domingo, 25 de diciembre de 2011

Can caffeine make us healthy?

We're always being told to cut down on caffeine for our wellbeing – yet new studies suggest it could protect against a range of diseases. Kate Hilpern filters fact from froth

For years we have been told to beware of caffeine. Now we seem to have swung in the opposite direction, with studies claiming that moderate amounts of coffee may reduce headaches and protect against diabetes, Alzheimer's and heart disease, among others. So where does the truth lie?

We don't all have the same reactions to caffeine, Mehul Dhinoja, a consultant cardiologist at BMI London Independent Hospital, says.

"Each of us has an enzyme in the liver that breaks down and metabolises caffeine. It's that process that enables caffeine to have its effect around the body," he says. "Some people are born with an enzyme that works extremely efficiently and others have quite the opposite. Because this isn't controlled in studies about caffeine, it's not surprising to find statistical contradictions."

Peter Rogers, head of experimental psychology, says some people are more sensitive to the effects of caffeine, while others develop a tolerance. "One of the things caffeine has been found to do is increase blood pressure and make your hands shake a little," he says. "But actually this depends if you're a person who regularly consumes caffeine."

You can even develop a dependence of caffeine so that without it, you can feel fatigued and headachey, he says. "That's why if coffee drinkers haven't had caffeine for a while – for example, overnight – the coffee they have in the morning is likely to make them feel more energetic and alert, while for a non-regular drinker, it will make them jittery."

So while some studies say coffee stimulates the brain and makes drinkers feel more awake, Rogers and his team have found the "caffeine high" may just be a reaction to the body craving the drug. Caffeine may even have radically different effects on the sexes. Studies from Bristol University have found that drinking caffeinated coffee boosted a woman's performance in stressful situations, but had the opposite effect on men, who became less confident and took longer to complete tasks once they had several coffees.

What caffeine is good for

Forget hair of the dog. If you want to cure a hangover, a good old cup of coffee and aspirin really is best, according to a new study from Thomas Jefferson University in Philadelphia. Confirming what many have suspected for years, the research found that the caffeine in coffee and the anti-inflammatory ingredients of aspirin reacted against the chemical compounds of ethanol, or pure alcohol, which – even in small doses – can bring on headaches.

Tim Grattan, who developed the technology for the new paracetamol and caffeine product, Panado Extra Advance, isn't surprised: "There's plenty of clinical evidence that shows caffeine actually speeds up the painkilling properties of various painkillers. In fact, caffeine has played a role in making our new product 37 per cent more tough on pain than ordinary paracetamol tablets."

Drinking lots of coffee can also boost sports performance by as much as 6 per cent – but, critically, only in any activity where muscles are not being worked to the limit, meaning coffee or tea could benefit a long-distance runner but not a sprinter.

Rob James, from the University of Coventry's department of Biomolecular and Sports Science, believes caffeine in the bloodstream may influence receptors on skeletal muscle, making a person temporarily more powerful. If you overdo it, fear not – caffeine can help here, too. A study from the University of Georgia found that caffeine can help reduce the soreness that discourages some people from keeping up their workouts.

What it's bad for

Contrary to popular opinion, one thing coffee doesn't do is sober you up – it may even further impair your judgement, scientists at Temple University in Philadelphia have found. Combining alcohol and caffeine at the same time produces a potentially lethal mix that makes it harder to realise you are drunk, according to the study published in Behavioural Neuroscience. Perhaps less of a surprise is the discovery that energy drinks – some of them, at least – are bad for our health. "There have been increasing instances of atrial fibrillation (AF), a heart-rhythm problem, among young people who consume large amounts of energy drinks," Dhinoja says. It's not just drinks that can cause this problem. In 2009, a 13-year-old boy needed hospital treatment after ingesting "energy" chewing gum that contained 320mg of caffeine – more than in three cups of coffee.

Large amounts of caffeine in pregnancy also appear to be risky. Back in 2008, the Food Standards Agency warned women to have no more than two cups of coffee a day after a study linked caffeine to low birth weight. Caffeine may affect your chances of getting pregnant in the first place, too, according to a Netherlands study that found that women who drank four cups of coffee a day were 26 per cent less likely than average to have conceived naturally.

Caffeine could even shrink some women's breasts. Swedish research found that too much of it can affect hormones, playing havoc with their bust size.

Cancer and heart disease

An analysis of 59 studies just published on the BioMed Central Cancer website suggests that coffee consumption may reduce your overall risk of getting cancer and that it may be inversely associated with the risk of bladder, breast, pharynx, pancreas and prostate cancers and leukaemia, among others. One study even discovered that caffeine can cut the risk of skin cancer by more than a third.

But women who drink more than four cups of coffee a day increase their risk of developing breast cancer by a third, according to Harvard University. A high caffeine intake can also increase the chance of developing larger tumours, which are harder to treat.

The jury is still out on caffeine's relationship with the heart, too. Arthur Klatsky, a cardiologist, and his team at the Kaiser Permanente Division of Research in California discovered that regular coffee drinkers were less likely to be treated in hospital for irregular heartbeats or rhythms. The more cups of coffee they drank each day, the less likely they were to suffer from the condition. Spanish research has even shown that women who drink three cups a day could reduce their risk of dying from heart disease by a quarter, whilst another study found that men who drank five or more cups a day were 44 per cent less likely to die from the disease.

Other factors

Women who drink tea were recently found by American researchers to be at greater risk of developing rheumatoid arthritis. Other studies have shown tea drinkers can halve their risk of dementia and cut their risk of a stroke. Yet the same cannot be said about coffee drinkers. "This highlights a really important point – that the other constituents in tea and coffee may have their very own impact on health and well-being," Rogers says.

Australian scientists found that drinking three to four cups of coffee a day can lower the risk of type 2 diabetes by 25 per cent, but those who drank decaffeinated coffee showed similar results. And a study of almost 50,000 men found that those who drank the most coffee were 60 per cent less likely to develop the most aggressive form of prostate cancer.

Should we give it up?

Doctors often tell patients to quit caffeine, but that may not be necessary, Rogers says. "It seems to me odd to be telling someone to give up something they enjoy and when there's no real evidence."


Rogers followed a group of people with tinnitus – a condition for which caffeine has traditionally been deemed by doctors as a big no-no. "We found that those who did give up caffeine didn't improve their condition in any way." He adds: "Not to undermine the importance of my own research, but tea and coffee are things to worry about so much less than if you're a smoker, overweight or have a poor diet."

Fuente: The Independent
http://www.independent.co.uk/life-style/food-and-drink/features/can-caffeine-make-us-healthy-2255635.html?
Fuente de la imagen: http://viviendosanos.com/wp-content/uploads/2...

Can caffeine make us healthy?

Navarra Quartet, Wigmore Hall

Beethoven’s deafness was a noisy affair, with his dying hearing-sensors sending dreadfully garbled messages to his brain, but you’d never know it from the magisterial poise of the music he went on writing.

Bedrich Smetana, on the other hand, made a deliberate choice to translate the tinnitus which heralded his deafness into an explicitly musical form.

The movement with which he concludes his String Quartet No 1 is marked ‘vivace’, and it really is vivacious until a sudden high E comes in like a dentist’s drill, bringing everything to a juddering halt, after which the instruments sound as if they are tiptoeing away.


image:bundanon.com.au

The young Navarra Quartet presented this moment with fine panache, after delivering a convincing account of this autobiographical work. ‘I wanted to paint in sounds the course of my life,’ wrote this Czech composer, and though the Prague chamber music society dismissed it as impossible to play, it is now deservedly one of the best-loved works in the chamber repertoire.
The Navarras didn’t quite catch the heel-clicking precision needed for the first of the country dances, but in every other respect they did it proud, bringing burning intensity to the ‘in memoriam’ for the composer’s dead wife, and a generous warmth to its evocations of village life.

They had begun their concert with Haydn’s Quartet Opus 54 No 2, and whoever penned the unsigned programme-note – one of the players? – deserves praise for a singular piece of illumination. It pointed out that in Haydn’s day quartets were mostly played by amateurs at home, where there would at best be just one skilled violinist: this work’s Adagio – one of the most sublime Haydn ever wrote – calls for extreme expressiveness from the first violin, while the other instruments provide the simplest of backdrops.

In point of fact, though the rest of the work was ably played, we didn’t get that sublimity from the Navarras: they had bags of vitality, but not that subtle synergy which distinguishes the most seasoned quartets. And by ending with an underwhelming account of Beethoven’s late A minor Quartet, with its transcendent Adagio, they demonstrated how far they have yet to go. This is holy ground, and only those able to penetrate its chiaroscuro mysteries should tread it.

Fuente: The Independent
http://www.independent.co.uk/arts-entertainment/classical/reviews/navarra-quartet-wigmore-hall-2235798.html?origin=internalSearch

Being Ernest: John Walsh unravels the mystery behind Hemingway's suicide

America's most celebrated writer, Ernest Hemingway, ended his life 50 years ago – in a manner his biographers have struggled to explain

Fifty years ago, in the early hours of Sunday 2 July, 1961, Ernest Hemingway, America's most celebrated writer and a titan of 20th-century letters, awoke in his house in the Sawtooth Mountains of Idaho, rose from his bed, taking care not to wake his wife Mary, unlocked the door of the storage room where he kept his firearms, and selected a double-barrelled shotgun with which he liked to shoot pigeons.

He took it to the front of the house and, in the foyer, put the twin barrels against his forehead, reached down, pushed his thumb against the trigger and blew his brains out.

His death was timed at 7am.

Witnesses who saw the body remarked that he had chosen from his wardrobe a favourite dressing gown that he called his "emperor's robe".

They might have been reminded of the words of Shakespeare's Cleopatra, just before she applied the asp to her flesh: "Give me my robe. Put on my crown; I have immortal longings in me".

His widow Mary told the media that it was an unfortunate accident, that Ernest had been cleaning one of his guns when it accidentally went off. The story was splashed on the front page of all American newspapers.

It took Mary Welsh Hemingway several months to admit that her husband's death was suicide; and it's taken nearly 50 years to piece together the reasons why this giant personality, this rumbustious man of action, this bullfighter, deep-sea fisherman, great white hunter, war hero, gunslinger and four-times-married, all-round tough guy, whom every red-blooded American male hero-worshipped, should do himself in.

How could he? Why would he? Successive biographers – AE Hochtner, Carlos Baker, KS Lynn, AJ Monnier, Anthony Burgess – have chewed over the available facts, his restless travelling, his many amours, the peaks and troughs of his writing career.

But eventually it took a psychiatrist from Houston, Texas, to hold up all the evidence to the light and announce his disturbing conclusions.

The idealised life of Ernest Hemingway, the one the writer himself wanted the world to buy, was simple: he was the perfect man, the perfect synthesis of brain and brawn.

Driven by a thirst for adventure, he was a swashbuckling, hard-drinking pugilist who loved being in the thick of the action, whether in the front line of battle or within charging distance of a water buffalo.

He also happened to be the finest writer around, disdaining the grandiose wordiness of Victorian prose for a clean, stripped-back simplicity, conveying emotion by what was not said as much as by what was.

Wounded on the Italian front in the First World War, he was a handsome convalescent who fell in love with a pretty nurse and wrote A Farewell to Arms as a result.

In the 1920s, he was at the forefront of American writers and artists who hung out in Paris, "being geniuses together". They included F Scott Fitzgerald, who (according to A Moveable Feast) once showed Hemingway his penis and confessed his worry that it was too small to satisfy his wife Zelda; Hemingway kindly reassured him it was OK.

In the 1930s, he went to Spain to fight for the republic against Franco and wrote For Whom the Bell Tolls, in which a brave American hero falls in love with a peasant guerrilla called Maria.

In the Second World War, he was at the Normandy landings and the liberation of Paris. After the war he retired with his fourth wife to Cuba, where he fished for marlins and wrote The Old Man and the Sea, won the Nobel Prize, was lionised wherever he went – but was killed in an unfortunate firearm accident.

That's the official story. In the years after his death, however, the jigsaw pieces of a counter-life gradually began to emerge. His war record, for instance. Hemingway was only 18 when he signed up for the First World War – but it was as a non-combatant. He had a defective left eye, inherited from his mother, which kept him out of battle. He went to Italy to man the Red Cross canteens and evacuate the wounded. Helping a wounded man to safety one evening, he was shot in the leg and hospitalised in Milan, with three other patients and 18 nurses. Though his dalliance with Sister Agnew von Kurovsky was unconsummated, he fell in love with European culture and manners, swanned about in an Italian cloak, drank wine and affected a clipped delivery borrowed from a British officer, Eric Dorman-Smith.

In Paris, where he enjoyed a temporary idyll with his first wife Hadley and their baby John (or "Bumby"), Hemingway started to make his name as a writer – but also to display dangerous mood swings, irascibility, spite and a compulsion to turn against those who helped him.

He dumped Hadley and the baby and took up with Pauline Pfeiffer, a decision for which he was racked with nightmares of guilt, and moved to Key West, Florida.

For some reason, he became obsessed with bullfighting: the glorification of blood, the spilt horse-guts, the matador's passes with the cape and sword, the art of killing.

In Death in the Afternoon, Hemingway seemed to be working out some personal philosophy about death, but it was hard to follow.

The critic Max Eastman complained that his prose style had become the equivalent of "false hair on the chest".

Unable to participate directly in killing bulls, Hemingway decamped to Mombasa where he could legitimately blaze away at lions and kudu.

Not content with land-based mayhem, he bought a 38-foot cruiser called the Pilar to fish, in Key West and Havana, for marlin and other aquatic creatures twice the size of himself.

Between 1928 and 1936, he seemed to spend months posing beside up-ended fish trophies, the self-burnished image of the muscular man of action, handsome, tanned, drinking with the sailors in Sloppy Joe's bar.

He went to Spain during the civil war, not to fight, like George Orwell, but because he was commissioned to report on it for the North American Newspaper Alliance – and because his new love, Martha Gellhorn, was going there.

He stressed many times that he wasn't taking sides, and didn't want to see the USA embroiled in a foreign war.

In Madrid, despite the bombardment, he had the time of his life – enjoying caviar and vodka at the Gaylord Hotel, the Russian HQ, making a movie called The Spanish Earth and supplying its gravelly commentary, writing his broadly fictional dispatches for newspapers that criticised them as "very inefficient".

He looked the part of a hunky warrior, but he was a lucky dilettante, who could have left Spain any time he liked.

He wrote a play about Madrid in 1936 called The Fifth Column, about Dorothy, a plucky female journalist, who falls for Philip, a tough, intrepid, hard-drinking spy masquerading as a war correspondent. Self-projection turned into self-parody.

When America entered the Second World War in 1944, Hemingway got himself to England on "priority war business" – writing pieces about the RAF for Collier's magazine. It was a tough assignment.

He took a room at the Dorchester, where he held court as the Great American Writer and went to parties, receiving compliments on his beardy, macho wonderfulness.

When he was concussed in a car accident that followed a drunken party with Robert Capa the photographer, Martha Gellhorn – who'd travelled to England in a ship packed with high explosives – visited him in hospital and laughed at his footling mock-heroics.

As though stung into action, he headed for the war, joining the invasion fleet to Normandy and, later, General Patton's armoured divisions.

He was a so-so war correspondent who was simultaneously a sort-of-warrior. At the liberation of Paris, he was found in a hotel with a small private army.

When asked to leave by a French general, he liberated the Traveller's Club and the Ritz, taking a room at the latter to entertain his new love, Mary Welsh...

It's easy to be spiteful about Hemingway.

All his posturing, his editing of the truth, his vainglorious fibbing can obscure his undoubted bravery.

He loved being in the thick of the war – the tank advance through the Ardennes, the Battle of the Bulge – dodging bullets, watching men being shot to hell all around him.

But it's hard to shake off the feeling that what he was doing wasn't bravery, but psychotic self-dramatisation.

And when you inspect the image of Hemingway-as-hero, you uncover an extraordinary sub-stratum of self-harming.

You discover that, for just over half of his life, Hemingway seemed hell-bent on destroying himself.

It was about the time he was finishing A Farewell to Arms, in 1928, when he learnt that his father Clarence had shot himself in the head with a Civil War revolver, that Hemingway's life first began to crack apart.

The most obvious external evidence was a succession of bizarre physical accidents, many of which were bashes on the head.

One, in Paris, left him with a split head needing nine stitches, after he yanked the chain in the bathroom, thinking it was the lavatory flush, and pulled the skylight down on top of him.

He became weirdly accident-prone. His car accident that occasioned his row with Martha saw him hurled through the windscreen, lacerating his scalp and requiring 57 stitches.

Three months later, he came flying off a motorbike evading German fire in Normandy. He suffered headaches, tinnitus, diplopia, showed speech and memory problems for months.

Back in Cuba after the war, he tore open his forehead on the rear-view mirror when his car skidded. Five years later, while drinking, he slipped on the deck of the Pilar, and concussed himself. Why, you'd almost think he was trying to emulate his late father, and his self-imposed head wound.

The most egregious injury, however, occurred in January 1954. He and Mary took off from Nairobi in a small plane, heading for the Belgian Congo.

Near Victoria Falls it crash-landed in a thorn thicket and Ernest sprained his shoulder. As rumours of his death spread, he and his companions were rescued and put in a 12-seater De Havilland Rapide which – incredibly – burst into flames on the runway.

Finding the door jammed, Hemingway volunteered to use his head as a battering ram, butted the door twice and got out.

He liked to present it as a classic example of superman pragmatism, but it nearly killed him.

He fractured his skull and lacerated his scalp; cerebrospinal fluid seeped from his ear.

In Nairobi he was diagnosed with grave overall concussion, temporary vision-loss in the right eye, deafness in left ear, paralysis of sphincter muscle, first degree burns on face, arms and head, sprained arm, shoulder and leg, crushed vertebra and ruptured liver, spleen and kidney.

Astonishingly, he was at it again only a month later: helping to extinguish a small fire, he fell into the flames and suffered second degree burns on legs, belly, chest, lips, left hand and right forearm.

Hemingway's taste for chronic self-immolation was matched by his prodigious feats of drinking: "The manager of the Gritti Palace in Venice tells me," wrote Anthony Burgess later, "that three bottles of Valpolicella first thing in the day were nothing to him, then there were the daquiris, Scotch, tequila, bourbon, vermouthless martinis.

The physical punishment he took from alcohol was ... actively courted; the other punishments were gratuitous – kidney trouble from fishing in chill Spanish waters, a torn, groin muscle from something unspecified when he was visiting Palencia, a finger gashed to the bone in a mishap with a punchbag..."

The drinking got worse after his father shot himself.

Ernest went to a doctor in 1937, complaining of stomach pains; liver damage was diagnosed and he was told to give up alcohol.

He refused. Seven years later, in 1944, when Martha Gellhorn visited him in hospital, she found empty liquor bottles under his bed.

In 1957, his doctor friend AJ Monnier wrote urgently, "My dear Ernie, you must stop drinking alcohol. This is definitely of the utmost importance." But even then, he couldn't stop.

What was bugging Hemingway? Why all the drinking, the macho excess, the manic displays of swaggering? Why was he so drawn to war, shooting, boxing and conflict? Why did he want to kill so many creatures? Was he trying to prove something? Or blot something out of his life?

Some answers were offered in 2006 by a long article in the American Psychiatry magazine, called "Ernest Hemingway: A Psychological Autopsy of a Suicide".

It was by Christopher D Martin, whose official title is Instructor and Staff Psychiatrist at the Menninger Department of Psychiatry and Behavioural Sciences at Baylor College of Medicine in Houston Texas.

Martin had read widely in the 15 or so biographies and memoirs of Hemingway and offered his expert analysis – based, inevitably, at second hand, but still a convincing evaluation.

He had no trouble in diagnosing the author as suffering from "bipolar disorder, alcohol dependence, traumatic brain injury, and probably borderline and narcissistic personality traits".

He notes that many in the Hemingway family – his father and mother, their siblings, his own son and his grand-daughter Margaux – were prone to manic-depression (Margaux's was the fifth, or possibly sixth, suicide in four generations) and suggests that it was Ernest's manic episodes that drove him to his astonishing feats of creativity. But he locates the writer's trauma in two childhood experiences.

It seems that it was his mother Grace's habit to dress him, as a child, in long white frocks and fashion his hair like a little girl's.

It was a 19th-century custom to dress infants alike, but she took it to extremes. She referred to him, in his cute lacy dress, as "Dutch dolly".

She said she was his Sweetie, or, as he pronounced it, "Fweetee". Once, when Ernest was two, Grace called him a doll once too often.

He replied, "I not a Dutch dolly... Bang, I shoot Fweetee".

But she also praised him for being good at hunting in the woods and fishing in the stream in boys' clothes.

It was too confusing for a sensitive kid. He always hated her, and her controlling ways. He always referred to her as "that bitch". He'd spend the rest of his life in a galloping parody of masculinity.

Dutch dolly indeed. He'd show the bitch there was no confusion in his head.

"I shoot Fweetee." The trouble was, he also wanted to shoot his father. Clarence Hemingway was a barrel-chested, six-foot bully, a disciplinarian who beat his son with a razor strop.

Ernest didn't retaliate directly. He bottled it up and subsumed it into a ritual, in which he'd hide in a shed in the family backyard with a loaded shotgun and take aim at his father's head.

Martin speculates that, when Clarence shot himself, Hemingway, aged 29, felt terrible guilt that he'd fantasised about killing him.

Unable to handle this, he took to blaming his mother for his father's death. "I hate her guts and she hates mine," he wrote in 1949. "She forced my father to suicide."

After Clarence's death, Hemingway told a friend, "My life was more or less shot out from under me, and I was drinking much too much entirely through my own fault".

He suffered a chronic identity crisis.

Henceforth he could be warm and generous or ruthless and overbearing. His friendships were often unstable (he could turn vicious or cruel, even with supposedly close pals) and his relations with women were full of conflict. He sulked like a child when, on his first safari, his wife Pauline shot a lion before he did.

And he was pursued, for the rest of his life, by a colossal death wish – either to join his late father, or to expatiate his guilt at his father's death by mirroring it.

Death took up residence at the heart of Hemingway's life, a constant spur to his creative imagination, a constant companion, a dark, secret lover.

Themes of violence and suicide informed his stories from the start.

His letters are full of references to his future suicide.

And when not contemplating his own death, he was putting himself into danger and combat as though to hasten it.

Wars, rebellion, bull-running in Pamplona, big-game hunting in Africa, fishing in Havana – they were all his way of throwing himself before the Grim Reaper. "I spend a hell of a lot of time killing animals and fish," he told Ava Gardner, "so I won't kill myself."

And of course writing was his way of evading the need to die.

He could polish his real-life experiences at war, in Italy, Spain, the Ardennes, and burnish his life in hindsight.

Being awarded the Nobel Prize in 1954 must have been a triumphant affirmation of his genius, but he worried that, after receiving the prize, most laureates never wrote anything worthwhile again.

Luckily, after finding two trunks of notes from the 1920s in a Paris hotel, he was able to manage one more book: A Moveable Feast, his touching memoir of being young, poor and happy in the French capital, with his first wife and baby, before everything started going to hell.

After 1960, however, he found he could no longer write.

The words wouldn't come. Depression came instead, and with it (as we learn from AE Hotchner's memoir, Papa Hemingway), paranoid delusions.

He thought that the two men he saw working late in a bank were "Feds", checking his bank account for irregularities.

He thought his friends were trying to kill him.

When his car slightly grazed another vehicle, he fretted that he'd be thrown in jail. It was a sorry thing, to see the epitome of "grace under pressure" succumbing to dementia.

He was given medication and, horribly, a course of electroconvulsive shock treatments.

In the spring of 1961, he was asked to contribute a single sentence to a presentation volume for John F Kennedy's inauguration.

Hemingway couldn't oblige. "It just won't come any more," he told Hotchner, and wept.

In April, his wife Mary found him sitting with a shotgun and two shells. He was sent to hospital in Ketchum, Idaho, his birthplace, but he tried twice more to end his life, once by walking into the path of a plane taxiing on the runaway.

There was a two-month period of hospitalisation and comparative peace and quiet, when he appeared sane to his doctor and deranged to his wife.

He seemed to be acting, right to the end.

He was released home one more time, had a picnic lunch with wine (he saw some state troopers and was sure they'd arrest him for possess of alcohol) and, the next morning, shot himself.

"The accumulating factors contributing to his burden of illness at the end of his life are staggering," writes Martin, listing Hemingway's bipolar mood disorder, depression, chronic alcoholism, repetitive traumatic brain injuries, the onset of psychosis.

But it seems clear that the defining problem of his life was his experience of childhood.

His confusion over gender, his Oedipal desire to kill his father for beating him, together led to what Martin calls "a retreat into a defensive façade of hyper-masculinity and self-sufficiency".

Building and sustaining the myth of Hemingway the Man's Man took courage and determination, but it was something he needed to do – and when it dwindled, along with the all-important capacity to write, he had no answer except to go the same way as his father.

The image of his father, a moody, bullying, depressive man, but a role model none the less, haunted his life.

He wanted to revivify him, in order to release himself from the responsibility for his death. He wanted to be the big, strong, heroic man that the world could call "Papa".

Fighter, writer, lover: a life in brief

1898 Ernest Hemingway is born in Oak Park, Illinois

1918 Wounded in Italy while working for the Red Cross during the First World War

1921 Marries first wife Hadley Richardson; they move to Paris

1923 First son John is born

1927 Divorced by Hadley, he marries Pauline Pfeiffer

1928 His father Clarence shoots himself in the head

1937 Works as a war correspondent during the Spanish Civil War

1940 For Whom the Bell Tolls is published; Hemingway marries Martha Gellhorn

1944 Reports on the liberation of Paris; begins relationship with Mary Welsh who he will marry in 1946

1952 The novella The Old Man and the Sea is published

1954 Awarded the Nobel Prize for Literature

1961 Shoots himself in the head in Ketchum, Idaho

FUENTE. THE INDEPENDENT
http://www.independent.co.uk/news/people/profiles/being-ernest-john-walsh-unravels-the-mystery-behind-hemingways-suicide-2294619.html?origin=internalSearch

Of mice and medicine: In defence of animal experiments

Animal experiments in the UK are on the rise.
Though controversial, these tests are transforming human lives, discovers Paul Vallely


Professor David McAlpine, Director of the UCL Ear Institute, where mice are used to investigate tinnitus

A sad-eyed, mournful-mouthed beagle stares out from a poster on a bus shelter by the front door of the Ear Institute of University College London. Below the melancholy dog blares the legend 'Boycott Vivisection'. It is clearly intended to be a reprimand to the scientists passing through the door into one of the world's leading research centres on hearing and deafness.

Not that there are any experiments on dogs going on in the Institute, but then facts are not always the first currency when it comes to the emotive subject of experiments on animals.

The number of research procedures on animals carried out in the UK rose by 3 per cent last year. The figure has risen steadily over the past decade to just over 3.7 million in 2010. 'Procedures' is the term used by the Home Office, which is looking at ways to meet a commitment in the Government's coalition agreement to reduce the use of animals in scientific research. And it is a significant word, for behind it lies a major shift in animal experimentation.

The headline figure disguises considerable changes. Experiments on many of the kind of animals which most inspire protest among animal rights activists were down: dogs by 2 per cent, rabbits by 10 per cent and cats by 32 per cent. Even the eponymous guinea pigs were down 29 per cent. There was also a fall of 11 per cent in the number of animals used in toxicity trials, as thanks to rule changes one test can now be used to satisfy several requirements.

Where there was an increase was in mice and fish – the latter up a whopping 23 per cent. What that reveals is a switch to animals whose genes can be easily modified. An extraordinary 44 per cent of those 'procedures' turn out not to be what most members of the public imagine as an 'animal experiment' but merely the act of breeding transgenic creatures, mostly done by allowing mice to do what male and female mice do naturally anyway. But the nature of the experiments has undergone a notable change.

For decades now, the terms of the debate on this subject have been set by the emotive, sentimental or absolutist intolerance of animal rights activists. We rarely hear the other side of the story, from the scientists who have for years kept themselves in the shadows, for fear of attacks from animal rights extremists, the most violent of whom are now in jail.

Inside the Ear Institute, research is being done by Professor David McAlpine and his colleagues into the problem of tinnitus – that odd buzzing sound in the ears which afflicts most of us when we leave a noisy rock concert. For more than five million people in the UK, however, that noise never goes away.

"People with tinnitus hear a constant noise in their ears, a buzzing, beeping or whining. It can get very distressing," says a senior researcher, Dr Roland Schaette. "Around 10 per cent of the population are chronic sufferers. And for 1 to 2 per cent, their quality of life is badly affected. They lose silence. Some can't relax or sleep. Social isolation and depression can follow. It can drive some people to suicide."

Dr Schaette uses mice in his research, to fill the gap between theoretical models and his experiments on human subjects. "We do behavioural training with the mice," he explains. "Obviously you can't ask them what they are experiencing so you have to train them to behave. We play a loud noise, and they jump. Next we play a low noise before the loud one and they learn not to jump when the big noise comes. Then you induce tinnitus in them and play a low constant noise at the same pitch as the first low noise. Mice with tinnitus don't hear [this] so they jump when the big noise comes; mice without, don't."

What happens then is that Dr Schaette and his research assistant use electro-physiological recording techniques to see how nerve activities are affected. "We place a tiny wire into the brain of a mouse that has been sedated with anaesthetic, and given a pain killer," he says. "Then we can record the reaction of a tiny area of the brain, even down to a single neurone, to see how nerve activities are affected, how it alters and what mechanisms alter it." At the end of the experiment the scientists increase the sedative to a fatal dose so that the mouse dies.

So couldn't they achieve the same ends without using an animal? "There are lots of ways of finding things out," interjects Prof McAlpine. "For some tasks you can use a dish of cells. For others you can used brain imaging like magneto-encephalography", which maps activity by the brain's natural electrical currents by recording the magnetic fields they generate.

"But that is a very limited technique. It is great for telling how the human brain lights up when the body is doing particular activities. But it won't tell you how neural pathways change in tinnitus. You can't tell without an animal model to investigate the neurones. There are more synapses – connections between neurones in the brain – than there are stars in the universe. We can look at which connections grow when a mouse learns a task."

But it is not research like this which accounts for the rise in animal experiments. Across the river at King's College London, in the school of biomedical sciences, research is being done manipulating mice genes in a search for a cure for Parkinson's Disease, the progressive disorder that causes problems with movement, including tremor and muscle rigidity.

This debilitating disease is caused by the death of nerve cells in the brain. It gets worse as more nerve cells die. Doctors don't know why. But through experiments on animals they have discovered drugs which dramatically alleviate the terrible shaking which characterises the disease. The problem is these only work for five years. So further experiments are underway as Roger Morris, Professor of Molecular Neurobiology and Head of the School of Biomedical Sciences at King's College explains.

"The primary cause of Parkinson's is the death of neurons that deliver an essential chemical called dopamine to the forebrain," he says. "The primary treatment is to provide a substitute chemical, L-DOPA. But in the healthy brain, dopamine is released only in very specific regions. L-DOPA, however, penetrates the whole brain, in a way that the body is not used to. Abnormal changes start to happen, resulting in continuous uncontrolled limb and body movements."

Scientists at King's – which has 22,000 experimental animals, 21,000 of them mice – have, over the past couple of decades, used marmosets – small, primitive New World monkeys – to discover the dose of L-DOPA which brings the fewest unwanted side effects. Work with such non-human primates is not quite so controversial as experiments with African monkeys. But this is the kind of work which most incenses animal rights activists.

Professor Morris is unapologetic. "There is a lot you can do without animals. Most scientists who use animals do so as part of a whole portfolio of techniques, which will include work with isolated molecules and genes, building up to whole cells growing on plastic dishes in tissue culture to study the more complex integration of cells to work together as a single tissue," he says. Some 90 per cent of his staff's work is done with individual molecules and cells in culture.

"At all these stages, extensive use is made of computational modelling, and analyses of databases, to bring together all the information available on how the particular aspect we work on functions in a living body," he continues. "And there are now non-invasive brain imaging techniques that tell us a lot. But real diseases are diseases of the whole body, and can only be studied in the whole body."

Dopamine deficiency is a key component of Parkinson's but the underlying cause is a complex set of interactions triggered by inflammation in the autoimmune system. "So we need to understand the interaction between two complex bodily systems – the brain, and the immune system – to understand this multi-tissue, multi-step disease. The body's controls on how those two systems interact are lost the moment both are cultured in a plastic dish. We need to look at living brain."

britain has the strictest rules in the world on such experiments, a House of Lords select committee has found. The Animals (Scientific Procedures) Act 1986 says they can only be performed where there is a clear potential benefit to either people, animals or the environment, and when there is no means of obtaining these benefits without using animals. The act also builds in a cost-benefit analysis which insists, in a very English test of reasonableness, that the good to humans must clearly outweigh the harm to animals.

Experiments must use the minimum number of animals, involve animals with the lowest degree of sensitivity, and cause the least suffering consistent with arriving at a clear scientific conclusion. Institutions, projects and scientists need three sets of licences. Home Office inspectors visit their labs around 12 times a year.

Evidence of proportionality is not hard to find. More than 120,000 people suffer from Parkinson's today in the UK. That seems a grievous problem set against the discomfort of a relatively small colony of marmosets – numbering just a few hundred over the past decade – whose suffering has dramatically improved the treatment of the disease. Moreover, when Parkinson's is induced in marmosets the disease does not progress as it does in human beings "and the animals live into old age, housed in pairs throughout their lives in an enriched environment," Prof Morris says.

All this is a big change from the bad old days. "I was appalled at some of what was allowed when I started my PhD in the United States in 1972," he recalls. "The kind of science done in living experiments with animals has completely changed." Thirty years ago a lot of experiments were with cats and dogs or primates.

Today there are more experiments recorded, but the animals used are mostly mice and fish and the procedures are considerably less severe. Before 1984, scientists could do anything with an animal that the Home Office had not specifically disallowed. Today the default is reversed; nothing is allowed that has not been specifically sanctioned.

In the old days the first line of experiment was often with the living animal, and the tests used were not very sophisticated. Now, before they get to an animal, scientists have refined the question they want to ask by extensive work with cells and computer modelling.

Previously, scientists had to breed a large number of animals just to get the type they needed – mice of the same age with the same parents. Now, thanks to genetic modification, they can generate precisely the number and kind they need for a particular experiment.

"We increase the number of animals used," says Professor Dominic Wells, of the neuromuscular disease group at the Royal Veterinary College, "but we decrease the overall severity of what we're doing." The technology allows a gene to be deleted so that an adult mouse appears to be normal until asked to remember something, which it cannot then do.

A scientist working elsewhere on spinal cord injuries, who asked to remain unnamed for fear of animal rights reprisals, elaborated on this. He is working on trying to stimulate the human body to regenerate nerves in the spinal cords of the 400,000 people in Europe who are paralysed after back or neck injuries from car accidents, violent falls or sports injuries.

"Human suffering is far more protracted and severe than anything we would allow in animals," he told me. "Procedures are done to reduce discomfort to a minimum. Our work is about understanding the early stages of the development of diseases, before irreversible brain damage has commenced, and understanding the subsequent disease mechanism so we can prevent it at an early stage. So we don't need to take animals to extremes. We can study the effects of that in humans."

What that means in practice is that, in his case, rats are partially paralysed – in one paw or to impair the tail. "You wouldn't enter a rat with a partial lesion of its spinal cord in a rat race," he told me, "but it can get around the cage well enough. What we are studying is mechanisms, so a 10 per cent paralysis will suffice to study what prevents a paraplegic human from recovering – and being condemned to 30 years in a wheelchair." Researchers have already discovered an enzyme which allows previously disabled rats to walk again almost normally.

There are both scientific and moral reasons that impel scientists to choose the simplest animal system that will give them the result they seek. "We do have a moral perspective about an animal's suffering," says David McAlpine. "There is a hierarchy. I'm unashamedly modernist about that. You take the animal that's the lowest in the hierarchy that will answer your question."

So basic studies on cell-division could be done to Nobel Prize level, as they were by Sir Paul Nurse, studying something as primitive as yeast, Prof Morris says. "It's very fast, very simple and you get clear answers quickly. But as you ask more detailed or complicated questions you need to go up the chain – to fish, mice, rats, bigger mammals and sometimes primates."

Prof McAlpine concurs. "Fruit flies go deaf for the same reasons you and I do," he says. "So you can do some basic work with them and do it much more quickly because they have simpler nervous systems. A mouse has a different hearing range from a human – it hears much higher sounds – but mice are close enough to us for use to study the range of hearing loss problems we have. For some things people use guinea pigs because they have a very similar hearing range to humans; you can do a cochlear implant in a guinea pig but not in mouse.

Despite the focus on dogs, cats and monkeys in the campaign posters of animal rights activists, those creatures were used in less than half of 1 per cent of all procedures in last year's official figures. A report by Professor Sir Patrick Bateson, president of the Zoological Society, in July found that 91 per cent of research on non-human primates between 1997 and 2007 was of high quality and scientifically and ethically justified. It is being conducted by 72 researchers working mainly on Alzheimer's and Parkinson's. Some animals were used in more than one procedure since the experiments had only minimal effect on the animals. Since then, The National Centre for the Replacement, Refinement and Reduction of Animals in Research has been brought into tighten up conditions to avoid even that 9 per cent failure rate. They vet each application for experiments involving primates.

But monkeys are not the area of innovative work in animal research. Fish are. Or to be more precise, zebrafish. In the Randall Division of Cell and Molecular Biophysics at King's College in London, Dr Claudia Linker is at her computer looking at a video made through a microscope of a small tear made in the tail of a zebrafish.

Zebrafish are those tiny, iridescent, black-striped creatures, originally natives of the Ganges River in India but popular now in Britain's home aquariums. But they are perfect creatures for the study of the early development of embryos. Not only do they grow up and reproduce in just three months, going through the same development stages as a human embryo, but their tiny eggs have clear shells that develop rapidly into translucent embryos so they can be studied using just an optical microscope.

They are easy to keep in a laboratory, lay around 200 eggs at a time which can be harvested without the need to kill the mother (as happens with lab mice). They develop from egg to fish within 18 hours. Scientists can not only look at a fish's heart beating under a microscope, they can mark individual cells with a fluorescent marker gene which they transfer from jellyfish. They can use different coloured markers for different cells and watch different cells participating in the embryo's development and multi-tag all the tissues. And their genes can be modified more easily than those of mice.

Dr Linker is enthralled by what she can see. The movement of blood cells towards the wound is clearly evident. "Can you see them moving?" she asks and shows me different examples of migratory cells. "My work is to find out how cells know when to start migrating, where to go, what to do when they arrive at their destination. I am not working on curing a particular disease but on understanding how the basic mechanism directing cell migration works. Once we understand it we might learn how to intervene to promote cells to do what we want, for example, stop the migration of cancer cells. It's very exciting, but it is open-ended."

Down the corridor, her colleague Professor Simon Hughes is doing something similar on skeletal muscle development. "We need to understand what is the signal mechanism within an embryo that says make a muscle here, a heart there, a liver over there – and you can't find that out from a test-tube."

Research on zebrafish published earlier in the year found that the fish are able to repair muscle within their hearts. "That's not something that happens in us, or mice. By experimenting with that it may well be possible to gain some insight that will enable human hearts to be regenerated," says Prof Hughes, who once researched with mice but switched to zebrafish. He is attempting to lay the groundwork for treatments for muscular dystrophy.

Wandering through a laboratory like this can be an exciting journey. By the stairs I meet Dr QueeLim Ch'ng who decided to study C elegans, a little worm almost too small to see with the naked eye, and discovered proteins which turn out to be involved in premature ageing, and which in man are critically involved in Alzheimer's.

Another King's scientist has discovered that coral produces a chemical which enables it to adapt to living in UV light – and that fish which eat the coral transfer that chemical to their eyes, so they don't get UV damage from light. The next step will be to see how the chemical moves from the fish's digestive system into its eyes by implanting the chemical in mice; the hope is that the research will lead to a treatment to prevent macular degeneration, which causes blindness in humans.

In another lab, a PhD student has identified the world's first therapy to partially reverse arm disabilities in strokes – and he did it by injecting a human molecule which naturally occurs in muscle into the upper arm muscles of rats. It even works 24 hours after a stroke.

Several of the range of drugs which have changed the lives of people with Aids have been based on animal experiments studying the mechanism of which cells it infects, how it gets into those cells, why it binds to particular receptors, and which drugs block that interaction. "Now," says Professor Morris, "we are working on something similar with Alzheimer's, trying to make a mouse model by altering three mouse genes to reproduce in mice some of the behaviour found in people with Alzheimer's."

For a nation of pet-lovers, we Britons take a surprisingly pragmatic attitude to all this. Most of us are aware of the ambiguity of our relationship with animals. Over 90 per cent of the population eats meat. As we are happy to breed animals for food, so we are content, too, to see them bred for experiments which improve human health. Polls consistently show that 60 per cent of the population are happy for any experiments to be done on animals. The proportion of Brits who accept animal experiments, subject to the kind of conditions now in place, is over 90 per cent. When you spend a little time with the scientists involved, you understand why.

fuente: http://www.independent.co.uk/news/science/

Language Impairment Associated With Arachnoid Cysts: Recovery After Surgical Treatment

Case Report
Image: radpod.org

Authors
Nicole Laporte BSca, Anne De Volder MD, PhDa, Christine Bonnier MD, PhDa, Christian Raftopoulos MD, PhDb, Guillaume Sébire MD, PhDc, Corresponding Author Contact Information, E-mail The Corresponding Author

a Service de Neuropédiatrie, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium
b Service de Neurochirurgie, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium
c Service de Neurologie Pédiatrique, Centre Hospitalier Universitaire de Sherbrooke, Faculté de Médecine, Université de Sherbrooke, Sherbrooke, Quebec, Canada

Available online 22 December 2011.
Abstract

Supporting data from the literature, we observe that large arachnoid cysts may affect cognitive function.

Neuropsychologic assessment plus magnetic resonance imaging allowed for documentation of associations between left temporal arachnoid cysts, language impairment, and other cognitive dysfunctions.

Significant cognitive improvements were evident soon after cysto-peritoneal shunting.

These observations reinforce the rationale for neuropsychologic assessments of patients with developmental delay and arachnoid cysts, and support the potential benefit of surgical decompression for arachnoid cysts associated with neurologic deficits, even if surgery is performed well after the occurrence of neurologic deficits.

Corresponding Author Contact InformationCommunications should be addressed to: Dr. Sébire; Service de Neurologie Pédiatrique; Centre Hospitalier Universitaire de Sherbrooke; Faculté de Médecine; Université de Sherbrooke; 3001 12ème Avenue Nord; Sherbrooke, Quebec J1H5N4, Canada.

FUENTE: Pediatric Neurology
Volume 46, Issue 1, January 2012, Pages 44-47
doi:10.1016/j.pediatrneurol.2011.10.001

EL USO DE PIROTECNIA PUEDE PROVOCAR DAÑO EN LOS OIDOS

22 de diciembre de 2011 • 11:15



El uso incorrecto de los artefactos de pirotecnia que se utilizan en la actualidad puede provocar traumas acústicos que derivan en pérdida auditiva permanente e irreversible, explicaron especialistas de la comisión de Ecología del Colegio de Fonoaudiólogos de la regional La Plata.

La pirotecnia en general, que se vende en el mercado produce sonidos de muy alta intensidad que al explotar pueden llegar hasta los 120 ó 140 decibeles, equivalente al producido por un arma de fuego o despegue de avión", explicó la entidad.

Los expertos señalaron que "está científicamente comprobado que toda intensidad sonora que supere los 90 decibeles resulta dañina para el oído.

De acuerdo con las últimas estadísticas oficiales, correspondientes a la atención de pacientes en la última Navidad, casi el 20% de los accidentados que ingresaron a las guardias presentaban alguna lesión auditiva.

De los 85 jóvenes y adultos atendidos en esa fecha, 15 tuvieron que recibir, además, atención en los servicios de audiología.

La secretaria del Colegio de Fonoaudiólogos, Noemí Díaz, explicó que al estallar un petardo por ejemplo, se produce un ruido corto, muy intenso e imprevisto, por lo tanto el oído de quien está cerca o lo manipula, pierde su capacidad de defensa".

"De esta manera es que puede producirse un `trauma acústico´ lo que provoca una pérdida auditiva permanente e irreversible y también resultan frecuentes las apariciones de zumbidos, en los momentos posteriores a la detonación", advirtió.

Díaz remarcó que "la pérdida súbita de la audición es una verdadera urgencia otorrinolaringológica que debe tratarse sin la menor dilación, en menos de 24 horas si es posible, para tener las mayores posibilidades de recuperación".

A partir de los resultados de estos estudios, el Colegio de Fonoaudiólogos de La Plata recomendó una manipulación responsable de este tipo de artefactos.

La presidenta del Colegio de Fonoaudiólogos de La Plata, Alejandra Morchón, expresó que "en esta época del año se intensifica el uso de pirotecnia y a veces los adultos no asumen los recaudos necesarios".

"Promovemos el uso responsable para preservar la salud de la población, aseguró.

Díaz explicó que los primeros síntomas de una afección en el aparato auditivo son el aturdimiento, molestia auditiva y en ocasiones, pérdida de equilibrio y zumbidos agudos.

Las autoridades explicaron que el riesgo es mayor aún si la explosión ocurre en lugares cerrados, como puede ser un balcón, un patio cubierto, un galpón ya que el sonido reverbera.

"Estamos hablando de que en algunos casos se duplica el ruido que se acepta como tolerable para un ser humano" dijeron los especialistas.

Silvia Bermúdez, responsable de la Comisión de Ecología del Colegio, explicó que "el oído está provisto en forma natural de un mecanismo protector que reduce la transmisión de los sonidos más intensos hacia las delicadas células del oído interno, pero actúa recién después de unos diez centésimos de segundo, por lo cual es ineficaz frente al ruido de los petardos".

"En general las personas asisten a consulta de guardias médicas, por otro tipo de consecuencias como quemaduras o heridas en ojos, y recién advierten el daño auditivo posteriormente, aseguró Díaz.

fuente: http://noticias.terra.com.ar

¿CUANTO TIEMPO DURAN LOS AUDÍFONOS?

¿Cuánto tiempo duran los audífonos ?


fuente de la imagen: timothybaril.com

Martes, 20 de diciembre 2011

Los audífonos normalmente duran de tres a cinco años, aunque en algunos casos pueden durar mucho más.

Los componentes en miniatura en los audífonos tienden a desgastarse con el tiempo, e incluso cuando son reparados, no tienen la misma integridad que los nuevos componentes.

Aunque los audífonos son frágiles aparatos electrónicos en miniatura, que están expuestos a la humedad, la transpiración,la cera de los oídos ya veces la lluvia, o la laca y otros factores - que no son ideales para los dispositivos médicos minúsculos.

Se ha demostrado que el uso de deshumidificadores especiales de audífonos , que ayudan a eliminar la humedad de los audífonos cuando no se utilizan, prolonga la vida de los audífonos.

Estos dispositivos pueden ser obtenidos a partir en su centro de ventade audífonos local . Además, la limpieza de sus audífonos con regularidad le ayudará a asegurarse que tengan una larga vida.

En muchos casos, la pérdida de la audición tiende a empeorar con el tiempo.

Por lo tanto, puede ser necesario usar audífonos nuevos para adaptarse a su pérdida de audición a medida que cambia.

Mientras que en muchos casos, los audifonos digitales modernos puede ser re-programados,para adaptarlos a cambios en la audición, algunas personas optan por comprar audífonos nuevos con el fin de beneficiarse de nuevas características que vienen con los avances en la tecnología de los audífonos.

FUENTE: http://www.healthyhearing.com

sábado, 24 de diciembre de 2011

Chronic intracranial hypotension.General Information

Intracranial Hypotension



Intracranial hypotension is a condition in which there is negative pressure within the brain cavity.
There are several possible causes:
Cerebrospinal fluid (CSF) leak from the spinal canal:
A leak following a lumbar puncture (spinal tap).
A defect in the dura (the covering the spinal tube).
Spontaneous, sometimes following exertion such as swinging a golf club.
A congenital weakness.
Following spinal surgery.
Following spinal trauma.
Following a shunt procedure for hydrocephalus.
Lumboperitoneal shunt.
Ventriculoperitoneal shunt with a low pressure valve.
In some cases, spinal CSF leaks can lead to a descent of the cerebellar tonsils into the spinal canal, similar to a Chiari malformation.
Large spinal dural defects can lead to herniation of the spinal cord into the defect.

Symptoms

The classic symptom is severe headache when upright, which is relieved when lying flat.
Other symptoms can include nausea, vomiting, double vision and difficulty with concentration.

Diagnosis

Diagnosis is usually suspected based on the postural dependency of the headache, although in many cases the diagnosis of intracranial hypotension is not considered for some time.
A contrast-enhanced brain magnetic response imaging (MRI) scan typically shows thickened and brightly enhancing meninges (pachymeningeal enhancement). Other findings include descent of the thalamus and cerebellar tonsils.
Continuous intracranial pressure monitoring is definitive for documenting abnormally negative intracranial pressures.
The identification of the site of CSF leak in the spinal canal can be very challenging. In some cases, the site cannot be identified. Methods include:
Dynamic myelography with fluoroscopy and computed tomography (CT).
Radioisotope cisternography.
Spinal MRI.

Treatment

If the site of the spinal CSF leak can be identified, then options include:
Epidural blood patch, performed by an anesthesiologist pain management specialist.
Surgical repair of the defect.
Over-draining CSF shunts are managed by replacing the valve with one that drains less.
Lumboperitoneal shunts may have to be removed or ligated.

Outcome

If the cause of the intracranial hypotension can be identified, the outcome following treatment is typically excellent.

fuente: UCLA
http://neurosurgery.ucla.edu/body.cfm?id=1123&ref=55&action=detail

Chronic intracranial hypotension.

Mackenzie RA, Lethlean AK, Shnier R, Blum PW




Acute intracranial hypotension can occur following lumbar puncture or a fall, and sometimes spontaneously.

Most cases resolve within weeks or months but some require surgical repair of the defect causing leakage of cerebrospinal fluid (CSF).

It is conceivable that such leaks could become chronic if the defect is incompletely sealed.

We report the case of a 49-year-old male who presented with a 10-month history of headache associated with a leaking thoracic extradural arachnoid cyst.

After this was repaired he reported relief not only of his recent headaches but also of chronic alcohol-related headaches.

A long-standing anaemia resolved and tinnitus hyperacusis improved.

It is suggested that an injury 30 years before may have initiated the leak of CSF resulting in chronic intracranial hypotension.

Fuente: J Clin Neurosci 1998 Oct; 5(4):457-60.

Alteraciones otorrinolaringológicas en el anciano

Aunque la afección más popular es la presbiacusia, debido a las alteraciones psicológicas y sociales que origina, el anciano puede presentar las mismas enfermedades del adulto, incluso algunas con mucha mayor frecuencia
En todo caso, estas enfermedades presentan en la persona mayor unas características especiales que hay que tener en cuenta a la hora de valorar al paciente

La sordera tiene un efecto adverso sobre las funciones cognitivas, conducta emocional y bienestar social, y puede ser un factor con peso específico considerable
para llevar una vida independiente.

Prevalencia
Cerca de un 25% de las personas de 65-74 años y hasta el 50% de los mayores de 75 años sufren una pérdida de audición.

Valoración de la discapacidad auditiva del anciano

Prueba de la voz susurrada

Se explica al paciente que se le pedirá que repita tres números. El examinador se coloca detrás del paciente para evitar que le lea los labios.
Se tapa el oído contralateral. A continuación el examinador espira completamente (lo que reduce el volumen de la voz) y, desde una distancia de unos 60 centímetros
de la oreja, le susurra tres números.
Si el paciente no puede repetir el 50% (tres números o más) en dos ensayos,
se considera que no ha superado la prueba.

Clasificación de la patología

Oído externo
1. Tapón de cerumen.
2. Otitis externa.
3. Otitis externa maligna.
4. Tumores benignos.
5. Lesiones precancerosas.
6. Tumores malignos.

Oído medio
1. Otosclerosis.
2. Otitis media aguda.
3. Otitis media crónica.
4. Tumores.

Oído interno
1. Presbiacusia.
2. Acúfenos.

Faringe
1. Faringitis crónica.

Oído externo


Tapón de cerumen

Motivo de consulta. Paciente que refiere hipoacusia (de transmisión) y/o inestabilidad y mareos, así como sensación de ocupación y autofonía.
Exploración y diagnóstico. Por otoscopia se visualizará el tapón de cerumen obstruyendo el conducto auditivo externo (CAE).
Actitud terapéutica. Extracción:
1. Reblandecimiento del tapón mediante gotas
tópicas disolventes.
2. Extracción con agua templada mediante jeringa
apropiada.
3. Nunca usar pinzas para su extracción.
Complicaciones de la extracción: breve crisis vertiginosa
por la introducción de agua muy caliente o fría.

Perforación timpánica
Motivo de consulta. Paciente que consulta por hipoacusia (de transmisión), otalgia, drenaje por el oído y acúfenos.
Entre sus antecedentes personales destaca otitis media o traumatismo mecánico o barotrauma.
Exploración y diagnóstico. En otoscopia se visualiza la perforación timpánica.
Actitud terapéutica. El tímpano roto o perforado tiende a recuperarse por sí solo en dos meses. Los objetivos del tratamiento son aliviar el dolor y prevenir
la infección.
La reparación quirúrgica está indicada cuando:
— Hipoacusia de conducción significativa.
— Infección crónica y otorrea.
— Presenta riesgo de aparición de colesteatoma.

La edad avanzada no es una contraindicación para la reparación en un paciente que esté por lo demás sano.

Otitis externa

Motivo de consulta. Paciente que consulta por OTALGIA (al presionar el trago), hipoacusia (de transmisión) y en ocasiones prurito (cuando la etiología es
otomicosis).
Exploración y diagnóstico. En la otoscopia se aprecia el oído enrojecido e inflamado, incluyendo el canal auditivo, el cual puede aparecer similar a un eccema
con descamación de la piel.
La palpación o manipulación del oído externo aumenta el dolor. El cultivo del drenaje del oído puede revelar la presencia de bacterias u hongos.
Tratamiento. Generalmente, la aplicación tópica de gotas que contienen antibióticos para combatir lainfección y corticoides para reducir el prurito y la inflamación
es efectiva. Ocasionalmente, los medicamentos tópicos se complementan con pastillas.
En casos en que el dolor sea muy severo, se pueden usar analgésicos, y también resulta útil la aplicación de calor sobre el área afectada para reducir dicho dolor.

Otitis externa maligna o necrotizante

Motivo de consulta. Anciano diabético o inmunodeprimido que consulta por otitis externa pertinaz y progresiva.

El cuadro se puede acompañar de focalidad neurológica (parálisis facial periférica).
Diagnóstico. El cuadro es producido por pseudomona aeruginosa.
En la otoscopia llama la atención la presencia de tejido de granulación con formación de pólipos y esfacelos en las paredes del conducto. Posteriormente
necrosis de tejidos adyacentes.

Realización de tac craneal.
Tratamiento. Es un cuadro poco frecuente, pero muy grave (mortalidad 50%).
Tratamiento con ciprofloxacino 400 mg/12 h iv o ceftacidima iv 2 g/8 h.
Cuidados locales con desbridamiento quirúrgico.

Tumores benignos

Queratosis seborreica

Motivo de consulta. Consulta por lesión elevada, irregular, untuosa al tacto, con formación de quistes y surcos que pueden sangrar.
Tratamiento. Extirpación quirúrgica.

Lesiones precancerosas


Cuerno cutáneo

Motivo de consulta. El paciente consulta por neoformación verrugosa claramente delimitada de la epidermis con superficie ligeramente rugosa, que, localizada en el pabellón auricular, no afecta al cartílago.
Tratamiento. Extirpación quirúrgica.

Queratosis senil

Motivo de consulta. Aparición de elevación de la piel sobre el pabellón auricular y el conducto auditivo externo mal delimitada y superficie áspera, intacta y
parcialmente cubierta con costras que no infiltra el cartílago. Carecen de fositas y surcos característicos de la queratosis seborreica.
Es la lesión precancerosa más frecuente en el anciano.
Tratamiento. Extirpación quirúrgica.

Tumores malignos

Carcinoma espinocelular

Motivo de consulta. El paciente presenta tumor exofítico mal delimitado, superficie ulcerada, localizado en el borde del pabellón, infiltra el cartílago. Crece lentamente y produce metástasis en ganglios linfáticos.

Tratamiento. Extirpación quirúrgica amplia y vaciamiento cervical ganglionar si hay extensión regional.

Pronóstico. Lesiones pequeñas del hélix o antehélix tienen una tasa de curación a los cinco años del 95%, mientras que las lesiones próximas al meato auditivo
tienen peor pronóstico.

Oído medio
Otitis media aguda

Motivo de consulta. El paciente presenta hipoacusia,
autofonía, acúfenos y otalgia.
Diagnóstico. Otoscopia: tímpano hundido y/o congestivo.
Ante todo anciano que presenta una otitis aguda o serosa, especialmente si es unilateral, se debe explorar el cavum para descartar patología tumoral.
Tratamiento. Tratamiento de la infección si existe.

Otitis media crónica

Motivo de consulta. Se caracteriza por la aparición de procesos infecciosos que se prolongan durante más de seis semanas o bien cuando los episodios se
presentan tres o más veces al año. Ausencia de dolor e hipoacusia.
Diagnóstico. Otoscopia: perforación del tímpano y supuración fétida.
Cultivo del exudado.
Tratamiento. Antibioterapia y plantear cirugía.

Oído interno

Presbiacusia
Motivo de consulta. El paciente presenta hipoacusia de percepción pura (3), es decir, no hay separación entre la conducción ósea y aérea. Es bilateral y
aproximadamente simétrica.
Comienzo insidioso, nunca bruscamente; precozmente aparecen dificultades para la audición de sonidos agudos (timbre del teléfono, pájaros...).
Alteraciones de discriminación en ambientes ruidosos o en conversaciones cruzadas. Oyen pero no entienden.

Diagnóstico. Audiometría tonal y verbal:
La curva total desciende gradualmente y bilateral de las frecuencias agudas con conservación de las graves.
Hay discordancia entre la inteligibilidad, la discriminación y la curva tonal.
Tratamiento. Médico: carece de terapia eficaz.
Refuerzo psicológico o pautas de comunicación:

1. Mire de frente a la persona que tiene pérdida de audición para que ella pueda ver su cara cuando usted hable. Esto le permite a una persona con deficiencia de la capacidad auditiva observar las expresiones faciales, los gestos y movimientos
corporales y de labios, todas claves que facilitan la comunicación.
2. Hable lentamente y pronunciando.
3. Durante las conversaciones, apague la radio o televisión. Ambiente silencioso.
4. Hable levemente más fuerte que lo normal, pero no grite. El grito puede distorsionar su habla.
5. Reformule las afirmaciones con oraciones más cortas y sencillas si cree que no están entendiendo lo que dice.
Rehabilitador: prótesis acústica.
Una persona con hipoacusia bilateral debería usar audífonos bilaterales, ya que permiten mejorar la discriminación, la localización del sonido y percibir mejor
las conversaciones en lugares con ruido. Sin embargo, muchas personas no pueden permitirse comprar dos aparatos. El coste normal de un audífono es de
1.000-2.500 euros.
Si la única opción es colocar un audífono, debe colocarse en el que tenga menor hipoacusia.

Acúfenos

Motivo de consulta. Los acúfenos, tinnitus o ruidos de oído, tan frecuentes en el anciano, representan uno de los problemas más difíciles de resolver.
Tratamiento. Pueden mejorar con medicación vasorreguladora.

Patología vestibular

Motivo de consulta. Cualquier alteración de estas estructuras origina un desequilibrio que se va a expresar en forma de crisis vertiginosa (sensación errónea
de giro de objetos), desequilibrio (pérdida del balance corporal en la bipedestación), mareo (sensaciones vagas o inespecíficas o vista nublada).
Muchos procesos pueden producir este cuadro.

Enfermedad de Meniére

Motivo de consulta. Crisis vertiginosas intensas,
cortejo vegetativo, hipoacusia brusca, acúfenos.
Sensación de plenitud auricular. Intercrisis libres de síntomas.

Tratamiento. Restricción de sal y el uso de diuréticos El uso episódico de antivertiginosos es útil para el tratamiento de los episodios de vértigos.

Faringe

Faringitis seca
Motivo de consulta. El paciente con procesos urémicos, diabéticos, con falta de hidratación o en fase terminal que presenta: sensación de sequedad, picazón, carraspeo y/o sensación de cuerpo extraño en faringe.
Diagnóstico. Mucosa atrófica, seca, brillante.
Secreciones costrosas.
Tratamiento. Hidratación e intensa humidificación.
Vitaminoterapia

Fuente: parte del articulo
DEPRIVACIÓN SENSORIAL
Isabel Ródenas Iruela
Mercedes García Moreno
Javier Bordas Guijarro
M.ª Ángeles Flores Carmona
Carlos Martínez Manzanares

Better Ways to Wire Your Ears for Music

By SAM GROBART
Published: December 21, 2011



Dollar for dollar, headphones are the best way to listen to music. They pack more sonic wallop than even the most face-meltingly amazing loudspeaker system, and they do it for a lot less money. Think about it: a truly magnificent home-speaker system can cost well into the tens of thousands of dollars. A screaming set of headphones? A few hundred bucks, tops — and those in the Really Quite Good category can cost less than $100.
The basic Apple earbuds are among a selection of listening options that range from simple to sophisticated.
Tony Cenicola/The New York Times
The AKG K 390 noise-canceling headphones.

And yet most people go along and listen to music on whatever headphones or earbuds came with their audio player. For not a lot of money (or, if you’d prefer, kind of a lot of money) you can make a real and lasting improvement to the music you hear when you’re on your own. What follows is not an exhaustive test of headphones, because what sounds good to one person may be just plain terrible to another. Instead, use the information below to find your own sonic bliss.

THE GOOD BRANDS There are dozens of headphone makers. If you’re beginning a search, consider models from these manufacturers: AKG, Audio-Technica, Beyerdynamic, Etymotic, Grado, Klipsch and Sennheiser. Are there other makers of good headphones? Sure, but even though furious debates rage on in audiophile circles, these are the names that keep coming up. As to which brand is best, it depends on your needs.

REGARDING BEATS BY DR. DRE It seems necessary to mention here why Beats by Dr. Dre, a popular and groundbreaking headphone brand, is not included in the above group. Some people love Beats, which are known for their (overly?) strong bass. Some people think they are overpriced and not that good. There’s too much disagreement out there to include them in the “universally liked/respected” camp. They sure do look nice, though, so by all means check out the shiny red or white Beats models and come to your own conclusion.

KNOW YOUR HEADPHONE TYPES “Earbuds” are those earphones that likely came with your phone or music player. Replacement pairs can be bought for as little as $5 and often top out at around $30. Earbuds sit somewhat in your ear, but not all the way in. They are usually a single piece of plastic. maybe with some softer rubber permanently attached. These are the coach class of headphones; they’ll get you there, but nobody raves about them.

“In-ear earphones” are a step up. These models consist of a hard part, which contains the mechanics and electronics, and a very soft, pliable earpiece that goes well into your ear, plugging up the canal and forming a seal. In-ear earphones can be amazing — and also costly. For example, some models, like Klipsch’s Lou Reed X10i Signature Edition headphones, cost $400. But other well-regarded models, like Klipsch’s comparatively downmarket headphones, the S3s, cost $50.

Just remember two things about in-ear earphones. They do form a nearly soundproof seal, so you won’t hear much, like, say, a fire truck rapidly approaching a crosswalk, and that seal is entirely dependent on little rubber or polyurethane earpieces, which have an annoying tendency to pop off and roll down a storm drain when you pull the earphones out of your pocket.

“On-the-ear” headphones start to get you into more serious territory. These models don’t fully enclose the ear, but sit on top of the outer ear; if you think of foam-covered, Walkman-era headphones, you’ve got a correct, if outdated, image in mind.

On-the-ear headphones strike a middle ground between superportable in-ear models and bulkier over-the-ear headphones. Since they neither plug up your ear canal nor encapsulate your entire ear, they do let external sounds creep in, but in a home setting or even in many portable situations, you may not want to be fully closed off from the world around you. Prices run from $50 to $200.

On-ear headphones can either have an open or closed back. Open-backed headphones allow air to circulate, which is more comfortable. They also can help give the impression that sound is coming from around you, as opposed to emanating from your corpus callosum, which is a characteristic of closed-back and in-ear headphones. Closed-back models are better at sealing off the outside world, but your ears may get hot from the lack of air circulation.

“Over-the-ear” headphones are the Nimitz-class of the category. These are large domes that fully sit around and over your ear. They are bulky, often expensive (you can spend $40, or nearly $2,000), hard to travel with, primarily meant for listening at home and — when they are good — completely amazing. Over-the-ear models can also be closed- or open-backed. Since they are generally designed for home use, they sometimes come with a larger plug (0.25 inches, or 6.35 mm) instead of the miniplug (3.5 mm) connections common to digital music players.
The Beyerdynamic T-1 headphones.
The AKG K 450 headphones.

UNDERSTAND NOISE CANCELING A subcategory of headphones provides noise-canceling (N.C.) features. Noise-canceling headphones can be active or passive, but wearing them won’t turn the world into a silent movie: some noise will get through. What will be eliminated is lower-frequency ambient noise, like the constant thrum in an airplane’s cabin. This means you can listen to your selected audio at a lower volume, saving your ears.

Passive noise cancellation isn’t very sophisticated — sealing off your ear canal or covering your whole ear are the most common methods — but it is fairly effective. What’s fancier is active N.C., in which the headphones detect ambient noise and emit a sound wave that cancels out the humming/buzzing you would otherwise hear.

Noise-canceling headphones are good for certain situations, but they aren’t necessary for everyday use and most people can do without them. They can also run from about $70 to a few hundred dollars. Bose is a big name in the active-N.C. world, but also consider the brands mentioned above, many of which offer active N.C. headphones in earbud, on-the-ear and over-the-ear models.

FIND YOUR PAIR (THE RIGHT WAY) Determining which kind of headphones to get is something only you can figure out. Some people, for example, prefer the portability that a pair of earbuds provide — just roll them up and stick them in your pocket. Other people can’t stand the idea of little rubber plugs sticking in their ears.

You won’t know your own preference until you try headphones out in person. Go to a store and try out a few different models. Bring your iPhone, iPod, Zune, whatever, and connect it to a pair and play a song you know really well. It may be more revealing if you’re listening to some obsessively engineered track that creates an unparalleled soundscape (I’m talking to you, Steely Dan fans), but even if your favorite song is “Jump” by Kriss Kross, it’s better to judge equipment with a song you know than something provided by the store.

Using your reference song, you can then determine which style and model of headphone sounds best. Pay no attention to the specs. It doesn’t matter what it says on the side of the box; if it sounds good to you, then it sounds good.

Fuente: The New York times, Personal Tech.
http://www.nytimes.com/2011/12/22/technology/personaltech/do-some-research-to-improve-the-music-to-your-ears.html?pagewanted=1&sq=ear%20sounds&st=cse&scp=1

Who Made That Sound?

By HILARY GREENBAUM

For the past week, I actually haven’t set foot on the sixth floor, as I’ve been serving my civic duty as a juror in the State of New York. Between each case that’s called, though, I can’t help hearing that sound. If you’ve ever watched an episode of “Law and Order,” you know exactly what I mean. It has been called, among other variations, the “doink doink,” the “dun dun” and the “chung chung.”


No, the courts of New York do not actually blast those two, distinctive notes through the speaker system (although that would be amazing), but I can’t get them out of my head. According to IMDb, “The distinctive thunk-thunk sound effect used in between scenes was created by combining close to a dozen sounds, including that of a group of monks stamping on a floor. The sound is intended to be reminiscent of both a jurist’s gavel and a jail-cell door slamming.” When the original “Law and Order” was canceled last year, Brandon Kim of I.F.C. referred it as the “sound that’s got to be the current title holder for Most Recognizable Sound on TV.”

That audible brand was created by Mike Post, who also wrote the theme to the show. He’s a Grammy and Emmy award-winning composer who has scored the themes of television shows like “The A-Team,” “Doogie Howser, M.D.,” “MacGyver,” “Magnum, P.I.,” “N.Y.P.D. Blue” and “The Greatest American Hero.” Multiple albums are available of Post’s work, including “Inventions from the Blue Line” and “The Essential Mike Post TV Theme Collection.”

Fuente: The New York times
http://6thfloor.blogs.nytimes.com/2011/03/28/who-made-that-sound/?scp=4&sq=head%20sounds&st=cse

To Sleep on the Subway, Maybe, but to Dream? Poor Chance

Dr. Brandon Foreman, a neurology fellow, was able to fall asleep on the A train to help a researcher study the quality of sleep obtained on the subway.
image: Marcus Yam for The New York Times


By CHRISTINE HAUGHNEY
Published: December 7, 2011


A ride on the New York subway can be a sensory overload: musicians perform for change; conductors plead to those who hold open train doors to relent; and passengers, often in unimaginably close proximity, subject one another to all sorts of sights, sounds, smells and touches, preferably inadvertent.

Milagro Benitez wired Dr. Foreman's head with electrodes to capture brain-wave data while he slept. He was asleep for 10 minutes on a 23.5-minute ride.

Amid all of that, some New Yorkers nevertheless manage to fall asleep. Seats are found, trains begin their rhythmic rattles of movement, and eyelids flutter closed. Gritted jaws loosen, furrowed brows release and heads nod.

People outside of New York may wonder how in a city that never sleeps, so many New Yorkers manage to doze on the subway.

There is no law against it, but those who take subway catnaps do so at their own risk; a recent Metropolitan Transportation Authority committee meeting featured a presentation on how criminals seeking iPhones slice open the pockets of dozing passengers.

So are these naps really worth the trouble?

Dr. Carl Bazil, director of the Epilepsy and Sleep Division at New York-Presbyterian Hospital/Columbia University Medical Center, offered to try to find out.

After Dr. Bazil stepped into an uptown A train on a recent morning, he tried to guess what stage of sleep the nappers onboard were in. He said that to reach Stage 1 sleep, the least restorative of the five stages, riders must be able to slow down their eye movements. To get Stage 2 sleep, riders must relax their muscles and stop moving their eyes entirely.

As Dr. Bazil watched the riders sitting across from him, the nappers’ eyelids fluttered when train doors opened. The riders also seemed to clench their messenger bags and backpacks with death grips.

“I suspect all you get is Stage 1 sleep; it’s not going to be restorative,” he said. “It’s kind of wasted sleep.”

At a reporter’s request, Dr. Bazil wired up a sleepy subway rider to study his brain waves as he tried to nap. He enlisted Dr. Brandon Foreman, a 30-year-old neurology fellow, whose 2-year-old son, Jude, still does not sleep through the night. Neither does Dr. Foreman.

But he has observed how the subway lulls his son to sleep, so he tries to replicate the train’s stops and jerks when he puts his son to bed. Dr. Foreman is no stranger to subway napping: He began doing so when commuting from Brooklyn during his residency, and said he coveted any sleep he could get.

“Lectures, classes, I can pretty much sleep anywhere,” Dr. Foreman said. “But it’s not usually a great sleep. It’s more the nodding off.”

Both doctors met at the end of a long workweek after Dr. Foreman had been up every night dealing with his son’s cold. As Dr. Foreman yawned, Dr. Bazil had a technician attach 25 multicolored plastic wires to Dr. Foreman’s head, connecting them to a monitor slightly larger than an iPod to track his brain waves. Then Dr. Foreman covered the wires with a long sock and a winter hat.

The pair got onto a southbound A train at 207th Street. After Dr. Foreman chose a corner seat, Dr. Bazil sat across from him to take notes. When the train left the station at 6:09 p.m., it seemed unlikely that Dr. Foreman would get any sleep. The train’s operator screeched the cars along as if she were training for Formula One. She shouted into the loudspeakers that her train was late, and peeled from stop to stop.

Dr. Foreman yawned, folded his arms, crossed his legs and shut his eyes. He opened his eyes when the train stopped. His eyes fluttered when several neurologists boarded and chatted over his shoulder. The train jostled. He opened his eyes and yawned deeply.

By 6:18 p.m., two minutes after Dr. Foreman left the 168th Street station, he looked as if he was falling asleep. He first held his head up and kept his arms crossed. But he let his head nod back and forth slightly. Then his head fell, and he dozed until 59th Street — no doubt aided by the uninterrupted run from 125th Street. As the doors opened at 59th Street, Dr. Foreman jumped up and hopped off the train.

After they briefly celebrated what looked like a successful subway nap, the doctors boarded an uptown train to see if Dr. Foreman could fall asleep again. Dr. Foreman found a seat lodged between two passengers. He put on his jacket hood, crossed his legs, folded his arms and let his head fall. While the conductor was quieter on this train, Dr. Foreman could not get back to sleep. At 145th Street, when a vendor stood before him and shouted that he was selling four DVDs for $10, Dr. Foreman opened his eyes widely.

“No luck,” he said.

Dr. Bazil was more pleased with the results. After downloading the data about Dr. Foreman’s brain waves, Dr. Bazil found that Dr. Foreman had slept for 10 minutes out of a 23.5-minute ride. For three and a half minutes, Dr. Foreman reached a Stage 2 level of sleep.

“It looks like it is definitely possible to get small amounts of restorative sleep on the subway, but only very small amounts,” Dr. Bazil said. He added that some studies show “even a brief nap that includes Stage 2 sleep can improve performance.”

But Dr. Foreman was less persuaded that he got any productive sleep.

“I don’t feel rested,” he said. “It’s not like I took a nap in bed.”
Fuente: The New York Times