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A case of multiple cranial nerve palsies
  1. Saranya Gomathy1,
  2. Arunmozhimaran Elavarasi1,
  3. Snigdha Komakula1,
  4. Manish Modi2,
  5. MC Sharma3,
  6. Kavneet Kaur3,
  7. Ajay Garg4,
  8. Madhavi Tripathi5,
  9. Anupam Kanodia6,
  10. Hitesh Verma6,
  11. Deepti Vibha1,
  12. Rajesh K Singh1,
  13. Bhargavi Ramanujam1,
  14. Manjari Tripathi1
  1. 1 Department of Neurology, All India Institute of Medical Sciences, New Delhi, Delhi, India
  2. 2 Department of Neurology, Post Graduate Institute of Medical Education and Research, Chandigarh, India
  3. 3 Department of Pathology, All India Institute of Medical Sciences, New Delhi, Delhi, India
  4. 4 Department of Neuroradiology, All India Institute of Medical Sciences, New Delhi, India
  5. 5 Department of Nuclear Medicine, All India Institute of Medical Sciences, New Delhi, India
  6. 6 Department of Otorhinolaryngology, All India Institute of Medical Sciences, New Delhi, India
  1. Correspondence to Dr Arunmozhimaran Elavarasi, Department of Neurology, All India Institute of Medical Sciences, New Delhi, India; arun_ela{at}yahoo.com

Abstract

Multiple cranial nerve palsies have many possible causes, including infective, inflammatory, neoplastic and infiltrative diseases of the meninges or skull base. We present the clinicopathological conference of a 27-year-old man with a smouldering course of sequential cranial nerve palsies. His imaging showed dural thickening and osteosclerosis of the skull base with otomastoiditis. Cerebrospinal fluid showed lymphocytic pleocytosis with reduced glucose and normal protein concentrations. There was a possible response to corticosteroids and anti-tubercular treatment. Initial biopsy from the thickened and enhancing dura was unremarkable. His condition deteriorated after the steroids were tapered; MR imaging showed progression of lesions and positron emission tomography showed intense hypermetabolism. Subsequently, a diagnostic test revealed the final diagnosis. This case was presented at the All India Institute of Medical Sciences’ monthly clinicopathological conference series in February 2021.

  • clinical neurology

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Footnotes

  • Contributors SG contributed to the diagnosis and management of the case and in writing the first draft of the manuscript. AE contributed to diagnosis, management, the conceptualisation of the report and in writing and critique of the manuscript. SK contributed to the diagnosis and management of the case and in writing the first draft of the manuscript. MM was involved in the discussion of the clinicopathological conference (CPC), writing and critique of the manuscript. MCS was involved in histopathological diagnosis, discussion of the pathology part of the CPC and in writing and critique of the manuscript. KK was involved in histopathological diagnosis, discussion of the pathology part of the CPC and in writing and critique of the manuscript. AG was involved in radiological diagnosis and discussion and writing and critique of the manuscript. Madhavi Tripathi was involved in positron emission tomography-CT interpretation and writing and critique of the manuscript. AK was involved in performing the biopsy and in diagnosis and writing and critique of the manuscript. HV was involved in performing the biopsy and in diagnosis and writing and critique of the manuscript. DV, RKS, BR and Manjari Tripathi were involved in the diagnosis and management of the case and critique of the manuscript.

  • 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 None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed by Michael Halmagyi, Sydney, Australia.

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