Abnormal gait واحدی هوشنگ دکترامیر

توانبخشی و فیزیکی متخصصطب

3قسمت

GAIT PATHOLOGY AND PROBABLE CAUSES1. Foot strike to foot flat 2.Foot strike through midstance3. Foot strike through toe off4. Foot flat through heel off5. Midstance through toe off6. Swing phase

1. Foot strike to foot flat

Gait Pathology Probable Causes

Foot slap Moderately weak dorsiflexors

Inadequate Dorsiflexion Control

In stance phase (Heel contact – Foot flat):Foot slap

In swing phase (mid-swing): Toe drag

Causes:Weak Tibialis Ant.Spastic plantarflexors

Flat foot strike/ Toe strike

Cause: Dorsiflexor weakness

Early Stance phase:

the forefoot falls to the ground without control and with a slapping sound

Foot slap gait

Toe Drag

Cause: Dorsiflexor weakness Plantarflexor

spasticity

Swing phase:

Forefoot cannot be adequately raised and is dragged along the ground

2-Foot strike through midstanceGait Pathology Probable Causes

Genu recurvatum Weak, short, or spastic quadriceps; compensated hamstring weakness; Achilles tendon contracture; plantarflexor spasticity

Excessive foot supination

Compensated forefoot valgus deformity; pes cavus; short limb; uncompensated external rotation of tibia or femur

Excessive trunk extension

Weak hip extensor or flexor; hip pain; decreased knee ROM

Excessive trunk flexion

Weak gluteus maximus and quadriceps

Excessive knee extension

Loss of normal knee flexion during stance phase Knee may go into hyperextension Genu recurvatum: hyperextension deformity of

knee Common causes:– Quadriceps weakness (mid-stance)– Quadriceps spasticity (mid-stance)– Knee flexor weakness (end-stance)

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Knee Hyperextension / Genu Recurvatum

During all stance phase of gait cycle

Observe from the side view, the normal knee is completely extended only at the end of stance phase

1. Bend trunk forward

2. Use hand to stabilize knee

3. Rotate the leg externally or internally

Increased Walking Base

Normal walking base: 5-10 cmCommon causes:

DeformitiesAbducted hipValgus knee

InstabilityCerebellar ataxiaProprioception deficits

Walking base

During all phases of gait cycle

If distance between centre of heels is greater or smaller than normal (5-10 cm) this is classified as abnormal

Abnormal walking base A broad walking base may be accompanied by

exaggerated side-to-side displacement of the pelvis, lateral pelvic tilt, or both

An excessively narrow walking base is often caused by internal hip rotation and exaggerated knee flexion in spasticity

Wide walking base:1. Contracture of hip abductors2. Unsteadiness due to anxiety3. Proprioceptive deficit4. General lower limb weakness5. Genu valgum6. Leg length discrepancy 7. Pressure effects, e.g. pain or tissue damage, on the

perineum

4. Foot flat through heel offGait Pathology Probable Causes

Excessive trunk lateral( Trendelenburg gait)

flexion Ipsilateral gluteus medius weakness; hip pain

Pelvic drop Contralateral gluteus medius weaknessWaddling gait Bilateral gluteus medius weakness

5. Midstance through toe offGait Pathology Probable Causes

Excessive foot pronation

Compensated forefoot or rearfoot varus deformity;uncompensated forefoot valgus deformity; pes planus; decreased ankle dorsiflexion; increased tibial varum; long limb; uncompensated internal rotation of tibia or femur; weak tibialis posterior

Bouncing or exaggeratedplantar flexion

Achilles tendon contracture; gastroc-soleus spasticity

Insufficient push-off

Gastroc-soleus weakness; Achilles tendon rupture; metatarsalgia; hallus rigidus

Inadequate hip extension

Hip flexor contracture; weak hip extensor

6. Swing phaseGait Pathology

Probable Causes

Steppage gait Severely weak dorsiflexors; equinus deformity; plantarflexor spasticity

Circumduction Long limb; abductor muscle shortening or overuse

Hip hiking Long limb; weak hamstring; quadratus lumborum shortening

Functional Leg-Length Discrepancy

Swing leg: longer than stance leg4 common compensations:

A. CircumductionB. Hip hikingC. SteppageD. Vaulting

Circumduction

1) Pes equinus2) Knee / ankle ankylosis3) Short contralateral 4) Leg Contralateral knee / hip

flexion contracture

Circumduction

Orothtic factor:–Knee lock– Inadequate dorsiflexion assist– Inadequate plantar flexion stop

Gait with dorsiflexor weakness: Compensatory deviation

Swing phase:

Patient can compensate for this only by exaggerated hip and knee flexion

High stepping gait

Hip “hiking “ or “vaulting”

During Swing phase, when foot not contact ground and is acting like a double pendulum

Hip hiking lengthens the stride on affected side since it permits greater rotation of the pelvis in transverse plane

Helping to increase pendulum movement

Hip Hiking:

Equinus deformity or ankle dorsiflexor weakness

Skeletal shortening on sound sideIt may be combined with circumduction in

order to give additional anterior movement to the flexion-impaired hip joint

Gait in Cerebral Palsy Patients

Spasticity Dynamic or fixed muscle contracture Lever arm dysfunction Joint contracture Impaired balance reactions and loss of

selective muscular control and equilibrium reactions, e.g. difficulty stopping if walking quickly

Common CP Knee Patterns in Gait Crouch knee gait Jump knee gait Stiff knee gait Recurvatum knee gait

Crouch Knee Characterised by:– Increased stance phase hip flexion– Persistent knee flexion >30 throughout stance– Excessive dorsiflexion throughout stance

Aetiology:– Weak ankle plantar flexors or over-lengthened TAs

or from increasingheight and weight– Overactive knee flexors (and/or rectus co-pasticity)– Overactive hip flexors Clinical examination – most have:– Hip flexion contractures– Knee flexion contractures– Severe hamstring tightness (popliteal angle >70)

Jump Knee Characterised by:– Increased knee flexion at initial contact

correcting to near normal in mid- to late stance

– Toe or flat foot strike– Increased stance phase hip flexion

Aetiology:– Overactive – hip flexors, knee flexors and/or rectus co-

spasticityand/or plantar flexors Physical examination:– Usually associated with dynamic contractures– Moderate hamstring tightness (mean popliteal angle

approximately50)

Stiff Knee Gait Characterised by:– Delayed and reduced peak knee flexion in swing– Associated with compensations to aid clearance– Mainly a swing phase problem Physical examination:– Positive Duncan-Ely test– Reduced ROM in swing– Delayed and reduced peak knee flexion in swing– EMG=rectus co-spasticity in swing

Recurvatum Knee Gait Characterised by:– Toe or flat foot strike– Recurvatum >2 in stance Aetiology:– Plantar flexor over-activity/contracture– Weak dorsiflexors– Overly aggressive hamstring lengthening Physical examination:– TA tightness– Hip flexion contracture– Some hamstring tightness (popliteal angle 40)

Typical pathological gaitANKLE / FOOTStance phase:– No heel strike ( Flat foot contact)– Toe strike ( Forefoot contact)– Excessive plantarflexion (Vaulting)– Varus (Inversion)– Valgus (Eversion)

Lack of heel rise (inadequate push off) Swing phase:– Drop foot– Toe drag

KNEEStance phase:– Inadequate knee extension (flex limited/excessive)– Recurvatum (hyperextension)– Knee varus (Genu varus)

Knee valgus (Genu valgus) Swing phase:

– Knee flexion absent– Reduced knee flexion – Increased Knee flexion

HIPStance or Swing phase:– Circumduction– Inadequate flexion– Inadequate extension– Exessive/ Not enough Adduction – Abduction of hip– Exessive/ Not enough External – Internal rotation

of hip

PELVIS / TRUNKStance or Swing phase:– Anterior – Posterior tilt of pelvis– Forward – Backward trunk leaning/Lumbar lordosis– Excessive Trunk rotation– Lateral trunk bending or Trendelenberg– Hip hiking

Five gait disorders caused by cerebral lesions

1. frontal gait disorders2. cortical-subcortical gait disorders3. subcortical gait disorders4. extrapyramidal gait disorders5. subcortical astatic disorders

1-Frontal gait disorders

caused by anterior cerebral artery strokemulti-infarct state Binswanger's diseasenormal pressure hydrocephalus bilateral frontal lobe lesions

Normal pressure hydrocephalus

• CADENCE ----------Slow• STEP LENGTH-------Short• BASE ------------Slightly wide• OTHER ASSOCIATED SIGNS-------Numerous

problems with handling axial body movement

Frontal lobe

• CADENCE ---------- Slow• STEP LENGTH------- Slow Greatly shortened• BASE ------------ Slightly wide(protective)• OTHER ASSOCIATED SIGNS------- Difficulty

starting and stopping; tendency for feet to “stick” to floor

2-Cortical-subcortical gait disorders

also been termed "gait ignition failure“ "primary progressive freezing gait“ "motor blocks“ or "trepidant abasia“ Etiologies vascular or degenerative lesions in the cerebral white

and gray matter "parkinsonian gait," - typically seen in patients with

parkinsonism

3-Extrapyramidal (hyperkinetic) gait

choreic gait, dystonic gait, action myoclonus, orthostatic tremor and other hyperkinetic movement disorders

present in – Huntington's disease– idiopathic torsion dystonia– tardive dyskinesia– cerebral palsy.

4-Subcortical astatic disorders

• are recognized previously as – thalamic astasia – thalamic ataxia – or subcortical disequilibrium

• they are caused by thalamic or basal ganglia lesions

5-Pyramidal gait disorders

hemiparetic and spastic patterncauses– stroke– demyelination– mass or trauma to the motor cortex or the

corticospinal tracts– focal epilepsy may cause a paroxysmal gait

disorder

„Cautious gait disorders„have been labeled with many different terms– "senile gait„– "pseudoagoraphobia," – "post-fall syndrome,„– "space phobia," – "adaptive gait," – "astasobasophobia.„

This is the most common abnormal gait pattern in the elderly

Classification Gait Findings in Gait Disorders of Older Adults

Peripheral sensory ‘‘steppage gait’• Sensory ataxia • Vestibular ataxia • Visual ataxia Peripheral motor (‘‘Trendelenburg’’

and‘‘waddling’’ gait)• Arthritic (antalgic,joint deformity) • Myopathic andneuropathic(weakness)

Spasticity • Hemiplegia/paresis circumduction, ‘‘scissor’’• Paraplegia/paresis Parkinsonism Cerebellar ataxia• Cautious gait • Frontal-related gait disorders, other white

matter lesions