Discussion of a Brain-Based Remedial Approach with ADHD and Executive Function Impairment
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Date: Wed, 18 Mar 2009 Time: 5:14 PM
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DISCUSSION OF A BRAIN-BASED REMEDIAL APROACH
WITH ADHD AND EXECUTIVE FUNCTION IMPAIRMENTS
“Overt Self Regulation 101”
By Robert DePaolo
A quick glance at the evolution of human culture would seem to suggest that new inventions, discoveries and progress itself typically arise from serendipitous mergers between previously disparate ideas. Whether it be Einstein imagining himself at a train station, stumbling upon Relativity Theory, Freud engaging in impromptu conversations with clients about their dreams and discovering the unconscious, or Charlie Parker drifting coincidentally from the classic swing tempo in developing the framework for bebop jazz, the process of divergence/convergence/innovation tends to repeat itself. One suspects a merger (accidental or otherwise) between ideas in Neuropsychology and Education might be just as fruitful. This might be especially true with regard to the remediation of students with Attention Deficit and Executive Function Disorders.
The terms Attention Deficit and Executive Function have become core elements in the modern educator’s vocabulary in recent times. At present nearly seven million students nationwide are diagnosed with Attention Deficit and/or Executive Function Disorder. While the ubiquitous nature of these disorders might imply that educators have a thorough familiarity with the cause and remediation of those syndromes, very little is actually known about attention and executive functions, other than in a topographical sense. Indeed so many words are typically used to describe the two faculties that it virtually precludes any sort of precision, either with respect to diagnosis or remediation.
Executive functioning is a real potpourri. Variously defined as a lack of planning ability, lack of anticipatory memory, inadequate self-regulation, lack of automaticity in skill acquisition, poor judgment and impaired social cue processing, it’s true essence remains somewhat vague. Meanwhile ADHD, which often includes executive function deficits, is also somewhat mysterious, particularly with regard to its overlap with factors like boredom-induced distractibility, auditory processing problems, learning disabilities and lower cognitive ability – all of which can lead to problems with activity, behavior, self- regulation and concentration. In that context, the diagnosis of such phenomena is often in the eyes of the beholder, based on overt behaviors and academic and social performance, and outside of a neuro-functional framework.
At present, not enough is known about the brains of individuals with executive function and attention deficits to paint a clear picture of causation. There is some evidence that the frontal lobes of children with ADHD exhibit delayed cellular maturation (Rappaport 2007) and that the disorders might have a genetic basis (Vance, 2009). But due in part to the small samples of subjects available to research studies, conclusions have been hard to come by. On the other hand, and to reiterate a point, sometimes a merger between different ideas can provide clarity.
To begin this discussion I’d like to reflect on two separate and completely unrelated events that nonetheless provide hints about the nature of these disorders, then extrapolate from that to a neuropsychological model of attention and executive function disorders that would lend itself to a particular remedial strategy.
Event No 1: The Strange Case of Phineas Gage
Mr. Gage was a rather straight-laced railroad worker from Lebanon, NH who suffered a serious head injury in 1848; the details of which are unfathomably grotesque. A tamping iron over three feet long and over an inch in diameter accidentally pierced his left cheek and continued its trajectory through the left frontal area of his brain – completely destroying the tissue therein. Ten days later, miraculously, he returned home, and while he exhibited changes in language and personality, including an uncharacteristic use of profanity, lack of social deference, capriciousness, and an inability to adhere to plans, he was able to function. Phineas’ overall health was essentially normal and he went to work subsequently as a coach driver. His case aroused the curiosity of the medical community but hard research was never conducted with regard to his post-morbid skills and functions, other than in the form of medical reports submitted by his treating physician. It left a lingering question about the functions of the frontal lobes.
It is now presumed that the frontal lobe of the brain somehow regulates behavior and provides inhibitory restraints on impulse (Arco, Cohen et. al 2004), creating a “pause function” that enables one to step back, look at the big picture and create schemes, rules and plans. Since the traditional premise is that frontal damage impairs attention and self regulatory capacities, one might expect to find neuropathy among individuals with executive and attention deficits. Unfortunately, the evidence for that is inconclusive.
It does appear that frontal lobe functioning has an inhibitory effect on inputs from various brain sites to which it is richly connected. Yet even if there is an irrefutably strong correlation between frontal dysfunction and ADHD and Executive Function Disorder, that wouldn’t explain very much about what those terms mean. Once again, it brings us back to questions about the essence of attention and of executive function disorders. With that comes the second vignette.
Event No. 2: Hull’s Model of Mind
Clark Hull began his tenure as a research professor of Psychology at Yale in 1929. He had read Isaac Newton’s integrative treatise on philosophy and mathematics, Principia, and decided to develop his own integrative ideas on behavior. Like Newton and Einstein he dabbled in diverse fields before embarking on his quest for a unified theory. He studied mental phenomena such as cognitive processes and hypnotism, developed aptitude test formats and over time became very interested in discovering the mechanisms underlying human thought. During his time not much was known about human cognition, at least in an empirical sense. The Zeitgeist in the field of psychology featured a clear separation between behaviorism, which measured specific responses to specific stimuli and was quantifiable, and Tolmanian cognitive psychology, which was still within the realm of theory. Hull sought to build a bridge between the two schools of thought by developing an objective formula by which to define and measure cognition.
His studies involved having rats run through a maze in order to obtain food. The animals had to decide on turns, direction and spatial elements to reach the goal. Such an endeavor took time, but the rats were able to learn. The question was; how, especially since the two prevalent behavior theories of the time (classical conditioning and operant conditioning) were both contradicted by the rats’ performances. For example, while in the maze, the rats were behaving – moving probing, changing direction etc. Yet there was no stimulus and no reinforcer in the tunnel during those times. What exactly kept the creatures going?
Hull believed he found an answer. By use of an electronic measuring device he was able to discern subtle, covert motor responses in the rats during the non stimulus, non reinforcement times. In other words it appeared the rats were providing their own motivational and perceptual continuity (tantamount to self regulation) by approximating the behavior they would use upon finding the food and by responding perceptually to the food stimuli as if it were within sight. Hull called these phenomena the fractional goal response and fractional stimulus. He could have just as easily said the rats used memory (which all mammals clearly have) to internalize the learning process but that would not have been measurable, at least not within the scope of the empirical research model.
Hull went on to describe an entire behavior/cognitive theory in mathematical terms, perhaps as an unwitting homage to Newton. Many of his ideas were subsequently refuted, in part because his mathematical variables were so precisely delineated that they could be easily tested. However the idea of the fractional goal response (or at least the concept that covert behavior drives cognition, habit and motivation) has stood the test of time (Grush 2004), Hesslow (2002). There is still some argument as to whether, as per Hull’s contention, thought is really behavior whittled down to covert levels, and that mentations such as imaginative thought and anticipation are really subliminal motor behaviors. What does seem clear is that brains, particularly the human brain, is not only able, but inclined to produce unobservable, inhibited versions of behavior that, in the Piagetian sense enable us to contemplate “as if” scenarios, through operational schemes.
That brings us back to the frontal lobe, and specifically the questions of what it does and how it does it. Research evidence presents a quandary. On one hand studies have shown that frontal lobe damage can effect a wide variety of functions, including language impairment (Brown 1972), impoverished facial expressions (Kolb and Milner 1981) and problems with initiation, judgment, impulse control, social and sexual behavior. On the other hand, Alexander, Benson et. al. have been able to conceptualize those various functions under the single rubric of language (1989). Taking into account the Phineas Gage experience, which saw fairly minimal impairment, and the research studies, which show widespread impairment, it would seem the frontal lobe has both a narrow and broad central purpose, which sounds paradoxical.
That’s where the Alexander-Benson study comes into play. It suggests all of the impaired functions incurred with frontal lobe damage can be viewed as a function of language and communication. It sounds feasible. For example, facial expressions can be considered narrow versions of communication. Social judgment comes from language-derived propositions on morality, altruism and other interactive rules. Rules themselves are function of language – for example laws are grammatical, logical and of course developed in a language format.
There are of course two frontal lobes – one on the left side, one on the right. The left has been shown to play a role in language, while the right is more propositional. Yet this too creates a dilemma. There is more than one language center in the human brain. One (Broca’s area) lies in the posterior frontal lobe, while another (Wermicke’s area) is situated in the temporal lobe. This language circuit drift suggests that language might function more broadly than the term “communication” implies.
Meanwhile, facial muscle control supposedly is regulated in the parietal motor strip, yet clearly can be effected by frontal damage, and emotions (also affected by frontal damage) appear to emanate from the limbic system, in the midbrain. Thus it would appear the frontal lobes do not foment or facilitate specific functions but rather provide a secondary function, perhaps serving as a gait keeper for expression, specifically by providing a capacity for covert, inhibited (language-fractionated) expression.
This brings us back to Hull’s fractional goal response. Rats have no language per se, and thus tend to internalize and register inhibited, covert versions of motor behavior as their prime mode of cognition. Humans do have language and therefore can run expression, as well as movement and perception through the frontal colander for refinement. In terms of brain evolution, the process wouldn’t have required a special function for the frontal lobes – only that they evolve through non specific brain expansion, and that impulses from other sites run through their networks via a garden-variety inhibitory process.
Perhaps that covert governance – that neural whittling process - is what provides the human learner with skills education theorists variously refer to as meta-cognition, self regulation, executive functions, attention span, task intitiative, a capacity to self reinforce and sustain interest and attention to academic tasks.
With regard to students with executive and attentive problems, brain studies have not consistently shown damage in the form or lesions or ventricular blood flow anomalies. On the other hand evidence is beginning to show that cellular dysplasia (a degree of brain cell immaturity) might be involved in not only executive and attention-related disorders but also Autism and Aspergers’s syndrome (Rubia, Overmeyer et al 1999), (Ahgren, Baldwin et al 2005). If cellular dysplasia is involved in attention and executive function disorders, then one possible contributing cause of those disorders can be said to be a frontal/inhibitory (internal language) deficiency. Certain trends would be predicted from that, including:
1. Problems with behavioral inhibition (impulsivity) social immaturity (based on poor processing and parsing of social-communicative cues that would normally come with stronger inhibitory capacities.
2. Internal language deficits, manifest as poor working memory leading to variable academic performance.
3. Difficulty with task initiative (due to the lack of internal motivation and regulatory skills that normally facilitate internal language guidance, as well as and planning and judgment skills.
One could conceivably compress what seems to be a complex neuropsychological process into a simple diagnostic premise; specifically that the student with attending or executive problems might lack the ability to covertly talk himself through tasks, and provide the attentive regulation, self reinforcements, start-up prompts and working memory capacities (Petrides, Alivistatos et. al 1993), (Paulescu, Frith et al 1993) that come with a fully mature frontal lobe, and more specifically, with fully developed internal language capacities.
A Remedial Concept
The above scenario implies certain things about remediation, and brings to mind the first grade student who is just learning to read and has not developed the word, syllabic, phonetic and comprehension skills to an automatic degree. Faced with such limitations. he is forced to read out loud, needs to receive feedback from his teacher and must utilize outside sources for not having internalized the process. It is conceivable that the symptoms associated with ADHD and executive disorders result from similar limitations. For example, while the young student cannot read silently, the ADHD or executively impaired student cannot talk to himself internally in ways that prompt a task focus and submit motivation-sustaining, self-provided feedback. In that context, he can be said to have, not an attention deficit or self-regulation problem, but a self-talk deficiency.
If that explains in part why and how ADHD and Executive Disorders affect learning and social adjustment, it might be helpful to incorporate not just classroom accommodations and alternative curricula but also a self regulatory plan into the student’s IEP, whereby he or she is coached in how to self-prompt, self-reinforce and self-sustain effort on task as well as in social situations. Just as a teacher might encourage an immature student to continue reading out loud prior to his reaching the level of automaticity, so too might the teacher help the ADHD or executively impaired student to develop overt self-talk regulatory skills to compensate for an internal language problem – at least initially. Perhaps with enough practice in overt self-talk guidance (including use of self-reinforcing comments) this could evolve into a covert skill, raising attention, self-regulation and task-initiative to the level of automaticity.
These assumptions are, of course, theoretical. Yet similar approaches have been advocated and used successfully in several school districts and university research projects (Munro, 2008), (Cowan, 2009), Harvey, Fagan et. al 2003). This article argues for a remedial approach that might not only be successful, but also provides a clearly defined neurological substrate for the two disorders.
References
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