LIMITS TO A LEFT-HEMISPHERE EXPLANATION FOR SPECIFIC LANGUAGE IMPAIRMENT

The hypothesis of unilateral left hemisphere damage as an explanatory model for the neurological basis of specific language impairment (SLI) does not appear to be sufficient for most children with SLI. Children with unilateral brain lesions have been shown to function significant ly lower than their neurologically intact peers on a variety of langua ge measures, yet few of the deficits noted are as persistent or severe as those seen in SLI. In at least two instances, however, language sy mptomatology following unilateral lesions in children does parallel so me types of SLI. The first occurs following subcortical damage to ante rior grey and white matter structures that typically results in pronou nced language and learning disorders. The second parallel lies in the similar developmental course shared by children with ''delayed'' langu age and children with known unilateral lesions, whereby language onset and development is slow in the preschool years but normalizes by scho ol age, with minimal long-term language-learning deficits.