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Principles and
Mechanisms of
Theruni Wijewardene

Lecture Objectives

the biomechanical principles of

common sports injuries related to
specific fields


is the study of the

structure and function of biological
systems by means of the methods
involved in mechanics - which is a
branch of physics that involves analysis
of the actions of forces


Within mechanics there are two sub fields of study:

1) statics: study of systems that are in a state of

constant motion either at rest (with no motion) or
moving with a constant velocity
2) dynamics: study of systems in motion if which
acceleration is present, may involve:

kinematics: study of motion of bodies with respect to

time, displacement, velocity, and speed of movement
either in a straight line or in a rotary direction
B) kinetics: study of forces associated with motion,
including forces causing motion and forces resulting from

Biomechanics & Sports Injuries

Biomechanics, put simply, is the study of how the
body moves
It can be used to analyse athlete movement to
improve technique and reduce risk of injury
Biomechanics allows us to understand how
muscles, tendons, ligaments, neural tissue and
bones will react to a given force
When the mechanism of injury is clear,
physiotherapists/medical professionals can
determine which tissues may have been damaged
and the severity of the injury

Biomechanics: 5 Important


of body or object in space with

respect to time
Described in terms of:



How fast was the athlete running when he

fell and in which direction (ie straight line or
side stepping)


influence that causes an object or person

to undergo a certain change which in turn
influences its:

Geometrical or anatomical structure


A tackle on the lateral aspect of the knee

can cause the knee to move medially and
deform the medial structures eg tear MCL


of mass and velocity

Eg a heavy rugby player running at full
speed has a large momentum and may
require large and prolonged force (eg in
the form of an external tackle) to either
reduce speed or stop

In the human body, arms and legs act as
levers, as does equipment such as racquets
and bats
3 parts to a lever:

Axis of rotation/fulcrum

Most muscles in the human body are 3 rd Class

Levers and create rotation of the distal

Alignment of COG over BOS
Balance influenced by:

Width of BOS
Height and motion of the COG
Weight of the person

Important for changing direction suddenly; generating

necessary force and momentum
Eg If balance or proprioception is reduced in a previously
injured ankle, the ability to correct alignment during
unstable movements is reduced and can lead to re-injury

Intrinsic Biomechanical Factors

Muscle imbalances eg VMO vs VL
Joint stiffness eg reduced DF
Joint instability/movement control disorder eg
unstable/hypermobile shoulders in swimmers
Muscle weakness or lack of endurance
Leg length discrepancies
Lower extremity alignment eg genu varus or valgus;
increased pronation of feet
Muscle tightness/inadequate flexibility eg hamstrings
Previous or untreated injuries

Extrinsic Factors

equipment eg shoes
Change in training surface eg hard vs
soft surfaces, non-shock absorbing, too
Sudden change in training load eg

Common Sports Injuries


RC tears / Impingement Syndrome

ACJ sprains


Lateral epicondyalgia/Tennis elbow

Common Sports Injuries



Patellofemoral pain syndrome



Common Sports Injuries


Lateral ankle sprain

Achilles tendinopathy

Rotator Cuff
Injury/Impingement Syndrome

main function of RC muscles: stabilise

the GH joint so that the larger shoulder
movers (eg, deltoid, latissimus dorsi) can
carry out their function without significant
motion of the humeral head on the glenoid.
Increased movement results in shearing
forces across the joint (especially to labrum)
and may result in humeral head migration
and impingement upon RC muscles and

Rotator Cuff
Weakness of RC increases demands on the static stabilizers (joint
capsule/labrum/GHJ/ ligaments).
If demands are long term or recurrent, static stabilizers may begin to fail
result in stretching or attenuation of the capsule greater shoulder laxity
greater demands on the already weak rotator cuff muscles.
Humeral head migration may occur with capsule laxity and weak RC RC
impingement and pain.
[Evidence to suggest that impingement may occur initially compromises
blood flow to SS and also relative avascularity at humeral attachment]
Pain may inhibit RC muscle firing, leading to disuse and further weakening
of the dynamic stabilizers with greater demands placed on the static
Other factors contributing to impingement/RC injuries: faulty postures;
capsular tightness; joint kinematics; structural abnormalities in
coracoacromial arch

Overhead Shoulder Movement

A similar type of motion is involved in a number of overhead sports activities
(eg, serving in tennis, spiking in volleyball, throwing a football or baseball). The
baseball throwing motion has been studied in detail and can be divided into 5
Stage 1 : Wind Up: EMG studies have determined that the rotator cuff muscles
are inactive during this initial stage.
Stage 2 : Early Cocking: involves shoulder external rotation and abduction
supplied primarily by the deltoid.
Stage 3 : Late Cocking: continues until maximal ER is achieved. The RC muscles
very active , especially subscapularis, which eccentrically contracts and acts as
a dynamic stabilizer.
Stage 4 : Acceleration: begins with internal rotation of the humerus and ends
with release of ball. Pectoralis major and the latissimus dorsi are very active,
whereas RC muscle are inactive.
Stage 5 : Follow Through: deceleration takes place. RC muscles and post.
deltoid are most active. The supraspinatus eccentrically contracts to decelerate
IR of the limb.

RC Injuries
Proper balance between concentrically contracting muscles that
generate force and the eccentrically contracting muscles that
control movement is important. Imbalance between these
opposing muscle groups results in overuse injuries.
During throwing movement where GHJ moves into considerable
abduction and ER, high SS forces required in this position
Role of RC is to synergistically resist distraction of the humeral
head therefore if injury or fatigue is present altering
throwing/movement pattern increases risk of further tissue
Note: Much of the force generated in overhead sports occurs in
the trunk and lower extremity, and require significant stability
and strength

RC Injuries

younger athletes with RC injuries

have a history of repetitive overhead
activities involving the rotator cuff or,
less commonly, a history of trauma
preceding clinical onset of symptoms.

RC: Mechanism of Injury

Enormous demands placed on shoulder mm during overhead
With repetitive movement when unable to supply the necessary
amount of force, speed and acceleration for necessary duration
fatigue and muscle weakness occurs
mm fatigue will reduce amount of contribution from active structures
and rely on passive structures for power output, especially anterior
band of IGHL
This increased demand can lead to overstretching and hypermobility
This hypermobility of passive structures increases demand on
stabilising mm (RC)
The inherently high muscular demands of the overhead movements
combined with acquired hypermobility leads to tensile failure in RC

RC: Common Mechanisms of

Fall: using arm to break fall eg GHJ abducted and IR
or more commonly on outstretched hand ( GHJ
flexed and IR) force directed anterior to posterior
and often inferior to superior
Heavy lifting: especially overhead or in hunched
position (Tx kyphosis and shoulders protracted
ant. displacement of GHJ)
Repetitive overhead movements eg throwing in
water polo; spiking volleyball; freestyle in swimmers
Most commonly involved RC mm in injury is

RC Injury/Impingement:
Clinical Signs
Mechanism of injury
Pain anterior shoulder and/or mid deltoid region
Pain with shoulder movement

Abduction painful arc: if impingement also present

Full Can (SS>IS)/Empty Can Test (IS>SS)+ve

Impingement: Hawkins/Kennedy +ve; Neer Test +ve
Observation: symmetry of mm bulk; scapulothoracic
position (winging medially or inferiorly)
Palpate: HOH position (1/3 HOH anterior is N); TOP greater
tuberosity; GHJ line; AC joint line; SS tendon; long head of
Passive movement: usually full

ACJ Sprain
Occurs when an applied force displaces the acromion
process from the distal end of the clavicle
Results from direct or indirect forces
Direct: force applied to the point of the shoulder (ACJ) with
GHJ in adduction

Eg when collides with solid object or person

Impact force drives acromion inferiorly relative to clavicle

Indirect: eg when person falls on outstretched hand.

contact force directed up the armhumerus acromion

Superior directed force causes separation of acromion from
Very rarely extreme traction force may cause separation of
acromion from clavicle

ACJ Injury

6 Types of ACJ Injuries

Type I: Isolated sprain of acromioclavicular ligament with pain over ACJ;
minimal pain with sh. movements and mild TOP
Type II: Widening of ACJ with elevation of distal end of clavicle and
disruption of acromioclavicular ligament; mod-severe pain with limited sh.
Type III: Dislocation of ACJ with superior displacement of clavicle;
disruption of coracoclavicular ligament; upper extremity depressed with
free floating clavicle; mod to severe pain
Type IV: Dislocated ACJ with posterior displacement of clavicle into or
through trapezius m; complete disruption of coracoclavicular ligament;
more pain than type III
Type V: Disruption of acromioclavicular and coracoclavicular ligaments;
gross displacement of ACJ joint; severe pain
Type VI: Disruption of acromioclavicular and coracoclavicular ligaments;
inferior displacement of clavicle into subacromial or subcoracoid position

ACJ Injury: Clinical Signs

Mechanism of injury
Observable swelling; deformity (eg tenting)
see previous slide for types
TOP over ACJ+/- Coracoclavicular spaces
Shoulder ROM: depending on severity
Hawkins/Kennedy or Cross Arm Test: +ve
Distraction: +ve
Reducibility: stabilise clavicle superiorly and
push superiorly at elbow

ACJ Injuries

Lateral Epincondyalgia:
Mechanism of Injury

due to increase in backhand stroke

playing or attempting to increase power or
incorrect backhand technique in
Relying on forearm force rather than on core,
rotator cuff, and scapular power:

Results in snapping the wrist with supination

and irritation of the extensor tendons
Doesnt have feet in correct ready position hits
the ball late or with a bent elbow

Lateral Epincondyalgia:
Mechanism of Injury

Other causes

new racquet
using a racquet that is
strung too tightly
using a racquet that is
too heavy
hitting wet or heavy balls
or hitting into the wind.
having a grip that is too large.
hitting with a 1-handed backhand versus a 2handed backhand

Lateral Epiconyalgia: Clinical

Mechanism or history of injury/pain
Isometric Tests: resisted wrist extension; 3 rd
digit extension +ve for pain reproduction
Functional Tests: gripping/shaking
hands/backhand/turning knob etc
TOP: lateral epicondyle/CEO/radial
head/extensor mm group/supinator
Reduced mm length: extensors+/- flexors
Reduced mm strength: extensors

Knee - Meniscus

Fibro-cartilaginous and relatively avascular: peripheral 1/3 receives

blood supply from capsule whilst medial 2/3 nourished by synovial fluid
from joint


Load transmission: elastic coupling enables effective transmission of

compression forces
In full extension, meniscii accomodates 45-50% of load, and in 90
flexion they accept 85% of load
Joint congruency: spread contact area between femoral condyles and
tibial plateau
Shock absorbency
Enhances stability
Changes in shape/distorts with knee flexion: elongates and flatten
posteriorly (lateral>medial)

Meniscus: Mechanism of Injury

Mensicii injury either traumatic (young, active individuals) or
degenerative (older) and occurs when subject to a
combination of flexion, rotation or extension and rotation
during WBing and resultant shear between tibial and femoral
Twist on a flexed knee

Squatting in awkward position

Rotational stress applied to flexed, WBing knee eg rapid change in
direction while running (foot is planted) internal femoral rotation
on a fixed tibia posterior displacement of medial meniscus
ER of foot and lower leg relative to femur risk of medial
meniscus injury
IR of foot and lower leg relative to femur risk of lateral
meniscus injury

Meniscus: Mechanism of Injury


extension: can cause longitudinal tear of

medial meniscus bucket handle tear (more
common with repeated trauma to a partial tear)
Low force or low velocity injuries

Relatively trivial movements in 30-50 yr olds common


common in more vulnerable older and/or

degenerative meniscii

Increased breakdown over time

Reduced ability to repair with increased age



Other major injuries eg ACL tear

Medial VS Lateral

has increased risk of injury due

to its tight connection with joint capsule;
MCL; and its frequent connection to ACL
LCL has only loose connection to joint
capsule and no direct connection to LCL
LCL is therefore more mobile in both the
loaded and unloaded position

Clinical Signs of Mensical

Mechanism of injury

Well localised to joint line

With loaded flexion eg squat

Can weight bear (but may be painful)


Slow, mild effusion/swelling due to low blood supply

Catching or Locking: loose fragment wedged

between condyles
McMurray Test +ve: pain/clicking with compression
and movement

Types of Meniscal Tears

Anterior Cruciate Ligament


Arises lateral femoral condyle to anterior tibia spiralling forward

from lateral to medial from femur to tibia


Primary (85%) restraint to limit anterior translation of the tibia. In this

role, ACL limits anterior translation of tibia relative to a fixed femur;
or conversely restricts posterior translation of femur to a fixed tibia.
Secondary restraint to tibial rotation and varus/valgus angulation at
full extension. Since the relationship between the tibia and femur
provides little bony stability, the ligamentous structures must provide
stability. When the ACL is injured, a combination of anterior
translation and rotation occurs.
Works in conjunction with PCL to limit knee hyperextension and

ACL: Mechanism of Injury

ACL injuries commonly occur during sport when sudden
stress is applied to the knee joint while the tibia is in contact
with the ground.
Typically, ACL is torn in a non-contact deceleration situation
that produces valgus and internal rotational moments
on the knee joint as it begins to to flex from near extension.
Eg high-risk pivoting sports when the athlete lands on the
leg and starts rotating to the opposite direction

Active quadriceps pull is considered to play an important role in

the pathomechanism of ACL injury. Reflective eccentric quads
contraction accompanied by apparent weakness of the HS mm
allows the extensor mechanism to strain the ACL during anterior
tibial translation. This mechanism can be observed during jump
stop landings

ACL: Mechanism of Injury

Less frequently, direct contact injuries occur
as a result of extensive valgus stress with
external tibial rotation; (eg tackle to
lateral aspect of knee) or hyperextension
of the knee joint (front on tackle)
Isolated disruption of the ACL is rare
condition; while complete or incomplete
ruptures accompanied by traumatic lesions to
the medial or lateral meniscus as well as to
MCL reported in 80% of all cases.

Mechanism of Injury


ACL Rupture: Non Contact

Classic twist with knee moving from flexion to
extesion and tibia internally rotating relative to
Tibia forced anteriorly into IR relative to femur

Knee hyperextension with internal tibial rotation

Eg rugby side step; sudden pivot, cut, deceleration,


eg basketball players; gymnasts after


May hear pop, crack, snap

ACL Injury: Contact


Eg tackle anterior around tibia

Motion can rupture layer by layer

capsule stretched ++ or torn




or varus force to knee: eg tackle

Valgus: MCLmedial mesniscusACL

Varus (less common): LCLACLfibres of
popliteusfracture medial tib condylelateral

Clinical Signs of ACL Injury

Mechanism of injury
Usually unable to weightbear due to intense pain
(may settle quickly)
Immediate hot effusion

Within 2 hrs
Haemathrosis: 80% chance ACL tear and most likely full

+ve Lachmans; Ant. Drawer; Pivot Shift

Not always isolated:

Lateral mensicus
ODonoghues / Unhappy Triad

rupture; MCL rupture; Med. mensicus

Posterior Cruciate

aspect of medial femoral

condyle in area of intercondylar notch and
inserts over tibial plateau 1cm distal to joint


Provides 95% restraint to posterior

translation of tibia relative to femur
Secondary function to resists varus,
valgus and external rotation

PCL: Mechanism of Injury


injured most commonly during knee

hyperflexion injury

eg heavy landing on tibia with KF and foot PF(eg

fall onto tibia) or forced KF with foot in DF (eg fall
on a flexed knee in squat position); blow forcing
tibia posteriorly in relation to femur (dashboard



usually accompanies ACL


Clinical Symptons of PCL Injury


drop visually: >12mm defect =

complete tear
Posterior tibial step off: from lateral view
+ve Posterior Drawer Test
Instability going down stars or hilss
PFJ pain
Associated LCL damage

Function: superficial MCL provides 57% of the restraining
valgus moment at 5 of knee flexion, and provides 78% of
the moment at 25 of knee flexion due to decreased
contribution from the posterior capsule. MCL strength ~
equal to ACL
After MCL rupture, the ACL may also tear, producing a more
extensive injury.
In one study of MCL injuries, Fetto and Marshall reported the
incidence of ACL tears to be 20% when there is no valgus
laxity on clinical exam, 53% with laxity only in 30 of knee
flexion, and 78% with valgus laxity in full extension.
Therefore, if the knee opens medially in extension, one must
suspect that an ACL injury is likely present

MCL: Mechanism of Injury



Contanct: direct blow to the outer aspect

of the lower thigh or upper leg
Non-contact valgus external rotation
injuries are common in skiing


to the position of the knee and the

force vectors, a combined flexion/
valgus/external rotation injury is usually
end result.

Clinical Signs of MCL

Mechanism of injury
MCL tender on palpation
Lack of extension pain ++
Postive to valgus stress test
Nil minimal swelling (unless capsular tear =
haemarthrosis (ie within 2 hours)
Pain worse with incomplete tears vs complete
Usually able to weightbear even with full tears
Associated Injuries: bone bruises, ACL tears, lateral
LCL tears, medial meniscus tears, lateral meniscus
tears, and PCL tears

LCL : Mechanism of Injury

Function: primary restraint to varus stress

across the knee
Injury: Rare; external tibial rotation or varus
stress eg MVA or tackle to inside knee; usually
varus loading, often in combination with
The postero-lateral capsule, which includes the
LCL, popliteofibular ligament, and
popliteus tendon, is the primary restraint
to external rotation stress across the knee.

Clinical Signs of LCL Injury


of injury
LCL tender on palpation
Lack of extension pain ++
Postive to varus stress test
Pain worse with incomplete tears vs
Grade III associated with posterloateral
corner instabilities: poplitues; PCL and
posterior capsule

Patellofemoral Pain Syndrome


knee pain
Biomechanics of injury:

direct trauma eg fall

overuse injury (repetitive knee bending eg
patella maltracking due to weak mm (quads esp VMO) and/or
tight mm (hamstrings/calf/ITB/ lateral retinaculum)
Poor foot biomechanics (overpronation or high arches)
Increased Q angle (ASIS to centre patella and centre patella
to tibial tuberosity)

External tibial torsion
Increased femoral anteversion

Clinical Signs of PFPS


around patella
Pain on knee flexion (eg
sitting/squatting etc); worse with
McConnels Functional Test: medial glide
of patella during functional test (eg
squat) improves function (eg ROM or

X-Ray of Knee Required...


2 or more of the following features are


>55 years old

Effusion of the joint

Knee feels tight/full; cant fix with milk/swipe


Unable to weight bear

Point tenderness on palpation

Patella; tibial plateau; femoral condyles or head of



of HS group, with exception of short

head of BF, has biarticular function.
This dictates that the muscle length is
determined by the conjoint action of both
the hip and knee
Hip flexion & knee extension: lengthen
SemiT; SemiM and BF (long head) and this
combined movement with mm in
lengthened position predisposes HS to injury

Hamstring Strains

It is concluded that hamstring strains during sprinting most likely

occur during terminal swing as a consequence of an eccentric
contraction (HS decelerate thigh and lower leg in preparation for
ground contact)

Increased speed increased peak biceps femoris force generated therefore

higher risk at higher speeds
Peak HS stretch at terminal swing and this effects greatest at biceps

HS strains also occur in early stance phase in running

HS contract eccentraically to decelerate knee extension followed by rapid

change to concentric contraction to extend hip

Poor glut max activation results in increased activation of HS to extend hip

predisposes to injury

Can also occur duing kicking and jumping

No sig differene in injury rate between kicking vs non-kciking leg in soccer

Hamstrings Strains

femoris (long head > short head)

most commonly injured near
muscle/tendon junctoin (~10cm distal to
ischial tuberosity)

Long and short head serpate nerve supply

asychnous contraction
Triarticular function: attachment to
sacrtuberous ligament

Hamstring Injury: Risk Factors

Extrinsic (environment related)

Inadequate warm up
Lack of literature for best practice guidelines
Warm up increases amount of force and
length a muscle can absorb prior to tearing

Training errors
Poor playing surfaces
Fatigue related to unsuitable structure and
content of training

Hamstring Injury: Risk Factors


(player related)

Muscle imbalances

H/S vs Quads

Lack of flexibility

Increasing age

and HS

yrs old 4x more likely than <20 year olds

Previous HS injury
Lack of neuromuscular control trunk/pelvis
Poor LL proprioception

Hamstring Injury: Risk Factors

Previous knee injury

Eg ACL or osteitis pubis

Injuries late in season or competition
Fatigued muscle absorbs less energy before

Inadequate fitness
Running style

Forward lean over stride increase HS length

Kicking technique

Hamstring Injury: Risk Factors

LBP (not proven)

Altered neural input L4/5; L5/S1

Age related factor: degen of L4-S1 most common

Altered lumbo-pelvic biomechanics (not proven)

Local ms response (eg increased tone) predisposes

to injury

Increased ant pelvic tilt increased lumbar

lordosis increased risk of HS injury

SIJ dysfunction

Early activation of BF in SIJ pain subjects during


Lateral Ankle Sprain:

Mechanism of Injury

injury: inversion; adduction

and mostly in plantarflexed position (eg
climbing down stairs; stepping off curb;
landing on forefoot)
However several studies showed lateral
ankle sprains occurring during DF: eg
during cutting/side stepping movements
where TCJ in ~20-25 deg DF

Lateral Ankle Sprain


commonly damaged structures:

Anterior talofibular ligament (weakest of lateral ligaments &

most commonly injured as ankle moves progressively through
Calcaneofibular ligament (most commonly injured when
inversion injury occurs w/ ankle in DF)
Posterior talofibular ligament (strongest of lat. ligaments;
fibres tensed only in max DF)



Medial STJ compression injury

Fracture of 5th metatarsal: fib brevis attachement avulsion
Malleolar fractures

Clinical Signs of Lateral Ankle


markers: swelling;

bruising; heat
Tenderness on palpation: lateral ankle,
distal to lat. Malleolus
Anterior Drawer Test +ve for ATFL in PF
Anterior Drawer Test +ve for CFL in DF
Talar Tilt Test +ve for ATFL

To Determine Whether X-ray


Ankle Rules:

Tenderness at following sites:


edge of fibular or tip of lateral

Posterior edge of tibia or tip of medial
Base of 5th MT
Navicular bone

Unable to weight bear at time of injury

Unable to walk 4 steps in ED/Clinic

Achilles Tendinopathy


Achilles tendon is a confluence of the gastrocnemius

and soleus muscles. It inserts into the posterior surface
of the calcaneus distal to the posterior superior
calcaneal tuberosity


Tendon responds to repetitive overload beyond

physiological threshold by inflammation of the sheath,
degeneration of the body or a combination of the two.
May also occur from stresses within physiological
limits, as repetitive microtrauma may not allow
adequate time for repair

Achilles Tendinopathy:
Contributing Factors

Altered weight bearing surfaces (slippery; uneven; excessively hard)

Inappropriate foot wear
Training errors
Type of activity/sport (involving stretch-shortening cycle eg


Previous injury
Increased age
Male gender
Increased adiposity/metabolic disorders
Pre-existing tendon abnormalities
Triceps surae inflexibility
Abnormal LL biomechanics

Achilles Tendinopathy & Over

One biomechanical factor commonly considered to be associated
with Achilles tendinopathy is the presence of excessive foot
Clement et al. originally proposed that excessive pronation of the
foot may lead to Achilles tendinopathy through two mechanisms

1) excessive pronation of the foot creates greater hindfoot

eversion motion resulting in excessive forces on the medial aspect
of the tendon and subsequent microtears.
2) abnormal pronation of the foot asynchronous movement
between the foot and ankle during the stance phase of gait
subsequent wringing effect within the Achilles tendon. This
wringing effect is theorised to cause vascular impairment within the
tendon and peritendon and elevated tensile stress subsequent
degenerative changes.

Biomechanical Factors

Azvedo et al (2009) showed that in runners with

Achilles Tendinopathy there was:

Reduced knee range of motion from heel strike to

midstance (to compensate for weak proximal hip mm
ie rec fem reduces shock absorbing capability
increases load on Achilles
Reduced preactivation of Tib Ant before heel strike:
reduces stiffness in tendo-muscular system and
impedes ability to tolerate impact forces increases
Achilles loading
Prolonged activation of gastroc and soleus
prolonged loading of Achilles

Biomechanical Factors

Muntaneu and Barton (2011) conducted a systematic review

of LL biomechanics of runners with Achilles tendinopathy and

increased eversion range of motion of the rearfoot

reduced maximum leg abduction
reduced ankle joint dorsiflexion velocity
reduced knee flexion during gait
altered plantar pressures and ground reaction forces as well as
reduced peak tibial external rotation moment.
Further, cases displayed differences in the timing and amplitude
of a number of lower limb muscles. Notably, the onset of tibialis
anterior was delayed and the duration of soleus and lateral
gastrocnemius was increased. In addition, cases displayed
reductions in the amplitude of gluteus medius and rectus femoris

Achilles Tendinopathy: Clinical


on waking; difficulty walking after getting

out of bed
Pain in the back of heel and ankle and Achilles
Pain with calf stretching or heel raise
Pain on DF
Pain with steps (down >up)/up
Antalgic gait pattern
Initial stage: pain may improve after warming up

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