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Objectives: If questionnaires contributing to the diagnosis of dry eye disease are to be recommended as alternatives to existing questionnaires, they must be comparable, with similar repeatability and treatment sensitivity. Comparability was thus examined for three common dry eye questionnaires along with identifying the individual questions that most strongly predicted overall scores. Methods: Anonymised data ( n = 329) collected via the Ocular Surface Disease Index (OSDI), 5-item Dry Eye Questionnaire (DEQ-5) and Symptom Assessment in Dry Eye (SANDE) questionnaires (including responses to individual questions) from consenting patients were drawn from real-world dry eye clinics/registries in the United Kingdom, Australia and New Zealand; at follow-up, normalised changes were evaluated in 54 of these patients. Treatment data were also analysed from a 6-month, randomised controlled trial assessing artificial tear supplement treatments with 43 responders and 13 non-responders to treatment identified. The questions extracted from the OSDI which form the abbreviated 6-item OSDI were also analysed. Results: The agreement between the questionnaires ranged from r = 0.577 to 0.754 (all p < 0.001). For the OSDI, three questions accounted for 89.1% of the variability in the total score. The correlation between the OSDI and OSDI-6 was r = 0.939, p < 0.001. For the DEQ-5, two questions accounted for 88.5% of the variance in the total score. Normalised treatment changes were also only moderately correlated between the questionnaires (r = 0.441 to 0.595, p < 0.01). For non-responders, variability was 7.4% with both OSDI and OSDI-6, 9.7% with DEQ-5, 12.1% with SANDE-frequency and 11.9% with SANDE-severity scale. For responders, improvement with drops was detected with a 19.1% change in OSDI, 20.2% in OSDI-6, 20.9% in DEQ-5, and 27.5%/23.6% in SANDE-frequency/severity scales. Conclusions: Existing commonly used dry eye questionnaire scores do not show high levels of correlation. Th

Pain associated with mechanical, chemical, and thermal heat stimulation of the ocular surface is mediated by trigeminal ganglion neurons, while cold thermoreceptors detect wetness and reflexly maintain basal tear production and blinking rate. These neurons project into two regions of the trigeminal brain stem nuclear complex: ViVc, activated by changes in the moisture of the ocular surface and VcC1, mediating sensory-discriminative aspects of ocular pain and reflex blinking. ViVc ocular neurons project to brain regions that control lacrimation and spontaneous blinking and to the sensory thalamus. Secretion of the main lacrimal gland is regulated dominantly by autonomic parasympathetic nerves, reflexly activated by eye surface sensory nerves. These also evoke goblet cell secretion through unidentified efferent fibers. Neural pathways involved in the regulation of meibomian gland secretion or mucin release have not been identified. In dry eye disease, reduced tear secretion leads to inflammation and peripheral nerve damage. Inflammation causes sensitization of polymodal and mechano-nociceptor nerve endings and an abnormal increase in cold thermoreceptor activity, altogether evoking dryness sensations and pain. Long-term inflammation and nerve injury alter gene expression of ion channels and receptors at terminals and cell bodies of trigeminal ganglion and brainstem neurons, changing their excitability, connectivity and impulse firing. Perpetuation of molecular, structural and functional disturbances in ocular sensory pathways ultimately leads to dysestesias and neuropathic pain referred to the eye surface. Pain can be assessed with a variety of questionaires while the status of corneal nerves is evaluated with esthesiometry and with in vivo confocal microscopy.

This report characterizes the neurobiology of the ocular surface and highlights relevant mechanisms that may underpin contact lens-related discomfort. While there is limited evidence for the mechanisms involved in contact lens-related discomfort, neurobiological mechanisms in dry eye disease, the inflammatory pathway, the effect of hyperosmolarity on ocular surface nociceptors, and subsequent sensory processing of ocular pain and discomfort have been at least partly elucidated and are presented herein to provide insight in this new arena. The stimulus to the ocular surface from a contact lens is likely to be complex and multifactorial, including components of osmolarity, solution effects, desiccation, thermal effects, inflammation, friction, and mechanical stimulation. Sensory input will arise from stimulation of the lid margin, palpebral and bulbar conjunctiva, and the cornea.