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Potential disease trigger as a therapeutic option: infliximab for paradoxical reaction in tuberculosis of the central nervous system
  1. Myriam Briner1,
  2. Michael Oberholzer1,
  3. Andrew Chan1 and
  4. Franca Wagner2
  1. 1Department of Neurology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland
  2. 2Diagnostic and Interventional Neuroradiology, Inselspital University Hospital Bern, 3010 Bern, Switzerland
  1. Correspondence to Dr Myriam Briner; myriam.briner{at}


A 36-year-old man of central Asian origin was diagnosed with subacute disseminated tuberculosis. Initially, central nervous system involvement was suggested by an encephalopathic condition and MRI showing extensive basal and spinal meningitis. After initiation of anti-tuberculosis drugs and corticosteroid therapy, clinical and radiological deterioration of spinal damage was noted. We interpreted this in the context of a paradoxical reaction, which is suggested to be an overshooting inflammatory response after reconstitution of the immune system. Despite increased dosage of corticosteroids, a gradual worsening of gait ataxia over several weeks was noted. After administration of infliximab, the patient’s condition progressively improved.

  • immunological products and vaccines
  • immunology
  • meningitis
  • TB and other respiratory infections
  • infection (neurology)

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  • MB and MO contributed equally.

  • Correction notice This article has been corrected since published online. The order of the authors has been corrected.

  • Contributors MB and MO contributed equally to this work. They gathered and interpreted clinical and laboratory findings, performed literature research and wrote the paper with input from all authors. AC supported MB and MO for writing the main part of the discussion and assisted them with literature interpretation. FW provided the neuroradiological images and revised their interpretation. She supported MB and MO in writing the part on radiological findings.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests MB received travel grants from Merck and Biogen, and research support from Burgergemeinde Bern. AC has received personal compensation for activities with Bayer, Biogen, Genzyme, Merck, Novartis, Roche and Teva. He received research support from the Swiss National Fonds (SNF, No. 310030_172952), Genzyme and UCB. FW received research support from Multiple Sklerose Gesellschaft Schweiz.

  • Provenance and peer review Not commissioned; externally peer reviewed.