Clinical motion analyses over eight consecutive years in a child with crouch gait: a case report.
BACKGROUND
This case report provides a unique look at the progression of crouch gait in a child with cerebral palsy over an 8-year time period, through annual physical examinations, three-dimensional gait analyses, and evaluation of postural balance. Our patient received regular botulinum toxin-A injections, casting, and physical therapy but no surgical interventions.


METHODS
A white American boy with spastic diplegic cerebral palsy was evaluated annually by clinical motion analyses, including physical examination, joint kinematics, electromyography, energy expenditure, and standing postural balance tests, from 6 to 13 years of age. These analyses revealed that the biomechanical factors contributing to our patient's crouch gait were weak plantar flexors, short and spastic hamstrings, moderately short hip flexors, and external rotation of the tibiae. Despite annual recommendations for surgical lengthening of the hamstrings, the family opted for non-surgical treatment through botulinum toxin-A injections, casting, and exercise. Our patient's crouch gait improved between ages 6 and 9, then worsened at age 10, concurrent with his greatest body mass index, increased plantar flexor weakness, increased standing postural sway, slowest normalized walking speed, and greatest walking energy expenditure. Although our patient's maximum knee extension in stance improved by 14 degrees at 13 years of age compared to 6 years of age, peak knee flexion in swing declined, his ankles became more dorsiflexed, his hips became more internally rotated, and his tibiae became more externally rotated. From 6 to 9 years of age, our patient's minimum stance-phase knee flexion varied in an inverse relationship with his body mass index; from 10 to 13 years of age, changes in his minimum stance-phase knee flexion paralleled changes in his body mass index.


CONCLUSIONS
The motor deficits of weakness, spasticity, shortened muscle-tendon lengths, and impaired selective motor control were highlighted by our patient's clinical motion analyses. Overall, our patient's crouch gait improved mildly with aggressive non-operative management and a supportive family dedicated to regular home exercise. The annual clinical motion analyses identified changes in motor deficits that were associated with changes in the child's walking pattern, suggesting that these analyses can serve to track the progression of children with spastic cerebral palsy.
The William H. Neukom Institute for Computational Science, Dartmouth College, Sudikoff Hall, Hanover, NH, 03755, USA. erin.e.butler@dartmouth.edu.
Erin E
EE
Butler
Department of Mechanical Engineering, University of Washington, 3600 E Stevens Way NE, Box 352600, Seattle, WA, 98195, USA.
Katherine M
KM
Steele
Motion & Gait Analysis Laboratory, Lucile Packard Children's Hospital at Stanford, 321 Middlefield Road, Menlo Park, CA, 94025, USA.
Leslie
L
Torburn
Department of Orthopaedic Surgery, Stanford University School of Medicine, 770 Welch Road, Suite 400, Palo Alto, CA, 94304, USA.
James G
JG
Gamble
Department of Orthopaedic Surgery, Stanford University School of Medicine, 770 Welch Road, Suite 400, Palo Alto, CA, 94304, USA.
Jessica
J
Rose
D000293:Adolescent; D019274:Botulinum Toxins, Type A / Q000627:therapeutic use; D002547:Cerebral Palsy / Q000150:complications*; D002648:Child; D004576:Electromyography / Q000379:methods; D020233:Gait Disorders, Neurologic / Q000150:complications / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D008297:Male; D010808:Physical Examination / Q000379:methods; D026741:Physical Therapy Modalities; D004856:Postural Balance / Q000502:physiology; D016059:Range of Motion, Articular
D019274:Botulinum Toxins, Type A
Botulinum toxin-A; Cerebral palsy; Clinical motion analysis; Crouch gait; Outcomes