A similar proposal can be made for the autistic syndrome in children. The autistic syndrome is a severe and chronic developmental disorder characterized by social and communicative deficits and by a reduced interest in the environment, towards which restricted and often stereotyped initiatives are taken . To be an autistic child means, with variable degrees of severity, to be incapable of establishing meaningful social communications and bonds, to establish visual contact with the world of others, to share attention with the others, and to be incapable of imitating others' behavior or of understanding others' intentions, emotions and sensations.
I would like to briefly focus on some of the early symptoms. Towards the end of the first year of life, autistic children experience difficulties or even impossibility in orientating themselves on the basis of cues provided by others. They are incapable of sharing attention with others, incapable of reacting in a congruent fashion to others' emotions. They are also highly impaired in their ability to recognize human faces or display imitative behaviors. All of these early manifestations of autism share a common root: the cognitive skills required to establish meaningful bonds with others are missing or seriously impaired.
My hypothesis is that these deficits are to be ascribed to a deficit or malfunctioning of "intentional attunement." If it is true-as held through-
out this chapter-that at the basis of our social competence is first of all the capacity to constitute an implicit and directly shared interpersonal meaningful space, enabling us to establish a link with the multiple intentional relations instantiated by others, then it follows that a disruption of this shared manifold should be the core problem of the autistic mind. Incapacity to develop a full and comprehensive intentional attunement with others implies as a consequence the development of an incomplete or malfunctioning shared manifold.
The lack of full-blown intentional attunement will produce various and diversified cognitive and executive deficits, all sharing the same functional origin: a lack or malfunctioning of embodied simulation routines, probably underpinned by impairments in connectivity and/or functioning of the mirror neuron system. If my hypothesis is correct, the posited intentional attunement deficit should become manifest at the various levels of social cognition it normally underpins. A series of experimental data seems to suggest this to be the case.
A recent study investigating postural adjustments in autistic children has shown that, unlike healthy individuals, they use motor strategies basically relying on feed-back information, rather than on feed-forward modes of control. This disturbance of executive control strategies prevents autistic children from adopting anticipatory postural adjustments . Given the functional characterization of forward models as simulation-based, it is difficult not to interpret these data as evidence of a simulation deficit. Such postural deficits are not intrinsically social; however, they stem from a disruption within the executive control domain of a functional mechanism-simulation-that I proposed to be at the root of the constitution of the shared experiential interpersonal space.
Two recent studies employing different techniques such as electroen-cephalography and TMS show that individuals with autistic spectrum disorder (ASD) might be suffering an action simulation deficit induced by a dysfunction of their mirror system for action. The study by Oberman et al.  showed that individuals with ASD, unlike healthy controls, did not show mu frequency suppression over the sensorimotor cortex during action observation. The study by Theoret et al.  showed that, again unlike healthy controls, individuals with ASD did not show TMS-induced hand muscle facilitation during hand action observation.
A further indication of simulation deficits in the autistic syndrome is exemplified by imitation deficits. Autistic children have problems in both symbolic and nonsymbolic imitative behaviors, in imitating the use of objects, in imitating facial gestures and in vocal imitation . These deficits characterize both high- and low-functioning forms of autism. Furthermore, imitation deficits are apparent not only in comparison with the performances of healthy subjects, but also with those of mentally disabled nonautistic subjects. According to my hypothesis, imitation deficits in autism are caused by the inability to establish a motor equivalence between demonstrator and imitator, most likely due to malfunctioning of the mirror neuron system, or because of disrupted emotional/affective regulation of the same system. Imitation deficits thus can be characterized as further examples of a disrupted shared manifold.
Let me now briefly turn to emotional/affective deficits. Several studies have reported the severe problems autistic children experience in the facial expression of emotions and the understanding of the same in others [80-83]. Furthermore, Hobson and Lee  reported that autistic children score much worse than healthy controls in reproducing the affective qualities of observed actions. All these deficits can be framed as affective attunement deficits, hence as further instantiations of a lacunate shared manifold.
My hypothesis for interpreting the autistic syndrome as an intentional attunement deficit is quite divergent from many of the mainstream ideas concerning the origin of this developmental disorder. One of the most credited theories on autism, despite its varying-and not always congruent-articulations, posits that autism is caused by a deficit in a specific mind module, the "theory of mind" module, selected in the course of evolution to build theories about the mind of others [85-87]. One of the problems of this theory is that it is hard to reconcile it with what we learn from the reports of some high-functioning autistic individuals. What they claim is that in order to understand how they supposedly should feel in given social contexts, and what others supposedly feel and think in those same contexts, they have to rely on theorizing. What these reports seem to suggest is that theorizing about the minds of others is not quite the basic deficit, but the only compensating strategy available in the absence of more elementary and basic cognitive skills enabling a direct experiential take on the world of others. Furthermore, a recent study carried out on a patient who suffered a focal bilateral lesion of the anterior cingulate cortex, previously identified as the candidate site for the theory of mind module, showed no evidence of mind-reading deficits .
The shared manifold of intersubjectivity and the intentional attune-ment it generates constitute a general hypothesis on social cognition [20-21,35] that can be empirically tested at multiple levels in both healthy and psychotic individuals. Furthermore, this proposal and the approach es it generates have the merit of revealing the possibility of establishing more insightful therapeutic bonds with psychotic patients.
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