Tendons of the ankle: Jose Tendons of the Ankle: o Normal NMR appearance: low signal on all pulse sequences

s T1 is good for anatomic detail T2 is useful for assessing increased fluid content often present in most pathologic conditions o Best evaluated in the axial plane EXCEPT the Achilles tendon sagittal! Tendon pathologies: o Tenosynovitis-fluid completely surrounding the tendon o Tendon degeneration/tendinosis- abnormal thinning or thickening o Partial tear- intratendinous high signal o Complete tear- complete tendon disruption o Subluxation/dislocation- abnormal tendon position Tendon tears o Interstitial tears- tears along the LA of the tendon (picture) Increased signal on T2 parallel to the LA Sequelae of mucoid degeneration o Partial thickness: tears along the transverse axis o Complete tears- aka full thickness, through and through across the transverse axis Tendons tend to contract proximally Mucoid degeneration (picture) o Abnormal collagen makeup of the tendon o Gray increased signal intensity, seen on T2, fusionform enlarged tendon w/ abnormal intra-substance signal intensity o Predisposes to tears along the LA True tears are partial and full thickness o Increased signal intensity on T2, perpendicular to the LA o Tendons tend to retract proximally

There are two bursae that are typically involved, there is the retrocalcaneal bursa and a retroachilles bursa which can also become inflamed. Dr. Glickman says that the sagittal is a great view to look at the AT, but its actually the axial which will help you to pick up all of the little tears; sometimes on the sagittal view you can miss little surface tears but on the axial images are cross sections through the tendon and that is where you are going to get your more precise information about the thickness of the tears and the extent of involvement. So this is showing tendinosis of the AT, the little bright foci are interstitial cavitation (mucoid degeneration), this isnt a focal area of mucoid degeneration, these are actually a multifocal diffuse areas of cavitation and there doesnt seem to be any surface tears. The structure on the axial view in front and to the right of the AT is the plantaris, and that is the tendon that goes along with the AT on the medial side (attaches to the medial aspect of the calcaneal tuberosity). There is also a Haglunds deformity (pump-bump) in this patient, sometimes you see it and there is no sequelae at all (there is no tendonitis, no edema), in other cases it is symptomatic and in this case this is diagnostic of Haglunds syndrome. So the surgical treatment for this patient was to de-bulk the tendon and sutured it with a krackow stitch, and we were thinking of taking a tendon that is nearby (FHL tendon) and augmenting it, but there was no need at this point. We also removed part of the huge bursa that you can see. We should have removed the bump because this is just going to recur, but the patient was n

ot interested in having any osseous work done. Calcium is usually really dark on all MR imaging, so this is not calcium, but there is a thin, linear focal area, as opposed to the other image where we saw lots of diffuse multifocal areas of those bright signals, so that is not multifocal mucoid degeneration, but it is actually diagnostic of an interstitial tear, so this is a little bit of a higher grade injury of the Achilles, we also have retrocalcaneal bursitis, not much of a Haglunds deformity.

He has loss of muscle power, which is key. Starting out at the top right picture: Retrocalcaneal bursitis is present, longitudinal interstitial tear in the AT, high signal intensity posterior to the tendon The thing about the AT that is different than every other tendon in your ankle is that it actually doesnt have a tendon sheath, so technically, you never really get tenosynovitis of the AT, it is either called peritendonitis or paratenonitis, because although it doesnt have a tendon sheath, it has the paratenon. Arrow in the picture in the bottom right corner is pointing to interstitial high signal (little interstitial tears or cavitations), but there is actually this little area that extends through the anterior surface of the Achilles, and that is actually a little surface tear. Back to the top right corner picture, there is this high signal that is actually inside the bone, which is bone marrow edema, this indicates that the symptoms are more severe, because bone marrow edema hurts. Where is the watershed area in the AT? 2-6 cm from the insertion! That is where the AT fibers begin to turn, and the watershed area is going to be on the lateral side of the tendon, so obviously there are more NVS on the medial side so it is going to be more vascular there.

Presence of an enthesophyte on the posterior aspect of the calcaneus (the difference between an enthesophyte and an osteophyte is that enthesophytes form at the insertions of tendons and ligaments, whereas osteophytes form at the margins of joints and they are not attached to tendons or ligaments).

Things that are bright on T1 are fat, blood, proteinacious material, melanin, and gadolinium (contrast agent), so in this case, theoretically, this could be a little tear with blood in it, but the fact that it looks so normal otherwise and that it seems to be continuous with the bone here means that it really just has to be os. If there is any doubt, an easy radiographical test to determine if this is blood or bone is an XR!

Side notes: Baxters neuropathy- what is the finding on imaging? Atrophy of the ADQM! That is the muscle on the lateral side, on the plantar aspect, sometimes you see high signal within it if it is an acute denervation or relatively acute, but the later stages are atrophy, that is chronic denervation and that comes from entrapment of the lateral branch of the inferior calcaneal nerve, which goes right by the spur that you see in plantar fasciitis and it is one of the things that can cause lateral plantar foot pain BUT be careful, because often you see atrophy of that muscle and it means nothing, you can get it with just senescent changes in older people, but if you have that combined with plantar fasciitis and otherwise unexplained plantar fasciitis pain, Baxters neuropathy is a good possibility. AT tendon xanthoma occurs with hypercholesterolemia. You will see young people with high cholesterol will have cholesterol deposits of crystals in the tendon, and they make the tendon look very enlarged, this would be a differential in the first case that we saw. Gout: diffuse, low signal thickening of the AT, sometimes with a little bit of high signal deposits. You like to see some other characteristics of gout like periarticular erosions, maybe some tophi, you want the patient to be in the right demographic group, have the right history.

Sesamoid pathology:

What would be the reason for sending this patient for an advanced imaging study? The patient had surgery 3 months ago- one of your main concerns is infection (some sort of OM), AVN, this sounds like a situation of hallux limitus so you would expect to find osteochondral defects at the first MPJ, not just at the metatarsal head or the base of the proximal phalanx, but also at the sesamoids- the sesamoids are being subluxed, especially the fibular sesamoid, so you would expect to find arthritic changes there. The sagittal T2 is the best place to look for your sesamoids and for arthritis of the

hallux-sesamoid complex, there is articular cartilage on the plantar aspect of the first metatarsal head, and there is also articular cartilage along the sesamoids, and you can get arthritis there just like you can at any joint, OA is the MC. On the sagittal view we are coming in from the medial side and we are first seeing the tibial sesamoid, and we can see arthritic change, degenerative change, subchondral cyst formation, chronic marrow edema, and there is thinning of the cartilage. The fibular sesamoid is where the action is clinically on this patient, and you can see (although barely) that there is some osteophyte formation, it is a little hard because of the angle and because the lateral sesamoid is laterally subluxed, as it often is in cases where there is arthritis of the joint. You can see on the axial that there is actually narrowing and osteophytes at the margin of the joint. There is no evidence of OM, on the T1 (bottom right) there is normal marrow signal within the sesamoid bones, if it were OM you would see a markedly hypointense signal on the T1 weighted images, marked confluent T1 hypointensity are the buzzwords in radiology, as opposed to reactive hyperemia (the main differential) when there is surrounding cellulitis but no OM; reactive hyperemia is a fine, reticulated pattern of T1 hypointensity. Other findings in this patient: there is no osteonecrosis (would be a really dark signal), no fragmentation, so there is basically just some DJD and lateral subluxation.

There is a lot of debate in the radiological literature about what sesamoiditis actually is, its kind of an ambiguous term, so you should understand that it is not a specific pathological process when you talk about sesamoiditis in a radiology report. This can either be a bipartite sesamoid or a fracture- this image shows regular edges so it is more likely a bipartite sesamoid, rather than an acute fracture which would have sharp, jagged edges. The problem is when you get into the cases of a subacute or a chronic fracture, over time the edges resorb, remodel, and smooth out. You can see on the T1 weighted image the fibular sesamoid is quite dark compared to the tibial, which is related to the bone marrow edema, so this is a case of sesamoiditis in an incidentally congenitally bipartite fibular sesamoid.

When you are ordering advanced imaging studies, what are you ruling out? Infection and AVN! First image: So we are coming in from the medial side and this is a fluid-sensitive sequence so its either a STIR or T2 Fat-Sat, so fluid is going to be bright, marrow edema is going to be bright. We see some changes at the head of the first metatarsal, it should be nice and smooth and it is very irregular, there is also a bright signal of marrow edema, in this picture you can see the tibial sesamoid, which has increased signal intensity, which could represent marrow edema, or infection, and edema is also the first sign of osteonecrosis. The distance between the sesamoid and the rest of the first MPJ seems a little increased, so we wonder about the joint capsule. You can also see on the next image that there is very bright signal on the tibial sesamoid, and at this point, looking at the T1 (not shown), its not really that dark, not really any evidence of OM, and looking at the T2 it is bright. The way radiology would read this is as non-specific marrow edema in the tibial sesamoid, it COULD be early osteonecrosis (this is due to the hypoxia, and the inflammatory changes in reaction to the hypoxia), there could be a capsular injury versus post-surgical change of the first MPJ, and in terms of the fibular sesamoid there are some inflammatory changes. Side note: two key findings in the late stages of osteonecrosis- 1) marked hypointensity on all sequences, T1 and T2, it is going to be really dark. 2) Fragmentation- in end-stage osteonecrosis the bone is so dead that it cant hold together under trauma anymore so it starts to fracture chronically.

Note the irregular, jagged edge of the proximal fragment of the tibial sesamoid. That, plus the signal intensity in between which is very high, as well as the history, which is highly suggestive of trauma. If this were turf toe, you would expect to see hyperintensity along the plantar plate, which kind of blends in with the joint capsule. In turf toe you are going to get a lot of hyperintensity, inflammation, and irregularity in the region of the distal attachment of the plantar plate, that is what the injury is.

Side note: ****Turf toe on XR: would the sesamoids be distal or proximal?

The bone marrow in the tibial sesamoid has an irregular serpiginous pattern, which is suggestive of AVN, it is a serpiginous pattern of hypointensity reflective of some dead bone with fragmentation. So how we would read this is old, not end-stage, osteonecrosis with marrow edema which could reflect the active symptomatology.

PTTD: Tendons of the ankle o Normal MR appearance o Should be low signal intensity on all mages o Magic angle effect- when viewing tendons When the fibrous of the tendons are 55 to the mian field Why ankle will be pf about 20 on MRI. Tendon pathologies: o Tenosynovitis-fluid completely surrounding the tendon o Tendon degeneration/tendinosis- abnormal thinning or thickening o Partial tear- intratendinous high signal o Complete tear- complete tendon disruption o Subluxation/dislocation- abnormal tendon position Anatomy: o The posterior tibial muscle takes origin from the posterior aspect of the tibia, fibula, and interosseous membrane, passes immediately posterior o the medial malleolus, and inserts into the navicular tuberosity, o Tendinous slips are also sent to the plantar aspect of the base of the metatarsals 2, 3, and 4, and the intermediate cuneiform o Right underneath the MM in a groove called the Medial Retromalleolar Sulcus or groove is the PTT. The tendon has its own synovial membrane over it. It shares a retinaculum with the tendon beneath it, FDL, and FHL.

o A zone of relative hypovasculariy exists posterior and distal to the medial malleolus. Function in gait o Its primary function is to decelerate and reverse pronation in the stance phase of gait by adducting and plantar-flexing the navicular on the talar head. o It directly opposes the midfoots abductory pull of the peroneus brevis. o It keeps the MTJ locked in early heel lift. Pathologic signs o When the tibialis posterior tendon ruptures, the talus plantarflexes, adducts, and moves anteriorly, possibly disrupting the navicular articulation. The longitudinal arch collapses, the spring ligament is placed under tension medially, Choparts joint abducts and the calcaneus everts. Therefore the pathomechanical presentation will appear as a flatfoot. In fact, a severe pes planovalgus foot with significant arch pain may be the presenting complaint after tibialis posterior tendon rupture. Symptoms o PTT acute rupture may not cause noticeable deformity and is often diagnosed as a medial ankle sprain. o The initial injury may or may not be recalled by the patient. o Usually the injury becomes more painful by continued activity and weight bearing. o The initial pain may be poorly localized. o Overtime the patient will notice continued flattening of the medial arch, which will prompt medical attention. Clinical signs o Pain, tenderness, warmth, and swelling will occur inferior to the medial malleolus. o The patient will have loss of forceful inversion. This is especially noticed when the foot is held in a plantarflexed position. o The tendon may not be palpable behind the medial malleolus as it courses to its insertion into the navicular. o The too many toes sign is also evident, such that when viewing the patient posteriorly more toes are seen on one foot versus the other, a factor of forefoot adduction. o Heel rise test aka Jacks test: patients are unable to invert the affected heel when they raise their toes. o Patients often states that they noticed one of the arches has collapsed.

Classification: Johnson and Strom Important to note that in stage 1 you still have NORMAL ALLIGNMENT. Elongation of the tendon- rearfoot valgus, too many toes FDL transfer FIXED deformity of rearfoot valgus FDL transfer or fusion of the TN, or calcaneal OT (MDCO)*** (Myerson) stage 3 + lateral ankle painonce it has progressed to a more rigid deformity, you are going to have sinus tarsi pain, STJ, CCJ arthrosis, CFL impingement, and possible osteophytic changes of the fibula.

Tendon is susceptible to dysfunction WITH INACTIVITY*** as opposed to most of the other tendons, which is overuse! o Caused by impingement and ischemia o Occurs in middle aged patients, F>M o Risk factors: DOHR- DM, HTN, Obesity, RA (RA patients have to take steroid medications) Tendon disorders o Tendinitis: tendon with active inflammation o Tendinosis: tendon with degenerative histological changes with the absence of inflammation Tendon tears o Interstitial tear: tears along the LA of the tendon, intratendinous Mucoid degeneration: a description of the collagen being degenerated. Seen on T2- Fusion-form enlarged tendon with abnormal intra-substance signal intensity (gray); pre-disposes to tears. This is usually seen in the Achilles tendon but it is not uncommon to see in the posterior tibial tendon. Parallel to the long axis Sequel of mucoid degeneration o Partial thickness tears- tears along transverse axis of the tendon o Complete tear- tear through and through along the transverse axis of the tendon o True tendon tears Partial and full thickness Perpendicular to the long axis Tendon tends to retract proximally Rosenberg Classification of Posterior Tibial Tendon Tears o Type 1 (hypertrophic/bulbular) Longitudinal splits with ischemia PT tendon is 4.5x the width of the FDL 4 tendons (TTDH, tom, tom, dick, and harry) sign occurs with severe swelling and splitting of the tendon, the PTT looks like two tendons with fluid in the middle. o Type 2 (atrophic/attenuated) Chronic interstitial tear with severe splitting that attenuates the tendon to 1/3 of its normal width. o Type 3 (full thickness) Complete rupture and proximal retraction Gap noted where the tendon used to be and is replaced by bright fluid intensity signal on T2. Conti- MRI classification o Type 1A- 1-2 long splits in the PT tendon without tendon degeneration o Type 1B- Multiple longitudinal splits and fibrosis without tendon degeneration o Type 2- Narrowing of the PTT, longitudinal splits, tendon degeneration o Type 3A- diffuse tendon swelling with uniform degeneration o Type 3B- Complete rupture o THIS IS FOR PREOPERATIVE PLANNING Funk Surgical Classification of PTT rupture- so you suspect a tear, you open it up and this is what youll see, and you will group it 1-4: o 1- Avulsion of tendon at the insertion o 2- Midsubstance tear at the level of the medial malleolus o 3- Longitudinal splits without complete rupture

o 4- Tenosynovitis without visible disruption Funk: this study examines the importance of intra-operative findings to qualify tibialis posterior tendon pathology and guide operative treatment accordingly, cautions against excessive emphasis on radiographic findings to predict pathology, and suggests that such pathology is not the only cause of AAFF. Lawson 1985/Coughlin: the tendon inserts into the Navicular o Type 1- os tibiale externum sesamoid o Type 2- articulating ossification center, accessory navicular: the medal ossification center never fuses to the body and you get a separate bone. There is a fibrous bridge in between the accessory navicular and the medial side of the navicular. 4% have accessory navicular. o Type 3- fused ossification center, gorilloid navicular, or arcuate-shaped navicular o This is important because this can cause an abnormal pull of the tendon in this area so you have more tendency to rupture, inflammation, or stress reaction. Watson Jones Navicular fracture- dont confuse this with an ossicle! It will have irregular borders. o Type I: Tuberosity fracture May be an isolated fracture or an avulsion by the PTT during acute eversion. Must be distinguished from a congenital os tibiale externum and possible MTJ subluxation should be considered. Treatment: Immobilization for 4 weeks. PTT impingement at insertion o Curnate shaped navicular or accessory navicular o The shape changes the course of the PTT and chronically irritates it and results in chronic impingement and ultimately tendon tear o Accessory navicular instability will have bone marrow edema noted at the level of the synchondrosis secondary to micromotion. Impingement at tibia (at the retromalleolar sulcus) o Caused by osteophyte o Every time the foot flexes the osteophyte impinges on the PTT

Note that the PTT is about 2x the size of the FDL, at this level the PTT is about normal size.

Far left picture: At the insertion of the PTT, you can see that there is some fluid in the tendon sheath, and the ligament running between the navicular and the calcaneus is the superomedial component of the spring ligament (can be seen on the axials and the coronals). This one looks more stretched out than usual and it also has some high signal within it, which is compatible with degeneration of that portion of the spring ligament. And there is no full thickness tear there, but maybe low-grade partial tear of the superomedial component. Right picture: As you come down below the Navicular, then you catch the other components of the spring ligament, so there is the medial plantar component, and then the longitudinal plantar component (can be seen on the axial images). Far left picture: The oblique axial images are also quite nice for looking at the PTT and the spring ligament, the superficial deltoid and the superomedial component of the spring ligament are kind of continuous, and this is easy to find because it is just deep to the PTT. In this case there is no complete tear of the spring ligament, but it looks a little more stretched out than usual and there is some high signal within it, and that is probably because of the PTTD in this case. Right picture: So back to the PTT: we already said that there is some fluid in the tendon sheath, so that is tenosynovitis, this is probably mild to moderate. The tendon itself is graded upon the signal intensity and its size, so this one is too thick distally, compared in size to the FDL you can see that it is reaching that 4.5x cross sectional area in size, and there is also some interspersed high signal within it, so this is a tendinosis of the tendon at this level. One of the important findings here is that there is sub-enthesial marrow edema in the medial navicular. So there is no accessory navicular, but clearly the navicular is reacting to the problems in the PTT, and that is called sub-enthesial marrow edema (sub-enthesial because it is the portion of the bone that is just sub-adjacent to the tendon attachment site). We dont see a through-and-through tear of the PTT, but this is not a happy PTT. Then, we should look for the osteophyte on the retromalleolar groove on the axial images, this patient does not have one that you can visualize. I think the main things to know how to look at the spring ligament because there are so many different components, but the main idea is: Axial and the Coronal for the superomedial band, and then in most patients you can catch the plantar components on the axial images, but those are really best seen on the oblique axial, in this plane you can see the longitudinal components of the spring ligaments quite well.

The key here is that the patient also has tenderness at the level of the sinus tarsi, this should give you an indication that either the PTT is partially torn or affected that the patient is getting arthritic symptoms, or symptoms in the STJ and possibly in the CCJ. When you first start looking at the images you should check to see the alignment of the tarsus- is the axis of the talus in line with the axis of the first metatarsal? Look at the alignment of the hindfoot in the coronal images, look at the valgus, look at how much of an angle there is between the talus and the calcaneus. So back to the PTT: this PTT has more than the typical amount of fluid, once youre above the MM and youre seeing fluid in the tendon sheath that is more than what should be seen, so this is another patient with tenosynovitis. Then you look at the size of the PTT and compare it to the FDL, at the level of the distal tibia, this PTT is about double the size of the FDL, so thats okay. As we get down further, and compare it again, it is not actually looking very large. When you get to the attachment of the PTT, remember it doesnt just attach to the Navicular, it also has attachments that go to the cuneiforms, so it is normal for it to widen slightly. Spring ligament (red dot)- this is the superomedial component, and this looks pretty normal, especially compared to the last patient. This component is supposed to be a thick band, so this looks okay, you look at the signal intensity, and its maintaining a pretty low signal throughout its course so thats good.

In this case the PTT has maybe mild tendinosis, but its not particularly enlarged, and there is no tear. Now this patient said that they had pain in the sinus tarsi so we should look at that.

You should use the sagittal T1 to look at the sinus tarsi, just to look at the fat, and sometimes you can get a good look at the tarsal sinus ligaments. On this patient, youre not seeing them too well, this is the cervical ligament (white arrow), the fat overall looks very good, there isnt any scar, doesnt seem to be any cartilage defects, so in this case, the imaging doesnt really match the exam very well.