From artificial tear drops to punctal plugs, steroids, and prescription medications, our dry eye treatment options continue to expand. Beginning in 1958, when the first implantable pacemaker was used, neurostimulation has been a meaningful part of healthcare (van Hemel and van der Wall, 2008). Since then, neurostimulation has been used to treat a host of conditions including Parkinson’s disease, psychiatric and neurological conditions, tremors, migraines, heart defects, epilepsy, retinitis pigmentosa, obesity, and hearing challenges (Gardner, 2013). Neurostimulation is also being investigated regarding how it can affect patients. And now, there is the option to utilize an electronic device that can alter an aspect of dry eye that has not been approached before.
How It Works
When it comes to the neural response for lacrimation, the trigeminal nerve (CN V) is responsible. The ophthalmic nerve branch innervates the lacrimal glands, meibomian glands, and the goblet cells. When triggered by either external or internal stimuli, the CN V system communicates with the central nervous system via afferent neurons. Then, both the parasympathetic and sympathetic signals are carried back from the cranial nerves via efferent neurons (Kossler et al, 2015; Beuerman et al, 2004; Brinton et al, 2016; Dartt, 2004). It is this pathway system that causes lacrimation and tear production. When the process is disrupted, tear production becomes altered. Neurostimulation directly signals the pathways that lead to increased tear production by triggering the central nervous system.
Having minimal clinical experience with this so far, eyecare practitioners (ECPs) hold out great hope that neurostimulation will become a new normal in our dry eye tool box. It won’t replace thermal pulsation, which opens plugged glands, but it could help keep those glands flowing afterward.
Its effect on the use of prescription medication is also unknown, but it is anticipated to be an adjunct treatment for patients who are currently taking these medications. Currently, ECPs use medication eye drops to manage T cell-mediated dry eye brought about by an altered lacrimal gland. While ECPs are unsure what the long-term effect of neurostimulation will be, we hypothesize that the treatment will help to upregulate and improve tear production—but only to a point; patients who are in the moderate or severe state of dry eye will still need to use prescription medication.
The patients who stand to benefit most are those who are significantly inconvenienced by their dry eye. In our limited clinical experience and investigation into the topic of neurostimulation, we believe that those who are using artificial tears will be able to use neurostimulation as an alternative that will likely reduce their dependence on drops. Instead, these patients can utilize the neurostimulation device throughout the day to bring about a more comprehensive tear film that is created by their own bodies. Over time, patients may reduce the number of times that they use the device as their nervous system may learn to produce tears in a more meaningful way. While this is speculation at this point, we are anxious for more clinical data—from patients and research—to teach us more.
The Verdict
For now, we encourage dry eye practitioners to look into neurostimulation as an adjunct therapy to their dry eye treatments. It may not be normal yet, but we anticipate it becoming normal very soon. CLS
For references, please visit www.clspectrum.com/references and click on document #271.