Differences in Cortical Surface Area in Developmental Language Disorder.

Approximately 7% of children have developmental language disorder (DLD), a neurodevelopmental condition associated with persistent language learning difficulties without a known cause. Our understanding of the neurobiological basis of DLD is limited. Here, we used FreeSurfer to investigate cortical surface area and thickness in a large cohort of 156 children and adolescents aged 10-16 years with a range of language abilities, including 54 with DLD, 28 with a history of speech-language difficulties who did not meet criteria for DLD, and 74 age-matched controls with typical language development (TD). We also examined cortical asymmetries in DLD using an automated surface-based technique. Relative to the TD group, those with DLD showed smaller surface area bilaterally in the inferior frontal gyrus extending to the anterior insula, in the posterior temporal and ventral occipito-temporal cortex, and in portions of the anterior cingulate and superior frontal cortex. Analysis of the whole cohort using a language proficiency factor revealed that language ability correlated positively with surface area in similar regions. There were no differences in cortical thickness, nor in asymmetry of these cortical metrics between TD and DLD. This study highlights the importance of distinguishing between surface area and cortical thickness in investigating the brain basis of neurodevelopmental disorders and suggests the development of cortical surface area to be of importance to DLD. Future longitudinal studies are required to understand the developmental trajectory of these cortical differences in DLD and how they relate to language maturation.

Can speech perception deficits cause phonological impairments? Evidence from short-term memory for ambiguous speech.

Poor performance on phonological tasks is characteristic of neurodevelopmental language disorders (dyslexia and/or developmental language disorder). Perceptual deficit accounts attribute phonological dysfunction to lower-level deficits in speech-sound processing. However, a causal pathway from speech perception to phonological performance has not been established. We assessed this relationship in typical adults by experimentally disrupting speech-sound discrimination in a phonological short-term memory (pSTM) task. We used an automated audio-morphing method (Rogers & Davis, 2017) to create ambiguous intermediate syllables between 16 letter name-letter name ("B"-"P") and letter name-word ("B"-"we") pairs. High- and low-ambiguity syllables were used in a pSTM task in which participants (N = 36) recalled six- and eight-letter name sequences. Low-ambiguity sequences were better recalled than high-ambiguity sequences, for letter name-letter name but not letter name-word morphed syllables. A further experiment replicated this ambiguity cost (N = 26), but failed to show retroactive or prospective effects for mixed high- and low-ambiguity sequences, in contrast to pSTM findings for speech-in-noise (SiN; Guang et al., 2020; Rabbitt, 1968). These experiments show that ambiguous speech sounds impair pSTM, via a different mechanism to SiN recall. We further show that the effect of ambiguous speech on recall is context-specific, limited, and does not transfer to recall of nonconfusable items. This indicates that speech perception deficits are not a plausible cause of pSTM difficulties in language disorders. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Microstructural Properties of the Cerebellar Peduncles in Children with Developmental Language Disorder.

Children with developmental language disorder (DLD) struggle to learn their native language for no apparent reason. While research on the neurobiological underpinnings of the disorder has focused on the role of cortico-striatal systems, little is known about the role of the cerebellum in DLD. Cortico-cerebellar circuits might be involved in the disorder as they contribute to complex sensorimotor skill learning, including the acquisition of spoken language. Here, we used diffusion-weighted imaging data from 77 typically developing and 54 children with DLD and performed probabilistic tractography to identify the cerebellum's white matter tracts: the inferior, middle, and superior cerebellar peduncles. Children with DLD showed lower fractional anisotropy (FA) in the inferior cerebellar peduncles (ICP), fiber tracts that carry motor and sensory input via the inferior olive to the cerebellum. Lower FA in DLD was driven by lower axial diffusivity. Probing this further with more sophisticated modeling of diffusion data, we found higher orientation dispersion but no difference in neurite density in the ICP of DLD. Reduced FA is therefore unlikely to be reflecting microstructural differences in myelination in this tract, rather the organization of axons in these pathways is disrupted. ICP microstructure was not associated with language or motor coordination performance in our sample. We also found no differences in the middle and superior peduncles, the main pathways connecting the cerebellum with the cortex. To conclude, it is not cortico-cerebellar but atypical olivocerebellar white matter connections that characterize DLD and suggest the involvement of the olivocerebellar system in speech acquisition and development.

Quantitative MRI reveals differences in striatal myelin in children with DLD.

Developmental language disorder (DLD) is a common neurodevelopmental disorder characterised by receptive or expressive language difficulties or both. While theoretical frameworks and empirical studies support the idea that there may be neural correlates of DLD in frontostriatal loops, findings are inconsistent across studies. Here, we use a novel semiquantitative imaging protocol - multi-parameter mapping (MPM) - to investigate microstructural neural differences in children with DLD. The MPM protocol allows us to reproducibly map specific indices of tissue microstructure. In 56 typically developing children and 33 children with DLD, we derived maps of (1) longitudinal relaxation rate R1 (1/T1), (2) transverse relaxation rate R2* (1/T2*), and (3) Magnetization Transfer saturation (MTsat). R1 and MTsat predominantly index myelin, while R2* is sensitive to iron content. Children with DLD showed reductions in MTsat values in the caudate nucleus bilaterally, as well as in the left ventral sensorimotor cortex and Heschl's gyrus. They also had globally lower R1 values. No group differences were noted in R2* maps. Differences in MTsat and R1 were coincident in the caudate nucleus bilaterally. These findings support our hypothesis of corticostriatal abnormalities in DLD and indicate abnormal levels of myelin in the dorsal striatum in children with DLD.

Seven percent of children struggle to learn their native language for no obvious reason. This condition is called Developmental Language Disorder (DLD). Children with DLD often have difficulty learning to read and write. They are at higher risk for academic underachievement and may struggle to find good jobs. Their language difficulties also contribute to difficulties making friends and emotional challenges. Scientists suspect children with DLD may have differences in areas deep in the brain that help people learn habits and rules. A new magnetic resonance imaging technique called multiparameter mapping (MPM) can help scientists determine if this is true. The technique measures the properties of brain tissue. It is particularly useful for measuring the amounts of a fatty protective sheath on brain cells called myelin. Myelin helps brain cells send information faster. Using MPM, Krishnan et al. show that children with DLD have less myelin in parts of the brain responsible for speaking, listening, and learning rules and habits. In the experiments, 56 children with typical language development and 33 children with DLD were scanned using MPM. Krishnan et al. then compared the two groups and found reduced myelin in these critical areas associated with learning a language in most of the children with DLD. But not all children with DLD had these differences. More studies are needed to determine if these brain differences cause language problems and how or if experiencing language difficulties could cause these changes in the brain. Further research may help scientists find new treatments that target these brain differences.

Functional organisation for verb generation in children with developmental language disorder.

Developmental language disorder (DLD) is characterised by difficulties in learning one's native language for no apparent reason. These language difficulties occur in 7% of children and are known to limit future academic and social achievement. Our understanding of the brain abnormalities associated with DLD is limited. Here, we used a simple four-minute verb generation task (children saw a picture of an object and were instructed to say an action that goes with that object) to test children between the ages of 10-15 years (DLD N = 50, typically developing N = 67). We also tested 26 children with poor language ability who did not meet our criteria for DLD. Contrary to our registered predictions, we found that children with DLD did not have (i) reduced activity in language relevant regions such as the left inferior frontal cortex; (ii) dysfunctional striatal activity during overt production; or (iii) a reduction in left-lateralised activity in frontal cortex. Indeed, performance of this simple language task evoked activity in children with DLD in the same regions and to a similar level as in typically developing children. Consistent with previous reports, we found sub-threshold group differences in the left inferior frontal gyrus and caudate nuclei, but only when analysis was limited to a subsample of the DLD group (N = 14) who had the poorest performance on the task. Additionally, we used a two-factor model to capture variation in all children studied (N = 143) on a range of neuropsychological tests and found that these language and verbal memory factors correlated with activity in different brain regions. Our findings indicate a lack of support for some neurological models of atypical language learning, such as the procedural deficit hypothesis or the atypical lateralization hypothesis, at least when using simple language tasks that children can perform. These results also emphasise the importance of controlling for and monitoring task performance.

Robust Sensorimotor Learning during Variable Sentence-Level Speech.

Sensorimotor learning has been studied by altering the sound of the voice in real time as speech is produced. In response to voice alterations, learned changes in production reduce the perceived auditory error and persist for some time after the alteration is removed [1-5]. The results of such experiments have led to the development of prominent models of speech production. This work proposes that the control of speech relies on forward models to predict sensory outcomes of movements, and errors in these predictions drive sensorimotor learning [5-7]. However, sensorimotor learning in speech has only been observed following intensive training on a handful of discrete words or perceptually similar sentences. Stereotyped production does not capture the complex sensorimotor demands of fluid, real-world speech [8-11]. It remains unknown whether talkers predict the sensory consequences of variable sentence production to allow rapid and precise updating of speech motor plans when sensory prediction errors are encountered. Here, we used real-time alterations of speech feedback to test for sensorimotor learning during the production of 50 sentences that varied markedly in length, vocabulary, and grammar. Following baseline production, all vowels were simultaneously altered and played back through headphones in near real time. Robust feedforward changes in sentence production were observed that, on average, precisely countered the direction of the alteration. These changes occurred in every participant and transferred to the production of single words with varying vowel sounds. The results show that to maintain accurate sentence production, the brain actively predicts the auditory consequences of variable sentence-level speech.

Cortico-cerebellar Networks Drive Sensorimotor Learning in Speech.

The motor cortex and cerebellum are thought to be critical for learning and maintaining motor behaviors. Here we use transcranial direct current stimulation (tDCS) to test the role of the motor cortex and cerebellum in sensorimotor learning in speech. During productions of "head," "bed," and "dead," the first formant of the vowel sound was altered in real time toward the first formant of the vowel sound in "had," "bad," and "dad." Compensatory changes in first and second formant production were used as a measure of motor adaptation. tDCS to either the motor cortex or the cerebellum improved sensorimotor learning in speech compared with sham stimulation ( n = 20 in each group). However, in the case of cerebellar tDCS, production changes were restricted to the source of the acoustical error (i.e., the first formant). Motor cortex tDCS drove production changes that offset errors in the first formant, but unlike cerebellar tDCS, adaptive changes in the second formant also occurred. The results suggest that motor cortex and cerebellar tDCS have both shared and dissociable effects on motor adaptation. The study provides initial causal evidence in speech production that the motor cortex and the cerebellum support different aspects of sensorimotor learning. We propose that motor cortex tDCS drives sensorimotor learning toward previously learned patterns of movement, whereas cerebellar tDCS focuses sensorimotor learning on error correction.