Intracranial abscesses

Intracranial abscesses.

cerebral or intracranial abscess

Topics covered:

  • Essentials
  • Introduction
  • Aetiology
  • Microbiology
  • Pathology
  • Clinical features
  • Diagnosis
  • Management
  • Prognosis
  • Further reading


The incidence of intracranial abscess is low in countries where antimicrobial treatment for infections is widespread (e.g. 2–3 per million in the United Kingdom), but they remain frequent causes of space-occupying masses in developing countries.

Aetiology—abscesses may be classified by (1) Route of transmission, including (a) direct—from a local source of infection, e.g. otitis media; (b) haematogenous—from a distant source, e.g. endocarditis, bronchiectasis, other septic lung conditions; or (c) following cranial surgery or fracture. (2) Microbiology—the commonest organisms are aerobic, anaerobic and micro-aerophilic streptococci, Staphylococcus aureus, and bacteroides, but up to 25% of abscesses are sterile. Immunodeficient patients are at increased risk.

Clinical features and investigation—typical presentations include headache, focal neurological symptoms/signs, seizures, meningism/meningitis, and signs of raised intracranial pressure. The investigations of choice are either CT scanning, with and without contrast, or MRI. Confirmation of diagnosis, usually by culture, follows aspiration/excision.

Treatment and prognosis—aside from supportive care and (where possible) identification and treatment of any underlying cause, treatment requires (1) abscess drainage by stereotactic surgical aspiration or excision by craniotomy, and (2) long-term antimicrobial therapy. Early intervention offers the best chance of recovery: without intervention, intracranial abscesses are fatal; appropriate treatment reduces overall mortality to about 10%, but long-term complications from neurological deficit and epilepsy remain frequent in survivors.


Intracranial abscesses, although less common since the introduction of antibiotics and improved treatment of systemic infections, still cause significant morbidity and mortality. The incidence is approximately 2 to 3 per million population per year in the United Kingdom, but far greater in developing countries where intracranial abscesses account for up to 8% of all intracranial space-occupying lesions, compared with 2% in developed countries. The use of modern imaging techniques and a combination of antibiotics and image-guided surgery has resulted in a reduction in morbidity and mortality in these patients. Abscesses can occur at any age but there is a peak at 30 to 50 years with a male:female ratio of 1.8:1 to 4:1.

Intracranial abscesses can be categorized according to their anatomical location, occurring in the extradural space, subdural space, or intraparenchyma. Occasionally, abscesses exist in more than one tissue plane. Intracerebral and subdural abscesses may rupture into the subarachnoid space and be accompanied by meningitis. Intracerebral pus may rupture into the ventricular system and produce ventriculitis.


The aetiology can be divided according to the route of transmission:

  • Direct—microorganisms spreading from a local source of infection such as otitis media, mastoiditis, paranasal sinusitis, or dental infection.
  • Haematogenous—microorganisms spreading from a distant source such as a right-to-left shunt secondary to cyanotic congenital heart disease in children or subacute endocarditis, bronchiectasis, and lung abscesses in adults.

Abscesses can also form after intracranial surgery or cranial trauma. Immunodeficient patients are at increased risk of developing abscesses, either secondary to conditions such as AIDS or leukaemia or iatrogenic. It is also thought that ischaemic brain tissue may encourage bacterial invasion and therefore abscesses can develop in closed head injuries and following cerebral infarcts, although this is rare.

The most common intracranial abscess is found within the intracerebral compartment, with about 60% related to middle-ear infection and 20% to frontal sinusitis. In about 10% of cases no primary source of infection can be identified. Owing to their strong connection with sinus and middle-ear disease, most intracerebral abscesses are found within the frontal or temporal lobes, or within the cerebellum. Infection disseminated through the bloodstream from more distant sites may result in multiple abscesses in any part of the brain.


The most common organisms associated with intracranial abscesses are aerobic, anaerobic, and microaerophilic streptococci, Staphylococcus aureus, and bacteroides. However, up to 25% of culture samples are sterile.

Cerebral abscesses associated with otitis media, mastoiditis, and nasal sinusitis usually show a mixed growth of anaerobic and aerobic organisms including anaerobic and microaerophilic streptococci and bacteroides, Strep. viridans and Staph. aureus are also frequently seen. Listeria tend to produce areas of focal cerebritis rather than true abscesses. Abscesses associated with frontoethmoidal sinusitis are usually due to Strep. milleri and Strep. angiosus. With trauma the organism is often Staph. aureus or one of the Enterobacteriaceae.


There are four distinct histological stages in the pathogenesis of intracranial abscesses. Spread of microorganisms, either direct or haematogenous, causes parenchymal damage after occlusion of the small vessels. The initial stage is early cerebritis (days 0–3) characterized by a local inflammatory response with perivascular and parenchymal neutrophil infiltration. During late cerebritis (days 3–9) a central necrotic area forms with macrophage infiltration. A reticulin network forms around the necrotic area in the early capsular stage (up to day 14) with parenchymal oedema. This is followed by the formation of a collagen capsule with distinct zones of neovascularization during the late capsular stage (after day 14). Perilesional cerebral oedema continues and gliosis takes place. The areas of oedematous brain may exert considerable mass effect.

In the case of direct spread, infection within an accessory air sinus or the petrous bone may cause an area of localized osteitis just above the dura. This can then spread intracranially. Initially it may be entirely confined to the extradural space, but will eventually penetrate the dura and spread subdurally. If the adjacent arachnoid is stuck to the inflamed patch of dura then it may spread into the subarachnoid space to give meningitis. If the subarachnoid space has been obliterated, it may penetrate the brain to produce initially a focal cerebritis. Large intracerebral abscesses can rupture into the ventricular system, producing a ventriculitis.

temporal lobe abscess

Above: Temporal lobe abscess

Clinical features 

Presentation depends upon the site, size, and number of lesions, and the involvement of neighbouring structures such as the cerebral ventricles and the venous sinuses. The signs are therefore legion, but the diagnosis should be considered in any case where there is an obvious primary source of infection associated with evidence of raised intracranial pressure, focal neurological signs, headache, epileptic seizures, or meningeal irritation.

Extradural abscess may be difficult to detect clinically, but can sometimes manifest as severe, unremitting, localized headache in association with sinusitis or mastoiditis. Patients with subdural empyema frequently appear toxic, with a swinging pyrexia, severe headache, a depressed level of consciousness, contralateral hemiparesis, papilloedema, meningeal irritation, and seizures. There is often an accompanying frontal sinusitis with tenderness of the forehead, erythema, and swelling of the eyelids.


Next If a brain abscess is suspected, predisposing sources of infection, including possible distant sites, should be carefully sought. Intracranial abscesses derived from haematogenous spread are often more fulminating in their course than those associated with direct spread. CT scans of the skull base, including views of the mastoids and other skull sinuses, should be performed. Plain radiographs of the mastoids and sinuses may reveal infection.

The investigations of choice for all forms of suspected intracranial abscess are either CT scanning, with and without contrast, or MRI. CT will normally demonstrate both extradural and subdural empyema and show intracerebral abscesses as ring-enhancing lesions with low-attenuation centres. The CT and MRI appearances correlate closely with the pathogenesis. During the early stages of cerebritis areas of hypodensity may be very subtle with minimal contrast enhancement. At this stage MRI may reveal oedema and some ring enhancement not evident on CT. Subdural empyema may initially be thinly spread over the cerebral cortex, producing relatively little midline shift, appearing virtually isodense with brain on CT. Under such circumstances, contrast-enhanced MRI (particularly with coronal views) is of great value. Diffusion-weighted imaging (DWI) with MRI can help differentiate a pyogenic abscess from other ring-enhancing lesions. Proton MR spectroscopy can be used to show peaks of lactate and cytosolic amino acids present in abscesses.

A left temporal cerebral abscess secondary to otitis media

Above: A left temporal cerebral abscess secondary to otitis media

The principal differential diagnoses in an intracranial abscess are meningitis, subdural haematoma, and intracranial tumour. It is not always possible to differentiate between intracerebral abscess and tumour on a CT scan, particularly when there is an appearance of ring enhancement, and it is largely for this reason that the biopsy of suspected cerebral tumour is advocated in nearly all such cases. MRI, however, tends to show a low-signal capsule on T 2-weighted images and may be helpful in making this differentiation.

One obvious concern is to differentiate between bacterial meningitis and intracerebral abscess. Both may present with pyrexia, neck stiffness, and some focal signs, but if there is any evidence of raised intracranial pressure, or any other supportive evidence of cerebral abscess, a lumbar puncture should be strictly avoided until a neurosurgical opinion has been sought. Lumbar puncture in the presence of cerebral abscess can lead to tonsillar or tentorial herniation. The cerebrospinal fluid can be entirely normal in intracranial abscesses. 


Treatment includes identifying and treating the underlying cause and image-guided stereotactic surgical aspiration or excision of the abscess by craniotomy combined with long-term antibiotics. Selected patients can be managed without surgical intervention. This tends to be limited to those who have multiple or inaccessible abscesses and those in whom surgery is contraindicated due to poor general medical condition. However, without biopsy the diagnosis cannot be confirmed and the pathogens cannot be identified. Therefore tissue should be obtained if at all possible.

Early diagnosis and treatment are essential to good outcome. The damaging effect of abscesses results from parenchymal displacement and oedema rather than destruction of tissue, so neurological deficits may be reversible. Treatment is aimed at identifying the causative agent, obtaining antibiotic sensitivities, and reducing mass effect. Early management includes the following steps: culturing blood and any extracranial infective lesion, obtaining tissue and starting appropriate intravenous antibiotics, administration of anticonvulsant agents, and, in cases of grossly depressed level of consciousness and massive cerebral oedema seen on a CT scan, giving intravenous dexamethasone. Steroids decrease cerebral oedma but are also thought to prevent antibiotic penetration. Therefore they should only be used in patients with mass effect on CT.

Pus from the suspected primary site of infection should be collected immediately and both aerobic and anaerobic cultures obtained. The intracranial pus must be similarly cultured. High dose intravenous empirical antibiotics should be commenced immediately without waiting for the culture report, and subsequently changed in the light of the sensitivity findings. The antimicrobial regimen should include penicillin, metronidazole, ampicillin, and either gentamicin or chloramphenicol, depending on the likely source of infection and the infective agent. Although antibiotics have good penetration into cerebrospinal fluid, the acidic environment of the abscess means that the efficacy of the antibiotic may be reduced. Intravenous antibiotics should be continued for more than 6 to 8 weeks before reverting to oral medication. Microbiologists should be involved in decisions regarding length and nature of antibiotic treatment.

Most supratentorial abscesses can be sterilized by aspiration through a burr hole. The direct administration of antibiotics through the burr hole, is sometimes employed. Aspiration is often repeated several times, but in about 30% of cases a single aspiration will suffice. Once the abscess is sterile, the capsule will shrink and finally form an irregular gliotic scar within the brain. Shrinkage of the abscess must be checked by serial CT scans. Subdural empyema should be evacuated through a craniotomy rather than burr holes, as very frequently the pus can spread widely, particularly alongside the falx cerebri. Extradural empyema is evacuated through a burr hole, or through a craniotomy for larger collections to allow complete excision of the abscess. Advances in image-guided stereotactic surgery have resulted in far more accurate and safe targeting of all intracranial lesions including abscesses and should be used to aid any surgical intervention.

Cerebellar abscesses, when diagnosed early, may be aspirated through a burr hole, but immediate total excision is often recommended because the small volume of the posterior cranial fossa leaves little latitude in terms of tonsillar herniation and death.


The mortality rate from intracranial abscesses has been reduced from 40 to 60% to around 10% since the introduction of CT scanners. The main problems remain those of late diagnosis and resistant bacteria. Epilepsy and permanent disability still occur in up to 50% of cases. Temporal lobe abscess, subdural empyema, and abscesses that rupture into the ventricles have a worse prognosis. Fungal abscesses can occur in transplant recipients and carry a mortality rate close to 100%.

Further reading


Kao PT, et al. (2003). Brain abscesses: Clinical analysis of 53 cases. J Microbiol Immunol Infect, 36, 129–36. 

Kastrup O, Wanke I, Maschke M (2008). Neuroimaging of infections of the central nervous system. Semin Neurol, 28, 511–22.

Lorber B (1997). Listeriosis. Clin Infect Dis, 24, 1–9. Mathisen GE, Johnson JP (1997). Brain abscess. Clin Infect Dis, 25, 763–79. Report of the Quality Standards Subcommittee of the American Academy of Neurology (1998). Evaluation and management of intracranial mass lesions in AIDS. Neurology, 50, 21–6.

Sharma R, Mohandas K, Cooke RPD (2009). Intracranial abscesses: changes in epidemiology and management over five decades in Merseyside. Infection, 37, 39–43.