Were such uratic deposits located at the site of _inflammatory_ as opposed to degenerative visceral foci, it would to our mind give more colour to the assumption that they were the outcome of a true gouty process; in other words, that, as in the joints, they were the _sequel_ or concomitant of _acute gouty inflammation_. But it is not so. As for the structural or organic degenerations met with in gouty subjects, very many, if not all, as Longstreth rightly says, “belong to some one of the great general classes of tissue changes, some of which are due to special causes, but the most of them own many causes. One of these many causes can be under certain circumstances gout, but there is really nothing special in the appearances by which we can unequivocally pronounce them of gouty origin.” With this view few would join issue, save only the reservation that the _scleroses_ so commonly met with in _gout_, if due thereto, must owe their origin to some more vital agent than _uric acid_, a few milligrammes more or less in the blood content thereof. It will be seen then that the _anatomical_ evidence that gout can affect the _internal_ organs is wholly lacking. The criteria then upon which the assumption is based that this or that functional disturbance is a manifestation of irregular or _visceral_ gout are wholly _clinical_. Doubtless the conception of irregular gout was derived from “the unaided operation of custom.” Thus, when one clinical event, A, was noticed frequently to precede another, B, the idea of an association between A and B was generated, and by virtue of this association A was said to be the cause of B. But obviously the fact that B has followed A does not establish any necessary connection between the two clinical events. In other words, the idea of a causal relation is in a sense a purely intellectual feat, a clinical inference _presumptive_ and _retrospective_. The evidence that a relationship exists between _irregular_ and _regular_ manifestations of gout rests upon the following sequences and alternations of clinical events:— (1) The subsidence or disappearance of functional visceral derangements following the development of articular gout; (2) Their occurrence directly after an articular paroxysm has been apparently suppressed; (3) Their recurrence and alternation with arthritic outbreaks, this in some instances repeatedly; (4) Lack of any appreciable cause for the functional derangements and their indefinite anomalous character; (5) Their favourable response to specific gouty therapy. As before noted, _digestive_ troubles frequently precede the initial outbreak of articular gout. The same likewise are frequent in chronic cases between the intervals of arthritic seizures.