Individuals with cerebral palsy commonly have gait pathologies that limit their mobility and hinder activities of daily living. One of the most common gait pathologies among individuals with cerebral palsy is crouch gait. Individuals who walk in a crouch gait have excessive hip and knee flexion which makes walking difficult and metabolically inefficient. If untreated, crouch gait can lead to joint pain, bone deformities, and a loss of independent mobility. Current treatments for crouch gait involve orthopaedic surgery and therapy;​ however, outcomes are inconsistent. Clinicians need a better understanding of how the complexities of the neuromuscular and musculoskeletal systems contribute to this pathologic gait pattern. The goal of this dissertation was to examine the musculoskeletal dynamics of crouch gait in individuals with cerebral palsy to better understand its biomechanical causes and improve treatment of individuals with crouch gait.

There are many proposed causes of crouch gait including excessive muscle activity from contracture or spasticity, muscle weakness, bone deformities, and impaired voluntary control. To determine which of these factors contribute to crouch gait requires an understanding of how individual muscles contribute to motion. We generated the first three-dimensional musculoskeletal simulations of crouch gait to evaluate how muscles contribute to joint and mass center acceleration. We found that individuals with crouch gait use the same muscles to support and propel the body as unimpaired gait. However, larger and more sustained muscle forces are required during crouch gait.

Many individuals with cerebral palsy and crouch gait also develop knee pain later in life. Since cartilage growth and maintenance is dependent upon the loads experienced during daily life, we sought to quanitfy how tibiofemoral forces change during crouch gait. We determined that the compressive tibiofemoral force increases quadratically with crouch severity and individuals who walk in a severe crouch gait experience three times the load experienced during unimpaired gait. Elevated tibiofemoral forces could compromise cartilage health and lead to knee pain.

Muscle weakness is commonly hypothesized as a cause of crouch gait and many individuals with crouch gait participate in strength training programs. We performed a meta-analysis of outcomes after strength training in individuals with cerebral palsy and crouch gait and found that although muscle strength increases after strength training, changes in gait kinematics are inconsistent. Some individuals with crouch gait had significantly more knee extension during gait after strength training;​ however, other individuals’ gait deteriorated. We determined that hamstring spasticity may be a contraindication for strength training among individuals with cerebral palsy and crouch gait;​ no individuals with hamstring spasticity had improved knee extension after strength training.

We also used musculoskeletal simulation to evaluate how much muscle strength is required to walk in a crouch gait compared to an unimpaired gait. We found that crouch gait requires more quadriceps strength than unimpaired gait but requires less hip abductor and ankle plantarflexor strength. These results suggest that weakness of the hip abductors or ankle plantarflexors may contribute to crouch gait and strengthening these muscles may lead to more consistent outcomes after strength training.

This dissertation examines the dynamics of crouch gait among individuals with cerebral palsy including muscle contributions to motion, changes in joint loads, and the effects of muscle weakness. This work provides a foundation for using musculoskeletal modeling and simulation to examine complex gait pathologies and also suggests exciting future areas of research to improve the care and treatment of individuals with cerebral palsy and crouch gait.