Thesis (Ph.D.) - Indiana University, Optometry, 2014Dry eye is a common condition that affects millions in the US and worldwide. It is considered to be a multifactorial disease of the tear film and ocular surface and is associated with symptoms of ocular discomfort and visual disturbance. Low blink rate has been identified as a potential risk factor for the development of dry eye because it can result in increased evaporative loss from the tear film. Failure of tear secretion has also been recognized as one of the main factors for dry eye development, characterized as low tear volume and slow tear turnover rate. Both factors in turn may lead to increased tear film hyperosmolarity and instability, which are considered core mechanisms of dry eye. In the natural condition, the ocular surface is mainly protected by blinking and tear secretion in that the newly secreted tears flow into the upper and lower meniscus and the blink spreads the new tear film from the meniscus to the ocular surface. Therefore, the ocular surface control over blinking and tear secretion is important in the etiology of the dry eye condition. In this proposal, we develop a laboratory model using human subjects to test how input from the ocular surface affects both blinking and tear secretion. We hypothesize that ocular surface stimuli will activate corneal receptors to signal a high blink rate, reflex tear secretion and ocular sensations of discomfort. These probably act together for the purpose of preventing ocular damage. These results will help us to understand the manner in which the ocular surface responds to adverse stimuli, which may ultimately lead toward further development of treatments or methods in dry eye patients.