Brain abscess pathophysiology

Revision as of 20:41, 29 July 2020 by WikiBot (talk | contribs) (Bot: Removing from Primary care)
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to navigation Jump to search

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farwa Haideri [2]

Abscess Main Page

Brain abscess Microchapters


Patient Information


Historical Perspective



Differentiating Brain abscess from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis


History and Symptoms

Physical Examination

Laboratory Findings



Other Imaging Findings

Other Diagnostic Studies


Medical Therapy


Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Brain abscess pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides


American Roentgen Ray Society Images of Brain abscess pathophysiology

All Images
Echo & Ultrasound
CT Images

Ongoing Trials at Clinical

US National Guidelines Clearinghouse

NICE Guidance

FDA on Brain abscess pathophysiology

CDC on Brain abscess pathophysiology

Brain abscess pathophysiology in the news

Blogs on Brain abscess pathophysiology

Directions to Hospitals Treating Brain abscess

Risk calculators and risk factors for Brain abscess pathophysiology


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:[1][2][3]

  • 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.

The most common organism recovered from cultures is the bacterium Streptococcus. A wide variety of other bacteria may cause brain abscess. These include:[4]

  • 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.[4]

Gross Pathology

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


  1. Macewan W (1893). Pyogenic Infective Diseases of the Brain and Spinal Cord. Glasgow: James Maclehose and Sons.
  2. Ingraham FD, Matson DD (1954). Neurosurgery of Infancy andChildhood. Springfield, Ill: Charles C Thomas. p. 377.
  3. Raimondi AJ, Matsumoto S, Miller RA (1965). "Brain abscess in children with congenital heart disease". J Neurosurg. 23: 588&ndash, 95.
  4. 4.0 4.1 "Brain abscess - Wikipedia, the free encyclopedia".

Template:WS Template:WH