[Efficacy and safety of transcranial magnetic stimulation in patients with non-fluent aphasia, following an ischaemic stroke. A controlled, randomised and double-blind clinical trial]. / Eficacia y seguridad de la estimulacion magnetica transcraneal en pacientes con afasia no fluente, posterior a ictus isquemico. Ensayo clinico controlado, aleatorizado y doble ciego.

INTRODUCTION: Non-fluent aphasia is a frequent complication in post-ischemic stroke patients, with repetitive transcranial magnetic stimulation (rTMS) being one of the possible treatment alternatives. AIM: To assess the efficacy and safety of rTMS in patients with non-fluent after-ischemic stroke aphasia. PATIENTS AND METHODS: Double blind, randomized controlled clinical trial in post-stroke patients who were assigned to receive 10 sessions (one daily) of active treatment or placebo of rTMS, without the addition of language therapy. The baseline characteristics were compared initially and the efficacy between the active group versus the placebo group at day 30 was evaluated through a Mann-Whitney U test. RESULTS: 82 patients were included: active group (n = 41) and placebo group (n = 41). At baseline, statistically significant differences were found between the groups in favor of the placebo in the domains of the Boston test of auditory compression (p = 0.024), denomination (p = 0.014) and praxis (p = 0.026), and also occurred on the 30th day in the naming domains (p = 0.037) and reading (p = 0.001). There were 39 adverse reactions: 23 (26.83%) in the active group vs 16 (21.96%) in the placebo group (p = 0.290); the majority corresponded to episodes of mild headache. CONCLUSION: rTMS is a safe therapy, however, given the conditions of this study, we could not demonstrate the efficacy of rTMS versus placebo in patients with non-fluent aphasia with involvement of Broca's area after an ischemic stroke.

TITLE: Eficacia y seguridad de la estimulacion magnetica transcraneal en pacientes con afasia no fluente, posterior a ictus isquemico. Ensayo clinico controlado, aleatorizado y doble ciego.Introduccion. La afasia no fluente es una complicacion frecuente en pacientes postictus isquemico y la estimulacion magnetica transcraneal repetitiva (EMTr) representa una de las posibles alternativas de tratamiento. Objetivo. Evaluar la eficacia y la seguridad de la EMTr en pacientes con afasia no fluente postictus isquemico. Pacientes y metodos. Ensayo clinico controlado doble ciego, aleatorizado, en pacientes postictus isquemico que fueron asignados a recibir 10 sesiones (una diaria) de tratamiento activo o placebo de EMTr, sin adicion de terapia del lenguaje. Las caracteristicas basales fueron comparadas inicialmente, y la eficacia entre el grupo activo frente al grupo placebo el dia 30 se evaluo a traves de una prueba U de Mann-Whitney. Resultados. Se incluyo a 82 pacientes: grupo activo (n = 41) y grupo placebo (n = 41). Se encontraron diferencias basales estadisticamente significativas entre los grupos a favor del placebo en los dominios del test de Boston de compresion auditiva (p = 0,024), denominacion (p = 0,014) y praxis (p = 0,026), e igualmente ocurrio el dia 30 en los dominios de denominacion (p = 0,037) y lectura (p = 0,001). Se presentaron 39 reacciones adversas, 23 en el grupo activo (26,83%) frente a 16 (21,96%) en el grupo placebo (p = 0,290), y la mayoria correspondia a episodios de cefalea leve. Conclusion. La EMTr es una terapia segura, pero dadas las condiciones de este estudio, no pudo demostrarse la eficacia de la EMTr frente al placebo en pacientes con afasia no fluente con afectacion del area de Broca posterior a un ictus isquemico.

[The role played by the autonomic nervous system in the relation between depression and cardiovascular disease]. / Papel del sistema nervioso autónomo en la relación entre depresión y enfermedad cardiovascular.

INTRODUCTION: Findings from several epidemiological studies have revealed that major depression is associated with an increased risk of developing cardiovascular diseases (CVD) and presenting complications and new events in subjects with already-established CVD. The pathophysiological mechanisms responsible for this increased cardiovascular risk in major depression remain unclear. DEVELOPMENT: The aim of this work is to review the literature on the possible pathophysiological mechanisms involved in the relation between major depression and CVD, with special emphasis on the studies dealing with cardiovascular autonomic dysfunction and heart rate variability. Likewise, recent hypotheses concerning the neural mechanisms underlying autonomic dysfunction in subjects with major depression are also discussed. CONCLUSIONS: The evidence that is currently available allows us to hypothesise that there are anomalies in the functioning of the central autonomic neural network in subjects with major depression, and more specifically in the hippocampus, prefrontal cortex and the brain stem nuclei. Such abnormalities, in association with lower central levels of serotonin give rise to a predominance of the sympathetic flow and a loss of cardiac vagal tone. The resulting cardiovascular autonomic dysfunction could be the main cause of the increased cardiovascular risk observed in major depression. In the future, studying the autonomic nervous system may be a useful tool in the development of new therapeutic strategies aimed at reducing cardiovascular morbidity and mortality in subjects with depression.

Papel del sistema nervioso autónomo en la relación entre depresión y enfermedad cardiovascular / The role playedby the autonomic nervous system in the relation between depression and cardiovascular disease

Introducción. Los resultados de varios estudios epidemiológicos han revelado que la depresión mayor está asociada con un riesgo incrementado de desarrollar enfermedades cardiovasculares (ECV) y presentar complicaciones y nuevos eventos en sujetos con ECV establecida. Los mecanismos fisiopatológicos responsables de este aumento del riesgo cardiovascular en la depresión mayor aún no se han esclarecido. Desarrollo. El objetivo del presente trabajo es revisar la literatura sobre los posibles mecanismos fisiopatológicos involucrados en la relación entre la depresión mayor y las ECV, con énfasis en los estudios relacionados con disfunción autonómica cardiovascular y variabilidad de la frecuencia cardíaca. Asimismo, se exponen hipótesis recientes acerca de los mecanismos neurales que subyacen en la disfunción autonómica en sujetos con depresión mayor. Conclusiones. La evidencia disponible permite establecer la hipótesis de que sujetos con depresión mayor presentan anormalidades en el funcionamiento de la red neuronal autonómica central, específicamente en el hipocampo, corteza prefrontal y núcleos del tallo cerebral, que asociadas a la disminución de los niveles centrales de serotonina ocasionan un predominio del flujo simpático y una pérdida del tono vagal cardíaco. La disfunción autonómica cardiovascular resultante podría ser la causa principal del riesgo cardiovascular aumentado observado en la depresión mayor. En el futuro, el estudio del sistema nervioso autónomo puede ser una herramienta útil en el desarrollo de nuevas estrategias terapéuticas enfocadas a disminuir la morbilidad y mortalidad cardiovascular en sujetos deprimidos

Introduction. Findings from several epidemiological studies have revealed that major depression is associated with an increased risk of developing cardiovascular diseases (CVD) and presenting complications and new events in subjects with already-established CVD. The pathophysiological mechanisms responsible for this increased cardiovascular risk in major depression remain unclear. Development. The aim of this work is to review the literature on the possible pathophysiological mechanisms involved in the relation between major depression and CVD, with special emphasis on the studies dealing with cardiovascular autonomic dysfunction and heart rate variability. Likewise, recent hypotheses concerning the neural mechanisms underlying autonomic dysfunction in subjects with major depression are also discussed. Conclusions. The evidence that is currently available allows us to hypothesise that there are anomalies in the functioning of the central autonomic neural network in subjects with major depression, and more specifically in the hippocampus, prefrontal cortex and the brain stem nuclei. Such abnormalities, in association with lower central levels of serotonin give rise to a predominance of the sympathetic flow and a loss of cardiac vagal tone. The resulting cardiovascular autonomic dysfunction could be the main cause of the increased cardiovascular risk observed in major depression. In the future, studying the autonomic nervous system may be a useful tool in the development of new therapeutic strategies aimed at reducing cardiovascular morbidity and mortality in subjects with depression