The Etiology of Autism;Metabolism and the Diffusion/Imbalance Problem

This article discusses the implications of metabolism and input diffusion on autistic development and behavior patterns in terms of possible causation and treatment possibilities.

Research on autism in recent years has provided valuable information with regard to its neurological underpinnings. For example, Haznedar, Buchsbaum et al (2000) found neuropathic features in limbic brain sites, which are typically implicated in the perception of pleasure, motivation, emotional regulation. Such findings would seem to suggest that one causative factor in autism is a disruption of (to use a generic term) “drive”, and perhaps a blunting of the capacity to express and perceive emotional experience.
If drive deficits are part of the problem that would coincide the findings of Courchesne (1995) who found underdeveloped (hypoplasic) neural structures in the cerebellum – a motor, regulatory and anchoring circuit that influences cognition and facilitates the automatic registering of skill memories so that the learner can take them for granted and move on to subsequent tasks.
In another study Courchesne discovered cellular hypoplasia in the pre-frontal lobe, (2011) which could lead to a disruption of self-regulatory, planning, inhibitory and language functions. Since language is a self-regulatory skill enabling us to separate “self” from “other” this would seem to coincide with Baron’s “theory of mind” concept (1995) espousing that at the core of autism is an empathy void, and more broadly, an incapacity to process both the figure and ground of social experience.
“Theory of Mind” offers a unique insight into language impairments inherent in autism, because by this line of reasoning, the autistic person might not see the point in communicating, making language learning both a neurological and motivational problem.
In a sense this raises a profound question regarding the nature of the disorder. To wit: Which comes first, a structural language problem or a social-perceptual problem, whereby extreme social insulation obviates the need and propensity to communicate?
Research evidence suggests the influence of neurological factors on perception and memory (Belmonte 2003) might be more descriptive of the disorder than the Theory of Mind concept, though the two are certainly not exclusive of one another. To become social and interactive requires not just intact neuro-linguistic software in the brain but also an ability to integrate various brain sites and functions so that the nuance and particulars of communication can be enacted; for example facial expressions, tonality, word meaning, word implications, gestures etc.
Belmonte’s studies indicate that autism does indeed feature sensory integration problems. Some of his research is especially relevant in sifting through the various brain sites and functions implicated in autistic etiology, because many of the findings discussed above have been challenged by follow up research findings contraindicating cerebellar, frontal and limbic dysfunction; for example Sundaram, Kumar et al (2008), Minshew, Beatriz et al (1999) and Connor (2005). On the other hand Belmonte’s findings seem incontrovertible. While this is part due to the functional rather than neurological nature of his inquiry (he was less concerned with brain cell anomalies than arousal levels and perceptual parsing of inputs) his conclusions provide a solid pivot point in discussing etiology and treatment.
Belmonte’s findings suggest the autistic individual does not efficiently, fluidly register inputs. He has what will be referred to here as a “diffusion problem” Ordinarily, when inputs impinge on brain there is a temporal correlation between their arrival and the brain’s response to them. Since inputs typically arrive in a sequence – for example language interactions are usually expressed one word at a time – the normal brain is able to time itself in line with the rhythm of the input, thereby catching the words and overall meaning of the statement. Belmonte found that this rhythm is disrupted in autism. In effect the perception of autistic individuals is smeared. They do not process fast enough to be able to handle all aspects of input in a rapid sequence. As a result they end up missing the forest for the trees and are relegated to working with burdensome input wholes without a sequential code or structure. Since this is the way the world presents itself to them it is not surprising that they have difficulty with both listening and verbal expression.
Depending on the of severity of the disorder that can result in either to a disheveled processing of inputs, rendering perception and comprehension delayed and non- contextual, or it can entail a virtually complete incapacity to understand words or inputs in general – especially those presented in rapid fashion and without specific cues by which to codify what is an otherwise un-codable message.
These findings have a wide variety of neurological and functional implications,. To illustrate, it might help to begin with what typically ensues when a person processes inputs, because certain mechanisms must be in place for us to make sense of our world.
Setting the Table
A first prerequisite for the perception of inputs occurs prior to actual perception. It takes the form of a preparatory arousal level with several functions. Pre-stimulus arousal is ongoing and forms a shield to meet the impetus of the input in a way that blunts its global impact on the brain. It operates in a way analogous to a hydroelectric dam, holding back a river, allowing only enough water to pass through to provide power to the town.. Without such a resistance mechanism the perceptual system and the brain itself would be too weak to handle incoming messages.
The weak shield hypothesis is not necessarily amenable to research paradigms although it is possible to describe it loosely in terms of the neurochemistry of preparatory arousal levels. For example The oft-tested and well supported Yerkes-Dodson Law (Broadhurst, 1957), (Duffy, 1957), (Anderson, 2000) describes a continuum of arousal patterns that are more or less conducive to accurate perception and efficient performance. The continuum ranges from waking state, to increasing alertness, to optimal arousal to increased arousal .
(Yerkes, Dodson 1908). The optimal state for perception and learning is somewhere in the middle range. Since, as Weil, Zhang et al have indicated, the driving force behind the functions of the brain is general arousal that is important.
The popular contention that autism is analogous to a sleep/dream state is interesting in that respect and coincides with the waxy flexibility, non responsiveness and apparently under-aroused state of many autistic children in early development. Certainly over time many autistic children are viewed as hyperactive, but their responsiveness in infancy is often muted, for example in responding to sights, sounds and faces. It could be argued that the first sign of autism is not language delay or sensory rituals but lethargy rooted in some sort of ergonomic deficiency
Perhaps one reason researchers have been unable to find an etiological neuro-chemical smoking gun to explain infantile lethargy, or hyperactivity in the toddler years is because an optimal arousal level is not something describable by discrete levels of norepinephrine, serotonin or other catecholamines. It is more likely the result of a neurochemical disproportion among various transmitters; an balance resembling the uneven distribution of excitatory and inhibitory neural activity in the brain that creates spikes…or “kindling” and makes perception difficult. If so, then a skewed neuro-chemical distribution might be involved in an arousal deficiency and concomitant input confusion.
That brings to mind the question of how neurochemicals are apportioned. To some extent this is reflected in the way in which brain metabolism is orchestrated. As Raichle & Gusnard (2002) have discussed, brain metabolism has a close connection to arousal levels and seems to obey the Yerkes-Dodson Law. They found that in order for the brain to function normally it is necessary for the brain to maintain ongoing activity, i.e. a basal arousal level, prior to the onset of the sodium pump mechanism that releases synaptic activity in response to a stimulus. One reason for having an ongoing arousal level is that it creates a state of associative preparedness, which ultimately conserves energy. In addition to its shield/resistance purpose it improves access to memory.
Arousal and Adaptation
The capacities to plan and anticipate are often discussed in evolutionary terms (for example by presuming such prescient cognitive capacities aided in hominid, then human evolution) but they also provide an ergonomic benefit. That is especially important for the human brain, which is disproportionately consumptive of the body’s energy. Thus basal, preparatory arousal grants metabolic as well as experiential and stimulus tolerance benefits.
Neurochemicals are ordinarily produced and dispersed in anticipation of specific circumstances. So-called pleasure chemicals such as endorphins and oxytocin are secreted during enjoyable activities, and to create relief from physical duress, whereas epinephrine and nor-epinephrine is produced during high stress, emergency situations. As discussed above, the dispersion of these chemicals runs parallel to the proportionate activation of excitatory and inhibitory neurons during any given activity or state of expectation.
As Rath, Rohde et al demonstrated (2012) a balanced and ongoing basal activation of both neuronal and neuro-chemical systems (a shield) is required in order to create connections among neurons and produce learning and memory.
In that context. the answer to the question of how neuro-chemical, synaptic and arousal balance are orchestrated can be found in the presence of an ongoing level of brain activity that provides a perceptual shield much like the resistance in an electrical current, keeps metabolic rates and energy within workable limits and activates and inhibits behavior proportionately to provide “do” and “don’t” behavioral options. In a sense this implies the existence of a neuro-relativity factor; whereby learning and memory are compromised in a brain system in which arousal levels go from extremely low to extremely and are maximized when the gap between arousal levels is narrower. Also, to the extent that basal levels provide semi-activation of access to memories and pathways even prior to task engagement, it also increases the speed of learning. In effect an ongoing arousal level gives the learner a frame of reference – a neuro-associative context in which to place experience.
Belmonte’s findings seem to suggest that autistic individuals are deficient with regard to the basal arousal/ shield capacity. Theirs is a brain of disproportion, featuring severe arousal shifts, an imbalance between activation and inhibition, inordinate energy consumption and a sporadic metabolic rate. All of that leads to their being unprepared for inputs, both neurologically and experientially. It also means that due to a dearth of synaptic connectivity resulting from these deficits, they cannot readily register the automaticity needed to learn progressively and in eventually render new inputs old and recognizable.
That leads to a rather awkward statement about etiology, because it implies that the essential cause of autism is autism; that autism is a self-propagating disorder, and that autistic individuals have trouble learning because, without being able to assemble building blocks of knowledge due to deficient basal arousal and neural connectivity deficits they are deprived of a frame of reference. In a Piagetian context they literally cannot assimilate or accommodate. A train with all cars in place but to engine to move forward.
Since autistic individuals tend to quasi-process inputs in terms of global, spiked, rather than apportioned arousal patterns those inputs will often be perceived as relatively new even if they has been encountered before. Autism could therefore be seen as a kind of global memory deficit, making life seem very threatening, forcing the child into obsessive, ritualistic compensations to reverse the uncertainty arising from interactions with people and other inputs that frame his every day existence.
Conversely, when the autistic child is able to establish pathways – for example through the use of narrow stimulus-response teaching formats (the so-called discrete trial method) – some of these problems can be ameliorated. The degree to which this occurs depends on a number of factors; most essentially whether the child has language capacities, because language provides among other things, a capacity to apportion and label experience and is itself an uncertainty-reducing mechanism. Yet while such teaching methods can lead to skill acquisition they obviously cannot address the arousal-metabolic-neural connectivity problem.
The Ergonomics of Autism
While energy conservation is less often mentioned in conjunction with autism, there is ample research suggesting metabolic factors are involved in the syndrome. For example an article in Science Daily discussed research pointing to mitochondrial involvement in autism (2010). There are also clinical examples of autistic children who have difficulty metabolizing gluten and other foods, and who have gastrointestinal disorders. Taking the evidence as a whole it does seem possible that in the near future autism will be viewed as primarily a metabolic disorder, with all other neuropathic signs being understood in that context. The autistic child’s apparent state of lethargy and nonresponsiveness could then be tied to an abnormal metabolic process, rooted in a dyspraxic disproportionate activation of neurochemicals, neurons and synapses – all resulting from lack of an ongoing arousal level or shield of brain activity that makes apportionment, perception, learning and memory possible.
Evidence for a core metabolic causation is mounting. In fact it might be considered a common factor explaining the vagarious results of neurological studies. For example the Courchesne study found hyper-density of neurons in the frontal lobe. In the first stages of child development this is a normal trend. However in later stages excessive brain tissue is discarded via a process called apoptosis. It is a good thing. The death of excess brain cells actually reduces noise in the central nervous system, making perception, thought and memory more streamlined and accessible. Metabolism plays a important role in this process and if insufficient, apoptosis is stifled, making for noisy, unwieldy brain function and a proneness to sensory overload.
Further support for a metabolic etiology is found in the work of Haznedar,, Buchsbaum et al. They demonstrated that the hypoplasia (lack of cellular maturation) typically seen in the brains of autistic subjects is accompanied by metabolic anomalies. In their MRI-PET study, children on the autistic spectrum showed hypo-metabolic characteristics. In addition a study by Russian researchers (Klembovskii, Ananenko et al showed that hypoplasia in general is caused by disorders of connective tissue resulting from metabolic dysfunction. Thus there seems to be evidence to suggest that a (hypoplasic) lack of maturation in brain cells can be caused by a metabolic dysfunction.
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The Etiology of Autism;Metabolism and the Diffusion/Imbalance Problem
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