This disorder has long been considered as a form of auto-intoxication and the theories propounded have been many and varied. Its similarity with uremia has led to the opinion that renal insufficiency was the prime cause but this does not explain many of its clinical features. It has been shown by the experiments of Blumreich (29) in which the kidneys of gravid rabbits were removed, that, the induced uremia did not cause eclampsia, and also that the brain of gravid animals is much more sensitive to irritation than that of the non-pregnant. In this latter conclusion we have an experimental realization of the well known fact that pregnant women are sensitive to influences that usually would have no effect, the nervous organism being markedly changed by their condition. Thinking that pregnancy might induce some peculiar change in the urine, Stewart (30) studied the urine of women in the later months of pregnancy but found that it showed no toxicity beyond that of ordinary urine.

Wells (31) has had the opportunity of observing the effects of gastric and intestinal catarrh in pregnant women, and finds that the auto-toxemia is more likely to appear in plethoric than anemic patients. The symptoms noted are pain about the eyes, headache, photophobia, malaise, frequent urination but diminished urinary quantity, mental dullness and casts and albumin in the urine. These observations are of importance, not in showing that the pregnant are liable to autointoxication, for that is evident as is also the fact that they are particularly susceptible to it, but as showing that the intoxication did not cause eclampsia even if the kidneys were affected.

Strumpf considers that acetone or some similar body is the materia peccans of eclampsia, and claims that it is invariably present in the breath and in large quantities in the urine. He would class this disease with diabetes as an acid intoxication. Massen believes the convulsions to be the result of a true auto-intoxication caused by non-oxidized cellular substances, which through faulty liver action are not destroyed.

But by far the most light has been thrown on this disorder by the researches of Ascoli (32) in which eclampsia has been produced experimentally. He found that when placental extract was injected into an organism, a reaction takes place with the formation of cyto-toxins, and when these are injected into other gravid animals a train of symptoms appear which closely resembles that of eclampsia. His serum was prepared by injecting into rabbits filtered emulsions of guinea pig placenta, and separating their blood serum. This when injected into the circulation of gravid guinea pigs caused no disturbance, but when injected under the dura the animals went into a state of coma which was interrupted by tetanic clonic and tonic convulsions which, without delivery, continued into profound coma and death. These experiments suggest that placental cells or soluble effluvium from them may be concerned in the etiology of eclampsia, and it is conceivable that immunity against these cyto-toxins might be developed. This is probably the case for we know that eclampsia occurs much more commonly in primipirae than in multipirae. In the case of puerperal eclampsia it matters not whether we consider that the poison proceeds from the fetal or the maternal organism, for they are made one through the circulation, each shares nutrition and tissue waste with the other, and we have a true auto-cyto-toxin, the advent of any heterogenous serum being impossible.