Abnormal gait
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Transcript of Abnormal gait
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Abnormal gait واحدی هوشنگ دکترامیر
توانبخشی و فیزیکی متخصصطب
3قسمت
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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
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1. Foot strike to foot flat
Gait Pathology Probable Causes
Foot slap Moderately weak dorsiflexors
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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
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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
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Toe Drag
Cause: Dorsiflexor weakness Plantarflexor
spasticity
Swing phase:
Forefoot cannot be adequately raised and is dragged along the ground
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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
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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
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1. Bend trunk forward
2. Use hand to stabilize knee
3. Rotate the leg externally or internally
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Increased Walking Base
Normal walking base: 5-10 cmCommon causes:
DeformitiesAbducted hipValgus knee
InstabilityCerebellar ataxiaProprioception deficits
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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
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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
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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
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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
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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
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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
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Functional Leg-Length Discrepancy
Swing leg: longer than stance leg4 common compensations:
A. CircumductionB. Hip hikingC. SteppageD. Vaulting
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Circumduction
1) Pes equinus2) Knee / ankle ankylosis3) Short contralateral 4) Leg Contralateral knee / hip
flexion contracture
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Circumduction
Orothtic factor:–Knee lock– Inadequate dorsiflexion assist– Inadequate plantar flexion stop
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Gait with dorsiflexor weakness: Compensatory deviation
Swing phase:
Patient can compensate for this only by exaggerated hip and knee flexion
High stepping gait
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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
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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
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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
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Common CP Knee Patterns in Gait Crouch knee gait Jump knee gait Stiff knee gait Recurvatum knee gait
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Crouch Knee Characterised by:– Increased stance phase hip flexion– Persistent knee flexion >30 throughout stance– Excessive dorsiflexion throughout stance
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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)
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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
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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)
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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
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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)
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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
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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
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HIPStance or Swing phase:– Circumduction– Inadequate flexion– Inadequate extension– Exessive/ Not enough Adduction – Abduction of hip– Exessive/ Not enough External – Internal rotation
of hip
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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
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Five gait disorders caused by cerebral lesions
1. frontal gait disorders2. cortical-subcortical gait disorders3. subcortical gait disorders4. extrapyramidal gait disorders5. subcortical astatic disorders
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1-Frontal gait disorders
caused by anterior cerebral artery strokemulti-infarct state Binswanger's diseasenormal pressure hydrocephalus bilateral frontal lobe lesions
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Normal pressure hydrocephalus
• CADENCE ----------Slow• STEP LENGTH-------Short• BASE ------------Slightly wide• OTHER ASSOCIATED SIGNS-------Numerous
problems with handling axial body movement
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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
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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
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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.
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4-Subcortical astatic disorders
• are recognized previously as – thalamic astasia – thalamic ataxia – or subcortical disequilibrium
• they are caused by thalamic or basal ganglia lesions
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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
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„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
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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)
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Spasticity • Hemiplegia/paresis circumduction, ‘‘scissor’’• Paraplegia/paresis Parkinsonism Cerebellar ataxia• Cautious gait • Frontal-related gait disorders, other white
matter lesions