Ganglioside-Related Disorders (GQ1b; Miller-Fisher Syndrome; CANOMAD),

Molecular mimicry between microbiologic agents and endogenous antigens that triggers dysimmunity has been well delineated in Guillain-Barré syndrome (GBS).1 The lipopolysaccharide (LPS) capsule of Campylobacter jejuni carries moieties that resemble gangliosides that are enriched in the nodal regions of nerves. The LPS configuration of the infecting bacteria and the immune constitution of the host determine the type of anti-ganglioside antibodies that are produced. The patients develop different subtypes of GBS contingent on the target of these antibodies. Miller Fisher syndrome and acute ophthalmoparesis are both associated with anti-GQ1b antibody. GQ1b is strongly expressed in the oculomotor, trochlear and abducens nerves, as well as muscle spindles in the limbs (the latter explaining the limb ataxia).