Michener Lori A, Subasi Yesilyaprak Sevgi S, Seitz Amee L, Timmons Mark K, Walsworth Matthew K
COOR Laboratory, Department of Physical Therapy, Virginia Commonwealth University, Rm 100, West Hospital Basement, Richmond, VA, 23298, USA,
Knee Surg Sports Traumatol Arthrosc. 2015 Feb;23(2):363-9. doi: 10.1007/s00167-013-2542-8. Epub 2013 Jun 5.
To characterize the supraspinatus tendon thickness, subacromial space, and the relationship between tendon thickness and subacromial space to further elucidate the mechanisms of subacromial impingement syndrome.
In a single-blind cross-sectional study, subjects were recruited with subacromial impingement syndrome (n = 20) and asymptomatic controls (n = 20) matched for age, gender, and hand dominance. Ultrasound images were collected using a 4-12-MHz linear transducer in B-mode of the supraspinatus tendon in the transverse (short axis) and the anterior aspect of the subacromial space outlet. Using image callipers, measurements of tendon thickness were taken at 3 points along the tendon and averaged for a single thickness measure. The subacromial space outlet was measured via the acromiohumeral distance (AHD) defined by the inferior acromion and superior humeral head. The occupation ratio was calculated as the tendon thickness as a percentage of AHD.
The subacromial impingement syndrome group had a significantly thicker tendon (mean difference = 0.6 mm, p = 0.048) and a greater tendon occupation ratio (mean difference = 7.5 %, p = 0.014) compared to matched controls. There were no AHD group differences.
The supraspinatus tendon was thicker and occupied a greater percentage of AHD, supporting an intrinsic mechanism. An extrinsic mechanism of tendon compression is theoretically supported, but future imaging studies need to confirm direct compression with elevation. Treatment to reduce tendon thickness may reduce symptoms, and surgical intervention to increase subacromial space may be considered if tendon compression can be verified.
描述冈上肌腱厚度、肩峰下间隙以及肌腱厚度与肩峰下间隙之间的关系，以进一步阐明肩峰下撞击综合征的发病机制。
在一项单盲横断面研究中，招募了患有肩峰下撞击综合征的受试者（n = 20）和年龄、性别及利手相匹配的无症状对照组（n = 20）。使用4-12MHz线性换能器以B模式在横断位（短轴）和肩峰下间隙出口的前位采集冈上肌腱的超声图像。使用图像卡尺，在肌腱上3个点测量肌腱厚度，并取平均值作为单一厚度测量值。通过肩峰下表面与肱骨头上方所定义的肩峰肱距离（AHD）测量肩峰下间隙出口。计算占据率，即肌腱厚度占AHD的百分比。
与匹配的对照组相比，肩峰下撞击综合征组的肌腱明显更厚（平均差值 = 0.6mm，p = 0.048）且肌腱占据率更高（平均差值 = 7.5%，p = 0.014）。AHD在两组间无差异。
冈上肌腱更厚且占AHD的百分比更高，支持一种内在机制。理论上支持肌腱受压的外在机制，但未来的影像学研究需要证实上举时的直接受压情况。减少肌腱厚度的治疗可能会减轻症状，如果能证实肌腱受压，可考虑手术干预以增加肩峰下间隙。
