Literature DB >> 23090334

Glycine receptor autoimmune spectrum with stiff-man syndrome phenotype.

Andrew McKeon1, Eugenia Martinez-Hernandez, Eric Lancaster, Joseph Y Matsumoto, Robert J Harvey, Kathleen M McEvoy, Sean J Pittock, Vanda A Lennon, Josep Dalmau.   

Abstract

OBJECTIVES: To determine whether glycine receptor α1 subunit-specific autoantibodies (GlyRα1-IgG) occur in a broader spectrum of brainstem and spinal hyperexcitability disorders than the progressive encephalomyelitis with rigidity and myoclonus phenotype recognized to date, and to ascertain disease specificity.
DESIGN: Retrospective, case-control study. SETTINGS: Mayo Clinic, Rochester, Minnesota, and University of Barcelona, Spain. PATIENTS: Eighty-one patients with stiff-man syndrome phenotype, 80 neurologic control subjects, and 20 healthy control subjects. INTERVENTION: Glycine receptor α1-transfected cells to test serum or cerebrospinal fluid from cases and control subjects. MAIN OUTCOME MEASURES: Frequency of GlyRα1-IgG positivity among stiff-man syndrome phenotype cases and control subjects. Comparison of GlyRα1-IgG seropositive and seronegative cases.
RESULTS: Seropositive cases (12% of cases) included 9 with stiff-man syndrome (4 classic; 5 variant; 66% were glutamic acid decarboxylase 65-IgG positive) and 1 with progressive encephalomyelitis with rigidity and myoclonus. Immunotherapy responses were noted more frequently in GlyRα1-IgG-positive cases (6 of 7 improved) than in seronegative cases (7 of 25 improved; P= .02). The single seropositive control patient had steroid-responsive vision loss and optic atrophy with inflammatory cerebrospinal fluid.
CONCLUSIONS: Glycine receptor α1-IgG aids identification of autoimmune brainstem/spinal cord hyperexcitability disorders and may extend to the glycinergic visual system.

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Year:  2013        PMID: 23090334      PMCID: PMC3718477          DOI: 10.1001/jamaneurol.2013.574

Source DB:  PubMed          Journal:  JAMA Neurol        ISSN: 2168-6149            Impact factor:   18.302


  21 in total

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