Migraine is a neurological disorder characterized by severe, often debilitating headaches, accompanied by visual disturbances, nausea, and sensitivity to light and sound. Dry Eye Disease (DED) is a common ocular surface condition defined by a loss of tear film stability, leading to discomfort, visual issues, and potential damage to the eye’s surface. Clinical studies suggest a significant link between these two conditions, indicating that migraines can indeed cause or exacerbate dry eye symptoms. This connection points toward a shared underlying mechanism rooted in the nervous system.
The Established Clinical Connection
Clinical data strongly supports the idea that migraines and dry eye disease frequently occur together, a phenomenon known as comorbidity. Population-based studies have demonstrated that individuals diagnosed with migraine have a significantly higher prevalence of DED compared to the general population. For instance, the odds of having a DED diagnosis were approximately 1.42 times higher in patients who had a history of migraine. This association appears to be particularly pronounced in people who experience chronic or high-frequency migraines, suggesting a dose-dependent relationship.
The link is often stronger for dry eye symptoms—such as burning, grittiness, or foreign body sensation—rather than measurable clinical signs like reduced tear production. This observation hints that the connection may be rooted more in the sensory experience and nerve processing than solely in the physical lack of tears. Furthermore, individuals whose migraines are accompanied by an aura often show an even stronger association with dry eye characteristics. These epidemiological findings establish a clear clinical pattern.
Neurological Pathways of Interaction
The functional bridge between migraine pain and dry eye symptoms lies in the trigeminal nerve, the fifth cranial nerve. This nerve is responsible for transmitting sensation from the face, including the eye’s surface, and is the primary pathway for migraine headache pain. Activation of the trigeminal system is a feature of a migraine attack, affecting the trigeminovascular network that innervates the blood vessels around the brain.
During a migraine, this activation can trigger neurogenic inflammation, which involves the release of potent neuropeptides. The most studied of these is Calcitonin Gene-Related Peptide (CGRP), a small protein that plays a central role in transmitting and amplifying pain signals. CGRP is released from the peripheral nerve endings of the trigeminal nerve, including those that densely innervate the cornea, the eye’s transparent outer layer. The release of CGRP and other inflammatory mediators along this shared neural pathway can sensitize the corneal nerves, changing how they respond to normal stimuli. This neuroinflammation can disrupt the delicate balance of the ocular surface, leading to increased nerve hypersensitivity, which the brain interprets as dryness, burning, and pain.
Shared Symptoms and Bidirectional Triggers
The intertwined nature of these conditions is highlighted by an overlap in patient-reported experiences, most notably photophobia, or extreme light sensitivity. Photophobia is a hallmark symptom of migraine, but it is also a frequent complaint among individuals with DED. This shared symptom is thought to be mediated, in part, by the same CGRP-related sensitization within the trigeminal system.
Beyond shared symptoms, the relationship is bidirectional, meaning the conditions can influence one another in a cyclical fashion. While migraines can initiate dry eye, severe and chronic dry eye disease can itself become a peripheral trigger for migraine attacks. The constant irritation and inflammation of the ocular surface in DED continuously activates the sensory fibers of the trigeminal nerve. This sustained activation provides input to the central pain processing centers, potentially lowering the threshold for a full-blown migraine attack or increasing its severity.
Integrated Treatment and Management
Because migraines and dry eyes are neurologically linked through a common inflammatory pathway, effective management requires an integrated approach that addresses both conditions simultaneously. For dry eye symptoms that are rooted in nerve inflammation, standard lubricating eye drops may not provide full relief. Targeted dry eye therapies, such as prescription anti-inflammatory agents like cyclosporine, are often used to stabilize the ocular surface and reduce the irritation that feeds back into the trigeminal system.
Treating the underlying migraine is also crucial for improving associated dry eye symptoms. Newer migraine preventive treatments, particularly those that block the activity of CGRP, offer a therapeutic benefit for both the headache and the related ocular discomfort. Even the consistent use of simple ocular lubricants has been shown to significantly reduce migraine-related disability in patients who also have DED, suggesting that calming the ocular surface can soothe the shared neural pathway. Comprehensive management also includes lifestyle adjustments beneficial to both, such as optimizing hydration and using light-filtering glasses to manage light sensitivity.