Author(s): Lisa Williams, MD, Brandon Hassid, MD
Originally published: February 3, 2012 Last updated: June 14, 2021
Jump to:

Disease/ Disorder

Definition

Immune mediated brachial plexopathy is characterized by acute severe attacks of neuropathic pain followed by multifocal weakness, atrophy and sensory changes of the affected shoulder or arm.1 It is also often referred to as Idiopathic Neuralgic Amyotrophy (INA). Symptom onset is often preceded by a traumatic event or immunologic insult such as a viral infection or immunization. INA was first reported in 1948 by Parsonage and Turner and has eponymously been called Parsonage Turner Syndrome (PTS).2 It is also known as neuralgic amyotrophy (NA) which is considered the most descriptive and preferred term to describe the pathology.2

Etiology

To date, the etiology of INA is not clearly understood. The cause is likely multifactorial. NA may be precipitated by a biomechanical traumatic event or by an iatrogenic or infectious insult, which may be followed by an inflammatory autoimmune pathophysiologic process.2,3,4 Certain forms of NA such as hereditary neuralagic amyotrophic (HNA) may be caused by genetic susceptibility.

NA has been associated with activities of repetition such as sports and manual labor. Traumatic insults from minor trauma, childbirth, gunshot wounds, burns, and surgeries have also been described, and up to 20% of patients with NA may have had one of these insults within the 4 weeks prior to symptom onset.4 Some incidences have been associated with improper positioning during surgery resulting in excessive neuronal traction.2,5,6,7

Some reports of up to approximately 15% of cases occur after immunization.8

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. Attacks occur more frequently in HNA and often involve peripheral nerves.7

Epidemiology including risk factors and primary prevention

NA considered to be rare with an estimated incidence of approximately 2-4 per 100,000 persons a year.4 However, more recent data suggests NA is not as rare as previously thought and is often a missed diagnosis.8,9,10 A prospective cohort study estimated the incidence rate to be 1 in 1000.11,12

The recurrence rate of NA is approximately 26.1% and as high as 75% in HNA. Recurrent attacks are a common feature of NA and may involve the same nerve(s) or may recur in an entirely different neuropathic pattern. Currently, there are no clinical diagnostic tools to predict or prevent recurrent attacks.4,12

There is a 3:2 predominance of men over women with the highest incidence occurring between the third and seventh decade of life.4 The median age is 40 years in INA and 25 years in HNA.4

Patho-anatomy/physiology

The exact pathophysiology is unknown and is thought to be multifactorial. An autoimmune pathogenic model has been described, although no distinct immunologic trigger has been identified. Nearly half of patients with NA will have preceding events associated with an immune response such as a viral or bacterial infection, childbirth, emotional or physical stress or immunization. It is theorized an immune-mediated response may be triggered by an event.7,8 Approximately 10 percent of cases have associated hepatitis E infection found at symptom onset.7,9,10

Autoantibodies targeting the nervous system have been detected in patients with neurologic symptoms such as paresthesias, weakness, and twitching. Humoral autoimmunity has been suggested by reports of multifocal mononuclear inflammatory cell infiltrates in brachial plexus biopsies, increased compliment factor as well as CD20+ B-lymphocyte germinal centers around dorsal ganglions.10,11,12 More recently, findings of the seroprevalence of antiganglioside antibodies have been found. Gangliosides are glycosphingolipids found throughout membrane components of the nervous system. Antiganglioside antibodies are thought to cause complement-dependent nerve damage. 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

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

Long term prognosis is variable depending on severity and hence the rate of recovery also varies. Reports of good recovery after 2-3 years was previously reported to be 80-90%, however, some studies have showed fewer positive outcomes. A large cohort study found only 10% full recovery after >3 years and 25% of patients were unable to work due to NA.7

A large proportion of patients have persistence of both neuropathic and musculoskeletal pain, fatigue and impaired activities of daily living. 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, 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

The acute phase is 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 plexus 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

The subacute phase can occur days to weeks after onset, weakness may develop with motor deficits predominating. Paresthesia and hypoesthesia can also develop in the subacute stage.4,18

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

Specific secondary or associated conditions and complications

Any peripheral nerve may be affected, although the upper trunk of the brachial plexus and the long thoracic, suprascapular, and anterior interosseous nerves are most commonly affected.3,14, In cases of HNA and INA extra-brachial involvement of peripheral nerves can be seen. Lumbosacral plexus, phrenic nerve and recurrent laryngeal nerve involvement have all been described.14,19

A recent retrospective imaging review suggests that the 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.33Autonomic symptoms have been described and occurs more commonly in brachial plexus lesions to the posterior cord and lower trunk.12

More than 75% of patients can develop a chronic neuropathic pain due to the hypersensitivity of the damaged nerves.12

A review of 246 cases indicated that 17% of patients developed adhesive capsulitis (frozen shoulder) of the affected extremity.14

Essentials of Assessment

History

The presentation of NA is highly variable. The hallmark presentation is acute onset severe pain lasting for days to weeks followed by weakness and muscle atrophy. These symptoms are often preceded by an antecedent event such as trauma, surgery, immunization, sports or work injury prior to the onset of symptoms.2,14

Pain is the presenting symptom in 90-95% of patients. A key feature of NA is a patchy distribution of pain not necessarily coinciding with a single neurologic source and often involves multiple muscles and dermatomal regions.4,17 Pain involvement can vary and can be quite severe. NA Pain is typically not positional and can commonly be worse at night and affect sleep.14,16

NA pain is often located in the upper extremities, neck, trunk or shoulder girdle. This 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

Nerve distribution is often patchy and may involve any nerve in the brachial plexus as well as nerves outside of the brachial plexus.14 Commonly involved sites include the upper and middle trunk distribution14,16 and long thoracic and/or suprascapular nerve occurred most frequently (71.1%).14 The most commonly affected nerve root patterns are C5 and C6; C4 and C7 are involved less frequently.14

Involvement of nerves outside the brachial plexus occurs more commonly in HNA. Nerves involved include the lumbosacral plexus (32.6%), phrenic nerve (14%), recurrent laryngeal nerve (18.6%) or other (7%).14 While extra-brachial nerve involvement is seen less in INA with recent findings of 8.2%, lumbosacral plexus; 6.6%, phrenic nerve; 2%, recurrent laryngeal nerve; 2.6%, other).14

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

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. van Alfen et al in 2006 found the infraspinatus (72%) and serratus anterior muscle (70%) to be more effected with the sternocleidomastoid (7.2%) or neck extensors (1.5%) infrequently involved.14,16

Sensory abnormalities, most commonly seen over the deltoid and lateral indicating 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 HIV, Lyme, and Syphilis) may be useful to evaluate for potentially reversible causes or precipitating viral or other illnesses .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 Cerebral spinal fluid (CSF) analysis may show seroprevalence of antimyelin 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 study, though it is unclear whether this plays a role in pathogenesis.25 Without further evidence at this time, CSF analysis may not have a relevant role in NA apart from ruling out other conditions, as its findings are typically non-specific.19,20

Imaging

Imaging has been useful to exclude other diagnoses, such as cervical and rotator cuff disease, that may be in the differential diagnosis. MRI or computed tomography can be used to rule out a Pancoast tumor. Although Pancoast tumors usually involve the lower trunk of the brachial plexus and are not commonly seen in NA, it is important to rule out as they may cause compression of vital structures such as the brachiocephalic vein, subclavian artery and phrenic nerve. A hemidiaphragm can be detected in 10% of patients with NA on MRI suggesting phrenic nerve involvement.21

MRI may detect abnormalities including dennervated muscles on MRI. T2-weighted imaging may demonstrate hyperintensity in clinically affected nerves.34 In the subacute or chronic phase, T1-weighted images may demonstrate atrophy and fatty infiltration. Magnetic resonance neurography (MRN) has been used and may demonstrate hyperintense thickening of the involved areas of the brachial plexus.4,8,35 The American College of Radiologists recent guidelines recommend the use of MRI as the primary imaging modality for visualizing the brachial plexus as it can help differentiate intrinsic from extrinsic causes of damage to a nerve.26More recently, high resolution ultrasound has been explored as a diagnostic tool in NA, however, to date there are no systematic studies of ultrasound findings in NA. Several case studies and case series have shown focal nerve swellings that mostly seem to affect the perineural compartment surrounding the fascicles as typically seen in other inflammatory neuropathies such as multifocal motor neuropathy.4,22,34 In advanced NA, focal constrictions and torsion can be seen.21

Supplemental assessment tools

Electrodiagnostic (EDX) testing is the most useful tool in assessing NA. Localization of the lesion in NA is possible with EDX and the most common pattern of NA appears to be either a single or multiple mononeuropathy affecting the suprascapular, long thoracic, phrenic, or axillary nerves on EDX.17 In particular, EDX findings can be seen in the distribution of the plexus, the upper and middle plexus, and/or in combination of peripheral nerves. 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 electrophysiologic evidence suggest that the neural insults are multifocal as well as bilateral.17 Sensory nerve and compound muscle action potentials studies are important for localization, determining the degree of axonal loss, and prognosis; side-to-side comparison is often useful in more mild cases.17

Early predictions of outcomes

Multiple attacks of NA, seen more frequently in HNA, may lead to a poor recovery. Additionally, the prognosis for recovery is affected by the severity of axonal involvement; greater axonal involvement is associated with a longer recovery period.2 With partial nerve lesions, reinnervation can take up to 6 to 12 months. Whereas with more severe lesions the recovery process can be delayed 1 to 3 years or longer and recovery may not be as good.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).

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.23 Steroids are currently recommended by multiple authors during the acute phase as below.23,24

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. Splinting may be useful. Edema control may be necessary. 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

Most patients are treated with a multidisciplinary approach including physical and occupational therapy, pharmacologic treatment and bracing.2 Surgical referral may also be considered.4,14

Treatment is an ongoing area of research and strategies vary depending on the phase. Oral corticosteroids in the acute phase have been shown in some studies to shorten the duration of painful symptoms,4,14,23 and although there have been no randomized trials, oral steroids have been recommended by several study authors when the condition is recognized within the early stage and still have pain.23,24 Patients receiving Intravenous Immunoglobulin (IVIG) have had improvement of symptoms, sometimes rapid, 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 Pain is usually self-limiting in the first two weeks from symptom onset. Prolongation of pain symptoms occurring less frequently.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. In addition to management of the acute neuropathic pain, care must also be given to assess and target muscular pain that may develop due to compensation for the abnormally functioning muscles.

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 options in cases refractory to pharmacologic and nonpharmacologic treatments include neurolysis, nerve grafts and nerve transfers. These are typically not performed until 6 months after symptom onset. Tendon and muscle transfers may facilitate function in cases of severe weakness.4,31

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 in muscles innervated by the brachial plexus. High suspicion for NA should also arise if in addition to these symptoms there are precipitating factors such as trauma, surgery, infection, and immunizations. Van Alfen et al provide a table to help providers recognize NA, suggesting that the presence of new onset shoulder pain, abnormal shoulder movement, and paresis of the long thoracic nerve, suprascapular nerve, and/or the anterior interosseous nerve within 3 weeks of onset should raise suspicion for NA.12

Routine laboratory studies are likely to be normal.

Electrodiagnosis may demonstrate single or multiple mononeuropathy or brachial plexopathy with motor and sensory abnormalities and may involve a very proximal nerve, including the long thoracic or phrenic nerves and nerve roots.

Rate of recovery is highly variable depending on severity. More recent data suggests ~25% unable to return to work after three years.3,5,17

Cutting Edge/ Emerging and Unique Concepts and Practice

Recent data has suggested that high-resolution ultrasound and MRN may be helpful in identifying abnormalities in patients with suspected AN. However, there are no guidelines for diagnostic criteria, and further research and recommendations may help these modalities play an additional role in diagnosis in the future.

Further research on the use of steroids and IVIG would be helpful to determine if use of these agents in the acute phase improves outcomes.

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. 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.
  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. Ophanet 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

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

Author Disclosures

Lisa Williams, MD
Nothing to Disclose

Brandon Hassid, MD
Nothing to Disclose