long thoracic nerve damage scapular winging

Clinical answer with reasoning, red flags and references. Clinically reviewed by Dr Kola Tytler MBBS CertHE MBA MRCGP.

Posted: 23 June 2026Updated: 23 June 2026 Clinically Reviewed
Dr Kola Tytler MBBS CertHE MBA MRCGPClinical Lead • iatroX

Causes

Long thoracic nerve (LTN) injury leading to scapular winging is most commonly caused by dysfunction of the LTN, which innervates the serratus anterior muscle. The primary aetiologies include spontaneous neuritis (often linked to Parsonage-Turner syndrome or amyotrophic neuralgia), blunt chest trauma, iatrogenic injury during surgeries like thoracic outlet decompression or breast surgery, compressive neuropathy at anatomical entrapment sites such as the scalenus muscle or serratus anterior fascia, and less commonly sharp nerve lacerations or prolonged pressure, such as long anesthesia in lateral decubitus position. Additionally, involvement due to muscular dystrophies like facioscapulohumeral dystrophy can present with bilateral involvement. Causes are varied, including viral illnesses, allergic drug reactions, overexertion, and autoimmune mechanisms ,.

Clinical Features

Patients with LTN injury typically present with weakness of shoulder elevation and protraction, and notable prominence of the medial border of the scapula during movement resulting in scapular winging. The characteristic signs include inability to raise the arm properly due to serratus anterior palsy, abnormal scapular kinematics with increased internal rotation and anterior tilt, and medial scapular border prominence especially on resisted forward flexion or protraction. Physical examination tests such as the boxer punch test, shoulder flexion resistance test at varying angles (30°, 60°, and 100°), and the scapular assistance test can help assess serratus anterior strength and function. Unlike other causes of scapular dyskinesia, in LTN injury, scapular winging is primarily due to serratus anterior paralysis while trapezius function remains intact. Electromyography (EMG) with nerve conduction studies (NCS), targeting specifically the LTN and periscapular muscles, may confirm the diagnosis but can occasionally be falsely negative, requiring adjunctive imaging such as MRI to detect serratus anterior atrophy or fatty infiltration ,.

Management Options

Conservative: Initial management consists of physical therapy focused on restoring shoulder range of motion, strengthening the trapezius, rhomboids, and serratus anterior muscles, as well as preventing secondary contractures of muscles like the pectoralis minor. Bracing to maintain scapular position can provide symptom relief. Due to the natural history, spontaneous recovery of serratus anterior function frequently occurs within 6 months to 2 years, particularly in inflammatory or traumatic neuropathies; thus, a nonoperative treatment period of 12–18 months is advised initially ,.

Surgical: Surgery is indicated in patients with persistent disabling symptoms after adequate conservative therapy or with documented nerve laceration. Surgical options include neurolysis to decompress the nerve, nerve transfer (e.g., thoracodorsal or intercostal nerves to reinnervate serratus anterior), and, in chronic cases with significant muscle atrophy or failed nerve surgery, tendon transfers. The current preferred tendon transfer is the direct transfer of the sternal head of the pectoralis major muscle to the inferior pole of the scapula, which provides dynamic scapular stabilization and improves shoulder function. This technique avoids graft interposition and reduces recurrence of winging. Postoperative immobilization followed by structured rehabilitation is essential. Scapulothoracic arthrodesis remains a salvage procedure for failed tendon transfers or specific muscular dystrophies ,.

In summary, LTN injury resulting in scapular winging presents clinically with medial scapular winging and shoulder weakness, is diagnosed chiefly by specific physical tests and EMG/NCS, and initially managed with physical therapy and bracing. Surgery is reserved for refractory cases, with neurolysis, nerve transfer, and tendon transfer tailored to stage and severity of palsy ,.

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