Revista de neurologia · 2009
[Pharmacological treatment of dyslexia].
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Artigas-Pallarés J
Аннотация
INTRODUCTION: Pharmacological approaches aimed at improving dyslexia are almost inexistent.
AIM: To analyse, based on the current theories of dyslexia, the possibility of applying some pharmacological measure.
DEVELOPMENT: The different theories on dyslexia are discussed. The multiple deficit model is then outlined, in opposition to the classical single dysfunction model. The model described provides a coherent explanation for several conceptual dilemmas that arise from the analysis of the comorbidity of dyslexia. The few pharmacological interventions that have been proposed to date are also analysed; with the exception of stimulants, however, they are not supported by any solid theoretical base about dyslexia. Lastly, we use the multiple deficit model as an aid to analyse the current data referring to the effect of stimulants on nuclear mechanisms in dyslexia.
CONCLUSIONS: It is suggested that it would be wise to monitor the response in reading skills in children with dyslexia and attention deficit hyperactivity disorder (ADHD) who are being treated with stimulants. We also recommend taking into consideration the comorbidity between dyslexia and ADHD as an argument in favour of pharmacological intervention in patients with apparently mild symptoms of ADHD. In any case, today, pharmacological intervention cannot be expected to go beyond its having a complementary and synergic effect on traditional methods of treatment.
AIM: To analyse, based on the current theories of dyslexia, the possibility of applying some pharmacological measure.
DEVELOPMENT: The different theories on dyslexia are discussed. The multiple deficit model is then outlined, in opposition to the classical single dysfunction model. The model described provides a coherent explanation for several conceptual dilemmas that arise from the analysis of the comorbidity of dyslexia. The few pharmacological interventions that have been proposed to date are also analysed; with the exception of stimulants, however, they are not supported by any solid theoretical base about dyslexia. Lastly, we use the multiple deficit model as an aid to analyse the current data referring to the effect of stimulants on nuclear mechanisms in dyslexia.
CONCLUSIONS: It is suggested that it would be wise to monitor the response in reading skills in children with dyslexia and attention deficit hyperactivity disorder (ADHD) who are being treated with stimulants. We also recommend taking into consideration the comorbidity between dyslexia and ADHD as an argument in favour of pharmacological intervention in patients with apparently mild symptoms of ADHD. In any case, today, pharmacological intervention cannot be expected to go beyond its having a complementary and synergic effect on traditional methods of treatment.