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January 15, 2013; 80 (3) Resident and Fellow Section

Teaching NeuroImages: Deep gray matter involvement in neurobrucellosis

Roopa Rajan, Dheeraj Khurana, Praveen Kesav
First published January 14, 2013, DOI: https://doi.org/10.1212/WNL.0b013e31827deb63
Roopa Rajan
From the Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
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Dheeraj Khurana
From the Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
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Praveen Kesav
From the Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
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Teaching NeuroImages: Deep gray matter involvement in neurobrucellosis
Roopa Rajan, Dheeraj Khurana, Praveen Kesav
Neurology Jan 2013, 80 (3) e28-e29; DOI: 10.1212/WNL.0b013e31827deb63

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A 27-year-old man, recent visitor to the Middle East, presented with 6-week history of fever (up to 102°F) followed by altered behavior and left hemiparesis. CSF was acellular with raised protein (138 mg/dL). CSF bacterial culture was sterile; adenosine deaminase normal (3 U/L); cryptococcal antigen, Venereal Disease Research Laboratory test, and Japanese B serology were negative. HIV serology and vasculitic workup were unremarkable. Serum Brucella agglutination titer was 320 IU (immunoglobulin M fraction 280 IU). Cranial MRI showed nonenhancing bilateral white matter and basal ganglia hyperintensities on T2-weighted images (figure, A–C). The patient was treated with IV ceftriaxone (1 month) along with oral doxycycline and rifampicin (4 months). At 3 months, Brucella agglutination titer was <20 IU and the patient became independent. Follow-up imaging showed a reduction in lesions (figure, D). Brucellosis frequently presents as chronic meningitis along with cranial neuropathies and spinal arachnoiditis.1 Demyelinating lesions are described in neurobrucellosis,1,2 involvement of the deep gray matter being unusual.

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Figure Imaging

Cranial MRI T2-weighted axial (A), T1-weighted axial (B), and T2 fluid-attenuated inversion recovery coronal (C) showing bilateral periventricular and basal ganglia hyperintensities with no contrast enhancement or mass effect. (D) Follow-up imaging at 11 months showing reduction in T2 hyperintensities in the right putamen, left caudate, and periventricular white matter.

AUTHOR CONTRIBUTIONS

Roopa Rajan: data collection, drafting of manuscript. Dheeraj Khurana: revision of manuscript, concept of manuscript. Praveen Kesav: data collection, review of literature.

STUDY FUNDING

No targeted funding reported.

DISCLOSURE

The authors report no disclosures relevant to the manuscript. Go to Neurology.org for full disclosures.

Footnotes

  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

  • © 2013 American Academy of Neurology

REFERENCES

  1. 1.↵
    1. Ceran N,
    2. Turkoglu R,
    3. Erdem I,
    4. et al
    . Neurobrucellosis: clinical, diagnostic, therapeutic features and outcome: unusual clinical presentations in an endemic region. Braz J Infect Dis 2011;15:52–59.
    OpenUrlCrossRefPubMed
  2. 2.↵
    1. Al-Sous MW,
    2. Bohlega S,
    3. Al-Kawi MZ,
    4. Alwatban J,
    5. McLean DR
    . Neurobrucellosis: clinical and neuroimaging correlation. AJNR Am J Neuroradiol 2004;25:395–401.
    OpenUrlAbstract/FREE Full Text
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