Dry eye disease (DED) is a common condition characterized by discomfort, visual disturbance, and tear film instability on the eye’s surface. Migraine is a prevalent neurological disorder marked by severe, recurring headaches, often accompanied by light and sound sensitivity. A significant clinical association exists between them; individuals with migraines have up to a 72% higher odds of also having a DED diagnosis. While dry eyes may not be the root cause of chronic migraine, they can act as a powerful trigger for an attack in susceptible individuals. This connection is best understood by exploring the shared biological pathways and systemic risk factors linking the eye and the brain’s pain centers.
The Trigeminal Nerve Connection
The most direct link between dry eye discomfort and migraine involves the trigeminal nerve (Cranial Nerve V). This nerve is the primary sensory pathway for the face, including the eye’s surface, and is also responsible for initiating migraine pain.
Chronic irritation and pain signals from a dry ocular surface are transmitted through the ophthalmic division of the trigeminal nerve. These signals travel inward to the brainstem, synapsing in the trigeminal nucleus caudalis. Constant, abnormal signaling from irritated corneal nerves causes peripheral and central sensitization.
This sensitization lowers the threshold for pain, making the brain’s pain centers hyper-responsive to stimuli, which is a hallmark of migraine development. The eye’s irritation activates the trigeminovascular system, the neural network integral to migraine attacks. A neuropeptide called calcitonin gene-related peptide (CGRP) plays a role in both DED and migraine pathogenesis. The release of CGRP contributes to neurogenic inflammation and helps explain why photophobia, or extreme sensitivity to light, is a common symptom in both conditions.
Shared Systemic Risk Factors
Dry eye disease and migraines frequently co-occur because they share systemic risk factors, suggesting a common underlying vulnerability beyond the direct neural trigger. Both conditions involve chronic systemic inflammation, with elevated levels of inflammatory molecules found in affected individuals. This inflammation predisposes the body to both ocular surface damage and neurological hyper-excitability.
A shared factor is central sensitization, where the central nervous system becomes overly reactive to various internal and external stimuli. This heightened sensitivity means a patient is prone to experiencing increased pain from non-painful stimuli (allodynia) and more intense pain from painful stimuli (hyperalgesia). This manifests as both severe migraine pain and chronic eye pain.
Certain underlying autoimmune disorders, such as Sjögren’s syndrome, cause both severe DED and a higher incidence of neurological symptoms, including migraine. In these cases, immune system dysfunction attacks multiple parts of the body, leading to the simultaneous presentation of both conditions. Furthermore, some medications used to treat systemic conditions, such as certain antidepressants, can inadvertently contribute to both dry eye symptoms and headache risk.
Integrated Management Approaches
Recognizing the strong neurobiological and systemic connection between DED and migraine has significant implications for treatment. Since dry eye irritation can act as a powerful migraine trigger, aggressively managing the ocular surface can reduce migraine frequency or severity. This requires eye care providers to incorporate questions about comorbid headaches, and neurologists to inquire about persistent dry eye symptoms.
Treatment often starts by targeting inflammation on the ocular surface, as this is a root cause of abnormal nerve signaling. First-line therapies for DED include anti-inflammatory prescription eye drops, such as topical corticosteroids, cyclosporine, or lifitegrast. Decreasing ocular surface inflammation aims to calm the peripheral trigeminal nerve and reduce pain signals traveling to the brain.
If initial anti-inflammatory treatments do not relieve symptoms, clinicians may consider therapies that directly target nerve dysfunction, such as nerve blocks or specific systemic medications. The effectiveness of treating DED symptoms in individuals with migraine underscores that a comprehensive approach must address both the eye and central nervous system sensitization. Effectively treating one condition often positively impacts the symptoms of the other.