Internal impingement in the shoulder

Gordon Edelson, MD, and Cecile Teitz, PhD, Tiberias and Tel Aviv, Israel

Current wisdom holds that the acromion is a major factor in

the development of rotator cuff impingement. From the examination of a large number of skeletal specimens (1232 shoulders), we conclude that this view may require some modification. It appears that internal impingement between the glenoid and the humeral head may also be a significant
mechanism in the development of rotator cuff pathosis. We
present here the evidence for this internal impingement, which
is expressed in characteristic telltale patterns impressed into
the bones on both sides of the joint. If this thesis is correct, the
rationale for some acromioplasty operations may be called
into question, currently the most popular procedure in shoulder surgery. (J Shoulder Elbow Surg 2000;9:308-15.)

Neer

surface bony mechanism does exist and may constitute

the missing link in the etiology of rotator cuff disruption
from the undersurface. The term internal impingement
aptly describes this process. This term has been used in
a similar but more limited extent in studies by Jobe,12
Walch,28 and others to describe what they observed
arthroscopically and experimentally as the greater
tuberosity contacts the superior posterior glenoid during
abduction maneuvers, particularly in athletes. These
observations have been extended recently by Budoff et
al2 to include contact along the anterior as well as the
posterior superior glenoid; those authors emphasized
that such contact also takes place during ordinary,
nonathletic activities. Our study will further expand and
illustrate these observations.

19

popularized the concept of external impingement of the rotator cuff against the overlying acromion
as the principal cause of rotator cuff tears. This concept
superseded the previous theory, associated with Codman,3 which held that rotator cuff tears originated from
wear and tear changes on the underside of the cuff
rim rents at the tuberosity insertions. This debate as to
etiology has occasioned much comment and research
over the years.1,16,21 It is of more than simple academic interest because the notion of the acromion as the
main culprit in producing tears underpins the operation
of acromioplasty, the most common surgical procedure
performed in the shoulder today.
Sophisticated recent histologic studies of the cuff 9,18
substantiate the contention that the vast majority of tears
originate from the undersurface rather than from the
acromial side. Similarly, the bulk of recent arthroscopic
observation tends to support this view.8 However, no
cogent mechanism has yet been proposed to rival or
replace the presence of hooks and exaggerated
curves on the overlying acromion and the fact that the
humeral head rises up to meet the corocoacromial arch
in the end stages of rotator cuff disease.
This work, based on the study of a large number of
skeletal specimens, seeks to demonstrate that an underFrom the Department of Orthopaedics, Poriya Government Hospital, Tiberias (Dr Edelman), and the Department of Anatomy and
Anthropology, Sackler School of Medicine, Tel Aviv (Dr Teitz).
Reprint requests: Gordon Edelson, MD, Kibbutz Deganya Bet,
M.P. Jordan Valley, 15130, Israel.
Copyright 2000 by Journal of Shoulder and Elbow Surgery
Board of Trustees.
1058-2746/2000/$12.00 + 0 32/1/105449
doi:10.1067/mse.2000.105449

308

MATERIALS AND METHODS

Specimens were obtained from the Terry Collection at
the Smithsonian Museum in Washington, DC, the Cobb
Collection at the Howard University in Washington, DC,
the Todd Collection at the Museum of Natural History in
Cleveland, Ohio, and the Department of Anatomy and
Anthropology of the Sackler School of Medicine in Tel Aviv,
Israel. Most of the specimens were collected for teaching
purposes during the first part of the last century. In all, more
than 6000 skeletons were available; from these, 616 individuals (1232 shoulders) were selected at random. The
age range of the selected specimens was 45 to 95 years;
the mean age was 51 years. A full skeleton was available
in each case. There were 206 females and 410 males.
Sex, age, occupation, and cause of death were available
in all but 15 cases. Work histories involving high levels of
occupational stress (such as laborer or laundress) were
noted in 374 specimens.
In every shoulder, with or without bony evidence of rotator cuff disease, the scapula and humerus were held manually in physiologic congruencyie, the midpoint of the
humeral head was maintained at the level of the midpoint of
the glenoid face (the dead meridian plane17); the joint was
then systematically taken into 11 different positions simulating common joint postures assumed during activities of daily
living (Table I). These postures were combined in varying
degrees: flexion, extension, abduction, horizontal adduction,
and internal and external rotation. Thirty (30) specimens, 15
with bony evidence of rotator cuff pathosis and 15 without
such evidence, were then examined in these positions in a
more quantitative fashion (Table II): the scapula was fixed in
a vice with the glenoid perpendicular to the floor, and humeral positioning was measured by means of transparent
goniometers. Areas of impingement between the humeral
head, glenoid, and acromion were recorded.
Two clinical tests were included in these range-of-motion

J Shoulder Elbow Surg

Volume 9, Number 4

studies: the Neer Impingement Sign,20 which consists of

full forward flexion of the humerus on a fixed scapula, and
the Hawkins Impingement Test,10 which consists of forward
flexion of the humerus to shoulder level plus forced internal
rotation. The Neer and Hawkins simulations were done in
2 forms: in the plane of the scapula (trial 1) and 45
degrees anterior to the scapular plane (trial 2). This was
done to take into account the variable ways in which these
tests are actually performed clinically.
Descriptive statistics were compiled for the mean, SEM,
SD, and minimum and maximum values (Table II). Each
measurement of humeral motion was rounded off to the
nearest degree. Contact positions on the glenoid were
expressed as a simulated right glenoid clock face and
rounded off to the nearest half hour.

OBSERVATIONS
Bony evidence of rotator cuff pathosis was noted in
34% of specimens (419 humeri). This evidence consisted of the following: on the humeral head side, craterlike
areas and bone resorption in the rotator cuff sulcus5,24;
areas of appositional new bone formation and osteophytes surrounding the head,4 irregularity, pitting, and
spur formation at the tendon attachment zones30 and
rounding off and eburnation of the tuberosities from
early to end stage degree.7 These changes on the
humeral head side were accompanied by characteristic
osteophytic changes on the glenoid side, subsequently
to be described.
Table I documents the areas of impingement between
the humeral head vis-a-vis the glenoid and/or the
acromion, which were seen when the 30 shoulders tested quantitatively were taken through the ranges of
motion selected for this study.
Some highlights of the results, which are summarized in Table I, are as follows:
With the scapula perpendicular to the floor and the
humerus in neutral rotation (test 1, Table I), abduction in
the scapular plane was only possible to approximately
90 degrees (Figure 1). Further motion was blocked by
forceful impingement between the supraspinatus facet
of the greater tuberositythe area where rotator cuff
tears usually first appearand the superior glenoid at
or just posterior to the biceps anchor site. External rotation allowed additional abduction (test 2, Table I), but
this too was eventually blocked by supraspinatus facet
impingement further posterior on the glenoid face (Figure 2). External rotation in abduction was thus obligated not to clear the greater tuberosity from impingement
under the acromion but rather to release it from
impaction against the superior aspect of the glenoid.
Impingement against the acromion took place only at
the extremes of external rotation and flexion, usually
outside a normal physiologic range of motion.13 Furthermore, no acromion, with or without a hook, made
actual contact with the rotator cuff insertional areas of
the head. Contact with the acromion, when it did occur,
took place farther down, at the surgical neck area of the

Edelson and Teitz

309

humeral shaft, well beyond the rotator cuff insertion (Figure 3; test 3, Table I).
Of crucial importance in substantiating the reality of
internal impingement was the fact that a number of the
head specimens showing evidence of rotator cuff disease (118 of 419) also demonstrated a telltale geographic pattern of osteophyte formation on their superior surfaces (Figure 4). This pattern fit like pieces of a
jigsaw puzzle to adjacent areas of impingement on the
glenoid side, as demonstrated during the range-ofmotion portion of the study. The pattern was not seen
distinctly in every case of rotator cuff disease. In the
early stages of disease, it had evidently not yet been
impressed into the bone; in the end stages of disease,
it was obscured by osteophyte proliferation and wearing away of the tuberosity (Figure 5). Only because of
the opportunity afforded here to examine a very large
number of specimens, demonstrating all stages of bony
rotator cuff pathosis, did this pattern become evident.
Of the specimens demonstrating bony signs of rotator cuff disease on the humeral side, it was observed
that the glenoid side showed a characteristic osteophytic pattern in 126 specimens. This pattern consisted
of a ring of osteophyte that was most evident in the posterior superior quadrant (Figure 6). This was the area
where internal impingement by the head against the
glenoid was most often demonstrated during the rangeof-motion tests. This posterior glenoid osteophyte was
usually not large, but in a number of cases (18 specimens) it was extremely prominent (Figure 7).
The most superior portion of the glenoidthat part
of the bone protected from direct impact with the head
by the overlying biceps insertionusually presented a
hiatus in the superior ring of glenoid osteophyte (Figure
8). In front of this biceps hiatus, along the anterior
superior quadrant, the ring of glenoid osteophyte was
less prominent but tended to regain substance distally,
reflecting most probably the internal impingement
demonstrated on the range-of-motion studies to take
place in this area. For example, in the arm at the side
position, internal rotation (necessary to reach a pocket
behind the back) resulted in impingement between the
chondral margin of the head just medial to the lesser
tuberosity and the middle glenoid rim (Figure 9). With
the addition of extension (necessary to reach higher up
the back) of the humerus to 45 degrees, the lesser
tuberosity itself was forced against the anterior inferior
glenoid rim (Figure 10; test 11, Table I).
Consistent signs of roughness and wear were noted
on or adjacent to the lesser tuberosity in most cases
(176 specimens) of moderate to severe rotator cuff disease (Figure 5). These changes sometimes spilled over
into the area of the bicipital groove (31 specimens),
with roughening and osteophyte formation along its
medial wall and, less commonly, along its lateral wall
(Figure 5 and Figure 8, B).
The Hawkins Impingement Test (test 10, Table I) usu-

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J Shoulder Elbow Surg

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Table I Internal and external impingement: summary of positions tested and demonstrated areas of contact
Test
no.

Position of glenohumeral joint

(glenoid fixed perpendicular to floor)

Position of
transepicondylar elbow axis

Full abduction in scapular plane

Anatomic position

Full abduction in scapular plane

Full abduction in scapular plane; Neer Sign trial #1

30 external rotation (anatomic position

+ 30 external rotation)
60 external rotation

Full abduction 45 anterior to scapular plane;

Neer Sign trial #2

60 external rotation

Full abduction 45 anterior to scapular plane

Anatomic position

Horizontal adduction beginning in scapular plane

Anatomic position

20 abduction in scapular plane; Arm at side position

Begin: anatomic position, then internally rotate

20 abduction in scapular plane; Arm at side position

Begin: anatomic position, then externally rotate

80 abduction in scapular plane; Hawkins Test trial #1

10

80 abduction, 45 anterior to scapular plane;

Hawkins Test trial #2

Begin: epicondylar axis parallel to floor,

then internally rotate
Begin: epicondylar axis parallel to floor,
then internally rotate

11

Abduction 20 and extension 45 from scapular plane

Begin: anatomic position, then internally rotate

*Beyond physiologic range of motion.13,14

ally created internal impingement between the lesser

tuberosity and the anterior superior glenoid (Figure 11).
During the Neer maneuver in the scapular plane (test 3,
Table I), acromial contact was not common, but did
occasionally take place within a physiologic range of
motion13 (Figure 12). This depended on anatomic variables, such as acromial size, slope, and offset from
glenoid.6 This acromial contact usually took place
simultaneously with an element of internal impingement
against the glenoid (Figures 3 and 12). When the Neer
maneuver was performed at 45 degrees anterior to the
scapular plane, acromial contact took place consistently, but only when the skeletal specimens were moved
well beyond a physiologic range of motion.

DISCUSSION
Although this type of work would benefit from
additional clinical correlation and could also be
strengthened by dissection, biomechanical, and
imaging studies, it nonetheless gives valuable information that cannot be observed by other means. The
unique patterns of osteophyte formation on both the
humeral head and the glenoid side, exactly paralleling the areas of impaction demonstrated between the
two during simulated range-of-imotion maneuvers,

appear to confirm the observation that internal

impingement is a real and substantial phenomenon.
Internal impingement may also provide an alternative mechanism underlying the Neer and Hawkins tests.
It appears that when bony contact occurs in these
maneuvers, it most commonly takes place between the
tuberosity insertion sites and the glenoid rim. When the
humeral head is maintained in the glenoid cavityas
is the case in vivo, except with significant preexisting
disease or inordinate stresses17the acromion itself
does not make actual contact with the rotator cuff insertional areas where tears begin (Figure 13).
At the extremes of normal shoulder motion, further
movement is constrained by the capsular-ligamentous
complex and/or by bony contact. It is this latter bony
backup that we have demonstrated. The acromion
does not appear to do this job. When the ordinary
range of motion concludes, the cartilage surfaces are
fully engaged29 and the head rides over the edges of
the glenoid onto the soft tissues.26,29 This presumably
provokes the bony changes we have noted. These
changes are probably added to by osteophytes stimulated particularly around the lower half of the humeral
head and the glenoid ring, where the most substantial
portions of the capsular ligamentous complex attach.

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J Shoulder Elbow Surg

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Contact between supraspinatus facet

of greater tuberosity and glenoid
Contact at 93 abduction with glenoid
at 12:00 oclock
Contact at 100 abduction with glenoid
at 11:00 oclock
Contact at 118 abduction with glenoid
at 10:00 oclock in 26 of 30 specimens

No contact
No contact
No contact
No contact
No contact within physiologic range
of rotation
No contact
Contact at 75 internal rotation
with glenoid at 12:30 oclock in
25 of 30 cases
No contact

Contact between lesser

tuberosity and glenoid

311

Contact between acromion

and proximal humerus

No contact

No contact

No contact

No contact

Contact at 112 abduction

with glenoid at 10:00 oclock
in 18 of 30 specimens

Contact anterior lateral acromion against lateral

biceps groove at surgical neck of humerus at
120* abduction in 18 of 30 specimens
simultaneous with tuberosity(s) contact in
14 of 30 cases, without tuberosity contact
in 4 cases
Contact anterior lateral acromoin against medial
bicipital groove at surgical neck of humerus at
146* abduction in 24 of 30 specimens
No contact

Contact at 130* abduction

with glenoid at 10:00 oclock
in 7 of 30 cases
Contact at 115 abduction with
glenoid at 12:30 oclock
Contact at 52 adduction with
glenoid at 1:30 oclock
Contact at 64 internal rotation with
glenoid at 2:00 oclock
No contact within physiologic
range of motion
No contact
Contact at 81 internal rotation with
glenoid at 3:00 oclock in 15 of 30
casessimultaneous with greater
tuberosity contact in 10 cases
Contact at 79 internal rotation with
glenoid at 5:00 oclock

No contact
No contact
No contact within physiologic range of motion
No contact
No contact

No contact

Table II Descriptive statistics (referable to tests summarized in Table I)

Test no.
1
2
3

4
5
6
7
8
9
10

11

No. of specimens
30
30
30
30
26
26
18
18
18
1
29
30
30
30
30
30
No contact
No contact
25
25
15
15
30
0

Point of impingement

Minimum

Maximum

Mean

SD

G
C
G
C
G
C
L
C
A
L
A
L
L
C
L
C

85
11:00
94
10:00
108
11:00
108
9:00
114

120
100
40
1:00
50
12:30

96
1:00
113
1:00
128
1:00
117
11:00
128

178
125
64
2:30
75
3:00

93
12:00
100
11:00
118
11:30
112
10:00
120
130
146
115
52
1:30
64
2:00

2.673
0.468
4.313
0.547
3.439
0.477
3.219
0.589
4.098

7.880
5.151
5.451
0.401
4.769
0.493

L
C
G
C
L
C

64
12:00
64
2:00
64
4:30

95
1:00
95
5:00
95
5:30

75
12:30
81
3:00
79
5:00

5.251
0.485
5.151
0.796
5.436
0.527

G, Greater tuberosityhumeral elevation or rotation at contact, expressed in degrees; L, lesser tuberosityhumeral elevation or rotation
at contact, expressed in degrees; A, acromionhumeral elevation at contact, expressed in degrees; C, point of contact on simulated
right glenoid clock face, expressed in hours.

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Figure 3 In this specimen (test 3, Table I), humeral scapular

Figure 1 Humerus abducted to 90 degrees in scapular plane with
scapula fixed so that glenoid is perpendicular to floor (test 1, Table
I). Arrows indicate area of internal impingement between supraspinatus facet of greater tuberosity and superior glenoid at approximately 12 oclock position. b, Bicipital groove.

abduction is blocked at 108 degrees by a combination of two factors that appear to occur simultaneously: (1) internal impingement
in jigsaw puzzletype fit between lesser tuberosity (l) and superior
posterior glenoid at 10:30 oclock position, where glenoid osteophyte (o) has formed; and (2) external impingement between anterior lateral acromion and surgical neck of humerus (arrowhead) in
area of bicipital groove.

Figure 2 With 30 degrees of external humeral rotation (test 2,

Table I), further humeral abduction in scapular plane to 100 degrees
is allowed before internal impingement again takes place (arrows)
between supraspinatus facet of greater tuberosity and superior glenoid at 10:30 oclock position in this specimen. b, Biceps groove.

The variability of this response is undoubtedly similar to

the wide variability among individuals in their tendency to lay down enthesopathic and/or osteophytic new
bone in other parts of the body.
This work offers a mechanical explanation and a
mechanism by which to explain the histologic and
arthroscopic observation that the rotator cuff begins
tearing from the underside. Our observations do not
replace etiologic considerations regarding age-related
changes or unique patterns of cuff blood supply15,22;
rather, they supplement these considerations. Nor does
such a concept deny that when the cuff is breached or
the muscles atrophy, the head then moves up to engage
in direct contact with the overlying acromion, the soft

Figure 4 Characteristic pattern of osteophyte formation on anterior superior aspect of humeral head suggestive of internal
impingement. Arrowheads indicate areas of impingement adjacent to greater and lesser tuberosities. These areas interdigitated
in jigsaw-puzzle fashion with superior posterior and/or superior
anterior rim of glenoid during range-of-motion testing. Area covered by biceps tendon as it emerges from its groove is relatively
free of osteophyte during this stage of disease process.

tissue arch, and occasionally the coracoid, resulting in

secondary external impingement and the production or
extension of tearing. As the head moves up and the
mechanics of the impingement process change, the
posterior superior glenoid osteophyte may increase in
size, especially in those individuals with a propensity to
lay down new bone (Figure 7).
This concept of internal impingement also provides

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Edelson and Teitz

313

Figure 7 Right scapulae from 2 different individuals. Arrows indicate more dramatic examples of posterior superior osteophyte formation in specimens demonstrating more advanced rotator cuff disease.

Figure 5 Later stage in evolution of humeral head osteophyte. Initial jigsaw-puzzle pattern (seen in Figure 4) has been superseded
by a more proliferative ring of osteophyte, which has spilled
across bicipital groove and extended onto lesser tuberosity. Note
also wearing away and rounding off of greater tuberosity.

Figure 6 Left scapulae from 2 different individuals. Arrows indicate characteristic posterior superior glenoid osteophyte reflecting
internal impingement of humeral head against this area.

additional food for thought regarding the etiology of

slap lesions,25 biceps tendon tears,23 and the increasing appreciation of the subscapularis component in
rotator cuff pathosis.27
If impingement, except in its latter stages, does not
involve the acromion, then perhaps acromioplasty, the
most common operation on the shoulder today, is a
procedure somewhat overdone. If we need to address
the acromion for its secondary role in exacerbating

Figure 8 A, Arrow indicates characteristic hiatus in glenoid osteophyte in area presumably protected by biceps anchor from direct
forces of internal impingement. B, Glenoid hiatus is articulated with
adjacent hiatus on humeral head side created by bicipital
groove (b), seen here in 90 degrees of humeral abduction.

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Figure 11 During Hawkins Test (test 10, Table I), internal

impingement takes place between lesser tuberosity and anterior
superior glenoid (arrow).

Figure 9 Internal rotation with arm slightly abducted (test 7, Table

1), as would be required for placement of an arm behind back, here
causes internal impingement between anterior glenoid margin and
humeral head adjacent to lesser tuberosity (1). b, Biceps groove.

Figure 12 Neer Sign (test 3, Table I) demonstrates imminent contact about to take place between lesser tuberosity and glenoid
(arrowhead indicates intemal impingement) and between anterior
lateral acromion and proximal humeral shaft (arrow indicates
external impingement).

Figure 10 Further extension, as would be required to reach higher up the back, jams lesser tuberosity into anterior inferior glenoid
(arrowhead), here illustrated in individual with bony evidence of
advanced rotator cuff disease.

rotator cuff disease, it may be sufficient to smooth the

bone down if it is roughas nature itself appears to try
to do. Alternatively, if we need to gain additional clearance after a malunited tuberosity fracture or an iatrogenically bulked-up rotator cuff repair, minimal bone
removal may be the wisest course. We might then
avoid many of the complications associated with overly aggressively surgery in this area.

The mechanisms of internal impingement noted here

can be confirmed on most office or departmental teaching skeletons. Care must be taken in this regard, however, because such skeletons are often assembled from
parts of different individuals and thus may not reflect
the true natural relationships. It is our good fortune to
have available large museum collections that offer the
opportunity for more careful and extensive observations, together with insights from the telltale patterns left
etched in the bones.
We greatly appreciate the help and contributions of the
following people: Drs D. Ortner and D. Hunt of the Smithsonian Institution, Washington, DC; Dr M. Blakey and M.
Mack, MA, of Howard University, Washington, DC; Dr B.
Latimer and L. Jellema, MA, of the Museum of Natural
History, Cleveland, Ohio; and Drs I. Herskovitz and J. Rak
of the Tel Aviv University, Israel. Sincere thanks as well to
Ms Lucy Yoram and Mrs Robyn Rubin for their technical
assistance and to D. Zirhen for his photographic help.
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Figure 13 Neer Impingement Sign, as seen fluoroscopically.

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