Acute inflammatory polyneuropathy classified according to symptoms and divided into axonal and demyelinating forms.
Two-thirds have a history of gastroenteritis or influenza-like illness weeks before onset of neurological symptoms.
Neurophysiology is confirmatory and is abnormal in 85% of patients, even early in the disease.
Up to 30% will develop respiratory muscle weakness requiring ventilation.
Lumbar puncture is useful, and the classic finding is elevated protein with normal cell count (albuminocytological dissociation).
Treatment combines supportive and disease-modifying therapy (plasma exchange or high-dose immunoglobulin).
Guillain-Barre syndrome (GBS) is a type of acute inflammatory neuropathy. It is a clinically defined syndrome characterised by motor difficulty, absence of deep tendon reflexes, paraesthesias without objective sensory loss, and increased CSF albumin with absence of cellular reaction (albuminocytological dissociation). Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is the most commonly encountered variant.
History and exam
- presence of risk factors
- muscle weakness
- respiratory distress
- speech problems
- back/leg pain
- facial weakness
- bulbar dysfunction causing oropharyngeal weakness
- extra-ocular muscle weakness
- facial droop
- non-reactive pupil
Queen Elizabeth Neurosciences Centre
University Hospital Birmingham
SJ declares that he has no competing interests.
Dr Saiju Jacob would like to gratefully acknowledge Dr John B. Winer, Dr Michael T. Torbey, Dr Dhruvil J. Pandya, and Dr Prem A. Kandiah, previous contributors to this monograph. JBW, MTT, DJP, and PAK declare that they have no competing interests.
Division of Pediatric Neurology
Columbia University College of Physicians and Surgeons
CA declares that he has no competing interests.
King's College Hospital
RH has been paid by Baxter Healthcare Ltd for membership of its neurology advisory board, and is a co-author of several studies referenced in this monograph.
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