- Email: [email protected]
Mirror neuron system based therapy for emotional disorders
Medical Hypotheses (2008) 71, 722–726
www.elsevier.com/locate/mehy
Mirror neuron system based therapy for emotional disorders Ti-Fei Yuan
a,*
, Robert Hoff
b,*
a
Department of Anatomy, Li Kai Shing Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Hong Kong b Department of Psychology, Mercyhurst College, 501 East 38th Street, Erie, PA 16546, USA Received 30 June 2008; accepted 2 July 2008
Summary Mirror neuron system (MNS) represents one of the most important discoveries in the area of neuropsychology of past decades. More than 500 papers have been published in this area (PubMed), and the major functions of MNS include action understanding, imitation, empathy, all of which are critical for an individual to be social. Recent studies suggested that MNS can modulate emotion states possibly through the empathy mechanism. Here we propose that MNS-based therapies provide a non-invasive approach in treatments to emotional disorders that were observed in autism patients, post-stroke patients with depression as well as other mood dysregulation conditions. c 2008 Elsevier Ltd. All rights reserved.
The mirror neuron system (MNS) has been regarded as one of the most important discoveries in cognitive neuroscience in recent years. The unique property of mirror neurons is that they discharge both during action execution and during observation of specific actions [1]. This property allows humans to understand the intentions of others through observation of their actions, and thereby plays a role in imitation-based learning and empathy.
Abbreviations: MNS, mirror neuron system; ASD, autism spectrum disorders; IFC, inferior frontal cortex; IPL, the inferior parietal lobule; STS, superior temporal sulcus; EEG, electroencephalography. * Corresponding authors. Tel.: +852 67362793 (T.-F. Yuan), +1 814 824 2380 (R. Hoff). E-mail addresses: [email protected] (T.-F. Yuan), rhoff@ mercyhurst.edu (R. Hoff).
Importantly, it has been found that the adult MNS is still plastic [2,3] and that artificially induced MNS activation could provide a basis for brain rehabilitation in patients with post-stroke motor defects [4]. In this manuscript, we discuss the possibility and some pioneer practices of MNS activation as a treatment modality for emotional disorders.
MNS dysfunction as a risk factor for autism and deficits in understanding emotion It has been suggested that developmental MNS dysfunction leads to disordered social cognition in humans, including autism spectrum disorders (ASD)
0306-9877/$ - see front matter c 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2008.07.004
Mirror neuron system based therapy for emotional disorders [5–7]. These disorders in theory are characterized by limitations of mind, imitation, and social communication, summarized by the phrase ‘‘seeing is not understanding’’ [8]. A number of studies, including EEG [9–11] and brain imaging studies [12,13] have suggested the presence of MNS dysfunction in ASD patients. For example, brain imaging studies showed significant thinning of areas that belong to the MNS, such as inferior frontal cortex (IFC), the inferior parietal lobule (IPL), superior temporal sulcus (STS) as well as other areas that constitute the distributed neural circuitry for social cognition [13], in individuals with ASD. Additionally, it appears that the MNS undergoes abnormal activation during visual information processing [12,14]. Collectively these findings suggest that MNS dysfunction might be an important neurobiological risk factor for autism spectrum disorders. Given the important contribution of face processing to emotion, it is likely that dysfunction of the MNS plays a role in the defective capacity of ASD patients to understand emotion [6,15–18]. With fMRI, it has been shown that there are reliable differences between normally developing children and children with ASD in the network comprising the frontal component of the MNS (namely, pars opercularis), the insula, and the amygdala, all of which enable emotion understanding via action representation [19,20]. Collectively, these data suggest that altered neural circuit activation in ASD patients includes emotion-processing brain areas. ASD patients was found to be correlated with mood disorders, both in children and adults [21–25], and the two diseases may share common genetic vulnerability, such as serotonin transporter genes that are one of the well-recognized family participating in anxiety and depression [26,27]. Consistently, patients with mood disorders show higher tendency to develop autism symptoms [28,29]. Thus the autism, possibly due to the mirror neuron dysfunction, can result in complex psychiatric conditions that include mood disorders. Can autism treatments elevate mood states simultaneously? Antidepressants have been used in combined therapies to some autism patients [23,30,31], with proved efficiency. It is possible that the antidepressants can rescue the normal neurotransmission in brain areas that correlated to mirror neuron system, as well as their global neurotrophic effects. Psychologically, the important contributions of mirror neuron defects in autism patients to mood disorder symptoms permit improved integration ability, and restore the social network function [5,32,33]. The noninvasive manipulation of MNS activity may provide a novel approach to improving emotion modulation in ASD
723
patients, and could possibly lead to overall clinical improvement in such patients.
Post-trauma emotional disorder: interpretation through the MNS Focal brain trauma, such as stroke, can result in post-trauma emotional disorders [34–36]. These emotional disorders can be separated into several groups: dysfunction in emotion comprehension/ understanding; dysfunction of those neurocognitive systems responsible for the experience of emotion; and dysfunction of emotion control and expression, which may be attributed to disrupted integration [37]. Given the putative role of MNS in emotion understanding, the impairment to MNS following stroke can lead to the first group of emotional disorders – the instrumental function of the MNS in the comprehension of emotion. Brain imaging studies on imitation of facial emotional expressions suggest a critical role for the motor system in emotional behavior [37]. Those mood disorder conditions represent more specific complications of stroke than simply psychological responses to the motor disability [38]. Mirror neuron thus may mediate this lost link. Some studies have shown co-activation of mirror-system and limbic circuits through insula [19], and the focal stroke that interrupts the mirror neuron system may cause loss of modulatory amygdala affect and, finally, catastrophic reactions [35,39]. Additional complications include athymhormia, reflecting flat affect and a loss of motivation in the execution of motor actions [35]. Moreover, some other brain areas of motor significance, if damaged, can lead to emotional disorders [40–42]. Currently, the neuropsychiatric diseases resulted from motor cortex ischemia, such as poststroke depression [43,44], could be treated with antidepressants and other general mood disorder therapies [45–47]. Here, the important role of MNS in post-brain trauma emotional disorders suggests a potential new avenue for treating stroke patients.
The MNS-based therapy: multi-functional and multi-modal Mirror neurons fire to both observed and performed actions, hence there exists a possibility for observed-learning based brain activation or even rehabilitation [48–50]. Mounting evidence indicates that many forms of experience, including
724 physical exercise, sensory perception, and even direct brain stimulation or drug administration, may alter existing synaptic connectivity or induce synaptogenesis. The physiological bases of experience-dependent plasticity have been only partly elucidated, but may include upregulated endogenous neurogenesis [51–53], changed neurochemical transmission [54], induced expression of neurotrophins and neuropeptides [55] or improved body immune responses. Though we currently lack a clear understanding of the underlying mechanism for brain activity-related plasticity, activation of MNS has already been successfully used for poststroke treatment and rehabilitation [4,56]. Considering the neurobiological role of MNS in emotional disorders inherent to both autism and post-stroke conditions, we believe that targeted MNS activation could be used to prevent and/or improve the experience of emotional disorders in such patients. First, the action-specific responses of mirror neurons provide a precise approach to activate related brain areas. Using computerized displays or virtual reality environments [57,58], it may be possible to design different scenes/actions in order to specifically modulate various brain regions. Observation therapy may therefore be useful in the prevention of emotional disorders with motor deficiency. Second, some mirror neurons may respond to sounds that are specific for actions– these have been termed ‘‘audio-visual’’ mirror neurons [59–61]. This suggests that combined therapies including both visual and auditory stimulations would maximize clinical efficacy. Furthermore, virtual reality may create such an environment. Recent neuroimaging studies indicate that music, like language, involves an intimate coupling between the perception and production of hierarchically organized sequential information, which links meaning to emotion via the mirror neuron system [62]. We believe that music could be a potent component in MNS-based therapies, as recent findings in the domain of stroke rehabilitation have shown [63]. Behavioral and psychiatric disturbances are frequent sequelae to traumatic brain injury and major limitations on patient quality of life [64]. Pharmaceutical approaches that improve depression and other negative mood states have been the usual, if limited, therapeutic modality. Alternatively, MNS-based therapy provides the promise of a novel and non-invasive approach to improving the physiological and psychological condition of brain-injured patients. It is hoped that in the future MNStargeted treatments can breathe fresh hopes for emotional disorders in autism children as well as post-brain trauma patients.
Yuan and Hoff
References [1] Rizzolatti G, Craighero L. The mirror-neuron system. Annu Rev Neurosci 2004;27:169–92. [2] Gillmeister H, Catmur C, Liepelt R, Brass M, Heyes C. Experience-based priming of body parts: a study of action imitation. Brain Res 2008. [3] Catmur C, Walsh V, Heyes C. Sensorimotor learning configures the human mirror system. Curr Biol 2007;17:1527–31. [4] Ertelt D, Small S, Solodkin A, Dettmers C, McNamara A, Binkofski F, et al. Action observation has a positive impact on rehabilitation of motor deficits after stroke. Neuroimage 2007;36(Suppl. 2):T164–73. [5] Williams JH, Waiter GD, Gilchrist A, Perrett DI, Murray AD, Whiten A. Neural mechanisms of imitation and ‘mirror neuron’ functioning in autistic spectrum disorder. Neuropsychologia 2006;44:610–21. [6] Williams JH, Massaro DW, Peel NJ, Bosseler A, Suddendorf T. Visual-auditory integration during speech imitation in autism. Res Dev Disabil 2004;25:559–75. [7] Williams JH, Whiten A, Suddendorf T, Perrett DI. Imitation mirror neurons and autism. Neurosci Biobehav Rev 2001;25: 287–95. [8] Fecteau S, Lepage JF, Theoret H. Autism spectrum disorder: seeing is not understanding. Curr Biol 2006;16: R131–3. [9] Oberman LM, Ramachandran VS, Pineda JA. Modulation of mu suppression in children with autism spectrum disorders in response to familiar or unfamiliar stimuli: the mirror neuron hypothesis. Neuropsychologia 2008;46:1558–65. [10] Oberman LM, Ramachandran VS. The simulating social mind: the role of the mirror neuron system and simulation in the social and communicative deficits of autism spectrum disorders. Psychol Bull 2007;133:310–27. [11] Oberman LM, Hubbard EM, McCleery JP, Altschuler EL, Ramachandran VS, Pineda JA. EEG evidence for mirror neuron dysfunction in autism spectrum disorders. Brain Res Cogn Brain Res 2005;24:190–8. [12] Hadjikhani N, Joseph RM, Snyder J, Tager-Flusberg H. Abnormal activation of the social brain during face perception in autism. Hum Brain Mapp 2007;28:441–9. [13] Hadjikhani N, Joseph RM, Snyder J, Tager-Flusberg H. Anatomical differences in the mirror neuron system and social cognition network in autism. Cereb Cortex 2006;16:1276–82. [14] Spezio ML, Adolphs R, Hurley RS, Piven J. Abnormal use of facial information in high-functioning autism. J Autism Dev Disord 2007;37:929–39. [15] Golarai G, Grill-Spector K, Reiss AL. Autism and the development of face processing. Clin Neurosci Res 2006;6:145–60. [16] Sasson NJ. The development of face processing in autism. J Autism Dev Disord 2006;36:381–94. [17] Dawson G, Webb SJ, Wijsman E, Schellenberg G, Estes A, Munson J, et al. Neurocognitive and electrophysiological evidence of altered face processing in parents of children with autism: implications for a model of abnormal development of social brain circuitry in autism. Dev Psychopathol 2005;17:679–97. [18] Moody EJ, McIntosh DN, Mann LJ, Weisser KR. More than mere mimicry? The influence of emotion on rapid facial reactions to faces. Emotion 2007;7:447–57. [19] Carr L, Iacoboni M, Dubeau MC, Mazziotta JC, Lenzi GL. Neural mechanisms of empathy in humans: a relay from neural systems for imitation to limbic areas. Proc Natl Acad Sci USA 2003;100:5497–502.
Mirror neuron system based therapy for emotional disorders [20] Dapretto M, Davies MS, Pfeifer JH, Scott AA, Sigman M, Bookheimer SY, et al. Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders. Nat Neurosci 2006;9:28–30. [21] Hemmings CP, Gravestock S, Pickard M, Bouras N. Psychiatric symptoms and problem behaviours in people with intellectual disabilities. J Intellect Disabil Res 2006;50: 269–76. [22] Begeer S, Meerum Terwogt M, Rieffe C, Stegge H, Koot HM. Do children with autism acknowledge the influence of mood on behaviour? Autism 2007;11:503–21. [23] Mandell DS, Morales KH, Marcus SC, Stahmer AC, Doshi J, Polsky DE. Psychotropic medication use among medicaidenrolled children with autism spectrum disorders. Pediatrics 2008;121:e441–8. [24] Scambler DJ, Hepburn S, Rutherford MD, Wehner EA, Rogers SJ, et al. Emotional responsivity in children with autism, children with other developmental disabilities, and children with typical development. J Autism Dev Disord 2007;37:553–63. [25] Lecavalier L. Behavioral and emotional problems in young people with pervasive developmental disorders: relative prevalence, effects of subject characteristics and empirical classification. J Autism Dev Disord 2006;36:1101–14. [26] Munesue T, Ono Y, Mutoh K, Shimoda K, Nakatani H, Kikuchi M. High prevalence of bipolar disorder comorbidity in adolescents and young adults with high-functioning autism spectrum disorder: a preliminary study of 44 outpatients. J Affect Disord 2008. [27] Muhle R, Trentacoste SV, Rapin I. The genetics of autism. Pediatrics 2004;113:e472–86. [28] Pine DS, Guyer AE, Goldwin M, Towbin KA, Leibenluft E. Autism spectrum disorder scale scores in pediatric mood and anxiety disorders. J Am Acad Child Adolesc Psychiatry 2008;47:652–61. [29] Towbin KE, Pradella A, Gorrindo T, Pine DS, Leibenluft E. Autism spectrum traits in children with mood and anxiety disorders. J Child Adolesc Psychopharmacol 2005;15: 452–64. [30] Unwin GL, Deb S. Use of medication for the management of behavior problems among adults with intellectual disabilities: a clinicians’ consensus survey. Am J Ment Retard 2008;113:19–31. [31] Pollard AJ, Prendergast M. Depressive pseudodementia in a child with autism. Dev Med Child Neurol 2004;46:485–9. [32] Aitken KJ. Intersubjectivity, affective neuroscience and the neurobiology of autistic spectrum disorders: a systematic review. Keio J Med 2008;57:15–36. [33] Harris JC. Social neuroscience, empathy, brain integration and neurodevelopmental disorders. Physiol Behav 2003;79: 525–31. [34] Chan KL, Campayo A, Moser DJ, Arndt S, Robinson RG. Aggressive behavior in patients with stroke: association with psychopathology and results of antidepressant treatment on aggression. Arch Phys Med Rehabil 2006;87:793–8. [35] Carota A, Staub F, Bogousslavsky J. Emotions, behaviours and mood changes in stroke. Curr Opin Neurol 2002;15: 57–69. [36] Clark PC, Dunbar SB, Aycock DM, Courtney E, Wolf SL. Caregiver perspectives of memory and behavior changes in stroke survivors. Rehabil Nurs 2006;31:26–32. [37] Bodini B, Iacoboni M, Lenzi GL. Acute stroke effects on emotions: an interpretation through the mirror system. Curr Opin Neurol 2004;17:55–60. [38] Folstein MF, Maiberger R, McHugh PR. Mood disorder as a specific complication of stroke. J Neurol Neurosurg Psychiatry 1977;40:1018–20.
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[39] Carota A, Rossetti AO, Karapanayiotides T, Bogousslavsky J. Catastrophic reaction in acute stroke: a reflex behavior in aphasic patients. Neurology 2001;57:1902–5. [40] Choi-Kwon S, Kim JS. Poststroke emotional incontinence and decreased sexual activity. Cerebrovasc Dis 2002;13: 31–7. [41] Kim JS, Choi S, Kwon SU, Seo YS. Inability to control anger or aggression after stroke. Neurology 2002;58:1106–8. [42] Kim JS, Choi-Kwon S. Poststroke depression and emotional incontinence: correlation with lesion location. Neurology 2000;54:1805–10. [43] Krishnan KR. Depression as a contributing factor in cerebrovascular disease. Am Heart J 2000;140:70–6. [44] Caeiro L, Ferro JM, Santos CO, Figueira ML. Depression in acute stroke. J Psychiatry Neurosci 2006;31:377–83. [45] Beckson M, Cummings JL. Neuropsychiatric aspects of stroke. Int J Psychiatry Med 1991;21:1–15. [46] Starkstein SE, Lischinsky A. The phenomenology of depression after brain injury. NeuroRehabilitation 2002;17: 105–13. [47] Chemerinski E, Levine SR. Neuropsychiatric disorders following vascular brain injury. Mt Sinai J Med 2006;73: 1006–14. [48] Buccino G, Solodkin A, Small SL. Functions of the mirror neuron system: implications for neurorehabilitation. Cogn Behav Neurol 2006;19:55–63. [49] Iacoboni M, Mazziotta JC. Mirror neuron system: basic findings and clinical applications. Ann Neurol 2007;62: 213–8. [50] Rossi EL, Rossi KL. The neuroscience of observing consciousness & mirror neurons in therapeutic hypnosis. Am J Clin Hypn 2006;48:263–78. [51] Kempermann G, van Praag H, Gage FH. Activity-dependent regulation of neuronal plasticity and self repair. Prog Brain Res 2000;127:35–48. [52] van Praag H. Neurogenesis and exercise: past and future directions. Neuromolecular Med 2008. [53] Fabel K, Kempermann G. Physical activity and the regulation of neurogenesis in the adult and aging brain. Neuromolecular Med 2008. [54] Meeusen R. Exercise and the brain: insight in new therapeutic modalities. Ann Transplant 2005;10:49–51. [55] Thakker-Varia S, Krol JJ, Nettleton J, Bilimoria PM, Bangasser DA, Shors TJ, et al. The neuropeptide VGF produces antidepressant-like behavioral effects and enhances proliferation in the hippocampus. J Neurosci 2007;27:12156–67. [56] Altschuler EL. Play with online virtual pets as a method to improve mirror neuron and real world functioning in autistic children. Med Hypotheses 2008;70:748–9. [57] August K, Lewis JA, Chandar G, Merians A, Biswal B, Adamovich S. FMRI analysis of neural mechanisms underlying rehabilitation in virtual reality: activating secondary motor areas. Conf Proc IEEE Eng Med Biol Soc 2006;1: 3692–5. [58] Merians AS, Poizner H, Boian R, Burdea G, Adamovich S. Sensorimotor training in a virtual reality environment: does it improve functional recovery poststroke? Neurorehabil Neural Repair 2006;20:252–67. [59] Bonaiuto J, Rosta E, Arbib M. Extending the mirror neuron system model. I. Audible actions and invisible grasps. Biol Cybern 2007;96:9–38. [60] Eng K, Siekierka E, Pyk P, Chevrier E, Hauser Y, Cameirao M, et al. Interactive visuo-motor therapy system for stroke rehabilitation. Med Biol Eng Comput 2007;45:901–7. [61] Kohler E, Keysers C, Umilta MA, Fogassi L, Gallese V, Rizzolatti G, et al. Hearing sounds, understanding actions:
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action representation in mirror neurons. Science 2002;297: 846–8. [62] Gridley MC, Hoff R. Do mirror neurons explain misattribution of emotions in music? Percept Mot Skills 2006;102:600–2. [63] Sarkamo T, Tervaniemi M, Laitinen S, Forsblom A, Soinila S, Mikkonen M, et al. Music listening enhances cognitive
recovery and mood after middle cerebral artery stroke. Brain 2008;131:866–76. [64] Jorge RE. Neuropsychiatric consequences of traumatic brain injury: a review of recent findings. Curr Opin Psychiatry 2005;18:289–99.
Available online at www.sciencedirect.com
www.elsevier.com/locate/mehy
Mirror neuron system based therapy for emotional disorders Ti-Fei Yuan
a,*
, Robert Hoff
b,*
a
Department of Anatomy, Li Kai Shing Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Hong Kong b Department of Psychology, Mercyhurst College, 501 East 38th Street, Erie, PA 16546, USA Received 30 June 2008; accepted 2 July 2008
Summary Mirror neuron system (MNS) represents one of the most important discoveries in the area of neuropsychology of past decades. More than 500 papers have been published in this area (PubMed), and the major functions of MNS include action understanding, imitation, empathy, all of which are critical for an individual to be social. Recent studies suggested that MNS can modulate emotion states possibly through the empathy mechanism. Here we propose that MNS-based therapies provide a non-invasive approach in treatments to emotional disorders that were observed in autism patients, post-stroke patients with depression as well as other mood dysregulation conditions. c 2008 Elsevier Ltd. All rights reserved.
The mirror neuron system (MNS) has been regarded as one of the most important discoveries in cognitive neuroscience in recent years. The unique property of mirror neurons is that they discharge both during action execution and during observation of specific actions [1]. This property allows humans to understand the intentions of others through observation of their actions, and thereby plays a role in imitation-based learning and empathy.
Abbreviations: MNS, mirror neuron system; ASD, autism spectrum disorders; IFC, inferior frontal cortex; IPL, the inferior parietal lobule; STS, superior temporal sulcus; EEG, electroencephalography. * Corresponding authors. Tel.: +852 67362793 (T.-F. Yuan), +1 814 824 2380 (R. Hoff). E-mail addresses: [email protected] (T.-F. Yuan), rhoff@ mercyhurst.edu (R. Hoff).
Importantly, it has been found that the adult MNS is still plastic [2,3] and that artificially induced MNS activation could provide a basis for brain rehabilitation in patients with post-stroke motor defects [4]. In this manuscript, we discuss the possibility and some pioneer practices of MNS activation as a treatment modality for emotional disorders.
MNS dysfunction as a risk factor for autism and deficits in understanding emotion It has been suggested that developmental MNS dysfunction leads to disordered social cognition in humans, including autism spectrum disorders (ASD)
0306-9877/$ - see front matter c 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2008.07.004
Mirror neuron system based therapy for emotional disorders [5–7]. These disorders in theory are characterized by limitations of mind, imitation, and social communication, summarized by the phrase ‘‘seeing is not understanding’’ [8]. A number of studies, including EEG [9–11] and brain imaging studies [12,13] have suggested the presence of MNS dysfunction in ASD patients. For example, brain imaging studies showed significant thinning of areas that belong to the MNS, such as inferior frontal cortex (IFC), the inferior parietal lobule (IPL), superior temporal sulcus (STS) as well as other areas that constitute the distributed neural circuitry for social cognition [13], in individuals with ASD. Additionally, it appears that the MNS undergoes abnormal activation during visual information processing [12,14]. Collectively these findings suggest that MNS dysfunction might be an important neurobiological risk factor for autism spectrum disorders. Given the important contribution of face processing to emotion, it is likely that dysfunction of the MNS plays a role in the defective capacity of ASD patients to understand emotion [6,15–18]. With fMRI, it has been shown that there are reliable differences between normally developing children and children with ASD in the network comprising the frontal component of the MNS (namely, pars opercularis), the insula, and the amygdala, all of which enable emotion understanding via action representation [19,20]. Collectively, these data suggest that altered neural circuit activation in ASD patients includes emotion-processing brain areas. ASD patients was found to be correlated with mood disorders, both in children and adults [21–25], and the two diseases may share common genetic vulnerability, such as serotonin transporter genes that are one of the well-recognized family participating in anxiety and depression [26,27]. Consistently, patients with mood disorders show higher tendency to develop autism symptoms [28,29]. Thus the autism, possibly due to the mirror neuron dysfunction, can result in complex psychiatric conditions that include mood disorders. Can autism treatments elevate mood states simultaneously? Antidepressants have been used in combined therapies to some autism patients [23,30,31], with proved efficiency. It is possible that the antidepressants can rescue the normal neurotransmission in brain areas that correlated to mirror neuron system, as well as their global neurotrophic effects. Psychologically, the important contributions of mirror neuron defects in autism patients to mood disorder symptoms permit improved integration ability, and restore the social network function [5,32,33]. The noninvasive manipulation of MNS activity may provide a novel approach to improving emotion modulation in ASD
723
patients, and could possibly lead to overall clinical improvement in such patients.
Post-trauma emotional disorder: interpretation through the MNS Focal brain trauma, such as stroke, can result in post-trauma emotional disorders [34–36]. These emotional disorders can be separated into several groups: dysfunction in emotion comprehension/ understanding; dysfunction of those neurocognitive systems responsible for the experience of emotion; and dysfunction of emotion control and expression, which may be attributed to disrupted integration [37]. Given the putative role of MNS in emotion understanding, the impairment to MNS following stroke can lead to the first group of emotional disorders – the instrumental function of the MNS in the comprehension of emotion. Brain imaging studies on imitation of facial emotional expressions suggest a critical role for the motor system in emotional behavior [37]. Those mood disorder conditions represent more specific complications of stroke than simply psychological responses to the motor disability [38]. Mirror neuron thus may mediate this lost link. Some studies have shown co-activation of mirror-system and limbic circuits through insula [19], and the focal stroke that interrupts the mirror neuron system may cause loss of modulatory amygdala affect and, finally, catastrophic reactions [35,39]. Additional complications include athymhormia, reflecting flat affect and a loss of motivation in the execution of motor actions [35]. Moreover, some other brain areas of motor significance, if damaged, can lead to emotional disorders [40–42]. Currently, the neuropsychiatric diseases resulted from motor cortex ischemia, such as poststroke depression [43,44], could be treated with antidepressants and other general mood disorder therapies [45–47]. Here, the important role of MNS in post-brain trauma emotional disorders suggests a potential new avenue for treating stroke patients.
The MNS-based therapy: multi-functional and multi-modal Mirror neurons fire to both observed and performed actions, hence there exists a possibility for observed-learning based brain activation or even rehabilitation [48–50]. Mounting evidence indicates that many forms of experience, including
724 physical exercise, sensory perception, and even direct brain stimulation or drug administration, may alter existing synaptic connectivity or induce synaptogenesis. The physiological bases of experience-dependent plasticity have been only partly elucidated, but may include upregulated endogenous neurogenesis [51–53], changed neurochemical transmission [54], induced expression of neurotrophins and neuropeptides [55] or improved body immune responses. Though we currently lack a clear understanding of the underlying mechanism for brain activity-related plasticity, activation of MNS has already been successfully used for poststroke treatment and rehabilitation [4,56]. Considering the neurobiological role of MNS in emotional disorders inherent to both autism and post-stroke conditions, we believe that targeted MNS activation could be used to prevent and/or improve the experience of emotional disorders in such patients. First, the action-specific responses of mirror neurons provide a precise approach to activate related brain areas. Using computerized displays or virtual reality environments [57,58], it may be possible to design different scenes/actions in order to specifically modulate various brain regions. Observation therapy may therefore be useful in the prevention of emotional disorders with motor deficiency. Second, some mirror neurons may respond to sounds that are specific for actions– these have been termed ‘‘audio-visual’’ mirror neurons [59–61]. This suggests that combined therapies including both visual and auditory stimulations would maximize clinical efficacy. Furthermore, virtual reality may create such an environment. Recent neuroimaging studies indicate that music, like language, involves an intimate coupling between the perception and production of hierarchically organized sequential information, which links meaning to emotion via the mirror neuron system [62]. We believe that music could be a potent component in MNS-based therapies, as recent findings in the domain of stroke rehabilitation have shown [63]. Behavioral and psychiatric disturbances are frequent sequelae to traumatic brain injury and major limitations on patient quality of life [64]. Pharmaceutical approaches that improve depression and other negative mood states have been the usual, if limited, therapeutic modality. Alternatively, MNS-based therapy provides the promise of a novel and non-invasive approach to improving the physiological and psychological condition of brain-injured patients. It is hoped that in the future MNStargeted treatments can breathe fresh hopes for emotional disorders in autism children as well as post-brain trauma patients.
Yuan and Hoff
References [1] Rizzolatti G, Craighero L. The mirror-neuron system. Annu Rev Neurosci 2004;27:169–92. [2] Gillmeister H, Catmur C, Liepelt R, Brass M, Heyes C. Experience-based priming of body parts: a study of action imitation. Brain Res 2008. [3] Catmur C, Walsh V, Heyes C. Sensorimotor learning configures the human mirror system. Curr Biol 2007;17:1527–31. [4] Ertelt D, Small S, Solodkin A, Dettmers C, McNamara A, Binkofski F, et al. Action observation has a positive impact on rehabilitation of motor deficits after stroke. Neuroimage 2007;36(Suppl. 2):T164–73. [5] Williams JH, Waiter GD, Gilchrist A, Perrett DI, Murray AD, Whiten A. Neural mechanisms of imitation and ‘mirror neuron’ functioning in autistic spectrum disorder. Neuropsychologia 2006;44:610–21. [6] Williams JH, Massaro DW, Peel NJ, Bosseler A, Suddendorf T. Visual-auditory integration during speech imitation in autism. Res Dev Disabil 2004;25:559–75. [7] Williams JH, Whiten A, Suddendorf T, Perrett DI. Imitation mirror neurons and autism. Neurosci Biobehav Rev 2001;25: 287–95. [8] Fecteau S, Lepage JF, Theoret H. Autism spectrum disorder: seeing is not understanding. Curr Biol 2006;16: R131–3. [9] Oberman LM, Ramachandran VS, Pineda JA. Modulation of mu suppression in children with autism spectrum disorders in response to familiar or unfamiliar stimuli: the mirror neuron hypothesis. Neuropsychologia 2008;46:1558–65. [10] Oberman LM, Ramachandran VS. The simulating social mind: the role of the mirror neuron system and simulation in the social and communicative deficits of autism spectrum disorders. Psychol Bull 2007;133:310–27. [11] Oberman LM, Hubbard EM, McCleery JP, Altschuler EL, Ramachandran VS, Pineda JA. EEG evidence for mirror neuron dysfunction in autism spectrum disorders. Brain Res Cogn Brain Res 2005;24:190–8. [12] Hadjikhani N, Joseph RM, Snyder J, Tager-Flusberg H. Abnormal activation of the social brain during face perception in autism. Hum Brain Mapp 2007;28:441–9. [13] Hadjikhani N, Joseph RM, Snyder J, Tager-Flusberg H. Anatomical differences in the mirror neuron system and social cognition network in autism. Cereb Cortex 2006;16:1276–82. [14] Spezio ML, Adolphs R, Hurley RS, Piven J. Abnormal use of facial information in high-functioning autism. J Autism Dev Disord 2007;37:929–39. [15] Golarai G, Grill-Spector K, Reiss AL. Autism and the development of face processing. Clin Neurosci Res 2006;6:145–60. [16] Sasson NJ. The development of face processing in autism. J Autism Dev Disord 2006;36:381–94. [17] Dawson G, Webb SJ, Wijsman E, Schellenberg G, Estes A, Munson J, et al. Neurocognitive and electrophysiological evidence of altered face processing in parents of children with autism: implications for a model of abnormal development of social brain circuitry in autism. Dev Psychopathol 2005;17:679–97. [18] Moody EJ, McIntosh DN, Mann LJ, Weisser KR. More than mere mimicry? The influence of emotion on rapid facial reactions to faces. Emotion 2007;7:447–57. [19] Carr L, Iacoboni M, Dubeau MC, Mazziotta JC, Lenzi GL. Neural mechanisms of empathy in humans: a relay from neural systems for imitation to limbic areas. Proc Natl Acad Sci USA 2003;100:5497–502.
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