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1 Department of Radiology, Thomas Jefferson University Hospital, 111 S 11th St.,
Ste. 3390, Gibbon Bldg., Philadelphia, PA 19107.
2 Present address: Department of Radiology, New York University Hospital for
Joint Disease, 3012 17th St., New York, NY 10003.
Received January 6, 2003;
accepted after revision July 30, 2003.
Address correspondence to W. B. Morrison
(William.Morrison{at}mail.tju.edu).
Abstract
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MATERIALS AND METHODS. Ninety-four 1.5-T MRIs of ankles of 90 individuals with histories of severe sprain were assessed by two musculoskeletal radiologists for syndesmosis injury (acute, edema of the syndesmosis; chronic, disruption or thickening of the syndesmosis without edema). We examined associated MRI findings, including anterior talofibular ligament injury (scar, chronic injury; edema, acute injury), bone bruise, osteochondral lesion, tibiofibular joint congruity, tibiofibular recess height, and osteoarthritis. The Fisher's exact test and analysis of variance test were used to evaluate the significance of the associations.
RESULTS. In 94 ankles, syndesmosis injury was seen in 63% (n = 59; 23 acute; 36 chronic). Anterior talofibular ligament injury (acute or chronic) was seen on MRIs in 74% (n = 70; 49 with syndesmosis injury; 21 without; p = 0.03). Bone bruises were present in 24% (n = 23; 18/23 acute; 4/36 chronic; 4/35 no injury; p < 0.0001). Of these, talar dome osteochondral lesions were present in 28% (n = 26; 11/23 acute; 14/36 chronic; 1/35 no injury; p = 0.0001; 13 medial; 13 lateral). The tibiofibular joint was incongruent in 33% (n = 31; 6/23 acute; 21/36 chronic; 4/35 no injury; p < 0.0001). The tibiofibular recess (mean ± SD) was 1.2 ± 0.92 cm in acute cases, 1.4 ± 0.57 cm in chronic cases, and 0.54 ± 0.68 cm in cases with no syndesmosis injury (p < 0.0001). Osteoarthritis was present in 10% (n = 9; 1/23 acute; 7/36 chronic; 1/35 no injury; p = 0.06).
CONCLUSION. Injury to the distal tibiofibular syndesmosis has a significant association with a number of secondary findings on MRI, including anterior talofibular ligament injury, bone bruises, osteochondral lesions, tibiofibular joint congruity, and height of the tibiofibular recess.
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Prior studies have documented the ability of MRI to visualize the ligaments of the distal tibiofibular syndesmosis [12, 13]; for the diagnosis of an anterior tibiofibular rupture, MRI has a sensitivity that ranges from 93% to 100%, with a specificity of 96–100% [12]. These figures showing high accuracy of MRI for diagnosis have been corroborated by others who report a 100% sensitivity and 93% specificity of MRI for injury to the anterior inferior syndesmotic ligament [14]. However, MRI is not performed routinely for diagnosis of ankle injuries; thus, sparse information pertains to MRI of syndesmosis injury. The purpose of this study was to characterize MRI findings associated with distal tibiofibular syndesmosis injuries, both acute and chronic.
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MRI was performed using a 1.5-T scanner (Signa, General Electric Medical Systems, Milwaukee, WI) with an extremity coil around the ankle; the foot was positioned at 90° in relation to the leg. The MRI protocol consisted of coronal and axial T2-weighted fast spin-echo images with fat suppression, axial proton density–weighted fast spin-echo images, sagittal fast spin-echo inversion recovery images, and sagittal T1-weighted spin-echo images. T2-weighted fast spin-echo images were acquired with a TR range/TEeff range of 3,000–7,500/60–90; echo-train length of 8; slice thickness of 4 mm; skip of 1 mm; 2–3 signal averages; field of view of 12–18 cm; and matrix of 256 x 192. T1-weighted spin-echo images were acquired with a TR range/TE range of 400–700/10–20; slice thickness of 4 mm; skip of 1 mm; 2 signal averages; field of view of 16–18 cm; and matrix of 256 x 192. Axial proton density–weighted fast spin-echo images were obtained with a TR range/TEeff range of 2,500–4,000/30-40; echo-train length of 4; slice thickness of 4 mm; skip of 1 mm; 2 signal averages; field of view of 14–16 cm; and matrix of 512 x 256. Sagittal fast spin-echo inversion recovery images were obtained with 2,000–5,000/20–40; inversion time of 150 msec, echo-train length of 8; slice thickness of 4 mm; skip of 1 mm; 2 signal averages; field of view of 16–18 cm; and matrix of 256 x 192. Frequency-selective fat saturation was used to acquire fat-suppressed sequences.
Two musculoskeletal radiologists, by consensus, retrospectively examined the MRIs. Syndesmosis injury (injury to the anterior tibiofibular ligament) was defined as acute (edema around or in the ligament) (Fig. 1A, 1B) or chronic (disruption or thickening of the ligament without edema) (Fig. 2A, 2B). Although there are numerous anatomic components of the distal tibiofibular syndesmosis, we evaluated the anterior tibiofibular ligament as a marker of injury to the complex as a whole because in our experience, compared with the other components, this portion is most commonly injured and is most reliably and consistently visualized on MRI.
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Anterior talofibular ligament injury was defined as acute (edema around or in the ligament) or chronic (disruption or thickening of the ligament without edema). Several associated MRI findings were examined. Bone bruises had ill-defined increased marrow signal intensity on T2-weighted images (Fig. 3A, 3B). The location of bone bruises and fractures was also recorded. Fractures were defined as a linear signal with surrounding bone marrow edema on T2-weighted images. We recorded the presence of an osteochondral lesion, defined as a solitary subchondral focus of signal on T2-weighted images in the talar dome without similar findings in the tibia (Fig. 4). The location of the osteochondral lesion (lateral or medial talar dome) was noted. In addition, on sagittal images, a line was drawn between articular surfaces of the ankle and divided into three equal zones representing anterior, middle anterior, and posterior thirds. Each osteochondral lesion was also categorized into one of these three locations. Distal tibiofibular joint congruity was examined on axial proton density–weighted images at the level of the distal tibiofibular joint (Fig. 5). A congruent joint consisted of a smooth articular surface and joint margins with no subluxation, diastasis, or enthesopathic proliferation. An incongruent joint was defined as a joint with an irregular surface, sharpened margins, articular offset of diastasis, or proliferation at the interosseous membrane (Fig. 6).
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The tibiofibular joint recess height was measured in centimeters on coronal T2-weighted images from the lateral talar dome to the maximal superior extent of joint fluid between the tibia and fibula (Fig. 7). Osteoarthritis was defined as marginal osteophytes or subchondral cysts (multiple or on both sides of the joint to distinguish osteoarthritis from solitary osteochondral lesions) on any sequence.
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On the basis of these data, three subpopulations were defined, consisting of patients with MRI evidence of acute syndesmosis injury, chronic syndesmosis injury, and normal syndesmosis. The number of times that an associated finding occurred for each of these groups was recorded, and the totals were compared between the three categories. The Fisher's exact test and analysis of variance test were used to evaluate for significance of the associations. A p value of less than 0.05 was considered to be statistically significant. Investigational review board approval was obtained for this retrospective study.
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In terms of associated findings, anterior talofibular ligament injury was seen on MRI in 70 (74%) (49 with syndesmosis injury; 21 without; p = 0.03). Bone bruises or fractures were present in 26 (28%) of the 94 ankles. Eighteen (78%) of the 23 ankles with acute syndesmosis injury had bone bruises as compared with four (11%) of the 35 ankles with no syndesmosis injury. Bone bruises were significantly associated with acute syndesmosis injury (p < 0.0001). Of the 22 ankles with both bone bruises and syndesmosis injuries (acute or chronic), 13 bone bruises occurred in the talus with nine in the medial talus (six in the medial talar dome and three in the anterior medial talus) and six bone bruises were located in the tibia (three in the posterior malleolus, one in the anterior tibia, and two in the medial malleolus). There were three fractures in the posterior malleolus.
Talar dome osteochondral lesions were present in 26 ankles (28%) studied (Table 1). Eleven (48%) of the 23 ankles with acute syndesmosis injury and 14 (39%) of the 36 ankles with chronic syndesmosis injury had osteochondral lesions. Only one (3%) of the 35 ankles with no syndesmosis injury had an osteochondral lesion. Osteochondral lesions were significantly associated with both acute and chronic syndesmosis injury (p = 0.0001 and p = 0.0003, respectively). Location of osteochondral lesions was equally distributed between the medial (n = 13) and lateral (n = 13) talar dome. Of the 13 medial talar dome osteochondral lesions, 12 (92%) were located in the middle third of the articular surface. One (8%) was located in the posterior third. Laterally, six (46%) of the 13 osteochondral lesions were located in the middle third. Two (15%) were in the anterior third, and five (38%) were in the posterior third.
The tibiofibular joint was incongruent in 31(33%) of the 94 ankles studied. Twenty-one (58%) of the 36 ankles with chronic syndesmosis injury had tibiofibular joint incongruity compared with only four (11%) of the 35 ankles with no syndesmosis injury and six (26%) of 23 ankles with acute injury (Table 1). Tibiofibular joint incongruity was significantly associated with chronic syndesmosis injury (p < 0.0001).
The tibiofibular recess height was significantly greater in both acute syndesmosis injuries (1.2 ± 0.92 cm) and chronic syndesmosis injuries (1.4 ± 0.57 cm) compared with the ankles with no syndesmosis injury (0.54 ± 0.68 cm) (p < 0.0001).
Osteoarthritis was present in nine (10%) of the 94 ankles. One case of osteoarthritis occurred in the group with acute syndesmosis injury. Seven cases of osteoarthritis occurred in the group with chronic syndesmosis injuries, and one case occurred in the group with no syndesmosis injury. Osteoarthritis was not significantly associated with acute or chronic syndesmosis injury (p = 0.06) (Table 1).
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Several of these findings are to be expected with severe ankle injury. For instance, an injury severe enough to disrupt the distal syndesmosis would also probably injure the anterior talofibular ligament. Bone bruise is an expected finding in an acute, severe injury that would also cause a syndesmosis injury. In the ankles with syndesmosis injuries, nine (47%) of the 19 bone bruises were in a medial location, suggesting an inversion mechanism as a major one associated with syndesmosis injury.
Another expected finding was the presence of osteochondral lesions, which were significantly more common in ankles with syndesmosis injury than in those without. Osteochondral lesions are a recognized complication of ankle sprain and fracture [15, 16]. The finding of an osteochondral lesion is one potential source of chronic pain in patients with prior ankle sprain. Osteochondral lesions were located in an equal distribution at the medial and lateral talar dome, which is similar to the findings of Canale and Belding [17]. Osteochondral lesions in our population were most common at the middle third of the talar dome, measured from the anterior to posterior articular surface. Eighteen (69%) of the 26 osteochondral lesions were at the middle third; however, others have shown that the most common location of osteochondral lesions is the anterolateral and posteromedial talar dome [15, 18, 19]. This difference in distribution may reflect a selection bias in our population, which included only patients with ankle sprain.
Radiographically, ossification at the distal tibiofibular joint or interosseous membrane has been described with chronic syndesmosis injury [20]. This corresponds to our finding of irregularity of the joint in patients with evidence of chronic syndesmosis injury. The same process that results in the radiographic appearance of heterotopic ossification (injury of the interosseous membrane) may cause an irregular appearance of adjacent cortical margins on MRI and result in the appearance of the distal tibiofibular joint incongruity that we observed.
In addition to joint incongruity, the tibiofibular joint recess would also be expected to become distorted if the syndesmosis was interrupted (Fig. 7). The tibiofibular recess begins above the small articular surface that joins these two bones. A cavity exists above the tibiofibular connections, which end proximally at the base of the interosseous ligament. The anterior part of this cavity forms a synovial recess that connects through a linear opening with the ankle joint. This recess is typically 1 cm in height [21]. Although the recess has been identified in prior anatomic and radiographic literature, there has not been thorough documentation of the normal measurement and abnormal appearance of the recess. A previous study noted that this recess becomes enlarged in patients with rheumatoid arthritis [22]. In our study, an average recess height (superior to inferior measurement) of 0.5 cm was seen in the subgroup with no syndesmosis injury, whereas average recess heights of 1.4 and 1.2 cm were measured in patients with chronic and acute syndesmosis injury, respectively. Although the SD of these measurements was large, in a patient without inflammatory arthropathy, a tibiofibular recess height greater than 1 cm might prompt consideration of prior syndesmosis injury.
Osteoarthritis was not significantly associated with syndesmosis injury in our population, although the p value approached 0.05. Possibly our population was not large enough to show significance or the observed syndesmosis injuries were not associated with ankle instability or there was not enough delay after injury to detect development of osteoarthritis.
Limitations of this study should be acknowledged. The retrospective study design was directed at establishing association between various MRI findings described previously. The purpose was not to associate these findings with the character of pain. Ligament injury, osteochondral lesion, osteoarthritis, and bone bruise and fracture all have been separately associated with pain, and many patients in our population had multiple findings. Therefore, attempting to separate the different findings into specific symptom patterns would be difficult in this population. Also, because ankle sprain is a common injury, especially in athletes, many individuals suffer recurrent injuries. Correlation of injury date with the MRI appearance would also have been limited in this population because of the potential for multiple episodes of injury with acute superimposed on chronic findings. Additionally, patients' recollections of ankle sprain histories are often unreliable. In contrast, morphologic and signal changes in ligaments on MRI have been correlated with injury presence and chronicity and are quantifiable [23]. In the same regard, patients with recurrent injuries could potentially have caused overlap of findings in the acute and chronic injury subgroups; no attempt was made to create a subgroup with acute superimposed on chronic injury. Lack of this subgroup could explain the presence of bone bruises in a small proportion of patients in the chronic injury subgroup.
The inability to have the reviewers blinded to the adjacent anatomic structures also limited the study. A selection bias is also expected. Past studies have reported the incidence of syndesmosis injury within a range of 1–20% [3, 5, 7, 8]. In this study, 63% of the ankles had syndesmosis injuries. There are several explanations. Patients referred for MRI after ankle sprain are usually those with more severe injuries or those who do not respond as expected to conservative treatment. Alternatively, because MRI can anatomically depict injury that is not clinically apparent, clinical assessments may be underestimating the true incidence of syndesmosis injury. Conversely, patients with radiographically or clinically apparent syndesmosis injury would probably have been treated acutely and are typically not referred for MRI. These theories are supported by a recent study that found a 46% incidence in their population with ankle sprain referred for MRI [14].
Several other limitations to this study include the lack of a control group. A control group is difficult to create because it would consist of individuals who never had an ankle injuries; these injuries are extremely common and are often forgotten by patients. A further limitation of this study is that there was no surgical follow-up; however, other studies using arthroscopy have shown the high accuracy of MRI in detecting syndesmosis injuries [12, 14]. These findings diminish the need to show surgical confirmation of the MRI findings. An additional limitation was that radiographs were not available for each MRI study to correlate findings. The volume of fluid in the tibiotalar articulation was not measured; variability of joint fluid volume in the tibiotalar articulation could possibly affect the height of the tibiofibular joint recess and might be responsible for the wide SD observed. A 3D analysis of ankle joint fluid volume or MR arthrography using a standard volume might be helpful to define this relationship.
In conclusion, on MRI, syndesmosis injury is associated with anterior talofibular ligament injury, osteochondral lesion, bone bruise (acute syndesmosis injury), and tibiofibular joint incongruity.
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