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Biomechanical

Principles and
Mechanisms of
Injury
Theruni Wijewardene
(t.wijewardene@gmail.com)

Lecture Objectives
Identify

the biomechanical principles of


common sports injuries related to
specific fields

Biomechanics
Biomechanics

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

Biomechanics

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:
A)

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
motion

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
Components
Motion
Force
Momentum
Levers
Balance

Motion
Movement

of body or object in space with


respect to time
Described in terms of:

Velocity
Acceleration
Displacement
Time

Eg.

How fast was the athlete running when he


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

Force
An

influence that causes an object or person


to undergo a certain change which in turn
influences its:

Movement
Direction
Geometrical or anatomical structure

Eg.

A tackle on the lateral aspect of the knee


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

Momentum
Product

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

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

Resistance
Force
Axis of rotation/fulcrum

Most muscles in the human body are 3 rd Class


Levers and create rotation of the distal
segment

Balance
Stability
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
New/different

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

Common Sports Injuries


Shoulder

RC tears / Impingement Syndrome


ACJ sprains

Elbow

Lateral epicondyalgia/Tennis elbow

Common Sports Injuries


Knee

Meniscus
Ligament
ACL
PCL
LCL
MCL

Patellofemoral pain syndrome


Muscles
Hamstring

strain/tear

Common Sports Injuries


Ankle/Foot

Lateral ankle sprain


Achilles tendinopathy

Rotator Cuff
Injury/Impingement Syndrome
The

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
tendons.

Rotator Cuff
Injury/Impingement
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
stabilizers.
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
stages.
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
injury
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
damage
Note: Much of the force generated in overhead sports occurs in
the trunk and lower extremity, and require significant stability
and strength

RC Injuries
Often,

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
movements
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
anteriorly
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


Injury
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
supraspinatus

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
biceps
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
clavicle
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.
Movement
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
Usually

due to increase in backhand stroke


playing or attempting to increase power or
incorrect backhand technique in
tennis/badminton/squash
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


Signs
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
Anatomy:

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


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

Function:

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
condyles
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


Rapid

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

More

common in more vulnerable older and/or


degenerative meniscii

Increased breakdown over time


Reduced ability to repair with increased age

Associated

injury:

Other major injuries eg ACL tear

Medial VS Lateral
Medial

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


Injury
Mechanism of injury
Pain

Well localised to joint line


With loaded flexion eg squat

Can weight bear (but may be painful)


Effusion

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

Anatomy:

Arises lateral femoral condyle to anterior tibia spiralling forward


from lateral to medial from femur to tibia

Function:

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
hyperflexion

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
2

Mechanisms:
Non-contact
Contact

ACL Rupture: Non Contact


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

Knee hyperextension with internal tibial rotation

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


landing

eg basketball players; gymnasts after


jumping/landing

May hear pop, crack, snap

ACL Injury: Contact


Hyperextension:

Eg tackle anterior around tibia


Motion can rupture layer by layer
Posterior

capsule stretched ++ or torn

ACL
PCL

Valgus

(partially)

or varus force to knee: eg tackle

Valgus: MCLmedial mesniscusACL


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

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
ACL

rupture; MCL rupture; Med. mensicus

Posterior Cruciate
Ligament
Anatomy:
Antero-lateral

aspect of medial femoral


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

Function:

Provides 95% restraint to posterior


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

PCL: Mechanism of Injury


PCL

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
injury)

Hyperextension

injury

usually accompanies ACL


injury

Clinical Symptons of PCL Injury


Posterior

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

MCL
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


Valgus

stress

Contanct: direct blow to the outer aspect


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

Due

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


Injury
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
hyperextension
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


Mechanism

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

Patellofemoral Pain Syndrome


Anterior

knee pain
Biomechanics of injury:

direct trauma eg fall


overuse injury (repetitive knee bending eg
running/jumping/squatting)
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)
Genu

valgum
External tibial torsion
Increased femoral anteversion

Clinical Signs of PFPS


TOP

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

X-Ray of Knee Required...


When

2 or more of the following features are


present:

>55 years old


Effusion of the joint
Haemarthrosis

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


technique

Unable to weight bear


Point tenderness on palpation

Patella; tibial plateau; femoral condyles or head of


fibula

Hamstrings
Muscles

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
femoris

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
Biceps

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


Intrinsic

(player related)

Muscle imbalances
Especially

eccentric
H/S vs Quads

Lack of flexibility
Quads

Increasing age
>25

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

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

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


SLS

Lateral Ankle Sprain:


Mechanism of Injury
Supination

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


Most

commonly damaged structures:

Anterior talofibular ligament (weakest of lateral ligaments &


most commonly injured as ankle moves progressively through
PF)
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)

Associated

injuries:

Medial STJ compression injury


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

Clinical Signs of Lateral Ankle


Sprain
Inflammatory

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


Required
Ottawa

Ankle Rules:

Tenderness at following sites:


Posterior

edge of fibular or tip of lateral


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

Unable to weight bear at time of injury


Unable to walk 4 steps in ED/Clinic

Achilles Tendinopathy

Anatomy:

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

Injury:

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
Extrinsic:

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


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

Intrinsic

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

Achilles Tendinopathy & Over


Pronation
One biomechanical factor commonly considered to be associated
with Achilles tendinopathy is the presence of excessive foot
pronation
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
showed:

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


Signs
Pain

on waking; difficulty walking after getting


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

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