[Miller-Fisher syndrome associated with acute motor axonal neuropathy: clinic-immunological correlation].

Miller-Fisher syndrome (MFS) is an extremely rare, autoimmune, axonal polyradiculoneuropathy which takes place during childhood. It is characterised by the clinical triad of ataxia, ophthalmoplegia and arreflexia. The annual incidence of Miller-Fisher syndrome is 0.09 cases per 100 000 inhabitants. The few published series that exist with children account for approximately 9% of the total of acute polyradiculoneuropathy cases. As in the case of Guillain—Barré syndrome, it is often triggered by certain strains of Campylobacter jejuni that induce the formation of anti-GQ1b antiganglioside, although there have also been cases described involving Haemophilus influenzae and Mycoplasma pneumoniae. Anti-GQ1b antibodies are elevated in 90—97% of Miller-Fisher syndrome cases. These antibodies recognise epitopes that are expressed specifically in the nodal regions of the oculomotor nerves, in the dorsal root ganglia and in the cerebellar neurons. All these structures are responsible for the symptoms of Miller-Fisher syndrome. Occasionally, Miller-Fisher syndrome and Guillain-Barré syndrome in its demyelinating, acute, motor axonal and acute sensorimotor variants may have an overlapping clinical spectrum, depending on the immunopathological cause. Moreover, motor axonal forms generally respect cranial nerves and present a predominantly distal involvement. Very few cases of this type of presentation have been studied in the light of current knowledge, improved antibody detection techniques and purification of new antigens from the nervous system. We present a study of a patient suffering from Miller-Fisher variant associated with an acute peripheral case of acute motor axonal neuropathy (AMAN). We