## 1 Introduction  
Leg length discrepancy (LLD), a common orthopedic condition, may be present either due to structural deformities originating from true bony leg length differences [1], or functional deformities originating from abnormal lower limb biomechanics [2] resulting from musculoskeletal abnormalities--such as joint contracture, static or dynamic mechanical axis malalignment, muscle weakness or muscular-tendon shortening.  
Recent studies have reported that gait deviations occur when LLD is <2 cm (hereafter, mild LLD) [3; 4; 5]; others have reported LLD as slight as 5-10 mm [6; 7]. Two main methodologies evaluating gait asymmetry as a result of LLD have been described in the literature. The subjects either existed anatomical LLD [8; 9] or LLD was acutely simulated with a shoe or heel lift in subjects assumed to have anatomically equal leg lengths [3; 7]. [PERSON] et al. assessed the impact of mild LLD on pathological gait deviations by correcting gait deviations using a sole lift of 12 mm among children diagnosed with spastic cerebral palsy diplegia and a relatively mild LLD of 16 mm (range 10-28) [5].  
Several studies have found that LLD is compensated by dynamic strategies aimed at achieving functional equalizations [1; 3; 7; 8], primarily when clearing the foot of the longer lower limb off the ground during the swing phase. Compensatory gait deviations can occur simultaneously in both the longer and shorter lower limb. Compensation of the shorter lower limb during the stance phase functionally elongates the limb by increasing hip and knee extension and ankle plantar flexion, whereas the longer leg utilizes deviations that functionally shorten the lower limb during the stance and swing phase with opposite kinematic deviations. According to the presence of the above asymmetric kinematic deviations, an anatomic LLD may be assumed. When assessing patients displaying neuromusculoskeletal abnormalities and exhibiting pathological gait deviations, additional clinical abnormalities such as spasticity, weak muscle strength and joint contracture deformities will either contribute to their functional LLD or limit their ability to compensate for anatomical LLD. Accordingly, the ability to measure the effect of LLD or to determine the lift height needed for correcting gait deviations is difficult. No attempt has been made to assess the impact of mild LLD on gait deviations in patients with pathological gait and its relationship to clinical abnormalities that might be present.  
The primary aim of this study was to analyze kinematical asymmetry of patients with mild LLD with and without other clinical abnormalities and compare the impact of LLD on their gait deviations. The secondary aim was to assess and quantify functional discrepancy based on dynamic leg length (DLL) measurements [7; 10; 11]. We hypothesized that patients with only LLD would achieve dynamic equalization with asymmetric kinematics by functionally shortening the longer side, and lengthening the shorter side, respectively. However, for patients with other abnormalities, LLD would not correlate with kinematic asymmetry due to their clinical abnormalities, and they would have a higher asymmetrical DLL, i.e., higher functional discrepancies.