Causes
When considering the underlying pathophysiology of Chronic Dry Eye, it is important to remember that it is not a condition of tear deficiency due to decreased tear production or increased tear evaporation. Clinical research suggests that the pathophysiology of Chronic Dry Eye is more complex in that the quality of tears is just as important – or maybe even more so – as the quantity of tears. Recent research also suggests that inflammation plays a role in tear quantity.
Several alterations in tear composition are now clearly associated with Chronic Dry Eye, including
- Altered protein and inflammatory cytokine profiles
- Increased osmolarity
- Decreased mucin content
These changes in the makeup of the tear film can, in turn, have profound effects on the ocular surface. Many aspects of tear production, tear composition, and the ocular surface appear to be interconnected by a neural feedback loop. Essentially, this neural loop controls tear production according to the composition of tears at the ocular surface. That is, tear composition is normally "sensed" by receptors on the ocular surface, and this information is transmitted via sensory (afferent) nerve fibers to the brain. In response, the brain then sends signals back via efferent nerve fibers to the tear-secreting glands. When stimulated by these secretomotor nerve impulses, the lacrimal glands secrete more tears.
Recent evidence suggests that there may be dysfunction of one or more aspects of this neural feedback loop in Chronic Dry Eye patients. For example, the increased osmolarity of tears in patients with dry eye can impact many aspects of the normal physiology of the ocular surface, affecting the ability of the sensory nerves to carry information to the brain. This results in a failure of the signaling system that would normally increase tear production.
Dry Eye can be an inflammatory cycle — underlying causes and signs are not always visible. In Dry Eye, a disrupted neural feedback loop appears to affect tear production:
- Abnormal tears inflame ocular surface
- Cytokines disrupt neural arc
- Brain signals lacrimal glands to activate T-cells
- Cytokines are delivered to ocular surface
Reference
- Stern ME, Beuerman RW, Fox RI, Gao J, Mircheff AK, Pflugelder SC. The pathology of dry eye: the interaction between the ocular surface and lacrimal glands. Cornea. 1998;17:584-589.
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RESTASIS® Ophthalmic Emulsion is indicated to increase tear production in patients whose tear production is presumed to be suppressed due to ocular inflammation associated with keratoconjunctivitis sicca. Increased tear production was not seen in patients currently taking topical anti-inflammatory drugs or using punctal plugs.
Important Safety Information:
RESTASIS® is contraindicated in patients with active ocular infections and has not been studied in patients with a history of herpes keratitis.
The most common adverse event was ocular burning (upon instillation) – 17%. Other events reported in 1% to 5% of patients included conjunctival hyperemia, discharge, epiphora, eye pain, foreign body sensation, pruritus, stinging, and visual disturbance (most often blurring).
Please see full prescribing information for RESTASIS® (cyclosporine ophthalmic emulsion) 0.05%.