This ARVO, there was a mini-symposium entitled An Overview to Ocular Surface Pain. This symposium reexamined dry eye disease with a focus on its main complaint, chronic symptoms of dryness, burning, aching, and/or tenderness that can all be classified under the umbrella of ocular surface pain. The focus was on examining the etiology, diagnosis, and treatment of both nociceptive and neuropathic causes of ocular surface pain. Nociceptive pain arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors. In the eye, many insults can cause nociceptive pain, including low tear production, epithelial disruption, and surgical injury. Nociceptive ocular pain is generally acute but can become chronic with persistent insult (i.e., low tear volume). On the other hand, neuropathic pain arises as a direct consequence of a lesion or disease affecting the somatosensory system. Research has shown that a variety of insults can change the morphology and function of nociceptors (i.e., surgical injury, ocular surface inflammation) and this can lead to chronic ocular surface pain, even in the absence of ocular surface abnormalities. While both pain types share several qualities (e.g., sensations of dryness), individuals with neuropathic pain often describe distinct pain characteristics, such as evoked pain to wind or light or burning, shooting, or stabbing pain.
Interestingly, knowledge from other disease entities, such as migraine, can be drawn upon to understand neuropathic ocular surface pain, as these two diseases share common underlying mechanisms. For example, evoked pain to light (i.e., photophobia) is a common symptoms in both diseases and likely results from activation of a distinct subset of retinal cells that transmit signals to the superior salivatory nucleus, which exerts parasympathetic innervation to ocular and meningeal vessels, creating a shared pathway between ocular pain and light processing. In turn, pain signaling is then transmitted to the trigeminal nucleus caudalis, posterior thalamus, and higher cortical centers.
Considering the multifaceted origins of ocular surface pain and shared pathways with other painful conditions such as migraine, providers have found some success by borrowing techniques from other specialties and applying them to the treatment of ocular surface pain. Examples include initiation of oral medications (gabapentin, pregabalin, duloxetine, and nortriptyline), periocular nerve blockades, botulinum toxin injections, transcutaneous electrical nerve stimulation, and calcitonin gene-related peptide inhibitors, as appropriate in the individual patient. In addition, an emotional component typically co-exists with ocular surface pain and needs to be addressed.
While the pathophysiology underlying ocular surface pain is complex and not entirely understood, the area is worthy of study as pain is a significant source of morbidity both in the U.S. and across the world. Patients with ocular surface pain have limitations in performing activities of daily living and the ability to work and the pain frequently negatively impacts mental health. As such, it is important to move the field forward and study pathophysiological mechanisms of ocular surface pain in animal models and humans, develop diagnostic tests to determine contributors to pain, and individualize treatment algorithms to improve pain and decrease suffering.