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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.
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.
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.
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.
Many people with autism spectrum disorders (ASDs) are remarkably proficient at remembering how things look and sound, even years after an event. They are also good at rote learning and establishing habits and routines. Some even have encyclopaedic memories. However, all individuals with ASD have difficulty in recalling personal memories and reliving experiences, and less able people may have additional difficulty in memorising facts. This book assembles research on memory in autism to examine why this happens and the effects it has on people's lives. The contributors utilise advances in the understanding of normal memory systems and their breakdown as frameworks for analysing the neuropsychology and neurobiology of memory in autism. The unique patterning of memory functions across the spectrum illuminates difficulties with sense of self, emotion processing, mental time travel, language and learning, providing a window into the nature and causes of autism itself.
Frith has argued that people with autism show “weak central coherence,” an unusual bias toward piecemeal rather than configurational processing and a reduction in the normal tendency to process information in context. However, the precise cognitive and neurological mechanisms underlying weak central coherence are still unknown. We propose the hypothesis that the features of autism associated with weak central coherence result from a reduction in the integration of specialized local neural networks in the brain caused by a deficit in temporal binding. The visuoperceptual anomalies associated with weak central coherence may be attributed to a reduction in synchronization of high-frequency gamma activity between local networks processing local features. The failure to utilize context in language processing in autism can be explained in similar terms. Temporal binding deficits could also contribute to executive dysfunction in autism and to some of the deficits in socialization and communication.
It is well established that people with autism have impaired face processing, but much less is
known about voice processing in autism. Four experiments were therefore carried out to
assess (1) familiar voice-face and sound-object matching; (2) familiar voice recognition; (3)
unfamiliar voice discrimination; and (4) vocal affect naming and vocal-facial affect matching.
In Experiments 1 and 2 language-matched children with specific language impairment (SLI)
were the controls. In Experiments 3 and 4 language-matched children with SLI and young
mainstream children were the controls. The results were unexpected: the children with
autism were not impaired relative to controls on Experiments 1, 2 and 3, and were superior
to the children with SLI on both parts of Experiment 4, although impaired on affect
matching relative to the mainstream children. These results are interpreted in terms of an
unexpected impairment of voice processing in the children with SLI associated partly, but
not wholly, with an impairment of cross-modal processing. Performance on the experimental
tasks was not associated with verbal or nonverbal ability in either of the clinical groups. The
implications of these findings for understanding autism and SLI are discussed.
Dienes & Perner's target article contains numerous but
unsystematic references to the implicit or explicit knowledge of the
temporal context of a known state of affairs such as may constitute the
content of a propositional attitude. In this commentary, the forms of
cognition that, according to D&P, require only implicit knowledge of
time are contrasted with those for which explicit temporal knowledge is
needed. It is suggested that the explicit representation of time may
have been important in human evolution and that certain developmental
disorders including autism may be (partly) caused by defective ability
to represent time.