The occurence of autistic phenomena, by and large, is noted in clnical reports. However, there are few reports documenting the way in which autism occurs. In other words, the actual process underlying the syndromal presentation has not as of yet been described in the literature.

How should we judge a theory as to autistic syndromal pictures ?

Our criteria should spring from the same source that allows us to judge other theories of neurophysiologic function.

We can then ask, what neurophysiologic theories exist of autism.

We will leave that question open. There appear to be specific theories for specific forms or features of atuism.

What is not evident, in the literature to date, is a theory that would describe why a single multiple element syndrome and at the same time account for how it is that som many various genetic changes result in a similar presentation.

In other words, if one sets out to explain a single syndrome, then it is not good science to propose multiple explanations for the same event. Multiple causes share a common end point, and the means by which they share that common end point must be provided.

To return to the articles provided prior, let's look at why providing a separate theory of acceleration for every heavenly body is poor science. The reason is, that the same theory of gravity and acceleration must apply to every heavnly body.

We also need to point out, that te reason that such a theory is proposed (the multiple special case theory) in the 21rst century, is that their is a profound social pathology that blocks the independent study of psychiatric illness. Unfortunately, the current psychiatric educational establishment seems to be wedded to this pathology, which is why if their is ever to be any real progress in psychiatry as a medical discipline, the internal and pervasive patholoiges of academic psychiatry must be examined in detail, and in public.

In the case of autistic spectrum syndromes, we must not some basic necessities.

Any theory must certainly explain not only the occurence of the basics of the syndrome, but the common comorbidities as well.

For instance, the elements of any autisitc spectrum synrome seem to begin with disturbances in communication capacity (often leading to phonation and word sequencing disturbances, echolalia, alterations of speech rhythm, and losses of recognition of the social and emotional content.

Similar disturbances occur in recognition not only of verbal content and its implications, but also of tone and facial expression. The disturbances, then, is in cognitive and verbal / communicatove process.

Because of the complexity of these organic functions, injuries to neural development in any of a multitude of pathways can lead to the initial features of the syndrome,.

This provides us with our first hint. Illness originating in the key interpretitive portions of the neocortex (presumably inlcuding frontal, temporal, and parietal lobes) then lead to losses of interpretitve capacity that appear to occur in mulitple circuits, but instead, occur in one complicated set of shared neocortex, for which, if any injuries occur, the entire mechanism fails. The immediate results include incongruent affect and disturbances in communicative process.

We can then, if we we wish, describe this portion of the neocortex as a virtual organ, which on failing, leads to a host of similar problems, regardless of the actual specific model of failure.

Only this mode of theory is in keeping with our judging criteria previously outlined.

Disturbance, then, in any of the interpretative mechanisms within this virtual organ, results in the subsequent findings.

For instance, as we know, obsesional features, compusional features, pica, impulsive features, and attraction to non - standard sensation, are all potential elements within autism.

The pervasiveness of autism, rather than being seen as a single epidemic, should rather be regarded as due to the fragility of the genetic assemblage that is necessary for interpreting human social data.

When that virtual organ fails or is severely impaired, the organism is forced to compensate.

In other words, the intact (and perhaps altered) psychic compensating mechanisms appear.

For patients with autistic spectrun syndromes, then, a host of motor effects and communicaton effects (and preferential sensory intakes) occur. These may include movements that the patient prefers, methods of communication that the patient prefers, maladaptive motoric and vocal responses to stress, avoidance patterns, and preferred sensory sources.

Distinguishing between inadequate compensatory approaches and the patient's response to inadequate compensatory response becomes part of the examination task.

When the compensatory pathways of the CNS are insufficient, the pataient realizes this, and as those experiences are brought into consciousness (and are also present in the unconscious, and are found to accompany their reasults -- anxiety, obsessions, compulsions, depression, mania, and psychosis.

The appearance of a treatment response to medications targeting these syndromes, misses that they are secondary to the organism attempting to compensate for losses of functioning that are severe impairments in the modern post - industrial world.

So, we see within the few paragraphs, an outline for autistic spectrum syndromes that allows us to meet the important criteria outlined elsewhere.

In addition, the theory outlined her outlined here, allows us to provide specifics as to what causal mechanisms lead to the course of illness.

The sequence of illness has been provided elsewhere (see citations), but has not allowed testing of the causal hypothesis because of the limited specificy and testability of the descriptions to date.

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