Sensorimotor demyelinating neuropathy with IgM antibody against gangliosides GD1a, GT1b and GM3.
We report a patient with sensorimotor demyelinating neuropathy with high-titer IgM antibody against gangliosides GD1a, GT1b and GM3. The patient was a 65-year-old male who was hospitalized with chief complaints of muscular weakness of all limbs and numbness of the hands and feet. Nerve-conduction studies revealed reduced conduction velocities of the motor nerves with increased temporal dispersion and loss of sensory nerve action potentials. Treatment with steroids was ineffective. IgM antibody against GD1a, GT1b and GM3, which are known to be the ligands for myelin-associated glycoprotein (MAG), might have played a role in the demyelination in this patient by inhibiting adhesion between myelin and axonal membrane.
Mizutani
K
K
Department of Neurology, Faculty of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Kyoto 606-8507, Japan.
Oka
N
N
Kusunoki
S
S
Kaji
R
R
Mezaki
T
T
Akiguchi
I
I
Shibasaki
H
H
D000368:Aged; D000906:Antibodies / Q000032:analysis*; D003711:Demyelinating Diseases / Q000276:immunology / Q000503:physiopathology*; D005679:G(M3) Ganglioside / Q000276:immunology; D005732:Gangliosides / Q000276:immunology*; D006801:Humans; D007075:Immunoglobulin M / Q000276:immunology*; D008297:Male; D009068:Movement; D012677:Sensation
D000906:Antibodies; D005679:G(M3) Ganglioside; D005732:Gangliosides; D007075:Immunoglobulin M; C021298:ganglioside, GD1a; C016481:trisialoganglioside GT1