Pain is a recognized association with LGI1-/ CASPR2-antibodies. Of 147 patients, pain was experienced by 17/33 (52%) CASPR2- versus 20/108 (19%) LGI1-antibody patients (p=0.0005), and identified as neuropathic in 89% versus 58% of these, respectively. Typically, normal nerve conduction studies and reduced intraepidermal nerve fibre densities were observed in subsets of both cohorts. In LGI1-antibody patients, pain responded to immunotherapy (p=0.008), often rapidly, with greater residual patient-rated impairment observed in CASPR2-antibody patients (p=0.019). Serum CASPR2-antibodies, but not LGI1-antibodies, bound in vitro to unmyelinated human sensory neurons and rodent dorsal root ganglia, suggesting pathophysiological differences which may underlie our clinical observations. This article is protected by copyright. All rights reserved.
Autoantibody, Autoimmune encephalitis, CASPR2, LGI1, Pain