term applied to the condition of the arteries as a result of irregular thickenings and deposits of lime salts in the walls. These changes give rise to marked tortuosity of the vessels. Occasionally such an obliterating process takes place in a larger artery. A thrombus forms and by a process of central softening, new channels permeate the thrombus, thus restoring to some extent the function of the vessel. That the same process leads at one time to thinning and at another time to thickening of the arterial walls has been noted above. Prof. Adami holds that the regular development of layer upon layer of new connective tissue is non-inflammatory. He calls it a "strain hypertrophy." It is analogous to the localized hypertrophy of bone where the muscle tendons are attached, as is so frequently seen in athletes. The increased tension on connective tissue, provided that it is not overstrained, leads to its overgrowth, but only when there is sufficient nourishment. Such conditions are adequately fulfilled in the arteries. When a local giving way under pressure occurs in the media, the intima is put on the stretch (see Fig. 8), and there results a hypertrophy of the intima until the volume of the new tissue and the resistance which this affords to the mean distending force, balances the loss sustained by the weakened media. When the balance is struck, the hypertrophy is arrested. The youngest tissue is thus found directly beneath the endothelium. Now should this local weakening of the media have an acute origin, instead of a stimulus to growth there is overstrain, and there is, in consequence, not hypertrophy but atrophy. The beginning process is here a mesaortitis, but the acuteness of the poison, and the pressure from within the artery so stretches the artery that there is no compensatory hypertrophy, but a thinning, and the ground is prepared for aneurysmal dilatation or pouching. [Illustration: Fig. 8.--I, media weakened at M' with overgrowth of intima filling in the depression. II, with postmortem rigor and contraction of the muscles of the media and removal of the blood pressure from within, the stretched media at M'' contracts; the intimal thickening thus projects into the arterial lumen. (After Adami.)] Again, one not infrequently encounters intimal nodosities when the underlying media appears of normal thickness. The explanation of this apparent exception is that the media in the living aorta is actually thinned, but the layers of subintimal tissue deposited over the weak spot due to strain hypertrophy become bulged inward when the pressure is relieved, as at postmortem. The media has not lost all of its elasticity (see Fig. 9), hence it contracts and there is the appearance of a nodule on the intima beneath which is a media equal in thickness to that of the healthy surrounding media.