Neurological Sciences | 2021
Aseptic meningitis after vaccination of the BNT162b2 mRNA COVID-19 vaccine
Abstract
Dear editor, Severe acute respiratory syndrome coronavirus 2 (SARSCoV2) infection has spread worldwide. The most promising strategy for successfully overcoming this coronavirus disease 2019 (COVID-19) pandemic is vaccination. Vaccination of the BNT162b2 messenger RNA (mRNA) against COVID-19 funded by Pfizer-BioNTech has recently started in Japan. The efficacy (94.8% against COVID-19) and safety are proven [1]. Although uncommon, serious adverse events have been reported. Herein, we report a first case of aseptic meningitis after the first dose of intramuscular injection of the BNT162b2 mRNA COVID-19 vaccine. A 42-year-old Japanese female nurse had a history of migraine, but she has had no obvious attack at least 9 months. She was just taking non-steroidal anti-inflammatory drugs (NSAIDs) and lomerizine hydrochloride orally as prophylaxis at that time. She has no history of allergy for food or cosmetics. Due to her professional history of contacting with patients who were treated with COVID-19, she had done SARS-CoV2 polymerase chain reaction (PCR) tests of a nasopharyngeal swab several times but never been positive before vaccination of the BNT162b2 mRNA vaccine. She received the first dose of the BNT162b2 mRNA vaccine (30 μg) at our hospital 1 week before the appearance of severe headache and high fever (38 °C). Although she took oral loxoprofen sodium hydrate as NSAIDs and acetaminophen because she thought that she had a migrane attack. Her headache getting worse, she injected sumatriptan succinate subcutaneously a day before the visit. In spite of the treatment, her headache was continued. Finally, she visited our hospital next day. On arrival, neck stiffness, Kernig sign, Brudzinski sign, eye ball tenderness, and other neurological signs were negative but only jolt accentuation was positive with headache and nausea. Her white blood cell count was 7,600 /μL (normal range 3,100–8,800 / μL; neutrophils 69.2%, eosinophils 1.7%, basophils 0.3%, lymphocytes 22.6%, monocytes 6.2%), although C-reactive protein level (CRP) was increased (9.85 mg/ dL; normal range 0–0.3 mg/dL). Computed tomography (CT) of chest showed no sign of pneumonia. A cerebrospinal fluids (CSF) analysis revealed pleocytosis (528/3 mm3; polynuclear cells 34.8%, mononuclear cells 64.1%, eosinophils 1.1%; Fig. 1), normal IgG index (0.54; normal range 0–0.73), and normal protein level (35.7 mg/dL; normal range 0–45.0 mg/dL) with high opening pressure (22 cmH2O). SARS-CoV2 PCR tests of a nasopharyngeal swab and CSF were both negative. We evaluated the presence of spike-specific (Sp) SARS-CoV2 IgG and IgM; she was slightly positive for the Sp SARS-CoV2 IgG (393.4 AU/mL; cutoff 0–50 AU/mL; (Chemiluminescent Enzyme Immunoassay; Architect Quant IgG II, Abbott)), but she was qualitatively negative for the Sp SARS-CoV2 IgM. Brain magnetic resonance imaging showed normal findings, including contrast enhancement. She was diagnosed with aseptic meningitis. Blood and CSF cultures were negative. Her CSF Sp SARS-CoV2 IgM was negative, although her CSF Sp SARS-CoV2 IgG was detected (17.1 AU/mL). Acyclovir (3 mg/kg/day) was administered for several days until other viral antibody titers were negative. Her headache showed no improvement. We therefore treated her with 5 days intravenous methylprednisolone (500 mg/day) after 3 days from admission. After 5 days from admission, her headache and nausea were significantly improved. Serum CRP level was rapidly decreased (0.36 mg/dL) and a pleocytosis (104/3 mm3) and protein * Kazuyuki Saito [email protected]