REVIEW URRENT C OPINION
Conceptual issues in autism spectrum disorders Shaun Gallagher a,b,c and Somogy Varga a
Purpose of review To provide an update on recent studies concerning social cognition in autism spectrum disorders (ASDs), to compare different theoretical approaches used to interpret empirical data, and to highlight a number of conceptual issues. Recent findings In regard to social cognition in ASDs, there is an emerging emphasis on early-onset and prolonged sensory–motor problems. Such sensory–motor problems may fit with the theories of social cognition that emphasize the importance of embodied interaction rather than deficits in mindreading, or they may reflect more general aspects of developmental disorders. Summary Different theoretical frameworks offer alternative perspectives on the central characteristics in ASDs and motivate different ways of conceptualizing diagnosis and intervention. Theory-of-mind approaches continue to appeal to false-belief paradigms, and debate continues about the performance of individuals with autism. Likewise, there is continuing debate and renewed skepticism about the role of simulation and deficits in the mirror system in ASDs. Growing evidence concerning sensory–motor problems, specifically disrupted patterns in re-entrant (afferent and proprioceptive) sensory feedback across the autistic spectrum, may not only provide support for more embodied interactive approaches, but also suggests that a single approach is unlikely able to explain all social cognition problems in autism. A pluralist approach understands ASDs as involving a variant range of cascading disrupted processes. Keywords ASDs, interaction theory, sensory–motor problems, simulation theory, theory of mind
INTRODUCTION Ongoing research on autism spectrum disorders (ASDs) is focused on the causes, including genetic and neurofunctional aspects; diagnosis; behavioral studies, with continuing emphasis on theory-ofmind deficits, but increasing focus on bodily (sensory–motor) processing, and therapy. In this article, we focus on the conceptual issues that pertain to the behavioral studies with some indication of how these issues also hold implications for the other areas of research. In the behavioral studies, we focus primarily on the questions about social cognition. The endeavor to work out explanations for various social cognition problems in ASDs continues to occupy a central position in contemporary debates; the research in this area has productively integrated empirical work on social cognition impairments and philosophically informed conceptual distinctions. The general theoretical approach most researchers have adopted links various social impairments to deficiencies in theory of mind (ToM) or ‘mindreading’ abilities, which may include deficits in
orienting to eye gaze and pointing gestures. Whereas prodromal symptoms of ASDs at 6 months include a diminished ability to attend spontaneously to people [1], the mindreading and joint attention deficits that appear later are regarded by many as universal for the whole spectrum. Many researchers continue to consider ‘mind blindness’ as the ‘core and possibly universal abnormality of autistic individuals’ (see [2] [2,p. 491], also see [3 ,4]). Others think that ‘singlecause’ explanations are untenable and prefer to speak about problems related to socialization, communication, and imagination [5 ,6]. &
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Department of Philosophy, University of Memphis, Memphis, Tennessee, USA, bSchool of Humanities, University of Hertfordshire, Hertfordshire, UK and cFaculty of Law, Humanities and the Arts, University of Wollongong, Wollongong, New South Wales, Australia Correspondence to Shaun Gallagher, Department of Philosophy, University of Memphis, Clement Hall 327, Memphis, TN 38152, USA. Tel: +1 321 438 1909; fax: +1 901 678 4365; e-mail: [email protected] Curr Opin Psychiatry 2015, 28:127–132 DOI:10.1097/YCO.0000000000000142
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KEY POINTS Attempts to work out the explanations for social cognition deficits in ASDs continue to occupy a central position in contemporary debates, and involve productive integration of empirical work and philosophically informed conceptual distinctions. Accounts of ASDs that continue to focus on theory of mind and false-belief tests or on simulation and mirror neurons remain controversial because of mixed results in empirical studies. Accounts of ASDs that highlight the problems with bodily aspects of social interaction have found recent support in the studies that show early manifestation of sensory–motor problems in infants later diagnosed with autism and across the autism spectrum. Studies of sensory–motor problems in ASDs still need to address the questions about the specific differences between sensory–motor problems in ASDs and those found in other developmental disabilities. Knowing the precise character of sensory–motor problems in ASDs may help to determine the proper methods for diagnosis and for developing therapies.
Although most agree on the nature of deficiencies in ASDs, the answer to a number of questions will depend on the theoretical framework within which researchers address the manifestations of impaired processes of social cognition. In this study, we give a brief overview of three theories that deal with the cognitive processes that underpin social cognition and the different perspectives they offer on central characteristics of ASDs. Theory theory claims that we make inferences about the mental states of others on the basis of a stored body of knowledge about the way mental states are usually connected to behavior. Simulation theory proposes that instead of recourse to a theory, we mentally ‘step into the shoes’ of the relevant person and model the mental states behind her behaviors by an internal simulation. Interaction theory highlights the (sometimes constitutive) role of social interaction and maintains that in many cases we do not need to theorize or to run a simulation in order to make sense of others.
and specifically failed to understand false beliefs and mentalistic stories [7]. Standard false-belief experiments show that the ability to explicitly attribute mental states to other people begins, on average, in typically developing children around the age of 4 years and is impaired in children with autism. More recent experiments of spontaneous or implicit false-belief comprehension show that infants as young as 13 months are seemingly able to distinguish behaviors related to false beliefs [8]. Individuals with ASDs, however, showed no evidence of implicit false-belief tracking [9,10]. Accordingly, Frith [11] [11,p. 2085] argues ‘it is the early-appearing, implicit form of ToM that points to a core problem in autism’. There is a continuing debate about whether the mindreading capability is innate and based on a domain-specific module that is activated at a certain stage of development [12] or whether children gradually acquire it [13,14]. According to some proponents of theory theory, the fact that younger infants can pass spontaneous false-belief tests supports the existence of an innate module or specific theory of mind mechanism (ToMM) [12]. Adams [3 ] further argues that thinking of autism as a spectrum disorder increases the plausibility of conceiving of ToM as involving a domain-specific module (although he remains neutral on whether it is innate). Adams points out that there are important differences in how we conceive of ASDs and in how we study it, depending on whether the aim is to develop diagnostic criteria, to design therapeutic interventions, or to discover cognitive architecture. To identify the diagnostic criteria, it is best to think of ASDs as composed of a set of overlapping deficits and to conduct large-scale, longitudinal studies of an ASD population. In contrast, to design therapeutic interventions one needs to focus on the individual and to think of ASDs as involving a set of deficits that may or may not overlap. If the aim is to discover cognitive architecture, however, Adams suggests we need to focus on individuals who have one isolated (or near isolated) deficit. To the extent that we can find individuals on the spectrum with isolated deficits – for example, deficits in ToM but not deficits in communication, social norms or problems in perception and motor behavior – we find evidence for a ‘domain-specific module’ [3 ] [3 ,p. 8]. Although Adams assumes (as a matter of definition of spectrum disorder) that ‘each symptom of a spectrum disorder can occur independently of the other symptoms’, he admits that empirically no one has identified individuals with just a ToM deficit in isolation from other deficits. The assumption that a spectrum disorder can be defined as a disorder in which symptoms can occur &
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THEORY THEORY Theory theory approaches to mindreading contend that we understand others by making inferences about their mental states on the basis of a stored body of knowledge, a ToM or ‘folk psychology’. Pioneers in autism research developed the theory theory approach by showing that a majority of children with ASDs failed at mindreading tasks, 128
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in isolation from each other [3 ] conflicts with the idea that in ASD deficits are highly interconnected – involving a ‘cascade and then a tangle of secondary effects that become causes of other effects, which in turn become causes of further effects. . .’ [5 ] [5 , p. 238]. But it also runs into the practical difficulty that an isolated symptom, by itself, cannot be diagnosed as belonging to ASDs. For example, one finds problems with ToM in schizophrenia as well as in autism. The logic of identifying one isolated deficit to establish its domain-specific nature runs counter to the fact that one needs to look at more than one symptom to distinguish ASDs from other disorders and this suggests that an understanding of cognitive architecture cannot be separated from the search for diagnostic criteria. One challenge for the theory theory account is that a substantial minority of children with ASDs regularly manage to pass false-belief tasks [15,16 ]. Also, high-functioning adults with ASDs can make use of theoretical inference to mental states, although, as noted, they do not implicitly track false-belief states of others [10]. Scheeren et al. [16 ] offer a slightly different interpretation. They explore ToM in children and adolescents with highfunctioning ASDs using advanced ToM stories (second-order false-belief stories, emotional display rule stories, double bluff, faux pas, and sarcasm) without finding significant differences to typically developing children. The study concludes that individuals with high-functioning ASDs ‘seem to master the concept of ToM without mastering the ability to use such insight in the service of their ongoing social interactions’ [16 ] [16 ,p. 633]. This may be explained in a variety of ways, but one possibility is to argue that such ToM and false-belief tasks might not give us a good picture of core characteristics in social cognition [17]. Fisch [18] summarizes a number of problems with the theory theory approach to ASDs and suggests that a neurobiological (rather than neurocognitive) approach may be more productive. He points to research on mirror neurons and their involvement in social behavior and language as promising. &
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SIMULATION THEORY Mirror neurons are activated during performance of one’s own intentional actions and when one observes another’s intentional actions. Their discovery in the 1990s gave a big boost to simulation accounts of social cognition. Simulation theory challenges the idea that ‘folk psychology’ should be granted a key role in social cognition. Rather than employing a theory, simulation theory maintains that mindreaders consult their own minds, that is,
they run their own mechanisms in a pretense mode in order to simulate what another person might be thinking. In other words, to mindread or make sense of others, we simply use our own minds as models [19]. Some simulation theory proponents [20,21] have argued that deficits in simulation processes may be at the core of autistic problems with social cognition; they link such processes to the proper functioning of mirror neuron networks. Following this approach, Sato et al. [22] presented dynamic and static facial expressions to high-functioning adults with ASDs; they found that regions of the mirror network demonstrated weaker activity compared with typically developing individuals. Gallese et al. [23 ] provide an extensive review of the mirror neurons hypothesis on autism and the idea of ‘an action simulation deficit in individuals with autism’ (p. 20). On the one hand, evidence in favor of this hypothesis includes EEG studies showing that the mu frequency (the suppression of which has some correlation with activation in the mirror system) was not suppressed in individuals with ASDs during relevant tasks. Diminished activation of mirror neurons in individuals with ASDs has been shown in a variety of social cognition tasks, including imitation of facial expressions of basic emotions [24,25]. On the other hand, Gallese et al. [23 ] are careful to point out that there are a number of critical challenges to the mirror neuron hypothesis. For example, in individuals with ASDs, mirror neuron activation is not diminished under certain circumstances, namely, when a familiar agent does the observed action and when an action has a clear goal [26–28]. Schwarzkopf et al. [29] show that highfunctioning autistic individuals do not have problems with implicit perspective-taking (which may involve mirror neuron activation) but do have problems with more explicit perspective-taking (which may involve ToM-related processes). Other studies show no difference in mu suppression during observation of goal-directed action between individuals with ASDs and controls [30]. Keysers et al. [31] [31, p. 254] note that ‘research on the observation of hand actions has not lent strong support to the mirror neuron hypothesis of autism’, a conclusion supported more generally by Hamilton’s review that suggests ‘little evidence for a global dysfunction of the mirror system in autism’ [32 ] [32 ,p. 91]. More conceptual concerns about the interpretation of the mirror system as instantiating simulations have been raised in the philosophical literature. Given the various definitions of simulation (as involving pretense, or matching, or reuse of motor control mechanisms) found in the literature [33], it is not always clear that mirror neurons
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should count as embodying a simulation process [34]. Thus, although Gallese et al. [23 ] regard mirror neurons as constituting an ‘action-perception matching mechanism’, it is not clear that, outside of instances of imitation, one’s everyday interactions with others call for matching one’s motor system to theirs [35]. Whether or not one accepts the simulation theory interpretation of mirror neuron data, or works out an alternative nonsimulative interpretation, however, it is still likely that mirror neuron activation plays an important role in social cognition and is diminished in some aspects of ASD behavior. This has motivated suggestions that one possible therapeutic approach to autism could involve the use of brain–computer interface games that combine neuro-feedback and bio-feedback to induce neuroplastic changes leading to normalization of the mirror neuron system [36]. &&
INTERACTION THEORY Although there are important differences between simulation theory and theory theory, they share a commitment to the idea that our understanding of others proceeds by an inferential or projective attribution of causally efficacious mental states. In contrast, interaction theory and enactive accounts of cognition put more emphasis on embodied processes in social interaction and the direct perception of at least some mental states [35,37–39]. Interaction theory draws on the recent embodied and enactivist theories of perception and cognition, taking seriously the idea that the mind is embodied, that perception and action are closely related, and cognition need not always be mediated by internal representations [40]. In accordance with these theoretical commitments, interaction theory not only emphasizes the embodied nature of social cognition, but also holds that, in social contexts, perception serves interaction and that for most of our ordinary everyday interactions, we are not required to engage in implicit or explicit processes of mindreading [41]. It also draws on work in developmental psychology that emphasizes primary intersubjectivity and the role of sensory–motor processes in the early development of social interaction [42–47,48 ,49,50]. Processes of primary intersubjectivity that involve perception of the other’s bodily postures, movements, gestures, facial expressions, vocal intonations, etc., as well as dynamic embodied interactions, often in rich pragmatic and social contexts, allow young infants, as well as adults, to gain a basic sense of the intentions and emotions of others. According to interaction theory, such primary intersubjective processes progressively become more refined to the extent that in &
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many everyday interactions, we immediately understand the intentions, emotions, and actions of others without having to infer or simulate. Interaction theorists cite evidence that before reaching the developmental age associated with ToM, infants later diagnosed with autism already display significant problems in the sensory–motor behavior that may affect the aspects of primary intersubjectivity [50–53]. These include postural instabilities, atypical gait, mistiming of motor sequences, motor coordination problems, problems with anticipatory postural adjustments and expressionless faces (Ref. [23 ] provides a good review of the literature on these motor problems, also see, for example [37,54–57,58 ]). These problems may be attributable to growth errors in the brain development of embryo, fetus and infant [52]. Regardless of the cause, these motor problems involve disrupted timing in prospective motor control that interferes with the efficient integration of sensory–motor coordination and may lead to well known perceptual difficulties found in some cases of ASDs [37,59]. Such disorders are clearly documented in early childhood, when typically developing children engage in joint attention and joint action with others and learn to communicate. As developmental disorders more generally may involve sensory– motor difficulties, one needs to ask whether such difficulties can be definitive for ASDs. The recent work of Torres and colleagues is noteworthy in this regard. In individuals with ASDs, Torres et al. [60 ,61] demonstrate the occurrence of disrupted patterns in re-entrant (afferent and proprioceptive) sensory feedback that usually contributes to the autonomous regulation and coordination of motor output. Such feedback supports volitional control and fluid, flexible transitions between intentional and spontaneous behaviors. In ASDs, there is a disruption in the maturation of this form of proprioception, and this is accompanied by behavioral variability in motor control. In contrast to typically developing individuals, the normalized peak (micro-movement) velocity and noise-to-signal ratios in the movement of all participants with ASDs, across different ages and across different verbal or nonverbal status, remained in a region corresponding to younger (3-year-old) typically developing children. Proprioceptive input is random (unpredictable), noisy, and unreliable. Accordingly, individuals with ASDs have difficulty distinguishing goal-directed from goal-less motions in most tasks [60 ,61,62]. This suggests that individuals with ASDs may have trouble anticipating the consequences of their own impending movements in a timely fashion. Such disruptions may also make it difficult if not impossible to &&
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apply fine-tuned discriminations to the actions and emotional facial expressions of others during realtime social interactions. In effect, essential aspects of primary intersubjectivity, a pervasive and basic component of social interaction (early developed and typically sustained), are disrupted. The use of ToM strategies by high-functioning autistic individuals, then, may be compensatory for the loss of the more primary processes. The specificity found in Torres’ research may support an embodied-interaction approach to autism if it can be shown that such sensorymotor problems are ASD-specific. Accordingly, this research is important for addressing two questions requiring further research. First, are kinematic disruptions in autistic individuals different from those found in other developmental disabilities (e.g., Down syndrome, cerebral palsy, attention deficit hyperactivity disorder, and cerebellar ataxia)? Indeed, one objection to the interaction theory account could be that not all cases of motoric abnormality lead to problems with social cognition [55]. Second, knowing the precise character of the motor problems in autism may also help to determine proper therapies. Further research is required to know precisely whether and why and what therapies, involving, for example, imitation, interactive music, or movement [37,52], might work.
CONCLUSION We presented a brief overview of different theoretical frameworks offering alternative perspectives on the central characteristics in ASDs. The philosophical and interdisciplinary debate on the nature of social cognition has important implications for psychiatry, as different approaches to social cognition will likely support different ways of conceptualizing diagnosis and intervention. The outline provided here suggests it is unlikely that a single approach is able to explain all social cognition problems in autism. It is more plausible to think that, depending on the circumstances and on where one is located on the autistic spectrum, deficits in capacity for theoretical inference, or in some cases, compensatory routines that rely on theoretical inference, or deficits in simulation ability, and in very basic embodied interactive processes, need to be included in a best understanding relative to each autistic individual. One advantage of a pluralist approach to social cognition is that it is possible to understand ASDs as involving a variant range of (cascading) disrupted processes. Acknowledgements None.
Financial support and sponsorship S.G.’s work was supported by a professorial fellowship at the University of Wollongong, by the Marie-Curie Initial Training Network, ‘TESIS: Toward an Embodied Science of InterSubjectivity’ (FP7-PEOPLE-2010-ITN, 264828), European Commission Research, and by the Humboldt Foundation’s Anneliese Maier Research Award. Conflicts of interest None.
REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. Chawarska K, Macari S, Shic F. Decreased spontaneous attention to social scenes in 6-month-old infants later diagnosed with autism spectrum disorders. Biol Psychiatry 2013; 74:195–203. 2. Baron-Cohen S. Is autism necessarily a disability? Dev Psychopathol 2000; 12:489–500. 3. Adams M. Explaining the theory of mind deficit in autism spectrum disorder. & Philos Stud 2013; 163:233–249. This study suggests, first, that the issue of domain-specific ToM mechanism relates directly to the specific characterization of autism as a spectrum disorder, and second that there are important differences in how we conceive of and study ASDs, depending on whether the aim is to develop diagnostic criteria, to design therapeutic interventions, or to discover cognitive architecture. 4. Kana RK, Libero LE, Hu CP, et al. Functional brain networks and white matter underlying theory-of-mind in autism. Soc Cogn Affect Neurosci 2014; 9:98– 105. 5. Boucher J. Putting theory of mind in its place: psychological explanations of & the socio–emotional–communicative impairments in autistic spectrum disorder. Autism 2012; 16:226–246. This study argues that although explanations of early impaired mindreading are untenable, impairments of dyadic interaction in ASDs can lead to impaired ToM ability. 6. Pellicano E. Individual differences in executive function and central coherence predict developmental changes in theory of mind in autism. Dev Psychol 2010; 46:530–544. 7. Baron-Cohen S, Leslie A, Frith U. Does the autistic child have a theory of mind? Cognition 1985; 21:37–46. 8. Onishi KH, Baillargeon R. Do 15-month-old infants understand false beliefs? Science 2005; 308:255–258. 9. Schneider D, Slaughter VP, Dux PE. What do we know about implicit falsebelief tracking? Psychon Bull Rev 2014. [Epub ahead of print]. doi: 10.3758/ s13423-014-0644-z. 10. Schneider D, Slaughter VP, Bayliss AP, Dux PE. A temporally sustained implicit theory of mind deficit in autism spectrum disorders. Cognition 2013; 129:410–417. 11. Frith U. Why we need cognitive explanations of autism? Q J Exp Psychol 2012; 65:2073–2092. 12. Carruthers P. Mindreading in infancy. Mind Lang 2013; 28:141–172. 13. Carpendale JIM, Lewis C. The development of social understanding: A relational perspective. In: Overton W.F., editor. The handbook of lifespan development Volume 1: Cognition, biology, and methods across the lifespan. Hoboken, NJ: Wiley; 2010. pp. 548–627. 14. Meltzoff AN, Gopnik A. Learning about the mind from evidence: children’s development of intuitive theories of perception and personality. In: BaronCohen S, Lombardo M, Tager-Flusberg H, Cohen D, editors. Understanding other minds: perspectives from developmental social neuroscience. Oxford: Oxford University Press; 2013. pp. 19–34. 15. Iao LS, Leekam SR. Nonspecificity and theory of mind: new evidence from a nonverbal false-sign task and children with autism spectrum disorders. J Exp Child Psychol 2014; 122:1–20. 16. Scheeren AM, de Rosnay M, Koot HM, Begeer S. Rethinking theory of mind in & high-functioning autism spectrum disorder. J Child Psychol Psychiatry 2013; 54:628–635. This study demonstrates that high-functioning individuals with ASDs performed equally well on ToM tasks as typically developing peers. Counter to the predictions of ToM accounts, individuals with ASDs can master advanced mental state reasoning, but may still fail to apply these theoretical principles during everyday social interactions. 17. Bowler D. Autism spectrum disorders: psychological theory and research. West Sussex: John Wiley and Sons; 2000.
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Neurodevelopmental disorders 18. Fisch GS. Autism and epistemology IV: does autism need a theory of mind? Am J Med Genet Part A 2013; 161A:2464–2480. 19. Goldman AI. Joint ventures: mindreading, mirroring and embodied cognition. Oxford: Oxford University Press; 2013. 20. Iacoboni M, Dapretto M. The mirror neuron system and the consequences of its dysfunction. Nat Rev Neurosci 2006; 7:942–951. 21. Oberman LM, McCleery JP, Hubbard EM, et al. Developmental changes in mu suppression to observed and executed actions in autism spectrum disorders. Soc Cogn Affect Neurosci 2013; 8:300–304. 22. Sato W, Uono S, Toichi M. Atypical recognition of dynamic changes in facial expressions in autism spectrum disorders. Res Autism Spectr Disord 2013; 7:906–912. 23. Gallese V, Rochat MJ, Berchio C. The mirror mechanism and its potential role && in autism spectrum disorder. Dev Med Child Neurol 2013; 55:15–22. This is a theoretically well balanced review of the evidence for the involvement of mirror neurons in ASDs with a focus on pervasive motor, emotion, imitation and communication deficits in ASDs. 24. Dapretto M, Davies MS, Pfeifer JH, et al. Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders. Nat Neurosci 2006; 9:28–30. 25. Williams JH, Waiter GD, Gilchrist A, et al. Neural mechanisms of imitation and ‘mirror neuron’ functioning in autistic spectrum disorder. Neuropsychologia 2006; 44:610–621. 26. 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; 46:1558–1565. 27. Martineau J, Cochin S, Magne R, Barthelemy C. Impaired cortical activation in autistic children: is the mirror neuron system involved? Int J Psychophysiol 2008; 68:35–40. 28. Enticott PG, Kennedy HA, Rinehart NJ, et al. Interpersonal motor resonance in autism spectrum disorder: evidence against a global ‘mirror system’ deficit. Front Hum Neurosci 2013; 7:218. 29. Schwarzkopf S, Schilbach L, Vogeley K, Timmermans B. ‘Making it explicit’ makes a difference: evidence for a dissociation of spontaneous and intentional level 1 perspective taking in high-functioning autism. Cognition 2014; 131:345–354. 30. Fan YT, Decety J, Yang CY, et al. Unbroken mirror neurons in autism spectrum disorders. J Child Psychol Psychiatry 2010; 5:981–988. 31. Keysers C, Thioux M, Gazzola V. Mirror neuron system and social cognition. In: Baron-Cohen S, Lombardo M, Tager-Flusberg H, Cohen D, editors. Understanding other minds: perspectives from developmental social neuroscience. Oxford: Oxford University Press; 2013. pp. 233–256. 32. Hamilton AFDC. Reflecting on the mirror neuron system in autism: a sys& tematic review of current theories. Dev Cogn Neurosci 2013; 3:91–105. A systematic review of 25 published studies that use neuroscience methods to examine the mirror system in autism. This review concludes that current data are inconsistent and there is little evidence for a global dysfunction of the mirror system in autism. 33. Gallese V. Bodily selves in relation: embodied simulation as second-person perspective on intersubjectivity. Philos Trans R Soc 2014; B369:20130177; http://dx.doi.org/10.1098/rstb.2013.0177. 34. Gallagher S. Reuse and body-formatted representations in simulation theory. Cogn Syst Res 2015 (in press). 35. Gallagher S, Varga S. Social constraints on the direct perception of emotions and intentions. Topoi 2014; 33:185–199. doi: 10.1007/s11245-013-9203-x. 36. Friedrich EV, Suttie N, Sivanathan A, et al. Brain–computer interface game applications for combined neurofeedback and biofeedback treatment for children on the autism spectrum. Front Neuroeng 2014; 7:21. 37. De Jaegher H. Embodiment and sense-making in autism. Front Integr Neurosci 2013; 7:15. doi: 10.3389/fnint.2013.00015. 38. De Jaegher H, Di Paolo E, Gallagher S. Does social interaction constitute social cognition? Trends Cogn Sci 2010; 14:441–447. 39. Gallagher S. In defense of phenomenological approaches to social cognition: interacting with the critics. Rev Philos Psychol 2012; 3:187–212. 40. Hutto D, Myin E. Radicalizing enactivism: basic minds without content. Cambridge, MA: MIT Press; 2013.
132
www.co-psychiatry.com
41. Schilbach L, Timmermans B, Reddy V, et al. Toward a second-person neuroscience. Behav Brain Sci 2013; 36:393–414. 42. Ambrosini E, Reddy V, de Looper A, et al. Looking ahead: anticipatory gaze and motor ability in infancy. PLoS One 2013; 8:e67916. 43. Beurkens NM, Hobson JA, Hobson RP. Autism severity and qualities of parent–child relations. J Autism Dev Disord 2013; 43:168–178. 44. Hobson RP, Hobson JA. Autism: self and others. In: Baron-Cohen S, Lombardo M, Tager-Flusberg H, Cohen D, editors. Understanding other minds: perspectives from developmental social neuroscience. Oxford: Oxford University Press; 2013. pp. 397–412. 45. Hobson JA, Hobson RP, Cheung Y, Calo´ S. Symbolizing as interpersonally grounded shifts in meaning: social play in children with and without autism. J Autism Dev Disord 2015; 45:42–52. 46. Hobson JA, Hobson RP, Malik S, et al. The relation between social engagement and pretend play in autism. Br J Dev Psychol 2013; 31:114–127. 47. Reddy V, Markova G, Wallot S. Anticipatory adjustments to being picked up in infancy. PLoS One 2013; 8:e65289. 48. Savarese RJ. Moving the field: the sensorimotor perspective on autism. & Commentary. Front Integr Neurosci 2013; 7:6. doi: 10.3389/fnint. 2013.00006. This article is part of a special issue on sensorimotor approaches to ASDs. The author, in summarizing the recently developing evidence for sensorimotor deficit in ASDs, and its explanatory power, suggests a sea change in the approaches for understanding ASDs. 49. Rochat P. The gaze of others. In: Banaji M, Gelman S, editors. Navigating the social world: what infants, children, and other species can teach us. New York, NY: Oxford University Press; 2013. pp. 205–211. 50. Trevarthen C. Embodied human intersubjectivity: imaginative agency, to share meaning. Cogn Semiotics 2012; 4:6–56. 51. Gallagher S. Understanding problems in autism: interaction theory as an alternative to theory of mind. Philos Psychiatry Psychol 2004; 11:199–217. 52. Trevarthen C, Delafield-Butt JT. Autism as a developmental disorder in intentional movement and affective engagement. Front Integr Neurosci 2013; 7:49. 53. Teitelbaum PO, Teitelbaum J, Nye J, et al. Movement analysis in infancy may be useful for early diagnosis of autism. Proc Natl Acad Sci USA 1998; 95:13982–13987. 54. Cattaneo L, Fabbi-Destro M, Boria S, et al. Impairment of actions chains in autism and its possible role in intention understanding. Proc Natl Acad Sci USA 2008; 104:17825–17830. 55. Cook JL, Blakemore SJ, Press C. Atypical basic movement kinematics in autism spectrum conditions. Brain 2013; 136:2816–2824. 56. Hilton C, Zhang Y, White M, et al. Motor impairment concordant and discordant for autism spectrum disorders. Autism 2012; 16:430–441. 57. Fabbri-Destro M, Cattaneo L, Boria S, Rizzolatti G. Planning actions in autism. Exp Brain Res 2009; 192:521–525. 58. Whyatt C, Craig C. Sensory–motor problems in autism. Front Integr Neurosci & 2013; 7:51. Kinematic studies of impaired use of perception–action coupling for guidance of movement shows inflexible and rigid motor profiles in ASDs. This study suggests that impairments of perception–action coupling are primary rather than secondary impairments and should be considered a fundamental aspect of ASDs. 59. David N, Schultz J, Milne E, et al. Right temporoparietal gray matter predicts accuracy of social perception in the autism spectrum. J Autism Dev Disord 2014; 44:1433–1446. 60. Torres EB, Brincker M, Isenhower RW, et al. Autism: the micro-movement && perspective. Front Integr Neurosci 2013; 7:32. doi: 10.3389/fnint.2013. 00032. This study shows the innovative use of methods for measuring deficits in reafferent kinesthetic features of movement in ASDs using a unifying statistical framework. This study shows that in ASDs, there is a disruption in the maturation of proprioceptive–kinesthetic feedback. 61. Torres EB. Atypical signatures of motor variability found in an individual with ASD. Neurocase 2013; 19:150–165. 62. Brincker M, Torres EB. Noise from the periphery in autism. Front Integr Neurosci 2013; 7:34.
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Conceptual issues in autism spectrum disorders Shaun Gallagher a,b,c and Somogy Varga a
Purpose of review To provide an update on recent studies concerning social cognition in autism spectrum disorders (ASDs), to compare different theoretical approaches used to interpret empirical data, and to highlight a number of conceptual issues. Recent findings In regard to social cognition in ASDs, there is an emerging emphasis on early-onset and prolonged sensory–motor problems. Such sensory–motor problems may fit with the theories of social cognition that emphasize the importance of embodied interaction rather than deficits in mindreading, or they may reflect more general aspects of developmental disorders. Summary Different theoretical frameworks offer alternative perspectives on the central characteristics in ASDs and motivate different ways of conceptualizing diagnosis and intervention. Theory-of-mind approaches continue to appeal to false-belief paradigms, and debate continues about the performance of individuals with autism. Likewise, there is continuing debate and renewed skepticism about the role of simulation and deficits in the mirror system in ASDs. Growing evidence concerning sensory–motor problems, specifically disrupted patterns in re-entrant (afferent and proprioceptive) sensory feedback across the autistic spectrum, may not only provide support for more embodied interactive approaches, but also suggests that a single approach is unlikely able to explain all social cognition problems in autism. A pluralist approach understands ASDs as involving a variant range of cascading disrupted processes. Keywords ASDs, interaction theory, sensory–motor problems, simulation theory, theory of mind
INTRODUCTION Ongoing research on autism spectrum disorders (ASDs) is focused on the causes, including genetic and neurofunctional aspects; diagnosis; behavioral studies, with continuing emphasis on theory-ofmind deficits, but increasing focus on bodily (sensory–motor) processing, and therapy. In this article, we focus on the conceptual issues that pertain to the behavioral studies with some indication of how these issues also hold implications for the other areas of research. In the behavioral studies, we focus primarily on the questions about social cognition. The endeavor to work out explanations for various social cognition problems in ASDs continues to occupy a central position in contemporary debates; the research in this area has productively integrated empirical work on social cognition impairments and philosophically informed conceptual distinctions. The general theoretical approach most researchers have adopted links various social impairments to deficiencies in theory of mind (ToM) or ‘mindreading’ abilities, which may include deficits in
orienting to eye gaze and pointing gestures. Whereas prodromal symptoms of ASDs at 6 months include a diminished ability to attend spontaneously to people [1], the mindreading and joint attention deficits that appear later are regarded by many as universal for the whole spectrum. Many researchers continue to consider ‘mind blindness’ as the ‘core and possibly universal abnormality of autistic individuals’ (see [2] [2,p. 491], also see [3 ,4]). Others think that ‘singlecause’ explanations are untenable and prefer to speak about problems related to socialization, communication, and imagination [5 ,6]. &
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Department of Philosophy, University of Memphis, Memphis, Tennessee, USA, bSchool of Humanities, University of Hertfordshire, Hertfordshire, UK and cFaculty of Law, Humanities and the Arts, University of Wollongong, Wollongong, New South Wales, Australia Correspondence to Shaun Gallagher, Department of Philosophy, University of Memphis, Clement Hall 327, Memphis, TN 38152, USA. Tel: +1 321 438 1909; fax: +1 901 678 4365; e-mail: [email protected] Curr Opin Psychiatry 2015, 28:127–132 DOI:10.1097/YCO.0000000000000142
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KEY POINTS Attempts to work out the explanations for social cognition deficits in ASDs continue to occupy a central position in contemporary debates, and involve productive integration of empirical work and philosophically informed conceptual distinctions. Accounts of ASDs that continue to focus on theory of mind and false-belief tests or on simulation and mirror neurons remain controversial because of mixed results in empirical studies. Accounts of ASDs that highlight the problems with bodily aspects of social interaction have found recent support in the studies that show early manifestation of sensory–motor problems in infants later diagnosed with autism and across the autism spectrum. Studies of sensory–motor problems in ASDs still need to address the questions about the specific differences between sensory–motor problems in ASDs and those found in other developmental disabilities. Knowing the precise character of sensory–motor problems in ASDs may help to determine the proper methods for diagnosis and for developing therapies.
Although most agree on the nature of deficiencies in ASDs, the answer to a number of questions will depend on the theoretical framework within which researchers address the manifestations of impaired processes of social cognition. In this study, we give a brief overview of three theories that deal with the cognitive processes that underpin social cognition and the different perspectives they offer on central characteristics of ASDs. Theory theory claims that we make inferences about the mental states of others on the basis of a stored body of knowledge about the way mental states are usually connected to behavior. Simulation theory proposes that instead of recourse to a theory, we mentally ‘step into the shoes’ of the relevant person and model the mental states behind her behaviors by an internal simulation. Interaction theory highlights the (sometimes constitutive) role of social interaction and maintains that in many cases we do not need to theorize or to run a simulation in order to make sense of others.
and specifically failed to understand false beliefs and mentalistic stories [7]. Standard false-belief experiments show that the ability to explicitly attribute mental states to other people begins, on average, in typically developing children around the age of 4 years and is impaired in children with autism. More recent experiments of spontaneous or implicit false-belief comprehension show that infants as young as 13 months are seemingly able to distinguish behaviors related to false beliefs [8]. Individuals with ASDs, however, showed no evidence of implicit false-belief tracking [9,10]. Accordingly, Frith [11] [11,p. 2085] argues ‘it is the early-appearing, implicit form of ToM that points to a core problem in autism’. There is a continuing debate about whether the mindreading capability is innate and based on a domain-specific module that is activated at a certain stage of development [12] or whether children gradually acquire it [13,14]. According to some proponents of theory theory, the fact that younger infants can pass spontaneous false-belief tests supports the existence of an innate module or specific theory of mind mechanism (ToMM) [12]. Adams [3 ] further argues that thinking of autism as a spectrum disorder increases the plausibility of conceiving of ToM as involving a domain-specific module (although he remains neutral on whether it is innate). Adams points out that there are important differences in how we conceive of ASDs and in how we study it, depending on whether the aim is to develop diagnostic criteria, to design therapeutic interventions, or to discover cognitive architecture. To identify the diagnostic criteria, it is best to think of ASDs as composed of a set of overlapping deficits and to conduct large-scale, longitudinal studies of an ASD population. In contrast, to design therapeutic interventions one needs to focus on the individual and to think of ASDs as involving a set of deficits that may or may not overlap. If the aim is to discover cognitive architecture, however, Adams suggests we need to focus on individuals who have one isolated (or near isolated) deficit. To the extent that we can find individuals on the spectrum with isolated deficits – for example, deficits in ToM but not deficits in communication, social norms or problems in perception and motor behavior – we find evidence for a ‘domain-specific module’ [3 ] [3 ,p. 8]. Although Adams assumes (as a matter of definition of spectrum disorder) that ‘each symptom of a spectrum disorder can occur independently of the other symptoms’, he admits that empirically no one has identified individuals with just a ToM deficit in isolation from other deficits. The assumption that a spectrum disorder can be defined as a disorder in which symptoms can occur &
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THEORY THEORY Theory theory approaches to mindreading contend that we understand others by making inferences about their mental states on the basis of a stored body of knowledge, a ToM or ‘folk psychology’. Pioneers in autism research developed the theory theory approach by showing that a majority of children with ASDs failed at mindreading tasks, 128
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in isolation from each other [3 ] conflicts with the idea that in ASD deficits are highly interconnected – involving a ‘cascade and then a tangle of secondary effects that become causes of other effects, which in turn become causes of further effects. . .’ [5 ] [5 , p. 238]. But it also runs into the practical difficulty that an isolated symptom, by itself, cannot be diagnosed as belonging to ASDs. For example, one finds problems with ToM in schizophrenia as well as in autism. The logic of identifying one isolated deficit to establish its domain-specific nature runs counter to the fact that one needs to look at more than one symptom to distinguish ASDs from other disorders and this suggests that an understanding of cognitive architecture cannot be separated from the search for diagnostic criteria. One challenge for the theory theory account is that a substantial minority of children with ASDs regularly manage to pass false-belief tasks [15,16 ]. Also, high-functioning adults with ASDs can make use of theoretical inference to mental states, although, as noted, they do not implicitly track false-belief states of others [10]. Scheeren et al. [16 ] offer a slightly different interpretation. They explore ToM in children and adolescents with highfunctioning ASDs using advanced ToM stories (second-order false-belief stories, emotional display rule stories, double bluff, faux pas, and sarcasm) without finding significant differences to typically developing children. The study concludes that individuals with high-functioning ASDs ‘seem to master the concept of ToM without mastering the ability to use such insight in the service of their ongoing social interactions’ [16 ] [16 ,p. 633]. This may be explained in a variety of ways, but one possibility is to argue that such ToM and false-belief tasks might not give us a good picture of core characteristics in social cognition [17]. Fisch [18] summarizes a number of problems with the theory theory approach to ASDs and suggests that a neurobiological (rather than neurocognitive) approach may be more productive. He points to research on mirror neurons and their involvement in social behavior and language as promising. &
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SIMULATION THEORY Mirror neurons are activated during performance of one’s own intentional actions and when one observes another’s intentional actions. Their discovery in the 1990s gave a big boost to simulation accounts of social cognition. Simulation theory challenges the idea that ‘folk psychology’ should be granted a key role in social cognition. Rather than employing a theory, simulation theory maintains that mindreaders consult their own minds, that is,
they run their own mechanisms in a pretense mode in order to simulate what another person might be thinking. In other words, to mindread or make sense of others, we simply use our own minds as models [19]. Some simulation theory proponents [20,21] have argued that deficits in simulation processes may be at the core of autistic problems with social cognition; they link such processes to the proper functioning of mirror neuron networks. Following this approach, Sato et al. [22] presented dynamic and static facial expressions to high-functioning adults with ASDs; they found that regions of the mirror network demonstrated weaker activity compared with typically developing individuals. Gallese et al. [23 ] provide an extensive review of the mirror neurons hypothesis on autism and the idea of ‘an action simulation deficit in individuals with autism’ (p. 20). On the one hand, evidence in favor of this hypothesis includes EEG studies showing that the mu frequency (the suppression of which has some correlation with activation in the mirror system) was not suppressed in individuals with ASDs during relevant tasks. Diminished activation of mirror neurons in individuals with ASDs has been shown in a variety of social cognition tasks, including imitation of facial expressions of basic emotions [24,25]. On the other hand, Gallese et al. [23 ] are careful to point out that there are a number of critical challenges to the mirror neuron hypothesis. For example, in individuals with ASDs, mirror neuron activation is not diminished under certain circumstances, namely, when a familiar agent does the observed action and when an action has a clear goal [26–28]. Schwarzkopf et al. [29] show that highfunctioning autistic individuals do not have problems with implicit perspective-taking (which may involve mirror neuron activation) but do have problems with more explicit perspective-taking (which may involve ToM-related processes). Other studies show no difference in mu suppression during observation of goal-directed action between individuals with ASDs and controls [30]. Keysers et al. [31] [31, p. 254] note that ‘research on the observation of hand actions has not lent strong support to the mirror neuron hypothesis of autism’, a conclusion supported more generally by Hamilton’s review that suggests ‘little evidence for a global dysfunction of the mirror system in autism’ [32 ] [32 ,p. 91]. More conceptual concerns about the interpretation of the mirror system as instantiating simulations have been raised in the philosophical literature. Given the various definitions of simulation (as involving pretense, or matching, or reuse of motor control mechanisms) found in the literature [33], it is not always clear that mirror neurons
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should count as embodying a simulation process [34]. Thus, although Gallese et al. [23 ] regard mirror neurons as constituting an ‘action-perception matching mechanism’, it is not clear that, outside of instances of imitation, one’s everyday interactions with others call for matching one’s motor system to theirs [35]. Whether or not one accepts the simulation theory interpretation of mirror neuron data, or works out an alternative nonsimulative interpretation, however, it is still likely that mirror neuron activation plays an important role in social cognition and is diminished in some aspects of ASD behavior. This has motivated suggestions that one possible therapeutic approach to autism could involve the use of brain–computer interface games that combine neuro-feedback and bio-feedback to induce neuroplastic changes leading to normalization of the mirror neuron system [36]. &&
INTERACTION THEORY Although there are important differences between simulation theory and theory theory, they share a commitment to the idea that our understanding of others proceeds by an inferential or projective attribution of causally efficacious mental states. In contrast, interaction theory and enactive accounts of cognition put more emphasis on embodied processes in social interaction and the direct perception of at least some mental states [35,37–39]. Interaction theory draws on the recent embodied and enactivist theories of perception and cognition, taking seriously the idea that the mind is embodied, that perception and action are closely related, and cognition need not always be mediated by internal representations [40]. In accordance with these theoretical commitments, interaction theory not only emphasizes the embodied nature of social cognition, but also holds that, in social contexts, perception serves interaction and that for most of our ordinary everyday interactions, we are not required to engage in implicit or explicit processes of mindreading [41]. It also draws on work in developmental psychology that emphasizes primary intersubjectivity and the role of sensory–motor processes in the early development of social interaction [42–47,48 ,49,50]. Processes of primary intersubjectivity that involve perception of the other’s bodily postures, movements, gestures, facial expressions, vocal intonations, etc., as well as dynamic embodied interactions, often in rich pragmatic and social contexts, allow young infants, as well as adults, to gain a basic sense of the intentions and emotions of others. According to interaction theory, such primary intersubjective processes progressively become more refined to the extent that in &
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many everyday interactions, we immediately understand the intentions, emotions, and actions of others without having to infer or simulate. Interaction theorists cite evidence that before reaching the developmental age associated with ToM, infants later diagnosed with autism already display significant problems in the sensory–motor behavior that may affect the aspects of primary intersubjectivity [50–53]. These include postural instabilities, atypical gait, mistiming of motor sequences, motor coordination problems, problems with anticipatory postural adjustments and expressionless faces (Ref. [23 ] provides a good review of the literature on these motor problems, also see, for example [37,54–57,58 ]). These problems may be attributable to growth errors in the brain development of embryo, fetus and infant [52]. Regardless of the cause, these motor problems involve disrupted timing in prospective motor control that interferes with the efficient integration of sensory–motor coordination and may lead to well known perceptual difficulties found in some cases of ASDs [37,59]. Such disorders are clearly documented in early childhood, when typically developing children engage in joint attention and joint action with others and learn to communicate. As developmental disorders more generally may involve sensory– motor difficulties, one needs to ask whether such difficulties can be definitive for ASDs. The recent work of Torres and colleagues is noteworthy in this regard. In individuals with ASDs, Torres et al. [60 ,61] demonstrate the occurrence of disrupted patterns in re-entrant (afferent and proprioceptive) sensory feedback that usually contributes to the autonomous regulation and coordination of motor output. Such feedback supports volitional control and fluid, flexible transitions between intentional and spontaneous behaviors. In ASDs, there is a disruption in the maturation of this form of proprioception, and this is accompanied by behavioral variability in motor control. In contrast to typically developing individuals, the normalized peak (micro-movement) velocity and noise-to-signal ratios in the movement of all participants with ASDs, across different ages and across different verbal or nonverbal status, remained in a region corresponding to younger (3-year-old) typically developing children. Proprioceptive input is random (unpredictable), noisy, and unreliable. Accordingly, individuals with ASDs have difficulty distinguishing goal-directed from goal-less motions in most tasks [60 ,61,62]. This suggests that individuals with ASDs may have trouble anticipating the consequences of their own impending movements in a timely fashion. Such disruptions may also make it difficult if not impossible to &&
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apply fine-tuned discriminations to the actions and emotional facial expressions of others during realtime social interactions. In effect, essential aspects of primary intersubjectivity, a pervasive and basic component of social interaction (early developed and typically sustained), are disrupted. The use of ToM strategies by high-functioning autistic individuals, then, may be compensatory for the loss of the more primary processes. The specificity found in Torres’ research may support an embodied-interaction approach to autism if it can be shown that such sensorymotor problems are ASD-specific. Accordingly, this research is important for addressing two questions requiring further research. First, are kinematic disruptions in autistic individuals different from those found in other developmental disabilities (e.g., Down syndrome, cerebral palsy, attention deficit hyperactivity disorder, and cerebellar ataxia)? Indeed, one objection to the interaction theory account could be that not all cases of motoric abnormality lead to problems with social cognition [55]. Second, knowing the precise character of the motor problems in autism may also help to determine proper therapies. Further research is required to know precisely whether and why and what therapies, involving, for example, imitation, interactive music, or movement [37,52], might work.
CONCLUSION We presented a brief overview of different theoretical frameworks offering alternative perspectives on the central characteristics in ASDs. The philosophical and interdisciplinary debate on the nature of social cognition has important implications for psychiatry, as different approaches to social cognition will likely support different ways of conceptualizing diagnosis and intervention. The outline provided here suggests it is unlikely that a single approach is able to explain all social cognition problems in autism. It is more plausible to think that, depending on the circumstances and on where one is located on the autistic spectrum, deficits in capacity for theoretical inference, or in some cases, compensatory routines that rely on theoretical inference, or deficits in simulation ability, and in very basic embodied interactive processes, need to be included in a best understanding relative to each autistic individual. One advantage of a pluralist approach to social cognition is that it is possible to understand ASDs as involving a variant range of (cascading) disrupted processes. Acknowledgements None.
Financial support and sponsorship S.G.’s work was supported by a professorial fellowship at the University of Wollongong, by the Marie-Curie Initial Training Network, ‘TESIS: Toward an Embodied Science of InterSubjectivity’ (FP7-PEOPLE-2010-ITN, 264828), European Commission Research, and by the Humboldt Foundation’s Anneliese Maier Research Award. Conflicts of interest None.
REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. Chawarska K, Macari S, Shic F. Decreased spontaneous attention to social scenes in 6-month-old infants later diagnosed with autism spectrum disorders. Biol Psychiatry 2013; 74:195–203. 2. Baron-Cohen S. Is autism necessarily a disability? Dev Psychopathol 2000; 12:489–500. 3. Adams M. Explaining the theory of mind deficit in autism spectrum disorder. & Philos Stud 2013; 163:233–249. This study suggests, first, that the issue of domain-specific ToM mechanism relates directly to the specific characterization of autism as a spectrum disorder, and second that there are important differences in how we conceive of and study ASDs, depending on whether the aim is to develop diagnostic criteria, to design therapeutic interventions, or to discover cognitive architecture. 4. Kana RK, Libero LE, Hu CP, et al. Functional brain networks and white matter underlying theory-of-mind in autism. Soc Cogn Affect Neurosci 2014; 9:98– 105. 5. Boucher J. Putting theory of mind in its place: psychological explanations of & the socio–emotional–communicative impairments in autistic spectrum disorder. Autism 2012; 16:226–246. This study argues that although explanations of early impaired mindreading are untenable, impairments of dyadic interaction in ASDs can lead to impaired ToM ability. 6. Pellicano E. Individual differences in executive function and central coherence predict developmental changes in theory of mind in autism. Dev Psychol 2010; 46:530–544. 7. Baron-Cohen S, Leslie A, Frith U. Does the autistic child have a theory of mind? Cognition 1985; 21:37–46. 8. Onishi KH, Baillargeon R. Do 15-month-old infants understand false beliefs? Science 2005; 308:255–258. 9. Schneider D, Slaughter VP, Dux PE. What do we know about implicit falsebelief tracking? Psychon Bull Rev 2014. [Epub ahead of print]. doi: 10.3758/ s13423-014-0644-z. 10. Schneider D, Slaughter VP, Bayliss AP, Dux PE. A temporally sustained implicit theory of mind deficit in autism spectrum disorders. Cognition 2013; 129:410–417. 11. Frith U. Why we need cognitive explanations of autism? Q J Exp Psychol 2012; 65:2073–2092. 12. Carruthers P. Mindreading in infancy. Mind Lang 2013; 28:141–172. 13. Carpendale JIM, Lewis C. The development of social understanding: A relational perspective. In: Overton W.F., editor. The handbook of lifespan development Volume 1: Cognition, biology, and methods across the lifespan. Hoboken, NJ: Wiley; 2010. pp. 548–627. 14. Meltzoff AN, Gopnik A. Learning about the mind from evidence: children’s development of intuitive theories of perception and personality. In: BaronCohen S, Lombardo M, Tager-Flusberg H, Cohen D, editors. Understanding other minds: perspectives from developmental social neuroscience. Oxford: Oxford University Press; 2013. pp. 19–34. 15. Iao LS, Leekam SR. Nonspecificity and theory of mind: new evidence from a nonverbal false-sign task and children with autism spectrum disorders. J Exp Child Psychol 2014; 122:1–20. 16. Scheeren AM, de Rosnay M, Koot HM, Begeer S. Rethinking theory of mind in & high-functioning autism spectrum disorder. J Child Psychol Psychiatry 2013; 54:628–635. This study demonstrates that high-functioning individuals with ASDs performed equally well on ToM tasks as typically developing peers. Counter to the predictions of ToM accounts, individuals with ASDs can master advanced mental state reasoning, but may still fail to apply these theoretical principles during everyday social interactions. 17. Bowler D. Autism spectrum disorders: psychological theory and research. West Sussex: John Wiley and Sons; 2000.
0951-7367 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved.
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Neurodevelopmental disorders 18. Fisch GS. Autism and epistemology IV: does autism need a theory of mind? Am J Med Genet Part A 2013; 161A:2464–2480. 19. Goldman AI. Joint ventures: mindreading, mirroring and embodied cognition. Oxford: Oxford University Press; 2013. 20. Iacoboni M, Dapretto M. The mirror neuron system and the consequences of its dysfunction. Nat Rev Neurosci 2006; 7:942–951. 21. Oberman LM, McCleery JP, Hubbard EM, et al. Developmental changes in mu suppression to observed and executed actions in autism spectrum disorders. Soc Cogn Affect Neurosci 2013; 8:300–304. 22. Sato W, Uono S, Toichi M. Atypical recognition of dynamic changes in facial expressions in autism spectrum disorders. Res Autism Spectr Disord 2013; 7:906–912. 23. Gallese V, Rochat MJ, Berchio C. The mirror mechanism and its potential role && in autism spectrum disorder. Dev Med Child Neurol 2013; 55:15–22. This is a theoretically well balanced review of the evidence for the involvement of mirror neurons in ASDs with a focus on pervasive motor, emotion, imitation and communication deficits in ASDs. 24. Dapretto M, Davies MS, Pfeifer JH, et al. Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders. Nat Neurosci 2006; 9:28–30. 25. Williams JH, Waiter GD, Gilchrist A, et al. Neural mechanisms of imitation and ‘mirror neuron’ functioning in autistic spectrum disorder. Neuropsychologia 2006; 44:610–621. 26. 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; 46:1558–1565. 27. Martineau J, Cochin S, Magne R, Barthelemy C. Impaired cortical activation in autistic children: is the mirror neuron system involved? Int J Psychophysiol 2008; 68:35–40. 28. Enticott PG, Kennedy HA, Rinehart NJ, et al. Interpersonal motor resonance in autism spectrum disorder: evidence against a global ‘mirror system’ deficit. Front Hum Neurosci 2013; 7:218. 29. Schwarzkopf S, Schilbach L, Vogeley K, Timmermans B. ‘Making it explicit’ makes a difference: evidence for a dissociation of spontaneous and intentional level 1 perspective taking in high-functioning autism. Cognition 2014; 131:345–354. 30. Fan YT, Decety J, Yang CY, et al. Unbroken mirror neurons in autism spectrum disorders. J Child Psychol Psychiatry 2010; 5:981–988. 31. Keysers C, Thioux M, Gazzola V. Mirror neuron system and social cognition. In: Baron-Cohen S, Lombardo M, Tager-Flusberg H, Cohen D, editors. Understanding other minds: perspectives from developmental social neuroscience. Oxford: Oxford University Press; 2013. pp. 233–256. 32. Hamilton AFDC. Reflecting on the mirror neuron system in autism: a sys& tematic review of current theories. Dev Cogn Neurosci 2013; 3:91–105. A systematic review of 25 published studies that use neuroscience methods to examine the mirror system in autism. This review concludes that current data are inconsistent and there is little evidence for a global dysfunction of the mirror system in autism. 33. Gallese V. Bodily selves in relation: embodied simulation as second-person perspective on intersubjectivity. Philos Trans R Soc 2014; B369:20130177; http://dx.doi.org/10.1098/rstb.2013.0177. 34. Gallagher S. Reuse and body-formatted representations in simulation theory. Cogn Syst Res 2015 (in press). 35. Gallagher S, Varga S. Social constraints on the direct perception of emotions and intentions. Topoi 2014; 33:185–199. doi: 10.1007/s11245-013-9203-x. 36. Friedrich EV, Suttie N, Sivanathan A, et al. Brain–computer interface game applications for combined neurofeedback and biofeedback treatment for children on the autism spectrum. Front Neuroeng 2014; 7:21. 37. De Jaegher H. Embodiment and sense-making in autism. Front Integr Neurosci 2013; 7:15. doi: 10.3389/fnint.2013.00015. 38. De Jaegher H, Di Paolo E, Gallagher S. Does social interaction constitute social cognition? Trends Cogn Sci 2010; 14:441–447. 39. Gallagher S. In defense of phenomenological approaches to social cognition: interacting with the critics. Rev Philos Psychol 2012; 3:187–212. 40. Hutto D, Myin E. Radicalizing enactivism: basic minds without content. Cambridge, MA: MIT Press; 2013.
132
www.co-psychiatry.com
41. Schilbach L, Timmermans B, Reddy V, et al. Toward a second-person neuroscience. Behav Brain Sci 2013; 36:393–414. 42. Ambrosini E, Reddy V, de Looper A, et al. Looking ahead: anticipatory gaze and motor ability in infancy. PLoS One 2013; 8:e67916. 43. Beurkens NM, Hobson JA, Hobson RP. Autism severity and qualities of parent–child relations. J Autism Dev Disord 2013; 43:168–178. 44. Hobson RP, Hobson JA. Autism: self and others. In: Baron-Cohen S, Lombardo M, Tager-Flusberg H, Cohen D, editors. Understanding other minds: perspectives from developmental social neuroscience. Oxford: Oxford University Press; 2013. pp. 397–412. 45. Hobson JA, Hobson RP, Cheung Y, Calo´ S. Symbolizing as interpersonally grounded shifts in meaning: social play in children with and without autism. J Autism Dev Disord 2015; 45:42–52. 46. Hobson JA, Hobson RP, Malik S, et al. The relation between social engagement and pretend play in autism. Br J Dev Psychol 2013; 31:114–127. 47. Reddy V, Markova G, Wallot S. Anticipatory adjustments to being picked up in infancy. PLoS One 2013; 8:e65289. 48. Savarese RJ. Moving the field: the sensorimotor perspective on autism. & Commentary. Front Integr Neurosci 2013; 7:6. doi: 10.3389/fnint. 2013.00006. This article is part of a special issue on sensorimotor approaches to ASDs. The author, in summarizing the recently developing evidence for sensorimotor deficit in ASDs, and its explanatory power, suggests a sea change in the approaches for understanding ASDs. 49. Rochat P. The gaze of others. In: Banaji M, Gelman S, editors. Navigating the social world: what infants, children, and other species can teach us. New York, NY: Oxford University Press; 2013. pp. 205–211. 50. Trevarthen C. Embodied human intersubjectivity: imaginative agency, to share meaning. Cogn Semiotics 2012; 4:6–56. 51. Gallagher S. Understanding problems in autism: interaction theory as an alternative to theory of mind. Philos Psychiatry Psychol 2004; 11:199–217. 52. Trevarthen C, Delafield-Butt JT. Autism as a developmental disorder in intentional movement and affective engagement. Front Integr Neurosci 2013; 7:49. 53. Teitelbaum PO, Teitelbaum J, Nye J, et al. Movement analysis in infancy may be useful for early diagnosis of autism. Proc Natl Acad Sci USA 1998; 95:13982–13987. 54. Cattaneo L, Fabbi-Destro M, Boria S, et al. Impairment of actions chains in autism and its possible role in intention understanding. Proc Natl Acad Sci USA 2008; 104:17825–17830. 55. Cook JL, Blakemore SJ, Press C. Atypical basic movement kinematics in autism spectrum conditions. Brain 2013; 136:2816–2824. 56. Hilton C, Zhang Y, White M, et al. Motor impairment concordant and discordant for autism spectrum disorders. Autism 2012; 16:430–441. 57. Fabbri-Destro M, Cattaneo L, Boria S, Rizzolatti G. Planning actions in autism. Exp Brain Res 2009; 192:521–525. 58. Whyatt C, Craig C. Sensory–motor problems in autism. Front Integr Neurosci & 2013; 7:51. Kinematic studies of impaired use of perception–action coupling for guidance of movement shows inflexible and rigid motor profiles in ASDs. This study suggests that impairments of perception–action coupling are primary rather than secondary impairments and should be considered a fundamental aspect of ASDs. 59. David N, Schultz J, Milne E, et al. Right temporoparietal gray matter predicts accuracy of social perception in the autism spectrum. J Autism Dev Disord 2014; 44:1433–1446. 60. Torres EB, Brincker M, Isenhower RW, et al. Autism: the micro-movement && perspective. Front Integr Neurosci 2013; 7:32. doi: 10.3389/fnint.2013. 00032. This study shows the innovative use of methods for measuring deficits in reafferent kinesthetic features of movement in ASDs using a unifying statistical framework. This study shows that in ASDs, there is a disruption in the maturation of proprioceptive–kinesthetic feedback. 61. Torres EB. Atypical signatures of motor variability found in an individual with ASD. Neurocase 2013; 19:150–165. 62. Brincker M, Torres EB. Noise from the periphery in autism. Front Integr Neurosci 2013; 7:34.
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