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Acute proximal weakness and paraesthesiae
  1. Lucia Maure Blesa1,
  2. Daniel López de Mota Sánchez1,
  3. Olalla Álvarez-Toledo2,
  4. Elena Montes Fernandez3,
  5. Montserrat Morales Conejo4,
  6. Teresa Díaz-Cardona5,
  7. Laura Olivie Garcia1,
  8. Ivana Zamarbide Capdepon1,
  9. Antonio Herranz Bárcenas1
  1. 1Neurology, Hospital Universitario Fundacion Jimenez Diaz, Madrid, Spain
  2. 2Internal Medicine Department, Hospital FREMAP Majadahonda, Madrid, Spain
  3. 3Neurophysiology Department, Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain
  4. 4Internal Medicine Department, Hospital Universitario Doce de Octubre, Madrid, Comunidad de Madrid, Spain
  5. 5Rehabilitation Centre, Hospital FREMAP Majadahona, Madrid, Spain
  1. Correspondence to Dr Lucia Maure Blesa, Neurology, Fundación Jiménez Díaz, Madrid, Spain; luciamaure.lm{at}gmail.com

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Case presentation

A man in his mid-50s was admitted to hospital after falling and fracturing his L2 and L4 vertebrae. He had a history of intestinal occlusion 20 years before that had resolved with conservative treatment in his country of origin, Peru. CT scan of head, abdomen and pelvis were normal.

While hospitalised and awaiting vertebroplasty, he developed mild confusion, vomiting and constipation, initially attributed to analgesics (opioids, dexketoprofen and metamizole). His symptoms progressed to oral intolerance with abdominal pain and distension, requiring a nasogastric tube. Given the clinical suspicion of an intestinal obstruction, an X-ray of abdomen showed dilation of intestinal loops. Blood tests identified severe hyponatraemia (serum sodium 123 mmol/L (137–144)) and elevated acute phase reactants including C reactive protein 9 mg/L (<0.05). CT scan of abdomen was compatible with an intestinal obstruction.

He promptly became haemodynamically unstable, developing hypotension (blood pressure 70/40 mm Hg), tachycardia (pulse 134 bpm) and fever (38.7°C), requiring intensive care unit admission for 3 days. An exploratory laparotomy found nothing pathological. His hyponatraemia (119 mmol/L) continued.

Two weeks after discharge from the intensive care unit, he developed numbness of his proximal lower limbs and trunk, progressing after 2 days to proximal weakness of all four limbs, with loss of deep tendon reflexes. He had no sphincter disturbance, facial numbness or weakness, no diplopia or other cranial nerves abnormalities. There was no fever or other features of infection. MR scan of brain showed no acute intracranial pathology and MR scan of spine showed only a fracture of the upper plate of L2.

He was admitted into the neurology department. On examination, he had a tachycardia (100 bpm). There was proximal muscle weakness, with moderate resistance in both arms and only movement against gravity in both legs. Reflexes were reduced in the upper limbs but absent in the lower limbs. He had hypoaesthesia …

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Footnotes

  • Contributors LMB attended clinically the patient, collected the data, wrote and edited the draft. DLdMS attended clinically to the patient and helped editing the draft. OA-T, EMF, TD-C, LOG, IZ helped collecting the data and editing the draft. MMC helped in genetic diagnosis. AH was in charge of the patient during hospitalisation and helped collect data and edit the draft.

  • 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 Jon Walters, Swansea, UK.

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