Attention-deficit/hyperactivity disorder (ADHD), a state of serious impairments in both learning ability and social functioning, is one of many labels for one of the most prevalent conditions in child psychiatry, and, undoubtedly, the most controversial, which partly persists into adulthood.
ADHD is conservatively estimated to occur in 3,0–7,5% of school-age children (Goldman et al., 1998), but more permissive criteria yield estimates of up to 17% (Barbaresi et al., 2002). Up to 20% of boys in some school systems receive psychostimulants for the treatment of ADHD (LeFever et al., 1999). Partly in response to legitimate concern about an apparent rapid increase in its prevalence in the 1990s, investigators have unsuccessfully attempted to formulate a single theory of ADHD, that would facilitate the development of an objective diagnosis test.
Aetiological factors of ADHD include not only genetic variations or mutations, but also environmental factors (brain injury and stroke, severe early deprivation, family psychosocial adversity and maternal smoking during pregnancy) and, most importantly and most difficult to identify, interactions between genes, and between genes and the environment. These factors are the initial causes of the multiple conditions that manifest symptomatically as ADHD, and their eventual identification should be accorded high priority.
The current criteria for the diagnosis of ADHD, published by the American Psychiatric Association in the 1994 Diagnostic and Statistical Manual of Mental Disorders (fourth edition; DSM-IV), are the most widely used and form our starting point. Other proposed criteria include those for the International Statistical Classification of Diseases and Related Health Problems (tenth revision; ICD-10) diagnosis of hyperkinetic disorder, which represents a more severe and ‘refined' subset of DSM-IV ADHD, but which does not recognize the DSM-IV predominantly inattentive subtype (Castellanos & Tannock, 2002).
Terms applied to ADHD include:
- attention-deficit disorder (ADD)
- hyperactivity
- hyperkinesis
- hyperkinetic syndrome
- minimal brain dysfunction and
- minimal brain damage.
ADHD & Working Memory
Research on ADHD has, mostly, been descriptive and atheoretical. The imperative to discover the genetic and environmental risk factors for ADHD is motivating the search for quantifiable intermediate constructs, termed endophenotypes. It could be concluded that such endophenotypes should be solidly grounded in the neurosciences.
Three such endophenotypes a specific abnormality in reward-related circuitry; deficits in temporal processing that result in high intrasubject intertrial variability; and deficits in working memory Are most amenable to integrative collaborative approaches that aim to uncover the causes of ADHD.
Working memory (WM) capacity is the ability to retain and manipulate information during a short period of time. This ability underlies complex reasoning and has generally been regarded as a fixed trait of the individual. Children with attention deficit hyperactivity disorder (ADHD) represent one group of subjects with a WM deficit, attributed to an impairment of the frontal lobe.
A previous preliminary study indicated that training of WM tasks can enhance executive functioning including working memory, response inhibition, and reasoning in children with ADHD (Klingberg et al., 2002b).
A randomized, controlled, double-blind trial to investigate the effect of improving working memory by computerized, systematic practice of WM tasks including 53 children with ADHD revealed a significant treatment effect both at intervention and follow-up (Klingberg et al., 2005).