[Multidrug resistant narcolepsy]. / Narcolepsia multirresistente.

INTRODUCTION: Narcolepsy type 1 is a focal degenerative disease of the hypothalamus that selectively affects orexin (hypocretin)-producing neurons. It presents multiple clinical manifestations, both in wakefulness and in sleep. The symptoms are often so disruptive that they cause enormous suffering and impair patients' quality of life. Although a non-pharmacological approach is sometimes sufficient, the vast majority of patients need medication for adequate clinical management. CASE REPORT: A male who, at 43 years of age, began to present acutely with excessive daytime sleepiness and episodes of cataplexy. After a thorough examination, he was diagnosed with narcolepsy type 1. Throughout the course of the disease, he was prescribed antidepressants, neurostimulants and sodium oxybate, in monotherapy or in combination. The response to pharmacological treatment was insufficient and accompanied by numerous side effects. Following the introduction of pitolisant, there was a marked improvement in his symptoms and a reduction in the dose of the other drugs and their adverse effects was achieved. CONCLUSION: A number of measures are now available to address the cardinal symptoms of the disease, although there are still cases that are resistant to anti-narcoleptic treatment. Drugs with mechanisms of action that act upon receptors in the histaminergic system can be very useful in these cases.

TITLE: Narcolepsia multirresistente.Introducción. La narcolepsia de tipo 1 es una enfermedad degenerativa focal del hipotálamo que afecta selectivamente a las neuronas productoras de orexina (hipocretina). Presenta múltiples manifestaciones clínicas, tanto en vigilia como en sueño. Con frecuencia, los síntomas son tan disruptivos que ocasionan enorme sufrimiento y deterioro de la calidad de vida de los pacientes. Aunque en ocasiones es suficiente con un abordaje no farmacológico, la gran mayoría de los enfermos necesita medicación para un adecuado control clínico. Caso clínico. Varón que a los 43 años comenzó a presentar de forma aguda excesiva somnolencia diurna y episodios de cataplejía. Tras un exhaustivo estudio se le diagnosticó narcolepsia de tipo 1. A lo largo de la evolución de la enfermedad se le prescribieron antidepresivos, neuroestimulantes y oxibato sódico, en monoterapia o en combinación. La respuesta al tratamiento farmacológico fue insuficiente y se acompañó de numerosos efectos secundarios. Tras la introducción de pitolisant se objetivó una franca mejoría de los síntomas, y se consiguió reducir la dosis de los otros fármacos y de sus efectos adversos. Conclusión. Son numerosas las medidas disponibles en la actualidad para abordar los síntomas cardinales de la enfermedad, aunque siguen existiendo casos resistentes al tratamiento antinarcoléptico. Los fármacos con mecanismos de acción sobre receptores del sistema histaminérgico pueden resultar de gran utilidad en estos casos.

[Neuropeptides in Alzheimer's disease]. / Neuropeptidos en la enfermedad de Alzheimer.

INTRODUCTION: Of approximately 200 peptides that are known to exist in the body, 80 carry out functions as neurotransmitters and about 20 have been linked to Alzheimer's disease (AD). DEVELOPMENT: In this article we review the most salient studies that have been conducted on neuropeptides such as corticotropin-releasing hormone, thyrotropin-releasing hormone, somatostatin, neuropeptide Y, oxytocin, arginine vasopressin, galanin and insulin, as well as the insulin-like growth factors, the glucagon-like peptides, vasoactive intestinal peptide, cholecystokinin, substance P, opioid peptides and the neuropeptide NAP. Although attempts are made to find a causal association with AD, in many cases the findings are contradictory or not very conclusive. CONCLUSIONS: The most notable points could be the reduction in substance P in the cerebral cortex, hippocampus, basal ganglia and cephalospinal fluid; the diminished levels of somatostatin in the same structures except for the basal ganglia; the reduction in the amount of vasopressin except in the temporal lobe; and the increased levels of dynorphin and leucine enkephalin.

Neuropéptidos en la enfermedad de Alzheimer / Neuropeptides in Alzheimer’s disease

Introducción. De los aproximadamente 200 péptidos que se sabe que existen en el organismo, 80 realizan funciones neurotransmisoras y unos 20 se han relacionado con la enfermedad de Alzheimer (EA). Desarrollo. En este artículo elaboramos una revisión de los principales estudios que se han realizado con neuropéptidos, tales como la hormona liberadora de corticotropina, la hormona liberadora de tirotropina, la somatostatina, el neuropéptido Y, la oxitocina, la arginina-vasopresina, la galanina, la insulina y los factores de crecimiento similares a insulina, los péptidos similares a glucagón, el péptido intestinal vasoactivo, la colecistoquinina, la sustancia P, los péptidos opiodes y el neuropéptido NAP. Aunque intentamos encontrar una asociación causal con la EA, hallamos en muchos casos resultados contradictorios o poco concluyentes. Conclusión. Lo más destacable podría ser la disminución de la sustancia P en corteza cerebral, hipocampo, ganglios basales y líquido cefalorraquídeo, la somatostatina disminuida en las mismas estructuras salvo en ganglios basales, la disminución de vasopresina salvo en el lóbulo temporal y el aumento en la corteza cerebral de la dinorfina y la leucoencefalina (AU)

Introduction. Of approximately 200 peptides that are known to exist in the body, 80 carry out functions as neurotransmitters and about 20 have been linked to Alzheimer’s disease (AD). Development. In this article we review the most salient studies that have been conducted on neuropeptides such as corticotropin-releasing hormone, thyrotropin-releasing hormone, somatostatin, neuropeptide Y, oxytocin, arginine vasopressin, galanin and insulin, as well as the insulin-like growth factors, the glucagon-like peptides, vasoactive intestinal peptide, cholecystokinin, substance P, opioid peptides and the neuropeptide NAP. Although attempts are made to find a causal association with AD, in many cases the findings are contradictory or not very conclusive. Conclusions. The most notable points could be the reduction in substance P in the cerebral cortex, hippocampus, basal ganglia and cephalospinal fluid; the diminished levels of somatostatin in the same structures except for the basal ganglia; the reduction in the amount of vasopressin except in the temporal lobe; and the increased levels of dynorphin and leucine enkephalin (AU)

[Intracranial haemorrhage secondary to a lightning strike: a case report]. / Hemorragia intracraneal secundaria a fulguración por rayo: presentación de un caso.

INTRODUCTION: The damage caused to the central nervous system by lightning can be immediate or delayed. Cerebrovascular accidents are usually an infrequent complication of lightning strikes. CASE REPORT: We report the case of a patient who was hit by lightning and then developed an acute bilateral intraparenchymatous haemorrhage in the basal ganglia and the left internal capsule. DISCUSSION: Few cases of intracranial haemorrhages secondary to lightning strikes have been reported. We carry out a review and analysis of the literature currently available on the subject. A number of theories have been put forward that attempt to explain the mechanism behind these haemorrhages in patients who have been hit by lightning. The reason why there is a predilection for the basal ganglia is unknown, although it could be linked to the particular features of the vascularisation of the area.