PNAS nexus · 2026
Reduced integrity in the frontal aslant tract's premotor connections is associated with dysfluency severity in stuttering.
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Michon Maëva, Hirsch Fabrice, Didirková Ivana, Giampiccolo Davide, Monfrais-Pfauwadel Marie-Claude, Lemaitre Anne-Laure, Deverdun Jérémy, Lebars Emmanuelle, Herbet Guillaume
Аннотация
Stuttering is a neurodevelopmental disorder marked by impaired speech production and substantial interindividual variability in symptom severity. Although neuroimaging studies have identified abnormalities in the basal ganglia-thalamocortical circuitry, the specific white matter pathways that underpin dysfluent speech production remain poorly understood. Here, we focus on the frontal aslant tract (FAT), a dorsoventral intralobar tract connecting the superior and inferior frontal cortices and proposed to support both cognitive and motor functions. Using diffusion MRI, we first compared the quantitative anisotropy of the FAT and relevant control tracts in individuals who stutter (n = 30, mean age = 35.67, SD = 13.03) and fluent speakers (n = 22, mean age = 35.64, SD = 10.87) and observed no significant group-level differences in either hemisphere. To delineate the role of FAT subbundles in speech dysfluency, we then segmented the tract at its dorsal and ventral cortical terminations and assessed their relationships with stuttering severity (Stuttering Severity Instrument-Fourth Edition). We identified left FAT subbundles connecting the posteroventral frontal structures, particularly the rostroventral precentral gyrus and, to a lesser extent, the pars opercularis to a dorsal prefrontal region whose integrity predicts stuttering severity. The left-lateralized nature of these associations suggests that stuttering results, in part, from abnormal connectivity between prefrontal systems governing volitional control and the motor circuits engaged in speech production. Together, these findings refine current neurobiological models of stuttering by implicating frontofrontal white matter pathways underlying speech dysfluency and highlight a potential anatomical target for individualized therapeutic interventions.