The terms axonal or demyelinating, traditionally disseminated in the classification of polyneuropathies, are electrophysiological interpretations that guide us to determine the pathogenic locus where the neuropathic lesion originates; this is an objective contribution to the knowledge of the etiology of the corresponding neuropathy. However, in some circumstances, a bimodal interpretation initially does not allow determining the possibility of involvement at the axolemma level, as can be identified in some immune-mediated polyneuropathies that compromise the Ranvier node or its different domains; These neuropathies are of autoimmune origin and are characterized by the presence of anti-ganglioside antibodies directed against antigenic epitopes at this anatomical locus.
This is a case report of a 66-year-old male patient with progressive weakness in all four limbs leading to prostration over a few weeks; no prior systemic infections were reported. Initially diagnosed with Guillain-Barré Syndrome (GBS), he was evaluated with electrophysiological studies that confirmed the existence of a sensorimotor demyelinating polyneuropathy and treated with intravenous immunoglobulin (IVIg), with partial clinical improvement. Two weeks later, he was readmitted with a new episode of global muscle weakness, due to a fluctuating response of GBS to immunomodulatory treatment; therefore, he received two cycles of IVIg with little response. Complementary immunological studies confirmed a diagnosis of Sjögren’s syndrome and showed positive IgM anti-GD1b antibodies.
