# Kinematic Relations during Double Support Phase in Parkinsonian Gait
## 4 Discussion  
It has been shown that the gait of PD patients differs from the gait of healthy controls in many motor aspects [4, 15, 16, 17, 18, 19, 20, 22, 23]. Our MoCap-based research supports the findings and provides greater insight into the topic by unveiling relations that have not been fully considered hitherto. It is often reported that the PD patients attain lower velocity compared to the healthy controls [20, 23, 30]. Higher gait velocity is associated with higher physical fitness [31] or higher life quality [32]. However, as our results surprisingly indicate, the PD patients are not slower throughout the whole gait cycle. During I, the PD CoG velocity was nearly 20% higher compared to CS. We explain this higher speed as a consequence of the preceding--less balanced--SSP resulting in a less controlled and therefore faster incursion into the I. Although the PD patients were faster during I phase compared to the CS, their speed was constant, unlike the speed of the CS whose speed was dynamically corresponding to the actual needs of the particular gait phase (i.e., slower during I and faster during \begin{table}
\begin{tabular}{c c c c} \hline
**Variable I** & **Variable II** & \(\rho\)**(PD)** & \(\rho\)**(CS)** \\ Step width index & I CoG v & 0.6702 & 0.0376 \\  & (medio-lateral) & & \\ T CoG v & I CoG v & & \\ (antero-posterior) & (antero-posterior) & 0.8957 & 0.4052 \\ TS shoulder \(\alpha\) & TO ankle \(\alpha\) & \(-0.4718\) & 0.4632 \\ TS shoulder \(\alpha\) & IO shoulder \(\alpha\) & 0.3660 & 0.9143 \\ IO shoulder \(\alpha\) & IS shoulder \(\alpha\) & \(-0.2488\) & 0.3795 \\  & I CoG v & & \\ DST \% & (antero-posterior) & \(-0.5469\) & \(-0.0337\) \\  & I CoG v & & \\ SST \% & (antero-posterior) & 0.5062 & 0.3120 \\ Walking cadence N/s & I Trunk lean & \(-0.3178\) & 0.3595 \\  & I CoG v & & \\ Step length index & (antero-posterior) & 0.7559 & 0.1081 \\ \hline \end{tabular}
\end{table} 
Table 2: Selected Spearman correlations in PD and CS. T, as seen in the Figure 2). Thus, the PD patients were nearly 20% faster at heel strike (0.921 m\(\cdot\)s\({}^{-2}\) compared to 0.795 m\(\cdot\)s\({}^{-2}\)); however, their velocity at heel off was about 28% slower compared to the CS (0.945 m\(\cdot\)s\({}^{-2}\) compared to 1.265 m\(\cdot\)s\({}^{-2}\)). In such fashion, the CS were periodically adjusting the gait velocity whereas the PD patients sustained rigid or careful speed that was chiselled also in a tight correlation between speed in the I and T phases, which was much fainter in the CS (Table 2). The possible reasons for the careful gait of PD patients have often been disputed [14; 33; 34]. Throughout the gait cycle, the CoG forward velocity for overcoming SSP is generated mostly by the pushing foot during T (along with the ongoing body mass inertia) [17]. This push-off is stronger in the CS, probably owing to stronger plantar flexors and better confidence in movement conduction [14; 34]. What is more, it is likely that where the CS can boldly predict, release, and utilise the force necessary for unrestrained smooth gait, the PD patients intentionally push-off less forcibly for fear of impeded balance control in the subsequent less stable SSP [34]. The lack of gait speed adaptability can represent an important root of many gait-related problems and could be thus considered by physiotherapists and neurologists. The extended DST is viewed as a pattern of disrupted gait control (in PD, it extends when in OFF state [17] and shortens when 3D cueing is provided [4]). The extension in the PD patients often breaks physiological ratio of SST:DST (4:1) [4; 15; 16; 17; 18; 19]; according to a meta-analysis [20], it changes to 3.93:1.08. In our sample, the SST:DST ratio in PD was even more shifted towards DST (3.45:1.55). The PD DST was nearly 27% longer compared to the CS. Is the DST extension an adaptation or rather a consequence? There is no clear answer among the authors yet.