Get The Elbow Up?


#1

A couple of days ago I got a question about whether a pitcher should be told to get his elbow up. I responded in this article that I think this is questionable advice…

Palo20 then PM’ed me and said that he thought that I was misinterpreting the nature of the question (which I took as being related to arm slot) and the logic behind the cue to “get your elbow up.” As I understand Palo20’s point, his thought is that the goal of the cue is to solve the problem where pitchers drop their elbows too far below the level of their shoulders. Kind of like this…

I guess I see the logic in this, because I do think that a pitcher’s elbow can be both too high and too low, but I have a couple of concerns…

  1. I very rarely see the above kind of elbow dropping, except in the youngest kids.

  2. I am concerned that the cue could be misinterpreted and lead to problems with pitchers getting their elbows too high.

As I have said before, I think a pitcher’s elbow should be just below the level of their shoulders; no higher, and no lower.

What do y’all think?


#2

[quote]As I have said before, I think a pitcher’s elbow should be just below the level of their shoulders; no higher, and no lower.

What do y’all think? [/quote]

I disagree. Otherwise you would have to conclude that all of these pitchers suffered from “poor mechanics”…


#3

In each of these photos, the pitcher’s elbow is actually below the level of their shoulders because their shoulders are tilted.


#4

Sorry folks but I have to ask the same question I’ve asked before.

When?
If you’re speaking of the acceleration phase of the arm, that’s related to shoulder tilt. If you’re speaking of the cocking phase, that’s another discussion altogether and we’ve had that one many times.

Also, how?

Chris, I don’t believe you are speaking of the tilt of the shoulders causing this. I posted before about this. Are you talking of the elbow being high relative to the acromial line, regardless of shoulder tilt? Or, are you talking about the elbow being higher than the shoulders because of shoulder tilt?

Clarity on the definition of this is critical to any meaningful discussion. Let’s make sure we’re all on the same page.


#5

It’s mostly, but not entirely related to shoulder tilt. In some cases pitchers have their elbows above the level of their shoulders after the acceleration phase and through the release point.

For example, I think that Steven Ellis did this and believe it is related to his shoulder problems (due to something called impingement syndrome). I have also seen this in scouting videos (that I unfortunately can’t share).

I agree, and that’s part of the problem with the cue to “get your elbow up”. It can be interpreted in many different ways.

I much prefer cues like “Tilt your shoulders.”


#6

So, do have it right that you believe that tilting the shoulders can cause shoulder impingement?


#7

i undertand what you mean by that even though i think glavine isn’t completly following a straight line, i don’t think it’s enough to be considered a problem.

making a M with your elbows is in my opinion asking for rushing problems since your forearm is staying down longer and people starting to turn their shoulders with a forearm not completly vertical but more orizontal is putting extra stress on his elbow since the elbow will bend backward a lot harder and further which can help for velocity (reason why pitchers doing it throw faster?) but will totally blow up your elbow in no time.

that’s why i think chris makes sense in his statements

exemple of what i’m trying to say:


#8

I’m with DM on this. I’d like to know when we’re talking about. To determine the potential for injury I think we need to know what parts of the body are involved and what they’re doing. So, is the humerous in external rotation or internal rotation? Is it in abduction or adduction? Is the elbow in flexion or extension? Or are we talking about the transition between internal and external rotation, between abduction and adduction, between flexion and extension?

Can we narrow this down to something more specific?


#9

Based on your description, I would say the shoulder would be the concern - not the elbow - since I believe the “bend backward” you’re talking about is really the external rotation of the upper arm (aka humerous). The elbow doesn’t really change its position at this point.

But this just proves my point in my previous post. Things can sound good yet really be meaningless if left too vague. We have to be very specific for this discussion to have meaning. IMHO, of course.


#10

No.

Tilting the shoulders prevents impingement.

I believe that impingement is caused (in part) by trying to get the PAS elbow up without tilting the shoulders; by taking the PAS elbow above the level of the shoulders.


#11

[quote=“4pie”]making a M with your elbows is in my opinion asking for rushing problems since your forearm is staying down longer and people starting to turn their shoulders with a forearm not completly vertical but more orizontal is putting extra stress on his elbow since the elbow will bend backward a lot harder and further which can help for velocity (reason why pitchers doing it throw faster?) but will totally blow up your elbow in no time.

that’s why i think chris makes sense in his statements

exemple of what i’m trying to say:

[/quote]

Exactly.

Notice how in the Wagner video that his shoulders start to turn…

  1. While his elbow is above the level of his shoulders.

  2. While his PAS forearm is horizontal.

Kerry Wood also does the second thing, and I think that is the root cause of his problems.


#12

I’ll be the first to admit that, while I think I have a good understanding of the root cause of shoulder problems, I have yet to find a good pattern when it comes to elbow problems.


#13

there is nothing that stretches in the elbow (tendon, muscles) while the forearm bounce back in the pitching motion? I would find it hard to believe.

the arm is like a wrecking ball the further you start it the more damages it causes.


#14

[quote=“Chris O’Leary”][quote=“4pie”]making a M with your elbows is in my opinion asking for rushing problems since your forearm is staying down longer and people starting to turn their shoulders with a forearm not completly vertical but more orizontal is putting extra stress on his elbow since the elbow will bend backward a lot harder and further which can help for velocity (reason why pitchers doing it throw faster?) but will totally blow up your elbow in no time.

that’s why i think chris makes sense in his statements

exemple of what i’m trying to say:

[/quote]

Exactly.

Notice how in the Wagner video that his shoulders start to turn…

  1. While his elbow is above the level of his shoulders.

  2. While his PAS forearm is horizontal.

Kerry Wood also does the second thing, and I think that is the root cause of his problems.[/quote]

EXACTLEY what is the root cause of his shoulder problems??? Not as in “he opens his shoulders to early” but moreso what does this do that puts stress on his shoulder? Where does this extra stress come from? Where EXACTLEY is it at? I want the names of the tendons, ligaments,muscles this effects not just some “notion” thats totally 100% meaningless and without proof which is all you have ever served up. In other words “WHERES THE BEEF CHRIS”?


#15

Here’s the current version of my theory.

The supraspinatus muscle, which is the muscle that is initially responsible for abducting the upper arm, is the one that is most frequently injured by pitchers. I don’t think it’s a coincidence that I have found that a state of hyperabduction (which is achieved using the Supraspinatus) is very often related to rotator cuff problems.

I am not sure what the exact mechanism is, but I believe that it could be related to impingement of the superior portion (top) of the Supraspinatus on the inferior portion (undersurface) of the Acromion.

http://www.exrx.net/Muscles/Supraspinatus.html


#16

[quote=“Chris O’Leary”]The supraspinatus muscle, which is the muscle that is initially responsible for abducting the upper arm, is the one that is most frequently injured by pitchers. I don’t think it’s a coincidence that I have found that a state of hyperabduction (which is achieved using the Supraspinatus) is very often related to rotator cuff problems.

I am not sure what the exact mechanism is, but I believe that it could be related to impingement of the superior portion (top) of the Supraspinatus on the inferior portion (undersurface) of the Acromion.[/quote]
I must say that I’m somewhat impressed by this. Yes, I did say that. 8) And yes, the supraspinatus HELPS in abducting the upper arm. Let’s add the middle deltoid to that.

Generally, the common cause of impingement written about is instability, not so much hyperabduction because of the supraspinatus but that would be a factor. Much is written about the problem being common in overhand actions, like throwing or tennis serves.

Now, on the instability front, you must take everything into account. For example, my son had impingement affecting his supraspinatus (I need a shorter name for that muscle). The root cause was determined to be a “winging scapula” caused by a weak serratus anterior. This instability was corrected by physiotherapy and he’s been fine ever since. So, let’s not forget scapular instability as a “root cause” of shoulder impingement.

Chris, you are correct about shoulder impingement being an issue but I’m not seeing the root cause being because of the particular mechanical features you’ve been describing. I recall reading somewere that Mike Marshall has even said that it’s impossible to hyper abduct the humerus above the acromial line. One has to rotate the humerus in the glenoid before it can go above that line.

So, my “theory” is that shoulder / rotator cuff issues are caused by instability or misalignment of the humerus in the glenoid during the throwing motion more than any mechanical flaw.

Geesh!! I think I kind of agreed with you here Chris. I gotta go lie down now and recover.
:lol:


#17

Heres a piece that should be of interest to all aspiring pitchers. Bottom line is pitching a baseball is a risk no matter what anybody says!

Rotational adaptation: Humeral head retroversion in throwing athletes.
Biomechanics; 4/1/2003; Chant, Chris B.

Search for more information on HighBeam Research for biomechanics of baseball pitching.

Byline: Chris B. Chant, MSc

The rotational stress placed on the shoulder while throwing a baseball is tremendous. During a normal overhead throw, the internal rotators and adductors of the shoulder generate large amounts of energy, which act on the humerus to forcefully rotate the shoulder internally from a position of abduction and extreme external rotation. In pitchers, during the cocking phase of throwing, the shoulder may be externally rotated as much as 180[degrees].1,2 During the acceleration phase, which begins when the shoulder is at maximal external rotation and ends at ball release, internal rotation can reach a peak angular velocity close to 7000[degrees]/sec and has been shown to be as high as 9000[degrees]/sec in professional major league pitchers.1,3 This translates into 80[degrees] of rotation occurring in as little as 30 ms.3 Elite pitchers can impart a velocity close to 160 km/h on a ball at the time of release, after which eccentric muscular forces completely stop arm motion within approximately 350 ms.1,3 Compressive forces on the shoulder averaging 1090 N have been reported during deceleration of the arm.4

Because the mechanics of pitching are repetitive and easily reproduced, most throwing studies have focused on the biomechanics and structural adaptations of the shoulder in elite pitchers. However, players at every position on the baseball field are required to throw a ball. Thus, arm and throwing strength are important to any successful player. Although pitchers spend more time overall throwing the ball, all players spend a considerable amount of time throwing before games and during practices.

As a result of greater repetitive stress being placed on one shoulder than the other, athletes who participate in overhead sports such as baseball and tennis display different flexibility patterns between their dominant and nondominant upper extremities.5-10 Much of the literature on this topic focuses on the decreased internal rotation found in the stroke arm of highly skilled tennis players compared to the nonstroke arm. Within this population, the loss of internal rotation seems to be progressive and correlates with increasing age and number of years of tournament play.7

Large differences in external and internal rotation between dominant and nondominant arms have also been demonstrated in baseball pitchers at both the professional and collegiate levels.5,6,8,10 In addition to the side-to-side differences in shoulder range of motion seen in pitchers, Brown and colleagues also reported increased external rotation and decreased internal rotation in the dominant arms of position players at the major league level compared to their nondominant, nonthrowing arms.8

Most investigators have deduced that these adaptations in glenohumeral flexibility occur as a result of changes in the soft tissue in and around the shoulder.6,8,10 The general belief has been that the increased external rotation results from stretching of the anterior capsule and glenohumeral ligaments, and that the decreased internal rotation results from tightening of the posterior capsule and surrounding musculature. However, recent studies of team handball players11 and baseball players5,12 suggest that an osseous adaptation, in the form of increased retroversion of the humeral head, may contribute to the different flexibility patterns of the throwing arm. In theory, a larger angle of retroversion would allow greater external rotation before the anterior capsule and glenohumeral ligaments limit additional movement. By the same token, a larger angle of retroversion would result in less internal rotation since the humeral head would be limited by the posterior capsule earlier in the throwing cycle. Such an osseous adaptation, along with changes in soft tissue, may indeed contribute to the differences in side-to-side ROM seen in throwing athletes.

Biomechanics

The overhead baseball pitch can be divided into five distinct phases: windup, arm cocking, arm acceleration, arm deceleration, and follow-through. The relative torques, forces, and muscle activity surrounding the shoulder during the wind-up and follow-through phases are relatively low.2,4 Most of the mechanical stress on the shoulder occurs during the arm cocking, arm acceleration, and arm deceleration phases of the baseball pitch.

The arm-cocking phase begins at the end of the windup and continues until the shoulder is at maximal external rotation. As the thrower drives the lead (stride) leg forward to generate momentum toward the desired target, the shoulder begins to horizontally abduct and externally rotate while the elbow remains in a flexed position. By the time the stride foot makes contact with the ground, the arm has been abducted to approximately 90[degrees] and is in an externally rotated position. The hips, trunk, and shoulders then rotate toward the target, and the trunk extends. As the upper body is turning toward the target, the throwing arm continues to externally rotate. Just prior to maximal shoulder external rotation, large shoulder internal rotation torques are generated. The internal rotators of the shoulder are eccentrically loaded during this period, as they are producing a substantial internal rotation torque on the proximal humerus while the upper arm, forearm, hand, and ball are still externally rotating.4

At the end of the arm-cocking phase, the combination of glenohumeral rotation, scapulothoracic rotation, and trunk extension result in the throwing arm achieving a maximal shoulder external rotation of 150[degrees] to 180[degrees].1,2 The extreme external rotation of the shoulder, coupled with 90[degrees] to 100[degrees] of abduction and significant horizontal extension at maximal shoulder external rotation, is thought to result in anterior capsule laxity and associated anterior instability.13 Although capsular laxity and shoulder instability may seem unfavorable to most athletes, it has been suggested that the extreme external rotation achieved during the pitching motion may be necessary for the performance of elite throwers.4 Specifically, the greater the maximal external rotation of the shoulder, the larger the angle over which the throwing athlete can accelerate the upper arm and ball prior to release.4

The arm-acceleration phase starts when the humerus begins to internally rotate about the shoulder and ends at the time of ball release. This is an extremely powerful and explosive part of the throw lasting less than 0.1 seconds.2 At the initiation of this phase, the trunk begins to flex from its previously extended position. The shoulder internal rotators continue to contract, now concentrically, to help produce an extremely high maximal internal rotation velocity, often close to 7000[degrees]/sec. Dillman3 reported a mean maximal angular velocity of 6940[degrees]/sec plus/minus 1080[degrees]/sec for internal rotation of the shoulder in 29 elite throwers. This maximal internal rotation velocity occurs just before the end of the arm acceleration phase (i.e., at ball release) while the shoulder is still at approximately 90[degrees] of abduction, as it has been throughout the entire phase.1,4

Arm deceleration begins at ball release. The primary purpose of this phase is to comfortably decelerate the throwing limb using eccentric muscular forces, which will completely stop arm motion within approximately 350 ms.1 During the first 50 ms after ball release, a vigorous active deceleration force is generated by the biceps and muscles of the posterior shoulder girdle while the shoulder continues to move into a position of horizontal flexion and internal rotation.1 Compressive forces placed on the shoulder while decelerating the arm have been reported to average as much as 1090 N in elite throwers.4

The final phase of the overhead throw, the follow-through, can be described as a passive phase, during which the body is merely catching up with the arm.

Musculoskeletal changes in athletes

In sports that require greater use of the dominant arm than the nondominant arm, there is overwhelming evidence demonstrating a number of different dominance-specific musculoskeletal changes in athletes. Greater muscle hypertrophy of the dominant arm compared to the nondominant arm is quite common in overhead sports such as tennis and baseball.8-10 Increased bone density and bone size in the one upper extremity compared to the other has also been documented for many athletes and has been related to both static and dynamic forces.14,15

A variety of different mechanical forces have been shown to affect the growth and development of the dominant humerus in athletes participating in overhead sports.15 Krahl14 presented evidence of an increase not only in bone density and diameter, but also in longitudinal bone growth in the stroke arms of 20 high-ranking professional tennis players. They attributed these adaptations to mechanical stimulation and hyperemia of the constantly strained extremity and thus regarded them as biopositive adaptations.

Neuromuscular disorders

Osseous changes due to imbalances in muscle size and strength are evident in many neuromuscular disorders. For instance, deformation of the femoral head in individuals with cerebral palsy has recently been attributed to specific disease-related muscular forces and pressures.16 Beck and colleagues16 reported on three case studies in which the muscle and tendon of the gluteus minimus caused lateral notching of the femoral head by hindering its migration out of the acetabulum.

Osseous deformities involving the glenohumeral joint have been associated with Erb’s palsy.17 Specifically, posterior displacement of the humeral head is quite common in these patients, who have a persistent brachial plexus palsy. The overall deformity of the joint has been found to progress with age during the growing years.18 Thus, evidence supports the theory of muscular forces affecting the growth and development of bone generally and of the humerus specifically.

Effects of muscular forces on humeral torsion

Krahl19 demonstrated the effects of muscle on the torsion of the humerus as early as 1947. In that paper, Krahl discussed the differences in humeral torsion observed between individuals with different-sized muscles and provided evidence that this torsion is subject to change during growth and until maturity. He suggested that there is a hereditary primary genetic torsion as well as a secondary torsion brought about by muscular forces acting above and below the proximal humeral physis. He felt that contraction of the internal and external rotators of the humerus caused a turning of the humeral shaft with respect to the proximal humeral epiphysis, directing the growth of the bone in a spiral fashion. Krahl also suggested that the torsion angle increases (retroversion decreases) by approximately 10[degrees] during childhood and adolescence, finally stabilizing at approximately age 20, coinciding with skeletal maturity.19 Thus, it is plausible that the increased humeral retroversion found in the dominant arm of many competitive baseball players occurred at the proximal physis as a result of repetitive throwing practice during adolescence.

The adolescent thrower

Due to the unique aspects of the developing skeleton, the effects of repetitive throwing on adolescents are not well understood. The weakest part of growing bone is the physis. Thus, although the adolescent athlete is vulnerable to the same injuries as the adult, the presence of the physis changes the patterns of injury. A mechanical stress that would cause injury to the soft tissue in an adult may fracture the physis in the adolescent.20 Fractures through the proximal physis in young baseball players are not uncommon and have been attributed to repetitive throwing of long duration and high frequency.21,22

Dotter22 first described Little Leaguer’s shoulder. He believed that pitching caused a fracture through the proximal physis of the humerus in a 12 year-old baseball player. Since this time there have been numerous case reports describing Little Leaguer’s shoulder, which is characterized by pain when pitching and is associated with widening of the epiphyseal plate shown on radiographic analysis.21,23

Barnett23 described this condition as being an inflammatory response and identical to adolescent capital femoral epiphyseolysis. It has been shown that an inflammatory process within the physis can have different and unpredictable effects on the linear growth of bone.24 Because as much as 80% of humeral length has been shown to occur at the proximal physis,25 and because the throwing athlete subjects this area to such high loads, it is not unreasonable to suspect some sort of osseous adaptation in the area of the proximal humeral physis in response to the same forces that can lead to injury.

Summary

Three major factors point toward humeral bone growth being shaped by the repetitive forces placed on the arm during the throwing motion. First, bone growth has been shown to increase in an athlete’s dominant arm due to consistent stress from sporting events.14,15 Second, the torsion angle of the humerus changes throughout the growth period, but stops once skeletal maturity is reached.19 Finally, rotational stress applied to the proximal humeral physis during throwing has been linked to changes in growth plate cartilage, such as Little Leaguer’s shoulder and widening of the physis.21-23 Therefore, it is reasonable to postulate that increased humeral head retroversion could be produced in athletes who frequently practice pitching prior to skeletal maturity.

Recognizing the possibility of osseous changes will aid in the prevention of throwing injuries. A lack of flexibility in the shoulder is often cited as being a cause of chronic shoulder pain. Stretching techniques are often prescribed to decrease tightness in the posterior capsule and surrounding musculature and to gain back some of the lost internal rotation that results from the repetitive microtrauma to the dominant shoulder of the throwing athlete. However, Pieper11 reported that the throwing arm of international handball players with chronic shoulder pain did not exhibit the increased humeral head retroversion that was present in those not suffering from chronic pain. He suggested that those athletes who do not undergo an osseous adaptation to the repetitive stress of overhead throwing have more strain on their anterior capsules with less external rotation and develop chronic shoulder pain due to anterior instability. Hence, the shoulder pain of athletes who do not exhibit an increase in humeral retroversion may not be relieved by stretching of the posterior capsule, and the possibility of underlying anterior instability should not be ignored.

Evidence of an osseous contribution to the loss of internal rotation should be taken into consideration during clinical evaluations of these athletes, and stretching of the shoulder complex should be closely monitored and individualized for each athlete. This knowledge could prove helpful in training prescriptions as well as in the treatment and prevention of injury.

Chris Chant, MSc, is a first-year medical student at The Flinders University of South Australia in Adelaide. Previously, he was a clinical kinesiologist at Physiotherapy One/Physiotherapy 2000 in Mississauga, ON.

References

  1. Pappas AM, Zawacki RM, Sullivan TJ. Biomechanics of baseball pitching: a preliminary report. Am J Sports Med 1985;13(4):216-222.

  2. Jobe FW, Tibone JE, Perry J, Moynes D. An EMG analysis of the shoulder in throwing and pitching: a preliminary report. Am J Sports Med 1983;11(1):3-5.

  3. Dillman CJ, Fleisig GS, Andrews JR. Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther 1993;18(2):402-408.

  4. Fleisig GS, Barrentine SW, Escamilla RF, Andrews JR. Biomechanics of overhand throwing with implications for injuries. Sports Med 1996;21(6):421-437.

  5. Kawamura S, Katsunori S, Yoshimoto H. Ultrasonographic evaluation of the humeral retroversion in baseball players: a correlation between range of motion and the humeral retroversion. Paper presented at the Japan Shoulder Society 25th Annual Meeting, Tokyo, October 1998.

  6. Bigliani LU, Codd TP, Connor PM, et al. Shoulder motion and laxity in the professional baseball player. Am J Sports Med 1997;25(5):609-613.

  7. Kibler WB, Chandler TJ, Livingston BP, Roetert EP. Shoulder range of motion in elite tennis players: effect of age and years of tournament play. Am J Sports Med 1996;24(3):279-285.

  8. Brown LP, Niehues SL, Harrah A, et al. Upper extremity range of motion and isokinetic strength of the internal and external shoulder rotators in major league baseball players. Am J Sports Med 1988;16(6):577-585.

  9. Chinn CJ, Priest JD, Kent BE. Upper extremity range of motion, grip strength, and girth in highly skilled tennis players. Phys Ther 1974;54(5):474-483.

  10. King JW, Brelsford HJ, Tullo HS. Analysis of the pitching arm of the professional baseball pitcher. Clin Orthop Rel Res 1969;67:116-123.

  11. Pieper H-G. Humeral torsion in the throwing arm of handball players. Am J Sports Med 1998;26(2):247-253.

  12. Makiuchi D, Tsutsui H, Mihara K, et al. The glenoid version and humeral head torsion in baseball players. Paper presented at the Japan Shoulder Society 25th Annual Meeting, Tokyo, October 1998.

  13. Dugas RW. Anterior shoulder subluxation in the throwing athlete. Orthopedics 1991;14(1):93-95.

  14. Krahl H, Michaelis U, Pieper H-G, et al. Stimulation of bone growth through sports: a radiologic investigation of the upper extremities in professional tennis players. Am J Sports Med 1994; 22(6):751-757.

  15. Qu X. Morphological effects of mechanical forces on the human humerus. Brit J Sports Med 1992;26(1):51-53.

  16. Beck M, Woo A, Leunig M, Ganz R. Gluteus minimus-induced femoral head deformation in dysplasia of the hip. Acta Orthop Scand 2001;72(1):13-17.

  17. Beischer AD, Simmons TD, Torode IP. Glenoid version in children with obstetric brachial plexus palsy. J Pediatr Orthop 1999;19(3):359-361.

  18. Waters PM, Smith GR, Jaramillo D. Glenohumeral deformity secondary to brachial plexus birth palsy. J Bone Joint Surg 1998;80-A(5):668-677.

  19. Krahl VE. The torsion of the humerus: its location, cause, and duration in man. Am J Anat 1947;80:275-315.

  20. Ireland M, Hutchinson MR. Upper extremity injuries in young athletes. Clin Sports Med 1995;14(3):533-569.

  21. Carson WG Jr, Gasser SI. Little Leaguer’s shoulder: a report of 23 cases. Am J Sports Med 1998;26(4):575-580.

  22. Dotter WE. Little leaguer’s shoulder: a fracture of the proximal epiphyseal cartilage of the humerus due to baseball pitching. Guthrie Clin Bull 1953;23:68-72.

  23. Barnett LS. Little league shoulder syndrome: proximal humeral epiphyseolysis in adolescent baseball pitchers. J Bone Joint Surg 1985;67-A(3):495-496.

  24. Skerry TM. The effects of the inflammatory response on bone growth. Eur J Clin Nutr 1994;48(Suppl 1):S190-S198.

  25. Pritchett JW. Growth plate activity in the upper extremity. Clin Orthop Rel Res 1991;(268):235-242.

Copyright [c] 2003 CMP Media LLC

COPYRIGHT 2003 All rights reserved. No part of this information my be reproduced, republished or redistributed without prior written consent of CMP Media Inc


#18

Here’s the current version of my theory.

The supraspinatus muscle, which is the muscle that is initially responsible for abducting the upper arm, is the one that is most frequently injured by pitchers. I don’t think it’s a coincidence that I have found that a state of hyperabduction (which is achieved using the Supraspinatus) is very often related to rotator cuff problems.

I am not sure what the exact mechanism is, but I believe that it could be related to impingement of the superior portion (top) of the Supraspinatus on the inferior portion (undersurface) of the Acromion.

HERES THE REAL SKINNY! wHAT YOU HAVE SURMISED IS NO SECRET BY ANY MEANS CHRIS. YOU DIDNT STUMBLE ONTO ANYTHING NEW WHATSOEVER. IN FACT YOU ARE WAY BEHIND WHAT THESE PEOPEL ALREADY KNOW. PAY CLOSE ATTENTION TO WHAT THE SCAPULA IS DOING CHRIS.

http://www.exrx.net/Muscles/Supraspinatus.html

http://en.wikipedia.org/wiki/Supraspinatus_muscle[/quote]Campagnolo, MD, MS , Director of Multiple Sclerosis Clinical Research, Investigator, Staff Physiatrist, Barrow Neurology Clinics, St Joseph’s Hospital and Medical Center

Disclosure

INTRODUCTION Section 2 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

Background: In 1834, Smith wrote the first description of a rupture of the rotator cuff tendon. Since then, with the work of such authors as Duplay, Von Meyer, Codman, and, more recently, Neer, degenerative changes to the rotator cuff have been better characterized; however, the exact mechanisms leading to the degeneration of the rotator cuff still are debated today. Moreover, despite numerous trials, questions still exist about the efficacy of different therapeutic modalities for rotator cuff disease. With the help of better methodology for studies, more successful treatment of degenerative rotator cuff disease can be expected.

Pathophysiology: The pathophysiology of rotator cuff degeneration is a controversial topic that still is not fully understood. Two hypotheses (ie, extrinsic, intrinsic) coexist and are supported by different authors.

The extrinsic hypothesis
In this theory, the lesion results mainly from repeated impingement of the rotator cuff tendon against different structures of the glenohumeral joint. The following 3 distinct impingement syndromes have been described:

The anterosuperior impingement syndrome

Impingement of the rotator cuff beneath the coracoacromial arch is an established cause of chronic shoulder pain. In 1972, Neer, in a landmark article, described and popularized the term impingement syndrome. Observations from cadaver studies and surgery gave evidence that impingement occurs against the under surface of the anterior third of the acromion, the coracoacromial ligament, and at times, the acromioclavicular joint. Located anterior to the coracoacromial arch in the neutral position, the supraspinatus tendon insertion to the greater tuberosity and the bicipital groove must past beneath the arch with forward flexion of the shoulder, especially if internally rotated, causing an impingement. His works showed that degenerative tendinitis and tendon ruptures were centered in the supraspinatus tendon, extending at times to the anterior part of the infraspinatus tendon and the long head of the biceps tendon.

Neer believed that 95% of tears of the rotator cuff were initiated by impingement wear, rather than circulatory impairment or trauma. He observed proliferative traction spurs at the undersurface of the anterior acromion that he explained by the repeated impingement of the cuff. He stated that the variation in shape and slope of the acromion could make people more susceptible to impingement and tear, making it appear logical to perform an anterior acromioplasty at the time of every cuff repair.

Later, the shape of the acromion has been studied in cadavers and roentgenographically. Biglianni has described 3 different shapes of acromia in cadavers, according to the anterior slope:

Type 1 - Flat

Type 2 - Curved

Type 3 - Hooked
Only 3% of tears are associated with a type 1 acromion. Although there is a strong association between cuff tears and hook acromia, it is unclear whether the shape is the cause or the result of the cuff tear or simply the result of aging; however, Ozaki’s study on cadavers showed that the undersurface of the acromion was normal when the incomplete tear was on the articular side. On the other hand, when the incomplete tear was on the bursal side of the cuff tendon, pathological changes of the under surface of the acromion were observed, suggesting that a hooked acromion is the result of the cuff tear on the bursal side of the tendon and not the cause. Nevertheless, curved and hooked acromia appear to be due to a degenerative process with formation of the osteophyte-enthesophyte complex at the acromion-coracoacromial ligament junction that is increasingly prevalent with age.

Neer described impingement lesions in the following 3 progressive stages:

In stage 1, edema and hemorrhage result from excessive overhead use and are observed in patients younger than 25 years.

In stage 2, fibrosis and tendinitis affect the bursa and the cuff following repeated episodes of mechanical inflammation in patients aged 25-40 years.

In stage 3, bone spurs and incomplete and complete tears of the rotator cuff and long head of the biceps tendon are found almost exclusively in patients older than 40 years.
Clinical course and treatment vary according to the stage of the disease process. Neer’s picture of the impingement syndrome may explain tears on the bursal (superficial) side of the tendon. However, partial tears most commonly involve the articular (deep) side of the tendon, as observed by many investigators. Other etiologies, then, must be considered to explain the rotator cuff degeneration.

The posterosuperior impingement syndrome

In 1991, Walch described, from arthrographic observations, an impingement occurring between the articular side of the supraspinatus tendon and the posterosuperior edge of the glenoid cavity. With the shoulder held at 120° of abduction, retropulsion, and in extreme external rotation (similar to the late cocking phase in throwers), the labrum moves away from the glenoid and the glenoid rim comes in contact with the deep surface of the tendon, producing repeated microtrauma and leading to partial tears. This process has been confirmed by MRI studies and may explain some of the articular side tears, especially in overhead sport athletes; however, it does not account for all the tears observed in older patients.

The anterointernal impingement syndrome

In 1985, Gerber described, from CT scan studies and from surgery observations, impingement of the cuff in the coracohumeral interval. He demonstrated that, when the shoulder is held in flexion and internal rotation, the coracohumeral distance is reduced from 8.6 mm when the arm is at the side to 6.7 mm. In this position, the lesser tuberosity, and also the biceps tendon and the supraspinatus tendon, become closer to the coracoid process, creating subcoracoid impingement and cuff lesions. Subcoracoid impingement can be idiopathic (eg, large coracoid tip), iatrogenic (eg, following a Trillat procedure) or following a fracture (eg, humeral head or neck fracture).

The intrinsic hypothesis
In this theory, the lesions result from progressive age-related degeneration of the tendon. Von Meyer was probably the first to introduce the concept that degeneration of the tendon plays a major role in the production of cuff lesions. Many histologic studies show the age-related degeneration of the cuff tendon; however, it is not the purpose of this article to describe those numerous changes. Observations from various sources (eg, cadaver, surgical, MRI, ultrasonographic, arthrographic studies) show that cuff tears rarely are seen in patients before 40 years and that the number observed after the patient has reached 50 years increases progressively.

In 1934, Codman introduced the concept that most tears originate on the articular side of the tendon. Since that time, many authors have come to support that theory from cadaver, surgery, and MRI observations. Most of the tears have been observed on the articular surface of the tendon, near its insertion on the greater tuberosity, in an area Codman called the critical zone. This zone appears to be at greater risk of developing a tear. To explain why the critical zone is more prone to tearing, some investigators have suggested that it is a poorly vascularized area. Histologic, cadaver, and Doppler studies show that the articular side of the tendon, near its insertion on the tuberosity, is relatively avascular when compared to the remainder of the cuff.

By contrast, some other authors did not support these observations and found no difference in vascularity when the critical zone was compared to the other parts of the cuff. On the other hand, Rathbun suggested that the relative avascularity of the cuff is position-dependent and observed a poor filling only when the shoulder is in adduction. Finally, Nixon stated that the critical zone is an area of anastomoses between the muscular vessels and the osseous vessels. The most recent studies suggest that the critical zone is not an avascular area. The normal degenerative process associated with aging, then, is the main factor to explain the lesions of the articular side of the cuff.

In all probability, both the intrinsic and the extrinsic theories coexist and explain the pathophysiology of rotator cuff degeneration. Nevertheless, this degeneration is the result of a continuum that is beautifully described by Matsen, Arntz, and Lippitt. The lesion starts where the load is presumably the greatest (eg, on the articular side of the anterior insertion of the supraspinatus tendon, near the tendon of the long head of the biceps muscle). Tendon fibers fail when the load exceeds their strength. The fibers tend to retract because they are under tension, causing rupture. Fiber failure causes at least the following 4 complications:

Increases the load on the neighboring, yet intact, fibers

Detaches muscle fibers from the bone, diminishing the force that the cuff muscles can deliver

Compromises the tendon fibers’ blood supply by distorting the anatomy, contributing to progressive local ischemia

Exposes increasing amounts of the tendon to joint fluid containing lytic enzymes, which remove any hematoma that could contribute to tendon healing
The scar tissue of the healing tendon lacks the normal resilience of tendon and, therefore, is under increased risk for failure. In the absence of repair, the degenerative process tends to continue through the substance of the supraspinatus tendon to produce a full thickness defect in the anterior supraspinatus tendon. The full thickness tear tends to concentrate loads at its margin, facilitating additional fiber failure with smaller loads than those that produced the initial defect.

Once a supraspinatus tendon defect is established, it typically propagates posteriorly through the remainder of the supraspinatus tendon, then into the infraspinatus tendon. With the increasing defect of the cuff tendon, the spacer effect of the cuff tendon is lost (as well as its stabilizing effect), allowing the humeral head to displace superiorly, placing increased load on the biceps tendon. As a result, the breadth of the long head tendon of the biceps is often greater in patients with cuff tears in comparison with uninjured shoulders. In chronic cuff deficiency, the long head tendon of the biceps frequently is ruptured.

Further propagation of the cuff defect crosses the bicipital groove to involve the subscapularis tendon, starting at the top of the lesser tuberosity and extending inferiorly. As the defect extends across the bicipital groove, it may be associated with rupture of the transverse humeral ligament and destabilization of the long head tendon of the biceps, allowing its medial displacement. The concavity compression mechanism of glenohumeral stability is compromised by cuff disease. Beginning with the early stage of cuff fiber failure, the compression of the humeral head becomes less effective in resisting the upward pull of the deltoid.

A partial thickness cuff tear causes pain on muscle contraction. This pain produces reflex inhibition of the muscle action. In turn, the combination of reflex inhibition and loss of strength from fiber detachment makes the muscle less effective for balance and stability; however, as long as the glenoid cavity is intact, the compressive action of the residual cuff may stabilize the humeral head. When the weakened cuff cannot prevent the humeral head from rising under the pull of the deltoid, the residual cuff becomes squeezed between the humeral head and the coracoacromial arch, contributing to further cuff degeneration.

Degenerative traction spurs develop in the coracoacromial ligament, which is loaded by pressure from the humeral head. Upper displacement of the humeral head also wears on the upper lip of the glenoid rim and labrum, reducing the effectiveness of the upper glenoid concavity. Further deterioration of the cuff allows the tendon to slide down below the center of the humeral head, producing a boutonnière deformity. The cuff tendons become humeral head elevators, rather than head compressor-depressors. Just as in the boutonnière deformity of the fingers, the shoulder with a buttonholed cuff is affected by the conversion of balancing forces into unbalancing forces.

This theoretical model on the continuum of the cuff degeneration demonstrates the result of many years of overuse, but this process is also the consequence of the phenomenon that happened thousands of years ago when man stood erect. That development has lead to use of the glenohumeral joint in an unusual and strange biomechanical way (eg, repetitive overhead activities, arm length activities, throwing). The extremely long lever arm of the upper limb leads the short lever arm cuff muscles to produce extremely high forces in order to stabilize the joint, in opposition to the upward pull of the humeral head by the deltoid and preventing the impingement of the cuff, but at the expense of overload and degeneration.

In summary, the pathophysiology of rotator cuff degeneration may be explained by a combination of extrinsic, intrinsic, and biomechanical factors; however, it is not understood why in some individuals those pathological changes cause pain, but not in some others. This question should keep investigators busy for the next decades (or centuries).

Frequency:

In the US: Shoulder pain is the third most common cause of musculoskeletal disorder after low back pain (LBP) and cervical pain. Estimates of the cumulative annual incidence of shoulder disorders vary from 7-25% in Western general population. The annual incidence is estimated at 10 cases per 1000 population, peaking at 25 cases per 1000 population in the age category of 42-46 years. In the population aged 70 years or more, 21% of persons were found to have shoulder symptoms, most of which were attributed to the rotator cuff.
In cadaver studies, the incidence of full thickness tears varies from 18-26%. The incidence of partial thickness tears varies from 32-37% after age 40 years. Before 40, tears rarely are observed. In MRI studies, tears have been observed in 34% of asymptomatic individuals of all ages. After 60 years, 26% of patients have partial thickness tears, and 28% demonstrate full thickness tears.

Internationally: The above data are derived from international literature. No known regional variation exists for the frequency of this disease.
Mortality/Morbidity: As mentioned before, shoulder pain is the third most common cause of musculoskeletal disorder after low back and neck pain. Although considered a benign condition, according to a study on the long-term outcome of rotator cuff tendinitis, 61% of the patients were still symptomatic at 18 months, despite receiving what was considered sufficient conservative treatment. Moreover, 26% of patients rated their symptoms as severe. Musculoskeletal disorders are the primary disabling conditions of working adults. The prevalence of rotator cuff tendinitis has been found to be as high as 18% in certain workers who performed heavy manual labor.

Webster and Snook estimated that the mean compensation cost per case of upper extremity work-related musculoskeletal disorder (MSD) was $8070 in 1993; the total US compensable cost for upper extremity, work-related MSDs was $563 million in the 1993 workforce. The compensable cost is limited to the medical expenses and indemnity costs (lost wages). When other expenses (eg, full lost wages, lost production, cost of recruiting and training replacement workers, cost of rehabilitating the affected workers) are considered, the total cost to the national economy becomes much greater. The impact of rotator cuff disease on the quality of life (QOL) is even more difficult to assess than its cost. Further studies using valid methods like the Medical Outcomes Study (MOS) 36-item short-form health survey (SF-36), measuring the impact of the disorder on the general health should assess this issue.

Race: No known race variation associated with rotator cuff disease is cited in the literature.

Sex: In one study, there is a predominance of male patients (66%) seeking consultation for rotator disease, but, in other studies, the male-to-female ratio is 1:1.

Age: Rotator cuff disease is more common after age 40 years. The average age of onset is estimated at 55 years.

CLINICAL Section 3 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

History: Without a good knowledge of the anatomy and biomechanics of the shoulder complex, the probability that a systematic history and physical examination leads to the correct diagnosis is reduced. The following paragraphs review these topics.

Focused anatomy
The shoulder joint is a complex structure comprising not 1, but 5 joints (ie, 3 synovial joints [sternoclavicular, acromioclavicular, glenohumeral joints] and 2 physiologic joints [scapulothoracic joint, subdeltoid joint]). The latter are called physiologic joints because they are not true anatomic joints with the usual joint characteristics (eg, capsule, ligament). Instead, they are gliding structures that play an important role in the biomechanics of the shoulder by positioning and stabilizing the shoulder complex. The 5 joints fall into the following 2 groups:

First group

Glenohumeral joint, a true joint

Subdeltoid joint, a physiologic joint

Second group

Sternoclavicular joint, a true joint

Acromioclavicular joint, a true joint

Scapulothoracic joint, a physiologic joint
In both groups, true joints are linked mechanically to physiologic joints and work simultaneously to produce movement.

The sternoclavicular joint

This joint represents the only bony connection between the trunk and the upper limb. The sternoclavicular joint is a synovial saddle-shaped joint composed of a capsule, the sternal side of the clavicle, the sternoclavicular joint surface, an articular disk, the costoclavicular ligament, the anterior and posterior sternoclavicular ligaments, and the interclavicular ligament. The fibrous capsule surrounds the joint and is attached around the clavicular and sternochondral articular surfaces. The concave clavicular surface fits snugly on the convex sternocostal surface similar to how a rider sits on a saddle and the saddle fits on the back of a horse.

The fibrocartilaginous articular disk increases the capacity for movement, cushions forces transmitted from the shoulder, improves the congruity of the surfaces, and resists upward dislocation of the clavicle. This costoclavicular ligament is a short flat band of fibers running between the cartilage of the first rib and the costal tuberosity on the undersurface of the clavicle. This ligament is the principal stabilizer of the sternoclavicular joint, opposing the upward pull of the sternocleidomastoid muscles, and it also resists the elevation of the clavicle.

The anterior sternoclavicular ligament is a broad anterior band linking the upper and anterior borders of the sternal end of the clavicle and the upper anterior surface of the manubrium of the sternum. Reinforced by the tendinous origin of the sternocleidomastoid muscle, it stabilizes the joint anteriorly. The posterior sternoclavicular ligament has similar origin and insertion and stabilizes the joint posteriorly. The interclavicular ligament attaches on the upper border of both clavicles and the sternum, strengthening the capsule above.

Acromioclavicular joint

The acromioclavicular joint is a synovial plane joint composed of a capsule, the lateral end of the clavicle, the medial border of the acromion, an articular disk, the acromioclavicular ligaments, the coracoclavicular ligaments, and the coracoacromial ligament. The joint stability is maintained by the surrounding ligaments rather than by the bony configuration of the joint. The plane joint surfaces slope downward and medially, favoring displacement of the acromion downward and under the clavicle. The articular capsule encloses the joint, attaching at the articular margins. The capsule is reinforced by the fibers of the deltoid and the upper trapezius muscles and the powerful superior acromioclavicular ligament superiorly, and the anterior, inferior, and posterior acromioclavicular ligaments. The wedge-shaped articular disk dips into the joint from the superior part of the capsule and makes the articular surfaces more congruent.

The coracoclavicular ligaments, although separated medially from the joint, are the primary joint stabilizers. Its 2 parts, named for their shape, are the posteromedial conoid ligament and the anterolaterally placed trapezoid ligament. The 2 ligaments lie in 2 planes, more or less at right angles to each other. A third part, the medial coracoclavicular ligament, is described inconsistently in anatomy textbooks. The coracoclavicular ligaments act to resist superior and, to a lesser extent, anterior dislocation of the acromioclavicular joint, resist axial compression at the distal clavicle, and indirectly limit excess rotation of the joint. The conoid ligament is fan-shaped with its apex lying inferiorly. This ligament inserts on the “tip of the elbow” of the coracoid process and the undersurface of the medial third of the clavicle.

During abduction and external rotation, the angle between the scapula and the clavicle widens and the conoid ligament is stretched, transmitting the force to the clavicle and, ultimately, to the strong acromioclavicular ligaments, preventing dislocation. The trapezoid ligament inserts on the medial border of the upper surface of the coracoid process and runs superiorly and laterally to attach on the undersurface of the clavicle. During adduction, the angle between the scapula and the clavicle is closed and the trapezoid ligament is stretched, preventing the dislocation of the acromioclavicular joint by the same force-transmission mechanism. In summary, the vertical stability of the acromioclavicular joint is provided mainly by the coracoclavicular ligaments, and the anteroposterior stability is provided mainly by the acromioclavicular ligament-capsule complex.

The scapulothoracic joint

The scapulothoracic joint is not a true anatomic joint because it lacks the usual joint characteristics. Except for its attachment to the axial skeleton at the acromioclavicular joint and with the coracoclavicular ligaments, the scapulothoracic joint is free gliding without any ligament restraint. Although it is not a true joint, the scapulothoracic joint plays an important role in the biomechanics of the shoulder complex. The scapula represents a mobile platform from which the upper limb operates.

The main role of the scapula is to orient the glenoid fossa in an optimal position to receive the humeral head and to provide a stable base of support for the controlled movement of the articular surface of the humeral head. It also allows increased shoulder mobility. In the resting position, the scapula lies between the second and seventh rib, over the serratus anterior and the subscapularis muscles. The superomedial angle corresponds to the first thoracic vertebra; the inferior angle corresponds to the seventh thoracic vertebra. The scapula runs obliquely, mediolaterally, and posteroanteriorly, forming an angle of 30° open anterolaterally with the frontal plane.

Five muscles directly control the scapula (trapezius, rhomboids, levator scapulae, serratus anterior, and, to a lesser extent, the pectoralis minor). These muscles act in a synchronous way to position the glenoid fossa.

The glenohumeral joint

The glenohumeral joint is a multiaxial ball and joint socket that is the most mobile and the least stable of all the joints. This joint is composed of a capsule, the head of the humerus, the glenoid fossa, the glenoid labrum, the glenohumeral ligaments, the coracohumeral ligament, and the transverse humeral ligament. The glenohumeral joint also is stabilized externally by the tendons of the rotator cuff muscles and the long head of the biceps tendon.

The joint capsule is a loose thin redundant sleeve that contributes to the mobility of the joint, but also to its instability. On the humeral head, the capsule attaches on the anatomic neck, immediately medial to the tuberosities, and then it extends onto the medial surface of the shaft, slightly below the articular head. The capsule has 2 openings. The upper end opening allows the passage of the long head of the biceps tendon; the anterior opening allows a communication between the joint cavity and the subscapular bursa. On the glenoid side, the capsule attaches to the labrum and, less frequently, to the scapular neck. Because of its laxity, the joint capsule is 2 times larger than the humeral head, and assistance is needed to stabilize the glenohumeral joint. This assistance is provided partly by the glenohumeral ligaments and the coracohumeral ligament.

Three intrinsic, yet distinct, capsular ligaments provide anterior stability to the joint. The anterior inferior, middle, and superior glenohumeral ligaments form a Z in front of the joint capsule. These ligaments become taut and restrict certain motions of the humerus. They are the last structures that provide stability after other static and dynamic stabilizers have been involved. The thin superior glenohumeral ligament arises from the anterosuperior edge of the glenoid and attaches to the top of the lesser tuberosity of the humerus, limiting inferior dislocation in the adducted shoulder and providing secondary restraint to posterior dislocation.

The middle glenohumeral ligament arises from the supraglenoid tubercle and the superior labrum, next to the superior ligament and attaches medially to the base of the lesser tuberosity, beneath the subscapularis tendon. The primary role of the middle glenohumeral ligament is to limit external rotation at 45° of abduction. This ligament also provides a secondary restraint to anterior dislocation.

The inferior glenohumeral ligament complex arises from the anteroinferior labrum and the glenoid border and attaches to the lesser tuberosity, just inferior to the middle ligament. This ligament is a hammock-shaped structure that consists of 3 parts, the axillary pouch and the anterior and posterior bands. The anterior and posterior bands reciprocally tighten as the humeral head is rotated. The anterior band is the primary restraint to anterior dislocation and external rotation at 90° of abduction. The loss of integrity of this ligament is a major cause of anterior instability in the throwing athlete.

The coracohumeral ligament is a broad band that arises from the lateral border of the horizontal arm of the coracoid process and attaches to the top of the greater and lesser tuberosities and the transverse humeral ligament. The primary role of this ligament is to stabilize the adducted shoulder and resist inferior subluxation of the humeral head.

The transverse humeral ligament stretches from the greater to the lesser tuberosity. The primary role of this ligament is to stabilize the long head of the biceps tendon in the bicipital groove.

The humeral head and glenoid fossa

The large humeral head articulates with the slender and shallow glenoid fossa, only a little more than one third its size. The axis forms an angle of 135° with the shaft and an axis of 30° with the frontal plane (retroversion angle). The head faces superiorly, medially, and posteriorly; the glenoid points anteriorly, laterally, and slightly superiorly. The concavity of the humeral head is irregular and less marked than the convexity of the humeral head. The irregular minimal bony contact between those 2 joint surfaces explains the lack of joint stability and the necessity for other mechanisms of stabilization.

The glenoid labrum is a rim of fibrocartilage that surrounds the glenoid fossa. This labrum serves many important functions for the glenohumeral joint, including the following:

Provides an extension to the concavity of the glenoid fossa and deepens the glenoid by 50%

Provides an increase in depth and, to a lesser extent in width, resulting in an increased stabilization against translating forces

Serves as an articular surface to the humeral head

Serves as an attachment for the capsule, the ligaments, and the long head of the biceps tendon
Rotator cuff muscles and the long head of the biceps tendon

The rotator cuff is made up of 4 interrelated muscles arising from the scapula and attaching to the tuberosities. Their tendons form a continuous cuff around the head that allows the cuff muscles to provide an infinite variety of moments to rotate and adjust the humeral head in the glenoid fossa, providing the optimal muscle balance for precise coordinated movements.

The supraspinatus muscle arises from the medial two thirds of the supraspinous fossa of the scapula. This muscle passes under the acromion and acromioclavicular joint and inserts onto the superior aspect of the greater tuberosity and joint capsule. The supraspinatus muscle is innervated by the suprascapular nerve (C4-C5-C6). Its primary role is to stabilize the head of the humerus in the glenoid fossa and to abduct the shoulder.

The infraspinatus muscle arises from the medial two thirds of the infraspinous fossa of the scapula and inserts on the middle facet of the greater tuberosity and joint capsule. This muscle is innervated by the suprascapular nerve (C4-C5-C6). Its primary role is to stabilize and externally rotate the head of the humerus.

The teres minor muscle arises from the upper two third of the dorsal aspect of the lateral border of the scapula and inserts onto the lower facet of the greater tuberosity and joint capsule. Its primary role is to stabilize and externally rotate the head of the humerus.

The subscapularis muscle arises from the subscapular fossa of the scapula and inserts to the lesser tuberosity and joint capsule. This muscle is innervated by the upper and lower subscapular nerve (C5-C6-C7). Its primary role is to stabilize and externally rotate the head of the humerus.

The long head of the biceps tendon arises from the supraglenoid tubercle of the scapula, runs between the supraspinatus and subscapularis muscles, exits the shoulder through the bicipital groove under the transverse humeral ligament, and inserts onto the tuberosity of the radius. The long head of the biceps is innervated by the musculocutaneous nerve (C5-C6). Its primary role is to stabilize and flex the humeral head and flex the elbow.

The subdeltoid joint

Like the scapulothoracic joint, the subdeltoid joint is not a true anatomic joint. The subdeltoid is composed of the undersurface of the acromion, the coracoacromial ligament, the subacromiodeltoid bursa, the rotator cuff, and the long head of the biceps tendon. Like the glenoid fossa, they form a concave structure that matches with the convex humeral head. Many authors have stressed the importance of this joint and have described it as the fifth joint of the shoulder. The subdeltoid joint serves the following 2 major roles:

Provides a gliding surface for the head of the humerus, especially during abduction and flexion

Resists the upward pull of the humeral head during abduction and flexion and provides superior stability
Degenerative changes observed on the undersurface of the acromion and coracoacromial ligament tend to confirm the involvement of this physiologic joint in shoulder motion.

Biomechanics of shoulder elevation

Most glenohumeral motion, especially in overhead activities, occurs around the plane of the scapula, which is approximately 30-45° anterior to the frontal plane. Any time the arm is raised in flexion or abduction, movements from the scapula and the clavicle accompany the glenohumeral joint. In the first 30° of abduction or 45-60° of flexion, the scapula moves either toward or away from the spine to seek a position of stability on the thorax. Consequently, the scapulothoracic joint does not participate in the early elevation of the arm, and the movement of the first 30° comes from the glenohumeral joint. After stabilization has been achieved, the scapula moves laterally, anteriorly, and superiorly, causing an upward rotation of the scapula and glenoid fossa. This scapular rotation serves the following 2 purposes:

Maintains the glenoid fossa in an optimal position to receive the head of the humerus, thus increasing the range of motion (ROM)

Permits the muscles acting on the humeral head to maintain a satisfactory length-tension relationship
Beyond the first 30° of abduction (or 45-60° of flexion), scapulothoracic motion occurs and contributes to the scapulohumeral rhythm. As the abduction progress, according to widely accepted belief, there is a 2:1 ratio of motion between the glenohumeral and scapulothoracic motion. Toward the end of the elevation, the scapula contributes more motion and the humerus less.

In total, the glenohumeral joint contributes 90-120° to shoulder abduction and the scapulothoracic joint supplies 60°. The contributing joint actions to the scapular motions are 20° produced by the acromioclavicular joint, 40° produced at the sternoclavicular joint, and 50° of clavicle elevation and 30° of posterior rotation. For the glenohumeral joint to realize 120° of abduction, external rotation of the humerus must occur. When internally rotated, the humerus can abduct to approximately 90° before the greater tuberosity hits the coracoacromial arch; however, when externally rotated, the greater tuberosity and cuff tendons avoid the coracoacromial arch, and 120° of abduction can be obtained. Full abduction cannot be achieved without trunk extension and contralateral flexion.

The muscle actions

The muscles contributing to shoulder abduction and flexion are similar. The glenohumeral abduction is performed primarily by the deltoid and the supraspinatus. Initially, it was assumed that the abduction was initiated by the supraspinatus and continued by the deltoid; however, studies in which selective nerve blocks were used to inhibit the deltoid and supraspinatus muscles showed that complete abduction still occurs, but with a 50% loss in power, when one muscle or the other is inhibited.

The contribution of the supraspinatus is greater at the initiation of abduction. As the abduction increases, the contribution of the deltoid increases because this muscle is more active through 90-180°. Therefore, the supraspinatus can be viewed not as an initiator of abduction, but as a useful and effective component of movement, particularly at the start of abduction. Simultaneous nerve blocks of both these muscles result in the inability to raise the arm.

In summary, each muscle can abduct the arm in a full ROM; each is more active in a certain ROM, but there is a loss of 50% in power if only one muscle is involved. As abduction occurs, the rotator cuff muscles act to stabilize the humeral head in the glenoid fossa.

In the early stages of abduction, the teres minor is active to depress and stabilize the humeral head and the muscle force of the teres minor is equal and opposite to that of the deltoid, forming a force couple. The subscapularis and the infraspinatus join a little later to assist the teres minor in the stabilization of the humeral head. The latissimus dorsi contracts eccentrically to assist the stabilization and increases in activity as the angle progresses. Above 90°, the rotator cuff force decreases, making the joint more susceptible to injury. The supraspinatus remains a major contributor to stabilization above 90°. As the arm is abducted, the scapula moves laterally, anteriorly, and superiorly to cause an upward rotation of the scapula. The serratus anterior and, to a lesser degree, the trapezius are responsible for this movement. Both muscles, along with the rhomboid muscles, stabilize the scapula on the thoracic wall and prevent winging of the scapula.

History

A complete medical history should be obtained in order to direct the physical examination and make the right diagnosis. Most of the time, the diagnosis can be made following a systematic history. Relevant past history, treatments, and test results should complement the history of the present injury. Sometimes, relevant social and family histories are necessary.

Patients with degenerative rotator cuff disease are almost always aged more than 40 years. Fifty percent of patients have a progressive onset of shoulder pain, whereas the other 50% can identify a specific event responsible for the onset of pain. The evolution of rotator cuff disease is characterized by variable episodes of recurrence following more intensive shoulder activities, followed by remission with rest or treatment.

As the disease progresses, shoulder pain becomes more constant. Overhead and arm-length activities typically increase the pain. Discomfort and night pain also can be present. With time, the individual can notice some weakness during shoulder elevation. Crepitus also can be noted. With the evolution of the disease, shoulder pain can be accompanied by cervical and mid back pain.

The following questions should help the physician in assessing the patient:

What is the patient’s age?

Shoulder pain in young overhead athletes suggests underlying shoulder instability.

In older patients, degenerative rotator cuff disease or frozen shoulder is suggested by shoulder pain.

What is the patient’s occupation or sport? Repetitive overhead activities and sports predispose to rotator cuff tendinitis.

What was the mechanism of injury?

A fall on an outstretched arm could indicate a dislocation of the glenohumeral joint or a fracture of the humeral neck.

Repetitive overhead motions can cause tendinitis and, in the long run, chronic degenerative changes.

A fall or a trauma on the tip of the shoulder can result in an acromioclavicular sprain.

What was the onset?

Insidious slow onset may suggest tendinitis or osteoarthritis.

Sudden onset usually is due to a trauma causing a fracture, dislocation, or a rotator cuff tear.

Where is the pain located?

Pain located on the superior or lateral aspect of the shoulder suggests rotator cuff tendinitis.

Pain on the anterior aspect of the shoulder may result from bicipital tendinitis, an acromioclavicular sprain, or anterior instability.

Neck pain and radicular pain or paresthesias suggest a cervical spine disorder.

What is the severity of the pain?

An acute burning pain could indicate an acute bursitis.

An intermittent dull pain may be due to a degenerative rotator cuff disease.

What is the type of pain?

Sharp burning pain suggests a neurologic origin.

Bone and tendon pain is deep, boring, and localized.

Muscle pain is dull and aching, not localized, and may be referred to other areas.

Vascular pain is aching, cramplike, poorly localized, and may be referred to other areas.

What is the duration of the symptoms?

Frozen shoulder goes through 3 stages that can last up to 3-4 years.

Acute bursitis has a short-term evolution and responds well to nonsteroidal anti-inflammatory drugs (NSAIDs).

What is the timing of the pain?

Predominantly night pain suggests frozen shoulder.

Morning pain and stiffness improved by activity may be caused by a synovitis.

Pain that increases with activity is usually the result of a rotator cuff tendinitis.

Which activities/positions increase the pain?

Pain increased by overhead activities or arm-length activities suggests rotator cuff tendinitis.

Pain increased when throwing is likely to be due to anterior instability.

Pain increased by lying on the affected shoulder may be caused by an acromioclavicular sprain.

Which activities/positions relieve the pain?

Is there any weakness or paresthesias in the upper extremities? Neurologic symptoms are caused by a cervical radiculopathy or peripheral nerve entrapment/lesion.

Are the symptoms constant or intermittent?

Intermittent symptoms usually result from soft tissues or joint disorders.

Constant symptoms suggest a neurologic lesion.

Are there any joint motion restrictions?

Passive and active joint restriction in all directions of ROM is caused by a frozen shoulder or glenohumeral synovitis.

Restriction in internal rotation suggests an impingement syndrome due to rotator cuff tendinitis.

Inability to perform active abduction suggests a rotator cuff tear or a frozen shoulder.

Is some crepitus noted?

Crepitus is the result of degenerative rotator cuff changes.

Crepitus is not a normal finding in the shoulder.

Are there any changes in the color of the arm?

Color changes may be due to ischemia secondary to vascular insufficiency.

Reflex sympathetic dystrophy (also called complex regional pain syndrome, type 1) can cause skin color changes.

Has the patient had any treatments like oral medication, injections, or physical therapy to date?

Has the patient had any diagnostic tests performed to date?

What is the evolution of the symptoms?

Has the pain changed?

Has the pain spread or moved?

Has the pain subsided or increased?
The last 3 questions help in deciding for the appropriate treatment and management.

The importance of obtaining a systematic detailed history cannot be overemphasized. Any attempt to shortcut the process leads to a nonfocused physical examination and inaccurate diagnosis. Remember that a recent study assessing the interobserver agreement of a diagnostic classification of shoulder disorders based on history and physical examination showed only moderate agreement between experienced observers.

Physical: A systematic examination of the shoulder region includes a careful observation, the palpation of the bones and soft tissues, passive and active ROM, impingement and topographic tests complemented, as needed, by instability tests, labrum tests, and special tests. The examination is completed by a cervical spine examination, along with neurologic and vascular examination.

Observation
The observation begins from the moment the patient enters the room. The smoothness and symmetry of the shoulders and the movements of the upper extremities are evaluated, as well as the patient’s gait. The examiner must be aware of any signs of painful posturing and irregularity of motion of the affected shoulder. Bilateral examination allows for comparison of the affected shoulder with the unaffected one.

The patient then must be asked to get suitably undressed so that an appropriate assessment of the bone and soft tissues can be performed. The shoulder, cervical region, and the entire upper extremity must be assessed. The examiner should assess bones and joints for possible asymmetry or deformities, as well as soft tissue changes suggesting vasomotor abnormalities, like swelling, erythema, white shiny skin, loss of hair, or atrophy. Scars and abrasions also must be noted. The observer should assess bony contours first and then soft tissues. Observation of the patient must be completed from the front, side, and back.

Anterior observation

Looking at bony contours, the examiner makes a general assessment. The dominant side may be lower than the nondominant one; the head and neck should be in the mid line; the clavicle should be symmetric without any deformity of the acromioclavicular joint and sternoclavicular joint.

Each of these parts is examined then in more detail. Because of its superficial location, a fracture of the clavicle or a subluxation or dislocation of both ends is easy to identify. A step deformity of the acromioclavicular or sternoclavicular joint, with the clavicle side of the joint migrating superiorly, is due to a dislocation of those joints.

Observation of the soft tissues is directed first at the contours of the deltoid. The mass of the deltoid should be round with the anterior and posterior aspects symmetrical. Flattening of the muscle suggests an atrophy of the deltoid usually due to a neurologic lesion like an axillary nerve neuropathy, an upper trunk brachial plexopathy (Erb palsy) or a C5-C6 radiculopathy. An anterior dislocation of the glenohumeral joint produces a flattening of the deltoid with a bulging of the anterior aspect of the muscle due to the dislocated head of the humerus, with the patient holding the shoulder in slight adduction and across the trunk. A bulge may be observed in the middle third of the belly of the biceps, when the elbow is flexed, suggesting a rupture of the long head of the biceps tendon.

Lateral observation

The side view allows the examiner to assess thoracic spine kyphosis, a protraction of the head or the shoulders. Deltoid atrophy also can be observed.

Posterior observation

Looking at bony contours, the examiner seeks evidence of a scoliosis of the thoracolumbar spine and then observes the scapulae. The scapula extends from the spinous process of T2 (superomedial angle) to the spinous process of T7 (inferomedial angle). Both scapulae should be at the same height and at the same distance from the spine. The examiner should check for a winging of the scapula (ie, a displacement of the medial side of the scapula away from the thorax). When the winging takes place with a medial displacement of the scapula toward the spine, a serratus anterior muscle palsy is suggested. This palsy usually is due to a long thoracic nerve injury. When the winging takes place with a lateral displacement of the scapula, a trapezius muscle palsy or, more rarely, a rhomboid muscle palsy must be suspected.

The trapezius muscle palsy can be due to a spinal accessory nerve (cranial nerve XI) injury, and the rhomboid muscle palsy can be due to a dorsal scapular nerve injury. A prominent spine of the scapula may be due to a supraspinatus and infraspinatus muscle atrophy caused by a suprascapular nerve injury in the suprascapular notch or a rotator cuff tear.

Observation of the soft tissues is directed at the posterior aspect of the deltoid muscle. The trapezius muscle then is observed. Atrophy resulting from palsy of the muscle has been discussed previously. Because the rhomboid is overlapped by the trapezius, atrophy of the rhomboids is more difficult to assess.

Palpation

Like observation, palpation must be performed in an orderly manner, beginning with the anterior structures and finishing with the posterior structures. Palpation must include bony structures and soft tissues. Irregular joint surfaces, swelling, heat, crepitus, pain, tenderness, and muscle tension and spasms must be looked for. Palpation can be performed more conveniently with the patient standing. In this position, it is easier for the examiner to move around the patient. The examiner should stand behind the patient for the palpation.

Beginning with the anterior structures, the examiner palpates the sternoclavicular joint. Superior migration of the medial end of the clavicle is palpated if there is a dislocation of the joint. The examiner must remember that the clavicle is superior to the manubrium. Always compare the affected side with the contralateral side. The sternocleidomastoid muscle also must be palpated, looking for tension and spasms. The muscle contracts to turn the head on the contralateral side. The muscle is easier to identify and palpate in this position. The sternal and clavicular heads of the muscle must be palpated. Hands can be moved medially to palpate the suprasternal notch. The first rib, the costochondral joints, and the sternum also should be assessed.

The clavicle should be palpated along its whole length, looking for bumps (suggesting callus formation resulting from fracture), loss of continuity, and crepitus. The acromioclavicular joint is a common site of pain and must be palpated with care. Because the acromioclavicular joint is a superficial joint, swelling and synovial thickening, as well as crepitus, can be felt under the fingers. Step deformities with superior migration of the lateral end of the clavicle, seen in dislocation or subluxation are easily palpable.

The coracoid process can be palpated approximately 2.5 cm (1 in) inferior and just medial to the acromioclavicular joint. The coracoid process is the site of origin of the short head of the biceps tendon, the coracobrachialis muscle, and the insertion of the pectoralis minor. The pectoralis major and minor also must be palpated. Muscle tension and spasms frequently are associated with shoulder disorders.

The acromion and subacromial space are palpated. The subacromiodeltoid bursa can be palpated indirectly in the subacromial space. Because it is overlapped by the deltoid muscle, the bursa cannot be felt under the fingers; however, the examiner, through pressure on the deltoid muscle, applies indirect pressure on the inflamed bursa, causing pain.

The examiner follows by palpating the greater tuberosity, the long head of the biceps tendon, and the lesser tuberosity. These structures can be identified easily in a lean patient by an experienced examiner. This identification may be more difficult in an overweight patient or one with abundant muscle mass. By rotating the shoulder medially (eg, by putting the dorsal aspect of the hand on the buttock), the examiner can feel the greater tuberosity on the anterior aspect of the shoulder, just inferior to the acromion. The supraspinatus, infraspinatus, and teres minor tendons all insert into this structure and, when inflamed, can produce pain on palpation of the greater tuberosity.

Keeping the fingers on the greater tuberosity, the examiner rotates the shoulder laterally. The fingers feel the bicipital groove where the long head of the biceps tendon can be palpated. Pain or thickening of the tendon sheet indicates an inflamed tendon, whereas its absence suggests a rupture or dislocation. By rotating the shoulder more laterally, the examiner can palpate the lesser tuberosity. The tendon of the subscapularis inserts on that structure and, when it is inflamed, the tendon is painful on palpation. With the shoulder back to a neutral position, extension of the shoulder allows the palpation of the subacromiodeltoid bursae under the anterior edge of the acromion.

All these structures must be palpated gently because they may be tender. Any painful palpation must be compared with the contralateral shoulder. A positive finding is when pain is more significant on the affected side compared with the contralateral shoulder. Any excessive pain caused by a vigorous palpation makes the examination less sensitive.

The biceps muscle should be palpated, looking for any bulging that indicates a long head of the biceps tendon rupture. The deltoid muscle also must be palpated to look for painful spasm or tension. Tone and atrophy also are assessed.

The examination is continued by palpation of the posterior structures. Bony structures can be rapidly assessed because they are rarely a source of pain. The spine of the scapula is palpated, followed by the palpation of the superior medial angle of the scapula. The levator scapulae muscle that inserts on this angle is a common site of pain. The medial border of the scapula then is palpated from the superior to the inferior medial angle. The bony palpation is completed by the palpation of the spinous processes of the dorsal and cervical spine.

Because muscle spasm and tension frequently are associated with a rotator cuff disease, the posterior muscles must be palpated with care to identify and treat those muscles. The superior trapezius is commonly tense and painful and must be palpated from its cervical and occipital origin to its insertion on the spine of the scapula and the acromion. Under this muscle, lying in the supraspinatus fossa, the supraspinatus muscle also should be palpated.

The rhomboid muscles, originating from C7 to T5, run downward to attach on the medial border of the scapula. These muscles, often a source of pain, are difficult to distinguish from the overlying middle trapezius muscle. The rhomboid muscles can be identified by asking the patient to put his/her hand behind the back, with the shoulder internally rotated and the elbow flexed, and to push posteriorly against a resistance. The muscle belly of the rhomboid muscles then becomes palpable. Muscle palpation is completed by assessing the infraspinatus and teres major and minor, as well as the latissimus dorsi muscles.

Range of motion

Both active and passive ROM must be evaluated. Although some authors suggest that there is no need to assess passive ROM if the patient is able to perform a complete active ROM without pain, passive ROM must be assessed systematically. Some patients with glenohumeral ROM restrictions have learned to compensate with increased scapulothoracic mobility and seem to have near normal active range. The following movements (with the normal ranges provided) should be assessed:

Abduction (70-180°)

Adduction (30-45°)

Flexion (160-180°)

Extension (45-50°)

External rotation (80-90°)

Internal rotation (90-110°)
Active movements are evaluated first. With the observer behind the patient who is standing, active abduction is performed. The reader is referred to the section on Biomechanics of shoulder elevation for a detailed description of the abduction.

The scapulohumeral rhythm is observed. If a painful arc (ie, pain or inability to abduct because of pain) is observed between 45-120°, a subacromial impingement syndrome is suggested. If the pain is greater after 120°, when full elevation is reached, an acromioclavicular joint disorder is suggested.

If a reverse scapulohumeral rhythm (ie, an abduction initiated by the scapulothoracic joint rather than by the glenohumeral joint) is observed, a frozen shoulder is suggested. Look for a winging of the scapula caused by a trapezius or rhomboid muscle weakness. Active flexion also is evaluated. In the presence of a subacromial impingement syndrome, this movement also can be painful. Active flexion also can elicit a winging of the scapula caused by a serratus anterior weakness.

Other motions can be evaluated through a combination of active movements. The Apley scratch test is probably the most well known of all. This test combines internal rotation and adduction of one shoulder with external rotation and abduction of the other.

Passive range of motion

The evaluation can be performed with the patient standing, sitting, or lying down. For practical purposes, the examination is performed with the patient standing. Passive abduction is assessed with the observer behind the patient. Full abduction is performed first to evaluate the combination of scapulothoracic and glenohumeral motion. Then, the scapulothoracic joint is locked by putting one hand over the scapula and the clavicle to resist any motion of this joint. This maneuver allows for a more selective evaluation of the glenohumeral joint (90-120°).

The same procedure can be used to evaluate full flexion that combines scapulothoracic and glenohumeral motion and flexion performed selectively by the glenohumeral joint. This maneuver is followed by the evaluation of the adduction. The external rotation is tested with the elbow held close to the waist and flexed at 90°. Then the arm is rotated externally. The examination is followed by an evaluation of the extension and an assessment of the internal rotation. The full range of internal rotation is achieved with the forearm passing behind the trunk with the shoulder slightly extended.

Impingement tests

Positive impingement tests result from the reproduction of the impingement of the rotator cuff tendon by different provocative maneuvers. In the case of an anterosuperior impingement syndrome, the impingement takes place underneath the coracoacromial arch; in the case of the posterosuperior impingement syndrome, the impingement is on the posterosuperior border of the glenoid cavity, whereas, in the case of the anterointernal impingement syndrome, the impingement takes place in the subcoracoid space or in the coracohumeral interval. For a better understanding of those syndromes, the reader is referred to the Pathophysiology section.

A recent study on cadaveric shoulders has shown that some provocative impingement tests, the Neer and Hawkins-Kennedy tests, appear to elicit contact consistent with impingement.

The Neer impingement test

With the examiner standing behind the patient, the shoulder is flexed passively. Although not originally described by Neer, the shoulder is positioned in internal rotation by this author.

When positive, this test produces pain that is caused by the contact of the bursal side of the rotator cuff on the anterior third of the undersurface of the acromion and the coracoacromial ligament, as well as by contact of the articular side of the tendon with the anterosuperior glenoid rim.

A positive test suggests an anterosuperior impingement syndrome.

The sensitivity of this test, assessed by operatively observed anatomic lesions, is 89%.

The Hawkins-Kennedy test

With the examiner standing behind the patient, the shoulder is flexed passively to 90°, followed by repeated internal rotation.

When positive, this test produces pain that is caused by the contact of the bursal side of the rotator cuff on the coracoacromial ligament and by the contact between the articular surface of the tendon and the anterosuperior glenoid rim.

Contact between the subscapularis tendon and the coracoid process also is observed.

A positive test suggests an anterosuperior or an anterointernal impingement test.

This author uses a modified version of this test with the shoulder positioned initially at 90° of abduction and 30° of flexion, in the plane of the scapula. Along with repeated internal rotation motion, the shoulder is brought progressively to 90° of flexion.

If pain is present when the shoulder is flexed at 30°, it is caused by an anterosuperior impingement syndrome.

If the pain is present only when the shoulder is brought to 90° of flexion, reducing the coracohumeral interval, an anterointernal impingement syndrome is suggested.

The sensitivity of this test is 87%.

The Yocum test

With the examiner standing behind the patient, the hand on the ipsilateral side of the examined shoulder is placed on the contralateral shoulder.

The elevation of the elbow is resisted by the examiner.

When positive, this test produces pain caused by the contact of the bursal side of the cuff tendon with the coracoacromial ligament and possibly the undersurface of the acromioclavicular joint.

A positive test suggests an anterosuperior or an anterointernal impingement syndrome.

The sensitivity of this test is only 78%; however, the sensitivity of the 3 tests together is 100%, which justifies that the 3 tests should be systematically performed together.

The posterior impingement test

With the patient lying down, the shoulder is positioned at 90-100° of abduction and maximally externally rotated.

When positive, this test produces pain in the posterior aspect of the shoulder that is caused by the impingement of the articular side of the cuff tendon between the greater tuberosity and the posterosuperior glenoid rim and labrum.

The relocation of the humeral head, performed by applying a posteriorly directed force to the humeral head, causes a reduction in pain.

The sensitivity of this test is 90%.

Impingement tests confirm an impingement syndrome; however, they do not determine the location of the rotator cuff lesion.

Topographic tests
Using resisted isometric contraction of specific muscles of the rotator cuff, it is possible to identify the location of the tendon lesion causing the impingement.

The supraspinatus tendon

The Jobe test

The shoulder is placed at 90° of abduction and 30° of flexion in the plane of the scapula.

Shoulder elevation is resisted.

The test is positive if pain is noted. When compared with surgical observations, the sensitivity of this test is 86%, and its specificity is 50%.

The positive predictive value (the ratio of true positive tests on all the positive tests) of the Jobe test is 96%, and its negative predictive value (the ratio of all the negative tests on all the negative tests) is 22%.

The full can test

The shoulder is placed at 90° of flexion and 45° of external humeral rotation (thumb pointing upward, like someone holding a full can, right-side-up).

Shoulder elevation is resisted.

The test is positive if it produces pain.

An electromyographic (EMG) study showed that this test results in the greatest supraspinatus activation with the least activation from the infraspinatus.
The infraspinatus tendon

The infraspinatus isolation test

The shoulder is positioned at 0° of elevation (elbows against the waist flexed at 90°) and 45° of internal rotation.

Shoulder external rotation is resisted.

The test is positive if it produces pain.

EMG shows that this is the optimal infraspinatus isolation test.

The Patte test

The shoulder is placed at 90° of abduction, neutral rotation, and in the plane of the scapula.

The examiner holds the elbow of the patient and the external rotation is resisted.

The test is positive if it produces pain.

The sensitivity of the test is 92%, but its specificity is only 30%.

The positive predictive value is 29%, and its negative predictive value is 93%.
A palsy of the external rotator also can be tested.

With the elbow held against the waist, the shoulder is positioned passively in external rotation.

The test is positive when the patient is unable to maintain the shoulder in external rotation, suggesting a full tear of the external rotators.
The teres minor tendon

No specific teres minor isolation tests exist.

The same tests used to test the infraspinatus tendon serves for the teres minor.
The subscapular tendon

The Gerber lift-off test

The shoulder is placed passively in internal rotation and slight extension by placing the hand 5-10 cm from the back with the palm facing outward and the elbow flexed at 90°.

The test is positive when the patient cannot hold this position, with the back of the hand hitting the patient’s back.

The sensitivity and specificity of this test are 100% when there is a full tear of the subscapularis.

The Gerber push with force test

The shoulder is placed in the same position as the lift-off test; however, the patient has to keep his hand away from the back and resists a push in the palm of the hand.

EMG shows that this is the optimal subscapularis isolation test with minimal activation of the pectoralis and latissimus dorsi muscles.
The long head of the biceps tendon

The Speed palm up test

The shoulder is placed at 90° of flexion with the elbow in e


#19

Just “somewhat” impressed??? I thought what I said was darn impressive. :wink:

That’s why I said “initially”. The supraspinatus gets the ball rolling and then the Deltoid finishes the job.

This is what led me in this direction. Also, guys like plumbers and sheet metal workers tend to have problems with their rotator cuffs for related reason (as does anyone who works with their arms above their heads for long periods of time).

How about SS (assuming you can ignore the whole Nazi thing). Infraspinatus then become IS and Teres Minor becomes TM.

I know that this can happen, but it’s more of an acute than a chronic problem.

I happen to think that Marshall is wrong about this. I also think that he goes too far on the scap loading thing. I think scap loading is safe as long as the elbows are below the level of the shoulders.

Could be.

This could tie into some of my ideas about Labrum problems (which would tend to exacerbate instability.

[quote=“dm59”]Geesh!! I think I kind of agreed with you here Chris. I gotta go lie down now and recover.
:lol:[/quote]

Let’s not make a habit of it. :wink:


#20

[quote=“Chris O’Leary”][quote=“dm59”]Geesh!! I think I kind of agreed with you here Chris. I gotta go lie down now and recover.
:lol:[/quote]

Let’s not make a habit of it. ;-)[/quote]

I said “kind of” now. It was a weak moment. I’ll get back to my old self soon. 8)

I still disagree with your cause and effect theory with respect to the culprit being the elbow above the shoulder. It makes a difference when the elbow is there.

It can’t be as the shoulders are squaring to the plate and max. ext. rotation of the humerus is reached because the elbow on all MLB pitchers we can look at is generally AT shoulder height or, more accurately put, in line with the acromial line, regardless of tilt.

It can’t be from high cocked onward for the same reason. Even the inverted W or M pitchers have the elbow in line with the acromial line by this time.

It can’t be from the horizontal W point onward either, for the same reason. The elbow’s at the acromial line by this time also.

So, the only time it CAN be is prior to the forearm reaching horizontal. Only that 80 - 90 degree time in the M guys.

Now, when the elbow is at that high point AND the forearm is pointing roughly downward, when the forearm starts rotating up toward horizontal, the elbow COMES DOWN simultaneously. By the time the forearm is horizontal, the elbow is back down.

Chris, what exactly is so dangerous in that scenario? The external rotation during this is very, very much within a “safe” range.

I’ve hypothesized about this one several months ago. I also don’t like the M but it’s just a “theory”. No science behind it. Theory. That being that the speed at which the external rotation happens because of the delay in doing it (someone just said the same thing recently) adds stress. That’s my amateur opinion or theory.