As to the _local_ inflammations typical of gout, Ord’s attitude was somewhat ambiguous. Thus he maintains, “The local inflammations do not necessarily depend upon the deposit of urate and the deposit is not a consequence of inflammation; at the same time, it is probable that excess of urate in the blood produces irritation of tissues.” Neither did he believe that the local inflammatory reactions were of necessity in every instance _specific_, viz., due invariably to mechanical irritation by _uratic deposits_, but that they might be initiated by injuries, exposure to cold, etc. Lastly, as to the migration of the disorder from place to place, he believed that for its explanation direct or reflex _nervous_ agencies had to be invoked, for he held the opinion that the local gouty “degeneration and inflammation tend to infect the rest of the system through the blood, and to set up similar actions elsewhere through reflex nervous influence.” We see, therefore, that for Ord gout, as Ewart observes, was “a mode of decay” or a “disease of degenerations.” “The local tissue degeneracies supply a basis for the uratic deposits and the general degenerative changes multiply the sites exposed to an infiltration from the contaminated blood; whilst reflex mechanisms step in as additional determining agents.”[4] Reminiscent of Ord’s view is the hypothesis associated with the name of Ebstein. As the outcome of experimental study he arrived at the conclusion that the primary factor in the causation of gout was a disturbance of tissue nutrition culminating in death or _necrosis_ of the damaged textures. The initial nutritional derangement was ascribed by him to the irritant effect of soluble _neutral sodium urate_. This necrotising agent, following the development of “free acid” during the process of necrosis, was transmuted into the acid urate. Subsequently this same was deposited in crystalline form in the necrosed area. He held these areas of necrosis quite as typical of gout as the uratic deposits, and postulated their combinations to be necessary for the production of a true gouty focus, claiming that he had detected such foci in cartilage, tendons, kidneys, and connective tissue. Experimentally, Ebstein endeavoured to induce a gouty condition in fowls by ligaturing both _ureters_, thus thrusting upon the circulation the dammed-up uratic secretion. In other instances he administered to the same animals subcutaneous injections of neutral _chromate_ of _potassium_, attributing to this substance the power of inhibiting the excretion of uric acid _viâ_ the kidneys through its action on the renal parenchyma. Subsequently, after death he noted the incidence of _uratic deposits_ in joints, muscles, tendon sheaths, and liver, the same being more copious in those animals subjected to chromate injections.