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Journal of Back and Musculoskeletal Rehabilitation -1 (2018) 1–5
DOI 10.3233/BMR-171037
IOS Press

Case Report

Atypical calcific tendinitis involving the long
biceps tendon: A rare cause of hemiplegic
shoulder pain
Jang Hyuk Choa,∗ , Sung Hwa Jungb , Shi Mo Yanga and Hyun Parka
Department of Rehabilitation Medicine, Daegu Veterans Health Service Medical Center, Daegu, Korea
Department of Radiology, Daegu Veterans Health Service Medical Center, Daegu, Korea

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Abstract.
BACKGROUND AND OBJECTIVE: Calcific tendinitis is commonly found in the rotator cuff; however, it is very rare in the
long biceps tendon (LBT). Furthermore, calcific tendinitis involving the LBT in the hemiplegic shoulder after a stroke has not
been previously reported.
MATERIALS AND METHOD: We present a case of a 63-year-old man who suffers from a stroke and atypical calcific tendinitis involving the LBT as a rare cause of hemiplegic shoulder pain. The patient had experienced intractable pain in the right
hemiplegic shoulder for more than 6 months with a waxing and waning course. Marked tenderness to palpation was present at
the biceps tendon adjacent to the bicipital groove. Ultrasound (US) and computed tomography revealed a long, blade-shaped,
circumscribed, cloudy and irregular dense calcific deposit in the LBT site, distal to the bicipital groove. The patient underwent
US-guided corticosteroid injection at the posterior intra-articular joint. The symptoms failed to resolve; we injected an additional corticosteroid into the biceps tendon sheath adjacent to the calcific deposit. This procedure provided satisfactory relief, and
follow-up US revealed mild diminution of the calcification through absorption.
CONCLUSION: This is the first report on atypical calcific tendinitis involving the LBT causing hemiplegic shoulder pain after
a stroke.

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Keywords: Calcific tendinitis, long biceps tendon, hemiplegic shoulder pain

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1. Introduction
Calcific tendinitis is a common disease affecting
the rotator cuff. The pathogenesis remains ambiguous;
some theories, such as degeneration, a cell-mediated
process within the less vascular area of the tendon, and
tendon overuse, have been proposed [1,2]. It mainly
affects the supraspinatus tendon; it affects the other

∗ Corresponding author: Jang Hyuk Cho, Department of Rehabili-

tation Medicine, Daegu Veterans Health Service Medical Center, 60,
Wolgok-ro, Dalseo-gu, Daegu, 42835, Korea. Tel.: +82 53 630 7191;
Fax: +82 53 630 7849; E-mail: jacob.chojh@gmail.com.

three tendons of the rotator cuff less frequently, and
seldomly the long biceps tendon (LBT) [3,4].
In patients with a stroke, weakness of the affected
shoulder girdle muscles results in hemiplegic shoulder pain and soft tissue injury, wherein the LBT involvement is often observed [5–9]. Hemiplegic shoulder pain can interfere not only with functional activities, but also motor recovery; thus, the appropriate
treatment route is decided as early as possible [5].
To the best of our knowledge, calcific deposition in
the LBT resulting in hemiplegic shoulder pain after a
stroke has not been previously reported. In this article,
we present a patient with atypical calcific tendinitis in-

ISSN 1053-8127/18/$35.00 c 2018 – IOS Press and the authors. All rights reserved

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2. Case report

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A 63-year-old man with a known right sided weakness after left thalamic infarction in 2004 gradually
experienced right shoulder pain over 6 months. No
trauma had occurred. He could move his right upper
limb through a partial range of motion against gravity,
and was graded as 2+ on a manual muscle test. Additionally, he had a markedly increased muscle tone of
his right upper limb throughout the range of motion,
and a spasticity grade of 2 according to the Modified
Ashworth Scale.
The shoulder pain progressively aggravated with a
waxing and waning course despite supportive physical
therapy and use of oral medications. He subsequently
experienced motion limitation and night pain, which
aggravated over time and made it impossible to sleep
at night. Subjective pain on the Visual Analogue Scale
(VAS) was 7 at rest and 9 during motion.
On physical examination, the skin over the anterolateral aspect of the shoulder joint was normal, and gentle palpation around the shoulder joint intensified the
tenderness to an intolerable degree of pain at the biceps tendon adjacent to the bicipital groove. Subluxation of the glenohumeral joint was examined by palpating the subacromial regions of both shoulders; the
palpated space between the acromion and the humeral
head of the right hemiplegic shoulder was wider than
the left shoulder by one-half finger width or more.
All laboratory results were within normal limits.
Plain radiographs demonstrated glenohumeral subluxation with displacement of the humeral head relative
to the glenoid fossa (Fig. 1). Ultrasound (US) revealed
a long, blade-shaped, circumscribed, cloudy and irregular dense calcific deposit in the LBT that measured
18 mm (long axis) with effusion of the tendon sheath
(Fig. 2A). To ensure an accurate diagnosis, he underwent computed tomography (CT) and magnetic resonance imaging (MRI). CT confirmed the presence of
a calcific deposit in the LBT site distal to the bicipital groove (Fig. 3), while MRI showed tendinosis of
the supraspinatus tendon without calcification. The radiologic records of the plain radiographs, US, CT and
MRI were reviewed for the presence of structural abnormalities in the painful shoulder.
On the basis of these findings, US-guided intraarticular corticosteroid injection was performed by

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volving the LBT as a rare cause of hemiplegic shoulder
pain.

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J.H. Cho et al. / Atypical calcific tendinitis involving the LBT

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Fig. 1. Plain radiographic anteroposterior view of the right (A) hemiplegic shoulder with subluxation shows the humeral head located
at the level of the inferior margin of the glenoid, while the left (B)
shoulder is normal.

penetrating the posterior joint capsule. A fluid mixture
composed of 0.5% lidocaine and 40 mg triamcinolone
was injected into the shoulder joint space by visualizing the posterior intra-articular space and the LBT [10].
After intra-articular injection, the night pain slightly
improved, but the patient complained of motion limitation with pain. His pain score on the VAS was 6 at
rest and 7 during motion. Compared with the scores on
his first visit, his pain score on the VAS slightly decreased from 7 to 6 at rest and from 9 to 7 during motion. Four weeks after the procedure was performed,
follow-up US revealed a similarly sized calcification
(Fig. 2B). The symptoms failed to resolve, although
they were abated; therefore, we injected additional corticosteroid into the biceps tendon sheath adjacent to the
calcific deposit. If the patient had intolerable pain after the injection, we planned US-guided barbotage targeted at the calcific deposit or surgical removal. Upon

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J.H. Cho et al. / Atypical calcific tendinitis involving the LBT

Fig. 2. Axial (A) and coronal (B) computed tomography scans
demonstrate a long calcification in the LBT site distal to the bicipital
groove. The arrows indicate the calcific deposit.
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re-evaluation two weeks after the additional injection,
the patient was satisfied with the pain relief after corticosteroid injection into the tendon sheath. His pain
score on the VAS was then 1 at rest and 2 during motion, and the tenderness at the biceps tendon adjacent
to the bicipital groove had disappeared. Two weeks after an additional injection was given, follow-up US revealed mild diminution by absorption in the previously
noted calcific deposit (Fig. 2C). The patient had no
complaints about pain or limited range of shoulder motion; thus, he did not require barbotage procedure or
surgical removal.

Fig. 3. Ultrasonography at the time of diagnosis through the long
axis of the biceps tendon reveals a blade-shaped, calcific deposit in
the LBT site distal to the bicipital groove with effusion of the tendon
sheath (A). Follow-up US 4 weeks after corticosteroid injection at
the posterior intra-articular joint shows a similar sized and dense calcification remaining (B). Two weeks after additional injection into
the biceps tendon sheath, follow-up US demonstrates mild diminution by absorption in the previously noted calcific deposit (C). The
arrows indicate the calcific deposit.

3. Discussion
This case report is noteworthy as it describes, in detail, the clinical manifestation of atypical calcific tendinitis involving the LBT site distal to the bicipital
groove. To the best of our knowledge, it is the first report of a pathology causing hemiplegic shoulder pain
after a stroke.

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motion impairment. To our knowledge, these injury
mechanisms in the hemiplegic shoulder remain unclear. The gravitational pull on the unsupported upper
limbs may lead to traction injuries, and increased muscle tone associated with spasticity may produce shortening of periarticular soft tissues [6]. In our case, the
patient had some conditions inciting hemiplegic shoulder pain such as glenohumeral subluxation, shoulder
girdle muscle weakness, and spasticity.
The widely accepted function of the LBT may be to
centre the humeral head in the glenoid fossa and reduce vertical translations. Likewise, this muscle probably plays a main role not only in glenohumeral joint
stabilization, but also in the elbow flexion spasticity associated with traction forces [6,8]. Clinically the most
common finding in hemiplegic shoulder pain is biceps
tendon tenderness, which suggests that the LBT is often involved [8]. The most common structural changes
on US in the hemiplegic shoulder were pathologies involving the LBT such as effusion, tenosynovitis, tendinitis, and tear [6,9].
In this case, our patient’s hemiplegic shoulder pain
was due to calcific tendinitis based on US and CT findings that revealed a calcific deposit in his LBT. Other
evidence to support this diagnosis was noticeable tenderness on palpation at biceps tendon adjacent to the
bicipital groove. There were also risk factors for hemiplegic shoulder pain present such as glenohumeral subluxation, weakness, and spasticity; these factors might
be conditions provoking the LBT injury. Excessive and
cumulative microtraumatic stresses at the LBT are associated with hemiplegic shoulder, which might have
caused localized injury within the tendon, and less vascular areas of the tendon resulting in calcific tendinitis.
Considering that the patient’s shoulder pain failed
to resolve after conventional intra-articular corticosteroid injection, we assume that the injection site in
the posterior joint capsule is distant from the site
of calcification; therefore, the infused corticosteroid
might not play a significant role due to effusion. The
glenohumeral joint cavity communicates with the LBT
sheath; therefore, copious effusion of the glenohumeral
joint may induce an increase of the effusion within the
tendon sheath [18]. To achieve an immediate effect of
availability, local administration of corticosteroid into
the LBT sheath adjacent to the calcification may be
more prudent. However, the patient described in this
report was only followed up for 2 months and longterm follow-up until complete diminution via absorption was not performed. This is a limitation of the current case report.

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Calcific tendinitis is a common disease with characteristic clinical and radiological findings. It is considered to be a self-healing condition that undergoes
spontaneous resolution and, in most cases, it can be
successfully treated non-operatively. The pathogenesis of calcific tendinitis has yet to be clarified; however, different theories have been proposed. Theories
for the degenerative aetiology have been suggested in
the past; Uhthoff and Loehr described a cell-mediated
process within the less vascular area of the tendon,
which is widely accepted [1,2]. According to recent reports, tendon overuse and excessive mechanical stimulation may be initial factors in the occurrence of calcification [2,11].
Calcific deposit in the shoulder is most often identified at the insertion of the supraspinatus tendon on the
greater tuberosity, or less frequently in the other three
tendons of the rotator cuff [3]. Although seldom affected, calcific tendinitis can also involve the LBT [4].
The LBT has two sites vulnerable to calcific tendinitis:
adjacent to its origin on the superior glenoid labrum
at the biceps-labial complex, and within the tendon
sheath at or site distal to the bicipital groove [4,12].
In our review of the English literature, a few reports
are available on calcific tendinitis involving the LBT
at its origin on the superior glenoid labrum [3,11–14].
The present authors found an acceptable past report involving in LBT at its origin or site distal to the bicipital groove; however, the authors identified calcific tendinitis by plain radiographs only [4]. Unlike this case,
we strived to examine the calcific deposit site distal to
the bicipital groove using US, CT, and MRI. The appearance of calcification was a long, blade-shaped, circumscribed, cloudy and irregular dense; compatible to
type II of the radiologic classification by Gartner and
Heyer [15] and Gartner and Simons [16].
Hemiplegic shoulder pain is a common problem in
patients with stroke. It results in limited shoulder motion because of the intolerance to active or passive
range of motion, and is thus associated with poorer motor recovery and functional performance. Risk factors
for pain include glenohumeral subluxation, range of
motion limitation, spasticity, flaccidity, poor arm motor
function, impaired sensation, and soft tissue injuries
of the shoulder joint [6,8]. Glenohumeral subluxation
refers to the static displacement of the humeral head
relative to the glenoid fossa; additionally, shoulder girdle muscle weakness has been suggested as the major
cause of this subluxation [5,7,17]. The ensuing weakness of the shoulder girdle muscles may result in damage to the protective structures that prevent shoulder

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In this report, we present the case of a patient who
experienced severe hemiplegic shoulder pain caused
by calcific tendinitis in the LBT site distal to the bicipital groove and was managed with US-guided corticosteroid injection. Repetitive microtraumatic stresses
at the LBT are associated with hemiplegic shoulder,
which might have caused localized tendon damage, deterioration of blood circulation, and calcific tendinitis
in the LBT. We believe that calcific tendinitis of the
LBT should also be considered in the differential diagnosis of hemiplegic shoulder pain. In addition, future
studies should standardize a detailed treatment protocol.

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Acknowledgments

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[2]

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References

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No potential conflict of interest relevant to this article was reported.

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Conflict of interest

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Uhthoff HK, Loehr JW. Calcific tendinopathy of the rotator
cuff: Pathogenesis, diagnosis, and management. J Am Acad
Orthop Surg. 1997; 5(4): 183-91.
Suzuki K, Potts A, Anakwenze O, Singh A. Calcific tendinitis
of the rotator cuff: Management options. J Am Acad Orthop
Surg. 2014; 22(11): 707-17.
Ji JH, Shafi M, Kim WY. Calcific tendinitis of the bicepslabral complex: A rare cause of acute shoulder pain. Acta Orthop Belg. 2008; 74(3): 401-4.
Goldman AB. Calcific tendinitis of the long head of the biceps brachii distal to the glenohumeral joint: Plain film radiographic findings. AJR Am J Roentgenol. 1989; 153(5): 10116.

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The authors would like to thank Tae Gyeong Son
for assistance in preparing the figures, and Editage
(www.editage.co.kr) for English language editing.

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[11]

Park GY, Kim JM, Sohn SI, Shin IH, Lee MY. Ultrasonographic measurement of shoulder subluxation in patients with
post-stroke hemiplegia. J Rehabil Med. 2007; 39(7): 526-30.
Pong YP, Wang LY, Huang YC, Leong CP, Liaw MY, Chen
HY. Sonography and physical findings in stroke patients with
hemiplegic shoulders: A longitudinal study. J Rehabil Med.
2012; 44(7): 553-7.
Vasudevan JM, Browne BJ. Hemiplegic shoulder pain: An approach to diagnosis and management. Phys Med Rehabil Clin
N Am. 2014; 25(2): 411-37.
Dromerick AW, Edwards DF, Kumar A. Hemiplegic shoulder pain syndrome: Frequency and characteristics during inpatient stroke rehabilitation. Arch Phys Med Rehabil. 2008;
89(8): 1589-93.
Idowu BM, Ayoola OO, Adetiloye VA, Komolafe MA. Sonographic evaluation of structural changes in post-stroke hemiplegic shoulders. Pol J Radiol. 2017; 82: 141-8.
Chung SG, Lee KJ, Kim HC, Seo KS, Lee YT. Intra-articular
pressure profiles of painful stiff shoulders compared with
those of other conditions. PM R. 2009; 1(4): 297-307.
Xue XH, Feng ZH, Li ZX, Pan XY. Calcifying tendinitis of
the long head of the biceps brachii and superior labrum: a
report of one case and literature review. J Sports Med Phys
Fitness. 2018; 58(7-8): 1090-5.
Kim KC, Rhee KJ, Shin HD, Kim YM. A SLAP lesion associated with calcific tendinitis of the long head of the biceps
brachii at its origin. Knee Surg Sports Traumatol Arthrosc.
2007; 15(12): 1478-81.
Lecoq B, Levasseur R, Fournier L, Schmutz G, Marcelli C.
Atypical pattern of acute severe shoulder pain: Contribution
of sonography. Joint Bone Spine. 2004; 71(6): 592-4.
Cho NS, Rhee YG. Calcification in superior glenoid labrum
of the shoulder: A case report. J Shoulder Elbow Surg. 2007;
16(6): e35-7.
Gartner J, Heyer A. Calcific tendinitis of the shoulder. Orthopade. 1995; 24(3): 284-302.
Gartner J, Simons B. Analysis of calcific deposits in calcifying tendinitis. Clin Orthop Relat Res. 1990; (254): 111-20.
Prato N, Banderali A, Neumaier CE, Dahmane M, Martinoli
C, Derchi LE. Calcific tendinitis of the rotator cuff as a cause
of drooping shoulder. Skeletal Radiol. 2003; 32(2): 82-5.
Park I, Lee HJ, Kim SE, Bae SH, Lee KY, Park KS, et al.
Evaluation of the effusion within biceps long head tendon
sheath using ultrasonography. Clin Orthop Surg. 2015; 7(3):
351-8.

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[14]

[15]
[16]
[17]

[18]

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