EXSS2021 Movement Analysis Week 2: Clinical Gait Full Study Notes
Introduction and Acknowledgement
Acknowledge of Country: Recognition of the Gadigal people of the Eora Nation as the Traditional Owners of the land. Respects are paid to Elders past, present, and emerging, as well as to Traditional Owners of other lands where participants are located.
Presenter Profile: Dr. Elizabeth Wojciechowski, PhD MIPEM CSci:
Biomedical Engineer and Deputy Director of the Paediatric Gait Analysis Service of NSW at The Children’s Hospital at Westmead.
Clinical Lecturer at the Faculty of Medicine and Health, School of Health Sciences, University of Sydney.
Educational Background:
BEng (2005–2009).
MSc in Biomedical Engineering (2009–2011).
Postgraduate Diploma with the Institute of Physics and Engineering in Medicine (IPEM) as an NHS Trainee Clinical Scientist (Engineer) (2009–2011).
PhD (2016–2020) focused on personalised orthotic therapy using 3D printing technologies.
Post-Doc Researcher (2021–present) exploring topics beyond the gait lab and wearable sensors.
Learning Objectives
LO5: Be familiar with the mechanical principles associated with normal and pathological gait, and understand how these principles change across the lifespan.
Clinical Gait Analysis (CGA) Overview
Definition: Clinical gait analysis is a process in which a patient’s movement patterns are measured, abnormalities are identified, causes are postulated, and treatment recommendations are developed (Davis, R.B.).
The Clinical Gait Analysis Process:
Background/History: Birth history, developmental milestones, GMFCS level, comorbidities, previous surgery, spasticity management, current therapies, and family concerns/goals.
Physical Exam: Assessment of spasticity and range of motion.
2D Video: Sagittal and coronal views, often using split-screen views; may include dynamic pedobarography.
3D Gait Analysis (3DGA): Collection of kinematic and kinetic data.
Electromyography (EMG): Optional wireless EMG to monitor muscle activity.
The Service Model at Westmead:
Data collection includes 3DGA, 2D video, physical exam, and optional pedobarography/EMG.
An impairment-focused interpretation is written into a report.
A multi-disciplinary reporting session (meeting) involving CHW, SCH, and JHH specialists leads to final recommendations.
Kinematic Data and Pathological Conditions
3DGA Kinematics: Measures the pelvis and three joints (Hip, Knee, Ankle) across three planes (Sagittal, Coronal, Transverse).
Conditions with Pathological Gait (Frequency Data):
Cerebral Palsy (CP): 960 cases (876 specifically spastic CP).
Hereditary Spastic Paraplegia (HSP): 49 cases.
Acquired or Traumatic Brain Injury: 48 cases.
Spina Bifida: 30 cases.
Muscular Dystrophy: 20 cases (DMD: 16; Emery-Dreifuss: 1; Limb girdle: 1; Other: 1).
Transverse Myelitis: 13 cases.
Aicardi-Goutieres Syndrome: 6 cases.
Incontinentia Pigmenti: 7 cases.
Neurofibromatosis: 6 cases.
Sjogren-Larsson Syndrome: 5 cases.
Charcot-Marie-Tooth Disease (CMT): Included as a frequent pathology.
10 Clinical Signs in Observational Gait Analysis
Clinical gait analysis uses observation tools like the Ranchos Los Amigos Observational Gait Assessment Form (Perry 1992) and the Edinburgh Visual Gait Scale. Whittle (2007) identifies 10 key signs:
1. Step Length Asymmetry
Potential Causes:
Weak push-off.
Weak hip flexor activity in early swing.
Hyperactive hamstrings in late swing.
Limited contralateral extension.
Parkinsonian steps.
2. Ankle at Contact - Loss of Dorsiflexion Function
Associated Conditions: Peroneal nerve palsy, diabetic neuropathy, or medial tibial stress syndrome (due to dorsiflexor overuse).
Observations:
Plantarflexed foot through swing followed by toe/forefoot contact.
Audible "foot slap" as the foot strikes the floor.
Biometrics: Forefoot strike creates an anterior Ground Reaction Force (GRF) and a plantarflexion moment (rather than dorsiflexion). This results in a large centre of pressure-ankle moment arm.
Clonus: A hyperactive stretch reflex can trigger ankle clonus (phasic contraction of plantarflexors) upon forefoot landing.
Clinical Recommendations: Dorsiflexion strengthening, Ankle Foot Orthosis (AFO) to support the limb and prevent swing-phase plantarflexion, Botulinum toxin (Botox) for calf spasticity, or calf lengthening surgery.
3. Knee Flexion at Initial Contact (IC)
Potential Indicators: Knee flexion contracture, hamstrings spasticity, tightness from muscle sprain, or poor foot positioning.
Associated Condition: Cerebral Palsy.
Clinical Recommendations: Botox into hamstrings or hamstring lengthening surgery.
4. Stance Phase Knee Flexion
Normal Profile: Knee is extended at contact, flexes to approximately , then extends again.
Pathology: Loss of flexion due to weak extensors or pain.
Jump Knee: The knee is flexed at initial contact but subsequently extends.
Clinical Recommendations: Spasticity management (Botox into calf/hamstrings) or surgery for contractures.
5. Single-Limb Support
Abnormalities:
Knee Collapse: Crouch gait.
Hyperextension: Genu recurvatum.
Premature Heel-Rise: Occurs before the contralateral limb swings past (around of the gait cycle or of stance). Suggests calf spasticity or equinus deformity.
Vaulting: Compensation for poor contralateral foot clearance.
6. Ankle and Foot during Push-off
Normal Function: Ankle ROM is approximately . Plantarflexion must occur while the limb is loaded. The foot should supinate for leverage.
Apropulsive Gait: Persistent pronation prevents firm leverage, resulting in weak push-off, reduced stride length, and decreased velocity.
Clinical Recommendations: AFO to improve lever arm and stability; strengthening of plantarflexors.
7. Swing Phase Knee Flexion
Reduced Flexion: Failure of swing initiation in late stance; often called "stiff knee gait." Caused by rectus spasticity or lack of ankle push-off.
Normal Flexion: during swing.
Excessive Flexion: Indicates a steppage gait to handle toe clearance issues.
8. Trunk Lean
Forward Lean: Places body weight/GRF ahead of the knee joint. This compensates for weak knee extensors (passive stability) and aids hip flexion (pull-off).
Posterior Lean: Occurs in early swing. The trunk is thrown backward to propel the swinging leg. Compensates for weak hip flexors or hip extensor spasticity. Also used if the knee cannot flex, requiring the leg to be moved as one unit.
9. Frontal Plane: Trendelenburg Sign
Normal: Hip abductors (gluteus medius/minimus) contract to prevent the pelvis from listing downward.
Trendelenburg Gait: Pelvis lists downward due to weak hip abductors or painful hip (e.g., OA).
Compensations: Leaning the trunk toward the weak side to reduce the hip abductor moment; using a contralateral cane.
Treatment: Strengthening abductors or using walking aids.
10. Transverse Plane
Signs: Medially rotated feet or femoral anteversion.
Femoral Anteversion: Defined by the angle the head and neck of the femur make with the shaft. It is at birth and reduces to in adults.
Upper-Limb Indicators: Reduced stance time on one side suggests pain. A flexed hemiplegic arm posture may suggest an ipsilateral lower-limb issue.
Special Topic: Cerebral Palsy and AFOs
Scenario 1: Weakness of Plantarflexion: Leads to the collapse of the plantarflexion-knee extension couple. An AFO restores this by preventing dorsiflexion, forcing the vertical GRF anterior to the knee to create an extensor moment.
Scenario 2: Plantarflexor Spasticity: Causes an exaggerated plantarflexion-knee extension couple. The AFO improves foot contact, forcing the GRF posterior to the ankle and knee at initial contact, which improves knee flexion and the flexor moment during loading response.
Detailed Compensatory Mechanisms for Clearing the Foot
Vaulting: Going up on the toes of the stance leg during the stance phase. Causes exaggerated vertical trunk movement; is energy-wasteful.
Circumduction: Swinging the leg outward in a circular motion during the swing phase. Used for weak hip flexors; allows adductors to act as flexors while the hip is extended.
Hip Hiking: Lifting the pelvis on the swing side by contracting spinal and lateral abdominal muscles.
Steppage: Exaggerated knee and hip flexion in swing to lift the foot higher, compensating for foot drop.
Case Study: Clinical Implementation
Patient Impairments ID'd: Excessive femoral anteversion, cavovarus R foot, increased R hip internal rotation, internal foot progression, and high pressure on the R lateral midfoot/forefoot.
Recommendations: R hip de-rotation (), R foot SPLATT/SPOTT, calf lengthening, and potential tibial derotation.
Surgical Outcome: R side SPLATT/SPOTT and R side femoral derotation osteoplasty () resulted in normalized barefoot kinematics in 2022 compared to 2018 data.