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A. Lora, J. Wang, J.-M. Parel, D. T. Tse; Lacrimal Nerve Stimulation by a Neurostimulator for Tear Production. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4244.
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Dry eye syndrome is a very common disorder most commonly caused by aqueous tear deficiency. It is postulated that tear secretion is controlled by a neural reflex arc; sensory nerves in the cornea and conjunctiva pass to the brain, and motor nerves from the brain terminate in the lacrimal gland to stimulate tear secretion. Recent studies indicate that chronic dry eye disease is inflammatory in nature. Inflammatory markers on the ocular surface inhibit sensory nerve input to the brain, leading to interruption of motor nerve impulses to the lacrimal gland, and thus lead to a decrease in the quality and quantity of tear production. Our purpose is to develop a new treatment option for dry eye syndrome. We propose to bypass ocular surface feedback inhibition by direct stimulation of the lacrimal nerve with an implantable neurostimulator.
An animal model was created to test safety and efficacy. Baseline anterior segment spectral domain optical coherence tomography (OCT) of the tear meniscus was performed on Dutch Belted rabbits to quantify basal tear volume. An implantable pulse generator was placed adjacent to the lacrimal nerve to stimulate tear production from the lacrimal gland. OCT was then used to quantify the change in tear volume before and after stimulation.
Stimulation of the lacrimal nerve with an implantable neurostimulator effectively increased tear volume. OCT demonstrated a 100% increase in tear production after stimulation compared to baseline. Additionally, there were no gross adverse effects to stimulation.
This study suggests that an implantable neurostimulator can effectively stimulate tear production and may be effective as a future treatment for dry eye syndrome.
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