# Postural Control in Children with Cerebellar Ataxia
## 4 Discussion  
The aim of this study was to describe the postural control adopted by children with PCA during quiet stance and gait initiation, in order to draw considerations on the role of the cerebellum in the development of postural control. As a main result, we observed that in patients with slow progressive PCA, i.e., SlowP, both the static and dynamic components of postural control were disturbed, while the postural behavior of children with non-progressive PCA, i.e., NonP, was much similar to that of healthy children. During the maintenance of upright posture, children with SlowP showed an increased ellipse area, mainly due to large mediolateral oscillations of the CoP. Considering CoP oscillations in anteroposterior direction too, this resulted in a general reduction of the ellipse eccentricity, outlining an omnidirectional decrease of stability. This finding was in agreement with the results described in adults with cerebellar lesions [26]. No statistical posturographic differences were instead found between children with NonP and H participants. Gait initiation parameters during the _imbalance_ and _unloading_ phases remained substantially unchanged in patients of both pathological groups compared to H controls. Also, this observation fitted with previous results obtained in adults with cerebellar ataxia [21,40]. First step length and velocity showed instead a marked reduction in children with SlowP with respect to H, possibly reflecting a compensatory strategy for their poor balance control, and in agreement with what has been previously described in adults [21]. Electromyographic data, despite the roughness of the descriptive approach, suggested that patients with NonP and SlowP suffered more alterations in the temporal (when) than in the spatial distribution (to what muscle) and in the sign of activity (how, i.e., excitation or inhibition). This aspect agreed with the general view that assigns to the cerebellum the role of a \"timing-machine\" [41, 42, 43, 44, 45] and leaves the pattern selection to other brain structures, like the basal ganglia. Such a perspective has been confirmed also for what regards APAs in adults [46, 47]. A short comment also deserves TA and SOL reciprocal activation. Despite our analysis was descriptive, patients with PCA and healthy children displayed the classical anticipatory postural pattern, characterized by SOL inhibition followed by TA activation of the stance limb (see Introduction). However, the latency between SOL and TA activity in the healthy group (about 40 ms) was consistent with what reported by [PERSON] et al. (2014) [18] and much lower than what has been found in adults (about 100 ms, [7]). This observation supported the choice of devoting a paper to gait initiation in children and, at the same time, suggested that the present H group, despite scarce, well represents the underlying population. On the contrary, indications of altered timing were observed in patients with PCA, in which the SOL-TA latency slightly increased to about 60 ms in children with NonP and attained about 100 ms in children with SlowP. This suggested a framework of abnormal feed-forward muscle synergies [21,24]. In summary, the reported differences in postural behavior between children with typical development and children affected by PCA support our hypothesis that the cerebellum plays a role also during the key phase of human maturation, in particular, in building internal models of gait initiation dynamics. This finding further stresses the importance of including postural training exercises in the rehabilitation programs for these pathologies [48]. Moreover, the observation that the gait initiation protocol allowed distinguishing motor deficits in children with SlowP vs. NonP, although the corresponding SARA scores were comparable, suggests that such protocol may be useful to monitor the evolution of motor deficits over time.