September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Mechanisms involved in tear break-up as revealed by pain response
Author Affiliations & Notes
  • Carolyn G Begley
    School of Optometry, Indiana University, Bloomington, Indiana, United States
  • Jun Zhang
    School of Optometry, Indiana University, Bloomington, Indiana, United States
  • Richard J Braun
    Dept of Mathematical Sciences, University of Delaware, Newark, Delaware, United States
  • Peter Ewen King-Smith
    College of Optometry, The Ohio State University, Columbus, Ohio, United States
  • Footnotes
    Commercial Relationships   Carolyn Begley, None; Jun Zhang, None; Richard Braun, None; Peter King-Smith, None
  • Footnotes
    Support  The project was supported by Grant Number R01EY021794 (Dr. Begley) from the National Eye Institute.
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 6166. doi:
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    • Get Citation

      Carolyn G Begley, Jun Zhang, Richard J Braun, Peter Ewen King-Smith; Mechanisms involved in tear break-up as revealed by pain response. Invest. Ophthalmol. Vis. Sci. 2016;57(12):6166.

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

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Abstract

Purpose : We postulate that two basic mechanisms are primary in many cases of tear break-up (TBU), evaporation and the lipid-driven Marangoni effect. Evaporation-dominated TBU would be expected to lead to a relatively gradual increase in the pain response due to increasing tear film osmolarity, whereas fluid flow dominated TBU would not be expected to produce pain until the area of TBU exposes or dries the corneal surface. The purpose of this pilot study was to examine the formation of TBU and the pain response to determine whether pain responses follow these patterns.

Methods : After instillation of 2 microliters of 2% sodium fluorescein dye, 10 subjects were seated behind a slit lamp biomicroscope and kept one eye open as long as possible (maximum blink interval=MBI) while turning a “pain knob” (0-10 scale) to indicate the discomfort level during blink suppression (3 trials for each subject). Images of the tear film were converted to grayscale and analyzed by custom MATLAB programs that analyzed the rate of changes in pixel intensity over time and compared it to the slope and rate of change of the pain response.

Results : Eight subjects (average MBI= 15.26±10.93s) with relatively long trials showed gradual decreases in fluorescence within areas of TBU and gradual increases in discomfort (average slope = 2.157±2.447, 1.331±0.906, respectively) initially. Two subjects with short trials (average MBI= 7.48±0.18s) showed very rapid formation of the percentage of TBU area (slope =4.043±3.700), with no discomfort for several seconds (average 4.634±1.528), followed by pain that induced rapid eye closure (average slope=4.742±4.502).

Conclusions : The relatively gradual increase in discomfort in the trials of 8 subjects is consistent with evaporation-dominated TBU, producing pain through increasing tear osmolarity. In contrast, TBU formed by Marangoni-driven fluid flow that rapidly exposes the corneal surface, producing sudden sharp pain is a likely explanation for the formation of TBU in the remaining 2 subjects. The rate of change of fluorescence within areas of TBU or thinning, and the associated pain response, suggest that more than one mechanism may be operative in the formation of TBU.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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