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Cns tuberculoma
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- 2. Mycobacterium Tuberculosis Pulmonary tuberculosis Extra-pulmonarytuberculosis TB Lymphadenitis Pleural TB Skeletal TB (Bones & Joints) CNS TB – 1% of all Tuberculosis Abdominal TB Genitourinary TB Pericardial TB
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- 4. Intracranial tuberculoma CNSTB almost always secondary to hematogenous spread Tuberculoma can occur either in association with meningitis or separately Tuberculoma are well defined focal masses that result from Mycobacterium Tuberculosis with central caseous necrotic core Etiology / Pathophysiology Hematogenous spread (gray-white matter junction lesions) Extension of meningitis into parenchyma
- 5. Clinical feature Symptomsand signs are non-specific Include Headache Fever Vomiting Seizures Neurological deficits e.g. altered sensorium, hemiparesis
- 6. Location Parenchyma (Supra/Infratentorial) Dural Subarachnoid space Brainstem infrequent, 2.5-8 % of intracranial tuberculomas. Size 1mm-6cm
- 7. Pathology 3 stages Area of cerebritis – focal non-caseating granuloma – caseation occurs later Histologically it consists of a central core of caseating necrosis with a surrounding wall of a florid granulomatous reaction containing Langerhans giant cells, epithelioid, histiocytes and lymphocytes Unlike tuberculous abscesses, organisms are uncommon or absent Usually, tuberculomas have a solid granulomatous core and some may undergo liquefaction
- 8. CSF Analysis Increasedprotein Increased lymphocyte count Low glucose May be negative for organisms
- 9. Imaging modalities CTScan MRI MRS
- 10. CT Scan NECT Non-caseating granuloma –isodense or mildly hyperdense, surrounded by perilesional low- density edema. Caseating granuloma – isodense or slightly hypodense, edema remains. CECT Non-caseating granuloma – dense nodular enhancement Caseating granuloma – ring enhancement. Target sign may be found in some cases, central area of enhancement surrounded by area of low attenuation then peripheral rim enhancement.
- 11. MRI T1WI Non-caseating– Iso/Hypointense Caseating granuloma Solid centre – hypo/isointense Necrotic centre – hypointense Rim – may be hyperintense T2WI Non-caseating – hyperintense Caseating granuloma Solid centre – hypointense Necrotic centre – hyperintense Rim - hypointense
- 12. Continue…. FLAIR Sameas T2WI DWI Usually shows no restriction May show hyperintense centre of tuberculoma Post-contrast Non-caseating granuloma – Nodular homogenous enhancement Caseating granuloma – Peripheral rim enhancement MRS Prominent lipid and lactate peaks Reduced NAA No amino acid
- 13. Case of 32yrs. Old male with complaints of headache, vomiting, seizures and blurred vision T1WI
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- 17. Case of Tuberculoma+ Meningitis 31 yrs. Old with complaints fever & seizures for 15 days FLAIR POST-CONTRAST
- 18. Tuberculomas with bothnodular and ring enhancing lesions in same patient
- 19. 6 yrs. Oldgirl Complaints of headache & deterioration of consciousness Dx- CNS military tuberculomas T2
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- 23. Natural history &prognosis of CNS Tuberculoma Long term morbidity Mental retardation Paralysis Seizures Rigidity Mortality high in immunocompromised patients Complications Hydrocephalus Stroke Cranial neuropathies Tuberculomas may take months to years to resolve
- 24. Tuberculoma Tubercular Abscess Central coreCaseating necrosis surrounded by granulomatous reaction. No DWI restriction Pus. So DWI restriction. Peripheral rim Comparatively thin Comparatively thicker Mycobacterium Tuberculosis May or may not present Must be present
- 25. Differentials for ring-enhancinglesions in CNS Common Some primary brain tumor (e.g. anaplastic astrocytoma) Metastatic brain tumor Abscess Granuloma Resolving hematoma Subacute infarct Less common Thrombosed vascular malformation Demyelinating disease (e.g. multiple sclerosis) Uncommon Thrombosed aneurysm CNS lymphoma in AIDS
- 26. Differentials for CNSTuberculomas Abscess Metastases Neurocysticercosis Meningioma (Dural tuberculomas)
- 27. Neurocysticercosis Common site– Subarachnoid> Parenchyma > Intraventricular (GM-WM junction) 4 pathological stages Vesicular Colloid vesicular Granular nodular Nodular calcified Variable time to progress through pathological stages = 1-9 yrs. Ring enhancing lesion with an eccentric hypodense dot (scolex) is typical for NCC NCC lesions follow CSF density/intensity in vesicular & colloid vesicular stages and are rim enhancing in granular nodular stage and calcified in nodular calcified stage.
- 28. 65 yrs. Oldmale complaints of unexplained progressive neurological symptoms Dx – NCC. NECT
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- 31. Post-contrast Vesicular & colloidvesicular stage
- 32. Brain Parenchymal metastases Patient may have known primary site Common location – GM-WM junction Metastases usually displace rather than infiltrate tissue Disproportionate edema and mass effect On DWI, most metastases do not restrict, but often have a high nuclear to cytoplasm ratio and sometimes show restricted diffusion Post-contrast Pattern varies = intense/punctate/nodular/ring enhancement. MRS Elevated choline Lipid/lactate peak often present 80-85% lack Creatine peak Reduced NAA peak
- 33. Cerebral abscess Has4 pathological stages Early cerebritis Late cerebritis Early capsule Late capsule T2WI Hypointense rim is typical (due to collagen) SWI Dual rim sign is typical Hyperintense inside & hypointense outside DWI Shows restriction MRS Central necrotic area may show peaks of amino acids, lactate, acetate & succinate.
- 34. T1 T1 T2 FLA IR T1C+ T1C+ 25yrs. male with headache Case of Cerebral Abscess
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Editor's Notes
- #36 Culture showed gram positive cocci