Article Text
Summary
An 81-year-old man presented with fever, confusion and rapidly-progressive flaccid tetraparesis. Clinical presentation and neurophysiology were consistent with a severe axonal polyneuropathy. Anti-GM1 and Campylobacter serology were both positive, consistent with postinfectious axonal-variant Guillain-Barré syndrome (GBS). GBS is characterised by albuminocytological dissociation, where an elevated protein and acellular cerebrospinal fluid are typical. However, in this case, CSF analysis revealed an exaggerated pleocytosis (72 white blood cells (WBC)/mm3). No source of central nervous system infection or inflammation was identified despite thorough investigation. The patient was treated with intravenous immunoglobulin and intensive rehabilitation.
Albuminocytological dissociation classically distinguishes GBS from infective causes of flaccid weakness (eg, enteroviruses, flaviviruses and HIV). Diagnostic criteria frequently cite a pleocytosis of <50 WBC/mm3 as required in the diagnosis of GBS. However, this case demonstrates that pleocytosis exceeding this level can occur in the presence of convincing evidence of GBS and without demonstrable neurotropic infection.
- neurology
- clinical neurophysiology
- infection (neurology)
- peripheral nerve disease
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Footnotes
Contributors GD: wrote the manuscript, performed literature analysis and obtained patient consent. SKA and AR: revised the manuscript. All authors: contributed to the clinical care of the patient.
Competing interests None declared.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.