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  In this Article
 »  Abstract
 » Introduction
 »  Pathogenesis and...
 »  Clinical Feature...
 » Chest Imaging
 » Neuroimaging
 »  Meningeal Inflam...
 » Infarcts
 » Angiography
 » Hydrocephalus
 »  Tuberculoma and ...
 » Cerebritis
 » Ventriculitis
 »  Spinal Cord Invo...
 » Paradoxical Response
 »  Human Immunodefi...
 »  Miliary Tubercul...
 »  Multidrug-Resist...
 »  Advanced Magneti...
 »  Differential Dia...
 » Conclusion
 »  References
 »  Article Figures
 »  Article Tables

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Table of Contents    
Year : 2016  |  Volume : 64  |  Issue : 2  |  Page : 219-227

Neuroimaging in tuberculous meningitis

1 Department of Neurology, King George Medical University, Lucknow, Uttar Pradesh, India
2 Department of Microbiology, King George Medical University, Lucknow, Uttar Pradesh, India

Date of Web Publication3-Mar-2016

Correspondence Address:
Ravindra Kumar Garg
Department of Neurology, King George Medical University, Lucknow - 226 003, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.177608

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 » Abstract 

Tuberculous meningitis is a serious infection caused by Mycobacterium tuberculosis. Early diagnosis is the key to success of treatment. Neuroimaging plays a crucial role in the early and accurate diagnosis of tuberculous meningitis and its disabling complications. Magnetic resonance imaging is considered superior to computed tomography. Neuroimaging characteristics include leptomeningeal and basal cisternal enhancement, hydrocephalus, periventricular infarcts, and tuberculoma. Partially treated pyogenic meningitis, cryptococcal meningitis, viral encephalitis, carcinomatous, and lymphomatous meningitis may have many similar neuroimaging characteristics, and differentiation from tuberculous meningitis at times on the basis of neuroimaging characteristics becomes difficult.

Keywords: Computed tomography; hydrocephalus; infarction; magnetic resonance imaging; radiculomyelitis; tuberculosis

How to cite this article:
Garg RK, Malhotra HS, Jain A. Neuroimaging in tuberculous meningitis. Neurol India 2016;64:219-27

How to cite this URL:
Garg RK, Malhotra HS, Jain A. Neuroimaging in tuberculous meningitis. Neurol India [serial online] 2016 [cited 2021 Jun 20];64:219-27. Available from:

 » Introduction Top

Tuberculous meningitis is a serious central nervous system infection caused by Mycobacteriumtuberculosis. The disease predominantly involves the brain and the meninges, but affects the spinal cord as well. The clinical diagnosis can be difficult; therefore, imaging plays an important role in establishing the diagnosis and in evaluating its complications.

According to the latest World Health Organization report, there were an estimated 11 million prevalent cases of tuberculosis. Of the estimated 9 million people who developed tuberculosis in 2013, more than half (56%) were in the South-East Asian and Western Pacific regions. There were an estimated 1.5 million tuberculosis deaths in 2013. Globally, an estimated 3.5% of new cases and 20.5% of previously treated cases have drug-resistant tuberculosis. In 2013, an estimated 1.1 million (13%) of the 9.0 million people who developed tuberculosis worldwide were human immunodeficiency virus (HIV)-positive.[1] Among the 6.1 million new cases notified in various National Tuberculosis Control Programmes, 0.83 million patients had extrapulmonary tuberculosis including central nervous system tuberculosis.[1] In the European Union/European Economic Area, from 2002 to 2011, 868,726 cases with tuberculosis were reported and of these, 167,652 (19.3%) had extrapulmonary tuberculosis. Tuberculous meningitis was seen in approximately 2.9% (3279) of the cases.[2] In the United States, among 253,299 cases, 18.7% were having extrapulmonary tuberculosis, including meningeal tuberculosis in 5.4% of patients.[3]

Approximately 50% of patients with tuberculous meningitis either die or become disabled. In Africa, adult tuberculous meningitis has a very high mortality (60%), which has not changed over several decades.[4],[5]

 » Pathogenesis and Pathology Top

Tuberculous meningitis is caused by M. tuberculosis, which spreads hematogenously to the meninges and brain parenchyma from the lungs (a primary site of infection). Subsequently, multiple small tuberculous granulomas are formed in the subpial and subependymal surfaces of the brain and spinal cord. Rupture of these tuberculomas and release of M. tuberculosis in the cerebrospinal fluid (CSF) results in pathogenic mechanisms responsible for tuberculous meningitis. The most characteristic pathologic feature of tuberculous meningitis is meningeal inflammation and formation of thick gelatinous exudates in the basal parts of the brain. The brain tissue underlying the tuberculous exudates shows varied degrees of inflammation which is termed as “border zone encephalitis.” Changes in cerebral vessels develop while arteries of the Circle of Willis pass through the basilar exudates and get strangulated. The vascular changes are characterized by inflammation, spasm, constriction, and eventually thrombosis of cerebral vessels. Occlusion of cerebral arteries leads to infarction of the brain parenchyma. Obstruction to the flow of CSF by thick exudates results in hydrocephalus. The optic chiasma and the roots of other cranial nerves arising from the ventral aspect of the brainstem are usually entrapped in thick exudates. Exudates can be seen surrounding the lower part of the spinal cord and cauda equina resulting in tuberculous radiculomyelopathy. Infrequently, tuberculous meningitis may results in the formation of tuberculomas consisting of caseous necrotic tissue, epithelioid cell granuloma, and mononuclear cell infiltration. Multiple small cerebral and spinal tuberculomas are seen when tuberculous meningitis is a manifestation of miliary tuberculosis.[6],[7],[8]

 » Clinical Features and Diagnostic Criteria Top

Headache, vomiting, meningeal signs, focal deficits, vision loss, cranial nerve palsies, and raised intracranial pressure are the characteristic clinical features of tuberculous meningitis. The sixth cranial nerve is the single most frequently involved cranial nerve. Visual loss, secondary to optic nerve involvement, is a disabling complication. If the patient remains untreated, confusion and coma follow over the ensuing days. CSF examination is crucial for an early and reliable diagnosis of tuberculous meningitis. Typical changes include lymphocytic pleocytosis, decreased glucose levels, and elevated protein levels. The gold standard for microbiological confirmation is the demonstration of M. tuberculosis in the CSF. Bacteriological confirmation is performed either by smear examination after Ziehl–Neelsen staining or by culture. All currently available definitive diagnostic tests for tuberculous meningitis are inadequate; hence empirical treatment is often needed.[9],[10]

 » Chest Imaging Top

Chest radiography is abnormal in a large number of patients with tuberculous meningitis. In one study, chest roentgenography demonstrated abnormal findings in 43% (32/74) cases. Hilar adenopathy, miliary pattern, and bronchopneumonic infiltrates were the more frequent abnormalities. The chest computed tomography (CT) scan was more sensitive (68/74) in detecting chest abnormalities. Mediastinal and hilar lymphadenopathy, miliary pattern, and bronchopneumonic infiltrate were frequent CT findings. The presence of tuberculosis elsewhere often provides a great help in establishing the diagnosis of tuberculous meningitis.[11]

 » Neuroimaging Top

Both CT and magnetic resonance (MR) scans are valuable for the assessment of the complications of tuberculous meningitis. MR imaging (MRI) is considered better. In early stages, neuroimaging may not reveal any abnormality. The neuroimaging characteristics of tuberculous meningitis classically include leptomeningeal and basal cisternal enhancement, ventriculomegaly due to hydrocephalus, periventricular infarcts, and the presence of tuberculomas.[12] A retrospective review of CT findings in 289 patients with tuberculous meningitis revealed that 254 (88%) patients had some form of imaging abnormality. The common changes included hydrocephalus (204 patients), parenchymal enhancement (62 patients), contrast enhancement of basal cisterns (49 patients), cerebral infarcts and focal or diffuse brain edema (39 patients), and one or more cerebral tuberculomas (14 patients).[13]

 » Meningeal Inflammation Top

Meningeal inflammation is defined as the enhancement of pia-arachnoid after administration of a contrast material. Abnormal meningeal enhancement extends into the subarachnoid spaces of the sulci, basal cisterns, along the inner table of the skull, and in dural folds of the falx and tentorium. Tentorial and cerebellar meningeal enhancement are much less common. The exudate is characterized by a thick area of enhancement in the region of the basal cistern and the Sylvian fissure. Basal meningeal enhancement, in fact, demonstrates thick basilar exudates. The interpeduncular fossa, pontine cistern, ambient cistern, suprasellar cisterns, and Sylvian fissures are the sites of predilection for the thick basilar exudates. Sulci over the convexities are less dominantly affected.[14] Andronikou et al., noted that the presence of high-density signal changes within the basal cisterns on non-contrast-enhanced CT is a very specific sign of tuberculous meningitis in children.[13]

Optochiasmatic arachnoiditis is a characteristic form of tuberculous meningitis that clinically manifests as severe visual loss. In patients with optochiasmatic arachnoiditis, thick basal exudates are dominantly present in the interpeduncular, suprasellar, and Sylvian cisterns. Contrast-enhanced CT scans may demonstrate the characteristic “spider leg appearance” because of intense homogenous enhancement of thick exudates in the basal cisterns. MRI depicts confluent enhancing lesions in the interpeduncular fossa, pontine cistern, and the perimesencephalic and suprasellar cisterns. The exudate encases the optic chiasma and the optic nerves. Optochiasmatic arachnoiditis may even develop paradoxically while the patient is being treated with antituberculous treatment. In patients with sellar tuberculomas, neuroimaging reveals a densely enhancing sellar mass with enhancement and thickening of the pituitary stalk. Frequently, optochiasmatic arachnoiditis is associated with marked hydrocephalus that further contributes to progressive vision loss [15],[16] [Figure 1] and [Figure 2].
Figure 1: Contrast-enhanced computed tomography reveals the thick basilar exudate with the “spider leg” appearance

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Figure 2: Contrast-enhanced magnetic resonance images show optochiasmatic arachnoiditis

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 » Infarcts Top

Infarcts in patients with tuberculous meningitis are characterized by an area of abnormal signal intensity in a vascular distribution without any evidence of mass effect. MR is more sensitive in detecting infarcts in these patients. Diffusion-weighted MR is especially sensitive in detecting infarcts when findings on the T2-weighted (T2W) MRI are normal.[17] In a meta-analysis that included 404 patients, infarcts, at the time of diagnosis, were present in approximately 25% of patients. Out of 33 patients who had a follow-up MRI, 5 (15%) had developed new infarcts. Infarcts, in tuberculous meningitis are often multiple, bilateral, and located in the periventricular regions of brain (affecting basal ganglia, thalamus, and internal capsule). Periventricular infarcts are often attributed to inflammation of deep penetrating vessels particularly the origin of the lenticulostriate arteries. The larger vascular distribution of the anterior and middle cerebral arteries is less commonly involved. Stroke can also occur due to the involvement of major vessels of Circle of Willis. Infarction may be asymptomatic, but can also cause severe disability and death [18] [Figure 3].
Figure 3: Magnetic resonance imaging of the brain depicts the presence of an acute infarct in the left basal ganglia on T2 (a), fluid attenuation inversion recovery (b), and diffusion-weighted (c) sequences. An old left border-zone infarct, leading to gliosis, may be noted in addition. Intracranial angiography (d) is suggestive of nonvisualization of the left middle cerebral artery (red arrows)

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 » Angiography Top

Angiography, frequently, reveals small segmental narrowing, uniform narrowing of large segments, irregular beaded appearance of vessels, or complete occlusion. The terminal portions of the internal carotid arteries and proximal parts of the middle and anterior cerebral arteries are the commonly involved vessel segments. Both MR and CT angiography have been found to be valuable in detecting vascular abnormalities.[19] Recently, transcranial Doppler imaging has been found to be an useful tool for the assessment of vessels of Circle of Willis in children. Basilar artery stenosis, secondary to vasculitis, was observed in the majority of pediatric patients suffering from tuberculous meningitis [20] [Figure 3].

 » Hydrocephalus Top

One of the common complications of tuberculous meningitis is hydrocephalus, which can readily be demonstrated by both MR and CT imaging. Hydrocephalus, on imaging, is defined as enlargement of the ventricles with the Evan's ratio (maximal width of frontal horns/maximal width of the inner skull) being more than 30%, and/or the size of one or both temporal horns being >2 mm. Hydrocephalus in tuberculous meningitis is of two types – the communicating, and the obstructive or noncommunicating types. On neuroimaging, communicating hydrocephalus is characterized by a dilated fourth ventricle. Fourth ventricle remains unaffected in obstructive or noncommunicating hydrocephalus. CT pneumoencephalography or contrast-enhanced cisternography, done via a lumbar puncture, may help in differentiating communicating and noncommunicating hydrocephalus.

In addition to ventriculomegaly, periventricular hypodensity on CT imaging, and periventricular hyperintense signal on fluid attenuation inversion recovery (FLAIR) and T2W images of MRI indicate the presence of interstitial edema caused by the periventricular ooze of CSF secondary to increase in intraventricular pressure [21] [Figure 4].
Figure 4: Axial T2 (a), fluid attenuation inversion recovery (b), and T1-gadolinium [GAD] (c) images, coronal T2 (d) image, and sagittal T2 (e) image of magnetic resonance scans of the brain show hydrocephalus and basal exudates in a patient having definite tuberculous meningitis. Magnetic resonance imaging of the spine depicts the presence of arachnoiditis in the same patient in sagittal T2 (f), sagittal T1-GAD (g, red arrows), and axial T2 images (h, red arrowheads)

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 » Tuberculoma and Tuberculous Abscess Top

Tuberculomas in patients with tuberculous meningitis are characterized as discrete or coalescing lesions, which demonstrate homogeneous or ring enhancement and have irregular walls of varying thickness. Tuberculomas are either solitary, multiple, or miliary. Numerous miliary tuberculomas are common in patients with miliary pulmonary tuberculosis. Miliary tuberculomas may be located anywhere within the brain parenchyma, although they most commonly occur within the frontal and parietal lobes [22],[23] [Figure 5].
Figure 5: Roentgenogram of the chest (a) and contrast-enhanced computed tomography of the thorax (b) depict the miliary shadowing observed in a patient having definite tuberculous meningitis. Axial T1-weighted fat-suppressed spoiled gradient-echo (SPGR) gadolinium (GAD)-enhanced magnetic resonance image of the brain (c) shows multiple tuberculomas of various sizes involving different parts of the brain parenchyma

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On the basis of MR characteristics, two predominant types of tuberculomas in tuberculous meningitis have been described. Caseating tuberculomas with a liquid core are often hypointense on T1W images. On T2W images, in central portion of the granuloma, there is hyperintensity along with a peripheral hypointense rim representing the capsule of the tuberculoma. Ring enhancement is usually seen after contrast administration. There is usually a variable amount of perilesional edema, which is hyperintense on T2W or FLAIR images. On diffusion-weighted imaging, the tuberculoma shows restriction with low intensity on apparent diffusion coefficient images. Noncaseating (nonnecrotizing) tuberculomas are usually hypointense on T1W images and hyperintense on T2W images. Often, there is homogeneous enhancement of the entire tuberculous lesion.

MR spectroscopy helps in differentiating tuberculous and nontuberculous brain lesions, since tuberculous lesions demonstrate a characteristic lipid peak. Disintegration of the mycobacterial cell wall and its lipid content within the tuberculoma is considered to be responsible for the marked elevation of the lipid peak.[22]

Tuberculous abscesses are rarely encountered complications of tuberculous meningitis. Tuberculous abscesses are usually larger in size than tuberculomas (often <3 cm in diameter), solitary, thin-walled, and multiloculated. Diffusion-weighted MRI in tuberculous abscesses demonstrates a restricted diffusion with low apparent diffusion coefficient values.[23]

 » Cerebritis Top

Tuberculous cerebritis on imaging appears as intense small areas of patchy enhancement with associated edema. Pathologically, cerebritis is characterized by a small tuberculous granuloma consisting of lymphocytic infiltrate, Langhans giant cells, epithelioid cells, and presence of occasional M. tuberculosis. Diffusion-weighted imaging helps in differentiating cerebritis from cerebral infarction. Restricted diffusion (hyperintense lesion) is seen in infarction, while cerebritis results in a more heterogeneous signal intensity on diffusion-weighted imaging and apparent diffusion coefficient imaging.[23],[24]

 » Ventriculitis Top

Ventriculitis is inflammation of the ependymal lining (ependymitis) and choroid plexus (choroid plexitis). On imaging, ependymitis presents with a thickened and enhanced ependymal lining, dilated ventricles, and presence of debris with irregular margins in dependent portions of the ventricles. Ventriculitis can also result in aqueductal obstruction due to inflammatory exudates. Inflamed choroid plexus appears as a unilaterally or bilaterally enlarged and intensely enhanced structure [25] [Figure 6].
Figure 6: Axial (a and b), coronal (c) and sagittal (d) T1-GAD images of magnetic resonance imaging of the brain depict multiple coalescing intraventricular tuberculomas associated with ventriculitis (red arrowheads)

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 » Spinal Cord Involvement Top

Tuberculous meningitis frequently affects the spinal cord and spinal nerve roots. Spinal cord involvement in tuberculous meningitis manifests in several forms, such as tuberculous radiculomyelitis, spinal tuberculoma, myelitis, syringomyelia, vertebral tuberculosis, and very rarely, spinal tuberculous abscess. Frequently, exceptionally high CSF protein content is a risk factor for spinal cord-related complications of tuberculous meningitis. Spinal cord and spinal nerve involvement, in contrast-enhanced MR, is demonstrated by diffuse enhancement of the cord parenchyma, nerve roots, and meninges. Other characteristic imaging features of spinal tuberculous meningitis include CSF loculations and obliteration of the spinal subarachnoid space with loss of outline of the spinal cord in the cervico-thoracic spine; CSF loculations often produce spinal cord compression. The spinal nerve roots in thoracic, lumbar, and sacral regions, may get matted in dense exudates and fibrous tissue in the subarachnoid space. Lumbosacral arachnoiditis is characterized by the irregularity of thecal sac, nodularity and thickening of nerve roots, and their clumping in later stages. Corticosteroids are often useful in these conditions.[26]

Syringomyelia is often a late complication of tuberculous arachnoiditis and is seen as cord cavitation that typically demonstrates CSF signal intensity on both T1- and T2-W images and does not enhance [26] [Figure 7] and [Figure 8].
Figure 7: T1-GAD magnetic resonance imaging of the brain of a patient having tuberculous meningitis depicts basal exudates (white arrowhead), tuberculomas, early hydrocephalus, and optochiasmatic arachnoiditis (white arrowhead) on axial (a) and coronal sections (b). Magnetic resonance imaging of the spine of the same patient shows the presence of hyperintense signals in the thoracic spinal cord (c, red arrow) on sagittal T2 sequence (e) and the presence of arachnoiditis along the entire extent of the spinal cord on sagittal T1-GAD sequence (d, red arrowheads)

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Figure 8: T1-GAD magnetic resonance imaging of the spine depicts intramedullary multiple coalescing tuberculous lesion along the cervical 4–6 segments on sagittal (a, red arrowhead) and coronal (b, red arrowhead) sections. Dural-based mulberry-shaped tuberculomas can be seen on sagittal (c, red arrowhead) and coronal (d, red arrowhead) sections of T1-GAD magnetic resonance imaging of the spine in a different patient

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In a prospective study, out of 71 patients, 33 (46.4%) had features suggestive of myeloradiculopathy and 22 (30.9%) patients had spinal cord involvement at inclusion. Eleven (15.4%) patients had a paradoxical spinal cord involvement. The most common imaging finding was spinal meningeal enhancement, seen in 40 (56.3%) patients; in 22 (30.9%) patients, enhancement was present in the lumbosacral region. Other MR abnormalities included myelitis in 16 (22.5%), tuberculoma in 4 (5.6%), CSF loculations in 4 (5.6%), cord atrophy in 3 (4.2%), and syringomyelia in 2 (2.8%) patients. A significant factor, that was frequently associated with myeloradiculopathy, was markedly raised CSF protein (>250 mg/dL).[27]

 » Paradoxical Response Top

Paradoxical reaction is defined as clinical worsening and/or appearance of newer imaging abnormalities of the brain and/or spinal cord after the initial improvement following antituberculous treatment. The paradoxical response usually occurs several weeks after starting antituberculous therapy. A variety of paradoxical complications have been reported in patients with tuberculous meningitis including enlargement of the preexisting brain tuberculomas and evolution of new tuberculomas, ventriculomegaly, and optochiasmatic and spinal arachnoiditis. Paradoxical response is thought to represent an exaggerated cell-mediated immune response against the mycobacterial antigens. Possibly, a massive release of mycobacterial proteins into the core of tuberculoma and subarachnoid space leads to intense inflammation causing an expansion of the existing tuberculous lesions [28] [Figure 9].
Figure 9: Computed tomography of the brain of two patients with definite tuberculous meningitis depicts the occurrence of hydrocephalus, as part of paradoxical reaction, in week 5 and week 6 after the initiation of anti-tuberculous treatment (a and b: Patient 1, c and d: Patient 2)

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 » Human Immunodeficiency Virus-Associated Tuberculous Meningitis Top

Most studies report no difference in the type or the presence of meningeal enhancement between the HIV-infected and HIV-uninfected tuberculous meningitis patients. The HIV-infected patients present more frequently with disseminated tuberculosis and systemic features of HIV infection. HIV infection, in a patient with tuberculous meningitis, does not change the clinical manifestations, laboratory, or neuroimaging findings, or the response to antituberculous treatment. However, diagnostic confusion prevails whenever neuroimaging shows a mass lesion within the cerebral parenchyma. In a HIV-uninfected tuberculous meningitis patient, such lesions are considered a tuberculoma, but in HIV-infected patients, several other differential diagnoses, such as toxoplasmosis, primary central nervous system lymphoma, and fungal granuloma, need to be considered. Another important issue in HIV-infected patients is that tuberculous meningitis and imaging abnormalities of the brain may also be a manifestation of paradoxical tuberculosis associated immune reconstitution inflammatory syndrome, following the start of antiretroviral therapy.[29],[30]

 » Miliary Tuberculosis and Disseminated Tuberculosis Top

Tuberculous meningitis and spinal cord tuberculosis are often a part of the disseminated tuberculosis and miliary tuberculosis syndrome. Miliary tuberculosis is defined as hematogenous spread of the tuberculous bacilli resulting in a widespread caseous tubercle formation with bilateral diffuse millet-sized pulmonary nodules. Miliary tuberculomas are usually associated with tuberculous meningitis. Miliary tuberculomas of the brain are usually <2 –5 mm in size and are often seen as tiny hyperintense foci on T2W images or may not be seen on conventional spin echo images. They show homogeneous enhancement on administration of gadolinium. Several diseases can mimic tuberculomas on conventional imaging, including neurocysticercosis, fungal granulomas, and tumors such as lymphomas, gliomas, and metastases. Disseminated tuberculosis is defined as tuberculous involvement of more than 2 noncontiguous body structures. Disseminated tuberculosis is usually seen in HIV-infected patients with a low CD4 count and has a high mortality rate [11],[31] [Figure 5].

 » Multidrug-Resistant Tuberculous Meningitis Top

Multidrug-resistant tuberculous meningitis is often associated with a high morbidity and mortality. The imaging appearances of multidrug-resistant tuberculous meningitis are the same as those of drug-susceptible tuberculous meningitis.[32]

 » Advanced Magnetic Resonance Imaging in Tuberculous Meningitis Top

Magnetization transfer MRI is a technique that is used for the detection and characterization of meningitis of infectious etiology. Demonstration of the meninges on precontrast T1W magnetization transfer images is considered indicative of tuberculous meningitis.[33] Other advanced MRI techniques such as perfusion-weighted MRI provide insights into the cerebral circulation (including capillary bed status), blood brain barrier, and the presence or absence of angiogenesis. In perfusion-weighted MRI, cerebral blood flow or cerebral blood volume is assessed following an injection of contrast material. MR perfusion may be used for the monitoring of response to antituberculous treatment in central nervous system tuberculosis. However, this imaging modality needs further investigation to unequivocally establish its usefulness in the diagnosis of tuberculous meningitis.[34]

 » Differential Diagnosis Top

Partially treated pyogenic meningitis, cryptococcal meningitis, viral encephalitis, as well as carcinomatous, and lymphomatous meningitis may have many similar neuroimaging characteristics and differentiation from tuberculous meningitis, at times, may become difficult [Table 1]. Points that suggest a diagnosis of neoplastic meningitis include absence of fever, presence of radicular pain, evidence of both cranial and spinal involvement, consistent CSF findings, and a characteristic neuroimaging picture, especially in patients in the older age group. Imaging findings such as cranial nerve enhancement, and intradural extramedullary enhancing nodules on spinal MR in the cauda equina region, are quite suggestive of neoplastic meningitis. Diagnosis is confirmed on positive CSF cytology for malignant cells.[35] Cryptococcal meningitis is another common differential diagnosis of tuberculous meningitis. The incidence of cryptococcal infection is high in the presence of HIV infection but it can occur in immunocompetent persons as well. Frequently, neuroimaging studies are normal. Dissemination of cryptococcal organisms may occur during the primary infection or during the reactivation spread from the basal cistern through the Virchow–Robin spaces to the basal ganglia, internal capsule, thalamus, and brainstem. The mucoid fungal material release may lead to the enlargement of perivascular spaces. MRI often reveals clusters of gelatinous pseudocysts in the periventricular white matter, basal ganglia, mammillary bodies, midbrain peduncles, and dentate nucleus with a “soap-bubble” appearance.[36],[37] In partially treated pyogenic meningitis, MRI typically shows complications of meningitis, such as leptomeningeal enhancement, hydrocephalus, subdural effusion, widening of the interhemispheric fissure, empyema, and infarction, and one must also look for parenchymal abscesses and ventriculitis. Neuroimaging can also detect bony conditions that may predispose to bacterial meningitis such as skull trauma, infection of the sinuses or mastoid air cells, skull base fractures, and many congenital anomalies of the skull.[38]
Table 1: Differential diagnosis (on the basis of neuroimaging) of the commonly encountered chronic meningitis

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 » Conclusion Top

The presence of basal exudates, hydrocephalus, infarcts, and tuberculoma are the four most characteristic features of tuberculous meningitis. Presence of these features on neuroimaging instills confidence in the clinical diagnosis even in the absence of bacteriological confirmation. Some imaging features such as optochiasmatic arachnoiditis are quite characteristic for tuberculous meningitis. Surgical intervention often requires a repeat neuroimaging. Neuroimaging is thus invaluable for assessing patients suffering from tuberculous meningitis at every stage of the disease.

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 » References Top

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]

  [Table 1]

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