How is evolving from new knowledge the concept of disorder attention deficit hyperactivity disorder ( ADHD) ?

Attention deficit hyperactivity disorder (ADHD) is a complex and still insufficiently known neurobiological disorder.

Although the first investigations date back to the first half of the twentieth century, it is from 1962 when in the scientific literature identify these patients with the name of minimal brain dysfunction (Clemens SD, Peters JE, 1962), concept that is modified from of the year 1965 (classification CIE 9) and 1968 (classification DSM II) with the name of hyperkinetic disorder, introducing the current concept of attention deficit hyperactivity disorder in the DSM III classification from the 80s. We currently use the DSM 5 classification.

From the etiological point of view, it is estimated that 50% to 82% of the variance of this disorder is of genetic origin (Goodman R, Stevenson J, 1989), Mardomingo MJ, 2002), (Barkley RA, 2005). The most important environmental factors are parents' education, family interaction systems and socioeconomic status.

The symptoms of ADHD are the final expression of neurobiological alterations that are born mainly in the prefrontal cortex and frontostriatal circuits. Currently, and based on this knowledge, a new explanatory model of ADHD has been developed, which attempts to explain its cognitive bases, known as the dual model of cognitive and motivational executive functions, also known as the model of aversion to delay (Sonuga-Barker EJ et al 2005). The aversion to delay maintains that children and adolescents with ADHD prefer to obtain immediate gratification, even if small, above a gratification of greater magnitude and far-reaching, but delayed. Within this model, impulsivity would have the objective of reducing the delay time to obtain gratification when the child with ADHD controls their environment.

When you have no control over the environment, choose to disconnect and let time go by , that is, try to ignore the delay. This model is based on brain cerebral reward circuits, modulated by catecholamines that connect frontal regions (anterior cingulate and orbitofrontal cortex) with the nucleus accumbens.. The amygdala is equally involved in this system, possibly playing a role in defining the motivational meaning of the incentives. Likewise, dopamine has a key role as a neuromodulator of reward.

The cognitive executive functions (dorsal frontal circuit) are the cognitive processes that deal with the control of the behavior directed to objectives through the planning and execution of the tasks and the motivational executive functions (ventral frontro-truss circuit) are related to the processes of impulse and reward in the performance of actions.

On the basis of what has been commented on and fundamentally affecting the prefrontal cortex and the dorsal and ventral frontal circutrostriates, the regulation of attention, work memory (among the various cognitive executive functions) and inhibitory control are conditioned.

Thus there are neuroanatomical, neurophysiological, neurobiochemical and genetic alterations, although partially known, that explain the etiopathogenesis of this disorder. The current publications are immense: (Castellanos FX et al 2002), (Krainer AL, Castellanos FX 2006), (Castellanos FX et al 2008), (Varela EM et al 2007), (Shaw P. et al 2007), (Shaw P. Te 2009), (Fransson P, Marrelec G 2008), (Rutter M 2007), (Faraone SV and 2001), (Li D et al 2006), (Faraone SV 2005), (Purper-Ouakil D et al 2005) , (Cheuk DK, Wong V 2006).