Vol. 2, #17   •   Thursday, July 22, 2021


Review's Chief Clinical Editor
Paul M. Karpecki, OD, FAAO

Provides you with cutting-edge clinical strategies for optimal management of ocular surface disease and beyond.


Another Cause of Dry Eye That Isn’t Dry Eye

Neurolens reading

Here is another case debunking the idea that DED is simple to manage and based heavily on symptoms.

A patient came in for an examination complaining that his LASIK surgery from two years prior was causing his dry eyes. His symptoms were worse late in the day and especially when he was reading or on a computer/digital device. It sounded like DED…until we started testing.

Osmolarity measured 296/295mOsmol/L, meibomian gland expression was a 3 in 8 of the 10 glands tested (clear, olive oil-type expression). The patient had inferior staining grade 1 and a 5-second TFBUT, but no conjunctival staining and an adequate tear meniscus. I told him he probably didn’t have dry eyes. He pulled out a bag of drops, pills, and devices he’d used over the last two years, and said he’d spent almost as much on DED treatments as his original LASIK surgery and nothing helped. I asked him if he experienced headaches, dizziness, or neck stiffness. He stated he had all of these symptoms but didn’t think it was related to his eyes. I asked if he wore contact lenses prior to having LASIK. He said he wasn’t able to as his “eyes were too dry” when he tried to wear contacts. I then tested his binocular vision, which revealed exophoria at distance and near. I asked him to bring the glasses he wore before LASIK. He dropped them off the next day, and we measured -4.50D OU with 0.50 of BI prism.

He was suffering from a condition known as trigeminal dysphoria (TD). When patients have small amounts of BI prism fusional requirements, their trigeminal nerve tends to get overstimulated during the numerous pursuits and saccades per day. A small amount of prism (4.5D of myopia alone induces BI prism) was aiding him prior to LASIK. After surgery and the loss of glasses, his fusional capabilities were not sufficient, leading to overstimulation of the nerve. Recall that one of the branches of the trigeminal nerve is the ophthalmic, which innervates the cornea. So it’s not uncommon to hear patients with TD describe dry eyes (along with frequent headaches, dizziness, and/or neck stiffness).

Treatment options include vision therapy or prescribing prism. This patient, like many patients with TD, had a far greater prismatic need at near than distance. Today, Neurolens technology can provide a contoured prism with greater prism at near than far. The patient’s neurolens test showed 1.8 EXO at distance and 8.0 EXO at near. He received a pair of neurolenses (with a plano Rx) that provided the ideal amount of prism at near and far—and all of his symptoms, including eye dryness, resolved.

One major clue to this diagnosis was that topical steroids—EYSUVIS is the only corticosteroid approved for the short term treatment of dry eye signs and symptoms—didn’t improve his symptoms. A short-term steroid trial showed that another condition was likely causing the dry eye symptoms.

KEY TAKEAWAY: DED is not a symptoms-only-based disease. When signs don’t correlate and topical agents like corticosteroids don’t help, consider another diagnosis. One of the often-overlooked causes of dry eye symptoms, when few or no signs are present, is trigeminal dysphoria.

Supported by an independent medical grant from Kala Pharmaceuticals

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