Brachial Plexus Neuritis Diagnosis: A Comprehensive Guide for Clinicians

Brachial neuritis, also known as neuralgic amyotrophy or Parsonage-Turner syndrome, presents a diagnostic challenge in the realm of neuromuscular syndromes affecting peripheral nerves. This condition, while considered inflammatory in nature, lacks a fully understood etiology, with potential contributions from immune-mediated, mechanical, and genetic factors. The hallmark of brachial neuritis is the sudden onset of severe pain in the shoulder girdle, typically unilateral but potentially bilateral, which is subsequently followed by muscle weakness. Sensory deficits may also accompany these primary symptoms in some individuals. The pain often radiates into the neck, arm, and forearm, and the symptomatic period can range from a few days up to approximately four weeks.

The diagnosis of brachial neuritis can be particularly complex due to its varied clinical presentations, the multifocal nature of symptoms, and the often-delayed appearance of pathological changes in diagnostic testing. Accurate diagnosis is paramount to prevent misdiagnosis, which can lead to unnecessary surgical interventions and increased patient complications. Therefore, a thorough understanding of the clinical progression of brachial neuritis and the ability to distinguish it from similar conditions are crucial for clinicians. This article aims to provide healthcare professionals with a detailed guide to enhance their competence in recognizing brachial neuritis, effectively navigating differential diagnoses, selecting and interpreting appropriate diagnostic evaluations, and ultimately improving patient outcomes through informed clinical decision-making.

Unraveling the Etiology of Brachial Plexus Neuritis

Despite extensive research, the precise etiology of brachial plexus neuritis remains elusive. Current consensus leans towards immune-mediated mechanisms as the primary underlying cause. This perspective is supported by the observation that a significant proportion of patients diagnosed with brachial neuritis have experienced events known to trigger immune responses prior to symptom onset. However, the specific factors that predispose individuals to this neuromuscular disorder are yet to be definitively identified. In addition to immune factors, both mechanical and genetic etiologies have been implicated in the development of brachial neuralgia.

Conditions that modulate or challenge the immune system have been observed to precede brachial neuritis in over half of diagnosed cases. Frequently reported immunological triggers in medical literature include a spectrum of infections (for example, hepatitis E virus, coxsackieviruses, COVID-19 virus, Escherichia coli, Staphylococcus aureus, and Aspergillus), surgical procedures, connective tissue disorders like systemic lupus erythematosus and temporal arteritis, vaccinations, pregnancy, and radiation therapy. Notably, hepatitis E virus stands out as one of the most consistently associated viral etiologies, identified in approximately 10% of patients diagnosed with brachial neuritis.

Mechanical stress impacting peripheral nerves is also considered a plausible etiological factor in brachial neuritis. A history of strenuous upper-body exercise has been noted in around 10% of patients with the condition. Other forms of mechanical injury, such as trauma to the shoulder girdle and physically demanding labor, are also considered potential triggers. Furthermore, the occurrence of recurrent brachial neuritis in some families points towards a potential genetic predisposition. Hereditary neuralgic amyotrophy (HNA), believed to be transmitted in an autosomal dominant pattern, suggests an underlying genetic component in a subset of patients. Genetic studies have identified point mutations and duplications on the SEPT9 gene in over half of HNA cases, although the precise mechanism by which these genetic alterations increase susceptibility to brachial neuritis remains to be fully elucidated.

Epidemiology and Prevalence of Brachial Plexus Neuritis

Brachial neuritis predominantly affects middle-aged individuals, with an average age of onset around 40 years. While it is more commonly diagnosed in males, individuals of any age and sex can be affected. In cases of hereditary neuralgic amyotrophy (HNA), the age of onset is typically younger, averaging around 20 years. The estimated incidence of brachial neuritis is approximately 1 in 1000 individuals, a figure that is higher than previous estimations, suggesting the condition might be underdiagnosed.

Studies examining pediatric populations have indicated a higher incidence of brachial neuritis in neonates and adolescents compared to other age groups. Recurrence of brachial neuritis is observed in about 25% of patients within 5 to 10 years of the initial episode. The recurrence rate is significantly elevated in individuals with HNA, reported to be as high as 75%, highlighting the chronic and potentially relapsing nature of the condition in genetically predisposed individuals.

Pathophysiology: Delving into the Mechanisms of Brachial Plexus Neuritis

While the exact pathophysiological mechanisms of brachial neuritis are not fully understood, a prevailing theory centers on an immune-mediated process. Research suggests that the immune system may directly target the brachial plexus nerves or initiate an indirect autoimmune response that leads to nerve damage. Even in cases where mechanical factors are implicated in the etiology, some experts propose that the immune system plays a secondary role. Mechanical injury could potentially disrupt the blood-nerve barrier, allowing inflammatory mediators to infiltrate and damage the nerves of the brachial plexus.

Ischemia, whether triggered by mechanical compression or inflammatory processes, is also considered a contributing factor to the sudden and intense pain characteristic of brachial neuritis. Reduced blood flow to the affected nerves can exacerbate nerve dysfunction and pain signaling, contributing to the clinical presentation of the condition.

Histopathological Findings in Brachial Plexus Neuritis

Histopathological data on brachial plexus neuritis is limited, but available reports from brachial plexus biopsies in sporadic cases reveal the presence of mononuclear inflammatory infiltrates. These infiltrates are indicative of an immune response within the nerve tissue. Furthermore, nerve biopsies conducted on post-surgical patients with brachial neuritis have demonstrated evidence of neovascularization (new blood vessel formation), perineural thickening, and focal fiber loss. These findings suggest ischemic changes, which, in turn, support the hypothesis of an immune-mediated pathogenesis.

Peripheral nerve biopsies from patients with brachial neuritis have also shown T-cell infiltrates within the endothelial vessels surrounding the nerves. The presence of T-cells, a type of immune cell, further reinforces the role of immune system involvement in the nerve damage associated with brachial neuritis.

Clinical Presentation: History and Physical Examination in Brachial Plexus Neuritis Diagnosis

The diagnosis of brachial neuritis is primarily clinical, relying heavily on the characteristic clinical features observed during patient history and physical examination. The clinical course of brachial neuritis is generally divided into acute and chronic phases, and the patient’s presenting symptoms can vary depending on the phase of the condition. Furthermore, the variable involvement of multiple nerves within the brachial plexus, affecting different locations and to varying degrees, contributes to the broad spectrum of clinical manifestations seen in brachial neuritis.

Clinical Symptoms of Brachial Plexus Neuritis

In approximately 70% of patients, the acute phase of brachial neuritis is marked by the sudden onset of severe shoulder pain, followed within days to weeks by the development of muscular weakness. The pain is typically unilateral, starting abruptly and described as continuous with burning, sharp, or throbbing qualities. Common locations of pain include the lateral aspect of the shoulder, the scapula, the superolateral thoracic wall, and the antecubital fossa. Pain frequently radiates to the neck and lateral forearm, reflecting the involvement of specific nerves such as the axillary, suprascapular, anterior interosseous, long thoracic, and musculocutaneous nerves. Notably, pain often intensifies at night, causing patients to awaken from sleep, and it is typically unrelieved by positional changes.

The acute pain phase is self-limiting and usually subsides within an average of 4 weeks. In rare instances, pain may resolve within 24 hours, while in about 10% of patients, pain can persist for longer than 8 weeks. Generally, a longer duration of pain is associated with a longer overall symptom resolution time. Muscle weakness in the shoulder and arm typically develops after the pain starts to diminish. While the forearm and hands can also be affected, involvement in these areas is less common. This temporal sequence of shoulder pain followed by muscular weakness is a key differentiating feature of brachial neuritis. In about 30% of patients, muscle weakness may manifest within 24 hours of pain onset, but in most cases, weakness is observed a few weeks after the pain begins. Sensory deficits may also be present in some patients, but they are rarely the sole presenting symptoms. If the phrenic nerve is involved, diaphragmatic dysfunction, orthopnea (shortness of breath when lying down), and severe fatigue may be noted. In the chronic phase of brachial neuritis, the clinical picture is characterized by persistent pain, sensory deficits, and musculoskeletal impairments. Some patients may also exhibit muscle atrophy, with a slow and gradual recovery of muscle function potentially occurring over 6 to 18 months.

Physical Examination Findings in Brachial Plexus Neuritis

A thorough neurological examination is essential during the physical assessment. This should include evaluation of scapular movement during abduction and anteflexion, as well as strength testing of the shoulder muscles. A distinctive feature that helps distinguish brachial plexus neuritis from other conditions is the involvement of muscles innervated by the same peripheral nerve, termed “pathy paresis”. Lower motor neuron signs, such as hypotonia (decreased muscle tone), areflexia (absent reflexes), atrophy, and fasciculations (muscle twitching), may become apparent later in the disease progression, particularly in cases affecting the upper brachial plexus (C5-C7 vertebral levels). During the weakness phase following acute pain, physical examination may reveal decreased shoulder abduction and external rotation, indicating involvement of the deltoid, supraspinatus, and infraspinatus muscles. When the long thoracic nerve is affected, medial scapular winging (protrusion of the scapula) can be observed. Sensory changes, including paresthesias (abnormal sensations like tingling or prickling) and hypoesthesia (decreased sensation) over the lateral arm, deltoids, and radial forearm, can occur in approximately 78% of patients. However, due to the intensity of the pain, patients may not readily notice sensory changes until a detailed sensory examination is performed.

Diagnostic Evaluation of Brachial Plexus Neuritis

Due to the potential for misdiagnosis of brachial neuritis, often confused with conditions like rotator cuff tendinitis, cervical cord compression, or nerve entrapment, it is crucial to recognize the characteristic clinical features and utilize appropriate diagnostic studies to confirm the diagnosis and rule out other possibilities. Accurate diagnosis is essential to avoid unnecessary treatments and ensure appropriate management. While brachial neuritis diagnosis is primarily clinical, diagnostic studies can provide supportive evidence and aid in excluding differential diagnoses.

Nerve Conduction Studies and Electromyography (NCS/EMG)

Nerve conduction studies (NCS) and electromyography (EMG) are valuable tools in confirming a clinical diagnosis of brachial neuritis and differentiating it from other neuromuscular disorders, especially in cases with atypical presentations. However, it is important to note that abnormalities on these studies may not be evident in the initial stages of the condition. On average, nerve conduction studies may take about a week to show abnormal findings, while EMG changes typically become apparent around 4 weeks after symptom onset. In 30% to 45% of patients with brachial neuritis, NCS findings may include reduced amplitudes of action potentials and an inability to precisely localize specific nerve branches. Because brachial neuritis is primarily an axonal disorder, nerve conduction velocities and distal latencies are typically normal, which helps to distinguish it from demyelinating neuropathies.

EMG studies are particularly useful in localizing the affected nerves and assessing the severity of nerve damage. In the acute phase of brachial neuritis, typically 3 to 4 weeks after symptom onset, EMG findings often reveal acute denervation with fibrillation potentials and positive sharp waves in the affected nerve roots and peripheral nerves. In later stages, approximately 3 to 4 months after symptom onset, EMG studies may demonstrate chronic denervation and polyphasic motor unit potentials, indicative of early reinnervation. Additional EMG findings can include prolonged motor latency and reduced movement amplitude, while sensory nerve testing may reveal decreased amplitude with normal conduction velocity.

Imaging Studies in Brachial Plexus Neuritis Diagnosis

Gadolinium-enhanced magnetic resonance imaging (MRI) of the shoulder and spine can be a valuable adjunct in the diagnostic evaluation of brachial neuritis. MRI can help visualize the brachial plexus and identify characteristic abnormalities. In affected nerves, MRI may show a hyperintense signal on T2-weighted images, suggesting inflammation or edema within the nerve. “Hourglass” constrictions, representing focal areas of nerve narrowing, may also be visualized on MRI. Non-contrast-enhanced MRI can be used to assess for structural abnormalities of the spine or shoulder that could mimic brachial neuritis, although the brachial plexus itself may appear normal on non-contrast imaging.

Recent studies have also highlighted the utility of ultrasound imaging in the diagnosis of brachial neuritis. Ultrasound can be a readily available and cost-effective imaging modality to assess the peripheral nerves. Key ultrasound findings in brachial neuritis include focal or diffuse nerve enlargement, incomplete or complete nerve constriction, hourglass-shaped nerves, and nerve entanglement. Ultrasound can provide dynamic assessment and may be particularly useful in visualizing superficial nerves of the brachial plexus.

Laboratory Studies

Serum laboratory studies, including complete blood count (CBC) and erythrocyte sedimentation rate (ESR), are typically normal in patients with brachial neuritis. These tests are primarily used to exclude other conditions in the differential diagnosis, such as systemic inflammatory disorders or infections. Similarly, cerebrospinal fluid (CSF) analysis is usually normal or may show a mild elevation of white blood cells in some patients. CSF analysis is mainly performed to rule out alternative etiologies, particularly if there is suspicion of central nervous system involvement. Further laboratory evaluation may include specific tests for infections that have been associated with brachial neuritis, such as Epstein-Barr virus, varicella-zoster virus, dengue virus, and hepatitis E virus, especially if the clinical history suggests a recent infection.

Management and Treatment Strategies for Brachial Plexus Neuritis

Brachial neuritis is generally a self-limiting condition with a tendency for spontaneous resolution. However, various therapies are employed to alleviate symptoms, promote recovery, and improve long-term outcomes. Management strategies are typically divided into acute and chronic phases, with treatment approaches tailored to the stage of the condition and the patient’s symptom profile. Common management modalities include supportive therapies, physical therapy, corticosteroids, and intravenous immunoglobulin (IVIg). It is important to note that the evidence base for many of these treatments is derived primarily from case studies, and robust clinical trials demonstrating definitive effectiveness are often lacking. Pharmacological therapies, such as opioids and corticosteroids, are often used during the acute phase to manage severe pain, but their impact on long-term outcomes and chronic symptoms is debated. Effective management often involves a multimodal approach combining pharmacological and non-pharmacological interventions. In selected cases with persistent symptoms, surgical procedures like neurolysis may be considered.

Acute Phase Management

Pain Management: The initial focus in the acute phase is effective pain management. Severe pain often requires analgesics, including opioids and nonsteroidal anti-inflammatory drugs (NSAIDs). Adjuvant neuropathic pain medications, such as tricyclic antidepressants or antiepileptic drugs, are generally less effective in the acute phase due to their slower onset of action. A relatively rapid-acting analgesic is preferred given the typically short duration of the acute pain phase. As pain symptoms begin to resolve, usually around 8 weeks, the need for pain medication may diminish. Corticosteroids and intravenous immunoglobulin (IVIg) have also been used in the acute phase and have shown potential to accelerate the resolution of acute pain. However, their effectiveness may be less pronounced if initiated more than 2 weeks after symptom onset.

Immobilization Therapy: In the acute phase, restricting movement of the affected extremity can help reduce severe pain and prevent symptom exacerbation. Immobilization is typically temporary and can be discontinued as the pain begins to subside.

Chronic Phase Management

Physical and Occupational Therapy: Once the acute pain is adequately controlled, physical and occupational therapy become crucial components of management. Range of motion, strengthening, and stretching exercises are essential to address muscle weakness and restore function. Physical therapy focuses on improving motor function and strength. Occupational therapy plays a vital role in teaching patients adaptive strategies to perform activities of daily living, household tasks, and recreational or athletic activities. Occupational therapists can also assist patients in returning to work by addressing specific job-related demands and tasks. Strengthening exercises are generally not recommended for completely denervated muscles. The role of electrical stimulation remains controversial, but it may be considered when denervation persists for more than 4 months. Follow-up EMG studies of the involved muscles can help assess the extent of reinnervation and guide rehabilitation strategies.

Surgical Therapy: Conservative therapies are typically recommended for at least 3 months, as spontaneous symptom resolution is common. Surgical interventions, such as neurolysis or nerve transfer, may be considered in patients with persistent symptoms despite conservative management. Neurolysis, the surgical release of a nerve from surrounding scar tissue or compression, has been reported to improve symptoms in approximately 90% of patients in some series. Some experts suggest using the degree of nerve constriction, as assessed by imaging, to guide surgical decisions. If nerve constriction is less than 75%, intrafascicular neurolysis (releasing constriction within the nerve fascicles) may be recommended. Nerve grafting, involving the transplantation of a segment of nerve, may be considered if constriction is 75% or greater. Another review recommends considering neurolysis if paralysis persists for more than 6 months, while nerve or tendon transfers may be considered if neurolysis is contraindicated or deemed less likely to be effective.

Differential Diagnosis of Brachial Plexus Neuritis

A comprehensive differential diagnosis is essential in evaluating patients presenting with symptoms suggestive of brachial plexus neuritis. Conditions that can mimic brachial neuritis include:

• Cervical radiculopathy (nerve root compression in the neck)
• Mononeuritis multiplex (damage to multiple individual peripheral nerves)
• Multifocal motor neuropathy (a motor nerve disorder)
• Tumors of the brachial plexus
• Transverse myelitis (inflammation of the spinal cord)
• Amyotrophic lateral sclerosis (ALS)
• Herpes zoster (shingles)
• Adhesive capsulitis (“frozen shoulder”)
• Acute calcific tendinitis
• Superior sulcus tumor (Pancoast tumor)
• Complex regional pain syndrome (CRPS)
• Myocardial infarction (heart attack)
• Pulmonary embolism (blood clot in the lung)
• Rotator cuff tear
• Entrapment neuropathy (nerve compression)

Careful clinical evaluation, along with appropriate diagnostic testing, is crucial to differentiate brachial plexus neuritis from these other conditions and ensure accurate diagnosis and management.

Prognosis and Long-Term Outcomes in Brachial Plexus Neuritis

The prognosis for patients with brachial plexus neuritis is variable and depends on the extent of nerve damage and the degree of reinnervation. Studies indicate that most patients experience some degree of recovery of nerve function within 2 to 3 years. However, a significant proportion, often exceeding 70%, may still experience some residual weakness or other symptoms even after several years. Many patients experience persistent symptoms that can impact their ability to return to work, particularly in the initial months after symptom onset. However, long-term studies suggest that while complete recovery is possible, a substantial percentage of patients may continue to experience functional limitations even after 3 years. Evidence suggests that timely and appropriate treatment may improve the prognosis of brachial plexus neuritis. Children tend to have a more favorable prognosis compared to adults, potentially due to greater nerve plasticity in younger individuals.

Diagnostic studies can provide insights into patient prognosis. EMG studies showing a significant reduction in the amplitude of motor action potentials (greater than 70%) are associated with a poorer prognosis, suggesting limited reinnervation capacity. Ultrasound findings, such as hourglass constrictions and fascicular entwinement, have also been linked to more severe nerve damage and a less favorable prognosis.

Potential Complications of Brachial Plexus Neuritis

While most patients with brachial plexus neuritis experience some degree of recovery, complications are not uncommon. Muscle atrophy and weakness associated with the condition can lead to joint instability in the shoulder, wrist, and hand, increasing the risk of subluxation (partial dislocation) or impingement syndromes. Adhesive capsulitis (“frozen shoulder”) can also develop as a secondary complication, resulting in persistent pain and restricted range of motion. Patients with persistent residual pain and weakness may experience limitations in performing everyday activities, including reaching, lifting, and repetitive arm or shoulder movements. Individuals with recurrent brachial neuritis are at an elevated risk of developing long-term complications.

Deterrence and Patient Education

Given the potentially prolonged course of brachial plexus neuritis, patient education is paramount. Clinicians should educate patients about the typical course of the condition, emphasizing that while symptoms may resolve over time, recovery can be lengthy, and residual symptoms are possible. Patients should be instructed on adaptive strategies to manage residual pain, fatigue, and weakness. The importance of physical therapy in the recovery process should be strongly emphasized. As with other peripheral neuropathies, lifestyle modifications such as avoiding smoking and excessive alcohol consumption, maintaining a healthy diet, and engaging in regular exercise can be beneficial. Brachial neuritis can also induce anxiety and emotional distress in patients. Counseling patients on relaxation techniques and stress management strategies can be helpful in mitigating the psychological impact of the condition.

Enhancing Healthcare Team Outcomes in Brachial Plexus Neuritis Management

Optimal management of brachial plexus neuritis often requires a collaborative interprofessional healthcare team approach. Given the diagnostic challenges and the multifaceted nature of the condition, effective teamwork is essential to ensure accurate diagnosis, comprehensive treatment, and optimal patient outcomes. The core team may include orthopedic surgeons, hand surgeons, neurologists, pain specialists, physical therapists, occupational therapists, and neurology-trained nurses. Rehabilitation therapies provided by physical and occupational therapists are critical for functional recovery. Pharmacists and pharmacy technicians play an important role in medication management, including reviewing prescriptions, monitoring for drug interactions, and ensuring patient medication adherence. Specially trained nurses are essential for patient education, symptom monitoring, and communication with the healthcare team. Recognizing the significant emotional distress and anxiety that brachial neuritis can cause, mental health clinicians are also valuable members of the interprofessional team, providing psychological support and counseling to patients and their families.

References

1. Kim TU, Chang MC. Neuralgic amyotrophy: an underrecognized entity. J Int Med Res. 2021 Apr;49(4):3000605211006542. [PMC free article: PMC8033465] [PubMed: 33823638]
2. Firmino GF, Schulze ML, Schlindwein MAM, Rampeloti B, Gonçalves MVM, Maçaneiro CH, Dos Santos RA. Neuralgic Amyotrophy: Its Importance in Orthopedics Practice. Spine Surg Relat Res. 2021;5(4):232-237. [PMC free article: PMC8356235] [PubMed: 34435146]
3. IJspeert J, Janssen RMJ, van Alfen N. Neuralgic amyotrophy. Curr Opin Neurol. 2021 Oct 01;34(5):605-612. [PubMed: 34054111]
4. Feinberg JH, Radecki J. Parsonage-turner syndrome. HSS J. 2010 Sep;6(2):199-205. [PMC free article: PMC2926354] [PubMed: 21886536]
5. Gonzalez-Alegre P, Recober A, Kelkar P. Idiopathic brachial neuritis. Iowa Orthop J. 2002;22:81-5. [PMC free article: PMC1888382] [PubMed: 12180618]
6. Duan L, Zhao L, Liu Y, Zhang Y, Zheng W, Yu X, Liu H, Li Z, Peng Z, Li X. Neuralgic amyotrophy: sensitivity and specificity of magnetic resonance neurography in diagnosis: A retrospective study. Medicine (Baltimore). 2023 Oct 27;102(43):e35527. [PMC free article: PMC10615388] [PubMed: 37904460]
7. Yamada H, Nakamori M, Kuga J, Hironaka A, Sugimoto T, Ueno H, Ohshita T, Morino H, Maruyama H. Nerve Ultrasonography for the Diagnosis and Evaluation of Neuralgic Amyotrophy. Intern Med. 2023 Jun 15;62(12):1843-1847. [PMC free article: PMC10332969] [PubMed: 36351573]
8. Bannasch JH, Berger B, Schwartkop CP, Berning M, Goetze O, Panning M, Fritz-Weltin M, Trendelenburg G, Gelderblom M, Lütgehetmann M, Stute F, Horvatits T, Dirks M, Antoni C, Behrendt P, Pischke S. HEV-Associated Neuralgic Amyotrophy: A Multicentric Case Series. Pathogens. 2021 May 30;10(6) [PMC free article: PMC8230081] [PubMed: 34070707]
9. Eubanks JD. Cervical radiculopathy: nonoperative management of neck pain and radicular symptoms. Am Fam Physician. 2010 Jan 01;81(1):33-40. [PubMed: 20052961]
10. Feinberg JH, Nguyen ET, Boachie-Adjei K, Gribbin C, Lee SK, Daluiski A, Wolfe SW. The electrodiagnostic natural history of parsonage-turner syndrome. Muscle Nerve. 2017 Oct;56(4):737-743. [PubMed: 28044362]
11. McCarty EC, Tsairis P, Warren RF. Brachial neuritis. Clin Orthop Relat Res. 1999 Nov;(368):37-43. [PubMed: 10613151]
12. Cignetti NE, Cox RS, Baute V, McGhee MB, van Alfen N, Strakowski JA, Boon AJ, Norbury JW, Cartwright MS. A standardized ultrasound approach in neuralgic amyotrophy. Muscle Nerve. 2023 Jan;67(1):3-11. [PMC free article: PMC10087170] [PubMed: 36040106]
13. Calvo-Lobo C, Unda-Solano F, López-López D, Sanz-Corbalán I, Romero-Morales C, Palomo-López P, Seco-Calvo J, Rodríguez-Sanz D. Is pharmacologic treatment better than neural mobilization for cervicobrachial pain? A randomized clinical trial. Int J Med Sci. 2018;15(5):456-465. [PMC free article: PMC5859768] [PubMed: 29559834]
14. Clarke CJ, Torrance E, McIntosh J, Funk L. 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 Dec;25(12):1997-2004. [PubMed: 27282731]