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.