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We are all headache doctors
There is a curious but undeniable connection between dry eye disease and migraine.
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One of my earliest columns on dry eye disease shared the sad news that each and every one of you is a red eye doctor. Yes, even you, esteemed Dr. Retina, are a red eye doctor, at least if you care about the things that your patient cares about. Well, I am back with more important albeit equally sad news about what kind of doctor you all are. I, you, we are all headache doctors.
Say it with me: “I am a headache doctor, and I am proud.”
Like the Four Horsemen of the Apocalypse, we have the Four Nags in the Clinic: headache, back pain, dry eye and “sinus.” Ophthalmologists own all four, although our ownership of back pain is because we personally suffer from back (or neck) pain. Objective dry eye signs are present in roughly 50% of patients who appear in an eye clinic for a routine exam (SkyVision Center data) and can be present in up to 80% of asymptomatic patients who are being seen for other eye care issues such as anterior segment surgery (hat tip to Preeya Gupta and Chris Starr). As I have oft stated, you ignore this reality at your own peril no matter what type practice you have.
Everyone, be they esteemed or not, sees patients who are referred to their clinic for the evaluation of headache. While some chronic headache patients have been seen by all manner of other specialists before they get to you, often is the case that you are the very first stop on their diagnostic odyssey. It goes like this: “My doctor sent me to see you to make sure that my headaches aren’t coming from my eyes. My CAT scan was normal. I’ve tried everything. Is it my eyes, or do you think I have sinus?”
I have no idea what “sinus” is, but apparently it is No. 2 on the differential diagnosis of every pain occurring above the collarbone.
Once again, I owe a deep debt for my growing understanding of the connection between headache and the eye to Kathleen Digre, MD, of Moran Eye Center in Utah and her 2017 Hoyt Lecture on the eye and migraine. Everyone should read it at least once; I have now read it at least five times and pull something new from each reading. There is a curious but undeniable connection between DED and migraine, one that was most recently described by the Bascom Palmer folks in a Veterans Affairs study. Did you know that 18% of women and 6% of men suffer from migraines, making migraine more common than diabetes and asthma combined? Does that 3:1 female:male ratio seem familiar? Looks an awful lot like the ratio we see in a DED clinic.
Dr. Digre lays out the shared neuroanatomy of the eye and the dura in exquisite detail, a task that is well beyond the ability of yours truly to reproduce. Suffice it to say that trigeminal activation gives rise to both eye pain and migraine (dural) pain, and that both are also tied to autonomic dysfunction in either the sympathetic or parasympathetic pathways (or both). Confocal microscopy shows a decrease in the density of corneal sensory nerves in both DED and migraine. Migraine is thought to be caused by a central sensitization in the pain pathways of the dura, pathways that are for the most part identical to those that innervate the eye and the orbital contents. More specific to DED, the autonomic innervation of the lacrimal functional unit is indistinguishable from that of the dura.
There is an incredible overlap in both the signs and symptoms of DED and migraine. In the simplest case, many chronic migraine headaches either include eye pain or have pain that is centered primarily around one eye. A burning sensation is a common description of the eye pain. Patients with both entities complain of light sensitivity (probably a topic worthy of a column all its own), often in the absence of any signs of inflammation. Blurred vision is a significant complaint as well. Indeed, DED is almost certainly the second most common cause of blurred vision in the developed world behind only uncorrected refractive errors. Classic migraine is associated with a pre-headache aura, often vision related. “Heat waves,” bright lights in the shape of a chevron, and scotomata of various types precede the stereotypical pain.
What about ocular signs, then? As noted above, there is a similar decrease in corneal sensory nerve density on confocal microscopy. Right. About that. Owing to its exorbitant cost and the fact that you cannot bill for the test, confocal microscopes are about as rare as amblyoscopes in eye clinics. (Google it. Gonna come up next month.) A more plebian exam will show that a decreased Schirmer test and decreased tear breakup time are seen in both DED and migraine. Due to the shared involvement of autonomic innervation, you can see conjunctival injection in the absence of staining in both entities. With or without the presence of redness, you can determine if photophobia is at least partially due to DED if a drop of Alcaine (proparacaine hydrochloride ophthalmic solution 0.5%, Novartis) provides relief.
Once you have gathered up all of your data, it is time to treat your patient’s headache. Yes, you the eye doctor, you must initiate at least a part of the headache solution. How? Well, this is The Dry Eye column: Treat the dry eye, however minimal the signs may be. Tear osmolarity and the presence or absence of meibomian gland dysfunction should allow you to make an informed choice of artificial tear. Go ahead and prescribe an omega-3 fatty acid supplement. Be super aggressive in the treatment of any signs of inflammatory DED, such as staining (cornea or conjunctiva), a positive InflammaDry (Quidel) or tear osmolarity that is elevated or asymmetric; put the patient on Restasis (cyclosporine ophthalmic emulsion 0.05%, Allergan), Cequa (cyclosporine ophthalmic solution 0.09%, Sun Pharma) or Xiidra (lifitegrast ophthalmic solution 5%, Shire), with or without a steroid. If you think there is a significant aspect of true neurogenic eye pain, consider Neurontin (gabapentin, Pfizer) or direct stimulation of the trigeminal nerve with TrueTear (Allergan). Go ahead and prescribe FL-41 lens filters for patients with photophobia (again, more next month).
It is quite possible that treating dry eye will effectively treat at least some part of a patient’s migraine. How about the other way around? If you aggressively treat migraine, will you also relieve eye pain otherwise thought to be due to DED? Sure, but that does not mean you and I should be writing prescriptions for medicines we have not used since medical school. Lamotrigine? Yikes! Make friends with a neurologist. Some of you may decide to go all in and learn about Botox (onabotulinumtoxinA, Allergan) injections to treat migraine. My only concern is that someone will discover that I am treating migraines with Botox and try to get me to treat their frown lines, too. We are all headache doctors, but I draw the line at treating whatever headaches caused those frown lines to appear in the first place.
Next thing you know, someone will try to make me a “sinus” doctor.
Next: Dry eye, migraine and the computer.
- References:
- Digre KB. J Neuroophthalmol. 2018;doi:10.1097/WNO.0000000000000660.
- Lee CJ, et al. Pain Rep. 2017;doi:10.1097/PR9.0000000000000629.
- For more information:
- Darrell E. White, MD, can be reached at SkyVision Centers, 2237 Crocker Road, Suite 100, Westlake, OH 44145; email: dwhite@healio.com.
Disclosure: White reports he is a consultant to Allergan, Shire, Sun, Kala, Ocular Science, Rendia, TearLab, Eyevance and Omeros; is a speaker for Shire, Allergan, Omeros and Sun; and has an ownership interest in Ocular Science and Eyevance.