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Related Experiment Videos

Functional imaging of working memory in obstructive sleep-disordered breathing.

Robert J Thomas1, Bruce R Rosen, Chantal E Stern

  • 1Division of Pulmonary Critical Care and Sleep Medicine, Department of Medicine, CC-866, Sleep Unit, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. rthomas1@bidmc.harvard.edu

Journal of Applied Physiology (Bethesda, Md. : 1985)
|January 29, 2005
PubMed
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Obstructive sleep-disordered breathing (OSDB) impairs working memory, particularly in the prefrontal cortex. Sleep fragmentation, not just hypoxia, may cause cognitive dysfunction in OSDB patients.

Area of Science:

  • Neuroscience
  • Sleep Medicine
  • Cognitive Psychology

Background:

  • Obstructive sleep-disordered breathing (OSDB) is linked to cognitive deficits.
  • The neural underpinnings of these deficits, especially in working memory, require further elucidation.
  • The roles of nocturnal hypoxia and sleep fragmentation in cognitive impairment are debated.

Purpose of the Study:

  • To investigate cerebral activation patterns during a working memory task in patients with OSDB compared to healthy controls.
  • To assess the effects of positive airway pressure treatment on cognitive performance and brain activity in OSDB patients.
  • To determine the contribution of nocturnal hypoxia versus sleep fragmentation to cognitive dysfunction in OSDB.

Main Methods:

  • Functional magnetic resonance imaging (fMRI) was employed to map brain activity.

Related Experiment Videos

  • A 2-back verbal working memory task was administered to 16 OSDB patients and 16 healthy controls.
  • Six OSDB patients underwent follow-up fMRI after 8 weeks of positive airway pressure treatment.

    • Main Results:

    • OSDB patients exhibited significantly slower working memory speed and absent dorsolateral prefrontal activation compared to controls.
    • Treatment with positive airway pressure led to subjective improvement in sleepiness but no significant change in behavioral performance or prefrontal activation.
    • Partial recovery of posterior parietal activation was observed post-treatment, alongside persistent hypofrontality.

    Conclusions:

    • Working memory impairment in OSDB is associated with disproportionate dysfunction in the dorsolateral prefrontal cortex (hypofrontality).
    • Sleep fragmentation, rather than nocturnal hypoxia alone, may be sufficient to cause cognitive dysfunction.
    • Dissociations exist between respiratory and cortical recovery, and between subjective and objective measures of improvement, suggesting complex recovery trajectories.