Not all Guillain Barré Syndrome (GBS) is the same. This will have been obvious to many patients with GBS and their families for some time. It has been official ever since the description of ''an acute axonal form'' of GBS by Tom Feasby and colleagues in what we call the “other” London (London, Ontario) in 1986. Our recent large multi-centre trial of intravenous immunoglobulin in GBS gave us the opportunity of studying just how common the different types are.

We had neurophysiological test results available from 369 patients within fifteen days after the onset of GBS. We used neurophysiological criteria to divide patients into groups with different types of abnormality of nerve conduction studies. Sixty nine percent were classified as demyelinating, three percent axonal, three percent were inexcusable (their nerves that is), two percent were normal and in twenty-three percent the results were abnormal but did not allow classification into either the demyelinating or axonal category. The demyelinating category would be consistent with damage to the myelin sheaths causing slowing of conduction. The axonal category would be consistent with damage to or abnormal function of the central conducting core, or axon, of the nerve fibers. This suggests that the immune system attacks different parts of the nerves in the different types.

Without pathological studies the truth of this deduction cannot be verified. However, the patients with axonal neurophysiology showed important biological differences from the demyelinating group. They were more likely to have had a preceding diarrhoeal illness, more likely to have normal sensory nerve function and more likely to have antibodies to ganglioside GM1. The patients with inexcusable nerves might have had such severe demyelinating neuropathy that conduction was completely blocked or such severe axonal neuropathy that all the axons had degenerated. Patients with inequitable nerves were more likely to be left disabled at the end of the study. The numbers of patients with axonal or inequitable nerves were too small for us to distinguish whether one of the three treatments being tested (plasma exchange, intravenous immunoglobulin, or plasma exchange followed by intravenous immunoglobulin) was superior in these types of GBS.

During the study we collected blood samples from patients before starting treatment and two weeks later. We still have a wealth of important information locked up in these samples and are currently studying the relationship between the different types of Guillain Barré Syndrome, different preceding infections, and different patterns of anti-ganglioside antibodies. We all owe a debt to the patients who agreed to be randomized in this trial to allow advances to be made in the understanding of the cause as well as the treatment of the disease. We would like to take this opportunity of thanking those patients again now. The full account of this study has been published.

Hadden RDM, Cornblath DR, Hughes RAC, Zielasek J, Hartugn H-P, Toyka KV, Swan AV, and the Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group. Electrophysiological classification of Guillain-Barré Syndrome: clinical associations and outcome. Ann Neurol 1998; 44:780-788