The most common source of CNS infections is hematogenous spread from an extracranial site. Infection can occur from direct extension from retrograde thrombophlebitis as in sinus infections. The infectious organisms may be pyogenic bacteria; and, in more than 33 percent more than one organism is involved.

The corticomedullary junction is the most common location and involves the frontal and parietal lobes most frequently. Less than 15% occur in the posterior fossa.

Complications of abscesses include daughter abscesses, ventriculitis, choroid plexitis and purulent leptomeningitis.

Four pathologic stages of cerebritis to abscess are described:
• early cerebritis(3-5 days),
• late cerebritis (4-5 days to 10-14 days)
• early capsule formation (2 weeks)
• late capsule (weeks to months).

Early cerebritis findings are poorly marginated, hypointense or isointense mass on T1WI, ill defined hyperintense mass on T2WI, and patchy enhancement on post contrast T1WI.

Late cerebritis demonstrates a hypointense center with isointense to mildly hyperintense rib on T1WI, hyperintense center and hypointense rim with hyperintense edema on T2WI and intense but irregular rim on post contrast T1WI.

Early capsule stage shows an isointense to hyperintense rim with a hyperintense center on T1WI, hypointense rim and hyperintense center on T2WI and thickened capule of rim enhancement on post contrast T1WI.

Late capsule stage includes decreased edema and mass effect on T2WI, collapse of the cavity and thickened capsular enhancement on post contrast T1WI.

Diffusion weighted imaging shows increased signal intensity; and, the Apparent Diffusion Coefficient maps show a decreased signal within the abscess.