Published online before print April 3, 2008, doi: 10.1161/STROKEAHA.107.502187
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(Stroke. 2008;39:1808.)
© 2008 American Heart Association, Inc.
Original Contributions |
MRI Findings in the Painful Poststroke Shoulder
From the Departments of Radiology (R.R.S.) and Physical Medicine and Rehabilitation (S.H., J.C.), Case Western Reserve University at MetroHealth Medical Center, Cleveland, Ohio; Kessler Medical Rehabilitation Research and Education Center (E.P.E.), West Orange, NJ; the Department of Rehabilitation Medicine (S.R.F., A.B.), Mt Sinai School of Medicine, New York, NY; the Department of Physical Medicine and Rehabilitation (N.V.), Carolina Rehabilitation, Charlotte, NC; the Department of Rehabilitation Sciences (S.J.P.), University of Cincinnati, Cincinnati, Ohio; and NeuroControl Corporation (Z.P.F.), North Ridgeville, Ohio. Z.P.F. is now affiliated with NBI Development, San Francisco, Calif.
Correspondence to John Chae, MD, Department of Physical Medicine and Rehabilitation, Case Western Reserve University, MetroHealth Medical Center, 2500 MetroHealth Drive, Cleveland, OH 44109. E-mail jchae{at}metrohealth.org
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Abstract |
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Background and Purpose— We describe the structural abnormalities in the painful shoulder of stroke survivors and their relationships to clinical characteristics.
Method— Eighty-nine chronic stroke survivors with poststroke shoulder pain underwent T1- and T2-weighted multiplanar, multisequence MRI of the painful paretic shoulder. All scans were reviewed by one radiologist for the following abnormalities: rotator cuff, biceps and deltoid tears, tendinopathies and atrophy, subacromial bursa fluid, labral ligamentous complex abnormalities, and acromioclavicular capsular hypertrophy. Clinical variables included subject demographics, stroke characteristics, and the Brief Pain Inventory Questions 12. The relationship between MRI findings and clinical characteristics was assessed through logistic regression.
Results— Thirty-five percent of subjects exhibited a tear of at least one rotator cuff, biceps or deltoid muscle. Fifty-three percent of subjects exhibited tendinopathy of at least one rotator cuff, bicep or deltoid muscle. The prevalence of rotator cuff tears increased with age. However, rotator cuff tears and rotator cuff and deltoid tendinopathies were not related to severity of poststroke shoulder pain. In approximately 20% of cases, rotator cuff and deltoid muscles exhibited evidence of atrophy. Atrophy was associated with reduced motor strength and reduced severity of shoulder pain.
Conclusions— Rotator cuff tears and rotator cuff and deltoid tendinopathies are highly prevalent in poststroke shoulder pain. However, their relationship to shoulder pain is uncertain. Atrophy is less common but is associated with less severe shoulder pain.
Key Words: magnetic resonance imaging • rotator ruff • shoulder pain • tendonopathy
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Introduction |
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Approximately one third of all stroke survivors experience shoulder pain some time during their recovery.1 Poststroke shoulder pain negatively impacts daily activities1 and is related to poor quality of life.2 Clinicians use a wide variety of approaches to treat poststroke shoulder pain.3,4 However, the large number of interventions and a lack of consensus as to which are effective suggest that both the etiology and rationale for the treatment of poststroke shoulder pain are poorly understood.
Many different etiologies for poststroke shoulder pain are postulated and include adhesive capsulitis, bicipital tendonitis, complex regional pain syndrome, brachial plexopathy, altered sensation, spasticity, and rotator cuff disease.5 These clinical entities, however, are likely end products of a complex cascade of events initiated by the biomechanical compromise of the poststroke glenohumeral joint.6 Although arthrograms have been used to evaluate structural abnormalities in the painful poststroke shoulder,7–12 the results of these studies have been inconsistent. For example, the prevalence of rotator cuffs tears was reported to be zero in one study11 and 40% in another.7 Given these inconsistencies and the invasiveness of arthrograms, Turner-Stokes and Jackson wrote, "It should be noted that all these studies were undertaken using arthrography, before the era of MRI, and the question should now be readdressed in larger numbers, in the light of more advanced and less invasive technology"(p 286).5
This report represents the first MRI-based evaluation of structural abnormalities in painful hemiplegic shoulders. The primary objective was to describe the structural abnormalities of the painful hemiplegic shoulder among chronic stroke survivors exhibiting pain duration greater than 3 months. The second objective was to relate these findings to clinical characteristics.
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Methods |
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Participants
The study population consisted of stroke survivors who responded to a request for participation in a clinical trial of a minimally invasive intervention for the treatment of poststroke shoulder pain. The study required exclusion of patients with rotator cuff tears and thus, those individuals who passed initial screening for the clinical trial received MRI evaluations. Inclusion criteria for entering into the MRI evaluation phase included (1) abduction strength of the affected shoulder of
4/5 as measured by the Medical Research Council scale13; (2) stroke occurring 
3 months before study entry; (3) sustained shoulder pain duration 3 months; and (4) shoulder pain on the Brief Pain Inventory (BPI)14,15 (question 124). Exclusion criteria included (1) prestroke shoulder pain; (2) use of more than one nonopioid or opioid analgesics for shoulder pain; (3) analgesics for any other acute or chronic pain; (4) corticosteroid steroid injection to the hemiparetic shoulder in the previous 6 weeks; (5) outpatient or home therapies for shoulder pain; (6) hemineglect; (7) complex regional pain syndrome; (8) MRI-related contraindications (eg, claustrophobia, ferrous metal, implanted electronic devices); (9) medical instability; (10) impaired memory; and (11) inability to rank 3 levels of pain in correct order (falling and breaking both ankles followed by a stubbed toe followed by a mosquito bite).
Participant Characteristics
Specific characteristics collected at baseline by a nurse coordinator included age, gender, time from stroke onset to study entry, duration of poststroke shoulder pain, stroke type (hemorrhagic versus nonhemorrhagic), side of hemiparesis, and severity of shoulder pain. Shoulder pain was quantified with the BPI 12, which asks subjects to rate their worst shoulder pain in the last 7 days on an 11-point numeric ration scale of 0 to 10, where "0" indicates "no pain" and "10" indicates "pain as bad as you can imagine."14,15
Subjects were further characterized at baseline with respect to physical examination findings by physician investigators. Inferior glenohumeral subluxation was documented based on "fingerbreadths" relative to the unaffected shoulder.16 Motor status was documented based on the Medical Research Council scale.13 Specific muscles/muscle groups that were measured included the upper trapezius, shoulder abductors, elbow extensors, wrist extensors, finger flexors, and finger abductors. The summary score was defined as percent of maximum (sum of all grades/maximum sumx100). Light touch and pin prick sensations were assessed with the volar surface of the finger tip and a sharp safety pin, respectively.17 Specific test areas included the skin overlying the acromioclavicular joint, lateral epicondyle, and medial epicondyle and the finger pads of digits 1, 3, and 5. Sensation to light touch and pin prick were coded as "normal" or "abnormal."
MRI Assessment
All subjects underwent T1- and T2-weighted multiplanar, multisequence MRI of the affected shoulder at a mean of 13.2±9.4 (SD) days after the baseline clinical assessments. All scans were reviewed by one radiologist based on standard radiological criteria18 for the following abnormalities: rotator cuff, biceps and deltoid tears, tendinopathies and atrophy, subacromial bursa fluid, labral ligamentous complex abnormalities, and acromioclavicular capsular hypertrophy. Specific criteria were as follows. Full-thickness tear of the rotator cuff muscles was defined as a gap in the entire width of the muscle on both coronal and sagittal images. A partial-thickness tear was defined as abnormal signal on T2-weighted images involving the articular or bursal side of the tendon on both coronal and sagittal images. Tendinopathy was defined as thickening and abnormal signal on proton density images, but not on heavy T2-weighted images. A muscle was deemed to exhibit atrophy if there was evidence of fatty infiltrates. Bursal fluid was defined as increased intensity in the bursa on T2-weighted images. Labral ligamentous abnormality was defined as a tear of the anterior or posterior aspect of the labrum. Biceps tendon tear and tendinopathy were defined based on criteria noted previously for the rotator cuff.
Analysis
Descriptive statistics were generated to quantify the prevalence of specific structural abnormalities as defined previously. All MRI-based structural abnormalities were coded as either "absent" or "present." To explore the relationship between clinical features and specific structural abnormalities, a series of simple bivariate correlations was calculated. Correlations were calculated for a specific structural abnormality only if that abnormality was present in more than 10% cases. A clinical variable was considered a correlate if the correlation coefficient exhibited a probability value of <0.1. Specific MRI structural abnormalities with more than one clinical correlate were further analyzed using logistic regression (forward) to identify independent predictors of the structural abnormality. The specific MRI finding was entered as the dependent variable and clinical correlates as independent variables. To assess the appropriateness of the P<0.1 criterion for acceptance of a variable into the logistic regression models, a sensitivity analysis was performed with P<0.05 and <0.20. To facilitate interpretation, a select number of independent predictors was presented graphically with respect to structural abnormalities.
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Results |
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A total of 89 stroke survivors received MRI scan evaluations of their painful poststroke shoulder. The mean age was 57.8±11.0 years (SD), 67% were men, mean BPI 12 score was 7.1±1.9, mean time from stroke onset to study entry was 61.1±79.3 weeks, and the mean duration of pain was 53.4±7.5 weeks. Sixty-seven percent sustained nonhemorrhagic strokes. Sixty-five percent exhibited left hemiparesis. The mean motor score was 49±29%. The mean glenohumeral subluxation was 0.89±0.56 fingerbreadth relative to the nonhemiparetic side with 61% exhibiting at least
fingerbreadth of subluxation. Light touch and pin prick sensations were impaired in 51% and 53% of subjects, respectively. Table 1 shows the prevalence of rotator cuff tears. There was one case of a biceps tear and no case of deltoid tear. Thirty-one (35%) subjects exhibited a tear of at least one muscle. Fourteen (16%) subjects exhibited tears of multiple muscles. Table 2 shows the prevalence of rotator cuff, deltoid and biceps tendinopathy and atrophy. Fifty subjects (56%) exhibited tendinopathy of at least one muscle. Eighteen (20%) exhibited tendinopathy of multiple muscles. Twenty-four subjects (27%) exhibited atrophy of at least one muscle. All subjects who exhibited atrophy exhibited atrophy in multiple muscles. Labral ligamentous complex abnormality was seen in 9%, subacromial bursa fluid in 26%, and acromioclavicular capsular hypertrophy in 67%.
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Table 3 shows the specific MRI structural abnormalities, the significant clinical correlates based on bivariate correlations, and the independent predictors of the structural abnormality based on logistic regression. Supraspinatus tears were more common among older subjects (Figure 1) and among those with better motor function (Figure 2). Supraspinatus and infraspinatus tears were more common among those with more recent strokes (Figure 3). Atrophy of the rotator cuff, biceps, or deltoids was more common with more severe motor impairments (Figure 4), less severe shoulder pain (Figure 5), older subjects (Figure 6), and women (Figure 7). Subacromial bursa fluid was more common with increased motor strength.
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Sensitivity analysis revealed minimal effect of entry criterion probability value. When P0.20 was used, minor changes related to gender were noted. Gender became a significant predictor of subscapularis tendinopathy but was no longer a significant predictor of atrophy of the supraspinatus. The use of the stricter criterion of P0.05 led to the exclusion of 3 variables that were significant predictors based on the P0.10 criterion. Specifically, motor status with regard to supraspinatus tears and age and gender with regard to supraspinatus atrophy were excluded. With the minor exceptions noted previously, the results of the logistic regression were unaffected by the entry criterion.
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Discussion |
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Poststroke shoulder pain is common and significantly impacts rehabilitation outcomes. However, the exact etiology remains unknown. A description of the structural abnormalities of the painful poststroke shoulder is fundamental to elucidating its etiology. The present report constitutes the first MRI-based description of the painful shoulder among chronic stroke survivors. Stroke survivors with shoulder pain demonstrate high prevalence of tears, tendinopathy and atrophy of various muscles around the glenohumeral joint, subacromial fluid collection, and acromioclavicular capsular hypertrophy. However, with the exception of atrophy, these structural abnormalities were not related to the severity of shoulder pain.
Rotator cuff pathology has been postulated as an etiology of poststroke shoulder pain.5 In the present series, 34% of subjects exhibited a tear of at least one rotator cuff muscle. Most were partial tears and the supraspinatus was most commonly affected. The prevalence of 34% is consistent with the 40% and 30% reported by Najensen et al7 and Nepomuceno and Miller,8 respectively, but higher than the 0% to 20% reported by others.9–11,19 Differences in prevalence may be due to the differences in patient selection. Among studies that reported low prevalence rates, the 2 studies with the largest sample sizes included all stroke survivors regardless of pain, whereas the present study included only those with pain.10,19 The age-dependent increase in the prevalence of supraspinatus tears is consistent with the profile observed in the able-bodied asymptomatic population.20 Given that the reported prevalence of rotator cuff tears among older asymptomatic able-bodied persons range between 22%20 and 40%,21 it would be difficult to definitively demonstrate a causative relationship between rotator cuff tears and poststroke shoulder pain.
Subjects with more recent strokes were more likely to exhibit rotator cuff tears. It is possible that shoulder pain in these groups represents different etiologies with different natural history. If rotator cuff tear is the etiology of shoulder pain in the "tear" group, data suggest that this type of pain resolves in the long-term. These data further suggest that poststroke shoulder pain that persists well into the chronic phase of stroke recovery is less likely to be due to a rotator cuff tear. Subjects with greater motor function were more likely to exhibit rotator cuff tears. Greater motor function in this population is still abnormal motor function, which may place the rotator cuff at increased risk for impingement, other traumas, and eventual tears.
Fifty-three percent of subjects exhibited tendinopathy of at least one rotator cuff, biceps or deltoid muscle. Tendinopathy or tendinosis refers to intratendinous atrophy and degeneration of the tendon.22 Although the term "tendinitis" is often applied loosely to a variety of shoulder problems that lead to focal pain and tenderness, the histological findings in the involved tissue are more compatible with an ischemic or degenerative process than an inflammatory one.18 Thus, for the purpose of MRI assessment, the term tendinopathy is preferred. Like with tears, the supraspinatus was most commonly involved followed by infraspinatus and subscapularis. Because tendinopathy is likely a precursor to tears, this parallel is not entirely surprising.
The prevalence of tendinopathy in the stroke population has not been well documented. Joynt23 injected local anesthetic into the subacromial bursa of stroke survivors with shoulder pain. Fifty percent reported significant reduction in pain or improvement in pain-free range of motion. This would be consistent with the results of the present series. However, it is uncertain whether the response to local anesthetic injection means that the pain was due to supraspinatus tendinopathy, subacromial bursitis, or both. In the only large-scale ultrasound-based study of poststroke shoulder, Lee et al19 reported significantly higher prevalence of rotator cuff "tendinitis" in the paretic shoulder (17%) versus the nonparetic shoulder (0%). Although these studies suggest a relationship between tendinopathy and shoulder pain, the present study did not corroborate their findings.
The prevalence of atrophy was similar among muscles studied, ranging between 20% and 23%. The exceptions were somewhat lower prevalence for the teres minor and biceps at 14% each and 0% for the subscapularis. As one might anticipate, atrophy was most commonly associated with reduced motor strength. However, atrophy was also associated with less pain. One might anticipate that greater atrophy leads to greater mechanical instability and greater pain. However, it is possible that atrophic muscles are also less spastic. Spasticity and poststroke shoulder pain have been strongly associated24 and may represent a cause and effect relationship. This may also explain why subscapularis atrophy was not observed in our series. Many stroke survivors exhibit significant reduction in external rotation range of motion of the shoulder, which has also been associated with shoulder pain.12,25–27 Some have speculated that this is due to adhesive capsulitis.12,26 However, spasticity of the subscapularis is an alternate consideration. Braun et al28 postulated that spasticity causes pain by traction on the periosteum at the muscle insertion. Spasticity may also present a greater risk for development of impingement.5 If the "spasticity hypothesis" is correct, then rendering the subscapularis "atrophic" through neurolysis might reduce poststroke shoulder pain. Earlier experience with phenol neurolysis of the subscapularis29,30 and results of a recent small randomized clinical trial of botulinum toxin injection to the subscapularis lend credence to this hypothesis.31
Subacromial bursa fluid was seen in 26% of cases and was associated with greater motor strength. Stroke survivors with greater motor strength are more likely to use their hemiparetic upper limb and thus may be at increased risk for repetitive movement trauma, leading to supraspinatus impingement and subacromial bursitis. A large percent of subjects had acromioclavicular capsular hypertrophy. However, this was not related to any clinical variables.
Although the present series represents the first large-scale MRI assessment of the painful poststroke shoulder, the study has a number of limitations. First, control comparisons were not included. Scans of the unaffected shoulder may provide invaluable comparative data to facilitate assessment of causative relationships. Similarly, a comparison group of motor impairment matched stroke survivors without shoulder pain may be invaluable. A lack of a relationship between structural abnormalities and shoulder pain in the present study may be an artifact of all subjects having shoulder pain. A longitudinal analysis of stroke survivors at risk for developing shoulder pain may provide further insights into the structure–pain relationship governing poststroke shoulder pain. Second, the clinical variables were not comprehensive. The study did not include pain-free range of motion,25 a measure of spasticity,32 a valid and reliable measure of poststroke motor impairment,33 or other specific physical examination assessments for shoulder pain.34 The addition of these variables may provide greater insight regarding the relationship between structure and clinical manifestations. Third, there was a selection bias in the study sample. By necessity, not all stroke survivors with shoulder pain were included due to the constraints of the clinical trial and MRI restrictions. Because the included subjects do not represent a random sampling of all stroke survivors with shoulder pain, the study results may not be generalizable to the broader stroke population.
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Acknowledgments |
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Source of Funding
This work was supported by grants from NeuroControl Corporation, North Ridgeville, Ohio, the National Center for Research Resource (M01RR0080), and the National Institute of Child Health and Human Development (K24HD054600).
Disclosures
Data presented in this study were part of an investigational device clinical trial sponsored by NeuroControl Corporation. However, the content of this report is not related to the investigational device. The following authors received clinical trials support from NeuroControl Corporation: R.S., E.P.E., S.R.F., A.B., V.N., S.P., and J.C.. At the time of the study, Z.P.F. was an employee of NeuroControl Corporation. NeuroControl Corporation terminated all business as of June 2007 and the clinical trial was terminated.
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Footnotes |
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This work was presented in part at the 2007 Annual Meeting of the Association of Academic Physiatrists, San Juan, PR, April 2007.
Received August 20, 2007; revision received October 5, 2007; accepted October 31, 2007.
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