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The development of neurological deterioration in the hours following the stroke onset occurs in somewhat more than 1 in 3 cerebral infarcts and is associated with an increase in morbidity and mortality. This early deterioration (0–48/72 h) entails the conversion of the ischemic penumbra area in an irreversible lesion, a process that is mediated as much by hemodynamic changes in the local cerebral circulation as by biochemical mechanisms. Late neurological deterioration (3–7 days) is more frequently associated with systemic causes. Knowledge of the various clinical, biochemical and imaging markers associated with neurological deterioration is consequently of fundamental importance. For their repercussion in clinical practice, we classify these predictors of deteriorating cerebral infarct into nonmodifiable, modifiable and possibly modifiable. The reduction in cerebral blood flow in a particular cerebral zone causes very early cerebral damage as a consequence of a significant liberation of neuroexcitatory amino acids, followed by an excessive entry of calcium into the interior of cells; this process causes lipid peroxidation, disintegration of the cellular membranes, nuclear destruction and neuronal death. Moreover, ischemia and posterior reperfusion induce an inflammatory response leading to further cellular destruction. It is therefore conceivable that therapeutic interventions aimed at decreasing proinflammatory cytokines and cell adhesion molecules might result in better outcome in this population.

Background and Purpose —The neurotoxic and neuroprotective role of nitric oxide (NO) in experimental cerebral ischemia has generated considerable debate. The aim of this study was to analyze the relationship between NO metabolite (NO-m) concentrations in cerebrospinal fluid (CSF) and clinical and neuroimaging parameters of brain injury in patients with acute ischemic stroke. Methods —We studied 102 patients and 24 control subjects who were included in a larger previous study conducted to analyze risk factors of progressing stroke. NO generation was calculated by quantifying nitrates and nitrites with a colorimetric assay in CSF samples obtained within the first 24 hours from symptoms onset. Early neurological deterioration was defined as a fall of 1 or more points in Canadian Stroke Scale score between admission and 48 hours after inclusion. Infarct volume was measured on days 4 to 7 by cranial CT. Results —Median NO-m concentrations [quartiles] were 2.1 [1.0, 4.5] μmol/mL in patients and 1.0 [1.0, 1.0] μmol/mL in control subjects ( P P P 5.0 μmol/mL were significantly associated with early neurological worsening (OR 5.7, 95% CI 1.2 to 27.4; P =0.030) independent of other important factors related to progressing stroke, such as CSF glutamate levels. Conclusions —Our clinical findings suggest an important role of NO generation in acute ischemic stroke. Increased NO-m in CSF are associated with a greater brain injury and early neurological deterioration.

Background and Purpose: High levels of glutamate in plasma and cerebrospinal fluid (CSF) have been demonstrated in patients with acute ischemic stroke. Whereas this glutamate increase in CSF is only evidenced during the first 6 h in stable ischemic stroke, it is sustained for 24 h in progressing stroke. The aim of this investigation was to study the evolution of serum glutamate levels after stroke in a rat model of permanent cerebral artery occlusion. Methods: Glutamate, glycine, aspartate, taurine and tryptophan were measured by high-performance liquid chromatography from serum samples taken before and at different times after permanent middle cerebral artery occlusion (MCAO) and from sham-operated rats. Results: After MCAO, a 3-fold increase in glutamate and a 2-fold increase in glycine and aspartate were observed in rat serum. The onset of this amino acid increase began 4–6 h after ischemic induction, reached peak values at 8–24 h and returned to preischemic values by 48–72 h. Serum concentrations of taurine and tryptophan were not modified after MCAO. Sham-operated rats did not exhibit changes of basal amino acid concentrations in serum. Conclusions: The serum excitatory amino acid profile in this experimental model confirms that the early detection of increased concentrations of glutamate and glycine at systemic circulation observed in patients with acute stroke is a consequence of the cerebral ischemic process.

Residue levels and degradation rates of procymidone residues were studied in green beans grown in a greenhouse. Experiments were planned to also assess the influence of planting density on the behavior of procymidone residues on this type of crop. The study was carried out in four random blocks considering three sub-blocks of different planting densities into each block. Plants were sprayed with Sumisclex 50 WP (1077.5 g of ai/ha) 52 days after the transplantation, and sampling was carried out daily during two different periods of 6 and 5 consecutive days, respectively, around the two harvest days (days 12 and 28 after the treatment). Residue levels of procymidone were determined by using the Luke extraction method and GC-NPD. The average residue levels of procymidone in the overall planting (mean of 12 determinations) were below 2 mg/kg (European maximum residue limit) for all the sampling days, obtaining values of 1.01 +/- 0.55 and 0.37 +/- 0.10 mg/kg, respectively, at the two harvest days. The decline behavior of procymidone residues in the overall plantation and in each block could be described as a pseudo-first-order reaction, obtaining half-life values (t(1/2)) of 10-11 days in all cases. The calculated residue level at the preharvest time (5 days) in the overall plantation was 1.7 mg/kg, but this value in the blocks depended on the block position along the greenhouse and ranged from 2.3 to 0.9 mg/kg. In this work, additional data on the residual behavior of the fungicide pyrazophos in green beans were also obtained.

El autor del presente artículo nos introduce en el tratamiento que nuestra legislación del Impuesto a laRenta contiene respecto de los contribuyentes no domiciliados en el Perú. Así, comenta como se encuentra regulada esta situación analizando la noción y regulación de la base jurisdiccional, los efectos de la condición de domiciliado, el criterio de renta peruana e internacional, para finalizar con los problemas de doble tributación.

Objective: To examine whether hyperthermia aggravates cerebral injury in acute ischemia by an excitotoxic mechanism, we studied the relationship between body temperature on admission and CSF concentrations of neuroexcitatory amino acids in 128 patients with acute ischemic stroke of less than 24 h duration. Methods: Stroke worsening was defined as the percent change between the Canadian Stroke Scale (CSS) at 48 h and the CSS on admission. Infarct volume was measured on days 4–7 on cranial computed tomography. Excitatory amino acids were analyzed using HPLC. Results: Glutamate concentration [median (min.-max.)] was 11 (2–19) µmol/l in hyperthermic patients (body temperature >37.5°C) and 5 (2–22) µmol/l in normothermic patients (p < 0.0001). Glycine concentration in hyperthermic and normothermic patients was 16 (3–21) µmol/l and 9 (3–50) µmol/l, respectively (p < 0.0001). Glutamate was significantly higher in patients with hyperthermia only during the first 12 h after the onset of symptoms. The CSF concentrations of glutamate (r = 0.52; p < 0.0001) and glycine (r = 0.62; p < 0.0001) correlated with body temperature. Body temperature was significantly related to stroke worsening and infarct size, but this effect was dependent on the glutamate effect. Conclusion: Glutamate and glycine release during the acute phase of cerebral ischemia could be responsible for the increased brain damage in hyperthermia.

Sin resumen

In the Introduction, Durand identified the general configuration of work organisation in the sector (Table 2 — ‘The four canonical models of work organisation’). He then distinguished three corresponding ideal typical forms of employee relations (Fordist, Japanese-lean production, Kalmarian), arguing that they are models in the double sense of the terms. Firstly, their systemic coherence allows us to make sense of particular situations at a particular moment. Secondly, they can be copied, imitated and reproduced by various actors who see in them the answer or answers to their problems.

Academic debate and literature on technological transfers, or transplants, has tended to focus on what are considered normal or standard instances of this. That is, attention has centred on the export of new forms of work, nearly always from countries labelled central or dominant, to others somewhat imprecisely and ironically described as ‘semi-’, or even completely, peripheral. Discussion of lean production, in turn, has revolved around the question of whether, and to what extent, new forms of productive organisation now being developed conform to the model in the core companies, regions or countries. Significantly, these models are often imaginary, or what might more kindly be described as ideal types [2]. In this context, it would appear exceptional for a multinational corporation to select one of its ‘semi-peripheral’ centres to play a leading role in the experimental introduction of a series of technological and organizational innovations in its strategy to, in their own words, ‘catch up with the Japanese’. It would also appear exceptional for the mother company to turn one of these centres of work and production into a laboratory for the new organisation in the search for the model of production for the 21st century — and for the company to invest its image and sufficient financial and human resources to enable the factory to meet a challenge of this scale. Exceptional but not unheard of, since this paper focuses on just such a case: Renault’s FASA plant in Spain.

To the Editor: Three major molecular events in brain damage from cerebrovascular occlusion are at present the focus of interest: calcium overload, excessive acidosis, and enhanced production of free radicals. Free radicals are generated in increased amounts under ischemic conditions and react with and damage proteins, nucleic acids, and membrane lipids, disrupting cellular integrity.1 This oxygen radical activity is especially intense during reperfusion after sustained ischemia. The generation of radical hydroxyl, the most toxic and reactive of free radicals, is catalyzed by ferrous iron released from intracellular stores during ischemia; thus, the sensitivity of neurons to oxidative stress depends on the availability of iron in the ischemic focus.2 3 Iron is released from large transport proteins, particularly from ferritin, which accounts for one third to three quarters of brain iron.4 In the absence of inflammation, cancer, and infectious diseases, the serum concentration of ferritin is thought to be directly proportional to tissue iron stores and can be used to assess their size.5 Despite the theoretical importance of iron in oxidative brain injury, very little direct evidence exists to implicate iron in stroke. In experimental models, iron depletion or chelation …

Background and Purpose High levels of glutamate in plasma and cerebrospinal fluid (CSF) have been demonstrated in patients with acute ischemic stroke. The duration of this excitatory amino acid release has not been studied, and therefore the window of opportunity of treatment with glutamate antagonists is unknown. The aim of this investigation was to study the duration of the glutamate increase in patients with stable and progressing ischemic stroke. Methods Glutamate in CSF was measured by high-performance liquid chromatography in 184 patients with an acute cerebral infarction of less than 24 hours’ duration and in 43 control subjects. Results Among the 120 patients with stable ischemic stroke, median glutamate levels were significantly lower—and within the reference range of control subjects—in those patients studied 6 to 24 hours from onset of symptoms than in patients studied in the first 6 hours (3 [range, 2 to 10] versus 5 μmol/L [range, 2 to 17]; P Conclusions The presence of glutamate increase in the CSF cannot be documented for greater than 6 hours in stable ischemic stroke. The sustained elevation of glutamate observed in progressing stroke suggests that the window to prevent neurological deterioration may be wider.

Mechanisms involved in progression of stroke are little understood. Studies in animals have shown an association between neuronal death mediated by excitatory aminoacids and deterioration in focal cerebral ischaemia. We looked for an association between concentrations of glutamate and glycine in plasma and cerebrospinal fluid (CSF) and early progression in a prospective study of 128 patients with acute ischaemic stroke.Of 556 consecutive admissions to our emergency unit, 128 eligible patients with ischaemic stroke were included in our study. Blood and CSF samples were taken within the first 24 h from stroke onset when cerebral oedema had been excluded on a previous cranial computed tomography. Ischaemic stroke was judged to be in progression if the Canadian stroke scale score (1.5 = maximum neurological deficit, 10 = no deficit) fell by 1 or more points during the first 48 h after inclusion. Glutamate and glycine concentrations in plasma and CSF were measured by high-performance liquid chromatography. The effect of plasma and CSF glutamate concentrations on progression was analysed by logistic regression.43 (33.6%) patients had progressing ischaemic stroke. Concentrations of glutamate and glycine in plasma and CSF were higher in patients with progressing stroke than in those with stable cerebral infarcts (p0.0001). There was a significant linear correlation between CSF and plasma concentrations of glutamate (r = 0.79, p0.001). The positive predictive value of a plasma glutamate concentration of more than 200 mumol/L for progression of ischaemic stroke was 97% (95% CI 85-100). Glutamate concentrations of more than 200 mumol/L in plasma and of more than 8.2 mumol/L in CSF were independently and significantly associated with progression of neurological deficit (26.1 [6.9-98.6] and 40.9 [7.6-220], respectively).Early neurological progression of acute ischaemic stroke is associated with high concentrations of glutamate in blood and CSF. Measurement of plasma glutamate may be useful for the early detection of those patients with acute stroke who will deteriorate during 48 h after onset.

En la primera parte de este trabajo se dan a conocer siete nuevas inscripciones en piedra de territorio riojano, conteniendo información novedosa principalmente sobre el ejército y las comunicaciones antiguas. En la segunda parte se recogen las inscripciones de nueve vasos cerámicos, hallados en Vareia (Varea, Logroño) y producidos en Calagurris Iulia por el officinator de esa ciudad G. Valerius Verdullus; son un magnífico exponente de la romanización del Ebro al final del período julio-claudio. The first part of this paper deals with seven new inscriptions over stone found in the territory of La Rioja, which give new information mainly about the army and the old communications. The second part deals with the inscriptions over nine ceramic vases found in Vareia (Varea, Logroño) and made in Calagurris Iulia by G. Valerius, the officinator of that town. They are a magnificent proof of the romanization of the Ebro at the end of the period JuliusClaudius.

Introduccion. El 15-30% de los ictus isquemicos son de origen cardioembolico. El ecocardiograma transtoracico desempena un papel fundamental en la evaluacion, diagnostico y manejo de la fuente embolica. La ausencia de recomendaciones oficiales para el empleo del ecocardiograma en pacientes con ictus isquemico lleva a una solicitud universal de la prueba, presentando una baja rentabilidad diagnostica. Objetivo. Analizar la rentabilidad diagnostica del ecocardiograma transtoracico en pacientes con ictus isquemico indeterminado tras la aplicacion de criterios clinicos predefinidos de riesgo. Pacientes y metodos. Se analizan los ecocardiogramas realizados a pacientes con ictus isquemico agudo solicitados durante 2009-2011 desde el servicio de neurologia. Se estudia la rentabilidad diagnostica y su aportacion al estudio etiologico. Se aplican unos �criterios de seleccion de paciente de alto riego con necesidad de realizacion de la prueba durante el ingreso� (edad < 60 anos, alteraciones en el ecocardiograma basal, cardiomegalia en la radiografia de torax basal, antecedentes de cardiopatia, sospecha clinica de endocarditis o neoplasia activa) y se analiza su validez. Resultados. De 930 pacientes, se realizo ecocardiograma a 201 (21,6%) y se detecto una fuente cardioembolica en el 9,95%. Tras la aplicacion de criterios de seleccion, el numero de ecocardiogramas paso a 97 (10,4%). Los criterios propuestos presentan: sensibilidad, 95%; especificidad, 56,9%; valor predictivo positivo, 19,6%, y valor predictivo negativo, 99%. Conclusiones. La aplicacion de nuestros criterios a pacientes con ictus indeterminado identifica con alta eficiencia la fuente cardioembolica, lo que permite la realizacion del ecocardiograma transtoracico ambulatorio en el resto de los pacientes.

Se estudia el efecto de la supresión del tratamiento con propranolol (0,5 mg/100 g rata/día) en solución acuosa, sobre la volemia y otras variables hemodinámicas en 20 ratas blancas. Paralelamente se llevaron 20 controles a los que se les administró agua destilada. La presión arterial sistólica se midió a los 20 días del tratamiento y a los 20 y 45 días de supresión de éste. A los 45 días de supresión de la droga a un subgrupo de 10 se le midió la volemia, utilizando como sustancia indicadora el Azul de Evans. Al otro subgrupo se le midió la presión arterial media, presión circulatoria media y presión venosa central en un polígrafo de 4 canales. Como resultado se obtuvo un aumento significativo del volumen sanguíneo, volumen de plasma y frecuencia cardíaca, y un aumento altamente significativo de la presión arterial media, presión arterial sistólica, presión venosa central y circulatoria media. De acuerdo con estos resultados se concluye que la supresión del propranolol provoca retención hidrosalina producto de hipertrofia tubular, lo cual pudiera esclarecer aún más el papel del riñón en la hipertensión arterial esencial.The effect of the suppression of the treatment with propranolol (0,5 mg/100 g rat/day) in aquous solution on blood volume and other hemodynamic variables was studied in 20 white rats. At the same time 20 con-trols were carried out to which distilled water was administered. The systolic arterial pressure was measured 20 days after the beginning of treatment, and 20 and 45 days after its suppression. 45 days after the drug's suppression, blood volume was measured in a subgroup of ten, using Evans' blue as an indicator substance. Mean arterial pressure, mean circulatory pressure, and central venous pressure were measured in the other subgroup by using a 4-channel polygraph. As a result, a marked increase of blood volume, plasma volume, and heart frequency was obtained. A highly significant rise of mean arterial pressure, systolic arterial pressure, central venous pressure, and mean circulatory pressure was also observed. According to the results, it is concluded that propranolol's suppression causes hydrosaline retention resulting from tubular hypertrophy, which could make even more clear the role of kidney in essential arterial hypertension.

Background and Purpose The participation of excitatory amino acids (EAAs) in the pathogenesis of ischemic neuronal lesion has been experimentally demonstrated, but clinical experience is scarce. Our objective was to examine EAA levels during the acute phase of cerebral infarction in relation to infarct size and intensity of neurological deficit. Methods Using high-performance liquid chromatography, we determined the glutamate, aspartate, taurine, and glycine concentrations in the plasma and cerebrospinal fluid (CSF) of 128 patients with ischemic cerebral infarction confirmed by CT and 43 control subjects. Blood and CSF samples were obtained on admission within the first 24 hours from symptom onset. The severity of the neurological deficit was assessed with the Canadian Stroke Scale immediately after these tests and at 48 hours after inclusion in the study. Infarct volume was determined in a second CT performed between the 4th and 7th day after the patient’s inclusion. Results The concentration of plasmatic glutamate was 121.39±80.89 μmol/L in the control group and 163.71±103.13 μmol/L in the patient group ( P =.015); in CSF it was 3.46±1.20 μmol/L in control subjects and 6.55±4.65 μmol/L in patients ( P P =.007); in CSF it was 6.18±2.28 μmol/L in control subjects and 11.23±6.96 μmol/L in patients ( P Conclusions Our results support the excitotoxic activity of glutamate and glycine in patients with cerebral infarction.

El papel del riñón en la génesis de la hipertensión arterial esencial se ha venido investigando desde hace más de 3 décadas. El propósito del presente trabajo fue valorar el comportamiento de algunas variables morfofuncionales renales en pacientes hipertensos. A voluntarios normales (40) y pacientes hipertensos (45), se les estudió el flujo plasmático renal efectivo (FPRE) mediante aclaramiento de paraminohipurato, intensidad de filtración glomerular (IFG) mediante aclaramiento de creatinina; el aclaramiento plasmático de litio (ApLi), la fracción de reabsorción de litio (FRLi), el manejo renal de sodio y potasio; así como la medición ultrasónica de los diámetros renales anteroposteriores, transversal y longitudinal con los cuales se determinó el volumen de los riñones mediante un programa de computación. Los resultados mostraron diferencias significativas en el FPRE, los diámetros renales y el volumen integrado, así como en el manejo renal del sodio. Estos resultados sugieren una retención hidrosalina en los hipertensos, lo que apoya las hipótesis que establecen la participación del riñón en la génesis de la hipertensión arterial.The role of the kidney in the genesis of essential arterial hypertension, has been investigated since more than three decades. The purposes of this article was to assess the behaviour of some renal morphofunctional variables in hypertensive patients. The effective renal plasma flow (ERPF) was studied in 40 normal volunteers and 45 hypertensive patients, by means of the paraamino-hippurate clearance, glomerular filtration rate (GFR) by means of creatinine clearance, lithium plasma clearance LiPC), lithium reabsorption fraction (LiRF), sodium and potassium renal management, as well as the ultrasonographic measurement of anteroposterior, transverse and longitudinal renal diameters, with which the kidneys volume was determined by a computed program. The results showed significant differences in ERPF, the renal diameters and the integrated volume, as well as in the sodium management. These outcomes suggest a hydrosaline retention in the hypertensive patients, and this advocates the hypothesis that they restore the kidney participation in the genesis of arterial hypertension.

Este artículo contextualiza la problemática actual de la administración de redes de comunicaciones considerando las profundas repercusiones, tanto de la internacionalización de la economía como del ritmo impetuoso del avance tecnológico sobre el sector teleinformática y la calidad en la prestación de los servicios de comunicaciones. Reseña someramente las actividades de los distintos frentes de estandarización; en particular a ISO, la ITU-T y la Internet. Se muestran, entonces, las características del soporte computacional para el desarrollo de aplicaciones, señalando los servicios de comunicaciones, interfaz gráfica y bases de datos teniendo en cuenta la naturaleza distribuida de la administración de redes. Finalmente, se muestran los atributos generales de las herramientas de desarrollo disponibles en la actualidad.

Sin resumen

Glutamate excitotoxicity, metabolic rate and inflammatory response have been associated to the deleterious effects of temperature during the acute phase of stroke. So far, the association of temperature with these mechanisms has been studied individually. However, the simultaneous study of the influence of temperature on these mechanisms is necessary to clarify their contributions to temperature-mediated ischemic damage. We used non-invasive Magnetic Resonance Spectroscopy to simultaneously measure temperature, glutamate excitotoxicity and metabolic rate in the brain in animal models of ischemia. The immune response to ischemia was measured through molecular serum markers in peripheral blood. We submitted groups of animals to different experimental conditions (hypothermia at 33°C, normothermia at 37°C and hyperthermia at 39°C), and combined these conditions with pharmacological modulation of glutamate levels in the brain through systemic injections of glutamate and oxaloacetate. We show that pharmacological modulation of glutamate levels can neutralize the deleterious effects of hyperthermia and the beneficial effects of hypothermia, however the analysis of the inflammatory response and metabolic rate, demonstrated that their effects on ischemic damage are less critical than glutamate excitotoxity. We conclude that glutamate excitotoxicity is the key molecular mechanism which is influenced by body temperature during the acute phase of brain stroke. This project has been partially supported by grants from the Spanish Ministry of Science and Innovation SAF2011-30517 and Fondo de Investigaciones Sanitarias, Instituto Salud Carlos III, RETICS-RD06/0026; Xunta de Galicia (Consellería de Innovación, Industria e Comercio: 09CSA057918PR; Consellería de Sanidade: PS09/32 and; Fundación Mútua Madrileña and by Red de Investigación Cooperativa Neurovascular SI

Trabajo publicado por Castillo J, Vivancos-Mora J, en nombre de los investigadores del registro EPICES

Trabajo publicado por Arias Rivas, Vivancos Mora y Jose Castillo, en nombre de los investigadores del registro EPICES

Trabajo publicado por Blanco, M., Vivancos-Mora J. y Castillo J, en nombre de los investigadores del registro EPICES

SYNOPSIS Clinical and pharmacological data suggest a derangement of central monoaminergic systems in tension‐type headache. Biochemical evidence has been rarely recognized. These findings may relate with pathophysiological mechanisms of headache or with underlying depression. We measured platelet‐rich plasma serotonin and plasma catecholamines (norepinephrine, epinephrine, and dopamine) in 30 patients with tension‐type headache and in 20 healthy controls, using High‐Pressure Liquid Chromatography. We studied differences between groups and the relation between biochemical parameters and clinical indices evaluating duration and severity of headache and depression. Platelet serotonin levels in tension headache patients were higher than in controls ( P

Introduccion. Los pacientes con enfermedad cerebrovascular (ECV) son un grupo de muy alto riesgo cardiovascular, ademas de por su propia patologia vascular, probablemente por un inadecuado control de factores de riesgo y por la presencia de comorbilidades. Pacientes y metodos. Estudio multicentrico, con participacion de 34 medicos de atencion primaria y registro de caracteristicas de 473 pacientes con historia de episodio de ECV que preciso hospitalizacion. Tras seguimiento clinico de la cohorte, se analizaron reingresos hospitalarios, mortalidad y causas. Resultados. La edad media de los pacientes (el 52% varones) fue de 75 ± 10 anos, y los factores de riesgo mas prevalentes fueron hipertension arterial (79%), dislipidemia (66%), obesidad (43%) y diabetes (29%). El 68% de los pacientes tenia diagnostico de ictus y el 32%, de ataque isquemico transitorio. El tiempo medio transcurrido desde el primer episodio de ECV fue de 6,6 ± 5,5 anos. Presentaban situacion de dependencia el 29% y solo un tercio mostraron buen control tensional y lipidico. Durante un seguimiento de 8,2 ± 2,3 meses, el 7,2% de los pacientes sufrio algun episodio cardiovascular (muerte u hospitalizacion), del que resultaron determinantes independientes la insuficiencia cardiaca previa (hazard ratio, HR = 2,74; intervalo de confianza del 95%, IC 95% = 1,3-5,9), la miocardiopatia (HR = 3,32; IC 95% = 1,4-8,2), la anemia (HR = 3,09; IC 95% = 1,6-6,2), la insuficiencia renal (HR = 2,4; IC 95% = 1,0-5,6), la situacion de dependencia (HR = 2,57; IC 95% = 1,3-5,7) y los ingresos cardiovasculares en el ultimo ano (HR = 3,05; IC 95% = 1,5-5,6). Conclusiones. Los pacientes con ECV seguidos en el ambito de atencion primaria presentan una prevalencia elevada y un escaso grado de control de hipertension arterial. Su pronostico esta condicionado por comorbilidades cardiovasculares y secuelas de su patologia cerebrovascular.

Introduccion. La isquemia cerebral desencadena una respuesta inflamatoria muy intensa que se caracteriza por la infiltracion de leucocitos en el parenquima cerebral. Entre estas celulas las primeras en llegar al cerebro son los neutrofilos. A pesar de ello, el papel de los neutrofilos y de la expresion de sus receptores de inmunidad innata TLR2 y TLR4 (toll-like 2 y 4) en la isquemia cerebral no esta claro. Objetivo. Estudiar la asociacion entre los niveles de neutrofilos y la expresion de TLR2 y TLR4 en dichas celulas y el pronostico de los pacientes con ictus isquemico. Pacientes y metodos. Incluimos a 110 pacientes con ictus isquemico de menos de 12 h de evolucion. Como variables principales consideramos la escala de Rankin modificada a los tres meses (mal pronostico > 2) y el volumen del infarto (medido mediante tomografia computarizada entre los dias 4 y 7). Analizamos el porcentaje de neutrofilos y la expresion media de TLR2 y TLR4 en neutrofilos a traves de citometria de flujo, al ingreso, a las 24 h, 72 h y a los 7 dias. Resultados. La expresion de TLR4 en neutrofilos a las 72 h (odds ratio, OR = 2,1; intervalo de confianza del 95%, IC 95% = 1,4-3,2) y a los 7 dias (OR = 3,2; IC 95% = 1,7-6,1) se asocio de forma independiente con el pronostico de los pacientes y con el volumen del infarto a las 72 h (B = 5,4; IC 95% = 2,9-7,8) y a los 7 dias (B = 7,0; IC 95% = 4,5-9,6). Conclusiones. Los neutrofilos a traves de la expresion de su TLR4 se asocian con el pronostico de los pacientes con ictus isquemico.

Introduccion. La gran prevalencia y morbimortalidad del ictus ha favorecido una consecuentemente amplia representacion en la medicina precientifica del pueblo gallego. Presentamos una interpretacion no estudiada hasta el momento, y que esta, por otra parte, ligada al fenomeno jacobeo: el ictus como resultado de la influencia maligna de un dragon. Otro dragon aparece citado en el Codice Calixtino como impedimento a la traslacion apostolica. Desarrollo. En el libro tercero del Codice Calixtino, donde se narran los hechos de la traslacion de los restos del apostol Santiago el Mayor desde Palestina hasta Santiago de Galicia, encontramos la principal referencia escrita de la figura del dragon del Pico Sacro. El simbolo pagano del dragon permanece acantonado en la medicina popular gallega, transmitida de forma predominantemente oral, como causante directo de procesos morbosos como el ictus. Conclusiones. En la medicina popular gallega, la patologia ictal se atribuye mayoritariamente a un subtipo del llamado `aojamiento´ o `mal de ojo´. Por vez primera, hasta donde sabemos, se revela el simbolo del dragon como explicacion magica directa de una patologia vascular cerebral. Por otra parte, la interpretacion precientifica del ictus en Galicia encuentra, en el mito del dragon, un puente de union con el relato legendario de la traslacion del apostol Santiago a Galicia. Tal relacion apoya la veracidad del relato de la traslacion del Codice Calixtino, en detrimento de reelaboraciones posteriores.

Many patients that survive stroke have to face serious functional disabilities for the rest of their lives, which is a personal drama for themselves and their relatives, and an elevated charge for society. Thus functional recovery following stroke should be a key objective for the development of new therapeutic approaches. In this series of two works we review the strategies and tools available nowadays for the evaluation of multiple aspects related to brain function (both in humans and research animals), and how they are helping neuroscientist to better understand the processes of restoration and reorganization of brain function that are triggered following stroke. We have mainly focused on magnetic resonance applications, probably the most versatile neuroimaging technique available nowadays, and that everyday surprises us with new and exciting applications. But we tackle other alternative and complementary techniques, since a multidisciplinary approach allows a wider perspective over the underlying mechanisms behind tissue repair, plastic reorganization of the brain and compensatory mechanisms that are triggered after stroke. The first of the works of this series is focused on methodological aspects that will help us to understand how it is possible to assess brain function based on different physical and physiological principles. In the second work we will focus on different practical issues related to the application of the techniques here discussed.

A pesar de la importante reduccion de su mortalidad, el ictus isquemico constituye la primera causa de morbimortalidad en el adulto en los paises industrializados. El tratamiento antiagregante ha conseguido reducir el riesgo de ictus y otros episodios vasculares. Aunque el tratamiento mas empleado es la aspirina, se han desarrollado otros antiagregantes con diferente mecanismo de accion. El clopidogrel bloquea la agregacion plaquetaria al inhibir el receptor de adenosin difosfato y la subsecuente activacion del complejo IIb/IIIa. Ademas de su poder antiagregante, tambien presenta efectos pleiotropicos, disminuyendo los mecanismos inflamatorios que se producen durante la isquemia. El clopidogrel ha demostrado un beneficio con respecto a la aspirina en la prevencion de episodios vasculares, sobre todo en pacientes de alto riesgo vascular. En este articulo revisamos los principales estudios que se han realizado con clopidogrel en la prevencion de ictus isquemico, tanto en monoterapia como en combinacion con otros antiagregantes.

Introduccion. Los modelos animales de isquemia cerebral son indispensables en la investigacion de la patologia cerebrovascular. Actualmente, no existe un modelo experimental que refleje perfectamente la fisiopatologia del ictus, por lo que la seleccion de este es fundamental para una interpretacion correcta de los resultados obtenidos. Objetivo. Caracterizar la evolucion temporal de tres modelos comunes de isquemia cerebral focal permanente mediante resonancia magnetica. Materiales y metodos. Treinta ratas macho Sprague-Dawley se dividieron en tres grupos, cada uno sometido a los siguientes modelos quirurgicos: sutura intracraneal de la arteria cerebral media (ACM), electrocoagulacion de la ACM y oclusion intraluminal de la ACM. Cada animal se sometio a una exploracion por resonancia magnetica los dias 1, 2, 3, 4, 7 y 14 tras la cirugia. A partir de imagenes adquiridas con secuencias potenciadas en T2 se calcularon tanto el volumen de lesion como el grado de edema. Resultados. El modelo intraluminal presento mayor volumen de infarto (media: 297 ± 163 mm3 de volumen maximo) y mayor edema (media: 17 ± 9% de edema maximo) frente al modelo de sutura intracraneal (178 ± 62 mm3 y 9 ± 6%, respectivamente) y electrocoagulacion (181 ± 45 mm3 y 9 ± 6%, respectivamente). Discusion. Pese a presentar una mayor mortalidad (28%), el modelo de oclusion intraluminal de la ACM es el mas adecuado para estudios a largo plazo al no precisar craneotomia, al contrario que los modelos transcraneales. El modelo de oclusion por electrocoagulacion muestra una region cerebral de lesion no isquemica y una evolucion de la lesion diferente a los otros dos modelos.

Muchos pacientes que sobreviven a un ictus se enfrentan a serias discapacidades funcionales durante el resto de sus vidas, lo que supone un drama personal para si mismos y sus allegados, y un elevado coste para la sociedad. Por ello, la recuperacion funcional del sujeto tras un ictus debe ser un objetivo esencial que habria que considerar en el desarrollo de nuevas aproximaciones terapeuticas. Este es el segundo de una serie de dos trabajos en los que revisamos las estrategias y herramientas disponibles hoy en dia para la evaluacion de multiples aspectos relacionados con la funcion cerebral (tanto en humanos como en animales de experimentacion), y que estan ayudando a los neurocientificos a entender mejor los procesos de restauracion y reorganizacion de la funcion cerebral que se inician tras un ictus, partiendo de la premisa de que una aproximacion multidisciplinar proporciona una perspectiva mas completa de los mecanismos que subyacen bajo los procesos de reparacion tisular, de reorganizacion plastica del cerebro y de los compensatorios que se desencadenan tras un ictus. En el segundo de los trabajos de esta serie nos centramos en una serie de tecnicas complementarias basadas en la imagen por resonancia magnetica y que no se engloban dentro de los grupos de tecnicas discutidos en el primer trabajo de esta serie, bien por abordar aspectos no relacionados directamente con la funcion cerebral, aunque si lo hacen de forma indirecta, bien por estar basados en principios fisicoquimicos o fisiologicos diferentes a los ya discutidos.

The MR findings in 27 patients with myotonic dystrophy were compared with those observed in 11 patients with other muscular dystrophies: six with limb-girdle dystrophy, three with facioscapulohumeral muscular dystrophy and two with Becker-type muscular dystrophy. Clinical status was graded into 10 stages. The MR study was performed at the medium third of the thigh, with a slice thickness of 7.5 mm (TR: 750/TE: 25 for T 1 ; TR: 2200/TE: 30/90 for DP/T 2 ). Muscle signal intensity was evaluated with a four-point grading scale using subcutaneous fat as a reference. Statistical analysis was done using the Mann-Whitney-Wilcoxon's test and simple linear regression. In the myotonic dystrophy group, 81.4% of the patients showed an abnormal signal at the crural muscle level, adopting a semilunar shape around the anteroexternal side of the femur. The presence and intensity of this hyperintense signal correlated positively with the duration of disease ( r =0.54) and the clinical stage ( r =0.69). Of the 11 patients with other muscular dystrophies, only three (27.2%) showed hyperintense signal at the crural muscle level. MR imaging of patients with muscle disease may contribute to the in vivo study of muscular dystrophy, its differential diagnosis and the detection of asymptomatic patients.

We measured platelet-rich plasma (PRP) serotonin in patients suffering from tension-type headache, before and after treatment with amitriptyline, comparing them with a healthy control group and patients with untreated depression. We evaluated the severity of headache and depression in each group. PRP serotonin levels were higher in patients with headache than in controls and depressed patients. We observed a fall of PRP serotonin in patients with tension-type headache to similar levels after treatment as the depressed group. This fall was correlated with the improvement of headache but not with depression scales. Our data suggest that the rise of platelet serotonin levels in tension-type headache is related to pain and not depression.

There is clinical and pharmacological evidence of the existence of sympathetic dysfunction in migraine. Adrenaline and noradrenaline concentrations were determined in plasma and CSF of patients during attacks of common or classic migraine, comparing them with controls suffering from stress. Plasma noradrenaline levels were significantly lower in the patients with common migraine than in controls (p < 0.05). Other catecholamine levels in plasma and CSF in both migraine groups were only slightly lower than in controls. Our results suggest that central sympathetic dysfunction exists in patients with migraine.

Taurine is the amino acid with the highest concentration in the human body. Its physiologic functions are not yet well understood. As a neurotransmitter or neuromodulator it may display inhibitory functions. We have measured taurine levels in plasma and cerebrospinal fluid of migraine patients during attacks, comparing them with controls. Patients with migraine had significantly higher concentrations than controls. No sex or age influence over the amino acid levels were observed. Plasma taurine levels in patients with classic migraine correlated negatively with severity of headache. Central taurine liberation during migraine crisis may be due to spontaneous depolarization or a defensive reaction in the context of cerebral homeostatic processes.