Foot And Ankle MRI: Tendons and Ligaments
Hi! This lecture is on foot and ankle MRI with emphasis on the tendons and ligaments. I am Steven Needell, and I am the Director of Musculoskeletal Imaging at the Boca Raton Community Hospital in Boca Raton, Florida.
Let us begin our lecture talking about MR sequences and image contrast. T1-weighted images are the best images for evaluating MR anatomy. On the T1-weighted image, the fat is bright and the fluid is dark. This is a patient with a Charcot foot. Note all the abnormal bone marrow changes in the mid foot. Abnormal bone marrow in a T1-weighted image appears dark.
Contrast that with T2-weighted image. On the T2-weighted image fat becomes darker and fluid becomes brighter. In modern imaging most T2-weighted sequences are performed with fast spin echo one of the problems with fast spin echo sequence is abnormal bone marrow is much less conspicuous than normal bone marrow on these fast T2-weighted sequences. Note how the gray scale on the mid foot in this patient is about the same as the normal bone marrow in hind foot.
Because of the limitations in the fast T2-weighted images, orthopedic MRI has largely turned to the fat suppressed or STIR sequence as the mainstay in detecting bone pathology. In the fat suppressed or STIR sequences, normal fat becomes dark black as in the hind foot and ankle bones on this patient. Note how abnormal bone marrow becomes conspicuously white as seen in the mid foot. Fluid is also quite bright on the STIR or fat suppressed sequences.
One of the most intimidating things about performing high quality MRI of the foot and ankle is the sheer volume of anatomy that you have to understand and to master. The foot and ankle contain 26 bones, 33 joints, 107 ligaments, and 19 muscles and tendons.
Now, we will talk about basic axial MR anatomy. On the left is an axial T1-weighted image taken at the level of the tibiotalar joint. I know this is a T1-weighted image because the subcutaneous fat and the bone marrow in the tibia and fibula are both bright white. On the right side, we have an axial T1-weighted image taken at the level of sinus tarsi and middle subtalar joint. Now, we will talk about the tendons. The tendons should always be dark black in signal intensity on all sequences. If the tendons are increased in signal, they are abnormal, either related to MR artifact or to tendinosis or tendon tearing. The most posterior tendon is the Achilles tendon. The Achilles tendon should always have a flat anterior margin. If the Achilles tendon has a convex anterior margin, it is abnormal. Of the tarsal tunnel tendons, tibialis posterior tendon is the largest, could be about one to two times the size of flexor digitorum and flexor hallucis longus. The posterior tibial neurovascular bundle lies in between these tendinous structures. Anteriorly, we have the tibialis anterior tendon, which can be about the same size as tibialis posterior tendon and never any larger than it. Lateral to these lie the extensor tendons. On the lateral side of the ankle, we have the peroneal tendons; posteriorly is peroneus longus tendon, anteriorly is the peroneus brevis tendon. The sinus tarsi should also be fatty in signal intensity.
This is a case presentation of a 38-year-old marathon runner with posterior ankle pain.
The differential diagnosis of posterior ankle pain can be quite extensive, it can include active Achilles tendinitis chronic Achilles tendinosis, Os Trigonum syndrome or posterior impingement, fracture of the posterior process of the talus, tendinitis of the flexor hallucis longus sheath, peroneal tendinitis, tendinitis of the posterior tibial tendon, sprain of the deltoid ligament, osteochondral lesions of the talus, and Haglund syndrome.
The discussion of tendon disorders may be approached in a stepwise or pyramid fashion. The pyramid is a useful analogy because all tendons in the foot and ankle with the exception of the peroneal tendons start out with tendinosis and proceed through a stepwise fashion ultimately to a full-thickness tearing. The term tendinosis is preferable to the term tendinitis. Tendinitis would imply active inflammation and active inflammation is distinctly absent under histologic evaluation in patients with tendinosis. The next step would be intersitial tearing which is a longitudinal tear. Partial thickness tears are along the transverse or short axis of the tendon and a full-thickness tear or complete tear is a complete transverse resection of the tendon along its short axis.
We will use the Achilles tendon as a good example to represent tendon disorders in general and what can go wrong. The Achilles tendon on an MRI should always be dark and straight, as I mentioned before, should always have a flat anterior margin. The Achilles tendon is the second longest tendon in the body behind plantaris; it is the largest and the strongest tendon of the body. It is most susceptible injury in its middle third which is watershed area representing where vasculature from superior and inferior meet resulting in a potential area of ischemia. The Achilles is the most frequent running injury and is most commonly injured in middle-aged elderly men.
The initial phase of Achilles tendon degeneration or chronic Achilles tendinitis presents as a round shape of the middle third of the Achilles tendon. Note here in the watershed area that the Achilles tendon is swollen, this is related to ischemia, hence the name hypoxic degeneration.
Hypoxic degeneration is the most common form of chronic Achilles tendinosis. It does present as a symptomatic enlarged or rounded tendon.
The next pathologic step of progression in Achilles tendon degeneration presents as a fusiform enlarged Achilles tendon with abnormal intrasubstance signal on the T2-weighted images. Note as indicated by the arrows, there are stippled foci of bright signal on the sagittal fat-suppressed T2-weighted image. These findings are known as the mucoid degeneration. Mucoid degeneration predisposes to frank tendon tearing and presents as bright intrasubstance T2 signal.
Intrasubstance tendon signal changes may then progress to the next stage where you have frank interstitial partial thickness tearing. Interstitial tearing presents as bright fluid intensity signal, which is longitudinal or parallel to the long axis of the tendon. Most commonly intersitial tears are sequela of mucoid degeneration.
While Achilles tendon pathology most commonly occurs in its watershed area and its middle third, the other area of large amount of stress is at the Achilles tendon insertion. Insertional tendinitis most commonly occurs in runners and presents as small longitudinal tear at the Achilles tendon insertion upon the os calcis. We are on the look out for subtendinous edema subtendinous edema within the os calcis, which is a secondary indicator of tendon pathology. This reactive bone marrow edema is generally a hyperemic process.
Full-thickness ruptures of the Achilles tendon may be apparent upon clinical examination. On the MRI, these findings may be quite conspicuous as well. We see a ruptured and often retracted tear of the tendon. We see a large amount of fluid and edema highlighting the ruptured tendon margins. Most commonly full thickness ruptures occur in watershed zone at the middle third of the tendon. In this case, we also see a full-thickness rupture at the tendon insertion. You can also see a rupture of tendon at its musculotendinous junction. Conspicuous findings on MRI are evidence of bleeding with hemorrhage and fluid highlighting the ruptured tendon margins. You can also see the evidence that this patient has longstanding underlying disease. Similar to the patient before, there is also evidence of hyperemic change within the subtendinous portion of the os calcis.
Not all pathology associated with the Achilles tendon relates to the tendon itself with regard to tendon tearing or tendon degeneration. There may also be inflammatory changes within the peritendinous soft tissues. In this patient, for example, we have a large amount of edema seen on fat -suppressed T2-weighted images within Kager pre-Achilles fat.
Ultrasound has received a large amount of attention in the literature recently in large part because of its highly portable nature. Ultrasound machines are also relatively inexpensive particularly when you compare them with MRI. I have personally found ultrasound to be most helpful in the foot and ankle in looking for foreign bodies. When the patient steps on a nail, it is very easy just to get an x-ray to see how deep the nail went and to confirm they have a nail or a needle that is in there, but when you do not have a radiopaque foreign body in there, MRI is not going to be very good because most foreign bodies do not have fat or water molecules in them; therefore, ultrasound is what we most commonly use look for foreign bodies that are not evident on x-ray. Ultrasound is very good when evaluating superficial tendons. It is limited, however, in its ability to look at the structures around the tendon, particularly the ligamentous and osteocartilaginous structures are very difficult to evaluate on ultrasound. The biggest limitation of using ultrasound is that it is highly user dependent. It requires a motivated and experienced technologist and physician when looking in
orthopedic cases using ultrasound. The anatomy is not obvious on ultrasound and the pathology is often at times difficult to quantify.
This an ultrasound of Achilles tendon performed on a patient with chronic tendinosis. I think it would be hard to press to show it to most people and have them differentiate whether this is a thyroid gland or pancreas or an ovary. Most people do not have lot of experience in evaluating tendons in ultrasound imaging, and this is one of its great limitations. However if you look carefully, you can see that tendon is the dark or hypoechoic region. On the left side is the longitudinal view of the tendon, and on the right side, we have a transverse view of the tendon. Just as we saw earlier on the MRI sequence, the anterior margin of a normal Achilles tendon should be flat; in this case, however, it is rounded. These are indicative of a hypoxic degeneration and again here on the right side you see a round anterior edge of the tendon. Note that the anterior edge on the ultrasound is the area that is farthest away from the transducer that is going to be at the bottom of this film.
Here is a patient with more extensive pathology seen in ultrasound. Note also that these images there are black bars dividing the ones on the top into three images because the ultrasound has a limited field of view and these are three different images that we took and pasted together. On the right side marked INS is the insertion of the Achilles tendons; on the left side, we have this large fat, dark, black Achilles tendon with a very disorganized shape. On the bottom image is a transverse image where you can see that there is actual fluid which is manifested by the dark or anechoic region around the tendon.
Here is another case of an insulin-dependent diabetic with inversion pain along the instep and swelling behind the ankle. The pain gets worse when walking and especially towards the end of the day.
This is a classic presentation of a patient with posterior tibial tendon dysfunction.
Abnormalities of the posterior tibial tendon can generally be divided into subdivisions of posterior tibial tendon dysfunction and posterior tibial tendon tears.
Posterior tibial tendon dysfunction tends to occur in middle-aged women and is a combination of both impingement and ischemic processes. Unlike other tendons in the body which are most susceptible to injury following over activity, the posterior tibial tendon is more susceptible to dysfunction with inactivity and subsequent ischemia, therefore patients who are sedentary including obese patients, diabetics, rheumatoid arthritis, and hypertensive patients are the ones that are most likely to be getting posterior tibial tendon dysfunction. This had led some to describe posterior tibial tendon dysfunction as the angina of the lower extremity.
Note this patient with a markedly enlarged posterior tibial tendon the tendon is at least 4 or 5 times the size of the flexor tendons and certainly much larger than anterior tibial tendon. The enlargement of this tendon relates to an underlying hypoxic degeneration similar to the pathology we saw at the Achilles tendon. Note also that there is abnormal signal within the substance of the tendon related to longitudinal or intersitial partial thickness tearing.
The most common classification used of tibialis posterior tendon tears divides the classification into 3 different types, type 1 or the hypertrophic tear results from longitudinal splitting of the tendon with underlying ischemia, the tendon is swollen 4 or 5 times the size compared to flexor digitorum longus tendon.
With extremely severe splitting of the tendon, this can actually result in the appearance of the 4 tendon sign or the Tom, Tom, Dick, Harry sign as noted here. Note also that there is a large amount of fluid distending the posterior tibial tendon sheath, which is a strong secondary indicator of dysfunction.
The type 2 or atrophic tear is a chronic interstitial tear which results in severe attritional changes which splint the tendon resulting in a width of about one-half to one-third its normal size.
The type 3 tears are full thickness tears with complete rupture and proximal retraction. On MRI, you see a gap where a tendon used to be and is now replaced by fluid intensity signal.
As I mentioned before, tibialis posterior tendon pathology results often times as a combination of both ischemia and impingement. Notice in this patient the accessory navicular bone has not completely separated and there is osseous union along its synchondrosis resulting in this hooked configuration in the navicular bone. This configuration is known as a cornuate configuration of the navicular. Anytime the posterior tibial changes its course or has spur formation irritating, it chronically will result in chronic impingement and ultimately may result in tendon tear.
The accessory navicular bone is a common secondary center of ossification, which may result in alteration of the normal course of posterior tibial tendon. This itself may result in impingement; however, the synchondrosis of the accessory navicular may also be susceptible to fracture as well as to pseudoarthrosis. Always look for a bone marrow
edema or fluid intensity signal within the synchondrosis which is a secondary indicator of the presence of micro instability in the synchondrosis itself.
Here is an example of a patient with extensive bone marrow edema at both sides of the synchondrosis. Note here the arrow indicating a gap in the synchondrosis which is unusually widened and the extensive bone marrow edema within the navicular as well as the within the ossicle itself. This is a patient who has had a fracture with ongoing micro instability. Note also posterior tibial tendon is unusually large in size related to dysfunction secondary to the changes here mentioned.
Note this axial T1-weighted sequence at the level of the distal tibia in another patient, which reveals a very large excrescence arising off the posterior medial margin of the distal tibia. This large bone spur acts as a dagger which chronically impinges upon the tendon whenever the foot is flexed or extended. Note how abnormal in both morphology and signal posterior tibial tendon appears just posterior to this long spur.
Flexor hallucis longus tendon courses in a groove along the posterior margin of the talus interposed between medial and lateral tubercles of the talus, the lateral tubercle is usually larger than the medial and may or may not be fused after puberty. If it remains separated, it is called the os trigonum. Posterior ankle impingement may be due to a large os trigonum, a thickened posterior capsule, calcific debris, or a large posterior calcaneal process.
This is an axial fat-sat T2-weighted sequence through the ankle joint. There is the large amount of fluid distending the flexor hallucis longus tendon sheath indicating stenosing tenosynovitis. Posterior ankle impingement is manifested by pain posteriorly in the ankle and may occur with or without FHL tenosynovitis. There are 3 anatomically tight sites for the FHL tendon which may have tenosynitis One is in the fibroosseous tunnel between the medial and lateral talar tubercles, the second is within the sheath behind the medial malleolus, and lastly between the sesamoid bones of the hallux.
The factors predisposing to FHL tenosynovitis include repetitive injury, direct blunt trauma and activities requiring extensive plantar flexion like ballet. Note that not all fluid distending the FHL tendon sheath is abnormal. Physiologically about 20% of patients may have the connection of the ankle joint to the FHL tendon sheath, so when u see an isolated or disproportionate amount of fluid distending the tendon sheath that is when you start thinking about tenosynovitis.
Here we have another case presentation case of a 14-year-old ballet dancer complaining of pain and tenderness posterolaterally in the ankle. Most common differential diagnoses here are peroneal tendon pathology, FHL tendon pathology, or Achilles tendinitis.
This is a nice example of a patient with os trigonum syndrome or posterior impingement syndrome. There is a large posterior process of the talus, which is actually an os trigonum, you can tell because on the sagittal T1-weighted image there is vertically oriented low intensity line indicating the synchondrosis. When you look on the STIR sequence, this corresponds with bright vertically oriented signa. This indicates that there is pseudoarthrosis, which suggests the presence of micro instability or micro motion along synchondrosis. A strong and secondary indicator of pathology in this location is the compartmentalized fluid between the FHL tendon sheath and surrounding the posterior process of the talus.
Tibialis anterior is the most medial of the extensor tendons, it serves as a dorsiflexor of the ankle and an inverter of the foot. It inserts distally upon the medial and plantar surfaces of the first cuneiform and on the base of the first metatarsal. Always look for the size of the tibialis anterior, it should be no larger than the tibialis posterior.
This is an axial fat-sat T2-weighted image obtained at the level of the superior margin of the talus. This patient presented with a large anterior ankle mass. On MRI, you see a huge amount of fluid distending the anterior tibial tendon sheath. The low intensity round structure in the center portion of this mass is the tendon itself surrounded by a large amount of fluid.
Tears of the anterior tibial tendon are most commonly related to lacerations. Tendon may spontaneously rupture, particularly in middle-aged or older individuals. When it ruptures, it often presents as a large, palpable, hard mass associated with foot drop. Ruptures most commonly occur between the superior and inferior extensor retinaculum.
Peroneal tendon disorders are often mis-diagnosed as lateral ankle sprains. As opposed to the tibialis posterior tendon, which is a disease of inactivity, peroneal tendon pathology most commonly occurs with trauma, acute, repetitive, or remote. The peroneus brevis tendon is anterior to peroneus longus tendon. Peroneus brevis inserts upon the base of the fifth metatarsal. Peroneus longus tendon courses through a fibroosseous tunnel in the cuboid bone to insert upon the first metatarsal base.
Tendinosis or tendon degeneration presents as an abnormal T1 signal within the peroneal tendons. One of the unusual things about the peroneal tendon is their tendency to sublux or dislocate. Several factors predispose the tendon subluxation including tear or atrophy of the superior peroneal retinaculum as well as a shallow or convex fibular peroneal groove or sulcus. Intraarticular calcaneal fractures can also cause lateral displacement, subluxation, or dislocation of the peroneal tendons. Notice on this MRI, peroneus longus tendon is laterally subluxed. We want to look for a nice secondary indicator of reactive bone marrow edema in the distal fibula, which is caused by chronic subluxation or banging of the tendon upon the distal fibula.
Small amounts of fluid may be seen physiologically within the peroneal tendon sheath. However, chronic tendinitis and overuse syndrome may be complicated by the thickening of the tendon sheath and constriction of the underlying peroneal tendons, which is known as stenosing tenosynovitis. Note here the large amount of fluid distending the peroneal tendon sheaths.
Laxity of the superior peroneal retinaculum may cause chronic peroneus brevis tendon subluxation with deformity and eventually longitudinal splitting of the tendon. Notice here how the peroneus brevis tendon has an unusual boomerang configuration caused by longitudinal splitting of the tendon, which typically occurs at the level of the lateral malleolus and propagates proximally. The peroneus longus tendon then is driven into the peroneus brevis tendon giving it this boomerang configuration.
Tears of the peroneus longus tendon most commonly occur within its fibroosseous tunnel along the cuboid bone. Note in this patient that the tendon is surrounded by a large amount of fluid and there is significant subtendinous reactive marrow change within the cuboid bone. This pathology is difficult to evaluate in any MR sequence but you have to localize the peroneus longus tendon in all three planes and make sure that it is intact as it courses in the mid foot.
MRI is very capable of evaluating the integrity of ligaments around the ankle. The ligamentous groups around the ankle, most commonly evaluated, are the medial and lateral collateral ligaments, the tibiofibular or the syndesmotic ligaments, and the interosseous ligaments within the sinus tarsi.
Normal-appearing ligaments should be thin, well-defined, low-intensity structures. The anterior talofibular ligament is the most commonly ruptured ligament in lateral ankle sprains followed by calcaneofibular ligament, which is affected in about 40% of ankle sprains. Posterior talofibular and syndesmotic ligaments are quite strong and typically do not rupture unless preceded by ATF and CF injuries.
Important secondary indicators of ankle sprain are bone contusions, which may accompany them. This is a coronal fat-sat T2-weighted image showing bone contusions in the medial malleolus, medial half of the talar dome, and in the sustentaculum. Bone bruises occur in one of the three patterns the ipsilateral contusions are tensile and relatively subtle and small. The compressive bone bruises seen here are contralateral, larger, and more obvious. The rotational bone bruises tend to occur on the neck of the talus.
The extent of lateral collateral ligament tears is best evaluated on MRI in the axial plane. On the left is a T1-weighted image and on the right is a fat-saturated T2-weighted image. Notice the usually low-intensity, well-defined anterior talofibular ligament is now amorphous and increased in signal intensity on the T1-weighted image. On the T2-weighted image, there is a large amount of fluid surrounding the tendon. Fluid distending the peroneal tendon sheath is an important secondary indicator of calcaneofibular ligament injury. Notice on this patient, there are contralateral bone contusions as well.
This patient presents following an inversion injury with lateral foot pain, tenderness, sensation of hind foot instability and weakness. Draw your attention to the sinus tarsi. Recall that the sinus tarsi should always be filled with the fat-intensity signal and the interosseous and cervical ligaments should be well defined and visualized, and here they are completely obscured and the sinus tarsi has been replaced by a low-intensity signal on the T1-weighted image and bright and intermediate intensity signal on fat-saturated T2-weighted image.
This is a typical appearance of a patient with sinus tarsi syndrome. Sinus tarsi syndrome may be acute or chronic. It may be idiopathic in etiology. However, in about 70%, it is associated with trauma. Sinus tarsi syndrome relates to the rupture of the interosseous and cervical ligaments. Often times, it is associated with tear of the lateral collateral ligamentous complex. These patients present with lateral pain and subtalar instability and often times this leads to a chronic synovitis.
In conclusion, I hope you have learned some basics about MRI sequences and imaging techniques. We have briefly reviewed anatomy and talked about the pathology of tendons and ligaments. Please look for my next lecture, which discusses bone marrow pathology and masses.
A patient arrives in your clinic 72 hours status post inversion sprain of the right ankle. The
conscientious emergency room physician ordered a MRI to rule out possible rupture of the collateral ligaments. The patient arrives with the MRI jacket, but
there is no report contained within. A trickle of sweat appears on your brow. Will you be able to distinguish between a well-defined anterior talofibular
ligament and an amorphous ligament with increased signal intensity on a T1 weighted image?
Relax!!! Dr. Steven Needel, Director of Musculoskeletal Imaging at Boca Raton Community Hospital, is here to help. He will clarify the difference between T1, T2, and Stir images; enlighten us on the distinction between tendonitis, tendonosis, dysfunction and tears. He will explain why fluid distending the peroneal sheath is an important secondary indicator of calcaneofibular ligament injuries. With Dr. Needel's help, you will be able to confirm or possibly rule out sinus tarsi or os trigonum syndrome.
This is a beautiful lecture filled with crystal clear MRI images, all evaluated and explained in detail by an excellent, enthusiastic practicing radiologist and teacher.
|Goals and Objectives|
After participating in this activity, the viewer should be better able to:
1. Enumerate MR sequences and contrast.
2. Describe MRI anatomy.
3. Determine pathology of various anatomical structures.
Estimated time to complete this activity is 41 minutes.
Physicians, diabetes educators, and other health care professionals who treat patients with diabetes.
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