Temporal disruption of upper-limb anticipatory postural adjustments in cerebellar ataxic patients

Abstract

Voluntary movements induce postural perturbations, which are counteracted by anticipatory postural adjustments (APAs) that preserve body equilibrium. Little is known about the neural structures generating APAs, but several studies suggested a role of sensory-motor areas, basal ganglia, supplementary motor area and thalamus. However, the role of the cerebellum still remains an open question. The aim of this present paper is to shed further light on the role of cerebellum in APAs organization. Thus, APAs that stabilize the arm when the index finger is briskly flexed were recorded in 13 ataxic subjects (seven sporadic cases, four dominant ataxia type III and two autosomal recessive), presenting a slowly progressive cerebellar syndrome with four-limb dysmetria, and compared with those obtained in 13 healthy subjects. The pattern of postural activity was similar in the two groups [excitation in triceps and inhibition in biceps and anterior deltoid (AD)], but apparent modifications in timing were observed in all ataxic subjects in which, on average, triceps brachii excitation lagged the onset of the prime mover flexor digitorum superficialis by about 27 ms and biceps and AD inhibition were almost synchronous to it. Instead, in normal subjects, triceps onset was synchronous to the prime mover and biceps and AD anticipated it by about 40 ms. The observed disruption of the intra-limb APA organization confirms that the cerebellum is involved in APA control and, considering cerebellar subjects as a model of dysmetria, also supports the view that a proper APA chain may play a crucial role in refining movement metria.

Postural Control in Children with Cerebellar Ataxia

“…On the contrary, children with SlowP suffer from a continuous cerebellar degeneration, which conflicts with the consolidation of compensatory functional strategies. This perspective not only fits with the gradual worsening of postural deficits we documented here when passing from healthy children to patients with NonP and to patients with SlowP but would also explain why patients with adult-onset cerebellar lesions show even more pronounced postural deficits [46]. Indeed, neural plasticity gradually but consistently decreases over the lifespan [50].…”

“…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].…”

“…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]. Evidence in this regard might come from functional MRI and diffusion tensor imaging techniques.…”

Transcranial direct current stimulation of SMA modulates anticipatory postural adjustments without affecting the primary movement

“…However, little is known about the precise role of each of these structures in governing APAs. In this regard it has been shown that the cerebellum is involved in APAs timing (Diedrichsen et al, 2005;Bruttini et al, 2015). Moreover, both excitatory and inhibitory APAs are already shaped in the primary motor cortex, M1 (Petersen et al, 2009;Caronni & Cavallari, 2009b).…”

APAs Constraints to Voluntary Movements: The Case for Limb Movements Coupling

“…Cerebellar lesions may selectively impair also the APAs subtending within-limb movements. For instance, in patients with cerebellar ataxia, simple brisk movements of the finger are associated with alterations of the APAs engaging proximal arm muscles (Bruttini et al, 2015; Cavallari et al, 2016). …”