Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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by Linda Geddes There's little doubt that smoking during pregnancy is bad for the baby. But besides stunting growth and boosting the risk of premature birth, it seems that tobacco smoke leaves a lasting legacy on the brain. Children whose mothers smoked during pregnancy have altered brain growth, which may put them at greater risk of anxiety and depression. Hanan El Marroun at Erasmus Medical Center in Rotterdam, the Netherlands, and her colleagues had previously seen impaired brain growth in babies born to women who smoked throughout their pregnancy, although no differences were seen if women stopped smoking soon after learning that they were pregnant. The question was whether these changes were permanent, or would correct themselves as the child developed. So El Marroun's team used MRI to look at the brains of 113 children aged between 6 and 8 years old whose mothers smoked during pregnancy, and another 113 children whose mums did not. The children's behavioural and emotional functioning was also tested. Depression link Those whose mothers smoked throughout pregnancy had smaller total brain volumes and reduced amounts of grey and white matter in the superior frontal cortex, an area involved in regulating moods. What's more, these structural differences correlated with symptoms of depression and anxiety in the children. Not every child whose mother smoked showed these symptoms, and the study could not definitively prove cause and effect. However, because we already know that smoking is bad for babies, pregnant women should continue to be advised not to smoke, El Marroun says. © Copyright Reed Business Information Ltd.
By Gary Stix Psychological depression is more than an emotional state. Good evidence for that comes from emerging new uses for a technology already widely prescribed for Parkinson’s patients. The more neurologists and surgeons learn about the aptly named deep brain stimulation, the more they are convinced that the currents from the technology’s implanted electrodes can literally reboot brain circuits involved with the mood disorder. Thomas Schlaepfer, a psychiatrist from the University of Bonn Hospital and a leading expert in researching deep brain stimulation, describes in the interview that follows the workings of the technique and why it may help the severely depressed. Can you explain what deep brain stimulation is and what it is currently used for? Deep brain stimulation refers to the implantation of very small electrodes in both hemispheres of the brain, which are connected to a neurostimulator, usually placed under the skin on the right chest. This device is in size and function very similar to a heart pacemaker. It allows stimulations of different pulse width and frequency. Depending on the chosen stimulation parameters the electrodes in the brain are able to “neuromodulate” – to reversibly alter the function – of the surrounding brain tissue. Deep brain stimulation has gained widespread acceptance as a successful treatment for tremor associated with Parkinson’s disease. More than 80,000 patients worldwide have been treated with this method. Some see deep brain stimulation as a much less invasive and fully reversibly alternative to historical neurosurgical interventions, which require tiny amounts of brain tissue to be destroyed in order to have clinical effects. © 2013 Scientific American
Link ID: 18747 - Posted: 10.05.2013
By NICHOLAS BAKALAR Depression may be an independent risk factor for Parkinson’s disease, a new study has found. In a retrospective analysis, researchers followed 4,634 patients with depression and 18,544 matched controls for 10 years. To rule out the possibility that depression is an early symptom of Parkinson’s disease, their analysis excluded patients who received a diagnosis of depression within five years of their Parkinson’s diagnosis. The average age of people with depression was 41, while it was 64 for those with both depression and Parkinson’s. The study, published online in Neurology, found that 66 patients with depression, or 1.42 percent, developed Parkinson’s disease, compared with 97, or 0.52 percent, among those who were not depressed. After controlling for age, sex, diabetes, hypertension and other factors, the researchers found clinical depression was associated with more than three times the risk for Parkinson’s disease. “Our paper does not convey the message that all depression leads to Parkinson’s disease,” said the senior author, Dr. Albert C. Yang, a professor of psychiatry at the National Yang-Ming University in Taiwan. “But particularly the depressed elderly and those with difficult-to-treat depression should be alert to the possibility of neurological disease and Parkinson’s.” Copyright 2013 The New York Times Company
By Travis Riddle Humans like being around other humans. We are extraordinarily social animals. In fact, we are so social, that simply interacting with other people has been shown to be use similar brain areas as those involved with the processing of very basic rewards such as food, suggesting that interacting with people tends to make us feel good. However, it doesn’t take much reflection to notice that the way people interact with each other has radically changed in recent years. Much of our contact happens not face-to-face, but rather while staring at screen-based digital representations of each other, with Facebook being the most prominent example. This raises a very fundamental question – how does online interaction with other people differ from interacting with people in person? One possible way these two interaction styles might differ is through how rewarding we find them to be. Does interacting with Facebook make us feel good as does interacting with people in real life? A recent paper suggests that the answer is “probably not.” In fact, the data from this paper suggest that the more we interact with Facebook, the worse we tend to feel. Researchers recruited participants from around a college campus. The participants initially completed a set of questionnaires, including one measuring their overall satisfaction with life. Following this, participants were sent text messages 5 times a day for two weeks. For each text, participants were asked to respond to several questions, including how good they felt at that moment, as well as how much they had used Facebook, and how much they had experienced direct interaction with others, since the last text. At the end of the two weeks, participants completed a second round of questionnaires. Here, the researchers once again measured participants’ overall satisfaction with life. © 2013 Scientific American
by Linda Geddes They say the early bird catches the worm, but night owls may be missing far more than just a tasty snack. Researchers have discovered the first physical evidence of structural brain differences that distinguish early risers from people who like to stay up late. The differences might help to explain why night owls seem to be at greater risk of depression. Around 10 per cent of people qualify as morning people or larks, and a further 20 per cent are night owls – with the rest of us falling somewhere in between. Your lark or night owl status is called your chronotype. Previous studies have suggested that night owls experience worse sleep, more tiredness during the day and consume greater amounts of tobacco and alcohol. This has prompted some to suggest that they are suffering from a form of chronic jet lag. To investigate further, Jessica Rosenberg at RWTH Aachen University in Germany and colleagues used diffusion tensor imaging to scan the brains of 16 larks, 23 night owls and 20 intermediate chronotypes. They found a reduction in the integrity of night owls' white matter – brain tissue largely comprised of fatty insulating material that speeds up the transmission of nerve signals – in areas associated with depression. "We think this could be caused by the fact that late chronotypes suffer from this permanent jet lag," says Rosenberg, although she cautions that further studies are needed to confirm cause and effect. © Copyright Reed Business Information Ltd.
By BRANDON A. GAUDIANO PROVIDENCE, R.I. — PSYCHOTHERAPY is in decline. In the United States, from 1998 to 2007, the number of patients in outpatient mental health facilities receiving psychotherapy alone fell by 34 percent, while the number receiving medication alone increased by 23 percent. This is not necessarily for a lack of interest. A recent analysis of 33 studies found that patients expressed a three-times-greater preference for psychotherapy over medications. As well they should: for patients with the most common conditions, like depression and anxiety, empirically supported psychotherapies — that is, those shown to be safe and effective in randomized controlled trials — are indeed the best treatments of first choice. Medications, because of their potential side effects, should in most cases be considered only if therapy either doesn’t work well or if the patient isn’t willing to try counseling. So what explains the gap between what people might prefer and benefit from, and what they get? The answer is that psychotherapy has an image problem. Primary care physicians, insurers, policy makers, the public and even many therapists are largely unaware of the high level of research support that psychotherapy has. The situation is exacerbated by an assumption of greater scientific rigor in the biologically based practices of the pharmaceutical industries — industries that, not incidentally, also have the money to aggressively market and lobby for those practices. For the sake of patients and the health care system itself, psychotherapy needs to overhaul its image, more aggressively embracing, formalizing and promoting its empirically supported methods. My colleague Ivan W. Miller and I recently surveyed the empirical literature on psychotherapy in a series of papers we edited for the November edition of the journal Clinical Psychology Review. It is clear that a variety of therapies have strong evidentiary support, including cognitive-behavioral, mindfulness, interpersonal, family and even brief psychodynamic therapies (e.g., 20 sessions). © 2013 The New York Times Company
Link ID: 18722 - Posted: 09.30.2013
If you look at the facts and figures on the mental health charity Mind's website, you'll find that around 1 in 4 people will experience some sort of mental health problem each year. About 10% of these people will see their doctor and be diagnosed as having a mental health problem, and of this group, a small proportion will in turn be referred to specialist psychiatric care. Of these people, precisely none resemble the breathtakingly ignorant costumes that have recently been withdrawn from Tesco and Asda. If you want to know what someone with a mental health issue looks like, just look around you. One of the most common types of mental health issue is anxiety – about 9% of people in Britain meet the criteria for mixed anxiety and depression, for example. We all feel anxious from time to time, and that's not necessarily a bad thing. Isaac Marks and Randy Nesse argued in 1994 that anxiety is an important emotion that has been shaped during the course of human evolution. If we are in a potentially dangerous environment, being anxious increases our awareness of our surroundings and puts us in a state of physiological readiness to deal with any threats. However, when an anxiety response kicks in too often, and in situations where it is not needed, it becomes a debilitating problem. In serious cases, anxiety can make it incredibly hard for the person to function. There's now a wealth of research that is trying to tap into the mechanisms involved in both sub-clinical and clinical forms of anxiety. By understanding what happens when we become anxious, we might be able to get a clearer idea of how and why things go wrong in anxiety disorders. For example, a new study published this week in the Journal of Neuroscience has suggested one potential contributing factor – how smells are processed. © 2013 Guardian News and Media Limited
By REED ABELSON THE first time Melissa Morelli was taken to the hospital, she was suicidal and cutting herself, her mother says. She was just 13, and she had been transferred to a psychiatric hospital, where she stayed for more than a week. Her doctors told her mother, Cathy Morelli, that it was not safe for Melissa to go home. But the family’s health insurance carrier would not continue to pay for her to remain in the hospital. The second time, the same thing happened. And the third and the fourth. Over the course of five months, Ms. Morelli took Melissa to the hospital roughly a dozen times, and each time the insurance company, Anthem Blue Cross, refused to pay for hospital care. “It was just a revolving door,” Ms. Morelli said. “You had not been getting better in a significant way,” Anthem explained in one letter sent directly to Melissa, then 14, in July 2012. “It does not seem likely that doing the same thing will help you get better.” Desperate to get help for her daughter, Ms. Morelli sought the assistance of Connecticut state officials and an outside reviewer. She eventually won all her appeals, and Anthem was forced to pay for the care it initially denied. All told, Melissa spent nearly 10 months in a hospital; she is now at home. Anthem, which would not comment on Melissa’s case, says its coverage decisions are based on medical evidence. Melissa’s treatment did not come cheap: it ultimately cost hundreds of thousands of dollars, Ms. Morelli said. Patients often find themselves at odds with health insurers, but the battles are perhaps nowhere so heated as with the treatment of serious mental illness. © 2013 The New York Times Company
By Michelle Roberts Health editor, BBC News online People prescribed anti-depressants should be aware they could be at increased risk of type 2 diabetes, say UK researchers. The University of Southampton team looked at available medical studies and found evidence the two were linked. But there was no proof that one necessarily caused the other. It may be that people taking anti-depressants put on weight which, in turn, increases their diabetes risk, the team told Diabetes Care journal. Or the drugs themselves may interfere with blood sugar control. Their analysis of 22 studies involving thousands of patients on anti-depressants could not single out any class of drug or type of person as high risk. Prof Richard Holt and colleagues say more research is needed to investigate what factors lie behind the findings. And they say doctors should keep a closer check for early warning signs of diabetes in patients who have been prescribed these drugs. With 46 million anti-depressant prescriptions a year in the UK, this potential increased risk is worrying, they say. Prof Holt said: "Some of this may be coincidence but there's a signal that people who are being treated with anti-depressants then have an increased risk of going on to develop diabetes. BBC © 2013
By John Horgan Once again, antidepressants have been linked to an episode of horrific violence. The New York Times reports that Aaron Alexis, who allegedly shot 12 people to death at a Navy facility in Washington, D.C., earlier this week, received a prescription for the antidepressant trazodone in August. When I first researched antidepressants almost 20 years ago, I encountered claims that they sometimes triggered violent episodes—for example, a 1989 incident in which a Kentucky man taking fluoxetine (brand name Prozac) shot to death eight co-workers and then himself. I dismissed the claims, reasoning that, because people prescribed psychiatric drugs are disturbed to begin with, it is not surprising that a tiny fraction hurt themselves and/or others. By 2004, however, in part because of lawsuits that forced pharmaceutical companies to disclose data on adverse effects, the FDA ordered antidepressant manufacturers to include a warning that antidepressants “increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults in short-term studies of major depressive disorder (MDD) and other psychiatric disorders.” Alexis, who was 34, was reportedly seeking treatment for insomnia when he received his prescription for trazodone. Originally marketed as an antidepressant after its approval by the FDA in 1981, trazodone is also prescribed for anxiety and insomnia. Trazodone was a precursor of the extremely popular selective serotonin reuptake inhibitors (SSRIs); like the SSRIs, trazodone boosts levels of the neurotransmitter serotonin. © 2013 Scientific American
By T. M. LUHRMANN STANFORD, Calif. — THE specter of violence caused by mental illness keeps raising its head. The Newtown, Conn., school killer may have suffered from the tormenting voices characteristic of schizophrenia; it’s possible that he killed his mother after she was spooked by his strange behavior and tried to institutionalize him. We now know that Aaron Alexis, who killed 12 people at the Washington Navy Yard on Monday, heard voices; many observers assume that he, too, struggled with schizophrenia. To be clear: a vast majority of people with schizophrenia — a disease we popularly associate with violence — never commit violent acts. They are far more likely to be the victims of violence than perpetrators of it. But research shows us that the risk of violence from people with schizophrenia is real — significantly greater than it is in the broader population — and that the risk increases sharply when people have disturbing hallucinations and use street drugs. We also know that many people with schizophrenia hear voices only they can hear. Those voices feel real, spoken by an external, commanding authority. They are often mean and violent. An unsettling question is whether the violent commands from these voices reflect our culture as much as they result from the disease process of the illness. In the past few years I have been working with some colleagues at the Schizophrenia Research Foundation in Chennai, India, to compare the voice-hearing experience of people with schizophrenia in the United States and India. The two groups of patients have much in common. Neither particularly likes hearing voices. Both report hearing mean and sometimes violent commands. But in our sample of 20 comparable cases from each country, the voices heard by patients in Chennai are considerably less violent than those heard by patients in San Mateo, Calif. © 2013 The New York Times Company
JoNel Aleccia NBC News A neurosurgery patient treated at a New Hampshire hospital this spring did have a rare brain disorder known as Creutzfeldt-Jakob Disease, health officials confirmed Friday. That means that 15 other people in three states may have been exposed to the invariably deadly infection through potentially tainted surgical equipment. Autopsy results came back positive for CJD from the National Prion Disease Pathology Surveillance Center and were reported to the New Hampshire Department of Health and Human Services and Catholic Medical Center, where the surgery took place. Earlier this month, New Hampshire officials notified eight patients who may have been exposed to CJD through shared equipment. Five others in Massachusetts and two in Connecticut were also warned of the risk, health officials in those states said. "Though we are not surprised by the test results, we are saddened by the toll this disease takes on families and our sympathies go out to all those affected," said Dr. Jose Montero, New Hampshire's director of public health, in a statement. The initial patient turned out to have sporadic CJD, which occurs spontaneously. It's not the variant form of the disease that causes a human type of "mad cow disease" and is associated with eating beef contaminated with the cattle version of the infection, called bovine spongiform encephalotpathy, or BSE, experts said. The problem arose because standard hospital disinfection techniques cannot eradicate the prion that causes CJD. A prion is a protein and the type that causes BSE and CJD is misfolded and somehow manages to transform other proteins into disease-causing shape.
Link ID: 18678 - Posted: 09.21.2013
Eliot Barford A parasite that infects up to one-third of people around the world may have the ability to permanently alter a specific brain function in mice, according to a study published in PLoS ONE today1. Toxoplasma gondii is known to remove rodents’ innate fear of cats. The new research shows that even months after infection, when parasites are no longer detectable, the effect remains. This raises the possibility that the microbe causes a permanent structural change in the brain. The microbe is a single-celled pathogen that infects most types of mammal and bird, causing a disease called toxoplasmosis. But its effects on rodents are unique; most flee cat odour, but infected ones are mildly attracted to it. This is thought to be an evolutionary adaptation to help the parasite complete its life cycle: Toxoplasma can sexually reproduce only in the cat gut, and for it to get there, the pathogen's rodent host must be eaten. In humans, studies have linked Toxoplasma infection with behavioural changes and schizophrenia. One work found an increased risk of traffic accidents in people infected with the parasite2; another found changes in responses to cat odour3. People with schizophrenia are more likely than the general population to have been infected with Toxoplasma, and medications used to treat schizophrenia may work in part by inhibiting the pathogen's replication. © 2013 Nature Publishing Group,
By NICHOLAS BAKALAR Five antidepressant drugs are approved by the Food and Drug Administration for treating obsessive-compulsive disorder. But they are sometimes ineffective, and guidelines suggest adding an antipsychotic drug to the regimen. Now scientists have found that adding cognitive behavioral therapy, or C.B.T., may be more effective than an antipsychotic. Researchers studied 100 people with O.C.D. who were taking antidepressants without sufficient improvement. They randomized 40 to the antipsychotic risperidone (brand name Risperdal), 20 to a placebo pill, and 40 to exposure and ritual prevention, a special form of C.B.T. delivered twice a week over eight weeks. All continued their antidepressants as well. The study was published online in JAMA Psychiatry, and several of the authors have financial relationships with pharmaceutical companies. Using well-validated scales and questionnaires, the researchers found that 80 percent of the C.B.T. patients responded with reduced symptoms and improved functioning and quality of life. About 23 percent got better on risperidone, and 15 percent on the placebo. “It’s important to discontinue antipsychotics if there isn’t continued benefit after four weeks,” said the lead author, Dr. Helen Blair Simpson, a professor of psychiatry at Columbia. “O.C.D. patients who still have symptoms should first be offered the addition of C.B.T., and some will achieve minimal symptoms. “There’s a hopeful message here,” she added. “There are good treatments.” Copyright 2013 The New York Times Company
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 18674 - Posted: 09.19.2013
By JEREMY W. PETERS and MICHAEL LUO WASHINGTON — Despite deep divisions that have kept Congress from passing new gun safety laws for almost two decades, there is one aspect of gun control on which many Democrats, Republicans and even the National Rifle Association agree: the need to give mental health providers better resources to treat dangerous people and prevent them from buying weapons. Yet efforts to improve the country’s fraying mental health system to help prevent mass shootings have stalled on Capitol Hill, tied up in the broader fight over expanded background checks and limits on weapons sales. Now the shooting at the Washington Navy Yard by a man who authorities say showed telltale signs of psychosis is spurring a push to move ahead with bipartisan mental health policy changes. The new debate over gun control is beginning to turn not on weapons or ammunition, but on the question of whether to spend more money on treating and preventing mental illness. Proponents again face a steep uphill push, but they see an opening even if it remains unclear whether any changes under consideration could have headed off the latest attack, in which the authorities say Aaron Alexis, a former Navy reservist, bought the shotgun he used in Virginia. “Given the clear connection between recent mass shootings and mental illness, the Senate should not delay bipartisan legislation that would help address this issue,” Senators Kelly Ayotte, Republican of New Hampshire, and Mark Begich, Democrat of Alaska, wrote Wednesday in a joint statement to the Senate leadership. The legislation they are pushing, which was held up when a more sweeping gun measure was defeated earlier this year, would establish programs to train teachers to recognize the signs of mental illness and how to defuse potentially violent situations. © 2013 The New York Times Company
By JIM DWYER Here are law students on a Tuesday morning in 2013, hearing that researchers hope over the next decade or so to map the wiring of the human brain, seeing how individual cells link to bigger circuits. A decade is a sprint, less time than since 9/11, to use one benchmark. The scientists want to lift the hood and get a look at the human mind. The students, in a seminar at Fordham University School of Law taught by Prof. Deborah W. Denno, wonder what that will mean for the law. Over and over, they put questions to a guest speaker, Joshua R. Sanes, director of the Center for Brain Science at Harvard, about the implications for society if and when brain science can identify with confidence a propensity for violence, or for lying. He bats it right back at them. “You tell me,” Dr. Sanes said. “It’s a huge issue. I wish I had something smart to say.” Last year, President Obama announced that the federal government would create a Brain Initiative to speed up the development of tools that can track how the brain works and how it breaks. It is not hard to imagine the benefits, beginning with more carefully targeted treatments for people afflicted with psychiatric ailments. “There has not been a brand new type of drug for antidepression or autism or schizophrenia, bipolar disorder or O.C.D. in something like 25 years,” Dr. Sanes said. “This is where we have to make a long-term investment and come up with some new types of help because what we are doing isn’t working.” Work on animals has shown in broad strokes how information gets into the head and processed, but current imaging tools cannot keep up with the brain’s processing speed, or are not powerful enough to follow the molecular transactions involved in passing information and creating thought. © 2013 The New York Times Company
Link ID: 18666 - Posted: 09.18.2013
By Sarah Amandolare Decades of research and billions of dollars go into developing and marketing drugs. Here's the life span of a typical brain drug—Cymbalta, a popular antidepressant Tuberculosis researchers discover that a drug that treats infections, called iproniazid, also boosts patients' mood. They learn that iproniazid slows the breakdown of three chemicals in the brain— serotonin, norepinephrine and dopamine. These molecules take center stage in the next two decades, as scientists search for antidepressants. 1974 Eli Lilly researchers develop fluoxetine (Prozac), the first selective serotonin reuptake inhibitor. Fluoxetine thwarts the absorption, or “reuptake,” of serotonin. This boosts levels of the chemical in the pockets of space between neurons. Prozac does not hit drugstore shelves until 1988. 1980s Scientists start tinkering with the reuptake of norepinephrine and dopamine, which, in addition to elevating mood, can relieve muscle and joint pain. They dub this new class of antidepressants serotonin-norepinephrine reuptake inhibitors (SNRIs). At Eli Lilly, scientists begin developing an SNRI with a special focus on norepinephrine. One of their molecules becomes known as duloxetine, later branded Cymbalta. 1986 © 2013 Scientific American
Link ID: 18660 - Posted: 09.18.2013
By PAULINE W. CHEN, M.D. One afternoon at a school not far from the hospital where I was working, a teacher opened a utility closet and found a staff member passed out on the floor. He was clutching a small bloody mass in one hand, a sharp knife in the other, she reported, a red stain spreading rapidly at his middle. He had amputated his genitals. Once he’d been brought to our emergency room and resuscitated, the man refused further treatment. Doctors and nurses, concerned that if they waited any longer to reattach the severed part the surgery might not work, took the necessary steps to deem him mentally incompetent to make such decisions. “The guy was seriously nuts,” I remember one of the doctors saying afterward. “He kept screaming that he didn’t want ‘it’ back.” For days after the successful operation, the gruesome story was all anyone at the hospital could discuss. Most of us chalked it up to his being “certifiable,” and several wondered if maybe they should have skipped the surgery. “After all,” said one clinician, “isn’t that what he wanted?” But in all the chatter none of us mentioned a key part of the patient’s story: the unbearable suffering that must have pushed him to commit so brutal an act. In fact, anyone overhearing our conversations might have been hard pressed to find any of the warmth and sensitivity we routinely displayed toward patients with cancer, AIDS or heart disease. I remembered the man and our reactions this past week while reading “Falling Into the Fire: A Psychiatrist’s Encounters With the Mind in Crisis,” a thought-provoking new book by Dr. Christine Montross. Of all the afflictions that fall upon us, few remain as misunderstood and stigmatized as those that affect the mind. Copyright 2013 The New York Times Company
By Philip Yam New Hampshire health officials announced last week that hospitals in three New England states may have accidentally exposed 15 people to prions, the infectious protein that ravages the brain and leaves it full of holes. Evidently, the hospitals involved used surgical tools that had previously been deployed on a patient who officials suspect later died from a particular prion infection called sporadic Creutzfeldt-Jakob disease (CJD). As disturbing as the revelation was, it pales in comparison with the announcement in 2002, when the University of Pittsburgh Medical Center Presbyterian announced that up to 4,000 patients might have been exposed to the prion. Both incidents show that the hospital transmission of prion diseases remains an ever-present possibility, if thankfully a very unlikely one. Prions are unusual pathogens distinct from parasites, fungi, bacteria and viruses. They are misfolded proteins that can transform healthy proteins into sickly versions, leading to the death of cells. Particularly abundant in the brain, they took center stage in the late 1980s, during the mad cow outbreak in the U.K. People who ate beef from infected cows ran the risk of contracting a variant of CJD. The panic brought to light the range of prion diseases that can affect humans and animals, including one that develops spontaneously. Called sporadic CJD, this spontaneous form strikes about one in every million people each year for no apparent reason. What’s more, the brain tissue from the unlucky few can infect healthy brains—hence, the worry over surgical transmission. © 2013 Scientific American
Link ID: 18643 - Posted: 09.14.2013
By Gary Stix New types of drugs for schizophrenia, depression and other psychiatric disorders are few and far between—and a number of companies have scaled back or dropped development of this class of pharmaceuticals. One exception stands out. Ketamine, the anesthetic and illegal club drug, is now being repurposed as the first rapid-acting antidepressant drug and has been lauded as possibly the biggest advance in the treatment of depression in 50 years. A few trials by large pharma outfits are now underway on a new, purportedly improved and, of course, more profitable variant of ketamine, which in its current generic drug form does not make pharmaceutical marketing departments salivate. Some physicians have decided they simply can’t wait for the lengthy protocols of the drug approval process to be sorted out. They have read about experimental trials in which a low-dose, slow-infusion of ketamine seems to produce what no Prozac-like pill can achieve, lifting the black cloud in hours, not weeks. With nothing to offer desperate, sometimes suicidal patients, physicians have decided against waiting for an expensive, ketamine lookalike to arrive and have started writing scripts for the plain, vanilla generic version that has been used for decades as an anesthetic. Ketamine, it seems, has captivated a bunch of white coats with the same grassroots energy that has propelled the medical marijuana movement. © 2013 Scientific American