Abstract
Purpose : Concussion-induced light sensitivity, or traumatic photalgia, is a lifelong debilitating problem for upwards of 50% of cases of mild Traumatic Brain Injury (mTBI). The retinal source of the pain of this persistent light sensitivity remains controversial and we found no previous reports of brain trauma affecting human retinal processing. We employed spectral analysis of electroretinographic (ERG) responses to assess unsuspected damage to the retina of the human eye and determine its retinal-cell source.
Methods : All participants had letter acuity of 20/40 or better in both eyes (LE: 22 ± 5, RE: 23 ± 6) and no visible ocular abnormalities. The mTBI participants had closed-head trauma resulting in a loss of consciousness for 5+ minutes, or loss of memory of the traumatic event; they were assigned to 1) the non-photalgic mTBI group if they experienced no discomfort on viewing the full-field flickering stimuli of the present study at their maximum intensities, and to 2) the photalgic mTBI group if they did experience visual discomfort. The control group included those with no past mTBI events.
Light-adapted ERG was recorded binocularly from skin electrodes at 200 ms on/off periods of full visual-field stimulation of equal radiance red (610 nm), green (540 nm), blue (470 nm) and white (610 + 540 + 480 nm) light, up to 750 Ph Td for the combination.
Results : Good quality ERGs were recorded under all conditions, with notable waveform changes, conforming to cone b-wave peak latencies for the control and non-photalgic groups, but shifting to rod b-wave latencies for the photalgic group (p<0.05, corrected.). In addition, the mTBI groups lacked the photopic negative response evident in control ERGs, implying reduced plexiform layer function.
Conclusions : The shift from a cone to a rod b-wave in photalgic mTBI implies an mTBI-driven blockage of the known photopic rod suppression mediated by the dopaminergic pathways (Akopian & Witkovsky, 1996, J Neurophysiol), which is a manifestation of the mutual mesopic cone-rod inhibition operating under normal conditions (Krizaj, 2016, Micr Res Tech). This novel insight into the retinal mechanisms of traumatic photalgia suggests that the primary etiology of the photalgic light sensitivity may be this inversion of cone/rod suppression, causing panretinal rod overactivation at moderate light levels, thus providing a non-invasive diagnostic biomarker for traumatic photalgia.