Frozen shoulder (FS) or adhesive capsulitis is a common disease, and most cases can be managed successfully with con-

servative treatments [1-3]. Inflammation and subsequent fibrosis of the joint capsule are thought to be one of the main pathologies of FS [4-7], although its etiology is not fully understood. The condition has long been considered self-limiting, and more recent literature has reported that less optimistic outcomes were achieved through conservative treatments such as a combination of anti-inflammatory medications, physical therapy, and domestic fitness regimens [1, 8]. Following FS diagnosis, physical therapy and intra-articular steroid injections have been found to decrease pain and assist in regaining range of motion (ROM) [9, 10]. Manipulation under anesthesia or arthroscopic capsular release may be considered upon failure of conservative treatments [7, 11, 12].

Medical history and physical examination findings, such as pain and restricted active and passive ROM in all planes, support the clinical diagnosis of FS [1, 13, 14]. However, imaging is commonly required to assist FS diagnosis as other shoulder problems might mimic FS [15]. Radiography is generally unremarkable and is only beneficial for ruling out other shoulder disorders [16]. Magnetic resonance imaging (MRI) is a noninvasive modality that could clarify changes in the joint capsule or synovial membrane, thereby distinguishing FS from other painful shoulder disorders [5, 13]. Previous studies using MRI as a diagnostic tool for detecting FS revealed features such as thickening of the joint capsule in the axillary pouch (AP), thickening of the coracohumeral ligament (CHL), and fibrosis of the subcoracoid fat in the rotator interval (RI) [16-20]. However, other investigators described that MRI alone showed no specific abnormalities with FS, but these alterations were often observed in other shoulder disorders, such as in rotator cuff tear [4, 21].

The usefulness of contrast-enhanced MRI (CE-MRI) in the diagnosis of FS has been widely recognized [5, 14, 15]. CE-MRI can display hypervascularity of the joint capsule in FS or other inflammatory conditions such as rheumatoid arthritis [4, 14, 16, 17, 22]. Additionally, observations of joint capsule enhancement have been made in most cases of FS, but not in cases of rotator cuff tears [17, 22]. During arthroscopic capsular release for FS, excessive bleeding from the capsule is often observed. Moreover, Okuno et al. recently reported that increased abnormal blood vessels were observed in patients with refractory FS, where angiography and transcatheter embolization of the abnormal vessels were found to be effective [23, 24]. Increased abnormal blood vessels are detected with CE-MRI and might be another pathologic feature of FS. However, this has to be elucidated through a comparatively large-scale study with respective normal opposite shoulder side counterparts.

The purpose of this study was to 1) compare CE-MRI features between the FS and contralateral non-affected shoulder and 2) compare AP joint capsule thickness, CHL thickness, and subcoracoid fat obliteration on both sides. We also performed a reliability analysis of the measurements, as no gold standard methods had been developed.

In this study, contrast-enhanced bilateral MRI was performed in 10 patients with unilateral refractory FS after failed conservative treatments. This study found global enhancement of the joint capsule to be significantly higher in the affected than the unaffected side, indicating abnormal blood flow in the joint capsule. Moreover, no differences were observed concerning the AP joint capsule thickness, CHL thickness, or subcoracoid fat obliteration when comparing affected to unaffected contralateral shoulders.

The diagnosis of FS is often based on physical findings rather than imaging studies. However, this is problematic as other shoulder diseases can mimic FS. Imaging is, therefore, likely to play an essential role in the avoidance of misdiagnosis [15]. AP capsular thickening, CHL thickening, subcoracoid fat obliteration in RI, and T2-weighted signal increase in the AP joint capsule have been identified as features of FS [14, 15, 17, 25]. Emig et al. previously measured the thickness of the AP joint capsule and reported a thickness greater than 4 mm to be a useful criterion for the diagnosis of FS [25]. Ahn et al. further suggested that a thickness of 5 mm provided the highest sensitivity and specificity [15]. In contrast, no significant difference in AP joint capsule thickness was observed by Mengiardi et al. and Manton et al. [19, 26]. Further, FS patients have been identified as having a thicker CHL than control subjects [19]. However, this finding has also not been consistent, as further findings discovered no significant CHL thickness differences between FS and control patients [25]. Thus, MRI outcomes of FS pathology studies have been controversial. In the current study, AP joint capsule thickness and CHL thickening differences between FS and contralateral shoulders were not significantly different, according to our CE-MRI results, which supported the current presumption that thickening of the joint capsule or CHL could be a natural aging phenomenon and not necessarily an FS pathology. Diagnosing patients as having FS because the joint capsule or CHL “looks” thickened is wrong.

A previous study using MRI has found subcoracoid fat obliteration in 50% of FS patients and 26% of controls [14]. Furthermore, Mengiardi et al. identified that partial or complete subcoracoid fat obliteration was significantly more frequent in FS patients [19]. In agreement with previous studies, Ahn et al. observed partial or complete obliteration in all FS patients, in addition to a lack of correlation with ROM limitation [16]. Our CE-MRI evaluation demonstrated no subcoracoid obliteration differences between the FS and contralateral shoulders, thereby suggesting that subcoracoid obliteration might be due to an aging process. Thus, clinicians are advised to consider the aging process upon identification of the thickened joint capsule in association with shoulder pain.

Carrillon et al., using CE-MRI to detect increased blood flow in the joint capsule, reported enhancement of the joint capsule in all FS patients (n = 25), but in only one of the 15 rotator cuff tear patients [22]. This finding was supported by Connell et al.’s study in which enhancement of the joint capsule was found in 22 of 24 surgically treated FS cases and two of the patients with rotator cuff tear as controls (n = 22) [17]. Furthermore, AP joint capsule enhancement was identified in 49 of 50 FS patients, but only 19 of 53 control subjects [15]. In our present study, all FS patients demonstrated global high-intensity changes in the joint capsule, but none in the contralateral shoulders. Hence, CE-MRI is able to detect the qualitative alteration of the joint capsule [27]. The procedure could, therefore, be performed in severe cases of failed conventional conservative therapy. Intra-articular steroid injections were considered useful in case of high enhancement, and surgery such as arthroscopic capsular release was required in patients with prolonged motion limitations despite having low enhancement [4]. However, in this study, global enhancement of the joint capsule was identified in all patients (n = 10), even after sufficient periods of conservative therapy, including several intra-articular steroid injections. Therefore, in some cases, inflammation was not resolved even after adequate conservative therapy. In contrast, when the joint capsule was not enhanced, extra-articular joint stiffness factors such as conditions of the scapula, muscle stiffness, or central problems should be considered. Recently, Okuno et al. described the results of angiography in patients with refractory FS [23, 24]. Neovessels were found to have been generated around the RI, mainly from the thoracoacromial artery or coracoid branch, and around the AP from the circumflex scapular artery or anterior or posterior circumflex artery. Moreover, the pain was found to improve rapidly after the embolization of the abnormal neovessels. These results indicate increased abnormal vessels to be the source of pain which is supported by findings of ongoing persistent inflammation in patients with refractory FS. Performing angiography in every FS patient is challenging. However, our study provided evidence in support of the possibility of predicting the existence of abnormal neovessels with the use of CE-MRI.

This study has several limitations. First, most FS patients recover sufficiently through conservative therapy and invasive therapy is no longer in use. Therefore, only a small number of patients could be included in this study. However, to ensure the characteristic findings of FS, most severe cases were chosen, which will be a strength of this study. Despite the limited sample size, the study findings are valuable for developing insight into FS as a guide for clinical practice. Since there is no established quantitative MRI evaluation technique to date, the method presented by Ahn et al. was applied in the current study. The overall reliability of the method was found to be acceptable, although some constituents had low reliability, suggesting evaluation methodology. Finally, characteristics of MRI might differ depending on the stages of frozen shoulder (i.e., freezing, frozen, or thawing), which determine the severity of the disease. As the current study focused exclusively on surgically treated refractory cases, associations between disease stage, pain intensity, and MRI features remain unknown. Future studies should aim to address this gap in current knowledge.

CE-MRI can detect the qualitative alteration of the joint capsule and could be used to assist the clinical diagnosis of FS. Significant differences, however, were not observable, regarding the AP joint capsule thickness, CHL thickness, or subcoracoid fat obliteration when compared to the contralateral shoulders, implying these observable changes in FS could be normal wear and tear which comes along with aging rather than the disease state.