Investigating Social Competence in a Pilot Randomized Clinical Trial of a Theatre-Based Intervention Enhanced for Adults with Autism Spectrum Disorder.

Autism spectrum disorder (ASD) is characterized by challenges in social competence that persist in adulthood, yet few treatment options exist. A pilot randomized clinical trial (RCT) of a peer-mediated, theatre-based intervention with established efficacy in youth with ASD was examined in autistic adults. The final sample consisted of forty-seven 18-to-40-year-old participants randomized to the experimental (EXP N = 23) or waitlist control (WLC N = 24) condition. A multimodal, social interdependent model was employed to examine social competence changes in brain (incidental face memory (IFM) using event-related potentials), cognition (Wechsler Memory Scale-III), behavior (Contextual Assessment of Social Skills) and function (Social Responsiveness Scale (SRS); Adaptive Behavior Assessment Scale (ABAS) Social Composite). Using analysis of covariance in which pretest was controlled in the model, posttest between-group differences were observed on IFM (p = 0.016, η2 = 0.139, d = 0.79) and several social and adaptive functional (SRS, ABAS) outcomes in social communication and interaction (SCI) (p = 0.019, η2 = 0.121, d = -00.45), communication (p = 0.044 η2 = 0.09, d = -00.31), and motivation (p = 0.001, η2 = 0.229, d = -0.79) domains. At two-month follow-up, gains in social motivation remained (p = 0.041, η2 = 0.100, d = -0.77). The results offer preliminary support for a unique theatre-based social skills intervention for autistic adults who have few treatment options to enhance social competence. The trial was pre-registered with ClinicalTrials.gov (Identifier: NCT04349644).

Quantitative sleep electroencephalogram and cognitive performance in Parkinson's disease with and without rapid eye movement sleep behavior disorder.

Introduction: Parkinson's disease (PD) patients with REM sleep behavior disorder (RBD) are at greater risk for cognitive decline and RBD has been associated with alterations in sleep-related EEG oscillations. This study evaluates differences in sleep quantitative EEG (qEEG) and cognition in PD participants with (PD-RBD) and without RBD (PD-no-RBD). Methods: In this cross-sectional study, polysomnography (PSG)-derived qEEG and a comprehensive level II neuropsychological assessment were compared between PD-RBD (n = 21) and PD-no-RBD (n = 31). Following artifact rejection, qEEG analysis was performed in the frontal and central leads. Measures included Scalp-slow wave (SW) density, spindle density, morphological properties of SW and sleep spindles, SW-spindle phase-amplitude coupling, and spectral power analysis in NREM and REM. The neurocognitive battery had at least two tests per domain, covering five cognitive domains as recommended by the Movement Disorders Society Task Force for PD-MCI diagnosis. Differences in qEEG features and cognitive performance were compared between the two groups. Stepwise linear regression was performed to evaluate predictors of cognitive performance. Multiple comparisons were corrected using the Benjamini-Hochberg method. Results: Spindle density and SW-spindle co-occurrence percent were lower in participants with PD-RBD compared to PD-no-RBD. The PD-RBD group also demonstrated higher theta spectral power during REM. Sleep spindles and years of education, but not RBD, were predictors of cognitive performance. Conclusion: PD participants with RBD have alterations in sleep-related qEEG compared to PD participants without RBD. Although PD-RBD participants had worse cognitive performance compared to PD-no-RBD, regression models suggest that lower sleep spindle density, rather than presence of RBD, predicts worse comprehensive cognitive score. Future studies should include longitudinal evaluation to determine whether sleep-related qEEG alterations are associated with more rapid cognitive decline in PD-RBD.

Peers, play, and performance to build social salience in autistic youth: A multisite randomized clinical trial.

OBJECTIVE: Individuals with autism spectrum disorder (ASD) have significant impairment in social competence and reduced social salience. SENSE Theatre, a peer-mediated, theater-based intervention has demonstrated posttreatment gains in face memory and social communication. The multisite randomized clinical trial compared the Experimental (EXP; SENSE Theatre) to an Active Control Condition (ACC; Tackling Teenage Training, TTT) at pretest, posttest, and follow-up. It was hypothesized that the EXP group would demonstrate greater incidental face memory (IFM) and better social behavior (interaction with novel peers) and social functioning (social engagement in daily life) than the ACC group, and posttest IFM would mediate the treatment effect on follow-up social behavior and functioning. METHOD: Two hundred ninety participants were randomized to EXP (N = 144) or ACC (N = 146). Per protocol sample (≥ 7/10 sessions) resulted in 207 autistic children 10-16 years. Event-related potentials measured IFM. Naive examiners measured social behavior (Vocal Expressiveness, Quality of Rapport, Social Anxiety) and functioning (Social Communication). Structural equation modeling was used to assess treatment effects. RESULTS: SENSE Theatre participants showed significantly better IFM (b = .874, p = .039) at posttest, and significant indirect effects on follow-up Vocal Expressiveness a × b = .064, with 90% CI [.014, .118] and Quality of Rapport a × b = .032, with 90% CI [.002, .087] through posttest IFM. CONCLUSIONS: SENSE Theatre increases social salience as reflected by IFM, which in turn affected Vocal Expressiveness and Quality of Rapport. Results indicate that a neural mechanism supporting social cognition and driven by social salience is engaged by the treatment and has a generalized, indirect effect on clinically meaningful functional outcomes related to core symptoms of autism. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Quantitative Sleep Electroencephalogram in Parkinson's Disease: A Case-Control Study.

BACKGROUND: Sleep disorders are common in Parkinson's disease (PD) and include alterations in sleep-related EEG oscillations. OBJECTIVE: This case-control study tested the hypothesis that patients with PD would have a lower density of Scalp-Slow Wave (SW) oscillations and higher slow-to-fast frequencies ratio in rapid eye movement (REM) sleep than non-PD controls. Other sleep-related quantitative EEG (qEEG) features were also examined, including SW morphology, sleep spindles, and Scalp-SW spindle phase-amplitude coupling. METHODS: Polysomnography (PSG)-derived sleep EEG was compared between PD participants (n = 56) and non-PD controls (n = 30). Following artifact rejection, sleep qEEG analysis was performed in frontal and central leads. Measures included SW density and morphological features of SW and sleep spindles, SW-spindle phase-amplitude coupling, and spectral power analysis in Non-REM (NREM) and REM. Differences in qEEG features between PD and non-PD controls were compared using two-tailed Welch's t-tests, and correction for multiple comparisons was performed per the Benjamini-Hochberg method. RESULTS: SW density was lower in PD than in non-PD controls (F = 13.5, p' = 0.003). The PD group also exhibited higher ratio of slow REM EEG frequencies (F = 4.23, p' = 0.013), higher slow spindle peak frequency (F = 24.7, p' < 0.002), and greater SW-spindle coupling angle distribution non-uniformity (strength) (F = 7.30, p' = 0.034). CONCLUSION: This study comprehensively evaluates sleep qEEG including SW-spindle phase amplitude coupling in PD compared to non-PD controls. These findings provide novel insights into how neurodegenerative disease disrupts electrophysiological sleep rhythms. Considering the role of sleep oscillatory activity on neural plasticity, future studies should investigate the influence of these qEEG markers on cognition in PD.

Effects of exercise on sleep spindles in Parkinson's disease.

Background: In a randomized, controlled trial, we showed that high-intensity rehabilitation, combining resistance training and body-weight interval training, improves sleep efficiency in Parkinson's disease (PD). Quantitative sleep EEG (sleep qEEG) features, including sleep spindles, are altered in aging and in neurodegenerative disease. Objective: The objective of this post-hoc analysis was to determine the effects of exercise, in comparison to a sleep hygiene, no-exercise control group, on the quantitative characteristics of sleep spindle morphology in PD. Methods: We conducted an exploratory post-hoc analysis of 24 PD participants who were randomized to exercise (supervised 3 times/week for 16 weeks) versus 26 PD participants who were assigned to a sleep hygiene, no-exercise control group. At baseline and post-intervention, all participants completed memory testing and underwent polysomnography (PSG). PSG-derived sleep EEG central leads (C3 and C4) were manually inspected, with rejection of movement and electrical artifacts. Sleep spindle events were detected based on the following parameters: (1) frequency filter = 11-16 Hz, (2) event duration = 0.5-3 s, and (3) amplitude threshold 75% percentile. We then calculated spindle morphological features, including density and amplitude. These characteristics were computed and averaged over non-rapid eye movement (NREM) sleep stages N2 and N3 for the full night and separately for the first and second halves of the recording. Intervention effects on these features were analyzed using general linear models with group x time interaction. Significant interaction effects were evaluated for correlations with changes in performance in the memory domain. Results: A significant group x time interaction effect was observed for changes in sleep spindle density due to exercise compared to sleep hygiene control during N2 and N3 during the first half of the night, with a moderate effect size. This change in spindle density was positively correlated with changes in performance on memory testing in the exercise group. Conclusions: This study is the first to demonstrate that high-intensity exercise rehabilitation has a potential role in improving sleep spindle density in PD and leading to better cognitive performance in the memory domain. These findings represent a promising advance in the search for non-pharmacological treatments for this common and debilitating non-motor symptom.

Taking the Time to Assess Cognition in Parkinson's Disease: The Clock Drawing Test.

BACKGROUND: Cognitive impairment is common and disabling in Parkinson's disease (PD). Cognitive testing can be time consuming in the clinical setting. One rapid test to detect cognitive impairment in non-PD populations is the Clock Drawing Test (CDT), which calls upon the brain's executive and visuospatial abilities to draw a clock designating a certain time. OBJECTIVE: Test the hypothesis that PD participants would perform worse on CDT compared to controls and that CDT would correlate with other measures of cognition. METHODS: This study evaluated two independent CDT scoring systems and differences in CDT performance between PD (N = 97) and control (N = 54) participants using a two-sample t-test. Pearson's correlations were conducted between the CDT and tests of sleepiness (Epworth Sleepiness Scale) and vigilance (Psychomotor Vigilance Test); executive function (Trails B-A); and global cognition (Montreal Cognitive Assessment). Receiver operating characteristic curves were used to determine cut points on the CDT that identify individuals who need additional cognitive testing. RESULTS: PD participants had worse performance on CDT compared to controls. The CDT was correlated with executive function (Trails B-A) and global cognition (Montreal Cognitive Assessment). The CDT correlated with vigilance (Psychomotor Vigilance Task) only in healthy controls. However, the CDT was not correlated with measures of sleepiness (Epworth Sleepiness Scale) in either group. A cut point of 9 on the Rouleau scale and 18 on the Mendez scale identified PD participants with cognitive impairment. CONCLUSION: The CDT is a rapid clinical cognitive assessment that is feasible in PD and correlates with other measures of cognition.

Greater Social Competence Is Associated With Higher Interpersonal Neural Synchrony in Adolescents With Autism.

Difficulty engaging in reciprocal social interactions is a core characteristic of autism spectrum disorder. The mechanisms supporting effective dynamic real-time social exchanges are not yet well understood. This proof-of-concept hyperscanning electroencephalography study examined neural synchrony as the mechanism supporting interpersonal social interaction in 34 adolescents with autism spectrum disorder (50% female), age 10-16 years, paired with neurotypical confederates of similar age. The degree of brain-to-brain neural synchrony was quantified at temporo-parietal scalp locations as the circular correlation of oscillatory amplitudes in theta, alpha, and beta frequency bands while the participants engaged in a friendly conversation. In line with the hypotheses, interpersonal neural synchrony was significantly greater during the social interaction compared to the baseline. Lower levels of synchrony were associated with increased behavioral symptoms of social difficulties. With regard to sex differences, we found evidence for stronger interpersonal neural synchrony during conversation than baseline in females with autism, but not in male participants, for whom such condition differences did not reach statistical significance. This study established the feasibility of hyperscanning during real-time social interactions as an informative approach to examine social competence in autism, demonstrated that neural coordination of activity between the interacting brains may contribute to social behavior, and offered new insights into sex-related variability in social functioning in individuals with autism spectrum disorders.

Slow Wave Sleep and EEG Delta Spectral Power are Associated with Cognitive Function in Parkinson's Disease.

BACKGROUND: Cognitive and sleep dysfunction are common non-motor symptoms in Parkinson's disease (PD). OBJECTIVE: Determine the relationship between slow wave sleep (SWS) and cognitive performance in PD. METHODS: Thirty-two PD participants were evaluated with polysomnography and a comprehensive level II neurocognitive battery, as defined by the Movement Disorders Society Task Force for diagnosis of PD-mild cognitive impairment. Raw scores for each test were transformed into z-scores using normative data. Z-scores were averaged to obtain domain scores, and domain scores were averaged to determine the Composite Cognitive Score (CCS), the primary outcome. Participants were grouped by percent of SWS into High SWS and Low SWS groups and compared on CCS and other outcomes using 2-sided t-tests or Mann-Whitney U. Correlations of cognitive outcomes with sleep architecture and EEG spectral power were performed. RESULTS: Participants in the High SWS group demonstrated better global cognitive function (CCS) (p = 0.01, effect size: r = 0.45). In exploratory analyses, the High SWS group showed better performance in domains of executive function (effect size: Cohen's d = 1.05), language (d = 0.95), and processing speed (d = 1.12). Percentage of SWS was correlated with global cognition and executive function, language, and processing speed. Frontal EEG delta power during N3 was correlated with the CCS and executive function. Cognition was not correlated with subjective sleep quality. CONCLUSION: Increased SWS and higher delta spectral power are associated with better cognitive performance in PD. This demonstrates the significant relationship between sleep and cognitive function and suggests that interventions to improve sleep might improve cognition in individuals with PD.

Randomized, Controlled Trial of Exercise on Objective and Subjective Sleep in Parkinson's Disease.

BACKGROUND: Sleep dysfunction is common and disabling in persons with Parkinson's Disease (PD). Exercise improves motor symptoms and subjective sleep quality in PD, but there are no published studies evaluating the impact of exercise on objective sleep outcomes. The goal of this study was to to determine if high-intensity exercise rehabilitation combining resistance training and body-weight interval training, compared with a sleep hygiene control improved objective sleep outcomes in PD. METHODS: Persons with PD (Hoehn & Yahr stages 2-3; aged ≥45 years, not in a regular exercise program) were randomized to exercise (supervised 3 times a week for 16 weeks; n = 27) or a sleep hygiene, no-exercise control (in-person discussion and monthly phone calls; n = 28). Participants underwent polysomnography at baseline and post-intervention. Change in sleep efficiency was the primary outcome, measured from baseline to post-intervention. Intervention effects were evaluated with general linear models with measurement of group × time interaction. As secondary outcomes, we evaluated changes in other aspects of sleep architecture and compared the effects of acute and chronic training on objective sleep outcomes. RESULTS: The exercise group showed significant improvement in sleep efficiency compared with the sleep hygiene group (group × time interaction: F = 16.0, P < 0.001, d = 1.08). Other parameters of sleep architecture also improved in exercise compared with sleep hygiene, including total sleep time, wake after sleep onset, and slow-wave sleep. Chronic but not acute exercise improved sleep efficiency compared with baseline. CONCLUSIONS: High-intensity exercise rehabilitation improves objective sleep outcomes in PD. Exercise is an effective nonpharmacological intervention to improve this disabling nonmotor symptom in PD. © 2020 International Parkinson and Movement Disorder Society.