Meningoencephalitis of Immune Origin; This is a literature report.  A 27-year-old female patient received BNT162b2 (BNT162B2), as dose 1, single (Batch/Lot number: unknown) for COVID-19 immunisation. The patient's relevant medical history and concomitant medications were not reported. The following information was reported: IMMUNE-MEDIATED ENCEPHALITIS (hospitalization, medically significant), 6 days after the suspect product administration, outcome "recovered", described as "Meningoencephalitis of Immune Origin". The clinical course was as follows: A 27-year-old woman presented to the ED with a 2-day history of acute-onset confusion and anxiety of unclear etiology. It started 6 days following the first dose administration of Pfizer-BioNTech SARS-CoV-2 vaccine that resulted in transient headache and fatigue. She had no prior neurological illness. She had a fever of 100.4 F without nuchal rigidity. Neurological examination revealed psychomotor agitation, dysfluent speech with paraphasic errors, and difficulty with writing. Serological assays were notable for a mildly elevated ESR to 21 mm/h (reference range 0-15 mm/h). There was no leukocytosis. Antibodies against COVID-19 Spike were positive (>250 U/ml) and nasopharyngeal COVID-19 PCR test was negative. Thyroid functions were normal. A Clinic serum autoimmune encephalitis panel (ID: ENS2) was negative. CSF analysis was notable for pleocytosis of 19 WBCs with 84% lymphocytic predominance, and normal protein and glucose. CSF infectious workup was negative, including bacterial and fungal cultures as well as viral PCR panel (which includes HSV-1, HSV-2, HHV-6, CMV, VZV, Enterovirus, Parechovirus). Anti-NMDA receptor antibody was not detected in the CSF; the remainder of CSF autoimmune encephalitis panel was not completed due to insufficient CSF quantity. CSF Oligoclonal bands were absent and IgG index was normal. Contrast enhanced brain MRI showed no abnormalities. Electroencephalography (EEG) showed mild generalized slowing without epileptiform abnormalities. Additional tests included anti Aquaporin-4 CSF antibody, anti Aquaporin-4 serum antibody, anti-Myelin Oligodendroglycoprotein CSF antibody, and anti-Myelin Oligodendroglycoprotein serum antibody, which were all unknown. She was started on a 5-day course of pulse IV methylprednisolone with a dose of one gram/day for presumed autoimmune meningoencephalitis with a significant clinical improvement. She was subsequently discharged on an oral tapering course of steroid with a steady improvement. She achieved a full recovery in about 1 month after discharge; thus, no further imaging of the brain or body was performed. This case involved a patient who presented with an acute encephalopathy associated with rapid cognitive decline within a week of vaccine administration. The diagnostic workup was notable for normal neuroimaging and CSF lymphocytic pleocytosis unexplained by infections or systemic autoimmunity. The rapid decline in mental status and cognitive functions, including working memory, in association with CSF inflammatory response together with the clinically meaningful response to steroids, suggest possible CNS autoimmunity such as seronegative autoimmune encephalitis. This is consistent with the rapidly increasing proportion of patients with encephalitis thought to be of immune origin despite undetectable neuronal surface autoantibodies in serum and CSF, and absent structural abnormalities on neuroimaging studies. The data linking vaccines to autoimmune encephalitis are very scarce and largely limited to sporadic cases of yellow fever vaccine. Therefore, it remained unclear whether this presentation is a coincidental event that occurred following, or an adverse event linked to, vaccination. Overall, adverse neuroinflammatory and immunological events across all the major clinical trials that assessed the safety profile of the various SARS-CoV-2 vaccines were reportedly very rare, with zero reported cases of CNS inflammatory/autoimmune disorders in the mRNA-based vaccine trials. The reported temporal association between inoculation with mRNA SARS-CoV-2 vaccine and the development of various CNS disorders of suspected inflammatory and immune origin is consistent with the clinical anecdotes associating other vaccines with short-term increase in CNS autoimmunity such as inflammatory demyelinating disease. The authors' findings suggest that the occurrence of post-mRNA SARS-CoV-2 vaccination CNS autoimmunity, new-onset or clinical relapse, might be more prevalent among those with pre-existing CNS autoimmunity or increased propensity for systemic autoimmune disorders. However, this short-term association should be interpreted with great caution. It neither proves a causal link nor implies a potential long-term risk increase in post-vaccination CNS autoimmunity. Clinicians should be aware of this potential association as early immune therapies may likely reverse these observed immunological events. Limitations to this study include the small sample size, given the brief period since SARS-CoV-2 vaccines have been available, data limited to a single hospital system, as well as the retrospective nature of the study.  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 information provide and plausible temporal association, the causality between BNT162B2 and IMMUNE-MEDIATED ENCEPHALITIS  cannot be completely excluded. 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-202200582985 same article and suspect drug, different patient and event