Suprascapular nerve anatomy during shoulder motion: a cadaveric proof of concept study with implications for neurogenic shoulder pain

Background prascapular nerve (SSN) carries sensory fibers which may contribute to shoulder pain. Prior anatomic study demonstrated that alteration in SSN course with simulated rotator cuff tendon (RCT) tears cause tethering and potential traction injury to the nerve at the suprascapular notch. Because the SSN has been implicated as a major source of pain with RCT tearing, it is critical to understand nerve anatomy during shoulder motion. We hypothesized that we could evaluate the SSN course with a novel technique to evaluate effects of simulated RCT tears, repair, and/or release of the nerve. s urse of the SSN was tracked with a dual fluoroscopic imaging system in a cadaveric model with simulated rotator cuff muscle forces during dynamic shoulder motion. s a simulated full-thickness supraspinatus/infraspinatus tendon tear, the SSN translated medially 3.5 mm at the spinoglenoid notch compared to the anatomic SSN course. Anatomic footprint repair of these tendons restored the SSN course to normal. Open release of the transverse scapular ligament caused the SSN to move 2.5 mm superior-posterior out of the suprascapular notch. sion ilot study demonstrated that the dynamic SSN course can be evaluated and may be altered by a RCT tear. Preliminary results suggest release of the transverse scapular ligament allowed the SSN to move upward out of the notch. This provides a biomechanical proof of concept that SSN traction neuropathy may occur with RCT tears and that release of the transverse scapular ligament may alleviate this by altering the course of the nerve.