Neurological Dry Eye

Neurological Dry Eye

Author: Diana Driscoll, OD, FAAO

Dry eye disease (DED) is commonly perceived as an eye-related issue; however, considering it as a more extensive problem involving inflammation throughout the body opens up new treatment possibilities. The autonomic nervous system, which controls inflammation and tear production, is key. A neurological approach to DED can address inflammation and tear production together by supporting the autonomic nervous system.

Neurological DED: A Widespread Issue

Chronic DED affects approximately 35 million people in the United States alone, causing significant morbidity. Most treatments available focus on managing ocular symptoms and local inflammation, perceiving DED solely as an eye problem. However, DED is a multifactorial disease with both local and systemic contributing factors that must be identified to achieve effective symptom resolution.

Controlling Inflammation in DED

Inflammatory processes are well-known contributors to DED, with autoimmune conditions like Sjogren's syndrome, Lupus erythematosus, and rheumatoid arthritis causing systemic inflammation that affects the eyes. In such cases, a combination of systemic and ocular treatments is often required to manage associated DED. Other factors, such as hormone fluctuations, menopause, and low androgenic hormone levels, also contribute to inflammation and should be addressed.

Furthermore, chronic systemic inflammation, which can stem from various sources such as normal aging, metabolic syndrome, endocrine disorders, and inflammatory bowel disease, is often overlooked in DED due to limited diagnostic and treatment options. Nevertheless, chronic inflammation can cause damage both locally (ocularly) and systemically, emphasizing the importance of addressing both types of inflammation for comprehensive patient recovery.

The Vagus Nerve: A Controller of Inflammation

The autonomic nervous system, specifically the vagus nerve, plays a vital role in controlling the body's inflammatory response. As the "anti-inflammatory" nerve, the vagus nerve releases acetylcholine to regulate the release of inflammatory cytokines and chemokines. When the vagus nerve is inhibited or damaged, it loses its ability to control inflammation, leading to chronic inflammation and the continued release of damaging inflammatory cytokines and chemokines.

For accurate measurement of inflammation in chronic inflammatory conditions, including DED, Type I and Type II cytokines provide more reliable indicators compared to traditional markers like CRP or SED rate. Studies have shown significantly increased concentrations of inflammatory cytokines such as IL-1b, IL-6, IL-8, IL-17, and TNF-alpha in the eyes of DED patients, reflecting the severity of the disease. However, the limited availability of tests for systemic and localized inflammatory cytokines and chemokines makes it challenging for practitioners to determine whether localized ocular inflammation corresponds to chronic systemic inflammation. Learning from other well-defined inflammatory diseases, it becomes clear that addressing both localized and systemic inflammation is crucial for optimal patient recovery.

FIGURE - available via license: Creative Commons Attribution 4.0 International

The Role of Acetylcholine

While the vagus nerve does not directly innervate the eyes, acetylcholine emerges as the common factor connecting both autonomic functions of inflammation control and tear production. Acetylcholine is the neurotransmitter utilized by the vagus nerve and the parasympathetic nervous system responsible for basal tear production.

The neurology of tear production involves both sensory and autonomic nervous systems. Sensory tear production occurs through various stimuli, including blinking, nasal stimulation, and ocular irritation. Damage to the trigeminal nerve, responsible for sensory innervation, can result in decreased tear response to sensory stimulation.

On the other hand, autonomic basal tear production relies on the parasympathetic nervous system, which releases acetylcholine to stimulate tear production. The parasympathetic fibers responsible for tear production originate in the superior salivatory nucleus and travel through the facial nerve to innervate the lacrimal gland, stimulating tear secretion.

The connection between acetylcholine and tear production suggests that optimizing acetylcholine levels could enhance tear production in patients with DED. Acetylcholinesterase inhibitors, which prevent the breakdown of acetylcholine, have shown promise in increasing tear production and improving symptoms of DED.

Systemic Treatment Approach

Considering DED as a systemic disorder allows for a more comprehensive treatment approach. Addressing both local and systemic inflammation and optimizing tear production through the modulation of acetylcholine levels can provide better outcomes for patients.

Treatment strategies for Neurological Dry Eye may include:

Anti-inflammatory interventions: Identifying and addressing sources of chronic systemic inflammation, such as autoimmune conditions, metabolic syndrome, or endocrine disorders, can help reduce the overall inflammation burden and improve DED symptoms.

Neurological modulation: Supporting the autonomic nervous system, particularly the vagus nerve, can help regulate inflammation. Techniques such as vagus nerve stimulation, acupuncture, or the use of acetylcholinesterase inhibitors can be considered.

Tear production optimization: Enhancing tear production through acetylcholine modulation may involve the use of acetylcholinesterase inhibitors, as well as addressing any underlying sensory deficits that may affect tear response to stimulation.

Combination therapy: A multimodal approach that combines systemic anti-inflammatory interventions, neurological modulation, and tear production optimization can provide synergistic effects and better outcomes for patients with neurological DED.

Introducing a Revolutionary Solution for Neurological Dry Eye Treatment

Experience the groundbreaking innovation of NeuroTearsTM, an exceptional over-the-counter supplement designed to address the challenges of neurological dry eye. This remarkable formula provides comprehensive support for acetylcholine, targeting both the nicotinic receptors of the vagus nerve and the muscarinic receptors of the lacrimal functional unit. Moreover, it goes beyond conventional limitations by effectively crossing the blood-brain barrier to enhance acetylcholine levels in the central nervous system, promoting cognitive function and short-term memory.

By stimulating the vagus nerve, this unique supplement aids in the regulation of inflammation, while simultaneously activating the nerves responsible for tear production within the lacrimal functional unit.

Originally developed and patented as ParasymPlus EyesTM to optimize vagus nerve function, including digestion and inflammation control, as well as brain health, its remarkable efficacy in significantly improving chronic dry eye led to further research and enhancements, culminating in the launch of NeuroTearsTM.

This advanced formula now provides stimulation to both nicotinic and muscarinic receptors, bypassing potential genetic issues and nutrient deficiencies associated with acetylcholine production. Importantly, NeuroTearsTM does not rely on functional nerves, instead directly targeting the receptors themselves.

Patients who incorporate this supplement into their routine typically experience noticeable relief from dry eye symptoms within weeks. Additionally, other symptoms related to low acetylcholine levels, such as brain fog, constipation, and fatigue, often show remarkable improvement within a day. Patients with enlarged pupils resulting from autonomic imbalance can expect normalization of pupil size in just a matter of days.

This approach to neurological dry eye treatment is truly groundbreaking, providing both systemic and ocular benefits. No existing medication can offer the unique combination of the vagus nerve and lacrimal functional unit stimulation, coupled with acetylcholine support for optimal brain function. NeuroTearsTM represents a revolutionary breakthrough, seamlessly complementing your current treatment protocols.

Neurological Dry Eye - Conclusion

Viewing DED as a systemic inflammatory disorder with neurological involvement opens up new possibilities for treatment. By addressing both local and systemic inflammation and optimizing tear production through the modulation of acetylcholine levels, practitioners can provide more comprehensive care for patients with DED.

The systemic treatment approach of NeuroTearsTM that considers the role of the autonomic nervous system can lead to improved outcomes and better quality of life for individuals suffering from neurological DED.


Calonge M, Enríquez-de-Salamanca A, Diebold Y, et al. Dry eye disease as an inflammatory disorder. Ocul Immunol Inflamm. 2010;18(4):244-253. doi:10.3109/09273941003721926.

Henrich CF, Ramulu PY, Akpek EK. Association of dry eye and inflammatory systemic diseases in a tertiary care-based sample. Cornea. 2014;33(8):819-825. doi:10.1097/ICO.0000000000000173.

Nguyen CQ, Peck AB. Unraveling the pathophysiology of Sjogren syndrome-associated dry eye disease. Ocul Surf. 2009;7(1):11-27. doi:10.1016/s1542-0124(12)70289-6.

Truong S, Cole N, Stapleton F, Golebiowski B. Sex hormones and the dry eye. Clin Exp Optom. 2014;97(4):324-336. doi:10.1111/cxo.12147.


De Martinis M, Franceschi C, Monti D, Ginaldi L. Inflamm-ageing and lifelong antigenic load as major determinants of ageing rate and longevity. FEBS Lett. 2005;579(10):2035-2039. doi:10.1016/j.febslet.2005.02.055

Tang YL, Cheng YL, Ren YP, Yu XN, Shentu XC. Metabolic syndrome risk factors and dry eye syndrome: a Meta-analysis. Int J Ophthalmol. 2016;9(7):1038-1045. Published 2016 Jul 18. doi:10.18240/ijo.2016.07.17

Chopra R, Chander A, Jacob JJ. The eye as a window to rare endocrine disorders. Indian J Endocrinol Metab. 2012;16(3):331-338. doi:10.4103/2230-8210.95659

Mrugacz M, Sredzińska-Kita D, Cyrta-Jarocka E, Bakunowicz-Lazarczyk A. Dry eye syndrome and cataract as ocular manifestations of Crohn's disease. Klin Oczna. 2005;107(7-9):509-510

V.A. Pavlov, K.J. Tracey; Controlling inflammation: the cholinergic anti-inflammatory pathway. Biochem Soc Trans 1 December 2006; 34 (6): 1037–1040


Pavlov VA, Wang H, Czura CJ, Friedman SG, Tracey KJ. The cholinergic anti-inflammatory pathway: a missing link in neuroimmunomodulation. Mol Med. 2003;9(5-8):125-134

Czura CJ, Tracey KJ. Autonomic neural regulation of immunity. J Intern Med. 2005;257(2):156-166. doi:10.1111/j.1365-2796.2004.01442.x.

Di Zazzo A, Micera A, Coassin M, et al. InflammAging at Ocular Surface: Clinical and Biomolecular Analyses in Healthy Volunteers. Invest Ophthalmol Vis Sci. 2019;60(5):1769-1775. doi:10.1167/iovs.18-25822.

Rogers RC, McTigue DM, Hermann GE. Vagal control of digestion: modulation by central neural and peripheral endocrine factors. Neurosci Biobehav Rev. 1996;20(1):57-66. doi:10.1016/0149-7634(95)00040-l.

Abit, Mahmut. (2015). Lacrimal Gland Pathologies from an Anatomical Perspective. Acta Medica Anatolia. 3. 113. 10.15824/actamedica.96512.


Dartt DA. Neural regulation of lacrimal gland secretory processes: relevance in dry eye diseases. Prog Retin Eye Res. 2009;28(3):155-177. doi:10.1016/j.preteyeres.2009.04.003.

Zoukhri D, Kublin CL. Impaired neurotransmitter release from lacrimal and salivary gland nerves of a murine model of Sjögren's syndrome. Invest Ophthalmol Vis Sci. 2001;42(5):925-932.

Driscoll, D. (2016). Correcting the Missing Piece in Chronic Fatigue Syndrome [white paper]. Genetic Disease Investigators, LLC.

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