AOA 2026: Why some patients with dry eye feel pain and others do not

Kaleb Abbott, OD, MS, FAAO, FOWNS, an assistant professor at the University of Colorado School of Medicine, discussed one of the central challenges in managing dry eye disease: the discordance between clinical signs and patient-reported symptoms. He emphasized that eye care providers frequently encounter patients who report severe discomfort—burning, grittiness, light sensitivity, and pain—while the ocular surface appears only mildly affected or even relatively normal. Conventional indicators such as corneal staining, tear breakup time, blepharitis severity, and meibomian gland dysfunction (MGD) often do not fully explain the symptom burden.

To account for this mismatch, Abbott focused on neural mechanisms and pain processing. He explains that in many such patients, the ocular symptoms may actually represent a peripheral manifestation of a systemic pain or sensitization condition, often referred to as central sensitization. In these cases, it is not simply “dry eye” driving symptoms, but broader systemic dysregulation of pain pathways. Another key entity he highlighted is neuropathic corneal pain or peripheral sensitization, in which hypersensitive corneal nerves generate disproportionate symptoms even in the absence of significant ocular surface damage.

Abbott stressed the importance of determining whether the pain is ocular or non-ocular in origin. The most practical clinical tool he recommends is a proparacaine challenge: clinicians assess baseline symptoms, instill topical anesthetic (proparacaine) in both eyes, wait approximately two minutes, then reassess symptoms. A substantial reduction in discomfort (around 50% or more) suggests that symptoms are predominantly driven by the corneal nerves—whether from traditional dry eye mechanisms, neuropathic corneal pain, or a combination such as “neuropathic dry eye.” Minimal or no improvement points to non-ocular, upstream pathways involving the trigeminal nerve or central pain processing centers.

The primary risk of misdiagnosis, Abbott noted, is not catastrophic ocular harm but ineffective care—wasted time, money, and treatment trials that fail to address the true pain source. He concluded by contrasting this scenario with neurotrophic keratitis, where patients may exhibit significant corneal staining and classic dry eye signs but report few or no symptoms. In these cases, diminished corneal sensation on testing (eg, with a cotton wisp or dental floss) reveals that the nerves are not adequately transmitting sensory information, indicating a nerve pathology that requires a fundamentally different management approach than standard dry eye therapy.