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Conventional Wisdom is an Obstacle to Developing Effective Treatments for Dry Eye

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Conventional Wisdom is an Obstacle to Developing Effective Treatments for Dry Eye
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Conventional Wisdom is an Obstacle to Developing Effective Treatments for Dry Eye

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Dry eye surfaces cause dry eye symptoms. On the other hand, observations that chronic dry eye symptoms can be experienced by patients whose eyes have an ample supply of and occasionally overflowing supply of tears, questions the canonical belief that tears (deficient in quality and/or quantity) is the underlying disease. Although chronic Meibomian gland dysfunction increases the rate of tear evaporation, the assumption that it can cause dry eye disease has been refuted by Galor and others (Invest Ophthalmol Vis Sci 2013, 54(2):1426-1433).  Shouldn’t this study have given pause to those whose research is focused on tears?  Instead, it has been ignored.

Dry eye symptoms are a specific type of corneal pain. Moreover, damaged/diseased pain nerves increase their sensitivity to irritants, a physiological response known as hyperalgesia. In this context it is reasonable to explain the uniquely high density of corneal pain nerves (200% greater than that of skin) as serving to protect the most powerful focusing lens of our eyes — the mirror-smooth tear layer. Because of the existential importance of preserving its integrity in the face of an ongoing battle with evaporation, a complex, powerful and sensitive monitoring/alarm system evolved to sustain and maintain it. When the specialized tear evaporation sensors incorporated in many of the terminals of the corneal nerves sense that the optical tear layer has thinned to the point of imminent break up, they normally trigger a cascade of unconscious reflexes that restores its robustness. However, if these sensors are not silenced the alarm escalates to conscious sensations of dry eye-like pain. Therefore it is not surprising that the corneal hypersensitivity developed by damaged corneal nerves (all of which are designed to carry pain signals) is focused on tear evaporation (that I describe as corneal evaporative hyperalgesia). That inserting scleral lenses on these eyes immediately suppresses dry eye symptoms regardless of the tear volume (personal observations) points to corneal evaporative hyperalgesia being caused by (rather than being the cause of) the underlying disease. Nevertheless, the primary disease must also explain the statistical fact that patients with chronic dry eye symptoms have less tears as a group. This can be explained if evaporative corneal hyperalgesia and impaired tear production are independent complications of an underlying corneal neuropathy in which the former precedes its effect on impairing tear secretion sometimes by a period of years (personal observations).

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