TextbookNeurologyBrain Abscess

Brain Abscess

Focal collection of pus within the brain parenchyma, usually caused by bacterial infection. Presents with headache, fever, and focal neurological deficit. Mortality ~10% with treatment. Requires combined surgical drainage and prolonged IV antibiotics.

Key Facts

Focal suppurative infection within brain parenchyma; incidence ~1-2 per 100,000/year; M:F 2-3:1 Sources: contiguous spread (otitis media, sinusitis, dental infection — most common), haematogenous (endocarditis, lung abscess, immunosuppression), direct inoculation (trauma, neurosurgery), cryptogenic (15-20%) Common organisms: Streptococcus spp. (most common), Staphylococcus aureus (trauma/surgery), anaerobes (Bacteroides), Gram-negatives; polymicrobial in 30% Classic triad: headache (most common — 70%) + fever (50%) + focal neurological deficit (50%); full triad in <50% CT/MRI: ring-enhancing lesion with surrounding oedema; restricted diffusion on DWI-MRI distinguishes abscess from tumour (high DWI signal in abscess) Treatment: IV antibiotics (ceftriaxone 2g BD + metronidazole 500mg TDS ± vancomycin if MRSA risk) for 6-8 weeks + stereotactic aspiration or excision for abscesses >2.5 cm

Overview

Key Facts

Brain abscess requires a high index of suspicion. Combined surgical and antibiotic treatment is standard. The source of infection must be identified and treated. DWI-MRI is key to distinguishing abscess from tumour.

Epidemiology

Incidence ~1-2 per 100,000/year. M:F 2-3:1. All ages but peak in 3rd-4th decade. Immunocompromised patients at higher risk (HIV, transplant, steroids).

Aetiology

  • Contiguous spread (~50%): otitis media/mastoiditis (temporal lobe, cerebellum), frontal sinusitis (frontal lobe), dental infection (frontal/temporal lobe)
  • Haematogenous (~25%): infective endocarditis, lung abscess, cyanotic congenital heart disease (right-to-left shunt), IV drug use
  • Direct inoculation (~10%): penetrating trauma, neurosurgery
  • Cryptogenic (15-20%): no source identified

Pathophysiology

Cerebritis stage (days 1-3): focal inflammation → early capsule (days 4-9) → late capsule (days 10-14+): well-formed capsule surrounded by oedema and gliosis. Ring enhancement on contrast imaging reflects capsule vascularity. Medial capsule is thinner than lateral (closer to white matter, less blood supply) → tendency to rupture into ventricle (ventriculitis — high mortality).

Clinical Presentation

Symptoms

  • Headache (70%): progressive, often localising
  • Fever (50%): may be absent, especially if on antibiotics
  • Nausea/vomiting: raised ICP
  • Seizures (25-30%): focal or generalised

Signs

  • Focal neurological deficit (50%): hemiparesis, dysphasia, visual field defect
  • Papilloedema: raised ICP
  • Meningism: if abscess close to meninges or ruptures

Red Flags

  • Rapid deterioration → abscess rupture into ventricle (ventriculitis — meningism, rapid GCS decline, very high mortality)
  • Multiple abscesses → haematogenous source (endocarditis, lung)
  • Immunosuppressed patient with ring-enhancing lesion → consider toxoplasma, fungal, TB

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Primary brain tumour (glioblastoma)Ring-enhancing, no restriction on DWI, progressiveMRI (DWI), biopsy
Cerebral metastasisMultiple lesions, known primary, ring-enhancingCT/MRI, staging
ToxoplasmosisHIV/immunosuppressed, multiple ring-enhancingToxoplasma serology, CD4, trial of treatment
CNS tuberculomaTB risk factors, basal meningeal enhancementCSF, biopsy
Cerebral lymphomaImmunosuppressed, homogeneous enhancement, periventricularMRI, biopsy
Demyelination (tumefactive MS)Young patient, incomplete ring, minimal mass effectMRI, CSF, clinical

Diagnosis / Investigation

Imaging

  • CT head with contrast: ring-enhancing lesion with surrounding oedema; urgent first-line
  • MRI brain with DWI: gold standard; restricted diffusion (high signal on DWI, low ADC) — distinguishes abscess from tumour (tumour shows no restriction)
  • MR spectroscopy: amino acid peaks (from bacterial breakdown products) — supports abscess diagnosis

Bloods

  • FBC: leucocytosis (may be normal)
  • CRP, ESR: raised
  • Blood cultures: positive in ~15-30% (especially haematogenous)
  • HIV test: if immunosuppression suspected

Source Identification

  • Echocardiography (TTE/TOE): endocarditis screening
  • CT sinuses/petrous bones: contiguous spread from sinusitis/otitis
  • Dental assessment: if dental source suspected
  • CT chest: lung abscess, pneumonia

Microbiology

  • Aspirate culture: from stereotactic drainage — essential for targeted antibiotic therapy
  • CSF: LP is generally CONTRAINDICATED (risk of coning); if performed — raised protein, lymphocytic pleocytosis, culture usually negative

Management

Antibiotics (Empirical — Then Targeted)

  • IV ceftriaxone 2g BD + IV metronidazole 500mg TDS: first-line empirical (covers streptococci, anaerobes, Gram-negatives)
  • Add IV vancomycin if MRSA risk (neurosurgery, trauma)
  • Duration: 6-8 weeks IV (minimum 4 weeks IV; may convert to oral after clinical and radiological improvement)
  • Adjust based on culture results from aspirate

Surgical

  • Stereotactic aspiration: CT/MRI-guided; diagnostic + therapeutic; first-line for most abscesses >2.5 cm
  • Craniotomy and excision: for superficial, well-encapsulated abscesses; fungal abscesses; failed aspiration
  • Conservative (antibiotics alone): small abscesses (<2.5 cm), cerebritis stage, surgically inaccessible location, multiple small abscesses
  • Repeat imaging: serial CT/MRI to monitor resolution (every 1-2 weeks initially)

Supportive

  • Dexamethasone: if significant oedema/mass effect (vasogenic oedema); controversial — may reduce antibiotic penetration and slow capsule formation
  • Anticonvulsants: if seizures (levetiracetam, phenytoin); prophylactic use is debated
  • ICP management: if raised (head elevation, osmotic agents, EVD if hydrocephalus)

Treat Source

  • Mastoidectomy for otogenic abscess; sinus surgery for sinogenic
  • Dental extraction for odontogenic
  • Treat endocarditis

Referral Criteria

  • All brain abscesses: neurosurgery + infectious diseases
  • ENT/dental if contiguous source
  • Cardiology if endocarditis suspected

Prognosis

Mortality ~10% with treatment (higher if ventricular rupture — ~80%). Seizures develop in ~30-50% (long-term antiepileptic therapy may be needed). Neurological sequelae in ~30-50%: focal deficits, cognitive impairment, epilepsy. Prognosis worse with: ventricular rupture, multiple abscesses, immunosuppression, deep/eloquent location, delayed treatment. Imaging resolution lags behind clinical improvement by weeks-months.

Other Relevant Information

Brain Abscess — Location by Source

SourceTypical LocationTypical Organism
Otitis media/mastoiditisTemporal lobe, cerebellumStreptococci, Bacteroides, Proteus
Frontal sinusitisFrontal lobeStreptococci, H. influenzae, anaerobes
Dental infectionFrontal/temporal lobeStreptococci, anaerobes
HaematogenousMultiple, MCA territoryVaries (S. aureus, Streptococci)
Trauma/neurosurgeryAt wound siteS. aureus, Gram-negatives

DWI-MRI: Abscess vs Tumour

FeatureBrain AbscessBrain Tumour
DWI signalHIGH (restricted diffusion)LOW/variable
ADC mapLOW (dark)HIGH (bright)
Ring enhancementSmooth, thin, uniformIrregular, thick
Surrounding oedemaYesYes