key: cord-0891753-i3wzq91f authors: Fortanier, Etienne; Le Corroller, Thomas; Hocquart, Marie; Delmont, Emilien; Attarian, Shahram title: Shoulder palsy following SARS‐CoV2 infection: 2 cases of typical Parsonage‐Turner syndrome date: 2022-04-16 journal: Eur J Neurol DOI: 10.1111/ene.15358 sha: d055fa25d4486556b7d2885afe6043eb2032f40b doc_id: 891753 cord_uid: i3wzq91f ‐ Neuralgic amyotrophy (NA), also named Parsonage-Turner (PT) syndrome, is an acute painful monophasic peripheral nerve injury triggered by mechanical or infectious stress. In addition, neuromuscular disorders such as Guillain-Barré syndrome 1 We present two acute painful shoulder weakness cases secondary to coronavirus 2 infection (SARS-CoV2) with electrophysiologic and plexus MRI abnormalities in favor of typical PT syndrome. Case 1. A 45-yo right-handed female schoolteacher was admitted for acute pain in the right shoulder, quickly followed by difficulty in raising her right arm. Her son was tested positive for SARS-CoV2 infection 10 days before, and she also presented fever with a positive PCR nasopharyngeal swab test the same day. Motor examination on the right side revealed weakness of shoulder abduction and elbow flexion (3/5 Medical Research Council grade). Right bicipital and brachioradialis reflexes were diminished. There was no other motor deficit, and sensory testing was strictly normal. Spinal cord MRI and cerebrospinal fluid analyses were unremarkable. The electrophysiological evaluation performed 35 days after symptoms onset showed preserved CMAP amplitudes in the right arm for ulnar, median, axillary, and musculocutaneous nerves and normal sensory evaluation including lateral and medial antebrachial cutaneous nerves. Electromyography showed acute dernervation without spontaneous activity in the biceps brachi and the deltoid muscles. The plexus MRI revealed a persistent hyperintense signal involving the right C6 root and the superior truncus of the brachial plexus, without contrast enhancement. Other viral serologies (HIV, CMV, B19 parvovirus, hepatitis B, C, and E) and antigangliosides antibodies were negative. She did not receive any treatment, and the evolution was favorable, with a complete disappearance of the symptoms three months later. This article is protected by copyright. All rights reserved Case 2. A 21-yo right-handed man complained of headache, nausea, and fever. He was hospitalized eight days later due to breathing difficulties. The PCR swab test was positive for SARS-CoV2 infection. Ten days after COVID-19 symptoms onset, he presented with severe right shoulder pain, associated with difficulty in raising the right arm. Right shoulder CT scan found no abnormality. The neurological evaluation found an isolated deficit of the serratus major muscle associated with a right scapula winging ( Figure 1A ). There was no sensory deficit, and the osteotendinous reflexes were all present. Electrophysiological evaluation performed five days later showed an isolated involvement of the right long thoracic nerve with reduced CMAP amplitudes compared to the left (2.8 vs. 4.5 mV, Figure 1C ) and a neurogenic recruitment pattern in the right serratus muscle without spontaneous activity (Fig 1D. ). Motor and sensory evaluations were normal in ulnar, median, axillary, anterior interosseous, radial, lateral and medial antebrachial cutaneous nerves. Plexus MRI showed a thickening and hyperintense signal involving the right long thoracic nerve within the scalenus medius muscle. Oral prednisone at 1mg/kg was initiated for seven days, followed by rapid tapering. Examination 4 months after symptoms onset still showed an isolated partial deficit of the serratus major muscle with a slight improvement of the winged scapula ( Figure 1B ) but persistent pain in the right shoulder. COVID-19 is now known to cause neurological complications in almost 9% of the cases 2 . We report two new cases of PT syndrome following SARS-CoV2 infection with explicit electrophysiologic and imaging pathologic features, underlining the possible association between COVID-19 and PT syndrome. To our knowledge, only a few cases of PT syndrome in the setting of COVID-19 have been detailed so far in the literature 3, 4, 5, 6, 7 . Only two of these cases showed typical brachial plexus involvement 3, 4 . Other previous reports consisted of a sole median nerve alteration 5 , a pure sensory deficit with left lateral antebrachial cutaneous electrophysiological abnormalities 6 , or an isolated weakness of trapezius muscle 7 . PT syndrome following viral infections. As in these two cases, time frame between viral infection and neurological symptoms is usually around 10 days, suggesting immune-mediated mechanisms triggered by the infection. A direct viral neuroinvasion have been suspected in cases where neurological symptoms occurred more rapidly during infection 3 . Our two cases do not allow us to conclude the exact relation between COVID-19 and PT syndrome, but temporal relation between infection and neurological symptoms may suggest a parainfectious pathogenesis. More extensive case-control studies are now required to better understand the biological process leading to PT syndrome in such cases. In conclusion, these two cases with classic clinical, MRI, and electrophysiological findings are in favor of typical PT syndrome triggered by SARS-CoV2 infection. The data that support the findings of this study are available from the corresponding author upon reasonable request. 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