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 significantly lower than their neurologically intact peers on a ... Research Article
Research Article  |   August 01, 1994
Limits to a Left Hemisphere Explanation for Specific Language Impairment
 
Author Affiliations & Notes
  • Dorothy M. Aram
    Division of Communication Disorders Emerson, College Boston, MA
  • Julie A. Eisele
    Department of Psychology, Skidmore College Saratoga Springs, NY
  • Contact author: Dorothy M. Aram, PhD, Division of Communication Disorders, Emerson College, 168 Beacon Street, Boston, MA 02116.
Article Information
Special Populations / Language Disorders / Specific Language Impairment / Language / Research Articles
Research Article   |   August 01, 1994
Limits to a Left Hemisphere Explanation for Specific Language Impairment
Journal of Speech, Language, and Hearing Research, August 1994, Vol. 37, 824-830. doi:10.1044/jshr.3704.824
History: Received August 26, 1993 , Accepted January 24, 1994
 
Journal of Speech, Language, and Hearing Research, August 1994, Vol. 37, 824-830. doi:10.1044/jshr.3704.824
History: Received August 26, 1993; Accepted January 24, 1994

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.

Acknowledgment
The research reported here was supported by NINCDS Grant 17366 and NS 20489 to the first author.
Order a Subscription
Pay Per View
Entire Journal of Speech, Language, and Hearing Research content & archive
24-hour access
This Article
24-hour access