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Background: Postural instability may result from altered sequencing of automatic motor programs for anticipatory postural corrections and/or impaired motor learning in Parkinson Disease (PD) patients. Comorbid white matter disease is a major determinant of axial motor impairment, leading to poorer stability than nigrostriatal dopaminergic denervation per se., Objective: To assess differences in anticipatory control of postural stability function between subjects affected by PD with comorbid leukoaraiosis (LPD), idiopathic Parkinson disease (IPD) and elderly healthy subjects (EHS) as control group., Methods: Eight patients with IPD, eight patients with LPD and eight age/weight matched elderly healthy subjects (EHS) were tested in standing position by measuring the Center of Pressure (CoP) along the anteroposterior axis (CoP-Y) while subjects were expecting three repeated backward surface translation., Results: LPD patients positioned the CoP-Y significantly backward while waiting for the second and third platform translations, with respect to their COP-Y position in preparation for the first translation. The IPD and EHS showed no significant differences in the COP-Y position among the repeated perturbation trials., Conclusions: LPD patients show inability to rescale an effective preparatory postural pattern to known, repeated postural perturbations suggesting impaired sensory-motor strategies in anticipating perturbations. Anticipatory postural patterns remain effective in IPD patients.

Most of the cerebral functions are asymmetrically represented in the two hemispheres. Moreover, dexterity and coordination of the distal segment of the dominant limbs depend on cortico-motor lateralization. In this study, we investigated whether postural control may be also considered a lateralized hemispheric brain function. To this aim, 15 young subjects were tested in standing position by measuring center of pressure (COP) shifts along the anteroposterior axis (COP-Y) during dynamic posturography before and after continuous Theta Burst Stimulation (cTBS) intervention applied to the dominant or non-dominant M1 hand area as well as to the vertex. We show that when subjects were expecting a forward platform translation, the COP-Y was positioned significantly backward or forward after dominant or non-dominant M1 stimulation, respectively. We postulate that cTBS applied on M1 may have disrupted the functional connectivity between intra- and interhemispheric areas implicated in the anticipatory control of postural stability. This study suggests a functional asymmetry between the two homologous primary motor areas, with the dominant hemisphere playing a critical role in the selection of the appropriate postural control strategy.

Botulinum neurotoxin type A (BoNT/A) is a metalloprotease that produces a sustained yet transitory blockade of transmitter release from peripheral nerve terminals. Local delivery of this neurotoxin is successfully employed in clinical practice to reduce muscle hyperactivity such as in spasticity and dystonia, and to relieve pain with long-lasting therapeutic effects. However, not all BoNT/A effects can be explained by an action at peripheral nerve terminals. Indeed, it appears that BoNT/A is endowed with trafficking properties similar to the parental tetanus neurotoxin and thus be able to directly affect the CNS. In this review, we present and discuss novel compelling evidence for a direct central effect of BoNT/A in both dorsal and ventral horns of the animal and human spinal cord after peripheral injection of the neurotoxin, with important consequences on pain and motor control. This new knowledge is expected to radically change the approach to the use of BoNT/A in the future. As BoNT/A central action appears to also contribute to functional improvement, for instance in human spastic gait, the challenge will be to develop new subtypes or BoNT derivatives with deliberate, cell-specific central effects in order to fully exploit the spectrum of BoNT/A therapeutic activity., (© The Author(s) 2014.)