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Axillary nerve

The axillary nerve is a peripheral nerve of the brachial plexus that originates from the posterior cord, primarily from the C5 and C6 spinal roots, and provides motor innervation to the deltoid and teres minor muscles while supplying sensory fibers to the skin over the lateral aspect of the shoulder.^[1]^[2] Emerging in the axilla posterior to the axillary artery and anterior to the subscapularis muscle, the axillary nerve travels posteriorly through the quadrangular space—bounded by the teres minor superiorly, teres major inferiorly, long head of the triceps medially, and surgical neck of the humerus laterally—before dividing into anterior and posterior branches near the surgical neck of the humerus, with the anterior branch coursing around 5-7 cm distal to the lateral acromion.^[1]^[2] The anterior branch innervates the anterior and middle deltoid for shoulder flexion and abduction, while the posterior branch supplies the posterior deltoid and teres minor for extension and external rotation, respectively; additionally, an articular branch provides sensory innervation to the glenohumeral joint capsule.^[1]^[2] Sensory function is mediated by the superior lateral brachial cutaneous nerve, a terminal branch that emerges from the posterior division and innervates the "regimental badge" area of skin over the deltoid region, enabling sensation in this superficial zone.^[1]^[2] Clinically, the axillary nerve is vulnerable to injury due to its close proximity to the humeral surgical neck and glenohumeral joint, with common mechanisms including anterior shoulder dislocations (reported in 9–55% of cases), proximal humerus fractures, or iatrogenic damage during surgical procedures like arthroscopy or proximal humerus nailing.^[1]^[2]^[3] Such injuries often result in deltoid weakness leading to impaired shoulder abduction beyond 15 degrees, teres minor dysfunction manifesting as positive Hornblower's sign, and numbness in the lateral shoulder, though many cases recover spontaneously without intervention due to the nerve's regenerative potential.^[1]^[2] In severe or persistent cases, associated with conditions like quadrangular space syndrome or Erb's palsy from upper trunk brachial plexus involvement, management may involve nerve conduction studies, physical therapy, or surgical exploration such as nerve grafting or transfer.^[1]^[2]

Anatomy

Origin and course

The axillary nerve arises as the terminal branch of the posterior cord of the brachial plexus within the axilla of the upper limb.^[4] It is primarily formed by contributions from the anterior rami of spinal nerves C5 and C6, though occasional contributions from C7 may occur.^[2] The nerve has an approximate length of 5 cm from its origin to the point of branching and a diameter of about 3 mm.^[5] From its origin, the axillary nerve emerges posterior to the axillary artery and anterior to the subscapularis muscle in the axilla.^[2] It then passes inferiorly and laterally, traversing the quadrangular space to reach the posterior aspect of the shoulder. The quadrangular space is bounded superiorly by the teres minor muscle, inferiorly by the teres major muscle, medially by the long head of the triceps brachii, and laterally by the surgical neck of the humerus.^[4] Accompanied by the posterior circumflex humeral artery and vein, the nerve winds posteriorly around the surgical neck of the humerus, positioned deep to the deltoid muscle and just inferior to the humeral head.^[6] Upon reaching the deltoid region, the axillary nerve enters the muscle belly, where it typically divides into its terminal branches near the mid-deltoid level.^[2] This positioning establishes its close association with the proximal humerus, facilitating its role in shoulder girdle innervation.^[1]

Branches

The axillary nerve divides into its two main terminal branches, the anterior and posterior divisions, typically within the quadrangular space or immediately distal to it upon entering the deltoid muscle.^[7] These terminal branches arise after the nerve has traversed the space bordered by the teres minor superiorly, the long head of the triceps medially, the surgical neck of the humerus laterally, and the teres major inferiorly.^[8] Prior to this bifurcation, the axillary nerve emits a small articular branch that penetrates the posterior capsule of the glenohumeral joint to supply its inferior and posterior aspects.^[9] This branch originates proximal to the quadrangular space and accompanies the posterior humeral circumflex artery in its course toward the joint.^[10] The anterior terminal branch courses medially and anteriorly around the surgical neck of the humerus, deep to the deltoid muscle, to reach and distribute to the anterior and middle fibers of the deltoid.^[11] In contrast, the posterior terminal branch extends posteriorly, piercing the teres minor muscle before distributing to its substance and continuing to the posterior fibers of the deltoid.^[8] From the posterior terminal branch, the superior lateral cutaneous nerve of the arm arises as a sensory division, traveling subcutaneously over the posterior aspect of the deltoid to supply the skin of the superolateral arm in the region known as the regimental badge area.^[8] The axillary nerve trunk itself lacks significant collateral branches along its course from the posterior cord of the brachial plexus up to the quadrangular space, maintaining a relatively undivided path through the axilla.^[12]

Anatomical relations

In the axilla, the axillary nerve courses posterior to the axillary artery and vein while lying anterior to the subscapularis muscle and the tendinous insertions of the latissimus dorsi muscle.^[7] This positioning places the nerve within the axillary fat pad, which envelops the axillary neurovascular structures deep to the superficial axillary fascia.^[13] The nerve's anterior branch crosses the inferolateral border of the subscapularis approximately 3 to 5 mm medial to its musculotendinous junction, maintaining close relation to the glenohumeral joint capsule during this segment.^[14] As it exits the axilla, the axillary nerve passes through the quadrangular space, bounded superiorly by the teres minor, inferiorly by the teres major, medially by the long head of the triceps brachii, and laterally by the surgical neck of the humerus.^[8] Within this space, the nerve is positioned lateral to the radial nerve and the profunda brachii artery, while its anterior branch is accompanied superiorly by the posterior circumflex humeral vessels.^[7] Around the proximal humerus, the axillary nerve winds posteriorly along the surgical neck, lying deep to the deltoid muscle and superficial to the teres minor muscle, with adjacency to the anterior and posterior circumflex humeral arteries.^[7] This course brings the nerve into intimate contact with the inferior glenohumeral joint capsule, at an average distance of about 1.1 cm from the glenoid labrum and 3.7 cm from the anteromedial tip of the coracoid process.^[15]

Variations

The axillary nerve typically arises from the posterior cord of the brachial plexus with contributions from the C5 and C6 spinal nerve roots, but variations in its formation include contributions from C5, C6, and C7 roots in approximately 20% of cases, as determined through nerve conduction studies on human cadavers.^[16] In some instances, the nerve originates as a common trunk with the radial nerve from the posterior cord, observed in 16% of upper limbs in a cadaveric dissection of 50 specimens.^[17] Communications or fusions between the axillary nerve and radial nerve are documented in cadaveric studies, with prevalence ranging from 5% to 15% depending on the population examined; for example, one study reported such connections in 8% of 100 adult cadavers, often forming a loop beneath the subscapular artery.^[18]^[19] Path anomalies are less common, including rare cases where the nerve courses anterior to the surgical neck of the humerus instead of the typical posterior path through the quadrangular space, reported in isolated cadaveric findings with an estimated prevalence below 5%.^[20] Duplication of the axillary nerve trunk has been noted sporadically in anatomical dissections but lacks large-scale prevalence data, occurring in fewer than 5% of examined specimens.^[21] Branching variations include occasional absence or hypoplasia of the superior lateral cutaneous nerve of the arm, the sensory continuation of the posterior division, though such anomalies are infrequently reported and primarily identified in case studies rather than population-level data.^[22] Additionally, variable motor branching to the subscapularis muscle occurs via the lower subscapular nerve, which arises directly from the axillary nerve in 25-57.5% of cases across cadaveric series, deviating from its more typical origin from the posterior cord.^[23]^[24] Overall, cadaveric studies indicate that anatomical variations in the axillary nerve affect 20-44% of individuals, with higher rates in the infraclavicular brachial plexus region, underscoring the diversity in human neuroanatomy.^[21]^[25]

Function

Motor functions

The axillary nerve provides motor innervation primarily to the deltoid and teres minor muscles, enabling key movements at the glenohumeral joint.^[8]^[1] The anterior branch of the axillary nerve supplies the clavicular (anterior) and acromial (middle) portions of the deltoid muscle, facilitating shoulder flexion and abduction.^[2]^[26] The posterior branch innervates the spinal (posterior) portion of the deltoid, contributing to shoulder extension and abduction.^[2]^[1] Additionally, the posterior branch innervates the teres minor muscle, which performs external rotation of the humerus and aids in stabilizing the glenohumeral joint.^[27]^[28] In shoulder abduction, the deltoid works in synergy with the supraspinatus muscle, where the initial 15–30 degrees are initiated primarily by the supraspinatus, followed by the deltoid as the primary abductor beyond this range.^[29]^[30] The axillary nerve has no autonomic or other non-motor functions.^[8]

Sensory functions

The axillary nerve provides sensory innervation primarily through its superior lateral cutaneous nerve of the arm, which emerges from the posterior division and pierces the deep fascia to supply the skin overlying the lower portion of the deltoid muscle and the upper lateral aspect of the arm. This cutaneous distribution covers the area commonly known as the "regimental badge" area, located on the inferolateral shoulder, and corresponds to the C5 dermatome with partial overlap from C6 roots of the brachial plexus. Sensory loss in this region can occur with axillary nerve injury, highlighting its role in superficial tactile sensation for the lateral shoulder.^[8]^[2]^[31] Unlike the posterior upper arm skin, which receives its primary sensory supply from the posterior cutaneous nerve of the arm arising from the radial nerve, the axillary nerve makes no major contribution to posterior cutaneous sensation in this region. This distinction underscores the axillary nerve's focused lateral distribution, avoiding overlap with the radial nerve's broader posterior coverage.^[32]^[8] In addition to cutaneous functions, the axillary nerve contributes articular sensory innervation via branches that supply the glenohumeral joint capsule and adjacent structures, including the inferior glenohumeral ligament. These articular branches, often originating from the posterior division, convey proprioceptive signals and pain sensations from the joint, enabling awareness of position and mechanical stress during shoulder movement. This sensory feedback plays a key role in maintaining shoulder joint stability by facilitating coordinated muscle responses to joint loading and positioning.^[33]^[34]

Clinical significance

Injury mechanisms

Injuries to the axillary nerve most commonly arise from traumatic events involving the shoulder, where the nerve's anatomical course through the quadrilateral space renders it susceptible to stretch or direct trauma.^[35] Anterior shoulder dislocations frequently cause axillary nerve damage due to excessive stretching as the humeral head displaces and compresses the nerve against the humeral neck or surrounding structures.^[3] The incidence of such nerve injury in anterior dislocations ranges from 9% to 65%, with the axillary nerve being the most commonly affected due to its close proximity to the glenohumeral joint.^[36] Proximal humerus fractures, particularly at the surgical neck, can lead to direct compression or laceration of the axillary nerve by bone fragments or hematoma formation.^[37] Iatrogenic injuries occur during surgical interventions around the shoulder, often from traction, retraction, or direct dissection.^[35] Procedures such as rotator cuff repairs or axillary lymph node dissections may inadvertently stretch or sever the axillary nerve, with reported overall nerve injury rates of 1-4% in shoulder surgeries, of which the axillary nerve is commonly affected.^[38]^[39] Reverse total shoulder arthroplasty also carries a risk of axillary nerve compromise due to retractor placement or excessive arm positioning during surgery.^[40] Compression syndromes represent non-traumatic causes of axillary nerve dysfunction, often involving chronic entrapment. Quadrilateral space syndrome results from compression of the axillary nerve (and sometimes the posterior humeral circumflex artery) within the quadrilateral space, typically due to fibrous bands, hypertrophy of the teres minor muscle, or space-occupying lesions like cysts.^[41] This leads to posterior shoulder pain, weakness in abduction and external rotation, and sensory deficits over the lateral deltoid.^[42] Parsonage-Turner syndrome, an idiopathic brachial neuritis, can selectively involve the axillary nerve through inflammatory demyelination or microvascular ischemia, often preceded by acute pain and followed by muscle atrophy in the deltoid or teres minor.^[43] The pathophysiology of axillary nerve injuries generally involves mechanical stretch, compression, or direct trauma, resulting in varying degrees of axonal disruption, demyelination, or ischemia.^[44] In stretch injuries, such as those from dislocations, the nerve may undergo neuropraxia (conduction block without axonal loss) or more severe axonotmesis, leading to Wallerian degeneration distal to the injury site, where the axon and myelin sheath break down over days to weeks.^[45] Complete transection (neurotmesis) from fractures or surgery causes immediate Wallerian degeneration and requires surgical intervention for potential regeneration.^[46] Ischemic mechanisms, as in compression syndromes, impair nerve perfusion, exacerbating demyelination and axonal transport failure.^[47]

Diagnosis and testing

Diagnosis of axillary nerve dysfunction begins with a thorough clinical examination focused on motor and sensory deficits in the affected shoulder. Patients typically present with weakness in shoulder abduction due to deltoid involvement and impaired external rotation from teres minor dysfunction, alongside potential atrophy of these muscles upon inspection.^[48] Specific strength testing includes resisted abduction at 90 degrees to assess deltoid power, often graded using the Medical Research Council scale, where grades below 4/5 indicate significant impairment.^[49] An external rotation lag sign, where the patient cannot actively hold the arm in maximal external rotation, helps evaluate teres minor integrity.^[48] Sensory examination involves testing light touch and pinprick over the lateral upper arm (regimental badge area), with hypoesthesia or anesthesia suggesting sensory branch involvement.^[35] Electrophysiological studies provide objective confirmation of axillary nerve injury. Electromyography (EMG) detects denervation in the deltoid and teres minor muscles, manifesting as fibrillation potentials and positive sharp waves, typically evident 2-3 weeks post-injury when Wallerian degeneration occurs.^[50] Nerve conduction studies (NCS) often reveal reduced compound muscle action potential amplitudes from the deltoid, while conduction velocities remain relatively preserved in axonal lesions, distinguishing them from demyelinating processes.^[51] These tests are most informative when performed serially, starting around 3-4 weeks after onset, to monitor for reinnervation via nascent motor unit potentials.^[48] Imaging modalities complement clinical and electrophysiological findings by visualizing structural abnormalities. Magnetic resonance imaging (MRI) is particularly valuable for detecting nerve edema, disruption, or associated soft tissue pathology, such as paralabral cysts compressing the nerve at the quadrilateral space; T2-weighted sequences highlight denervation edema in affected muscles with high signal intensity.^[37] High-resolution ultrasound enables dynamic assessment of the axillary nerve, identifying compression or focal thickening in the quadrilateral space, and is useful for guiding interventions when MRI is contraindicated.^[52] Differential diagnosis requires distinguishing axillary nerve lesions from other conditions causing similar shoulder deficits. Key alternatives include cervical radiculopathy (C5-C6), which may involve additional myotomes and radicular pain, brachial plexopathy with broader upper extremity involvement, suprascapular nerve entrapment affecting both supraspinatus and infraspinatus without deltoid weakness, and radial nerve injury featuring wrist drop absent in isolated axillary cases.^[35] Rotator cuff tears can mimic abduction weakness but spare external rotation and sensory loss.^[48] Comprehensive evaluation, integrating history, exam, and targeted testing, ensures accurate localization.^[53]

Treatment and management

The management of axillary nerve injuries prioritizes conservative approaches for milder cases, such as neurapraxia, where spontaneous recovery is common. Initial treatment involves immobilization of the shoulder for 2-4 weeks to protect the nerve, followed by physical therapy focused on restoring range of motion and strengthening the deltoid muscle through progressive exercises like pendulum swings and isometric contractions.^[35] This conservative regimen is effective for low-grade injuries, with full recovery rates of 85-100% within 6-12 months, though initial improvements in motor function may appear in 3-6 months for neurapraxic lesions.^[54] Observation with serial electromyography (EMG) monitoring every 3 months guides progression, as lack of recovery signs by 3 months may prompt escalation to surgical evaluation.^[55] Pharmacological interventions complement conservative care by addressing pain and inflammation associated with axillary nerve dysfunction. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, are first-line for reducing acute pain and swelling, while corticosteroids may be administered orally or via injection for cases of inflammatory neuritis to mitigate edema around the nerve.^[56] For persistent neuropathic pain manifesting as burning or tingling in the shoulder region, gabapentin or pregabalin is recommended, starting at low doses (e.g., 300 mg daily for gabapentin) and titrating based on response, as these agents modulate nerve hyperexcitability.^[57] These medications are typically used short-term, with multidisciplinary input to avoid side effects like gastrointestinal issues from NSAIDs or sedation from gabapentinoids.^[58] When conservative measures fail after 3-6 months, surgical interventions are indicated for moderate to severe injuries, tailored to the lesion's location and extent. Neurolysis, involving dissection and decompression of the nerve from scar tissue or compressive structures like the quadrilateral space, is preferred for entrapment or partial injuries, often yielding good functional restoration when performed early.^[55] For complete disruptions or avulsions, nerve grafting using sural nerve segments reconstructs the deficit, while nerve transfers—such as from the long head of the triceps branch of the radial nerve to the anterior branch of the axillary nerve—provide innervation to the deltoid when direct repair is infeasible, with optimal timing within 6-12 months post-injury to maximize axonal regrowth potential.^[59] Postoperative rehabilitation mirrors conservative protocols, emphasizing protected mobilization to prevent adhesions.^[46] Prognosis for axillary nerve recovery depends on injury severity, patient demographics, and intervention timing. Using the Sunderland classification, grade I (neurapraxia) and II (axonotmesis) injuries generally recover fully without surgery, whereas grades III-V (neurotmesis) require operative repair for any meaningful regeneration, with poorer outcomes in higher grades due to disrupted endoneurium or complete transection.^[60] Younger patients under 30 years exhibit better regenerative capacity, with success rates declining after age 50 due to reduced axonal sprouting and muscle atrophy.^[45] Early intervention within 6 months improves deltoid strength recovery to M4/M5 levels on the Medical Research Council scale in up to 80% of cases, while delays beyond 12 months correlate with permanent deficits.^[54]

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