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Table of Contents
LETTER TO THE EDITOR
Year : 2019  |  Volume : 10  |  Issue : 4  |  Page : 231-232

Vanishing splenium of corpus callosum hyperintensity in a case of tuberculous meningitis


Department of Neurology, SMS, Jaipur, Rajasthan, India

Date of Submission10-Sep-2019
Date of Decision30-Sep-2019
Date of Acceptance02-Oct-2019
Date of Web Publication06-Nov-2019

Correspondence Address:
Dr. Divya Goel
4Ba19, Jawahar Nagar, Jaipur - 302 004, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/INJMS.INJMS_119_19

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How to cite this article:
Jain R S, Goel D. Vanishing splenium of corpus callosum hyperintensity in a case of tuberculous meningitis. Indian J Med Spec 2019;10:231-2

How to cite this URL:
Jain R S, Goel D. Vanishing splenium of corpus callosum hyperintensity in a case of tuberculous meningitis. Indian J Med Spec [serial online] 2019 [cited 2019 Dec 14];10:231-2. Available from: http://www.ijms.in/text.asp?2019/10/4/231/270426



Dear Editor,

A 35-years-old female presented with 15 days' history of moderate-to-high grade fever, headache, vomiting, and altered behavior in the form of occasional irrelevant talks. On examination, neck stiffness and bilateral papilledema were noted. Magnetic resonance imaging (MRI) brain with contrast revealed a hyperintensity in splenium of corpus callosum with diffusion restriction [Figure 1] and [Figure 2]. Cerebrospinal fluid examination showed 260 cells with lymphocytic predominance (95%), raised proteins (254 mg/dl), and low sugar (22 mg/dl) indicative of tuberculous meningitis. The patient was started on antitubercular therapy (HRZES regimen) with injectable steroids (injection dexamethasone 4 mg tid). She showed improvement in her symptoms but developed intermittent vertigo for which her MRI brain was repeated after 6 days, which showed resolution of the corpus callosal hyperintensity [Figure 3] and [Figure 4]. Injection streptomycin was withheld after which her vertigo subsided. The patient became asymptomatic in the next 4 days and was discharged on antitubercular therapy and tapering doses of oral steroids (tablet dexamethasone 4 mg tid with a weekly taper).
Figure 1: Magnetic resonance imaging brain diffusion-weighted imaging axial image shows diffusion restriction in the splenium of the corpus callosum with corresponding apparent diffusion coefficient fall

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Figure 2: Magnetic resonance imaging brain T2 axial image shows well-defined hyperintense lesion in the splenium of the corpus callosum

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Figure 3: Magnetic resonance imaging brain diffusion-weighted imaging axial image shows resolution of diffusion restriction in the splenium of the corpus callosum

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Figure 4: Magnetic resonance imaging brain T2 axial image shows resolution of hyperintense lesion in the splenium of the corpus callosum

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The lesions in the splenium of the corpus callosum supervene only rarely in tuberculous meningitis. Hirotani et al. reported a case of tuberculous meningitis with abnormal signal intensities in splenium, internal capsule, and basal ganglia which resolved after a few days of therapy.[1] Kimura et al.[2] reported reversible hyperintense lesions in white matter and splenium of the corpus callosum in a case of influenza-associated encephalitis. Jain et al.,[3] in his case report, found a vanishing splenial lesion presenting as alexia with dysgraphia. The exact pathogenesis of the splenial lesion in the corpus callosum in this case of tuberculous meningitis is uncertain. The reversible lesion in the splenium of the corpus callosum is postulated to be caused by an increase in cytokines such as interleukin-6, interleukin-10, and intramyelinic edema.[2] These raised inflammatory cytokines decrease following treatment of the tuberculous meningitis[4],[5] with anti-inflammatory action of steroids, resulting in the resolution of the intramyelinic edema. This explains why the lesion in the splenium of the corpus callosum in tuberculous meningitis is only transient, as seen in this patient. To conclude, isolated vanishing splenial hyperintensity may be seen in a case of tuberculous meningitis, is an uncommonly documented entity, and carries a good prognosis with routine management.

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.

Financial support and sponsorship

None.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Hirotani M, Yabe I, Hamada S, Tsuji S, Kikuchi S, Sasaki H. Abnormal brain MRI signals in the splenium of the corpus callosum, basal ganglia and internal capsule in a suspected case with tuberculous meningitis. Intern Med 2007;46:505-9.  Back to cited text no. 1
    
2.
Kimura E, Okamoto S, Uchida Y, Hirahara T, Ikeda T, Hirano T, et al. Areversible lesion of the corpus callosum splenium with adult influenza-associated encephalitis/encephalopathy: A case report. J Med Case Rep 2008;2:220.  Back to cited text no. 2
    
3.
Jain RS, Kumar S, Paul M, Agrawal R. Vanishing splenial lesion presenting as alexia with dysgraphia. J Neurol 2015;262:1058-62.  Back to cited text no. 3
    
4.
Yadav A, Chaudhary C, Keshavan AH, Agarwal A, Verma S, Prasad KN, et al. Correlation of CSF proinflammatory cytokines with MRI in tuberculous meningitis. Acad Radiol 2010;17:194-200.  Back to cited text no. 4
    
5.
Mansour AM, Frenck RW Jr., Darville T, Nakhla IA, Wierzba TF, Sultan Y, et al. Relationship between intracranial granulomas and cerebrospinal fluid levels of gamma interferon and interleukin-10 in patients with tuberculous meningitis. Clin Diagn Lab Immunol 2005;12:363-5.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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