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.