Abstract
Controlling posture, i.e., governing the ensemble of involuntary muscular activities that manage body equilibrium, represents a demanding function in which the cerebellum plays a key role. Postural activities are particularly important during gait initiation when passing from quiet standing to locomotion. Indeed, several studies used such motor task for evaluating pathological conditions, including cerebellar disorders. The linkage between cerebellum maturation and the development of postural control has received less attention. Therefore, we evaluated postural control during quiet standing and gait initiation in children affected by a slow progressive generalized cerebellar atrophy (SlowP) or non-progressive vermian hypoplasia (Joubert syndrome, NonP), compared to that of healthy children (H). Despite the similar clinical evaluation of motor impairments in NonP and SlowP, only SlowP showed a less stable quiet standing and a shorter and slower first step than H. Moreover, a descriptive analysis of lower limb and back muscle activities suggested a more severe timing disruption in SlowP. Such differences might stem from the extent of cerebellar damage. However, literature reports that during childhood, neural plasticity of intact brain areas could compensate for cerebellar agenesis. We thus proposed that the difference might stem from disease progression, which contrasts the consolidation of compensatory strategies.
Highlights
Postural adjustments are involuntary muscular activities that accompany the voluntary movement.These activities spread over adjacent muscles and create “chains” that reach the available support points
Very little attention has been given to the linkage between the development of postural control and the maturation of such neural structure. Aiming to elucidate this topic, we explored quiet stance and gait initiation in children affected by Pediatric Cerebellar Ataxia (PCA), used as a model of cerebellar dysfunction vs. a healthy control group of comparable age
It has been observed that the compensatory role of the cerebellum contributes to preventing the full manifestation of the typical motor symptoms during the initial stage of Parkinson’s disease (PD); this compensatory ability saturates with time, leading these patients to develop cerebellar symptoms too [58]. These pieces of evidence allow arguing that, reciprocally, intact basal ganglia may compensate for cerebellar deficits. This hypothesis is still to be demonstrated, but should it be proved, it would provide a straightforward explanation for the graded postural impairments we found in children affected by PCA, as well as for the worse impairments reported in adult patients with cerebellar ataxia [46]
Summary
Postural adjustments are involuntary muscular activities that accompany the voluntary movement. These activities spread over adjacent muscles and create “chains” that reach the available support points (in many cases, the ground). Such chains allow fine-tuning the body equilibrium, in order to adapt it to the mechanical needs of the ensuing movement. When flexing both arms at the shoulder, postural actions develop in a dorsal muscle chain, including Erector Spinae (ES), Biceps. Instead, when rising on tiptoes, involuntary bursts of activity develop in Tibialis Anterior (TA) muscles, so as.
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