Studies of structural language in individuals with autistic spectrum disorder (ASD) are reviewed, and theories of the causes of structural language anomalies and impairments in ASD are presented and discussed. It is concluded that the factors that may contribute to language impairment in individuals with ASD are many and various; that impaired mindreading is always implicated, but that some additional and critical causal factor remains to be conclusively identified.

Introduction

Languages, defined in formal or structural terms, are systems of mainly arbitrary items (e.g. sounds, signs or written letters; morphemes; words) with rules for combining items to convey meaning to others with shared knowledge of the language. Language can be analysed and characterised at the level of grammar (morphology and syntax) and meaning (semantics); and, in the case of spoken language, phonology.

Communication, on the other hand, involves the use of language in social interaction, whether directly in face-to-face talk, or indirectly as in, for example, a recorded phone message or a Last Will and Testament. Thus, language is a means, or method, of communicating. Non-linguistic, or non-verbal, signals including facial expression, gesture, and body language also provide means, or methods, of communicating. Prosody, which involves the use of vocal tone, pitch, rhythm and inflexion during speech also comes under the heading of non-verbal communication. Factors influencing the communicative use of language and non-verbal communication signals in specific instances can be analysed and characterised in the study of pragmatics.

Introduction

Memory can be impaired by brain damage at any age. Developmental memory disorders can result from genetic factors or genetic/environmental interactions which prevent the brain from developing normally; or from early-acquired brain lesions. Developmental memory problems are likely to resemble adult memory problems with respect to specific deficits in information processing that depend on dedicated brain structures where there is little scope for transfer of function, as may be true of the medial temporal lobes (MTL) (Bachevalier, this volume, Chapter 2).

The effects of developmental memory problems are, however, likely to differ from the effects of adult-acquired memory problems in several ways. On the one hand, they may have a cumulative effect in so far as they slow or prevent the acquisition of knowledge critical for the development of social skills, language and crystallized intelligence. As a result, developmental memory problems may produce much more severe social, linguistic and cognitive disruption than adult memory problems, as appears to be the case in infant-lesioned as opposed to adult-lesioned primates (Bachevalier, this volume, Chapter 2). Conversely, early-acquired disorders could allow the acquisition of better compensatory strategies and coping skills than occurs in adult-acquired disorders. Also, if a structure has never been functional or even present, other brain structures will not have to adapt to working with it and then without it, so that their functioning may be more optimal.

Introduction

Over the last two decades most psychological and neuropsychological research into autism has focused on individuals with Asperger syndrome or high-functioning autism (HFA), rather than on individuals with low functioning autism (LFA) or what is termed autistic disorder in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV; American Psychiatric Association, 1994). The core symptoms of autism, namely impairments of social interaction, communication and behavioural flexibility, are more likely to occur in pure form in people with HFA than people with LFA, and it makes sense, therefore, to focus on HFA to improve understanding of the core impairments.

A consequence of this strategy, however, has been a relative neglect of the impairments of language and intellectual ability that distinguish LFA from HFA. This is regrettable for both practical and theoretical reasons. From a practical point of view the combined effects of cognitive and linguistic impairments with autism are devastating for individuals themselves, and for their families and carers. Better understanding of the additional impairments is needed to provide optimal interventions and care. From a theoretical point of view, familial and genetic studies indicate that vulnerability to language impairment is related to vulnerability to autism (e.g. Bolton et al., 1994; Piven & Palmer, 1997; Folstein et al., 1999; Tomblin, Hafeman & O'Brien, 2003; Bartlett et al., 2004). Understanding the bases of the language impairment in LFA should therefore contribute to understanding autism as a whole.

Despite the fact that memory in people with autism spectrum disorders (ASD) has been researched for over fifty years, there has been very little in the way of attempts to synthesize or codify the findings. The two most notable such attempts are the seminal monographs Psychological Experiments with Autistic Children (Hermelin & O'Connor, 1970) and Seeing and Hearing and Space and Time (O'Connor & Hermelin, 1978), now over thirty years old. The period since the publication of these two books has seen considerable changes in the landscape of autism research, the most important of which have been an enlargement of the concept of ‘autism’ to encompass a spectrum of conditions that includes but is not limited to that first described by Kanner (1943), and the mushrooming of research into all aspects of the spectrum.

Memory research has grown in parallel with this general increase. One of us (JB) was heavily involved in the early phase of this growth, in particular developing the hypothesis that the patterning of memory functions, at least in lower-functioning individuals with ASD, had some parallels with that seen in the amnesic syndrome. This work continued into the 1980s but then diminished, partly because of the lack of a community of scholars interested in the topic, but also because memory was not seen as a particular problem in those high-functioning individuals who were becoming the main focus of research.