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.

中文翻译：

---

基于因果脑损伤的口吃定位


大约百分之一的成年人患有口吃，并可能导致严重的沟通问题和社交焦虑。它最常作为发育障碍发生，但也可能由局灶性脑损伤引起。后一种情况可能会为导致口吃的大脑区域提供独特的见解。在这里，我们使用三个独立的数据集研究了口吃的神经解剖学基础：（i）来自已发表文献的中风后获得性神经源性口吃的病例报告（n = 20，14 名男性/6 名女性，16-77 岁）； (ii) 中风后获得性神经源性口吃的临床单一研究队列（n = 20，13 名男性/7 名女性，45-87 岁）； (iii) 患有持续性发育性口吃的成年人（n = 20，14 名男性/6 名女性，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这个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脑区域，但这些病变位置都在功能上连接到以左壳核为中心的共同网络，包括屏状核、杏仁核纹状体过渡区和其他邻近区域。这一发现被证明对于口吃具有特异性 (PFWE < 0.05)，并且在我们的中风诱发口吃患者的独立临床队列 (PFWE < 0.05) 中可重复，从而在两个中风数据集中形成共同的获得性口吃网络。 在常见的获得性口吃网络中，我们发现对于左侧后腹壳核持续性发育性口吃的成年人来说，灰质体积与口吃影响之间存在显着相关性，并延伸到邻近的屏状核和杏仁核纹状体过渡区（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一个共同的大脑网络，以左壳核、屏状核和杏仁核纹状体过渡区为中心。这种基于病变的网络与发育性口吃症状严重程度的关联表明跨病因学具有共同的神经解剖学特征。