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Think neuropathic pain when dry eye symptoms, findings misalign
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Some 70 years ago, Dr. Theodore Woodward, a professor in the University of Maryland’s School of Medicine, first uttered the phrase: “When you hear hoofbeats, think of horses, not zebras.” It was Dr. Woodward’s way of impressing upon his students the importance of logically linking patient symptoms with clinical findings ... and then pursuing the most probable diagnosis first.
For certain, this is sage advice that has undoubtedly stood the test of time. Even today, the concept of “think horses, not zebras” is woven into every health care providers’ training, regardless of their discipline. It is a philosophy that not only serves us well, but also provides us with a greater level of confidence and comfort – confidence in knowing that when subjective symptoms and objective findings agree, the differential diagnosis is less complicated, and comfort in knowing that we have tangible metrics upon which to gauge the efficacy of our treatment. Unfortunately, as we all know, subjective symptoms and objective findings do not always align.
Perhaps this discrepancy between symptoms and findings is no more evident than in the case of dry eye. In certain dry eye patients, there is reasonably good concordance between symptoms and findings, and therapeutic endeavors are easily gauged, while for others there is a tremendous disconnect. For these folks, symptoms are disproportionate for clinical findings and, accordingly, therapeutic efforts are often futile at best. It is in precisely these situations that it behooves us to actually think zebras. And in the case of the dry eye sufferer, the zebra might well be neuropathic pain.
The concept of neuropathic pain is not a new one and goes well beyond medicine. As far back as the 1600s, rationalist philosophers referenced the most rudimentary form of neuropathic pain – phantom limb pain – as evidence that empiricism was inherently flawed. Even today, neuropathic pain remains a philosophical and medical enigma. At best, we can describe it as a complex, chronic pain resulting from some form of somatosensory dysregulation.
In the case of dry eye, it might well result from some form of antecedent ocular trauma such as longstanding contact lens abuse, previous photorefractive surgery, or even prior herpes zoster ophthalmicus. In the absence of an overt ocular trigger, it might well be related to an underlying systemic driver such as diabetes, vitamin B deficiency or fibromyalgia. And in other cases? We just do not have an answer.
Our concerns with neuropathic pain are multifaceted. Is the site of dysregulation and associated pain mediated centrally or peripherally? Should our therapies be targeted to the ocular surface or certain higher cortical processing centers? If not treated promptly, can neuropathic pain become “hard wired” and more recalcitrant to future therapeutic efforts? One thing is clear: The stakes are high, as evidenced by the tremendous impact neuropathic pain has on quality of life, dry eye patients included.
In this month’s issue, our feature article “Dry eye pain without clinical signs could be neuropathic” takes a closer look at this complex disorder. While unable to provide every answer to the neuropathic pain puzzle, it does give us a better understanding of proposed mechanisms, differential diagnosis, treatment strategies and, perhaps, most importantly, when to think zebras.