EFFECT OF SLEEPER STRETCH AND EXERCISE IN

GLENOHUMERAL INTERNAL ROTATION DEFICIT

BY

ASIYATH FIDA AFNAN K [ PT ]

Project submitted to the Rajiv Gandhi University of Health Sciences,

Bangalore, Karnataka

In partial fulfillment of the requirements for the degree of

BACHELOR OF PHYSIOTHERAPY

Under the guidance of

DR. RAKSHITH BANGERA K

ASSOCIATE PROFESSOR

KANACHUR COLLEGE OF PHYSIOTHERAPY

KANACHUR COLLEGE OF PHYSIOTHERAPY,MANGALORE,

KARNATAKA,575018

1
DECLARATION BY THE CANDIDATE

I hereby declare that this project work entitled, “EFFECTS OF SLEEPER

STRETCH AND EXERCISE IN GLENOHUMERAL INTERNAL
ROTATION DEFICIT” is a bonafide and genuine work carried out by me
under the guidance of DR.RAKSHITH BANGERA

DATE: SIGNATURE OF CANDIDATE

PLACE: NAME:ASIYATH FIDA AFNAN K

2
CERTIFICATE BY THE GUIDE

This is to certify that the project untitled, “EFFECTS OF SLEEPER

STRETCH AND EXERCISE IN GLENOHUMERAL INTERNAL
ROTATION DEFICITE” is a bonafied project work done by ASIYATH
FIDA AFNAN K in a partial fulfillment of the requirement of the degree of
BACHELOR OF PHYSIOTHERAPY.

SIGNATURE OF THE GUIDE

DATE: NAME : DR.RAKSHITH BANERA K

PLACE:

3
ENDORSEMENT BY THE PRINCIPAL OF THE INSTITUTION

This is to certify that the project work entitled, “EFFECTS OF

SLEEPER STRETCH AND EXERCISE IN GLENOHUMERAL
INTERNAL ROTATION DEFICITE” is a bonafied work done by
ASIYATH FIDA AFNAN K under the guidance of DR.
RAKSHITH BANGERA K, ASSOCIATE PROFESSOR, Kanachur
College of Physiotherapy.

SEAL AND SIGNATURE OF THE PRINCIPAL

NAME: DR.MOHAMMAD SUHAIL

DATE:

PLACE: MANGALORE

4
DECLARATION BY THE CANDIDATE

I, ASIYATH FIDA AFNAN K of KANACHUR COLLEGE OF

PHYSIOTHERAPY, hereby declare that the RAJIV GANDHI UNIVERSITY
OF HEALTH SCIENCES, KARNATAKA shall have the perpetual rights to
preserve, use, and disseminate this project work in print or electronic format for
academic/research purpose.

SIGNATURE OF CANDIDATE

DATE : NAME: ASIYATH FIDA AFNAN K

PLACE:

5
 ACKNOWLEDGEMENT

I thank the Almighty, my beloved husband mohammed jawad my beloved

parents my siblings and my loved ones who have been the foundation source of
the strength and inspiration. It gives an immense pleasure in expressing my
most profound sincere gratitude and indebtedness to my learned guide DR.
RAKSHITH BANGERA K, ASSOCIATE PROFESSOR -KANACHUR
COLLEGE OF PHYSIOTHERAPY for all guidance, able supervision and
invaluable suggestions throughout thetexture of this project.

My sincere thanks to all my lecturers of Kanachur College of Physiotherapy for

providing me all the help and facilities required for conducting this project. My
thanks to all my colleagues for helping and supporting me, each in their own
special waythroughout the course of my studies. I wish to convey my special
thanks to my responsible teacher DR MOHAMMAD SUHAIL,DEAN,
KANACHUR COLLEGE OF PHYSIOTHERAPY, MANGALORE, for the
meticulous guidance, encouragement and support..

Last but not the least, I thank all my classmates for being there with me and
supporting me

6
SL.NO TITLES PAGE

1 INTRODUCTION 8

2 DEFINITION 9-11

3 CINICAL RELEVENT 11-13

ANATOMY
4 EPIDEMILOGY 14

5 ETIOLOGY 14-16

6 CLINICAL PRESENTATION 17-18

7 DIFFERENTIAL DIAGNOSIS 18-19

8 DIAGNOSTIC PROCEDURE 20-24

9 PATHOLOGY 25-29

10 MANAGEMENT 30-38

11 REVIEW OF LITRATURE 39-42

12 REFERENCE 43-46

7
1.INTRODUCTION

Glenohumeral internal rotation deficit (GIRD) is a term used in the literature to

describe the physiological adaptation that occurs in the dominant arm of the
overhead-throwing athlete. The meaning of this term and the clinical
significance and the rationale for its treatment have all been described with
some ambiguity within the literature. GIRD as a measurement is multivariate.
There is an adaptive bony component in humeral retroversion (HR) and
muscular contributions in the form of thixotropy which can confound the
capsular component of GIRD. Emerging diagnostic tools such as ultrasound can
help differentiate between the bony and soft tissue contributions as well as
provide a dynamic assessment in the throwing shoulder. The purpose of this
review is to describe and differentiate between anatomical GIRD (aGIRD) and
pathological GIRD (pGIRD), discuss the clinical significance of pGIRD and
values reported within the literature, and describe its measurement and clinical
treatment.

8
 2.DEFNITION

Gelnohumeral internal rotation deficit is defined as a loss of internal rotation

when the posterior structures of the glenohumeral joint are shortened this may
compromise the hammock function of the inferior glenohumeral ligament
[ IGHL] and increase the risk of impingement symptoms during throwing.

However, not all GIRD is pathological and decreased IR [compared to non-

throwing shoulder] can exist without concomitant shoulder pathology when
total rotational motion [TRM] of the shoulder is symmetric.[1]

This is partly due to increased retatosion [decreased ante version] of the

humerus, which shifts the are of motion more posteriorly [external].

Pathological GIRD in contrast, exists when there is a loss of TRM > 5̊

compared to the contralateral shoulder. This 5̊ change has been associated with
decreased shoulder strength and increased injury rates in baseball players.

9
Definitions for common terminology used in the diagnosis and treatment of
GIRD[2]

Term Definition
GIRD (glenohumeral Loss of internal rotation (IR) of ≥20° or greater
internal rotation compared to contralateral shoulder
deficit)
TRM (total rotational Summation of internal and external rotation (ER)
shoulder motion) measured at 90° of shoulder abduction; should not
exceed 187°
Internal impingement Contact between the greater tuberosity of the humerus
and the posterior superior glenoid rim leading to
impingement of the posterosuperior labrum and
articular side of the rotator cuff
External impingement Contact between and greater tuberosity of the humerus
and the acromion leading to impingement on the bursal
side of rotator cuff
SLAP (superior Tear of superior labrum from anterior to posterior
labrum, anterior to
posterior)
ABER (abduction and Position of the shoulder in the cocking phase of
ER) throwing where shoulder abduction is ≥90° and ER can
achieve up to 160°
IGHL (inferior Capsular thickening that provides restraint to
glenohumeral translation of the humeral head; anterior band prevents
ligament) posterior translation in ABER and posterior band
prevents anterior translation
PASTA (partial Articular-sided partial-thickness tear of the posterior

10
Term Definition
articular-sided supraspinatus tendon caused by internal impingement
supraspinatus tear) of the greater tuberosity on the posterior labrum.
3.CLINICALLY RELEVENT ANATOMY

The scapula is a flat blade lying along the thoracic wall. Because of the wide
and thin configuration, it’s possible for the scapula to glide smoothly on the
thoracic wall and provides a large surface area for muscle attachments, both
distally and proximally.

The coracoacromial arch and the subacromial elements are important elements
of anatomy related to GIRD. As the name implies, the coracoacromial arch is
formed by the coracoid and the acromion processes and the connecting
coracoacromial ligaments. It protects the humeral head and subacromial
structures from direct trauma and superior dislocation of the humeral head.
Impingement may occur when the rotator cuff and other subacromial structures
become encroached between the greater tuberosity and the coracoacromial arch.

The tendons of the rotator cuff are:

• Subscapular is tendon (anterior)

• Supraspinatus tendon (superior)

• Infraspinatus tendon (posterior)

• Teres minor tendon (posterior)

11
12
is located on the articular side of the rotator cuff, typically at the
intersection of the infraspinatus and supraspinatus insertions onto the
humeral head.

The scapulothoracic articulation is a prime example of the dynamic stability

of the human body. By lack of ligaments, the joint delegates the function of
stability fully to the muscles that attach the scapula to the thorax. So their
proper function is essential to the normal biomechanics of the shoulder.

These muscles include:

 Serratus anterior
 Trapezius
 Levator scapula
 Rhomboid major
 Rhomboid minor
 Latissimus dorsi
 Pectoralis major and minor
 Supraspinatus and Infraspinatus

The serratus anterior and the trapezius has been suggested to be the most
important muscles acting upon the scapulothoracic articulation. [3]

13
4.EPIDEMIOLOGY

The incidence of internal impingement is unknown due to the variety of

associated pathologic lesions and diagnostic difficulty. ]The majority of
patients who have been identified as having internal impingement are
overhead athletes or throwing athletes (tennis, volleyball players, swimmers,
or baseball players). These patients participate in activities requiring
repetitive external rotation and (hyper) abduction. The majority of the
research on internal impingement has been done on elite baseball players.
However, non-elite athletes, as well as non-athletes may also be affected by
internal impingement. With the non-elite athletic population, it is important
to realize that older patients are more likely to have concurrent shoulder
conditions. Since internal impingement is often involved with other
pathology of the shoulder the incidence of it in isolation has not been
established.[4]

5.ETIOLOGY

PATHOPHYSIOLOGY

The leading pathologic process in GIRD is posterior capsular and rotator-cuff

tightness, due to the repetitive cocking that occurs with the overhead throwing
motion. Achieving increased ER in the maximally abducted position is thought
to help increase throwing velocity. During pitching, biomechanical studies have
shown shoulder ER can exceed 160°, IR acceleration can exceed 6,000°/second,
and IR torque can exceed 60 N/these kinematic extremes place a high amount of
stress on the static and dynamic stabilizers of the shoulder, including the rotator
cuff, joint capsule, and labrum. With each pitch, these structures are loaded to
levels that approach their ultimate load to failure, making them extremely
vulnerable to injury. Although a single traumatic event can lead to a shoulder

14
injury, more commonly it is repetitive overuse that leads to numerous
pathologic conditions, including posterior labral tears, partial articular-sided
posterosuperior rotator-cuff tears, and superior labral anterior-to-posterior
(SLAP) tears. In addition to shoulder pathology, patients also display scapular
dyskinesia and are predisposed to ulnar collateral ligament (UCL) tears at the
elbow.[5]

The throwing motion is an extremely complex process in which remarkable

velocities and extreme forces are repetitively generated. Mobility and stability
are often directly at odds with each other, leading to the idea of the “thrower’s
paradox” coined by Wilk et al. While throwers may not complain of frank
instability, they do have a component of pathologic laxity or micro instability
that predisposes them to injury.

15
 PATHOANATOMY

 tightening of posterior capsule or posteroinferior capsule leads to translation of

humeral head (capsular constraint mechanism)
 translation of humeral head is in the OPPOSITE direction from area of capsular
tightening
 posterior capsular tightness leads to anterosuperior translation of humeral head
in flexion
 posterorinferior capsular tightness leads to posterosuperior translation of
humeral head in ABER
 anterior capsule is stretched[6]

16
6.CLINICAL PRESENTATION

The diagnosis of GIRD based on history alone is extremely difficult, and

symptoms tend to be variable and fairly nonspecific.GIRD patients present
with any of the following:

 Posterior Shoulder Pain

o Chronic - diffuse posterior shoulder girdle pain is the chief

complaint in the throwing athletes with internal impingement,
but the pain may also be localised to the joint line. The patient
may describe the onset of posterior shoulder pain, particularly
during the late-cocking phase of throwing, when the arm is in
90° of abduction and full external rotation.
o Acute - non-throwing athletes, who present with this syndrome,
have a chief complaint of acute shoulder pain following an
injury

 Decrease in throwing velocity - a progressive decrease in throwing

velocity or loss of control and performance in the overhead athlete.
 Dead arm - Some signs of the pathologic process include a so-called
“dead arm,” the feeling of shoulder and arm weakness after throwing,
and a subjective sense of slipping of the shoulder
 Muscular Asymmetry - Overhead athletes and throwers in particular
often have muscular asymmetry between the dominant and the non-
dominant shoulder. [7]

17
  Muscular/Neuromuscular Imbalance – A common finding is muscle
imbalances in the shoulder complex as well as improper
neuromuscular control of the scapula.

 Increased Laxity - A patient with isolated internal impingement may

have an increase in global laxity or an increase in anterior laxity alone
of the dominant shoulder.
 Anterior Instability - Patients may have instability symptoms, such as
apprehension or the sensation of subluxation with the arm in a position
of abduction and external rotation
 Rotator Cuff Pathology - Patients may also present with symptoms
similar to those associated with other rotator cuff pathologies (tears,
other impingements). Younger patients with such symptoms,
particularly throwing athletes, should raise the clinician’s index of
suspicion for internal impingement. In fact, some authors have
identified internal impingement as the leading cause of rotator cuff
lesions in athletes.
 .A combination of internal derangement-popping, clicking, catching,
sliding.
 Rotator cuff weakness Rotator cuff is a common name for the group
of 4 distinct muscles (infraspinatus, supraspinatus, teres minor and
subscapularis) and their tendons that provide strength and stability
during motion of the shoulder. The four rotator cuff muscles may
separately provide a disturbed muscle balance [8]

7.DIFFRENTIAL DIAGNOSIS

18
It is important to understand that the common findings for GIRD have been
found in asymptomatic shoulders so it is key to evaluate the patient's entire
clinical scenario. The patient's age, profession, activity level, symptom
severity, degree of disability and the effects of this condition on their athletic
performance need to be part of the clinician's decision-making process. When
examination findings are somewhat unremarkable, and when the patient
presents with signs of numerous pathologies, yet do not seem to fit any one
pathology exclusively, this should raise the clinician's suspicion for a case of
internal impingement. During the diagnostic process it is helpful to understand
that GIRD has a similar presentation to numerous pathologic shoulder
conditions, including but not limited to:[9]

 Partial- or full-thickness rotator cuff tears

 Anterior or posterior capsular pathologies
 SLAP (Superior Labrum Anterior to Posterior) lesion
 Subacromial Impingement
 Glenoid chondral erosion
 Chondromalacia of the posterosuperior humeral head
 Anterior GH instability
 Biceps tendon lesion
 Scapular Dysfunction
 Each of these disorders can exist alone or as a concomitant pathological
condition.

19
8.DIAGNOSTIC PROCEDURE:

In athletes with pathologic GIRD, shoulder stiffness, the need for a prolonged
warm-up, and loss of velocity (dead arm) are often the initial complaints. Pain is
often aspecific, localizing to the posterior shoulder, and the late cocking
position is often provocative. Palpation of the posterior joint line and
surrounding soft tissue can reproduce pain. Due to the high prevalence of GIRD
in overhead throwers, a high index of suspicion is necessary for any throwing
athlete who presents with shoulder symptoms. Therefore, all throwers with
shoulder pain must be assessed for passive IR and TRM of the shoulder. The
authors’ preferred method to assess loss of IR of the shoulder is to have the
patient lie supine on the examination table. The examiner can then bring both
arms into 90° of shoulder abduction and 90° of elbow flexion. Maximum
passive ER and IR are then assessed in the throwing shoulder compared to the
contra-lateral extremity, and differences can be measured using a goniometer .
Importantly, maximum passive IR is defined as the point just before the scapula
begins to lift from the examining surface. Although the exact definition is
debated, a difference of 20° or more when compared to the contralateral side is
generally considered diagnostic of GIRD. The sum of maximum ER and IR
equals the TRM of the shoulder. In most overhead-throwing athletes, TRM
should be symmetric bilaterally. This method is preferred to measuring IR by
assessing the vertebral level that can be reached when rotating the arm up the
back, because it has been shown to have greater reliability and is not affected by
scapulothoracic or elbow motion.[10]

20
21
Posterior-shoulder tightness can be assessed as described by Tyler et al. This is
performed by having the subject lie in the lateral decubitus position with the
throwing shoulder up. With the shoulder in 90° of abduction and neutral
rotation (scapula stabilized), the arm is maximally adducted (lowered toward
the floor). The distance that the medial epicondyle of the humerus travels in
centimeters is recorded. Posterior-shoulder tightness is then calculated as the
difference between the throwing and nonthrowing shoulders. Every 1 cm loss of
adduction correlates with an ~ 5° loss of IR. Therefore, a 4 cm deficit would
equate to a 20° loss of IR and a diagnosis of GIRD. Myers et al confirmed this
in a series of throwers, showing the average amount of posterior-shoulder
tightness was 4.2 cm in subjects with internal impingement compared to 0.9 cm
in subjects throwers without impingement. To assess internal impingement in a
throwing athlete with GIRD further, Meister et al developed a test termed
“posterior impingement sign” to look for posterosuperior labral tears and partial
articular-sided supraspinatus tear (PASTA) lesions. The shoulder is brought into
maximum passive abduction and ER (late cocking). The presence of deep
posterior-shoulder pain is considered positive.[11]

In addition to posterior-shoulder tightness, approximately two-thirds of pitchers

with GIRD display a sulcus sign on exam. This is thought to be due to laxity of
the rotator interval structures (coracohumeral and superior GH ligament), due to
repetitive cocking while throwing. Another classic pathologic finding in the
examination of the throwing athlete includes so-called SICK scapula, which
consists of scapular malposition, inferior medial border prominence, coracoid
pain and malposition, and dyskinesis of scapular movement. Static position of
the scapula is best assessed from behind, and it is often helpful to draw the bony
prominences bilaterally for comparison. Active motion can then be assessed by
having the patient perform maximum forward elevation, and any dyskinesia can

22
be detected. Finally, all throwers with shoulder pain in our clinic are evaluated
for active and passive motion in all planes (forward flexion, extension,
abduction, cross-body adduction), manual muscle-strength testing of the rotator
cuff, impingement findings (Hawkins–Neer testing), SL and bicep pathology
(active compression and Speed’s test), and instability (apprehension, load and
shift, and jerk testing). Specifically, for throwers with painful shoulders,
evaluation of the entire kinetic chain of throwing is performed by a team of
trained physical therapists and includes assessments of core strength and hip
mechanics.

IMAGING

Radiography can be nondiagnostic in athletes with GIRD. We routinely

obtain a standard shoulder series (AP, Grashey, axillary, and scapular
Y) in patients who present to our clinic with a new complaint of
shoulder pain. Occasionally, a posterior glenoid osteophyte (Bennett’s
lesion) can be seen on axillary radiography and sclerosis of the
posterior glenoid rim seen on computed tomography. MRI is the
modality of choice for the diagnosis of GIRD to rule out any
concomitant pathology. The MRI features of posterior glenoid internal
impingement have been described, and include supraspinatus and
anterior infraspinatus partial undersurface tears, bony cystic changes
at the posterosuperior humeral head, glenoid chondral wear, and
labral pathology, including posterior SL tears and type II SLAP
tears.Superoposterior subluxation of the humeral head and thickened
appearance of the posterior band of the IGHL can also be seen. MR
arthrography (MRA) of the shoulder offers increased sensitivity for
the detection of articular-surface partial-thickness rotator-cuff tears
23
and SLAP lesions over conventional MRI. Additionally, MRA
performed in the abduction and external rotation (ABER) position
allows the posterosuperior rotator cuff to relax, permitting better
visualization of a rotator-cuff tear Placing the shoulder in ABER puts
the biceps anchor on tension, allowing for visualization of otherwise
nondisplaced SLAP tears. For these reasons, MRA in the ABER position
should be considered in all symptomatic overhead athletes.[12]

24
8.PATHOLOGY

Although GIRD in isolation is not a pathologic process, throwers with GIRD

often present to the clinic due to the development of shoulder pathology. The
pathologic process in throwing shoulders with GIRD can be divided into intra-
articular shoulder pathology (labrum, joint capsule, articular-sided rotator cuff),
extra-articular shoulder pathology (bursal-sided rotator cuff, acromion), and
pathology of the throwing kinetic chain (lower extremity, core, scapula, and
elbow). We discuss each in detail.[13]

Posterior-shoulder tightness and humeral retrotorsion

Traditionally, the major pathologic process in GIRD was thought to be

contracture of the posterior GH-joint capsule and the posterior band of the
IGHL.2,16,42–45 In high-level throwers, the posterior capsule was found to be
thicker in the dominant shoulder compared to the contralateral extremity.46
Experimentally, posterior capsular plication has replicated the biomechanical
changes that occur in the throwing shoulder.47 Following simulated
posteroinferior capsular tightness (with resultant GIRD), GH contact pressure
and rotator-cuff impingement significantly increases. Additionally, with as little
as 5% GIRD, translational changes in the humeral head occur, including
increased superior displacement of the humeral head in maximum abduction
and ER (ABER).16,43 These shifts in humeral head center of rotation have
implications for injury, due to altered joint kinematics.3 Interestingly, more
recent data have shown that posterior rotator-cuff tightness, not just capsular
contracture, may contribute to GIRD.48 This idea is also supported by studies
showing GIRD can change as much as 15% after a single throwing

25
exposure,49,50 making the loss of IR too rapid for capsular contracture alone.
Therefore, the terminology of posterior-shoulder tightness to include all soft
tissue (capsule and cuff) has been proposed as a better descriptor of the
pathology that occurs.[14]

Although the adaptive changes seen in GIRD were historically thought to affect
only soft tissue, studies have shown bony changes, including increased humeral
retrotorsion (decreased anteversion) in collegiate and professional baseball
pitchers. A recent study showed professional baseball pitchers displayed
significantly greater humeral retrotorsion in their dominant arm compared with
those without GIRD. Pitchers also displayed a greater side-to-side difference in
humeral torsion. In youth and high school pitchers, age-related increases in
GIRD were correlated with increased humeral retrotorsion, not soft-tissue
changes. Bony changes to the scapula also occur in the dominant arm, with
significantly increased glenoid retroversion seen in baseball players compared
to controls.[15] Interestingly, many authors believe increased bony adaptation is
protective to the soft-tissue stabilizers of the shoulder the idea being increased
ER gain through bony changes protects the shoulder from excess stress on the
anterior capsuloligamentous structures.

Rotator-cuff pathology

Tears of the rotator cuff are common in the throwing athlete, and MRI of the
dominant shoulder in asymptomatic throwers shows cuff tears in up to 40%.In
this population, failure of the rotator cuff is multifactorial, caused by
supraphysiological strain, defects in the kinetic chain (notably the scapula), and
26
anterior insability.[16] Rotator-cuff pathology in patients with GIRD can be
separated into two categories: acute traumatic tears due to overload during
deceleration (minority of tears), and partial- or full-thickness degenerative tears
due to impingement (internal > external). The degenerative fraying on the
articular side of the rotator cuff that is seen in throwers was first described in
the first half of the twentieth century12 and better defined at the time of
arthroscopy by Andrews et al and Walch et al. The etiology of articular-sided
tears is thought to be caused by a tight posterior capsule, leading to internal
impingement, repetitive microtrauma, and shear stress on under-surface fibers,
which have limited intrinsic repair potential.58 Importantly, the shoulder
capsule maintains a broad insertion on greater tuberosity; therefore, by
definition any articular-sided partial-thickness rotator-cuff tears must involve
compromise of the superior capsule and subsequently permit increased GH
translation and shoulder laxity.[17]

Although much of the focus on GIRD centers around the cocking phase of
throwing (Figure 1), biomechanical studies have shown that enormous forces
are placed upon the shoulder stabilizers during ball release. During arm
deceleration, posterior sheer force can reach 400 N and compression of the
humeral head against the glenoid can exceed 1,000 N.19 For this reason, the
instant just before ball release has been defined as a critical phase of throwing.
After ball release, extreme force and torque is placed upon the rotator cuff as
the arm decelerates, which can result in tensile failure and an acute traumatic
rupture.

27
Labral pathology

The hallmark lesion of GIRD and internal impingement is a posterosuperior

labral tear. Impingement of the greater tuberosity against the glenoid rim during
late cocking causes lesions to the posterosuperior labrum and articular side of
the supraspinatus tendon. Although this can be a normal physiological
occurrence in maximum ABER, the biomechanics of repetitive throwing
intensify this contact. In addition to posterior labral tears, subjects with GIRD
develop SLAP tears. Andrews et al and Snyder et al pioneered our
understanding of these tears in throwing athletes. Although the function of the
superior labrum is still debated, most agree it is important for concavity
compression of the shoulder as well as an attachment site for soft-tissue
stabilizers. The mechanism of SLAP tears in overhead athletes is thought to be
multifactorial, but most authors agree the “peel back” that occurs during
ABER65 contributes to SLAP pathology. During the throwing motion, superior
migration of the humeral head can increase the stress on the superior labrum
and bicep anchor. Kinematic studies have shown that during the cocking phase
of throwing, superior shear forces can exceed 250 N.Additionally, bicep
contraction in a lengthened position places tensile stress on the bicep anchor,
which may lead to SL tears. Some authors argue that SLAP lesions are adaptive
and allow for supraphysiological ER, as the biceps anchor is a stabilizer in the
late-cocking position.

Kinetic chain

28
As described by Burkhart et al in the kinetic chain of throwing, the legs and
trunk generate force, the shoulder regulates and funnels force, and the arm
delivers force to the ball.15 Approximately half of the kinetic energy generated
during throwing is transferred to the arm through the scapulothoracic joint,
making the scapula crucial in the kinetic chain for throwing.15 A SICK scapula
can lead to altered kinematics in the GH and acromioclavicular joints, leading to
anterior-shoulder pain, coracoid tenderness, acromioclavicular-joint pain with
overhead activities, and decreased range of motion, specifically forward
flexion.15 Another aspect of the kinetic chain that can be injured in overhead
throwing with GIRD is the elbow. Many studies have shown a correlation
between GIRD and injuries to the elbow UCL in throwers.22,55,66 Increasing
the amount of ER increases the valgus load seen at the elbow in the cocking
phase. However, a recent study showed there was no significant difference in
mean dominant-arm humeral retrotorsion between pitchers with previous UCL
reconstructions compared to uninjured controls.67 Therefore, it may be
decreased TRM, and not just GIRD, that predisposes pitchers to UCL injuries.

29
9.MANAGEMENT:

MEDICAL MANAGEMENT

Rest from throwing and physical therapy for 6 months.

Medical management will hinge on the specifics of the patient presentation

including the mechanism of injury , severity, patient goals, etc.In some cases,
particularly those with a traumatic mechanism, surgical intervention may be
warranted to restore joint stability.

Conservative management of internal impingement is an appropriate initial

approach, particularly in patients who do not report an acute traumatic event
We can divide the medical management in non-surgical treatment and
surgical treatment.
Non-surgical treatment [18]

Interventions that are recommended in the literature in early disease when

the shoulder is stiff and can be poorly localized are:

 Rest
 Ice (cryotherapy)
 NSAID’s (or other oral-anti-inflammatory meds)
 Corticosteroid injection

All these interventions will be used in addition to a structured, supervised

physical therapy regimen

30
SURGICAL MANAGEMENT

Surgery for internal impingement may be indicated if improvements have

not been seen with a prolonged rehab protocol specifically designed to
correct any impairments, imbalances, deficiencies and/or pathologic
findings.[19]

Indications ;

1. Failed nonoperative treatment

2. Partial thickness rotator cuff tear (PASTA-Partial articular
supraspinatus tendon avulsion) compromises the integrity of the
rotator cuff
3. Partial rotator cuff tears >50%
4. Bennett lesion
5. Peel-back labral lesion
6. SLAP lesion
7. Dislocation

For the surgical treatment, we have different approaches:

 Arthroscopic interventions -It is the preferred type of surgery. Prior to

any surgical procedure, it is highly recommended that a thorough
exam under anesthesia (EUA) is done, as well as a diagnostic
arthroscopy. Due to the often-confusing physical findings that may be
associated with internal impingement, the final therapeutic surgical
plan should be aimed at specific pathologic lesions related to patient
symptoms that have been identified from an EUA and diagnostic
arthroscopy. It’s recommended that the EUA specifically assess for

31
 GH ROM, any kind of subluxation, as well as a meticulous analysis
for the presence of any instability.

 Posteroinferior capsule release

 Anterior stabilization

some advocate posterior capsule release while others advocate anterior

stabilization

repair thinned rotator cuff if significantly thinned (transcuff or takedown and

repair)

technique controversial

for throwing athlete with posteroinferior capsular contracture, release posterior

inferior capsule and posterior band of IGHL

electrocautery inserted through posterior portal, camera from anterior portal

from 9 to 6 o'clock position

at level of glenoid rim

until rotator cuff fibers (behind the capsule) can be seen from within joint

insert arthroscopic shaver to widen gap in capsule (prevents recurrence)

gentle manipulation at the end completes release of any remaining fibers,

maximizes IR and flexion

results

will immediately gain 65° of internal rotation postop

32
PHYSIOTHERAPY

PREVENTION/EARLY MANAGEMENT

If an overhead athlete report feelings of tightness, stiffness, or not loosening

up, the pitcher should be removed from participation and started in a rehab
program. It is important, before treatment is undertaken, to rule out other
anterior instability pathology, including SLAP lesions, labral tears, and
partial rotator cuff tears.

Strengthening the shoulder:

 Closed kinetic chain exercises for stabilizing the rotator cuff muscles.
 Strengthening program for posterior capsule
 Muscle imbalance and/or improper neuromuscular control of the
shoulder complex
 Strengthening periscapular musculature and the rotator cuff muscles to
prevent over-angulation in the late cocking phase of throwing.

Stretching the shoulder

 Sleeper stretch

Several stretching techniques have been described and are purported

to provide stretching or mobilization of the posteroinferior soft tissue
structures. One such method that has gained interest recently has
been called the “sleeper stretch”.To perform the sleeper stretch the
patient is placed in the side lying position with the weight of the body
stabilizing the scapula against the table. The shoulder and elbow are
flexed to 90°. A passive IR moment is applied at the wrist of the
involved upper extremity via the opposite extremity. This
33
stretch/mobilization can be done at both 90° and at 45°of
glenohumeral joint elevation. When the sleeper stretch is performed
at 90° with IR, it has the potential to iatrogenically impinge the
shoulder. The roll‐over sleeper stretch is similar to the standard
sleeper stretch except that the shoulder is only flexed to 45° and the
patient rolls forward (placing the glenohumeral joint in a more
horizontal adducted position) to approximately 30–40° from vertical
side lying . The authors feel that in many athletes the roll over sleeper
stretch may be too aggressive of a technique and can create pain, and
should be used with caution. The modified sleeper stretch (30° of
scaption) has been demonstrated with cadaveric models to produce
the best stretch on the posterior capsule. [20]This is the position
recommended by the authors of this commentary since it better
isolates the posterior shoulder and decreases risk of impingement due
to 45° position rather than standard sleeper at 90°. A recent second
modification of the sleeper stretch that the authors would like to
introduce is performed with the patient sideling and the glenohumeral
joint at 90° of abduction. Instead of staying directly in side lying
(vertical body position) the patient performs a quarter turn toward
their back‐placing their glenohumeral joint in the scapular plane and .
This has been observed clinically to reduce glenohumeral joint
impingement complaints.

34
35
 Cross body stretch
Another popular stretch is the cross‐body stretch. In this stretch the
shoulder is elevated to approximately 90° of flexion and then pulled
across the body into horizontal adduction with the opposite arm. This
stretching method has been criticized in the past due to its inability to
selectively stretch the posterior capsule. Clinicians believe that
scapulothoracic tissues may also be stretched with this technique,
although no biomechanical studies or tissue strain studies have been
performed to prove or disprove this theory. If stretching the posterior soft
tissues (rather than posterior capsule) is indicated, then this stretch may
be one to consider. The horizontal adduction stretch with scapular
stabilization described by Wilk et al is a stretching technique that appears
to selectively stretch the posterior structures of the glenohumeral
joint. The patient lies supine while the clinician stabilizes the patient’s
scapula with one hand and imparts a horizontal adduction moment to the
humerus with the other hand. Because the clinician is stabilizing the
scapula, less tissue stretch should be imparted to the posterior scapular
muscles, and more to the posterior cuff muscles.

36
Each of these stretching techniques should be held for approximately 30
seconds, in younger athletes, which has been determined to be the optimal time
frame for stretching musculoskeletal structures. [20]Prior to attempting to throw, a
dynamic form of stretching may be more appropriate as research has indicated
that static stretching results in decreased muscle strength and performance
acutely.

 Joint mobilizations (mobs)

GH anterior-posterior joint mobs can be used to help stretch the posterior

capsule and increase internal rotation; however, if instability is noted on the
initial exam, joint mobs should be avoided. Grade IV, end range, dorsal-
glide mobilizations are performed with the patient supine with shoulder
placed into 90 abduction, and either in neutral or end range internal rotation
of the humerus (refer to pictures).

 Thoracic and cardiothoracic manipulation

Spinal manipulations can be used to improve mobility in these regions and

have proven therapeutic short and long term effects. Several studies have
shown a significant improvement in symptoms of shoulder impingement
syndrome when a thoracic manipulation was combined with exercise. The
benefits of a thoracic or cardiothoracic manipulation for internal
impingement have yet to be studied, but based on the similar presentation of
these two syndromes and the low-risk to benefit ratio of manipulation, these
procedures may add a huge benefit to treatment.

37
  Whole body kinetic chain exercise

Incorporating this early in rehab has been recommended in order to prepare

the athlete's whole body for return to activity. Core stability, leg balance,
and diagonal movement patterns can be used to incorporate the entire kinetic
chain while simultaneously involving the shoulder as well. One example of
this is simply adding a degree of instability to an exercise; doing external
rotation exercises while sitting on an exercise ball or while performing a
single leg stance by standing on the opposite leg of the arm you are
working..

38
10. REVIEW OF LITRATURE
1.Robert A Keller , Anthony F De Giacomo , Julie A Neumann conducted a
study on Glenohumeral Internal Rotation Deficit and Risk of Upper Extremity
Injury in Overhead Athletes they concluded that The pooled results of this
systematic review and meta-analysis did not reach statistical significance for
any shoulder motion measurement and its correlation to shoulder or elbow
injury. Results, though not reaching significance, favored injury in overhead
athletes with GIRD, as well as rotational loss and external rotational gain. [21]

2.Mohsen Moradi , Malihe Hadadnezhad , Amir Letafatkar conducted a study

on Efficacy of throwing exercise with TheraBand in male volleyball players
with shoulder internal rotation deficit they concluded that Throwing exercise
with a TheraBand improved shoulder muscle activation, IR ROM, rotator cuff
muscle strength ratio and GH joint position sense in participants with GIRD.
These findings may improve the treatment of GIRD in a clinical setting.
Although the results are significant, further studies should follow up the long-
term effects of the Throwing exercise with a TheraBand on GIRD[22].

3. Ann M ,Amir Letafatkar conducted a study on prevention of shoulder injury

in overhead athetes they concluded that shoulder is at high risk for injury during
overhead sports which can be prevented by designing preventative training
programe.[23]

39
4.Omar Gharisia 1, Everett Lohman 1, Noha Daher conducted a study on Effect
of a novel stretching technique on shoulder range of motion in overhead athletes
with glenohumeral internal rotation deficits they cncuded that Both stretches
appear to be effective at improving IR ROM in overhead athletes with GIRD.
However, the novel stretching might be more effective at reducing shoulder
pain and thus may be more appropriate for symptomatic patients.[24]

5.Kyle Gouveia 1, Jeffrey Kay 2, Muzammil Memon they conducted a study on

Glenohumeral Internal Rotation Deficit in the Adolescent Overhead Athlete: A
Systematic Review and Meta-Analysis they concluded that The adolescent
overhead athlete has roughly 10° of IR deficit in their dominant arm,
accompanied by nearly 7° of ER gain, with similar ROM measurements for
injured and uninjured athletes. Those with pathological GIRD have a greater
degree of IR deficit, but without an accompanying compensatory increase in
ER, leading to a TROM deficit of nearly 15°. Surgical treatment in the absence
of other indications is rare, whereas physiotherapy and sleeper stretches remain
the first-line treatment[25]
.

6. Ahmed Mohammed Alqarni 1, Shibili Nuhmani 1, Qassim Ibrahim Muaidi

conducted a study on Glenohumeral internal rotation deficit in volleyball
players with and without a history of shoulder pain they concuded that There
was no correlation between the level of pain and the presented ROM
adaptations. The study showed that for volleyball players, pathological GIRD
should be defined at 10-18⁰ degrees of GIRD that are accompanied by
differences in the TROM that exceeds 8⁰.[26]

40
7. Ralf J Doyscher 1 2, Leopold Rühl 1, Benjamin Czichy conducted a study on
Bilateral glenohumeral internal rotation deficit (GIRD) in elite gymnasts they
concluded that A new bilateral form of GIRD was identified in higher age
groups of youth and senior elite gymnasts enrolled in this study. Despite to
former definition of GIRD there was no compensatory increase in external
rotation range of motion (ERRM) but an association with posterior capsular
thickening, while there was no periscapular muscle hypertrophy. Humeral
retrotorsion was also slightly increased in the gymnasts group.[27]

8. Andri Mt Lubis 1 2, Rizky P Wisnubaroto 1 2, Ermita I Ilyas conducted a

study on Glenohumeral internal rotation deficit in non-pitcher overhead athletic
athletes: case series analysis of ten athletes they concuded that Glenohumeral
internal rotation deficit could be present in non-pitcher overhead athletics
athletes.[28]

9. Kota Tanaka 1, Hiroki Funasaki 2, Yusuke Murayama they conducted a study

on Age-related differences in glenohumeral internal rotation deficit, humeral
retrotorsion angle, and posterior shoulder tightness in baseball players they
concuded that The difference in HTA between the dominant and nondominant
sides increased with age until 16 years old regardless of symptoms. STE in the
dominant side was observed only in symptomatic baseball players after the age
of 13 years and increased with age, plateauing around the age of 16 years.
Posterior shoulder muscle elasticity was not indicated as a cause of STE. [29]

41
10. Hyung Jun Park 1, Jin Ho Jeon 1, Dae Keun Suh conducted a study on
Correlation of glenohumeral internal rotation deficit with shear wave ultrasound
elastography findings for the posterior inferior shoulder capsule in college
baseball players they concuded that The SW velocity is closely associated with
posterior shoulder capsular tightness and may be of quantitative value in
baseball players.[30]

42
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