Abstract

Motor signs are increasingly acknowledged as candidate transdiagnostic endophenotypic features in different clinical stages of severe mental disorders, such as schizophrenia spectrum and mood disorders.1–4 At the same time, motor signs in children and adolescents are widely recognized as proxy features of an altered neurodevelopmental trajectory associated with a higher risk of psychopathological manifestations. These motor abnormalities, spanning from developmental motor delays (eg, sitting, walking) to motor signs (eg, dyscoordination, psychomotor retardation, and psychomotor agitation), presumably reflect complex, cumulative and diachronically stratified interactions between genetic load for severe mental illness and early environmental adversities. Indeed, there is a robust empirical evidence from familial high-risk studies indicating that the genetic risk for schizophrenia is associated with a delayed/altered motor development, whereas comparable evidence for the genetic risk for unipolar and bipolar depression is much less robust. For example, longitudinal studies indicate that impaired motor coordination in offspring of patients with schizophrenia is predictive of subsequent psychosis.5–7 Similarly, the recent Danish VIA78 study found that offspring of parents with schizophrenia (but not those of parents with bipolar disorder) had 2.02 times higher odds of having motor performance in the clinical range at the Movement Assessment Battery for Children (ie, the gold standard for the diagnostic assessment of Developmental Coordination Disorder in children and adolescents). This is partly echoed in preliminary studies based on polygenic risk scores, which showed that the higher is the score for schizophrenia the more severe is the delay in motor development in first years of age,9 a pattern less evident for bipolar score9 and in agreement with the finding of less severe motor signs in the premorbid developmental anamnesis of mood disorders.10

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