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Incidence Definition Pathophysiology TB and arteries Diagnostic clue Location Ct findings Other modalities Differential diagnosis

CNS involvement is thought to occur in 2 - 5% of patients with tuberculosis and up to 15% of those with AIDS related tuberculosis Male-to-female ratio is 1:1

Although CNS involvement by tuberculosis is seen in all age groups, there is a predilection for younger patients, with 60 - 70% of cases occurring in patients younger than 20 years of age In endemic regions, tuberculomas account for as many as 50% of all intracranial masses

Definitions Infection by Mycobacterium tuberculosis (TB), an acid-fast bacillus causes tuberculous meningitis General Features Most TB CNS infections are secondary result of hematogenous spread (often pulmonary)

Meningitis is most frequent manifestation of CNS TB and is more common in children


Childhood TB is typically a primary infection Adult TB is most often post primary infection up to 30% due to primary infection

Potential manifestations include: Tuberculous meningitis : most common Intracranial tuberculous granuloma (tuberculoma) Focal tuberculous cerebritis Intracranial tuberculous abscess Tuberculous encephalopathy Complications secondary cerebral infarction from obliterative end arteritis arachnoid fibrosis with resultant hydrocephalus

CNS TB almost always secondary to pulmonary TB rarely GI or GU tract TBM pathophysiology Penetration of meningeal vessel walls by hematogenous spread Rupture of subependymal or subpial granulomata into the CSF Tuberculoma pathophysiology Hematogenous spread (GM-WM junction lesions) Extension of meningitis into parenchyma via cortical veins or small penetrating arteries

Arteritis: More common in children & HIV+ Arteries directly involved by basilar exudate or indirectly by reactive arteritis (up to 40% of patients) Infection causes arterial spasm resulting in thrombosis and infarct Lenticulostriate arteries, MCA, thalamoperforators most often affected Infarcts most common in basal ganglia, cerebral cortex, pons, cerebellum

Best diagnostic clue


Basilar meningitis + extracerebral TB (pulmonary) Meningitis + parenchymal lesions highly suggestive. TBM: Basal meningitis Tuberculomas: Typically parenchymal, supratentorial (often parietal lobes) Infratentoriallesions are less common, can involve brainstem (up to 8%) Dural tuberculomas may occur Size:Tuberculomas range from 1 mm to 6 cm

CT Findings NECT: May be normal early (10-15%) Isodense to hyperdense exudate effaces CSF spaces, fills basal cisterns, sulci. CECT: Intense basilar meningeal enhancement

CT Findings Hypodense to hyperdense round or lobulated nodule/mass with moderate to marked edema Solid or ring-enhancing "Target sign with contrast

BASAL MENIGITIS WITH COMMUNICATING HYDROCEPHALUS

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 in active stage.

Extensive infarcts of the right basal ganglia and internal capsule after the appearance of vasculitis in the thalamoperforating arteries in a child treated for tuberculous meningitis

Focal tuberculous cerebritis CT scan will show intense focal gyral enhancement Tuberculous encephalopathy severe unilateral or bilateral cerebral edema is seen

Magnetic Resonance Imaging MRI is more sensitive than CT scanning in determining the extent of meningeal and parenchymal involvement.

T1-weighted gadoliniumenhanced MRI in a patient with multiple enhancing tuberculomas in both cerebellar hemispheres.

T2-weighted MRI of a biopsy-proven, right parietal tuberculoma. Note the low-signalintensity rim of the lesion and the surrounding hyperintense vasogenic edema.

T1-weighted gadoliniumenhanced MRI in a child with a tuberculous abscess in the left parietal region. Note the enhancing thick-walled abscess.

MR spectroscopy with a single-voxel proton technique can be used to characterize tuberculomas and differentiate them from neoplasms 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.

Proton spectroscopy trace of a patient with an intracerebral tuberculoma demonstrating an elevated lactate peak (LA) with diminished N-acetyl aspartate (NAA) and choline (CH) peaks typical of an inflammatory mass in the brain.

Nuclear Imaging 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. Angiography 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.

The primary differential diagnoses are fungal meningitis, Other bacterial meningitis, carcinomatous meningitis neurosarcoidosis

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CHOROID PLEXITIS

Skull radiographic findings are usually normal. Rarely, in healed tuberculosis meningitis, faint parenchymal calcification is evident