Brachial Plexus Injuries

• Neurapraxia (First-degree injury): Demyelination without axonal loss or loss of continuity. Conduction block occurs across the injury site while the axon and endoneurium remain intact. Complete spontaneous recovery typically occurs within 6–12 weeks as remyelination progresses. Electrophysiologically, compound motor action potentials (CMAPs) show normal amplitude distal to the lesion but absent response across the injury site.

• Axonotmesis (Second- and third-degree injuries): Axonal disruption with preservation of some connective tissue framework. Second-degree injuries preserve the endoneurium; third-degree injuries disrupt the endoneurium but spare the perineurium. Wallerian degeneration begins within 48–72 hours of injury, with progressive loss of motor endplate contacts and muscle fiber atrophy. Regeneration proceeds at approximately 1 mm per day, with motor recovery dependent on reinervation distance and time (critical window is 12–18 months before irreversible muscle atrophy and motor endplate degeneration occur).

• Neurotmesis (Fourth- and fifth-degree injuries): Complete disruption of the axon and connective tissue sheaths (fourth-degree) or complete anatomical transection (fifth-degree). Fourth-degree injuries may spontaneously reorganize if scar tissue does not completely block regeneration. Fifth-degree injuries necessitate surgical repair for any possibility of functional recovery. The mechanical disruption prevents axonal growth cones from reaching distal targets, resulting in permanent neurological deficit without intervention.

• High-energy motor vehicle accidents (motorcycle crashes most common): Account for 50–60% of brachial plexus injuries through violent shoulder abduction combined with lateral neck flexion or by direct shoulder trauma during impact. Extreme traction forces (>60 pounds) exceed the plexus's tensile strength.
• Penetrating trauma (knife wounds, gunshot wounds, iatrogenic injury during vascular access, thoracic surgery, or supraclavicular block): Direct laceration or transection accounts for 10–15% of cases. Iatrogenic injury risk is heightened during first rib resection or axillary artery cannulation.
• Blunt trauma and falls (sports injuries, falls from height): Occur in up to 25% of cases, particularly involving shoulder dislocation or fracture of the first rib, clavicle, or scapula.
• Crush injuries (industrial accidents, heavy weight compression): Cause combined neurotmesis and ischemic injury through vascular compromise.

• Birth brachial plexus palsy: Occurs in 0.4–3 per 1000 live births, associated with shoulder dystocia, macrosomia, cephalopelvic disproportion, and difficult operative delivery. Excessive lateral traction during delivery causes upper trunk (Erb's palsy) or lower trunk (Klumpke's palsy) injury. Most cases (90%) resolve spontaneously within 3 months.

Non-traumatic causes

• Compression neuropathy: Thoracic outlet syndrome (TOS) from scalene muscle hypertrophy, cervical rib, fibrous bands, or anatomical compression of the plexus between the anterior and middle scalene muscles.
• Neoplastic: Primary or metastatic tumors, lymphoma, or pancoast tumors causing progressive plexopathy.
• Radiation injury: Delayed plexopathy occurring 6 months to >10 years after radiation therapy for breast cancer or lymphoma (dose-dependent; risk increases significantly above 60 Gy).
• Inflammatory/infectious: Brachial plexitis (neuralgic amyotrophy), herpes zoster, Lyme disease, HIV.
• Vascular: Subclavian artery dissection, aneurysm, or thrombosis causing ischemic injury.

• Loss of shoulder abduction (supraspinatus, deltoid denervation via axillary nerve)
• Loss of external rotation at the shoulder (infraspinatus)
• Loss of forearm supination (biceps)
• Classic "waiter's tip" position: arm hangs at the side with shoulder adducted and internally rotated, forearm pronated

• Intrinsic hand muscle weakness and atrophy (interossei, lumbricals)
• Claw hand deformity (hyperextension at metacarpophalangeal joints; flexion at interphalangeal joints)
• Loss of grip strength
• Sensory loss over the hypothenar eminence and medial one-and-a-half fingers
• Horner's syndrome (ptosis, miosis, anhidrosis) present if T1 root is avulsed

• Triceps and wrist extensor weakness
• Loss of elbow extension and wrist dorsiflexion

Posterior cord injuries

• Global weakness of elbow, wrist, and finger extension
• Axillary nerve involvement causing deltoid paralysis

• Flaccid paralysis of the entire upper extremity
• Sensory loss from shoulder to fingertips
• Horner's syndrome if T1 root avulsion present
• Early muscle atrophy becomes evident by 2–3 weeks

Associated physical examination findings

• Sensory deficits: Distributed according to dermatome (C5: lateral shoulder; C6: lateral forearm/thumb; C7: middle finger; C8: medial forearm/ulnar digits; T1: medial arm/axilla)
• Tinel's sign: Percussion over the injury site produces tingling in the distal distribution (indicates regenerating axons)
• Horner's sign: Ptosis, miosis, anhidrosis, loss of ciliospinal reflex indicating preganglionic (root) injury
• Nerve root avulsion signs: Severe pain, early muscle atrophy, abnormal EMG findings
• Clavicular prominence or step-off: May indicate underlying fracture contributing to plexus compression

Clinical evaluation

• Electromyography (EMG): Establishes the presence and distribution of denervation (fibrillations, positive sharp waves appearing 2–3 weeks post-injury). Interference pattern analysis assesses motor unit recruitment. Serial EMG studies (baseline, 3 weeks, 8 weeks, 12 weeks) demonstrate denervation evolution and early reinnervation (nascent motor units, polyphasia).
• Nerve conduction studies (NCS): Document conduction velocity slowing, conduction blocks, and reduced compound motor action potential (CMAP) amplitudes. Distal CMAP preservation (normal amplitude distal to lesion) indicates neurapraxia with preserved axonal continuity; absent or severely reduced distal CMAP suggests axonotmesis or neurotmesis. Sensory nerve action potentials (SNAPs) help localize the injury relative to the dorsal root ganglia: preserved SNAPs with absent motor responses indicate preganglionic (root) avulsion since sensory neurons have their cell body in the dorsal root ganglion, proximal to the injury site.

Imaging studies

• Magnetic resonance imaging (MRI) with dedicated brachial plexus protocol: High sensitivity for detecting root avulsion (absence of nerve root exiting the neural foramen), pseudomeningoceles (cerebrospinal fluid collection indicating avulsion), edema and signal abnormality within nerve roots/trunks, and space-occupying lesions. MRI is superior for evaluation of soft tissue and nerve involvement but has limited sensitivity for acute transection.
• High-resolution ultrasound: Real-time imaging allowing dynamic assessment, detection of neural transection (gap between nerve ends), hypoechoic edema, and measurement of retraction. Increasingly used as first-line imaging due to accessibility and no radiation.
• CT imaging: Identifies associated skeletal injuries (first rib fracture, clavicle fracture, scapular fracture) and may reveal mass lesions; lower sensitivity for nerve-specific pathology.
• Myelography or CT myelography: Gold standard for detecting nerve root avulsion (demonstrates absent nerve root or pseudomeningocele), reserved for cases where surgery is planned.

Diagnostic criteria for specific injury patterns

• Preganglionic injury (root avulsion): Clinical Horner's syndrome + preserved SNAP with absent CMAP + MRI/myelography confirmation of root avulsion or pseudomeningocele
• Postganglionic injury: Absent SNAP and CMAP + normal or edematous-appearing roots on imaging
• Neurapraxia: Conduction block on NCS (absent CMAP across lesion, normal amplitude distally) + normal or minimally abnormal EMG + clinical recovery within expected timeline
• Complete transection: Wide gap between nerve ends on ultrasound/MRI + no recovery after 6 months + progressive muscle atrophy

• Immobilization and supportive care: Protect the flaccid extremity from additional trauma; use sling, padding, and careful handling to prevent contracture formation. Educate patient on skin care to prevent pressure ulcers.
• Pain management: Multimodal analgesia including gabapentin (300–3600 mg daily in divided doses) or pregabalin (150–600 mg daily) for neuropathic pain. Severe acute pain may require opioid analgesia and regional anesthesia blocks for comfort.

First-line therapeutic approach by injury severity

• Conservative management: Observation with serial clinical and electrodiagnostic examinations at 3, 8, and 12 weeks. Physical therapy emphasizing passive range-of-motion exercises to prevent contracture during denervation period.
• Mechanism: Spontaneous remyelination (neurapraxia) or axonal regrowth (axonotmesis) proceeds without intervention.

• Early surgical consultation (ideally within 3 months, but urgent if transection or avulsion confirmed): Establishes candidacy for nerve repair and appropriate timing.
• Nerve repair techniques:
• Primary repair (best outcomes): Microsurgical approximation of nerve ends or cable grafting if gap exists (performed within 72 hours to 3 weeks for optimal outcomes; up to 12–18 months possible but with diminishing returns). Autologous nerve grafts remain the gold standard for segmental defects (harvested from sensory nerves such as sural nerve).
• Nerve transfer (increasingly popular): Redirecting healthy nerve fascicles to reinnervate critical muscles, reducing regeneration distance and improving motor recovery timing. Example: spinal accessory (CN XI) to suprascapular nerve for shoulder abduction recovery.
• Neurolysis: Microsurgical release of scar tissue if conduction block present without complete transection.
• Muscle transfer: Reconstructive surgery for paralyzed muscles when nerve repair unsuccessful or recovery incomplete (e.g., pectoralis major transfer for shoulder abduction if axillary nerve irreparably damaged).

• Not directly repairable: Conventional nerve repair impossible as the root has been pulled from the spinal cord. Root reimplantation is experimental and rarely successful.
• Nerve transfer strategy: Utilize intact proximal nerves or donor nerves (e.g., contralateral C7 root transfer, intercostal nerve transfer) to provide distal reinnervation.
• Surgical reconstruction: Multiple staged procedures often necessary, including muscle transfers for functional restoration.

Second-line and adjunctive therapies

• Electrical stimulation (intraoperative): Electrolocation of regenerating axons during exploration; improves precision of repair.
• Corticosteroids: Role remains controversial; some evidence supports high-dose methylprednisolone (1 g IV daily × 3–5 days) within 72 hours for traumatic injury to reduce inflammation and edema, though benefit in brachial plexus injury specifically is limited.
• Physical and occupational therapy: Critical for maintaining joint mobility, strengthening recovering muscles, developing compensatory strategies, and functional retraining.

Non-pharmacological measures

• Range-of-motion exercises: Passive range-of-motion 2–3 times daily to prevent contracture of joints and muscles.
• Splinting and bracing: Custom-fitted orthoses to support weak joints and prevent contracture deformity.
• Functional electrical stimulation (FES): Stimulates partially denervated muscles to maintain bulk and potentially improve recovery; evidence for benefit remains limited.
• Constraint-induced movement therapy: For partial recovery, forcing use of affected limb to promote neuroplasticity.
• Mirror therapy: Visual feedback techniques to enhance motor recovery.
• Psychosocial support: Counseling for adjustment to potential chronic disability; management of depression common in severe injuries.

Monitoring parameters

• Serial clinical examination (strength testing using Medical Research Council [MRC] scale, sensory testing) at baseline, 4–6 weeks, 8–12 weeks, and 6 months.
• Repeat EMG/NCS at 8–12 weeks to assess for reinnervation potentials; additional study at 4–6 months if incomplete recovery.
• Imaging (ultrasound or MRI) at 3 months to assess nerve healing and scar formation if surgical repair performed.

• Muscle contracture: Muscle fibrosis and joint stiffness develop within 4–8 weeks of denervation if passive range-of-motion not maintained. Prevention through aggressive physical therapy is essential; established contractures require surgical release.
• Pressure ulceration: Flaccid, anesthetic limb at high risk for skin breakdown, particularly over bony prominences (shoulder, elbow). Requires meticulous skin care, frequent repositioning, and protective padding.
• Reflex sympathetic dystrophy (complex regional pain syndrome type 1): Occurs in up to 10% of patients; presents with disproportionate pain, edema, vasomotor changes (skin color/temperature changes), and progressive functional impairment. Treated with physical therapy, topical agents (lidocaine patches, capsaicin cream), regional anesthesia blocks, and systemic agents (gabapentin, amitriptyline).

• Motor unit loss and chronic atrophy: Irreversible if reinnervation does not occur within 12–18 months. Progressive motor endplate degeneration and muscle fiber death occur; later-stage muscle transfer becomes necessary for functional restoration.
• Chronic neuropathic pain: Persists in 20–50% of patients despite motor recovery. Treated with gabapentin, pregabalin, duloxetine, tricyclic antidepressants (amitriptyline), topical lidocaine, and interventional pain management (sympathetic blocks, spinal cord

The two named palsies

• Erb–Duchenne (C5–C6, upper trunk): waiter's tip posture — adducted, internally rotated shoulder, extended elbow, pronated forearm. On the newborn exam the Moro is asymmetric but the grasp reflex is intact; this grasp/Moro dissociation is the single most testable discriminator from Klumpke palsy.
• Klumpke (C8–T1, lower trunk): claw hand from intrinsic loss, with an absent grasp. Add Horner syndrome and the stem is telling you T1 is involved.

The association examiners test

• Horner syndrome = preganglionic (root avulsion), because the sympathetic fibers leave T1 before the plexus. It signals a lesion not amenable to direct repair and predicts poor spontaneous recovery — nerve transfer, not neurorrhaphy.
• Preserved SNAPs in an anesthetic dermatome is the electrophysiologic equivalent of the same message: the dorsal root ganglion is distal to the avulsion, so the sensory axon never degenerates. A stem pairing numb skin with a normal sensory response is testing preganglionic localization (AANEM electrodiagnostic principles).
• Erb palsy plus respiratory distress should prompt a look for ipsilateral phrenic nerve (C3–C5) injury with an elevated hemidiaphragm.

Best next step

• In a neonate with shoulder dystocia and a flaccid arm, the immediate step is radiography of the clavicle and humerus to exclude fracture, then supportive positioning and range-of-motion therapy; ACOG's shoulder dystocia guidance emphasizes that most obstetric palsies are not preventable and that the majority recover spontaneously. Referral to a specialized brachial plexus center is triggered by failure of biceps (elbow flexion) recovery over the first few months.
• In an adult after trauma, defer EMG until roughly 3 weeks, when fibrillations and positive sharp waves appear; an immediate study cannot distinguish neurapraxia from axonotmesis.

Common distractors

• Painless upper-plexus plexopathy with myokymia after breast/lymphoma radiation = radiation fibrosis; painful lower-plexus plexopathy with Horner = tumor infiltration (Pancoast).
• Abrupt severe shoulder pain followed days later by patchy weakness and scapular winging is **neuralgic amyotrophy (Parsonage–Turner)**, not traumatic traction injury.
• A football burner/stinger is transient upper-trunk neurapraxia; bilateral symptoms mean cervical cord, not plexus.