This document discusses Mycobacterium tuberculosis and central nervous system tuberculosis, focusing on intracranial tuberculomas. It describes the etiology, clinical features, imaging appearance and characteristics of tuberculomas on CT and MRI. Tuberculomas appear as ring-enhancing lesions on imaging and can be distinguished from other ring-enhancing lesions like abscesses, metastases and neurocysticercosis based on their imaging characteristics and presence of a caseous necrotic core. Differential diagnosis and pathology of tuberculomas are also discussed.

1. 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
 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
 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
FLA
IR
T1C+ T1C+
25 yrs. male with headache
Case of Cerebral Abscess

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