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The neuroanatomy of developmental language disorder
Poster B62 in Poster Session B and Reception, Thursday, October 6, 6:30 - 8:30 pm EDT, Millennium Hall
Michael T. Ullman1, Gillian M. Clark2, Mariel Y. Pullman3, Jarrett T. Lovelett4, Elizabeth I. Pierpont5, Xiong Jiang1, Peter E. Turkeltaub1; 1Georgetown University, Washington, DC, USA, 2Deakin University, Geelong, Victoria, Australia, 3New York-Presbyterian/Columbia University Medical Center, New York, NY, USA, 4University of California, San Diego, La Jolla, CA, USA, 5University of Minnesota Medical Center, Minneapolis, MN, USA
Developmental language disorder (DLD) is a common neurodevelopmental disorder whose adverse impacts continue into adulthood. However, its neural substrates remain unclear. To address this lacuna we systematically identified and quantitatively synthesized neuroanatomical studies of DLD. Analyses of structural brain data (22 papers, 577 participants) revealed highly consistent anomalies in the basal ganglia (100% of studies that examined this structure, weighted by study sample sizes; 99.8% permutation-based likelihood that the anomaly clustering was not due to chance). These anomalies were further localized to the neostriatum, in particular the anterior portion (again 100% and 99.8%). No other structure showed as consistent abnormalities, including frontal cortex (82.6% weighted proportion; 97.7% permutation-based likelihood), which showed the next highest rate of abnormalities. The structural abnormalities were distributed similarly across the two hemispheres. As expected given the task-dependence of activation, functional neuroimaging data (11 papers, 414 participants) yielded less consistency. Nevertheless, the highest weighted proportion of functional imaging anomalies also occurred in the basal ganglia (80.9%; 97.2%), with the parietal lobes showing a similar rate (80.0%; 98.2%). Functional imaging abnormalities were found at similar proportions across the hemispheres with the exception of the basal ganglia, which showed a higher rate of anomalies in the right than left side. Multiple sensitivity analyses revealed that both the structural and functional neuroanatomical patterns were robust. The findings are likely more reliable and generalizable than single study results, since the number of participants is by definition larger than in any one study in the synthesis, and because the diversity of the included studies suggests greater generalizability of the findings. The results reveal clear patterns regarding the neuroanatomy of DLD. A key finding is that DLD is associated with striking structural neuroanatomical consistency, despite the etiological and behavioral diversity linked to the disorder. We suggest that, analogous to the acquired aphasias, DLD may be best explained by its pattern of neuroanatomical abnormalities, rather than by etiological (e.g., genetic polymorphism or toxic insult) or linguistic/cognitive factors, even if these may also contribute to the phenotype of the disorder. Indeed, one such neuroanatomical account has previously been proposed, the Procedural circuit Deficit Hypothesis (PDH), which largely—though not completely—predicted the pattern of observed abnormalities, in particular in the basal ganglia. The results are interpreted with respect to the PDH and other explanatory accounts of DLD. We discuss limitations as well as basic research and translational implications both for DLD and for language more generally.
Topic Areas: Disorders: Developmental, Development