Gait

IntroductionGait pattern.jpg

Human gait depends on a complex interplay of major parts of the nervous, musculoskeletal and
cardiorespiratory systems.

The individual gait pattern is influenced by age, personality, mood and sociocultural factors.

The preferred walking speed in older adults is a sensitive marker of general health and survival.

Safe walking requires intact cognition and executive control.

Gait disorders lead to a loss of personal freedom, falls and injuries and result in a marked reduction in
the quality of life[1].

Definitions

Gait - the manner or style of walking.

Gait Analysis - An analysis of each component of the three phases of ambulation is an essential part of
the diagnosis of various neurologic disorders and the assessment of patient progress during
rehabilitation and recovery from the effects of neurologic disease, a musculoskeletal injury or disease
process, or amputation of a lower limb.

Gait speed

The time it takes to walk a specified distance, usually 6 m or less. Slower speeds correlate with an
increased risk of mortality in geriatric patients.[2]

Normal walking speed primarily involves the lower extremities, with the arms and trunk providing
stability and balance.

Faster speeds - body depends on the upper extremities and trunk for propulsion, balance and stability
with the lower limb joints producing greater ranges of motion.[3]

Gait cycle is a repetitive pattern involving steps and strides[4]

Step is one single step

Stride is a whole gait cycle.

Step time - time between heel strike of one leg and heel strike of the contralateral leg[4].

Step width - the mediolateral space between the two feet[4].

The demarcation between walking and running occurs when periods of double support during the
stance phase of the gait cycle (both feet are simultaneously in contact with the ground) give way to two
periods of double float at the beginning and the end of the swing phase of gait (neither foot is touching
the ground)[5].

The Gait CycleWalk.jpg

The sequences for walking that occur may be summarised as follows:[6]

Registration and activation of the gait command within the central nervous system.

Transmission of the gait systems to the peripheral nervous system.

Contraction of muscles.

Generation of several forces.

Regulation of joint forces and moments across synovial joints and skeletal segments.

Generation of ground reaction forces.

The normal forward step consists of two phases: stance phase; swing phase,

The Stance phase occupies 60% of the gait cycle, during which one leg and foot are bearing most or all of
the bodyweight

The Swing phase occupies only 40% of it[4], during which the foot is not touching the walking surface
and the bodyweight is borne by the other leg and foot.

In a complete two-step cycle both feet are in contact with the floor at the same time for about 25 per
cent of the time. This part of the cycle is called the double-support phase.Gait cycle phases: the stance
phase and the swing phase and involves a combination of open and close chain activities.[3]

The 90 second video below gives the basics of this cycle

[7]
Figure2.jpg

Phases of the Gait Cycle (8 phase model):[4][8]

Initial Contact

Loading Response

Midstance

Terminal Stance

Pre swing

Initial Swing

Mid Swing

Late Swing.[9]

Heel Strike (or initial contact) -

Short period, begins the moment the foot touches the ground and is the first phase of double support.
[3]

Involves:

30° flexion of the hip: full extension in the knee: ankle moves from dorsiflexion to a neutral (supinated
5°) position then into plantar flexion.[3][4]

After this, knee flexion (5°) begins and increases, just as the plantar flexion of the heel increased.[4]

Plantar flexion is allowed by eccentric contraction of the tibialis anterior

Extension of the knee is caused by a contraction of the quadriceps

Flexion is caused by a contraction of the hamstrings,

Flexion of the hip is caused by the contraction of the rectus femoris.[4]

Foot Flat (or loading response phase)

Body absorbs the impact of the foot by rolling in pronation.[3]

Hip moves slowly into extension, caused by a contraction of the adductor magnus and gluteus maximus
muscles.

Knee flexes to 15° to 20° of flexion. [4]

Ankle plantarflexion increases to 10-15°.[3][4]

Midstance

Hip moves from 10° of flexion to extension by contraction of the gluteus medius muscle.[4]

Knee reaches maximal flexion and then begins to extend.

Ankle becomes supinated[3] and dorsiflexed (5°), which is caused by some contraction of the triceps
surae muscles.[3]

During this phase, the body is supported by one single leg.

At this moment the body begins to move from force absorption at impact to force propulsion forward.
[3]

Heel Off

Begins when the heel leaves the floor.

Bodyweight is divided over the metatarsal heads.[3]

10-13° of hip hyperextension, which then goes into flexion.

Knee becomes flexed (0-5°)[4]

Ankle supinates and plantar flexes.[4]

Toe Off/pre-swing

Hip becomes less extended.

Knee is flexed 35-40°

Plantar flexion of the ankle increases to 20°.[3][4]

The toes leave the ground.[4]

Early Swing

Hip extends to 10° and then flexes due to contraction of the iliopsoas muscle[4] 20° with lateral rotation.
[3][4]

Knee flexes to 40-60°

Ankle goes from 20° of plantar flexion to dorsiflexion, to end in a neutral position.[3]

Mid Swing

Hip flexes to 30° (by contraction of the adductors) and the ankle becomes dorsiflexed due to a
contraction of the tibialis anterior muscle.[4]

Knee flexes 60° but then extends approximately 30° due to the contraction of the sartorius muscle.[3][4]
(caused by the quadriceps muscles).[3][4]

Late Swing/declaration

Hip flexion of 25-30°

Locked extension of the knee

Neutral position of the ankle.[3]

Range of Motion during Gait

[10]

Ground Reaction Force during Gait

[11]
Muscular Activity during Gait

[12]

Gait Cycle - Anatomical Considerations

Pelvic region - anterior-posterior displacement, which alternates from left to right. Facilitates anterior
movement of the leg (each side anterior-posterior displacement of 4-5°).[3][4][8]

Frontal plane - varus movement in the: foot between heel-strike and foot-flat and between heel-off and
toe-off; hip, in lateral movements (when the abductors are too weak, a Trendelenburg gait can be
observed).[3][8] Valgus movement between foot-flat and heel off in the feet.

A disorder in any segment of the body can have consequences on the individual's gait pattern.[13]

Gait Disorders

Gait disorders - altered gait pattern due to deformities, weakness or other impairments eg loss of motor
control or pain[14].

Human falls.jpg

Prevelence increases with age and the number of people affected will substantially increase in the
coming decades due to the expected demographic changes.

Lead to a loss of personal freedom and to reduced quality of life.

Precursors of falls and therefore of potentially severe injuries in elderly persons[1].

Gait DescriptionsTrendelenburg gait.jpg

This is not an exhaustive list.

Antalgic gait a limp adopted so as to avoid pain on weight-bearing structures, characterized by a very
short stance phase.
Ataxic gait an unsteady, uncoordinated walk, with a wide base and the feet thrown out, coming down
first on the heel and then on the toes with a double tap.This gait is associated with cerebellar
disturbances and can be seen in patients with longstanding alcohol dependency. People with
'Sensory'Disturbances may present with a sensory ataxic gait. Presentation is a wide base of support,
high steps, and slapping of feet on the floor in order to gain some sensory feedback. They may also need
to rely on observation of foot placement and will often look at the floor during mobility due to a lack of
proprioception

Equine gait a walk accomplished mainly by flexing the hip joint; seen in crossed leg palsy.

Parkinsonian Gait (seen in parkinson's disease and other neurologic conditions that affect the basal
ganglia). Rigidity of joints results in reduced arm swing for balance. A stooped posture and flexed knees
are a common presentation. Bradykinesia causes small steps that are shuffling in presentation. There
may be occurrences of freezing or short rapid bursts of steps known as ‘festination’ and turning can be
difficult.

Trendelenburg gait, the gait characteristic of paralysis of the gluteus medius muscle, marked by a listing
of the trunk toward the affected side at each step.

Hemiplegic gait a gait involving flexion of the hip because of footdrop and circumduction of the leg.

Steppage gait the gait in footdrop in which the advancing leg is lifted high in order that the toes may
clear the ground. It is due to paralysis of the anterior tibial and fibular muscles, and is seen in lesions of
the lower motor neuron, such as multiple neuritis, lesions of the anterior motor horn cells, and lesions
of the cauda equina.

Stuttering gait a walking disorder characterized by hesitancy that resembles stuttering; seen in some
hysterical or schizophrenic patients as well as in patients with neurologic damage.

Tabetic gait an ataxic gait in which the feet slap the ground; in daylight the patient can avoid some
unsteadiness by watching his feet.

Waddling gait exaggerated alternation of lateral trunk movements with an exaggerated elevation of the
hip, suggesting the gait of a duck; characteristic of muscular dystrophy.

Diplegic Gait (Spastic gait). Spasticity is normally associated with both lower limbs. Contractures of the
adductor muscles can create a ‘scissor’ type gait with a narrowed base of support. Spasticity in the lower
half of the legs results in plantarflexed ankles presenting in ‘tiptoe’ walking and often toe dragging.
Excessive hip and knee flexion is required to overcome this

Neuropathic Gaits. High stepping gait to gain floor clearance often due to foot drop[13][14][15][2]

[16]
Causes of gait disorders

They include neurological, orthopedic, medical and psychiatric conditions and multifactorial etiology
becomes more common with advancing age, making classification and management more complex. Any
gait disorder should be thoroughly investigated in order to improve patient mobility and independence,
to prevent falls and to detect the underlying causes as early as possible. Thorough clinical observation of
gait, careful history taking focussed on gait and falls and physical, neurological and orthopedic
examinations are basic steps in the categorization of gait disorders and serve as a guide for ancillary
investigations and therapeutic interventions.

Musculoskeletal Causes

Pathological gait patterns resulting from musculoskeletal are often caused by soft tissue imbalance, joint
alignment or bony abnormalities affect the gait pattern as a result[14].

Hip Pathology

Arthritis is a common cause of pathological gait. An arthritic hip has reduced range of movement during
swing phase which causes an exaggeration of movement in the opposite limb ‘hip hiking[14].

Excessive Hip Flexion can significantly alter gait pattern most commonly due to; • Hip flexion
contractures • IT band contractures, • Hip flexor spasticity, • Compensation for excessive knee flexion
and ankle DF, • Hip pain • Compensation for excess ankle plantar flexion in mid swing. The deviation of
stance phase will occur mainly on the affected side. The result is forward tilt of the trunk and increased
demand on the hip extensors or increased lordosis of the spine with anterior pelvic tilt. A person with
reduced spinal mobility will adopt a forward flexion position in order to alter their centre of gravity
permanently during gait.

Hip Abductor Weakness. The abductor muscles stabilise the pelvis to allow the opposite leg to lift during
the swing phase. Weak abductor muscles will cause the hip to drop towards the side of the leg swinging
forward. This is also known as Trendelenburg gait[15]

Hip Adductor Contracture. During swing phase the leg crosses midline due to the weak adductor
muscles, this is known as ‘scissor gait’[15]

Weak Hip Extensors will cause a person to take a smaller step to lessen the hip flexion required for initial
contact, resulting in a lesser force of contraction required from the extensors. Overall gait will be slower
to allow time for limb stabilisation. Compensation is increased posterior trunk positioning to maintain
alignment of the pelvis in relation to the trunk[15]
Hip Flexor Weakness results in a smaller step length due to the weakness of the muscle to create the
forward motion. Gait will likely be slower and may result in decreased floor clearance of the toes and
create a drag

Knee Pathologies

Weak Quadriceps. The quadriceps role is to eccentrically control the knee during flexion through the
stance phase. If these muscles are weak the hip extensors will compensate by bringing the limb back
into a more extended position, reducing the amount of flexion at the knee during stance phase.
Alternatively heel strike will occur earlier increasing the ankle of plantar flexion at the ankle, preventing
the forward movement of the tibia, to help stabilise the knee joint[15].

Severe Quadriceps Weakness or instability at the knee joint will present in hyperextension during the
initial contact to stance phase. The knee joint will ‘snap’ back into hyperextension as the bodyweight
moves forwards over the limb[15]

Knee Flexion Contraction will cause a limping type gait pattern. The knee is restricted in extension,
meaning heel strike is limited and step length reduced. To compensate the person is likely to ‘toe walk’
during stance phase. Knee flexion contractures of more than 30 degrees will be obvious during normal
paced gait. Contractures less then this will be more evident with increased speeds[14][15].

Ankle Pathologies

Ankle Dorsiflexion Weakness results in a lack of heel strike and decreased floor clearance. This leads to
an increased step height and prolonged swing phase[15].

Calf Tightening or Contractures due to a period of immobilisation or trauma will cause reduced heel
strike due to restricted dorsiflexion. The compensated gait result will be ‘toe walking’ on stance phase,
reduced step length, and excessive knee and hip flexion during swing phase to ensure floor
clearance[14].

Foot Pathologies

Hallux Rigidus results in a lack of dorsiflexion of the great toe. The MPJ uses the windlass effect to raise
the arch and stiffen the foot during dorsiflexion of the hallux. This stiffness increases the efficiency of the
propulsion portion of the gait cycle. To be efficient in creating stiffness, the hallux should be able to
dorsiflex at least 65 degrees.

Leg length discrepancy

Leg length discrepancy can be as a result of an asymmetrical pelvic, tibia, or femur length or for other
reasons such as scoliosis or contractures. The gait pattern will present as a pelvic dip to the shortened
side during the stance phase with possible ‘toe walking’ on that limb. The opposite leg is likely to
increase its knee and hip flexion to reduce its length[14].

Antalgic Gait
Antalgic gait due to knee pain presents with decreased weight bearing on the affected side. The knee
remains in flexion and possible toe weight-bearing occurs during stance phase[14]

Antalgic gait due to ankle pain may present with a reduced stride length and decreased weight bearing
on the affected limb. If the problem is pain in the forefoot then toe-off will be avoided and heel weight-
bearing used. If the pain is more in the heel, toe weight-bearing is more likely. General ankle pain may
result in weight-bearing on the lateral border[14][15].

Antalgic gait due to hip pain results in a reduced stance phase on that side. The trunk is propelled
quickly forwards with the opposite shoulder lifted in an attempt to even the weight distribution over the
limb and reduce weight-bearing. Swing phase is also reduced[14].

Summary of Gait Deviations

Observed Gait DeviationLikely ImpairementCompensation/Mechanical Rationale

Hip

Backward leaning of the trunk during loading phaseWeak Hip ExtensorsThe line of gravity of the trunk
moves behind the hips thereby reducing the need for hip extension torque

Forward bending of the trunk during loading responseWeak QuadricepsThe trunk is moved forward to
bring the line of gravity anterior to the axis of rotation of the knee and reducing the need for knee
extensors

Lateral trunk lean towards the stance (Compensated Trendelenburg Gait)Marked weakness of the hip
abductors

Hip pain

Shifting of the trunk over the unaffected lower extremity reduces the demand of the hip abductors

Hip Circumduction

(semicircle movement of the hip during swing phase)

Hip flexor weaknessSemicircle movement includes the combination movement of hip flexion, hip
abduction and forward rotation of the pelvis

Knee

Flexed position of the knee during stance despite normal range of motion at the knee jointImpairement
at the ankle or the hip joint
(Compensation occurring at the knee joint)

Exaggerated hip flexion or ankle dorsiflexion during stance results in flexion of the knee

Excessive knee flexion during swing phaseReduced ankle dorsiflexion of the swing limbIncrease toe
clearance of the swing limb.

(This is accompanied with increased hip flexion)

Knee is kept in extension during loading phase

(No extension thrust is observed)

Weak quadricepsAnterior trunk lean is observed during early stance, thereby moving the line of gravity
of the trunk slightly anterior to the axis of rotation

Reduced knee flexion during swing phaseKnee extension contractureHip hiking or hip circumduction will
be observed as compensation

Ankle

Foot slap

Quick ankle plantar flexion occurring after heel contact

Weakness in ankle dorsiflexorsNone/less active dorsiflexion occurs during swing phase

Normal dorsiflexion can occur during stance phase (if there is normal range of motion at the ankle joint)

Drop Foot

Ankle remains in plantar flexion during swing phase

Weakness in ankle dorsiflexorsTo prevent toes from dragging during the swing phase hip circumduction,
hip hiking or exaggerated hip and knee flexion will be noted
[17]

Below are links to videos demonstrating normal gait and various gait abnormalities:

[18]

[19]

Age-Related Gait Changes

Ageing is marked with cognitive decline, reduction in joint motion due to osteopenia and osteoporosis.
[20] And most especially plantar flexors loss that reduce stance phase in this population with reduction
in acuity for auditory, vestibular, visual and somatosensory system.[21] [22] This factors interplay to
results in increase in prevalence of gait disorders among older adults.

Also, any threat to balance induces changes in the strategies for standing and walking - the stance and
gait base is widened, bipedal floor contact is prolonged, step length becomes shorter, the feet are lifted
less high during the swing phase, walking becomes slower and the posture becomes stooped.

Bianca-jordan-IPjWtxPJUQc-unsplash.jpg

The fear of falling and the actual risk of falling increase with age.

Older persons are therefore more likely to use these protective gait strategies.

As muscle power diminishes and proprioception and vision become impaired with age,

body sway on standing, which is constantly present to a slight degree, increases.

In younger persons this sway can be compensated by activating the muscle groups around the upper
ankle joints. Older persons shift this compensation to the proximal muscle groups around the hips due
to loss of distal proprioception.

This requires an increased reliance on vestibular afferent, which undergo less change during the ageing
process.

The preferred walking speed in apparently healthy elderly subjects declines by 1 % per year from a mean
of 1.3 m/s in the seventh decade to a mean of 0.95 m/s in those aged over 80 years (caused by a
decrease in step length rather than by a change in cadence).

Gait changes are to some degree a consequence of normal ageing however individual walking speed in
elderly subjects is a strong indicator of general health and survival[1]

Some specific changes observed in elements of gait as affected in older adults are not limited to:

reduction in gait velocity (speed of walking) due to shorter steps but at the same rate (cadence).

And increase in time spent in double stance phase

Because of multi-decline in body physiological functions and prevalent of multi-morbidity among this
population it is not uncommon to have mixtures of neurological and musculoskeletal related gait
disorders in this population.[23] Common gait disorders in older adults under neurological causes are
sensory ataxia, Parkinsonism & frontal gait disorders. While non-neurological ( includes hip and knee
osteoarthritis.[24]

Gait Analysis

The analysis of the gait cycle is important in the biomechanical mobility examination to gain information
about lower limb dysfunction in dynamic movement and loading.[25]

When analyzing the gait cycle, it is best to examine one joint at a time.[3]

Objective and subjective methods can be used.[26][27]

Subjective

Different gait patterns - We might ask the individual to walk normally, on insides and outsides of feet, in
a straight line, running (all the time looking to compare sides and understanding of "normal").

Ask/observe the type of footwear the patient uses (a systematic review suggests shoes affect velocity,
step time, and step length in younger children's gait[28]).
Objective

Gait Analysis CP.jpg

An objective approach is quantitative and parameters like time, distance, and muscle activity will be
measured. Other objective methods to assess the gait cycle that use equipment include:[29][27]

Video Analysis and Treadmill

Electronic and Computerized Apparatus

Electronic Pedometers

Satellite Positioning System[26]

Qualitative methods to assess and analyse gait include: [27]

Rancho Los Amigos Hospital Rating List[30]

Ten Meter Walking Test[31]

6 Minute Walk Test

2 Minute Walk Test

Dynamic Gait Index

Emory Functional Ambulation Profile[32]

Timed Up and Go Test[33] This test is statistically associated with falling in men, but not in women.

Functional Ambulation Categories[34]

Tinetti-Test[35]

Clinical Bottom LineGait assessment.png

Good knowledge of anatomy and biomechanics is important to understand the different phases of the
gait cycle. When you know the normal pattern, you can see what’s going wrong!

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Related articles

The Gait Cycle - Physiopedia

The Gait Cycle The action of walking may be summarised by the following sequence:[1] Registration and
activation of the gait command within the central nervous system. Transmission of gait signals to the
peripheral nervous system. Contraction of muscles. Generation of forces across joints Regulation of joint
forces and moments by skeletal segments. Generation of ground reaction forces (GRF). Normal gait
consists of two phases: stance phase; swing phase. These phases are further divided into a total of 8
sub-phases.[2] The gait cycle involves a combination of open- and closed-chain activities.[3] Stance
Phase The stance phase occupies 60% of the total gait cycle, during which some part of the foot is in
contact with the ground. It is further divided into five sub-phases: Initial contact (heel strike) Loading
response (foot flat) Mid-stance Terminal stance (heel off) Pre-swing (toe off) Swing Phase The swing
phase occupies 40% of the total gait cycle [4], during which the foot is not in contact with the ground
and the bodyweight is borne by the other leg and foot. It is further divided into three sub-phases: Initial
swing Mid-swing Late swing[5] In a complete two-step cycle both feet are in contact with the ground at
the same time for 20% of the total gait cycle, 10%at the beginning of the stance phase and 10% at the
end of the stance phase.[2] These are termed 'double-support periods'. The rest of the time is spent in
single support, when only one foot is in contact with the ground. The 90-second video below gives the
basics of this cycle: [6] Breakdown of Gait Cycle Sub-Phases[edit | edit source] Initial Contact (or Heel
Strike) - 0% The moment the foot touches the ground and begins the first phase of double support.[3] Its
function is to establish contact with the ground surface and initiate weight acceptance. [2]
Kinematics/Joint Motion Muscle Action Ankle Neutral, 0° Concentric to eccentric dorsiflexors Knee 5°
flexion Eccentric extensors Hip 30° flexion Concentric extensors and eccentric flexors Loading Response
(or Foot Flat) - 0-10% Begins with initial contact and continues until the contralateral foot leaves the
ground. The foot continues to accept weight and absorb shock by rolling into pronation.[3]
Kinematics/Joint Motion Muscle Action Ankle Rapid plantarflexion to 10° Eccentric dorsiflexors Knee
Flexes to 10-15° Eccentric extensors and concentric flexors Hip Gradual extension Concentric extensors
[2] Midstance - 10-30% Begins when the contralateral foot leaves the ground and continues until
ipsilateral heel lifts off the ground. The body is supported by a single leg and begins to move from force
absorption at impact to force propulsion forward.[3] Kinematics/Joint Motion Muscle Action Ankle
Gradual dorsiflexion Eccentric plantarflexors and concentric dorsiflexors Knee Begins to extend
Concentric extensors Hip Gradual extension Concentric extensors [2] Terminal Stance (or Heel Off) - 30-
50% Begins when the heel leaves the floor and continues until the contralateral foot contacts the
ground. In addition to single limb support and stability, this event serves to propel the body forward.
Bodyweight is divided over the metatarsal heads.[3] Kinematics/Joint Motion Muscle Action Ankle
Gradual dorsiflexion until a maximum of 10° before beginning to plantarflex Eccentric plantarflexors,
then concentric plantarflexors Knee Continues extending until a maximum of 5° of flexion before
beginning to flex Concentric extensors, then eccentric extensors and concentric flexors Hip Extends until
a maximum of 10° extension Eccentric flexors [2] Pre-Swing (or Toe Off) - 50-60% Begins when the
contralateral foot contacts the ground and continues until the ipsilateral foot leaves the ground.
Provides the final burst of propulsion as the toes leave the ground.[4] Kinematics/Joint Motion Muscle
Action Ankle Begins to plantarflex rapidly before foot leaves the ground Concentric plantarflexors Knee
Begins to flex rapidly Eccentric extensors Hip Begins to flex before foot leaves the ground Concentric
flexors [2] Early Swing - 60-75% Begins when the foot leaves the ground until it is aligned with the
contralateral ankle. This event functions to advance the limb and shorten the limb for foot clearance.
Kinematics/Joint Motion Muscle Action Ankle Continues to plantarflex until a maximum of 20° before
moving back towards a neutral position Eccentric dorsiflexors, then concentric dorsiflexors and eccentric
plantarflexors Knee Rapid knee flexion until a maximum of about 60° Eccentric extensors and concentric
flexors Hip Gradually flexes Concentric flexors [2] Mid-Swing - 75-85% Begins from the ankle and foot
alignment and continues until the swing leg tibia is vertical. As in early swing, it functions to advance the
limb and shorten the limb for foot clearance. Kinematics/Joint Motion Muscle Action Ankle Maintains a
neutral position Concentric dorsiflexors Knee Begins to extend Eccentric flexors Hip Continues to flex
until a maximum of just over 30° Concentric flexors [2] Late Swing/Deceleration - 85-100% Begins when
the swing leg tibia is vertical and ends with initial contact. Limb advancement slows in preparation.
Kinematics/Joint Motion Muscle Action Ankle Maintains a neutral position Concentric dorsiflexors Knee
Extends until full extension, and flexes just slightly before initial contact Eccentric flexors, then
concentric flexors Hip Hip remains flexed to around 30 ° Concentric flexors and eccentric extensors, then
concentric extensors [2] Clinical Application[edit | edit source] Understanding the gait cycle allows for
effective gait analysis. When analysing gait, it should be done systematically, looking at each joint
separately throughout the entire gait cycle and detecting deviations from normal.[2] Injury or disease
can alter any of the sub-phases of the gait cycle, resulting in distinct characteristics of the gait pattern.
[7]

Muscle Activity During Gait - Physiopedia

Gait Kinetics and Joint Moment Gait kinetics investigates the forces and moments of the gait cycle. This
includes the study of ground reaction forces (GRF), joint torque, plantar pressure distribution and
muscle activity.[1] The body should be in equilibrium during gait, therefore, the external ground reaction
forces (GRF) (external moment) should be balanced by the internal muscle forces (internal moment).[2]
Different muscles perform different actions at every phase to create an internal moment against the
external joint moment. Ground reaction force vectors create the direction of moment and the muscle
will act in the opposite direction. If the ground reaction force falls anterior to the axis of the joint, the
proximal segment of the joint will move anteriorly; if the ground reaction force falls posterior to the axis
of the joint, the proximal segment of the joint with move posteriorly. Muscles can contract
concentrically or eccentrically to overcome the external moment. During a concentric muscle
contraction, the muscle shortens and there is movement at the joint, whereas during an eccentric
contraction the muscle lengthens while producing force. Read more: Types of Skeletal Muscle Actions
Ground Reaction Forces Breakdown of Kinematics and Kinetics During the Gait Cycle[edit | edit source]
Stance Phase[edit | edit source] Initial Contact (or Heel Strike) The moment the foot touches the ground
and begins the first phase of double support. Its function is to establish contact with the ground surface
and initiate weight acceptance.[3] Sagittal Plane: Kinematics and Kinetics at Initial Contact[4] Joint
Kinematics Kinetics External Forces Internal Forces/ Muscle Action Ankle Ankle moves from 0° neutral at
initial contact to 5° of plantarflexion at foot flat GRF posterior to axis of rotation of the ankle joint
External plantar flexor moment created Internal dorsiflexor moment Eccentric contraction of
dorsiflexors (tibialis anterior, extensor digitorum longus, extensor hallucis longus) Knee Knee moves
from 0° extension at initial contact to 15° flexion at foot flat GRF anterior to axis of rotation of the knee
joint External extensor moment created Internal flexor moment Concentric contraction of knee flexors
(hamstrings) Eccentric contraction of knee extensors (quadriceps) The range of motion change in the
knee joint (0° - 15°), results in the shifting of GRF from anterior to posterior - this will result in external
flexor torque, and the knee extensors will work eccentrically to control the knee Hip Hip moves from 20°
flexion at initial contact to 15° of flexion at foot flat GRF anterior to axis of rotation of the hip joint
External flexor moment created Internal extensor moment Concentric contraction of hip extensors
(gluteus maximus) Frontal Plane: Muscle Activity and Motion in the Frontal Plane from Initial Contact to
Foot Flat[5] Joint Motion Muscle Activity Pelvis Forward rotation on right side of pelvis at initial contact
Left side of pelvis begins to move forward *Reference limb is the right lower extremity Hip Medial
rotation of the femur on pelvis Knee Valgus thrust Medial rotation of tibia Gracilis, vastus medialis,
semitendinosus Long head of biceps femoris to control medial rotation of tibia Ankle Valgus thrust with
increasing pronation Subtalar joint pronation - maximum at end of loading response Transverse tarsal
pronation Eccentric contraction of tibialis posterior to control valgus thrust on foot Foot Flat (Loading
Response) Begins with initial contact and continues until the contralateral foot leaves the ground. The
foot continues to accept weight and absorb shock by rolling into pronation.[3] Sagittal Plane: Kinematics
and Kinetics at Foot Flat[4] Joint Kinematics Kinetics External Forces Internal Forces/Muscle Action Ankle
Ankle moves from 5° of plantarflexion during foot flat to 5° of dorsiflexion at midstance GRF posterior to
axis of rotation of ankle joint External plantar flexor moment created Internal dorsiflexor moment
Concentric contraction of dorsiflexors Eccentric contraction of plantarflexors (gastrocnemius, soleus)
The range of motion change in the ankle from 5° plantarflexion to 5° dorsiflexion results in the shifting of
GRF from posterior to anterior, thus the posterior musculature (plantarflexors) is used eccentrically to
control dorsiflexion. Knee Knee moves from 15° flexion at foot flat to 5° flexion at midstance GRF
posterior to axis of rotation of the knee joint External flexor moment created Internal extensor moment
Concentric contraction of knee extensors Hip Hip moves from 15° flexion at foot flat to 0° at midstance
GRF anterior to axis of rotation of the hip joint External flexor moment created Internal extensor
moment Concentric contraction of hip extensors Frontal Plane: Muscle Activity and Motion in the
Frontal Plane from Foot flat to Midstance[5] Joint Motion Muscle Activity Pelvis Right side rotates
backward to reach neutral at midstance Lateral tilt towards swinging extremity *Reference limb is right
lower extremity Hip abductors active to prevent excessive lateral tilt (gluteus medius and tensor fascia
latae) Hip Medial rotation of the femur on the pelvis continues to a neutral position at midstance.
Adduction moment continues throughout single limb support Minimal or no activity Knee Reduction in
valgus thrust and tibia begins to rotate laterally Minimal or no activity Ankle Foot begins to move into
supination direction from pronation at end of loading response Foot neutral position at midstance
Tibialis posterior helps to produce supination Midstance Begins when the contralateral foot leaves the
ground and continues until the ipsilateral heel lifts off the ground. The body is supported by a single leg
and begins to move from force absorption at impact to force propulsion forward.[3] Sagittal Plane:
Kinematics and Kinetics at Midstance[4] Joint Kinematics Kinetics External Forces Internal forces/Muscle
Actions Ankle Ankle moves from 5° dorsiflexion at midstance to 0° of dorsiflexion at heel off GRF
anterior to axis of rotation of the ankle External dorsiflexor moment Internal plantarflexor moment
Concentric contraction of plantarflexors Knee Knee moves from 5° flexion at midstance to 0° flexion at
heel off GRF anterior to axis of rotation of the knee joint External extensor moment Internal flexor
moment Eccentric contraction of knee flexors Hip Hip moves from 0° flexion at midstance to 10° - 20° of
extension at foot flat GRF posterior to axis of rotation of the hip joint External extensor moment Internal
flexor moment Eccentric contraction of hip flexors (iliopsoas) Frontal Plane: Muscle Activity and Motion
in the Frontal Plane from Midstance to Heel Off[5] Joint Motion Muscle Activity Pelvis Right side moves
posteriorly from neutral *Reference limb is the right lower extremity Minimal or no muscle activity Hip
Lateral rotation of femur and adduction Inconsistent hip adductor activity Knee Lateral rotation of tibia
No activity Ankle Increased supination of subtalar joint Concentric plantarflexor activity Heel Off (or
Terminal Stance) Begins when the heel leaves the floor and continues until the contralateral foot
contacts the ground. In addition to single limb support and stability, this event serves to propel the body
forward. Bodyweight is divided over the metatarsal heads.[3] Sagittal Plane: Kinematics and Kinetics at
Heel Off[4] Joint Kinematics Kinetics External Forces Internal Forces/Muscle Actions Ankle Ankle moves
from 0° at heel off to 20° plantarflexion at toe off GRF anterior to the axis of rotation of the ankle
External dorsiflexor moment Internal plantarflexor moment Concentric contraction of plantarflexors
Knee Knee moves from 0° at heel off to 30° flexion at toe off GRF anterior to the axis of rotation of the
knee External extensor moment Internal flexor moment Concentric contraction of knee flexors Hip Hip
moves from 10° extension at heel off to 20° extension at toe off GRF posterior to the axis of rotation of
the hip joint External extensor moment Internal flexor moment Eccentric contraction of hip flexors
Frontal Plane: Muscle Activity and Motion in the Frontal Plane from Heel Off to Toe Off(End of Preswing)
[5] Joint Motion Muscle Activity Pelvis Left side moving forward until left heel contact (right toe off)
Lateral tilting to swing side ceases as contralateral limb begins stance phase and start of double support
period *Reference limb is the right lower extremity Eccentric control by adductors Hip Abduction as
weight is shifted onto opposite extremity. Lateral rotation of femur Knee Lateral rotation tibia
( inconsistent motion) Ankle Weight is shifted to toes. Supination of subtalar joint Plantarflexors Toe Off
(or Preswing) Begins when the contralateral foot contacts the ground and continues until the ipsilateral
foot leaves the ground. Provides the final burst of propulsion as the toes leave the ground.[3] Sagittal
Plane: Kinematics and Kinetics at Toe Off[4] Joint Kinematics Kinetics External Forces Internal
Forces/Muscle Actions Ankle Ankle moves from 20° plantarflexion at toe off to 10° plantar flexion at
early swing GRF anterior to the axis of rotation of the ankle joint External dorsiflexor moment Internal
plantarflexor moment Eccentric contraction of plantarflexors Concentric contraction of dorsiflexors to
propel the foot up Knee Knee moves from 30° flexion at toe off to 60° flexion at early swing GRF
posterior to the axis of rotation of the knee joint External flexor moment Internal extensor moment
Eccentric contraction of knee extensors Concentric contraction of knee flexors Hip Hip moves from 10° -
20° extension at toe off to 20° flexion at early swing GRF posterior to the axis of rotation of the hip joint
External extensor moment Internal flexor moment Concentric contraction of hip flexors Swing
Phase[edit | edit source] Ground reaction forces are not applicable to the swing phase as there is no
contact with the ground. However, the muscles still contract concentrically or eccentrically as needed.
[2] Early Swing Begins when the foot leaves the ground until it is aligned with the contralateral ankle.
This event functions to advance the limb and shorten the limb for foot clearance.[3] Sagittal Plane:
Muscle Actions at Early Swing[6] Kinematics/Joint Motion Muscle Action Ankle Ankle moves from 20° of
plantarflexion at toe off to 10° of plantarflexion at early swing Concentric contraction of dorsiflexors
Knee Knee moves from 30° flexion at toe off to 60° flexion at early swing Eccentric contraction of knee
extensors and concentric contraction of knee flexors Hip Hip moves into flexion Concentric contraction
of hip flexors Frontal Plane: Muscle Activity and Motion in the Frontal Plane from Initial Swing through
Midswing[5] Joint Motion Muscle Activity Pelvis Lateral pelvic tilt to the right Right side moving forward
*Reference limb is the right lower extremity Left gluteus medius Hip Rotation from lateral to medial
rotation Knee From lateral to medial rotation Ankle Subtalar joint (no weight) returns to slight
supination Mid-Swing Begins from the ankle and foot alignment and continues until the tibia of the
swing leg is vertical. As in early swing, it functions to advance the limb and shorten the limb for foot
clearance.[3] Sagittal Plane: Muscle Action at Mid-Swing[6] Kinematics/Joint Motion Muscle Action
Ankle Ankle moves from 10° of plantarflexion at early swing to 0° of plantarflexion at mid-swing
Concentric contraction of dorsiflexors Knee Knee moves from 60° flexion at early swing to 30° flexion at
mid-swing Eccentric contraction of knee flexors Hip Hip moves from 20° flexion at early swing to 30°
flexion at mid-swing Concentric contraction of hip flexors Frontal Plane: Muscle Activity and Motion in
the Frontal Plane from Mid -Swing through Late Swing (Deceleration)[5] Joint Motion Muscle Activity
Pelvis Right side moving anteriorly *Reference limb is right lower extremity Right gluteus medius Hip
Lateral tilting to the left medial rotation Knee Medial rotation Ankle Late Swing/Deceleration Begins
when the swing leg tibia is vertical and ends with initial contact. Limb advancement slows in
preparation.[3] Muscle Action at Late Swing[6] Kinematics/Joint Motion Muscle Action Ankle Maintains
a neutral position Concentric and isometric contraction of dorsiflexors Knee Knee moves from 3o°
flexion at mid-swing to o° flexion at late swing Eccentric contraction of knee flexors, then concentric
contraction of knee flexors Hip Hip moves from 20°-30° flexion at mid-swing to 30° flexion at late swing
Concentric contraction of hip flexors [7] [8]

Joint Range of Motion During Gait - Physiopedia

Introduction Merriam-Webster dictionary defines gait as “a manner of walking or moving on foot."[1] It

involves the interaction between the nervous, musculoskeletal, and cardiorespiratory systems and is
heavily impacted by human age, personality, mood, and sociocultural factors.[2][3] Normal gait function
is determined by the optimal operation of the following: “locomotor function (for initiating and
sustaining rhythmic gait), balance, postural reflexes, sensory function and sensorimotor integration,
motor control, the musculoskeletal apparatus and cardiopulmonary functions."[2][4] Stance Versus
Swing Phase[edit | edit source] The typical forward stride consists of two phases: stance phase and
swing phase.[5] The stance phase occupies 0-60% of the gait cycle. During stance phase, one leg and
foot bear most or all of the body weight.[6] The swing phase occupies 60-100% (total 40%) of the gait
cycle. During swing phase, the foot does not touch the walking surface and the body weight is borne by
the other leg and foot.[7] In a complete two-step cycle, both feet are in contact with the floor at the
same time for about 25% of the time. This part of the cycle is called the double-support phase.[6] Gait
cycle phases: the stance phase and the swing phase involve a combination of open and close chain
activities.[8][9] Read more here: The Gait Cycle Phases of Gait[edit | edit source] The stance and swing
phases of gait can be subdivided into eight sub-phases.[6][9] Initial contact (heel strike) Foot flat
(loading response) Midstance (single-leg support) Heel off (terminal stance) Toe off (preswing) Initial
swing Mid swing Late swing (deceleration) See below for a diagram of the gait cycle: The video below
shares a 90-second description of the basics of the gait cycle: [10] Range of Motion Involved in Gait
Phases[edit | edit source] Initial contact (heel strike) Occurs at 0% of the gait cycle Previously referred to
as "heel strike", but in some pathological gaits, the heel strike may not be the initial contact [6]
Function: To establish contact with the surface and initiate weight acceptance[11] Range of Motion
(ROM) at Initial Contact Body part ROM requirements Ankle 0° (neutral position) Knee 0° (full extension)
Hip average 20° of flexion Foot flat (loading response) Occurs at 8-10% of the gait cycle Function: Weight
acceptance and shock absorption Range of Motion (ROM) Requirements During Foot Flat Body part
ROM requirements Ankle 0-5° plantarflexion Knee 15° of flexion Hip 15° of flexion (hip is moving into
extension) Midstance (single-leg support) The greater trochanter is vertically above the mid-point of the
foot Function: Single limb support and stability Range of Motion (ROM) Requirements During Midstance
Body part ROM requirements Ankle 5° of dorsiflexion Knee 5° of flexion Hip 0° of flexion (neutral
position) Heel off (terminal stance) Occurs at around 30-40% of the gait cycle Function Single limb
support, stability, and propulsion Range of Motion (ROM) Requirements During Heel Off Body part ROM
requirements Ankle 0° (neutral position) Knee 0° of flexion (complete extension) Hip 10-20° of
hyperextension Toe off (preswing) Occurs at 60% of the gait cycle (final phase of stance) Function Final
burst of propulsion to propel the body forward Range of Motion (ROM) Requirements During Toe Off
Body part ROM requirements Ankle 20° of plantarflexion Knee 30° of flexion Hip 10-20° of
hyperextension Early swing Occurs at 60-75% of the gait cycle (beginning of swing phase) Toe off until
the swinging limb is even with the stance limb Function To propel the lower extremity forward and
shorten the limb for foot clearance Range of Motion Requirements During Early Swing Body part ROM
requirements Ankle 10° of plantarflexion Knee 60° of flexion Hip moves into 20° of flexion Mid swing
Occurs at 75-85% of the gait cycle Swinging limb is opposite the stance limb Function To clear the lower
extremity from the ground in order to advance into initial contact Range of Motion (ROM) Requirements
During Mid Swing Body part ROM requirements Ankle 0° (neutral position) Knee moves into 30° of
flexion Hip 30° of flexion (hip is moving into extension) Late swing Occurs at 85-100% of the gait cycle
Tibia vertical to initial contact Function To decelerate the lower extremity to establish contact with the
ground Range of Motion (ROM) Requirements During Late Swing Body part ROM requirements Ankle 0°
(neutral position) Knee 0° (complete extension) Hip 30° of flexion The following video describes the
range of motion requirements involved in the different gait phases: Range of Motion during Gait [12]
Maximum Values[edit | edit source] It is important for clinicians to be aware of the range of motion
values necessary as the minimum prerequisites for a normal gait pattern.[13] It is also important to
know during which subphase of the gait cycle these ranges of motion occur as this will aid in gait
analysis and enable clinicians to observe for specific gait pathology. Maximum Range of Motion (ROM)
at Lower Extremity Joints during the Gait Cycle Body part Maximum ROM values Hip 20° of extension;
20° of flexion Knee 0° (complete extension); 60° of flexion Ankle 5° of dorsiflexion; 20° of plantarflexion
Gait Kinetics[edit | edit source] Definitions[edit | edit source] Ground reaction force (GRF) = forces
applied by the ground to the foot, when the foot is in contact with the ground[14] Creates an external
plantarflexion or dorsiflexion torque If GRF is anterior to the joint axis - this causes an anterior motion of
the proximal segment If GRF is posterior to the joint axis - this causes a posterior motion of the proximal
segment Read more: Ground Reaction Forces Lower extremity gait musculature - creates an internal
torque Centre of pressure - point of application of pressure to the foot segment Read more: Gait
Definitions Initial contact (heel strike)[edit | edit source] Ankle At initial contact - lateral calcaneus
strikes the ground first. Ground reaction forces are slightly posterior to the axis of rotation of the foot
and ankle joint. This creates a plantarflexion moment at the ankle.[9] Ankle dorsiflexors oppose this
plantarflexor torque - internal torque is controlled by tibialis anterior, extensor digitorum longus and
extensor hallucis.[6] Knee At initial contact - GRF is anterior to the knee joint creating anterior rotation
of the femur.[9] GRF wants to move into extension. Utilise flexor musculature - hamstrings - in order to
control progression. Hip GRF is anterior to the hip joint - this creates an external torque (anterior
rotation) at the pelvis.[9] Utilise extensor musculature - gluteal musculature - to oppose/control the
progression or external torque. Foot flat (loading response)[edit | edit source] Ankle Centre of pressure
remains at the posterior calcaneus - GRF remains posterior to the ankle.[9] Utilise dorsiflexors to
prevent plantarflexion from occurring at the ankle. Hip Centre of pressure and GRF remains the same -
anterior to the axis of rotation.[9] Anterior pelvic tilt creates a flexion torque. Utilise extensor
musculature to control this torque. Knee Range of motion moves from 0-15°. GRF posterior to the axis of
rotation of the knee joint - creates a flexion torque.[9] Utilise extensor musculature to control the knee
from moving into flexion. Midstance (single-leg support)[edit | edit source] Ankle GRF creates a
clockwise torque of the proximal segment (on top of distal segment) - causing a dorsiflexion moment at
the talocrural joint.[9] Utilise plantarflexors to oppose the external torque. Knee GRF creates an anterior
(clockwise) torque of the proximal segment (on top of distal segment) - wants to move into extension by
the femur moving anteriorly on the tibia.[9] Utilise flexors to oppose this torque - this activates the
hamstrings. Hip GRF is posterior to the axis of rotation - wants pelvis to move into a posterior pelvic tilt
(extension).[9] Utilise flexors to oppose extension torque. Heel off (terminal stance)[edit | edit source]
Ankle GRF is anterior to the axis of rotation of the ankle joint - wants the tibia to flex on the talus.[9]
Creates an external dorsiflexion moment at the talocrural joint. Utilise plantarflexors to oppose this
moment. Knee GRF is anterior to the knee joint - this pulls the femur into extension, creating an external
extensor torque.[9] Counteracted by an internal flexor torque. Hip GRF is posterior to the hip joint - this
creates an external extensor moment.[9] Counteracted by an internal flexor moment. Toe off (preswing)
[edit | edit source] Ankle Centre of pressure/GRF stay anterior to the axis of rotation of the ankle joint.
[9] Creates an external dorsiflexion moment. Counteracted by an internal plantarflexion moment. Knee
GRF is posterior to the axis of rotation of the knee joint as the knee is moving into flexion.[9] Creates an
external flexion moment. Counteracted by an internal extensor (quadriceps musculature) moment. Hip
GRF is posterior to the axis of rotation of the hip joint as the hip is moving into extension.[9] Creates a
posterior pelvic tilt. Utilise flexor musculature (iliopsoas) to counteract this moment. Internal Torque
Peaks[edit | edit source] The sagittal internal torque peaks at the hip, knee and ankle are[15]: Hip: Foot
flat - extensor torque Heel off - flexor torque Knee: Initial contact - flexor torque (hamstrings
musculature active) Foot flat - extensor torque (quadriceps musculature active) Heel off - flexor torque
(hamstrings musculature active) Ankle: Initial contact/foot flat - dorsiflexion torque Heel off -
plantarflexion torque (gastrocnemius/soleus active)
Gait in prosthetic rehabilitation - Physiopedia

Normal Gait Gait is a term used to describe a walking pattern. ‘Normal gait’ is used to define a pattern
which has been generalised from the general public across many variables, including age and sex[1]. A
complete cycle of gait begins at initial contact of one limb and ends at the repeated initial contact of the
same limb, performing all phases of gait in doing so. This full cycle can be described as a stride. A step is
sometimes incorrectly used to describe this cycle. A step however, is different; it is described as the
distance of heel strike from one leg to the heel strike of the opposite leg[2]. Step and stride in human
gait The gait cycle can be split into 2 stages.[3] Stance Phase -Time the foot is in contact with the floor,
weight acceptance and single leg stance (i.e. the "heel-to-toe contact sequence of the foot"[4]), which
makes up 60% of the cycle[1] Swing Phase – The period of time where the limb is lifted from the floor,
limb advancement (i.e. when the foot is suspended[4]). This makes up 40% of the cycle[1] In order to
describe the elements of gait, the cycle can be broken down further into 8 sub factors[1][2][5]: Initial
Contact Loading Response Midstance Terminal Stance Preswing Initial Swing Midswing Terminal Swing
The diagram demonstrates this division of the gait cycle. Divisions of Gait Cycle Initial Contact[edit | edit
source] Also known as heel strike. This is the first moment the foot comes into contact with the floor.
The hip is flexed approximately to 30 degrees, knee extended between 0-5 degrees and ankle
dorsiflexed to a neutral position, giving contact with the floor at approximately a 25-degree angle. This is
the first phase of double limb support. The aim of initial contact is to stabilise the limb in preparation for
it to take the impending forward translation of body weight[2][6]. Loading Response[edit | edit source]
The foot flattens on the floor through pronation. The hip begins to extend and propels the body
forwards and over the foot, using the heel as a ‘rocker’. The knee then flexes to allow shock absorption.
The aim of this phase is shock absorption, weight bearing stability and preservation of progression[2][6].
Mid Stance[edit | edit source] This is the first half of single limb support. Weight is aligned fully over the
supporting foot through ankle dorsiflexion, while the hip and knee extend, as the other foot lifts off the
floor. The body weight is fully supported on one leg[2][6]. Terminal Stance[edit | edit source] This is the
second half of single leg support; it begins as the other leg lifts off the floor. The heel of the loaded limb
lifts off the floor and the body weight moves forward past the forefoot, as the hip increases in extension.
The knee gains full extension and begins to flex again. This phase is completed when the non-loaded
limb makes contact with the floor[2][6]. Pre-swing[edit | edit source] Also known as ‘toe off’ and is the
final phase of stance. The other limb has now begun a new stance phase and is in the initial contact
phase. The limb is rapidly off loaded with a forward push to transfer the weight onto the opposite limb.
The knee is flexed and the ankle plantarflexes as the toe leaves the ground[2][6]. Initial Swing[edit | edit
source] The foot is lifted off the floor by hip and knee flexion, as the ankle begins to dorsiflex. The other
foot will be in midstance phase. When the offloading limb is level with the leg in stance phase the initial
swing phase is complete[2][6]. Mid Swing[edit | edit source] The limb swings forward of the body
through hip flexion as the knee begins to extend. The foot is clear of the floor[2] Terminal Swing[edit |
edit source] Also known as late swing, the knee becomes fully extended and the ankle dorsiflexes to
neutral as the foot prepares to make contact with the floor[2]. The diagram below demonstrates the 8
phases of the gait cycle: [7] Prosthetic Gait[edit | edit source] After an amputation, the amputee uses
different muscle groups in order to create a smoother gait pattern. Overall energy consumption required
is higher, due to the increased effort required to compensate for the loss of the limb. While progress has
been made in the design of prostheses, "the replacement of lower-limb segments with a prosthesis
affects the efficiency of this locomotion."[8] The amount of metabolic oxygen consumption in a non-
amputee correlates directly to increased walking distance and speeds. In the amputees, however, this
metabolic cost is higher even at normal speed. On average these increased requirements are[9]:
Traumatic Transtibial Gait - 25% increased energy requirement Vascular Transtibial Gait - 40 % increased
energy requirement Traumatic Transfemoral Gait - 68% increased energy requirement Vascular
Transfemoral Gait -100% increased energy requirement Transtibial Gait[edit | edit source] The average
gait pattern will vary dependent on the type of prosthesis used for mobility, however, generalisations
can be made. The ankle of the prosthesis has a reduced range of movement compared to the anatomical
ankle. This results in prolonged heel strike and weight bearing through the heel before flat foot contact,
with delayed forefoot loading[10] Knee flexion is decreased at initial contact and the overall maximum
flexion achieved is reduced as the foot moves to floor contact to[10].During swing phase of the non-
prosthetic limb the body weight begins to move forward over the prosthetic limb, which is in stance
phase. In order to gain adequate step length of the non-prosthetic limb, heel rise on the prosthesis
occurs earlier. The heel rise achieved is greater than that of a normal gait pattern[10]. This creates an
elevation of the body and results in a greater loading force on the non-prosthetic side (or sound side)
(approx 130% compared to average 111%) as the body weight drops more rapidly onto the limb. Greater
quadriceps contraction is needed to absorb the force[9][10]. The ‘toe off’ force generated from the
prosthetic limb is reduced, which is compensated for by the hip flexors. Flexion of the knee on the
prosthetic limb occurs with some hamstring contraction but mainly eccentric contraction of the
quadriceps[11] During the stance phase, the energy generated by the prosthetic limb is reduced by 50%
to that which would be generated by the normal limb, this is compensated by greater energy
expenditure in muscles higher up the limb. The rocker effect of the prosthesis results in increased
instability and the reduced knee flexion achieved on the prosthetic side requires hip muscles to generate
greater energy to ensure stability. As the body transfers weight in a forward motion this energy
generation is then transmitted to the trunk muscles in order to generate enough force to propel the
body forward and to compensate for the loss of energy through the prosthesis[9]. Due to the reduced
ankle movement of the prosthesis the range of extension at the hip is reduced to approx half of that of
the opposite limb. The stance time on the non-prosthetic side is also increased compared to the
prosthetic side[10]. Transfemoral Gait[edit | edit source] A person with a transfemoral amputation has
to compensate for the loss of both the knee and ankle joint[9]. The gait cycle is affected by the quality of
the surgery, the type and alignment of the prosthesis, the condition of the stump and the length of the
remaining muscular structure and how well these are reattached[11]. The main focus of the gait cycle is
to prevent the knee from buckling during stance phase. A ‘fixed knee’ prosthesis will counteract this
issue. A ‘free knee’ will need to remain in extension for longer throughout the stance phase approx 30-
40% to ensure buckling does not occur[9]. This extension causes prolonged heel strike and the body will
move forward over the prosthetic leg as one unit for stance phase. The hip extensors on the prosthetic
side will work to stabilise the limb in prosthetic weight bearing[9]. During the swing phase of the
prosthetic limb, the hip extensors and calf muscles on the sound side help to generate force for the
sound limb to swing forwards. Hip flexors on the prosthetic limb must generate the same force required
during normal gait. Although the prosthesis is generally 30% lighter than the limb would be, speed
generated by the hip flexors is required in order to snap the prosthesis of a ‘free knee’ into extension for
heel strike[9][10]. General control and strength are reduced in a transfemoral amputation due to the
shortened lever length of the thigh muscles, which reduces the force of contraction[9]. For amputees
with a fixed knee (locked knee) prosthesis floor clearance is reduced during swing phase, due to the lack
of knee flexion and ankle dorsi flexion. Elevation of the hip using trunk and hip muscles is required to
prevent dragging on the floor known as ‘hip hitching’ or ‘hip hiking’[10]. Stance time on the sound limb
is increased as it is for transtibial amputees, because of the instability resulting from the prosthesis and
the reduced range of motion available. Overall energy expenditure is higher than is required for a
transtibial amputee due to the energy which is lost through the prosthesis over two joints and not one.
Greater compensation is required by the hip and trunk muscles and the contralateral limb to generate
the energy required for stability and movement throughout the gait cycle[9]. A person with a
transfemoral amputation will walk 30% slower than someone without an amputation. The sound limb
will have higher ground reaction force and more hip range with single limb stance than the prosthetic
side. The sound ankle, knee and hip also have bigger joint moments. This all leads to asymmetry that can
lead to low back pain and sound limb osteoarthritis. [12] Harandi et al. [12] found the following with
regards to people with transfemoral amputations: Compensatory strategies are used during walking The
sound limb muscles are essential in mediolateral balance The prosthesis is providing support,
progression and breaking during the stance phase of gait When there is an increased pelvic tilt to the
prosthetic side the person will also have a reduction in hip motion.[12] Gait Deviations[edit | edit
source] While assessing amputee gait it is important to be aware of normal gait and how normal gait in
the amputee is affected. Furthermore, there may be deviations which an amputee will adopt to
compensate for the prosthesis, muscle weakness or tightening, lack of balance and fear. These
deviations create an altered gait pattern and it is important that these are recognised, as rehabilitation
of the gait will need to encompass corrections of these deviations[11][10]. [13] Learn about common
gait deviations on the Gait deviations in amputees page. Summary[edit | edit source] Amputees should
have a fully functional and physical assessment and rehabilitation should be based around personalised
functional goals. Individualised exercise programmes are developed after a thorough assessment.
Awareness of normal gait and the deviations and their cause formulates the basis of the correct
rehabilitation of the individual[14][15]. There are numerous techniques that can be used during
rehabilitation and not all of them will be appropriate for each individual, therefore the programme and
technique must be applied to each individual and reviewed regularly to ensure it remains adequate[10]
[14]. The amputee’s previous level of activity, overall health and potential to improve needs to be taken
into consideration when formulating a rehabilitation programme and should aim at translating the
function gained in a controlled environment into their own home functional environment[14][15].

Gait Deviations - Physiopedia

Introduction A gait deviation is an abnormality in the gait cycle that can affect the trunk, hip, knee, or
ankle joint. Gait deviations can stem from increased age and/or certain pathologies. These pathologies
can be musculoskeletal or neurological in nature.[1] The etiology can be determined through lab work,
clinical presentation, and diagnostic testing. Furthermore, this entity can be subdivided into episodic and
chronic deviations. Gait deviations can have a tremendous impact on patient's quality of life, morbidity,
and mortality.[2] The variety of gait deviations calls for different treatments. Etiology[edit | edit source]
The causes of gait deviations include neurological conditions (e.g. sensory or motor impairments),
orthopedic problems (e.g. osteoarthritis and skeletal deformities) and medical conditions (e.g. heart
failure, respiratory insufficiency, peripheral arterial occlusive disease and obesity). In older age, gait
deviations typically have several causes, which may include impaired proprioceptive function in
polyneuropathy, poor vision, frontal gait disorder associated with vascular encephalopathy and
osteoarthritis of the hips or knees. If a gait disorder has an acute onset, cerebrovascular, spinal and
neuromuscular causes should be considered, as should adverse drug effects and psychiatric deviations.
[3] Some common causes are: A degenerative disease (such as arthritis) An inner ear disorder Stroke
Foot conditions A neurologic condition like Parkinsonism. Something as simple as ill-fitting shoes
Epidemiology[edit | edit source] Studies have demonstrated that gait deviations occur as an individual
age; these deviations stemming from neurological and non-neurological causes. Studies have shown
that while 85% of individuals 60-year-old have a normal gait, by the time they reach the age of 85, only
20% maintains normal gait. Gait deviations are not commonly seen in the younger population unless
they stem from a developmental or musculoskeletal etiology.[2] Physiological Basis of Gait[edit | edit
source] For normal gait many all of the following functions and systems are required to be intact:
locomotor function (for initiating and sustaining rhythmic gait), balance, postural reflexes, sensory
function and sensorimotor integration, motor control, the musculoskeletal apparatus and
cardiopulmonary functions. Afferent nerves from the visual, vestibular and proprioceptive systems
provide essential information on the position of the body and its parts. Efferent system comprises
descending pathways including the pyramidal tract, peripheral nerves, neuromuscular end plate and
muscles. The gait cycle is divided into a stance and swing phase. The stance phase constitutes
approximately 60 % of the gait cycle and is subdivided into initial contact, loading response, mid-stance,
terminal stance and pre-swing. The swing phase constitutes 40% and is subdivided into initial swing (toe-
off), mid-swing (tibia vertical) and terminal swing, terminated by the heel striking the ground. Both feet
are on the ground at the beginning and end of the stance phase, these two double support periods lasts
for approximately 10–12 % of the gait cycle.[3] Pathological Gait Deviations[edit | edit source]
Pathological gait deviations can be caused by decreases in joint pathology, ROM, muscular strength,
balance, and proprioception or a combination of them all. They can cause varying compensations at the
trunk, hip, knee, or ankle joint, and can be musculoskeletal or neurological in nature.[1]
Musculoskeletal[edit | edit source] Antalgic gait. Antalgic gait is due to pain in the lower extremities
that results in a limp that is associated with a shortened stance phase relative to the swing phase. This
gait deviation, asymmetry, can be caused by issues that originate in the trunk, hip, knee, or ankle.[2] Leg
Length Discrepancies. Leg length discrepancies can either be structural of functional. This can cause
pelvic drop, decreased hip, knee, and ankle plantarflexion. To compensate, the patient may use vaulting
or toe-walking.[1] [4] [5] Trendelenburg Gait. Trendelenburg gait occurs when the gluteus medius is
weak. Gluteus medius weakness can be the result of dysfunctions or diagnoses related to back pain or
lumbopelvic pain, chronic hip dysfunctions, or lumbopelvic surgery. The weakness of the involved side
causes a contralateral pelvic hip drop during swing phase. This contralateral hip drop might cause the
quadratus lumborum, on the stance leg, to bring the pelvis back in neutral.[6] Posterior Lurch Gait.
Posterior lurch gait is when the trunk leans posteriorly with a hyperextended hip, especially during the
loading response due to a weak gluteus maximus.[7]Hence it is also known as gluteus maximus gait.
Circumduction of the Hip. Circumduction of the hip during swing phase occurs for several reasons
including weak hip flexors, contralateral hip dysfunction, or leg length discrepancy. This is a combination
of hip hiking, forward rotation of the pelvis, and abduction of the hip. Hip flexor weakness is caused by
L2-L3 nerve compression or possibly upper motor neuron lesion.[8] [9] [10] [11] Neurological[edit | edit
source] Spastic hemiparetic gait. It is characterized by unilateral leg extension and circumduction, in
which the paretic leg performs a lateral motion (circumduction ) during the swing phase. This is also
known as circumductory gait. Spastic diplegic gait (scissors gait). It is characterized by bilateral leg
extension and adduction, the legs appear to be stiff. When spasticity in the adductors is marked it
results in a scissoring gait where the legs cross in the scissors-like pattern. Steppage gait. In this gait, the
patient must lift the leg higher than usual and the patient is unable to stand or walk on their heel. It is
caused by weakness in the ankle dorsiflexors. This gait is also known as a slapping gait. Waddling gait
(myopathic gait). In waddling gait weakness in the gluteus medius muscles leads the hip on the swinging
side to drop during gait, in an attempt to counteract, the patient bends the trunk towards the other side,
resulting in the gait to appear waddling. Parkinsonism gait. The gait is slow with a short step length and
a narrow base. The feet are lifted less high than normal resulting in shuffling. Patients with parkinsonism
can develop a Freezing gait in which there is blockage of movement during turning or when approaching
obstacles or narrow passages such as doors. This gait is also known as festinating gait. Cerebellar ataxic
gait. The gait is broad based, insecure and lacks coordination. Leg movements and step length are
irregular and variable. Senosory Ataxic gait. In this gait the patient’s proprioception is disturbed resulting
the gait to appear broad-based and insecure. The patient uses visual control to compensate for the
disturbed proprioception. Hyperkinetic gait. this gait is seen in basal ganglia deviations including chorea,
dystonia and Wilson's disease.[2][3] [12] [13] Examination[edit | edit source] The gait should be
observed from all sides, while the patient walks a distance of at least several meters without obstacles
and preferably without shoes. Normal walking appears to be rhythmical, flowing, and effortless, with
freely swinging legs and with an upright body posture. Normal walking is accompanied by movements of
the head, the trunk and the arms. The parameters that should be clinically examined include step
length, stride length, step width, rhythm, speed, posture, swinging of arms and legs and the duration
and type of contact with the floor. A general neurological examination should follow evaluation of gait.
The examination is advised to be done most of the patient’s clothes removed to detect any orthopedic
abnormalities such as asymmetries or postural abnormalities. [3] Treatment[edit | edit source] It
depends on the cause. Assistive devices such as canes and walkers may help in some cases in which
balance is a problem. Physical therapy: may be appropriate in other cases to improve balance, strength
and flexibility. You should also receive instruction in fall prevention. Maintaining proper foot alignment
may require in-shoe splints or leg braces. A shoe lift may help in cases of an unequal leg length.
Medicines are available to treat arthritis, Parkinson’s disease and multiple sclerosis. Surgery or
prostheses may be recommended, such as hip and knee replacement for persons with osteoarthritis[14]
See also comprehensive links in Resources below Differential Diagnosis[edit | edit source] There are
numerous etiologies that could lead to gait deviations. The following potential causes should be ruled
out and to come up with a final diagnosis. Neurologic: Parkinson, dementia, delirium, stroke, cerebellar
dysfunction, multiple sclerosis, amyotrophic lateral sclerosis Metabolic: Diabetes mellitus,
encephalopathy, obesity, vitamin B12 deficiency, uremia Psychiatric: Substance abuse, depression,
anxiety, malingering[2] Prognosis[edit | edit source] The prognosis depends on the aetiology. Metabolic
etiologies of gait deviations have a relatively good prognosis. If the metabolic disorder is addressed the
patient mostly recovers without lasting symptoms. While neurologic conditions often have a poor
prognosis, some neurologic conditions have no cure and must be treated symptomatically. [2]
Resources[edit | edit source] See also Gait Gait and Lower Limb Observation of Paediatrics - (GALLOP)
Gait deviations in amputees Gait Training in Stroke Gait: Antalgic Gait Re-education in Parkinson's Gait
Re-education in Multiple Sclerosis(MS)

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