Neuralgic Amyotrophy

A Commonly Overlooked Cause of Acute Shoulder Pain

Background: Neuralgic amyotrophy (NA) is a multifactorial, monophasic neuritis that mainly affects the nerves of the shoulder girdle. It is characterized by very severe pain and by weakness that arises some time after the pain. Its reported incidence is high (100 cases per 100 000 persons per year), but our data suggest that many or most cases are diagnosed late or not at all.

Methods: This review of the epidemiology, pathophysiology, diagnosis, and treatment of NA is based on pertinent publications retrieved by a selective literature search, and on data provided by the scientific institute of AOK, a German statutory health-insurance carrier.

Results: It is currently thought that the combination of a genetic predisposition, an immunological trigger factor, and mechanical stress on the affected nerve segment(s) is pathophysiologically determinative. The prognosis of untreated NA is poor, with 25% of patients remaining unable to work at three years. The main form of treatment is with corticosteroids that are administered as early as possible. If there is evidence of nerve constriction or torsion, surgery may also help. There have only been six controlled cohort studies on the treatment of NA, and no randomized trials. It is not uncommon for the acute phase to develop into a chronic pain syndrome requiring multidimensional treatment.

Conclusion: Particularly in view of the high incidence and improved therapeutic options, NA should be included in the differential diagnosis of all patients with suggestive symptoms.

Neuralgic amyotrophy (NA) is a monophasic, autoimmune-triggered neuritis that is typically associated with very severe arm and/or shoulder pain, followed after a time by weakness. NA was first reported at the end of the 19th century. Parsonage and Turner, who lent their names to the disorder primarily in the Anglo-American world, defined a separate disease entity for the first time in 1948, based on a larger patient population (1).

The inflammatory process does not usually involve the brachial plexus itself but rather proximal segments of the arm nerves arising from the plexus (2, 3, 4). For this reason, terms such as “brachial plexus neuritis”, “plexus neuritis”, and “brachial plexus neuropathy” do not really reflect the true nature of the disease. Given that nerves of the lumbosacral plexus are involved in four to 11 percent of patients, the term “neuralgic shoulder amyotrophy” should also be avoided in favor of the pathophysiologically more accurate term “neuralgic amyotrophy” as used in this article (5, 6).

Although NA was long considered a rare disease, a prospective study in 2012 found a high incidence of 100 cases per 100 000 persons per year (7). On the other hand, in a large population of patients insured with the AOK, a German statutory health-insurance carrier, the diagnosis of NA was coded with an incomparably lower incidence of 21 cases per 100 000 (8) (Table). This discrepancy suggests that NA still often goes undiagnosed and is also not adequately treated as a result.

Table

Compilation of controlled studies on the therapy of neuralgic amyotrophy

The aim of the present review article is to familiarize the reader with the clinical presentation, pathophysiological concept, treatment options, as well as the clinical course and prognosis of the disorder.

Methods

A selective literature search was conducted using the Google Scholar search service and the Cochrane Library and PubMed databases. This included the most relevant and most recent studies of the highest quality and with the highest possible level of evidence. The chosen search string was “neuralgic amyotrophy” OR “Parsonage Turner syndrome” OR “brachial plexopathy” OR “brachial plexus neuropathy”. The last inquiry was on March 24, 2024. The publications were screened by two independent investigators. Furthermore, the scientific institute of AOK conducted a data request on the incidence of the corresponding ICD-10 code G54.5 among their approximately 26 000 000 AOK insured persons over the last ten years.

Pathophysiology

The pathophysiology of NA is due to a combination of genetic predisposition, an immunological trigger factor, and mechanical stress on the affected nerve segment(s) (due to unusual physical activity, for example) (Figure 3). It is not a classic autoimmune disease since the inflammatory process is limited to a few days or weeks of attacks. The resulting nerve damage, however, can lead to chronic symptoms.

Figure 3

Pathophysiological concept of neuralgic amyotrophy

First-degree relatives with a history of NA are identified in about ten percent of patients (6). These cases are referred to as hereditary NA, usually with an autosomal dominant hereditary trait which appears to be associated in many cases with mutations in the SEPT9 gene (9). It has a high recurrence rate of 75 percent. However, even in the sporadic form, there is a significantly higher recurrence rate of 20 to 25 percent as compared with the general population, so there appears to be a genetic predisposition here too (6, 10).

In principle, many immunostimulatory factors are potential triggers of an NA attack. These factors include infection, vaccines, immunotherapy (such as interferons and immune checkpoint inhibitors (11)), surgical procedures, pregnancy and childbirth, trauma, and mental stress (6). It should be noted, however, that the benefits of preventive vaccination generally outweigh the risk of NA, even if an attack has already occurred. The list of pathogens that have been identified as triggers of NA is becoming increasingly longer. Hepatitis E virus is particularly noteworthy, being associated with 10 to 15 percent of all NA cases and often resulting in an extensive phenotype with bilateral manifestation and involvement of extraplexal nerves such as the phrenic nerve (12, 13).

It is still uncertain whether it is a T or B cell-mediated disease entity. The few available histopathological examinations now suggest the former following the detection of endoneurial T-cell infiltrates (14, 15). However, antiganglioside antibodies can be detected in the serum of 26 percent of those affected (6, 16). These antibodies are directed against membrane components of nerve cells and are also encountered in other inflammatory neuropathies (17). However, it remains uncertain whether these are actually pathogenetically relevant or merely epiphenomena of non-specific immune stimulation. According to current knowledge, an additional factor is required, namely the involvement of microtrauma of the affected nerves which leads to a temporary increase in the permeability of the blood-nerve barrier. Only then is it possible for cellular or humoral components of the immune system to reach the endoneurial space and initiate an autoimmune-inflammatory process (18). Given that the anatomy of the shoulder joint permits a very large range of motion, the proximal nerves of the upper extremities are at times subjected to high tensile loads in everyday life. This could explain the predominant occurrence of NA in this region of the body (10).

Constrictions or torsions of the clinically affected nerves or individual nerve fascicles are found in 50 to 90 percent of patients who do not achieve spontaneous recovery. These alterations appear to be a specific characteristic of NA and can predict a poor spontaneous outcome (19, 20, 21, 22). It is assumed that inflammatory swelling and connective tissue adhesions in combination with limb movements lead to kinking and local twisting of fascicles or even an entire nerve (23, 24).

Clinical presentation

Basically, neuralgic amyotrophy can develop at any age. The median age of onset is around 40 years for the sporadic form and around 25 years for the hereditary form. Published case collections show that men are more frequently affected with a ratio of 2:1. The ratio reported in the cohort of patients covered by the AOK health-insurance carrier described above, however, is largely balanced at 1:1.2 (8) (eTable 1). Since there are no conclusive laboratory or other additional examinations, crucial importance is attached to patient history and clinical examination.

eTable 1

Number of insured AOK members with a confirmed ICD-10 diagnosis G54.5 “Neuralgic amyotrophy” in the years 2013 to 2016* in comparison with a study from the year 2006

Initial symptoms of NA typically occur at night or in the early hours of the morning. In over 90 percent of those affected, onset is characterized by severe pain in the shoulder and neck area which can radiate diffusely to the back and arm. Painless attacks appear to be very rare (6, 25). Pain intensity is generally reported to be at least seven out of ten on the analogue scale and is characterized as boring or aching. This initial pain persists continuously for days to a few weeks and in around 75 percent of cases is followed by two further pain episodes (6). On the one hand, classic neuropathic pain syndrome can develop, manifesting as burning or shooting and electrifying pain. The majority of patients also report a third entity, however, in the form of musculoskeletal pain syndrome, usually involving the origins and insertions of the paretic or compensating muscles. With persistent paresis of the rotator cuff muscles or pain-related reduced joint excursion, there arises the additional risk of developing secondary pathology of the shoulder joint. This results in true frozen shoulder (glenohumeral adhesive capsulitis) in 17 percent of cases and glenohumeral subluxation or dislocation in 8.4 percent. Overall, 29 percent of those affected complain of chronic pain (6).

Paresis typically arises a while after the pain, within 24 hours in 34 percent of patients and not until two weeks later in 27 percent (6). A patchy distribution pattern of paralysis is also typical and does not correspond to the distribution area of a specific nerve root. The classic phenotype of NA particularly involves the nerves of the upper and middle brachial plexus. The suprascapular and long thoracic nerves are most commonly affected. For this reason, it is of paramount importance to assess abduction and external rotation of the shoulder joint, together with shoulder blade mobility, during the physical examination of the patient with the upper body exposed. For this purpose, the patient is asked to abduct both arms simultaneously above the head and then lower them parallel in front of the upper body. If the long thoracic nerve is involved, together with paresis of the serratus anterior muscle, winged scapula, which is often already visible in the resting position, becomes more pronounced, especially during the second phase of the maneuver (Figure 1). Atrophy of the affected muscles can develop over the course of weeks to months, from which the name of the disease is derived.

Figure 1

Right-sided winged scapula secondary to involvement of the long thoracic nerve

In 25 to 50 percent of patients, only one nerve is clinically involved in the form of a mononeuropathy (2, 25). More recent studies, for example, show that anterior interosseous nerve syndrome, which has been regarded for decades as a nerve compression syndrome and subsequently treated as such, is in fact a variant of NA in almost every case (26). Particular attention should be paid to involvement of the phrenic nerve which can occur unilaterally or bilaterally in eight percent of cases (27). For this reason, the patient’s medical history should be explicitly explored for new onset dyspnea and further diagnostics should be initiated if there are any indications of this. In particular, this would include lung function tests in an upright and lying position as well as diaphragm ultrasound. On the other hand, in cases presenting idiopathic diaphragmatic paresis, underlying NA should be included in the differential diagnostic considerations (28).

In summary, therefore, the typical clinical findings of NA consist of an acute presentation of very severe pain, particularly in one or both shoulders, associated with paresis which manifests with a time delay and cannot be assigned to the area supplied by a particular nerve root. Sensitive symptoms are not paramount, and passive limitation of motion is not evident. If NA is suspected, a prompt neurological consult should be immediately obtained.

Diagnostic investigations

Usually, NA is a purely clinical diagnosis based on the above mentioned criteria. However, over recent years, the introduction of various additional examinations has to some extent fundamentally changed this situation.

Laboratory methods are of limited help only. The serological identification of a (sub-)acute infection as a potential immunological trigger increases the likelihood of the presence of NA. Tests to detect the presence of IgM and IgG antibodies against hepatitis E in particular should be undertaken. Serological examinations for Borrelia and the varicella-zoster virus (VZV) can also be of help during the differential diagnostic workup. A more recent study has shown a significantly higher incidence of anti-ganglioside antibodies in patients with a severe clinical course, rendering their detection a potential prognostic marker (16).

Neurophysiological methods such as electroneurography and electromyography, however, are rarely of any help for diagnosing NA. Thus, for example, less than 20 percent of those affected presented abnormal sensory neurography results (29). With persistent paresis, however, an appropriate examination to better assess prognosis is useful.

A paradigm shift has brought with it the application of MR neurography and high-resolution neuro-ultrasound. Structural abnormalities of the affected nerves were detected within the first month of developing NA in 90 percent of the patients involved in recent studies (30, 31). Increased diameters of thickened nerve fascicles, with and without evidence of nerve constrictions or torsions, were discovered. An important discovery was that, given the strict somatotopic organization within the fascicles, proximal partial lesions not involving the entire nerve cross-section can clinically imitate a more distal lesion (26). The respective advantages and disadvantages of a particular examination modality should be borne in mind when selecting imaging techniques. While MR neurography is especially suitable for deeper nerves, peripheral nerve ultrasound impresses with its particularly good resolution in the near field and the possibility of dynamic examination of larger nerve sections. For the first time, a standardized approach to the diagnostic workup of NA using peripheral nerve ultrasound has been recently published (32). Diagnostic imaging modalities are therefore increasingly regarded as valuable instruments for confirming the diagnosis. They also allow visualization of nerve and fascicular torsions and can therefore contribute decisively towards justifying therapeutic surgical measures (Figure 2).

Figure 2

Demonstration of an hourglass-like constriction neuropathy

Treatment

For a long time, only individual retrospective case series were available which suggested positive effects of oral treatment with corticosteroids in the acute phase of NA (33). There are still only case reports and one single retrospective case series on the intravenous administration of human immunoglobulins (6, 34, 35). Back in 2009, a systematic Cochrane review of the available literature concluded that there is no evidence backed up by randomized studies to support any particular form of treatment (36).

In the meanwhile, several, some prospective, studies have produced further indications for the efficacy of corticosteroid administration in providing earlier pain relief, recovery of motor function, and shortening the length of incapacity to work (37, 38). In the study conducted by Covtun (38), mean pain intensity three weeks after onset of symptoms was 3.7 in the corticosteroid group versus 6.8 in the control group. The proportion of participants with subjectively free range of motion after six months also differed with 74 percent versus 18 percent. Prednisolone was given orally at a dose of 60 mg for five days or 100 mg for 14 days, followed by a tapering regime. A crucial aspect appears to be the early start of treatment within four weeks at the utmost, still during the acute stage of the pain syndrome. Dose-finding studies and a comparison of the current oral dose with a higher dosed intravenous administration are still lacking.

When paresis persists and if, at the same time, nerve or fascicle torsions are detected, several studies show that a surgical approach is associated with recovery of motor function in a large proportion of patients (15, 39). Thus, the very recent publication by Krishnan reported that 82 percent of the operated patients, but only 23 percent of those treated conservatively, experienced significant clinical improvement (40). Apart from simple (micro-)neurolysis, excision of the involved nerve segment was performed, followed by direct suture or the use of an autologous nerve interposition. The Table provides an overview of all controlled studies on NA published to date.

In summary, therefore, it is recommended to obtain a high-resolution ultrasound scan to assess the presence of nerve torsions in those patients who have not experienced any improvement of their paresis grade by three months after onset of symptoms (eTable 2).

eTable 2

Summary of diagnosis and treatment of neuralgic amyotrophy

Those affected often initially emphasize pain as the main cause of their complaints, so adequate pain management is always part of the treatment concept for NA. This approach will vary, however, depending on the stage of the disease: Apart from the administration of prednisolone, the short-term combination of non-opioid and opioid analgesics has proven itself for the treatment of this initial pain. If classic neuropathic pain syndrome develops during the course of the disease, then administration of co-analgesics (e.g., pregabalin) has often been found beneficial. Musculoskeletal pain secondary to paresis-related persistent scapular dyskinesia is most difficult to treat. Specific physiotherapeutic interventions with a focus on movement technique and less on strength or endurance training have the highest level of evidence here. Primary emphasis is on correcting maladaptive cerebral neuroplasticity (e1) (Figure 4).

Figure 4

Multimodal pain management of neuralgic amyotrophy

Future prospects

At the time this article was published, a number of questions were still unanswered with regard to the clinical condition of NA, including:

• Are we taking too narrow a view of the phenotype NA?
• Is the incidence of low-pain/painless courses actually higher than previously thought?
• Is NA a possible cause of other mononeuropathies, such as that involving the phrenic nerve, for example?
• What exactly is the pathophysiology of NA?
• Is the disease associated with B or T-cells?
• What role does the genotype play?
• Are there any better methods for early diagnostics?
• Which corticosteroid dose is the right one and which mode of application?
• Can recurrences be avoided?

It is therefore essential to include more affected patients in prospective studies than has been the case so far. However, in view of current and future projects—some of them from our own working group—we are confident that our understanding of the disease will broaden significantly in the coming years.

Conflict of interest statement

WW is President of the German Society for Pneumology and Respiratory Medicine (DGP) and member of the executive board of the German Airways League.

The other authors declare that there are no conflicts of interest.

Manuscript received on15 January 2024, revised version accepted on 16 April 2024

Translated from the original German by Dr. Grahame Larkin

Corresponding author

Dr. med. Johannes Fabian Holle

Department of Neurology, Hospitals of the City of Cologne

Health Faculty/Department for Human Medicine

University of Witten/Herdecke

Ostmerheimer Str. 200,
51109 Cologne

Cite this as:
Holle JF, Limmroth V, Windisch W, Zimmermann M: Neuralgic amyotrophy: a commonly overlooked cause of acute shoulder pain. Dtsch Arztebl Int 2024; 121: 483–9. DOI: 10.3238/arztebl.m2024.0077

References

1. Parsonage MJ, Aldren Turner JW: Neuralgic amyotrophy—the shoulder-girdle syndrome. Lancet 1948; 1: 973–8

2. Ferrante MA, Wilbourn AJ: Lesion distribution among 281 patients with sporadic neuralgic amyotrophy. Muscle Nerve 2017; 55: 858–61

3. Abraham A, Izenberg A, Dodig D, Bril V, Breiner A: Peripheral nerve ultrasound imaging shows enlargement of peripheral nerves outside the brachial plexus in neuralgic amyotrophy. J Clin Neurophysiol 2016; 33: e31–3

4. Ferrante MA: The distribution of neuralgic amyotrophy lesions is overwhelmingly extraplexal. Muscle Nerve 2018; 58: 325–6

5. Collins MP, Dyck PJB, Hadden RDM: Update on classification, epidemiology, clinical phenotype and imaging of the nonsystemic vasculitic neuropathies. Curr Opin Neurol 2019; 32: 684–95

6. van Alfen N, van Engelen BGM: The clinical spectrum of neuralgic amyotrophy in 246 cases. Brain 2006; 129: 438–50

7. van Alfen N, van Eijk JJ, Ennik T, et al.: Incidence of neuralgic amyotrophy (Parsonage Turner syndrome) in a primary care setting—a prospective cohort study. PLoS One 2015; 10: e0128361

8. Wissenschaftliches Institut der AOK: Anzahl an AOK-Versicherten mit einer (gesicherten) ICD-10 Diagnose G54.5 „Neuralgische Amyotrophie“. Wissenschaftliches Institut der AOK 2023.

9. Collie AMB, Landsverk ML, Ruzzo E, et al.: Non-recurrent SEPT9 duplications cause hereditary neuralgic amyotrophy. J Med Genet 2010; 47: 601–7

10. Van Alfen N: Clinical and pathophysiological concepts of neuralgic amyotrophy. Nat Rev Neurol 2011; 7: 315–22

11. Porambo ME, Sedarsky KE, Elliott EJ, Theeler BJ, Smith JK: Nivolumab induced neuralgic amyotrophy with hourglass like constriction of the anterior interosseous nerve. Muscle Nerve 2019; 59: E40–2

12. Arányi Z, Szpisjak L, Szőke K: Multiphasic presentation of neuralgic amyotrophy associated with hepatitis E virus infection. Muscle Nerve 2020; 61: 108–10

13. Van Eijk JJJ, Dalton HR, Ripellino P, et al.: Clinical phenotype and outcome of hepatitis E virus–associated neuralgic amyotrophy. Neurology 2017; 89: 909–17

14. Suarez GA, Giannini C, Bosch EP, et al.: Immune brachial plexus neuropathy: suggestive evidence for an inflammatory-immune pathogenesis. Neurology 1996; 46: 559–61

15. Pan Y, Wang S, Zheng D, et al.: Hourglass-like constrictions of peripheral nerve in the upper extremity: a clinical review and pathological study. Neurosurgery 2014; 75: 10–22

16. Glos D: Immunologische und klinische Aspekte der Pathophysiologie der Neuralgischen Amyotrophie: Prävalenz von Anti-Gangliosid-Antikörpern (Inaugural-Dissertation zur Erlangung des Medizinischen Doktorgrades). Freiburg im Breisgau: Albert-Ludwigs-Universität 2015.

17. Cutillo G, Saariaho AH, Meri S: Physiology of gangliosides and the role of antiganglioside antibodies in human diseases. Cell Mol Immunol 2020; 17: 313–22

18. van Eijk JJ, Groothuis JT, Van Alfen N: Neuralgic amyotrophy: an update on diagnosis, pathophysiology, and treatment. Muscle Nerve 2016; 53: 337–50

19. Arányi Z, Csillik A, DéVay K, et al.: Ultrasonography in neuralgic amyotrophy: sensitivity, spectrum of findings, and clinical correlations. Muscle Nerve 2017; 56: 1054–62

20. Arányi Z, Csillik A, Dévay K, et al.: Ultrasonographic identification of nerve pathology in neuralgic amyotrophy: enlargement, constriction, fascicular entwinement, and torsion. Muscle Nerve 2015; 52: 503–11

21. Sneag DB, Urban C, Li TY, et al.: Hourglass-like constrictions on MRI are common in electromyography confirmed cases of neuralgic amyotrophy (Parsonage–Turner syndrome): a tertiary referral center experience. Muscle Nerve 2023; DOI: 10.1002/mus.27961. Epub ahead of print

22. Sneag DB, Rancy SK, Wolfe SW, et al.: Brachial plexitis or neuritis? MRI features of lesion distribution in Parsonage-Turner syndrome. Muscle Nerve 2018; 58: 359–66

23. Nagano A: Spontaneous anterior interosseus nerve palsy. J Bone Joint Surg Br 2003; 85: 313–8

24. Ochi K, Horiuchi Y, Tazaki K, Takayama S, Matsumura T: Fascicular constrictions in patients with spontaneous palsy of the anterior interosseous nerve and the posterior interosseous nerve. J Plast Surg Hand Surg 2012; 46: 19–24

25. Cruz-Martínez A, Barrio M, Arpa J: Neuralgic amyotrophy: variable expression in 40 patients. J Peripher Nerv Syst 2002; 7: 198–204

26. Pham M, Baumer P, Meinck HM, et al.: Anterior interosseous nerve syndrome: fascicular motor lesions of median nerve trunk. Neurology 2014; 82: 598–606

27. Van Alfen N, Doorduin J, Van Rosmalen MHJ, et al.: Phrenic neuropathy and diaphragm dysfunction in neuralgic amyotrophy. Neurology 2018; 91: e843–9

28. Zimmermann M, Wollsching-Strobel M, Majorski DS, et al.: Die neuralgische Amyotrophie: eine häufige Ursache uni- oder bilateraler Zwerchfellparesen. Pneumologie 2023; 77: 814–24

29. Van Alfen N, Huisman WJ, Overeem S, van Engelen BGM, Zwarts MJ: Sensory nerve conduction studies in neuralgic amyotrophy. Am J Phys Med Rehabil 2009; 88: 941–6

30. Ripellino P, Arányi Z, van Alfen N, et. al.: Imaging of neuralgic amyotrophy in the acute phase. Muscle Nerve 2022; 66: 709–14

31. Wang T, Qi H, Wang Z, et al.: The role of ultrasonography in diagnosis of neuralgic amyotrophy. Skeletal Radiol 2023; 52: 1305–11

32. Cignetti NE, Cox RS, Baute V, et al.: A standardized ultrasound approach in neuralgic amyotrophy. Muscle Nerve 2023; 67: 3–11

33. Tsairis P, Dyck PJ, Mulder DW: Natural history of brachial plexus neuropathy. Report on 99 patients. Arch Neurol 1972; 27: 109–17.

34. Naito K, Fukushima K, Suzuki S, et al.: Intravenous immunoglobulin (IVIg) with methylprednisolone pulse therapy for motor impairment of neuralgic amyotrophy: clinical observations in 10 cases. Intern Med 2012; 51: 1493–500

35. Fukahori K, Saito N, Abe Y, Ikuse T, Tohyama J, Saitoh A: Neuralgic amyotrophy after COVID-19 vaccination in an adolescent: successful intravenous immunoglobulin treatment. Pediatr Neurol 2023; 140: 50–1

36. van Alfen N, van Engelen BG, Hughes RA: Treatment for idiopathic and hereditary neuralgic amyotrophy (brachial neuritis). Cochrane Database Syst Rev 2009; 3: CD006976

37. van Eijk JJ, van Alfen N, Berrevoets M, van der Wilt GJ, Pillen S, van Engelen BGM: Evaluation of prednisolone treatment in the acute phase of neuralgic amyotrophy: an observational study. J Neurol Neurosurg Psychiatry 2009; 80: 1120–4

38. Covtun S: Studie zur Beurteilung der Therapieergebnisse einer neuralgischen Schulteramyotrophie: Spielt eine frühzeitige Kortisontherapie für das bessere Outcome eine Rolle? (Dissertation zum Erwerb des Doktorgrades der Medizin). München: Medizinische Fakultät der Ludwig-Maximilians-Universität zu München 2018.

39. Wu P, Yang JY, Chen L, Yu C: Surgical and conservative treatments of complete spontaneous posterior interosseous nerve palsy with hourglass-like fascicular constrictions: a retrospective study of 41 cases. Neurosurgery 2014; 75: 250–7

40. Krishnan KR, Sneag DB, Feinberg JH, et al.: Outcomes of microneurolysis of hourglass constrictions in chronic neuralgic amyotrophy. J Hand Surg 2021; 46: 43–53

e1. Lustenhouwer R, Van Alfen N, Cameron IGM et al.: NA-CONTROL: a study protocol for a randomised controlled trial to compare specific outpatient rehabilitation that targets cerebral mechanisms through relearning motor control and uses self-management strategies to improve functional capability of the upper extremity, to usual care in patients with neuralgic amyotrophy. Trials 2019; 20: 48