Murdoch Childrens Research Institute, Flemington Road, Parkville, Victoria 3052, Australia.
Brain. 2013 Feb;136(Pt 2):646-57. doi: 10.1093/brain/aws355. Epub 2013 Jan 31.
Severe and persistent speech disorder, dysarthria, may be present for life after brain injury in childhood, yet the neural correlates of this chronic disorder remain elusive. Although abundant literature is available on language reorganization after lesions in childhood, little is known about the capacity of motor speech networks to reorganize after injury. Here, we examine the structural and functional neural correlates associated with chronic dysarthria after childhood-onset traumatic brain injury. Forty-nine participants aged 12 years 3 months to 24 years 11 months were recruited to the study: (i) a group with chronic dysarthria (n = 17); matched for age and sex with two control groups of (ii) healthy control subjects (n = 17); and (iii) individuals without dysarthria after traumatic brain injury (n = 15). A high-resolution 3D T(1)-weighted whole-brain data set was acquired for voxel-based morphometry analyses of group differences in grey matter. Functional magnetic resonance imaging was used to localize activation associated with speaking single words (baseline: listening to words). Group differences on voxel-based morphometry revealed widespread grey matter reductions in the dysarthric group compared with healthy control subjects, including in numerous speech motor regions bilaterally, such as the cerebellum, the basal ganglia and primary motor cortex representation of the articulators. Relative to the non-dysarthric traumatic brain injury group, individuals with dysarthria showed reduced grey matter bilaterally in the ventral sensorimotor cortex, but this reduction was concomitant with increased functional activation only in the left-hemisphere cluster during speech. Finally, increased recruitment of Broca's area (Brodmann area 45, pars triangularis) but not its right homologue, correlated with better speech outcome, suggesting that this 'higher-level' area may be more critically involved with production when associated motor speech regions are damaged. We suggest that the bilateral morphological abnormalities within cortical speech networks in childhood prevented reorganization of speech function from the left- to right-hemisphere. Rather, functional reorganization involved over-recruitment of left-hemisphere motor regions, a reorganization method that was only partly relatively effective, given the presence of persisting yet mild speech deficits. The bilateral structural abnormalities found to limit functional reorganization here, may also be critical to poor speech prognosis for populations with congenital, degenerative or acquired neurological disorders throughout the lifespan.
严重且持久的言语障碍,构音障碍,在儿童期脑损伤后可能会持续一生,但这种慢性障碍的神经相关性仍难以捉摸。尽管有大量关于儿童期病变后语言重组的文献,但对于运动言语网络在损伤后的重组能力却知之甚少。在这里,我们研究了与儿童期创伤性脑损伤后慢性构音障碍相关的结构和功能神经相关性。招募了 49 名年龄在 12 岁 3 个月至 24 岁 11 个月的参与者参加研究:(i)一组患有慢性构音障碍(n = 17);与年龄和性别匹配的两组对照:(ii)健康对照组(n = 17);和(iii)创伤性脑损伤后无构音障碍的个体(n = 15)。为了进行灰质的基于体素形态计量学分析,我们采集了高分辨率 3D T1 加权全脑数据集。功能磁共振成像用于定位与说话单字相关的激活(基线:听单词)。基于体素形态计量学的组间差异显示,与健康对照组相比,构音障碍组的灰质普遍减少,包括双侧的许多言语运动区域,如小脑、基底节和主要运动皮层代表发音器官。与非构音障碍性创伤性脑损伤组相比,患有构音障碍的个体双侧的腹侧感觉运动皮层灰质减少,但这种减少仅在左侧语言区的集群中伴随着功能激活的增加。最后,Broca 区(Brodmann 区 45,三角区)的募集增加,但不是其右侧同源物的募集增加,与更好的言语结果相关,这表明当相关的运动言语区域受损时,这个“更高层次”的区域可能更关键地参与言语的产生。我们认为,儿童时期皮质言语网络中的双侧形态异常阻止了言语功能从左半球到右半球的重组。相反,功能重组涉及左半球运动区域的过度募集,这种重组方法只是部分相对有效,因为存在持续但轻微的言语缺陷。这里发现的双侧结构异常限制了功能重组,对于一生中患有先天性、退行性或获得性神经障碍的人群来说,可能对言语预后也很关键。