been found in other forms of disease apart from goitre or exophthalmos. The late appearance of goitre in many cases shows that it cannot be the primary cause of the symptoms by pressure on the sympathetic cord.

It is, on the whole, much more likely that the disease is central, and the coexistence of other more general disturbances-nervousness, hysteria, etc. -supports this view. Dr. Hale White called attention to the persistence of the thymus, and the changes in Peyer's patches in some cases.

Diagnosis.-Occasionally a simple goitre may actually press upon the sympathetic in the neck, and produce dilatation of the pupil, paralysis of accommodation, slight exophthalmos, and depression of the temperature in the external meatus. It will be seen that these symptoms agree with those of Graves' disease only in the exophthalmos. The difference would be most obvious if they occurred on one side only.

Prognosis. The majority of cases are of some years' duration, beginning insidiously, and only slowly recovering; or improving up to a certain point, and then remaining stationary; or dying from exhaustion, from mitral disease, from intercurrent complaints, or suddenly, and then probably from heart failure. Of twelve cases collected by Dr. Hale White from the Guy's Hospital records from 1877 to 1884, seven had died by 1886. Treatment. A cure can only be expected from prolonged treatment, and no drug can be said to have been uniformly successful. Digitalis and belladonna seem to have done most good, and ergot has been recommended. Iron is of little value. Many cases have benefited under galvanism, the constant current being applied with the kathode on the cervical spine, and the anode over the sympathetic in the neck, or over the thyroid; and a weak current may be similarly applied to the eyes. The application of ice to the thyroid is also of value.

DISEASES OF THE BLOOD-VESSELS.

The diseases of arteries are mainly comprised in inflammation and degeneration, and the mechanical results of those lesions. Inflammation of the veins or phlebitis, and thrombosis and embolism will also be considered in this section.

ARTERITIS.

Etiology. The following are recognized causes of arterial inflammation (1) Local contact with inflammatory and septic foci, as in arteritis. from suppuration or embolism; (2) over-strain, which acts especially as a cause of inflammation of the aorta and large vessels; (3) syphilis, affecting the small vessels generally, and also vessels actually in contact with gum

matous deposits; (4) tubercle, which attacks the vessels in the various organs it invades. In tubercular meningitis the vessels are often first attacked, and in phthisis the tubercle, by involving the outer wall of the vessels, leads to their rupture, or to the formation of aneurism.

Anatomical Changes.-Inflammation of the arteries may be acute or chronic, local or general. One form of acute local arteritis occurs when a vessel is exposed in a wound, or in contact with a suppurating centre; or when a vessel is the subject of embolism, and the impacted embolus gradually leads to inflammation of the inner coat; or the inner coat of the aorta may become inflamed from vegetations on its valves, such as are seen in ulcerative endocarditis. The change in the aortic lining closely resembles that which takes place in the valve already described. A general acute aortitis also occurs, in which all the coats of the vessel become thickened with cellular infiltrations, especially about the vasa vasorum, as well as on the surface, and in the meshes of the inner coat. In chronic arteritis, which may begin as an acute disease, the inner surface presents broad, grayishwhite, slightly raised patches, which may be soft, mucoid and gelatinous, or more or less sclerosed from the presence of fibrous tissue. In later stages there may be a semi-cartilaginous thickening, affecting the inner coat mainly. But the same changes involve also the middle coat, destroying the muscular and elastic elements, and the outer coat, causing fibrous thickening and condensation of the tissue. The results of arteritis are: (1) Degeneration and atheroma; (2) constriction and even obliteration of the arterial channel, which occurs mainly in the small and medium-sized arteries; (3) dilatation, either general or irregularly distributed, or purely local. In the latter case it constitutes aneurism.

Symptoms.-Acute aortitis is probably not revealed by symptoms; but cases of acute arteritis have been recorded affecting the vessels of the extremities. In one such case pain and tenderness, limited to the course of the vessels, gradually spread down the limbs to the extremities. In others there have been pain, tenderness, loss of pulse in the affected vessels, gangrene of portions of skin in the area corresponding to their distribution, or shedding of the nails. General arteritis has also been seen in a chronic form, leading again to pains in the limbs along the course of the arteries, and followed by obliteration or such narrowing of the channel as to abolish the pulse.

ARTERIAL DEGENERATIONS.

The most important is that known as atheroma, which frequently follows upon and complicates the arteritis of the inner coat (endarteritis) above described. The gray semi-cartilaginous patches become mixed with others. of a yellow color, which arise from a fatty change taking place in the inflamed tissue. A pasty mass results, which contains fat granules and

cholesterin crystals. It affects chiefly the deeper layers of the inner coat, but may approach to the surface, so that the innermost layers finally give way, and an atheromatous ulcer results. In some cases calcareous granules are deposited and form plates or spicules, upon which fibrin may be deposited from the circulating blood. The combination of patches of early inflammation, atheroma and calcareous deposits, with the irregular dilatation of the vessel which occurs as the various weakened spots yield to the bloodpressure, constitutes endarteritis deformans. Simple fatty degeneration of the cells of the innermost layers of the inner coat, and calcareous deposits in the same, are seen as a senile change.

Symptoms. When at all extensive, atheromatous degeneration can be recognized by its effect upon those arteries which are accessible to examina

B. LEFT RADIAL PULSE IN THE SAME CASE.

C. RADIAL PULSE IN COMPRESSION OF THE SUBCLAVIAN ARTERY.

D. ATHEROMATOUS ARTERY. PRESSURE, SIX OUNCES.

tion during life. Firstly, the artery wall becomes rigid; secondly, yielding to the pressure of the blood current the walls become stretched, and make the vessel both larger in its transverse diameter, and at the same time longer; and the increased length is accommodated by the vessel becoming tortuous instead of nearly straight. At each beat of the heart the artery is not only expanded, but bent still more out of a straight course. To the finger the artery feels hard, rigid and rough, while the pulse consists of a sudden expansion, and a slow almost unbroken collapse. Fig. 21, D, shows the characters of a sphygmographic tracing.

It can hardly be said that any general condition of illness necessarily accom

panies atheromatous arteries. Many persons in advanced life with this form of degeneration are in the enjoyment of perfect health. But such diseased vessels frequently coexist with chronic Bright's disease; by their want of elastic tissue they tend to hypertrophy and dilatation of the heart; and they lead to serious results in several ways, by rupture (cerebral hemorrhage), by thrombosis and obstruction (hemiplegia, gangrene of the limbs), or by local dilatation (aneurism). Thus while itself often an indication of senility of tissues, atheroma should forewarn us as to possible accidents.

The lardaceous or amyloid change is a form of degeneration affecting vessels, of which more will be said under Lardaceous Disease of the Liver.

ANEURISM.

This name is applied to dilatation of an artery for a more or less limited extent of its course. Aneurisms have been divided, according to their shape, into fusiform and sacculated; the fusiform being a more or less uniform dilatation of the whole circumference of the vessel; the sacculated forming a globular projection from one side of the vessel, and connected with it in advanced cases by a constriction or neck. They have been divided into true and false, according to the number of the arterial coats still present in the sac; but it appears that the inner coat never persists in aneurisms over a certain size, and hence this distinction has no apparent value. Sometimes, especially in the limbs or the abdomen, a sacculated aneurism ruptures at a prominent point, blood oozes slowly out into the tissue around and forms a coagulum, bounded by a kind of cyst of inflam matory tissue. This has been called a diffused aneurism. Lastly, a dissecting aneurism is formed when at a part of the artery affected with atheroma the blood penetrates the inner and middle coats, and forces its way outside these two, between them and the outer coat.

Etiology.-Aneurisms arise from any cause that weakens the vessel at one point. The most common cause is atheroma, especially in the large vessels, in which the inner and middle coats are weakened, and the whole wall yields to the pressure of the blood at that point. In smaller vessels— for instance, those of the brain and lungs-the vessel may be weakened by the local causes of arteries already spoken of, viz., impacted embolus, or the invasion of tubercle. Surgical injuries of the outer coat also lead to aneurism. Of the more general causes predisposing to aneurism, syphilis holds an important place; and probably also excessive muscular strain acting through the circulation.

Results. These are mostly seen in the sacculated forms. One result is the coagulation of blood in the sac itself. As this is out of the direct current, it moves more slowly and has a tendency to coagulate. The sac is thus frequently lined, or nearly filled with successive layers of pale buff, fibrinous

deposits; and it is by the complete filling of the sac with these fibrinous layers that aneurisms are mostly obliterated and cured. The greater the freedom of communication with the main vessel the less the liability to fibrin formation, and in the case of a fusiform aneurism no deposits take place.

Another result of aneurism is its pressure upon the parts around it. The sac may attain an enormous size; an aneurism, of which there is a model in the Museum of Guy's Hospital, springing from the aortic arch, measured eight inches in diameter. As it enlarges, the growth presses with irresistible force upon adjacent parts, displacing the various organs, compressing and obstructing the blood-vessels, the trachea, the bronchi, or the oesophagus, flattening and stretching nerves, and causing thereby pain, numbness, or paralysis, according to the nerve involved, and the degree of its compression. When it comes in contact with unyielding bone, an aneurism causes absorption of the osseous tissue, and excavates or actually perforates it. The vertebræ are frequently eroded in this way, and it is remarkable that the intervertebral cartilages are more resistant than the bone, so that when the aneurism is large enough to cover more than one vertebra the cartilage projects between the two cavities which have been made in the adjacent vertebræ. The ribs and sternum, at first slightly raised by the advance of an aneurism, are subsequently perforated, and allow the pulsation of the tumor directly under the skin. Analogous results occur in other parts of the body, but it is chiefly in the thorax that the pressure effects of aneurism are manifested, because the bony walls allow no room for their important contents to escape.

A third effect of aneurism is hemorrhage, which is the cause of death in a large percentage of cases. The great distention of the coats, and the degeneration which precedes this, sufficiently explain why hemorrhage occurs. Even the deposit of layers of fibrin within the sac will not always prevent it; the clot, if at all abundant, does not organize, and the blood may force its way into fissures and meshes of the coagulum, and so finally reach the surface, and slowly ooze out. The rapidity and extent of the hemorrhage further depend upon the support the aneurism has from without. Ruptures into hollow viscera are rapidly fatal; ruptures into connective tissue or inter-muscular spaces are often much slower, and in the limbs may allow time for successful treatment.

Symptoms. They may be divided into those common to all aneurisms, and those determined by the locality; and here will be considered only the special symptoms of thoracic aneurism, those characteristic of abdominal aneurism being discussed elsewhere (see Abdominal Tumors).

The symptoms common to aneurism in any part of the body are: (1) Tumor; (2) Pulsation; (3) Murmur; (4) Pain; and other effects of pressure. Tumor, or some kind of swelling, is a necessary part of an aneurism, but it may, of course, be entirely unrecognizable during life in such parts as the cranium, the thorax, the deeper parts of the abdomen, or the gluteal region.