(Radiology. 2000;215:497-503.)
© RSNA, 2000
Posterior Ankle Impingement Syndrome: MR Imaging Findings in Seven Patients1
Nathalie J. Bureau, MD, FRCPC,
Étienne Cardinal, MD, FRCPC,
Roger Hobden, MD and
Benoit Aubin, MD, FRCPC
1 From the Department of Radiology, Hôpital Saint-Luc, Centre hospitalier de l'Université de Montréal, 1058, rue Saint-Denis, Montréal, Québec Canada, H2X 3J4 (N.J.B., E.C., B.A.), and the Clinique de Médecine Familiale, Montréal, Québec (R.H.). From the 1997 RSNA scientific assembly. Received February 19, 1999; revision requested April 8; final revision received September 21; accepted October 20. Address correspondence to N.J.B. (e-mail: bureaun@ere.umontreal.ca).
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Abstract
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PURPOSE: To report the magnetic resonance (MR) imaging findings in seven patients with posterior ankle impingement (PAI) syndrome.
MATERIALS AND METHODS: Seven patients—three ballet dancers, one badminton player, one soccer player, one hockey player, and one construction worker—who presented with posterior ankle pain were assessed with MR imaging. Their clinical records and imaging studies were reviewed. The MR imaging studies were assessed for the presence of abnormal bone marrow signal intensity, osseous lesions, and soft-tissue abnormalities.
RESULTS: One patient was treated surgically. In all patients, MR imaging demonstrated abnormal bone marrow signal intensity in the os trigonum and/or lateral talar tubercle, consistent with bone contusions. Two patients had a fragmented os trigonum or lateral tubercle, and two had a pseudoarthrosis of the posterolateral talus. Increased signal intensity was seen with distention of the posterior recess of the tibiotalar joint in two patients and with distention of the posterior recess of the subtalar joint in four patients. Three patients had fluid accumulation in the flexor hallucis longus tendon sheath.
CONCLUSION: Bone contusions of the lateral talar tubercle and os trigonum are prevalent MR imaging findings of PAI syndrome. MR imaging clearly depicts the osseous and soft-tissue abnormalities associated with PAI syndrome and is useful in the assessment of this condition.
Index terms: Ankle, abnormalities, 463.252, 463.415, 463.486, 463.785 • Ankle, anatomy • Ankle, injuries, 463.415, 463.486 • Ankle, MR, 463.121411, 463.121412, 463.121413, 463.121415, 463.121416 • Magnetic resonance (MR), pulse sequences, 463.121411, 463.121412, 463.121413, 463.121415, 463.121416 • Synovitis, 463.252, 463.785
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Introduction
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Pain in the posterior ankle can result from many causes and may represent a diagnostic challenge. Posterior ankle impingement (PAI) syndrome refers to a group of pathologic entities that result from repetitive or acute forced plantar flexion of the foot (1). The talus and surrounding soft tissues are compressed between the tibia and the calcaneus, resulting in bone and/or soft-tissue lesions. This syndrome in classical ballet dancers (2–5) has been extensively described, but it also has been recognized in individuals who are active in sports, including soccer, basketball, running, and volleyball, as well as in those who participate in non–sport-related activities (1,6).
The diagnosis of PAI syndrome is based primarily on the patient's clinical history and physical examination results (1) and is supported by findings at radiography, scintigraphy, and computed tomography (CT) (7). Radiographs may demonstrate the presence of an os trigonum, which may or may not be the source of the problem (4). Scintigraphy may depict abnormal radionuclide uptake in the bone or soft-tissue structures of the posterior ankle (8). CT may depict chronic chondro-osseous injury between the talus and the os trigonum or a fracture of the talar lateral tubercle or os trigonum (9), but it is less sensitive for the depiction of soft-tissue involvement.
Magnetic resonance (MR) imaging is useful in the assessment of a wide range of soft-tissue and osseous disorders of the ankle (10). To our knowledge, however, the value of MR imaging in the evaluation of PAI syndrome has not been fully established because there exists to our knowledge only one series involving this condition—that of three patients—reported in the literature (11). The purpose of our study was to report the MR imaging findings of PAI syndrome that we observed in seven patients.
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MATERIALS AND METHODS
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Between November 1995 and July 1998, seven patients (three female, four male; mean age, 28 years; age range, 15–46 years) who were referred to our institution for MR imaging of the ankle had a diagnosis of PAI syndrome. In four patients—three ballet dancers and a competitive badminton player—who were referred by two sports medicine physicians, the diagnosis of PAI syndrome was established on the basis of clinical presentation and physical examination results. The other three patients—a soccer player, hockey player, and construction worker—were referred for investigation of indeterminate pain in the posterior ankle, and the diagnosis of PAI syndrome was established on the basis of the MR imaging findings. In the case of the hockey player, the diagnosis was also confirmed at surgery. The clinical charts and imaging studies of these seven patients were retrospectively reviewed.
The MR imaging studies were performed by using a 1.0- or 1.5-T MR unit (Signa; GE Medical Systems, Milwaukee, Wis) with a dedicated quadrature or linear extremity coil; the foot and ankle were in the neutral position (linear extremity coil) or in plantar flexion (quadrature extremity coil).
The following MR imaging sequences were used: transverse, sagittal, and coronal T1-weighted spin-echo (300–600/13–20 [repetition time msec/echo time msec]); transverse and coronal T2-weighted spin-echo (4,000/98); T2-weighted fast spin-echo with fat suppression (3,000–4,000/92–98; echo train length, eight) or gradient-echo (600/20, 30° flip angle); and sagittal fast multiplanar inversion-recovery or fast spin-echo inversion-recovery (4,000/54–69; inversion time, 130–150 msec). Other sequence parameters used were a 12–17-cm field of view, 256 x 192 matrix, 3–4-mm section thickness, 1.0–1.5-mm section spacing, and two to three signals acquired. In two cases, three-dimensional spoiled gradient-echo MR imaging (50/5, 40° flip angle) with a 12-cm field of view, 1.8-mm section thickness, 28 sections, 256 x 128 matrix, and two signals acquired also was performed.
The clinical chart of each patient was reviewed for information on clinical presentation—that is, symptoms at presentation, duration of symptoms, results of physical examination, and diagnosis based on clinical evaluation) and outcome—that is, conservative treatment versus surgery and findings at follow-up. The same physician (N.J.B.) reviewed the clinical charts of all seven patients, and in three cases, this was done conjointly with another physician (R.H.). The MR imaging studies were reviewed by two radiologists (N.J.B., E.C.), and any disagreement was resolved by means of consensus. The imaging studies were assessed for abnormal bone marrow signal intensity, osseous lesions, and soft-tissue lesions, including synovitis, tenosynovitis, and tendinitis. We did not grade the severity of the abnormalities; rather, we simply classified them as being present or absent.
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RESULTS
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The MR imaging findings are summarized in the Table. Three ballet dancers presented with pain in the posterior ankle, which occurred mainly with jumping and while assuming en pointe and demi-pointe positions. In all three cases, the symptoms had been present for at least 1 year and were gradually increasing. At physical examination there was limited plantar flexion of the foot compared with that of the nonaffected side, palpation of the posterior ankle was painful, and the pain could be reproduced by placing the ankle and foot in extreme plantar flexion. A competitive badminton player was referred for pain in the posterior ankle that manifested after he sprained his ankle 2 months earlier and had not resolved despite adequate conservative treatment for the ankle sprain. The pain was exacerbated by jumping. At physical examination, there was limited plantar flexion of the affected foot, and palpation of the posteromedial aspect of the subtalar joint was painful; however, palpation of the ankle ligaments did not trigger any pain. The pain could be reproduced by placing the ankle and foot in extreme plantar flexion.
The above four patients were referred for MR imaging to confirm a clinical diagnosis of PAI syndrome. In all four cases, the MR imaging findings confirmed the diagnosis of PAI syndrome. MR imaging also had a marked effect on the clinical care by enabling the determination of the exact nature of the osseous and soft-tissue lesions and by excluding other causes of posterior ankle pain.
Two of the three ballet dancers were treated successfully with conservative treatment and could resume dancing. The third ballet dancer had a fragmented lateral talar tubercle that was diagnosed at MR imaging. This patient did not improve with conservative treatment. She was referred to an orthopedist experienced with ballet dancer injuries who, after evaluation, did not recommend surgery. The patient finally quit dancing because of intractable ankle pain. In the case of the badminton player, surgical excision of the os trigonum was recommended by an orthopedist who specialized in sports medicine. The patient refused surgery and has had partial resolution of pain symptoms with conservative treatment; he continues to play badminton despite persistent pain.
Among the other three patients, the hockey player presented with pain in the posterior ankle of 3 weeks duration. There was no history of trauma. At physical examination, palpation of the posterior ankle was painful, but the origin of the pain was indeterminate. The construction worker complained of chronic ankle pain that had existed since he was aged 15 years. He could not recall any history of trauma. Palpation of the posterior ankle was painful, but the physical examination results were otherwise nonspecific. The soccer player complained of pain in the posterior ankle that started after a soccer game 2 weeks earlier. The pain was exacerbated by kicking and could be reproduced by palpating the posterior ankle.
On the basis of our clinical chart review, no presumptive clinical diagnosis was determined in any of these three patients before they underwent MR imaging for assessment of the cause of their symptoms. In these three patients, a diagnosis of PAI syndrome was established on the basis of MR imaging findings. MR imaging had a marked effect on clinical care by excluding other causes of posterior ankle pain and by helping to establish a clinical diagnosis that led to the appropriate treatment in at least two patients. In the case of the hockey player, a pseudoarthrosis of the lateral talar tubercle was diagnosed and successfully resected at surgery. Three months after surgery, the patient was free of symptoms and able to resume his activities. In the case of the soccer player, MR imaging depicted bone marrow edema of the os trigonum and lateral talar tubercle and subtalar synovitis. This patient received conservative treatment, and the clinical examination findings and symptoms resolved completely. After MR imaging, the construction worker was referred to an orthopedic surgeon for potential surgical resection of a posterior ankle ossicle. This patient was involved in a car accident and suffered severe cervical trauma. Review of this patient's clinical chart revealed that orthopedic consultation was delayed, and no further follow-up information on his condition was available at the time of this study. Repeated MR imaging was not performed in any of the seven patients.
In all seven cases, MR imaging depicted low signal intensity of the os trigonum and/or lateral talar tubercle on T1-weighted images and high signal intensity of these structures on fat-suppressed T2-weighted (ie, fast multiplanar inversion-recovery, fast spin-echo inversion-recovery, and fast spin-echo with fat saturation) images, consistent with bone marrow edema. The images obtained in one patient showed abnormal signal intensity isolated to the os trigonum, and those obtained in two patients showed abnormal signal intensity of the os trigonum and the adjacent lateral talar tubercle, without evidence of other associated osseous abnormalities (Fig 1). The abnormal signal intensity of these structures was best appreciated on the sagittal MR images.
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Figure 1a. PAI syndrome in a 20-year-old male soccer player. (a) Lateral radiograph of the right ankle demonstrates a well-defined os trigonum (arrow). (b) Sagittal T1-weighted image (366/14) shows area of low signal intensity (arrow) within the os trigonum. (c) Sagittal, fast spin-echo inversion-recovery image (4,000/69; inversion time, 130 msec) medial to b demonstrates bone marrow high signal intensity (arrows) in the posterior talus, consistent with a bone contusion.
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Figure 1b. PAI syndrome in a 20-year-old male soccer player. (a) Lateral radiograph of the right ankle demonstrates a well-defined os trigonum (arrow). (b) Sagittal T1-weighted image (366/14) shows area of low signal intensity (arrow) within the os trigonum. (c) Sagittal, fast spin-echo inversion-recovery image (4,000/69; inversion time, 130 msec) medial to b demonstrates bone marrow high signal intensity (arrows) in the posterior talus, consistent with a bone contusion.
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Figure 1c. PAI syndrome in a 20-year-old male soccer player. (a) Lateral radiograph of the right ankle demonstrates a well-defined os trigonum (arrow). (b) Sagittal T1-weighted image (366/14) shows area of low signal intensity (arrow) within the os trigonum. (c) Sagittal, fast spin-echo inversion-recovery image (4,000/69; inversion time, 130 msec) medial to b demonstrates bone marrow high signal intensity (arrows) in the posterior talus, consistent with a bone contusion.
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One patient had a fragmented lateral talar tubercle (Fig 2). One patient had osseous fragments with irregular margins in the posterior ankle, but it was difficult to determine, both at MR imaging and CT, whether the fragments were the result of a fragmented os trigonum or a fragmented lateral talar tubercle. These osseous fragments showed abnormal signal intensity consistent with bone marrow edema. One patient had a pseudoarthrosis of the lateral talar tubercle that was proved at surgery (Fig 3). Another patient presented with a large ossicle in the posterior ankle, with irregular margins and abnormal signal intensity of this ossicle and the adjacent lateral talar tubercle. The appearance was consistent with a pseudoarthrosis, but it was difficult to establish whether the pseudoarthrosis was through the os trigonum synchondrosis or the result of an old lateral talar tubercle fracture.
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Figure 2a. (a, b) Lateral radiographs of the (a) right and (b) left feet in the demi-pointe position, obtained in a 15-year-old female ballet dancer with pain in the posterior left ankle, limited plantar flexion, and a clinical diagnosis of PAI syndrome. (b) The limited plantar flexion of the left foot can be appreciated at a greater tibiocalcaneal angle (60° in the left foot compared with 50° in the right foot). An increased distance between the posterior malleolus of the tibia and the margin of the posterior facet of the calcaneus also is seen. Note the presence of bone fragments (arrow) in the posterior aspect of the left ankle. (c) Sagittal T1-weighted MR image (400/20) of the left ankle shows an area of low signal intensity within the posterior talus and adjacent bone fragments (open arrows). Note the spur (solid arrow) at the margin of the posterior facet of the calcaneus. (d) Sagittal fast multiplanar inversion-recovery image (4,000/56; inversion time, 150 msec) of the left ankle demonstrates an area of high signal intensity within the posterior talus and adjacent osseous fragments (curved arrows), in the posterior recess (straight solid arrow) of the subtalar joint, and in the FHL tendon sheath (open arrow), consistent with inflammation. (e) Findings on transverse CT image of the left ankle confirm fragmentation of the lateral talar tubercle (arrow).
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Figure 2b. (a, b) Lateral radiographs of the (a) right and (b) left feet in the demi-pointe position, obtained in a 15-year-old female ballet dancer with pain in the posterior left ankle, limited plantar flexion, and a clinical diagnosis of PAI syndrome. (b) The limited plantar flexion of the left foot can be appreciated at a greater tibiocalcaneal angle (60° in the left foot compared with 50° in the right foot). An increased distance between the posterior malleolus of the tibia and the margin of the posterior facet of the calcaneus also is seen. Note the presence of bone fragments (arrow) in the posterior aspect of the left ankle. (c) Sagittal T1-weighted MR image (400/20) of the left ankle shows an area of low signal intensity within the posterior talus and adjacent bone fragments (open arrows). Note the spur (solid arrow) at the margin of the posterior facet of the calcaneus. (d) Sagittal fast multiplanar inversion-recovery image (4,000/56; inversion time, 150 msec) of the left ankle demonstrates an area of high signal intensity within the posterior talus and adjacent osseous fragments (curved arrows), in the posterior recess (straight solid arrow) of the subtalar joint, and in the FHL tendon sheath (open arrow), consistent with inflammation. (e) Findings on transverse CT image of the left ankle confirm fragmentation of the lateral talar tubercle (arrow).
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Figure 2c. (a, b) Lateral radiographs of the (a) right and (b) left feet in the demi-pointe position, obtained in a 15-year-old female ballet dancer with pain in the posterior left ankle, limited plantar flexion, and a clinical diagnosis of PAI syndrome. (b) The limited plantar flexion of the left foot can be appreciated at a greater tibiocalcaneal angle (60° in the left foot compared with 50° in the right foot). An increased distance between the posterior malleolus of the tibia and the margin of the posterior facet of the calcaneus also is seen. Note the presence of bone fragments (arrow) in the posterior aspect of the left ankle. (c) Sagittal T1-weighted MR image (400/20) of the left ankle shows an area of low signal intensity within the posterior talus and adjacent bone fragments (open arrows). Note the spur (solid arrow) at the margin of the posterior facet of the calcaneus. (d) Sagittal fast multiplanar inversion-recovery image (4,000/56; inversion time, 150 msec) of the left ankle demonstrates an area of high signal intensity within the posterior talus and adjacent osseous fragments (curved arrows), in the posterior recess (straight solid arrow) of the subtalar joint, and in the FHL tendon sheath (open arrow), consistent with inflammation. (e) Findings on transverse CT image of the left ankle confirm fragmentation of the lateral talar tubercle (arrow).
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Figure 2d. (a, b) Lateral radiographs of the (a) right and (b) left feet in the demi-pointe position, obtained in a 15-year-old female ballet dancer with pain in the posterior left ankle, limited plantar flexion, and a clinical diagnosis of PAI syndrome. (b) The limited plantar flexion of the left foot can be appreciated at a greater tibiocalcaneal angle (60° in the left foot compared with 50° in the right foot). An increased distance between the posterior malleolus of the tibia and the margin of the posterior facet of the calcaneus also is seen. Note the presence of bone fragments (arrow) in the posterior aspect of the left ankle. (c) Sagittal T1-weighted MR image (400/20) of the left ankle shows an area of low signal intensity within the posterior talus and adjacent bone fragments (open arrows). Note the spur (solid arrow) at the margin of the posterior facet of the calcaneus. (d) Sagittal fast multiplanar inversion-recovery image (4,000/56; inversion time, 150 msec) of the left ankle demonstrates an area of high signal intensity within the posterior talus and adjacent osseous fragments (curved arrows), in the posterior recess (straight solid arrow) of the subtalar joint, and in the FHL tendon sheath (open arrow), consistent with inflammation. (e) Findings on transverse CT image of the left ankle confirm fragmentation of the lateral talar tubercle (arrow).
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Figure 2e. (a, b) Lateral radiographs of the (a) right and (b) left feet in the demi-pointe position, obtained in a 15-year-old female ballet dancer with pain in the posterior left ankle, limited plantar flexion, and a clinical diagnosis of PAI syndrome. (b) The limited plantar flexion of the left foot can be appreciated at a greater tibiocalcaneal angle (60° in the left foot compared with 50° in the right foot). An increased distance between the posterior malleolus of the tibia and the margin of the posterior facet of the calcaneus also is seen. Note the presence of bone fragments (arrow) in the posterior aspect of the left ankle. (c) Sagittal T1-weighted MR image (400/20) of the left ankle shows an area of low signal intensity within the posterior talus and adjacent bone fragments (open arrows). Note the spur (solid arrow) at the margin of the posterior facet of the calcaneus. (d) Sagittal fast multiplanar inversion-recovery image (4,000/56; inversion time, 150 msec) of the left ankle demonstrates an area of high signal intensity within the posterior talus and adjacent osseous fragments (curved arrows), in the posterior recess (straight solid arrow) of the subtalar joint, and in the FHL tendon sheath (open arrow), consistent with inflammation. (e) Findings on transverse CT image of the left ankle confirm fragmentation of the lateral talar tubercle (arrow).
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Figure 3a. Surgically proved lateral talar tubercle pseudoarthrosis in a 32-year-old male hockey player. (a) Sagittal T1-weighted MR image (350/16) shows low-signal-intensity area (arrow) within the posterior aspect of the talus. (b) Sagittal fast multiplanar inversion-recovery image (4,000/56; inversion time, 150 msec) shows corresponding area of high signal intensity (solid straight arrow) consistent with bone marrow edema. Note the vertical linear area of low signal intensity (open arrow) that corresponds to the pseudoarthrosis. There also is evidence of inflammation of the posterior recess of the tibiotalar and subtalar joints (curved arrows). (c) Transverse CT image shows an incomplete fracture (arrow) with osteosclerosis of the margins, consistent with a pseudoarthrosis.
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Figure 3b. Surgically proved lateral talar tubercle pseudoarthrosis in a 32-year-old male hockey player. (a) Sagittal T1-weighted MR image (350/16) shows low-signal-intensity area (arrow) within the posterior aspect of the talus. (b) Sagittal fast multiplanar inversion-recovery image (4,000/56; inversion time, 150 msec) shows corresponding area of high signal intensity (solid straight arrow) consistent with bone marrow edema. Note the vertical linear area of low signal intensity (open arrow) that corresponds to the pseudoarthrosis. There also is evidence of inflammation of the posterior recess of the tibiotalar and subtalar joints (curved arrows). (c) Transverse CT image shows an incomplete fracture (arrow) with osteosclerosis of the margins, consistent with a pseudoarthrosis.
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Figure 3c. Surgically proved lateral talar tubercle pseudoarthrosis in a 32-year-old male hockey player. (a) Sagittal T1-weighted MR image (350/16) shows low-signal-intensity area (arrow) within the posterior aspect of the talus. (b) Sagittal fast multiplanar inversion-recovery image (4,000/56; inversion time, 150 msec) shows corresponding area of high signal intensity (solid straight arrow) consistent with bone marrow edema. Note the vertical linear area of low signal intensity (open arrow) that corresponds to the pseudoarthrosis. There also is evidence of inflammation of the posterior recess of the tibiotalar and subtalar joints (curved arrows). (c) Transverse CT image shows an incomplete fracture (arrow) with osteosclerosis of the margins, consistent with a pseudoarthrosis.
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Increased signal intensity and distention of the posterior capsular recess, consistent with the presence of fluid or synovitis, was detected in the tibiotalar joint in two patients and in the subtalar joint in four patients. An increased amount of synovial fluid was also detected within the FHL tendon sheath in three patients. In one of these patients it was associated with subtalar joint synovitis, in one patient it was the only abnormality found in the soft tissues, and in the third patient it was associated with a tibiotalar synovitis. In the latter case, the fluid accumulation was restricted to the segment of the FHL tendon sheath that was proximal to the lateral talar tubercle, which was consistent with stenosing tenosynovitis.
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DISCUSSION
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Different names have been given to PAI syndrome, including os trigonum syndrome, talar compression syndrome, and posterior block of the ankle (4–6). The mechanisms of injury have been likened to a nut in a nutcracker because the posterior talus and surrounding soft tissues are compressed between the tibia and the calcaneus during plantar flexion of the foot (1). Classical ballet can be viewed as an experimental model for PAI syndrome. Because of the repetitive movements required in the choreography—especially the en pointe and demi-pointe positions of the foot—ballet dancers impose chronic stress on the posterior ankle and are at increased risk of developing osseous and soft-tissue injuries. PAI syndrome may also occur with acute plantar flexion of the foot and has been recognized in association with a number of sports and non–sports-related activities (1,6).
The anatomy of the posterior aspect of the ankle is a key factor in the occurrence of PAI syndrome. The talar posterior process extends both posteriorly and medially from the body of the talus and protrudes posteriorly to the ankle joint surface (Fig 4). The posterior process is grooved by the tendon of the FHL muscle. This groove separates the medial and lateral tubercles of the talus. The medial talocalcaneal and posterior tibiotalar ligaments insert on the medial tubercle. The lateral tubercle, which is more prominent than the medial tubercle, serves as a site for attachment of the posterior talofibular ligament. The lateral tubercle may be short or long, or it may articulate with a separate ossification center called the os trigonum (Fig 5). If the lateral tubercle is long, it is called the Stieda process (6).
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Figure 4a. Drawings of the lateral talar tubercle in the left ankle. (a) Drawing in the transverse plane illustrates the lateral talar tubercle (straight black arrow) extending posteriorly from the body of the talus (T) over the calcaneal tuberosity (C). The FHL tendon (white arrow) is illustrated in cross section, in the groove between the medial (curved arrow) and lateral talar tubercles. The lateral talar tubercle is normally more prominent than the medial talar tubercle. (b) Drawing in the sagittal plane illustrates the profile of the lateral talar tubercle (black arrow). The posterior malleolus of the tibia (white arrow) may have a more or less pronounced down slope and contribute to the impingement.
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Figure 4b. Drawings of the lateral talar tubercle in the left ankle. (a) Drawing in the transverse plane illustrates the lateral talar tubercle (straight black arrow) extending posteriorly from the body of the talus (T) over the calcaneal tuberosity (C). The FHL tendon (white arrow) is illustrated in cross section, in the groove between the medial (curved arrow) and lateral talar tubercles. The lateral talar tubercle is normally more prominent than the medial talar tubercle. (b) Drawing in the sagittal plane illustrates the profile of the lateral talar tubercle (black arrow). The posterior malleolus of the tibia (white arrow) may have a more or less pronounced down slope and contribute to the impingement.
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Figure 5a. Drawings of the os trigonum in the left ankle. (a) Drawing in the transverse plane shows a short lateral talar tubercle (white arrow) articulating with the os trigonum (black arrow). (b) Drawing in the sagittal plane illustrates the profile of the os trigonum (straight arrow). There may be a prominence (curved arrow) at the dorsum of the calcaneal tuberosity, which may contribute to the impingement.
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Figure 5b. Drawings of the os trigonum in the left ankle. (a) Drawing in the transverse plane shows a short lateral talar tubercle (white arrow) articulating with the os trigonum (black arrow). (b) Drawing in the sagittal plane illustrates the profile of the os trigonum (straight arrow). There may be a prominence (curved arrow) at the dorsum of the calcaneal tuberosity, which may contribute to the impingement.
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The term "os trigonum" is often used inappropriately. According to McDougall (12), between the ages of 11 and 13 years in boys and 8 and 10 years in girls, a separate ossification center forms in the posterior region of the talus. Grogan et al (13) observed at histologic analysis that this ossification center forms within a cartilaginous extension from the posterior portion of the talus. Normally, this ossification center fuses with the rest of the talus within 1 year of its appearance (12). In approximately 7% of the population, however, this ossification center remains separate and is referred to as the os trigonum (14). It is bilateral in approximately 1.4% of individuals (15). The os trigonum is totally corticated and articulates with the lateral talar tubercle through a synchondrosis.
Two other bone structures that are involved in the impingement mechanism are the posterior tibial articular surface (ie, posterior malleolus) (Fig 4b), which may have a more or less prominent down slope, and the superior surface of the calcaneal tuberosity, which may have a prominence (4) (Fig 5b). The soft-tissue components of this anatomic interval—especially the synovial sheath of the FHL and the posterior synovial recess of the tibiotalar and subtalar joints, which, respectively, extend superiorly and inferiorly to the lateral talar tubercle—also can be involved.
PAI syndrome may manifest as an inflammation of the posterior ankle soft tissues, as an osseous injury, or as a combination of both (16). The osseous injuries include fracture, fragmentation, and pseudoarthrosis of the os trigonum or lateral talar tubercle (1,7,16). In this study, we observed the isolated occurrence of abnormal signal intensity within the os trigonum and lateral talar tubercle, consistent with bone marrow edema or bone contusion.
Typically, the patient with PAI syndrome presents with posterior ankle pain exacerbated by plantar flexion of the foot. The differential diagnosis of PAI syndrome is extensive. PAI syndrome is one of many conditions that may account for ankle and/or hind foot pain; other causes include the following entities: achilles tendinitis, achilles tendon rupture, retrocalcaneal bursitis, FHL tendinitis (ie, stenosing tenosynovitis, which may be part of PAI syndrome), peroneal tendon subluxation, ankle joint arthritis, ankle sprain, lateral ankle instability, tarsal tunnel syndrome, talofibular arthritis, osteochondral lesion, Haglund deformity, Mortise diastasis, calcaneal fracture, tarsal coalition, and Sever disease (5,11,16).
Radiographs may show the presence of a Stieda process or os trigonum, which may or may not be the cause of the problem. Lateral radiographs obtained with the foot in plantar flexion may show the os trigonum or lateral talar tubercle impinged between the posterior tibia malleolus and the calcaneal tuberosity. It is not always possible to differentiate between an os trigonum and a fractured lateral talar tubercle on radiographs. Although an os trigonum is usually round or oval with well-defined corticated margins, and a fracture of the lateral tubercle has irregular serrated margins between the ossicle and the posterior talus, a fracture fragment may also have smooth borders (6). CT, with its high spatial resolution, may be helpful in evaluating the osseous structures. Technetium 99m diphosphonate bone scans may show increased blood flow and active bone repair (8).
MR imaging, with its multiplanar capabilities, exquisite soft-tissue and bone marrow contrast, and large field of view availability, is particularly well suited to investigate foot and ankle disorders (10). In this study, as in that by Wakeley et al (11), MR imaging was useful in establishing the diagnosis of PAI syndrome. In all seven cases, sagittal T1-weighted and fat-suppressed T2-weighted (ie, fast multiplanar inversion-recovery, fast spin-echo inversion-recovery, and fast spin-echo with fat saturation) images showed abnormal low and high signal intensity, respectively, in the lateral talar tubercle and/or os trigonum, consistent with bone marrow edema. In three cases, this area of abnormal signal intensity was the only osseous lesion demonstrated. Wakeley et al (11) also reported this abnormal signal intensity in one of their three cases and thought it represented bone marrow edema. Considering the mechanisms of injury in PAI syndrome, we believe that this abnormal signal intensity is the result of bone impaction and thus represents bone contusions or occult fractures. Bone contusions, which represent microtrabecular fractures, edema, and/or hemorrhage of the bone marrow without disruption of the cortex, have been well recognized at MR imaging (17–19). They are not visible on radiographs or CT images. It is important to diagnose bone contusions because they are usually painful and their presence may influence treatment (20).
In the other four cases in this study, a fracture or pseudoarthrosis of the lateral talar tubercle or os trigonum also was diagnosed. In two cases it was not possible to determine whether the injury occurred in the os trigonum or the lateral talar tubercle. We do not believe that this is a shortcoming of MR imaging. As long as there is abnormal signal intensity in these osseous structures consistent with bone contusions and evidence of traumatic injury, the exact nomenclature of the osseous structures is secondary.
The MR imaging studies in our study were obtained with the foot in flexion in three patients and with the foot in a neutral position in four patients. In their study, Wakeley et al (11) obtained sagittal images both with the foot in flexion and with it extended, and in one case, they determined the mobility of the os trigonum in relation to the posterior talus, which was consistent with a pseudoarthrosis through the synchondrosis.
In this study, MR imaging also depicted inflammatory changes in the posterior ankle soft tissues—namely, the posterior synovial recess of the subtalar and tibiotalar joints and the FHL tendon sheath. An increased amount of fluid is a sign of synovitis. Although the FHL tendon sheath may communicate with the ankle joint, in one of our study patients, FHL synovitis was an isolated finding. Because of its location between the medial and lateral talar tubercles, the FHL tendon is subject to inflammation in patients with PAI syndrome. FHL tenosynovitis is a common and well-recognized injury in classical ballet dancers that is caused by extreme plantar flexion of the foot that assumes the en pointe and demi-pointe positions (3).
The treatment of PAI syndrome is initially conservative. In the case of isolated soft-tissue involvement, as in the case of an os trigonum or lateral talar tubercle fracture, a below-the-knee cast is applied for 4–6 weeks or longer if necessary. Once the cast is removed, a rehabilitation program is instituted. If conservative treatment fails, then surgical excision of the osseous fragments, with potential release of the FHL tendon, may be indicated (4). Surgical excision of the os trigonum in classical ballet dancers has resulted in good prognoses (5).
In conclusion, bone contusions of the lateral talar tubercle and os trigonum are MR imaging findings of PAI syndrome. Conventional radiographs and CT images cannot demonstrate these occult fractures. In addition, MR imaging clearly depicts the soft-tissue abnormalities associated with PAI syndrome. We believe that MR imaging is useful in the assessment of PAI syndrome.
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Footnotes
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Abbreviations: FHL = flexor hallucis longus
PAI = posterior ankle impingement
Author contributions: Guarantor of integrity of entire study, N.J.B.; study concepts and design, N.J.B., E.C.; definition of intellectual content, N.J.B.; literature research, N.J.B., E.C.; clinical studies, all authors; data acquisition and analysis, N.J.B., E.C., R.H.; manuscript preparation, N.J.B.; manuscript editing, N.J.B., E.C.; manuscript review, E.C., B.A.
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Abstract
Introduction
