Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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Sara Reardon Suicide is a puzzle. Fewer than 10% of people with depression attempt suicide, and about 10% of those who kill themselves were never diagnosed with any mental-health condition. Now, a study is trying to determine what happens in the brain when a person attempts suicide, and what sets such people apart. The results could help researchers to understand whether suicide is driven by certain brain biology — and is not just a symptom of a recognized mental disorder. The project, which launched this month, will recruit 50 people who have attempted suicide in the two weeks before enrolling in the study. Carlos Zarate, a psychiatrist at the US National Institute of Mental Health in Bethesda, Maryland, and his colleagues will compare these people's brain structure and function to that of 40 people who attempted suicide more than a year ago, 40 people with depression or anxiety who have never attempted suicide and a control group of 40 healthy people. In doing so, the researchers hope to elucidate the brain mechanisms associated with the impulse to kill oneself. Zarate's team will also give ketamine, a psychoactive ‘party drug’, to the group that has recently attempted suicide. Ketamine, which is sometimes used to treat depression, can quickly arrest suicidal thoughts and behaviour — even in cases when it does not affect other symptoms of depression1. The effect is known to last for about a week. © 2015 Nature Publishing Group,
By Nicholas Bakalar Bright light therapy has been used effectively for seasonal affective disorder, the kind of depression that comes on at a specific time every year, often the dark days of late fall and winter, and then lifts. Now a new study has found that it may work to treat nonseasonal depression as well. Researchers randomly assigned 122 patients, 19 to 60 years old, with major depression to receive one of four treatments: 30 minutes of daily exposure to fluorescent light; 20 milligrams of Prozac daily; both light and Prozac; and a control group that received a dummy pill and exposure to an electric air purifier. The study, in JAMA Psychiatry, lasted eight weeks. Using well-validated scales that quantify depression severity, the researchers found improvements in all four groups. The difference between Prozac alone and the placebo was not statistically significant, but light therapy alone was significantly better than placebo, and light therapy with medication was the most effective treatment of all. “This is the first study to show that light treatment is an option for people with nonseasonal depression, which is much more common than seasonal depression,” said the lead author, Dr. Raymond W. Lam, a professor of psychiatry at the University of British Columbia. “Light treatment can be combined with medicine and psychotherapy, and it’s a safe treatment without a lot of side effects.” © 2015 The New York Times Company
By Jonathan Webb Science reporter, BBC News A study of 153 brain scans has linked a particular furrow, near the front of each hemisphere, to hallucinations in schizophrenia. This fold tends to be shorter in those patients who hallucinate, compared with those who do not. It is an area of the brain that appears to have a role in distinguishing real perceptions from imagined ones. Researchers say the findings, published in Nature Communications, might eventually help with early diagnosis. The brain wrinkle, called the paracingulate sulcus or PCS, varies considerably in shape between individuals. It is one of the final folds to develop, appearing in the brain only just before birth. "The brain develops throughout life, but aspects such as whether the PCS is going to be a particularly prominent fold - or not -may be apparent in the brain at an early stage," said Jon Simons, a neuroscientist at the University of Cambridge, UK. "It might be that a reduction in this brain fold gives somebody a predisposition towards developing something like hallucinations later on in life." If further work shows that the difference can be detected before the onset of symptoms, for example, Dr Simons said it might be possible to offer extra support to people who face that elevated risk. But he stressed that schizophrenia is a complicated phenomenon. Hallucinations are one of the main symptoms, but some patients are diagnosed on the basis of other irregular thought processes. "We've known for some time that disorders like schizophrenia are not down to a single region of the brain. Changes are seen throughout various different areas. "To be able to pin such a key symptom to a relatively specific part of the brain is quite unusual." © 2015 BBC.
Link ID: 21644 - Posted: 11.18.2015
By Elahe Izadi The days growing shorter and colder can be more than just a nuisance; the seasonal change can also trigger clinical depression. Those who suffer from seasonal affective disorder, or SAD, may turn to a light box to help make them feel better. But a new study suggests another form of therapy could be more powerful and enduring: talking. The benefits of cognitive behavioral therapy — a form of talk therapy — outlasted light therapy sessions for people suffering from SAD, according to a study published Thursday in the American Journal of Psychiatry. "Light therapy is a treatment that suppresses symptoms as long as you're using it," said lead author Kelly Rohan, a psychology professor at the University of Vermont. "So if you're not using it, there's no reason to expect the continued benefit for a treatment that works that way, whereas cognitive behavioral therapy teaches skills." And the people who learn those skills can use them long after their therapy sessions. For the study, researchers tracked 177 people who suffer from major depression that follows a recurring seasonal pattern. About half of the subjects received six weeks of daily light therapy; the others received 12 sessions of cognitive behavioral therapy over the same period of time.
By Nicholas Bakalar A person with depression is at higher risk for heart disease, and a person with heart disease is at higher risk for depression. The link between the two diseases is complex and not entirely understood. Many of the effects of depression — feeling unable to exercise or eat properly, for example — and the behaviors associated with depression, like smoking and abusing alcohol, are well established risk factors for heart disease. Some studies have suggested that insomnia, another symptom of depression, may also increase the risk for cardiovascular illness. Depression can also make heart disease worse. Heart patients with depression may find it more difficult to take medications and comply with the behavioral demands of living with heart disease. Depression may also have destructive physiological effects on heart rhythm, blood pressure, stress hormone levels and blood clotting, studies have shown. These may be among the reasons why depressed patients with stable cardiovascular disease, or those who have survived a heart attack or had coronary bypass surgery, are at two to three times higher risk of dying than similar patients without depression. Treating depressed heart patients with drugs like Prozac may help. These drugs, known as selective serotonin reuptake inhibitors, or S.S.R.I.’s, in addition to relieving depression, have blood-thinning effects that may be beneficial against heart disease. “It is clear that treatment with an S.S.R.I. reduces cardiac mortality in depressed patients post heart attack,” said Dr. Steven P. Roose, a professor of psychiatry at Columbia. “What is not clear is whether the reduction in mortality results from the antidepressant effect of the medication or the anti-platelet effect of the medication.” © 2015 The New York Times Company
By DAVE ITZKOFF and BENEDICT CAREY For the first time in more than a year, the widow of the actor Robin Williams is speaking publicly about the circumstances that preceded Mr. Williams’s death, and sharing details about a disease he had when he died. Stories from Our Advertisers In interviews with People magazine and with ABC News, the widow, Susan Schneider Williams, laid the blame for her husband’s suicide in 2014 not on depression but on diffuse Lewy body dementia. “It was not depression that killed Robin,” Mrs. Williams said in the People magazine interview. “Depression was one of let’s call it 50 symptoms and it was a small one.” She added: “This was a very unique case and I pray to God that it will shed some light on Lewy bodies for the millions of people and their loved ones who are suffering with it. Because we didn’t know. He didn’t know.” Parts of an interview with Mrs. Williams were shown Tuesday on ABC’s “Good Morning America,” with further segments scheduled for that evening on the network’s “World News Tonight” and “Nightline” programs, and Friday on its morning talk show “The View.” Robin Williams was one of the most explosively, exhaustingly, prodigiously verbal comedians who ever lived, says film critic A. O. Scott. And the only thing faster than Williams’s mouth was his mind. By Adam Freelander on Publish Date August 12, 2014. Photo by ABC, via Associated Press. Watch in Times Video » Mr. Williams, the stand-up comic and star of “Mork & Mindy,” “Good Morning, Vietnam,” “Good Will Hunting” (for which he won an Oscar) and “Dead Poets Society,” killed himself on Aug. 11, 2014, in the home he shared with Mrs. Williams in Tiburon, Calif. He was 63. © 2015 The New York Times Company
By Simon Makin Most people have felt depressed or anxious, even if those feelings have never become debilitating. And how many times have you heard someone say, “I'm a little OCD”? Clearly, people intuitively think that most mental illnesses have a spectrum, ranging from mild to severe. Yet most people do not know what it feels like to hallucinate—to see or hear things that are not really there—or to have delusions, persistent notions that do not match reality. You're psychotic, or you're not, according to conventional wisdom. Evidence is growing, however, that there may be no clear dividing line. Psychiatrists have long debated whether psychosis exists on a spectrum, and researchers have been investigating the question for more than a decade now. A 2013 meta-analysis, combining much of the existing data, by Jim van Os of Maastricht University in the Netherlands and Richard Linscott of the University of Otago in New Zealand, found the prevalence of hallucinations and delusions in the general population was 7.2 percent—much higher than the 0.4 percent prevalence of schizophrenia diagnoses found in recent studies. Now the most comprehensive epidemiological study of psychotic experiences to date, published in July in JAMA Psychiatry, has given researchers the most detailed picture yet of how many people have these experiences and how frequently. The results strongly imply a spectrum—and suggest that the standard treatment for a psychotic episode might be due for an overhaul. After ruling out experiences caused by drugs or sleep, the researchers determined that 5.8 percent of the respondents had psychotic experiences. Two thirds of these people had had only one type of episode, with hallucinations being four times more common than delusions. © 2015 Scientific American
Link ID: 21591 - Posted: 11.02.2015
? Joanne Silberner Each year, nearly three times as many Americans die from suicide as from homicide. More Americans kill themselves than die from breast cancer. As Thomas Insel, longtime head of the National Institute of Mental Health, prepared to step down from his job in October, he cited the lack of progress in reducing the number of suicides as his biggest disappointment. While the homicide rate in the US has dropped 50 percent since the early 1990s, the suicide rate is higher than it was a decade ago. "That to me is unacceptable," Insel says. It hasn't been for lack of trying. The US has a national suicide hotline and there are suicide prevention programs in every state. There's screening, educational programs, and midnight walks to raise awareness. Yet over the last decade or so, the national suicide rate has increased. In 2003, the suicide rate was 10.8 per 100,000 people. In 2013, it was 12.6. An effort that began in Detroit in 2001 to treat depression, the most common cause of suicide, is offering hope. With a relentless focus on finding and treating people with depression, the Henry Ford Health System has cut the suicide rate among the people in its insurance plan dramatically. The story of the health system's success is a story of persistence, confidence, hope and a strict adherence to a very specific approach. © 2015 npr
Link ID: 21589 - Posted: 11.02.2015
By Diana Kwon | In the human form of mad cow disease, called Creutzfeldt-Jakob, a person's brain deteriorates—literally developing holes that cause rapidly progressing dementia. The condition is fatal within one year in 90 percent of cases. The culprits behind the disease are prions—misfolded proteins that can induce normal proteins around them to also misfold and accumulate. Scientists have known that these self-propagating, pathological proteins cause some rare brain disorders, such as kuru in Papua New Guinea. But growing evidence suggests that prions are at play in many, if not all, neurodegenerative disorders, including Alzheimer's, Huntington's and Parkinson's, also marked by aggregations of malformed proteins. Until recently, there was no evidence that the abnormal proteins found in people who suffer from these well-known diseases could be transmitted directly from person to person. The tenor of that discussion suddenly changed this September when newly published research in the journal Nature provided the first hint such human-to-human transmission may be possible. (Scientific American is part of Springer Nature.) For the study, John Collinge, a neurologist at University College London, and his colleagues conducted autopsies on eight patients who died between the ages of 36 and 51 from Creutzfeldt-Jakob. All the subjects had acquired the disease after treatment with growth hormone later found to be contaminated with prions. The surprise came when the researchers discovered that six of the brains also bore telltale signs of Alzheimer's—in the form of clumps of beta-amyloid proteins, diagnostic for the disease—even though the patients should have been too young to exhibit such symptoms. © 2015 Scientific American,
Bret Stetka Sometime around 1907, well before the modern randomized clinical trial was routine, American psychiatrist Henry Cotton began removing decaying teeth from his patients in hopes of curing their mental disorders. If that didn't work he moved on to more invasive excisions: tonsils, testicles, ovaries and, in some cases, colons. Cotton was the newly appointed director of the New Jersey State Hospital for the Insane and was acting on a theory proposed by influential Johns Hopkins psychiatrist Adolph Meyer, under whom Cotton had studied, that psychiatric illness is the result of chronic infection. Meyer's idea was based on observations that patients with high fevers sometimes experience delusions and hallucinations. In 1921 he published a well-received book on the theory called The Defective Delinquent and Insane: the Relation of Focal Infections to Their Causation, Treatment and Prevention. A few years later The New York Times wrote, "eminent physicians and surgeons testified that the New Jersey State Hospital for the Insane was the most progressive institution in the world for the care of the insane, and that the newer method of treating the insane by the removal of focal infection placed the institution in a unique position with respect to hospitals for the mentally ill." Eventually Cotton opened a hugely successful private practice, catering to the infected molars of Trenton, N.J., high society. © 2015 npr
By Roni Jacobson After many lawsuits and a 2012 U.S. Department of Justice settlement, last month an independent review found that antidepressant drug Paxil (paroxetine) is not safe for teenagers. The finding contradicts the conclusions of the initial 2001 drug trial, which the manufacturer GlaxoSmithKline had funded, then used its results to market Paxil as safe for adolescents. The original trial, known as Study 329, is but one high-profile example of pharmaceutical industry influence known to pervade scientific research, including clinical trials the U.S. Food and Drug Administration requires pharma companies to fund in order to assess their products. For that reason, people who read scientific papers as part of their jobs have come to rely on meta-analyses, supposedly thorough reviews summarizing the evidence from multiple trials, rather than trust individual studies. But a new analysis casts doubt on that practice as well, finding that the vast majority of meta-analyses of antidepressants have some industry link, with a corresponding suppression of negative results. The latest study, published in the Journal of Clinical Epidemiology, which evaluated 185 meta-analyses, found that one third of them were written by pharma industry employees. “We knew that the industry would fund studies to promote its products, but it’s very different to fund meta-analyses,” which “have traditionally been a bulwark of evidence-based medicine,” says John Ioannidis, an epidemiologist at Stanford University School of Medicine and co-author of the study. “It’s really amazing that there is such a massive influx of influence in this field.” © 2015 Scientific American
Link ID: 21546 - Posted: 10.22.2015
By BENEDICT CAREY More than two million people in the United States have a diagnosis of schizophrenia, and the treatment for most of them mainly involves strong doses of antipsychotic drugs that blunt hallucinations and delusions but can come with unbearable side effects, like severe weight gain or debilitating tremors. Stories from Our Advertisers Now, results of a landmark government-funded study call that approach into question. The findings, from by far the most rigorous trial to date conducted in the United States, concluded that schizophrenia patients who received smaller doses of antipsychotic medication and a bigger emphasis on one-on-one talk therapy and family support made greater strides in recovery over the first two years of treatment than patients who got the usual drug-focused care. The report, to be published on Tuesday in The American Journal of Psychiatry and funded by the National Institute of Mental Health, comes as Congress debates mental health reform and as interest in the effectiveness of treatments grows amid a debate over the possible role of mental illness in mass shootings. Its findings have already trickled out to government agencies: On Friday, the Centers for Medicare & Medicaid Services published in its influential guidelines a strong endorsement of the combined-therapy approach. Mental health reform bills now being circulated in Congress “mention the study by name,” said Dr. Robert K. Heinssen, the director of services and intervention research at the centers, who oversaw the research. In 2014, Congress awarded $25 million in block grants to the states to be set aside for early-intervention mental health programs. So far, 32 states have begun using those grants to fund combined-treatment services, Dr. Heinssen said. © 2015 The New York Times Company
Link ID: 21532 - Posted: 10.20.2015
Could brain inflammation be to blame for schizophrenia? People with the disorder seem to have more active immune cells inside their brains, and now this activity has been spotted even before the disorder develops. This link could be a breakthrough in developing new treatments that better target the causes of the disorder. The idea that the immune system might play a part in schizophrenia was first floated 10 years ago. Since then, a couple of studies have found that people with schizophrenia seem to have more active microglia – the immune cells of the brain. Peter Bloomfield at Imperial College London wondered if this increased immune system activity might be detectable before a person is diagnosed with schizophrenia. His team examined 14 people who had been identified as being at “ultra-high risk” of developing the disorder – they had already seen a doctor about symptoms like paranoia or hallucinations, but hadn’t yet had a psychotic episode. Typically, between 20 and 35 per cent of such individuals will go on to be diagnosed with schizophrenia. By injecting a dye that labels active cells and using a PET scanner, Bloomfield’s team compared the activity of these people’s microglial cells with those of people with schizophrenia, as well as healthy people. They found increased microglial activity in both those who had schizophrenia, and those who had been classified as ultra-high risk. “What’s interesting is that the level of activity correlated with the severity of symptoms,” says Bloomfield. During the study, two of the 14 at ultra-high risk went on to develop schizophrenia and schizotypal disorder – these people had the highest levels of microglial activity, says Bloomfield. © Copyright Reed Business Information Ltd.
Elaine Korry Efforts to protect children in foster care from being inappropriately medicated with powerful antipsychotic drugs got a big boost forward on Tuesday, when California Gov. Jerry Brown signed three bills into law designed to reform prescribing. Overprescribing of psychiatric meds for foster youth is a persistent problem nationwide, with children given the drugs at double or triple the rate of those not in foster care. In 2011, the federal Government Accounting Office found nearly 1 in 4 children in foster care was taking psychotropic medications, which include antipsychotics, antidepressants, mood stabilizers and stimulants. Hundreds of children were found to be taking five or more psychotropic medications at a time, and thousands were prescribed doses that exceeded FDA-approved guidelines. According to the report, monitoring programs fell short of guidelines established by the American Academy of Child and Adolescent Psychiatry. Many of the medications have side effects that include lethargy, weight gain, diabetes and tremors. The California legislation, which covers 63,000 children and teens in foster care, will allow public health nurses access to medical records to monitor the foster children who are prescribed psychotropic drugs; identify the group homes that rely most on these medications and potentially require them to take corrective action; and provide child welfare workers with better training and oversight tools to spot dangerous prescribing practices. © 2015 NPR
By Miriam E. Tucker Before he got sick, Whitney Dafoe was an award-winning photographer and a world traveler. He’d helped build a nunnery in India, ridden a motorcycle in the Himalayas and visited all 50 American states. He also worked on Barack Obama’s 2008 presidential campaign, and although he was already ill by January 2009, pushed himself to travel to Washington from his California home to photograph the inauguration. But now, at 31, Whitney lies in bed in a darkened room in his parents’ home, unable to talk, walk or eat. He is fed intravenously and is barely able to tolerate light, sounds or being touched. His parents and the medical personnel who see him wear plain clothing when they enter his room because bright colors, shapes or any kind of print make him feel even worse, as does any movement that he’s not expecting. “It’s hard to explain how fragile he is,” says his mother, Janet Dafoe. This isn’t the picture that people imagine when they hear “chronic fatigue syndrome,” which is often viewed by the public and the health-care community as a trivial or primarily psychological complaint. In a February report, the Institute of Medicine gave the illness a new name — systemic exertion intolerance disease. Many patients have long criticized the name “chronic fatigue syndrome” for not reflecting the seriousness of the illness. The new name, some say, is not much of an improvement. Some patients call it by an older name, “myalgic encephalomyelitis.” Most official documents refer to it with a compromise term, “myalgic encephalomyelitis/chronic fatigue syndrome,” or ME/CFS.
Link ID: 21479 - Posted: 10.06.2015
By BENEDICT CAREY Medical literature has overstated the benefits of talk therapy for depression, in part because studies with poor results have rarely made it into journals, researchers reported Wednesday. Their analysis is the first effort to account for unpublished tests of such therapies. Treatments like cognitive behavior therapy and interpersonal therapy are indeed effective, the analysis found, but about 25 percent less so than previously thought. Doctors have long known that journal articles exaggerate the benefits of antidepressant drugs by about the same amount, and partly for the same reason — a publication bias in favor of encouraging findings. The new review, in the journal PLOS One, should give doctors and patients a better sense of what to expect from various forms of talk therapy, experts said, if not settle long-running debates in psychiatry about the relative merits of one treatment over another. Five million to six million Americans receive psychotherapy for depression each year, and many of them also take antidepressant drugs, surveys find. Most people find some relief by simply consulting a doctor regularly about the problem, experts said. Engaging in a course of well-tested psychotherapy, according to the new analysis, gives them an added 20 percent chance of achieving an even more satisfying improvement, or lasting recovery. Before accounting for the unpublished research, that figure was closer to 30 percent, a difference that suggests that hundreds of thousands of patients are less likely to benefit. The new paper is the latest chapter in a broad retrenchment across science in which researchers are scrutinizing past results to weed out publication bias and other, more deliberate statistical manipulations. © 2015 The New York Times Company
Link ID: 21464 - Posted: 10.01.2015
Jon Hamilton A mind-altering drug called ketamine is changing the way some doctors treat depression. Encouraged by research showing that ketamine can relieve even the worst depression in a matter of hours, these doctors are giving the drug to some of their toughest patients. And they're doing this even though ketamine lacks approval from the Food and Drug Administration for treating depression. "It became clear to me that the future of psychiatry was going to include ketamine or derivatives of ketamine," says David Feifel, a professor of psychiatry at the University of California, San Diego, who began administering the drug to patients in 2010. Ketamine was developed as an anesthetic and received FDA approval for this use in 1970. Decades later, it became popular as a psychedelic club drug. And in 2006, a team from the National Institute of Mental Health published a landmark study showing that a single intravenous dose of ketamine produced "robust and rapid antidepressant effects" within a couple of hours. Since then, thousands of depressed patients have received "off-label" treatment with ketamine. One of those patients is Paul, 36, who lives in San Diego and is a patient of Dr. Feifel. We're not using his last name to protect his medical privacy. © 2015 NPR
By Karen Weintraub Depression makes people more vulnerable to alcoholism and vice versa, said Dr. Shelly Greenfield, a professor of psychiatry at Harvard Medical School and director of McLean Hospital’s Alcohol and Drug Abuse Clinical and Health Services Research Program. About a third of depressed people also have a problem with alcohol, she said, adding that the depression usually comes first. Genetics makes some people more vulnerable to each — and perhaps the combination, Dr. Greenfield said, “but it’s not the whole story.” Social environment, particularly in childhood, also plays a key role. People who are the victims of physical or sexual abuse, for example, are at higher risk for both alcoholism and depression later in life, she said. Depressed people who drink will most likely see their depression worsen, because alcohol is a depressant, tamping down the nervous system, said Dr. Kathleen Brady, a distinguished university professor at the Medical University of South Carolina. Abstinence will be harder for alcoholics who are depressed, because of the hopelessness that comes with depression. Getting help promptly may make recovery from alcoholism easier, Dr. Greenfield said. Needing help to quit drinking or to resolve depression is not a sign of weakness or personal failure, she noted. In families with a history of either depression or alcoholism, it is important to be vigilant about drinking, particularly in adolescence. © 2015 The New York Times Company
By BENEDICT CAREY Fourteen years ago, a leading drug maker published a study showing that the antidepressant Paxil was safe and effective for teenagers. On Wednesday, a major medical journal posted a new analysis of the same data concluding that the opposite is true. That study — featured prominently by the journal BMJ — is a clear break from scientific custom and reflects a new era in scientific publishing, some experts said, opening the way for journals to post multiple interpretations of the same experiment. It comes at a time of self-examination across science — retractions are at an all-time high; recent cases of fraud have shaken fields as diverse as anesthesia and political science; and earlier this month researchers reported that less than half of a sample of psychology papers held up. “This paper is alarming, but its existence is a good thing,” said Brian Nosek, a professor of psychology at the University of Virginia, who was not involved in either the original study or the reanalysis. “It signals that the community is waking up, checking its work and doing what science is supposed to do — self-correct.” The authors of the reanalysis said that many clinical studies had some of the same issues as the original Paxil study, and that data should be made freely available across clinical medicine, so that multiple parties could analyze them. The dispute itself is a long-running one: Questions surrounding the 2001 study played a central role in the so-called antidepressant wars of the early 2000s, which led to strong warnings on the labels of Paxil and similar drugs citing the potential suicide risk for children, adolescents and young adults. The drugs are considered beneficial and less risky for many adults over 25 with depression. © 2015 The New York Times Company
Neel V. Patel The concept of the insanity defense dates back to ancient Greece and the Roman Empire. The idea has always been the same: Protect individuals from being held accountable for behavior they couldn’t control. Yet there have been more than a few historical and recent instances of a judge or jury issuing a controversial “by reason of…” verdict. What was intended as a human rights effort has become a last-ditch way to save killers (though it didn’t work for James Holmes). The question that hangs in the air at these sort of proceedings has always been the same: Is there a way to make determinations more scientific and less traditionally judicial? Adam Shniderman, a criminal justice researcher at Texas Christian University, has been studying the role of neuroscience in the court system for several years now. He explains that neurological data and explanations don’t easily translate into the world of lawyers and legal text. Inverse spoke with Shniderman to learn more about how neuroscience is used in today’s insanity defenses, and whether this is likely to change as the technology used to observe the brain gets better and better. Can you give me a quick overview of how the role of neuroscience in the courts, has changed over the years? Especially in the last few decades with new advances in technology. Obviously, [neuroscientific evidence] has become more widely used as brain-scanning technology has gotten better. Some of the scanning technology we use now, like functional MRI that measures blood oxygenation as a proxy for neurological activity, is relatively new within the last 20 years or so. The nature of brain scanning has changed, but the knowledge that the brain influences someone’s actions is not new.