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Table of Contents    
Year : 2019  |  Volume : 67  |  Issue : 2  |  Page : 614-615

Cerebral hemiatrophy: A delayed sequalae of multidrug-resistant tuberculous meningitis

1 Department of Neurology, King George Medical University, Lucknow, Uttar Pradesh, India
2 Department of Microbiology, King George Medical University, Lucknow, Uttar Pradesh, India

Date of Web Publication13-May-2019

Correspondence Address:
Dr. Ravindra K Garg
Department of Neurology, King George Medical University, Lucknow - 226 003, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.257985

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How to cite this article:
Garg RK, Rizvi I, Jain A, Malhotra HS, Kumar N, Pandey S. Cerebral hemiatrophy: A delayed sequalae of multidrug-resistant tuberculous meningitis. Neurol India 2019;67:614-5

How to cite this URL:
Garg RK, Rizvi I, Jain A, Malhotra HS, Kumar N, Pandey S. Cerebral hemiatrophy: A delayed sequalae of multidrug-resistant tuberculous meningitis. Neurol India [serial online] 2019 [cited 2020 Aug 3];67:614-5. Available from:

The diagnosis of multidrug-resistant tuberculous meningitis is difficult, and differentiation from a paradoxical reaction is crucial. A 16-year old girl presented with fever, headache vomiting, and diplopia of 10-day duration in 2010. She improved after 2 weeks of treatment. Two months later, she presented with vision loss, drooping of the left eyelid, and difficulty in walking. Cranial computed tomography showed a thick abnormal leptomeningeal enhancement and hydrocephalus [Figure 1]. In the hospital, she had right-sided hemiparesis and right focal seizures. Neuroimaging revealed an infarct in the left basal ganglia, internal capsule, and thalamus. She also developed right supraclavicular lymphadenopathy. Aspirate from the lymph node demonstrated the presence of multidrug-resistant Mycobacterium tuberculosis [Figure 2]. A five-drug antituberculous regimen was started. Seven years later, she came for follow-up, and the latest magnetic resonance imaging showed a left cortical hemiatrophy and some enhancing lesions on the left side [Figure 3]. After 8 years of diagnosis, she is bed-ridden with right hemiparesis and marked spasticity. A new lesion or enlarging cerebral mass lesions in tuberculous meningitis is not always because of paradoxical reaction, and a possibility of drug resistance should be considered. Drug susceptibility testing, in specimens from extra central nervous system sites, should always be performed.
Figure 1: At the time of initial diagnosis, the normal cranial computed tomography is shown (a). One and a half month later, there is a paradoxical worsening in imaging, as evidenced by optochiasmatic arachnoiditis and left perimesencephalic tuberculoma (b), infarct in the left basal ganglia and thalamus extending upto the posterior limb of internal capsule (c), and computed tomography angiogram showing the narrowed A1 segmment of the left anterior cerebral artery and P1 segment of the left posterior cerebral artery, along with increased collaterals in the posterior circulation (d)

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Figure 2: Acute inflammatory supraclavicular lymphadenopathy

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Figure 3: Cranial magnetic resonance imaging showing left cortical hemiatrophy, dilation of both lateral ventricles with marked asymmetry, with irregular margin and enhancing septations on the left side (a and b). Exudates and granulation tissue were also noted in the interpeduncular, prepontine, and suprasellar cisterns (c and d)

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Drug-resistant tuberculous meningitis is difficult to recognize and treat. Mortality in multidrug-resistant tuberculous meningitis is exceptionally high.[1] Clinical characteristics and neuroimaging features of drug-resistant and drug-susceptible tuberculous meningitis cases were similar. A paradoxical reaction is an important differential diagnosis and may lead to wrong conclusions (e.g., possibility of a mycobacterial drug resistance).[2] Marked cerebral hemiatrophy as a sequel of tuberculous meningitis is extremely rare. There is only one report available about cerebral hemiatrophy secondary to tuberculous meningitis. Cerebral hemiatrophy, in the autopsy, was noted after 15 years of illness. Cerebral hemiatrophy was associated with hemiparesis as a squeal and considered as being due due to a severe cerebrovascular disease.[3] Our patient also developed severe left cerebral hemiatrophy involving in the region of both anterior and posterior circulation due to the large-sized arterial involvement. In tuberculous meningitis, vasculitis mostly affects deep perforating arteries causing infarction mainly in the region of basal ganglia, thalamus, and internal capsule.[4],[5]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Heemskerk AD, Nguyen MTH, Dang HTM, Vinh Nguyen CV, Nguyen LH, Do TDA, et al. Clinical outcomes of patients with drug-resistant tuberculous meningitis treated with an intensified antituberculosis regimen. Clin Infect Dis 2017;65:20-8.  Back to cited text no. 1
Singh AK, Malhotra HS, Garg RK, Jain A, Kumar N, Kohli N, et al. Paradoxical reaction in tuberculous meningitis: Presentation, predictors andimpact on prognosis. BMC Infect Dis 2016;16:306.  Back to cited text no. 2
Garg RK, Malhotra HS, Kumar N. Paradoxical reaction in HIV negative tuberculous meningitis. J Neurol Sci 2014;340:26-36.  Back to cited text no. 3
Itoh M, Sunahara M, Kurata K, Satoh J, Fueki N, Yamada K, et al. An autopsy case of cerebral hemiatrophy with tuberculous meningitis sequelae. Brain Dev 1995;17:371.  Back to cited text no. 4
Modi M, Goyal MK, Jain A, Sawhney SS, Sharma K, Vyas S, et al. Tuberculous meningitis: Challenges in diagnosis and management: Lessons learnt from Prof. Dastur's article published in 1970. Neurol India 2018;66:1550-71.  Back to cited text no. 5
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