[Footnote 12: The reader may consult with advantage Dr. Morris Longstreth's fourth chapter in his recent excellent monograph upon _Rheumatism, Gout, and some Allied Disorders_, New York, 1882.] The latest modification of the lactic-acid theory of Prout is founded upon the modern physiological teaching that during muscular exercise sarcolactic acid and acid phosphate of potassium are formed, and carbon dioxide set free, in the muscular tissue, and that cold, acting on {24} the surface under such circumstances, may check the elimination of these substances and cause their accumulation in the system. This view, it is held, explains why the muscles and their associated organs, the joints and tendons, suffer first and chiefly, because the morbific influence is exerted upon them when exhausted by functional activity; and it further accounts for the visceral manifestations and the apparent excess of acid eliminated during the course of the disease. The circumstance that in three cases of diabetes (Foster,[13] Kuelz[14]) the administration of lactic acid appeared to induce polyarticular rheumatism favors the idea that acid is the materies morbi in rheumatism. [Footnote 13: _Brit. Med, Jour._, ii. 1871.] [Footnote 14: _Beiträge zur Path. und Therapie des Diabetes_, u. s. w., ii. 1875.] Now it must be admitted that, as yet, no sufficient proof is forthcoming that a considerable excess of lactic acid exists in the fluids or solids of the body or in the excretions in rheumatism (it is true the point has not been sufficiently investigated). On the other hand, that acid has been found in the urine of rickets, and its excess in the system is regarded by Heitzmann and Senator[15] as the cause of the peculiar osteoplastic disturbances of that disease--an affection altogether different from rheumatism. It is quite improbable that the amount of sarcolactic acid produced by over-prolonged muscular exertion, and whose elimination has been prevented by a chill or a mental emotion, is sufficient to maintain the excessive acidity of the urine and other fluids during a long rheumatic fever; and arguments can be adduced favorable to the view that excessive formation of acid is an effect rather than the cause of rheumatism: cases of that disease occur in which neither excessive muscular exertion nor exposure to chill have preceded the rheumatic outbreak. Lastly, lactic acid is not the only principle retained when the functions of the skin are arrested by cold, the usual exciting cause of rheumatism; why should not the retained acetic, formic, butyric, and other acids, for example, play their rôle in the production of the symptoms observed under such conditions? [Footnote 15: _Ziemssen's Cyclop._, xvi. p. 177.]