Brain Abscess

Brain abscess is a life-threatening condition that involves the collection of pus in the brain parenchyma caused by infection from bacteria, fungi, parasites, or protozoa. The most common presentation is headache, fever with chills, seizures, and neurological deficits. Diagnosis is mainly based on imaging, as it is difficult to arrive at a definitive diagnosis based on clinical presentation alone. Management includes administration of empiric antibiotic therapy and surgical intervention. Immediate management is necessary; otherwise, severe neurologic complications ensue.

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Brain abscess is an uncommon but life-threatening infectious collection of pus in the brain parenchyma.


  • Rare in developed countries but the incidence is high in developing countries 
  • More predominant in men than women (2:1) 
  • Higher incidence in patients with AIDS
  • Mortality rate has improved with advances in brain imaging.


There are 2 routes of the spread of infection to the brain: 

  1. Direct spread from adjacent infections of the head and neck region typically presents as a single abscess:
    • Otitis media (spread to the inferior temporal lobe and cerebellum)
    • Mastoiditis (spread to the inferior temporal lobe and cerebellum)
    • Paranasal sinus infection (spread to the frontal lobes)
    • Dental infection (spread to the frontal lobes)
    • Head/facial trauma 
    • Neurosurgical procedure
  2. Hematogenous spread from infections from other regions of the body typically presents with multifocal abscesses in middle cerebral artery distribution:
    • Bacterial endocarditis 
    • Chronic pulmonary infection: 
      • Lung abscess
      • Empyema
    • Pelvic infection 
    • Intraabdominal infection

Organisms causing brain abscess:

  • Bacteria:
    • Staphylococcus aureus (most common)
    • Streptococcus viridans (2nd most common)
    • Bacteroides 
    • Prevotella 
    • Nocardia 
  • Fungi:
    • Candida 
    • Aspergillus 
    • Rhizopus arrhizus
    • Coccidioides 
    • Blastomyces dermatitidis
    • Histoplasma capsulatum
  • Protozoa:
    • Toxoplasma gondii
    • Trypanosoma cruzi 
    • Entamoeba histolytica 
    • Naegleria 
    • Acanthamoeba 
  • Helminths: 
    • Taenia solium
    • Schistosoma
    • Paragonimus

Risk factors:

  • Patients on immunosuppressants 
  • Immunocompromised individuals
  • Recent head injury or surgery
  • Recent dental procedure 
  • IV drug abusers

Pathophysiology and Clinical Presentation


  • Brain tissue damage is caused by the acute inflammatory response.
  • Early phase:
    • Cerebritis
    • 1–2 weeks
    • Presents with vascular congestion and localized edema
    • No tissue necrosis 
  • Late phase:
    • Develops in 2–3 weeks
    • Liquefaction and tissue necrosis
    • Development of fibrotic capsule made up of 3 layers:
      • Outer astroglial layer
      • Middle collagenous layer 
      • An inner layer of granulation tissue

Stages of development of brain abscess after infection

Early cerebritis (days 1–3):

  • Acute inflammatory infiltrate
  • Visible ogranisms on staining
  • Surrounding edema

Late cerebritis (days 4–9):

  • Predominant macrophage
  • Lymphocyte infiltrate

Early capsule formation (days 10–13):

  • Necrotic center decreases in size.
  • Edema
  • Collagenous capsule develops.

Late capsule formation (day 14 +):

Capsule becomes thick and is amenable to excision.

Locations (in order of frequency)

  • Frontal-temporal
  • Frontal-parietal
  • Parietal 
  • Cerebellar
  • Occipital

Clinical presentation

  • Classical triad: 
    1. Headache (most common presenting symptom; 70% of patients):
      • Pain is usually localized to the side of the abscess.
      • Does not abate with analgesics 
    2. Fever with chills (50%)
    3. Focal neurological deficits (50%):
      • Aphasia 
      • Hemiparesis 
      • Visual field defects  
  • Seizures (25%):
    • Especially if lesion is located in frontal lobe
    • May be due to focal lesion or increased intracranial pressure
  • Neck stiffness (15%): 
    • Abscess located in occipital lobe
    • Leakage into lateral ventricle 
  • Increased intracranial pressure (ICP):
    • Nausea and vomiting
    • Altered sensorium     
    • 3rd and 6th cranial nerve palsies 
    • Papilledema (25%)


Physical exam

  • Fever
  • Focal/unilateral headache
  • Signs of increased ICP:
    • Papilledema (optic disc swelling)
    • Unilateral cranial nerve deficits
    • Hemiparesis


  • MRI:
    • More sensitive than CT scan
    • Performed with gadolinium
    • Useful in early cerebritis and to detect satellite lesions
    • Estimates extent of necrosis and cerebral edema 
    • Classic “ring enhancement” is observed.   
  • CT scan:
    • Not as sensitive as MRI and therefore mostly used only in emergencies
    • Performed with and without contrast 
    • Early cerebritis appears as an irregular area of low density.
    • Ring enhancement is not as clear as in MRI.

Lumbar puncture

  • Performed to:
    • Exclude meningitis/meningoencephalitis from differential
    • Obtain CSF for serologic analysis
  • Obtain brain imaging first to rule out intracerebral mass due to risk of brainstem herniation.
  • Contraindicated if papilledema or focal neurologic deficits are present due to risk of brainstem herniation

Abscess aspirate/biopsy

  • Obtained via image-guided aspiration or during surgical intervention
  • Tests performed on the specimen: 
    • Gram stain
    • Aerobic and anaerobic bacterial culture
    • Fungal and mycobacterial culture 
    • Histopathology:
      • Gives a definitive diagnosis 
      • Specimen is obtained during surgery or via image-guided brain biopsy.

Serology of blood and CSF

  • Indicated if parasitic abscess is suspected
  • Can detect antibodies against T. gondii
  • Can detect anti-cysticercal antibodies


Management is based on a combination of medical and surgical treatment.

Medical management


  • Empiric treatment is directed toward the suspected etiology and source of the abscess. 
  • Administration is via the IV route for a minimum duration of 4–8 weeks.
  • Infection from a direct source:
    • Metronidazole + ceftriaxone/cefotaxime
  • Infection from hematogenous spread:
    • MRSA: vancomycin + metronidazole + ceftriaxone/cefotaxime 
    • MSSA: nafcillin/oxacillin + metronidazole + ceftriaxone/cefotaxime 
  • Postsurgical infection (head and neck area): 
    • MRSA: vancomycin + ceftazidime/cefepime or meropenem
    • MSSA: naficillin/oxacillin + ceftazidime/cefepime or meropenem
  • Infection due to penetrating trauma:
    • MRSA: vancomycin + ceftriaxone/cefotaxime 
    • MSSA: nafcillin/oxacillin + ceftriaxone/cefotaxime
    • Suspected Pseudomonas infection: vancomycin + cefepime 
  • Unknown source:
    • Normal regimen: vancomycin + metronidazole + ceftriaxone/cefotaxime
    • Suspected Pseudomonas infection: vancomycin + metronidazole + cefepime 


  • Glucocorticoids are considered in the setting of substantial mass effect.
  • Should be discontinued once mental status and neurologic manifestations have improved due to associated complications

Surgical management

Needle aspiration:

  • Associated with fewer complications than surgical excision (preferred)
  • A burr hole is drilled under image guidance.
  • An aspiration needle is passed through the burr hole.
  • Aspirate is sent for laboratory/pathologic analysis. 
  • Contraindications: 
    • Early cerebritis without evident central necrosis (liquification)
    • Abscess in vital regions or inaccessible regions 

Surgical excision:

  • Associated with more complications than needle aspiration
  • Treatment of choice in:
    • Traumatic brain abscess (with bone chips/ foreign bodies)
    • Multiloculated abscesses 
    • Encapsulated fungal brain abscess
  • Indications for surgical excision after needle aspiration:
    • Lack of clinical improvement 1 week after needle aspiration
    • Depressed sensorium
    • Increased intracranial pressure
    • Progressive increase in the diameter of the abscess

Surgical intervention could be avoided if:

  • Patient presents with early cerebritis without evidence of necrosis
  • Abscess is in a vital location or inaccessible


  • Mortality is approximately 10%.
  • Full recovery rate is 70%.
  • Most common neurologic sequelae is seizures.

Differential Diagnosis

  • Neurocysticercosis: cysts in the brain caused by an infection from the parasite Taenia solium. Presents with epilepsy, headache, raised intracranial pressure, dementia, and dysarthria. Confirmatory diagnosis is by imaging. Management includes antiparasitics and possible surgical intervention.
  • Intracranial tumor: a benign or malignant growth of cells in the brain that presents as headache, unexplained nausea or vomiting, blurred vision, and difficulty in speech or hearing. The main diagnosis is by imaging (MRI or CT) and a neurological examination. Management includes radiation, chemotherapy, and surgery.
  • Encephalitis: infectious inflammation of the brain parenchyma. Presents with fever, headache, pain in muscles and joints, and fatigue. Diagnosed by imaging, CSF analysis, lab tests, and electroencephalogram. Rarely presents with nuchal rigidity and photophobia. Seizures are common. Supportive management, antiinflammatory drugs, and antiviral drugs are used to manage encephalitis.
  • Meningitis: inflammation of the meninges usually caused by a bacterial or viral infection. Clinically presents with headache, fever, and nuchal rigidity and is diagnosed by clinical presentation, blood tests, CSF analysis, and imaging. Management includes supportive treatment and antimicrobials directed against the infectious agent.


  1. Southwick FS. (2020). Pathogenesis, clinical manifestations, and diagnosis of brain abscess. UpToDate. Retrieved April 22, 2021, from
  2. Southwick FS. (2019). Treatment and prognosis of bacterial brain abscess. UpToDate. Retrieved April 22, 2021, from
  3. Brook I. (2021). Brain Abscess. Medscape.
  4. Cerebral Abscess. John Hopkins Medicine.
  5. Bokhari MR, Mesfin FB. (2020). Brain Abscess. NCBI.

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