Autism and attention deficit hyperactivity disorder (ADHD) are often accompanied by sleep problems. Longitudinal studies hint towards a greater proportion of persisting sleep problems across early development in neurodivergent compared to neurotypical individuals. Within the context of a prospective infant sibling study of autism and ADHD (n = 209), we compared early caregiver-rated sleep trajectories of individuals diagnosed with autism, ADHD or cooccurring autism and ADHD (AuDHD) at 36 months with two groups that did not meet diagnostic criteria-one group of individuals with and one without elevated likelihood of autism and/or ADHD. Sleep behaviors assessed at 10 and 14 months (i.e., number of night awakenings and settle durations) did not differ between individuals with and without a diagnosis of autism and/or ADHD. At 24 and 36 months, individuals diagnosed with autism and/or ADHD took longer to fall asleep, had less sufficient sleep, more parasomnia-related behaviors and had greater overall sleep disturbance than those without a diagnosis, suggesting that their sleep problems are more circumscribed than often reported for older age ranges. In autism specifically, bedtime resistance improved from 24 to 36 months. While additional studies incorporating objective sleep measures are needed, the current results indicate that sleep involvement in neurodevelopmental conditions may mainly reflect transdiagnostic rather than diagnosis-specific processes in early childhood.
Eva-Maria Kurz, S. Bölte, T. Falck-Ytter· Autism Research· 0 citations
Sensory processing differences are a core feature of autism, affecting 60-95% of individuals, yet the associated neural mechanisms remain unclear. An excitation-inhibition (E/I) imbalance in brain circuits has been proposed, but in vivo evidence linking genetic variation in E/I pathways, regional neurochemistry, neural circuit function, and sensory behaviour has been lacking. Here we performed a multimodal investigation in 206 individuals (130 autistic), integrating gene-set polygenic scores for excitatory glutamatergic and inhibitory gamma-aminobutyric acid (GABA)-ergic pathways, magnetic resonance spectroscopy (MRS) measures of regional GABA and Glx (glutamate + glutamine) levels, vibrotactile psychophysical measures of tactile perception, and questionnaire measures of behavioural sensory reactivity. We found that glutamatergic polygenic scores predicted thalamic glutamate levels in neurotypical but not autistic individuals, suggesting altered genotype-neurochemistry coupling in autism. Thalamic Glx:GABA levels associated with tactile perception in both groups, but with opposing directions of effect, indicating that autistic and neurotypical individuals achieve similar perceptual outcomes with potentially differing thalamocortical circuit mechanisms. Within autistic individuals, tactile perceptual differences further related to behavioural sensory reactivity. Together, these findings suggest that autistic sensory processing potentially relies on distinct circuit mechanisms linking genetic variation, neurochemistry and perception. This work thus has important implications for how sensory differences are conceptualised, studied, and interpreted, and ultimately for how interventions and support are developed.
A. Thomson, V. Hollestein, M. Arenella et al.· medRxiv· 0 citations
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