Abstract
Guillain-Barré syndrome, a clinical syndrome of rapidly progressive weakness attributable to polyradiculoneuro-pathy and reaching its nadir within 4 weeks, is now recognised to be due to any one of several pathological processes.1 The commonest underlying pathological change in Europe and North America is acute inflammatory demyelinating polyradiculoneuropathy, which affects mainly the anterior spinal roots and motor nerve fibres and causes more weakness than sensory loss. The inflammation causes demyelination and, when severe, axonal degeneration as well.
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