About ADHD

Introduction to ADHD in children and adolescents

Diagnostic and Classificatory Systems in Use

There are two sets of diagnostic criteria in regular use currently to diagnose psychiatric and behavioural disorders in children: DSM-IV and ICD-10. ADHD is a DSM-1V diagnosis, that is, it is a diagnosis found in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders published by the American Psychiatric Association (1994). ADHD does not appear in ICD-10 - the classificatory system published by the World Health Organisation (WHO, 1992) and the preferred system used in the UK and Europe. In ICD-10 the nearest equivalent diagnosis to ADHD is that of hyperkinetic disorder (HKD).

Both classifications utilise lists of behaviours to consider in the process of diagnosing hyperactive conditions. The list of behaviours is essentially the same in both, however, the DSM-IV lists of items, allow for the existence of sub-types of ADHD depending on the balance of symptoms of inattention and hyperactivity-impulsiveness. The majority of children receiving the diagnosis of ADHD in the UK are both inattentive and hyperactive/impulsive (i.e. ADHD-combined-type). This is roughly equivalent to the ICD-10 diagnosis of hyperkinetic disorder (HKD). It is these children with a combined picture of inattention, over-activity and impulsivity which the term ADHD refers to from here on in this site, and not those with the less severe subtypes of ADHD as defined in DSM-IV.

What is Attention Deficit Hyperactivity Disorder (ADHD)?

The three core areas of impairment seen in ADHD are generally considered to be:

Necessary criteria for a diagnosis of ADHD:

Severity

The National Institute for Health and Clinical Excellence guidelines on diagnosis and management of ADHD in children, young people and adults (2008, p.5/6 www.nice.org.uk/CG072) define severity of ADHD in children and young people as follows:

Key information about ADHD

Epidemiology

Potential causes of ADHD

Genetic factors

The underlying causes of ADHD are not fully understood although it is likely that both psychosocial and biological factors play a part (Cantwell, 1996). Whilst there is evidence to support the role of genetic factors in ADHD (heritability estimates range from between 0.7 to 0.9 of the phenotypic variance in twins), the mode of inheritance is still unclear and is likely to be moderated by factors such as environment and gender. Molecular genetic studies suggest that the dopamine DRD-4 receptor gene and the dopamine transporter gene (DAT) may be involved (Thapar et al. 1999; Curran and Taylor 2000); Martin, McDougall and Hay, 2008).

Environmental factors

Environmental factors which also seem to have a causative role in ADHD include adverse events during pregnancy and birth e.g. drug exposure in utero; brain infections, e.g. encephalitis; neurotoxin exposure e.g. lead poisoning; and some forms of psychosocial adversity e.g. where there is history of child abuse or neglect, or multiple foster placements (American Psychiatric Association, 1994; Haddad and Garralda, 1992). There is little evidence however that ADHD can arise purely out of social or environmental factors such as poverty, family chaos, diet or poor parent management (Barkley, 1990).

It is thought that the genetic and/or environmental factors which lead to ADHD do so by altering the brain structures and functions associated with cognitive executive functioning. For example: deficits in dopamine-decarboxylase in the anterior frontal cortex, leading to reduced dopamine availability and diminished focusing and attention; more symmetrical brains; smaller-sized brains in the area of the prefrontal cortex (caudate, globus pallidus).

Long term outcomes of ADHD

When ADHD is recognised and managed at an early stage, many of the educational and psychosocial difficulties can be addressed (Cantwell, 1996). Untreated however, the prognosis is poor with anti-social behaviour, underachievement in school, social and peer problems, substance misuse, criminal activity and later psychiatric diagnoses commonly occurring, particularly where there is coexistent conduct disorder (Swanson et al. 1998; Cantwell, 1996).

To date, there are no long-term studies looking at the efficacy (and safety) of stimulants or psychosocial treatments. In addition, no information is available on long-term educational, psychosocial or occupational outcomes of individual's who have received treatment (National Institutes of Health, 2000). Clinical experience however points to the majority of children requiring medication to be continued for many years (Overmeyer and Taylor, 1999; Greenhill et al. 1999).