l)ILATATtON 01' AKTERIES. — ANEURISM. 259 



tioii of the ■vessoLs of the lioud which follows division of the 

 cervical sympathetic, not to suggest a 2)artial disturbance of the 

 vasomotor system as its probable cause. All these howe^■er are 

 rare cases, and therefore comparatively unimportant. 



^ 224. What is shortly called aneurism at the bed-side — an 

 ectasy confined to a short part of the aorta or some other 

 artery, has its causes shrouded in great obscurity. It is usually 

 complicated with chronic endoarteritis. We must endeavour to 

 ascertain how far this change is capable of contributing to the 

 dilatation of an arterial tube. In the first place, we must reflect 

 that an overgrow^th of the intima as such, augments the super- 

 ficial area as well as the thickness of the inner wall of the vessel. 

 The circumscribed patches of newly-formed connective tissue are 

 not merely superimposed on one another; they likewise pene- 

 trate horizontally between the existing lamellae of the intima, 

 forcing them actively asunder as they grow. We are surely 

 entitled to regard the growth of the inflamed intima in a hori- 

 zontal plane as at least one factor in the dilatation of the vessel. 

 For even thouo^h we assimi but a small value to its active co- 

 operation, yet we must regard the intima, while it is under- 

 going the fluctuations of internal change, as less capable of 

 resisting the dilating impulse and increased tension of the blood, 

 than it is in its normal state. I have already pointed out that 

 atheromatous changes in the arterial walls cause a rise in the 

 blood-pressure above and at the affected jDoints of the vascular 

 system. To this must be ascribed in the first place that uniform 

 dilatation of the aorta which is nearly always found in cases of 

 extensive endoarteritis. For the production of a true aneurism 

 however, it is the systolic rise in the blood-pressure which is 

 chiefly important. This differs from that which occurs normally. 

 The diseased condition of the arterial walls hinders that pro- 

 visional transformation of velocity into elastic tension, which 

 causes the systolic rise in the blood*pressure and its ^' other' 

 mode,'' velocity, to be distributed over a longer interval of time* 

 Accordingly, both these manifestations of energy culminate at 

 the moment when the systole commences, and collapse imme- 

 diately afterwards to a proportionate extent. With each ven- 

 tricular contraction, the diseased artery is subjected to a dilating 

 impulse, to which it can only oppose a passive, not, as before, 

 an active resistance. The patient's throbbing pulse informs us 



