100174576 Describe the key features, terms and concepts of the Developmental approach to Psychopathology and discuss how the approach can aid the understanding of Attention-Deficit Hyperactivity Disorder
Developmental Psychopathology (DP) is an integrative, multidisciplinary approach focusing on individuals’ adaptive and maladaptive patterns of behaviour across the lifespan, with respect to normal developmental markers at given developmental periods. Sroufe and Rutter (1984), defined DP is as the study of the origins and course of behavioural maladaptation, whatever the age of onset, causes and transformations, however complex the course of developmental pattern. Claiming that DP is concerned with child pathology, enhanced by the study of nondisordered behaviour and also interested in the aetiology of disordered behaviour that becomes clinically recognisable only in adulthood. The ‘DP’ perspective is characterised by a synthesis of a number of aetiological models, each differing in their emphasis on causal mechanisms and with distinct ideas about the risk/vulnerability; maintenance; resilience/protective and continuity/discontinuity factors implicated in the pathways to pathology (Mash & Dozois, 2003). Rendering the task of diagnosis and treatment, particularly affine to a dimensional construct of dynamic organisms in multiple contexts and time-points (i.e., children), with varying stressors acting upon them from a myriad of sources (environment & biology), all of which need to be operationalised, measured and taken into account during assessment and implementation of intervening treatment programmes Santostefano (1978) introduces two propositions defining the Developmental Perspective: (1) the meaning of behaviour can only be determined within the total psychological context (‘Holism’); (2) individuals are not mere passive recipients of environmental input: they selectively perceive, respond to and create their experiences through the lens of the past (‘Directedness’) The problem of ‘continuity and change’ is of central value to DP. It has import for the difficult task of classifying disordered behaviour, which is complicated by the dynamic nature of both the developmental trajectory to pathology, and the continually changing nature of the child. Hence, a particular pattern of adaptation at one time could forecast possible vulnerabilities in the face of a particular set of environmental challenges; this predictive possibility impacts strongly on the validity of the DP approach as a whole. Garmezy et al., (1984) established ‘competence’ and ‘vulnerability’ as key concepts within the DP approach. Investigating protective characteristics, attitudes, skills and persuasions that encouraged coping and how they change over time and across contexts is an area that DP stands alone in its core emphasis. Mash & Dozois (2003), reviewed a decade of research into ‘risk factors’ and listed: insecure attachment; difficult behaviour; socio-cognitive deficits; emotion dysregulation; neuropsychobiological dysfunction; maladaptive parenting; maternal depression; marital discord and low SES were among them. Risk is clearly not a unitary issue, and this explains why DP research tends not to grant aetiological status to single causal agents. Luthar, (2000), describes ‘resilience’ as a dynamic process of positive adaptation within the context of significant adversity, making it very sensitive to environmental and homeostatic change. Werner (1995) lists easy temperament, good nature, early coping
strategies combining autonomy and interdependence, high intelligence, effective communication and positive self-image as protective factors for most children. ‘Adaptational Failure’, from a DP perspective, equates to deviation away from ageappropriate norms of behaviour. It could be caused by interference, failure to master salient developmental tasks, functions or regulatory mechanisms (Loeber, et al., 1991). These failures are understood, differentially within Biological (genetic mutations/neuroanatomical dysfunction), Psychodynamic (intrapsychic conflicts, defences, attachment models, internal representations of self and other), Behavioural (reinforcement), Social Learning, Cognitive (deficient or distorted cognitive structures and processes), Affective (emotional dysregulation) and Family Systems (intra and intergenerational systems, structural/functional factors of family) models: the integration of which involves going beyond unitary theories of causality and pulls together a more holistic picture of the individual. Contextual issues such as Gender, Ethnicity and Culture are all given centrality within a DP system and will be considered alongside the other tenets of the DP approach in the case of ADHD in the penultimate part of this essay. Paradoxically, the factors and pathways to disorder, which are either exaggerated or mediated by the environmental context, can be equifinal and varied, yet lead to a similar expression of PP, or they may be multifinal and appear synonymous at onset but result in different forms of PP. Loeber (1991) think that systematic delineation of ‘developmental trajectories’, ‘comorbidity’ and sensitivity to ‘diverse outcomes’ and aetiologies, is the only way to capture the changing expression of a disorder over time. This fusion of detail defines the Developmental approach to Child Psychopathology (CP). DP deals primarily in dimensional constructs of individuals’ personalities, yet the medical model of mental illness, dictates that there must be some threshold, above which an individual is considered to ‘have’ a certain disorder and below which they do not. DSM is a categorical system, but provides a rich descriptive base from which further exploration into the way PP manifests in children, and draws a focus to the potential discontinuities between early problems and later disorder. Dimensional systems like the Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood (0-3/National Centre for Clinical Infant Programs, 1994) assume that a number of independent dimensions or traits of behaviour exist in all children to a greater of lesser extent. Garber (1984), refers to the loose application of diagnostic criteria as opposed to completely rejecting traditional nosology because of its emphasis on static traits, as children’s personality structures, symptoms and traits are all still developing and changeable. Garber (1984) also proposes: ‘Intensity’ (excessive magnitude of behaviour at either end of the continuum); ‘Frequency’ (rate of emission of certain behaviours as criterion of severity) and ‘Duration’ (deviating from the normal course and duration of behavioural expression in childhood), with the number and combination of symptoms, as aids to determining the degree of deviation and thus to diagnosis. Finally, Comorbidity is understood as the existence of two or more disorders, the co-occurrence of which is significantly more likely than chance (Mash & Dozois 2003), suggesting that certain developmental pathways may cross to produce a unique combination of different
disorders that have been found to co-exist in particular cases more than others. DP is capable of asking -- at what point in time and for what reasons do developmental pathways diverge from the normal course? And what explains the fact that not all ‘atrisk’ young people develop PP? The answers require accounting for normal development, vulnerability and risk as well as the factors leading to extinction or persistence (continuity versus discontinuity). In the case of Attention-Deficit Hyperactivity Disorder, the more studied concepts of developmental approach to CP will be used as an example of their facility in helping to understand such an historically contentious disorder as ADHD.
Over six million children were diagnosed with ADHD by the end of the 1990’s, in America alone, with a large proportion of them being treated with a Schedule II central nervous system stimulants, classified by the Drug Enforcement Agency (DEA) as the most dangerous and addictive drugs that can be prescribed legally. From 1990 to 1997 annual production in Ritalin increased by 700%. 500,000 2-5 yr olds are now being treated with powerful drugs for ADHD even though nobody has any idea of the effects these drugs have on children so young. (Baughman & Hovey, 2006) When the bigger picture of this disorder is clear for all to see, the role of the DP approach can be appreciated. With a multiaetiological base, ADHD can be understood and interrupted in numerous ways, all of which have the potential to do less harm than psychiatric prescription stimulant medications, which as yet have produced no reliable evidence that drug treatment extinguishes the causal factors of the behavioural disorder. Genetic studies show that environmental factors such as parent-child relationship and interpersonal context account for only 10-15% of variance in ADHD, suggesting that these factors are more important in the severity and persistence of the disorder. Heredity has been shown to play a major role with twin studies finding convincing .80 average heritability for symptoms (Faraone & Biederman, 1998). Neurological accounts of ADHD implicate brain impairment and historically this model has been the main impetus for stimulant drug treatment, despite constant revisions to the adequacy of unfounded ‘minimal brain damage’ hypotheses of dysfunction (Mash & Barkley, 1996) Wenar & Kerig (2000), confirm that the medical model of ADHD is not satisfactory because of the organic context (general hypothesis that certain expressions of PP result from organic dysfunctions and can be classified in the same way as physical diseases). They state the strong potential of psychogenic aetiology, in that ADHD has a significant genetic predisposition and transmission component, but prefer to view the developmental disorder more holistically. Behavioural models also seem to account well for the behavioural excess of higher frequency, maladaptive, intense and continuous manifestations of ADHD. The beauty of the DP approach is that it continues to consider the potential of the environment, as with Bandura’s Observational Learning theory from the mid 1960s which would argue for reciprocal determinism, and the active interaction with the social context and ‘significant others’ as causal factors in the expression of ADHD. Eriksson modelled the psychosocial development of the child, corresponding to
the psychosexual stages of Freud’s psychodynamic theory, and from his Ego psychological viewpoint, the developmental trajectory of ADHD would be assumed to spring forth from a particular crisis/resolution during childhood, lending support to social causal agent hypotheses. Attachment theory and Object Relations emerging from the earlier work of psychoanalysis, emphasise the quality of the child’s relationship with primary caregivers, again, suggesting a social element in the expression of the ‘inappropriate’ externalising behaviours typically seen in cases of ADHD. Finally, the Family Systemic Model centralises the role of the entire family system, as a dynamic whole and provides a potential realm of origin for CP. With increasing divergence and convergence between these theories, a unified model emerges, as integrative DP. Mash and Wolfe (2005) claim that ADHD describes children displaying persistent ageinappropriate symptoms of inattention, hyperactivity and impulsivity sufficiently to cause impairment in major life activities, admitting that it is a blanket term referring to differing patterns and combinations of behaviour that could have distinct aetiologies. Douglas (1972) believes that sustained attention is the primary deficit area in ADHD. Teicher et al (1996) found that ADHD children displayed more motor-activity when they slept than a non-ADHD cohort. Solanto et al (2001) think that children with ADHD may experience difficulty in resisting temptation or delaying gratification. ADHD samples consistently show deficits in one or more executive functions (Pennington & Ozonoff, 1996). 80% of children with ADHD qualify for Learning Disability (LD) by late childhood and Rappaport et al., (1999) explain that different pathways may underlie the comorbidity of ADHD with LD: the child’s cognitive and intellectual deficits may directly lead to learning problems or ADHD may predispose the child to conduct problems in school that may result in poor academic performance. The literature suggests ADHD comorbidity with Developmental Co-ordination Disorder (DCD) and Tic Disorders – Gillberg 2003b; Conduct Disorder (CD) and Oppositional Defiant Disorders (ODD) – Kadesjo & Gillberg, 2001; Depression – Spencer et al., (2000), at alarming rates ranging from 20-80% across comorbidities. Prevalence is said to be between 3-5% (Briggs-Gowan et al 2000) with a higher incidence in males (Breton et al 1999). Even in adolescence, when overall rates of ADHD drop for males and females, boys outnumber girls 3:1 in nonclinical samples and 6:1 in clinical samples (Lahey et al 1999). One explanation of this androcentrism may be the socialisation bias of boys being treated more roughly and thus displaying more externalising behaviours than girls. When girls did display more oppositional symptoms, they were referred at an earlier age than boys, suggesting lower tolerance and greater concern (Silverthorne et al, 1996). ADHD relates to risk for early initiation of substance abuse (Molina & Pelham, 2003). Environmental adversity was found significantly amongst ADHD compared with proband controls (Biederman et al, 1995), stressing the importance of familyenvironmental variables as risk factors for children with ADHD. ADHD is only identifiable after the age of 3 years with difficult temperament, extreme and unpredictable activity, irritability, under/over stimulation, erratic sleep and feeding difficulties. During preschool, impulsive activity, rapid change of activity, preference for
immediate gratification and strong reactions to routine events are linked with the expression of ADHD, which continues into adolescence for approximately 50% of those children diagnosed (Campbell 2002). Inattention emerges around the age of 5-7, becoming especially evident when the child starts school (Hart et al 1996). The age of onset, developmental course and outcomes of ADHD, obviously differ, depending on the sample, measures, co-morbidity as well as the sub-type of ADHD (Hyperactive/Impulsive/Inattentive) Jacobvitz and Sroufe (1987) found overstimulated mother-child interactions early in life as primary in ADHD within impoverished inner-city families, where a pattern of intrusive caregiving predicted ADHD several years later. Most ADHD is likely to constitute a complex synergy of intraindividual, familial and broader systems factors than a purely environmental or genetic causal route (Hinshaw, 1994). With substantially different pathways, leading to similar patterns of behaviour known as ADHD, the concept of ‘equifinality’ would seem to best describe the disorder. However, robust predictors of ADHD have thus far, evaded detection and it could be that the school failure feature of the disorder is more reflective of the rigidity of the education system than the child’s inability to learn. It could be that the temperament of the child and subsequent parent-child dynamic leads to low-self-esteem, parents don’t have time to read to the child at night and rarely have much attention for the child altogether, leading to a negativism within the school and home environment, being picked up on later by teachers as an ‘unwillingness to learn’ and therefore achieving the status of ADHD, when obvious psychosocial interventions would solve the problems of inattention and hyperactivity. On the other hand, neurological deficits may, in some cases, play a more significant determining role, and mild stimulant medications may be the most effective treatment and may produce more benefits to the child’s learning, but not necessarily to curing the ‘problem’. Poverty presents a particularly salient vulnerability factor in ADHD as the prevalence and concentration of low-income neighbours is known to increase the incidence of externalising behaviour problems, commonly seen in cases of ADHD (Duncan et al., 1994). Wilson (1991) posits that it is the structural changes in postindustrial society that has increased the number of poor and jobless people and thus affected the behaviour of residents in impoverished neighbourhoods; perhaps this explains the gradual but steady and recently phenomenal increase in cases of ADHD. The effects of poverty are cumulative, with persistent poverty having a 60-80% larger influence than transient poverty on problem behaviour at the age of 5 (Haveman et al., 1991). SES intuitively is a powerful determinant of cognitive, emotional, intellectual and behavioural development of children. Economic disadvantage has tangible effects on children via the provision of educational resources and through the negative effects the class struggle has on their parents; it is little wonder then, that ADHD is found more often amongst the lower strata of the class society. Each society, has its own tolerance practices around diagnosing children with PP, but on the whole, ADHD is a rare occurrence, affecting anywhere between 2-7% of children.
Risk and protective factors are thought to be similar across the board for most disordered behaviour (positive caregiver relations, higher SES, good academic performance) with few studies demonstrating unique factors for ADHD. Santostefano (1978) recommends we view the child wholly and within its total psychological, sociobiological context, to appreciate that developmental trajectories can begin early under the principle of directedness, whereby children do a certain amount of choosing responding and reacting to the stimuli around them. There seems to be considerable discontinuity of ADHD between preschool and school ages suggesting it is particularly sensitive to the school environment and imposing doubts as to the organic nature of the disorder, but more alarmingly, treatment methods have been focussed on stimulant therapy which has not yet been shown to target the causal factors of the disorder, merely making children more adjusted in school whilst being dependent on highly addictive and potentially harmful in the long-term, stimulants which are seen to break the cycle of deprivation that ensues from the low academic performance associated with ADHD. ADHD has a unique relationship with SES. (Miech et al, 1999) and Achenbach et al., (1991) also found a significant tendency for lower SES children to score higher on many problem items, a result that was more significant than ethnicity and home location, suggesting than class may play a bigger role than ethnicity in ADHD. Is it possible that ADHD, is simply a reflection of the harsh reality of the class system and of the relative disparity of resources (time, money, attention) given to different children in different social class backgrounds? Research, to date, is inconsistent, but shows a disturbing trend in finding higher prevalence of ADHD amongst the more disadvantaged social groups. A failure to adapt to novel or changing environmental demands is a core feature of ADHD (Cools & Robbins, 2004). Rutter (1980) explains, “…the process of development constitutes the crucial link between genetic determinants and environmental variables…sociology and individual psychology...physiogenic and psychogenic causes…” (pp 110). It seems clear that ADHD a complex, multi-determined, perhaps socially convenient label, that is most effectively viewed from a DP standpoint and from this position to conclude that a disease or medical syndrome must have a physical or chemical abnormality or it is not a disease (or a medical syndrome or anything physical or biologic). ADHD has no robust measurable physical or chemical abnormalities, making it a theory in search of validation (Baughman & Hovey 2006). The best methods for treatment for ADHD must involve first understanding where it comes from within the macroparadigm of DP and then interrupting detrimental processes leading towards ageinappropriate and pathological relationships to the total environment. Thus far, youngsters have been disproportionately labelled and drugged, for what seems to be a failure of the education system, than for failures in their ability to learn and adjust to the relatively oppressive nature of mandatory schooling, in understaffed and inattentive institutions that expect children to behave more like adults, despite their biological predisposition to be more energetic and less seriously focussed.
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