Article Text

other Versions

Download PDFPDF
Primary position upbeat nystagmus in thiamine deficiency
  1. Denison Alves Pedrosa,
  2. René de Araújo Gleizer,
  3. Raphaela Coelho Veloso Gomes,
  4. José Marcos Vieira de Albuquerque Filho,
  5. Breno Assunção Matos,
  6. Rafaela Almeida Alquéres
  1. Hospital Israelita Albert Einstein, São Paulo, Brazil
  1. Correspondence to Dr. Denison Alves Pedrosa, Hospital Israelita Albert Einstein, São Paulo, Brazil; denisonpedrosa{at}hotmail.com

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

A 34-year-old woman presented to the emergency department with symptoms of encephalopathy, characterized by visual hallucinations, gait disturbance, and oscillopsia. She had a previous diagnosis of schizophrenia and a 3-month history of severely restricted food intake and self-induced vomiting, but no known alcohol abuse or use of tobacco or recreational drugs. On examination, she was disorientated in time and space, with apathy and reduced attention span. Funduscopy was normal. There was upbeat nystagmus in the primary position (figure 1), which was amplified on upgaze and attenuated by a horizontal–torsional component on lateral gaze (online supplemental video 1). Muscle strength, deep tendon reflexes and sensations were normal, with flexor plantar responses. She showed incoordination in all limbs and a broad-based ataxic gait. There were no signs of meningeal irritation. Investigations including full blood count, fasting glucose, serum B12, electrolytes, and serological tests for syphilis (venereal disease research laboratory), viral hepatitis B and C, and HIV serology were normal or negative. CT scan of the whole body and CSF analysis, including a meningoencephalitis panel, were normal. MR scan of the brain showed symmetric hyperintensities in the medial thalami and periaqueductal grey matter (figure 2). The clinical …

View Full Text

Footnotes

  • Contributors DAP: drafting/revision of the manuscript for content, including medical writing for content; major role in the acquisition of data; study concept or design; analysis or interpretation of data; RG: major role in the acquisition of data; analysis or interpretation of data; RCVG: major role in the acquisition of data; analysis or interpretation of data; JMVAF: major role in the acquisition of data; analysis or interpretation of data; BAM: major role in the acquisition of data; study concept or design; analysis or interpretation of data; RAA: drafting/revision of the manuscript for content, including medical writing for content; major role in the acquisition of data; study concept or design; analysis or interpretation of data.

  • 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 Luke Bennetto, Bristol, UK.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

Other content recommended for you