ArticleNeurology2012
Chronic pain as a manifestation of potassium channel-complex autoimmunity.
Article in Neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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Who cites it
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 178 citations in OpenAlex.
- Systematic review of the clinical spectrum of CASPR2 antibody syndrome.Journal of neurology · 2020Pooled it
- Inhibition of Janus kinase/signal transducer and activator of transcription reduces nociceptive sensitization in a murine model of complex regional pain syndrome.Pain reports · 2026Article
- The neuroimmune microenvironment of peripheral nerve injury: mechanisms, pathophysiology, and therapeutic implications.Frontiers in surgery · 2026Review
- UNC5A IgG in a Previously Reported CASPR2/LGI1-Negative VGKC-Associated Peripheral Nerve Hyperexcitability Syndrome: Long-Term Clinical and Electrophysiological Follow-Up.Case reports in neurological medicine · 2026Article
- Article
- Fibromyalgia syndrome-am I an autoimmune condition?Pain reports · 2025Review
- Neuropathic Pain and Distinct CASPR2 Autoantibody IgG Subclasses Drive Neuronal Hyperexcitability.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Satellite Glial Cells in Human Disease.Cells · 2024Review
- Case report: Recurring potassium channel complex autoimmunity-related neuropathic pain.Frontiers in immunology · 2024Article
- The serum metabolomic profile of a distinct, inflammatory subtype of acute psychosis.Molecular psychiatry · 2022Article
- Autoantibodies against NCAM1 from patients with schizophrenia cause schizophrenia-related behavior and changes in synapses in mice.Cell reports. Medicine · 2022Article
- The associations between ADHD, pain, inflammation, and quality of life in children and adolescents-a clinical study protocol.PloS one · 2022Article
- Potential Neuroimmune Interaction in Chronic Pain: A Review on Immune Cells in Peripheral and Central Sensitization.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- Sex-Specific B Cell and Anti-Myelin Autoantibody Response After Peripheral Nerve Injury.Frontiers in cellular neuroscience · 2022Article
- Leucine-Rich Glioma-Inactivated 1 versus Contactin-Associated Protein-like 2 Antibody Neuropathic Pain: Clinical and Biological Comparisons.Annals of neurology · 2021Article
- Overlapping central and peripheral nervous system syndromes in MOG antibody-associated disorders.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- Paraneoplastic Neuropathies: What's New Since the 2004 Recommended Diagnostic Criteria.Frontiers in neurology · 2021Review
- Autoimmune regulation of chronic pain.Pain reports · 2021Review
- Neuropsychiatric Disorders Due to Limbic Encephalitis: Immunologic Aspect.International journal of molecular sciences · 2020Review
- Assembly and Function of the Juxtaparanodal Kv1 Complex in Health and Disease.Life (Basel, Switzerland) · 2020Review
2 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveAutoantibodies targeting voltage-gated potassium channel (VGKC) complexes cause a spectrum of neuronal hyperexcitability disorders. We investigated pain as a manifestation of VGKC-complex autoimmunity.
methodsWe reviewed the prevalence and characteristics of pain in VGKC-complex-immunoglobulin G (IgG)-seropositive patients in 25 months of comprehensive service testing for neural autoantibodies, subtyped positive sera for LGI1-IgG and CASPR2-IgG specificities, and reviewed pain prevalence in autoimmune control patients.
resultsVGKC-complex-IgG was identified in 1,992 patients of 54,853 tested (4%). Of 316 evaluated neurologically at Mayo Clinic, 159 (50%) had pain, in isolation (28%) or with accompanying neurologic manifestations (72%), and not attributable to alternative cause. Pain was subacute in onset, chronic in course, neuropathic, nociceptive, regional, or diffuse and sometimes attributed to fibromyalgia (6%) or psychogenic cause (13%). Most patients had normal peripheral nervous system function, measured by neuropathy impairment scores and nerve conduction. Evidence of neuronal hyperexcitability (hyperhidrosis, quantitative heat-pain hyperalgesia, or electromyographic excitability) was 25-fold more common in pain patients. Pain management required multiple medications in 70% (narcotics, 30%); 13 of 16 patients reported pain relief with immunotherapy. Pain was significantly associated with CASPR2-IgG-positivity (16% positive with pain, 7% without pain; p = 0.014) but not with LGI1-IgG. Less than 10% of 167 patients with neural autoantibodies other than VGKC-complex-IgG reported pain.
conclusionsChronic idiopathic pain is a syndromic manifestation of VGKC-complex autoimmunity. Hyperexcitability of nociceptive pathways is implicated. CASPR2-IgG significantly associates with pain, but in most patients the antigenic VGKC-complex molecule remains to be determined. VGKC-complex autoimmunity represents an important new direction for pain research and therapy.
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