UCL Great Ormond Street Institute of Child Health, London, UK.
Population Health and Immunity Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville 3052, Australia.
Brain. 2022 Apr 29;145(3):1177-1188. doi: 10.1093/brain/awab364.
Developmental stuttering is a condition of speech dysfluency, characterized by pauses, blocks, prolongations and sound or syllable repetitions. It affects around 1% of the population, with potential detrimental effects on mental health and long-term employment. Accumulating evidence points to a genetic aetiology, yet gene-brain associations remain poorly understood due to a lack of MRI studies in affected families. Here we report the first neuroimaging study of developmental stuttering in a family with autosomal dominant inheritance of persistent stuttering. We studied a four-generation family, 16 family members were included in genotyping analysis. T1-weighted and diffusion-weighted MRI scans were conducted on seven family members (six male; aged 9-63 years) with two age and sex matched controls without stuttering (n = 14). Using Freesurfer, we analysed cortical morphology (cortical thickness, surface area and local gyrification index) and basal ganglia volumes. White matter integrity in key speech and language tracts (i.e. frontal aslant tract and arcuate fasciculus) was also analysed using MRtrix and probabilistic tractography. We identified a significant age by group interaction effect for cortical thickness in the left hemisphere pars opercularis (Broca's area). In affected family members this region failed to follow the typical trajectory of age-related thinning observed in controls. Surface area analysis revealed the middle frontal gyrus region was reduced bilaterally in the family (all cortical morphometry significance levels set at a vertex-wise threshold of P < 0.01, corrected for multiple comparisons). Both the left and right globus pallidus were larger in the family than in the control group (left P = 0.017; right P = 0.037), and a larger right globus pallidus was associated with more severe stuttering (rho = 0.86, P = 0.01). No white matter differences were identified. Genotyping identified novel loci on chromosomes 1 and 4 that map with the stuttering phenotype. Our findings denote disruption within the cortico-basal ganglia-thalamo-cortical network. The lack of typical development of these structures reflects the anatomical basis of the abnormal inhibitory control network between Broca's area and the striatum underpinning stuttering in these individuals. This is the first evidence of a neural phenotype in a family with an autosomal dominantly inherited stuttering.
发展性口吃是一种言语不流畅的状况,其特征为停顿、阻滞、延长以及声音或音节重复。它影响约 1%的人口,可能对心理健康和长期就业产生不利影响。越来越多的证据表明其具有遗传病因,但由于缺乏受影响家族的 MRI 研究,基因-大脑关联仍未得到充分理解。在这里,我们报告了第一个在具有常染色体显性遗传持续性口吃的家族中进行的发展性口吃的神经影像学研究。我们研究了一个四代同堂的家族,对 16 名家族成员进行了基因分型分析。对 7 名家族成员(6 名男性;年龄 9-63 岁)和 2 名年龄和性别匹配的非口吃对照者(n = 14)进行了 T1 加权和弥散加权 MRI 扫描。使用 Freesurfer,我们分析了皮质形态(皮质厚度、表面积和局部脑回指数)和基底节体积。还使用 MRtrix 和概率追踪法分析了关键言语和语言束(即额斜束和弓状束)的白质完整性。我们发现左侧脑岛 opercularis (Broca 区)皮质厚度存在显著的年龄与组间交互效应。在受影响的家族成员中,该区域未能遵循对照组中观察到的与年龄相关的变薄的典型轨迹。表面积分析显示家族双侧额中回区域减少(所有皮质形态学显著水平设定在顶点阈值 P < 0.01,校正多重比较)。家族中左侧和右侧苍白球均大于对照组(左侧 P = 0.017;右侧 P = 0.037),且右侧苍白球越大与口吃越严重相关(rho = 0.86,P = 0.01)。未发现白质差异。基因分型鉴定出染色体 1 和 4 上的新基因座,与口吃表型相关。我们的研究结果表明,皮质基底节-丘脑-皮质网络内存在破坏。这些结构的典型发育缺失反映了这些个体中口吃所基于的 Broca 区与纹状体之间异常抑制控制网络的解剖学基础。这是首个具有常染色体显性遗传口吃的家族的神经表型证据。