By Robert DePaolo


The article proposes that attention, memory and cognition are dependent on an energy apportioning pre-input capacity that provides a shield against input and facilitates engagement in the learning process. The shield mechanism is described as an essential component in normal learning, while deficiencies in the shield mechanism are attributed to autistism, attention and learning disorders.


In discussing brain function as pertains to normal individuals, those with learning disabilities and also those on the autistic spectrum it is important to consider a possible foundational mechanism that creates a readiness for perception, language, memory and broad cognition. Since, despite its immense associative and mnemonic capacities, the brain is most fundamentally an electro-chemical device it might be possible to describe that foundation in terms of energy dynamics.

Whenever stimuli impinge upon the brain an energy dispersion process occurs, as it does in all electrochemical structures. In such circumstances it is important for input not to exceed the load/resistance capacities of the structure. One reason for this can be seen in the second law of thermodynamics, which holds that energy always flows from a high state to a low state (whether the differentials pertain to heat, pressure or material elements). In simpler terms, whenever a high energy source is adjacent to and interacts with an extremely low resistance source, the former will tend to overwhelm and hyper-influence the latter. Conversely, when two systems are more equal in terms of energy content the flow will be less forceful. As a result less information will be lost (entropy reduced) and the systemic organization of the recipient source will remain intact. A shield mechanism in the brain would ensure that resistance could adequately meet input head-on.

The suggestion here is that since the brain operates by an electro-chemical energy dispersion process it would tend to obey the 2nd law of thermodynamics. While that assumption is somewhat general, there is research to suggest that an energy source in the brain operates outside the realm of neurons and in the absence of direct stimulus arousal to provide a backdrop of energy reserves and maintain homeostatic functions (Magistretti, Pellerin et al 2000). While that study does not directly address the concept of a shield mechanism, it would appear that to be adaptive the brain must handle inputs and submit behavior with some precision. To do so would require an energy flow apportioning mechanism. Assuming that is the case, one can speculate as to the possible involvement of this mechanism in learning and developmental disorders.


Various researchers, ostensibly beginning with Pavlov, discussed the importance of inhibitory neural circuits as a mechanism by which input and arousal levels could be modulated. Pavlov’s notion of protective inhibition (called into question by some) postulated that the brain will tend to shut down in the face of hyper-arousal. His primary concern was with cortical hyper-arousal, particularly with regard to its impact on schizophrenia. In the aftermath of his writings, some Russian psychiatrists used stimulants like caffeine to treat psychotic patients as a means of re-activating the cortex, (the so-called higher brain structure that is indigenous to mammals and quite massive in humans) and restoring lucid, integrative thought and language. While there were some claims of success, the practice is now practically nonexistent. The problem with cortical stimulation has always revolved around the question of whether stimulating the cortex re-invigorates or further depletes its energy resources. Thus the question arises as to whether the stimulant in itself would become a possible antecedent to hyper-arousal, thereby creating overload in the brain and exacerbate the patient’s symptoms.

At present caffeine is now more likely to be viewed as a pathogen than a cure (Bolton, 1981). Yet caffeine-induced cortical stimulation has been shown to enhance cognition (Kelly, Gomez-Ramirez et al 2008).

Thus, it appears that while the treatment derived from Pavlov’s notion of protective inhibition was somewhat questionable his description of this process had merit, Now of course it is a well established fact that neural inhibition is crucial in learning, perception and also the prevention of overload in the brain.

With regard to its possible role in the input-shielding process, post-synaptic neural inhibition seems less than complete. One reason is that inhibition depends largely on prior learning. There are of course pathways in the brain with inherent inhibitory and excitatory functions, but just how they are applied and recruited to specific experience depends to an extent on learning, memory, expectations and even the brain’s extant chemical status. Furthermore, inhibition would tend to arise after stimulus impingement, e.g. after relevance and impact have been determined within the brain. By then it might be too late to forestall an unbalanced proper (input-heavy) flow of energy into the brain.

Because brains need to be efficient to have evolutionary value that would seem to require an a priori mechanism providing a built-in, versatile and readily available means by which to ensure that the energy dispersion is immediate, thus conducive to perception, learning and cognition.


One way to conceptualize how this works can be seen in the example of a water pump. For it to work efficiently, water must flow through with a certain rhythmic regularity. The only way for that to happen is for the hose to have sufficient resistance to prevent the walls from lumping up or breaking down. The relationship between water pressure and internal resistance creates a synchronous flow that enables the pump and the machine it drives to operate fluidly. A simila example would be the fuselage of an airplane.

With respect to “brain mechanics” that implies that one of the most important initial capabilities of the brain is a built-in device (a kind of wall or shield) providing stimulus resistance, submitting its own ongoing counter-force to ensure that mental functions can ensue properly.

While analogical, the concept of a shield is not at all mysterious. It can and has been indirectly discussed in terms of norepinephrine and epinephrine levels in the brain, specifically with regard to the resting levels of these neurotransmitters/hormones and learning prowess. For example Berridge and Waterhouse (2003) demonstrated a relationship between norepinephrine levels and cognitive efficiency.

It has also been discussed with regard to neuro-developmental disorders. For example in research on autistic subjects Akshoomoff (1989) and Brunea (2003) found that subjects’ responses to inputs were characterized by both overload and delayed perception. Both outcomes would be predicted in a high energy-to low energy transition in the brain and also imply that unless the brain is itself sufficiently energized and able to “meet input at the door” internal/neural overload (or possibly experiential chaos) could occur.

Other research studies have pointed to a low level of norepinephrine in children with Attention Deficit Disorder, (Biederman, Spencer, 1999), (Shekin, Bylund et al 1994). Their results imply that terms like “hyperactive” and “inattentive” might be something of a misnomer; the phrase insufficiently pre-activated being perhaps a bit more accurate.

The potentially broad influence of a shield mechanism is implied in other studies, particularly if norepinephrine is assumed to play a role in the structure and functions of the shield. For example Sahehi was able to reverse cognitive dysfunction in mice with Down Syndrome by administering Norepinephrine (2009). Meanwhile Matsuishi and Yamashita (1999) found correlations between low norepinephrine and both attention-deficient and learning disabled students, which suggests the possibility that their subjects lacked an inadequate a priori arousal (shield) mechanism.

That norepinephrine has a major impact on various mental faculties is well established. Yet it is unlikely to comprise the total foundation of the shield. There are several reasons for this. First, if as Courchesne has stated, autistic individuals use repetitive, rhythm-inducing behaviors as a substitute for an internal shield mechanism, one would expect resting norepinephrine levels to be lower in autistic subjects. At least one study by Young and Kavanaugh et al (1982) suggests this is not the case. Another reason to suspect a more complex neurochemical structure for the shield is the nature of cognitive ability.


Whenever one engages in an activity involving attention, associative or integrative skills a number of cognitive and affective processes come into play. Attending requires mobilization of various brain circuits – which could be provided by norepinephrine output. It also requires inhibition of peripheral motor activity and another other, crucially important element. Attending is not unlike any form of exercise in that it involves arousal and a certain amount of duress. When the body incurs stress it produces neurochemistry that enhances pleasure, ostensibly as a means of overriding stress and buffering the arousal levels that might produce aversive states and withdrawal. That suggests a dopaminergic influence beyond norepinephrine could be part of the shield structure. Perhaps, due to the need for associations and closure to alleviate uncertainty so too would cholinergic systems. In that context the shield mechanism referred to here would be comprised of a pan-supportive, neurochemical soup.

The idea that proper brain function and the fine tuning of excitory/inhibitory differentials that facilitate mental faculties depend on an even energy flow and adequate neuro-chemical resistance seems consistent with the symptoms inherent in ADHD and autism, which can include an aversion to input, underdeveloped self regulation, dependency on external cues, stimulus-bound impulsivity and deficits in internal/social skills such as empathy, contemplation and self awareness.

Interestingly, Courchesne’s Overstimulation Theory of Autism holds that the child shields himself against outside inputs. His theory revolves around the idea of deficient brain circuits (for example in the cerebellum) which ordinarily facilitate perceptual shifting, attention and memory. (1999).

Self Regulation is of particular interest, not just for ADHD and autism but for human learning in general. Like the term “executive function,” self regulation is somewhat difficult to define without exhausting every verb in the dictionary. For example skills such as planning ability, decision making, moral judgment, self monitoring, self awareness and empathy are all encompassed in the term. One way to streamline the concept is to attribute related deficits to a weak shield mechanism. For example, with low internal arousal comes low resistance to input. As a result, the capacities for self examination, post processing of experience, imagination and empathy would all be overwhelmed from the outside and under-stimulated from within. A vacuum-like, low resistance neuro-humoral predisposition, (or inadequate shield) would not only make the individual subservient to outside stimuli but would also preclude the processing of internal stimuli (ie. thoughts, feelings and operational cognition per se) that ordinarily lead to self regulation.


Another behavioral feature of interest in the context of Shield Theory is aggression. Tantrums have long been viewed as “behavior problems” subject to and remediable by behavior teaching methods. When it comes to autism spectrum and attention-related disorders, there might be more to it than that. The body has a somewhat compensatory way of distributing chemicals around its internal environment. For example when the pancreas does not produce adequate levels of insulin, diabetes can result. That usually means blood sugar levels rise, often requiring medication for treatment. However the relationship between elevated blood sugar levels and medication treatments is a bit more complicated than one might assume. For example low blood sugar might lead to a stress response, in which case sugar levels will spike, in what amounts to a compensatory response – even in the absence of sugar intake. This is particularly true after exercise or duress and it signifies that the body has a signal system that can correct for neurochemical depletions. In this particular instance lactose would be released in considerable volume, thus converting low sugar levels into high sugar levels.

Something similar could occur with norepinephrine and other neurotransmitter/hormone outputs that comprise the shield. In somewhat of a neuro-behavioral irony, aggression might simply represent a compensatory spike prompted by low neurotransmitter/shield resistance and high energy task demands. If so, that would suggest the cause of the tantrum is not just habit and/or frustration but also a neurobiological compensation originating in a mismatch between stimulus levels and attention requirements, coupled with a deficient shield mechanism.

Theoretically (some might argue, too theoretically), this model could be applied to everyone from the autistic individual to the client with depression, or even individuals with conduct disorders and socioopathy. It could also be used to explain the unique juxtaposition of antisocial behavior and autistic symptoms seen in Aspergers Syndrome.

Perhaps in that sense it casts too wide a net. On the other hand, a neuropsychological principle discovered by Yerkes and Dodson (1908) offers support. In their classic experiment, they demonstrated that behavioral efficiency and performance depend on a close correlation between the level of activation and the nature of the task. The Yerkes-Dodson law was not applied strictly to the neuro-developmental population but might have relevance in that regard. In that sense the shield could be viewed as a very significant determinant of intellectual ability, memory, attention, motivation, language and other mental faculties affecting not just those on the spectrum but all of us.

If that hypothesis is feasible then it might be interesting to see if clinical approaches focusing on shield-enhancement might make a difference in the lives of individuals with ADHD, Autism, learning disabilities, depressive clients and anyone who finds it hard to function on a day to day basis vis a vis the demands of the outside world. That of course would require a greater understanding of the process of neuro-humoral preparedness in the brain.

In a previous article this writer wrote about the potential benefits of norepinephrine as a pan-curative element that helps us cope not just with learning problems but also medical problems. The above-mentioned study by Sahehi on Down Syndrome is interesting in that respect. Whether any research has been conducted regarding input/brain energy differentials and neuro-humoral conglomerates is not known to this writer. Of particular interest would be how those factors correlate with symptom severity, attentive faculties, memory and cognition. Such an undertaking might help provide a more thorough understanding of developmental disorders and human intelligence per se.


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Berridge, CW, Waterhouse, BD (2003) Locus Coeruleus Noradrenergic System and Modulation of Behavioral State and State-dependent Cognitive Processes. Brain Research Review. April 42 (1) 33-84

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Sahehi, A (2009) Cognitive Dysfunction Reversal in Mouse Model of Down Syndrome. Science Translates Medicine. Article 11/19/2009 in Science Daily.

Shekin, WO, Bylund, DB, Hodges. K. Glaser, R. Ray-Prenger, C & Oetting, G. (1994) Platelet alpha 2 adrenergic receptor binding and the effects of d-amphetamine in boys with attention deficit hyperactivity disorder. Neuropsychiatry,: 29 (3) 120-124

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Young, JG, Kavanaugh, ME. Anderson, GM. Shaywitz, BA. Cohen, DJ. (1982) Clinical Neurochemistry of Autism and Associated Disorders. Journak of Autism and Developmental Disorders. 12: 147-165



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