Posts tagged mental illness
Articles and news from the latest research reports.
Bipolar Disorder Discovery at the Nano Level
A nano-sized discovery by Northwestern Medicine® scientists helps explain how bipolar disorder affects the brain and could one day lead to new drug therapies to treat the mental illness.
Scientists used a new super-resolution imaging method — the same method recognized with the 2014 Nobel Prize in chemistry — to peer deep into brain tissue from mice with bipolar-like behaviors. In the synapses (where communication between brain cells occurs), they discovered tiny “nanodomain” structures with concentrated levels of ANK3 — the gene most strongly associated with bipolar disorder risk. ANK3 is coding for the protein ankyrin-G.
“We knew that ankyrin-G played an important role in bipolar disease, but we didn’t know how,” said Northwestern Medicine scientist Peter Penzes, corresponding author of the paper. “Through this imaging method we found the gene formed in nanodomain structures in the synapses, and we determined that these structures control or regulate the behavior of synapses.”
Penzes is a professor in physiology and psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine. The results were published Oct. 22 in the journal Neuron.
High-profile cases, including actress Catherine Zeta-Jones and politician Jesse Jackson, Jr., have brought attention to bipolar disorder. The illness causes unusual shifts in mood, energy, activity levels and the ability to carry out day-to-day tasks. About 3 percent of Americans experience bipolar disorder symptoms, and there is no cure.
Recent large-scale human genetic studies have shown that genes can contribute to disease risk along with stress and other environmental factors. However, how these risk genes affect the brain is not known.
This is the first time any psychiatric risk gene has been analyzed at such a detailed level of resolution. As explained in the paper, Penzes used the Nikon Structured Illumination Super-resolution Microscope to study a mouse model of bipolar disorder. The microscope realizes resolution of up to 115 nanometers. To put that size in perspective, a nanometer is one-tenth of a micron, and there are 25,400 microns in one inch. Very few of these microscopes exist worldwide.
“There is important information about genes and diseases that can only been seen at this level of resolution,” Penzes said. “We provide a neurobiological explanation of the function of the leading risk gene, and this might provide insight into the abnormalities in bipolar disorder.”
The biological framework presented in this paper could be used in human studies of bipolar disorder in the future, with the goal of developing therapeutic approaches to target these genes.
(Source: northwestern.edu)
Schizophrenia not a single disease but multiple genetically distinct disorders
New research shows that schizophrenia isn’t a single disease but a group of eight genetically distinct disorders, each with its own set of symptoms. The finding could be a first step toward improved diagnosis and treatment for the debilitating psychiatric illness.
The research at Washington University School of Medicine in St. Louis is reported online Sept. 15 in The American Journal of Psychiatry.
About 80 percent of the risk for schizophrenia is known to be inherited, but scientists have struggled to identify specific genes for the condition. Now, in a novel approach analyzing genetic influences on more than 4,000 people with schizophrenia, the research team has identified distinct gene clusters that contribute to eight different classes of schizophrenia.
“Genes don’t operate by themselves,” said C. Robert Cloninger, MD, PhD, one of the study’s senior investigators. “They function in concert much like an orchestra, and to understand how they’re working, you have to know not just who the members of the orchestra are but how they interact.”
Cloninger, the Wallace Renard Professor of Psychiatry and Genetics, and his colleagues matched precise DNA variations in people with and without schizophrenia to symptoms in individual patients. In all, the researchers analyzed nearly 700,000 sites within the genome where a single unit of DNA is changed, often referred to as a single nucleotide polymorphism (SNP). They looked at SNPs in 4,200 people with schizophrenia and 3,800 healthy controls, learning how individual genetic variations interacted with each other to produce the illness.
In some patients with hallucinations or delusions, for example, the researchers matched distinct genetic features to patients’ symptoms, demonstrating that specific genetic variations interacted to create a 95 percent certainty of schizophrenia. In another group, they found that disorganized speech and behavior were specifically associated with a set of DNA variations that carried a 100 percent risk of schizophrenia.
“What we’ve done here, after a decade of frustration in the field of psychiatric genetics, is identify the way genes interact with each other, how the ‘orchestra’ is either harmonious and leads to health, or disorganized in ways that lead to distinct classes of schizophrenia,” Cloninger said.
Although individual genes have only weak and inconsistent associations with schizophrenia, groups of interacting gene clusters create an extremely high and consistent risk of illness, on the order of 70 to 100 percent. That makes it almost impossible for people with those genetic variations to avoid the condition. In all, the researchers identified 42 clusters of genetic variations that dramatically increased the risk of schizophrenia.
“In the past, scientists had been looking for associations between individual genes and schizophrenia,” explained Dragan Svrakic, PhD, MD, a co-investigator and a professor of psychiatry at Washington University. “When one study would identify an association, no one else could replicate it. What was missing was the idea that these genes don’t act independently. They work in concert to disrupt the brain’s structure and function, and that results in the illness.”
Svrakic said it was only when the research team was able to organize the genetic variations and the patients’ symptoms into groups that they could see that particular clusters of DNA variations acted together to cause specific types of symptoms.
Then they divided patients according to the type and severity of their symptoms, such as different types of hallucinations or delusions, and other symptoms, such as lack of initiative, problems organizing thoughts or a lack of connection between emotions and thoughts. The results indicated that those symptom profiles describe eight qualitatively distinct disorders based on underlying genetic conditions.
The investigators also replicated their findings in two additional DNA databases of people with schizophrenia, an indicator that identifying the gene variations that are working together is a valid avenue to explore for improving diagnosis and treatment.
By identifying groups of genetic variations and matching them to symptoms in individual patients, it soon may be possible to target treatments to specific pathways that cause problems, according to co-investigator Igor Zwir, PhD, research associate in psychiatry at Washington University and associate professor in the Department of Computer Science and Artificial Intelligence at the University of Granada, Spain.
And Cloninger added it may be possible to use the same approach to better understand how genes work together to cause other common but complex disorders.
“People have been looking at genes to get a better handle on heart disease, hypertension and diabetes, and it’s been a real disappointment,” he said. “Most of the variability in the severity of disease has not been explained, but we were able to find that different sets of genetic variations were leading to distinct clinical syndromes. So I think this really could change the way people approach understanding the causes of complex diseases.”
(Source: news.wustl.edu)
Mind and body: Scientists identify immune system link to mental illness
Children with high everyday levels of a protein released into the blood in response to infection are at greater risk of developing depression and psychosis in adulthood, according to new research which suggests a role for the immune system in mental illness.
The study, published today in JAMA Psychiatry, indicates that mental illness and chronic physical illness such as coronary heart disease and type 2 diabetes may share common biological mechanisms.
When we are exposed to an infection, for example influenza or a stomach bug, our immune system fights back to control and remove the infection. During this process, immune cells flood the blood stream with proteins such as interleukin-6 (IL-6), a tell-tale marker of infection. However, even when we are healthy, our bodies carry trace levels of these proteins – known as ‘inflammatory markers’ – which rise exponentially in response to infection.
Now, researchers have carried out the first ever longitudinal study – a study that follows the same cohort of people over a long period of time – to examine the link between these markers in childhood and subsequent mental illness.
A team of scientists led by the University of Cambridge studied a sample of 4,500 individuals from the Avon Longitudinal Study of Parents and Children – also known as Children of the 90s – taking blood samples at age 9 and following up at age 18 to see if they had experienced episodes of depression or psychosis. The team divided the individuals into three groups, depending on whether their everyday levels of IL-6 were low, medium or high. They found that those children in the ‘high’ group were nearly two times more likely to have experienced depression or psychosis than those in the ‘low’ group.
Dr Golam Khandaker from the Department of Psychiatry at the University of Cambridge, who led the study, says: “Our immune system acts like a thermostat, turned down low most of the time, but cranked up when we have an infection. In some people, the thermostat is always set slightly higher, behaving as if they have a persistent low level infection – these people appear to be at a higher risk of developing depression and psychosis. It’s too early to say whether this association is causal, and we are carrying out additional studies to examine this association further.”
The research indicates that chronic physical illness such as coronary heart disease and type 2 diabetes may share a common mechanism with mental illness. People with depression and schizophrenia are known to have a much higher risk of developing heart disease and diabetes, and elevated levels of IL-6 have previously been shown to increase the risk of heart disease and type 2 diabetes.
Professor Peter Jones, Head of the Department of Psychiatry and senior author of the study, says: “Inflammation may be a common mechanism that influences both our physical and mental health. It is possible that early life adversity and stress lead to persistent increase in levels of IL-6 and other inflammatory markers in our body, which, in turn, increase the risk of a number of chronic physical and mental illness.”
Indeed, low birth weight, a marker of impaired foetal development, is associated with increased everyday levels of inflammatory markers as well as greater risks of heart disease, diabetes, depression and schizophrenia in adults.
This potential common mechanism could help explain why physical exercise and diet, classic ways of reducing risk of heart disease, for example, are also thought to improve mood and help depression. The group is now planning additional studies to confirm whether inflammation is a common link between chronic physical and mental illness.
The research also hints at interesting ways of potentially treating illnesses such as depression: anti-inflammatory drugs. Treatment with anti-inflammatory agents leads to levels of inflammatory markers falling to normal. Previous research has suggested that anti-inflammatory drugs such as aspirin used in conjunction with antipsychotic treatments may be more effective than just the antipsychotics themselves. A multicentre trial is currently underway, into whether the antibiotic minocycline, used for the treatment of acne, can be used to treat lack of enjoyment, social withdrawal, apathy and other so called negative symptoms in schizophrenia. Minocycline is able to penetrate the ‘blood-brain barrier’, a highly selective permeability barrier which protects the central nervous system from potentially harmful substances circulating in our blood.
The ‘blood-brain barrier’ is also at the centre of a potential puzzle raised by research such as today’s research: how can the immune system have an effect in the brain when many inflammatory markers and antibodies cannot penetrate this barrier? Studies in mice suggest that the answer may lie in the vagus nerve, which connects the brain to the abdomen. When activated by inflammatory markers in the gut, it sends a signal to the brain, where immune cells produce proteins such as IL-6, leading to increased metabolism (and hence decreased levels) of the ‘happiness hormone’ serotonin in the brain. Similarly, the signals trigger an increase in toxic chemicals such as nitric oxide, quinolonic acid, and kynurenic acid, which are bad for the functioning of nerve cells.
Discovery of new pathways controlling the serotonergic system
With the aid of new methods, a research team at Karolinska Institutet have developed a detailed map of the networks of the brain that control the neurotransmitter serotonin. The study, published in the scientific journal Neuron, may lead to new knowledge on a number of psychiatric conditions and the development of new pharmaceuticals.
The neurotransmitter serotonin controls impulsivity, mood and our cognitive functions, among other things, and comes from the serotonergic neurons – the neurons that produce serotonin. So that we have good mental health and normal behaviour, it is important that there is correctly regulated activity among these neurons. The activity is governed by other neurons from different regions of the brain via direct links, known as synapses, on the serotonergic neurons. Imbalance in the serotonergic system can lead to depression, Parkinson’s disease, schizophrenia and autism, among other things.
So far it has been impossible to study in detail how different types of nerve cells are interlinked and how the brain’s networks control behaviour. Consequently, there has also been a lack of knowledge of which nerve cells control the activity of the serotonergic neurons. But with the help of new methods, researchers at Karolinska Institutet can now investigate how the various networks of the brain are organised and how they work. The research team, led by Konstantinos Meletis of the Department of Neuroscience, has established which networks of the brain control the serotonergic neurons.
“We have been able to create a new type of map of the neurons’ contacts and discovered new pathways that control the serotonergic system. These networks were previously unknown and are very interesting in terms of how they help us to understand how the serotonergic system works, which could also help us to understand certain mental illnesses,” Konstantinos Meletis explains.
In order to map out which neurons have direct contact with serotonergic neurons, the researchers established a method in which these cells were marked with a rabies virus which produced a fluorescent marker. Via genetic manipulation, the rabies virus was then spread to all of the neurons directly linked to the serotonergic neurons. The researchers thereby gained a very detailed, three-dimensional image of the networks of the brain that control serotonin. Using optogenetics, a method in which light is used to control the activity of neurons, the researchers were then able to manipulate select networks and thus study their effect on the serotonergic neurons.
Via mapping, the researchers discovered a network in the frontal lobe which is associated with cognition and well-being and which controls the serotonergic neurons. Researchers also found that serotonin can be controlled from new types of neurons in the basal ganglia, an area of the cerebrum which among other things controls movement, well-being and decision-making; a discovery which may have significance for conditions such as Parkinson’s disease.
“We are very optimistic that the revolution we are now seeing in brain research could also lead to entirely new and effective medicine in the field of psychiatry,” Konstantinos Meletis explains.
Working to Loosen the Grip of Severe Mental Illness
A neuroscientist at Rutgers University-Newark says the human brain operates much the same whether active or at rest – a finding that could provide a better understanding of schizophrenia, bipolar disorder and other serious mental health conditions that afflict an estimated 13.6 million Americans.
In newly published research in the journal Neuron, Michael Cole, an assistant professor at the Center for Molecular and Behavioral Neuroscience, determined that the underlying brain architecture of a person at rest is basically the same as that of a person performing a variety of tasks.
This is important to the study of mental illness because it is easier to analyze a brain at rest, says Cole, who made the discovery using functional magnetic resonance imaging (fMRI).
“We can now observe people relaxing in the scanner and be confident that what we see is there all the time,” says Cole, who initially feared his team might find that the brain reorganizes itself for every task. “If that had been the case, we would have had less hope that we could understand mental illness in our lifetime.”
Instead, Cole says, scientists can now make their search for causes of mental illness more focused – and he suggests at least one target of opportunity. The prefrontal cortex is a portion of the brain involved in high level thinking, as well as remembering what a person’s goal is and the task being performed.
Cole says it would be useful to explore whether connectivity between the prefrontal cortex and other areas of the brain is altered – while the brain is at rest – in people with severe mental illness. “And then we can finally say something fundamental,” he predicts, “about what’s different about the brain’s functional network in schizophrenia and other conditions.”
Those differences, in turn, could explain certain symptoms. For instance, what if a patient has visual hallucinations because poor connectivity between the prefrontal cortex and the portion of the brain that governs sight causes the hallucinations to override what the eyes actually see? Cole suggests that’s just one of the questions that analysis of the brain at rest might help to answer. Others include a person’s debilitating beliefs, such as overly negative self-assessment when depressed.
Opportunities to find better ways to improve patients’ lives might then follow. Cole notes that current medications for severe mental illness, when they help at all, typically do not relieve cognitive symptoms. It is possible the drugs will reduce hallucinations or depressing thoughts, but patients continue to have difficulty concentrating on the task at hand, and often find it hard to find or hold a job. Cole says that even solving that one issue would be a major step forward – and he hopes his new work has helped advance science toward achieving this goal.
(Source: news.rutgers.edu)
Sleep deprivation leads to symptoms of schizophrenia
Psychologists at the University of Bonn are amazed by the severe deficits caused by a sleepless night
Twenty-four hours of sleep deprivation can lead to conditions in healthy persons similar to the symptoms of schizophrenia. This discovery was made by an international team of researchers under the guidance of the University of Bonn and King’s College London. The scientists point out that this effect should be investigated more closely in persons who have to work at night. In addition, sleep deprivation may serve as a model system for the development of drugs to treat psychosis. The results have now been published in “The Journal of Neuroscience”.
In psychosis, there is a loss of contact with reality and this is associated with hallucinations and delusions. The chronic form is referred to as schizophrenia, which likewise involves thought disorders and misperceptions. Affected persons report that they hear voices, for example. Psychoses rank among the most severe mental illnesses. An international team of researchers under the guidance of the University of Bonn has now found out that after 24 hours of sleep deprivation in healthy patients, numerous symptoms were noted which are otherwise typically attributed to psychosis or schizophrenia. “It was clear to us that a sleepless night leads to impairment in the ability to concentrate,” says Prof. Dr. Ulrich Ettinger of the Cognitive Psychology Unit in the Department of Psychology at the University of Bonn. “But we were surprised at how pronounced and how wide the spectrum of schizophrenia-like symptoms was.”
The scientists from the University of Bonn, King’s College London (England) as well as the Department of Psychiatry and Psychotherapy of the University of Bonn Hospital examined a total of 24 healthy subjects of both genders aged 18 to 40 in the sleep laboratory of the Department of Psychology. In an initial run, the test subjects were to sleep normally in the laboratory. About one week later, they were kept awake all night with movies, conversation, games and brief walks. On the following morning, subjects were each asked about their thoughts and feelings. In addition, subjects underwent a measurement known as prepulse inhibition.
Unselected information leads to chaos in the brain
"Prepulse inhibition is a standard test to measure the filtering function of the brain,” explains lead author Dr. Nadine Petrovsky from Prof. Ettinger’s team. In the experiment, a loud noise is heard via headphones. As a result, the test subjects experience a startle response, which is recorded with electrodes through the contraction of facial muscles. If a weaker stimulus is emitted beforehand as a “prepulse”, the startle response is lower. “The prepulse inhibition demonstrates an important function of the brain: Filters separate what is important from what is not important and prevent sensory overload,” says Dr. Petrovsky.
In our subjects, this filtering function of the brain was significantly reduced following a sleepless night. “There were pronounced attention deficits, such as what typically occurs in the case of schizophrenia,” reports Prof. Ettinger. “The unselected flood of information led to chaos in the brain.” Following sleep deprivation, the subjects also indicated in questionnaires that they were somewhat more sensitive to light, color or brightness. Accordingly, their sense of time and sense of smell were altered and mental leaps were reported. Many of those who spent the night even had the impression of being able to read thoughts or notice altered body perception. “We did not expect that the symptoms could be so pronounced after one night spent awake,” says the psychologist from the University of Bonn.
Sleep deprivation as a model system for mental illnesses
The scientists see an important potential application for their results in research for drugs to treat psychoses. “In drug development, mental disorders like these have been simulated to date in experiments using certain active substances. However, these convey the symptoms of psychoses in only a very limited manner,” says Prof. Ettinger. Sleep deprivation may be a much better model system because the subjective symptoms and the objectively measured filter disorder are far more akin to mental illnesses. Of course, the sleep deprivation model is not harmful: After a good night’s recovery sleep, the symptoms disappear. There is also a need for research with regard to persons who regularly have to work at night. “Whether the symptoms of sleep deprivation gradually become weaker due to acclimatization has yet to be investigated,” says the psychologist from the University of Bonn.
(Image: Getty)
How the brain processes visual information
MSU’s Behrad Noudoost was a co-author with Marc Zirnsak and other neuroscientists from the Tirin Moore Lab at Stanford University in publishing a recent paper on the research in Nature, an international weekly journal for natural sciences.
Noudoost and the team studied saccadic eye movements—those movements where the eye jumps from one point of focus to another—in an effort to determine exactly how this happens without us being overcome by our brains processing too much visual information.
To introduce the study, Noudoost first gets his audience to think about eye movements at the most basic level. “Look in the mirror and stare at one eye,” Noudoost said. “Then look at the other eye. We are essentially blind during eye movement as we cannot see our eyes move, even though we know they did.”
According to Noudoost, scientists have been trying to learn exactly how the brain processes these visual stimuli during saccadic eye movement and this research offers new evidence that the prefrontal cortex of the brain is responsible for visual stability.
"Visual stability is what keeps our vision stable in spite of changing input. It is similar to the stabilizer button on a video camera," Noudoost said.
"We wanted to know what causes the brain to filter out un-necessary information when we shift our vision from one focal target to another," Noudoost said. "Without that filter the visual information would overwhelm us."
According to the scientists, the study offers evidence neurons in the prefrontal cortex of the brain start processing information in anticipation of where we are going to look before we ever do it, suggesting that selective processing might be the mechanism for visual stability.
Noudoost said this new information can help scientists better understand the underlying causes of problems such as dyslexia and attention deficit disorders.
According to Frances Lefcort, the head of the Department of Cell Biology and Neuroscience, the team’s basic research may have implications for understanding a myriad of mental health issues.
"Schizophrenia and attention deficit disorders have been linked to visual stability, so the work Behrad is doing offers valuable knowledge to other scientists working in cognitive neuroscience," Lefcort said.
"Understanding how a healthy brain works is important in terms of knowing its impact on cognitive functions such as memory, learning and in this case attention," Noudoost said. "By exploring normal brain function, we can better understand what happens in someone with a mental illness."
According to Lefcort, Noudoost and neuroscience professor Charles Gray are strengthening MSU’s contribution to the field of cognitive neuroscience.
"Behrad is an exquisitely trained neuroscientist. He offers students a viewpoint as both scientist and a physician," Lefcort said. "We are thrilled to have him and he has already brought new energy and is bolstering our impact on the growing field of brain research."
Noudoost joined MSU’s Department of Cell Biology and Neuroscience last summer from Stanford University and has already been awarded a $225,000 Whitehall Foundation grant for neuroscience. Whitehall Foundation grants are awarded to established scientists working in neurobiology.
"I am colorblind and I wanted to see the world as others could see it," Noudoost said explaining why he was first drawn into this type of research. "Although I still don’t see the world in the same colors as everyone else, I am more amazed everyday by the brain."
Attention deficits are central to psychiatric disorders such as schizophrenia or bipolar disorder, and are thought to precede the presentation of the illnesses. A new study led by Wayne State University School of Medicine researcher Vaibhav Diwadkar, Ph.D. suggests that the brain network interactions between regions that support attention are dysfunctional in children and adolescents at genetic risk for developing schizophrenia and bipolar disorder.
The brain network mechanisms that mediate these deficits are poorly understood, and have rarely been tackled using complex image analytic methods that focus on how brain regions communicate, said Dr. Diwadkar, associate professor of psychiatry and behavioral neurosciences and co-director of the departments Brain Imaging Research Division
The desire to understand dysfunctional brain mechanisms motivated Dr. Diwadkar and his team of colleagues and WSU medical students in the study titled, “Dysfunction and dysconnection in cortical-striatal networks during sustained attention: genetic risk for schizophrenia or bipolar disorder and its impact on brain network function, featured in the May issue of Frontiers in Psychiatry.
The study is clinically significant because the estimated lifetime incidence of schizophrenia or bipolar disorder in the groups studied is approximately 10-20 times what is generally observed. We believe that genetic risk may confer vulnerability for dysfunctional brain network communication. This abnormal network communication in turn might amplify risk for psychiatric illnesses. By identifying markers of network dysfunction we believe we can elucidate these mechanisms of risk. This knowledge may in turn increase focus on possible premeditative intervention strategies, Dr. Diwadkar said.
The researchers identified dysfunctional brain mechanisms of sustained attention using functional Magnetic Resonance Imaging data and complex modeling of fMRI signals. Data were collected in 46 children and adolescents ages 8 to 20, half at genetic risk for schizophrenia or bipolar disorder by virtue of having one or both parents with either illness. During the 20-minute fMRI, participants completed a sustained attention task, adapted to engage specific brain regions.
The researchers induced variations in the degree of demand on these brain regions a method of assessing how genetic risk might impair the brains ability to respond to attention challenges by varying task difficulty. Increased attention demand led to increased engagement in the typical control group. The genetically at-risk group did not respond the same. Instead, interactions between the dorsal anterior cingulate, a principal control region in the brain, and the basal ganglia were highly dysfunctional in that group, suggesting impaired communication between specific brain networks.
The study indicates that brain networks supporting basic psychological functions such as attention do not communicate appropriately in young individuals at genetic risk for illnesses such as schizophrenia or bipolar disorder.
Genetics and neurodevelopment are inextricably linked. How psychiatric illnesses emerge from their combination is a central question in medicine. Analytic tools developed in the last few years offer the promise of answers at the level of how these processes impact brain network communication, Dr. Diwadkar said.
Study shows increasing rates of premature death and violent crime in people with schizophrenia since 1970s
New research, published in The Lancet Psychiatry journal, shows that rates of adverse outcomes, including premature death and violent crime, in people with schizophrenia are increasing, compared to the general population.
The results come from a unique study, led by Dr Seena Fazel, at Oxford University, UK, which analyses long-term adverse outcomes – including conviction for a violent crime (such as homicide or bodily harm) premature death (before the age of 56), and death by suicide – between 1972 and 2009 in nearly 25,000 people in Sweden diagnosed with schizophrenia or related disorders.
For the first time, the researchers compared adverse outcomes in people with a diagnosis of schizophrenia to both the general population and to unaffected siblings, allowing them to account for risk factors within families (such as parental criminality or violence) which might be expected to affect the risk of suicide or violent behaviour in siblings.
Overall, the results show that within five years of diagnosis, around 1 in 50 men and women with schizophrenia (2.3% of men and 1.7% of women) died by suicide; around one in 10 (10.7%) of men and around one in 37 (2.7%) of women with schizophrenia were convicted of a violent offence within five years of diagnosis. Overall, men and women with schizophrenia were eight times more likely to die prematurely than the general population.
Analysing the changing rate of adverse outcomes across the study period (1972 – 2009), the researchers found that the risk of premature death, suicide, and conviction for a violent offence has increased for men and women with schizophrenia in the last 38 years, compared with both the general population, and their unaffected siblings.
By tracking the number of nights spent in hospital by people with schizophrenia during the study period, the study shows that these increased rates of adverse outcomes appear to be associated with decreasing levels of inpatient care for these patients, although the study does not provide any evidence for a causal connection between decreasing inpatient care and adverse outcomes.
The researchers also analysed risk factors for adverse outcomes in both people with schizophrenia, the general population, and unaffected siblings. Across all three groups, the risk factors for violence and premature death were broadly similar, and included drug use disorders, criminality, and self-harm, all before diagnosis – suggesting that improved strategies to address these risk factors have the potential to reduce violence and premature deaths across the population, and not just in those with schizophrenia.
According to Dr Fazel, “In recent years, there has been a lot of focus on primary prevention of schizophrenia – preventing people from getting ill. While primary prevention is clearly essential and may be some decades away, our study highlights the crucial importance of secondary prevention – treating and managing the risks of adverse outcomes, such as self-harm or violent behaviour, in patients. Risks of these adverse outcomes relative to others in society appear to be increasing in recent decades, suggesting that there is still much work to be done in developing new treatments and mitigating risks of adverse outcomes in people with schizophrenia.”*
Dr Eric Elbogen and Sally Johnson, at the University of North Carolina-Chapel Hill School of Medicine, USA, write in a linked Comment that, “One of the unique aspects of this study—that violence and suicide were analysed simultaneously—has an important implication for how we as a society perceive people with mental illness. News coverage of schizophrenia and other psychiatric disorders often focuses on violence and crime. Much less attention is paid to suicide and self-harm in people with severe mental illnesses.”
However, they add that, “Importantly, we should remember that, when reporting about the intricate links between schizophrenia and these adverse outcomes, most people with schizophrenia and related disorders are neither violent nor suicidal. Despite the need to ensure people with schizophrenia are provided help to reduce their risks of suicide, violence, or premature death, researchers reporting findings also bear the burden of ensuring that most people with schizophrenia and related disorders, who are not violent, are not left to contend with stigma and discrimination. Policy makers, researchers, and clinicians need to remember the importance of appropriately weighing up the issue of schizophrenia relative to the myriad of other factors that contribute to increased risk of violence and suicide.”
(Source: alphagalileo.org)
Antipsychotic medication during pregnancy does affect babies
A seven-year study of women who take antipsychotic medication while pregnant, proves it can affect babies.
The observational study, published in the journal PLOS ONE, reveals that whilst most women gave birth to healthy babies, the use of mood stabilisers or higher doses of antipsychotics during pregnancy increased the need for special care after birth with 43 per cent of babies placed in a Special Care Nursery (SCN) or a Neonatal Intensive Care Unit (NICU), almost three times the national rate in Australia.
As well as an increased likelihood of the need for intensive care, the world-first study by experts from the Monash Alfred Psychiatry Research Centre (MAPrc) and Monash University, shows antipsychotic drugs affects babies in other ways; 18 per cent were born prematurely, 37 per cent showed signs of respiratory distress and 15 per cent developed withdrawal symptoms.
Principal investigator, Professor Jayashri Kulkarni, Director of MAPrc, said the study highlights the need for clearer health guidelines when antipsychotic drugs are taken during pregnancy.
“There’s been little research on antipsychotic medication during pregnancy and if it affects babies. The lack of data has made it very difficult for clinicians to say anything conclusively on how safe it is for babies,” Professor Kulkarni said.
“This new research confirms that most babies are born healthy, but many experience neonatal problems such as respiratory distress.”
With no existing data to draw on, MAPrc established the world-first National Register of Antipsychotic Medications in Pregnancy (NRAMP) in 2005. Women who were pregnant and taking antipsychotic medication were recruited from around Australia through clinical networks in each state and territory. In all 147 women were interviewed every six weeks during pregnancy and then followed until their babies were one year old.
Antipsychotic drugs are currently used to treat a range of psychiatric disorders including schizophrenia, major depression and bipolar disorder. About 20 per cent of Australian women experience depression in their lifetime, compared to 10 per cent of men. In Australia 25 per cent of women experience postnatal depression and 20 per cent experience severe menopausal depression.
Women have much higher rates of anxiety disorders and there are equal percentages of men and women with schizophrenia (2 per cent) and bipolar disorder (about 3 per cent).
Professor Kulkarni said the emergence of new antipsychotic drugs means that many women with a well controlled psychiatric disorder are able to contemplate having babies, but there have always been concerns about the effect of treatment on their offspring.
“The potentially harmful effects of taking an antipsychotic drug in pregnancy have to be balanced against the harm of untreated psychotic illness. The good news is we now know there are no clear associations with specific congenital abnormalities and these drugs,” Professor Kulkarni said.
“However clinicians should be particularly mindful of neonatal problems such as respiratory distress, so it’s critical that Neonatal Intensive Care Units, or Special Care Nurseries are available for these babies.”
(Source: monash.edu)