A brain abscess develops from either direct extension from a contiguous suppurative focus of infection (frontoethmoidal sinusitis, chronic otitis media, mastoiditis, or dental infections), hematogenous dissemination from a distant site of infection (lungs, skin, endocarditis, intra-abdominal abscess, urinary tract infection), or from direct inoculation (head trauma or a neurosurgical procedure). In 20 to 30% of cases, no source of infection is identified.[26–28]
The most common pathogens in brain abscess associated with paranasal sinusitis are aerobic (usually Streptococcus milleri group) and anaerobic streptococci, Haemophilus species, Bacteroides species, Staphylococcus aureus, and Enterobacteriaceae. The most common pathogens in brain abscess from dental infections are streptococci, Bacteroides fragilis, and Fusobacterium species. The majority of brain abscesses that are associated with chronic otitis media are due to streptococci, Bacteroides species, Pseudomonas aeruginosa, and Enterobacteriaceae.
The most common site of infection outside of the CNS for hematogenous dissemination and brain abscess formation are the lungs. A brain abscess associated with a pyogenic lung infection (lung abscess and empyema) is often due to Streptococcus species, staphylococci, Actinomyces species, Fusobacterium species, and Nocardia asteroides. When endocarditis is the source of a brain abscess, the causative organism is often viridans streptococci or Staphylococcus aureus.
The most common symptoms of a brain abscess are fever, headache, and vomiting. Patients may also present with new-onset seizures or focal neurological deficits.
A brain abscess may be diagnosed by either CT or MRI. The preferred neuroimaging study is MRI as the early cerebritis stage of a brain abscess (Figure 1A) can be better imaged by MRI than CT. A brain abscess typically appears as a ring-enhancing lesion on a T1-weighted MRI image after the administration of gadolinium (Figure 1B). DWI is the preferred modality for distinguishing brain abscess from tumor (Figure 1C). In the majority of cases, a brain abscess demonstrates restricted diffusion with hyperintensity on DWI and corresponding hypointensity on apparent diffusion coefficient images (Figure 1D).
(A) Brain abscess. T1-weighted magnetic resonance imaging (MRI) postcontrast demonstrating early abscess with surrounding edema in the right temporal lobe. (B) Brain abscess. T1-weighted MRI postcontrast demonstrating abscess with thick rim of enhancement in the right temporal lobe. (C) Brain abscess on diffusion-weighted imaging (DWI). There is abnormal bright restricted diffusion typical of the necrotic center of an abscess. (D) Brain abscess on apparent diffusion coefficient (ADC) demonstrates associated low ADC signal.
The etiological organism(s) of a brain abscess may be identified by Gram's stain and culture of brain abscess pus obtained by stereotactic CT-guided needle aspiration. Empiric therapy is based on predisposing and/or associated condition that predict the most likely causative organism similar to meningitis (Table 1 and Table 2), and antimicrobial therapy is modified when the results of culture and antimicrobial sensitivities are known. Intravenous antibiotic therapy should be continued for 6 to 8 weeks, followed by a 2- to 3-month course of oral antimicrobial therapy. Complete excision of an abscess is rarely necessary. Corticosteroid therapy is recommended only for patients with cerebral edema causing mass effect, increased ICP, and impending cerebral herniation. Prophylactic antiepileptic therapy is recommended during treatment and for a minimum of 3 months after surgery.[30–32]
Semin Neurol. 2019;39(3):334-342. © 2019 Thieme Medical Publishers