June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
How Does Tear Breakup Trigger the Ocular Surface Sensory Response?
Author Affiliations & Notes
  • Jun Zhang
    School of Optometry, Indiana University, Bloomington, IN
  • Carolyn G Begley
    School of Optometry, Indiana University, Bloomington, IN
  • Arthur Bradley
    School of Optometry, Indiana University, Bloomington, IN
  • Ping Situ
    School of Optometry, Indiana University, Bloomington, IN
  • Trefford L Simpson
    University of Waterloo, Waterloo, ON, Canada
  • Footnotes
    Commercial Relationships Jun Zhang, None; Carolyn Begley, None; Arthur Bradley, None; Ping Situ, None; Trefford Simpson, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 361. doi:https://doi.org/
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      Jun Zhang, Carolyn G Begley, Arthur Bradley, Ping Situ, Trefford L Simpson; How Does Tear Breakup Trigger the Ocular Surface Sensory Response?. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):361. doi: https://doi.org/.

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

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Purpose: Previous studies in our laboratories have shown that increasing tear breakup (TBU) was associated increased discomfort during blink suppression (Varikooty et al, 2009, Begley et al, 2013) and that increased hyperosmolarity within areas of TBU may be a factor in causing the discomfort (Liu et al, 2010) . The purpose of this study was to use changes in fluorescence intensity within areas of TBU to estimate increases in osmolarity over time, and to compare these estimates to the pain response.

Methods: After instillation of 2 microliters of sodium fluorescein dye, 10 subjects were seated behind a slit lamp biomicroscope and kept one eye open as long as possible while turning a “pain knob” (0-10 scale) to indicate the discomfort level during blink suppression. Images of the tear film were converted to grayscale and analyzed by custom MATLAB programs that (1) analyzed the area of TBU over time and (2) the percent changes in pixel intensity (PI%) in the leading area of TBU. Changes in osmolarity within areas of TBU were estimated, with the assumption that evaporation is the main mechanism in TBU (King-Smith et al, 2008) and that tear film thickness is proportional to the square root of the fluorescence intensity (Nichols et al, 2012).

Results: The TBU area ranged from 0.41% to 76.4% of the corneal area, with an average of 13.0%±17.0%. The range and average slope of the pain knob, the TBU% area and the %PI was 0.9-2.9/sec (average of 1.5±0.6sec), 0.01 to 7.86%/sec (average of 2.81±2.41), 2.87-18.35% (average of 7.41±4.87), respectively. The pain was significantly correlated with the decrease in PI% and TBU slope (Pearson's, r=0.673 and 0.592, respectively; p<0.05). Using this method, most subjects exhibited a linear decrease in PI%, suggesting an increase in hyperosmolarity that exceeded the following: 500mOsm/Kg at pain knob level 4, 600MOsm/Kg at level 6, 900mOsm/kg at level 8 and 1000mOsm/Kg at level 10.

Conclusions: Although more accurate estimates could include other factors, such as local fluid flow, osmosis and diffusion (Braun et al, Prog Retin Eye Res, in press), these results provide a connection between pain and “ballpark” estimates of increases in tear film hyperosmolarity within areas of TBU.


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