[Paroxysmal dyskinesias]. / Discinesias paroxísticas.

INTRODUCTION: Paroxysmal dyskinesias are uncommon movements disorders that consist on recurrent brief episodes characterized by attacks with any combination of dystonia, chorea, athetosis or ballismus. DEVELOPMENT AND CONCLUSIONS: The pathophysiology of paroxysmal dyskinesias is unclear at the present time. An epileptic mechanism and basal ganglia disorders have been proposed although channelopathy due to ion channel mutations have been recently suggested. These disorders were classified by Demirkiran and Jankovic into two main groups: paroxysmal kinesigenic dyskinesia if the attacks were induced by sudden movement and paroxysmal nonkinesigenic dyskinesia if they were not. In addition to these groups, two more types have been known, namely paroxysmal exercise-induced dyskinesia and hypnogenic paroxysmal dyskinesia. As well association between benign infantile familial convulsions and paroxysmal choreoathetosis, or rolandic epilepsy, episodes of exercise induced dystonia, and writers' cramp have been described. Also others paroxysmal movements disorders have been known, we mention below. Paroxysmal dyskinesias can further be divided into idiopathic (familiar in most of the cases) or secondary cases depending on underlying cause.

Discinesias paroxísticas / Paroxysmal Diskinesias

Resumen. Introducción. Las discinesias paroxísticas consisten en trastornos del movimiento infrecuentes, que ocurren de forma brusca y recurrente, manifestadas como posiciones distónicas, movimientos coreicos, atetósicos, balísticos o una combinación de éstos. Desarrollo y conclusiones. No conocemos con exactitud su fisiopatología. Se sugiere tanto un mecanismo epiléptico como una alteración de la modulación de los ganglios basales, aunque como alteración común se plantea que se trate de canalopatías por mutaciones en genes de canales iónicos. En función del precipitante de las discinesias podremos hablar de discinesias no cinesogénicas, cinesogénicas, inducidas por ejercicio o hipnogénicas, siguiendo la última clasificación propuesta por Demirkiran y Jankovic. Además, se han descrito asociaciones como el síndrome de convulsiones infantiles y coreoatetosis paroxística o la asociación de epilepsia rolándica, distonía paroxística inducida por el ejercicio y calambre del escribiente. También se han descrito otros trastornos del movimiento paroxísticos; aunque no entraremos en detalles, se nombrarán posteriormente. Las discinesias paroxísticas también se diferencian, dependiendo de su etiología, en idiopáticas (familiares en la mayoría de los casos) y secundarias (sintomáticas de una enfermedad subyacente (AU)

Summary. Introduction. Paroxysmal dyskinesias are uncommon movements disorders that consist on recurrent brief episodes characterized by attacks with any combination of dystonia, chorea, athetosis or ballismus. Development and conclusions. The pathophysiology of paroxysmal dyskinesias is unclear at the present time. An epileptic mechanism and basal ganglia disorders have been proposed although channelopathy due to ion channel mutations have been recently suggested. These disorders were classified by Demirkiran and Jankovic into two main groups: paroxysmal kinesigenic dyskinesia if the attacks were induced by sudden movement and paroxysmal nonkinesigenic dyskinesia if they were not. In addition to these groups, two more types have been known, namely paroxysmal exercise-induced dyskinesia and hypnogenic paroxysmal dyskinesia. As well association between benign infantile familial convulsions and paroxysmal choreoathetosis, or rolandic epilepsy, episodes of exercise induced dystonia, and writers’ cramp have been described. Also others paroxysmal movements disorders have been known, wemention below. Paroxysmal dyskinesias can further be divided into idiopathic (familiar in most of the cases) or secondary cases depending on underlying cause (AU)

[Pharmacology of neuroprotection in acute ischemic stroke]. / Farmacología de la neuroprotección en el ictus isquémico agudo.

INTRODUCTION: Stroke leads the list of causes of disability in adults and represents the second leading cause of death worldwide. Knowledge about the pathophysiology of ischemic stroke has improved substantially over the past 25 years, and, as a result of this, new therapeutic strategies have been developed with two main aims: restoration of cerebral flow and the minimization of the deleterious effects of ischemia on neurons. Although so far there are no drugs approved for the neuroprotection therapy in stroke, there are some compounds with promising results. DEVELOPMENT: This paper makes a critical review of several studies on the preclinical stroke neuroprotection with drugs aimed to protect the brain tissue adjacent to the damaged central area or ischemic penumbra zone until either the physiological mechanisms or the treatment stop the ischemic insult. We expose the potential neuroprotective properties of these treatments mainly based on inhibiting excitotoxicity processes mediated by gamma-aminobutyric acid receptors, glutamate release and interacting with ion channels such as calcium and sodium. We focus on drugs which have shown to be capable of modulating intracellular degenerative pathways in mitochondria mediated apoptosis or the expression of apoptotic proteins in experimental models. CONCLUSION: It is very likely that the neuroprotective effects require a poly-drug therapy that combines different mechanisms of action.

Farmacología de la neuroprotección en el ictus isquémico agudo / Pharmacology of neuroproctection in acute ischemic stroke

Introducción. El ictus es el primer motivo de discapacidad en adultos y la segunda causa de mortalidad en el mundo. El conocimiento sobre la fisiopatología del ictus isquémico ha mejorado sustancialmente durante los últimos 25 años y, como consecuencia de ello, se han desarrollado nuevas estrategias terapéuticas con dos objetivos fundamentales: restablecer el flujo sanguíneo lo antes posible y minimizar los efectos deletéreos de la isquemia sobre las neuronas mediante terapias neuroprotectoras. Hasta el momento, no hay fármacos aprobados para esta indicación, pero con algunos compuestos se han obtenido resultados prometedores. Desarrollo. Este trabajo realiza una revisión crítica de diferentes estudios preclínicos de neuroprotecciónen el ictus con fármacos que tienen como finalidad salvaguardar el tejido cerebral adyacente a la zona central de daño isquémico o zona de penumbra, hasta que los mecanismos fisiológicos o el tratamiento detengan la agresión isquémica. Se expone el potencial de las propiedades citoprotectoras de dichos tratamientos, principalmente mediante la interacción con los procesos excitotóxicos: a través de la modulación del ácido gamma-aminobutírico, los receptores glutamatérgicoso el bloqueo de canales iónicos como los de calcio y sodio. Destacamos aquellos fármacos que han demostrado su capacidad de actuar en vías intracelulares degenerativas como la apoptosis mediada por la mitocondria o por la expresión de proteínasproapoptóticas. Conclusión. Es muy probable que los efectos neuroprotectores requieran un tratamiento basado en unapoliterapia que combine fármacos con diferentes mecanismos de acción

Introduction. Stroke leads the list of causes of disability in adults and represents the second leading cause of death worldwide. Knowledge about the pathophysiology of ischemic stroke has improved substantially over the past 25 years, and, as a result of this, new therapeutic strategies have been developed with two main aims: restoration of cerebral flow and theminimization of the deleterious effects of ischemia on neurons. Although so far there are no drugs approved for the neuroprotection therapy in stroke, there are some compounds with promising results. Development. This paper makes a critical review of several studies on the preclinical stroke neuroprotection with drugs aimed to protect the brain tissue adjacent to the damaged central area or ischemic penumbra zone until either the physiological mechanisms or the treatment stop the ischemic insult. We expose the potential neuroprotective properties of these treatments mainly based on inhibiting excitotoxicity processes mediated by gamma-aminobutyric acid receptors, glutamate release and interacting with ion channels such ascalcium and sodium. We focus on drugs which have shown to be capable of modulating intracellular degenerative pathways in mitochondria mediated apoptosis or the expression of apoptotic proteins in experimental models. Conclusion. It is very likely that the neuroprotective effects require a poly-drug therapy that combines different mechanisms of action