CNS Tuberculosis Imaging

Updated: Oct 03, 2023
  • Author: Richard C Lee, MD; Chief Editor: James G Smirniotopoulos, MD  more...
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Practice Essentials

Tuberculosis (TB) of the central nervous system (CNS) is a severe granulomatous infection caused by Mycobacterium tuberculosis. M tuberculosis is responsible for about 6% of community-acquired CNS infections worldwide. CNS tuberculosis occurs as a diffuse form (tuberculous meningitis), a focal form (tuberculoma), or spinal arachnoiditis, with tuberculous meningitis causing 70-80% of infections.Tuberculous meningitis occurs when a caseating meningeal or subcortical focus (Rich focus) ruptures into the subarachnoid space. Major diagnostic features include extensive basilar leptomeningeal enhancement and exudates in 38-89%, hydrocephalus in 60-75%, cerebral infarcts in 15-28%, and tuberculoma in 27%. [1, 2, 3, 4, 5, 6, 7, 8]

CNS TB predominantly manifests in the brain and meninges as tuberculomas, abscess formation, or meningeal enhancement. Occasionally, it can also affect the spinal cord. Clinical diagnosis can be difficult, as clinical presentation is nonspecific; therefore, imaging has an important role in establishing the diagnosis. Treatment consist of a 4-drug regimen of isoniazid, rifampin, pyrazinamide, and ethambutol, with adjunctive corticosteroid therapy. [1, 2, 3, 4, 5, 6, 7, 9, 10, 11]

(See the images below.)

Axial contrast-enhanced CT scan in a patient with Axial contrast-enhanced CT scan in a patient with tuberculous meningitis demonstrating marked enhancement and basilar exudate in the interpeduncular cisterns and meninges.
Axial T1-weighted contrast-enhanced MR image in a Axial T1-weighted contrast-enhanced MR image in a child with a tuberculous abscess in the left parietal region. Note the enhancing thick-walled abscess.

The hallmark feature of tuberculous meningitis (TBM) is the formation of thick, gelatinous exudates. The most common sites of involvement are the interpeduncular cisterns, the ambient cisterns, and the chiasmatic region.

Other characteristic pathologic changes are meningeal inflammation; vasculitis of the arteries of the circle of Willis while traversing the basilar exudates; and obstruction of the flow of cerebrospinal fluid, resulting in hydrocephalus. When the thick, inflammatory exudates of TBM surround the spinal cord, complications include spinal tuberculoma, myelitis, syringomyelia, vertebral tuberculosis, and rarely spinal tuberculous abscess. Tuberculous arachnoiditis leading to myeloradiculopathy is the most characteristic spinal complication of TBM. [7]  Abnormal signal hyperintensities along the cerebellar folia on fluid-attenuated inversion recovery (FLAIR) have also been reported. [12]  

Imaging modalities

Magnetic resonance imaging (MRI) with gadolinium enhancement is the preferred method of initial investigation. [13, 14] MR is the most sensitive test for detecting the extent of leptomeningeal disease and is superior to computed tomography (CT) in detecting parenchymal abnormalities, such as tuberculomas, abscesses, and infarctions. MR also readily depicts hydrocephalus. [15, 16, 17, 18]  CSF analysis  shows a decreased glucose level, elevated protein levels, and mild pleocytosis. Results of CSF polymerase chain reaction (PCR) assays may be diagnostic. [19, 20, 21, 22]

Follow-up CT and MR images at 1 week and 1 month after the initial scan are useful for early identification of complications, as well as for tracking the response to treatment; however, most abnormalities persist beyond 6 months despite clinical improvement. [23]

Although not routinely used for CNS TB, cerebral angiography can demonstrate findings of vasculitis, including vascular irregularity, vascular narrowing, and vascular occlusion. Vessels commonly affected include the terminal portions of the internal carotid arteries and the proximal parts of the middle and anterior cerebral arteries. Imaging features of vasculitis and/or vascular occlusion are detected in other inflammatory and ischemic cerebral conditions.

Skull radiographic findings are usually normal. Rarely, in healed tuberculosis meningitis, faint parenchymal calcifications are evident. Calcifications on skull radiographs in patients with healed TBM or healed tuberculomas are nonspecific findings. Skull calcification may indicate choroid plexus and pineal or habenular calcification.

Single-photon emission CT scanning with hexamethylpropyleneamine oxime (HMPAO) can be used to assess the degree and extent of cerebral ischemia resulting from TBM cerebral vasculitis. Findings are specific only for diminished cerebral perfusion. This is rarely used with the advent of MR imaging.

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Computed Tomography

In cases of tuberculous meningitis (TBM), contrast-enhanced CT of the brain depicts prominent leptomeningeal and basal cistern enhancement. With ependymitis, linear periventricular enhancement is present. Ventricular dilatation (eg, dilatation of the third and fourth ventricles) due to hydrocephalus is usually seen. Often, low-attenuating focal infarcts are seen in the deep gray matter nuclei, deep white matter, and pons; these infarcts result from associated vasculitis. The primary differential diagnoses are fungal meningitis, bacterial meningitis, carcinomatous meningitis, and neurosarcoidosis. CSF analysis often helps in establishing the diagnosis.

(See the images below.)

Axial contrast-enhanced CT scan in a patient with Axial contrast-enhanced CT scan in a patient with tuberculous meningitis demonstrating marked enhancement and basilar exudate in the interpeduncular cisterns and meninges.
Axial contrast-enhanced CT of a child with tubercu Axial contrast-enhanced CT of a child with tuberculous meningitis demonstrating acute hydrocephalus and meningeal enhancement.
Axial CT shows extensive infarcts of the right bas Axial CT shows extensive infarcts of the right basal ganglia and internal capsule after the sequelae of vasculitis in the thalamoperforating arteries in a child treated for tuberculous meningitis.

Tuberculomas (see the images below) demonstrate various patterns and are the most common form of CNS parenchymal involvement of tuberculosis. Noncaseating granulomas are homogeneously enhancing round or lobulated lesions. Caseating granulomas are rim enhancing; if these have a central calcific focus, they may form a targetlike lesion, which is suggestive of, but not pathognomonic for, tuberculosis. Granulomas may also form a miliary pattern with multiple tiny nodules scattered throughout the brain. Active lesions can be surrounded by hypodensity (edema). The differential diagnoses include fungal infections, bacterial infections, neurocysticercosis, and cerebral metastases.

Axial contrast-enhanced CT shows a tuberculoma at Axial contrast-enhanced CT shows a tuberculoma at the posterior left midbrain extending into the supracerebellar cistern.
Axial contrast-enhanced CT shows multiple enhancin Axial contrast-enhanced CT shows multiple enhancing tuberculomas at the right frontal brain parenchyma.

 

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Magnetic Resonance Imaging

MRI is more sensitive than CT scanning in determining the extent of meningeal and parenchymal involvement. [22, 24, 5]

In tuberculous meningitis (TBM), gadolinium-enhanced T1-weighted images demonstrate prominent leptomeningeal and basal cistern enhancement. With ependymitis, linear periventricular enhancement is present. Ventricular dilatation due to hydrocephalus is usually seen. Deep gray matter nuclei, deep white matter, and pontine infarctions resulting from vasculitis are hyperintense on T2-weighted images. Diffusion-weighted MRI is especially sensitive in depicting early ischemic lesions when findings on the T2-weighted MR images are normal. The primary differential diagnoses are fungal meningitis, bacterial meningitis, carcinomatous meningitis, and neurosarcoidosis.

(See the images below.)

Axial contrast-enhanced MR shows prominent dural t Axial contrast-enhanced MR shows prominent dural thickening and enhancement over the left frontal lobe with a small amount of parenchymal and leptomeningeal enhancement as well.
Axial diffusion-weighted MR shows multiple foci of Axial diffusion-weighted MR shows multiple foci of restricted diffusion involving the bilateral thalami and lentiform nuclei.

 

Axial T2-weighted MR image of a biopsy-proven, rig Axial T2-weighted MR image of a biopsy-proven, right parietal tuberculoma. Note the low–signal-intensity rim of the lesion and the surrounding hyperintense vasogenic edema.
Axial T1-weighted contrast-enhanced MR image in a Axial T1-weighted contrast-enhanced MR image in a patient with multiple enhancing tuberculomas in both cerebellar hemispheres.
Axial T1-weighted contrast-enhanced MR image in a Axial T1-weighted contrast-enhanced MR image in a child with a tuberculous abscess in the left parietal region. Note the enhancing thick-walled abscess.
Sagittal T1-weighted contrast-enhanced MR image of Sagittal T1-weighted contrast-enhanced MR image of the thoracic spinal cord in a patient with acquired immunodeficiency syndrome (AIDS) and leptomeningeal tuberculosis. Note the numerous granulomas on the dorsal surface of the cord and the dural enhancement.
Sagittal T2-weighted magnetic resonance image of t Sagittal T2-weighted magnetic resonance image of the thoracic spinal cord of a patient with 2 hyperintense intramedullary tuberculomas.

Parenchymal tuberculomas demonstrate various patterns. They are typically hypointense on T2-weighted images, but they may be hyperintense as well. Tuberculomas, like bacterial cerebral abscesses, have a hypointense rim on T2-weighted MR images. The cause is unknown, but free oxygen radicals released by the inflammatory process are believed to decrease T2 values. Noncaseating granulomas are homogeneously enhancing lesions. Caseating granulomas are rim enhancing. Granulomas may also form a miliary pattern with multiple tiny, enhancing nodules scattered throughout the brain. Lesions are typically surrounded by hyperintense edema on T2-weighted images. The differential diagnoses include fungal infections, bacterial infections, neurocysticercosis, and cerebral metastases.

(See the images below.)

Axial T1-weighted contrast-enhanced MR shows multi Axial T1-weighted contrast-enhanced MR shows multiple enhancing caseating and non-caseating tuberculomas.

 

Axial contrast-enhanced MR shows multiple enhancin Axial contrast-enhanced MR shows multiple enhancing tuberculomas throughout the cerebral and cerebellar hemispheres with faint leptomeningeal enhancement.

MR spectroscopy (see the image below) with a single-voxel proton technique can be used to characterize tuberculomas and differentiate them from neoplasms. Tuberculomas show elevated fatty-acid spectra that are best seen by using the stimulated-echo acquisition mode technique and a short echo time. The necrosis of the waxy walls of mycobacteria within the granuloma is believed to cause the elevation of fatty-acid peaks. The lactate peak is caused by anaerobic glycolysis and is found in inflammatory, ischemic, and neoplastic lesions of the brain; this finding is nonspecific.

Proton spectroscopy trace of a patient with an int Proton spectroscopy trace of a patient with an intracerebral tuberculoma demonstrating an elevated lactate peak (LA) with diminished N-acetyl aspartate (NAA) and choline (CH) peaks typical of an inflammatory mass in the brain.

MRI is especially useful in detecting leptomeningeal involvement of the spinal cord; cauda equina; and intramedullary tuberculomas, which, although rare, can be detected in patients with AIDS. MR imaging findings of spinal tuberculous meningitis consist of CSF loculation and obliteration of the spinal subarachnoid space, with loss of outline of the spinal cord in the cervicothoracic spine and matting of the nerve roots in the lumbar region. [25]  Contrast-enhanced imaging reveals nodular, thick, linear intradural enhancement, which can completely fill the subarachnoid space.

Syringomyelia may also occur as a complication of arachnoiditis.

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Ultrasonography

In infants, brain ultrasonography can be used to detect hydrocephalus. [19]   Many patients with TBM develop intracranial vasculopathy, which can be diagnosed and monitored using transcranial Doppler ultrasonography (TCD). 

TCD provides accurate information on intracranial blood flow velocities and identifies areas of intracranial stenosis.

TCD is a noninvasive and a relatively inexpensive test and can be performed at the bedside, making it a valuable tool for critically ill and ventilated patients. In addition, TCD monitoring in TBM may guide the management of elevated intracranial pressure. [26]

 

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