Last Updated: March 27, 2020
Abscesses begin as focal areas of infected brain called cerebritis, which may result from direct spread (commonly iatrogenic or from mastoiditis, sinusitis, or meningitis) or from hematogenous spread. There are four characteristic zones of an abscess that include a cavity of central necrosis, a capsule composed of fibroblasts, reticulin and collagen, peripheral edema, and areas of extraparenchymal spread (meninges, ventricles, CSF spaces, bone, blood vessels).
There are 4 stages of brain infection between cerebritis and abscess, which are as follows:
- Early cerebritis
- Late cerebritis
- Early capsule
- Late capsule
The lesions are either located near extra-axial infection or at common sites of hematogenous spread that are usually supratentorial, usually in the anterior circulation (ACA and MCA), and usually at the grey-white matter junctions and basal ganglia.
The most distinguishing characteristics of abscesses are peripheral enhancement around a cavity of central necrosis and pus. Without further information, however, the finding of solitary or multiple ring-enhancing lesions is not specific and the differential diagnosis is broad, including neoplasms, demyelinating disorders, other infections, and subacute insult to the brain parenchyma like contusion or stroke.
- Early cerebritis
- Ill-defined low-density area
- Possible patchy enhancement
- Ill-defined low-density area with mass effect
- Subtle ring-like enhancement PLUS persistent central enhancement
- Discrete low-density lesion with mass effect and surrounding ill-defined low-density of the brain tissue reflecting edema
- Discrete ring-like enhancement of the capsule
- Decreasing size of the low-density mass and decreasing mass effect
- Decreasing hypodense surrounding edema
- Thickening of the enhancing capsule but decreased size of the cavity
- Possible development of satellite abscesses
- Early cerebritis
- Early cerebritis:
- T1: Ill-defined area of decreased signal
- T2/FLAIR: Ill-defined area of increased signal
- DWI/ADC: increased signal on both (edema, NOT restricted diffusion)
- T1 post-contrast: Patchy enhancement
- T1: low signal center, iso-intense rim
- T2: high signal center, hypointense rim (presumed to be due to high concentration of free oxygen radicals causing local disruption of the magnetic field and loss of signal)
- FLAIR: increased signal within and surrounding the lesion
- DWI/ADC: increased signal within and surrounding the lesion on both (edema, transitioning to restricted diffusion)
- T1 post-contrast: irregular rim enhancement
- T1: Discrete iso- to hyperintense rim, low signal center
- T2: High signal center, low-signal rim, surrounding high signal of edema
- FLAIR: Increased signal within and surrounding the lesion
- DWI/ADC: Central increased DWI signal and decreased ADC signal (restricted diffusion due to high degree of cellular debris – bacteria and inflammatory response cells).
- T1 post-contrast:
- Thin, avidly enhancing rim, absent central enhancement (necrotic center).
- The ventricular side of the capsule is often thinner and more prone to rupture, allowing for the development of satellite abscesses and intraventricular extension. The cause is felt to be relatively poorer blood flow and poorer fibroblast migration from the deep white matter.
- Typical findings of ventriculitis include intraventricular restricted diffusion, intraventricular debris (incomplete suppression of the CSF fluid signal on FLAIR sequence), periventricular edema and enhancement of the ventricular walls (usually mild and thin).
- MR spectroscopy: Central necrosis shows increased lactate and amino acids.
- T1: Thicker capsule, decreased size of the cavity
- T2/FLAIR: decreased surrounding edema
- DWI/ADC: Persistent restricted diffusion in the necrotic center (high DWI, low ADC), decreased surrounding edema (high DWI and high ADC)
- T1 post-contrast: Thick enhancing capsule, decreased size of the non-enhancing central cavity
- Early cerebritis:
- Abscesses show peripheral uptake of F-18 fluorodeoxyglucose and C-11 methionine.
- Infarct (subacute infarcts can present as nodular or ring-enhancing lesions with restricted diffusion, mimicking cerebritis or abscess, as in this case of infarct in the left corona radiata)
- Atypical Infections (neurocysticercosis, cryptococcosis, toxoplasmosis, tuberculosis and many others) and this case, which is tuberculous meningitis with intraparenchymal extension in the inferior frontal lobes that presents as multiple, cystic ring-enhancing lesions, but these do not cause restricted diffusion)
- Cerebral Parenchymal Contusion
- Primary CNS Lymphoma, particularly in the immunocompromised setting
- Demyelinating disease
- Radiation necrosis
Contributor: Jordan McDonald, MD
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