Causes and treatment

So far the underlying condition of autism has been untreatable though many meliorative forms of treatment have been tried, with limited success. There is no consensus about the fundamental causes of autism. It is more clear what autism is not rather than what it is. Autism is not just a variety of mental retardation or a form of childhood schizophrenia. There are three principal theories, competing but not necessarily mutually incompatible. The first is that autism is the product of faulty emotional attachment between the parent and the infant. Treatment flowing from this approach concentrates on breaking down parent/child emotional barriers. This approach is not accepted by most of those working professionally with autistic children insofar as it implies that parents are to blame for their children's autism. The second theory is that there is an important genetic component - this indeed seems likely but does not go far to explain the character of autism or to indicate how it should be treated. The third theory is that there are faults in pre-natal and post-natal neural development, in the maturation of the brain. Neural connections which make possible the transfer of experience from one sensory modality to another are not made or are not functional. In the absence of the normal translation of sensations into percepts and concepts, the autistic child is unable to organise appropriate response to the outside world. It has been suggested that the faulty brain development may be due to excessive neurone proliferation; in post-mortem examination of autistic patients, increased neurone density has been found. This could reflect abnormality in the process of selective cell death, by which the appropriate pattern of connections is established. Some practical treatment is based on this; it takes the form of controlled patterning of the movements of autistic children in the hope that this will establish the neural connections that should have resulted from normal development.
The plausibility of this developmental view of autism depends on the extent to which it is coherent with current theory of normal pre-natal and post- natal cerebral development. Some of the most valuable work on this has been by Trevarthen(1990), from whom the following account is largely derived. In normal development the child acquires before birth an array of communication capabilities, for imitation, motor control, response to facial expression, systematic links between vision and action. These capabilities are essential for maturation of the infant's brain through interaction with the parent; the infant's communication abilities are matched to those of the parent. Applied to autism, this account would bring together the concept of autism as a developmental neural failure and autism as related to emotional communication between parent and child; the parent is not the cause of the child's autism but is the agent responsible for normal development. The autistic child, for genetic or other reasons, lacks the neural connections which would enable it to take part in co-ordinated communication with the parent.
The failure of development in autism can be contrasted with what is known or hypothesised about normal pre-natal and post-natal cerebral development. A brain that is already very elaborate soon after birth, reaches full maturity with exceptional slowness. After a maximum rate of growth from the mid-fetal stage, the human brain continues a rapid size increase for one and one-half years after birth. Between birth and one year, it more than doubles in weight, by three it reaches 80 per cent of the adult brain size Other processes proceed almost as if birth had never happened: proliferation of synapses, branching of dendrites, changes in the density of dendritic spines, changes in connectivity.
Trevarthen (1984: 253 ff.) says that the neural basis for empathic response would underlie imitation in both directions. Although infants do learn by imitation, the structural foundations for the imitative movements cannot be learned. It is necessary to assume an innate structure that at least partly matches the structure of the adult models to explain both imitation and more complex reciprocal or complementary interactions which are characteristic of communication between child and adult from immediately after birth. This theory would explain transmission of culture in terms of a specific and highly active epigenetic program for brain growth that needs brain- brain interaction, a companionship formed by emotions,in the context of an intimate relationship between infant and mother: immature brains and mature brains entering into a long program of emotion-guided communication. Before a baby gains postural stability, it has refined awareness of other persons and their emotions. By the end of the first month, a full-term infant can join in a 'proto-conversation' looking at the mother intently. The evidence indicates that infants are born with a considerable part of the neural structures that will coordinate the functional patterns of muscle activity in adults,
How does this kind of approach relate to, have points of contact with what the motor theory proposes? For language, the theory suggests, there must be the development of neural connections linking perception, motor control and language. Only if this happens will the child find it easy, natural, to acquire the phonemes of whatever happens to be the mother-language. Only if these neural connections are made will there be an easy and natural relation between the structures of words and the visual (or other) percepts or actions to which the words relate. Only if the necessary neural connections between neural motor sequencing and language sequencing will the infant be able easily and naturally to acquire grammatical features,, the concept of word-order, the use of function-words, etc. The emphasis laid by the motor theory on the cross-modal aspects of language, on language in use as a continual neural restructuring, on the vital importance of the primitive motor-elements, seems to have very direct relevance.