Imaging in CNS Tuberculosis
- Author: Peter D Corr, MD, MB, ChB, FRCR, FRCPC; Chief Editor: James G Smirniotopoulos, MD more...
Tuberculosis (TB) of the central nervous system (CNS) is a granulomatous infection caused by Mycobacterium tuberculosis. The disease predominantly involves the brain and meninges, but occasionally, it affects the spinal cord. Clinical diagnosis can be difficult; therefore, imaging has an important role in establishing the diagnosis (see the images below).
Magnetic resonance imaging (MRI) with gadolinium enhancement is the preferred method of initial investigation.[1, 2] MRI is the most sensitive test for detecting the extent of leptomeningeal disease and is superior to computed tomography (CT) scanning in detecting parenchymal abnormalities, such as tuberculomas, abscesses, and infarctions. MRI also readily depicts hydrocephalus.[3, 4, 5, 6] Cerebrospinal fluid (CSF) analysis is usually used to detect a decreased glucose level, elevated protein levels, and a slight pleocytosis. Results of CSF polymerase chain reaction (PCR) assays may be diagnostic.[7, 8, 9, 10]
Limitations of techniques
Conventional MRI may cause early meningitis and early infarcts to be missed, and no MRI findings are pathognomonic for TBM. Diffusion-weighted imaging, if available, depicts infarctions in the hyperacute stage.
For excellent patient education resources, visit eMedicineHealth's Infections Center and Brain and Nervous System Center. See also eMedicineHealth's patient education articles Tuberculosis and Brain Infection.
Skull radiographic findings are usually normal. Rarely, in healed tuberculosis meningitis, faint parenchymal calcification is evident.
Degree of confidence
Calcifications on skull radiographs in patients with healed TBM or healed tuberculomas are nonspecific findings.
Skull calcification may indicate choroid plexus, pineal, and/or habenular calcification.
In tuberculosis meningitis (TBM), contrast-enhanced CT scanning 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. Basal cistern and meningeal enhancement are seen in the first 2 images below. Vasculitis-associated infarcts are seen in the third image.
Parenchymal cerebritis may cause hypoattenuation with little or no enhancement. Parenchymal tuberculomas demonstrate various patterns. Noncaseating granulomas are homogeneously enhancing lesions. Caseating granulomas are rim enhancing; if these have a central calcific focus, they may form a targetlike lesion. Granulomas may also form a miliary pattern with multiple tiny nodules scattered throughout the brain. All lesions are surrounded by hypoattenuating edema. The differential diagnoses include fungal infections, bacterial infections, neurocysticercosis, and cerebral metastases.
Cryptococcal meningitis also occurs in patients with acquired immunodeficiency syndrome (AIDS); however, the history is longer (ie, months) than that of TBM, and perivascular cysts are often seen in the region of the basal ganglia. Perivascular cysts do not occur with TB. Toxoplasmosis usually causes a focal abscess in patients with AIDS.
Degree of confidence
CT scan findings are typical of granulomatous meningitis with parenchymal involvement. Fungal infections and neurosarcoidosis may appear similar to CNS TB. At times, bacterial infections and metastatic disease also may mimic CNS TB. CSF analysis often helps in establishing the diagnosis.
Magnetic Resonance Imaging
MRI is more sensitive than CT scanning in determining the extent of meningeal and parenchymal involvement.[11, 12, 10]
In tuberculosis 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 MRIs are normal. The primary differential diagnoses are fungal meningitis, bacterial meningitis, carcinomatous meningitis, and neurosarcoidosis. (See the images below.)
Parenchymal cerebritis may show hyperintensity with little or no enhancement on T2-weighted images.
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 hypointense walls or rims on T2-weighted MRIs. 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.
MR spectroscopy with a single-voxel proton technique can be used to characterize tuberculomas and differentiate them from neoplasms (see the image below). 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.
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.
Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the Medscape Reference topic Nephrogenic Systemic Fibrosis. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or magnetic resonance angiography scans.
NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see Medscape.
Degree of confidence
MRI improves diagnostic confidence, but images in patients with fungal infections can appear identical to those in patients with neurosarcoidosis. At times, metastatic disease and bacterial infections also can mimic CNS TB.
In infants, brain ultrasonography can be used to detect hydrocephalus.
Degree of confidence
Usually, CT scanning or MRI is required for definitive diagnosis.
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.
Degree of confidence
Findings are specific only for diminished cerebral perfusion.
Although not currently in routine use in patients with CNS TB, cerebral angiography demonstrates findings of vasculitis. These findings include vascular irregularity, vascular narrowing, and vascular occlusion. Vessels commonly affected include the terminal portions of the internal carotid arteries, as well as the proximal parts of the middle and anterior cerebral arteries.
Degree of confidence
Features of vasculitis and/or vascular occlusion are detected in other inflammatory and ischemic cerebral conditions.
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