Finkelstein assumes that "the abnormal changes that take place in the bodies which are normally produced in the catabolism of the foocl and in a healthy child are at once rendered harmless, arc the S01.11Te of the symptoms." It is probable that the disturbance has nothing to do with casein, rnilk-fat, and sugar, since no harm appears to be done by adding these substances (casein in the form of plasmon or nutrose) to a diet consisting of substances (breast-milk, flour, etc.) which tend to diminish irritability. Undoubtedly, however, whey has the same effect as COW'S milk in increasing the irritability, and it may therefore be inferred that it contains in solution a substance which is in some way eoncerned in the production of the anonialy.
Finkelstein's contention that COW'S milk is almost invariably harmful is not quite in accord with my own experience, for I have seen symptoms of spasmophilia in breast-fed children who received either nothing but breast-milk, or, in addition to breast-milk, nourishment entirely free from cow's milk (as, for example, rolls soaked in water, with butter and sugar, or soup made with flour). However, cases of this kind are rare exceptions, and we are not inclined on their account to deny the iniportance of diet.
Finkelstein correctly pointed out that the "army of children afflicted with the spasmophile diathesis can he divided into two dif ferent types, which arc closely connected by intermediate forms." One type is seen in the obese, overfed child, in whom, as a rule, a C111.0 can readily be effected by cutting clown the diet; the other finds its repre sentative in the lean, the subjects of chronic gastro-enterie disease, in whom spasmophilia cannot be prevented by restricting the amount of food and is not always curable.
This very knowledge, that the spasmophile affections vary in their manifestations, their degree of severity and clinical course, should pre vent us from neglecting other factors of etiologic importance which we learn by clinical observation and which we are in danger of overlooking because of the importance we attach to the influence of diet.
One of these factors, direct homologous transmission of spasmo Philia front parents to children, has already been mentioned. The significance of this factor is beautifully illustrated by the interesting observation of Finkelstein that children who, without any demon strable alimentary weakness or, at the most, very- slight symptoms of indigestion, acquire spasmophilia, are born of mothers who have them selves had spasmophilia in their childhood and in some instances still present distinct latent sy-mptoms.
Filially, it is probable that the spasmophile diathesis may be produced by protracted diseases of the respiratory organs leading to cachexia, suppurative processes and the like.
Having thus attempted to make elear the predisposing causes of the spasinophile diathesis according to our present knowledge, let us inquire how and in what manner, in a given case of spasmophilia, the individual clinical manifestations ftetany, eclampsia, laryngospasm, expiratory' apneva) are produced. Thc obvious answer is by- reflex action. It will be remembered that Soltmann used the terms "spas mophilia" and "increased predisposition to reflex irritation" synony mously; but it is difficult to make this interpretation harmonize with the absi•nee of exaggeration of the tendon, cutaneous, and mucous membrane reflexes, which ought to be present regularly or at least frequently. Clinical observation supports Thiemich's theory that, in the case of laryngospasm at least, and probably- also of celampsia, some disturbance of the respiration and therefore of the normal ventilation of the blood foxygenation).is the most important etiologic factor. An attack may be brought on by crying from any cause, by the reflex cessation of respiration which accompanies depression of the tongue to allow inspection of the pharynx, or the introduction of a stomach tube, the practical importance of which requires no further elucidation. It is possible that orerfilling of the stomach by a too copious meal, which clinical observation would naturally- incline us to regard as a cause of eonvolsions, may act in a similar manner. The eases of sud den death from arrest of the heart in spasmophile children occur so very frequently after a copious meal that we cannot regard it merely as a coincidence.
Reflex irritation in any part of the body cannot be regarded as the immediate cause of the convulsions. It would he almost superfluous to state in so many words that NYC (10 not acknowledge eruption of a tooth as a possible cause of the convulsions. were it not that quite re cently some authors (Spiegelberg and Bendix for instance) have again taken up this fallacy, which had been successfully vanquished by Fleisch mann, Kassowitz and others.
Finally-, fever must be mentioned as a possible exciting cause. The signifieance of this, factor is very difficult to estimate correctly-, although clinical observation shows that fever is frequently coincident with the occurrence of the convulsions. The time-honored theory that convulsions take the place of chills in infants is untenable, for we note that the so-called fever convulsions occur practically without exception in children of a spasmophile diathesis, and furthermore also in mild tions, such as varicella, and in association with slight febrile elevations.
The diagnosis and prognosis have been sufficiently discussed in the preceding, and all that remains is a short discussion of the