## 4 Discussion  
Our study demonstrates that anatomic LLD is correlated with compensatory kinematic asymmetry only when no additional clinical abnormalities are present. The presence of clinical abnormalities, such as joint contractures, muscle-tendon shortening and weak muscle strength will most probably have more of an effect on gait, making the mild anatomic LLD of <2 cm inconsequential. In pathological gait deviations, a functional measurement based on DLL might assist in assessing functional LLD during gait. When examining the relationship between kinematic symmetry for movements known to compensate for LLD and anatomic LLD measured by X-ray, no correlation was found in Group B with pathological gait and clinical abnormalities. However, a high correlation was found in five kinematic parameters in Group A that had only LLD as a clinical finding, consistent with others [1; 3; 4; 8]. This suggests that kinematic asymmetry in pathological gait where clinical abnormalities were present, was not associated with LLD. Group A exhibited a uniform gait pattern, demonstrating that a higher classification accuracy attained by the random forest method might suggest that LLD was the main factor influencing their gait deviations. An 80% accuracy level obtained by the classifier in Group A is considered high. It is well-known that decision-making in pathological gait is variable [21]. Both groups presented different classification variables for LLD displaying a different kinematic profile, despite a similarity in LLD. In addition, evaluating the 3 cases in group B which were incorrectly classified by the model, revealed that they were relatively \"normal\" subjects: two with an LLD of 3 mm and one with an LLD of 11 mm, which seems reasonable to be classified incorrectly. However, in group B, the model incorrectly classified 6 subjects, with significant clinical abnormalities leading to difficulty in classifying them according to their gait pattern. The clearance index, based on the relationship between maximal stance and contralateral minimal swing phase DLL revealed several differences between the groups. A relatively different clearance index between sides was seen in group B, which might be related to their clinical abnormalities since the two groups did not differ in their anatomic LLD. Group A achieved compensatory asymmetry in their gait pattern which equalized their DLL. The asymmetry in their anatomic LLD was associated with their clearance index, except for Group A with longer left lower limb, where a relative symmetry was found despite the anatomic LLD. This might be due to the fact that some subjects with LLD were able to--or chose to--compensate for their LLD and change their DLL, while others are not able to--or do not to--compensate. This might depend on the amount of LLD or factors that we are still not aware of. However, group B exhibited a pathological gait with significant clinical abnormalities affecting their DLL, leading to an asymmetrical clearance index, unrelated to their anatomic leg length. In addition, Group B with longer right lower limb presented higher asymmetry in their HDL and ADLL, which may imply that this group was severe with significantly more clinical abnormalities that affect gait and lead to asymmetry. FDLL performed differently and presented a relatively symmetrical DLL, which might be due to its dependency on ankle joint movement [11] due to compensation strategies used along with the clinical abnormalities. The effect of the functional discrepancy, as a result of the clinical abnormalities, considerably affects gait more than LLD, and thus, this should be the basis on which asymmetry is quantified and equalization determined. Although this research was methodically planned, the authors are aware of its limitations. The polyvalence of the primary diagnosis of the patients demonstrates a potential limitation which may have produced some inconclusive results.