Información y Formación Médica.

19/03/2017

La Residencia Médica: el paraíso anhelado por todo médico:

https://youtu.be/P8RQSpTtAAA

Los residentes médicos son vulnerables a un trato violento y discriminatorio por la organización militar que se aplica en los hospitales, lo que aunado a sem...

23/11/2015

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23/11/2015

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New research finds cortical lamination speeds up neuronal circuit formation, but is not an essential feature for circuit function.

03/11/2015

Médicos, jueces y brujos en el siglo XVII

Los etnólogos saben perfectamente que la medicina puede ser analizada desde el punto de vista de su funcionamiento social, y dicho análisis no concierne exclusivamente a la persona del médico -con su poder, sus secretos, sus amenazas, sus prescripciones y toda la fuerza inquietante que posee- sino también a las formas que adopta su práctica y a los objetos que pueden ser medicalizados.

Cada cultura define de una forma propia y particular el ámbito de los sufrimientos, de las anomalías, de las desviaciones, de las perturbaciones funcionales, de los trastornos de conducta que corresponden a la medicina, suscitan su intervención y le exigen una práctica específicamente adaptada. En último término no existe un ámbito que pertenezca de pleno derecho y de modo universal a la medicina.

La medicina del siglo XIX creyó que establecía lo que se podría denominar las normas de lo patológico, creyó conocer lo que en todos los lugares y en todos los tiempos debería ser considerado como enfermedad, creyó poder diagnosticar retrospectivamente todo aquello que debería haber sido discernido como patológico pese a que se le confirió, por ignorancia, un estatuto distinto.

La medicina de hoy ha llegado a ser consciente de la relatividad de lo normal y de las considerables variaciones a las que se ve sometido el umbral de lo patológico: variaciones que radican en el propio saber médico, en sus técnicas de investigación y de intervención, en el grado de medicalización alcanzado por un país, pero también en las normas de vida de la población, en su sistema de valores y en sus grados de sensibilidad, en su relación con la muerte, con las formas de trabajo impuestas, en fin, con la organización económica y social. En último término la enfermedad es, en una época determinada y en una sociedad concreta, aquello que se encuentra práctica o teóricamente medicalizado. Ya es hora de que esta nueva conciencia de la medicina pase a ser objeto de análisis histórico. Durante demasiado tiempo la historia de la medicina ha sido una cronología de los descubrimientos: se contaba cómo la razón o la observación habían triunfado sobre los prejuicios, sorteando los obstáculos e iluminando las verdades ocultas.

En realidad, si de verdad se quiere que la historia de las ciencias o de las ideas adquiera un mayor rigor y pueda articularse con otras disciplinas tales como la sociología o la historia económica, es preciso sin duda alguna desplazar su territorio tradicional y sus métodos. Hay que intentar sin que se pueda evidentemente lograrlo por completo- etnologizar la mirada que nosotros dirigimos sobre nuestros propios conocimientos: captar no sólo la forma mediante la cual se utiliza el saber científico, sino también el modo en el que son delimitados los ámbitos que este saber científico domina, así como el proceso de formación de sus objetos de conocimiento y el ritmo de creación de sus conceptos.

Hay que restituir, en el interior de una formación social, el proceso mediante el cual se constituye un "saber", entendiendo éste como el espacio de las cosas a conocer, la suma de los conocimientos efectivos, los instrumentos materiales o teóricos que lo perpetúan. De este modo la historia de una ciencia ya no será la simple memoria de sus errores pasados, o de sus medias verdades, sino que será el análisis de sus condiciones de existencia, de sus leyes de funcionamiento y de sus reglas de transformación. (Foucault)

03/11/2015

Chronic fatigue syndrome: what is it and how to treat? Ever since neurologist George Miller Beard coined the term neurasthenia in the 19th century,1 dozens of names have been used to describe illnesses resembling chronic fatigue syndrome. The diverse nomenclature refl ects heterogeneity in the disorder’s conceptualisation, spawning terms as divergent as chronic Epstein–Barr virus, epidemic neuro myasthenia, systemic exertion intolerance disease, post-viral fatigue syndrome, myalgic encephalomyelitis, and chronic fatigue immune dysfunction syndrome. The diversity in nomenclature parallels the diversity in therapies assessed for this frequently refractory cluster of symptoms, which include pharmacological (eg, fl uoxetine, rintatolimod, galantamine), psychological (eg, cognitive therapy, adaptive pacing therapy), and lifestyle interventions (eg, exercise).2 In Lancet Psychiatry, Michael Sharpe and colleagues3 report the 2·5 year long-term follow-up of the PACE trial, a 2011 multicentre, four-arm, randomised controlled trial of 641 individuals with diagnosed chronic fatigue syndrome to compare the eff ect of four nonphamacological therapies (standard medical care alone [SMC]), adaptive pacing therapy [APT], graded exercise therapy [GET], and cognitive behavioural therapy [CBT]) on self-rated levels of fatigue and physical functioning.4 Initial results of the trial showed clear superiority of augmenting SMC with CBT or GET, but not APT, to SMC alone on fatigue and physical function at 12 months.4 For their follow-up study, Sharpe and colleagues3 accumulated postal responses from 481 of the original 641 participants, who reported their level of fatigue, physical functioning, and whether they had received any further study treatments since study conclusion. Interestingly, individuals who originally received CBT and GET maintained improvement in fatigue and physical functioning at follow-up (median 31 months after randomisation; range 24–53), irrespective of whether they received any further treatment. Individuals who received APT or SMC alone displayed improvement in fatigue and physical functioning irrespective of receiving further treatment, such that no diff erence in outcomes was evident between any of the original treatment groups at long-term follow-up. Finally, individuals allocated to APT or SMC alone in the original trial were more likely than other participants to receive CBT, GET, or both treatments, during the followup period.3 The authors hypothesise that the improvement in the APT and SMC only groups might be attributed to the eff ects of post-trial CBT or GET, because more people from these groups accessed these therapies during follow-up. However, improvement was observed in these groups irrespective of whether these treatments were received, and thus this hypothesis remains unproven. Overall, our interpretation of these results is that structured CBT and GET seems to accelerate improvement of self-rated symptoms of chronic fatigue syndrome compared with SMC or SMC augmented with APT, an important fi nding in an illness with few treatment options and substantial morbidity. But why would these therapies accelerate symptom improvement? The boundaries of chronic fatigue syndrome and related entities are not clear and considerably overlap with other neuropsychiatric disorders (eg, depression). Theories about the patho physiology of chronic fatigue syndrome might be best considered when divided into aetiopathogenic (casual) factors and neurobiological manifestations. Hypothesised causal factors might include infection, environmental exposures, translocation of gut commensal bacteria, allergies, and physiological and psychosocial stress.5 These factors theoretically aff ect neurobiological processes involved in a wide range of neuropsychiatric disorders, including neuro endocrinology, neuro trans mission, neuroplasticity, oxidative and nitrosative stress regulation, mitochondrial function, and neuro immunology.6 The neuroimmunology of fatigue is increasingly researched, showing associations with increased concentrations of proinfl ammatory cytokines, oxidative stress, and activated Toll-like receptors.6 Single nucleotide polymorphisms for genes representing the complement cascade, chemokines, and Toll-like receptor signalling have been associated with altered immune responses seen in chronic fatigue syndrome.5 Additionally, a 2014 neuroimaging study in patients with chronic fatigue syndrome used positron emission tomography to show evidence of widespread glial activation (representing neuroinfl ammation) with degree of activation associated with severity of neuropsychological symptoms (eg, cognitive impairment, pain, and depression).7 These neuroimmunological f i ndings could assist understanding for eff ectiveness of the PACE trial treatments, as well as other novel interventions for chronic fatigue syndrome. For example, exercise therapy might improve symptoms of chronic fatigue syndrome thorough benefi cial eff ects on neuronal functions via anti-infl ammatory and antioxidant actions.8 Intriguingly, CBT has also been suggested to have antiinfl ammatory properties.9 An increased understanding of the pathogenesis of chronic fatigue syndrome could lead to development of new diagnostic and therapeutic interventions. An early example of this is rituximab, a B-cell-depleting monoclonal antibody against the B-cell protein CD20, which has shown promise in early trials10 for chronic fatigue syndrome and is now being examined in a randomised controlled trial (ClinicalTrials.gov identifi er: NCT02229942). New treatments like this have been sparse for many neuropsychiatric disorders over the past few decades. An increasing appreciation of the pathophysiological role of neuroimmunological pathways in these disorders opens many new avenues to explore. Recent evidence that suggests the eff ectiveness of mechanistically inspired therapies such as antioxidants and anti-infl ammatory agents in diverse neuropsychiatric disorders supports the potential of this approach. Steven Moylan, Harris A Eyre, Michael Berk School of Medicine, Deakin University, Geelong, VIC, Australia (SM, HAE, MB); Discipline of Psychiatry, University of Adelaide, Adelaide, SA, Australia (HAE); Department of Psychiatry, Orygen Research Centre, and the Florey Institute for Neuroscience Mental Health, The University of Melbourne, Parkville, VIC, Australia (MB); and Barwon Health, Geelong, VIC 3220, Australia (SM, HAE, MB) [email protected] MB reports grants from Deakin University, Cooperative Research Centres (CRC) for mental health, National Institutes of Health, National Health and Medical Research Council, Stanley Medical Research Institute, CRE in Clinical Research, Meat and Livestock Australia, University of British Columbia–Research & International, and National Natural Science Foundation of China, and reports personal fees from Janssen, Lundbeck, AstraZeneca, GlaxoSmithKline, Servier, and Lilly. SM and HAE declare no competing interests. 1 2 3 4 5 6 7 8 9 10 Beard G. Neurasthenia, or nervous exhaustion. Boston Medical and Surgical Journal 1869; 80: 217–21. Smith ME, Haney E, McDonagh M, et al. Treatment of myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review for a national institutes of health pathways to prevention workshop. Ann Intern Med 2015; 162: 841–50. Sharpe M, Goldsmith KA, Johnson AL, Chalder T, Walker J, White PD. Rehabilitative treatments for chronic fatigue syndrome: long-term follow-up from the PACE trial. Lancet 2015; published online Oct 28. http://dx.doi.org/10.1016/S2215-0366(15)00317-X. White PD, Goldsmith KA, Johnson AL, et al, for the PACE trial management group. Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial. Lancet 2011; 377: 823–36. Rajeevan MS, Dimulescu I, Murray J, Falkenberg VR, Unger ER. Pathway-focused genetic evaluation of immune and infl ammation related genes with chronic fatigue syndrome. Hum Immunol 2015; published online June 24. DOI:10.1016/j.humimm.2015.06.014 2015. Morris G, Berk M, Walder K, Maes M. Central pathways causing fatigue in neuro-infl ammatory and autoimmune illnesses. BMC Med 2015; 13: 28. Nakatomi Y, Mizuno K, Ishii A, et al. Neuroinfl ammation in patients with chronic fatigue syndrome/myalgic encephalomyelitis: An (1)(1)C-(R)-PK11195 PET Study. J Nuc Med 2014; 55: 945–50. Moylan S, Eyre HA, Maes M, Baune BT, Jacka FN, Berk M. Exercising the worry away: how infl ammation, oxidative and nitrogen stress mediates the benefi cial eff ect of physical activity on anxiety disorder symptoms and behaviours. Neurosci Biobehav Rev 2013; 37: 573–84. Irwin MR, Olmstead R, Breen EC, et al. Cognitive behavioral therapy and tai chi reverse cellular and genomic markers of infl ammation in late life insomnia: a randomized controlled trial. Biol Psychiatry 2015; published online Feb 4. DOI:10.1016/j.biopsych.2015.01.010. Fluge O, Risa K, Lunde S, et al. B-lymphocyte depletion in myalgic encephalopathy/ chronic fatigue syndrome. an open-label phase II study with rituximab maintenance treatment. PloS One 2015; 10: e0129898.
www.thelancet.com/psychiatry Published online October 28, 2015 http://dx.doi.org/10.1016/S2215-0366(15)00475-7

02/11/2015

The Ghost in my Brain Clark Elliott Viking, NY, USA Pp 312. ISBN 978-0-525-42656-1
showArticle Info
Summary
Concussion varies in severity and persistence of symptoms. In fact, the damage to the brain is almost impossible to predict. A computational metaphor to describe the organization and design of the brain's software is how Clark Eliott introduces us to his autobiographical account of a concussion that stole his life, and, in his words, caused a breakdown of the machine that allowed him to feel and function as human. The Ghost in my brain offers an acutely descriptive narrative about the alienating and debilitating effects of a relatively minor car crash, an impact with long-term repercussions on cognitive functioning—memory, spatial awareness, movement—with ongoing pain, chronic fatigue, and confusion.

Eliott is a highly distinguished professor of artificial intelligence at DePaul University (IL, USA), and it appears that his computer science training, together with an utmost determination to override his injury, contribute to his remarkable achievement of managing his responsibilities. He continues to work and raise his children, and appears to do this independently, with minimal assistance, although acknowledging the support from family, friends, and his employer. To understand the challenges there are many anecdotes where he describes in painful detail, with an analytical slant, the extent of his disability. The tone of this book is predominately written in this way. Eliot writes about himself like a case study—his fascination with the symptoms, the cognitive disruptions and impairments, often supersede the personal or subjective narrative. This does not compromise the emotional impact of his story, but his keenness to explore the complexities of traumatic brain injury and convey this experience to a diverse readership, makes for a compelling insight into a damaged mind, but one that can still function on some levels.

The first chapter opens with a scenario (one of many), two and a half years after the accident. Following a three-hour lecture, Elliott crawls through the University hallways, taking two hours to leave the building. “I was by now shuffling along with a strange, slightly pigeon-toed gait and only managing a few inches with each step. My jaw hung down, and my head bobbed from side to side as I moved. I felt the onset of a visual impairment similar to what cinematographers call the ‘Dolly Zoom Effect’,…with each step I took forward, the distant goal toward which I was walking appeared two steps further away. Despite the frightening challenges such breakdowns engendered, I often perversely experienced a kind of existential wonder during these episodes as well, as I watched the great machine disintegrating before my eyes.” As his brain resources emptied he was eventually unable to move at all.

Eliott draws on all of his experiences in order to learn, adapt, and adjust. He is repeatedly told that medical science can not fix him, and the invisibility of his illness means that people around him can not make sense of it, creating a wall of isolation, misunderstandings, and at times hostility. He explains how the automatic sensory filtering process is affected, how doing more than one thing at a time becomes impossible, how cognitive slowing interfered with communication, and how the balance and visual system is shot to pieces. The nightmarish situations that Eliott describes provide the reader with an overwhelming sense that the functioning of the brain is inscrutable, a cryptogram that defies nature and science. Only when it stops working can you appreciate just how incredible it is.

Finally, after 8 years, Eliott reaches an impasse. He then stumbles upon two inspirational and brilliant minds: a cognitive restructuring specialist of brain plasticity, Dr Donalee Markus, who refers him to Deborah Zelinsky for neuro-optometric rehabilitation. Markus is confounded by the extent of Eliott's brain damage; “how can you possibly work at all?” she says, concluding he is the “guy that never gives up—ever!”. With his resilience, she knows she can work with him, and the “brain-plasticity miracle” begins.

Markus focuses on restructuring the cognitive aspects based on neuroscientific principles, using specific exercises (included in the book) starting with simple join the dot figures and gradually increasing in difficulty. Find the rule, follow instructions, and repeat again: a task that Eliott willingly jumps into, until he reaches saturation point, complaining that they no longer present challenges. Markus, identifying attention difficulties as a weakness, tells him he must continue, however frustrating. Eliott notices that with time his ability to think is expanding; he can visualize symbols, organize visual scenes, balance background context, and solve real-life problems.

Zelinksy performs extensive visual-neurological tests, and evidence-based options are presented: prescription solutions would balance the relationship between target (centre vision, attention, and peripheral vision, awareness); nonyoked prisms would affect peripheral awareness processing; yoked prisms postural mechanisms; and filters (such as tints, occlusions, and blocking tear duct drains), would help regulate body systems. Eliott is instructed to wear glasses, Phase 1 to 4, and immediately experiences a positive shift in his brain. This continues with everyday wear, and in the closing epilogue of his book he writes: “I am, except in a few small ways, free from concussion symptoms”. It is difficult to imagine how a knock on the head could take so much away, but Eliott's book is an accolade to the cutting-edge scientists who strive towards performing clinical miracles. Eliott is to be greatly admired for this extraordinary story—the message is never give up, because the brain is plastic, and it can rehabilitated.

02/11/2015

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02/11/2015

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02/11/2015

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27/10/2015

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22/10/2015

Discusión mente-cerebro: la necesidad de reintegrarlos

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20/01/2015

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