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:
- Hyperactivity
- Impulsivity
- Attention problems
Necessary criteria for a diagnosis of ADHD:
- ADHD is characterised by a triad of behaviours which include over-activity, inattention and impulsivity.
- For a diagnosis of ADHD to be applied, these behaviours should be present to an extent which is unwarranted for the developmental age of the individual concerned and which significantly impairs their social, educational and emotional well-being.
- The behaviours will have lasted for more than 6 months and will usually have been present before the age of 7 years.
- They will also be evident in more than one setting, e.g. at home and at school i.e. the behaviours are pervasive.
Key information about ADHD
Epidemiology
- The prevalence rate of ADHD is usually estimated at 3%-5% in school -aged children (American Psychiatric Association, 1994) although recent systematic reviews report ADHD prevalence estimates as wide as 2-18% (Rowland et al. 2002).
- Around 1% of school-aged children have severe combined type ADHD (DSM-1V)/ hyperkinetic disorder (HKD - ICD-10); equivalent to approximately 73,000 children aged 6-16 in England and Wales.
- Taking all forms of ADHD into account, perhaps 5% of school-aged children are affected - or 366,000 in England and Wales. Significant numbers remain undiagnosed.
- The ratio of boys to girls is 4:1, with no social, economic or ethnic group bias in the general child population.
- One third of affected individuals have at least one parent who suffers from similar symptoms.
- ADHD is associated with: low birth weight (<1500g); environmental toxins; tobacco, alcohol and cocaine abuse during pregnancy (Milberger et al, 1996).
- Although in the past it was thought that ADHD did not continue beyond adolescence, research has shown that a childhood diagnosis of ADHD has long term implications. More than 70% of those diagnosed with ADHD as children continue to fulfill diagnostic criteria in adolescence, and up to 65% of adolescents with ADHD still present with the disorder as adults (Jadad et al. 1999).
- The number of prescriptions written for Methylphenidate in the UK increased from ~about 6000 in 1994 to ~ 345,000 children in 2003.
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).
- Approximately one-half of parents who themselves have ADHD have a child with the disorder.
- 10-35% of children with ADHD have a first-degree relative with ADHD.
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).
