Postprandial attenuation of gastric slow waves in anxiety-depression, with and without functional dyspepsia: associations with heart rate variability and sleep quality.

Attention-deficit/hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder affecting approximately 5% of children globally and 6.26% in China (, ), often—but not always—characterized by inattention, hyperactivity/impulsivity, and deficits in executive functions (EFs) such as response inhibition and working memory (, ). Beyond these core features, mounting evidence indicates that some individuals with ADHD may also exhibit sensorimotor dysfunction, including deficits in sensory input, motor output, and sensorimotor integration (, ). For example, South African primary school children with ADHD have shown impaired fine motor skills (), and Belgian children with ADHD and autism spectrum disorder displayed motor abnormalities associated with regional gray matter volumes (). These sensorimotor deficits are not merely peripheral; they interact with higher-order cognitive processes, suggesting that the sensorimotor network (SMN) may play a critical role in the pathophysiology of ADHD. Neuroimaging studies have consistently identified anatomical and functional alterations within sensorimotor regions in ADHD (–). For instance, U.S. children with ADHD showed atypical motor and sensory cortex activation during finger tapping (), Canadian adolescents and adults with ADHD exhibited altered cortical morphology in sensorimotor processing regions (), and Chinese youth with ADHD demonstrated distinct cortical thickness alterations (). Early work in drug-naïve South Korean boys (aged 7–12 years) documented altered regional cerebral blood flow in bilateral sensorimotor cortices (), whereas Chinese boys of the same age range showed increased amplitude of low-frequency fluctuations in the left sensorimotor cortex (). More recent investigations using magnetoencephalography in Canadian adults with ADHD revealed atypical oscillatory activity (), and resting-state fMRI studies in Chinese ADHD patients identified abnormal dynamic brain entropy within the SMN (). Structurally, the SMN encompasses core sensorimotor cortices (precentral and postcentral gyri, supplementary motor area) as well as associated regions in the frontal, parietal, and insular cortices that collectively mediate sensorimotor integration and motor control (, ). Genetic and neurophysiological evidence also links SMN dysfunction to the severity of hyperactive/impulsive symptoms and inhibitory control deficits (, ). Specifically, Chinese early adolescents with ADHD showed multimodal SMN alterations predictive of diagnosis (), and Chinese children carrying the DRD4 2-repeat allele exhibited prefrontal cortex network abnormalities related to SMN function (). Despite these advances, the functional connectivity (FC) patterns of the SMN in ADHD remain incompletely characterized and inconsistently reported. Some studies observe increased intra-SMN or SMN–default mode network (DMN) connectivity associated with milder symptoms or better EF (, ). For example, Chinese children with ADHD (N > 60) demonstrated that increased dynamic FC between DMN and SMN was associated with reduced symptoms (), and Chinese children with ADHD showed altered neurovascular coupling in SMN regions (). Conversely, other studies report reduced connectivity between sensorimotor and striatal regions correlated with motor overflow and poor integration (). Notably, Canadian children with ADHD and developmental coordination disorder (half of whom were on psychostimulants) exhibited reduced FC between M1 and somatosensory/striatal regions (). These discrepancies likely reflect methodological diversity—including seed-based versus independent component analysis (ICA) approaches, varying age ranges (children vs. adults), medication status, and motion-correction strategies—as well as the inherent developmental heterogeneity of brain networks (). Notably, a recent systematic review and meta-analysis of rs-fMRI studies in ADHD highlighted substantial methodological variability across sites and emphasized the need for carefully controlled, medication-naïve pediatric samples to improve reproducibility (). Whether increased or decreased SMN connectivity represents a pathological signature, a compensatory adaptation, or a neurobiological subtype remains unresolved, particularly in drug-naïve children. As summarized in , neuroimaging findings in ADHD indicate that SMN functional activity and connectivity vary by developmental stage, clinical status, and methodological approach.