Attention deficit and hyperkinetic disorders in childhood and adolescence
Eric Taylor
Introduction
The concept of ADHD arose from neurological formulations, but does not entail them, and the modern definition simply describes a set of behavioural traits. The historical evolution of the concept was described by Schachar.(1) It began with the idea that some behavioural problems in children arose, not from social and familial adversity, but from subtle changes in brain development. The term ‘minimal brain dysfunction (MBD)’ was often applied, and covered not only disorganized and disruptive behaviour but other developmental problems (such as dyspraxias and language delays) presumed to have an unknown physical cause. MBD, however, stopped being a useful description when studies of children with definite and more-than-minimal brain damage made it plain that they showed a very wide range of psychological impairment, not a characteristic pattern (see Harris, this volume); and therefore it was invalid to infer the presence of brain disorder from the nature of the psychological presentation.
The successor to the concept of MBD was attention deficit and hyperactivity: defined, observable behaviour traits without assumption of cause. ‘Attention Deficit/Hyperactivity Disorder’ (ADHD) in DSM-IV, and ‘Hyperkinetic Disorder’ in ICD-10, describe a constellation of overactivity, impulsivity and inattentiveness. These core problems often coexist with other difficulties of learning, behaviour or mental life, and the coexistent problems may dominate the presentation. This coexistence, to the psychopathologist, emphasizes the multifaceted nature of the disorder; to the sociologist, a doubt about whether it should be seen as a disorder at all; to the developmentalist, the shifting and context-dependent nature of childhood traits. For clinicians, ADHD symptoms usually need to be disentangled from a complex web of problems. It is worthwhile to do so because of the strong developmental impact of ADHD and the existence of effective treatments. Public controversy continues, but professional practice in most countries makes ADHD one of the most commonly diagnosed problems of child mental health.
Clinical features
Overactivity
The idea of overactivity refers simply to an excess of movement. It is not totally dependent on context and cannot be reduced to non-compliance: physical measures of activity level have indicated that it is higher in children with ADHD than in controls, even during sleep.(2) It is, however, partly dependent upon context: it is often inhibited by a novel environment, creating a pitfall for the inexperienced diagnostician who may exclude it incorrectly because it is not manifested during observation at a first clinic visit. It may not be evident in situations where high activity is expected, such as the games field. The key situations where it is evident are familiar to the child and where calm is expected, such as visiting family friends, attending church, mealtimes, homework and—often the most troublesome—at school, during class.
(a) Impulsivenes
Impulsiveness means action without reflection—often described as a failure to ‘stop and think’. The term covers premature, unprepared and poorly timed behaviours—such as interrupting others, and giving too little time to appreciate what is involved in a school task or a social situation.
(b) Inattentiveness
Inattentiveness means disorganized and forgetful behaviour: short-sequence activities, changing before they are completed, with a lack of attention to detail and a failure to correct mistakes. All these are behavioural observations, not psychological constructs. At a cognitive level, ‘Attention deficit’ is a rather poor descriptor; the performance of affected children does not fade with time on a task any more than that of ordinary people and the presence of irrelevant information (‘distractors’) does not worsen their performance disproportionately to that of other people.(3) There are cognitive changes of a different kind (see ‘Aetiology’ below); but the diagnosis of inattentiveness depends on descriptions and observations of behaviour rather than on tests of performance.
Many other behavioural changes characterize some children with ADHD. They are, for instance, often irritable and their emotions can flash very rapidly when provoked. They may sleep badly (and this in turn can contribute to poor concentration). They can be aggressive to other people and non-compliant to authority. They can also be charming, humourous, inquisitive and intuitive. None of these, however, are either constant in ADHD or confined to those with ADHD. They are worth noting, but they do not make the diagnosis.
Classification
Attention Deficit/Hyperactivity Disorder in DSM-IV is defined as the presence of a number, above a cut-off, of behaviours considered to reflect the cardinal features described above to a degree that is developmentally inappropriate and gives rise to some impairment in more than one setting (e.g. school and home).(4) Overactive and impulsive behaviours are considered together as a single construct of ‘hyperactivity-impulsiveness’, and for convenience the combined dimension will be referred to in this chapter as ‘hyperactivity’. Examples of inattentive behaviour are added together and form a separate dimension. There are therefore three subtypes: hyperactive-impulsive, inattentive and combined.
The same problems characterize the ICD-10 definition of ‘Hyperkinetic Disorder’ (HD),(5) but with added requirements: especially, that all three cardinal features are present, pervasively across home, school and other situations. HD is therefore, in effect, a subtype of ADHD.(6, 7) The subtypes of hyperkinetic disorder are based on the presence or absence of conduct disorder—and indeed the presence of conduct disorder is an important factor with which to reckon in the course.
Diagnosis
Description of the symptoms makes them sound easy to recognize, and indeed the problems are usually very salient, disruptive to
other people, and common causes of referral to health and special education services. Nevertheless, there are pitfalls in the diagnosis, making it necessary for a specialist assessment to be undertaken before the diagnosis is given.
other people, and common causes of referral to health and special education services. Nevertheless, there are pitfalls in the diagnosis, making it necessary for a specialist assessment to be undertaken before the diagnosis is given.
Ambiguous criteria
The behavioural problems, described in outline above, are translated into detailed criteria in DSM-IV and ICD-10, and some of them can be ambiguous. For example, ‘does not follow instructions’ is a DSM item intended to imply that instructions are forgotten or not attended to; but the behaviour can also be shown for reasons of wilfulness and therefore a part of oppositional/defiant disorder. Careful description or witnessing the behaviours complained of is necessary.
Confusion of cardinal and associated features
Many behavioural problems—such as temper tantrums, sleeplessness, aggression and disobedience to adult authority—are common in children with ADHD, and may be the key reasons for presentation. It is easy to make the mistake of diagnosing ADHD when only disruptive behaviour is present. Much of the confusion comes from the way impulsiveness is operationalized in the diagnostic schemes. Behaviours, such as calling out in class and interrupting others, can indeed come from a difficulty in holding oneself back; but they can also represent deliberate flouting of the rules, and in a London survey of 6- to 8-year-old boys they were as common in nonhyperactive but defiant children as in the hyperactive.(8) Direct observation can usually make the distinction—watching either the children tackling tasks requiring them to stop and think in the clinic, or their natural behaviour in the classroom. Inattentive behaviour also helps to make the diagnosis of ADHD and is less confounded by oppositionality.
(a) Reliance on non-expert judgements
The behaviours of ADHD are continuously distributed in the population (see ‘Epidemiology’). The level that is considered normal or acceptable will vary from one culture to another and from one rater to another. To be diagnosed, they should be excessive not only for the child’s age but also for the developmental level; and this demands considerable familiarity with the usual range of variation. The diagnostician will acquire this in the course of training and experience; experienced teachers will be excellent judges; but inexperienced or overstressed parents may identify the problems at a low level of hyperactive behaviour, or suppose that an abnormal level is only to be expected in childhood. It is usually helpful to obtain a detailed behavioural account rather than rely on an overall judgment of ‘overactivity’ or ‘failure to concentrate’. Contradiction between sources may occur, and leads to arguments between parents and teachers. This may be due to different expectations, the emotional relationship of raters with the child, or children behaving very differently in contexts that vary in the demands placed on the children. The clinician needs to understand the full context of the way involved adults describe the child.
(b) Problems of recognition in the presence of coexistent problems
It is commonplace for children whose problems meet the criteria for ADHD to show other patterns of disturbance as well. This is often, confusingly, called ‘comorbidity’ – confusing because it assumes that the other pattern is a distinct disorder, which is only one of the explanations for coexistent problems. Clinicians need to understand the relationships for two reasons; so that they do not make or miss the diagnosis of ADHD; and so that they can make good strategies for treating ADHD in the presence of other disorders and other disorders in the presence of ADHD (see ‘Treating Complex cases’, below).
(c) Conduct and oppositional disorders
The commonest association and the best researched is with conduct and oppositional disorders. Nearly half the children with hyperactive behaviour in a community survey showed high levels of defiant and aggressive conduct as well; but the associations of the two problems were different, with hyperactivity (but not conduct problems) being associated with delays in motor and language development.(8) Genetic research indicates higher heritability for hyperactivity than for defiant and aggressive behaviour; but there are some genetic influences that are common to both.(9) Hyperactivity is more responsive to stimulant medication than are less hyperactive forms of conduct problem.(10)
When both ADHD and conduct problems are present, then the combined diagnosis (‘hyperkinetic conduct disorder’ in ICD-10) shows the associations of both disorders. ADHD is therefore not to be diagnosed by the absence of conduct disorder features, but by the clear presence of the core problems of inattentivess and disorganization.
(d) Tourette disorder and multiple tics
A different kind of differential is presented by children with Tourette disorder. Their motor restlessness may indeed represent the coexistence of ADHD, but can result directly from tics. If a child’s tics are very frequent and there are a large number of them, then their repetitive and stereotyped nature may not be apparent and they may be seen simply as restless fidgetiness. Again, direct observation of the pattern of overactivity is the key. When there is doubt, videorecording the child and subsequent slow-motion review may make repetitive patterns evident.
(e) Autism spectrum disorders
Children with autism have clear and characteristic impairments of language, communication, and social development. Spectrum disorders, however, can raise diagnostic challenges. Children with ADHD alone often show language delays (usually of an expressive nature with over-simple utterances, by contrast with the receptive difficulties and idiosyncratic patterns of autism). Their attention difficulties may make them unresponsive to the overtures of others in a way that can simulate the social obliviousness of people in the spectrum of autism, and they are often friendless—not because of lack of interest in others but because of the capacity of hyperactive behaviour to irritate other people. Indeed, attention problems can extend to perseverativeness on certain activities such as video games that may be mistaken for the restricted interests of autism. All these factors can lead to ADHD being mistaken for autism, but the reverse can happen too. There are other reasons for overactive behaviour in autism. First, stereotyped patterns of driven overactivity can be seen: they are not disorganized or impulsive and are often made worse by change and novelty (which usually reduce the overactivity of ADHD). Second, episodic bursts of extreme activity can be seen and may be best regarded and treated as catatonic. Third, akithisia may result from neuroleptic medication, or irritable
restlessness from anticonvulsants, and it will be necessary to establish a clear history that ADHD has been a persistent trait.
restlessness from anticonvulsants, and it will be necessary to establish a clear history that ADHD has been a persistent trait.
(f) Attachment disorders
Reactive attachment disorder (RAD) may share with ADHD a disinhibited style of relating to other people (an unreserved but shallow making of social contact). Children with RAD, however, tend to be controlling rather than disorganized, and vigilant rather than inattentive; and inattention and impulsiveness are not cardinal features of RAD; so it is not difficult to recognize both patterns when present in an individual child. The confusion in practice often comes from theoretical misconceptions. Those caring for neglected or abandoned children may consider that the diagnosis of ADHD cannot be accurate because the cause of the children’s problems is clearly to be found in their early deprivation. The causal pathway may indeed be that of neglect (though genetic inheritance and fetal exposure to toxins also need considering); but ADHD is a descriptive category, not an explanatory one. If the pattern of ADHD is present it still needs recognizing—not least because the cause of the ADHD behaviour does not seem to determine the response to stimulant medication, and children who have encountered neglect or abnormal early attachment may still have their ADHD problems reduced by medication.(10)
(g) Bipolar disorders
Both ADHD and manic conditions are characterized by overactivity, overtalkativeness, a sensation of whirling thoughts, and often by irritable mood. The distinction is made by the presence in bipolar disorder of episodicity, euphoria, and grandiosity. A suggestion that these distinguishing features are not in fact present in childhood bipolar disorder has naturally led to great overlap between the expanded childhood bipolar diagnosis and ADHD with poor emotional regulation, and further research will be needed to clarify whether there is a distinction.
In all these differential diagnoses, the principle is to establish that the child shows not only overactive behaviour, but the specific pattern of ADHD. Experienced judgement may be required, and the practice of diagnosing on the basis of questionnaire scores alone risks overidentification.
In adult life, there are still more possibilities for misdiagnosis. The commonest reasons for uncertainty are in distinguishing from atypical bipolar disorder and the effects of substance misuse. ‘Personality disorder’ is sometimes applied; and indeed ADHD shares with personality disorders a long-standing trait quality, but can also be a more precise way of describing the difficulties presented. Differentiation from the normal range of variation can be difficult in the absence of clear standards. The task of the diagnostician is harder when adults are presenting for the first time if only self-report is available; the self-description of hyperactivity may be a form of self-depreciation.
Methods of recognition
(a) Rating scales and informant interviews
Questionnaire ratings by parents or teachers are very useful for screening purposes, and in group studies they give a fairly good discrimination between people with a clinical diagnosis of ADHD and controls from the ordinary population.(11) Many are available(12,13) and the most famous are those from Conners, which yield several different scoring systems; and derivatives such as the Iowa Conners, the SWAN and SNAP scales.(14) They do however leave a fair number of individuals misclassified, and are not suitable as the sole means of establishing a diagnosis. A detailed interview with parents establishes what actual behaviours are the basis for ratings, allows professional judgement to be included, and remains the most informative single method.
(b) Psychiatric interview
Interview with the child is valuable for the observation of attention and social interaction that it yields, and for understanding a child’s view of their predicament. Children, however, are not good witnesses about their own concentration and impulse control, and even affected adults are not good at describing themselves in these terms. The experience of ADHD is usually one of suffering the reactions evoked from other people, or an experience of repeated failure. Adults often describe an experience of whirling and interrupted thoughts (in the absence of manic features); and some children will say the same, especially if treatment has enabled them to make a comparison with another way of being.
(c) Investigating underlying causes
Assessment needs not only to distinguish ADHD from related disorders, but to consider whether the ADHD pattern may result from remediable causes. The anamnestic history is by far the most productive investigation. It should include whether hearing problems have been excluded by previous testing (and, if not, an expert assessment should be arranged), and any injuries or diseases are potentially damaging the brain. The strengths and weaknesses of the family environment need to be assessed; they may dictate the choices of treatment. Physical examination should be sufficient to detect congenital anomalies, skin lesions, and motor abnormalities that can be the pointers to a neurological cause. Psychometric assessment is desirable whenever there are problems at school, both to generate an idea of developmental level against which the ‘developmental inappropriateness’ of behavioural symptoms can be judged, and to detect barriers to learning that may be the reason for inattentiveness. Special physical investigations are not routinely necessary. EEG often yields evidence of immaturity, but this does not advance assessment much and is not routinely indicated. It is valuable in the investigation of epilepsy and in the rare cases when deterioration of function suggests the possibility of a degenerative disorder. Blood tests should be planned only on the basis of history and examination, but may include tests of thyroid function, lead (in high-lead areas) chromosomal integrity (including fragile-X probe) when there is other evidence of developmental delay, and specific DNA tests when there is clinical suspicion of a phenotype such as that of Williams syndrome.
Epidemiology
Prevalence estimates vary widely; but most of the variation between studies comes from differences in definition(6) A community survey in London of more than 2000 6-8-year-old boys found a continuum of severity on rating scales: at each successively higher level of hyperactive behaviour there were successively fewer number of children(8) The genetic evidence also supports a continuum: in a population-based twin study, the influences on hyperactive behaviour were similar over the whole range of variation.(15) Estimates of prevalence are therefore critically dependent upon the cut-off point chosen.
Two major influences on the cut-off are the diagnostic criteria applied and the cultural attitudes of raters. Attention Deficit/Hyperactivity Disorder has a rate in the school age population usually given at about 5 per cent, but varies from 2.4 to 9 per cent(6, 16) probably depending on how rigorously ‘impairment’ is defined. The ICD-10 diagnosis of Hyperkinetic disorder yields rates around 1 to 2 per cent of the school age population.(6, 17) Sex differences are marked: population surveys suggest that 2-3 boys are affected for every girl.(18)
The frequency of hyperactive behaviour in the population, at least as indexed by rating scales in surveys, has not been increasing over the last two decades.(19) By contrast, there have been large increases in the frequency with which hyperactivity as a medical condition has in practice been recognized—most obviously evidenced by a great increase in the rates of stimulant prescription between 1995 and 2005 in the UK (Wong et al, in submission) and a continuing increase in the USA.(20) The studies suggest that stimulant medication is given for about 3 children per 1000 in the UK (i.e. about 12 per cent of those in the community meeting ADHD criteria with impairment) and about 40 per 1000 in the USA. It is likely that health service organization plays a part in determining recognition. In the USA survey, a diagnosis of ADHD was more likely to have been made for children whose families Carried Health Insurance.(20) In a UK survey, children with high hyperactivity as rated by teachers and parents seldom received a diagnosis, with the main filter coming at the level of recognition by primary health care services.(21)
In adult life, those who were hyperactive as children still have an elevated rate of hyperactivity and related social impairment (reviewed systematically by Faraone et al.).(22) Indeed, a cross-sectional population survey of adults described a surprisingly high prevalence rate of about 4 per cent, with a high rate of co-existent psychological morbidity.(23) More evidence is needed on the extent of the adult problem. It is however clear that a substantial number of adults, who were not diagnosed in childhood, may be affected, and an increasing number are presenting for the first time to adult services.
Aetiology
Genetic inheritance
Genetic influences are strong: Twin studies suggest a heritability around 80 per cent, making it one of the psychological disorders most strongly influenced by genetic inheritance,(24, 25) and adoptive family studies concur in emphasizing the strength of association with biological relatives.(26) Indeed, several DNA variants in genes coding for relevant proteins have now been identified and replicated.(27) In particular, the genes coding for the dopamine D4 and D5 receptors, the dopamine transporter, SNAP25 (affecting synaptosomal protein), the serotonin 1b receptor and the serotonin transporter have all been associated with ADHD by more than one group of investigators. Several kinds of caution are, however, needed in interpreting these findings. The odds ratios are all quite small (between 1.1 and 1.5), no polymorphism so far found is either necessary or sufficient; it is possible that there are subtypes of ADHD with different genetic influences(28)
Current research continues to seek more associated genes, especially by genome scans and positional cloning and to emphasize the likely importance of gene-environment interactions. Individual studies have reported that the risk alleles for genes in the dopamine system magnify the effects on the foetus of maternal smoking and alcohol consumption during pregnancy,(29, 30) and catechol o-methyl transferase (COMT) of low birth weight(31)
Environment
Environmental influences are reviewed by Taylor & Warner Rogers.(32) There are associations with several kinds of adversity in fetal and early postnatal life; and genetic factors may influence the exposure to some hazards (e.g. to lead, via playing in contaminated areas) as well as their impact. Many of the insults have generalized effects on brain development and can also lead to low IQ.
Prenatal
The prenatal factors implicated include smoking and drinking in pregnancy,(33) cocaine,(34) maternal stress during pregnancy,(35) anticonvulsant use(36) and the factors causing very low birth weight.(37) For some of these, there is experimental evidence for a harmful effect in animals. Smoking, for example, has high biological plausibility: the substances inhaled have an effect in animal models, and there is a dose-response relationship in human studies.(38) It is important to recognize these risk factors in assessing a referred child, because one may be able to prevent a subsequent child from suffering the same injury. Interpretation of a positive history, however, is not straightforward, because of the likely effects of genetic influences as well. There is no doubt of the existence of the fetal alcohol syndrome, nor that it can include ADHD symptoms, but the effect of lesser degrees of exposure is uncertain. Apparent associations could be magnified by gene-environment correlations. Maternal drinking may be influenced by the same genes that influence ADHD; the genes and the pregnancy toxin may be handed down together. Knopic et al.(39) investigated this by studying the offspring of mothers who were identical twins yet differed in whether they had a history of alcohol abuse: ADHD was common in both groups: the suggestion was that the genes were more important than the presumed exposure to alcohol.

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