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Genetic and environmental factors Over the past decades, concepts of ADHD have evolved from narrow behavioural symptom clusters to broader notions of deficient self-regulation; and from a focus on lower brain centres to theories that involve frontal and prefrontal regulation (Hinshaw 1994; Hynd, Horn, Voller et al 1991). Conceptions of underlying mechanisms must be able to account for a wide range of problems including those of academic, social and cognitive dimensions. For example, DSM-IV field trials separated dimensions of inattentive/restless from impulsive/hyperactive behaviours. It is possible that varying subgroups of ADHD (and co-morbid conditions) may relate to various vulnerability factors, which may push the child past the threshold of disorder. Further large-scale genetic studies are needed to determine genetic versus environmental influences on ADHD, Oppositional Defiant Disorder and Conduct Disorder as well as relationships to language and learning disabilities (Levy, Hay, McLaughlin et al 1996). Neurophysiology Biological brain differences have been reported in children and adults with learning/language, behaviour and attention difficulties including ADHD and slow learning disability (SLD). Differences have been described in anatomy, electrical activity, psychological functions, brain metabolism and blood flow and these may show Înormalisationâ with medical treatment (Matochik, Liebenauer, King et al 1994). These findings largely fall within the spectrum of normal. Genetic factors There is evidence for genetic factors as shown by higher concordance in monozygotic than dizygotic twins for increased ADHD (Levy, Hay, McStephen et al 1997; Levy, Hay, McLaughlin et al 1996; Gilles, Gilger, Pennington et al 1992; Goodman and Stevenson 1989). Recent reports indicate possible mutations in dopamine transporter genes (Cook, Stein, Krakowski et al 1995) or receptor genes (D4 receptor gene ÷ Ebstein, Novick, Umansky et al 1996) which may predispose to ADHD. Congenital factors Retrospective accounts suggest numerous congenital factors may be related to ADHD. However, there is no compelling evidence for specificity of perinatal (Levy, Hay, McLaughlin et al 1996) or congenital factors (Cantwell and Hanna 1989). Maternal substance abuse during pregnancy may be associated with ADHD (Steinhausen, Willms and Spohr 1993). Substances such as cocaine and nicotine (Nichols and Chen 1981) may also induce ADHD-related symptoms. Diet and environmental agents Available evidence does not strongly support the role of food additives in ADHD (Kavale and Forness 1983; Conners 1980; Levy, Dumbrell, Hobbes et al 1978). Recent evidence from a population study has failed to confirm a relationship between allergy and ADHD (McGee, Stanton and Sears 1993). There is, however, evidence that exposure to lead, even at subclinical toxicity levels, is associated with small but significant decrements in intellectual performance and with distractible impulsive behaviour (Fergusson, Horwood, Lynskey 1997 and 1993a; Needleman, Schell, Bellinger et al 1990). Familial factors Familial factors are very difficult to separate from genetic factors, but the concept of Îgoodness of fitâ between parent and child temperament may be important (Thomas and Chess 1977). The interaction of family, genetic and psychosocial factors are discussed by Biederman, Faraone, Keenan et al (1990) and by Biederman, Millberger and Faraone et al (1995). The interaction of child and family factors influencing referral of children with hyperactivity is discussed by Woodward, Dowdney and Taylor (1997).
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