Axillary Nerve Palsy: Causes, Symptoms, and Acupuncture Treatment

Axillary nerve paralysis is a clinical syndrome resulting from injury or compression of the axillary nerve due to various causes, leading to paralysis of the muscles and cutaneous nerves within its innervation territory.

The axillary nerve arises from the distal portion of the posterior cord of the brachial plexus, originating from spinal nerves C5–C6. It initially courses posterior to the axillary artery, then descends around the surgical neck of the humerus from behind, and passes anteriorly between the humerus and the deltoid muscle. The axillary nerve gives off an articular branch to innervate the shoulder joint capsule and muscular branches to the deltoid muscle. The deltoid originates from three parts: the anterior part from the lateral third of the clavicle, the middle part from the acromion of the scapula, and the posterior part from the inferior border of the scapula. All muscle fibers converge to insert onto the deltoid tuberosity in the middle portion of the humerus. Contraction of the anterior part flexes the arm forward, the middle part abducts the arm to the horizontal level, and the posterior part extends the arm backward. Additionally, the axillary nerve innervates the teres minor muscle, which assists in external rotation of the arm. The superior lateral cutaneous nerve of the arm (a branch of the axillary nerve) supplies the skin over the deltoid muscle and the lateral and posterior aspects of the arm.

The main causes of axillary nerve palsy include: shoulder joint dislocation, humeral fracture injury or local hematoma compression, trauma to the shoulder joint capsule, gunshot wounds, blunt or sharp instrument injuries causing tearing of the shoulder joint capsule, and suppurative inflammation of the shoulder joint capsule, all of which can lead to axillary nerve palsy.

Diagnostic Key Points

When the axillary nerve is paralyzed, the arm is unable to perform movements such as horizontal abduction, forward extension, or external rotation. The upper limb hangs downward, the shoulder joint loses its tension, the acromion is notably depressed, and skin sensation over the deltoid region is markedly diminished. In later stages, atrophy of the deltoid muscle occurs.

Treatment

1. Acupoints and Acupuncture Techniques

1. LI16 (Jugu) (affected side): Located in the depression between the acromial end of the clavicle and the scapular spine. Use a 30-gauge, 2-cun filiform needle; routinely disinfect the local area. Insert obliquely toward the shoulder joint to a depth of approximately 1.8 cun. Needle.

Sensation: Localized distending pain.

2. LI15 (Jianyu) (affected side): Located in the upper part of the deltoid muscle, between the acromion and the greater tubercle of the humerus. When the arm is abducted to a horizontal position, two depressions appear; the point lies in the anterior depression. Use a gauge-30, 2-cun filiform needle. After routine local disinfection, insert obliquely toward the elbow to a depth of approximately 1.8 cun. Needling sensation: local distension and pain, or a radiating sensation toward the elbow.

**3. SI9 (Jianzhen) (Affected Side):** Located posterior and inferior to the shoulder joint, 1 cun above the posterior axillary crease when the arm is adducted. Using a 30-gauge, 2-cun filiform needle, after routine local disinfection, insert perpendicularly toward the shoulder joint to a depth of approximately 1.8 cun. Needle sensation: local distension and pain.

4. **LI14 (Binao)** (affected side): Located on the line connecting LI11 (Quchi) and LI15 (Jianyu), 7 cun above LI11 (Quchi), at the lower border of the deltoid muscle. Use a 0.30 mm × 50 mm (gauge 30, 2 cun) filiform needle. Perform routine local disinfection. Insert perpendicularly toward the axilla to a depth of approximately 1.8 cun. Needling sensation: local distension and pain.

II. Methods

The patient is seated. The above acupoints are needled following the appropriate method and connected to electrical stimulation. The needles are retained for 40 minutes and then removed. Cupping (fire cupping) is applied for about 1 minute. The treatment is administered once daily, with 10 sessions constituting one course of treatment. After a 5-day rest, the next course is begun.

Commentary

For such patients, electroacupuncture combined with the above method yields good results, particularly in promoting faster and better recovery of atrophied scalene and deltoid muscles. For those with muscle atrophy and shoulder joint laxity, a longer course of treatment is required, yet the therapeutic outcome remains quite satisfactory. During treatment or after recovery, patients should be advised to perform shoulder and neck exercises regularly, which can help accelerate the recovery of atrophied muscles.

Etiology and Mechanisms of Axillary Nerve Palsy

Axillary nerve palsy arises from a spectrum of axillary nerve palsy causes, predominantly involving traumatic injury or compressive neuropathy. The nerve’s anatomical course—winding around the surgical neck of the humerus—renders it highly vulnerable in shoulder dislocations, proximal humeral fractures, and direct blows to the deltoid region. Iatrogenic damage during shoulder arthroscopy, open reduction of fractures, or intramuscular injections into the deltoid comprises a significant subset of causes. Less frequent etiologies include prolonged compression from crutch use, nerve entrapment at the quadrilateral space, or stretch injuries during violent arm abduction. Systemic conditions such as brachial neuritis, diabetes mellitus, and vasculitic neuropathies are occasional contributors. The axillary nerve primarily innervates the deltoid and teres minor muscles, along with a cutaneous branch supplying the regimental badge area over the lateral shoulder. Disruption of these motor and sensory fibers leads to characteristic deficits. Understanding these diverse causes is essential for targeted prevention, especially in athletes, trauma patients, and surgical candidates. Early identification of the specific mechanism—whether neuropraxia, axonotmesis, or neurotmesis—guides subsequent management strategies.

Clinical Manifestations and Diagnostic Evaluation

Patients present with hallmark axillary nerve palsy symptoms that reflect both motor and sensory loss. The most prominent motor deficit is inability to abduct the arm beyond the first 15–30 degrees due to deltoid weakness, though supraspinatus function may partially compensate. Atrophy of the deltoid muscle often becomes visible within weeks. Strength in external rotation is reduced because of teres minor involvement. Sensory disturbances manifest as numbness, paresthesia, or hypoesthesia over the lateral shoulder region—the regimental badge area. These symptoms may be subtle in early stages, delaying diagnosis. A thorough neurological examination includes manual muscle testing of deltoid and teres minor, assessment of external rotation strength with the arm adducted, and sensory mapping of the axillary nerve’s cutaneous territory. Electromyography and nerve conduction studies are crucial for confirming the diagnosis, localizing the lesion, and distinguishing axillary nerve palsy from C5–C6 radiculopathy or suprascapular nerve injury. Magnetic resonance imaging may reveal denervation changes in deltoid or teres minor and can identify structural causes such as hematomas or quadrilateral space syndrome.

Therapeutic Interventions and Prognostic Outcomes

Management of axillary nerve palsy is tailored to the severity and etiology of the injury. Conservative axillary nerve palsy treatment is the mainstay for neuropraxic lesions and includes rest, activity modification, and physical therapy focusing on maintaining passive range of motion and preventing shoulder stiffness. As recovery progresses, strengthening exercises for deltoid and teres minor are introduced. Surgical intervention—nerve decompression, neurolysis, nerve grafting, or tendon transfer—is indicated for complete axonal disruption, persistent deficits beyond 3–6 months, or progressive deterioration. Prognosis strongly depends on the nature of the injury. Axillary nerve palsy recovery time varies widely: for mild axonotmetic injuries, functional improvement often occurs within 4–6 months, while severe neurotmetic injuries may require 12–18 months or longer, with incomplete recovery possible. Close serial follow-up with electrodiagnostic studies and muscle strength assessments guides prognosis. Patient education regarding realistic expectations and adherence to rehabilitation protocols is critical to optimize outcomes. Multidisciplinary care involving neurologists, orthopedic surgeons, and physiotherapists offers the best chance for restoring shoulder function.