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      Off-Label Use of Intravenous Immunoglobulin with Methylprednisolone to Treat Parsonage–Turner Syndrome in a United States Marine

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      1 , 2 ,   3 , 4 ,
      Case Reports in Medicine
      Hindawi

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          Abstract

          Neuralgic amyotrophy (NA) also known as Parsonage–Turner syndrome is an inflammatory disorder of the brachial plexus characterized by sudden, acute onset of severe pain of the arm and/or shoulder followed by muscle weakness and sensory abnormalities. Although management may involve physical therapy, immunomodulatory drugs, and analgesics, there is nothing specific for the treatment of NA. Full functional recovery can take months to years, but recurrence and/or persistence of symptoms and disability are frequent. This case reports a 22-year-old male who recovered from NA within 3 months following treatment with 1000 mg of methylprednisolone and off-label use of 0.5 g/kg of intravenous immunoglobulins (IVIG) for four consecutive days. Three years later, the patient experienced soreness and paresthesia of the shoulder following a military shooting exercise, and 0.75 g/kg of IVIG and 1000 mg of MP were prescribed for 2 consecutive days resulting in complete recovery and no recurrences to date. EMG findings, 3.5-year postinitial treatment, revealed improvement in the brachial plexopathy. This provides support for the combined use of IVIG and glucocorticoids in the treatment of NA and highlights the need for further studies investigating whether this combined treatment regimen may accelerate recovery and improve long-term outcomes for patients diagnosed with NA.

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          Most cited references24

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          The clinical spectrum of neuralgic amyotrophy in 246 cases.

          We investigated the symptoms, course and prognosis of neuralgic amyotrophy (NA) in a large group of patients with idiopathic neuralgic amyotrophy (INA, n = 199) and hereditary neuralgic amyotrophy (HNA, n = 47) to gain more insight into the broad clinical spectrum of the disorder. Several findings from earlier smaller-scale studies were tested, and for the first time the potential differences between the hereditary and idiopathic phenotypes and between males and females were explored. Generally, the course of the pain manifests itself in three consecutive phases with an initial severe, continuous pain lasting for approximately 4 weeks on average. Sensory involvement was quite common and found in 78.4% of patients but was clinically less impairing than the initial pain and subsequent paresis. As a typically patchy disorder NA can affect almost any nerve in the brachial plexus, although damage in the upper and middle trunk distribution with involvement of the long thoracic and/or suprascapular nerve occurred most frequently (71.1%). We found no correlation between the distribution of motor and sensory symptoms. In INA recurrent attacks were found in 26.1% of the patients during an average 6 year follow-up. HNA patients had an earlier onset (28.4 versus 41.3 years), more attacks (mean 3.5 versus 1.5) and more frequent involvement of nerves outside the brachial plexus (55.8 versus 17.3%) than INA patients, and a more severe maximum paresis, with a subsequent poorer functional outcome. In males the initial pain tended to last longer than it did in females (45 versus 23 days). In females the middle or lower parts of the brachial plexus were involved more frequently (23.1 versus 10.5% in males), and their functional outcome was worse. Overall recovery was less favourable than usually assumed, with persisting pain and paresis in approximately two-thirds of the patients who were followed for 3 years or more.
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            Neuralgic amyotrophy: An update on diagnosis, pathophysiology, and treatment

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              Mutations in SEPT9 cause hereditary neuralgic amyotrophy.

              Hereditary neuralgic amyotrophy (HNA) is an autosomal dominant recurrent neuropathy affecting the brachial plexus. HNA is triggered by environmental factors such as infection or parturition. We report three mutations in the gene septin 9 (SEPT9) in six families with HNA linked to chromosome 17q25. HNA is the first monogenetic disease caused by mutations in a gene of the septin family. Septins are implicated in formation of the cytoskeleton, cell division and tumorigenesis.
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                Author and article information

                Contributors
                Journal
                Case Rep Med
                Case Rep Med
                CRIM
                Case Reports in Medicine
                Hindawi
                1687-9627
                1687-9635
                2021
                1 April 2021
                : 2021
                : 6663755
                Affiliations
                1Campbell University, Jerry M. Wallace School of Osteopathic Medicine, P.O. Box, Buies Creek, NC 27506, USA
                2Neurology Department, Gundersen Health System, 1900 South Avenue, La Crosse, WI 54601, USA
                3Department of Anatomy, Campbell University, Jerry M. Wallace School of Osteopathic Medicine, P.O. Box 4280, Buies Creek, NC 27506, USA
                4Department of Microbiology and Immunology, Campbell University, Jerry M. Wallace School of Osteopathic Medicine, P.O. Box 4280, Buies Creek, NC 27506, USA
                Author notes

                Academic Editor: Mamede de Carvalho

                Author information
                https://orcid.org/0000-0002-1265-8171
                https://orcid.org/0000-0001-8854-8860
                Article
                10.1155/2021/6663755
                8035001
                c615f998-4f11-45c5-a2a6-11b8583cc164
                Copyright © 2021 Carissa M. Sedlacek et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 9 December 2020
                : 5 March 2021
                : 14 March 2021
                Categories
                Case Report

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