SUBACROMIAL

ANATOMY AND
BIOMECHANICS
RELATED TO THE
IMPINGEMENT SYNDROME
CHARLES

E. NEAGLE, MD, and JAMES B. BENNETT,

MD

Shoulder girdle evolution, anatomy, biomechanics, and potential etiologies of impingement are reviewed. It is
apparent that shoulder impingement can occur as a secondary phenomenon in the presence of certain intrinsic
shoulder pathology.
Rotator cuff lesions frequently involve tendon degeneration.
Subacromial impingement is
believed to play a major role in this degenerative process. In addition, it is postulated that cuff degeneration
precedes subacromial impingement more frequently than is commonly believed. A multifactorial etiology in
which the relative importance of a specific element varies from case to case best explains tendon degeneration.
KEY WORDS: biomechanics, etiology, subacromial impingement

Anatomically
and biomechanically,
the human shoulder most closely resembles that of a tree-swinging,
quaAdditional modification of this condrupedal mammal.
struct was necessitated by mans bipedal upright posture.
On assumption of the erect position, a series of complex
adaptive changes were required to facilitate the exchange
of stability for mobility to improve prehension and other

demands of the upright posture.

This process is best
illustrated by comparing the pectoral girdle with the pelvic girdle, where a stronger, more stable, and less mobile
articulation is noted.
A basic pattern for the mammalian shoulder girdle was
initiated in the primitive bony fish. The human forelimb
was derived from a pair of longitudinal dermal folds, the
cleithrum, which formed the posterior edge of the gill
opening and attached to the skull.
Muscle buds and
spinal nerves migrated into the proximal portion of the
ridge as they developed into pectoral fins. Between
these muscle buds cartilage rays, termed radials, arose to
form a support structure whose proximal portions coalesced to form the basilia. This construct formed the
Migration
ventrally of the
primitive pectoral girdle.
paired basilia toward the midline formed a ventral bar, a
precursor of the paired clavicles. The dorsal projections
of the basilia over the thorax were the precursors of the
scapulae. At the junction of the ventral and dorsal segments an articulation developed, representing the glenoid fossa. The remainder of the pectoral fin developed
into the glenohumeral joint.
The first increase in mobility of this pectoral girdle occurred in amphibians,

the attachment

of the cleithrum

The basic mammalian

pattern

where

to the skull was lost?

consisted

of a well-

From Southwest
Orthopedic
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and Department
of
Orthopedic
Surgery,
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College
of Medicine,
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82

Operative

developed clavicle, which articulated with the sternum,

and a flat wide scapula with a moderate-sized coracoid.
This basic design diverged in four directions.3
Shoulder
girdles modified for running lost their clavicle to further
mobilize the scapula, which is relatively narrow.
Mammals adapted for swimming also lost their clavicles but
developed a wider scapula. Shoulder girdles modified
for flying have a prominent, well-developed clavicle with
a concomitantly
small, narrow, curved scapula.
The
fourth was modified for brachiating.
This subgroup includes man, in whom a strong clavicle, large coracoid,
and wide scapula have developed.
Compared with the
active brachiators, mans shoulder girdle is less mobile.
Additional adaptations reflected in mans erect posture
were a relative flattening of the thorax in the anteriorposterior dimension and the evolution of the pentadactyl
limb.
To appreciate the evolutionary specificity of the human
shoulder girdle, the particulars of each component will be
addressed separately.
The human scapula is suspended by muscles and is
shifted caudally from its cervical position in lower animals.

Additionally,

the scapular

index,

a ratio of the

width of the base of the scapular spine compared with the

height of the scapula as measured from the superior to
inferior angle, is decreased.
This largely results from an
increase in the infraspinous fossa.
The broadening of
the infraspinatus fossa alters the vector of the infraspinaThis increases their biomechanical
tus and teres minor.
advantage as depressors and external rotators of the humeral head.5
An extension of the scapular spine, the acromion process, is also significantly larger in humans compared with
that in pronograde animals.
This reflects the increased
role of the deltoid muscle with respect to shoulder function. The enlarged acromion increases the area of the
deltoid origin and shifts the origin laterally, which affords
a biomechanical advantage.
This increased advantage is
furthered by distal advancement of the deltoid insertion
Techniques

in Sports

Medicine,

Vol

2, No 2 (April),

1994:

pp 82-88

The evolution of the scapulohumeral

on the humerus.
muscles notes a greater than twofold increase in the proportional representation of the deltoid.6
The above emphasizes the importance of the deltoid in human shoulder function.
As an important origin and insertion site for musculature, the coracoid process is larger in humans compared
with that in pronograde animals.4

EMBRYOLOGY
The embryonic period, which comprises the first 8 weeks
of prenatal development, will be reviewed with respect to
the shoulder girdle.
By the end of the 4th week of gestation, small elevations are noted on the ventral lateral
body wall, which are termed limb buds.7 During the 5th
week, peripheral nerves grow into the limb mesenchyme.
This stimulates the development
of limb musculature;
concomitantly, the clavicle begins to ossify. The mesenthyme condenses to form digital rays, and the scapulae
enlarge and extend from C-4 to approximately T-7 during
the 6th week of gestation.
Ventral extension and external rotation of the upper limb buds are noted during the
seventh week.7 By the 8th week, the shoulder joint has
the form of the adult glenohumeral joint.7 The fetal period of prenatal development
is largely concerned with
the upper extremity, including enlargement of the structures formed during the embryonic period.
Postnatal shoulder girdle development is characterized
by the development of secondary centers of ossification.
The clavicle has two separate ossification centers, with
the lateral being more prominent.
The body and spine
of the scapula are ossified at birth, but the coracoid, glenoid, acromion, vertebra border, and inferior angle are
not. Two and occasionally three centers of ossification
are noted in the development
of the coracoid process.
The acromion has two and occasionally three centers of
ossification.
They develop during puberty and are usually fused by 22 years of age. These three separate centers are termed preacromion,
mesoacromion, and metaacromion.*,9
Failure of these centers to unite is termed
OS acromiale.
First described in the literature in 1936,
Liberson
noted a 2.7% incidence of OS acromiale; of
these, 62% were bilateral.
Best visualized on an axillary
view, the lesion is most commonly seen as a failure of
fusion between the mesoacromion and meta-acromion.
The glenoid fossa has two ossification centers. The
proximal humerus has three centers of ossification, representing the head of the humerus, greater tuberosity,
and lesser tuberosity.

PERTINENT BIOMECHANICS
Space permits a brief review of shoulder biomechanics;
thus, only those issues germane to shoulder impingement will be discussed.
Integrated motion of the sternoclavicular, acromioclavicular,
scapulothoracic, and glenohumeral joints is required for adequate shoulder girdle
function.
Twenty-six muscles are required to control
these various joints for optimal shoulder function.i*
SUBACROMIAL

BIOMECHANICS

IN IMPINGEMENT

The intricate interaction of these four joints and numerous muscles affords the shoulder more movement than
any other joint.
Thus, the soft tissues provide stability.
This allows the arm to move through 0 to 180 of elevation and approximately 150 of internal and external rotation, with anterior and posterior rotation in a horizontal
plane approaching 170.13
Shoulder motion has been a topic of controversy for
more than 100 years. In his 1934 paper, Codman14 specifically addresses this in great detail. Additionally,
he
describes a pivotal paradox.
This pivotal paradox is
best explained by the concept that three-dimensional
rotation is sequence dependent.
Glenohumeral motion results from three basic components: spin, slide, and ro11.15
Pure translation of a moving segment against the fixed
segment is termed sliding.
Here, the contact point of
the moving surface does not change; however, the corresponding fixed segment contact point does change.
Spinning motion occurs when the moving segment rotates, but the contact point on the fixed surface is unchanged.
Finally, rolling occurs when contact points on
both the fixed and moving segment surfaces change.
Arm elevation is considered to be the most important
function of the shoulder.
Relative contributions of glenohumeral and scapulothoracic motion in this respect has
received significant attention.
Initial observations relegated the first 90 of motion to the glenohumeral
contribution.
Subsequently,
an overall glenohumeralscapulothoracic ratio of 2:l was described.4
More recently, sophisticated
investigational
techniques have
depicted an inconsistent ratio during the first 30 of elevation.16 Bergmann17 summarizes the results of recent
studies in this regard.
Invariably, greater motion occurs
at the glenohumeral joint during the first 30 of elevation;
however, the last 60 occur with roughly equivalent contributions
by the glenohumeral
and scapulothoracic
joints.
An obligatory external rotation of the humerus is necessary for maximum elevation of the arm. The rationale
for this includes (1) external rotation clears the greater
tuberosity preventing impingement,
(2) rotation optimizes contact for the glenohumeral
articulation, and (3)
greater stability is noted in full elevation and maximal
external rotation compared with the elevated position.

MUSCLE FORCES ACROSS THE

GLENOHUMERAL JOINT
The functional result of a particular muscle activation depends on the muscles size, orientation, and level of fiber
recruitment.
As alluded to earlier, the articulations and
muscles involved in shoulder girdle motion render their
analysis a formidable task. However, investigation can
be facilitated by the examination of this construct in isolated planes of motion.4,18,20 The majority of upper extremity use occurs between the planes of forward flexion
and scapular elevation.*r
Scapular elevation requires a combined action of the
deltoid and rotator cuff musculature.4
Specifically, electromyographic
studies emphasize the importance of coordinated supraspinatus and deltoid activity.**
The del83

toid and supraspinatus are considered the primary elevaTheir action is facilitated by
tors of the upper extremity.
the subscapularis, teres minor, and infraspinatus, which
This describes a force coustabilize the glenohumeral joint.
ple that allows abduction by the deltoid muscle instead of superior translation as the humerus is held in the glenoid by the
rotator cuff.
Bechto13 describes the relationship
between the supraspinatus and deltoid muscles.
A uniform decrease in
abduction strength independent of joint position was noted
along with the absence of the deltoid. In contrast, without
the rotator cuff, initial abduction strength was normal,
with a rapid decrease at elevations beyond 30. Howell
et a123 used an isokinetic dynamometer
in concert with
isolated paralysis of the suprascapular and axillary nerves
and reported different findings.
In this report, an equal
role of the supraspinatus and deltoid muscles was found
with respect to torque production about the shoulder in
the functional planes of motion.23

PATHOPHYSIOLOGY OF IMPINGEMENT
Impingement refers to the compression of the rotator cuff
mechanism by its surrounding local anatomic structures.
Specifically,
the acromion,
coracoacromial
ligament,
coracoid process, posterior superior glenoid, and fibrocartilaginous or bony projections from the anterior acromion or acromioclavicular
joint may be involved.
A number of authors during this century address
shoulder impingement.24,25
However, in Neers2* 1972
article the term impingement syndrome is advanced.
This
report emphasizes the importance of proliferative
spurs
on the undersurface of the anterior acromion.
Additionally, he emphasizes that with the arm in an anatomic
position, the biceps tendon, supraspinatus tendon, and
anterior portion of the infraspinatus tendon lie anterior to
the acromion.
In activities of daily living, where the arm
is often internally rotated, these structures become more
anterior.
With external rotation, the insertion of the supraspinatus is immediately lateral to the anterior third of
the acromion.
Hence, with elevation of the arm in internal or external rotation, this critical area passes under
the coracoacromial ligament or the anterior acromial process. With 80 of abduction, this critical area of the supraspinatus
is beneath the acromioclavicular
joint.
Thus, joint excrescences may impinge on the cuff. Additionally, the concept of a continuum of pathology from
chronic bursitis and partial rotator cuff tear to complete
rotator cuff tear is described.
Recent studies that employ more sophisticated techniques substantiate Neers conclusion that the anterior
acromion is involved
in subacromial
impingement.
Jalovaara26 used a pietzoresistive sensor and determined
that the highest pressures were found under the anterolateral acromion and were significantly higher in patients
with impingement
than in those with acromioclavicular
joint dislocation.
The pressure increased gradually with
an increase in the abduction angle; humeral rotation had
a minor effect. The increased pressure zone started approximately 14 to 18 mm posterior to the anterior margin
of the acromion.
Flatow et a127 applied stereophoto84

grammetry to investigate subacromial contact in cadavers. Soft tissue contact started at the anterolateral edge
of the acromion with the arm in neutral elevation and
shifted medially with elevation.
With respect to the humerus, the contact pattern shifted from the proximal end
to the distal end of the supraspinatus tendon with arm
elevation.
Maximal proximity of the rotator cuff tendons to the acromial undersurface occurred between 60
and 120 of arm elevation and was located at the supraspinatus insertion.
In conclusion, subacromial contact centered on the supraspinatus
insertion and increased with type III acromions.
Neer and Poppen
advanced the term supraspinatus
outlet to describe the space between the acromion, coracoacromial ligament, coracoid, acromioclavicular
joint,
and glenoid through which the supraspinatus
muscle
passes. It is their belief that narrowing of this outlet is
the primary cause of impingement.28
The coracoacromial arch includes the two scapular processes, coracoid and acromion, and the coracoacromial
ligament.
This broad, fin-shaped ligamentous structure
spans the interval between the coracoid and acromion.
The subacromial bursa contains two serosal surfaces lubricated by synovial fluid, which facilitates cuff motion
between the humerus and the coracoacromial
arch.
The rotator cuff is comprised of the subscapularis, supraspinatus,
infraspinatus,
and teres minor.
These
muscles blend together as they transverse the glenohumeral space and insert into the lesser tuberosity, the
greater tuberosity, and the transverse humeral ligament.
Rotator cuff functions include stabilization of the shoulder against the actions of the prime movers (force couple
effect) and the enhancement of glenohumeral torque during rotation and arm elevation.

ETIOLOGIES OF IMPINGEMENT
A variety of factors have been described and proposed in
the development and exacerbation of the subacromial impingement syndrome. These can be grouped into structural, vascular, dynamic, traumatic, and functional events.

Structural
Acromial shape has received significant attention with
respect to causation of the impingement
syndrome.
Earlier in this century, clinicians focused treatment on
complete or lateral acromionectomies.29
However, Neer
emphasizes the importance of the anterior acromion.
Subsequently, Aoki et aim examined acromial slope relative to a line connecting the posterior acromion with the
tip of the coracoid to determine the propensity for impingement.
They found that the acromial slope in patients with impingement
was significantly less than that
in normal volunteers.
This was confirmed by Zuckerman et a1,31 who found a significantly lower angle in cadaveric shoulders with full-thickness
rotator cuff tears
compared with shoulders having intact rotator cuffs.
Acromial shape variations occur more commonly in patients with impingement and cuff tears.21 One hundred
NEAGLE

AND BENNETT

forty shoulders in 71 cadavers whose average age was

74.4 years were reviewed by Bigliani.32 Three types of
acromia were identified: the flat, type I, was seen in 17%;
curved, type II, in 43%; and hooked, type III, in 40%.
Bilateral concurrence of shape was seen in 58% of the
cadavers.
One third of the rotator cuffs had fullthickness tears, of which 73% were seen in type III acromions, 24% in type II, and 3% in type I. This cadaveric
study then was su ported in a clinical review by Morrison and Bigliani,3 r who reviewed 200 modified lateral
scapular radiographs.
Eighty percent of patients with
full-thickness rotator cuff tears had hooked acromia; the
remainder had curved acromia.
A normal distribution
of acromial shapes was seen in patients with a clinical
diagnosis of impingement.
Recent cadaveric investigations
by Barthel et al% attempted to verify Morrison and Biglianis report.
Radiographs were analyzed and sections were made along the
coracoacromial
ligament.
After being transfixed in a
polyurethane
mold, the sections were inspected.
The
anatomic dissection yielded a 46% incidence of curved
acromia, with the remainder described as flat. Radiographically, a curved acromion was seen in 85%, with the
remainder categorized as flat. These authors were unable to identify a hooked form of acromial shape in either
the anatomic or radiographic studies.
However, Morrison and Bigliam 33 did acknowledge a dramatic variability
in radiographic technique when radiographs from other
institutions were reviewed and compared with their technique .
Zuckerman et a131investigated the spatial relationship
of the coracoacromial arch and the humeral head. This
was a cadaveric study in which 14 measured parameters
were used to determine a series of 24 calculated parameters to characterize the anatomy.
Shoulders with fullthickness rotator cuff tears were compared with those
without visibly detectable cuff tears. This study did not
specifically address impingement.
However,
using
Neers concept of a continuum of subacromial bursitis to
impingement
to full-thickness rotator cuff tear and perception of outlet impingement,
one could argue the
relevance of Zuckermans study to impingement.
Conversely, Morrison and Bigliani33 found no difference in
the incidence of acromial shape in Stage I and Stage II
impingement
compared with that in normal shoulders.
Pertinent findings by Zuckerman et al include a significantly greater anterior projection of acromia in shoulders
with rotator cuff tears and a significantly decreased acromial tilt angle. This, together with an unchanging acromial length, supports the relationship that as the acromial
tilt angle decreases, the anterior projection increases and
the coracoacromial ligament length decreases. The findings referable to the acromial projection and tilt support
Neers emphasis on the acromial portion of the coracoacromial arch with respect to rotator cuff tear pathogenesis. The authors were able to quantify the supraspinatus outlet, and they documented
a 22.5% decrease in
available area in shoulders with rotator cuff tears.31
Reviewed earlier, the incidence of OS acromiale is
2.7%.
The downward
sloping of the unfused acromion and the spurs or soft tissue proliferation at the nonunion site may cause impingement.
An unfused fragSUBACROMIAL

BIOMECHANICS

IN IMPINGEMENT

ment as large as 5 x 2 cm21 has been reported.

Several
authors have noted an association of an unfused acromial
epiphysis with the impingement syndrome.35,36
In a review of 145 shoulders, 6% with full-thickness rotator cuff
tears were found to have an OS acromiale37; this was
higher than the 2.7% incidence found in the general population.ii
Histological studies performed by Ozaki et a138demonstrate that the anterior acromion has four separate layers:
synovial, cartilaginous, fibrocartilaginous,
and osseous.
As one moves posteriorly on the acromion, two layers are
noted: synovia and bone. The cartilaginous fibers in the
anterior portion of the acromion represent the coracoacromial ligament insertion.

Coracoacromial ligament. Burns and Whipple39

performed a study on cadaveric shoulder specimens, and
they concluded that impingement
more commonly occurs with the coracoacromial ligament rather than the
acromion.
Specifically, they note that the supraspinatus
and biceps tendon contact the superior lateral and inferior lateral edge of the coracoacromial ligament, respectively.
This occurs during the combination of flexion at
15 with abduction of 15, flexion at 45 with internal rotation of 45, and pure shoulder abduction between 45
and 60. Movements involving extension and abduction
isolate the supraspinatus tendon in contact with the inferolateral edge of the coracoacromial ligament.
Using
photographic
documentation,
maximum
contact and
compression of the rotator cuff occur during flexion of 30
with 45 of internal rotation and 30 of abduction.
These
authors only note acromial-rotator
cuff compression in
abduction with external rotation; thus, their emphasis on
the coracoacromial ligament.
On dissection of 40 coracoacromial ligaments, Harris
and Blackney4 noted that the classical triangular ligament was present in 40%. Additionally,
anterior and
posterior bands were described in 40% and an oblong
band in 20%. Prolongation of the short head of the biceps to the acromion was found in 30%. The subacromial extension of the ligament averaged between 10 and
20 mm, with maximum extension of 35 mm. Spur formation at the anterior edge of the acromion was intimately associated with the coracoacromial ligament, and
a progression from a fibrocartilaginous
ridge to a bony
projection was seen. Instron testing of the scapula demonstrated that up to 15 mm of separation between the
coracoid and acromion from a resting state occurred with
a distractive force of 30 kg. The authors propose that in
vivo tension forces occur within the ligament during activities of daily living.
These traction forces are concentrated at the subacromial attachment.
It is through this
mechanism that the genesis of acromial enthesopath
and subsequent supraspinatus outlet narrowing occur. L
Recent histological cadaveric investigation of the coracoacromial
arch41,42 shows that the ultrastructural
changes in the coracoacromial ligament in patients with
chronic impingement
syndrome possibly occur as secondary events. They are likely to be induced by alterations in soft tissue structures of the subacromial compartment.
Additionally,
their findings support that rotator cuff tears are more likely to develop as an intrinsic
85

degenerative tendinopathy
rather than being initiated by
impingement.
Acromial enthesopathy
appears to be
secondary to the development of partial or complete rotator cuff tears. Specifically, 34 of 36 partial tears were
observed at the articular side; 86% of these specimens
showed an abnormal undersurface of the acromion.*

Subcoracoid impingement.
Goldthwait43
raises
the possibility of a subcoracoid site of impingement.
Gerber et al@ revived interest in this earlier publication in
1985. A space occurs anterior to the coracoacromial ligament between the coracoid process and the lesser tuberosity. This space averages 8.7 mm in resting position
and decreases to 6.8 mm in flexion with medial rotation.
With flexion and medial rotation, the soft tissues in the
These tissues include the subspace becomes folded.
scapularis tendon, superior and middle parts of the glenohumeral ligament, and nearby insertion of the long
head of the biceps tendon.&
The pathogenesis of this
syndrome could be traumatic, such as avulsion fractures
of the coracoid process or lesser tuberosity or an incorrectly placed bone block to correct instability.
This space
can be crowded by a traumatic tear of the subscapularis
with calcification of this tendon.
Diffuse laxity of the
anterior capsule and ligaments allowing anterior humeral
displacement also has been implicated.45
It appears that
this proposed syndrome was frequently a consequence of
trauma, which resulted in some type of superior labrum
anterior to posterior lesion or anterior instability.
Thus,
treatment should be designed to correct these underlying
sources of pathology.
Superior

glenoid

impingement.

Attention
recently has been given to the throwing athlete who presents with posterior shoulder pain, a positive impingement sign, and signs of rotator cuff rupture.
Jobe and
Sidles6 examined 10 frozen cadaveric specimens that had
no signs of instability.
They noted an indentation in the
articular surface of the supraspinatus tendon, which represented contact with the glenoid labrum; a labral deformation by the tendon and greater tuberosity also was
noted.
Computer graphic representation
of 8 subjects
demonstrated that the greater tuberosity approached the
articular surface of the glenoid with potential rotator cuff
and glenolabrum contact. Additional findings on magnetic resonance imaging scans confirmed superior labral
contact with the greater tuberosity.
Arthroscopic confirmation in 17 throwing athletes demonstrated
impingement between the posterosuperior
border of the glenoid
and the undersurface of the tendinous supraspinatus and
infraspinatus insertions.47
All 17 patients had evidence
of a partial rotator cuff tear.

Other structural factors. Malunion of the greater

tuberosity,
distal clavicle, or acromion as a result of
trauma can narrow the supraspinatus outlet, which may
incite rotator cuff impingement.
Additionally,
diseases
or processes that cause inflammatory
bursitis (rheumatoid arthritis), a thickening of the rotator cuff (calcific tendinitis), or a flap partial rotator cuff tear can be involved
in the impingement
process.
Finally, the concept of

congenital subacromial stenosis advanced by Burkhart**

states that a congenitally narrowed subacromial space can
exist. Previous investigations49,50 suggest that the lower
limit of normal with respect to the acromial-humeral
interval is 7 mm. Burkhart identified 6 patients of 25 who
had impingement
syndrome without rotator cuff tears
whose average acromial-humeral
interval was 4.7 mm.
This suggests a predisposition
to subacromial impingement.
However, these findings were noted in patients
with pathology.
Thus, a weakened rotator cuff, rather
than congenital predisposition,
may have allowed superior humeral translation and subsequent decrease in the
acromial-humeral
interval.

Vascular
The vascularity of the rotator cuff has been explored over
the last 50 years. Lindblom5i advances the notion of an
avascular area of the supraspinatus tendon near its insertion site at the greater tuberosity.
However, Iannotti et
a152 detected substantial blood flow in this zone of the
rotator cuff using laser Doppler.
Despite hypotheses
suggesting that this area is exsanguinated with various
shoulder motions and activities,53,s it is unlikely that this
produces sufficient ischemia for tendon damage.
However, it was demonstrated
in recent neurohistological
studies that the usually abundant blood and nerve supply
in the subacromial bursa was deficient in areas of partial
rotator cuff tears.55

Traumatic and Dynamic Factors

Violent trauma can cause complete rotator cuff tears as
evidenced by that fact that this complication accompanies
anterior and inferior glenohumeral dislocation.56
Other
authors57 propose the occurrence of a full-thickness rotator cuff tear after significant trauma without suspected
glenohumeral dislocation.
However, Neer5s does not support trauma as a significant etiological factor in the impingement
lesion.
He
attributes acute traumatic subacromial bursitis to a single
injury that impacts the humerus against the acromion.59
He describes this process as a short-lived impairment of 3
to 6 weeks duration.
It is conceivable that this could
result in a chronic thickening of the subacromial bursa,
which could lead to impingement
syndrome.
Avocational and vocational activities can initiate or exacerbate rotator cuff impingement.
Athletic participation in throwing sports as well as occupations that require
frequent overhead lifting or repetitive activity in the
plane of scapular elevation, are more common precursors.6o These activities can lead to an overuse syndrome
or recurrent microtrauma to the rotator cuff that results in
tendinitis.
If the humeral head depression mechanism
is weakened, superior migration of the humerus can occur. In addition, the supraspinatus outlet can be narrowed by edema and inflammation.
Athletic technique
is crucial to avoid symptoms.61,62
Neer59 describes altering technique to limit symptoms as seen in pitchers who
have learned to throw three-quarters side-arm and swimmers who change from breathing only on one side to
alternating sides.
NEAGLE

AND BENNETT

Loss of glenohumeral
motion in conjunction with impingement signs can present simultaneously.
Specifically, stiffness of the posterior capsule prevents the rotation of the humeral head posteriorly on elevation.
This
causes a superior translation of the humeral head and can
potentially exacerbate impingement
of the rotator cuff
against the coracoacromial arch. Q
Jobe et a163 describe a mechanism by which glenohumeral instability can lead to secondary impingement
of
the rotator cuff against the acromion and coracoacromial
ligament.
This anterior instability also is described as a
potential mechanism for subcoracoid impingement.45
Thus, to effectively treat impingement
in this scenario,
attention must be focused on the underlying problem of
instability.
Altchek et al& demonstrated
radiographically
that a
statistically significant upward translation of the humeral
head relative to the glenoid occurs during arm elevation
in patients with chronic impingement.
This emphasizes
the rotator cuff function as the stabilizer of the shoulder
against the actions of the deltoid and pectoralis major
muscles.
Thus, cuff weakness from a suprascapular
nerve palsy, C5-6 radiculopathy,
partial rotator cuff tear,
or disuse will weaken this function.
Thus, impingement
can be initiated or exacerbated.

Functional
The remaining factors that can influence the impingement syndrome include abnormal positioning
of the
scapula secondary to thoracic kyphosis or acromioclavicular separation.
Dynamic scapular abnormalities,
as a
result of weakness or paralysis of the suspensory musculature (trapezius), can be potential factors in the development of impingement.

CONCLUSION
Numerous potential factors have been implicated as having a potential etiological role in rotator cuff lesions.
Evidence has been presented supporting each of these
factors and their potential clinical relevance.
Central to these proposed pathogenic mechanisms is
the concept of cuff degeneration.
Codmani4 concludes
that intrinsic rotator cuff degeneration is responsible for
the majority of cuff lesions.
However, Neer2r advances
the concept that degeneration is secondary to subacromial impingement in 95% of patients with full-thickness rotator cuff tears.
Structural factors in the development
of rotator cuff
impingement
have been emphasized by a number of
authors.
Aoki et a13 found a significantly
increased
propensity for impingement
with lower acromial slope
angles. Although Norris et aP6 found a significant correlation between acromial shape and the presence of a
full-thickness rotator cuff tear, no significant correlation
was found in patients with a clinical diagnosis of impingement.
The presence of an unfused acromion is
found more commonly in patients with full-thickness rotator cuff tears than in the general population.
Despite
Burns and Whipples39 belief that the coracoacromial ligament is more important than the anterior acromion in
impingement,
recent sophisticated studies using presSUBACROMIAL

BIOMECHANICS

IN IMPINGEMENT

sure sensors and stereophotogrammetry

support the role
of the acromion as advanced by Neer. Anterior acromial
enthesopathy appears to be related to repetitive distractive forces experienced by the coracoracromial ligament.
Conversely, Ozaki et al,38 Sarkar et aL4 and Ogata and
Uhthoff42 interpret the results of their investigations to
support the concept of intrinsic rotator cuff degeneration
as the primary event, with subacromial changes occurring secondarily.
This intrinsic cuff degeneration
can
decrease the force couple effect so that the humeral head
can translate superiorly in shoulder function.
Superior
translation in conjunction with posterior capsular tightness then can cause the rotator cuff to impinge on the
coracoracromial arch. Nonoperative
measures employing cuff strengthening and capsule stretching techniques
are frequently effective in symptom resolution.
This
clinical response tends to support impingement
as a secondary phenomenon.
Subcoracoid impingement,
superior glenoid impingement, impingement
related to malunions
around the
shoulder girdle, and impingement
seen in conjunction
with glenohumeral instability are situations in which rotator cuff impingement occurs as a result of other intrinsic
shoulder pathology.
Rotator cuff vascularity does not appear to play a primary role in cuff degeneration.
However, the deficiency
in the usually abundant blood and nerve supply in the
subacromial bursa adjacent to partial rotator cuff tears
may propagate degeneration once it is initiated.
It appears that either microtrauma or macrotrauma can
participate in the development or exacerbation of rotator
cuff lesions through partial or full-thickness tears or as a
causative role in subacromial bursitis.
Authors differ as
to the relative importance of trauma.
Suprascapular nerve palsy and fixed or dynamic scapular abnormalities can be involved in the initiation or exacerbation of impingement.
A multifactorial etiology of rotator cuff lesions, including the impingement
syndrome, is evident.
It is likely
that the relative importance
of the numerous factors
listed vary from patient to patient.
However, essential
roles can be ascribed to a decrease in the humeral head
depressor mechanism of the rotator cuff and capsular
tightness.
Rotator cuff impingement
can be primary or
secondary.
After a thorough review, it appears that secondary occurrence is more common than traditional concepts dictate. Once initiated a vicious cycle can ensue,
with further loss of motion, decrease in cuff strength, and
subacromial crowding, thus exacerbating impingement.

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AND BENNETT