The ocular surface, by virtue of its dense innervation, is one of the most sensitive tissues in the body.1 Indeed, many of the millions of patients with ocular disease experience symptoms ranging from mild discomfort and “dryness” to frank pain, which can in some cases be debilitating. However, for a significant number of patients, there is a discordance between the signs seen on physical examination and the sensory symptoms felt by these patients. Nerve sensitization, genetic susceptibility to pain, neuropathic pain mechanisms, and psychological status have been proposed as mechanisms for this incongruity between signs and symptoms in dry eye disease (DED).2