domingo, 10 de abril de 2011
TIC y EDUCACIÓN... ¿Cambiará la escuela?
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TIC y EDUCACIÓN... ¿Cambiará la escuela?
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El Futuro del Aprendizaje
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El Futuro del Aprendizaje
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Brain And Hypertension
Brain And Hypertension
The risk of stroke is directly related to arterial pressure, and this graded relationship appears to be maintained even within the normal range of diastolic blood pressure. Meta-analysis of nine prospective observational studies confirmed that there is no convincing evidence of a ‘threshold’ level of diastolic blood pressure at which risk begins. In general, with sustained increases in diastolic blood pressure of 5, 7.5 and 10 mmHg, there are corresponding increases in stroke risk of 34, 46 and 56%, respectively. Of the factors that predict stroke, blood pressure is dominant, although other independent risk factors have been identified and these include smoking, obesity and plasma levels of fibrinogen.
The incidence of stroke remains particularly low in some lessdeveloped countries where the average diastolic blood pressure may be only 60 mmHg. In China, Japan and parts of Africa, high blood pressure and stroke are common but coronary artery disease is relatively infrequent. This discrepancy, at least in the Far East, is probably due to differences in prevailing levels of blood cholesterol and low-density lipoproteins (LDL).
Just over 10% of all clinical strokes are caused by cerebral hemorrhage. Hemorrhages in hypertension are caused by rupture of microaneurysms that develop on the short penetrating branches of the main cerebral arteries. Such small aneurysms have been identified on arteries 50–220 μm in diameter, principally at sites of branching, and are particularly frequently seen in the distribution of the lateral lenticulostriate artery. The density of lesions tends to be highest in the putamen, globus pallidus, caudate nucleus, thalamus, external capsule and basis pontis. Hemorrhage into the putamen is especially frequent , and presents as weakness of the contralateral face, arm and leg, sometimes with hyperreflexia at an early stage.
Large lesions cause hemisensory loss and hemianopia with conjugate deviation of the eyes, reduced consciousness and aphasia, or visuospatial . Another brain lesion associated with uncontrolled hypertension is a small infarct which evolves into a slit-like space or lacune 0.5–15.0 mm in diameter. These small deep
infarcts are often undetectable on computed tomography (CT), and are the result of occlusion of one of the same perforating arteries that rupture in hypertensive cerebral hemorrhage.
The arteries immediately proximal to small infarcts show segmental disorganization of the vessel wall, possibly resulting from mechanical disruption of the intima and insudation of plasma constituents. Such changes are seen in small arteries that are close to high-pressure arteries, but not in vessels of the same caliber at more remote sites.
The relative underdevelopment of the muscle and elastic tissue layers of these particular small brain arteries may contribute to their vulnerability. Intraluminal pressures may also be higher in these arteries immediately proximal to small infarcts show segmental disorganization of the vessel wall, possibly resulting from mechanical disruption of the intima and insudation of plasma constituents. Such changes are seen in small arteries that are close to high-pressure arteries, but not in vessels of the same caliber at more remote sites. The relative underdevelopment of the muscle and elastic tissue layers of these particular small brain arteries may contribute to their vulnerability. Intraluminal pressures may also be higher in these countries and most usually present as episodes of pure motor hemiparesis, pure sensory stroke or ataxic hemiparesis.
Symptoms may evolve progressively over a period of 24–48 hours. Because subcortical white matter is involved, there are no signs of cortical dysfunction such as dysphagia, neglect, agnosia, or apraxia. Transient ischemic attacks may also occur. It is not difficult to understand that the incidences of hemorrhage and lacunar infarction are greatly reduced by effective treatment of chronic hypertension.
Most strokes in Western populations are due to atheromatous disease, often affecting extracranial vessels, especially the origin of the internal carotid artery. This predilection to atheroma is probably explained by the turbulent blood flow at a point of arterial bifurcation causing alterations in endothelial function.
Atheroma within the proximal internal carotid artery most often causes cerebral infarction in the distribution of the middle cerebral artery. Vascular occlusion is initiated by rupture of the fibrous cap of an atherosclerotic plaque with superimposed thrombosis. Artery-to-artery embolism is the predominant mechanism of transient ischemic attacks (TIAs) in carotid artery stenosis. In some cases, the fragmented emboli can sometimes be
visualized as refractile cholesterol-rich deposits at points where the retinal arterioles branch.
The velocity of blood flow in narrowed vessels is increased, and this acceleration may be detected by Doppler ultrasonography in combination with a two-dimensional image of the structures referred to as the duplex method with color flow imaging. Because Doppler misclassifies a proportion of carotid artery lesions, computed tomographic angiography or magnetic resonance angiography is increasingly used to supplement or
replace ultrasonography. Most TIAs in the territory of a stenosed internal carotid artery are caused by either atheroembolism with resultant hemiparesis or amaurosis fugax.
Clinical trials have clearly shown that drug treatment of hypertension reduces the incidence of stroke by about 40% and benefit accrues after relatively short periods of reduction in blood pressure. Benefits are especially seen in men or women of African-American origin and in elderly patients with isolated systolic hypertension or diabetes. Monotherapy is not effective in about 40% of patients; these patients require more than one drug and sometimes several different drugs.
Treatment trials have not differentiated between hemorrhagic stroke, lacunar events and large artery disease and cardioembolism. In primary prevention, there is some evidence from the Hypertension Optimal Treatment (HOT) study that aspirin in patients with well-controlled arterial pressures reduces the risk of myocardial events but, if pressures are poorly controlled, then there is little evidence that aspirin is of benefit. In secondary prevention of stroke, results of the PROGRESS trial showed that treatment based on an angiotensin converting enzyme (ACE) inhibitor and thiazide diuretics were effective in reducing risk of re-occurrence of major vascular events, but treatment was not started until at least 2 weeks from the acute event. Benefits extended to patients with normal levels of blood pressure. There have been concerns about antihypertensive therapy immediately after stroke when cerebral autoregulation is impaired, but there is, as yet, little evidence from clinical trials about the safety (or otherwise) of early antihypertensive therapy.
Antiplatelet agents such as aspirin or clopidogrel are also routinely used for prevention of ischemic
strokes, and the combination of aspirin and dipyridamole may also be effective. In the presence of large artery atherosclerosis causing carotid or extracranial vertebral artery stenosis, antihypertensive drugs have the potential to cause ischemic events if the degree of narrowing is critical. In practice, such events seem to occur rather infrequently. Symptomatic carotid stenoses greater than 70% are treated by endarterectomy and trials of angioplasty and stent insertion are ongoing. There is less certainty about the role of surgery in asymptomatic patients and various algorithms have been proposed to quantify risk in individual patients.
The incidence of stroke remains particularly low in some lessdeveloped countries where the average diastolic blood pressure may be only 60 mmHg. In China, Japan and parts of Africa, high blood pressure and stroke are common but coronary artery disease is relatively infrequent. This discrepancy, at least in the Far East, is probably due to differences in prevailing levels of blood cholesterol and low-density lipoproteins (LDL).
Just over 10% of all clinical strokes are caused by cerebral hemorrhage. Hemorrhages in hypertension are caused by rupture of microaneurysms that develop on the short penetrating branches of the main cerebral arteries. Such small aneurysms have been identified on arteries 50–220 μm in diameter, principally at sites of branching, and are particularly frequently seen in the distribution of the lateral lenticulostriate artery. The density of lesions tends to be highest in the putamen, globus pallidus, caudate nucleus, thalamus, external capsule and basis pontis. Hemorrhage into the putamen is especially frequent , and presents as weakness of the contralateral face, arm and leg, sometimes with hyperreflexia at an early stage.
Large lesions cause hemisensory loss and hemianopia with conjugate deviation of the eyes, reduced consciousness and aphasia, or visuospatial . Another brain lesion associated with uncontrolled hypertension is a small infarct which evolves into a slit-like space or lacune 0.5–15.0 mm in diameter. These small deep
infarcts are often undetectable on computed tomography (CT), and are the result of occlusion of one of the same perforating arteries that rupture in hypertensive cerebral hemorrhage.
The arteries immediately proximal to small infarcts show segmental disorganization of the vessel wall, possibly resulting from mechanical disruption of the intima and insudation of plasma constituents. Such changes are seen in small arteries that are close to high-pressure arteries, but not in vessels of the same caliber at more remote sites.
The relative underdevelopment of the muscle and elastic tissue layers of these particular small brain arteries may contribute to their vulnerability. Intraluminal pressures may also be higher in these arteries immediately proximal to small infarcts show segmental disorganization of the vessel wall, possibly resulting from mechanical disruption of the intima and insudation of plasma constituents. Such changes are seen in small arteries that are close to high-pressure arteries, but not in vessels of the same caliber at more remote sites. The relative underdevelopment of the muscle and elastic tissue layers of these particular small brain arteries may contribute to their vulnerability. Intraluminal pressures may also be higher in these countries and most usually present as episodes of pure motor hemiparesis, pure sensory stroke or ataxic hemiparesis.
Symptoms may evolve progressively over a period of 24–48 hours. Because subcortical white matter is involved, there are no signs of cortical dysfunction such as dysphagia, neglect, agnosia, or apraxia. Transient ischemic attacks may also occur. It is not difficult to understand that the incidences of hemorrhage and lacunar infarction are greatly reduced by effective treatment of chronic hypertension.
Most strokes in Western populations are due to atheromatous disease, often affecting extracranial vessels, especially the origin of the internal carotid artery. This predilection to atheroma is probably explained by the turbulent blood flow at a point of arterial bifurcation causing alterations in endothelial function.
Atheroma within the proximal internal carotid artery most often causes cerebral infarction in the distribution of the middle cerebral artery. Vascular occlusion is initiated by rupture of the fibrous cap of an atherosclerotic plaque with superimposed thrombosis. Artery-to-artery embolism is the predominant mechanism of transient ischemic attacks (TIAs) in carotid artery stenosis. In some cases, the fragmented emboli can sometimes be
visualized as refractile cholesterol-rich deposits at points where the retinal arterioles branch.
The velocity of blood flow in narrowed vessels is increased, and this acceleration may be detected by Doppler ultrasonography in combination with a two-dimensional image of the structures referred to as the duplex method with color flow imaging. Because Doppler misclassifies a proportion of carotid artery lesions, computed tomographic angiography or magnetic resonance angiography is increasingly used to supplement or
replace ultrasonography. Most TIAs in the territory of a stenosed internal carotid artery are caused by either atheroembolism with resultant hemiparesis or amaurosis fugax.
Clinical trials have clearly shown that drug treatment of hypertension reduces the incidence of stroke by about 40% and benefit accrues after relatively short periods of reduction in blood pressure. Benefits are especially seen in men or women of African-American origin and in elderly patients with isolated systolic hypertension or diabetes. Monotherapy is not effective in about 40% of patients; these patients require more than one drug and sometimes several different drugs.
Treatment trials have not differentiated between hemorrhagic stroke, lacunar events and large artery disease and cardioembolism. In primary prevention, there is some evidence from the Hypertension Optimal Treatment (HOT) study that aspirin in patients with well-controlled arterial pressures reduces the risk of myocardial events but, if pressures are poorly controlled, then there is little evidence that aspirin is of benefit. In secondary prevention of stroke, results of the PROGRESS trial showed that treatment based on an angiotensin converting enzyme (ACE) inhibitor and thiazide diuretics were effective in reducing risk of re-occurrence of major vascular events, but treatment was not started until at least 2 weeks from the acute event. Benefits extended to patients with normal levels of blood pressure. There have been concerns about antihypertensive therapy immediately after stroke when cerebral autoregulation is impaired, but there is, as yet, little evidence from clinical trials about the safety (or otherwise) of early antihypertensive therapy.
Antiplatelet agents such as aspirin or clopidogrel are also routinely used for prevention of ischemic
strokes, and the combination of aspirin and dipyridamole may also be effective. In the presence of large artery atherosclerosis causing carotid or extracranial vertebral artery stenosis, antihypertensive drugs have the potential to cause ischemic events if the degree of narrowing is critical. In practice, such events seem to occur rather infrequently. Symptomatic carotid stenoses greater than 70% are treated by endarterectomy and trials of angioplasty and stent insertion are ongoing. There is less certainty about the role of surgery in asymptomatic patients and various algorithms have been proposed to quantify risk in individual patients.
BIBLIOTECA MEDICA
BIBLIOTECA MEDICA |
Posted: 09 Apr 2011 09:55 PM PDT ¿Qué es? Un trastorno alimenticio inverso a la anorexia: Las personas se ven delgadas pero en realidad están excedidas de peso. Es sabido que el sobrepeso y la obesidad son grandes problemas de salud mundial que se han incrementado a tal punto en los últimos años, incluso entre los más jóvenes y los niños, que han llegado a transformarse en una gran epidemia. En este contexto es que una |
Arts
Arts
THEATER
Putting the Juice in 'Jerusalem'
By PATRICK HEALY
Mark Rylance is back on Broadway for the second time this season, in the attention-getting role of Rooster Byron in "Jerusalem."
MUSIC
He Can Sing It, if Not Speak It
By BEN RATLIFF
Bill Callahan, 44, sinks into his baritone on his latest album, "Apocalypse," though he still mostly avoids face-to-face interviews.
A Composer Not Afraid to Mash Things Up
By ALLAN KOZINN
Avner Dorman, who is known for outlandish musical combinations, will unveil a new work this week at the 92nd Street Y.
James Brown and Al Pacino, Salsa Added
John Leguizamo draws from the dances of decades (and from a movie star or two) for his kinetic movement in his Broadway show "Ghetto Klown."
Receptores GABA-A como dianas moleculares de los anestésicos generales: identificación de los sitios de unión provee pistas para la modulación alostérica.
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sábado, 9 de abril de 2011
Validación de una escala de medición del dolor en pacientes sometidos a ventilación mecánica
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[Comenta este artículo] [Primera página: http://medicina-intensiva.com]
[Comenta este artículo] [Primera página: http://medicina-intensiva.com]
Artículo nº 1621. Vol 11 nº 4, abril 2011.
Autor: José Manuel Velasco Bueno
Autor: José Manuel Velasco Bueno
Validación de una escala de medición del dolor en pacientes sometidos a ventilación mecánica
Artículo Original: Latorre Marco I, Solís Muñoz M, Falero Ruiz T, Larrasquitu Sánchez A, Romay Pérez A.B, Millán Santos I. Validación de la Escala de Conductas Indicadoras de Dolor para valorar el dolor en pacientes críticos, no comunicativos y sometidos a ventilación mecánica: resultados del proyecto ESCID. Enferm Intensiva 2011; 22: 3-12. [Resumen] [Artículos relacionados]
Introducción: La valoración y control del dolor cobra especial importancia en el cuidado de los pacientes críticos. En pacientes conscientes y con sus capacidades comunicativas conservadas el mejor instrumento de medición del mismo y de sus características es la manifestación del propio paciente. En pacientes sometidos a ventilación mecánica y con dificultad para expresarse son necesarios otros métodos de valoración y cuantificación de la intensidad del dolor. El Grupo de Trabajo de Analgesia y Sedación de la SEMYCIUC en un documento de consenso propone la utilización de la escala de Campbell para este fin, reconociendo la necesidad de su validación [1] .
Resumen: La escala sobre Conductas Indicadoras de Dolor (ESCID) es una propuesta de modificación de la escala de Campbell cuya diferencia radica en que sustituye la valoración de la respuesta verbal del paciente por la adaptación a la ventilación mecánica. Este estudio tiene como objetivo determinar la validez y fiabilidad de la ESCID para valorar el dolor en pacientes no comunicativos sometidos a ventilación mecánica. Para ello se midió el dolor por parte de evaluadores independientes, con esta escala y con otra validada y aceptada para tal fin (Behavioural Pain Scale), ante dos procedimientos dolorosos y en distintos momentos (antes, durante y después del procedimiento). Realizaron 480 observaciones en 42 pacientes. Se obtuvo una adecuada consistencia interna para cada uno de los cinco ítems que conforman la escala (coeficiente alfa de Cronbach entre 0,70 y 0,80). Se observó una buena concordancia intra e interobservador con las dos escalas en los tres momentos en que se aplicaron sin que aparecieran diferencias significativas entre las mediciones. Igualmente se observó una buena correlación entre la escala a validar y la ya validada (correlación de Pearson de 0,97 antes del procedimiento, 0,94 durante y 0,95 después).
Comentario: A la luz de los resultados del presente estudio podría recomendarse el uso de esta escala para la detección y medición del dolor en pacientes críticos, no comunicativos y sometidos a ventilación mecánica. Lógicamente esta valoración no tiene mucho sentido si no va acompañada de una adecuación de la pauta analgésica para cada caso. Otros estudios han destacado la tendencia de los profesionales sanitarios a infravalorar el grado de dolor de los pacientes señalando que un porcentaje considerable refirió dolor de intensidad moderada a grave durante más del 50% de su estancia hospitalaria.
Tabla I. Escala de Conductas Indicadoras de Dolor (ESCID)
0 | 1 | 2 | Puntuación parcial | |
Musculatura facial | Relajada | En tensión, ceño fruncido/gesto de dolor | Ceño fruncido de forma habitual/ dientes apretados | |
“Tranquilidad” | Tranquilo, relajado, movimientos normales | Movimientos ocasionales de inquietud y/o posición | Movimientos frecuentes, incluyendo cabeza o extremidades | |
Tono muscular | Normal | Aumentado. Flexión de dedos de manos y/o pies | Rígido | |
Adaptación a ventilación mecánica (VM) | Tolerando ventilación mecánica | Tose, pero tolera VM | Lucha con el respirador | |
Confortabilidad | Confortable, tranquilo | Se tranquiliza al tacto y/o a la voz. Fácil de distraer | Difícil de confortar al tacto o hablándole | |
Puntuación total (máximo 10): | ||||
0: no dolor | 1-3: dolor leve-moderado | 4-6: dolor moderado-grave | > 6: dolor muy intenso | |
Considerar otras posibles causas |
José Manuel Velasco Bueno
Hospital Clínico Universitario, Málaga.
REMI. http://medicina-intensiva.com. Abril, 2011.
Hospital Clínico Universitario, Málaga.
REMI. http://medicina-intensiva.com. Abril, 2011.
Enlaces:
- Pardo C, Muñoz T, Chamorro C; Grupo de Trabajo de Analgesia y Sedación de la SEMICYUC. Monitoring of pain. Recommendations of the Analgesia and Sedation Work Group of SEMICYUC. Med Intensiva 2008; 32(S1): 38-44. [PubMed]
- Sessler CN, Grap MJ, Ramsay MA. Evaluating and monitoring analgesia and sedation in the intensive care unit. Crit Care 2008; 12(Suppl 3): S2. [PubMed]
Búsqueda en PubMed:
- Enunciado: Medición del dolor en pacientes críticos sometidos a ventilación mecánica
- Sintaxis: pain measurement[mh] AND mechanical ventilation AND critical illness[mh]
- [Resultados]
Lo que pasa en nuestros cerebros cuando leemos, en pantalla o papel, una historia
Lo que pasa en nuestros cerebros cuando leemos, en pantalla o papel, una historia
Dolors Reig | Friday, April 8th, 2011 | 1 Comentario / Referencia »“El sentimiento que experimentamos al contemplar un cuadro, no se puede distinguir del cuadro ni de nosotros mismos. El sentimiento, el cuadro y nosotros mismos estamos reunidos en nuestro misterio”
René Magritte en una carta a P. Colinet en 1975
Hay mucho de la idea de flujo de Csíkszentmihályi en la lectura, uno de los formatos más universales para contar historias unos cuentos, relatos, que son, según múltiples investigaciones, casi vividos a juzgar por nuestra actividad cerebral.
Es probable que esté en ese aspecto, en el hecho de que percibamos la historia en cuestión como si la estuviéramos viviendo, una de las claves del éxito de la aplicación de la perspectiva del storytelling a juegos, compras, lecciones y cualquier otro tipo de narrativa que requiera motivación.
Me ha gustado especialmente la entrevista a Livia Blackburne, autora de From Words To Brain, acerca de qué procesos cerebrales están implicados en la lectura, procesos que ya observábamos en cuanto a los juegos en Digital Nation y que pueden generalizarse a lo que ocurre cuando nos acercamos y nos sumergimos en cualquier tipo de historia.
De este modo, el autor recomienda que al escribir usemos palabras que evoquen emociones, descripciones vívidas y un lenguaje preciso que permita al lector dibujarse una imagen de lo que está ocurriendo. Debemos conseguir que el lector se identifique con los personajes, que empatice con ellos, nos dice. Crear situaciones que guarden similitudes con lo que el lector haya experimentado en algún momento de su vida provocará mayor empatía.
Leer una página o pantalla puede activar nuestros cerebros al menos de dos modos distintos. Primero las palabras activarán una red específica para el lenguaje en nuestros hemisferios izquierdos. Después, a un nivel más profundo, los lectores mostrarán actividad cerebral en distintas zonas, dependientes del significado de las palabras. Como decíamos al comenzar, algunas áreas de la imaginación son las mismas que utilizamos para procesar los eventos que efectivamente experimentamos.
Por ejemplo, una descripción visual vívida activará regiones visuales, mientras que descripciones de los pensamientos y motivaciones de un personaje activarán porciones del cerebro relacionadas con el razonamiento social. Y eso de forma parecida a lo que pasa cuando vemos películas, escuchamos una historia, jugamos un videojuego o, añado, interactuamos en redes sociales virtuales (lo explicamos en el enlace).
¿Porqué nos gustan tanto las historias?
Todavía más interesante resulta su explicación acerca de la potencia de las historias, del también llamado “storytelling”, centrada en cómo las vivenciamos, en qué funciones cumplen:
Nuestros cerebros parecen programados para buscar significados, las causas de lo que va ocurriendo a nuestro alrededor. Queremos dar sentido al mundo y las historias siguen esa lógica, la de ayudar a dar sentido y estructurar el mundo.
En segundo lugar, somos animales sociales. Nos gusta pasar tiempo con otros, escuchar acerca de las cosas que les pasan, lo cual crea un interés evidente sobre las historias que nos llegan.
En tercero, tal y como hemos explicado antes aquí al hablar de las neuronas espejo y su función adaptativa, las historias son una forma de traspasar información a los demás, de enseñar. Aprendemos de lo que ocurre a los demás, sobre situaciones que no hemos experimentado.
En fin… os dejo con los interesantísimos derechos del lector:
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