A young male patient in his mid-20s was recently referred to our office by his neuro-ophthalmologist to evaluate his dry eye symptoms. He had been diagnosed with multiple sclerosis (MS) one year ago. Although he was fairly symptomatic (Ocular Surface Disease Index: 68.2), the majority of his slit lamp examination was completely normal. His tear prism was adequate, and a phenol red thread test showed >30mm of wetting in 15 seconds.

Vital dye staining of the cornea and conjunctiva (with sodium fluorescein and lissamine green) was completely negative; however, other indications of inadequate lubricity and tear film instability were present: mild flakes in the upper lashes, asymmetric and elevated tear film osmolarity, a positive InflammaDry (Rapid Pathogen Screening, Inc.) test (which indicates elevated levels of matrix metalloproteinase-9), reduced tear breakup time, and grade 1 lid wiper epitheliopathy. He also presented with incomplete blinks and lagophthalmos. Approximately 30% of his meibomian glands were capped. The lids showed adequate apposition to the globe, without notching or scalloping; mild posterior lid margin inflammation was observed.

Meibography revealed the biggest surprise and, undoubtedly, the largest contributor to his symptoms: only about six meibomian glands remained in his upper lids, all in various stages of atrophy. His lower glands were faring much better, with 90% present, although again, all at various degrees of truncation. Of the glands that expressed with digital pressure, the meibum was normal to slightly turbid.

MS and the Ocular Surface

Patients who have MS are at particular risk for developing dry eye disease. Inflammation in the central nervous system can cause myelin sheath damage. Because myelin protects and insulates the underlying nerve axon, disruptions in this coating cause reduced processing times. Ultimately, damage to the underlying nerve fiber can occur, resulting in some neurological signs associated with MS (i.e., fatigue, tingling, numbness, spasticity, gait changes, reduction in higher-level brain function, dysarthria, and dysphonia, to name a few) (National Multiple Sclerosis Society).

These changes can also result in the potential development of sensory issues with the cornea, reduced ocular motor responses to environmental stimuli (including reduced aqueous production), and exposure due to lid closure failure because of muscle limitations (Lewandowska-Furmanik et al, 2011; Prasad and Galetta, 2010; Jung et al, 2000).

Although there is almost no information specifically linking meibomian gland dysfunction with MS, it makes sense that it has a higher likelihood of developing alongside MS. Reduced corneal sensitivity, exposure, and a decreased response to environmental stimuli can disrupt ocular surface homeostasis. If the tears are unstable, evaporation rates increase, and osmolarity rises. Chronically elevated osmolarity initiates inflammatory cascades, which become detrimental to the delicate meibomian glands over time.


Our patient was treated with lid margin exfoliation via BlephEx (BlephEx, LLC); 2,000mg of oral omega-3s daily; nonpreserved, lipid-based artificial tears; blink exercises; and daily warm compresses with a commercial mask, followed by lid massage and commercial lid scrubs. We also initiated a short course of topical corticosteroids until the InflammaDry test was negative.

Although it may seem controversial due to the high degree of meibomian gland atrophy in this case, Lipiflow (TearScience) was prescribed to help preserve his remaining glands. Daily cyclosporine ophthalmic emulsion was also prescribed. This medication has a better safety profile compared to long-term corticosteroids in managing chronic inflammation, and it improves tear film stability, reduces meibomian gland inclusions, and increases goblet cell density (Prabhasawat et al, 2012; Perry et al, 2006; Pflugfelder et al, 2008). CLS

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