Syphilis by producing a specific cerebral lesion may be the cause of symptomatie epilepsy. Other signs of focal disease besides the con vulsions arc practieally always found in such eases. In others, which appear to be cases of genuine epilepsy, congenital syphilis probably has the same etiologic importance as any constitutional injury that affects the central nervous system, such as various intoxications, aleohol, lead and the like.
The relation existing between epilepsy and eelampsia infantum calls for special discussion.
Since it may be regarded as certain that the two diseases are funda mentally different, the transition from eelampsia to epilepsy is no more conceivable than a transition, for example, from hysteria to epilepsy. The question is whether eclamptic patients, or those who have suffered froin eclampsia, possess a certain predisposition to epilepsy. The statistics which we find in the literature (see Finckh's analysis), and which without exception answer this question in the affirmative, are marred by two serious defects. In the first place, genuine and symp tomatic epilepsy are not differentiated with sufficient accuracy: and in the seeond place, it is impossible, when a history of convulsions in infancy is obtained, to secure sufficient proof that the convulsions were eclamptie in character.* The only way in which positive conelusions can be reached is by keeping a series of eclamptic children under observation for a period of years instead of depending on retrospective examinations of epileptics, but this method has never been systematically employed. My own numerous observations, although they have not as yet been carried on for a sufficient length of time, tend to show that eelampsia does not indicate any predisposition to epilepsy. this I do not mean to deny that a child who has had eclampsia may later become epileptic; but such eases are rare in comparison with the frequeney of eclampsia in childhood.
When the ease is merely reported by a layman and has not been under accurate medical observation, it is always possible that the first attacks during infancy may have been epileptic; or conversely, attacks occurring in the second or third period of childhood may be attacks of late eelampsia (eomparc page 343).
Quito independently of the data obtained by questioning the patient, which we have used as a starting point, we may speculate theoretically whether the convulsive attack itself, judged by its severity or frequent reeurrenee, may have been capable of producing the epileptic changes in the brain indirectly through the circulatory disturbances to which it may have given rise. Although this possibility cannot be altogether
denied, there are so many well-founded objections to (for the literature see Freud) this view that its adherents are constantly diminishing in numbers.
Many authors see in autointoxicatiom of the organism an important etiologic factor of epilepsy. As yct this doctrine of autointoxication is based on such a small number of authentic cases that we need not dis cuss it here and may refer the reader to the text books on epilepsy.
The same is true of the rare reflex epflepsies, the study of which must be begun all over again, taking into account what we now know of the spasmophile diathesis.
The diagnosis of epilepsy in its well-developed forms is easy when the chronic character of the disease has become manifest by the peri odical recurrence of the motor or psychic attacks at intervals of months or years, and permanent intcrparoxysmal changes have perhaps already developed. It is much more difficult, and frequently quite impossible, on the other hand, to diagnose epilepsy from the first convulsive phe nomena or psychic equivalents as observed by the patient's friends or family. The clinical expression of this emotional or inhibitory explosion is not in itself eharacteristic of epilepsy, and becomes so only by the periodical recurrence of the attacks.
In the present state of our knowledge. we are tillable in every individual ease, even after a careful examination of the patient, to decide whether a convulsive attack represents the first manifestation of an organic disease of the brain or merely a functional disturbance. There are functional convulsions the origin of which is absolutely unin telligible—at least none of the well-known causes, such as uraimia, for example, can be discovered—and such attacks we are inclined to regard as the first manifestations of epilep.sy. In the subsequent course of these cases, however, we are often surprised to find that the convulsions remain limited to one or a very few attacks, and recur either »ot at all, or only after the lapse of many years.