FIG. 48.-Toxic Migraine. Male. Aged forty-three. From a member of a family in which typical migraine headaches are common, having occurred in the patient's father, mother, aunt and sister. In this patient these attacks come on with great regularity, at seven- or eight-day intervals. When first seen these headaches were causing great annoyance by interfering with his daily activities. Refractive errors have been corrected. The Wassermann reaction is negative. The patient is of sedentary habits and is a large eater. His work is purely mental. The patient is constipated and the urine, upon frequent examinations showed evidence of intestinal toxemia. Therapeutic efforts were directed solely toward elimination of toxemia and resulted in considerable relief until the patient at (A) returned from a ten days' business trip. During this time he had several headaches and a number of dizzy spells. Dietetic measures were again instituted with the following result, namely, a moderate decrease in systolic pressure with a great fall in pulse pressure incident to an approximation of systolic and diastolic pressures. The rise at (B) seemed to be incident to a return of constipation which was relieved by exercises.

may be elicited, such as fleeting dizziness, throbbing temples, tinnitus aurium, disturbed sleep, cold hands and feet, gastric distress and flatulency, constipation, lack of interest and of power of concentration, diminished desire to be up and doing, distaste for physical exertion and weakened tolerance for substances which affect the brain, such as alcohol and tobacco.

The blood-pressure does not need to be greatly increased in order to injure the heart and cause permanent change in the blood-vessels and in the kidneys. The additional amount of work required of the heart to overcome the resistance of a few millimeters of mercury mounts up surprisingly (see page 275).

Concerning the actual systolic pressure level encountered in hypertension as contrasted with that found in cases where arteriosclerosis and degenerative changes have developed, most authorities agree upon 160 to 170 mm. Hg. as the dividing line, although this is by no means arbitrary, since it is well known that well-developed cases of arteriosclerosis and nephritis may exist with systolic pressures averaging lower than 170, and that apoplexy has occurred in patients who have never shown a systolic pressure of over 170.

The diastolic pressure will be found elevated, but to a less degree than the systolic pressure, this giving a moderately increased pulse pressure, but the difference is rarely as great in proportion as shown by the pulse pressure usually met in arteriosclerosis and nephritis. A typical case might present the following: systolic pressure 160, diastolic pressure 100, pulse pressure 60. It would be an error to base a diagnosis upon this alone as only repeated study

and the careful weighing of all evidence, permits the arrival at a safe and correct opinion.

Diagnosis. This requires fine judgment, is always difficult and becomes additionally so as the boundary line between hypertension and arteriosclerosis is approached.

It will be a great aid to diagnosis to keep the fact constantly before the mind that hypertension is a cardiovascular (largely vascular) function of a temporary nature, which we now recognize and correct, while arteriosclerosis is a permanent pathologic change of the tissues of the arterial walls for which we know no remedy.

The eliciting of a group of otherwise unexplainable symptoms as enumerated above, in the absence of demonstrable (after careful and repeated search) lesions of the heart and kidneys, and with only a moderately elevated systolic pressure (below 170) and a slightly increased pulse pressure, in persons susceptible to auto-intoxication, as those of sedentary habits or accustomed to overeating, especially when blood-pressure reducing measures rapidly reëstablish normal blood-pressure values, should afford the clinician a reliable diagnosis. A note of warning should be sounded here, which is that one should not be too ready to make a positive diagnosis of pure hypertension, as it is safer to err on the side of the more grave condition and so proceed in the treatment. This will avoid a too sanguine view of a possibly serious case which at first being considered trivial, later develops into one of true arterial or renal disease.

Syphilis is well recognized as a cause of hypertension; it acts in the same manner as other circulating toxins and

therefore may be looked for as one factor in the production of hypertension (see also Chapter XIII).

Concerning the relationship between true hypertension and permanent renal and arterial changes, we are coming more and more to the view that high blood-pressure is primary and the involvement of the kidneys and arteries only incidental.1

This seems only natural when we realize the great surface area of arterial walls which are exposed to the action of irritating substances in the circulating blood, as compared with which the kidneys actually only receive a small portion of these toxic irritants.

1A. W. Hewlett, Jour. A. M. A., May 25, 1912, lviii, No. 21. V. Bie, Ugeskriftm f. Sarger., Mar. 4, lxxxvii, No. 9.

Cottentot and Sergent, Jour. A. M. A., Mar. 28, 1914, lxii, No. 13, p.

1032.

CHAPTER XVII

ARTERIOSCLEROSIS

In any consideration of this subject we should primarily insist upon an absolute distinction between hypertension and arteriosclerosis. Arterial hypertension is a cardiovascular phenomenon having perversions and abnormalities which the diagnostician can now recognize and in many instances successfully arrest and correct (see Chapter XVI, page 243). Arteriosclerosis is a permanent pathologic change of tissue for which there is no remedy. The source of danger in arteriosclerosis is not primarily in the thickened artery but in the amount of permanent bloodpressure elevation accompanying it. The thickened artery itself is a physiologic development of a protective nature and represents a factor of safety rather than a source of danger.

Latterly our conceptions concerning the origin and development of arteriosclerosis have undergone great changes, largely due to the fact that during the past few years much experimental work has been carried on and many clinical investigations made, which in great measure prove the causative relation of a large number of exciting agents, the effect of which, either directly or indirectly, on the vessel walls is the provocative cause of arteriosclerosis. In another direction, studies have demonstrated the relation of this condition to abnormally and persistently high