Sex: F
Vaccine: COVID19
Symptoms: SARS-CoV-2 test, Serology test, Vital signs measurement, White blood cell count
Clinical narrative: Neuromyelitis Optica Spectrum Disorder; This is a literature report for the following literature source(s): "A Single-Health System Case Series of New-Onset CNS Inflammatory Disorders Temporally Associated With mRNA Based SARS CoV 2 Vaccines", Frontiers in Neurology, 2022; Vol:13, DOI:10.3389/fneur.2022.796882.  A 63-year-old woman with hypothyroidism and hyperlipidemia presented with a 2-week history of severe back pain, rapidly progressive paraparesis, and urinary retention. The onset of neurological symptoms was about 1 week following the first dose of the Pfizer-BioNTech vaccine. General examination was unremarkable with normal vital signs. She was found to have leukopenia (2.55 K/µL). Neurological examination revealed moderate paraparesis of the lower extremities, mild weakness of the right arm, and reduced right facial sensation. The remainder of the segmental neurological examination was unremarkable. MRI with gadolinium of the brain, cervical and thoracic cords revealed a contrast-enhancing left thalamic lesion, and a non-enhancing, longitudinally extensive T2 hyperintensity extending from T6 to T12 levels, consistent with longitudinally extensive transverse myelitis (LETM). Nasopharyngeal COVID-19 PCR testing was negative. Serum spike protein antibodies were detectable at titers >250 U/mL. Serological and immunological assays were notable for elevated titers of anti-nuclear antibody (ANA) of 1:2560 (reference <1:80), and double-stranded DNA antibody (anti-DsDNA) of 158 IU/ml (reference <29). The remainder of the immune assays were normal, including serum levels of anti-aquaporin 4 (anti-AQP4) antibody utilizing enzyme linked immunosorbent assay (ELISA) technique, angiotensin convertingenzyme (ACE), and C3 and C4 complement. CSF analysis demonstrated a pleocytosis of 33 cells/µL with 91% lymphocytic predominance and an elevated protein of 57 mg/dL, a negative paraneoplastic panel, undetectable anti-MOG antibody, absent oligoclonal bands, and normal IgG index. Biopsy of the left thalamic lesion demonstrated a histiocytic inflammatory process, focal perivascular lymphocytosis and reduced astroglial density at the center of the lesion. Based on the subsequent detection of CSF anti-AQP4 antibody utilizing cell-based assay (CBA) with titers of 1:16 (reference <1:2) and reduced astroglial staining reflective of astroglial injury known to be associated with anti-AQP4 antibody, the diagnosis of NMOSD was entertained. The patient demonstrated a notable clinical response to an extended course of pulse IV methylprednisolone therapy followed by oral steroid tapering course, and plasmapheresis. Follow-up MRI of the brain and spinal cord at 6-months demonstrated persistent T2 hyperintense lesions in the left thalamus and thoracic cord. At 10 months follow-up, serum anti-AQP4 antibody utilizing a CBA was found to be positive, solidifying the diagnosis of NMOSD.  No follow-up attempts are possible; information about lot/batch number cannot be obtained. No further information is expected.; Sender's Comments: Based on the currently available information the possibility of causal association between the event NMOSD and the suspect drug BNT162B2  cannot be ruled out. The case will be reassessed once new information is available. The impact of this report on the benefit/risk profile of the Pfizer product is evaluated as part of Pfizer procedures for safety evaluation, including the review and analysis of aggregate data for adverse events. Any safety concern identified as part of this review, as well as any appropriate action in response, will be promptly notified to regulatory authorities, Ethics Committees, and Investigators, as appropriate. ,Linked Report(s) : US-PFIZER INC-202200583170 Same drug and different patient/event.;US-PFIZER INC-202200582985 Same drug and different patient/event.