Journal Information
Vol. 13. Issue 1.
Pages 60-61 (January - February 2017)
Vol. 13. Issue 1.
Pages 60-61 (January - February 2017)
Letter to the Editor
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Parsonage–Turner Syndrome: A Case Report
Síndrome de Parsonage-Turner: a propósito de un caso
Itxasne Cabezón
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Corresponding author.
, Guillermo Barreiro, María Victoria Egurbide
Servicio de Medicina Interna, Hospital Universitario de Cruces, Baracaldo, Vizcaya, Spain
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To the Editor,

Parsonage–Turner syndrome (PTS) is a neuritis of the idiopathic brachial plexus.1 We report the case of a patient affected by this disorder, which had no triggering factor.

The patient was 67-year-old man with type 2 diabetes mellitus, with good metabolic control and obstructive sleep apnea hypopnea syndrome. He had been diagnosed with a lung squamous cell carcinoma, stage pT1apN0, in March 2015. He was treated with left upper lobectomy and lymphadenectomy. He was admitted to our hospital in November after several days of severe pain in the right scapular region, followed by paresis involving extension of his 4th finger, with no history of traumatic injury or infection. Physical examination revealed weakness in dorsal interossei and in all the extensor carpi, with slight amyotrophy. He underwent cervicothoracic computed tomography, which ruled out lung apex disease, as well as cervical magnetic resonance imaging (MRI), which revealed spondyloarthrosis without myelopathy, and MRI of the brachial plexus, which showed no changes. An electromyogram performed 2 weeks after symptom onset indicated right brachial plexopathy with inferior predominance (C8-T1). Cerebrospinal fluid was normal. Suspecting PTS, we began treatment with analgesics, glucocorticoids and rehabilitation, which achieved resolution of the pain and nearly complete recovery of the movement of the 4th finger 2 months later.

Parsonage–Turner syndrome (amyotrophic neuralgia) is an acute neuritis of the brachial plexus characterized by shoulder pain, followed by a motor deficit and muscle atrophy, generally in the shoulder and the area of the elbow.1 There are idiopathic and hereditary forms.2 In the idiopathic form, 50% of the patients are exposed to a previous event (infection, surgery, systemic disease or vaccination), which would activate lymphocytes sensitized to the brachial plexus in individuals with a genetic predisposition.1,3,4 A number of cases of PTS have been reported after different types of surgery.1,5,6 Some authors suggest that surgical stress could activate an unidentified virus that remains latent in the peripheral nervous system, as occurs in some cases of postoperative reactivation of herpes zoster.5 Others propose a mechanical lesion affecting the plexus during general anesthesia. Our patient was subjected to pulmonary surgery (contralateral to the clinical findings) during the previous months. However, we do not consider that to be a triggering factor, since the clinical signs develop soon after surgery (1–13days) in all the reported cases.6

It especially affects men, ranging from 20 to 60 years old, with an incidence of 1.6–3cases/100000population/year.7 The typical clinical signs and symptoms consist of severe pain in the shoulder, that develops suddenly and is not traumatic, and frequently radiates toward the cervical region and the outside of the arm. After a variable period of time, muscle atrophy appears, followed by paresis; the latter is flaccid, patchy and progressive, and its distribution does not always coincide with the painful area. It can affect several peripheral nerves and nerve roots (especially C5 and C6) or a combination of both.4 A third of the patients develop bilateral and symmetrical symptoms.7 The diagnosis is based on the medical records, physical examination and the electromyogram, which typically shows acute denervation in a specific nerve or a patchy nerve loss throughout the entire plexus.8 Magnetic resonance imaging of the cervical spine and brachial plexus can, in the initial phases, look normal or have hyperintense signals in T2 due to muscle edema, and, once atrophy is established, there can be an increased intramuscular linear signal intensity in T1 due to fatty infiltration.9 The attempt is made to treat the symptoms with analgesics, immobility of the limb and rehabilitation.4 The use of moderate doses of glucocorticoids at the initiation seems to relieve the pain and accelerate recovery, which is generally slow (from months to years).2 After 3years, a third of the patients have chronic pain and 2 thirds have a functional deficit, and the recurrence rate is 26%.10

Conflicts of Interest

The authors declare they have no conflicts of interest.

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Please cite this article as: Cabezón I, Barreiro G, Egurbide MV. Síndrome de Parsonage-Turner: a propósito de un caso. Reumatol Clin. 2017;13:60–61.

Copyright © 2016. Elsevier España, S.L.U. and Sociedad Española de Reumatología y Colegio Mexicano de Reumatología
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