During the first half of twentieth century, there were variety of descriptions for autistic-like syndromes. The terminology was primarily used to reflect the general assumption that autism was the very early onset of adult-type psychoses. The syndrome identified in 1943 by a psychiatrist, Leo Kanner, who distinguished the characteristics and symptoms of autism so that it could be differentiated from mental retardation or childhood schizophrenia. The most fundamental symptom of autism as he described it was “extreme autistic aloneness” and he spent further emphasis on the emotional coldness and obsessive qualities that he saw in the parents.
In his research, Kanner’s description of the syndrome of infantile autism was an exception to preceding misconceptions. He set his diagnostic criteria based on specific child behaviors as he observed them rather than in terms of modifications of adult-psychosis criteria. Furthermore, it is often hard to differentiate between autism and mental retardation because most of autistic children score below 70 on IQ tests. Patients of Autism were characterized by an inability to relate themselves to other people, a delay in the acquisition of speech together with abnormalities of language, an excellent rote memory, and an obsessive desire for the maintenance of sameness.
Kanner also suggested that although patients had some inborn unitary defect, the disorder was, in part, due to lack of affection from parents and concluded that Autism was partly psychogenic due to “emotional refrigeration”. It is considered as a serious abnormality in the developmental process that manifest in early infancy, therefore it also differed from symptoms of childhood schizophrenia. It is for this reason that the American Psychiatric Association (1980) classification, DSM-III, categorized autism under pervasive developmental disorders. APA and the World Health Organization concentrated on four main sets of diagnostic criteria.
The first requirement for the criteria was that the disorder be manifested before 30 months of age. This criterion led to some confusion because it is often hard to distinguish between specific autistic features from other developmental disorders but it is useful to separate those late onset conditions from autism. However, it doesn’t answer the question that whether autism that has been preceded by normal development differs in any fundamental way from autism with developmental abnormality from the outset. The second diagnostic criteria “…concerns various aspects of deviance in the development of social relationships” (Rutter & Schopler, 1987). It is important to take in to account that some delay or impairment in social development could also be caused by mental handicap independent from autism. It is crucial that social abnormalities are defined by deviance and by their relation to child’s age and cognitive abilities.
Moreover, it is important to identify the features of the social abnormalities and distinguish them from nonspecific features that could be the product of something other than autism. The third diagnostic criterion comprises abnormalities in communicative process. The basic deficit is the lack of capacity, creativity and spontaneity to use language for social communication. Further more, autistic children fail to initiate or sustain conversational exchange, and they have repetitive and stereotyped use of language. It is important to make the distinction here that autistic children not only fail to use language but their communicative process is impaired. The fourth set of diagnostic criteria deals with the restricted, repetitive and compulsive patterns of behavior. These behavioral patterns include; preoccupation with restricted patterns of interest, attachments to unusual objects, compulsive rituals, and distress over changes in details of environment (Rutter and Schopler, 1987).
As pointed out there is no apparent recognizable separation point between autism and other disorders that share some behavioral features but not all of the diagnostic criteria. Therefore, it is a better method to understand this behavioral disorder in terms of conceptualized dimensions rather than categorical terms. The features that separate autistic children from nonautictic children of comparable mental age are then important to point out. These features are: abnormalities in the detection of socioemotinal cues, cognitive deficits of abstract meaning, the association of seizures that develop in early childhood rather than in adolescence, and language-related cognitive impairments. Language and verbal deficits in autism vary according to the stage of development and the severity of the syndrome (Damasio ; Maurer, 1978).
Defects in comprehension range from failure to understand or attend to speech, and impaired ability to comprehend abstractions and complex associations. Written language is often better processed than spoken, as indicated by interest in reading and ability to read outloud. However, reading comprehension is usually defected. In addition, defects in nonverbal communication (gesture, facial expression, and posture) differentiate autistic from children with developmental impairments. Autistic children’s comprehension and expression are defected and they do not use gesture or facial expression for what they cannot communicate verbally. Two prominent features of the verbal defects of autism are mutism and echolalia. There is a great resemblance between the verbal defects of autism and the syndromes of mutism or relative speech inhibition that appear during recovery from mesial frontal lobe lesions which is usually accompanied by profound defects of nonverbal communication (Damasio&Maurer, 1978).
These defects don’t seem to derive from damage to the primary language processing area of the brain, instead these defects seem to derive from a lack of initiative to communicate, orientation towards stimuli, and are suggestive of impairment in higher motor or perceptual control, or overall cognitive organization. In spite of their inability to communicate verbally, their lack of mimicry, and their failure to attend to stimuli in the environment and proper orientation, and their ability to repeat speech are many features of childhood autism. Even when recovery takes place, they are unable to regain creative use of language, or proper propositional organization of speech.
In order to classify psychotic disorders, which develop in childhood, we have to define the disorder in terms of the age of onset. First, if the disorder begins in early adolescence or in the year or so preceding the onset of puberty, it will similarly be schizophrenia. A degenerative brain disease best explains the type of psychosis, which begins at about the age of 3, 4, 5 (normal development until that age) then the child’s condition. And third, is the description Kanner provided in 1943 that disorder begins in infancy, usually very early infancy but often as late as 2 years old (Rutter, 1968). The major characteristics that can be observed in severe infantile psychosis, or autism are; avoidance of eye-to-eye gaze, disturbance in personal relationships, aloofness and distance (Kanner, 1943), lack of interest in people, failure to form relationships, the little use of facial expression, and lack of sympathy or empathy for other people (Rutter, 1968). It is important to point out that some of these features can be greatly modified or not found at all in the older child.
Aside from the behavioral impairments there are additional cognitive defects that affect primarily attention and perception of autistic children. Specifically, autistic children have shorter visual inspection than normally developed children do (Damasio & Maurer, 1978). Their ability to scan the environment is less comprehensive and systematic, also they have less sustained orientation towards visual stimuli. They seem to use their peripheral vision more than they do central vision and avoiding focusing attention on specific targets is the primary feature of the disorder.
The dominant approach to the understanding and treatment of autism has included psychodynamic (psychogenic), biological, and genetic models. Autism has been viewed as the child’s response to general qualities in his parents’ personality. Researchers commented that most parents of autistic children appear detached, cold and obsessive (Kanner, 1943). Kanner also pointed out that parents of autistic children have exceptional intelligence level and usually high socioeconomic status. It is important to keep in mind that if the etiology of the disorder would totally depend on the characteristic of parental personality, then the siblings of autistic children would also be autistic. This is not the case, but it is well known that parents usually have very different attitudes towards each of their children even if they don’t want to admit. Therefore, it is reasonable to suggest that there might be a specific kind of abnormality in the parental behavior toward only one child in the family.
However, questions still remain about the origins of psychogenic factors. For example, it is accepted that there has to be some kind of abnormality between the parent and the child but there is no evidence as to what kind of abnormality. In addition, it is quite possible that the parental abnormality may be due to the child’s abnormalities rather than the other way around. Bettelheim’s view (1967) which constitutes the most clearly expressed psychogenic hypothesis suggests that autism develop as a response to extreme negative feelings shown by the parent (feelings so significant that draws the child to hopelessness). He points out critical periods in development, namely first 6 months when object relationships begin, 6-9 months when language and locomotion are beginning to turn the infant into a child, and 18-24 months when the child starts to shape his relations with the environment.
The child lacks speech and lacks emotional expression because there is a lack of a receptive audience as perceived by the child. The siblings are not affected he suggests because the parental reaction was specific to the one child, and because only the autistic child experienced the rejection at the critical period in development. “I can now be more specific about what essentially the autistic Anlage consists of: it is the conviction that one’s own efforts have no power to influence the world, because of the earlier conviction that the world is insensitive to one’s reactions.” (Battelheim, 1967 pg. 46) he points out that original convictions create the notion that there is nothing one can do about a world that offers no satisfaction towards one’s desires that passivity and withdrawal becomes inevitable. Children attempt to retain access to satisfaction only through the mother, never or rarely by themselves.
If the child fails to gain satisfaction, then he is left with frustration and destructive convictions. Critical experiences to account for autism may be the period from 6-9 months, where anxiety towards meeting social and individual standard begins. During this period, the child begins to recognize other people as individuals, and he begins to recognize himself as one, too. He suggests that if the child’s attempts to relate himself to the other are left unresponsive then not having found the other may get in the way of finding himself. In his research, Battelheim also suggested that emotional disturbance and the lack of response to outside stimuli is due to faulty conditioning. Many researchers observe that autistic children show improvement when treated with love, affection and acceptance, therefore he suggests that, they must have lacked love and acceptance in earlier life.
The behavioral model suggests that the problem of the autistic child is external, meaning that the child’s observed behavior is the problem rather than an unobservable, internal emotional disturbance or conflict. The child’s disorder behavior is not regarded as a symptom or an underlying disturbance, but rather as a direct consequence of external stimulus events. The heteropathy therapy for behavioral model for treatment and causation are separated in which the primary emphasis is on the present determinants of the child’s disordered behavior and less with past and perhaps irrelevant circumstances. Treatment is then conducted in terms of child’s present deficits.
Treatment in that sense concentrates on teaching the child the behavior patterns (play, speak, or cooperate) necessary for his participation in the social community, and patterns that are crucial for realizing his own intellectual and emotional capabilities. The two main behavioral approaches to the understanding and treatment of autism are operant conditioning and social exchange theory.
“Operant conditioning theory focuses upon those classes of behavior (called operants) whose future occurrence is thought to be a function largely of those stimulus events which follow the response, that is, consequences” (Kozloff 1973, pg. 16). The processes of operant conditioning are the basis upon which the principles of social exchange theory is based on. The autistic child’s behavior in an exchange with his parents, or environment, is determined by the consequences for him in terms of reinforcement and punishment of the response he receives. The child will tend to repeat those behavioral responses which result in his being reinforced or rewarded, or escaping or avoiding a negative reinforcer.
The biological model for understanding the disorder assumes that the child’s disorder is internal because child’s behavior indicate an emotional disturbance, a disturbance in the child’s conception or perception of reality, a metabolic imbalance, structural defect or inherited predisposition to respond in maladaptive ways. The basis of the autism syndrome is the child’s impaired ability to relate new stimuli to remembered experience and inability to associate that information to make cognitive decisions (cognitive dysfunction). The most significant feature of this dysfunction is the failure to transfer information between sensory modalities. In that sense the research is directed towards the reticular activating system which is a cluster of neurons at the top of spinal column connected to fibers from each of the sensory pathways. The role of RAS is to arouse the cerebral cortex based on the information that come from sensory receptors.
Information traveling from the cerebral cortex through RAS activates the body’s reactive mechanisms and gets it ready for action. It is hypothesized that a lesion in the RAS of autistic children leads to a chronic state of underarousal, limiting their ability to respond to external stimuli. Alternatively, chronic overarousal of RAS causes autistic children to defensively filter out external stimuli, and avoid situations like changes in the detail of the environment. Electroencephalogram studies of autistic children have also helped to understand the correlation between neurological dysfunction and autism.
The primary focus of EEG research is the response of brain waves to auditory and visual stimuli. EEG responses of autistic children significantly differed from normal, but without a distinguishable pattern to autism. One possible explanation for this difference was that autistic children experience a delay in neurological maturation (Ollendick ; Hersen 1983). Also EEG responses without any given outside stimuli indicate that autistic children do not exhibit the higher voltages over one of the two brain hemispheres. This may suggest that autistic have a failure to develop functional lateralization of brain hemispheres. Also other researches indicated that EEG responses progressively became more indicative of high arousal and behavior became more stereotyped as the environment became increasingly complex (Coleman, 1985).
Many researchers laid emphasis on autism in relation to a basic constitutional defect or abnormality, and discussed that some of these defects may be inborn. Although researchers argue that these defects may be genetically determined, the hypothesis remains inconclusive. Chromosomal studies have not revealed pathological abnormalities in autistic children. Kanner reported as mentioned earlier that parents of autistic children have high intelligence. Some researchers proposed that intelligence is directly correlated with the amount of blood circulation. They contend that infants who inherited genes for exceptionally high blood circulation in the brain may be vulnerable to brain damage caused by high concentration of oxygen (Achenbach, 1974).
In the present state of knowledge only tentative conclusion are possible. Yet, there is no established treatment of autistic children but current knowledge helps us to distinguish specific features of the disorder to apply proper course of treatment. Behavioral and psychodynamic treatment provides promising results. Eventhough they are not proven to completely remove autistic syndromes, they help the patients to develop tools to be able function within the social environment.
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