Teaching Case

A 49-year-old man with a history of alcohol abuse presented to the Emergency Department with fever, headache and productive cough for the past 4 days. The day before his clinical conditions were aggravated by confusion and motor slowing. No relevant previous medical history. Laboratory analysis found leukocytosis and increased c-reactive-protein.

Non-enhanced CT (NECT) showed a hypodense area in the right centrum semiovale and hyperdense material in the right ventricle (Fig. 1a-c). Obliteration of paranasal sinuses was an associated finding (Fig. 1d). At contrast-enhanced CT (CECT) the lesion presented a ring enhancement communicating with the right ventricle (Fig. 2a-c).

At MRI, a hyperintense nodular lesion on T2WI/FLAIR with hypointense ring was found in the right centrum semiovale, with punctiform diffusion restriction and rim enhancement after contrast injection (Fig. 3a-d).

FLAIR and DWI evidenced hyperintense material in the ventricles and prepontine cistern (Fig. 4a-e). Ependymal contrast enhancement was appreciated at the right ventricle (Fig. 4f). A diagnosis of cerebral abscess with ventriculitis was suspected.

 At one-month MR follow-up, after antibiotic therapy and external ventricular drainage, reduction of the focal lesion and material in the ventricular system was detected; moreover, disappearance of the subependymal enhancement of the right ventricle was evidenced (Fig. 5a-d).

Background: Pyogenic brain abscesses are rare but potentially fatal infections of the central nervous system which occur more frequently in men at any age although the median age of presentation is 34 years. [1] Predisposing factors are present in the majority of patients and include penetrating trauma, neurosurgery, infections of the ear, paranasal sinuses or teeth, endocarditis, congenital heart disease, lung infections and immunosuppression. [1] In our case the patient had paranasal sinusitis and periodontitis and Campylobacter rectus was isolated from CSF.

Clinical perspective: Clinical manifestation depends on several factors (systemic condition, virulence of the organism, size and location of the abscess) and is often nonspecific with fever in less than 50% of the patients; other typical symptoms are headache, focal neurologic deficit, confusion and nausea/vomiting. Laboratory data often show higher inflammatory markers, but the absence will not exclude the diagnosis. After rupture in ventricular system a sudden worsening of the clinical status often occurs. [1, 2]

Imaging perspective: CT and MR imaging are essential for early diagnosis and better outcome since mortality is high (13.4-21%) [3-5] and it rises up to 40% after intraventricular rupture. [6, 7]

Imaging findings depend on the stages of the abscess development (early cerebritis, late cerebritis, abscess with early capsule and late capsule formation). [8]

In the early capsule stage NECT shows the presence of a hypodense area while a ring enhancement is found on CECT. In case of intraventricular rupture, ventriculomegaly with a debris level is evidenced on NECT; ventricular walls may enhance after contrast media injection. [8]

At MR examination, the capsule is typically hypointense on T2WI and on SWI it shows the suggestive “dual rim sign” [9] characterised by two concentric rims, the outer hypointense and the inner hyperintense. Furthermore, the capsule could be hyperintense on T1WI and after the contrast media injection is responsible of the ring enhancement. The central suppurated core of the abscess is characterised by hyperintensity on T2WI/FLAIR and high restriction a DWI. The capsule is surrounded by oedema characterised by hyperintensity on T2WI/FLAIR and hypointensity on T1WI. After intraventricular rupture, the pus is present in the ventricular system and can be reliably evidenced with FLAIR and DWI; post-contrast T1WI may show enhancement of the ventricular walls. [8]

Take home message: CT and MR findings in the early capsule stage of brain abscess are fundamental for correct diagnosis in accordance to the clinical manifestation and predisposing factors of the patient.

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