ADHD and its comorbidity: an example of gene–environment interaction and its implications for...

ADHD and its comorbidity: an example ofgene–environment interaction and its implications forchild and family social workcfs_666 265..275

David HoweProfessor of Social Work, The School of Social Work and Psychology, University of East Anglia, Norwich, UK

ABSTRACT

In many of their cases, child and family social workers, particularlythose involved with abuse and neglect, will find themselves alsoworking with children who have been diagnosed with attentiondeficit hyperactivity disorder (ADHD). The paper reviews currentunderstandings and debates about the nature and causes of ADHD.Although modern evidence suggests the neurobiological basis of thecondition and the effectiveness of medication in treating the behav-iour, it is also recognized that the quality of the child’s caregiving andsocial environment plays a significant role in the aetiology, mainte-nance and treatment of ADHD. Recognizing the part that psychoso-cial elements play in understanding the condition, child and familysocial workers can be valued members of multidisciplinary teamstreating ADHD in which they offer support to parents, helping themto understand and manage their ADHD-diagnosed child.

Correspondence:David Howe,The School of Social Work andPsychology,Elizabeth Fry Building,University of East Anglia,Room EFB 2.23,Norwich NR4 7TJ,UKE-mail: [email protected]

Keywords: ADHD, comorbidity,environment, genes, social work

Accepted for publication: October2009

Published online: March 2010

INTRODUCTION

Although the exact figures are not known, many chil-dren in cases where there are concerns about abuse,neglect and family dysfunction also have a diagnosis ofattention deficit hyperactivity disorder (ADHD).Children with ADHD or hyperkinesis are also morelikely to be removed from home and placed with eitherfoster carers or adopters (Foreman et al. 2005).Higher than normal rates of children with ADHDhave been found in populations of fostered andadopted children (Simmel et al. 2001). Pentecost &Wood (2002) surmised that it was reasonable toassume that given the prevalence of ADHD in caseswhere there are behavioural and emotional difficulties,child and family social workers would be working on aregular basis with children diagnosed with ADHD.

It is often not clear what social workers in suchcases are supposed to do with this information,particularly when the child has been prescribed a psy-chostimulant such as the commercial drug Ritalin(Novartis, Basel, Switzerland). Sometimes there is the

inference that because ADHD has biological causes,the parents and family have no part to play in itsaetiology, management or treatment. A pharmacologi-cal response is the only appropriate intervention.

However, there are other views that do see parentsand their caregiving playing a role in the cause, main-tenance and treatment of ADHD. There are strongand weak versions of this ‘environmental’ perspective.The strong view argues that the quality of caregiving,particularly in cases where there is abuse, neglect andtrauma, accounts for much of the causation of ADHD.The weak view suggests that suboptimal caregiving isa direct response to the child’s ADHD; that is, ADHD‘causes’ poor parenting. For example, impulsive,hyperactive and non-compliant children are morelikely to provoke stronger controlling disciplinarystrategies and reduced responsiveness in parents(Barkely et al. 1992). Although mothers ofchildren with CD tend to show the highest levelsof coercive discipline coupled with the mostimpaired family functioning (Johnson & Mash 2001),higher than average rates are also observed in parents

doi:10.1111/j.1365-2206.2009.00666.x

265 Child and Family Social Work 2010, 15, pp 265–275 © 2010 Blackwell Publishing Ltd

whose children have ADHD (Finzi-Dottan et al.2006).

The classic investigations by Barkely & Cunning-ham (1979) shed interesting light on the possiblecausal direction.They observed suboptimal caregivingby parents of children diagnosed with hyperactivity.However, when the children received stimulant medi-cation and their compliance increased, the parentingimproved. Parents of hyperactive children who weregiven a placebo continued to display poor parent–child interaction. When the hyperactive children wereswitched from placebo to medication, the negative andcontrolling behaviour previously shown by mothersreduced, suggesting that parenting is a reaction to thechild’s hyperactivity and non-compliance. Neverthe-less, suboptimal parenting maintains, and possiblyexacerbates, the symptoms of ADHD.

There is a third strand to the debates surroundingADHD that queries whether all cases of ADHD havebeen correctly diagnosed. The behaviours associatedwith many other childhood disorders have similaritieswith the ADHD profile but might be better under-stood as post-traumatic stress disorder (PTSD), anattachment disorder or even attachment disorganiza-tion. It is certainly the case that ADHD has highcomorbidity with several other childhood disordersincluding conduct disorder (CD), oppositional defiantdisorder (ODD) and PTSD (Nigg et al. 2006).

DESCRIPTION OF ADHD

Even as early as the beginning of the 20th century,clinicians were observing that some children hadproblems keeping still and keeping their attentionfocused.They were fidgety and restless and had prob-lems sustaining focus and mental effort. Of course,this was a time of increasing compulsory education.Therefore, until these children found themselves inenvironments where sitting still and paying attentionwere required, these problems often went unnoticed,which is to say these behaviours, though present, werenot necessarily being perceived as problems. In thissense, the disorder exists only when the child’s behav-iour fails to meet social expectations, particularly inthe context of the school classroom.

In the Diagnostic and Statistical Manual of MentalDisorder (DSM-III-R; American Psychiatric Associa-tion 1987) and DSM-IV (American PsychiatricAssociation 2000), the syndrome was eventuallynamed ADHD, in which three types are recognized: apredominantly inattentive type, a predominantlyhyperactive–impulsive type and a combined type in

which both symptom clusters are recognized. Thesubtypes hint at the likelihood that ADHD is a het-erogeneous phenomenon (Taylor 2009, p. 130).

More boys are diagnosed with ADHD than girls,with ratios varying from 2 : 1 to as high as 9 : 1(Waschbusch et al. 2006, p. 54).The peak age of refer-ral is between 7 and 9 years, although initial onset istypically observed in the pre-school years.The rates ofdiagnosis of childhood ADHD and the associated pre-scription of stimulant medications have risen signifi-cantly since the early 1990s. In a meta-analysis, theworldwide prevalence was estimated at around 5%,making it one of the commonest childhood psychiatricdisorders (Polanczyk et al. 2007). Taylor (2009)believes that ‘the rise in the prevalence of ADHD isattributable to changes in recognition and diagnosticpractice rather than a true increase in the disorder’ (p.130). In contrast, Haber (2003) argues that the hugeincrease in cases of ADHD is a result of a significantincrease in misdiagnosis.

The main diagnostic criteria for ADHD includeearly onset of extreme problems of inattention, hyper-activity and impulsiveness (remembering that prob-lems of inattention and impulsivity are common inmost young children).These problems occur at home,at school and with peers. In general, children withADHD tend to have serious social difficulties.Relationships with family members and peers aretypically poor. In all, there are about 18 diagnosticcriteria. DSM-IV and International Classification ofDiseases-10 (World Health Organization 1992)require that when present, each behaviour must occuroften and must persist for at least 6 months to a degreethat is maladaptive and inconsistent with the child’sdevelopmental level.

Problems of attention and impulse control arelinked at various levels. Both attention and impulsecontrol are affected by the child’s level of arousal ortendency to arousability. Executive function (EF),cognitive control and ‘effortful control’, though differ-ent concepts, each refers to a child’s ability to regulatehis or her responses, suppress inappropriate behav-iours and adjust responses to the context. They alsoinvolve the children’s ability to keep on track in orderto achieve goals. EF and cognitive control are criticalto maintaining attention and controlling impulses.

Both genes and socialization experiences are likely toaffect EF development. Language development alsobecomes implicated in these processes. For example,poor language development may upset children’sability to regulate behaviour by the use of self-talkstrategies. Children whose language and comprehen-

ADHD and its comorbidity D Howe


sion development is delayed might increase parentalfrustration. Indeed, there is some evidence thatlanguage problems are a correlate of ADHD (e.g.Tannock & Schachar 1996).Children withADHD alsohave impaired social cognitive abilities. As a conse-quence, they misperceive and misread social situations.

Thus, a number of ‘within-child’ factors, such asarousability, EF and effortful control, can affectparent–child relationships, socialization and languagedevelopment. In turn, the dynamic interactionbetween these elements – genes and environment –contributes to the genesis and maintenance of ADHD(Garbarino & Thompson 2000). Furthermore,various parental characteristics – anger, emotionaldysregulation, hostility and misattunement to childcues – can interact with both ‘within-child’ factors andthe previous dynamic transactions that contributed topoor language development, weak socialization, atten-tional problems and impulsivity.

However, it must be noted that there is considerablepotential for confounding these various genetic andpsychosocial factors. If, for example, heritability is afeature of ADHD, parental characteristics, themselvesgenetically influenced, are also involved in creating thepsychosocial environment. In this sense, it is difficultto disentangle what part genes and (social) environ-ment are playing in a child’s ADHD.

DIAGNOSIS , MISDIAGNOSISAND PROGNOSIS

Accurate assessment and diagnosis ideally requiretaking a careful history from multiple adult infor-mants (particularly parents and teachers), coupledwith direct observation of the child in the family andschool environment using well-normed rating instru-ments. It is possible that less thorough and robustassessments, particularly those that fail to distinguishADHD from other childhood disorders, might in partaccount for some of the disorder’s apparent increase.Clinicians who base their assessments on relativelyshort periods of observation using non-standard,subjective criteria are most likely to misdiagnose thecondition.

Young children diagnosed with ADHD are at long-term risk of a number of problems including learningdifficulties and behaviour problems (Fonagy et al.2002, p. 198) Prospective studies show that ADHDoften persists into adolescence and even adulthood(Manuzza & Klein 2000). Children with ADHDare at increased long-term risk of poor academic

achievement, school dropout, family dysfunction, peerrejection, accidental injury, aggressive behaviourand unemployment.

COMORBIDITY

A diagnosis of ADHD often occurs along with severalother child psychiatric conditions (Tuvblad et al.2009). These include disruptive disorders (ODD,CD), learning disorders, anxiety disorders, PTSDs,and attachment disorders. For example, rates ofcomorbidity between ADHD and conduct problemsrange between 30% and 50% (Waschbusch et al.2006, p. 53). Hyperactivity specifically is more likelyto be comorbid with CD. Moreover, when ADHD isfound with other antisocial behaviours, both problemstend to be more severe and persistent, have a worseprognosis and show a stronger association withcognitive deficits and lower verbal abilities than whenthey occur alone (Thapar et al. 2006, 2007). Severalstudies also report that children diagnosed withADHD are more likely to have an attachment classi-fication of ‘disorganised-controlling’ (e.g. Clarke et al.2002).

The substantial overlap and comorbidity of disor-ders, particularly the externalizing disorders, raisesthe question of whether there might be somecommon, underlying causes, including genetic causes,and/or neuropsychological features associated withADHD, CD and attachment difficulties. Tyrer (2009)believes that when there is up to 70% comorbiditybetween psychiatric diagnoses, a common underlyinggenetic condition is strongly indicated. Tuvblad et al.(2009, p. 163) found that genetic influences explained57% of the covariance of the externalizing problembehaviour seen in ADHD, CD and ODD. Neverthe-less, there are some unique genetic and environmentalinfluences in each disorder. This suggests that,although there are some common genetic risk factors,there are also independent effects that produce theslightly different symptomatologies associated witheach condition.

GENETIC AND ENVIRONMENTAL CAUSES

Heritability

High levels of heritability have been found for ADHD(e.g. Levy et al. 2001). The disorder does appear torun in families. Many genes are likely to be involved,but those related to dopamine neurotransmission andserotonin pathways in the brain have been strongly



implicated. Dopamine receptors, in particular, seemto play a part in the aetiology of the disorder. (Dopam-ine is a key neurotransmitter in motor action and thereward system; too much dopamine can result inmood changes, increased motor behaviour and dis-turbed frontal lobe functioning, an area of the braininvolved in attention and keeping focus).

Antenatal environments

A number of antenatal environmental risk factors forADHD have also been suggested. These includetobacco smoking and alcohol consumption by themother during pregnancy, prenatal maternal stress,prematurity and low birth weight (e.g. Bhutta et al.2002; Langley et al. 2005; Banerjee et al. 2007;Thapar et al. 2007). Children’s post-birth diets havealso been identified as a possible risk.

The caregiving environment

Poor quality caregiving and inadequate parental dis-cipline have also been suggested as causal (Carlsonet al. 1995). In Carlson et al.’s (1995) study, parentswho were ‘misattuned’ and poor at reading their chil-dren’s cues predicted ADHD-related symptoms.However, although hostile, harsh, rejecting and coer-cive parenting has been associated with ADHD, thesefamily environmental risk factors tend to be associatedwith most areas of child psychopathology. This sug-gests that their links with ADHD, though relevant, areprobably non-specific. As suggested above, it is morelikely that social environmental risks interact with spe-cific arrays of genetic factors that affect, among others,brain chemistry, neurological sensitivity and tempera-ment, leading to the development of either ADHD,CD or ODD. But again, to further complicatematters, some researchers and clinicians suggest thatenvironments interacting with genes can also affectthe brain’s chemistry, including dopamine production(e.g. Halasz & Vance 2002; Crittenden & Barne2007). This might be particularly true in caregivingenvironments where the child experiences danger andstress, which would be the case in abuse, neglect andrejection.

Insecure, anxious and disorganized attachments,including those in which the child experiencestrauma, abuse, neglect and high levels of stress, notonly hypersensitize children’s reactions to stress butalso affect the neurological development of the orb-itofrontal cortex, which plays a key role in helpingchildren recognize and self-regulate emotions and

their arousal (e.g. Schore 1996, 2001a,b). Abuse andneglect, associated with increased risks of disorga-nized and controlling attachments, are therefore alsoassociated with poor emotional self-regulation andhence impulsivity and hyperactivity. In a further devel-opment of these associations, Lakatos and his team(2000) found links between the dopamine D4 recep-tor gene (also linked to ADHD) and attachmentdisorganization.

In an attempt to reconcile what they believe is thecurrently dominant biodeterministic model of ADHDand brain development with one that includesenvironmental influences, Crittenden & Barne(2007) offer further refinements to an attachmentperspective:

This suggests an interaction between genetic vulnerability and

early attachment experiences, expressed in the form of the

symptoms that define ADHD. Based on this idea, Ladnier and

Massanrani (2000) proposed that ADHD resulted from

‘bonding breaks’.Their review of the histories of children with

ADHD indicated that, in every case, the histories contained

one or more bonding breaks. That is, attachment concerns

might be a necessary component of the etiology of ADHD.

(p. 1223)

The different patterns of attachment organizationreflect the different strategies employed by children inorder to increase safety and regulation (Ainsworthet al. 1978). Survival is always the bottom line ofexistence. Crittenden’s particular attachment model,which she calls the dynamic maturational model, pro-poses that any threat to survival in humans involvesthe use of a range of survival and behavioural strate-gies that become more extreme the more dangerousthe environment (e.g., child abuse and neglect).

These strategies function to raise or lower arousal, signal need

to others, and elicit both feelings in and responses from others.

The more an individual focuses on survival, using relatively

extreme strategies, the less they can turn attention to other

activities, e.g. peer friendships, academic work. Further,

extremely high or low arousal will be reflected in neurological

functioning and behaviour. That is, some neurological and

behavioral symptoms of ADHD may be part of a self-

protective strategy (e.g. high arousal, hypervigilant-scanning

attention) whereas others (e.g. lack of focus on school work)

may be inherent ‘side effects’ of the strategy. (Crittenden &

Barne 2007, p. 1223)

Relational trauma

Perry & Szalavitz (2006) also explore the possibilitythat some cases of ADHD might be precipitated byrelational trauma, particularly maltreatment in theearly years. They also wonder whether, in fact, some



cases of diagnosed ADHD might be better understoodas examples of PTSD; that is, ADHD is a misdiagno-sis. Either way, they examine the effects of earlytrauma on brain organization. This analysis does notrule out genetic susceptibility factors, but it doesrequire environmental risk factors to set in train theconsequences of an initial genetic vulnerability.

In discussing the case ofTina, a 7-year-old who hadbeen sexually abused, Perry & Szalavitz (2006, pp.7–30) describe symptoms of attention deficits, coor-dination and language problems. Perry’s work on theeffects of stress on early brain development suggestedto him that children who suffer repeated activation ofthe stress response system will have altered brainreceptors that will affect sensitivity. He began to thinkthat the cause of Tina’s attention and impulse prob-lems was the result of developmental trauma:

due to a change in the organisation of her stress response

neural networks, a change that might have once helped her

cope with her abuse, but was now causing her aggressive

behaviour and inattention to her class work in school. It made

sense: a person with an overactive stress system would pay

close attention to the faces of people like teachers and class-

mates, where threat might lurk, but not to benign things like

classroom lessons. (Perry & Szalavitz 2006, pp. 24–25)

Perry observes that in the classroom many trauma-tized children’s tendency to dissociate and todevelop hyperarousal looks ‘remarkably like attentiondeficit disorder, hyperactivity or oppositional dis-order . . . While not all ADD, hyperactivity andoppositional-defiant disorder are trauma-related, it islikely the symptoms that lead to these diagnoses aretrauma-related more than anyone has begun tosuspect’ (Perry & Szalavitz 2006, p. 51).

Severe neglect

There is evidence that early and long-lasting severeand extreme neglect and deprivation, coupled withmajor disruptions of care (e.g., in poor quality insti-tutional care), is associated with disinhibited attach-ments; quasi-autism; and inattentivity, overactivityand impulse control problems (e.g. Kreppner et al.2001). This population of deprived children showshigh rates of inattention/overactivity that share manyfeatures with ADHD.

The study by Colvert et al. (2008) found thatRomanian children who experienced early and pro-longed global deprivation in institutional care suffereddeficits in EF and that EF partially mediated thehigher rates of ADHD seen in these children.

These findings suggest the possibility that early andextreme neglect or trauma might play a part in thecause of ADHD, at least in the case of some mal-treated children who carry a genetic susceptibility. Forexample, Stevens et al.’s (2008) study of adoptedRomanian children whose early years were character-ized by extreme deprivation found that the symptomsof inattentiveness and overactivity persisted into earlyadolescence despite the radical and positive change ofenvironment involved in adoption. This points to thepossibility that early environmental deprivation canalter neurological development in the early years,resulting in ADHD-like symptoms.

This finding supports a growing body of evidencethat early and prolonged stress affects brain develop-ment and therefore psychological and behaviouralfunctioning (Stevens et al. 2008, p. 394). Althoughthe detail is likely to be complicated, this neurode-velopmental speculation goes some way to explainwhy early and prolonged abuse, neglect and traumalead to a range of associated disorders includingADHD, disinhibited attachments, disorganizedattachments and CD. In short, environments,particularly in cases where children carry a geneticsusceptibility, can affect brain development at thelevel of both neurological organization and brainchemistry (e.g. dopamine and adrenaline systems).In turn, compromised brain development willadversely affect cognition, emotional regulation andbehaviour.

GENE–ENVIRONMENT INTERACTION

Biological causes of ADHD have been in the ascen-dancy over recent years. ‘Even so’, reflect Waschbuschet al. (2006), ‘virtually every influential conceptualiza-tion of ADHD emphasizes that ADHD is multiplydetermined, with both biological and environmentalcontributions to the disorder’ (p. 59). Thus, althoughADHD has been found to be a neurodevelopmentaldisorder with high heritability, its development andcontinuation has been found to be strongly influencedby family environmental factors, including parentalrejection (Lifford et al. 2008).This appears to be mostlikely when ADHD is comorbid with externalizingproblem behaviours such as CD. The bidirectionalityof these examples again reminds us that the geneticfactors for ADHD affect the child’s environment (inthis case, the quality of parenting) and that parentingaffects the expression of the genetic susceptibility todevelop and display ADHD symptoms and other dis-ruptive behaviours.



The concept of gene–environment interaction offersa dynamic picture of the relationship between genesand environment. No longer is the nature–nurturedebate simply one of nature or nurture, or indeed oneof ‘this much nature’ and ‘that much nurture’, butrather one in which genetically determined traits (e.g.temperament) effect and are affected by environmen-tal factors. For example, each individual has a geneticpotential to reach a certain height. However, whetherthat genetic potential is reached depends on a numberof environmental factors such as maternal smokingduring pregnancy, the child’s diet and exposure todisease and illness.

Similar processes have been found to be at work fora range of mental-health and psychiatric problems.For example, although there is no single gene fordepression, some people appear to have a heightenedgenetic risk of getting depressed. However, whether ornot they actually get depressed might also depend ona range of environmental experiences includingquality of early caregiving, and the number and inten-sity of life stressors they meet.

We need to have these ideas in mind when thinkingabout ADHD and its comorbidity. This is a reminderthat these disorders are recognized on the basis of setsof behavioural descriptions and not clearly identifiedunderlying causes (or aetiology). However, given thatmore than half of the genetic risks are shared byADHD, CD and ODD, Tuvblad et al. (2009, p. 164)wonder if environmental experiences actually influ-ence which particular disorder gets expressed. Thissuggestion introduces the currently prevalent viewthat genes express themselves in the context of theenvironment in which they happen to find themselves.In other words, similar but slightly different behav-iours, conditions and strategies such as ADHD, CDand attachment disorganization might share many(though not all) of the same genetic risk factors, butthe way these ‘susceptibility’ genes are expresseddepends on the characteristics of the environment,particularly the social and caregiving environment.The fast growing science of epigenetics looks at howenvironmental experiences, including those in thewomb, determine which genes get switched on or off.This suggests that children who suffer high levels ofstress in the caregiving environment and who alsocarry a genetic risk of ADHD would be more likely todevelop the disorder. Support for this ‘correlated riskfactors model’ for ADHD and CD is provided byRhee et al. (2008), who suggest ‘that there are signifi-cant shared genetic and environmental influencesbetween ADHD and CD’ (p. 38).

Genes, as has been often said, although powerfulforces in our development, are not destiny. The envi-ronment plays its own unique role. Biederman et al.(1995) found that the ‘reactivity’ of the early caregiv-ing environment affected the chances of whethergenetically at risk children developed ADHD. Severemarital discord, paternal criminality, paternal antiso-cial personality disorder and maternal mental disorderhave all been found to increase the risk of ADHD.Some studies suggest that children with ADHD andCD are more likely to have parents with CD, ADHD,antisocial behavioural problems, avoidant attach-ments, depression and marital dysfunction (also seeBiederman et al. 1995; Garbarino &Thompson 2000;Waschbusch et al. 2006). In other words, the psycho-social environment can mediate gene expressionduring key developmental stages, particularly in thefirst years of life.These are examples of what is knownas the ‘developmental origin of health and disease’ orthe DOHaD hypothesis that postulates that ‘theenvironment during various critical developmentalperiods is crucial in determining onset of diseases inlater life’ (Mill & Petronis 2008, p. 1026). Thishypothesis has been explored for a wide range ofphysical and mental-health diseases ranging from dia-betes, heart diseases, longevity and ADHD.

It will be apparent from this brief review ofADHD’s varied symptomatology, extensive comor-bidity, number of proposed risk factors and range ofpossible causes that it is a heterogeneous phenomenonaround which there remains much debate.

TREATMENTS, SUPPORTSAND INTERVENTIONS

Medication

Most clinical trials and evidence-based research findthat stimulant pharmacological treatments are effec-tive in about 75% of cases, at least in the short term,currently defined as 1 or 2 years (e.g. Connors et al.2001). Medication is less effective in the presence ofcomorbidity and developmental delay (Barkely 1998).The long-term efficacy and effect of these drugs [e.g.methylphenidate (MPH) of which the commercialform, Ritalin, is an extended-release form of the drug,and dexamphetamines, of which Adderall (Teva Barr,Petach Tikva, Israel) is an example] on children,including possible adverse effects on the brain, is notyet known (see Breggin 2008; Bentall 2009; Moncrieff2009 for recent critiques of psychiatric medicine’sheavy use of drug-based interventions in the treat-



ment of many mental-health and behavioural prob-lems, including ADHD). Because children withADHD appear to need high levels of stimulation toachieve arousal, the administration of a stimulant drugincreases the sensitivity of children’s neurologicalsystems. This reduces their need to behave hyperac-tively and act impulsively. Medication also increasestheir ability to sustain attention.

In summary, therefore, regardless of age, 75% of children with

ADHD show normalization of inattention, hyperactivity, and

impulsivity when treated with stimulants. It is not possible to

predict reliably which children will show a good response. In

addition, 70% of children with ADHD with comorbid aggres-

sion will show significant improvement in aggressive behaviors

to the level of controls. However, prosocial behaviors do not

improve . . . (Fonagy et al. 2002, p. 204)

Behaviour modification

Behaviour modification, though showing some posi-tive effects, when used on its own is less effective thanstimulant medication when used on its own.With theaim of improving attention and productivity, examplesof behaviour modification include positive reinforce-ment and response–cost treatments in which the childcan accumulate points (traded for free time or otherbenefits) for staying still and keeping to the task. Theproblem of sustaining these improvements in behav-iour remains the main shortcoming of behaviourmodification programmes for ADHD (AmericanAcademy of Child and Adolescent Psychiatry OfficialAction 1997). Booster sessions are often required.

Combined treatments

The most effective treatments, albeit measured over therelatively short term, seem to be those that combinestimulant medication (e.g. MPH) and behaviourtherapy (Pelham et al. 1998). Stimulant medicationplus behaviour therapy is more effective than eithertreatment alone (e.g. Fabiano et al. 2000). Neverthe-less, there is no evidence that these treatments and thebehavioural improvements they engender actually leadto normalization, even though long-term outcomes forchildren who took medication are better than controlgroups of children with ADHD who did not.

Treatments based on a neurosequential approach

If some abused and neglected children’s ADHD-likesymptoms are actually better understood as PTSD ordevelopmental trauma that affect the brain’s earlydevelopment, organization and chemistry, then treat-

ments must aim to repair the developmental damage(Perry & Svalavitz 2006). This is achieved by helpingchildren experience and rework healthy developmen-tal opportunities, particularly under conditions ofarousal, in the order that the brain would normallyand optimally experience them. This usually involvesworking up from the level of the senses and motororganization, through the emotions, and finally up tothe level of cognitive–reflective functioning in aprocess described as a ‘neurosequential’ approach.

Parental support, guidance and education

Given the active debates about the nature, origins anddevelopments of ADHD in which both genes andenvironment are implicated, it seems clear that as wellas behaviour therapies, there is a role for a variety ofother psychosocial interventions. Psychostimulantmedications treat the symptoms, but in so doing theyalso change the quality and character of child–parent,child–peer and child–teacher interactions. In manycases, this facilitates better quality relationshipsbetween the child and key others in his or herenvironment.

However, it is also the case that some types ofstressful parent–child interaction, particularly in casesof maltreatment, might mediate gene expressionduring key developmental stages, particularly in thefirst years of life. This can increase the risk of com-promised early neurological development and ADHD.This complex gene–environment aetiology indicates avariety of interventions and supports, some of whichmight be provided by health and social care workers(e.g. Olds et al. 2004; Slade et al. 2005). Stress reduc-tion, education about young children’s developmentand parental support could play a preventative role inpopulations where there are increased risks of childabuse, neglect and associated ADHD.

In their study, Pentecost & Wood (2002) found thatthe majority of social workers understood the diagnos-tic criteria for ADHD. However, there was moreuncertainty about the appropriateness of varioustreatments, with the majority favouring psychosociallybased interventions including parental guidance,support and training. Other researchers have foundthat in cases where ADHD is already suspected ordiagnosed, increased support and more specific psy-chosocial interventions should be offered includingfamily therapy and attachment-based interventions(e.g. Berlin et al. 2005; Crittenden 2008). Clarke et al.(2002) found an association between insecure attach-ments and ADHD.They therefore recommended that



the quality of attachment with primary caregiversfor children who present with symptoms of ADHDshould be assessed. In the case of insecure attach-ments, relationship-based treatment should be offeredto help parents improve their sensitivity and respon-sivity (Oppenheim & Goldsmith 2007; Juffer et al.2008; Lieberman & Van Horn 2008).

If the arguments about the quality of parent–childrelationships in which children are anxious, if notfrightened by the behaviours of their parents, have anymerit, then the treatment focus shifts from symptomreduction (which is the case in drug and behaviourmodification treatments) to ‘strategic adaptation andthe need for children to feel that their home is safe andcomforting’ (Crittenden & Barne 2007, p. 1227). Inpractice, this means working not only with the childbut also with the parents’ memories, fears and anxi-eties as it is these that elicit the child’s fears andanxieties, increased vigilance and distractability, andstruggles to stay focused.

Sunderland (2006) further reminds us that youngchildren need to run and play. She advises parents onthe need for pre-school children to have many oppor-tunities to be playful and active, particularly with theirpeers, if children are to avoid developing ADHD.

Parent training programmes have had some success.The aim is not to cure ADHD but to help parents andschools cope and work with the disorder. Early inter-vention, guidance and support help reduce symptomsand the risk of future behavioural problems (Taylor &Overmeyer 1999). Training can also support parentsto become more attuned and responsive as they try tohelp their children learn to regulate their own arousal(e.g. Olfson et al. 2003; Finzi-Dottan et al. 2006).Courses typically involve between six and 12 sessions.The nature of ADHD is explained. With the under-standing gained about the condition, more appropri-ate disciplinary techniques are taught. Parents areencouraged to recognize and praise compliant behav-iour. As a result of the programme, improvements inboth parent and child functioning have beenobserved, including decreases in parental stress andincreases in child self-esteem (e.g. Anastopoulos et al.1993).

Multimodal interventions

Multimodal interventions combine a range of treat-ments and supports. They might include stimulantmedication, study skills training, social skills training,parent skills training, group therapy and educationalprogrammes. Although promising, there is yet insuffi-

cient evidence to say whether or not these multimodalinterventions are effective. However, some multimo-dal studies have suggested that these combinedapproaches can maintain their effectiveness even witha 20% reduction in the use of medication comparedwith medication used on its own (Pelham 1999). Forexample, dosReis et al. (2004) describe, compare andevaluate a multimodal treatment intervention foryouth in three Medicaid groups – children who aredisabled, children in foster care and children in low-income families – noting the differences in treatmentsdelivered to each group.

More specifically, from a social work point of view,Pentecost & Wood (2002) recommend that socialworkers liaise more with their mental-health, psychi-atric and disability team colleagues.They also suggestthat social workers make more use of ADHD supportgroups and organizations, which can be a great sourceof information and potential support for parentswhose children have a diagnosis of ADHD.

Summary of treatments and interventions

Stepping back from this review of evidence-based andclinically based treatments, it seems that stimulantmedication does help children increase attention anddecrease their symptoms of hyperactivity and impul-siveness, at least over the short term. Parents andteachers feel less stressed when their children are lesshyperactive and impulsive, and, as a result, the chil-dren tend to respond more positively to advice andguidance. However, a clear role for environmental andpsychosocially based interventions is emerging, par-ticularly when ADHD is associated with concernsabout child abuse, neglect and trauma. Evidence-based research suggests these interventions should becombined with stimulant medication. There is lessrobust evidence to support the use of stimulants forimprovements in academic performance and prosocialbehaviours with peers and others.

CONCLUSION

Current thinking and research evidence suggest thatmental illness has its origins in the interactionbetween biology and early life experience. The neu-rodevelopmental processes that go awry in early devel-opment and that increase the risks of mental-healthproblems are governed by both genetic and environ-mental factors, which is to say that gene expression isinfluenced by the quality of the environment,including the social and relationship environment,



particularly in the early years. This understandingexplains some of the success of the various drug thera-pies, but it also outlines a role for a range of psycho-social treatments, many of which could be carried outby social workers, particularly those who are membersof multidisciplinary child and adolescent mental-health teams.

Behaviourally based interventions combined withmedication have received the most support fromevidence-based research, but there are promisingprospects for psychosocial interventions that aim tosupport, guide and educate children, their parents,families and schools. Given the nature of the earlyneurodevelopmental models underpinning currentthinking about ADHD, CD, attachment disturbancesand PTSD, early supportive and preventative inter-ventions, many provided and managed by child andfamily social workers, have a clear role to play. This isparticularly true in the case of abuse, neglect andtrauma cases where there is the risk of ADHD and CDcomorbidity. The environmental and relationshipchanges that such supports and guidances canpromote in parent-child interactions have the capacityto affect brain organization and maturation in popu-lations of children otherwise at-risk of ADHD andother behavioural problems.

Because ‘most mental illnesses have their origins inchildhood’, March (2009) writes, ‘it follows that theprevention of mental illness will necessitate early iden-tification and treatment of mentally ill youth as well asearly life prevention-intervention strategies’ (p. 174).In his discussion of the long-term future of psycho-therapy for mentally ill children and adolescents,March (2009) sees a range of psychosocial interven-tions, particularly those pitched at young children andtheir parents, combining with increasingly better tar-geted drug-based treatments. Whether or not childand family social work gets swept up in March’s visionof a new, unitary discipline based on the fast-movingneurodevelopmental sciences is less certain, but aclear role is seen for social workers, particularly thosewho embrace an evidence-based approach to practice(McNeil 2006).

The unexpected support for psychosocial-basedinterventions emerging out of developments in genet-ics and the neurosciences is relevant to child andfamily social workers. The realization that the waygenes express themselves depends on the quality andcharacter of the environment, particularly the socialand caregiving environment in the case of children’sneurodevelopment, means that those professionswhose business is to improve and bring about changes

in relationships, parenting, family life, social interac-tion, community resources and material well-beinghave a strong part to play in promoting mental health.Perhaps the strongest message to emerge out of recentreviews is the value of promoting early, psychosociallybased interventions by health and social care workersin the lives of at-risk populations of young children.

To repeat, genes are not destiny. ‘Genes’, writesNoble (2006), ‘are merely a data-base and cannotdo anything without other systems interpretingthem . . . the environment affects the way genes work’(p. 5). By promoting healthy psychosocial environ-ments in the early years, social workers can help chil-dren who are at risk of ADHD, particularly when thedisorder is associated with abuse and neglect, findmore optimal pathways as they begin life’s journey.

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