Meanings and causes in ADHD

D. B. Double

Eric Taylor dismisses Sami Timimi’s critique of attention-deficit hyperactivity disorder (ADHD) as an oversimplified polemic (Timimi/Taylor, 2004). He admits he may have been biased because he viewed it as an antipsychiatry tract. I find it unfortunate that the threat of ‘antipsychiatry’ means that a serious attempt does not appear to have been made to resolve the controversy surrounding ADHD (Double, 2002a). Is there a dispute about the facts as well as their interpretation? For example, it is not clear whether brain differences have been shown in unmedicated children, with the protagonists stating opposite views. From the article, it is difficult to see who is correct because Professor Taylor merely quotes the chapter on ADHD from his co-edited textbook (viz. Schachar & Tannock, 2002).

Furthermore, Professor Taylor makes various statements, again with the authority of this textbook chapter, which seem to need further clarification. For example, he says there are known physical counterparts of hyperactivity in brain structure and function, and then does not say what these abnormalities are. If we know what they are, they should be stated and we can then debate their role in aetiology. Similarly, he says that some molecular genetic variations have been robustly replicated, but then does not name the genes, except to say that they especially affect dopamine systems.

There is surely an onus on Professor Taylor to justify his response to Dr Timimi’s challenge that the medical model of ADHD ‘offers a decontextualised and simplistic idea that leads to all of us – parents, teachers and doctors – disengaging from our social responsibility to raise well-behaved children’. Instead, Taylor proposes increased recognition of the disorder, at least in the UK, ‘because there are several good ways of supporting children with severe hyperactivity’. If the central issue is the role of medication in treatment, this is clearly a matter of values (Double, 2002b). The recently published collection edited by Fulford et al (2003) argues that meanings as well as causes are essential to good psychiatric care. One way of viewing the ADHD controversy is that Dr Timimi is more concerned about the meaning rather than the physical cause of the disorder. Such a position should not be dismissed as antipsychiatry, but acknowledged as a valuable contribution to the debate about the extent to which the use of medication exploits people’s emotional problems.

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Author’s reply

I am grateful to Dr Double for giving me the opportunity to cite more references than are allowed in a debate; but the biological basis of hyperactivity is one of the most researched questions in psychiatry and a letter cannot do justice to it. The chapter I cited previously gives references, and interested readers might also like to consult the recent reviews cited below.

The best-established findings are probably the associations with DNA variations in genes coding for the dopamine receptor (DiMaio et al, 2003) and dopamine transporter, and neuroimaging findings of altered brain structures including frontal lobe and striatum.

Castellanos et al (2002), for example, report the altered neuroanatomy of ADHD, with the brains of those who have never been medicated being more abnormal than those of children who have received stimulants.

Dr Double extends the debate to the question of the use of medication. A large controlled trial (MTA Collaborative Group, 1999) has shown significant advantages of medication over psychological therapy (although I believe that psychological treatment still has an important place). I should therefore like to emphasise that there are dangers in being too reluctant to diagnose and treat ADHD. Children then often receive more destructive labels. Treatment can restore normal function, so it seems to me unacceptable to withhold its benefits from individual children for the sake of a preference for a different form of society.

References