Parsonage-Turner Syndrome Following COVID-19 Vaccination; This is a literature report, 2021, DOI: 10.1148/radiol.2021211374, entitled Parsonage-Turner Syndrome Following COVID-19 Vaccination: MR Neurography.  Vaccination is one of the several known triggers of Parsonage-Turner syndrome (PTS). This report describes 2 individuals with clinical presentations of PTS whose symptoms began 13 hours and 18 days following receipt of the Pfizer-BioNTech BNT162b2 and Moderna mRNA-1273 COVID-19 vaccine, respectively. The diagnosis of PTS was confirmed using both electrodiagnostic testing and 3 Tesla magnetic resonance (MR) neurography. While research is needed to understand the association between PTS and COVID-19 vaccination, MR neurography may be used to confirm suspected cases of PTS as COVID-19 vaccines continue to be distributed worldwide. Parsonage-Turner syndrome (PTS; neuralgic amyotrophy) is a rare peripheral neuropathy typically characterized by sudden onset, severe upper arm pain followed by muscle weakness. Muscle weakness can be debilitating and up to two-thirds of patients experience long-term functional deficits. Materials and Methods: Two patients were referred for MR neurography between February and March 2021 due to clinically suspected PTS that developed 13 hours following the Pfizer-BioNTech (BNT162b2) COVID-19 vaccine and 18 days following the Moderna (mRNA-1273) COVID-19 vaccine. With informed consent from each participant, medical records were retrospectively reviewed for pertinent clinical and electrodiagnostic testing data as part of an ongoing, institutional review board- approved PTS registry compliant with the Health Insurance Portability & Accountability Act. A single musculoskeletal radiologist with greater than 7 years of MR neurography experience (DBS) reviewed 3-Tesla MR neurography and cervical spine MRI examinations. Results: Patient 1: A 49-year-old man was awoken by severe, electric shooting pain in his left volar forearm, 13 hours after receiving the first dose of the BNT162b2 vaccine (Pfizer-BioNTech) in his contralateral, right shoulder. Due to persistent, severe pain, he went to the emergency room where he received intravenous, non-steroidal anti-inflammatory medications, but these provided only mild relief. Laboratory tests performed in the emergency room, including C-reactive protein, erythrocyte sedimentation rate, complete blood count and comprehensive metabolic panels were all normal. His past medical history was significant for Lyme disease manifesting with an erythema migrains lessions, fatigue and myalgias 2 months prior and treated with doxycycline, although Lyme IgM and IgG antibodies also obtained in the emergency room were negative, The patient was discharged and treated with an oral, 8-days prednisone taper, at the end of which his pain subsided. Electrodiagnostic testing performed 9 days post onset was normal; specifically, no median nerve abnormality was identified on the nerve conduction or electromyography portions of the exam. The patient developed weakness in wrist flexion and forearm pronation the day after electromyography, along with numbness along a 1-inch strip in the middle, volar forearm region. Cervical spine and brachial plexus MRI performed 9 days post onset of initial pain symptoms did not demonstrate any findings to account for the patient's symptoms. Eight weeks post onset of initial pain, physical examination by a neurologist revealed mild atrophy in the left volar forearm and mild weakness in forearm pronation and wrist flexion (British Medical Research Council Scale strength 4+/5). MR neurography demonstrated prominent denervation edema pattern of the pronator teres (PT) and flexor carpi radials (FCR) muscles within the forearm. Within the arm, 4 severe hourglass-like constrictions and T2-weighted signal hyperintensity of the anteromedially positioned fascicular bundle of the median nerv0. Repeat e were detected; this bundle represents the PT/FCR bundle based on the known topographical, fascicular arrangement of the median nerve. Repeat electromyography, consistent with imaging findings, demonstrated severe denervation and no motor unit recruitment within the PT or FCR muscles. Muscles in the anterior interosseous nerve distribution were normal on MRI and electromyography. At 3 months' follow up post onset, the patient reported no residual pain but increased weakness. He had not yet received the second dose of his COVID-19 vaccine. Post-vaccination PTS typically ensure within 28 days of immunisation and has been reported as early as the same day as vaccination. Intrinsic, hourglass-like constrictions of affected nerves or nerve fascicles have been recognized in the acute phase of PTS10 and to date, they have not been observed in other spontaneous neuropathies. Patients 1 and 2 developed symptoms 13 hours and 18 days respectively, after receiving a COVID-19 vaccine, with MR neurography confirming the diagnosis by 8 and 5 weeks, respectively. While approximately half of all individuals with PTS report no identifiable trigger,1 the close temporal association between events suggests that vaccination may have been linked to PTS in these patients. Patient 1 received a clinical diagnosis of Lyme disease 2 months prior to PTS symptom onset despite negative OgM and IgG serologic tests, which have low sensitivity during early infection. He was treated with doxycycline and recovered prior to receiving the COVID-19 vaccine. In the report, 3 COVID-19 vaccines have received FDA Emergency Use Authorization. These include mRNA vaccines developed by Pfizer/BioNTech (BNT162b2) and Moderna (mRNA1273), as well as a one-dose, replication-incompetent human adenovirus vector vaccine developed by Johnson & Johnson/Janssen (Ad26.COV2.S). Additionally, some individuals will develop PTS within the post-vaccination window by chance alone. MR neurography is a useful diagnostic tool for PTS and may be particularly relevant as worldwide COVID-19 vaccinations increase. While there are currently no approved treatments, early, oral prednisone may reduce PTS symptom duration and severity. In recalcitrant cases, surgical neurolysis has also demonstrated efficacy. The timely and accurate diagnosis of PTS, which is often delayed, can help alleviate any undue stress for the patient and direct appropriate management. Patient 1. A 49-year-old man with Parsonage-Turner syndrome that developed 13 hours following the 1st dose of the Pfizer-BioNTech (BNT162b2) COVID-19 vaccine. Axial T2- weighted fast-spin echo (FSE) fat suppressed image 8 weeks post symptom onset (A) demonstrates denervation edema pattern of the pronator teres (PT) and flexor carpi radialis (FCR) muscles. Axial T2-weighted gradient echo image (B) demonstrates abnormal signal hyperintensity of the PT/FCR, anteromedially positioned, fascicular bundle (arrow, magnified inset) of the median nerve (oval) within the distal arm. Oblique sagittal, curved multiplanar reformatted T2-weighted gradient echo image (C) demonstrates multiple, severe intrinsic constrictions (arrows) of the PT/FCR bundle of the median nerve (bracket).  No follow-up attempts are possible; information about lot/batch number cannot be obtained. No further information is expected.; Sender's Comments: Based on available information and a possible contributory role of suspect product BNT162B2 to the development of event neuralgic amyotrophy cannot be totally 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 RAs, Ethics Committees, and Investigators, as appropriate.