title: [Dyslexia: a disease, a disorder or something else?].
abstract: BACKGROUND
  Although dyslexia is widely diagnosed and affects a very important portion of the childhood population, a conceptual definition of the condition is still lacking. This paper analyses different contributions from molecular genetics, neurocognitive research and evolutionary psychology so as to provide a series of reflections that may further our understanding of the nature of dyslexia and make it easier to categorise. Genetics has shown that dyslexia is linked to quantitative, pleiotropic genes. Moreover, dyslexia is not linked to a single gene, but is polygenic. Another genetic characteristic is its heterogeneity, that is to say, dyslexia may be due to a variety of different genetic combinations. This model, which has recently been put forward to make sense of and lend coherence to the data provided by genetics and neurocognitive research, has been called the multiple deficit model. Writing, on the other hand, is seen as a cultural technique that was invented only recently, if we compare it with whole process of human evolution. In order to learn to read and write successfully, the brain has had to adapt structures that were designed by the process of natural selection to perform functions that are typical of our species and have absolutely nothing to do with reading.
  
  
  CONCLUSIONS
  Taking the multiple deficit model as its starting point, this article analyses the therapeutic response to stimulant medication as a way of improving nuclear aspects of dyslexia, when dyslexia and attention deficit hyperactivity disorder coincide.
authors.affiliation: Unidad de Neuropediatría, Corporació Sanitària Parc Taulí, Barcelona, España. 7280jap@comb.es
authors.forename: J
authors.initials: J
authors.lastname: Artigas-Pallarés
mesh_terms: D001289:Attention Deficit Disorder with Hyperactivity / Q000235:genetics; D000697:Central Nervous System Stimulants / Q000627:therapeutic use; D002648:Child; D004410:Dyslexia / Q000175:diagnosis* / Q000235:genetics / Q000503:physiopathology* / Q000628:therapy; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008774:Methylphenidate / Q000627:therapeutic use; D011932:Reading; D014956:Writing
chemical_list: D000697:Central Nervous System Stimulants; D008774:Methylphenidate