# Postural Control in Children with Cerebellar Ataxia
## 3 Results
### EMG
\begin{table}
\begin{tabular}{l l c c c c c} \hline  & & \multicolumn{2}{c}{**SlowP**} & \multicolumn{2}{c}{**NonP**} & \multicolumn{2}{c}{**H**} \\ \hline  & **Phase duration (s)** & 0.41 & (0.25 to 1.03) & 0.42 & (0.31 to 1.90) & 0.31 & (0.25 to 0.53) \\  & **CoP length (mm)** & 34 & (24 to 100) & 70 & (33 to 134) & 42 & (17 to 68) \\  & **ML CoP shift (mm)** & 15.99 & (13 to 28) & 39.80 & (\(-\)6 to 67) & 25.95 & (8 to 49) \\  & **AP CoP shift (mm)** & \(-\)18 & (\(-\)43 to \(-\)5) & \(-\)25 & (\(-\)43 to \(-\)11) & \(-\)14 & (\(-\)14 to \(-\)8) \\  & **ML COM shift (mm)** & \(-\)7.33 & (\(-\)14.67 to \(-\)20.3) & \(-\)6 & (\(-\)9.67 to 2) & \(-\)7 & (\(-\)13.67 to \(-\)2.33) \\  & **AP COM shift (mm)** & 4.33 & (\(-\)0.67 to 20.33) & 6 & (2 to 8.67) & 6 & (2.33 to 11.67) \\  & **ML CoP\(\rightarrow\) COM (mm)** & \(-\)25 & (\(-\)54.67 to \(-\)16.67) & \(-\)30.75 & (\(-\)49.25 to 54) & \(-\)37.33 & (\(-\)56.67 to \(-\)18) \\  & **AP CoP \(\rightarrow\) COM (mm)** & 24.67 & (2.67 to 62.67) & 28.83 & (12 to 47.33) & 21 & (12 to 56) \\ \hline \multirow{4}{*}{**Cop**} & \multirow{2}{*}{**Phase duration (s)**} & \multirow{2}{*}{0.46} & \multirow{2}{*}{(0.21 to 1.53)} & \multirow{2}{*}{0.33} & \multirow{2}{*}{(0.23 to 1.20)} & \multirow{2}{*}{0.41} & \multirow{2}{*}{(0.21 to 0.56)} \\  & **CoP length (mm)** & 172 & (112 to 202) & & & & \\ \cline{1-1}  & **ML CoP shift (mm)** & \(-\)104 & (\(-\)147 to \(-\)48) & \(-\)127 & (\(-\)168 to \(-\)9) & \(-\)121 & (\(-\)152 to \(-\)76) \\ \cline{1-1}  & **AP CoP shift (mm)** & 9 & (\(-\)12 to 28) & \(-\)1 & (\(-\)26 to 17) & \(-\)9 & (\(-\)59 to 9) \\ \cline{1-1}  & **ML COM shift (mm)** & \(-\)34.67 & (\(-\)6.66 to \(-\)21) & \(-\)34.37 & (\(-\)49 to \(-\)17) & \(-\)35.67 & (\(-\)53.33 to \(-\)22) \\ \cline{1-1}  & **AP COM shift (mm)** & 43 & (21.67 to 47.33) & 35.08 & (12 to 55.5) & 38.67 & (28 to 55.33) \\ \cline{1-1}  & **ML CoP \(\rightarrow\) COM (mm)** & 44.25 & (33.67 to 90.33) & 50.96 & (\(-\)7 to 62.67) & 46.67 & (23 to 61.67) \\ \cline{1-1}  & **AP CoP \(\rightarrow\) COM (mm)** & 51 & (37.33 to 94.33) & 67.75 & (29.33 to 106) & 80 & (57.33 to 108.5) \\ \hline \end{tabular}
\end{table} 
Table 3: Postural parameters during the imbalance and unloading phases. Data are shown as _median value (range)_ for children _median value (range)_ for children with slow progressive PCA (SlowP), children with non-progressive PCA (NonP), and healthy children (H). ML: mediolateral, positive towards the swing foot; AP: anteroposterior, positive when forwards; CoP\(\rightarrow\)COM: horizontal distance from CoP to COM. timing distribution of the muscular actions was found in the three groups (Table 5). In the stance limb side, healthy subjects showed a clear craniocaudal progression, for both the inhibitory (first ES and BF, then SOL) and excitatory (first RF, then TA) chains. Such a progression was lost both in children with NonP and in those affected by SlowP; moreover, in SlowP, the recruitment of the excitatory chain was delayed. On the contralateral side with respect to the swing limb, both chains had a caudocranial progression in the H group (first SOL, then BF and ES; first TA, then RF), while children with NonP displayed a disrupted progression of the inhibitory chain, where SOL de-activated after BF and ES, followed by an almost synchronous activation of RF and TA. Instead, in children with SlowP, the inhibitory chain still maintained a caudocranial progression but was overall delayed. Also, in this group, the excitatory actions in RF and TA were synchronous. Of note, in the control group, the inhibition of the stance leg SOL started about 40 ms prior to TA excitation. While this timing was overall preserved in the children of the NonP group (about 60 ms), it was effectively increased in children with SlowP (about 100 ms, Figure 2). Similar changes were detected also for the swing leg. Figure 2: EMG (electromyographic) of shank muscles of the stance leg.