The target article focuses on the phenomenology of neonatal imitation, a topic that has received considerable attention in the past decades. Its wide appeal results in part from the suggestion that neonatal imitation has a crucial role not only in the development of more complex imitative skills, but also as a building block of social cognition (Meltzoff & Decety Reference Meltzoff and Decety2003). This view would imply that humans – at least to some extent – are wired to imitate and socially interact. At the neural level, some theorists – as also reported by Keven & Akins (K&A) – implicate mirror mechanisms in neonatal imitation (Simpson et al. Reference Simpson, Murray, Paukner and Ferrari2014a) and imitative phenomena in general (Iacoboni Reference Iacoboni2009b). As such, anomalies in brain mechanisms supporting imitation may trigger a cascade of effects on the acquisition of imitative and social skills, ultimately contributing to social interaction difficulties, such as those characterizing autism spectrum disorder (ASD; e.g., Casartelli & Molteni Reference Casartelli and Molteni2014; Kana et al. Reference Kana, Wadsworth and Travers2011). Although this perspective on the functional and developmental role of imitation has long been the mainstream view in developmental brain sciences, we posit, in line with K&A, that conceptual and experimental caveats continue to undermine the notion of imitation. For instance, the reliability of neonatal imitation in predicting future social skills is controversial, and recent longitudinal evidence even challenges the existence of neonatal imitation in humans (Oostenbroek et al. Reference Oostenbroek, Suddendorf, Nielsen, Redshaw, Kennedy-Costantini, Davis, Clark and Slaughter2016; Simpson et al. Reference Simpson, Miller, Ferrari, Suomi and Paukner2016). Furthermore, following K&A's proposal, behaviors such as orofacial stereotypies are crucial to the maturation of the neonate's skillset, but they are not necessarily imitative instances. We may question whether the reasons that have sustained interest in the concept of imitation (i.e., its role as building block in social skills) would survive in the absence of a nativist model for neonatal imitation. Indeed, to consider neonatal imitation as innate is the classical way to bridge the gap between elementary and more complex (i.e., socially relevant) imitative phenomena. To contribute to this debate and, more generally, to understand the functional and developmental role of imitation in typical and atypical brain development, we stress the need to conceptually clarify the definition of imitation and reframe it in more operational terms. This may prove meaningful not only from a basic research perspective, but also from a clinical viewpoint. Below, we propose three initial considerations in this direction.
1. Separating origin and function of imitation
Since Meltzoff and Moore (Reference Meltzoff and Moore1977) first uncovered the ability of newborns to imitate adults' facial gestures, the study of neonatal imitation has aimed to define its contribution to the emergence of subsequent complex imitative and social skills. The questions of how and when the social value of imitation appears are surely interesting, but are secondary to understanding its function. Accordingly, we should not confound the origin and function of imitation. We claim that regardless of when the social properties of imitation emerge across maturation, and irrespective of their underlying mechanisms (e.g., genetics, learning, or both), the study of its features is crucial to describe (a)typical developmental trajectories. For example, this may help shed light on the pathophysiological mechanisms of ASD.
2. Imitation as a multi-level concept
We argue for an update to the concept of imitation into more basic components with distinct, although potentially interconnected, layers. This could reduce the ambiguities of experimental findings on imitation (for a similar debate on theory of mind, see Schaafsma et al. Reference Schaafsma, Pfaff, Spunt and Adolphs2015). Addressing imitation as a multi-level construct will facilitate the identification (and empirical testing) of specific sub-processes, reflecting different degrees of abstraction. In line with studies on motor cognition focused on mirror-based motor action/intention understanding (for a review, see Rizzolatti & Sinigaglia Reference Rizzolatti and Sinigaglia2010), we propose a similar conceptual framework for imitation. Thus, to imitate can refer to the imitation of proximal goal/motor act (e.g., to grasp an apple), or of distal goal/motor action (e.g., to grasp an apple to eat it). To imitate can also refer to the imitation of “motor prosody” or “motor style” (e.g., to grasp an apple to eat it gently; see also Casartelli & Molteni Reference Casartelli and Molteni2014). As long as we consider imitation as a monolithic process, these levels are neglected, and in turn, imitative phenomena (whether impaired or preserved) can potentially be misinterpreted. This is critical in the context of ASD in which misleading results or misinterpretations may bias clinical practice.
3. Imitative phenomena, motor interference, and ASD.
Reformulating the concept of imitation as a multi-layer construct offers additional opportunities to evaluate markers that differentiate how neurotypical and ASD individuals encode (imitative) actions. Compelling studies describe how the social and nonsocial cues may affect motor output (e.g., during imitative tasks), raising alternative hypotheses on how social cues affect action production and/or action understanding mechanisms in ASD individuals. Thus, either ASD individuals do not attend to social cues that influence motor output, or they atypically select and/or process such cues. Studies on gaze processing and action in ASD individuals support a sort of immunity of the motor system to social cue interference (Becchio et al. Reference Becchio, Pierno, Mari, Lusher and Castiello2007). However, studies on visuo-olfactomotor interference propend for atypical social cue interference. Indeed, children with ASD show preserved automatic imitation (namely, the kinematics of their movement are facilitated following the observation of a model performing the same action) only when action observation occurs in the presence of the maternal body odor (Parma et al. Reference Parma, Bulgheroni, Tirindelli and Castiello2013). In other words, an olfactory social cue is able to kinematically perturb an imitative action (see the notion of “motor interference” in Casartelli et al. Reference Casartelli, Molteni and Ronconi2016) in an anomalous way with respect to neurotypical individuals. Systematically assessing if and how social stimuli interfere with imitation, and whether this is explained by mirror mechanisms, may be an effective way to characterize atypical developmental trajectories in ASD.
The present commentary praises K&A's assessment of the development of imitation through a sensorimotor lens, and extends it with a perspective on how motor cognition may shape the concept of imitation. We propose a revision of the concept of imitation centered on its multi-layer nature. Besides revealing typical developmental trajectories, this approach represents an intriguing tool to study the pathophysiology of ASD with potential impacts on clinical practice (Ronconi et al. Reference Ronconi, Molteni and Casartelli2016).
The target article focuses on the phenomenology of neonatal imitation, a topic that has received considerable attention in the past decades. Its wide appeal results in part from the suggestion that neonatal imitation has a crucial role not only in the development of more complex imitative skills, but also as a building block of social cognition (Meltzoff & Decety Reference Meltzoff and Decety2003). This view would imply that humans – at least to some extent – are wired to imitate and socially interact. At the neural level, some theorists – as also reported by Keven & Akins (K&A) – implicate mirror mechanisms in neonatal imitation (Simpson et al. Reference Simpson, Murray, Paukner and Ferrari2014a) and imitative phenomena in general (Iacoboni Reference Iacoboni2009b). As such, anomalies in brain mechanisms supporting imitation may trigger a cascade of effects on the acquisition of imitative and social skills, ultimately contributing to social interaction difficulties, such as those characterizing autism spectrum disorder (ASD; e.g., Casartelli & Molteni Reference Casartelli and Molteni2014; Kana et al. Reference Kana, Wadsworth and Travers2011). Although this perspective on the functional and developmental role of imitation has long been the mainstream view in developmental brain sciences, we posit, in line with K&A, that conceptual and experimental caveats continue to undermine the notion of imitation. For instance, the reliability of neonatal imitation in predicting future social skills is controversial, and recent longitudinal evidence even challenges the existence of neonatal imitation in humans (Oostenbroek et al. Reference Oostenbroek, Suddendorf, Nielsen, Redshaw, Kennedy-Costantini, Davis, Clark and Slaughter2016; Simpson et al. Reference Simpson, Miller, Ferrari, Suomi and Paukner2016). Furthermore, following K&A's proposal, behaviors such as orofacial stereotypies are crucial to the maturation of the neonate's skillset, but they are not necessarily imitative instances. We may question whether the reasons that have sustained interest in the concept of imitation (i.e., its role as building block in social skills) would survive in the absence of a nativist model for neonatal imitation. Indeed, to consider neonatal imitation as innate is the classical way to bridge the gap between elementary and more complex (i.e., socially relevant) imitative phenomena. To contribute to this debate and, more generally, to understand the functional and developmental role of imitation in typical and atypical brain development, we stress the need to conceptually clarify the definition of imitation and reframe it in more operational terms. This may prove meaningful not only from a basic research perspective, but also from a clinical viewpoint. Below, we propose three initial considerations in this direction.
1. Separating origin and function of imitation
Since Meltzoff and Moore (Reference Meltzoff and Moore1977) first uncovered the ability of newborns to imitate adults' facial gestures, the study of neonatal imitation has aimed to define its contribution to the emergence of subsequent complex imitative and social skills. The questions of how and when the social value of imitation appears are surely interesting, but are secondary to understanding its function. Accordingly, we should not confound the origin and function of imitation. We claim that regardless of when the social properties of imitation emerge across maturation, and irrespective of their underlying mechanisms (e.g., genetics, learning, or both), the study of its features is crucial to describe (a)typical developmental trajectories. For example, this may help shed light on the pathophysiological mechanisms of ASD.
2. Imitation as a multi-level concept
We argue for an update to the concept of imitation into more basic components with distinct, although potentially interconnected, layers. This could reduce the ambiguities of experimental findings on imitation (for a similar debate on theory of mind, see Schaafsma et al. Reference Schaafsma, Pfaff, Spunt and Adolphs2015). Addressing imitation as a multi-level construct will facilitate the identification (and empirical testing) of specific sub-processes, reflecting different degrees of abstraction. In line with studies on motor cognition focused on mirror-based motor action/intention understanding (for a review, see Rizzolatti & Sinigaglia Reference Rizzolatti and Sinigaglia2010), we propose a similar conceptual framework for imitation. Thus, to imitate can refer to the imitation of proximal goal/motor act (e.g., to grasp an apple), or of distal goal/motor action (e.g., to grasp an apple to eat it). To imitate can also refer to the imitation of “motor prosody” or “motor style” (e.g., to grasp an apple to eat it gently; see also Casartelli & Molteni Reference Casartelli and Molteni2014). As long as we consider imitation as a monolithic process, these levels are neglected, and in turn, imitative phenomena (whether impaired or preserved) can potentially be misinterpreted. This is critical in the context of ASD in which misleading results or misinterpretations may bias clinical practice.
3. Imitative phenomena, motor interference, and ASD.
Reformulating the concept of imitation as a multi-layer construct offers additional opportunities to evaluate markers that differentiate how neurotypical and ASD individuals encode (imitative) actions. Compelling studies describe how the social and nonsocial cues may affect motor output (e.g., during imitative tasks), raising alternative hypotheses on how social cues affect action production and/or action understanding mechanisms in ASD individuals. Thus, either ASD individuals do not attend to social cues that influence motor output, or they atypically select and/or process such cues. Studies on gaze processing and action in ASD individuals support a sort of immunity of the motor system to social cue interference (Becchio et al. Reference Becchio, Pierno, Mari, Lusher and Castiello2007). However, studies on visuo-olfactomotor interference propend for atypical social cue interference. Indeed, children with ASD show preserved automatic imitation (namely, the kinematics of their movement are facilitated following the observation of a model performing the same action) only when action observation occurs in the presence of the maternal body odor (Parma et al. Reference Parma, Bulgheroni, Tirindelli and Castiello2013). In other words, an olfactory social cue is able to kinematically perturb an imitative action (see the notion of “motor interference” in Casartelli et al. Reference Casartelli, Molteni and Ronconi2016) in an anomalous way with respect to neurotypical individuals. Systematically assessing if and how social stimuli interfere with imitation, and whether this is explained by mirror mechanisms, may be an effective way to characterize atypical developmental trajectories in ASD.
The present commentary praises K&A's assessment of the development of imitation through a sensorimotor lens, and extends it with a perspective on how motor cognition may shape the concept of imitation. We propose a revision of the concept of imitation centered on its multi-layer nature. Besides revealing typical developmental trajectories, this approach represents an intriguing tool to study the pathophysiology of ASD with potential impacts on clinical practice (Ronconi et al. Reference Ronconi, Molteni and Casartelli2016).
ACKNOWLEDGMENTS
LC was supported by a grant by the Italian Ministry of Health (Ricerca Corrente 2016–2018). We sincerely thank Elizabeth McDevitt for her useful suggestions.