Adult ADHD as a dimensional disorder

Moncrieff & Timimi argue that there is no specific evidence to link adult attention-deficit hyperactivity disorder (ADHD) with childhood ADHD. ¹ They also question the increase in the use of stimulants for the condition and the role of the pharmaceutical industry in this. We can all lament the way in which the pharmaceutical industry has tried to increase the use of their products, yet the mere fact that they have done so does not invalidate their use.

The authors seem to ignore that most clinicians and academics see ADHD as a dimensional disorder. Just as with depression, the cut-off point for treatment is essentially arbitrary. This is the case in many psychiatric and other medical illnesses and conditions. We all recognise a patient when the illness is severe but it is less clear whether treatment is the appropriate course of action in less severe cases.

Majority opinion clearly suggests that the reason for the symptoms of ADHD is an increased density of dopamine transporter (DAT) complexes. ^2,3 With increasing age, there is a natural decline of these complexes, which causes a reduction of core symptoms. This leads to a change of prioritisation of core difficulties in adults, which does not represent a completely different set of symptoms as the authors suggest. The other argument the authors pursue is the high rate of comorbidity which they argue invalidates the diagnosis. However, untreated ADHD is likely to cause secondary difficulties such as conduct problems, personality disorder and substance misuse. Of course these difficulties cause some symptoms that are similar to the core symptoms of ADHD, but this hardly invalidates the primary diagnosis. More research is needed to find out whether adult treatment of ADHD mitigates the impact of acquired secondary problems. The current evidence would suggest that this is probably not the case. Therefore, the authors are certainly correct when they urge caution in the use of stimulants in adults if the main reason for the treatment would be to treat secondary diagnoses.

The authors argue that the wide variation of prevalence rates in difference studies is an argument against the validity of the concept of ADHD. However, such varieties are found in many dimensional syndromes. Depression and personality disorder are only two examples where this is the case. The American studies usually show higher prevalence rates because of their lower cut-off point for caseness of ADHD. In Europe, because the cut-off point is arbitrary and researches usually have it set higher, the prevalence figures appear different.

Moncrieff & Timimi mention a follow-up study which, they claim, shows that any beneficial effects from stimulant use are not sustained at long-term follow-up. ⁴ Careful analysis of this study would have shown that the reported lack of sustained benefit had to do with the relatively high drop-out rate in the intention-to-treat analysis. This is not surprising as most psychiatric studies over 3 years have high drop-out rates. However, the subgroup of children that stayed in this study and continued with their medication actually maintained the benefits throughout the 3-year period. I fully agree with the authors that the evidence in adults is rather less clear, although on current evidence the effect sizes of stimulant drugs are certainly among the highest in medicine.

At the end of the day, the decision to treat adult ADHD with stimulants is a clinical one that should take into account the severity of symptoms, potential side-effects, and the likelihood of reasonable improvement.