Axillary Nerve Injury

Axillary nerve injury is the most common nerve injury in the shoulder region and shoulder anterior dislocation represents the predominant causative mechanism.

The axillary nerve represents one of the most vulnerable neural structures in the shoulder region, deriving from the posterior cord of the brachial plexus (C5-C6). This critical peripheral nerve provides motor innervation to the deltoid and teres minor muscles while supplying sensory innervation to the lateral aspect of the upper arm.

Related Anatomy

The axillary nerve originates from the posterior cord of the brachial plexus, composed primarily of nerve roots from the fifth and sixth cervical segments. After emerging from the brachial plexus, the nerve courses anteriorly to the subscapularis muscle before traversing the quadrilateral space. This anatomically confined region is bounded by the teres minor superiorly, teres major inferiorly, long head of triceps medially, and the surgical neck of the humerus laterally.

Upon exiting the quadrilateral space, the axillary nerve divides into anterior and posterior branches. The anterior branch innervates the anterior and middle portions of the deltoid while providing cutaneous sensation to the lateral shoulder. The posterior branch supplies the posterior deltoid and the teres minor muscle, with some sensory fibers contributing to the superior lateral cutaneous nerve of the arm.

See Also: Brachial Plexus Anatomy

The anatomical course of the axillary nerve predisposes it to injury during shoulder trauma. As the nerve wraps around the surgical neck of the humerus at a distance of approximately 5-7 cm from the lateral acromion, it becomes particularly vulnerable during anterior dislocations and proximal humeral fractures. The nerve’s relatively fixed position within the quadrilateral space further increases its susceptibility to traction injuries during shoulder displacement.

Mechanisms of Injury

The axillary nerve is the most commonly injured nerve in the shoulder region, with anterior dislocation of the shoulder representing the predominant causative mechanism. Studies indicate that approximately 9-18% of traumatic anterior shoulder dislocations result in some degree of axillary nerve dysfunction. The nerve injury may occur during the initial dislocation event or subsequently during reduction procedures, particularly when excessive force or improper technique is employed. Fractures involving the surgical neck of the humerus constitute the second most frequent cause, with the nerve vulnerable to both direct compression and traction forces.

Beyond these primary mechanisms, axillary nerve injury may result from penetrating trauma such as gunshot or stab wounds, iatrogenic injury during shoulder surgery, compression from improper crutch usage, or as a component of broader brachial plexus injuries. Quadrilateral space syndrome represents a less common but significant cause of axillary nerve compression, often associated with repetitive overhead activities or fibrous band formation within the quadrilateral space. Rarely, the nerve may be compromised by space-occupying lesions, including ganglion cysts, lipomas, or vascular malformations in proximity to its anatomical course.

Axillary Nerve Injury Symptoms & Signs

The clinical manifestations of axillary nerve injury primarily reflect dysfunction of its innervated muscles and sensory distribution. Motor deficits constitute the most apparent and functionally significant findings. Patients typically present with weakness or complete inability to abduct the arm due to deltoid paralysis. Upon careful examination, compensatory mechanisms may be observed as patients attempt to achieve shoulder abduction through alternative means. This typically involves lateral rotation of the arm and utilization of the long head of the biceps brachii, commonly referred to as a “trick movement.” Similarly, weakness of lateral rotation indicates teres minor involvement, with patients often compensating through exaggerated scapular movements utilizing the trapezius or serratus anterior muscles.

Physical examination reveals characteristic findings. Progressive deltoid atrophy leads to flattening of the lateral shoulder contour, contrasting with the normal rounded appearance. This becomes particularly evident when comparing the affected shoulder with the contralateral side. Sensory deficits present as diminished or absent sensation over the lateral deltoid region, with the most pronounced loss occurring in a circumscribed area approximately 2-3 cm in diameter at the deltoid insertion.

Interestingly, some patients with partial axillary nerve injury remain relatively asymptomatic during routine activities but demonstrate rapid fatigue during sustained or strenuous use of the affected arm. This presentation often leads to delayed diagnosis, emphasizing the importance of comprehensive neuromuscular examination in all cases of shoulder trauma.

Diagnostic Approaches

Accurate diagnosis of axillary nerve injury requires a systematic approach combining detailed clinical assessment with appropriate diagnostic studies. The initial evaluation should include a comprehensive history focusing on the mechanism of injury, symptom progression, and functional limitations. Physical examination must assess deltoid strength through resisted shoulder abduction, teres minor function via resisted external rotation, and sensory perception over the lateral arm. Careful observation for compensatory mechanisms and comparison with the unaffected side enhances diagnostic sensitivity.

Electrodiagnostic studies represent the cornerstone of objective assessment. Nerve conduction studies may demonstrate reduced compound muscle action potential amplitudes in the deltoid and teres minor, while needle electromyography can reveal fibrillation potentials and positive sharp waves in denervated muscles. These studies not only confirm the diagnosis but also provide valuable information regarding the severity of nerve injury, chronicity, and potential for spontaneous recovery.

Advanced imaging modalities complement electrodiagnostic findings. Magnetic resonance imaging of the shoulder provides detailed visualization of soft tissue structures, potentially identifying nerve compression, edema, or surrounding pathology contributing to axillary nerve dysfunction. Ultrasound offers a dynamic assessment option with the advantages of lower cost and real-time evaluation. In cases with uncertain etiology, magnetic resonance neurography may specifically highlight nerve signal abnormalities indicative of compression or intrinsic pathology.

Management Strategies

The management of axillary nerve injury follows a tiered approach based on injury severity, chronicity, and associated pathology. Initial treatment typically employs conservative measures, particularly for neuropraxic injuries with a favorable prognosis for spontaneous recovery. This approach includes physical therapy focusing on maintaining passive range of motion, preventing contractures, and strengthening unaffected muscle groups. Electrical stimulation may be incorporated to minimize muscle atrophy during the recovery period.

For axillary nerve injury with evidence of axonotmesis or neurotmesis, or those failing to demonstrate improvement after 3-4 months of conservative management, surgical intervention warrants consideration. Surgical options include neurolysis for compressed nerves with preserved continuity, direct nerve repair when feasible, or nerve grafting for segmental defects exceeding a few centimeters. Recent advances in peripheral nerve surgery have introduced nerve transfers as a viable alternative when conventional repair options prove inadequate.

In cases of chronic axillary nerve palsy with established deltoid atrophy and minimal potential for neural recovery, functional reconstruction may be achieved through tendon transfers. The most commonly employed technique involves transferring the upper portion of the trapezius to the proximal humerus, providing substitute power for shoulder abduction. Alternatively, the latissimus dorsi or portions of the pectoralis major may be rerouted to compensate for deltoid dysfunction.

Prognosis and Outcomes

The natural history and recovery potential of axillary nerve injury vary considerably depending on multiple factors. Injuries classified as neuropraxia, characterized by local conduction block without axonal disruption, typically demonstrate excellent recovery within 6-12 weeks. In contrast, axonotmesis injuries involving axonal disruption with preserved neural sheath structures show variable recovery patterns, with significant improvement possible over 3-6 months as axonal regeneration proceeds at approximately 1-2 mm per day.

Complete nerve transection (neurotmesis) carries the least favorable prognosis, with functional recovery largely dependent on timely surgical intervention. Even with optimal management, complete restoration of deltoid function remains challenging due to the extended reinnervation distance and potential for muscle fibrosis during the denervation period.

Several prognostic indicators have been identified. Patient age significantly influences recovery potential, with younger individuals demonstrating superior neural regenerative capacity. The timing of intervention represents another critical factor, with surgical exploration ideally undertaken within 3-6 months of injury for optimal outcomes. Electrophysiological studies provide valuable prognostic information, with the presence of motor unit potentials or evidence of ongoing reinnervation suggesting favorable recovery potential.

References & More

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4. Safran MR. Nerve injury about the shoulder in athletes. Part 1: suprascapular nerve and axillary nerve.Am J Sports Med. 2004;32:803–819. Pubmed