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).

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.