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Abstract Previous research has suggested that short‐term immobilization of the arm may be a low‐cost, non‐invasive strategy to enhance the capacity for long‐term potentiation (LTP)‐like plasticity in primary motor cortex (M1). Short‐term immobilization reduces corticospinal excitability (CSE) in the contralateral M1, and interhemispheric inhibition (IHI) from ipsi‐ onto contralateral M1 is increased. However, it is unclear whether reduced CSE and increased IHI are associated with changes in intracortical inhibition, which has been shown to be important for regulating neuroplasticity in M1. The current study used transcranial magnetic stimulation to evaluate the effects of short‐term (6 h) arm immobilization on CSE, IHI, and intracortical inhibition measured bilaterally in 43 neurotypical young adults (23 immobilized). We replicated previous findings demonstrating that immobilization decreased CSE in, and increased IHI onto, the immobilized hemisphere, but a significant change in intracortical inhibition was not observed at the group level. Across individuals, decreased CSE was associated with a decreased short‐interval intracortical inhibition, an index of GABAA‐ergic inhibition, within the immobilized hemisphere only in the immobilization group. Previous research has demonstrated that decreases in GABAA‐ergic inhibition are necessary for the induction of LTP‐like plasticity in M1; therefore, decreased intracortical inhibition after short‐term arm immobilization may provide a novel mechanism to enhance the capacity for LTP‐like plasticity within M1 and may be a potential target for strategies to augment plasticity capacity to enhance motor learning in health and disease.

Sensory loss involves irreversible behavioral and neural changes. Paradigms of short-term limb immobilization mimic deprivation of proprioceptive inputs and motor commands, which occur after the loss of limb use. While several studies have shown that short-term immobilization induced motor control impairments, the origin of such modifications is an open question. A Fitts’ pointing task was conducted, and kinematic analyses were performed to assess whether the feedforward and/or feedback processes of motor control were impacted. The Fitts’ pointing task specifically required dealing with spatial and temporal aspects (speed-accuracy trade-off) to be as fast and as accurate as possible. Forty trials were performed on two consecutive days by Control and Immobilized participants who wore a splint on the right arm during this 24 h period. The immobilization modified the motor control in a way that the full spatiotemporal structure of the pointing movements differed: A global slowdown appeared. The acceleration and deceleration phases were both longer, suggesting that immobilization impacted both the early impulse phase based on sensorimotor expectations and the later online correction phase based on feedback use. First, the feedforward control may have been less efficient, probably because the internal model of the immobilized limb would have been incorrectly updated relative to internal and environmental constraints. Second, immobilized participants may have taken more time to correct their movements and precisely reach the target, as the processing of proprioceptive feedback might have been altered.

Sensory loss involves irreversible behavioral and neural changes. Paradigms of short-term limb immobilization mimic deprivation of proprioceptive inputs and motor commands, which occur after the loss of limb use. While several studies have shown that short-term immobilization induced motor control impairments, the origin of such modifications is an open question. A Fitts' pointing task was conducted, and kinematic analyses were performed to assess whether the feedforward and/or feedback processes of motor control were impacted. The Fitts' pointing task specifically required dealing with spatial and temporal aspects (speed-accuracy trade-off) to be as fast and as accurate as possible. Forty trials were performed on two consecutive days by Control and Immobilized participants who wore a splint on the right arm during this 24 h period. The immobilization modified the motor control in a way that the full spatiotemporal structure of the pointing movements differed: A global slowdown appeared. The acceleration and deceleration phases were both longer, suggesting that immobilization impacted both the early impulse phase based on sensorimotor expectations and the later online correction phase based on feedback use. First, the feedforward control may have been less efficient, probably because the internal model of the immobilized limb would have been incorrectly updated relative to internal and environmental constraints. Second, immobilized participants may have taken more time to correct their movements and precisely reach the target, as the processing of proprioceptive feedback might have been altered. [ABSTRACT FROM AUTHOR]

Prolonged limb immobilization deprives sensorimotor cortical areas of an important source of excitatory input, as well as of motor output. Previous work has described effects on motor excitability but it is unclear whether motor plasticity is also influenced. In two groups of eight healthy human subjects, the left hand was immobilized for 8 h to induce sensorimotor deprivation of the cortical representation of the abductor pollicis brevis muscle. We used transcranial magnetic stimulation protocols to evaluate motor excitability with motor-evoked potentials, input- output (IOcurve) and short-latency intracortical inhibition (SICI) recruitment curves, as well as long-term potentiation (LTP)/long-term depression (LTD)-like plasticity with paired-associative stimulation (PAS) of the median nerve and motor cortex using an interstimulus interval of 25 ms (PAS25) or 10 ms (PAS10), respectively, in two sessions at least 7 d apart (baseline and after immobilization). After immobilization, the slope of the IOcurve decreased, and SICI at lower conditioning pulse intensities was reduced. The LTP-like effects of PAS25 and the LTD-like effect of PAS10 were both significantly enhanced. The effects differed among individuals: the more IOslope decreased after immobilization, the greater the increase of PAS25 and the smaller the increase of PAS10 effects. We suggest that sensorimotor deprivation has two effects. It increases the sensitivity to remaining sensory inputs and therefore increases the effectiveness of both PAS protocols. In addition, it reduces neuronal excitability to an individually different level, as reflected in the reduced IOslope and leads to an interdependent modulation of synaptic plasticity as such as it shifts the threshold of LTP/LTD-like plasticity induction. [ABSTRACT FROM AUTHOR]

Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Recent evidence suggests that immobilization of the upper limb for 2-3 weeks induces changes in cortical thickness as well as motor performance. In constraint induced (CI) therapy, one of the most effective interventions for hemiplegia, the non-paretic arm is constrained to enforce the use of the paretic arm in the home setting. With the present study we aimed to explore whether non-paretic arm immobilization in CI therapy induces structural changes in the non-lesioned hemisphere, and how these changes are related to treatment benefit. 31 patients with chronic hemiparesis participated in CI therapy with (N = 14) and without (N = 17) constraint. Motor ability scores were acquired before and after treatment. Diffusion tensor imaging (DTI) data was obtained prior to treatment. Cortical thickness was measured with the Freesurfer software. In both groups cortical thickness in the contralesional primary somatosensory cortex increased and motor function improved with the intervention. However the cortical thickness change was not associated with the magnitude of motor function improvement. Moreover, the treatment effect and the cortical thickness change were not significantly different between the constraint and the non-constraint groups. There was no correlation between fractional anisotropy changes in the non-lesioned hemisphere and treatment outcome. CI therapy induced cortical thickness changes in contralesional sensorimotor regions, but this effect does not appear to be driven by the immobilization of the non-paretic arm, as indicated by the absence of differences between the constraint and the non-constraint groups. Our data does not suggest that the arm immobilization used in CI therapy is associated with noticeable cortical thinning.