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Autism and Linear Cognition: Neuro-psychological implications

November 20th, 2020 by Robert DePaolo | Posted in Psychology | No Comments » | 47 views | Send article | Print this Article |


by Robert DePaolo

This article discusses the literal, linear cognitive style typically seen in individuals with autism. Similarities between this thought process and the cognitive styles seen in obsessive compulsive disorders, anxiety disorders and clients with traumatic brain injury are considered and dismissed. Meanwhile, autistic linearity is deemed a special kind of cognitive rigidity caused in part by neuropsychological dyspraxia.

Stop and Go Neurology…

Autistic cognition is a difficult subject to wrap one’s mind around, in part because the functional levels of individuals diagnosed with autism can vary so much. While those disparities arguably make the term autistic diagnostically mystifying, if not downright untenable, it is a reality researchers, educators and writers have to deal with. Despite those vagaries, there are fairly pervasive features within the spectrum. One is cognitive rigidity, i.e. the tendency to think and act as though life consists of only ‘stop and go’ thoughts and behaviors. (D’Cruz, Raggino 2013). For the most part autism precludes the ability to see nuance, gray areas of experience, to accommodate changes in routine and to alter behaviors to deal with changes in stimulus conditions and social circumstances. (Watanabe, Lawson, et al. (2019)

Patterns similar to these are seen in individuals with psychiatric disorders such as schizophrenia and obsessive compulsive disorder, as well as organic disorders such as traumatic brain injury. (Whiting, Deane et al. 2017)

The single track mindedness inherent in these disorders results from several sources. In schizophrenia, neurotransmitter depletion blocks the flow of neurochemical activity that under normal circumstances enables it to extend, branch off laterally and integratively and facilitate figure-ground thought and perception (Walz J.A. 2017).

Similar connectivity deficits are seen in traumatic brain injured patients. In their case damage to brain tissue and the superposition of enlarged ventricles (liquid sacks) over synaptic tissue prevents proper conductivity.(Poca, Sahuquillo,et al.2005). That leads to fragmentation, uncertainty and the need for the TBI patient to compensate through cognitive rigidity.

Cognitive rigidity and compulsiveness present differently for the individual with emotional disorders. While cognitive and behavioral tendencies within that rubric vary from person to person there are common symptomatic antecedents. One of which is anxiety.

When anxiety is intense and chronic, arousal levels create rigid fight/flight tendencies. Those high levels of arousal mobilize what Cannon called emergency reactions on such a regular basis as to block integrative thought. (1932). By analogy, rather than seeing both forest and trees the hyper-anxious individual is forced to attend to narrow stimuli he perceives as threatening.

The picture changes a bit with regard to autism. I believe this is largely because of the language factor. The typical diagnostic criteria for autism include substantial language deficits. In discussing that factor it is helpful to consider both the neurological and functional aspects of language.

As Luria and Trotsky have pointed out, language is both an external communicative faculty and an internal, regulatory faculty (Derovesne (2011). Seldom discussed is that language functions seem to extend beyond the social and interpersonal domains. They also help to maintain neural stability.

The human brain is vast, with billions of neurons and many billions of connections among and between those neurons. That provides advantages: for example enabling us to label and distinguish between and among a wide variety of phenomena, to research, combine and separate objects and conceive of relationships within the natural world. In the process we can create that marvelous thing called culture.

However, there is a drawback. With billions of neurons sending signals around the brain each experience will entail potential confusion or… “noise.” That noise must be modulated or the vastness of the brain would be highly disadvantageous.

In that context language seems function as a search light in the brain, providing focus and closure through the neuro-symbolic targeting of circuits that separate event-relevant networks from circuits that are peripheral to any given task at hand.

There are several means through which modulation is provided. One is through the binary mechanism of excitatory and inhibitory neurons. (Lakna 2018) One type halts conductivity, the other stimulates conductivity. As long as the brain can coordinate the timing of the two ( for example when certain neural clusters are activated, others inhibited) it is possible to engage in effective thought and behavior patterns.

Some timing comes from brain wave activity: the rhthmic quality of which seems to have a probative effect on learning and memory (Pribram, 1971). However, much of it comes from learning. With experience, the brain establishes fixed circuits corresponding to learned behaviors and cognitions. If circuit A stores the memory for turning on a faucet, circuit B will not. With learning circuits become functionally differentiated so that with added experience one doesn’t interfere with another. Somewhat ironically, human learning (ostensibly deriving from the vastness of the human brain) actually occurs by reducing the effective size and volume of the brain through the process of elimination. This is seen in the course of cognitive development.

In child development the first year is characterized by longitudinal connections within the brain. During that phase simple associations are accrued and the child shows a rigid cognitive style.
Around age two a branching process begins, whereby neural connections spread around the brain in multi-dimensional manner. In effect the single neural highway of year one becomes a multiple series of off-roads and bypasses in the second year. (Lenrout, Giodd 2007). Interestingly around this time the child also begins to develop a sense of self. This comes about because in being able to crawl, then walk, he finds he can move toward goals without being carried by another person. He becomes functionally, motorically separate from the caretaker. Rather than being merely a symbiotic extension of mom or dad, he becomes a distinctive “me.” From that sense of self comes what some have referred to as a “theory of mind,” (Korkmaz 2011). Being able to separate himself from others psychologically allows the child to understand that being separate means others can be studied, imitated and learned from. In a sense, they become objectified, didactic vehicles.

The motor aspect of self development is not the only determinant of self and other perception. Language development (which also occurs during the first and second years) is even stronger. With increasing language capacities the child can gain and enhance a sense of self, and develop a theory of mind.

Interestingly, language development also depends on the branching mechanism that occurs between the first and second year. With a disruption in that branching process there will tend to a deficient sense of self, and of others. The child will lack a theory of mind and will tend to think and act in terms of the first associative stage of neural development featuring chained, linear associative behavior and cognition.

Linearity is not the only factor in autism. Without the benefits of fluid neural branching the brain of an autistic individual will be prone to intensive and pervasive noise. Arousal episodes will be excruciating, which can make learning new tasks highly frustrating and produce an avoidant mindset. That has educational implications. The learning problems seen in autism often lead to high power teaching methods that can elevate arousal levels, which are the autistic child’s Achille’s heel. in that sense it is not surprising that some research has shown hat for some autistic students, attempts at new learning are often accompanied by arousal induced behavior problems and even seizure activity. (Billeci, Tonacci et al 2018), Prince, Kim et al (2016).

Because the preferred state of arousal for autistic individuals is manageably low, they will tend to resist new teaching and when prompted to cooperate will do so by use of self-regulatory behaviors such as behavioral perseveration, hand flapping, humming, rocking etc. These seem to be monotony/stability restoring behaviors to offset the noise and concomitant arousal in the brain.
Note, here the word ‘arousal’ doesn’t necessarily refer to spike activity or excessive autonomic activity. It refers more generally to unresolved neural activation, i.e. a disproportion between arousal ands closure – what Goldstein referred to as the “catastrophic reaction” (Klonoff, Lage et al 1993). It is possible that in addition to controlling arousal levels these behaviors are used as a substitute for language regulation; indeed might be a form of para-linguistic expression.

As seen in the psychiatric therapeutic process, language is a soothing mechanism, not just because it can talk us into equanimity by relabeling stressful events but because it can ameliorate noise within the brain. That suggests without language the individual will tend toward an intently avoidant mindset.
Some individuals with autism have language but it is topographically similar to their behavior patterns, perhaps featuring a lack of contextual understanding, a proneness to literal cognition and difficulty augmenting language with peripheral communicative gestures (facial and manual expressions) and body language. (Grafton (2013).

In line with the above factors it would seem a central issue in autism revolves around why they think and act in linear fashion.

The answer is not clear, at least neurologically. It is obvious that cross connections that in the normal brain allow for the multi-access among neurons and provide for conceptual thought and contextual cognition. But just why those interconnections are blocked in autism is unknown. Possible causes could be neuro-chemical, related to tissue damage or as some have suggested caused by a hyper-volume of neurons in the brain resulting from interruption of the “pruning” process in childhood, whereby deletion of neurons occurs to streamline the brain and facilitate access among various brain sites. (Pederson, 2018).

Still, another possibility is that since navigating fluidly among billions of neural connections requires extraordinary coordination among expiatory and inhibitory neurons, there is some something highly dysrhythmic about the autistic brain.

What creates the rhythm and orchestration in the brain? While language serves that purpose (all languages, including human language have cadence and sequential, orderly grammatical features) even that would require a governing mechanism. Might it be found in aberrant brain wave activity, or perhaps in a tendency toward double firing in the sensory motor domains so that feedback is not registered properly?

The idea of redundant or skewed feedback in autism has been discussed in the past. (Mosconi Mohanty et al 2015). In fact sensory instruments with delayed feedback have been used with autistic populations with some but certainly not overwhelming success. Such double, redundant or diffuse neuronal firing would be consistent with excessive-neural volume in the brain since neural systems would tend to collide and replicate rather then parse efficiently in the course of learning.

Another question revolves around whether linear cognition is a built-in feature of the autistic brain, forcing them both structurally and functionally to think and act that way, or whether linearity is a compensatory cognitive style used by the autistic individual to control extreme arousal diffusion as the brain addresses the normal figure/ground, conceptual features of the environment.

I tend to believe much of autistic behavior and cognition is an attempt at adaptation by a fragile central nervous system that lacks the inhibitory/excitatory neural orchestration to address the world in normal terms. Once again, this suggests autism is primarily a severe form of psycho-neural dyspraxia.
In a previous article I referred to a prime cause of autism through the idea of the “Bad Maestro.” I still believe autism is a most fundamentally a profound type of dyspraxia. Whether this has any validity can only be determined by research on the coordination among impulses in the brain following stimulus presentations. Whether this is valid there is no structural reason why autistic people would lack language ability. Their hyoid bones are present, their larynx is situated normally, and they do not typically display hearing loss (Beers, McBoyle et. al. 2014). Absent such deficits a significant factor could be a deficient orchestration mechanism that can juggle some 25 billion neural connections efficiently enough to produce flexible cognition, contextual emotions and normal language.


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