RESUMO
BACKGROUND: Adolescents with cerebral palsy often complain about a Duchenne gait, which increases the load on the spine, the energy consumption and therefore decreases gait efficiency. However the underlying causes of a Duchenne gait in patients with CP are not clearly researched yet. Nevertheless there is an assumption that excessive trunk lean might assist foot clearance to compensate for muscle weakness or contractures of the legs. In particular weakness, secondary to surgical soft tissue muscle tendon lengthening in childhood, might predispose patients to greater compensatory movements of the trunk. Therefore the aim of this study was to estimate the prevalence, underlying causes and calculated predictors for a Duchenne gait on CP patients with and without previous muscle tendon lengthening. PATIENTS, MATERIALS AND METHODS: 50 CP patients between 12 and 22 years with diplegia and GMFCS II (GMFCS: Gross Motor Function Classification System) participated in this study. 25 patients had no previous surgeries (CP-0). 25 patients had previous calf, hamstrings and/or adductor muscle tendon lengthening surgeries (CP-1). Data of 20 typically developed adolescents served as controls (TD). Gait was analysed using an instrumented gait analysis system (Vicon, Oxford, UK) The parameter "thorax obliquity range" (TOR) investigated the dimension of Duchenne gait. RESULTS: CP-0 showed a prevalence of 72â%, CP-1 of 66â% for Duchenne gait. TOR was 5 ± 2°, 16 ± 8° and 16 ± 8°, for TD, CP-0 and CP-1, respectively. CP-0 and CP-1 showed significant differences in TOR between TD (both p < 0.001), but not between CP-0 and CP-1 (p = 1.0). Passive hip abduction range of motion (ROM) showed no significant correlation to TOR in both groups, whereas hip abduction muscle strength revealed significant correlation (rs = - 0.37) in CP-0. Best gait predictors in CP-0 patients were increased hip generation work (stance = st) and ankle dorsi flexion (swing = sw), together explaining 47â% of the variance in TOR. In CP-1 best gait predictors were increased hip generation work (st) as well as reduced knee flexion (sw) and ankle generation work (st), explaining 31â% of the variance in TOR. CONCLUSION: With a prevalence of 66â% or higher Duchenne gait is a serious gait pathology in CP. Neither the hypothesis that previous muscle tendon lengthening nor that hip adductor contractures increase Duchenne gait could be confirmed in this study. Weak hip abductor muscle strength only showed a small correlation in CP-0. Best predictor in both groups was hip generation work (st). Certain hip abductors (M. gluteus medius ventral; M. gluteus minimus; M. tensor fasciae latae) function also as hip flexors and internal rotators. This leads to the hypothesis that during stance the Duchenne gait unloads the hip abductor muscles and therefore decreases the effect of internal rotation and hip flexion which leads to improved dynamic power of the hip for propulsion. In consequence the resultant hip extension moment increases by reducing the hip flexion moment. Presumably this is due to the fact that patients with CP show a reduced selective muscle control. For CP patients the negative effects of the common pelvis drop and internal rotation of the hip during gait decrease.
