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During goal-directed arm movements, the eyes, head, and arm are coordinated to look at and reach the target. We examined whether the expectancy of visual information about the target modifies Anticipatory Postural Adjustments (APAs). Ten standing subjects had to (1) move the eyes, head and arm, so as to reach, with both gaze and index-finger, a target of known position placed outside their visual field (Gaze-Reach); (2) look at the target while reaching it (Reach in Full Vision); (3) keep the gaze away until having touched it (Reach then Gaze) and (4) just Gaze without Reach the target. We recorded eye, head, right arm, and acromion kinematics, EMGs from upper- and lower-limb muscles, and forces exerted on the ground. In Gaze-Reach, two coordination strategies were found: when gaze preceded arm muscle recruitment (Gaze-first) and when the opposite occurred (Reach-first). APAs in acromion kinematics, leg muscles, and ground forces started significantly earlier in Gaze-first vs. Reach-first (mean time advance: 44.3 ± 8.9 ms), as it was in Reach in Full Vision vs. Reach then Gaze (39.5 ± 7.9 ms). The Gaze-first to Reach-first time-shift was similar to that between Reach in Full Vision and Reach then Gaze (p = 0.58). Moreover, Gaze without Reach data witnessed that the head-induced postural actions did not affect the APA onset in Gaze-first and Reach-first. In conclusion, in Gaze-first, the central control of posture considers visual information while planning the movement, like in Reach in Full Vision; while Reach-first is more similar to Reach then Gaze, where vision is not required.

The literature reports that anticipatory postural adjustments (APAs) are programmed according to movement velocity. However, the linkage between APAs and velocity has been highlighted within single subjects who were asked to voluntarily change movement velocity; therefore, till now, it has been impossible to discern whether the key factor determining APA latency was the intended movement velocity or the actual one. Aim of this study was to distinguish between these two factors. We analyzed the APA chain that stabilizes the arm during a brisk index finger flexion in two groups of subjects: (1) 29 who composed our database from previous experiments and were asked to "go-as-fast-as-possible" (go-fast), but actually performed the movement with different speeds (238-1, 180°/s), and (2) ten new subjects who performed the go-fast movement at more than 500°/s and were then asked to go-slow at about 50% of their initial velocity, thus moving at 300-800°/s. No correlation between APA latency and actual movement speed was observed when all subjects had to go-fast (p > 0.50), while delayed APAs were found in the ten new subjects when they had to go-slow (p < 0.001). Moreover, in the speed range between 300 and 800°/s, the APA latency depended only on movement instruction: subjects going fast showed earlier APAs than those going slow (p < 0.001). These data suggest a stronger role of the intended movement velocity versus the actual one in modifying the timing of postural muscles recruitment with respect to the prime mover. These results also strengthen the idea of a shared postural and voluntary command within the same motor act.

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.

Voluntary movement is known to induce postural perturbations that are counteracted by unconscious anticipatory postural adjustments (APAs). Thus, for every movement, two motor commands are dispatched: a voluntary command recruiting the prime mover and a postural command driving the APAs. These commands are classically thought to be separated; this study investigates whether they could be instead considered as two elements within the same motor program. We analyzed the APAs in biceps brachii, triceps brachii and anterior deltoid that stabilize the arm when briskly flexing the index finger (prime mover flexor digitorum superficialis). APAs and prime mover activation were recorded before, under and after ischemic block of the forearm. Ischemia paralyzed the prime mover, thus suppressing the finger movement and the ensuing postural perturbation. If the two commands had been separated, it would have been expected that after a few failed attempts to flex the index finger, the APAs were suppressed too, being purposeless without postural perturbation. APAs were still present under ischemia even after 60 movement trials. No significant changes were found in APA amplitude in biceps and triceps among different conditions, or in the average APA latency. Inhibitory APA in anterior deltoid was reduced but still present under ischemia. In addition, the pharmacologic block of the sole median nerve produced similar effects. APAs were instead almost abolished when applying a fixation point to the wrist. The observation that APAs remained tailored to the expected perturbation even when that perturbation did not occur supports the idea of a functionally unique motor command driving both the prime mover and the muscles of the APA chain.

It is a common experience, immediately after the removal of a cast or a splint, to feel motor awkwardness, which is usually attributed to muscular and joint immobilization. However, the same feeling may also be perceived after a brief period of immobilization. We provide evidence that this last effect stems from changes in the cortical organization of the focal movement as well as in the associated anticipatory postural adjustments. Indeed, these two aspects of the motor act are strongly correlated, although scaled in different manners. In fact, they are both shaped in the primary motor cortex, they both undergo similar amplitude and latency modulation and, as we will show, they are both impaired by the immobilization of the lone prime mover. Neuromuscular effects of limb immobilization are well known; however, most papers focus on changes occurring in the pathways projecting to the prime mover, which acts on the immobilized joint. Conversely, this study investigates the effect of immobilization on anticipatory postural adjustments. Indeed, we show that 12 h of wrist and fingers immobilization effectively modify anticipatory postural adjustments of the elbow and the shoulder, that is, those joints not immobilized within the fixation chain. Accordingly, the motor impairment observed after short-term immobilization most likely stems from the unbalance between anticipatory postural adjustments and the focal movement.