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IMAGES IN RADIOLOGY
Year : 2011  |  Volume : 57  |  Issue : 2  |  Page : 143-144

Unusual clinical presentation of tuberculoma


Department of Neurology, Chhatrapati Shahuji Maharaj Medical University, Lucknow, U.P., India

Date of Submission01-Jan-2010
Date of Decision10-Dec-2010
Date of Acceptance21-Dec-2010
Date of Web Publication4-Jun-2011

Correspondence Address:
R Verma
Department of Neurology, Chhatrapati Shahuji Maharaj Medical University, Lucknow, U.P.
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0022-3859.81878

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How to cite this article:
Verma R, Sharma P. Unusual clinical presentation of tuberculoma. J Postgrad Med 2011;57:143-4

How to cite this URL:
Verma R, Sharma P. Unusual clinical presentation of tuberculoma. J Postgrad Med [serial online] 2011 [cited 2019 Nov 18];57:143-4. Available from: http://www.jpgmonline.com/text.asp?2011/57/2/143/81878


A 24-year-old gentleman presented acutely with gait disturbances, nausea, vomiting, and dizziness. He was also complaining of dysphagia, dysarthria, and decreased sweating on right half of face. Detailed neurological examination revealed right-sided Horner syndrome, horizontal nystagmus with torsional component beating toward left, right 9 th , and 10 th cranial nerve palsy, gait ataxia with swaying toward right side along with impairment of thermal, and pain sensation over the right face and left side of the body. Suspecting an acute ischemic event involving posterior circulation, a magnetic resonance imaging (MRI) was performed which showed a ring-enhancing intra-axial lesion in right medulla oblongata. The lesion was showing hyperintense signals on T1 contrast and FLAIR images with surrounding edema [Figure 1] and [Figure 2]. No apparent restriction of diffusion was present and magnetic resonance angiography was also normal. To ascertain the nature of the lesion, cerebrospinal fluid (CSF) examination was done which yielded 28 cells/mm 3 of lymphocytes, 56 mg% of protein, and 32 mg% of glucose. CSF culture and CSF polymerase chain reaction (PCR) were positive for Mycobacterium tuberculosis. India ink preparation and Elisa test for neurocysticercosis were negative in CSF. Thus, a tubercular etiology was established and a diagnosis of brain stem tuberculoma presenting as lateral medullary syndrome was considered. He was treated with standard four drug antitubercular regimen with corticosteroids. He showed good response to the treatment, and repeat MRI after one month of treatment showed regression of lesion [Figure 3] and [Figure 4]. He was almost asymptomatic at one-year follow-up and the lesion was remarkably reduced in size with atrophy of surrounding medulla in repeat MRI after one year [Figure 5].
Figure 1: Magnetic resonance imaging cranium T2 flair axial image revealing hyperintense lesion in right-sided medulla oblongata

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Figure 2: Magnetic resonance imaging cranium T1 contrast coronal image showing ring-enhancing lesion in brainstem

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Figure 3: Repeat MRI cranium after a month showed regression of lesion

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Figure 4: Repeat MRI of same area (coronal image) depicting reduction in size of lesion

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Figure 5: MRI studies after a year demonstrated near resolution of lesion with surrounding atrophy

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Lateral medullary syndrome is characterized by a constellation of neurological symptoms and signs due to injury of lateral part of the medulla. Most commonly, it results from a vascular insult secondary to vertebral artery or posterior inferior cerebellar artery occlusion. The critical location of the lesion in right lower medulla in our patient explains all the clinical manifestations. Positive CSF culture and PCR for mycobacteria, characteristic neuroimaging finding, and response to antitubercular treatment supported the diagnosis of tuberculoma. The main clinical and radiological differential diagnosis is given in [Table 1]. MRI characteristics of intracranial tuberculoma are extremely diverse. The MR features of the individual tuberculoma depend on presence of caseation in the granuloma. A hypointense core with a hyperintense rim was the most common signal characteristic on T2-weighted MRI. The central hypointensity on T2-weighted and FLAIR images reflect widespread necrosis and hypercellularity. [1] Many clinical syndromes depending upon site of intracranial tuberculoma are reported in the literature. Kumar et al. reported a patient presenting as isolated bilateral ptosis due to midbrain tuberculoma. [2] Pontine tuberculoma presenting as horizontal gaze palsy is also described [3] To the best of our knowledge, lateral medullary syndrome due to brainstem tuberculoma has not been previously reported. We conclude that tuberculoma should be considered as an etiology in brainstem space-occupying lesions presenting as lateral medullary syndrome, particularly in developing countries.
Table 1: The main clinical and radiological differential diagnosis

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 :: References Top

1.Wasay M, Kheleani BA, Moolani MK, Zaheer J, Pui M, Hasan S, et al. Brain CT and MRI findings in 100 consecutive patients with intracranial tuberculoma. J Neuroimaging 2003;13:240-7.  Back to cited text no. 1
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2.Kumar S, Rajshekhar G, Prabhakar S. Isolated bilateral ptosis as the presentation of midbrain tuberculoma. Neurol India 2008;56:212-3.  Back to cited text no. 2
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3.Saxena R, Menon V, Sinha A, Sharma P, Kumar DA, Sethi H. Pontine tuberculoma presenting with horizontal gaze palsy. J Neuroophthalmol 2006;26:276-8.  Back to cited text no. 3
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