TY - JOUR
T1 - Guillain-Barré syndrome
T2 - An update
AU - Vucic, Steve
AU - Kiernan, Matthew C.
AU - Cornblath, David R.
N1 - Funding Information:
Funding support from the Motor Neuron Disease Research Institute of Australia (MNDRIA) and National Health and Medical Research Council of Australia is gratefully acknowledged.
PY - 2009/6
Y1 - 2009/6
N2 - Guillain-Barré syndrome (GBS) is an acute polyneuropathy consisting of different subtypes. Acute inflammatory demyelinating polyradiculoneuropathy, the classic demyelinating form of GBS, accounts for 90% of all GBS cases in the Western world. Acute motor axonal neuropathy (AMAN) and acute motor and sensory axonal neuropathy (AMSAN) are axonal forms of GBS that are more prevalent in Asia, South and Central America, often preceded by infection by Campylobacter jejuni. AMAN and AMSAN may be mediated by specific anti-ganglioside antibodies that inhibit transient sodium ion (Na+) channels. The efficacy of plasmapheresis and intravenous immunoglobulin has been established in large international randomised trials, with corticosteroids proven ineffective. Although axonal demyelination is an established pathophysiological process in GBS, the rapid improvement of clinical deficits with treatment is consistent with Na+ channel blockade by antibodies or other circulating factors, such as cytokines. This review provides an update on the epidemiology, clinical features, diagnosis, pathogenesis and treatment of GBS.
AB - Guillain-Barré syndrome (GBS) is an acute polyneuropathy consisting of different subtypes. Acute inflammatory demyelinating polyradiculoneuropathy, the classic demyelinating form of GBS, accounts for 90% of all GBS cases in the Western world. Acute motor axonal neuropathy (AMAN) and acute motor and sensory axonal neuropathy (AMSAN) are axonal forms of GBS that are more prevalent in Asia, South and Central America, often preceded by infection by Campylobacter jejuni. AMAN and AMSAN may be mediated by specific anti-ganglioside antibodies that inhibit transient sodium ion (Na+) channels. The efficacy of plasmapheresis and intravenous immunoglobulin has been established in large international randomised trials, with corticosteroids proven ineffective. Although axonal demyelination is an established pathophysiological process in GBS, the rapid improvement of clinical deficits with treatment is consistent with Na+ channel blockade by antibodies or other circulating factors, such as cytokines. This review provides an update on the epidemiology, clinical features, diagnosis, pathogenesis and treatment of GBS.
KW - Acute inflammatory demyelinating polyradiculoneuropathy
KW - Acute motor and sensory axonal neuropathy
KW - Acute motor axonal neuropathy
KW - Guillain-Barré syndrome
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U2 - 10.1016/j.jocn.2008.08.033
DO - 10.1016/j.jocn.2008.08.033
M3 - Review article
C2 - 19356935
AN - SCOPUS:67349199109
SN - 0967-5868
VL - 16
SP - 733
EP - 741
JO - Journal of Clinical Neuroscience
JF - Journal of Clinical Neuroscience
IS - 6
ER -