Guillain-Barre syndrome is a well-defined clinical entity correspondin
g to primary inflammatory demyelinating lesions of peripheral nerves a
nd spinal roots in the majority of cases seen in Western Europe and No
rth America. Documentation of conduction abnormalities characteristic
of demyelination in the context of rapidly developing weakness confirm
s the clinical diagnosis of acute inflammatory demyelinating polyradic
uloneuropathy. These abnormalities include(1) conduction block, (2) ma
rkedly prolonged distal latencies, (3) marked slowing of motor conduct
ion velocities, and (4) absent or impersistent F responses. Other abno
rmalities are of ambiguous significance : (1) low amplitude compound m
uscle responses, (2) absent sensory nerve potentials, (3) reduction in
the maximum EMG recruitment pattern, which may all (1, 2, and 3) indi
cate conduction block or axonal degeneration, and (4) fibrillation pot
entials due to breakdown of motor axons, a frequent non-specific effec
t of primary inflammatory demyelination, A Guillain-Barre va riant due
to immune-mediated primary axonal degeneration has also been recently
described.