Looking back: A continuing journey

Patricia Howlin considers where more than 70 years of research and intervention has left us in understanding autism

It is now more than 70 years since Kanner (1943) first described the condition he named ‘childhood psychosis’ but which is now known today as autism or autism spectrum disorder (APA, 2013). This special issue therefore presents a timely opportunity to consider the many changes that have taken place in psychologists’ understanding of autism over the past seven decades.

Epidemiology
Initially considered to be a very rare condition, prevalence estimates for autism have increased steadily over the decades. Early epidemiological studies were fairly consistent in suggesting rates of around 0.4 per 1000. However, following the inclusion of autism as a specific disorder in the DSM-III in 1980, clinicians and educators became increasingly aware of the condition. It was also evident that autism occurred in individuals of all levels of ability, from profound intellectual disability to superior IQ, and that it affected adults as well as children. Thus, prevalence estimates have been steadily revised upwards over the years, with recent figures from the Centers for Disease Control and Prevention in the US (CDCP, 2014), for example suggesting rates of 14.7 per 1000 (i.e. 1 in 68 children, although it should be noted that the estimate range varies widely from around 5 to 21 per 1000). There is as yet no evidence that this increase in prevalence estimates reflects a real rise in incidence and, although that remains a possibility, the change in estimates is generally thought to represent increased awareness of autism among many different groups of professionals as well as by the general public. Suggestions of an ‘epidemic of autism’ remain without foundation.

Classification
When autism was first described in the 1940s psychodynamic theories of causation and treatment pervaded much of psychology and psychiatry. Kanner, along with others at the time, regarded autism as ‘the earliest manifestation of childhood schizophrenia’ noting that ‘I do not believe that early infantile autism will at any future time… be separated from the schizophrenias’ (1949). Indeed, one of the leading journals in this field (now the Journal of Autism and Developmental Disorders) was originally called the Journal of Autism and Childhood Schizophrenia.

Experimental and clinical studies conducted during the late 1960s and 1970s contributed to increasing awareness of the distinction between autism and other psychiatric or developmental disorders. Early research and reviews by Michael Rutter (1968, 1972) for example, provided clear evidence of the differences between autism and schizophrenia. In 1970, Hermelin and O’Connor published their classic text Psychological Experiments with Autistic Children in which, via a series of innovative and imaginative experiments, they demonstrated the many cognitive differences between children with autism and children with intellectual disabilities. Their work, and subsequent experimental studies by Uta Frith (cf. Frith, 1989) also highlighted particular areas of skill among children with autism, as well as areas of deficit.

Many other studies of the characteristic cognitive phenotype associated with autism, and how this differed from other disorders, also emerged during the 1970s. Rutter (1968) had already highlighted the central role of social communication deficits in autism, while Uta Frith’s studies of cognitive processing first brought attention to the deficits in ‘mentalising’ or understanding others’ minds that are characteristic of the disorder (Frith, 1989). Her work was a spur to many other studies of cognitive functioning by individuals such as Francesca Happé and Simon Baron-Cohen, leading to theories about the potential roles of ‘theory of mind’, weak central coherence or executive functioning deficits in determining how individuals with autism experience and relate to the world about them. Frith was also responsible for translating Hans Asperger’s accounts of autistic psychopathy in childhood (Frith, 1991) and in highlighting both the similarities and differences between his accounts and those of Kanner.

As functional imaging techniques became increasingly available to experimental psychologists, it became possible to explore the difference between autism and other conditions in much greater depth. However, although resulting in various different theories about cognitive and social processing, brain localisation and function (and lots of pretty pictures), many of these studies have involved very small or poorly ascertained groups of participants, and use experimental paradigms that only distally represent real-world interactions. Thus, although it is now evident that changes in brain structure, functioning and connectivity are associated with autism (Ecker & Murphy, 2014) the condition is characterised by wide aetiological and phenotypic heterogeneity. There are currently no imaging techniques that can reliably identify autism at an individual level, and claims for various other biologically based diagnostic techniques (e.g. blood samples or measurement of head circumference) remain without foundation.

Causation
As with schizophrenia, autism was initially viewed by many as being caused by disruptions to early ego development, which, in turn, were attributed to inadequate or insensitive parenting. Although Kanner himself initially believed that the signs of autism appeared so early in life that they must be due to ‘inborn disturbances of affective contact’ he subsequently wrote extensively on the ‘coldness and obsessiveness’ of many parents (Kanner, 1949). He viewed the condition as a combination of biologically based perturbations of development combined with unfavourable environmental factors; but a much more extreme, and widely popularised theory, was that of Bettelheim (1967). He considered autism to be directly caused by parental pathology and that it could only be cured by separating children from their parents – a theory that resulted in unnecessary distress for parents in many countries of the world.

Psychoanalytical views about parents’ role in aetiology proved very difficult to dispel despite growing recognition of the association between autism and organic conditions (e.g. links with epilepsy, thalidomide, or rubella virus, etc.)

Early suggestions that autism might be due to genetic causes were also dismissed, but twin and family studies conducted by teams of psychologists and psychiatrists in the 1970s and 80s began to provide strong evidence of the highly heritable nature of autism. However, despite recurrent media claims that the ‘gene for autism’ has been discovered, the genetic mechanisms involved in autism remain uncertain. Both common and rare genetic variations have been identified in families with a child with autism, but the role of these variants is unknown. Moreover, many of these variants have also been identified in other psychiatric conditions, such as schizophrenia, depression, bipolar disorder and ADHD (Smoller et al., 2013).

Intervention
Theories about the role of ‘refrigerator’ parents took many years to dispel and resulted in early-intervention programmes frequently being psychodynamic in approach. The first empirical psychological studies to disprove the theory of parental inadequacy/pathology were conducted by Rutter and colleagues (Cox et al., 1975). They were able to demonstrate that there were no differences in parenting style, parenting characteristics or psychopathology in parents of children with autism compared with parents of children with other communication disorders. The comparative lack of effectiveness of psychoanalytic-based therapies compared with more structured educational approaches for school-aged children was also confirmed by the same research group (Rutter & Bartak, 1973). 

In the US, too, from the late 1960s onwards, there was a rapid growth in the use of operant-based techniques with children with autism. These initially focused on the elimination of ‘challenging behaviours’ (often using aversive procedures including electric shock), with a very mechanistic approach to teaching developmental skills, and somewhat simplistic notions of reinforcement (food rewards predominated). However, they did provide evidence that the behaviours of children with autism, far from being irreversible, could be significantly modified. Unfortunately most of the children involved in these programmes were treated as inpatients, often over long periods of time, with the result that when they returned to their families any advances that they had made while in hospital tended to disappear.

Eric Schopler was among the first to emphasise the importance of working with parents as co-therapists (Schopler et al., 1982). His TEACCH programme (Treatment and Education of Autistic and related Communication handicapped Children), whilst based on behavioural principles, focused on the generalisation of life skills to the child’s regular environment. Ivar Lovaas, one of the earliest proponents of operant techniques for children with autism also became aware that the direct involvement of parents was necessary in order to achieve successful generalisation and maintenance of behaviours. However, his claim (Lovaas. 1987) that 40 hours a week of early, intensive home-based behavioural intervention (EIBI) for two years or more could result in ‘normal’ functioning has continued to generate much controversy. Although, when compared with ‘treatment as usual’, early intensive programmes supervised by highly trained (and expensive) consultants have been found to result in greater intellectual and/or behavioural improvements at a group level, individual change is much more variable (Magiati et al., 2012).

Over the last two decades interventions based on behavioural strategies have continued to be the predominant approach to psycho-social problems. However, these have moved a long way from the mechanistic approaches of the early 1970s, which paid little attention to normal developmental trajectories, or the importance of learning in naturalistic settings. The Early Start Denver Model (Rogers & Dawson, 2010) for example is founded on behavioural principles but also takes account of normal developmental processes and sequences. In particular, there is a strong focus on reciprocal social interaction, and evidence from a randomised control trial suggests that children involved in the programme (20 hours a week over two years) showed greater improvement in cognitive and language abilities and adaptive behaviour and fewer autism symptoms than did non-treated children. Several other recent randomised control trials add to the evidence base for early social communication focused programmes, designed to encourage parental synchrony (see Kasari and Patterson, 2012). Language training programmes, too, have moved a long way from the very mechanistic sound imitation procedures of the 1970s, with the focus being much more on reciprocity between adult and child, using multiple communication forms.

For older children, there is now a wide range of different approaches available to enhance social skills or deficits related to ‘theory of mind’ (Green et al., 2010; Kasari & Patterson, 2012); the effectiveness of cognitive behavioural therapy is also being explored in the treatment of comorbid mental health problems (Moree and Davis, 2010).

Although initial findings from such research are encouraging, there remains great variation in treatment response (both among individual children and according to the different domains assessed); evidence of generalisation of treatment effects to new skills or new settings is limited, and there is no evidence of long-term impact or significant improvements in functioning in later childhood/adolescence. Claims, for example, that two years of EIBI result in significant lifetime savings are both spurious and misleading. Research into the individual characteristics of children or families that are related to outcome is also in its infancy although more recent treatment trials are beginning to focus much more on moderating and mediating factors that are associated with treatment outcomes.

It is important, too, to recognise that most intervention research continues to focus on children who come predominantly from relatively high-functioning, middle-class families who have the resources to participate in clinical studies. This excludes the majority of children with autism, and future research needs to include these underrepresented groups to broaden our understanding of intervention effectiveness (Kasari & Patterson, 2012). A further need is to focus more on the development of effective short-term programmes that will help to improve access to high-quality treatment for a majority of children with autism, not just the privileged few.

Finally, it is crucial to recognise that autism is not a childhood disorder. Individuals are adults with autism much longer than they are children with autism. Autism does not disappear at age 18, but unfortunately most interventions and support networks do! Several recent studies and systematic reviews have highlighted both the scarcity of studies of adults with autism and the poor quality of what little intervention research does exist. As highlighted by Piven and colleagues (2011), we need systematic studies on the characteristics (behavioural, neuropsychiatric and medical) associated with ageing in autism, and potential interventions, both individual and societal, that may improve outcome and quality of life. If the advances in comprehensive treatment programmes for very young children can be applied across the lifespan, then the current generation of children with autism may face a more positive future.

Patricia Howlin is Emeritus Professor of Clinical Child Psychology at the Institute of Psychiatry, London
[email protected]


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