Images below require Macromedia's Flash Player to view

Neuroradiology Case of the Week

Case 195

Anthony Conde, MD, MPH and Per-Lennart Westesson, MD, PhD, DDS

Clinical Presentation: Patient is a 59-year-old male presenting with a brain abscess.

Radiological Findings: There is a poorly marginated mixed hypo-isointense mass at the right posterior frontal lobe in the T1WI (Fig. 1).  On the T2WI (Fig. 2) and FLAIR (Fig. 3) images the lesion demonstrates a hyperintense center surrounded by hyperintense edema.  The lesion displays patchy enhancement in the T1C+ (Fig 4.).  Finally, the lesion demonstrates marked signal intensity on the DWI (Fig. 5) and decrease intensity on the ADC map (Fig. 6) images typical of restricted diffusion. 

Diagnosis: Brain abscess

Differential diagnosis and distinguishing features:

• Primary of metastatic neoplasm
• May have either a low or high signal on DWI.
• Resolving hematoma
• History will usually reveal a trauma or other pertinent data.
• Blood has a different classic appearances on MRI depending on the time.
• Demyelination
• There may be an incomplete enhancement of a ring.
• Other similar lesions will usually be found.
• Mass effect caused by the lesions will be minimal.
• Subacute infarct
• Signs and symptoms of a stroke.
• Vascular distribution.

Discussion: Brain abscesses usually present as headaches (90%) with fevers (50%). However, other symptoms may include seizures, altered mental status and focal neurological deficits. Lab values may show an increased erythrocyte sedimentation rate in 75% of the cases and leucocytosis in 50% of the cases. Their prognosis is directly proportional to the location and size of the lesion as well as the virulence of the infecting organism. They may occur at any age but are most common in the third and fourth decades of life.
     Approximately 20-30% of abscess have no identifiable source. However, there are many known etiologies. It may be caused by a hematogenous route from an extracranial location such as the urinary track (i.e. urinary track infections), the heart (i.e. endocarditis) or the lungs (i.e. upper or lower respiratory infections). A right-to-left shunt may also result in the hematogenous spread of infection to the brain coming from either the heart (congenital malformations) or even the lung (through AVMs ). The infection causing a brain abscess may also spread via direct extension from either the calvarium or the meninges. Some common infections that result in direct extension include the paranasal sinuses, the middle ear, and teeth infections. A third cause of an abscess may be through seeding caused by foreign bodies such as metal fragments from bullets or bone fragments from the calvarium that disrupt the blood brain barrier. This may explain their 2:1 male to female ratio prevalence. Other intentional disruptions of the blood brain barrier include surgical interventions.
     The most common culprits are streptococci, staphylococcus and pneumococcus. Klebsiella is predominant in the diabetic population. In transplant patients, Nocardia, Aspergillus and Candida predominate. In the AIDS populations the most common culprits include toxoplasmosis and tuberculosis. In neonates we find sources such as Citrobacter, Proteus, Pseudomonas, Serratia, and Staphyloccocus aureus. If untreated abscesses may be fatal usually as a result of ventriculitis. Complications include meningitis that are spawned by the lesion or mass effects that may result in hernation (and is also potentially a life threatening complication as well). Mortality rate still hovers from 0-30%. Treatment consists of surgical drainage and/or excision as a first line of therapy. Antibiotics are considered for abscesses less than 2.5 cm. or early phase lesions (i.e. early cerebritis). Steriods may be used for the edema and/or mass effect.
     Brain abscesses are usually found in the supratentorial region at the grew/white matter junction of the frontal and parietal lobes. The lesions prefer the anterior and middle cerebral artery distributions. They are classified by their pathological stages depending on the timing of the lesion. These include the early cerebritis (3-5 days), late cerebritis (4 days to 2 weeks), early capsule (usually takes weeks) and late capsule (from weeks to months). The cerebritis stage is characterized by an unencapsulated zone of vessels, inflammatory cells accompanied by edema. As time goes on the necrotic foci will gradually coalesce. The capsular stage is characterized by a well defined capsule that develops around the necrotic core. As the abscess matures the surrounding edema and mass effect will decrease.

Typical imaging findings based on staging

References:

1. Osborn A. Diagnostic Imaging: Brain. 1st ed. Philadelphia: W.B. Saunders, 2004: Section I-8:24-26.
2. Castillo, M.  Neuroradiology:  The Core Curriculum.  Lippincott Williams and Wilkins, 2002: 274.