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Werry, Reeves & Elkind (1987) investigated whether or not particular risk factors discriminated between different disorders. They found that whilst most factors distinguished between children and adolescents with and without disorder, there were few significant differences between the disorders themselves. They did identify some small differences according to sex, whereby boys were more likely to report externalising behaviours than girls. In support of this, other studies have found adolescent girls to report more depressive symptomatology than boys (Angold & Worthman, 1993; Nolen- Hoeksma & Girgus, 1994; Hankin et al., 1998; Ko vacs, 2001). It is likely, therefore, that the risk factors considered here are not specific to any one disorder and will overlap. Also, it is likely that the accumulation of risk factors is influential and deleterious, rather than the nature of the risk as a single entity (Rutter et al., 1970).

Attention Deficit Hyperactivity Disorder/Hyperkinetic Disorder (ADHD/HD)

The heterogeneity of ADHD/HD is well documented, as are the diverse array of different risk factors which may result in different manifestations of the disorder (eg inattentive or impulsive/hyperactive behaviour, aggression, impaired educational performance), as well as variability in the nature of its comorbid relationships with other disorders. A number of predisposing variables are consistently reported, including neurobiological, genetic and environmental risk factors that are more likely to co-occur than arise independently. For example, neurobiological factors may impact on cognitive development and account for some of the associations with learning difficulties that are discussed in Section 2.5. (Although, whether or not low academic attainment is a risk factor or a consequence of this disorder

remains uncertain.) However, as a consequence of the additional interplay with environmental factors, the ensuing behaviour of the young person may sustain and/or lead to the exacerbation of these difficulties. Evidence in support of this type of scenario comes from studies showing that stimulant medication typically prescribed for these children does not ameliorate the poor peer relationships or impaired educational performance that are commonly associated with this disorder (eg Barkley et al., 1990a). Thus, although these neural mechanisms play a significant role in the onset and development of ADHD, they do not account for all its manifestations and associated impaired outcomes.

Further support for the interplay between neurobiological and environmental factors comes from Szatmari et al (1989), who found a higher prevalence of ADHD in urban rather than rural communities. Also, children and adolescents with hyperactivity have been reported to show a wide range of adverse environmental circumstances from family dysfunction (including divorce and/or separation), low socio-economic status, negative parenting, parental mental health and psychosocial factors (such as overcrowding and deprivation) (Shachar, 1991). Although these findings are remarkably consistent between studies overall, some studies report that the lower socio-economic status (SES) identified in a large percentage of children with ADHD may be attributable to the high levels of comorbid conduct disorder and aggression in these populations (eg Barkley, 1996).

It has also been suggested that some factors, such as family dysfunction, may not only predispose young people to hyperactive behaviours, but serve to maintain the disorganised and aggressive behaviours reported during the preschool and early school years (eg Campbell, March, Pierce, Ewing et al., 1991). Other studies indicate that the relationship between ADHD and negative family relationships may be a response to the disruptive behaviours manifest by the child (Barkley, 1996). Under these conditions, the use of medication to alter the behaviour alone of the young person has been

successful in improving the attitude of the parents towards the child (Barkley, 1996).

Conduct Disorder (CD)

There are some indications that there is a genetic component to the onset of CD in the familial aggregation of early onset conduct and antisocial behaviours, although patterns of inheritance and which behaviours are inherited has proven difficult to ascertain (Earls & Mezzacappa, 2002). It is likely that these genetic factors may predispose a child towards the development of disorder, and some environmental factors act to increase or sustain that risk.

Other factors that have been associated with the onset of CD include family dysfunction, parental mental health and low socio-economic status (eg Thomas, Byrne, Of ford & Boyle, 1991). They also identified associated factors, including male gender and large sibship, as well as finding that antisocial behaviours appear to be particularly heavily influenced by family conflict, especially amongst boys. Violence at home is a strong contributor to the early development of antisocial behaviour and delinquency (Kruttschnitt & Dornfield, 1993), and children exposed to violence in the home are more likely to progress to committing more serious crimes later on. Nonviolent marital discord also has its ramifications. In a study by Emery & Kitzmann (1995), they found that whilst divorce preceded the onset of many behaviours associated with CD, it was not the actual separation but the exposure to high levels of inter-marital conflict prior to the breakdown of the marriage that provided the greatest risk to psychopathology. In particular, boys seem to be particularly vulnerable, even taking socio-economic factors (ie family income) and early levels of aggression into account (Vaden-Kiernan, Lalonga, Pearson & Kellam, 1995).

Parental mental health, in particular antisocial personality disorder, is an important concern as a risk factor for CD (Lahey et al, 1995). They found

strong correlations between antisocial personality disorder in the parent and CD in the child, both at initial presentation to the clinic and four years later. The behaviours associated with antisocial personality disorder are likely to provide an inconsistent pattern of parenting for the child, which appears to both increase the risk of disorder and serves to maintain it.

Influence of social disadvantage is strongly associated with a number of mental health problems, and there are consistent reports that low socio­ economic status is a risk factor for CD (eg Farrington & Loeber, 1998). Moreover, this relationship to deprivation may have some bearing on finding that a higher proportion of young people with conduct disorder are identified in inner cities than rural areas. For instance, Rutter, Cox, Tupling, Berger et al (1975) found the prevalence rate for this disorder to be twice as high in inner London compared to the Isle of Wight.

Depression

Risk factors for depression are likely to encompass predominantly familial and environmental factors, with only a limited number of studies investigating genetic predispositions to the development of depression. Biologically determined familial factors are strong determinants in the development of depression, suggesting a genetic component. Harrington, Fudge, Rutter, Bredenkamp et al (1993) found that relatives of children with depression were twice as likely to have a lifetime prevalence of depression themselves, than relatives of children who were not depressed. Much of the evidence surrounding genetic mechanisms, however, suggests that combined genetic and environmental factors interact in a way that increases the risk of a child developing depression (eg Silberg, Pickles, Rutter, Hewitt et al., 1999).

As such, there is strong evidence for a relationship between family risk factors and the development of depression. For example, a community based longitudinal study found a number of risk factors including family size, birth order and parental age significantly contributed to the onset of

depressive symptoms, and that girls were particularly vulnerable (Reinherz et al., 1993). Other studies have found high levels of depression In young people from families who have divorced or separated (eg Downey & Coyne, 1990), although marital conflict prior to the break-up may well explain the association, as previously mentioned.

Studies Investigating the Influence of environmental factors have been heavily weighted In favour of evidence suggesting that low socio-economic status Is likely to predispose children and adolescents to develop depression (eg Kandel & Davies, 1982; Schoenbach et al., 1982). Loss or bereavement Is also likely to lead to depression (eg Clark et al., 1996), although the precise nature of this link Is somewhat difficult to determine due to the associated outcomes. For example, as well as the loss Involved with losing someone close, additional factors are likely to contribute to grief reactions and the onset of depression. These may Include the break down of the family unit, possible upheaval In a move to another home, changes to financial circumstances and/or arrival of a step-parent each of which are likely to contribute additional risk to the development of disorder.

Tourette Syndrome (TS)

Risk factors associated with this neurodevelopmental disorder have predominantly focused on genetic vulnerabilities to the development of TS, as well as some non-genetic factors. These are reviewed In some detail In Section 2.2.4.5, and only a brief synopsis Is provided here.

Genetic risk factors focus on models of familial Inheritance for TS (eg Pauls & Leckman, 1986; Kurlan et al., 1994a; Comings, 1996; Walkup et al., 1996), although the pattern of Inheritance has yet to be determined. However, non- genetlc risk factors have examined the Influence of adverse perinatal factors to Include birth complications (Robertson, 2000) and lower birth weights In monozygotic co-twins (Leckman et al., 1987). Other evidence for Increased risk for tics and TS comes from a study by Leckman et al (1990), who found

higher rates of maternal stress and increased levels of nausea and vomiting during the first trimester of pregnancy. A number of studies have also reported that children who develop streptococcal infections are more vulnerable to the development of this disorder (eg Swedo et al., 1998), although the findings are inconclusive.

Aside from genetic or non-genetic factors, it is also suggested that psychological factors may also predispose individuals to the manifestation of tics. These range from the well documented exacerbation of tics under stressful conditions or as a direct consequence of experiencing stressful life events (eg dagger et al., 1982) including parental disharmony (Leckman et al., 1990). However, whilst these psychological factors are unlikely to constitute risk in causing the initial development of TS, they may contribute to the maintenance of this condition.

2.3.3 Summary

Clearly there are a number of risk factors associated with each of the disorders under investigation in this study, which are only briefly considered in this section. Overall, however, this vast literature has determined that few factors are able to distinguish between disorders or pinpoint single causal mechanisms, perhaps with the exception of some of the genetic and non- genetic risk factors associated with TS. Instead, disorders are likely to arise as a consequence of increased vulnerability and susceptibility from the interrelationships between a number of different risk factors. Moreover, Rutter (2000) suggested that the cumulative effect of both multiple environmental and genetic factors were likely to pose the greatest risk to the onset of psychopathology.

Also, the influence of different risk factors on mental health may begin long before the risk factor itself is identified. For example, divorce is often the culmination of longstanding parental conflict, which the child may routinely witness prior to the decision of the parents to separate (eg Emery &

Kitzmann, 1995). There is little evidence to suggest that a child will develop psychopathological problems as a direct consequence of a specific set of adverse circumstances. As such, the literature embodies evidence that there are marked individual differences in young people’s responses to circumstances, and their levels of vulnerability and resilience are dependent on various factors (Rutter, 1996). Risk factors do seem to distinguish reasonably well between those with and without psychopathology, and provide consistent background information for community based studies comparing these two groups, although the information is likely to be limited in terms of giving a true indication of causal direction.