Childhood obsessive-compulsive disorder (OCD) stems from a bunch of restricted and repetitive behaviors, which are part of normal behavioral repertoire up to the age of 7. The persistence of compulsive-like behaviors after that age is often associated with unique comorbidity patterns, which are age-at-onset dependent and reflect different developmental stages. In particular, OCD synchronically co-occurs with a broad constellation of neurodevelopmental disorders, whereas diachronically it is related to an increased risk of major adult psychoses. Moreover, OCD is associated with trait-like sensory phenomena, suggesting a common disrupted sensorimotor grounding.
The present study is aimed at exploring the hypothesis that this specific temporal and comorbidity OCD profile may be due to a developmental heterochronic mechanism of delay in attenuation of ontogenetically early behavioral patterns. The developmental shift of highly evolutionarily conserved behavioral phenotypes might be regulated by epigenetic changes induced by different conditions of sensory unbalance. This evolutionary and developmental model allows capturing childhood OCD in light of the ultimate causes of ritual behavior throughout phylogeny, namely its “homeostatic” function over conditions of unpredictability. Moreover, it may have important clinical implications, as OCD symptoms could represent putative biomarkers of early divergent developmental trajectories, with a pathoplastic effect on course and outcome.