Gait in RA

Gait in RA

RA a systemic inflammatory disease process, characterized by B/L symmetrical pattern of joint involvement and chronic inflammation of the synovium

*According to a study in J Biomechanics in 1988, “Gait in RA” following results were concluded on a study of 17 female RA patients.

• Stride length & duration of g art cycle were decreased .
• Mobility (ROM) of ankle joint was significantly less in both rotation & adduction among RA patients.

AT HIP JOINT

• Rotation of the hip joint increased.
• Adduction at hip joint decreased

AT KNEE JOINT

• No ssd were ascertained in ROM of knee joint.

AT ANKLE JOINT

• Maximum angular execution of ankle at toe off.

• Pattern of ankle flexion- different in RA patients.

• Smaller PF at toe off than normals.

• In advanced stages of disease, tendency to valgus deformity.

• Inflammation of ankle joint prevented the normal mechanism of adduction in subtlar joint at the end of stance, for an energetic push off (by rigid lever)

*According to a study by D Laroche et al in J Biomechanics, 2005 on “Effect of loss of MTP joint mobility on gait in RA”, it was concluded.

• Walking velocity & stride length were decreased +vely related to MTP DF ROM
• Decreased MTP ROM –esp in DF rom
• Pain during walking was exp by 5/9 patients and DF tended to be decreased in these patients
• Negative relationship b/w MTP DF rom & maximal hip and knee flexion during walking.

OA marked by two localized , pathological features

Progressive destruction of articular & formation of bone at the margins of joint.

Confines itself to affected joint.

Mechanical factors play a significant role in the ethology of the disease by giving rise to instating

joint damage.

High loading rates-increases risk if OA.

*According to study by H.S. Gill of Biomechanics, 2003 on”Heel strike & pathomechanics of OA” it was concluded that;

The test population was divided into two gps

Displayed markedly different loading during H S phrase of gait- attributed to differences in the vertical velocity of the ankle at HS.

Differences in loading -more apparent in saggital plane.

Subtle differences in the trajectories appeared to produce large difference on ankle velocity at HS .

The Non -loader gp lifted their ankle higher (ssd) than loader gp during early swing phase.

Antalgic Gait

It reflects the body’s efforts to compensate for pain or instability in the stance- phase limb by minimizing the duration and magnitude of loading. It is a gait pattern characterized by diminished single limb stance time.

• Habitual limp
• Distinguished by awkward displacement of shoulder &
• Characteristic rhythm

*According to a study in JBJS, 1939

Probable cause

1. Shortening – a sufficiently large number of coxalgic patient are cured with affected limb, the same length as the other

• i.e. there is no shortening but patients continue to limp
• patients with shortening following fracture of the thigh do not commence to limp (unless 3-4 cm)

2. Ankylosis – Bony ankylosis of hip, consequent to a true osseous fusion of femur to pelvis causes only a very slight limp

- the less complete the ankylosis the more attentuated limp

3) Deformity – (flexion, abduction, adduction, irotation)

• deformities when very marked – render walking almost impossible

• compensatory attitude – ascent of pelvis, accentuated lorsosis – too render walking possible but with awkward and painful limp

• with correction of deformity antalgic gait reappears

Trendelenburg Limp – mechanical phenomenon

• insufficiency of the gluteus medius
• causes pivoting of the pelvis around femoral head
• descent of iliac spine on the contra-lateral side, as a result
• lack of opposition of this descent
• may be associated with CDH

HIP JOINT

Inadequate Extension/ Excessive Flexion

1. Stance phase

1. Primary causes – hip flexor spasticity/contracture

• hams/hip extensor weakness
• iliotibial band contracture as in DMD
• hip joint pain

2. Secondary cause – excessive DF
3. Consequence – associated anterior pelvic tilt and forward trunk lean.
4. Compensated by inc lumbar lordosis –more strain on L.S
5. IncompletParkinson's Disease

• Chronic, progressive disease of the nervous system
• Characterized by cardinal features of rigidity, akinesia, bradykinesia, tremors & postural instability
• Damage to BG results in motor dysfunction's of voluntary movements & control of associated postural adjustments.
• Characterized by - shuffling gait with small steps.

6. e compensation leads to inc (external) extension moment at knee DF moment at ankle.

B) Swing Phase

1. Primary cause - hip flexor spasticity/contracture

Excessive Adduction

A) Stance Phase

1. Primary cause – adductor muscle spasticity/contracture

• ipsilateral abductor muscle weakness

2. Secondary cause – c/l hip abductor contracture
3. Consequences – dec BOS (coronal plane)

- dec limb stability

B) Swing Phase

1. Primary cause – adductor muscle spasticity
2. Secondary cause – limb-length inequality – short c/l limb causes adduction in swing
3. Compensation for weak hip flexor to assist in limb clearance.
4. Consequences – relative lengthening of limb

• Scissor gait (in cp)
• Trendelenburg gait / uncompensated gluteus medius gait pattern,

With c/l pelvic drop during single limb support,

Lateral trunk lean over stance limb so c.o.m is effectively moved closer to stance phase hip joint, decreased demand on gluteus medius – abductor lurch.

Excessive Abduction

A) Stance phase

1. Primary cause – abductor muscle contracture
2. Secondary cause - limb-length inequality
3. Consequences - inc BOS

- dec in relative length of stance limb

B) Swing Phase

1. Primary cause- ipsilateral abductor contracture
2. Subsitute for weak hip flexors
3. To clear long limb with pelvic rotation – circumduction
4. Consequence – dec functional length of ipsilateral limb.

Gait abnormalities in CEREBRAL PALSY

C.P- is a non-progressive, CNS disorder with pre-natal , peri-natal or post-natal etiology ( that may occur up to 2 yrs of age).

*Damage to cerebral cortex-

*Loss of cortical inhibition over sub cortical centers - manifested as UMN lesion

* release of abn patterns of reflex movements

* inability to perform certain purposeful movements

* Inefficient gait pattern due to absence of synchronization of various muscle groups- poor co-ordinations of movements.

* hyperactive stretch reflex - clonus- a spinal level response in which hyper active stretch

reflex ,lacks UMN control & is poor prognosticator.

* impaired sensory or proprioceptive loss.

Abnormalities in Gait

• impaired muscle action or loss of mobility
• inefficient gait pattern, due to inc energy expenditure
• lack of reciprocal relaxation of antagonist
• steps length- shortened on involved side
• co-contraction of opposing muscle gps is frequent

1. Pelvic Rotation – transverse plane, related to stride length, prevents excessive vertical displacement of COM

• limited by motor dysfunction, joint contracture, abnormal muscle sequencing

SAGGITAL PLANE

2. Hip Joint

• hams, adductors – markedly increased periods of phasic activity that dec. hip flexion & increases med rotation
• Pts walk slowly with shorter step, med rotated leg.
• When hip flexion contractures have developed

Lumbar lordosis

Flexion of knees – slower gait, short step.

3. Knee Joint

at I.C, flexion of knee- important shock absorber -normally

if knee flexion contracture- compensation by flexion at hip or DF at ankle

Or - compensatory equinnus, which eliminate heel contact

Dec stride-length, speed & ankle DF, with inc energy consumption..

If prolonged phasic activity of quads & hams - circumductory gait may develop.

4. Ankle Joint

. prolonged phasic activity of calf muscles- (common) leads to equinnus gait , and toe -heel contact

. If lack of ankle DF, compensates hyper extending knee or flexion at hip & knee joints.

. Crouch gait- manifested by flexion at hips & knee & maximal DF of ankle in stance phase, called flatfoot gait may be a result of surgical lengthening of TA- if they result in weak post muscle & prolonged phasic activity of anterior muscle.

Frontal Plane

Hip Joint

-hip adduction spasticity- relative shortening of the involved limb.

-Compensated by dec step-width, equinnus, genu-valgum of c\l knee.

Knee joint

-prolonged activity of medial hams & adductors- may create appearance of genu valgum & in-toed position.

- B\L genu valgum, there may be pelvic rotation to keep the knees from knocking.

Recurvatum Gait- hyper extension of the knee in stance phase, consequence of over active medical & lateral distal hams lengthening in children with CP

1. Acc to a study by Catherine Tardieu et at in 1989.

Toe walking in cerebral palsy requires detailed evaluation prior to Rx.

• Toe walking may be due to excessive muscle contraction of triceps surae.
• Toe walking due to contracture of triceps surae although they may similar walking pattern

2. According to a study by Cheryl J Hanson et al 1989.

The use of tone inhibiting cast, orthosis permits the development of a more normal gait pattern in a child with hyperactive reflexes & reduce the abn tome reflexes.

Parkinson's Disease- Gait

Parkinson's Disease

• Chronic, progressive disease of the nervous system
• Characterized by cardinal features of rigidity, akinesia, bradykinesia, tremors & postural instability
• Damage to BG results in motor dysfunction's of voluntary movements & control of associated postural adjustments.
• Characterized by - shuffling gait with small steps.

HIP JOINT

Inadequate Extension/ Excessive Flexion

1. Stance phase

1. Primary causes – hip flexor spasticity/contracture

• hams/hip extensor weakness
• iliotibial band contracture as in DMD
• hip joint pain

2. Secondary cause – excessive DF
3. Consequence – associated anterior pelvic tilt and forward trunk lean.
4. Compensated by inc lumbar lordosis –more strain on L.S
5. Incomplete compensation leads to inc (external) extension moment at knee DF moment at ankle.

B) Swing Phase

1. Primary cause - hip flexor spasticity/contracture

Excessive Adduction

A) Stance Phase

1. Primary cause – adductor muscle spasticity/contracture

• ipsilateral abductor muscle weakness

2. Secondary cause – c/l hip abductor contracture
3. Consequences – dec BOS (coronal plane)

- dec limb stability

B) Swing Phase

1. Primary cause – adductor muscle spasticity
2. Secondary cause – limb-length inequality – short c/l limb causes adduction in swing
3. Compensation for weak hip flexor to assist in limb clearance.
4. Consequences – relative lengthening of limb

• Scissor gait (in cp)
• Trendelenburg gait / uncompensated gluteus medius gait pattern,

With c/l pelvic drop during single limb support,

Lateral trunk lean over stance limb so c.o.m is effectively moved closer to stance phase hip joint, decreased demand on gluteus medius – abductor lurch.

Excessive Abduction

A) Stance phase

1. Primary cause – abductor muscle contracture
2. Secondary cause - limb-length inequality
3. Consequences - inc BOS

- dec in relative length of stance limb

B) Swing Phase

1. Primary cause- ipsilateral abductor contracture
2. Subsitute for weak hip flexors
3. To clear long limb with pelvic rotation – circumduction
4. Consequence – dec functional length of ipsilateral limb.

Gait abnormalities in CEREBRAL PALSY

C.P- is a non-progressive, CNS disorder with pre-natal , peri-natal or post-natal etiology ( that may occur up to 2 yrs of age).

*Damage to cerebral cortex-

*Loss of cortical inhibition over sub cortical centers - manifested as UMN lesion

* release of abn patterns of reflex movements

* inability to perform certain purposeful movements

* Inefficient gait pattern due to absence of synchronization of various muscle groups- poor co-ordinations of movements.

* hyperactive stretch reflex - clonus- a spinal level response in which hyper active stretch

reflex ,lacks UMN control & is poor prognosticator.

* impaired sensory or proprioceptive loss.

Abnormalities in Gait

• impaired muscle action or loss of mobility
• inefficient gait pattern, due to inc energy expenditure
• lack of reciprocal relaxation of antagonist
• steps length- shortened on involved side
• co-contraction of opposing muscle gps is frequent

1. Pelvic Rotation – transverse plane, related to stride length, prevents excessive vertical displacement of COM

• limited by motor dysfunction, joint contracture, abnormal muscle sequencing

SAGGITAL PLANE

2. Hip Joint

• hams, adductors – markedly increased periods of phasic activity that dec. hip flexion & increases med rotation
• Pts walk slowly with shorter step, med rotated leg.
• When hip flexion contractures have developed

Lumbar lordosis

Flexion of knees – slower gait, short step.

3. Knee Joint

at I.C, flexion of knee- important shock absorber -normally

if knee flexion contracture- compensation by flexion at hip or DF at ankle

Or - compensatory equinnus, which eliminate heel contact

Dec stride-length, speed & ankle DF, with inc energy consumption..

If prolonged phasic activity of quads & hams - circumductory gait may develop.

4. Ankle Joint

. prolonged phasic activity of calf muscles- (common) leads to equinnus gait , and toe -heel contact

. If lack of ankle DF, compensates hyper extending knee or flexion at hip & knee joints.

. Crouch gait- manifested by flexion at hips & knee & maximal DF of ankle in stance phase, called flatfoot gait may be a result of surgical lengthening of TA- if they result in weak post muscle & prolonged phasic activity of anterior muscle.

Frontal Plane

Hip Joint

-hip adduction spasticity- relative shortening of the involved limb.

-Compensated by dec step-width, equinnus, genu-valgum of c\l knee.

Knee joint

-prolonged activity of medial hams & adductors- may create appearance of genu valgum & in-toed position.

- B\L genu valgum, there may be pelvic rotation to keep the knees from knocking.

Recurvatum Gait- hyper extension of the knee in stance phase, consequence of over active medical & lateral distal hams lengthening in children with CP

1. Acc to a study by Catherine Tardieu et at in 1989.

Toe walking in cerebral palsy requires detailed evaluation prior to Rx.

• Toe walking may be due to excessive muscle contraction of triceps surae.
• Toe walking due to contracture of triceps surae although they may similar walking pattern

2. According to a study by Cheryl J Hanson et al 1989.

The use of tone inhibiting cast, orthosis permits the development of a more normal gait pattern in a child with hyperactive reflexes & reduce the abn tome reflexes.