Attention- deficit /hyperactivity disorder (ADHD) is currently one of the most common disorders of childhood occurring in 9% of children (Halperin, 2010). In Western society’s search for empirical truth a tendency to label everything has been developing. Being able to categorize and classify everyone and everything into neat boxes makes for clear cut parameters, but it has its downfalls. More specifically, when we get into the habit of classifying different behaviours and labelling them as mental disorders, at what point do we stop ourselves and question the methods we use in both diagnosing and treating these behaviours? There is already literature that maintains that diagnostic categories are constitutive: they construct, rather than represent reality (Cosgrove, 2005). The moment I realized the truth validity of this statement was when we were made aware that my brother was misdiagnosed with Attention Deficit Hyperactive Disorder. He received the diagnosis when he was six years old. Medication was strongly recommended to treat his condition, as the psychiatrist said that ADHD was the cause of his inability to regulate his behaviour. My mother refused to put him on medication, but it left me wondering what the ramifications would have been, should she have chosen to treat this misdiagnosis with what is currently available in the market?
ADHD is a disorder that is managed and not cured (Goldstein, 2008). Considering the permanence of the condition, how, in the span of four years can a child go from not only being diagnosed with ADHD, but having a strong recommendation of being medicated as a result, to having another professional adamantly deny that there was any basis to the initial diagnosis? Based on the DSM-IV, ADHD is said to have a neuropsychological profile and yet, the diagnostic criteria continue to reflect behavioural rather than cognitive or neuropsychological manifestations (Goldstein, 2008). So which is it? Many researchers start from the assumption that research hypotheses, data analyses, and diagnostic labels are neutral, objective and free of bias; this assumption sustains the science/politics binary because it is based on the belief that science, in contrast to politics, is uncontaminated by power and particular interests (Cosgrove, 2005). How much of what we read in the DSM is socially constructed, and how much of it is based on real neuropsychological disorders? The objective of this research paper is to determine if whether or not ADHD is a social construct or has neuropsychological basis.
In conducting my research I will primarily focus my attention on the history of ADHD and how it has progressed from when it was first introduced into society until now. Secondly, I will be looking at the nature of ADHD, as well as some of its defining characteristics as agreed by the APA (American Psychiatry Association), and the DSM-IV. The paper will bring to focus three sub-components of ADHD being ADHD-HI, ADHD-I and ADHD-C, identifying their behavioural manifestations as well as differences and similarities between the three sub-diagnosis. The paper will also be identifying current theories and strategies that are in place as modes of intervention and treatment for these three separate forms of Attention Deficit Hyperactivity Disorder. Once we have identified both the history, and the foundation of the disorder itself, the paper will bring to focus the literature that supports there being a neuropsychological basis to the diagnosis of ADHD.
The paper will be focusing on consistencies within the literature as well as disparities. Upon outlining the schools of thought that support there being a neuropsychological basis for ADHD, we will then look at the literature that considers the claim that ADHD as a neuropsychological disorder is unfounded, and critically assess their reasons for believing that ADHD is nothing more than a construct established by society to generate yet another label. We will then turn our focus to the treatment used for children suffering from ADHD, both medicinal and behavioural therapies that are available, and discuss the benefits and setbacks of the available treatments. Lastly, I will draw on the strengths and weaknesses of both arguments, ADHD as a disorder supported by having a neuropsychological basis, and ADHD as nothing more than a social construct, to determine which of the two premises hold more truth in what they are trying to discount. It is important to note that mental disorders, ADHD included, do not necessarily have to derive from neurophysiology to hold as true disorders. Attempts to explain a client’s distress by appealing to primarily or solely to intra-individual factors e.g. cognitive distortions, neurotransmitter dysfunction, weak ego boundaries, obscures the role of social injustice in the development of personal distress or disability (Cosgrove, 2005). I would not make such a strong claim that there would need to be some deficit in the physical brain in order to conclude that the disorder exists.
The objective of this study is to determine if ADHD is a manifestation of the sort as subscribed by the DMS-IV, as well as the APA. This study appreciates the history and controversies that surround many DSM diagnoses, that also bring to bear on the disorder in question, being ADHD. Many personality disorders listed in the DSM readily fit stereotypes of marginalized groups […] the creation of diagnosis such as Premenstrual Dysphoric Disorder (PMDD), Dependent Personality Disorder (DPD), and Gender Identity Disorder (GID) demonstrate what a psychologised society North America has become (Cosgrove, 2005). It is important to look at what society deems as ‘mental’ disorders and critically assess the diagnosis and determine if symptoms are created to match with the diagnosis, or if the diagnosis is a sum of its symptoms. It is also very important to note that once we have established that a disorder exists, that we are then identifying the disorder efficiently and treating people effectively. If one of these three criteria is not met, that in itself would not be sufficient to conclude that ADHD is nothing more than a social construct, but it would be enough to say that we need to reorganize and redefine the parameters in place in order to avoid misdiagnosing, and unnecessarily treating healthy individuals. My hope is to review the available literature without bias, understanding that there will be no clear-cut answers in discovering my objective and perhaps conclude by determining that ADHD has some components of both neuropathology and components that are more socially constructed.
The History of ADHD
In May 1968, the second edition of the DSM was published and under the category of Behaviour Disorders of Childhood and Adolescence a condition referred to as Hyperkinetic Reaction of Childhood (or adolescence) was introduced (Goldstein, 2008). The symptomology of this behaviour was characterized by ‘over activity, restlessness, distractibility and short attention span, especially in young children; the behaviour usually diminishes in adolescence” (p.50 DSM-II). The manual noted that these conditions “are more stable, internalized and resistant to treatment than transient situational disturbances but less so than psychoses, neuroses, and personality disorders (p.50, DSM-II). Once these behaviours were observed, at that point a diagnosis was made. The identifiers used to subscribe someone as suffering from ADHD is interesting. How do we determine normal activity from over activity? What are the qualifiers for restlessness, distractibility and short attention span? It would seem that from the very beginning ADHD was subject to the observer relative biases of the clinician.
Another cause for concern is the fact that there is no defined parameter of exactly what is meant by the terms used to diagnose children with Hyperkinetic Reaction of Childhood. The third edition of the DSM defined two sub-types of ADHD; ADD with hyperactivity and ADD without hyperactivity (Chhabildas et al, 2001). Thirty-two years from the second edition, DSM-IV of the APA was published, and the manual had grown from 134 pages to 943 pages (Goldstein, 2008). The diagnosis of Hyperkinetic Reaction of childhood evolved to be referred to as ADHD, Attention Deficit and Hyperactivity Disorder, the original description of eight lines for this condition grew to a set of diagnostic criteria and accompanying descriptions of eight pages (Goldstein, 2008). Despite the fact that characteristics that would lead to a diagnosis of ADHD went from eight lines to eight pages, none of the necessary conditions used to identify a subject with ADHD supported there being a neuropsychological basis to the disorder. All of the descriptions were behavioural characteristics of children that were and are broad enough to easily classify a child who would not otherwise be characterized as suffering from ADHD.
With the fourth edition, there are currently three sub-types of ADHD, ADHD-C, ADHD HI, and ADHD I (Goldstein, 2008). Even still, the diagnostic process has remained unchanged (Goldstein, 2008). Despite the many changes and editions that they’ve made to the diagnosis itself, no adjustments have been made to ensure that the diagnosis subscribed to children who are labelled as suffering from ADHD, was more than just the subjective opinion of the clinician. With such a huge list of supporting behavioural characteristics, and no formalized tools in order to apply them as needed, it is left to wonder why there are huge controversies surrounding how much of the diagnosis of ADHD is emitting from the child’s behaviour, and how much of ADHD is moulded by the DSM?
What is Attention Deficit Disorder?
The definition of ADHD as applied in this segment of the study was purposely structured to not incorporate a neuropsychological definition. Both the neuropsychological definition, as well as components of the definition that are considered as being socially constructed will be revisited later on in the study. Rather than providing a biased definition that would either be, “I support the neuropsychological side,” or, “the side that deems the disorder to be socially constructed,” the definition provided here will be as objective as possible. The essential feature of ADHD is currently described as a “persistent pattern of inattention and/or hyperactivity impulsivity that is more frequently displayed and more severe than is typically observed in individuals at a comparable level of development” (p.85, DSM-IV). This condition is increasingly being identified and defined as a disorder resulting from impaired behavioural inhibition leading to executive function deficits (Goldstein, 2008). Children with ADHD are characteristically impulsive and make hasty responses in situations where care and caution are needed, and make slow, inaccurate responses when speed is called for (Nigg, 2006). This finding seems to imply that there is definitely some type of reversed order going on when children suffering from ADHD are subject to tasks that normal subjects would have completed with the opposite results. By executive functions, ADHD is being characterized as a disorder that specifically affects abilities to plan effectively, incorporate self-discipline in order to regulate and modify behaviour according to the social settings.
ADHD appears to be distinct from other psychiatric and developmental conditions because of its intensity and persistence as well as the clustering of symptoms rather than the simple presence or absence of symptoms that drives impairment and ultimately confirms the diagnosis (Goldstein, 2008). As will be mentioned later on in the paper, a lot of what is characterizing ADHD as different from other disorders actually lend to support characteristics of disorders that also seem to overlap with ADHD, such as bi-polar, and depression. Most if not all psychiatric disorders that are characterized as developmental rather than situational, are disorders that are chronic and linger throughout the life span of the individual. Some disorders that come to mind are things like learning disabilities such as dyslexia. ADHD reflects an exaggeration of what is normal behaviour, either too much or not enough of what is expected in certain settings (Goldstein, 2008). Since the 1970s research has increasingly suggested that the core problem for ADHD is not excessive activity but deficits in executive functions […] representing a profound disturbance in self-regulation and organization behaviour across time (Goldstein, 2008).
ADHD-H is congruent with issues in executive functions, whereas ADHD-I would be dealing with selective attention problems (Goldstein, 2008). ADHD-I based on current studies, isn’t ADHD at all. Recent debates surround if whether or not this sub-type should be completely removed as what would be characteristically described as ADHD as the symptomology is completely different. They have an impairment in selective attention and these children appear “daydreamy,” hypoactive, passive, apathetic, lethargic, confused, and sluggish as well as socially passive and withdrawn (Goldstein, 2008). These characteristics seem to be completely opposite of what ADHD is normally recognized as portraying in behaviour, characteristics that would follow the standard descriptions of ADHD would include examples showing hyperactivity, high strung, strong emotional fluctuations, with an inability to regulate emotions. ADHD-I is different from inhibition needed to control behaviour, a problem for persons with ADHD-HI, in that attentional inhibition means focus on relevant stimuli and resistance to responding to distracters in the environment (Goldstein, 2008).
At this point, people are starting to question the very label of ADHD-HI since their deficiencies lie predominantly in behavioural control and do not suffer from attentional deficits, using such a descriptor leads to the logical assumption that these children are poor in attention; it would be more logical and consistent with the symptomology to describe children with ADHD-I as attention deficit as they have problems with selective attention, but those with ADHD-HI be given a different label , something along the lines of self-regulation deficit (Goldstein,2008)
Neuropsychological definition of ADHD
The three sub-types of ADHD have differing neuropsychological profiles. ADHD was first classified, as we saw earlier into two sub categories being ADD- H and simply ADD. The latter being Attention Deficit Disorder with Hyperactivity and the former being simply ADD without the added Hyperactivity, this was the diagnostic criteria established in DMS-III. DSM-IV defines ADHD based on elevations of two separate but correlated symptom dimensions, those of inattention (IA) and hyperactivity/impulsivity (H/I), children meet criteria for the disorder by having six or more symptoms of either IA or of H/I, or both (C) (Chhabildas et al, 2001). DSM-IV describes three diagnostic subtypes of ADHD based on differential elevations of symptoms on these two dimensions (Chhabildas et al, 2001). Essentially, those with ADHD experience a constitutional predisposition to struggle with attention, effort, inhibitory control, and fully modulated arousal, and have a need to seek stimulation (Goldstein, 2008).
Children with ADHD Combined Type (ADHD C) and ADHD Hyperactive/ Impulsive Type (ADHD HI) are characterized as having poor behavioural inhibition, their symptoms include problems with inhibition of prepotent responses, which limits control of behaviour, which leads to poor planning and anticipation; reduced sensitivity to errors; poor organization; impaired verbal problem solving and self-directed speech; poor rule governed behaviour and self-regulation of emotion; problems developing, using and monitoring organizational strategies; and self-regulation and inhibition problems (Barkely, 2003). Most of the above-mentioned research focuses on the behavioural aspect of ADHD, and then they are drawing inferences to the brain processes that are known to be involved with the functions that are affected by the disorder. Neuroimaging studies suggest an important role for frontostriatal circuits along with a wide array of other cortical ADHD (Halperin, 2010).
Similarly, studies have found reduced caudate nucleus size, and reduced volume in the globus pallidus and reduced callosal area in ADHD (Halperin, 2010). Based on prior exposure, I know that the caudate nucleus is involved with learning and memory, the article didn’t say specifically what the correlation of learning and memory had to do with evidence that its’ reduced size also corresponding to the presence of ADHD which is more about behavioural inhibition, and hyperactivity. ADHD is not a learning disability, it can be characterized as an inefficiency to use what they know to behave accordingly, but their ability to learn and retain information is not affected. Located below and behind the prefrontal cortex lays the basal ganglia; neural loops exist between the prefrontal cortex and the basal ganglia especially the putamen and the caudate (Nigg, 2006). The feedback structure is meant to modulate and maintain goal directed behaviour and to control unwanted response tendencies; these structures assist with motor control, emotion, motivation as well as maintenance of attention and suppression of motor responses (Nigg, 2006).
This is an interesting correlation, as the feedback structure seems to have a strong overlap with some of the defining characteristics of ADHD. They are not good at behavioural inhibition, neither with the suppression of motor responses. The fact that the system is also meant to modulate and maintain goal directed behaviour and control unwanted response tendencies makes a strong argument that deficits to this structure would lead to a lesser ability to maintaining control of these functions. Structural anomalies have also been reported in several brain regions outside of the frontal lobes and striatum; studies have also noted reduced volume in several parts of the cerebellum in ADHD as well as posterior cortical anomalies (Halperin, 2010). The cerebellum is known mostly for its role in motor control. It also has some involvement with cognitive functions such as language and attention. To say that the volume of the cerebellum is reduced and that it correlates specifically to ADHD, without any explanation for there not being deficits in language production leaves open questions about how far this evidence goes to support the claim that the volume decrease in the cerebellum plays a role in the neuropsychological profile of ADHD.
Recently, studies have begun to use MRI to examine differences in cortical thickness between individuals with and without ADHD, Shaw et al (2006, 2007a,b) reported that children with ADHD followed a similar sequential pattern of cortical development, yet were delayed by as much as 2-3 years, depending on the specific cortical region (Halperin, 2010). These studies didn’t make mention exactly how big of a disparity there was and if it was consistent amongst participants. Up until this study the profile of ADHD as a disorder has always corresponded with it being a long-term disorder that one developed strategies of coping with. In saying that ADHD is a developmental delay would suggest that the disorder itself will disappear over time. This is a clear contradiction to how the majority of the literature would characterize the disorder. The DSM-IV field trials indicated that the current subtypes differ significantly on variables such as age of onset, gender ratio, and level of social and academic impairment (Chhabildas et al, 2001).
There really is not much literature that defines the neuropsychological profiles of the subtypes of ADHD, but more is known about ADHD as a global category (Chhabildas et al, 2001). Interesting that they use the term “global category” to subscribe to ADHD; if it can be described globally, then why are the symptomologies for each subtype of the model so different? Not to say that a neat correlation should be expected between the neurophysiology and behaviour, but it is a bit odd to have three sub-types that have different behavioural manifestations derive out of a single set of neurophysiological deficits. A finding of differential neuropsychological profiles would not only lend external validity to the subtypes, but also could suggest that the different subtypes develop along different etiologic pathways, may require varying treatments, and may have differential outcomes (Chhabildas et al, 2001).
Another interesting overlap that needs to be mentioned is that the prefrontal structures are implicated in many psychiatric disorders, as they are involved with what has been termed “executive function” and memory […] (Nigg, 2006). We will be looking later on at the comorbidities that are also associated with ADHD, to critically asses how much of the neuropsychological that has been reduced to the mentioned brain areas are specific to ADHD or can be, or most likely are attributed to another disorder.
ADHD as a social construct
After having looked at all the literature had to say with respects to ADHD correlating with deficits in executive functions, it seems an interesting objective to try and undermine all the prior research and go forwarded with saying that all the claims are unfounded. Yet there is just as much research that provides evidence that this is the case. Experimental work shows that executive function deficits do not explain ADHD (Furman, 2008). Most ADHD review confuse “familial” with “genetic” and trivialize the potential role of nongenetic factors with short lists such as “food additives/ diet, lead contamination, cigarette and alcohol exposure, maternal smoking through pregnancy and low birth weight; nongenetic familial factors are powerful and difficult to measure and include the effects of culture, religion, learning, parenting and socioeconomic adversity (Furman, 2008).
These are some of the factors that research written to support claims that ADHD has neuropsychological basis fail to even make mention of. There is absolutely no focus put on potential environmental factors that can lead to the onset of the behavioural manifestations of the disorder. Yet, with other psychiatric disorders, the nature-nurture debate is usually thoroughly investigated. Interestingly, with all the evidence that purports that ADHD is of a biological kind, the DSM still only establishes diagnoses of the disorder based on observable behaviour. Psychiatric geneticists initially embraced genome scans and candidate gene studies as ways to identify a genetic cause of ADHD, these have yielded negative results (Furman, 2008).
Candidate molecular gene research has focused primarily on neurotransmitters affected by ADHD medications; this literature is largely inaccessible to those not schooled in epidemiologic analysis of molecular genetic studies, creating reliance on reviews that are excessively enthusiastic and frankly misleading, describing results as having ‘produced substantial evidence implicating several genes in the etiology of ADHD (Furman, 2008). Already at this point we are seeing truths a priori to these claims prior to do investigations. A lot of the literature that focuses on ADHD being of a biological sort are technical in nature, and the majority of the public does end up having to rely on the experts to get the gist of the findings without being able to make sense of the reports on their own.
This means that small effect sizes can clearly be construed as large effect sizes and we wouldn’t know differently. Not much of the literature demonstrated in this study focused on molecular genealogy, yet we can see even with the studies mentioned that some of the claims that are made i.e. with the cerebellum, are made without any explanation of why other mechanisms in which these parts of the brain are involved in processing are left unscathed. The major contributing factor to ADHD that was consistent across studies was deficits in executive functions yet current studies are showing that there was not a significant difference in these regions after controlling for brain volume; rather, a difference in cerebellar volume was noted (Furman, 2008). The studies of overall and region-specific cerebellar volumes showed inconsistent rather than confirmatory results (Furman, 2008). This is an inquiry that I made earlier on in my study. The fact that the effect sizes weren’t readily available to determine how great the disparity was between agents suffering from ADHD and normal subjects. Based on these findings, there is not any significant trend, also, what was failed to be mentioned in the neuropsychological literature is that it is highly likely that complex brain functions recruit neural networks throughout the cortex and are not mapped identically in all individuals (Furman, 2008).
This would make it all the more challenging to find correlations consistent across individuals when there isn’t an actual deficit or lesion that is commonplace with the specific disorder. Since ADHD is a deficit in higher order cognitions, any correlations that we draw from the neurophysiology will only be probabilistic in nature. If they can only be probabilistic in nature then how are we so ready to define it as a treatable disorder? The original unifying neuropsychological theory postulated for ADHD was a deficiency in executive function, specifically inhibitory control; studies have been conducted that matched 75 boys with “severe” ADHD with 70 controls, and there were no group differences on executive functions and inhibitory control tests (Furman, 2008). What does this tell us about the articles printed that prove that ADHD is of a biological nature? Essentially it is telling us, that perhaps ADHD is strictly behavioural, and scientists are grasping into thin air to make the diagnosis of ADHD an empirical one in order to perhaps lend further support to there needing to be a pharmacological treatment to suppress the behavioural component.
If we recall the history of ADHD started out as being purely behavioural, and later on as it grew as a disorder, it would seem psychiatrists felt the need to defend ADHD by necessarily reducing their explanations to actual deficits in cognition, and it brain organization. This is most likely due to the rise of prescription drugs that are being recommended to treat this disorder, as well as questions that parents are very well asking, to determine the validity of the diagnosis. Neuropsychological research on ADHD has largely ignored environmental and personality factors, which have been important to the understanding of other childhood pathologies; test results are analyzed without consideration for emotional factors; investigators use reward points for task success as a proxy for affect, motivation and task saliency (Furman, 2008).
One has to question why research conducted to support the neuropsychological bases of ADHD are leaving out so many variables that have proven to be important in properly establishing parameters for other psychiatric disorders? We’ve taken a look at the research and see that there is bias that makes it seem as though interaction with the environment does not play a role in the manifestation of the disorder. Yet other research is saying differently, other factors that are said to associate with the diagnosis of ADHD include lower socioeconomic level; family conflict; punitive parenting methods; parental affective disorders, such as maternal depression and anxiety; parental substance abuse; parental disruptive, antisocial and criminal behaviour, increased TV viewing; and intellectual disability (Furman, 2008). This research is painting a wholly different picture of ADHD, not to say that any of the associations between environmental, psychosocial, and parenting influences establish themselves as the cause of the disorder, but they are still factors that should not be ignored (Furman, 2008).
An issue that we fall into when incorporating the medical model with trying to set defining parameters around mental disorders is that it necessarily has to reduce to a lesion or a deficit in the physical brain. If there is no physical manifestation of the mental disorder, then it can be argued that anything strictly mental is beyond the realm of physicians and clinicians; people who generally specialize in physical ailments and injuries. So, then we look at what psychiatrists use, and we are brought back to the DSM. In looking at the history of the DSM, we begin to see why it is so easy to establish that many of the disorders, ADHD included, are socially constructed and we are also able to identify motivators who would benefit from these diagnoses. The potential for conflict arises when DSM committee members are receiving funding, stocks or honoraria from pharmaceutical companies while they are conducting research on the efficacy of psychotropic medications or when they are providing testimony to the Federal Drug Administration (FDA) about whether a new mental disorder should be included in the DSM (Cosgrove, 2005).
There is a clear conflict of interest here. What this information is relaying is that not only is it a possibility that disorders are created simply to make money off of treating them, it is telling us that this is the case a good part of the time. It might also explain why a description of eight lines to identify ADHD, grew to eight pages within two editions. Something that shouldn’t be taken lightly is this “uneasy alliance” between the pharmaceutical industry and clinical investigators, a number of research physicians and public policy experts have raised concerns about the association between funding source and study outcome (Cosgrove, 2005). These are all concerns that bring to bear on the issue of ADHD specifically, as a result of the prescription medication that is being administered to treat the condition.
There are now seemingly many controversial reasons that seem to support ADHD as a disorder, and none to do with any evidence of an actual dysfunction in the child’s ability to interact. We not only have to question if whether or not there is a basis of there being a neuropsychological foundation to the disorder, but we also now have to question who is conducting the study and how is the study itself being funded, before believing there to be any truth validity to the arguments in support of the diagnosis. The very common behaviours described in the DSM-IV criteria for ADHD can be conceptualized as symptoms of childhood mental, emotional and cognitive problems rather than a neurobehavioural disease (Furman, 2008).
Comorbidities or Etiologies?
At this point, there are some other questions that we need to ask ourselves, if it isn’t ADHD, what else could it be? Apparently, children who meet criteria for ADHD may have one or more urgent and treatable conditions including;
- Ongoing or past physical or sexual abuse, ranging from punitive parenting to explicit abuse;
- Mental retardation, cognitive limitations, one or more specific learning disabilities;
- Hypervigilance and apprehension because of an unsafe or unpredictable environment at home or school;
- Psychiatric diagnoses, including depression and anxiety;
- Emotional and developmental difficulties because of conflicts or life stresses that would benefit from psychotherapy; and
- A mismatch between parental or educator expectations and child behaviour and performance–this may be due to developmentally inappropriate or child inappropriate expectations (Furman, 2008).
The list of other potential contributing factors to the child’s behaviour has too many options that are easily treated by psychosocial interventions, to have so many professionals jump to ADHD as a common denominator. A mainstream ADHD researcher noted that the “costs of ADHD treatment reflect dramatic underutilization of psychosocial treatments” and recommended the use of behavioural treatments, including educational interventions and parent education before medication (Furman, 2008). Putting the debate to rest for a moment, this statement made by the professional denotes many things. One of them being, even if there was such a condition formally known as ADHD, we aren’t treating the condition appropriately by automatically prescribing medication to mask conditions. Children with apparently “pure” attentional problems whose grades improve with stimulant treatment may have short-term improvement without long-term benefit, and the child’s apparent improvement (or worsening) can mask need for treatment of an underlying problem (Furman, 2008).
The potential of masking the actual issue should be a major concern to psychiatrists and clinicians who we would assume are in the industry to help treat and cure people of whatever physical or psychological distress they may be suffering from. The biggest factor in this is the fact that the topic of consideration is children themselves. The study will be taking a look at the medicinal treatments as well as their effects later on, but a priori without any further investigation we know that anything involving a disruption of neurotransmitters and dopamine intertakers in children is a risky event, as the drugs administered is causing a direct interference within the inner communications of the child’s developing brain. How much of a concern should this be? The range of “comorbidities” described in ADHD includes oppositional defiant disorder (30% to 60%); conduct disorder (9% to 19%); mood disorders, including depression (18%- 60%); anxiety disorders (23%-34%); and learning disorders (10%-90%) (Furman, 2008).
The overlap between some of these disorders is significant. It would be very easy, without the use of standardized tools in order to test the validity of diagnoses to confuse any one of the disorders with ADHD. Yet when ADHD seems to be the diagnosis in question, there are no tools currently being used, that provide any additional support to preconceived notions that the child might very well be suffering from ADHD. Almost all children younger than 12 years of age who meet criteria for ODD [oppositional defiant disorder] or CD [conduct disorder] will almost always meet the criteria for ADHD (Furman, 2008). ODD and CD are not conditions that are treated with medication. Rather, these children undergo behavioural interventions and treatments to curb the behaviour. Based on this statistic 90% of these children will be misdiagnosed and treated with medication.
Pharmacological Treatments for ADHD
The primary method of treatment for children suffering from ADHD is the administration of Ritalin. Ritalin (methylphenidate hydrochloride, MP) is a non-amphetamine psychostimulant and is the drug of choice to treat children and adults diagnosed with attention deficit hyperactivity disorder (Ferreira et al, 2010). Clinical studies have showed that even therapeutic doses of MP can induce severe manic-like or psychotic-like symptoms in children for which MP is used as a treatment for ADHD; this is attested by retrospective data showing high prevalence rates of schizophrenia or bipolar disorder in children under MP treatment (Ferreira et al, 2010). Already, we are seeing that the side effects that are highly prevalent are showing that there is minimal cost effectiveness in treating children suffering from ADHD, whether it is a social construct or otherwise. How do we justify treating behavioural symptomology that more poses as a nuisance and a disturbance to individuals around the child, by providing them with treatment that has been statistically proven to increase their chances of developing schizophrenia and bipolar disorder?
MP has a neuropharmacological profile similar to that of cocaine, releasing catecholamines and also inhibiting their reuptake, primarily the use of dopamine (DA), through its inhibitory action on the DA transporter (Ferreira et al, 2010). Despite the large number of children being treated with MP it is surprising that few studies have addressed the consequences of chronic MP exposure or withdrawal after long- or even short-term use (Ferreira et al, 2010). For a condition that has so many controversies surrounding its validity, I’m not sure why someone has not questioned or revoked the use of such strong medications that have such strong side effects in children who are under its influence. Also, the fact that there are so many children who are misdiagnosed with ADHD in a given year, nearly 900,000 children under the age of 18 were misdiagnosed with ADHD (Journal of Health Economics). Also, the misdiagnosis of ADHD is costing $320 to $500 million a year in unnecessary medication (Deanna Sletten).
It seems a bit conspicuous that pharmaceutical agencies are generating so much revenue gaining from the ambiguity and generalizations that are surrounding the current diagnosis. The fact that so many children are receiving unnecessary treatment hasn’t yet been considered as an epidemic is all the more alarming.
Ritalin was introduced into the market in the 1950s as treatment for fatigue, depression and associated psychosis, abnormal senile behaviour and narcolepsy (Svetlove, 2007). A medication that was initially introduced into the market to treat known neurophysiological disorders that do result from a disruption in the chemical balances in the brain to treating behavioural exuberances is hardly explainable. How does one justify using a psychostimulant to treat inattention and hyperactivity? Are we to say that these types of issues run parallel to disorders like narcolepsy and senile behaviour? I would hope that the answer is no. Because of its structural and pharmacological similarity to amphetamine, it has been suggested that the abuse liability of methylphenidate is similar to amphetamine, as an example MP was self-administered by dogs, evoked comparable discriminative effects in various animals and discriminative and subjective effects in humans (Svetlov, 2007).
A 1996 U.S. Drug Enforcement Administration (DEA) survey found that between 30 and 50 percent of adolescents in drug treatment centres reported Ritalin abuse—taken orally, through snorting and injection […] since 1991 prescriptions for all drugs to treat Attention Deficit Disorder have quintupled, in 2004, about six million children were prescribed Ritalin or other forms of ADHD medication (Svetlov, 2007). Despite the alarming findings that were presented in this study, the study itself depicted Ritalin as a harmless intervention method to treat ADHD. I see a huge disparity in this logic. Of those six million children who have been prescribed the drug it leads me to wonder how many of them didn’t need a prescription at all, and from that sample, how many of these children developed psychiatric illness as a direct result to this treatment.
What is our society doing to our children? We are providing a prescription medication that children have found methods to ingest orally, by snorting and injecting? These findings are hugely alarming to me. Regardless of whether or not we determine that ADHD has a neuropsychological basis one thing is clear, the current methodologies to treat ADHD need to be revolutionized. As it is right now, the drug is doing far more harm than good.
When looking at life impairments in adults with medication treatment ADHD we see that they have been shown to experience a variety of functional impairments, such as unemployment, or underemployment, economic problems and relationship difficulties (Safren, 2010). Beyond functional impairment, adults with ADHD have directly reported significantly lower quality of life than adults without ADHD with quality of life being negatively correlated with ADHD severity (Safren, 2010). Not only are the adverse effects of the medicinal treatments apparent with children suffering from this condition, but it has residual effects into adulthood. Medicinal treatment is being correlated with having a negative impact on the people’s self-esteem and overall morale. These quality of life impairments may be ameliorated with psychosocial interventions to augment effects of medication management (Safren,2010). It seems as though when incorporating medicinal treatment, the process of treatment become all the more complex. Not only are we treating the ADHD disorder, but also now we’re treating the psychological effects that come with the primary treatment. This seems counter intuitive and counterproductive as more resources are being used than necessary it would seem dealing with the residual effects of the initial treatment.
In childhood, ADHD has repeatedly been linked with academic, social and behavioural impairments, in adolescence there are parental concerns about poor schoolwork, peer difficulties, and behaviour toward parents or other authority figure are more often the reason for referral rather than the core system of ADHD per se, as adults, people with ADHD are involved in an even wider variety of settings that can be impacted by ADHD symptoms and also have more independent responsibility for their behaviour in such settings; not surprisingly, adults with ADHD report more impairment than their non-ADHD peers across domains including academic, occupational, home , marital and social functioning (Safren, 2010).
It would seem that there is a lot that the medicinal treatment lacks the capacity to treat when it comes to all that needs to be considered with people having to deal with ADHD as a life-long condition. Unfortunately, it is not optimal to sedate these individuals into adulthood, because as they develop, society expects that they are able to self-regulate and engage within their environments as autonomous agents. Perhaps at this point it would be beneficial to search out alternatives that have a more holistic approach to treating this condition effectively.
Cognitive Behavioural Treatments for ADHD
Having reviewed the literature on the medicinal treatments for ADHD and seeing some of the detrimental effects that it poses, it makes sense to seek out plausible alternatives that also have the capacity to effectively treat this disorder. Based on the research reviewed in this study, it would seem that the medicinal treatment only has masking effects on the symptoms that manifest with ADHD. This is apparent because as soon as the medication is removed, the behavioural symptomologies are back. Since there are such adverse effects to treating especially younger children who suffer from this disorder it is important to look for alternatives in treatments. An alternative method that I found in my research is known as “cognitive behavioural therapies”.
These therapies manifest because of the basic premise that current empirically supported interventions are generally successful in reducing ADHD symptoms, but treatment effects are rarely maintained beyond the active intervention (Halperin, 2010). ADHD is now generally thought of as a chronic disorder that is often present well into adolescence and early adulthood, the need for continued treatment throughout the lifetime is both costly and problematic for a number of logical reasons; therefore, it would be highly beneficial if treatments would have lasting effects that remain after the intervention is terminated (Halperin, 2010). These cognitive behavioural strategies still impose that there is some level of neurophysiological basis of ADHD, but one that can be moderated through intensive interventions ultimately aiming to have longer lasting positive effects from the treatments. The majority of these approaches have either targeted attention or working memory (Halperin, 2010).
The basic premise of these approaches is that deficits in the targeted cognitive domain are causally related to ADHD symptoms and that remediation of these deficits will lead to lasting improvements; collectively these studies have shown that cognitive interventions for children with ADHD improve working memory, inhibition, attention, and nonverbal reasons ability and may reduce behavioural symptoms of ADHD as reported by parents and/or teachers (Halperin, 2010). One thing that cannot be argued is that there is a clear pattern of behaviour that is persistent enough to categorize that pattern of behaviour as “something.” If we would like to refer to that something as ADHD that would not be the issue, the issue is in the diagnostics and treatment process. As we have seen, there are many studies that have found truth in the premise that ADHD is a direct result of deficits in the executive functions.
Should we assume this to be true, we would then need to find the best fit treatment type to aid these individuals deal with these symptoms effectively and integrate into society. The literature reads that the cognitive behavioural therapies are an effective means of treating the main functional deficits of the disorder, and to further my support of these therapies, the effects are long lasting. This would mean that the children diagnosed with ADHD are provided with the tools and resources they need to successfully manage themselves as an autonomous agent within their given environment. This is the definition of effective treatment. The effects of the medicinal treatment are hardly as optimistic as this. Despite that fact a recent review conducted found only 3 randomized controlled trails of psychosocial interventions for adult ADHD (Safren, 2010). It is unclear to me as to why, other than to the advantage of corporate and political gain, why there is so little attention given to the alternative cognitive behavioural strategy method.
The mere fact that there is so little attention and resources going into developing less intrusive methods of treatment, especially for such a chronic condition is disturbing. To note, those who were randomized to cognitive behavioural therapy showed significantly better outcomes than those randomized to relaxation with education support, additional, among those who showed at least a partial response to cognitive behavioural therapy, improvements were maintained at the follow-up assessments, up to 9 months post treatment (Safren, 2010). The research is providing a clear indication that the preferred mode of treatment should be with the cognitive behavioural therapies. We have the positive and long-lasting effects of treatment without also exposing subjects to the additional risks that are associated with using medicinal treatments.
Discussion
Because diagnostic decisions shape treatment choices, bias or inconsistency in assessment poses a potentially serious problem for effective clinical practice and service delivery; the assessment process generally involves an early decision about whether an individual is suffering from a mental disorder (Pottick et al, 2007).To summarize, we have outlined the history of ADHD as well as drawn comparisons between its’ past and present characteristics, we have reviewed both the neurophysiological definition of this disorder, as well as arguments that would rather ADHD be considered as a social construct.
In completing our analysis of current research we also took a look at some of the medicinal treatments and have drawn a comparison between the positive and negative effects of this form of treatment. It is clear that cognitive behavioural strategies have proven to be greater if not equally effective in the treatment of the behavioural characteristics of this disorder and would hope that it is clear that to treat these symptoms medicinally, is overly excessive and lacks the capacity to provide the resources and tools that people suffering with ADHD need to live healthy lives and integrate successfully in society. At this point, it would seem that to completely disregard ADHD as a social construct would be an oversight, and not at all helpful to the individuals who share the same pattern of behaviour that have proven to be disruptive to themselves and those around them.
It perhaps would work to our benefit to keep into consideration the notion of multiple realizability and what that means specifically in the case of ADHD a cognitive syndrome. Generally speaking, cognitive syndromes can only be addressed at a cognitive level and will not always reduce nicely to a single neurophysiological cause. A different assortment of deficits at the neuroscientific level in each individual could all equate to the same persistent set of behavioural characteristics. Trying to explain ADHD at a neurophysiological level, could simply be the wrong way of trying to find a solution to this dilemma. Also, there are undefined notions when defining a mental disorder such as symptoms that are ‘clinically recognizable,” “symptoms,” and “dysfunction” (Bolton, 2001). With such an undefined foundation to work with, we need to be cautious when assigning treatment to disorders like ADHD that, as it stands currently, whose symptomologies are open to the interpretations and misinterpretations of psychiatrists and clinicians alike.
Conclusion
When starting this research, the intended conclusion would be to summarize with a clear-cut decision that ADHD was definitely the cause of some neurophysiological deficit or was socially constructed for the financial gain of the pharmaceutical companies. Naïve as I was when commencing this undertaking, there are too many unknown variables to lend myself to either hand of this argument without doing so irresponsibly. The current research that supports ADHD as being a result of executive dysfunction have been proven to be false or inconclusive.
There are other things to be taken into consideration, namely the fact that regardless of how we choose to define ADHD the behavioural symptomologies exist, and they persist. This fact cannot be ignored, there are symptoms that can be masked by medicinal treatment or eliminated through intensive cognitive behavioural therapies. That being said, ADHD cannot be said to be or not be an actual disorder. Whether it be result of a neurophysiological deficit, that remains to be told, whether we should consider it to be socially constructed, not entirely.
At this point, the markedly major flaws in terms of ADHD lie in the diagnostic criteria and the preferred treatment strategies in place. Based on my findings, I’ve reached the conclusion that ADHD as a clinical disorder, needs to be redefined by both the DSM and the APA in order to avoid running risk of being considered as a social construct. The parameters need to be reconstructed in order for there to be less ambiguity in determining whether a subject does or does not suffer for this condition. Also, until we are able to find a clear definition of the disorder, at this point, we should regard any pharmaceutical intervention as an excessive and inefficient means of treatment. It is important that effective treatment addresses the issue at hand and does not simply mask the symptoms present.
The effects of the medicinal treatment are harsh and the benefits short-lived. At this point, we should focus on the cognitive behavioural strategies that are currently in place and work to developing those strategies in order to both gain a better understanding of the disorder, and effectively treating both the symptomologies and providing individuals who suffer on so many levels of their lives because of the behavioural manifestations the tools and resources to integrate into society and function normally as do individuals who are not suffering from this condition.
References
Bolton, D. (2001). Problems in the Definition of ‘Mental Disorder’. The Philosophical Quarterly, 51, 162-199.
Chhabildas, N., Pennington, B. F., & Willcutt, E. G. (2001). A Comparison of the Neuropsychological Profiles of the DSM-IV Subtypes of ADHD. Journal of Abnormal Child Psychology, 29(6), 529-540. Retrieved November 12, 2010, from the PSYCINFO database.
Cosgrove, L. (2005). When Labels Mask Oppression: Implications for Teaching Psychiatric Taxonomy to Mental Health Counselors. Journal of Mental Health Counselling, 27(4), 283-296.
Faraone, S. V. (2004). The scientific foundation for understanding attention-deficit/hyperactivity disorder as a valid psychiatric disorder. European Child & Adolescent Psychiatry, 10, 1-10.
Ferreira, R., Bassi, G., Cabral, A., & Nobre, M. (2010). Withdrawal from methylphenidate increases neural reactivity of dorsal midbrain. Neuroscience Research, 68, 290-300. Retrieved November 5, 2010, from http://www.elsevier.com/locate/neures
Furman, L. M. (2008). Attention-Defecit Hyperactivity Disorder (ADHD): Does Research Support Old Concepts. Journal of Child Neurology, 23(7), 775-784. Retrieved November 6, 2010, from the PSYCINFO database.
Goldstein, S., & Naglieri, J. A. (2008). The School Neuropsychology of ADHD: Theory, Assessment, and Intervention. Psychology in the Schools,45(9), 859-874. Retrieved November 21, 2010, from the PSYCINFO database.
Halperin, J. M., & Healey, D. M. (2010). The influences of environmental enrichment, cognitive enhancement, and physical exercise on brain development: Can we alter the developmental trajectory of ADHD?. Neuroscience and Biobehavioral Reviews, 10, 14. Retrieved November 12, 2010, fromwww.elsevier.com/locate/neubiorev
Nigg, J. T. (2006). What Causes ADHD?: Understanding what goes wrong and Why. New York: The Guildford Press.
Pottick, K. J., Kirk, S. A., Hsieh, D. K., & Tian, X. (2007). Judging Mental Disorder in Youths: Effects of Client, Clinician and Contextual Differences. Journal of Consulting and Clinical Psychology, 75(1), 1-8. Retrieved November 19, 2010, from the PSYCINFO database.
Safren, S. A., Sprich, S. E., Cooper-Vince, C., Knouse, L. E., & Lerner, J. A. (2010). Life Impairments in Adults with Medication-Treated ADHD. Journal of Attention Disorders, 13(5), 524-531. Retrieved November 17, 2010, from jad.sagepub.com
Safren, S. A., Sprich, S., & Mimiaga, M. J. (2010). Cognitive Behavioral Therapy vs Relaxation With Educational Support for Medication-Treated adults With ADHD and Persistent Symptoms: A Randomized Controlled Trial. JAMA, 304(8), 875-880. Retrieved November 17, 2010, from jama.ama-assn.org/cgi/content/full/304/8/875
Svetlov, S. I., Kobeissy, F. H., & Gold, M. S. (2007). Performance Enhancing, Non-Prescription Use of Ritalin: A Comparison with Amphetamines and Cocaine. Journal of Addictive Diseases, 26(4), online.
Musings of a CogSci Nerd 