[Migraine and evolutionary theory: paths for a clinical approach]. / Migraña y teoria evolutiva: vias para un acercamiento clinico.

INTRODUCTION: Migraine is a very common disorder with a raising incidence. The theory of evolution allow us to explain the emergence of the disorder, due to the advantages that the overreactivity to stimulus provided to ancestral groups of Homo sapiens, and a greater presence of the disorder in modern societies, based in the interactions with external factors. Herein we analyze these points. DEVELOPMENT: Design of organisms and their responses to environmental factors emerge to improve survival. Thus pain and headache can be contemplated as homeostatic and adaptative responses. Below 10% of the population has no experience with headache and the migrainous phenotype is quite frequent in secondary headaches and in syndromic forms of migraine. These features can be understood under the next undergrounds: specific neurophysiological data (lack of habituation, sensibilization and low preactivation), genetic features (polygenic disorder with the implication of many gens with a low penetrance, that interact with the environment and are shared with comorbid disorders such as depression and anxiety); and environmental interactions in modern societies (increase in the number of estrogenic cycles and particularly overexposition to stress). CONCLUSIONS: A feature that was an evolutionary advantage has been transformed in a highly prevalent and disabling disorder in modern societies. It is the result of the interaction with internal (estrogenic cycles) and external (stress) stimuli. As a consequence, it becomes a mismatch disorder. The effects appear in childhood through epigenetics. Therefore, therapeutic interventions would yield greater benefits if whole populations were included in educative interventions incorporating these aspects.

TITLE: Migraña y teoria evolutiva: vias para un acercamiento clinico.Introduccion. La migraña es un trastorno muy comun, con incidencia en aumento. La teoria evolutiva permite explicar su aparicion, dadas las ventajas que aportaba a grupos originarios de Homo sapiens una mayor reactividad a estimulos, y la presencia creciente de interaccion con factores ambientales. Analizamos estos aspectos a traves de los mecanismos potenciales que los explican. Desarrollo. El diseño de los organismos y sus respuestas ambientales surgen para mejorar la supervivencia. Asi, el dolor y la cefalea pueden entenderse como respuestas homeostaticas y adaptativas. Menos del 10% de la poblacion no tiene experiencia de cefalea, y el fenotipo migrañoso es una repuesta dolorosa comun en formas secundarias y sindromicas de cefalea. Estas caracteristicas se entienden segun rasgos neurofisiologicos especificos (falta de habituacion, sensibilizacion y baja preactivacion), caracteristicas geneticas (trastorno poligenico con multiples genes de baja penetrancia, que interaccionan con el ambiente y que son comunes a los de los trastornos comorbidos, como depresion-ansiedad) e interaccion ambiental en las sociedades modernas (aumento del numero de ciclos estrogenicos, y especialmente sobreexposicion al estres). Conclusiones. Lo que fue una ventaja evolutiva se ha transformado en la sociedad moderna en un trastorno muy prevalente y frecuentemente incapacitante. Es el resultado de una interaccion con sobrecarga de estimulos externos (estres) e internos (hormonales), lo que, de acuerdo con la teoria evolutiva, convertiria a la migraña en una enfermedad por desajuste. Los efectos ocurririan precozmente, en la infancia, a traves de mecanismos de epigenetica. Se obtendria un gran beneficio terapeutico mediante intervenciones poblacionales y educativas que incorporen estos aspectos.

[Inflammatory mechanisms, arteriosclerosis and ischemic stroke: clinical data and perspectives]. / Mecanismos inflamatorios, arteriosclerosis e ictus isquémico: datos de interés clínico y perspectivas.

OBJECTIVE: The atherosclerosis is the most common cause of death and disability in developed countries by causing ischemic cardiopathic and stroke. The ischemic atherotrombotic stroke is the most frequent form of the last one. In this sense we review herein the mechanisms underlying the artherosclerotic process. DEVELOPMENT: It is understood as an inflammatory disease, by taking into account the widely accepted hypothesis by Ross: it was firstly stated in structural terms, as macrophages and T/B linfocities were present in the arterial wall from the first stages of the disease (fatty streak) to the last and complicated ones. The starting point is a functional endothelial damage, secondary to mechanical or vascular risk factors and called response to injury hypothesis . The next step is an inflammatory cascade that involves humoral (citokines, growth factors) and cellular (increased quimiotaxis, adherece and infiltration of inflamatory cells) mechanisms. They interact among them, outbalanced and in a progresssive way that leads to the final fibroproliferative response. Every stage has his own inflammatory components and interactive pathways. The following elements are outstanding in this process: 1) Adhesion molecules, including E selectin, ICAM 1 and VCAM 1, that are increased locally in the plaques and as circulating elements; plaquetary receptors of the type IIb/IIIa are integrins wich belong to the same family; 2) Citokines with either proinflammatory activity like IL 1, the TNF a and linfocitary ligands like the CD 40, or with antiinflammatory activity like the gamma interpheron; 3) Growth factors, with plaquetary (PDGF) and fibroblastic (FGF) variants as the cornerstone; 4) Markers of systemic inflammation, overall plasma C reactive protein and fibrinogen, that predict the risk of stroke and cardiovascular death; IL 6, complement, thrombin and heat shock proteins (HSP) would act in a similar but less conclusive way. CONCLUSIONS: The evidences of the pivotal role of the inflammation in the stroke allow to develop therapeutical strategies to prevent the disease: fostering natural antiinflamatory mechanisms, or inhibiting inflammatory elements by selective (monoclonal antibodies) or non selective (IIb/IIIa receptors, antiinflammatory drugs) pathways are distinctily glimpsed, ongoing or fully developed.

Mecanismos inflamatorios, arteriosclerosis e ictus isquémico: datos de interés clínico y perspectivas / Inflammatory mechanisms, arteriosclerosis and ischemic stroke: clinical data and perspectives

Objetivo. La arteriosclerosis es la causa más común de muerte y discapacidad en los países desarrollados, debido a su papel principal en la cardiopatía isquémica e ictus, del cual la forma aterotrombótica resulta la más frecuente. Revisamos aquí los mecanismos subyacentes a la enfermedad arteriosclerótica. Desarrollo. Consideramos ésta un proceso inflamatorio de acuerdo con la hipótesis de Ross, inicialmente descrita en términos estructurales, ya que macrófagos y linfocitos T/B están presentes en la pared arterial desde los primeros (fatty streak) hasta los últimos y complicados estadios de la enfermedad. El punto de inicio es un daño endotelial funcional, secundario a factores de riesgo vascular o mecánicos, definido como ` response-to-injury hypothesis'. El siguiente paso es una cascada inflamatoria que incluye factores humorales (citocinas y factores de crecimiento) y celulares (aumento de quimiotaxis, adherencia e infiltración de células inflamatorias), que interactúan entre ellos de manera progresiva, dando lugar a la respuesta fibroproliferativa. Cada estadio tiene sus propios componentes inflamatorios e interacciones. Los siguientes elementos destacan en este proceso: 1) Moléculas de adhesión, incluyendo la E-selectina, ICAM-1 y VCAM-1, que están aumentados localmente en las placas y en el plasma; los receptores plaquetarios del tipo IIb/IIIa son integrinas pertenecientes a la misma familia; 2) Citocinas con actividad proinflamatoria -tales como la IL-1 o el TNF-alfa- y ligandos inflamatorios -como el CD-40-, o con actividad antiinflamatoria, como interferón- gama; 3) Factores de crecimiento: las variantes plaquetarias (PDGP) y fibroblástica (FGF) serían los elementos claves; 4) Marcadores de inflamación sistémica, sobre todo la proteína C reactiva plasmática y el fibrinógeno, que predicen el riesgo de ictus y de muerte cardiovascular; la IL-6, complemento, trombina y proteinas de `golpe de calor' (HSP) actuarían de modo similar pero menos decisivo. Conclusiones. Las evidencias del papel fundamental de la inflamación en el ictus permiten desarrollar estrategias terapéuticas para prevenir la enfermedad, ya sea fomentando los mecanismos antiinflamatorios o inhibiendo los elementos inflamatorios por vías selectivas (anticuerpos monoclonales) o no selectivas (receptores IIb/IIIa, fármacos antiinflamatorios); se vislumbra su desarrollo completo en un futuro próximo (AU)

[Arterial thoracic outlet syndrome and diagnostic angioresonance]. / Síndrome de apertura torácica superior y angiorresonancia diagnóstica.

INTRODUCTION: The anatomy of the upper cervical region, in the presence of structural anomalies favours the compression of the brachial plexus and/or subclavian vessels, giving rise to the thoracic inlet syndrome (SATS). Neurological involvement is more common than vascular involvement (95 and 5% respectively); the latter is known as the arterial SATS. The forms of clinical presentation of arterial SATS are very variable and have different prognoses: it may present as acute distal ischaemia with a variable course, peripheral embolism or as a non-serious condition such as Raynaud's phenomenon. CLINICAL CASE: We present a case with arterial involvement only, associated with a clavicular osteophyte, in a patient with episodes of acute, transient weakness of the arm which were initially thought to be transient strokes with brachial monoparesis. CONCLUSION: Classically, the basic examination to diagnose arterial SATS has been conventional angiography, an invasive test which is not without complications; in our case it was magnetic angioresonance which showed changes in blood flow on forced arm movement. This avoided having to do a conventional angiogram. Angioresonance, rarely cited in this syndrome, is worthy of study and comparison with the 'standard' diagnostic method of conventional angiography.