Rod sensitivity and photic history: response to Spitschan’s letter

In his letter, Dr. Spitschan [2] raises the possibility that our dark-adapted ERG recording could not be interpreted as an electrical signal that arises from rods and post-rods retinal pathways only because a 20 minutes adaptation time may not be sufficient for a full adaptation, especially when considering the “photic history” in our experimental design [1]. Based on the above, he suggests that our findings may reflect a fundamental difference between migraineurs and control subjects in the ability of their rods to adapt to dark. While his proposal is interesting and definitely worthwhile the time and effort it may take to address in yet another clinical study, we would like to call attention to the following: 1) Photic history is known to affect the degree to which subsequent exposure to light acts to shift circadian rhythm. This effect, however, is independent of rod light sensitivity, which is simply a function of instantaneous rhodopsin concentration within the rods. 2) Rhodopsin is synthesized at a nearly constant rate. At high light levels, it is destroyed as fast as it is regenerated. At lower luminances, rhodopsin concentration equilibrates with light level and thus provides a light sensitivity appropriate to the luminance. 3) After 20 minutes of dark adaptation, normal individuals achieve a light sensitivity which will not increase significantly with longer adaptation times, even when measured with psychophysical techniques. 4) The electrophysiological methods used in our study for recording ERG would be able to detect any improvement in adaptation after the 20-min adaptation period as the differences would be too small to resolve. 5) Because high levels of dark adaptation are almost instantly reversed upon exposure to photopic conditions, duration and history of dark adaptation is best normalized by dark adapting a patient who has been previously exposed to normal photopic conditions for a fixed length of time. Accordingly, we strongly believe that our findings represent a true difference in sensitivity to low luminance conditions in migraineurs vs. health control subjects. Finally, if rods ability to adapt to dark is in fact compromised in the migraine eye, one would predict that migraineurs will be more prone to night-blindness than non-migraineurs as dysfunctions in this adaptation process (which involves a recombination of free opsin with an untransformed retinal and the resultant regeneration of rhodopsin) is often associated with this night blindness. To the best of my knowledge, there is no evidence for different prevalence of night blindness in migraineurs as compared to non-migraineurs. Logically, since migraineurs are more sensitive than non-migraineurs to low luminance, one could suggest that their adaptation process is completed faster. This would suggest that the incidence of night blindness is lower in the migraineurs than in the non-migraineurs. Lack of epidemiological data on this topic limits this discussion.