traditional and psychiatric RBD, intermediate in treated psychiatric controls, and lowest in untreated psychiatric and OSA controls (P < 0.01). RSWA distribution and type also differed between antidepressant-treated patients having higher values in anterior tibialis, and PD-RBD with higher submentalis and tonic RSWA. Psychiatric RBD had significantly younger age at onset than traditional RBD patients (P < 0.01).ConclusionsAntidepressant treatment was associated with elevated REM sleep without atonia (RSWA) even without REM sleep behavior disorder (RBD), suggesting that antidepressants, not depression, promote RSWA. Differences in RSWA distribution and type were also seen, with higher anterior tibialis RSWA in antidepressant-treated patients and higher tonic RSWA in Parkinson disease-RBD patients, which could aid distinction between RBD subtypes. These findings suggest that antidepressants may mediate different RSWA mechanisms or, alternatively, that RSWA type and distribution evolve during progressive neurodegeneration. Further prospective RSWA analyses are necessary to clarify the relationships between antidepressant treatment, psychiatric disease, and RBD.
| S-EPMC4434557 | biostudies-literature
Project description:BackgroundRapid eye movement (REM) sleep behavior disorder (RBD) occurs occasionally in essential tremor (ET), but polysomnographic REM sleep without atonia (RSWA) analyses have been sparse.ObjectiveTo characterize the amount and distribution of polysomnographic RSWA, the electrophysiologic substrate of RBD, in patients with Parkinson's disease (PD) and ET.MethodsWe 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.ResultsSM 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.ConclusionsElevated 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.
| S-EPMC7780943 | biostudies-literature
Project description:Idiopathic rapid eye movement (REM) sleep behavior disorder (RBD) is a harbinger of synuclein-mediated neurodegenerative diseases. It is unknown if this also applies to isolated REM sleep without atonia (RWA). We performed a long-term follow-up investigation of subjects with isolated RWA.Participants were recruited from 50 subjects with isolated RWA who were identified at the sleep laboratory of the Department of Neurology at the Medical University of Innsbruck between 2003 and 2005. Eligible subjects underwent follow-up clinical examination, polysomnography, and assessment of neurodegenerative biomarkers (cognitive impairment, finger speed deficit, impaired color vision, olfactory dysfunction, orthostatic hypotension, and substantia nigra hyperechogenicity).After a mean of 8.6 ± 0.9 y, 1 of 14 participating subjects (7.3%) progressed to RBD. Ten of 14 RWA subjects (71.4%) were positive for at least one neurodegenerative biomarker. Substantia nigra hyperechogenicity and presence of mild cognitive impairment were both present in 4 of 14 subjects with isolated RWA. Electromyographic activity measures increased significantly from baseline to follow-up polysomnography ("any" mentalis and both anterior tibialis muscles: 32.5 ± 9.4 versus 52.2 ± 16.6%; p = 0.004).This study provides first evidence that isolated RWA is an early biomarker of synuclein-mediated neurodegeneration. These results will have to be replicated in larger studies with longer observational periods. If confirmed, these disease findings have implications for defining at-risk cohorts for Parkinson disease.
| S-EPMC4623125 | biostudies-literature
Project description:ObjectiveThe objective of this cross-sectional study was to test the hypothesis that patients with Parkinson disease (PD) and freezing of gait (PD+FOG) would demonstrate sleep disturbances comparable to those seen in patients with REM sleep behavior disorder (RBD) and these changes would be significantly different from those in PD patients without FOG (PD-FOG) and age-matched controls.MethodsWe conducted overnight polysomnography studies in 4 groups of subjects: RBD, PD-FOG, PD+FOG, and controls. Tonic and phasic muscle activity during REM sleep were quantified using EMG recordings from the chin, compared among study groups, and correlated with disease metrics.ResultsThere were no significant differences in measures of disease severity, duration, or dopaminergic medications between the PD+FOG and PD-FOG groups. Tonic muscle activity was increased significantly (p < 0.007) in the RBD and PD+FOG groups compared to the PD-FOG and control groups. There was no significant difference in tonic EMG between the PD+FOG and RBD group (p = 0.364), or in tonic or phasic EMG between the PD-FOG and control group (p = 0.107). Phasic muscle activity was significantly increased in the RBD group compared to all other groups (p = 0.029) and between the PD+FOG and control group (p = 0.001), but not between the PD+FOG and PD-FOG groups (p = 0.059).ConclusionsThese findings provide evidence that increased muscle activity during REM sleep is a comorbid feature of patients with PD who exhibit FOG as a motor manifestation of their disease.
| S-EPMC3795590 | biostudies-literature
Project description:Compare nocturnal REM sleep without atonia (nRWA) and REM sleep behavior disorder (RBD) between pediatric patients with and without narcolepsy and determine if the nRWA index is a valid diagnostic biomarker for narcolepsy.Retrospective cohort study of children ages 6 to 18 years who completed a nocturnal polysomnogram (PSG) and Multiple Sleep Latency Test (MSLT). Our study sample included 11 patients with narcolepsy type 1 (NT1), 6 with narcolepsy type 2 (NT2), 12 with idiopathic hypersomnia (IH), and 11 with subjective hypersomnia (sHS). We compared group nRWA indices (epochs of RWA/total stage R sleep epochs) from the nocturnal PSGs and analyzed nRWA index receiver operating curve (ROC) statistics for narcolepsy diagnosis.The median nRWA index of patients with NT1 was 15 to 30 times higher compared to sHS and IH (Ps < .005) but similar to that of the NT2 group (P = .46). RBD was present in 25% of patients with narcolepsy (NT1 and NT2). In comparing those with and without narcolepsy, the nRWA index area under the curve was 0.87 (0.6), 95% confidence interval (CI) = 0.75 to 0.99, P < .001. The threshold of having ? 1% of stage R sleep epochs with nRWA yielded a sensitivity of 88.2%, 95% CI = 63.6-98.5 and specificity of 60.9%, 95% CI = 38.5 to 80.3 for diagnosis of narcolepsy. In contrast, a threshold of ? 8% yielded a specificity of 95.7%, 95% CI = 78.1 to 99.9 and sensitivity of 52.9%, 95% CI = 27.8 to 77.The nRWA index is a very good diagnostic biomarker of pediatric narcolepsy. Depending on the clinical cutoffs utilized, this biomarker can identify more children/adolescents with narcolepsy using just the PSG or reduce false-positive diagnostic results.
| S-EPMC5786844 | biostudies-other
Project description:BackgroundSialic acid-protein interactions are involved in regulating central nervous system immunity; therefore, derangements in sialylation could be involved in neurodegeneration.ObjectivesWe evaluate the differences in serum transferrin sialylation in prodromal and early-stage Parkinson's disease (PD), its relation to substantia nigra degeneration, and the risk of phenoconversion to manifest disease.MethodsSixty treatment-naive PD patients; 72 polysomnography-confirmed isolated rapid eye movement sleep behavior disorder (iRBD) patients, that is, patients with prodromal synucleinopathy; and 46 healthy volunteers aged ≥45 years and drinking ≤60 standard drinks per month were included. The proportion of serum low-sialylated, carbohydrate-deficient transferrin (CDT) isoforms was assessed using high-performance liquid chromatography, and the values were adjusted for alcohol intake (CDTadj ). Dopamine transporter single-photon emission computed tomography (DaT-SPECT) imaging was performed. In iRBD, phenoconversion risk of DaT-SPECT and CDTadj was evaluated using Cox regression adjusted for age and sex.ResultsMedian CDTadj was lower in PD (1.1 [interquartile range: 1.0-1.3]%) compared to controls (1.2 [1.1-1.6]%) (P = 0.001). In iRBD, median CDTadj was lower in subjects with abnormal (1.1 [0.9-1.3]%) than normal (1.3 [1.2-1.6]%) DaT-SPECT (P = 0.005). After a median 44-month follow-up, 20% of iRBD patients progressed to a manifest disease. Although iRBD converters and nonconverters did not significantly differ in CDTadj levels (P = 0.189), low CDTadj increased the risk of phenoconversion with hazard ratio 3.2 (P = 0.045) but did not refine the phenoconversion risk associated with abnormal DaT-SPECT yielding hazard ratio 15.8 (P < 0.001).ConclusionsDecreased serum CDTadj is associated with substantia nigra degeneration in synucleinopathies. iRBD patients with low CDTadj are more likely to phenoconvert to manifest disease. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson Movement Disorder Society.
| S-EPMC9305135 | biostudies-literature
Project description: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.
| S-EPMC5412719 | biostudies-literature
Project description:ObjectivesTo develop a polysomnographic video-based scale for rating the severity of REM sleep behavior disorder (RBD), to classify the severity of RBD and to determine the intraindividual variability of RBD in patients with Parkinson disease (PD).MethodsTwenty PD patients identified with RBD were investigated with video-supported polysomnography (PSG). Seventy-three motor behavior events during REM sleep were graded visually and polysomnographically on an event-to-event basis according to categorical location of movements: "0" = no visible movement; "1" = slight movements or jerks "2" = movements involving proximal extremities, including violent behavior; "3" = axial involvement including bed falls. Vocalizations were rated as "1" for present or "0" for absent. Ratings were performed by 2 blinded raters. Reliability was calculated with Cohen's ?. Final RBD severity was determined by the highest score given. This rating scale was then used to compare RBD severity and density, calculated as RBD episodes per REM sleep minute over 2 consecutive nights in 10 additional PD patients with RBD. Statistical significance was determined by effect size (Hedges' g) and calculation of the confidence interval.ResultsInterrater reliability of the scale was 0.8 for movement data and 0.89 for vocalization data. Intraindividual RBD density varied significantly (effect size 0.5 ± 0.22; confidence interval 0.2 to 0.79) by factor 2.5 between the 2 PSG nights. Final RBD severity score differed in 60% of patients between nights 1 and 2. Forty percent of patients showed violent behavior, but only on one night. All patients had severely disturbed sleep with reduced sleep efficiency, loss of slow wave sleep, sleep fragmentation, and an increased periodic limb movement (PLM) index.ConclusionThe RBD severity scale (RBDSS) is a reliable, easy-to-use tool for assessing motor events during REM sleep with PSG. Severity and phenomenology of RBD shows a significant variability in the individual PD patient.
| S-EPMC3041623 | biostudies-literature