Intracranial pus may be extradural, subdural, or intracerebral.

Extradural pus is associated with osteomyelitis due to frontal sinusitis, middle ear disease, or to compound fractures. Local swelling (Pott's puffy tumour) occurs, and treatment requires removal of the infected bone (Fig. 1) 2298. The dura is a remarkable barrier to infection: intradural extension of an infection associated with osteomyelitis is rare, but can occur.

Subdural pus usually arises from frontal sinusitis. Once pus enters the subdural space it diffuses widely, not only over the hemisphere, but also alongside the falx. Thrombosis of the draining cortical veins produces the characteristic picture of severe epilepsy and profound hemiplegia (and aphasia if on the dominant side). The causative organism is usually Streptococcus milleri. Strict anaerobes, such as Bacterioides, may occasionally be found if appropriate laboratory methods are used.

The clinical feature are those of severe, progressive ‘sinus’ headache; the patient is febrile and unwell, and epilepsy and severe focal neurological signs develop within 24 or 48 h. Intracranial pressure becomes raised later in the course of the illness. CT scanning usually shows a parafalcine collection of pus, but if the diagnosis is in doubt a burr hole should be made.

An extensive craniotomy extending laterally from the midline, enables parafalcine pus to be evacuated. High doses of parenteral penicillin (20 Mu per day) and metronidazole (400–600 mg twice daily) should be administered before the results of bacteriological investigations are known. The frontal sinus may also require drainage.

The majority (75 per cent) of intracerebral abscesses are caused by spread of an infection in a nearby site, usually in the frontal sinuses or middle ear. The remainder are caused by haematogenous spread of micro-organisms, particularly in patients with congenital cyanotic heart disease.

Initially there is a zone of suppurative encephalitis; this is followed by necrosis with frank pus formation surrounded by granulation tissue (acute abscess). After 5 to 6 weeks a zone of fibrous tissue develops (chronic abscess). Frontal sinusitis produces a frontal lobe abscess, while middle ear infection passes through the roof of the middle ear cavity into the temporal lobe; haematogenous spread produces multiple and often deep abscesses. Cerebellar abscess is now rare; the causative organism is usually Streptococcus milleri (microaerophilic) or Bacteroides (anaerobic).

Raised intracranial pressure occurs early in the course of the illness, because of the considerable oedema surrounding the abscess. Papilloedema is often present without other features of raised pressure; frequent fundoscopic examination is important not only for the diagnosis but also the assessment of patients during treatment (Fig. 4) 2301. Focal signs are sometimes difficult to elicit in a drowsy patient, but if carefully looked for these will be found. A frontal lobe abscess may cause a lack of facility or a drift of an outstretched arm, suggestive of mild weakness. A temporal lobe abscess causes a homonymous quadrantopia which can be demonstrated by asking the patient to take hold of the examiner's hands: the hand on the side of the defect is ignored.

The CT scan is the best method of confirming the diagnosis. This shows a cystic lesion with a fine but regular capsule which enhances with contrast due to the zone of granulation tissue. There is considerable surrounding oedema. Cystic gliomas sometimes have a similar appearance: if there is doubt a diagnostic burr hole and aspiration (performed stereotactically, with CT guidance for deep and inaccessible lesions) is indicated. The oedema surrounding a cerebral abscess is dramatically reduced by treatment steroids (dexamethasone). This may improve the patient's headache and drowsiness and mask the CT scan appearances by reducing the oedema and compression of adjacent structures. A false negative diagnosis may be made if the patient has received steroid treatment before CT scanning has been performed.

The treatment of a cerebral abscess is the same as that for collections of pus anywhere in the body. The inflammation is treated by antibiotics. Penicillin (20 Mu IV/day) and metronidazole (600 mg twice daily) are reasonable choices until the bacteriological diagnosis and antibiotic sensitivities are known. Removal of the pus is best achieved by burr hole aspiration. This should be repeated each day until no further pus is obtained. The oedema persists for several weeks or months and repeat CT scans are advisable to confirm that there is no recrudescence of pus. If aspiration fails because of reinfection or because the capsule is too thick, craniotomy and excision of the abscess is necessary. Drainage is sometimes used, but this has not found general favour.

The effects of the abscess must be treated. If the patient has greatly raised intracranial pressure and shows signs of tentorial coning, judicious administration of high doses of dexamethasone may be life-saving especially if emptying the abscess of pus fails to reduce the intracranial pressure rapidly. The comatose patient requires appropriate nursing case with maintenance of the airway, and care of the skin, bladder, and bowels. About one-third of patients develop epilepsy, and anticonvulsants should be given to all patients with an intracerebral abscess. If chronic epilepsy results despite adequate drug treatment this can be sometimes effectively treated, for instance by excising the frontal lobe containing the abscess scar. The cause of infection also requires treatment; this is often frontal sinus disease, middle ear infection, or congenital heart disease.