Cerebral abscess

Last revised by Arlene Campos on 20 May 2024

A cerebral abscess is a focal area of necrosis starting in an area of cerebritis surrounded by a membrane. It is a potentially life-threatening condition requiring prompt radiological identification and rapid treatment. Fortunately, MRI is usually able to convincingly make the diagnosis, distinguishing abscesses from other ring-enhancing lesions

Demographics reflect at-risk groups (see below) with all age groups being affected.

Risk factors for hematogenous spread include 3:

Clinical presentation is non-specific, with many cases having no convincing inflammatory or septic symptoms. Symptoms of raised intracranial pressure, seizures and focal neurological deficits are the most common forms of presentation. Eventually, many abscesses rupture into the ventricular system, which results in a sudden and dramatic worsening of the clinical presentation and often heralds a poor outcome. 

Cerebral abscesses result from pathogens growing within the brain parenchyma. Initial parenchymal infection is known as cerebritis, which may progress into a cerebral abscess. Historically direct extension from sinus or scalp infections was the most common source. More recently, hematological spread has become most common. Direct introduction by trauma or surgery accounts for only a small minority of cases 3.

Cerebral infection is commonly divided into four stages with distinct imaging and histopathologic features:

  1. early cerebritis (a focal infection without a capsule or pus formation,can resolve or develop into frank abscess)

  2. late cerebritis

  3. early abscess/encapsulation - may occur 10 days after infection

  4. late abscess/encapsulation - may occur >14 days after infection

  • Streptococcus spp.: 35-50% 3

    • especially S. pneumoniae 4

  • sterile: 25%

  • mixed: variable, 10-90% of cases depending on source 3

  • Staphylococcus aureus and epidermidis: following neurosurgery

  • Gram-negative spp. more common in infants

  • Listeria in pregnant women and older patients

  • group B Streptococcus (GBS) and E. coli in neonates

  • Fusobacterium nucleatum : rare 15

The immunocompromised patient is susceptible to a host of other organisms including 3:

Both CT and MRI demonstrate similar features, although MRI has a greater ability to distinguish a cerebral abscess from other ring-enhancing lesions:

  1. early cerebritis - please see cerebritis article

  2. late cerebritis - please see cerebritis article

  3. early encapsulation

    • ​​a discrete lesion with a thin enhancing rim

    • the rim may be less-well defined along the peripheral aspect of the lesion (away from ventricles)

    • +/- additional "daughter" collections

    • +/- ventricular extension, with accompanying ventriculitis

  4. late encapsulation - progressive central necrosis, cavity shrinks, decreasing surrounding edema

In patients with suspected intraparenchymal sepsis, pre- and post-contrast scans should be obtained, unless the plan is to proceed to MRI regardless of the CT findings. Typical appearances include:

  • outer hypodense and inner hyperdense rim (double rim sign) in most cases

  • ring of iso- or hyperdense tissue, typically of uniform thickness

  • central low attenuation (fluid/pus)

  • surrounding low density (vasogenic edema) 

  • ventriculitis may be present, seen as enhancement of the ependyma

  • obstructive hydrocephalus will commonly be seen when intraventricular spread has occurred

MRI is more sensitive than CT. Although peripherally-enhancing lesions may be non-specific by imaging, diffusion-weighted sequences (less commonly MR spectroscopy) showing central diffusion restriction are critical for suggesting the diagnosis of a cerebral abscess.

  • T1

    • central low intensity (hyperintense to CSF)

    • peripheral low intensity (vasogenic edema) 

    • ring enhancement 

    • ventriculitis may be present, in which case hydrocephalus will commonly also be seen

  • T2/FLAIR

    • central high intensity (hypointense to CSF, does not attenuate on FLAIR)

    • peripheral high intensity (vasogenic edema)

    • the abscess capsule may be visible as an intermediate to slightly low signal thin rim 1


    • high DWI signal is usually present centrally 11

    • represents true restricted diffusion.

    • peripheral or patchy restricted diffusion may also be seen; this finding is however not as constant as one may think, with up to half of the rim-enhancing lesions demonstrating some restriction not proving to be abscesses.

    • in some immunocompromised states, central content may not restrict diffusion (e.g. tuberculoma, cerebral toxoplasmosis) 13

  • SWI

    • low-intensity rim 9

      • complete in 75% 

      • smooth in 90%

      • mostly overlaps with contrast-enhancing rim

    • dual rim sign: a hyperintense line located inside the low-intensity rim 

  • MR perfusion: rCBV is reduced in the surrounding edema cf. to both normal white matter and tumor edema seen in high-grade gliomas 2

  • MR spectroscopy: elevated peaks are seen corresponding to lipids/lactate, succinate, acetate, and amino acids (alanine, valine, leucine, and isoleucine) 14

The mainstay of treatment for cerebral abscesses is neurosurgical intervention and drainage of the collection. This can be performed either by stereotactic aspiration or craniotomy 7. Broad-spectrum intravenous antibiotics are also needed and can later be changed to agents tailored to the specific organisms. 

In cases where the abscess cavity does not completely obliterate, follow-up with MRI including DWI is useful and lack of restricted diffusion is reassuring. Demonstration of ongoing restricted diffusion in a cavity suggests persistent infection 8.  

The differential diagnosis typically includes other ring-enhancing lesions:

When a lesion demonstrates both ring enhancement and central restricted diffusion the differential is very much narrowed, and although cerebral abscess is by far the most likely diagnosis, the following should also be included on the differential 6

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