Anti-HNK1 antibodies were assessed with the GanglioCombi™ MAG ELISA test (Buhlmann) in 41 anti-MAG neuropathies and in 118 controls: 34 chronic inflammatory demyelinating polyradiculoneuropathies, 3 Miller Fisher syndromes, 12 sensory neuronopathies, 63 length-dependent axonal sensory polyneuropathies, 6 healthy controls.
Anti-HNK1 antibodies were assessed with the GanglioCombi™ MAG ELISA test (Buhlmann) in 41 anti-MAG neuropathies and in 118 controls: 34 chronic inflammatory demyelinating polyradiculoneuropathies, 3 Miller Fisher syndromes, 12 sensory neuronopathies, 63 length-dependent axonal sensory polyneuropathies, 6 healthy controls.
GATA2 mutation-related immunodeficiency may predispose to EBV-associated subacute demyelinating polyradiculoneuropathy by both viral susceptibility and immune dysregulation.
Compared to ANNA1 alone, CRMP5 neuropathy has a higher prevalence of pain (79% vs 46%, <i>p</i> = 0.008), asymmetric polyradiculoneuropathy (54% vs 12%, <i>p</i> < 0.001), and inflammatory spinal fluids (elevated CSF protein or nucleated cell count 92% vs 60%, <i>p</i> = 0.022).
IgM autoantibodies against neurofascin-155 were detected by ELISA in five patients, four with inflammatory demyelinating polyradiculoneuropathy (CIDP) and one with Guillain-Barré syndrome (GBS), and were confirmed by ELISA-based preabsorption experiments and Western blot.Titres ranged from 1:100 to 1:400.
Compared to ANNA1 alone, CRMP5 neuropathy has a higher prevalence of pain (79% vs 46%, <i>p</i> = 0.008), asymmetric polyradiculoneuropathy (54% vs 12%, <i>p</i> < 0.001), and inflammatory spinal fluids (elevated CSF protein or nucleated cell count 92% vs 60%, <i>p</i> = 0.022).
Compared to ANNA1 alone, CRMP5 neuropathy has a higher prevalence of pain (79% vs 46%, <i>p</i> = 0.008), asymmetric polyradiculoneuropathy (54% vs 12%, <i>p</i> < 0.001), and inflammatory spinal fluids (elevated CSF protein or nucleated cell count 92% vs 60%, <i>p</i> = 0.022).
Hereditary neuropathy with liability to pressure palsy (HNPP) is an inherited disease caused by a deletion or point mutation in the peripheral myelin protein 22 (PMP22) gene, which may manifest as a recurrent polyradiculoneuropathy.