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 the 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. Initial parenchymal infection is known as cerebritis, which may progress 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.

Cerebral infection is commonly divided into four stages with distinct imaging and histopathologic features:

1. early cerebritis( a focal infection without a capsule or pus formation,can resolve or develop into frank abcess)
2. late cerebritis
3. early abscess/encapsulation - may occur 10 days after infection
4. late abscess/encapsulation - may occur >14 days after infection

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
  • pneumonia ¹²
• 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 species more common in infants
• Listeria in pregnant women and older patients
• group B Streptococcus (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 lesions:

1. early cerebritis - please see cerebritis article
2. late cerebritis - please see cerebritis article
3. early encapsulation
   • ​​discrete lesion with thin enhancing rim
   • rim may be less-well defined along peripheral aspect of lesion (away from ventricles)
   • +/- additional "daughter" collections
   • +/- ventricular extension, with accompanying ventriculitis
4. late encapsulation - progressive central necrosis, cavity shrinks, decreasing surrounding oedema

CT

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

• outer hypodense and inner hyperdense rim (double rim sign) in most cases
• 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 than CT. Although peripherally-enhancing lesions may be non-specific by imaging, diffusion-weighted sequences (less commonly MR spectroscopy) showing central diffusion restriction are critical for suggesting the diagnosis of cerebral abscess.

• 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.
  • in some immunocompromised states, central content may not diffusion restrict ¹³
• SWI
  • low-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 rim⁹
• MR perfusion: rCBV is reduced in the surrounding oedema cf. to both normal white matter and tumour oedema seen in high-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 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 diagnosis typically includes other ring-enhancing lesions:

• metastasis or high-grade glioma (e.g. GBM)
  • abscesses tend to have smoother inner wall ²
  • satellite lesions favour infection ²
  • abscesses may have low-intensity capsule ^1-2
  • rCBV elevated in high-grade gliomas, reduced in abscesses ²
  • low-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, subacute haemorrhage or contusion
• demyelinating lesion
• 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