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Neural anomaly and reorganization in speakers who stutter
Published Web Locationhttps://doi.org/10.1212/wnl.0b013e31826356d2
ObjectivesThe aim of the current study was to differentiate between neural activity that represents neural anomalies that are responsible for persistent developmental stuttering (PDS) from the activity that is a result of compensating for stuttering. This was done by investigating alterations to the intrinsic functional architecture of speech-language processes of patients with PDS before and after a short-term intervention.
MethodsThe resting-state functional connectivity (RSFC) and cortical thickness were examined before and after the intervention. The structural data were used to validate the functional results. Fifteen stuttering patients who received intervention (PDS+), 13 stuttering patients who did not receive intervention (PDS-), and 13 fluent controls participated.
ResultsBefore the intervention, both groups of PDS patients showed significant RSFC and cortical thickness reductions in the left pars-opercularis (PO) and RSFC increases in the cerebellum, as compared to fluent controls. The intervention was effective in reducing stuttering in PDS+ patients and lowering their RSFC in the cerebellum to the level of fluent controls. The intervention effect was specific to the PDS+ group (it was not evident in the PDS- group). The intervention did not change RSFC and cortical thickness in the left PO, which remained at its preintervention level.
ConclusionsThe results suggest that the left PO is a locus where the intrinsic functional architecture of speech-language processes is altered in PDS patients, suggesting an etiologic role of this region in PDS. The cerebellum showed intervention-induced neural reorganization, suggesting a compensatory response when stuttering occurs.
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