American Society for Peripheral Nerve

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Computational Biomechanical Study of the Contributions of Posterior Deltoid and Teres Minor to Shoulder Strength and Function
Dustin L. Crouch, BS; Johannes F. Plate; Zhongyu Li, MD, PhD; Katherine R. Saul, PhD
Wake Forest School of Medicine, Winston Salem, NC, USA

Neurotmesis injury of the axillary nerve paralyzes the deltoid and teres minor muscles and substantially weakens the shoulder. Nerve transfer has emerged as an alternative to traditional nerve graft repair, even though posterior deltoid and teres minor are left paralyzed following nerve transfer. Therefore, the objective of this study was to determine how persistent paralysis of posterior deltoid and teres minor may adversely affect shoulder strength and function. We used a generic computational musculoskeletal model representing the upper limb of a 50th percentile adult male. The model included the muscle properties and origin-to-insertion paths of 32 muscles and muscle compartments crossing the shoulder and elbow. We determined the relative contributions of posterior deltoid and teres minor to 1) maximum joint strength during a simulated static strength assessment, and 2) joint moments generated during simulations of abduction, extension against 5 lbs resistance, and external rotation against 5 lbs resistance. Movement simulations were performed with and without paralysis of posterior deltoid and teres minor to determine whether other non-paralyzed muscles could biomechanically compensate for their paralysis. Muscle forces and activations produced during movement simulations were assumed to minimize metabolic effort. Teres minor and posterior deltoid collectively accounted for approximately 15% of the total maximal shoulder extension and external rotation strength generated during the static strength assessment. During the three movement simulations, posterior deltoid produced less than 20% of the mean shoulder extension joint moments, while teres minor accounted for less than 5% of all shoulder joint moments. When posterior deltoid and teres minor were paralyzed, joint moments generated by supraspinatus, the long head of triceps, latissimus dorsi, and middle deltoid increased to compensate. Muscles that compensated for posterior deltoid and teres minor paralysis were not fully activated, suggesting that the shoulder had additional capacity to compensate during tasks demanding greater strength. Our simulation results suggest that posterior deltoid and teres minor are lesser contributors to maximal and sub-maximal tasks. Therefore, nerve transfer may be a biomechanically suitable alternative to nerve graft repair even when posterior deltoid and teres minor are left paralyzed. More extensive peripheral nerve injury at the shoulder may limit the ability of the shoulder musculature to compensate for weakened or paralyzed muscles. Nerve graft repair may be preferred if shoulder extension strength is severely reduced. Quantifying the biomechanical role of muscles during maximal and sub-maximal tasks can inform pre-operative planning and permit more precise predictions of functional outcomes.


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