Cns tuberculoma

CNS Tuberculoma.
Radiology and Imaging

1. CNS Tuberculoma Dr. Mac For Radiology

2. Mycobacterium Tuberculosis Pulmonary tuberculosis Extra-pulmonary tuberculosis TB Lymphadenitis Pleural TB Skeletal TB (Bones & Joints) CNS TB – 1 % of all Tuberculosis Abdominal TB Genitourinary TB Pericardial TB

3. CNS Tuberculosis Leptomeningitis Pachymeningitis Cerebritis Tuberculoma TB Abscess

4. Intracranial tuberculoma CNS TB 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 Symptoms and 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 1 mm-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 Increased protein Increased lymphocyte count Low glucose May be negative for organisms

9. Imaging modalities CT Scan 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 Same as 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 32 yrs. Old male with complaints of headache, vomiting, seizures and blurred vision T1WI

14. T2WI

15. FLAIR

16. Post-contrast

17. Case of Tuberculoma + Meningitis 31 yrs. Old with complaints fever & seizures for 15 days FLAIR POST-CONTRAST

18. Tuberculomas with both nodular and ring enhancing lesions in same patient

19. 6 yrs. Old girl Complaints of headache & deterioration of consciousness Dx - CNS military tuberculomas T2

20. Axial Post-contrast

21. Coronal Post-contrast

22. Sagittal Post-contrast

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 core Caseating 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-enhancing lesions 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 CNS Tuberculomas 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. Old male complaints of unexplained progressive neurological symptoms Dx – NCC. NECT

29. T1

30. FLAIR

31. Post-contrast Vesicular & colloid vesicular 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 Has 4 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 FLAIR T1C+ T1C+ 25 yrs. male with headache Case of Cerebral Abscess

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