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Related Experiment Videos

Limits to a left hemisphere explanation for specific language impairment

D M Aram1, J A Eisele

  • 1Division of Communication Disorders, Emerson College, Boston, MA.

Journal of Speech and Hearing Research
|August 1, 1994
PubMed
Summary

Unilateral left hemisphere damage is insufficient to explain most cases of specific language impairment (SLI). However, some language deficits in children with unilateral brain lesions parallel certain aspects of SLI.

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Comprehension and imitation of syntax following early hemisphere damage.

Brain and language·1994

Area of Science:

  • Neurolinguistics
  • Developmental Psychology
  • Pediatric Neurology

Background:

  • Specific Language Impairment (SLI) presents complex language deficits in children.
  • Unilateral brain lesions in children can cause language impairments, but their severity and persistence often differ from SLI.
  • Existing models struggle to fully account for the neurological underpinnings of SLI.

Purpose of the Study:

  • To evaluate the sufficiency of unilateral left hemisphere damage as the sole neurological basis for SLI.
  • To compare language deficits in children with unilateral brain lesions to those observed in SLI.
  • To identify specific instances where unilateral lesions may parallel SLI symptomatology or developmental trajectories.

Main Methods:

  • Review of existing literature on language disorders following unilateral brain lesions in children.

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  • Comparative analysis of language measures in children with unilateral brain damage versus children diagnosed with SLI.
  • Examination of developmental language trajectories in children with unilateral lesions and those with delayed language acquisition.

    • Main Results:

    • Unilateral left hemisphere damage alone is not a sufficient explanation for the majority of SLI cases.
    • While unilateral lesions can cause language deficits, they are typically less persistent and severe than those seen in SLI.
    • Two parallels between unilateral lesions and SLI were identified: subcortical damage leading to pronounced disorders and similar developmental courses in some cases.

    Conclusions:

    • The neurological basis of SLI is likely more complex than simple unilateral left hemisphere damage.
    • Specific patterns of subcortical damage and certain developmental trajectories following unilateral lesions may offer insights into SLI.
    • Further research is needed to fully elucidate the neurological underpinnings of SLI.