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Musculoskeletal Imaging |
1 From the Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, Mo. From the 1998 RSNA scientific assembly. Received April 28, 1999; revision requested June 14; final revision received November 16; accepted November 24. Address correspondence to M.D.L., Caritas Medical Center, 1850 Bluegrass Ave, Louisville, KY 40215 (e-mail: davidlinkous@home.com).
| ABSTRACT |
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MATERIALS AND METHODS: Bilateral wrist arthrograms were reviewed for 30 consecutive patients with a history of wrist trauma and unilateral wrist pain who had at least one scapholunate ligamentous communicating defect and unremarkable conventional radiographs. The location and size of each ligamentous defect was recorded. Differences between symptomatic and asymptomatic wrists were analyzed with the
2 or Fisher exact test.
RESULTS: Most communicating defects in both groups were incomplete and ranged from pinhole size to large. There was a higher frequency of complete disruption in the symptomatic wrists (nine [32%] of 28 wrists) than in the asymptomatic wrists (two [10%] of 20 wrists; P = .092). Communicating defects involved the dorsal portion in 18 (64%) of the 28 symptomatic cases and in five (25%) of the 20 asymptomatic cases (P = .007).
CONCLUSION: The data suggest that the demonstration of a complete ligamentous disruption or involvement of the dorsal portion of the ligament may indicate a traumatic cause rather than a degenerative change.
Index terms: Ligaments, injuries, 434.483 Wrist, abnormalities, 434.483 Wrist, arthrography, 434.122 Wrist, injuries, 434.483
| INTRODUCTION |
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Findings of various cadaveric and arthrographic studies have demonstrated that defects occur within the substance of the scapholunate and lunotriquetral ligaments, as well as within the triangular fibrocartilage, as senescent changes in asymptomatic wrists (7,1118). Therefore, the discovery of a communicating defect through any of the ligaments could represent either a symptomatic disruption or an asymptomatic perforation as the result of degeneration.
We have recognized this dilemma and have adapted our arthrographic technique to better assess intercarpal ligamentous defects by performing contralateral arthrography (8,11,12) when a communicating defect is discovered and by performing a focused physical examination in each patient. Both of these strategies most likely improve the chances for the referring clinician to predict whether the discovered ligamentous defect is clinically important, but neither strategy offers a direct method to distinguish symptomatic from asymptomatic communicating defects.
No researchers in arthrographic or arthroscopic studies, to our knowledge, have investigated the characteristics of individual scapholunate ligamentous communicating defects in symptomatic and asymptomatic wrists to determine if there are significant differences between the two groups. We undertook this study to test our hypothesis that defects through the scapholunate ligament have different characteristics in symptomatic wrists (possibly the result of trauma) than in asymptomatic wrists (presumably the result of degeneration).
| MATERIALS AND METHODS |
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Since the convention in the orthopedics literature is to refer to symptomatic intercarpal ligamentous perforations as "tears" and because we selected patients who had experienced unilateral wrist trauma, we chose to use the terms "traumatic lesion" and "degenerative perforation" to describe communicating defects of the scapholunate ligament in the symptomatic posttraumatic group and the asymptomatic group, respectively. Thus, in this article, the term "traumatic lesion" is used in certain contexts to refer to symptomatic perforations or communicating defects.
Study Design
We reviewed the arthrographic data sheets, reports, and arthrograms of 213 consecutive patients who underwent bilateral wrist arthrography over 15 months, from November 1995 through February 1997. Included in this cohort were patients with a history of wrist trauma and unilateral wrist pain in whom at least one communicating scapholunate ligamentous defect could be demonstrated. Those patients who had alternative radiographic explanations for wrist pain (unhealed fracture, arthritis, osteonecrosis, etc) or a history of prior surgery at a location in proximity to the scapholunate ligament were excluded. Thirty of the 213 patients met the criteria for inclusion.
The sixty wrist arthrograms in the 30 patients (30 symptomatic wrists; 30 asymptomatic wrists) were reviewed retrospectively by two musculoskeletal radiologists (M.D.L., L.A.G.) without knowledge of the presence of symptoms in each case. All interpretations were by consensus. The following characteristics were assessed.
1. The presence of a scapholunate ligamentous defect was recorded. The size of the defect was recorded as pinhole, small, medium, large, or complete. A pinhole defect was defined as a visible punctate column of contrast material through the ligament. Small, medium, and large communicating defects were defined as those defects estimated to extend through less than one-third, one-third through two-thirds, and greater than two-thirds, respectively, of the sagittal dimension of the ligament. Complete defects were those that involved the entire sagittal dimension of the ligament (disruption).
2. The location of the communicating defect in the coronal plane was categorized as through the scaphoid attachment, through the lunate attachment, or through the substance of the ligament.
3. The location in the sagittal plane was categorized by noting whether the communicating defect involved the dorsal, middle, and/or volar (ventral) thirds of the ligament.
Examination Technique
All patients underwent a three-compartment assessment of the symptomatic wrist in the following sequence: midcarpal injection of contrast material; distal radioulnar joint injection; and, finally, radiocarpal injection, which was delayed until contrast material had been resorbed from the adjacent compartments. Communication with, and full distention of, adjacent compartments during an injection usually obviated separate injection into those compartments. All patients in the study underwent tailored arthrography of the asymptomatic wrist when a communicating defect through one of the intercarpal ligaments in the symptomatic wrist was discovered. The arthrographic evaluation of the contralateral wrist in such cases has been the standard of practice at our institution for some time. The tailored examination consisted of evaluation of the compartments on either side of the same ligament that had a communicating defect in the symptomatic wrist.
The technique of wrist arthrography in this study was standard for all patients and follows the technique outlined by Linkous and Gilula (19). For each injection, the hand was secured in a pronated position, and the skin along the dorsal aspect of the wrist was prepared and draped by using an aseptic technique. Local anesthesia was achieved with 1% lidocaine (Xylocaine; AstraZeneca, Wilmington, Del) without epinephrine.
By using fluoroscopic guidance and depending on the suspected area of abnormality, one of two sites for injection into the midcarpal compartment was selected. As a rule, the needle is placed as far from the patients site of maximal symptoms as possible. Sites included (a) between the scaphoid and capitate, just proximal to the trapezoid, and (b) at the clear space formed by the intersection of the lunate, triquetrum, hamate, and capitate.
Similarly, injection was performed at one of two sites in the radiocarpal joint space, depending on the location of wrist pain. In the case of radial-sided pain, the ulnar aspect of the joint was entered at a point proximal to the triquetrum at the radial edge of the pisiform. For ulnar-sided pain, the radioscaphoid space was entered at a point away from the scapholunate ligament but proximal to the scaphoid tubercle, typically adjacent to the radial styloid.
A 25-gauge needle was coupled via connective tubing to a syringe filled with contrast material: two parts 43% meglumine and one part 1% lidocaine. Following confirmation of an intraarticular location of the needle tip, the scapholunate joint was profiled, the contrast material was injected under direct fluoroscopic control, and multiple spot images were obtained. The joint space was distended until there was slight widening of the capitolunate space (midcarpal injection) or radiolunate space (radiocarpal injection), at which point the needle was removed and the track was obliterated.
The wrist was then examined in the prone position and in neutral, radial, and ulnar deviations with fluoroscopy to assess for any abnormal communications. Standard pronated oblique (profiling the scaphotrapezial joint), neutral lateral, supinated oblique (profiling the pisotriquetral space), and supinated views were also obtained with the wrist in the neutral, radial, and ulnar positions.
If scapholunate or lunotriquetral ligamentous defects were identified or suspected, additional imaging was performed, with each of these two ligaments individually profiled. Imaging was then performed with the wrists held in half and full flexion in the supinated position and half and full extension in the pronated position; these maneuvers facilitated the evaluation of the volar and dorsal segments, respectively, by bringing these areas of each examined ligament tangent to the x-ray beam (Fig 1).
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2 analysis was used for the comparison of parameters between the symptomatic and the asymptomatic groups, unless the number of cases was less than five. The Fisher exact test was used when the number of cases was less than five. | RESULTS |
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Communicating defects at the scaphoid attachment also occurred frequently in both groups, accounting for nine (32%) of 28 defects in the symptomatic group and six (30%) of 20 defects in the asymptomatic group (Fig 2). There was no significant difference between the two groups in the frequency of communicating defects at either of these two locations (P = .67).
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| DISCUSSION |
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The volar segment is intimately associated with the strong volar extraosseous ligamentous network and is separated from the central segment by the radioscapholunate ligament, a structure that is more akin to a vascular pedicle than a true ligament (20).
Multiple authors (7,1218) have demonstrated that perforations occur in the scapholunate ligaments of asymptomatic patients and are found in cadavers with no known history of wrist injury. These perforations rarely are present before 20 years of age but occur more frequently with advancing age and reach approximately a 50% prevalence by the 8th decade of life (7,16). However, very few authors have investigated characteristics that might help distinguish traumatic tears of the scapholunate ligament from attritional lesions. Wright et al (18) observed in cadavers with no history of wrist abnormality that 77% of scapholunate perforations involved either the central portion or the full ventral to dorsal extent. A minority of perforations involved the ventral or dorsal components in isolation. Berger (20) has observed that the fibers are thinner at the scaphoid attachment of the scapholunate ligament. Smith (6) speculated from these data that traumatic avulsions should occur more frequently at the scaphoid attachment.
Our data do not support the hypothesis that a communicating defect through the scaphoid attachment of the scapholunate ligament is an indicator of a traumatic cause. Instead, we found that defects in the scapholunate ligament occur frequently within the substance of the ligament and at its scaphoid attachment in both symptomatic and asymptomatic wrists. We postulate from these results that the inherent weakness of the ligament in these two locations makes it susceptible to perforation at these sites from both traumatic and degenerative forces. Therefore, we believe, the identification of a communicating defect at the scaphoid attachment should not be used in exclusion as a criterion for diagnosing a scapholunate ligamentous tear.
Although the difference was not statistically significant in our small study population, communicating defects through the lunate attachment of the scapholunate ligament were not observed to occur in the asymptomatic group but accounted for 11% of the scapholunate ligamentous communicating defects in the symptomatic group. This raises the question of whether the bulkier fibers of the lunate attachment make it less susceptible to degeneration. We believe that further investigation should be undertaken to test the hypothesis that a scapholunate ligamentous communicating defect at the lunate attachment may be an indicator of a traumatic cause rather than a degenerative perforation.
The discovery that a significantly greater percentage of communicating defects involved the dorsal segment of the scapholunate ligament in the symptomatic group raises some interesting questions. Is the involvement of the dorsal segment simply related to the fact that the defects in the symptomatic group were generally larger than those in the asymptomatic group? Does involvement of the fibrous dorsal segment produce subtle symptomatic instability patterns? Or is it possible that defects that extend into this segment (which, unlike the collagenous central segment, contains nerve fibers) are more likely to be painful? These questions raise an even bigger question: Are all symptomatic intercarpal ligamentous perforations the result of trauma, or can degenerative perforations be symptomatic as well? Currently, to our knowledge, there is little evidence or agreement in the orthopedics literature to answer this question.
Finally, scapholunate ligamentous communicating defects that involve the ventral portion of the ligament in isolation were a very infrequent finding, occurring in only one of the 60 wrists examined. This finding reinforces the findings of the anatomic work by Berger (20) and suggests that the volar segment is strengthened by the adjacent strong extracapsular volar extrinsic ligamentous complex and by the radioscapholunate ligament, which terminates at the junction of the volar and central segments of the ligament.
We recognize several limitations of this study. First, although we excluded cases in which other radiographic abnormalities, such as healing fractures and degenerative changes, existed, several of the patients had concurrent arthrographic abnormalities, such as triangular fibrocartilaginous or lunotriquetral ligamentous communicating defects. These, like scapholunate ligamentous communicating defects, are known to occur as a result of degeneration but could be contributors to the patients symptoms.
Second, even in those patients in whom we diagnosed isolated scapholunate ligamentous defects, there is no assurance that this defect was the cause of the patients pain. Third, it is possible that some of the communicating defects in the asymptomatic wrists were the result of trauma that occurred many years earlier that the patients were unable to recall and that were no longer symptomatic.
Fourth, despite our meticulous attempts to evaluate the location and extent of each defect by using the various maneuvers described in the Materials and Methods section, the exact anatomic boundaries between segments are not radiographically discernible. Finally, the small study size reduces our ability to prove or disprove statistically significant differences between the groups.
In this pilot study, however, we believe that we have achieved our goal of initiating an evaluation of the characteristics of scapholunate ligamentous communicating defects. Findings in this article show that defects in the dorsal portion of the scapholunate ligament were more common in symptomatic wrists than in asymptomatic wrists.
In addition, findings in this article lead us to question whether defects through the lunate atachment of the scapholunate ligament are more important clinically than defects through the scaphoid attachment or within the substance of the ligament. We hope that this project will spur further imaging, arthroscopic, or anatomic research in this area and that certain characteristic differences will be proved in the sizes and locations of scapholunate ligamentous defects between symptomatic and asymptomatic wrists that will improve our ability to predict whether an observed communicating defect represents degenerative change or a symptomatic, trauma-induced defect.
| FOOTNOTES |
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| REFERENCES |
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