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Hello everybody, this is Don Resnick coming

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to you from Cincinnati, Ohio.

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It's a privilege to be back with you this year

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and to be able to participate in a course

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that should be really, really good.

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I'm joined by other speakers who I know

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and I know are excellent.

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Our job is to cover the upper extremity,

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beginning approximately with the shoulder

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and heading in a distal direction with stops at the elbow,

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the wrist, the hand, the finger,

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and then learning about the nerves in the upper extremity.

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My job with the first lecture is in fact

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to cover the rotator cuff tendons discussing their anatomy

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and pathologic uh, findings.

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There are three general objectives.

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They're listed here to review the anatomic features

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of the tendons of the rotator cuff

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to describe pathologic abnormalities of these tendons,

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including such things as degeneration, infiltration,

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calcification, impingement, and of course tendon tearing.

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And then at the end I'm going to introduce the terminology

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that we use at the University of California San Diego.

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We apply it to the various patterns of failure that occur

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with the rotator cuff tendons.

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Let's start with some general anatomy,

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and I'm gonna use this drawing

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that I made several years ago.

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It shows you the very simple arrangement of a muscle, tendon

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and bone unit, as I will describe at

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the end of this lecture.

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Although it is simple, unfortunately it is also anatomically

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incorrect in a lot of various sites in the human skeleton.

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But in this particular drawing we can see in fact a single

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tendon entering a single fusiform muscle belly at the

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proximal myo tendonous junction.

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And as we follow it to the right, we can see it exits

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as a single tendon at the distal myo Tendonous junction

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continues to attach to a bone

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and an area we call a footprint and enis

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or an enal organ

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tendons are important anatomic structures.

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They typically are smooth and white.

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They connect obviously muscles to bones as shown here

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and they control joint motion

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and shown at the bottom of this particular slide.

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You can appreciate that they have great tensile strength.

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Well, let's go ahead

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and show the histologic appearance of the tendon,

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which is in red here.

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And I'm showing you cross sections.

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You can see collagen fibers, which are in dark blue,

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are arranged in fales or bundles, which are in light blue.

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And they are oriented along the long axis of the tendon,

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which is terrific for us

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because you see by the major force applied to a tendon

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is a tensile force.

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And these collagen bundles with their collagen

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fibers are oriented ideally to resist

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a tensile force supplied along the length of the tendon.

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Located among the collagen bundles is cellular tissue shown

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here as the background

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and kind of light orange separating the collagen bundles.

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Now let's do an experiment.

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Let's apply a tensile force to the red tendon.

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I'm showing you a cross section of two bundles separated

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by cellular tissue.

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Each of the bundles elongates,

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but as shown by the double-headed arrows, the degree

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of the elongation

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of each bundle is different from the ones next to it.

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And because of that, what occurs is something called

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interfa movement.

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And that movement between these collagen bundles leads

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to friction in the cellular tissue that separates them.

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So you can imagine what may occur in fact, is

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that friction may produce failure,

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but the body recognizes this by providing us

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with a lubricating factor known as luin.

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And that luin shown here on the left

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with several pictures taken from the literature that

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luin shown in dark brown

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lubricates the collagen bundles in that region

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where the cellular tissue separates them.

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So that is a good thing, preventing ideally failure

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between the collagen bundles.

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Now as we get older, a lot of bad things happen,

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not the worst of which is the loss of lubricant.

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And because of that loss, friction may develop again in

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that cellular tissue

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and that friction can lead to failure between

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and among the collagen bundles, not through them

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but between and among them.

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And that pattern of failure is known as delamination.

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It's shown on the left in a coronal section falling a

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arthrogram that we did in this cadaver,

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the we injected blue latex.

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You can see that in the background

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and you can see here beautifully

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that there is a full thickness tear

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right here at the footprint.

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These are the bursal sided fibers.

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These are the articular sided fibers.

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So delamination

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or sliding between the collagen bundles in the deep

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and superficial fibers has occurred.

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Now this is a baseball picture.

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We've examined that picture with an autogram

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and we're showing you a coronal image on your left

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and an abducted, externally rotated image on your right.

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And you can see that the contrast material is passing from

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the joint through the articular side fibers reaching the

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intra region.

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As we look on the right, an abducted, externally rotated

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uh image shows you in fact that delamination,

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these are the articular sided fibers.

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These, the bursal sided fibers

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and contrast material is running

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between those two groups of fibers.

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This is tendon de degeneration.

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Now let's look at some further anatomy

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and look at the anatomy of the greater tuberosity

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we're classically taught.

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If you look at that anatomy here, shown in a drawing

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of a sagittal section with this anterior, in this posterior,

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you will identify three facets.

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The anterior facet is also called the superior facet,

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shown at the top, it is a flat region.

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On the greater tuberosity, the only tendon that connects

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to the sup facet is the supraspinatus tendon.

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As you go to the next facet, it's obliquely oriented,

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shown here in this region, we go to the middle image

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and we can see here the oblique facet, the middle facet

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of the greater tuberosity anter.

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The supraspinatus tendon attaches to that facet,

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which we can see here more posteriorly,

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the in infraspinatus tendon.

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So let's go to the bottom of our three images.

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This the more posterior image here is the in infraspinatus

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tendon attaching to the oblique facet

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of the greater to veracity.

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The final facet, the inferior

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or vertical facet shown here, the only tendon that attaches

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to it is the Terry's minor tendon.

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Now there have been some recent articles in the literature

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that have indicated in fact that if you look closely,

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we're not giving enough credit to the footprint

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of the infraspinatus.

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And in that article it was shown

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that the infraspinatus tendon footprint shown in purple here

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extends far anteriorly on the greater tuberosity.

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Here's what it would look like in some sections we did

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of our own cadaveric material.

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This is far anteriorly on the greater tuberosity

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and that is the in infraspinatus tendon

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that is attaching to it.

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So it does extend more anteriorly than

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what we originally believed.

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Now take a look at this case

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where I'm showing you four coronal images.

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These are fat suppressed.

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The most posterior one is at the bottom,

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the mo most anterior one is at the top.

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This is clearly as we look at the bottom,

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the in infraspinatus tendon,

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and I'm putting arrows on where I think it is.

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As we move anteriorly,

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here's the tear shown here in these old

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images as bright signal.

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Now you might originally have called this a supraspinatus

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tendon tear, but I wonder if what we're looking at

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because of the new extended footprint

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of the infraspinatus is an infraspinatus tendon

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there to prove that point.

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Others have looked at the anatomy in greater detail

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and they have identified a separate impression

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or uh, area of elevation known

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as the lateral impression shown here, triangular in shape

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between the superior and middle facets.

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This is the area of attachment

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of the infraspinatus tendon anteriorly on the greater

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to porosity.