This article was migrated. The article was marked as recommended. The term neurophobia was defined by Jozefowicz as "a fear of the neural sciences and clinical neurology that is due to the students' inability to apply their knowledge of basic sciences to clinical situations, leading to a paralysis of thought or action". In this paper we review what we see as the key aspects of neurophobia. What gives rise to it? Notable among multiple causes are how basic and clinical neurosciences are taught, the peculiarities of neurological patient history, examination and differential diagnosis in the field, and how neurology and neurologists are seen from outside the field. We will also review the extent of the issue, for in view of its prevalence, many students will reject a specialty in increasing demand (as the incidence of neurological disorders will not cease to grow), along with its consequences: more patient referrals to neurology (owing to neurophobia or defensive medicine), or over-prescription of ancillary tests for diagnosis. Finally we will look at the solutions proposed, especially those aiming to bring about changes in the form and content of teaching, how the teaching of neurological examination and of new technologies is to be approached, and the use of those technologies as teaching aids.

Aims. To present a review of the so- called 'Mozart effect', to explain why Mozart and his sonata K. 448 were chosen, and to review the available literature on the treatment of epilepsy with that sonata. Development. Profuse literature exists on the cerebral mechanisms that allow us to perceive, process and respond to the musical stimulus. Cerebral plasticity, especially in people with musical training, has also been demonstrated. The ` Mozart effect' arose from the finding that hearing the sonata K. 448 improved cognitive abilities, but the fact that these results may be due not to the music itself but to the listener increasing arousal or enjoyment generated controversy. In this context of debate, a large number of papers about the 'Mozart effect' in the field of epilepsy were published, and are reviewed in this work. Conclusions. The 'Mozart effect' has a scientific basis but its nature limits the methodological quality of the research. The music of Mozart, chosen for its exquisite structure, has been able to increase even more the controversy because also it is of the taste of a great majority. It is still far from being consolidated as a non-pharmacological antiepileptic treatment, but it could increase the scientific evidence with studies whose design minimizes the cited confounding factors.

La demencia, estrechamente ligada a factores predisponentes ambientales como la dieta, supone un problema de salud pública de magnitud creciente: actualmente más de 35 millones de pacientes con demencia tipo alzhéimer, y se espera que superen los 135 millones en 2050. Si conseguimos retrasar el desarrollo de la demencia 5 años, reduciremos su prevalencia en un 50%. Los pacientes con demencia alteran su dieta y se han reportado déficits, entre otros, de ácido fólico, vitaminas B12, B6, C, E, A, D, K, betacarotenos y omega tres, que deben ser resueltos con una dieta adecuada y, en según qué casos, con aportes extra. Pero para reducir o al menos retrasar la prevalencia debemos preconizar la prevención mediante una dieta adecuada desde el inicio de la vida, idea reforzada por el hecho de que los factores de riesgo cardiovascular se relacionen de forma directa con el desarrollo de demencia. Disponemos de abundante bibliografía que, aunque con límites, nos permite hacer recomendaciones nutricionales para prevenir el deterioro cognitivo. Se han conseguido mejores resultados cuando se han estudiado dietas completas que cuando se han considerado nutrientes específicos. De especial interés es la dieta mediterránea, que garantiza un aporte elevado de vegetales, frutas, frutos secos, legumbres, cereales, pescado y aceite de oliva, y moderado de carne, productos lácteos y alcohol, y en la que nos centraremos en este artículo.

One of the accepted factors of antiseizure medication resistance is the action of P-glycoprotein (P-gp), limiting the access of drugs to the nervous system. But if we ask which antiseizure medications are substrates of P-gp and which are not, the available bibliography will not allow us to obtain a clear answer. In this review, we focus on clarifying this response. The reviewed studies have been conducted both in cell lines and in mice that have been administered a P-gp inhibitor, artificially induced with drug-resistant epilepsy, or had a P-gp gene knockout. A limited number of studies have been conducted in dogs, primates, brain sections of known epilepsies, or human volunteers, including pharmacokinetic studies in healthy volunteers and symptomatic response to treatment. Notably, in human cases, allele variation studies check if having one allele or another of P-gp varies the pharmacokinetics in question. As we see, the approach to P-gp and antiseizure medication can be done using very different methods, which undoubtedly complicates the interpretation of the findings. We cannot be categorical in our results, but we can mention probabilities. Regarding the weighting of studies, we will consider those conducted in humans as more important, followed by animal studies, and we will give less weight to studies showing contradictory results compared to the general bibliographic base. Based on the published bibliography, we propose that, among the anticrisis medications, the following are likely substrates of P-glycoprotein: Phenytoin, Phenobarbital, Oxcarbazepine, Lamotrigine, Topiramate, and Lacosamide (less evidence). The following are probably not substrates: Brivaracetam, Zonisamide, Valproic acid, Perampanel, Gabapentin, and Vigabatrin. We have not obtained enough information about: Carbamazepine, Eslicarbazepine, Levetiracetam, Tiagabine, Felbamate, Pregabalin, Rufinamide, Ezogabine, and Retigabine.