vessel through the thickening of its walls and the swelling of the internal coat. Again, by weakening the vessel-wall, it may produce dilatation and lead to an aneurysm. The small arteries arising at the seat of atheromatous invasion may be occluded, though the parent vessel remains pervious. Collateral territories are thus cut off, while the ultimate distribution remains active. The rigidity and brittleness of the artery favor rupture and hemorrhage.

Atheroma may be considered as a purely senile condition in many cases, a part of the involutionary changes of the organism in advanced years. There is no doubt that gout, rheumatism, great muscular straining, overindulgence in alcohol, lead poisoning, and syphilis are additional causes. Lancereaux says chronic malarial infection may cause atheroma. These causes are frequently combined in a given case, as gout and senility. Atheroma, though usually found after middle life, has been noted in the aorta and large systemic vessels in children and even in infants.

The symptoms of atheroma of the cerebral vessels are usually vague and uncertain until thrombosis, aneurysm, or hemorrhage has been added. It may be reasonably suspected when the condition in the heart, aorta, and palpable systemic arteries indicates its generalized distribution. Lesion of the optic chiasm by bilateral atheromatous thickenings of the carotids pressing upon it has been noted. Double temporal hemianopia may thus be produced. The formation of an aneurysmal tumor gives rise to its own localizing symptoms. Resulting hemorrhage and thrombosis present symptoms related to the structures that are injured or destroyed.

The treatment of atheroma is practically the same as that of arteriosclerosis.

Arteriosclerosis (arteriocapillary fibrosis) is always a generalized systemic condition, but it may be more accentuated in certain bodily organs and there give rise to local symptom groups. Its effect upon cerebral activity is most important. According to Sansom, the changes brought about are due to a poison circulating in the blood, which acts upon the fibroid elements of various tissues, but preeminently upon those of the arterial channels. The essential histological modification consists of a fibroid proliferation or fibrosis. In certain locations this acts mechanically to strangulate associated structures, as, for instance, in the arteries, where the muscular fibers are thus invaded and even displaced. The walls of the entire arterial system become thickened. This may be due: (1) To thickening of the internal coat, which may go on to complete obliteration of small vessels, or (2), commencing first in the external wall, the disease may spread inward, usually causing at first some hypertrophy of the muscular coat, or (3) the fibrosis may originate outside of the arterioles, which are involved secondarily by extension of the process to them. The various initial locations of the disease seem to depend upon the mode of the poisonous invasion. In one instance it affects the intima directly from the blood-stream, in another the outer coat from the perivascular or lymphatic space, and in the third variety the fibrous structures of parenchymatous organs are disturbed

through the lymph-channels. All these varieties may be found in the

same case.

This condition has a number of pathological associations. Atheroma is present in about one-half the cases. Cardiac hypertrophy and dilatation, Bright's disease, asthma, angina pectoris, and mitral stenosis are frequently associated and due to identical changes. The effect of arteriosclerosis is to diminish the arterial caliber and thereby lessen nutrition. This may reach a complete degree and in the brain give rise to localized anemia and softening.

The nature of the poison which stimulates the fibroid activity is obscure. Loomis says the "general fibrosis has its origin in a fibroid diathesis either hereditary or acquired," but this explains nothing. By some writers defective elimination, particularly that from the kidney, is accused. Arteriosclerosis is certainly an accompaniment of old age and is a fair index of the wear and tear the individual has undergone and of

the remaining vital capacity. We find it often a marked family characteristic. It is also clear that chronic intoxications by alcohol, lead, gout, rheumatism, and syphilis favor it strongly. Overeating, repeated muscular strains, and intestinal, renal, muscular, and cutaneous sluggishness count for something in its causation.

The cerebral symptoms produced by arteriosclerosis cover a wide range, but are all due to faults of brain-nutrition. They embrace those of senility, premature senility, and degenerative processes, both chronic and acute. The highest and most delicate brain-functions are likely to be first affected. We, therefore, find lessened mentality, aphasia, and monoplegias or mere clumsiness of the hands. Paresthesias are very common. Hemiplegic and diplegic manifestations are observed. At first these symptoms are temporary and recurrent, but unless the arterial condition improves, they tend to become more and more continuous and permanent. Slight attacks of hebetude or sleepiness may eventuate in

stupor, coma, and even in death. Jacksonian and generalized convulsions, syncopic attacks, and periods of mental confusion are all within the range of this protean malady. If the fibroid change occludes a cerebral vessel, it acts like a thrombus, to which, indeed, it often leads, and a softened infarct results, with permanent loss of localized brainfunction. Many islands of softening and many sclerotic patches may be due to this cause and present multiple symptoms. Diffuse sclerotic processes in the cortex are associated with it, and it underlies some of the cerebral lesions of general paresis and tabes. Associated minor symptoms, such as vertigo, headache, insomnia, irritability, lack of mental energy and muscular force, and the craving for stimulants, all point to the lowered nutrition of the brain. All the manifestations of cerebral

arteriosclerosis are likely to come at first in gusts and waves.

Symptoms. The physical examination of a case of arteriosclerosis usually demonstrates a tortuous, rigid, frontal artery, sometimes moving under the skin in a vermicular manner at each pulse-wave. The cornea is the seat of a marked senile arcus. The radials, brachials, femorals, and all palpable arterial trunks are tense and rigid. The pulse is one of high tension. A light finger imperfectly detects it, but it seems to increase as pressure is applied and can hardly be extinguished. There is usually an enlarged, laboring heart, and often roughened valvular sounds. The urine is likely to show albumin and the formed elements that mark chronic nephritis. Often the quantity of urea is scanty or markedly deficient. A constipated habit is the rule, and the general health is below par. In less advanced cases the general indications of the arterial state may be very slight and yet the cerebral mischief may be extensive. This is especially true in the syphilitic varieties. The same processes that take place in cerebral structures affect the cord, and may, and often do, give rise to organic mischief, furnishing the basis of many systematized and unsystematized cord-lesions.

The treatment of arteriosclerosis affecting the brain must be undertaken at an early stage if much is to be accomplished. Toxic causes, if present, must be eliminated. Syphilis, gout, lead poisoning, alcoholism, renal, pulmonary, and cardiac conditions must receive their appropriate management. The arterial spasm due to the local irritation of the muscular tunic, and perhaps also to uric products in the circulation, must be overcome. To relieve the spasm the nitrites, especially nitroglycerin, may be given at short intervals. Mercurials and much water to cleanse the intestines and stimulate the kidneys are valuable aids. Alkaline waters such as Vichy and the lithia waters are good. Care of the digestive tract and of the diet is of the first importance. All excesses must cease. A simple, easily digested regimen, with a very limited amount of red meats, starches, and sugars, should be ordered. The skin should be kept active by baths, frictions, and massage. If muscular exercises are for any reason contraindicated or not available, massage may take their place. An outdoor habit should be cultivated, and change of scene may do much to reduce the mental distress and vague broodings. Of all medicine directed toward improving the arterial condition the iodids easily hold first rank, but it should

be remembered that the potassium salts depress the heart's action and perhaps add to the arterial sluggishness. Sodium iodid is much to be preferred and is usually better tolerated. This should be given in doses of from five to twenty grains after meals, and continued for months and years, with short intervals. A good plan is to order the iodid discontinued during every fifth week. Tonics are almost invariably required. Arsenic can be readily given with the iodid, and strychnin is perhaps the best aid to the laboring heart. Avoid digitalis and everything else that tends to increase arterial tension. No harm seems to come from the frequent use of amyl nitrite or trinitrin, and the prompt, though transient, relief produced is often very gratifying, besides in a way confirming the diagnosis.

Under such a plan of treatment, aphasias, mental disturbance, hemiparesis, and many other symptoms of brain disturbance will sometimes rapidly clear up and, if not cured, remain in abeyance for years, provided moderation in all things be the rule of life. The prognosis, however, should be guarded, as we know that brain-cells degenerate beyond recovery if entirely deprived of their blood-supply for about forty-eight or, at the most, seventy-two hours at a time. At best it is evident that the presence of arteriosclerosis signifies a shortened lifelease.

Syphilitic Arteritis. It is now generally recognized that cerebral arteritis from syphilitic infection may be a comparatively early manifestation of the disease. Ogilvie shows from Naunyn's statistics that syphilitic diseases of the cerebrospinal axis present the greatest proportion of cases during the first year following the initial lesion. They may appear even after a score of years. The basilar, carotids, circle of Willis, and large cerebral arteries are those usually implicated, but smaller brain-arteries may be similarly diseased. The specific inflammation may produce a peri-arteritis and nodular plaques that look something like those of atheroma, or it may invade and infiltrate all the arterial walls with gummy products, commencing either as an endarteritis or a peri-arteritis. Long-standing syphilitic arteritis, especially of the large vessels of the base, produces a sclerous degeneration that does not calcify. It is generally circumscribed in small patches, causing bulging of the internal and external coats, deforming the artery and altering its capacity.

Syphilitic arteritis leads to: (1) Obstruction of the vessel by the production of thrombosis or by an obliterating endarteritis; (2) rupture and hemorrhage, and (3) aneurysm. It may appear at any age and may follow inherited syphilis in children and even in adults.

The most prominent indications of syphilitic disease of the cerebral arteries are the prodromata. Of these the syphilitic headache, coming on usually toward evening and lasting until midnight, is the most distinctive. Except that due to tumor, it is the most intense and unmanageable headache with which the physician is called upon to deal. Ordinarily it is not confined to any portion of the head, but is described as being somewhat superficial, unlike the deep-seated pain of tumor. less the condition is now recognized or, as is rarely the case, sponta

Un

neously subsides, disturbances in the cortex are likely to appear, marked by paresthesias and loss of power in the extremities or disturbance of speech and the special senses. After vacillating symptoms of this character, which have a tendency to recur at intervals of a few days or weeks, a sudden apoplectic stroke, due to sudden rupture of the vessel, may ensue, or a complete thrombosis lead to cerebral softening. When hemorrhage or thrombosis takes place the headache usually disappears, or sometimes it disappears a few days before the onset of serious results. The symptoms are those of cortical irritation and the eventual onset of paralysis is usually not marked by complete loss of consciousness, except in the hemorrhagic form, and coma is the great exception. Aphasia, facial paralysis, monoplegia, paresthetic tinglings, preceded by a history of violent headache, with nocturnal exacerbations, strongly indicate syphilitic disease of the cerebral arteries, even in the absence of any history of specific infection. As has been shown by Charcot, almost invariably there is some degree of basilar syphilitic meningitis in these cases and transient or permanent disturbance of the ocular apparatus is often added.

According to Charrier and Klippel, the chief groups of cerebral manifestations of syphilitic disease of the arteries are: (1) Apoplexy; (2) paralysis from obliterating arterial disease; (3) slight aphasia and transitory varying palsies, and (4) intellectual disturbance somewhat similar to that of general paresis. There is also reason to suppose that it is the true though remote basis of general paresis.

The treatment of the condition should be energetic even when it is diagnosed early, and will be discussed at length under the consideration of General Syphilitic Diseases of the Nervous System.

Acute arterial degenerations of an amyloid and fatty character affecting the cerebral vessels may follow numerous states marked by various systemic infections. Only in very rare instances do they give rise to marked cerebral symptoms, and these are usually overshadowed by the general state. Rupture and hemorrhage or thrombosis and softening may be due to them.

CHAPTER VI.

CEREBRAL HEMORRHAGE AND THE HEMIPLEGIC

STATE.

EXCEPTING traumatic cases, hemorrhage into the substance of the brain is a secondary or terminal effect of degenerative or inflammatory disease of the cerebral blood-vessels, almost invariably of the arteries. Usually of comparatively slight seriousness in itself, the resulting injury or destruction of important brain-structures entails permanent disability if an early fatality is escaped. All parts of the