A physically fit 26-year-old man presented for evaluation of right shoulder weakness and instability. His symptoms began after starting a weight-lifting program 2 months before presentation. Exercises included repetitive military presses and leverage incline chest presses with high resistance. He initially noticed “aching and burning” at the superior and posterior aspect of the right shoulder, which gradually progressed to include shoulder weakness with overhead motion and instability. His pain interfered with sleep and was worse at the end of the day. After 4 to 6 weeks, the pain resolved, but the patient continued to have weakness and instability of his shoulder. He reported occasional faint aching and tingling sensations radiating into the proximal arm but not distal to the elbow. 

Initial examination of the musculoskeletal system revealed postural deficiency with forward-positioned head and anteriorly rolled shoulders, normal muscle bulk and tone, and no tenderness on palpation to the cervical, thoracic, or lumbar regions. Tissue texture changes and taut bands were present along the right medial border of the scapula. Examination of the right shoulder revealed a painless restricted range of motion of flexion and abduction to approximately 145° in the sagittal and coronal planes, respectively. Scapula assessment with SICK (scapular malposition, inferior medial border prominence, coracoid pain/malposition, and dyskinesis of movement) demonstrated scapular dyskinesis and prominent medial winging (Figure 1, eVideo). A positive scapular assist maneuver eased the action of full overhead abduction. Serratus anterior function, which is the primary scapular protractor, can be adequately assessed with the wall push-up.⁷ In the present case, a wall push-up further demonstrated medial scapular winging with marked prominence of the medial scapular border (Figure 2, eVideo). Neurologic examination demonstrated 5/5 strength throughout the major muscle groups of the upper extremity, including the rotator cuff. The remainder of the physical examination demonstrated grossly intact sensation to light touch, negative Spurling maneuver bilaterally, negative Hoffman test bilaterally, and grossly intact cranial nerves II through XII. 

The leading differential diagnosis was mononeuropathy of the long thoracic nerve secondary to overhead weight lifting. The expanded differential diagnosis included rotator cuff tear, SICK scapula, glenohumeral instability, SLAP (superior labral from anterior to posterior) tear, acromioclavicular disease, biceps tendonitis, Parsonage Turner syndrome (brachial neuritis, neuralgic amyotrophy), and scapular osteochondroma. Right upper extremity electromyography (EMG) and a nerve conduction study (NCS) were ordered to assess the long thoracic nerve and periscapular musculature, and standard radiographic imaging of the shoulder and scapula were ordered to rule out osseous abnormality. 

The EMG found evidence of a right long thoracic nerve injury by increased insertional activity with positive sharp waves and fibrillations in the serratus anterior on the right, which indicated active denervation. The remainder of muscles tested demonstrated normal insertional activity and motor unit action potential configuration. Results of motor NCSs of the right long thoracic, median, and ulnar nerves as well as the left long thoracic nerve were normal. No electrodiagnostic evidence of cervical radiculopathy, brachial plexopathy, or peripheral neuropathy was found in the right upper extremity. The shoulder/scapular radiographs revealed no remarkable findings. The results confirmed the diagnosis of long thoracic nerve injury resulting in scapular dyskinesis. 

A conservative treatment plan was initiated and included an active scapular physical therapy program focusing on strengthening the serratus anterior, lower-middle trapezius, and rhomboid muscles, with a focus on functional tasks with proper scapular positioning and integration of closed kinetic chain exercises. The program also included stretching of the anterior chain, specifically the pectoralis minor muscle, education on home exercises, and rib mobilization. A follow-up appointment was scheduled at 6 weeks. 

In athletes, damage to the long thoracic nerve commonly occurs when there is traction on the arm in the overhead position with the neck turned to the contralateral direction.⁸ Actions such as throwing a baseball or taking a breath during freestyle swimming may increase the risk of damage to the long thoracic nerve. The current patient’s weight-lifting program included repetitive military presses and leverage incline chest presses. Military presses require an overhead lift of weight, and it can be varied to incorporate both arms simultaneously or 1 at a time. Depending on the height of the incline, the leverage incline press can also incorporate a press movement greater than 90° from the trunk of the body. Both actions can injure the long thoracic nerve. The type of nerve injury in the current patient was classified as axonotmesis because denervation potentials were found on needle examination. However, some motor axons were still intact, indicated by a compound motor action potential found during the NCS. This finding led us to believe that the patient had a good prognosis, owing to the intact perineurium and epineurium. A good prognosis is implied with an axonotmesis nerve injury as long as the distance between the lesion site and end organ is not too long.⁹ 

A few key factors explain how we arrived at the diagnosis of long thoracic nerve injury despite the normal results on motor NCS. The EMG showed increased insertional activity with positive sharp waves and fibrillation potentials in the serratus anterior muscle. These findings are indicative of active denervation. During the NCS, the long thoracic nerve was assessed by stimulating the Erb point and recording over the serratus anterior with surface electrodes. The serratus anterior is a large muscle spanning multiple intercostal levels; therefore, it is possible that the electrodes were placed over intact endplate zones and not directly over an area of denervation. We determined that the data collected during the EMG portion of the study provided compelling evidence to confirm denervation of the long thoracic nerve, as there is no other physiologic basis for the presence of positive sharp waves and fibrillation potentials within the serratus anterior muscle. Therefore, further NCSs were deemed unnecessary for confirmation of the diagnosis. 

The long thoracic nerve originates from C5-C7. Cervical vertebrae 5-6 nerve branches pass through the scalenus medius and merge with C7 nerve branches, which travel anterior to the scalenus medius.^10-12 The path continues to pass over the first rib and then enters a fascial sheath and travels down the lateral component of the thoracic wall to the serratus anterior.^10,12,13 This long course, averaging a total length of 24 cm, is hypothesized to be a reason for an increased susceptibility to mechanical damage.¹⁴ Although it is difficult to establish a consensus on where the lesion typically occurs, one mechanism suggests a traction injury, which occurs when the long thoracic nerve exits the fascial sheath that encompasses it along the thoracic wall.¹³ Another plausible mechanism involves chronic and repetitive overhead arm raising that ends up lengthening and potentially fraying the long thoracic nerve. One study demonstrated doubling of the length of the long thoracic nerve in cadavers by putting the cadavers’ arms overhead with the head simultaneously tilted laterally away from the involved shoulder.¹ An additional mechanism involves the scalenus medius going into spasm, compressing the long thoracic nerve, and reducing conduction.¹ 

Initial treatment should involve a conservative, nonsurgical approach.⁸ The general consensus is to allow 6 to 24 months of conservative treatment, because most cases spontaneously resolve during this time.^10,15 Axonal regeneration is typically estimated to occur at a rate of 1 mm per day, but it can vary. A lack of improvement after 24 months may indicate that paralysis is permanent; in that case, surgical intervention is the best course of action.^10,15 

Rehabilitation, as in the current case, should focus on alleviating the scapular dyskinesis with proper strengthening exercises for the muscles that stabilize the scapula. Patients should also be encouraged to undergo osteopathic manipulative treatment, including correction of somatic dysfunction in the cervical, thoracic, rib, and upper extremity regions. Rib motion should be assessed with suspected exhalation dysfunction of ribs 6 to 9 (normal bucket handle motion), which could result from the impaired activation of the serratus anterior. Additional techniques include inhibition of myofascial tenderpoints along the right medial scapular border and scapular mobilization, supine pectoral traction, and thoracic mobilization to facilitate correction of postural derangement. 

Consistent follow-up with patients who have long thoracic nerve injury is necessary during the therapeutic process to maximize the potential for functional recovery. 

Although it is a rare phenomenon, an injury to the long thoracic nerve should be included in the differential diagnosis for a patient with scapular dyskinesis and medial scapular winging. If the patient also has a history of participating in activities that require repetitive motions of the arm in the overhead position, the likelihood of damage to the long thoracic nerve is greater.