Periodic Reporting for period 1 - MOTOR SIMULATION (Motor simulation: Evaluating the role of mirror neurons in humans through ECOG and Lesion Studies)
Reporting period: 2015-07-01 to 2017-06-30
"My research focuses on different aspects of social cognitive neuroscience – from the behavioral level, to the hormonal and brain levels, in healthy individuals as well as in those with brain damage. Since I come from a cognitive neuroscience background, I am interested in the interactions between the social and cognitive aspects of our mind and brain.
One of the most intriguing, yet still controversial discoveries in the neuroscience field in the past two decades, is the discovery of the mirror neuron system (MNS). The essence of the mirror mechanism is thought to be the following: each time an individual observes another individual performing an action, a set of neurons that encode that action is activated in the observer’s cortical motor system. The result of this mechanism is thought to be the capacity to recognize that an individual is performing an action, to differentiate this action from others analogous to it, and to use this information in order to act appropriately. While many studies indirectly measured mirror neuron activity in humans using fMRI and MEG/EEG (as I did in my PhD) – two important methods of studying the human MNS and its significance were scarcely used, and can give us valuable information about this system:
(a) Intracranial recordings, or electrocorticography (ECoG) of human brain signals. For purely clinical reasons, patients with epilepsy are sometimes implanted with such electrodes to localize their seizure onset prior to surgical therapy. This gives us the chance to study brain processes with unmatched temporal and spatial resolution in combination with wide brain coverage. I’ve recently published a paper describing what we've learned from our ECoG study which was focused on different aspects of the mirroring mechanism: We found regions with ""mirror"" properties in parietal, inferior frontal and sensorimotor cortices. We revealed that the parietal regions were active before the rest, and probably decode arm movements or the initiation of the movement, rather than the exact grasp. Lastly, we showed that within the different mirror regions, there are both ""pure mirroring"" sites, active both for viewing and for imitating, but not in between, and, what we called ""mnemonic mirroring"" sites, which were also active in between viewing and imitating, perhaps taking part in rehearsal of the action to be imitated
(b) Lesion patients: If indeed this brain network is important for action recognition, damage to regions in this network should be followed, at least in part, by deficits in action recognition. For the last 3 years, I studied a group of brain injury patients (following stroke, tumor resection or traumatic brain injury) with lesions to different regions associated with the mirror neuron network. This work was done in collaboration with Oslo University. This collaboration enabled us to recruit 17 patients with lesions to the lateral prefrontal cortex and 18 matched controls. We showed that lateral prefrontal cortex damage results in deficits in recognizing emotions, as seen both by longer reaction times and reduced accuracy. Accuracy in these tasks also correlated with EEG mu suppression, thought to be a correlate of the human mirror neuron system. This research was also published this year.
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One of the most intriguing, yet still controversial discoveries in the neuroscience field in the past two decades, is the discovery of the mirror neuron system (MNS). The essence of the mirror mechanism is thought to be the following: each time an individual observes another individual performing an action, a set of neurons that encode that action is activated in the observer’s cortical motor system. The result of this mechanism is thought to be the capacity to recognize that an individual is performing an action, to differentiate this action from others analogous to it, and to use this information in order to act appropriately. While many studies indirectly measured mirror neuron activity in humans using fMRI and MEG/EEG (as I did in my PhD) – two important methods of studying the human MNS and its significance were scarcely used, and can give us valuable information about this system:
(a) Intracranial recordings, or electrocorticography (ECoG) of human brain signals. For purely clinical reasons, patients with epilepsy are sometimes implanted with such electrodes to localize their seizure onset prior to surgical therapy. This gives us the chance to study brain processes with unmatched temporal and spatial resolution in combination with wide brain coverage. I’ve recently published a paper describing what we've learned from our ECoG study which was focused on different aspects of the mirroring mechanism: We found regions with ""mirror"" properties in parietal, inferior frontal and sensorimotor cortices. We revealed that the parietal regions were active before the rest, and probably decode arm movements or the initiation of the movement, rather than the exact grasp. Lastly, we showed that within the different mirror regions, there are both ""pure mirroring"" sites, active both for viewing and for imitating, but not in between, and, what we called ""mnemonic mirroring"" sites, which were also active in between viewing and imitating, perhaps taking part in rehearsal of the action to be imitated
(b) Lesion patients: If indeed this brain network is important for action recognition, damage to regions in this network should be followed, at least in part, by deficits in action recognition. For the last 3 years, I studied a group of brain injury patients (following stroke, tumor resection or traumatic brain injury) with lesions to different regions associated with the mirror neuron network. This work was done in collaboration with Oslo University. This collaboration enabled us to recruit 17 patients with lesions to the lateral prefrontal cortex and 18 matched controls. We showed that lateral prefrontal cortex damage results in deficits in recognizing emotions, as seen both by longer reaction times and reduced accuracy. Accuracy in these tasks also correlated with EEG mu suppression, thought to be a correlate of the human mirror neuron system. This research was also published this year.
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Using different research methodology and analytic tools, I spent the last 2 years studying the brain mechanisms enabling us to understand others. As detailed in my proposal, I have used two different approaches:
(a) Intracranial recordings, or electrocorticography (ECoG): I investigated the spatial and temporal dynamics of mirror neurons during imitation, and differentiated for the first time between two kinds of ‘mirroring’ populations (pure mirroring, versus mnemonic / rehearsing neurons). This work was recently published in Cerebral Cortex (2017);
(b) Lesion studies: If simulation via a mirror neuron network is necessary for understanding others, patients with lesions to core regions in this network should show deficits in understanding others’ actions, intentions or emotions. For the last two years of the project I studied neurological patients with focal lesions centered in lateral prefrontal (LPFC) regions as they performed 5 different tasks that measure one’s understanding of others. Results showed a behavioral deficit in LPFC lesioned patients in tasks requiring inferring others emotions, but not intentions. This deficit correlated with a reduction in EEG mu suppression, a proposed EEF marker for mirror neuron activity. This work was also published this year (Brain, 2017).
(a) Intracranial recordings, or electrocorticography (ECoG): I investigated the spatial and temporal dynamics of mirror neurons during imitation, and differentiated for the first time between two kinds of ‘mirroring’ populations (pure mirroring, versus mnemonic / rehearsing neurons). This work was recently published in Cerebral Cortex (2017);
(b) Lesion studies: If simulation via a mirror neuron network is necessary for understanding others, patients with lesions to core regions in this network should show deficits in understanding others’ actions, intentions or emotions. For the last two years of the project I studied neurological patients with focal lesions centered in lateral prefrontal (LPFC) regions as they performed 5 different tasks that measure one’s understanding of others. Results showed a behavioral deficit in LPFC lesioned patients in tasks requiring inferring others emotions, but not intentions. This deficit correlated with a reduction in EEG mu suppression, a proposed EEF marker for mirror neuron activity. This work was also published this year (Brain, 2017).
This work has broad clinical implications, and will affect the way researchers think of interventions for patients with social deficits (e.g. autism, social anxiety, schizophrenia).
Moreover, people are increasingly faced with situations in which they must understand outgroup members from different backgrounds and cultures. This is due to both to globalization and to demographic changes, as most western countries have large minorities and diverse, constantly changing populations. A better understanding of how we recognize the affective states of others, what drives accurate understanding, and the neural mechanisms underlying these social processes could lead to creating better interventions for understanding others, for accepting others in the community and allow for improved adjustments to social change.
Moreover, people are increasingly faced with situations in which they must understand outgroup members from different backgrounds and cultures. This is due to both to globalization and to demographic changes, as most western countries have large minorities and diverse, constantly changing populations. A better understanding of how we recognize the affective states of others, what drives accurate understanding, and the neural mechanisms underlying these social processes could lead to creating better interventions for understanding others, for accepting others in the community and allow for improved adjustments to social change.