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Brachial Plexopathy


Basics


Description


  • Dysfunction of any region of the brachial plexus due to injury, lesion, or idiopathic etiologies
  • The brachial plexus is a complex network of peripheral nerves arising from the lower neck that provide the sensory and motor innervation to the upper extremity.
  • A brachial plexopathy should be considered in the differential diagnosis of any patient presenting with shoulder or upper extremity pain, weakness, or paresthesia.
  • Brachial plexopathies are easy to confuse with cervical radiculopathies. Radiculopathies are usually sensorimotor dominate, and plexopathies are motor dominate and may have a decline in pain symptoms as motor weakness evolves.
  • Clinical anatomy
    • The complex nerve network travels from the neck to the axilla before sending its terminal branches down the arm. In its course, it transverses through the anterior and middle scalene muscles, encircles the subclavian artery, and sends off several peripheral branches and nerves.
    • The brachial plexus arises from the ventral rami of spinal nerve roots C5-T1. The ventral rami travel distal and branch together to form the three main trunks (upper, middle, and lower). Fibers of the trunks then divide and reunite as they progress through the shoulder to form the cords (medial, lateral, and posterior). The cords then branch out to form the major nerves that supply motor and sensation to the upper extremity. The posterior cord forms the axillary and radial nerves. The lateral cord branches to form the musculocutaneous nerve and joins a branch of the medial cord to form the median nerve. The ulnar nerve arises from terminal end of the medial cord.
    • Some peripheral nerves of the brachial plexus arise directly from the ventral rami (long thoracic and dorsal scapular nerves) and some from the roots and cord levels (suprascapular, medial, and lateral pectorals; axillary, thoracodorsal, and lower subscapular).

Epidemiology


Incidence
  • The most common etiology is traumatic.
  • It is the most common peripheral nerve injury seen in athletes. It occurs at a rate as high as 49-61% of collegiate football players.
  • Traumatic brachial plexopathy is more likely to occur in young athletes and males.
  • Idiopathic brachial plexopathy (IBP), also known as Parsonage-Turner syndrome (PTS), brachial neuritis, or neuralgic amyotrophy, is rarer. It occurs with an overall incidence of 1.64 cases per 100,000. It occurs at all ages but is more common between the 3rd and 7th decades (1).

Etiology and Pathophysiology


  • The pathologic basis can vary with the different etiologies: compression, transection, idiopathic, inflammatory, or idiopathic. However, the underlying mechanism can be traced to a dysfunction in nerve conduction: conduction block, failure, or slowing.
  • Nerve compression or stretch may occur during contact sports; focal forces to the shoulder region result in brief compression of the ipsilateral plexus. Stretch of the shoulder and neck result in traction of the ipsilateral plexus or compression of the contralateral plexus. Nerve conduction returns to normal in matter of minutes or hours. An athlete may describe "shaking the arm out" and this often referred to as a burner or a stinger (2).
  • High-force trauma can cause a direct disruption of the nerve through transection from stretch or penetrating injury or it can injure the brachial plexus secondarily through disruption of blood supply or swelling around the brachial plexus (3).
  • Idiopathic or PTS, the pathology may be autoimmune or inflammatory mediated. Up to 25% of nontraumatic brachial plexopathies have been linked to preceding infections, and up to 15% have been reported to occur following vaccinations. The majority of nontraumatic cases have no associated etiologies.
  • Cancer-related brachial plexopathies; metastatic brachial plexopathies can result from compression by a lesion or invasion of cancer into the plexus or surrounding connective tissue. Radiation treatment for cancer can result in brachial plexus injury.

Diagnosis


History


Brachial plexopathy should be considered in any patient presenting with shoulder or upper extremity pain, weakness or paresthesia with insidious, sudden onset or after trauma.  
  • The common traumatic events that injure the brachial plexus are a fall on a shoulder that stretches or compresses the neck, direct compression from a hit during a contact sport, a motor vehicle accident, or athletic injury in which the shoulder and neck were stretched or compressed.
  • In cases of the mildest form of stretch injury, neurapraxia, the pain and weakness may be transient and is often called a burner or stinger if full recovery occurs within a few hours of injury. A patient may describe shaking the arm out to get strength or sensation back.
  • In cases of PTS, severe shoulder girdle pain develops suddenly, usually without identifying causation and classically presents with pain that wakes the patient up at night.
  • The symptoms will correlate to the portion of the brachial plexus involved. It usually involves a region of the brachial plexus such as the posterior cord, thus one would have weakness and pain in the distribution of the axillary and radial nerves. In cases of a brachial neuritis, it may involve just one nerve, but it is usually multiple nerves.
    • In cases of trauma-induced injury, pain and weakness usually develop concomitantly.
    • In cases of IPB or PTS, weakness may follow the pain by 1-2 weeks.
  • Traumatic brachial plexopathies are almost always unilateral and bilateral symptoms should prompt C-spine precautions and workup.
  • Nontraumatic cases usually present unilateral but may be bilateral.

Physical Exam


  • Symptoms correlate with the nerves affected by the injury. Consider that in some cases, motor weakness may follow pain and paresthesia by 1-2 weeks.
  • Neck, bilateral shoulders, and upper extremities should be inspected for atrophies. Wasting can occur within a few weeks after onset.
  • Sensory in dermatomal (C5-T1) and peripheral nerve distributions should be inspected and compared.
  • Motor testing for strength and fatigue should be tested from C5 through T1 and peripheral distributions as well.
  • Symptoms consistent with a nerve root distribution versus peripheral nerves can help you distinguish cervical injury from a brachial plexopathy.
  • Neck palpation, neck range of motion, or Spurling maneuver that reproduces symptoms is more consistent with a nerve root injury and may also help distinguish a nerve root injury from a brachial plexopathy.
  • A thorough shoulder exam should also be performed to rule out shoulder joint and rotator cuff etiology.
  • The axillary nerve is the most commonly affected by PTS and corresponding sensory deficits on cap of the shoulder and weakness of arm adduction can be elicited.
    • Suprascapular involvement is the second most common and presents with weakness in initiation of adduction or resisted "empty can" test for supraspinatus weakness as well as external rotation deficits from a weak infraspinatus.
    • Long thoracic involvement is common and presents with a winging scapula.

Differential Diagnosis


  • Cervical spine injuries
  • Cervical nerve root injury (e.g., herniation, compression, stenosis)
  • Herpes zoster
  • Shoulder joint arthropathy
  • Rotator cuff pathology
  • Adhesive capsulitis
  • Hereditary neuropathy

Diagnostic Tests & Interpretation


Initial Tests (lab, imaging)
A proper history and physical should lead to a reasonable conclusion with diagnostic tests helping to rule out lesions, tumors, fractures, etc.  
  • Radiologic
    • Plain films can help to rule out C-spine or shoulder fractures or anatomic anomalies that may be causing a compressive neuropathy.
    • Spine magnetic resonance imaging (MRI) may help identify extraspinal lesions, C-spine herniation, or stenosis.
    • A specialized magnetic resonance neurography can visualize individual roots, segments of the plexus, and peripheral nerves. It has low specificity but is more sensitive than conventional MRI for plexus lesions. It can identify local factors relevant to possible demyelination, nerve edema, thickening, and T2 hyperintensities.
  • Electrodiagnostic studies
    • Electromyography and nerve conductions studies are helpful in localizing, classifying severity of the injury, and distinguishing a demyelinating injury such as PTS and stretch injury from a compression injury. However, they will not be useful for 3-4 weeks after onset of symptoms.

Treatment


General Measures


Treatment varies depending on varying factors such as etiology and severity. The goal of treatment should be restoring motor and sensory function and alleviating pain. All acute onset, nontraumatic cases, and burner syndrome should be treated conservatively (3)[C].  
  • Initial
    • Pain can be treated pharmacologically and with physical therapy (4)[B].
  • Rehabilitation
    • It is important to prevent secondary complications of both pain and weakness in the shoulder such as adhesive capsulitis. Thus, exercises directed toward the muscles affected by the injury should be started as soon as tolerated by the patient. Physical and occupational therapy is often indicated for functional return and pain management (4)[B].
  • Surgery
    • Surgery is rarely indicated but should be considered in cases of traumatic plexopathy and cases with no long-term recovery in function or pain. Surgeries have variable results and include major reconstructive surgeries, implantable devices to control pain, muscle transfers, and arthrodesis (5)[B].
  • Return to activity or sport
    • Full function, sensation, and strength should be restored before a patient can safely return to a sport that requires contact. Consider limiting overhead activities that may lead to further injury if patient continues to use a limited upper extremity (6)[C].

Medication


First Line
  • Neuropathic pain can be treated with gabapentin or tricyclic antidepressants.
  • Pain is usually worse at onset and may subside after 1-2 weeks. In some cases, pain may continue for several weeks. Medication should be adjusted accordingly to severity of pain.
  • The severe pain of an acute brachial plexopathy may require the higher end dosing such as 600 mg of gabapentintid.

Second Line
  • Other analgesics such as tramadol or opiates may also be useful.
  • Opiates help reduce overall pain but have been shown to have varying efficacy for neuropathic pain.
  • Corticosteroids have no proven benefit but have been used and may help shorten duration of pain (7)[A].

Ongoing Care


Follow-up Recommendations


  • Physical therapy or occupational therapy is required for an optimal recovery of function and for managing pain.
  • Close monitoring of strength and symptoms should be performed. If anticipated recovery is delayed or symptoms worsen, further imaging or a referral may be indicated (6)[C].
  • Psychological impact of loss of function can be significant and require intervention with behavioral management.

Prognosis


Traumatic injures  

Complications


  • Weakness of any of the brachial plexus can lead to joint instability, contractures, and chronic pain in the upper extremity.
  • Depression secondary to loss of function and chronic pain may develop.

References


1.Khadikar  SV, Khade  SS. Brachial plexopathy. Ann Indian Acad Neurol.  2013;16(1):12-18.  
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2.Neal  S, Fields  KB. Peripheral nerve entrapment and injury in the upper extremity. Am Fam Physician.  2010;81(2):147-155.  
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3.Wilbourn  AJ. Plexopathies. Neurol Clin.  2007;25(1):139-171.  
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4.Smith  CC, Bevelaqua  AC. Challenging pain syndromes: Parsonage-Turner syndrome. Physl Med Rehabil Clin N Am.  2014;25(2):265-277.  
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5.Bertelli  J, Ghizoni  MF. Results and current approach for Brachial Plexus reconstruction. J Brachial Plex Peripher Nerve Inj.  2011;6(1):2.  
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6.Kuhlman  GS, McKeag  DB. The "burner": a common nerve injury in contact sports. Am Fam Physician.  1999;60(7):2035-2040.  
[]
7.van Alfen  N, van Engelen  BG, Hughes  RA. Treatment for idiopathic and hereditary neuralgic amyotrophy (brachial neuritis). Cochrane Database Syst Rev.  2009;(3):CD006976.  
[]

Codes


ICD09


  • 353.0 Brachial plexus lesions
  • 953.4 Injury to brachial plexus
  • 353.5 Neuralgic amyotrophy

ICD10


  • G54.0 Brachial plexus disorders
  • S14.3XXA Injury of brachial plexus, initial encounter
  • G54.5 Neuralgic amyotrophy

SNOMED


  • 3548001 Brachial plexus disorder (disorder)
  • 6836001 injury of brachial plexus (disorder)
  • 26609002 Neuralgic amyotrophy (disorder)
  • 76691009 Brachial plexus neuralgia (disorder)

Clinical Pearls


  • Brachial plexopathies should be considered with any insidious or sudden onset of upper extremity pain, weakness, or paresthesia.
  • Most cases are posttraumatic, but several are idiopathic and require a high degree of suspicion for proper diagnosis.
  • The course is usually self-limiting but requires astute clinical skills for diagnosis, monitoring, and rehabilitation of full pain-free function.
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