Chronic Dry Eye and Pain

Laura Periman, MD

#EvenCowgirlsGetTheBlues – Part III

Originally Published on Ophthalmology Management

Part III: Ocular Surface Disease as seen through lessons learned on the Montana Ranch.

Chronic Dry Eye Pain is like being saddle sore, blistered up and with no end to the ride in sight. The last thing your long-suffering patient needs to hear is just stay the course.

All may look well on the ocular surface to your exam, yet your patient describes significant pain and impacts on their quality of life. Confocal microscopy gives us insight into real disease that your careful examination cannot reveal. Neuroscientific advances reveal that central processing of pain is remarkably complex. It seems like eye pain can be distilled into four main buckets: pain stimuli, signaling, amplification and central processing (aka the Big Black Box).

Optimize the surface. Think Physiologic Restoration. By controlling inflammation, you also control a chronic wound healing response and an innate upregulatory nociceptive mechanism. It is a good mechanism for protecting the cornea during acute phases of healing, but in the face of chronic inflammation of dry eye disease, it becomes dysfunctional. Cytokine mischief makers IL-1 and TNF upregulate NGF (nerve growth factor). NGF receptors induce epithelial cell “fence” damage (via apoptosis) and corneal nerve dysmorphology as seen on confocal microscopy.

Messages from the surface to the brain are carried by interesting corneal nerve subtypes polymodal, mechanical, temperature nerves and nacent nerves that lie in reserve ready to upregulate, respond.

For your patient, the stampede noise from the corneal pain receptors can be thunderous. Nociceptors that tell the brain which direction the stampede is coming from include:

•  Thermoreceptors (fire at lower temperature deltas in CDED)
•  Osmoreceptors (fire at increasing amplitudes to a certain point then stop…almost like if there’s no one listenin’, I’ll just stop talkin’)
•  Mechanoreceptors; and my personal favorite…
•  Inflammation-inducible nociceptors (like an amplifier that reminds me of the classic rockumentary spoof, Spinal Tap #ThisOneGoesToEleven).

Along with optimizing the surface and addressing the corneal sub basal plexus dysmorphology of Chronic Dry Eye Disease, think about teaming up with other medical subspecialties to address more central pain mechanisms. Loss of descending inhibitory pain pathways are implicated in Neuropathic Dry Eye Pain and our fine colleagues in Neurology, Pain Management and Psychiatry can be asked to help so that you and your patient don’t have to ride alone.

The original diagram can be found in the TFOS DEWS II pain and sensation report.

Me and my grandpa on the ranch.

The entire TFOS DEWS II report is available to all for free at

Laura M. Periman, MD is Director of Dry Eye Services and Clinical Research at Evergreen Eye Center in Seattle, WA. Relevant to this series, she discloses relationships with Allergan, Bio-Tissue, Eyedetec, Lumenis, Science Based Health, Sun Pharmaceuticals, TearLab, Topcon and Visant.