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Here s a 51-year-old man

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with the specific history of

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chronic knee pain getting worse.

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I hate those histories because I

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I use the history

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to focus my efforts and work backwards,

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and I always try and match my report

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to what the clinician needs to know,

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and that comes from the history.

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So you're going to need to train your

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clinicians to give you histories,

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and the best way to do that is for them to

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know that you are accurate, interested,

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passionate in their success.

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So we're going to start out with

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an axial T2 weighted image.

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The first thing that might strike you is this

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ridge that is extending off the lateral femoral

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condyle so that ridge can contribute to notch

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stenosis and therefore, secondary ACL deficiency.

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So that is one of the causes of notch problems,

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so called acquired dysplasia. Now,

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you normally have a little bit of a bump there,

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but this one is just too large.

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Normally, the bump protrudes out maybe two to 3.

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As you look at the case, say, okay, well,

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there is the round cross sectional view of the

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PCL, and you say, okay, the ACL is there.

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It's just a little fat and very black.

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But I can follow contiguous black dark hypointense

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signal all the way from the tibial spines

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back to this ridge, and then I lose it.

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So it's a little bit confusing.

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Maybe that's a little bit more

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of the ACL right there,

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coming all the way into the high inside

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edge of the lateral femoral condyle.

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And you might not be suspicious

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that the ACL is diseased.

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And the reason for that is,

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it's a T2 weighted image, and the ACL is diseased.

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Now, why is that? Well,

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it's because this patient has extensive scarring,

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and you have seen probably in

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some of the other vignettes.

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There's one specific vignette

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I hope you get to look at,

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where PVns just buries a torn chronic acl

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and obscures it. But in that example,

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you actually see some blooming,

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some real shift in the signal character,

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geography,

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and shape of the signal inside the joint

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from one sequence to another.

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This is especially conspicuous when you go from a

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spin echo to a gradient echo or from a

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spin echo to a fat suppression pd.

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Fat, sad, or spur or stir.

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In this case,

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the signal is dark and bland on everything.

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So let's go to our sagittal and let's scroll.

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Admittedly,

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there are enough findings here to sink a ship.

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The medial compartment has failed.

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There's chondromalacia.

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There's penetrating class four chondromylasic

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erosions. There's a deficient,

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small macerated meniscus remnant.

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Most likely it has been partially resected.

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There are multiple speckled foci inside the joint.

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I'm going to ignore those for now.

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And there are innumerable heterogeneous

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signal intensities inside the joint,

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some of which related, perhaps,

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to prior instrumentation.

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There is a mass posterior,

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and that mass is in the midline.

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Now, I don't want to make light of the mass,

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even though that isn't the point of the case.

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I mean, we're all doctors,

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and this mass is right smack dab in the middle.

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It is coming out of the capsule,

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so it's possible it's a ganglion pseudocyst

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that is lined by fibrous tissue,

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but it's hard not to say that it's a capsule

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synovial cyst lined by synovia.

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So on this one, I'm not sure,

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but it is pressing on the neurovascular bundle.

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This is exactly the type of baker's cyst,

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of which there are twelve types,

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this one being in the midline,

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that could wreak havoc with the papateal vein.

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So there are two major teaching points here.

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One, we've got a midline mass.

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We've got to pay very close attention

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to the neurovascular bundle.

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And now let's turn our attention

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to our scarred ACl.

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Now, on the proton density fat suppression image,

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we see a small defect in the distal ACl,

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but look at where it goes.

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The ACl goes here and then never goes any further.

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It is glued to the PCl,

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and there's not very much anterior tibial

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translation relative to the back of the femur.

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In other words,

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they almost line up perfectly posterior cortex

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of the tibia, posterior cortex of the femur,

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same thing on the lateral side.

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That is not uncommon, by the way.

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In fact,

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many individuals will heal their acl to the pcl,

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or inner wall of the condyle,

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and they will be stable for years or for their

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full life. That is not an uncommon phenomenon.

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Contrary to the original,

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previous classic teaching from a quarter of

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a century ago, in which it was thought,

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acls can never heal.

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Just like men and women can never be friends,

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acls can heal and they can

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heal to other structures.

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So let's look at the T2 Now,

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unlike our siderotic case,

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where things are really black

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and really disorganized,

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we can pick out what's left

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of the acl right there.

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And unlike ceteraic material,

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which has a geographic distortion,

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effect on the image.

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The low signal intensity is very concrete in

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its position from sequence to sequence.

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It has a very consistent signal intensity from

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sequence to sequence. Now, admittedly,

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there's a lot more inflammation that shows

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up on the PD. Fat suppression,

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but on the T2 dark signal intensity,

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not as black as hemocytrine, not as dark as air,

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not geometrically distorted.

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No mass effect by pigmented villanodular tissue,

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although there is mass effect in the

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back by this nasty little ganglion.

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Pseudocyst or capsulose synovial cyst.

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And our acl is now glued right there to the

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posterior cruciate ligament and this patient's

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knee, while having innumerable other findings.

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Chondromalasia, an effusion,

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an inflamed hoffus fat space.

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Let's look at the coronal.

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A failed medial compartment with penetrating

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chondromalacia. Class four, no cartilage.

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Let's blow it up.

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Cartilage, no cartilage.

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Just inflamed tissue and synovium and

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very little meniscal tissue left.

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So medial compartment failure,

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and the femur not lining up with the tibia.

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Look how it shifted over.

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And the patient isn't even standing up.

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This conformity change. When she stands up,

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it gets. Gets worse.

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The femur will go over even more.

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So she's got all kinds of problems.

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But the case is meant to show you,

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along with a few other tidbits and benefits.

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Friends with benefits. We've got a chronic,

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full thickness but stable ACl tear

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scarred snugly to the PCL