Acute ataxic neuropathy with cross‐reactive antibodies to GDlb and GD3 gangliosides
HJ Willison, A Almemar, J Veitch, D Thrush - Neurology, 1994 - AAN Enterprises
HJ Willison, A Almemar, J Veitch, D Thrush
Neurology, 1994•AAN EnterprisesWe report a patient with an acute, self-limiting neuropathy consisting of ataxia and areflexia,
but without ophthalmoplegia or limb weakness, with transient, high-titer serum IgG
antibodies to a single NeuAc (α2–8) NeuAc-linked disialosyl epitope, as found on GDlb and
GD3 gangliosides. The serum did not react with GQlb, GTla, or GTlb. This atypical case,
which most closely represents an incomplete Miller Fisher syndrome, indicates that anti-
GDlb/GDs antibodies may be able to induce sensory ataxia.
but without ophthalmoplegia or limb weakness, with transient, high-titer serum IgG
antibodies to a single NeuAc (α2–8) NeuAc-linked disialosyl epitope, as found on GDlb and
GD3 gangliosides. The serum did not react with GQlb, GTla, or GTlb. This atypical case,
which most closely represents an incomplete Miller Fisher syndrome, indicates that anti-
GDlb/GDs antibodies may be able to induce sensory ataxia.
We report a patient with an acute, self-limiting neuropathy consisting of ataxia and areflexia, but without ophthalmoplegia or limb weakness, with transient, high-titer serum IgG antibodies to a single NeuAc(α2–8)NeuAc-linked disialosyl epitope, as found on GDlb and GD3 gangliosides. The serum did not react with GQlb, GTla, or GTlb. This atypical case, which most closely represents an incomplete Miller Fisher syndrome, indicates that anti-GDlb/GDs antibodies may be able to induce sensory ataxia.
American Academy of Neurology