AbstractObjectiveIn some patients with apraxia of speech (AOS), we observed impaired perceptual timing abilities, which lead us to propose a shared mechanism of impaired perceptual timing underlying impaired rhythm discrimination (perceptual processing) and AOS (motor speech output). Given that considerable white matter damage is often observed in these patients, we here investigate whether white matter changes are related to impaired rhythm processing as one possible mechanism underlying AOS.MethodsWe applied deformation-based morphometry (DBM) and diffusion tensor imaging (DTI) in 12 patients with the nonfluent variant (NFV) of Primary Progressive Aphasia (PPA) with AOS, as well as 11 patients with the semantic variant and 24 controls.ResultsSeventy-five percent of the patients with NFV displayed impaired rhythm processing and the severity of their impairment correlated with their degree of AOS. Moreover, left frontal white matter volume loss adjacent to the supplementary motor area (SMA) correlated with impaired rhythm processing. In addition, we obtained tract-based metrics of the left Aslant tract, which is typically damaged in NFV. The structural integrity of the left Aslant tract also correlated with rhythmic discrimination abilities in NFV.ConclusionsOur data suggest that a shared white matter substrate adjacent to the SMA contributes to impaired rhythm perception and motor speech impairments. This indicates that impaired perceptual timing may be one of the neurocomputational mechanisms underlying AOS. Our observation that regional variations in left frontal lobe atrophy are linked to the phenotypical heterogeneity in NFV may lead the way for earlier diagnosis.
Left frontal white matter atrophy links to timing mechanisms relevant for apraxia of speech
