Brain abscess pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
|
Brain abscess Microchapters |
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Brain abscess pathophysiology On the Web |
|
American Roentgen Ray Society Images of Brain abscess pathophysiology |
|
Risk calculators and risk factors for Brain abscess pathophysiology |
Overview
Pathophysiology
Brain abscesses are usually polymicrobial in nature.
The most common organism recovered from cultures is the bacterium Streptococcus. However, a wide variety of other bacteria (Proteus, Pseudomonas, Pneumococcus, Meningococcus, Haemophilus), fungi and parasites may also cause the disease. 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. The location of the primary lesion may be suggested by the location of the abscess: infections of the middle ear result in lesions in the middle and posterior cranial fossae;[1] congenital heart disease with right-to-left shunts often result in abscesses in the distribution of the middle cerebral artery[2][3]; and infection of the frontal and ethmoid sinuses usually results in collection in the subdural sinuses.
Brain abscesses usually start as a focal area of cerebritis that eventually develops into a collection of puss, surrounded by a well-vascularized capsule.
- In general, the brain is relatively resistant to infection due to the presence of the abundant blood supply, and the relatively impermeable blood-brain barrier.
- Although underlying pathology (tumor, blood etc.) can sometimes be a nidus for infection, the majority of cases occur in a previously ‘healthy’ brain.
- Experimental models have identified four stages for abscess formation:
- Early cerebritis (days 1 – 3): focal inflammation and edema.
- Late cerebritis (d 4 – 9): development of a necrotic center.
- Early capsular (d 10 – 14): formation of a well-vascularized, ring-enhancing capsule with peripheral gliosis and / or fibrosis.
- Late capsular: (after 2w): formation of a well-formed fibrous capsule.
- Approximately 47% of cases arise from a contiguous infection, most commonly in the middle ear, the paranasal sinuses and teeth.
- ~ 25% result from hematogenous seeding from an extracranial infection.
- Penetrating trauma accounts for ~ 10% of cases.
- 20 – 30% of cases are idiopathic, and no obvious focus can be identified.
- The location of the abscess obviously depends on the source of infection, as does the specific microbial flora.
References
- ↑ 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. Unknown parameter
|paes=ignored (help) - ↑ Raimondi AJ, Matsumoto S, Miller RA (1965). "Brain abscess in children with congenital heart disease". J Neurosurg. 23: 588&ndash, 95.