the possibility of sinus occlusion. If meningeal or focal symptoms are present, coupled with local edema about the eye or face, over the vertex, in the mastoid or occipital region, a diagnosis may be made.

The prognosis will depend upon the nature of the initial illness, the probability of cortical softening, and the vital prospects. When the cachexia or exhausting disease can be controlled and life maintained, the tendency to resorption of the clot presents a favorable outlook, except for the softened areas of brain-tissue. When these have been produced, permanent disability of a motor or mental character, or both, may be expected. The treatment is that of the general condition.

Infective sinus thrombosis, inflammatory thrombosis or secondary thrombosis, is the result of the invasion of pathogenic infectious organisms. It is, therefore, a secondary process and occurs usually in adults. Generally it is located in one of the paired sinuses and in the one nearest the infection atrium. It is likely to produce meningitis or give rise to cerebral abscess, or both, and it is frequently attended or followed by systemic infection and pyemia. It arises from septic traumatic conditions of the face, scalp, cranial and facial bones, and from septic processes in the nose, mouth, pharynx, in the various bony sinuses, and in the middle ear and mastoid process. By far the most common source of infection is suppurative middle-ear disease. Anthrax of the face and lips, facial and scalp erysipelas, dental caries, and carbuncles have been noted as causes. The sinus always becomes infected by extension of the septic process to it, either by direct invasion or by propagation along a venous tributary. Inflammation of the sinus-walls is followed by thrombotic coagulation of the contained blood, and a septic plug is formed that closely adheres to the diseased and softened vessel.

The septic, soft, and disintegrating thrombotic clot, swarming with pathogenic and pyogenic bacteria, sets up infection of the immediate territory, and, yielding particles to the blood-stream, often induces disseminated and systemic infection. Thus arise the numerous pyogenic foci throughout the body that are frequently present. The thrombus once formed is prone to extend, and the internal jugular is often invaded, presenting itself in its upper third as an indurated cord that can be palpated in the neck. Even the superior vena cava has been invaded. The sinus-walls being softened, the neighboring leptomeninges are infected and a localized or disseminated septic meningitis is added. In a similar way the infective process travels along the veins into the substance of the encephalon and sets up abscesses. Macewen thus tabulates the principal differences between marantic and infective sinus thrombosis:

4. Tendency to produce brain softening. 5. There is seldom purulent infection as a sequence.

6. No accompanying leptomeningitis, cerebral or cerebellar abscess.

4. No tendency to brain softening.
5. Purulent infection common from
septic or infective emboli.

6. Often coincident purulent leptomen-
ingitis, cerebral or cerebellar ab-

scess.

The symptoms of infective sinus thrombosis are local and systemic. The local ones are due to circulatory disturbance, such as circumscribed edema and brain symptoms. They will be given in detail in the description of thrombosis of special sinuses. The systemic symptoms are those of septicemia; intense headache, often localized at the seat of disease; vomiting, fluctuating and remittent temperature; small, thready pulse; rigors, profuse perspiration, dry tongue, anorexia and diarrhea, or constipation.

Depending upon the preponderance of symptoms and their grouping, the septicemia shows different clinical varieties. When the lungs are first or mainly involved by the plugging of pulmonary vessels, localized or diffuse pain is occasioned, cough is induced, and the expectoration may change to "prune-juice" appearance, and then becomes purulent, fetid, and extremely offensive as the pulmonary process increases. Abscesses form and gangrene occurs. In this way septic pneumonia also is

induced.

When the brunt of the attack falls upon the abdominal organs, the typhoid type of septicemia, which closely mimics enteric fever and is sometimes mistaken for it, is presented. In another and much smaller group of cases meningeal symptoms dominate the picture and are actually due, in large part at least, to the infective leptomeningitis. All three of the symptom groups, or any combination of their various. features, may be presented by the same case.

Infective cavernous sinus thrombosis arises from septic invasion, reaching the sinus usually by way of the ophthalmic vein. It may also be due to a forward extension of a septic process in the lateral or petrosal sinuses. The secondary meningitis to which it gives rise is basilar. Fractures of the cranial base and blows on the head have furnished its starting-point. Erysipelas of the face, especially about the eye and nose; abscess of the orbit; infections of the nasal, buccal, and pharyngeal cavities or of their sinuses; ulceration of the tonsillar glands, and caries or periosteitis of the facial, especially of the maxillary bones, have led to it.

Symptoms: One sinus is usually first involved, and the local manifestations are one-sided. There is, however, a pronounced tendency for the process to invade the opposite sinus, and then the case presents bilateral signs. Such a sequence is highly diagnostic. The first affected side may even show improvement through the establishment of the collateral return circulation before the second side is invaded. There is usually considerable pain of a supra- or infra-orbital neuralgic sort, and diffuse headache. Mental symptoms are wanting, unless meningitis is set up, and then delirium, hebetude, and coma may appear. When the sinus is plugged the return circulation through the

ophthalmic veins is cut off. The orbital contents become edematous, the ocular globe is thrust forward, the lids are swollen, and the swelling extends to the nose, brow, and cheek. There may also be swelling on the same side of the pharynx. The optic disc is congested or choked, the retinal veins are distended, and pressure is exerted on the ocular nerves that enter the orbital apex. This causes more or less ophthalmoplegia. The third, fourth, sixth, the ophthalmic division of the fifth, and the optic nerves are more or less affected. Ptosis, strabismus, pupillary stasis, and defective vision in varying degrees are thereby added to the exophthalmos.

The invasion may be abrupt or insidious and the disease may last from a few days to several months, but infective cases are practically fatal. When the second eye is involved, it usually is very rapidly affected. The appearance of basilar meningitis and the development of septicemia add immediate gravity to the already serious condition.

Infective lateral sinus thrombosis is the form most frequently encountered. Its origin is nearly always in a septic condition of the middle ear. The petrosal sinuses and the internal jugular are usually invaded. It is commonly encountered in young adults, and is rare in the two extremes of age. While ordinarily due to middle-ear disease, it may arise from a mouth or throat infection by way of the Eustachian tube and tympanum, from extension of thrombosis in other sinuses, from basilar fractures involving the petron, and from infections about the occiput, nucha, and mastoid.

Symptoms: The lateral sinus is usually affected from a chronic middle-ear suppuration which has caused more or less erosion of the tympanic bony structure. An acute process may cause it, but this is exceptional. In the chronic cases of purulent otitis media it is a constant menace. Frequently there is a lessening or cessation of the ear-discharge, pain develops in the ear, and headache follows. The fluctuating temperature mounts up, and vomiting and rigors indicate the involvement of the sinus or an intracranial extension. Local signs of lateral sinus thrombosis depend on the obstruction of its lumen and the location or extent of the thrombus and phlebitis. Occlusion of the sinus, blocking the inlet of the mastoid vein, gives rise to a circumscribed edema extending from the auricle over the mastoid. Pain on percussion of the mastoid is present only when the bone or periosteum is inflamed. If the thrombosis is situated lower in the sinus and shuts off the condylar veins, through which the superficial circulation of the lateral lower occipital region drains, a brawny hardness and edema may be made out in the upper part of the posterior cervical triangle. Should the phlebitis extend into the internal jugular, extreme local tenderness is found over the upper portion of this vessel on palpation, or may be experienced by the patient in swallowing. The head is usually inclined to the affected side to lessen muscular pressure on the jugular. When the thrombosis follows down into the jugular, it may be easily palpated as a firm, cord-like structure. Disintegration of the thrombus may cause it to disappear in a few days. The lymphatic glands in the neck are frequently engorged and easily palpable. Gerhardt has pointed out

that during inspiration the external jugular vein on the affected side is less prominent. This is due to the occlusion of the internal jugular, which allows rapid drainage of the external branch into the common trunk. If, however, the thrombus extends into the common trunk, the external vessel is then engorged and more prominent than on the sound side.

If the inflammatory thickening at the jugular foramen is sufficiently great, it involves, by extension or pressure, the cranial-nerve trunks, which make their exit at this opening. Pneumogastric, spinal accessory, and glossopharyngeal symptoms are then produced. Respiratory, laryngeal, cardiac, and vocal disturbances; difficulty in swallowing, spasm or paresis in the sternomastoid and trapezius point to this condition. Abscesses sometimes form in the neck, under the sternomastoid or in the nuchal region.

Almost from the first there are distinct cerebral symptoms. The cephalalgia is attended by somnolence, which may deepen into coma. Delirium is often an early symptom. Phlebitis is likely to extend into the temporosphenoidal lobe and cerebellum, giving rise to diffuse inflammation or rapidly producing softening and abscesses. At the seat of the sinus thrombosis the softened dural wall no longer protects the soft meninges, and a localized septic meningitis, with a tendency to become diffuse is occasioned. Even the bone under the sinus is eroded, and definite discolorations are left, both on the cranial wall and on the cerebral surface, to mark the site of the sinus disease.

A disease presenting so many complications and possibilities necessarily lacks clinical uniformity. While lateral sinus thrombosis is usually confined to one side, it may propagate itself into the venous channels of the opposite side and infect both internal jugulars. The appearance of cerebritis, meningitis, or intracranial abscess greatly reduces the life chances. Septicemia is particularly likely to develop, with its own serious import. The virulence of the infection, however, seems to vary between wide extremes. Some cases run a rapid course to fatal termination in four to seven days, others last weeks and months, and exceptional ones may recover. The gravity of the disease can not well be overestimated.

Infective thrombosis of the longitudinal sinuses is extremely rare, while marantic thrombosis finds its most common location in these venous passages and especially in the superior one. Infectious conditions in the nasal vault, in the scalp, and in the cranial diploë of the vertical region are capable of extension to the superior longitudinal sinus. Phlebitis may then extend to the cortical veins. Occlusion of the sinus leads to local edema in the scalp and probably in the brain also, but the collateral circulation obviates any serious results from this mechanical feature. The danger lies in the likelihood of septic cerebral phlebitis and septic meningitis. Usually the obtrusive meningitic features predominate, and suggestions of cortical phlebitis and even of abscess formation are obscured or overlooked.

The treatment of infective cranial sinus thrombosis is primarily surgical. The infection atrium is to be determined and rendered

thoroughly aseptic. Whenever possible, it must be eradicated. In the case of the cavernous sinuses little more can be done by the surgeon, but aggressive interference is allowable, and indicated when the lateral and longitudinal sinuses are invaded. Many cases of lateral sinus thromboses have probably been saved by prompt and radical interference. The sinus has been opened, the infective thrombus removed, and abscesses in the temporal lobe and in the cerebellum drained. Often as a preliminary measure the mastoid antrum and the middle ear have been surgically dealt with, but when there is evidence of sinus thrombosis it is a waste of time and opportunity to stop at this step.

In

Local applications of heat and cold to the head may be used, and serve sometimes to relieve the headache and modify the delirium. view of the septic nature of the disease, supportive measures are emphatically indicated from the first. Against the septicemia we may bring measures to bear that favor elimination by the skin, bowels, and kidneys. The administration of antiseptics, such as the salicyl preparations and the mercurials, are of doubtful value, but are strongly advised by many and should not be omitted.

CHAPTER IX.

CEREBRITIS, ENCEPHALITIS, AND ABSCESS OF THE

BRAIN.

INFLAMMATION of the brain proper may be local or generalized, acute or chronic.

Acute Localized Cerebritis.-Etiology.-The brain is subject to inflammatory processes the same as any other parenchymatous organ, yet generalized cerebritis is rare, and only recently have we learned to recognize it. Localized acute cerebritis, on the other hand, occurs with frequency, but is practically, if not invariably, a secondary condition. Meningitis always entails some underlying cerebritis. A circumscribed cerebritis occurs about a hemorrhagic focus or spot of thrombotic softening if infection is added. Without the additional infection such as is furnished by septic endocarditis or other infective focus the zone surrounding a cerebral tumor, hemorrhage, or area of softening is one of congestion, edema, and pressure necrosis. Blows on the head may cause localized meningitis and cerebritis at the point of violence, or on the opposite side of the head by the action of contre coup. In some cases the local cerebritis alone follows, and this may only affect the white matter below the cortex. Apparently the traumatism favors the local action of bacteria by reducing the resistance of the tissues, as proved by Ehrnrooth in an interesting series of experiments.1 Cranial frac tures, punctured wounds, and perhaps severe concussion may cause it. Bone disease, septic processes in the diploë, and in the cranial bony and venous sinuses, may lead to cerebral inflammation and be followed by 11"Rev. Neurolog.," Aug., 1900.