Going Back One Car in the Train: Evaluation of the Relative Afferent Pupillary Defect in the Era of Tele-Neuro-Ophthalmology

Letters to the Editor Going Back One Car in the Train: Evaluation of the Relative Afferent Pupillary Defect in the Era of Tele-Neuro-Ophthalmology T he recent pandemic has forced us from our usual practice of medicine to alternative means including telehealth visits for the safety of the patients and practitioners. These virtual office visits have left us with few of the tools that we normally rely on. Therefore, there is a greater reliance on clinical skills that can translate in the virtual visit and be helpful for diagnosis. Here we bring to attention the evaluation of a relative afferent pupillary defect (RAPD), a sign of optic neuropathy, through an old-fashioned method. Galen's second century observation about pupillary reactivity was remarked on by Hirschberg in 1901 (1) that the uncovered eye's dilation was worth observing. Although alternate cover testing was not explicitly described by Gunn, he was doing it in bright light to describe his observation that completely covering the good eye would paradoxically dilate the bad eye. Alfred Kestenbaum measured this difference in pupil size (2), and it was termed Kestenbaum's pupil number (KPN) by Dr. H. Stanley Thompson in his beautifully written treatise in the Second Hoyt Lecture on the history of pupillary function (3). This method is still perfectly suited for today's available technology in the era of tele-neuro-ophthalmology that we outline below: Evaluation of an RAPD in the tele-neuro-ophthalmology video examination as follows: 1. With bright diffuse daylight oriented at the patient's face ask the patient to orient a camera framed closely on both eyes while they fixate at a distant target. 2. Using a large kitchen spoon that can block light ask the patient to alternatively cover each eye. 3. Observe the revealed pupil. If it dilates rather than constricts, this is evidence of an RAPD. 4. Pupils in saved images can be compared and their difference in size documented as KPN, a quantitative measurement is validated against neutral density filters (4). Prothrombin G20210A Mutation Causing Nonarteritic Anterior Ischemic Optic Neuropathy in a Young Patient W e read with interest the article by Francis and Patel (1) and wish to share our experience of managing 7nonarteritic anterior ischemic optic neuropathy (NAION) in young patients. A 47-year-old man presented 442 5. To visualize dark irides, patients' alternately illuminating each eye with a closely held bright light in a dark room is effective and familiar. To quote H.S. Thompson, "When almost every 'discovery' turns out to be a rediscovery, our modern clinical contributions begin to seem like just another car at the end of a long and magnificent train of observations." We have the fortune to walk back one train car length and recall a forgotten but useful clinical skill for our patients today. Linus D. Sun, PhD, MD Departments of Ophthalmology and Neurology, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, New York Jeffrey G. Odel, MD Department of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, New York The authors report no conflicts of interest. REFERENCES 1. Hirschberg J. Ueber die Pupillen-Bewegung bei schwerer Sehnerven-Entzündung. Berliner Klinischer Wochenschrift. 1901;38:1173-1175. 2. Fineberg E, Thompson H, Quantitation of the afferent pupillary defect. In: Smith J, ed. Neuro-ophthalmology Focus 1980. New York, NY: Masson Publishing, 1979:25-29. 3. Thompson HS. The vitality of the pupil: a history of the clinical use of the pupil as an indicator of visual potential. J Neuroophthalmol. 2003;23:213-224. 4. Jiang MQ, Thompson HS, Lam BL. Kestenbaum's number as an indicator of pupillomotor input asymmetry. Am J Ophthalmol. 1989;107:528-530. to our hospital with sudden onset painless defective vision in the left eye of 10 days' duration. His best-corrected visual acuity was 20/20 in the right eye (RE) and 20/ 500 in the left eye (LE). Anterior segment was normal in the RE, and a relative afferent defect was present in the LE. Fundus examination of the RE showed a crowded disc, and the LE showed a pallid disc edema (Fig. 1). Visual-evoked potential showed reduced amplitude of P100 in the LE with normal latency. Fundus fluorescein Letters to the Editor: J Neuro-Ophthalmol 2020; 40: 442-443 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.