Neural consequences of sleep disordered breathing: The role of intermittent hypoxia

  • Morrell M
  • Twigg G
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Sleep disordered breathing is characterised by periodic breathing,
episodes of hypoxia and repeated arousals from sleep; symptoms include
excessive daytime sleepiness, impairment of memory, learning and
attention. Recent evidence from animal studies suggests that both
intermittent hypoxia and sleep fragmentation can independently lead to
neuronal defects in the hippocampus and pre frontal cortex; areas known
to be closely associated with neural processing of memory and executive
function. We have previously shown that sleep disordered breathing is
associated with loss of gray matter concentration within the left
hippocampus (47). We have now confirmed and extended this finding in 22
right handed, newly diagnosed male patients (mean (sd): age 51.8 (15.4)
yrs, apnea/hypopnea index 53.1 (14.0) events/hr, minimum nocturnal
oxygen saturation 75 (8.4) %) and 17 controls matched for age and
handedness. Voxel-based morphometry, an automated unbiased technique,
was used to characterise changes in gray matter concentration. The
magnetic resonance images were segmented and grey matter concentration
determined voxel by voxel. Analysis of variance was then preformed,
adjusted for overall image intensity, with age as a covariant.
Additional to the deficit in the left hippocampus, we found more
extensive loss of gray matter bilaterally in the parahippocampus. No
additional focal lesions were seen in other brain regions. Based on our
findings and data from other human and animal studies, we speculate that
in patients with sleep disordered breathing intermittent hypoxia is
associated with neural deficit, and further that such lesions may lead
to cognitive dysfunction.

Author-supplied keywords

  • Cognitive
  • Memory
  • Periodic breathing
  • Sleep apnea

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  • Mary J. Morrell

  • Gillian Twigg

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