School of Psychology, Speech and Hearing, University of Canterbury, 8140 Christchurch, New Zealand.
New Zealand Institute of Language, Brain and Behaviour, University of Canterbury, 8140 Christchurch, New Zealand.
Brain. 2024 Jun 3;147(6):2203-2213. doi: 10.1093/brain/awae059.
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.
口吃影响大约每 100 人中的 1 人,可能导致严重的沟通问题和社交焦虑。它最常发生在发育障碍中,但也可能由局灶性脑损伤引起。这些后者的情况可能为口吃的脑区提供独特的见解。在这里,我们使用三个独立的数据集研究口吃的神经解剖学基础:(i)来自中风后获得性神经源性口吃的已发表文献的病例报告(n = 20,男性 14 人/女性 6 人,年龄 16-77 岁);(ii)一项具有中风后获得性神经源性口吃的临床单研究队列(n = 20,男性 13 人/女性 7 人,年龄 45-87 岁);和(iii)持续性发育性口吃的成年人(n = 20,男性 14 人/女性 6 人,年龄 18-43 岁)。我们使用前两个数据集和病变网络映射来测试导致获得性口吃的病变是否映射到共同的大脑网络。然后,我们使用第三个数据集来测试基于病变的网络是否与发育性口吃相关。在我们的文献数据集中,我们发现导致口吃的病变发生在多个异质的脑区,但这些病变位置均与以左侧壳核为中心的共同网络功能连接,包括屏状核、杏仁纹状体过渡区和其他相邻区域。这一发现被证明是口吃特异性的(PFWE < 0.05),并在我们中风后引起口吃的独立临床患者队列中具有可重复性(PFWE < 0.05),从而在两个中风数据集中产生了共同的获得性口吃网络。在共同的获得性口吃网络中,我们发现持续性发育性口吃的成年人左侧后腹壳核灰质体积与口吃影响之间存在显著关联,延伸至相邻的屏状核和杏仁纹状体过渡区(PFWE < 0.05)。我们得出的结论是,导致获得性神经源性口吃的病变映射到以左侧壳核、屏状核和杏仁纹状体过渡区为中心的共同大脑网络。该基于病变的网络与发育性口吃症状严重程度的关联表明,不同病因的口吃具有共同的神经解剖结构。