Neurostimulation for Tear Production

Ji Kwan Park; Sandra Cremers; Andrea Lora Kossler

Disclosures

Curr Opin Ophthalmol. 2019;30(5):386-394. 

In This Article

Abstract and Introduction

Abstract

Purpose of review: Dry eye disease (DED) is a chronic multifactorial disease that affects millions of people worldwide. Despite ongoing research, treatment for DED remains a challenge. Neurostimulation for tear production is a rapidly evolving field that culminated in the development of the intranasal tear neurostimulator (ITN). In this article, we review the neuroanatomy and pathophysiology of tear production and the evolution of neurostimulation for the treatment of DED.

Recent findings: The ITN was approved for commercial use in April 2017. This innovation stemmed from the success of lacrimal nerve and anterior ethmoid nerve stimulation animal studies. Since then, numerous pilot studies and multicenter randomized controlled trials demonstrate increased aqueous tear production, improved DED-related symptoms, and device safety. Recent studies also report the positive effects of intranasal stimulation on mucin and lipid secretion.

Summary: Neurostimulation for enhanced tear production is a promising new treatment option for DED. Stimulation of the lacrimal nerve and anterior ethmoid nerve both effectively increase tear volume. The ITN is a noninvasive device that effectively increases aqueous tear volume and may improve tear composition, including mucin and lipid concentrations. Further studies are needed to determine proper patient selection and the long-term efficacy of neurostimulation for DED.

Introduction

Dry eye disease (DED), also known as keratoconjunctivitis sicca, is a multifactorial condition with a global prevalence ranging between 5 and 50% among the adult population. In the United States, 3.2 million women and 1.7 million men over the age of 50 years have been estimated to have moderate-to-severe DED.[1,2,3] The disease is increasing among the younger population between 18 and 34 years of age because of the frequent use of contact lenses, computer, smartphones, and tablets.[4,5]

A vicious cycle of aqueous tear deficiency and excessive tear evaporation from inflammation and somatosensory abnormalities can result in visual disturbances, ocular irritation, pain, photophobia, excessive tearing, and decreased quality of life.[2,5] Previous modalities focused on lubricating the ocular surface with artificial tears, ointments, and punctal plugs, and inhibiting the inflammatory response with agents, such as cyclosporine and lifitegrast.[2,3,6,7] Advances in understanding the neural control of the tear film and the dynamic interplay between the nasolacrimal reflex (NLR) and lacrimal functional unit (LFU) has led to a paradigm shift in the treatment of DED.[3,5] Neurostimulation utilizes the NLR to stimulate tear production via the afferent or efferent branches of the neural reflex arc.[8,9–11] This article aims to review the neural pathways involved in tear production and the evolution of neurostimulation for the treatment of DED.

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