A voxel-based morphometry (VBM) analysis of regional grey and white matter volume abnormalities within the speech production network of children who stutter.

It is well documented that neuroanatomical differences exist between adults who stutter and their fluently speaking peers. Specifically, adults who stutter have been found to have more grey matter volume (GMV) in speech relevant regions including inferior frontal gyrus, insula and superior temporal gyrus (Beal et al., 2007; Song et al., 2007). Despite stuttering having its onset in childhood only one study has investigated the neuroanatomical differences between children who do and do not stutter. Chang et al. (2008) reported children who stutter had less GMV in the bilateral inferior frontal gyri and middle temporal gyrus relative to fluently speaking children. Thus it appears that children who stutter present with unique neuroanatomical abnormalities as compared to those of adults who stutter. In order to better understand the neuroanatomical correlates of stuttering earlier in its development, near the time of onset, we used voxel-based morphometry to examine volumetric differences between 11 children who stutter and 11 fluent children. Children who stutter had less GMV in the bilateral inferior frontal gyri and left putamen but more GMV in right Rolandic operculum and superior temporal gyrus relative to fluent children. Children who stutter also had less white matter volume bilaterally in the forceps minor of the corpus callosum. We discuss our findings of widespread anatomic abnormalities throughout the cortical network for speech motor control within the context of the speech motor skill limitations identified in people who stutter (Namasivayam and van Lieshout, 2008; Smits-Bandstra et al., 2006).

Neuromotor speech deficits in children and adults with spina bifida and hydrocephalus.

Acquired cerebellar lesions are associated with motor speech deficits. Spina bifida with hydrocephalus (SBH) is a neurodevelopmental disorder that involves significant dysmorphology of the cerebellum. Videotaped narratives produced by 40 children and adults with SBH and their 40 age-matched controls were coded for three motor speech deficits: dysfluency, ataxic dysarthria (articulatory inaccuracy, prosodic excess, and phonatory-prosodic insufficiency) (Brown, Darley, & Aronson, 1970; Darley, Aronson, & Brown, 1969a), and speech rate. Individuals with SBH had more motor speech deficits than controls. Dysfluency was related to an interaction between chronological age and SBH. Speech rate was related independently to chronological age and SBH. Ataxic dysarthria was related to the biology of SBH, and was associated with both physical phenotype (level of spinal cord lesion) and medical history (number of shunt revisions). The data show that developmental as well as acquired lesions of the cerebellum disrupt motor speech, and add to the developmental role of the cerebellum in the automatization of motor skills, including speech.