12th : Is much the same, no special pain, but the tenderness on pressure remains; perspiration slight hut distinctly acid ; pulse 100, temperature 101.3. Continue powders. Has had 750 grains of salicin.
13th : Feels much better; pain and tenderness gone; pulse 90, temperature 98'. Has taken 930 grains of salicin.
14th : Feels quite well, only weak; pulse 76, temperature 98 . Has a good appetite.
He was more careful on this occasion, remained in bed for a week, took salicin for a fortnight, and made a good recovery without any drawback.
In this case the pain was decidedly relieved within six, and was gone within twenty, hours of the time that he came under notice. The temperature, too, had fallen to the normal standard.
It will be noted that during the first attack neglect of the salicin, on December 2d, led to a rise of the temperature from 98.4° in the morning to 101° iu the evening. The resumption of the remedy in hourly doses led to a speedy fall of the temperature to the normal. The second attack was clearly attributable to the early omission of the salicin.
Reference has already been made to a morbid condition to which the term rheumatism is usually applied, but which is more properly a sequence of rheumatism than a distinct form of the disease. The condition referred to essentially consists in chronic thickening and irritability of fibrous textures which have been the seat of frequent attacks of rheumatic inflammation. The usual history of such cases is that each attack has been less perfectly recovered from, leaving behind it a legacy of increased disability. Their history indeed shows, what a knowledge of pathology would indicate, that the tex tures which have been the seat of inflammation do not recover their natural tone as soon as the inflammation ceases. There remains for a time, which varies with the and severity of the seizure, some thickening of the fibrous textures of the affected joints, causing the stiffness which is felt after the acute symptoms have disappeared. If the attacks are frequent and obstinate this morbid change in the fibrous textures is less and less perfectly recovered from, by each succeeding seizure a little more damage is done, and ultimately there is induced a condition of chronic thickening of these textures, which is perthanent.
That such a change should take place as a result of frequent and long-continued rheumatic attacks consists with what we know of the mode of production of similar pathological changes iu other organs.
Clinical experience teaches that when an organ has been the seat of repeated attacks of inflammation, the local symptoms to which such inflammation gives rise are apt to recur in a minor degree from the operation of causes which would not have sufficed to induce the original attack. What more common than for chronic bronchitis to
be developed as a sequence of one or more acute attacks; and for the course of the chronic malady to be interrupted by subacute seizures brought on by causes which would not have sufficed to induce the original malady? A similar instance we have in the readiness with which dysenteric symptoms may be developed in those who have once suffered from the acute form of the disease. Exposure to cold, over fatigue, mental disturbance—causes which never could have originated the disease—will often bring back some of the local symptoms of the original attack in a milder but still quite characteristic form. So it is with fibrous textures which have been weakened and altered by re peated rheumatic attacks. They are rendered irritable and weak by the changes which have taken place in them, and are apt to be dis turbed by agencies which have no such effect on healthy fibrous tex tures. Irritation of fibrous textures, no matter how induced, causes pain in the affected part. Hence such disturbance as arises in these altered textures from exposure to cold and damp gives rise to the same symptoms as would result from the action of the rheumatic poison. Originating in true rheumatic attacks, occurring in those who have given decided evidence of being of rheumatic constitution, and characterized by symptoms which are associated with true rheu matism, it is not unnatural that the symptoms should be regarded as due to the action of the rheumatic poison. But such a view is patho logically inaccurate and pregnant with therapeutic errors. The con dition which has to be dealt with is one which, though originally induced by repeated rheumatic attacks, exists, after it has been de veloped, independently of the cause which gave rise to it. Pain, swelling, slight rise of temperature, even increased formation of lactic acid, may thus result from inflammation of these altered fibrous tex tures induced by cold, just as like symptoms would result from simi lar disturbance set agoing by the rheumatic poison. We may thus have all the symptoms of subacute rheumatism without any action of the rheumatic poison. Over such an attack the salicyl compounds can exercise no control.