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nfection by Mycobacterium tuberculosis has affected human-kind for thousands of years. It is believed that Aristotle was

he first to recognize the disease; however, the discovery ofhe specific infectious agent took several centuries, until882, when Dr. Koch isolated the bacillus.1,2

Due to the poor socioeconomic conditions of most of theopulation in the Western countries at the end of the 18thnd beginning of the 19th centuries, the morbidity and mor-ality related to infection by tuberculosis (TB) was very high.3

t the end of the 19th and beginning of the 20th centuries,ith the improvement of the socioeconomic environment,

he appearance of better diagnostic tools, including the use of-rays (1895), and the discovery of antibiotics such as strep-

omycin (1940), the disease was thought to be virtually underontrol, persisting endemically only in underdevelopedountries.4 Nevertheless, the global increase in the incidencef tuberculosis in the 1990’s, in immunocompetent as well asn immunocompromised patients, led the World Health Or-anization (WHO) to declare TB as a global emergency.5 It isstimated that between 1997 and 2020 approximately 1 bil-ion people will acquire the infection and that 70 millioneople will die of TB.2,6 The two factors that have contributedo the reappearance of TB include infection in HIV� patientsnd the appearance of multidrug-resistant TB.7-15

In countries with low incomes the predisposing factors areoverty and HIV-associated TB. Examples of this are sub-aharan Africa and Southeast Asia.16,17 In highly developedountries, 80% of TB affects the elderly and is directly relatedo poverty.15,18 The HIV/AIDS epidemic is also a determiningactor in the increase of TB incidence in developed countries,here the incidence of TB may be as high as 3%.6,19-21 Theresence of HIV/AIDS increases the risk of TB by a factor of30%, in contrast with other disorders that are accompaniedy immunodeficiencies such as diabetes, renal insufficiency,ancer, and immunosuppressive therapies where the risk ofB is 3 to 17 times higher.8

Since 1940, when streptomycin was introduced as the only

Departments of Radiology, Instituto Neurológico de Antioquia (INDEA),Hospital Pablo Tobón Uribe and Universidad de Antioquia, Medellín,Colombia.

University of North Carolina School of Medicine, Chapel Hill, NC, USA.ddress reprint requests to: Andrés Arbeláez, MD, Instituto Neurológico de

Antioquia (INDEA), Calle 55 46-36, Medellín, Colombia. E-mail:

1andres.arbelaez@rilan.org.

74 0037-198X/04/$-see frontmatter © 2004 Elsevier Inc. All rights reserved.doi:10.1053/j.ro.2004.06.003

rug for TB treatment, resistance was observed and controlledith the simultaneous use of two other drugs. As a result, virtu-

lly no cases of resistance were observed between 1960 and980.22 In 1990, mycobacterium strains resistant to isoniazide

n 14.2% of patients and to isoniazide and Rifampicin in 3.5% ofatients were observed in USA. In New York, as much as 20% ofases with TB-HIV are resistant to the traditional drugs.23 Thelinical profile of patients with multidrug-resistant TB is similaro that of the nonresistant form; however, mortality is higher,eaching up to 20%, in immunocompetent subjects and up to0% in immunocompromised subjects even with aggressivereatments.24

Although TB is usually limited to the lungs, it can affectny organ system.7 TB infection of the central nervous systemCNS) is almost always the result of a hematogenous dissem-nation and can present in different forms, including menin-itis, tuberculoma(s), abscess(es), and cerebritis.9,11,21,25,26 Inractical terms, CNS TB may be divided into a diffuse typeuch as meningitis, or a localized type such as parenchymalesions.

Infection of the CNS is present in 2.5% of patients with TBnd in 10% of patients with TB associated with AIDS and isonsidered one of the most severe and feared forms of theisease due to its high mortality and complications and se-uelae associated with it.20

Brain imaging studies allow for early diagnosis of CNS TB,nd contrast enhanced magnetic resonance imaging (MRI) ishe method of choice for diagnosis and follow-up. In thisrticle we review the different forms of presentation of cere-ral TB and their imaging manifestations.

eningeal Tuberculosiseningeal tuberculosis is the most common presentation ofNS TB and is seen most frequently in children and adoles-ents.11,20,26,27 Isolated tuberculous meningitis is infrequentnd represents less than 5% of all meningitis in children andess than 17% of all cases of CNS TB. Meningeal TB is foundenerally in undernourished patients, with protein and ca-oric malnutrition and with a low socioeconomic level, par-icularly in the Black and Hispanic populations and in pa-ients older than 65 years of age.28,29 The majority of childrenith TB meningitis also have a diffuse miliary infection and

1% of patients have parenchymal and meningeal le-

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ions.25,27,30 In a series of 54 patients evaluated in one of ournstitutions (HUSVP, Medellín, Colombia), 73.9% of thehildren and 28.5% of the adults with meningeal TB pre-ented with concomitant pulmonary TB.

The infection disseminates hematogenously from a distantocal point and the meningeal compromise is considered toccur due to rupture in the subarachnoid space of a micro-copic cortical, subependymal, and/or subpial lesions calledcenter of Rich.”26,27,31,32,33 The meningeal compromise canlso be secondary to the rupture of a tuberculoma into alood vessel, to miliary TB, or be acquired from tuberculousastoiditis.In meningeal TB, the subpial exudate is primarily located

n the inferomedial surface of the frontal, the anteromedialurface of the temporal lobes, the superior aspect of the cer-bellum, and the floor of the third ventricle (Figs. 1 and 2).rom these sites it disseminates to the interpeduncular cis-

igure 1 Axial contrast enhanced CT shows thick enhancing exudaten the Sylvian fissure and hydrocephalus.

igure 2 Coronal post contrast T1-weighted image shows enhance-ent of the right Sylvian fissure and a mild degree of hydrocepha-

mus.

ern and to the anterior part of the pontomesencephalic cis-erns.26 This granulomatous process is characterized by ahick exudate composed of neutrophils, mononuclear cells,rythrocytes, and bacilli in the basal portions of the brain, thenterpeduncular, ambiens, and suprasellar cisterns. In theate stages of the disease, the leptomeningeal process extendso the convexities and to the ependymal surfaces of the ven-ricles.20 Morbidity due to TB is high and a delay in treatmentesults in severe sequelae; therefore, early diagnosis andreatment are important to diminish the morbidity and mor-ality.11,27

Clinical manifestations of meningeal TB are photophobia,ever, cephalea, nausea, vomiting, and nuchal rigidity. Theisease may present with seizures, signs of intracranial hy-ertension, focal motor deficits, or with paralysis of the cra-ial nerves. The CSF shows lymphocytic pleocytosis, aarked increase in proteins, and decreased glucose level.Despite the lack of specific signs, neuroimaging studies

an be useful in the early diagnosis of meningeal TB. CThows obliteration of the basal cisterns and plaque-like duralhickening. In some cases of chronic TB meningitis, duralalcifications in the basal cisterns may be found.11,34 Afterontrast administration, there is diffuse enhancement of theasal cisterns, which may extend to the convexities, tento-ium, and Sylvian fissures30,32 (Figs. 1-3).

MRI findings vary depending on the stage of the disease. Inarly stages, T1-weighted images without contrast may beormal. Later, there may be widening of the subarachnoidpaces with associated T1 and T2 shortening of the CSF.27,35

ost contrast T1-weighted images show enhancement which

igure 3 Axial post contrast T1-weighted image shows thick andomewhat nodular enhancement of the tentorium.

ay be pronounced in the basal cisterns and Sylvian fis-

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ures7,9,11,20,32,36 (Fig. 2). Extension of the inflammatory pro-ess to the ventricular system may result in choroid plexitis.37

Complications of meningeal tuberculosis include hydro-ephalus, focal infarctions, atrophy, and very rarely syrin-obulbia7,35 (Figs. 4 and 5). Hydrocephalus is the most fre-uent complication and develops mainly in children (in oureries, 100% of the children developed some degree of ven-ricular dilation). Hydrocephalus portrays a poor prognosis,specially in children. Involvement of the cisterns may resultn “communicating” hydrocephalus. Additionally, extensionnd narrowing of the fourth and third ventricles and of thequeduct may result in “noncommunicating” hydrocepha-us.26,29 The hydrocephalus produced by tuberculous men-ngitis is usually persistent and progressive and leads to tran-ependymal edema. CT is a good method for the sequentialollow-up of hydrocephalus.25,30

Parenchymal infarcts are also a common complication ofasal tuberculous meningitis.11,26,27 The presence of exudate

n the basal cisterns may compromise the blood vessels, re-ulting in stenosis or occlusion, leading to ischemia. Theost affected blood vessels are the deep perforating arterieshich may lead to infarctions in the basal ganglia, internal

apsules, brainstem, and cerebellum. In 20 to 38% of pa-ients with CNS TB, CT shows poorly defined hypodensenfarcts that occasionally may enhance25,38 (Fig. 4). In MRI,he infarcts are typically hypointense on T1 and hyperintensen T2; edema and enhancement with contrast media varyepending on the age of the lesions. FLAIR images are moreensitive in the detection of acute and chronic infarctions in

30

igure 4 Axial post contrast CT shows enhancement and obliterationf cortical sulci, hydrocephalus, and an acute infarction in the rightasal ganglia.

he supratentorial brain. Diffusion-weighted images are the o

gold standard” for the diagnosis of acute infarctions. MRngiography may show stenoses of the major arteries (Fig. 5).

Another potential complication is involvement of the cra-ial nerves, which occurs in 17 to 70% of patients. Theirompromise may be secondary to ischemia or mass effect byuberculomas. The most affected cranial nerves are II, III, IV,I, and VII. MRI shows thickening and enhancement of theffected cranial nerves, particularly in their cisternal por-ions.39,40

The differential diagnosis of tuberculous meningitis includesther infections such as viruses, fungi, and parasites. Noninfec-ious causes, such as rheumatoid disease and sarcoidosis, andrimary or secondary neoplasias compromising meningeal sur-aces, should also be considered.11,20,21,27

arenchymal Tuberculosisarenchymal disease may be isolated or associated with basaleningitis and presents usually as tuberculomas. It can alsoanifest as cerebral abscesses, focal areas of cerebritis, or

arely as TB encephalopathy. Focal intracranial lesions oftenoexist with low CD4� counts, typically less than 100 cells/L.41,42

uberculomashese lesions originate as a conglomerate of microgranulo-as in areas of TB cerebritis. Later they form a mature non-

aseating tuberculoma. Tuberculous granulomas (or tuber-ulomas) usually disseminate hematogenously and areocated at the cortico-medullary (gray/white) junctions. Mostre infratentorial in children and supratentorial in adults andffect the frontal and parietal lobes mainly.43 Their occur-ence in other locations may be explained by extension alonghe perivascular spaces.11 Histologically they are rounded orval masses or sometimes multilobulated due to the fusion ofeveral smaller nodules. They are not necrotic initially, butheir center becomes necrotic eventually. They present with aelatinous capsule that contains collagen fibers and giantells associated with surrounding gliosis.

Due to the nonspecificity of the clinical manifestations andecause CSF studies tend to be negative, diagnosis is oftenased on neuroimaging findings. The “target” sign, which isharacterized by a central area of calcification surrounded by

igure 5 Frontal view from an MR angiogram shows multiple areas

f stenoses in the middle and anterior cerebral arteries.

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Cerebral tuberculosis 477

rim of enhancement, is considered to be typical of tubercu-ous lesions. Noncaseating granulomas usually appear solid,re hypodense or isodense on CT, and enhance homoge-eously with contrast media. On MRI they are hypointense tohe brain on T1 and T2 sequences, probably due to the pres-nce of free oxygen radicals in macrophages.11 They may also

Figure 6 A. Axial post contrast CT shows an irregular ensurrounding edema, mass effect, and mild prominenT1-weighted image shows similar findings. C. Axial T2and the focal central hypointensity within the lesion. D.in the lesion.

e hyperintense on T2-weighted images and have homoge- s

eous enhancement.44 Caseating granulomas have varyingppearances depending on whether their contents are solidr liquid. On CT, solid granulomas are heterogeneous lesionsnhancing peripherally, and on MRI they are iso- or hypoin-ense on T1 and T2 sequences with ring enhancement afteradolinium administration and are typically accompanied by

g lesion in the left posterior temporal region. There ishe lateral ventricles. B. Corresponding post contrastted image shows the hyperintense surrounding edemaLAIR image also shows the focal central hypointensity

hancince of t-weighAxial F

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hypointense capsule, a center that is hypointense on T1,yperintense on T2, and ring enhancement7,27,40,45,46,47 (Fig.). The degree of hypointensity of the central caseum de-ends on the presence of fibrosis/gliosis, macrophage (andheir free oxygen radicals) infiltration.21,27,46,47 The caseumas high lipid content that may be identified on proton MRpectroscopy.47,48 Images obtained with magnetization trans-er may be useful in the diagnosis of tuberculomas.21 Theifferential diagnosis of tuberculous granulomas includesther infectious granulomatous lesions such as cysticercosis,ungal lesions, and primary and metastatic tumors.49,50

uberculous Abscessesuberculous abscesses are rare. They occur in less than 10%f patients with CNS TB.20,51 They may be solitary or multiplend are more frequent in the elderly or in immunocompro-ised patients.27,32,52 These abscesses are similar to pyogenic

nes. TB abscesses contain a purulent center that is rich inubercular bacilli, unlike a caseous tuberculoma, which con-ains few bacilli. Clinical signs are usually severe and includeever, neurological deficits, and headaches. The final diagno-is depends on the following criteria: macroscopic evidencef pus in the abscess cavity, presence of AFB, or growth of M.uberculosis in culture.41,51 The CD4� counts of patients witherebral TB abscesses are between 112 and 270 cells/�L.53,54

IV� patients need to be managed with antituberculous andetroviral drugs.55

In imaging studies, a TB abscess may be indistinguish-ble from a caseating tuberculoma or a pyogenic abscess.owever, a TB abscess has thinner and smoother walls, is

igure 6 E. Axial trace diffusion weighted image shows that theesion is of relatively low signal intensity unlike a pyogenic abscesshat would have been very bright.

ommonly multiloculated, and is larger (generally more s

han 3 cm in diameter), its walls enhance and it has pe-ipheral edema41,48 (Fig. 7 and 8). The end result of manyocal parenchymal brain TB infections is calcificationFig. 9).

igure 7 Axial contrast enhanced CT shows multilobulated lesionrobably arising in the left thalamus. There is surrounding edemand mass effect as well as hydrocephalus.

igure 8 Axial contrast enhanced CT showing a multilobulated, ringnhancing mass in the right periventricular region with extensive

urrounding edema and mass effect.

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iliary Tuberculosisiliary TB or disseminated TB presents when the host’s im-une system is unable to contain the infection. This type ofB is generally associated with meningeal involvement. Theajority of patients present with pulmonary disease or an-

ther site of primary involvement.56 Brain lesions are locatedt the cortical–medullary junctions due to hematogenous dis-emination. The lesions are usually small (3 mm in diameter)nd generally asymptomatic. MRI shows small lesions thatre hypointense on T2-weighted sequences and which mayave ring enhancement21,56 (Fig. 10). CT may also show these

esions (Fig. 11).

B Encephalopathyhis type of TB is typically found in preschool and school-ge children and presents with diffuse compromise of thehite matter and no masses or meningeal involvement. Its

tiology seems to be due to a type IV hypersensitivityeaction, which depends on T-lymphocytes, which are re-ctive to a tuberculin protein. Neuroimaging studies, bothT and MR, show severe uni- or bilateral cerebral edema.he T2 signal hyperintensity in the white matter is due toyelin loss with depletion of oligodendroglia and astro-

26,57

igure 9 Axial non contrast CT shows heavily calcified mass in theedial left frontal lobe and possibly also in the genu of the corpus

allosum. This mass is the sequelae of a treated tuberculoma. Theres diffuse atrophy and prominent ventricles.

yte increases. l

onclusionhe incidence of tuberculosis of the central nervous sys-

em has recently increased, in both immunocompetentnd immunocompromised patients. The involvement issually complex and potentially devastating. Imaginganifestations are often nonspecific; however, it is impor-

ant to be familiar with the patterns manifested by theisease to provide an accurate diagnosis, which may leado rapid initiation of treatment and to the appropriateaboratory and histological tests to diminish morbiditynd mortality. It is also to be remembered that in addition

igure 10 Contiguous coronal post contrast T1-weighted imageshow left-sided meningeal enhancement with an underlying area oferebritis and early abscess formation. There are also focal enhanc-ng lesions in the pons and superior right temporal region (the latteras extensive surrounding edema). Some meningeal enhancement

s also present elsewhere.

igure 11 Axial post contrast CT shows multiple small enhancing

esions that have little or no surrounding edema.

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o the brain (which was the main topic of this review), TBay involve also the spinal cord, spinal column, eyes,

kull, paranasal sinus, and the upper aero-digestive tract.

cknowledgmente thank Isabel Barbal for help in translating this paper.

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