Alterations in aperiodic and periodic EEG activity in young children with Down syndrome.

Down syndrome is the most common cause of intellectual disability, yet little is known about the neurobiological pathways leading to cognitive impairments. Electroencephalographic (EEG) measures are commonly used to study neurodevelopmental disorders, but few studies have focused on young children with DS. Here we assess resting state EEG data collected from toddlers/preschoolers with DS (n=29, age 13-48 months old) and compare their aperiodic and periodic EEG features with both age-matched (n=29) and cognitive-matched (n=58) comparison groups. DS participants exhibited significantly reduced aperiodic slope, increased periodic theta power, and decreased alpha peak amplitude. A majority of DS participants displayed a prominent peak in the theta range, whereas a theta peak was not present in age-matched participants. Overall, similar findings were also observed when comparing DS and cognitive-matched groups, suggesting that EEG differences are not explained by delayed cognitive ability.

Clinical high risk for psychosis syndrome is associated with reduced neural responding to unpleasant images.

Deficits in emotion processing are core features of psychotic disorders. Electrophysiology research in schizophrenia suggests deficits in sustained engagement with emotional content (indexed by the late positive potential [LPP]) may contribute to emotion processing impairments. Despite similar behavioral emotion processing dysfunction in those at clinical high risk (CHR) for psychosis, limited research has examined neural mechanisms of impaired emotion processing in the high-risk period, where research can inform risk models. To examine mechanisms of emotion processing deficits in those at CHR for psychosis, the present study used a passive viewing task to elicit the LPP in response to emotionally engaging and neutral stimuli in 28 CHR and 32 control participants (60% female). Relative to controls, CHR participants showed reduced LPP amplitude when viewing unpleasant images (d = 0.75, p = .005) but similar LPP amplitude in response to both neutral (d = 0.35, p = .19) and pleasant images (d = 0.31, p = .24). This pattern suggests that individuals at CHR for psychosis exhibit a deficit in sustained engagement with unpleasant stimuli. Clinical and trait questionnaires were administered to examine potential exploratory explanations for group differences in LPP amplitude. Consistent with evidence suggesting LPP amplitude reflects engagement of approach/avoidance motivational systems, greater LPP amplitude was associated with greater trait-level behavioral avoidance in control participants (r = .42, p = .032) but not CHR participants (r = -.21, p = .40). Together, the present research is consistent with LPP studies in psychosis and implicates reduced sustained engagement with emotional content in the high-risk period. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Neural mechanisms of motor dysfunction in individuals at clinical high-risk for psychosis: Evidence for impairments in motor activation.

Motor abnormalities are a core feature of psychotic disorders observed from the premorbid period through chronic illness, suggesting motor dysfunction may reflect the pathophysiology of psychosis. Electrophysiology research in schizophrenia suggests impaired motor activation and preparation may underlie these motor abnormalities. Despite behavioral studies suggesting similar motor dysfunction in those at clinical high-risk (CHR) for psychosis, there have been no studies examining neural mechanisms of motor dysfunction in the CHR period, where research can inform pathophysiological and risk models. The present study used the lateralized readiness potential (LRP), an event-related potential index of motor activation and preparation, to examine mechanisms of motor dysfunction in 42 CHR and 41 control participants (N = 83, 56% female). Response competition was manipulated to determine whether deficits are secondary to cognitive control impairments or reflect primary motor deficits. Behaviorally, CHR participants exhibited overall slower responses than controls. Further, relative to controls, CHR participants showed reduced activation of correct but not incorrect responses, reflected in blunted LRP amplitude under weak response competition and no difference in amplitude associated with the incorrect response under strong response competition. This pattern of results suggests individuals at CHR for psychosis exhibit primary motor deficits in activating and preparing behavioral responses and are contrary to a deficit in cognitive control. Further, blunted LRP amplitude was associated with worsening of negative symptoms at 12-month follow-up. Together, these findings are consistent with LRP studies in psychosis and implicate motor activation deficits as potential mechanisms of motor dysfunction in the high-risk period. (PsycInfo Database Record (c) 2022 APA, all rights reserved).