Brachial Plexus Injuries

Overview

Anatomy

The brachial plexus is a network of nerves from which all the motor and sensory nerves of the upper extremity arise. It is formed by the nerve roots from C5 to T1 and divides into:

• Trunks:
  • Upper trunk: formed by the C5 and C6 roots
  • Middle trunk: formed by the C7 root 
  • Lower trunk: formed by the C8 and T1 roots
• Divisions: Each trunk divides into an anterior and posterior division.
• Cords, branches, and nerves:
  • Lateral cord branches into:
    • Musculocutaneous nerve 
    • Median nerve
  • Posterior cord branches into:
    • Axillary nerve
    • Subscapular nerve
    • Thoracodorsal nerve
    • Radial nerve
  • Medial cord branches into: 
    • Median nerve 
    • Ulnar nerve
    • Medial cutaneous nerves of the arm and forearm
  • Suprascapular nerve: arises from the upper trunk
  • Dorsal scapular nerve: arises from the C5 root
  • Long thoracic nerve: arises from the C5, C6, and C7 roots

Epidemiology

• Brachial plexus syndromes are rare:
  • Occur in 0.4% of patients with cancer
  • Occur in 2% to 5% of patients exposed to radiation
• Incidence of idiopathic brachial plexopathy or brachial amyotrophy is 2–3 per 100,000.
• The incidence ratio for traumatic injuries is 2:1, men to women.

Classification

• Based on the location of the injury
• Supraclavicular preganglionic:
  • Associated with avulsion of nerve roots
  • Usually results in permanent motor and sensory deficits
  • Denervation of neck muscles is common.
• Supraclavicular postganglionic:
  • Often due to traction injuries
  • Nerve roots remain intact.
• Infraclavicular: involves individual branches of the plexus

Pathogenesis

The brachial plexus can be injured by several mechanisms:

• Nerve traction:
  • Also known as stretch injury (as seen in delivery of infants)
  • Occurs from sudden severe pull or tension of the nerves
• Nerve compression: 
  • Uncommon: The brachial plexus is protected by bony structures.
  • Occurs in contact sports
• Overt nerve transection with major trauma
• Ischemia resulting from occlusion of small intraneural vessels due to:
  • Inflammation 
  • Radiation
  • Metabolic abnormalities
• Direct nerve invasion by cancer cells 

Clinical Presentation

Clinical symptom onset may vary from acute to insidious, with shoulder or upper arm pain described as “electric shock-like” or a burning sensation. 

Traumatic plexopathies

• Trauma from injuries:
  • Open: knife or gunshot wounds, animal bites
  • Closed: motorcycle/automobile accidents, falls from a height, hematomas
  • Manifestations correlate to the nerve(s) affected by the injury.
• Trauma from sports injuries: burner (also called stinger)
  • Caused by downward traction of the shoulder, involving the upper trunk of the brachial plexus
  • Most often due to tackling
  • Manifests as transient numbness, paresthesias, or weakness in the arm
  • Usually brief and self-limited; occasionally, recovery may take days to weeks
• Backpack palsy (also known as rucksack paralysis or cadet palsy):
  • Affects the upper trunk (C5–C6)
  • Presents after wearing a backpack or similar apparatus
  • Usually painless, due to stretch or compression of the nerve fibers
  • Symptoms: 
    • Weakness of shoulder abduction and elevation
    • Weakness in extension of the forearm, wrist, and fingers 
    • Some sensory loss in the same distribution
    • Most patients recover fully in a few months.
• Obstetric brachial plexus palsies:
  • Erb palsy:
    • More common than Klumpke palsy
    • Affects C5 and C6 nerve roots
    • Deformity: arm hanging by the side, adducted, and medially rotated
  • Klumpke palsy:
    • Affects C8 and T1 nerve roots 
    • “Claw hand” deformity: hyperextension at the metacarpophalangeal joints and flexion at the interphalangeal joints

Nontraumatic plexopathies

Neuralgic amyotrophy (progressive wasting of muscle tissues):

• Inflammatory disorder of the brachial plexus
• Also known as Parsonage-Turner syndrome or idiopathic brachial plexopathy
• May affect both children and adults
• Sudden onset of shoulder/upper arm pain → progressive weakness and atrophy

Hereditary brachial plexopathy:

• Autosomal dominant 
• Characterized by painful, recurrent brachial plexopathies
• Features: short stature, hypotelorism, unusual skin folds, creases on the neck
• Rare 

Neoplastic brachial plexopathy:

• Presents with pain in the shoulder/axilla
• Types:
  • Primary: due to neurogenic tumors (e.g., schwannomas, neurofibromas)
  • Secondary: due to regional lymph nodes causing nerve compression; most commonly due to breast and lung cancers
  • Paraneoplastic: due to demyelinating injury from antibodies against the myelin sheath, associated with Hodgkin lymphoma
• C8 or T1 nerve root involvement:
  • Seen with Pancoast tumors (usually non–small cell lung carcinoma (NSCLC))
  • Sympathetic neurons run through the brachial plexus over the lung apex.
  • Clinical symptoms: Horner syndrome (ptosis, miosis, and anhidrosis) due to an interruption of the cervical sympathetic chain supply to the eye

Radiation-induced brachial plexopathy:

• May not present until months or years after radiation
• Due to direct axonal damage, demyelination, microvascular infarction, and fibrosis
• Risk ↑ with concurrent chemotherapy

Thoracic outlet syndrome (TOS):

• Due to compression of blood vessels and nerves as they pass between the clavicle and the 1st rib 
• Causes:
  • Accidents
  • Repetitive-use type of occupational injuries
  • Anatomic variants
  • Hypertrophy of the scalene or pectoralis minor muscle in weight lifters and athletes
• Symptoms vary but may include:
  • Muscle weakness
  • Numbness
  • Ischemic changes
  • Edema of the upper extremities
  • Venous thrombosis

Diabetes-related brachial plexopathy:

• Not as common as lumbosacral plexopathy
• May be mononeuropathies of the ulnar and median nerves

Iatrogenic plexopathies:

• Classic postoperative paresis:
  • Caused by traction or pressure during surgery
  • Presents with painless weakness and paresthesia
  • Recovery is rapid and complete.
• Post-median sternotomy plexopathy:
  • Occurs after open-heart surgery 
  • Caused by injury to the anterior ramus C8 
  • Presents with hand weakness, paresthesia, and pain in the C8 dermatome
• Anesthetic block plexopathy:
  • Occurs after regional infraclavicular brachial plexus blockade
  • Due to trauma from the infusion needle, hematoma formation, or neurotoxicity from the local anesthetic
• Medial brachial fascial compartment syndrome:
  • Occurs after puncture of the axillary or brachial artery during procedures such as arteriography or axillary regional anesthetic blocks
  • Expanding hematoma causes nerve compression of the median or ulnar nerves most commonly.

Diagnosis

The primary pathologic lesion in most plexopathies is axonal loss, whether due to trauma, demyelination, or compression. Diagnosis is based on clinical presentation and testing.

History

• Duration of symptoms
• Characteristics of pain, sensory changes, weakness, and muscle atrophy
• Infection, activity, or injury associated with the onset
• Change in symptoms with a change in head, neck, or arm position
• Autonomic symptoms
• Change in functionality of the arm 
• Past medical history:
  • Malignancy, radiation, chemotherapy
  • Demyelinating disorders
  • Diabetes 
  • Previous brachial plexopathy
• Details of pregnancy and delivery in neonatal patients (e.g., stretching/traction)

Physical examination

• Visual inspection for skin changes: 
  • Surgical scars or wounds 
  • Muscle atrophy
• Palpation of the muscles of the shoulder and arm
• Range of motion (ROM) of the cervical spine and upper extremity
• Pupil exam for possible Horner syndrome
• Neurological exam:
  • Motor strength
  • Sensory exam
  • Deep tendon reflexes (DTRs)
• Neonatal patients: Clinical diagnosis is made when arm weakness at birth fits a distribution consistent with a brachial plexus injury.

Imaging and tests

• Cervical spine X-ray for bony abnormalities
• Chest X-ray if concern for lung malignancy
• MRI for structural abnormalities (e.g., disc herniation, tumor)
• Ultrasound may distinguish preganglionic from postganglionic traumatic lesions noninvasively.
• Electromyography (EMG)/nerve conduction studies:
  • Assesses for axonal damage in motor nerves 
  • Gives information regarding other diagnoses (e.g., nerve entrapment syndromes)
  • Sensory nerve conduction studies are more sensitive to axonal loss than motor nerve studies.

Management

Acute traumatic injuries may lead to plexopathies that are self-limited within a few months. Specific treatments for nontraumatic plexopathies include PT and medications.

Traumatic plexopathies

• Some situations may require emergent surgical intervention.
• Nonemergency surgery: indicated if no improvement after 3–4 months 
• Types of procedures:
  • Neurolysis
  • Nerve grafts
  • Nerve transfers
  • Tendon and muscle transfers
• Prognosis: improved function noted in approximately 60% of patients after surgical intervention

Nontraumatic plexopathies

Neuralgic amyotrophy:

• Conservative management:
  • PT
  • Glucocorticoids 
  • Analgesics
• Prognosis:
  • Recovery is slow over 1–3 years.
  • Some patients may have persistent disability.

Hereditary brachial plexopathy:

• Glucocorticoids
• Analgesics
• PT

Neoplastic plexopathy:

• Radiation therapy (RT) to reduce pain
• Analgesics 

Radiation-induced plexopathy:

• Gabapentinoids (inhibit neurotransmission)
• Glucocorticoids
• Tricyclic antidepressants (TCAs)

TOS:

• Conservative measures:
  • Weight reduction
  • Analgesics
  • Strengthening program
• Surgery:
  • True neurogenic TOS → surgical release of the fibrous band or resection of the rudimentary cervical rib
  • Vascular TOS → decompressive surgery

Iatrogenic plexopathies:

• Conservative management
• Surgical decompression

Neonatal brachial plexus palsy:

• PT to promote muscle strengthening
• Surgery indications include:
  • Pan-plexopathy and preganglionic nerve root lesion
  • Complete nerve disruption and nerve root avulsions
  • Incomplete functional recovery
• Botulinum toxin injection: may be helpful for contractures/muscle imbalances 
• Psychosocial support for ongoing disability in childhood
• Prognosis:
  • Spontaneous recovery occurs over 1–3 months in most cases.
  • More favorable prognosis if early clinical improvement in a few weeks
  • Good prognosis with normal or near-normal strength in elbow flexion, shoulder external rotation, and forearm supination by 3 months of age

Differential Diagnosis

• Cervical radiculopathy: refers to pain and neurologic symptoms in the upper extremities due to injury or inflammation of the cervical spine nerve roots. The causes of cervical radiculopathy include cervical disc herniation, infection, tumor infiltration, and demyelination. The clinical features vary depending on the location and degree of cervical nerve root involvement. Diagnosis is made based on clinical exam, MRI, and electrodiagnostic studies. Treatment can be conservative with PT and pain control, or with surgical decompression if there’s no improvement.
• Guillain-Barré syndrome (GBS): refers to a family of immune-mediated polyneuropathies that occur after infections (e.g., Campylobacter jejuni). Typical GBS is characterized by acute monophasic neuromuscular paralysis, which is symmetric and ascending and may progress to respiratory failure requiring prolonged hospitalization. Management is mostly supportive and may require either plasma exchange or IV immunoglobulin (IVIG). 
• Multiple sclerosis (MS): chronic inflammatory autoimmune disease leading to demyelination of the CNS. The etiology is uncertain, but both genetic and environmental factors are believed to play a role. Diagnosis is made by MRI as well as CSF examination. Management involves corticosteroids for acute exacerbations and disease-modifying agents to reduce exacerbations and slow the progression of the disease.
• Spinal cord injury: associated with complete or incomplete syndromes due to vertebral fracture, disc herniation, or, in some cases, arterial occlusion/ischemia. The cardinal sign is a discrete injury level, above which neurologic function is intact, and below which it is absent or markedly diminished. Diagnosis is by clinical exam and MRI. Management depends on the cause of the spinal cord syndrome and involves long-term symptomatic care and rehabilitation.