UNASSIGNED: Traumatic injury to the long thoracic nerve causes paralysis of the serratus muscle, clinically expressed as winged scapula and functional impairment of the shoulder girdle. Treatment varies according to the severity of the injury, with a focus on early intervention for best results; however, the therapeutic approach remains a challenge at present.
UNASSIGNED: We present the case of a 32-year-old male patient, athlete, right-handed, presented with bilateral paresis predominantly in the right arm, associated with paresthesia and changes in the coloring of the upper limbs. After being diagnosed with Thoracic Outlet Syndrome and undergoing surgery, vascular symptoms persisted with a significant loss of strength in the right shoulder. Winged scapula was observed and structural lesions were excluded on magnetic resonance imaging. Electromyographic studies confirmed the presumption of traumatic nerve involvement of the long thoracic nerve. Notwithstanding 6 months of physical therapy, there was no improvement, so a nerve transfer from the thoracodorsal nerve to the right long thoracic nerve was chosen. At 12 months, complete resolution of the winged scapula and functional recovery were observed. The patient also experienced a decrease in preoperative pain from 5/10 to 2/10 on the visual analog scale.
UNASSIGNED: Nerve transfer from the thoracodorsal nerve to the long thoracic nerve is a safe and effective technique to treat winged scapula due to long thoracic nerve injury.

BACKGROUND: Two main hypotheses have been proposed for the pathophysiology of long thoracic nerve (LTN) palsy: nerve compression and nerve inflammation. We hypothesized that critical reinterpretation of electrodiagnostic (EDX) studies and MRIs of patients with a diagnosis of non-traumatic isolated LTN palsy could provide insight into the pathophysiology and, potentially, the treatment.
METHODS: A retrospective review was performed of all patients with a diagnosis of non-traumatic isolated LTN palsy and an EDX and brachial plexus or shoulder MRI studies performed at our institution. The original EDX studies and MR examinations were reinterpreted by a neuromuscular neurologist and musculoskeletal radiologist, respectively, both blinded to our hypothesis.
RESULTS: Seven patients met the inclusion criteria as having a non-traumatic isolated LTN palsy. Upon reinterpretation, all of them were found to have findings not consistent with an isolated LTN. On physical examination, three of them (43%) presented with weakness in muscles not innervated by the LTN. Four of them (57%) had additional EDX abnormalities beyond the distribution of the LTN. Five of them (71%) had MRI evidence of enlargement of nerves or denervation atrophy of muscles outside the innervation of the LNT, without evidence of compression of the LTN in the middle scalene muscle.
CONCLUSIONS: In our series, all 7 patients, originally diagnosed as having an isolated LTN, on reinterpretation, were found to have a more diffuse muscle/nerve involvement pattern, without MR findings to suggest nerve compression. These data strongly support an inflammatory pathophysiology.