Patient was diagnosed with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP); This is a report.  A 26-year-old male patient received BNT162b2 (BNT162B2), as dose 2, single (Batch/Lot number: unknown) for covid-19 immunisation. The patient's relevant medical history and concomitant medications were not reported. Vaccination history included: Bnt162b2 (DOSE 1, SINGLE), for COVID-19 immunisation. The following information was reported: CHRONIC INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY (medically significant), 21 days after the suspect product(s) administration, outcome "recovering", described as "Patient was diagnosed with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)". The patient presented with bilateral lower motor neuron facial weakness and numbness followed by numbness in the hands and feet that progressed to generalized weakness and pain. Initial symptom onset was 21 days after administration of his second Pfizer-BioNTech COVID-19 vaccination. Within a few hours of receiving the second dose, he developed chills, myalgias, and bone pain which were followed by fatigue for 1-2 weeks before symptom onset. Neurologic evaluation 9 weeks after symptom onset revealed moderate facial diplegia, diffuse symmetric, distal-predominant bilateral upper and lower extremity weakness including bilateral foot drop, and diffuse areflexia with preserved patellar reflexes. Laboratory investigation revealed positive SARS-CoV-2 nucleocapsid and receptor binding domain-specific antibodies, consistent with a history of prior natural COVID-19 infection as opposed to vaccination alone. CSF analysis demonstrated albuminocytologic dissociation with cell count 4/mm3 and protein 485 mg/dL and mildly elevated angiotensin-converting enzyme but was otherwise normal. The following laboratory results were normal or negative: CBC; CMP; SARS-CoV-2 RNA PCR; HgbA1c; ESR, C-reactive peptide; SPEP with immunofixation; complement; ANA; antineutrophil cytoplasmic antibodies; rheumatoid factor; vitamins B1, B6, B9, B12, and E; homocysteine; methylmalonic acid; HIV; West Nile Virus, syphilis, and GM1 and GQ1b antibodies. Magnetic resonance imaging (MRI) of full spine revealed marked cauda equina nerve root enhancement. Electrophysiologic studies 9 weeks after symptom onset demonstrated absent to low amplitudes of the upper extremity sensory responses (sural sparing pattern) and diffuse prolonged distal latencies with decreased amplitudes and slow conduction velocities of all motor responses on NCS and fibrillation potentials and large, long duration motor units with decreased recruitment in the distal leg and hand muscles on needle EMG. The findings were consistent with chronic and active demyelinating polyradiculoneuropathy with chronic axon loss. The patient was diagnosed with CIDP and treated with IVIg 2 g/kg divided over 5 days followed by 0.5 g/kg every 2 weeks. At the follow-up visits 1 month after initiation of treatment, he had moderate improvement in facial and proximal and distal extremity weakness, numbness, paresthesia, and balance. Although there are unusual features such as acute onset of facial weakness the abnormal electrophysiologic findings to support demyelination, elevated CSF protein and good responses to immunotherapy strongly suggest demyelinating neuropathy after COVID-19 vaccination. The presence of cranial nerve symptoms is consistent with demyelinating neuropathy that has antecedent events, particularly infections, reported elsewhere. In addition, there is no established pathophysiologic association between infection or vaccination and CIDP. However, recent studies suggested that approximately 10% of CIDP cases were associated with antecedent infectious illness and 1% with preceding vaccination. Among the CIDP cases associated with antecedent infection or vaccine, clinical presentations were more likely to be acute-onset CIDP, defined as those initially diagnosed with GBS with subsequent clinical deterioration beyond 8 weeks, and associated with cranial nerve involvement. It is imperative to remember that as with any other vaccination, any proposed association between COVID-19 vaccinations and demyelinating neuropathies cannot be considered causal because these case reports have been very few compared with the number of cases vaccinated.; Sender's Comments: Considering a plausible drug-event temporal association, a reasonable possibility that the event chronic inflammatory demyelinating polyradiculoneuropathy is related to BNT162B2 cannot be excluded. This case will be reassessed should additional information become 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-202300097179 Same article/ drug and different patient/event;US-PFIZER INC-PV202300041685 Same article/ drug/event and different patient;