Brain abscess

Pathogenesis and pathophysiology
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By John E Greenlee MD

Brain abscesses may be single or multiple. Each abscess begins as a microscopic focus of septic, microvascular injury, usually within white matter or at the gray-white junction. Growth of bacteria within this focus produces a localized encephalitis or "cerebritis," which undergoes liquefaction (Britt and Enzmann 1983; Enzmann et al 1983; Pendlebury et al 1989; Brouwer et al 2014a). The developing abscess elicits an inflammatory response of lymphocytes and polymorphonuclear leukocytes, with localized, frequently intense cerebral edema. Over time, an abscess capsule forms, consisting of both fibrotic and gliotic elements. The abscess capsule tends to be thickest on its cortical surface and thinnest medially, causing the abscess to expand toward and rupture into the ventricular system (Kastenbauer et al 2004). Death in brain abscess may result from tonsillar herniation, caused by the mass effect of the abscess and its surrounding cerebral edema, or from rupture of the abscess into the ventricular system.

Brain abscesses most frequently arise following hematogenous dissemination of organisms from distant sites of infection. The most common associated systemic infections are chronic lung infections, in particular bronchiectasis and lung abscess, and acute bacterial endocarditis (Greenlee and Mandell 1973; Bleck and Greenlee 2000; Kastenbauer et al 2004; Pruitt 2013). Brain abscess is particularly likely in conditions in which a right-to-left cardiac shunt allows organisms to move directly from the venous circulation into left-sided systemic circulation. For this reason, children with cyanotic congenital heart disease are at particular risk for hematogenous brain abscess (Cole et al 2012; Ozsurekci et al 2012), as are patients with hereditary hemorrhagic telangiectasia (Tabakow et al 2005; Galitelli et al 2006a; 2006b; Sell et al 2008; Corre et al 2011). Rarely, brain abscess may also complicate pulmonary arteriovenous fistulae not associated with hereditary hemorrhagic telangiectasia or in the setting of a patent foramen ovale (Kawano et al 2009).|{picture:dgba.bmp}{caption:Classic appearance of a brain abscess on MRI}{label:This 49-year-old male was told that he no longer needed SBE prophylaxis for dental procedures despite the presence of his patent foramen ovale. Three weeks after undergoing routine teeth cleaning, this patient developed a seizure. Axial MR imaging of a pathologically proven brain abscess in this patient reveals (A) marked restricted diffusion on diffusion-weighted images, (B) high T2 signal, and (C) FLAIR signal due to edema and a well circumscribed mass in the right frontal lobe. Once the capsule has formed (usually within 2 to 3 weeks), the walls of the mass are often (D) clearly delineated even without on T1 weighted imaging, and (E) the walls show brisk enhancement with contrast and demarcates the wall from the necrotic center. (Contributed by Dr. Diana Gomez-Hassan.)}| Less frequently, brain abscesses result from spread of organisms through emissary veins during sinusitis, otitis, or mastoiditis (Bleck and Greenlee 2000). Historically, otitis represented the major pericranial infection associated with brain abscess; at present, however, brain abscess is more frequently associated with frontal, ethmoidal, and sphenoidal sinusitis (Kastenbauer et al 2004), and the most common site of brain abscess is the frontal lobe (Roche et al 2003). Less frequent causes of brain abscess include penetrating trauma, neurosurgical procedures, facial infections, and dental sepsis (Kastenbauer et al 2004). A single case report lists brain abscess as a complication of tongue piercing (Herskovitz et al 2009). Brain abscesses of hematogenous origin are most common in the distribution of the middle cerebral artery, followed by those of the anterior cerebral artery and posterior circulation (Kastenbauer et al 2004). Abscesses arising from frontal and ethmoidal sinusitis are most commonly located within the frontal lobe (Bleck and Greenlee 2000). Sphenoid sinusitis may cause frontal or temporal lobe abscesses. Infections of the middle ear or mastoid may spread through emissary veins into the middle fossa to cause temporal lobe abscesses or into the posterior fossa to cause cerebellar abscess (Bleck and Greenlee 2000; Kastenbauer et al 2004).

In This Article

Historical note and nomenclature
Clinical manifestations
Clinical vignette
Pathogenesis and pathophysiology
Differential diagnosis
Diagnostic workup
Prognosis and complications
References cited