Pioneering Study Demonstrates Benefit of Imaging Technique in Identifying Mental Illness

MRI may be an effective way to diagnose mental illnesses such as bipolar disorder, according to experts from the Icahn School of Medicine at Mount Sinai. In a landmark study using advanced techniques, the researchers were able to correctly distinguish bipolar patients from healthy individuals based on their brain scans alone. The data are published in the journal Psychological Medicine.

Currently, most mental illnesses are diagnosed based on symptoms only, creating an urgent need for new approaches to diagnosis. In bipolar disorder, there may be a significant delay in diagnosis due to the complex clinical presentation of the illness. In this study, Sophia Frangou, MD, Professor of Psychiatry and Chief of the Psychosis Research Program at the Icahn School of Medicine at Mount Sinai teamed up with Andy Simmons, MD, of the Kings College London and Janaina Mourao-Miranda, MD, of University College London, to explore whether brain imaging could help correctly identify patients with bipolar disorder.

“Bipolar disorder affects patients’ ability to regulate their emotions successfully, which puts them at great disadvantage in their lives,” said Dr. Frangou. “The situation is made worse by unacceptably long delays, sometimes of up to 10 years, in making the correct diagnosis. Bipolar disorder may be easily misdiagnosed for other disorders, such as depression or schizophrenia. This is why bipolar disorder ranks among the top ten disorders causing significant disability worldwide.”

Dr. Frangou and her team used MRI to scan the brains of people with bipolar disorder and of healthy individuals. Using advanced computational models, they were successful in correctly separating people with bipolar disorder from healthy individuals with 73 percent accuracy using their brain imaging scans alone. They replicated their finding in a separate group of patients and healthy individuals and found a 72 percent accuracy rate.

Dr. Simmons added, “The level of accuracy we achieved is comparable to that of many other tests used in medicine. Additionally, brain scanning is very acceptable to patients as most people consider it a routine diagnostic test.”

“This approach does not undermine the importance of rigorous clinical assessment and the importance of building relationships with patients but provides biological justification for the type of diagnosis made,” said Dr. Frangou. “However, diagnostic imaging for psychiatry is still under investigation and not ready for widespread use. Nonetheless, our results together with those from other labs are a harbinger of a major shift in the way we approach diagnosis in psychiatry.”

N.C. Coal Plant Emissions Might Play Role in State Suicide Numbers

New research from Wake Forest Baptist Medical Center finds that suicide, while strongly associated with psychiatric conditions, also correlates with environmental pollution.

Lead researcher John G. Spangler, M.D., M.P.H., a professor of family medicine at Wake Forest Baptist, looked specifically at the relationship between air pollution and emissions from coal-fired electricity plants.

"This study raises interesting questions about suicide rates in counties where coal-fired electrical plants operate and suggests that the quality of air can affect people suffering from different mood disorders," Spangler said.

For this ecological study, Spangler evaluated air level contaminates in 20 North Carolina counties where coal-fired electricity plants existed, using data from the 2000 U.S. Census, 2001-2005 mortality rates from the N.C. State Center for Health Statistics and the U.S. Environmental Protection Agency.  

County-level suicide rates were higher overall in North Carolina (12.4 per 100,000 population) compared to the U.S. population (10.8 per 100,000). The study found that for each additional coal-fired electricity plant per N.C. county, there were about two additional suicides per 100,000 population annually per county. As there were 20 coal-fired electricity plants in North Carolina when this study was carried out, that means there were about 40 suicides a year per 100,000 population related to the plants. When applied to the state’s year 2,000 population of 8,049,313, this equals about 3,220 suicides a year associated with coal-fired electricity plants.

The study is published in the most recent online edition of the Journal of Mood Disorders.

"The presence of a coal-fired electricity plant correlated with airborne levels of nickel, mercury, lead, chromium, cadmium, beryllium and arsenic," Spangler said.

While prior research has evaluated the association between environmental contamination and mood disorders and suicide, coal emissions have not been looked at in this fashion, Spangler said. “This is the first study to show that the existence of coal-fired electricity plants is related to population-level suicide rates. Because suicide might be associated with environmental pollution, this study may help inform regulations not only of air pollutants, but also of coal-fired electrical power plant emissions.”

Spangler has conducted previous ecological research into environmental heavy metals, looking at their correlation to diabetes mortality, chronic liver disease death, cancer mortality and infant mortality. Spangler said the study was subject to a number of limitations because it only looked at county-level characteristics and could not control for factors in individual residents.

"Still, it raises the interesting question of whether suicide in a given population is related to the presence or absence of coal-fired electricity plants and the air quality," he said. "Further research is needed to understand what factors related to coal burning actually are at play and suggest that tighter regulation of coal-fired power plant emissions might cut down on county suicide rates in North Carolina."

(Image: David Freund)

'Strikingly similar' brains of man and fly may aid mental health research

A new study by scientists at King’s College London’s Institute of Psychiatry and the University of Arizona (UA) published in Science reveals the deep similarities in how the brain regulates behaviour in arthropods (such as flies and crabs) and vertebrates (such as fish, mice and humans).

The findings shed new light on the evolution of the brain and behaviour and may aid understanding of disease mechanisms underlying mental health problems.

Based on their own findings and available literature, Dr Frank Hirth (King’s) and Dr Nicholas Strausfeld (UA) compared the development and function of the central brain regions in arthropods (the ‘central complex’) and vertebrates (the ‘basal ganglia’).

Research suggests that both brain structures derive from embryonic stem cells at the base of the developing forebrain and that, despite the major differences between species, their respective constitutions and specifications derive from similar genetic programmes.

The authors describe that nerve cells in the central complex and the basal ganglia become inter-connected and communicate with each other in similar ways, facilitating the regulation of adaptive behaviours. In other words, the response of a fly or a mouse to internal stimuli such as hunger or sleep, and external stimuli such as light/dark or temperature, are regulated by similar neural mechanisms.

Dr Hirth from the Department of Neuroscience at King’s Institute of Psychiatry says: “Flies, crabs, mice, humans: all experience hunger, need sleep and have a preference for a comfortable temperature so we speculated there must be a similar mechanism regulating these behaviours. We were amazed to find just how deep the similarities go, despite the differences in size and appearance of these species and their brains.”

Dr Strausfeld, a Regents Professor in the UA’s Department of Neuroscience and the Director of the UA’s Center for Insect Science, says: “When you compare the two structures, you find that they are very similar in terms of how they’re organized. Their development is orchestrated by a whole suite of genes that are homologous between flies and mice, and the behavioral deficits resulting from disturbances in the two systems are remarkably similar as well.”

In humans, dysfunction of the basal ganglia can cause severe mental health problems ranging from autism, schizophrenia and psychosis, to neurodegeneration - as seen in Parkinson’s disease, motor neurone disease and dementia - as well as sleep disturbances, attention deficits and memory impairment. Similarly, when parts of the central complex are affected in fruit flies, they display similar impairments.

Dr Hirth (King’s) adds: “The deep similarities we see between how our brains and those of insects regulate behaviour suggest a common evolutionary origin. It means that prototype brain circuits, essential for behavioural choice, originated very early and have been maintained across animal species throughout evolutionary time. As surprising as it may seem, from insects’ dysfunctional brains, we can learn a great deal about how human brain disorders come about.”

The findings suggest that arthropod and vertebrate brain circuitries derive from a common ancestor already possessing a complex neural structure mediating the selection and maintenance of behavioural actions.

Although no fossil remains of the common ancestor exist, trace fossils, in the form of tracks criss-crossing the seafloor hundreds of millions of years ago, reveal purposeful changes in direction.

Dr Strausfeld (UA) says: “If you compare these tracks to the tracks left behind by a foraging fly larva on an agar plate or the tunnels made by a leaf-mining insect, they’re very similar. They all suggest that the animal chose to perform various different actions, and action selection is precisely what the central complex and the basal ganglia do.”

The trace fossils may thus support the early existence of brains complex enough to allow for action selection and a shared ancestry of neural structures between invertebrates and vertebrates.

Evidence Mounts for Role of Mutated Genes in Development of Schizophrenia

Johns Hopkins researchers have identified a rare gene mutation in a single family with a high rate of schizophrenia, adding to evidence that abnormal genes play a role in the development of the disease.

The researchers, in a report published in the journal Molecular Psychiatry, say that family members with the mutation in the gene Neuronal PAS domain protein 3 (NPAS3) appear at high risk of developing schizophrenia or another debilitating mental illnesses.

Normally functioning NPAS3 regulates the development of healthy neurons, especially in a region of the brain known as the hippocampus, which appears to be affected in schizophrenia. The Johns Hopkins researchers say they have evidence that the mutation found in the family may lead to abnormal activity of NPAS3, which has implications for brain development and function.

"Understanding the molecular and biological pathways of schizophrenia is a powerful way to advance the development of treatments that have fewer side effects and work better than the treatments now available," says study leader Frederick C. Nucifora Jr., Ph.D., D.O., M.H.S., an assistant professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine. "We could definitely use better medicines."

A New Focus on the ‘Post’ in Post-Traumatic Stress

Psychological trauma dims tens of millions of lives around the world and helps create costs of at least $42 billion a year in the United States alone. But what is trauma, exactly?

Both culturally and medically, we have long seen it as arising from a single, identifiable disruption. You witness a shattering event, or fall victim to it — and as the poet Walter de la Mare put it, “the human brain works slowly: first the blow, hours afterward the bruise.” The world returns more or less to normal, but you do not.

In 1980, the Diagnostic and Statistical Manual of Mental Disorders defined trauma as “a recognizable stressor that would evoke significant symptoms of distress in almost everyone” — universally toxic, like a poison.

But it turns out that most trauma victims — even survivors of combat, torture or concentration camps — rebound to live full, normal lives. That has given rise to a more nuanced view of trauma — less a poison than an infectious agent, a challenge that most people overcome but that may defeat those weakened by past traumas, genetics or other factors.

Now, a significant body of work suggests that even this view is too narrow — that the environment just after the event, particularly other people’s responses, may be just as crucial as the event itself.

The idea was demonstrated vividly in two presentations this fall at the Interdisciplinary Conference on Culture, Mind and Brain at the University of California, Los Angeles. Each described reframing a classic model of traumatic experience — one in lab rats, the other in child soldiers.

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Bullying by childhood peers leaves a trace that can change the expression of a gene linked to mood

A recent study by a researcher at the Centre for Studies on Human Stress (CSHS) at the Hôpital Louis-H. Lafontaine and professor at the Université de Montréal suggests that bullying by peers changes the structure surrounding a gene involved in regulating mood, making victims more vulnerable to mental health problems as they age. The study published in the journal Psychological Medicine seeks to better understand the mechanisms that explain how difficult experiences disrupt our response to stressful situations. “Many people think that our genes are immutable; however this study suggests that environment, even the social environment, can affect their functioning. This is particularly the case for victimization experiences in childhood, which change not only our stress response but also the functioning of genes involved in mood regulation,” says Isabelle Ouellet-Morin, lead author of the study.

A previous study by Ouellet-Morin, conducted at the Institute of Psychiatry in London (UK), showed that bullied children secrete less cortisol—the stress hormone—but had more problems with social interaction and aggressive behaviour. The present study indicates that the reduction of cortisol, which occurs around the age of 12, is preceded two years earlier by a change in the structure surrounding a gene (SERT) that regulates serotonin, a neurotransmitter involved in mood regulation and depression.

To achieve these results, 28 pairs of identical twins with a mean age of 10 years were analyzed separately according to their experiences of bullying by peers: one twin had been bullied at school while the other had not. “Since they were identical twins living in the same conditions, changes in the chemical structure surrounding the gene cannot be explained by genetics or family environment. Our results suggest that victimization experiences are the source of these changes,” says Ouellet-Morin. According to the author, it would now be worthwhile to evaluate the possibility of reversing these psychological effects, in particular, through interventions at school and support for victims.

(Image: mentalhealthsupport.co.uk)