Hi, I have HNF1-alpha type monogenic diabetes. I have the "aura" (flashing lights) somewhat regularly -- I think I have all of my life, possibly -- as far back as I can remember, although I only diagnosed myself as a diabetic after the age of fifty and have been using insulin therapy for less than a decade.
In contrast to what many have described herein for themselves, I have found that I only experience the aura when I am near normal glycemia (~80mg/dL, or 4.4mmol/L) but either transitioning downward or upward. Usually these transitions are related to peripheral flux from earlier subcutaneous insulin administration, sometimes in combination with portal flux from a meal.
I never have aura when I have significantly lower than normal fed-state BG -- say, mid sixties (mg/dL) or lower. In this state portal glucagon secretion should be high, guaranteeing appropriate fuel (ketones and glucose) for brain and eyes. In those who are not normally keto-adapted the primary response (glucagon) may be ineffective, however. This produces the adrenal response, which is unpleasant, and involves a fuel crisis sensed by the brain.
Based upon my own experience I believe that the aura is likely an effect confined to certain tissues of the eye, and unrelated to the brain. I never experience any other symptoms of glycemia, including "hypoglycemia" -- when the primary response is working well the brain has more than adequate fuel. However T1Ds, within a few years after diagnosis, generally do NOT have normal or healthy primary response.
The alpha cells change due to the sustained absence of an insulin signal. This is referred to in the islet research literature as "loss of intraislet insulin decrement", and similar terms. When endogenous insulin production/secretion drops to near zero there can no longer be an "intraislet decrement" sensed by the alpha cells, as in a non-diabetic, driven by a drop in BG.
Many tissues, especially those not expressing insulin such as many of the cells in the eyes, cannot respond quickly to rapid changes/transients in BG. This is one of the fundamental reasons for diabetic complications in general, and in eyes in particular. This damage occurs dominantly during prandial glycemic transients which a diabetic cannot control endogenously.
Possibly the aura is related to vascular glycocalyx in eyes, for instance. These nanostructures reportedly are destabilized by BG transients or disequilibrium.
I suspect that the aura I remember from younger years may have been induced by physical exercise and depletion of muscle glycogen. I associate the auras from this time with the outdoors, making it likely that I was engaged in strenuous activity.
If available, I might drink a cup of bone broth, inducing a gentle hyperglucagonemic stinulus to the islets. Otherwise, the aura never lasts very long -- usually less than a half hour or so. In the worst case I might be working under a microscope or something like that, in which case I will just wait things out until presumably the eye tissues and glucose stabilize.
I never have headaches, and so I cannot personally compare any aura from this condition.