Typical knee extension range is 0 degrees (full knee extension).

Posterior capsular contracture can result from the imbalance between spastic or contracted hamstrings and knee extensor dysfunction (often associated with patella alta).

Distal femoral anatomy is normal, although torsional deformity (excessive femoral anteversion) is commonly seen in neuromuscular conditions, especially cerebral palsy.

The pathogenesis of knee flexion deformity and crouch gait in cerebral palsy will be described, as it is the most common condition to be treated with this technique. However, other causes of knee flexion deformity and persistent crouch could be treated similarly.

Preterm, perinatal, or infantile brain injury leads to static encephalopathy.

This neurologic disorder causes hypertonia (commonly spasticity), impaired motor control, and weakness.

Typical muscle growth results from the tension produced by normal bone growth and age-appropriate, typical gross and fine motor activities.

Musculotendinous growth in children with cerebral palsy is delayed because spastic muscle does not grow normally in response to stretch and delays in attainment of typical functional activities.

Bone growth and joint development are also adversely affected by a lack of normal functional activities as well as spasticity and musculotendinous contracture.

Crouch gait is not uncommon at 5 to 7 years of age. At these ages, the primary causes are spasticity, weakness, and impaired balance mechanisms.

If crouch persists during later childhood, musculotendinous contractures of the two-joint muscles (psoas, hamstrings, rectus femoris, and gastrocnemius) develop. Persistent alignment in a crouch position leads to excessive elongation of the one-joint muscles (gluteus maximus, quadriceps, and soleus), which are primarily responsible for normal upright posture.¹

The soleus, in particular, is responsible for restraining the forward movement of the tibia over the plantigrade foot (also known as the plantarflexion-knee extension couple).¹ As a result, the ground reaction force vector typically falls near the knee joint in midstance, minimizing the demand on the quadriceps to maintain knee extension.

If weak or elongated, the ankle plantarflexors are no longer able to restrain the forward movement of the tibia over the plantigrade foot (loss of the normal plantarflexion-knee extension couple).

Further growth leads to loss of knee joint mobility and the development of posterior capsular contracture.

For some patients in adolescence, pain from stress fractures or from excessive stress in the patellofemoral joint itself can lead to a precipitous worsening of crouch.

Knee pain, decreased ambulatory function, or the loss of walking ability in adulthood in individuals with cerebral palsy is common.³

Physical examination methods include the following:

A complete examination of the patient should also include evaluation of associated abnormalities to identify all potential contributors to crouch gait, including hip flexion deformity, hamstring contracture, femoral anteversion, tibial torsion, foot deformity or instability, balance disorder, and visual or sensory disturbances.

A plain lateral radiograph of the knee in maximum extension should be obtained to assess for fixed knee flexion contracture and patella alta (FIG 1).

If the knee is held in maximum extension, the femoral-tibial angle on the lateral radiograph represents the degree of true knee flexion deformity.

The knee is extended maximally with a bolster just below the patella to assess the true degree of patella alta. Patella alta can be documented using the Insall ratio or the Koshino index.²

Inferior pole sleeve avulsion injuries of the patella are common in children with spastic cerebral palsy and can be identified on the lateral radiograph. The development of a stress fracture is typically painful and can lead to the rapid progression of crouch over a short period.

Computerized gait analysis provides much needed insight to create a problem list to guide treatment decision making by identifying the numerous other contributors to crouch gait listed earlier.

Physical therapy (stretching and strengthening) helps minimize the development of musculotendinous contracture secondary to spasticity and weakness.

Botulinum toxin injections or oral spasmolytic agents can help manage spasticity.

Functional strengthening of the muscle groups that contribute to crouch (ankle plantarflexors, knee extensors, and hip extensors) can help correct muscle imbalance.

Nighttime knee extension splinting with knee immobilizers or bivalved casts can help prevent a flexed knee position during the night, thereby minimizing the development of knee capsular contracture.