Intracranial tuberculous abscess
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At the time the article was created Frank Gaillard had no recorded disclosures.View Frank Gaillard's current disclosures
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The epidemiology of patients with tuberculous abscesses is essentially the same as that of other CNS manifestations of tuberculosis (see CNS tuberculosis), although they are more frequently encountered in patients who are immunocompromised 2.
Patients with tuberculous abscesses present non-specifically, with focal neurological deficits, seizures or sign and symptoms of raised intracranial pressure 1.
In contrast to tuberculomas, tuberculous abscesses are filled with pus and have distinct microscopic changes: vascular granulation tissue in the wall, absence of epithelioid granulomatous reaction (seen in tuberculoma) 1,3,4. Furthermore, Mycobacterium tuberculosis can be isolated from the pus, which is sometimes unable to be isolated from tuberculomas 1.
Tuberculous abscesses have appearances very similar, and often identical, to pyogenic cerebral abscesses. They tend to be solitary, but can be multiloculated, and are relatively large and faster growing, compared to tuberculomas, that are usually a little smaller 4. They are surrounded, as is the case with pyogenic abscesses, by abundant vasogenic edema 1. Tuberculous meningitis may or may not co-exist 3.
Appearances are those of a cerebral abscess: a peripherally-enhancing lesion with low attenuation center surrounded by vasogenic edema.
As is the case with CT, MRI appearances are those of a cerebral abscess 1-3.
- central low intensity (hyperintense to CSF)
- peripheral low intensity (vasogenic edema)
- T1 C+ (Gad): ring enhancement
- central high intensity (hypointense to CSF, does not fully attenuate on FLAIR)
- peripheral high intensity (vasogenic edema)
- the abscess capsule may be visible as an intermediate to slightly low signal thin rim
- high DWI signal is usually present centrally
Treatment and prognosis
Surgical drainage is often curative, with concurrent multiagent antituberculous antibiotics.
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