Tuberculosis of the central nervous system can result from either hematogenous spread from distant systemic infection (e.g. pulmonary tuberculosis) or direct extension from local infection (e.g. tuberculous otomastoiditis).
Intracranial manifestations of tuberculosis are protean and can affect all compartments and are discussed individually in separate articles. Manifestations include:
The remainder of this article is a general discussion of CNS tuberculosis. For a general discussion on systemic tuberculosis, please refer to the article on tuberculosis.
Tuberculosis remains a leading cause of morbidity and mortality in the developing world. It may account for ≈1/6th of the 3 million global mortality due to Mycobacterium tuberculosis infection. CNS involvement is thought to occur in 2-5% of patients with tuberculosis and up to 15% of those with AIDS-related tuberculosis 6,7.
Although CNS involvement by tuberculosis is seen in all age groups, there is a predilection for younger patients, with 60-70% of cases occurring in patients younger than 20 years of age 7.
In endemic regions, tuberculomas account for as many as 50% of all intracranial masses 8.
Clinical presentation depends on the particular manifestation, although in all cases symptoms and signs are nonspecific and include fever, seizures, meningism and focal neurological deficits (e.g. altered sensorium, hemiparesis).
Hematogenous spread from the lungs or gastrointestinal tract is most common, leading to small subpial or subependymal infective foci. These are termed Rich foci and form a reservoir from which intracranial manifestations may arise 5,7,8. This can occur either during the primary infection (uncommon, and more frequently seen in children) or be reactivated later and cause a post-primary infection.
There is a wide radiological and pathological spectrum of CNS disease. Tuberculous meningitis and intracranial tuberculous granuloma (tuberculoma) are the most common manifestations and these are discussed in detail in separate articles. Below is a brief discussion of the main imaging features of each presentation.
Tuberculous meningitis may manifest in two forms:
TB leptomeningitis is common and presents with thick tuberculous exudate within the subarachnoid space, particularly pronounced at the base of the brain (especially in the interpeduncular fossa, anterior to the pons and around the cerebellum) and may also extend into the Sylvian fissures. In contrast to bacterial meningitis, extension over the surfaces of the cerebral hemispheres is relatively uncommon 8. Eventually, mass-like regions of caseous necrosis can form within this exudate, representing extra-axial tuberculomas.
Not surprisingly CSF flow is disrupted, and obstructive hydrocephalus is common.
An additional complication is arteritis that may result in ischemic infarcts, which are seen in approximately a third of cases, especially in children 7.
In contrast, TB pachymeningitis is rare and is characterized by thick plaque-like regions of pachymeningeal enhancement. This term should be reserved for cases where it is an isolated abnormality, and not confused with the sometimes dramatic thickening of dura adjacent to a tuberculoma 8.
Intracranial tuberculomas may occur either in isolation or combined with extra-axial TB infection. They typically appear as ring-enhancing lesions with surrounding vasogenic edema. Centrally they tend to have only intermediate or even low signal on T2 weighted images (helpful in distinguishing them from the less common tuberculous abscess) 9. They may be associated with extensive adjacent leptomeningeal and/or pachymeningeal enhancement.
For further discussion, please refer to separate articles on intracranial tuberculoma.
Treatment and prognosis
Treatment of CNS tuberculosis is based on an anti-tubercular treatment regimen. However, multidrug-resistant tuberculosis remains a major hurdle in treatment.
- 1. Leonard JM, Des prez RM. Tuberculous meningitis. Infect. Dis. Clin. North Am. 1990;4 (4): 769-87. Pubmed citation
- 2. Gupta RK, Gupta S, Singh D et-al. MR imaging and angiography in tuberculous meningitis. Neuroradiology. 1994;36 (2): 87-92. Pubmed citation
- 3. Salgado P, Del brutto OH, Talamás O et-al. Intracranial tuberculoma: MR imaging. Neuroradiology. 1989;31 (4): 299-302. Pubmed citation
- 4. Brismar J, Hugosson C, Larsson SG et-al. Imaging of tuberculosis. III. Tuberculosis as a mimicker of brain tumour. Acta Radiol. 1996;37 (4): 496-505. Pubmed citation
- 5. Engin G, Acunaş B, Acunaş G et-al. Imaging of extrapulmonary tuberculosis. Radiographics. 20 (2): 471-88. Radiographics (full text) - Pubmed citation
- 6. Burrill J, Williams CJ, Bain G et-al. Tuberculosis: a radiologic review. Radiographics. 27 (5): 1255-73. doi:10.1148/rg.275065176 - Pubmed citation
- 7. Kornienko VN, Pronin IN. Diagnostic Neuroradiology. Springer Verlag. (2009) ISBN:3540756523. Read it at Google Books - Find it at Amazon
- 8. Gupta RK, Lufkin RB. MR imaging and spectroscopy of central nervous system infection. Springer Us. (2001) ISBN:0306465515. Read it at Google Books - Find it at Amazon
- 9. Kim TK, Chang KH, Kim CJ et-al. Intracranial tuberculoma: comparison of MR with pathologic findings. AJNR Am J Neuroradiol. 1995;16 (9): 1903-8. AJNR Am J Neuroradiol (abstract) - Pubmed citation
- 10. Khanna PC, Godinho S, Patkar DP et-al. MR spectroscopy-aided differentiation: "giant" extra-axial tuberculoma masquerading as meningioma. AJNR Am J Neuroradiol. 2006;27 (7): 1438-40. AJNR Am J Neuroradiol (full text) - Pubmed citation
- 11. Garg RK. Tuberculosis of the central nervous system. Postgrad Med J. 1999;75 (881): 133-40. doi:10.1136/pgmj.75.881.133 - Free text at pubmed - Pubmed citation
Related Radiopaedia articles
- causative agent
- tuberculoma (tuberculous granuloma)
- tuberculous abscess
- miliary tuberculosis
- pulmonary tuberculosis
- intracranial tuberculosis
- tuberculous otomastoiditis
- tuberculous lymphadenopathy
- cardiac tuberculosis
- tuberculous mastitis
- gastrointestinal tuberculosis
- tuberculous peritonitis
- visceral tuberculosis
- hepatic tuberculosis
- gallbladder tuberculosis
- pancreatic tuberculosis
- splenic tuberculosis
- genitourinary tuberculosis
- skeletal tuberculosis
Infections of the central nervous system
- classification by etiology
- Eastern equine encephalitis
- enterovirus rhombencephalitis
- flavivirus encephalitis
- herpes virus family
- HIV CNS manifestations
- HTLV-1-associated myelopathy
- JC virus
- measles encephalitis
- Nipah virus (NiV) encephalitis
- rabies encephalitis
- CNS listeriosis (Listeria monocytogenes)
- CNS nocardiosis (Nocardia spp)
- CNS tuberculosis (Mycobacterium tuberculosis)
- Lyme disease (Borrelia burgdorferi)
- neurobrucellosis (Brucella sp.)
- neurosyphilis (Treponema pallidum)
- Rocky Mountain spotted fever (Rickettsia rickettsii)
- cerebral amoebiasis
- cerebral malaria (Plasmodium falciparum)
- cerebral sparganosis (Spirometra mansonoides)
- neurocysticercosis (Taenia solium)
- neurohydatidosis (Echinococcus spp)
- neurotoxoplasmosis (Toxoplasma gondii)
- Creutzfeldt-Jakob disease (sporadic, variant, familial, and iatrogenic)
- fatal familial insomnia
- Gerstmann-Straussler-Scheinker disease
- variably protease-sensitive prionopathy
- others or those with possible infectious etiologies
- classification by location
- classification by etiology