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Related Experiment Videos

The irrelevant speech effect and working memory load.

Jens Gisselgård1, Karl Magnus Petersson, Martin Ingvar

  • 1Cognitive Neurophysiology, MR Research Centre, Department of Clinical Neuroscience, N-8, Karolinska Hospital, Stockholm 17176, Sweden. jens.gisselgard@cns.ki.se

Neuroimage
|June 29, 2004
PubMed
Summary
This summary is machine-generated.

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Irrelevant speech disrupts memory recall by altering brain activity. Increased working memory load recruits additional brain regions, suggesting complex compensatory mechanisms are involved in the irrelevant speech effect.

Area of Science:

  • Cognitive Neuroscience
  • Neuroimaging
  • Psychology

Background:

  • Irrelevant speech impairs immediate serial recall of visual information.
  • Previous studies linked the irrelevant speech effect (ISE) to reduced blood flow in the superior temporal cortex.
  • Verbal working memory relies on specific cortical regions.

Purpose of the Study:

  • To investigate the neural correlates of the irrelevant speech effect (ISE) under increased working memory load.
  • To explore how working memory load modulates brain activity in response to irrelevant speech.
  • To understand the network-based nature of the ISE.

Main Methods:

  • Functional neuroimaging (likely fMRI or PET) was used to measure regional blood flow.
  • Participants performed a verbal working memory task with varying loads.

Related Experiment Videos

  • Irrelevant speech was presented during task performance.

    • Main Results:

    • Increased working memory load led to heightened activity in the dorsolateral prefrontal cortex in response to irrelevant speech.
    • No single brain region was identified as the sole locus of the ISE.
    • Brain areas sensitive to ISE are also activated by the verbal working memory task itself.

    Conclusions:

    • The irrelevant speech effect (ISE) is not localized to a single brain area but involves dynamic networks.
    • Brain activity related to ISE is modulated by working memory load.
    • Mechanisms include top-down inhibition (low load) and recruitment of compensatory processes (high load).