PubMed · 14936735
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K KOLLE, G SCHALTENBRAND, F TOBEL. 1952. [Infectious polyneuritis].. https://pubmed.ncbi.nlm.nih.gov/14936735/
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Autoimmune-mediated disorders belong to the main causes of neuropathies worldwide. During recent years much progress has been achieved in the understanding of the underlying pathomechanisms, associated with implications for therapeutic approaches. Here we will briefly review the pathogenesis and discuss treatment options of the Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and neuropathies associated with paraproteinemias. In most of these disease entities intravenous immunoglobulins play a major role as effective and safe treatment options.
Guillain-Barré syndrome (GBS) is an autoimmune acute peripheral neuropathy. Frequently a flu-like episode or a gastroenteritis precede GBS, and the cross-reactivity between microbial and neural antigens partly explains the pathophysiology of the disease and the possible detection of antiganglioside antibodies. The weakness reaches its nadir in 2-4 weeks: the patients may be chair- or bed-bound, may need artificial ventilation and frequently experience dysautonomic dysfunction; 5-15% of the patients die and more patients are left with a disabling motor deficit and/or fatigue. Electrophysiology and cerebrospinal fluid evaluation support the diagnosis. The treatment of GBS is multidisciplinary, and both plasma exchange and high dose immunoglobulin (IVIg) are effective in reducing both the severity of the disease and the residual deficits. Finally, steroids are not effective in GBS.
Guillain-Barré syndrome typically presents with an acute ascending areflexic weakness, progressing over 4 weeks or less. The most common form of the disease is an acute inflammatory demyelinating polyneuropathy, but other forms with primarily axonal pathologies are well documented. The association of Guillain-Barré syndrome with a range of antecedent infections, particularly Campylobacter jejuni enteritis, is also established. A range of serological and neurophysiological investigations can assist in making an accurate diagnosis. Background information about the syndrome and the evidence base for such treatments are discussed herein.