Anterior shoulder instability identifying neuromotor control patterns during overhead arm motions

1 CHAPTER ONE: INTRODUCTION. “Neuromotor control is a function about which we may know a great deal but, in reality, we understand very little.” Garrett Jr & Kirkendall (2000) page 53. During dynamic arm elevation, the passive and active restraint systems at the glenohumeral joint ensured the proper alignment of the humerus within the glenoid fossa throughout the range of shoulder movements (Calliet 1981; Lephart et al 2000). Forceful and traumatic dislocation at the glenohumeral joint (GH) disrupted the structural congruency of the passive restraints and altered the force equilibriums generated primarily by the active systems. Anterior dislocation of the humeral head is common after trauma to the shoulder and occurs in ninety eight percent of patients with shoulder instability (Hayes et al 2002). Eighty three percent of patients were less than twenty years old while 20% were aged 60 and more (Rowe 1956; Gumina & Postaccini 1997; Robinson et al 2002). After a first shoulder dislocation, as much as 60% of patients sustained a re-dislocation over a 10-year period, usually when performing non-traumatic activities such as putting on their tshirt or during quick trivial overhead arm movements (Hovelius et al 1996; Robinson et al 2002; Deitch et al 2003). A high prevalence of nerve palsy was present after the first dislocation (Robinson et al 2002). Twenty-two percent of recurrent shoulder dislocations occurred among elderly patients who are less likely to be involved in overhead arm associated sports (Gumina & Postacchini 1997). Anterior Shoulder Instability – Rajaratnam B S (2007) Shoulder stabilization surgeries such as re-tensioning of the lax capsule prevented recurrent dislocations and facilitated transmission of kinesthesia and joint position signals to the brain for neuromotor control processing (Hovelius et al 1996). However, a recent Cochrane review stated that there was limited evidence to support primary surgery to prevent recurrent dislocations for patients with anterior shoulder instability (Handoll et al 2005). Despite having undergone a stabilization procedure and correction of structural deficits, of 16 adolescents patients (31%) experienced postoperative shoulder dislocation (Deitch et al 2003) while arthroscopic stabilization decreased recurrence to 5% to 22% (Lawton et al 2002). Saha (1983) was of the opinion that when there was no history of shoulder injury and when no Bankart lesion was demonstrable, recurrent shoulder dislocation occurred due to a lack of the stabilizing factors. Superimposed trauma may cause the GH joint to undergo spontaneous dislocation with or without minimal stress. Furthermore, two factors that contributed to negative outcomes after surgery other than damages to osseous restraints were the presence of multidirectional instability features and injuries to the rotator cuff muscles (Robinson et al 2002; Meehan & Petersen 2005). Poor functional return may be anticipated even after surgery if uncorrected mixed pathologies of muscle imbalances and altered muscle activation patterns are present (McAuliffe et al 1988; Sharkey & Marder 1995; McMahon & Lee 2002; Lewis et al 2004; Myers et al 2004; Morris et al 2004; Barden et al 2005). Albeit, no study has quantified neuromotor control strategies at the unstable shoulder during overhead arm motion even though studies have Anterior Shoulder Instability – Rajaratnam B S (2007) quantified defective activation patterns among patients with chronic low back and neck pain (Panjabi 1992; Hodges & Richardson 1999; Sahrmann 2002; Krishnamoorthy et al 2003; Ko et al 2003; Falla et al 2004a; Silfes et al 2005). The findings among patients with spinal disorders led to better rehabilitation programs and functional outcomes for them. Current rehabilitation strategies for patients with anterior shoulder instability (ASI) are focused mainly on strengthening of the rotator cuff and scapula-thoracic muscles after shoulder injury and surgical correction of shoulder instability (Gibson et al 2004). Understanding how quickly minimal practice of inappropriate muscle activation patterns alters the cortical maps and synaptic connections is important (Hayashi et al 2002; Falla et al 2004a & b; On et al 2004). Quantifying temporal-spatial characteristics of the muscle activation patterns at the shoulder among patients with ASI also provides an insight to how the central nervous system activates feed forward and feedback neuromotor controls to regulate GH joint stability throughout the range of arm elevation. Understanding these quantifiable evidences of altered neuromotor control strategies can lead to more effective musculoskeletal rehabilitation for better management of the unstable shoulder (van Vliet & Heneghan 2006). Rehabilitation programmes for the unstable shoulder also advocated correction of deficits in proprioception. However, neurophysiological studies highlighted that proprioceptive signal from mechanoreceptors within the labral-ligamentous junctions of the unstable shoulder were undamaged and Anterior Shoulder Instability – Rajaratnam B S (2007) maintained direct afferent neurological pathways to the cerebral cortex (Lephart et al 1994; Tibone et al 1997). The mechanoreceptor arrangement of muscle spindles and Golgi Tendon Organs (GTO) senses changes in length and force respectively during arm elevation (Nichols 2002). The central nervous system utilized signals from mechanoreceptors to co-ordinate the actions of the rotator cuff muscles and generated compressive forces in excess of 0.92 times body weight for maximal concavity compression between the humeral head and the glenoid fossa (Poppen & Walker 1976; Howell & Kraft 1991; Inman et al 1944; Itoi et al 1996; Apreleva et al 2000). Anecdotal evidence suggests that the central nervous system priority is to maximize concavity compression and restrain abnormal humeral head translation at all cost (Latash & Anson 1996; Apreleva et al 2000; Magarey & Jones 2003). However, cadaver studies not evaluate the regulatory role of the neuromotor control system during motion even though placing the unstable arm in overhead arm positions has been reported to stimulate muscle imbalances that contribute to GH joint instability (Lee et al 2000; An 2002; McMahon & Lee 2002; Labriola et al 2004 and 2005). A conceptual model of stability in the spine described by Panjabi (1992) that involved the dynamic interactions between the passive, active and neuromotor control systems can be adopted to study central nervous system of shoulder stability (Figure 1.1). Anterior Shoulder Instability – Rajaratnam B S (2007) NEUROMOTOR CONTROL SYSTEM (spinal cord and central ner vous s ystem) ACTIVE SYSTEM (muscles) PASSIVE SYSTEM (anatomical structures) (rotator cuff and periscapular muscl es including long head of biceps, pectoralis, latissmus, deltoids, trapezius , serratus anterior, rhomboids) (bone, glenoid labrum and caps ule, glenohumeral ligaments, interarticular pressure) Figure 1.1: Conceptual model of dynamic shoulder stability at the glenohumeral joint (model adopted from Panjabi M.M. The stabilizing system of the spine. 1. Function, dysfunction, adaptation and enhancement. Journal of Spinal Disorders 1992; 5/4: 383-389) Panjabi (1992) proposed that 80% of cervical spine stability was attributed to the muscular system (active system) while the ligaments, capsules and other passive structures accounted for the remaining 20%. Patients with chronic recurrent low back pain had altered anticipatory neuromotor control of their proximal spine and this adversely affected lumbar spinal stability (Hodges & Richardson 1999). Patients with chronic neck pain delayed the activation of their deep cervical flexors, contralateral sternocleidomastoid and anterior scalene muscles during neck flexion (Falla et al 2004a). The neuromotor control system subconsciously can compensate for structural deficits or local dysfunctions by activating atypical muscle patterns, synergistic muscle alliances and substitution muscle actions that create new subsets of temporary neuromotor maps (Latash & Anson 1996; Lieber & Friden 2000; Schmidt & Wrisberg 2000; O’Sullivan 2000). Anterior Shoulder Instability – Rajaratnam B S (2007) The minimally constrained ball and socket GH joint requires significant intra-socket negative pressure and GH ligament-muscle alliances to keep the humeral head centered within the glenoid fossa for stability (Howell & Kraft 1991; Bigliani et al 1996). Unlike the ligaments in the knee, the glenohumeral ligaments not have the strength characteristics to stabilize the GH joint alone. They function in concert with the dynamic shoulder stabilizers and align themselves with numerous scapulo-thoracic and rotator cuff muscles (Bigliani et al 1996). Also structurally, at least half of the glenohumeral ligaments intermingle with the rotator cuff muscles to contribute to GH joint stability (Clark et al 1990; Lippitt et al 1993; Thompson et al 1996). Atypical neuromotor control among patients with ASI during elevation was observed as altered muscle recruitment patterns included suppression of the activities of the pectoralis major, supraspinatus and subscapularis, increased peak activation of other rotator cuff muscles and delayed reflex latency of the biceps brachii (Myers et al 2004). Patients with shoulder laxity increased the magnitudes of their biceps and supraspinatus and decreased the recruitment of their pectoralis major, subscapularis, latissimus dorsi and serratus anterior during performance of throwing (Glousman et al 1988). Patients with multidirectional instability also altered the activation patterns of their deltoids and pectoralis major during arm elevation (Morris et al 2004; Barden et al 2004 & 2005). The hallmark of an intact cortical neuromotor maps is it ability to precisely inhibit and excite the agonist and antagonist Anterior Shoulder Instability – Rajaratnam B S (2007) shoulder and rotator cuff muscles throughout the range of arm movement for maximal concavity compression (Voigt et al 1998; Diederichen et al 2004). Re-establishing the appropriate actions of the dynamic shoulder stabilizers before and during shoulder motion are essential neuromotor control strategies that influence articular stability (Ide et al 1996; Hogervorst & Brand 1998; Hodges & Richardson 1999; David et al 2000). Atypical muscle activation patterns also hint towards disrupted feed forward and feedback central nervous system control mechanisms. Cadaver studies reported that failure to correct atypical muscles patterns in the unstable shoulder led to further instability (Figure 1.2). However, the identification of atypical shoulder muscle patterns among patients with ASI as they perform overhead elevation tasks has eluded us, probably due to the failure by researchers to quantify the various neuromotor control strategies the central nervous system activates in various planes and ranges of arm elevation during motion. Anterior Shoulder Instability – Rajaratnam B S (2007) GOOD STABILITY Rehabilitation + appropriate neuromotor retraining Surgical Correction + appropriate neuromotor retraining At ypical neuromotor control strategies INSTABILITY Rehabilitation Trauma Mechanoreceptor damage + Increase sensitivity of nociceptors + Atypical Neuromotor Control POOR STABILITY Surgical Correction Figure 1.2: Paradigm of shoulder instability. Even though surgical correction and rehabilitation aims to re-establish stability at the glenohumeral joint, failure to address atypical neuromotor control strategies due to altered cortical neuromotor maps will lead to further shoulder instability. When the shoulder was placed in the elevated and apprehension arm position and selected shoulder muscles mechanically stimulated, cadaver studies reported reduced infraspinatus activity and increased pectoralis major activity that together increased the anterior shear forces at the GH joint by 143% and pulled the humeral head into an unstable anterior-inferior position (McMahon & Lee 2002; Labriola et al 2005). To compensate for weakened infraspinatus in the late cocking phase of throwing, pitchers with chronic ASI increased their supraspinatus activity (Glousman et al 1988), while patients Anterior Shoulder Instability – Rajaratnam B S (2007) with generalized shoulder laxity activated peak supraspinatus activity earlier (Kronberg et al 1991). However, cadaver models indicated that increased supraspinatus activity during overhead elevation generated significant anterior directed translational or shear forces on the head of the humerus that have the potential to destabilize the GH joint (Lee et al 2000). The contradictory findings between cadaver and EMG studies reflect the importance of studying shoulder neuromotor control in vivo. Cadaver studies are unable to replicate real-world setting and not permit the study of how the central nervous system maintains GH joint stability in the presence of shoulder dysfunction. Morphological changes to muscle fibers with increased age affected shoulder muscle strength and movement speed even among the most active older person (Hughes et al 1999). The elderly above 60 years of age experienced a high recurrent shoulder dislocation rate of 22% that was not associated with participation in overhead arm sports or further damages to peripheral structures at the shoulder (Gumina & Postacchini 1997). Hence, age-related peripheral muscle skeletal changes may contribute to altered neuromotor control strategies among the elderly. The association between changes within the active and passive systems and neuromotor control is not well established even thought it is important for the development of better clinical outcomes for patients with ASI. Identifying shoulder muscle activation patterns in the different planes of arm elevation provides critical information to understand how the central nervous system establishes cortical neuromotor maps from neural signals recorded by Anterior Shoulder Instability – Rajaratnam B S (2007) 10 mechanoreceptors located at the passive and active systems. The results could lead to better shoulder rehabilitation programs and thus, better functional outcomes after acute ASI and after surgical correction of the unstable shoulder. A thorough quantification of neuromotor control strategies adopted by patients with ASI during the performance of everyday functional reaching tasks is currently lacking. The aim of this thesis was to identify the muscle activation patterns at the shoulder when patients with ASI perform everyday overhead tasks in two planes of arm elevation. Their results were compared with healthy young and elderly subjects to evaluate confounding factors that may influence GH joint stability during overhead arm motions. Anterior Shoulder Instability – Rajaratnam B S (2007) 142 Figure 6.5 Schematic of the principles of inverse and forward dynamics musculo-skeletal models (from Chadwick & van der Helm 2003. Musculo-skeletal modeling of the shoulder. Proceeding at the ISB 2003: Shoulder biomechanics tutorial) The present study chose the forward dynamics musculoskeletal model to predict joint reaction forces due to muscle contractions in the overhead arm position. Experimental studies cannot replicate this extreme arm position accurately due to the fear of re-dislocating the shoulder. Moreover, conducting such an experimental study would be unethical as it compromise patient’s safety. The forward dynamic musculoskeletal model provides predictable values of joint reactions forces at the GH joint for improved patient care. Anterior Shoulder Instability – Rajaratnam B S 2007 143 6.4.2 Predicting forces generated by the supraspinatus and infraspinatus at the overhead arm position. Cadaver studies indicated that as the joint moved into the overhead and apprehension positions, some muscles generated large translational (shear) forces that have the potential to dislocate the unstable shoulder (Hugh & An 1996; Lee et al 2000; Lee & An 2002; McMahon & Lee 2002; Labriola et al 2005). However, results of cadaver studies were found to be significantly different to EMG data during performance of overhead functional tasks such as throwing. Cadaver studies reported decreased activation of the infraspinatus and an increased recruitment of pectoralis major in the overhead arm position (McMahon & Lee 2002; Labriola et al 2005). The unrestrained muscle imbalance on cadavers resulted in anterior translation of the humeral head and decreased concavity compression. However, athletes with shoulder instability decreased their activation of infraspinatus and pectoralis major between 150º-180º of arm elevation in the cocking phase of throwing when compared with asymptomatic athletes (Glousman et al 1988; McMahon et al 1996). The different muscle activation patterns compared with cadaver studies may have been regulated by neuromotor control systems that minimize the risk of shoulder re-dislocation. Thus, cadaver studies cannot quantify neuromotor control strategies. EMG studies, on the other hand, can quantify atypical neuromotor control strategies adopted to maintain joint stability when anatomical deficits exist. Anterior Shoulder Instability – Rajaratnam B S 2007 144 The present study like others made reasonable assumptions that the internal force magnitudes of the selected shoulder muscles were proportional to their physiological cross-sectional area (Poppen & Walker 1978; Labriola et al 2004). The force magnitude of each muscle can be estimated by multiplying its predicted maximal muscle force with the ratio of the recorded EMG in the various phases of arm elevation (Labriola et al 2004). The lines of action of muscles not change with muscle tension. Recorded EMG is compared with maximal muscle tension that is a constant (32.2N/cm2) derived from previous studies (Wuelker et al 1998). Therefore, the predicted joint reaction forces exerted by the supraspinatus and infraspinatus were calculated by the formulae: Predicted Joint Reaction Forces of a muscle = PCSA x maximal muscle tension x EMG activation at various ranges of arm elevation This basic assumption was supported by the finding that increased posterior deltoid and psoas major EMG activities at the shoulder and hips respectively were associated with increased joint reaction forces at the hip (Ringelberg 1985; Gatton et al 1999). The PCSA values in Table 2.2.2, force values in Table 2.2.5 and the maximal muscle tension constant of 32.2N/cm2 allowed comparison of force magnitudes of the infraspinatus and supraspinatus with results of other similar studies (Table 6.4). Anterior Shoulder Instability – Rajaratnam B S 2007 145 Table 6.4: Force magnitudes (in N) of the supraspinatus and infraspinatus during elevation in coronal plane (data compiled from Labriola et al 2004; Glousman et al 1988; Hughes & An 1996; McMahon et al 1996). Muscles Force magnitude (N) Elevation 90º abd @90°abd & max ER (predicted) 120º 150º +180° (predicted) *App #Max 60 175 49 723 Supraspinatus (PCSA=5.21 cm-2) Anterior Shoulder Instability 61.3 71.4 43.2 34.4 23.4 Control Young 66.7 38.2 37.8 50.3 36.9 Infraspinatus -2 (PSCA=9.51 cm ) Anterior Shoulder Instability 199.0 266.3 199.6 195.9 160.2 Control Young 20.6 170.6 28.3 24.5 21.6 *App=Apprehension position or 60º of glenohumeral abduction, 30º of scapulothoracic rotation and maximal external rotation. # max isometric strength in scapular plane; @ late cocking phase of throwing. The maximal magnitude of the two dynamic shoulder stabilizers among patients and subjects in the present study were less than their maximal isometric values reported by Hughes & An (1996). The differences may be because the measurement of muscle forces in the present study were during motion while the latter study measured muscles activities during isometric maximal contraction. Maximal magnitudes of both muscles occurred at 90° of arm elevation in the present study, which concurred with findings of others that concavity compression peaked at this range (Apreleva et al 2000). After 90º arm elevation, the resultant joint reaction forces decreased to 0.4 times body weight (Poppen & Walker 1978). The present study also found similar trends as Anterior Shoulder Instability – Rajaratnam B S 2007 146 the predicted infraspinatus and supraspinatus forces at 180º of elevation was significantly less than the forces generated at 90º of arm elevation. Reduction of rotator cuff muscle magnitudes by 50% resulted in less concavity compression and a 46% increase in anterior displacement of the humeral head (Wuelker et al 1998). The findings of the present study imply that the GH joint is vulnerable to instability in the upper quadrant of overhead arm elevation due to less active dynamic stabilizers. The current findings reflect the importance of rotator cuff muscles activities at the end ranges of arm elevation. Strong rotator cuff muscle actions in this vulnerable arm position compressed the humeral head into the glenoid concavity to provide stability and resist humeral head translation (Lippitt & Matsen 1993; Illyes & Kiss 2005). Amateur pitchers generated the greatest force at the GH joint in the overhead arm position just before they explosively released the ball (Gowan et al 1987). However, only 40% of compressive forces of the rotator cuff muscles will resist humeral head translation (Matsen et al 1991). Using Matsen et al (1991) calculated model, the compressive forces of the supraspinatus and infraspinatus at 180º of elevation in the present study among patients with ASI would be less than 0.14 times body weight. The low glenohumeral compressive force in the overhead arm position partially explains why patients with ASI are more likely to re-dislocate their unstable shoulder when performing spontaneous and effortless functional tasks such as putting on a t-shirt or when they raise their hand overhead during sleep. Thus, atypical muscle patterns generated by poor neuromotor control contribute to further shoulder instability. Anterior Shoulder Instability – Rajaratnam B S 2007 147 The predicted results of asymptomatic subjects in the present study confirmed that the supraspinatus contributes to stability at the higher ranges of arm elevation (Kuechle et al 2000; Graichen et al 2001). However, obligatory arm external rotation of an unstable shoulder reduced the GH joint dynamic stability index (Lee et al 2000). Repetitive external rotation and increased supraspinatus activities in the overhead arm position also increases the incidence of supraspinatus tendonitis and subacromial impingement. One-third of patients with ASI in the present study demonstrated positive Neers and Hawkins special tests that reflected impaired perfusion of the supraspinatus tendon at its muscle-tendon junction (Nakajima et al 2004). With repetitive overhead activity, joint laxity, muscle weakness, atypical shoulder muscle patterns and pseudoparesis would develop and contribute to the pathoetiology of multidirectional instability (Janda 1986; Barden et al 2005). However, the increase activity of the infraspinatus in the vulnerable apprehension arm position increased concavity compression by 96% and raised the dynamic stability index from 13% to 41% (Lee et al 2000). The results of the present study suggest that rehabilitation for patients with ASI should include strengthening the infraspinatus in the upper quadrant of arm elevation (Baeyens et al 2001), and less emphasis should be placed on strengthening the supraspinatus. This strategy may increase the GH joint stability in the vulnerable overhead arm position among patient with unstable shoulders. Anterior Shoulder Instability – Rajaratnam B S 2007 148 Thus, the unstable glenohumeral joint behaved in a similar manner to the lumbar spine as both joints are vulnerable to instability when they experience high mechanical loads and/or low muscle activities (Cholewicki & McGill 1996). Greater supraspinatus activity increases the mechanical load on the GH joint and if concurrent muscle weakness of the infraspinatus and the internal rotators exist, re-dislocation could occur during performance of trivial functional tasks. The results of the present study provide further support to the view that maximal activation of the infraspinatus during overhead arm performances has profound positive effects to maintain GH joint stability in the unstable shoulder (Lee et al 2000). Anterior Shoulder Instability – Rajaratnam B S 2007 149 Objective 3: To determine if altered muscle activation patterns at the GH joint during overhead reaching tasks were confounded by peripheral factors associated with aging such as muscle atrophy and decline in joint proprioception. 6.5 Differences in peak muscle magnitudes with increase age. The present study found that older asymptomatic subjects’ peak muscle magnitudes at the GH joint were similar to younger asymptomatic subjects, although the literature indicated that they demonstrate clinical features of decrease shoulder muscle strength, atypical muscle imbalances, and muscle activation patterns (section 2.3). One likely reason is the present study investigated a functional task that placed a minimal or sub-maximal biomechanical demand on shoulder muscles. The only exception was older subjects demonstrated less supraspinatus muscle activity compared to the asymptomatic young. The results indicated that morphological changes due to age were not confounding factors that influenced activation of atypical shoulder muscle patterns during arm elevation. Thus, age-related changes in muscle morphology did not account for the reported high rate of shoulder recurrent dislocation among individuals 60 years and older. Rather, the high incidence of rotator cuff tears among the elderly with shoulder dysfunction would be a more likely source that led to muscle weakness and Anterior Shoulder Instability – Rajaratnam B S 2007 150 imbalances, particularly in the overhead positions. This hypothesis requires further investigation. 6.6 Limitation. One of the limitations of the current study was the capturing capacity of the data collection system. The system could only capture a maximum of seven muscles at any one time even though more than 25 muscles are involved in shoulder elevation. We would like to have evaluated the activation patterns of more muscles, particularly the antagonist muscles of the selected current muscles. Other researchers chose these seven muscles too and thus our results were compared with these studies (Poppen & Walker 1978; Glousman et al 1988; Kronberg et al 1991; McMahon et al 1996; David et al 2000; Cools et al 2003; Myers et al 2004; Alpert et al 2000; Morris et al 2004; Barden et al 2005). The experiment design could not exclude soft tissue artifacts that would influence the calculation of humeral axial rotation. As peripheral landmarks not correspond accurately to the axis of joint articulation, the axial rotation of the humerus was underestimated by as much as 35% by Cutti and colleagues (2005). To obtain accurate kinematic data, invasive techniques to secure electrodes on body landmarks have been proposed. Such techniques would generate more confounding factors including pain due to the insertion of these invasive electrodes that would alter the natural movement and activation patterns of the upper limb muscles during arm elevation. Anterior Shoulder Instability – Rajaratnam B S 2007 151 Furthermore, patients are unlikely to participate in any experimental studies that heighten their risk of re-dislocating their unstable shoulders. Thus, the present experimental set-up did not force patients with unstable shoulder into the overhead arm position. Cadaver studies indicated that maximal arm elevation was associated with at least 35º of external rotation to clear the humeral tuberosity from beneath the acromion (Browne et al 1990). Shoulder external rotation greater than 67.5º encouraged the supraspinatus and infraspinatus to generate significant superior and anterior directed shear forces that dislocated the GH joint (Lee et al 2000). Our 3-D pilot study found that the maximal obligatory external rotation during both planes of arm elevation was less than 50° and theoretically unlikely to destabilize the GH joint. Therefore, the experimental protocol was safe and captured natural arm movement. The predicted model of joint reaction forces at the GH joint in the overhead arm position is modeled on physiological features of each muscle’s PCSA. The model does not consider altered lines of muscle action that occurs with increased arm elevation. Researchers tend to assume that EMG temporal and magnitude data account for these variables (Labriola et al 2004). The current model is thus a simplified predictive computation of joint reaction forces at the GH joint by two important rotator cuff muscles. Finally, ASI is a multi-factorial pathological condition. Our assessments indicated that approximately a third of patients with ASI have positive signs of subacromial Anterior Shoulder Instability – Rajaratnam B S 2007 152 impingement syndrome with fewer numbers showing symptoms of biceps tendonitis. The incidence of shoulder impingement among the patients with ASI in the current study was higher than the 18% reported by Rafii and colleagues (1988). This may be attributed to the different selection criteria of patients by the two studies. The present study also took the precaution of not including patients with severe shoulder pain and deficits in external rotation to minimize the likelihood of including shoulder pain as a confounding factor that is known to influence neuromotor control. Thus, the patterns of neuromotor control presented by patients with ASI in the present study are accurate reflection of underlying biomechanical factors directly associated with GH joint stability. 6.7 Clinical implications. The findings of the present study recommend that during rehabilitation and after surgical stabilization procedures, patients with ASI should be guided to rectify their atypical temporal shift in shoulder muscles activation patterns early and before strengthening the shoulder muscles. Motor relearning programs rectify neuromotor control of intact feedback mechanism from the passive and active stabilizers and normalize temporal characteristics of shoulder muscle onset and peak magnitude patterns. However, strengthening the supraspinatus in the overhead arm position would amplify anterior humeral translation, and decreases the activity of the infraspinatus that would led to less concavity compression (Wuekler et al 1998; Otis et al 1994; Lee et al 2000; Labriola et al 2005). Rehabilitation should focus on selectively strengthened the Anterior Shoulder Instability – Rajaratnam B S 2007 153 infraspinatus and subscapularis to facilitate posterior translation of the humeral head for better GH joint stability during arm elevation. Selective, strengthening programs performed in the functional elevated positions would also reinforce typical neuromotor recruitment patterns. Other proposed strategies include facilitating co-activation and synergistic actions of the shoulder muscles throughout the ranges of arm elevation, and introducing novel and functional upper limb activities that stimulate neuromotor control (Nyland et al 1998; Swanik et al 2002). Early rectification of atypical neuromotor control strategies after ASI and surgical correction of shoulder instability may also limit the development of secondary shoulder complications and recurrent shoulder dislocations. 6.8 Future directions. The present study is the first to quantify the temporal and magnitude characteristics of muscle activation patterns among patients with ASI during performance of overhead arm motion. Comparisons were performed with asymptomatic aged matched younger and older subjects and patients with mild upper limb hemiparesis after stroke. The EMG results of the present study utilized forward dynamics modeling to predict the joint reaction forces at the GH joint by two important dynamic shoulder stabilizers in the overhead arm position. Anterior Shoulder Instability – Rajaratnam B S 2007 154 Two possible future studies could be: 1. To correlate the amount of translation of the humeral head during arm elevation among patients with ASI with their EMG muscle activation patterns. An opencoil magnetic resonance imaging would measure humeral head translation before and after surgical correction of a Bankart lesion. Anatomical data together with kinematic and muscle activation patterns would provide important dynamic biomechanical data to develop a comprehensive neuromotor control model of the unstable shoulder (Veeger et al 2004). The model could indicate if surgery and rehabilitation has re-established typical neuromotor control strategies for better outcomes. 2. Recent biomechanical models of the shoulder have acknowledged the importance of the special role of the rotator cuff muscles and shoulder prime movers to direct joint reaction forces into the glenoid, to stabilize and constrain the GH joint movement, to provide feed forward and feedback for typical neuromotor control and more (Veeger et al 1997; van Vliet & Heneghan 2006). The relationship between proprioception and joint stability in the pathological shoulder has not been studied in detail and should be explored further. Altered proprioception is likely to influence feed forward and feedback mechanisms associated with neuromotor control. Studies could also explore inter-subject differences in neuromotor control of GH joint stability and could ultimately lead to the development of more effective shoulder rehabilitation programs. Anterior Shoulder Instability – Rajaratnam B S 2007 155 CHAPTER SEVEN: CONCLUSION The conclusions of the present study are: 1. Arm elevation performed in the sagittal or coronal planes adopted a common neuromotor control strategy that simplified shoulder control, probably by freezing the degrees of freedom at the GH joint (Bernstein’s redundancy theory) and developing common patterns of muscle alliances (Kelso’s dynamical systems theory). 2. Different neuromotor control strategies were activated throughout the ranges of arm elevation to match the biomechanical changing demands and priorities at the GH joint during motion. In the lower ranges of arm elevation, temporal characteristics of muscle onsets were pre-programmed to activate a “stability before mobility” strategy. GH dynamic stabilizers were activated early and some even before initiation of arm elevation, probably to compensate for limited scapula excursion. The mechanical demand of the mid-range of elevation activated a “stability at all cost” strategy as peak activations of all selected shoulder muscles occurred in this range. Both strategies have been described for the first time based on accurate EMG data of unconstrained arm elevation among patients with ASI and compared with asymptomatic Anterior Shoulder Instability – Rajaratnam B S 2007 156 aged match subjects. The present study also found that the teres major could perform a novel role as a dynamic shoulder stabilizer among patients with unstable shoulders. 3. Age-related morphological changes did not influence the above two- named neuromotor control strategies. However, patients with mild hemipareis demonstrated different and unpredictable neuromotor control strategies compared to patients with ASI during arm elevation. 4. When the present EMG data at 1500 of arm elevation was transposed to predict joint reaction forces at the GH joint at the overhead arm position, it was found that infraspinatus activities were calculated to be significantly more active than the supraspinatus among patient with ASI compared to asymptomatic aged match subjects. In this position, rotator cuff muscle activities were also significantly less among patients with ASI. 5. The predicted compressive forces generated by the weak dynamic shoulder stabilizers would be insufficient to maintain concavity compression and negate shear forces that are directed outside the effective glenoid arch in the overhead arm position. The low level of rotator cuff muscle activities predicted in the overhead arm position may explain why trivial but sudden arm rotations such as reaching over your Anterior Shoulder Instability – Rajaratnam B S 2007 157 head during sleep and taking your t-shirt off can re-dislocate the shoulder of patients with ASI. The main clinical implication of the present findings is that rehabilitation programs should focus on rectifying temporal and magnitude characteristics of shoulder muscles early after injury and after surgical intervention. Selective muscle strengthening programs for patients participating in rehabilitation and after surgical stabilization procedures should commence after correction of atypical temporal muscle activation patterns. This opinion has been expressed, but not proven with scientific evidences. The present study is the first published evidence to support this clinical opinion based on altered temporal EMG data of muscle activation onsets and times of peak activities among selected shoulder muscles of patients with ASI. Muscles are important “sensors of the joint instability.” More evidence-based clinical investigations of the unstable shoulder could improve our understanding of neuromotor control at the complex shoulder joint. This may ultimately lead to the development of rehabilitation programs that will minimize the likelihood of shoulder redislocation after a Bankart lesion. “Central nervous system ‘knows’ how to develop and control movement with respect to unconstrained multi-joint movements whereas we are just starting to formulate viable hypothesis in this field” Latash & Anson (1996) page 59. Anterior Shoulder Instability – Rajaratnam B S 2007 [...]... further injury However, repetitive overhead activities by the unstable shoulder elicit inappropriate neuromotor control strategies that alter shoulder muscle activation patterns that further destabilized the shoulder joint Anterior Shoulder Instability – Rajaratnam B S (2007) 29 2.2 Muscle alliances at the shoulder joint The central nervous system regulates the neuromotor control system to create synergisms... shoulder musculature to perform explosive and injury free shoulder elevation motions Anterior Shoulder Instability – Rajaratnam B S (2007) 12 The following discussions are limited to the kinematics of the scapula and, the translation and rotation actions of the humeral head within the glenoid fossa during arm elevation 2.1.1 Scapula kinematics During elevation, the scapula rotates and tilts about its... continuously during motion and through the rull range of arm elevation in the clinical setting The GH:ST relationship also varied when there were deficits to the passive and active systems of the shoulder When suprascapular nerve blocks paralyzed the supraspinatus and infraspinatus, the scapula rotated more than normal (McCully et al 2006) Patients with shoulder instability also Anterior Shoulder Instability. .. stability angle implies that typically shoulder muscles regulate safe humeral translation during arm elevation (Figure 2.1.4) However, strong contraction of a muscle such as pectoralis major when the arm in placed in the apprehension position would generate a large anterior humeral translation outside the balance stability angle (McMahon & Lee 2002) Anterior Shoulder Instability – Rajaratnam B S (2007)... the shoulder during arm elevation, the muscle alliances at the shoulder joint, and the effects of increased age and changes after stroke on muscle morphology 2.1 Biomechanics of shoulder elevation More than 30 muscles coordinate the synchronized actions of the sternoclavicular, acromioclavicular, GH and scapulothoracic (ST) joints to produce smooth and efficient shoulder motions in various planes of arm. .. presence of altered shoulder muscle activations in the apprehension position among patients with atraumatic shoulder instability may explain why they commonly experience shoulder dislocation in this position (Eisenhart-Rothe et al 2002) In the same study, patients who experienced shoulder instability due to trauma recruited the dynamic stabilizers to recenter their humeral head in the overhead arm position... the glenoid fossa minimizes the mechanical energy required to stabilize the GH joint during arm elevation (Saha 1983, Cheng 2005) Hence, any change to scapula excursion during arm elevation would require more humeral axial rotation for joint stability through range (Saha 1983, Karduna et al 2000) Anterior Shoulder Instability – Rajaratnam B S (2007) 13 Figure 2.1.1: Schematic representation of the... nervous system 45% of Anterior Shoulder Instability – Rajaratnam B S (2007) 23 the superior glenohumeral ligament, 42% of the middle glenohumeral ligament and 48% of the inferior glenohumeral ligament have mechanoreceptors (Guache et al 1999) The properties of the different types of shoulder joint mechanoreceptors have been extensively studied (Table 2.1.1) Anterior Shoulder Instability – Rajaratnam... the shoulder s position sense (Janwantanakul et al 2001) However, capsular laxity initiates abnormal muscle activation patterns that resulted in excessive humeral translation during forceful throwing actions in the vulnerable overhead position (Myer & Lephart 2002) The administration of lidocaine to paralyze the shoulder muscles elicited inappropriate muscle activation patterns that led to signs of shoulder. .. controversy associated with shoulder instability Studying the excursion of the ST and GH joints during unrestricted arm motions provides insight to how the central nervous system maintains shoulder joint stability by: a Altering scapulo-humeral rhythm to generate a safe and effective concavity compression zone between the glenoid and the humerus; b Coordinating the activity of shoulder musculature to perform . Albeit, no study has quantified neuromotor control strategies at the unstable shoulder during overhead arm motion even though studies have Anterior Shoulder Instability – Rajaratnam B S (2007). the neuromotor control system during motion even though placing the unstable arm in overhead arm positions has been reported to stimulate muscle imbalances that contribute to GH joint instability. to evaluate confounding factors that may influence GH joint stability during overhead arm motions. Anterior Shoulder Instability – Rajaratnam B S (2007) 11 CHAPTER TWO: REVIEW OF THE LITERATURE.