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Musculoskeletal Imaging |
1 From the Department of Radiology, Cappagh National Orthopaedic Hospital, Finglas, Dublin 11, Ireland. Received January 8, 2004; revision requested March 12; revision received May 27; accepted July 1. Address correspondence to S.E. (e-mail: seustace@iol.ie).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Ethics review board approval was not required for studies involving retrospective image or case record review; informed consent for review was not required. Eighteen male athletes (mean age, 24 years; age range, 19–32 years) were included for study. All patients underwent radiography and MR imaging (coronal fast spin-echo T1-weighted, transverse fast spin-echo T2-weighted, and coronal turbo short inversion time inversion-recovery [STIR] imaging) of the pelvis. Subsequent image-guided nonionic contrast material injection was followed by a 0.5% bupivacaine hydrochloride (1 mL) and methyprednisolone acetate (20 mg) injection into the central cleft of the symphysis pubis. Comparison was made between imaging findings at symphyseal cleft injection and appearances at preprocedure MR imaging, with specific reference to the presence of a secondary cleft. The sensitivity and specificity of MR imaging in demonstrating the secondary cleft sign were compared with those of the reference standard, imaging at symphyseal cleft injection. MR images from a reference group of 70 asymptomatic athletes who underwent STIR imaging of the pelvis were analyzed for evidence of a secondary cleft.
RESULTS: Osteitis pubis was diagnosed in six patients on the basis of radiography and/or MR imaging. A secondary cleft was identified in 12 of 18 patients at MR imaging, was best visualized at coronal STIR imaging, and was confirmed in each patient during contrast material injection into the central physiologic symphyseal cleft. In no patient was a secondary cleft identified at symphyseal cleft injection and not identified at MR imaging (sensitivity and specificity, 100%). In each patient, the side of the secondary cleft corresponded to the side of symptoms that responded to local anesthetic and steroid injection. Four of the six patients with osteitis pubis had evidence of a secondary cleft. In one patient, a secondary cleft was not identified at MR imaging or symphyseal cleft injection, but adductor avulsion was identified at MR imaging. No evidence of a secondary cleft sign at MR imaging was identified in the reference group.
CONCLUSION: The secondary cleft sign demonstrated at MR imaging is a marker of groin injury in athletes presenting with groin pain.
© RSNA, 2005
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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The symphysis pubis is a fibrocartilaginous joint in which a central cleft or cavity may be present. The adjacent medial pubic bones are the origins for multiple tendons, including those of the adductor muscles. The medial pubic bones are also the origins for the gracilis and the conjoined tendon, the common aponeurosis of which supports the joint anteriorly.
Efforts by clinicians to determine the cause of groin pain have focused predominantly on the interpretation of clinical examination findings and appearances at radiography and bone scanning. Previously, authors have emphasized the role of magnetic resonance (MR) imaging and symphyseal cleft injection, which is performed with fluoroscopic guidance after administration of contrast material (6–8). The purpose of this study was to determine whether the secondary cleft sign demonstrated in the symphysis pubis at MR imaging is a marker of injury in athletes presenting with groin pain.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Radiography
Anteroposterior radiographs of the pelvis, including collimated flamingo views (alternate weight bearing on one leg) of the symphysis pubis, were obtained and evaluated jointly by two musculoskeletal radiologists (D.B. and S.E., with 5 and 15 years experience, respectively).
MR Imaging
MR imaging was performed with a 1.5-T system (Gyroscan; Philips Medical Systems, Best, the Netherlands) and a phased-array surface coil. Pelvis and groin imaging included coronal fast spin-echo T1-weighted imaging (770/20 [repetition time msec/echo time msec]), transverse fast spin-echo T2-weighted imaging (3000/80), and coronal turbo short inversion time inversion-recovery (STIR) imaging (2000/20/160 [repetition time msec/echo time msec/inversion time msec]). Section thickness was 4 mm for both fast spin-echo T1-weighted imaging and fast spin-echo T2-weighted imaging; section thickness was 6 mm for STIR imaging. The rectangular field of view was 365 mm.
Symphyseal Cleft Injection
Symphyseal cleft injection was performed by a radiologist (D.B., S.E.) as a diagnostic intervention and temporary treatment. With the patient in a supine position, an initial skin mark was placed, and the joint cleft was subsequently accessed by using fluoroscopic guidance, which was performed by directing the needle perpendicular to the fluoroscopic beam in the midline at the central portion of the joint. After 2 mL of 1% lignocaine (Braun, Dublin, Ireland) was injected subcutaneously, a 22-gauge spinal needle (Spinocan; Braun) was introduced into the symphyseal cleft midway between the upper and lower margins of the symphysis pubis. The needle was passed through the subcutaneous fat, and, once the needle reached the outer margin of the joint, which was indicated by increased resistance, the needle was advanced 1 cm farther into the cleft of the fibrocartilaginous disk. A subsequent injection of 1 mL of nonionic contrast material (iopramide, Ultravist 300; Schering, Berlin, Germany) was performed. During injection, note was made of symptom provocation and whether the injection induced symptoms that were lateralized to the side of the described groin pain. In addition, note was made of whether contrast material extended beyond the physiologic central cleft, which was determined by the inferior margin of the symphysis pubis, or whether contrast material extended lateral to the midline, that is, to a so-called secondary cleft. A local analgesic composed of an aqueous suspension of 20 mg of methylprednisolone (Depo Medrol; Pharmacia, Dublin, Ireland) and 1 mL of 0.5% bupivacaine hydrochloride (Astra Zeneca, Dublin, Ireland) was subsequently injected into the cleft.
In each patient, radiography, MR imaging, and symphyseal cleft injection were performed within a 3-week period in the same order. All patients were routinely followed up within a 6-week period; during follow-up, clinical correlation was made between symptoms, clinical examination findings (including symptoms elicited by lateral pressure on the hip joints), and findings during exercises to elicit symptoms (resisted internal rotation and adduction of the hip). No follow-up imaging was performed.
Image Interpretation
All acquired symphyseal cleft injection and MR images were reviewed by two radiologists (D.B., S.E.), one of whom performed each of the symphyseal cleft injections. Each reviewer initially examined symphyseal cleft injection images followed by MR images independently and noted whether a secondary cleft was identified. At a separate sitting, the two reviewers reexamined images together in a different patient order for each modality and agreed on a final diagnosis by consensus. Note was made of identification of a secondary cleft at symphyseal cleft injection and at MR imaging. At this time, radiographs and MR images were also reviewed for evidence of osteitis pubis. Diagnosis of osteitis pubis was made at radiography on the basis of joint space narrowing or widening, joint malalignment, and articular surface irregularity or erosions. Diagnosis of osteitis pubis was made at MR imaging on the basis of high-signal-intensity abnormalities consistent with bone edema in the medial pubic bones, joint malalignment, and articular surface irregularity or erosions. The physiologic central cleft was defined as a midline potential space confined within the superior and inferior margins of the joint. The secondary cleft was defined as any evidence at symphyseal cleft injection of the extension of contrast material either lateral to the midline or inferior to the joint. There was a 3-week interval between each image review session to eliminate recall bias. During MR image review, note was made of the optimum imaging plane and tissue weighting used to identify the symphyseal cleft and the secondary cleft. Correlation was also made with clinical outcome.
Reference Group
Seventy male athletes who were asymptomatic for groin pain and who had enrolled in a separate research protocol were used as a reference group for MR imaging of the secondary cleft sign. All athletes were college-level or post–college-level rowers (age range, 17–34 years; mean age, 24 years). All athletes who were enrolled in the separate research protocol, which had institutional review board approval, had given informed consent, including consent for the use of data for other studies at our institution. All athletes had undergone coronal STIR imaging of the pelvis (as part of a whole-body MR imaging protocol), which was performed by using parameters identical to those used in the athletes with groin pain.
Statistical Analysis
The sensitivity and specificity of MR imaging in demonstrating the secondary cleft sign were calculated by using symphyseal cleft injection as a reference standard. A 
statistic was recorded for interobserver agreement regarding the presence of a secondary cleft at symphyseal cleft injection and MR imaging.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Symphyseal Cleft Injection
In all patients, injection of contrast material reproduced the symptom of groin pain. In each patient, symptoms were subsequently relieved with local anesthetic and steroid injection. At cleft injection, a secondary symphyseal cleft was identified in 12 of the 18 patients (Fig 1), including one patient in whom bilateral clefts were identified ( = 1.0). In six patients, a midline physiologic cleft was identified without the extension of contrast material below the inferior margin of the symphysis pubis. In each of the 12 patients with a secondary cleft, contrast material extended to the side of symptomatic groin pain. In one patient with a midline physiologic cleft, symptoms were lateralized to the right side of the groin. In the remaining five patients with a midline physiologic cleft, symptoms were localized to the midline overlying the symphysis pubis.
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= 1.0). In each instance, the physiologic and secondary symphyseal clefts were best identified at coronal STIR imaging. The secondary cleft demonstrated fluid signal intensity and was continuous with the physiologic cleft. In seven patients, the cleft extended to the inferior margin of the right side of the pubic ramus. In four patients, the secondary cleft extended to the inferior margin of the left side of the pubic ramus. In one patient, a bilateral cleft was identified that corresponded to an abnormality demonstrated at symphyseal cleft injection. In the remaining six patients, no secondary cleft was identified. In each of these six patients, there was complete correlation between the recorded findings at symphyseal cleft injection and the findings at MR imaging. In each instance, the cleft that was identified at MR imaging lateralized to the side of the patients’ symptoms. In one patient who had no evidence of a secondary cleft, review of STIR images revealed the presence of focal traction bone edema at the adductor longus and gracilis tendon attachment on the side of symptoms (Fig 5). Osteitis pubis was diagnosed in six patients on the basis of radiographic appearances of symmetric sclerosis and articular surface irregularity (n = 4) and/or bilateral diffuse pubic bone edema at MR imaging (n = 6). Four of the six patients with osteitis pubis had evidence of a secondary cleft. A secondary cleft was not identified in any of the 70 athletes from the reference group. When reviewed in isolation, the secondary cleft sign allowed accurate diagnosis and correct lateralization of symptoms at MR imaging in all 12 patients who had abnormalities that were identified at symphyseal cleft injection (sensitivity and specificity, 100%). At 6-week clinical follow-up, no discrepancy was found between findings at symphyseal cleft injection and outcome.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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We describe the development of a secondary cleft that is continuous with the physiologic cleft within the symphyseal fibrocartilage. A secondary cleft could develop as a result of chronic maceration of the central fibrocartilage owing to abnormal stress in the pelvic ring. In this study, the lateralization of symptoms corresponding to the side of cleft abnormality and the extension of the cleft beyond joint margins raises the possibility that the cleft could be a consequence of prolonged traction force on the pubic rami and the common aponeurosis anterior to the joint. This traction force imposed by the hip adductors, gracilis, and possibly the conjoined tendon could explain a loss of morphologic features in the fibrocartilaginous disk. Chronic injury leads to communication between this secondary cleft and the physiologic central cleft. At symphyseal cleft injection, the secondary cleft extends beyond the margins of the fibrocartilaginous disk and into the enthesis of the adductor and gracilis muscles; this finding was confirmed at MR imaging. Because of the limitations of resolution at MR imaging, it is possible that this extension is between fascial planes rather than in the tendon substance, but, in either case, the finding is abnormal and suggests tendon injury. The relationship between adductor or gracilis tendon dysfunction and a secondary cleft is not proved in this study because surgical correlation was not performed in the patient group. In addition, one patient in this series had evidence of substantial adductor and gracilis avulsion injury without cleft abnormality. This may reflect acute injury as opposed to chronic repetitive strain. Communication between the secondary cleft and the site of tear is likely to account for symptom relief in patients after injection of local anesthetic and steroid.
In this study, a subset of four patients with osteitis pubis had a secondary cleft, whereas two additional patients with osteitis pubis had a normal central cleft. In pregnancy, hormone-induced ligamentous laxity allows increased motion at the symphysis pubis, with impaction of bone on bone to produce osteitis pubis. Increased ligamentous laxity or muscle imbalance has been proposed as a mechanism for the development of osteitis pubis in athletes (4). Acquired laxity as a result of adductor and/or gracilis dysfunction is a prospective mechanism for abnormal symphyseal motion and, hence, for the development of traumatic osteitis pubis. This sequence is suggestive of a spectrum of changes in those who experience groin pain, commencing with microavlusion injury at the anterior or inferior surface of the pubic rami, with the development of a secondary cleft, continuing to subsequent tendon tear, and finally progressing to florid osteitis pubis. Such a spectrum might assist in the triage of patients into groups of those who are likely to recover following short-term rest, prolonged rest, exercise programs, or tenotomy (11,12). Other patients, however, appear to develop osteitis pubis without a preceding secondary cleft that is consistent with the multifactorial causes for this condition. Further research is needed to determine if a secondary cleft can predict outcome or response to treatment.
In previous studies, researchers who have reviewed MR images of patients with groin pain have concentrated on the presence or absence of edema in affected muscles and pubic bones. The presence of a cleft has not been discussed. In one study of Australian Rules football players, an alteration of pubic bone signal intensity was present in most patients with clinically diagnosed osteitis pubis (10). Although an alteration in the signal intensity of the public bones is a sensitive marker of osteitis pubis, in the same study a similar finding was also identified in the asymptomatic reference group, thereby reducing specificity. Researchers from a North American study of 32 patients with pubalgia (defined as pubic pain of indeterminate origin) also reported signal intensity abnormalities in the marrow of the pubic bone in 70% of patients; however, the change in signal intensity was often unilateral despite bilateral symptoms (9). Other investigators have focused on the morphologic characteristics of the rectus abdominus muscles and have documented an alteration in the size and symmetry of the rectus abdominis muscles in patients who experience groin pain (13,14). Other investigators (15,16) have concluded that injury to the adductor muscle origin is important in the pathogenesis of osteitis pubis, a conclusion similar to that in our current study, and have emphasized the development of an imbalance in the stabilizing structures of the symphysis pubis following injury. The secondary cleft sign as a marker of symphyseal injury provides a potential explanation for groin pain because multiple causes of groin pain frequently coexist.
When used as a single diagnostic sign, the secondary cleft was identified correctly at symphyseal cleft injection in each patient with a secondary cleft. The results of this study suggest that the identification of a secondary cleft replaces the need for diagnostic symphyseal cleft injection, although this procedure remains valuable when combined with local anesthetic and steroid injection. O’Connell et al (7) demonstrated the correlation between provoked symptoms at symphyseal cleft injection and clinical outcome. It remains unclear, however, whether therapeutic cleft injection, when used as a short-term treatment, results in treatment of osteitis pubis or adductor and/or conjoined tendon avulsion injury prior to the development of osteitis pubis.
This study is limited by its small size. The method of patient selection has inherent bias because only athletes with severe symptoms were likely to undergo MR imaging and symphyseal cleft injection. In this series, the 100% sensitivity and specificity (12 of 12 patients) of MR imaging in demonstrating the secondary cleft sign is unlikely to be reproduced in a larger case series. The larger, asymptomatic reference group was standardized for approximate age; however, this group was not standardized for the same sports practiced, and all athletes in both groups were male. Lack of the secondary cleft sign in the reference group excludes this sign as a common normal variant; a rare, normal variant cannot be excluded but is unlikely. It is possible that the secondary cleft sign could be present in asymptomatic individuals who practice the same sports (soccer and rugby) as the study group practiced. In addition, the reference group was reviewed separately, thereby introducing bias. It was not ethically possible to perform symphyseal cleft injection in the reference group, and, therefore, this group could not be a true control. Surgery was not indicated in any patient in this series.
In conclusion, we describe the secondary cleft sign demonstrated at MR imaging in athletes who are referred with nonspecific groin pain. Although not specifically proved in this study, the secondary cleft sign may imply dysfunction of the adductor, gracilis, or conjoined tendon. The sign can be identified in the absence of recognized features of osteitis pubis and, therefore, should be specifically sought on coronal STIR images in athletes presenting with groin pain. The presence of the secondary cleft sign at MR imaging may obviate an extensive search for other causes of groin pain, thereby reducing potentially unnecessary interventions.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Authors stated no financial relationship to disclose.
Author contributions: Guarantors of integrity of entire study, D.B., M.J.O., P.C., S.E.; study concepts and design, D.B., M.J.O., M.R., D.T., C.C., P.O., S.E.; literature research, D.B., M.J.O., P.C., S.E.; clinical studies, D.B., S.E., D.T., C.C., M.R.; experimental studies, D.B., M.R., S.E.; data acquisition, D.B., M.J.O., M.R., D.T., C.C., P.O., S.E.; data analysis/interpretation, all authors; statistical analysis, D.B., M.J.O., S.E.; manuscript preparation, all authors; manuscript definition of intellectual content, D.B., M.J.O., M.R., D.T., C.C., P.O., S.E.; manuscript editing, D.B., M.J.O., M.R., S.E.; manuscript revision/review and final version approval, all authors
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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