CASE REPORT

Intravenous Corticosteroid Therapy for Bilateral Parsonage-Turner Syndrome A Case Report and Review of the Literature Daniel Philip Wiser Smith, DO,* Jennifer A. Elliott, MD,* and James H. Helzberg† Objective: Parsonage-Turner syndrome (PTS) is a distinct clinical disorder characterized by pain, sensory loss, and impaired mobility of the upper extremities and, less commonly, the lower extremities. Manifestations vary from minor to fairly extensive involvement of the brachial and/or lumbosacral plexus. No evidence-based treatment protocol exists, with only anecdotal support of varied palliative efforts. Case Report: We describe a case of PTS in an otherwise healthy 19-year-old man presenting with severe neuropathic pain in the right upper extremity progressing to include weakness and contralateral extremity involvement. Intravenous corticosteroids were initiated with resolution of the pain after the first day of therapy and improvement in muscular strength throughout his hospitalization. Conclusions: This case supports the use of intravenous corticosteroids in the literature as a treatment option for PTS to ameliorate intractable pain as well as to impede the progression of motor dysfunction. (Reg Anesth Pain Med 2014;39: 243–247)

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arsonage-Turner syndrome (PTS), initially characterized in the 1940s, classically presents with the sudden onset of severe pain, typically in the shoulder, without a history of trauma or injury. The pain is followed by rapidly progressive paresis in the involved limb. The etiology is thought to be an autoimmune process related to a variety of triggering events including infections, trauma, surgery, childbirth, drug exposures, immunizations, and radiation therapy. Two types of PTS have been described, namely, an idiopathic form and a hereditary form. Risk factors for the development of PTS have been extensively reported; however, randomized controlled studies describing the treatment of this debilitating disorder are lacking.1 We describe a case involving progressive intractable upper extremity pain followed by the loss of motor strength bilaterally that was treated with high-dose intravenous (IV) corticosteroids, resulting in a significant reduction of pain and improvement in the patient’s motor function.

CASE REPORT The patient consented to educational publication of this case. A 19-year-old right-hand dominant man presented initially to the pain management center 2 weeks after undergoing arthroscopic knee surgery and patellar grafting. The patient initially noticed pain in his right shoulder 24 hours after surgery, which became progressively worse over time. He had been given From the *Department of Anesthesiology, Kansas City School of Medicine, University of Missouri, Kansas City, MO; and †Davidson College, Davidson, NC. Accepted for publication August 26, 2013. Address correspondence to: Jennifer A. Elliott, MD, 4401 Wornall Rd, Kansas City, MO 64111 (e‐mail: [email protected]). The authors declare no conflict of interest. Copyright © 2014 by American Society of Regional Anesthesia and Pain Medicine ISSN: 1098-7339 DOI: 10.1097/AAP.0000000000000070

tramadol, which decreased his pain for a short period, along with oxycodone and hydrocodone. Nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids were avoided at the request of his surgeon. He started physical therapy (PT) for his knee and shoulder; however, he was unable to tolerate therapy due to his shoulder pain. No muscle weakness was noted during his PT treatments until a few days before his visit to the pain management center. A magnetic resonance imaging (MRI) of the shoulder showed minor intrasubstance tearing of the infraspinatus but no other abnormalities. Magnetic resonance imaging of the cervical spine was normal. On physical examination, the patient had a significant decrease in the range of motion of his right shoulder with no involvement of the left shoulder. No sensory loss or paresthesias were noted. Muscle strength during external rotation and abduction of the right upper extremity at the shoulder was graded 2+/5. Otherwise, normal motor strength was noted in the right upper extremity. Examination findings suggested that the supraspinatus and infraspinatus muscles (suprascapular nerve) and deltoid and teres minor muscles (axillary nerve) were primarily affected. Reflexes were normal and rated as 2+/4. Normal muscle mass and tone of the affected upper extremity were noted. The patient’s overall pain was greatly exacerbated with palpation over the area of the suprascapular notch. A diagnosis of suprascapular neuropathy was initially made, and a suprascapular nerve block with 0.25% bupivacaine and 40 mg of triamcinolone was performed. Gabapentin was also prescribed and titrated to 300 mg 3 times daily. The patient initially had near-total relief of his pain after the injection. However, 2 to 3 days later, the pain returned, having spread into his right upper arm and beginning to include the left shoulder. In addition, his right arm was noted to have increased weakness on manual muscle testing, graded 1+/5 with external rotation and abduction at the shoulder and 3+/5 grip strength, flexion and extension at the shoulder. Then, physical examination indicated progression of muscle weakness to involve the coracobrachialis (musculocutaneous nerve), latissimus dorsi (thoracodorsal nerve), teres major (lower subscapular nerve), and forearm flexors (anterior interosseous nerve). The patient was subsequently hospitalized due to pain and progressive muscle weakness. The patient’s pain continued to be severe and refractory to any of the previous therapies. The left upper extremity began to show 3+/5 weakness with external rotation, indicating involvement of the infraspinatus muscle (suprascapular nerve) and teres minor muscle (axillary nerve) on that side. Opioid medications were discontinued, as adverse effects outweighed the minor benefit achieved from their use. A diagnosis of PTS was made based on the clinical characteristics of progressively worsening pain and weakness isolated to the upper extremities. Because the patient’s pain and weakness continued to worsen, the care team elected to initiate steroid therapy as the limited medical literature on PTS indicated potential benefit from this treatment. The patient was started on 1 g of methylprednisolone IV given every 24 hours. After day 1 of the steroid therapy, the patient showed slight improvement in his grip strength in the right hand to 4+/5, with a

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significant reduction in his bilateral upper extremity pain. The 1-g dose was continued for 5 days and the patient was discharged on an oral prednisone taper lasting 12 days. Physical examination upon discharge showed minor residual left upper extremity dysfunction with 4+/5 weakness in external rotation. The right upper extremity showed 3+/5 motor strength with abduction, external rotation, flexion, and extension at the shoulder and 4+/5 grip strength and flexion/extension at the elbow. Physical therapy was continued, and a low-dose fentanyl patch and tapentadol for breakthrough pain were prescribed to help facilitate ongoing rehabilitation. The patient was weaned off all analgesics after 1 month of IV corticosteroid therapy; he continued PT with slow improvement in muscle weakness. On follow-up, 12 months after the initial onset of pain, the patient reported no pain and had resumed most daily activities. His right shoulder girdle muscle function showed minimal improvement since his initial discharge, but he regained full use of the distal portions of his right upper extremity.

DISCUSSION Parsonage-Turner syndrome, also known as neuralgic amyotrophy (NA) or idiopathic brachial plexitis, was described in detail by Parsonage and Turner2 in 1948 as a disease process of the shoulder girdle. It is now classified as having an idiopathic form (INA) and a hereditary form (HNA). The criteria for the diagnosis of HNA are outlined in Table 1.1,3 The estimated incidence of INA is 2 to 4 cases per 100,000 population per year, with a much lower incidence for HNA. ParsonageTurner syndrome may occur from infancy to old age, and more commonly affects men. Recurrence of PTS after an initial episode has been described. The diagnosis of PTS may be delayed due to attribution of symptoms to other disorders such as cervical radiculopathy or shoulder joint pathology.1,4–7 The differential diagnosis of PTS involves a number of neurological and orthopedic conditions and is summarized in Table 2. Susceptibility to this syndrome may relate to a combination of factors, including genetic predisposition, autoimmune triggers, and mechanical vulnerability.4 This diagnosis of PTS is based primarily upon its clinical course. Parsonage-Turner syndrome consists of sudden onset of severe neuropathic pain in 96% of cases, followed by the development of a patchy progressive weakness of the involved extremity that may commence within days to weeks after the onset of pain.4,5 Historically, no inciting trauma is identified before the onset of PTS, and pain often recedes once weakness develops.8 Parsonage-Turner syndrome is distinguished from other neurological disorders by the fact that the pain, weakness, and sensory disturbances typically do not manifest in a single nerve root or peripheral nerve distribution.4,9,10 It most frequently involves one of the upper extremities, but can involve the lower extremities (lumbar plexus), and can be bilateral (although typically asymmetric) in up to one third of episodes.4 Most commonly, the symptoms start in the upper brachial plexus, affecting primarily the proximal shoulder girdle, but can involve any portion of the brachial plexus. The nerves typically affected in PTS include the long thoracic, suprascapular, axillary, musculocutaneous, anterior interosseous, and the lateral antebrachial cutaneous.4,7 Involvement of other nerves such as the phrenic, recurrent laryngeal, facial, spinal accessory, hypoglossal, and intercostals has also been reported.4–11 Although speculative, the current etiological hypothesis for the development of PTS is that mechanical injury or a genetic predisposition lead to an immune-mediated reaction causing damage to the brachial plexus. As many cases are identified

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after surgery is performed on an unrelated body region or limb (particularly after lower extremity surgery),12,13 this commonly leads to attribution of nerve injury to improper patient positioning, with attendant medicolegal implications.9,13 Other potential provocative factors include neoplasm,14 immunosuppressants,15 viral infection,9 antibiotic use,9 antiretroviral use,16 or autoimmune disease.9 In many cases, no antecedent provocative factors can be identified.17 Peripheral nerve biopsies in patients with PTS have shown epineural perivascular mononuclear infiltrates associated with active axonal degeneration.4,7,18 Other findings include focal decreases in myelinated fibers within individual nerve fascicles and apparent constrictive bands along the course of an affected nerve.7,10 Parsonage-Turner syndrome may be most completely described by the phrase, “multifocal multifascicular inflammatory and constrictive brachial neuritis.”10 Neither nerve biopsy nor any other diagnostic test is required for diagnosis. Parsonage-Turner syndrome is diagnosed primarily from its characteristic clinical presentation. Parsonage-Turner syndrome is a diagnosis of exclusion, and no test can definitively confirm or refute its occurrence.8 Parsonage-Turner syndrome may be confused with complex regional pain syndrome (CRPS), another clinically diagnosed pain syndrome; however, in CRPS, pain is not typically as sudden in onset, tends to be poorly localized, and is associated with edema and color changes of the affected extremity. Diagnostic tests may be useful to differentiate PTS from other conditions. Magnetic resonance imaging of the cervical spine or shoulder can be used to exclude disc herniation or rotator cuff/shoulder joint pathology as sources of the presenting symptoms. Electromyography (EMG) and nerve conduction studies have historically been the only diagnostic tests that provide support for the diagnosis of PTS.5 Electromyography often shows evidence of denervation with positive sharp waves, high amplitude, and long duration motor unit potentials and fibrillations on needle electrode examination.11 Distal peripheral nerves exhibit decreased conduction velocities. More recently, MRI using T2 weighting and short τ inversion recovery imaging has been used to assess for evidence of high signal intensity representing edema of denervated muscles.19–23 Edematous changes may be seen within 2 to 4 weeks after denervation occurs20; therefore, changes may not be apparent if imaging is obtained very early after symptom onset. Later, changes of atrophy and fatty infiltration of the affected muscles may be seen.19–21 Several studies using MRI in classic PTS have found that the most commonly affected muscles are the supraspinatus and infraspinatus, correlating with suprascapular nerve involvement.19–22 Although the onset of symptoms in PTS tends to be abrupt, recovery typically takes considerable time. The initial acute phase of pain lasts an average of 4 weeks, which is often replaced by a secondary neuropathic pain that may last for several more months.4 One study of 246 PTS cases presented data regarding different modalities of pain control.6 Acetaminophen, NSAIDs, opioids, combination opioid/NSAID, or any of the previously mentioned with coanalgesics (amitriptyline, carbamazepine, or gabapentin) were used. The greatest degree of relief was obtained with a combination of an NSAID and an opioid, and the least with an NSAID alone. Interestingly, 31.6% found opioids to provide good control of their pain, whereas only 2.2% felt similar relief from an NSAID alone. The NSAID and opioid combination afforded good pain control in 60.7% of the subjects. Rest and immobilization of the affected extremity during the acutely painful phase of PTS may help decrease pain exacerbations.17 Although many other treatments may exist, including regional anesthetic techniques, there is little evidence to support other methods of pain management. © 2014 American Society of Regional Anesthesia and Pain Medicine

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TABLE 1. Summary of the 1999 ENMC Criteria for Hereditary Neuralgic Amyotrophy Inclusion Clinical criteria Family history Age at onset Clinical manifestations

Compatible

Autosomal dominant inheritance with high penetrance Second to third decade Acute, recurrent unilateral or bilateral brachial plexopathy

Isolated cases may be due to de novo mutations Earlier or later onset is possible Lumbar plexus may be affected

Severe pain precedes the onset of weakness by days to few weeks

Cranial nerves may be affected (most commonly facial or recurrent laryngeal nerves) Phrenic nerve may be affected Abortive attacks may present with pain not followed by weakness Intervals between attacks can be long (up to many years) Motor symptoms > sensory loss Sensory abnormalities

Deficits are predominantly motor Number of episodes may vary from 1 to many (up to 20) Complete recovery without any residual deficits Relapsing/remitting course Recovery occurs within month to 2 y

Exclusion

Absence of pain before or during attacks (absence may very rarely occur in subsequent attacks) Signs of a generalized neuropathy

Autonomic symptoms Tendon reflexes diminished/absent Weakness/atrophy may be noted in previously affected limbs Hypotelorism, epicanthal folds, short stature may be present Recovery often incomplete with residual neurodeficit persisting especially after repeated attacks affecting the same limb Chronic undulating course without completely symptom-free interval Electrophysiological criteria

Molecular genetics

EMG shows signs of denervation or reinnervation in muscles innervated by affected nerves Slightly reduced distal nerve conduction velocity in affected nerves Reduced amplitude of affected sensory nerve action potentials Linkage to the HNA locus (SEPT9) on chromosome 17q25

Electrophysiological signs of generalized neuropathy

Absence of linkage to the HNA (SEPT9) locus on 17q25

Presence of mutations in the PMP22 gene Presence of HNPP deletion on 17p11.2

EMG indicates electromyography; ENMC, European Neuro Muscular Centre; HNPP, hereditary neuropathy with liability to pressure palsy. Reproduced with modifications with permission from van Alfen et al.1 Copyright © 2000–2013 by John Wiley & Sons, Inc or related companies. All rights reserved. Also reproduced from Kuhlenbäumer et al,3 copyright 2000, with permission from Elsevier. Adaptations are themselves works protected by copyright. So in order to publish these adaptations, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

Long-term, up to one third of patients with PTS will continue to experience significant pain and fatigue, with up to two thirds of patients reporting difficulties in performing activities of daily living such as grooming or household chores.24 A substantial number may also experience some degree of work-related disability due to residual symptoms.24 It seems that patients experiencing pain for longer durations and those with lower plexus lesions tend to have a slower rate of recovery.25 It has been estimated that recovery is complete in 36% of patients after 1 year, 75% after 2 years, and 89% after © 2014 American Society of Regional Anesthesia and Pain Medicine

3 years.17,25 Therefore, more than 3 years may elapse before a final assessment of residual impairments can be made.4 The hypothesis that an autoimmune reaction causes the brachial plexopathy suggests that steroid therapy would be optimal treatment for PTS, but only anecdotal evidence exists. One observational study showed improvement in the acute phase with oral steroids.26 Very little literature exists regarding the use of IV corticosteroids for this condition.18,27,28 In 1 case series, use of high-dose IV methylprednisolone (500–1000 mg/d) resulted in dramatic improvement in pain symptoms within hours of

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TABLE 2. Differential Diagnosis of Neuralgic Amyotrophy Differential Diagnosis Neurological disorders Cervical radiculopathy, degenerative Cervical radiculopathy, disc rupture Mononeuritis multiplex/vasculitis Multifocal motor neuropathy Asian tick-borne encephalitits, poliomyelitic form Focal motor neuron disease (Hirayama, brachial amyotrophic diplegia, distal spinal muscular atrophy) Entrapment neuropathies (carpal tunnel, ulnar neuropathy at the elbow) Pancoast tumor with brachial plexus involvement Thoracic outlet syndrome Hereditary neuropathy with liability to pressure palsy (HNPP) Nonneurological disorders Shoulder or elbow joint pathology Cervical spondylosis with referred brachialgia CRPS

Features Distinguishing Disorder From Neuralgic Amyotrophy Insidious onset, slowly progressive or fluctuating course Acute onset, pain varies with posture; pain, sensory, and motor symptoms occur in same dermatome Symptoms also occur in legs or distal arm, subacute onset, progressive Painless, no sensory symptoms, distal predominance, progressive After viral prodrome, severe headache and back pain, flaccid shoulder girdle paralysis, death by respiratory involvement Insidious onset, no sensory symptoms, painless, progressive Subacute onset, mild to moderate pain, prominent sensory symptoms Insidious onset, progressive pain, symptoms spread from lower plexus to middle and upper parts; Horner syndrome Painless wasting of thenar > hypothenar musculature, slowly progressive, hypesthesia in medial forearm Often painless, can resolve rapidly, concomitant entrapment neuropathies, polyneuropathy in elderly patients Pain brought on by joint movement or posture, usually relief at rest, passive restriction of movement Often posture-dependent or activity-dependent, no focal deficits, fluctuating course Vasomotor features predominate, diffuse pain and weakness, subacute onset with progression

Reprinted by permission from Macmillan Publishers, Ltd: Nature Reviews: Neurology. Van Alfen N. Clinical and pathophysiological concepts of neuralgic amyotrophy, copyright 2011. Also with kind permission from Springer Science+Business Media: Journal of Neurology, The neuralgic amyotrophy consultation, vol. 254 (6), 2007, page 701, Van Alfen N, figures 1 & 2. Adaptations are themselves works protected by copyright. So in order to publish these adaptations, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

administration in 2 of the 4 subjects with HNA studied.28 In both of these subjects, symptoms recurred when steroids were tapered or discontinued.28 Our patient similarly exhibited dramatic pain reduction in the first 24 hours of treatment with IV corticosteroid therapy but did not experience significant return of pain or recurrent weakness after the prednisone taper was completed. The course of our patient’s treatment was complicated by the concerns about patellar graft failure after steroid use, resulting in delay of corticosteroid administration. It is likely that his pain would have been controlled more quickly had corticosteroid treatment been begun earlier. Although steroids may help provide rapid symptom resolution, they may not reduce the weakness associated with PTS25,27,28; however, our patient did experience acute improvement in weakness with steroid therapy. Use of IV immunoglobulin (IVIg) to treat the weakness associated with PTS has been reported.27,29 In 1 case, corticosteroids were helpful in treating pain from PTS, but weakness continued to progress during the course of 2 weeks.27 This patient demonstrated improvement in strength after infusion of IVIg 2 g/kg during period of 4 days.27 A recent prospective study of the use of prophylactic corticosteroids in 3 subjects with HNA who had experienced previous episodes of brachial plexitis with surgery or childbirth demonstrated that none of the individuals experienced a recurrence of symptoms perioperatively when prophylactic steroids were given.30 One patient who underwent elective cesarean delivery received 1 g of methylprednisolone IV before cesarean delivery and 6 infusions of IVIg postpartum.30 The other 2 patients were treated solely with steroids; one received oral prednisone 60 mg daily for 1 week before surgery and

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dexamethasone 8 mg IV intraoperatively, and the other received 1 g of methylprednisolone on the day before, the day of, and the day after surgery.30 The need for randomized controlled clinical trials for the treatment of pain and weakness in PTS is obvious but difficult due to its sporadic occurrence.1 One trial under way is assessing oral corticosteroid use, which may be helpful in guiding a specific treatment protocol in the future.1 The finding (in a limited number of patients) that prophylactic steroid use may prevent recurrence of PTS is promising. This may prompt the administration of perioperative steroids to patients at risk for recurrent attacks, especially those with identified HNA. Because there is always a potential for recurrent attacks even in individuals with a history of INA, this may become a standard preoperative treatment for such patients in the future. Additional study of this treatment as well as the use of IVIg to treat steroid nonresponders and patients with severe PTS-associated weakness is needed.

CONCLUSIONS Because PTS can be a debilitating condition, it is important to recognize its symptoms and achieve a diagnosis early in its course. Although a number of therapies have been attempted with varying success, no evidence-based treatment for PTS exists. Further comprehension of the pathophysiologic basis of PTS has led to the use of treatments commonly used in the management of other disease processes that share a similar © 2014 American Society of Regional Anesthesia and Pain Medicine

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autoimmune basis. Our case supports the use of IV corticosteroid therapy leading to rapid amelioration of pain and improvement in motor function. Further study of this treatment, perhaps compared with other modalities that have shown promise, will help develop a universal protocol to treat PTS.

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15. Arias M, Arias-Rivas S, Dapena D. Brachial plexitis and myelitis and herpes zoster lumbar plexus disorder in a patient treated with infliximab [in Spanish]. Neurologia. 2005;20:374 –376. 16. Bellagamba R, Tomassi C, De Marco M. Parsonage-Turner syndrome: a rare case of abacavir hypersensitivity reaction in HIV-infected patients. J Infect. 2008;57:88–90.

ACKNOWLEDGMENTS The authors thank Dr Eugene Fibuch for his comments, proofreading, and assistance in composing this article.

17. McCarty EC, Tsairis P, Warren RF. Brachial neuritis. Clin Orthop Relat Res. 1999;368:37– 43.

REFERENCES

19. Bredella MA, Tirman PFJ, Fritz RC, Wischer TK, Stork A, Genant HK. Denervation syndromes of the shoulder girdle: MR imaging with electrophysiologic correlation. Skeletal Radiol. 1999;28:567–572.

1. van Alfen N, van Engelen BGM, Hughes RAC. Treatment for idiopathic and hereditary neuralgic amyotrophy (brachial neuritis). Cochrane Database Syst Rev. 2009;CD006976. 2. Parsonage MJ, Turner JW. Neuralgic amyotrophy: the shoulder-girdle syndrome. Lancet. 1948;1:973–978.

18. Suarez GA, Giannini C, Bosch EP, et al. Immune brachial plexus neuropathy: suggestive evidence for an inflammatory-immune pathogenesis. Neurology. 1996;46:559–561.

20. Elsayes KM, Shariff A, Staveteig PT, Mukundan G, Khosla A, Rubin DA. Value of magnetic resonance imaging for muscle denervation syndromes of the shoulder girdle. J Comput Assist Tomogr. 2005;29:326–329.

3. Kuhlenbäumer G, Stögbauer F, Timmerman V, De Jonghe P (on behalf of the European CMT Consortium). Diagnostic guidelines for hereditary neuralgic amyotrophy or heredofamilial neuritis with brachial plexus predilection. Neuromuscul Disord. 2000;10:515–517.

21. Gaskin CM, Helms CA. Parsonage-Turner syndrome: MR imaging findings and clinical information of 27 patients. Radiology. 2006;240:501–507.

4. Van Alfen N. Clinical and pathophysiological concepts of neuralgic amyotrophy. Nat Rev Neurol. 2011;7:315–322.

22. Scalf RE, Wenger DE, Frick MA, Mandrekar JN, Adkins MC. MRI findings of 26 patients with Parsonage-Turner syndrome. AJR Am J Roentgenol. 2007;189:W39 –W44.

5. van Alfen N. The neuralgic amyotrophy consultation. J Neurol. 2007;254:695–704. 6. van Alfen N, van Engelen BGM. The clinical spectrum of neuralgic amyotrophy in 246 cases. Brain. 2006;129:438– 450. 7. van Alfen N, Hannibal MC, Chance PF, van Engelen BGM. Hereditary neuralgic amyotrophy. 2008 Feb 27 (Updated 2012 Dec 6). In: Pagon RA, Adam MP, Bird TD, et al, eds. GeneReviews (Internet). Seattle, Wash): University of Washington, Seattle; 1993–2014. Available at http://www.ncbi.nlm.nih.gov/books/NBK1395/. Accessed April 18, 2013. 8. Misamore GW, Lehman DE. Parsonage-Turner syndrome (acute brachial neuritis). J Bone Joint Surg Am. 1996;78:1405–1408. 9. Feinberg JH, Radecki J. Parsonage-Turner syndrome. HSS J. 2010;6:199–205. 10. Sumner AJ. Idiopathic brachial neuritis. Neurosurgery. 2009;65:A150–A152. 11. Schreiber AL, Abramov R, Fried GW, Herbison GJ. Expanding the differential of shoulder pain: Parsonage-Turner syndrome. J Am Osteopath Assoc. 2009;109:415– 422. 12. Fibuch EE, Mertz J, Geller B. Postoperative onset of idiopathic brachial plexus neuritis. Anesthesiology. 1996;84:455–458. 13. Simon JP, Fabry G. Parsonage-Turner syndrome after total-hip arthroplasty. J Arthroplasty. 2001;16:518–520. 14. Symonds RP, Hogg RB, Bone I. Paraneoplastic neurological syndromes associated with lymphomas. Leuk Lymphoma. 1994;15:487– 490.

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23. Zara G, Gasparotti R, Manara R. MR imaging of the peripheral nervous system involvement: Parsonage-Turner syndrome. J Neurol Sci. 2012;315:170 –171. 24. van Alfen N, van der Werf SP, van Engelen BG. Long-term pain, fatigue, and impairment in neuralgic amyotrophy. Arch Phys Med Rehabil. 2009;90:435– 439. 25. Tsairis P, Dyck PJ, Mulder DW. Natural history of brachial plexus neuropathy. Arch Neurol. 1972;27:109–117. 26. van Eijk JJ, van Alfen N, Berrevoets M, et al. Evaluation of prednisolone treatment in the acute phase of neuralgic amyotrophy; an observational study. J Neurol Neurosurg Psychiatry. 2009;80:1120 –1122. 27. Johnson NE, Petraglia AL, Huang JH, Logigian EL. Rapid resolution of severe neuralgic amyotrophy after treatment with corticosteroids and intravenous immunoglobulin. Muscle Nerve. 2011;44:304 –305. 28. Klein CJ, Dyck PJB, Friedenberg SM, Burns TM, Windebank AJ, Dyck PJ. Inflammation and neuropathic attacks in hereditary brachial plexus neuropathy. J Neurol Neurosurg Psychiatry. 2002;73:45–50. 29. Moriguchi K, Miyamoto K, Takada K, Kusunoki S. Four cases of anti-ganglioside antibody-positive neuralgic amyotrophy with good response to intravenous immunoglobulin infusion therapy. J Neuroimmunol. 2011;238:107–109. 30. Klein CJ, Barbara DW, Sprung J, Dyck PJ, Weingarten TN. Surgical and postpartum hereditary brachial plexus attacks and prophylactic immunotherapy. Muscle Nerve. 2013;47:23–27.

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Intravenous corticosteroid therapy for bilateral parsonage-turner syndrome: a case report and review of the literature.

Parsonage-Turner syndrome (PTS) is a distinct clinical disorder characterized by pain, sensory loss, and impaired mobility of the upper extremities an...
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