[Cognitive models in attention deficit hyperactivity disorder].
BACKGROUND
Attention deficit hyperactivity disorder (ADHD) is a condition that is currently identified almost exclusively by the simultaneous presence of a set of symptoms that tend to coincide in a more or less homogenous manner in a large number of patients. Yet, to be able to advance in the consolidation of a model of ADHD, based on genetic, neurofunctional and cognitive features, the symptoms need to be understood as being the result of one or more nuclear deficiencies.


METHODS
This work reviews the most significant and up-to-date proposals put forward with the aim of providing a cognitive understanding of ADHD. Although the involvement of the executive functions is widely accepted today, it is not unanimously agreed that they are the only exclusive factor at play or that there is a possible interaction between the executive functions and other cognitive impairments. The study outlines the single deficit proposals, that is to say, deficient inhibitory control, regulation of the status and aversion to delay. The multiple deficit models are also discussed: the energetic cognitive model, the Sonuga-Barke model and models based on comorbidity with dyslexia and with autism.


CONCLUSIONS
Advances in genetics and in neurological functioning are offering very valuable data that will undoubtedly help to shape the cognitive model or models underlying ADHD. Lastly, a greater understanding of the effects of pharmacological agents is also needed. Apart from improving the symptoms, the pharmacological agents employed also have an effect on cognitive mechanisms. In line with this assumption, very promising research is being carried out on the indication of methylphenidate in dyslexia and autism that are comorbid with ADHD.
Artigas-Pallarés
J
J
Hospital de Sabadell. Corporacio Sanitaria Parc Tauli, 08208 Sabadell, Espana. 7280jap@comb.es
D001289:Attention Deficit Disorder with Hyperactivity / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology*; D001321:Autistic Disorder / Q000453:epidemiology / Q000503:physiopathology; D003071:Cognition / Q000502:physiology*; D003072:Cognition Disorders / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology*; D015897:Comorbidity; D004410:Dyslexia / Q000453:epidemiology / Q000503:physiopathology; D006801:Humans; D008959:Models, Neurological