Ocular Surface Pain: A Narrative Review

Abstract

Ocular surface pain is a frequent cause of visits to an eye care provider and has a substantial impact on healthcare cost, yet a complete understanding of its causative factors and tools for diagnostic workup are notably missing in many eye clinics. The cornea has the densest sensory innervation in the human body and has the potential to be a powerful producer of pain. Pain can manifest as a result of a noxious stimulus or disruption in the ocular surface anatomy (nociceptive pain), or it can result from abnormalities in the ocular surface neurosensory apparatus itself (neuropathic pain). Novel advances in neurobiology have sought to differentiate the two entities, particularly to identify when chronic dry eye symptomatology is driven by neuropathic ocular pain. In this review, we seek to provide an overview of the prevalence, physiologic factors, and management of ocular surface pain complaints.

Keywords: Dry eye; Neuropathic pain; Nociceptive pain; Ocular pain; Ocular surface pain.

Fig. 1

A simplified depiction of the ocular surface sensory pathway. Neuronal cell bodies of corneal nociceptors are located in the trigeminal ganglion. These first-order neurons synapse at the trigeminal subnucleus caudalis/upper cervical transition zone and the subnucleus interpolaris/subnucleus caudalis. Second-order neurons project from trigeminal subnuclei to the thalamus, and third-order neurons terminate in the primary somatosensory cortex and other cortical areas. The thalamus also projects descending inhibitory fibers that are involved in neural pain modulation