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• W2096911516 abstract "A 36-year-old primiparus woman with no previous significant medical history presented with painless acute impairment in elevation of the right arm above head level. Three days before onset, she had delivered a full-term 7 pound girl after 5 h of labor, under epidural anesthesia. Neurological examination showed right scapular winging characterized by slight medial and superior shift that increased with arm abduction. Three weeks after symptom onset needle electromyography showed fibrillation potentials in the right serratus anterior muscle. Complete blood tests, including autoimmune screening, were unremarkable. A chest radiograph was normal. Brachial plexus MRI showed increased signal intensity with contrast enhancement of the right long thoracic nerve, suggesting inflammation (Fig. 1). The patient was given oral prednisolone, 1 mg/kg daily for 21 days, with dose tapering over the next month. Three months later, her symptoms were stable, but electrophysiological follow-up showed a slight reduction of fibrillation potentials in right serratus anterior muscle. Scapular winging is caused by imbalanced action of scapular muscles. The clinical examination based on the muscle group affected (trapezius, rhomboids, serratus anterior) is still the first guide for interpretation both of “pure” and “complicated” phenotypes.1 Isolated scapular winging due to serratus anterior weakness is usually caused by traumatic or postsurgical long thoracic nerve injury, or it can occur as a manifestation of neuralgic amyotrophy, also known as Parsonage-Turner syndrome (PTS). PTS is a clinical syndrome characterized by attacks of extreme pain at onset, patchy weakness in the upper extremities, and atrophy of affected muscles.2 The available evidence suggests that PTS has a complex pathophysiology that includes an underlying predisposition, susceptibility to dysfunction of some peripheral nervous system structures, and an autoimmune trigger.3 Cases of PTS are described after an immune event, such as pregnancy, childbirth, vaccination, or infection.2 Our patient did not have a history of previous surgery or trauma involving the thoracic area. Other possible causes were excluded by the laboratory evaluation. Moreover, she did not experience acute pain at onset, but only subsequent musculoskeletal pain due to compensation for the deficit. Since childbirth, an immunological trigger, occurred 3 days before symptom onset and approximately 4% of patients with PTS do not experience pain,2 we made a diagnosis of post-partum PTS. Currently, neuralgic amyotrophy cannot be diagnosed confidently by a single test, and often the presence of extreme pain of the upper limb together with patchy paresis helps in the diagnosis. In PTS without pain at onset, neuroimaging studies can be very useful, because they can exclude other causes such as intervertebral disc disease, tumors, or entrapment neuropathies. Furthermore, the evidence of contrast enhancement on MRI suggests a possible inflammatory etiology, thus supporting early administration of corticosteroids even in absence of pain, to block further evolution of the clinical picture and to possibly speed up functional nerve recovery. In conclusion, contrast-enhanced MRI can provide crucial help in identifying different phenotypes of PTS and can guide therapy. Viviana Nociti, MD, PhD1 Mauro Monforte, MD,2 Alessia Perna, MD2 Francesca Madia, MD, PhD2 Giovanni Melchiorri, MD3 Massimiliano Mirabella, MD, PhD2 1Don Carlo Gnocchi Onlus Foundation, Milan, Italy 2Institute of Neurology, Catholic University, Rome, Italy 3Motor Science Degree, Tor Vergata University, Rome, Italy" @default.
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• W2096911516 date "2013-12-03" @default.
• W2096911516 modified "2023-10-16" @default.
• W2096911516 title "Case of postpartum Parsonage-Turner syndrome" @default.
• W2096911516 cites W2025778948 @default.
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• W2096911516 doi "https://doi.org/10.1002/mus.24073" @default.
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