The effect of motor imagery on corticospinal excitability and inhibition in healthy adults: a systematic review.

BackgroundBoth motor imagery (MI) and motor execution (ME) can facilitate motor cortical excitability. Although cortical excitability is modulated by intracortical inhibitory and excitatory circuits in the human primary motor cortex, it is not clear which intracortical circuits determine the differences in corticospinal excitability between ME and MI.MethodsWe recruited 10 young healthy subjects aged 18−28 years (mean age: 22.1 ± 3.14 years; five women and five men) for this study. The experiment consisted of two sets of tasks involving grasp actions of the right hand: imagining and executing them. Corticospinal excitability and short-interval intracortical inhibition (SICI) were measured before the interventional protocol using transcranial magnetic stimulation (baseline), as well as at 0, 20, and 40 min (T0, T20, and T40) thereafter.ResultsFacilitation of corticospinal excitability was significantly greater after ME than after MI in the right abductor pollicis brevis (APB) at T0 and T20 (p < 0.01 for T0, and p < 0.05 for T20), but not in the first dorsal interosseous (FDI) muscle. On the other hand, no significant differences in SICI between ME and MI were found in the APB and FDI muscles. The facilitation of corticospinal excitability at T20 after MI correlated with the Movement Imagery Questionnaire (MIQ) scores for kinesthetic items (Rho = −0.646, p = 0.044) but did not correlate with the MIQ scores for visual items (Rho = −0.265, p = 0.458).DiscussionThe present results revealed significant differences between ME and MI on intracortical excitatory circuits of the human motor cortex, suggesting that cortical excitability differences between ME and MI may be attributed to the activation differences of the excitatory circuits in the primary motor cortex.

BackgroundMotor imagery (MI) improves motor skill learning, which is further enhanced when MI is paired with primary motor cortex transcranial brain stimulation or with electrical stimulation of the peripheral median nerve. Applying both stimulation types (here with 25 ms intervals) is called paired associative stimulation (PAS25). The final primary motor cortex output is determined by combined excitatory and intracortical inhibitory circuits, and reducing the latter is associated with enhanced synaptic transmission and efficacy. Indeed, short‐interval intracortical inhibition (SICI) inhibits motor evoked potentials (MEPs), and motor learning has been associated with decreased SICI and increased cortical excitability. Here, we investigated whether cortical excitability and SICI are altered by PAS25 applied after MI‐induced modulation of motor learning.MethodsPeak acceleration of a hand‐grasping movement and MEPs and SICI were measured before and after MI alone, PAS25 alone, and MI followed by PAS25 in 16 healthy participants to evaluate changes in motor learning, corticospinal excitability, and intracortical inhibition.ResultsAfter PAS25 alone, MEP amplitude increased while peak acceleration was unchanged. However, PAS25 applied following MI not only significantly enhanced both peak acceleration (p = 0.011) and MEP amplitude (p = 0.004) but also decreased SICI (p = 0.011). Moreover, we found that this decrease in SICI was significantly correlated with both the peak acceleration (r = 0.49, p = 0.029) and the MEP amplitude (r = 0.56, p = 0.013).ConclusionsThese results indicate that brain function altered by PAS25 of the motor cortex enhances MI‐induced motor learning and corticospinal excitability and decreases SICI, suggesting that SICI underlies, at least in part, PAS25 modulation of motor learning.

Modulation of hand motor skill performance induced by motor practice combined with matched or mismatched hand posture motor imagery

Deficits in voluntary activation of the quadriceps muscle are characteristic of knee osteoarthritis (OA), contributing to the quadriceps weakness that is also a hallmark of the disease. The mechanisms underlying this central activation deficit (CAD) are unknown, although cortical mechanisms may be involved. Here, we utilize transcranial magnetic stimulation (TMS) to assess corticospinal and intracortical excitability in patients with knee OA and in a comparably aged group of healthy older adults, to quantify group differences, and to examine associations between TMS measures and pain, quadriceps strength, and CAD. Seventeen patients with knee OA and 20 healthy controls completed testing. Motor evoked potentials were measured at the quadriceps by superficial electromyographic recordings. Corticospinal excitability was assessed by measuring resting motor threshold (RMT) to TMS stimulation of the quadriceps representation at primary motor cortex, and intracortical excitability was assessed via paired-pulse paradigms for short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF). No statistically significant differences between patients with knee OA and healthy controls were found for RMT, SICI or ICF measures (p > 0.05). For patients with knee OA, there were significant associations observed between pain and RMT, as well as between pain and ICF. No associations were observed between CAD and measures of corticospinal or intracortical excitability. These data suggest against direct involvement of corticospinal or intracortical pathways within primary motor cortex in the mechanisms of CAD. However, pain is implicated in the neural mechanisms of quadriceps motor control in patients with knee OA.

It is not known whether individuals with Parkinson disease (PD) can practice movements mentally. Before this question can be addressed, a reliable imagery assessment tool must be established. The recently developed Kinesthetic and Visual Imagery Questionnaire (KVIQ) is valid for non-disabled individuals and individuals with stroke. We have extended this work by examining the test-retest reliability and concurrent validity of the KVIQ in individuals with PD. Eleven individuals with mild to moderate PD were assessed, while on medication, by the same examiner at 2 sessions (5-12 days apart). Test-retest reliability was measured using intraclass correlation coefficients (ICCs). To examine concurrent validity, KVIQ scores from the second session were compared with a gold standard, the revised Movement Imagery Questionnaire, using Spearman rank order correlation coefficients. There was no significant difference between total KVIQ scores for the test-retest sessions (P > 0.05). Overall, test-retest reliability of the KVIQ was good (ICC = 0.87), and reliability of the subscale of the KVIQ for indexing visual imagery and kinesthetic imagery was also good (ICC = 0.82 and 0.95, respectively). However, the subscale indexing axial visual imagery showed less reliability (ICC = 0.74), suggesting that individuals with PD were not as reliable when imagining axial visual movements as they were for imagining limb movements. Concurrent validity between the second session KVIQ score and the revised Movement Imagery Questionnaire score (gold standard) was excellent (rho = 0.93). Our data support the conclusion that the KVIQ is a reliable and valid test for indexing mental imagery ability in individuals with PD. The KVIQ is easy to administer, and the movements (both real and imagined) required are appropriate for individuals with neuropathology. Our data suggest that the KVIQ is a good choice for clinicians who may wish to index motor imagery ability before implementing imagery as a rehabilitation intervention.

Motor imagery (MI) is similar to overt movement, engaging common neural substrates and facilitating the corticomotor pathway; however, it does not result in excitatory descending motor output. Transcranial magnetic stimulation (TMS) can be used to assess inhibitory networks in the primary motor cortex via measures of 1-ms short-interval intracortical inhibition (SICI), long-interval intracortical inhibition (LICI), and late cortical disinhibition (LCD). These measures are thought to reflect extrasynaptic GABAA tonic inhibition, postsynaptic GABAB inhibition, and presynaptic GABAB disinhibition, respectively. The behavior of 1-ms SICI, LICI, and LCD during MI has not yet been explored. This study aimed to investigate how 1-ms SICI, LICI, and LCD are modulated during MI and voluntary relaxation (VR) of a target muscle. Twenty-five healthy young adults participated. TMS was used to assess nonconditioned motor evoked potential (MEP) amplitude, 1-ms SICI, 100- (LICI100) and 150-ms LICI, and LCD in the right abductor pollicis brevis (APB) and right abductor digiti minimi during rest, MI, and VR of the hand. Compared with rest, MEP amplitudes were facilitated in APB during MI. SICI was not affected by task or muscle. LICI100 decreased in both muscles during VR but not MI, whereas LCD was recruited in both muscles during both tasks. This indicates that VR modulates postsynaptic GABAB inhibition, whereas both tasks modulate presynaptic GABAB inhibition in a non-muscle-specific way. This study highlights further neurophysiological parallels between actual and imagined movement, which may extend to voluntary relaxation.NEW & NOTEWORTHY This is the first study to investigate how 1-ms short-interval intracortical inhibition, long-interval intracortical inhibition, and late cortical disinhibition are modulated during motor imagery and voluntary muscle relaxation. We present novel findings of decreased 100-ms long-interval intracortical inhibition during voluntary muscle relaxation and increased late cortical disinhibition during both motor imagery and voluntary muscle relaxation.

Modulation of lower limb muscle corticospinal excitability during various types of motor imagery

T49. Motor cortical circuit interactions in Parkinson’s disease

Unravelling the Modulation of Intracortical Inhibition During Motor Imagery: An Adaptive Threshold-Hunting Study

Inhibitory neural control of antagonist muscle is one of the fundamental neural mechanism of coordinated human limb movement. Previous studies have revealed that motor execution (ME) and motor imagery (MI) share many common neural substrates; however, whether inhibitory neural activity occurs during MI remains unknown. In addition, recent studies have demonstrated that a combined MI and action observation (MI + AO) produces strong neurophysiological changes compared with MI or AO alone. Therefore, we investigated inhibitory changes in cortical and spinal excitability of the antagonist muscle during MI + AO and ME. Single-pulse transcranial magnetic stimulation (TMS) experiments revealed that corticospinal excitability of the antagonist muscle was decreased during MI + AO. Conversely, F-wave experiments showed that F-wave persistence of the antagonist muscle increased. Paired-pulse TMS experiment also demonstrated that short-interval intracortical inhibition (SICI) did not contribute to this inhibition. Therefore, cortical mediated inhibition, except for SICI, may be related to this inhibition. Conversely, such clear inhibition of the antagonist muscle was not observed during ME, presumably owing to the effects of muscle contraction to decelerate the movements and/or sensory input accompanying the joint movements. These findings provide important insights into the neurophysiological differences between MI + AO and ME.

Unravelling homeostatic interactions in inhibitory and excitatory networks in human motor cortex

Motor imagery (MI) is the mental rehearsal of a motor act without overt movement. Using transcranial magnetic stimulation (TMS), we tested the effect of MI on corticospinal excitability in patients with writer's cramp. In 10 patients with writer's cramp and 10 healthy controls, we applied focal TMS over each primary motor area and recorded motor evoked potentials (MEPs) from contralateral hand and arm muscles while participants imagined a tonic abduction of the index finger contralateral to the stimulated hemisphere. In healthy controls and patients, the MEP amplitude in the relaxed first dorsal interosseus muscle (FDI) showed a muscle-specific increase during MI; however, the increase was less pronounced in patients than in healthy controls. In addition, in patients but not in controls, the MEP amplitude also increased in hand and forearm muscles not involved in the imagined movement. This abnormal spread of facilitation was observed in the affected and unaffected upper limb. MI of simple hand movements is less efficient and less focussed in patients with writer's cramp than it is in normal subjects.

Attentional focus and imagery vividness facilitate corticospinal excitability during contralateral action observation and motor imagery.

There is sparse evidence in the literature that the combination of neuromuscular electrical stimulation (NMES) and motor imagery (MI) can increase corticospinal excitability more that the application of one or the other modality alone. However, the NMES intensity usually employed was below or at motor threshold, not allowing a proper activation of the whole neuromuscular system. This questions the effect of combined MI + NMES with higher intensities, closer to those used in clinical settings. The purpose here was to assess corticospinal excitability during either MI, NMES or a combination of both at different evoked forces. Seventeen healthy participants were enrolled in one session consisting of 6 conditions targeting flexor carpi radialis muscle (FCR): rest, MI, NMES at 5% and 20% of maximal voluntary contraction (MVC) and MI and NMES performed simultaneously (MI + NMES). During each condition, corticospinal excitability was assessed by evoking MEP of FCR by using transcranial magnetic stimulation. Maximal M-wave (Mmax) was measured by using the stimulation of the median nerve. MEPs during MI were greater as compared to rest (P = 0.005). MEPs during MI were significantly lower than during MI + NMES at 5% (P = 0.02) and 20% (P = 0.001). Then, MEPs during NMES 5% was significantly lower than during MI + NMES 20% (P < 0.005). The present study showed that MI + NMES increased corticospinal excitability more than MI alone. However, corticospinal excitability was not higher as the intensity increase during MI + NMES. Therefore, MI + NMES targeting FCR may not significantly increase the corticospinal excitability between different low-submaximal contractions intensities.

Motor imagery (MI) combined with electrical stimulation (ES) enhances upper-limb corticospinal excitability. However, its after-effects on both lower limb corticospinal excitability and spinal reciprocal inhibition remain unknown. We aimed to investigate the effects of MI combined with peripheral nerve ES (MI + ES) on the plasticity of lower limb corticospinal excitability and spinal reciprocal inhibition. Seventeen healthy individuals performed the following three tasks on different days, in a random order: (1) MI alone; (2) ES alone; and (3) MI + ES. The MI task consisted of repetitive right ankle dorsiflexion for 20 min. ES was percutaneously applied to the common peroneal nerve at a frequency of 100 Hz and intensity of 120% of the sensory threshold of the tibialis anterior (TA) muscle. We examined changes in motor-evoked potential (MEP) of the TA (task-related muscle) and soleus muscle (SOL; task-unrelated muscle). We also examined disynaptic reciprocal inhibition before, immediately after, and 10, 20, and 30 min after the task. MI + ES significantly increased TA MEPs immediately and 10 min after the task compared with baseline, but did not change the task-unrelated muscle (SOL) MEPs. MI + ES resulted in a significant increase in the magnitude of reciprocal inhibition immediately and 10 min after the task compared with baseline. MI and ES alone did not affect TA MEPs or reciprocal inhibition. MI combined with ES is effective in inducing plastic changes in lower limb corticospinal excitability and reciprocal Ia inhibition.