Intracranial cerebral abscess
Epidemiology and pathogenesis
Cerebral abscesses are focal suppurative intracranial infections that start as an area of focal cerebritis, eventually demarcating into discrete collections of encapsulated pus surrounded by a well-vascularized capsule. They progress through four classic stages: early cerebritis, late cerebritis, early capsular, and late capsular. In the later stage, there is a rim of granulation tissue surrounded by increasing angiogenic neovascularity, which causes increasing cerebral edema.
The most common etiology is direct extension from the sinuses, eyes, and dental infections, followed by hematogenous seeding (more often multifocal due to endocarditis or chronic pulmonary infections) or rarely direct trauma (sometimes iatrogenic). Up to 25% to 35% of cases in children may have an unknown, cryptic source. Increased risk is associated with immunosuppression, congenital heart conditions, including patent foramen ovale and arteriovenous fistulas. Numerous different pathogens are associated, most commonly mixed species, including Streptococcus pneumoniae, Staphylococcus aureus and S. epidermidis, Actinomyces, HACEK bacteria, gram-negative species in infants, and group B streptococcus in nenonates. In immunocompromised patients, additional pathogens include toxoplasmosis, Nocardia, Candida, Listeria, Mycobacterium, and Aspergillus. The incidence is estimated at 0.3 to 0.9 per 100,000 with a 2-3:1 preponderance in males compared with females.
The classic triad, including headache (approximately 69%), fever (53%), and focal neurologic deficit (48%), is seen in only approximately 20% of cases, with symptoms occurring about eight days prior to diagnosis. Other neurological deficits include seizures (25%) and altered mental status (48%). The abrupt onset of meningeal signs with worsening headache and neurological status is associated with rupture of an abscess into the ventricular space causing ventriculitis, which is associated with high mortality.
Approximately 80% of brain abscesses are solitary, and they are most commonly seen in the frontal and temporal lobes.
Early cerebritis is often invisible on CT but may demonstrate an area of poorly marginated subcortical hypodensity.
Late cerebritis and early capsular stages will demonstrate irregular rim enhancement on contrast-enhanced CT and MRI.
Contrast-enhanced CT and MRI in the late capsular stage will show a capsular ring that is T1 hyperintense and T1 hypointense, with a complete ring of enhancement with a central area of necrosis.
In later stages, there will also be a large amount of surrounding vasogenic edema due to vascular permeability (seen as white-matter hypoattenuation on CT and high T2/FLAIR signal on MRI).
On MRI, the central necrotic area is hypointense on T1 and hyperintense on T1 with restricted diffusion.
Susceptibility-weighted imaging (SWI) may show a low-intensity rim of increased susceptibility that mostly overlaps with the contrast-enhancing rim, sometimes with a double rim sign (two concentric rims inside and outside abscess cavity), distinguishing it from glioblastoma.
In some cases, MRI spectroscopy and MR perfusion can be helpful for distinguishing an abscess from a high-grade glioma with a necrotic core. Relative cerebral blood volume (rCBV) is elevated in high-grade gliomas and reduced in abscesses, while elevated succinate peak is specific for an abscess.
Treatment and prognosis
Intracranial abscesses progress rapidly and lead to devastating and permanent neurological deficits.
The mainstay treatment is with neurosurgical intervention to drain the collection, either by aspiration or craniotomy.
This is combined with IV antibiotics, which is first broad and then tailored to the specific organisms involved.
Given the high risk of seizures, seizure prophylaxis is recommended in all patients.
In cases of abscesses secondary to septic emboli from cardiac infections, heart valve surgery may be necessary to treat persistent vegetations.
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