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Related Experiment Videos

Subcortical aphasia

S E Nadeau1, B Crosson

  • 1Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, Gainesville, FL 32608-1197, USA.

Brain and Language
|July 1, 1997
PubMed
Summary
This summary is machine-generated.

Subcortical aphasia is not primarily caused by basal ganglia damage or disconnection. Instead, language deficits may stem from cortical hypoperfusion or thalamic pathway disruption affecting attentional processes and working memory.

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Area of Science:

  • Neuroscience
  • Neurolinguistics
  • Cognitive Neurology

Background:

  • Traditional views on subcortical aphasia mechanisms are challenged by recent findings.
  • Basal ganglia's direct role in language and disconnection/diaschisis theories lack consistent evidence.
  • Striatocapsular infarction cases show variable language deficits, questioning established models.

Purpose of the Study:

  • To critically review literature on subcortical aphasia mechanisms.
  • To propose new hypotheses reconciling existing data with current understanding.
  • To investigate the role of cortical and thalamic structures in subcortical aphasia.

Main Methods:

  • Literature review of subcortical aphasia, focusing on striatocapsular and thalamic infarcts.
  • Analysis of reported cases and associated linguistic impairments.

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  • Examination of vascular events and anatomical pathways involved in infarcts.

    • Main Results:

    • Absence of aphasia in some dominant hemisphere striatocapsular infarcts contradicts direct basal ganglia involvement.
    • Linguistic deficits are linked to cortical hypoperfusion and potential thalamic disconnection.
    • Thalamic lesions affecting the frontal lobe-inferior thalamic peduncle system disrupt attentional gating and working memory.

    Conclusions:

    • Subcortical aphasia is unlikely due to direct basal ganglia damage.
    • Cortical hypoperfusion and thalamic pathway disruption are key mechanisms.
    • Deficits in selective engagement and working memory underlie language impairments in subcortical lesions.