Thus, they maintain that the fleeting attacks of lumbar fibrositis or lumbago which ensue after dietetic indiscretions have no relation to gout, but are simply indicative of some digestive disability on the part of the individual for certain articles of diet. Hardly to our mind a satisfactory mode of differentiation; much less can it be held to put out of court the influence of _gout_. For are not the gouty precisely the very persons who display this inability to cope satisfactorily with unusual or excessive meals? Hence the frequency with which in their instance attacks of lumbar fibrositis, often transient, almost invariably ensue when any unwonted excess of purin-containing food has to be disposed of, and especially when at the same time katabolic changes have been stimulated in the body by the ingestion of alcohol, not necessarily excessive in amount. That the _lumbar_ regions should have been singled out is the more remarkable, for, if there be one form of fibrositis more than another prone to be associated with gout, it is precisely _lumbago_. Our difficulty, moreover, in appreciating the cogency of this plea for excluding the influence of gout in muscular fibrositis is the more accentuated in that those who advocate it claim that this very gout is the salient etiological factor in _sciatica_ and _brachialgia_. This position is untenable, and for the following reasons: the pathological lesion in both instances is the same—viz., _fibrositis_; in lumbago and deltoid rheumatism it implicates the sheaths and interstitial tissues of the _muscles_, in sciatica and brachialgia the similar investments of the _nerves_. Strictly speaking, therefore, any differentiation that we can effect between muscular and neuralgic types of fibrositis is perforce merely _topographical_. To draw _etiological_ distinctions is well-nigh impossible, for the very continuity of the fibrous tissues favours the passage of one type into the other. Hence clinically we find that the bulk of our cases of sciatica are preceded by lumbago, and similarly many cases of brachial neuralgia or neuritis develop by extension out of a pre-existing deltoid fibrositis. In light of such transitions of _muscular_ into _neuralgic_ types of fibrositis, it seems inconsistent to postulate a gouty origin for the latter and at the same time to deny it any share in the production of the former. For ourselves, we fully recognise gout as the most potent predisposing factor in sciatica and brachialgia, and _ergo_ in the closely associated and often antecedent muscular types of fibrositis. While insisting on the importance of gout as a _predisposing_ factor in _fibrositis_, we feel called upon to emphasise the fact that we are not sheltering ourselves under that nebulous term “latent” gout, for our contention is based on the ground that in the vast majority of the cases for which we claim a gouty origin unequivocal proofs of gout, such as _tophi_, etc., were present.