Abstract
The Inflammatory Polyneuropathies (IPN) are an important group of acquired neuropathies characterized pathologically by the presence of inflammatory lesions scattered throughout the peripheral nervous system associated with segmental demyelination and remyelination, high protein content and normal cell count in the CSF, and low nerve conduction velocities. Clinically, patients may present with an acute or subacute onset of weakness and areflexia and recovery in weeks or months (Acute Inflammatory Polyneuropathy (AIPN) or the (Guillain-Barre Syndrome), or with an insidious onset of a distal sensory-motor polyneuropathy with a progressive or relapsing-remitting course (Chronic Inflammatory Polyneuropathies (CIPN)). Their pathogenesis is unclear though related to abnormal immune responses with the possible implication of both cell-mediated and humoral-mediated immunity. The efficacy of modifiers of the immune response in the management of the IPN is controversial. Corticosteroids and cytotoxics have not proven a benefit in the acute cases, but they seem effective in the chronic ones. Plasma exchange therapy has been reported effective in uncontrolled trials in AIPN and in some CIPN cases, but failures have also been reported.