Surgical Restoration of Shoulder Function in 270 Patients With Scapulothoracic Abnormal Motion (STAM, Type 3) due to Serratus Anterior Palsy

Background Scapulothoracic abnormal motion (STAM) describes any abnormal scapular position or movement that results in pain and dysfunction, commonly referred to as dyskinesia or scapular winging. These abnormalities may arise from musculoskeletal, neurological, or genetic etiologies. Subtype 3 (STAM 3) is characterized by weakness and functional impairment of the serratus anterior (SA) muscle, typically due to injury of the long thoracic nerve (LTN) and the brachial plexus upper trunk (BPUT). Objectives Reporting on our experience in surgical restoration of STAM 3 in 270 patients with serratus anterior palsy. Patients and Methods We report outcomes of surgical decompression and microneurolysis of the LTN and BPUT in 270 STAM 3 patients unresponsive to prior interventions. The average time between the onset of injury and surgery was 3.8 years. Results STAM 3 was fully corrected in 194 shoulders (70%), while 80 (29%) recovered well with minimal winging after surgery (a mean follow‐up of 1 year; range 3 months to 9 years). The extent of the scapular winging (ESW) grading scale (range 1–4) significantly improved postoperatively to a median score of 4 (IQR = 3‐4) from the preoperative median score of 2 (IQR = 1‐2). Two hundred and seventy‐four of 278 STAM 3 (99%) had excellent or good improvement. The overall improvement in shoulder forward flexion and abduction (mean 169° ± 24° and 167° ± 27°) after surgery was statistically significant compared to the preoperative mean of 127 ± 41° and 122 ± 42°, respectively ( p < 0.0001). Conclusions Decompression and microneurolysis of the LTN and BPUT reduced the severity of STAM 3 and/or improved active shoulder range of motion in 99% of patients (274 of 278 shoulders). We demonstrate that the extent of internal and external microneurolysis maintained the BPUT and LTN healthy in their course to supply the serratus anterior muscle and its function by improving the axonal transport of the cofounding neurotrophic factors and motor signals from the cerebral cortex.