Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_138_библиотеки_им_акад_М_И_Перельмана
.pdf
in elite throwing athletes when compared to their
https://t.me/med1917
non-throwing counterparts, with both glenoid and
humeral retroversion. ese occur in conjunction
Figure 2.
with soft tissue adaptations and potentially play
a role in internal impingement in the overhead
14
athlete.
Humeral retroversion does not contribute to
15
instability as much as glenoid changes.
But, there
is potential for increased mechanical compression
of the supraspinatus tendon at 60° and 90° of
shoulder elevation and pathogenesis of articular
sided rotator cuff disorders with increased humeral
16
retroversion.
It has been well documented that
humeral retroversion is commonly increased on the
2,4
dominant side and more pronounced in throwers.
For the throwing athlete, there is a significant sideto-side difference in external and internal rotation
ROM secondary to humeral retroversion on the
4
throwing arm.
Increased humeral retroversion is
associated with a loss of IR and concomitant increase
15
in ER ROM.
It is important for the clinician
to understand the potential bony morphological
A, In abducted and external rotation end ranges, the glenoid pushes
the cuff tendon at its insertion by 16% of the glenoid width, the
remaining 84% of the glenoid articulates with the humeral head,
defined as the glenoid track. B, When a glenoid defect exists, the
defect width (a) should be subtracted from the 84% length to obtain
a true glenoid track width (b).
*Adapted from Yamamoto et al.22 Illustration by Kinslter Design.
changes that may affect ROM and to know when
and why interventions may not be effective.
In addition to soft tissue disruption following
a traumatic instability event, osseus injuries may
occur. e Hill-Sachs lesion, compression fracture of the
posterosuperior aspect of the humeral head, occurs in the
majority of anterior-inferior shoulder dislocation as the humeral
head contacts the dense cortical glenoid when displaced.
17
Reverse Hill-Sachs lesions, a compression fracture of the
anterosuperomedial side of the humeral head, can occur up to
17
86% of the time in cases of posterior shoulder instability.
It
has been shown that defects as small as 12.5% of the humeral
18
head surface area may affect biomechanical stability.
Surgery
may be warranted in cases of recurrent instability to address
both compromised capsulolabral complex and osseus lesions.
17
After instability incidents, the glenoid can also sustain a
bone loss. While some bone defects are common, glenoid bone
loss greater than 20-25% should be addressed surgically with
bone augmentation procedures to restore normal anatomy.
19-21
In 62% of cases of recurrent dislocation, both a glenoid and
20
humeral bone lesion were identified.
us, an interaction
(combination) of both glenoid and humeral bone lesions can be
problematic and has been described with the “Glenoid Track”
18,22
concept.
e glenoid track consists of 84% of the width of
the normal glenoid where the humerus contacts, with the 16%
remaining for the rotator cuff insertion when in an abducted
22
and externally rotated shoulder position (Figure 2).
Bony
defects of the anterior glenoid would decrease the glenoid track
width. A Hill-Sachs lesion that is smaller than and within the
track is thought to maintain contact with the glenoid, with
18
lower risk of recurrent instability (“on track”).
A shoulder with
Glenoid Track Concept
a Hill-Sachs lesion that is larger than the glenoid track is at
increased risk of instability and the lesion can engage with the
anterior glenoid rim (“off track”).
18
Patients undergoing surgical
soft tissue capsulolabral repair procedures (Bankart repair) are
at risk for recurrence of instability with off track lesions because
bony lesions are not adequately addressed with these procedures.
Surgeons frequently address bone deficits using procedures like
the Latarjet
21
surgical reconstruction that is discussed later in
this monograph.
Acromioclavicular and sternoclavicular anatomy
e acromioclavicular (AC) joint is comprised of the distal
end of the clavicle and the medial portion of the acromion.
23
Static restraints to movement include a lax capsule that surrounds
the joint as well as individual portions of the AC ligaments.
e AC ligaments include superior, inferior, anterior, and
24
posterior structures and attach from the anteromedial edge
of the acromion to the lateral edge of the clavicle. e AC
ligaments provide stability in an anterior posterior direction.
Further stability is provided by the coracoclavicular (CC)
ligaments though these are not directly attached to the AC
joint or capsule.
23
e CC ligaments have 2 portions, the
conoid ligament medially and trapezoid ligament laterally.
Both CC ligaments provide restraint to superior inferior forces;
however, the conoid more than the trapezoid.
23
Movement in
the AC joint is relatively small when compared to GH joint
or scapulothoracic joint motion. In addition to motion around
the sternoclavicular (SC) joint, the clavicle rotates posteriorly
Academy of Orthopaedic Physical erapy, APTA.
For personal use only. No other uses without permission.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
9
5-8° in relation to the acromion during humeral elevation in
https://t.me/med1917
the scapular plane.
25
e SC joint is the only direct articulation between the
shoulder and axial skeleton. e clavicle articulates with the
sternum and superior surface of the first costal cartilage. As
with the AC joint, the articulation between the clavicle and
26
sternum is not congruent.
Between the articular surfaces
resides a fibrocartilaginous disc that attaches to both the clavicle
and first costal cartilage. Elevation and depression occurs
primarily between the clavicle and articular disc; protraction
and retraction occurs primarily between the articular disc and
26
sternum.
In addition, posterior rotation of the clavicle occurs
on the sternum during humeral elevation.
Acromioclavicular and sternoclavicular pathoanatomy
Acromioclavicular joint injuries occur secondary to
trauma, such as a direct fall on the shoulder. Rockwood
described AC joint injuries with Type I injuries involving a
sprain to the AC ligament that may be stretched or partially
27
No appreciable displacement is noted. A type II injury
torn.
is considered when the AC ligament is completely torn, while
27
the CC ligaments are stretched but remain intact.
ere may
be mild displacement of the AC joint that may not be obvious
during a physical examination. With Type III sprains, both AC
and CC ligaments are ruptured and there is complete separation
27
of the AC joint.
When the AC ligaments, CC ligaments, and
the capsule surrounding the AC joint are torn, the displacement
of the distal end of the clavicle is usually obvious on clinical
examination. Without any ligamentous support, the shoulder
falls under the weight of the arm and the distal clavicle may
appear to be elevated, termed step deformity, and demonstrate
23
up to 25% separation on a radiograph.
Secondary to the
proximity to the brachial plexus, concurrent plexus injuries
should be appropriately screened.
e AC joint is a diarthrodial joint, with a concave-convex
relationship of the acromion to clavicle, respectively. e joint
space contains an intraarticular disc; interestingly, the inherent
incongruency of this disc contributes to the high rate of early
24
degenerative changes at the AC joint.
At 70° of GH joint
abduction, the rotator cuff contacts the inferior surface of the
28
AC joint.
is proximity to potential degenerative changes
of the AC joint (bone growth and osteophytes) may implicate
its role in the development of subacromial impingement in the
older population.
24
e SC joint has incongruent joint surfaces, a location
close to midline, and the presence of 4 ligaments (anterior SC,
posterior SC, costoclavicular, and interclavicular) that encase the
26
joint making it an inherently stable joint.
Traumatic injuries
to the SC joint are rare in comparison to GH joint or AC joint
injuries. In fact, more often the clavicle will fracture before the
26
surrounding SC joint ligaments fail.
Anterior dislocations,
that occur via indirect forces, greatly outnumber posterior
dislocations, which occur via direct forces such as motor vehicle
collisions and sports related injuries. Posterior dislocations can
have life threatening consequences such as pneumothorax,
26
vascular injury, or brachial plexus injury.
Atraumatic causes of
SC joint pain are frequently accompanied by OA changes which
29
in cadaveric studies show a high prevalence with age.
Like other
peripheral synovial joints, the SC joint may demonstrate signs
of inflammation due to systemic inflammatory conditions such
as rheumatoid arthritis, psoriatic arthritis, and septic arthritis.
26
Glenohumeral ligaments
Glenohumeral ligaments and the long head of the biceps
attach to the labrum. e superior, middle, and inferior GH
ligaments insert around the periphery of the glenoid and the
anatomic neck of the humerus. ese ligaments are considered
focal thickenings of the GH joint capsule. In the anterosuperior
portion of the glenoid, the superior GH ligament can extend
from the anterosuperior labrum, the biceps tendon attachment,
30
or the middle GH ligament.
Due to its orientation, the
superior GH ligament provides contributions to inferior GH
stability in neutral rotation and 0° shoulder abduction. e
superior GH ligament, coracohumeral ligament, and distal
subscapularis tendon blend to form a “pulley” that stabilizes
the biceps tendon prior to its entry to the bicipital groove.
31
e coracohumeral ligament is extracapsular but fuses with the
32
capsule at the rotator cuff interval.
e rotator cuff interval is a
triangular portion of the capsule between the supraspinatus and
subscapularis that additionally stabilizes the GH joint as shown
32
in Figure 3.
Capsular anatomy can vary here also, with 59%
of individuals demonstrating a rotator cuff interval opening
32
superolateral to the middle GH ligament.
Inferior to the superior GH ligament, the middle GH
ligament stretches obliquely from the mid-anterior labrum
and glenoid fossa to the inferior aspect of the lesser tuberosity
of the humerus. Of the ligaments of the shoulder, the middle
GH ligament is the most variable in morphology. Commonly,
it may have a conjoined origin with the superior GH ligament
or the biceps tendon; it also may be thickened and cordlike
in conjunction with a Buford complex (congenital labrum
variant where the anterosuperior labrum is absent from 1 to 3
1
“o-clock”).
e middle GH ligament contributes to GH joint
stability most when the shoulder is abducted 45° and externally
rotated.
e inferior GH ligament consists of an anterior and
posterior band with redundant capsular tissue between the two.
e inferior GH ligament complex can have a “collar-like” or
33
“V-shaped” attachment on the humerus.
Originating from
the glenoid rim and labrum, its anterior band is between the
2 and 4 o’clock position and posterior band between the 7 and
1
9 o’clock position.
e inferior GH ligament complex is the
main GH joint stabilizer resisting inferior GH joint translation.
e anterior band resists anterior translation of the humeral
head when the shoulder is abducted to 90° and externally
34
rotated.
e anterior band is thicker and has the highest
10
Academy of Orthopaedic Physical erapy, APTA.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
For personal use only. No other uses without permission.
Figure 3.
https://t.me/med1917
e Rotator Cuff Interval (dashed line)
is Located Between the Supraspinatus and
Subscapularis*
Abbreviations: CHL, coracohumeral ligament; IGHL, anterior
inferior glenohumeral ligament; LBT, long biceps tendon; LCHL,
lateral coracohumeral ligament; MCHL, medial coracohumeral
ligament; MGHL, middle glenohumeral ligament; SGHL,
superior glenohumeral ligament; SSC, subscapularis tendon; SSP,
supraspinatus tendon
*Adapted from Tamborrini et al.
455
Illustration by Kinstler Design.
tensile strength of the inferior GH ligament complex fibers.33
e posterior band resists posterior translation with the arm
flexed and internally rotated.
34
Glenohumeral ligamentous pathoanatomy
e axillary pouch, coracohumeral ligament, and
rotator cuff interval are often implicated in idiopathic frozen
shoulder.
33,35
e thickness and enhancement of these tissues
can be noted on magnetic resonance imaging (MRI) and
demonstrate a negative association with ER ROM.
35
If
arthroscopic surgery is warranted for this condition, the rotator
cuff interval will often be released.
GH ligament contracture, limited ER ROM is evident.
32
With anterior inferior
30
If
the posterior band of the inferior GH ligament is shortened
or contracted, it can lead to internal impingement as well as
increased shear forces on the labrum.
33
e effects of GH joint hypomobility on upper extremity
kinematics will be discussed later in the section labeled
scapulohumeral rhythm. Regarding GH joint instability,
historically injuries have been placed into 2 categories or “labels”:
Traumatic, Unilateral, Bankart lesion, Surgery (TUBS) and
Atraumatic, Multidirectional, Bilateral, Rehabilitation, Inferior
capsular shift (AMBRI).
36
However, it may be more beneficial
and all-encompassing to consider categorization based on:
direction (uni- or multi-directional instability [MDI]), etiology
(traumatic or atraumatic), frequency (primary or recurrent),
37,38
and severity (subluxation or dislocation).
e presence or
absence of underlying soft tissue laxity or connective tissue
disorder should be a consideration. e parameters that define
MDI continue to be debated; however, are conventionally
defined as instability in at least 2 directions.
39
Capsulolabral injuries are common with trauma and
unidirectional subluxation/dislocation incidents. Anterior
instability events typically implicate the anterior inferior
GH ligament and account for 95% of all shoulder instability
39
diagnoses.
e anterior inferior GH ligament can be
compromised in positions of combined shoulder abduction
and ER. Posterior instability events, though far less common,
typically implicate the posterior inferior GH ligament. e
posterior inferior GH ligament stabilizes the shoulder when in
a position of flexion and IR, as seen when football linemen are
5
blocking.
An avulsion of the anterior band of the inferior GH
ligament that occurs with the labrum is called a Bankart lesion;
if this occurs with an avulsion of the anterior aspect of the
glenoid, the term Bony Bankart is used. e impact of glenoid
bone loss on recurrent instability is discussed later in this
monograph. A “Reverse Bankart” is defined as a capsulolabral
lesion involving the posterior labrum and posterior inferior GH
ligament and likewise, with an avulsion fracture of the glenoid,
the term “Bony Reverse Bankart” is used.
5
Less common capsulolabral injuries can occur after a
traumatic GH joint dislocation. Isolated GH joint ligament
tears are commonly seen in patients over 40 years of age and are
40
associated with rotator cuff tears in those over the age of 50.
Isolated inferior GH ligament tears has been shown to account
for 9% of cases of anterior instability and 35% of patients
33
presenting with anterior instability without labral pathology.
Injuries to the inferior GH ligament are varied. In a cadaveric
biomechanical study, proximal glenoid avulsion injuries were
shown to occur in 40% of inferior GH ligament injuries, distal
humeral avulsion injuries (HAGL) occurs in 25% of them, and
mid-substance or axillary pouch tears occurs in another 35% of
41
those ligament injuries.
Variations in the location of avulsion
can occur as well, with a “reversal” of the injury involving the
33
posterior inferior GH ligament complex.
Recurrent instability
following a surgical soft tissue anterior stabilization (Bankart
repair), can be due to these other subtle variations in injury
presentation.
Labrum
e labrum is a fibrocartilaginous structure that outlines
the periphery of the pear-shaped glenoid. e cross-sectional
profile of the labrum is triangular and slopes upwards around
the periphery of the glenoid. e labrum acts as a buttress to
excessive translation of the humeral head on the glenoid. e
depth of the glenoid fossa is increased by 50% due to the
orientation and profile of the labrum, providing stability to
Academy of Orthopaedic Physical erapy, APTA.
For personal use only. No other uses without permission.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
11
an inherently unstable GH joint.
https://t.me/med1917
42,43
Superiorly, the labrum
is more loosely attached while inferiorly the labrum is firmly
affixed to the articular cartilage.
to the supraglenoid tubercle as well as to the superior labrum.
42
e biceps footprint extends
42
Dynamic stability of the labrum is controlled by the attachment
of the long head of the biceps tendon.
Labral pathoanatomy
With acute or repetitive trauma, the labrum can be torn
and the stability of the GH joint compromised. Labral tears
in the anterosuperior quadrant of the glenoid are recognized as
“superior labrum, anterior to posterior” (SLAP) lesions.
44
High
eccentric biceps activity, as noted in overhead throwing athlete,
contributes to the prevalence of SLAP lesion.
45
A theorized
“peel back” mechanism is also thought to contribute to the
prevalence of SLAP lesion.
46
With the shoulder positioned in
maximum shoulder abduction and ER during the late cocking
phase of throwing, the biceps insertion undergoes a torsional
force that subsequently pulls (or ‘peels’) back the labrum.
44
To
further highlight the complexity of the superior labrum and
biceps complex, a simulated SLAP lesion in a cadaveric model
was shown to increase the strain in the inferior GH ligament
complex and decrease its ability to resist ER forces.
47
us, the
clinician should ensure their prescribed rehabilitation program
addresses dynamic constraints to motion globally in efforts to
optimize stability of the GH joint.
Vascularization of the labrum has historically been reported
as sparse or poorly defined. But, in general, vascularization
is dense in the periphery of the labrum. Recent studies on
cadaveric labrum specimens (age range 76-90 years old) suggest
the anterosuperior labrum as having a “rich blood supply,”
with contributions from surrounding vasculature as well as the
underlying glenoid bone. is would suggest that certain labral
tears have the potential to heal.
43
However, it is difficult to make
conclusions based on the data from cadaveric studies because
only intact labral specimens were investigated. ere are other
contributing factors that may often reduce the success of nonoperative management including the type of labral tears, GH
joint instability, and a rotator cuff tear.
44
Free nerve endings are present within the labrum, providing
rationale as to why tears induce pain. It is speculated that the
sensory fibers may also play a role in GH joint proprioception.
48
A decrease in proprioception has been documented in cases of
shoulder instability and subsequent injury; and restoration of
proprioception occurs after stabilization surgery.
49
Additionally,
altered proprioception may be found not only on the affected
side, but also on the unaffected side, suggesting central
mechanisms may also be a factor in labral pathology.
49
Active Structures and Constraints to Movement
Rotator cuff anatomy
e layer of tissue directly above the GH joint capsule
is comprised of the rotator cuff. e rotator cuff consists
of 4 muscles: supraspinatus, infraspinatus, teres minor, and
subscapularis. e supraspinatus muscle originates on the
supraspinous fossa of the scapula, and inserts on the superior
and middle facets of the greater tuberosity.
50
e infraspinatus
and teres minor muscles originate on the infraspinous fossa
and insert on the middle and inferior facets of the greater
50
tuberosity.
e subscapularis muscle originates on the scapular
fossa and projects anteriorly to insert on the lesser tuberosity of
the humerus, medial to the bicipital groove, and has the largest
51
footprint of the rotator cuff tendons.
Traditionally, the rotator
cuff is described as having distinct insertion points as noted
above, however, surgical and cadaveric investigations suggest
there is interdigitation of the rotator cuff tendon insertions
with the capsule. us, defects of the rotator cuff, such as acute
or degenerative tears, affect all tissues in close proximity to the
lesion.
At the greater tuberosity, the supraspinatus and
infraspinatus tendons interdigitate and slightly overlap. Five
52
layers of tissue exist at this overlap zone.
Each layer has a
slightly different histological presentation, orientation of fibers,
and function, which allows for appropriate force transfer from
muscle to tendon to bone. e 5 layers distribute both the
compressive and tensile loads that the rotator cuff tendons
experience. Within the supraspinatus tendon, there are anterior
50
and posterior subregions.
e modulus of elasticity (measure
of stiffness) differs between these 2 regions, which can preserve
the shape of the tendon with multiaxial movements. Stiffness of
the supraspinatus tendon is higher on the bursal side as opposed
to the articular side, and higher anteriorly than posteriorly.
50
Within the rotator cuff tendons is a cable-crescent complex
that enhances the mechanical properties of the supraspinatus
tendon with important clinical implications for tendon tears.
e rotator cable is a thin, crescent shaped capsuloligamentous
structure, that runs posteriorly from the anterior insertion
of the supraspinatus footprint to the inferior border of the
infraspinatus footprint, perpendicular to the rotator cuff
50
tendons (Figure 3).
is cable connects the supraspinatus and
infraspinatus tendons to the head of the humerus. e rotator
cable has been considered as the “suspension bridge” for the
rotator cuff, with the suggestion that tears that do not involve
the cable insertions have less of an impact on function and
53
progression than those involving the cable.
Located between
the rotator cable and the tendinous insertions on the greater
tuberosity is the rotator crescent. is area is relatively avascular;
though it has been noted that vascular supply is greater on the
50,54
bursal side of the tendon.
Anatomically, the cable is 2.59
times thicker than the rotator crescent. e cable can “stress
shield” the thinner tissue within the crescent and increase the
32
area in which forces are distributed.
Stress shielding refers
to a stress transfer from the rotator cuff to the cable, which
shields stress from the thinner capsular and tendinous tissue
within the crescent. e cable-crescent morphology changes
12
Academy of Orthopaedic Physical erapy, APTA.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
For personal use only. No other uses without permission.
with age. In younger patients, the crescent is more robust and
https://t.me/med1917
not stress shielded as much by the cable. With age, the crescent
is much thinner compared to the cable and the cable is better
able to stress shield. us, this explains the nomenclature for
a crescent dominant rotator cuff in younger patients, and the
cable dominant rotator cuff in older patients.
Force couples
Force couples are defined as 2 forces directed in opposite
directions that create rotation of a joint in a specific direction.
If the forces are equal and opposite, the instantaneous center of
rotation is maintained. If the instantaneous center of rotation
is maintained, dynamic stability is intact throughout the ROM.
Several force couples specific to the shoulder are not directly
opposite to one another. However, the summation of the forces
about the GH joint are enough to cause compression of the
humerus on the glenoid. With compression of the humeral
head, the rotator cuff can function to generate torque necessary
for rotation of the humerus on the glenoid.
e subscapularis and infraspinatus muscles function
together as a force couple to provide dynamic stability to the
GH joint. ese muscles create a resultant compressive joint
reaction force within the transverse plane. e transverse
plane force couple resists the superior pull of the deltoid with
abduction and is a fulcrum for rotation of the humeral head
55
on the glenoid.
Within the force couple, the infraspinatus
prevents superior and anterior translation of the humeral head
56
and the subscapularis is involved in forward flexion.
e collective rotator cuff and deltoid muscles form
another force couple around the GH joint. e compression
force offered from the resultant force vector from the rotator
cuff offsets the forces of the deltoid and pectoralis muscles which
tend to destabilize the GH joint anteriorly and superiorly.
56
is mechanism is termed concavity-compression and applies
to muscles being the stabilizers in lower and mid-range GH
joint motions when capsuloligamentous structures are relatively
6
loose.
As mentioned previously, the long head of the biceps is
thought to provide stability to the GH joint. While a larger
role is still debated, there is general consensus that it specifically
provides stability to the GH joint when the shoulder is in a
57
combined position of abduction and ER.
Biomechanical
studies have shown that some superior and anterior humeral
head translation occurs during shoulder elevation without an
intact long head of the biceps.
57
Rotator cuff pathoanatomy
Pathology of the rotator cuff is common, and the spectrum
of cuff disease is wide-ranging. Prevalence rates of rotator cuff
injuries are associated with age: 5-10% of rotator cuff injuries
occur in patients younger than 20 years old, compared to more
58
than 60% in patients older than 80 years of age.
Rotator cuff
pathology has been attributed to both extrinsic factors and
59,60
intrinsic factors.
Extrinsic factors originate from outside
of the tendon, causing mechanical compression or shearing
on the tendons of the rotator cuff.
59,60
Neer’s classic theory on
subacromial impingement is an example of a mechanism of
injury related to an extrinsic factor.
61
Intrinsic factors of rotator
cuff pathology include alterations in biology, mechanical
properties, morphology, and vascularity.
60,62
Tendon changes
occur secondary to age, excessive tensile and shear forces, and
local cellular changes.
60,62
Other factors that increase the risk
for rotator cuff pathology are smoking, hypercholesterolemia,
and a family history of rotator cuff tears.
63
It is important
to understand the pathogenesis of rotator cuff disease is a
combination of these factors, unique to each individual.
Extrinsic mechanisms
e extrinsic impingement model was hypothesized
to be the mechanism behind rotator cuff pathology.
65
Neer
proposed that 95% of rotator cuff tears were caused by
61,64,65
impingement. As the subacromial space narrows with shoulder
elevation, the long head of the biceps tendon, GH ligament,
coracohumeral ligament, GH joint capsule, rotator cuff tendons,
and subacromial bursa impinge under the coracoacromial arch.
Subacromial impingement of these structures would occur
due to compression under the anterior aspect of the acromial
arch, resulting in inflammation, pain, and progressive tendon
degeneration. Variations in extrinsic factors, including acromial
arch shape, posture, and muscle performance impairments,
were thought to be the primary contributions to the progression
of rotator cuff disease. While these factors do contribute to
pathology secondary to mechanical compression, pathology is
most likely an interplay between extrinsic and intrinsic factors.
e pathoetiology of rotator cuff disease occurring as
a direct and primary result of extrinsic factors, subacromial
impingement, has been challenged. Objections to this causal
relationship are derived from in vivo shoulder kinematic studies
and surgical outcome data.
50,66-68
If the mechanical impingement
model held true for the majority of cases, modification of
extrinsic factors, including the acromion shape and space via
surgical interventions, would decrease symptoms and increase
function. But, comparison between non-operative and surgical
treatment of subacromial impingement syndrome demonstrates
surgical treatment is no better than non-operative treatment.
67
In addition, combined removal of the acromion and bursectomy
was no more beneficial than a bursectomy alone.
68
Some have
argued that improvement after acromioplasty or subacromial
decompression could be attributed to the relative rest incurred
in the post-operative rehabilitative process and a gradual
restoration of ROM and strength.
69
Rotator cuff impingement under the coracoacromial arch
has been confirmed in healthy asymptomatic shoulders.
50,70
Kinematic data suggest that subacromial impingement on the
rotator cuff does not occur beyond 70° of shoulder elevation.
e shortest distance between the acromion and supraspinatus
footprint is between 30-70° of elevation.
66
At 90° of flexion and
Academy of Orthopaedic Physical erapy, APTA.
For personal use only. No other uses without permission.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
13
scapular plane elevation, the proximal humerus and bicipital
https://t.me/med1917
groove approximates the acromion, not the supraspinatus tendon
66
(Figure 4).
us, pain that occurs with shoulder elevation past
90° cannot be attributed to subacromial compression of the
supraspinatus (or other rotator cuff tendons).
e cause of pain with special tests purportedly designed to
assess for subacromial impingement, such as the Neer sign, has
also been challenged. With the Neer sign, the lateral surface of
the greater tuberosity and proximal humeral shaft approximate
the lateral-inferior edge of the acromion at end-range elevation.
71
But, at end-range elevation, the articular surface of the rotator
cuff folds in on itself and is caught between the humeral head
and the posterior/superior aspect of the glenoid rim, leading
72
to what has been called “internal impingement.”
us, the
Neer sign may be more indicative of internal impingement
which occurs with full shoulder elevation. Consequently, given
the likely non-specific and multifactorial causes of rotator cuff
pathologies, the diagnostic term, subacromial impingement
is no longer favored, with preference given to terms such as
subacromial pain syndrome, rotator cuff related shoulder pain,
or other similar terms.
Posterior internal impingement is primarily attributed
6
to extrinsic factors.
It is a diagnosis that was first recognized
in throwing athletes due to the impingement of the posterior
rotator cuff between the glenoid rim and humeral head
6
during the late cocking phase of throwing.
Extrinsic factors
of consideration can include the presence of GH joint laxity/
instability, posterior capsule stiffness, posterior rotator cuff
stiffness, or reduced scapular retraction or posterior tilt during
humeral abduction.
60
Intrinsic mechanisms
Intrinsic factors influence rotator cuff tendon morphology
and the ability for the tendon to withstand compressive loads
and distribute tensile loads. Age is a primary intrinsic factor. An
aging tendon demonstrates disorganized and thinning collagen,
73
myxoid degeneration, and hyaline degeneration.
changes are more pronounced in the middle and deep layers
73
versus superficial layers of the tendon.
e frequency and
ese
distribution of these changes suggest they are common changes
73
involved in the early phase of rotator cuff tendinopathy.
Rotator cuff vascularity, that is significantly decreased after
the age of 40 as compared to those under the age of 40, is an
74
intrinsic factor to injury.
Histopathological studies confirm
neovascularization in response to low levels of oxygen in the
59
tissue.
Other intrinsic mechanisms implicate the internal or
systemic environment. Evidence suggests that patients with
hypercholesteremia and diabetes are at a higher risk for
75
developing tendinopathy.
Smoking inhibits delivery of oxygen
to tissues and is associated with increased risk of cuff tear, tear size
63
progression,
and failure of surgical rotator cuff repair to heal.76
Smoking is also associated with poorer scores on shoulder selfreported pain and function, a time and dose dependent relation
with rotator cuff tears, and a relationship with rotator cuff
77
tendinopathy.
ere is evidence that genetic predisposition
plays a small role in rotator cuff degeneration.
78
Figure 4.
Acromiohumeral Distance, as Defined as the Distance
Between the Acromion and Humerus*
A, At elevation angles below 34° the minimum distance between
surfaces is on the articular surface of the humeral head. B, With
elevation, the minimum distance between surfaces is located on the
greater tuberosity within the supraspinatus footprint. C, At elevation
angles greater than 72° the minimum distance between surfaces is
located on the proximal humeral shaft outside of the glenohumeral
joint.
*Adapted from Giphart et al.66 Illustration by Kinstler Design.
factors that cause macro or microtrauma to the
78
tendon.
Preexisting, age related, degenerative
changes in association with macro or microtrauma
73
is most likely the main cause of rotator cuff tears.
Rotator cuff tears
Differences in the presentation of rotator cuff
tears exist based on location, thickness, width,
tendon morphology, chronicity of injury, muscle
quality, and/or the presence of tendon retraction.
59
Location of partial-thickness rotator cuff tears are
categorized as bursal-sided, articular-sided, intratendinous, or a combination of these presentations.
79
Degenerative changes to the tendon with age are
80
associated with structural compromise,
thinning,
and partial thickness tears. A cadaveric investigation
found that of the 13% of specimens that had
partial rotator cuff tears, 55% of tears were intratendinous, 27% were articular-sided, and 18% were
81
bursal sided.
Intra-tendinous tears may correlate
with the degenerative changes noted in the middle
and deep layers of the tendon. Greater stiffness
and vascularity on the bursal side compared to the
14
Academy of Orthopaedic Physical erapy, APTA.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
For personal use only. No other uses without permission.
articular side
https://t.me/med1917
50,54
may create stress differentials contributing to
the etiology of partial-thickness tears. Additionally, the risk of
tear progression is relative to the percentage of partial tendon
thickness involvement. In patients with tears involving >50%
of the tendon thickness, 55% had tear progression; but if the
tear was <50% of the tendon thickness, only 14% had tear
62
progression at 4.4 years.
Full-thickness tears, involving all 5 layers of the tendon,
have been shown to progress in size and propagate in both
82
anterior and posterior directions over time.
Degenerative
tears were thought to initiate at the anterior portion of the
supraspinatus due to the amount of contractile load that is
82
transmitted in that region.
However, more recent evidence
suggests degenerative tears initially occur within the crescent,
and at the junction between the supraspinatus and infraspinatus
82,83
tendons.
anterior cable insertion of the supraspinatus.
e location of the tear in the crescent spares the
83
Only 30% of full-
thickness tears involved the most anterior aspect of the tendon
83
footprint and anterior cable attachment.
Consideration should
be given for rotator cuff tears and where their location is in
relationship to the rotator cable. A full thickness tear involving
the infraspinatus would disrupt the posterior rotator cable;
a tear involving the upper half of the subscapularis tendon
56
would disrupt the anterior rotator cable.
For tears within the
rotator crescent, function is well maintained because there is no
56
disruption in the rotator cable.
Full-thickness rotator cuff tendon tears tend to result
in progressive rotator cuff muscle atrophy, fibrosis, and fat
84
infiltration.
muscles is typically evaluated with MRI. Goutallier et al
Fat infiltration and atrophy of the rotator cuff
85
described 4 progressive stages of rotator cuff fat infiltration
which are used to determine the chronicity of a tear and is
highly associated with clinical outcomes following a rotator cuff
repair. Supraspinatus and infraspinatus muscle atrophy can also
be evaluated with MRI as a ratio of the cross-sectional size of
the muscle compared to that of the surrounding scapular fossa,
86
defined as occupation ratio.
has been correlated to higher post-operative re-tear rates.
Rotator cuff atrophy (<.40 ratio)
87
Patients who have a re-tear or unhealed repair have slightly
compromised functional outcomes compared to those with
88
intact rotator cuff repairs.
In a systematic review from 2017,89
rotator cuff fat infiltration, indicative of chronic tear, was shown
to be the greatest predictor (odds ratio [OR] = 9.3) of failed
healing of a surgical repair. Multiple tendon involvement (OR
= 6.0), larger tear size (OR = 4.3), and lower pre-operative
muscle strength (OR = 4.0) also had moderate negative effects
on outcomes. Older age also has a negative, albeit modest, effect
on cuff integrity at follow-up after surgical repair (OR = 2.8),
but no significant effect on function. Duration of symptoms
before surgery has no significant effect on outcomes, likely due
to presence of asymptomatic tears with age.
Rotator cuff tears, particularly those that include the cable,
increase the risk for further pathoanatomic changes. Rotator
cuff tears alter direction of the resultant joint reaction force.
If the force couples around the GH joint are unbalanced, the
56
deltoid will create an upward migration of the humeral head.
With a change in the instantaneous center of rotation of the
humerus and increase in superior humeral head migration
due to a rotator cuff tear, there is an increased strain on the
50
labrum and bicipital attachment.
Cartilage degeneration also
increases with progressive loading. In addition to changes in the
fibrocartilaginous labrum, changes in the articular cartilage of
the humeral head can be seen as early as 12 weeks after rotator
50
cuff transection.
Due to changes in mechanics, narrowing of
the acromiohumeral distance and superior migration of the
humeral head on the glenoid and secondary GH joint OA,
a condition termed “cuff tear arthropathy,” occurs in some
patients. In patients with asymptomatic small to medium sized
rotator cuff tears, 22% showed GH joint OA progression at an
8-year follow-up.
90
Long head of the biceps tendinopathy and injuries are also
common with rotator cuff tears. e larger the size of the rotator
cuff tear, the greater the extent of bicipital damage and change
50
in its mechanical properties.
In addition, the long head of the
biceps is highly innervated at the tendon origin as opposed to its
57,91
musculotendinous junction.
us, a long head of the biceps
tenodesis or tenotomy as part of the surgical rotator cuff repair
is done in an effort to reduce pain, with potentially causing a
50
small negative effect on GH joint movement.
Scapulothoracic anatomy
Of the 17 muscles that attach to the scapula, 6 are
responsible for stabilization of the scapulothoracic joint. ose 6
muscles include the trapezius, serratus anterior, levator scapulae,
92
rhomboid major and minor, and pectoralis minor.
e serratus
anterior can be divided into 3 functioning segments. Of note
is the lower segment that assist with both upward rotation
and ER of the scapula. e middle segment of the serratus
anterior protracts the scapula, and the upper segment stabilizes
92
the scapula to allow for upward rotation.
Consideration for
serratus anterior function in closed kinetic chain function would
be movement of the thorax in relation to a fixed scapula, such
as when performing a push-up. e trapezius spans the upper
occiput through T12, with insertion sites along the clavicle and
93
spine of the scapula.
e upper trapezius originates from the
occiput, superior nuchal ligament, and spinous processes from
vertebrae as low as C6, with insertion on the distal third of
the clavicle. e middle trapezius arises from C7–T4 spinous
processes and inserts on the acromion and spine of the scapula,
93
with the majority of muscle fibers in an horizontal orientation.
e lower trapezius arises from T5-12 spinous processes and
attaches to the medial base of the scapular spine. e fibers of
the lower trapezius are superiorly and obliquely oriented.
93
Biomechanics of the scapula
Scapular movements are comprised of 2 translations
(protraction/retraction, elevation/depression) and 3 rotations
(upward/downward; anterior/posterior tilt; internal/external).
Academy of Orthopaedic Physical erapy, APTA.
For personal use only. No other uses without permission.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
15
Movement from the scapulothoracic joint is
https://t.me/med1917
achieved through a combination of these 6
degrees of freedom in efforts to optimize the
Figure 5.
position of the glenoid for articulation with
94
the humeral head.
e scapulohumeral
rhythm is defined as the sequence of events
between the interaction of the GH joint and
scapulothoracic joint in efforts to raise the
upper extremity overhead. e length-tension
relationship of the muscular attachments can
be maintained with a proper scapulohumeral
rhythm which then allows for adequate force
production. e scapulohumeral motion also
impacts the size of the subacromial space.
ere is a complex interaction that occurs
as a result of muscle timing, strength, and
coordination in efforts to provide efficiency of
95
movement.
Classically, the scapulohumeral
rhythm is defined as a 2:1 ratio comprised of
60° of scapular upward rotation and 120° of
GH joint movement to achieve 180° of total
96
shoulder elevation.
ere is variable pattern
of scapular motion up to 30 to 60° of flexion
or abduction, then a more consistent 2:1
motion ratio is maintained. Recent studies
have suggested the key component to the
scapulohumeral rhythm is scapular upward
rotation, followed by posterior tilt with coupled
motions of the AC and SC joints.
97
e serratus anterior and trapezius are
responsible for a force couple that produces
scapular upward rotation, posterior tilt, and
A, eoretical mechanism of how the serratus anterior (SA) and middle
trapezius (MT) and lower trapezius (LT) muscles can control the posterior
tilt and external rotation of the upwardly rotating scapula during scapular
plane abduction. B, e SA and LT act in a force-couple to posteriorly
tilt the scapula relative to the axis of rotation at the acromioclavicular
joint (indicated by the green circle). C, e SA and MT act in a forcecouple to externally rotate the scapula relative to the axis of rotation at
the acromioclavicular joint (indicated by the blue circle). Each muscle’s
moment arm is indicated as a dark black line, originating at the axis of
rotation of the acromioclavicular joint.
*Reprinted with permission from Neumann and Camargo.98 Copyright 2019, Brazilian
Journal of Physical erapy.
ER during shoulder elevation (flexion and
98
abduction) (Figure 5).
e serratus anterior
is the primary upward rotator and protractor of
the shoulder girdle, consequently contribution
from the middle trapezius, a scapular retractor, is essential to
counterbalance the protraction action of the serratus anterior
and control the location of the instantaneous center of rotation
98
of the scapula.
e lower trapezius externally rotates the
scapula, depresses the shoulder girdle, and assists to upwardly
93
rotate the scapula.
e upper trapezius has commonly been
included in the force couple between the lower trapezius and
serratus anterior. However, the upper trapezius only modestly
93
contributes to scapular upward rotation.
Due to the upper
trapezius insertion on the clavicle and due to kinematic coupling
of the SC and scapulothoracic joints, the upper trapezius is
thought to provide greater contribution to scapular ER and
93
scapular elevation.
It is important to consider that scapular
muscle function is often referenced to a stable spine. In a closed
chain position with the scapula theoretically stabilized, the
trapezius can laterally flex and contralaterally rotate the thoracic
93
In summary, to simplify function and the scapular force
spine.
Force Couples Around the Scapulothoracic Joint*
couple, the serratus anterior is the primary mover, while the
trapezius is the primary stabilizer of the scapula.
93
Scapular dyskinesis
Scapular dyskinesis, defined as altered dynamic scapular
control, is present in as many as 67-100% of athletes with
shoulder injuries, with prevalence in overhead athletes
outnumbering that of non-throwing athletes 2:1.
99
there is conflicting evidence as to whether or not scapular
100
dyskinesis is a risk factor for future injury
resulting in clinical
debates regarding its relevance with shoulder pain.
Patterns of scapular dyskinesis have been proposed
including medial border or inferior angle winging, and excessive
101
elevation termed “hiking,” to name a few.
Scapular muscle
imbalances and altered motor control believed to contribute
to dyskinesis include (1) excessive upper trapezius activation,
and (2) decreased or delayed activation of lower and middle
trapezius and serratus anterior muscles. If the GH joint
However,
16
Academy of Orthopaedic Physical erapy, APTA.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
For personal use only. No other uses without permission.
demonstrates hypomobility, due to arthritic changes or adhesive
https://t.me/med1917
capsulitis for example, the scapula is forced to play a larger role
in shoulder ROM
upward rotation motion.
102
with potentially excessive hiking, ER, or
103
Scapular dyskinesis can occur due to a variety of reasons,
both neurological and structural. Neurological causes can
include cervical radiculopathy or long thoracic nerve or spinal
accessory nerve palsy.
95
Long thoracic nerve injury causes
serratus anterior weakness associated with medial border
winging.
92
e long thoracic nerve may be susceptible to
compression injury secondary to its superficial location on the
lateral wall of the thorax. It can also be injured with traction,
spinal cord compromise, or idiopathic neuropathy.
98
e spinal
accessory nerve innervates the sternocleidomastoid as well as the
trapezius muscles.
93
Injury to this nerve can occur secondary
to surgical procedures around the neck, such as lymph node
removal or radical neck dissection due to cancerous tumors.
92
Spinal accessory nerve injuries result in excessively depressed,
protracted, and downwardly rotated scapula.
93
Loss of
innervation to the trapezius removes several primary stabilizers
of the scapula and predisposes the patient to shoulder pain.
93
Structural changes can include but are not limited to an
abnormal thoracic kyphosis or reversal of kyphosis, AC joint
instability,
92,95
or thoracic outlet brachial plexus symptoms.
In absence of occult trauma or deformity, the presence of
obvious scapular dyskinesis may indicate impairments related
to neuromuscular control and/or muscle length, strength, or
endurance.
e effect of scapular dyskinesis is theorized to be an
extrinsic factor and potentially modifiable impairment
associated with subacromial pain syndrome.
103
Decreased
scapular posterior tilt and ER during elevation has been noted
in those with subacromial pain syndrome.
103
Fewer studies
have investigated the effect of scapular kinematics on internal
(posterior) impingement. However, one study concluded that
95% of athletes with posterior superior labral injuries showed
increased scapular IR.
103
Challenges to the clinical relevance
of scapular dyskinesis and interventions specific to address the
condition are discussed later in this monograph.
Summary and Implications for Practice
In efforts to effectively examine, diagnose, and treat
shoulder injuries, it is imperative for the clinician to understand
pathophysiological mechanisms pertinent to the shoulder.
Consideration for extrinsic mechanism(s) to injury, with
understanding of concurrent intrinsic mechanism(s), can help
the clinician to prescribe treatment to address these deficits, as
well as effectively communicate prognosis to the patient. As
mentioned earlier, the conventional subacromial impingement
theory has been challenged and may highlight the importance
of controlling the load on the tendon versus focusing excessively
on “creating space” under the acromion. Regarding rotator cuff
tears, understanding the variation in the layers of the tendon
with stress shielding capabilities and the relative location
of the tear in relation to the rotator cuff interval, may help
explain why some partial- and full- thickness rotator cuff tears
respond to non-operative treatment and others do not. Lastly,
understanding the pathoanatomical changes that occur with
GH joint OA can help the clinician to educate the patient on
joint protection strategies.
CLINICAL EXAMINATION
AND DECISION-MAKING PROCEDURES
Patient History and Interview
e patient’s history and interview should provide
information to generate the diagnostic hypotheses and movement
related classification for shoulder pain. e clinician should
initially start broad and consider all diagnostic hypotheses.
Local nociceptive sources and other more remote sources that
may refer pain to the shoulder should be considered. Pain in the
shoulder can include somatic referred pain from cervical spine
104
facet
and disc,
nerve root involvement. Potential visceral or vascular systems
sources can also refer pain to the shoulder.
A detailed history taking should include a pain diagram
completed by the clinician to identify the pattern of the patient
complaints and rule out other regional involvement. On the
pain diagram, the description of the patient’s symptoms (eg,
burning, catching) is identified and regional distribution of
symptoms is mapped. Nociceptive pain patterns for subacromial
structures and GH joint disorders are commonly located distal
to the acromion in the lateral deltoid region.
pain from the AC joint is located on the top of the acromion
surrounding the AC joint and may extend to the anterior
aspect of the shoulder.
labeling these by the patient’s primary (P1) and secondary
(P2) complaint may assist with questioning to determine if a
single source of symptoms is related to both pain locations or
if more than 1 source of symptoms should be considered. e
pain diagram is used in combination with information on the
mechanism of injury, age, and pain behavior to identify patterns
for diagnostic hypotheses. Pain behavior includes aggravating
and alleviating factors, 24-hour pattern, pain severity and
irritability, and chronicity. Common patterns of symptoms,
associated with specific conditions, identified with the history
and interview can help refine (to narrow down) the number
of hypothesized shoulder diagnoses to inform the physical
examination (Table 1).
Not all shoulder pain is attributed to local tissue sources.
More than 40% of patients have persistent pain and disability
a year after the onset of shoulder symptoms.
evidence suggests a substantial proportion of individuals
with shoulder pathology have features of sensitization.
research on the effectiveness of interventions have largely been
designed for specific pathoanatomic diagnoses. Nociceptive
pain arises from damage to non-neural tissues and is due to
105
or peripheral neuropathic pain with C5
106
In contrast,
107
When more than 1 region is involved,
108
More recently,
109
Yet,
Academy of Orthopaedic Physical erapy, APTA.
For personal use only. No other uses without permission.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
17
Table 1.
https://t.me/med1917
Common History Findings and Symptoms Associated with Shoulder Pathologies
Hypothesized
Pathoanatomic Diagnosis
Adhesive
capsulitis - primary
Glenohumeral joint
osteoarthritis - primary
Subacromial pain
syndrome
Rotator cuff tear
Persistent pain anterior-lateral shoulder region accompanied by inability to sleep due to pain
and gradual loss of motion attributed to pain. Higher risk in females, age 40-65, presence of
diabetes or hypothyroidism.
Gradual onset of pain and associated loss of motion, age 60 or older.
May complain of crepitus or catching with end range motions and stiffness that is worse in
the morning.
Anterior/lateral shoulder pain, pain with motions at or above shoulder height, complains of
pain with mid-range active shoulder elevation (painful arc), and pain that increases at night.
Anterior or lateral shoulder pain, with loss of strength, pain that wakes the patient during
sleep, pain that is worse at night, and age of 40 or greater.
Associated History and Symptoms
Reports of anterior shoulder pain, apprehension, and/or pain in positions of end-range
Anterior instability/
labral tear
shoulder abduction and external rotation, a history of anterior/inferior trauma, recurrent
anterior/inferior subluxations and/or dislocations, joint clicking/clunking, complaints of joint
locking, and a history of “dead arm syndrome.”
Complaints of instability, apprehension, and/or pain in positions of combined shoulder
Posterior instability
flexion and horizontal adduction with posterior directed force on humerus - pushing or
closed chain activities. A history of trauma with or without recurrent subluxations and/or
dislocations.
SLAP lesions
Posterior internal
impingement
Long head of the biceps
tendinopathy
Deep anterior shoulder pain with clicking/clunking/joint locking, pain with throwing or
biceps loading (shoulder flexion and arm supination).
Posterior shoulder pain during combined shoulder abduction and external rotation
particularly with horizontal plane hyperabduction. Overhead athletes complain of reduced
performance.
Anterior pain isolated to the long head of the biceps in the bicipital groove particularly with
shoulder flexion and arm supination.
Shoulder pain at top of the shoulder near AC joint that increases with end-range shoulder
AC joint arthropathy/
injury
elevation and/or horizontal adduction. History may include heavy weightlifting. History of
trauma with a contact force that displaced the shoulder girdle inferiorly. A visual deformity at
the top of the shoulder may be apparent.
Abbreviations: AC, acromioclavicular; SLAP, superior labral anterior to posterior
the activation of nociceptors.
pain is more likely to reflect pain locally at the shoulder.
Neuropathic pain is caused by a lesion or disease of the central
or peripheral somatosensory nervous system.
shoulder pain might follow a radicular pattern (eg, cervical
C5 radiculopathy) that is located along the upper arm or in
other locations specific to a peripheral nerve (eg, suprascapular
neuropathy) distribution and could potentially be reproduced
with neurodynamic tests. A neurological screen is a necessary
part of the examination in patients with suspected neuropathic
pain. Nociplastic pain arises from altered nociception, despite
no clear evidence of actual or threatened tissue damage causing
110
A pain diagram for nociceptive
111
Neuropathic
the activation of peripheral nociceptors or evidence for disease
110
or lesion of the somatosensory system.
Nociplastic pain may
be attributed to enhanced central excitability and/or diminished
pain inhibition, often referred to as central sensitization.
Nociplastic shoulder pain may be diffuse pain, potentially
beyond the shoulder region, in anatomic areas non-characteristic
of shoulder pain. ere may be disproportionate aggravating
and easing pain responses and diffuse areas of tenderness with
112
palpation.
Pain presentation should be identified according to
the neurophysiological mechanism responsible for its etiology
or maintenance, realizing that more than 1 pain mechanism
113
can co-exist.
18
e predominant pain presentation can inform
Academy of Orthopaedic Physical erapy, APTA.
© 2021 Academy of Orthopaedic Physical erapy, APTA, Inc. All rights reserved.
For personal use only. No other uses without permission.
110
Соседние файлы в папке Библиотека им академика М.И. Перельмана