Frontal and Parietal Lobes' Structure Is Associated with Impairments in Motor and Social Skills in Children with Autism Spectrum Disorder

Friday, May 16, 2014
Atrium Ballroom (Marriott Marquis Atlanta)
R. Mahajan1,2, B. Dirlikov3, D. Crocetti3 and S. H. Mostofsky3,4,5, (1)Department of Psychiatry, Kennedy Krieger Institute, Baltimore, MD, (2)Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, (3)Laboratory for Neurocognitive and Imaging Research, Kennedy Krieger Institute, Baltimore, MD, (4)Department of Psychiatry, Johns Hopkins School of Medicine, Baltimore, MD, (5)Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD
Background: Electrophysiological and functional imaging studies suggest that frontal and parietal regions may be critical for guiding learning and ongoing behavioral control in children (Gazzaley et al., 2005; Schumacher et al., 2007). Furthermore, the ability to use sensory information to form internal representations of behavior is critical to guiding skilled movements and complex behaviors. Frontal-parietal networks (FPNs), therefore, appear to be important for 1) transposing sensory representations into motor commands, 2) selecting goal oriented movements, and 3) executing movement.  FPNs are thereby central in the control of a person's interaction with his/her environment including the planning and organization of sequences of movements necessary to engage in complex social and communicative behavior. Children with autism spectrum disorder (ASD) may have deficits in these abilities. Several studies have implicated frontal and parietal lobe dysfunction in children with ASD (Muller et al., 2001; Haswell et al., 2009) prompting researchers to emphasize the potential contribution of FPNs to the pathophysiology of autism (Just et al., 2007).

Objectives: To examine the structure of frontal and parietal regions relevant for formation of internal models of action and their associations with measures of motor function and symptom severity in children with ASD and typically-developing (TD) children.

Methods: High resolution T1-weighted MPRAGE images (Slice thickness=1.0 mm) images were acquired in 50 children (42 M) with ASD and 50 (42 M) age, gender, SES, and PRI (WISC-IV) matched TD children, aged 8-12 years. Cortical measurements (thickness, surface area, volume) were examined in Freesurfer using motor, premotor, and parietal ROIs derived from the Desikan (Desikan et al., 2006) and Ranta (Ranta et al., 2009) atlases. MANOVA and MANCOVA were used to examine group effects while covarying for total brain volume (TBV). Pearson's correlations were used to examine motor relevant ROI associations with measures of motor function, assessed using the Physical and Neurological Examination for Soft Signs (PANESS) and the Florida Apraxia Battery, modified for children (Mostofsky, 2006), and autism symptom severity assessed using the ADOS-G and the ADI-R.         

Results: Children with ASD showed significant bilateral increases in both cortical grey matter volumes (GMV) and cortical surface area (SA) in the inferior parietal cortex, post-central gyrus, and precentral gyrus before and after covarying for TBV. Pearson correlations revealed significant relationships between bilateral primary motor cortex SA and total PANESS scores, with higher (worse) PANESS score associated with increased SA (r=0.25, p = 0.019).  Additionally, bilateral inferior parietal cortex GMV (r=0.268, p=0.062) and bilateral postcentral gyrus GMV (r=0.305, p=0.033) were correlated with higher total ADOS scores.

Conclusions: Consistent with previous literature, children with ASD showed increased brain volumes and SA in the frontal and parietal cortices.  Furthermore, these increases in regions pertinent to internal action model formation were associated with impaired motor skill learning and control, as well as increased ASD symptom severity. These results support the growing literature on motor dysfunction in ASD and suggest that for children with ASD, dysfunction within FPNs may contribute to impaired development of a range of skilled behavior, including motor and social skills.