To Get Good Grades, Get Good Sleep.

You’d think that college students would be experts at sleeping.  But odd hours, parties, cramming for tests, personal problems, self-medication with drugs or alcohol and general  can wreck a student’s sleep habits. Which can be bad for the body and the mind.

60-Second Psych from Scientific American podcasts
8 December 2008

A neural link between intelligence and self-control

If you had a choice between receiving $1,000 right now or $4,000 ten years from now, which would you pick? Psychologists use the term "delay discounting" to describe our inability to resist the temptation of a smaller immediate reward in lieu of receiving a larger reward at a later date. Discounting future rewards too much is a form of impulsivity, and an important way in which we can neglect to exert self-control.

Previous research suggests that higher intelligence is related to better self-control, but the reasons for this link are unknown. Psychologists Noah A. Shamosh and Jeremy R. Gray, from Yale University, and their colleagues, were interested in testing the idea that certain brain regions supporting short-term memory play a critical role in this relationship. "It has been known for some time that intelligence and self-control are related, but we didn't know why. Our study implicates the function of a specific brain structure, the anterior prefrontal cortex, which is one of the last brain structures to fully mature," said Dr. Shamosh.

In this study, 103 healthy adults were presented with a delay discounting task to assess self-control: a series of hypothetical choices where they had to choose between two financial rewards, a smaller one which they would receive immediately or another, larger reward which would be received at a later time. The participants then underwent a variety of tests of intelligence and short term memory. On another day, subjects' brain activity was measured using fMRI, while they performed additional short-term memory tasks.

The results show that participants with the greatest activation in the brain region known as the anterior prefrontal cortex also scored the highest on intelligence tests and exhibited the best self-control during the financial reward test. This was the only brain region to show this relation. The results appear in the September issue of Psychological Science, a journal of the Association for Psychological Science.

Previous studies have shown that the anterior prefrontal cortex plays a role in integrating a variety of information. The authors suggest that greater activity in the anterior prefrontal cortex helps people not only to manage complex problems, resulting in higher intelligence, but also aids in dealing with simultaneous goals, leading to better self-control.

Knowledge of the neural mechanisms underlying the relationship between short term memory, intelligence and delay discounting may result in improved techniques of increasing self-control. This is particularly applicable in regulating behavior related to gambling and substance abuse. "Understanding the factors that support better self-control is relevant to a host of important behaviors, ranging from saving for retirement to maintaining physical and mental health," the authors conclude.

Findings help identify mechanism of age-related memory deficits, highlight the importance of sleep for memory

Aging impairs the consolidation of memories during sleep, a process important in converting new memories into long-term ones, according to new animal research in the July 30 issue of The Journal of Neuroscience. The findings shed light on normal memory mechanisms and how they are disrupted by aging.

During sleep, the hippocampus, a brain region important in learning and memory, repeatedly "replays" brain activity from recent awake experiences. This replay process is believed to be important for memory consolidation. In the new study, Carol Barnes, PhD, and colleagues at the University of Arizona found reduced replay activity during sleep in old compared to young rats, and rats with the least replay activity performed the worst in tests of spatial memory.

Barnes and colleagues recorded hippocampal activity in 11 young and 11 old rats as they navigated several mazes for food rewards. Later, when the animals were asleep, the researchers recorded their hippocampal activity again. In the young animals, the sequence of neural activity recorded while the animals navigated the mazes was repeated when they slept. However, in most of the old animals, the sequence of neural activity recorded during sleep did not reflect the sequence of brain activity recorded in the maze. "These findings suggest that some of the memory impairment experienced during aging could involve a reduction in the automatic process of experience replay," said Michael Hasselmo, DPhil, at Boston University, an expert unaffiliated with the study.

Animals with more faithful sleep replay also performed better on memory tests. The researchers tested the same 22 rats on a spatial learning and memory task. Consistent with previous research, the young rats recalled the solution to the spatial task faster and more accurately than the old rats. In the old group, the researchers found that the top performers in the spatial memory task were also the ones that showed the best sleep replay. Irrespective of the animal's age, the researchers found that animals who more faithfully replayed the sequence of neural activity recorded in the maze while asleep also performed better on the spatial memory task. "This is the first study to suggest that an animal's ability to perform a spatial memory task may be related to the brain's ability to perform memory consolidation during sleep," said study author Barnes.

Identification of the specific memory deficit present in the aging brain may be a first step to preventing age-related memory loss. "This study's findings could inspire the development and testing of pharmacological agents designed to enhance memory replay phenomena," Hasselmo said.

Can we train ourselves to be compassionate? A new study suggests the answer is yes. Cultivating compassion and kindness through meditation affects brain regions that can make a person more empathetic to other peoples' mental states, say researchers at the University of Wisconsin-Madison. Published March 26 in the Public Library of Science One, the study was the first to use functional magnetic resonance imaging (fMRI) to indicate that positive emotions such as loving-kindness and compassion can be learned in the same way as playing a musical instrument or being proficient in a sport. The scans revealed that brain circuits used to detect emotions and feelings were dramatically changed in subjects who had extensive experience practicing compassion meditation.

The research suggests that individuals - from children who may engage in bullying to people prone to recurring depression - and society in general could benefit from such meditative practices, says study director Richard Davidson, professor of psychiatry and psychology at UW-Madison and an expert on imaging the effects of meditation. Davidson and UW-Madison associate scientist Antoine Lutz were co-principal investigators on the project. The study was part of the researchers' ongoing investigations with a group of Tibetan monks and lay practitioners who have practiced meditation for a minimum of 10,000 hours. In this case, Lutz and Davidson worked with 16 monks who have cultivated compassion meditation practices. Sixteen age-matched controls with no previous training were taught the fundamentals of compassion meditation two weeks before the brain scanning took place.

Many contemplative traditions speak of loving-kindness as the wish for happiness for others and of compassion as the wish to relieve others' suffering. Loving-kindness and compassion are central to the Dalai Lama's philosophy and mission," says Davidson, who has worked extensively with the Tibetan Buddhist leader. "We wanted to see how this voluntary generation of compassion affects the brain systems involved in empathy."

Various techniques are used in compassion meditation, and the training can take years of practice. The controls in this study were asked first to concentrate on loved ones, wishing them well-being and freedom from suffering. After some training, they then were asked to generate such feelings toward all beings without thinking specifically about anyone. Each of the 32 subjects was placed in the fMRI scanner at the UW-Madison Waisman Center for Brain Imaging, which Davidson directs, and was asked to either begin compassion meditation or refrain from it. During each state, subjects were exposed to negative and positive human vocalizations designed to evoke empathic responses as well as neutral vocalizations: sounds of a distressed woman, a baby laughing and background restaurant noise.

"We used audio instead of visual challenges so that meditators could keep their eyes slightly open but not focused on any visual stimulus, as is typical of this practice," explains Lutz. The scans revealed significant activity in the insula - a region near the frontal portion of the brain that plays a key role in bodily representations of emotion - when the long-term meditators were generating compassion and were exposed to emotional vocalizations. The strength of insula activation was also associated with the intensity of the meditation as assessed by the participants. "The insula is extremely important in detecting emotions in general and specifically in mapping bodily responses to emotion - such as heart rate and blood pressure - and making that information available to other parts of the brain," says Davidson, also co-director of the HealthEmotions Research Institute.

Activity also increased in the temporal parietal juncture, particularly the right hemisphere. Studies have implicated this area as important in processing empathy, especially in perceiving the mental and emotional state of others. "Both of these areas have been linked to emotion sharing and empathy," Davidson says. "The combination of these two effects, which was much more noticeable in the expert meditators as opposed to the novices, was very powerful."

The findings support Davidson and Lutz's working assumption that through training, people can develop skills that promote happiness and compassion. "People are not just stuck at their respective set points," he says. "We can take advantage of our brain's plasticity and train it to enhance these qualities." The capacity to cultivate compassion, which involves regulating thoughts and emotions, may also be useful for preventing depression in people who are susceptible to it, Lutz adds. "Thinking about other people's suffering and not just your own helps to put everything in perspective," he says, adding that learning compassion for oneself is a critical first step in compassion meditation.

The researchers are interested in teaching compassion meditation to youngsters, particularly as they approach adolescence, as a way to prevent bullying, aggression and violence. "I think this can be one of the tools we use to teach emotional regulation to kids who are at an age where they're vulnerable to going seriously off track," Davidson says. Compassion meditation can be beneficial in promoting more harmonious relationships of all kinds, Davidson adds. "The world certainly could use a little more kindness and compassion," he says. "Starting at a local level, the consequences of changing in this way can be directly experienced."

Lutz and Davidson hope to conduct additional studies to evaluate brain changes that may occur in individuals who cultivate positive emotions through the practice of loving-kindness and compassion over time.

Neuroanatomist Jill Bolte Taylor had an opportunity few brain scientists would wish for: One morning, she realized she was having a massive stroke. As it happened -- as she felt her brain functions slip away one by one, speech, movement, understanding -- she studied and remembered every moment. This is a powerful story about how our brains define us and connect us to the world and to one another.

Jill Bolte Taylor: My Stroke of Insight

The theory that depression is caused by a chemical imbalance is often presented in the media as fact even though there is little scientific evidence to support it, according to a new study co-authored by a Florida State University visiting lecturer. Jeffrey Lacasse, an FSU doctoral candidate and visiting lecturer in the College of Social Work, and Jonathan Leo, a neuroanatomy professor at Lincoln Memorial University in Tennessee, found that reporters who included statements in news articles about depression being caused by a chemical imbalance, or a lack of serotonin in the brain, were unable to provide scientific evidence to support those statements.

Lacasse and Leo spent about a year in late 2006 and 2007 monitoring the daily news for articles that included statements about chemical imbalances and contacting the authors to request evidence that supported their statements. Several reporters, psychiatrists and a drug company responded to the researchers' requests, but Lacasse and Leo said they did not provide documentation that supported the chemical imbalance theory. Their findings were published in the journal Society.

"The media's presentation of the theory as fact is troublesome because it misrepresents the current status of the theory," Lacasse said. "For instance, there are few scientists who will rise to its defense, and some prominent psychiatrists publicly acknowledge that the serotonin hypothesis is more metaphor than fact. As the current study documents, when asked for evidence, reporters were unable to cite peer-reviewed primary articles in support of the theory." Moreover, the researchers said, several of the responses received from reporters seem to suggest a fundamental misunderstanding of the theory's scientific status. The "Diagnostic and Statistical Manual of Mental Disorders," which almost all psychiatrists use to diagnose and treat their patients, clearly states that the cause of depression and anxiety is unknown, according to Lacasse and Leo.

The Society article builds on the pair's 2005 study, which focused on pharmaceutical advertisements that claim depression is caused by an imbalance of serotonin—an imbalance the drug companies say can be corrected by a class of antidepressants called Selective Serotonin Reuptake Inhibitors (SSRIs). "The chemical imbalance theory, which was formulated in the 1960s, was based on the observation that mood could be artificially altered with drugs, rather than direct observation of any chemical imbalances," Leo said. "Since then there has been no direct evidence to confirm the theory and a significant number of findings cast doubt on the theory."

The researchers said the popularity of the theory is in large part based on the presumed efficacy of the SSRIs, but they say that several large studies now cast doubt on this efficacy. A review of a full set of trial data published in the journal PLoS (Public Library of Science) Medicine last month concluded that much of the perceived efficacy of several of the most common SSRIs was due to the placebo effect. Other studies indicate that for every 10 people who take an SSRI, only one to two people are truly receiving benefit from the medication, according to Lacasse and Leo.

Still, the National Center for Health Statistics found that antidepressants are the most prescribed drugs in the United States, with doctors writing more than 31 million prescriptions in 2005. Both Lacasse and Leo emphasized the importance of patients being given factual information so they can make informed decisions about medications and the role of other potentially useful interventions, such as psychotherapy, exercise or self-help strategies. "Patients might make different choices about the use of medications and possibly use alternative approaches to their distress if they were fully informed," Lacasse said. "We believe the media can play a positive role by ensuring that their mental health reporting is congruent with scientific literature."

FSU News
March 2008

Eric Chudler at Neuroscience for Kids has recently added Neuroscience on Stamps.

Queensland Brain Institute (QBI) scientists have found another important clue to why nerve cells die in neurodegenerative diseases, based on studies of the developing brain. Neuroscientists at The University of Queensland have just published findings, which add more weight to the "use it or lose it" model for brain function.

QBI's Dr Elizabeth Coulson said a baby's brain generates roughly double the number of nerve cells it needs to function; with those cells that receive both chemical and electrical stimuli surviving, and the remaining cells dying. In research published in the "Journal of Neuroscience", Dr Coulson and her colleagues have identified a crucial step in the cell-death process. "It appears that if a cell is not appropriately stimulated by other cells, it self-destructs," Dr Coulson said.

This self-destruct process is also known to be an important factor in stroke, Alzheimer's and motor neuron diseases, leading to the loss of essential nerve cells from the adult brain. "We know that a lack of both chemical and electrical stimuli causes the cells to self-destruct," Dr Coulson said. "But we believe that nerve cells will survive if appropriate electrical stimuli are produced to block the self-destruct process that we have identified." The researchers' next step is to test whether dying cells receiving only electrical stimulation can be rescued.

More than three years' research has gone into understanding these crucial factors regulating nerve cell survival, but it is a major step in the long process of discovery needed to combat neurodegeneration. QBI Director, Professor Perry Bartlett said the research is an extremely exciting finding because it also provides the missing piece of information as to how the brain likely keeps alive the new neurons it generates in some brain areas as an adult. "Combining this with our knowledge of how to stimulate new neurons in the brain of adults following to disease processes such as stroke, it provides new mechanisms for the treatment of a variety of diseases from depression to dementia," he said.

Very young brains process memories of fear differently than more mature ones, new research indicates. The findings appear in the Feb. 6 issue of The Journal of Neuroscience. The work significantly advances scientific understanding of when and how fear is stored and unlearned, and introduces new thinking on the implications of fear experience early in life.

“This important paper raises questions that are the ‘tip of the iceberg’ related to the very complex series of events that occur as we learn to fear something. In the real world, we become fearful, extinguish that fear, reacquire it at another time, and then conquer it yet again,” says John Krystal, MD, of Yale University and director of the clinical neuroscience division of the VA National Center for Post-Traumatic Stress Disorder. “Typically, we think about long-term, negative impact of fear learning, such as lifelong problems with anxiety. But this work highlights an avenue for adapting to early stresses that apparently can occur only early in life: to erase a learned fear from memory.” Krystal was not affiliated with the research.

Study co-authors Jee Hyun Kim and Rick Richardson, PhD, of the University of New South Wales in Sydney, homed in on the amygdala, using anesthesia to temporarily inactivate it and therefore isolate its role. The amygdala is critical for emotional learning and plays a central role in dulling the memory of a fear. Kim and Richardson trained rats that were 16 and 23 days old—the human equivalent of children and budding adolescents—to associate a specific sound with a mild shock to the foot. After subsequent training, when the sound was not followed by a shock, the animals’ fearful reaction to hearing the sound faded. Technically, this is known as “extinction,” and depended on the function of the amygdala.

In a second round of training, the researchers reintroduced the fear and tried to re-extinguish it. This time around, they found, only the older rats were able to do so without the amygdala. The researchers concluded that the age at which the initial extinction training occurred was critical to whether or not the rats’ fear faded the second time independently of the amygdala. The authors suggest that in the very young, it is primarily the amygdala that extinguishes fearful memories, but that mechanisms independent of the amygdala develop later.

This raises the possibility that fears unlearned at an early enough age are, in fact, erased. As brains develop, however, and related structures near the amygdala mature, these structures take on a greater role. Thus, fear in adolescence and later in life may not be erased, but instead be, for example, inhibited by a process of overlaying neutral memories on top of the initial fear reaction. The initial memory could still exist and be called on again. “Extinction in the young brain might forever erase early traumatic learning—but accepting this hypothesis will have to wait for more research,” says Mark Bouton, PhD, of the University of Vermont, who did not participate in the esearch. “What might change as the brain develops is where and how fear learning and extinction are stored and how they can be retrieved.”

Another crack at non-addictive opioids? Why we don't get hooked on our own endorphins.
by Maia Szalavitz at 60-Second Science
29 January 2008

Turner, E.H., Matthews, A.M., Linardatos, E., Tell, R.A., & Rosenthal, R. (2008). Selective Publication of Antidepressant Trials and Its Influence on Apparent Efficacy. New England Journal of Medicine, 358(3). 252-260.

ABSTRACT
Background: Evidence-based medicine is valuable to the extent that the evidence base is complete and unbiased. Selective publication of clinical trials — and the outcomes within those trials — can lead to unrealistic estimates of drug effectiveness and alter the apparent risk–benefit ratio.

Methods: We obtained reviews from the Food and Drug Administration (FDA) for studies of 12 antidepressant agents involving 12,564 patients. We conducted a systematic literature search to identify matching publications. For trials that were reported in the literature, we compared the published outcomes with the FDA outcomes. We also compared the effect size derived from the published reports with the effect size derived from the entire FDA data set.

Results: Among 74 FDA-registered studies, 31%, accounting for 3449 study participants, were not published. Whether and how the studies were published were associated with the study outcome. A total of 37 studies viewed by the FDA as having positive results were published; 1 study viewed as positive was not published. Studies viewed by the FDA as having negative or questionable results were, with 3 exceptions, either not published (22 studies) or published in a way that, in our opinion, conveyed a positive outcome (11 studies). According to the published literature, it appeared that 94% of the trials conducted were positive. By contrast, the FDA analysis showed that 51% were positive. Separate meta-analyses of the FDA and journal data sets showed that the increase in effect size ranged from 11 to 69% for individual drugs and was 32% overall.

Conclusions: We cannot determine whether the bias observed resulted from a failure to submit manuscripts on the part of authors and sponsors, from decisions by journal editors and reviewers not to publish, or both. Selective reporting of clinical trial results may have adverse consequences for researchers, study participants, health care professionals, and patients.

NEJM: 17 January 2008

9 December 2007 — You study the menu at a restaurant and decide to order the steak rather than the salmon. But when the waiter tells you about the lobster special, you decide lobster trumps steak. Without reconsidering the salmon, you place your order—all because of a trait called “transitivity.”

“Transitivity is the hallmark of rational economic choice,” says Camillo Padoa-Schioppa, a postdoctoral researcher in HMS Professor of Neurobiology John Assad’s lab. According to transitivity, if you prefer A to B and B to C, then you ought to prefer A to C. Or, if you prefer lobster to steak, and steak to salmon, then you will prefer lobster to salmon.

Padoa-Schioppa is lead author on a paper that suggests this trait might be encoded at the level of individual neurons. The study, which appears online Dec. 9 in Nature Neuroscience, shows that some neurons in a part of the brain called the orbitofrontal cortex encode economic value in a “menu invariant” way. That is, the neurons respond the same to steak regardless if it’s offered against salmon or lobster.

“People make choices by assigning values to different options. If the values are menu invariant preferences will be transitive. The activity of these neurons does not vary with the menu options, suggesting that these neurons could be responsible for transitivity,” Padoa-Schioppa explains.

“This study provides a key insight into the biology of our frontal lobes and the neural circuits that underlie decision-making,” Assad adds. “Despite the maxim, we in fact can compare apples to oranges, and we do it all the time. Camillo’s research sheds light on how we make these types of choices.”

Frontal lobe damage has been linked to “choice deficits” such as eating disorders, compulsive gambling and abnormal social behavior. For example, in the first documented case of brain injury impacting behavior, the infamous railroad construction foreman Phineas Gage became unsociable after a tamping iron passed through his skull in 1848, damaging his frontal lobes. This area of the brain has also been implicated in drug abuse.

Labs are just beginning to probe normal decision-making at the level of individual neurons, venturing into a new field called neuroeconomics. Such research might eventually help to explain choice deficits associated with frontal lobe functions.

The new study builds on an April 2006 Nature paper in which Padoa-Schioppa and Assad identified neurons that encode the value macaque monkeys assign to juice they choose independent of its type, providing a common currency of comparison for the brain.

In that study, the scientists found that although monkeys generally prefer grape juice to apple juice, sometimes they choose the latter, if it is offered in large amounts. When presented with 3 units of apple juice and 1 unit of grape juice, for example, a monkey might take the grape juice only 50 percent of the time. This indicates that the value of the grape juice is 3 times that of the apple juice. A particular group of neurons in the orbitofrontal cortex fire at roughly the same rate, regardless of the monkey’s decision because the animal values both choices equally. These neurons also fire at the same rate if the monkey chooses 6 units of apple juice or 2 units of grape juice. Thus, these neurons encode the value the monkey receives in each trial.

Now, by adding a third juice to the mix, the team has tested whether these neurons reflect transitivity. The three juices were offered to a monkey in pairs dozens of times over the course of a session, the quantity of each juice varying from trial to trial.

In general, monkeys preferred 1 unit of juice A to 1 unit of juice B, 1B to 1C, and 1A to 1C. During each session, Padoa-Schioppa recorded the activity of a handful of neurons in the orbitofrontal cortex, and he discovered their firing rate did not depend on whether B was offered against A or against C, indicating that these neurons respond in a menu invariant way.

“The stability of these neurons could help to explain why we make decisions that are consistent over the short term,” Padoa-Schioppa says. “In our study, the neural circuit was not influenced by the short-term behavioral context.”

Padoa-Schioppa is now examining the possibility that value-encoding neurons may adapt to different value scales over longer periods of time.

Columbia scientists use fMR technology, find brain changes when viewing violent media

Violence is a frequent occurrence in television shows and movies, but can watching it make you behave differently? Although research has shown some correlation between exposure to media violence and real-life violent behavior, there has been little direct neuroscientific support for this theory until now.

Researchers at Columbia University Medical Center’s Functional Magnetic Resonance Imaging (fMRI) Research Center have shown that watching violent programs can cause parts of your brain that suppress aggressive behaviors to become less active.

In a paper in the Dec. 5 on-line issue of PLoS ONE (published by the Public Library of Science), Columbia scientists show that a brain network responsible for suppressing behaviors like inappropriate or unwarranted aggression (including the right lateral orbitofrontal cortex, or right ltOFC, and the amygdala) became less active after study subjects watched several short clips from popular movies depicting acts of violence. These changes could render people less able to control their own aggressive behavior. Indeed the authors found that, even among their own subjects, less activation in this network was characteristic of people reporting an above average tendency to behave aggressively. This characteristic was measured through a personality test.

A secondary finding was that after repeated viewings of violence, an area of the brain associated with planning behaviors became more active. This lends further support to the idea that exposure to violence diminishes the brain’s ability to inhibit behavior-related processing.None of these changes in brain activity occurred when subjects watched non-violent but equally engaging movies depicting scenes of horror or physical activity.

“These changes in the brain’s behavioral control circuits were specific to the repeated exposure to the violent clips,” said Joy Hirsch, Ph.D., professor of Functional Neuroradiology, Psychology, and Neuroscience and Director of the Center for fMRI at CUMC, and the PLoS ONE paper’s senior author. “Even when the level of action in the control movies was comparable, we just did not observe the same changes in brain response that we did when the subjects viewed the violent clips.”

“Depictions of violent acts have become very common in the popular media,” said Christopher Kelly, the first author on the paper and a current CUMC medical student. “Our findings demonstrate for the first time that watching media depictions of violence does influence processing in parts of the brain that control behaviors like aggression. This is an important finding, and further research should examine very closely how these changes affect real-life behavior.”

From the List Universe -- Top 10 Bizarre Mental [/neurological] Disorders

The theory explains how the brain compensates for damage from injuries such as stroke

Carnegie Mellon University neuroscientist Marcel Just and Stanford postdoctoral fellow Sashank Varma have put forward a new computational theory of brain function that provides answers to one of the central questions of modern science: How does the human brain organize itself to give rise to complex cognitive tasks such as reading, problem solving and spatial reasoning? Just and Varma's theory, called 4CAPS, is described in the fall issue of the journal Cognitive, Affective, and Behavioral Neuroscience.

More than a decade of research involving functional Magnetic Resonance Imaging brain scans in hundreds of laboratories has yielded a tremendous amount of information about what parts of the brain are activated when a person performs various tasks. Some researchers have been tempted to conclude that a simple one-to-one relationship exists between high-level mental tasks and brain areas. For example, some believe that a specific brain area is responsible for a specific cognitive task, such as identifying a face.

Just and Varma, however, propose that the evidence reveals a more complex picture in which thinking is a network function - a collaboration of several brain areas that is constantly adapting itself, based on the task at hand and the brain's own resources and biological limitations. The collaborating parts of the brain, according to Just, are like members of a sports team whose players substitute in and out of the action. 4CAPS (an acronym for Capacity Constrained Concurrent Cortical Activation-based Production System), proposes a decentralized process by which members of the cortical team volunteer themselves when their strengths are called for, but also permits less efficient but capable members to step forward when the primary player is injured or disabled, as might occur as a result of a stroke. Just and Varma have constructed a number of computational models to demonstrate this process, such as a model that understands English sentences.

A unique characteristic of the theory is that it can accurately predict the change in brain activation that results from some types of brain damage or disease. For example, if a stroke damages the part of the brain known as Broca's area - which is located in the left prefrontal cortex and is involved in language processing - the corresponding site on the right side of the brain often becomes activated during language processing, even within hours after a stroke. According to 4CAPS, the same dynamic allocation mechanism that allows brain areas to volunteer themselves on a moment-by-moment basis would also come into play if Broca's area were damaged, and would allow any excess computational load to spill over to the right hemisphere mirror site on a more permanent basis. Another example occurs with Alzheimer's disease, where the damage to some brain areas causes additional "helper" areas to be recruited to perform a task, additional areas that are not typically used by control subjects who do not have the disease.

"Many brain-imaging studies have shown as the nature of the task changes, so does the set of activating brain areas," said Just, the D.O. Hebb Professor of Psychology. "It is as though substitutions of team players are being made dynamically in response to changes in the game."

"We credit this dynamic mechanism with the fluidity or adaptability of human intelligence, and with much of the plasticity that occurs with learning or with recovery from brain damage," Just said.

4CAPS provides a framework for scientists and medical researchers to better understand nascent topics in neuroscience, such as how brain areas communicate and collaborate with one another during the thought process and how this can go awry. For example, Just and his colleagues have proposed an influential theory of autism, called the underconnectivity theory, that attributes the disorder to poor connectivity and hence communication between frontal areas of the brain and more posterior areas. The individual areas still have their specializations, according to the theory, but they cannot communicate as well with each other, and may develop a tendency to operate more independently of each. The theory also provides an account of what limits our ability to do multitasking.

"The thousands of facts that scientists have learned from brain imaging studies cry out for some sort of organization, some way to impose coherence, and ultimately to understand the brain system that is producing the results," Just said. "The theory provides a new conceptual framework for understanding how the fluidity of thought arises from the dynamics of brain activity.

"As neurological issues arise in education, aging and development, and as a basis for a knowledge-based economy, it will become increasingly important that human brain function be understood by students, parents and educators, patients and doctors, trainees and managers, citizens and policy-makers."

Carnegie Mellon Press Release
15 November 2007

Scientists are finding new evidence that a good night's rest plays a crucial role in cementing memories formed during the day.

One new study has identified a brain region involved, along with the hippocampus, in creating memories of the day's activities during sleep. Another study suggests melatonin, a hormone involved in regulating our day-night cycle, or "circadian rhythm," acts to suppress the formation of new memories as bedtime nears, perhaps in an effort to give memories made earlier in the day a chance to be prepared for long-term storage.

Both studies are detailed in the Nov. 16 issue of the journal Science.

Duke University Medical Center neuroscientists say the places a memory is processed in the brain may determine how someone can be absolutely certain of a past event that never occurred. These findings could help physicians better appreciate the memory changes that accompany normal aging or even lead to tools for the early diagnosis of Alzheimer's disease, according to Duke neuroscientist Roberto Cabeza, Ph.D.

Information retrieved from memory is simultaneously processed in two specific regions of the brain, each of which focuses on a different aspect of an past event. The medial temporal lobe (MTL), located at the base of the brain, focuses on specific facts about the event. The frontal parietal network (FPN), located at the top of the brain, is more likely to process the global gist of the event. The specific brain area accessed when one tries to remember something can ultimately determine whether or not we think the memory is true or false, the researchers found.

"Human memory is not like computer memory -- it isn't completely right all the time," said Cabeza, senior author of a paper appearing in the Journal of Neuroscience. "There are many occasions when people feel strongly about past events, even though they might not have occurred." Cabeza wanted to understand why someone could have such strong feelings of confidence about false memories. In his experiments, he scanned the brains of healthy volunteers with functional MRI as they took well-established tests of memory and false memory. Functional MRI is an imaging technique that shows what areas of the brain are used during specific mental tasks.

During the brain scans, Cabeza found that volunteers who were highly confident in memories that were indeed true showed increased activity in the fact-oriented MTL region. "This would make sense, because the MTL, with its wealth of specific details, would make the memory seem more vivid," Cabeza said. "For example, thinking about your breakfast this morning, you remember what you had, the taste of the food, the people you were with. The added richness of these details makes one more confident about the memory's truth."

On the other hand, volunteers who showed high confidence in memories that turned out to be false exhibited increased activity in the impressionistic FPN. The people drawing from this area of the brain recalled the gist or general idea of the event, and while they felt confident about their memories, they were often mistaken, since they could not recall the details of the memory.

These findings, coupled with the findings of other studies, can help explain what happens to the human brain as it ages, Cabeza said. "Specific memories don't last forever, but what ends up lasting are not specific details, but more general or global impressions," Cabeza said. "Past studies have shown that as normal brains age, they tend to lose the ability to recollect specifics faster than they lose the ability recall impressions. However, patients with Alzheimer's disease tend to lose both types of memories equally, which may prove to be a tool for early diagnosis."

Cabeza's colleague for this research was Hongkeun Kim at Daegu University in South Korea. The research was supported by the National Institutes of Health and Daegu University.

By activating multiple fluorescent proteins in neurons, neuroscientists at Harvard University are imaging the brain and nervous system as never before, rendering their cells in a riotous spray of colors dubbed a "Brainbow."

The technique, described in the cover story of the Nov. 1 issue of the journal Nature, has been developed by a team led by Harvard's Jean Livet, Joshua R. Sanes, and Jeff W. Lichtman and  allows researchers to tag neurons with roughly 90 distinct colors, a huge leap over the mere handful of shades possible with current fluorescent labeling. (read article; view slide show)

You may not be fully dressed without a smile, but a look of horror will make a faster first impression. Vanderbilt University researchers have discovered that the brain becomes aware of fearful faces more quickly than those showing other emotions. "There are reasons to believe that the brain has evolved mechanisms to detect things in the environment that signal threat. One of those signals is a look of fear," David Zald, associate professor of psychology and a co-author of the new study, said. "We believe that the brain can detect certain cues even before we are aware of them, so that we can direct our attention to potentially threatening situations in our environment." Randolph Blake, Centennial Professor of Psychology, and Eunice Yang, doctoral student, were co-authors of the study, which will appear in the November 2007 issue of Emotion.

The researchers set out to determine if we become aware of fearful, neutral or happy expressions at the same speed, or if one of these expressions reaches our awareness faster than the others. To do this, they needed to find a way to slow down the speed at which subjects processed facial information -- which usually takes less than 40 milliseconds. At those high speeds it is difficult to tell which images rise to awareness the fastest.

Yang, the lead author of the study, realized that a technique being used in Blake's lab might provide a solution to the problem. The technique, continuous flash suppression, keeps people from becoming aware of what they are seeing for up to 10 seconds. Using this technique, the team had research subjects look at a screen through a viewer, similar to the eyepieces on a microscope, which allowed different images to be presented to each eye. Many images were rapidly presented to one eye while a static image of a face was presented to the other. The multiple images served as visual 'noise,' suppressing the image of the face. The subjects indicated when they first became aware of seeing a face, enabling the researchers to determine if the expression on the face had any impact on how quickly the subject became aware of it.

The team found that subjects became aware of faces that had fearful expressions before neutral or happy faces. They believe a brain area called the amygdala, which shortcuts the normal brain pathway for processing visual images, is responsible. "The amygdala receives information before it goes to the cortex, which is where most visual information goes first. We think the amygdala has some crude ability to process stimuli and that it can cue some other visual areas to what they need to focus on," Zald said.

Zald and his colleagues believe the eyes of the fearful face play a key role. "Fearful eyes are a particular shape, where you get more of the whites of the eye showing," he said."That may be the sort of simple feature that the amygdala can pick up on, because it's only getting a fairly crude representation. That fearful eye may be something that's relatively hardwired in there."

A surprising finding was that subjects perceived happy faces the slowest. "What we believe is happening is that the happy faces signal safety. If something is safe, you don't have to pay attention to it," Zald said.

Next, the researchers will explore how this information influences our behavior. "We are interested in now exploring what this means for behavior," Yang said. "Since these expressions are being processed without our awareness, do they affect our behavior and our decision making? If so, how?"

Suggests that loss of treatment response is likely due to loss of placebo response

Providence, RI – A new study by Rhode Island Hospital researchers indicates that a relapse during antidepressant continuation treatment may be due to a relapse in patients who were not true drug responders. The loss of drug response may be due to loss of placebo response (a positive medical response to taking a placebo as if it were an active medication.). The study was published in the August issue of the Journal of Clinical Psychiatry.

Historically, the treatment of depression is divided into three phases – initial/acute, continuation and maintenance. During the initial phase, the goal is to reduce symptoms and psychosocial impairment. During the continuation phase, usually six months to one year after initial treatment response, the goal is to maintain the gains and prevent a relapse. In the maintenance phase, which occurs after a sustained period of improvement, the goal is to further maintain the gains and prevent recurrence of the disorder.

Mark Zimmerman, MD, director of outpatient psychiatry at Rhode Island Hospital and associate professor of psychiatry and human behavior at the Warren Alpert School of Medicine at Brown University, is the paper’s lead author. Zimmerman, along with his colleague Tavi Thongy, MD, also of Rhode Island Hospital and Brown University, conducted a meta-analysis of continuation studies of new generation antidepressants that began as placebo-controlled acute phase studies. Treatment studies of depression have found that approximately 50 to 65 percent of patients respond to medication and that approximately 25 to 35 percent respond to placebo.

Past studies have indicated that a number of patients who respond to treatment in the initial phase experience a relapse or recurrence despite ongoing pharmacotherapy during the two latter phases of treatment. This return of symptoms is often interpreted as a loss of efficacy of antidepressant activity, and is referred to as tachyphylaxis or the “poop-out” effect. Zimmerman says, “When a patient improves after being prescribed an antidepressant medication you do not know if they got better because of the medication or because they had a placebo response.”

The researchers used formulas developed by Quitkin and colleagues more than a decade ago to calculate the relapse rate attributable to relapse in presumptive placebo responders. “Our study suggests that the return of symptoms despite ongoing treatment during the continuation and maintenance phases of treatment may not represent a loss of drug effect because the patient may not have experienced a true drug response in the first place.” Zimmerman also notes, “While our conclusion is limited to the continuation phase of treatment, our results suggest that these findings probably also apply to the maintenance phase of treatment.”

The researchers note that these findings are not inconsistent with conclusions that continuation and maintenance studies of antidepressants have clearly established the benefit of ongoing treatment beyond the acute phase.

Exercise has a similar effect to antidepressants on depression. This has been shown by previous research. Now Astrid Bjørnebekk at Karolinska Institutet has explained how this can happen: exercise stimulates the production of new brain cells.

In a series of scientific reports, she has searched for the underlying biological mechanisms that explain why exercise can be a form of therapy for depression and has also compared it with pharmacological treatment with an SSRI drug.

The experiment studies were conducted on rats. The results show that both exercise and antidepressants increase the formation of new cells in an area of the brain that is important to memory and learning. Astrid Bjørnebekk's studies confirm previous research results, and she proposes a model to explain how exercise can have an antidepressant effect in mild to moderately severe depression. Her study also shows that exercise is a very good complement to medicines.

"What is interesting is that the effect of antidepressant therapy can be greatly strengthened by external environmental factors," she says.

Previous studies have shown that drug abusers have lowered levels of the dopamine D2 receptor in the brain's reward system. It has been speculated that this may be of significance to the depressive symptoms drug abusers often suffer from. These rat studies show that genetic factors may influence how external environmental factors can regulate levels of the dopamine D2 receptor in the brain.

"Different individuals may have differing sensitivity to how stress lowers dopamine D2 receptor levels, for example. This might be significant in explaining why certain individuals develop depression more readily than others," she says.

Why does putting our feelings into words - talking with a therapist or friend, writing in a journal - help us to feel better? A new brain imaging study by UCLA psychologists reveals why verbalizing our feelings makes our sadness, anger and pain less intense. [complete press release from UC News Wire]

Disturbed sleep is a commonly reported symptom among individuals diagnosed with anxiety disorders. However, the direct cause of disrupted sleep is poorly understood. Proper sleep is critical for cognitive and daily functioning, and reduced quality of sleep has the potential to exacerbate pre-existing psychological conditions, according to a research abstract presented Wednesday at SLEEP 2007, the 21st Annual Meeting of the Associated Professional Sleep Societies (APSS).

To effectively evaluate differences in sleep architecture after induced stress, Robert Ross MacLean, of Boston University, utilized an objective measure of anxiety and recorded subsequent sleep-wake behavior in rats. In the rodent model, many previous studies had observed differences in sleep-wake behavior after shock exposure, but the level of anxiety was merely assumed or absent.

MacLean's study exposed naïve rats to one of three paradigms: escapable shock, inescapable shock or fear conditioning. Immediately after experimental manipulation, individual level of anxiety was assessed using the elevated-plus maze apparatus, and polygraphic signs of sleep-wake behavior were recorded for six hours.

By measuring individual anxiety level prior to recording sleep, MacLean was able to make comparisons between sleep architecture and level of anxiety. In doing so, MacLean intended to establish a direct link between variation in sleep architecture and heightened anxiety in the rodent model.

"These changes could elucidate sleep-wake behavior associated with the subjective complaint of disrupted sleep, thus creating the potential for new diagnostic and assessment criteria for anxiety disorders," said MacLean. "This information is relevant given the recent influx of psychological disorders in Iraq war veterans, particularly generalized anxiety and post-traumatic stress disorder."

The amount of sleep a person gets affects his or her physical health, emotional well-being, mental abilities, productivity and performance. Recent studies associate lack of sleep with serious health problems such as an increased risk of depression, obesity, cardiovascular disease and diabetes.

Experts recommend that adults get between seven and eight hours of sleep each night to maintain good health and optimum performance.

Washington — Young adults with a short temper or mean disposition also tend to have compromised lung function, says a recent study published in the journal Health Psychology, by the American Psychological Association (APA). This occurred even when asthma and smoking were ruled out as possible causes of lung dysfunction.

In a study of 4,629 Black and White 18-30 year olds from four metropolitan areas (sampled from the Coronary Artery Risk Development in (Young) Adults Study cohort (CARDIA), psychologists examined whether the tendency to be hostile went along with having decreased lung function in otherwise healthy young adults. The results indicated that the more hostile one’s personality—characterized by aggression or anger, for example—the lower levels one’s of lung function even after controlling for age, height, socioeconomic status, smoking status and presence of asthma.

People with higher levels of general frustration predicted statistically significant reductions in pulmonary function for Black women, White women, and Black men. The only marginally strong finding occurred among the White men sampled. The authors speculate that people in lower status roles, Black women, White women, and Black men, who display hostility (and may be pushing against social expectations), elicit stronger social consequences than White men, resulting in higher levels of internalized stress that can make them sick. Further research is required to rule out if environmental toxins such as air pollution may contribute to both higher hostility and lower lung function.

Hostility was measured using the Cook-Medley Questionnaire which is derived from the items on the Minnesota Multiphasic Personality Inventory. Pulmonary function was measured while participants were standing and wearing a nose clip, blowing into a machine to measure their lung capacity, which can indicate upper airway obstruction.

“Recent research demonstrates that greater hostility predicts lung function decline in older men. This is the first study of young adults to offer a detailed examination of the inverse link between hostility and pulmonary function,” states lead author and psychologist Benita Jackson PhD MPH, Smith College. “It’s remarkable to see reductions in lung function during a time of life we think of as healthy for most people. Right now, we can’t say if having a hostile personality causes lung function decline, though we now know that these things happen together. More research is needed to establish whether hostility is associated with change in pulmonary function during young adulthood.” This research has implications for future research exploring the possible influence of social status on personality functioning and pulmonary health.

---

Article: Does Harboring Hostility Hurt" Associations Between Hostility and Pulmonary Function in the Coronary Artery Risk Development in (Young) Adults (CARDIA) Study, Journal of Health Psychology, Vol. 26 No. 3

Full text of the article is available at http://www.apa.org/journals/releases/hea263333.pdf

All anxiety is not created equal, and a research team at the University of Illinois now has the data to prove it. The team has found compelling evidence that differing patterns of brain activity are associated with each of two types of anxiety: anxious apprehension (verbal rumination, worry) and anxious arousal (intense fear, panic, or both).

Their work appears this month online in Psychophysiology. [press release from UIUC]

Eternal sunshine
It's sold as happiness in a blister pack - a cure-all that has changed the way we think about wellbeing. As Prozac reaches its 20th birthday, Anna Moore presents 20 things you need to know about the most widely used antidepressant in the world

13 May 2007
The Observer

Memorizing a series of facts is one thing, understanding the big picture is quite another. Now a new study demonstrates that relational memory – the ability to make logical “big picture” inferences from disparate pieces of information – is dependent on taking a break from studies and learning, and even more important, getting a good night’s sleep.

Led by researchers at Beth Israel Deaconess Medical Center (BIDMC) and Brigham and Women’s Hospital (BWH), the findings appear on-line in today’s Early Edition of the Proceedings of the National Academy of Sciences (PNAS).

“Relational memory is a bit like solving a jigsaw puzzle,” explains senior author Matthew Walker, PhD, Director of the Sleep and Neuroimaging Laboratory at BIDMC and Assistant Professor of Psychology at Harvard Medical School (HMS). “It’s not enough to have all the puzzle pieces – you also have to understand how they fit together.”

Adds lead author Jeffrey Ellenbogen, MD, a postdoctoral fellow at HMS and sleep neurologist at BWH, “People often assume that we know all of what we know because we learned it directly. In fact, that’s only partly true. We actually learn individual bits of information and then apply them in novel, flexible ways.” For instance, if a person learns that A is greater than B and B is greater than C, then he or she knows those two facts. But embedded within those is a third fact – A is greater than C – which can be deduced by a process called transitive inference, the type of relational memory that the researchers examined in this study.

Earlier research by Walker and colleagues had shown that sleep actively improves task-oriented “procedural memory” – for example, learning to talk, to coordinate limbs, musicianship, or to play sports. Because relational memory is fundamental to knowledge and learning, Walker and Ellenbogen decided to explore how and when this “inferential” knowledge emerges, hypothesizing that it develops during “off-line” periods and that, like procedural memory, would be enhanced following a period of sleep.

So, the researchers tested 56 healthy college students, each of whom was shown five pairs of unfamiliar abstract patterns – colorful oval shapes resembling Faberge eggs. The students were then told that some of the patterns were “correct” while others were “incorrect,” for example, Shape A wins over Shape B, Shape B wins over Shape C, and so on. All of the students learned the individual pairs but were not told that there was a hidden “hierarchy” linking all five of the pairs together.

After a 30-minute study period, the students were separated into three groups to test their understanding of the larger “big picture” relationship between the individual patterns: Group One was tested after a period of 20 minutes; Group Two was tested after a 12-hour period; and Group Three was tested after a 24-hour time span. In addition, approximately half of the students in Group Two slept during the 12-hour period, while the other half remained awake. All of the students in Group Three had a full night’s sleep.

The test results showed striking differences among the three groups, especially between the students who had a period of sleep and those who remained awake. “Group One, the students who were tested soon after their initial learning period, performed the worst,” says Walker. “While they were able to learn and recall the component pieces [for example, Shape A is greater than Shape B, Shape B is greater than Shape C] they could not discern the hierarchical relationships between the pieces [Shape A is greater than Shape C] – they couldn’t yet see ‘the big picture.’” Groups Two and Three, on the other hand, demonstrated a clear understanding of the interrelationship between the pairs of shapes.

“These individuals were able to make leaps of inferential judgment just by letting the brain have time to unconsciously mull things over,” he says. But, perhaps most notable, he adds, when the inferences were particularly difficult, the students who had had periods of sleep in between learning and testing significantly outperformed the other groups. “This strongly implies that sleep is actively engaged in the cognitive processing of our memories,” notes Ellenbogen. “Knowledge appears to expand both over time and with sleep.”

Concludes Walker, “These findings point to an important benefit [of sleep] that we had not previously considered. Sleep not only strengthens a person’s individual memories, it appears to actually knit them together and helps realize how they are associated with one another. And this may, in fact, turn out to be the primary goal of sleep: You go to bed with pieces of the memory puzzle, and awaken with the jigsaw completed.”


20 April 2007
Beth Israel Deaconess Medical Center News

A Brown University-led research team has, for the first time, recorded activity inside the cells of the hippocampus while simultaneously measuring activity in the neocortex. Recordings from these two brain regions – seats of memory creation and storage – revealed a surprisingly complex pattern of activity. These findings, in the Proceedings of the National Academy of Sciences, are part of a growing body of evidence that challenges traditional theories of the role of sleep in learning and memory. [read more]

Spending on prescription drugs to treat depression, anxiety, pain, schizophrenia and other conditions climbed from $7.9 billion in 1997 to $20 billion in 2004 - over a 150 percent increase, according to the latest News and Numbers from the Agency for Healthcare Research and Quality.

• The sharpest increase was for antipsychotic agents, medications used to manage schizophrenia, bipolar disorder and other psychoses. They saw an increase from $1.3 billion to $4.1 billion from 1997 to 2004.
  
  
• Spending for central nervous system stimulants to treat pain and control seizures, nearly tripled over the same time period, increasing from $0.6 billion to $1.7 billion.
  
  
• Spending on antidepressants more than doubled from 1997 to 2004, increasing from $5.1 billion to $12.1 billion, as did expenditures for anxiolytics, sedatives, and hypnotics for anxiety and sleep disorders. Spending for these drugs rose from $.9 billion to $2.1 billion.
  
  
• During the same time period, overall prescriptions for psychotherapeutic drugs increased from 141.9 million to 244.3 million; the number of people prescribed at least one such drug rose from 21 million to 32.6 million; and the average price per purchase increased from $55.80 to $82.00.

AHRQ, a part of the U.S. Department of Health and Human Services, works to improve the quality, safety, efficiency and effectiveness of health care in the United States. The data in this AHRQ News and Numbers comes from the Agency's Medical Expenditure Panel Survey, a highly detailed source of information on the health services that Americans use, how frequently they use them, the cost of these services, and how they are paid.

For more information on this AHRQ News and Numbers see Trends in the Use and Expenditures for the Therapeutic Class Prescribed Psychotherapeutic Agents and All Subclasses, 1997 and 2004 (PDF).

http://www.ahrq.gov

* * * * * * * * * * *
Medical News Today
30 March 2007

Alcohol and tobacco more harmful than cannabis and ecstacy.

A new study published in the Lancet proposes that drugs should be classified by the amount of harm that they do, rather than the sharp A, B, and C divisions in the UK Misuse of Drugs Act. The new ranking places alcohol and tobacco in the upper half of the league table. These socially accepted drugs were judged more harmful than cannabis, and substantially more dangerous than the Class A drugs LSD, 4-methylthioamphetamine and ecstasy.

Harmful drugs are currently regulated according to classification systems that purport to relate to the harms and risks of each drug. However, these are generally neither specified nor transparent, which reduces confidence in their accuracy and undermines health education messages.

Professor David Nutt from the University of Bristol, Professor Colin Blakemore, Chief Executive of the Medical Research Council, and colleagues, identified three main factors that together determine the harm associated with any drug of potential abuse:

   1. the physical harm to the individual user caused by the drug
   2. the tendency of the drug to induce dependence
   3. the effect of drug use on families, communities, and society

Within each of these categories, they recognized three components, leading to a comprehensive 9-category matrix of harm. Expert panels gave scores, from zero to three, for each category of harm for 20 different drugs. All the scores for each drug were combined to produce an overall estimate of its harm. In order to provide familiar benchmarks, for comparison with illicit drugs, five legal drugs of potential misuse (alcohol, khat, solvents, alkyl nitrites, and tobacco) and one that has since been classified (ketamine) were included in the assessment. The process proved simple, and yielded roughly similar scores for drug harm when used by two separate groups of experts.

Professor David Nutt, lead author on the paper, said: “Drug misuse and abuse are major health problems. Our methodology offers a systematic framework and process that could be used by national and international regulatory bodies to assess the harm of current and future drugs of abuse.”

Professor Colin Blakemore added: “Drug policy is primarily aimed at reducing the harm to individual users, their families and society. But at present there is no rational, evidence-based method for assessing the harm of drugs. We have tried to develop such a method. We hope that policy makers will take note of the fact that the resulting ranking of drugs differs substantially from their classification in the Misuse of Drugs Act and that alcohol and tobacco are judged more harmful than many illegal substances.”

Press release: 23 March 2007
University of Bristol

Humans acquire fears using similar neural processes whether they’ve personally experienced an aversive event or only witnessed it, according to a study by researchers at New York University’s Departments of Psychology. This is the first study examining the brain basis of fears acquired indirectly, through the observation of others. The study shows that the amygdala, which is known to be critical to the acquisition and expression of fears from personal experience, is also involved during the acquisition and expression of fears obtained indirectly through social observation. The findings appear in the most recent issue of the journal Social Cognitive and Affective Neuroscience (SCAN).

The research team, from the laboratory of NYU Professor Elizabeth Phelps, also includes Andreas Olsson, now a post-doctoral fellow at Columbia University’s Department of Psychology, and Katherine Nearing from NYU’s School of Medicine.

Previous research has shown how people develop fears after first-hand experience of an aversive event—getting stung by a bee or being burned by a hot pan. In acquiring these fears, a process known as fear conditioning, the brain’s amygdala plays a critical role. However, it’s unclear if fear conditioning can occur indirectly—that is, through social observation with no personal experience. It is also uncertain what neural processes take place in the acquisition of fears stemming from events or circumstances not experienced first-hand.

In this study, subjects witnessed a short video of another individual participating in a fear-conditioning experiment. In the video, subjects saw another person responding with distress when receiving mild electric shocks paired with a colored square. The subjects watching the video were then told they would take part in an experiment similar to the one they just viewed. Unlike the experiment in the video, these subjects never received shocks.

The results showed that the participants had a robust fear response when they were presented with the colored square that predicted electric shocks in the video, indicating that such a response resulted from merely observing—rather than directly experiencing—an aversive event. In addition, using brain imaging techniques, the researchers found that the amydgala response was equivalent with both when watching others receive a shock and when presented with the colored square that was previously paired with shock in the video. This finding demonstrates that similar neural systems are engaged when fears are learned through first-hand experience or by merely observing others.

"In our daily lives, we are frequently exposed to vivid images of others in emotional situations through personal social interactions as well as the media," explained Phelps. "The knowledge of somebody else’s emotional state may evoke empathic responses. However, as our results reveal, when others’ emotions are accompanied with vivid expressions and perceived as potentially relevant to our own future well being, we may engage additional learning mechanisms."

Olsson added: "In a way, learning by observing others’ emotional responses is like exploiting their expertise without being directly exposed to the potential risks associated with the direct learning. This seems a very adaptive thing to do for most social animals, which could explain why it is commonly seen across species. However, it remains to be explored in what way uniquely human social abilities contribute to learning fears through social observation."

A common drug [propranolol] administered in the first hours following trauma to patients deemed to be at risk of developing post-traumatic stress disorder (PTSD) reduced the occurrence of PTSD, according to a study led by researchers at the University of Lille, France [in 2003].

While the study involved a small number of subjects, its results are encouraging, says its senior author, Charles Marmar, MD, associate chief of staff for mental health at the San Francisco VA Medical Center and professor and vice chair of psychiatry at University of California, San Francisco.

"The study is based on the new theory that PTSD is most likely to occur in patients who experience a particularly severe and prolonged response to trauma. If this model proves accurate after five or ten replications of studies like this one, it could have very profound ramifications. From a public health perspective, if you could identify the subgroup of people who are susceptible to PTSD, giving them this course of medication -- which is brief, very well tolerated and inexpensive -- could be very effective prevention [following major trauma] and may have great social relevance." The study appears in the November 1 issue of Biological Psychiatry. [read rest of article]

Also: The Memory Pill (60 Minutes video -- 26 Nov 2006)
Bad Memory? Wipe It Clean With New Pill (16 Jan 2006)

A drug company was last week accused of concealing evidence about the safety of the antidepressant Seroxat. According to leading psychiatrist Professor David Healy, this is just the latest in a string of cases where patients and medical professionals have been misled about a drug's adverse effects. [read more]