by Michael S. Cooper, OD
Dry eye may initially be pretty low on the list of medical concerns for patients recovering from traumatic brain injury, with much more emphasis placed on regaining critical functions like mobility and speech.
However, it is very common for there to be ocular surface consequences to a traumatic brain injury (TBI), sometimes for years afterwards. Awareness of the link may help solve some mysteries — and bring welcome relief — to patients in your practice.
There can be neurological, mechanical and even inflammatory causes behind dry eye in post-TBI patients.
Michael S. Cooper
For example, we know that there is an eye-brain feedback loop that is critical for healthy tear production and tear film homeostasis. The nerves in the cornea originate from the ophthalmic branch of the trigeminal nerve, also known as the fifth cranial nerve. Together, these cranial and corneal nerves are responsible for detecting sensation and reporting pain — actions that signal tear production, the blink reflex, and the release of important immune factors and nutrients into the tears.
Damage to the brain can disrupt this cycle, dramatically reducing the production of aqueous. Work done with Allergan’s TrueTear device suggests that neurostimulation of the trigeminal nerve can increase production of mucins and lipids, in addition to aqueous (Dieckmann et al., Green et al.). For problems with a disrupted tear feedback loop, lubrication and hydration can be beneficial. Depending on the patient’s status and access to other treatments, the clinician may want to add topical anti-inflammatory medications or in-office procedures, such as punctal occlusion, nasal neurostimulation or thermal pulsation therapy.
Nerve injury in the brain can lead to trigeminal neuralgia, a chronic, neuropathic form of ocular pain, dryness or other discomfort that often seems out of proportion to ocular surface signs. And of course, optic nerve damage can lead to vision loss.
We can also find that brain injury leads to corneal denervation. This may be due to nerve loss in the brain or to a reduction in the release of neurotrophic factors into the tear film. In any case, it can result in a loss of sensation and a neurotrophic form of dry eye that, untreated, may progress to neurotrophic ulcers.
Oxervate (cenegermin-bkbj ophthalmic solution 0.002%, Dompé) is a recombinant form of human nerve growth factor that targets this nerve pathology. Autologous serum harvested from the patient or viable donor can also be of assistance in these cases as a compound (suggestion 20% concentration) containing a hyperdose of sorts in natural tears such as growth factors, neuromediators, cytokines and vitamins (Matsumoto et al.). Additionally, there is evidence seen in my clinic and in the literature illustrating that Bio-Tissue’s Prokera, a cryopreserved wet amniotic membrane technology, has a valid place in the management of these patients (Chen et al., Lee et al.).
Sometimes, other conditions can mimic dry eye symptoms, adding to the discomfort. Misalignments and problems with eye tracking, which are extremely common following a TBI, can overstimulate the trigeminal nerve. Tracking problems can be quantified using an eye tracking device such as the RightEye Brain Health EyeQ test. Misalignments can be evaluated and relieved by the Neurolens Measurement Device and the company’s contoured prism lenses. In other cases, other neuro-rehabilitation tools (prisms, selective occlusion, tints, filters) or even, in some cases, a simple change in the spectacle prescription can be effective.
Patients may also have lagophthalmos after TBI, causing punctate keratopathy that is exposure-related rather than due to any underlying disease. When I see post-TBI patients who are in rehabilitation or skilled nursing facilities, it is not uncommon for a care giver to tell me that the patient’s eyes are constantly tearing and, upon examination, I find severe punctate keratopathy, particularly in the inferior region. A night mask or taping the lids closed at night can help prevent exposure keratopathy.
Not everyone will be treating TBI patients in a rehabilitation setting. However, even after recovery, dry eye symptoms can persist and may be seen in your clinic.
I recently saw a new patient who came in complaining of a decline in vision over the past 2 years, as well as ocular irritation and headaches. After examining him thoroughly, I asked him if he had ever been in a car accident or had a head injury. When I asked that question, he immediately took off his hat to show me an old injury in which he had been hit in the head by an assailant wielding a crowbar. The incident had occurred more than 6 years ago, and he had not connected it to the more recent onset of symptoms, but, in fact, that fight led to traumatic optic neuropathy and other related problems.
This case is a good illustration of the benefit of just adding a few questions to your history about concussions, accidents and head injuries. If we don’t ask, we don’t know.
Chen HJ, et al. Br J Ophthalmol. 2000;doi:10.1136/bjo.84.8.826.
Dieckmann G, et al. Ophthalmol Vis Sci. 2017;58(8):2694.
Dua HS, et al. Prog Retin Eye Res. 2018;doi:10.1016/j.preteyeres.2018.04.003.
Green KB, et al. Ophthalmol Vis Sci. 2017;58(8):2693.
Lee SH, et al. Am J Ophthalmol. 1997;doi:10.1016/s0002-9394(14)70125-4.
Matsumoto Y, et al. Ophthalmology. 2004;doi:10.1016/j.ophtha.2003.10.019.
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Michael S. Cooper, OD, is in practice at Solinsky Eye Care in West Hartford, Conn., where he specializes in anterior segment disease, including dry eye, lid disease, allergy and uveitis. He serves as an adjunct professor at Midwestern University in Downers Grove, Ill., and Massachusetts College of Pharmacy and Health Sciences in Boston. Cooper is the current president of the Intrepid Eye Society.
Disclosure: Cooper reports the following relevant financial disclosures: Alcon, Allergan, Bausch + Lomb, Bio-Tissue, Eyevance Pharmaceuticals, Glaukos, Johnson & Johnson Vision Care, The Mentholatum Company, Novabay Pharmaceuticals, Novartis Eye and Ear (formerly Takeda/Shire) and TearScience.
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