In the time since the condition was originally labelled in 1943, a wide range of theories have been put forward to explain the emergence, maintenance, and treatment of autism. There is often controversy in this area, as different paradigms often disagree about the aetiology of autism and its subsequent treatment. This paper reviews and compares conceptualisations of autism based on the psychoanalytic and cognitive paradigms, exploring separate theories within these models such as weak central coherence, theory of mind, executive function, autistic identification, drives and attachment in autism, and refrigerator mother theory. The cognitive and psychoanalytic models approaches to treatment and their subsequent effectiveness are also reviewed, and consideration is given to controversies in the treatment of this pervasive developmental disorder. It is concluded based on the available literature that the psychodynamic model focuses primarily on the emergence and causes of autism, whereas the cognitive model is more concerned with the maintenance of the disorder and its cognitive consequences and symptoms, whilst neither give sufficient consideration to its treatment.
Autism is a pervasive developmental disorder characterised by deficits in social behaviour and communication and unusual and restricted, repetitive behaviours (APA, 2000). Since Leo Kanner first labelled and described the condition in 1943, there have been a number of attempts to explain this disorder. Two important paradigms that have made contributions are the cognitive and the psychodynamic paradigm. This paper will examine and critically evaluate the contribution that these models have made to the understanding of the emergence, maintenance, and treatment of autism.
The Cognitive Model and Autism
Since its rise to popularity in recent decades, the cognitive model has contributed considerably to the understanding of autism. Autism is characterised not only by social deficits but also by deficits in cognitive control (Dichter & Belger, 2007), with most autistic children having impairments in at least one area of cognitive functioning (Szelag et al., 2004). Cognitive symptoms and social symptoms may in fact overlap and be related to one another; Shah & Wing (1986) argue that the social deficit observed in autism is directly related to the level of general cognitive function. Cognitive “scripts” of specific events and the usual procedures surrounding them have been found to be deficient in autism, in particular in terms of scripts for social routines, which may account for a number of the social deficits observed ( Trillingsgaard, 1999).
The most common view of autism is that it is primarily a deficit in communication skills, with deficits such as stereotyped conversations, echolia, and a lack of understanding of metaphors and non-verbal behaviour (e.g., Siegel, 1998). Autistic individuals are poor at remembering verbal sounds (Gervais et al., 2004), which may explain the limited attention paid to voices and the inability to infer emotional meaning from voices (Gervais et al., 2004). Autistic individuals also have trouble recognising emotional expressions (Dichter & Belger, 2007). Autistic children also have abnormal sensory input, in particular integrating different sensory modalities, and thinking and interests are rigid, with poor conceptual reasoning ( Bjorne & Balkenius, 2005; Rumsey & Hamburger, 1988) .
Cognitive development in autism
A number of computational models of autism have been developed to explain the processes involved in the abnormal cognitive development of autism ( Bjorne & Balkenius, 2005). Such models have been used to suggest that a single cognitive impairment early in life can lead to an array of problems along the cognitive developmental pathway, eventually leading to the collection of cognitive deficits known as autism ( Bjorne & Balkenius, 2005). Focusing on the cognitive developmental pathway of autism can lead to a greater understanding in terms of causes and potential treatment ( Bjorne & Balkenius, 2005), as a number of cognitive variables have been found to predict long-term outcome (Nordin & Gillberg, 1998). It has been suggested that autism is a combination of a number of cognitive disorders (Baron-Cohen & Swettenham, 1997). However, there are 3 main cognitive theories of autism which will be examined in this paper; weak central coherence, deficient theory of mind, and executive dysfunction.
The weak central coherence theory of autism (Frith, 1989) suggests that symptoms observed in autism are due to a style of cognition termed weak central coherence. This refers to a limited ability to understand the context in which events occur, an inability to see the “big picture.” This results in autistic individuals taking things literally, such as not being able to understand metaphors or sarcasm. Computational models have used the principles of weak central coherence to account for both the poor generalisation and poor context processing observed in autism (Cohen, 1994; Bjorne & Balkenius, 2005 ). Weak central coherence seems to be a separate factor in autistic cognition ( Teunisse et al., 2004). However, it may not be related to the behavioural symptoms of the disorder as weak central coherence is not related to either social competence or severity of symptoms ( Teunisse et al., 2004). Thus it may be a consequence of autism rather than a cause.
Theory of mind
“Theory of mind” refers to the ability to infer what others are thinking so that it is possible to predict their behaviour (Happé, 1999). Baron-Cohen (1995) originally proposed that autistic individuals do not have this important part of social cognition. They cannot tell what others are thinking, hence the reason they do not respond to facial expressions or tone of voice. According to Baron-Cohen (1995), a lack of a theory of mind is the main cognitive component of autism and can explain a number of the observable social deficiencies in autism, such as low levels of social eye contact. This lack of a theory of mind has been found consistently in autism and has been argued to be crucial in the cause of the disorder (Travis & Sigman, 1998). However, others have argued that it does not account for all of the deficits observed (Smukler, 2005). Happé et al. (2001) argue that the theory of mind account of autism is useful in explaining many of the social and communication deficits observed, however it cannot account for other symptoms such as repetitive behaviours and restriction of interests. Furthermore there is evidence that a lack of a theory of mind cannot explain all of the deficit social behaviour in autism; for example it has been shown that training to improve theory of mind does not improve social skills (Ozonoff & Miller, 1995). Thus it may be that theory of mind is an important factor in the cognitive aspects of autism, however it is unlikely to account for the range of symptoms associated with the disorder.
Ozonoff et al. (1991, 1994) first proposed the executive dysfunction model for autism. “Executive function” refers to the complicated cognitive capacities used to control action and motor co-ordination, in particular in unusual circumstances. Included in this therefore is planning behaviour, observing behaviour, using working memory, and inhibiting automatic reactions. This model has been used to successfully explain a number of symptoms, in particular such executive impairment can account for the repetitive and restricted behaviour observed in autistic children (Pennington et al., 1997). Cognitive shifting, an important part of executive function, has been found to predict poor social abilities in adulthood and is the only factor that can predict improved social intelligence in autistic individuals (Nordin & Gillberg, 1998). However, whilst executive dysfunction can explain certain deficits, it cannot account for the areas of cognition that are intact or superior (Happe et al., 2001).
Cognitive accounts of autism have lead to a number of cognitive approaches to its treatment. A number try to improve the sensory abnormalities in autistic children, with an important therapy being auditory integration training that attempts to reduce sensitive hearing (Smith, 1996). This has been argued to improve a number of cognitive deficits such as memory and language comprehension (Stehli, 1991), though others only suggest very limited or no benefits (Rimland & Edelson, 1995; Mudford et al., 2000). Due to the nature of autism Cognitive Behaviour Therapy (CBT) has not been considered to be appropriate, however evidence suggests that a modification of CBT techniques may be useful for the treatment of autism (Laskaridou & Tagouli, 2007). A number of aspects of cognitive functioning such as cognitive shifting and central coherence have been found to predict long-term outcome, yet have not been applied to treatment programmes despite having significant potential (Berger et al., 1993; Teunisse et al., 2004). Improving social functioning is one of the most important goals in terms of the treatment of autism (Teunisse et al., 2004); whilst certain treatments have been found to have a positive impact on social skills (Howlin, 1997), those using cognitive principles have been less effective (Ozonoff & Miller, 1995). Because aspects of cognition vary considerably between individuals, a purely cognitive treatment for all may be inefficient (Baron-Cohen & Swettenham, 1997).
Psychoanalysis and Autism
Since autism was first described by Kanner in 1943, psychoanalysis has contributed to understanding the emergence, maintenance, and treatment of autism. Psychoanalysts view autism as a disorder in which the development of a sense of self and a sense of others is altered dramatically (Mayes & Cohen, 1994). Autism is explained through psychoanalytic concepts such as a dysfunctional emergence of the self, internalization, identification, and introjection (Mayes & Cohen, 1994). Autism can be conceptualised through object relations theory as the prolonging of a stage in normal development where object relations feature prominently in perception (Hobson, 1990). Psychoanalytic explanations focus less on the cognitive symptoms and more on the social deficits observed (Hobson, 1990). Autism differs from other childhood psychiatric disorders as there is a significant disconnection from the outside world, and there are two main psychoanalytic explanations for this aspect of autism (Fendik, 2005). One is that the disorder is a regression to an earlier stage of development; another holds that autistic behaviour is a defence mechanism in response to extremely stressful situations.
There are a number of sources of evidence that support psychoanalytic views of autism (Volkmar, 2000). Early psychoanalysts believed that the experience of autistic children played a role in the pathology, and a number of studies have suggested that autistic children have a qualitatively different experience in psychoanalytic terms, with problems in object relations and other aspects of ego development, which are responsible for the social abnormalities observed in the condition (Volkmar, 2000). Many early psychoanalysts believed that autism is psychogenic, and this can still be found in such approaches today (Hobson, 2005).
It has been argued that the mechanisms of social engagement, which lead to identification as outlined by Freud are crucial in autistic development (Hobson, 2005). Meltzer (1975) developed a model of autism based on three main ideas: the dismantling of the ego, adhesive identification, and the bio-dimensionality of object relations. The dismantling of the ego refers to the notion that autistic children split their ego across the different senses so that they can never properly perceive the world around them, and all sensations are combined. The biodimensionality of object relations refers to how the autistic child relates to libidinal objects, with an inability to see beyond the surface of objects. This relates in biodimensionality whereby the self identifies with only the surface of objects, which leads to a difficulty of articulating thoughts. Tustin (1977) similarly explained autism in terms of an infant having a fear of a discontinuity between their body and the outside world. The infant protects itself from this fear by constructing the illusion that is merged as one with the outside world.
Drives and autism
Freud’s original concepts of drives have been especially influential in psychodynamic explanations of the causes of autism. Adhesive identification is often seen in autism and results from the transfer of energy from the death drive and the libido when these drives are being defused (Ribas, 1998). Thus autism can be viewed as the diffusion of drives, in particular the death drive. The role of the libido in autism in terms of the diffusion of energy has been neglected, but it may explain the phenomenon of adhesiveness and auto-sensuality observed in autism (Ribas, 1998). There is a lack of unity in terms of the integration of the self, and there is a lack of projection in autistic children.
Refrigerator mother theory
Bettelheim argued that autism is caused by “refrigerator” mothers; autism is a defence mechanism against cold, emotionless, and detached mothers (Gardner, 2000). Autistic children are been raised in unstimulating and uncaring homes during the early stages of development where language and social skills usually develop. Mothers do not interact with their children enough, and this is the underlying cause of autism. A number of psychoanalysts such as Tustin (1981) agree with this conceptualisation, claiming that problems in the behaviour of mothers to their children are responsible for autistic behaviour. Bettelheim claimed that using this principle he was able to cure 85% of his autistic patients, however this has been subsequently shown to be inaccurate (Pollak, 1997). Despite no experimental research to provide evidence for the refrigerator mother theory of autism, a number of psychoanalysts continue to follow these ideas (Roser, 1996).
The relevance of attachment to autism has been noted since the first description of the disorder by Kanner (1943) who noted the inability to form emotional affection with others. The DSM-III made the distinction between childhood schizophrenia and autism in terms of attachment behaviour (APA, 1980). Rutgers et al. (2004) argue that a lack of early and secure attachment leads to the social isolation observed in autism. Although autistic children show attachment behaviours, they are significantly less securely attached (Rutgers et al., 2004) and cannot be comforted by their caregiver (Shirataki, 1994). Such disturbances in the mother-daughter relationship have been shown to have severe and long-lasting effects (Robson, 1972), and socially isolated monkeys behave in such a similar way to autistic children that it has been argued that autism is a result of a social isolation from parents (Harlow & McKinney, 1971). However differences in attachment behaviour in autism have been refuted by a number of studies (Sigman & Ungerer, 1984; Dissanayake & Rossley, 1996), and the cause-effect nature of any relationship is unclear.
Despite a number of objections, psychoanalytic theories continue to be applied to the treatment of autism (Bromfield, 2000). Psychodynamic interventions concentrate on the worker-child relationship, rather than directly attempting to induce behavioural change (Helm, 1976), and the importance of a close encounter between the practitioner and child is stressed (Dessiex et al., 2001). Holding therapy focuses on the autistic child’s relationship with the mother, with physical affection being encouraged (Welch, 1988). The refrigerator mother theory of autism has been particular important in influencing interventions, and in the 1950’s and 60’s psychoanalytic play therapy based on these principles was the most common treatment used for autism (Howlin, 1997). It has been argued that intensive psychoanalytic psychotherapy can improve autistic children’s long-term prognosis, but that this is often overlooked (Langdell, 1973) and that using counter-transference is especially useful in improving prognosis ( Parada, 1996 ). However others argue that the blame that is put on parents and the lack of goals and structure can in fact worsen behaviour in autistic children (Smith, 1996).
Controversies in Treatment
Regardless of the approach used, whether autism can be treated at all is controversial (Charman, 1999). Autism has long been seen as a disorder with lifelong morbidity, with such a poor prognosis to the extent that it has been deemed to be incurable (Rutter, 1970). Autism has been described for a long time as a disorder for which the cause is unclear, and treatment even less clear (Moore & Shiek, 1971). The American Academy of Child and Adolescent Psychiatry’s official policy is that "it now appears that the usefulness of psychotherapy in autism is very limited" (AACAP, 1999). Psychotherapy for autism may not be effective regardless of whether the cognitive or psychodynamic approach is used. As with all treatments for autism, neither approach has received sufficient empirical study of its effectiveness (Howlin, 1997; Campbell et al., 1996).
The psychodynamic and cognitive models have both been used to explain the emergence and maintenance of autism and attempted subsequently to suggest treatments. These theories focus on very different aspects of autistic behaviour, with the cognitive model concentrating on deficits in areas such as theory of mind and executive function, whilst the psychodynamic model concentrates primarily on parent relationships and upbringing. It seems that the psychodynamic model focuses primarily on the emergence and causes of autism, whereas the cognitive model is more concerned with the maintenance of the disorder and its cognitive consequences and symptoms. Neither in fact gives much attention to its treatment, though this maybe simply due to the previously stated assumption that autism is incurable. It has been argued that the cognitive account of autism is the more accurate representation of the disorder, and that psychodynamic explanations focus too heavily on specific aspects of the disorder (Frith, 1989). However this criticism could work both ways. Both psychodynamic and cognitive models tend to explain autism in terms of a single unitary deficit accounting for all of the observed symptoms. However there is insufficient evidence to suggest that autism is the result of a unitary deficit, and it may be that no single theory or approach can adequately account for the wide-ranging symptoms of the disorder (Szelag et al., 2004). This author believes that the cognitive model provides a more accurate account of the emergence and maintenance of autism, though this may simply appear to be the case due to the difficulty in testing psychodynamic conceptualisations of this disorder. This paper concludes that the cognitive model needs to focus on combinations of cognitive symptoms, and begin to move away from the unitary deficit theories that dominate the paradigm today. In terms of the treatment, though the two models examined here propose very different treatments, it seems that neither can cure autism, though there is more evidence at present to suggest that cognitive approaches have the greatest potential to improve the prognosis of autistic children.
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