J Neurol Neurosurg Psychiatry 73:344 doi:10.1136/jnnp.73.3.344
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Miller-Fisher syndrome and Hodgkin’s disease

  1. E Rubio-Nazabal,
  2. J Marey-Lopez,
  3. J P Torres-Carrete,
  4. P Alvarez-Perez,
  5. P Rey Del Corral
  1. Departments of Neurology and Haematology, Hospital Juan Canalejo, La Coruña, Spain
  1. Correspondence to:
 Dr E Rubio-Nazabal, Servicio de Neurología, Hospital Juan Canalejo, As Xubias sn, 15006 La Coruña, Spain;

    Miller-Fisher syndrome (MFS) is a rare clinical entity classically regarded as a variant of Guillain-Barré syndrome (GBS) and characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia.1 In MFS, paralysis is restricted to extraocular and occasionally other craniobulbar muscles. We report on a patient with a relapsing Hodgkin’s disease who developed MFS. Conventional immunosuppressive and intravenous immunoglobulin treatments improved the neurological deficits.

    This 27 year old white man who had an eight year history of Hodgkin’s disease (type mixed cellularity, pathological stage IVB) had been receiving a salvage ESHAP regimen (etoposide VP-16 68 mg/day, methylprednisolone 500 mg/day, and cisplatin 42.5 mg/day for four days and cytosinearabinoside 3.4 g/day on the fifth day) since the first disease relapse four months before admission. He was admitted to the hospital for constitutional symptoms (39°C fever, recurrent night sweats, fatigue, malaise, and weakness). There was no history of infection. General examination was unremarkable except for bilateral inguinal adenopathy (1.5 × 1.5 cm). Haemoglobin concentration was 63 g/l, packed cell volume 17.8%, platelet count 89 × 109/l, white cell count 3.34 × 109/l (neutrophils 2.42 × 109/l), and lactate dehydrogenase 461 U/l. Results of the following investigations were normal: glucose, cholesterol, triglycerides, and ions; renal, liver, and thyroid function tests; vitamin B12 and folic acid; and tests for Campylobacter …

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