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LETTER TO EDITOR
Year : 2014  |  Volume : 62  |  Issue : 1  |  Page : 73-75

Third ventricular tuberculoma


1 Department of Neurosurgery, All India Institute of Medical Sciences, New Delhi, India
2 Department of Neuroradiology, All India Institute of Medical Sciences, New Delhi, India

Date of Submission14-Nov-2013
Date of Decision26-Jan-2014
Date of Acceptance02-Feb-2014
Date of Web Publication7-Mar-2014

Correspondence Address:
Hitesh Kumar Gurjar
Department of Neurosurgery, All India Institute of Medical Sciences, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.128329

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How to cite this article:
Garg K, Gurjar HK, Joseph S G, Shashikant RC, Sharma BS. Third ventricular tuberculoma. Neurol India 2014;62:73-5

How to cite this URL:
Garg K, Gurjar HK, Joseph S G, Shashikant RC, Sharma BS. Third ventricular tuberculoma. Neurol India [serial online] 2014 [cited 2019 Nov 17];62:73-5. Available from: http://www.neurologyindia.com/text.asp?2014/62/1/73/128329


Sir,

Tuberculosis (TB) is among the most lethal infectious diseases and is still rampant in the developing world. The intraventricular tuberculomas of the brain are extremely rare, with only few reported cases. [1],[2],[3],[4]

A 16-year-old girl presented to an emergency department in altered mental state (Glasgow Coma Scale (GCS) score E2V2M5). She had a 6 month history of low-grade fever. Computed tomography brain revealed a rounded isodense lesion in the third ventricle with rim contrast enhancement and obstructive hydrocephalus [Figure 1]a. A right frontal external ventricular drain was inserted with which there was an improvement in the neurological status (GCS: E4VtM6) within 24 h. Magnetic resonance imaging (MRI) revealed a third ventricular lesion with isointense and hypointense signals on T1- and T2-weighted images (WI) respectively [Figure 1] and [Figure 2]. [5] T1-isointense rim of the lesion was hyperintense on magnetization transfer (MT) sequence [Figure 2]. There was intense peripheral rim enhancement with contrast administration. MR-spectroscopy showed lipid lactate peak with increased choline/N-acetyl-aspartate ratio (1:3) [Figure 2]. In addition, multiple ring enhancing lesions were seen in the cerebellum and left temporal lobe with leptomeningeal enhancement. Diagnosis of intraventicular tuberculoma with tubercular meningitis was made and the patient was started on five drugs anti tuberculosis therapy. External ventricular drain was removed and a ventriculoperitoneal shunt was inserted. Patient showed gradual improvement and doing well at 2 months follow-up.
Figure 1: (a) Non-contrast computed tomography axial section showing isodense lesion in the third ventricle with dilated lateral ventricles, (b) magnetic resonance imaging (MRI) T1 weighted axial section showing isointense lesion in the third ventricle, (c) MRI T2 weighted axial section showing hyperintense central core with inner isointense and peripheral hypointense rim. Edema is seen in bilateral thalamus, posterior limb of bilateral internal capsule. Small air pocket in right frontal horn of lateral ventricle due to shunt surgery, (d) MRI T2 weighted sagittal section showing intraventricular
lesion with mass effect on superior convexity of midbrain with elevation of internal cerebral veins, (e) T1 magnetization transfer images coronal section showing a lesion in the third ventricle with hyperintense rim suggestive of caseating tuberculoma


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Figure 2: (a) Magnetic resonance imaging (MRI) diffusion weighted image (WI) axial section showing no diffusion restriction, (b) MRI susceptibility WI axial section showing no blooming, (c) T1 magnetization transfer images axial section showing hyperintense rim suggestive of caseating tuberculoma, (d-f) T1 fat-saturated post contrast shows peripheral intense enhancement with enhancing tuberculomas in the cerebellum and in left temporal pole. Leptomeningitis along cerebellar folia and in bilateral sylvian fi ssure, (g) MR perfusion showing no increased perfusion in lesion relative cerebral blood volume (rCBV-61) as compared to normal temporal white matter (rCBV-350), (h) MR spectroscopy (multi-voxel) in lesion shows prominent lipid lactate peak with choline: N-acetyl-aspartate 1:3

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Central nervous system (CNS) -TB accounts for 5-15% of extrapulmonary disease and is the most severe form of the disease. [6] In patients with advanced CNS-TB, mortality rate is close to 50%. The CNS-TB includes tuberculous meningitis, tuberculoma, tubercular abscess and disseminated military lesions. [7] The common location of tuberculomas is in the cerebellum and cerebral hemispheres, particularly in the frontoparietal region and basal ganglia. Intraventricular tuberculoma is rare and the exact route of entry of tubercle bacilli into the ventricles is controversial. Hematogenous spread through the choroid plexus appears to be the most likely route. [1]

The CT appearances of tuberculoma are low or high-attenuation rounded or lobulated mass that commonly demonstrate ring enhancement on contrast-enhanced images. [5] MRI appearances of tuberculoma depends on whether its non-caseating or caseating. Non-caseating tuberculomas are relatively hypointense on T1-WI, hyperintense on T2-WI and show homogeneous enhancement after gadolinium administration. Caseating granulomas with a solid center appear relatively hypointense or isointense on T1-WI and iso- to hypointense on T2-WI. Caseating tuberculomas show rim enhancement on contrast-enhanced images. Tuberculomas with necrotic center demonstrate central hyperintensity on T2-WI. In addition, the presence of basal enhancing exudates, other parenchymal tuberculoma and asymmetric hydrocephalus strongly suggest the possibility of tuberculous pathology. MT imaging and MR-spectroscopy are helpful in the differential diagnosis of tuberculoma. [5]

Multidrug chemotherapy is highly efficacious in the management of intracranial tuberculomas and total cure rates are very high. Transient paradoxical tuberculoma expansion on starting chemotherapy can lead to a sudden increase in the intracranial pressure. [8] Cerebrospinal fluid diversion may be required to treat hydrocephalus. Endoscopic or stereotactic biopsy of lesions may provide definite diagnosis in cases where radiological features are equivocal. Indications for surgery include: Uncontrolled intracranial pressure due to obstructive hydrocephalus, lesions with mass effects and elevated intracranial pressure and failure of medical treatment. [9]

 
  References Top

1.Berthier M, Sierra J, Leiguarda R. Intraventricular tuberculoma. Report of four cases in children. Neuroradiology 1987;29:163-7.  Back to cited text no. 1
    
2.Van Allen MI, Kalousek DK, Chernoff GF, Juriloff D, Harris M, McGillivray BC, et al. Evidence for multi-site closure of the neural tube in humans. Am J Med Genet 1993;47:723-43.  Back to cited text no. 2
    
3.Desai K, Nadkarni T, Bhatjiwale M, Goel A. Intraventricular tuberculoma. Neurol Med Chir (Tokyo) 2002;42:501-3.  Back to cited text no. 3
    
4.Desgeorges M, Tranier J, Mercier P, Masselot A, Gendron Y. Intraventricular cerebral tuberculoma. Apropos of a case. Ann Med Interne (Paris) 1977;128:541-4.  Back to cited text no. 4
    
5.Osborn A. Tuberculosis and Fungal Infection. St. Louis, Baltimore, Boston: Mosby; 1994.  Back to cited text no. 5
    
6.Hernández Pando R. Modelling of cerebral tuberculosis: Hope for continuous research in solving the enigma of the bottom Billion′s disease. Malays J Med Sci 2011;18:12-5.  Back to cited text no. 6
    
7.Grange J, Zumla A. Tuberculosis. In: Cook G, Zumla A, editors. Manson′s Tropical Diseases. London: Saunders; 2003. p. 995-1053.  Back to cited text no. 7
    
8.Vajramani GV, Devi BI, Hegde T, Santosh V, Khanna N, Vasudev MK. Intraventricular tuberculous abscess: A case report. Neurol India 1999;47:327-9.  Back to cited text no. 8
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9.Gropper MR, Schulder M, Sharan AD, Cho ES. Central nervous system tuberculosis: Medical management and surgical indications. Surg Neurol 1995;44:378-84.  Back to cited text no. 9
    


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