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Leucine-Rich Glioma-Inactivated 1 versus Contactin-Associated Protein-like 2 Antibody Neuropathic Pain: Clinical and Biological Comparisons.
Ramanathan, Sudarshini; Tseng, Mandy; Davies, Alexander J; Uy, Christopher E; Paneva, Sofija; Mgbachi, Victor C; Michael, Sophia; Varley, James A; Binks, Sophie; Themistocleous, Andreas C; Fehmi, Janev; Anziska, Yaacov; Soni, Anushka; Hofer, Monika; Waters, Patrick; Brilot, Fabienne; Dale, Russell C; Dawes, John; Rinaldi, Simon; Bennett, David L; Irani, Sarosh R.
Affiliation
  • Ramanathan S; Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Tseng M; Neuroimmunology and Brain Autoimmunity Groups, Kids Neuroscience Centre, Children's Hospital at Westmead; Brain and Mind Centre and Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.
  • Davies AJ; Department of Neurology, Concord Hospital, Sydney, New South Wales, Australia.
  • Uy CE; Neural Injury Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Paneva S; Inflammatory Neuropathy Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Mgbachi VC; Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Michael S; Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
  • Varley JA; Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Binks S; Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Themistocleous AC; Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Fehmi J; Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Anziska Y; Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Soni A; Neural Injury Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Hofer M; Inflammatory Neuropathy Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Waters P; Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Brilot F; Wellcome Centre for Integrative Neuroimaging, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Dale RC; Department of Neuropathology, Oxford University Hospital, National Health Service Foundation Trust, Oxford, UK.
  • Dawes J; Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.
  • Rinaldi S; Neuroimmunology and Brain Autoimmunity Groups, Kids Neuroscience Centre, Children's Hospital at Westmead; Brain and Mind Centre and Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.
  • Bennett DL; School of Medical Sciences, University of Sydney, Sydney, New South Wales, Australia.
  • Irani SR; Neuroimmunology and Brain Autoimmunity Groups, Kids Neuroscience Centre, Children's Hospital at Westmead; Brain and Mind Centre and Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.
Ann Neurol ; 90(4): 683-690, 2021 10.
Article in En | MEDLINE | ID: mdl-34370313
ABSTRACT
Pain is a under-recognized association of leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein-like 2 (CASPR2) antibodies. Of 147 patients with these autoantibodies, pain was experienced by 17 of 33 (52%) with CASPR2- versus 20 of 108 (19%) with LGI1 antibodies (p = 0.0005), and identified as neuropathic in 89% versus 58% of these, respectively. Typically, in both cohorts, normal nerve conduction studies and reduced intraepidermal nerve fiber densities were observed in the sampled patient subsets. 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 that may underlie our clinical observations. ANN NEUROL 2021;90683-690.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Autoantibodies / Membrane Proteins / Nerve Tissue Proteins / Neuralgia Type of study: Risk_factors_studies Limits: Humans Language: En Journal: Ann Neurol Year: 2021 Document type: Article Affiliation country: Reino Unido
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Autoantibodies / Membrane Proteins / Nerve Tissue Proteins / Neuralgia Type of study: Risk_factors_studies Limits: Humans Language: En Journal: Ann Neurol Year: 2021 Document type: Article Affiliation country: Reino Unido