Answer for BIR CoW 14 Jul 2024
DISSEMINATED TUBERCULOSIS
FINDINGS IN MRI BRAIN
Evidence of multiple ill defined hypointense lesions with surrounding edema noted in bilateral hippocampus,right anterior temporal region ,bilateral frontal region,left thalamus,right medial temporal lobe and hippocampus,bilateral basi frontal regions and right hypothalamus showing no diffusion restriction/gradient blooming. On contrast administration, multiple conglomerate lesions noted with peripheral ring enhancement in the bilateral basifrontal region with bilateral frontal region ,right anterior temporal region ,hippocampus, vermis and perimesencephalic cistern.
FINDINGS IN MRI SPINAL CORD
Evidence of long segment expansile T2 hyperintense lesion noted extending from D1 to D11 vertebrae with cord edema. Evidence of multiple(2) T2 hypointense intramedullary lesions noted at D7 and D9 vertebral levels. On contrast administration,significant pial enhancement with nodular thickening noted in cervical and dorsal cord with enhancement of intramedullary lesion. Visualised cuts shows ,peripherally enhancing collection with surrounding marrow edema in sacrum and coccyx Multiple enhancing collections noted within the left iliac bone, left sacral ala, extending into the left sacroiliac joint. Anteriorly the collection is noted extending into the left iliac muscle and retroperitoneum. Posteriorly the collection is noted extending into left paraspinal muscles, left gluteal muscles and forming a subcutaneous collection showing peripheral enhancement. Diagnosis : Multiple cerebral and spinal tuberculomas with spinal tuberculous arachnoiditis , sacral and left iliac bone ostesomyelitis with intramuscular and subcutaneous abscess - Features suggestive of disseminated Tuberculosis.
DISCUSSION
CNS TB is a rare manifestation of extra-pulmonary TB. It occurs in only around 10% of patients with systemic TB. It commonly occurs in immunocompromised individuals such as those with HIV infection or on immunosuppressive therapy. Tuberculosis of the central nervous system can result from either hematogenous spread from distant systemic infection or direct extension from local infection . Intracranial manifestations of tuberculosis are protean and can affect all compartments. Manifestations include: extra-axial Tuberculous meningitis(leptoneningitis)most common Tuberculous pachymeningitis rare intra-axial Intracranial tuberculous granuloma(tuberculoma) Focal tuberculous cerebritis Intracranial tuberculous abscess Tuberculous rhombencephalitis Tuberculous encephalopathy Complications of CNS tuberculosis infection can include: Hydrocephalus (communicating or non-communicating),ventriculitis,choroid plexitis,arterial vasculitis and dural sinus thrombosis.
STAGES OF TUBERCULOMA Tuberculomas occur in four stages – non caseating granuloma, caseating granuloma, caseating granuloma with central liquefaction, and calcified granuloma. Pathologically tuberculoma consist of a typical granuloma with epithelioid cells, Langhans giant cells, and a peripheral rim of lymphocytes. Central caseous necrosis followed by liquefaction develops in subsequent stages. Post treatment a paradoxical increase in size of tuberculoma can occur. They may resolve completely, but in most cases they resolve with the formation of calcified granulomas. The definitive diagnosis is necessary, as most tuberculomas respond to medical management. On MR imaging, tuberculoma’s appearance varies depending on its stage of maturation (ie, whether noncaseating, caseating with solid or liquid center). The noncaseating tuberculoma usually appears as hyperintense on T2-weighted and slightly hypointense on T1-weighted images. Metastases, lymphoma, and other infective granulomas also have similar imaging features. On T1-weighted magnetization transfer (MT) imaging, the cellular component of the lesion appears brighter and is considered relatively specific for the disease . The solid caseating tuberculoma appears isointense to hypointense on both T1-weighted and T2-weighted images. On T1-weighted MT images, the solid center appears hypointense with hyperintense rim. The significantly lower MT ratio (MTR) of the rim of T2 hypointense tuberculoma than cysticercosis granuloma helps in its differentiation. When the solid center of caseating lesion liquefies, it appears hyperintense with a hypointense rim on T2-weighted images with edema. On T1-weighted and T1-weighted MT images, the peripheral hyperintense rim may be visualized beyond the T2 hypointensity and shows enhancement on postcontrast study. In their final stage of resolution, tuberculomas often undergo calcification, and the perilesional oedema resolves completely.
SPINAL MANIFESTATIONS Spinal involvement is rare, seen in 2% of all CNS TB cases and 0.2-5% of all CNS tuberculomas. The ratio of intramedullary tuberculoma to intracerebral tuberculoma is approximately 1:42, and 72% of lesions are located in the thoracic cord . For spinal intramedullary tuberculosis, MRI is the optimal measure because it can accurately show location, size, and number of lesions, as well as whether there is degeneration and necrosis around the lesions. In the acute phase, symptoms of intramedullary spinal tuberculoma may predominate. Tuberculomas may resolve completely, but mostly they undergo calcification with the resolution of perilesional edema. They appear hypointense on T1WI and T2WI with no enhancement. Gradient recalled echo/susceptibility-weighted imaging (GRE/SWI) sequences show susceptibility artifact . The “target sign” is a valuable indicator that helps differentiate spinal tuberculoma from other intramedullary lesions. Rim enhancement is usually observed in spinal tuberculosis. Compared with tumors, spinal tuberculoma has a sharper margin and lower T2WI signals, and it is particularly easy to differentiate the disease when there is a “target sign.” Tuberculoma vs. other ring enhancing lesions 1H proton spectroscopy plays a major role in differentiating tuberculomas from other ring enhancing lesions, especially in atypical cases. A prominent lipid peak at 1.3 ppm is characteristic of tuberculomas . Recent studies also show the presence of a guanidinoacetate peak at 3.8 ppm to be characteristic of tuberculomas . Tuberculomas with heterogeneous signal intensity on T1W and T2W with heterogeneous post-contrast enhancement show a choline peak at 3.32 ppm in addition to the lipid peak at 1.3 ppm and suggested high cellularity in this variety of tuberculoma as a possible cause for the same . Tuberculosis and neurocysticercosis (NCC) are close differentials in countries where both infections are endemic. Other forms of parenchymal TB include cerebritis, cerebral abscess, miliary TB, or tuberculous encephalopathy. TB cerebritis or abscess may appear similar to that of pyogenic infection. Miliary form of disease is seen in severely immunocompromised patients with multiple tiny (2-3 mm) scattered lesions located at the corticomedullary junction. These may be invisible on non-contrast MRI or appear hypointense on T2WI and show ring enhancement. Tuberculous encephalopathy usually affects children who present with convulsions or coma. MRI shows cerebral edema and demyelination seen as hyperintensity on T2WI The Differential diagnosis for ring-enhancing lesions includes Neurocysticercosis, Metastasis, CNS lymphoma (immunocompromised individuals), Toxoplasmosis Tumors (astrocytoma, ependymoma, and hemangioblastoma), Pyogenic abscesses.
References
Rehman S, Rehman AU, Naveed MA, Iftikhar A. Intracranial and Spinal Tuberculosis: A Rare Entity. Cureus. 2021 Dec 28;13(12):e20787. doi: 10.7759/cureus.20787. PMID: 35111471; PMCID: PMC8795229. Khatri GD, Krishnan V, Antil N, Saigal G. Magnetic resonance imaging spectrum of intracranial tubercular lesions: one disease, many faces. Pol J Radiol. 2018 Dec 29;83:e524-e535. doi: 10.5114/pjr.2018.81408. PMID: 30800191; PMCID: PMC6384409.
FINDINGS IN MRI BRAIN
Evidence of multiple ill defined hypointense lesions with surrounding edema noted in bilateral hippocampus,right anterior temporal region ,bilateral frontal region,left thalamus,right medial temporal lobe and hippocampus,bilateral basi frontal regions and right hypothalamus showing no diffusion restriction/gradient blooming. On contrast administration, multiple conglomerate lesions noted with peripheral ring enhancement in the bilateral basifrontal region with bilateral frontal region ,right anterior temporal region ,hippocampus, vermis and perimesencephalic cistern.
FINDINGS IN MRI SPINAL CORD
Evidence of long segment expansile T2 hyperintense lesion noted extending from D1 to D11 vertebrae with cord edema. Evidence of multiple(2) T2 hypointense intramedullary lesions noted at D7 and D9 vertebral levels. On contrast administration,significant pial enhancement with nodular thickening noted in cervical and dorsal cord with enhancement of intramedullary lesion. Visualised cuts shows ,peripherally enhancing collection with surrounding marrow edema in sacrum and coccyx Multiple enhancing collections noted within the left iliac bone, left sacral ala, extending into the left sacroiliac joint. Anteriorly the collection is noted extending into the left iliac muscle and retroperitoneum. Posteriorly the collection is noted extending into left paraspinal muscles, left gluteal muscles and forming a subcutaneous collection showing peripheral enhancement. Diagnosis : Multiple cerebral and spinal tuberculomas with spinal tuberculous arachnoiditis , sacral and left iliac bone ostesomyelitis with intramuscular and subcutaneous abscess - Features suggestive of disseminated Tuberculosis.
DISCUSSION
CNS TB is a rare manifestation of extra-pulmonary TB. It occurs in only around 10% of patients with systemic TB. It commonly occurs in immunocompromised individuals such as those with HIV infection or on immunosuppressive therapy. Tuberculosis of the central nervous system can result from either hematogenous spread from distant systemic infection or direct extension from local infection . Intracranial manifestations of tuberculosis are protean and can affect all compartments. Manifestations include: extra-axial Tuberculous meningitis(leptoneningitis)most common Tuberculous pachymeningitis rare intra-axial Intracranial tuberculous granuloma(tuberculoma) Focal tuberculous cerebritis Intracranial tuberculous abscess Tuberculous rhombencephalitis Tuberculous encephalopathy Complications of CNS tuberculosis infection can include: Hydrocephalus (communicating or non-communicating),ventriculitis,choroid plexitis,arterial vasculitis and dural sinus thrombosis.
STAGES OF TUBERCULOMA Tuberculomas occur in four stages – non caseating granuloma, caseating granuloma, caseating granuloma with central liquefaction, and calcified granuloma. Pathologically tuberculoma consist of a typical granuloma with epithelioid cells, Langhans giant cells, and a peripheral rim of lymphocytes. Central caseous necrosis followed by liquefaction develops in subsequent stages. Post treatment a paradoxical increase in size of tuberculoma can occur. They may resolve completely, but in most cases they resolve with the formation of calcified granulomas. The definitive diagnosis is necessary, as most tuberculomas respond to medical management. On MR imaging, tuberculoma’s appearance varies depending on its stage of maturation (ie, whether noncaseating, caseating with solid or liquid center). The noncaseating tuberculoma usually appears as hyperintense on T2-weighted and slightly hypointense on T1-weighted images. Metastases, lymphoma, and other infective granulomas also have similar imaging features. On T1-weighted magnetization transfer (MT) imaging, the cellular component of the lesion appears brighter and is considered relatively specific for the disease . The solid caseating tuberculoma appears isointense to hypointense on both T1-weighted and T2-weighted images. On T1-weighted MT images, the solid center appears hypointense with hyperintense rim. The significantly lower MT ratio (MTR) of the rim of T2 hypointense tuberculoma than cysticercosis granuloma helps in its differentiation. When the solid center of caseating lesion liquefies, it appears hyperintense with a hypointense rim on T2-weighted images with edema. On T1-weighted and T1-weighted MT images, the peripheral hyperintense rim may be visualized beyond the T2 hypointensity and shows enhancement on postcontrast study. In their final stage of resolution, tuberculomas often undergo calcification, and the perilesional oedema resolves completely.
SPINAL MANIFESTATIONS Spinal involvement is rare, seen in 2% of all CNS TB cases and 0.2-5% of all CNS tuberculomas. The ratio of intramedullary tuberculoma to intracerebral tuberculoma is approximately 1:42, and 72% of lesions are located in the thoracic cord . For spinal intramedullary tuberculosis, MRI is the optimal measure because it can accurately show location, size, and number of lesions, as well as whether there is degeneration and necrosis around the lesions. In the acute phase, symptoms of intramedullary spinal tuberculoma may predominate. Tuberculomas may resolve completely, but mostly they undergo calcification with the resolution of perilesional edema. They appear hypointense on T1WI and T2WI with no enhancement. Gradient recalled echo/susceptibility-weighted imaging (GRE/SWI) sequences show susceptibility artifact . The “target sign” is a valuable indicator that helps differentiate spinal tuberculoma from other intramedullary lesions. Rim enhancement is usually observed in spinal tuberculosis. Compared with tumors, spinal tuberculoma has a sharper margin and lower T2WI signals, and it is particularly easy to differentiate the disease when there is a “target sign.” Tuberculoma vs. other ring enhancing lesions 1H proton spectroscopy plays a major role in differentiating tuberculomas from other ring enhancing lesions, especially in atypical cases. A prominent lipid peak at 1.3 ppm is characteristic of tuberculomas . Recent studies also show the presence of a guanidinoacetate peak at 3.8 ppm to be characteristic of tuberculomas . Tuberculomas with heterogeneous signal intensity on T1W and T2W with heterogeneous post-contrast enhancement show a choline peak at 3.32 ppm in addition to the lipid peak at 1.3 ppm and suggested high cellularity in this variety of tuberculoma as a possible cause for the same . Tuberculosis and neurocysticercosis (NCC) are close differentials in countries where both infections are endemic. Other forms of parenchymal TB include cerebritis, cerebral abscess, miliary TB, or tuberculous encephalopathy. TB cerebritis or abscess may appear similar to that of pyogenic infection. Miliary form of disease is seen in severely immunocompromised patients with multiple tiny (2-3 mm) scattered lesions located at the corticomedullary junction. These may be invisible on non-contrast MRI or appear hypointense on T2WI and show ring enhancement. Tuberculous encephalopathy usually affects children who present with convulsions or coma. MRI shows cerebral edema and demyelination seen as hyperintensity on T2WI The Differential diagnosis for ring-enhancing lesions includes Neurocysticercosis, Metastasis, CNS lymphoma (immunocompromised individuals), Toxoplasmosis Tumors (astrocytoma, ependymoma, and hemangioblastoma), Pyogenic abscesses.
References
Rehman S, Rehman AU, Naveed MA, Iftikhar A. Intracranial and Spinal Tuberculosis: A Rare Entity. Cureus. 2021 Dec 28;13(12):e20787. doi: 10.7759/cureus.20787. PMID: 35111471; PMCID: PMC8795229. Khatri GD, Krishnan V, Antil N, Saigal G. Magnetic resonance imaging spectrum of intracranial tubercular lesions: one disease, many faces. Pol J Radiol. 2018 Dec 29;83:e524-e535. doi: 10.5114/pjr.2018.81408. PMID: 30800191; PMCID: PMC6384409.
Note:
We do not discourage differential diagnosis. But all the differentials must satisfy the findings noted in the case.
If you feel you have answered rightly but cannot find your name in the above list, please call 09551942599.
Did you Know?
The order in which the names appear in this winner's list is based on the time of submission. The first person to send the correct answer gets his/her name on top of the list!
We do not discourage differential diagnosis. But all the differentials must satisfy the findings noted in the case.
If you feel you have answered rightly but cannot find your name in the above list, please call 09551942599.
Did you Know?
The order in which the names appear in this winner's list is based on the time of submission. The first person to send the correct answer gets his/her name on top of the list!