Researchers have determined that the presence of photophobia in dry eye, migraine and traumatic brain injury (TBI) suggests a shared pathophysiologic mechanism. As such, they suggest that practitioners inquire about the presence of migraine, TBI and other pain complaints in patients with dry eye.
During a literature review, the researchers found that the neural dysregulation of peripheral and central nervous system components is implicated in photophobia in various animal models and in humans. In particular, enhanced activity of the neuropeptide calcitonin gene-related peptide (CGRP) is closely linked to photophobia. CGRP mediates central neuroplasticity and hypersensitivity in the three conditions’ trigeminothalamic pathophysiologic mechanisms.
Current therapies for photophobia include glasses that shield the eyes from specific wavelengths, botulinum toxin and inhibition of CGRP and its receptor. However, the researchers note that a paucity of evidence exists on the effects in dry eye and TBI patients.
The review concludes that practitioners should consider using therapy strategies that target neural pathways, such as oral neuromodulators and transcutaneous nerve stimulation, in patients with persistent photophobia, specifically in individuals whose symptoms are not controlled with traditional therapies.
Diel RJ, Mehra D, Kardon, et al. Photophobia: shared pathophysiology underlying dry eye disease, migraine and traumatic brain injury leading to central neuroplasticity of the trigeminothalamic pathway. Br J Ophthalmol. July 23, 2020. [Epub ahead of print].