2.1 T HE CHANGING FACE OF ADHD
2.1.5 The 1990s
smaller in children with ADHD (Hynd, Semrud-Clikeman, Lorys, Novey, Eliopulos &
Lyytinen, 1991). However, in a later study, only the posterior region was found to be significantly smaller (Semrud-Clikeman, Filipek, Biederman, Steingard, Kennedy, Renshaw & Bekken, 1994).
Additional studies were reported by Hynd, Hern, Novey, Eliopulos, Marshall, Gonzalez and Voeller (1993), who found a smaller left caudate region in children with ADHD, and Giedd, Castellanos, Casey, Kozuch, King, Hamburger and Rapoport (1994), who found smaller anterior regions of the corpus callosum.
More recently, two research teams published studies using MRI with considerably larger samples of ADHD children (Castellanos, Giedd, Eckburg, Marsh, Vaituzis, Kaysen, Hamburger & Rapoport, 1994; Castellanos, Giedd, Marsh, Hamburger, Vaituzis, Dickstein, Sarfatti, Vauss, Snell, Lange, Kaysen, Krain, Ritchie, Rajapakse
& Rapoport, 1996; Filipek, Semrud-Clikeman, Steingard, Renshaw, Kennedy &
Biederman, 1997). These studies documented significantly smaller right prefrontal lobe and striatal regions in children with ADHD. Castellanos et al. (1996) also found smaller right-sided regions of structures in the basal ganglia, such as the striatum, as well as the right cerebellum. Filipek et al. (1997) observed the left striatal region to be smaller than the right. Despite some inconsistencies across these studies, most have implicated the prefrontal-striatal network as being smaller in children with ADHD, with the right prefrontal region being smaller than the left. Such studies have placed on a considerably firmer foundation the view that ADHD does, indeed, involve impairments in the development of the brain, particularly in the prefrontal-striatal regions, and that the origin of these differences from normal are likely to have occurred in embryological development (Castellanos et al., 1996). Advances in neuroimaging technology will continue to provide exciting and revealing new developments in the search for the structural differences in the brain that underlie this disorder.
2.1.5.2 Genetic research
In the 1990s a number of studies, particularly those by Biederman and colleagues strengthened the evidence of the familial nature of ADHD. Between 10% and 35% of the immediate family members of children with ADHD were found to have the disorder, with the risk to siblings of the ADHD children being approximately 32%
(Biederman, Faraone & Lapey, 1992; Biederman, Keenan & Faraone, 1990; Pauls, 1991; Welner, Welner, Stewart, Palkes & Wish, 1977). Even more striking, recent
research shows that if a parent has ADHD, the risk to the offspring is 57%
(Biederman, Faraone, Mick, Spencer, Wilens, Kiely, Guite, Ablon, Reed &
Warburton, 1995). Thus, family aggregation studies find that ADHD clusters among biological relatives of children or adults with the disorder, strongly implying a hereditary basis to this condition.
At the same time these studies were appearing, a number of twin studies were being reported that focused on the heritability of the dimension(s) of behaviour underlying ADHD, that being hyperactive-impulsive-inattentive behaviour, or on the clinical diagnosis of ADHD itself. Large-scale twin studies on this issue have been quite consistent in their findings of a high heritability for this trait or for the clinical diagnosis with minimal or no contribution made by the shared environment (Edelbrock, Rende, Plomin & Thompson, 1995; Levy & Hay, 1992). For instance, Gilger, Pennington and DeFries (1992) found that if one twin was diagnosed as ADHD, the concordance of the disorder was 81% in monozygotic twins and 29% in dizygotic twins. Recent large scale studies with twins demonstrate that the majority of variance (70-90%) in the trait of hyperactivity-impulsivity is due to genetic factors (averaging approximately 80%) and that such a genetic contribution may increase the more extreme the scores along this trait happen to be, although this latter point is debatable (Faraone, 1996;
Gjone, Stevenson & Sundet, 1996; Gjone, Stevenson, Sundet & Eilertsen, 1996;
Rhee, Waldman, Hay & Levy, 1995, Silberg, Rutter, Meyer, Maes, Hewitt, Simonoff, Pickles, Loeber & Eaves, 1996; Thapar, Hervas & McGuffin, 1995; van den Oord, Verhulst & Boomsma, 1996). Thus twin studies add substantially more evidence to that already found in family aggregation studies, supporting a strong genetic basis to ADHD and its behavioural symptoms.
Also in this decade, a few studies began to be published that used molecular genetic techniques to analyse DNA taken from ADHD children and their family members to identify genes that may be associated with the disorder. The focus of research initially was on the dopamine type 2 gene, given findings of its increased association with alcoholism, Tourette syndrome and ADHD (Blum, Cull, Braverman & Comings, 1996; Comings, Comings, Muhleman, Dietz, Shahbahrami, Tast, Knell, Koesis, Baumgarten, Kovacs, Levy, Smith, Borison, Evans, Klein, MacMurray, Tosk, Sverd, Gysin & Flanagan, 1991).
More recently, the dopamine transporter gene was implicated in ADHD (Cook, Stein, Krasowski, Cox, Olkon, Kieffer & Leventhal, 1995; Cook, Stein & Leventhal, 1997).
Dopamine, a chemical in the brain that relays messages, is typically broken down quickly after it is released in the body. If for some reason the breakdown and reabsorption is delayed, it is theorized that high levels of hyperactivity, inattention, and impulsivity result. Due to the success of medications that regulate the reabsorption of dopamine in patients with ADHD, the authors of this study were interested in the part dopamine plays in the disorder. Coming from the perspective that ADHD is familial, they designed their study with a focus on families with ADHD and administered intelligence tests, behaviour rating scales, and DNA testing. The family units consisted of the mother, father, and the affected child or children. Cook and his colleagues concluded that, although these results need to be replicated to determine if there are any defective gene patterns, there appears to be some association between mutations in the dopamine transporter gene and the manifestation of ADHD within families. This is an indication of a difference in brain chemistry among individuals with ADHD and those without the disorder, and it reinforces the theory of heritability.
Another gene related to dopamine, the D4RD (repeater gene) was recently found to be overrepresented in the seven-repetition form of the gene in children with ADHD (Lahoste, Swanson, Wigal, Glabe, Wigal, King & Kennedy, 1996).
Research into the molecular genetics involved in the transmission of ADHD across generations offers the promise of the eventual development of genetic tests for, and subtyping of, ADHD into potentially more homogenous and useful genotypes, as well as the promise of developing more specific pharmacological agents for treating ADHD (Barkley, 1998).
2.1.5.3 Essential fatty acid research
The nineties have also seen an interest in the role that essential fatty acid (EFA) plays in ADHD. EFA plays an important part in the structure and function of the cells in the human body. Stevens and colleagues (Stevens, Zentall, Deck, Abate, Watkins, Lipp & Burgess, 1995) conducted a study to determine if essential fatty acid (EFA) is associated with ADHD in boys. Subjects included in the study consisted of boys with ADHD and a control group of healthy boys (all between the ages of 6 and 12 years).
The ADHD diagnosis was confirmed through parent and teacher completion of behaviour rating scales. EFA levels were determined by blood tests.
ADHD subjects were found to have lower levels of EFA than controls. In addition, they had some of the symptoms of EFA deficiency, such as thirst (greater fluid intake), more frequent urination, and drier skin than the control group.
Some studies have indicated a possible association between deficiencies in zinc and EFA and hyperactivity or maladjusted behaviour. There has also been a great deal in the press in recent years about serotonin and melatonin and their effects on mood and behaviour. Zinc and fatty acids are believed to influence the production of serotonin and melatonin, which in turn affect dopamine function. So it seems reasonable to study deficiencies in zinc and EFA in relationship to ADHD. Bekaroglu, Aslan, Gedik, Deger, Mocan, Erduran, and Karahan (1996) looked at the levels of both elements in patients with ADHD. The research was conducted by establishing a diagnosis of ADHD for the target group and by analysing free fatty acid (FFA) and zinc levels from blood samples. The subjects included boys and girls between the ages of six-and-a-half and 12 years.
The authors found that children with ADHD had significantly lower levels of zinc and FFA than the control group. It is not clear whether the zinc deficiency is responsible for the lowered FFA levels; further studies are needed to establish FFA as a primary or perhaps secondary cause of ADHD.
2.1.5.4 ADHD in adults
The 1990s saw a broader acceptance of ADHD in adults. According to Barkley (1998) this is in part due to studies that documented the persistence of the disorder into adolescence in up to 70%, and into adulthood in up to as many as 66% of childhood cases (Barkley, Fischer, Edelbrock & Smallish, 1990; Fischer, 1997;
Mannuzza, Gittelman-Klein, Bessler, Malloy & LaPadula, 1993; Weiss & Hechtman, 1993). It can also be attributed to published studies on clinically referred adults diagnosed with the disorder (for example Biederman, Faraone, Spencer, Wilens, Norman, Lapey, Mick, Lehman & Doyle, 1993; Murphy & Barkley, 1996).
Also notable in this decade was the publication of more rigorous studies that demonstrated the efficacy of the stimulants (Spencer, Wilens, Biederman, Faraone, Ablon & Lapey, 1995) and the antidepressants (Wilens, Biederman, Prince, Spencer, Faraone, Warburton, Schleifer, Harding, Linehan & Geller, 1996) in the management of adult ADHD. Thus, the adult form of the disorder was found to not only share many
of the same patterns of symptoms and comorbid disorders as did the childhood form, but also to respond just as well to the same medications (Barkley, 1998).
2.1.5.5 Other developments in the1990s
In 1994, new diagnostic criteria for the disorder were set forth in DSM-IV (DSM-IV, American Psychiatric Association, 1994). These criteria contained several improvements over those in the DSM III-R. They reintroduced criteria for the diagnosis of a purely inattentive form of ADHD, similar to ADD without hyperactivity which first appeared in DSM-III. The diagnostic criteria also now required evidence of symptom pervasiveness across settings, as well as the demonstration of impairment in a major domain of life functioning (home, school, work). Based on a much larger field trial than any of its predecessors, the DSM-IV criteria are the most empirically based in the history of this disorder (Barkley, 1998).
A further development in this decade was the undertaking of the NIMH multisite study of ADHD that focused on various combinations of long-term treatments (Arnold, Abikoff, Cantwell, Connors, Elliot, Greenhill, Hechtman, Hinshaw, Hoza, Jensen, Kraemer, March, Newcorn, Pelham, Richters, Schiller, Severe, Swanson, Vereen &
Wells, 1997). The Swedish government also commissioned the longest treatment study of stimulant medication ever undertaken, the results of which indicated that amphetamine treatment remained effective for the entire 15 months of the investigation. More sobering was a report that a year-long intensive treatment programme using primarily cognitive–behavioural treatment produced no substantial treatment effects either at post-treatment or at follow-up (Braswell, August, Bloomquist, Realmuto, Skare & Crosby, 1997). Barkley (1998) reports a year-long intensive early intervention programme for hyperactive-aggressive children that found no significant impact of training either at post-treatment or at a two-year follow-up.
The school-based portion of this multimethod programme produced some immediate gains, but by two-year follow-up these had dissipated. Finally, a multisite study of stimulant medication with and without intensive behavioural and psychosocial interventions was reported to have found that the psychosocial interventions added little or nothing to treatment outcome beyond that achieved by stimulant medication alone (Abikoff & Hechtman, 1995). According to Barkley (1998), these studies do not so much undermine the earlier studies on the effectiveness of behavioural interventions with ADHD children, as suggest that some of those interventions produce minimal or no improvements when used on a large-scale basis, that the extent of improvement is difficult to detect when adjunctive stimulant medication is
also used, and that treatment effects may not be able to be maintained over time following treatment termination.
This decade also witnessed the emergence of new trends such as renewed interest in theory development related to ADHD. There was a recognition that deficits in behavioural inhibition may be the most distinguishing characteristic of this disorder from other mental and developmental disorders. Russell Barkley put forth the view that the frontal lobes of individuals with ADHD do not function properly, resulting in deficiencies in the executive functions that allow us to plan and control our behaviour and to inhibit unwise responses (Barkley, 1997a, 2000). There was also recognition that the subtype of ADHD comprising chiefly inattention without impulsive- hyperactive behaviour may possibly be a qualitatively distinct disorder entirely from those children who have hyperactive-impulsive behaviour (Barkley, Grodzinsky &
DuPaul, 1992; Goodyear & Hynd, 1992; Lahey & Carlson, 1992).
A new stimulant medication, Adderall, appeared on the market in this decade that shows promise as being as effective for ADHD as the other stimulants. The 1990s also saw an increasing interest in the use of peers as treatment agents for academic performance and peer conflict in school settings in several new behavioural intervention programmes (Cunningham & Cunningham, 1998; DuPaul & Henningson, 1993).
Although the 90s saw a shift to viewing ADHD as far more influenced by neurological and genetic factors than by social or environmental ones, some critics still regard it as a label. The year 1999 saw the publication of the book The Indigo Children (Caroll & Tober, 1999). The authors describe the Indigo child as a new kind of child who comes into the world “knowing” who they are. According to them these children:
§ Come into the world with a feeling of royalty (and often act like it)
§ Have a feeling of "deserving to be here," and are surprised when others don't share that.
§ Have no problem with self-worth. They often tell the parents "who they are."
§ Have difficulty with absolute authority (authority without explanation or choice).
§ Simply will not do certain things; for example, waiting in line is difficult for them.
§ Get frustrated with systems that are ritually oriented and don't require creative thought.
§ Often see better ways of doing things, both at home and in school, which makes them seem like "system busters" (nonconforming to any system).
§ Seem antisocial unless they are with their own kind. If there are no others of like consciousness around them, they often turn inward; feeling like no other human understands them. School is often extremely difficult for them socially.
§ Will not respond to "guilt" discipline ("Wait till your father gets home and finds out what you did").
§ Are not shy in letting you know what they need.
The authors believe that society copes with this new kind of child by diagnosing him/her with ADHD and legally drugging the child. According to the authors, these unusually bright and active children must be recognised and celebrated for their exceptional qualities and must be guided with love and care.