Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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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
By ERIC R. KANDEL THESE days it is easy to get irritated with the exaggerated interpretations of brain imaging — for example, that a single fMRI scan can reveal our innermost feelings — and with inflated claims about our understanding of the biological basis of our higher mental processes. Such irritation has led a number of thoughtful people to declare that we can never achieve a truly sophisticated understanding of the biological foundation of complex mental activity. In fact, recent newspaper articles have argued that psychiatry is a “semi-science” whose practitioners cannot base their treatment of mental disorders on the same empirical evidence as physicians who treat disorders of the body can. The problem for many people is that we cannot point to the underlying biological bases of most psychiatric disorders. In fact, we are nowhere near understanding them as well as we understand disorders of the liver or the heart. But this is starting to change. Consider the biology of depression. We are beginning to discern the outlines of a complex neural circuit that becomes disordered in depressive illnesses. Helen Mayberg, at Emory University, and other scientists used brain-scanning techniques to identify several components of this circuit, two of which are particularly important. One is Area 25 (the subcallosal cingulate region), which mediates our unconscious and motor responses to emotional stress; the other is the right anterior insula, a region where self-awareness and interpersonal experience come together. These two regions connect to the hypothalamus, which plays a role in basic functions like sleep, appetite and libido, and to three other important regions of the brain: the amygdala, which evaluates emotional salience; the hippocampus, which is concerned with memory; and the prefrontal cortex, which is the seat of executive function and self-esteem. All of these regions can be disturbed in depressive illnesses. © 2013 The New York Times Company
By Brian Mossop A fine line separates creativity and madness. Bipolar disorder teeters along that line, with patients experiencing moments of impulsive thought, which can yield bold insights or quickly descend into confusion or rage. In her new book, Haldol and Hyacinths, Iranian-American author and activist Moezzi presents a captivating autobiographical account of her struggle with bipolar disorder. Using a series of vignettes, she reconstructs her downward spiral into psychosis, which eventually led to a suicide attempt and multiple stays in mental health facilities. From seemingly innocuous bouts of insomnia to full-blown hallucinations, Moezzi describes how she descended into madness. Moezzi's medical issues first emerged in her sophomore year of college, when she began to experience severe abdominal pain, later diagnosed as pancreatitis. Doctors decided to remove her pancreas to save her life and prevent a cyst from festering. Everyone she knew rallied alongside her during this time. Things were much different when Moezzi's bipolar disorder took hold in the years following her physical illness. She soon discovered that mental illness has no heroes, no celebrity spokesperson, no champions. Relying solely on the support of her immediate family and a devoted husband, Moezzi saw that the disorder carries a stigma, exacerbated by inaccurate media portrayals. Even worse is the plight of patients in places such as Moezzi's homeland of Iran, where mental illness is simply ignored. Despite bipolar disorder being the sixth leading cause of disability in the world, there is not even a word for the disease in Farsi. © 2013 Scientific American
Link ID: 18559 - Posted: 08.26.2013
Linda Carroll TODAY contributor Whether it’s “One Flew Over the Cuckoo’s Nest,” “Girl Interrupted,” or “Homeland,” Hollywood’s portrayals of electroconvulsive therapy have never been pretty. And the images from those movies and TV shows have only added to a stigma that keeps many desperate patients from opting for a therapy that might turn their lives around, experts say. “We can’t get past the stigma of all the visuals we’ve seen from movies and the fact that it seems so antiquated when you consider modern medicine,” NBC chief medical editor Dr. Nancy Snyderman told TODAY’s Matt Lauer. “But time and time and time again if you look at patients who have severe depression who don’t respond to medications, they will tell you that ECT works.” That’s certainly true in Denise Stewart’s case. Stewart, a mother of two, suffers from schizoaffective disorder. Her hallucinations were pushing her closer and closer to suicide each day. “There would be voices in my head that would sit there and say, ‘Denise, see the knife in the kitchen? Cut your wrists. Denise, see those pills over there? Take all those pills,’” she told TODAY. After antidepressants made Stewart’s condition worse, her doctors suggested ECT. And the change was dramatic. “If it hadn’t been for the electroconvulsive therapy, I wouldn’t be alive right now,” Stewart said. These days an estimated 100,000 Americans undergo ECT each year – and the process is a lot different from what you see in the media, experts say.
By RICHARD A. FRIEDMAN, M.D. Fully 1 in 5 Americans take at least one psychiatric medication. Yet when it comes to mental health, we are facing a crisis in drug innovation. Sure, we have many antidepressants, antipsychotics, hypnotic medications and the like. But their popularity masks two serious problems. First, each of these drug classes is filled with “me too” drugs, which are essentially just copies of one another; we have six S.S.R.I. antidepressants that essentially do the same thing, and likewise for the 10 new atypical antipsychotic drugs. Second, the available drugs leave a lot to be desired: patients with illnesses like schizophrenia, major depression and bipolar disorder often fail to respond adequately to these medications or cannot tolerate their side effects. Yet even though 25 percent of Americans suffer from a diagnosable mental illness in any year, there are few signs of innovation from the major drug makers. After a series of failed clinical trials in which novel antidepressants and antipsychotics did little or no better than placebos, the companies seem to have concluded that developing new psychiatric drugs is too risky and too expensive. This trend was obvious at the 2011 meeting of the American Society for Clinical Pharmacology and Therapeutics, where only 13 of 300 abstracts related to psychopharmacology and none related to novel drugs. Instead, they are spending most of their research dollars on illnesses like cancer, heart disease and diabetes, which have well-defined biological markers and are easier to study than mental disorders. © 2013 The New York Times Company
What if a psychiatrist could tell whether someone was about to commit suicide simply by taking a sample of their blood? That’s the promise of new research, which finds increased amounts of a particular protein in the bloodstream of those contemplating killing themselves. The test was conducted on only a few people, however, and given that such “biomarkers” often prove unreliable in the long run, it’s far from ready for clinical use. Suicide isn’t like a heart attack. People typically don’t reveal early symptoms to their doctor—morbid thoughts, for example, instead of chest pain—and there’s no equivalent of a cholesterol or high blood pressure test to identify those at most risk of killing themselves. "We are dealing with something more complex and less accessible," says Alexander Niculescu III, a psychiatrist at the Indiana University School of Medicine in Indianapolis. So some researchers are eager to find physical signs, called biomarkers, that can be measured in the bloodstream to signal when a person is at a high likelihood of committing suicide. Over the past decade, Niculescu and his colleagues have been refining a method for identifying biomarkers that can distinguish psychological states. The technique depends on blood samples taken from individuals in different mental states over time—for example, from people with bipolar disorder as they swing between the disorder’s characteristic high and low moods. The researchers test those samples for differences in the activity, or expression, of genes for of different proteins. After screening the blood samples, the scientists “score” a list of candidate biomarker genes by searching for related results in a large database of studies by other groups using a program that Niculescu compares to the Google page-ranking algorithm. In previous published studies, Niculescu and other groups have used the technique to probe for biomarkers in disorders such as bipolar disorder, psychosis, and alcoholism. © 2012 American Association for the Advancement of Science.
Link ID: 18530 - Posted: 08.20.2013
By Bruce Bower NEW YORK CITY — Psychiatrists regularly get criticized for turning typical life problems into medical disorders. But in an odd reversal, many mental health clinicians are trying to transform one certified mental illness, borderline personality disorder, into a label for needy, manipulative people who don’t need treatment, a sociologist reported at the American Sociological Association’s annual meeting on August 11. Patients with borderline personality disorder, unlike people with schizophrenia or other serious mental conditions, are often viewed by mental health providers as having cynically planned out rash acts and even suicide attempts, sociologist Sandra Sulzer of the University of North Carolina at Chapel Hill found in extensive interviews with 22 psychiatrists and psychologists in the United States. The condition includes difficulty controlling emotions, intense but unstable relationships, recklessness, cutting and other acts of self-harm, along with attempted and completed suicides. Before Sulzer’s study, little was known about how mental health professionals discuss and deal with this troubling set of symptoms. “Clinicians frequently view borderline personality disorder symptoms as signs of badness, not sickness, and as a code to route patients out of mental health care,” Sulzer said. That finding goes a long way toward explaining why many borderline personality disorder patients receive no treatment despite the availability of effective forms of psychotherapy (SN: 6/16/07, p. 374), she suggested. © Society for Science & the Public 2000 - 2013
Link ID: 18511 - Posted: 08.15.2013
By RONI CARYN RABIN Over the past two decades, the use of antidepressants has skyrocketed. One in 10 Americans now takes an antidepressant medication; among women in their 40s and 50s, the figure is one in four. Experts have offered numerous reasons. Depression is common, and economic struggles have added to our stress and anxiety. Television ads promote antidepressants, and insurance plans usually cover them, even while limiting talk therapy. But a recent study suggests another explanation: that the condition is being overdiagnosed on a remarkable scale. The study, published in April in the journal Psychotherapy and Psychosomatics, found that nearly two-thirds of a sample of more than 5,000 patients who had been given a diagnosis of depression within the previous 12 months did not meet the criteria for major depressive episode as described by the psychiatrists’ bible, the Diagnostic and Statistical Manual of Mental Disorders (or D.S.M.). The study is not the first to find that patients frequently get “false positive” diagnoses for depression. Several earlier review studies have reported that diagnostic accuracy is low in general practice offices, in large part because serious depression is so rare in that setting. Elderly patients were most likely to be misdiagnosed, the latest study found. Six out of seven patients age 65 and older who had been given a diagnosis of depression did not fit the criteria. More educated patients and those in poor health were less likely to receive an inaccurate diagnosis. Copyright 2013 The New York Times Company
Link ID: 18499 - Posted: 08.13.2013
By D. D. GUTTENPLAN LONDON — With its battered desks, fluorescent lights and interactive whiteboard showing an odd creature that, depending on how you look at it, could be either a duck or a rabbit, this could be a class in any university philosophy department. But this is a class with a difference. It is the Maudsley Philosophy Group, a seminar that meets regularly on the grounds of the Maudsley Hospital, Britain’s largest mental health teaching hospital, which is affiliated with the Institute of Psychiatry at King’s College London. Participants at the last session included psychiatrists, psychologists, philosophers and an actor who had just finished working as a chaplain in a locked men’s ward at the hospital and who was about to organize a storytelling group there. “We started out as a reading group for trainee psychiatrists,” said Gareth S. Owen, a researcher at the Institute of Psychiatry who co-founded the group in 2002. “Then, gradually, we developed and started inviting philosophers — at first it was quite low key. We would talk about our clinical experiences and then they would relate those experiences to their way of thinking.” Robert Harland, another co-founder of the group, said he had known Dr. Owen since they “cut up a corpse together at medical school.” “The analytic philosophers brought a real clarity to our discussions,” Dr. Harland said. “We were looking at various models to help us understand what we were doing as psychiatrists. “There is lots of applied science now in psychiatry: neuroimaging, genetics, epidemiology. But they don’t have much to say about sitting with a patient and trying to understand that person’s experiences.” © 2013 The New York Times Company
Some colors humans are exposed to late at night could cause symptoms of clinical depression. That is the conclusion of a study that builds on previous findings that individuals exposed to dim levels of light overnight, such as from a glowing television set, can develop signs of clinical depression. Investigators, curious as to whether the color of light contributed to depressive symptoms in humans, designed an experiment that exposed hamsters to different colors. They chose hamsters because they are nocturnal, meaning they sleep during the day and are active at night. One group of hamsters was kept in the dark during their nighttime period. Another group of rodents was exposed to blue light and a third group slept in the presence of white light. A fourth group of hamsters was exposed to glowing red light. After four weeks, researchers noted how much sugary water the hamsters drank. The more depressed rodents consumed the least amount of water. Randy Nelson, chair of Ohio State University’s Department of Neuroscience and co-author of the study, said animals that slept in blue and white light appeared to be the most depressed. “What we saw is these animals didn’t show any sleep disruptions at all but they did have mucked up circadian clock genes and they did show depressive phenotypes whereas if they were in the dim red light, they did not,” Nelson said. Nelson explained that photosensitive cells in the retina, which don’t have much to do with vision, detect light and transmit signals to the master circadian clock in the brain that controls the natural sleep-wake cycle.
By Fred Guterl Myths can be more harmful than lies, Nobel laureate Harry Kroto has said, because they are more difficult to recognize and often go unexamined. For many years, a diagnosis of schizophrenia was like a prison sentence, because many people (some of them in the medical profession) held to the notion that a schizophrenic could not recover from the illness and was condemned to an inexorable decline into madness. Like any myth, this one had some truth to it. Many people with severe symptoms do not recover. But some can, as Eleanor Longden discovered for herself. Longden began hearing voices when she was an undergraduate. At first they were somewhat benign, making mostly neutral, factual comments, but they grew more troublesome as she struggled to adjust to college life. Longden was diagnosed as schizophrenic and underwent conventional treatment. By her own account, in “Listening to Voices” in the September/October 2013 issue of Scientific American MIND, the label of schizophrenic and the attitudes of those around her to that label exacerbated her own internal struggles. The voices grew more menacing. Longden began her own slide into madness. But then something odd happened: she began to recover. She did so in part, she says, by accepting the voices in her head as an aspect of her own personality. She listened to them, and tried to understand them. In this way she was able to tame them, and she got enough control over her life to attend school and pursue her graduate studies. © 2013 Scientific American
Link ID: 18481 - Posted: 08.10.2013
by Nora Schultz A unique population in northern Finland has helped reveal that schizophrenia, some autism spectrum disorders and other forms of cognitive impairment may all share a common genetic pathway. In Finland, there exist several small communities that used to live for years in isolation. Amongst the descendants of these groups, otherwise rare genes occur more regularly than elsewhere in the country because a level of inbreeding was almost inevitable. Nelson Freimer at the University of California, Los Angeles, and colleagues studied one of these communities, where schizophrenia and other neurological disorders are unusually common. His team first searched for any genetic deletions – chunks of DNA that are missing from a chromosome – that were more common in this group than in the general population. They found a promising candidate on chromosome 22. A deletion on this chromosome was present in 18 of 173 people from this isolated group, but in just one of the 1586 samples taken from people spread throughout the rest of Finland. Tests confirmed that people with schizophrenia or cognitive impairments were more likely to be missing this chunk of DNA. Identifying this deletion as a risk factor for schizophrenia and cognitive impairment puts us one step closer to understanding the biological processes at the root of such complex syndromes, says Freimer. © Copyright Reed Business Information Ltd.
Women living in urban centres in Canada with more than 500,000 inhabitants are at higher risk of postpartum depression than women in other areas, suggests a new study in the Canadian Medical Association Journal. Looking at the experiences of over 6,000 women who lived in rural, semi-rural, semi-urban or urban areas from the 2006 Canadian Maternity Experiences Survey, the study suggests that women in urban areas were at higher risk, with almost 10 per cent reporting postpartum depression compared with six per cent of women in rural areas, almost seven per cent of women in semirural areas and about five per cent in semiurban areas. Urban areas were found to have higher numbers of immigrant populations, and more women in these areas reported lower levels of social support during and after pregnancy. "We found that Canadian women who lived in large urban areas … were at higher risk of postpartum depression than women living in other areas," said Dr. Simone Vigod, psychiatrist at Women's College Hospital and scientist at Women's College Research Institute in Toronto. "The risk factors for postpartum depression [including history of depression, social support and immigration status] that were unequally distributed across geographic regions accounted for most of the variance in the rates of postpartum depression." The reason why immigrant woman appear to be at higher risk is not really known, she said. "Some theories are that it's related to social support or being away from their family." They could also have cultural barriers or needs that are not being met, she added. © CBC 2013
By Scicurious Most current treatments for depression target the serotonin system, a chemical messenger that plays a role in mood (though it also plays a role in many, many other things). Most of the antidepressant drugs on the market (such as Prozac, Celexa, and Zoloft) that target serotonin do it by blocking the recycling of serotonin, keeping it in the spaces between neurons and allowing it to be active for far longer than it might otherwise. The problem is, these drugs take a long time to work. Often many weeks. In that time, patients may grow frustrated as side effects happen and the needed effects don’t. Patients may be in very desperate straights when they first go on medication, and any extra time before the drugs work becomes that much more dangerous. The drugs may not work at all, causing doctors and patients to have to go through the entire, weeks long process over and over again. Scientists are looking for new antidepressant mechanisms, and trying to create more effective drugs. But there are various ways to go about it. You can go looking for an entirely new way of working, but you can also look at ways to make the current drugs work faster. One target that might help antidepressant drugs work faster is one of the many receptors for serotonin, the 5-HT1A receptor. Receptors are proteins that sit on cell surfaces, and bind chemicals. When they bind a chemical, they cause change, maybe by opening a channel, or starting a signal to make a neuron fire more, or less. What a receptor does depends on its type, but also where in the brain it is located and on what type of cell. © 2013 Scientific American
Link ID: 18463 - Posted: 08.06.2013
By CHRISTINE MONTROSS PROVIDENCE, R.I. — M is a 33-year old woman who swallowed silverware. She wasn’t psychotic, or out of touch with reality. She knew it was not a good idea to swallow forks and knives and she wasn’t trying to kill herself. In fact, each time she ingested utensils, she went to the emergency room so that doctors could remove them from her esophagus and stomach. Then the hospital transferred M to the psychiatric unit, where she was assigned to my care. Enlarge This Image Robert Frank Hunter When I met M she had already been hospitalized 72 times. She’d swallowed silverware — and batteries — before. Sometimes she inserted sharp objects or large doses of medication into her vagina. There are psychiatric patients who cut or burn themselves in an attempt to relieve mental anguish; M did both of these things, too, periodically, but she had primarily developed a maladaptive habit of ingesting or inserting dangerous objects into her body as a means of coping with stress. Each time, she said, she felt better afterward. Then she brought herself to the emergency room for treatment. M’s case is dramatic. But she is one of countless psychiatric patients who have nowhere to turn for care, other than the E.R. It is well known that millions of uninsured Americans, who can’t afford regular medical care, use the country’s emergency rooms for primary health care. The costs — to patients’ health, to their wallets, and to the health care system — are well documented. Less visible is the grievous effect this shift is having on psychiatric care and on the mentally ill. © 2013 The New York Times Company
Link ID: 18457 - Posted: 08.05.2013
Steve Connor A gene thought to be involved in nerve development can double the risk of schizophrenia when it is damaged, according to a pioneering study into one of most costly mental illnesses. The findings are further evidence of a genetic basis for schizophrenia – which affects about one in every 100 people at some time of their lives – and could lead to a greater understanding of the physical faults that might lead to the psychiatric disorder in some susceptible people. The chronic, long-term illness, which results in persistent delusions and hallucinations, is estimated to cost the NHS about £2bn a year in care and treatment alone. But the extra burden on patients, their families and the criminal justice system is thought to be at least twice as high. Scientists said the genetic fault they have discovered is also associated with a separate inherited disorder that results in learning difficulties and autism. This link, they said, is probably the result of them sharing a common biological pathway at the genetic level. The gene linked to schizophrenia, called TOP3B, is normally involved in unwinding the DNA double helix to allow other genes to function, especially when the nerve cells of the brain are developing, both in the womb and during the crucial first years of life. © independent.co.uk
Researchers have reverse-engineered the outlines of a disrupted prenatal gene network in schizophrenia, by tracing spontaneous mutations to where and when they likely cause damage in the brain. Some people with the brain disorder may suffer from impaired birth of new neurons, or neurogenesis, in the front of their brain during prenatal development, suggests the study, which was funded by the National Institutes of Health. “Processes critical for the brain’s development can be revealed by the mutations that disrupt them,” explained Mary-Claire King, Ph.D. External Web Site Policy, University of Washington (UW), Seattle, a grantee of NIH’s National Institute of Mental Health (NIMH). “Mutations can lead to loss of integrity of a whole pathway, not just of a single gene. Our results implicate networked genes underlying a pathway responsible for orchestrating neurogenesis in the prefrontal cortex in schizophrenia.” King, and collaborators at UW and seven other research centers participating in the NIMH genetics repository, report on their discovery Aug. 1, 2013 in the journal Cell. “By linking genomic findings to functional measures, this approach gives us additional insight into how early development differs in the brain of someone who will eventually manifest the symptoms of psychosis,” said NIMH Director Thomas R. Insel, M.D. Earlier studies had linked spontaneous mutations to non-familial schizophrenia and traced them broadly to genes involved in brain development, but little was known about convergent effects on pathways.
By PAM BELLUCK For some people with severe mental illness, life is a cycle of hospitalization, skipped medication, decline and then rehospitalization. They may deny they have psychiatric disorders, refuse treatment and cascade into out-of-control behavior that can be threatening to themselves or others. Now, a study has found that a controversial program that orders these patients to receive treatment when they are not hospitalized has had positive results. Patients were much less likely to end up back in psychiatric hospitals and were arrested less often. Use of outpatient treatment significantly increased, as did refills of medication. Costs to the mental health system and Medicaid of caring for these patients dropped by half or more. The study evaluated the program run by New York State, known as Kendra’s Law because it was enacted after Kendra Webdale was pushed to her death on the New York City subway tracks by a man with untreated schizophrenia in 1999. Forty-four other states have some form of Kendra’s Law, but New York’s is by far the most developed because the state has invested significant resources into paying for it, experts say. From the start, Kendra’s Law has had staunch defenders and detractors. But the new analysis, led by researchers at Duke University and published in The American Journal of Psychiatry, joins a series of studies that suggest the program can be helpful for patients who, while they constitute only a small number of the people with mental illness, are some of the most difficult and expensive to care for. © 2013 The New York Times Company
By Simon Makin One common complaint about psychiatry is its subjective nature: it lacks definitive tests for many diseases. So the idea of diagnosing disorders using only brain scans holds great appeal. A paper published recently in PLOS ONE describes such a system, although it was presented only as an initial proof of concept. News reports, however, trumpeted the advent of “objective” psychiatric diagnoses. The paper used data from several earlier studies, in which researchers outlined key brain regions in MRI scans of people with bipolar disorder, ADHD, schizophrenia or Tourette's syndrome; people with low or high risk of developing major depressive disorder; and a healthy group. The scans were also labeled with the disorder or depression risk level of the original study participant. In the new study, scientists divided the scans randomly into two sets, one to build the diagnostic system and the other to test it. Their software then grouped the scans in the first set by the shape of various regions. Each group was labeled with the most common diagnosis found within it. During testing, the system analyzed the shapes of brain regions in each test scan and assigned it to the group it most resembled. The scientists checked its work by comparing the new labels on the test scans with the original clinical diagnoses. They repeated the procedure several times with different randomly generated sets. When the system chose between two disorders or one ailment and a clean bill of health, its accuracy was nearly perfect. When deciding among three alternatives, it did much worse. © 2013 Scientific American
Jaak Panksepp, the inventor of the term "affective neuroscience", is regarded as a radical in his field, with ground-breaking insights into emotional issues ranging from depression to playfulness. What makes him radical? First, his study of animal emotions, and his data-supported assertion that animals experience feelings as humans do. Using electrical stimulation of the brain, Panksepp has shown that all mammals have the same basic emotional system: i.e. underlying neural networks that are linked to feelings of raw emotion, and respond positively or negatively when aroused. For example, Panksepp has tickled rats to hear them 'laugh' ; in other species, he has conducted extensive experiments on what he calls "separation distress." Today's neuroscientists generally do not bother to consider the emotional life of animals, or put it on par with that of humans. But as Panksepp eloquently argues: "Animals do have emotional systems that generate feelings, even though hardly a neuroscientist yet acknowledges this fact." Second: Panksepp looks at what causes our feelings: the primary, instinctual networks in the brain that make them happen. Most neuroscientists, he confided in our phone conversation between Paris (where I teach) and Washington (where he teaches), look only at symptoms. "They are behaviorists. They follow the tradition of early psychologist William James, who looked at emotion as a mental after-effect, a cognitive read-out of autonomic bodily arousals, rather than as the brain system which drives us." He has been at odds with these behaviorists for most of his career, this despite the fact that Panksepp's major contributions to the field of emotion are now widely accepted, especially by psychotherapists treating patients for emotional concerns such as depression. © 2013 TheHuffingtonPost.com, Inc.