Full-field electroretinograms (ERGs) are a well-characterised method to indirectly study the clinical function of the visual system from the level of the photoreceptors to the ganglion cells. In past research, the a-wave and b-wave components have been studied separately (Thomas and Lamb, 1999; Cameron, Mahroo and Lamb, 2006), however, few sources evaluate them together.  In this study, we aimed to address the rod contribution to the full-field ERG response for both the A-wave and B-wave components. This was done by comparing the responses from normal subjects to the responses of subjects with a range of genetic and acquired retinal diseases to dissect the different components of the full-field ERG response.   Patients with Vitamin A deficiency experience night blindness and ERGs typically show abolished rod system responses and preserved cone system responses, two main hypotheses have been put forward to explain this phenomenon: Vitamin A deficiency reduces quantal catch (total number of photons absorbed per unit time) due to lack of chromophore in the outer photoreceptor segment. The presence of significant quantities of free opsin weakly activating the phototransduction cascade, leading to the shut-off of circulating current. These two hypotheses cannot easily be tested, as the rod driven ERG responses are normally completely abolished in most cases of Vitamin A deficiency. This study used a patient with moderate Vitamin A deficiency where the ERG response is only partially reduced.   According to the first explanation, a response to a flash stimulus  in Vitamin A deficiency would be identical to a response to a dimmer flash delivered when Vitamin A levels are normal. In the second case, the flash response would resemble the response obtained in the presence of a light-adapting background (which similarly causes a reduction in photoreceptor circulating current).  In our patient, we found rod-driven responses were more consistent with the second explanation, indicating that loss of rod sensitivity in Vitamin A deficiency is largely a result of shut-off of circulating current due to sustained activation of the phototransduction cascade, probably by free rod opsin.