The close association of the exudative and neuropathic diatheses suggests a causal relationship. The frequent anaphylactic nature of the former 1 would seem to point toward a similar cause in the latter.It is my purpose in this paper to discuss certain nervous manifestations in infants and children from the standpoint of anaphylactic cause.It is hardly necessary to call attention to the frequent occurrence of the exudative and neuropathic diatheses in the same individual. All observers recognize the common association. However, it seems to have been generally held that this relationship is nothing more than accidental. Czerny considered it so.2 He felt that the almost universal presence of the neuropathic diathesis in one or both parents of children with the exudative diathesis led, as a natural result, to the neurotic child. The degree to which the infant was affected by this nervous environment determined, to a certain extent, the obstinacy and severity of the exudative manifestations. Pfaundler 3 stated that the sneezing in coryza, pertussoid in bronchitis, asthma in bronchiolitis, severe colic in enteritis, etc., were dependent, to a certain degree, on the coexistence of a neuropathic diathesis along with the exudative diathesis.This common association, together with the fact that frequently in the same individual the symptoms of one, and again the symptoms of the other diathesis, will seem to predominate, led me to the opinion that not infrequently the symptoms of both conditions might be due to the same underlying factor. Inquiry revealed the fact that often nervous patients have a history, either personal or familial, of exudative dis¬ turbances, and the frequent anaphylactic basis for the exudative phenomena suggested that the nervous symptoms might also be due to this cause. Therefore, this investigation was undertaken to see if this might not be the case clinically.The cases presented are of three types ; first, the type in which the symptoms of both diatheses were plainly present; second, the type in

Our forefathers believed that foods ingested by the nursing mother might affect the child through the breast milk. We, however, have discarded that belief almost universally, and have relegated it to the shelves of superstition simply because we have not succeeded in proving it to be true. Having seen several cases of food disturbance in

Eczema in breast fed babies has been even more puzzling to physicians than that occurring in the artificially fed, or in adults. Its etiology has been almost wholly a mystery; treatment has been empirical, and results have been as unsatisfactory as one would expect. Recent researches give promise of a rational explanation of the cause and a

Objectives-Raised concentrations of antimony have been found in infants dying of sudden infant death syndrome (SIDS). The presumed source of this antimony is toxic gases generated from fire retardants that are present in cot mattresses. The aim of this study was to determine the role of antimony in SIDS. Design-Samples of liver, brain, serum, and urine were collected from all patients dying from SIDS and a group of aged matched control infants who had died of other causes. Setting-Nationwide study in Ireland. Subjects-52 infants dying from SIDS and 19 control infants aged > 7 days and < 1 year. Results-The median concentration of antimony in the liver and brain of infants dying of SIDS was < 1 ng/g, with no diVerence detected between the infants dying from SIDS and the control infants. The range of antimony in the serum of infants dying of SIDS was 0.09-0.71 µg/ litre (median, 0.26). Although no diVerence was found between infants dying from SIDS and control infants, SIDS infants were found to have higher concentrations when compared with healthy infants in the 1st year of life, probably as a result of release of antimony into serum after death. Urine antimony concentrations in infants dying from SIDS were < 3.91 ng/mg (corrected for creatinine) and similar to values found both in control infants and healthy infants. Conclusion-There is no evidence to support a causal role for antimony in SIDS.

No abstract