and undoubtedly is due to disturbances of nutrition in the intima. Except for the remote danger of clot formation on the uneven or eroded spot, these places are of no special significance, and are not to be confused with the atheroma of nodular sclerosis.

The lesions of arteriosclerosis are of a different character. It has been customary to differentiate three types: (1) nodular; (2) diffuse; (3) senile. It must be understood that this is not a classification of distinct types. As a rule in advanced arteriosclerosis, lesions representing all types and all grades are found. The nodular type, however, may occur in the aorta alone, the branches remaining free. This is most often found in syphilitic sclerosis where the lesion is confined to the ascending portion of the arch of the aorta.

The retrogressive changes of advancing years can not be rightly termed disease, yet it becomes necessary to regard them as such, for the senile changes, as we shall see, may be but the advanced stages of true arteriosclerosis. Much depends on the nature of the arterial tissue and much on the factors at work tending to injure the tissue. A man of forty years may therefore have the calcified, pipe stem arteries of a man of eighty. Our parents determine, to great extent, the kind of tissue with which we start life. The arteries are elastic tubes capable of much stretching and abuse. In the aorta and large branches there is much elastic tissue and relatively little muscle. When the vessels have reached the organs, they are found to be structurally changed in that there is in them a relatively small amount of elastic tissue but a great deal of smooth muscle. This is a provision of nature to increase or decrease the supply of blood at any point or points.

The aorta and the large branches are distributing tubes only. It is after all in the arterioles and smaller arteries that the lesions of arteriosclerosis do the most damage. A point to be emphasized is that the whole arterial system is rarely, if ever, attacked uniformly. That is, there may be a marked degree of sclerosis in the aorta and coronary arteries with very little, if any, change in the radials. On the contrary, a few peripheral arteries only may be the seat of disease. A case in point was seen at autopsy in which the aorta in its entirety and all the large peripheral branches were absolutely smooth. In the brain, however, the arteries were tortuous, hard, and were studded with miliary aneurysms. It is not possible to judge accurately the state of the whole arterial system by the stage of the lesion in any one artery; but on the whole one may say that an undue thickening of the radial artery indicates analogous changes in the mesenteric arteries and in the aorta.

So far as the anatomical lesions in the aorta and branches are concerned, there is much uniformity even though the etiologic factors have been diverse. The only difference is one of extent. To Thoma we owe the first careful work on arteriosclerosis. He regarded the lesion in arteriosclerosis as one situated primarily in the media; there is a lack of resistance in this coat. His views are now chiefly of historical interest. As the author understands him, he considered a rupture in the media to be the cause of a local widening and consequently the blood could not be distributed evenly to the organ which was supplied by the diseased artery or arteries. Moreover, there was danger of a rupture at the weak spot unless this were strengthened. It was essential for the even distribution of blood that the lumen be restored to its former size. Nature's method of repair was a hypertrophy of the subintimal connective tissue and the formation of a nodule at that point. The thickening was compensatory, resulting in the establishment of the normal caliber of the vessel. Thoma showed that by injecting an aorta in the subject of such changes, with paraffin at a pressure of 160 mm. of mercury, these projections disappeared and the muscle bulged externally. He recognized the fact that the character of the artery changed as the years passed, and to this form he gave the name, primary arteriosclerosis. To the group of cases caused by various poisonous agents, or following high peripheral resistance and consequent high pressure, he gave the name, secondary arteriosclerosis. This is a useful but not essential division, as the changes which age and high tension produce may not be different from those produced in much younger persons by some circulating poison. And most important to bear in mind, octogenarians may have soft, elastic arteries.

As the body ages, certain changes usually take place in the arteries leading to thickening and inelasticity of their walls. This is a normal change, and in estimating the palpable thickening of an artery, such as the radial, the age of the individual must always be considered.

Thayer and Fabyan, in an examination of the radial artery from birth to old age, found that, in general, the artery strengthens itself, as more strain is thrown upon it, by new elastica in the intima and connective tissue in the media and adventitia. Up to the third decade there is only a strengthening of the media and adventitia. During the third and fourth decades there is also distinct connective tissue thickening in the intima. "In other words, the strain has begun to tell upon the vessel wall, and the yielding tube fortifies itself by the connective tissue thickening of the intima and to a lesser extent of the media." By the fifth decade the connective tissue deposits in the intima are marked, there is an increase of fibrous tissue upon the medial side of the intima and, in lesser degree, throughout the media. "Finally, in these sclerotic vessels degenerative changes set in, which are somewhat different from those seen in the larger arteries, consisting, as they do, of local areas of coagulation necrosis with calcification, especially marked in the deep layers of the connective tissue thickenings of the intima, and in the muscle fibers of the media, particularly opposite these points. These changes may ... go on to actual bone formation." The mesenteric artery differs in some respects from the radial, but in the main, the changes brought about by age are the same. Thayer and Fabyan note two striking points of difference: "(1) calcification is apparently much less frequent than in the radials; (2) in several cases plaques were seen with fatty softening of the deeper layers of the intima and superficial proliferation—a picture which we have never seen in the radial." (See Fig. 2.)