These are different manifestations of infection, the clinical picture differing according to the tissues and localities involved. For the production of these infectious conditions no special bacteria other than those already catalogued in Chapter III are comprehended. Their method of activity is there discussed at sufficient length, and we need here only consider the various paths of infection. These may lie along the bloodvessels, the lymphvessels, nerve sheaths, and prolongations of the membranous sacs which extend from the cranial cavity proper.

The most common of all the paths of infection is afforded by the middle ear, especially when involved in a chronic suppurative lesion, which is by no means necessarily connected with a patulous tympanic membrane, and which may consequently be undiscovered, though in more or less constant activity.

A. Abscess of the Brain.

—This may be traumatic or non-traumatic. The former variety is most often due to the direct result of injury, infection displaying its consequences promptly or sometimes not until long periods have elapsed. The ordinary form occurs within the first two weeks, usually as an acute cortical abscess beneath a more or less compromised membrane, surrounded by a zone of red softening, and this by another of brain edema. The chronic traumatic abscesses are less often cortical, but are deeper. They are marked by prolonged suppuration of the external wound, but may occur through some mechanism not understood. Only the chronic abscesses show encapsulation, the capsule partaking of the character of the pyophylactic membrane, elsewhere described. (See [Chapter VIII].) It may cover a long period—to my personal knowledge at least nine years, while others have mentioned twenty and more. The non-traumatic abscesses are in the main due to middle-ear disease. When the roof of the tympanum breaks down it is the middle fossa of the skull which is infected; when the posterior wall, naturally the posterior fossa. The most common result of perforation of the tympanic roof is involvement of the mastoid antrum or the sigmoid groove and sinus. In the former case we have temporosphenoidal abscess; in the latter, cerebellar, if any. Previous to actual perforation there is thinning of bone with thrombosis along the minute veins connected with the sinuses. When the dura is exposed by the carious process, granulation tissue often protects it against further inroads, while masses of the same projecting into the tympanum have been mistaken for prolapse. If the sigmoid groove be the site of the first disturbance, extradural abscess may form between the sinus and the remaining bone, the granulating process then involving the whole bony groove. Its later consequence is sinus phlebitis, sinus thrombosis, or intradural infection. If there be adhesion between the dura and the cortex we have actual brain ulceration without formation of a true abscess; but if once the perivascular sheaths have carried infection to the substance of the brain there is a rapid purulent disintegration of the same, and formation of a true subpial or deep abscess, which latter is in effect a purulent encephalitis. Macewen has shown how important it is not merely to evacuate such abscesses, but to eradicate the path of infection from the point of origin, which is rarely easy.

Extradural pus may escape into the mastoid cells by erosion of their inner walls. Such pus may escape suddenly, and serious symptoms thus be mitigated. Even abscess of the bone may thus empty itself by the process of adhesion and pointing toward the surface. Pus from the mastoid cells may perforate the temporomaxillary joint or escape along the digastric groove and form deep cervical abscesses.

When the arachnoidal tissue is involved, both subdural and subarachnoidal spaces participate in the infection, and the brain floats upon a pus-bed rather than a water-bed. Leptomeningitis under these circumstances becomes quickly diffused and fatal. Serous fluid may accumulate so quickly as to produce death by mere obstruction to the cerebral bloodvessels, while distention of the ventricles and an acute infectious internal hydrocephalus is possible. Leptomeningitis may be propagated wherever anatomical paths may carry it, even to the cauda equina and along the spinal nerve sheaths.

The pus within cerebral abscesses is often discolored, sometimes offensive. A greenish color is usually imparted by the Bacillus pyocyaneus, while the offensive odor comes mostly from the Bacillus coli. Around such an abscess is a zone of inflamed cerebral tissue. If within this zone a pyophylactic membrane is produced by condensation the abscess may become encapsulated and life be prolonged. When a capsule fails to form, the process being too acute or rapid, death is the speedy termination of such a case. These abscesses are generally single, but may be multiple. There is also a metastatic expression of abscess formation, seen in typical cases of pyemia, where numerous miliary abscesses are found within the brain. Pressure symptoms are less likely from abscess than from a tumor of the same bulk, while there is much greater liability to edema and sudden infection. Gradually extending paralysis implies pathological activity around the abscess. Large collections of pus are often met in the least vital parts of the brain, as in the frontal or temporosphenoidal lobes.

Symptoms.

—Aside from causal indications (e. g., injury to the head, middle-ear disease, recent operations upon the air-containing cavities, etc.) the first symptoms may be slight. They consist usually of headache, often ascribed to cold or trifling injury, becoming exaggerated, rarely definitely located, radiating widely. In time it is spoken of as “excruciating,” and may be continuous or intermittent. Vomiting is not infrequent, rarely accompanied by nausea. Chills come on early in the history of the case, varying in intensity, duration, and frequency. The more frequent, the more likely is it that the abscess results from some general infection. Temperature is seldom much elevated; it is often subnormal. When exalted it is in proportion to the degree of meningeal involvement. If pressure symptoms become marked we get the usual slow pulse due to increased tension. After evacuation of pus pressure symptoms may subside, but temperature rise. Such discharge from the middle ear as may have been previously noted usually diminishes. A history of cessation of discharge and of increased pain and fever occurring at irregular intervals is very characteristic.