This meta-analysis examined 36 studies comparing autism spectrum disorder (ASD) and control groups in reading comprehension. Three moderators (semantic knowledge, decoding skill, PIQ) and two text types (high vs. low social knowledge) were examined as predictors of reading comprehension in ASD. The overall standardized mean difference for reading comprehension was g = -0.7 SD. The strongest individual predictors of reading comprehension were semantic knowledge (explaining 57 % of variance) and decoding skill (explaining 55 % of variance). Individuals with ASD were significantly worse at comprehending highly social than less social texts. Having ASD alone does not predict reading comprehension deficits. Instead, individual skills, especially language ability, must be considered before one can accurately predict whether a given individual with ASD will experience difficulties in reading comprehension.

Mutations in FOXP2 cause developmental verbal dyspraxia (DVD), but only a few cases have been described. We characterize 13 patients with DVD--5 with hemizygous paternal deletions spanning the FOXP2 gene, 1 with a translocation interrupting FOXP2, and the remaining 7 with maternal uniparental disomy of chromosome 7 (UPD7), who were also given a diagnosis of Silver-Russell Syndrome (SRS). Of these individuals with DVD, all 12 for whom parental DNA was available showed absence of a paternal copy of FOXP2. Five other individuals with deletions of paternally inherited FOXP2 but with incomplete clinical information or phenotypes too complex to properly assess are also described. Four of the patients with DVD also meet criteria for autism spectrum disorder. Individuals with paternal UPD7 or with partial maternal UPD7 or deletion starting downstream of FOXP2 do not have DVD. Using quantitative real-time polymerase chain reaction, we show the maternally inherited FOXP2 to be comparatively underexpressed. Our results indicate that absence of paternal FOXP2 is the cause of DVD in patients with SRS with maternal UPD7. The data also point to a role for differential parent-of-origin expression of FOXP2 in human speech development.

No abstract

We report detailed clinical, cytogenetic, and molecular findings in a girl with a deletion of chromosome 7q31-q32. This child has a severe communication disorder with evidence of oromotor dyspraxia, dysmorphic features, and mild developmental delay. She is unable to cough, sneeze, or laugh spontaneously. Her deletion is on the paternally inherited chromosome and includes the FOXP2 gene, which has recently been associated with speech and language impairment and a similar form of oromotor dyspraxia in at least three other published cases. We hypothesize that our patient's communication disorder and oromotor deficiency are due to haploinsufficiency for FOXP2 and that her dysmorphism and developmental delay are a consequence of the absence of the other genes involved in the microdeletion. We propose that this patient, together with others reported in the literature, may define a new contiguous gene deletion syndrome encompassing the 7q31-FOXP2 region. Cytogenetic and molecular analysis of this region should be considered for other individuals displaying similar characteristics.

Deficient rapid temporal processing may contribute to impaired language development by interfering with the processing of brief acoustic transitions crucial for speech perception. Using magnetoencephalography, evoked neural activity (M50, M100) to two 40 ms tones passively presented in rapid succession was recorded in 10 neurologically normal adults and 40 8-17-year-olds with autism, specific language impairment, Asperger syndrome or typical development. While 80% of study participants with intact language (Asperger syndrome, typical development, adults) showed identifiable responses to the second tone, which presented rapid temporal processing demands, 65% of study participants with impaired language (autism, specific language impairment) did not, despite having shown identifiable responses to the first tone. Rapid temporal processing impairments may be fundamentally associated with impairments in language rather than autism spectrum disorder.

No abstract

This study investigated the magnetic mismatch field elicited by changes in streams of vowels or spectrally matched tones in children with autism spectrum disorder (ASD) relative to children with typical development to explore whether impaired sound discrimination may contribute to language impairments in autism spectrum disorder. Using magnetoencephalography, we recorded evoked neural activity to 300-Hz and 700-Hz tones (and /u/ and /a/ vowels) presented in an oddball paradigm with deviant stimuli (15%) occurring within a train of standards (85%). The magnetic mismatch field was robustly observed in both groups, but children with autism spectrum disorder demonstrated a significantly delayed magnetic mismatch field compared with typically developing peers. Difficulty parsing transient differences in sounds may lead to impaired acoustic or phonological representations and subsequent language impairment in autism spectrum disorder.

This study investigated the 50 ms (M50) and 100 ms (M100) components of the auditory evoked field to explore their change during development. Using MEG, neuromagnetic fields elicited by a 1 kHz sinusoidal tone were recorded in adults and two groups of children and adolescents with typical development or autism spectrum disorder. M50 amplitude was larger in children than in adults, suggesting a developmental trajectory with M50 amplitude decreasing and M100 increasing with age. Child M50 and M100 latencies were prolonged relative to adults. Children with autism did not differ from control children with respect to these observations. The M50 in relation to the M100 is a robust index of early auditory system maturation suitable for future developmental investigations.