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Keywords:

  • attention deficit hyperactivity disorder;
  • early intervention;
  • parenting;
  • pre-school children;
  • psychosocial support

Abstract

  1. Top of page
  2. Abstract
  3. Aetiology
  4. Genetics of attention deficit hyperactivity disorder
  5. Co-morbidity
  6. Developmental course
  7. Intervention
  8. Conclusions
  9. References

Attention deficit hyperactivity disorder (ADHD) is a complex disorder, where both genetic and environmental influences make a substantial contribution to the risk for the disorder. One of the challenges facing clinicians is to simplify for parents the multifaceted reasons why their child may have developed ADHD, explain the associated symptoms, and encourage parents to participate in intervention. Increasing parents understanding about ADHD should make them better informed about the disorder, more likely to consent to intervention, and increase adherence to both psychosocial and pharmacological treatment. The aim of this review is to provide clinicians with a brief synopsis of our current understanding about the aetiology of ADHD, co-morbidity and associated problems, developmental course and intervention options.

Despite several name changes over the past 50 years, the current diagnosis of attention deficit hyperactivity disorder (ADHD) shares the core group of symptoms, impulsivity, inattention, and motor restlessness, with earlier terms such as minimal brain dysfunction, hyperactive child syndrome and attention deficit disorder with or without hyperactivity (APA 1980). The disorder is relatively common, affecting approximately 4% of all children, although estimates vary widely from 3% to 11% or more (Zametkin & Ernst 1999). The disorder usually begins in early childhood and is characterized by excessive activity, even when developmental level and limited behavioural control are taken into consideration. (Elia et al. 1999).

Classification of what constitutes ADHD has changed dramatically over the last 20 years, with each successive revision of the Diagnostic and Statistical Manual, the diagnostic criteria used to describe the disorder. Current classification for combined type ADHD (DSM IV; APA 1994) require a minimum of six out of nine symptoms of inattention and a minimum of six out of nine symptoms of hyperactivity/impulsivity. In addition there must be some impairment from symptoms in two or more settings (e.g. home and school) and clear evidence of significant impairment in social, school or work functioning. The DSM IV also allows the classification of two sub-type disorders: (i) predominantly inattentive where the child only meets criteria for inattention; and (ii) predominantly hyperactive–impulsive where only the hyperactive–impulsive criteria are met.

Aetiology

  1. Top of page
  2. Abstract
  3. Aetiology
  4. Genetics of attention deficit hyperactivity disorder
  5. Co-morbidity
  6. Developmental course
  7. Intervention
  8. Conclusions
  9. References

Underlying aetiological explanations of ADHD can be simply divided into biological and environmental. In simple terms biological explanations include genetics, brain structure and their influence on neuropsychology, while predominant environmental explanations include parenting and diet.

Genetics of attention deficit hyperactivity disorder

  1. Top of page
  2. Abstract
  3. Aetiology
  4. Genetics of attention deficit hyperactivity disorder
  5. Co-morbidity
  6. Developmental course
  7. Intervention
  8. Conclusions
  9. References

There is now little doubt that ADHD is a condition in which genetic differences between children make a substantial contribution to the risk of the disorder (Stevenson et al. 2005). Initially genetic studies demonstrated that ADHD was highly heritable (Thapar et al. 1999) while more recent studies have begun to examine which particular genes might be implicated in ADHD. Interest in a potential genetic mechanism underlying AD/HD increased with reports of an association with a single dopamine transporter gene (Cook et al. 1995), and with reports of variations within the D4 receptor gene (LaHoste et al. 1996). Genetic studies have focused mainly on candidate genes involved in dopaminergic transmission. Several reasons exist for this particular focus, dopaminergic drugs (methylphendiate) are clinically efficacious in addressing the core problems associated with ADHD. Imaging studies using Positron Emission Tomography (PET), and Magnetic Resonance Imaging (MRI) techniques have implicated the frontostriatal circuitry in AD/HD, an area rich in dopaminergic activity. However recent meta-analysis have questioned the robust association between dopaminergic genes and ADHD (Purper-Ouakil et al. 2005). Other candidate genes have also been investigated including serotonin transporter genes (Manor et al. 2001). Current genetic investigations aim to examine whether different genes contribute to specific aspects of ADHD. For example, a recent meta-analysis by Waldman and Faraone (2002) has shown that the dopamine transporter gene DAT1 is more closely associated with ADHD combined sub-type than with the inattentive sub-type. While future molecular genetic studies aim to examine gene–environment interactions, the extent to which environmental factors moderate genetic risks for ADHD. As well as gene–gene interactions, the extent to which having a cocktail of different genetic influences might elevate risk for ADHD.

Brain structure of attention deficit hyperactivity disorder

A wealth of recent literature has examined the anatomical structure of the brain in children with ADHD. Using brain scanning technology such as MRI these studies suggest that the brain circuits linking the prefrontal cortex, striatum and cerebellum are not functioning normally in children with ADHD (Castellanos & Acosta 2002). Further evidence has examined the relationship between brain structure and behavioural measures of inhibition and attention. These results suggest that compromised brain morphology of selected regions related to behavioural measures of inhibition and attention. (Semrud-Clikeman et al. 2000). Further investigations of anatomical structure may allow the development of pharmacological interventions for ADHD which are better targeted to the specific site of action in the brain.

Neuropsychology of attention deficit hyperactivity disorder

Studies examining the neuropsychology of ADHD provide an opportunity to understand the relationship between underlying biological processes and symptoms of ADHD. For many years it was accepted that ADHD symptoms were the result of cognitive dysregulation (Nigg 2001). The ADHD child's behaviour resulted from insufficient forethought, planning and control (Schachar et al. 2000). Evidence to support this view point came from many studies using neuropsychological tests which demonstrated that ADHD children performed less well on these tests than did matched controls (Inoue et al. 1998). ADHD children asked to match familiar figures demonstrated more impulsive responding and higher error rates than did matched controls. (Sonuga-Barke et al. 1994a). A summary of ADHD as a disorder of cognitive dysregulation suggested that the relationship between biology and behaviour in ADHD was mediated by inhibitory dysfunction (Sonuga-Barke 2002). In contrast to the dominant view, Sonuga-Barke and colleagues (1994a) offered an alternative view of ADHD, not as a disorder of cognitive dysregulation, but as a motivational style. This viewed ADHD as a functional response by the child, aimed at avoiding delay. This alternative viewpoint of ADHD was based on studies by Sonuga-Barke and colleagues (1994a) which showed that most of the neuropsychological evidence to support ADHD as a result of cognitive dysregulation was confounded by delay. To demonstrate this, Sonuga-Barke and colleagues (1994a) got ADHD and match control children to participate in the matching familiar figures test, and found the same results as previous studies. ADHD children made more impulsive responses and more errors. However, Sonuga-Barke and colleagues (1994a) pointed out that all these studies involved trial constraints where as soon as one trial ended the next began and were confounded with delay. In order words, ADHD children made more impulsive responses because it allowed them to complete the task quicker and therefore escape delay. When Sonuga-Barke and colleagues (1994a) re-ran their study under time constraint (for a fixed period of time where early or impulsive responses had no influence on delay), ADHD children performed no differently from controls. Results of these studies lead to the development of the delay aversion hypothesis (Sonuga-Barke et al. 1996) which characterized the influence of delay on behaviour dependent upon whether the child has control over their environment or not. When the child is in control of their environment they can choose to minimize delay by acting impulsively, e.g. by skipping the queue at the end of the slide! When the child is not in control of their environment, or at least where they are expected to behave in certain ways or face sanctions, the child would choose to distract themselves from the passing of time. For example, in a classroom context during literacy lessons the child could achieve this either by daydreaming (inattention) or by fidgeting (hyperactivity). A summary of ADHD as a motivational style suggests that the relationship between biology and behaviour in ADHD is mediated by delay aversion.

Traditionally these two different accounts of ADHD have both sought to independently explain the disorder. However, a study by Solanto and colleagues (2001) compared the measurement of both of these hypotheses in a head-to-head study. Results of this study showed that measures used to test each hypothesis were uncorrelated, demonstrating that they measured different constructs. Both sets of measures were correlated with ADHD, and when combined were highly diagnostic, correctly distinguishing 87.5 of cases from non-cases. These results suggested that both accounts appeared to help to explain ADHD, but that neither explanation was the ‘single theory of ADHD’ which both theoretical camps had been searching for. Based on these findings, Sonuga-Barke (2002) proposed his dual pathway model of ADHD. This model proposed two possible routes between biology and ADHD behaviour. One via cognitive dysregulation and the other via motivational style. Clinically the dual pathway model suggests that there may be merit in targeting different sub-types with specific treatments, as well as allowing the development of novel interventions, perhaps aimed at desensitizing delay (Sonuga-Barke 2002). Sonuga-Barke (2004) has suggested ways in which the greater understanding about the influence of delay aversion on the development of ADHD could be used to develop alternative interventions. His suggestions include the use of delay fading, a technique to systematically reorganize the child's delay experience, as a means of increasing tolerance for delay, and reducing ADHD symptoms.

Environmental influences on attention deficit hyperactivity disorder

Attention deficit hyperactivity disorder is best viewed as a gene × environment interaction (Larsson et al. 2004). Children who have a genetic predisposition will express the disorder when put in the correct environment, typically one characterized by chaotic parenting (Johnston & Mash 2001). The best evidence for environmental influences on ADHD come from intervention studies which have demonstrated improvements in ADHD symptoms, when parents have been taught alternative parenting skills (Sonuga-Barke et al. 2001; Bor et al. 2002). Results of these studies do not necessarily imply that parents of children with ADHD are bad parents. In fact, influence of parenting on ADHD is best viewed from an interactionist viewpoint. The relationship between ADHD and parenting may result from both negative aspects of the child influencing the parents behaviour, and negative aspects of the parents influencing the child's behaviour. Studies examining mother–child interaction have found that ADHD children are, less often on task, less compliant, less responsive and more active than controls (Mash & Johnston 1982; Befera & Barkley 1985). Buhrmester and colleagues (1992) investigate both mother–son and father–son interactions and found that parents of ADHD boys were more demanding, aversive and power assertive, while the findings of Gardner (1994) have demonstrated that mothers of ADHD children have been found to be more negative, controlling, intrusive and disapproving, and less rewarding and responsive than mothers of non-ADHD children. So while parents of children with ADHD may engage in less than optimal parenting, it is easy to see how such responses might have evolved.

In addition genetic studies highlight the familial basis of AD/HD (Biederman et al. 1992; Smalley et al. 2000). Children with ADHD are more likely to have an ADHD parent. ADHD symptoms in parents usually interfere with consistent and appropriate parenting. Evans and colleagues (1994) found that ADHD in parents prevented effective parental monitoring and consistent use of constructive parenting techniques. Harvey and colleagues (2003) found that parental ADHD symptoms were associated with lax discipline, while Sonuga-Barke and colleagues (2002) found that high ADHD symptoms in mothers were a barrier to successful psychosocial intervention for pre-school children with ADHD.

Diet is another environmental influence, often cited by parents as having an adverse influence on their child's ADHD symptoms. Specifically, food additives, refined sugars and fatty acid deficiencies have all been associated with ADHD symptoms (Schnoll et al. 2003). However, the majority of this literature comes from older studies, with a variety of methodological problems, and small sample sizes (Schnoll et al. 2003). In fact a large recent randomized control trial examined the influence of food colourings and benzoate preservatives on pre-school hyperactivity. Results demonstrated a general adverse effect of food colouring and benzoate preservatives on hyperactive behaviour of pre-school children, based on parental reports, but not on simple clinic assessment. Children with high levels of hyperactivity were no more vulnerable to this effect than children with low levels of hyperactivity (Bateman et al. 2004).

While improving children's diet might impact on their general health and improve their overall behaviour, the clinical importance of dietary change as a means of remediating ADHD remains doubtful (Eigenmann & Haenggeli 2004).

Co-morbidity

  1. Top of page
  2. Abstract
  3. Aetiology
  4. Genetics of attention deficit hyperactivity disorder
  5. Co-morbidity
  6. Developmental course
  7. Intervention
  8. Conclusions
  9. References

It is widely accepted that ADHD is a co-morbid disorder, what is actually meant by this is far from clear. Gillberg and colleagues (2004) points out that co-morbidity can mean a common underlying aetiology which leads to two or more different disorders, or that one disorder leads to another, or even that two unrelated disorders co-occur. The term co-morbid also implies that their entities are morbid conditions, i.e. diseases. In fact, the vast majority of co-morbidities with ADHD represent functional impairments and symptoms, which are not rooted in specific diseases (Gillberg et al. 2004). It therefore seems more prudent to discuss associated problems rather than co-morbidity.

Attention deficit hyperactivity disorder appears to be associated with a wide variety of other psychiatry problems. Notable associations exist with Oppositional Defiant Disorder (ODD), Conduct Disorder (CD), depression and anxiety. About 50–60% of children with ADHD meet criteria for ODD, even in the pre-school period (Kadesjo et al. 2001). Busch and colleagues (2002) reported that ADHD children in primary care settings were significantly more likely than non-ADHD clinic controls to demonstrate mood disorders (57%) such as depression, multiple anxiety disorders (31%), and substance use disorders (11.5%). However, in the recent British Child Mental Health Survey (Ford et al. 2003), anxiety was not associated with ADHD when adjustment was made for the presence of a third disorder. In addition to associations with other psychiatric disorders children with ADHD are also more likely than their non-ADHD counterparts to experience a substantial array of developmental, social and health risks; these include:

Motor co-ordination

Children with ADHD often demonstrate poor motor co-ordination and balance (Moffitt 1990; Mariani & Barkley 1997). Studies by Kadesjo and colleagues (2001) have demonstrated that up to 60% of ADHD children demonstrate problems with motor co-ordination or deficits in developmental co-ordination compared with 35% of control children.

Impaired academic functioning

Children with ADHD are usually at an educational disadvantage upon school entry. ADHD children are more likely than their non-ADHD peers to demonstrate difficulties with basic maths and pre-reading skills during their first year at school (Lahey et al. 1988; Mariani & Barkley 1997). Even pre-school children with ADHD demonstrate educational disadvantage, DuPaul and colleagues (2001) demonstrated that their sample of pre-school ADHD children demonstrated deficits in pre-academic skills even prior to formal school entry. The pre-school ADHD children in their sample scored on average one standard deviation lower on the Battelle Developmental Index (Newborg et al. 1988) than did their non-ADHD control group.

Low IQ

Clinic-referred children with ADHD often present with lower scores on intelligence tests than control groups, specifically verbal intelligence with differences ranging from 7 to 10 standard score points (McGee et al. 1992). Studies with community samples of ADHD children (Sonuga-Barke et al. 1994b; Peterson et al. 2001) have also demonstrated negative associations between ADHD and intelligence.

Psychosocial functioning

Children with ADHD demonstrate serious difficulties with psychosocial functioning. Social adjustment is often given little attention on assessment protocols, given its designation as an associated feature of ADHD (APA 1994). However, the high levels of disruptive behaviour demonstrated by ADHD children increases the likelihood of negative reactions from parent, teachers and also peers (Cunningham 1990). In addition, negative social interactions with peers ultimately leads to peer rejection (Olson & Brodfeld 1991). Because these social difficulties are often resistant to psychosocial and pharmacological treatment (Pelham et al. 1998), they are expected to continue into adolescence, and even adulthood when criteria for the disorder may no longer be met (Slomkowski et al. 1995).

Unintentional injury

Children with ADHD appear to be at a greater risk for physical injury and accidental poisoning (DuPaul et al. 2001). Rowe and colleagues (2004) found that children with ADHD were at a greater risk for suffering fractures, most likely as a result of hyperactive and impulsive behaviour. Children with ADHD are also more likely than their non-ADHD counterparts to be injured as pedestrians, to inflict injuries to themselves, to sustain injuries to multiple body regions and to experience head injury (DiScala et al. 1998). Knowledge about safety does not appear to be lower in these children, implying interventions aimed at increasing knowledge about safety may have little impact (Mori & Peterson 1995).

Sleep problems

Studies report an association between ADHD and sleep disturbances (Gruber et al. 2000). Corkum and colleagues (1999) found that sleep problems occurred twice as often in AD/HD as in control children. The problems are mainly more behavioural and include settling difficulties, a longer time to fall asleep, instability of sleep duration, tiredness at awakening or frequent night waking.

While knowledge about the associations between ADHD and other related variables is useful in terms of diagnostic profiles, less is known about the impact of related variables on long-term outcome for the disorder. A recent study by Newcorn and colleagues (2004) demonstrated that the co-occurrence of conduct disorder and anxiety disorder with ADHD in childhood predicted a more severe course for ADHD in adolescence. Even less is known about the specificity of these associated problems to ADHD. In fact it may be that most of these associated problems are non-specific to ADHD, but more associated with psychiatry caseness in general (Angold et al. 1999).

Developmental course

  1. Top of page
  2. Abstract
  3. Aetiology
  4. Genetics of attention deficit hyperactivity disorder
  5. Co-morbidity
  6. Developmental course
  7. Intervention
  8. Conclusions
  9. References

While originally conceived of as a disorder of childhood and adolescence, recent evidence suggest scientific merit and clinical value in examining AD/HD in adulthood (Weiss et al. 1999; Faraone et al. 2000) and during the pre-school period (Sonuga-Barke et al. 2005). AD/HD symptoms have been shown to persist into later life with up to 40% of childhood cases continuing to meet full criteria in the adult years (Fischer et al. 1993). Adult ADHD appears to share many characteristics of the childhood disorder. Similar to their childhood counterparts, adults with ADHD display impairment in the interpersonal, vocational and cognitive domains (Biederman et al. 1990; Murphy & Barkley 1996; Schweitzer et al. 2000; Dinn et al. 2001). The adult and childhood disorders also appear to share a common neuropathology (Muglia et al. 2000; Hesslinger et al. 2001) and demonstrate a similar response to treatment (Sachdev 1999).

In the pre-school years a wealth of evidence now exists comparing pre-school ADHD symptoms to its school-aged counterpart. Children with a pre-school variant of ADHD present with the same symptom structure (Gadow & Nolan 2002), similar associated impairment and developmental risk (Lahey et al. 1988; Gadow & Nolan 2002) and similar patterns of neuropsychology (Sonuga-Barke et al. 2003a). Despite the similarities between pre-school ADHD and school-aged ADHD, little is known about what constitutes impairment during the pre-school years although school readiness should be what clinicians focus on. And even less is known about the relationship between early hyperactivity and later expression of the ADHD disorder (Sonuga-Barke et al. 2005).

Intervention

  1. Top of page
  2. Abstract
  3. Aetiology
  4. Genetics of attention deficit hyperactivity disorder
  5. Co-morbidity
  6. Developmental course
  7. Intervention
  8. Conclusions
  9. References

Inventions for ADHD are a relatively controversial topic, and dominated by the results of one large American study, the Multi-modal Treatment Study of ADHD (MTA) (Jensen et al. 1999). The controversy surrounds whether or not it is appropriate to medicate children with ADHD. On one hand, medication appears to yield significant improvements in symptoms (Konrad et al. 2005). However, a number of concerns have been raised regarding the use of psychostimulant medication for children with ADHD, especially younger children. These range from ethical objections to utilizing medication to modify children's behaviour (Perring 1997) to concerns about the lack of evidence for the long-term effectiveness of stimulant medication (Pelham et al. 1998). Side effects of stimulant medication have also been a cause of concern. Research has indicated that pre-school children seem to be at increased risk of developing short-term side effects (Ghuman et al. 2001). There is also a lack of research evidence regarding the long-term effects of stimulant medication on pre-school children's physical and neurological development (Sonuga-Barke et al. 2003b).

The MTA study set out to compare the efficacy of medication management, psychosocial intervention, combined (medication and psychosocial intervention) against routine community care. Results of the MTA study suggested that medical management alone was found to be significantly more effective for the core symptoms of ADHD compared with psychosocial treatment alone and routine community care (Jensen et al. 1999). In addition, psychosocial intervention did not significantly improve outcome when combined with medical treatment. The results of this study influenced recommendations made in the British National Institute of Clinical Excellence report (NICE 2000) on interventions for ADHD, which recommended medication as the front line intervention to be followed by psychosocial intervention, if necessary. However, later analysis using different outcome measures of ADHD symptoms indicated the superiority of combined intervention over medical management alone in the long term (Swanson et al. 2001), while sub-group analysis suggests large effects for psychosocial intervention in certain groups and settings (Swanson et al. 2002).

However, the relevance of the MTA study results to intervention in clinical settings remains unclear. The study compared a drug intervention tailored to each child's needs using a sophisticated titration protocol to a psychosocial intervention much less tailored to children's needs (Greene & Ablon 2001). The psychosocial intervention used could never be replicated clinically, as it involved a multitude of individual sessions for the child, summer camps, additional classroom help, support for the child's teacher and group and individual sessions for the child's parents (Green & Ablon 2001). More important is the fact that no theoretical rational for the content of the behavioural intervention has ever been published, and it is possible that elements of the intervention were counterproductive (Morrell & Murray 2003). Morrell and Murray (2003) suggest that interventions for ADHD should include strategies for reducing adult demands and intrusion when interacting with ADHD children, elements not included in the MTA intervention.

In addition since the publication of the NICE report, two recent studies evaluating parent-based interventions for pre-school children with ADHD have highlighted the value of early intervention. Sonuga-Barke and colleagues (2001) evaluated the treatment outcomes of a parent training (PT) intervention designed specifically to address the key components of ADHD against parent counselling and support (PC & S) and a waiting list (WL) control group. Results indicated that in comparison with PC & S and WL, PT reduced ADHD symptoms and increased mother's sense of well-being at the end of intervention, with reductions in ADHD symptoms being maintained 15 weeks after the end of intervention. For this pre-school sample the magnitude of the effects were similar to those achieved using stimulant medication with older children. Bor and colleagues (2002) compared standard and enhanced behavioural family intervention with WL control for pre-school children with ADHD and behavioural problems. Lower levels of behaviour problems and increased parental competence were found in both behavioural family intervention groups compared with the WL. These studies suggest that psychosocial intervention is a valuable treatment alternative to stimulant medication, when, intervention is tailored to the problems that children with ADHD experience, delivered in a timely way (i.e. early) and when the interventions are informed by theories about the aetiology of ADHD.

Conclusions

  1. Top of page
  2. Abstract
  3. Aetiology
  4. Genetics of attention deficit hyperactivity disorder
  5. Co-morbidity
  6. Developmental course
  7. Intervention
  8. Conclusions
  9. References

Attention deficit hyperactivity disorder is a complex disorder, therefore, it is not surprising that there are no simple solutions. The aim of this paper was to provide clinicians with a short and concise review which they could use to inform their patients about the disorder. By including in this review information about the connection between biology and behaviour, it is hoped that clinicians at all levels will feel more confident about explaining to parents of ADHD children, and older ADHD children themselves (i) how ADHD develops; (ii) what the intervention options are; and (iii) why these interventions are likely to address the symptoms of ADHD.

This review also highlights the need for greater consideration about the developmental course of ADHD. There is a desperate need for more attention to be paid to early intervention services for children with ADHD. With a wealth of studies now demonstrating the validity of the disorder in the pre-school years, and randomized control trials demonstrating the effectiveness of early intervention (Sonuga-Barke et al. 2001; Bor et al. 2002), now is the time for the development of a nationwide early intervention programme. What is the sense in delaying intervention until the school age period when the child's behaviour has become associated with antisocial tendency and school failure (Claude & Firestone 1995) and when greater effort, and resources will have to be expended to achieve less. In developing early intervention programmes, services might want to consider training needs and the role of specialization. A recent paper (Sonuga-Barke et al. 2004) demonstrated that psychosocial intervention for pre-school ADHD was much more effective when delivered by specialized therapists, than when it was delivered as routine care, by trained health visitors as part of their everyday case load.

Greater innovation is also required in terms of service development. Tight budgetary constraints will remain a reality for years to come. In order to meet the increased demands on future services, both self-directed interventions and telephone-based interventions involving minimal therapist contact require development and evaluation. A self-directed version of the early intervention implemented by Sonuga-Barke and colleagues (2001) has been developed and is currently being evaluated in North Wales. Early results from this evaluation look promising. While self-directed interventions will never achieve the same results as therapist-led interventions, they may provide services with useful tools for dealing with clients on waiting lists, or as an adjunct to conventional therapist-led intervention.

Greater attention also needs to be paid to the development of services for adults with ADHD. There are currently few clinical services available to adults with ADHD. Yet considerable evidence now exists, which demonstrates the disorder continues into adulthood with high levels of symptoms and impairment for some individuals (Fischer et al. 1993). The greatest challenge we face is the development and refinement of effective interventions for adults with ADHD, especially psychosocial interventions. A promising start has been made (Young 1999). Our greater understanding about the aetiology of ADHD, especially the role of delay aversion, indicates that novel interventions such as delay fading (Sonuga-Barke 2004) as a means of increasing tolerance for delay may prove useful in future interventions for adults.

A nationwide adult ADHD service should also be developed. In developing new clinical services for adults with ADHD, it will be important to recognize both the existing expertise of clinicians in child services, the strong developmental nature of the disorder, the wealth of existing research findings and the need for integrated services. At present child services have no place to refer on their clients when they reach adulthood, and adult services struggle to know what to do with individuals with ADHD. Greater collaboration between adult and child services is needed to facilitate future service development for individuals with ADHD.

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  1. Top of page
  2. Abstract
  3. Aetiology
  4. Genetics of attention deficit hyperactivity disorder
  5. Co-morbidity
  6. Developmental course
  7. Intervention
  8. Conclusions
  9. References
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