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Risk factors for treatment related clinical fluctuations in Guillain-Barré syndrome
  1. J H REES
  1. National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. Telephone 0171 837 3611; fax 0171 829 8720

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    The efficacy of immunomodulatory treatments, either plasma exchange or intravenous immune globulin (IVIg), is now well established in the management of Guillain-Barré syndrome. However, about 5% of patients deteriorate after a period of initial improvement or stabilisation, and two independent reports drew attention to a worryingly high relapse rate after treatment with IVIg.1 2 A second unrelated issue revolved around the severity of disease that required intervention and in particular whether patients should be treated while still ambulant. Cost and safety considerations preclude widespread adoption of this practice, but it is also possible that early treatment may be associated with a higher relapse rate. These issues have been partly considered by the study of Visser et al 3 (pp 242–4 of this volume) who report their data on 16 patients who relapsed after either plasma exchange or IVIg and compared the clinical characteristics with 156 patients who did not relapse. Their findings go some way to reassure us that treatment modality—namely, plasma exchange or IVIg—seems not to have any influence on the risk of relapse. Secondly, the time from onset of weakness to treatment was similar in both groups although, as all patients had to be unable to walk 10 m independently to be randomised, we are still in the dark as to whether ambulant patients tend to relapse more often. A third interesting finding, but not entirely unexpected, is that those patients who have an “acute motor Guillain-Barré syndrome” characterised by a rapid onset of weakness and progression to tetraplegia without any associated sensory loss do not relapse. This may be because this variant of Guillain-Barré syndrome is caused by acute axonal degeneration. As the axons once destroyed cannot regenerate sufficiently quickly to be attacked again by the original immune effector mechanisms (which may have subsided long before), clinical relapse would not be expected to occur. The authors also suggest that fluctuations tended to occur in those patients with a more protracted disease course, as defined by a slightly longer time until the nadir, although the difference did not reach significance. Inevitably, significant results will appear if enough variables are examined and if a Bonferroni correction of 20 (No of variables examined) is applied to these data, then none exceeds the 5% significance level. The authors rightly point out that the numbers are small and so care must be taken not to draw too many conclusions from this study alone. Nevertheless it would be interesting to confirm or refute these findings by testing the data from the other large treatment study carried out by the Plasma Exchange/Sandoglobulin Guillain-Barré syndrome Trial group4 to define a subgroup of patients more likely to relapse. The next challenge is to determine the best treatment for relapsing patients and trials are ongoing to answer this question.

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