central nervous system tuberculosis · floor, main block, 3 lok man road, chai wan, hong kong. tel:...

JLS Khoo, KY Lau, CM Cheung, TH Tsoi

J HK Coll Radiol 2003;6:217-228 217

J HK Coll Radiol 2003;6:217-228

PICTORIAL ESSAY

Correspondence: Dr Jennifer Lai-San Khoo, Department ofRadiology, Pamela Youde Nethersole Eastern Hospital, GroundFloor, Main Block, 3 Lok Man Road, Chai Wan, Hong Kong.Tel: (852) 2595 6179; Fax: (852) 2975 0432;E-mail: [email protected]

Submitted: 18 June 2003; Accepted: 29 August 2003.

Central Nervous System TuberculosisJLS Khoo,1 KY Lau,1 CM Cheung,2 TH Tsoi2

1Department of Radiology, and 2Department of Medicine,Pamela Youde Nethersole Eastern Hospital, Hong Kong

ABSTRACTThe imaging findings of 9 patients with central nervous system tuberculosis are presented to highlightthe typical findings and some complications. Lesions may involve the meninges, brain, and spinal cord.Contrast-enhanced magnetic resonance imaging is the best imaging modality for detection and follow-up oflesions and assessment of complications.

Key Words: Central nervous system, Computed tomography, Magnetic resonance imaging, Meningitis, Tuberculosis

INTRODUCTIONTuberculosis (TB) is an infectious disease that contin-ues to be a significant public health concern in HongKong. According to the statistics published by theDepartment of Health, there were 7262 notified casesin 2001, which accounted for 28% of the total notifi-able infectious diseases, and the number of deaths fromTB was reported to be 311. The cumulative numberof notifications was 6665 in the year 2002.1 Accordingto the 2001 Annual Report of the Tuberculosis andChest Service of the Department of Health, 25 cases of“tuberculosis of the meninges” were reported.2

Central nervous system (CNS) TB infection causes agranulomatous inflammatory reaction that involves theCNS meninges and parenchyma. This paper presentsthe computed tomography (CT) and magnetic resonanceimaging (MRI) features of 9 patients with CNS TBmanaged at the Pamela Youde Nethersole EasternHospital during the past 7 years.

PATHOLOGYIn most patients, TB involving the leptomeninges isthought to spread by haematogenous disseminationfrom a primary source outside the CNS such as the lung

or gastrointestinal tract. The meningitic process mayaffect the cranial cerebrospinal fluid (CSF) pathway, thespinal subarachnoid pathway, or both.3 CNS involvementby the tuberculous bacilli can also manifest as hard orsoft granulomas, tuberculous abscess, tuberculouscerebritis, pachymeningitis, spinal arachnoiditis, andintraspinal tuberculoma.4

Hydrocephalus may result from blockage of the basalsubarachnoid cisterns by the dense basal exudate, ornarrowing of the aqueduct and third ventricle bytuberculomas. Extension of the inflammatory exudatealong proliferating blood vessels into the brain substancecauses ischaemic brain damage due to vasculitis.5

Parenchymal disease usually presents as either solitaryor multiple tuberculoma, and can occur with or withoutmeningitis.3,6 Tuberculomas are histologically round oroval masses, or they may assume a more lobular con-figuration with the fusion of several smaller nodules.7

A tuberculous granuloma is typically small, measuringapproximately 0.5 to 2.0 mm in size.4 The granulomaconsists of epithelioid cells harbouring tuberculousbacilli, with a peripheral collar of fibroblasts and mono-nuclear inflammatory cells. Langhans’ giant cells, whichcontain multiple nuclei, is a characteristic feature. Ahard tubercle does not show central necrosis, but withcell-mediated delayed hypersensitivity reaction, thecore undergoes caseous necrosis, which is a coagulat-ive and liquefactive necrosis resembling cheesy material.This forms the soft tubercle of tuberculosis.4

CME

Central Nervous System Tuberculosis

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Spinal tuberculous meningitis (STBM) may originatein 3 ways:• haematogenous spread from a source outside the CNS• caudal extension of intracranial tuberculous basal

meningitis• intraspinal extension from osseous or discal TB.3,8

IMAGING FEATURESCranial Tuberculous MeningitisOn CT scan, the most common finding in cranial tuber-culous meningitis (CTBM) is obliteration of the basalcisterns by isodense or mildly hyperdense exudate.After the administration of contrast medium, there isdense homogeneous enhancement of the basal menin-ges (Figure 1). Extension of the meningeal enhance-ment over the surface of the cerebral and cerebellarhemispheres may also be observed.4,7 Extension into theventricular system with ependymitis may be seen as alinear enhancement along the ventricular margin.4,7,9

Communicating hydrocephalus, the most frequentcomplication of CTBM, usually caused by obstructionof CSF flow by the meningeal exudate in the basalcisterns, may also be seen at the time of diagnosis.3,4 Innon-contrast enhanced CT and MRI, hydrocephalusmay be the only clue for diagnosis at the initial pres-entation (Figure 2).

At MRI, although the meningeal inflammation or basalexudate may not be readily apparent on the pre-contrast

Figure 2. Hydrocephalus in a 34-year-old man with cranial tuber-culosis. Axial T1-weighted magnetic resonance imaging revealsdilatation of the lateral ventricles.

Figure 1. Tuberculous meningitis in a 48-year-old woman. (a) Non-contrast enhanced computed tomography scan shows effacement ofthe basal cisterns caused by the presence of exudate. (b) Contrast-enhanced computed tomography scan shows dense enhancement ofthe thickened inflamed basal meninges.

(a) (b)

MR images, post-contrast T1-weighted MR imagesshow diffuse meningeal enhancement, mainly at thebasal cisterns (Figure 3).4,10,11

With extension into the ventricular system, abnormalenhancement of the ependymal lining of the ventriclesand the choroid plexi may be seen (Figure 4).3


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Figure 3. Leptomeningeal tuberculosis and granuloma affectingthe basal meninges in 2 patients. (a) Axial T1-weighted magneticresonance imaging of a 34-year-old man shows abnormal com-plex hyperintensity in the suprasellar and perimesencephaliccisterns. (b) Axial T1-weighted image after intravenous gadolin-ium injection in the same patient as Figure 3a demonstrates dif-fuse enhancement of the cisterns, and nodular enhancement inthe right temporal region suggestive of tuberculosis granuloma.(c) Coronal post-contrast T1-weighted magnetic resonanceimaging of a 14-year-old woman demonstrates dense meningealenhancement at the suprasellar cistern.

(a) (b)

(c)

Parenchymal involvement is another complication ofCTBM, manifesting as TB cerebritis and granulomaformation (Figure 5). This will be further discussed laterin this article, together with parenchymal involvementof the spinal cord.

Vasculitis may be caused by direct invasion of thevessel by mycobacteria, or from extension of adjacentarachnoiditis. These may lead to spasm or thrombosisof the vessels, with resulting infarction, most frequentlyseen at the basal ganglia and internal capsule.3,4,12 OnCT scan, infarctions are demonstrated as areas of

Figure 4. Ventriculitis in a 34-year-old man. Coronal T1-weightedmagnetic resonance imaging after intravenous gadolinium injec-tion shows ependymal enhancement in the right lateral ventricleconsistent with ventriculitis. The tentorium cerebelli is also denselyenhanced due to meningeal involvement.


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Figure 6. Granulomatous tuberculous meningitis, ventriculitis, andspinal arachnoiditis in a 34-year-old man. Sagittal paramedianT1-weighted magnetic resonance imaging after intravenousgadolinium injection reveals irregular lumpy enhancement ofthe tentorium cerebelli suggestive of granulomatous meningitis.Enhancement of the walls of the lateral ventricle and spinal canalare consistent with ventriculitis and spinal arachnoiditis.

Figure 5. Tuberculosis causes midbrain signal change in a 25-year-old woman. (a) Axial T1-weighted magnetic resonanceimaging after intravenous gadolinium injection reveals multipletuberculosis granulomas in the right temporal lobe, and menin-geal enhancement in the right ambient cistern. (b) Axial T2-weightedmagnetic resonance imaging shows hyperintense changes inthe right midbrain, which may represent cerebritis or infarction. (c)Follow-up scan performed 19 months later. Axial T2-weightedmagnetic resonance imaging shows resolution of the hyperintensesignals in the midbrain, suggesting that the signal change wasdue to cerebritis rather than infarction.

(a) (b)

(c)

hypodensities, while on MR images, areas of highsignal intensity on T2-weighted images are observed.MRI is more sensitive than CT for the demonstrationof areas of infarction.4,12

Granulomatous basal meningitis is another complicationof intracranial tuberculosis. This is characterised by dif-fuse or circumscribed granulomatous involvement of themeninges at the skull base.4,13 On CT scan, an irregularlumpy enhancing mass can be seen superimposed onthe dense basal enhancement. On MR imaging, T1-weighted images reveal a mass isointense to brain, andpost-gadolinium scans show intense heterogeneouslumpy enhancement of the basal cisterns (Figure 6).4


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Caseation of the granuloma will produce rim-enhancinglesions. Contrast-enhanced MRI is superb for lesiondemonstration and offers the advantage of multiplanarcapability (Figure 7). In the chronic phase of CTBM,calcification of the granulomas will be demonstratedas hyperdense foci on non-contrast CT scan, while on MRI,lesions are hypointense on T1-weighted and T2-weightedimages due to the calcium deposition (Figure 8).

Spinal Tuberculous MeningitisThe unenhanced MR images of spinal tuberculousmeningitis (STBM) may appear unremarkable, ormay show CSF loculation and obliteration of the

Figure 7. Caseating dural/epidural tuberculosis granuloma orabscess in the same patient as in Figure 6. (a) Axial T2-weightedmagnetic resonance imaging demonstrates nodular hyperintensityposterior to the clivus and anterior to the medulla (arrow). (b)Axial T1-weighted image after intravenous gadolinium injectiondemonstrates dural/epidural rim enhancement suggestive ofcaseating tuberculosis granuloma or abscess. (c) Sagittal enhancedT1-weighted magnetic resonance imaging demonstrates thecaseating dural/epidural tuberculosis granuloma or abscess pos-terior to the clivus. Abnormal meningeal enhancement is presentat the prepontine and interpeduncular cisterns, over the superioraspect of the cerebellum, surrounding the brainstem at the foramenmagnum and the cervical spinal cord, consistent with cranio-spinal meningeal tuberculosis.

spinal subarachnoid space with loss of outline of thespinal cord in the cervico-thoracic spine, and thicken-ing and clumping of the nerve roots in the lumbarspine.3,14,15

Gadolinium-enhanced MR images show linear enhance-ment of the surface of the spinal cord and nerve roots,or plaque-like enhancement of the dura-arachnoid matercomplex which obliterates the subarachnoid space(Figures 9 and 10).3,14,15

Parenchymal Tuberculosis in the Brain andSpinal CordParenchymal TB granulomas or abscesses may beseen in the brain and spinal cord, and may be singleor multiple. The changes may be seen in associationwith leptomeningitis.3,4,6 Intracranially, parenchymalTB may be in the form of cerebritis and tuberculomas(Figure 11). Tuberculomas may appear in varioussizes and locations. They may appear as non-enhancing

(a) (b)

(c)


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Figure 8. Calcified granuloma in a 47-year-old woman. (a) Non-contrast enhanced computed tomography scan shows hyperdensities atthe interpeduncular cistern and anterior to the left temporal lobe, consistent with calcified foci. (b) Axial T2-weighted magnetic resonanceimaging shows a low signal intensity focus at the interpeduncular cistern, corresponding to the calcified focus seen on computedtomography. Dilatation of the temporal horns indicated hydrocephalus.

Figure 9. Spinal tuberculosis meningitis in a 62-year-old woman.Sagittal T1-weighted magnetic resonance imaging after intra-venous gadolinium injection shows intense enhancement ofthe subarachnoid space indicating arachnoiditis. Loculation ofcerebrospinal fluid is demonstrated posteriorly in the thoracicspinal canal (arrow).

(a) (b)

or enhancing lesions, as solid enhancing or ring-enhancing lesions, and as disseminated tuberculoma.3,4

A variable degree of vasogenic oedema surrounds thelesions, which is better appreciated on T2-weighted MRimages.4 Enhancement of the granulomas on thepost-gadolinium scans improves their conspicuity andenables their differentiation from the adjacent vasogenicoedema (Figures 12 and 13). Parenchymal tuberculo-mas can also obstruct the CSF pathways and causehydrocephalus (Figure 14).5

Tuberculous abscess is an uncommon complication ofbrain tuberculosis. There is usually irregular perilesionaloedema adjacent to the lesion. Dense peripheral ringenhancement of the wall is demonstrated on post-contrast studies (Figure 15).4 It may be difficult todifferentiate tuberculous abscesses from caseatingtuberculous granulomas and pyogenic abscesses, sincerim enhancement may be seen in all 3 conditions.3,4,6

The spinal cord may be involved with parenchymalTB myelitis and tuberculoma formation, or as compli-cations of arachnoiditis (e.g. infarction or syrinomyelia)[Figures 16 and 17].3,14

Contrast-enhanced MRI is superior to CT scanning orunenhanced MRI for the demonstration of CNS TB,4


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Figure 10. Spinal tuberculosis meningitis affecting the lumbar spine in a 34-year-old man. (a) Sagittal T1-weighted magnetic resonanceimaging of the lower thoracic and lumbar spine shows no abnormality. (b) Sagittal T2-weighted magnetic resonance imaging is alsounremarkable. (c) Sagittal and (d) axial enhanced T1-weighted magnetic resonance imaging with fat suppression show intense enhance-ment of the subarachnoid space indicating arachnoiditis. Loculation of cerebrospinal fluid is demonstrated posteriorly in the lowerthoracic spinal canal (arrows).

(a) (b)

(c)

(d)


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Figure 11. Caseating tuberculosis granuloma involving the lefttemporal lobe in a 48-year-old woman. Contrast-enhanced com-puted tomography scan shows a rim-enhancing lesion in the lefttemporal lobe consistent with a caseating tuberculosis granuloma.

Figure 12. Tuberculosis granulomas and cerebritis in a 21-year-oldwoman. (a) Axial T2-weighted magnetic resonance imaging demon-strates a mixed hypo- and hyperintense mass in the left posteriorparasagittal region, associated with hyperintense oedema. Other smallhyperintense foci are noted in the left periventricular region. (b) Axial T1-weighted magnetic resonance imaging after intravenous gadoliniuminjection reveals irregular rim enhancement of the caseating tuberculo-sis granuloma. Other periventricular foci of T2 signal changes shown inFigure 12a, which did not show enhancement, are presumably foci oftuberculous cerebritis.

Figure 13. Miliary cerebral and cerebellar tuberculosis in a21-year-old woman. Coronal enhanced T1-weighted magneticresonance imaging reveals intense nodular enhancement in thecerebrum and cerebellum.

Figure 14. Caseating tuberculosis granuloma involving the leftthalamus and causing obstructive hydrocephalus in a 21-year-oldwoman. Coronal T1-weighted magnetic resonance imaging afterintravenous gadolinium injection reveals thick irregular rim en-hancement of the caseating tuberculosis granuloma compressingonto the third ventricle and causing obstructive hydrocephalus.

(a)

(b)


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(a) (b)

Figure 15. Tuberculosis abscess and granulomas in a 21-year-old woman. (a) Axial T2-weighted magnetic resonance imaging reveals alarge hypointense left cerebellar lesion with associated oedema. Another small low-signal lesion containing a central dot-like high signalis noted in the right cerebellar hemisphere (arrow), also with surrounding hyperintense oedema. (b) Axial T1-weighted magnetic reso-nance imaging after intravenous gadolinium injection reveals a uniformly thin smooth wall of enhancement surrounding the large leftcerebellar lesion consistent with a tuberculosis abscess, and solid nodular enhancement of several contiguous tuberculosis granulomas.The tiny right cerebellar lesion shows rim enhancement and is consistent with a caseating soft tuberculous granuloma.

Figure 16. Non-caseating tuberculous granulomas involving the cervical spinal cord, with associated oedema, in a 63-year-old man. (a)Sagittal T2-weighted magnetic resonance imaging shows hyperintensity in the cervical spinal cord extending from C2 to C7 levels con-sistent with oedema. A hypointense nodule representing the granuloma is noted at the C4 level. Underlying cervical spondylotic changesare present. (b) Sagittal T1-weighted magnetic resonance imaging and (c) axial T1-weighted magnetic resonance imaging with fat sup-pression after intravenous gadolinium injection reveal an area of solid nodular enhancement representing non-caseating tuberculosisgranuloma of the spinal cord. A smaller enhancing granuloma is also noted at the C2 level on the sagittal image.

(a) (b) (c)


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Figure 17. Spinal tuberculosis meningitis in a 64-year-old woman. (a) Sagittal T1-weighted magnetic resonance imaging after intravenousgadolinium injection shows intense enhancement of the subarachnoid space indicating arachnoiditis. (b) Sagittal T2-weighted magneticresonance imaging shows hyperintense changes in the cervical spinal cord that did not enhance on the post-contrast study, presumablyrepresenting myelitis and associated oedema.

(a) (b)

and is currently the best imaging modality for thedemonstration of the meningeal disease, parenchymalabnormalities, complications, and for the follow-upof lesions. The multiplanar capability of MRI offersadditional advantage for the localisation of lesions(Figure 18).

Other conditions which may give rise to MRI findingssimilar to cranial and spinal TB include other infectiousand non-infectious inflammatory diseases such asfungal infection and sarcoidosis, metastatic tumours(arising within or outside the CNS), and multicentricprimary neoplastic disease (such as gliomata).3

CONCLUSIONImaging features of CNS TB have been outlined. MRIwith contrast administration is more sensitive than CTscanning or unenhanced MRI for the detection of lesions,and has the advantage of multiplanar capability. Densebasal meningeal enhancement is a typical finding, andcomplications include hydrocephalus, abscess for-mation, and vasculitis leading to infarction. TB menin-gitis and parenchymal tuberculosis are important

differential diagnoses when hydrocephalus and multi-ple enhancing lesions are noted in the CNS. Radio-logists and clinicians should be familiar with the imagingfeatures of this disease entity in order to achieve earlydiagnosis and treatment. Radiological imaging playsan important role in the diagnosis and monitoring ofthe disease, and for assessment of complications.

ACKNOWLEDGEMENTSThe authors thank Ms Elaine Chan, Ms Shalla Liu, MsKarman Wong, Mr Gilbert Lee, and Mr Peter Lim ofthe Department of Radiology, and Mr Cheng Kai Chiof the Medical Media Unit, Pamela Youde NethersoleEastern Hospital, for their assistance.

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Figure 18. Combined tuberculosis of basal meninges and cerebral parenchyma in a 25-year-old-woman. (a) Axial and (b) coronal T1-weighted magnetic resonance imaging after intravenous gadolinium injection shows multiple small right temporal lobe granulomata, andintense meningeal enhancement in the right ambient cistern consistent with leptomeningeal tuberculosis. (c) Contrast-enhanced com-puted tomography scan and (d) axial T1-weighted magnetic resonance imaging after intravenous gadolinium injection, performed 10months later for follow-up, show striking nodular enhancing lesions in the right temporal lobe, indicating unsatisfactory response totreatment. Mild linear enhancement in the right ambient cistern is suggestive of partial resolution of the tuberculosis meningitis.

(a) (b)

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spinal tuberculous variety. In: Spillane JD, editor. Tropicalneurology. London: Oxford University Press; 1973:63-72.

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