|
|
Frenkel-Toledo, S., Liebermann, D. G., Bentin, S., & Soroker, N. (2016). Dysfunction of the Human Mirror Neuron System in Ideomotor Apraxia: Evidence from Mu Suppression. J Cogn Neurosci, .
Abstract: Stroke patients with ideomotor apraxia (IMA) have difficulties controlling voluntary motor actions, as clearly seen when asked to imitate simple gestures performed by the examiner. Despite extensive research, the neurophysiological mechanisms underlying failure to imitate gestures in IMA remain controversial. The aim of the current study was to explore the relationship between imitation failure in IMA and mirror neuron system (MNS) functioning. Mirror neurons were found to play a crucial role in movement imitation and in imitation-based motor learning. Their recruitment during movement observation and execution is signaled in EEG recording by suppression of the lower (8-10 Hz) mu range. We examined the modulation of EEG in this range in stroke patients with left (n = 21) and right (n = 15) hemisphere damage during observation of video clips showing different manual movements. IMA severity was assessed by the DeRenzi's standardized diagnostic test. Results showed that failure to imitate observed manual movements correlated with diminished mu suppression in patients with damage to the right inferior parietal lobule and in patients with damage to the right inferior frontal gyrus pars opercularis-areas where major components of the human MNS are assumed to reside. Voxel-based lesion symptom mapping revealed a significant impact on imitation capacity for the left inferior and superior parietal lobules and the left post central gyrus. Both left and right hemisphere damages were associated with imitation failure typical of IMA, yet a clear demonstration of relationship to the MNS was obtained only in the right hemisphere damage group. Suppression of the 8-10 Hz range was stronger in central compared with occipital sites, pointing to a dominant implication of mu rather than alpha rhythms. However, the suppression correlated with De Renzi's apraxia test scores not only in central but also in occipital sites, suggesting a multifactorial mechanism for IMA, with a possible impact for deranged visual attention (alpha suppression) beyond the effect of MNS damage (mu suppression).
|
|
|
|
Frenkel-Toledoa, S., Bentin, S., Perry, A., Liebermann, D. G., & Soroker, N. (2014). Mirror-neuron system recruitment by action observation: Effects of focal brain damage on mu suppression. NeuroImage, 87, 127–137.
Abstract: Mu suppression is the attenuation of EEG power in the alpha frequency range (8-12 Hz), recorded over the sensorimotor cortex during execution and observation of motor actions. Based on this dual characteristic it is thought to signalize activation of a human analogue of the mirror neuron system (MNS) found in macaque monkeys, though much uncertainty remains concerning its specificity and full significance. To further explore the hypothesized relationship between mu suppression and MNS activation, we investigated how it is affected by damage to cortical regions, including areas where the MNS is thought to reside. EEG was recorded in 33 first-event stroke patients during observation of video-clips showing reaching and grasping hand movements. We examined the modulation of EEG oscillations at central and occipital sites, and analyzed separately the lower (8-10 Hz) and higher (10-12 Hz) segments of the alpha/mu range. Suppression was determined relative to observation of a non-biological movement. Normalized lesion data were used to investigate how damage to regions of the fronto-parietal cortex affects the pattern of suppression. The magnitude of mu suppression during action observation was significantly reduced in the affected hemisphere compared to the unaffected hemisphere. Differences between the hemispheres were significant at central (sensorimotor) sites but not at occipital (visual) sites. Total hemispheric volume loss did not correlate with mu suppression. Suppression in the lower mu range in the unaffected hemisphere (C3) correlated with lesion extent within the right inferior parietal cortex. Our lesion study supports the role of mu suppression as a marker of MNS activation, as suggested by findings gathered in previous studies in normal subjects.
|
|
|
|
Goodman, D., & Liebermann, D. G. (1992). Time-to-contact as a determiner of action: vision and motor control. In D. Elliott, & J. Proteau (Eds.), Vision and Motor Control (pp. 335–349). Amsterdam, Holland: Elsevier Pub. Co.
|
|
|
|
Grinberg, A., Strong, A., Strandberg, J., Selling, J., Liebermann, D. G., Bjorklund, M., et al. (2024). Electrocortical activity associated with movement-related fear: a methodological exploration of a threat-conditioning paradigm involving destabilising perturbations during quiet standing. Exp Brain Res, .
Abstract: Musculoskeletal trauma often leads to lasting psychological impacts stemming from concerns of future injuries. Often referred to as kinesiophobia or re-injury anxiety, such concerns have been shown to hinder return to physical activity and are believed to increase the risk for secondary injuries. Screening for re-injury anxiety is currently restricted to subjective questionnaires, which are prone to self-report bias. We introduce a novel approach to objectively identify electrocortical activity associated with the threat of destabilising perturbations. We aimed to explore its feasibility among non-injured persons, with potential future implementation for screening of re-injury anxiety. Twenty-three participants stood blindfolded on a translational balance perturbation platform. Consecutive auditory stimuli were provided as low (neutral stimulus [CS(-)]) or high (conditioned stimulus [CS(+)]) tones. For the main experimental protocol (Protocol I), half of the high tones were followed by a perturbation in one of eight unpredictable directions. A separate validation protocol (Protocol II) requiring voluntary squatting without perturbations was performed with 12 participants. Event-related potentials (ERP) were computed from electroencephalography recordings and significant time-domain components were detected using an interval-wise testing procedure. High-amplitude early contingent negative variation (CNV) waves were significantly greater for CS(+) compared with CS(-) trials in all channels for Protocol I (> 521-800ms), most prominently over frontal and central midline locations (P </= 0.001). For Protocol II, shorter frontal ERP components were observed (541-609ms). Our test paradigm revealed electrocortical activation possibly associated with movement-related fear. Exploring the discriminative validity of the paradigm among individuals with and without self-reported re-injury anxiety is warranted.
|
|
|
|
Grip, H., Tengman, E., Liebermann, D. G., & Hager, C. K. (2019). Kinematic analyses including finite helical axes of drop jump landings demonstrate decreased knee control long after anterior cruciate ligament injury. PLoS One, 14(10), e0224261.
Abstract: The purpose was to evaluate the dynamic knee control during a drop jump test following injury of the anterior cruciate ligament injury (ACL) using finite helical axes. Persons injured 17-28 years ago, treated with either physiotherapy (ACLPT, n = 23) or reconstruction and physiotherapy (ACLR, n = 28) and asymptomatic controls (CTRL, n = 22) performed a drop jump test, while kinematics were registered by motion capture. We analysed the Preparation phase (from maximal knee extension during flight until 50 ms post-touchdown) followed by an Action phase (until maximal knee flexion post-touchdown). Range of knee motion (RoM), and the length of each phase (Duration) were computed. The finite knee helical axis was analysed for momentary intervals of ~15 degrees of knee motion by its intersection (DeltaAP position) and inclination (DeltaAP Inclination) with the knee's Anterior-Posterior (AP) axis. Static knee laxity (KT100) and self-reported knee function (Lysholm score) were also assessed. The results showed that both phases were shorter for the ACL groups compared to controls (CTRL-ACLR: Duration 35+/-8 ms, p = 0.000, CTRL-ACLPT: 33+/-9 ms, p = 0.000) and involved less knee flexion (CTRL-ACLR: RoM 6.6+/-1.9 degrees , p = 0.002, CTRL-ACLR: 7.5 +/-2.0 degrees , p = 0.001). Low RoM and Duration correlated significantly with worse knee function according to Lysholm and higher knee laxity according to KT-1000. Three finite helical axes were analysed. The DeltaAP position for the first axis was most anterior in ACLPT compared to ACLR (DeltaAP position -1, ACLPT-ACLR: 13+/-3 mm, p = 0.004), with correlations to KT-1000 (rho 0.316, p = 0.008), while the DeltaAP inclination for the third axis was smaller in the ACLPT group compared to controls (DeltaAP inclination -3 ACLPT-CTRL: -13+/-5 degrees , p = 0.004) and showed a significant side difference in ACL injured groups during Action (Injured-Non-injured: 8+/-2.7 degrees , p = 0.006). Small DeltaAP inclination -3 correlated with low Lysholm (rho 0.391, p = 0.002) and high KT-1000 (rho -0.450, p = 0.001). Conclusions Compensatory movement strategies seem to be used to protect the injured knee during landing. A decreased DeltaAP inclination in injured knees during Action suggests that the dynamic knee control may remain compromised even long after injury.
|
|
