A. and C.-Section of abdominal aortas at bifurcation, showing lime deposits.
B. Outside view of aortic valves; athroma and obstruction of a coronary.
D.—Inside view of aortic valves; chalky placques back of valves.

F.-A coronary with aortic cusp attached; sudden death from obstruction of this vessel.

G.-Degenerated and aueurismal coronary; ruptured and caused sudden death by filling pericardium with blood.

equal, seem most liable to the trouble.

The disease is often a

primary condition, a clinical entity, presenting a definite and diagnosable picture. While text books treat separately fibrosis and atheroma, it seems that the latter is but the terminal stage of the other, that the same causes operate to produce these stages of one pathological process. Degeneration and deposits take place where strain is greatest, more decidedly in tortuosities, at the bifurcation of vessels, at the sphyncter-like entrance to vessels, offering here a nidus for the formation of thrombi or becoming detached as emboli.

I beg to exhibit specimens from autopsies on persons who suffered from nervous and mental disorders; while illustrating extreme degrees of atheroma and contributing largely to cause death in the subjects from which taken, they are suggestive of the grave injuries to organs which must have been going on for years before death. It is impossible to say whether this state was initiated by an acute arteritis not recognized or lost sight of as time went on, or whether it was a sub-chronic and slowly progressing state; certainly it was the leading pathological state and explained the nervous and mental phenomena present, as well as the cause of death in these cases.

It is a long time and a long way from the alteration of the lumen of a vessel which disorders the more sensitive and vulnerable cerebro-spinal centers to the obstruction which causes gangrene, and for years before, altered elasticity or slightly altered lumen may have seriously affected those numerous subtle osmotic processes, which we call collectively metobolism.

I am convinced from the findings of many autopsies that chronic Brights, melancholy, hypochondria, premature physical and psychical decay are most frequently the direct result of changes in the nephritic and cerebral nutrition caused by this degeneration, even in its early stages of impaired elasticity. The condition when established is likely to cause such nervous symptoms is vertigo, insomnia, neurasthenia, irritability, some degree of amnesia or dementia, sudden, short, partial or complete losses of consciousness, slight aphasia, arythmia and dyslexia or hemianopsia, and intermittence of the pulse, pseudo or true apoplexy, anguina-pectoris and sudden death from plugging of a

coronory or bursting of a cerebral artery. In the presenile, in melancholia with hypochondria after 35, it is rare to do an autopsy and not find atheromatous change in some degree, particularly at the base of the brain. Many of the nervous disorders we have called functional, trophic and vaso-motor may come in time to be regarded as due to this condition and reverse our views as to cause and effect, stamping the disease as organic. It is to be borne in mind that central atheroma of the larger vessels may be the cause of vaso-motor spasms of smaller peripheral ones.

Opinion is shifting from the view that sclerosed kidneys cause atheroma to the view that the fibrosed artery oftener causes the sclerosed kidney. The effect on the brain of renal inadequacy is attracting just attention as a cause of hysterical attacks, mania and melancholia. Arterial degeneration, renal cirrosis, mental failure and the post-mortem findings of opacque or adherent dura are frequent associations, and more and more is it noted how often bulbar and other basal cerebral troubles depend on atheroma.

There is a recognizable symptom complex, indicative of atheroma of the basilar and other cerebral vessels and prodromal of apoplexy; cerebral shocks from change in the lumen of a vessel, the formation of a chalky nodule or a minute dilation at a weak spot, slight hemipligic attacks with short or no loss of consciousness, a unitateral numbness or weakness, vertigo, etc.

To cite an illustrative case: The middle of April last Mrs. F. W. B. presented herself at the clinic for nervous diseases, University of Denver, and gave the following history. "I am 55, widow, retired nurse, passed change of life six years ago, my father and mother lived to good age. The only disease I have suffered from was rheumatism. For the last two years I seem to have failed in strength; two months ago I had numbness in my left thumb and first finger; a few days later I awoke one morning weak; felt like falling to the left; there was a tingling in my tongue and face on the left. For three days I could not talk well; for a while my son had to assist me at things. I had a little swelling of my feet; the left worse, and it felt pricky and cold to touch. I am nervous; any little thing will make me cry. I have a weak feeling about the heart and dizziness when I stoop. My sleep and appetite are rather poor; when alone I feel uneasy and depressed."

Examinations of the urine were negative; some accentuation of the aortic 2nd sound, no oedema, no arcus senilis, but radials and temporals a trifle hard; her symptoms were attributed to atheroma of cerebral vessels, with liability to a cerebral hemorrhage; she attends the clinic occasionally and is on diet of milk, cereals and vegetables; she has taken small doses of iodide of sodium and nitroglycerine.

How often are we told after a fatal or disabling cerebral hemorrhage, that there had been for long, dizziness when stooping, slight amnesia, flushing of face, etc., which failed to impress patient or family.

Many cases of dementia and of epilepsy in persons in advanced life depend on circumscribed softenings or cicitrices after thrombic of embobic injuries, slight enough to escape notice or long enough ago to have been lost sight of as a possible cause. The condition described by Erb and Charcot and called intermittent clandication or augina cruris, consisting of cramps, rheumatoid pains, tingling and weakness of the leg and limping following slight exertion, and relieved by rest, elevation and gentle friction, is now admitted to be not spinal, but failure of adequate blood supply from athroma of the abdominal aorta or the iliacs. In the latter case the symptoms may be unilateral.

The related conditions of Mitchell's red-neuralgia, Erythromelalgia, Raynaud's superficial gangrene and the attacks of sudden failure of the muscles of the legs and back called astasiaabasia, are often dependent upon similiar causes. The early diagnosis of atheroma is important; not only does it make clear obscure nervous symptoms, but anticipates by prognosis or delays by management and treatment the disabling or fatal hemorrhage. Important medico-legal questions may arise as to the responsibility for moral and intellectual lapses, testamentary capacity, etc., persons in whom this condition of the cerebral vessels existed.

of

Apart from the nervous and mental symptoms enumerated, high tension which can be felt by the finger or shown by the sphygmograph and a lowering of the point of the greatest intensity of the aortic 2nd sound posteriorly, from the curve of the spine of the scapula to a line from the lower angle of the scapula to the 2nd dorsal vertebra, are the admitted points in diagnosis.