April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Visual perception and oculomotor control are robust to acute hypoxia
Author Affiliations & Notes
  • Charlotte Joy Waikauri Connell
    Exercise Neurometabolism Laboratory, University of Auckland, Auckland, New Zealand
  • Jhordaine B Charlton
    Exercise Neurometabolism Laboratory, University of Auckland, Auckland, New Zealand
  • Clare E Turner
    Exercise Neurometabolism Laboratory, University of Auckland, Auckland, New Zealand
  • Joanna M Black
    Department of Optometry and Vision Science, University of Auckland, Auckland, New Zealand
  • Gustav Kuhn
    Department of Psychology, Goldsmiths, University of London, London, United Kingdom
  • Michael P Claffey
    Department of Psychology, University of California, San Diego, CA
  • Benjamin Thompson
    Department of Optometry and Vision Science, University of Auckland, Auckland, New Zealand
  • Nicholas Gant
    Exercise Neurometabolism Laboratory, University of Auckland, Auckland, New Zealand
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 2577. doi:
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      Charlotte Joy Waikauri Connell, Jhordaine B Charlton, Clare E Turner, Joanna M Black, Gustav Kuhn, Michael P Claffey, Benjamin Thompson, Nicholas Gant; Visual perception and oculomotor control are robust to acute hypoxia. Invest. Ophthalmol. Vis. Sci. 2014;55(13):2577.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Hypoxia impairs cerebral metabolism and represents a significant challenge to brain homeostasis and cognitive function. Therefore, experimentally-induced hypoxia provides a model for brain injuries that impair cellular energy provision. The aims of this study were 1) to investigate the effect of acute, severe hypoxia on visual perception and saccadic eye movements, and 2) compare the effects of hypoxia on visual and cognitive function.

Methods: Within a single-blind, randomized, matched-pairs design, 26 healthy participants (10 male) inspired either a hypoxic (FIO2 = 0.10) or sham (FIO2 = 0.21, atmospheric air) gas mixture for 90 min. Saccadic eye movements, assessed within the context of an established social attention paradigm, were measured at baseline and intervention. Global motion perception and cognitive performance were assessed using random dot kinematograms and the CNS Vital Signs test battery respectively. In addition, chromatic discrimination (Farnsworth-Munsell 100-hue test), perceived symptoms of hypoxia (environmental symptoms questionnaire), cardiovascular responses and oxygen saturation were recorded at regular intervals throughout the protocol.

Results: Hypoxia significantly reduced arterial oxygen saturation (SaO2 = 79 ± 6%, p < 0.001) and severely impaired a wide range of cognitive processes, compromising neurocognitive index scores by -20 ± 13% (p = 0.025). Saccadic eye movements (peak velocity, latency and accuracy), global motion perception, and chromatic discrimination were not affected by hypoxia. However, visual disturbances including blur and dimmed vision were reported on the environmental symptoms questionnaire during the hypoxic condition.

Conclusions: Oculomotor control and visual perception are robust to a severe hypoxic insult that significantly impairs higher order cognition. Visual disturbances reported by participants during hypoxia did not influence objective measures of visual function. Energy provision to networks responsible for controlling saccadic eye movements, global motion perception and color perception appear to be protected during a severe, acute oxygen deficit.

Keywords: 522 eye movements • 548 hypoxia • 641 perception  
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