1.4 percent: Behind the numbers of ADHD prevalence

A question closely tied to the issue of prescribing ADHD medication is the actual growth of the disorder. Media reports have cited substantial increases in Ritalin use in the UK, and from looking at prescribing trends in the US one possibility is that the diagnosis of ADHD increases in parallel with growing Ritalin prescriptions. It is particularly important to understand how the increased prescribing of ADHD medication in the UK relates to the actual prevalence of the disorder. However, a key issue in the ADHD debate is whether the diagnosis represents a core developmental disorder. The growth in Ritalin prescriptions and the disproportionately high rates of ADHD in the US in particular have often been used to suggest that ADHD diagnosis is socially motivated.

When we look more closely at the numbers around ADHD, however, three important observations emerge.  First, we can see that although there has been a consistent growth in ADHD medication prescriptions in the UK, there is no evidence speaking to whether this also corresponds to an increase in ADHD diagnoses. Second, the common perception of the US being disproportionately affected by ADHD is surprisingly unsupported. Rather, we can see that different methods and approaches to ADHD diagnosis are what best explain its relative prevalence.  Third, thinking about ADHD as a label for a highly heterogeneous group can perhaps more readily account for the differential rates of ADHD based on the diagnostic criteria used.

Has the prevalence of ADHD in the UK increased in line with Ritalin prescriptions?

As we saw in our previous blog post, the number of Ritalin prescriptions dispensed in England increased by 156% from 2004 to 2014. However, this does not mean that the prevalence of ADHD has increased by a similar proportion. Why? Factors that can influence the number of prescriptions for ADHD medication written include GPs being more likely to prescribe such medication due to more positive peer-reviewed articles about its effects, changes in prescription protocols (such as more frequent repeat prescriptions being provided), and more awareness amongst parents and the public about the possible benefit of ADHD medication meaning a higher proportion of people ask for medication¹. Further, although NICE guidelines published in 2013 recommended treatment for ADHD with medication as part of a comprehensive treatment programme (including psychological, behavioural and educational support), reductions in funding available for such support may contribute to a higher prescription of medication by GPs as an alternative. All of these factors can lead to a higher number of prescriptions being written, and this means the number of prescriptions does not necessarily align with the number of individuals diagnosed with ADHD.

So we need to take a different approach to estimating the prevalence of ADHD diagnoses, by looking at the proportion of actual ADHD diagnoses in the population. However, there are currently no available public health records about ADHD prevalence in the UK. Instead, one useful source of data come from population-based studies, which take a large sample of children (often around 8000-14,000) and estimate the prevalence of ADHD through the percentage of children with parent reports of symptoms and/or ADHD diagnoses. These studies have the benefit of estimating the prevalence of ADHD through a non-referred sample, avoiding the biases arising from estimates reached by only counting the number of children brought to medical attention.

One such study conducted by Green and colleagues in 2004² estimated the UK prevalence of ADHD in 5-15 year-olds at approximately 1.5%. (A similar report from 2003 estimated the prevalence in this age group at 2.2%³). A more recent report by Russell et al. (2014)⁴ based on the Millenium Cohort Study estimated ADHD prevalence in the UK at 1.4%. This estimate came from data collected in 2008-2009 when children were 6-8 years old, and parents reported whether ADHD had been identified by a doctor or other health professional.

At face value, these figures are a striking contrast to the prescription data: the parent-report data suggest no increase in ADHD diagnoses (from 2004-2009, at least), in contrast to the yearly increase in Ritalin prescriptions over the same time period. However, it is important to consider that the more recent Millennium Cohort Study figures may slightly underestimate the prevalence of children affected by ADHD: this is because the Millennium Cohort sample children were younger, and more children are likely to be diagnosed when they are older.

So whilst it is possible that ADHD diagnoses in the UK have increased, we do not have the data to accurately evaluate this change. As we saw in our previous blog post, data from the US would suggest that growing use of ADHD medication does align with increasing diagnoses, but it is difficult to evaluate this relationship for the UK because we do not have statistics from comparable samples of children at different time points. It is particularly important to verify if the actual number of individuals diagnosed with ADHD has increased to understand whether such a growth in prescriptions stems from more diagnoses, a growing trend to provide medication in lieu of other treatment options, or a combination of the two.

But the current wave of Millennium Cohort Study data were recently collected when children were 11 years old, and using these data researchers can assess if more children in the sample have now been diagnosed with ADHD as they have gotten older – so we might have an answer soon.

Is the United States disproportionately affected by cases of ADHD, and does this tell us anything about causality?

The growth of ADHD medication use and the concurrent prevalence of the disorder is closely related to the debate around whether it reflects an increase in a genuine developmental disorder, or whether such growth is part of a cultural trend towards diagnosis. The geographical vagaries of ADHD in the US particularly have often been invoked as an argument against its legitimacy as a disorder, with some suggestion that the US peak in ADHD rates indicates its diagnosis can be culturally motivated. Sir Ken Robinson, an author, speaker and education adviser, gave a popular TED talk in 2010 in which he showed a map of ADHD prescription rates across the USA, indicating that they increased as one moved east across the country – or as put by Sir Ken, “people start losing interest in Oklahoma, they can hardly think straight in Arkansas, and by the time they get to Washington they’ve lost it completely.”

This brings us to our next question: is it really the case that ADHD is over diagnosed in the US relative to the rest of the world, as media discussion often suggests? The geographical distribution of ADHD is important for two reasons. First, consistent differences in the geographical spread of ADHD may offer clues as to its aetiology: possible environmental causation in areas of high rates, and preventative factors in areas of low rates. Second, the worldwide distribution of ADHD informs the debate on whether it stems from cultural factors which make it an ‘American’ disorder – whatever this may mean – in which case we would expect it to be more prevalent in the US than anywhere else.

When we look at just the US and UK, it appears that US does have higher diagnosis rate of 6.3% (as reported by Russell et al., 2014). This is the closest estimate using the same sampling methods as the UK figure of 1.4% from the Millennium Cohort Study. However, as pointed out in the Millennium Cohort report by Russell et al., there is an explanation for this: a difference in the measurement of ADHD between the US and UK. When the data were collected the DSM-IV was used in the US, but researchers in the UK from whom the data were collected mainly used the ICD-10. The ICD-10 is more stringent, in which a child must show symptoms in all three dimensions of inattention, hyperactivity, and impulsivity to be diagnosed with ADHD, with no comorbid disorders. The DSM-IV is less stringent in the classification of ADHD, whereby children can be diagnosed with symptoms in one dimension only (such as inattention) alongside comorbid disorders. This difference in relative preference of diagnostic criteria can at least partly explain why the DSM-IV-using US has an epidemic compared to the relative calm of the ICD-10-preferring UK⁵.

When we look at the geographical spread of ADHD across the rest of the world, the figures are particularly striking. A meta-analysis by Polanczyk et al. in 2007⁶ combined 102 studies, comprising data from 171,756 children, to estimate the average prevalence rates reported from samples worldwide in the previous 25 years. This figure was 5.3%. Second, they evaluated whether the US prevalence rates really did exceed everywhere else in the world, relative to Africa, Asia, Europe (excluding the UK), the Middle East, Oceania, and South America. The US rate of 6.2% did not significantly differ from the European rate (4.6%), or the highest rate in South America (11.8%). And importantly, there was no overall association between geographic location and ADHD prevalence rates when the methodology of the studies was controlled for. The figure below shows the prevalence estimates for each region (the bars represent the variability in this estimate).

Finally, Polanczyk and colleagues verified that the different ADHD prevalence estimates between the US and Europe in particular were indeed explained by the different diagnostic criteria of the DSM and ICD. They did this by coding for all the methodological features in each study, and found that US diagnoses were more frequently made on DSM criteria, and European diagnoses more so on ICD-10 criteria. Another meta-analysis by Willcutt (2012)⁷ also found that differences in ADHD prevalence across countries were not significant after diagnostic approaches were controlled for. So these data suggest that ADHD is not disproportionately prevalent in the US; rather, its relative prevalence seems to depend more on the diagnostic tool used.

But on an individual level, any parent of a child with ADHD, or any individual with ADHD, is unlikely to attest that their difficulties with learning, concentration and communication are because they are living in Bolivia rather than Finland. The critical ongoing issue is therefore what constitutes our diagnosis of ADHD. In practice, a child is likely to be identified with ADHD because of how their various cognitive difficulties are expressed, and how this expression is interpreted by clinicians. Part of this interpretation may be due to less quantifiable environmental, social and cultural factors: in particular, Conrad and Bergey (2014)⁸ recognise that the historical approach to ADHD and medication use in a country can greatly influence whether clinicians classify children’s difficulties under the ADHD diagnostic label. But the different diagnostic criteria of the DSM and ICD do play a role. As noted by Russell et al. (2014), children with hyperactive behaviour and social difficulties may be more likely to be diagnosed with autism spectrum disorder in the UK (due to ICD-10 criteria ruling out a combined diagnosis), and ADHD in the US (due to the DSM-IV allowing ADHD to be diagnosed alongside other developmental disorders). It therefore seems that ADHD is not disproportionately prevalent in the US when we take diagnosis methods into account, but that fact that different tools can yield different prevalence rates makes it important to verify what the ADHD diagnostic label is mapping onto.

A dimensional approach to ADHD

At first glance, quantifying the prevalence of ADHD would suggest counting all children and adults struggling with attention, hyperactivity, and impulsivity and suggesting those individuals reflect the relative rate of ADHD in a particular population. In practise, however, there is no natural threshold between affected and unaffected individuals with ADHD. ADHD can frequently co-occur with other developmental disorders, such as autism spectrum disorder (ASD); in the Millennium Cohort dataset, 24% of the children with ADHD were also diagnosed with ASD. This individual variation supports a dimensional approach to classifying developmental disorders, which considers the extent to which various cognitive difficulties are present rather than a clear-cut diagnostic label.

This is critical in deciding how we give children help in the classroom. For example, we have seen previously that children with poor working memory and children with ADHD have highly similar working memory and executive function deficits, indicating that these shared difficulties are not limited to children with ADHD. Further, although an estimated 25-40% of children with ADHD also have dyslexia⁹, the treatment approaches for ADHD do not usually address reading difficulties, even though these can be a main constraint on a child’s progress at school. The diagnostic label of ADHD thus represents a highly heterogeneous group of children, and what best helps one child with ADHD may not be what best helps another.

But one might argue that neuroimaging data suggesting reduced prefrontal cortex activity in ADHD is indicative of a clear group of children who suffer from a specific neurobiological disorder. However, even such neurobiological ‘markers’ of ADHD are present to a varying degree in individuals without ADHD. Shaw et al. (2007)¹⁰ reported that the age of reaching peak cortical thickness – a measure of brain maturation, before cortical thinning proceeds throughout late childhood and adolescence – was delayed in children with ADHD relative to typically developing children. This finding suggested that ADHD may reflect a delay in typical brain development, rather than a qualitative difference between children with and without an ADHD diagnosis. And Shaw et al. (2011)¹¹ found that this rate of cortical thinning was related to the degree of hyperactive and impulsive symptoms in typically developing children without an ADHD diagnosis. Children with higher ratings of hyperactive/impulsive symptoms had a slower rate of cortical thinning, similar to what was observed in children with ADHD. These data align with the idea that ADHD may be a disorder that is better understood dimensionally, with those who are affected being at the end of a continuum of inattention and/or hyperactivity symptoms, rather than there being a distinct cut-off between ADHD and ‘typical’ development.

How does this inform the question on whether ADHD exists as a developmental disorder? From the evidence above it seems that the label of ADHD does not identify a separate category of children who are inattentive and hyperactive. Rather, what we think of as ADHD is a complex cluster of cognitive and behavioural difficulties which fall on a scale for all children, from unaffected to severe. It is how these difficulties are expressed by children and interpreted by different diagnostic approaches, in different cultural contexts, which determine the cut-off at which a child is diagnosed. Whilst difficult to unpick, these factors may best capture how ADHD is identified and why prescriptions have steadily grown; however, we critically need further data to accurately evaluate ADHD growth in the UK. And on an individual level, the symptoms of ADHD have a substantial impact on the day-to-day lives of those who are affected. It is important we ensure that diagnosis appropriately reflects individual differences between children, and think about how to best to commission education and health services to help affected children and adults.

References

1. Prescribing in primary care: Understanding what shapes GPs’ prescribing choices and how might these be changed, RAND Technical Report. Available at http://www.nao.org.uk/wp-content/uploads/2007/05/TR443_3C.pdf
2. Green, H., McGinnity, A., Meltzer, H., & Ford, T. G., R. (2004). Mental health of children and young people in Great Britain, 2004. Report commissioned by the Office for National Statistics.
3. Reported in the NICE Guidelines pp. 26, available here: https://www.nice.org.uk/guidance/cg72/resources/cg72-attention-deficit-hyperactivity-disorder-adhd-full-guideline-2
4. Russell, G., Rodgers, L. R., Ukoumunne, O. C., & Ford, T. (2014). Prevalence of parent-reported ASD and ADHD in the UK: findings from the Millennium Cohort Study. J Autism Dev Disord, 44(1), 31-40. doi: 10.1007/s10803-013-1849-0
5. For interested readers, there is also an excellent timeline here depicting ADHD rates in the US as diagnostic tools have changed from 1970 to the present day.
6. Polanczyk, G., de Lima, M. S., Horta, B. L., & Biederman. J. (2007). The Worldwide Prevalance of ADHD: A Systematic Review and Metaregression Analysis. American Journal of Psychiatry, 164(6). 942-948.
7. Willcutt, E. G. (2012). The prevalence of DSM-IV attention-deficit/hyperactivity disorder: a meta-analytic review. Neurotherapeutics, 9(3), 490-499. doi: 10.1007/s13311-012-0135-8
8. Conrad, P., & Bergey, M. R. (2014). The impending globalization of ADHD: notes on the expansion and growth of a medicalized disorder. Soc Sci Med, 122, 31-43. doi: 10.1016/j.socscimed.2014.10.019
9. Reported in Eden, G. F., & Vaidya, C. J. (2008). ADHD and developmental dyslexia: two pathways leading to impaired learning. Ann N Y Acad Sci, 1145, 316-327. doi: 10.1196/annals.1416.022
10. Shaw, P., Eckstrand, K., Sharp, W., Blumenthal, J., Lerch, J. P., Greenstein, D., . . . Rapoport, J. L. (2007). Attention-deficit/hyperactivity disorder is characterized by a delay in cortical maturation. Proc Natl Acad Sci U S A, 104(49), 19649-19654. doi: 10.1073/pnas.0707741104
11. Shaw, P., Gilliam, M., Liverpool, M., Weddle, C., Malek, M., Sharp, W., . . . Giedd, J. (2011). Cortical development in typically developing children with symptoms of hyperactivity and impulsivity: support for a dimensional view of attention deficit hyperactivity disorder. Am J Psychiatry, 168(2), 143-151. doi: 10.1176/appi.ajp.2010.10030385
    

Ritalin and ADHD: What is the story so far?

The use of Ritalin to treat ADHD has become a highly contentious issue over the past decade. Part of this contention stems from a marked growth in use, with a 156% increase in the number of Ritalin prescriptions dispensed in England over the last ten years. Another source of contention comes from fragmented information about what the precise effects of Ritalin are (and ADHD medications in general) and what governs whether it is prescribed. We can unpick at least some of this debate by asking two questions: what is the evidence for what Ritalin does, and the extent to which it can help children with ADHD? And why could the number of Ritalin prescriptions have steadily increased over the past decade?

Methylphenidate medication in ADHD: What does Ritalin do, and can it help children with ADHD?

ADHD is a developmental disorder which, despite having a single diagnostic label, presents substantial individual differences between children who are affected. ADHD is characterised by deficits of inattention, impulsiveness, and hyperactive behaviour. These difficulties are often understood to be tied to reduced functionality of the prefrontal cortex (PFC) in individuals with ADHD. The PFC is important for attentional control and executive functions – a broad term for cognitive functions governing organised and controlled behaviour – and this reduced PFC functionality is suggested to result in the core ADHD symptoms of attentional and behaviour control deficits. However, ADHD also frequently co-occurs with other developmental disorders, such as dyslexia and autism. This means that children who are diagnosed with ADHD will range from those severely affected by difficulties in concentrating and sitting still, to those who struggle to pay attention and have comorbid difficulties in areas such as reading and communication. From the outset it is therefore important to recognise that there is huge individual variation in the children (and adults) whom fall under the ADHD diagnostic umbrella.

Ritalin, also known as methylphenidate, is a stimulant medicine which is commonly used to treat ADHD symptoms of inattention and hyperactivity. To understand the effects of Ritalin on cognition, research studies compare performance on tasks when participants have taken Ritalin to when they have taken a placebo. A meta-analysis of these studies by Coghill et al. (2014)¹ combined papers investigating the effects of Ritalin in children and adolescents with ADHD. They found that the medication improved short term memory accuracy, working memory capacity, response speeds, and response inhibition relative to a placebo. Because the meta-analysis combined results across at least ten published studies for each aspect of cognition, these results are more representative than findings from a single study. A similar review by Epstein et al. (2014)² assessed the effects of Ritalin medication in adults with ADHD, and observed that it improved inattentiveness, hyperactivity and impulsive behaviour. These findings overall suggest that Ritalin has positive effects on cognition and controlled behaviours compared to a placebo, in both children and adults with ADHD.

A suggested neurophysiological mechanism for Ritalin’s effect on cognition and hyperactivity is via increased functionality of the prefrontal cortex (Spencer et al., 2015)³. Ritalin prevents the reuptake of the neurotransmitters dopamine and norepinephrine in the PFC. Because these neurotransmitters allow nerve cells to communicate, their increased levels in the PFC strengthen its signalling and therefore improve its functionality. This increased activity of the PFC is measured in studies using fMRI, and is suggested to be tied to Ritalin’s effects of improving PFC-dependent cognitive skills such as attentional control, working memory, impulse control, and organised behaviour (Berridge & Devilbiss, 2011)⁴.

Importantly, however, these effects do not mean that the Ritalin treats the causes of ADHD. A key piece of evidence comes from the finding that Ritalin has the same ‘cognition-enhancing’ effects on individuals without ADHD. A review by Linssen et al. (2014)⁵ found that when adults without ADHD were given Ritalin their performance improved on tests of working memory and processing speed, and to a lesser extent attention and vigilance. Whilst these data do not allow us to assess if the magnitude of these methylphenidate effects were statistically identical to those in individuals with ADHD, they are an important indicator that Ritalin can improve these cognitive markers irrespective of an ADHD diagnosis (as current American college trends may also attest). These findings suggest that whilst Ritalin can be beneficial, it does not operate on the root aetiology of ADHD.

But interestingly, despite the cognitive benefits measured in short-term studies, Ritalin does not seem to improve children’s academic achievement in the long term. A large-scale longitudinal study reported by Molina et al. (2009)⁶ assessed the long-term outcomes of 579 children with ADHD who were randomly allocated to one of four treatment groups: methylphenidate medication, behaviour therapy, combined medication and behaviour therapy, or community care. At the end of the fourteen-month treatment period, all groups had improved relative to their pre-treatment baseline on a range of outcomes including parent and teacher-rated ADHD symptoms, teacher-rated social skills, and reading and maths achievement. Interestingly, the greatest improvements were for the medication group and combined medication plus behaviour therapy group. At the first follow-up ten months after treatment, the initial advantage of the medication and combined groups was still present (although the magnitude of this effect was about half what it had been immediately after treatment).

However, when the children were followed up several years later, this added benefit of medication had levelled out. At the three-year follow-up the four treatment groups remained above their pre-treatment baseline, but there was no difference between the treatment options; that is, the relative advantage of the medication groups was no longer present. After eight years the groups continued to perform above a pre-treatment baseline, but there remained no differential treatment benefit of medication. These findings suggest that medication can have a benefit during a relatively short-term treatment period, but beyond this initial treatment there is no evidence for a lasting medication advantage for the majority of children.

It is particularly interesting that there was no evidence for medication specifically improving long-term academic attainment in light of its short-term improvement of attention, short-term memory, and working memory. Because we know these cognitive skills are significant predictors of educational outcomes, we might have expected their improvement with Ritalin to also boost educational outcomes. Of course, the reason for no longer-term effects of medication may simply be that it can improve cognitive control during treatment, but these effects of the drug do not continue to have additive benefits after treatment is discontinued. There is also relatively little existing research on the effects of taking Ritalin for a longer time period, which limits our understanding of its effects from longer-term use.

However, another interesting explanation for the lack of such an effect may come from the heterogeneity of children diagnosed with ADHD. In their report Molina et al. (2009) identified three subgroups of children in the three-year follow-up, each with different ADHD trajectories as a result of treatment. One group showed an increasing steady benefit of medication use over three years; a second group showed a very large initial benefit for medication use which then plateaued, and was maintained three years after treatment; and a final group returned to pre-treatment levels with no ongoing benefit of treatment. These different profiles of children continued to be associated with their performance on the outcome measures of cognitive, social, and academic attainment at the eight-year follow-up. Importantly, these findings suggest that children’s longer-term outcomes may be determined more by their individual profile of symptoms than the specific type of treatment they receive.

So overall, what do these data us about the decision to use Ritalin for individuals with ADHD? Whilst research studies conducted over the short-term indicate that Ritalin can improve aspects of controlled cognition such as working memory and attention relative to a placebo, there is no evidence that medication continues to have an added benefit to non-medication treatments (such as behavioural therapy) after about two years following the start of treatment. The varying effects of medication may come from the heterogeneity of children diagnosed with ADHD. For many children, comorbid difficulties with reading or communication, for example, could be a key limiter on their performance at school, which Ritalin may do little to redress. Although Ritalin can undoubtedly be beneficial for children who substantially suffer with attention or behavioural control difficulties, the fact it is not universally helpful is an indicator of how much children diagnosed with ADHD can differ in their profile of strengths and weaknesses. Importantly, the effects of medication may therefore depend more on the symptoms of an individual child than the presence of an ADHD diagnosis.

156 percent: What are the reasons behind growing Ritalin use?

A herein lies the controversy: despite the above findings, and an anecdotal lack of consensus about its effects, the number of Ritalin prescriptions dispensed in England increased by 156% between 2004 and 2014. These data, published by the Health and Social Care Information Centre in 2015 and shown on the figure below, show Ritalin prescriptions at 359,068 in 2004 and 922,206 in 2014⁷. (Interestingly, whilst the HSCIC data show that prescriptions for Ritalin are of a larger quantity than the other ADHD medicines on the market, the average use of other ADHD medicines also increased by a modest 136%).

But could it just be the case that all prescriptions have increased this much in general over the last decade? No; the average number of prescriptions dispensed across England rose by 55.2% over the same ten-year period. This discrepancy prompted the National Institute for Health and Care Excellence (NICE) to release guidelines in 2013 that initial treatment of moderate ADHD should not include methylphenidate medication, prompting substantial debate as to what constituted ‘moderate’. So whilst it is agreed that the prescription of ADHD medication has grown substantially, there is no consensus on what is driving this change.

What reasons could there be behind a growing number of Ritalin prescriptions? One obvious reason is an increase in the number of children (and adults) diagnosed with ADHD. In the United States at least, this argument for a relationship between prescription rates and ADHD diagnoses seems to hold. The Centre for Disease Control and Prevention collected comprehensive data on the percent of 4-17 year-olds with parent-reported ADHD diagnoses in each state, and the percent of children taking ADHD medication in each state, in 2007 and 2011⁸. These data mean we can look at whether there is a relationship between each state’s change in ADHD diagnoses in this period, and their simultaneous change in medication use. The figure below shows the relationship between the change in the percentage of children with ADHD diagnoses and percent of children taking ADHD stimulant medication in each state, and there is indeed a significant positive correlation between the two. This positive correlation means that states with a larger increase in ADHD diagnoses also had a larger increase in the number of children prescribed stimulant medication. Whilst we cannot infer causality from these data (that is, we cannot assume that more ADHD diagnoses cause more medication prescriptions) they do suggest that the growth in diagnoses and prescriptions are related.

The main question these data raise – apart from what is going on in Texas – is why ADHD diagnoses have increased. In a recent paper investigating reasons behind the global expansion of ADHD diagnoses and medication use, Conrad and Bergey (2014)⁹ suggested that increased promotion of ADHD drugs by the pharmaceutical industry, the increased adoption of DSM (the Diagnostic and Statistical Manual of Mental Disorders, an American publication) diagnostic criteria, and more accessible information about ADHD online could all contribute to its steady growth. ADHD information being more visible and accessible online can prompt more individuals to seek and thus obtain a diagnosis, and promotions by pharmaceutical companies can result in medication treatment being more frequently offered to individuals diagnosed with ADHD. Further, the diagnostic criteria used are particularly important: Conrad and Bergey suggested that a shift towards the DSM criteria in the 1990s contributed to increasing rates of ADHD, as the DSM uses a lower threshold for diagnosis and allows the co-occurrence of ADHD with other developmental disorders. Whilst these are broad brush strokes for reasons for which Ritalin use has grown, they nonetheless suggest possible mechanisms for the increase in prescriptions.

However, it is important for us to recognise that measuring the number of prescriptions dispensed may not be the best indicator of how many individuals are actually taking the medication. A good example of this comes from looking at the headline finding from a 2008 study which reported huge variation in the number of Ritalin prescriptions dispensed across England, with as much as a ­23-fold difference between the lowest and highest-prescribing areas of the UK (Stoke-on-Trent and Wirral, respectively). However, the prescription rate for each region was measured by the number of prescriptions dispensed as a proportion of the population in that region. These figures meant that differences in prescribing practises across regional primary care trusts, such as the standard frequency of repeat prescriptions, could contribute to a lot of this variation. The overall population of a region also influenced its ‘rate’ of prescribing; this might explain why the relatively small Isle of Wight had the second-highest rate at 107 prescriptions per 1000 children. Although just one example, this points to the need to look at Ritalin use in terms of the number of individuals prescribed Ritalin and ask how this aligns with the number of individuals actually diagnosed with ADHD.

So the story about Ritalin seems to have two parts: first, it can have beneficial effects on cognition, but these benefits may critically depend on children’s individual profile of symptoms. Second, it is possible that Ritalin use has increased in line with growing ADHD diagnoses, but we need to carefully evaluate the evidence we have to assess this. Possible vehicles for growth include more individuals seeking a diagnosis due to the information now available about ADHD, promotion by pharmaceutical companies for the use of medication, and a shift in diagnostic criteria meaning a higher proportion of people are identified as having ADHD. In the UK, however, we know relatively little about how increasing Ritalin use relates to the number of individuals with ADHD taking medication, and the wider growth of ADHD as a disorder. This is the question we will turn to in our next post.

References

1. Coghill, D. R., Seth, S., Pedroso, S., Usala, T., Currie, J., & Gagliano, A. (2014). Effects of methylphenidate on cognitive functions in children and adolescents with attention-deficit/hyperactivity disorder: evidence from a systematic review and a meta-analysis. Biol Psychiatry, 76(8), 603-615. doi: 10.1016/j.biopsych.2013.10.005
2. Epstein, T., Patsopoulos, N. A., & Weiser, M. (2014). Immediate-release methylphenidate for attention deficit hyperactivity disorder (ADHD) in adults. The Cochrane Review, (9). Retrieved from http://www.cochrane.org/CD005041/BEHAV_ritalin-for-adult-attention-deficit-hyperactivity-disorder-adhd
3. Spencer, R. C., Devilbiss, D. M., & Berridge, C. W. (2015). The cognition-enhancing effects of psychostimulants involve direct action in the prefrontal cortex. Biol Psychiatry, 77(11), 940-950. doi: 10.1016/j.biopsych.2014.09.013
4. Berridge, C. W., & Devilbiss, D. M. (2011). Psychostimulants as cognitive enhancers: the prefrontal cortex, catecholamines, and attention-deficit/hyperactivity disorder. Biol Psychiatry, 69(12), e101-111. doi: 10.1016/j.biopsych.2010.06.023
5. Linssen, A. M., Sambeth, A., Vuurman, E. F., & Riedel, W. J. (2014). Cognitive effects of methylphenidate in healthy volunteers: a review of single dose studies. International Journal of Neuropsychopharmacology, 17(6), 961-977. doi: 10.1017/S1461145713001594
6. Molina, B. S., Hinshaw, S. P., Swanson, J. M., Arnold, L. E., Vitiello, B., Jensen, P. S., . . . Group, M. T. A. C. (2009). The MTA at 8 years: prospective follow-up of children treated for combined-type ADHD in a multisite study. J Am Acad Child Adolesc Psychiatry, 48(5), 484-500. doi: 10.1097/CHI.0b013e31819c23d0
7. http://www.hscic.gov.uk/catalogue/PUB17644/pres-disp-com-eng-2004-14-rep.pdf, pp. 139-140. Data available in ‘Appendix 2 Tables’ Excel Spreadsheet here: http://www.hscic.gov.uk/catalogue/PUB17644
8. The researchers measured medication prevalence by the number of individual children who were prescribed ADHD medication, rather than the number of prescriptions being written.
9. Conrad, P., & Bergey, M. R. (2014). The impending globalization of ADHD: notes on the expansion and growth of a medicalized disorder. Soc Sci Med, 122, 31-43. doi: 10.1016/j.socscimed.2014.10.019

Why should we take a dimensional approach to studying developmental disorders?

Developmental disorders like attention deficit disorder, attention deficit hyperactivity disorder (ADD/ADHD), autism spectrum disorder (ASD), language, learning and movement disorders are relatively common, more common then we might think. Furthermore, these disorders have a considerable impact upon the daily lives of those who struggle with them. Because some of these disorders are more apparent in some contexts than others, and their severity is highly variable, they may go unrecognised for some time. Indeed, in many cases these disorders are only formally recognised when a child has already progressed through years of formal schooling. This means that they may already have had a largely negative experience of learning, may have lost motivation, and may already have fallen far behind their peers.

When trying to study these disorders, researchers normally use a case-control approach. It’s an observational study in which two groups differing in outcome are identified and compared on the basis of some presumed causal attribute. Researchers use this method to identify factors that may contribute to a medical condition with the help of comparing subjects who have that condition (“cases”) with patients who do not have the condition but are otherwise similar (“controls”).

Case-control studies are relatively cheap and they are a frequently used type of epidemiological study that can be carried out by small teams or individual researchers in single facilities in a way that more complex experimental studies often cannot be. This design is often used in the study of rare diseases or as an exploratory study where little is known about the connection between the risk factor and the disease. In several cases they have bigger statistical power than cohort studies. This approach has largely been translated from the clinical sphere to study developmental disorders.

Well-designed observational studies, like case-control designs, can provide valuable evidence. It is however worth noting that they are quasi-experimental in nature and thus do not bring the same level of evidence as randomized controlled experiments. That said, case-control designs can sit well alongside complementary randomized controlled experiments. There are however other problematic features of case-control designs, which are particularly highlighted when studying developmental disorders. Selecting an outcome of choice, indeed the basis for choosing one particular group, may produce unintended biases that can have a strong effect in overall findings.

One such example is the exclusion of children with any comorbid symptoms – this is routine practice when using a case-control design to study developmental disorders. The most important disadvantage in case-control studies relates to the problem of acquiring reliable information about an individual’s status over time, and then using this as a basis for choosing some children whilst excluding others. The children actually included may be atypical of those with a particular disorder. This exemplifies why this design does not always translate well into the study of developmental disorders; in developmental disorder comorbidity is more the rule than the exception. This approach can also give a false impression of the nature of these disorders, which can be graded rather than discrete.

However, it also is possible to use a dimensional approach instead of the case-control approach. A dimensional approach puts focus on the kind of problem a person is experiencing and on the extent to which that aspect of cognition is impaired. It doesn’t place people into diagnostic categories but along dimensions. Diagnosis then becomes not a process of deciding the presence or absence of a symptom or disorder, but the degree to which particular characteristic is present. This is entirely the approach taken by the Centre for Attention Learning & Memory (CALM; http://calm.mrc-cbu.cam.ac.uk/). Children are referred not on the basis of any discrete disorder or diagnosis, but because they are experiencing problems in the areas of attention, learning and memory. The researchers are taking a dimensional approach to exploring the nature of these impairments.

Instead of making judgements of “present or not?” the dimensional approach asks the question “how much?”. It ranks disorder on a continuum based upon multiple domains of cognition, assessed using standardised materials. A dimension is viewed as a cluster of related psychological/behavioural characteristics that occur together. This approach generates profiles, rather than discrete diagnostic categories. Of course, one could argue that this approach is far ‘messier’ than a simple case-control approach. However, one might also argue that this unique profiling is far more informative about the nature and extent of the impairments themselves, and provides a far clearer picture about the pattern of deficits actually present in a population of children with problems of learning.

Whilst working at CALM I have been trying to understand how children attend, listen and remember and how these skills impact on learning. These include difficulties in language, literacy and maths. By improving our understanding of the cognitive and brain processes involved in learning, we hope to develop ways of identifying and overcoming problems that might appear during childhood. We also hope to provide an information hub for researchers and professionals in children’s services, and to run regular workshops.

A child visiting the CALM clinic is profiled by grading the severity of symptoms from a number of dimensions using standardised tests. For example these dimensions include working memory, attentional control, short-term memory, phonological skills, the ability to inhibit and control responses, to initiate, plan, organise and set goals, inattention, hyperactivity, aggression, conduct problems, emotional symptoms, peer relations, prosocial behaviour, as well as aspects of communication (speech, syntax, semantics, coherence, initiation, use of context and non-verbal communication). This information can be fed back to the referrer and can then be used to help guide the support that the child receives. In parallel to this we are building a large and rich dataset. A dimensional approach is better able to capture the complexities that a categorical approach may miss. Of course, this approach is not without its challenges also. How does one define a dimension? What statistical approaches ought we to use? And what kind of scores would warrant some form of intervention?

Despite these challenges, we think that the dimensional approach will provide a way of capturing the rich complexities of these data. Whilst other disciplines may strongly favour an approach with rigid categorical boundaries, this approach is not always appropriate for studying developmental disorders. Whilst strict case-control studies can be valuable, reliance on these designs alone can provide a biased and unrealistic view of the children with problems of learning.

References

Gelder M, Harrison P, Cowen P. Classification and diagnosis. In: Shorter oxford textbook of psychiatry. 5 th ed. Oxford: Oxford University Press; 2006. p. 21-34.

Helzer, J. E., Kraemer, H. C., & Krueger, R. F. (2006). The feasibility and need for dimensional psychiatric diagnoses. Psychological Medicine(36), 1671–1680. http://psych.colorado.edu/~willcutt/pdfs/Helzer_2006.pdf

Kendell RE. Five criteria for an improved taxonomy of mental. In: Helzer JE, Hudziak J, editors. Defining psychopathology in the 21 st century: DSM-V and beyond. Washington DC: American Psychiatric Publishing; 2002. p. 3-18.

Lewallen, S., & Courtright, P. (1998). Epidemiology in Practice: Case-Control Studies. Community Eye Health(11(28)), 57–58. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1706071/

http://www.healthknowledge.org.uk/elearning/epidemiology/practitioners/introduction-study-design-ccs

ADHD and sugar: new avenues for an old question?

There is something about sugar consumption and hyperactivity that seems very intuitive. Perhaps, because everyone has experienced kids going crazy at a birthday party after having consumed industrial amounts of sugar through cakes, sweets, and lemonade. According to questionnaire studies, this opinion is also shared by parents of children with attention deficit hyperactivity disorder (ADHD). For some parents, dietry restrictions that cut-out all refined carbohydrates are preferred over gold standard stimulant treatment (Sciutto, 2015). However, the evidence that sugar has any effect on children’s behaviour and cognitive performance is not well supported. A number of studies were conducted in the 1980s and 1990s that investigated the link between sugar consumption and behaviour in children. The general design of these studies involved having children consume food items that contained either sugar or an artificial sweetener (aspartame or saccharine) without the child or the experimenter being aware which group the individual child was assigned to (double blind experiment). Next, the outcome of the food intake was measured as performance on a particular cognitive task (mostly standard assessments of general cognitive ability). A meta-analysis of these studies found no effect on test performance or observed behaviour (Wolraich, Wilson, & White, 1995). These results suggest that there is no effect of sugar consumption on general measures of behaviour and performance in typical children. But what about children with an ADHD diagnosis?

Some studies that looked at associations between environmental influences and ADHD in a large number of people found links between a diet high in carbohydrates and saturated fats and ADHD scores in independent samples in the UK, Western Australia, and Korea (Howard et al., 2011; Woo et al., 2014). However, it is difficult to draw firm conclusions from these population-based studies as both dietary patterns and ADHD behaviours may be influenced by a common underlying factor, e.g. differences in family lifestyle or socio-economic status. Conversely, some studies investigated the effect of specific diets as a treatment for ADHD. A recent review reported no effects of sugar vs apartame/saccharine on ADHD symptoms in 3 out of 4 studies (Heilskov Rytter et al., 2015). Interestingly, the one study that found differences reported differences on a measure of attention, while a behavioural assessment of aggressive behaviour was not influenced by sugar ingestion (Wender & Solanto, 1991). The other studies were based on playroom observations or assessments of general learning and memory (Gross, 1984; Milich & Pelham, 1986; Wolraich, Milich, Stumbo, & Schultz, 1985). The possibility that sugar consumption only affects performance on certain cognitive tasks but not general behaviour remains to be further investigated. In addition, research in the last decades has established that children diagnosed with ADHD present a very heterogeneous sample. This lead to the inclusion of subtypes in the last revision Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). It is possible that different subtypes of the disorder are differently affected by sugar consumption and that different studies find different results due to differences in the inclusion of subtypes within the study sample. The scientific interest in links between sugar and ADHD has ebbed away in the new millennium, while parents and educators continue to belief in a link. It seems that future work should address the questions that have not been satisfyingly answered in the previous work.

Some support for an association between ADHD and sugar comes from studies on the physiological level. Children are typically less able to regulate blood sugar levels compared to adults and this seems to be especially the case for children with ADHD (Lindblad, Eickhoff, Forslund, Isaksson, & Gustafsson, 2015). The brain is the most energy-hungry organ consuming 25% of the energy while only accounting for 2% of the body’s mass. Differences in energy metabolism are also known to influence behaviour, e.g. in the case of hypoglycemia (Millichap & Yee, 2012). Sugar intake was also found to increased EEG beta activity over frontal regions in children with “food-induced” hyperactivity (Uhlig, Merkenschlager, Brandmaier, & Egger, 1997), which related to measures of problematic behaviour. Based on these findings and others, a recent extensive review suggested that differences in energy metabolism are at the heart of ADHD symptomatology (Killeen, Russell, & Sergeant, 2013). According to the neuroenergetics theory, ADHD is characterised by a less efficient regulation of energy supply to neurons, which results in a reduction of around 15% in energy capacity. Further, based on this model inconsistencies between studies are also expected when the demands of the task vary. However, it is currently not clear from the model how differences in neuronal energy metabolism relate to dietary patterns. It is possible that attraction to high energy foods is an attempt of the system to counter-balance inefficient energy supply, but further empirical and theoretical work will be needed to fully understand the link between dietary preferences and brain metabolism.

In summary, the discussed studies do not support that there is a strong link between sugar consumption and ADHD. However, evidence from populations studies and physiological investigations indicate that energy regulation is affected in children with ADHD. These studies highlight that ADHD needs to be understood as a complex systemic disorder that affects many different levels of observation from cell biology to behaviour, which will hopefully be addressed in future research.

This line of investigation also poses questions that are extremely important for parents and educators, but it also raises concerns about current research practices. If food intake has an immediate effect on behavioural performance that differs systematically between ADHD and comparison groups, any study that aims to investigate neuro-cognitive differences should be controlling this factor.

Photo credit: Moyan Brenn (https://www.flickr.com/photos/aigle_dore/)

References:

Gross, M. D. (1984). Effect of sucrose on hyperkinetic children. Pediatrics, 74(5), 876–878.

Heilskov Rytter, M. J., Andersen, L. B. B., Houmann, T., Bilenberg, N., Hvolby, A., Mølgaard, C., et al. (2015). Diet in the treatment of ADHD in children – a systematic review of the literature. Nordic Journal of Psychiatry, 69(1), 1–18. doi:10.3109/08039488.2014.921933

Howard, A. L., Robinson, M., Smith, G. J., Ambrosini, G. L., Piek, J. P., & Oddy, W. H. (2011). ADHD is associated with a “Western” dietary pattern in adolescents. Journal of Attention Disorders, 15(5), 403–411. doi:10.1177/1087054710365990

Killeen, P. R., Russell, V. A., & Sergeant, J. A. (2013). A behavioral neuroenergetics theory of ADHD. Neuroscience & Biobehavioral Reviews, 37(4), 625–657. doi:10.1016/j.neubiorev.2013.02.011

Lindblad, F., Eickhoff, M., Forslund, A. H., Isaksson, J., & Gustafsson, J. (2015). Fasting blood glucose and HbA1c in children with ADHD. Psychiatry Research. doi:10.1016/j.psychres.2015.01.028

Milich, R., & Pelham, W. E. (1986). Effects of sugar ingestion on the classroom and playground behavior of attention deficit disordered boys. Journal of Consulting and Clinical Psychology, 54(5), 714–718.

Millichap, J. G., & Yee, M. M. (2012). The diet factor in attention-deficit/hyperactivity disorder. Pediatrics, 129(2), 330–337. doi:10.1542/peds.2011-2199

Sciutto, M. J. (2015). ADHD knowledge, misconceptions, and treatment acceptability. Journal of Attention Disorders, 19(2), 91–98. doi:10.1177/1087054713493316

Uhlig, T., Merkenschlager, A., Brandmaier, R., & Egger, J. (1997). Topographic mapping of brain electrical activity in children with food-induced attention deficit hyperkinetic disorder. European Journal of Pediatrics, 156(7), 557–561. doi:10.1007/s004310050662

Wender, E. H., & Solanto, M. V. (1991). Effects of sugar on aggressive and inattentive behavior in children with attention deficit disorder with hyperactivity and normal children. Pediatrics, 88(5), 960–966.

Wolraich, M. L., Wilson, D. B., & White, J. W. (1995). The Effect of Sugar on Behavior or Cognition in Children: A Meta-analysis, 274(20), 1617–1621. doi:10.1001/jama.1995.03530200053037

Wolraich, M., Milich, R., Stumbo, P., & Schultz, F. (1985). Effects of sucrose ingestion on the behavior of hyperactive boys. The Journal of Pediatrics, 106(4), 675–682.

Woo, H. D., Kim, D. W., Hong, Y.-S., Kim, Y.-M., Seo, J.-H., Choe, B. M., et al. (2014). Dietary patterns in children with attention deficit/hyperactivity disorder (ADHD). Nutrients, 6(4), 1539–1553. doi:10.3390/nu6041539

ADHD and Low Working Memory: A comparison

I was recently directed to a paper titled ‘Children with low working memory and children with ADHD: same or different?’ From the title alone this paper piqued my curiosity. As scientists we often focus on collecting large amounts of data, and in some cases forget the importance of forming new theories and ideas. For me, this paper casts the profiles of an ADHD diagnosis and a deficit in working memory, a common childhood issue, in a new light. What does it mean (if anything) to have a clinical diagnosis? And what is the best way of characterising children with problems of attention and memory?

Whilst I will summarise the main findings below, for those that want to read the paper for themselves it can be accessed here:

http://journal.frontiersin.org/Journal/10.3389/fnhum.2014.00976/full

This paper provides a novel comparison of cognitive skills, executive function, educational attainment and behaviour between those with a low WM and those with a diagnosis of ADHD. It utilised three groups of children (8-11yrs): one group identified by routine screening as having a low WM, one group with diagnoses of ADHD and one group of typically developing children.

Age was controlled for across the groups and for each group the following measures were taken: Working memory (Automated working memory assessment); Executive function (Delis-Kaplan Executive Function System, The K-test of the Continuous Performance Test and Walk/Don’t Walk from the Test of Everyday Attention for Children); Academic ability (Wechsler reading, spelling, reading comprehension, mathematical reasoning and number operations and the four WASI subtests); And classroom behaviour problems (Connors teacher rating and the Behaviour rating inventory of executive function). Those children taking medication for their ADHD stopped taking it at least 24hrs prior to the session to ensure the effects of the drugs were eliminated by the time of testing.

The theory that makes up the basis for the research, includes the fact that both ADHD and low WM in childhood are significantly associated with poor educational attainment. It has also been established in the literature that there are associations between poor WM and inattentive behaviour and poor WM and executive function deficits. These elements combined suggest a high degree of overlap between the profiles of those with a deficit in WM and those with an ADHD diagnosis. In ADHD, we see executive function problems (deficits in response inhibition, attentional switching, planning and sustained attention) and also excessively high levels of motor activity and impulsive behaviour.

Some have argued that the executive function deficits in ADHD are a result of an underlying low WM, whilst others have proposed that ADHD involves two distinct neurodevelopmental systems:

1) a ‘cool/cognitive system’ that affects executive functions and WM

and

2) a ‘hot/affective system’ that leads to ‘aversion to delay that manifests as impulsive behaviour’.

It is this impulsive behaviour that manifests as excessive motor activity and problems in impulse control that are core characteristics of ADHD and are not associated with low WM. Thus, this study hypothesised that the two groups share a common deficit in the ‘cool executive function system’ reflected in the fact that both profiles exhibit lack of attentional control, but only those with the ADHD diagnosis have impairments in the ‘hot executive function system’ that results in hyperactivity and impulsivity.

The ADHD and low WM group, as expected, performed more poorly than the typically developing children on the tests of working memory (necessarily so for the latter group, because they were selected on this basis). Performance was significantly decreased for the low WM group in the two WM subtests that they were initially screened on. This suggests a selection artefact as ‘the two groups did not differ on the verbal WM task that was not used at screening’. In the executive function switching task no significant difference was seen between the low WM and ADHD group when considering accuracy, however, the low WM group showed a significantly slower performance than the ADHD and typical group. The sustained attention executive function task showed that both the ADHD and low WM children were significantly less accurate than the typically developing group and that they both made a significantly greater number of omissions than the typically developing group. The ADHD group also further made a significantly greater number of commission errors than the other two groups. No other significant differences were seen between the low WM group and the ADHD group on any other test of executive function. It is also worth noting that although there are a number of different models proposed for the functional structure of WM, the findings of this paper remain consistent across models on the basis that the ‘storage-only capacities of short-term memory (STM) and the capacity-limited attentional control functions of WM can be distinguished’.

They concluded that the ADHD and low WM groups have very similar profiles of WM ability and executive function impairment. They did however find two important differences: the low WM group were ‘slower to respond on several tasks’ and the ADHD group were ‘more hyperactive and exhibited more difficulties in controlling impulsivity in sustained attention’.  The processing speed impairments in the low WM group were an unexpected finding. They state that ‘it does not appear to be a part of a broader problem in fluid intelligence, as controlling statistically for performance IQ had little impact’. They present the idea that the impairment in response time may be a result of sluggish cognitive tempo (SCT). Sluggish cognitive tempo is a ‘set of symptoms strongly associated with the predominantly inattentive form of ADHD that includes high levels of daydreaming, slow response times, poor mental alertness and hypoactivity.’ It could perhaps be the case that those with a low WM may correspond to those with SCT, a predominantly inattentive subtype of ADHD. At present SCT is not a commonly utilised diagnosis in the UK. The more hyperactive behaviour in the ADHD children however was expected. ‘They violated rules more frequently during a planning task, and made more commission errors on the Continuous Performance Test of sustained attention’. This elevated hyperactivity was also shown in the Connor’s teacher rating as increased impulsivity and oppositional behaviour.

Interestingly they found the two groups to have equivalently high levels of inattentive behaviour. Whilst it has been shown before that children with low WM often exhibit inattentiveness, this paper is the first to show that this inattentive behaviour is of a very similar degree to that of  children with ADHD. In terms of the deficits in working memory, both groups exhibited deficits in the same regions and of a similar magnitude. They had impairment in ‘visuospatial short term memory, verbal working memory and visuo-spatial working memory’; but ‘their verbal short term memory scores fell within the typical age range’. The novel finding here is that there is such a high degree of correspondence between the profile and severity of the WM impairments in the two groups.

Previous research has also suggested a close relationship between ‘controlled cognitive attention and working memory’. This paper takes this understanding one step further suggesting that it is now looking more likely that there is a ‘link between poor working memory and overt inattentive and distractible behaviours’ as seen through the inattentiveness in the behaviour of those children with a low WM. In addition to being comparable in inattentiveness and working memory impairment, the two groups both exhibited ‘high rates of problem behaviours across a wide range of executive function behaviours’. Previous studies have also indicated that problem behaviours associated with executive function are seen in children with a low WM. This paper supports and extends this idea by showing that both groups ‘performed poorly on direct measures of switching, inhibition, sorting, planning, sustained attention and response suppression’.

When considering again, the cool (cognitively based) and the hot (affective) model of executive function, the pattern found in the results from this study suggest that there is some shared general executive deficit between the ADHD and low WM groups. The cool deficits manifest as inattention and low WM in both groups whilst the hot deficits, only present in the ADHD group, manifests as the hyperactivity. The additional delay in response times in the low WM group is the only component that does not fit with this theory, but the authors have identified that it ‘may be symptomatic of a subgroup of children with the predominantly inattentive form of ADHD who are characterised by SCT’.

In conclusion, this paper shows some very interesting preliminary findings into two conditions that are generally considered distinct. Both groups showed equal levels of underachievement when IQ differences were taken into account (‘they are indistinguishable in terms of their poor learning progress in mathematics and reading’). This is of great significance as those with a diagnosis of ADHD will almost certainly have learning support provided to them whilst those with a low WM will not. The educational needs of the group of children with a low WM are being overlooked as they do not show the disruptive hyperactivity of ADHD, even though in many respects the groups are indistinguishable.

Holmes J, Hilton KA, Place M, Alloway TP, Elliott JG and Gathercole SE (2014) Children with low working memory and children with ADHD: same or different? Front. Hum. Neurosci. 8:976. doi: 10.3389/fnhum.2014.00976