Links for Keyword: Schizophrenia
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
People with schizophrenia are six times more likely to develop epilepsy, says a study which finds a strong relationship between the two diseases. Writing in Epilepsia, researchers in Taiwan say this could be due to genetic, neurobiological or environmental factors. The study followed around 16,000 patients with epilepsy and schizophrenia between 1999 and 2008. An epilepsy expert says it is an interesting and convincing study. The study used data from the Taiwan National Health Insurance database and was led by researchers from the China Medical University Hospital in Taichung. They identified 5,195 patients with schizophrenia and 11,527 patients with epilepsy who were diagnosed during the nine years period. These groups of patients were compared to groups of the same sex and age who did not have either epilepsy or schizophrenia. The findings show that the incidence of epilepsy was 6.99 per 1,000 person-years in the schizophrenia patient group compared to 1.19 in the non-schizophrenia group. The incidence of schizophrenia was 3.53 per 1,000 person-years for patients with epilepsy compared to 0.46 in the non-epilepsy group. Previous studies had suggested a prevalence of psychosis among epilepsy patients. BBC © 2011
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 15815 - Posted: 09.19.2011
RandyeKaye, a former radio personality in Connecticut, has just written a book, “Ben Behind His Voices: One family’s journey from the chaos of schizophrenia to hope,’’ about life with her son. A. I had always wanted to share our family’s story. One of the things that was so hard for us is I felt so alone - like nobody else’s kid had a mental illness, what’s wrong with my son, what did I do wrong? I wanted to spread the message of exactly what families go through and that recovery is possible, and some of the ways to deal with things. Q. Your son wasn’t diagnosed until years after he started acting oddly and had psychotic episodes that potentially damaged his brain. Do you resent the fact that he wasn’t diagnosed sooner? A. A lot of symptoms of mental illnesses overlap. I look back now [at the] typical pattern of gradual onset schizophrenia, and my son hit every single point: from extreme brightness, to being slightly anxious as a child, to having difficulty organizing his thoughts, to mood swings, and then to isolation from his peers. But if you look at any of those symptoms, it could be plain old adolescence, it could be drug use. There’s no way to test [for] it. Q. Mental illness can also be a financial catastrophe as well as an emotional one for a family. Did you experience that? A. My son’s college fund went to cure symptoms of an illness I didn’t know was there. A lot of families [facing mental illness] say you either have no money and the system can help you, or you have money and the system will help you when you’re out of money. Medications alone can be $6,000 a month. © 2011 NY Times Co
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 15746 - Posted: 08.30.2011
By Nicole Gray A mother's age is often considered a genetic risk factor for offspring, but research is now pointing the finger at fathers, too—particularly when it comes to the mental health of their progeny. Males may have the advantage of lifelong fertility, but as they grow older, the rate of genetic mutations passed on via their sperm cells increases significantly—putting their children at increased risk for psychiatric disorders, especially autism and schizophrenia. Two recent studies support this link at least associatively, but experts remain uncertain if age is the cause of these problems. The Malaysian Mental Health Survey (MMHS) results, which were published online in March 2011, for instance, revealed that people with older parents as well as those whose fathers were at least 11 years older than their mothers, were at increased risk for certain mental health disorders, including anxiety, depression, obsessive-compulsive disorder and phobias. Offspring whose fathers were 19 or younger when the child was born had just a 9 percent prevalence of mental health disorders. Regardless of paternal age, however, if the father was 11 years or older than the mother, that rate jumped to 24 percent. The greatest risk of mental health disorders—42 percent—was seen in the children of fathers aged 50 and older, with wives at least 11 years younger than their husbands. The link between paternal age and increased risk of mental illness has long been recognized by practitioners, but researchers are beginning to unravel more details: "We have known that the children of older men have higher susceptibility to sporadic disease since the 1970s, but there has been an explosion of research in this area," says Dolores Malaspina, a professor of psychiatry and environmental medicine at New York University and a leader in the field of paternal age-related schizophrenia (PARS). © 2011 Scientific American,
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 15738 - Posted: 08.30.2011
By Kenneth I. Kaitin and Christopher P. Milne Schizophrenia, depression, addiction and other mental disorders cause suffering and cost billions of dollars every year in lost productivity. Neurological and psychiatric conditions account for 13 percent of the global burden of disease, a measure of years of life lost because of premature mortality and living in a state of less than full health, according to the World Health Organization. Despite the critical need for newer and better medications to treat a range of psychiatric and neurodegenerative diseases, including Alzheimer’s and Parkinson’s, drugs to treat these diseases are just too complex and costly for big pharmaceutical companies to develop. The risk of spending millions on new drugs only to have them fail in the pipeline is too great. That’s why many big drug companies are pulling the plug on R&D for neuropsychiatric and other central nervous system (CNS) medicines. Our team at the Tufts Center for the Study of Drug Development has arrived at this conclusion after conducting surveys of pharmaceutical and biotechnology companies about the drug development process. These surveys allow us to generate reliable estimates of the time, cost and risk of designing new drugs. Our analyses show that central nervous system agents are far more difficult to develop than most other types. © 2011 Scientific American,
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 15671 - Posted: 08.11.2011
By James Gallagher Health reporter, BBC News US scientists say they have "fundamentally transformed" the understanding of the genetics of schizophrenia. A report in the journal Nature Genetics showed that "fresh mutations" in DNA are involved in at least half of schizophrenia cases, when there is no family history of the illness. Researchers found mutations in 40 different genes. They say their findings explain the high number of cases around the world. Schizophrenia is quite common, it affects one in every 100 people during their lifetime. Genes play a part in the illness. A tenth of people with schizophrenia also have a parent with the condition. However, researchers now say there is a genetic role even in cases which have not been inherited. A person's DNA is not a perfect copy of their parents' genetic code - there are mutations when eggs and sperm are formed. A team at Columbia University Medical Center analysed the genetic code of 225 people, some with and some without the condition. They found mutations in 40 genes were linked to schizophrenia. Lead researcher Dr Maria Karayiorgou said: "The fact that the mutations are all from different genes is particularly fascinating. BBC © 2011
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 15659 - Posted: 08.09.2011
By BENEDICT CAREY LEE’S SUMMIT, Mo. — The job was gone, the gun was loaded, and a voice was saying, “You’re a waste, give up now, do it now.” Mr. Holt and his wife, Patsy, who has been one of his main resources in his struggle with mental illness. It was a command, not a suggestion, and what mattered at that moment — a winter evening in 2000 — was not where the voice was coming from, but how assured it was, how persuasive. Losing his first decent job ever seemed like too much for Joe Holt to live with. It was time. “All I remember then is a knock on the bedroom door and my wife, Patsy, she sits down on the bed and hugs me, and I’m holding the gun in my left hand, down here, out of sight,” said Mr. Holt, 50, a computer consultant and entrepreneur who has a diagnosis of schizophrenia. “She says, ‘Joe, I know you feel like quitting, but what if tomorrow is the day you get what you want?’ And walks out. I sat there staring at that gun for an hour at least, and finally decided — never again. It can never be an option. Patsy deserves for me to be trying.” In recent years, researchers have begun talking about mental health care in the same way addiction specialists speak of recovery — the lifelong journey of self-treatment and discipline that guides substance abuse programs. The idea remains controversial: managing a severe mental illness is more complicated than simply avoiding certain behaviors. The journey has more mazes, fewer road signs. © 2011 The New York Times Company
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 15654 - Posted: 08.08.2011
By DUFF WILSON Warnings for Seroquel will soon recommend that the drug be avoided in combination with 12 drugs linked to arrhythmia. The revised label, posted without fanfare last week on the F.D.A. Web site, says Seroquel and extended-release Seroquel XR “should be avoided” in combination with at least 12 other medicines linked to a heart arrhythmia that can cause sudden cardiac arrest. Sandy Walsh, a spokeswoman for the F.D.A., said the statement was only a precaution for doctors, and should not be considered a complete ban against prescribing Seroquel with the other drugs. Ms. Walsh said the label was changed after the F.D.A. received new information about reports of arrhythmia in 17 people who took more than the recommended doses of Seroquel. Though it should not be a problem at a normal dosage, she said, it may still be good advice to avoid using the drugs together. The arrhythmia, known as prolongation of the QT interval, referring to two waves of the heart’s electrical rhythm, is estimated to cause several thousand deaths a year in the United States. As AstraZeneca prepares to report its second-quarter earnings at the end of this month, it faces additional scrutiny this week. The F.D.A. is considering the London-based company’s dapagliflozin, a proposed diabetes drug with Bristol-Myers Squibb, and is expected to decide soon on Brilinta, an anticoagulant. The company is facing the loss of patents for Seroquel next year and for the heartburn drug Nexium in 2014. © 2011 The New York Times Company
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 15583 - Posted: 07.19.2011
Alison Abbott Epidemiologists showed decades ago that people raised in cities are more prone to mental disorders than those raised in the countryside. But neuroscientists have avoided studying the connection, preferring to leave the disorderly realm of the social environment to social scientists. A paper in this issue of Nature represents a pioneering foray across that divide. Using functional brain imaging, a group led by Andreas Meyer-Lindenberg of the University of Heidelberg's Central Institute of Mental Health in Mannheim, Germany, showed that specific brain structures in people from the city and the countryside respond differently to social stress (see pages 452 and 498). Stress is a major factor in precipitating psychotic disorders such as schizophrenia. The work is a first step towards defining how urban life can affect brain biology in a way that has a potentially major impact on society — schizophrenia affects one in 100 people. It may also open the way for greater cooperation between neuroscientists and social scientists. "There has been a long history of mutual antipathy, particularly in psychiatry," says sociologist Craig Morgan at the Institute of Psychiatry in London. "But this is the sort of study that can prove to both sides that they can gain from each others' insights." Meyer-Lindenberg works on risk mechanisms in schizophrenia, and previously focused on the role of genes. But although a dozen or so genes have been linked to the disorder, "even the most powerful of these genes conveys only a 20% increased risk", he says. Yet schizophrenia is twice as common in those who are city-born and raised as in those from the countryside, and the bigger the city, the higher the risk (see 'Dose response?'). © 2011 Nature Publishing Group
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 15476 - Posted: 06.23.2011
By RICHARD A. FRIEDMAN, M.D. No sooner had Dominique Strauss-Kahn been arrested on sexual assault charges in New York than a parade of psychiatrists stepped forward to offer their expert opinion in the news media. Mr. Strauss-Kahn, who subsequently resigned as chief of the International Monetary Fund, will experience “a terrible grief because he is in prison,” said one. Another offered that he would have “terrible mourning” for “the loss of social status, image and glory.” Of course, it’s only natural for the media to seek comment from experts. But as a psychiatrist, I cringe at statements like these, for they cross an ethical line that goes back to a presidential campaign nearly half a century ago. Just before the 1964 election, a muckraking magazine called Fact decided to survey members of the American Psychiatric Association for their professional assessment of Senator Barry Goldwater of Arizona, the Republican nominee against President Lyndon B. Johnson. Ralph Ginzburg, the magazine’s notoriously provocative publisher, had heavily advertised the issue in advance, saying it would call Mr. Goldwater’s character into question. A.P.A. members were asked whether they thought Mr. Goldwater was fit to be president and what their psychiatric impressions of him were. It was not American psychiatry’s finest hour. © 2011 The New York Times Company
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 15356 - Posted: 05.24.2011
By Jamie Horder The search for the genetic roots of psychiatric illnesses and behavioral disorders such as schizophrenia, autism and ADHD has a long history, but until recently, it was one marked by frustration and skepticism. In the past few years, new techniques have begun to reveal strong evidence for the role of specific genes in some cases of these conditions but in a way few people expected. To understand what makes the new discoveries so novel, it’s necessary to appreciate how our genes can go wrong. The human genetic code can be thought of as an encyclopedia in multiple volumes. Our normal genome contains 46 chromosomes, so that’s 46 volumes. Each chromosome is a long string of the chemical DNA and the information is “written” in the form of a molecular alphabet with just four letters: A, T, C and G. There are three ways in which something can go wrong here. First, a whole chromosome can be either missing or duplicated. This drastic change is almost always fatal. (The exceptions include Downs Syndrome.) Second, single-nucleotide polymorphisms (SNPs, or “snips” as everyone calls them) are when a single base-pair is different, corresponding to a misprinted character. Finally, copy-number variants (CNVs) are when a stretch of DNA is either missing (deleted), or repeated (duplicated), a bit like a page that’s either fallen out or been printed twice. As you can imagine, CNVs tend to be more serious than SNPs, because they affect more of the DNA. This is only a general rule, however. There are plenty of serious SNPs, and plenty of harmless CNVs. It all depends on where they happen, and whether they interfere with important genes. © 2011 Scientific American
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 15341 - Posted: 05.19.2011
Analysis by Nic Halverson "A mental breakdown in the relation between thought, emotion and behavior, leading to faulty perception, inappropriate actions and feelings, withdrawal from reality and personal relationships into fantasy and delusion, and a sense of mental fragmentation." Sound like what your brain feels like after an Angry Birds marathon or an 8-hour binge of searching for the end of the Internet? Maybe. But this is actually the definition of schizophrenia. Ubiquitous computing might send schizophrenic ripples through your frontal lobes whenever you log on, but researchers at the University of Texas at Austin are taking that a step further by actually using computers to simulate the mental disorder. One theory about the cause of schizophrenia suggests that an afflicted brain remembers too many irrelevant things, due to an excessive release of dopamine. Overwhelmed by vast caches of facts, thoughts and memories all junk-piled in their heads, schizophrenics start processing them into delusional conclusions not based in reality. Uli Grasemann, a graduate student in the University of Texas' Department of Computer Science, used a synthetic neural network to simulate these delusions, often called hyperlearning hypothesis. Designed by his adviser, professor Risto Miikkulainen, Graseman used the network, dubbed DISCERN,to mimic the effects that different neurological dysfunction have on human language function. © 2011 Discovery Communications, LLC
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 15321 - Posted: 05.12.2011
Ewen Callaway Before committing suicide at the age of 22, an anonymous man with schizophrenia donated a biopsy of his skin cells to research. Reborn as neurons, these cells may help neuroscientists to unpick the disease he struggled with from early childhood. Experiments on these cells, as well as those of several other patients, are reported today in Nature1. They represent the first of what are sure to be many mental illnesses 'in a dish', made by reprogramming patients' skin cells to an embryonic-like state from which they can form any tissue type. Recreating neuropsychiatric conditions such as schizophrenia and bipolar disorder using such cells represents a daunting challenge: scientists do not know the underlying biological basis of mental illnesses; symptoms vary between patients; and although psychiatric illnesses are strongly influenced by genes, it has proved devilishly hard to identify many that explain more than a fraction of a person's risk. "All of us had been contacted by patients asking 'when can I get my stem cells to solve my schizophrenia'. It's not as simple as that," says Russell Margolis, a psychiatrist and neurogeneticist at Johns Hopkins University in Baltimore, Maryland, who was not involved in the study. "It's an additional piece to the puzzle as opposed to the answer." © 2011 Nature Publishing Group,
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 15214 - Posted: 04.14.2011
Scientists are eyeing a rare genetic glitch for clues to improved treatments for some people with schizophrenia (http://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml) — even though they found the mutation in only one third of 1 percent of patients. In the study, funded in part by the National Institutes of Health, schizophrenia patients were 14 times more likely than controls to harbor multiple copies of a gene on Chromosome 7. The mutations were in the gene for VIPR2, the receptor for vasoactive intestinal peptide (VIP) — a chemical messenger known to play a role in brain development. An examination of patients' blood confirmed that they had overactive VIP activity. Discovery of the same genetic abnormality in even a small group of patients buoys hopes for progress in a field humbled by daunting complexity in recent years. The researchers’ previous studies (http://www.nimh.nih.gov/science-news/2008/rates-of-rare-mutations-soar-three-to-four-times-higher-in-schizophrenia.shtml) had suggested that the brain disorder that affects about 1 percent of adults might, in many cases, be rooted in different genetic causes in each affected individual, complicating prospects for cures. "Genetic testing for duplications of the VIP receptor could enable early detection of a subtype of patients with schizophrenia, and the receptor could also potentially become a target for development of new treatments," explained Jonathan Sebat, Ph.D., of the University of California, San Diego, who led the research team. "The growing number of such rare duplications and deletions found in schizophrenia suggests that what we have been calling a single disorder may turn out, in part, to be a constellation of multiple rare diseases."
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 15043 - Posted: 02.24.2011
Evidence that prescription drugs shrink patients' brains would, one might think, suggest only one course of action: stop prescribing them. But the matter turns out to be much more complicated, according to research published today in Archives of General Psychiatry on the effects of antipsychotic drugs in people with schizophrenia1. In the past 15 years, research has indicated that people with schizophrenia have smaller cerebral volumes than the general population, and that this reduction is particularly large in 'grey-matter' structures, which contain the cell bodies of neurons. For instance, one meta-analysis points to 5–7% reductions in the size of the amygdala, hippocampus and parahippocampus2, which are all involved in memory storage and retrieval. But scientists have debated whether the decrease is caused by the disease alone, or whether powerful antipsychotic drugs also have a role. According to the latest findings, the more antipsychotics patients receive, the more likely they are to have a decreased amount of grey matter. The research was led by Beng Choon Ho, a psychiatrist and neuroscientist at the University of Iowa in Iowa City. His team used magnetic resonance imaging (MRI) to scan the brains of 211 patients, administering on average 3 scans per patient over a 7.2-year period1. They found that treatment length and the type and dose of antipsychotic drugs taken were both relatively good predictors of total brain volume change. Use of antipsychotics explained 6.6% of the change in total brain volume and 1.7% of the change in total grey-matter volume. © 2011 Nature Publishing Group,
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 14973 - Posted: 02.08.2011
By DWIGHT GARNER Judith Guest’s 1976 novel, “Ordinary People,” and the 1980 film adaptation starring Timothy Hutton, were groundbreaking because they underscored Ms. Guest’s title. Mental illness could occur in the most ordinary families, these works suggested. It could happen to anyone. The appeal of the Irish journalist Patrick Cockburn’s distressing new memoir, written with his son Henry, is quite the opposite, because the large Cockburn family is completely extraordinary. “Henry’s Demons” is about how Henry Cockburn, in 2002, at the age of 20, received a diagnosis of schizophrenia. He was enrolled at the University of Brighton at the time. Trees began talking to him; he leapt naked into frozen lakes; he soiled his pants on a regular basis; he ate raw garlic; his hair became matted into a single mephitic dreadlock; he roamed the woods, his crotch becoming infested with insects; he began to resemble Jesus or a caveman. He would be in and out of mental institutions, all across England, for nearly the next decade. The charming young man his family had known was largely gone. This is an awful, hard-to-witness, downbound train of a story. The book’s last sentence, written by Henry, is as startling as the moment in a horror movie when the mutilated monster, long presumed dead, flicks opens its green eyes. © 2011 The New York Times Company
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 14953 - Posted: 02.05.2011
By Julie Steenhuysen CHICAGO — Although first approved to treat schizophrenia, new antipsychotic medications are increasingly being prescribed for a host of other uses, even when there is little evidence they work, U.S. researchers said on Friday. The drugs, known as "atypical antipsychotics," have quickly eclipsed older-generation or "typical" antipsychotics and are increasingly used to treat conditions like bipolar disorder, depression and even autism. "What we see is wide adoption for the use of these medications far beyond the evidence base to support it," said Dr. Caleb Alexander of the University of Chicago and a consultant for IMS Health, a company that collects data on prescription drugs. He said more than half of all atypical antipsychotic prescriptions written in 2008 were based on flimsy evidence. "We're talking millions of prescriptions a year for antipsychotics in settings where there is uncertain evidence to support them," said Alexander, whose study appears in the journal Pharmacoepidemiology and Drug Safety. The drugs are not harmless, Alexander said in a telephone interview. They can cause weight gain, diabetes and heart disease and are far more costly than the older antipsychotics, which cause disorders such as involuntary movements. Atypical antipsychotics accounted for more than $10 billion in U.S. retail pharmacy drug costs in 2008 — nearly 5 percent of all prescription drug spending. Copyright 2011 Thomson Reuters.
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 14849 - Posted: 01.10.2011
By Steven E. Hyman It can fairly be said that modern psychiatric diagnosis was “born” in a 1970 paper on schizophrenia. The authors, Washington University psychiatry professors Eli Robins and Samuel B. Guze, rejected the murky psychoanalytic diagnostic formulations of their time. Instead, they embraced a medical model inspired by the careful 19th-century observational work of Emil Kraepelin, long overlooked during the mid-20th-century dominance of Freudian theory. Mental disorders were now to be seen as distinct categories, much as different bacterial and viral infections produce characteristic diseases that can be seen as distinct “natural kinds.” Disorders, Robins and Guze argued, should be defined based on phenomenology: clinical descriptions validated by long-term follow-up to demonstrate the stability of the diagnosis over time. With scientific progress, they expected fuller validation of mental disorders to derive from laboratory findings and studies of familial transmission. This descriptive approach to psychiatric diagnosis -- based on lists of symptoms, their timing of onset, and the duration of illness -- undergirded the American Psychiatric Association’s widely disseminated and highly influential Diagnostic and Statistical Manual of Mental Disorders, first published in 1980. Since then, the original “DSM-III” has yielded two relatively conservative revisions, and right now, the DSM-5 is under construction. Sadly, it is clear that the optimistic predictions of Robins and Guze have not been realized. © 2010 Scientific American
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 14831 - Posted: 12.29.2010
by Paul Raeburn Lithium is as puzzling as it is potent. It was the first drug used to treat mental illness, and more than 50 years later, it is still one of the most widely used psychiatric medications. But the doctors who prescribe lithium to their patients still do not know how it works or even why it works. “It is the most mysterious drug in psychiatry,” says De-Maw Chuang, a biologist at the National Institute of Mental Health. “It’s so small, but it is so powerful.” Unlike other psychoactive chemicals—large, complex molecules like Prozac (fluoxetine) or Abilify (aripiprazole)—lithium is extremely simple. It is an element, the lightest of the metals, and its chemical properties are similar to those of the sodium in table salt. Nonetheless, researchers have recently found that lithium could be something close to a psychiatric wonder drug. It has two remarkable powers in the brains of mentally ill patients: protecting neurons from damage and death and alleviating existing damage by spurring new nerve cell growth. Far beyond its current application as a mood stabilizer, lithium could be helpful in treating or preventing Alzheimer’s disease, schizophrenia, stroke, glaucoma, Lou Gehrig’s disease (amyotrophic lateral sclerosis), and Huntington’s disease—an impressive tally that earned it the nickname “the aspirin of the brain” in the journal Nature. The mood-stabilizing powers of lithium were discovered by accident in the 1940s by John F. J. Cade, a lone psychiatrist working in Melbourne, Australia. Cade had noticed that some substance in the urine of patients with mania was particularly toxic and was investigating uric acid as the potential culprit. © 2010, Kalmbach Publishing Co.
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 14824 - Posted: 12.29.2010
Wendy Zukerman and David Cohen There's been a slight over-reaction in the media to the publication of a study exploring the fascinating effects of the drug ketamine on people's perception of reality. Most reports got bogged down in hyped outrage over paying students £250 to take part in the trial, and the side effects experienced by one participant. Paying participants is a common practice in scientific research and risks would have been weighed by an ethical review board. The side effects reported in a local Cambridgeshire newspaper seemed to have stirred things up, even though that report also admits it is not the first of its kind - at least two other studies involving ketamine were conducted at Cambridge over the last two years. But there's a far more interesting story here. Hannah Morgan at Cambridge University and Philip Corlett at Yale University, Connecticut, found that ketamine increased susceptibility to an illusion that makes people believe a rubber hand is their own. The finding illustrates how easily our sense of self can be manipulated, and could illuminate the underpinnings of schizophrenia - a condition where sufferers often believe actions, thoughts and even limbs are not their own. Over 10 years ago, researchers found that if they put a rubber hand on a table in front of a person and stroked the rubber hand and the person's hand simultaneously, they could convince the volunteer the rubber hand was their own. Subsequent research found that this rubber hand illusion (RHI) is more easily induced in schizophrenics than in healthy people. © Copyright Reed Business Information Ltd.
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 14809 - Posted: 12.22.2010
By Rachael Rettner In recent years, we've been bombarded with studies about the hormone oxytocin — researchers have demonstrated it increases trust and helps aid in social bonding. It has even garnered a reputation as the "love hormone." But what good is it for? Despite all these findings, the hormone's medical use remains limited to obstetrics — it is used to induce labor and aid in breastfeeding. But researchers are now trying to apply these findings, and are investigating oxytocin as a treatment for psychiatric illnesses. They say its unique ability to adjust our wiring could remedy symptoms of schizophrenia, post-traumatic stress disorder(PTSD) and anxiety, and improve social abilities among those with autism. A number of oxytocin studies have even reached the stage of clinical trials — which test the effectiveness and safety of a substance before it can become an approved drug — with promising findings. "The idea of augmenting … the way we connect to and with each other, would just be so helpful for so many people," said Dr. Kai MacDonald, an adjunct professor of psychiatry at the University of California, San Diego, who has studied oxytocin as a treatment for schizophrenia. However, the results so far, while hopeful, have not been "earthshaking," MacDonald said. There are hurdles to such research. Because oxytocin is a large molecule, it doesn't cross from the bloodstream into the brain very easily. It is also rapidly degraded in both the stomach and the blood. MyHealthNewsDaily Copyright © 2010.
Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 14741 - Posted: 12.06.2010




