Subclassification of Autism
A review of the most carefully controlled neuroscientific studies (Bachevalier, 1994) using various methods such as autopsy material, brain scanning and imaging (MRI, CAT, PET, SPECT, rCBF) suggest that it may be helpful to divide autism into two distinct subclasses: Type1, where there are distinct neurologic signs and varying ranges of mental retardation (encompassing approximately 60-70% of the autistic population); Type 2, where the CNS is anatomically intact and there is no mental retardation (encompassing approximately 30-40% of the autistic population). Obviously a continuum from severe functioning deficits to very minor exists in the autism population. DeLong (DeLong and Nohria, 1994) has appropriately described this phenomenon as the "spectrum" of disorders in autism. The two sub-types should be seen as fitting into such a spectrum or continuum.
It makes greater sense to subclassify autism in the above manner when the neurodevelopmental evidence is taken into consideration. For example, we know from the earlier discussion about critical periods, particularly during 8-16 weeks of gestation, that mental retardation is most likely to occur if any event interferes with the process of neuronal migration. This earlier onset disruption of the developing fetus, regardless of the cause, would produce more severe consequences. This type of disruption would affect many brain areas and have definite abnormalities such as those seen by Kemper and Bauman (1993). Cells in the limbic system (amygdala, hippocampus, cingulate, septum) would most likely be affected. The development of the Purkinje cells and deep cerebellar nuclei would also undoubtedly be affected. In this case, many neural circuits would not be properly formed and brain functioning would therefore be compromised later in life. The blend with mental retardation would make it difficult to reverse the brain functioning difficulties found with such people. Level of improvement would obviously be influenced to a very large extent by the degree of brain impairment.

In the second type of autism proposed, any disruptive event would have to occur later in the gestational timetable and would, therefore, hardly disrupt brain development at all. In this case there would be no anatomical abnormalities as the neural structures would be fully formed. Therefore, we would expect to find very subtle anatomical signs, if any, as has been reported by Kemper and Bauman (1993) and Tsai (1983). Most likely the major problem related to brain functioning would be dysfunction of the neurotransmitter system where the chemical substances responsible for conducting nerve impulses across synapses would be affected. Such a situation is much easier to reverse or correct, either through pharmacological therapy, by activating the correct pathways in the young brain that produce normative brain development, or both.
Predicting Successful Outcomes
The neurodevelopmental findings discussed previously, when combined with the growing clinical and experimental evidence on the memory systems necessary for learning, can help us understand the most effective ways to teach youngsters with autism and produce more successful outcomes. For example, the work of Mishkin and others (Mishkin and Appenzeller, 1987; Zola-Morgan and Squire, 1993; Bachevalier, 1990) has shown that there are basically two types of memory systems which underlie successful learning. The first has been referred to as "habit, rote, or procedural" memory. This system develops early and becomes functional during the first months of life in humans. It is the kind of memory we use for skill learning and is acquired by repeated presentation of the same stimulus until the task is correctly stored and accessed in memory and thereby learned. The striatum and neocortex of the cerebral hemispheres are the areas which mediate this kind of memory. It will be recalled that both of these brain structures have been found to be anatomically intact and normal in the brains of children with autism.
The second type of memory evident from the work of Mishkin and his colleagues has been termed the "representational, associative, or cognitive" system, which is anatomically distinct from the "habit or procedural" type mentioned previously. Most importantly though, Mishkin states that the "representational" system coordinates all of the sensory modalities, including the processing of experiences and events, and the generalization of such information which leads to higher-order cognition and learning. This "representational" system depends on the integrity of the lmbic system, especially the amygdala and hippocampus and areas connected to them. Any disruption to these connections or limbic areas would interfere with the acquisition and meaning of information obtained from the continual presentation of novel stimuli typical in the daily life of a developing infant and child. There is little doubt that disturbances in the CNS which would disrupt the "representational" system would lead to disorganized cognition, problems with modulation of sensory events, inapproprite social interaction and abnormal language development. These are the features so typical of autism.
From what has beeen discussed so far in this paper, conclusions can be drawn as follows: a). Children with autism, particularly those that fall into the Type 2 classification (probably also a large number of the Type 1) have intact brain cortices and, therefore, their habit, rote, or procedural memory systems should be intact. They should be fully capable of acquiring skills through repeated presentation of stimuli until tasks are properly learned. They will appear to be quite normal during their first few years of life and then show difficulty acquiring language and social skills because of disorders in their limbic system and cerebellum disrupting "representational" memory functions. However, due to the nature of the late onset of disturbances in brain development, they should be prime candidates for recovery if given the appropriate treatment early in life (certainly starting at around two years of age or soon thereafter) so that their limbic and cerebellar circuits can be activated and they can utilize their associative or representational learning systems. This would allow them to form basic cause-effect relationhips, associations and generalizations so crucial to adaptive behavior functioning. b). Children with autism falling into the Type 1 class who most likely had earlier onset disruption of a critical period of brain development (most likely starting early in gestation during the 8-16 week period) and therefore different levels of mental retardation complicating their autism, would have less probability for full recovery. However, if their cortical brain areas are intact, they too would be quite normal in their first two years of development and they would have normal rote or habit learning. They should, therefore, acquire early rote learning skills easily, provided they are placed in an environment ideally suited to maximize such learning through repeated presentations of stimuli. Once they acquired the necessary rote learning, which is a prerequisite to the higher-order or associative learning sytem, they could then be taught to use the latter, depending on the integrity of their limbic circuits. The best way to determine how much these children would be constrained in their learning would be by screening them comprehensively with neurodiagnostic techniques. Those children discovered to be neuroanatomically "intact" would undoubtedly experience the most success following intensive teaching and training. Those with neurological involvement would learn skills to a lesser extent, yet still profit greatly from intensive early intervention.
What follows, therefore, from the above discussion is the critical need to carefully screen children suspected of having autism, at the earliest possible moment in life, using thorough neurodiagnostic methods. This will assist in predicting learning potential and recovery to a great extent. Also, just as important, is the need for early intervention or therapy which will allow the youngster with autism to maximize rote learning capabilities and then move on to higher-order, associative, learning. Since the ability to transfer skills from the rote to the associative stages is critically dependent upon the interaction of brain maturation and stimulation from the outside environment, it is crucial that the correct teaching strategies be started early, that they be presented consistently and repeatedly over most of the time the child is awake and functioning, and for several years in duration. We know from neuroscientific evidence that neuronal networks develop and mature very slowly over time in humans. Any lasting changes to such a slow developing system takes many years (Hudspeth and Pribram, 1992). Given what we know of brain development and what has been discussed in this paper, it is hard to conceive of any techniques of teaching or remediation that will be effective with the autistic child unless they meet these conditions. This kind of knowledge ertainly argues very strongly against any short, or brief, therapies being capable of establishing long-lasting changes in brain functioing and behavior.
Fortunately, several recent studies (Lovaas, 1987; Perry, Cohen and DeCarlo, 1995; Wetherby, Koegel and Mendel, 1981; Luce, Niemann, Wright, and Dyer, 1995) support the notion that early, intensive therapy of several years duration are most effective in treating autism. These methods not only meet the criteria of early intervention and intensity over time but also start out by teaching rote learning skills in an ideal format of repeated presentation, at the correct pace, along with numerous contingencies of optimal reinforcement. Following the acquisition of basic rote skills, such programs then move on to the higher-order associative skills which allow generalization and the development of more adaptive behaviors necessary for independent daily functioning. These studies, in effect, follow the ideal course of brain development and employ the best principles of brain maturation and development. Little wonder, then, that they can achieve such good outcomes and report various levels of recovery from earlier autistic behaviors.
From what has been presented in this paper, it can be argued that autism should be reversible, possibly in at least 40 to 50% of cases, provided they are properly identified, carefully screened neurologically, and provided early intervention that is intensive on a daily basis and lasts several years. This is the encouraging news. However, it also raises a dilemma because we know from brain development that there is a narrow window of opportunity to achieve optimal results. Waiting until the child is five or six years old may be too late because the brain may already have passed the stage of plasticity which would allow it to benefit from any remedial technique, no matter how intensive. Any child with autism who is not given early intervention of an intensive nature may, therefore, be deprived of an opportunity to change later in life. This may lead to permanent disabilities that will continue to exact more costly emotional and economic costs on the individual, his family, and society. It also raises the issue of neglect for those cases that never get appropriate therapy. Such issues will undoubtedly keep debate alive in this area for years to come. Nevertheless, it is hoped that the recent findings in the neurosciences that have been reviewed in this paper and offer so much hope for improvement, will lead to more urgently needed research and to a greater understanding of autism and how best to maximize functioning for people born with this syndrome.
References
Bachevalier, J. (1994). Medial temporal lobe structures and autism: A review of clinical and experimental findings. Neuropsychologia, 32, 627-648.
Bachevalier, J. (1990). Ontogenetic development of habit and memory formation in primates. In Development and Neural Bases of Higher Cognitive functions. A Diamond (Ed.), New York Academy of Science, New York, pp.457-484.
Bauman, M.L. (1993). Understanding autism through neuropathologic studies. Keynote address; Annual Conference of the New Jersey Center for Outreach & Community Services, Princeton, NJ,
Clarren, S.K. (1990). Fetal alcohol syndrome: diagnosis, treatment and mechanisms of teratogenesis. In Transplacental disorders: Perinatal Detection, Treatment and Management. Alan R. Liss, Inc., pp. 37-55.
Coleman, P.D., Romano, J., Lapham, L., & Simon, W. (1985). Cell counts in cerebral cortex in an autistic patient. Journal of Autism and Developmental disorders, 15, 245-246.
DeLong, G. R., and Nohria, C. (1994). Psychiatric family history and neurologic disease in autistic spectrum disorders. Developmental Medicine and Child Neurology, 36, 441-448.
Hudspeth, W.J., and Pribram, K.H. (1992). Psychophysiological indices of cerebral maturation. International Journal of Psychophysiology, 12, 19-29.
Kemper, T.L., and Bauman, M.L. (1993). The contribution of neuropathologic studies to the understanding of autism. Behavioral Neurology, 11, 175-187.
Luce, S.C., Niemann, G.W., Wright, S., and Dyer, K. (1995). A comparison of two delivery models of early and intensive intervention with young autistic children; preliminary data. World Congress of Behavioral & Cognitive Therapy, Copenhagen, Denmark.
Lovaas, O. I. (1987). Behavioral treatment and normal educational and intellectual functioning in young autistic children. Journal of Consulting and Clinical Psychology, 55, 3-9.
Mishkin, M., and Appenzeller, T. (1987). The anatomy of memory. Scientific American, 256, 80-89.
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Perry, R., Cohen, I, and DeCarlo, R. (1995). Case Study: Deterioration, autism and recovery in two siblings. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 232-237.
Schull, W.J., and Otake, M. (1986). Effects of radiation on the developing nervous system. In Radiation risks to the developing nervous system, K. Krieger et. al., (Eds.) Gustav Fischer Verlag, Stuttgart, pp. 399-419.
Streissguth, A.P., Barr, H.M., and Martin, D.C. (1984). Alcohol exposure in utero and deficits in children during the first four years of life. In R. Porter, M. O"Conner, and J. Whelan (Eds.), Mechanisms of alcohol damage in utero. Pitman Publisihing, London, pp.176-196.
Tsai, L.Y. (1989). Recent neurobiological findings in autism. Paper presented at the State-of-the-Art Conference on Diagnosis & Treatment of Infantile Autism. Gothenberg, Sweden.
Wetherby, A.M., Koegel, R.L., and Mendel, M. (1981). Central auditory nervous system dysfunction in echolalic autistic individuals. Journal of Speech and Hearing, 24, 420-429.
Zola-Morgan, S., and Squire, L.R. (1993). The neuroanatomy of memory. Annual Review of Neurosciences, 16, 547-563.
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