Pathological Physiology

Abstract

As we said at the beginning, during the early decades the study of cretinism was confronted with the confusing impression that cretinism on the one hand was bound geographically to those regions of most severe goitres, while on the other hand a large number of cretins do not present goitre. Initially, the clinical relationship linking cretinism with cachexia thyropriva discovered by J. and A. Reverdin, Th. Kocher and P. von Bruns in particular, and the myxœdema described by English authors, redirected research for the last 50 years in the direction of the thyroid gland. The fact that a normal thyroid gland had not been found in a single cretin demonstrated that cretinism is in actual fact a thyroid gland problem to a great extent. The non-goitrous cretin turned out to be a person with an atrophic thyroid gland. This atrophy showed the same geographical spread as did the severe endemic goitres. Transitions between thyroid gland atrophies without goitre, and those with goitre, are fluid, and occasionally, within the same family, we find one child stricken purely with thyroid gland atrophy, and the others stricken with cretinous feeble-mindedness with goitre and atrophy of the remnants of the thyroid gland. We therefore had to broaden the idea of goitre endemic disease into that of endemic thyropathy encompassing both endemic atrophy of the thyroid gland and the endemic goitrous enlargement of it. Admittedly, that still did not solve the problem but simply defined it more sharply.