There are 4 stages of brain abscess evolution: early and late cerebritis, early capsule formation, and late capsule. Common causes include hematogenous spread, direct extension from infections like otitis or sinusitis, and trauma. Presentation includes headache, fever, seizures, and neurological deficits. Imaging shows evolving appearance on CT and MRI from ill-defined lesion to encapsulated mass. Treatment involves surgical drainage with antibiotics and steroids.

1. M A H T A B M U R A D
G B S N , S E M - I V
F A C U L T Y : S I R R A F I Q U E S Y A I L
Brain Abscess

2. Introduction
Abscess is initiated by focal intracranial
infection as an area of cerebritis and
evolves into a collection of pus surrounded
by a vascularized capsule
 Males are more commonly affected
 Infants and neonates its rare (may occur as
 complication of bacterial meningitis)

3. Causative agents
Adults
Streptococci, Staphylococci
Gram-negative (Escherichia coli, Klebsiella,Proteus,Pseudomonas, H. influenzae)
Neonates and children:
Citrobacter, Proteus, Pseudomonas, Serratia and Staphylococcus aureus
Mostly the causative agents are bacteria but there can be fungal or
granulomatous or Parasitic agents
In 20-30% of abscesses, cultures are sterile and no specific organism is
identified

4. Hematogenous dissemination
Cyanotic heart disease Cardiac(infective endocarditis)
 Drug abuse
 Pulmonary infection Sepsis
 Urinary tract infection
Causes of brain abscess

5. Causes of brain abscess
Direct extension
 Otitis
 Paranasal
 sinus
 Mastoditis
 Calvarial or meningeal infection

6. Causes of brain abscess
Trauma
 Penetrating injury
 Postsurgical
 No predisposing factors in 25% of cases

7. Location
 Corticomedullary(gray-white junction) most common location
 Frontal and parietal lobes are most frequent sites
 Subdural space
 Temporal lobe and cerebellum (OM & mastoiditis)
 15% posterior cranial fossa
 Multiple uncommon except in immunocompermised

8. Presentation
Most Common
Headache most common symptom (up to 90%);
Fever in approximately 50%
Other signs:
Seizures, altered mental status, focal neurologic
deficits Increased erythrocyte sedimentation rate
(ESR)
(75%), elevated WBC count (50%)
CSF study- increase protein &increase white cell
count

9. Pathology: four stages of evolution
Early cerebritis (3-5 days)
 Infection is focal but not localized
 Unencapsulated mass of PMNs, with edema
 Scattered foci of necrosis and petechial hemorrhage
Late cerebritis (4-5 days up to 2 weeks)
 Necrotic foci coalesce
 Rim of inflammatory cells, macrophages, granulation tissue, fibroblasts
surrounds central necrotic core
 Vascular proliferation, surrounding vasogenic edema

10. There is a focal unencapsulated mass of
petechial hemorrhage, inflammatory
cells, and edema
Autopsy case demonstrates typical
pathologic findings of late cerebritis
with significant mass effect, edema.
The coalescing lesion shows some
central necrosis and an illdefined rim of
petechial hemorrhage .

11. Pathology: 4 stages of evolution
Early capsule (begins at around 2 weeks)
Well-delineated collagenous capsule
Liquefied necrotic core, peripheral gliosis
Late capsule (weeks to months) characteristic 3 layers
1. An inner inflammatory layer of granulation tissue &
macrophages
2. A middle collagenous layer
3. An outer gliotic layer

12. Autopsy case shows typical findings of a
cerebral abscess at the early capsule
stage. The liquefied necrotic core of the
lesion is surrounded by a well-developed
capsule
Autopsy case shows late capsular
stage with well delineated
collagenous core that surrounds the
necrotic core.

13. Test
 CT
 MRI
 DWI
 MRS
 NUCLEAR MEDICINE STUDIES

14. COMPUTED TOMOGRAPHY
Early cerebritis:
 Ill-defined hypodense subcortical lesion with mass effect
 May be normal early
Late cerebritis:
 Central low density area; peripheral edema,
 Mass effect increase
Early capsule:
 Hypodense mass with moderate vasogenic edema & mass effect
 Thin well delineated capsule
Late capsule:
 Edema, mass effect diminish

15. MRI
Early cerebritis:
Poorly marginated, mixed hypointense/isointense mass
Late cerebritis: Hypointense center, isointense/mildly hyperintense
rim, edemapresent nearly always
Early capsule: Thick irregular rim; isointense to hyperintense to white matter;
center hyperintense to CSF
Late capsule: Cavity shrinks, capsule thickens

16. DWI, MRS AND NUCLEAR MEDICINE
STUDIES
DWI : Increased signal intensity in cerebritis and abscess
ADC map: Markedly decreased signal centrally within abscess
MRS: Central necrotic area may show presence of acetate, lactate, alanine,
 succinate, pyruvate, and amino acids
Nuclear Medicine Findings
PET: FDG and Carbon-ll-Methionine have shown increased uptake in brain
abscess

17. Treatment
 Surgical drainage and/or excision primary therapy
 Antibiotics only, if small « 2.5 cm) or early phase of cerebritis
 Steroids to treat edema and mass effect
 Lumbar puncture hazardous, pathogen often can't be determined
from CSF