A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Localization of stuttering based on causal brain lesions
Tekijät: Theys, Catherine; Jaakkola, Elina; Melzer, Tracy R; De Nil, Luc F; Guenther, Frank H; Cohen, Alexander L; Fox, Michael D; Joutsa, Juho
Kustantaja: Oxford University Press
Julkaisuvuosi: 2024
Journal: Brain
Tietokannassa oleva lehden nimi: Brain : a journal of neurology
Lehden akronyymi: Brain
Vuosikerta: 147
Numero: 6
Aloitussivu: 2203
Lopetussivu: 2213
ISSN: 0006-8950
eISSN: 1460-2156
DOI: https://doi.org/10.1093/brain/awae059
Verkko-osoite: https://academic.oup.com/brain/article/147/6/2203/7667029
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/454774237
Stuttering affects approximately 1 in 100 adults and can result in significant communication problems and social anxiety. It most often occurs as a developmental disorder but can also be caused by focal brain damage. These latter cases may lend unique insight into the brain regions causing stuttering. Here, we investigated the neuroanatomical substrate of stuttering using three independent datasets: (i) case reports from the published literature of acquired neurogenic stuttering following stroke (n = 20, 14 males/six females, 16-77 years); (ii) a clinical single study cohort with acquired neurogenic stuttering following stroke (n = 20, 13 males/seven females, 45-87 years); and (iii) adults with persistent developmental stuttering (n = 20, 14 males/six females, 18-43 years). We used the first two datasets and lesion network mapping to test whether lesions causing acquired stuttering map to a common brain network. We then used the third dataset to test whether this lesion-based network was relevant to developmental stuttering. In our literature dataset, we found that lesions causing stuttering occurred in multiple heterogeneous brain regions, but these lesion locations were all functionally connected to a common network centred around the left putamen, including the claustrum, amygdalostriatal transition area and other adjacent areas. This finding was shown to be specific for stuttering (PFWE < 0.05) and reproducible in our independent clinical cohort of patients with stroke-induced stuttering (PFWE < 0.05), resulting in a common acquired stuttering network across both stroke datasets. Within the common acquired stuttering network, we found a significant association between grey matter volume and stuttering impact for adults with persistent developmental stuttering in the left posteroventral putamen, extending into the adjacent claustrum and amygdalostriatal transition area (PFWE < 0.05). We conclude that lesions causing acquired neurogenic stuttering map to a common brain network, centred to the left putamen, claustrum and amygdalostriatal transition area. The association of this lesion-based network with symptom severity in developmental stuttering suggests a shared neuroanatomy across aetiologies.
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Julkaisussa olevat rahoitustiedot:
C.T., T.R.M. and F.H.G. received funding from the Royal Society of New Zealand Marsden Fund (M1180). E.J. reports research funding from the Finnish Medical Foundation and the Finnish Parkinson Foundation. T.R.M. also received funding from a Health Research Council of New Zealand Charles Hercus Career Development Fellowship. F.H.G. received funding from the National Institute on Deafness and Other Communication Disorders, National Institutes of Health (R01 DC007683). L.F.D. received funding from the Natural Sciences and Engineering Research Council. A.C. received funding from the NIMH (K23MH120510) and the Simons Foundation Autism Research Initiative. M.D.F. was supported by grants from the NIH (R01MH113929, R21MH126271, R56AG069086, R21NS123813, R01NS127892), the Kaye Family Research Endowment, the Ellison/ Baszucki Family Foundation, and the Manley Family. J.J. received funding from the Finnish Medical Foundation, Sigrid Juselius Foundation, Instrumentarium Research Foundation, University of Turku, and Turku University Hospital.
