Editorials

Intravenous IgG in Guillain-Barre syndrome

BMJ 1996; 313 doi: https://doi.org/10.1136/bmj.313.7054.376 (Published 17 August 1996) Cite this as: BMJ 1996;313:376
  1. R A C Hughes, Professor
  1. Department of Neurology, Guy's and St Thomas's Medical and Dental School, London SE1 9RT

    <it>Same short term benefit as plasma exchange but easier to administer</it>

    The commonest misdiagnosis of Guillain-Barre syndrome by the doctor of first contact is hysteria. This is understandable when most doctors have not seen a case since medical school. However, the syndrome is neither rare nor trivial. With an incidence of one or two cases per 100 000 population per year, new cases are about half as common as new cases of multiple sclerosis—a disease confined to the central nervous system as closely as Guillain-Barre syndrome is restricted to the peripheral nervous system. A quarter of adult patients require artificial ventilation, 10% die as a result of complications of the disease, and 10% are left with such severe disability that they cannot walk unaided a year later.1

    The pathological process underlying Guillain-Barre syndrome is heterogeneous. Most patients have an acute multifocal lymphocytic infiltration in their peripheral nerves and spinal roots causing primary demyelination, which will recover quickly. Severely affected patients usually have additional axonal degeneration, which causes delayed and often incomplete recovery. About 10% of patients have an acute motor, or motor and sensory, axonal neuropathy in which macrophages invade the axons, especially in the spinal roots.2 3 Both types of Guillain-Barre syndrome are thought to be due to an autoimmune response triggered …

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