17575
A ‘Bottom-up' Approach to ASD: The Anatomy of Precision Grasping Deficits in ASD: Focus on a Newly Described Set of Fronto-Parietal Connections
It is commonly reported that individuals with ASD have abnormalities in motor co-ordination (dyspraxia), and that these frequently precede clinical signs in ASD. This is of importance as fine motor skill such as precision grasping ability can be rapidly and objectively measured by clinicians. Furthermore, advanced neuroimaging methods based on diffusion imaging tractography give direct access to networks underlying sensory-motor integration. In this study we test the hypothesis that impaired precision grasping in ASD is associated with specific abnormalities of the connections between the primary motor (M1) and somatosensory (S1) cortices specialised in sensory-motor integration of the fingers.
Objectives:
To perform virtual in vivo dissections of the U-shaped connections between M1 and S1 and investigate whether white matter abnormalities correlate with performances in precision grasping in ASD.
Methods:
We included 120 individuals from the Autism Imaging Multicentre Study (MRC AIMS Consortium). Sixty right-handed adult male participants with ASD (above cut off on the Autism Diagnostic Interview-Revised (ADI-R) and Autism Diagnostic Observation Schedule (ADOS)) and 60 age-matched controls (age 18-50, IQ > 70). The Purdue Pegboard Test was administered as a measure of precision grasping. Diffusion Tensor Imaging-Tractography (DTI) was used to compare, in vivo, the microstructural organization of the FPUTs bilaterally between subjects with ASD and healthy controls – as indexed by fractional anisotropy, mean diffusivity and perpendicular diffusivity.
Results:
The ASD group performed significantly less well on the Purdue Pegboard test in the right hand (t=2.08, p = .040) and both hands assembly measure (t=3.98, p < .001). Compared to healthy controls, individuals with ASD showed significantly greater mean diffusivity and perpendicular diffusivity and lower fractional anisotropy on both left and right FPUT (p < 0.025 in all cases). In the control group higher scores on the pegboard test correlated significantly with increased microstructure of the left-hemisphere FPUT (increased fractional anisotropy, decreased mean diffusivity and decreased perpendicular diffusivity). In the ASD group pegboard scores did not correlate with left FPUT structure, but did correlate significantly with increased microstructure of the right-hemisphere FPUT (increased fractional anisotropy, decreased mean diffusivity and decreased perpendicular diffusivity).
Conclusions:
We found that precision grasping impairment in ASD is associated with altered structure of the FPUTs. We found an association between Pegboard performance and the structure of the left hemisphere tracts in the control group, which is in line with left-hemisphere dominance of praxis. We did not find this left-hemisphere association in ASD, and found an anomalous right-hemisphere association. This suggests the loss of neurotypical lateralization of sensory-motor integration for precision grasping in ASD. Precision grasping assessment may be a reliable proxy measure for assessing generalised brain abnormality in ASD.