A crucial role for the cortico-striato-cortical loop in the pathogenesis of stroke-related neurogenic stuttering

Abstract

Neurogenic stuttering is an acquired speech disorder characterized by the occurrence of stuttering-like dysfluencies following brain damage. Because the onset of stuttering in these patients is associated with brain lesions, this condition provides a unique opportunity to study the neural processes underlying speech dysfluencies. Lesion localizations of 20 stroke subjects with neurogenic stuttering and 17 control subjects were compared using voxel-based lesion symptom mapping. The results showed nine left-hemisphere areas associated with the presence of neurogenic stuttering. These areas were largely overlapping with the cortico-basal ganglia-cortical network comprising the inferior frontal cortex, superior temporal cortex, intraparietal cortex, basal ganglia, and their white matter interconnections through the superior longitudinal fasciculus and internal capsule. These results indicated that stroke-induced neurogenic stuttering is not associated with neural dysfunction in one specific brain area but can occur following one or more lesion throughout the cortico-basal ganglia-cortical network. It is suggested that the onset of neurogenic stuttering in stroke subjects results from a disintegration of neural functions necessary for fluent speech.

CNV amplitude as a neural correlate for stuttering frequency: A case report of acquired stuttering

“…However, all these studies concern developmental stuttering. Although neurogenic and developmental stuttering are suggested to share common neural substrates (Theys et al, 2012), its translation in CNV amplitude seems to be different. The neural network involved in fluent (and stuttered) speech is suggested to be differently interrupted causing the opposite observation in MH.…”

“…Many of these areas are also assumed to be involved in developmental stuttering (e.g. Chang et al, 2009; originally thought to be two different entities, it now seems that both types of stuttering may share common neural characteristics (Theys et al, 2012).…”

Computational modeling of stuttering caused by impairments in a basal ganglia thalamo-cortical circuit involved in syllable selection and initiation

“…This group of nuclei, which takes part in speech production (Crosson, 1992; Gracco & Abbs, 1987; Guenther, 2008), was first linked to stuttering indirectly: the association was made due to the BG’s interconnection with the supplementary motor area (SMA), which may also be involved in the disorder (Caruso, Abbs, & Gracco, 1988). Basal ganglia lesions are associated with the presence of acquired (neurogenic) stuttering following strokes (Theys et al, 2012) and traumatic brain injuries (Ludlow et al, 1987), and several case studies showed that such a scenario (acquired stuttering after a BG lesion) leads to speech disturbances similar to developmental stuttering in various behavioral and clinical dimensions (Heuer, Sataloff, Mandel, & Travers, 1996; Koller, 1983; Krishnan & Tiwari, 2011; Tani & Sakai, 2011). The BG also have critical role in sequence skill learning, which is deficient in PWS (e.g., Smits-Bandstra & De Nil, 2007).…”

Acquired stuttering due to recurrent anaplastic astrocytoma

“…Though the mechanism remains unclear, stuttering has been attributed to lesions in the supplementary motor area, pons, putamen, the left and right parietal lobes, the thalamus and the corpus callosum 18–21. Using voxel-based lesion-symptom correlates, Theys et al 22 showed that acquired stuttering from infarcts is not due to one specific lesion but rather a dysfunction in the left-sided neural network compromised of the cortex-basal ganglia-cortex.…”