Motion Analysis-Sai Wei Yang, Ph.D.

Pathological Gait-1

Pathological Mechanics Pathological Gait

Gait analysis; Perry (p171-p347)
Deformity Contracture Muscle weakness Impaired control
sensory loss Impaired motor control (Spasticity)

Pain

Deformity
Contracture structural change within the fibrous connective tissue component of Muscles, ligaments or joint capsule following prolonged inactivity or scarring from injury. elastic/rigid Elastic contracture

abnormal joint contours and ankylosis(bony rigidity) resists all stretching efforts.Its effects will be consistent throughout the stride.

rigid contracture

Motion Analysis-Sai Wei Yang, Ph.D.

Pathological Gait-1

A knee flexion contracture *blocks progression during stance by inhibiting the advancement of the thigh. *increases the level of muscular activity required to stabilize the knee.

*the trunk is placed forward of the vertical midline *this introduces additional strain on the back and hip extensors. Limb must retract and trunk lean forward

Hip stability during stance is impaired by a flexion contracture.

Muscle weakness (insufficient muscle strength to meet the demands of walking) *Disuse muscular atrophy/neurological impairment LMN disease/muscular pathology(polio/GBS/muscular dystrophy/ Primary muscular dystrophy) has the excellent capacity to substitute(with normal sensation and selective neuromuscular control)

Muscle Weakness
Insufficient muscle strength, Disuse muscular atrophy as well as neurological impairment Poliomyelitis, Guillain-Barres syndrome, muscular dystrophy, primary muscular atrophy Lower walking speed is expected. Prediction of walking ability is difficult because of the limitation of MMT.
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Pathological Gait-1

Guillain-Barr (Ghee-yan Bah-ray) Syndrome

Guillain-Barr?syndrome (GBS) is an inflammatory disorder of the peripheral nerves. The peripheral nerves convey sensory information (e.g., pain, temperature) from the body to the brain and motor (i.e., movement) signals from the brain to the body. GBS is characterized by weakness and numbness or tingling in the legs and arms, and possible loss of movement and feeling in the legs, arms, upper body, and face.

Causes
Guillain-Barr?syndrome is not hereditary or contagious. What causes GBS is not known; however, in about half of all cases the onset of the syndrome follows a viral or bacterial infection, such as the following: flu, common cold gastrointestinal viral infection infectious mononucleosis viral hepatitis campylobacteriosis (usually from eating undercooked poultry) porphyria (rare disease of red blood cells)

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Grade 5 () Grade4() Grade3 Grade2,, Grade1,, Grade0 >3 - <3 -

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Muscle strength at different resistance

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Pathological Gait-1

modifying the timing of muscle action to avoid threatening postures and induce protective alignment during stance each major muscle group has a postural substitution also reduce the demend by walking at a slower speed.

Sensory loss
Proprioception is most important. Intact motor control: able to substitute Impaired muscle strength: slow and cautious walking.

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Sensory Loss(absent/impaired/normal) Proprioceptive impairment obstructs walking prevents it from knowing the position of the hip, knee, ankle or foot and the type of contact with the floor. does not know when it is safe to transfer body weight onto the limb. even with moderate sensory impairment, walking is slow and cautious.

Pain
Pain(excessive tissue tension musculoskeletal pain) *joint distension related to trauma or arthritis is the common situation. physiological reactions to pain deformity and muscular weakness
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Pathological Gait-1

Pain
Excessive tissue tension (trauma or arthritis) Induced obstacles: deformity and weakness
Deformity: natural resting position. Weakness: muscle activation difficulty for joint protection

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Impaired Motor Control (spasticity) ( CP/stroke/TBI/incomplete SCI/MS spastic gait) Central neurological lesion (brain/spinal cord) spastic paralysis an overaction to stretch(i.e. spasticity) Obstructs the yielding quality of eccentric muscle action during stance impaired selective motor control(mimic flaccid paralysis with intact reflexes) prevents the patient from controlling the timing and intensity of muscle action. Involved whole limb severe in distal primitive locomotor patterns commonly become an alternate source of voluntary control- using mass flexion pattern The primitive pattern allows vary the intensity of muscle but incompleteness of the patterns results in insufficient strength 19

mass flexion pattern hip-knee flexion+hip abduction+hip external rotation +ankle dorsiflexion mass extension pattern hip-knee extension+hip adduction+hip internal rotation +ankle plantarflexion muscles change their phasing ( the sum of the control errors and spasticity) altered proprioception muscular control is altered by limb position and body alignment

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Motion Analysis-Sai Wei Yang, Ph.D.

Pathological Gait-1

spasticity(resistance to passive motion velocity-dependent) mild/moderate/severe *klasp-knife pattern *lead-pipe *cog-wheel(characteristics of PD)

spasticity obstructs the yielding quality of eccentric muscle action during stance.
Soleus and gastrocnemius spasticity persistent ankle plantarflexion loss of the ankle rocker and inability to rise on the metatarsal heads for the forefoot rocker hamstrings spasticity persistent knee flexion limits the effectiveness of terminal swing and restricts thigh advancement in stance hip flexor spasticity restricts progression in mid- and terminal stance sustained quadriceps action inhibits pre-swing preparation for limb advancement.
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quick stretch

elicits clonus

Generates sustained muscle action

Impaired motor control (spasticity)

CP,CVA, Brain injury, iSCI, Multi-sclerosis

Loss of selective control:

unable to control the timing and intensity of muscle action

Overreaction to stretch
Plantar flexor spasticity
limited progression & push-off difficulty

Primitive locomotion pattern

Take a step by using a mass flexion pattern Attain stance stability by mass extension pattern Unable to make a smooth transition from stance to swing. Unable to vary the intensity of muscle action

Knee flexor spasticity

ineffective terminal swing & thigh advancement limitation.

Hip flexor spasticity

mid and terminal stance progression restriction

knee extensor spasticity

limitation of pre-swing preparation for limb advancement
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Inappropriate phasing
muscle action is inconsistent.
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Motion Analysis-Sai Wei Yang, Ph.D.

Pathological Gait-1

Terminology Calcaneus excessive dorsiflexion Equinue toe walkers (inadequate plantarflexion) Drop foot flaccid foot in swing (inadequate plantarflexion) but except for excessive plantarflexion
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Ankle and Foot Gait Deviations

Excessive plantar flexion Excessive dorsiflexion Arcs of normal ankle motion: 10o

excessive ankle plantarflexion causes:

1.pre-tibial muscle weakness 2.plantarflexion contracture 3.soleus and gastrcnemius spasticity 4.voluntary excessive ankle plantarflexion

loss of progression (during stance) shortened stride length reduced gait velocity threatened stability( difficulty in attaining an upright posture) obstructs limb advancement(during swing) substitutive actions that required increased limb or body effort shortened step( delayed floor clearance/initiate an effective substitution)

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Pathological Gait-1

Excessive Ankle Plantar Flexion

Stance: loss of progression shortened stride length, reduced gait velocity, decreased stability. Swing: Obstruct limb advancement gait cycle involves 10-20plantar flexion

1. **Initial contact Low heel contact 1.when the foot strikes the floor with the ankle in 15 degrees PF and the knee fully extended 2.while the heel still initiates floor contact, the foot is nearly parallel with the floor Forefoot contact 1.represents a mixture of ankle equinus and knee flexion 2.A 20 degrees posture at each joint is sufficient to place the forefoot lower than the heel at the time the floor is contacted

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loading response

normal initial heel contact instantaneous foot drop when pretibial control of the heel rocker is weak Low heel contact markedly reduced the heel rocker(as the foot has only a 10 degrees arc rather than the usual 25-30 degrees to travel) the knee flexion thrust is markedly reduced.
Three loading patterns A.the foot will rapidly drop onto the heel while the tibia stays vertical if there is good ankle mobility. B. Rigid plantarflexion can lead to two possible reactions, the heel off posture may continue C.The tibia is driven backward as the heel drops to the floor.
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Pathological Gait-1

Loading Response

**Mid-Stance 1. Excessive plantarflexion in mid stance inhibits tibial advancement. 2. Any limitation that restricts dorsiflexion to less than 5 by the 30% point in the gait cycle represents an abnormal restraint. 3. Loss of the ankle rocker proportionally limited progression short step length A.premature heel off B.foot flat with a posteriorly restrained tibia C.substitution for lack of tibial progression by forward trunk lean.
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Mid stance
Restricted tibia advancement short step length. Three substitutions as showed by the figure
**terminal stance * *depend on the patient`s ability to roll onto the forefoot. **if the patient can not attain a heel rise the advancement of the body is limited to the extent that knee hyperextension or trunk lean and pelvic rotation improve the forward reach of the opposite limb. (shortened step-length mild in vigorous walker but can be severe in patients who never attain good stability on the forefoot)

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Pathological Gait-1

Terminal stance
The advancement of the body is limited for patients do not have heel rise Normal pattern for vigorous walker with low heel strike

Swing phase
Pre-: normal pattern if forefoot support was attained. Initial-: no clinical significant Mid-: toe drag & inhibition of limb advancement
hip flexion, knee flexion circumlocution, lateral trunk lean, contralateral vaulting.

Terminal:hip flex & knee ext help lift the foot.

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1.

Pre-swing

Initial Swing 1.if forefoot support was attained during terminal stance, there will no insignificant gait abnormalities in pre-swing.The alignment to initiate knee flexion is present. 2.patients who had maintained heel contact throughout terminal stance may develop a late heel rise after body weight has been transferred to the other limb. Otherwise, the heel will not rise until the thigh begins to advance for initial swing. **no clinical significance. **the trailing posture of the tibia tends to minimize the effect increased ankle plantar flexion has on toe drag.

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Pathological Gait-1

**mid-swing drops the foot below horizontal. toe drag on the floor and inhibition of limb advancement swing is prematurely terminated

**terminal swing the flexed hip and extended knee place the forefoot above the floor. Persistent toe-drag indicates a mixture of excessive ankle plantarflexion and inadequate knee extension

substitution: increased hip flexion to lift the limb and hence the foot no adequate hip flexion circumduction, lateral trunk lean, and contralateral vaulting
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Cause of excessive PL

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Pathological Gait-1

excessive ankle dorsiflexion

Excessive ankle dorsiflexion

Abnormal event in all of the gait phases except mid stance and terminal stance. 5deviation is normal. Lack of normal plantar flexion More functional significance in stance than swing.

causes: soleus weakness ankle locked at neutral

1.dorsiflexion beyond neutral is an abnormal event in all of the gait phases except mid-stance and terminal stance. 2.A 5 degree deviation can be considered within the normal variance, yet it also may have functional significance as it still leads to considerable tibial tilt.

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IC, LR
Instability, exaggerated heel rocker flat foot IC passive form of ED accelerated tibial advancement. Ankle fixes at neutral same tibia advance rate knee flex quadriceps demand .

Initial Contact 1.infrequent 2.a position of instability 3.forefoot will be higher above the floor than normal exaggerated heel rocker.

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Motion Analysis-Sai Wei Yang, Ph.D.

Pathological Gait-1

Loading Response 1.an abnormal form in initial contact 2.inhibition of the normal ankle plantarflexion increased quadriceps demands floor contact with the flat foot has eliminated the 10 degrees plantarflexion a passive form of excessive dorsiflexion as the limb is loaded the potential for accelerated tibial advancement.

MS (inadequate soleus response), TS

ankle dorsiflexion at LR instability at stance. Gradual increase of dorsiflexion through stance with peak at TS instability increased quadriceps demand and knee may be flexed. Prolong heel contact and knee flexion

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Mid Stance

Terminal Stance
1.excessive dorsiflexion of the ankle during terminal stance is difficult to identify by observation because two actions tilt the tibia forward. (heel rise and ankle dorsiflexion) 2.when HC continues through terminal stance, the ankle position because visible ,even the normal 10 degrees dorsiflexion may appear excessive. 3.as elevation of the ankle is more conspicuous than an increase in tibial angle , the combination of heel rise and excessive dorsiflexion masks the change in ankle position

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Pathological Gait-1

Pre-swing
Prolong heel contact as the body draws the tibia forward The foot never rise above neutral during swing deviate position of ankle at the time of IC

Pre-swing

1.whenever the normal 20 degrees plantarflexion is reduced, the ankle is in excessive dorsiflexion. 2.This most often occurs with prolonged heel contact as the body, by being well forward of the foot, draws the tibia forward once the ankle`s passive range has been reached.

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Cause of Excessive Ankle Dorsiflexion

Soleus weakness
Initial swing/Mid swing/and terminal swing Normal quadriceps walks with knee flexed Weak quadriceps knee control inadequacy reduction of heel rocker knee extended shorter steps & slower walking
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1.seldom does the foot rise above neutral during swing. 2.the only clinical significance relates to the position the ankle will be in at the time of initial contact

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Pathological Gait-1

Cause of EAD
Ankle locked at neutral
increase heel rocker action knee flexed at the same rate as the foot falls quadriceps demand increases

Common Causes of Inadequate triceps surae action

Disuse, paralysis Excessive surgical lengthening of a tight Achilles tendon Insufficient neurological control of restoration of normal range motion Physiological muscle lengthening by the addition of sarcometers to the muscle fiber in response to the repeated eccentric stretch in gait
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Cause of EAD
Stance knee flexion
knee flexion contracture requires ankle dorsiflexion beyond neutral.

Foot dysfunction
Pattern of foot contact during the stance phase malalignment of the foot in swing

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Pathological Gait-1

Sagittal plane deviations

Prolong heel only

painful forefoot, marked imbalance between ankle dorsi and plantar flexor decrease excessive dorsiflexion

Premature heel off ( forefoot contact)

loading response, mid stance spastic hamstring and the calf
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Delayed heel contact: tight tissues yield as a greater load is applied to the limb later in stance Prolonged heel on: terminal stance or preswing
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Coronal plane deviation

curtailed heel-only: shortened heel-only support, followed by

foot slap: weak tibialis anterior Delayed heel contact: follows after forefoot contact

Excessive inversion (varus)

Heel: medial tilt of calcaneus Forefoot: 1st metatarsal head deviation, increased arch height, adduction. Floor contact by lateral surface of the foot, premature heel-off

Toe drag: delayed limb advancement Premature heel rise: follows after initial forefoot contact( excessive PF or KF)

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Pathological Gait-1

Cause of coronal plane deviations

Abnormal muscular control static deformities proximal limb control causing torsion

Excessive eversion(valgus)
total heel contact or medial surface contact, shortened heel-on interval Fifth metatarsal head contact at midstance, depression of mid-foot, push-off by whole forefoot
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Dynamic varus
Swing with varus with good ankle DF
strong TA without TE: spastic patient May reverse to valgus in stance (extensor synergy)

Dynamic Valgus
Total weakness of inverters: spastic or paralysis rather than peroneal action Strong toe extensor and peroneus tertius muscles can suspend the lateral side of the foot Weak TA allow medial side toe drop. Less complete foot clearance

Tibialis posterior: inconsistency Soleus: Strong extensor synergist, premature onset at terminal swing FHL &FD: primitive extensor pattern, primitive activation in terminal swing. Peroneus longus and brevis: varus or valgus
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Pathological Gait-1

Knee abnormal gait

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Inadequate flexion
more stable desirable for quadriceps weakness lack of shock absorption capability microtrauma toe off difficulty greater hip flexor toe drag limb advancement difficulty, display of peak knee flexion until mid swing

Excessive Extension
Extensor thrust:excessive extension force, first reaction to limb loading Hyperextension: slow, passive, or active; mid stance or terminal stance
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Pathological Gait-1

Cause of EKF & EKE -- quadriceps weakness

Too much gluteus maximus, premature ankle plantar flexion. HE at MS and TS:balance between soleus and anterior vector, slower ankle dorsiflex, prolong heel contact.
prolong GM & soleus action, slight forward trunk lean

Cause of EKF & EKE

Pain
Same mechanism as for quadriceps weakness To escape shear force to reduce compressive force from a contracting Q less complete flexion at LR, inadequate arc of flexion at IW.

Continue knee extension until preswing, momentary toe drag.

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Extension contractures

spastic quadriceps
premature knee extension at LR, trunk forward lean, ankle PF Rectus femoris (hip flexor): due to slow velocity Persistent vastus intermedius activity into swing Prolonged action of all vasti into a major portion of swing

capsular scarring or quadriceps contractures Normal PROM but tissue can not yield rapidly enough ( 60 degree knee flexion within 0.2 seconds)

Cause of EKF & EKE -- excessive APF

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Pathological Gait-1

Excessive Knee Flexion

In LR: more than 25 degree flexion In MSW: secondary effect of increased hip flexion, not a clinical concern

Inadequate extension
In MSD & TSD:A continuation of excessive flexion displayed in loading response. In TSW: incomplete recovery of knee extension following peak knee flexion

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Causes of EKF & IKE

Inappropriate hamstring activity
Spasticity: primitive activity in MSW and through MSD MSW and TSW:flexor momentum stretch spastic hamstring, inhibited knee ext in MSW LR: floor contact continue hamstring pull but wt bearing stability is preserved because of primitive extensor pattern. MSD & TSD: continue hamstrings activity or a response to forward trunk lean (due to inadequate ankle DF 79

Knee Flexion contracture

Flexion 30 is the resting for a swollen knee.
All phase of gait cycle will be abnormal except ISW.

Penalty for loss of extension in TSW is shortening of step length Inability to appropriately extend the knee in mid and terminal stance increase demand on Q.

Soleus weakness ineffective tibia control

tibia fall forward as body vector advance, the tibia advance faster than femur continue knee flex quadriceps can't reestablish knee ext , whole limb advance with inadequate knee extension.
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Pathological Gait-1

Associated with excessive ADF, sustained heel contact.

Excessive APF
Hip flexion is the basic and primary action, while knee flexion is a passive because gravity action on tibia.

Wobble
Small , alternating arc of flex and ext during stance for search of stability in a joint with impaired proprioception or spastic clonus.

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Cause of coronal plane bait devotions

Static factor: congenital or traumatic deformity Dynamic factor
OA persist medial body weight vector unequal load deformity trunk sway RA: unload painful hip or valgus foot deformity trunk lateral lean. Paralytic gait: lateral trunk lean to stabilize hip with abductor weakness.

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