Brain abscesses typically present as rim-enhancing lesions that evolve through four stages: early and late cerebritis, early capsule formation, and late capsule. Imaging plays a key role in diagnosis, with CT showing a hypodense lesion and MRI demonstrating a central hyperintense region on T2-weighted imaging surrounded by a hypointense rim. Treatment involves surgical drainage and long-term antibiotics, while complications may arise if left untreated such as meningitis, daughter lesions, or mass effect on brain structures. Differential diagnoses include tumors, demyelinating diseases, and infarcts.

1. Brain Abscess
Dr. Manmohan Bir Shrestha
For Radiology

2. Objectives
 Introduction
 Causative agents
 Etiology
 Location
 Presentation
 Pathology
 Imaging modalities
 Tuberculous cerebral abscess
 Fungal cerebral abscess
 Gas containing cerebral abscess
 Ruptured cerebral abscess
 Treatment
 Complications
 Differential diagnosis

3. 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.
 Size- 5 mm up to several centimeters
 Age – most common in 3rd and 4th decades.
25% occurs < 15 years.
 Males are more commonly affected (2:1)
 Infants and neonates - its rare (may occur as complication of bacterial meningitis)

4. 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
 AIDS patient – toxoplasmosis, Mycobacterium tuberculosis.
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.

5. Etiology
 Hematogenous
Pulmonary infection, endocarditis, UTI
 Direct extension from calvarial or meningeal infection
Paranasal sinus, middle ear, teeth infections ( via emissary veins)
 Postoperative
 Penetrating trauma
 Right to left shunts
Cong. Cardiac malformations, pulmonary arteriovenous meningitis.
 Neonatal
2/3rd associated with meningitis
20-30% have no identifiable source.

6. Location
 Typically supra-tentorial, up to 14% infratentorial
 Gray-White junction is common ( usually if hematogenous)
 Subdural space
 Frontal lobe – sinusitis, odontogenic infection
 Temporal lobe - OM & mastoiditis
 Multiple uncommon except in immunocompromised

7. Presentation
Most Common
Headache most common symptom (up to 90%);
Fever in approximately 50%
Other signs:
Seizures, altered mental status, focal neurologic deficits,
Nausea & vomiting
Increased erythrocyte sedimentation rate (ESR)
(75%), elevated WBC count (50%)
Absence of leukocytosis does not exclude the diagnosis.

8. 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

9. 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 .

10. 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
Central cavity shrinks
Thick wall (collagen granulation tissue, macrophages, gliosis)
**Medial or ventricular wall
Thinner and more uniform
Probably an effect of differential blood supply

11. 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

12. Imaging modalities
 CT Scan
 MRI
 NUCLEAR MEDICINE STUDIES

13. 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

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

16. 25yrs male

17. 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

18. 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

19. 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

20. DWI, MRS AND NUCLEAR MEDICINE STUDIES
 DWI : Increased signal intensity in cerebritis and abscess
(due to pus, viable macrophages)
 ADC map: Markedly decreased signal centrally within abscess
 T2* GRE: Dual rim sign on SWI (hypointense outside, hyperintense inside)
Helpful to distinguish
 MRS: Central necrotic area may show presence of acetate, lactate, alanine, succinate
and amino acids
 Nuclear Medicine Findings
 PET: FDG and Carbon-ll-Methionine have shown increased uptake in brain
abscess

21. T1
T1 T2
FLAI
R
T1C+ T1C+
25 yrs male with headache

23. 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.
CASE

24. 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.
Late Capsule Stage

25. Dual rim sign in SWI

26. Tubercular cerebral abscess
 CNS TB always secondary to hematogenous spread (often pulmonary)
 Manifestation include -tuberculous meningitis
-tuberculoma
-TB abscess
 Size of abscess usually - >3 cm
 Large, solitary often multiloculated ring enhancing
 TB meningitis may or may not coexist.

27. Imaging
 Similar characteristics as pyogenic abscess
T2 – hyperintense lesion with hypointense rim & marked vasogenic
edema
DWI – restricted diffusion
Post contrast – rim enhancing
 Difference is –
Clinical profile
Comparatively less edema than pyogenic abscess
MRS helpful – TB abscess has prominent lipid, lactate but no amino
acid resonance.

28. Fungal cerebral abscess
60 yrs old patient with occipital headache, blurred vision.
CT shows rim enhancing lesion in left occipital lobe with surrounding edema with
effacement of sulci. Histology revealed - Aspergillus

29. Gas containing abscess
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
Gas may be present adjacent to or within an abscess
Indicates – Tapping of the cavity
- Infection with gas forming organism
- Fistulous connection with the exterior

30. Case of bifrontal lobe abscess
36 yrs old male with pansinusitis

31. Ruptuted cerebral abscess
20 yrs old male with fever & altered consciousness for 2 weeks

32. Treatment – Pyogenic abscess
 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

33. Complications of inadequately treated or
untreated abscess
Meningitis
Daughter lesions
Mass effect
Herniation
Intraventricular rupture, ventriculitis
Epilepsy – common in paediatric patients
Mortality – 0-30%

34. Differential diagnosis-
Rim enhancing lesions
 Common
Some primary brain tumor (e.g. anaplastic astrocytoma)
Metastatic brain tumor
Abscess
Granuloma
Resolving hematoma
Subacute infarct
 Less common
Thrombosed vascular malformation
Demyelinating disease (e.g. multiple sclerosis)
 Uncommon
Thrombosed aneurysm
CNS lymphoma in AIDS

35. Glioblastoma
Thick nodular enhancement
Low signal on DWI

36. Necrotic neoplasm

37. Demyelinating disease
Multiple sclerosis , ADEM
Ring enhancement often incomplete- open ring sign
Characteristic lesion elsewhere.

38.  Resolving intracerebral hematoma-
 H/O trauma or vascular lesion
 Blood products present on MRI
 Subacute cerebral infarction-
 H/O stroke , vascular distribution
 Gyriform >ring enhancement.

41. CT Case
12 yrr old girl presented with the complaints
Headache for 1 month over right side, worse in morning, aggravated
by coughing, bending of head
Seizure 1 episode 25 days back
Pain in right ear 1 month prior headache lasting for 10 days, no
discharge from ear and fever then
Blood tests
Hb – 12.5
WBC -20500 26000 10000
ESR – 15
CRP - normal

44. Take home message
 Age – most common 3rd and 4th decade
 80% supra-tentorial
 Mostly GM-WM junction
 4 stages
 Avascular rim enhancing lesion
 T2 – hypo rim with hyper centre
 DWI & ADC – diffusion restriction, low signal in ADC
 MRS – presence of amino acid, lactate, acetate & succinate
 Post contrast- Complete rim enhancing
 D/D’s –Glioblastoma, metastases, demyelinating disease, resolving
hematoma, subacute infarct
Questions are welcomed