Limits to a left hemisphere explanation for specific language impairment

Abstract

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 significantly lower than their neurologically intact peers on a variety of language measures, yet few of the deficits noted are as persistent or severe as those seen in SLI. In at least two instances, however, language symptomatology following unilateral lesions in children does parallel some types of SLI. The first occurs following subcortical damage to anterior grey and white matter structures that typically results in pronounced language and learning disorders. The second parallel lies in the similar developmental course shared by children with "delayed" language and children with known unilateral lesions, whereby language onset and development is slow in the preschool years but normalizes by school age, with minimal long-term language-learning deficits.