Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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By Scicurious Depression is a disease with a difficult set of symptoms. Not only are the symptoms difficult to describe (how do you really describe anhedonia, before you know the word for it?), symptoms of depression manifest in different ways for different people. One person will eat more, sleep all the time, move slowly. Another will eat almost nothing, never sleep, and be irritable and nervous. They are both depressed. The only universal symptom is the feeling of…depression, and the need for successful treatment. Treatments which often take several weeks to work, are often ineffective, and which come with a host of side effects. So I was particularly intrigued when Nature published two papers this week looking at the role of dopamine in depressive-like behavior. What I particularly like is that these two papers have somewhat opposite results, due to different behavioral methods, something which I think highlights some of the problems associated with studying depression. Ed Yong covered both of the studies together fabulously over at Not Exactly Rocket Science, but I’d like to look at them both separately, to take a deeper look at each one, see what they’ve achieved, and what other questions they raise. Today we are on the second of the two papers, one which has a similar angle to the first paper, but an entirely different result. Yesterday’s paper looked at how changes in dopamine cell firing from the ventral tegmental area (which projects to areas like the prefrontal cortex and the nucleus accumbens) can impact depressive-like behaviors in mice and rats. Today’s paper looks at the ventral tegmental area as well, but instead of cutting on or turning “off” cell firing, the authors of this study looked at different types of neuronal activity, and the effects in socially defeated mice. © 2012 Scientific American
Link ID: 17621 - Posted: 12.19.2012
By Judy Stone We’ve touched on some of the many disturbing things that happened during the clinical trial on which Dan Markingson committed suicide. In my first post, I asked how a psychotic, homicidal patient who was involuntarily hospitalized in a psychiatric hospital could give an informed consent for participation in a clinical trial. There appeared to have been abuse of a vulnerable patient and extraordinary coercion—participate in this trial or be committed to a psych hospital seems to have been the bottom line. In my second post, we looked at investigator responsibilities, delegation of authority, and Good Clinical Practice tenets, all of which were violated with no consequences. Now we turn to the need to disclose conflicts of interest (COI), again a basic clinical research ethics principle that was violated. There are so many obvious conflicts of interest that it is hard to know quite where to start. The most obvious and egregious COI was that shown by Dr. Stephen Olson, who acted as both Dan Markingson’s treating physician and as Principle Investigator on the CAFÉ study. As Dr. Harrison Pope, a Harvard expert, concluded in his testimony, Olson “failed to meet the standards for good clinical practice both as a principal investigator and as the study physician for Mr. Markingson.” He failed his ethical responsibilities to Dan. © 2012 Scientific American
Link ID: 17619 - Posted: 12.19.2012
By Scicurious Depression is a disease with a difficult set of symptoms. Not only are the symptoms difficult to describe (how do you really describe anhedonia, before you know the word for it?), symptoms of depression manifest in different ways for different people. One person will eat more, sleep all the time, move slowly. Another will eat almost nothing, never sleep, and be irritable and nervous. They are both depressed. The only universal symptom is the feeling of…depression, and the need for successful treatment. Treatments which often take several weeks to work, are often ineffective, and which come with a host of side effects. So I was particularly intrigued when Nature published two papers this week looking at the role of dopamine in depressive-like behavior. What I particularly like is that these two papers have somewhat opposite results, due to different behavioral methods, something which I think highlights some of the problems associated with studying depression. Ed Yong covered both of the studies together fabulously over at Not Exactly Rocket Science, but I’d like to look at them both separately, to take a deeper look at each one, see what they’ve achieved, and what other questions they raise. So I will start with one today, and post the other tomorrow, looking at both sides. While you often hear about serotonin in studies of depression (serotonin is, after all, a target of many current antidepressants), there are many other neurotransmitters and systems that are also under investigation, and many of them are bearing some fruitful results. Ketamine, for example. And of course there is the role of dopamine. © 2012 Scientific American
Link ID: 17613 - Posted: 12.18.2012
By JAMES DAO Reviving a 20-year debate over illnesses of veterans of the 1991 Persian Gulf war, a new scientific paper presents evidence that nerve agents released by the bombing of Iraqi chemical weapons depots just before the ground war began could have carried downwind and fallen on American troops staged in Saudi Arabia. The paper, published in the journal Neuroepidemiology, tries to rebut the longstanding Pentagon position, supported by many scientists, that neurotoxins, particularly sarin gas, could not have carried far enough to sicken American forces. The authors are James J. Tuite and Dr. Robert Haley, who has written several papers asserting links between chemical exposures and gulf war illnesses. They assembled data from meteorological and intelligence reports to support their thesis that American bombs were powerful enough to propel sarin from depots in Muthanna and Falluja high into the atmosphere, where winds whisked it hundreds of miles south to the Saudi border. Once over the American encampments, the toxic plume could have stalled and fallen back to the surface because of weather conditions, the paper says. Though troops would have been exposed to low levels of the agent, the authors assert that the exposures may have continued for several days, increasing their impact. Though chemical weapons detectors sounded alarms in those encampments in the days after the January 1991 bombing raids, they were viewed as false by many troops, the authors report. © 2012 The New York Times Company
A specific pattern of neuronal firing in a brain reward circuit instantly rendered mice vulnerable to depression-like behavior induced by acute severe stress, a study supported by the National Institutes of Health has found. When researchers used a high-tech method to mimic the pattern, previously resilient mice instantly succumbed to a depression-like syndrome of social withdrawal and reduced pleasure-seeking — they avoided other animals and lost their sweet tooth. When the firing pattern was inhibited in vulnerable mice, they instantly became resilient. "For the first time, we have shown that split-second control of specific brain circuitry can switch depression-related behavior on and off with flashes of an LED light," explained Ming-Hu Han, Ph.D. External Web Site Policy, of the Mount Sinai School of Medicine, New York City, a grantee of NIH’s National Institute of Mental Health (NIMH). "These results add to mounting clues about the mechanism of fast-acting antidepressant responses." Han, Eric Nestler, M.D., Ph.D. External Web Site Policy,of Mount Sinai, and colleagues, report on their study in the journal Nature. In a companion article, NIMH grantees Kay Tye, Ph.D. External Web Site Policy, of the Massachusetts Institute of Technology, Cambridge, Mass., and Karl Deisseroth, M.D., Ph.D. External Web Site Policy, of Stanford University, Stanford, Calif., used the same cutting-edge technique to control mouse brain activity in real time. Their study reveals that the same reward circuit neuronal activity pattern had the opposite effect when the depression-like behavior was induced by daily presentations of chronic, unpredictable mild physical stressors, instead of by shorter-term exposure to severe social stress.
by Peter Aldhous IT HAS been more than a decade in the works, but finally we know the main changes that will be introduced next May, when the American Psychiatric Association publishes the next edition of its Diagnostic and Statistical Manual of Mental Disorders, known as DSM-5. Those changes, which could influence the way millions are treated, include new definitions of autism and related conditions, and a shift in the criteria for depression to include some people grieving after bereavement. Debate over DSM-5 seems likely to rumble on. But now there is a deeper problem to ponder: while discoveries about the genes and brain circuits that underlie human behaviour are accumulating rapidly, they haven't led to major clinical advances. That's largely because these findings don't map well on to the constellation of conditions described in the DSM. When the last major revision was completed in 1994, its authors hoped that neurobiologists would soon home in on specific disruptions to brain circuitry involved in the main psychiatric disorders. "I was naive enough to think that it was just a matter of time," says Michael First of Columbia University in New York City. It hasn't worked out that way. Take schizophrenia: what was once considered to be a distinct psychotic disorder actually seems to cover a variety of disruptions to normal brain functioning. This suggests that many of psychiatry's diagnostic labels do not describe coherent conditions with common underlying causes. No wonder, then, that many conditions are so hard to treat. © Copyright Reed Business Information Ltd.
By Laura Sanders Signs of depression can be turned on and off in mice with the flip of a switch. Activating or silencing the behavior of certain brain cells with laser light causes the animals to change their depressive behavior, two new studies find. Although the experiments were done in rodents, the results have direct relevance to human depression, says neurologist Helen Mayberg of the Emory University School of Medicine in Atlanta. The new work may point out places in the human brain that doctors can similarly stimulate to treat depression. The results, published online December 13 in Nature, took advantage of a technique called optogenetics, which allows scientists to control nerve cell behavior with a tiny fiber-optic light. In the studies, mice were genetically engineered to harbor nerve cell proteins that respond to light. The researchers could make certain nerve cells fire off messages by shining blue light, and quiet them by shining yellow light. These cells, which produce the chemical messenger dopamine, nestle in a brain region called the ventral tegmental area, a spot known for handling rewards. This system may be skewed in people with depression, since the disorder often keeps people from responding normally to things that used to be enjoyable. One tiny fiber-optic flash had an instant and profound effect on the mice’s behavior, says psychiatrist and neuroscientist Karl Deisseroth of Stanford University, who coauthored both papers. “That was pretty amazing for us.” © Society for Science & the Public 2000 - 2012
Link ID: 17601 - Posted: 12.13.2012
By Ed Yong In a lab at Stanford University, a mouse is showing signs of depression. For around 10 weeks, it has experienced a series of irritations, from bouts without food or water, to erratic sleep patterns. Now, its motivation is low—when picked up by the tail, it makes few attempts to escape, and it doesn’t try to explore new spaces. It’s also less willing to sip from a sugary liquid– a sign that it gets less pleasure from normally pleasurable activities. It is never easy to assess the mental health of an animal, but this mouse is clearly showing some of the classic symptoms of depression. But not for long. Earlier, Kay Tye and Julie Mirzabekov altered the mouse so that a flash of light can activate a small part of its brain—the ventral tegmental area (VTA), near the bottom of the brain and close to the midline. A burst of light, and the mouse’s behaviour changes almost instantly. It struggles when held aloft, it explores open areas, and it regains its sweet tooth. A burst of light, and its symptoms disappear. But on the other side of the country, at the Mount Sinai School of Medicine, Dipesh Chaudhury and Jessica Walsh are doing the same thing to completely different effect. Their mice have been altered in a similar way, so that light can also switch on their VTA neurons. But these rodents have endured a shorter but more intense form of stress—10 days of being placed in cages with dominant, aggressive rivals. Because of the resulting attacks, some of them have developed depressive symptoms. Others are more resilient. But when Chaudhury and Walsh flashed the VTAs of these mice, resilient individuals transformed into susceptible ones.
Link ID: 17600 - Posted: 12.13.2012
A drug that works through the same brain mechanism as the fast-acting antidepressant ketamine briefly improved treatment-resistant patients' depression symptoms in minutes, with minimal untoward side effects, in a clinical trial conducted by the National Institutes of Health. The experimental agent, called AZD6765, acts through the brain's glutamate chemical messenger system. Existing antidepressants available through prescription, which work through the brain’s serotonin system, take a few weeks to work, imperiling severely depressed patients, who can be at high risk for suicide. Ketamine also works in hours, but its usefulness is limited by its potential for dissociative side-effects, including hallucinations. It is being studied mostly for clues to how it works. "Our findings serve as a proof of concept that we can tap into an important component of the glutamate pathway to develop a new generation of safe, rapid-acting practical treatments for depression," said Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health, which conducted the research. Zarate, and colleagues, reported on their results online Dec. 1, 2012 in the journal Biological Psychiatry. AZD6765, like ketamine, works by blocking glutamate binding to a protein on the surface of neurons, called the NMDA receptor. It is a less powerful blocker of the NMDA receptor, which may be a reason why it is better tolerated than ketamine.
Link ID: 17594 - Posted: 12.11.2012
By BENEDICT CAREY They plotted a revolution, fell to debating among themselves, and in the end overturned very little except their own expectations. But the effort itself was a valuable guide for anyone who has received a psychiatric diagnosis, or anyone who might get one. This month, the American Psychiatric Association announced that its board of trustees had approved the fifth edition of the association’s influential diagnostic manual — the so-called bible of mental disorders — ending more than five years of sometimes acrimonious, and often very public, controversy. The committee of doctors appointed by the psychiatric association had attempted to execute a paradigm shift, changing how mental disorders are conceived and posting its proposals online for the public to comment. And comment it did: Patient advocacy groups sounded off, objecting to proposed changes in the definitions of depression and Asperger syndrome, among other diagnoses. Outside academic researchers did, too. A few committee members quit in protest. The final text, which won’t be fully available until publication this spring, has already gotten predictably mixed reviews. “Given the challenges in a field where objective lines are hard to draw, they did a solid job,” said Dr. Michael First, a psychiatrist at Columbia who edited a previous version of the manual and was a consultant on this one. Others disagreed. “This is the saddest moment in my 45-year career of practicing, studying and teaching psychiatry,” wrote Dr. Allen Frances, the chairman of a previous committee who has been one of the most vocal critics, in a blog post about the new manual, the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, or DSM5. © 2012 The New York Times Company
Cognitive behavioural therapy (CBT) can reduce symptoms of depression in people who fail to respond to drug treatment, says a study in the Lancet. CBT, a type of psychotherapy, was found to benefit nearly half of the 234 patients who received it combined with normal care from their GP. Up to two-thirds of people with depression do not respond to anti-depressants. Patients should have access to a range of treatments, the charity Mind said. CBT is a form of talking psychotherapy to help people with depression change the way they think to improve how they feel and alter their behaviour. The study followed 469 patients with treatment-resistant depression picked from GP practices in Bristol, Exeter and Glasgow over 12 months. One group of patients continued with their usual care from their GP, which could include anti-depressant medication, while the second group was also treated with CBT. After six months, researchers found 46% of those who had received CBT reported at least a 50% reduction in their symptoms. This compared with 22% experiencing the same reduction in the other group. The study concluded CBT was effective in reducing symptoms and improving patients' quality of life. The improvements had been maintained for a period of 12 months, it added. BBC © 2012
Link ID: 17582 - Posted: 12.08.2012
by Greg Miller On Saturday, the board of trustees of the American Psychiatric Association (APA) voted to approve the final text of the DSM-5, the next revision to the leading manual for diagnosing mental illness. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, which originated in 1952, will be released next May at the APA's annual meeting in San Francisco. The revision process leading to DSM-5 began in 1999, and APA says it consulted more than 1500 experts in 39 countries in updating the criteria for diagnosing hundreds of psychiatric conditions. It has been a bumpy ride. Controversy has dogged the revision process for years. Even before the first draft of proposed changes was released in 2010, critics alleged that too much of the deliberation was conducted in secret and that too many of those involved had ties to drug companies that stood to benefit from changes to diagnostic criteria—APA has repeatedly rejected these charges. And many of the diagnostic proposals have elicited a strong reaction. A proposal to combine several autism-related disorders into a single diagnosis raised concerns among some critics that it would radically alter who gets diagnosed with those disorders and angered advocates for Asperger syndrome, a milder form of autism that would be eliminated in the new scheme. A new childhood condition called disruptive mood dysregulation disorder, characterized by irritability and violent outbursts, was intended to stem the perceived overdiagnosis of childhood bipolar disorder, but critics have argued that the diagnosis lacks scientific validity. Yet another controversial proposal, to remove language that excludes people who've recently experienced the loss of a loved one from being diagnosed with major depression, elicited complaints that it would lead to the medicalization of normal grief. These changes will stand, APA said in a press release. © 2010 American Association for the Advancement of Science.
Scicurious Guest Writer, Nicole Baganz! 4:02 PM. It took every ounce of energy I had to drag myself to the bathroom. Arriving in the room that is located 2 feet from my bed felt like a victory. I rifled through the medicine cabinet, stuck the thermometer in my mouth and collapsed on the bathroom floor. 103.2° F. Yep, I’m sick. Sleepiness. Fatigue. Loss of appetite and motivation. Lethargy. Leave me alone. We all know what it feels like to be sick. Clinicians collectively describe this group of symptoms as “sickness behavior”. Evolutionarily speaking, the idea that the immune system would produce these symptoms makes sense. An organism infected with a pathogenic bug should retreat from its social group to protect others from the spread of infection. The organism essentially shuts down in order to send every ounce of energy to the immune system to battle the bug that has invaded the body’s cells. This sickness state would facilitate recovery of the organism and also protect the community from the spread of the infection by limiting the interaction of the infected party from its entire social group. All of the symptoms of sickness behavior are displayed not only by people who have an infection, but also by those who have been diagnosed with Major Depressive Disorder (MDD). Could sickness behavior and MDD be linked? What happens in the brain to produce sickness behaviors, and how might these relate to depression? Mice are good models for scientists to use to study the effect of immune system activation on brain function and behavior (research studies that subject people to infectious agents before probing their brains in the name of science draw few willing volunteers). Laboratory mice also display sickness behavior when their immune systems are turned on. Sick rodents sleep more, eat less, and lose interest in drinking sugary water (usually a scrumptious treat for mice). They also stop interacting socially – mice are, by nature, very social creatures that like to sniff, groom, lick and cuddle up to their roommates. © 2012 Scientific American
Link ID: 17551 - Posted: 11.29.2012
By David Levine People with depression or other mental illnesses often report trouble sleeping, daytime drowsiness and other sleep-related issues. Now a growing body of research is showing that treating sleep problems can dramatically improve psychiatric symptoms in many patients. Much of the latest work illustrates how sleep apnea, a common chronic condition in which a person repeatedly stops breathing during sleep, may cause or aggravate psychiatric symptoms. In past years sleep apnea has been linked to depression in small studies and limited populations. Now a study by the Centers for Disease Control and Prevention strengthens that connection. The CDC analyzed the medical records of nearly 10,000 American adults with sleep apnea. Men diagnosed with this disorder had twice the risk of depression—and women five times the risk—compared with those without sleep apnea. Writing in the April issue of Sleep, lead author Anne G. Wheaton and her colleagues speculate that in addition to interrupting sleep, the oxygen deprivation induced by sleep apnea could harm cells and disrupt normal brain functioning. Treating this disorder shows promise for reducing symptoms of depression, a recent study at the Cleveland Clinic suggests. In the experiment, patients went to bed wearing a mask hooked up to a machine that increases air pressure in their throat. The increased pressure prevents the airway from collapsing, which is what causes breathing to cease in most cases of this disorder. Using this machine, psychiatrist Charles Bae and his colleagues treated 779 patients who had been diagnosed with sleep apnea. After an average of 90 days of sleeping with the machine, all the patients scored lower on a common depression survey than before the treatment—regardless of whether they had a prior diagnosis of depression or were taking an antidepressant. The data were presented in June at the SLEEP 2012 conference in Boston. © 2012 Scientific American
By BENEDICT CAREY For years they have lived as orphans and outliers, a colony of misfit characters on their own island: the bizarre one and the needy one, the untrusting and the crooked, the grandiose and the cowardly. Their customs and rituals are as captivating as any tribe’s, and at least as mystifying. Every mental anthropologist who has visited their world seems to walk away with a different story, a new model to explain those strange behaviors. This weekend the Board of Trustees of the American Psychiatric Association will vote on whether to adopt a new diagnostic system for some of the most serious, and striking, syndromes in medicine: personality disorders. Personality disorders occupy a troublesome niche in psychiatry. The 10 recognized syndromes are fairly well represented on the self-help shelves of bookstores and include such well-known types as narcissistic personality disorder, avoidant personality disorder, as well as dependent and histrionic personalities. But when full-blown, the disorders are difficult to characterize and treat, and doctors seldom do careful evaluations, missing or downplaying behavior patterns that underlie problems like depression and anxiety in millions of people. The new proposal — part of the psychiatric association’s effort of many years to update its influential diagnostic manual — is intended to clarify these diagnoses and better integrate them into clinical practice, to extend and improve treatment. But the effort has run into so much opposition that it will probably be relegated to the back of the manual, if it’s allowed in at all. © 2012 The New York Times Company
Link ID: 17542 - Posted: 11.27.2012
The long-held view that a full moon or even a new moon triggers psychological problems has been debunked by a study from Montreal. Researchers at the University of Laval's School of Psychology evaluated patients visiting Montreal's Sacré-Coeur Hospital and Hôtel-Dieu de Lévis between March 2005 and April 2008 and found no correlation between anxiety disorders and the phases of the moon — despite, it seems, what 80 per cent of nurses and 64 per cent of doctors surveyed believe. These researchers analyzed 771 individuals who had shown up at the emergency room with chest pains for which no medical cause could be determined. Psychological evaluations indicated many were suffering anxiety, panic attacks, mood disorders or suicidal thoughts. The time of their visit was then correlated with the phase of the moon at that moment. "We observed no full-moon or new-moon effect on psychological problems," said lead researcher Genevieve Belleville whose study is published in General Hospital Psychiatry. The study went on to suggest that health professionals may think there are more mental problems during a full-moon phase due to "self-fulfilling prophecies." © CBC 2012
The search for genes predisposing people to depression has taken an unexpected twist, according to Canadian researchers who found a clue in an obesity gene. Studies on families and twins suggest depression has a genetic component, but for 15 years, scientists haven't been able to find genes associated with the illness. Researchers at McMaster University in Hamilton, Ont., took a different approach by testing how obesity genes may be linked with depression. "We found the first gene predisposing to depression with consistent results," said David Meyre, an associate professor in clinical epidemiology and biostatistics at McMaster and a Canada Research Chair in genetic epidemiology. In Monday's issue of the journal Molecular Psychiatry, Meyre and his co-authors reported that a variant of the FTO gene may be associated with a lower risk of depression independent of the gene's effect on obesity. The common perception is that obese people become depressed because of their appearance and poor self-esteem or discrimination. Another common thought is that those who are depressed are less likely to be physically active or follow healthy eating habits. Taking antidepressants can also lead to weight gain. But the genetic findings challenge that thinking, Meyre said, since those with the genetic mutation predisposing to obesity were protected from depression. "This suggests that the FTO gene may have a broader role than initially thought with an effect on depression and other common psychiatric disorders," the researchers wrote. © CBC 2012
Richard A. Lovett Scientists have known for years that human medications, from anti-inflammatories to the hormones in birth-control pills, are ending up in waterways and affecting fish and other aquatic organisms. But researchers are only beginning to compile the many effects that those drugs seem to be having. And it isn't good news for the fish. One such drug, fluoxetine, is the active ingredient in the antidepressant Prozac. Like some other pharmaceuticals, fluoxetine is excreted in the urine of people taking it, and reaches lakes and waterways through sewage-treatment plants that are unequipped to remove it. To investigate the effects of fluoxetine, researchers have turned to a common US freshwater fish species called the fathead minnow (Pimephales promelas). Normally, fathead minnows show a complex mating behaviour, with males building the nests that females visit to lay their eggs. Once the eggs are laid and fertilized, the males tend to them by cleaning away any fungus or dead eggs. But when fluoxetine is added to the water, all of this changes, said Rebecca Klaper, an ecologist at the University of Wisconsin-Milwaukee's Great Lakes Water Institute. Klaper presented her results this week at the 2012 meeting of the North American division of the Society of Environmental Toxicology and Chemistry in Long Beach, California. © 2012 Nature Publishing Group,
In 2009, Susannah Cahalan was a healthy 24-year-old reporter for the New York Post, when she began to experience numbness, paranoia, sensitivity to light and erratic behavior. Grasping for an answer, Cahalan asked herself as it was happening, "Am I just bad at my job — is that why? Is the pressure of it getting to me? Is it a new relationship?" But Cahalan only got worse — she began to experience seizures, hallucinations, increasingly psychotic behavior and even catatonia. Her symptoms frightened family members and baffled a series of doctors. After a monthlong hospital stay and $1 million worth of blood tests and brain scans that proved inconclusive, Cahalan was seen by Dr. Souhel Najjar, who asked her to draw a clock on a piece of paper. "I drew a circle, and I drew the numbers 1 to 12 all on the right-hand side of the clock, so the left-hand side was blank, completely blank," she tells Fresh Air's Dave Davies, "which showed him that I was experiencing left-side spatial neglect and, likely, the right side of my brain responsible for the left field of vision was inflamed." As Najjar put it to her parents, "her brain was on fire." This discovery led to her eventual diagnosis and treatment for anti-NMDA receptor encephalitis, a rare autoimmune disease that can attack the brain. Cahalan says that doctors think the illness may account for cases of "demonic possession" throughout history. Cahalan's new memoir is called Brain on Fire: My Month of Madness. ©2012 NPR
By Charles Q. Choi People with schizophrenia often experience the unnerving feeling that outside forces are controlling them. Other times they feel an illusory sense of power over uncontrollable events. Now scientists find these symptoms may arise from disabilities in predicting or recognizing their own actions. The findings suggest new therapies for treating schizophrenia, which afflicts an estimated 1 percent of the world population. To see where this confusion might stem from, researchers tested two ways people are known to link actions and their outcomes. We either predict the effects of our movements or retrospectively deduce a causal connection. Healthy participants and schizophrenic patients were asked to look at a clock and occasionally push a button. Most of the time the button push was followed by a tone. The participants then told researchers what time they had pushed the button and when the tone had occurred. Healthy volunteers reported later times for each button push if it was followed by a tone. This result suggests that awareness of a link between the two events causes people to perceive less time between them. Participants also tended to estimate later button pushes even in the few cases when no tone was emitted, revealing that the subjects were predicting they would hear the sound, says psychiatrist and cognitive neuroscientist Martin Voss of Charité University Hospital and St. Hedwig Hospital in Berlin. © 2012 Scientific American