Georg Royl1,2, Tsafack Judicael Fokou3, Rittika Chunder4, Rakad Isa3, Thomas F Münte3,5, Klaus-Peter Wandinger3,6, Markus Schwaninger5,7,8, Oliver Herrmann8, José Manuel Valdueza9, Jan Brocke9, Martin Willkomm10, Dietrich Willemsen11, Gerd U Auffarth12, Swantje Mindorf4, Britta Brix4, Angel Chamorro13,14, Anna Planas14,15, Xabier Urra13,14. 1. Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Germany. georg.royl@neuro.uni-luebeck.de. 2. Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany. georg.royl@neuro.uni-luebeck.de. 3. Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Germany. 4. Euroimmun Medizinische Labordiagnostika, Lübeck, Germany. 5. Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany. 6. Institute of Clinical Chemistry, University Hospital of Schleswig-Holstein, Holstein, Germany. 7. Institute of Experimental and Clinical Pharmacology and Toxicology, University of Lübeck, Lübeck, Germany. 8. Department of Neurology, University of Heidelberg, Heidelberg, Germany. 9. Neurological Center, Segeberger Kliniken, Bad Segeberg, Germany. 10. Geriatric Research Group, Krankenhaus Rotes Kreuz, Lübeck, Germany. 11. SANA Kliniken Ostholstein, Middelburg, Germany. 12. Department of Ophthalmology, University of Heidelberg, Heidelberg, Germany. 13. Department of Neuroscience, Comprehensive Stroke Center, Hospital Clinic, Barcelona, Spain. 14. August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. 15. Department of Brain Ischemia and Neurodegeneration, Institut d'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas, Barcelona, Spain.
Abstract
BACKGROUND AND PURPOSE: Ischemic stroke (IS) and hemorrhagic stroke (HemS) typically lead to a breakdown of the blood-brain barrier with neural antigen presentation. This presentation could potentially generate destructive auto-immune responses. Pre-existing antineuronal and antiglial antibodies (AA), predominantly NMDA receptor antibodies, have been reported in patients with stroke. This article summarizes three independent prospective studies, the Lübeck cohort (LC), Barcelona cohort (BC), and Heidelberg cohort (HC), exploring the frequency and clinical relevance of AA in patients with acute stroke (AS). METHODS: In all cohorts together, 344 consecutive patients admitted with AS (322 × IS, 22 × HemS) were screened for AA in serum at admission. Clinical outcome parameters as well as a second AA screening were available at 30 days in the LC or at 90 days in the BC. A control group was included in the BC (20 subjects free from neurological disease) and the HC (78 neurological and ophthalmological patients without evidence for stroke). RESULTS: The rate of positivity for AA was similar in control subjects and AS patients (13%, 95% CI [7%, 22%] vs. 13%, 95% CI [10%, 17%]; p = 0.46) with no significant difference between cohorts (LC 25/171, BC 12/75, HC 9/98). No patient had developed new AA after 30 days, whereas 2 out of 60 patients had developed new AA after 90 days. AA positive patients did not exhibit significant differences to AA negative patients in stroke subtype (LC, BC), initial stroke severity (BC, LC, HC), infarct volume (BC), and functional status at admission (BC, LC, HC) and follow-up (BC, LC). CONCLUSIONS: AS does not induce AA to a relevant degree. Pre-existing AA can be found in the serum of stroke patients, but they do not have a significant association with clinical features and outcomes.
BACKGROUND AND PURPOSE:Ischemic stroke (IS) and hemorrhagic stroke (HemS) typically lead to a breakdown of the blood-brain barrier with neural antigen presentation. This presentation could potentially generate destructive auto-immune responses. Pre-existing antineuronal and antiglial antibodies (AA), predominantly NMDA receptor antibodies, have been reported in patients with stroke. This article summarizes three independent prospective studies, the Lübeck cohort (LC), Barcelona cohort (BC), and Heidelberg cohort (HC), exploring the frequency and clinical relevance of AA in patients with acute stroke (AS). METHODS: In all cohorts together, 344 consecutive patients admitted with AS (322 × IS, 22 × HemS) were screened for AA in serum at admission. Clinical outcome parameters as well as a second AA screening were available at 30 days in the LC or at 90 days in the BC. A control group was included in the BC (20 subjects free from neurological disease) and the HC (78 neurological and ophthalmological patients without evidence for stroke). RESULTS: The rate of positivity for AA was similar in control subjects and AS patients (13%, 95% CI [7%, 22%] vs. 13%, 95% CI [10%, 17%]; p = 0.46) with no significant difference between cohorts (LC 25/171, BC 12/75, HC 9/98). No patient had developed new AA after 30 days, whereas 2 out of 60 patients had developed new AA after 90 days. AA positive patients did not exhibit significant differences to AA negative patients in stroke subtype (LC, BC), initial stroke severity (BC, LC, HC), infarct volume (BC), and functional status at admission (BC, LC, HC) and follow-up (BC, LC). CONCLUSIONS: AS does not induce AA to a relevant degree. Pre-existing AA can be found in the serum of strokepatients, but they do not have a significant association with clinical features and outcomes.
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