remarkable feebleness of the heart’s action, irritability of the stomach, and a peculiar change in the colour of the skin.” On account of this discoloration of skin, which Dr. Addison at first conceived always to accompany the disease, it was originally named “melama super-renale.” At a later period, however, Dr. Addison stated, at a meeting of the Medico-Chirurgical Society, that cases might and did occur without any such discoloration. The newly-discovered malady was nevertheless afterwards called bronzed-skin disease, but has now become generally known by the more appropriate and convenient name of Addison’s disease; appropriate because it commemorates the name of the discoverer, in accordance with the custom which has connected the names of Bright and Pott with the diseases which they first recognised, and convenient because it involves no theory as to the ill-understood nature of the disease itself. Dr. Addison’s book contains the record of eleven cases, some of which he had not seen during life, and several of which where certainly not true examples of the disease now known by his name. Indeed, he appears at that time, to have thought that any disease involving the structure of the supra-renal capsules would be accompanied by the symptoms he described. Subsequent observation appears to show that the symptoms, peculiar to Addison’s disease, only occur in connexion with that form of disease of the supra-renal capsules which has commonly been called tubercular, a term perhaps not precisely accurate, but which, for want of a better, I shall on this occasion continue to employ. I do not, however, mean you to infer that the deposit found in the capsules in these cases is identical with tubercle as we meet with it in other organs, but only that it has an apparent resemblance to it, and undergoes degenerative changes of so similar a character, that this term is, in the present state of our knowledge, the most convenient for clinical purposes; more particularly as we find it, in a very large proportion of cases, occurring in persons of a tubercular diathesis. Evidence of inflammation, afforded by adhesion to neighbouring organs and by thickening of the connective tissue surrounding the capsules, are, indeed, common in Addison’s disease, but are always associated either with abscess or with tubercular affection of the capsules themselves. abscess - or at least transformation of the capsules into cysts filled with creamy-looking fluid, or with thinner fluid containing flocculi - have been found associated with the symptoms of Addison’s disease in few instances. It appears to me, however, that there are good grounds for believing that in such cases the abscesses have been formed by the softening down of the deposit, and that they

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