The very disparity between the local lesions seems to exclude the possibility of their being due to one and the same cause: in the joint, acute _inflammation_; in the heart and brain, _degenerative_ changes. Where then the nexus? Surely it is but a _time relation_, a coincidence, the outcome of, _concurrent_ though _unrelated cardiac_ and _vascular_ lesions. In short, the cases of so-called retrocedent “cardiac” and “cerebral” gout usually resolve themselves into _cardio-mural degeneration_, _arterio-sclerosis_, or _renal disease_. OTHER IRREGULAR MANIFESTATIONS The more dramatic examples of retrocedent gout, as before stated, occur mainly in the _acute_ varieties of the disorder. But the same visceral metastases are occasionally linked up with the less severe articular manifestations, or with that vague clinical entity known as “goutiness,” the same being frequently known as “wandering” or “flying” gout. Most of the examples met with in the present day belong to the last category. This may possibly find its explanation in the growing infrequency of the more acute or sthenic types of gout. Both of the mild and of the severe forms of metastasis the same pathological interpretation is hazarded. The gout is described as “suppressed” or “retrocedent.” According to the former conception, the gouty process itself suffers _inhibition_, while the latter term signifies _deflection_ of the _materia peccans_ of gout from the joint into the viscera. Of the twain the former hypothesis seems to me the more plausible. Thus, given an acute gout at its inflammatory zenith, it is conceivable that, if _abruptly checked_, the same might _reflexly_ precipitate the occurrence of internal lesions in structures undermined by insidious and _pre-existing degenerative_ changes. In other words, the aborted attack is not the cause, but the _occasion_, of the cardiac failure, the apoplectic stroke, the uræmia, etc. On the other hand, given that such were due to actual _transference_ of the gouty poison, one would expect that it would induce the same _inflammatory_ phenomena in the viscera as in the joint. But there is no _anatomical_ proof that such occurs, no evidence of an actual invasion of the impeached viscus by the _gouty inflammation_. _Uratic deposits_ have, it is true, been found _post mortem_ at the site of visceral lesions, but, be it noted, generally in _degenerating_ tissue altered by other morbid processes. Some, however, affirm that in such the gouty process has _quâ_ the uratic deposits left, so to speak, its attestation behind it. But any _degenerative_ focus may in a _gouty_ subject become the seat of such a _deposition_. Yet it would be presumptuous to infer its gouty origin from this fact alone. Such are common in _chronic nephritis_, and this apart from gout. What need for wonder then that the same should occur in gouty subjects, with their blood surcharged with uric acid?