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Case 163 year old male, previously healthy with recent bout of pneumonia now presents with mental status changes

Differential Diagnosis ofRing Enhancing Lesions

Metastasis

Abscesses

Multi-focal GBM

Subacute or resolving infarcts

Demyelinating Disease (M.S.)

Resolving contusion or hematoma

Differential Diagnosis of Lesions with restricted Diffusion

Infarct/Ischemia

Demyelinating

Infection/pus

Epidermoid

Tumor

Blood products

Brain Abscess

Caused by a variety of organisms

Most common: Streptococci and Staphylococci

In neonates: Citrobacter, Proteus, Psuedomonas, Serratia, Staph aureus

Other: Tuberculosis, Actinomyces, Nocardia, Parasites

Brain Abscesses (cont’d)

Abscesses follow a predictable progression of formation: Early cerebritis (3-5 days), Late cerebritis (4-14 days), Early capsule phase (begins around 14 days after initial infection), Late capsule phase

Form by hematogeneous spread or local invasion (mastoiditis, meningitis, post-surgical)

At gray-white jxn. Uncommon in post. fossa

Imaging Features of Brain Abscesses

Rim closer to gray matter usually thicker than medial rim due to better vascularization

Dark T2 signal rim

Frequently have “daughter” or “satellite” lesions budding off

Restricted (bright) on diffusion images

Nocardia Brain Abscess

Accounts for only 2% of all brain abscesses

Extra-neural site of disease in 66% of patients (lung > skin)

Single lesion is more common than multiple lesions

Around 1/3 patients immunocompromised (organ transplant>HIV>leukemia/lymphoma)

Mortality rate 3X higher than bacterial brain abscesses

Nocardia brain abscess

Risk factors for increased mortality: immunocompromised (more than double), multiple lesions

Treatment: rare disease with lack of established optimal treatment plan. Some advocate more aggressive, craniotomy with debridement early

Retrospective case review of 120 cases from 1950-1993; Mortality rates: crani/excision 24%, stereo aspiration 50%, non-operative therapy 30%