International Committee of the Red Cross

Physical Rehabilitation Programme

Lower Limb Orthotics

"The human foot is a masterpiece of engineering
and a work of art."
Leonardo da Vinci
 WARNING!
This document is a compilation of
articles from different sources.
The document is NOT to be
published or sold.
The document is intended
STRICTLY for personal uses as a
training guide and/or reference.
Table of Contents
I. INTRODUCTION TO ORTHOTICS................................................................................... 1
1.1 ORTHOTIC SCIENCE ........................................................................................................................1
1.2 ORTHOTIC BIOMECHANICS ..........................................................................................................5

II. ANATOMY OF THE FOOT ................................................................................................ 21

2.1 INTRODUCTION................................................................................................................................21
2.2 ANATOMY REVIEW: LEG, ANKLE AND FOOT........................................................................21
2.3 MOVEMENTS OF THE FOOT AND ANKLE COMPLEX.........................................................61

III. PATHOLOGY OF THE FOOT ........................................................................................... 67

3.1 FLAT FOOT (PES PLANUS)............................................................................................................67
3.2 PES CAVUS ........................................................................................................................................73
3.3 FOOT PAIN..........................................................................................................................................77
3.4 METATARSALGIA .............................................................................................................................78
3.5 BUNION (HALLUX VALGUS) .........................................................................................................81
3.6 SESAMOIDITIS..................................................................................................................................89
3.7 HAMMER TOE ...................................................................................................................................95
3.8 CLAW TOE ..........................................................................................................................................98
3.9 MORTON'S NEUROMA .................................................................................................................103
3.10 TALALGIA (HEEL SPURS)............................................................................................................107
3.11 NEUROPATHIC JOINT DISEASE ..............................................................................................108
3.12 DIABETES MELLITUS ..................................................................................................................116
3.13 CHARCOT FOOT ............................................................................................................................119
3.14 CLUB FOOT .....................................................................................................................................123

IV. CLINICAL ASSESSMENT ................................................................................................ 126

4.1 CLINICAL ASSESSMENT OF THE FOOT AND ANKLE .......................................................126
4.2 SUBJECTIVE ASSESSMENT ......................................................................................................127
4.3 OBJECTIVE ASSESSMENT.........................................................................................................130
4.4 RANGE OF MOTION ......................................................................................................................133
4.5 MUSCLE TESTING .........................................................................................................................153
4.6 JOINT STABILITY ...........................................................................................................................171
4.7 LEG LENGTH MEASUREMENT .................................................................................................180

V. BIOMECHANICS................................................................................................................. 182
5.1 MECHANICS – LEVERAGE/MOMENT ....................................................................................182
5.2 MECHANICS – STRESS ................................................................................................................184
5.3 MECHANICS – TORSION .............................................................................................................188
5.4 APPLIED BIOMECHANICS ..........................................................................................................190

VI. ORTHOTIC SCIENCE ....................................................................................................... 223

6.1 INTRODUCTION..............................................................................................................................223
6.2 INSOLES............................................................................................................................................224
6.3 ORTHOPAEDIC SHOES................................................................................................................265
6.4 SHOE MODIFICATIONS ...............................................................................................................268

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 I. INTRODUCTION TO ORTHOTICS

1.1 ORTHOTIC SCIENCE

Definition
The word "orthosis" comes from the Greek "ortho", which means "straight", "upright" or "correct".
An Orthosis is an external appliance or apparatus used to support, align, prevent, or correct
deformities or to improve the function of movable parts of the body. In some cases, it has an antalgic
effect as well.
Archaeologists have uncovered specially fabricated braces in Egypt that date back from 2500 BC.
Later there are records that some blacksmiths and armour makers became known for fabricating
devices for injured people. As the need grew due to improvements in health care and increasing life
expectancy, craftsman began to specialise in fabrication of devices. These specialists tended to come
from trade backgrounds such as ship builders and metal workers.
Ambroise Paré, the "father of modern surgery", who published his work in 1575, made a perforated
steel orthosis for the correction of scoliosis and an ankle foot orthosis to correct club foot.

Classification According to Anatomical Level

As for lower limb prosthetics, lower limb orthotics have been classified according to the body
segments and according to joints involved.

Table 1: Classification of Lower-Limb Orthotics (ISO1 / ISPO2)

Short Body Segments Main Lower-Limb
Denomination
Name involved Joints Involved

Foot Orthosis FO Foot -

Knee Orthosis KO Thigh, Leg Knee

Hip Orthosis HpO Pelvis, Thigh Hip

Ankle Foot Orthosis AFO Leg, Foot Ankle

Knee Ankle Foot Orthosis KAFO Thigh, Leg, Foot Knee, Ankle

Hip Knee Ankle Foot Orthosis HKAFO Pelvis, Thigh, Leg, Foot Hip, Knee, Ankle

Thoracic Hip Knee Ankle Foot Trunk, Pelvis, Thigh,

THKAFO Hip, Knee, Ankle
Orthosis Leg, Foot

1
ISO - International Standards Organisation
2
ISPO – International Society for Prosthetics and Orthotics

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Classification According to Function

The general functions of orthotics are:

• to control, guide, limit and/or immobilize an extremity, joint or body segment for a particular
reason
• to restrict movement in a given direction
• to assist movement generally
• to reduce weight bearing forces for a particular purpose
• to aid rehabilitation from fractures after the removal of a cast
• to otherwise correct the shape and/or function of the body, to provide easier movement
capability or reduce pain
Biomechanically, orthoses can be classified according to the following functions:
a) Correction orthoses:
• To correct a deviation of bones or
joints. The application of an
appropriate 3-point force system on
leg segments will aim to re-align the
segment(s).

b) Fixation / accommodation orthoses:

• to resist or block an unwanted
movement in order to bring a stable
position;
• to prevent further deformities,
unbalanced forces;
• To prevent or to alleviate pain.

c) Extension / relieve orthoses:

• to discharge or to unload the body
weight partially or completely with
the aim of minimizing bad posture or
to relieve pain

d) Compensation orthoses:
• to compensate leg length
discrepancy

Multi-Disciplinary Team

The interdisciplinary health care team has

become essential in the rehabilitation of patients
whose function would be enhanced by an
orthosis. The complexity of the rehabilitation
process and the multidimensional needs of
patients frequently require the expertise of many
different profession disciplines. The
rehabilitation team often shaped by the typical
needs and characteristics of the patient
population that it is designed to serve. The
professionals most often represented on the
team include an orthopaedic or vascular
surgeon, neurologist, the patient's primary
physician, an orthotist, nurses, a physical and/or
occupational therapist, a dietician, a social
worker, a vocational counsellor, and, most
important, the patient. Each of the professionals
has an important role to play in the rehabilitation

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of the patient. Patient education is often one of the primary concerns of the team; understanding the
condition's process and prognosis and the available treatment options helps patients be active
partners in care. Patients and their families are best able to define their needs and concerns and
communicate them to the other team members. Each member of the team has the responsibility to
contribute to this education so that patients have the information needed for an effective partnership
and positive outcome of rehabilitation efforts.
Research studies across a wide variety of medical conditions and health discipline contain evidence
that those patients who feel prepared and informed are most likely to invest in and comply with
recommended interventions and often have most positive health outcome.
A "mini-team" consisting of patient's physician, a physical therapist and an orthotist can usually be
assembled, even in a small town with fewer facilities. Regardless of its size, an effective team views
the patient and family for a holistic perspective, with an input from each specialty being of equal
importance.
In summary, the team is a diverse group of health care professionals, each with particular skills to
address the needs of the patient. Each member of the team must understand the role and
responsibilities of the other members. Clear and frequent communication is essential for this team to
function effectively.

Materials Used in Orthotics

Orthoses can be classified in 3 main families according to material used: rigid, semi-rigid and flexible
orthoses. The choice will depend on the function and on the goal to achieve.
Wood
The only application of wooden product used in orthotics is cork used in insole.
Leather
Used for suspension straps, belts, protective coverings. Also used in the manufacture of footwear,
orthopaedic shoes and insoles.
Fabric
Wool, cotton, silk, and a number of synthetic materials such as nylon, olefin, polyester, rayon, vinyl. It
can be woven or knitted, moulded. Used in corsets, belts and stockings.
Rubber
The elastic properties and high friction coefficient of rubber materials make them useful in orthotic
devices. They are mainly used for footwear.
Metal
The 3 types of metals that are commonly used in
orthotics are aluminium, steel, and alloys of titanium
and magnesium. The figure shows a comparison of
their maximum strength, stiffness, and weight per unit
volume (density).
Steel and stainless steel have the advantage of low-
cost, ready availability and relative ease of fabrication.
It is strong, rigid, and fatigue resistant. However,
unfortunately, it is also relatively heavy. Widely used in
orthotics for joints, metal bands, cuffs, cables, springs,
bearings, etc.
Aluminium is much lighter than steel with a high strength-to-weight ratio. The main disadvantage of
aluminium is its relatively poor resistance to fatigue at high load levels.
Titanium and magnesium alloys have strength comparable to steel but are much lighter and have a
good corrosion resistance. Their main disadvantage is their relatively high cost.
Most components manufacturers adopted a system of classification consistent with patient weight and
functional activity level. This allows the practitioners to order components optimized for each patient's
weight and functional activity level.

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Plastics
Plastics include any synthetic material that can be moulded, extruded, laminated or hardened into any
form. Plastics are lightweight, can be readily formed into complex anatomical shapes, tend to be non-
toxic, and are generally impervious to body fluids. There are two categories of plastics: thermoplastics
and thermosetting.
Thermoplastic materials (such as polypropylene) become soft when heated and hard when cooled.
They can be repeatedly heated and re-moulded. Thermoplastics are referred to as high-temperature
or as low-temperature thermoplastics. High-temperature thermoplastics become soft above 80°C and
low-temperature thermoplastics below 80°c. The latter can be formed directly on a body segment and
is used for temporary upper-limb splints.
Thermosetting materials (such as polyester) develop a permanent shape once they solidify and they
cannot be reheated and reformed. They are usually laminated with layers of natural or synthetic cloth
and can be sanded, trimmed, drilled and riveted. They can also be pigmented to match the patient's
basic skin colour. Addition of glass or carbon fiber (see "composites" below) dramatically increases its
maximum strength and stiffness.
Composites
Newer materials include composites such as graphite. Graphite is very strong and very light. It is
impossible to modify its shape after being heated and shaped. The most commonly used is carbon
fibre (pictures).

Silicones, thermoplastic elastomers, and urethanes are mainly used in comfort liners (mainly
prosthetics).

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1.2 ORTHOTIC BIOMECHANICS

Lower limb orthoses are orthopaedic devices that are designed to promote structural integrity of the
joints of the foot and lower limb. Some lower extremity orthoses function by resisting ground reaction
forces that cause abnormal skeletal motion to occur during the stance phase of gait while others
function by applying forces to the body and thereby affecting joint moments. The therapeutic benefit of
the force application may be to resist or assist motion, transfer force, or protect a body part. The
amount of force and the area of the body subjected to the force influence the comfort of the orthosis.

Common Causes of Gait Deviation

The most common causes of gait deviations are:

• Muscle weakness
• Deformity (bony or soft tissue)
• Impaired control including sensory loss
• Fear or anxiety
• Pain
• Ill-fitting or poorly aligned orthosis
1. Muscle weakness
Weak muscles can cause numerous postural and gait deviations:
Example 1: Weak abductors on the stance limb can result in increased pelvic drop on the swing
side as shown in Figure 1. This is relative adduction of the stance limb and relative
abduction of the swing limb. A person with weak abductors is likely to have a
trendelenburg gait pattern.

Figure 1: Weak abductor muscles allow the pelvis on the opposite side to tilt down during stance phase.

Example 2: An exaggerated lordosis or an anterior pelvic tilt may result from weakness of the
abdominals. The abdominals and gluteus maximus (hip extensors) normally work as a
force couple to tilt the pelvis posteriorly. If either are weak, it essentially allows the
pelvis to "fall" into an anterior pelvic tilt.

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 Example 3: Weak dorsiflexors of the foot might result in foot-slap on loading if they are unable to
control the plantarflexion moment created by the ground reaction force (GRF). In
swing, weak or absent dorsiflexors would result in toe-drop.
Example 4: Weakness of the plantarflexors of the foot causes a lack of control of the advancing
tibia in stance and excessive knee flexion. Weakness of the plantarflexors might also
cause loss of heel-off for terminal stance.
Example 5: Excessive pronation on loading and throughout midstance may result from weakness
of the posterior tibialis or tibial anterior.
Example 6: Weakness of the peroneals results in excessive varus at the subtalar joint. There is a
loss of some stabilization of the forefoot during stance, allowing the medial foot to lift
off the ground as the foot is supinating.
Frequently, individuals with muscle weakness may try to adapt the position of the trunk to manipulate
the position of the GRF (ground reaction force) in relation to the joint axes. It is common to see
individuals lean the trunk to make up for lower-extremity weakness. The direction of the lean depends
on the weakness present. Some examples of muscle weaknesses and patient compensation
mechanisms are:
Example A: Weakness of the gluteus medius may result in a lateral trunk lean toward the side of
weakness. Leaning the trunk toward the weakness brings the GRF closer to the joint
axis as shown in the Figure 2. This decreases the moment-arm associated with the
GRF. A shorter moment arm means less moment is created by the GRF about the hip
joint, and in turn, the gluteus medius does not have to generate as much force to
counter the GRF moment and stabilize the hip joint.

Figure 2: Lateral trunk lean in a person with weak gluteus medius.

Example B: A person with hip extensor weakness may lean the trunk posteriorly (Figure 3) in
order to change the GRF from a flexor moment to an extensor moment, obviating the
need for the gluteus maximus to work.

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 Figure 3: Posterior trunk lean creating more extension moment at the hip and increasing hip joint stability.

Example C: An anterior trunk lean due to weakness in the quadriceps: leaning the trunk forward
moves the GRF anterior to the knee to give an extension moment, and therefore
adding stability to the knee (Figure 4). Generally, with weak quadriceps, the individual
will try to limit the amount of knee flexion during stance.

Figure 4: Anterior trunk lean creating more extension moment at the knee and increasing knee stability.

2. Deformity (bony or soft tissue)

Many deformities create a leg length difference. Whether the difference is a true anatomic leg length
discrepancy or something that effectively creates a leg length difference, walking may be affected.
Example 1: Hip flexion contracture and/or knee flexion contracture can create short limb.

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 Example 2: Insufficient dorsiflexion at the ankle, as occurs with weakness of the dorsiflexors or
contracture of the plantarflexors, effectively lengthens the limb.
Example 3: Insufficient flexion at the hip and knee can prevent the necessary shortening of the
limb in swing, thereby creating a long limb. This makes it difficult to clear the ground
during swing.
Example 4: In the frontal plane, gait can be affected by deformities of varus and valgus at the
knee. Varus and valgus deformities can alter the width of the base of support. In some
cases, varus and valgus deformities at the knee can result in varus and valgus
deformities of the calcaneus and forefoot as the individual adjusts the foot position to
get the foot flat on the floor. The moment created by the GRF passing through a joint
with a varus or valgus deformity is greater than that in a normally aligned joint as
shown in Figure 5. This increased moment tends to worsen the deformity and stress
the collateral ligaments of the knee or the ankle.

Figure 5: GRF resulting in increased varus and valgus moments in individuals with varus and valgus knee
deformities respectively.

Example 5: In the presence of a significant plantarflexion contracture, an individual may be forced

to land on the toe or footflat rather than the heel at initial contact.
Example 6: In the transverse plane, contractures can occur in the medial or lateral rotators of the
hip. These contractures can affect the degree of toe-in or toe-out. Rotation
contractures will affect the degree of forward and backward pelvic rotation (Figure 6):
a right lateral rotation contracture would limit the left forward rotation of the pelvis
while a right medial rotation contracture would limit the left backward rotation of the
pelvis.

Figure 6: Relationship of hip rotational contractures to pelvic forward and backward rotation.

As in the case of individuals with muscle weaknesses, individuals with bony or soft tissue deformities
will employ different compensation mechanisms to accommodate for the deformities.
Example A: An individual with leg length discrepancies may use one of the following options to
accommodate for the discrepancy when swinging the leg with the longer length: raise
the pelvis on the long leg side by hip hiking or by laterally leaning trunk to the side
opposite the long leg, circumduct the long limb to gain clearance from the ground,
excessively flex the hip and knee of the long limb, vault on the shorter limb side.

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 Figure 7: Gait deviations to accommodate a long leg.

Example B: In double stance, a wide walking base may help accommodate a longer limb in an
individual with limb length discrepancy. For smaller differences in length, an individual
may accommodate by pronating the foot on the long side and supinating the foot on
the short side.
Example C: A hip flexion contracture of 15° or less may be accommodated by an increased
anterior pelvic tilt or increased lumbar lordosis.
3. Impaired muscle control including sensory loss
Some of the factors that can cause gait deviation are:
• Pathologic states involving either upper or lower motor units
• Central nervous system lesions as in cerebral palsy, cerebral vascular accident, or spinal cord
injury
o Peripheral nerve damage that results in motor and/or sensory damage
In case where there is significant paralysis or lack of muscle control, gait can become impossible. In
other instances however, orthoses can compensate for the loss of voluntary control of the muscles.
4. Fear or anxiety
Fear of falling is the typical reason that cause gait deviation in individuals. Fear of falling may cause
the individual to:
1. Walk with a wide base of support and/or
2. Decrease the step length of their gait. At heel strike, the shorter step length causes a reduced
horizontal component of the force at the heel as shown in Figure 8.

Figure 8: Heel forces associated with a shorter step length compared to those during a normal step length.

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5. Pain
A painful limb can cause gait deviation. The natural response to pain is to try to move away from it, to
take the weight or pressure off the painful area.
Example 1: An individual with pain on the heel may avoid landing on the heel, bypassing heel
strike and moving directly into footflat to get weight off the area.
When motion about a joint is painful, a contracture may develop. This can lead to deformity of the
limbs.
With the application of orthoses, pain can develop from the stress and strain of the device on the
tissues of the body. The forces applied to the body may exceed the tolerance of the tissue, leading to
pain and gait deviations.

Functions of Orthoses

1. Correction
Orthoses are used to realign skeletal segments whose normal alignments in three-dimensional space
or in relation to each other has been disturbed by congenital or acquired factors. An individual with
genu varus may wear a KO with a 3-point pressure system (Figure 9) to counteract the deforming
forces and realign the deformity.

Figure 9: Orthosis in use for correction of genu varus.

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A person with knee contracture, a condition disallowing for the physiological degree of extension of the
knee joint, may wear a KO with a 3-point pressure system (Figure 10) to stretch the contracted
structures and to realign the joint.

Figure 10: A knee orthosis used to correct knee contracture.

2. Fixation
Orthoses are used to control excessive or unwanted motion. A woman who has quadriceps paralysis
may wear a KAFO (Figure 11) that has a mechanical lock to stabilize the knee.

Figure 11: KAFOs used to stabilize the leg.

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A child who sustained a spinal cord injury may be fitted with a THKAFO (Figure 12) that supports him,
immobilizing the hips, knees, and ankles so he can stand. In a patient with spina bifida, the same
device can be used for walking as well.

Figure 12: Reciprocating Gait Orthosis (RGO).

In addition to resisting motion, orthoses can maintain a particular alignment. A hip orthosis similar to
that shown in Figure 13 can keep the femoral head in the acetabulum for a youngster with Leg-Calve-
Perthes disease.

Figure 13: A pediatric hip abduction orthosis used for managing the range of motion of the hip in a patient with
Leg-Calve-Perthes Disease.

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3. Extension
Orthoses can be designed to transfer forces from one portion of the body to another (example, a foot
orthosis that shifts load from a heel spur to the forefoot). An orthosis that incorporates an ischial seat
(Figure 14) transfers weight-bearing stress from the pelvis to the distal end of the orthosis, bypassing
the skeleton of the lower limb.

Figure 14: KAFO with ischial seat.

Load transfer is often used in FOs. A woman with metatarsalgia (Figure15) will be more comfortable
with an FO that includes a pad underneath the metatarsal shafts (Figure 16). The pad transfers force
from the painful metatarsal heads to the less sensitive shafts.

Figure 15: Metatarsalgia: pain in the front part of Figure 16: Metatarsal pad.
the foot, under the heads of the metatarsal bones
(the ball of the foot)

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4. Compensation
Orthoses can be used to compensate for structural or functional leg length discrepancies. These
orthoses (Figure 17) will be in the form of heel lifts or full shoe lifts on the shorter leg and function by
raising the short leg and levelling it with the other leg. The orthoses therefore compensate for the leg
length discrepancy and level the pelvis.

Figure 17: Heel lifts and full shoe lifts to compensate for LLD.

Important Design Aspects of Orthoses

1. Comfort
Regardless of its purpose, the orthosis must be comfortable; otherwise, the patient is unlikely to wear
it. If an uncomfortable orthosis is worn, it may irritate or injure the skin and underlying structures. A
major element in ensuring comfort is minimizing pressure by maximizing the area covered by the
orthosis. Another way to improve comfort is to provide sufficient leverage through which the
longitudinal segments of the orthosis apply force.
Maximizing Area
The greater the portion of the body that the orthosis covers, the lower is the unit pressure. For
example, the calf band of an AFO is likely to be more comfortable when it wider than smaller. For
the same amount of force to be applied by the orthosis, the pressure per unit area decreases as
the area through which force is applied is increased.
Force
Pr essure =
Area
Snug Fit
Regardless of material or design, some portion of an orthosis must touch the body. The contact
should be snug, rather than constricting. An excessively tight band will compress superficial blood
vessels and cause pain and abrasions. Equally important, the contact should not be loose. For
example, an AFO that has an overly loose calf band will irritate the skin as the individual passes
through the stance phase of gait.
Leverage
The longer the longitudinal segment of an orthosis, the less pressure exerted at each end to
provide the same functional benefits. In an AFO, a calf band with a relatively long forearm applies
less pressure on the proximal forearm than a band with a shorter forearm.
2. Orthotic Effectiveness
Although comfort is a prime prerequisite of all orthoses, the therapeutic benefit of the device will be
realized only if the device applies forces effectively. An orthosis worn over a malaligned body segment
can exert force to correct or reduce the deformity if the deformity is not rigid and anatomic joint yields
to passive force. If the deformity cannot be reduced passively, then the orthosis must accommodate
the malalignment. For examples, a patient may have a knee that rests in a position of genu valgum.
When the clinician applies appropriate manual force, the knee achieves a straighter alignment. In such
an instance, the patient would benefit from a corrective orthosis that will maintain the improved

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position. Alternatively, a person may have fixed hallux valgus (Figure 18) deformity that does not
change when corrective force is exerted. The individual will benefit from an accommodative shoe that,
although it does not change foot alignment, will be comfortable.

Figure 18: Hallux Valgus.

Pressure Systems
Supportive systems involve a series of forces and counterforces which are known as pressure
systems. The basic pressure system for an orthosis is the three-point force system. The system
consists of a principal force acting in one direction and two counterforces acting in the opposite
direction, located proximal and distal to the principal force. For example, a patient who has genu
valgum will have the deformity controlled by wearing a KAFO, which exerts laterally directed force
on the medial aspect of the knee and medially directed counterforces on the lateral aspect of the
thigh and leg. This is shown in Figure 19.

Figure 19: Three-point pressure system in a left KAFO to control genu valgum.

Some orthoses exert a four-point force system. The parapodium, a THKAFO, applies posteriorly
directed forces from the chest band and the anterior leg bands, and also applies anteriorly directed
forces from the dorsolumbar band and the back of the shoe supports as shown in Figure 20.

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 Figure 20: Four-point pressure system (two sets of 3PP system) in a parapodium to assist standing.

Ground Reaction Force

When one walks, the floor reaction is resultant of the vertical force, which represents the
interaction of gravity and acceleration; the horizontal force, which represents the tendency of the
foot to slide forward; and the rotational force, which prevents the torsional movement of the leg. All
wearers of lower limb orthoses must contend with floor reactions while standing or during the
stance phase of gait.
At the time of heel contact, the floor reaction normally passes behind the ankle, exerting a plantar
flexion moment of force (shown in Figure 21). In a normal person, contraction of the dorsiflexors
controls ankle plantarflexion in response to this external force.

Figure 21: GRF on an AFO with solid ankle and anterior calf band.

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Use of 3PP and 4PP Systems in Orthotic Design

Most orthotic designs use a balanced parallel force system to control joint motion. These force
systems operate, in effect, as a first-class lever system (a lever system where the forces are applied
on opposite sides of a fulcrum or point of rotation). In a three-point control system, a proximal and a
distal force applied in the same direction are countered by (or balanced against) a third force applied
in the opposite direction at a point somewhere in between the proximal and distal forces. Each plane
and direction of motion that the orthosis attempts to control has a three-point loading system as shown
in Figure 22.

Figure 22: Force system in solid-ankle AFOs.

Some orthotic designs (Figure 23) use an additional force, acting as a balanced four-point pressure
system, to allow better control of rotatory and translatory motion of the joint or to provide effective
control of motion in multiple planes. Distributing the counterforce (central force) on either side of an
anatomical joint axis reduces shearing forces at the joint while simultaneously controlling the joint
movement.

Figure 23: An orthosis with a 4-point pressure system.

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Force(s) applied at specific points on the limb by the use of lower limb orthoses impact the joint
indirectly through the contact between orthosis (via straps, pads, bands, or total contact fit) and the
soft tissue structures (skin, muscle, fat, fascia, tendons) and bones of the limb. Many molded AFOs
are designed to use the shoe as a means of closure to apply the desired force to the foot. The loading
forces of a three- and four-point control system on a limb segment or joint may be substantial; even
low pressure sustained over long periods of time can lead to tissue deformation and breakdown. For
this reason, orthotic forces are often distributed over as much surface area of the limb as possible, to
keep pressures applied by the orthosis within levels that are tolerable to soft tissue and comfortable
for the patient during wear. This is especially important for patients with sensory loss, cognitive
impairment, or compromised circulation, who may have increased vulnerability to skin breakdown.
Most orthotic designs incorporate "relief" for areas of bony prominence or use padding to cushion or
distribute forces that would otherwise be excessive.
As a first-class lever system, the magnitude of each of the forces in the control system is inversely
related to the distance between its point of application and the axis of movement. For the system to be
in equilibrium, the forces must sum to zero and the bending moments created must sum to zero.
Consider, as an example, a knee orthosis designed to control genu recurvatum (Figure 24). The
central force in the system is an anteriorly directed force applied at the posterior knee. The opposing
paired posteriorly directed forces located above and below the central force are applied at the anterior
femur and the anterior tibia. Although these forces can be applied anywhere along the shaft of the
femur and tibia, the magnitude of the required force decreases as the point of application is moved
upward on the femur and downward on the tibia. If the forces are in equilibrium, the central force
applied at the posterior knee will be twice the magnitude of either of the other forces.

Figure 24: Forces applied by an orthosis used to control recurvatum.

Because most human movement is multiplanar, with an axis of joint motion offset from any single
plane, no orthosis can perfectly match or mimic the biomechanical motion of the anatomical joint. As a
result, the reactive forces that originate from the limb segment and the forces directed by the orthosis
will be mismatched. Because these applied and reactive forces are, to some extent, noncollinear, any
multiple-point force system applied by an orthosis to a limb in an effort to control joint motion will have
a desired (corrective, controlling) and undesired (deforming) impact. These effects are best
understood in terms of bending moments and shearing forces.
Characteristic features of this three-point system are the bending moment and transverse shear forces
created by the applied forces. These loads are created when forces applied to a "rigid" structure are
not collinear with the reacting forces. Both the bending moments and the transverse shear forces are
important to the design and intended purpose of the orthosis.
The bending moment varies along the length of the structure (leg), being zero under the end forces
and greatest under the middle force. This moment can be graphically represented by the triangular
bending moment diagram shown in Figure 25. The maximum corrective or control potential is applied
at the apex of the diagram.

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 Figure 25: Bending moment and shear force diagrams for an orthosis that applies maximum moment at the
anatomical knee joint.

If the central force is moved away from the joint center toward one end of the limb, reaction forces of
different magnitudes are required to maintain equilibrium. These changes in the location of the
maximum bending moment and shear force are demonstrated in Figure 26.

Figure 26: Variations in the magnitudes and locations of the bending moment and shear force relative to the
location of the central force exerted by an orthosis.

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Figures 25 and 26 also illustrate the transverse shear forces that displace one segment relative to
another along the plane of action of the forces. The location and magnitude of the shear forces
depend on the external support reactions generated by the brace and mechanisms of loading. The
forces are controlled through orthotic design features such as strap location, selective strap tightness,
and depth/shallowness of the bands. In order to minimize shear force at any one point along a
segment, the sum of the forces on opposite sides of the segment must be equal to zero.

Figure 27: Bending moment and shear force diagrams of a four-point system.

In the four-point system shown in Figure 27, two horizontal or parallel forces (Fproximal, Fdistal) are
applied on one side of the segment and two forces (Fcentral, Fcentral) are applied on the other side. In the
simplest cases in which the forces are equal and arranged symmetrically, part of the leg between the
inner pairs of forces (Fcentral, Fcentral) is subjected to a constant bending moment and minimum shear
force.
When the goal of an orthosis is to support motion, rather than to immobilize a joint, the relationship
between the anatomic and orthotic joint is an important consideration in orthotic design as well.
Because most anatomic joints have a triplanar or polycentric axis and most orthotic joints are single
axis designs, incongruence necessarily occurs between the axes of the joint and the orthosis at some
point in the range of motion, even in the most carefully designed orthosis. The torque that results from
this mismatch can, over time, have significant impact on the integrity of soft tissue and articulating
surfaces of the joint that the orthosis is trying to control.
Ideally, the force system used in an orthotic design is able to apply judiciously only the amount of force
necessary to accomplish its goal, and the forces are applied in such a way that bending moments are
effective and shearing or torque forces that act on the joint are minimal.

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 II. ANATOMY OF THE FOOT

2.1 INTRODUCTION

Centuries of evolution allows the human body to perform movements in the surrounding planet hearth
in most diversifying environments. The human body is build to interact with the different environments
according to the following principles: adaptability, ergonomic, strength, stability, flexibility and velocity.
The human osteo-muscular system, which is the ultimate means of movement of the "human body'
system" enclosed all these characteristic. Most of the activities of the human relations are performed
in vertical position, such as standing, walking and running. The foot may be considered the first
contact of the body with the environment (ground) and source of information and mobility.
The module will review firstly the human anatomical segment of the leg and foot, such as bones, joint
and muscles, successively will explain how this segments perform movements in the different motor
performance i.e. walking.

2.2 ANATOMY REVIEW: LEG, ANKLE AND FOOT

Bones of the Leg: Tibia and Fibula

The tibia, also known as the shinbone, is a long bone of the lower leg. The tibia is found between the
patella and the ankle. Like the femur, the tibia bears much of the body’s weight and plays an essential
role in movement and locomotion. In males, the tibia is relatively vertical whereas in females, the tibia
is more slanted to account for wider hips in females. Additionally, the tibia is the second largest bone
in the human skeleton, following the femur.
The fibula, also known as the calf bone, is a long bone of the lower leg running parallel to the tibia.
This bone is located between the patella and the ankle. Although the fibula is thinner than the other
leg bones, the fibula still plays a role in supporting the body’s weight and allowing movement.

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Bones of the Foot
Structurally, the foot has three main parts: the Hind foot, the Mid foot, and the Fore foot.
The Hind foot is composed of two bones the Talus and Calcaneous. The top of the talus is
connected to the two long bones of the lower leg (tibia and fibula), forming a hinge that allows the foot
to move up and down. The heel bone (Calcaneus's) is the largest bone in the foot. The two bones are
connected trough the Sub-Talar Joint.
The Mid foot has five irregularly shaped tarsal bones. From medial to lateral, these bones are:
Cuboid bone, Navicular bone, Lateral Cuneiform bone, Intermediate Cuneiform bone, Medial
Cuneiform bone. They form the foot's arch which serves as a shock absorber. The bones of the
midfoot connected the forefoot and the hindfoot by muscles and the plantar fascia (arch ligament).

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 List of all Hind foot & Mid foot Bones (Tarsal
Bones):
A. calcaneus (heel bone) (2)
B. talus (2)
C. cuboid bone (2)
D. navicular bone (2)
E. lateral cuneiform bone (2)
F. intermediate cuneiform bone (2)
G. medial cuneiform bone (2)

The Fore foot is composed of the five toes (called phalanges) and their connecting long bones
(metatarsals). Each toe (phalanx) is made of several small bones. The big toe (also known as the
hallux) has two phalanx bones—distal and proximal. It has one joint, called the inter-phalangeal joint.
The big toe articulates with the head of the first metatarsal and the articulation is called the first
metatarsophalangeal joint (MTPJ for short).

Fore foot: List of all Metatarsus Bones

Metatarsal bone (5 × 2)

Fore foot: List of all Digits of the feet

(Phalanges)
Proximal phalanges (5 × 2)
Intermediate phalanges (4 × 2)
Distal phalanges (5 × 2)

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Segmental division:
• Hind foot (Rear foot)
• Mid foot
• Fore foot

Hind foot, Tarsal bones: Calcaneus

The Calcaneus, also known as the heel bone, is the largest bone of the tarsal or ankle region. The
calcaneus also constitutes the region known as the heel. This bone is very important in movement of
the foot and support of the body. Additionally, the calcaneus consists of important structures, such as
the Achilles tendon, tarsal sinus, and the tuber calcanei.

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Hind foot, Tarsal bones: Talus
The Talus bone, also known as the astragalus, is an irregularly shaped bone of the tarsal or ankle
region. This is the second largest of the ankle bones and forms part of the ankle joint. The talus
functions in allowing motion of the foot and transfers the body’s weight to the foot. Additionally, the
talus is divided into three regions: the head, neck, and body.

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Mid foot, Metatarsal bones: Navicular
The Navicular bone is one of the bones of the tarsal or ankle region. The Navicular is a relatively small
bone that plays a function in locomotion and body support. It touches five other bones: the three
cuneiform bones, the talus bone, and the Cuboid bone. Additionally, the Navicular resembles a boat
due to its concavity.

Mid foot, Metatarsal bones: Cuboid

The cuboid bone is found one the lateral side of the tarsal bones. The function of the cuboid is support
of the body’s weight, locomotion, and maintaining lateral foot stability. Additionally, the cuboid bone
forms part of many joints in the foot, such as the tarsometatarsal and calcaneocuboid joints.

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Mid foot, Metatarsal bones: Medial Cuneiform
Like other tarsal bones, this bone plays a role in motion and support of the body. Additionally, the
medial cuneiform touches four other bones: the intermediate cuneiform bone, the Navicular, and two
metatarsal bones.

Mid foot, Metatarsal bones: Intermediate Cuneiform

The intermediate cuneiform is wedge shaped and also known as the second cuneiform bone or middle
cuneiform bone. The bone plays a role in movement and support of the body.

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Mid foot, Metatarsal bones: Lateral Cuneiform
The lateral cuneiform is a wedge shaped bone located in between the intermediate cuneiform and
cuboid bones. Like the other tarsal bones, the lateral cuneiform plays a role in motion and support.
Furthermore, the lateral cuneiform is also known as the third cuneiform or external cuneiform.

Fore foot: Metatarsal Bones

Each foot consists of five metacarpal bones and thus the entire human skeleton consists of ten
metatarsal bones. The metatarsal bones are located between the tarsus and the phalanges (toes).
The metatarsal bones’ primary functions include foot motion, body support, and providing the shape of
the foot.
Fore foot: Phalanges
The phalanges consist of three sections: The proximal phalanges, the intermediate phalanges, and
the distal phalanges. Collectively, these bones make up the structure known as the toes.
Proximal Phalanges
The proximal phalanges are found at the base of the toes, closest to the tarsus. These bones are
longer than the play an important role in movement of the foot.
Intermediate Phalanges
The intermediate phalanges are found in
between the proximal phalanges and distal
phalanges. There are four intermediate
phalanges found on each foot, the only toes
that lacks the intermediate phalanges are the
thumbs. Like the distal phalanges, the
intermediate phalanges play an important role
in motion of the foot.

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Joints of the Leg and Foot

Tibia and Fibular joints are divided in two joints: the proximal Tibio-Fibular joint and distal
Tibiofibular Syndesmosis.
Proximal Tibia fibular joint: This is a plane type of synovial joint between the head of the fibula and
lateral condyle of the tibia. The flat, oval-to-circular facet on the head of the fibula articulates with a
similar facet located postero-laterally on the inferior aspect of the lateral condyle of the tibia.
Slight movement occurs at the superior tibiofibular joint during dorsiflexion of the foot at the ankle joint.
This presses the lateral malleolus laterally and causes movement of the body and head of the fibula.
Some movement of the joint also occurs during plantarflexion of the foot.
The joint is surrounded by the fibrous capsule and is attached to the margins of the articular facets
on the fibula and tibia. It is strengthened by the anterior and posterior ligaments of the head of the
fibula. The fibres of these ligaments run superomedially from the fibula to the tibia.
The tendon of the popliteus muscle is intimately related to the posterosuperior aspect of the proximal
tibiofibular joint.
The synovial membrane lines the fibrous capsule. The pouch of synovial membrane passing under
the tendon of the popliteus muscle, known as the popliteus bursa, sometimes communicates with the
synovial cavity of the proximal tibiofibular joint though an opening in the superior part of the synovial
capsule.
Consequently, the proximal tibiofibular joint may be indirectly in communication with the synovial
cavity of the knee joint.

The Distal Tibiofibular Joint (Tibiofibular syndesmosis)

It is located between the inferior ends of the tibia and fibula. The articular surface of the Distal
Tibiofibular Joint is a rough, convex, triangular articular area on the medial surface of the inferior end
of the fibular, it articulates with a facet on the inferior end of the tibia.
A strong interosseous ligament continuous superiorly with the interosseous membrane forms the
principal connection between the tibia and fibula at this joint.
It consists of strong bands that extend from the fibular notch of the tibia to the medial surface of the
distal end of the fibula.

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The strong anterior and posterior tibiofibular ligaments also strengthen the distal tibiofibular joint
anteriorly and posteriorly.
They extend from the border of the fibular notch of the tibia to the anterior and posterior surfaces of
the lateral malleolus, respectively.
The inferior, deep part of the posterior tibiofibular ligament is called the transverse tibiofibular
ligament. This strong band closes the posterior angle between the tibia and fibula.
This articulation forms a strong union between the distal ends of the tibia and fibula; much of the
strength of the ankle joint is dependent on this union.
Slight movement of the distal tibiofibular joint occurs to accommodate the talus during dorsiflexion of
the foot at the ankle joint.

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The ankle joint:
The Ankle is a hinge joint. It is a joint between: the lower end (1) and medial malleolus of the tibia (2)
and the lateral malleolus of the fibula (3) and the trochlear surface of the talus (4)

The ankle joint is a hinge type joint that participates in movement and is involved in lower limb stability.

The lateral ligaments consists of :

• The anterior talofibular ligament, between the neck of the talus and the lateral malleolus;
• The calcaneofibular ligament;
• The posterior talofibular ligament, between the talus and the malleolar fossa.

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The medial and lateral ligaments prevent anterior and posterior slipping of the talus. They may be torn
in injuries to the ankle, with the lateral ligaments being significantly weaker and more liable to sprain. If
the ligaments do not yield, one or both malleoli may be broken off in dislocations of the ankle joint. The
shape of the surfaces at the ankle is such that, aided by the ligaments of the tibiofibular syndesmosis,
the malleoli grip the talus tightly in dorsiflexion. Therefore, most sprains of the ankle occur with the
ankle in some degree of flexion.
The medial, or deltoid ligament runs from the medial malleolus to the talus, navicular, and calcaneus.
It is crossed by the tendons, vessels, and nerves that have entered the foot by passing posterior to the
medial malleolus.

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The Hind foot is composed of the Talus and Calcaneus, which are connected through the Sub-talar
joint.
The sub-talar joint includes three articulating surfaces and has 3 different articulations:
1. Anterior talar – calcaneuos surface
2. Middle talar – calcaneuos surface
3. Posterior talar – calcaneuos surface

The Calcaneus is the largest tarsal bone, and forms the heel. The talus rests on top of it, and forms
the pivot of the ankle.

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The shape of calcaneus is complex. On its upper surface are three smooth facets, posterior, middle,
and anterior, which articulate with corresponding facets on the lower surface of the talus to form the
subtalar joint. Of these three talocalcaneal facets, the posterior is the largest, covering almost the
entire width of the calcaneal body. The middle and anterior facets are located on the medial side of the
upper calcaneal surface, and are usually continuous with each other. The middle and posterior facets
are separated from each other by a deep groove, which together with a corresponding groove on the
talus, forms a channel between the two bones called the sinus tarsi.
The lateral wall of calcaneus is nearly flat, except for a small ridge called the peroneal tubercle. The
medial wall has a shelf-like projection, the sustentaculum tali. This shelf carries the middle
talocalcaneal facet on its upper surface. The undersurface of the shelf has a groove for the flexor
hallucis longus tendon.
The front or anterior process of calcaneus articulates with the cuboid bone to form the calcaneocuboid
joint. The rear part of calcaneus consists of a large rounded projection, the calcaneal tuberosity, which
forms the back of the heel and provides attachment for the Achilles tendon. The undersurface of the
tuberosity forms the bottom of the heel; this surface comes into contact with the ground during
weightbearing, cushioned by a fibroelastic fat pad.
The talus, which rests on top of calcaneus, also has a complex shape. The main part or body of the
talus is roughly cubical. Its smooth, dome-shaped upper surface (the talar dome) articulates with the
distal ends of the tibia and fibula (the two bones of the lower leg) to form the ankle joint (see The
ankle, below).
The rear surface of the talar body protrudes backward to form a posterior process. In some
individuals, the posterior process ossifies (develops into bone) independently, and may remain
separate from the talar body as a small accessory bone called the os trigonum (see also Ossicles,
below).
Projecting forward from the talar body is the head of the talus, which is separated from the body by a
slight constriction called the neck. The talar head articulates with the navicular bone, forming the
talonavicular joint.
The lower surface of the talus contains three smooth facets, posterior, middle, and anterior, which
articulate with the corresponding facets on the upper surface of calcaneus. The posterior facet (the
largest of the three) covers the undersurface of the talar body; the anterior and middle facets are
located on the undersurface of the talar head. Together, these three talocalcaneal articulations form
the subtalar joint.
The subtalar joint is bound together by several talocalcaneal ligaments. They are classified as:
The Anterior Talocalcaneal Ligament extends from the front and lateral surface of the neck of the
talus to the superior surface of the calcaneus. It forms the posterior boundary of the
talocalcaneonavicular joint, and is also described as the anterior interosseous ligament.
The Posterior Talocalcaneal Ligament connects the lateral tubercle of the talus with the upper and
medial part of the calcaneus; it is a short band, and its fibers radiate from their narrow attachment to
the talus.
The Lateral Talocalcaneal Ligament is a short, strong fasciculus, passing from the lateral surface of
the talus, immediately beneath its fibular facet to the lateral surface of the calcaneus. It is placed in
front of, but on a deeper plane than, the calcaneofibular ligament, with the fibers of which it is parallel.
The Medial Talocalcaneal Ligament connects the medial tubercle of the back of the talus with the
back of the sustentaculum tali. Its fibers blend with those of the plantar calcaneonavicular ligament
In addition, the subtalr joint is supported by portions of the medial and lateral ligaments of the ankle,
which span both the ankle and the subtalar joint. The calcaneocuboid and talonavicular joints, together
referred to as the midtarsal joint, form the boundary between hindfoot and midfoot.
Midfoot Joints
The mid foot is composed of 5 bones, Navicular, Cuboid and 3 Cuneiforms. The main joints
articulating in the mid foot are:
• Transverse tarsal joint
• Tarso metatarsal joint

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The Transverse tarsal joint (Chopart joint): the transverse tarsal joint is divided into two joints, the
calcaneo-cuboid joint and the talo-navicular joint. These 2 joints form an "S" shape that transects the
foot diving the rear foot to the mid-foot.

We can also notice, independently from the two main joints, that the 3 cuneiforms are articulating with
the navicular proximally and each cuneiform is articulating with corresponding Metatarsal bones. For
th th
the Cuboid it articulates with the calcaneus and Metatarsal bone 4 and 5 .

The midfoot is composed of five of the seven tarsal bones, the navicular, cuboid, and three cuneiform
bones. These can be thought of as being arranged in two irregular rows, with the cuboid occupying
space in both rows. The proximal row contains the navicular (on the medial side of the foot) and the

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cuboid (on the lateral side). The distal row contains the three cuneiforms (medial, intermediate, and
lateral) and the cuboid (lateral to the lateral cuneiform).
The boundary between the midfoot and forefoot consists of five tarsometatarsal (TMT) joints, the joints
between the distal row of the midfoot and the bases of the metatarsals. (The medial, intermediate,
and lateral cuneiforms articulate with the first, second, and third metatarsals, respectively; the
cuboid articulates with the fourth and fifth metatarsals.)
There are also multiple joints within the midfoot itself. The distal row of the midfoot has two
intercuneiform joints (between adjacent cuneiforms) and a cuneocuboid joint (between the lateral
cuneiform and the cuboid). Proximally, the three cuneiforms articulate with the navicular bone (the
cuneonavicular joints). In some individuals, there is also a small articulation between the cuboid and
navicular.
In addition to its articular surfaces, each tarsal bone has specific features adapted for function. For
example, the medial surface of the navicular projects downward to form a tuberosity, which serves as
an attachment for the tibialis posterior tendon. The lateral surface of the cuboid also has a tuberosity,
which serves as a ligament attachment. The cuboid bone has no major tendon attachments; however,
the peroneus longus tendon passes across the cuboid tuberosity, to run in a groove on the plantar
surface of the bone. The peroneus longus tendon often contains a sesamoid bone, which articulates
with a small facet (articular surface) on the tuberosity.

Forefoot Joints
The fore foot includes the Metatarsal bones and the phalanges.
• Tarso metatarsal joint (TMJ)
• Metatarso phalangeal joint (MTP)

The framework of the forefoot is formed by five metatarsal bones, along with the phalanges (the bones
of the digits or toes). Each digit has three phalanges (proximal, middle, and distal), except for the big
toe, which has two (proximal and distal). The digits and their metatarsal rays are numbered from one
to five, starting with the big toe.

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The metatarsals and phalanges are long bones. Each has a diaphysis (shaft) with slightly flaring ends.
The proximal end or base of each bone has a smooth articular surface where it forms a joint with the
adjacent bone. The distal end or head also has an articular surface, except for the distal phalanges,
whose distal ends provide attachment for the soft tissue (pulp) of the digit tips.
Of the metatarsal bones, the first bears the most weight and plays the most important role in
propulsion; it is therefore the shortest and thickest. It provides attachment for several tendons,
including tibialis anterior and peroneus longus (see below, under Muscles and tendons). The fifth
metatarsal has a tuberosity (protuberance) on the lateral side of its base, to which the
peroneus brevis tendon is attached. (The tuberosity of the fifth metatarsal can be felt halfway along
the lateral side of the foot.) The second, third, and fourth (called the internal metatarsals) are the most
stable of the metatarsals, in part because of their protected position; but also because they have only
minor tendon attachments, and therefore are not subjected to strong pulling forces.
The joints between the metatarsals and the proximal phalanges are called the metatarsophalangeal
(MTP) joints. Each digit also has two interphalangeal (IP) joints, proximal (PIP) and distal (DIP),
except for the big toe, which has only one IP joint. Each MTP and IP joint is bound together by several
ligaments,one on each side of the joint (medial and lateral collateral ligaments), and one along the
plantar (sole) surface (plantar ligament).
The first MTP joint has an additional feature. Near the head of the first metatarsal, on the plantar
surface of the foot, are two sesamoid bones. (A sesamoid is a small, oval-shaped bone which
develops inside a tendon, where the tendon passes over a bony prominence. In this case, the tendon
is that of flexor hallucis brevis, as it passes over the first metatarsal head.) These sesamoid bones
articulate with the head of the first metatarsal, and function as part of the first MTP joint. They are held
in place by their tendons, and are also supported by ligaments. These include the sesamoid collateral
ligaments (which bind the sesamoids to the metatarsal head) and the intersesamoidal ligament (which
connects the sesamoids to each other).

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Muscles Acting on the Ankle and Foot

Movements of the foot and ankle, either to stabilize or to control are realised through the muscles
activity during the gait cycle.
Muscles of the leg and foot might be divided primarly into:
Extrinsic: All muscles originating on the lower leg except the popliteus muscle and are
attached to the bones of the foot.
Intrinsic: These muscles lie deeper to the extrinsic muscles. They origin and insert within the
foot.
Muscles of the leg are divided in 3 compartments, anterior, posterior and lateral and have their own
function toward the ankle and foot. In order to keep the ankle and foot in neutral position, muscles
have to be in balance.

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Tibialis Posterior

Posterior aspect of interosseous

membrane, superior 2/3 of
medial posterior surface of fibula,
superior aspect of posterior
Origin surface of tibia, and from
intermuscular septum between
muscles of posterior
compartment and deep
transverse septum

Splits into two slips after passing

inferior to plantar
calcaneonavicular ligament;
superficial slip inserts on the
tuberosity of the navicular bone
Insertion
and sometimes medial
cuneiform; deeper slip divides
again into slips inserting on
plantar surfaces of metatarsals 2
- 4 and second cuneiform

Principal invertor of foot; also

adducts foot, plantar flexes
Action
ankle, and helps to supinate the
foot

Innervation Tibial nerve (L4, L5)

Muscular branches of sural,

Arterial
peroneal and posterior tibial
Supply
arteries

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Tibialis Anterior

Lateral condyle of tibia, proximal

1/2 - 2/3 or lateral surface of tibial
Origin
shaft, interosseous membrane, and
the deep surface of the fascia
cruris

Medial and plantar surfaces of 1st

Insertion cuneiform and on base of first
metatarsal

Dorsiflexor of ankle and invertor of

Action
foot

Innervation Deep peroneal nerve (L4, L5, S1)

Arterial
Anterior tibial artery
Supply

Soleus

Posterior aspect of fibular head, upper 1/4 - 1/3 of

posterior surface of fibula, middle 1/3 of medial
Origin border of tibial shaft, and from posterior surface of a
tendinous arch spanning the two sites of bone origin

Eventually unites with the gastrocnemius aponeurosis

Insertion to form the Achilles tendon, inserting on the middle
1/3 of the posterior calcaneal surface

Action Powerful plantar flexor of ankle

Innervation Tibial nerve (S1, S2)

Arterial
Posterior tibial, peroneal, and sural arteries
Supply

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Plantaris

Origin Inferior aspect of lateral supracondylar line of distal femur

Middle 1/3 of the posterior calcaneal surface, just medial to Achilles

Insertion
tendon

Action Plantar flexor of ankle; also flexes knee

Innervation Tibial nerve (L5, S1, S2)

Arterial
Sural arteries
Supply

Peroneus Tertius

Arises with the extensor digitorum longus from the medial

fibular shaft surface and the anterior intermuscular septum
Origin
(between the extensor digitorum longus and the tibialis
anterior)

Insertion Dorsal surface of the base of the fifth metatarsal

Works with the extensor digitorum longus to dorsiflex, evert and

Action
abduct the foot

Innervation Deep peroneal nerve

Arterial
Anterior tibial artery
Supply

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Peroneus Longus

Head of fibula, upper 1/2 - 2/3 of lateral fibular shaft

Origin surface; also anterior and posterior intermuscular septa of
leg

Plantar posterolateral aspect of medial cuneiform and

Insertion
lateral side of 1st metatarsal base

Everts foot and plantar flexes ankle; also helps to support

Action
the transverse arch of the foot

Superficial peroneal nerve (L5, S1, S2); may also receive

Innervation additional innervation from common or deep peroneal
nerves

Arterial
Anterior tibial and peroneal arteries
Supply

Peroneus Brevis
Inferior 2/3 of lateral fibular surface; also
Origin anterior and posterior intermuscular septa
of leg

Lateral surface of styloid process of 5th

Insertion
metatarsal base

Action Everts foot and plantar flexes ankle

Innervation Superficial peroneal nerve (L5, S1, S2)

Arterial
Muscular branches of peroneal artery
Supply

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Flexor Hallucis Longus

Inferior 2/3 of posterior

surface of fibula, lower
Origin
part of interosseous
membrane

Plantar surface of base

Insertion of distal phalanx of great
toe

Flexes great toe, helps to

supinate ankle, and is a
Action
very weak plantar flexor
of ankle

Innervation Tibial nerve (S2, S3)

Muscular branch of
Arterial
peroneal and posterior
Supply
tibial artery

Flexor Digitorum Longus

Posterior surface of tibia distal to

Origin
popliteal line

Splits into four slips after passing

through medial intermuscular septum
Insertion of plantar surface of foot; these slips
then insert on plantar surface of bases
of 2nd - 5th distal phalanges

Flexes toes 2 - 5; also helps in plantar

Action
flexion of ankle

Innervation Tibial nerve (S2, S3)

Arterial Muscular branch of posterior tibial

Supply artery

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Extensor Hallucis Longus

Anterior surface of the fibula and the adjacent interosseous

Origin
membrane

Insertion Base and dorsal center of distal phalanx of great toe

Action Extends great toe and dorsiflexes ankle

Innervation Deep peroneal nerve (L4, L5, S1)

Arterial
Anterior tibial artery
Supply

Extensor Digitorum Longus

Lateral condyle of fibula, upper 2/3 - 3/4 of medial fibular shaft surface,
Origin upper part of interosseous membrane, fascia cruris, and anterior
intermuscular septum

Splits into 4 tendon slips after inferior extensor retinaculum, each of

Insertion which insert on dorsum of middle and distal phalanges as part of
extensor expansion complex

Action Extend toes 2 - 5 and dorsiflexes ankle

Innervation Deep peroneal nerve (L4, L5, S1)

Arterial
Anterior tibial artery
Supply

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Table 2: Muscles of the leg acting on the ankle and foot by function

Muscle Function Muscle Name

• Tibialis Anterior
• Extensor Digitorum Longus
Dorsiflexion of the ankle / foot
• Extensor Hallucis Longus
• Peroneus Tertius
• Triceps Surae
• Tibial Posterior
• Flexor Digitorum Longus
Plantarflexion of ankle / foot
• Flexor Hallucis Longus
• Peroneus Longus
• Peroneus Brevis
• Peroneus longus
Pronation of foot • Peroneus brevis
• Peroneus tertius
• Tibialis anterior
Supination of foot • Tibialis posterior
• Extensor hallucis longus

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Intrinsic Muscles of the Foot
Definitions: muscles fully contained (origin, belly, insertion) in the foot and toes. These muscles are
arranged in 4 layers; all are innervated by the plantar branches of the tibial nerve. Although they may be
capable of producing the actions described under their individual entries, as a group the primary function of
the intrinsic muscles of the foot is to provide dynamic support of the longitudinal arch of the foot, resisting
those forces that act momentarily to spread the arch during walking and running.

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FOURTH LAYER:
The Interossei plantares (Plantar interossei), three in number, lie beneath rather than between the
metatarsal bones, and each is connected with but one metatarsal bone. They arise from the bases
and medial sides of the bodies of the third, fourth, and fifth metatarsal bones, and are inserted into the
medial sides of the bases of the first phalanges of the same toes, and into the aponeuroses of the
tendons of the Extensor digitorum longus.

Interossei plantares Interossei dorsales

The Interossei dorsales (Dorsal interossei), four in number, are situated between the metatarsal
bones. They are bipenniform muscles, each arising by two heads from the adjacent sides of the
metatarsal bones between which it is placed; their tendons are inserted into the bases of the first
phalanges, and into the aponeurosis of the tendons of the Extensor digitorum longus. In the angular
interval left between the heads of each of the three lateral muscles, one of the perforating arteries
passes to the dorsum of the foot; through the space between the heads of the first muscle, the deep
plantar branch of the dorsalis pedis artery enters the sole of the foot. The first is inserted into the
medial side of the second toe; the other three are inserted into the lateral sides of the second, third,
and fourth toes.

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 Muscle Origin Insertion Action Innervation

abductor digiti medial and lateral lateral side of the abducts the 5th toe; lateral plantar
minimi (foot) sides of the base of the flexes the nerve
tuberosity of the proximal phalanx metatarsophalageal
calcaneus of the 5th digit joint

abductor medial side of the medial side of the abducts the great toe; medial plantar
hallucis tuberosity of base of the flexes the nerve
calcaneus proximal phalanx metatarsophalageal
of the great toe joint
(hallux)

adductor oblique head: bases lateral side of adducts the great toe deep branch of
hallucis of metatarsals 2-4; base of the (moves it toward the lateral plantar
transverse head: proximal phalanx midline of the foot; nerve
heads of of the great toe i.e.toward the 2nd digit)
metatarsals 3-5

dorsal shafts of adjacent bases of the abduct digits 2-4 (move deep branch of
interosseous metatarsal bones proximal these digits away from the lateral plantar
(foot) phalanges for midline as defined by a nerve
digit 2 (both plane passing through
sides) & digits 3,4 the 2nd digit); flex the
(lateral side) metatarsophalangeal
joints and extend the
interphalangeal joints
of those digits

extensor superolateral extensor extends toes 1-4 deep fibular

digitorum surface of the expansion of toes (peroneal) nerve
brevis calcaneus 1-4

extensor lateral condyle of dorsum of the extends the deep fibular

digitorum the tibia, anterior lateral 4 toes via metatarsophalangeal, (peroneal) nerve
longus surface of the extensor proximal
fibula, lateral expansions interphalangeal and
portion of the (central slip distal interphalangeal
interosseous inserts on base of joints of the lateral 4
membrane middle phalanx, toes
lateral slips on
base of distal
phalanx)

extensor superolateral dorsum of base extends the great toe deep fibular
hallucis brevis surface of the of proximal (peroneal) nerve
calcaneus phalanx of the
great toe

extensor middle half of the base of the distal extends the deep fibular
hallucis anterior surface of phalanx of the metatarsophalangeal (peroneal) nerve
longus the fibula and the great toe interphalangeal joints
interosseous of the great toe
membrane

flexor digiti base of 5th lateral side of flexes the lateral plantar
minimi brevis metatarsal bone base of proximal metatarsophalangeal nerve
(foot) phalanx of 5th joint of the 5th digit
digit

flexor tuberosity of the base of the flexes the medial plantar

digitorum calcaneus, plantar middle phalanx of metatarsophalangeal & nerve

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 brevis aponeurosis, digits 2-5 after proximal
intermuscular splitting to allow interphalangeal joints
septae passage of the of digits 2-5
flexor digitorum
longus tendons

flexor middle half of the bases of the flexes the tibial nerve
digitorum posterior surface of distal phalanges metatarsophalangeal,
longus the tibia of digits 2-5 proximal
interphalangeal and
distal interphalangeal
joints of digits 2-5;
plantar flexes the foot

flexor hallucis cuboid, lateral medial belly: flexes the medial plantar
brevis cuneiform, medial medial side of metatarsophalangeal nerve (lateral
side of the first proximal phalanx joint of the great toe belly occasionally
metatarsal of the great toe; receives
lateral belly: innervation from
lateral side of the the lateral plantar
proximal phalanx nerve)
of the great toe

flexor hallucis lower 2/3 of the base of the distal flexes the tibial nerve
longus posterior surface of phalanx of the metatarsophalangeal
the fibula great toe and proximal
interphalangeal joints
of the great toe; plantar
flexes the foot

interosseous, shafts of adjacent bases of the abduct digits 2-4 (move deep branch of
dorsal (foot) metatarsal bones proximal these digits away from the lateral plantar
phalanges for midline as defined by a nerve
digit 2 (both plane passing through
sides) & digits 3,4 the 2nd digit); flex the
(lateral side) metatarsophalangeal
joints and extend the
interphalangeal joints
of those digits

interosseous, base and medial bases of proximal adduct digits 3-5 (move deep branch of
plantar side of metatarsals phalanges and these digits toward the the lateral plantar
3-5 extensor midline of the foot as nerve
expansions of defined by a plane
digits 3-5 through the second
digit); flex the
metacarpophalangeal
and extend
interphalangeal joints
of digits 3-5

lumbricals tendons of the medial side of the flex the medial (1st)
(foot) flexor digitorum extensor metatarsophalangeal lumbrical: medial
longus expansion of joint, extend the plantar nerve;
digits 2-5 proximal lateral three
interphalangeal & distal lumbricals: lateral
interphalangeal joints plantar nerve
of digits 2-5

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 plantar base and medial bases of proximal adduct digits 3-5 (move deep branch of
interosseous side of metatarsals phalanges and these digits toward the the lateral plantar
3-5 extensor midline of the foot as nerve
expansions of defined by a plane
digits 3-5 through the second
digit); flex the
metacarpophalangeal
and extend
interphalangeal joints
of digits 3-5

plantaris above the lateral dorsum of the flexes the leg; plantar tibial nerve
femoral condyle calcaneus medial flexes the foot
(above the lateral to the calcaneal
head of tendon
gastrocnemius)

quadratus anterior portion of tendons of the assists the flexor lateral plantar
plantae the calcaneus and flexor digitorum digitorum longus in nerve
the long plantar longus m. flexing the toes
ligament

Arches of the Foot

The foot is composed of four main arches.

• Medial longitudinal arch
• Lateral longitudinal arch
• Transverse tarsal arch
• Transverse metatarsal arches

Functions of the Arches of the Foot

The medial longitudinal arch in particular creates a space for soft tissues with elastic properties, which
act as springs, particularly the thick plantar aponeurosis, passing from the heel to the toes.
Because of their elastic properties, these soft tissues can spread ground contact reaction forces over a
longer time period, and thus reduce the risk of musculoskeletal wear or damage, and they can also
store the energy of these forces, returning it at the next step and thus reducing the cost of walking
and, particularly, running, where vertical forces are higher.
However, human feet, and the human medial longitudinal arch, differ in that the anterior part of the
foot is medially twisted on the posterior part of the foot, so that all the toes may contact the ground.

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Longitudinal arches:
The main arches are the antero-posterior arches, which may, for descriptive purposes, be regarded as
divisible into two types a medial and a lateral.

Medial Arch:
The medial arch is made up by the calcaneus, the talus, the navicular, the three cuneiforms, and the
first, second, and third metatarsals.

Its summit is at the superior articular surface of the talus, and its two extremities, on which it rests in
standing, are the tuberosity on the plantar surface of the calcaneus posteriorly and the heads of the
first, second, and third metatarsal bones anteriorly. The chief characteristic of this arch is its elasticity,
due to its height and to the number of small joints between its component parts.

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Medial Arch Support
Its weakest part is the joint between the talus and navicular, but this portion is braced by the plantar
calcaneonavicular ligament a spring ligament, which is elastic and is thus able to quickly restore the
arch to its pristine condition when the disturbing force is removed. The ligament is strengthened
medially by blending with the deltoid ligament of the ankle-joint, and is supported inferiorly by the
tendon of the Tibialis posterior, which is spread out in a fanshaped insertion and prevents undue
tension of the ligament or such an amount of stretching as would permanently elongate it.

The arch is further supported by the plantar aponeurosis, by the small

muscles in the sole of the foot, by the tendons of the Tibialis anterior
and posterior and Peronæus longus, and by the ligaments of all the
articulations involved.

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Lateral Arch
The lateral arch is composed of the calcaneus, the cuboid, and the fourth and fifth metatarsals.

Its summit is at the talocalcaneal articulation, and its chief joint is the calcaneocuboid, which
possesses a special mechanism for locking, and allows only a limited movement. The most marked
features of this arch are its solidity and its slight elevation; two strong ligaments, the long plantar and
the plantar calcaneocuboid, together with the Extensor tendons and the short muscles of the little toe
(abductor digiti minimi), preserve its integrity.

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Transverse arches:
In addition to the longitudinal arches the foot presents two transverse arches.
At the posterior part of the metatarsus and the anterior part of the tarsus the arches are complete, but
in the middle of the tarsus they present more the characters of half-domes the concavities of which are
directed downward and medialward, so that when the medial borders of the feet are placed in
apposition a complete tarsal dome is formed. The transverse arches are strengthened by the
interosseous, plantar, and dorsal ligaments, by the short muscles of the first and fifth toes (especially
the transverse head of the Adductor hallucis), and by the Peronæus longus, whose tendon stretches
across between the piers of the arches.

The transverse arch of the foot is primarily formed by

the 5 metatarsal bones
Every ligament that connects the bones of the foot plays a
part in the maintenance of the arches, but some which
pass across two or more joints are especially important.
Among these are the long plantar ligament, the plantar
calcaneocuboid ligament and the plantar calcaneonavicular
ligament, on which the head of the talus rests.
While the normal tone of the small intrinsic muscles of the
foot also plays an essential part in keeping the arches
intact, the long muscles which are inserted by tendons into
the bones of the foot have an even more important role.
These are the tendon of the tibialis anterior muscle, the
tendon of the tibialis posterior muscle, the tendon of the
peroneus longus and the tendons of the flexor hallucis
longus and flexor digitorum longus muscles.
Finally, more superficially, the plantar aponeurosis also
plays an important part in maintaining the medial
longitudinal arch.

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2.3 MOVEMENTS OF THE FOOT AND ANKLE COMPLEX

Introduction

For better understanding, we will present the movements of ankle and foot joints initially at segmental
level and according to the passive range of motion (PROM) and active range of motion (AROM).
Successively, we will connect these movements with functional action (i.e. walking) and following the
principle of open/closed muscles chains.

Movements of the Tibiofibular Joints

The tibiofibular joint consists of the junction between the tibia and fibula.
Proximally, this joint is classified as a plane synovial joint in which gliding occurs between the
articulating surfaces. The proximal joint has got micro movements primarily affected by movement of
the knee, but can also be affected by traumatic inversion forces directed at the ankle.
The distal tibiofibular joint is the articulation between a concave tibial facet and a convex fibular facet.
Movement at the foot will have a direct effect on the distal tibiofibular joint. During foot dorsiflexion, the
fibula must glide superiorly and rotate laterally. This movement occurs to accommodate the wider
anterior portion of the talus as it moves into the mortise. Actual separation of the distal tibiofibular joint
with dorsiflexion varies from 1 mm to 4 mm of spread.
During plantar flexion, the accessory movement is reversed with the fibula gliding inferiorly and
internally rotating toward the tibia.

Movements of the Talocrural Joint (Ankle Joint)

The talocrural joint is a uniaxial modified hinge synovial joint designed for stability. It is comprised of
the proximal articular surface of the talus (trochlea) and the distal articular surfaces of the tibia and
fibula. Motion at the talocrural joint is primarily dorsiflexion and plantar flexion. Because the trochlea of

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the talus is wider anteriorly than posteriorly and the radius of curvature is longer laterally, a helical
movement occurs during plantar flexion-dorsiflexion rather than a pure swing.
During dorsiflexion the talus glides in a posteromedial direction on the tibia, while in plantar flexion the
talus glides in an anterolateral direction. Consequently, weight-bearing dorsiflexion of the ankle is
accompanied by internal rotation of the limb, and weight-bearing plantar flexion is accompanied by
external rotation of the limb. Accessory component movements for plantar flexion and dorsiflexion are
listed in Table 3.

Table 3: Component movements for plantarflexion and dorsiflexion

Dorsiflexion Plantarflexion

Proximal Tibiofibular Joint Fibula glides superiorly Fibula glides inferiorly

Distal Tibiofibular Joint Superior glide of tibia and fibula Inferior glide of tibia and fibula

Talocrural Joint Talus posteromedial glide on tibia Talus anterolateral glide on tibia

The axis of the ankle joint is slightly oblique

(through the malleoli) and allowed
movements on three planes:
• Dorsiflexion (10° to 30°) = upwards
movement = extension & external
rotation
• Plantarflexion (20° to 50°) =
downwards movement = flexion &
internal rotation
The triceps surae and fibularis longus
muscles plantar-flex the foot. The tibialis
anterior and extensor digitorum longus
muscles dorsiflex the foot. It should be
appreciated that, physiologically, plantar
flexion of the foot and toes is an extensor
response, whereas dorsiflexion of the foot and toes is a flexor response.
Try this on yourself - as you lift up your ankle, notice how your toes rotate outwards. This happens
because of the shape of the talus - it has a smaller radius of curvature on the lateral side than the
medial side.

Movements of the Subtalar Joint

The subtalar joint consists of a bicondylar articulation between the talus and calcaneus. The
arthrokinematics of the subtalar joint can be very complicated due to its triplanar movement. Subtalar
joint motion in weight bearing and non weight bearing are described differently." The non weight
bearing subtalar joint motion is described strictly by calcaneal movement. Pronation consists of
calcaneal eversion, calcaneal dorsiflexion, and calcaneal abduction (medial tilt), whereas supination
involves calcaneal inversion, calcaneal plantar flexion, and calcaneal adduction (lateral tilt).
The main Subtalar joint motions are pronation and supination. They occurs around a single, oblique
axis on the sagittal, frontal, and transversal planes.

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The arrows in this transverse plane (cross-sectional) view of the right foot illustrate the three
components of open chain movement in the right subtalar joint. The line represents the subtalar joint
axis.
Plane of movement for PRONATION and SUPINATION
• FRONTAL (cross-section of foot) eversion / inversion
• SAGITTAL dorsiflexion plantar flexion
• TRANSVERSE abduction adduction
The gastrocnemeus and soleus, and each of the foot's extrinsic muscles attach distal to the talus and,
therefore, produce motion at the subtalar joint. Muscles whose lines of application pass on the subtalar
joint axis' lateral side produce pronation. Muscles whose lines of application pass on the axis' medial
side produce supination. The latter group includes the gastrocnemeus and soleus, which attach near
the calcaneus' midline, on the medial side of the joint axis

Movements of the Midtarsal Joint

The midtarsal joint is composed of the talonavicular and calcaneocuboid joints. When the subtalar joint
is supinated, the midtarsal joint becomes locked. It unlocks when the subtalar joint is pronated.
Supination requires inferior and medial glide of the navicular on the talar head, while a superior and
lateral glide of the navicular accompanies eversion.
Table 4 presents the accessory joint components of supination and pronation.

Table 4: Component movements for supination and pronation

Supination Pronation

Subtalar Joint (nonweight Calcaneal inversion, plantar Calcaneal eversion,

bearing) flexion, and adduction dorsiflexion, and abduction
Calcaneal eversion, talar
Subtalar Joint (weight Calcaneal inversion, talar
adduction, and plantar
bearing) abduction, and dorsiflexion
flexion
Inferior and medial glide of the Superior and lateral glide of the
Midtarsal Joint
navicular on the talus navicular on the talus

In addition to basic range-of-motion measurement, strength assessment, and joint stress testing, the
athletic trainer's evaluation of the ankle-foot complex should include assessment of joint play
movements. Each joint should be assessed for normal accessory movements. Any disturbance along
the lower extremity chain causing alteration of normal arthrokinematics will result in compensation at
any or all other lower extremity joints.

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Movements of the Tarsal-Metatarsal Joint (Lisfrancs)

These are plane joints. The first metatarsal bone articulates with the medial cuneiform bone; the
second is dovetailed in between the medial and lateral cuneiform bones, articulating by its base with
the intermediate cuneiform bone; the third articulates with the lateral cuneiform bone; the fourth, with
the cuboid and lateral cuneiform bones; and the fifth with the cuboid bone. The bones are connected
by dorsal, plantar, and interosseous ligaments.
The dorsal ligaments are strong, flat bands. The first metatarsal is joined to the medial cuneiform
bone by a capsular ligament; the second metatarsal receives three bands, one from each cuneiform
bone; the third, one from the lateral cuneiform bone; the fourth, one from the lateral cuneiform bone,
and another from the cuboid bone; and the fifth, one from the cuboid bone.
The plantar ligaments consist of longitudinal and oblique bands, disposed with less regularity ban the
dorsal ligaments. Those for the first and second metatarsal bones are the strongest; the second and
third metatarsal bones are joined by oblique bands to the medial cuneiform bone; the fourth and fifth
metatarsal bones are connected by a few fibers to the cuboid bone.
The interosseous ligaments are three in number. The first is the strongest and passes from the
lateral surface of the medial cuneiform bone to the adjacent angle of the second metatarsal bone (fig,
576). The second connects the lateral cuneiform bone with the adjacent angle of the second
metatarsal bone. The third connects the lateral angle of the lateral cuneiform bone with the adjacent
side of the base of the third metatarsal bone.
Movements: The movements permitted between the tarsal and metatarsal bones are limited to slight
gliding of the bones upon each other.

Movements of the Intermetatarsal Joint

The base of the first metatarsal bone is not connected with that of the second by any ligaments; in this
respect the great toe resembles the thumb. A small bursa is often interposed between the lateral aide
of the base of the first metatarsal bone and the medial side of the shaft of the second (fig. below).
The bases of the second, third, fourth, and fifth metatarsal bones are connected by dorsal, plantar,
and interosseous ligaments.
The heads of all the metatarsal bones are connected indirectly by the deep transverse ligaments of the
sole.
The dorsal and plantar ligaments pass transversely between the bases of the adjacent bones.

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The interosseous ligaments consist of strong transverse fibers which connect the rough nou-artieular
portions of the adjacent surfaces (fig. 576).
Movements-The movements permitted between the tarsal ends of the metatarsal bones are limited to
a slight gliding of the articular surfaces one upon another.

SYNOVIAL CAVITIES OF THE TARSUS AND METATARSUS

The synovial cavities (Fig. 576) present in the joints of the tarsus and metatarsus are six in number:
1. for the talocaleanean
2. for the talocalcaneonavicular
3. for the calcaneocuboid;
4. for the euneonavicular, intercuneiform, and cuneocuboid articulations, the articulations of the
intermediate and lateral cuneiform bones with the bases of the second and third metatarsal
bones, and the adjacent surfaces of the bases of the second, third, and fourth metatarsal
bones;
5. for the medial cuneiform bone with the metatarsal bone of the great toe
6. for the articulation of the cuboid bone with the fourth and fifth metatarsal bones. A small
synovial cavity is sometimes found between the contiguous surfaces of the navicular and
cuboid bones; it usually communicates with that between the cuboid and third cuneiform
bones.

Movements of the Metatarsophalangeal Joints

The metatarsophalangeal joints are of the condyloid kind, formed by the reception of the rounded
heads of the metatarsal bones in shallow cavities on the bases of the proximal phalanges.
The ligaments are the plantar and collateral.
The plantar (accessory plantar) ligaments are thick, dense, fibrous structures. They are placed on the
plantar surfaces of the joints in the intervals between the collateral ligaments, to which they are
connected; they are loosely united to the metatarsal bones, but are firmly fixed to the bases of the
proximal phalanges. Their margins are continuous with the deep transverse ligaments of the sole, and
their plantar surfaces are grooved for the flexor tendons, the fibrous sheaths of which are connected to
the sides of the grooves; the deep surfaces of the ligaments form parts of the articular facets for the
heads of the metatarsal bones.
The deep transverse ligaments of the sole (ligamenta capitulorum transversa) consist of four short,
wide, flattened bands which connect the plantar ligaments of adjoining metatarsophalangeal joints to
one another. Their dorsal aspects are related to the interosseous muscles and their plantar aspects to
the lumbricals and the digital vessels and nerves. They correspond closely to the deep transverse
ligaments of the palm, but, in addition, they are connected to the plantar ligament of the first
metatarsophalangeal joint.
The collateral ligaments are two strong, rounded cords, placed on the sides of the joints; each is
attached by one end to the dorsal tubercle on the side of the head of the metatarsal bone, and by the
other to the corresponding side of the base of the phalanx.
The extensor tendons supply the place of dorsal ligaments.
Movements: The movements permitted in the metatarsophalangeal articulations are flexion,
extension, adduction, abduction and circumduction.
Muscles producing the movements:
• Flexion - Flexores digitorum longus, brevis et accessorius (Quadratus plantae), Lumbricales,
Interossei dorsales et plantares, Flexores hallucis longus et brevis, Flexor digiti minimi brevis.
• Extension - Extensores digitorum longus et brevis, Extensor hallucis longus.
• Adduction - Interossei plantares, Adductor hallucis, long flexors of toes.
• Abduction - Interossei dorsales, Abductor hallucis, Abductor digiti minimi.

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THE JOINTS OF THE DIGITS
The digital or interphalangeal articulations are hinge-joints, and each has a plantar and two collateral
ligaments. The arrangement of these ligaments is similar to that in the metatarsophalangeal
articulations. The extensor tendons supply the places of dorsal ligaments.
Movements: The only movements permitted in the joints of the digits are flexion and extension; these
movements are more free between the proximal and middle phalanges than between the middle and
distal. The amount of flexion is very considerable, but extension is limited by the plantar ligaments.
Muscles producing the movements
• Flexion.-Flexores digitorum longus, brevis et accessorius (Quadratus plantae), Flexor hallucis
longus.
• Extension.-Lumbricales, Interossei dorsales et plantares, Extensor hallucis longus.

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 III. PATHOLOGY OF THE FOOT

3.1 FLAT FOOT (PES PLANUS)

Figure 28: A flat foot.

A Flat Foot (also called pes planus or fallen arches) is a formal reference to a medical condition in
which the arch of the foot collapses, with the entire sole of the foot coming into complete or near-
complete contact with the ground. In some individuals (an estimated 20–30% of the general
population) the arch simply never develops in one foot (unilaterally) or both feet (bilaterally).
Three studies of military recruits have shown no evidence of later increased injury, or foot problems,
due to flat feet, in a population of people who reach military service age without prior foot problems.
However, these studies cannot be used to judge possible future damage from this condition when
diagnosed at younger ages. They also cannot be applied to persons whose flat feet are associated
with foot symptoms, or certain symptoms in other parts of the body (such as the leg or back) possibly
referable to the foot.

Overview

About one in four people in the United States has flat feet – “pes planus”, also referred to as fallen
arches or pronated feet (when one or both feet roll inward). Simply defined, flatfoot is when the sole of
your foot is in full contact with the ground. The bottom of the foot lacks the normal arch.
In most cases, flatfoot does not cause symptoms, nor does it adversely affect the ability to carry on
with daily activities. It’s normal for children to have flat feet until about age ten, as the bones and
ligaments in the foot slowly form an arch. Flatfoot can persist into adulthood, often without symptoms.
But flatfoot causes pain for some people, and can affect the ability to walk, run, climb stairs or engage
in sports.
1. There are four types of flatfoot:
2. Flexible flatfoot
3. Flexible flatfoot with short Achilles Tendon
4. Rigid flatfoot
5. Aduclt-acquired flafoot

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Flexible Flatfoot

This appears in childhood. When full weight is placed on the foot, the sole of the foot rests completely
on the ground. When weight is taken off the foot, the arch returns. This is the most common type of
flatfoot, and in the majority of cases, no long-term consequences or pain follow, even into adulthood.
Treatment Options for Flexible Flatfoot: Most cases are not painful, but for those who experience
pain, custom shoe inserts can provide relief. Over-the-counter, non-steroidal anti-inflammatory
(NSAIDs) medications reduce pain and inflammation. Changing activities – for example, limiting
prolonged walking or standing – is helpful. For those who are overweight, diet and exercise might
bring relief.

Flexible Flatfoot with Short Achilles Tendon

A short Achilles, the tendon that runs down the back of your ankle to connect the calf muscle to the
heel bone, causes the heel to lift off the ground earlier than normal during each step. This can develop
into a painful condition.
Treatment Options for Flexible Flatfoot: Surgery to lengthen the tendon can be very helpful in
reducing pain.

Rigid Flatfoot

This type of flat footedness arises from bone malformations or fusions that prevent the arch from
forming during childhood. A dislocated talus bone at the top of the arch can result in rigid flatfoot. This
can occur at any stage of life.
Treatment Options for Flexible Flatfoot: Multiple surgeries can help alleviate the pain of rigid
flatfoot, depending on its cause. Procedures include bone fusions, reconstruction of the arch, and soft
tissue repair.

Adult-acquired Flatfoot

This type of flatfoot occurs in adults when the posterior tibial tendon becomes inflamed, overstretched
or otherwise injured or damaged. This tendon runs from the calf muscle along the inside of the ankle
and foot, ending at the arch. The tendon is crucial to support the arch. Posterior tibial tendon
dysfunction, which is the medical name for adult-acquired flatfoot, usually occurs in one foot but can
emerge in both. It’s a debilitating condition that worsens unless it’s treated early.
Treatment Options for Flexible Flatfoot: Treatment options depend on how advanced the condition
is. In the early stages, rest, foot immobilization, physical therapy and over-the-counter pain
medications can be used. If the condition worsens, total immobilization with a foot brace is the next
step. Surgery is often the last alternative but one that is quite successful. If the tendon is torn, the ends
may be sutured back together. Tendon-lengthening surgery or tendon transfers are two procedures
that may be considered.
Operating on the bones to restore arch height and heel position may be appropriate, along with soft
tissue surgery.

Flatfoot in Children

Figure 29: Foot with a typical arch.

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Flatfoot of a child is usually expected to develop into high or proper arches, as shown by feet of the
mother.
The appearance of flat feet is normal and common in infants, partly due to "baby fat" which masks the
developing arch and partly because the arch has not yet fully developed. The human arch develops in
infancy and early childhood as part of normal muscle, tendon, ligament and bone growth. Training of
the feet, especially by foot gymnastics and going barefoot on varying terrain, can facilitate the
formation of arches during childhood, with a developed arch occurring for most by the age of four to
six years. Flat arches in children usually become proper arches and high arches while the child
progresses through adolescence and into adulthood. A survey of 297 school children at Allahabad,
Uttar Pradesh, India revealed that 40.32% of children under 5, 22.15% of children between 5 and 10,
and, 15.48% of children older than 10 suffered bilateral flat foot.
Because young children are unlikely to suspect or identify flat feet on their own, it is a good idea for
parents or other adult caregivers to check on this themselves. Besides visual inspection, parents
should notice whether a child begins to walk oddly or clumsily, for example on the outer edges of the
feet, or to limp, during long walks, and to ask the child whether he or she feels foot pain or fatigue
during such walks. Children who complain about calf muscle pains or any other pains around the foot
area, may be developing or have flat feet. Pain or discomfort may also develop in the knee joints. A
recent randomized controlled trial found no evidence for the efficacy of treatment of flat feet in children
either for expensive prescribed orthoses (shoe inserts) or less expensive over-the-counter orthoses.
Treatment:
Going barefoot, particularly over terrain such as a beach where muscles are given a good workout, is
good for all but the most extremely flatfooted, or those with certain related conditions such as plantar
fasciitis. One medical study in India with a large sample size of children who had grown up wearing
shoes and others going barefoot, found that the longitudinal arches of the bare footers were generally
strongest and highest as a group, and that flat feet were less common in children who had grown up
wearing sandals or slippers than among those who had worn closed-toe shoes.

Flatfoot in Adults

Flat feet can also develop as an adult ("adult acquired flatfoot") due to injury, illness, unusual or
prolonged stress to the foot, faulty biomechanics, or as part of the normal aging process. This is most
common in woman over 40 years of age. Known risk factors include obesity, hypertension and
[5]
diabetes . Flat feet can also occur in pregnant women as a result of temporary changes, due to
increased elastin (elasticity) during pregnancy. However, if developed by adulthood, flat feet generally
remain flat permanently.

Figure 30: Flatfoot in a 55 years old female with ankle and knee arthritis.

If a youth or adult appears flatfooted while standing in a full weight bearing position, but an arch
appears when the person dorsiflexes (stands on heel or pulls the toes back with the rest of the foot flat
on the floor), this condition is called flexible flatfoot. This is not a true collapsed arch, as the medial
longitudinal arch is still present and the Windlass mechanism still operates; this presentation is
actually due to excessive pronation of the foot (rolling inwards), although the term 'flat foot' is still
applicable as it is a somewhat generic term. Muscular training of the feet, while generally helpful, will
usually not result in increased arch height in adults, because the muscles in the human foot are so
short that exercise will generally not make much difference, regardless of the variety or amount of
exercise. However, as long as the foot is still growing, it may be possible that a lasting arch can be
created.

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Causes of Adult Flatfoot:
Ø Posterior tibial tendon rupture
Ø Deficiency of the spring ligament complex:
Ø Morphometric Dimensions of the Calcaneonavicular (spring) Ligament

Pathophysiology

Research has shown that tendon specimens from people who suffer from adult acquired flat feet show
evidence of increased activity of proteolytic enzymes. These enzymes can break down the
constituents of the involved tendons and cause the foot arch to fall. It is possible that in future these
enzymes will become targets for new drug therapies.
Clinical Manifestations:
Must distinguish between flexible flat foot & rigid / spastic flat foot;
Ø Hypermobile Foot:
o The suspended foot will regain a normal appearing arch;
o As the patient stands on his toes, the arch will reappear & heel will move out of a valgus
position.
This is a good indirect test for nl subtalar motion;
Ø Forefoot Varus:
o Once foot is placed in subtalar neutral position assess whether there is relative forefoot varus
(see exam of subtalar joint);
Ø Differentiate between midfoot collapse and posterior tibial tendon insufficiency;
o If patient can perform a single limb heel rise, then the posterior tibial tendon is functioning;
Complicating Factors:
Ø heel cord contracture:
o lateral deviation of Achilles with wt bearing;
o severe Achilles contracture is associated with midfoot break down;
• Hyperpronation of hindfoot
• Supination of the forefoot which does not correct when hindfoot is reduced;
• Everted heel with fails to invert w/ toe raise;
• Abducted forefoot;

Diagnosis

Many medical professionals can diagnose a flat foot by examining the patient standing or just looking
at them. On going up onto tip toe the deformity will correct when this is a flexible flat foot in a child with
lax joints. Such correction is not seen in the adult with a rigid flat foot.
An easy and traditional home diagnosis is the "wet footprint" test, performed by wetting the feet in
water and then standing on a smooth, level surface such as smooth concrete or thin cardboard or
heavy paper. Usually, the more the sole of the foot that makes contact (leaves a footprint), the flatter
the foot.
In more extreme cases, known as a kinked flatfoot, the entire inner edge of the footprint may actually
bulge outward, where in a normal to high arch this part of the sole of the foot does not make contact
with the ground at all.

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Radiographic Analysis:
Ø standing lateral:
o Normally there is a straight line relationship between talus & first metatarsal;
o in flat foot this relationship will be lost & there will be a sag at either the talonavicular
or naviculocuneiform joint;
Ø standing AP:
o degree of heel valgus is important to assess;
o talocalcaneal angle is measured and if > 35 deg, heel valgus is said to be present;
o note the degree of talo-navicular uncoverage / subluxation;
Ø oblique views
o To rule out tarsal colatition;

Treatment

Most flexible flat feet are asymptomatic, and do not cause pain. In these cases, there is usually no
cause for concern, and the condition may be considered a normal human variant. Flat feet were
formerly a physical-health reason for service-rejection in many militaries.
However, three military studies on asymptomatic adults (see section below), suggest that persons with
asymptomatic flat feet are at least as tolerant of foot stress as the population with various grades of
arch. Asymptomatic flat feet are no longer a service disqualification in the U.S. military.
Rigid flatfoot, a condition where the sole of the foot is rigidly flat even when a person is not standing,
often indicates a significant problem in the bones of the affected feet, and can cause pain in about a
quarter of those affected. Other flatfoot-related conditions, such as various forms of tarsal coalition
(two or more bones in the midfoot or hindfoot abnormally joined) or an accessory navicular (extra bone
on the inner side of the foot) should be treated promptly, usually by the very early teen years, before a
child's bone structure firms up permanently as a young adult. Both tarsal coalition and an accessory
navicular can be confirmed by x-ray. Rheumatoid Arthritis can destroy tendons in the foot (or both feet)
which can cause this condition, and untreated can result in deformity and early onset of Osteoarthritis
of the joint.Such a condition can cause severe pain and considerably reduced ability to walk, even with
orthoses. Ankle fusion is usually recommended.
Treatment of flat feet may also be appropriate if there is associated foot or lower leg pain, or if the
condition affects the knees or the lower back. Treatment may include using Orthoses such as an arch
support, foot gymnastics or other exercises as recommended by a podiatrist/orthotist or physical
therapist. In cases of severe flat feet, orthoses should be used through a gradual process to lessen
discomfort. Over several weeks, slightly more material is added to the orthosis to raise the arch. These
small changes allow the foot structure to adjust gradually, as well as giving the patient time to
acclimatise to the sensation of wearing orthoses. Once prescribed, orthoses are generally worn for the
rest of the patient's life. In some cases, surgery can provide lasting relief, and even create an arch
where none existed before; it should be considered a last resort, as it is usually very time consuming
and costly.
Ø Non Operative Treatment:
• flexible flatfoot is generally a benign condition that rarely requires treatment;
• heel cord stretching should be the main emphasis of treatment;
be sure to supinate the foot while stretching inorder to "lock the midfoot" (avoids
worsening midfoot collapse);
• foot orthotics:
in most cases orthotics will not alter osseous relationships and are ineffective in many
patients;
• furthermore, arch supports may actually make the patient's symptoms worse, until a
concomitant heel cord contracture is relieved;

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 • in patients with talonavicular subluxation, consider taking a wt bearing AP of the
patients feet with and without the inserts;
• if the talonavicular joint subluxation is not corrected w/ inserts then the inserts
are probably not doing their job;
in some cases, patients with a calcaneovalgus deformity can "normalize their wt bearing
pattern" w/ a medial heel wedge;
• children and adolescents:
many feet improve as the child ages, at least until 5 to 6 yrs old;
flexible flatfeet are asymmetic for most pts, & its impossible to predict which planovalgus
feet will become painful in adulthood;
Ø Indications for Surgery:
• Cerebral Palsy
equino-valgus foot deformities with heel cord contracture in patients with cerebral
palsy will generally tend to have break down of mid-foot and longitudinal arch;
these patients are best treated w/ tendo-achilles lengthening (w/ severe contracture) or a
sub-talar fusion before mid-foot break down occurs;
• once mid-foot break down occurs, a triple arthrodesis is required;
• Painful Rigid Flatfoot
small number of flexible flatfeet do not correct w/ growth & will become rigid due to
adaptive changes occur;
painful rigid flat foot will require triple arthrodesis
• Painful Flexible Flatfoot
in this situation, it is important to determine the anatomic cause of the pain;
as noted by JTC Lau and TR Daniels, a tarsal tunnel release w/ a concomitant pes
planus may have the effect of increasing posterior tibial nerve tension, which may
explain the high rate of poor surgical results;
in the same study, distraction calcaneo-cuboid arthrodesis reduced nerve tension;
Ø Contra-Indications for Surgery:
• hyper-mobile joints (such as Marfan's, Ehler's Danlos, Down's);
• in adults, if feet are asymptomatic, surgery is almost never indicated;

Running

It is generally accepted by professionals that a person with flatfeet tends to over pronate in his or her
running form. Pronation is a natural form of shock absorption during running and walking, when the
ankle rolls inward and the weight distribution in the foot shifts medially. Overpronation is excessive
pronation; it disrupts the alignment of the leg and may result in injuries due to over-stressing of the
knee and leg. With normal, or neutral, running shoes, a person who overpronates in his or her running
form may be more susceptible to shin splints, back problems, and tendonitis in the knee. Running in
shoes with extra medial support or using special shoe inserts, orthoses, may help correct one's
running form by reducing pronation and may reduce risk of injury.

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3.2 PES CAVUS

Figure 31: High arch in a foot of a person with a hereditary neuropathy.

High arch (also high instep, pes cavus in medical terminology) is a human foot type in which the
sole of the foot is distinctly hollow when bearing weight. That is, there is a fixed plantar flexion of the
foot. A high arch is the opposite of a flat foot, and somewhat less common.

History

The term pes cavus is Latin for hollow foot and is synonymous with the terms talipes cavus, cavoid
foot, high-arched foot, and supinated foot type. Pes cavus is a multiplanar foot deformity characterised
by an abnormally high medial longitudinal arch. It also commonly features a varus (inverted) hindfoot,
a plantarflexed position of the first metatarsal, an adducted forefoot and dorsal contracture of the toes.
Despite numerous anecdotal reports and hypothetical descriptions, very little rigorous scientific data
exist on the assessment or treatment of pes cavus.
Pes cavus, as shown in the images below, is a high arch of the foot that does not flatten with weight
bearing. No specific radiographic definition of pes cavus exists. The deformity can be located in the
forefoot, midfoot, hindfoot, or a combination of these sites.

Figure 32: Pes cavus with severe hindfoot involvement.

Figure 33: Pes cavus with plantarflexion of the first ray.

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Types of Pes Cavus

The term pes cavus encompasses a broad spectrum of foot deformities. Three main types of pes
cavus are regularly described in the literature: pes cavovarus, pes calcaneocavus and ‘pure’ pes
cavus. The three types of pes cavus can be distinguished by their aetiology, clinical signs and
radiological appearance.
Pes cavovarus, the most common type of pes cavus, is seen primarily in neuromuscular disorders
such as Charcot-Marie-Tooth disease, and in cases of unknown aetiology, conventionally termed as
‘idiopathic’. Pes cavovarus presents with the calcaneus in varus, the first metatarsal plantarflexed and
a claw-toe deformity.
Radiological analysis of pes cavus in Charcot-Marie-Tooth disease shows the forefoot is typically
plantarflexed in relation to the rearfoot.
In the pes calcaneocavus foot, which is seen primarily following paralysis of the triceps surae due to
poliomyelitis, the calcaneus is dorsiflexed and the forefoot is plantarflexed. Radiological analysis of
pes calcaneocavus reveals a large talo-calcaneal angle. In ‘pure’ pes cavus the calcaneus is neither
dorsiflexed or in varus, and is highly-arched due to a plantarflexed position of the forefoot on the
rearfoot. A combination of any or all of these elements can also be seen in a ‘combined’ type of pes
cavus that may be further categorized as flexible or rigid. Despite various presentations and
descriptions of pes cavus, all are characterised by an abnormally high medial longitudinal arch, gait
disturbances and resultant foot pathology.

Epidemiology of Pes Cavus

There are few good estimates of prevalence for pes cavus in the general community. While pes cavus
has been reported between 2 and 29% of the adult population, there are several limitations of the
prevalence data reported in these studies. Population based studies suggest the prevalence of the
cavus foot is approximately 10%. Common complaints associated with pes cavus include pain under
the metatarsal heads and the heel, lateral ankle sprains, and footwear issues.

Cause of Pes Cavus

High foot arches are much less common than flat feet. They are more likely to be caused by a bone
(orthopedic) or nerve (neurological) condition.
Unlike flat feet, highly arched feet tend to be painful because more stress is placed on the section of
the foot between the ankle and toes (metatarsals). This condition can make it difficult to fit into shoes.
People who have high arches usually need foot support. A high arch may cause disability.
Pes cavus may be hereditary or acquired, and the underlying cause may be neurological, orthopedic
or neuromuscular. Pes cavus is sometimes—but not always—connected through Hereditary Motor
and Sensory Neuropathy Type 1 (Charcot-Marie-Tooth disease) and Friedreich's Ataxia; many other
cases of pes cavus are natural.
The cause and deforming mechanism underlying pes cavus is complex and not well understood.
Factors considered influential in the development of pes cavus include muscle weakness and
imbalance in neuromuscular disease, residual effects of congenital clubfoot, post-traumatic bone
[12]
malformation, contracture of the plantar fascia and shortening of the Achilles tendon.
Among the cases of neuromuscular pes cavus, 50% have been attributed to Charcot-Marie-Tooth
[13]
disease which is the most common type of inherited neuropathy with an incidence of 1 per 2,500
[14]
persons affected. Also known as Hereditary Motor and Sensory Neuropathy (HMSN), it is
genetically heterogeneous and usually presents in the first decade of life with delayed motor
milestones, distal muscle weakness, clumsiness and frequent falls. By adulthood, Charcot-Marie-
Tooth disease can cause painful foot deformities such as pes cavus. Although it is a relatively
common disorder affecting the foot and ankle, surprisingly little is known about the distribution of
muscle weakness, severity of orthopaedic deformities, or types of foot pain experienced. Currently,
there are no cures or effective treatment to halt the progression of any form of Charcot-Marie-Tooth
disease.
The development of the cavus foot structure seen in Charcot-Marie-Tooth disease has been
previously linked to an imbalance of muscle strength around the foot and ankle. A hypothetical model
proposed by various authors describes a relationship whereby weak evertor muscles are overpowered

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by stronger invertor muscles causing an adducted forefoot and inverted rearfoot. Similarly, weak
dorsiflexors are overpowered by stronger plantarflexors causing a plantarflexed first metatarsal and
anterior pes cavus.
Pes cavus is also evident in people without neuropathy or other neurological deficit. In the absence of
neurological, congenital or traumatic causes of pes cavus, the remaining cases are classified as being
‘idiopathic’, because their aetiology is unknown.

Symptoms

• Shortened foot length

• Difficulty fitting shoes
• Foot pain with walking, standing, and running (not everyone has this symptom)

Pain and Disability in Pes Cavus

As with certain cases of flat feet, high arches may be painful due to metatarsal compression; however,
high arches— particularly if they are flexible or properly cared-for—may be an asymptomatic condition.
People with pes cavus sometimes—though not always—have difficulty finding shoes that fit and may
require support in their shoes. Children with high arches who have difficulty walking may wear
specially-designed insoles, which are available in various sizes and can be made to order.
Individuals with pes cavus frequently report foot pain, which can lead to a significant limitation in
function. The range of complaints reported in the literature include metatarsalgia, pain under the first
metatarsal, plantar fasciitis, painful callosities, ankle arthritis and Achilles tendonitis.
There are many other symptoms believed to be related to the cavus foot. These include shoe-fitting
problems, lateral ankle instability, lower limb stress fractures, knee pain, iliotibial band friction
syndrome (back pain and tripping).
Foot pain in people with pes cavus may result from abnormal plantar pressure loading because,
structurally, the cavoid foot is regarded as being rigid, non-shock absorbent and having reduced
ground contact area. There have previously been reports of an association between excessive plantar
pressure and foot pathology in people with pes cavus.

Exams and Tests

When the person stands on the foot, the instep looks hollow and most of the weight is on the back and
balls of the foot (metatarsals head).
Your health care provider will check to see if the high arch is flexible, meaning it can be moved
around.
Tests that may be done include:
• Electromyography
• MRI of the spine
• Nerve conduction studies
• X-ray of the feet
• X-ray of the spine

Treatment

Surgical treatment is only initiated if there is severe pain, as the available operations can be difficult.
Otherwise, high arches may be handled with care and proper treatment.
Suggested conservative management of patients with painful pes cavus typically involve strategies to
reduce and redistribute plantar pressure loading with the use of foot orthoses and specialised
cushioned footwear. Other non-surgical rehabilitation approaches include stretching and strengthening
of tight and weak muscles, debridement of plantar callosities, osseous mobilization, massage,
chiropractic manipulation of the foot and ankle and strategies to improve balance. There are also

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numerous surgical approaches described in the literature aimed at correcting the deformity and
rebalancing the foot. Surgical procedures fall into three main groups: (1) soft-tissue procedures (e.g.
plantar fascia release, Achilles tendon lengthening, tendon transfer); (2) osteotomy (e.g. metatarsal,
midfoot or calcaneal); (3) bone-stabilising procedures (e.g. triple arthrodesis).

Medical Therapy
The goal of treatment is to allow the patient to ambulate without symptoms. The underlying cause
must be identified in order to determine if the disorder is progressive. The patient must understand the
rationale for treatment and that surgical reconstruction does not provide a normal foot. The goal of
surgery is to produce a plantigrade foot and pain relief. Repeat surgical procedures may be necessary,
especially if the deformity is progressive. Preoperative patient education is essential for patient
satisfaction.
Nonoperative treatment may provide patients with significant relief. Physical therapy to stretch tight
muscles and strengthen weak muscles may provide early relief. Orthotics with extra-depth shoes to
offload bony prominences and prevent rubbing of the toes may improve symptoms. For varus
deformities, a lateral wedge sole modification can improve function. Bracing for supple deformities or
foot drop may allow patients to ambulate; however, in patients with sensation deficits, Plastazote
linings in the brace are required and frequent inspection of the skin.

Clinical Goal for Orthotic Treatment

The orthosis for the treatment of pes cavus foot must accomplish several specific goals:
Increase plantar surface contact area. The overload on the metatarsal heads is a result of limited
plantar surface contact due to the high arch and limited ankle joint dorsiflexion. Increasing plantar
surface contact with an orthosis ensures that more of the foot is bearing weight in the arch and the
metatarsal heads are bearing less weight for less time.
Resist excessive supination. Lateral ankle instability and a laterally deviated subtalar joint axis (STJ)
are frequently associated with high arched feet. This lateral position of the STJ axis results in
excessive supinatory torque around the subtalar joint axis. The prescribed orthosis should be
designed to resist this excessive supination.
Resist both excessive pronation and supination forces. Rearfoot instability is an extension of the
laterally deviated subtalar axis. However, in flexible pes cavus feet, midtarsal flexibility complicates the
later portion of the stance phase of gait. The forefoot pathology produces midtarsal joint supination
that leads to excessive pronation of the rearfoot. Some pes cavus feet suffer from both lateral ankle
instability at midstance and rearfoot pronation at late midstance.
It is essential that the prescribed orthoses is designed to provide resistance to both excessive
pronation and supination forces.

Possible Complications

• Chronic pain
• Difficulty walking

Prevention
People with highly arched feet should be checked for nerve and bone conditions. Identifying these
other conditions may help prevent or reduce arch problems.

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3.3 FOOT PAIN

There are many causes of foot pain, but when most people talk about foot pain they are describing
symptoms that cause pain under the "ball of the foot." When foot pain occurs under the ball of the foot,
the medical term is metatarsalgia.
There are many other causes of foot pain in other parts of the foot:
Toe pain and bunions
Arch pain
Heel pain (underneath the heel)
Posterior heel pain (behind the heel)
Metatarsalgia occurs in the region between the arch and the toes. The medical term for foot pain,
metatarsalgia, comes from the name of the bones that are in this part of the foot: the metatarsals. The
metatarsals are long bones at the base of each toe. Sometimes pressure on the ends of the
metatarsal bones causes symptoms in the ball of the foot.

Problems Causing the Symptoms of Foot Pain

Foot pain can be caused by increased pressure on the metatarsal heads. This can be due to
constricting foot wear or high heel shoes. If you have pain under the ball of your foot, try wearing
shoes that have a wider toe box.
Other conditions that can cause foot pain include ligament injuries and joint irritation. These problems
can also be relieved with more accommodating footwear.

Treatments Available for Foot Pain

Treatment of foot pain often consists of anti-inflammatory medications, footwear modifications, and
inserts for your shoes.
When buying footwear, look for shoes with a wide toebox, good support, and avoid high heels. Simple
inserts can help with many types of foot pain. Metatarsal pads are best for the treatment of
metatarsalgia. These pads help to take pressure off the ball of the foot. If some simple steps do not
alleviate your symptoms, you should see your doctor to ensure you are receiving adequate treatment.
Foot Pain Treatments
Shoe Inserts
Anti-Inflammatory Medications
Buying Shoes

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3.4 METATARSALGIA

Figure 34: Metatarsalgia.

Definition of Metatarsalgia
Metatarsalgia, a form of neuralgia, is an inflammation of the nerve that runs between the third and the
fourth metatarsal (foot) bones.

Description of Metatarsalgia

Metatarsalgia is caused by the compression of a small toe nerve between two displaced metatarsal
bones. Inflammation occurs when the head of one displaced metatarsal bone presses against another
and they catch the nerve between them. With every step, the nerve is pushed together by the bones
and then rubbed, pressed again, and irritated without relief. Consequently, the surrounding nerve
tissue becomes enlarged, with a sheath of scar tissue that forms to protect the nerve fibers.
Metatarsalgia really covers a group of foot disorders. The classic symptom is pain in the front (ball) of
the foot. Many people say that it is "like walking on pebbles," but x-rays usually show nothing irregular.
The problem affects males and females from adolescents to older adults. It is most common in middle-
aged women.
Metatarsalgia (literally metatarsal pain, colloquially known as stone bruise) is a general term used to
refer to any painful foot condition affecting the metatarsal region of the foot. This is a common problem
that can affect the joints and bones of the metatarsals. Metatarsalgia is most often localized to the first
metatarsal head (the ball of the foot just behind the big toe). There are two small sesamoid bones
under the first metatarsal head. The next most frequent site of metatarsal head pain is under the
second metatarsal.
This can be due to either too short a first metatarsal bone or to "hypermobility of the first ray"
(metatarsal bone + medial cuneiform bone behind it), both of which result in excess pressure being
transmitted into the second metatarsal head.
Metatarsalgia is a condition marked by pain and inflammation in the ball of your foot.
You may experience metatarsalgia if you're physically active and you participate in activities that
involve running and jumping. You may develop metatarsalgia by wearing ill-fitting shoes also. There
are other causes as well.
Although generally not serious, metatarsalgia can sideline you. Fortunately, conservative treatments,
such as ice and rest, can often relieve metatarsalgia symptoms. And proper footwear, along with
shock-absorbing insoles or arch supports, may be all you need to prevent or minimize future problems
with metatarsalgia.

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Causes and Risk Factors of Metatarsalgia

The most common causes are:

Heredity: Narrow, high-arched feet can focus stress on the balls of the feet. Also, if the legs are not
equal in length, the metatarsal-phalangeal joints of the shorter leg receive additional stress.
Skin Irritation: Metatarsalgia often occurs with bunions or tender calluses under the metatarsal-
phalangeal joints.
Foot Disorders: Rheumatoid arthritis, stress fractures, fluid accumulation and muscle fatigue can
help cause metatarsalgia. If one is born with - or develops - flat feet, there is also a risk.
"Overloaded" Feet: Excess weight from pregnancy or obesity can contribute to metatarsalgia. So
can persistent and abnormal stress on the feet. For example, soldiers, letter carriers and dancers are
at risk because of extensive standing and walking.
Nerve Disorders: Morton's neuroma is a benign growth that can develop on a nerve in the foot. The
neuroma can cause a burning sensation that may radiate to other parts of the foot. Soreness can
persist even when resting.

Clinical Features

Figure 35: Metatarsalgia pain occurs on the ball of the foot.

Figure 36: Metatarsalgia. This condition refers to pain under the ball (front) of the foot. Symptoms of
metatarsalgia may often diminish with rest.

Figure 37: Metatarsalgia is a condition marked by pain and inflammation.

Figure 38: Metatarsalgia and Mortons Neuroma are most common in women aged 25-55 years.

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 Figure 39: Why Metatarsalgia may not be what it seems.

Figure 40: Ball of foot pain / Metatarsalgia.

Treatment of Metatarsalgia

In most cases, simple measures will lessen pain at the front of the foot.
Foot freedom: If you wear tight shoes with thin soles and high heels, give them away. If you have
symptoms of a Morton's neuroma, remove the shoes periodically and gently massage the painful area.
If you pinch or rub vigorously, you may experience pain as intense as when you hit your "funny bone."
Orthotics (or metatarsal pads): Consult your podiatrist or physician for a footpad that relieves
pressure on the metatarsal area.
Medications: Your doctor may prescribe nonsteroidal anti-inflammatory medications such as
ibuprofen or sulindac. This is the most common treatment. Ibuprofen, sulindac, or diclofenac sodium,
prescription astringents, emollients or ointments can help treat bunions or calluses, which sometimes
are associated with metatarsalgia. Rarely, injections of a corticosteroid into the tender area may be
used.
Surgery: An operation seldom is necessary. In severe cases of Morton's neuroma, surgeons remove
the nerve associated with painful symptoms. Surgical options for other types of metatarsalgia include
reshaping joints and modifying irregularly shaped bones.

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3.5 BUNION (HALLUX VALGUS)

Figure 41: Hallux Valgus.

Definition:
A bunion (hallux valgus) is a deformity characterized by lateral deviation of the great toe, often
erroneously described as an enlargement of bone or tissue around the joint at the head of the big toe
(metatarsophalangeal joint). As the great toe (hallux) turns in toward the second toe (angulation) the
tissues surrounding the joint may become swollen and tender.

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The term is used to refer to the pathological bump on the side of the great toe joint. The bump is partly
due to the swollen bursal sac and/or an osseous (bony) anomaly on the mesophalangeal joint (where
the first metatarsal bone and hallux meet). The larger part of the bump is a normal part of the head of
first metatarsal bone that has tilted sideways to stick out at its top.
There are many causes of bunions, but the primary one is tight, ill-fitting shoes, shoes that constrict
the forefoot over a long period of time. High heels and constricting forefoot shoe gear are the primary
causes of Hallux Valgus.
There are many things that you can do to lessen the pain associated with this condition:
1. A good, well-supported, wide toe box shoe, along with good insoles or orthotic.
2. Anti-inflammatory medications such as aspirin, Tylenol, etc.
3. Cold compresses
4. Soaking the foot in Epsom salts, Johnson and Johnson foot soaks, or Dome-Boro type
solutions, massage, paraffin bath therapy
5. Support wraps and pads, such as the Bunion Splint, Silopad Gel Bunion Pad, and the Bunion
Shield are also good palliative measures.
Diabetes, vascular insufficiency, arthritis complicate the condition.

Pathogenesis
The etiology of hallux valgus is somewhat controversial. Some cases are congenital, perhaps
secondary to a sloping surface of the first tarsometatarsal joint. When this joint is hypermobile, with or
without the normal angle, it is often referred to as an "atavistic" tarsometatarsal joint. Other cases are
almost certainly due to environmental factors, such as poorly fitting footwear. The fashionable shoes
worn by many women are more constraining than the shoes worn by men and are felt by many
authors to be the etiologic factor in most cases of hallux valgus. This would help to explain the 10:1
ratio of females to males seen with this disorder.

Figure 42: 25 years old female with normal feet and no shoes.

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 Figure 43: Same patient as figure above, but now in shoes with 3 inch heels. The intermetatarsal angle has
widened in both feet, and a functional hallux valgus has developed due to her constricting shoes.

Bunions are mostly genetic and consist of certain tendons, ligaments, and supportive structures of the
first metatarsal that are positioned differently. This bio-mechanical anomaly may be caused by a
variety of conditions intrinsic to the structure of the foot – such as flat feet, excessive flexibility of
ligaments, abnormal bone structure, and certain neurological conditions. These factors are often
considered genetic. Although some experts are convinced that poor-fitting footwear is the main cause
of bunion formation, other sources concede that footwear only exacerbates the problem caused by the
original genetic structure.
Bunions are commonly associated with a deviated position of the big toe toward the second toe, and
the deviation in the angle between the first and second metatarsal bones of the foot. The small
sesamoid bones found beneath the first metatarsal (which help the flexor tendon bend the big toe
downwards) may also become deviated over time as the first metatarsal bone drifts away from its
normal position. Arthritis of the big toe joint, diminished and/or altered range of motion, and discomfort
with pressure applied to the bump or with motion of the joint, may all accompany bunion development.

Symptoms

The symptoms of bunions include irritated skin around the bunion, pain when walking, joint redness
and pain, and possible shift of the big toe toward the other toes. Blisters may form more easily around
the site of the bunion as well.
Having bunions can also make it harder to find shoes that fit properly; bunions may force a person to
have to buy a larger size shoe to accommodate the width the bunion creates. When bunion deformity
becomes severe enough, the foot can hurt in different places even without the constriction of shoes
because it then becomes a mechanical function problem of the forefoot.
Pain is focused under the great toe on the ball of the foot. With sesamoiditis, pain may develop
gradually; with a fracture, pain will be immediate.
Swelling and bruising may or may not be present.
You may experience difficulty and pain in bending and straightening the great toe.

Diagnosis

During the examination, the physician will look for tenderness at the sesamoid bones. Your doctor may
manipulate the bone slightly or ask you to bend and straighten the toe. He or she may also bend the
great toe up toward the top of the foot to see if the pain intensifies.
Your physician will request X-rays of the forefoot to ensure a proper diagnosis. In many people, the
sesamoid bone nearer the center of the foot (the medial sesamoid) has two parts (bipartite). Because
the edges of a bipartite medial sesamoid are generally smooth, and the edges of a fractured sesamoid

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are generally jagged, an X-ray is useful in making an appropriate diagnosis. Your physician may also
request X-rays of the other foot to compare the bone structure. If the X-rays appear normal, the
physician may request a bone scan.

Treatment

Bunions may be treated conservatively with changes in shoe gear, different orthotics (accommodative
padding and shielding), rest, ice, and medications. These sorts of treatments address symptoms more
than they correct the actual deformity.
Surgery, by an orthopedic surgeon or a podiatrist, may be necessary if discomfort is severe enough or
when correction of the deformity is desired.
Orthotics
Orthotics are splints, regulators while conservative measures include various footwear like gelled toe
spacers, bunion / toes separators, bunion regulators, bunion splints, and bunion cushions.
Surgery

Figure 44: A podiatrist performing surgery to remove the bony enlargement and restore normal alignment of the
toe joint.

Procedures are designed and chosen to correct a variety of pathologies that may be associated with
the bunion. For instance, procedures may address some combination of:
• removing the abnormal bony enlargement of the first metatarsal,
• realigning the first metatarsal bone relative to the adjacent metatarsal bone,
• straightening the great toe relative to the first metatarsal and adjacent toes,
• realigning the cartilagenous surfaces of the great toe joint,
• addressing arthritic changes associated with the great toe joint,
• repositioning the sesamoid bones beneath the first metatarsal bone,
• shortening, lengthening, raising, or lowering the first metatarsal bone, and
• correcting any abnormal bowing or misalignment within the great toe.
At present there are many different bunion surgeries for different effects. The age, health, lifestyle, and
activity level of the patient may also play a role in the choice of procedure.
Bunion surgery can be performed under local, spinal, or general anesthetic. The trend has moved
strongly toward using the less invasive local anesthesia over the years. A patient can expect a 6- to 8-
week recovery period during which crutches are usually required for aid in mobility. An orthopedic cast

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is much less common today as newer, more stable procedures and better forms of fixation (stabilizing
the bone with screws and other hardware) are used.
History of the Procedure
In the 19th century, the prevalent understanding of the bunion—hallux valgus—was that it was purely
an enlargement of the soft tissue, first metatarsal head, or both, most commonly caused by ill-fitting
footwear. Thus, treatment had varying results, with controversy over whether to remove the overlying
bursa alone or in combination with an exostectomy of the medial head. These surgeries were
considered to be beneath many surgeons, so the understanding of the pathology of hallux valgus was
gradual in its development. Surgeons slowly began to recognize that bunions could develop as a
result of numerous different factors, that they tended to be familial, and that they often were
associated with other foot deformities.
As the school of thought began to shift, the first surgical treatment to address deforming pathology
was developed and presented on May 4, 1881, when J. L. Reverdin gave a report on hallux
abductovalgus to the Medical Society of Genfer. He described a procedure in which a curved incision
medial to the extensor hallucis longus was followed by incision of the periosteum, chiseling off of the
exostosis, removal of a wedge of bone from behind the capitulum of the metatarsus, and suturing of
the bone with catgut. This operation is considered to be the forerunner of all operations that aim to
correct hallux valgus via osteotomy.

Figure 45: Lateral release sequence: (1) release of the conjoined adductor hallucis tendon, (2) release of the fibular
sesamoid ligament, (3) tenotomy of the lateral head of the flexor hallucis brevis, and (4) excision of the fibular
sesamoid.

.
Figure 46: Preoperative radiograph shows degenerative joint disease.

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 Figure 47: Postoperative radiograph obtained after resectional arthroplasty and total joint implant placement.

Since its inception, the Reverdin procedure has undergone many variations and modifications,
including the addition of lateral releases and proximal osteotomies, in an effort to address deformity.
Indeed, more than 100 procedures have been attempted and developed for the correction of hallux
valgus. However, many of these variations have been developed out of ignorance; some are even
repetitions of previous procedures, both failed and successful. Surgeons have continued to reevaluate
the osteotomy in search of the most stable procedure with the fewest complications.
Recent Studies
Shima et al investigated the intraobserver and interobserver reliability of different radiographic
methods used to measure the hallux valgus and intermetatarsal angles and to determine the most
reliable method for making those measurements before and after a proximal crescentic
osteotomy of the first metatarsal. The method that yielded the highest intraobserver and interobserver
correlation coefficients for the preoperative hallux valgus and intermetatarsal angles and the
postoperative hallux valgus angle was that in which a line connected the centers of the first metatarsal
head and the proximal articular surface of the first metatarsal to define the longitudinal axis of the first
metatarsal. The authors therefore recommended that this method be used for evaluating radiographs
before and after a proximal crescentic osteotomy for the treatment of hallux valgus.
Schuh et al studied the changes of plantar pressure distribution during the stance phase of gait in
patients who underwent hallux valgus surgery followed by a multimodal rehabilitation program. The
study included 30 patients who underwent Austin and scarf osteotomy for correction of mild to
moderate hallux valgus deformity and began a rehabilitation program 4 weeks postoperatively (once
per week for 4-6 wk). Plantar pressure analysis was performed preoperatively and at 4 weeks, 8
weeks, and 6 months postoperatively. Range of motion of the first metatarsophalangeal joint was also
measured. Surgery and the first metatarsophalangeal joint range of motion increased at 6 months,
with a significant increase in isolated dorsiflexion.

Physical Exam

• vascular status: dorsalis pedis and posterior tibial artery;

• ankle equinus deformity (loss of ankle dorsiflexion may accentuate forefoot pain);
• determine the correctability of the deformity:
• degree to which standing accentuates the deformity;
• passive correctability of the hallux valgus and determine the ROM of the MTP joint in both the
corrected and uncorrected positions;

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 • toe stiffness: note whether the toe is stiff once placed in the corrected position?
• a mildly symptomatic hallux valgus is preferable to a stiff corrected MTP joint;
• note that a technically correct surgical procedure may leave toe stiff once placed in corrected
position (due to soft tissue contractures);
• the result may be pain w/ toe off during gait;
• amount of 1st toe pronation (associated w/ severity);
• first MT-cuneiform joint is evaluated for hypermobility and tenderness (involves pushing the
MT head into dorsiflexion & plantar flexion);

Radiographic Findings

Hallux valgus is often associated with abnormalities in two planes. In such cases, the first metatarsal
head is not only deviated medially, but also dorsally. As the first metatarsal splays dorsally, greater
stress is placed on the central metatarsals, especially the second, leading to hyperostosis and
occasionally stress fractures.

Figure 48: Normally, the 1st and 2nd metatarsals are parallel to each other, and their superior surfaces appear
within 1 - 2 mm of each other, as shown here.

Figure 49: Some patients with metatarsus primus varus demonstrate not only medial angulation of the first
metatarsal head, but also dorsal angulation as well. Here the first metatarsal is elevated several mm above the
second metatarsal head.

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Figure 50: This patient has a marked hallux valgus deformity in both feet. As the first toe migrates more and more
to valgus, it presses against the second toe, and may aggravate dorsal clawing of the second toe, which is usually
initiated by overload of the second metatarsal and synovitis of the metatarsophalangeal joint. Also note the relative
hyperostosis of the second metatarsal shafts compared to the third and fourth, as well as dorsal rotation of the
fibular sesamoids.

Figure 51: Preoperative film showing hallux valgus and clawtoe deformities of the second and third toes. Medial
subluxation of the head off the sesamoids is shown, as well as marked hyperostosis of the second metatarsal shaft.

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Non-operative Treatment

Ø pts with out DJD of MTP joint may benefit from lace up shoes w/ a wide toe box;
Ø pts with equinus contracture may benefit from stretching, which may unload the forefoot and
relieve pain;
Ø ts with DJD of MTP (hallux rigidus) may benefit from a stiff soled shoe;

Complications

Ø hallux varus:
o excessive resection of medial metatarsal head;
o excision of medial sesamoid;
o excessive capsular plication;
o immobilization of the toe in excessive varus during the post op period;

3.6 SESAMOIDITIS

Figure 52: Human sesamoid bones.

Most bones in the human body are connected to each other at joints. But there are a few bones that
are not connected to any other bone
Instead, they are connected only to tendons or are embedded in muscle. These are the sesamoids.
The kneecap (patella) is the largest sesamoid. Two other very small sesamoids (about the size of a
kernel of corn) are found in the underside of the forefoot near the great toe, one on the outer side of
the foot and the other closer to the middle of the foot.
Sesamoids act like pulleys. They provide a smooth surface over which the tendons slide, thus
increasing the ability of the tendons to transmit muscle forces. The sesamoids in the forefoot also
assist with weightbearing and help elevate the bones of the great toe. Like other bones, sesamoids
can break (fracture). Additionally, the tendons surrounding the sesamoids can become irritated or

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inflamed. This is called sesamoiditis and is a form of tendinitis. It is common among ballet dancers,
runners and baseball catchers.

Anatomy
st
The 1 metatarso-phalangeal joint is found at the base of the big toe (where the big toe joins the foot),
and is made up of:
1. The base of the proximal phalanx, which is the big toe
bone closest to the foot.
st
2. The head of the 1 metatarsal, or the foot bone that
attaches to the big toe.
3. The medial (tibial) sesamoid, a pea sized bone that
st
lies on the undersurface of the 1 metatarsal head. It is
the sesamoid closest to the inner edge of the foot.
4. The lateral (fibular) sesamoid, also pea sized, lies
next to the medial sesamoid on the side closest to the
nd
2 metatarsal and toe.
5. The joint capsule surrounds these bones, including the
st
sesamoids, at the joint. It stabilizes the 1 metatarso-
phalangeal joint.
6. The muscles that flex or bend the big toe down are called the flexor hallucis muscles. These
st
muscles pass underneath the 1 metatarso-phalangeal joint, crossing over the sesamoids before
attaching to the bottom of the big toe.

Primary Function of Sesamoids

st
Because the sesamoids protrude down, underneath the head of the 1 metatarsal, they act as a
fulcrum for the big toe flexors, giving these muscles extra leverage and power. This power allows the
big toe to ""push"" us forward with extra force each time we take a step forward. Without the medial
and lateral sesamoids, the big toe loses some of its power and force.
Sesamoiditis is the inflammation of the sesamoid bones, along with the surrounding tissues. As with
any inflammation of tissue and bone, it can cause intense pain. In the case of sesamoiditis, pain it is
felt directly below the first metatarsal joint in the big toe, in the ball of the foot. The pain usually gets
worse over a period of time, helping with the diagnosis and differentiating it from other ball of foot
problems. The sudden onset of pain is possible however, when the condition is caused by trauma
such as a stress fracture to the sesamoid bones. Due to the small size of the bones, it is sometimes
difficult to diagnose the condition with an x-ray, and a bone scan is the most reliable way of getting an
accurate diagnosis, and also determining the severity of the condition.
Usually periostitis (new bone growth) occurs along with sesamoiditis, and the suspensory ligament
may also be affected. Sesamoiditis results in inflammation, pain, and eventually bone growth.
Humans will also experience inflammation and pain. Sometimes the sesamoid bone will even fracture
and can be difficult to pick up on X-ray. A bone scan is a better alternative

Causes

In the human excessive forces caused by sudden bending upwards of the big toe, high heels, or a
stumble can contribute to sesamoiditis. Once the sesamoid bone is injured it can be very difficult to
cure because every time you walk you put additional pressure on the sesamoid bone. Treatment in
humans consists of anti-inflammatory medication, cortisone injections, strapping to immobilize the big
toe and orthotics with special accommodations to keep pressure off the affected bone.
Sesamoiditis typically can be distinguished from other forefoot conditions by its gradual onset. The
pain usually begins as a mild ache and increases gradually as the aggravating activity is continued. It
may build to an intense throbbing. In most cases there is little or no bruising or redness. One of the
major causes of sesamoiditis is increased activity. You've probably stepped up your activity level
lately, which has forced you to put more pressure on the balls of your feet. Speedwork, hillwork, or
even increased mileage can cause this. If you have a bony foot, you simply may not have enough fat

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on your foot to protect your tender sesamoids. Also, if you have a high arched foot, you will naturally
run on the balls-of-your-feet, adding even more pressure.
There are a number of causes of sesamoiditis, although the age of patients can indicate which is most
likely. In the older age ranges the condition is most commonly due to arthritic changes to the sesamoid
bones, usually at the point where they articulate with the head of the first metatarsal.
Osteoarthritis of the sesamoid bones is the most likely cause in older patients, and may involve the
formation of additional bone in the form of a bone spur. This bone fragment can cause inflammation of
the surrounding muscles and tendons as well as the sesamoid bones themselves becoming inflamed.
Osteoporosis is another factor, which weakens the bones, reducing their ability to cope with the forces
from walking. Whilst this is common with older patients, it can also be a cause of sesamoiditis in
younger women, especially those with a history of eating disorders or irregular menstruation.
For most healthy young to middle aged adults the condition is usually the result of a single trauma to
the sesamoid bones, or repeated stresses over time. Women who frequently wear high heels place an
increased stress on the forefoot, as do athletes and dancers. Any job which requires squatting or
carrying heavy loads can also trigger the condition over time.
Some people can be prone to develop sesamoiditis due to abnormalities of the bones themselves, and
those people with large sesamoid bones are particularly prone to the condition. The larger the bones,
the greater the force they have to take, and the result of injury is far more likely. People with high
arches also place a greater strain on the forefoot, and runners who overpronate – excessive roll their
feet inwards when running – are more likely to develop the condition.

In the horse it occurs at the horse's fetlock. The sesamoid bones lie behind the bones of the fetlock, at
the back of the joint, and help to keep the tendons and ligaments that run between them correctly
functioning.
Usually periostitis (new bone growth) occurs along with sesamoiditis, and the suspensory ligament
may also be affected. Sesamoiditis results in inflammation, pain, and eventually bone growth.
Humans will also experience inflammation and pain. Sometimes the sesamoid bone will even fracture
and can be difficult to pick up on X-ray. A bone scan is a better alternative.

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Clinical Features

The most common sesamoiditis symptom is pain experienced when walking, although any load
bearing exercise is likely to cause pain. The pain is strongest during the “toe off” when walking, as the
body weight transfers onto the toes. Pain is felt directly underneath the first metatarsal head in the ball
of the foot, at the base of the big toe.
Sesamoiditis is usually accompanied by tenderness of the surrounding tissues, and intensifies when
direct pressure is applied. The pain is usually only felt during activity, and whilst the pain may persist
for a short time when the weight is taken off the feet, it usually rapidly subsides. As the condition
deteriorates, the pain persists for longer, and in severe cases, pain is present most of the time.
Sesamoiditis also can cause a small degree of swelling under the first metatarsal joint.
The most common symptoms of sesamoiditis include:
Ø Early Stage:
o Sesamoids are tender when direct pressure is applied to them.
o Mild pain occurrs when walking barefoot or in thin soled shoes. Pain is worse when running
and jumping.
o Pain subsides quickly with rest.
o Mild swelling under the sesamoids that usually subsides with rest and elevation of the foot.
Ø Later Stage:
o Constant pain may be present under the sesamoids. This pain becomes worse when:
§ Walking, running, and especially jumping, even in well padded shoes.
§ Applying direct pressure to the sesamoids.
§ Bending the toe up.
o Swelling is increased, and may not subside with rest and elevation of the foot.
st
o Eventually, the entire 1 metatarso-phalangeal joint may become swollen. This may cause
stiffness in the big toe.
If the above symptoms occur abruptly, or after an injury to the forefoot, one or both sesamoids may be
fractured. Fractured sesamoids should be cared for by your physician or by a foot and ankle specialist.
The most common causes of Sesamoiditis include:
Ø Injury to the sesamoids may occur in one of two ways:
o Direct injury to the sesamoids (such as stepping on a rock while walking or running barefoot).
o Micro-trauma is an overuse injury due to excessive or repetitive stress on the sesamoids. This
type of injury occurs over a period of time. Examples include:
§ Dancing barefoot or in shoes with thin soles.
§ Squatting for long periods of time (such activities may be performed by a baseball catcher,
plumber, or carpet installer).
§ Running and jumping on the balls of the feet.
§ Wearing high heel shoes while standing or walking for long periods of time.
Ø Age-related changes. As we age, we all develop osteoarthritis and osteoporosis to one extent or
another. Both of these conditions can cause sesamoiditis:
o Osteoarthritis may cause small bone spurs to form on the sesamoids. These spurs may irritate
the flexor tendon that the sesamoids lie in. When this occurs, the results are inflammation,
swelling, and pain in the sesamoid and tendon.
o Osteoporosis occurs when bones lose calcium and become weaker and thinner. If the
sesamoids become weak, they may not be able to withstand the force applied to them with
each step we take. If this should occur, small stress fractures may form within the sesamoid

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 (small, shallow cracks in the bone). Stress fractures produce pain, swelling and inflammation
of the sesamoid.
Ø Hereditary Defects are those defects that we are born with, which predisposes us to sesamoiditis:
o Feet with high arches are usually more rigid than normal and will not allow the high arch to
come into contact with the ground when we step down. Therefore, as we step forward, all of
our weight is thrown on to the balls of the feet, rather than some of the weight being carried by
the arch. This will force the bones in the balls of the feet to bear excessive weight, especially
the big toe and first metatarsal head. The result of this repetitive and excessive weight on the
big toe and sesamoid bones under the first metatarsal head is compression, deterioration,
inflammation, and pain in the sesamoids.
o A plantarflexed first metatarsal is one of the most common predisposing hereditary factors
of sesamoidtis. This condition occurs when the first metatarsal head is tilted down in the
forefoot, rather than lying straight. Because the first metatarsal head and sesamoids are lower
than the other forefoot bones, each time we take a step forward, the sesamoids are forced to
bear more of the body's weight than is normal. Over time, this results in the sesamoids
becoming over-stressed, which may lead to inflammation, erosion of the sesamoids, and pain.
o Pronation occurs when the foot rolls outward at the ankle, forcing us to walk more on the
inner border of the foot than is normal. Therefore, as we walk, pronation causes us to place
excessive weight and pressure on the big toe, the first metatarsal head, and the sesamoids.
This extra weight and pressure will eventually over-stress the sesamoids causing them to
become compressed, inflamed, and painful.
o Enlarged sesamoids. When we are born with larger than normal sesamoids, they are forced
to bear abnormal amounts of the body's weight each time we take a step forward. Eventually,
due to this excessive weight and pressure forced on these bones, they begin to deteriorate
and become inflamed and painful.
Tips
• Stop the activity causing the pain.
• Take aspirin or ibuprofen to relieve the pain.
• Rest and ice the sole of your feet. Do not apply ice directly to the skin, but use an ice
pack or wrap the ice in a towel.
• Wear soft-soled, low-heeled shoes. Stiff-soled shoes like clogs may also be
comfortable.
• Use a felt cushioning pad to relieve stress.
• Return to activity gradually, and continue to wear a cushioning pad of dense foam
rubber under the sesamoids to support them. Avoid activities that put your weight on
the balls of the feet.
• Tape the great toe so that it remains bent slightly downward (plantar flexion).
• Your doctor may recommend an injection of a steroid medication to reduce swelling.
• If symptoms persist, you may need to wear a removable short leg fracture brace for 4
to 6 weeks.
Fracture of the Sesamoid
• You will need to wear a stiff-soled shoe or a short, leg-fracture brace.
• Your physician may tape the joint to limit movement of the great toe.
• You may have to wear a J-shaped pad around the area of the sesamoid to relieve
pressure as the fracture heals.
• Pain relievers such as aspirin or ibuprofen may be recommended.
• It may take several months for the discomfort to subside.
• Cushioning pads or other orthotic devices are often helpful as the fracture heals.

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Treatment and Prevention

Treatment for sesamoiditis is almost always noninvasive. Minor cases call for a strict period of rest,
along with the use of a modified shoe or a shoe pad to reduce pressure on the affected area. This may
be accomplished by placing a metatarsal pad away from the joint so that it redistributes the pressure
of weight bearing to other parts of the forefoot. In addition, the big toe may be bound with tape or
athletic strapping to immobilize the joint as much as possible and allow for healing to occur. It is
recommended to decrease or stop activity for awhile. This will give your sesamoids time to heal. You
should apply ice to the area for 10 to 15 minutes after exercise, or after any activity that aggravates
the area. As with icing, anti-inflammatories will help the swelling go down so healing can begin. While
the injury is healing, women should wear flat shoes on a daily basis. If home remedies do not work,
see your doctor for a correct diagnosis.

Self-Treatment or Prevention
The old adage, ""An ounce of prevention is worth a pound of cure,"" is most apropos when trying to
prevent the debilitating effects of sesamoiditis. If this disease is not prevented or treated in its earliest
stages, it may produce such debilitating pain that surgery will be required to allow the foot to function
normally again.
Long Term Treatment must be directed towards:
• Stabilizing the foot. When the foot is maintained in its normal, or neutral position, it cannot
pronate and roll out. When pronation is controlled, the big toe, the first metatarsal head, and
the sesamoids no longer bear excessive weight. This reduces forceful and destructive
compression of the sesamoids. Thus, the sesamoids remain healthy and pain free.
• Supporting high arches in order to relieve excess pressure on the balls of the feet,
especially the first metatarsal head and the sesamoids. When these structures no longer must
bear excessive amounts of weight as they help ""push"" us forward, the sesamoids are
protected from excessive weight and force. This will result in healthy sesamoids, free of
deterioration and pain.
• Elevating the plantarflexed first metatarsal head and sesamoids will prevent them from
bearing abnormal and excessive amounts of weight. When this is achieved, the sesamoids
under the first metatarsal head will no longer be subjected to excessive weight and
pressure. This will prevent the sesamoids from being over-stressed and eroding. The results
are healthy and pain free sesamoids.
• Providing shock absorption for the foot. The arches of our feet are the body's main shock
absorbers. As we take each step, the arch of the foot helps to absorb and disperse the
tremendous force that occurs when our foot strikes the ground. This force can equal 3 to 7
times our body weight, depending on whether we are walking or running. When the arch is
higher than normal, shock absorption by the arch is reduced. When this occurs, the big toe,
sesamoids, forefoot, and heel of the foot, must absorb this shock. The effect on the
sesamoids is to forcefully jam them into the under surface of the first metatarsal head, which
may cause them to eventually fracture.
Make sure that your shoes are:
• Wide enough across the ball of the foot and toe area, so that there is no pressure on the big
toe joint and sesamoids.
• The shoes must be the correct length for your foot.
• The heel of the shoe should be no higher than 1"".
• The innersole of the shoe should be well padded in order to cushion and protect the
sesamoids.
Immediate Treatment must be directed towards reducing the inflammation, swelling, and pain in the
sesamois. In the very early stages of sesamoiditis, the following self-help treatments may be effective:
• Rest the foot by keeping weight off of it. Each time you take a step, the sesamoids
are aggrevated and abused. They cannot calm down if you do not keep weight off of the foot.

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 • Shoes can help to protect the sesamoids if they have the following features:
o A well padded innersole. This will help to cushion the sesamoids with each step that is
taken.
o A wide and deep toebox prevents side-to-side squeezing of the sesamoids.
o A flat shoe reduces the pressure and weight that the sesamoids must bear when
walking. As the heel is raised, the sesamoids are forced to carry more of the body's
weight.
• Proper length shoes will also go a long way in reducing sesamoid pain.
• Reduce pressure on the sesamoids with a Dr. Jill's gel pad. This soft gel pad cushions the
ball of the foot and reuces pressure on the sesamoids. Self-stick, re-usable pad makes for
easy application. For more information about these pads click here.
• Soaking the foot in warm water may help to soothe the inflamed and painful sesamoids. The
soaking water must be comfortably warm and not hot, as hot water will usually cause
discomfort, skin burns, and increased pain and swelling. Soaking for 10 to 15 minutes two or
three times a day is usually suggested. If soaking increases pain, swelling, or inflammation,
stop immediately.
• Gentle massage with a topical pain reliever can help to provide comfort. By combining the
pain relieving properties of Tripod Labs Flexstat Topical Pain Reliever with gentle massage,
pain, swelling, and inflammation can be reduced or eliminated.
If the pain becomes worse, the foot more swollen or inflamed, or if you think that you have a
serious problem, see a doctor immediately.

3.7 HAMMER TOE

Figure 53: A mallet toe is evident on the 3rd digit.

A hammer toe or contracted toe is a deformity of the proximal interphalangeal joint of the second,
third, or fourth toe causing it to be permanently bent, resembling a hammer. Mallet toe is a similar
condition affecting the distal interphalangeal joint. A hammer toe is a deformity of the second, third or
fourth toes. In this condition, the toe is bent at the middle joint, so that it resembles a hammer.
Initially, hammer toes are flexible and can be corrected with simple measures but, if left untreated,
they can become fixed and require surgery.
People with hammer toe may have corns or calluses on the top of the middle joint of the toe or on the
tip of the toe. They may also feel pain in their toes or feet and have difficulty finding comfortable
shoes.
Claw toe is another similar condition, with dorsiflexion.

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Causes

Hammer toe results from shoes that don't fit properly or a muscle imbalance, usually in combination
with one or more other factors. Muscles work in pairs to straighten and bend the toes. If the toe is bent
and held in one position long enough, the muscles tighten and cannot stretch out.
Shoes that narrow toward the toe may make your forefoot look smaller. But they also push the smaller
toes into a flexed (bent) position. The toes rub against the shoe, leading to the formation of corns and
calluses, which further aggravate the condition. A higher heel forces the foot down and squishes the
toes against the shoe, increasing the pressure and the bend in the toe. Eventually, the toe muscles
become unable to straighten the toe, even when there is no confining shoe. Hammer toe usually
affects the second toe. However, it may also affect the other toes. The toe moves into a claw-like
position.
Hammer toe is more likely to occur in:
• Women who wear shoes that do not fit well or have high heels
• Children who keep wearing shoes they have outgrown
The condition may be present at birth (congenital) or develop over time.
In rare cases, all of the toes are affected. This may be caused by a problem with the nerves or spinal
cord.
Hammer toe most frequently results from wearing poorly fitting shoes that can force the toe into a bent
position, such as excessively high heels or shoes that are too short or narrow for the foot. Having the
toes bent for long periods of time can cause the muscles in them to shorten, resulting in the hammer
toe deformity. This is often found in conjunction with bunions or other foot problems. It can also be
caused by muscle, nerve, or joint damage resulting from conditions such as osteoarthritis, rheumatoid
arthritis, stroke, Charcot-Marie-Tooth disease or diabetes.

Symptoms

The middle joint of the toe is bent. The end part of the toe bends down into a claw-like deformity. At
first, you may be able to move and straighten the toe. Over time, you will no longer be able to move
the toe.
A corn often forms on the top of the toe. A callus is found on the sole of the foot.
Walking or wearing shoes can be painful.

Exams and Tests

A physical examination of the foot confirms that you have hammer toe. The health care provider may
find decreased and painful movement in the toes.

Treatment

Figure 54: Corrective surgery for hammer toe.

In many cases, conservative treatment consisting of physical therapy and new shoes with soft,
spacious toe boxes is enough to resolve the condition, while in more severe or longstanding cases
orthopedic surgery may be necessary to correct the deformity. The patient's doctor may also prescribe
some toe exercises that can be done at home to stretch and strengthen the muscles. For example, the

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individual can gently stretch the toes manually, or use the toes to pick things up off the floor. While
watching television or reading, one can put a towel flat under the feet and use the toes to crumple it.
Conservative treatment starts with new shoes that have soft, roomy toe boxes. Shoes should be one-
half inch longer than your longest toe. (Note: For many people, the second toe is longer than the big
toe.) Avoid wearing tight, narrow, high-heeled shoes. You may also be able to find a shoe with a deep
toe box that accommodates the hammer toe. Or, a shoe repair shop may be able to stretch the toe
box so that it bulges out around the toe. Sandals may help, as long as they do not pinch or rub other
areas of the foot.
Hammer toe can be corrected by surgery if conservative measures fail. Usually, surgery is done on an
outpatient basis with a local anesthetic. The actual procedure will depend on the type and extent of the
deformity. After the surgery, there may be some stiffness, swelling and redness and the toe may be
slightly longer or shorter than before.
Mild hammer toe in children can be treated by manipulating and splinting the affected toe.
The following changes in footwear may help relieve symptoms:
• Wear the right size shoes or shoes with wide toe boxes for comfort, and to avoid making
hammer toe worse.
• Avoid high heels as much as possible.
• Wear soft insoles to relieve pressure on the toe.
• Protect the joint that is sticking out with corn pads or felt pads
A foot doctor can make foot devices called hammer toe regulators or straighteners for you, or you can
buy them at the store.
Exercises may be helpful. You can try gentle stretching exercises if the toe is not already in a fixed
position. PIcking up a towel with your toes can help stretch and straighten the small muscles in the
foot.
For severe hammer toe, you will need an operation to straighten the joint.
• The surgery often involves cutting or moving tendons and ligaments.
• Sometimes the bones on each side of the joint need to be connected (fused) together.
Most of the time, you will go home on the same day as the surgery. The toe may still be stiff afterward,
and it may be shorter.

Outlook (Prognosis)

If the condition is treated early, you can often avoid surgery. Treatment will reduce pain and walking
difficulty.

Possible Complications

• Foot deformity
• Posture changes caused by difficulty in walking

Prevention

Avoid wearing shoes that are too short or narrow.

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3.8 CLAW TOE

People often blame the common foot deformity claw toe on wearing shoes that squeeze your toes,
such as shoes that are too short or high heels. However, claw toe also is often the result of nerve
damage caused by diseases like diabetes or alcoholism, which can weaken the muscles in your foot.
Having claw toe means your toes "claw," digging down into the soles of your shoes and creating
painful calluses. Claw toe gets worse without treatment and may become a permanent deformity over
time.

Symptoms

• Your toes are bent upward (extension) from the joints at the ball of the foot.
• Your toes are bent downward (flexion) at the middle joints toward the sole of your shoe.
• Sometimes your toes also bend downward at the top joints, curling under the foot.
• Corns may develop over the top of the toe or under the ball of the foot.

Evaluation

If you have symptoms of a claw toe, see your doctor for evaluation. You may need certain tests to rule
out neurological disorders that can weaken your foot muscles, creating imbalances that bend your
toes. Trauma and inflammation can also cause claw toe deformity.

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Treatment

Claw toe deformities are usually flexible at first, but they harden into place over time. If you have claw
toe in early stages, your doctor may recommend a splint or tape to hold your toes in correct position.
Additional advice:
• Wear shoes with soft, roomy toe boxes and avoid tight shoes and high-heels.
• Use your hands to stretch your toes and toe joints toward their normal positions.
• Exercise your toes by using them to pick up marbles or crumple a towel laid flat on the floor.
If you have claw toe in later stages and your toes are fixed in position:
• A special pad can redistribute your weight and relieve pressure on the ball of your foot.
• Try special "in depth" shoes that have an extra 3/8" depth in the toe box.
• Ask a shoe repair shop to stretch a small pocket in the toe box to accommodate the deformity.
If these treatments do not help, you may need surgery to correct the problem.

Definition

A claw toe is a toe that is contracted at the PIP and DIP joints (middle and end joints in the toe), and
can lead to severe pressure and pain. Ligaments and tendons that have tightened cause the toe's
joints to curl downwards. Claw toes may occur in any toe, except the big toe. There is often discomfort
at the top part of the toe that is rubbing against the shoe and at the end of the toe that is pressed
against the bottom of the shoe.
Claw toes are classified based on the mobility of the toe joints. There are two types - flexible and rigid.
In a flexible claw toe, the joint has the ability to move. This type of claw toe can be straightened
manually.
A rigid claw toe does not have that same ability to move. Movement is very limited and can be
extremely painful. This sometimes causes foot movement to become restricted leading to extra stress
at the ball-of-the-foot, and possibly causing pain and the development of corns and calluses.

Cause

Claw toes result from a muscle imbalance which causes the ligaments and tendons to become
unnaturally tight. This results in the joints curling downwards. Arthritis can also lead to many different
forefoot deformities, including claw toes.

Treatment and Prevention

Changing the type of footwear worn is a very important step in the treatment of claw toes. When
choosing a shoe, make sure the toe box (toe area) is high and broad, and can accommodate the claw
toes. A shoe with a high, broad toe box will provide enough room in the forefoot area so that there is
less friction against the toes.
Other conservative treatments include using forefoot products designed to relieve claw toes, such as
toe crests and hammer toe splints. These devices will help hold down the claw toe and provide relief to
the forefoot. Gel toe shields and gel toe caps are also recommended to eliminate friction between the
shoe and the toe, while providing comfort and lubrication.

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Ø claw toe consists of hyperextension at the metatarsophalangeal joint, and flexion at the proximal
(and distal interphalangeal joints);
o all of the toes are usually affected, although contracture of the great toe can be the most
severe;
o there is an imbalance between the extrinsic extensor tendons (which indirectly extend the
MP joint and the intrinsics which flex the MP joint);
Ø claw toes result from simultaneous contraction of extensors & flexors with weak or insufficient
intrinsic muscles;
Ø hyperextension deformity of the MP joint is caused by excessive relative pull of the extensor
tendons;
o PIP hyperflexion is caused by excessive pull of the long flexors;
o hyperextension of the MT joints and flexion of the IP joints, are common features of a
neuropathic clawfoot or pes cavus;
o dorsiflexion of the MP joint causes the metatarsal fat pad to be pulled distally through its
attachments to the proximal phalanx;
o flexed IP joints are constantly irritated by shoe, & painful metatarsal callosities develop;
o deformity will become permanent.

Differential Diagnosis

Hammer Toes
Ø characteristics include: MPT joints extended, flexed at the PIP joint, and hyperextended at the
distal interphalangeal joint;
Ø in contrast to hammer toes which may or may not have MPT joint hyper-extension, a claw toe is
always associated w/ MTP hyperextension;

Inciting Conditions

Ø rheumatoid arthritis
Ø advanced age (decreased muscle tone and reliance of toe gripping for balance)
Ø diabetes
Ø compartment syndrome involving deep posterior compartment
Ø polio: claw toes
Ø Charcot Marie Tooth
Ø stroke
Ø cavus foot
o when the claw toe deformities are associated with a cavus deformity, tarsal deformity should
be corrected first, since clawing of toes may correct spontaneously;

Exam

Ø note presence of pes cavus deformity;

Ø determine degree of MTP hyperextension and PIP flexion;
Ø note presence of metatarsalgia w/ associated skin changes (plantar keratosis);

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Ø determine whether claw toes are flexible or fixed;
o assess flexibility of toes w/ ankle in plantar flexion and dorsiflexion;
§ if the claw toe deformity disappears w/ plantar flexion then the deformity is considered
flexible;
o apply pressure underneath the metatarsal heads and note degree of correction;
Ø assessment during gait:
o note whether the clawing becomes worse during gait (stance phase vs swing phase);
o clawing during swing phase: may indicate weak ankle dorsiflexors and over-compensation of
toe extensors;
o clawing during stance phase: may indicate weak triceps surae and over-compensation of long
toe flexors;

Radiographs

Ø subluxation is indicated on AP radiographs by narrowing of the apparent joint space (which occurs
from the overlap of the proximal phalanx over the metatarsal;

Non Operative Treatment

Ø includes corn padding, soft metatarsal pads (when metatarsalgia is present), & shoe w/ high, wide
toe box, often succeeds;

Flexible Claw Toes

Ø implies that there is no contraction of MTP or PIP joints;

Ø Girdlestone-Taylor Procedure:
o indicated for flexible claw toes w/ dorsally subluxated MP joints;
Ø transfers long flexor to extensor hood over proximal phalanx) is performed along with extensor
tenotomies and dorsal capsulodesis of MTP;
Ø clawed hallux:
o authors carried out a cross-sectional study in 51 patients (81 feet) with a clawed hallux in
association with a cavus foot after a modified Robert Jones tendon transfer;
o in all feet, concomitant procedures had been undertaken, such as extension osteotomy of the
first metatarsal and transfer of the tendon of the peroneus longus to peroneus brevis, to
correct the underlying foot deformity;
o overall rate of patient satisfaction was 86%, and the deformity of the hallux was corrected in 80
feet;
o catching of the big toe when walking barefoot, transfer lesions and metatarsalgia, hallux flexus,
hallux limitus and asymptomatic nonunion of the interphalangeal joint were the most frequent
complications;
o hallux limitus was more likely when elevation of the first ray occurred (p = 0.012);
o additional transfer of the tendon of peroneus longus to peroneus brevis was a significant risk
factor for elevation of the first metatarsal.
o deforming force of extensor hallucis longus is effectively eliminated by the Jones transfer, but
the mechanics of the first metatarsophalangeal joint are altered.

Fixed Claw Toe Deformity

Ø inform pt that toe ischemia sometimes follows correction of severe deformity;

Ø w/ neurologic disorder such as Charcot Marie Tooth disease, consider transfer of the long
extensors to the neck of metatarsals along with fusion of the PIP joints;

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MTP Joint Subluxation

Ø often associated with metatarsalgia;

Ø once MP joint is dislocated, result is never entirely satisfactory, & joint is always slightly stiff;
o contracted extensor tendons (which are the main deforming force) may have to be
tenotomized to allow correction of dorsal subluxation of MP joints;
§ first extend EDL, then EDB;
§ if MP joint is still extended, then release collateral ligaments;
§ note that reduction of MP joint, may cause ischemia of the digit, due to stretching of the
N/V bundle across contracted soft tissues;
• hence, toe cannot be relocated w/o bone resection;
shortening at base of proximal phalanx;
o resection of base of proximal phalanx may lead to instability, which is may require
syndactylization to an adjacent toe;
shortening at metatarsal head;
o resect bone from or distal metatarsal head shaving or partial resection of distal portion of
metatarsal head alone;
o joint ishould immobilized for three to four weeks postoperatively;

PIP Deformity

Ø deformity at PIP joint is best treated w/ resection arthroplasty, removing distal one third of proximal
phalanx;
Ø arthrodesis is indicated only in the presence of severe or recurrent deformity, or when associated
w/ neurologic disturbance of forefoot;
o when performing arthrodesis of the interphalangeal joint, toe should be slightly plantarflexed,
because this position is better tolerated than a stiff straight toe;

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3.9 MORTON'S NEUROMA

Figure 55: The plantar nerves.

Morton's neuroma (also known as Morton's metatarsalgia, Morton's neuralgia, plantar neuroma and
intermetatarsal neuroma) is a benign neuroma of an intermetatarsal plantar nerve, most commonly of
the third and fourth intermetatarsal spaces.
This problem is characterised by pain and/or numbness, sometimes relieved by removing footwear.
[1]
Despite the name, the condition was first correctly described by a chiropodist named Durlacher, and
although it is labeled a "neuroma", many sources do not consider it a true tumor, but rather a
perineural fibroma (fibrous tissue formation around nerve tissue).

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Morton's Neuroma in Popular Culture

Figure 56: Morton's Neuroma.

Morton's neuroma is a painful condition that affects the ball of your foot, most commonly the area
between your third and fourth toes. Morton's neuroma may feel as if you are standing on a pebble in
your shoe or on a fold in your sock.
Morton's neuroma involves a thickening of the tissue around one of the nerves leading to your toes. In
some cases, Morton's neuroma causes a sharp, burning pain in the ball of your foot. Your toes also
may sting, burn or feel numb.
Morton's neuroma may occur in response to irritation, injury or pressure. Common treatments for M
If you sometimes feel that you are "walking on a marble," and you have persistent pain in the ball of
your foot, you may have a condition called Morton's neuroma. A neuroma is a benign tumor of a
nerve. Morton's neuroma is not actually a tumor, but a thickening of the tissue that surrounds the
digital nerve leading to the toes.

Morton's neuroma occurs as the nerve passes under the ligament connecting the toe bones
(metatarsals) in the forefoot.
Morton's neuroma most frequently develops between the third and fourth toes, usually in response to
irritation, trauma or excessive pressure.
The incidence of Morton's neuroma is 8 to 10 times greater in women than in men.

Symptoms and Signs

• Normally, there are no outward signs, such as a lump, because this is not really a tumor.
• Burning pain in the ball of the foot that may radiate into the toes. The pain generally intensifies
with activity or wearing shoes. Night pain is rare.
• There may also be numbness in the toes, or an unpleasant feeling in the toes.
Runners may feel pain as they push off from the starting block. High-heeled shoes, which put the foot
in a similar position to the push-off, can also aggravate the condition. Tight, narrow shoes also
aggravate this condition by compressing the toe bones and pinching the nerve. Other Symptoms
include: pain on weight bearing, frequently after only a short time. The nature of the pain varies widely
among individuals. Some people experience shooting pain affecting the contiguous halves of two toes.

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Others describe a feeling like having a pebble in your shoe. Burning, numbness, and paresthesia may
also be experienced.
Morton's neuroma lesions have been found using MRI in patients without symptoms.

Diagnosis/ Differential Diagnosis

Negative signs include no obvious deformities, erythema, signs of inflammation, or limitation of

movement. Direct pressure between the metatarsal heads will replicate the symptoms, as will
compression of the forefoot between the finger and thumb so as to compress the transverse arch of
the foot. This is referred to as Mulder’s Sign.
There are other causes of pain in the forefoot. Too often all forefoot pain is categorized as neuroma.
Other conditions to consider are capsulitis, which is an inflammation of ligaments that surrounds two
bones, at the level of the joint. In this case, it would be the ligaments that attach the phalanx (bone of
the toe) to the metatarsal bone. Inflammation from this condition will put pressure on an otherwise
healthy nerve and give neuroma-type symptoms. Additionally, an intermetatarsal bursitis between the
third and fourth metatarsal bones will also give neuroma-type symptoms because it too puts pressure
on the nerve. Freiberg's disease, which is an osteochondritis of the metatarsal head, causes pain on
weight bearing or compression.

Histopathology

Microscopically, the affected nerve is markedly distorted, with extensive concentric perineural fibrosis.
The arterioles are thickened and occlusion by thrombi are occasionally present.

Imaging

Though a neuroma is a hard tissue abnormality and won’t be visualized on standard radiographs, the
first step in the assessment of forefoot pain is an X-ray in order to evaluate for the presence of arthritis
and exclude stress fractures/reactions and focal bone lesions, which may mimic the symptoms of a
neuroma. Ultrasound (sonography) accurately demonstrates thickening of the interdigital nerve within
the web space of greater than 3 mm, diagnostic of a Morton’s neuroma. This typically occurs at the
level of the intermetatarsal ligament. Frequently, intermetatarsal bursitis coexists with the diagnosis.
Other conditions that may also be visualized with ultrasound and can be clinically confused with a
neuroma include synovitis/capsulitis from the adjacent metatarsophalangeal joint, stress
fractures/reaction, and plantar plate disruption. MRI can similarly demonstrate the above conditions;
however, in the setting where more than one abnormality coexists, ultrasound has the added
advantage of determining which may be the source of the patient’s pain by applying direct pressure
with the probe. Further to this, ultrasound can be used to guide treatment such as cortisone injections
into the webspace, as well as alcohol ablation of the nerve.

Treatment

Initial therapies are nonsurgical and relatively simple. They can involve one or more of the following
treatments:
• Changes in footwear. Avoid high heels or tight shoes, and wear wider shoes with lower heels
and a soft sole. This enables the bones to spread out and may reduce pressure on the nerve,
giving it time to heal.
• Orthoses. Custom shoe inserts and pads also help relieve irritation by lifting and separating
the bones, reducing the pressure on the nerve.
• Injection. One or more injections of a corticosteroid medication can reduce the swelling and
inflammation of the nerve, bringing some relief.
Several studies have shown that a combination of roomier, more comfortable shoes, nonsteroidal anti-
inflammatory medication, custom foot orthoses and cortisone injections provide relief in over 80
percent of people with Morton's Neuroma. If conservative treatment does not relieve your symptoms,
your orthopaedic surgeon may discuss surgical treatment options with you. Surgery can resect a small
portion of the nerve or release the tissue around the nerve, and generally involves a short recovery
period.

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Orthotics and corticosteroid injections are widely used conservative treatments for Morton’s neuroma.
In addition to traditional orthotic arch supports, a small foam or fabric pad may be positioned under the
space between the two affected metatarsals, immediately behind the bone ends. This pad helps to
splay the metatarsal bones and create more space for the nerve so as to relieve pressure and
irritation. It may however also elicit mild uncomfortable sensations of its own, such as the feeling of
having an awkward object under one's foot. Corticosteroid injections can relieve inflammation in some
patients and help to end the symptoms. For some patients, however, the inflammation and pain recur
after some weeks or months, and corticosteroids can only be used a limited number of times because
they cause progressive degeneraton of ligamentous and tendinous tissues.
Sclerosing alcohol injections are an increasingly available treatment alternative if the above
management approaches fail. Dilute alcohol (4%) is injected directly into the area of the neuroma,
causing toxicity to the fibrous nerve tissue. Frequently, treatment must be performed 2-7 times, with 1-
3 weeks between interventions.
An 82-90% success rate has been achieved in clinical studies, equal to or exceeding the success rate
for surgical neurectomy with fewer risks and less significant recovery.
If such interventions fail, patients are commonly offered surgery known as neurectomy, which involves
removing the affected piece of nerve tissue. Postoperative scar tissue formation (known as stump
neuroma) can occur in approximately 20% of cases, causing a return of neuroma symptoms
Neurectomy can be performed using one of two general methods. Making the incision from the dorsal
side (the top of the foot) is the original, traditional method but requires cutting the deep transverse
rd th
metatarsal ligament that connects the 3 and 4 metatarsals in order to access the nerve beneath it.
rd th
This results in exaggerated postoperative splaying of the 3 and 4 digits (toes) due to the loss of the
supporting ligamentous structure. This has aesthetic concerns for some patients and possible though
unquantified long-term implications for foot structure and health. Alternatively, making the incision from
the ventral side (the sole of the foot) allows more direct access to the affected nerve without cutting
other structures. However, this approach requires a greater post-operative recovery time where the
patient must avoid weight bearing on the affected foot because the ventral aspect of the foot is more
highly enervated and impacted by pressure when standing.
Cryogenic neuroablation is a lesser known alternative to neurectomy surgery. Cryogenic neuroablation
(also known as cryo injection therapy or cryosurgery) is a term that is used to describe the destruction
of axons to prevent them from carrying painful impulses. This is accomplished by making a small
incision (~3mm) and inserting a cryoneedle that applies extremely low temperatures of between •50C
to •70C to the nerve/neuroma. This results in degeneration of the intracellular elements, axons, and
myelin sheath (which houses the neuroma) with wallerian degeneration. The epineurium and
perineurium remain intact, thus preventing the formation of stump neuroma.
The preservation of these structures differentiates cryogenic neuroablation from surgical excision and
neurolytic agents such as alcohol. An initial study showed that cryo neuroablation is initially equal in
effectivenesss to surgery but does not have the risk of stump neuroma formation. However, the results
from this procedure are not considered permanent.

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3.10 TALALGIA (HEEL SPURS)

Talalgia with plantar heel or in clinical term, is defined tallodinia inflammatory disease, painful heel,
namely the region of the foot that corresponds to the back and bottom of the heel, also called the heel.
The causes of the disease vary depending on the affected areas, namely: soft areas (tendon
inflammation, fasciitis, bursitis, etc..) areas bone (stress fractures, heel spurs, arthritis talus-calcaneus,
tumors, etc.).
It is not uncommon that even the pain occurs due to postural alterations that somehow alter the
structure and breech loading on this area. This can happen for various reasons such as overweight or
obesity, unsuitable footwear, sporting activities.
The sports most at risk are running, soccer, volleyball, basketball, walking and all those disciplines that
involve substantial efforts to heel region. Do not underestimate these shoes used for sports activities
that need to be equipped with a special heel, called a shock absorber, capable of reducing vibration
and impact stresses. Women who move from high-heeled shoes to flat shoes may suffer because the
pressure on the heel bone and ligamentous structures of the heel increases with the decrease in
height of the heel.

Several Types of Bead

The hooker may be located at the longitudinal arch, with or without concomitant pain in the heel, and
in this case is called plantar fasciitis. Typically, the pain originates in the middle of the arch and by
palpation of the nodules can also detect, in turn painful. The pain appears in the morning when you
start to walk before moving on, although it may take suddenly during the course of the day.
One of the most frequent causes of plantar talalgia, however, is the heel spur, also called heel spur, a
bony protrusion of the heel that may be of congenital origin or occur later. The heel spur is generated
because, for various reasons that will be seen later, pronation, ie the support of the foot during gait is
altered and this causes inflammation through a continuous traction of the plantar fascia at the insertion
point on the heel.
There are various causes of this disease and between the main physical activity which increases the
stress and repeated microtrauma possible - perhaps turning wrong shoe shod (narrow or hard edges)
or moving on land not suitable - which increases the pressure and irritation causes bruising of the heel
and plantar surface of the foot. Not to mention, the overweight or erroneous and distorted postures.
But, of course, the disease can also be caused by systemic and metabolic diseases including it should
be noted:
• rheumatoid arthritis
• Gout
• the collagen
• rheumatic diseases, etc..
The calcaneus, where there is a secondary center of ossification of the tendon which inserts the heel
(Achilles tendon), can be also exposed to osteochondrosis, a disease that is characterized by an
alteration of the degenerative-necrotic ossification in the growth. It is striking, in fact, young people
between 8 and 13 years, with localized pain in the back of the heel, especially after a long walk.
Evolution is always benign and does not cause local deformity even if the duration of the condition can
be quite long. In these cases, just an arch support that limits the rear shock, giving at times when the
pain becomes more acute anti-inflammatory drugs.
In the elderly, the cause of the heel can find, however, the progressive atrophy of the fat pad
infracalcaneare, due to the aging of tissues.

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Haglund's Deformity and Bursitis Diagnosis

The heel spurs, also called Haglund's deformity, or "pump bump" consists of an exostosis, which is a
congenital bone growths, which most often appears at the posteromedial side of the bone.
This form of bone change very frequently due to bursitis, or inflammation of the bursa anterior to the
Achilles tendon and back of the heel, since it causes abnormal pressure on the point where it is and
resulting in pain.
The back of the Achilles tendon bursitis can be diagnosed either by X-ray investigations,
which directly experiencing the painful part that usually has a diffuse swelling and the
formation of a thick callus on the back surface of the calcaneus.

Possible Therapies
Of course the treatment depends largely on the nature and extent of any damage talalgia the heel
bone. Keep in mind that a mild disease heals within a few days. If the pain persists beyond two weeks
is necessary to use a specialist.
The main piece of advice, especially if the patient is involved in physical activity continues, is to
suspend it immediately, waiting to resume its normal function. The heel pain, in fact, should not be
underestimated under any circumstances, but above all we must avoid the risk of possible
deterioration that can occur if you do not suspend the motor activity, because of what are called
compensatory paramorphisms. People who suffer from heel tend to limit the load on the foot sore, but
by adopting a particular posture or incorrect change in an unnatural way of walking. Which, in the long
run, can cause problems, even serious, pelvis, spine and knees.
The first intervention during the acute phase of illness is, as always, the application of a bag of ice on
the painful area. In cases of plantar fasciitis can be effectively undergo stretching exercises that, in
addition to the plantar fascia, involving the calf and the Achilles tendon. Later, you can resort to the
use of orthotics, so-called "discharge", guardians night, knee-highs.

3.11 NEUROPATHIC JOINT DISEASE

Figure 57: A 68 year-old diabetic female on dialysis presented with a chronic right heel ulcer (3.4 cm X 3.1 cm) of
greater thatn 3 months duration. Photograph of the wound after through wound bed preparation over the course of
2 weeks.

Neuropathic Arthropathy (or Neuropathic Osteoarthropathy), also known as Charcot Joint (often
"Charcot Foot"), refers to progressive degeneration of a weight bearing joint, a process marked by
bony destruction, bone resorption, and eventual deformity. Onset is usually insidious.
If this pathological process continues unchecked, it could result in joint deformity, ulceration and/or
superinfection, loss of function, and in the worst case scenario: amputation or death. Early
identification of joint changes is the best way to limit morbidity.

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Pathogenesis

Any condition resulting in decreased peripheral sensation, proprioception, and fine motor control:
• Diabetes mellitus neuropathy (the most common in the U.S. today, resulting in destruction of
foot and ankle joints), with Charcot joints in 1/600-700 diabetics. Related to long-term poor
glucose control.
• Alcoholic neuropathy
• Cerebral palsy
• Leprosy
• Syphilis (tabes dorsalis), caused by the organism Treponema pallidum
• Spinal cord injury
• Myelomeningocele
• Syringomyelia
• Intra-articular steroid injections
• Congenital insensitivity to pain

Underlying Mechanisms

Two primary theories have been advanced:

1. Neurotrauma: Loss of peripheral sensation and proprioception leads to repetitive microtrauma
to the joint in question; this damage goes unnoticed by the neuropathic patient, and the
resultant inflammatory resorption of traumatized bone renders that region weak and
susceptible to further trauma. Indeed, it is a vicious cycle. In addition, poor fine motor control
generates unnatural pressure on certain joints, leading to additional microtrauma.
2. Neurovascular: Neuropathic patients have dysregulated autonomic nervous system reflexes,
and de-sensitized joints receive significantly greater blood flow. The resulting hyperemia leads
to increased osteoclastic resorption of bone, and this, in concert with mechanical stress, leads
to bony destruction.
In reality, both of these mechanisms probably play a role in the development of a Charcot joint.

Joint Involvement
Diabetes is the foremost cause in America today for neuropathic joint disease, and the foot is the most
affected region. In those with foot deformity, approximately 60% are in the tarsometatarsal joints
(medial joints affected more than lateral), 30% Metatarsophalangeal joints and 10% have ankle
disease. Over half of diabetic patients with neuropathic joints can recall some kind of precipitating
trauma, usually, minor.
Patients with neurosyphilis tend to have knee involvement, and patients with syringomyelia of the
spinal cord may demonstrate shoulder deformity.
Hip joint destruction is also seen in neuropathic patients.

Clinical Finidings

Clinical findings include erythema, edema and increased temperature in the affected joint. In
neuropathic foot joints, plantar ulcers may be present. Note that it is often difficult to differentiate
osteomyelitis from a Charcot joint, as they may have similar tagged WBC scan and MRI features (joint
destruction, dislocation, edema). Definitive diagnosis may require bone or synovial biopsy.

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Radiologic Findings

First, it is important to recognize that two types of abnormality may be detected. One is termed
atrophic, in which there is osteolysis of the distal metatarsals in the forefoot. The more common form
of destruction is hypertrophic joint disease, characterized by acute peri-articular fracture and joint
dislocation. According to Yochum and Rowe, the "6 D's" of hypertrophy are:
1. Distended joint
2. Density increase
3. Debris production
4. Dislocation
5. Disorganization
6. Destruction
The natural history of the joint destruction process has a classification scheme of its own, offered by
Eichenholtz decades ago:
Stage 0: Clinically, there is joint edema, but radiographs are negative. Note that a bone scan may be
positive before a radiograph is, making it a sensitive but not very specific modality.
Stage 1: Osseous fragmentation with joint dislocation seen on radiograph ("acute Charcot").
Stage 2: Decreased local edema, with coalescence of fragments and absorption of fine bone debris
Stage 3: No local edema, with consolidation and remodeling (albeit deformed) of fracture fragments.
The foot is now stable.
Destroyed Tarsometatarsal joints in the medial left foot, with fracture and dislocation of fragments;
these are classic findings. Also note loss of the foot arch and acquired flat foot (pes planus) deformity.
Atrophic Features:
1. "Licked candy stick" appearance, commonly seen at the distal aspect of the metatarsals
2. Diabetic osteolysis
3. Bone resorption

Treatment

Once the process is recognized, immobilization with a total contact cast will help ward off further joint
destruction. Pneumatic walking braces are also used. Surgical correction of a joint is rarely successful
in the long-term in these patients.
It can take 6–9 months for the edema and erythema of the affected joint to resolve.

Hansen Disease (Mycobactrium Leprae)

Hansen disease (leprosy) is a chronic disease resulting from infection with Mycobacterium leprae and
the ensuing host response. The organs most prominently affected are the respiratory mucosa, skin,
and the peripheral nervous system, but testicular and ocular involvement are described. Humans were
long believed to be the sole host of M. leprae, but naturally acquired infection has been documented in
armadillos in the southeastern United States, and experimental infection has been established in
primates, nude mice, and armadillos.
Chronic skin lesions, madarosis, sensory neuropathy resulting in the loss of digits or limbs, and
paresis secondary to motor nerve dysfunction are among the sequelae
of leprosy. The highly visible nature of these debilities led to the historical stigmatization of the “leper.”
The psychologic and sociologic sequelae of this stigma can be as debilitating as the disease itself and
may result in delays in seeking medical attention. To combat this prejudice, the term leprosy patient
has replaced the word leper, and Hansen disease, after Armauer Hansen who identified M. leprae as
the cause of leprosy in 1873, has become an accepted designation.

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Etiology
M. leprae, an obligate intracellular pathogen with a generation time of 14 days, is an acid-fast bacillus
of the family Mycobacteriaceae. M. leprae grows optimally at 27–30°C and cannot be cultured in vitro.
The incubation period of leprosy in humans ranges from 3 mo–20 yr (average 3–5 yr). The rare
occurrence of leprosy in infants as young as 3 mo of age suggests that in utero transmission may
occur or that very short incubation periods may be possible in certain situations.

Epidemiology

After the introduction of multidrug therapy (MDT) by the World Health Organization (WHO) in 1982,
there has been a steady decline in the prevalence of leprosy. On a global scale, the estimated
prevalence rate has been reduced 85% from >20 cases/10,000 persons in 1985 to 1.25 cases/10,000
persons in 2000. Approximately 11 million leprosy patients have been cured over the past 15 yr.
However, the new case detection rate has remained nearly steady since 1985 with 750,000 new cases
detected and registered for treatment in 2000. The World Health Organization estimates that an
additional 2.5 million cases will be detected between the years 2000–2005. The goal by 2005 is to
decrease the global prevalence rate to =1 case/10,000 persons. Currently, >90% of the world's
leprosy patients reside in 10 major endemic countries in Africa, Southeast Asia, and Central and South
America, with 70% residing in India. Approximately 100 cases are reported annually in the United
States, of which 85% are in immigrants. Small numbers of endemic cases are reported from Texas,
Hawaii, and Louisiana.
Human-to-human transmission accounts for an overwhelming majority of cases; a high percentage of
them occur in family members or in close contacts of known patients. Leprosy occurs at all ages, but
infections in infants are extremely rare; incidence rates peak during childhood and early adulthood in
endemic areas. HIV infection has not been documented to alter the risk of leprosy in areas of high
prevalence for both pathogens.

Pathogenesis

The entry of M. leprae into the human host is poorly understood. Possible modes of transmission
include contact with desquamated infected epidermis, ingestion of infected breast milk, and bites of
mosquitos or other vectors. At present, however, the basis for most infections appears to be
transmission from untreated lepromatous patients by means of prolonged contact with infected nasal
secretions containing a high bacterial load. Little is known of the host immune responses in the initial
period after infection, but skin testing and serologic studies suggest that up to 80–90% of those
infected develop immunity without ever manifesting clinical disease. Studies in endemic areas using
polymerase chain reaction (PCR) show widespread presence of the organism in nasal secretions from
asymptomatic individuals.
From the nasal mucosa, M. leprae appears to be transported hematogenously to skin and peripheral
nerves. Using the armadillo model of neuritis, M. leprae has been shown to colonize the perineural
space and gain access to the interstitium of the endoneural space.
Once there, it is available for phagocytosis by Schwann cells surrounding peripheral nerve axons and
interstitial macrophages. Intracellular replication of M. leprae follows with varying degrees depending
on the host cellular immune response. M. leprae attachment to and ingestion by Schwann cells has
been shown to depend on receptors on the lamin-2 glycoprotein in the basal lamina and the a-
dystroglycan complex in the Schwann cell basement membrane. M. leprae specific phenolic glycolipid-
1 appears to be the ligand mediating this binding. With the recent mapping of the genome of M.
leprae, more details of this important binding will become available.
Once M. leprae has colonized the surface of nerves and has infected endoneural macrophages and
Schwann cells, several mechanisms of skin and nerve injury occur depending on the host immune
response. One end of the spectrum is tuberculoid leprosy, in which there is a vigorous and specific
cell-mediated immune response to M. leprae antigens. In tissue biopsies there are tightly organized
granulomas composed of epithelioid cells and lymphocytes but bacilli are scant or absent.
Macrophages, when present, do not contain intracellular organisms. Caseation is rare. Heavy cellular
infiltration is found in the dermis with destruction of cutaneous nerve fibers.
At the other end of the spectrum is lepromatous leprosy, in which there is total and specific anergy to
M. leprae both by skin testing and by in vitro assays of cell-mediated immunity. Large amounts of

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circulating and tissue-based antibody to mycobacterial antigens are present, but they afford no
protective immunity. Bacilli are found in enormous numbers in the skin, nasal mucosa, and peripheral
nerves. There is continual bacillemia as well as bacillary invasion of all major organs except the
central nervous system. Tissue granulomas are poorly formed and are composed chiefly of loose
aggregates of foamy histiocytes.
Macrophages teeming with undigested bacilli are common. There is extensive, symmetric involvement
of peripheral nerves, although the cutaneous nerve endings are usually spared.
An M. leprae–specific suppressor T-cell population is found in the circulation of patients with
lepromatous leprosy, and increased numbers of suppressor T cells are found in their skin granulomas.
T cells from lepromatous patients also produce less interleukin 2 and less interferon-? after stimulation
with M. leprae antigens than do T cells from tuberculoid patients or normal controls.
Borderline or dimorphous leprosy is subdivided into three subclasses that lie between the
tuberculoid and lepromatous poles.

Clinical Manifestations

INDETERMINATE LEPROSY (IL)

Indeterminate leprosy is the earliest clinically detectable form of leprosy. Although it is observed in
only 10–20% of infected individuals, it is a stage through which most patients with advanced leprosy
have passed. Usually there is a single hypopigmented macule, 2–4?cm in diameter, with a poorly
defined border but having no erythema or induration. Anesthesia is minimal or absent, particularly if
the lesion is on the face. Tissue samples may contain granulomas, but bacilli are rarely demonstrable.
The histopathology is not distinctive; the diagnosis is usually made by exclusion of other skin disorders
in contacts (especially children) of leprosy patients. In 50–75% of patients with indeterminate leprosy,
the lesions heal spontaneously; in the remainder, they progress to one of the classic forms.
TUBERCULOID LEPROSY (TL)
There is usually a single, large (often >10?cm in diameter) lesion with a well-demarcated, elevated
erythematous rim.
The interior of the lesion is flat, atrophic, hypopigmented, occasionally scaly, and anesthetic. Rarely,
there may be as many as four lesions. The closest superficial nerve is often impressively thickened.
The ulnar, posterior tibial, and great auricular nerves are most commonly affected. Periodic
examination of all leprosy patients and their contacts should include palpation of these nerves. Without
therapy, the skin lesion tends to enlarge slowly, but documented instances of spontaneous resolution
exist. The coloration of the rim slowly fades with therapy and the induration resolves, resulting in a flat
lesion with central hypopigmentation and a ring of postinflammatory hyperpigmentation. Loss of hair
follicles, sweat glands, cutaneous nerve receptors, and sensation in the central portion of the lesion is
irreversible. Marked improvement should be apparent within 1–2 mo after initiating therapy, but
complete resolution may take up to 8–12 mo. There is an entity of “pure neural” tuberculoid leprosy,
which presents as either pure sensory or combined sensory and motor nerve dysfunction with
prominent nerve thickening but no cutaneous lesions. Histopathology is mandatory to establish this
diagnosis.
Nerve trunk size varies widely, and over diagnosis of “enlarged” nerves is common among
inexperienced observers. Nodular or fusiform nerve thickening has greater diagnostic value than a
palpable nerve that is smooth and symmetric.
BORDERLINE LEPROSY
The clinical and histologic criteria for the three subdivisions of borderline leprosy are less well defined
than are those of the two polar categories. In contrast to the tuberculoid and lepromatous patterns,
those in the borderline divisions are unstable. For example, host or bacterial factors can result in
immunologic downgrading of the clinical condition toward the lepromatous pattern or upgrading it
toward the tuberculoid pattern.
Therapy is the most common cause of upgrading reactions; downgrading can be seen in conditions
that compromise host immunity, for example, pregnancy. Clinical characteristics of the three generally
accepted borderline subclasses are as follows.

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In the borderline tuberculoid (BT) pattern, the lesions are greater in number but smaller in size than
in tuberculoid leprosy. There may be small satellite lesions around older lesions, and the margins of
the borderline tuberculoid lesions are less distinct. There is usually thickening of two or more
superficial nerves.
In the borderline (BB) pattern, the lesions are more numerous and more heterogeneous in
appearance. They may become confluent, and plaques may be present.
The borders are poorly defined, and the erythematous rim fades into the surrounding skin. There may
be anesthesia, but hypesthesia is more common. Mild to moderate nerve thickening is common, but
severe muscle wasting and neuropathy are unusual.
In the borderline lepromatous (BL) pattern, a large number of asymmetrically distributed lesions are
heterogeneous in appearance. Macules, papules, plaques, and nodules may all coexist. Individual
lesions are small unless confluent. Anesthesia is mild and superficial nerve trunks are spared. The
initial response to therapy is often dramatic; nodules and plaques flatten within 2–3 mo. With
continued therapy, the lesions become macular and almost invisible.
LEPROMATOUS LEPROSY (LL)
The lesions are innumerable, often confluent, and symmetric. Initially there may be only vague
macules or even uniform, diffuse skin infiltrations without discernible lesions. As the disease
progresses, the lesions become increasingly papular and nodular, so that with the diffuse thickening
and infiltration of the skin, the characteristic leonine facies accompanied by loss of the eyebrows and
distortion of the earlobes becomes apparent. Anesthesia of the lesions is less severe than in
tuberculoid leprosy, but a symmetric peripheral sensory neuropathy usually develops late in the course
of the disease. Testicular infiltration leading to azoospermia, infertility, and gynecomastia is common in
adults but not in children. Bacilli are demonstrable in most internal organs other than the central
nervous system, but tissue damage or interference with function is infrequent. Glomerulonephritis,
when it occurs, is believed to be secondary to immune complex deposition rather than to infection per
se. The initial response to therapy may be encouraging but is often followed by a long (2–5 yr) period
of very slow improvement. In true lepromatous leprosy, the specific anergy to the leprosy bacillus
persists despite therapy, thus making the patient theoretically susceptible to relapse if even a single
viable bacillus remains at the end of therapy.
REACTIONAL STATES
Acute clinical exacerbations are common in leprosy and are believed to reflect abrupt changes in the
host-parasite immunologic balance. Although these reactional states do occur in the absence of
therapy, they are especially common during the initial years of treatment. Approximately 30% of
patients receiving effective chemotherapy can develop reactions, and, unless adequately treated, they
will result in crippling deformities. Two major variants are recognized.
Type 1 (reversal) reactions are observed predominantly in borderline leprosy and result from a
sudden increase in effective cell-mediated immunity in response to M. leprae antigens in dermis and
Schwann cells. Acute tenderness and swelling at the site of existing cutaneous and neural lesions and
the development of new lesions are the major manifestations. Existing or new skin lesions often
ulcerate to leave hideous scars.
Fever and systemic toxicity are uncommon, but the acute neuritis that can present either as a severe
painful episode or be insidious and painless can lead to irreversible nerve injury (anesthesia, facial
paralysis, claw hand, footdrop) if not treated immediately. Reversal reactions constitute perhaps the
only medical emergency related to leprosy per se. Patients should be instructed to contact their
physicians immediately if signs of a reaction appear.
Type 2 (erythema nodosum leprosum) reactions (ENL) occur in lepromatous and borderline
lepromatous cases as a systemic inflammatory response to deposition of extravascular immune
complexes of antibody and M. leprae antigen. Tender red dermal papules or nodules, clinically
resembling erythema nodosum, are the hallmarks of this syndrome. They develop in a few hours and
last only a few days. High fever, migrating polyarthralgia, painful swelling of lymph nodes or spleen,
orchitis, iridocyclitis, and, rarely, nephritis may occur. Leukocytosis and albuminuria may be present.
Circulating and tissue-based immune complexes are frequently present and may explain the
resemblance to other immune complex disorders, but the underlying mechanism appears to involve
the activation of a helper T-cell subset. There is a strong tendency to recurrence (45% of patients),
and there is a risk of amyloidosis and renal failure if treatment is inadequate.

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Diagnosis

The critical factor in the diagnosis of leprosy is its inclusion in the differential diagnosis of a skin
disorder in anyone who has resided in an endemic leprosy region.
Anesthetic skin lesions with or without thickened peripheral nerves are virtually pathognomonic of
leprosy. A full-thickness skin biopsy from an active lesion (stained with both a standard histologic stain
and an acid-fast stain such as Fite-Faraco) is the optimal procedure for confirmation of the diagnosis
and accurate disease classification. Acid-fast bacilli are rarely found in patients with indeterminate or
tuberculoid disease, but the presence of granulomas and lymphocytic infiltration of nerves in
anesthetic skin lesions essentially confirms the diagnosis. For purposes of assigning patients to the
appropriate WHO MDT regimen, slit skin smears are assessed to determine whether patients have
paucibacillary infection (=5 skin lesions and no bacilli on skin smears) or multibacillary infection (=6
skin lesions and bacilli on skin smears). The bacterial index can range from zero (no bacilli in 100 oil-
immersion fields) to 6+ (>1,000 bacilli per field). Other routine clinical, microbiologic, and radiologic
tests have little or no role in the diagnosis of leprosy, although they may be useful in the exclusion of
other diagnoses. Various assays for serum antibodies directed against unique antigens of M. leprae
have been developed, but current tests lack sufficient sensitivity and specificity for active disease to be
useful for clinical diagnostic purposes. PCR analysis has been found to detect M. leprae only when
biopsy specimens are positive for acid-fast bacilli.
DIFFERENTIAL DIAGNOSIS
Many diseases endemic in developing countries can mimic the appearance of leprosy; these include
secondary syphilis, cutaneous leishmaniasis, yaws, and cutaneous fungal infections. None of these
entities involve paresthesia/anesthesia localized to the skin lesions or cause thickening of peripheral
nerves. The presence of nerve thickening with skin lesions also differentiates leprosy from primary
neurologic disease. Indeterminate leprosy may present as minimal anesthesia, no nerve thickening,
and equivocal histopathology, suggesting a superficial fungal infection, particularly tinea versicolor.
The diagnosis of indeterminate leprosy should be considered one of exclusion and will rarely be
established in anyone other than a close contact of a known lepromatous patient.

Treatment

Only three antimycobacterial agents have proven to be consistently effective in the treatment of
leprosy. Since the early 1940s, dapsone has remained the cornerstone of therapy because of its low
cost, minimal toxicity, and wide availability. However, secondary resistance develops when it is used
as the sole agent.
Dermatitis, hepatitis, and methemoglobinemia are the most common side effects; granulocytopenia is
rare but potentially fatal. Dose-related hemolytic anemia, which can be severe, is seen in patients with
glucose-6-phosphate dehydrogenase deficiency, methemoglobin reductase deficiency, or hemoglobin
M. Pregnancy studies have not shown an increased risk of fetal abnormalities.
Rifampin is the most rapidly mycobactericidal drug for M. leprae, achieving excellent levels inside
cells, where most leprosy bacilli reside. Resistance develops when Rifampin is used as the sole agent.
The widespread use of rifampin has been limited by cost more than by toxicity. Hepatitis is the most
common side effect that necessitates discontinuance.
Clofazimine, a phenazine dye with both antimycobacterial and anti-inflammatory activity, has been
particularly useful in decreasing the incidence of reactional states.
The pharmacokinetics are poorly understood, but the half-life is several days. The drug is avidly taken
up by epithelial cells, a feature that may be important for its activity but also results in cutaneous
hyperpigmentation, ichthyosis, xerosis, and enteritis. The intense reddish-brown discoloration of the
skin is cosmetically a deterrent to use and often results in discontinuation or poor compliance.
Minocycline, certain second-generation quinolones, and some new macrolide derivatives such as
clarithromycin have shown promise in experimental models but limited human treatment data exist.
Introduced by the WHO in 1982, multidrug therapy has been very successful with a high cure rate and
a relapse rate of 1%/yr following a full course of therapy.
For adults with multibacillary leprosy (all BL and lepromatous patients), therapy is recommended for
12–24 mo to include rifampin (600?mg once monthly PO, directly observed), dapsone (100?mg once
daily PO, self-administered), and clofazimine (300?mg once monthly, directly observed, and 50?mg

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once daily PO, self-administered). For adults with paucibacillary leprosy (all indeterminate, TT, and
most BT patients), therapy is recommended for 6 mo with rifampin (600?mg once monthly PO, directly
observed) and dapsone (100?mg once daily PO, self-administered). Patients who experience relapse
are re-treated with the same regimens. To date there have been no patients treated with WHO
recommended MDT who have experienced secondary Rifampin resistance in contrast to those treated
with Rifampin monotherapy or multidrug therapy not recommended by WHO. Resistance is difficult to
determine at present, requiring an in vivo mouse footpad test of 12 mo duration. Newer genetic testing
models evaluating for resistance-associated mutations in the rpoB gene of M. leprae are much faster
and appear very accurate.
Patients treated in the United States may be advised to receive regimens that vary from WHO
recommendations. Adults with paucibacillary disease receive dapsone (100?mg once daily PO) and
rifampin (600?mg once daily PO)for 12 mo; those with multibacillary disease receive dapsone
(100?mg once daily PO), rifampin (600?mg once daily PO), and clofazimine (50?mg once daily PO)
for 24 mo. Daily pediatric doses are dapsone 1?mg/ kg, rifampin 10?mg/kg, and clofazimine 1?mg/kg,
not to exceed the recommended adult doses.
Therapy for reactional states can be complicated and generally requires expert consultation.
Management depends on maintenance of antimycobacterial drugs, effective and prolonged anti-
inflammatory therapy, and adequate analgesia and physical support during the phase of active
neuritis.
Mild ENL may respond to nonsteroidal anti-inflammatory agents. More severe ENL usually requires
corticosteroid therapy (prednisolone 1?mg/kg/24?hr) but often relapses when the drug is discontinued.
Clinical remission of acute or suppression of chronic ENL can be achieved with thalidomide. A dose of
100?mg qid will usually control the reaction within 48?hrs. The dose is then tapered to a maintenance
level of around 100?mg/24?hr, and every few months an attempt should be made to wean patients off
the drug altogether. Thalidomide is absolutely contraindicated in women of child-bearing age;
otherwise it is much safer than corticosteroids for chronic use. The major side effect is fatigue.
Pediatric dosages have not been established. Clofazimine 300?mg/24?hr tapering to 100?mg/24?hr or
less for 12 mo is also useful in managing chronic ENL. Type 1 reversal reactions are optimally treated
with high-dose corticosteroids (prednisolone 20–40?mg/ 24?hr PO in adults, and 1?mg/kg/24?hr PO in
children) tapered over several months. Alternate-day regimens may be effective in patients with
frequent relapses requiring prolonged treatment.

Prognosis

The prognosis for arresting progression of tissue and nerve damage is good, but recovery of lost
sensory and motor function is variable and generally incomplete; hyperpigmentation,
hypopigmentation, and loss of hair follicles or sweat glands persist. Intercurrent reactional states, poor
compliance, and emergence of drug resistance can all lead to clinical exacerbations or relapses
necessitating close follow-up of patients. Much of the chronic debility results from repeated trauma to
anesthetic digits and limbs. Careful counseling of patients and consultation with physical and
occupational therapy services is essential for an optimal outcome.

Prevention

Two approaches are advocated for interrupting leprosy transmission in endemic areas. The first is
directed at the risk of infection among household contacts of leprosy patients, especially those with
multibacillary disease. It is based on regular periodic examination of contacts and early treatment at
the first evidence of leprosy. The second is the use of bacille Calmette-Guerin (BCG) vaccination. One
dose of BCG appears to be 50% protective against leprosy; a second dose increases the protective
benefit.
One historical practice that has fortunately been abandoned is the forcing of leprosy patients into a
leprosarium. Mouse footpad inoculation studies have demonstrated that viability of M. leprae in skin
biopsies decreases sharply within 3 wk of initiating therapy with dapsone and rifampin. This rapid
decrease in infectivity combined with the high probability that family members have already had
prolonged exposure to the patient before the diagnosis makes physical isolation of leprosy patients.

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3.12 DIABETES MELLITUS

Etiology

Diabetes mellitus (DM) comprises a group of metabolic disordersthat share the common phenotype of
hyperglycemia. DM is currently classified on the basis of the pathogenic process that leads to
hyperglycemia.
Under this classification, the terms type 1 DM and type 2 DM have replaced insulin-dependent
diabetes mellitus (IDDM)and non-insulin-dependent diabetesmellitus (NIDDM), respectively.
Type 1 DM is characterized by insulin deficiency and a tendency to develop ketosis, whereas type 2
DM is a heterogeneous group of disorders characterized by variable degrees of insulin resistance,
impaired insulin secretion, and excessive hepatic glucose production.
Other specific types include DM caused by genetic defects [maturity-onset diabetes of the young
(MODY)], diseases of the exocrine pancreas (chronic pancreatitis, cystic fibrosis, hemochromatosis),
endocrinopathies (acromegaly,Cushing’s syndrome, glucagonoma, pheochromocytoma,
hyperthyroidism),drugs (nicotinic acid, glucocorticoids, thiazides, protease inhibitors), and pregnancy
(gestational diabetes mellitus).

Diagnosis

Criteria for the diagnosis of DM include one of the following:

• Fasting plasma glucose _ 7.0 mmol/L (_126 mg/dL)
• Symptoms of diabetes plus a random blood glucose concentration _ 11.1 mmol/L (_ 200 mg/dL)
• 2-h plasma glucose _ 11.1 mmol/L (_ 200 mg/dL)during a 75-g oral glucose tolerance test.
These criteria should be confirmed by repeat testing on a different day, unless unequivocal
hyperglycemia with acute metabolic decompensation is present.
Two intermediate categories have also been designated:
1. Impaired fasting glucose (IFG)for a fasting plasma glucose between 6.1 and 7.0 mmol/L (110
and 126 mg/dL)
2. Impaired glucose tolerance (IGT)for plasma glucose levels between 7.8 and 11.1 mmol/L (140
and 200 mg/dL)2 h after a 75-g oral glucose load
Individuals with IFG or IGT do not have DM but are at substantial risk for developing type 2 DM and
cardiovascular disease in the future. The hemoglobin A1c (HbA1c)level is useful for monitoring
responses to therapy but is not recommended for screening or diagnosis of DM.

Risk Factors for Type 2 Diabetes Mellitus

• Family history of diabetes (i.e., parent or sibling with type 2 diabetes)

• Obesity (BMI _ 25 kg/m2)
• Habitual physical inactivity
• Race/ethnicity (e.g., African American, Hispanic American, Native American, Asian American,
Pacific Islander)
• Previously identified IFG or IGT
• History of GDM or delivery of baby _4 kg (_9 lb)
• Hypertension (blood pressure _ 140/90 mmHg)

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• HDL cholesterol level _ 35 mg/dL (0.90 mmol/L)and/or a triglyceride level_250 mg/dL (2.82
mmol/L)
• Polycystic ovary syndrome or acanthosis nigricans
• History of vascular disease
Note: BMI, body mass index; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; GDM,
gestational diabetes mellitus; HDL, high-density lipoprotein.
The metabolic syndrome, the insulin resistance syndrome, and syndrome X are terms used to
describe a commonly found constellation of metabolic derangementsthat includes insulin resistance
(with or without diabetes), hypertension,dyslipidemia, central or visceral obesity, and endothelial
dysfunctionand is associated with accelerated cardiovascular disease.

Clinical Features

Common presenting symptoms of DM includepolyuria, polydipsia, weight loss, fatigue, weakness,

blurred vision, frequentsuperficial infections, and poor wound healing. A complete medical history
should be obtained with special emphasis on weight, exercise, ethanol use, familyhistory of DM, and
risk factors for cardiovascular disease.
In a patient with established DM, assessment of prior diabetes care, HbA1c levels, self-
monitoringblood glucose results, frequency of hypoglycemia, and pt’s knowledge about DM should be
obtained. Special attention should be given on physical exam to retinal exam, orthostatic bp, foot
exam (including vibratory sensation and monofilament testing), peripheral pulses, and insulin injection
sites. Acute complicationsof diabetes that may be seen on presentation include diabetic ketoacidosis
(DKA)and hyperglycemic hyperosmolar state.
The chronic complications of DM are listed below:
• Ophthalmologic: nonproliferative or proliferative diabetic retinopathy, mascular oedema
• Renal: proteinuria, end-stage renal disease (ESRD), type IV renal tubular Acidosis
• Neurologic: distal symmetric polyneuropathy, polyradiculopathy, mononeuropathy, autonomic
neuropathy
• Gastrointestinal: gastroparesis, diarrhea, constipation
• Genitourinary: cystopathy, erectile dysfunction, female sexual dysfunction
• Cardiovascular: coronary artery disease, congestive heart failure, peripheral vascular disease,
stroke
• Lower extremity: foot deformity (hammer toe, claw toe, Charcot foot), ulceration, amputation

Treatment

Optimal treatment of diabetes requires more than plasma glucose management.

Comprehensive diabetes care should also detect and manage DM-specific complications and modify
risk factors for DM-associated diseases. The pt with type 1 or type 2 DM should receive education
about nutrition, exercise, care of diabetes during illness, and medications to lower the plasma glucose.
In general, the target HbA1c level should be _7.0%, though individual considerations (age, ability to
implement a complex treatment regimen, and presence of other medical conditions)should also be
taken into account. Intensive therapy reduces long-term complications but is associated with more
frequent and more severe hypoglycemic episodes.
In general, pts with type 1 DM require 0.5–1.0 U/kg per day of insulin divided into multiple doses.
Combinations of insulin preparations with different times of onset and duration of action should be
used.
Commonly used regimens include twice-daily injections of an intermediate insulin combined with a
short-acting insulin before the morning and evening meal, injection of glargine at bedtime and
preprandial lispro or insulin aspart, and continuous subcutaneous insulin using an infusion device.

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Pts with type 2 DM may be managed with diet and exercise alone or in conjunction with oral glucose-
lowering agents, insulin, or a combination of oral agents and insulin. A reasonable treatment algorithm
for initial therapy proposes either a sulfonlyurea or metformin as initial therapy because of their
efficacy (1–2% decrease in HbA1c), known side-effect profile,and relatively low cost (Fig. 176-1).
Metformin has the advantage that it promotes mild weight loss, lowers insulin levels, improves the lipid
profile slightly, and does not cause hypoglycemia when used as monotherapy, though it is
contraindicated in renal insufficiency, congestive heart failure, any form of acidosis, liver disease, or
severe hypoxia, and should be temporarily discontinued in pts who are seriously ill or receiving
radiographic contrast material.
Combinations of two oral agents may be used with additive effects, with stepwise addition of bedtime
insulin or a third oral agent if adequate control is not achieved. As endogenous insulin production falls,
multiple injectionsof intermediate-acting and short-acting insulin may be required, asin type 1 DM.
Individuals who require _1 U/kg per day of intermediateacting insulin should be considered for
combination therapy with an insulinsensitizing agent such as metformin or a thiazolidinedione.
The morbidity and mortality of DM-related complications can be greatly reduced by timely and
consistent surveillance procedures. A routine urinalysis may be performed as an initial screen for
diabetic nephropathy.
If it is positive for protein, quantification of protein on a 24-h urine collection should be performed. If the
urinalysis is negative for protein, a spotcollection for microalbuminuria should be performed (present if
30–300 _g/mg creatinine on two of three tests within a 3- to 6-month period).

Guidelines for Ongoing Medical Care for Patients with Diabetes

• Self-monitoring of blood glucose (individualized frequency)

• HbA1c testing (2–4 times/year)
• Patient education in diabetes management (annual)
• Medical nutrition therapy and education (annual)
• Eye examination (annual)
• Foot examination (1–2 times/year by physician; daily by patient)
• Screening for diabetic nephropathy (annual urine microalbumin)
• Blood pressure measurement (quarterly)
• Lipid profile (annual)
• Influenza/ pneumococcal immunizations

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3.13 CHARCOT FOOT

What is Charcot Foot?

Charcot foot is a condition causing weakening of the bones in the foot that can occur in people who
have significant nerve damage (neuropathy). The bones are weakened enough to fracture, and with
continued walking the foot eventually changes shape. As the disorder progresses, the joints collapse
and the foot takes on an abnormal shape, such as a rocker-bottom appearance.
Charcot foot is a very serious condition that can lead to severe deformity, disability, and even
amputation. Because of its seriousness, it is important that patients with diabetes—a disease often
associated with neuropathy—take preventive measures and seek immediate care if signs or
symptoms appear.

Causes

Charcot foot develops as a result of neuropathy, which decreases sensation and the ability to feel
temperature, pain, or trauma. Because of diminished sensation, the patient may continue to walk—
making the injury worse.
People with neuropathy (especially those who have had it for a long time) are at risk for developing
Charcot foot. In addition, neuropathic patients with a tight Achilles tendon have been shown to have a
tendency to develop Charcot foot.

Symptoms

The symptoms of Charcot foot may include:

• Warmth to the touch (the affected foot feels warmer than the other)
• Redness in the foot
• Swelling in the area
• Pain or soreness

Diagnosis

Early diagnosis of Charcot foot is extremely important for successful treatment. To arrive at a
diagnosis, the surgeon will examine the foot and ankle and ask about events that may have occurred
prior to the symptoms. X-rays and other imaging studies and tests may be ordered.
Once treatment begins, x-rays are taken periodically to aid in evaluating the status of the condition.

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Non-Surgical Treatment

It is extremely important to follow the surgeon’s treatment plan for Charcot foot. Failure to do so can
lead to the loss of a toe, foot, leg, or life.
Non-surgical treatment for Charcot foot consists of:
• Immobilization. Because the foot and ankle are so fragile during the early stage of Charcot,
they must be protected so the weakened bones can repair themselves. Complete non-
weightbearing is necessary to keep the foot from further collapsing. The patient will not be able
to walk on the affected foot until the surgeon determines it is safe to do so. During this period,
the patient may be fitted with a cast, removable boot, or brace, and may be required to use
crutches or a wheelchair. It may take the bones several months to heal, although it can take
considerably longer in some patients.
• Custom shoes and bracing. Shoes with special inserts may be needed after the bones have
healed to enable the patient to return to daily activities—as well as help prevent recurrence of
Charcot foot, development of ulcers, and possibly amputation. In cases with significant
deformity, bracing is also required.
• Activity modification. A modification in activity level may be needed to avoid repetitive
trauma to both feet. A patient with Charcot in one foot is more likely to develop it in the other
foot, so measures must be taken to protect both feet.

When is Surgery Needed?

In some cases, the Charcot deformity may become severe enough that surgery is necessary. The foot
and ankle surgeon will determine the proper timing as well as the appropriate procedure for the
individual case.

Preventive Care

The patient can play a vital role in preventing Charcot foot and its complications by following these
measures:
• Keeping blood sugar levels under control can help reduce the progression of nerve damage in
the feet.
Get regular check-ups from a foot and ankle surgeon:
• Check both feet every day—and see a surgeon immediately if you notice signs of Charcot foot.
• Be careful to avoid injury, such as bumping the foot or overdoing an exercise program.
• Follow the surgeon’s instructions for long-term treatment to prevent recurrences, ulcers, and
amputation.

Diabetic Charcot Foot

Diabetic Charcot Foot, or neuropathic arthropathy, is a condition that affects some diabetic patients
with peripheral neuropathy (loss of sensation) after 8 to 10 years of the disease.
Neuropathy is a term used to describe problems with the nervous system. In diabetics this is called
peripheral neuropathy and affects the sensory nervous system to the peripheral, or farther, points of
the body (i.e. feet and hands) causing loss of feeling or numbness. Diabetic neuropathy also involves
the autonomic (involuntary) nervous system which controls regulation of blood vessels and may result
in increased blood flow to the limb, contributing to swelling and osteoporosis of the bones as the
Charcot process occurs. Arthropathy is a term used to describe a problem with a joint. Therefore,
neuropathic arthropathy is used to describe problems with joints related to lack of nerve system input.
It is believed that as the peripheral neuropathy progresses in long-standing diabetes, the joints are
unable to recognize the forces put across them and the relative positions of the various joints,
sustaining microtrauma or microfractures because the body does not adjust to these forces and
positions.

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It would therefore be reasonable to assume that most cases of neuropathic arthropathy would occur in
the lower extremities, with their weight-bearing function. This is indeed the case, although on occasion
other joints can be involved.
When Does the Charcot Foot Occur?
Most patients who develop neuropathic arthropathy have peripheral neuropathy after being diabetic
about 10 years or longer. So a patient with juvenile-onset diabetes (as a child) may develop this in his
20s or 30s. However, most patients with Charcot arthropathy are in their 40s or older, as more patients
have adult-onset diabetes.
Signs & Symptoms of the Charcot Foot
There are three stages to Charcot arthropathy. The first stage is a fragmentation or destruction stage.
During this stage, as the process begins, the joint and surrounding bone is destroyed. The bone
fragments, the joint becomes unstable and in some cases the bone is completely reabsorbed. This
stage is clinically identified by significant swelling (often with little pain to the patient) erythema
(redness), and warmth or heat to the area. It is easy to see why this is often confused with an
infection, especially as there is often no history of injury or trauma. As the bones and joint are affected,
fractures and instability develop and the joints can dislocate or shift the bones in relationship to each
other. This can lead to severe deformity of the foot and ankle. Often the midfoot joints are affected and
the result is a very flat foot which is wide where the normal foot narrows in the arch. Bony
prominences often develop on the plantar (bottom) surface of the foot. Diagnosis and early treatment
at this stage is important to try to minimize the bone destruction and deformity. This process may last
as long as six to 12 months.
Acute Phase Destructive Process
The second stage is termed coalescence. During this stage the acute destructive process slows down
and the body begins to try and heal itself. The swelling and heat begin to disappear. Once the acute
process is resolved and the healing on-going, the third stage begins. This is a consolidation or
reconstruction phase during which the bones and joints heal. Unfortunately, the foot is often deformed,
and if there has been enough destruction, there may be residual instability. Fitting shoes may be very
difficult, and prescription footwear and diabetic orthotics (shoe inserts) are important to help prevent
ulcer formation over deformed areas.
Treatment of the Charcot Foot
Once the diagnosis is made (for most patients in the first stage) there are several important treatment
goals. The first is to get the heat and swelling under control. The second is to support or stabilize the
foot to minimize deformity. A total contact cast is applied by trained personnel. This cast has more
padding than a standard cast and is often applied with the toes completely covered to prevent foreign
objects (gravel, stones, etc.) from getting in the cast. The cast will need to be changed frequently
initially as it will get loose very quickly as the swelling is controlled. Once the initial swelling is
controlled and the patient is tolerating the casts without skin problems, the cast change interval may
be lengthened to two to four weeks. Another alternative is fabrication of a custom walking boot for
diabetics. The foot must be supported until all heat and swelling has resolved. This may occur in
several months but more commonly requires six to 12 months. Minimizing weight-bearing on the
affected foot/ankle is also important. Realistically this is extremely difficult for the patient with diabetic
neuropathy and should be encouraged.
Assistive aides such as a walker or cast are recommended. During this period the patient will be seen
frequently in the office. Continued education about diabetic foot care and Charcot arthropathy is
necessary. Also, support of the various stages of anger and denial concerning this rather profound
change is necessary. After the first stage is completed, molds for appropriate diabetic footwear,
orthotics and braces (if needed) are made. During treatment it is important to check the noninvolved
foot and protect it, as that foot is doing much more work.
For patients who develop deformities that are unshoeable or bracable, or who develop unbracable
instability, surgery may be considered. The timing for this surgery is important. Surgery done during
stage one has a high complication rate, often with fragmentation of any grating done. Sometimes,
however, surgery must be done during this stage due to joint instability. Another option for severe
deformity/instability is amputation and prosthetic fitting. Patients often have multiple medical problems
which must be taken into account in consideration for any surgery.

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Long-term management of patients with Charcot Arthropathy is important. Once the patient is stable,
periodic checkups (six to twelve month intervals) with a qualified foot and ankle specialist is important
to identify early complications, address footwear, orthotic and brace issues, and continue patient
education regarding the care of diabetic feet and the special needs of the patient with Charcot
arthropathy. Patients should be counseled to seek medical care if they develop any redness, selling,
or heat in their feet, as this could be the start of another Charcot process.

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3.14 CLUB FOOT

Figure 58: Bilateral Club Foot.

[1]
A club foot, or congenital talipes equinovarus (CTEV), is a congenital deformity involving one foot
[2]
or both. The affected foot appears rotated internally at the ankle. TEV is classified into 2 groups:
Postural TEV or Structural TEV.
Without treatment, persons afflicted often appear to walk on their ankles, or on the sides of their feet. It
is a common birth defect, occurring in about one in every 1,000 live births. Approximately 50% of
cases of clubfoot are bilateral. In most cases it is an isolated dysmelia. This occurs in males more
often than in females by a ratio of 2:1.

Deformities

The deformities affecting joints of the foot occur at three joints of the foot to varying degrees. They are
• Inversion at subtalar joint
• Adduction at talonavicular joint, and
• Equinus at ankle joint, that is, a plantarflexed position
The deformities can be remembered using the mnemonic, "InAdEquate" for Inversion, Adduction and
Equinus.

Causes

There are different causes for clubfoot depending on what classification it is given. Structural cTEV is
caused by genetic factors such as Edwards syndrome, a genetic defect with three copies of
chromosome 18. Growth arrests at roughly 9 weeks and compartment syndrome of the affected limb
are also causes of Structural cTEV. Genetic influences increase dramatically with family history. It was
previously assumed that postural cTEV could be caused by external influences in the final trimester
such as intrauterine compression from oligohydramnios or from amniotic band syndrome. However,
this is countered by findings that cTEV does not occur more frequently than usual when the
[5] [citation needed]
intrauterine space is restricted. Breech presentation is also another known cause. cTEV
occurs with some frequency in Ehlers Danlos Syndrome and some other connective tissue disorders,
such as Loeys-Dietz Syndrome. TEV may be associated with other birth defects such as spina bifida
cystica.

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Prenatal Screening

Screening for club foot prenatally is a debatable topic. However, this is commonly done as it is easily
identified using a ultrasound scan. Most fetuses undergo a 20 weeks gestation fetal abnormality scan
[6] in which club foot is one of the abnormalities that can be picked up. Some doctors have argued that
club foot may occasionally be associated with a syndromic disease and should therefore be screened.
If no syndromic association is found prenatally, most fetuses with club foot are born and can live a
normal life with medical treatment.

Treatment

Clubfoot is treated with manipulation by podiatrists, physiotherapists, orthopedic surgeons, specialist

Ponseti nurses, or orthotists by providing braces to hold the feet in orthodox positions, serial casting,
or splints called knee ankle foot orthoses (KAFO). Other orthotic options include Dennis-Brown bars
with straight last boots, ankle foot orthoses and/or custom foot orthoses (CFO). In North America,
manipulation is followed by serial casting, most often by the Ponseti Method. Foot manipulations
usually begin within two weeks of birth. Even with successful treatment, when only one side is
affected, that foot may be smaller than the other, and often that calf, as well.
Extensive surgery of the soft tissue or bone is not usually necessary to treat clubfoot; however, there
are two minimal surgeries that may be required:
1. Tenotomy (needed in 80% of cases) is a release (clipping) of the Achilles tendon – minor
surgery – local anesthesia
2. Anterior Tibial Tendon Transfer (needed in 20% of cases) – where the tendon is moved from
the first ray (toe) to the third ray in order to release the inward traction on the foot.
Of course, each case is different, but in most cases extensive surgery is not needed to treat clubfoot.
Extensive surgery may lead to scar tissue developing inside the child's foot. The scarring may result in
functional, growth and aesthetic problems in the foot because the scarred tissue will interfere with the
normal development of the appendage. A child who has extensive surgery may require on average
two additional surgeries to correct the issues presented above.
In stretching and casting therapy the doctor changes the cast multiple times over a few weeks,
gradually stretching tendons until the foot is in the correct position of external rotation. The heel cord is
released (percutaneous tenotomy) and another cast is put on, which is removed after three weeks. To
avoid relapse a corrective brace is worn for a gradually reducing time until it is only at night up to four
years of age.

Non-Surgical Treatment and Ponseti Method

Ponseti Method
Treatment for clubfoot should begin almost immediately to have the best chance for a successful
outcome without the need for surgery. Over the past 10 to 15 years, more and more success has been
achieved in correcting clubfeet without the need for surgery. The clubfoot treatment method that is
[7]
becoming the standard in the U.S. and worldwide is known as the Ponseti Method. Foot
manipulations differ subtly from the Kite casting method which prevailed during the late 20th century.
Although described by Dr. Ignacio Ponseti in the 1950s, it did not reach a wider audience until it was
re-popularized around 2000 by Dr. John Herzenberg in the USA and in Europe and Africa by NHS
surgeon Steve Mannion while working in Africa. Parents of children with clubfeet using the Internet
also helped the Ponseti gain wider attention. The Ponseti method, if correctly done, is successful in
>95% of cases in correcting clubfeet using non- or minimal-surgical techniques. Typical clubfoot cases
usually require 5 casts over 4 weeks. Atypical clubfeet and complex clubfeet may require a larger
number of casts. Approximately 80% of infants require an Achilles tenotomy (microscopic incision in
the tendon requiring only local anesthetic and no stitches) performed in a clinic toward the end of the
serial casting.
Throughout the past decade, physicians at Texas Scottish Rite Hospital for Children have been
studying the effectiveness of both the Ponseti casting method and the French functional (physical
therapy) method of stretching, massaging and taping and comparing the results with patients who
have undergone surgery. Results of these studies have been presented at national and international
conferences, such as the Pediatric Orthopaedic Society of North America annual meeting, the

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International Clubfoot Symposium, Brandon Carrell Visiting Professorship and the American Academy
of Orthopaedic Surgeons annual meeting, and have been published in the Journal of Pediatric
Orthopaedics.
After correction has been achieved, maintenance of correction may require the full-time (23 hours per
day) use of a splint—also known as a foot abduction brace (FAB)—on both feet, regardless of whether
the TEV is on one side or both, for several weeks after treatment. Part-time use of a brace (generally
at night, usually 12 hours per day) is frequently prescribed for up to 4 years. Without the parents'
participation, the clubfoot will almost certainly recur, because the muscles around the foot can pull it
back into the abnormal position. Approximately 20% of infants successfully treated with the Ponseti
casting method may require a surgical tendon transfer after two years of age. While this requires a
general anesthetic, it is a relatively minor surgery that corrects a persistent muscle imbalance while
avoiding disturbance to the joints of the foot.
The developer of the Ponseti Method, Dr Ignacio Ponseti, was still treating children with clubfeet
(including complex/atypical clubfeet and failed treatment clubfeet) at the University of Iowa Hospitals
and Clinics well into his 90s. He was assisted by Dr Jose Morcuende, president of the Ponseti
International Association.
The long-term outlook for children who experienced the Ponseti Method treatment is comparable to
that of non-affected children.
Botox is also being used as an alternative to surgery. Botox is the trade name for Botulinum Toxin type
A. a chemical that acts on the nerves that control the muscle. It causes some paralysis(weakening) of
the muscle by preventing muscle contractions (tightening). As part of the treatment for clubfoot, Botox
is injected into the child’s calf muscle. In about 1 week the Botox weakens the Achilles tendon. This
allows the foot to be turned into a normal position, over a period of 4–6 weeks, without surgery.
The weakness from a Botox injection usually lasts from 3–6 months. (Unlike surgery it has no lasting
effect). Most club feet can be corrected with just one Botox injection. It is possible to do another if it is
needed. There is no scar or lasting damage.
On occasion, stretching, casting and bracing are not enough to correct a baby's clubfoot. Surgery may
be needed to adjust the tendons, ligaments and joints in the foot/ankle. Usually done at 9 to 12
months of age, surgery usually corrects all clubfoot deformities at the same time. After surgery, a cast
holds the clubfoot still while it heals. It is still possible for the muscles in the child's foot to try to return
to the clubfoot position, and special shoes or braces will likely be used for up to a year or more after
surgery. Surgery will likely result in a stiffer foot than nonsurgical treatment, particularly over time.
Without any treatment, a child's clubfoot will result in severe functional disability, however with
treatment, the child should have a nearly normal foot. He or she can run and play without pain and
wear normal shoes. The corrected clubfoot will still not be perfect, however; a clubfoot usually stays 1
to 1½ sizes smaller and somewhat less mobile than a normal foot. The calf muscles in a leg with a
clubfoot will also stay smaller. Long-term studies of adults with post-club feet, especially those with
substantial numbers of surgeries, may not fair as well in the long term, according to Dobbs, et. al., A
percentage of adults may require additional surgeries as they age, though there is some dispute as to
the effectiveness of such surgeries, in light of the prevalence of scar tissue present from earlier
surgeries.

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 IV. CLINICAL ASSESSMENT

4.1 CLINICAL ASSESSMENT OF THE FOOT AND ANKLE

When manufacturing an insole, the technician must be perfectly aware of the effect of the different
correcting elements used on the foot. Indeed, the foot being the base of the lower limb, any
modification of its static alignment will affect the alignment of the entire lower limb and the body
posture in general.
That is why the conception of an orthopaedic insole supposes that the foot has been analysed, not as
an isolated element of the body, but as a part belonging to the lower limb.
It is also to be mentioned that a clinical assessment must be done in the best conditions: spacious
room; privacy and comfort for the patient; enough time for a comprehensive examination to be done;
use of an assessment form where all necessary information are written down.
A good clinical assessment should give the orthotist and the assessment team, the possibility to
determine (or to confirm) the diagnostic, and to determine (or confirm) the appropriate prescription and
rehabilitation program.
Ideally, the clinical assessment of the patient should be performed within a multidisciplinary
rehabilitation team, including:
• an orthopaedic surgeon
• an orthotic and/or prosthetic technician
• a physiotherapist
• an occupational therapist
• an orthopaedic shoe specialist
• a social worker
At the end of the clinical examination, the rehabilitation team must be able to identify the main
problems of the patient and to define a realistic and individual treatment plan (e.g. pre-fitting
physiotherapy, prescription of a P&O device, referral to specialist, etc).
The information and results gathered in the assessment must be clearly and precisely recorded in the
patient’s file.
The clinical assessment of a patient allows the Rehabilitation Team to record the physical condition of
a patient at a given moment. It is the first step towards the physical rehabilitation of the patient and it
provides the baseline data for further evaluation of changes (improvements).
The clinical assessment procedure is divided in two phases:
1. The subjective assessment
2. The objective assessment

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4.2 SUBJECTIVE ASSESSMENT

The subjective assessment involves questioning the patient to obtain information about his / her
condition including the main complaint, when the problems started to appear, the present symptoms,
the effects of a previous treatment, possible reasons for not doing any orthosis, patient’s goals,
patient’s concerns and questions.
The subjective assessment not only gives important information to the orthotist, but also creates a
climate of trust and comfort for the patient.
The subjective assessment of a patient includes several steps:
1. Anamnesis: during this step, the Assessor consults any relevant documents related to the
patient (X-ray, surgical report, etc.) and asks the patient several questions on his medical
history, the history of the disability, his living conditions, etc.
2. Inspection: this is the step where the Assessor visually evaluates several points:
a. Body static of the patient (general, spine, lower limbs, upper part of the body)
b. Basic activities of daily life (sitting on the floor, standing up, squatting down, etc.)

Anamnesis
During the anamnesis, the Assessor gathers information on the patient and his related past by
interviewing the patient and consulting any relevant documents (X-rays, surgical reports, referral
documents, etc.)
The anamnesis should contain the following information:
• Personal data of the patient
o Patient’s name, age and gender
o Civil status (civilian, military)
o Place of residence (kebele, wooreda, regional state)
o Profession (before and after disability, if different)
o Family situation (single, married, number of children)
o Living environment (urban, rural)
o Any specific activity the patient has besides normal ADL (activities of daily living) and
his profession
o Any specific activity for which the patient feels limited because of his disability
o Assistance needed for ADL
• Medical history of the patient
o History of the disability (when did it start? what did cause it?)
o Medical or surgical treatments and follow-up (surgeries, medication, complications,
etc.)
o Current medical status and general condition
o Associated or other diseases and illnesses
o Pain (where? what does cause the pain?

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 • Orthotic device
o Has the patient been fitted before?
o If yes, what is the problem with the old device? What is his independence with the old
device (walking distance, etc.)?
o If the patient has never been fitted before, what are his expectations of the new
device?

Patient Observation

a. Body statics and dynamics of the patient

General:
• General physical condition, overweight, general weakness, body posture.
• Way of moving, dependence on walking aids, degree of inipendence.

Spine:

Presence of Deformities:

Gibbus of Thoracic Spine Hyperlordosis of Hyperkyphosis of

Lumbar Spine Thoracic Spine Scoliosis

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Lower Limbs:

Lower
Limbs

Knee Valgus (Genu Knee Hyperextension

Knee Varus (Genu Varum)
Valgum) (Genu Recurvatum)

Foot

Flat Foot (Pes Planus) Cave Foot (Pes Cavus)

Foot Valgus or Foot
Varus

b. Basic activities of daily living (ADL)

Can the patient do these activities alone, does he need help?
• Standing à sitting on a chair à standing up
• Standing à sitting on the floor à standing up
• Squatting on the floor
• Going up and down stairs
• Getting dressed
• Body hygiene (cleaning his body, going to the toilet)
• Feeding

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4.3 OBJECTIVE ASSESSMENT

The objective assessment involves the Physical Examination of the patient including a series of tests
3
to evaluate the neurological and muscular-skeletal status of the patient, such as tendon reflex test ,
range of motion, muscle strength, sensation and gait analysis oedema, etc.
Physical Examination:
During physical examination, the evaluator observes the skin and palpates the leg and foot.
Look at the skin leg and feet one by one, and pay attention to:
• skin: colour, temperature, consistency, callosities, sensation
• swellings: soft tissues, bony areas
• wound, blister, scars
• vascularisation, skin discoloration
• temperature of the skin
• Note if there is any painful area (hot: is there an infection? cold: blood circulation problems?)
Check the Muscle tone
• Muscles wasting (circumference)
• Muscles hypotonic/hypertonic
Check the Pressure Areas
While palpating the leg and foot, it is necessary to understand the difference between pressure
tolerant and pressure sensitive areas.
The pressure tolerant areas are weight-bearing areas. They are used to bear the whole weight of the
patient in the orthesis during the midstance of gait. The pressure tolerant areas are the areas where
plaster will be taken off during the rectification of the positive cast. If major weight-bearing areas are
painful, it is more difficult, in some cases even impossible, to fit the patient.
During palpation, the evaluator has to make sure that the patient can support pressure on those
pressure-tolerant areas. Therefore, the pressure given during palpation should be equivalent to the
pressure the patient will feel when standing on the orsthesis. Any pain or uncomfortable sensation of
the patient during this palpation has to be reported on the assessment form.
List of pressure Tolerant areas of the Leg
• Patella tendon
• Medial flare of the Tibia
• Lateral flare of the Tibia
• Lateral flare of Fibula
• Posterior flare of the leg
List of pressure Tolerant area of Ankle and Foot
• Calcaneus
• Plantar part of the foot
• Longitudinal arches
• Transversal Arches

3
(See Nervous System Section)

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The pressure sensitive areas are all the places that should be protected from pressure. During the
rectification of the positive cast, there areas need a build-up. Hypersensitive areas are always possible
to fit, if they are taken into account already during the rectification and manufacturing of the device.
During palpation of pressure sensitive areas, the objective is not to hurt the patient, but to know if an
area is hypersensitive or provoking excessive pain. In this case, the information has to be registered
on the assessment form.
List of pressure Sensitive areas of Leg:
• Patella
• Lateral Tibial Condyle
• Tibial tuberosity
• Tibial crest
• Tiabial malleoli
• Fibula malleoli
List of pressure Sensitive area of Ankle and Foot
• Medial condyle of the tibia
• Lateral condyle of fibula
• Achilles Tendom
• Navicular Tuberosity
• Distal end of metatarsal
• Lateral sides of Metatarsal I &V
Assessment of the shoes:
The patient’s shoes often reveal the presence of pathological gait, abnormal pressures, etc. Check the
out sole, the heel and the insole. Also, ask the patient, which kind of shoes he / she is wearing usually,
because some patient might not come to the consultation with their “every day” shoes.
Assessment of the patient:
The patient must take off shoes and socks, as well as trousers.
1. Examination with patient sitting:
The patient sits on the examination bed and the assessor sits on a stool in front of him.
Check the legs:
• hip joint range of movement
• stability of knees
• alignment of patella and malleoli (tibial torsion)
• legs length
• lower limb reflexes.
2. Examination with the patient standing
The patient stands with the feet about 15 cm apart and looks straight ahead
Look from front (frontal):
• the knees (valgus or varus?)
• the shape of the foot in general
• the medial border in particular
• the position of the toes

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Look from back (posterior):
• position of the heel and achilles tendon
• position of the heel and medial arch shape when the patient stands on tip-toe
3. Examination with the patient walking
Observe:
• stride length
• cadence
• which part of the foot hits the ground first
• degree of pronation and supination
• the toes function

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4.4 RANGE OF MOTION

When testing the range of motion of the lower limb joints of the patient, the Assessor will know the
mobility limitations or contractures of the patient, which will have to be taken into account when
manufacturing the orthopaedic device.
Range of motion is divided in Passive Range of Motion (PROM) and Active Range of Motion
(APROM). During clinical examination the evaluator, checks primarily the PROM and secondarily the
APROM together with the muscles function.
Principles for ROM Test
• The patient has to be comfortably installed in the position in which the Assessor wants to test the
joint
• When testing the ROM of a joint, one segment has to be stabilised, while the other segment is
mobilised.
Example: when testing the ROM of the knee flexion, the femur has to be stabilised while the
Assessor is mobilising the tibia. The stabilising hand on the femur will avoid any compensation
movement by the hip and give the exact ROM of the knee flexion
• Always only test one movement at the time
• At the end of the ROM, identify the quality of the end of motion: soft or hard, provoking pain?
• At the end of the ROM, measure the exact angle of motion with the goniometer and report the
measure on the assessment sheet
Neutral Zero Method
Range of motions are recorded with the standardized neutral zero method.
In the neutral zero method the joints are in zero position when the patient is standing, feet parallel.
The extended knee = 0° (not 180°), the angle between the foot and lower leg = 0° (not 90°).
The range of motion is recorded with three figures. The figure in the middle is the zero position, or the
angle measured for a contracture.
Examples:
• Measure of the hip flexion and extension of a patient without contractures.
The recorded measures will be:
Hip flexion/extension: 120° / 0° / 5°
This means that the patient has 120° flexion, can reach the neutral zero position and has 5° of
extension of the hip.
• Measure of the hip flexion and extension of a patient with a hip flexion contracture of 40°.
The recorded measure will be:
Hip flexion/extension: 120° / 40° / 0°
This means that the patient has 120° flexion, can not reach the neutral zero position (due to the
contracture), which is at 40°, and has 0° extension (measured from the contracture)
Causes of Joint Limitations
Every limitation of range of motion in a joint has a cause. When testing the ROM, the Assessor has to
define this cause, and decide whether it is reversible or not.
Reversible causes of ROM limitations:
• Scars or burns that limit the elasticity of the skin
• Retraction of the joint capsule or ligaments

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• Muscle shortening : shortening of the muscle performing the antagonist (opposite) movement
Example: knee extension can be limited because the hamstrings (performing knee flexion) are too
short
• Spasticity (hypertonicity of the antagonist muscle with stretching resistance, due to a central
nervous system disorder)
Non-reversible causes
• Calcification or fibrosis of peri-articular structures (capsule, ligaments, tendons)
• Destruction of intra-articular structures (articular space)
• Old fixed articular dislocations
The reversible causes can be treated with Physiotherapy: stretching of the concerned structure,
decrease spasticity, etc.

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Hip Flexion
Normal range of Motion: 0° - 120°

Patient: In supine position

Fixation: Hand on anterior

superior iliac spine to
fix the pelvis

Mobilization: Hand distal on thigh

and Mobilise in flexion

Compensation: Lumbar kyphosis

Flexion of the opposite
hip

Hip Flexion:
Measurement Tool: Universal Goniometer
Testing Position: Supine with hips and knees in neutral rotation
Stabilization: Trunk stabilized by body position
Goniometer Axis: Femoral Greater Trochanter
Proximal Arm: Parallel to midaxillary line of the trunk
Distal Arm: Parallel to longitudinal axis of the femur in line with lateral femoral
condyle
Movement: Hip flexion with knee flexion allowed
Expected ROM: 120°
Substitutions: Lumbar Spine flexion

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Hip Extension
Normal range of Motion: 0° - 30°

Patient: In prone position

Fixation: Hand on posterior

iliac crest to fix the
pelvis

Mobilization: Hand distal on thigh

and mobilise in
extension

Compensation: Lumbar lordosis

Hip Extension:
Measurement Tool: Universal Goniometer
Testing Position: Prone with hips & knees in neutral and feet extending off end of the table
Stabilization: Pelvis is stabilized through straps or manual fixation
Goniometer Axis: Greater Trochanter
Proximal Arm: Parallel to midaxillary line of the trunk
Distal Arm: Parallel to longitudinal axis of femur in line with lateral femoral condyle
Movement: Hip extension with knee extended. ASIS must remain on table.
Expected ROM: 30°
Substitutions: Lumbar spine extension

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Thomas Test
The Thomas test allows checking very quickly and easily if there is a hip contracture. This test can be
done just after testing the hip flexion.

Patient: In supine position

Fixation: Opposite hip in maximum flexion, lumbar spine flat on the table

Mobilization: Hand distal on thigh and mobilise in extension. If the thigh touches
the table, the patient has no hip contracture (this corresponds to
approximately 20° of hip extension)

Compensation: Lumbar lordosis

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Hip Abduction
Normal range of Motion: 0° - 45°

Patient: In supine position

Fixation: Other leg in full

abduction
or
Hand on iliac crest
to fix the pelvis

Mobilization: The limb of the patient

rests on the Assessor's
arm, hand on medial
side of distal thigh,
controlling rotations
(patella looks to
zenith), mobilising
in abduction

Compensation: Pelvis moves with

abduction, lateral
flexion of lumbar spine

Hip Abduction:
Measurement Tool: Universal Goniometer
Testing Position: Supine with hips and knees in neutral and pelvis level
Stabilization: Opposite hip abduction
Goniometer Axis: ASIS on measured side
Proximal Arm: Along a line between the two anterior superior iliac spines
Distal Arm: Parallel to the long axis of the femur
Movement: Abduction until motion is detected at the opposite anterior superior iliac spine
Expected ROM: 45°
Substitutions: Hip external rotation, knee flexion/internal rotation, or lateral pelvic tilt

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Hip Adduction
Normal range of Motion: 0° - 30°

Patient: In supine position

Fixation: Hand on iliac crest

to fix the pelvis

Mobilization: The limb of the patient

rests on the Assessor's
arm, hand on medial
side of distal thigh,
controlling rotations
(patella looks to
zenith), mobilising
in adduction

Compensation: Pelvis moves with

abduction, lateral
flexion of lumbar spine

Hip Adduction:
Measurement Tool: Universal Goniometer
Testing Position: Supine with the opposite extremity abducted
Goniometer Axis ASIS on measured side
Proximal Arm: Along a line between the two anterior superior iliac spines
Distal Arm: Parallel to the long axis of the femur
Movement: Adduction
Expected ROM: 30°
Substitutions: Hip internal rotation or lateral pelvic tilt

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Hip Internal Rotation
Normal range of Motion: 0° - 35°

Patient: In supine position,

hip and knee flexed
at 90°, neutral
abduction/adduction

Fixation: Hand on iliac crest

to fix the pelvis

Mobilization: The limb of the patient

rests on the
Assessor's arm, hand
on medial femoral
condyle, mobilising in
internal rotation (foot
moves towards lateral)

Compensation: Pelvis rotation

Note: be careful to keep 90º of hip and knee flexion during the whole mobilisation, without abduction /
adduction of the hip

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Hip External Rotation
Normal range of Motion: 0°- 45°

Patient: In supine
position, hip and
knee flexed at 90°,
neutral abduction
/ adduction

Fixation: Hand on iliac

crest to fix the
pelvis

Mobilisation: The limb of the

patient rests on
the Assessor's
arm, hand on
medial femoral
condyle,
mobilising in
external rotation
(foot moves
towards medial !)

Compensation: Pelvis rotation

Note: be careful to keep 90º of hip and knee flexion during the whole mobilisation, without abduction /
adduction of the hip

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Hip Internal and External Rotation:
Measurement Tool: Universal Goniometer
Testing Position: Sitting with the hip and knee flexed 90°. Opposite extremity abducted
and resting on a foot' stool
Stabilization: prevent thigh abduction/adduction
Goniometer Axis: mid-patella
Proximal Arm: Perpendicular to the floor
Distal Arm: Parallel to long axis of the tibia
Movement: internal and external ROM
Expected ROM: 35° internal and 45° external ROM
Substitutions: thigh abduction/adduction

Alternate Test Position for Hip Internal/External Rotation:

Test Position: prone with knees flexed 90°
Stabilization: strap or manual fixation of pelvis
Diagnostic Findings: similar measurements with hips flexed or extended indicate structural
limitations while different amounts of motion in each position may
indicate soft tissue tightness of the hip flexors/extensors

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Knee Flexion
Normal range of Motion: 0° - 140°

Patient: In supine
position

Fixation: Not necessary

in this position

Mobilisation: On the distal

part of the
tibia,
mobilising in
flexion

Compensation: Extension of
the hip

Note: During knee flexion, the quadriceps muscle is stretched. If knee flexion is tested with the
hip in neutral position, it is possible that the quadriceps is stretched to its maximum.
Therefore, always test knee flexion in a position where the patient has some amount of
hip flexion.

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Knee Flexion:
Measurement Tool: Universal Goniometer
Testing Position: Supine or reclined with hip and knee in neutral rotation
Stabilization: Trunk and pelvis stabilized by body weight and position
Goniometer Axis: Lateral epicondyle of the femur
Proximal Arm: Parallel to the long axis of the femur & pointing at the greate
trochanter
Distal Arm: Parallel to the long axis of the fibula and pointing at the lateral
malleolus
Movement: The hip and knee are flexed as the heel moves toward the buttock
Expected ROM: 140°
Alternate Position: Prone lying with the femur stabilized. Knee flexion motion may be
decreased as the rectus femoris is now stretched over two joints.
Prevent substitute motion of hip abduction and/or hip flexion.

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Knee Extension
Normal range of Motion: 0° - 3°

Patient: In supine position

Fixation: Hand on distal

femur (NOT on
patella !)

Mobilisation: On the distal part of

the tibia, mobilising
in extension

Compensation: Flexion of the hip

Note: During knee extension, the hamstring muscles are stretched. If knee extension is tested
with the hip flexed, it is possible that the hamstring muscles restrict the full extension of
the knee. Therefore, always test knee extension with the hip being in extension or neutral
position.
Knee Extension:
Measurement Tool: Universal Goniometer
Testing Position: Supine with hips and knees in neutral rotation; distal leg on bolster
Stabilization: Trunk and pelvis stabilized by body weight and position
Goniometer Axis: Lateral Epicondyle of the femur
Proximal Arm: Parallel to the long axis of the femur & pointing at the greater
trochanter
Distal Arm: Parallel to the long axis of the fibula and pointing at the lateral
malleolus
Movement: Knee extension
Expected ROM: 0° - 3°. Hyperextension may be present up to 10-15°
Alternate Position: Prone lying heel height technique

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Knee Flexion Contracture

A knee flexion contracture can

occur for several reasons:
o If the quadriceps muscle is
paralysed or weak, it can
not counteract upon the
constant pull in flexion of
the hamstring muscles.
This can result in a flexion
contracture of the knee, if
the patient does not
regularly exercise to
maintain full ROM of his
joints.
o An untreated knee
dislocation can result in a
non-reversible knee flexion
contracture.
o Any trauma injuring the
knee joint can, if not
treated well, result in a
knee flexion contracture.

Excessive Knee Extension

An excessive knee extension (over 5°) is called knee hyperextesion or Genu Recurvatum

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Patella Movements

Cranial-caudal movements
Patient: in supine position,
limb relaxed (no
quadriceps
contraction!)
Mobilisation: Therapist holds
patella between
thumb and index
finger and gently
moves patella caudal
and cranial.

Lateral-medial movements
Patient: in supine position,
limb relaxed (no
quadriceps
contraction!)
Mobilisation: Therapist holds
patella between
thumb and index
finger and gently
moves patella medial
and lateral.

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Ankle Plantar Flexion
Normal range of Motion: 0° - 50°

Patient: in supine position,

foot out of the table

Fixation: hand and arm on

the tibia

Mobilisation: on the dorsal side

of the foot, just
below the ankle (on
the head of the
talus)

Compensation: flexion of the knee

Talocrural Plantarflexion:
Measurement Tool: Universal Goniometer
Testing Position: Prone or supine with the knee in slight flexion
Stabilization: Therapist stabilizes the lower leg
Goniometer Axis: Lateral calcaneus at bisection of fibula and 5th metatarsal
Proximal Arm: Parallel to the long axis of the fibula and pointing towards the fibular
head
Distal Arm: Parallel to the long axis of the 5th metatarsal
Movement: The ankle is actively plantarflexed
Expected ROM: 30-50 degrees.
Alternate Position: Prone lying

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Ankle Dorsal Flexion
Normal range of Motion: 0° - 20°

Patient: In supine position,

foot out of the table

Fixation: Hand on posterior

distal part of the
tibia

Mobilisation: Holding the foot on

the medial side,
mobilising in dorsal
flexion

Compensation: None knee

hyperextension

Talocrural Dorsiflexion:
Measurement Tool: Universal Goniometer
Testing Position: Prone with ankle off edge of table and knee extended
Stabilization: Manual stabilization of tibia against the supporting surface
Goniometer Axis: Lateral calcaneus at bisection of fibula and 5th metatarsal
Proximal Arm: Parallel to the long axis of the fibula and pointing towards the fibular
head
Distal Arm: Parallel to the long axis of the 5th metatarsal
Movement: The ankle is actively dorsiflexed
Expected ROM: 10° with knee extended; increased to 20 with the knee flexed
Substitutions: Therapist must monitor for subtalar pronation. Watching for calcaneal
eversion can monitor this.
Alternate Test: The above procedure should be repeated with the knee flexed 90° to
isolate soleus flexibility. A 10° increase in ROM to 20° should be
expected

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Foot Inversion
Normal range of motion: 0° - 30°/40°

Patient: In supine position,

foot out of the
table

Fixation: Hand on distal

part of the tibia

Mobilisation: Holding the

calcaneus,
mobilising in
inversion

Compensation: None (Leg

Abduction)

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Foot Eversion
Normal range of motion: 0° - 15/25°

Patient: In supine position,

foot out of the table

Fixation: Hand on distal part of

the tibia

Mobilisation: Holding the

calcaneus, mobilising
in eversion

Compensation: None (Leg Abduction)

Subtalar Inversion/Eversion (alternative test position):

Measurement Tool: Universal Goniometer
Testing Position: Standing with bilateral stance
Stabilization: No stabilization necessary
Goniometer Axis: Just proximal to the achilles insertion on the calcaneus
Proximal Arm: Parallel to the distal bisection of the lower leg
Distal Arm: Parallel to the bisection of the calcaneus
Movement: Patient can perform trunk and/or tibial rotation to maximally invert and
evert the calcaneus
Expected ROM: Approximately 10° of calcaneal eversion (pronation) and 20° of
calcaneal inversion (supination) from the subtalar neutral position
Alternate Position: Prone lying or unilateral stance positions. Maximal motion and
greatest test-retest reliability has been demonstrated in the bilateral
stance position

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Metatarsophalangeal and Interphalangeal Flexion/Extension

Metatarsophalangeal and Interphalangeal Flexion/Extension:

Measurement Tool: Universal or Digit Goniometer
Testing Position: Ankle in resting position of mild plantarflexion and the STJ is in
neutral.
Stabilization: Careful stabilization of metatarsals without metatarsal compression
Goniometer Axis: Over the dorsum of the measured joint. If measuring the 1st or 5th the
axis can be placed over the medial or lateral aspect of the joints,
respectively.
Proximal Axis: Parallel to the longitudinal axis of the metatarsal of the digit being
measured
Distal Axis: Parallel to the longitudinal axis of the metatarsal of the digit being
measured
Movement: Active flexion and/or extension of the distal digit being measured
Expected ROM: 1st MTP dorsiflexion - 20° passively and 60-70° actively; 1st MTP
plantarflexion - 45° 2-5 MTP - 40° plantar/dorsiflexion; 2-5 PIP flexion -
35°; 2-5 DIP flexion - 60°
Substitutions: The long toe flexors and extensors will effect ROM according to the
positioning of the more proximal joints that they cross.

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4.5 MUSCLE TESTING

What is the purpose of muscle testing?

Muscle testing is a mean to evaluate the strength and function of muscles or muscle groups. It allows
to know the strong muscles of a patient, but also to define those who need strengthening exercises
and the ones who are paralysed.
The "academic" muscle testing tests each single muscle of the body separately, but most of the time,
especially in terms of orthotics and prosthetics, testing the muscle by functional groups is sufficient
(e.g. testing the extensors of the hip as a group, instead of testing the Gluteus Maximus, the
Semimembranosus, the Semitendinosus and the Biceps Femoris separately). Therefore, in this
course, we will only talk about the functional testing of groups of muscles performing the same
movement on a joint.
Some muscles of the body cross more than one joint and act on the movements of all the crossed
joints. Therefore, the position of the testing has to be adapted to the movement and the joint that are
tested.
Muscle shortening and consequent contractures occur if there is a muscular imbalance in a joint. For
example, if the extensors of the knee (quadriceps) are paralysed while the flexors (hamstrings) are still
strong, the constant pull of the hamstrings on the posterior side of the knee will result in a flexion
contracture (flexum) if no preventive action is taken.
What are the indications for muscle testing?
Muscle testing is a specific tool to diagnose the muscular activity. Besides in orthotics and prosthetics,
it is mainly used for injuries and illnesses of the Peripheral Nervous System such as poliomyelitis,
Guillain-Barré paralysis, polyneuropathies, muscular dystrophies, etc.
In the field of Central Nervous System lesions, it is only used to assess the exact level of a spinal cord
injury. In the case of an injury of the central nervous system, such as cerebral palsy for example,
muscle testing can not be used, as the disease alters the normal muscle tone. The different tests
would provoke muscle tremor and increase the spasticity, rendering the muscles assessment
meaningless.
What are contraindications and precautions to muscle testing?
As said above, contra-indications include several lesions of the Central Nervous System. Furthermore,
a muscle testing should not be done in the following cases:
• inflammation of the region to be tested
• pain in the region to be tested: pain would alter the muscle contraction and would not give an
accurate indication of the real strength of the muscles
• conditions that might worsen with fatigue of the patient: malnutrition, multiple sclerosis,
poliomyelitis in the acute phase, myopathies, etc.

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Levels of Muscle Strength: Grading (Oxford Scale)

0 No visible and/or palpable muscle contraction

0% of the normal muscle strength

1 No movement, but visible and/or palpable muscle contraction

10% of the normal muscle strength

1+ Movement without gravity, less than ½ of the complete range of motion

2- Movement without gravity, more than ½ of the complete range of motion

2 Movement without gravity, complete range of motion

25% of the normal muscle strength

2+ Movement with gravity, less than ½ of the complete range of motion

3- Movement with gravity, more than ½ of the complete range of motion

3 Movement with gravity, complete range of motion

50% or normal muscle strength

4 Movement in the complete range of motion, with minimal manual resistance

75% of normal muscle strength

5 Movement in the complete range of motion, with maximal manual resistance

100% of normal muscle strength

Remark: if you are not sure if the resistance is minimal (level 4) or strong (level 5) as
compared to the normal force of the patient, test the same muscle on the other limb

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Principles of Testing
The muscle testing has to be adapted to the pathology and the general health of the patient. If he/she
is not able to perform the muscle test in the "normal" position, this has to be mentioned on the chart.
Furthermore, in order not to weaken the patient too much, the best is to perform all the muscle tests in
one given position (i.e. sitting, lying prone, etc.) before asking the patient to change position. In order
to facilitate this procedure, you will find below a summary of what muscle groups are to be tested in
which position.
The normal proceeding of a muscle testing is the following:
1. Place the patient in the correct position to test the muscles at strength 3 (see above)
If the patient can not take this position, mention the testing position on the chart.
2. Stabilise the segment of the body that has to remain fixed during the test, in order to allow only the
tested segment to move.
3. Test the muscle length by testing the passive range of motion of the joint.
If there is a limitation of the range of motion, it has to be mentioned on the chart.
4. Perform the muscle test
If the patient can not move the joint in the complete range of motion, or compensates the
movement, test the active insufficiency.
5. Palpate the muscle in mid-range of motion to feel its contraction and be sure that it is the tested
muscle that is performing the movement.
6. If the patient can move the joint in the complete range of motion in the position of strength 3, then
oppose a manual resistance to the movement to test strength 4 and 5
- If the test in position of strength 3 is negative (i.e. incomplete range of motion,
compensation, etc.), test the muscle in position of strength 2

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Hip Flexion

Main muscle: Ilio-psoas (L2-L3)

Position 3-4-5

Patient: sitting on the table, whole thighs resting on

the table, legs hanging down. Hands hold the edge of
the table while the patient performs flexion of the hip

Fixation: on the pelvis

Resistance (4-5): anterior, just above the knee

(never on the patella !)

Palpation: on the anterior side of the thigh, just above

the knee or just below the flexion crease at the hip

Compensation: posterior tilt of the pelvis

Position 2

Patient: lying on infra-lateral side, the therapist holds

the supra-lateral (upper) leg in abduction

Fixation: on the infra-lateral pelvis

Positions 1 – 0

Patient: lying in supine position, the therapist holds

the limb in flexion, while the patient tries to contract
the hip flexion muscle

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Hip Extension

Main muscles:

1. Gluteus maximus (L5-S2)

2. Semi-tendinosus (L4-S2)

3. Semi-membranosus (L5-S2)

4. Biceps femoris(S1-S3)

Positions 3 – 4 – 5

Patient: lying in prone position (on the belly), knees

in extension, extends the hip

Fixation: on the pelvis

Resistance (4-5): posterior, just above the knee

Palpation: on the buttock

Compensation: anterior tilt of the pelvis and lumbar

hyperextension

Position 2

Patient: lying on infra-lateral side, the therapist holds

the supra-lateral (upper) leg in abduction

Fixation: on the pelvis

Positions 1 – 0

Patient: same as position 3, trying to contract the hip

extensor muscles

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Hip ABDuction

Main muscle: Gluteus medius (L4-S1)

Positions 3 – 4 – 5

Patient: lying on supra-lateral side, infra-lateral knee

slightly flexed (for stability of the position) performs
complete abduction of the supra-lateral hip, in the
axis of the body

Fixation: on the pelvis

Resistance (4-5): lateral, just above the knee

Palpation: on the lateral side of the pelvis, just above

the greater trochanter

Compensation: flexion or extension or external

rotation of the hip

Position 2

Patient: lying in supine position (on the back), other

leg slightly abducted

Fixation: on the pelvis

Positions 1 – 0

Patient: same as position 2, trying to contract the

hip abductor muscles

Clinical test: When walking, during the single stance phase, the hip abductor muscles of the
supporting leg have to contract to keep the pelvis level. In case of weakness or paralysis of the hip
abductors, the pelvis on the contra-lateral side will drop. This is called the Trendelenburg sign.

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Hip ADDuction

Main muscles:

1. Adductor magnus (L2-L4)

2. Adductor brevis (L2-L3)

3. Adductor longus (L2-L4)

4. Pectinueus (L2-L4)

5. Gracilis (L3-L4)

Positions 3 – 4 – 5

Patient: lying on the infra-lateral side,

physiotherapist supports the supra-lateral leg

Fixation: on the pelvis

Resistance (4-5): medially, just above the knee

Palpation: on the medial face of the thigh, just below

the ischio-pubic rami

Compensation: flexion or external rotation of the hip

Position 2

Patient: lying in supine position (on the back), other

leg largely abducted

Fixation: on the pelvis

Positions 1 – 0

Patient: same as position 2, trying to contract the

hip adductor muscles

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Hip External (Lateral) Rotation

Main muscles:

1 + 2. Obturator muscles (L3-S3) (external and

internal)

3. Quadratus femoris (L5-S1)

4. Piriformis (S1-S2)

5 + 6. Gemellus muscles (L5-S3) (inferior and

superior)

Positions 3 – 4 – 5

Patient: sitting on the table, whole thighs resting on

the table, legs hanging down. Hands hold the edge of
the table. While performing the external rotation, the
leg and foot will move medially

Fixation: on the pelvis

Resistance (4-5): medially, just above the ankle

Palpation: posterior of the great trochanter, deep

palpation

Compensation: abduction and extension of the hip

Position 2

Patient: lying in supine position (on the back), leg in

internal rotation

Fixation: on the pelvis

Positions 1 – 0

Patient: same as position 2, trying to contract the

external rotator muscles

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Hip Internal (Medial) Rotation

Main muscles: Gluteus minimus (L4-S1)

Positions 3 – 4 – 5

Patient: sitting on the table, whole thighs resting on

the table, legs hanging down. Hands hold the edge of
the table. While performing the internal rotation, the
leg and foot will move laterally

Fixation: on the pelvis

Resistance (4-5): laterally, just above the ankle

Palpation: just behind a line between the anterior-

superior iliac spine and the great trochanter

Compensation: abduction and flexion of the hip

Position 2

Patient: lying in supine position (on the back), leg in

external rotation

Fixation: on the pelvis

Positions 1 – 0

Patient: same as position 2, trying to contract the

internal rotator muscles

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Knee Extension

Main muscles: Quadriceps, composed of:

1. Rectus femoris (L2-L4)

2. Vastus intermedius (L2-L4)

3. Vastus medialis (L2-L4)

4. Vastus lateralis (L2-L4)

Positions 3 – 4 – 5

Patient: sitting on the table, whole thighs resting on

the table, legs hanging down. The patient leans
backwards and rests on his hands behind his back

Fixation: on the pelvis (but avoid the anterior

superior iliac spine, origin of the rectus femoris
muscle)

Resistance (4-5):manterior, just above the ankle

Palpation: the muscle fibres are palpated just above

the knee, the tendon between the patella and the tibial
tuberosity

Compensation: posterior tilt of the pelvis

Position 2

Patient: lying on infra-lateral side, the therapist holds

the supra-lateral (upper) leg in abduction

Fixation: above the infra-lateral knee

Positions 1 – 0

Patient: lying in supine position, therapist holds knee

in slight flexion while the patient tries to contract the
knee extension muscles

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Knee Flexion

Main muscles: Hamstrings, composed of:

1. Biceps femoris (L4-S3)

2. Semi-tendinosus (L4-S3)

3. Semi-membranosus (L4-S3)

Positions 3 – 4 – 5

Patient: lying in prone position (on the belly), legs

straight

Fixation: on the pelvis

Resistance (4-5): posterior, just above the ankle

Palpation: on the posterior face of the knee, lateral

and medial of the popliteal area

Compensation: anterior tilt of the pelvis

Position 2

Patient: lying on infra-lateral side, the therapist

holds the supra-lateral (upper) leg in abduction

Fixation: above the infra-lateral knee

Positions 1 – 0

Patient: same as position 3, therapist holds knee in

slight flexion while the patient tries to contract knee
flexion muscles

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Ankle Dorsal Flexion

Muscle: Tibialis anterior (L4-S1)

(Dorsal flexion by the tibialis anterior muscle always

includes inversion !)

Positions 3 – 4 – 5

Patient: sitting on the table, whole tights resting on

the table, legs hanging down

Fixation: on the leg, above the ankle

Resistance (4-5): on the dorsal side of the foot, on

the metatarsals

Palpation: on the anterior-medial face of the ankle

Compensation: extension of the toes

Position 2

Patient: same as position 3, but incomplete range of

motion

Fixation: same as for position 3

Positions 1 – 0

Patient: same as position 3, trying to contract the

ankle dorsal flexor muscle.

Clinical test: make the patient walk on his heels

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Ankle Plantar Flexion

Main muscles: Triceps sural, composed of

1. Gastrocnemius (S1-S2)

2. Soleus (S1-S2)

Positions 3 – 4 – 5

Patient: standing on the limb to test and lifts himself up

on the toes.

Rating: 1x = 3; 5x = 4; 10x = 5

OR

Patient is lying in supine position (on his back). The

therapist resists the plantar flexion by attracting the
calcaneus downwards. This position of test can not get a
rating of 5, as only the bearing of the body-weight can
test the normal strength of the triceps sural.

Palpation: the muscle fibers are palpated below the

popliteal area of the knee, the tendon just above the
calcaneus

Compensation: inversion/eversion of the foot

Position 2

Patient: lying on infra-lateral side, knee in extension,

and performs plantar flexion

Fixation: on the leg, above the ankle

Positions 1 – 0

Patient: same as position 2, trying to contract the

plantar flexion muscles

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Foot Inversion

Main muscle: Tibialis posterior (L5-S1)

Positions 3 – 4 – 5

Patient: lying on infra-lateral side, ankle in plantar

flexion

Fixation: on the leg, above the ankle

Resistance (4-5): hand on the medial part of the foot,

pushing towards eversion

Palpation: between the medial malleoli and the

navicular tuberosity

Compensation: dorsal flexion, flexion/extension of

toes, internal rotation of the knee

Position 2

Patient: lying in supine position (on the back), ankle

in plantar flexion, foot out of the table

Fixation: on the leg, above the ankle

Positions 1 – 0

Patient: same as position 2, trying to contract the

foot inversion muscle

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Foot Eversion

Main muscles:

1. Peroneus longus (L4-S1)

2. Peroneus brevis (L4-S1)

Positions 3 – 4 – 5

Patient: lying on supra-lateral side, ankle in plantar

flexion

Fixation: on the leg, above the ankle

Resistance (4-5): hand on the lateral part of the foot,

pushing towards inversion

Palpation: just posterior to the lateral malleoli

Compensation: dorsal flexion of the ankle, external

rotation of the knee, flexion/extension of the toes

Position 2

Patient: Patient lying in supine position (on the

back), ankle in plantar flexion, foot out of the table

Fixation: on the leg, above the ankle

Positions 1 – 0

Patient: Same as position 2, trying to contract the

foot eversion muscles

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Extension of the Toes

Main muscles:

1. Extensor digitorum longus (L4-S1)

2. Extensor digitorum brevis (L5-S1)

3. Extensor hallucis longus (L4-S1)

Positions 3 – 4 – 5

Patient: lying in supine position (on the back)

Fixation: on the metatarsals

Resistance (4-5): on the dorsal part of the toes,

pushing towards flexion

Palpation: the tendons of the ext. digitorum longus

can be palpated on the dorsal face of the
metatarsals, the muscular fibers of the ext.
digitorum brevis just in front of the lateral malleoli
and the tendons of the ext. hallucis longus on the
dorsal face of the first metatarsophalangeal joint

Compensation: plantar flexion of the ankle

Position 2

Patient: same as position 3, incomplete range of

motion

Positions 1 – 0

Patient: same as position 3, trying to contract the

extensors of the toes

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Flexion of the Metatarsal-Phalangeal Joint

Main muscles:

1. Lumbricales (L4-L5)

2. Flexor hallucis brevis (S1-S2)

Positions 3 – 4 – 5

Patient: lying in supine position (on the back)

Fixation: on the metatarsals

Resistance (4-5): on the plantar part of the toes,

pushing towards extension

Palpation: not possible

Compensation: abduction of the toes, extension of

the toes

Position 2

Patient: same as position 3, incomplete range of

motion

Positions 1 – 0

Patient: same as position 3, trying to contract the

flexors of the toes

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Positions for Muscle Testing of the Lower Limb
A. Sitting
• Hip: flexion – 3
• Hip: external rotation – 3
• Hip: internal rotation – 3
• Knee: extension – 3
• Ankle: dorsal flexion – 3 + 2

B. Lying in supine position (on the back)

• Hip: abduction – 2
• Hip: adduction – 2
• Hip: external rotation – 2
• Hip: internal rotation – 2
• Foot: eversion – 2
• Foot: inversion – 2
• Foot: extension of the toes – 3 + 2
• Foot: flexion of the toes – 3 + 2

C. Lying in prone position (on the belly)

• Hip: extension – 3
• Knee: flexion – 3

D. Lying on the supra-lateral side

• Hip: abduction – 3

E. Lying on the infra-lateral side

• Hip: flexion – 2
• Hip: extension – 2
• Hip: adduction – 3
• Knee: extension – 2
• Knee: flexion – 2
• Ankle: plantar flexion - 2
• Foot: eversion – 3
• Foot: inversion – 3

F. Standing
• Ankle: plantar flexion

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4.6 JOINT STABILITY

The stability of a joint depends on the good and strong active (muscles) and passive (ligaments,
capsule, etc.) structures surrounding the joint. Stability is essential for a physiological functioning and
a good alignment of the joint.
A lack of stability in a joint, whether due to active or passive structures deficiencies, can cause:
• Misalignment of the joint
• Overstress of the passive and active structures of the joints, resulting in dislocations, non-
inflammatory arthritis (over-use of the joint), etc.
• Various gait deviations

Valgus of the Knee Knee Hyperextension

Knee Dislocation Hip Dislocation

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Hip Joint

Instability of the hip joint can occur as a result of:

• Active insufficiency (muscular weakness or paralysis)
• Passive insufficiency (rupture or weakness of ligaments, joint capsule)
The lack of stability will manifest itself by:
• Misalignment of the hip joint in the different planes
• Overstress of the joint structures (•degeneration)
• Luxation of the hip joint (dislocation)
• Gait deviations

The Trendelenburg test (lateral instability of the hip and pelvis)

When standing on one leg, the pelvis is stabilized in the frontal plane by the M. Gluteus medius of the
stance leg, who works in a closed chain: the distal segment (femur) being stable, it is the proximal
segment (pelvis) that is mobilised by the contraction of the muscle. This means that the pelvis, instead
of dropping on the unsupported side, will remain horizontal, or even rises a little.
A positive Trendelenburg test means that the pelvis drops on the unsupported side. This is due to an
impaired function of the weight bearing hip in terms of insufficient muscular stabilisation by the M.
Gluteus medius.

A. Normal, patient standing on both legs

B. Negative Trendelenburg test: when the patient stands on the right leg, the left pelvis rises a
little: his right hip is stable, the Gluteus medius muscle is functional.
C. Positive Trendelenburg test: when the patient stands on the right leg, the left pelvis drops: his
right hip is not stable, the Gluteus medius muscle is not functional.

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Knee Joint

The knee has a very important position in the statics of the lower limb and is relatively often subject to
trauma.
As the bones do not offer any stability of the knee joint, due to their shape, it gets its stability
exclusively from ligaments (passive structures) and muscles (active structures).
In full knee extension, the collateral ligaments, parts of the cruciate ligaments and the posterior
capsule are tight. In flexion of the knee, the collateral ligaments are mainly relaxed. This is an
important point to bear in mind when testing the knee for instability. In a fully extended knee there
must be no anterior-posterior glide and no medial-lateral movement !

The drawer test (anterior – posterior instability of the knee)

The patient is lying on the table in supine position,

the tested knee flexed at 90°.

The assessor stabilises the foot of the patient by

sitting very close in front of the foot (the ischial
tuberosity of the Assessor sits just in front of the foot
of the patient).

The Assessor tries to mobilise the tibia anterior-

posterior.

Positive anterior drawer sign: when pulling the tibia anterior,

the displacement under the femur is excessive (2-3cm).

This means that the anterior cruciate ligament, and probably

the posterior capsule of the knee are injured.

1. Anterior cruciate ligament

2. Posterior capsule of the knee

Positive posterior drawer sign: when pushing the tibia

posterior, the displacement under the femur is excessive (over
5mm).

This means that the posterior cruciate ligament is injured.

3. Posterior cruciate ligament

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The valgus-varus test: (medial – lateral instability of the knee)
The patient sits or lies on the table. The Assessor holds the patient's limb with a slight flexion of the
knee (20°-30°).
With one hand, the Assessor stresses on the lateral side of the knee, testing the medial collateral
ligament stability, and then on the medial side, testing the lateral collateral ligament stability.

A. Positive valgus test: when pushing from the lateral side, the medial collateral
ligament can not ensure the medial stability of the knee. The knee will bend into
valgus during the test
B. Positive varus test: when pushing from the medial side, the lateral collateral ligament
can not ensure the lateral stability of the knee. The knee will bend into varus during
the test.

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Tibio Fibular Joints (Anterior and Posterior Tibiofibular Ligaments)

Tibiofigular Joint

Proximal Tibiofibular Joint

(Anterior/Posterior Glide)

• Indication: To test joint micro

movements at the tibiofibular
joint. The fibular head must
move anteriorly on knee flexion
and posteriorly on knee
extension.

• Patien: Supine with the knee

flexed to 90° with foot flat.

• Operator: Stabilize the knee

with the medial hand. Grasp
the head and neck of the
proximal fibula with the lateral
hand, the thumb contacting
anteriorly, and the index and
long finger pads contacting
posteriorly. (Be cautious of the
peroneal nerve.)

• Mobilizing Force: The lateral

hand may glide the proximal
fibula posteriorly or anteriorly.

Distal Tiobiofibular Joint

(Posterior Glide)

• Indication: To test the joint

mortise spread during
dorsiflexion.

• Patient: Supine with knee in

extension.

• Operator: Place the fingers of

the medial hand under the
tibia and the thumb over the
tibia to stabilize it. Place the
lateral hand using thenar
eminence over the lateral
malleolus, with fingers
underneath.

• Mobilizing Force: Glide the

lateral malleolus posteriorly
directing force through the left
thenar eminence.

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Ankle Joint (Talo-Crural Joint)

The stability of the ankle depends on an intact function of the muscles and ligaments surrounding the
ankle. Insufficiency of the active or passive stabilizers results in misalignment of the joint.
The stability tests of the ankle assess the integrity of the lateral ligaments stabilising the lateral
malleolus. These ligaments are often injured during a sprain of the ankle.

The anterior drawer test: (anterior talo-fibular ligament) (Ventral glide)

• Indication: To test
anterior talofibular
ligament (increased
plantar flexion).

• Patient: Prone with

knee relaxed and foot
over the edge of the
plinth.

• Operator: Operator's
cranial hand grasps the
anterior/distal surface
of the tibia and fibular.
The caudal hand
contacts the posterior
talus/calcaneus with
the web space.

• Mobilizing Force:
Glide the calcaneus
and talus downward in
an anterior direction.

The Assessor fixes the

distal tibia with one hand,
while the other hand,
holding the calcaneus, is
pulling the foot anterior.

If the anterior displacement

of the foot under the tibia is
excessive (more than
0.5cm), the test is positive,
meaning that the anterior
talo-fibular ligament is
injured.

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The posterior drawer test (Dorsal glide) (Posterior Talofibular ligament)

• Indication: To Test Posterior

talofibula ligament, incresed
dorsiflexion.

• Patient: Supine and relaxed with

heel over the edge of the plinth.

• Operator: Stabilize the distal tibia

against the plinth with the cranial
hand, wrapping the fingers around
posteriorly. The web of the caudal
hand grasps the neck of the talus
with the fingers wrapped around
the foot.

• Mobilizing Force: Glide the talus

posteriorly on the tibia.

The lateral drawer test: (talo-fibular and calcaneo-fibular ligaments)

The Assessor fixes the lateral

malleolus with his thumb. The other
thumb is placed on the
Sustentaculum Tali, pushing the talus
into inversion (from medial towards
lateral).

If the inversion is excessive, the test is

positive, meaning that the anterior
talo-fibualr and the calcaneo-fibular
ligaments are both injured.

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Subtalar Joint

Medial Glide (Lateral Ligaments)

• Indication: To Test lateral

ligaments. Increased medial glide
of the calcaneus on the talus.

• Patient: Sidelying with leg

supported on the table and lateral
side up.

• Operator: Align shoulder and arm

parallel to the bottom of the foot.
Stabilize the talus with your
proximal hand. Place the base of
the distal hand on the side of the
calcaneus laterally and wrap the
fingers around the plantar
surface.

• Mobilizing Force: Apply a glide

medially.

Lateral Glide (Medial Ligaments)

• Indication: To Test medial
ligaments. Increase lateral
glide of the calcaneus on the
talus.

• Patient: Sidelying with leg

supported on the table and
the medial side up.

• Operator: Align shoulder

and arm parallel to the
bottom of the foot. Stabilize
the talus with your proximal
hand. Place the base of the
distal hand on the side of the
calcaneus medially and wrap
the fingers around the
plantar surface.

• Mobilizing Force: Apply a

glide laterally.

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Midtarsal Joint

These test can be used for the talonavicular joint, calcaneocuboid joint, naviculocuneiform joint, or the
cuneiformmetatarsal joints.
Plantar Glide
• Indication: To test (increased) the
medial arch of the foot.

• Patient: Supine with the knee

relaxed.

• Operator: Fixate the more

proximal bone with your finger by
grasping dorsally at the level of the
talar neck, the thumb wraps
around laterally and the rest of
the fingers wrap around medially.
The other hand grasps the
navicular, the thumb contacts
dorsally and the hand and fingers
wrap around the foot medially and
plantarly.

• Mobilizing Force: Move the distal

bones plantarly.

Dorsal Glide

• Indication: To test (decreased) the

medial arch of the foot.

• Patient: Prone with knee flexed.

• Operator: Fixate the calcaneus

with one hand. With your other
hand, wrap your fingers around
the lateral side of the foot.

• Mobilizing Force: Move the distal

bones in a dorsal direction.

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4.7 LEG LENGTH MEASUREMENT

It is very important to measure the leg length of any non-amputated patient. A discrepancy in the leg
length can, after a while, create compensatory problems in the back or the different joints of the lower
limb.
When measuring the leg length discrepancy, the Assessor has to make the difference between real
leg length discrepancy and apparent leg length discrepancy.

Real Leg Lenth Discrepancy

The real leg length discrepancy is

measured from one fixed bony
reference point to another fixed
bony reference point.

The measure is taken from the

anterior superior iliac spine (ASIS)
to the medial malleolus, passing
the measuring tape through the
medial side of the knee.

If there is a leg length discrepancy, it is possible to measure if this discrepancy comes

from the femur or from the tibia:

• Measure the length of the femur from the ASIS to the medial knee joint line

• Measure the length of the tibia from the medial knee joint line to the medial
malleolus

It is also possible to visually identify which bone is responsible for the shortening. When
the patient is lying on the table with both knees flexed at 90° and the feet at the same
level, watch the knees:

• If the knee is lower when observed from the front, it is the tibia which is shorter

• If the knee is lower when observed from the side, it is the femur which is shorter

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Apparent Leg Length Discrepancy

The apparent leg length discrepancy is

measured from a non-fixed reference
point to a fixed bony reference point.

The measure is taken from the navel

(umbilicus) to the medial malleolus,
passing the measuring tape through
the medial side of the knee.

Measuring the apparent leg length

discrepancy is only useful for a patient
having a severe pelvis obliquity.

Example:

The patient on the right seems to have

a severe shortening of the left leg.
Indeed, when measuring the apparent
leg length, it appears that the
difference between both legs is several
cm.

Nevertheless, when measuring the real

leg length discrepancy, from ASIS to
malleoli, it appears that the patient
has no leg length discrepancy at all.

The cause of his apparent leg length

discrepancy comes from the oblique
pelvis.

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 V. BIOMECHANICS

5.1 MECHANICS – LEVERAGE/MOMENT

Leverage

Mechanical leverage refers to the amplification of force with the use of levers. It is comprised of three
elements, namely, a fulcrum, an input effort, and an output load or resistance. Depending on the
relative locations of these elements, the lever has three categories – first class, second class, and
third class.
In a first class lever, the fulcrum is located between the input effort and resistance as shown in Figure
59.

Figure 59: First class lever.

In a second class lever, the output force or resistance is located between the input force and the
fulcrum, shown in Figure 60.

Figure 60: Second class lever.

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In a third class lever, the input force is located between the output force and the fulcrum as shown in
Figure 61.

Figure 61: Third class lever.

Moment

Moment is the tendency of a force to rotate an object about a fulcrum (pivot point). It can be expressed
as M = Fd, where F is the applied force and d is the perpendicular distance between the force and the
fulcrum as shown in Figure 62.

Figure 62: Moment.

As an object rotates around a fulcrum, points farther from the pivot have a longer lever arm than points
closer to the pivot. A force applied to a point farther from the pivot must be less than the force located
at a point closer in order to create the same amount of moment about the fulcrum. For the system
shown n Figure 63 to be in equilibrium, M1 must be heavier than M2 as M1 has a shorter lever arm.

Figure 63: A lever in equilibrium.

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5.2 MECHANICS – STRESS

Stress measures the average force per unit area of a surface within a deformable body on which
internal forces act. The internal forces are produced between the particles in a body as a reaction to
external forces.
Stress is therefore expressed as the force applied to a surface divided by the area of the surface. It is
measured in psi (English unit) or in Pa (SI unit).

Stress = Force / Area

Stress can be classified as normal stress, shear stress, and bearing stress.

Normal Stress

Normal stress develops when a force is applied perpendicular to the cross-sectional area of the
material as shown in Figure 64. It is expressed by
F
δ =
A
where F is the applied normal (perpendicular) load in Newton and A is the area on which the force is
2
applied in m .

Figure 64: Normal stess.

There are two types of normal stress; tensile stress and compressive stress. A material is subjected to
a tensile stress when the applied force pulls the material and compressive stress is developed hen the
material is being compressed by two opposing forces (Figure 65).

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 Figure 65: Direction of an applied force relative to the cross-sectional area through which it is applied
determines the type of stress experienced by the body.

Shear Stress

Figure 66: Shear stress..

Shear stress is developed if the applied force is parallel to the resisting area (Figure 66 and 67). Shear
stress is also known as tangential stress and is expressed as:

Fs
τ =
A
where Fs is the resultant force which passes through the centroid of the area A being sheared.

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 Figure 67: Types of shearing.

Shearing Deformation
Shearing forces cause shearing deformation as shown in Figure 68. An element subject to shear does
not change in length but undergoes a change in shape.

Figure 68: Shearing deformation.

Bearing Stress

Bearing stress is the contact pressure between two separate bodies (Figure 69). It differs from
compressive stress, as it is an internal stress caused by compressive forces.

Figure 69: Bearing stress.

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Strain

Figure 70: Bearing stress.

Strain is the ratio of the change in length caused by the applied force, to the original length. It is also
known as unit deformation.
Based on Figure 70,
δ
Strain(ε ) =
L

Stress-Strain Diagram
The graph of the normal stress • and the strain •, with the stress • along the y-axis and the strain •
along the x-axis is called the stress-strain diagram (Figure 71). Different materials have different
stress-strain diagram that is unique to the physical properties of the material.
Elastic Limit: is the maximum stress that may be developed such that there is no permanent or
residual deformation when the load is entirely removed. In other words, it is the limit beyond which the
material will no longer go back to its original shape when the load is removed.
Elastic Range: is the region from the origin to the elastic limit in the stress-strain diagram shown in
Figure 71.
Ultimate Strength: is the maximum stress that a material can withstand while being stretched or
pulled before necking, which is when the specimen's cross-section starts to significantly contract.
Failure: is the stress at which a material ruptures/fractures/breaks.

Figure 71: Stress-strain diagram.

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5.3 MECHANICS – TORSION

Torsion

Torsion is the twisting of an object due to an applied torque. It is expressed in N·m (SI unit). In
sections perpendicular to the torque axis, the resultant shear stress is perpendicular to the radius.
Consider a rod to be rigidly attached at one end and twisted at the other end by a torque or twisting
moment T equivalent to F x d, which is applied perpendicular to the axis of the bar as shown in Figure
72.

Figure 72: A rod in torsion.

Torsional Shearing Stress, •

For a solid or hollow circular shaft subject to a twisting moment T, the Torsional shearing stress • at a
distance • from the center of the shaft is

Tρ Tr
τ = and τ max =
J J

where J is the polar moment of inertia of the section and r is the outer radius.

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For solid cylindrical shaft:

For a hollow cylindrical shaft:

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5.4 APPLIED BIOMECHANICS

Introduction

Definition of Foot Orthosis: A foot orthosis is an in-shoe medical device which is designed to
change the magnitudes and temporal patterns of the reaction forces acting on the plantar aspect of
the foot. This allows a more normal foot and lower extremity functions and decreases pathologic
loading forces on the structural components of the foot and lower extremity during weight bearing
activities.
As shown in Figure 73, effectively managing the pathological foot with the use of foot orthosis can
have positive effects not only within the foot itself but also more proximally on the rest of the lower limb
and the trunk.

Figure 73: Effects of foot pathology and proper foot orthosis on the foot and the more proximal joints.

Categories of Foot Orthosis:

1. Non-prescription Foot Orthoses: fabricated in average sizes and shapes of feet within a
population.
2. Prescription Foot Orthoses: specifically constructed for an individual.
a. Functional Foot Orthoses: alter the function of the joints of the foot and the lower extremity
during weight-bearing activities.
b. Accommodative Foot Orthoses: alter the magnitude and temporal loading patterns of
symptomatic or injured plantar structures of the foot during weight-bearing activities.
c. Functional/Accommodative Foot Orthoses: alter both the function of the joints of the foot and
lower extremity and the magnitude and temporal loading patterns of symptomatic or injured
plantar structures of the foot during weight-bearing activities.

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Unlike most other orthotic devices, foot orthoses invariably work by realigning the ground reaction
force rather than by applying forces or moments directly to joints. For a mobile foot, in which the
deformity or malalignment is correctable, the aim of the realignment is to place the foot in its optimum
functional position. This essentially involves placing the subtalar and midtarsal joints in their neutral
positions. For a rigid foot with fixed deformities, the aims may be to accommodate deformity, to
redistribute plantar pressure, to relieve dorsal pressure, or to realign the plantar surface of the shoe in
order to obtain more normal contact forces.

Biomechanics of the Ankle-Foot Complex

The biomechanics of the foot and ankle are important to the normal function of the lower
extremity. The foot is the terminal joint in the lower kinetic chain that opposes external
resistance. Proper arthrokinematic movement within the foot and ankle influences the ability of
the lower limb to attenuate the forces of weight bearing.
It is important for the lower extremity to distribute and dissipate compressive, tensile,
shearing, and rotatory forces during the stance phase of gait. Inadequate distribution of these
forces could lead to abnormal stress and the eventual breakdown of connective tissue and
muscle. The combined effect of muscle, bone, ligaments, and normal foot biomechanics will
result in the most efficient force attenuation in the lower limb. To better understand the
biomechanics we have also to consider how the structures of the human body interact with the
surrounding environment and its forces.
The movement of the human body are seldom segmental (only one joint) but most of the time, are
multi-segmental involving more segments in the limbs and more than one joint and muscle at the
same time. Because of this, the movements of the human body are classified as kinetic chain
movement. Kinetic chain movements can be divided into "Open Chain" and "Closed chain
movements".
Open Chain: When the chain is open, a twisting force at one end causes rotation of the other. As it
rotates it "untwists" the chain and so no torsion stress occurs.
Closed Chain: If the end of the chain is fixed, the chain will not be able to “untwist”. Any rotation at
one end (joint) produces tortional stress across the joints in the chain. The greater the rotation, the
higher the tortional stress.
Combination: The lower limb frequently acts as a closed chain when the foot is fixed to the ground
by the body weight. However, if the foot is free, as it is during the “swing” phase of walking, it becomes
an open chain. It is important to realize that either the distal (furthest from the trunk) or proximal
(closest to the trunk) end of a limb may be free to move and so “open” the chain. Take for example, a
foot fixed to the ground – if the rotation force is strong enough it will move the proximal segment (the
trunk) and this trunk rotation will untwist the chain.

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Functional Components of the Foot

The foot can be divided into the following three functional regions:
1. the rearfoot: composed of the talus and calcaneus
2. the midfoot: consists of the navicular, cuboid, and cuneiform bones
3. the forefoot: includes the metatarsals and their respective phalanges

Figure 74: The bones and functional components of the foot.

The regions of the foot function as interdependent units during the stance phase of gait. Alterations in
mobility and function of any region have an impact on structures both intrinsic and extrinsic to the foot.

Important Articulations of the Ankle-Foot Complex

1. Ankle Joint: articulation between the tibia, fibula, and talus

2. Subtalar Joint (STJ): articulation between the calcaneus and talus
3. Midtarsal Joint (MTJ): the talonavicula and calcaneocuboid articulations between the midfoot and
rearfoot

Figure 75: The joint structures of the foot. The Talonavicular Joint and the Calcaneocuboid Joint make up the
Midtarsal Joint of the foot.

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Motions of the Ankle-Foot Complex

The motions of the ankle-foot complex can be defined operationally by motion in the sagittal, frontal,
and transverse planes.
1. Sagittal Plane Motions of the Ankle-Foot Complex: dorsiflexion and plantarflexion
2. Frontal Plane Motions of the Ankle-Foot Complex: eversion and inversion
3. Transverse Plane Motions of the Ankle-Foot Complex: abduction and adduction
Although the motions of the foot and ankle are defined in terms of the cardinal planes, the true
mechanical axes of the joints of the foot complex for the most part are not perpendicular to these
cardinal planes but lie at some oblique orientation to these planes (Figure 76). Because motions of the
foot occur perpendicular to the axis of rotation, it follows that these motions occur in planes other than
the cardinal planes. The motions that occur in planes that pass through all three cardinal planes are
known as triplanar motions.

Figure 76: Details of joint axes in the foot indication their orientation projected onto the Sagittal plane and
the transverse plane respectively.

The terms pronation and supination are used to describe the triplanar motions of the foot. Pronation
refers to the combined movements of abduction, dorsiflexion, and eversion. Supination refers to
adduction, plantarflexion, and inversion. The nonweigth-bearing motions of the foot can be described
in relationship to the relatively "fixed" tibia and fibula, shown in Figure 77 and Figure 78.

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 Figure 77: Pronation and supination of a nonweigth-bearing foot.

Figure 78: Triplanar motions of the foot.

During the stance phase of the gait (when the foot is bearing load), movements of the STJ cause
rotational movements of the leg, and indirectly, the thigh. Pronation of the STJ results in the medial
rotation of the talus and therefore internal rotation of the leg. Conversely, supinating movements of the
STJ cause external rotation of the leg. The ankle mortise shown in Figure 79 is responsible for this
mechanism of the foot during the stance phase of the gait.

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 Figure 79: The principle of the ankle mortise.

Static and Dynamic Structures of the Ankle-Foot Complex

(This section of this document is a reading assignment for students)
Normal biomechanics of the foot and ankle can be divided into static and dynamic components. The
static structures include the bones, joint surface congruity, ligaments, and fascia. The dynamic
components include the arthrokinematics of the tarsal bones and muscle function.
Static Structures
Muscle activity is not necessary to support the fully loaded foot at rest. The maintenance of the arch in
the static foot is attributed to ·passive ligamentous and osseous support.
When analysing the static structure of the foot, the importance of the "beam action" of the metatarsals
and the tension strength of the plantar aponeurosis have to first be emphasized. I n the static stance
position, the beam action of the meta-tarsals takes up approximately 25% of the stress of weight
bearing and the plantar aponeurosis takes up approximately 60% of the stress. The ability of the
plantar aponeurosis to absorb stress increases as the aponeurosis becomes taut with toe extension
(the widlass effect).
The short and long plantar ligaments and the calcaneonavicular ligament (spring ligament) also assist
in the passive maintenance of the arch.

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 Truss-and-beam Mechanics of the Foot
A curved beam and a truss (Figure below) are frequently used when
modeling the medial arch of the foot. Beams are designed to withstand
bending under an applied force. A truss is a triangular framework with 2 rigid
supports connected together at its base. Because the ends of the foot are not
secure at the beginning of stance, the foot functions like a beam. As the
weight of the body transfers forward, the calcaneus and the heads of the
metatarsals are pressed to the ground, with the arch functioning as a truss.
Truss-and-beam mechanics of the foot rely on the first ray to function as the
pillar for the medial arch. The first ray, therefore, is a critical element in
controlling the structural integrity of the foot.

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 The Windlass Effect
At maximum extension of the toes, during the push-off phase of gait, the
aponeurosis winds around the metatarophalangeal joints (MTPJs). This
twisting effect increases the tension of the tissue, allowing the plantar
aponeurosis to take on greater amounts of stress. Tension within the plantar
aponeurosis, in addition ot absorbing more stress, assists in supination of the
subtalar join.

The beam action of the metatarsals, as

described, represents the supportive
aspect of the long bones of the foot
and the metatarsal are the main
stabiliser of the foot. This is obvious
when observing the trabecular
patterns, which indicate the direction of
force transmission into the foot.
The trabecular systems follow the
alignment of the medial and lateral
arch. The surface congruity is
described as a stabilizing factor of the
tarsal bones. Joint congruity has
classically been described as a stabilizing influence in synovial joints. The joint alignment and
congruity of the metatarsal and tarsal bones are critical in establishing the medial and lateral arches.
This joint relationship is also important for normal arthrokinematics of the foot and ankle.
In summary, the static mechanisms responsible for force attenuation within the foot include the
windlass effect of the plantar aponeurosis, the tensile strength of the plantar ligaments, the beam
effect of the metatarsals, and the joint congruity of the tarsal and metatarsal bones. The dynamic
aspects of foot and ankle biomechanics work in conjunction with, and are dependent upon, the static
mechanisms.

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Dynamic Structures
Movement of the foot and ankle is a complex action involving many joints. Functionally, the foot and
ankle are similar to a closed kinetic chain. A closed kinetic chain is defined as "a combination of
several successively arranged joints constituting a complex motor unit, where the terminal joint of the
chain meets with considerable resistance."
The lower extremity is frequently described as a closed kinetic chain during the gait cycle. However,
the foot, independent of the lower extremity, may also be considered as a unit so arranged that motion
at one joint influences mechanisms of other joints within the chain.
The complex motions of the foot and ankle, which promote the interdependence of joint movement are
called pronation and supination. Pronation and supination (shown in the following figure) are described
as triplanar motions. For example, pronation includes the body plane movements of abduction,
dorsiflexion, and eversion. These three motions are derived from the transverse, sagittal, and frontal
planes, respectively. However, because the axes of motion of the triplanar joints are oblique,
traversing all three body planes, the movement of abduction, dorsiflexion, and eversion occur
simultaneously.
Supination is the triplanar motion including adduction, plantar flexion, and inversion. Supination and
pronation as described above occur in an open kinetic chain. This open kinetic chain movements are
described by observing the calcaneous in the non-weight bearing position.

The functional biomechanics of the foot and ankle are important in the weight bearing position or the
closed kinetic chain. Sixty percent of the gait cycle is weight bearing, better described as the stance
phase of gait. Supination and pronation occur at certain points in the stance phase to assist
movement, stabilize joints, and reduce forces within the foot and lower limb.
Five triplanar joints have been identified within the foot that allow pronation and supination to occur.
The triplanar joints include: the talocrual, the subtalar, the midtarsal, the first ray (first
metatarsal/cuneiform), and the fifth ray (fifth metatarsal).
Pronation: Heel Strike/Toe Strike (Closed Chain)
Pronation occurs in the stance phase of gait to allow for shock absorption, ground terrain changes,
and equilibrium. From heel strike to toe strike there are four basic forces acting on the foot and
lower limb which need to be attenuated.
Upon heel strike, 80% of body weight is directly over the calcaneous, producing a vertical force
against the ground. Bone is a specialized connective tissue designed to reduce compressive
forces. The alignment of the tibia, talus, and calcaneous at heel strike (shown in the following
figure) are important to distribute the vertical compressive forces safely.

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 From heel strike to toe strike the compressive force of
weight bearing is distributed between the calcaneous
and the metatarsal. The tarsals and the metatarsals at
footflat are in a mutual compression, very similiar to a
stone arch.
The midfoot carries virtually no weight during the
stance phase. There is also an anterior shearing force,
within the foot, of the tibia on the talus. This anterior
movement is decelerated mainly by the gastroc/soleus
muscle group. A medial shearing to the foot is
described to result from an internal rotation of the
lower limb.
The subtalar joint, consisting of the talus and the calcaneous, responds to the internal rotation and
medial shear by allowing the calcaneous to move laterally or into Valgus. The talus rolls in a medial
direction (plantarflexes and adducts) to fully articulate with the middle facet on the calcaneous. This
middle facet is formed by the medial process on the calcaneous called the sustentaculum tali.
Therefore, as the posterior aspect of the calcaneous rolls laterally, the sustentaculum tali falls
medially along with the talus (shown in the following figure). This rotation of the talus and the
calcaneous has been described as the torque converter of the lower limb.

Ambulation is a series of rotations, starting in the lumbar spine, that propel the body through space.
The transverse rotations of the tibia and the femur are transmitted and reduced at the subtalar joint.
During the stance phase of the gait the foot does not rotate. The tibia rotates medially at heel strike

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 and the talus follows resulting in pronation of the subtalar joint or a valgus heel (as shown in the
previous figure). The transverse rotations of the lower limb are converted into the triplanar motions
of pronation and supination. The midtarsal joint, which consists of the talonavicular and the
calcaneal cuboid articulations, unlocks with subtalar joint pronation. The cuboid and the navicular
become more parallel allowing the forefoot to become a loose bag of bones. The forefoot is now a
more efficient mobile adaptor to changes in ground terrain, thus facilitating equilibrium. The
midtarsal area is where the lowering and raising of the medial arch can observe.
In summary, there are many forces acting on the foot and lower limb from heel strike to toe strike.
The four we have reviewed include compression, rotation, anterior shear, and medial shear.
Normal pronation is important in attenuation of these forces. It is a passive activity, in the closed
kinetic chain, that results from internal rotation of the lower limb and a medial shear to the foot.
Pronation is initiated at heel strike and controlled by an eccentric contraction of the supinators. The
three muscles that are active from heel strike to toe strike, include tibialis anterior, extensor
digitorium longus, and extensor hallicus longus. These muscles are classified as supinators of the
foot.

Suspination: Toe Strike/Push Off (Closed Chain)

Supination occurs at the end of the stance phase of gait. It enables the extrinsic muscles to
function more efficiently and sets up a rigid lever from which to push off. This rigid lever is
established by a locking of the bones of the foot and ankle. The fixed position of the tarsals and
metatarsals allow for a muscle pulley system to be set up. Several of the extrinsic muscles are
dependent upon bony levers for proper function. For example, the peroneus longus during push-off
stabilizes the first ray. The ability of the muscle to act in this manner is dependent upon the cuboid
pulley.

Supination of the foot results from several mechanisms. First, from toe strike to push-off
(midstance) the activity of the extrinsic muscles initiate supination. EMG studies have shown during
midstance the increase in activity of the gastroc/soleus, posterior tibialis, flexor digitorium longus,
and the flexor hallicus longus. EMG studies have demonstrated the significance of the intrinsic
muscles from toe strike to push-off. The abductor digiti quinti, flexor digitorium brevis, flexor hallicus
brevis, abductor hallicus brevis, dorsal interossei, and the extensor digitorium brevis are all
important in stabilization of the midtarsal joint during the final 50% of the stance phase.
The second factor influencing supination of the foot is the external rotation of the lower limb. The
contralateral limb swings forward past the weightbearing limb initiating an external rotation force.
This external rotation causes a lateral shearing force within the foot promoting supination. The
subtalar joint initiates supination by inversion of the calcaneous. The talus is pushed into a lateral
position (abduction and dorsiflexion) by the sustentaculum tali (as shown in the following figure).
The midtarsal joint locks upon supination of the subtalar joint. This locking mechanism occurs when
the cuboid and the navicular are perpendicular to each other.The bones now act as rigid levers for
more efficient pull of peroneus longus and the posterior tibialis, respectively.Thus, a synergistic
contraction of these two muscle groups stabilize the midfoot and first ray. First ray stabilization
affords good alignment of the first MTP joint and a rigid lever for push-off.

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 The third factor influencing supination is the mobility of the first MTP joint. Dorsiflexion of the MTP
produces increased tension of the plantar aponeurosis assisting subtalar joint supination. This
mechanism was described previously as the windlass effect. The normal amount of joint range of
motion needed to facilitate this mechanism is 60-70° of passive MTP dorsiflexion.

In summary, supination of the foot is dependent upon a combination of dynamic and static
mechanisms. The activity of the intrinsic and extrinsic muscles, in conjunction with external rotation
and MTP extension produce a supination movement.

Neutral
The neutral position of the subtalar joint is described as in two-thirds from inversion and one-third
from eversion of the calcaneous. The normal foot needs to pronate and supinate 6-8° from the
neutral position. The amount of supination and pronation that is available can be measured by
lining up the longitudinal axis of the lower limb and the vertical axis of the calcaneous (shown in the
following figure). Passive movement of the calcaneous into inversion is normally 20°. This
represents the amount of supination available at the subtalar joint. Conversely, the amount of
eversion is normally 10°. This represents the amount of pronation available.

Another method of determining neutral position of the subtalar joint uses the position of the talar
head as a guide. The talar head in a pronated foot can be palpated as a medial bulge. Conversely,
in a supinated foot the talar head bulges laterally. In the neutral position, the talar head can be
palpated equally on the medial and lateral aspect of the ankle. The neutral position described
above, is usually present when the longitudinal axis of the lower limb and the vertical axis of the
calcaneous are parallel as shown in the figure above.

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 Summary:
Pronation and Supination:

PRONATION SUPINATION

Calcaneus everts inverts

plantar flexes dorsiflexes

Talus
adducts abducts

Tibia rotates internally rotates externally

Knee flexes extends

Comparison of Open and Closed Chain Subtalar Movements:

PRONATION SUPINATION

OPEN CHAIN CLOSED CHAIN OPEN CHAIN CLOSED CHAIN

(Talus is Stable) (Talus is Mobile) (Talus is Stable) (Talus is Mobile)

Calcaneus Everts Everts Inverts Inverts

Adducts Abducts
Talus (stable) (stable)
Plantarflexes Dorsiflexes

Abducts Adducts
Forefoot (stable) (stable)
Dorsiflexes Plantarflexes

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Biomechanics of some of the Muscles and the Plantar Fascia of the Foot

Muscular activity and soft tissues control movements about the various joints of the foot. Figure 80
shows the locations of the muscles of the foot relative to the longitudinal, subtalar and ankle axes of
the foot.

Figure 80: The location of the muscles of the foot relative to the three axes of the foot.

1. Tibialis anterior
The tendon of this muscle passes nearly perpendicular to the axis of the ankle joint and the first
ray and produces large moment about both, hence its dorsiflexion function. It also passes medial
to the STJ and longitudinal MTJ axes with a large moment arm about the latter, hence its
supinatory function. The moment arm of the tendon about the oblique MTJ is negligible.
2. Triceps surae (gastrocnemius and soleus)
The gastrocnemius passes posteriorly and almost perpendicularly to the ankle joint axis with a
large moment arm and, when the knee is extended, produces strong plantarflexion about this axis.
It also has a reasonably large moment arm about the STJ, but because it crosses this axis at
about 48° its supinatory effect is reduced. When the knee is flexed all of these actions are reduced
in strength because of the origin of the muscle on the femoral condyles. The soleus muscle can be
considered as the same in function as the gastrocnemius having much the same position and
direction. Due to its different origin from the tibia, it is not affected by knee flexion.
3. Extensor hallucis longus
The tendon of this muscle passes anteriorly and almost perpendicularly to the ankle joint axis and
is a strong dorsiflexor about this axis. It does this without pronating or supinating the foot about the
STJ because it runs nearly parallel to and very close to the STJ axis. In addition, this tendon
passes dorsally and perpendicular to the first MTPJ axis, which enables it to function as a
stabilizer of this joint during the final stages of stance.

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 4. Flexor hallucis longus
The tendon of this muscle passes posteriorly to the ankle joint, around the talus and under the
sustentaculum tali, attaching distally on the foot. The long moment arm created by the talus results
in a strong plantarflexion action of the foot about the ankle or, conversely, a strong deceleration of
the forward motion of the tibia. It also has a large moment arm about the STJ axis which, being at
an acute angle, reduces its supinatory action. This muscle also plantarflexes the hallux at the first
MTPJ axis, as well as flexing the IP joint of the hallux.
5. Tibialis posterior
The tendon of this muscle passes posterior to the ankle joint axis around the medial malleolus. As
this gives the muscle only a small moment arm, it is thus a weak plantarflexor of the foot. It has,
however, a large moment arm about the STJ axis and is thus a strong supinator about this axis. In
addition, it passes almost perpendicularly to the oblique MTJ axis with a large moment arm and
also produces strong supination about this axis. It has little or no action about the longitudinal MTJ
axis.
6. Peroneus longus and brevis
Both peronei pass posterior to the lateral malleolus with a small moment arm about the ankle joint
axis and are thus weak ankle plantarflexors. Peroneus longus has a large moment arm about the
STJ axis producing pronation, but passes through the oblique MTJ axis and has no effect here.
Peroneus brevis acts similarly about the STJ axis but has a small moment arm about the oblique
MTJ axis and acts perpendicularly to this axis to produce pronation.
Functions of these muscles are summarized in Table 5.

Table 5: Primary specific functions of some foot muscles

Muscle Primary Function

Tibialis anterior Dorsiflexion of toe at toe-off

Dorsiflexion of foot in swing
Assist supination of foot prior to heel-strike
Prevent excessive pronation during swing and stance
phases
Assist plantarflexion of foot after heel-strike

Gastrocnemius Plantarflexion of foot during late stance phase

Assistance with STJ supination during middle and late
stance
Externally rotates the leg
Prevents excessive internal rotation of the leg towards the
end of stance

Soleus Assist the gastrocnemius

Stabilization of the lateral forefoot during late stance

Extensor hallucis longus Stabilize the first MTPJ for propulsion

Dorsiflex the foot during early swing phase
Maintain the hallux dorsiflexed in early swing

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 Tibialis posterior Supinate the STJ during midstance
Assist the soleus
Decelerate STJ pronation during early stance
Stabilize the MTJ
Assist with heel-lift

Peroneus longus and brevis Stabilize the first ray

Assist with medial weight transfer in late stance
Assist, weakly, ankle joint plantarflexion
Pronation of the STJ

7. Plantar Fascia
In addition to the muscles discussed above,
the plantar fascia has an important role in
relation to the function of the foot.The plantar
fascia has three parts, medial, lateral and
central, the latter being the major one and
having the role of maintaining the longitudinal
arch of the foot.
The plantar aponeurosis is triangular in shape
and originates from the medial calcaneal
tuberosity and inserts into the plantar plate of
the metatarsophalangeal joints, flexor tendon
sheaths and the base of the proximal
phalanges of the toes (Figure 81). When the
toes are dorsiflexed in terminal stance, the
aponeurosis is shortened causing the
calcaneus to rotate inwards (into varus) and
the medial arch to elevate (windlass
mechanism shown in Figure 82). The tension
in the plantar fascia and the internal rotation of
the calcaneus draw the two ends of the foot
together and lock the ankle joint complex. This
stabilizes the moving foot and converts it from
a flexible adapter (necessary in the early
phase of gait) to a rigid lever (which is
essential for the propulsive phase of gait;
Figure 81: The Plantar Fascia. smooth transition of forces from the rearfoot to
the forefoot).
Summary: The following effects occur simultaneously during passive first MPJ dorsiflexion:
1. An increase in medial longitudinal arch height.
2. Inversion of the rearfoot (as the PF draws the calcaneus anteriorally).
3. External rotation of the tibia.
4. Appearance of a tight band in the PF region.

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 Figure 82: The windlass mechanism of the foot.

Functions of the Foot in Gait

1. Absorb shock from the ground reaction forces

2. Maintain Equilibrium
3. Allow forward propulsion of the body by becoming a rigid lever (Transmit Propulsive Forces)
Tables 6, 7 and 8 describe the motions of the leg and the three functional components of the foot in
order for the foot to function properly throughout the stance phase of the normal human gait cycle.

Table 6: Leg and foot kinematics during weight acceptance

Weight Acceptance:
Initial Contact to Loading Response (0%-12% of Gait Cycle)

Leg and Rearfoot Midfoot Forefoot

Tibia rotates from a position of MTJ pronation (about oblique Forefoot contact by end of
external rotation at heel axis) with "unlocking" of loading response
contact to internal rotation cuboid and navicular
Supinated relative to midfoot
Ankle plantarflexes and rearfoot (about
approximately 10° longitudinal axis)
Calcaneus everts as STJ
pronates

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Table 7: Leg and foot kinematics during single limb supporrt

Single Limb Support:

Midstance to Terminal Stance (12%-50% of Gait Cycle)

Leg and Rearfoot Midfoot Forefoot

Anterior movement of tibia MTJ pronation relative to Plantarflexion of medial

rearfoot forefoot to maintain forefoot
Reversal of tibial rotation from contact by end of this phase
maximum internal rotation to Osseous "locking" of
external rotation by terminal calcaneocuboid joint stabilizes Osseous locking of
stance forefoot against rearfoot by calcaneocuboid joint in
end of this period combination with ligamentous
Ankle dorsiflexed to 10° by tension stabilizes forefoot on
end of terminal stance rearfoot
STJ pronation maximum
between 25% and 50% of
stance
Calcaneus inverts to
accompany STJ supination to
neutral position by end of this
period

Table 8: Leg and foot kinematics during swing limb advancement

Swing Limb Advancement:

Preswing (50%-62% of Gait Cycle)

Leg and Rearfoot Midfoot Forefoot

Tibia external rotation reaches MTJ supination (about oblique Significant first ray
maximum prior to toe-off axis) accompanies STJ plantarflexion at this phase
supination
Ankle plantarflexion to 20° by May be described as
end of preswing "pronation twist" of forefoot
relative to midfoot
STJ supination
Calcaneus inversion

The following picture summarises the weight transfer according to the different stages of the stance
phase of the gait cycle.

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Biomechanical Examinations of the Ankle and Foot

Biomechanical examinations of the ankle-foot complex include:

1. Nonweight-bearing Assessment
2. Static Weight-bearing Assessment
3. Dynamic Gait Analysis
(Details of the biomechanical examinations are can be found in the clinical assessment section of this document)

Deformities in the Ankle-Foot Complex

Abnormal Pronation

Abnormal pronation of the foot can result from bone abnormalities in the foot, trauma, or weakness of
the muscles. Abnormal pronation may also occur as a compensation for abnormalities that are
extrinsic to the foot.

Figure 83: Possible deformities in a foot with abnormal pronation.

A foot with a non-rigid abnormal pronation deformity will, upon weight bearing, adopt a pronated
position. This produces a pattern of deformity in the foot which may include internal rotation of the
tibia, plantarflexion and adduction of the talus, and a calcaneovalgus deformity (Figure 83). As a
result,

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 1. The the line of action of the Achilles shifts laterally. This then reduces the supinating moment
that can be produced by the triceps surae, further contributing to the deformity created due to
the weak or absent supinators..
2. The tendon of tibialis anterior is deflected laterally, reducing its supinatory ability particularly at
the STJ.
3. The forefoot is unable to pronate because of the presence of the ground and thus is forced into
a relatively supinated position and may also be slightly adducted.
As a result of the abnormal force distribution in both the rearfoot and the forefoot of a person with
weak or absent supinators, the following secondary changes tend to be produced in the midfoot.
1. The talonavicular joint is disturbed by the navicular being displaced medially and distally.
2. The cuboid is displaced laterally and distally.
3. The medial and intermediate cuneiforms are internally rotated and also displaced distally.
In general, there is a tendency for the bones on the medial side of the foot to be distracted
(adducted) while those on the lateral border are compressed.
Listed below are deviations to the normal foot that can possibly result as a consequence of the
abnormal orientations of the bones of the foot discussed above.
1. The medial longitudinal arch can be depressed and the deltoid ligament get stretched.
2. Contractions can occur in the ankle joint capsule and the calcaneocuboid ligament.
3. The peroneal tendons can get contracted and as a resulttend to resist supination at the STJ.
4. The short plantar muscles can get stretched by the action of the depression of the arch and
are thus become less effective.

Deformities causing Abnormal Pronation of the Foot:

Rearfoot Varus
This condition is defined as an intrinsic frontal plane deformity whereby the calcaneus is inverted
relative to the lower leg when the foot is maintained in STJ neutral position. Because of this
excessively inverted position of the rearfoot, initial ground contact occurs along the posterolateral
edge of the calcaneus. In order for the medial condyle of the calcaneus to contact the supporting
surface, the STJ must pronate beyond normal, moving the calcaneus from a varus to a vertical
position.

Figure 84: Rearfoot varus.

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 Forefoot Varus
This is an intrinsic frontal plane deformity; the forefoot is inverted with respect to the rearfoot when
the foot is maintained in STJ neutral position. Forefoot varus may be compensated by abnormal
STJ pronation, manifested by calcaneal eversion beyond vertical. This motion occurs during the
phase of gait when the foot should be reaching a stable position in preparation for propulsion.
Forefoot varus deformity is frequently associated with hypermobility or dorsal shifting of the first
metatarsal and inadequate stabilization of the first ray. Inadequate stabilization may predispose the
metatarsophalangeal joint to problems such as hallux limitus or hallux rigidus. When there is
insufficient compensation by STJ pronation, compensation may occur at the midfoot and first ray.
These include midfoot abduction and excessive first ray plantarflexion, respectively.

Figure 85: Forefoot varus.

Ankle Joint Equinus

This intrinsic sagittal plane deformity is defined as a lack of talocrural joint dorsiflexion when the
foot is maintained in STJ neutral position. The most common cause of ankle joint equinus is limited
flexibility of the gastrocnemius and soleus muscle groups. Compensations for insufficient talocrural
joint dorsiflexion include excessive STJ and MTJ pronation or an increase in the toe-out foot
placement angle in gait. Impingement exostoses may occur over time with repeated contact
between the talar neck and distal tibia.
Structural or Functional Leg Length Discrepancies
Structural leg length discrepancies are true anatomic differences in the length of the femur, tibia, or
both. Functional leg length discrepancies may be described as the shortening or lengthening of a
limb secondary to muscle imbalance or joint contracture.
Acquired Pes Planus Deformities Resulting from Trauma and Laxity
Rupture of the tibialis posterior tendon is described as a cause of acquired adult pes planus foot
deformity. The calcaneus can be described as subluxing under the talus. Ligamentous laxity is also
considered and acquired pes planus deformity of the adult foot and is due to insufficient tensile
strength within short and long plantar ligaments, the spring ligament, and plantar fascia.
Rotational Malalignment: Tibial Torsion, Femoral Anteversion/Retroversion
These extrinsic sources of exaggerated transverse plane rotational malalignments may result in
compensatory pronation.

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 Figure 86: Femoral anteversion and retroversion respectively.

GRF on a Foot with Varus Deformity:

In a segment of the foot with varus deformity, the line of action of the ground reaction force will be
medial to the line of action of the weight force as the segment contacts the ground (as shown in Figure
87). This produces a varus moment which forces the STJ into supination. A person with a flexible
deformity therefore pronates the foot during the stance phase in order to compensate for the varus
moment.

Figure 87: GRF on an inverted foot section.

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Abnormal Supination

A foot with an abnormal supination will, during swing phase and at foot contact, adopt a supinated
position. This supinated position of the foot may continue throughout the stance phase of the gait. As
a result of a supinated foot,
1. The ankle dorsiflexes and the short flexors on the plantar surface of the foot contract. The talus is
thus dorsiflexed (Figure 88) and the plantar fascia tightens producing a high arched cavus foot.
2. The angle of the MTJ is made more acute which leads to a tightness in the long extensors and this
in turn causes the toes to become retracted and clawed, i.e. hyperextended, at the MTPJs and
fixed at the IP joints.

Figure 88: Possible deformities in a foot with abnormal supination.

In a non-weight bearing foot with abnormal supination,

1. High longitudinal medial and lateral arches are evident.
2. The forefoot is everted.
3. The first and sometimes the fifth rays are plantarflexed.
4. The plantar fascia is tighter and the metatarsal bones are adducted.

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In a weight bearing foot with abnormal supination,
1. The calcaneus adopts a varus posture.
2. The fifth ray is forcefully dorsiflexed and bears excessive weight.
3. The triceps surae is able to more actively supinate the foot at the STJ because of the varus
rearfoot. This effect is reinforced by the increase in the ability of the tibialis anterior to supinate the
STJ and MTJ.
4. The area of the MTPJ is overloaded by the hyperextension of the STJ and MTJ joints.

Foot Deformities causing Abnormal Supination of the Foot:

Rearfoot Valgus
In this intrinsic frontal plane deformity, the calcaneus is everted relative to the lower leg when the
foot is maintained in the STJ neutral position.. In the compensated foot, this position may be
maintained during the weight-bearing condition. This deformity also is present during the weight-
bearing examination in cases of posterior tibialis tendon rapture.

Figure 89: Rearfoot valgus.

Forefoot Valgus
This intrinsic frontal plane deformity occurs when the forefoot is everted with respect to the rearfoot
when the foot is maintained in STJ neutral position. A flexible forefoot valgus may develop
secondary to a rearfoot varus that is not compensated by STJ pronation. This flexibility of the
forefoot allows the plantar forefoot to be brought to the ground by means of eversion about the
longitudinal MTJ axis. A rigid forefoot valgus is compensated by abnormal STJ supination.

Figure 90: Forefoot valgus

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 Plantarflexed First Ray Deformity
In an intrinsic sagittal plane deformity of the first ray (first metatarsal, medial cuneiform), the
position of the first ray is in equinus or plantarflexion. A fixed plantarflexed first ray results in a rapid
transfer of weight laterally and abnormal STJ supination.

Figure 91: Plantarflexed first ray.

It is common for any combination of forefoot or rearfoot deformities to coexist. The manifestations
of the combined foot deformities may be different from the manifestations of the individual
structural deformities. Orthotic management for combinations of malalignments can be a confusing
but challenging process when one is deciding management strategies to address the deformities.

GRF on a Foot with Valgus Deformity:

In a segment of the foot with valgus deformity, the line of action of the ground reaction force will be
lateral to the line of action of the weight force as the segment contacts the ground (as shown in Figure
92). This gives rise to a destabilizing valgus moment about the STJ. A person with a flexible deformity
therefore supinates the foot during the stance phase in order to compensate for the valgs moment.

Figure 92: GRF on a valgus foot section.

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Abnormal Toe Extension and Flexion
Abnormal toe extension and flexion can be caused by weak flexors and extensors of the toes
respectively. Weakness of the toe flexor muscles, particularly those associated with the first ray and
hallux, may cause significant foot pathology. Although this problem is often associated with an inability
to plantarflex the foot at the ankle, the destabilization of the hallux during walking may lead to a
number of sequelae.
Weakness of the toe extensors is usually associated with an inability to dorsiflex the foot at the ankle
joint.
Deformities of the MTPJs and the IP joints may result in a foot with weak or absent toe extensors and
flexors:
1. Clawing of the toes may result from weak or absent extensors of the toe, with subluxation of the
MTPJs and an increase in pressure applied under the metatarsal heads. Associated dorsal lesions
over the IP joints may also develop. This is more problematical when the hallux is involved
because of the importance of the first ray for locomotion.
2. Hammer toes, which is a plantarflexion deformity of the proximal IP joint, or mallet toes (an
abnormal plantarflexion of the distal phalanx only) can alsobe produced as a result of weak or
absent toe extensors.
3. Weakness in the flexors and extensors of the toes can lead to a malalignment of the metatarsal
heads. This leads to the prominent heads being subjected to increased pressure and the creation
of plantar callosities and discomfort.

Abnormal Structural Alignment

Structural malalignments are often congenital and in general result in a foot in which the joints are
mobile, but function about abnormal positions. Such a foot will be less capable of providing an energy
efficient gait pattern. The compensatory processes adopted by the body of an individual with structural
malaligments in the foot may result in long-term pain both in the foot and at the more proximal joints.

Abnormal Structural Integrity

The structural integrity of the foot is commonly compromised by an arthritic condition,trauma, and
repetitive injury from high levels of sporting activity.
In rheumatoid arthritis for example,
1. Tendons become soft and therefore lose their mechanical stabilizing effect.
2. Cartilage becomes soft and eroded, and the joints (the MTPJs) start to dislocate.
3. Deformities of the toes lead to metatarsal overloading with the underlying skin degenerating and
becoming susceptible to ulceration due to the occurrence of pressures of up to the three times
normal levels.
The consequence of structural integrity in the foot is that the foot is painful even during normal
activities.

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Biomechanics of Foot Orthoses

Different forms of foot orthoses are used to change the biomechanics of a foot with deformity. Foot
orthoses function primarily by altering the alignment of the ground reaction force on the foot in order to
achieve the desired joint moments and realign anatomical joints into their optimum functioning
positions.
This section of this document discusses the biomechanics of foot orthoses that can possibly be used
to correct or compensate for the deformities discussed in the previous section.

Wedges
Wedges are forms of foot orthoses that can be utilized to correct deformities in the foot. Figure 93(A)
shows a foot with varus forefoot. This type of deformity can lead to internal rotation of the tibia causing
the knee to move medially as the forefoot pushes down to meet the ground (Figure 93(B)). This in
return causes an abnormally pronated foot during weight bearing.
A wedge on the medial side of the foot with a varus forefoot can be used to place the foot in a neutral
STJ position and alter the moment created by the GRF about the STJ. This will also reduce the strain
on the knee as shown in Figure 93(C).

Figure 93: Use of wedge to correct for varus forefoot.

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The simplest way to adjust the position of the calcaneus relative to the ground is to wedge the heel of
the shoe. However, much more accurate control over the final heel position can be achieved if the
wedging required is built into an in-shoe foot orthosis: the foot orthosis is manufactured to a cast of the
foot from which the required angles can be obtained relatively accurately and the presence of the
orthosis, which is moulded to the plantar surface of the foot, adds significantly to the control of the foot
within the shoe. These two methods of wedging are shown in Figure 94.

Figure 94: Adjustment of the position of the calcaneus with the use of wedge on the heel of a shoe and on an in-
shoe foot orthoses respectively.

Shoe Modifications (Rocker Sole)

In cases where the foot has rigid (uncorrectable) deformities, different forms of foot orthoses are used
to alleviate high localized pressures both on the dorsal and plantar surfaces of the foot. These types of
foot orthoses are also used to reduce shear stresses in areas of the foot with abnormally high loads.
A rocker sole is a type of shoe modification used to reduce peak pressures on the susceptible
metatarsal heads by slowing down the forward progression of the center of pressure of the ground
reaction force. As shown in Figure 95, a shoe rocker results in a 'hesitating' progression of the center
of pressure at the point of contact of the rocker with the ground. The rocker thereby reduces the
moment about a stiff and painful MTPJ.

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 Figure 95: The use of a rocker sole to delay the forward progression of the ground reaction force between the foot
and the ground.

Flares/ Extensions
Flares are a type of foot orthoses that can alter alignment of ground reaction forces to change the
moment about the subtalar joint.
Example 1: In Figure 96, the moment arm of the ground reaction force is increased from 'r' to 'R' by
using a foot orthosis with medial heel extension. This helps increase the supination
moment of the foot.

Figure 96: A foot orthosis with a medial heel extension.

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Example 2: In Figure 97(A) the line of action of the GRF is aligned lateral to the subtalar joint resulting
in a large eversion moment.
The application of a supramalleolar AFO with a medial flare (Figure 97(B)) moves the line
of action of the GRF medial to the STJ at foot contact. A corrective inversion moment is
generated to position the calcaneus in a corrected vertical position before weight
acceptance at foot flat.

Figure 97: A supramalleolar orthosis with a medial flare.

Example 3: Figure 98 shows how adding a flare to the medial side of a shoe can be used to move the
point of initial contact medially in an everted foot. This allows for the ground reaction force
to produce a correcting varus moment which swings the heel round into its correct
alignment.

Figure 98: Medial shoe flare.

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Example 4: Similar to the previous example, Figure 99 shows how adding a flare to the lateral side of
a shoe can be used to move the point of initial contact laterally in an inverted foot.

Figure 99: Lateral shoe flare.

Three-point Pressure Systems

Deformities associated with weak toe extensors and flexors are good examples where three-point
pressure systems could possibly be used as correction methods. Figure 100 illustrates how forces P1,
P2, and P3 are applied to correct a flexion deformity at the proximal IP joint of the hallux. Lower part of
Figure 100 shows how an interdigital orthosis can be used to redistribute high pressure on the apices
of the flexed toes by spreading the loads over larger areas.

Figure 100: Three-point pressure system use to correct toe deformity.

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Pads
Example 1: Deformities in the toes due to weak flexors and extensors can lead to malalignment of the
metatarsal heads. This in turn leads to increased pressure on the prominent heads and
associated pain. To relieve this pain, the prominent head may be re-aligned with the
others by applying a corrective force under the shaft of the affected metatarsal using a
metatarsal pad (Figure 101).

Figure 101: A metatarsal pad used to correct a plantarflexed metatarsal.

If the deformity in the toe is only partially correctable or non-correctable, then the area of
increased pressure should be relieved. As shown in Figure 102, accommodative pad is
used to evenly spread the pressure around the problem area, over a wider surface area
of the foot (all the metatarsal heads of the foot) so that the initially high pressure under a
single metatarsal head is reduced.

Figure 102: An accommodative pad used to distribute pressure.

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 It is convenient to consider the plantar surface of the foot divided into nine areas (Figure
103). For each of these regions there is a specific pad type that is appropriate.

Figure 103: Types of functional pads based on their application on the areas of the plantar surface of the foot.

Example 2: In a foot with Hallux Abducto Valgus (HAV) shields can be used to relief of pressure
between the foot and shoe (Figure 104) and prevent the hallux from overriding or
underriding on the second and third toes.

Figure 104: Hallux Abducto Valgus (HAV).

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 VI. ORTHOTIC SCIENCE

6.1 INTRODUCTION

Definition
A foot orthosis (FO) is a mechanical device used to align and support the foot; prevent, correct, or
accommodate foot deformities; or improve the overall functions of the foot.

Function

The foot orthosis may have one or several of the following functions:
• evenly distribute the weight-bearing stresses over the entire plantar surface of the foot;
• indirectly reduce the stress and strain on ankle, knee, hip and spine;
• alleviate pain from sensitive and painful areas of the sole;
• support the various foot arches;
• provide relief for metatarsalgia of various causes;
• decrease the amount, degree, and rate of foot hyperpronation during walking and running;
• improve foot alignments;
• accommodate congenital or developmental foot anomalies;
• serve as an addition to an ankle-foot orthosis (AFO);
• equalize foot length discrepancy;
• compensate for mild leg length discrepancy;
• limit the motion and weight-bearing stresses of various painful foot joints;
• minimize the pressure and irritation from external (shoe) or internal (bony prominence)
sources.

Types

We will differentiate 3 types of foot orthoses & orthopaedic footwear: insoles, orthopaedic shoes,
and shoe modification. In this course, we will see the manufacture of insoles in details and we will do
an introduction to orthopaedic shoes and shoe modifications.

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6.2 INSOLES

Definition and Types

The insole is an insert made after accurate measures, and placed in a standard (commercial) shoe.
It can have different roles, but generally speaking we can say that it has an effect on the foot itself and
also on the more proximal parts of the body (knee and hip articulations, spine, etc.). Insoles can be
corrective, stabilise, be palliative or antalgic.
There are three different types of insoles: rigid, semi-rigid, and soft. Their use will depend on the
pathology of the patient and on the result expected by the insole, but soft insoles are the most
commonly accepted due to their less traumatising effect on the soft tissues of the foot.
a. Rigid Insole: made from a single layer of material, such as stainless steel, acrylic, or
polypropylene sheet, and are usually metatarsal length.
The advantage of the rigid insole is its small thickness and the consequent little space it takes in the
shoe. Another positive consequence of this rigidity is the fact that the material does not deteriorate
easily.
The main disadvantages of the rigid insole include:
• its traumatising effect on the soft tissues of the foot and the compression it creates on the plantar
veins of the foot, with negative consequences on the plantar muscles;
• poor shock absorption ability;
• inability to make fine adjustments on them.
Therefore, it is less and less used by the orthotists. Due to its stiffness, it can not be used for elderly
patients or for patients who have poor or no sensibility in their feet.
Stainless steel Whitman plate and Shatter plate, polypropylene, and acrylic Insoles are examples of
rigid insoles.
Four Basic types of rigid insoles based on overall length: (see picture below)

A: Metatarsal Length; B: Sulcus Length; C: Morton extension; D: Full Length

b. Semi-rigid Insole: made out of thin thermoplastic (1mm thick) and soft material such as EVA.
They come in all three lengths and are made of a combination of materials with a wide range of rigidity
depending on the functions these materials are designed to perform. The materials used in fabricating
semi rigid Insoles include leather, felt, spring steel, natural and rubberized cork, thermoplastic cork,
cellular rubber, plastazote, and polyethylene.
Semi-rigid insoles are sometimes used for sportive patients who have a rigid plantar arch and who do
sports with multi-directional movements (badminton, tennis, etc.)

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The advantage is the durability of its plastic base. They are more comfortable to wear and can also
provide pressure relief, shock absorption, improvement
of weight-bearing transfer, and support and stabilization
of various foot deformities. In addition, semi rigid
Insoles can also be moulded against the positive model
or cast of the foot.
The disadvantage is its bigger thickness compared to
the rigid insoles (use of EVA) and the fact that they are
usually weaker, softer, more flexible, and less durable.
The figure on the right shows a pair of custom-made
full-length semi rigid insoles. They are made of multiple
layers of plastic foam materials, and their top covers
are made of vinyl.

c. Soft Insole: made out of leather and EVA.

They are the most commonly used by the orthotists for their various use possibilities.
Their main advantages are the fact that they have the best shock-absorbing ability and are quite
effective in reducing shear, compression, and tension stresses. They are also comfortable to wear.
Disadvantages are their limited support action due to their softness, and their limited durability.
In comparison with rigid and semi-rigid insoles, soft insoles usually come in a full-length form and are
often made of plastazote, polyurethane foam, polyvinyl chloride foam, or latex foam.

Functions of Insoles

Correction - stimulation
When the foot presents a deformity that can be corrected, the insole will have a corrective or even
stimulation role. Correction / stimulation insoles are used only with children and teenagers, never with
adults for whom deformities can only be stabilized. An insole can also correct more proximal joints'
deviations, such as genu varus / valgus.
Stabilisation - support
When the foot presents a deformity which is progressing and/or which cannot be corrected, the insole
will help maintain the foot in a stable position and prevent further deformity.
Palliative
When the foot presents important deformities, the insole counterbalances the deformities without any
corrective purpose.
Antalgic
When they are used to reduce excessive pressures or to maintain the foot structure with the aim to
relieve pain, plantar supports have an antalgic action.

Elements of Insoles

Different elements can be used in an insole. The thickness of the elements and their exact shape are
made according to the foot size and the action required by the insole.
Many possibilities and variations exist but we are going to see the most commonly used elements of
the soft insoles.
The following figure shows some examples of insoles with different elements combinations:

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 Intervention Time of the Different Elements of an Insole During the Stance Phase of
the Gait Cycle

Heel strike Foot flat Heel off / toe off

Period Period Period
=• 5 % =• 40 % =• 22 %
Metatarsal bars

Metatarso-Palangeal bar

Heel pads

Posterior Supinator Wedge

Posterior Pronator Wedge

Pronator bar
st
Metatarso-Phalangeal – 1 M-P
(Supinator)

Anterior Pronator Wedge

Metatarsal Pronator Wedge

Navicular and Cuboïd pads

Posterior Supinator and Pronator

Wedges for stimulation

Internal Median Arch Support

for Unload

Heel Cup for Unload

Heel Cup

Metatarso-Phalangeal Elements
for Unload

Phalangeal elements

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 Transverse Metatarsal Eement for Unloading
Metatarsal Bar (SAE Type)

Anterior Limit:
Curved line, tangent to the back of the
five metatarsal heads, concave forward
in its 2/6 internal, then convex in its
3/6 medium and concave in its 1/6
external, 2/3 posterior

Postero-internal Limit:
On the outline of the sole in line with
the first metatarsal base

Postero-external Limit:
On the outline of the sole, in line with
the styloid of the fifth metatarsal.

Posterior Limit:
Concave line backward and inward.

Top:
Along a transverse line on the
metatarsal necks, 6mm at the back of
the metatarsal heads, parallel to the
anterior limit.

Profile:
From the top, convex in front under
the metatarsal necks and inclined
backward.

Materials:
Agglomerated cork or compressible
rubber.

Main indication:
• Complete unload of
metatarso-phalangeal
articulations;
• Extension of the toes

Intervention Period:
• Foot flat
• Heel off
Intensity:
• High in foot flat.
• Low at heel off

Action Time:
• Total Action ± 40 % + 2à4%
• Optimal Action ± 40 %

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 Transverse Metatarsal Element for Compensation
Metatarsal Bar (Hollow Foot Type)

Limits are identical to the previous

one, except for the postero-internal,
which is located in line with the
astragalo-navicular articulation.

Top:
In line with the 1st. cuneiform

Profile:
Inclined from inside to outside and
from posterior to anterior according to
each metatarsal angular coefficient.

Materials:
Compressible rubber.

Main indication:
• Compensation for irreducible
foot
• Global unload of the
metatarso-phalangeal
articulations
• Toes extension

Intervention Period:
Same as previous

Intensity:
Same as previous

Action Time:
Same as previous

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 Transverse Metatarsal Element for Pronation
Pronator Metatarsal Bar

What is different:

Postero-external Limit:
On the outline of the sole, in line with the
Chopart articulation.

Top:
Lateral external limit.

Profile:
From the top:
• Inclined from outside to inside
without coming down to zero to
keep the unload potential at the
nd
level of the 1st and 2 metatarsal
heads.
• Convex in front under the
metatarsal necks and sharply
inclined backward.

Materials:
Agglomerated cork.

Main indication:
• Correction or compensation of a
supination of the anterior tarsal
and metatarsal;
• Unload of lateral metatarso-
phalangeal articulations

Intervention Period:
Same as previous

Intensity:
Same as previous

Action Time:
Same as previous

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 Transversal Metatarso-Phalangeal elements
Metatarso-Phalangeal Bar

Anterior Limit:
Curved convex line in front and
outside located in line with the middle
of the proximal phalangeal diaphyses

Posterior Limit:
Identical to metatarsal bar

Lateral Limit:
On the outline of the sole

Top:
• Following a horizontal plane in
the 2/3 posterior of the length
of the element (1);
• Or, without height difference
between the posterior and
anterior parts of the bar (2)

Profile:
From the top, inclined forward in the
1/3 anterior of the metatarso-
phalangeal area, and backward for the
metatarsal area, as for the metatarsal
bar.

Materials:
Agglomerated cork; foam

Main Indication:
• Correction of pes cavus for
children.
• Opposition to Achilles tendon
retraction (heel off gait)
• Antero-posterior re-alignment
of the pelvis and spine.

Intervention Period:
In foot flat and in heel off.

Action Time:
Total optimal action ± 62%

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 Median Metatarsal Element
Metatarsal Pad

Anterior Limit:
Curved line, convex in front and tangent
posterior of the 2nd., 3rd., and 4th. metatarsal
heads

Posterior Limit:
In the middle of the 3rd. cuneo-metatarsal
articulation

Lateral Limit:
Convex lines inside and outside in the 1st.
and 4th. inter-metatarsal spaces.

Top:
Following a horizontal plane at the back of
the metatarsal necks on the second quarter
of its length and transversally.

Profile:
From the top:

• Convex under metatarsal necks and

on 5mm inward and outward.
• Inclined backward.

Materials:
Compressible rubber.

Main Indication:
• Unload the median metatarsal
heads
• Active load of the 1st. and 5th.
metatarsal heads.
• Toes extension

Intervention Period:
Foot flat and beginning of heel off

Action Time:
• Total action time ± 40% + 2 to 4%
• Optimal Action time ± 40.

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 Raising Posterior Element
Heel Pad (Raising Type)

Following a transverse line on the Chopart

articulation (can go until metatarsals heads
for a pes equinus). 1/3 posterior.

Lateral Posterior Limit:

Follows the insole and heel counter

Top:
Posterior limit

Profile:
From the top:

• Inclined from back to front.

• Transversally, horizontal or slightly
concave

Materials:
Agglomerated cork

Main Indication:
• Compensation of leg length
discrepancies
• Frontal re-alignment of the pelvis
and spine

Intervention Period:
Heel strike and foot flat.

Action Time:
Optimal total action time ± 45%.

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 Posterior Antalgic Element
Heel Pad (Talalgia Type)

Identical to those of the raising heel pad. A

hole is made on the painful area.

Top:
In an horizontal place
On the ¾ posterior of the element's length
and transversally.

Profile:
From the top:

• Inclined in the ¼ anterior of its

length

Materials:
Compressible rubber.

Main Indication:
• Inflammation of the plantar
aponevrosis insertion

• Calcaneus spur

Intervention Period:
Same as previous

Action Time:
Same as previous

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 Posterior Supinator Element for Stabilization
Posterior Supinator Wedge / Stabilization

Anterior Limit:
On the outline of the insole, on the
astragalo-navicular articulation. 1/3
posterior.

Posterior Limit:
On the outline of the insole at ¾
external of the insole width.

Latero-internal Limit:
Following the shoe heel counter.

Latero-external Limit:
Curved line, first convex outside in
its ½ anterior, in the middle tangent
to the antero-posterior axis of the
foot, then concave to join the
posterior limit point.

Top:
On the internal limit.

Profile:
From the top, inclined inward and
outward.

Materials:
Agglomerated cork

Main Indication:
• Compensation or correction
of posterior valgus.

• External rotation of the

lower-limb (hip, knee,
ankle/foot)

• Compensation for pelvis

rotations.

Intervention Period:
Heel strike and foot flat.

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 Posterior Supinator Element for Stimulation
Posterior Supinator Wedge / Stimulation

Anterior Limit:
Outline of the insole, at the external
¾ of the insole's width.

Lateral Postero-internal Limit:

Follows the shoe heel counter

Lateral Antero-external Limit:

Straight line joining anterior and
posterior limit points

Top:
Middle of the lateral postero-internal
limit.

Profile:
Inclined from back to front and
outward.

Material:
Agglomerated cork.

Main Indication:
Correction of a postural pes valgus
for children

Intervention Periods:
Heel strike and foot flat

Intensity:
High at the beginning of the heel
strike.

Low at foot flat.

Action Time:
• Total action time 45%
• Optimal Action time at heel
strike 5%

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 Posterior Pronator Element for Stabilization
Posterior Pronator Wedge / Stabilization

Anterior Limit:
Outline of the insole, at the level of the
calcaneo-cuboïd articulation

Posterior Limit:
Outline of the insole at ¾ internal side of the
insole width.

Lateral External Limit:

Follows the shoe heel counter

Lateral Internal Limit:

Straight line joining the anterior and posterior
limit points.

Top:
On the lateral external limit.

Profile:
From the top, inclined from outside to inside.

Main Indications:
Compensation or correction of a posterior
varus.

Intervention Periods:
Heel strike and foot flat.

Action Time:
Optimal total action time ± 45 %.

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 Posterior Pronator Element for Stimulation
Posterior Pronator Wedge / Stimulation

Symmetrical compared to the foot axis to

the supinator wedge.

Material:
Agglomerated cork

Main Indications:
Correction of a postural pes varus for
children

Intervention Periods:
Same as previous

Action Time:
Same as previous

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 Total Pronator Element
Pronator Bar

Antero-external Limit:
In the second inter-metatarsal space, just
behind the 2 adjacent heads.

Anterior Limit:
Follows a line first convex anteriorly in its
2/6 internal then concave in its 1/6
external and tangent to the posterior
aspect of the external metatarsal heads.

Posterior Limit:
On the outline of the insole, in the middle
of the insole's width.

Lateral External Limit:

Follows the shoe heel counter

Lateral Internal Limit:

Curved line with a large radius concave
inside, and in its middle tangent to the
antero-posterior foot.

Top:
Follows the internal limit.

Profile:
From the top, inclined from outside to
inside, and convex under metatarsal
necks.

Material:
Agglomerated cork.

Main Indication:
Compensation of a global varus of the
foot.

Intervention Period:
Heel strike and foot flat + heel off

Action Time:
Optimal total action time ± 45 %

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 Anterior Supinator Element
Internal Metatarso-Phalangeal Wedge / 1st. Metatarso-phalangeal Articulation

Anterior Limit:
Transversal line located at the middle of
the proximal phalangeal diaphysis of the
hallux.

Posterior Limit:
On the outline of the shoe insole, in line
with the base of the first metatarsal.

External Lateral Limit:

Parallel line with the antero-posterior foot
axis located in the first metatarso-
phalangeal space, than convex backward
and outward to join the posterior limit
point.

Internal Lateral Limit:

Follows the insole.

Top:
On the internal lateral limit in the ½ of its
length.

Profile:
Inclined from inside to outside, than
inclined in front and backward from the ½
median.

Material:
Agglomerated cork

Main Indications:
• Pronation of the metatarsal and
anterior tarsal (postural flat foot)
with implication of the entire foot
balance.

• External rotation of the lower-limb

(hip, knee, ankle/foot) and
compensation of pelvic rotations.

Intervention Periods:
Foot flat and heel off

Action Time:
Optimal total action time ± 62%

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 Anterior Pronator Elements
Anterior Pronator Wedge (1)
Metatarso-Phalangeal Pronator Wedge (2)

Antero-internal Limit:
In the second inter-metatarsal space, just
behind the two adjacent heads
Anterior Limits:
Three designs:
• Straight line
• First convex anteriorly in its 2/3
internal, than concave in its 1/6
external, and tangent to the
posterior outline of the external
metatarsal heads
• Convex anteriorly, inline with the
middle of the 4th. and 5th. proximal
phalangeal diaphyses.
Posterior Limit:
Follows the outline of the insole, in line with
the Chopart articulation.
External Lateral Limit:
Follows the shoe shank
Internal Lateral Limit:
Straight line joining antero and postero
internal limits.
Top:
External lateral limit
Profile:
From the top, inclined from outside to
inside than convex under metatarsal necks
and than sharply inclined backward.
Material: Agglomerated cork
Main Indications:
• Correction or compensation of
anterior tarsal and metatarsal
supination
• Internal rotation of the lower-limb
(hip, knee, ankle/foot) and
compensation of pelvis rotations
Intervention Periods:
• Foot flat and heel off (1)
• Foot flat and heel off – toe off (2)
Intensity:
• High at foot flat and low at
beginning of heel off (1)
• High at foot flat and at heel off – toe
off (2)
Action Time: Total action time ± 40% + 2 à
4%. (1)

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 Cuboïd Element
Cuboïd Pad

Anterior Limit:
On the outline of the insole, at the union
between the body and the base of the 5th
metatarsal.

Posterior Limit:
On the outline of the insole, at the 1/3
posterior of the foot length.

Lateral Internal Limit:

Line convex internally and in its middle
tangent to the antero-posterior axis of the
foot.

Lateral External Limit:

Follows the shoe shank

Top:
Middle of the lateral external limit

Profile:
From the top, convex from outside to inside
and from back to front.

Material:
Agglomerated cork

Main Indications:
Correction or compensation of:
• Pes varus
• Genu varus
• Internal rotation of the lower-limb
(hip, knee, ankle/foot) and
compensation of pelvic rotations

Intervention Periods:
End of heel strike and foot flat.

Action Time:
Optimal total action time ± 40% + 1 or 2%

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 Navicular Element = Correction Element
Navicular Pad for Correction (Active Element for Children)

For Children Only

Symmetrical compared to the foot axis and to

the cuboïd pad.

Material:
Agglomerated cork

Main Indications:
• Correction or compensation of genu
valgus
• External rotation of the lower-limb
(hip, knee, ankle/foot) and
compensation of pelvic rotations +
genu valgus

Intervention Period:
Foot flat

Action Time:
Optimal total action time ± 40 %.

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 Internal Unloading Element for Support
Navicular Pad for Unloading

Anterior Limit:
Concave line just behind the head of the first
metatarsal. All other characteristics are
identical to those described before.

Profile:
.

Top:
½ of its length

Material:
Compressible rubber

Main Indication:
Unload of the first metatarsal head

Intervention Period:
Foot flat

Action Time:
Optimal total action time ± 40%

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 Medio-internal Element for Support and Comfort

Navicular Pad for Support

Anterior Limit:
On the outline of the insole, at the union
between the 1/3 posterior and middle of the
first metatarsal.

Posterior Limit:
On the outline of the insole, at the union
between the 1/3 anterior and middle of the
posterior 1/3 of the foot length.

External Lateral Limit:

Curved line with a large radius outside and
tangent in its middle to the antero-posterior
foot axis.

Internal Lateral Limit:

Follows the shoe shank.

Top:
Internal lateral limit at the union of the 1/3
posterior and middle of its length (under the
navicular)

Profile:
From the top, convex from inside to outside,
and from back to front.

Material:
Compressible rubber or agglomerated cork.

Main Indications:
• Compensate medio-tarsal collapse

• Comfortable plantar support

• Problems of blood return circulation

Intervention Periods:
Foot flat

Action Time:
Optimal total action time ± 40%

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 Posterior stabilizing element
Heel Cup

Antero-internal Limit:
On the outline of the insole, at the level of the
astragalo-navicular articulation.

Antero-external Limit:
On the outline of the insole, behind the 5th
metatarsal base.

Anterior Limit:
Concave anteriorly and parallel to the
posterior outline of the insole, at a distance
equal to 1/6 of its width.

Lateral and Posterior Limits:

Flared out following the shoe shank

Top:
Lateral and posterior limits

Profile:
Slightly concave upward until the anterior
limit

Material:
Agglomerated cork

Main Indications:
• Stabilize the rear foot;

• Keep the insole in a proper position

with the foot, avoiding sliding toward
the front part of the shoe.

Intervention Periods:
Heel strike and foot flat

Action Time:
Total action time ± 45%

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 Metatarso-Phalangeal Element for Unload
Metatarso-phalangeal Elements

Located longitudinally under one or several

metatarso-phalangeal articulations

Anterior Limit:
Transversal line located under the middle of the
proximal phalanges diaphyses.

Posterior Limit:
Together with the anterior limit of the metatarsal
bar.

Lateral Limits (according to the considered

segment):
• Against the shank of the shoe, without
flare;

• In an inter metatarso-phalangeal space,

parallel to the foot antero-posterior axis.

Profile:
From the top: inclined on 1/3 of its length

Material:
• Agglomerated cork;

• Compressible rubber

Main Indication:
Selective unload of metatarso-phalangeal area

Intervention Period:
Foot flat and heel off

Action Time:
Optimal total action time ± 62%

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Insole Design According to Pathology

Flat Foot (Pes Planus)

a) Stimulation insole, for postural (valgus) flat foot for children and adolescents:
This type of insole stimulates the foot proprioception and does not give any bony support. It is used for
children and teenagers; not for adults. Reminder: Never treat a postural flat foot for a child younger
than 4 years old!

Elements used:
• Posterior Supinator Wedge / stimulation
• Internal Metatarso-Phalangeal Wedge
• Metatarsal Pad (6 to 10mm high)
Mode of action of the insole:
1. Places the foot in a balanced position, close to its theoretical equilibrium;
2. Triggers the activation of the tibio-peroneal muscles, the intervention of the flexor hallucis, actions
that impact the plantar ligament structures;
3. Stimulates the articular and muscular proprioceptive mechanisms;
4. Pre-loads the medial longitudinal arch through the bending in torsion of the longitudinal arches;
5. Opposes the locking of the bones that results from ligament and muscular tensions and that
induces a certain neuro-motor laziness of the foot.
b) Stabilization insole, for (valgus) postural flat foot with children, adolescents and adults:
Used with children and adolescents every time the stimulation insole does not bring any effect. For
adults this is the first choice insole for stabilizing a flat foot.

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Elements used:
• Posterior Supinator Wedge / stabilization
• Metatarsal Pad
• (Anterior Pronator Wedge)
Mode of action of the insole:
• The Posterior Supinator Wedge is more lateral than the one used for stimulation. It re-aligns
the calcaneus in a vertical position;
• The Metatarsal Pad helps the fore foot to have a well balanced position with regard to the
rear foot;
• The addition of an Anterior Pronator Wedge will be used only if the forefoot is supinated due
to an over correction of the posterior valgus. The anterior Pronator wedge associated to the
Posterior Supinator Wedge will induce a torsion of the foot in its longitudinal axis, that helps
re-create the arches.
c) Palliative insole, for (valgus) flat foot with children, adolescents and adults:
This type of insole is used for flat feet that cannot be corrected anymore. Used with children and
adolescents every time both the stimulation and the stabilization insoles do not bring any effect, which
is very rare. For adults, this insole is used when the stabilization insole does not bring any effect
anymore.

Elements used:
• Posterior Supinator Wedge / stabilization
• Navicular Pad
• (Metatarsal pad)
• (Anterior Pronator Wedge)
Mode of action of the insole:
• The Posterior Supinator Wedge re-aligns the calcaneus in vertical position (whenever
possible); it helps re-adjusting the lateral muscles and ligaments' tension;
• The Navicular Pad supports the collapsed medial longitudinal arch; avoids the dislocation of
the navicular bone; reduces the extension of the plantar ligaments thereby avoiding pain;
• The Metatarsal Pad can be used to help improve the amortisation of the step and to better
share the load on the forefoot at the level of the metatarso-phalangeal hinge;
• If the forefoot remains supinated, the addition of an Anterior Pronator Wedge will help re-
balancing the forefoot

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d) "Derotation" insole, for valgus flat foot for children and adults:
This type of insole is used when the entire lower-limb is externally rotated.

Elements used:
• Posterior Supinator Wedge (Stabilisation type)
• Internal Metatarso-Phalangeal Wedge (Supination)
Mode of action of the insole:
By supinating the foot posteriorly and anteriorly, the proximal articulations (i.e. knee and hip joints) will
rotate externally.

Hollow Foot (Pes Cavus)

For a hollow foot we have the choice between 2 types of insoles: correction (Children in reducible
deformity) or stabilisation (Children and adults in fixed deformity). Both types may have an Antalgic
effect as well.

Elements used:
Correction:
• Metatarso-Phalangeal Bar, to extend the phalanges;
• (in case of valgus of the heel: Posterior Supinator Wedge; in case of varus of the heel:
Posterior Pronator Wedge)
• (in case of pain at the medial longitudinal arch: soft navicular pad)

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Stabilization:
• Metatarsal Bar, to reduce the difference of levels (not too high, it should not be painful!) (in
the case of painful callosities on the metatarsals, they should be relieved from pressure)
• (in case of valgus of the heel: Posterior Supinator Wedge; in case of varus of the heel:
Posterior Pronator Wedge)
• (in case of pain at the medial longitudinal arch: soft navicular pad)
Mode of action of the insole:
As the hollow foot creates a difference of level between the forefoot and the rear foot, the insole
should reduce or eliminate this difference by moving the metatarsals up, widening the contact on the
metatarsal heads, and correct a deviation of the heel.

Metatarsalgia
Type of insole:
Stabilisation and unload, with an antalgic effect. The figures below show different options according to
the localisation of the callosities.

Elements used:
• Metatarso-Phalangeal Bar with relieve on callosities
• (Navicular pad)
Mode of action of the insole:
The pressure must be reduced under the metatarsal heads; the metatarsal arch can also be supported
if callosities are mainly located medially.

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Hallux Valgus
Orthoses do not cure the hallux valgus but it can limit its
progression. Only surgery can bring a correction.
Type of foot orthosis:
The Hallux Valgus is not treated by the means of an insole.
Adapted shoes with a space to accommodate the widening
of the forefoot; night splint (for small deformities).

Sesamoiditis
Type of insole:
Same as for hollow foot and metatarsalgia
Elements used:
Same as hollow foot and metatarsalgia

Hammer Toes
Type of insole:
Insoles will be used for flexible hammer toes only. Their action will be correction, with an antalgic
effect.

Elements used:
• Phalangeal Bar
• Metatarsal Pad
• Heel Cup
Mode of action of the insole:
• The Phalangeal Bar will extend the toes;
• The Metatarsal Pad will "open" the metatarso-phalangeal articulations;
• The heel Cup can always be added to stabilize the calcaneus and keep the foot in proper
position on the insole.

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Morton's Neuroma
Type of insole:
Stabilisation, with an antalgic effect

Elements used:
• Metatarsal Pad
• (Navicular Pad)
• (Heel Cup)
Mode of action of the insole:
•
rd th
The Metatarsal Pad helps "opening" the 3 / 4 inter-phalangeal space thereby releasing the
pressure on the nerve

Talalgia
Type of insole:
Unload with an antalgic effect. Elastomers ("energy absorbing") prefabricated insoles can also be used
if available.

Unload insole with 2cm EVA heel pad

Elastomer off-the-shelve insole for
treatment of talalgia

Elements used:
• Heel Pad (2 cm EVA).
• A hole can be done in the Heel Pad on the painful area to eliminate pressure on that spot.
• A navicular pad for unloading can also be added to reduce load on the internal aspect of the
calcaneus, if needed.

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Mode of action of the insole:
The heel pad distributes the pressure on the entire heel and reduces it on the painful place; it also
reduces the tension on the plantar aponevrosis through the elevation of the heel.

Sensibility Loss
The goal of the orthopaedic treatment for non-sensitive feet is first to protect the tissues from
mechanical pressures until complete recovery.
Orthopaedic shoes
Especially adapted to the affected foot and protecting
the ulcers. Materials used must be soft enough to
offer both support and comfort. Slippers made out of
EVA after a cast mould are a very good solution to
wear at home. The heel must be held in neutral
position by the shoe heel counter.
Let us add that the out sole of the shoe must be rigid
in order to reduce the friction forces between the skin
and the shoe, and to reduce the movements of
flexion and extension at the metatarso-phalangeal
articulation.

Insole
The insoles for non-sensitive feet are palliative. They must be done
after a cast in order to respect the anatomical shape of the foot
without bringing any correction. The material used is EVA and
covers the entire foot sole. Callosities and / or ulcers should be
relieved from pressure.

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Shoe modification
The use of a rocker sole or of a metatarsal bar reduces the vertical forces on the metatarsal heads
and facilitates the gait.

Club Foot and Metatarsus Adductus

In case of equinus of the foot, the heel of the shoe is taken away and the front part of the shoe sole is
increased.
Type of insole:
Stabilisation. The correction obtained by orthopaedic splints or other methods is maintained by the
insole.
Elements used:
• Metatarsal Pad
• Total Pronator Wedge

Measurment Methods

The two usual measurements methods for foot orthoses are the footprint and the plaster mould.
The footprint gives a picture of the pressure distribution on the plantar surface of the foot. It will help us
prescribe and manufacture an appropriate foot orthosis.

A plaster mould is necessary for the manufacture of rigid and semi-rigid insoles. It is also used to
manufacture soft insoles for non-sensitive feet (diabetes). For other soft insoles, often the orthotist will
use other methods to record the footprint.

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Plaster Mould
The cast is taken with the patient lying in prone (or in supine, according to the method used) position
on the examination table and the orthotist sitting on a stool in front of him.

Cast taken in supine position

Cast taken in prone position

Podoscope
The podoscope is a device that gives the image of the plantar side of the foot in standing position
through an assembly of glass and mirrors. It gives a visual footprint It is a good diagnostic instrument.

The range and the level of the pressure under the feet are seen thanks to the effect of ischemia (hypo-
vascularization) of the foot sole (the regions under pressure become white).

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Podograph (Foot Pressure Graph)
The podograph gives an ink footprint on paper. It is composed of
an ink box covered by a rubber sheet and in which the paper to
be printed is introduced. The patient stands on the rubber sheet
and his footprint is copied on the paper.
Draw the shape of the foot with a pencil held perpendicular to the
ground. Draw marks behind the metatarsal heads medially and
laterally, and at the level of the malleoli. Full weight bearing is
being performed. Various foot parameters can be taken now.

Podograph – alternative method

If there is no podograph available, there is a very simple and economical way, using a regular A4 size
white paper (thick paper is better than regular printing paper) vaseline (petroleum jelly) and colorant
powder or sand, and that will give a decent footprint:
• Cover the plantar surface of the patient's foot with a thin layer of Vaseline;
• Place the foot a thick white paper in the same way you would do with the podograph;
• Draw the foot outline with a ball pen held vertically;
• Mark the points: just behind the first and fifth metatarsal heads; at the level of the navicular;
at the level of medial and lateral malleoli;
• Remove the foot from the paper;

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 • Spread colorant powder or sand over the paper and remove the extra by blowing it off
carefully (do not touch with hands or you will alter the print)
The foot print is realized and gives a good picture of the pressure distribution (see picture below)

Foot print using vaseline and colorant powder / sand

Left: foot print with reference marks
Right: drawing of different elements

Foam Impression
The footprint is taken using a block of compressible foam.
By standing with one foot on the foam, the patient compresses the
foam and it gives a negative footprint.
Liquid plaster is poured into the print, giving a positive plaster mould
of the foot.

Computerized: PodoView and SoleScan

The newest methods of measurements are computerised. The patient stands on a podoscope which is
video connected to a computer. The footprint can be seen on the computer screen and elements built
up according to the correction required. The computer is itself connected to a robot (computerised
milling machine) which actually manufactures the insole.
In the most sophisticated systems, the foot is scanned and seen in three dimensions on the computer.
Corrections are made “virtually” and the result is seen immediately on the computer screen.

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Insoles Fabriction Method

Casting Technique
Material needed
Indelible pencil, scissors, plaster of Paris bandage (1 piece of 80cm and 1 piece of 60cm), water,
assessment form, tape measure.
Casting procedure
1. Patient lies in prone (or in supine) position
on the examination table;
2. Fold the 80cm PoP bandage into 2 to
obtain a double layer & make a 1cm fold
on the length to reinforce that one side.
Dip the bandage into lukewarm water;
3. Rinse out the excess of water;
4. Apply the PoP starting from the heel, to
enclose the calcaneus entirely just below
the malleoli;
5. Fold one side of the PoP on the plantar
surface of foot;
6. Fold the opposite side so that they overlap
nicely;
7. Prepare the 60cm PoP the same way as
the first one;
8. Apply the PoP starting from the toes and
joining the first PoP on both sides. Do not
push hard on the toes or the toes will flex;
9. Fold one side of the PoP than the
opposite side so that they overlap nicely;
10. Hold the 5 toes in your 2 hands and move
them slightly up and down;
11. Massage gently the cast all over without
modifying its shape. Make sure that the
toes are aligned in a neutral position;
12. When the cast is hard, remove it pulling the heel out first.
Rectification procedures
It is important to do modifications in an orderly way. In orthotics the cast is very important. A good cast
will give an easier time at modification. With the negative mould the alignment of the rear foot and
forefoot is done at time of casting (subtalar neutral / midfoot locked). The walking pattern and
muscular weakness have been recorded on the chart. The material used in fabrication of the Foot
orthosis helps to determine how the cast is modified.
Cast modification involves 6 steps:
1. evaluation of the positive mould before modification
2. modification of the heel and forefoot
3. modification of the medial and lateral longitudinal arches
4. addition of a metatarsal bar
5. addition of plaster build-ups
6. smoothing and evaluation of cast

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1. Evaluation of the positive mould
Positive moulds are checked on a flat surface. The following landmarks are especially checked:
• the heel and forefoot are parallel, and the calcaneus is perpendicular to the base
• the medial border of the foot is straight (not pronated)
• the lateral forefoot is in neutral alignment (no bulge)
• both casts are similar in shape and alignment (right and left feet)
Once this has been done, the orthotist can decide what changes are necessary to give the support
needed with minimal changes to the cast. It is important not to modify the cast too much or the shape
will be lost and there are no accurate measurements to compare to.
The orthotist should know which material will be used to make the foot orthosis as it will determine
what small changes are needed in plaster technique: a metatarsal pad or bar is not built into a rigid
plastic insole as adjustment is not possible after fabrication. The metatarsal pad is added afterward
with this selected material. Other materials like EVA permit a metatarsal bar to be built into the cast
during modification.
2. Modification of the heel and forefoot
Using a flat surform blade in the holder, flatten the heel and the
forefoot (only) so that the desired alignment is obtained. The
metatarsal heads and the heel base are parallel in both coronal and
sagittal planes. The cast sits stable on a flat surface.

3. Modification of the medial and lateral longitudinal arches

Once the rear foot and forefoot are parallel, the next step is to shape and blend the medial and lateral
longitudinal arches. Using a half round surform follow the shape of the medial longitudinal arch that
you formed while casting the foot. Blend it into the medial border of the foot. The medial arch is
defined by the distance from the distal third of the heel to the metatarsal heads.
Now that you know the length of the arch, the lateral
longitudinal arch can be carved into the cast. Generally,
this arch is not very high but is needed to properly support
the foot. Over modification can be done if a lateral ground
reaction force is needed to assist in correcting the knee –
ankle - foot alignment.
Using a half round file carve a lateral arch into the plantar
lateral surface of the foot, while paying attention to the
position of the medial longitudinal arch. Blend the arches
so that there are no ridges. Blend the arch into the lateral
border of the foot being careful not to remove plaster from
the base of the fifth metatarsal.
Addition of a metatarsal bar
Sometimes the patient requires a metatarsal bar to be built into the foot orthosis. This is required when
they have pain on the plantar surface of the foot underneath the metatarsal heads. This usually
happens because the metatarsal arch has collapsed and the weight is now pressing on the metatarsal
heads.
The arch needs to be recreated by pushing on the proximal edge of the metatarsal heads themselves.
This position can be marked by dividing the 1st and 5th metatarsal heads in half and drawing a line

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across the plantar surface of the foot. The arch position is drawn out by curving the line around the 1st
and 5th head, then arcing around the 2nd to 4th metatarsal heads so that the line is just distal to the
mid-line drawn previously.

The arch is cut into the cast using a scarpers knife. The arch should be deeper on the big toe side and
blend proximally into the medial and lateral longitudinal arches. The depth should be at least 1 cm at
the high point. If at time of fitting there is too much support it can be reduced by sanding. It takes more
time and work to add onto a metatarsal arch than it does to sand it down.

4. Addition of plaster build-ups

The foot requires build-ups on the bony prominence and borders so that the foot orthosis does not put
pressure on sensitive areas.
Addition of plaster to the toes ensures that the final orthosis is larger than the foot on weight bearing
and that the orthosis does not slide around in the shoe. Again addition of plaster to the mould is done
with care so that the shape of the mould is not lost.
The plaster should be mixed so that it is not runny. Water is used in small amounts to smooth the
plaster to the mould. If the same step by step procedure is used each time you modify the cast the
process becomes routine.
• add a small amount of plaster to the base of the fifth metatarsal and the navicular. Blend to
cast with fingers wet with water;
• •add plaster to the medial and lateral borders of the foot, starting at the metatarsal heads and
working from the dorsum side of the foot towards the plantar surface Add the plaster in small
amounts so that you do not loose the shape of the mould. Work proximally to the level of the
malleoli, no plaster is added to the mould posterior to this point. Blend and smooth;
• •using a footboard add plaster to the toes starting at the metatarsal heads and working distally
so that the toe box area is similar in shape to the shoe profile. Approximately 2.5 cm should be
added distally to the toes so that there is enough material to trim to match the shoe liner;
• •after the plaster has hardened use a flat surform in a holder to realign the plantar surface of
the forefoot.
For supra malleolar types of insoles then there is also addition of plaster to the malleoli so that there is
room for padding and no pressure is placed on the malleoli themselves.
If a forefoot abduction or adduction stop is required then should be a plaster build-up over the
appropriate metatarsal head so that the final plastic trim line is deep enough.

5. Smoothing and evaluation of the casts

When the cast modification is complete, the casts are smoothed using screening and the shape and
alignment is compared between the two feet. As mentioned previously the desired alignment is neutral
subtalar and parallel rear foot / forefoot. The two feet are held so that the plantar surfaces are together
and the shape, position and depth of the medial / lateral / metatarsal arches are compared. If they are
different, changes should be made to reach symmetry.

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We are now ready for the fabrication. Drying time depends on the type of material used in fabrication.
EVA is done on slightly damp cast; polypropylene must be done on a dry cast or else it will bubble.
If the patient requires FO made of plastic and they also require a rear foot post (medial or lateral), then
the desired post must be built into the cast before fabrication. This specific modification is done with a
flat surform and the amount of the post depends on the amount of control needed.

Fabrication of Rigid Insoles

Rigid insoles can be made of various materials. Here is a non exhaustive list:
- thermoplastics: acrylic resins, polyethylene, polypropylene, polyester resins
- metal: duralumin, stainless steel, titanium
Manufacture of polypropylene insoles:
Once the positive plaster mould has been rectified, mould a 3 or 4 mm polypropylene sheet.
The hard PP insole is cut at the level of the metatarsal heads so that gait is not disturbed and toes are
not squeezed in the shoe.

Fabrication of Semi-rigid Insoles

Semi-rigid insoles can be made of moulded leather or thin thermoplastic, covered inside by a softer
material such as polyethylene foam (EVA).
Manufacture of PP and EVA insoles:
Once the positive plaster mould is rectified, mould a 3 mm EVA on the cast and eventually add some
pads where the insole should be more soft (for example metatarsal pad, navicular pad, ...). Than cover
with a 3 mm PP.
The semi-rigid insole is cut at the level of the metatarsal heads for the same reasons as for the rigid
insole.

Fabrication of Soft Insoles

The soft insole is done using the podograph footprint and the prescription. The podograph footprint
gives the shape of the foot, its size, and the exact place of the metatarsal heads. It also shows the
repartition of pressure under the foot.

1. Preparation of the base of the insole:

The base of the insole is made of rigid leather. The base is cut using prefabricated models.
The base of the insole will be 1 to 1.5 cm longer than the footprint. Laterally it will be about 8 mm
thinner than the forefoot (4 mm on each side).

2. Drawing of the elements of the insole:

The elements have been already determined during the patient’s evaluation.
Draw the different elements directly on the footprint.

3. Preparation of the elements of the insole:

The elements are cut in EVA 6 or 12 mm, depending on the prescription. They are cut slightly bigger
than the drawing so that it can later be trimmed to the exact shape. Prefabricated elements can be
used, if available.

4. Gluing of the elements on the base of the insole:

The elements are glued and then trimmed one after the other on the base at their exact position.

5. Adjustment of the elements of the insole:

The different elements of the insole are grinded to their final shape.

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The heel pad as well as all elements touching the borders of the insoles must keep a lateral inclination
(not vertical).

6. Fitting of the insole:

The insole is tried by the patient before finishing it.
• Patient standing on the insole:
o check the right place, shape and height of the elements: ask the patient to lift the heel in
order to be able to check the place of the metatarsal pad or bar.
o ask the patient if there is any discomfort and / or abnormal pressure.
• Patient sitting
o place the insole on the foot and repeat the previous tests
o If necessary, some elements must be adjusted in their shape, height or position.

7. Finishing of the insole:

The base and elements are covered by a thin leather, artificial leather (stronger and cleaner), or thin
EVA (1 mm).

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6.3 ORTHOPAEDIC SHOES

Generally made after a plaster mould, they are manufactured by

specialists called orthopaedic shoemakers. Orthopaedic shoes
protect the foot and maintain or correct foot deformities.
A standard shoe for a foot orthosis is usually made of leather
with a blucher pattern, leather lining, plain toe, high and broad
toe box, roomy vamp, high lacing, extended heel counter, broad
and low rubber heel, wide and strong shank reinforced with a
spring steel shank, and a thick leather or neoprene sole with or
without a rocker bar.

Footwear Functions

The shoe should provide several basic functions:

• protection for the foot from the surrounding environment
• provide friction between the foot and the ground
• stabilise the foot through all stages of the gait cycle
• assist the foot by providing shock absorbing capabilities
• help maintain and / or correct various foot deformities
• act as a distal attachment for the lower extremity orthoses

Parts of the Shoe

The shoe is separated into upper and lower sections:

Upper Part Includes Lower Part Includes

• Vamp • Outer Sole
• Quarter • Inner Sole
• Toe Box • Shank
• Throat • Heel
• Tongue
• Heel Counter

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Fit of the Shoe

Best judged on a weight bearing foot. Shoe should provide support, cushioning to the ball of the foot,
firm arch support, flexibility of the forefoot for easy push off. The shoe should contain and support the
foot, not squeeze or compress it. The toe box should provide free movement of the toes without
pressure. Recommend approximately 1 cm space between the end of the longest toe and the end of
the shoe.
Pointed or sloping toe box is not a good idea as it puts pressure on the toes.
The shoes should have the following characteristics:
• firm heel counter
• firm upper
• deep and wide toe box
• stiff in torsion
• lace-up

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Measurements of Orthopaedic Footwear

The following picture shows the different measurements taken for the manufacture of orthopaedic
shoes of different designs.

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6.4 SHOE MODIFICATIONS

Functions

There are two reasons for shoe modifications:

a) support the foot for improved balance in standing and walking.
b) relieve painful areas from abnormal pressure.
The foot deformities are supported or accommodated depending on the type. If the deformity is fixed it
should be accommodated rather than corrected. Flexible deformities should be actively corrected.

Elements

Different types of modifications exist. Here are the main ones: see drawings on following pages.
Here are the most common ones and their function:
1. Thomas heel: lengthening of the medial distal part of the heel to increase the base of support
medially.
2. Wedging: addition of material to medial or lateral side of the shoe to act as a post. This will use
ground reaction force to correct excessive body weight being borne on the medial or lateral side of
the foot.
3. Buttress: medial or lateral flare of the sole that extends up to support the side of the shoe. This
increases ankle stability. This can help to control excessive pronation or supination from heel
strike - mid stance by acting as a lever arm that stops the unwanted motion.
4. Metatarsal bar: this prevents extension of the metatarso-phalangeal joint and reduces the vertical
forces to the forefoot at heel off. It also shortens the weight bearing area. This can be used in
treating metatarsalgia, fractures of the toes, callous formation on the metatarsal heads, ulcers.
5. Rocker sole: modification of the shoe to allow for easier rollover. This smoothes out the walking
pattern particularly if the person wears a rigid AFO or KAFO. Prevents too much weight being
borne on the metatarsal heads.
6. SACH heel: (bevelled heel) helps with shock absorption on the heel strike and rates when foot flat
(stability) is reached. Similar to SACH in prosthetic feet.
7. Sole lift: permanent, external modification of the midsole and outsole to add a prescribed amount
of height to one or both shoes. Used in leg length discrepancy.

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 Acknowledgements :

- Franck Joumier Prosthetist Orthotist

- Girma Bireda Prosthetist Orthotist

- Hiywot Zerihun Biomedical Engineer

- Dr. Johanes Abraham Pathologist

- Bernard Matagne Prosthetist Orthotist

- Jean Pierre Schepens Prosthetist Orthotist

- Roberto Ciconne Physiotherapist

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