AOCCN2017

Presentation information

Parallel Session

[PS1] Parallel Session 1: ASD / ADHD 1

Thu. May 11, 2017 10:00 AM - 11:50 AM Room A (1F Argos A・B)

Chair: Virginia Chun-Nei Wong (The University of Hong Kong, Queen Mary Hospital ), Tatsuya Koeda (National Center for Child Health and Development)

Cosponsored by Janssen Pharmaceutical K.K.

[PS1-1A-K] Autism Spectrum Disorders and Attention Deficit and Hyperactivity Disorder

Paolo CURATOLO (Department of Pediatric Neuroscience, Tor Vergata University of Rome, Italy)

Autism Spectrum Disorders (ASD) and Attention Deficit and Hyperactivity Disorder
(ADHD) are common neurodevelopmental disorders that have undergone important revisions in the DSM-5 both in the diagnosis and the classification. Converging evidence suggest that ASD and ADHD share genetic underpinning vulnerabilities, factors and symptoms domain. ASD and ADHD concur since childhood age, and pick during adolescence because social adaptation and executive function skills become more significant at these age.
Behavioural indicators of risk for later ASD and ADHD may be present early in development, and therefore improve early detection and treatment of these disorders. Effective screening in preschool age children may allow early interventions strategy for both ASD and ADHD.
Recent progresses in neuroimaging techniques have shown neuronal correlates in both disorders that explain both the convergent and divergent clinical and behavioural manifestations.
ASD and ADHD are the most common comorbid conditions associated with childhood epilepsy. This concurrence may results from several modified neurobiological mechanisms involved in early brain development and altering synaptic plasticity, functional connectivity and neuronal transmission.
Since both these conditions include a set of heterogeneous neurodevelopmental disorders the ultimate goal is to identify more homogeneous subgroups for a better understanding of the underlying biological mechanism, clinical outcome and treatment response.
Recently, the delineation of the biochemical signalling pathways in single gene disorders, such as Tuberous Sclerosis Complex, suggests strategies for developing target therapies, which are now being evaluated in clinical trials.