atypical demyelinating polyneuropathy temporally associated with SARS-CoV2 mRNA vaccination; chronic inflammatory demyelinating polyradiculoneuropathy (CIDP); This is a literature report.  A 62-year-old female patient received BNT162b2 (BNT162B2 NOS), as dose number unknown (booster), single (Batch/Lot number: unknown) for covid-19 immunisation. The patient's relevant medical history and concomitant medications were not reported. Vaccination history included: Covid-19 vaccine (Primary Immunization series complete; unknown manufacturer), for COVID-19 immunisation. Patient developed distal, symmetric upper and lower extremity sensorimotor impairments and areflexia three weeks after SARS-CoV2 booster vaccination (Pfizer-BioNTech). Initial cerebrospinal fluid analysis demonstrated cytoalbuminologic dissociation (protein 76mg/dL). Intravenous immunoglobulin (IVIg) (2 gm/kg total) was prescribed. The patient's symptoms and signs resolved. Asymmetric, proximal appendicular weakness, distal appendicular sensory loss, gait impairment, and areflexia reoccurred approximately one week later. Plasma exchange (PLEX) was completed, resulting in marked clinical improvement. Clinical worsening again reoccurred in the weeks following PLEX completion. Electrodiagnostic and serologic studies were obtained. Immunomodulatory therapies were escalated with IVIg (repeat 2 gm/kg), corticosteroid, and rituximab therapies prescribed. Sustained symptom improvement was evidenced. Nerve conduction and electromyography studies demonstrated absent F-waves, prolonged distal motor latencies, and reduced recruitment of normal motor units consistent with a demyelinating polyneuropathy. Ga1NAc-GD1a IgG, beta-tubulin IgG, and neurofascin155 IgG antibodies were detected in serum samples obtained prior to IVIg therapy .  Conclusion(s): The patient's clinical syndrome was ultimately consistent with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). The asymmetric pattern of weakness, robust initial treatment response(s), and severe fluctuations were atypical for classical CIDP, but consistent with demyelinating disease marked by specific auto antibodies. Uniquely, Ga1NAc-GD1a IgG, beta-tubulin IgG, and neurofascin-155 IgG antibodies were identified. Antibodies against axons and myelin proteins have been recently reported in patients with acute and chronic demyelinating polyneuropathies. Antibodies to neurofascin isoforms, anti-tubulin and Ga1NAc-GD1a can result in severe phenotypes with variable treatment responses, including robust treatment response to Bcell targeted therapies. To our knowledge, this is a novel case due to multiple co-existing, potentially pathogenic, auto antibodies. A possible immunemediated mechanism precipitated by SARS-CoV2 vaccination requires further investigation.; Sender's Comments: Based on known drug safety profile, there is reasonable possibility of causal association between the events (Demyelinating polyneuropathy, Chronic inflammatory demyelinating polyradiculoneuropathy) and BNT162B2.  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.