Thursday, September 27, 2007

Arizona Teen Becomes Sixth Victim This Year of Brain-Eating Amoeba

Thursday , September 27, 2007


It seemed like a headache, nothing more. But when pain killers and a trip to the emergency room didn't fix Aaron Evans, the 14-year-old asked his dad if he was going to die.

"No, no," David Evans remembers saying. "We didn't know. And here I am: I come home and I'm burying him."

What was bothering Aaron was an amoeba, a microscopic organism called Naegleria fowleri that attacks the body through the nasal cavity, quickly eating its way to the brain. The doctors said he probably picked it up a week before while swimming in the balmy shallows of Lake Havasu.

Such attacks are extremely rare, though some health officials have put their communities on high alert, telling people to stay away from warm, standing water.

"This is definitely something we need to track," said Michael Beach, a specialist in recreational water-born illnesses for the Centers for Disease Control and Prevention.

"This is a heat-loving amoeba. As water temperatures go up, it does better," Beach said. "In future decades, as temperatures rise, we'd expect to see more cases."

According to the CDC, Naegleria infected 23 people from 1995 to 2004. This year health officials say they've noticed a spike in cases, with six Naegleria-related cases so far — all of them fatal.

Though infections tend to be found in southern states, Naegleria has been found almost everywhere in lakes, hot springs, even some swimming pools. Still, the CDC knows of only several hundred cases worldwide since its discovery in Australia in the 1960s.

The amoeba typically live in lake bottoms, grazing off algae and bacteria in the sediment. Beach said people become infected when they wade through shallow water and stir up the bottom. If someone allows water to shoot up the nose — say, by doing a cannonball off a cliff — the amoeba can latch onto the person's olfactory nerve.

The amoeba destroys tissue as it makes its way up to the brain.

People who are infected tend to complain of a stiff neck, headaches and fevers, Beach said. In the later stages, they'll show signs of brain damage such as hallucinations and behavioral changes.

Once infected, most people have little chance of survival. Some drugs have been effective stopping the amoeba in lab experiments, but people who have been attacked rarely survive, Beach said.

"Usually, from initial exposure it's fatal within two weeks," Beach said.

Researchers still have much to learn about Naegleria, Beach said. For example, it seems that children are more likely to get infected, and boys are infected more often than girls. Experts don't know why.

"Boys tend to have more boisterous activities [in water], but we're not clear," he said.

In addition to the Arizona case, health officials reported two cases in Texas and three more in central Florida this year. In response, central Florida authorities started an amoeba telephone hot line advising people to avoid warm, standing water, or any areas with obvious algae blooms.

Texas health officials also have issued news releases about the dangers of amoeba attacks and to be cautious around water. People "seem to think that everything can be made safe, including any river, any creek, but that's just not the case," said Doug McBride, a spokesman for the Texas Department of State Health Services.

Lake Havasu City officials also are discussing how to deal with rare amoeba attacks in the wake of Aaron Evans' death. "Some folks think we should be putting up signs. Some people think we should close the lake," city spokesman Charlie Cassens said. City leaders haven't yet decided what to do.

Beach warned that people shouldn't panic about the dangers of brain-eating amoeba. Infections are extremely rare when compared with the number of times a year people come into contact with water. And there have been occasional years during the past two decades that experts noticed a similar spike in infections.

The easiest way to prevent infection, Beach said, is to simply plug your nose when swimming or diving in fresh water.

"You'd have to have water going way up in your nose to begin with" to be infected, he said.

David Evans has tried to learn as much as possible about amoebas during the past month. But it still doesn't make much sense. The questions keep swirling around his head. Why now? His family has gone to Lake Havasu countless times without a problem. Have people always been in danger? Did city officials know about amoebas? Can they do anything to kill them off?

"It's been pretty heavy-duty," he said.

Evans lives within eyesight of Lake Havasu, a bulging strip of the Colorado River that separates Arizona from California. Temperatures hover in the triple digits all summer, and like almost everyone else, the Evans family looks to the lake to cool off.

On Sept. 8, he brought Aaron, his two other children and his parents to Lake Havasu to celebrate his birthday. They ate sandwiches and spent a few hours splashing around one of the beaches.

"For a week, everything was fine," he said.

Then Aaron got the headache that wouldn't go away. Evans took him to the hospital, and doctors thought his son was suffering from meningitis. Aaron was rushed to another hospital in Las Vegas.

Evans tried to reassure his son, but he had no idea what was wrong. On Sept. 17, Aaron stopped breathing as David held him in his arms.

"He was brain dead," David said. Only later did doctors realize the boy had been infected with Naegleria.

"My kids won't ever swim on Lake Havasu again."

Tuesday, September 25, 2007

Pedophiles ' brains 'different'

Scientists say distinct differences in the brain activity of pedophiles have been found using scanning technology.

A Yale University team found activity in parts of pedophiles' brains were lower than in other volunteers when shown adult, erotic material.

The journal Biological Psychiatry said this was the first real-time evidence of differences in thought patterns.

A forensic psychologist from the UK said drug treatments for pedophilia might be possible.

This deficit may predispose individuals who are vulnerable to pedophilia to seek other forms of stimulation
Dr John Krystal, Editor, Biological Psychiatry

There is increasing evidence that problems in certain areas of the brain may contribute to feelings of sexual attraction towards children.

In a few cases, patients with a brain tumor in a particular part of the brain have developed such feelings, only for them to go away when the tumor was removed.

The Yale study used functional Magnetic Resonance Imaging (fMRI), a technique which allows the activity within the brain to be recorded as the patient is thinking.

They found that when known patients with pedophilia feelings were asked to look at adult pornography, a part of the brain called the hypothalamus, which is known to be involved in arousal and hormone release, was less active than in other volunteers.

More generally, the more extreme the pedophilia behavior was rated, the lower the activation in a part of the brain called the "frontal cortex".

However, Dr John Krystal, the journal's editor, said he didn't know whether this particular pattern of brain activity could be used to predict someone's risk of pedophilia.

But he said: "The findings provide clues to the complexity of this disorder, and this deficit may predispose individuals who are vulnerable to pedophilia to seek other forms of stimulation."

Drug treatment

Lead researcher Dr Georg Northoff added: "Our results may thus be seen as the first step towards establishing a neurobiology of pedophilia which ultimately may contribute to the development of new and effective means of therapies for this debilitating disorder."

In the UK, many experts are looking to the biology of the brain to explain not just pedophilia, but other types of compulsive criminality.

Dr Keith Ashcroft, a forensic psychologist at the Center for Forensic Neuroscience, in Lancashire, said that other evidence pointed to problems in the pre-frontal cortex of the brain being linked to pedophilia thoughts.

He said: "Sexual behavior is very complex, especially as some people are not aroused by visual stimuli, but by touch instead.

"I am campaigning for the use of anti-schizophrenia drugs in pedophilia, as these act on a similar part of the brain and may be useful."

Story from BBC NEWS:

Strange but True: Less Sleep Means More Dreams

September 20, 2007

Missing sleep tonight may just boost your dreams tomorrow night.

By Christie Nicholson

About three years ago Eva Salem got into some trouble with a
crocodile. It snapped her hand in its jaws. In a panic, she managed to
knock out the crocodile and free herself. Then, she woke up.
"I imagine that's what it's like when you're on heroin. That's what my
dreams were like—vivid, crazy and active," she says. Salem, a new
mother, had been breast-feeding her daughter for five months before
the croc-attack dream, living on four hours of sleep a night. If she
did sleep a full night, her dreams boomeranged, becoming so vivid that
she felt like she wasn't sleeping at all.

Dreams are amazingly persistent. Miss a few from lack of sleep and the
brain keeps score, forcing payback soon after eyelids close. "Nature's
soft nurse," as Shakespeare called sleep, isn't so soft after all.
"When someone is sleep deprived we see greater sleep intensity,
meaning greater brain activity during sleep; dreaming is definitely
increased and likely more vivid," says neurologist Mark Mahowald of
the University of Minnesota and director of the Minnesota Regional
Sleep Disorders Center in Minneapolis.

The phenomenon is called REM rebound. REM refers to "rapid eye
movement," the darting of the eyes under closed lids. In this state we
dream the most and our brain activity eerily resembles that of waking
life. Yet, at the same time, our muscles go slack and we lie
paralyzed—a toe might wiggle, but essentially we can't move, as if our
brain is protecting our bodies from acting out the stories we dream.
Sleep is divided into REM and four stages of non-REM; each has a
distinct brain wave frequency. Stage one of non-REM is the nodding off
period where one is between sleeping and waking; it's sometimes
punctuated with a sensation of falling into a hole. In stage two the
brain slows with only a few bursts of activity. Then the brain
practically shuts off in stages three and four and shifts into
slow-wave sleep, where heart and breathing rates drop dramatically.
Only after 70 minutes of non-REM sleep do we experience our first
period of REM, and it lasts only five minutes. A total non-REM–REM
cycle is 90 minutes; this pattern repeats about five times over the
course of a night. As the night progresses, however, non-REM stages
shorten and the REM periods grow, giving us a 40-minute dreamscape
just before waking.

The only way scientists can study REM deprivation is by torturous
sleep deprivation. "We follow the [electroencephalogram] tracing and
then when we see [subjects] moving into REM, we wake them up," says
psychologist Tore Nielsen, director of the Dream and Nightmare Lab at
the Sacré-Coeur Hospital in Montreal. "As soon as you start to rob
them of REM, the pressure for them to go back into REM starts to
build." Sometimes Nielsen will have to wake them 40 times in one night
because they go directly into REM as soon as they are asleep.
Of course there is non-REM rebound as well, but the brain gives
priority to the slow-wave sleep and then to REM, suggesting that the
states are independent of each other.
In a 2005 study published in Sleep, Nielsen showed that losing 30
minutes of REM one night can lead to a 35 percent REM increase the
next night—subjects jumped from 74 minutes of REM to a rebound of 100

Nielsen also found that dream intensity increased with REM
deprivation. Subjects who were only getting about 25 minutes of REM
sleep rated the quality of their dreams between nine and eight on a
nine-point scale (one being dull, nine being dynamite).
Of course, REM deprivation, and the subsequent rebound, is common
outside the lab. Alcohol and nicotine both repress REM. And blood
pressure drugs as well as antidepressants are also well known REM
suppressants. (Take away the dreams and, curiously, the depression
lifts.) When patients stop the meds, and the vices, they're rewarded
with a scary rebound.

But the persistence of REM begs the question: Why is it so insistent?
When rats are robbed of REM for four weeks they die (although the
cause of death remains unknown). Amazingly, even though we spend about
27 years dreaming over the course of an average life, scientists still
can't agree on why it's important.
Psychiatrist Jerry Siegel, head of the Center for Sleep Research at
the University of California, Los Angeles, recently proved that REM is
nonexistent in some big-brained mammals, such as dolphins and whales.
"Dying from lack of REM is totally bogus," Siegel says. "It's never
been shown in any species other than a rat."
Some theories suggest that REM helps regulate body temperature and
neurotransmitter levels. And there is also evidence that dreaming
helps us assimilate memories. Fetuses and babies spend 75 percent of
their sleeping time in REM. Then again, platypuses experience more REM
than any other animal and researchers wonder why, because, as
Minnesota's Mahowald puts it, "Platypuses are stupid. What do they
have to consolidate?"

But, given that rats run through dream mazes that precisely match
their lab mazes, others feel that there must be some purpose or
meaningful information in dreams.
John Antrobus, a retired professor of psychology and sleep research at
the City College of New York says that dream content is tied to our
anxieties. But he never found the extreme vividness in REM rebound
that others assume is there, based on a higher level of brain activity
which likely means more action-packed dreams.
"The brain is an interpretive organ, and when regions are less
connected as they are in sleep, we get bizarre narratives," he says.
"But its purpose? For that we have to ask what is the purpose of
thought. We can't answer one without answering the other."

Taken from: Scientific America

Sunday, September 23, 2007

Unearthing Brain Cells

A new trick for viewing brain cells—without a scalpel
By: Laura Allen

Physicist Hans-Ulrich Dodt, a visiting professor at the Max Planck Institute in Germany, has figured out how to see nerve cells deep in mice brains as clearly as little neon motel signs. His technique could advance research on Alzheimer's disease by quickly showing how new drugs affect nerve degeneration in rodent brains. It could also make three-dimensional fly-through animations of the brain possible for the first time, Dodt says. To see deeper than a millimeter inside a brain, scientists currently have to slice it into hundreds of thin sections and reconstruct the distorted neurons in 3-D on a computer. Dodt's solution is to first render the whole brain transparent by immersing it in an oily solution that prevents any light-scattering that might cloud the image. Then he slices with light instead of a knife, shining a laser on the tissue, which has been genetically engineered to fluoresce. Observed under a microscope, the result is a stunning 3-D view of neurons. "The technique could scale up considerably," says Dodt, who teaches full-time at the Vienna University of Technology. Next he'll try higher-resolution cameras, among other tweaks, to see all of the organs inside a mouse embryo.
Taken from /

Happiness is a Warm Electrode

Gregory Mone

In the middle of room #11 in the Cleveland Clinic's surgical center, Diane Hire lies on an operating table, the back half of her shaven head hidden behind a plastic curtain. Four pins, one driven into either side of her forehead, the other two in back, hold a titanium halo fast to her skull. An anesthesiologist, several nurses and her psychiatrist cluster around the bed.

Behind the curtain, neurosurgeon Ali R. Rezai surveys Hire's brain, white and snaked with thin red arteries, through a pair of small holes he's drilled in the top of her skull. Because so few pain receptors are located in the brain, only local anesthetic numbs Hire's head. She is awake during the procedure—or as awake as she can be. For the past 20 years, she has suffered from severe depression, a crippling strain of the disease that afflicts as many as four million people. Years of therapy, at least 10 different drugs and six courses of the whole-brain shock technique known as electroconvulsive therapy (ECT) all failed to bring Hire lasting relief. Her final hope is this operation, a radical form of neurosurgery called deep-brain stimulation, or DBS. Whereas ECT—a treatment that's been demonized in movies like One Flew over the Cuckoo's Nest but is still used on roughly 100,000 patients a year—floods the brain with electricity from the outside, this technique delivers a smaller dose of better-targeted current to an area of the brain believed to be a key regulator of mood. Wires thread beneath the skin from their place in the brain and plug into two battery-run stimulators implanted in the chest. About the size of an iPod nano, each stimulator constantly pumps out current, bathing a small region of brain tissue in electricity. If ECT is the equivalent of slapping defibrillators against a heart-attack victim's chest, deep-brain stimulation is the pacemaker that prevents the attack in the first place.

On the operating table, Hire closes her eyes. Rezai slowly inserts a wire as thin as a fishing line through the left hole in her skull, using the halo as a guide. His team has already mapped out his route using a precise 3-D reconstruction of Hire's brain compiled from 180 MRI scans. His target is a chunk of neurons associated with energy and mood. After the tip of the wire is in the right spot, he repeats the process on the other side. Within 90 minutes of the first cut, Hire has two electrodes lodged in the center of her brain. Now it's time to charge them up. On the other side of the curtain, Donald A. Malone, Jr., Hire's psychiatrist, tells her that everything's ready. Malone has a clear, soothing voice and a comforting, boyish face. He's the kind of person you'd want to talk to if someone was about to shock your brain.

At his signal, two volts of electricity, enough to power a wristwatch, course through the wires and radiate outward from the tip a few millimeters in every direction. Millions of neurons bask in the electricity, and the effect is fairly immediate. Hire feels warm at first, a bit flushed.

And then it happens. The room looks brighter to her. The faces, the big, circular lights overhead, the ceiling—they all seem clearer. Malone asks her how she feels. "I'm really happy," she replies, clearly surprised. "I feel like I could get up and do all sorts of things." But even more telling than her words is the look on her face. For the first time in 20 years, with a halo bolted to her head and two freshly drilled holes in her skull, Hire smiles.

Prescription Voltage
Deep-brain stimulation began as a treatment for movement disorders in the mid-1990s, and the surgery has been performed on more than 40,000 patients, most of them Parkinson's sufferers, since then. In those cases, the current normalizes activity in the basal ganglia and thalmus—which dictate motor control, among other things—and can calm their shaking hands and limbs.

But the clinical trial in which Hire is enrolled, along with 16 other patients, is among the first to tackle depression. Other major trials are under way at Emory University and the University of Toronto. Exact numbers are hard to ascertain, but it's estimated that fewer than 50 patients in North America are walking around with wires in their brain.

In some ways, severe depression is a far more challenging disease to treat than Parkinson's. It can manifest in dozens of different ways and arises from a variety of complex factors, some genetic and some environmental. For instance, scientists are just starting to identify a class of what they call vulnerability genes. In essence, they come in two forms: lucky and unlucky. "If you have one version, you are relatively resilient in the face of stress," says Brown University psychiatrist Ben Greenberg, who is collaborating with the Cleveland Clinic group. "But if you have another, the more severe the stress you have in your life, the more likely you are to develop depression."

Most depression therapies address the disease as a kind of communications problem in the brain. When all is healthy, a neuron receives a chemical message from a neighboring neuron and dispatches a corresponding electrical signal along a nerve fiber called an axon. Then, at the other end, the neuron pumps chemicals on to the next cells.

Drugs attempt to improve communication by altering chemical signals. Prozac, the popular antidepressant, blocks the action of a pump that sucks serotonin, a key mood-regulating chemical, out of the gaps between two neurons. This leaves more serotonin in those spaces, supposedly improving the flow of messages between neurons. But why (or whether) this makes people happy remains unclear. Antidepressants may generate billions of dollars in revenue for pharmaceutical companies, but recent studies suggest that pills work only 50 percent of the time—and they don't do much at all for the millions like Hire who are severely depressed.

The New Lobotomy?
But first Rezai must convince his colleagues that attacking depression with electrical current is a good idea. Patients like Hire, who don't respond to drugs, therapy or ECT, reveal how little modern science really understands about depression, which is one reason why DBS tends to raise thorny scientific and ethical questions. Most Parkinson's patients are in their 60s or older, but victims of depression might only be in their 20s. Will it be safe, wonders psychiatrist Neal Swerdlow of the University of California at San Diego, for them to have the hardware implanted for six or seven decades?

Then there's the fundamental problem of delivering happiness on demand. Hire's psychiatrist uses a handheld device to tune the voltage and frequency of the stimulators implanted in her chest. Although some patients might wish to manipulate the device themselves, Malone says self-control is unlikely. There's a risk of cranking the volts too high, potentially causing brain damage. "This is not cosmetic neurology," he says. "This is about treating a fatal illness." Yet the trial-and-error process of banishing depression is still as much art as it is science.

To some, acting on this rudimentary understanding of DBS and its effects on the brain recalls the notorious history of operating on the brain to treat mental disorders. One psychiatrist, Jeffrey Schwartz of the University of California at Los Angeles, has compared the procedure to a lobotomy. Swerdlow is more hopeful. He thinks DBS, or some future derivation of it, truly could help patients and advance neuroscience along the way. His main concern is that the trials are happening too fast.

But Malone can't imagine going much slower. Time is dangerous in depression, with suicide—the eleventh leading cause of death in the U.S.—claiming more than 32,400 lives every year. For Hire, DBS isn't about unlocking the mysteries of the brain; it's about being able to get out of bed in the morning.

Some Rare Good News
Depression started controlling Hire's life in her early 30s. At 36, after 12 years of service in the Navy, she was medically discharged because of the disease. She went back to school and became a physical therapist. She worked and worked, trying to ignore her growing unease and inability to relate to family and friends, let alone strangers. She tried various drugs and met frequently with therapists. Yet the depression only grew stronger.

In 1999 she stopped working for good. She started semi-regular courses of ECT. The treatment failed to improve her mood and affected her short-term memory, a common side effect. Then, in 2005, Hire heard about Malone's work with DBS and applied to be part of one of the first clinical trials of its use to treat depression. She and her therapist submitted a dictionary-thick stack of papers to Malone, documenting Hire's long battle with mental illness, but they got no reply.

By 2006, Hire rarely left her sofa, spent most days in sweatpants, and watched television from morning to night. It took her four weeks to work up the motivation to clean the house. That fall, she called her therapist and told her that she couldn't handle it anymore. "It was a really black, dismal existence," Hire recalls. "I just couldn't function."

As fate would have it, the very next day Malone called Hire's therapist with some excellent news: He wanted to meet Hire, if she was still interested, to begin the long process of determining whether she was a suitable candidate for the trial. The vetting could take months, but Hire didn't care. "I was at the end of my rope," she says.

Mood Swings in an MRI
The day after her surgery, with her scalp sewn up but the wires still sticking out, Hire is moved to the Cleveland Clinic's main imaging center, where she's wheeled into a tightly packed room containing a functional magnetic-resonance-imaging (fMRI) machine. The device generates powerful magnetic fields to measure the metabolic activity in different areas of the brain in real time. It's shaped like a giant, nine-foot-wide doughnut and has a narrow bed inserted through the center hole. The imaging technician, John Cowan, helps Hire position her head inside the opening and outfits her with earphones and a microphone, while neurophysiologist Kenneth Baker squeezes behind the machine to attach the wires from her head to an external stimulator in another room.

From an adjacent room, Cowan, Malone and Baker watch Hire through a window and on a small video screen, talking to her frequently to keep her calm. For the next 48 minutes, while she tries to remain relaxed and perfectly still, Baker turns the voltage on and off as the machine scans her brain. For 30 seconds, she's happy. Then Baker shuts off the electrodes, Hire's smile fades, and the machine maps how her brain reacts. Another 30 seconds pass, and the happiness returns. Cowan later marvels at the effect of the stimulation on Hire and the other depression patients. "They're always laughing, and I'm wondering, how can you be laughing like this so soon after surgery?"

Regardless of how or even whether DBS is curing Hire's depression, the fMRI scans show that physiological changes in her brain accompany the emotional changes. The scientists can watch different brain areas—which they refer to as "nodes" or "hubs" in a larger circuit—become active, one after the other, in a repetitive pattern. "We're putting electrical impulses into a hub that connects large parts of the brain involved in your mood, your anxiety and your energy level," Rezai says. The more that scientists understand about how the diseased brain functions, he explains, the more they will know how to find the faulty wiring or circuits responsible for it, and from there they can design the therapies to fix it.

Keep on Smiling
The results of these limited tests of DBS are impressive so far. In 2005 the Toronto group found that four out of six patients showed significant improvements. Earlier this year, psychiatrist Thomas Schlaepfer's group at the University of Bonn in Germany announced that all three of his patients were benefiting from the surgery. And the Cleveland-Brown collaboration reports improvements in 70 percent of their patients, half of whom are in complete remission.

Medtronic, a company in Minneapolis that manufacturers the hardware for DBS, is working with the Food and Drug Administration to plan the largest study yet of depression and DBS—a 100-patient trial in which the scientists may delay stimulation in half the patients for six months, switch it on in the other half, and compare the results. Emory is also planning to conduct a blind trial.

The Cleveland-Brown group is even starting to think about next-generation versions of the technology. Rezai, for instance, envisions implanted sensors that could detect abnormal activity in key brain circuits and deliver the necessary jolts to correct it. With the help of Cleveland Clinic biomedical engineer Charles Steiner, he's also developing versatile electrodes that send current in a specific direction. These would create a more targeted pulse, enabling the psychiatrist to further fine-tune the stimulation to suit the patient.

In Hire's case, though, the existing technology seems to be working just fine. When I meet with her six months after the surgery, she doesn't look like a person who spent 20 years trapped in a dark mental cave. She's energetic. She shakes my hand firmly and looks me straight in the eye—something she says she simply wouldn't have been able to do before. She laughs often (and my jokes aren't even really funny). She now walks 50 miles a week, talks to her family constantly, chats with strangers at the post office. And her smile is a regular, everyday thing, not a freakish, fleeting appearance in a crowded operating room.

The stimulation has been active since a month after the surgery, when, over the course of several visits, Malone adjusted the electricity, searching for and finding the optimal pulse. Yet Hire's depression hasn't been vanquished. The disease could still be triggered by life events—a death in the family, for example—which is why Malone and the other psychiatrists stay so heavily involved in each patient's life. But now if Hire starts feeling despairing or apathetic again, Malone can adjust the stimulation enough to ward off the darkness.

I ask Diane whether it bothers her to have her mental health regulated by a machine, and she shakes her head. For the most part, she says, she forgets there's a stimulator stuffed under her chest muscles and two wires snaking up her neck, into the depths of her brain. "I wake up every morning and feel like I control how the day's going to be and don't even think about, 'Oh, gosh, I hope it's still on,' " she says. "It feels like I have the power."

Saturday, September 22, 2007

Humans mispredict their emotions after decision making

Behavioral research over the past 15 years has confirmed what anyone who has purchased a house or dumped a significant other could tell you: When people make decisions, they anticipate that they may regret their choices. It is important that we maintain this ability, because as the aforementioned house-buyers and spouse-dumpers know, regret can be a terrible feeling.

How accurate are people in their anticipations of regret and of other post-decisional emotions, such as disappointment" It is a topic has been rather neglected by scientists, but new research reported in the recent issue of Psychological Science, a journal of the Association for Psychological Science, aims to fill this gap.

In the first of two experiments, participants took part in a two-person negotiation for money that would allow the scientists to observe negotiation style as well as measure how much regret the participants would feel if their tactics failed. The scientists observed that participants across the board tended to over-predict their post-negotiation regret and disappointment if their transaction was rejected. However, those who negotiated reasonably (i.e., less aggressive or greedy) were less prone to experience regret than the latter, as they had provided sensible offers.

In the second experiment, participants who had just completed a course assignment were asked to predict how they would feel if the grades that they received for their assignments exceeded, matched, or were lower than their expectations. On average, participants received higher than expected grades. However, the scientists observed that participants over-predicted the rejoicing and somewhat under-predicted the regret that they experienced when they received the grades.

In the light of such misprediction of emotions, Nick Sevdalis and Nigel Harvey the University College London scientists who authored the study argue that when people make decisions they should perhaps discount the regret, rejoicing, and other post-decisional emotions that they anticipate will be linked to potential outcomes arising from those decisions.

Posted by: Beverly Source

Thursday, September 20, 2007

Researchers Develop Intelligence Model

By SUE MAJOR HOLMES – 2 days ago

ALBUQUERQUE, N.M. (AP) — Rex Jung says researchers need to understand how the brain is put together to better understand how it unravels.

To that end, Jung — a research scientist at the Mind Research Network — and psychology professor Richard Haier of the University of California Irvine's School of Medicine scoured the neuroscience literature and analyzed studies of reasoning and measures of intelligence to put together a theoretical model aimed at letting researchers study intelligence in a more systematic way.

There's a lot of interest in measuring intelligence and how people solve tasks that require reasoning, said Jung.

"The terms intelligence and IQ are just so infused in our culture. ... We like to know fundamentally how our brains differ from others," he said.

Intelligence — the capacity of the brain to function well in a given setting — can be affected by such diseases as schizophrenia or Alzheimer's.

"Understanding how the brain produces intelligent behavior may allow us to address the cognitive decline associated with some of these devastating diseases," Jung said.

Jung and Haier, looking at the network of gray and white matter that comprises human intelligence, concluded there is significant consistency in brain structure and function related to intelligence.

From their review, they created the Parieto-Frontal Integration Theory, or P-FIT, which Jung said is the first testable, physical model of where intelligence resides in the human brain and what neural factors might affect cognitive performance.

Jung became interested in the topic prior to attending graduate school, when he started volunteering to work with Special Olympics, an international nonprofit organization dedicated to helping people with intellectual disabilities become physically fit, productive members of society through sports training and competition.

"I became attached to this group of individuals as a coach and as a friend, and I wanted to do something for that group of individuals," he said.

"It would be really nice if we could figure out ways to mitigate the damage done by neurological brain disorders that result in mental retardation. ... It would be great if we could help adults and youngsters who require a lot of help just to get through the day," Jung said.

A lot of researchers are looking for ways to cure Alzheimer's, schizophrenia or mental retardation, but not many are looking at the other side of the coin — research into what brains do well and how that can help research into what brains don't do well, Jung said.

With the P-FIT, researchers will now be able to test their studies against a model.

"Instead of having a piecemeal approach at looking at intelligence ... we now have a unified model to move forward with," said Jung, who expects the model to become more refined over time.

The neuroimaging studies they looked at analyzed both brain structure and function, including white matter and gray matter correlates of intelligence.

To explain those, Jung likens gray matter and white matter to the Internet in which computers connect to other computers so they can function at a higher rate than they could function alone. Gray matter can be compared to a computer's central processing unit, while white matter functions like the cables that allow the processing centers to communicate with each other.

Some of the 19 peer reviews published with the article faulted the limitations of the theoretical model. But Jung and Haier note that overall, those commentaries recognize P-FIT as "a reasonable empirical framework to test hypotheses about the relationship of brain structure and function with intelligence and reasoning."

"Some researchers out there ... may be able to tap into what we've done here and really improve people's lives in a dramatic fashion. That would be fantastic," Jung said.