Author(s): Lisa Williams, MD
Originally published: February 3, 2012 Last updated: April 30, 2025
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Disease/Disorder

Definition

Immune mediated brachial plexopathy is a multifocal inflammatory neuropathy affecting the upper limbs. It was first described in 187940 and later reported in 1948 by Parsonage and Turner and has eponymously been called Parsonage Turner Syndrome (PTS).2 Current favored terminology includes Neuralgic amyotrophy (NA), Idiopathic (INA) or Hereditary (HNA). NA encompasses a broad phenotype characterized by acute attack(s) of neuropathic pain, often severe, followed by multifocal weakness, atrophy and sensory changes of the affected shoulder or arm.1,2,3,4 Symptom onset is often preceded by a traumatic event or immunologic insult such as a viral infection or immunization. Recovery is not always satisfactory for patients, and many patients may not achieve full recovery as previously thought.40

Etiology

To date, the etiology of NA is not clearly understood. Leading theories include an inflammatory autoimmune attack on selected peripheral nerves after a predisposing event and can be identified in up to 20-50% of caseswithin four weeks of symptoms onset4,44. The clinical features are similar in both INA and HNA. Genetic predisposition is seen in HNA with recurrent attacks, whereas the exact cause of INA is unknown. A mutation in the SEPTIN9 (SEPT9) is implicated in HNA and it follows an autosomal dominant inheritance pattern. HNA is not as common as INA or may be underdiagnosed due to lack of access to genetic testing. However, on history there is usually a strong family history of recurrent episodes of neuralgic amyotrophy in multiple generations at a younger age.

Epidemiology including risk factors and primary prevention

NA is not as rare as previously thought and likely underdiagnosed.8,9,10,40 Recent advances in neuromuscular ultrasound have suggested NA may be the most common cause of acute anterior and posterior interosseus neuropathy.40 A prospective cohort study estimated the one-year incidence rate to be 1 in 1000, more common than ulnar neuropathy at the elbow and as common as cervical radiculopathy.11,12,40 The average age of onset of INA is 40 and HNA is 20with a male predominance of 3:2.4,2,40 HNA may be predictive of recurrent attacks.4,12

Patho-anatomy/physiology

The exact pathophysiology is unknown and is thought to be multifactorial with an interplay between autoimmune, biomechanical, stress, infection and genetic factors.

Autoimmune pathogenic model: No distinct immunologic trigger has been identified. Although vaccine exposure and infections are posed as potential triggers.

Autoantibodies targeting the nervous system have been detected in patients with neurologic symptoms such as paresthesia, weakness, and twitching. Humoral autoimmunity has been suggested by reports of multifocal mononuclear inflammatory cell infiltrates in brachial plexus biopsies, including increased complement factor as well as CD20+ B-lymphocyte germinal centers around dorsal ganglia leading to axonal degeneration.10,11,12,40 Antibodies against gangliosides, glycosphingolipids found throughout membrane components of the nervous system, are thought to cause complement-dependent nerve damage.20,25 In another study, complement fixing antibodies to peripheral nerve myelin were found to be increased in the acute phase of the condition.4,7,13 High titers of anti-GA1 (asialo-GM1 ganglioside) antibodies have been associated with a variety of motor syndromes such as Guillain-Barré, multifocal motor neuropathy and motor neuron disease.13

Biomechanical or Stressful Factors: Biomechanical or stressful events such as sports/strenuous exercise, manual labor, surgery and peripartum have been implicated.2,3,4,44 Vaccine exposure and infectious insult have been reported including 10% of cases after hepatitis E infection (HEI)44 and case reports after COVID-19 vaccines and infections.8,41,42 15% of cases of NA are associated with a recent vaccine exposure.8 HEI, found in pork derived products, is associated with a more severe disease course and symptoms are often bilateral.

Other theories include repeated microtraumas to the brachial plexus, due to its exceptional mobility, resulting in increased permeability of the blood-nerve barrier, allowing autoimmune susceptibility to the endoneurial space.40

Genetic susceptibility: HNA has been well described and involves an autosomal dominant inheritance pattern associated with a mutation of septin 9 gene (SEPT9) on chromosome 17q23. Ten percent of patients with NA have a positive family history. The SEPT9 gene has been found to account for 55% of inherited cases, more genes are likely to be discovered in the future as biomolecular genetic testing advances.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

The clinical phenotype is broad and long-term prognosis is variable depending on severity. Recovery outcomes are not as positive as previously thought and long-term follow-up studies have showed less favorable outcomes.40,44 A large cohort study found only 10% full recovery after >3 years and that 25% of patients were unable to work due to NA.7

Early intraoperative reports identified nerve constriction and torsion. Inflammation leads to intraneural edema and swelling on the nerve resulting in reduced mobility of the nerve. Neuromuscular ultrasound and MRI have reinforced this theory and studies have shown that structural changes of affected nerve may portend poor recovery from pain and paresis in many cases.44,45,46 Neuropathic and musculoskeletal pain, fatigue and impaired activities of daily living are commonly reported. Reports of residual paresis and exercise intolerance are variable and as high as 70% in some studies.3,7,14,15

Neuralgic amyotrophy disease progression is classically categorized into three phases: Acute, Subacute, and Chronic/Stable. Hallmark findings of NA are characterized as an initial episode of pain, followed by weakness. In the later stages amyotrophy and sensory disturbances are seen.2,3,16

Acute Phase: Characterized by constant and intense sharp pain localized around the shoulder or scapular region related to the portion of the plexus affected.17 Upper brachial plexopathy with or without the involvement of the long thoracic nerve is the most common pattern.3,4 Pain duration on average lasts 1-2 weeks and is highly variable lasting from several hours to months. Lingering pain beyond the acute episode is not uncommon.4,18

Subacute Phase: Weakness may develop with motor deficits predominating in the days to weeks following acute attack. Paresthesia and hypoesthesia can also develop in the subacute stage.4,18

Chronic phase: In the later stages of recovery and chronic/stable phase pain and autonomic dysfunction including vegetative and trophic skin and nail changes, edema, and temperature dysregulation and contractures have been reported.2,4,18

Recurrence can occur in up to 25% in INA and occur more frequently in HNA. A positive family history is associated with a 75% increased risk of recurrent attack within 5-10 years after initial attack.7,44

Specific secondary or associated conditions and complications

Associated conditions include autonomic symptoms, associated with posterior cord and lower trunk, adhesive capsulitis and chronic neuropathic pain.12,14 Extra-brachial involvement of peripheral nerves including lumbosacral plexus, phrenic nerve and recurrent laryngeal nerve involvement have all been described.14,19 Pediatric NA may be underdiagnosed as it is difficult to recognize the symptoms in a child who is not able to communicate their symptoms. Presentation in children is more often painless. In neonates less than 6 months old, a specific phenotype including septic osteomyelitis of the humerus along with NA may exist. Pediatric cases may represent a more favorable prognosis.

Essentials of Assessment

History

The classic phenotype in 70% of cases include acute onset severe pain lasting for days to weeks followed by weakness and muscle atrophy. A preceding event such as trauma, surgery, immunization, sports or work injury is common.2,14 The pain is often patchy involving multiple dermatomal regions and does not necessarily coincide with a single neurologic lesion.4,17 Weakness and sensory disturbances follow suit. NA pain is typically not positional and can commonly be worse at night and affect sleep.14,16 The pain may last up to 4 weeks with pain dissipating in 5% of the cases in 24 hours. In 10% it can last greater than 2 months.1 Pain may be bilateral in 28.5% of patients.4,9

Although less common, autonomic symptoms have been described, including edema of the involved extremity, trophic changes of the skin and temperature dysregulation.

Physical examination

On inspection, abnormal symmetry of the shoulder girdle may be seen. Medial or lateral scapular winging may be present. If presenting in the chronic phase, atrophy of the involved muscles may be visualized.

Weakness results in dysfunction of coordinated shoulder girdle movement resulting in scapular dyskinesis.4 As NA is a patchy disorder, essentially any muscle can be involved. The most commonly affected nerves include the long thoracic, suprascapular, superficial radial and anterior interosseous nerves.3,14 A less common “distal variety” is also seen, involving the lower trunk of the brachial plexus.40

Sensory abnormalities are most commonly seen over the deltoid and lateral arm consistent with upper trunk involvement of the brachial plexus. Dysesthesias may also be present.14,16 Reflexes may be absent or normal and there should be no upper motor neuron findings such as hyperreflexia or increased tone.

HNA may have additional findings of mild dysmorphic features, including up slanting palpebral fissures, long nasal bridge, and hypotelorism.17

Functional assessment

Patients may have difficulty with proximal muscle movements that can interfere with daily activities. Such activities include the following: grooming, hygiene, self-feeding, and bathing. Referral to occupational or physical therapy for upper limb functional assessment may be beneficial.

Laboratory studies

The diagnosis of NA remains a clinical diagnosis. Electrodiagnostic evaluation may demonstrate brachial plexopathy and is also useful in ruling out other causes of symptoms such as cervical radiculopathy or a mononeuropathy of the median or ulnar nerves.

All laboratory studies are typically normal. Occasionally, elevation in liver function tests can be seen in associated viral infections. Some lab tests (complete blood count, serum glucose, hemoglobin A1c, erythrocyte sedimentation rate, and serology for Hepatitis panel, HIV, Lyme, and Syphilis) may be useful to evaluate for precipitating viral illnesses or other risk factors.36,37,38,39

Monocular inflammatory infiltrates have been noted on brachial plexus biopsy and complement-fixing antibodies to peripheral nerve myelin though biopsy is not typically pursued.10

Routine cerebrospinal fluid (CSF) analysis is typically non-specific and may show seroprevalence of anti-myelin and antiganglioside antibodies and disruption of the blood-brain barrier; 36% of patients with NA had anti-ganglioside IgM present in CSF compared to 2% of controls in one cohort.

Imaging

Imaging has been useful to exclude other diagnoses, such as cervical and rotator cuff disease and tumors.4,8,26,35

MRI findings are localized to the peripheral nerves themselves rather than to a portion of or the entire plexus, suggesting that NA is characterized by a single or by multiple mononeuropathies.33,34In the subacute or chronic phase, T1-weighted images may demonstrate atrophy and fatty infiltration. T2-weighted imaging may demonstrate hyperintensity.34

High resolution neuromuscular ultrasound (NMUS), >12MHz linear array transducer, is a non-invasive diagnostic tool and may be predictive of recovery. Hourglass constrictions and fascicular entwinement are characteristic. Studies have shown a favorable recovery at six months with ultrasound findings of nerve swelling with incomplete constriction47. Perineural swelling as seen in inflammatory neuropathies such as multifocal motor neuropathy can also be seen in immune mediated brachial plexopathy.4,22,34 In advanced NA, focal constrictions and torsion can be seen.21

Supplemental assessment tools

Electrodiagnostic (EDX) testing is a useful tool to localize the lesion(s) and rule out other causes.  When sensory abnormalities are involved, the lateral antebrachial cutaneous nerve is most commonly affected.8 Needle electromyography of the affected muscles demonstrates fibrillation potentials and positive sharp waves.4,17 The electromyographer must be careful to avoid sampling error and misdiagnoses if only using “routine muscle” screening.

Pulmonary function tests are useful in evaluating phrenic nerve involvement and may reveal restrictive lung disease pattern including low mean inspiratory and expiratory pressures (MIP/MEP) and low peak cough. The forced vital capacity may also be low, especially in the supine position, a difference of greater than 15-20% between seated to supine is considered significant. A chest x-ray may also reveal an elevated hemidiaphragm and a “sniff test” can demonstrate paradoxical movement of the diaphragm.

Early predictions of outcomes

HNA may lead to multiple attacks and a poor recovery. Additionally, greater axonal involvement is associated with a longer recovery period, 1-3 years.2,14 With partial nerve lesions, reinnervation can take up to 6 to 12 months.2,14

Social role and social support system

Some patients may require assistance with their activities of daily living and if they are severely affected, they may need caregivers to help with mobility and impairments in daily living. In addition, patients may have difficulties with maintaining their occupational functions and if unable to return to work may benefit from resources provided by the Americans with Disability Act (ADA) and the Department of Rehabilitation (DOR).

Professional issues

Given the hypothesis of an autoimmune etiology, patients have been treated with high dose steroids and/or intravenous immunoglobulin (IVIG), as mentioned below. These treatments have not been approved by the U.S. Food and Drug Administration, thus could be considered an “off label” use of these agents.

Rehabilitation Management and Treatments

Available or current treatment guidelines

A 2009 Cochrane review identified 1 open-label, retrospective series suggesting that oral methylprednisolone during the first month of an attack could shorten the duration of painful symptoms, however, evidence is inconclusive.23,24 In several case studies, Intravenous Immunoglobulin (IVIG may help alleviate symptoms, as shown in several case studies. However, to date there have been no randomized trials that support either of these pharmacologic therapies in NA.27,28,29,30

Peripheral nerve surgery is an emerging area of interest with advances in NMUS showing structural changes in NA.44 However, clear surgical guidelines are needed.

A multidisciplinary approach is optimal and includes physical and occupational therapy, pharmacologic treatment for pain management and bracing.2 Surgical referral may also be considered.4,14,31 The focus of rehabilitation includes addressing the altered biomechanics and functional deficits of the affected limb with physical and occupational therapy to prevent joint contractures, protect the limb from subluxation, and address activity of daily living issues. Transcutaneous electrical nerve stimulation and acupuncture, as in other conditions, may be helpful with pain control, but have not been shown to aid in recovery.

At different disease stages

Pain is usually self-limiting in the first two weeks from symptom onset. Prolonged pain can occur however it is less frequently observed.14,16 In cases of severe pain, a short course of opioids may be used. In the chronic phase, pain relief may be provided by acetaminophen, non-steroidal medications, gabapentin or pregabalin, tricyclic antidepressants. Topical analgesics or a course of transcutaneous electrical stimulation (TENS) may be used. Acupuncture has also been suggested but is less studied.

Physicians may need to consider addressing the risks of immobilization/decreased limb usage and using appropriate rehabilitation measures for these patients: skin breakdown prevention, venous thromboembolism treatment, and prevention of contractures.

Surgical treatment treatments including neurolysis, nerve grafts and nerve transfers may be considered in refractory cases. These are typically not performed until after 3 months of conservative treatment.44

Coordination of care

Optimal care of patients with NA requires the integrated management of a team that may include a physiatrist, electrodiagnostician, pediatrician, neurologist, physical and occupational therapist, and pain specialist. Referral to surgery may be indicated in certain cases.

Patient & family education

Patients and families need to be educated on the etiology, signs and symptoms, treatment, and prognosis of the disorder. Prevention of complications needs to be addressed with the patients and their caregivers. In particular, patients with HNA are at increased risk for recurrence and should be counseled on avoidance of precipitating causes. If initial presentation follows vaccination, a discussion on the risks and benefits of vaccination is crucial.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

NA should be included in the differential diagnosis of acute upper limb pain in the brachial plexus distribution followed by weakness. High suspicion for NA should also arise if in addition to these symptoms there are precipitating factors such as trauma, surgery, infection, and immunizations.

Routine laboratory studies are likely to be normal and EMG/NCS may miss the diagnosis if a thorough study of the brachial plexus is not performed.

Rate of recovery is highly variable depending on severity and outcomes are not as favorable as previously thought. More recent data suggests ~25% unable to return to work after three years.3,5,17

Cutting Edge/Emerging and Unique Concepts and Practice

High-resolution ultrasound is a growing area of interest and current research suggests it may be a useful tool in diagnosis and prognostication. Emerging surgical interventions targeting neuronal torsion and adhesions is also a promising area of research.

COVID-19 infections and vaccinations have been identified as a potential risk factor for NA.

Gaps in the Evidence-Based Knowledge

The treatment of neuralgic amyotrophy with the administration of oral steroids and high dose IVIG has not been recognized by the U.S. FDA.2,14,16 There have been no randomized trials to date to support either of these treatments.

References

  1. Ikeda S. Pathogenesis and treatment of brachial plexus neuritis. Shinkeigaku Rinsho. 2013;53(11):969-73.
  2. Seror P. Neuralgic Amyotrophy. An Update. Joint Bone Spine. 2016. Accepted March 10th, 2016.
  3. Fukushima K, Ikeda S. Neuralgic Amyotrophy. Brain Nerve. 2014;66(12): 1421-8
  4. Jeroen J, Van Eijk J, Groothuis J. Neuralgic amyotrophy: An update on diagnosis, pathophysiology, and treatment. Muscle & nerve. 2016;53(3)337 -350
  5. Foncea N, Yurrebaso I, Gómez Beldarrain M et al. Postoperative bilateral brachial plexopathy mimicking the “man-in-the-barrel” syndrome. Neurologia. 2002 Aug-Sep;17(7):388-90.
  6. Tomas J. Post-operative brachial plexus neuropraxia: A less recognized complication of combined plastic and laparoscopic surgeries. Indian J Plast Surg. 2014 Sep-Dec; 47(3): 460–464.
  7. van Alfen N. Clinical and pathophysiological concepts of neuralgic amyotrophy. Nat Rev Neurol. 2011;7:315-322.
  8. Smith C, Bevelaqua A. Challenging Pain Syndromes Parsonage-Turner Syndrome. Phys Med Rehabil Clin N Am. 2014; (25)265–277 .
  9. Silva M, Wicki B, Tsouni P, et al. Hepatitis E virus infection as a direct cause of neuralgic amyotrophy. Muscle Nerve. 2016 Mar 3. doi:10.1002/mus.25096
  10. Suarez GA, Giannini C, Bosch EP, et al. Immune brachial plexus neuropathy: suggestive evidence for an inflammatory-immune pathogenesis. 1996;46:559-561.
  11. Vriesendorp FJ, Dmytrenko GS, Dietrich T, Koski CL. Anti-peripheral nerve myelin antibodies and terminal activation products of complement in serum of patients with acute brachial plexus neuropathy. Arch Neurol. 1993;50:1301-1303.
  12. van Alfen N, van Eijk J, Ennik T, et al. Incidence of neuralgic amyotrophy (Parsonage Turner syndrome) in a primary care setting–a prospective cohort study. PLoS One. 2015 May 27;10(5)
  13. Lopez PH, Comin R, Villa AM, Di Egidio M et al. A new type of anti-ganglioside antibodies present in neurological patients. Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease. 2006. Mar 1762(3), 357–361.
  14. van Alfen N, van Engelen BGN. The clinical spectrum of neuralgic amyotrophy in 246 cases. Brain (2006) (129) 438-450.
  15. I Kolev. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004. http://www.orpha.net/data/patho/GB/uk-Turner.pdf.
  16. Clarke CJ, Torrance E, McIntosh J et al. Neuralgic amyotrophy is not the most common neurologic disorder of the shoulder: a 78-month prospective study of 60 neurologic shoulder patients in a specialist shoulder clinic. J Shoulder Elbow Surg. 2016 Jun 6.
  17. Dumitru D, Amato AA, Zwarts MJ, eds. Electrodiagnostic Medicine. 2nd ed. Philadelphia, PA: Hanely & Belfus; 2002.
  18. Stutz CM. Neuralgic amyotrophy: Parsonage-Turner Syndrome. J Hand Surg Am. 2010;35:2104-2106.
  19. Geibler k, Klingner C. Neuralgic amyotrophy associated with temporary vocal fold paralysis: successful treatment by vocal fold augmentation with hyaluronic acid. Journal of laryngology and otology. 2015; 129 (4)1-3.
  20. Stich O, Glos D, Brendle M, Dersch R et al. Cerebrospinal fluid profile and seroprevalence of antiganglioside reactivity in patients with neuralgic amyotrophy. Journal of the Peripheral Nervous System. 2016;21:27-32.
  21. Scalf RE, Wenger DE, Frick MA, Mandrekar JN, Adkins MC. MRI fndings of 26 patients with Parsonage-Turner Syndrome. AJR Am J Roentgenol. 2007;189:W39-44.
  22. Aranyi Z, Csillik A, Devay K, et al. Ultrasonographic identification of nerve pathology in neuralgic amyotrophy: enlargement, constriction, Fascicular entwinement, and torsion. Muscle and Nerve. 2015;52: 503-511.
  23. van Alfen N, van Engelen BG, Hughes RA. Treatment for idiopathic and hereditary neuralgic amyotrophy (brachial neuritis). Cochrane Database Syst Rev. 2009 Jul 8;(3):CD006976.
  24. van Eijk JJJ, 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 Psychiatr. 2009;80(10):1120-1124. doi:10.1136/jnnp.2008.163386
  25. Stich O, Glos D, Brendle M, Dersch R, Rauer S. Cerebrospinal fluid profile and seroprevalence of antiganglioside reactivity in patients with neuralgic amyotrophy. J Peripher Nerv Syst. 2016;21(1):27-32. doi:10.1111/jns.12157
  26. Expert Panel on Neurologic Imaging:, Bykowski J, Aulino JM, et al. ACR appropriateness criteria® plexopathy. J Am Coll Radiol. 2017;14(5S):S225-S233. doi:10.1016/j.jacr.2017.02.002
  27. 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(1-2):107-109. doi:10.1016/j.jneuroim.2011.08.005
  28. 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(2):304-305. doi:10.1002/mus.22100
  29. 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(12):1493-1500. doi:10.2169/internalmedicine.51.7049
  30. Chuk R, Sheppard M, Wallace G, Coman D. Pediatric hereditary neuralgic amyotrophy: successful treatment with intravenous immunoglobulin and insights into SEPT9 pathogenesis. Child Neurology Open. 2016;3:2329048X16668970. doi:10.1177/2329048X16668970
  31. Shanina E, Liao B, Smith RG. Brachial plexopathies: update on treatment. Curr Treat Options Neurol. 2019;21(5):24. doi:10.1007/s11940-019-0562-5
  32. Smith DPW, Elliott JA, Helzberg JH. Intravenous corticosteroid therapy for bilateral parsonage-turner syndrome: a case report and review of the literature. Reg Anesth Pain Med. 2014;39(3):243-247. doi:10.1097/AAP.0000000000000070
  33. 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(3):359-366. doi:10.1002/mus.26108
  34. Lieba-Samal D, Jengojan S, Kasprian G, Wöber C, Bodner G. Neuroimaging of classic neuralgic amyotrophy. Muscle Nerve. 2016;54(6):1079-1085. doi:10.1002/mus.25147
  35. Duman I, Guvenc I, Kalyon TA. Neuralgic amyotrophy, diagnosed with magnetic resonance neurography in acute stage: a case report and review of the literature. Neurologist. 2007;13(4):219-221. doi:10.1097/NRL.0b013e31805778bb
  36. Etgen T, Bischoff C, Resch M, Winbeck K, Conrad B, Sander D. Obstacles in the diagnosis and treatment of syphilitic amyotrophy. Neurology. 2003;60(3):509-511. doi:10.1212/01.wnl.0000046584.72672.d3
  37. Finney KA, David L. Brachial plexus neuritis in the context of acute HIV seroconversion illness: a case report. Int J STD AIDS. 2012;23(2):143-144. doi:10.1258/ijsa.2011.011176
  38. Schmitt M, Daubail B, Bohm A. Parsonage-Turner syndrome secondary to Lyme disease. Joint Bone Spine. 2018;85(3):387-388. doi:10.1016/j.jbspin.2017.05.018
  39. Wendling D, Sevrin P, Bouchaud-Chabot A, et al. Parsonage-Turner syndrome revealing Lyme borreliosis. Joint Bone Spine. 2009;76(2):202-204. doi:10.1016/j.jbspin.2008.07.013
  40. IJspeert J, Janssen RMJ, van Alfen N. Neuralgic amyotrophy. Curr Opin Neurol. 2021 Oct 1;34(5):605-612. doi: 10.1097/WCO.0000000000000968. PMID: 34054111.
  41. Ameer MZ, Haiy AU, Bajwa MH, Abeer H, Mustafa B, Ameer F, Amjad Z, Rehman AU. Association of Parsonage-Turner syndrome with COVID-19 infection and vaccination: a systematic review. J Int Med Res. 2023 Jul;51(7):3000605231187939. doi: 10.1177/030006053
  42. 31187939. PMID: 37523491; PMCID: PMC10392513.
  43. Sookaromdee P, Wiwanitkit V. Parsonage-Turner syndrome and SARS-CoV-2 vaccination. Turk J Phys Med Rehabil. 2023 Feb 7;69(1):125. doi: 10.5606/tftrd.2023.12196. PMID: 37200997; PMCID: PMC10186010.
  44. Hagemann C, Antoniadis G, Pham M, Bischoff C, Ghosh T, Grieser T, Naumann M, Holzapfel K. Diagnostik und Therapie sanduhrförmiger Nervenstrikturen und -torsionen bei neuralgischer Amyotrophie [Diagnostics and treatment of hourglass-like nerve constrictions and torsions in neuralgic amyotrophy]. Nervenarzt. 2023 Dec;94(12):1157-1165. German. doi: 10.1007/s00115-023-01562-9. Epub 2023 Nov 9. PMID: 37943327.
  45. Salminger S, Sturma A, Aman M, Harhaus L, Platzgummer H, Aszmann OC. Neuralgic amyotrophy: a paradigm shift in diagnosis and treatment. J Neurol Neurosurg Psychiatry. 2020 Aug;91(8):879-888. doi: 10.1136/jnnp-2020-323164. Epub 2020 Jun 2. PMID: 32487526.
  46. 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.
  47. wang Y, Liu T, Song L, et al. Spontaneous peripheral nerve palsy with hourglass- like fascicular constriction in the upper extremity. J Neurosurg. Published online 2019:1–11.
  48. Similar to motor findings, anatomical distribution of sensory symptoms is also variable. Sensory disturbances are most commonly found over the deltoid and lateral upper arm (48.9%) which correlates with the predominant involvement of the upper trunk.14,15,16

Original Version of the Topic

Karina Bouffard, MD, John Harrell, MD. Immune Mediated Brachial Plexopathy. 2/03/2012

Previous Revision(s) of the Topic

Lisa Williams, MD. Immune Mediated Brachial Plexopathy. 9/19/2016

Lisa Williams, MD, Brandon Hassid, MD. Immune Mediated Brachial Plexopathy. 6/14/2021

Author Disclosures

Lisa Williams, MD
Nothing to Disclose