Brain abscess pathophysiology
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Brain abscesses are usually polymicrobial in nature. Swelling and irritation (inflammation) develop in response to this infection. Infected brain cells, white blood cells, live and dead bacteria, and fungi collect in an area of the brain. Tissue forms around this area and creates a mass. While this immune response can protect the brain by isolating the infection, it can also do more harm than good. Infected material can block the blood vessels of the brain. Although underlying pathology (tumor, blood etc.) can sometimes be a nidus for infection, the majority of cases occur in a previously healthy brain.
The location of the primary lesion may be suggested by the location of the abscess. It depends on the source of infection, as does the specific microbial flora. Roughly 25% of brain abscess result from hematogenous seeding from extra-cranial infection. Penetrating trauma accounts for nearly 10% of cases. About 20 to 30% of cases are iodiopathic, and no obvious focus can be identified. Common locations include:
- Infections of the middle ear result in lesions in the middle cranial fossal.
- Approximately 47% of cases arise from a contiguous infection, most commonly in the middle ear, the paranasal sinuses and teeth.
- Posterior cranial fossae
- Congenital heart disease with right-to-left shunts often result in abscesses in the distribution of the middle cerebral artery.
- Infection of the Frontal and Ethmoid sinuses usually results in collection in the subdural sinuses.
- Proteus, Pseudomonas, Pneumococcus, Meningococcus, Haemophilus
- Fungi and parasites are especially associated with immunocompromised patients.
- Organisms that are most frequently-associated with brain abscess in patients with AIDS are Mycobacterium tuberculosis, Toxoplasma gondii and Cryptococcus neoformans, though in infection with the latter organism, symptoms of meningitis generally predominate.
- Bacterial abscesses rarely (if ever) arise de novo within the brain. There is almost always a primary lesion elsewhere in the body that must be sought assiduously, because failure to treat the primary lesion will result in relapse. In cases of trauma, for example in compound skull fractures where fragments of bone are pushed into the substance of the brain, the cause of the abscess is obvious. Similarly, bullets and other foreign bodies may become sources of infection if left in place.
Experimental models have identified four stages for abscess formation. These include:
- Early cerebritis (days 1 – 3): focal inflammation and edema
- Late cerebritis (days 4 – 9): development of a necrotic center
- Early capsular (days 10 – 14): formation of a well-vascularized, ring-enhancing capsule with peripheral gliosis and/or fibrosis
- Late capsular: (after 2 weeks): formation of a well-formed fibrous capsule
- Macewan W (1893). Pyogenic Infective Diseases of the Brain and Spinal Cord. Glasgow: James Maclehose and Sons.
- Ingraham FD, Matson DD (1954). Neurosurgery of Infancy andChildhood. Springfield, Ill: Charles C Thomas. p. 377.
- Raimondi AJ, Matsumoto S, Miller RA (1965). "Brain abscess in children with congenital heart disease". J Neurosurg. 23: 588&ndash, 95.
- "Brain abscess - Wikipedia, the free encyclopedia".