Eye-contact and complex dynamic systems--论文代写范文精选

早些时候的直接目光接触，提出的失败可能导致自闭症,包括电视/视频,因此会统计这与自闭症有关。最近证实,自闭症与室内活动和电缆的引入有关。这是最合理的解释吗?早期接触电视/视频与自闭症有关。下面的essay代写范文将进行详述。

Abstract
Estimates of autism’s incidence increased 5-10 fold in ten years, an increase which cannot be genetic. Though many mutations are associated with autism, no mutation seems directly to cause autism. We need to find the direct cause. Complexity science provides a new paradigm - confirmed in biology by extensive hard data. Both the body and the personality are complex dynamic systems which spontaneously self-organize from simple dynamic systems. Autism may therefore be caused by the failure of a simple dynamic system.

We know that infants who cannot track their mother’s face often become autistic, that eye-contact initiates intersubjectivity which is blocked in autism, and that the infant-mother pair seems designed to promote eye-contact, as does the eye’s appearance. This author earlier proposed that failure of eye-contact might directly cause autism and that early non-maternal childcare, including television/video, would therefore be statistically linked to autism.

Waldman et al. (2008; 2006) recently proved that autism is strongly linked to precipitation (indoor activity) and to the introduction of cable. The most plausible explanation? Early exposure to television/video is linked to autism. Furthermore a normal developmental cascade (blocked in autism) has been deciphered: (a) Infant-mother eye-contact triggers increased maternal attention. (b) Early maternal attention permanently increases not only baseline vasopressin but also that oxytocin release which is triggered by subsequent maternal attention. (c) Vasopressin and oxytocin promote face recognition, gazing-at-the-eyes, emotion recognition, and social bonding.

Introduction
This paper attempts to show why an experimental hypothesis is plausible and merits testing. In brief the hypothesis is that autism begins with a failure in early learning and that changing the environment of early learning would dramatically change the incidence of the syndrome. Strong statistical evidence which supports this hypothesis has already been published by Waldman et al. (2008) but to date that evidence has largely been ignored, perhaps because it challenges prevalent beliefs about autism.

This paper also suggests that the current epidemic of autism is serious enough, and intellectually mysterious enough, to merit attention from a wider community of cognitive scientists: new ideas are needed. A confirmation of this paper’s hypothesis would have interesting implications for cognitive science.

Most clinicians and researchers in the field of autism (Hobson 2002; Klin and Jones 2007; Johnson and Morton 2009; Baron-Cohen 1994) agree that autism is a pervasive developmental disorder, that is, that a primary deficit in the fetus or infant begins (to a greater or lesser degree) a cascade of secondary developmental failures which constitute the autistic syndrome. After decades of research, however, the primary deficit has not been identified (Ungerer 1989; Muratori & Maestro 2007). This paper departs from the work of the researchers listed above only in arguing that the primary deficit which begins the cascade of developmental failures is not a genetic defect but is instead a failure in early learning.

Autism calls for an interdisciplinary approach; such an approach is difficult because insights from unfamiliar disciplines may not be well understood. Geneticists have found that autism is strongly associated with a large variety of genetic lesions. Understandably, geneticists emphasize the relevance of their own results for research in autism. Researchers who are not themselves geneticists have tended to overlook the important distinction between a genetic association and a genetic cause. This has led to the widespread assumption that autism is initiated/caused by a genetic defect.

Current research on the first causes of autism
Working with infants (or older children), several teams of researchers have recently described anatomical or behavioral traits which are correlated with autism. These researchers tend to assume that such traits are genetically determined. In no case, however, have they eliminated the possibility that the trait might be acquired by experience in the first days, months, or years after birth.

In their discussion of ‘embodied psychoanalysis’ Klin and Jones (2007) elaborate Hobson’s (2002) view that autism needs to be understood in the context of an ‘enactive mind’, that is, a mind which emerges as a result of the interactions an infant almost inevitably has with his/her environment. When these interactions are disrupted, autism may be the result. However Ami Klin and his associates (Kaiser et al. 2010) assume that such disruptions are initially caused by ‘strongly genetic neurodevelopmental’ defects. Kaiser et al. used functional magnetic resonance imaging with 4 to 17-year-old children and detected neural signatures which characterize ‘the disruption in brain circuitry’ associated with autism spectrum disorders.

Working with 30-month-old children Chawarsaki et al. (2010) showed that children with autism show atyptical ease of disengagement from attending to faces. In a 15-month-old infant with autism Klin and Jones (2008) observed altered face scanning and impaired recognition of biological motion. In two-year-olds with autism, Klin et al. (2009) identified abnormalities eye-tracking behavior and abnormalities in tracking of point-light displays of biological motion. Drawing upon an earlier claim by Simion et al. (2008) that ‘newborns have a predisposition for biological motion’, Klin et al. suggested that autism may result from ‘neurobiological anomalies that predispose’ an infant not to attend preferentially to biological motion.

Simion et al. (2008) claimed that two-day-old infants show spontaneous preferences for biological vs. nonbiological point-light animations. A viewing of Simion et al.’s point-light animations (available online, ibid), however, suggests that their results may be an artifact of experimental design. What they term ‘biological motion’ may be any motion in which the movement of points of light is coordinated to create contrasts of direction and speed, that is, in which visual stimuli reinforce each other: the authors may simply be detecting a newborn’s stronger response to stronger stimuli. These authors also observed a (smaller) preference for upright vs upside-down ‘biological motion’, but this observation might also be an artifact: a newborn might, for example, respond more strongly to stimuli in the lower half of its visual field.

Baron-Cohen et al. (2005) suggest that some aspects of autistic neuroanatomy may be extremes of typical male neuroanatomy. This extends Baron-Cohen’s (2003) argument that impaired empathizing and enhanced systematizing, both of which are characteristic of autism, are extremes of normal male characteristics. Chakrabarti et al. (2009) showed that sex steroid-related gene variations are associated with autistic traits in adults. As I explain later in this paper, such associations, if confirmed, would say nothing about direct causes: they would prove only that there is an indirect link.

Auyeung et al. (2010), associates of Simon Baron-Cohen, have shown that elevated foetal testosterone levels are positively correlated with psychological autistic traits in 18 to 24-month toddlers. They conclude that ‘given that sex steroid-related gene variations are associated with autistic traits in adults, this new finding suggests that the brain basis of autistic traits may reflect individual differences in prenatal androgens and androgen-related genes.’ It has not been proven, however, that autism originates in brain anatomy: differences in brain anatomy may be secondary to an early disruption in learning. Furthermore this research does not give evidence of direct causation. Prenatal androgen levels might promote autism indirectly by affecting post-natal learning processes.

Bergman (1985) documented the healing of an autistic child through psychoanalytic treatment. Deborah Fien (Poitras 2010) recently documented that at least 10%, and perhaps 20% of children who have clearly satisfied the criteria for a diagnosis of autism or autism spectrum disorder are able, given intensive behavioral therapy before age 4 or 5, to ‘move off the autism spectrum’. These results are not consistent with genetic causation because a genetic deficit is unlikely to be reversed by psychoanalytic or behavioral therapy.

Autism spectrum disorders and intelligence
The autistic syndrome varies greatly in severity. A child with Asperger’s syndrome (mild or high-functioning autism) has normal intelligence and language but has a social deficit and a narrow range of interests and activities (Rapin 1997). A child with classic autism may sometimes have high intelligence, but has more severe social symptoms including:

marked impairment ... of nonverbal behavior such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interactions; failure to develop peer relationships; ... lack of showing, bringing, or pointing out objects of interest; lack of social or emotional reciprocity; failure to distinguish among persons; language that is not used for ... interpersonal communication, but is characterized by echolalia and references to the self in third person (ibid).
Hans Asperger (1944; Frith 1991) found that Asperger’s individuals could be highly successful in intellectual pursuits:

To our own amazement, we have seen that autistic individuals, as long as they are intellectually intact, can almost always achieve professional success, usually in highly specialized academic professions, often in very high positions, with a preference for abstract content. We found a large number of people whose mathematical ability determines their professions; mathematicians, technologists, industrial chemists and high-ranking civil servants.
It is common for scientists and mathematicians to show some degree of Asperger’s traits (Baron-Cohen et al. 2001). According to standard criteria it seems very likely that Newton, Einstein, and Cavendish had Asperger’s syndrome (James 2003). Because autism is sometimes associated with high intelligence its immediate cause does not necessarily affect intelligence: it’s immediate cause must specifically target social abilities.

Endnotes

1. The terms ‘mother’ and ‘maternal’ refer to the very early mothering function, which may sometimes be fulfilled by a person other than the mother.

2. Earlier I proposed that the failure was to acquire or retain the image of the mother’s eye. Eye-contact itself is a more measurable phenomenon. Eye-contact requires recognition which requires that the infant acquire an image, in some sense, of the mother’s eye. 

3. Molecular biologists have described in fine detail the mechanisms by which macromolecules self organize. In their writing, however, molecular biologists do not always distinguish between the invariance of primary structure (invariant because it is directly specified by genes) and the invariance of secondary, tertiary, and quaternary structure (invariant because, in the normal intracellular environment, the outcome of macromolecular self-organization is predictable). 

4. This account, including my use of ordinal numbers, is highly schematic. My purpose is to clarify the hierarchical nature of complexity in biological systems. 

5. This inclusive definition is compatible with most theories of personality, for example with trait, type, psychoanalytic, behaviorist, social cognitive, and humanistic theories. It also recognizes that psychological life is in large part interpersonal, that is, residing in the exchange between people as they relate to each other. I give objective evidence for the centrality of the interpersonal in section 8.6.3.

6. Some of the personality emerges though interactions with impersonal factors in the environment. （essay代写)

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