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Using neurostimulation to treat dry eye


Neurostimulation could be the “next big thing” in dry eye disease (DED). A new neurostimulation device called TrueTear (Allergan) is a patient-directed, non-pharmacologic option.

Neurostimulation could be the “next big thing” in dry eye disease (DED). A new neurostimulation device called TrueTear (Allergan) is a patient-directed, non-pharmacologic option.

TrueTear is inserted into the nostril; two prongs contact the ophthalmic branch of the trigeminal nerve. An electrical signal from the device signals the trigeminal nerve (5V1) and travels to cranial nerve VII, which stimulates the lacrimal glands. The nervous pathway, not reflect tears, ultimately drives secretion of basal tears.

Optometrists have questions about how the device works, patient use, and safety concerns. Let’s answer them.

What is neurostimulation?

Much like the word implies, neurostimulation describes supplying stimulation to a nerve. Neurostimulation in used in several applications in medicine, including pain management, treatment of post-traumatic stress disorder, and cognitive neurologic conditions, such as Alzheimer disease.

Previously from Dr. Hom: Why ODs should care about antibiotic resistance

As it pertains to the treatment of DED, neurostimulation using the TrueTear device initiates an afferent signaling pathway that culminates in secretion of tears by one or more proposed mechanisms.

For instance, the electrical signal received by the ethmoidal nerve may travel through the trigeminal afferent nerve fibers in the nasal cavity to the superior salivatory nucleus region of the brain, the area that controls tears.1

A second theoretical mechanism is TrueTear may induce changes in the meibomian glands that restore their ability to contribute to tears.2

Researchers have also described a pathway through which TrueTear prompts activity in glands responsible for secretion of lipids and proteins that contribute to tear development.3

TrueTear may also induce the nasal-ocular tear reflex-the stimuli might initiate a secondary signaling pathway to the pterygopalatine ganglion, a parasympathetic ganglion that has axonal projection to the lacrimal glands and nasal mucosa, which then shifts to the parasympathetic pathway to stimulate facial nerve VII, which connects to the goblet cells and meibomian glands.4


Is the device difficult to use in the clinic?

In my experience as a clinical investigator, it is not difficult, and the learning curve is minimal. A certain amount of training is required for the patient, but optometrists are already comfortable with education protocols, such as with contact lens training and fitting. If your staff can perform contact lens training with patients, they can use TrueTear.

Because TrueTear has a novel mechanism of action, I think it fits naturally with other treatment approaches. There should be no need to discontinue use of other forms of DED therapy. For some patients, especially those with inadequate response to pharmacotherapy, TrueTear may be an alternative to topical drops.

Related: Antibiotic resistance in the eyecare practice

Are there safety concerns?

TrueTear demonstrated excellent safety in clinical trials. To my knowledge the only adverse event study patients experienced was rhinitis.

If TrueTear restores physiologic function, it may also stimulate adaptation; patients who use the device long term may need to increase the signal intensity or usage frequency. I am not certain this theory is entirely plausible, but device has power settings, and it is reasonable to start on the lowest setting and titrate as needed.

Related: Is it all about itch?

What is the “True Tear without TrueTear Test?”

More practically for the clinician, use of a provocative test appears to have utility in determining whether someone is a candidate for the device. I call it the “True Tear without TrueTear Test.” 

Insert a cotton tip into the nostril (by either patient or clinician) to press on the middle turbinate. If the stimuli evokes tear production, the TrueTear device likely will be successful. If the test does not work, there may be an anatomical defect, such as a deviated septum or residual trauma from a previously broken nose.

For the braver clinician, a more invasive version of the provocative test can be performed in patients without a tear response. With a nasal speculum, open the nostril and look with a light. Any restrictions or deviations will be revealed. Note: tell the patient to blow his nose before performing the test.

Based on my clinical trial experience with TrueTear, I had a 100 percent success rate with study patients who passed this test showing dry eye symptom improvement after usage.


What’s the big deal?

The ability to offer patients a drug-free yet effective and safe treatment for DED is a win. The fact that TrueTear may affect long-term pathway remodeling makes it even more intriguing. At a minimum, the device offers patients the prospect of short-term relief from DED symptoms-and when used adjunctively and in combination with other modalities, TrueTear becomes part of an overall strategy to address the multiple mechanisms and triggers of DED.

The DED treatment space has expanded significantly in recent years, adding several highly effective platform-based and pharmacologic options to address DED and related entities, such as meibomian gland dysfunction. As more and more patients look for options to gain relief from ocular pain and other symptoms due to DED, and as we continue to learn about its multifactorial etiology having multiple treatment options increases the likelihood of matching patients with the best possible treatment approach.

I usually think of DED treatments as anti-inflammatory or as relieving obstruction. TrueTear adds a brand new category: neurostimulation.

Related: Treat rosacea by treating the cause: demodex


1. Friedman NJ, Burton K, Robledo N, et al. A nonrandomized, open-label study to evaluate the effect of nasal stimulation on tear production in subjects with dry eye disease. Clin Ophthalmol. 2016;10 795-804.

2. Pondelis JN, Dieckmann G, Kataguiri P, et al. Intranasal Neurostimulator Induces Morphological Changes in Meibomian Glands in Patients with Dry Eye Disease. Poster presented at ARVO 2017. May 8, 2017; Baltimore.

3. Brinton M, Chung JL, Kossler A, Kook KH, Loudin J, Franke M, Palanker D. Electronic enhancement of tear secretion. J Neural Eng. 2016;13(1):016006.

4. Hom MM, Bielory L. The anatomical and functional relationship between allergic conjunctivitis and allergic rhinitis. Allergy & Rhinology. 2013;4.3:e110-e119.

Read more from Dr. Hom here

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