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 Table of Contents  
PICTORIAL ESSAY - CLINICS IN NEURORADIOLOGY
Year : 2017  |  Volume : 4  |  Issue : 3  |  Page : 174-185

Central nervous system tuberculosis: Rare presentations of a common disease


Department of Radiodiagnosis, Vardhaman Mahavir Medical College and Safdarjung Hospital, New Delhi, India

Date of Web Publication30-Jan-2018

Correspondence Address:
Mahesh Kumar Mittal
Department of Radiodiagnosis, Safdarjung Hospital, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/astrocyte.astrocyte_71_17

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  Abstract 


Tuberculosis (TB) is a highly prevalent disease in developing countries of the world such as India. Central nervous system (CNS) involvement by TB can produce devastating effects and can be parenchymal, meningeal, intraventricular, subdural, or extradural. Common modes of CNS involvement include leptomeningitis and intracranial tuberculomas. Similar involvement of the spinal cord can produce tubercular arachnoiditis and intramedullary spinal tuberculomas. Atypical locations of tuberculomas include basal ganglia, brainstem, corpus callosum, and extra-axial and suprasellar locations. Uncommon modes of CNS involvement include tubercular pachymeningitis, focal tubercular cerebritis, cerebral abscess formation, and miliary TB. Tubercular pachymeningitis can also involve the dural lining of the spinal cord. We have presented cases of CNS TB, both atypical forms of common presentations as well as uncommon presentations with findings on magnetic resonance imaging (MRI) presenting a diagnostic dilemma. The radiologist plays a central role in the diagnosis of CNS TB in such cases, and careful tailoring of the MRI examination based on the clinical picture of the patient can play a vital role in making the diagnosis, even in atypical presentations.

Keywords: Central nervous system tuberculosis, miliary central nervous system tuberculosis, magnetic resonance imaging, magnetic resonance spectroscopy, tuberculosis, tubercular cerebritis, tubercular pachymeningitis, tubercular brain abscess, tuberculoma


How to cite this article:
Krishnan V, Mittal MK, Sinha M, Kumar M, Thukral BB. Central nervous system tuberculosis: Rare presentations of a common disease. Astrocyte 2017;4:174-85

How to cite this URL:
Krishnan V, Mittal MK, Sinha M, Kumar M, Thukral BB. Central nervous system tuberculosis: Rare presentations of a common disease. Astrocyte [serial online] 2017 [cited 2020 Jun 3];4:174-85. Available from: http://www.astrocyte.in/text.asp?2017/4/3/174/224198




  Introduction Top


Tuberculosis (TB), a chronic granulomatous infection caused by Mycobacterium tuberculosis, is a highly prevalent disease in developing countries of the world such as India. Based on Western data from Center for Disease Control, about 1.3% of all cases of TB and 6.3% of cases of extrapulmonary TB have central nervous system (CNS) involvement.[1] CNS involvement by TB can produce devastating effects. It can manifest in a variety of patterns, which can be parenchymal, meningeal, intraventricular, subdural, or extradural.

Common modes of CNS involvement include tubercular leptomeningitis and intracranial tuberculomas.[2] Tubercular leptomeningitis is the most common presentation of tubercular meningitis. However, leptomeningeal involvement of the spinal cord in the form of spinal arachnoiditis is uncommon. Tuberculomas most commonly occur within the frontal and parietal lobes. These granulomas usually involve the cortico-medullary junction and periventricular region as expected from hematogenous dissemination.[2] Rarer sites of tuberculomas include involvement of the basal ganglia, brainstem, corpus callosum, and the extra-axial and suprasellar locations. Tuberculomas are usually small and can be solitary or multiple and conglomerate. Large tuberculomas more than 2.5 cm in size (giant tuberculomas) are also unusual. Likewise, intramedullary tuberculomas in the spinal cord are uncommon.

Rarer presentations of CNS TB include focal tubercular cerebritis, cerebral abscess formation, and tubercular pachymeningitis.[3],[4] Tubercular cerebritis refers to a focal, ill-defined area of involvement of the cerebral parenchyma. Cerebral abscess may form either from focal tubercular cerebritis in an immunocompromised patient or from liquefaction of a tuberculoma.[2] Tubercular pachymeningitis refers to focal inflammation of the dural lining and is frequently associated with underlying chronic tubercular leptomeningitis.[2] It is even more unusual to find pachymeningitis involving the dural layers of the spinal cord.

Miliary TB of the brain is a rare entity which usually develops in severely immunocompromised patients and is usually associated with pulmonary miliary TB.[5] Numerous miliary granulomas can be demonstrated and it can occur as a clinically silent event. Only one case of isolated miliary CNS TB in a healthy patient has been reported to date.

Tuberculous encephalopathy is another rare entity that consists of a diffuse cerebral disorder occurring in young children and infants with extensive white matter demyelination due to a delayed type-IV hypersensitivity mechanism of cell-mediated immunity to tuberculoprotein.[2]

Here, we present a series of rare and atypical cases of CNS TB including both brain and spine TB. These forms of TB are particularly important to recognize because of the difficulty in diagnosing these atypical patterns, which are unusual for TB as well as the clinical importance of timely diagnosis as a delay in diagnosis and treatment can have devastating consequences. The onus of timely diagnosis in such cases frequently lies with the radiologist.


  Materials and Methods Top


A total of 10 cases of CNS TB with unusual imaging appearances were observed and analyzed over a period of 6 months and are presented. Magnetic resonance imaging (MRI) was done on Philips 1.5 Tesla Achieva scanner. Intravenous gadolinium contrast was administered in all cases for better characterization of the visualized lesions and for identifying more subtle lesions.

Case 1

A 14-year-old female patient presented with complaints of persistent headache with low-grade fever. She had no other significant complaints or any other significant history. Her routine laboratory test results were within normal limits. MRI of the brain was performed in order to rule out any organic lesion. Her noncontrast MRI scan revealed a normal brain study on all sequences with no evidence of any focal lesion [Figure 1](a-d). Due to history of low-grade fever, contrast (gadolinium) was administered for further evaluation. Postcontrast scan revealed numerous tiny 1–2 mm-sized disc enhancing lesions diffusely involving the entire brain parenchyma, including bilateral cerebral cortex, cerebellum, and brainstem. Majority of the lesions were noted to be located at the gray–white matter junction [Figure 1](e-f). Based on history, a provisional diagnosis of miliary TB of the brain was made.
Figure 1: (a) T2W axial image (b) FLAIR axial image at the level of basal ganglia and thalamus is normal. (c) T1 axial image is normal. (d) T1CE shows numerous tiny enhancing lesions, (e) T1 postcontrast axial image at the level of corona radiata and (f) posterior fossa with cerebellum and brainstem shows numerous tiny enhancing lesions, (g) Chest X-ray PA view shows paraspinal soft tissue density at the level of D10–D11 vertebral bodies, (h) Axial sections at the level of corona radiata. Bilateral parietal regions show gyral swelling with T2 hyperintensity and (i) leptomeningeal enhancement with gyral enhancement on postcontrast T1.

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The patient was further evaluated with a Chest X-ray posteroanterior (PA) view, which showed normal lung fields but showed the presence of a paraspinal soft tissue density at the level of D10–D11 vertebral bodies [Figure 1](g). Ultrasound scan of the abdomen was normal. Tests for HIV I and HIV II were nonreactive. Random blood sugar levels were normal. No cause of immunosuppression could be identified in the patient. Mantoux test was found to be positive (18 mm). Cerebrospinal fluid (CSF) examination showed elevated protein, elevated leukocytes, and reduced sugar. Adenosine deaminase was elevated (13.24 U/L). On microbiological examination, however, no acid-fast bacilli (AFB) could be detected in the CSF. Patient was started on antitubercular therapy (ATT) and showed rapid clinical improvement.

Case 2

An 11-year-old male child presented with complaints of seizures, altered sensorium, fever, and vomiting. MRI examination of the brain revealed a well-defined, thick-walled lesion in the right basifrontal region which appeared hypointense on T1 and hyperintense on T2 with heterogeneously hypointense signal intensity on fluid-attenuated inversion recovery (FLAIR). Postcontrast scan showed peripheral rim enhancement of the lesion [Figure 2](a-d). Diffusion weighted imaging (DWI) sequence at b1000 showed the lesion to be hyperintense, while apparent diffusion coefficient (ADC) maps showed the lesion to be hypointense, suggesting diffusion restriction [Figure 2](e-f). These features were consistent with brain abscess. Single-voxel proton MRI spectroscopy of the lesion showed lipid-lactate peak [Figure 2](g). Mass effect by the lesion with contralateral midline shift to the left was also present.
Figure 2: (a) T2W axial image and (b) FLAIR axial image at the level of thalami show a hyperintense lesion with heterogeneous suppression on FLAIR in the right basifrontal region. Mass effect with mild midline shift to left also seen. (c) On T1 axial image the lesion is hypointense. (d) T1CE (1 week later) shows peripheral rim enhancement of the lesion with hydrocephalus and leptomeningeal enhancement, Axial sections at the level of fourth ventricle. The lesion shows (e) hyperintensity on DWI at b1000 (left) which (f) appears hypointense on ADC map s/o diffusion restriction, (g) Single-voxel proton MRI spectroscopy from the lesion shows lipid-lactate peak.

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Further, the bilateral frontal and parieto-occipital regions also showed diffuse leptomeningeal enhancement with focal gyral enhancement and gyral swelling with hyperintensity on T2/FLAIR, also showing restricted diffusion s/o cerebritis with edema [Figure 1](h-i). The postcontrast scan which was performed after a gap of 1 week due to technical factors also showed the development of hydrocephalus with periventricular CSF ooze. Based on the imaging features, he was provisionally diagnosed with tubercular cerebritis and leptomeningitis with tubercular abscess formation and hydrocephalus.

In view of significant mass effect due to the brain abscess, the child underwent neurosurgical drainage of the abscess. Microbiological examination of the pus showed the presence of tubercular AFBs. A diagnosis of tubercular cerebritis and leptomeningitis with tubercular abscess formation was made and patient was started on ATT.

Case 3

A 40-year-old patient presented with complaints of focal seizures with headache and fever. MRI revealed a focal region of T2 hypointensity involving the cortex and adjacent white matter of the perirolandic region which appeared isointense on T1. Surrounding moderate edema was seen. Mild gyral swelling was also noted in the region. On postcontrast scan, focal gyral enhancement was seen in the region of T2 hypointensity [Figure 3](a-d). No other focal lesion was identified in the brain. On single-voxel proton MRI spectroscopy, lipid-lactate as well as choline were found to be elevated [Figure 3]e.
Figure 3: (a) T2W axial image and (b) FLAIR axial image at the level of rolandic sulcus show a hypointense region in the right perirolandic region. Large area perilesional edema is also seen. (c) On T1 axial image the region is isointense with surrounding hypointense edema. (d) T1CE shows focal gyral enhancement of the region, (e) Single-voxel proton MRI spectroscopy from the lesion shows elevated lipid-lactate and choline,

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CSF examination revealed elevated proteins and leukocytes. Microbiological examination, however, showed no AFBs in CSF. Mantoux test was positive (21 mm). He was provisionally diagnosed with focal tubercular cerebritis and started on ATT. Significant clinical improvement was observed.

Case 4

A 24-year-old female patient who was a known case of tuberculous meningitis for 2 weeks and had been started on ATT presented with complaints of worsening of symptoms and development of quadriparesis and paresthesias for 1 week. MRI of the cervical spine revealed mild swelling of the cervical spinal cord from C3 to C7 vertebral levels on T1W. On T2/short-tau inversion recovery (STIR), long-segment hyperintensity in the cord was noted at these levels s/o cord edema. On postcontrast scan, diffuse enhancement of the leptomeningeal lining of the spinal cord was noted [Figure 4](a-d). Further, a focal lesion was noted along the posterior spinal cord at the C2–C3 intervertebral disc (IVD) level abutting the pia-arachnoid, appearing isointense on T1 and hypointense on T2. This was seen to show ring enhancement on postcontrast scan [Figure 4](e-f). A provisional diagnosis of spinal arachnoiditis with spinal tuberculoma and associated spinal cord edema was made.
Figure 4: (a) T2W sagittal and (b) STIR sagittal images show long-segment hyperintensity in the cord extending from the C3 to C7 levels which appears isointense with mild cord swelling on (c) T1 sagittal image. Diffuse leptomeningeal enhancement also noted in the cervical spinal cord on postcontrast (d) T1 sagittal image with a focal enhancing lesion along the posterior spinal cord abutting the pia-arachnoid at the C2–C3 IVD level, (e) T2 axial image shows focal T2 hypointense lesion along the posterior spinal cord abutting the pia-arachnoid at the C2–C3 IVD level, which shows enhancement on postcontrast (f) T1 axial image.

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Case 5

A 14-year-old female patient, who had been previously diagnosed with tubercular arachnoiditis of the spinal cord 3 months back and the diagnosis having been confirmed by detection of AFBs in the CSF obtained by lumbar puncture 3 months back, came for follow-up MRI scan of the spinal cord to look for resolution, having been on ATT since 3 months. She had significant clinical improvement from the time of the previous scan 3 months back, but had persisting weakness in the bilateral lower limbs. The follow-up MRI showed focal thickening of the posterior dura at the level of the D6 vertebral body. A focal region T2/STIR hyperintensity was seen in the underlying cord which appeared hypointense on T1. On postcontrast scan, homogeneous enhancement of the thickened dura was present [Figure 5](a-f). No other focal lesion could be identified in the spinal cord. A diagnosis of focal tubercular pachymeningitis was made.
Figure 5: (a) T2W sagittal and (b) STIR sagittal images show focal thickening of the posterior dura at D6 level (arrow) with focal hyperintensity in the underlying cord. The focal lesion in the cord appears mildly hypointense on (c) T1 sagittal image. Enhancement of the thickened dura on postcontrast (d) T1 sagittal image seen, (f) Postcontrast T1W axial image shows focal enhancement of the posterior dura compared with the (e) noncontrast T1 axial image.

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Case 6

A 6-year-old male patient presented with complaints of seizures. MRI of the brain revealed typical T1 isointense, T2 hypointense tuberculomas, some of them showing central T2 hyperintensity incompletely suppressed on FLAIR, suggestive of tuberculomas. On postcontrast scan, ring enhancement of the lesions was present. The lesions were conglomerated in the rostrum, genu, and anterior body of the corpus callosum with perilesional FLAIR hyperintense edema [Figure 6] and [Figure 7]. Patient was started on ATT and showed significant clinical improvement.
Figure 6: (a) T2W axial images show multiple hypointense as well as hyperintense lesions not suppressed on (b) FLAIR conglomerated in the rostrum, genu, and anterior body of the corpus callosum. Lesions appear isointense to hypointense on (c) T1W axial images and (d) show ring enhancement on postcontrast images.

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Figure 7: (a) T2W and postcontrast (b) T1W show conglomerate ring-enhancing lesions in the rostrum, genu, and anterior body of the corpus callosum.

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Case 7

Another companion case of a 15-year-old female who presented with multiple cranial nerve palsies. MRI brain showed multiple tuberculomas conglomerated in the pons [Figure 8]. Single-voxel MR spectroscopy from the lesion showed lipid lactate peak [Figure 9].
Figure 8: (a) T2W images showing extensive hyperintensity in the midbrain and pons with few focal hypointensities within. (b) Postcontrast T1W images show conglomerate ring-enhancing lesions in the pons with swelling of the pons.

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Figure 9: Single-voxel MR spectroscopy from the lesions shows lipid-lactate peak.

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Case 8

An 11-year-old female patient presented with paraparesis of bilateral lower limbs with swelling in the upper back. MRI of the cervicodorsal spine showed T2/STIR hyperintensity involving the posterior elements of D1 vertebra, involving the posterior spine, laminae, transverse processes, and pedicles as well as focal regions of the posterior vertebral body with involvement of the adjacent paraspinal musculature. A large collection was also present in the subcutaneous plane of the back overlying the posterior spinous process, with extension along the process into the epidural space with associated compression of the spinal cord [Figure 10]. Microbiological examination of the pus in the collection revealed Mycobacterium tuberculosis bacilli.
Figure 10: (a) STIR sagittal and (b) T2W sagittal show hyperintensity involving the posterior elements and paraspinal soft tissues of the D1 vertebra with a collection in the subcutaneous plane of the back extending into the posterior epidural space. (c) T1W axial and (d) T1W axial postcontrast show enhancement of the involved tissues.

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Case 9

Another companion case with MRI of the LS spine reveals focal bone marrow edema involving only the posterior spinous process of the L3 vertebral body with focal extension into the bilateral laminae. Mild surrounding T2/STIR hyperintensity is present in the paraspinal muscles. Postcontrast enhancement is also present in the spinous process and the adjacent paraspinal muscles [Figure 11]. Microbiological examination of the tissue from the region revealed TB involving the posterior neural arch of L3.
Figure 11: (a) T2W sagittal and (b) STIR sagittal showing hyperintensity involving the posterior spine of L3 vertebra and adjacent paraspinal soft tissues. (c) T1W axial and postcontrast (d) T1W axial show enhancement of the involved tissues.

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Case 10

A 31-year-old male patient presented with complaints of fever with quadriparesis. MRI of the cervical spine was performed, which revealed T2 hyperintensity in the odontoid process that showed postcontrast enhancement with associated soft tissue compressing the cervical spinal cord at the level of the odontoid process [Figure 12]. Patient was started on ATT and showed eventual clinical improvement.
Figure 12: (a) T2W sagittal and (b) coronal show altered signal intensity in the odontoid process with dense surrounding hypointense soft tissue compressing the cervical spinal cord. (c) T1W sagittal and (d) postcontrast T1W show enhancement of the involved tissues.

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  Discussion Top


CNS TB is a devastating infection with high rates of morbidity and mortality worldwide. It can affect both the brain and spinal cord and manifest in many different forms. It can involve the meninges, the parenchymal tissues, or both. The most common manifestation of CNS TB is tubercular leptomeningitis and is most frequently seen in children and adolescents.[6] Another form of meningeal involvement in CNS TB is tubercular pachymeningitis. The most common form of parenchymal TB is tuberculoma.[6] Other parenchymal forms of TB include focal tubercular cerebritis, tubercular abscess formation, miliary TB, and tubercular encephalopathy. In most of these cases, the lesions are usually readily recognized on noncontrast MRI scans, which are made more obvious by the administration of intravenous contrast (gadolinium).[2] Calvarial TB and tubercular spondylitis may also occur with secondary neurological involvement by collection or inflammatory tissue.

Meningeal tuberculosis

Tubercular leptomeningitis and its complications

This is the most common presentation of CNS TB and can occur either through hematogenous spread or by rupture of subpial tubercular focus into the subarachnoid spaces or basal cisterns.[6] Tuberculous meningitis often has an insidious course with a nonspecific clinical presentation in its early stages, especially in children and may present with fever, vomiting, and general listlessness. In later stages, the characteristic features of meningeal irritation set in, such as neck stiffness, altered sensorium, and focal neurological deficits. Eventually, the clinical features of the complications set in.

Enhancing exudates in the basal cisterns is the most common manifestation of leptomeningeal TB on MRI, and is also obvious in Case 2. Meningeal enhancement is considered to be the most sensitive feature and is found in up to 90% of the cases.[7] The subpial exudate is primarily located in the inferomedial surface of the frontal lobes, the anteromedial surface of the temporal lobes, the superior aspect of the cerebellum, and the floor of the third ventricle. Extension to suprasellar, interpeduncular, and pontomesencephalic cisterns may also occur from these primary sites. In most cases, some degree of meningeal involvement is seen within the sulci over the cerebral convexities, the Sylvian fissures, and also the ependymal surfaces of the ventricles; the latter usually occurs in the later stages of the disease. Other radiologic manifestations of tuberculous meningitis may be related to its possible complications, including progressive hydrocephalus, vasculitis, infarction, and cranial neuropathies.[6]

Tuberculous spinal leptomeningitis presents on MRI with obliteration of the spinal subarachnoid space or CSF loculation, thick, linear enhancement of the meningeal pia-arachnoid lining, which may completely fill the subarachnoid spaces as seen in Case 2. Longstanding arachnoiditis may result in the development of syringomyelia (spinal cord cavitation) that typically demonstrates CSF signal intensity on all MR sequences. CSF analysis often reveals features typical of tuberculous meningitis such as lymphocytic pleocytosis, elevated CSF protein, and reduced CSF sugar. AFBs can sometimes be detected in the CSF in active infection. Possible differentials to be considered include infective meningitis, inflammatory diseases such as rheumatoid arthritis, sarcoidosis, or carcinomatous meningitis.[6]

Tubercular pachymeningitis

Chronic infection of the duramater secondary to underlying leptomeningitis may lead to tubercular pachymeningitis. Pachymeningitis is an unusual manifestation of cerebral TB that can be diffuse or, more commonly, localized and known as dural tuberculoma en plaque. The clinical features depend on the location of the pathology. They may present with headache, seizures, focal neurological deficits, or cranial nerve palsies and can involve the brain or, as in Case 5, the spinal cord.[4]

On MRI, the lesions often present as focal plaque-like or less commonly diffuse, dural thickening, which shows postcontrast enhancement. Often, the underlying white matter edema is noted, as in Case 5. The presence of sulcal enhancement in some cases presumably indicates leptomeningeal involvement. Diagnosis based on radiologic findings is presumptive, however, there are no imaging features unique to tuberculous pachymeningitis.[8] CSF analysis may be normal or may reveal mildly elevated protein concentration with mild lymphocytic pleocytosis. Biopsy is the only method for definitive diagnosis of tubercular pachymeningitis by the detection of granulomatous inflammation with Langhan's giant cells.[9] An important differential diagnosis to be considered is a meningioma en plaque.[10] Other differentials to be considered include neurosarcoidosis and lymphoma.

Parenchymal tuberculosis

Tuberculomas

This is the most common form of parenchymal TB.[7] The lesion may be solitary or multiple and may occur anywhere in the parenchyma of the brain or, as in Case 4, even in the spinal cord. Lipid-lactate peak occurs on MRI spectroscopy. Calcification may occur, especially in the healing stages. The patients usually present with focal neurological deficit or seizures.[11] The tuberculoma can exist in three different stages:[12]

Noncaseating granuloma

It is usually isointense or hypointense on T1W and hyperintense on T2W images. Homogeneous disc enhancement is seen with gadolinium.

Caseating solid granuloma

It is usually isointense or hypointense on T1W and strikingly hypointense on T2W images. This is attributed to the granulation tissue and compressed glial tissue in the central core, resulting in greater cellular density than the brain parenchyma. It shows ring enhancement with gadolinium.

Granuloma with central liquefaction

It appears centrally hypointense on T1, and hyperintense with a peripheral hypointense rim on T2W images. The low-signal intensity of the capsule may be related to a layer of collagenous fibers with high protein concentration and low water content and a layer of outer inflammatory cells. The central hyperintensity is due to liquefaction with increased water content. Ring enhancement is seen with gadolinium.

Histologically, the mature tuberculoma is composed of a necrotic caseous center surrounded by a capsule that contains fibroblasts, epithelioid cells, Langhan's giant cells, and lymphocytes.[13] Important differentials include other inflammatory granulomas such as neurocysticercosis or toxoplamosis and metastases. Unusual locations of tuberculomas such as conglomeration in the corpus callosum or pons can also occur as in Cases 6 and 7. Cases have been reported of brainstem tuberculomas presenting with cranial nerve palsies.[14]

Focal tubercular cerebritis

This is a rare form of presentation of cerebral parenchymal TB, first described by Jenkins as a separate entity.[15] A similar presentation can occur in the spinal cord in the form of tubercular myelitis. It represents focal infection of the brain parenchyma by tuberculous bacilli. On MRI, focal tuberculous cerebritis appears hypointense on T1W and hyperintense on T2W images, with postcontrast images showing small areas of patchy enhancement with underlying cerebral edema,[16] as is evident in Case 3. Very limited literature is available regarding this form of parenchymal TB.

Tubercular abscess

Tubercular abscess is also one of the rarer presentations of cerebral parenchymal TB. They have been observed in immunocompromised as well as immunocompetent individuals. However, they are more frequent in immunocompromised patients and at the extremes of age. Farrar believes that if the quantity of bacilli is high enough or the immunity is depressed, a focal cerebritis may progress to an abscess.[17] On the contrary, some authors consider abscesses to be the result of liquefaction of tuberculomas.[18] Patients usually present with fever, focal neurological deficits depending on the site of the abscess and features of raised intracranial tension.

On MRI, tubercular brain abscesses are circular or elliptical lesions, which are T1 hypointense and T2 hyperintense and classically rim-enhancing on contrast administration. T2-weighted scans show surrounding hyperintense signals from the perilesional edematous brain. Restricted diffusion on DWI sequence is present with hypointensity on ADC maps. An important differential is pyogenic brain abscess, especially in acute presentations. On the basis of conventional MRI, it is difficult to differentiate between these two entities.[19] According to Luthra et al., pyogenic and tuberculous abscesses may be differentiated by their unique metabolite pattern on MR spectroscopy, with recognition of amino acids, acetate, and succinate, in pyogenic abscesses and lipid-lactate peak in tuberculous abscesses.[20] In Case 2, diagnosis on radiological imaging was confirmed by the presence of lipid-lactate peak and absence of amino acids on MR spectroscopy.

Tuberculous brain abscesses show significantly lower magnetization transfer (MT) ratios compared with those of pyogenic abscesses. When MT MRI is combined with in vivo MR spectroscopy, it might be possible to differentiate tuberculous brain abscesses from pyogenic brain abscesses with a high degree of accuracy. However, definitive conformation of diagnosis can be done only by histopathological examination. The abscess wall is composed of vascular granulation tissue, containing acute and chronic inflammatory cells, and AFBs of tuberculous origin can be detected within.[21]

Miliary tuberculosis

Miliary TB is a rare form of CNS TB, which has only been reported in single case reports or as variants of short case series. Almost all of the cases have been reported in association with severe immunosuppression and associated pulmonary or systemic involvement.[11],[22] The lesions are usually diffusely scattered in the brain parenchyma, predominantly in the gray–white matter junction, which is highly suggestive of hematogenous spread to the brain. Further, the lesions may be completely invisible on plain MRI scans and only recognized after the administration of contrast, as in Case 1. In visible lesions, MRI shows small lesions that are hypointense on T2W sequences. These lesions can be seen occasionally as small hypodensities on computed tomography scan. Postcontrast T1W MR images show numerous, round, small, homogeneous, enhancing lesions.[6]

The most common clinical presentation of usual tuberculomas is signs of intracranial hypertension, focal neurological deficit, and seizures.[23] These effects usually occur because the tuberculoma with the perilesional edema acts to produce mass effect on the adjacent brain parenchyma. Miliary tuberculomas, on the other hand, can have a variety of unusual presentations due to their small size and insignificant mass effect. There have been reports of miliary tuberculomas presenting with headaches, seizures, meningeal signs, and even anxiety.[24],[25]

Gupta et al. have also reported a case of miliary TB of the brain without any neurological symptoms or signs in a known patient of pulmonary miliary TB. The radiological picture was, however, classical of miliary TB of the brain.[26]

Isolated miliary TB of the brain in a healthy patient without any other systemic involvement is, however, exceedingly rare. In patients without any known cause of immunosuppression, miliary TB usually presents in very young children or old debilitated patients. There has been only one reported case of isolated miliary TB in a healthy patient without any other systemic involvement.[22] In that case, the patient's neurological examination revealed wide-based ataxic gait and mental depression. In the discussed case, however, the patient's only complaint was headache with low-grade fever, and neurological examination was normal. There have been no similar cases reported in the literature to the best of our knowledge.

The fact that plain MRI without contrast was normal in this case on all sequences also underlines the importance of administration of contrast for diagnosis. As standard scan protocols for headache in most institutions do not include contrast sequences, careful elicitation of history of fever prior to scan proved vital in this case. A standard scan protocol for headache would have revealed a normal scan. This also makes a case for consideration of contrast administration as a standard component of every MRI examination. However, further studies on the risk benefit ratio of such a protocol modification is necessary.

The various differentials to be considered in a case of miliary enhancing lesions in the brain include, besides neuroTB, also neurosarcoidosis, metastases, lymphoid granulomatosis, Erdheim Chester disease, Lyme's disease, histoplasmosis, Bechet's disease, and Susac's syndrome. The assessment of distribution of lesions, involvement of the perivascular space, associated findings, and clinical and laboratory picture is vital in order to narrow down the diagnosis.[27]

Tubercular spondylitis

This refers to TB of the spinal column, which can lead to collections or inflammatory tissues which may secondarily involve or compress the spinal cord causing neurological symptoms. It typically presents with back pain and/or neurological deficit and deformity. Spinal lesions affect only 1% of TB patients and 6% of those with extrapulmonary lesions; only 1% of these spinal lesions involve the upper cervical spine and craniovertebral junction.[28] Vertebral TB is usually located in the anterior body and involvement of the posterior elements is considered rare, particularly in isolation. Its incidence is estimated to be 2–3% in spinal TB patients.[29]


  Conclusion Top


TB of the CNS can present in a wide variety of ways, some of which are common such as tubercular leptomeningitis and tuberculomas, while some are rare such as tubercular pachymeningitis and focal tubercular cerebritis. Tuberculomas can also conglomerate in unusual sites. Each of these can also affect the spinal cord in a manner similar to involvement of the brain. Some rarer types such as tubercular abscess and miliary TB are mostly associated with immunosuppression. In very rare cases, miliary TB of the brain can present with indolent symptoms with normal neurological examination in a healthy patient. Further, the lesions of miliary TB may also be invisible on noncontrast MRI scans, necessitating the administration of contrast for the diagnosis. The radiologist plays a central role in the diagnosis of CNS TB, and careful tailoring of the MRI examination based on the clinical picture of the patient can play a vital role in making the diagnosis, even in atypical presentations.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patients have given their consent for the images and other clinical information to be reported in the journal. The patients understand that name and initial will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12]



 

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