Uneasiness in the right hypochondrium and even slight swelling of the liver was noted by Trousseau and also by Scudamore. Such congestion of the portal system and hepatic enlargement may be only fugacious, but often the same is permanent, a penalty of the same cause—free living—which leads to the production of gout. For in many instances but too true is it that “for years together,” as Sydenham said, “a man has drunk and feasted, has omitted his usual exercise, has grown slow and sluggish, has been over-studious or anxious, in short, has gone wrong in some important point of life.” But more palpable to his friends than to himself are the concomitant changes in his disposition and character. From being good-natured and easy-going he becomes morose and irritable. The irascibility of the gouty is proverbial, and the explosive mental outbursts to Duckworth appeared at times to be “a metamorphic substitution for a more overt and regular attack,” or, as Sydenham expressed it, “Non rectius podagræ quam iracundiæ paroxysmus omnis dici potest.” Sometimes his mental vagaries are exchanged for or accompanied by neuralgia, painful cramps in the limbs, etc. In truth, the premonitory phenomena of gout are protean, inasmuch as, given any prior weakness or functional derangement of any viscus, the symptoms of oncoming gout are masked by aggravation of the same, it may be by cardiac irregularities, vesical irritability, or in an old bronchial subject by increase of cough, etc. But it may be objected, there is nothing _specific_ about these various _functional_ disturbances. They are not more common in the _gouty_ than in others. Moreover, the habits of life productive of gout favour the development of gastric and hepatic derangements. The mental irritability, the gastric disturbances, etc., may be quite as well accounted for by overeating and overdrinking as by gout. Now, if there be nothing _specific_ of gout in these so-called prodromata—“heartburn, acidity, flatulence, etc.”—then what is their true significance? For, obviously recognition of their true import is most essential. Now to my mind the said “dyspeptic” symptoms should be regarded not as symptomatic of gout, but as _etiologically_ related thereto. For, though the etiology of gout is still much debated, the same obscurity will certainly not be clarified, if we merely content ourselves with dubbing such “dyspeptic” symptoms as “gouty.” On the other hand, if we, at this early stage, endeavour to elucidate the _true origin_ of the “dyspeptic” symptoms, who will deny that this is the more rational and scientific mode of procedure? The timely elimination of _septic foci_ in the mouth, tonsils, and naso-pharynx conjoined with modification or restriction of food intake and recognition betimes of the signs of intestinal infection and constipation would perhaps stave off or avert the threatened articular outbreak.