Amir Moezzi is a clinical scientist at the Centre for Contact Lens Research, in the School of Optometry and Vision Science, University of Waterloo, Canada.
Belmonte C, Nichols JJ, et al. TFOS DEWS II pain and sensation report. Ocul Surf 2017;15(3): 404-37.
The view of the TFOS DEWS II Pain and Sensation subcommittee was that unpleasant (and sometimes painful) sensations (e.g. dryness, discomfort) associated with ocular surface diseases such as dry eye disease should be considered and studied as a specific form of eye pain, as these unpleasant sensations appear to share the same underlying neurobiological mechanisms as in pathological ocular pain conditions such as microbial keratitis and iridocyclitis.
The corneal sensory neurons are categorized into three groups according to their functions: polymodal nociceptors, specific mechano-nociceptors and cold thermoreceptors.
Polymodal nociceptors sense chemical, mechanical and thermal stimuli. Mechano-nociceptors are sensitive to mechanical stimuli. Polymodal and mechano nociceptors are silent in normal conditions. Polymodal nociceptors re sensitized by the inflammatory mediators from ocular surface injury. Most cold thermoreceptors are continuously active at normal temperature with dependency of their firing frequency upon cooling or warming. Corneal cold thermoreceptors are also sensitive to osmolarity changes and thereby contributing to reflex control of basal tear production and blinking. This is by sensing cooling temperature during inter-blink tear evaporation.
Nociceptive vs. neuropathic pain
In general, pain can be categorized into nociceptive and neuropathic pain. Nociceptive pain is signaled through normal activation of nociceptors (sensory receptors of the peripheral nervous system) as a result of damage to tissues in their receptive field by noxious mechanical, thermal and chemical stimuli. In contrast, neuropathic pain is caused by a lesion or disease of the somatosensory nervous system itself.
Although neuropathic pain should not be diagnosed as dry eye disease, this differentiation may improve clinical diagnosis and treatment efficacy as treatment for nociceptive pain in dry eye disease (e.g. artificial tears) will likely be ineffective for ocular neuropathic pain.
Lack of correlation between signs and symptoms
The lack of correlation between signs and symptoms of dry eye disease has puzzled researchers and clinicians for many years. As the time course from onset of ocular surface disease to the reporting of symptoms in any particular patient is unknown, possible peripheral and or central nervous sensitization and hyper-excitability from chronic inflammation and nerve damage in chronic dry eye disease may contribute to this imbalance between signs and symptoms.
Incomplete understanding
Compared with other tissues, such as skin, our knowledge is incomplete with respect to the effects of ocular surface dryness on the activation of inflammatory mechanisms and their effects on peripheral sensory terminals. Increased osmolarity, along with rapid cooling from increased tear film evaporation in chronic tear film deficiency, can affect the ocular surface, leading to local inflammation and peripheral nerve injury. Local inflammation has a significant role in the sensitization of peripheral nerves and chronicity in dry eye disease. Epithelial cells are stimulated by persistent desiccation in dry eye disease, releasing inflammatory mediators that can increase the activity of sensory nerve terminals and sensitize them, thereby potentially leading to chronic pain.
REFERENCES:
Belmonte C, Nichols JJ, et al. TFOS DEWS II pain and sensation report. Ocul Surf 2017;15(3): 404-37.
For further details, please refer to The TFOSÂ DEWS II Pain and sensation report
