It is only logical to suppose that with anatomo-pathological alterations of the thyroid, indicating a condition of hyperactivity, there must be corresponding clinical symptoms and that these must necessarily be similar to those found in another condition of hyperactivity of the thyroid gland—i.e., in Graves’s disease, the condition of hyperthyroidia. And, indeed, such must be the case, for, as we shall try to show, fever and Graves’s disease have similar clinical symptoms. Thus their most typical symptom is the same: tachycardia or increased frequency of the pulse, without which no case of Graves’s disease should be diagnosed. There is a sensation of heat in most of the cases of Graves’s disease, and the temperature sometimes reaches a dangerous degree in fully developed cases of this disorder. Thirst, frequent in fever, is also a frequent symptom in Graves’s disease (polydipsia in 14 out of 59 cases recorded by Albert Kocher[62]), and can also be produced by thyroid feeding (Lanz,[63] Georgiewski,[64] and others). After a certain duration of fever further symptoms of an increased activity of the thyroid appear, such as abundant perspiration—a typical feature of Graves’s disease. Vaso-dilatation and excessive perspiration can also be produced by thyroid feeding. The latter symptom of fever is a device by which nature tries to eliminate toxic products, and accordingly there generally follows upon it a fall in the temperature and an amelioration of the symptoms of fever. The diarrhœa which we find in some infectious diseases, like that of typhoid fever, trypanosomiasis, etc., is also a typical symptom in Graves’s disease. When the fever subsides there appears another typical symptom of this condition: polyuria. To complete this analogy we may mention toxic decomposition of proteins, diminution in the body weight, great muscular weakness, and increased elimination of urea and uric acid as typical symptoms of both conditions. As in Graves’s disease, there is also in fever an augmentation of the processes of oxidation. Glycosuria is frequent in both conditions, and acetonuria may occur in fever and also in Graves’s disease. Glycosuria and diabetes in consequence of infectious diseases are, as we have shown in a paper read before the London Pathological Society,[65] probably due to the increased activity of the thyroid, and their disappearance, occasionally after a high fever, may be ascribed to the exhaustion of the thyroid after a previous hyperactivity. We know that a condition of Graves’s disease may be followed by a myxœdematous condition in which, as we have shown previously, glycosuria is very rare. In the few hitherto published cases there was no complete myxœdema. Footnote 62: A. Kocher: “Mittheilungen aus den Grenzgebeiten,” etc., 1901. Footnote 63: Lanz: Quoted after Buschau, Wein, 1895. Footnote 64: Georgiewski: Zeitschrift für klin. Medicin, Bd., xxxiii, f. 1-2, p. 153, 1897. Footnote 65: