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
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- 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