This document provides information about brain abscesses: 1. Brain abscesses usually begin as a focal intracranial infection that evolves into a collection of pus surrounded by a capsule. Common causative agents are streptococci, staphylococci, and various gram-negative bacteria. 2. Brain abscesses most often occur in the first four decades of life and are more common in males. Location is commonly the corticomedullary junction. Presentation includes headache, fever, seizures, and altered mental status. 3. Treatment involves surgical drainage, excision, and long-term antibiotics. Differential diagnosis includes tuberculomas, which appear as round or lobulated masses

1. Brain Abscess
Dr. Mahesh Chaudhary
Resident Phase B
MD Radiology & Imaging
BSM Medical University, Dhaka

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.
 Most common in first four decades of life
 Males are more commonly affected
 Infants and neonates its rare (may occur as
complication of bacterial meningitis)

3. Causative agents (1/3rd mixed)
 Adults :
Streptococci, Staphylococci
Gram-negative (Escherichia coli, Klebsiella, Proteus, Pseudomonas, H. influenzae)
 Neonates and children :
Citrobacter, Proteus, Pseudomonas, Serratia and Staphyloccocus 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. Causes of brain abscess
 Hematogenous dissemination
Cyanotic heart disease
Cardiac(infective endocarditis)
Drug abuse
Pulmonary infection
Sepsis
Urinary tract infection
 Congenital or acquired dural
dehiscence
 Direct extension
Otitis
Paranasal sinus
Mastoditis
Calvarial or meningeal infection
 Trauma
Penetrating injury
Postsurgical
No predisposing factors in 25% of
cases

5. 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

6. 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

7. 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

8. 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 .

9. 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

10. 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.
Daughter lesion is also seen

11. Imaging modalities
 CT
 MRI
 DWI
 MRS
 NUCLEAR MEDICINE STUDIES

12. COMPUTED TOMOGRAPHY (NECT)
 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

13. COMPUTED TOMOGRAPHY (CECT)
 Early cerebritis: +/- Mild patchy enhancement
 Late cerebritis: Irregular peripheral rim enhancement
 Early capsule: Low density center with thin distinct enhancing capsule
Deep part of capsule is thinnest(near ventricle); thickest near cortex
 Late capsule: Cavity shrinks, capsule thickens
May be multiloculated and have "daughter"abscesses

14. MRI
 T1WI
 Early cerebritis: Poorly marginated, mixed hypointense/isointense mass
 Late cerebritis: Hypointense center, isointense/mildly hyperintense rim,
edema present nearly always
 Early capsule: Thick irregular rim; isointense to hyperintense to white matter;
center hyperintense to CSF
 Late capsule: Cavity shrinks, capsule thickens

15. MRI
 T2WI
 Early cerebritis: Ill-defined hyperintense mass
 Late cerebritis: Hyperintense center, hypointense rim; hyperintense edema
 Early capsule: Hypointense rim ; Related to collagen, hemorrhage, or
paramagnetic free radicals
 Late capsule: Edema and mass effect diminish

16. MRI
 Tl C+
 Early cerebritis: Patchy enhancement
 Late cerebritis: Intense but irregular rim enhancement
 Early capsule: Well-defined, thin-walled enhancing rim
 Late capsule: Cavity collapses, thickened enhancement of capsule
Capsule is thinnest on the ventricular side

17. 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

18.  Resolving abscess
• Hyperintense on T2WI, FLAIR; hypointense rim resolves
• Small ring/punctate enhancing focus may persist for months
 Complication of Brain Abscess
• Formation of satellite lesions
• Ventriculitis
• Choroid plexitis
• Purulent leptomeningitis

19. A tiny ill defined enhancing focus
is present in left frontal lobe
9 days later pre and post contrast axial scan MRI shows a predominantly
low signal left frontal mass with irregularly enhancing rim , edema and
mass effect.

20. 5 weeks after drainage and antibiotic therapy axial CECT scans shows a small ring enhancing
residual left frontal lobe mass. Some edema persists but is diminished. This is the late capsule
stage of abscess formation. Enlarged ventricle with persistent choroid plexitis.

21. Abscess caused by gas-forming organism. Gas is seen with a surrounding low-density
area on noncontrast CT scan. Contrast CT scan shows irregular, ring like enhancement;
gas is visible within the cavity. The causative organism was Escherichia coli

22. Mature abscess: T2-weighted image shows a mature abscess with hypointense rim, central
cavity, and adjacent surrounding edema. A small satellite lesion is also seen. Gadolinium-
enhanced MRI study demonstrates smooth, ring like enhancement corresponding to the
hypo intense rim seen on T2-weighted images.

23. 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

24. Differential diagnosis
Tuberculoma

25. Tuberculoma
 The second most common manifestation of neurotuberculosis
 Parenchymal infection with central caseating necrosis
 Secondary to pulmonary TB rarely GI or GU tract.
 Occurs at any age; most commonly in first three decades
 Location :
Cerebral hemispheres(frontal and parietal & basal ganglia
Less commonly brainstem and dura

26. Pathology
 Non caseating with solid center or caseating with necrotic center
 Rarely progresses to TB abscess
 Lobulated mass with thick rim in parenchyma subarachnoid space or
dura
 Size: range from 1mm to 6cm
 Clinical presentation
 Seizures, increased intracranial pressure, papilledema

27. Imaging
 NECT
Hypodense to hyperdense round or lobulated nodule/mass with
moderate to marked edema.
 CECT
Solid or ring enhancing
Target sign : central calcification or enhancement followed by
enhancing rim

28. MRI
 T1WI:
Non caseating granuloma: Hypointense to brain
Caseating granuloma with solid/necrotic center: Hypointense or isointense
Caseating granuloma may have hyperintense rim
T2WI:
 Noncaseating granuloma: Hyperintense to brain
 Caseating granuloma with solid center: Iso- to hypointense with hypointense
rim
 Caseating granuloma with necrotic center: Central hyperintensity with
hypointense rim
 Hypointense rim + surrounding edema common

29. FLAIR
Similar to T2 characteristics
TI C+
Noncaseating granuloma: Nodular, homogeneous enhancement
Caseating granuloma with solid center: Peripheral rim enhancement
Caseating granuloma with necrotic center: Peripheral rim-enhancement,
central low signal
MRA: vessel narrowing, irregularity, occlusion
 MRS : prominent lipid, lactate but no amino acid resonances

30. Two small lesions with thick ring enhancement

31. T2WI shows multifocal tuberculomas as hypointense
foci surrounded by edema
T1C+ scan in the same case illustrates
additional lesions with punctate , ring
enhancement

32. Thank You