33 Impingement Syndrome
Michael D. Rosenthal, PT, DSc, SCS, ECS, ATC, CSCS  |  Josef H.
Moore, PT, PhD  |  Joseph R. Lynch, MD
IMPINGEMENT SYNDROME
The clinical diagnosis of “impingement syndrome” was intro-
duced in 1972 by Dr. Charles Neer II and comprised a spec-
trum of disease ranging from chronic bursitis and partial tears
of the supraspinatus tendon to complete tears (Neer 1972).
It was hypothesized that the rotator cuff underwent progres-
sive pathologic change due to compression against a rough
undersurface of the coracoacromial arch made up of the ante-
rior third of the acromion, the coracoacromial ligament, and
the AC joint (Fig. 33.1). Since Neer’s original report, greater
understanding of the shoulder has led to further growth in the
diagnosis and treatment of this clinical syndrome that we now
understand to represent a continuum of rotator cuff pathology
(Neer 1983).
Impingement syndrome—or more accurately rotator cuff
pathology—can produce shoulder pain, weakness, and referred
pain or paresthesias into the region of the deltoid insertion and
upper lateral arm. A thorough examination of the upper extrem-
ity and axial spine is necessary to rule out other pathology that
can produce similar symptoms or co-exist with impingement
syndrome. The role of proximal segments (i.e., trunk and hips)
should also be considered and assessed in the comprehensive
evaluation of the patient with impingement syndrome. When
impingement syndrome is suspected it is important to dif-
ferentiate between the possible types of rotator cuff pathol-
ogy: primary subacromial (coracoacromial arch), secondary
subacromial (coracoacromial arch), and internal (Hayworth
2009). The majority of impingement syndrome cases are attrib-
uted to either primary or secondary (Bigliani 1997). Accurate
diagnosis is necessary to guide the most appropriate course of
management.
Rotator cuff impingement, regardless of the type, alters mus-
cular function of the cuff and results in diminished dynamic
control of the glenohumeral (GH) joint (Michener 2003). Until
optimal strength and neuromuscular control are established,
continued use of the arm at or above the level of the shoulder
will produce further impingement of the rotator cuff (Manske
2013). If cuff impingement is not recognized and corrected early
the problem can progress to degradation of tissue and resultant
tears in the rotator cuff. The Neer classification is still widely
used and described in Box 33.1.
Primary Impingement
Primary subacromial impingement is the result of an abnormal
mechanical relationship between the rotator cuff and the cora-
coacromial arch (acromion, coracoacromial ligament, and/or
coracoid process) (Bigliani 1997, Cavallo 1998). It also includes
other “primary” factors that can lead to narrowing of the sub-
acromial outlet (Table 33.1). Patients with primary impingement
210
are usually older than 35 years and complain of anterolateral
shoulder and upper lateral arm pain, with an inability to sleep
on the affected side. They have complaints of shoulder weak-
ness, which may be due to pain inhibition or true cuff pathol-
ogy, and difficulty performing activities at or above the level
of the shoulder. Physical examination should include pos-
tural assessment of the thoracic region, scapula, and GH joint
because faulty posture is thought to contribute to a diminished
subacromial outlet space (Kibler 1998, Lewis 2005). Range of
motion (ROM) assessment often demonstrates limitations and
pain with forward elevation (flexion or abduction) and hori-
zontal adduction. Evaluation of rotator cuff strength with the
patient’s arm at his or her side is often normal, whereas testing
performed in positions of shoulder elevation more consistently
reproduces symptoms of pain and weakness. The Hawkin’s sign,
Neer impingement sign, empty can sign (Jobe’s test), pain-
ful arc, external and internal rotation resistance strength tests
are often positive, and the clinician should assess for localized
symptom reproduction while recognizing that these tests can
elicit symptoms when other shoulder pathology exists as well
(Cavallo 1998, Diercks 2014, Michener 2009, Tennent 2003,
Zaslav 2001). The Neer impingement test, performed by inject-
ing 10 ml of 1% lidocaine (Xylocaine) into the subacromial
space, can be useful in diagnosing impingement (Neer 1983,
Tennent 2003). Meticulous palpation of the GH joint, acro-
mioclavicular joint (AC), and coracoid region can also assist in
determining the source of the patient’s symptoms. Patients with
primary impingement may have associated AC joint arthritis
or a history of an AC joint sprain, which may ultimately con-
tribute to pathologic compression of the rotator cuff. Patients
often report discomfort in the anterior subacromial region
and AC joint region with internal rotation maneuvers, such as
scratching their back, or experience pain superiorly with shoul-
der abduction. Findings on physical examination that confirm
AC joint pathology include localized tenderness at the AC joint
with palpation, symptom reproduction (localized to the AC
joint) with cross-body adduction, reproduction of pain with
O’Brien’s test (resisted elevation with the arm forward elevated
90 degrees, internally rotated, and horizontally adducted), and
resolution of the pain with an injection of lidocaine into the
AC joint. Radiologic evaluation including an anteroposterior,
axillary, and supraspinatus outlet views may support the diag-
nosis of primary or “outlet” impingement by demonstrating
bony abnormality contributing to narrowing of the subacromial
space from acromial morphology, spurring, or hypertrophy of
the AC joint (Balke 2013, Cavallo 1998) (Fig. 33.2). 
Secondary Impingement
Secondary impingement is a clinical phenomenon that
results in a “relative narrowing” of the subacromial space.

Acromion
Arch
CA ligament
Fig. 33.1  The normal coracoacromial (CA) arch. (From F.W. Jobe, Ed:
Operative Techniques in Upper Extremity Sports Injuries. St. Louis, Mos-
by, 1996.)
BOX 33.1  (NEER’S) PROGRESSIVE STAGES OF
SHOULDER (PRIMARY) IMPINGEMENT
STAGE 1: EDEMA AND INFLAMMATION
Typical age: Younger than 25 yr but may occur at any age.
Clinical course: Reversible lesion.
Physical signs:
• Tenderness to palpation over the greater tuberosity of the
humerus.
• Tenderness along anterior ridge or acromion.
• Painful arc of abduction between 60 and 120 degrees,
increased with resistance at 90 degrees.
• Positive impingement sign.
• Shoulder ROM may be restricted with significant subacro-
mial inflammation. 
STAGE 2: FIBROSIS AND TENDINITIS
Typical age: 25–40 yr.
Clinical course: Not reversible by modification of activity.
Physical signs: Stage 1 signs plus the following:
• Greater degree of soft tissue crepitus may be felt because
of scarring in the subacromial space.
• Catching sensation with lowering of arm at approximately
100 degrees.
• Limitation of active and passive ROM. 
STAGE 3: BONE SPURS AND TENDON RUPTURES
Typical age: Greater than 40 yr.
Clinical course: Not reversible.
Physical signs: Stages 1 and 2 signs plus the following:
• Limitation of ROM, more pronounced with active motion.
• Atrophy of infraspinatus.
• Weakness of shoulder abduction and external rotation.
• Biceps tendon involvement.
• AC joint tenderness.
This often results from excessive GH joint mobility or scapu-
lar dyskinesis (Kibler 1998, Kibler 2013) (Fig. 33.3). In those
patients who have underlying GH hypermobility, with or
without instability, the symptoms of secondary rotator cuff
impingement are caused by excessive demands placed on
the rotator cuff to dynamically stabilize the shoulder. While
the rotator cuff may effectively stabilize the hypermobile
33  Impingement Syndrome 211
TABLE Structural Factors That May Increase
33.1 Subacromial Joint Impingement
Structure Abnormal Characteristics
Acromioclavicular Congenital anomaly
joint Degenerative spur formation
Acromion Unfused acromion (Os acromiale)
Coracoid Degenerative spurs on undersurface
Rotator cuff Malunion/nonunion of fracture
Humerus Congenital anomaly
Congenital Abnormal shape after surgery or trauma
Thickening of tendon from calcific
deposits
Tendon thickening after surgery or
trauma
Upper surface irregularities from partial
or complete tears
Increased prominence of greater
tuberosity from
anomalies or malunions
Modified from Matsen FA III, Arntz CT: Subacromial Impingement. In
Rockwood CA Jr, Matsen FA III (eds): The Shoulder. Philadelphia, WB
Saunders, 1990.
GH joint, when this requirement is coupled with repetitive
overhead movement (i.e., swimming or throwing) muscular
fatigue is often produced. Rotator cuff fatigue leads to the
loss of the stabilizing function and allows superior migration
of the humeral head (decreased depression of the humeral
head during throwing and less “clearance”) and is thought
to result in mechanical compression of the rotator cuff on
the coracoacromial arch (Chen 1999, Michener 2003, Royer
2009) (Fig. 33.4).
In patients with scapular dyskinesis (limited or exces-
sive scapular mobility), impingement results from improper
positioning of the scapula with relation to the humerus.
This loss of neuromuscular scapular control produces insuf-
ficient retraction along with inadequate upward rotation and
posterior tilting of the scapula resulting in earlier abutment
of the acromion and coracoacromial arch on the underly-
ing rotator cuff (Kibler 1998, Kibler 2013, Ludewig 2009,
Michener 2003).
Patients with secondary impingement are usually younger
and often participate in overhead sporting activities such as
baseball, swimming, volleyball, tennis, or weight lifting. Pain
and weakness with overhead motions are a common com-
plaint and they may even describe a feeling of the arm going
“dead.” Physical examination should include observation of
postural or soft tissue asymmetries about the shoulder girdle,
ROM symmetry, strength testing of the rotator cuff and scapu-
lar stabilizing muscles, and special provocative tests such as
Hawkin’s test and Neer’s sign. Furthermore, assessment of
spinal mobility restrictions, primarily in the cervical and/or
thoracic spine, should be assessed based on their potential role
in impacting scapulothoracic and GH joint mobility (Kabae-
tse 1999, Ludewig 1996). Regional interdependence has been
shown to influence shoulder symptoms and outcomes (Berg-
man 2004). The examiner should look for possible associ-
ated pathology, including GH joint instability, with a positive
apprehension and relocation test or abnormal scapular func-
tion such as scapular winging or asymmetrical motion. Gleno-
humeral joint hyperlaxity, without instability, can be further
assessed by the sulcus and Gagey hyperabduction tests. The
scapular retraction and scapular assistance tests can effectively
212 SECTION 3  Shoulder Injuries

Type I Type II Type III

Fig. 33.2  Different acromion morphologies. (From F.W. Jobe, Ed: Operative Techniques in Upper Extremity Sports Injuries. St. Louis, Mosby, 1996.)

Scapulothoracic Rotor cuff

muscle weakness weakness or
or fatigue fatigue

Overload of
passive
restraints

Functional
scapulothoracic
instability

Glenohumeral
instability
A B
Fig. 33.4  The supraspinatus tendon (rotator cuff) helps to stabilize the
Disruption of head of the humerus against the upward pull of the deltoid. A, Subacro-
scapulohumeral mial impingement is prevented by the normal cuff rotator function. B,
rhythm Deep surface tearing of the supraspinatus tendon weakens the ability of
the cuff to hold the humeral head down (i.e., depress the humeral head
Relative subacromial to allow clearance under the acromion) resulting in impingement of the
space narrowing tendon at the acromion with overhead activities. (A and B, Redrawn
from Matsen FA III, Arntz CT: Subacromial impingement. In Rockwood
CA Jr, Matsen FA III, Eds.: The Shoulder. Philadelphia, WB Saunders,
1990, p. 624.)

Secondary subacromial impingment

Fig. 33.3  Development of secondary impingement.

demonstrate the impact of altered scapular neuromuscular
control as a source of the patient’s symptoms and indicate the
potential for improved shoulder function by correcting this
deficiency (Burkhart 2003, Tate 2008). Patients with tight-
ness in the posterior shoulder will have a loss of internal
rotation. Posterior capsular tightness leads to an obligate
anterosuperior translation of the humeral head and resul-
tant diminished subacromial outlet space, which is thought
to contribute to the impingement problem (Burkhart 2003,
Tyler 2000).
In patients with secondary impingement, treatment of the
underlying problem should result in resolution of the “second-
ary impingement” symptoms. Clinicians should be aware of the
potential for proximal kinetic chain deficits (i.e., lumbo-pelvic-
hip complex) to contribute to secondary impingement (Kibler
1998, McMullen 2000). Often, recognition of the underlying
GH joint laxity or scapular instability is missed, and the “sec-
ondary impingement” is incorrectly treated as a “primary”
impingement. A subacromial decompression may worsen
the symptoms because the shoulder is rendered even more
“unstable” and does not address the primary mechanical
problem. 

Internal Impingement
Posterior shoulder pain produced by contact of the greater
tuberosity with the posterosuperior aspect of the glenoid, when
the shoulder is abducted to approximately 90 degrees and fully
externally rotated, produces impingement of the posterior rota-
tor cuff, capsule, and labrum (Gold 2007, Walch 1992). While
this “internal impingement” is present in normal physiologic
motion it may become pathologic with repetitive overhead activ-
ities. The pathology consists of undersurface tears of the poste-
rior supraspinatus and/or anterior aspect of the infraspinatus
tendon and often includes superior labrum anterior to posterior
(SLAP) tears (Heyworth 2009). There is debate regarding causa-
tion of this syndrome (Heyworth 2009, Manske 2013). Anterior
instability and inadequate neuromuscular control, enabling cuff
tendon entrapment with the glenoid during excessive anterior
humeral head translation, is one proposed mechanism (Cavallo
1998). Another reported mechanism is tightness within the
posterior GH joint, restricting normal GH rotation and produc-
ing a posterosuperior shift in the GH contact point creating the
pathologic “peel-back mechanism” (Burkhart 2003).
Patients with pathologic internal impingement are usually
under 35 years of age and involved in repetitive overhead abduc-
tion and external rotation demand activities. Patient complaints
often include posterior shoulder pain (specifically in the late
cocking position), stiffness, and decreasing performance (i.e.,
loss of throwing velocity or control) (Manske 2013). Physical
examination should focus on localized symptom reproduction
with special tests, posterior GH joint palpation, and ROM. Pos-
terior impingement signs and Jobe’s relocation test, with specific
resolution of posterior GH joint pain, are recommended (Meister
2004). Increased external rotation and decreased internal rotation
are common in patients with internal impingement (Morrison
2000, Myers 2006, Tyler 2010, Tyler 2000). Concurrent shoul-
der pathology often exists in the presence of pathologic internal
impingement so a thorough shoulder examination is important
to ascertain the possibility of co-existing conditions.  2003). Anterior GH joint stretching should not be performed
TREATMENT
The key to the successful treatment of subacromial impinge-
ment is defining the underlying cause, whether it is primary
or secondary to the pathologic relationship between the
coraco­acromial arch and the rotator cuff or due to internal
impingement. Identification of the true cause is critical when
conservative management fails and surgical intervention is
indicated, because the operative procedures are different for
these clinical entities. For primary impingement, surgical
treatment is directed toward addressing primary rotator cuff
pathology such as bursitis, partial thickness or full thickness
cuff tears, and abrasive or prominent surfaces of the underly-
ing acromion and acromioclavicular joint. The surgical treat-
ment for secondary impingement and internal impingement
must address the primary mechanical abnormality, which is
often not the rotator cuff or undersurface of the acromion
but rather is a problem with shoulder hypermobility. For
example, if impingement symptoms develop secondary to mul-
tidirectional instability, the surgical treatment is a stabiliza-
tion surgery, not an acromioplasty. Performing a rotator cuff
procedure or acromioplasty in the setting of GH instability will
not cure the shoulder problem and may serve only to make the
underlying condition worse.
33  Impingement Syndrome 213
Nonoperative Treatment
Nonoperative treatment is frequently successful and involves
a combination of treatment modalities including anti-inflam-
matory medications and a well-organized rehabilitation pro-
gram (Box 33.2). While comprehensive rehabilitation for both
primary and secondary impingement syndrome is similar, opti-
mal outcomes are most likely to be attained with an individu-
alized program that addresses patient-specific impairments as
opposed to applying a general protocol (Bang 2000). The initial
goals of the rehabilitative process are to obtain pain relief, regain
motion, and promote scapulothoracic and rotator cuff neuro-
muscular control (Manski 2013). Along with oral medications,
use of a subacromial injection with a corticosteroid may help to
control the discomfort in the acute stages of the inflammatory
process (Diercks 2014, Krabak 2003). Modalities such as heat
and cryotherapy, while lacking in supporting research evidence,
are often utilized for pain management. Research does not sup-
port the use of ultrasound or electrical stimulation, although
still commonly applied, for enhancing outcomes. Improving
comfort may promote more successful advances in motion and
strengthening.
Because the rotator cuff tendons are intact, ROM exer-
cises can be passive, active-assisted, and active. Initially, these
are done within the patient’s available pain-free range, usu-
ally below 90 degrees of abduction, to avoid reproduction of
impingement symptoms. As symptoms improve, the ROM
is increased. During the performance of ROM exercises it is
important to ensure quality of shoulder girdle motion and
avoidance of compensatory shoulder shrugging. ROM and
stretching exercises should be performed at least daily (Kuhn
2009). Selection of stretching exercises should be based on
postural impairments and movement limitations. Pectoralis
minor stretching is important for both primary and second-
ary impingement to allow posterior tilting of the scapula and
to improve subacromial outlet space (Borstad 2005, Burkhart
in patients with secondary impingement. If a GH joint internal
rotation deficit (GIRD) is identified, posterior capsular stretch-
ing should be initiated. Cross-chest (horizontal adduction)
and “sleeper” stretches have been shown to restore normal pos-
terior GH joint mobility (Tyler 2010). Scapular stabilization
while performing these exercises is key to selectively stretching
the posterior GH joint and minimizing stretch of the medial
scapular stabilizers. Correction of GIRD is a key component
in the treatment of both primary and internal impingement
(Burkhart 2003).
Localized manual therapy techniques to address GH joint,
scapulothoracic, and/or spinal mobility restrictions may also be
necessary to optimize shoulder girdle complex mobility. Mul-
tiple studies have demonstrated efficacy in improving shoul-
der impingement symptoms by addressing spinal impairments
(regional interdependence model) (Bang 2000, Bergman 2004,
Boyles 2009, Rhon 2014). Soft tissue mobilization techniques
can also serve as a useful adjunct in the resolution of impinge-
ment symptoms (Haahr 2005, Senbursa 2007).
Initial strength training consists of scapular control, closed
chain exercises, multidirectional isometrics, and isotonics
(Escamilla 2014, Kibler 2001, Kibler 1998, McMullen 2000).
Scapula stabilizing exercises are important for patients with
all types of impingement (Figures 33.5 and 33.6). The scap-
ula forms the stable base from which the rotator cuff and
214 SECTION 3  Shoulder Injuries
scapular stabilizing muscles originate. Reciprocal motion
is required between the GH and scapulothoracic joints for
proper cuff function and correct positioning of the coraco­
acromial arch. Abnormal scapular movement (dyskinesis)
can be corrected, and impingement symptoms ameliorated,
with manual assistance (clinician-applied scapular retraction
or upward rotation) or with a scapular taping program as part
of the exercise regimen (Burkhart 2003, Kibler 1998) (Fig.
33.7). Although scapular taping has become popular, further
research is necessary to substantiate widespread use of this
treatment technique (Hsu 2009, Thelen 2008). Restoration of
normal scapular neuromuscular control should be achieved
by application of a progressive dynamic strengthening pro-
gram that includes coordinated movement of the trunk with
the scapulothoracic and GH joints (Kibler 2001, Kibler 2013,
McMullen 2000).
Closed chain exercises assist in developing proximal sta-
bility and enhancing neuromuscular control of the scapula
(Fig. 33.8) while effectively strengthening the rotator cuff
(Burkhart 2003, McMullen 2000, Uhl 2003). Progression of
closed chain exercises from limited axial loading in kneel-
ing or standing to greater magnitudes of axial loading will
increase muscular recruitment and preparation for return to
preinjury activities.
Isometric exercises begin with the arm at the side and
may progress to varying angles of pain-free shoulder elevation
(Escamilla 2014). Isotonic exercises, performed with the use
BOX 33.2  CONSERVATIVE (NONOPERATIVE) TREATMENT OF SHOULDER IMPINGEMENT
Exercise progression is based on functional improvement and pain
reduction, not a specific time frame. Patient education throughout all
phases is important to ensure restoration of optimal shoulder girdle
neuromuscular control and performance.
MODALITIES
• Heat applied before exercise may facilitate gains in ROM.
• Ice application following resistance exercises  • Isotonics: flexion, extension, adduction, abduction, IR/ER at 45
RANGE OF MOTION (PERFORMED 1–2 TIMES DAILY)
• Active and active-assisted ROM in the scapular plane
• Posterior capsule stretching (Fig. 33.10)
• Progression to end-range stretching. End-range stretching
should continue to be performed once full range of motion is
achieved (i.e., through the late stage of rehabilitation).  • Late phase: Focus on restoration of shoulder girdle strength,
MANUAL THERAPY
• Techniques applied by clinician to address specific GH joint cap-
sular, scapulothoracic joint, or spinal mobility limitations. Manual
therapy techniques should be initiated in the initial phase and
may be necessary throughout all stages of rehabilitation.  (i.e., single leg or on a physioball) and figure 8 exercises. Closed
STRENGTH TRAINING (PERFORMED ON ALTERNATING DAYS;
I.E., 3 TO 4 DAYS PER WEEK)
• Initial phase: scapular neuromuscular control, closed chain
exercises, rotator cuff isometrics, and limited range isotonics
(1–3 sets of 10–15 repetitions)
• Scapular retraction, depression, PNFs, shoulder dump, scapular
clocks, prone row, and low row
• Rotator cuff isometrics progressing from arm at the side to varying
angles of shoulder elevation
• Begin isotonics, limited to 0 to 90 degrees of shoulder elevation,
when cuff isometrics can be performed without pain.
• Progress to intermediate phase when normal scapulothoracic
and glenohumeral motion are present through a 0- to-150 degree
arc of shoulder elevation (concentric and eccentric control).
of resistance bands, cable machines, or light dumbbells, are
initially focused on rotator cuff strengthening with the arm at
the side. These exercises help restore the ability of the rota-
tor cuff to dynamically depress and stabilize the humeral
head, resulting in a relative increase in the subacromial
space (Reinold 2009, Sharkey 1995). Progression involves
functional movement patterns of the shoulder (Fig. 33.9)
within the available pain-free range of mobility while ensuring
quality of the movement pattern. In general, isolated flexio
n and abduction movements are limited in the early reha-
bilitation phase to avoid impingement symptoms (McClure
2004). Isokinetic exercises may be introduced once good rota-
tor cuff strength and scapular stability are achieved. Isokinetic
training, variable resistance at a constant predetermined speed
of movement, can be helpful in maximizing return of shoul-
der girdle power and muscular endurance (Ellenbecker 2000).
Incorporation of eccentric loading training of the rotator cuff
and deltoid may also contribute to functional improvements
and reduction in pain for patients with nonoperative manage-
ment (Jonsson 2006).
In patients with secondary impingement, strengthening
is started with the arm near the patient’s side and advanced
through greater ranges of motion while avoiding positions that
provoke symptoms of impingement or instability (i.e., com-
bined abduction and external rotation). As dynamic stabili-
zation (neuromuscular control) of the scapula and GH joint
improves, exercises can be advanced into greater ranges of
• Intermediate phase: Progression of strengthening and attain-
ment of full range of motion
• Scapular retraction with horizontal abduction (“T”) (Fig. 33.11),
scapular “Y” (Fig. 33.12), shoulder punches, wall circles
• PNFs and rhythmic stabilization exercises
• Seated press-ups and push-up “plus” progression (wall to incline
to traditional)
to 90 degrees abduction, rows in standing
• Plyometric exercises (see Fig. 33.13)
• Progress to late phase when the patient is pain free and
demonstrates normal scapulothoracic and glenohumeral
mechanics throughout the full range of motion (both concentric
and eccentric control) and 5/5 strength.
neuromuscular control, and maintenance of normal mobility.
• Individualize the rehabilitation progression to prepare the patient
for specific occupational and athletic demands.
• Isokinetic exercises and testing
• Closed kinetic chain: push-up plus with diminishing support
kinetic chain testing
• Strength training may include changing the stability of the
base of support (i.e., double to single-leg stance and perform-
ing exercises while standing on a wobble board or foam mat).
Modification of lower extremity and core support and integrated
demands by performing various shoulder movements while in
a split stance or athletic stance (Fig. 33.14), while squatting or
lunging (Fig. 33.15), whole body diagonal movements (lift and
chop) (Fig. 33.16), and unilateral lifting (dumbbells)
• Gradual return to traditional weightlifting exercises. Caution is
recommended when returning to barbell pressing movements
(bench, incline, and military presses) and dips because these
movements can result in a return of symptoms. Behind the neck
pull-downs and military press should be avoided.
 Fig. 33.8  Closed kinetic chain flexion–extension.

Fig. 33.5  Resistance band low row.

Fig. 33.6  Scapular clocks.

Fig. 33.9  PNF D2 pattern.

Fig. 33.10  Posterior capsule stretching.

Fig. 33.7  Example of scapular taping.

216 SECTION 3  Shoulder Injuries

Fig. 33.11  “T” exercise, scapular retraction with horizontal abduction.

Fig. 33.13  Plyometric chest pass.

Fig. 33.12  “Y” exercise, scapular depression and retraction with

shoulder flexion.

shoulder elevation, abduction, and external rotation (Escamilla

2014, Manske 2013).
Strengthening of both the scapular musculature and rota-
tor cuff should include increasing levels of resistance and vol-
ume of activity to improve muscular endurance. Readiness for
return-to-overhead activities (sports or occupational demands)
should be based on demand-specific analysis for optimal
return of strength and mobility (Kibler 2001). Return to high-
demand activities based solely on absence of pain, without
full return of requisite strength and mobility throughout the
kinetic chain, will put the patient at risk for eventual return
of impingement symptoms.
Historically, nonoperative treatment was considered unsuc-
cessful if no improvement occurred after a year of proper
conservative management. Today, nonoperative treatment
should be considered unsuccessful if the patient shows no
Fig. 33.14  Plate press in athletic stance.
improvement after 3 to 6 months of a comprehensive and
coordinated medical and rehabilitative program. After 6
months of appropriate conservative treatment, most patients
have achieved maximal improvement from the nonoperative
treatment program (Bigliani 1997, Cavallo 1998). Adherence
to nonoperative care is critical because subacromial decom-
pression has not been shown to produce superior outcomes to
nonoperative management (Gebremariam 2011, Haahr 2005,
Ketola 2013, Kuhn 2009). In patients with an accurate diagno-
sis, failed conservative management or a plateau in recovery at

Fig. 33.15  Lift and chop, whole body PNF.
an undesirable level of function can be an indication for surgical
intervention.  labrum or a capsular shift (capsulorrhaphy), depending on
Operative Treatment
The success of operative treatment is dependent upon an accu-
rate diagnosis, a thorough understanding of the underlying
mechanical abnormality, and the technical skill of the surgeon
performing the procedure designed to correct the mechani-
cal problem. For primary impingement syndrome, it is
believed that rotator cuff pathology is the primary problem;
therefore, surgical treatment aimed at addressing the rotator
cuff and surrounding anatomy is the current procedure of
choice (Bigliani 1997). Rehabilitation after surgery focuses on
pain control, improved ROM, and muscle strengthening and
can be dependent on the severity of the pathology found at
the time of surgery (bursitis vs. full thickness rotator cuff tear)
(Box 33.3). Return to high demand sports can be limited and
a comprehensive postoperative rehabilitation program must
be emphasized. Outcomes from subacromial decompression
have been noted to be similar in both groups that underwent
arthroscopic decompression as well as those that underwent
open subacromial decompression (Davis 2010, Gebremariam
2011, Husby 2003).
For secondary impingement, surgical treatment must be
directed at the primary problem. For instance, if GH insta-
bility is identified as the primary problem and is associated
with the development of secondary impingement type symp-
toms, surgical treatment should focus on addressing shoul-
der stability. Open or arthroscopic stabilization procedures
33  Impingement Syndrome 217
Fig. 33.16  Lunge and lift.
may be performed, with either a repair of a torn or avulsed
the underlying primary etiology. The potential advantages of
arthroscopic procedures include decreased operative time,
less operative morbidity, less loss of motion, and a quicker
recovery (Davis 2010). The rehabilitation principles after an
arthroscopic stabilization procedure that includes a labral
repair or suture capsulorrhaphy are similar to those after an
open stabilization procedure. The biology of healing tissue is
the same whether the procedure is done open or arthroscopi-
cally. The rehabilitation protocol after an open or arthroscopic
Bankart repair for anterior shoulder instability is fundamen-
tally the same (with the only notable difference of protect-
ing the subscapularis tenotomy following a traditional open
Bankart procedure).
When internal impingement is suspected a thorough bilat-
eral examination under anesthesia is conducted along with
diagnostic arthroscopy (Heyworth 2009). Surgical manage-
ment of internal impingement may include anterior capsular
plication, posterior capsular release, débridement or repair of
the rotator cuff tear, and débridement or repair of the postero-
superior labral pathology (Heyworth 2009). The rehabilitation
protocol implemented is pathology specific (i.e., post anterior
capsulorrhaphy protocol) with special focus on maintenance
of posterior capsule mobility. Clinical outcomes for surgical
treatment of patients with internal impingement—particularly
overhead athletes—can be guarded, particularly as it relates
to return to presurgical levels of play. As such, every effort is
made to correct these patients’ pathology through nonsurgical
means.
218 SECTION 3  Shoulder Injuries

BOX 33.3  PROGRESSIVE, SYSTEMATIC INTERVAL PROGRAMS FOR RETURNING TO SPORTS AFTER ARTHROSCOPIC
SUBACROMIAL DECOMPRESSION (WITH MODIFICATION FOR DISTAL CLAVICLE RESECTION AND/OR ROTATOR
CUFF DÉBRIDEMENT)
PHASE 1: WEEKS 0–4 Immobilization
Restrictions • None. 
• ROM Pain Control
• 140 degrees of forward flexion.
• 40 degrees of external rotation. • NSAIDs—for patients with persistent discomfort.
• 60 degrees of abduction. • Therapeutic modalities (ice, HVGS).
• ROM exercises begin with the arm comfortably at the patient’s side, • Moist heat before therapy, ice at end of session.
progress to 45 degrees of abduction and eventually 90 degrees. • Subacromial injection: lidocaine/steroid—for patients with acute
Abduction is advanced slowly depending on patient comfort level. inflammatory symptoms that do not respond to NSAIDs. 
• No combined abduction and rotation until 6 wk after surgery. Exercises
• No resisted motions until 4 wk postoperative.
• No cross-body adduction until 8 wk postoperatively if distal Motion
clavicle resection.  • Progress from active-assisted to active ROM in all directions.
• Focus on prolonged, gentle passive stretching at end ranges to
Immobilization increase shoulder flexibility.
• Early motion is important. • Thoracic extension to promote proximal kinetic chain function
• Sling immobilization for comfort only during the first 2 wk. and postural awareness.
• Sling should be discontinued by 2 wk after surgery. • Joint mobilizations (manual therapy) for capsular restrictions,
• Patients can use sling at night for comfort.  especially the posterior capsule. 
Muscle Strengthening (performed on alternating days)
Pain Control
• Scapular stabilizer strengthening: retraction, protraction,
• Reduction of pain and discomfort is essential for recovery depression.
• Medications • Scapular proprioceptive neuromuscular facilitation (PNFs)
• Narcotics—10 day–2 wk following surgery. exercises.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) for patients with • Progress to open chain scapular stabilizer strengthening.
persistent discomfort following surgery. • Closed chain strengthening exercises—delay until 6 wk when
• Therapeutic modalities (ice, HVGS). RTC débridement is performed.
• Moist heat before therapy, ice at end of session.  • Multidirectional isometric shoulder strengthening: IR, ER,
extension, adduction, flexion (performed with the elbow flexed
Motion: Shoulder
to 90 degrees).
Goals • Open chain strengthening with resistance bands and/or dumb-
• 140 degrees of forward flexion. bells—delay until 6 to 8 wk when RTC débridement is per-
• 40 degrees of external rotation. formed.
• 60 degrees of abduction.  • Starting position is with the arm at the patient’s side and using a
Exercises short lever arm (elbow flexed to 90 degrees) advancing to
• Begin with Codman pendulum exercises to promote early motion. motions with a long lever arm (elbow extended).
• Passive ROM exercises (Fig. 33.17). • Exercises are performed through a pain-free arc of motion while
• Manual therapy (capsular stretching) for anterior, posterior, and ensuring normal GH and scapulothoracic movement patterns.
inferior capsule (Fig. 33.18). • Patients should not progress to greater level of resistance if
• Active-assisted ROM exercises (Fig. 33.19). there is any discomfort or suboptimal movement patterns at the
• Shoulder flexion, extension, internal and external rotation. present level.
• Progress to active ROM exercises as comfort improves. • Progress to resistance band and light dumbbell exercises, which
• Address proximal kinetic chain motion restrictions (i.e., limited permit both concentric and eccentric strengthening of the
thoracic extension).  shoulder muscles and are a form of isotonic exercises
(characterized by variable speed and fixed resistance)
Motion: Elbow • IR, ER, abduction, adduction, flexion, and extension
• Active • Note: Do not perform more than 15 repetitions for each set or
• 0 to 130 degrees. more than three sets of repetitions. If this regimen is easy for the
• Pronation and supination as tolerated.  patient, then increase the resistance not the repetitions. Upper
body strengthening with excessive repetitions can be
Muscle Strengthening counterproductive during this subacute phase of recovery. 
• Gripping exercises. PHASE 3: WEEKS 8–12
• Scapular control exercises (retraction, depression, and low row)
• Light resistance isometric IR and ER (delay until 3-4 weeks if RTC Criteria for Progression to Phase 3
débridement is performed)  • Full painless ROM.
• Minimal or no pain.
PHASE 2: WEEKS 4–8 • At least 4/5 strength
Criteria for Progression to Phase 2 • Absence of scapular dyskinesis 
• Minimal pain and tenderness. Goals
• Nearly complete motion.
• Scapular muscle control  • Improve shoulder complex strength, power, and endurance.
• Improve neuromuscular control and shoulder proprioception.
Restrictions • Prepare for gradual return to functional activities. 
• Progress ROM goals to Motion
• 160 degrees of forward flexion.
• 45 degrees of internal rotation (vertebral level L1). • Achieve motion equal to contralateral side.
• 60 degrees of external rotation. • Utilize both ROM exercises and manual therapy to maintain
• 140 degrees of abduction.  ­motion. 
 33  Impingement Syndrome 219

BOX 33.3  PROGRESSIVE, SYSTEMATIC INTERVAL PROGRAMS FOR RETURNING TO SPORTS AFTER ARTHROSCOPIC
SUBACROMIAL DECOMPRESSION (WITH MODIFICATION FOR DISTAL CLAVICLE RESECTION AND/OR ROTATOR
CUFF DÉBRIDEMENT)—cont’d
Muscle Strengthening is recommended when returning to barbell pressing movements
• Advance strengthening of the shoulder complex (rotator cuff and (bench, incline, and military presses) and dips as these movements
scapular stabilizers) can result in a return of symptoms. Behind the neck pull-downs
• Progression should include a gradual increase in resistance and/ and military press should be avoided. 
or training volume. Progressive, Systematic Interval Program for Returning to Sports
• Continue strengthening on alternating days to enable
neuromuscular recovery.  • Throwing athletes.
• Tennis players.
Functional Strengthening • Golfers.
• PNFs and rhythmic stabilization exercises. • Institute “Thrower’s Ten” program for overhead athlete with
• Push-up progression (wall to incline to traditional). progression to the advanced thrower’s ten.
• Plyometric exercises.  • Maximum improvement is expected by 4 to 6 months following
an acromioplasty and 6 to 12 months following an acromioplasty
For Patients with Concomitant Distal Clavicle Resection or RTC combined with a distal clavicle resection. 
débridement
Warning Signals
• Now begin cross-body adduction exercises
• First passive, advance to active motion when AC joint pain is • Loss of motion—especially internal rotation.
minimal.  • Lack of strength progression—especially abduction.
• Continued pain—especially at night.
PHASE 4: WEEKS 12–16
Treatment of Above “Problems”
Criteria for Progression to Phase 4 • These patients may need to move back to earlier routines.
• Full, painless ROM. • Return to supervised rehabilitation to address subtle losses of
• No pain or tenderness. motion, aberrant movement patterns, and insufficient strength.
• 4+ to 5/5 strength. • May require increased utilization of pain control modalities as
• Satisfactory clinical examination.  outlined above.
• If no improvement, patients may require repeat surgery
Goals • It is important to determine that the appropriate surgical proce-
• Progressive return to unrestricted activities. dure was done initially.
• Maintenance of full ROM • Issues of possible secondary gain must be evaluated.
• Advancement of strength training may include isokinetic training
and gradual return to traditional weightlifting exercises. Caution

Fig. 33.17  Passive range of motion in the scapular plane. Fig. 33.18  Inferior mobilization of the glenohumeral joint.
220 SECTION 3  Shoulder Injuries

Fig. 33.19  Active-assisted range of motion.

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