Suprascapular nerve block results in a compensatory increase in deltoid muscle activity

Abstract

A balance exists between the deltoid and rotator cuff contribution to arm elevation. Both cadaver and computer models have predicted an increase in deltoid muscle force with dysfunction of the rotator cuff. The goal of the present study was to verify this phenomenon in vivo by examining the effects of paralysis of the supraspinatus and infraspinatus muscles with a suprascapular nerve block on the electrical activity of seven shoulder muscles. Electromyographic data were collected before and after the administration of the block. The block resulted in a significant increase in muscle activity for all heads of the deltoid, with a higher percentage increase noted at lower elevation angles. Although the deltoid activity was reduced as the subjects recovered from the block, even low levels of cuff dysfunction were found to result in increased deltoid activity. These results suggest that even small disruptions in the normal function of some rotator cuff muscles (e.g., due to fatigue or impingement syndrome), may result in an increase in deltoid activity. It is possible that such compensation may result in higher superior loads at the glenohumeral joint, possibly increasing the risk of tendon damage.

Introduction

During normal shoulder function, there exists a delicate balance between the forces exerted by the deltoid and rotator cuff muscles. Weiner and MacNab (1970) first suggested that an impairment of this balance was responsible for the observed decrease in subacromial space width associated with rotator cuff tears, both in vivo (Golding, 1962; Weiner and Macnab, 1970) and in cadavers (Cotton and Rideout, 1964). More recently, several X-ray studies have demonstrated that patients with full-thickness rotator cuff tears exhibit greater superior translation of the humeral head when compared to healthy controls (Deutsch et al., 1996; Paletta et al., 1997; Yamaguchi et al., 2000; Bezer et al., 2005). Additionally, simulated paralysis (Sharkey and Marder, 1995; Hurschler et al., 2000) and tears (Thompson et al., 1996; Halder et al., 2001; Mura et al., 2003) of the rotator cuff muscles in a cadaver model have also consistently resulted in an increase in humeral head superior migration.

It has been established in cadaver (Sharkey et al., 1994; McMahon et al., 1995) and computer (Magermans et al., 2004) models that reducing the contribution of the rotator cuff muscles places a higher demand on the deltoid. While the elevation moment arms of the middle deltoid and supraspinatus are very similar (Liu et al., 1997), the line of action of the deltoid is directed more superiorly. Consequently, this increase in deltoid force results in a more superiorly directed joint reaction force at the glenoid in a cadaver model (Parsons et al., 2002). This unbalanced superior force is believed to be responsible for the above-mentioned superior translation. Without proper regulation, this can result in a positive feedback loop, where damage leads to increased translation that leads to even further damage. This theoretical increase in deltoid activity has not been demonstrated in vivo.

Although the rotator cuff consists of four muscle-tendon units, the supraspinatus and infraspinatus are the most commonly injured tendons (Sher, 1999; Matsen et al., 2004). Previous work in our laboratory has focused on simulated rotator cuff dynsfunction with a fatigue model (Tsai et al., 2003; Ebaugh et al., 2006). However, one of the key problems with this approach is that it is very difficult to isolate the rotator cuff musculature. Since the suprascapular nerve innervates both the supraspinatus and infraspinatus, a pharmacological block of this nerve offers an appropriate model to better understand rotator cuff dysfunction (Colachis and Strohm, 1971; Howell et al., 1986; Kuhlman et al., 1992; Werner et al., 2006b). The aim of this study was to examine the effect of a suprascapular nerve block on shoulder muscle activity. We hypothesized that this block would result in a compensatory increase in deltoid activity, similar to what has been observed in cadaver models.