ADHD Symptomatology and White Matter Development in Autism Spectrum Disorder

Poster Presentation
Friday, May 11, 2018: 11:30 AM-1:30 PM
Hall Grote Zaal (de Doelen ICC Rotterdam)
A. K. Converse1, D. C. Dean1, B. G. Travers1, M. B. Prigge2, E. Bigler3, N. Lange4, A. L. Alexander1 and J. E. Lainhart1, (1)University of Wisconsin - Madison, Madison, WI, (2)University of Utah, Salt Lake City, UT, (3)Brigham Young University, Provo, UT, (4)McLean Hospital, Cambridge, MA
Background: The symptoms that characterize attention deficit hyperactivity disorder (ADHD) are often found in individuals with autism spectrum disorder (ASD). Abnormal brain white matter has been associated with both ASD and ADHD, however, greater knowledge of white matter abnormalities in comorbid ADHD in ASD may further illuminate the neurobiological substrates of these disorders. Such understanding may help to advance diagnosis and therapy in both of these developmental disorders. We therefore asked whether white matter development differs in ASD according to the degree of comorbid ADHD symptomatology.

Objectives: To examine the influence of comorbid ADHD and ASD symptomatology on developmental trajectories of white matter microstructure.

Methods: Diffusion tensor imaging (DTI) data from male participants (3-45 years, 220 time points) were acquired up to 4 times across 9 years using a 3 Tesla Siemens Tim Trio. ADHD symptom level was measured by the ADHD index and inattentive scores from the Conners' ADHD/DSMIV Scale. Following acquisition, imaging data were corrected for subject head motion and eddy-current distortions and quantitative parameter maps of fractional anisotropy (FA), mean diffusivity (MD), radial diffusivity (RD) and axial diffusivity (AD) were computed. Mean values of these parameters were then computed for a group of five regions of interest from a published meta-analysis of studies relating FA and symptom levels in individuals with ADHD (van Ewijk et al. 2012). Using a linear mixed effects model, DTI measures from these regions were described as a function of age and ADHD symptom level.

Results: In preliminary analyses, no relationships between ADHD symptom level and FA were observed in these regions. However, MD, RD, and AD were correlated with ADHD symptom level across these white matter locations.

Conclusions: Although published reports of reduced FA in the regions examined may partially reflect deficits in the general ADHD population, the present results suggest that it may not be responsible for ADHD symptoms in comorbid ASD. Future work will use voxelwise analysis to search for regions in which altered DTI parameters are associated with elevated ADHD symptomatology in individuals with ADHD. Further study would also be helpful to determine whether or not ADHD with comorbid ASD shares aspects of the neurobiological etiology of ADHD without comorbid ASD.