domingo, 28 de agosto de 2011

Do You Suffer From Decision Fatigue?


Three men doing time in Israeli prisons recently appeared before a parole board consisting of a judge, a criminologist and a social worker.

The three prisoners had completed at least two-thirds of their sentences, but the parole board granted freedom to only one of them. Guess which one:

Case 1 (heard at 8:50 a.m.): An Arab Israeli serving a 30-month sentence for fraud.
Case 2 (heard at 3:10 p.m.): A Jewish Israeli serving a 16-month sentence for assault.
Case 3 (heard at 4:25 p.m.): An Arab Israeli serving a 30-month sentence for fraud.

There was a pattern to the parole board’s decisions, but it wasn’t related to the men’s ethnic backgrounds, crimes or sentences.

It was all about timing, as researchers discovered by analyzing more than 1,100 decisions over the course of a year.

Judges, who would hear the prisoners’ appeals and then get advice from the other members of the board, approved parole in about a third of the cases, but the probability of being paroled fluctuated wildly throughout the day.

Prisoners who appeared early in the morning received parole about 70 percent of the time, while those who appeared late in the day were paroled less than 10 percent of the time.
The odds favored the prisoner who appeared at 8:50 a.m. — and he did in fact receive parole.

But even though the other Arab Israeli prisoner was serving the same sentence for the same crime — fraud — the odds were against him when he appeared (on a different day) at 4:25 in the afternoon.

He was denied parole, as was the Jewish Israeli prisoner at 3:10 p.m, whose sentence was shorter than that of the man who was released. They were just asking for parole at the wrong time of day.

There was nothing malicious or even unusual about the judges’ behavior, which was reported earlier this year by Jonathan Levav of Stanford and Shai Danziger of Ben-Gurion University.

The judges’ erratic judgment was due to the occupational hazard of being, as George W. Bush once put it, “the decider.”

The mental work of ruling on case after case, whatever the individual merits, wore them down.

This sort of decision fatigue can make quarterbacks prone to dubious choices late in the game and C.F.O.’s prone to disastrous dalliances late in the evening.

It routinely warps the judgment of everyone, executive and nonexecutive, rich and poor — in fact, it can take a special toll on the poor.

Yet few people are even aware of it, and researchers are only beginning to understand why it happens and how to counteract it.

Decision fatigue helps explain why ordinarily sensible people get angry at colleagues and families, splurge on clothes, buy junk food at the supermarket and can’t resist the dealer’s offer to rustproof their new car.

No matter how rational and high-minded you try to be, you can’t make decision after decision without paying a biological price.

It’s different from ordinary physical fatigue — you’re not consciously aware of being tired — but you’re low on mental energy.

The more choices you make throughout the day, the harder each one becomes for your brain, and eventually it looks for shortcuts, usually in either of two very different ways.

One shortcut is to become reckless: to act impulsively instead of expending the energy to first think through the consequences.

(Sure, tweet that photo! What could go wrong?) The other shortcut is the ultimate energy saver: do nothing. Instead of agonizing over decisions, avoid any choice.

Ducking a decision often creates bigger problems in the long run, but for the moment, it eases the mental strain.

You start to resist any change, any potentially risky move — like releasing a prisoner who might commit a crime.

So the fatigued judge on a parole board takes the easy way out, and the prisoner keeps doing time.

Decision fatigue is the newest discovery involving a phenomenon called ego depletion, a term coined by the social psychologist Roy F. Baumeister in homage to a Freudian hypothesis.

Freud speculated that the self, or ego, depended on mental activities involving the transfer of energy.

He was vague about the details, though, and quite wrong about some of them (like his idea that artists “sublimate” sexual energy into their work, which would imply that adultery should be especially rare at artists’ colonies).

Freud’s energy model of the self was generally ignored until the end of the century, when Baumeister began studying mental discipline in a series of experiments, first at Case Western and then at Florida State University.

These experiments demonstrated that there is a finite store of mental energy for exerting self-control.

When people fended off the temptation to scarf down M&M’s or freshly baked chocolate-chip cookies, they were then less able to resist other temptations.

When they forced themselves to remain stoic during a tearjerker movie, afterward they gave up more quickly on lab tasks requiring self-discipline, like working on a geometry puzzle or squeezing a hand-grip exerciser.

Willpower turned out to be more than a folk concept or a metaphor.

It really was a form of mental energy that could be exhausted.

The experiments confirmed the 19th-century notion of willpower being like a muscle that was fatigued with use, a force that could be conserved by avoiding temptation.

To study the process of ego depletion, researchers concentrated initially on acts involving self-control ¬— the kind of self-discipline popularly associated with willpower, like resisting a bowl of ice cream.

They weren’t concerned with routine decision-making, like choosing between chocolate and vanilla, a mental process that they assumed was quite distinct and much less strenuous.

Intuitively, the chocolate-vanilla choice didn’t appear to require willpower.

But then a postdoctoral fellow, Jean Twenge, started working at Baumeister’s laboratory right after planning her wedding.

As Twenge studied the results of the lab’s ego-depletion experiments, she remembered how exhausted she felt the evening she and her fiancé went through the ritual of registering for gifts.

Did they want plain white china or something with a pattern? Which brand of knives? How many towels? What kind of sheets? Precisely how many threads per square inch?
“By the end, you could have talked me into anything,” Twenge told her new colleagues.

The symptoms sounded familiar to them too, and gave them an idea.

A nearby department store was holding a going-out-of-business sale, so researchers from the lab went off to fill their car trunks with simple products — not exactly wedding-quality gifts, but sufficiently appealing to interest college students.

When they came to the lab, the students were told they would get to keep one item at the end of the experiment, but first they had to make a series of choices.

Would they prefer a pen or a candle? A vanilla-scented candle or an almond-scented one? A candle or a T-shirt? A black T-shirt or a red T-shirt?

A control group, meanwhile — let’s call them the nondeciders — spent an equally long period contemplating all these same products without having to make any choices.

They were asked just to give their opinion of each product and report how often they had used such a product in the last six months.

Afterward, all the participants were given one of the classic tests of self-control: holding your hand in ice water for as long as you can.

The impulse is to pull your hand out, so self-discipline is needed to keep the hand underwater.

The deciders gave up much faster; they lasted 28 seconds, less than half the 67-second average of the nondeciders.

Making all those choices had apparently sapped their willpower, and it wasn’t an isolated effect.

It was confirmed in other experiments testing students after they went through exercises like choosing courses from the college catalog.

For a real-world test of their theory, the lab’s researchers went into that great modern arena of decision making: the suburban mall.

They interviewed shoppers about their experiences in the stores that day and then asked them to solve some simple arithmetic problems.

The researchers politely asked them to do as many as possible but said they could quit at any time.

Sure enough, the shoppers who had already made the most decisions in the stores gave up the quickest on the math problems.

When you shop till you drop, your willpower drops, too.

Any decision, whether it’s what pants to buy or whether to start a war, can be broken down into what psychologists call the Rubicon model of action phases, in honor of the river that separated Italy from the Roman province of Gaul.

When Caesar reached it in 49 B.C., on his way home after conquering the Gauls, he knew that a general returning to Rome was forbidden to take his legions across the river with him, lest it be considered an invasion of Rome.

Waiting on the Gaul side of the river, he was in the “predecisional phase” as he contemplated the risks and benefits of starting a civil war.

Then he stopped calculating and crossed the Rubicon, reaching the “postdecisional phase,” which Caesar defined much more felicitously: “The die is cast.”

The whole process could deplete anyone’s willpower, but which phase of the decision-making process was most fatiguing?

To find out, Kathleen Vohs, a former colleague of Baumeister’s now at the University of Minnesota, performed an experiment using the self-service Web site of Dell Computers.

One group in the experiment carefully studied the advantages and disadvantages of various features available for a computer — the type of screen, the size of the hard drive, etc. — without actually making a final decision on which ones to choose.

A second group was given a list of predetermined specifications and told to configure a computer by going through the laborious, step-by-step process of locating the specified features among the arrays of options and then clicking on the right ones.

The purpose of this was to duplicate everything that happens in the postdecisional phase, when the choice is implemented.

The third group had to figure out for themselves which features they wanted on their computers and go through the process of choosing them; they didn’t simply ponder options (like the first group) or implement others’ choices (like the second group).

They had to cast the die, and that turned out to be the most fatiguing task of all.

When self-control was measured, they were the one who were most depleted, by far.

The experiment showed that crossing the Rubicon is more tiring than anything that happens on either bank — more mentally fatiguing than sitting on the Gaul side contemplating your options or marching on Rome once you’ve crossed.

As a result, someone without Caesar’s willpower is liable to stay put.

To a fatigued judge, denying parole seems like the easier call not only because it preserves the status quo and eliminates the risk of a parolee going on a crime spree but also because it leaves more options open: the judge retains the option of paroling the prisoner at a future date without sacrificing the option of keeping him securely in prison right now.

Part of the resistance against making decisions comes from our fear of giving up options.

The word “decide” shares an etymological root with “homicide,” the Latin word “caedere,” meaning “to cut down” or “to kill,” and that loss looms especially large when decision fatigue sets in.

Once you’re mentally depleted, you become reluctant to make trade-offs, which involve a particularly advanced and taxing form of decision making.

In the rest of the animal kingdom, there aren’t a lot of protracted negotiations between predators and prey.

To compromise is a complex human ability and therefore one of the first to decline when willpower is depleted.

You become what researchers call a cognitive miser, hoarding your energy. If you’re shopping, you’re liable to look at only one dimension, like price: just give me the cheapest.

Or you indulge yourself by looking at quality: I want the very best (an especially easy strategy if someone else is paying).

Decision fatigue leaves you vulnerable to marketers who know how to time their sales, as Jonathan Levav, the Stanford professor, demonstrated in experiments involving tailored suits and new cars.

The idea for these experiments also happened to come in the preparations for a wedding, a ritual that seems to be the decision-fatigue equivalent of Hell Week.

At his fiancée’s suggestion, Levav visited a tailor to have a bespoke suit made and began going through the choices of fabric, type of lining and style of buttons, lapels, cuffs and so forth.

“By the time I got through the third pile of fabric swatches, I wanted to kill myself,” Levav recalls. “I couldn’t tell the choices apart anymore.

After a while my only response to the tailor became ‘What do you recommend?’ I just couldn’t take it.”

Levav ended up not buying any kind of bespoke suit (the $2,000 price made that decision easy enough), but he put the experience to use in a pair of experiments conducted with Mark Heitmann, then at Christian-Albrechts University in Germany; Andreas Herrmann, at the University of St. Gallen in Switzerland; and Sheena Iyengar, of Columbia.

One involved asking M.B.A. students in Switzerland to choose a bespoke suit; the other was conducted at German car dealerships, where customers ordered options for their new sedans.

The car buyers — and these were real customers spending their own money — had to choose, for instance, among 4 styles of gearshift knobs, 13 kinds of wheel rims, 25 configurations of the engine and gearbox and a palette of 56 colors for the interior.

As they started picking features, customers would carefully weigh the choices, but as decision fatigue set in, they would start settling for whatever the default option was.

And the more tough choices they encountered early in the process — like going through those 56 colors to choose the precise shade of gray or brown — the quicker people became fatigued and settled for the path of least resistance by taking the default option.

By manipulating the order of the car buyers’ choices, the researchers found that the customers would end up settling for different kinds of options, and the average difference totaled more than 1,500 euros per car (about $2,000 at the time).

Whether the customers paid a little extra for fancy wheel rims or a lot extra for a more powerful engine depended on when the choice was offered and how much willpower was left in the customer.

Similar results were found in the experiment with custom-made suits: once decision fatigue set in, people tended to settle for the recommended option.

When they were confronted early on with the toughest decisions — the ones with the most options, like the 100 fabrics for the suit — they became fatigued more quickly and also reported enjoying the shopping experience less.

Shopping can be especially tiring for the poor, who have to struggle continually with trade-offs.

Most of us in America won’t spend a lot of time agonizing over whether we can afford to buy soap, but it can be a depleting choice in rural India.

Dean Spears, an economist at Princeton, offered people in 20 villages in Rajasthan in northwestern India the chance to buy a couple of bars of brand-name soap for the equivalent of less than 20 cents.

It was a steep discount off the regular price, yet even that sum was a strain for the people in the 10 poorest villages.

Whether or not they bought the soap, the act of making the decision left them with less willpower, as measured afterward in a test of how long they could squeeze a hand grip.

In the slightly more affluent villages, people’s willpower wasn’t affected significantly.

Because they had more money, they didn’t have to spend as much effort weighing the merits of the soap versus, say, food or medicine.

Spears and other researchers argue that this sort of decision fatigue is a major — and hitherto ignored — factor in trapping people in poverty.

Because their financial situation forces them to make so many trade-offs, they have less willpower to devote to school, work and other activities that might get them into the middle class.

It’s hard to know exactly how important this factor is, but there’s no doubt that willpower is a special problem for poor people.

Study after study has shown that low self-control correlates with low income as well as with a host of other problems, including poor achievement in school, divorce, crime, alcoholism and poor health.

Lapses in self-control have led to the notion of the “undeserving poor” — epitomized by the image of the welfare mom using food stamps to buy junk food — but Spears urges sympathy for someone who makes decisions all day on a tight budget.

In one study, he found that when the poor and the rich go shopping, the poor are much more likely to eat during the shopping trip.

This might seem like confirmation of their weak character — after all, they could presumably save money and improve their nutrition by eating meals at home instead of buying ready-to-eat snacks like Cinnabons, which contribute to the higher rate of obesity among the poor.

But if a trip to the supermarket induces more decision fatigue in the poor than in the rich — because each purchase requires more mental trade-offs — by the time they reach the cash register, they’ll have less willpower left to resist the Mars bars and Skittles.

Not for nothing are these items called impulse purchases.

And this isn’t the only reason that sweet snacks are featured prominently at the cash register, just when shoppers are depleted after all their decisions in the aisles.

With their willpower reduced, they’re more likely to yield to any kind of temptation, but they’re especially vulnerable to candy and soda and anything else offering a quick hit of sugar.

While supermarkets figured this out a long time ago, only recently did researchers discover why.

The discovery was an accident resulting from a failed experiment at Baumeister’s lab.

The researchers set out to test something called the Mardi Gras theory — the notion that you could build up willpower by first indulging yourself in pleasure, the way Mardi Gras feasters do just before the rigors of Lent.

In place of a Fat Tuesday breakfast, the chefs in the lab at Florida State whipped up lusciously thick milkshakes for a group of subjects who were resting in between two laboratory tasks requiring willpower.

Sure enough, the delicious shakes seemed to strengthen willpower by helping people perform better than expected on the next task.

So far, so good. But the experiment also included a control group of people who were fed a tasteless concoction of low-fat dairy glop.

It provided them with no pleasure, yet it produced similar improvements in self-control.

The Mardi Gras theory looked wrong.

Besides tragically removing an excuse for romping down the streets of New Orleans, the result was embarrassing for the researchers.

Matthew Gailliot, the graduate student who ran the study, stood looking down at his shoes as he told Baumeister about the fiasco.

Baumeister tried to be optimistic.

Maybe the study wasn’t a failure. Something had happened, after all.

Even the tasteless glop had done the job, but how? If it wasn’t the pleasure, could it be the calories?

At first the idea seemed a bit daft. For decades, psychologists had been studying performance on mental tasks without worrying much about the results being affected by dairy-product consumption.

They liked to envision the human mind as a computer, focusing on the way it processed information.

In their eagerness to chart the human equivalent of the computer’s chips and circuits, most psychologists neglected one mundane but essential part of the machine: the power supply.

The brain, like the rest of the body, derived energy from glucose, the simple sugar manufactured from all kinds of foods.

To establish cause and effect, researchers at Baumeister’s lab tried refueling the brain in a series of experiments involving lemonade mixed either with sugar or with a diet sweetener.

The sugary lemonade provided a burst of glucose, the effects of which could be observed right away in the lab; the sugarless variety tasted quite similar without providing the same burst of glucose.

Again and again, the sugar restored willpower, but the artificial sweetener had no effect.

The glucose would at least mitigate the ego depletion and sometimes completely reverse it.

The restored willpower improved people’s self-control as well as the quality of their decisions: they resisted irrational bias when making choices, and when asked to make financial decisions, they were more likely to choose the better long-term strategy instead of going for a quick payoff.

The ego-depletion effect was even demonstrated with dogs in two studies by Holly Miller and Nathan DeWall at the University of Kentucky.

After obeying sit and stay commands for 10 minutes, the dogs performed worse on self-control tests and were also more likely to make the dangerous decision to challenge another dog’s turf.

But a dose of glucose restored their willpower.

Despite this series of findings, brain researchers still had some reservations about the glucose connection.

Skeptics pointed out that the brain’s overall use of energy remains about the same regardless of what a person is doing, which doesn’t square easily with the notion of depleted energy affecting willpower.

Among the skeptics was Todd Heatherton, who worked with Baumeister early in his career and eventually wound up at Dartmouth, where he became a pioneer of what is called social neuroscience: the study of links between brain processes and social behavior.

He believed in ego depletion, but he didn’t see how this neural process could be caused simply by variations in glucose levels.

To observe the process — and to see if it could be reversed by glucose — he and his colleagues recruited 45 female dieters and recorded images of their brains as they reacted to pictures of food.

Next the dieters watched a comedy video while forcing themselves to suppress their laughter — a standard if cruel way to drain mental energy and induce ego depletion.

Then they were again shown pictures of food, and the new round of brain scans revealed the effects of ego depletion: more activity in the nucleus accumbens, the brain’s reward center, and a corresponding decrease in the amygdala, which ordinarily helps control impulses.

The food’s appeal registered more strongly while impulse control weakened — not a good combination for anyone on a diet.

But suppose people in this ego-depleted state got a quick dose of glucose? What would a scan of their brains reveal?

The results of the experiment were announced in January, during Heatherton’s speech accepting the leadership of the Society for Personality and Social Psychology, the world’s largest group of social psychologists.

In his presidential address at the annual meeting in San Antonio, Heatherton reported that administering glucose completely reversed the brain changes wrought by depletion — a finding, he said, that thoroughly surprised him.

Heatherton’s results did much more than provide additional confirmation that glucose is a vital part of willpower; they helped solve the puzzle over how glucose could work without global changes in the brain’s total energy use.

Apparently ego depletion causes activity to rise in some parts of the brain and to decline in others.

Your brain does not stop working when glucose is low.

It stops doing some things and starts doing others.

It responds more strongly to immediate rewards and pays less attention to long-term prospects.
The discoveries about glucose help explain why dieting is a uniquely difficult test of self-control — and why even people with phenomenally strong willpower in the rest of their lives can have such a hard time losing weight.

They start out the day with virtuous intentions, resisting croissants at breakfast and dessert at lunch, but each act of resistance further lowers their willpower.

As their willpower weakens late in the day, they need to replenish it.

But to resupply that energy, they need to give the body glucose. They’re trapped in a nutritional catch-22:

1. In order not to eat, a dieter needs willpower.

2. In order to have willpower, a dieter needs to eat.

As the body uses up glucose, it looks for a quick way to replenish the fuel, leading to a craving for sugar.

After performing a lab task requiring self-control, people tend to eat more candy but not other kinds of snacks, like salty, fatty potato chips.

The mere expectation of having to exert self-control makes people hunger for sweets.

A similar effect helps explain why many women yearn for chocolate and other sugary treats just before menstruation: their bodies are seeking a quick replacement as glucose levels fluctuate.

A sugar-filled snack or drink will provide a quick improvement in self-control (that’s why it’s convenient to use in experiments), but it’s just a temporary solution.

The problem is that what we identify as sugar doesn’t help as much over the course of the day as the steadier supply of glucose we would get from eating proteins and other more nutritious foods.

The benefits of glucose were unmistakable in the study of the Israeli parole board. In midmorning, usually a little before 10:30, the parole board would take a break, and the judges would be served a sandwich and a piece of fruit.

The prisoners who appeared just before the break had only about a 20 percent chance of getting parole, but the ones appearing right after had around a 65 percent chance.

The odds dropped again as the morning wore on, and prisoners really didn’t want to appear just before lunch: the chance of getting parole at that time was only 10 percent.

After lunch it soared up to 60 percent, but only briefly.

Remember that Jewish Israeli prisoner who appeared at 3:10 p.m. and was denied parole from his sentence for assault?

He had the misfortune of being the sixth case heard after lunch.

But another Jewish Israeli prisoner serving the same sentence for the same crime was lucky enough to appear at 1:27 p.m., the first case after lunch, and he was rewarded with parole.

It must have seemed to him like a fine example of the justice system at work, but it probably had more to do with the judge’s glucose levels.

It’s simple enough to imagine reforms for the parole board in Israel — like, say, restricting each judge’s shift to half a day, preferably in the morning, interspersed with frequent breaks for food and rest.

But it’s not so obvious what to do with the decision fatigue affecting the rest of society.

Even if we could all afford to work half-days, we would still end up depleting our willpower all day long, as Baumeister and his colleagues found when they went into the field in Würzburg in central Germany.

The psychologists gave preprogrammed BlackBerrys to more than 200 people going about their daily routines for a week.

The phones went off at random intervals, prompting the people to report whether they were currently experiencing some sort of desire or had recently felt a desire.

The painstaking study, led by Wilhelm Hofmann, then at the University of Würzburg, collected more than 10,000 momentary reports from morning until midnight.

Desire turned out to be the norm, not the exception.

Half the people were feeling some desire when their phones went off — to snack, to goof off, to express their true feelings to their bosses — and another quarter said they had felt a desire in the past half-hour.

Many of these desires were ones that the men and women were trying to resist, and the more willpower people expended, the more likely they became to yield to the next temptation that came along.

When faced with a new desire that produced some I-want-to-but-I-really-shouldn’t sort of inner conflict, they gave in more readily if they had already fended off earlier temptations, particularly if the new temptation came soon after a previously reported one.

The results suggested that people spend between three and four hours a day resisting desire.

Put another way, if you tapped four or five people at any random moment of the day, one of them would be using willpower to resist a desire.

The most commonly resisted desires in the phone study were the urges to eat and sleep, followed by the urge for leisure, like taking a break from work by doing a puzzle or playing a game instead of writing a memo.

Sexual urges were next on the list of most-resisted desires, a little ahead of urges for other kinds of interactions, like checking Facebook.

To ward off temptation, people reported using various strategies.

The most popular was to look for a distraction or to undertake a new activity, although sometimes they tried suppressing it directly or simply toughing their way through it.

Their success was decidedly mixed.

They were pretty good at avoiding sleep, sex and the urge to spend money, but not so good at resisting the lure of television or the Web or the general temptation to relax instead of work.

We have no way of knowing how much our ancestors exercised self-control in the days before BlackBerrys and social psychologists, but it seems likely that many of them were under less ego-depleting strain.

When there were fewer decisions, there was less decision fatigue.

Today we feel overwhelmed because there are so many choices.

Your body may have dutifully reported to work on time, but your mind can escape at any instant.

A typical computer user looks at more than three dozen Web sites a day and gets fatigued by the continual decision making — whether to keep working on a project, check out TMZ, follow a link to YouTube or buy something on Amazon.

You can do enough damage in a 10-minute online shopping spree to wreck your budget for the rest of the year.

The cumulative effect of these temptations and decisions isn’t intuitively obvious.

Virtually no one has a gut-level sense of just how tiring it is to decide.

Big decisions, small decisions, they all add up.

Choosing what to have for breakfast, where to go on vacation, whom to hire, how much to spend — these all deplete willpower, and there’s no telltale symptom of when that willpower is low.

It’s not like getting winded or hitting the wall during a marathon.

Ego depletion manifests itself not as one feeling but rather as a propensity to experience everything more intensely.

When the brain’s regulatory powers weaken, frustrations seem more irritating than usual.

Impulses to eat, drink, spend and say stupid things feel more powerful (and alcohol causes self-control to decline further).

Like those dogs in the experiment, ego-depleted humans become more likely to get into needless fights over turf.

In making decisions, they take illogical shortcuts and tend to favor short-term gains and delayed costs.

Like the depleted parole judges, they become inclined to take the safer, easier option even when that option hurts someone else.

“Good decision making is not a trait of the person, in the sense that it’s always there,” Baumeister says.

“It’s a state that fluctuates.” His studies show that people with the best self-control are the ones who structure their lives so as to conserve willpower.

They don’t schedule endless back-to-back meetings.

They avoid temptations like all-you-can-eat buffets, and they establish habits that eliminate the mental effort of making choices.

Instead of deciding every morning whether or not to force themselves to exercise, they set up regular appointments to work out with a friend.

Instead of counting on willpower to remain robust all day, they conserve it so that it’s available for emergencies and important decisions.

“Even the wisest people won’t make good choices when they’re not rested and their glucose is low,” Baumeister points out.

That’s why the truly wise don’t restructure the company at 4 p.m. They don’t make major commitments during the cocktail hour.

And if a decision must be made late in the day, they know not to do it on an empty stomach. “The best decision makers,” Baumeister says, “are the ones who know when not to trust themselves.”

John Tierney ( is a science columnist for The Times.

His essay is adapted from a book he wrote with Roy F. Baumeister, “Willpower: Rediscovering the Greatest Human Strength,” which comes out next month.
Editor: Aaron Retica (
Fuente: The New york Times; 17 de agosto, 2011

£10 million raised for GSK hearing disorder spin-out

World News | August 23, 2011

Kevin Grogan

£10 million raised for GSK hearing disorder spin-out

Autifony Therapeutics, a UK-based biotechnology start-up specialising in hearing loss and tinnitus which has been set up by ex-GlaxoSmithKline senior scientists, has received financial backing from a couple of major investors plus the drugs giant itself.

GSK noted that it has received a 25.4% minority equity stake, representing nearly a £1.3 million investment, in Autifony, while Imperial Innovations Group and SV Life Sciences have committed to invest £5 million each. Following the £10 million funding round, GSK will own 13.2% of the firm, which has preclinical assets targeting voltage-gated ion channels, the modulation of which is thought to have potential in the treatment of hearing disorders.

Charles Large, Autifony’s co-founder and former director of molecular and cellular biology at GSK, noted that “there are currently no pharmacological treatments available for hearing loss or tinnitus despite the increasingly large number of patients, both old and young, that suffer from these conditions". He claimed the start-up represents "an important opportunity to bring together our drug-discovery experience with the expertise of academic groups in this field", in particular University College London’s Ear Institute (UCL is a founding shareholder in Autifony).

Susan Searle, Imperial Innovations’ chief executive, said that "this is a creative approach to building new companies, leveraging established pharmaceutical assets together with the world class scientific expertise that exists at the UCL Ear Institute.” Proceeds from the funding will be used to accelerate preclinical development with the objective of commencing human trials in early 2013.


Recovery after acute unilateral vestibular loss and predictors for remaining symptoms

Fuente de la imagen:
Ann-Sofi C. Kammerlind RPT, PhDa, Torbjörn E.A. Ledin MD, PhDc, Lars M. Ödkvist MD, PhDd and Elisabeth I.B. Skargren RPT, PhDb

a Physiotherapy, Ryhov County Hospital, Jönköping, Sweden

b Division of Physiotherapy, Department of Medicine and Health, Faculty of Health Sciences, Linköping University, Linköping, Sweden

c Division of Otorhinolaryngology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden

d Department of Otorhinolaryngology, University Hospital, Linköping, Sweden
Received 27 February 2010.
Available online 2 October 2010.



The aims of this study were to follow recovery during the first 6 months after acute unilateral vestibular loss (AUVL) and to determine predictors for self-rated remaining symptoms.

Materials and methods

Forty-two subjects were included less than 10 days after AUVL.
Static and dynamic clinical balance tests, visual analogue scales, University of California Los Angeles Dizziness Questionnaire, Dizziness Beliefs Scale, European Quality of Life questionnaire, Dizziness Handicap Inventory, and Hospital Anxiety and Depression Scale were performed at inclusion and at 7 follow-ups over 6 months. Subjects rated their symptoms on visual analogue scales daily at home. Videonystagmography was performed in the acute stage and after 10 weeks.


Decrease of symptoms and improvement of balance function were larger during the first compared with the latter part of the follow-up period.

Visual analogue scale ratings for balance problems were higher than those for dizziness.

A prediction model was created based on the results of 4 tests in the acute stage:
1- standing on foam with eyes closed,
2-standing on 1 leg with eyes open,
3-visual analogue scale rating of vertigo at rest,
4- and European Quality of Life questionnaire rating of health-related quality of life.

The prediction model identified subjects at risk of having remaining symptoms after 6 months with a sensitivity of 86% and a specificity of 79%.


Recovery mainly takes place during the first weeks after AUVL.

Subjects rate more balance problems than dizziness.

Self-rated remaining symptoms after 6 months may be predicted by clinical balance tests and subjective ratings in the acute stage.

Corresponding Author Contact Information
Corresponding author.
Physiotherapy T7, Ryhov County Hospital,
SE-581 85 Jönköping, Sweden. Tel.: +46 70 518 23 40.

Fuente: American Journal of Otolaryngology
Volume 32, Issue 5, September-October 2011, Pages 366-375

Benign paroxysmal positional vertigo following whiplash injury: a myth or a reality?

fuente de la imagen:


Francesco Dispenza MDa, Alessandro De Stefano MDb, Navneet Mathur MSc, Adelchi Croce MDb and Salvatore Gallina MD, PhDd

a Dipartimento Discipline Chirurgiche ed Oncologiche–UO Otorinolaringoiatria, Università degli Studi di Palermo, Italia

b Dipartimento di Scienze Chirurgiche, Sperimentali e Cliniche–UO Otorinolaringoiatria, Università degli Studi “G. d'Annunzio” Chieti-Pescara, Italia

c RNT Medical College, Udaipur, India

d Dipartimento Neuroscienze Cliniche–UO Otorinolaringoiatria, Università degli Studi di Palermo, Italia


The aim of the study was to evaluate the true incidence, diagnosis, and treatment of benign paroxysmal positional vertigo (BPPV) arising after whiplash injury and to distinguish this type of posttraumatic vertigo from other types of dizziness complained after trauma.


This was a retrospective study comprising patients referred to our center after whiplash injury. The patients were evaluated with neurotologic examination including bedside and instrumental tests. A Dizziness Handicap Inventory evaluating the symptoms of patients was submitted before and after treatment and was evaluated. The BPPV patients were separately evaluated from those with cervicogenic vertigo, and a comparison between our data about idiopathic BPPV was done.


Eighteen patients of whiplash who had BPPV were evaluated.
The mean age was 38.2 years.
BPPV was the cause of vertigo in 33.9% of total whiplash patients.
In 16 cases, the posterior semicircular canal was involved; the lateral semicircular canal was involved in 2 cases.
The instrumental neurotologic assessment did not show any alteration of either vestibulospinal reflexes or dynamic ocular movements.
Duration of symptoms before treatment ranged from 3 to 26 days.

A total of 55.5% of patients had relief from their symptoms after first repositioning maneuver.
The Dizziness Handicap Inventory score improved in all patients treated with repositioning maneuvers, but no difference emerged with idiopathic BPPV data.


BPPV after whiplash injury could be unveiled with a simple bedside examination of peripheral vestibular system, and a treatment could be done in the same session.

The diagnosis of posttraumatic BPPV is not different from the idiopathic form, but the treatment may require more maneuvers to achieve satisfactory results.

Corresponding Author Contact Information Corresponding author.
Dipartimento Discipline Chirurgiche ed Oncologiche–UO Otorinolaringoiatria, Università degli Studi di Palermo,
Via Paolo Emiliani Giudici 37, 90127
Palermo–Italy. Tel.: +393334565471.

: American Journal of Otolaryngology
Volume 32, Issue 5, September-October 2011, Pages 376-380

Single-shot, low-dose intratympanic gentamicin in Ménière disease: role of vestibular-evoked myogenic potentials and caloric test in the prediction of outcome

fuente de la imagen:
Sercan Gode MDa, Nese Celebisoy MDb, Aycan Akyuz MDa, Feray Gulec MDb, Hale Karapolat MDc, Cem Bilgen PhDa and Tayfun Kirazli MDa

a Department of Otolaryngology, Ege University Medical School, Izmir, Turkey

b Department of Neurology, Ege University Medical School, Izmir, Turkey

c Department of Physical Medicine and Rehabilitation, Ege University Medical School, Izmir, Turkey


The aim of this study was to assess the efficacy and safety of single and low-dose intratympanic gentamicin therapy in patients with Ménière disease and who were monitored both with caloric tests and vestibular-evoked myogenic potentials (VEMPs) to see if VEMPs have an additional role in predicting the efficacy of the drug.
Study design

This is a prospective cohort study.

Tertiary referral center is the study setting.

Twenty-five intractable Ménière disease patients were included as the study group.

Low-dose (16 mg/mL), single-shot intratympanic gentamicin was applied. VEMP and caloric test were applied 2 weeks after the application.
Main outcome measure(s)

Safety and efficacy of protocol were evaluated at the sixth month postoperatively with tonal audiogram and visual analog scale, respectively.

Mean average pure-tone hearing threshold at 0.5, 1, 2, 4, and 8 kHz was 49.6 and 51.0 dB before and after the application, respectively (P > .05).

Mean pretreatment and posttreatment visual analog scale scores of patients were 17.6 mm (10–30 mm) and 74.6 mm (41–100 mm), respectively (P < .01). Posttreatment VEMPs were absent in 17, deteriorated in 2, and not changed in 6 patients.

VEMP was a significant predictor of posttreatment visual analog scale score, whereas caloric test was not (P < .01). Conclusions

Low-dose, single-shot intratympanic gentamicin treatment proved to be effective and safe among intractable Ménière patients.

VEMPs obtained at posttreatment second week were significant predictors of patients posttreatment sixth-month dizziness status and vertigo control.

Corresponding Author Contact Information
Corresponding author. Ege Universitesi Hastanesi,
Kulak Burun Bogaz Bolumu, 35100,
Bornova, Izmir, Turkey.
Tel.: +902323902600; fax: +902323902670.

Fuente: American Journal of Otolaryngology
Volume 32, Issue 5, September-October 2011, Pages 412-416

Nos publicitan en "Taringa"

Tratamiento para acufenos en Buenos Aires

Taringa! es una comunidad virtual donde los usuarios comparten todo tipo de información a través de un sistema colaborativo de interacción.

Hola gente de taringa,hace unos meses comenze a tener un acufeno en mi oido derecho,muy molesto y no me deja dormir por las noches creando sensaciones de angustia y ansiedad.

Feisimo,cualquiera q lo sufra me sabra entender.

Empeze a buscar informacion a lo loco por internet.

Obviamente tomando todo con pinzas ya que sabemos como es la informacion que uno lee en internet y encontre el Centro Acufenos de Bs.As. donde se lleva a cabo un tratamiento llamado T.R.T,en EEUU funciono en el 80% de los casos.

Esto me tranquilizo bastante y no lo encontre en taringa asi que me parecio util subirlo para cualquiera q lo necesite.

En el sitio tienen la explicacion detallada del tratamiento.
Aca les dejo el link si quieren mas informacion sobre el tema,mandamenme un MP que lo contesto al toque,saludos!!!
Espero les sirvan!!!

Centro de acufenos Bs.As


sábado, 27 de agosto de 2011

Enlarged Vestibular Aqueducts and Childhood Hearing Loss

On this page:

* What are vestibular aqueducts?
* How are enlarged vestibular aqueducts related to childhood hearing loss?
* What causes enlarged vestibular aqueducts?
* How are enlarged vestibular aqueducts diagnosed?
* Can enlarged vestibular aqueducts be treated to reduce hearing loss?
* What research is being conducted on enlarged vestibular aqueducts and hearing loss?
* Where can I find additional information?

What are vestibular aqueducts?

Diagram of normal inner ear and enlarged vestibular aqueduct, showing the cochlea, endolymphatic sac, endolymphatic duct, vestibular aqueduct, enlarged vestibular aqueduct, and enlarged endolymphatic sac.

Diagram of the inner ear.

Vestibular aqueducts are narrow, bony canals that travel from the inner ear to deep inside the skull (see figure). The aqueducts begin inside the temporal bone, the part of the skull just above the ear. The temporal bone also contains two sensory organs that are part of the inner ear. These organs are the cochlea, which detects sound waves and turns them into nerve signals, and the vestibular labyrinth, which detects movement and gravity. These organs, together with the nerves that send their signals to the brain, work to create normal hearing and balance. Running through each vestibular aqueduct is a fluid-filled tube called the endolymphatic duct, which connects the inner ear to a balloon-shaped structure called the endolymphatic sac.

A vestibular aqueduct is considered enlarged if it is greater than 1.5 millimeters in size, roughly the diameter of the head of a pin. If a vestibular aqueduct is enlarged, the endolymphatic duct and sac usually grow large too. The functions of the endolymphatic sac and duct are not completely understood. Scientists currently believe that the endolymphatic sac and duct help to ensure that the fluid in the inner ear contains the correct amounts of certain chemicals called ions. Ions are needed to help start the nerve signals that send sound and balance information to the brain.

How are enlarged vestibular aqueducts related to childhood hearing loss?

Research suggests that most children with enlarged vestibular aqueducts (EVA) will develop some degree of hearing loss. Scientists also are finding that five to 15 percent of children with sensorineural hearing loss, or hearing loss caused by damage to sensory cells inside the cochlea, have EVA. However, scientists do not think that EVA causes hearing loss. Instead, scientists regard EVA as an important clue about hearing loss and its possible causes. This information helps physicians talk with families about how their child’s hearing loss may change over time.

The presence of EVA can be a symptom of a genetic disorder called Pendred syndrome, a cause of childhood hearing loss. According to a study by the National Institute on Deafness and Other Communication Disorders (NIDCD), approximately one-third of individuals with EVA and hearing loss have Pendred syndrome. With Pendred syndrome, the hearing loss is progressive, which means that a child will have less hearing over time. Some children may become totally deaf.

In addition to its association with hearing loss, EVA may also be linked with balance symptoms in a small percentage of people. However, the brain is very good at making up for a weak vestibular system, and most children and adults with EVA do not have a problem with their balance or have difficulty doing routine tasks.

What causes enlarged vestibular aqueducts?

EVA has many causes, not all of which are fully understood. The most well-known cause of EVA and hearing loss is mutations to a gene known as SLC26A4 (also referred to as the PDS gene) on chromosome 7. Two mutations in the PDS gene can result in Pendred syndrome. Scientists believe that other, currently unknown genetic or environmental factors also may result in EVA.

How are enlarged vestibular aqueducts diagnosed?

Medical professionals use different clues to help them determine the cause of an individual’s hearing loss. Two tests that are often used to identify the cause of hearing loss are magnetic resonance imaging (MRI) and computed tomography (CT) imaging of a person’s inner ear. One or both tests are often recommended to evaluate a child with sensorineural hearing loss. This is particularly true when a child’s hearing loss occurs suddenly, is greater in one ear than the other, or varies or gets worse over time. Although most CT scans of children with hearing loss are normal, EVA is the most commonly observed abnormality.

Can enlarged vestibular aqueducts be treated to reduce hearing loss?

No treatment has proven effective in reducing the hearing loss associated with EVA or in slowing its progression. Although some otolaryngologists recommend steroids to treat sudden sensorineural hearing loss, there are no scientific studies to show that this treatment is effective or ineffective when an individual also has EVA. In addition, surgery to either drain liquid out of the endolymphatic sac and duct or to remove the endolymphatic sac and duct is not only ineffective in treating EVA, it can be harmful. Research has shown conclusively that these surgeries can destroy hearing.

To reduce the likelihood of progression of hearing loss, individuals with enlarged vestibular aqueducts should avoid contact sports that might lead to head injury; wear head protection when engaged in activities that might lead to head injury (such as bicycle riding or skiing); and avoid situations that can lead to barotrauma (extreme, rapid changes in pressure), such as scuba diving or hyperbaric oxygen treatment.

Identifying hearing loss as early as possible is the best way to reduce its effect. The earlier hearing loss is identified in children, the sooner they can develop the skills that will help them learn and communicate with others. Children with permanent and progressive hearing loss, which often is linked with EVA, will benefit from learning other forms of communication, such as sign language or cued speech, or using assistive devices, such as a hearing aid or cochlear implant.
What research is being conducted on enlarged vestibular aqueducts and hearing loss?

While mutations of the SLC26A4 gene are known to cause EVA, not all EVA cases are the result of an SLC26A4 mutation. Some cases may be caused by other genetic or environmental factors. For these reasons, NIDCD researchers are currently conducting a clinical trial to identify and understand the various factors that can lead to EVA and hearing loss. For more information on this study, visit, and enter "enlarged vestibular aqueducts" in the search box.
Where can I get more information?

NIDCD maintains a directory of organizations that can answer questions and provide printed or electronic information on enlarged vestibular aqueducts. Please see the list of organizations at

Use the following keywords to help you search for organizations that are relevant to enlarged vestibular aqueducts:

* Early identification of deafness in children
* Genetic diseases/disorders

For more information, additional addresses and phone numbers, or a printed list of organizations, contact:
NIDCD Information Clearinghouse
1 Communication Avenue
Bethesda, MD 20892-3456
Toll-free Voice: (800) 241-1044
Toll-free TTY: (800) 241-1055
Fax: (301) 770-8977

fuente: NIH Pub. No. 06-6053, NIDCD Information Clearinghouse
October 2006

Síndrome del acueducto vestibular dilatado. A propósito de cuatro casos


Taha, Muhamad; Plaza, Guillermo; Montojo, José; Urbasos, María; Hernando, Ana

Fuente de la imagen:

Aunque el síndrome del acueducto vestibular dilatado (SAVD) ha sido considerado una de las anomalías más frecuentemente asociadas a la pérdida auditiva neurosensorial en la infancia, el mecanismo fisiopatológico que conduce a dicha pérdida aún no está claro, y no hay criterios establecidos para su diagnóstico.

Presentamos a 4 pacientes con hipoacusia neurosensorial que fueron diagnosticados de SAVD en nuestro servicio el último año.

Revisamos los criterios diagnósticos de esta enfermedad.
Palabras clave Síndrome del acueducto vestibular dilatado. Hipoacusia neurosensorial. Tomografía computarizada. Resonancia magnética.

Texto completo

El síndrome del acueducto vestibular dilatado (SAVD) fue descrito por primera vez por Valvassori et al1 en 1978.

Es una malformación congénita del hueso temporal que implica tanto al sistema auditivo como al vestibular, ocasionando pérdidas auditivas neurosensoriales y alteraciones vestibulares a una edad muy temprana en los pacientes afectos 2-4.

El proceso fundamental que causa la deformidad del acueducto vestibular es el crecimiento anormal de su contenido: el saco y el conducto endolinfáticos 1,2,5. Sin embargo, la fisiopatología de la pérdida auditiva aún no está clara 6-8.

Algunos estudios han encontrado relación entre el SAVD y otras anomalías del oído interno como el canal semicircular horizontal dilatado 9 o la displasia de Mondini 10,11, así como entre el SAVD e hipoacusias sindrómicas como el síndrome CHARGE12, síndrome de Alagille 13, enfermedad de Von Hippel-Lindau 14,15 o el síndrome de Pendred 16,17.

Con los continuos avances en las técnicas de imagen, esta entidad está cobrando en los últimos años más interés 18,19.

Presentamos a 4 pacientes con hipoacusia neurosensorial debida al SAVD que fueron diagnosticados en el último año en nuestro servicio.


Varón de 25 años, sin antecedentes medicoquirúrgicos de interés, que acudió a consulta por hipoacusia del OD desde hace 3 años. No presentaba otra clínica audiológica.

En la audiometría tonal (AT) presentaba normoacusia en el OI e hipoacusia mixta en el OD, con umbral tonal liminar (PTA) de 60 dB y un umbral diferencial tonal (gap) de 20 dB.

Una audiometría verbal confirmó los hallazgos, con umbral de recepción verbal (URV) de 53 dB. La acumetría era normal. El timpanograma era normal.

La resonancia magnética (RM) demostró un acueducto vestibular aumentado en el oído derecho (fig. 1).

Figura 1. Secuencia ecográfica de gradiente (FIESTA). Saco endolinfático derecho dilatado, de 1,8 mm, como hallazgo aislado.

Caso 2

Varón de 54 años que acudió por hipoacusia bilateral de varios años de evolución, siendo portador de audífonos bilaterales desde hace aproximadamente 15 años. Ocasionalmente presentaba clínica de vértigo giratorio.

La AT mostraba una hipoacusia neurosensorial moderada bilateral asimétrica, más acusada en el OD con PTA en vía aérea de 60 dB y un umbral diferencial tonal de 10 dB. Una audiometría verbal presentaba un URV a 55 dB.

El timpanograma era normal. La imagen del acueducto vestibular derecho dilatado en una RM confirmó el diagnóstico (fig. 2).

Figura 2. Reconstrucción de proyección de intensidad máxima, en visión axial y coronal. Saco endolinfático dilatado, de 1,9 mm, dentro del acueducto vestibular óseo, separado del líquido cefalorraquídeo por la duramadre de la fosa posterior, hasta su extensión posterior extraósea. Vestíbulo normal.

Caso 3

Varón de 36 años que acudió manifestando hipoacusia del OD desde la infancia.
No refería otra clínica añadida.
La AT mostraba una hipoacusia mixta moderada-severa unilateral del OD, con PTA de 72 dB y un umbral diferencial tonal de 17 dB.
La audiometría verbal evidenció una URV del 65 dB.
La imagen de un acueducto vestibular dilatado en la RM confirmó el SAVD.

Caso 4

Mujer de 32 años que acudía por episodios de vértigo giratorio desde hace 4 años, con hipoacusia del OD progresiva desde la infancia.

Como antecedentes personales de interés, refería estenosis subaórtica operada durante la infancia.

La exploración otoneurológica, incluida una videonistagmografía, era normal.
La AT reflejaba una caída en 4 y 8 kHz de 40 y 85 dB respectivamente.
Una audiometría verbal presentaba una discriminación del 100 % de las palabras a 60 dB.
La RM confirmó el diagnóstico de dilatación del acueducto vestibular (fig. 3).

Figura 3. Reconstrucción de proyección de intensidad máxima axial oblicua. Dilatación del acueducto vestibular derecho de 3,1 mm de diámetro máximo.


Entre las anomalías congénitas del oído interno, el SAVD es la detectada con más frecuencia en estudios de imagen 2,16,
Con una prevalencia estimada en sujetos con hipoacusia neurosensorial de un 1-25 % dependiendo de los estudios 4,5,18-20.

Su diagnóstico se establece mediante la asociación de un contexto clínico adecuado, la existencia de hipoacusia neurosensorial unilateral o bilateral y la visualización de los signos característicos en los métodos de imagen correspondientes, tomografía computarizada (TC) y RM, de las que ésta es la técnica que aporta los datos más importantes para su diagnóstico 21.

La edad de presentación de este cuadro clínico es variable 1,18.

Aunque más frecuente en mujeres, en esta enfermedad no suelen haber antecedentes familiares 3,6, aunque algunos autores han encontrado antecedentes de primera o segunda generación en 1 de cada 3 pacientes 22.

Sin embargo, estudios recientes no han podido demostrar correlación clara entre la malformación anatómica y mutaciones o alteraciones genéticas 23.

De hecho, algunas publicaciones han presentado a pacientes con acueducto vestibular dilatado y estudios genéticos normales 24.

En este síndrome, la TC proporciona detalles del laberinto óseo, mientras que la RM presenta imágenes de su contenido1-3.

Dahlen et al 25 han encontrado una buena correlación entre el diámetro del laberinto óseo mediante el uso de TC y el diámetro de su contenido usando la RM.

El acueducto vestibular se considera aumentado de tamaño cuando mide más de 1,5 mm de anchura, medido en el punto medio de su trayecto, desde la crura común hasta su apertura externa1,3,7,8,18,26. Antonelli et al22 han clasificado el SAVD en cinco grados

El tamaño del acueducto vestibular en nuestros casos oscilaba entre 1,8 y 3,1 mm

La RM permite demostrar la presencia del conducto y saco endolinfáticos dilatados, así como su proyección extraósea sobre la fosa posterior.

La existencia de pacientes con hipoacusia neurosensorial, con TC normal y conducto y saco endolinfáticos dilatados (falsos negativos de la TC) permite afirmar que la RM es el método de imagen más adecuado para detectar esta malformación17.

Tabla II. Resumen de los síntomas y signos de los pacientes

hipoacusia neurosensorial uni o bilateral

Los pacientes con el SAVD suelen presentar un déficit auditivo moderado en la infancia, que va aumentando progresivamente hasta ser diagnosticado tras varios años de evolución 4,19.

Estos pacientes pueden beneficiarse de un implante coclear, tal como se demuestra en la literatura re-ciente 18,27.

En ocasiones, la hipoacusia neurosensorial es fluctuante y se asocia a clínica vestibular 28-30, como en 2 de nuestros casos.

En conclusión, el SAVD es una entidad relativamente frecuente, que debe sospecharse en pacientes con hipoacusia neurosensorial unilateral o bilateral cuya RM demuestre el acueducto vestibular aumentado de tamaño (> 1,5 mm de anchura), especialmente si es progresiva desde la infancia.

Su diagnóstico precoz es importante, puesto que pueden beneficiarse de un implante coclear .

Dr. M. Taha. Servicio de Otorrinolaringología.
Hospital de Fuenlabrada. Camino del Molino, 2. 28942 Fuenlabrada. Madrid. España. Correo electrónico:


1. Valvassori GE, Clemis JD. The large vestibular aqueduct syndrome. Laryngoscope. 1978;88:723-8.
2. Jackler RJ, De La Cruz A. The large vestibular aqueduct syndrome. Laryngoscope. 1989;99:1238-43.
3. Levenson MJ, Parisier SC, Jacobs M, et al. The large vestibular aqueduct syndrome in children. Arch Otolaryngol Head Neck Surg. 1989;115:54-8.
4. Arcand P, Desrosiers M, Dube J, et al. The large vestibular aqueduct syndrome and sensorineural hearing loss in the pediatric population. J Otol. 1991; 20:247-50.
5. Emmett JR. The large vestibular syndrome. Am J Otol. 1985;6:387-403.
6. Griffith AJ, Arts HA, Downs C, et al. Familial large vestibular aqueduct syndrome. Laryngoscope. 1996;106:960-5.
7. Kodama A, Sando I. Postnatal development of the vestibular aqueduct and endolymphatic sac. Ann Otol Rhinol Laryngol Suppl. 1982;96:3-12.
8. Kodama A, Sando I. Dimensional anatomy of the vestibular aqueduct and the endolymphatic sac in human temporal bones. Ann Otol Rhinol Laryngol Suppl. 1982;96:13-20.
9. Ieda Maria I, Makoto S. Lateral semicircular canal and vertigo in patients with large vestibular queduct syndrome. Otol Neurotol. 2006;27:788-92.
10. Gussen R. The endolymphatic sac in the Mondini disorder. Arch Otorhinolaryngol. 1985;242:71-6.
11. Chen-Chi W, Yuh-Shyng C. Common clinical features of children with enlarged vestibular aqueduct and Mondini dysplasia. Laryngosope. 2005;115: 132-7.
12. Murofishi T, Ouvrier RA, Parker GD, et al. Vestibular abnormalities in CHARGE association. Ann Otol Rhinol Laryngol. 1997;106:129-34.
13. Okuno T, Takahashi H, Shibahara Y, et al. Temporal bone histopathologic findings in Alagille’s syndrome. Arch Otolaryngol Head Neck Surg. 1990;116:217-20.
14. De Minteguiaga C, García Ibáñez L, Tran Ba Huy P. Tumor del saco endolinfático y enfermedad de Von Hippel-Lindau. Revisión de la literatura. Acta Otorrinolaringol Esp. 2002;53:515-20.
15. Williamson RA, Coker NJ. Endolymphatic sac tumor in von Hippel-Lindau disease. Otol Neurotol. 2003;24:832.
16. Phelps PD, Coffey RA, Trembath RC, et al. Radiological malformations of the ear in Pendred syndrome. Clin Radiol. 1998;53:268-73.
17. Moshe G, Glaser M. CT of the ear in Pendred syndrome. Radiology. 2005; 235:537.
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21. Damborenea T, Hernandez D, Fraile R, Llorente A, Garcia A, Vicente G, et al. Síndrome del acueducto vestibular dilatado en la infancia. A proposito de un caso. An Otorrinolaringol Ibero Am. 2001;28:5-11.
22. Antonelli PJ, Nal AV, Lemmerling MM, et al. Hearing Loss with coclear modiolar defects and large vestibular aqueducts. Am J Otol. 1998;19:306-12.
23. Ramirez-Camacho R, Garcia Berrocal JR, Arellano B, Trinidad A. Familial isolated unilateral larg vestibular aqueduct syndrome. ORL J Otorhinolaryngol Relat Spec. 2003;65:45-8.
24. Gonzalez-Garcia JA, Ibanez A, Ramirez-Camacho R, Rodríguez A, Garcia-Berrocal JR, Trinidad A. Enlarged vestibular aqueduct: looking for genotypic-phenothpic correlations. Eur Arch Otorhinolaryngol. 2006;263: 971-6.
25. Dahlen RT, Harnsberger HR, Gray SD, Shelton C, Allen R, Parkin JL, et al. Overlapping thin-section fast spin-echo MR of the large vestibular aqueduct syndrome. AJNR. 1997;18:67-75.
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27. Claros P, Sanz JJ, Claveria MA, Costa C, Claros A. Implante coclear en paciente con dilatación del saco endolinfático y del acueducto del vestíbulo. Acta Otorrinolaringol Esp. 2005;56:132-4.
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fuente: Publicado en Acta Otorrinolaringol Esp. 2008;59:506-8. - vol.59 núm 10
Taha, Muhamada; Plaza, Guillermoa; Montojo, Joséa; Urbasos, Maríab; Hernando, Anab

aServicio de Otorrinolaringología. Hospital de Fuenlabrada. Fuenlabrada. Madrid. España.

bServicio de Radiodiagnóstico. Hospital de Fuenlabrada. Fuenlabrada. Madrid. España.

Consenso sobre el diagnóstico y tratamiento de la sordera subita


Plaza, Guillermo a; Durio, Enrique b; Herráiz, Carlos c; Rivera, Teresa d; García-Berrocal, José Ramóne

aServicio de Otorrinolaringología, Hospital Universitario de Fuenlabrada, Fuenlabrada, Madrid, España

bServicio de Otorrinolaringología, Hospital Universitario de Getafe, Getafe, Madrid, España

cServicio de Otorrinolaringología, Hospital Universitario de Alcorcón, Alcorcón, Madrid, España

dServicio de Otorrinolaringología, Hospital Universitario Principe de Asturias, Alcalá de Henares, Madrid, España

eServicio de Otorrinolaringología, Hospital Universitario Puerta de Hierro-Majadahonda, Majadahonda, Madrid, España


Mediante revisión sistemática de la literatura sobre sordera súbita, desde 1966 hasta junio de 2010, sobre los términos MESH “(acute or sudden) hearing loss”, llegando a las siguientes sugerencias:

En cuanto al diagnóstico, ante una sospecha clínica de sordera súbita, las pruebas diagnósticas que se consideran necesarias son:

audiometría tonal,
audiometría verbal y

Una vez hecho el diagnóstico clínico de sordera súbita, antes de comenzar el tratamiento, se solicitará una batería analítica, debiendo completarse más tarde el estudio con RM de oído interno.

Se recomienda que el tratamiento de la sordera súbita esté basado fundamentalmente en los corticoides sistémicos, generalmente por vía oral, apoyados en los corticoides intratimpánicos como rescate.

Respecto al seguimiento, se realizará un control a la semana del inicio del mismo, incluyendo audiometría tonal y verbal, y a los 15, 30 y 90 días del diagnóstico, y 12 meses después.

La sordera súbita idiopática es aquella hipoacusia neurosensorial de inicio súbito, en menos de 72 horas, sin otros antecedentes otológicos previos.

Presentamos un consenso sobre el diagnóstico, tratamiento y seguimiento de la sordera súbita, surgido desde la Asociación Madrileña de ORL.

Como consenso, el resultado de los tratamientos aplicados debería presentarse, tanto en cuanto a la cantidad de dBs recuperados en el umbral auditivo tonal, como siguiendo la tasa de recuperación en los casos unilaterales, así como con parámetros de audiometría verbal.
Palabras clave Sordera súbita. Acumetría. Audiometría. Corticoides. Efectos secundarios.

Texto completo

Durante el III Congreso de la Asociación Madrileña de ORL (AMORL), celebrado en 2008, en la Mesa Redonda de Sordera Súbita se manifestó la necesidad de crear entre los hospitales de Madrid un documento de consenso sobre el diagnóstico y tratamiento de la misma, ya que se trata de una patología controvertida, y a la vez relativamente frecuente.

Por otra parte, recientemente se han publicado varias revisiones sobre sordera súbita (SS) en revistas de interés general1,2, por lo que parece conveniente hacer una revisión sobre el tema, al objeto de proponer aunar criterios sobre esta enfermedad.

Respecto a la metodología, este grupo de consenso, avalado por la AMORL, ha realizado una revisión sistemática de la literatura publicada desde 1966 hasta junio de 2010, sobre los términos MESH “(acute or sudden) hearing loss”, recogiendo 4.180 artículos en español, inglés, alemán y francés.

Es llamativo que, entre tanta publicación, no exista una guía de práctica clínica publicada sobre el tema, y sean tan pocos los estudios randomizados y metanálisis realizados.

A través de diversas reuniones, el grupo evalúo la literatura de forma independiente destacando aquellos trabajos de mayor calidad científica, especialmente en relación con el tratamiento.

Por ello, este documento trata de recoger y aunar las experiencias de varios hospitales, y revisar sistemáticamente la evidencia científica disponible, para llegar a un consenso común acerca de esta patología, en beneficio de los pacientes adultos con hipoacusia súbita.


Por consenso, se considera como SS, aquella hipoacusia neurosensorial o perceptiva de inicio súbito, en menos de 72 horas, con pérdida de más de 30 dBs, al menos en tres frecuencias consecutivas de la audiometría tonal, sin otros antecedentes otológicos previos1,2,3,4,5.

En caso de disponer de una audiometría previa, se utilizará ésta como referencia basal; si no hay audiometrías previas, en casos unilaterales, se utilizará el oído contralateral sano como referencia.

Sin embargo, algunos estudios también consideran “SS probable” aquella hipoacusia neurosensorial o perceptiva que sólo afectan 2 o 3 frecuencias, con pérdidas de 10-20 dBs, aparecidas hace menos de 12 horas, incluyendo las sorderas apreciadas al levantarse por la mañana, que se recuperan rápidamente6,7.


Desde su primera descripción en 19448, la incidencia de la SS ha ido incrementándose progresivamente a lo largo de los años, y supone un 1,2% de las Urgencias Hospitalarias de ORL1,3,9.

Si atendemos a las publicaciones sobre su epidemiología, su incidencia puede establecerse en 5-20 casos por 100.000 habitantes y año1,6,9,10.

Recientemente, otros autores han descrito una incidencia todavía mayor, de 160 casos por 100.000 habitantes y año11,12, especialmente cuando existen registros nacionales de SS como en Japón.

Probablemente, estas diferencias se deban a distintos criterios de inclusión definitorios de la sordera súbita y al infradiagnóstico que se hace de esta entidad a nivel de atención primaria1,5,7,12.

Etiopatogenia y fisiopatología

Se han postulado tres posibles causas de SS idiopática1,2,3,4,5,6,7,10,13,14:

Teoría viral

Es la teoría más documentada, tanto anatomopatológicamente en necropsias con hallazgos relacionados con infección por el virus del herpes simple tipo 115, como por el frecuente antecedente de catarro de vías aéreas superiores o su mayor incidencia en determinadas épocas del año16.

Sin embargo, no se han demostrado perfiles serológicos concretos 17 ni respuesta a tratamientos antivirales habituales como aciclovir15,18,19,20,21,22,23,24.

Teoría de la alteración en la microcirculación del oído interno

Algunos estudios han encontrado una cierta susceptibilidad genética pretrombótica 25,
mientras que otros han demostrado una mayor incidencia de SS en pacientes con riesgo cardiovascular 26,27,28,29,30,31,32,
especialmente con el prolapso mitral l33,34
o el síndrome antifosfolípido 35.

Por otra parte, la SS ha sido descrita tras fenómenos de isquemia transitoria en el oído interno, como durante una anestesia genera l36,37,

O confirmada tras un episodio de hemorragia intralaberíntica, objetivada mediante RM 38,39,40.

Asimismo, se ha descrito que la frecuencia de ictus es mayor en los 5 años posteriores tras haber padecido una SS 41.

Estas alteraciones en la microcirculación del oído interno han sido la base de tratamientos como la administración de heparinas de bajo peso molecular 42,

la plasmaféresis para limpieza de LDL del plasma 43,44,45,46,47,48,49,

El uso de carbógeno inhalado 50,51,52 o de cámaras hiperbáricas de oxígeno 53,54,55,56,57,58,59,60,61,62,

o la administración de prostaglandinas como la PGE152,63,64, con resultados diversos.

Teoría de la enfermedad inmuno-mediada

Los estudios anatomopatológicos, las curaciones espontáneas y la respuesta al tratamiento con esteroides pueden apoyar esta teoría 1,2,3,4,5,6,7,14,65,66.

Sin embargo, en algunos pacientes con SS no hay datos de alteración en la inmunidad, y la evolución clínica no siempre es compatible con un cuadro autoinmune 67,68.

Además, en muchas ocasiones un cuadro de SS que queda catalogado como idiopático acaba con el tiempo por ser diagnosticado de una patología autoinmune determinada 69.

Por otra parte, aunque no se trataría de una SS idiopática, se ha descrito la “teoría de la ruptura de membranas cocleares” 70,71, debido a una posible fístula perilinfática, aparecida en relación con:
Ejercicio físico,
o una maniobra de Valsalva.

Esta teoría podría justificar la recuperación espontánea de algunos pacientes, y para algunos autores, sienta la indicación de la timpanotomía exploradora precoz para su sellado 72,73.

Ante una sospecha clínica de SS, y antes de plantear un posible tratamiento, las pruebas diagnósticas necesarias serían:

En el ámbito de Atención Primaria y Urgencias de ORL son necesarias dos pruebas: otoscopia
y acumetría


La otoscopia, que debe ser normal en los dos oídos; sin embargo, el hecho de encontrar un tapón de cera no excluye una posible SS.
Hay que retirar el tapón y preguntar por la normalización de la audición 1,5,13.

La acumetría (diapasones) nos dará un patrón neurosensorial: Rinne positivo en el oído enfermo y Weber lateralizado al oído sano , lo que permite descartar causas de SS por patologías del oído medio: otitis media serosa, etc. con patrón transmisivo (Rinne negativo en oído enfermo y Weber hacia el oído enfermo) 1,5,74.

Sin embargo, en SS severas, cofosis, puede darse el llamado falso Rinne negativo (el paciente no oye el diapasón en absoluto).

Acumetría en la sordera súbita:
A: Rinne aplicando el diapasón junto al pabellón auricular para explorar la vía aérea.
B: Rinne aplicando el diapasón sobre mastoides para explorar la vía ósea.
C: Weber, percibiendo la conducción ósea hacia el oído sano.OS: oído sano; OE: oído enfermo.

En las Consultas Externas de ORL: además de confirmar la otoscopia normal y la acumetría neurosensorial, son necesarias una audiometría tonal y verbal, y un timpanograma


Mediante la audiometría tonal, se determinará el umbral auditivo tonal puro (PTA), tomando la media del umbral en dBs de las frecuencias 0.25, 0.5, 1, 2, 4, y 8kHz como PTA, que deberá ser mayor de 30 dBs en la vía ósea para confirmar el diagnóstico de SS.

Por otra parte, la audiometría verbal evaluará la comprensión verbal determinando el umbral de recepción verbal (URV) y la máxima discriminación (DMax)75.

Con estas pruebas, realizamos ya el diagnóstico inicial, por lo que se puede comenzar el tratamiento; además, servirán como dato basal, para evaluar la respuesta al mismo.

De forma electiva se puede ampliar la exploración audiológica realizando:
audiometría tonal supraliminar,
otoemisiones acústicas, o
potenciales auditivos (PEATC, PEAee), o
mediante pruebas vestibulares, calóricas, y VEMP.

En cuanto al proceso diagnóstico, se aconseja completarlo mediante:


Reflejo estapedial, incluyendo el test de Metz, para descartar reclutamiento coclear y enfermedad de Meniere 76.

Batería analítica 66,68,77,78,79, “cuya extracción debería realizarse previamente al tratamiento”, incluyendo, al menos, los siguientes parámetros:

hemograma, velocidad de sedimentación globular (VSG),
serología luética (VDRL y FTAabs) y
anticuerpos antinucleares (ANA),
según revisiones sistemáticas previas 66,77.

Puede ser útil solicitar también el fenotipo inmunológico, mediante las subpoblaciones linfocitarias CD4+ y CD8+, y sus isoformas CD45RO+ y CD45RA+66,80.

Resonancia magnética de oído interno con gadolinio, para descartar patología retrococlear o demostrar hemorragia intracoclear 81,82,83,84,85,86.

Para una revisión más extensa acerca del proceso diagnóstico de la SS, se recomienda revisar los trabajos de Chau y cols 14, y Nosrati-Zarenoe y cols 83.

Diagnóstico diferencial

La SS puede ser un síntoma de muchas enfermedades, tanto como forma de debut de las mismas, como en el curso de su evolución.
Lo difícil es determinar la relación causal en cada paciente individual.

Exponemos en la Tabla 1 la relación de la patología con la localización anatómica1,2,3,4,5,6,7, con el objetivo de reducir los casos que quedan como SS idiopática.

Tabla 1. Causas de sordera súbita

Inflamatorias: virus, bacterias, espiroquetas (sífilis)
Hematológicas (anemia, embolia, trastornos de la circulación)
Enfermedades inmunomediadas (Cogan, esclerodermia, colitis ulcerosa, sarcoidosis), vasculitis
Hydrops endolinfático, incluida la enfermedad de Menière
Enfermedades metabólicas (diabetes)
Enfermedades óseas de la cápsula ótica (metástasis, mieloma, histiocitosis X)

Esclerosis multiple
Ataxia de Friederich
Esclerosis lateral amiotrófica
Síndrome de Vogt-Koyanagi-Harada
Xeroderma pigmentosum
Tumores de la fosa posterior (neurinoma de acústico)
Sordera central


Por otra parte, es obligado hacer un correcto diagnóstico diferencial entre la SS y otras entidades de presentación parecida, como la ototubaritis catarral, el barotrauma, etc.1,5, para lo que es fundamental la otoscopia y la acumetría.

Formas clínicas

Entre las formas de presentación nos podemos encontrar las siguientes curvas audiométricas de hipoacusia neurosensorial (HNS), con diferente implicación pronóstica 87 , ya que aquellas que afectan más a graves tienen habitualmente mejor respuesta al tratamiento.

Formas de presentación de la sordera súbita.

A: Sordera súbita con HNS en frecuencias graves (mejor pronóstico).
B: Sordera súbita con HNS pantonal.
C: Sordera súbita con HNS en frecuencias agudas.
D: Sordera súbita con HNS en frecuencias medias.
E: Sordera súbita con restos auditivos (cofosis).

Por otra parte, existen tres formas atípicas de SS 88:

Formas infantiles

En caso de antecedente traumático, aunque sea mínimo, hay que investigar un síndrome del acueducto vestibular dilatado, mediante TC de oído 89,90.

Formas bilaterales

En estos casos, los ANA suelen encontrarse elevados, si se trata de formas autoinmunes, como sarcoidosis, esclerosis multiple, enfermedad de Crohn, síndrome de Cogan, enfermedad inmunomediada de oído interno, etc.

Otras posibles causas de SS bilateral son infecciosas (mononucleosis infecciosa, sífilis, meningitis, infección por VIH, etc.), neoplásicas (linfomatosis malignas, meningitis carcinomatosas, leucemia, etc.) o vasculares (aneurisma intracraneal, hidrocefalia, ictus, periarteritis nodosa, antecedente de raquianestesia, etc.).

Formas evolutivas

Se trata de casos de SS como síntoma de presentación de una hipoacusia neurosensorial fluctuante, o de una enfermedad de Menière, sobre todo cuando afecta a las frecuencias graves 83,91,92.

Sin embargo, cuando afecta sobre todo a los agudos, la SS puede ser el primer síntoma de un neurinoma del acústico 81,82, aun cuando se recupere la audición totalmente.


La historia natural de la SS es variable, debido a que las causas son múltiples. Algunos pacientes se recuperan completamente sin intervención médica, habitualmente durante los tres primeros días (recuperación espontánea) y, generalmente, no acuden al médico 93,94,95.

Otros mejorarían lentamente en un periodo de 1 a 2 semanas, habiéndose publicado la mejoría o recuperación espontánea en hasta el 65% de los casos en las series más clásicas de los años 70 y 80 96,97,98,99.

No obstante, la mayoría de los pacientes no van a recuperar audición sin tratamientos, e, incluso, hasta un 10% de los pacientes experimentan un empeoramiento de su audición en el tiempo, a pesar de la instauración del tratamiento adecuado 100.

Los factores de mal pronóstico en la SS que son más aceptados en la literatura son los siguientes:


Edad avanzada del paciente.

Factores de riesgo cardiovascular (hipertensión arterial, etc.).

Exposición a traumas sonoros.

Intensidad de la pérdida inicial: a mayor grado de pérdida, peor es el pronóstico de recuperación de la función auditiva.

Tipo de curva audiométrica: las sorderas pantonales o en agudos tienen menor porcentaje de recuperación.

Función auditiva del oído sano: cuando el oído contralateral tiene otra patología, la SS del oído afecto presenta un peor pronóstico de recuperación.

Sintomatología asociada: la presencia de síntomas vestibulares representa un mayor compromiso de todo el laberinto, y tiene peor pronóstico.

Precocidad en la instauración del tratamiento: cuanto antes se intervenga sobre el proceso, mayores serán las posibilidades de recuperación.

Rapidez en la aparición de mejoría clínica: cuanto antes se presente la mejoría de la sintomatología clínica, mejor será el pronóstico funcional de la SS.


El tratamiento de la SS es muy controvertido, debido a la ausencia de evidencia científica sólida que avale claramente alguna de las opciones planteadas103, siendo además las dosis empleadas muy variables 104,105.

Las medidas generales clásicas como el reposo absoluto o la dieta con restricción de ingesta de sal no han demostrado efectividad, por lo que el ingreso hospitalario para guardar reposo es discutible.

Por este motivo, no hay acuerdo sobre la necesidad de una primera fase de tratamiento hospitalario de 4 a 7 días, seguida de un tratamiento ambulatorio1,2.

A pesar del exceso de literatura existente sobre la SS, hay pocos ensayos clínicos controlados aleatorizados doble ciego, que han sido revisados por la Cochrane104 y resumidos en un meta-análisis 106.

Destacan el ensayo clásico de Wilson et al 107 quiénes en 1980 compararon esteroides orales frente a placebo, sentando las bases del uso de los mismos (OR 3,22; 1,18-8,76), a pesar de que el grupo de Cinamon et al50 no encontró un efecto significativo con los esteroides (0,89; 0,1-7,86).

Respecto al tratamiento antiviral, aunque teóricamente los agentes antivirales deberían tener un efecto positivo en la SS, los ensayos clínicos aleatorizados llevados a cabo por Stokross et al en 199820, Tucci et al en 200221 y Westerlaken et al en 200323 no han podido hallar que existan diferencias estadísticamente significativas entre ambos antivirales y placebo.

Otros tratamientos muy utilizados, sobre la base de la etiología vascular, como los vasodilatadores, el carbógeno, o el oxígeno hiperbárico han sido revisados recientemente en un meta-análisis55 y por la Cochrane 60, sin poder destacar un una efectividad significativas en la SS.

Por ello, revisada la literatura, en opinión de este grupo de consenso, una vez diagnosticada la SS, podemos aconsejar el siguiente esquema terapéutico
, basado fundamentalmente en los corticoides sistémicos:
apoyados en los corticoides intratimpánicos como rescate, con un gran volumen de publicaciones recientes al respecto:

* - “Si el diagnóstico ha sido posible antes de 30 días del inicio de los síntomas”, el tratamiento será mediante corticoides orales durante 1 mes, siendo tres las opciones más habituales 152,153:

• Prednisona (Prednisona Alonga®, Dacortin®),1mg/kg peso/día, en pauta descendente cada 5 días (por ejemplo, en un paciente de 80kg de peso, 80mg x 5 días, 60mg x 5 días, 40mg x 5 días, 20mg x 5 días, 10mg x 5 días, 5mg x 5 días).

• Metilprednisolona (Urbason ®), 1mg/kg peso/día, en pauta descendente cada 5 días (por ejemplo, en un paciente de 80kg de peso, 80mg x 5 días, 60mg x 5 días, 40mg x 5 días, 20mg x 5 días, 10mg x 5 días, 5mg x 5 días).

• Deflazacort (Dezacor®, Zamene®), en pauta descendente similara, 1,5mg/kg peso/día, en pauta descendente cada 5 días (por ejemplo, en un paciente de 80kg de peso, 120mg x 5 días, 90mg x 5 días, 60mg x 5 días, 30mg x 5 días, 15mg x 5 días).

- “Si se trata de una SS severa (>70 dBs), en oído único o con vértigo intenso asociado (sospecha de neuritis vestibular)”, se ofrecerá tratamiento intravenoso con corticoides durante 7 días, en régimen de Hospital de Día Médico o mediante ingreso hospitalario, con dosis de 500mg de metilprednisolona al día, a pasar en una dosis, lentamente, en suero en 30 minutos 154,155. Posteriormente se reintroduciría la pauta oral anteriormente descrita.

- “Si hay contraindicación para el uso de corticoides sistémicos, o si no hay respuesta al tratamiento con corticoides sistémicos, orales o intravenosos, pasados 7 días desde su instauración”, se ofrecerá tratamiento intratimpánico con esteroides de rescate 121,148, mediante 1 dosis semanal durante 3 semanas, en consultas externas de ORL (y se mantendrá la pauta descendente oral), siendo dos las pautas más utilizadas (previa anestesia tópica con fenol sobre la membrana timpánica, con aguja abocath n° 22) 150:

– Metilprednisolona, 0,9 cc de un vial de 40mg, mezclado con lidocaína al 1%, 0,1ml.

– Dexametasona, 0,9 cc de un vial de 8mg.

Durante el tratamiento esteroide sistémico, sea oral o intravenoso, se realizará profilaxis gastroduodenal con inhibidores de bomba de protones, tipo omeprazol, a dosis de 40mg /día, durante 1 mes.

En pacientes mayores de 65 años, si el tratamiento glucocorticoide se prolonga más de 15 días, será necesario asociar vitamina D (800 UI/día) y calcio (800-1.000mg/día), como pauta preventiva de la pérdida de masa ósea y osteoporosis (es opcional pedir una densitometría ósea) 156,157.

Por otra parte, dada la relativa frecuencia de los efectos adversos asociados a los tratamientos habituales de la SS 158,159,160,161,162, este consenso sugiere el uso de un consentimiento informado específico, especialmente cuando se recurre a tratamientos intravenosos con corticoides a altas dosis (consentimiento informado validado, que puede solicitarse a los autores).

En casos de sospecha de etiología vascular (factores de riesgo cardiovascular conocidos, etc.), se podrán asociar vasodilatadores 42,163,164,165,166,167, como nimodipino, por vía intravenosa (5-15 cc en 500ml de suero salino, a pasar lentamente, cada 8 horas), o como trimetazidina, por vía oral (especialmente si el paciente ya está en tratamiento antihipertensivo, 1 comp/8h durante 1 mes), y se remitirá el paciente al Servicio de Medicina Interna, para su valoración y posible tratamiento antiagregante.


- “Si el diagnóstico es tardío”, entre 30 días y 90 días desde el inicio de los síntomas, el tratamiento será mediante corticoides orales durante 1 mes, siguiendo el esquema previo.

- “Si el diagnóstico es muy tardío”, más de 90 días desde el inicio de los síntomas, el tratamiento se discutirá de forma individualizada.


Una vez instaurado el tratamiento, se realiza un control a la semana del inicio del mismo, incluyendo audiometría tonal y verbal, para valorar la tolerancia al tratamiento y sus resultados:


- Si el paciente ha recuperado totalmente la audición y presenta normoacusia, se sigue la pauta prescrita (corticoides orales en pauta descendente durante un mes).

- Si el paciente ha recuperado parcialmente la audición, con mejoría de menos de 15 dBs, se sigue la pauta prescrita (corticoides orales en pauta descendente durante un mes), y se recomendará de forma individualizada el tratamiento intratimpánico simultáneamente.

- Si la audición ha empeorado, se recomendará tratamiento intravenoso de rescate.

Se realiza control, incluyendo audiometría tonal y verbal, a los 15, 30 y 90 días del diagnóstico 167,168,169,170, si bien para descartar hipoacusias autoinmunes o enfermedad de Menière sería conveniente revisar los pacientes hasta 12 meses después del diagnóstico, especialmente en SS que afectan a frecuencias graves 89,171.

Evaluación de resultados

Tras tratamiento, la recuperación sería total si se logra alcanzar una diferencia máxima de 10 dBs con el PTA óseo del oído sano contralateral, mientras que se considera que hay respuesta parcial al tratamiento si se obtiene una mejoría de menos del 50% de la pérdida inicial.

Sin embargo, para la mayoría de los autores, el éxito del tratamiento de la SS queda definido de forma arbitraria, ante una “recuperación auditiva promedio del umbral auditivo” (tomando la media del umbral a 0.25, 0.5, 1, 2, 4, y 8kHz como PTA) de más de 30 dBs, o siguiendo esquemas graduales como el propuesto en EE.UU en los años 70 por Siegel 172, por el Comité de Sordera Subita de Japón en los años 80 173,174,175, o por el registro nacional de Suecia 176.

Sin embargo, otros autores utilizan criterios más restrictivos como la “tasa de recuperación” (recovery rate), descrita en trabajos ya publicados en los años 70. Dicha tasa queda establecida teniendo en cuenta el grado de recuperación del oído enfermo respecto al oído sano, de forma sólo es aplicable en aquellos casos cuya audición contralateral sea normal (< 25 dBs), siguiendo este cociente: Fórmula Por otra parte, resulta esencial constatar la mejoría en la comprensión verbal mediante la audiometría verbal seriada, determinando el umbral de recepción verbal (URV) y la máxima discriminación (DMax o SDS). Como consenso, el resultado de los tratamientos aplicados debe presentarse de ambas formas, tanto en cuanto a la cantidad de dBs recuperados en PTA (escala de Siegel), como siguiendo la tasa de recuperación en los casos unilaterales, así como con parámetros de logoaudiometría como el URV y la DMax, como se postula en los estudios más recientes 101,104,177. Conclusiones

La sordera súbita (SS) es aquella hipoacusia neurosensorial o perceptiva de inicio súbito, en menos de 72 horas, con pérdida de más de 30 dBs, al menos en 3 frecuencias consecutivas de la audiometría tonal, sin otros antecedentes otológicos previos.

Es una entidad de incidencia creciente, afectando a 5-20 casos por 100.000 habitantes y año, y su diagnóstico requiere una mayor implicación de la red de Atención Primaria,

Ante una sospecha clínica de SS, y antes de plantear un posible tratamiento, las pruebas diagnósticas necesarias serían, en el ámbito de Atención Primaria y Urgencias ORL, una otoscopia, normal, y acumetría, que mostrará un patrón neurosensorial (Rinne positivo en el oído enfermo y Weber lateralizado al oído sano).

En las Consultas Externas ORL: además serían necesarias una audiometría tonal, para determinar el umbral auditivo, una audiometría verbal, para hallar el umbral de recepción verbal y la máxima discriminación, y un timpanograma.

Una vez hecho el diagnóstico clínico de SS, antes de comenzar el tratamiento; se solicitará una batería analítica, cuya extracción debería realizarse previamente al tratamiento, incluyendo, al menos, los siguientes parámetros:

hemograma, velocidad de sedimentación globular, serología luética y anticuerpos antinucleares, debiendo completarse más tarde el estudio con RM de oído interno.

El tratamiento de la SS es muy controvertido; sin embargo, como consenso, una vez diagnosticada la SS, podemos aconsejar un esquema terapéutico, basado fundamentalmente en los corticoides sistémicos, generalmente por vía oral, apoyados en los corticoides intratimpánicos como rescate.

Por otra parte, dada la relativa frecuencia de los efectos adversos asociados a los tratamientos habituales de la SS, este consenso sugiere el uso de un consentimiento informado específico.

Respecto al seguimiento, una vez instaurado el tratamiento, se realizará un control a la semana del inicio del mismo, incluyendo audiometría tonal y verbal, para valorar la tolerancia al tratamiento y sus resultados, y a los 15, 30 y 90 días del diagnóstico, si bien es conveniente revisar los pacientes hasta 12 meses después del diagnóstico.

Como consenso, el resultado de los tratamientos aplicados a pacientes con SS debe presentarse, tanto en cuanto a la cantidad de dBs recuperados en el umbral auditivo tonal, como siguiendo la tasa de recuperación en los casos unilaterales, así como con parámetros de audiometría verbal.
Registro de Sordera Súbita

Siguiendo las iniciativas de otros países como Japón 173 o Suecia 176, sería conveniente crear un registro de SS en nuestros hospitales, de forma unitaria en la Comunidad de Madrid o en aquellas comunidades que lo estimen oportuno.

Para ello, existe un conjunto mínimo de datos que sería necesario recoger de cada paciente , y enviar al registro comunitario, mediante correo electrónico a la SEORL (pueden enviarse al correo electrónico de los autores).

Registro de Sordera Súbita: datos iniciales

Caso Iniciales
Fecha SS
Fecha Nacimiento
Antecedentes generales HTA, DM, etc.
Antecedentes ORL Oído único, secuela otorreica
Lado Derecho, izquierdo
Recidiva Sí/No
Acúfenos Sí/No
Hiperacusia Sí/No
Vértigo Sí/No

PTA peor Media aritmética de las frecuencias
PTA mejor 0,5; 1, 2, 4 y 8 KHz

URV peor
URV mejor
DMax peor
DMax mejor
Tipo de curva Graves/Pantonal/Agudos/Medias/Cofosis
Grado de sordera Leve/Moderada/Severa

Tabla 6. Registro de sordera súbita: datos evolutivos

Oído peor Oído mejor
7 días
PTA peor
PTA mejor
URV peor
URV mejor
DMax peor
DMax mejor

30 días
PTA peor
PTA mejor
URV peor
URV mejor
DMax peor
DMax mejor

90 días
PTA peor
PTA mejor
URV peor
URV mejor
DMax peor
DMax mejor

Recuperacion en dBs de media y en tasa de recuperación.
Estudio etiológico: RM, analítica, etc.

Conflicto de intereses: Los autores declaran no tener ningún conflicto de intereses.

☆ Trabajo desarrollado bajo la dirección de la Asociacion Madrileña de Otorrinolaringologia (AMORL).

a Debe tenerse en cuenta la equivalencia entre ambos esteroides en cuanto a potencia de efecto antinflamatorio: 4mg metilprednisolona equivalen a 6mg de deflazazort.

Autor para correspondencia.

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Fuente: Publicado en Acta Otorrinolaringol Esp.2011; 62 :144-57 - vol.62 núm 02
Fuente de la imagen: