scholarly journals C-65 Transdiagnostic Factors of Social Impairment in Comorbid Autism Spectrum Disorder and Attention Deficit Hyperactivity Disorder

2019 ◽  
Vol 34 (6) ◽  
pp. 1094-1094
Author(s):  
A Garagozzo ◽  
L Katz ◽  
M Scott ◽  
S Hunter

Abstract Objective Comorbid Autism Spectrum Disorder (ASD) and ADHD are associated with greater symptom severity, including social impairment. Furthering work by Lerner, Pothoff, and Hunter (2015), we sought to identify unique and shared factors that contribute to parent-reported social deficits in children with ADHD, ASD, and ADHD+ASD. We hypothesized attention, hyperactivity, and motor skills would predict social deficits in ADHD, while functional communication and motor skills would predict social deficits in ASD; and additively, all factors would predict social deficits in ADHD+ASD. Method Utilizing a clinical database, we identified 236 participants (4-21 years; Mage = 10.6; 71% male; 28% African American; FSIQ M = 94.31) with diagnoses of ADHD, ASD, and ADHD+ASD. We examined FSIQ from the WISC-4/5, WPPSI-3, or DAS-2, motor skills and social impairment from the SIB-R and attention, hyperactivity, and functional communication from the BASC-2/3. Results Using hierarchical linear regression and controlling for FSIQ, hypotheses were partially supported. FSIQ was controlled for in each group. For ADHD, hyperactivity, functional communication, and motor skills contributed significantly to the model (p < .001), while for ASD, motor skills contributed significantly to the model (p < .001). For ASD + ADHD, functional communication and motor skills contributed significantly to the model (p < .001) Conclusion Results support previous findings that motor deficits and functional communication are associated with social impairment in children with ADHD and ASD, independently and comorbidly. This suggests that targeting motor dysfunction and functional communication concurrently may be effective for improving social interaction skills in children with ADHD +ASD.

2021 ◽  
pp. 1-11
Author(s):  
Denis Pavăl ◽  
Ioana Valentina Micluția

Autism spectrum disorder (ASD) comprises a group of neurodevelopmental disorders characterized by social deficits and stereotyped behaviors. Despite intensive research, its etiopathogenesis remains largely unclear. Although studies consistently reported dopaminergic anomalies, a coherent dopaminergic model of ASD was lacking until recently. In 2017, we provided a theoretical framework for a “dopamine hypothesis of ASD” which proposed that autistic behavior arises from a dysfunctional midbrain dopaminergic system. Namely, we hypothesized that malfunction of 2 critical circuits originating in the midbrain, that is, the mesocorticolimbic and nigrostriatal pathways, generates the core behavioral features of ASD. Moreover, we provided key predictions of our model along with testing means. Since then, a notable number of studies referenced our work and numerous others provided support for our model. To account for these developments, we review all these recent data and discuss their implications. Furthermore, in the light of these new insights, we further refine and reconceptualize our model, debating on the possibility that various etiologies of ASD converge upon a dysfunctional midbrain dopaminergic system. In addition, we discuss future prospects, providing new means of testing our hypothesis, as well as its limitations. Along these lines, we aimed to provide a model which, if confirmed, could provide a better understanding of the etiopathogenesis of ASD along with new therapeutic strategies.


2021 ◽  
Author(s):  
Laura E. Quiñones‐Camacho ◽  
Frank A. Fishburn ◽  
Katherine Belardi ◽  
Diane L. Williams ◽  
Theodore J. Huppert ◽  
...  

mSphere ◽  
2020 ◽  
Vol 5 (6) ◽  
Author(s):  
Yu Chen ◽  
Hui Fang ◽  
Chunyan Li ◽  
Guojun Wu ◽  
Ting Xu ◽  
...  

Gut microbiota may contribute to the pathogenesis and development of autism spectrum disorder. The maternal gut microbiota influences offspring gut microbial structure and composition.


Sign in / Sign up

Export Citation Format

Share Document