patient was diagnosed with CIDP; This is a literature report for the following literature source(s):   A 64-year-old female patient received BNT162b2 (BNT162B2), as dose 1, single (Batch/Lot number: unknown) for covid-19 immunization. The patient's relevant medical history included: "mild COVID-19 infection" (unspecified if ongoing), notes: 2 months before vaccination. The patient's concomitant medications were not reported. Clinical course: The patient presented with acute onset of bilateral lower motor neuron facial weakness, dysarthria, dysphagia, acroparesthesia worse on the left, and impaired balance 8 days after her first Pfizer-BioNTech COVID-19 vaccination. On initial evaluation in an emergency department, a stroke workup was negative and she was treated with valacyclovir and prednisone for a presumptive diagnosis of Bell's Palsy. However, further neurologic assessment revealed albuminocytologic dissociation on CSF analysis with cell count 6/mm³ and protein 217 mg/dL. She was diagnosed with AIDP and treated with a 3-day course of IVIg with no significant improvement. There was a history of prior mild COVID-19 infection about 2 months before vaccination. The patient reported progression of neurological symptoms beyond 8 weeks. Neurologic examination at our institution 5 months after symptom onset was remarkable for flaccid dysarthria, facial diplegia with Bell's phenomenon, areflexia in the lower extremities, absent vibratory sensation and proprioception and diminished light touch and pain sensation in the lower extremities, and normal motor strength. Laboratory workup revealed mildly elevated ESR, HgbA1c 6.0%, and hypertriglyceridemia. The following serum laboratory results were normal or negative: CBC, CMP, SPEP with immunofixation, folate, anti- Sjogren syndrome antibodies (SSA and SSB), angiotensin-converting enzyme, ANA, and motor and demyelinating neuropathy antibody panels. MRI of the brain was notable for mild asymmetric enhancement of the left facial nerve (Fig. 3C). Repeat electrophysiologic studies 6.5 months after symptom onset demonstrated prolonged distal latencies and slowed conduction velocities in motor studies in the upper and lower extremities and face, abnormal diffuse low amplitudes of the sensory responses in the lower extremities, and significantly prolonged F-wave latencies. Blink reflexes revealed prolonged R1 and R2 latencies bilaterally. Fibrillation potentials and large, long-duration motor units with decreased recruitment were noted in the distal leg and frontalis muscles on needle EMG. These findings were consistent with diffuse, chronic, and active demyelinating polyradiculoneuropathy. The patient was diagnosed with CIDP and was restarted on IVIg 1 g/kg every 2 weeks. At the most recent follow-up after 3 IVIg treatments, she has had resolution of facial weakness but continued to have sensory loss in the bilateral lower extremities. 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. 11,16 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.11 Two of our 4 cases had a history or laboratory evidence of prior COVID-19 infection, although quantitative antibody testing for the SARS-CoV-2 nucleocapsid and receptor proteins (which theoretically ought to distinguish patients with prior infection vs. vaccination because the latter should only confer receptor antibodies) was only performed in 1 patient. Whether occult COVID-19 infection may have contributed to our patients' demyelinating disease is therefore unclear. 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/event and different patient;US-PFIZER INC-202300097174 Same article/ drug/event and different patient;