Persistent Neurobehavioral Markers of Developmental Morphosyntax Errors in Adults.

Purpose Child language acquisition is marked by an optional infinitive period (ages 2-4 years) during which children use nonfinite (infinitival) verb forms and finite verb forms interchangeably in grammatical contexts that require finite forms. In English, children's errors include omissions of past tense /-ed/ and 3rd-person singular /-s/. This language acquisition period typically ends by the age of 4 years, but it persists in children with language impairments. It is unknown if adults still process optional infinitives differently than other kinds of morphosyntax errors. Method We compared behavior and functional brain activation during grammaticality judgments across sentences with developmental optional infinitive tense/agreement errors ("Yesterday I play the song"), nondevelopmental agreement errors ("He am tall") that do not occur in typical child language acquisition, and grammatically correct sentences. Results Adults (N = 25) were significantly slower and less accurate in judging sentences with developmental errors relative to other sentences. Sentences with developmental errors yielded greater activation in bilateral inferior frontal gyri relative to nondevelopmental error sentences in both auditory and visual modalities. Conclusions These findings suggest that the heightened computational demands for finiteness extend well beyond early childhood and continue to exert their influence on grammatical mental and brain function in adulthood.

Amygdala-medial prefrontal cortex connectivity relates to stress and mental health in early childhood.

Early life stress has been associated with disrupted functional connectivity between the amygdala and medial prefrontal cortex (mPFC), but it is unknown how early in development stress-related differences in amygdala-mPFC connectivity emerge. In a resting-state functional connectivity (rs-FC) analysis with 79 four- to seven-year-old children, we found a significant correlation between more adverse experiences and weaker amygdala-mPFC rs-FC. We also found that weaker amygdala-mPFC rs-FC was associated with higher levels of aggressive behavior and attention problems. These findings suggest that the impact of stress on emotional circuitry is detectable in early childhood and that this impact is associated with mental health difficulties. Connectivity in this circuit may be useful as a marker for mental health risk and for tracking the efficacy of early interventions.

Brain bases of reading fluency in typical reading and impaired fluency in dyslexia.

Although the neural systems supporting single word reading are well studied, there are limited direct comparisons between typical and dyslexic readers of the neural correlates of reading fluency. Reading fluency deficits are a persistent behavioral marker of dyslexia into adulthood. The current study identified the neural correlates of fluent reading in typical and dyslexic adult readers, using sentences presented in a word-by-word format in which single words were presented sequentially at fixed rates. Sentences were presented at slow, medium, and fast rates, and participants were asked to decide whether each sentence did or did not make sense semantically. As presentation rates increased, participants became less accurate and slower at making judgments, with comprehension accuracy decreasing disproportionately for dyslexic readers. In-scanner performance on the sentence task correlated significantly with standardized clinical measures of both reading fluency and phonological awareness. Both typical readers and readers with dyslexia exhibited widespread, bilateral increases in activation that corresponded to increases in presentation rate. Typical readers exhibited significantly larger gains in activation as a function of faster presentation rates than readers with dyslexia in several areas, including left prefrontal and left superior temporal regions associated with semantic retrieval and semantic and phonological representations. Group differences were more extensive when behavioral differences between conditions were equated across groups. These findings suggest a brain basis for impaired reading fluency in dyslexia, specifically a failure of brain regions involved in semantic retrieval and semantic and phonological representations to become fully engaged for comprehension at rapid reading rates.