Cerebral abscess

Brain abscess is a potentially life threatening condition requiring rapid treatment, and prompt radiological identification. Fortunately, MRI is usually able to convincingly make the diagnosis, distinguishing abscesses from other ring enhancing lesions. 

Epidemiology

Demographics reflect at-risk groups (see below) with all age groups being affected.

Clinical presentation

Clinical presentation is non-specific with many cases having no convincing inflammatory or septic symptoms. Symptoms of raised intracranial pressure, seizures and focal neurological deficits are the most common forms of presentation. Eventually, many abscesses rupture into ventricular system, which results in a sudden and dramatic worsening of the clinical presentation and often heralds a poor outcome. 

Pathology

Cerebral abscesses result from pathogens growing within the brain parenchyma, initially as a cerebritis and then eventually demarcating into a cerebral abscess. Historically direct extension from sinus or scalp infections was the most common source. More recently haematological spread has become most common. Direct introduction by trauma or surgery accounts for only a small minority of cases ³. 

Four stages are recognised, which distinct pathological and radiological features:

1. early cerebritis
2. late cerebritis
3. early capsule
4. late capsule

Risk factors

Risk factors for haematogenous spread include ³:

• right to left shunt
  • congenital heart disease
  • pulmonary AVM and AVFs as seen in hereditary haemorrhagic telangiectasia (HHT)
• infective endocarditis
  • intravenous drug use (IVDU)
• lung infection
  • lung abscess
  • bronchiectasis
  • empyema
• sinonasal infections
• dental abscess
• systemic sepsis

Microbiology

• Streptococcus sp: 35-50% ³
  • especially S. pneumoniae ⁴
• sterile: 25%
• mixed: variable, 10-90% of cases depending on source ³
• Staphylococcus aureus and epidermidis: following neurosurgery
• Gram negative-negative species more common in infants
• Listeria in pregnant women and older patients
• group B strep (GBS) and E coli in neonates

The immunocompromised patient is susceptible to a host of other organisms including ³:

• Toxoplasma gondii
• Nocardia asteroides
• Candida albicans
• Listeria monocytogenes
• Mycobacterium sp
• Aspergillus fumigatus

Radiographic features

Both CT and MRI demonstrate similar features, although MRI has a greater ability to distinguish a cerebral abscess from other ring enhancing-enhancing lesions. 

By stage

1. early cerebritis

• may be invisible on CT
• poorly marginated cortical or subcortical hypodensity with mass effect with little or absence of enhancement

2. late cerebritis

• irregular rim enhancing-enhancing lesion with a hypodense centercentre, better defined than early cerebritis

3. early capsule

• well-defined rim enhancing-enhancing mass, an outer hypodense and inner hyperdense rim (double rim sign) is seen in most cases

4. late capsule

• rim enhancing-enhancing lesion with thickened capsule and diminished hypodense central cavity

CT

In patients with suspected intraparenchymal sepsis, pre- and postcontrast scans should be obtained, unless the plan is to proceed to MRI regardless of the CT findings. Typical appearances include:

• ring of iso- or hyperdense tissue, typically of uniform thickness
• central low attenuation (fluid/pus)
• surrounding low density (vasogenic oedema) 
• ventriculitis may be present, seen as enhancement of the ependyma
• obstructive hydrocephalus will commonly be seen when intraventricular spread has occurred

MRI

MRI is more sensitive and especially with the addition MRS and DWI far more specific for the diagnosis of cerebral abscesses. 

• T1
  • central low intensity (hyperintense to CSF)
  • peripheral low intensity (vasogenic oedema) 
  • ring enhancement 
  • ventriculitis may be present, in which case hydrocephalus will commonly also be seen
• T2/FLAIR
  • central high intensity (hypointense to CSF, does not attenuate on FLAIR)
  • peripheral high intensity (vasogenic oedema)
  • the abscess capsule may be visible as an intermediate to slightly low signal thin rim ¹
• DWI/ADC
  • high DWI signal is usually present centrally ¹¹
  • represents true restricted diffusion (low signal on ADC, typically ~650 +/- 160 x 10^-6 mm²/s ¹⁰⁾
  • peripheral or patchy restricted diffusion may also be seen; this finding is however not as constant as one may think, with up to half of rim enhancing lesions demonstrating some restriction not proving to be abscesses ²
  • ADC values increase as treatment is successful even if cavity remains ⁹
• SWI
  • low intensity-intensity rim ⁹
    • complete in 75% 
    • smooth in 90%
    • mostly overlaps with contrast enhancing rim
  • dual rim sign: a hyperintense line located inside the low intensity-intensity rim ⁹
• MR perfusion: rCBV is reduced in the surrounding oedema cf. to both normal white matter and tumour oedema seen in high grade-grade gliomas ²
• MR spectroscopy: elevation of a succinate peak is relatively specific but not present in all abscesses; high lactate, acetate, alanine, valine, leucine, and isoleucine levels peak may be present; Cho/Crn and NAA peaks are reduced

Treatment and prognosis

The mainstay of treatment for cerebral abscesses is neurosurgical intervention and drainage of the collection. This can be performed either by stereotactic aspiration or craniotomy ⁷. Broad spectrum-spectrum intravenous antibiotics are also needed and can later be changed to agents tailored to the specific organisms. 

In cases where the abscess cavity does not completely obliterate, follow-up with MRI including DWI is useful and lack of restricted diffusion is reassuring. Demonstration of ongoing restricted diffusion in a cavity suggests persistent infection ⁸.  

Differential diagnosis

The differential of an established abscess is essentially that of a ring enhancing lesion, and therefore includes:

• metastasis or high grade-grade glioma (e.g. GBM)
  • abscesses tend to have smoother inner wall ²
  • satellite lesions favour infection ²
  • abscesses may have low intensity-intensity capsule ^1-2
  • rCBV elevated in high grade-grade gliomas, reduced in abscesses ²
  • low intensity-intensity SWI rim of GBM  ⁹
    • incomplete and irregular in 85% 
    • within (rather than overlapping) the peripheral enhancement
    • absent dual rim sign 
  • cystic component does not show restricted diffusion unlike abscess
• subacute infarction, haemorrhage or contusion
• demyelination
• radiation necrosis

When a lesion demonstrates both ring enhancement and central restricted diffusion the differential is very much narrowed, and although cerebral abscess is by far the most likely diagnosis, the following should also be included on the differential ⁶: 

• cerebral metastases: particularly necrotic adenocarcinoma