Electro-shock therapy sees a resurgence

The procedure is widely accepted by the medical community, although it lingers in the public imagination as a crude medical holdover.

The patients are rolled on gurneys into a small screened-off area at Park Royal Hospital every 15 minutes with assembly line regularity.

One is a woman in her 60s, who, like the others, gets a momentary jolt of electricity sent through her head, causing a brain seizure and her body to tense for several seconds. The hope: That this treatment — the electroconvulsive, or “electro-shock,” therapy — will ease the symptoms of her bipolar disorder that has so far not responded well to drugs.

The procedure, one of thousands performed at Park Royal since the 76-bed hospital opened last year, has worked on the woman in the past, says Dr. Ivan Mazzorana, who performs all of them on patients here. And, he said, it’s likely to do so again.

These days, the treatment goes by its more clinical-sounding acronym, “ECT.”

"When you bring it up, most people say, ‘Oh my God! Not ECT, that’s something from the past,’" Mazzorana said. "It’s a very simple procedure, safer, and it’s a lot quicker than the medication."

Electroconvulsive therapy today is a procedure widely accepted by the medical community and one, absent a rare court order, that is done with patient consent. But it is also a treatment that lingers in the public imagination as a crude medical holdover almost as dated as bloodletting. Many outside of psychiatry are surprised to learn that the procedure still exists at all.

Despite that, ECT has seen a resurgence at many health centers in recent decades, experts say.

Park Royal, the only inpatient psychiatric hospital in Lee County, Fla., has already treated nearly 200 people with ECT, most receiving multiple treatments. The number represents roughly 10 percent of all of Park Royal’s admissions since it opened in early 2012.

The hospital is a for-profit facility owned by the Tennessee-based Acadia Healthcare Co.

Most of those who have received ECT at Park Royal — patient ages have ranged from 18 years to those in their 90s — suffer from severe depression or bi-polar disorders. About 90 percent are inpatients. Others are referred from other parts of Florida, according to the hospital. A few are snowbirds who come in for ETC “maintenance” treatments.

The Mayo Clinic calls the treatment, which has a reported success rate of 70 percent to 80 percent, the “gold standard” treatment for severe depression. The most common side effect, according to proponents, is temporary short-term memory loss.

"I was afraid, to be honest with you," said Ron Spesia, a 71-year-old Fort Myers Beach retiree who suffered a deep, multiyear depression that did not respond to medication. He had 12 treatments and said he started feeling better after the third. "Then one day I decided, ‘Hey, you know what? It’s time to put the big boy pants on and pursue this.’ Smartest move I ever made."

Still, ECT has its critics. Some, including patients of decades past and anti-ECT groups, say it is little more than intentional brain damage. This, despite the psychiatric community’s endorsement of it and positive testimonials from many of the estimated 100,000 Americans who get the treatment each year.

A Fort Myers News-Press reporter was recently allowed to witness about a half dozen such procedures at Park Royal.

But even hospital administrators remain sensitive to the ECT stigma. Though a patient agreed to be photographed during one such procedure, and to have it recorded on video, the hospital overruled that consent.

The hospital also prohibited patient interviews inside the building, though other medical facilities routinely allow such interactions if patients are willing. David Edson, Park Royal’s director of business development, cited concerns about privacy and “the very delicate nature of the ECT treatment.”

Despite that, Mazzorana said he wants to demystify the treatment and those who get it.

"It seems like an extreme, dramatic treatment," Mazzorana said. "It’s a matter of really educating the psychiatric community, so then we can educate patients."

Mundane process

The treatments at Park Royal begin at 7 a.m. Mondays, Wednesdays and Fridays, and continue throughout the mornings. Staff usually see up to 10 ECT patients on these days.

The process bears little resemblance to its horrific depictions in popular culture. At Park Royal, it starts when patients come to a medical preparation area adjacent to the ECT treatment room, where staff hook them up to IVs — they will eventually get medication to paralyze their muscles during the treatment — as well as heart and brain monitors attached to their skin.

After a quick chat with medical staff, who assess their conditions, patients bite down on foam “bite blocks” before they are put fully under.

Flashlight-shaped paddles coated with a blue conductive gel are placed on each temple (bilateral treatment) or one goes on the right temple and one on the top of the head (unilateral treatment), depending on the type of ECT the patients need. Bilateral ECT is recommended in more severe cases of mental illness and may produce more memory loss, experts say.

Following a quick buzzing sound, patients’ bodies tense for about five seconds. Patients typically wake a minute or so after the procedure and are sent off to a recovery area until the anesthesia fully wears off. They remember nothing of the treatment itself.

New patients must typically stay in the hospital for the first half of the standard dozen ECT treatments.

Spesia, the former ECT patient, said the IV injection was the most painful part of the process. The most unpleasant, he said was the hospital stay. Now, months after the process, he said the only lingering side effect has been some short-term memory loss.

"All I can remember is them giving me the rubber bite block and then them putting the (anesthesia) mask on and telling me to breathe deeply." he said. "Absolutely painless."

Nancy Kish, a 74-year-old Fort Myers resident who has received dozens of treatments over the years, said her memory of treatments from years past is fuzzy but her mind is otherwise as sharp as it has ever been. She said the treatment is a better alternative to the high doses of medication she otherwise took, drugs that largely left her bed-ridden.

"I feel pretty good," said Kish. "I get upset easy, and I get anxiety attacks. But other than that, I’m better than what I was."

Much like the therapeutic mystery behind anti-depressant medication experts are not exactly sure why ECT works for some patients.

Mazzorana said two theories dominate: One says that electroconvulsive therapy enhances certain beneficial brain chemicals that are lacking in different parts of the brain. Another states that it causes the release of hormones that have a beneficial effect on mood and promote the growth of healthy brain cells, he said. Other recent research suggests that ECT works by reducing “hyper-connectivity” in the minds of severely depressed patients.

Endorsements

Whatever the exact mechanism, ECT’s endorsements include the American Psychiatric Association, the American Medical Association, and the U.S. Surgeon General.

"When you raise ECT, people’s eyes always roll up in their heads and their family says, ‘Oh my God, you’re a monster!’" said Fort Myers psychiatrist Steve Machlin, who performed the procedure more than a decade ago. "There’s always going to be people on the outside who say it’s not proven but, if you’ve looked at the science, it’s been proven to be effective."

Another Southwest Florida psychiatrist and researcher, Fred Schaerf, said opposition to the treatment is largely anti-psychiatry bias and from the treatment’s early days, when it was performed without anesthesia.

"I think there is a misconception about the treatment — that it’s barbaric, cruel," Schaerf said. "It has to do with that stigma and people’s belief system with psychiatry."

Most insurance, including Medicare, covers the treatment.

Edson, the Park Royal Hospital business development director, said the health center generally charge insurers $500 a treatment, though that does not include the costs of the anesthesiologist and hospital stay. Mazzorana said the total cost is about $1,000.

Opposition

Medical and patient endorsements aside, some patient groups believe it does little more than cause brain damage. A quick Internet search turns up a long list of anti-ECT websites, many of which include testimonials from people claiming to have suffered negative effects from the treatments.

Among the most vocal opponents is the Philadelphia-based National Mental Health Consumers’ Self Help Clearinghouse, which urged the U.S. Food and Drug Administration in 2011 not to reduce federal oversight of ECT devices. It also sharply criticized the Surgeon General’s endorsement of ECT in 1999.

The group points to published studies suggesting that ECT leads to memory loss and may be far more dangerous for the elderly than medication alone. Susan Rogers, the organization’s director, said patients aren’t warned enough about the risks.

"People are not given the opportunity for truly informed consent," said Rogers, who has not had the procedure herself. "People are not advised of the enormous risks as well as the benefits. They’re given a whitewashed version of the facts. They’re not told it might cause permanent cognitive impairment, and I think that’s wrong."

She said she is not opposed to the treatment itself.

"Apparently about 100,000 people a year receive ECT in the United States and, I’m sure for many of those people, they’re satisfied with those results," she said. "There are also many people who feel that ECT has destroyed their lives."

The psychiatric community commonly uses the one in 10,000 patients mortality figure (or one per 80,000 treatments), figures anti-ECT groups say dramatically under-estimate the risk, particularly among older patients. A 1995 USA TODAY investigation found that it may have been as high as one in 200 among elderly patients, based on some state reports at the time and some earlier studies.

A recent Department of Veterans Affairs review of ECT between 1999 and 2010 found no ECT deaths at VA hospitals during that period. It placed the mortality risk at one per 14,000 patients, or one per 73,400 treatments.

Florida does not closely track ECT usage. But Texas, which does, reported that none of the 2,079 patients receiving ECT last year died during the procedure. Two died shortly after treatment in 2012, the state report noted, but neither case was related to the treatment.

Five years of reports show that roughly 2 percent of patients experience some level of memory loss shortly after treatment.

None of Park Royal’s ECT patients have died during the procedure, said Christina Brownwood, the hospital’s ECT coordinator. Nor have any needed emergency medical care immediately after a treatment, she said.

What Is the Brain Telling Us About the Diagnoses of Schizophrenia and Bipolar Disorder?

We live in the most exciting and unsettling period in the history of psychiatry since Freud started talking about sex in public.

On the one hand, the American Psychiatric Association has introduced the fifth iteration of the psychiatric diagnostic manual, DSM-V, representing the current best effort of the brightest clinical minds in psychiatry to categorize the enormously complex pattern of human emotional, cognitive, and behavioral problems. On the other hand, in new and profound ways, neuroscience and genetics research in psychiatry are yielding insights that challenge the traditional diagnostic schema that have long been at the core of the field.

“Our current diagnostic system, DSM-V represents a very reasonable attempt to classify patients by their symptoms. Symptoms are an extremely important part of all medical diagnoses, but imagine how limited we would be if we categorized all forms of pneumonia as ‘coughing disease,” commented Dr. John Krystal, Editor of Biological Psychiatry.

A paper by Sabin Khadka and colleagues that appears in the September 15^th issue of Biological Psychiatry advances the discussion of one of these roiling psychiatric diagnostic dilemmas.

One of the core hypotheses is that schizophrenia and bipolar disorder are distinct scientific entities. Emil Kraepelin, credited by many as the father of modern scientific psychiatry, was the first to draw a distinction between dementia praecox (schizophrenia) and manic depression (bipolar disorder) in the late 19^th century based on the behavioral profiles of these syndromes. Yet, patients within each diagnosis can have a wide variation of symptoms, some symptoms appear to be in common across these diagnoses, and antipsychotic medications used to treat schizophrenia are very commonly prescribed to patients with bipolar disorder.

But at the level of brain circuit function, do schizophrenia and bipolar differ primarily by degree or are there clear categorical differences? To answer this question, researchers from a large collaborative project called BSNIP looked at a large sample of patients diagnosed with schizophrenia or bipolar disorder, their healthy relatives, and healthy people without a family history of psychiatric disorder.

They used a specialized analysis technique to evaluate the data from their multi-site study, which revealed abnormalities within seven different brain networks. Generally speaking, they found that schizophrenia and bipolar disorder showed similar disturbances in cortical circuit function. When differences emerged between these two disorders, it was usually because schizophrenia appeared to be a more severe disease. In other words, individuals with schizophrenia had abnormalities that were larger or affected more brain regions. Their healthy relatives showed subtle alterations that fell between the healthy comparison group and the patient groups.

The authors highlight the possibility that there is a continuous spectrum of circuit dysfunction, spanning from individuals without any familial association with schizophrenia or bipolar to patients carrying these diagnoses. “These findings might serve as useful biological markers of psychotic illnesses in general,” said Khadka.

Krystal agreed, adding, “It is evident that neither our genomes nor our brains have read DSM-V in that there are links across disorders that we had not previously imagined. These links suggest that new ways of organizing patients will emerge once we understand both the genetics and neural circuitry of psychiatric disorders sufficiently.”

(Image: ALAMY)

Imaging in mental health and improving the diagnostic process

What are some of the most troubling numbers in mental health? Six to 10 — the number of years it can take to properly diagnose a mental health condition. Dr. Elizabeth Osuch, a Researcher at Lawson Health Research Institute and a Psychiatrist at London Health Sciences Centre and the Department of Psychiatry at Western University, is helping to end misdiagnosis by looking for a ‘biomarker’ in the brain that will help diagnose and treat two commonly misdiagnosed disorders.

Major Depressive Disorder (MDD), otherwise known as Unipolar Disorder, and Bipolar Disorder (BD) are two common disorders. Currently, diagnosis is made by patient observation and verbal history. Mistakes are not uncommon, and patients can find themselves going from doctor to doctor receiving improper diagnoses and prescribed medications to little effect.

Dr. Osuch looked to identify a ‘biomarker’ in the brain which could help optimize the diagnostic process. She examined youth who were diagnosed with either MDD or BD (15 patients in each group) and imaged their brains with an MRI to see if there was a region of the brain which corresponded with the bipolarity index (BI). The BI is a diagnostic tool which encompasses varying degrees of bipolar disorder, identifying symptoms and behavior in order to place a patient on the spectrum.

What she found was the activation of the putamen correlated positively with BD. This is the region of the brain that controls motor skills, and has a strong link to reinforcement and reward. This speaks directly to the symptoms of bipolar disorder. “The identification of the putamen in our positive correlation may indicate a potential trait marker for the symptoms of mania in bipolar disorder,” states Dr. Osuch.

In order to reach this conclusion, the study approached mental health research from a different angle. “The unique aspect of this research is that, instead of dividing the patients by psychiatric diagnoses of bipolar disorder and unipolar depression, we correlated their functional brain images with a measure of bipolarity which spans across a spectrum of diagnoses.” Dr. Osuch explains, “This approach can help to uncover a ‘biomarker’ for bipolarity, independent of the current mood symptoms or mood state of the patient.”

Moving forward Dr. Osuch will repeat the study with more patients, seeking to prove that the activation of the putamen is the start of a trend in large numbers of patients. The hope is that one day there could be a definitive biological marker which could help differentiate the two disorders, leading to a faster diagnosis and optimal care.

In using a co-relative approach, a novel method in the field, Dr. Osuch uncovered results in patients that extend beyond verbal history and observation. These results may go on to change the way mental health is diagnosed, and subsequently treated, worldwide.

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.”

Do drugs for bipolar disorder “normalize” brain gene function?

Every day, millions of people with bipolar disorder take medicines that help keep them from swinging into manic or depressed moods. But just how these drugs produce their effects is still a mystery.

Now, a new University of Michigan Medical School study of brain tissue helps reveal what might actually be happening. And further research using stem cells programmed to act like brain cells is already underway.

Using genetic analysis, the new study suggests that certain medications may help “normalize” the activity of a number of genes involved in communication between brain cells. It is published in the current issue of Bipolar Disorders.

The study involved brain tissue from deceased people with and without bipolar disorder, which the U-M team analyzed to see how often certain genes were activated, or expressed. Funding support came from the National Institutes of Health and the Heinz C. Prechter Bipolar Research Fund.

“We found there are hundreds of genes whose activity is adjusted in individuals taking medication – consistent with the fact that there are a number of genes that are potentially amiss in people with bipolar,” says senior author Melvin McInnis, M.D., the U-M psychiatrist, U-M Depression Center member and principal investigator of the Prechter Fund Projects who helped lead the study. “Taking the medications, specifically ones in a class called antipsychotics, seemed to normalize the gene expression pattern in these individuals so that it approached that of a person without bipolar.”

Digging deeper into bipolar genetics

Scientists already know that bipolar disorder’s roots lie in genetic differences in the brain — though they are still searching for the specific gene combinations involved.  

McInnis and his colleagues have now embarked on research developing several a lines of induced pluripotent stem cells derived (iPSC) from volunteers with and without bipolar disorder, which will allow even more in-depth study of the development and genetics of bipolar disorder.

The newly published study looked at the expression, or activity levels, of 2,191 different genes in the brains of 14 people with bipolar disorder, and 12 with no mental health conditions. The brains were all part of a privately funded nonprofit brain bank that collected and stored donated brains, and recorded what medications the individuals were taking at the time of death.

Seven of the brains were from people with bipolar disorder who had been taking one or more antipsychotics when they died. These drugs include clozapine, risperidone, and haloperidol, and are often used to treat bipolar disorder. Most of the 14 brain donors with bipolar disorder were also taking other medications, such as antidepressants, at the time of death.

When the researchers compared the gene activity patterns among the brains of bipolar disorder patients who had been exposed to antipsychotics with patterns among those who weren’t, they saw striking differences.

Then, when they compared the activity patterns of patients who had been taking antipsychotics with those of people without bipolar disorder, they found similar patterns.

The similarities were strongest in the expression of genes involved in the transmission of signals across synapses – the gaps between brain cells that allow cells to ‘talk’ to one another. There were also similarities in the organization of nodes of Ranvier – locations along nerve cells where signals can travel faster.

McInnis, who is the Thomas B. and Nancy Upjohn Woodworth Professor of Bipolar Disorder and Depression in the U-M Department of Psychiatry, worked with U-M scientists Haiming Chen, M.D. and K. Sue O’Shea, Ph.D., of the U-M Department of Cell and Developmental Biology. They also teamed with Johns Hopkins University researcher Christopher Ross, M.D., Ph.D. on the new research; U-M and Johns Hopkins have a long history of collaboration on bipolar disorder research.

The research used brain tissue samples from the Stanley Brain Collection of the Stanley Medical Research Institute in Maryland.

Using “gene chip” analysis to measure the presence of messenger RNA molecules that indicate gene activity, and sophisticated data analysis, they were able to map the expression patterns from the brains and break the results down by bipolar status and medication use. The bipolar and control (non-bipolar) brains were matched by age, gender and other factors.

“In bipolar disorder, it’s not just one gene that’s involved – it’s a whole symphony of them,” says McInnis, who has helped lead U-M’s bipolar genetics research for nearly a decade. “Medications appear to nudge them in a direction that aligns more with the normal expression pattern.”

Among those that were “nudged” were genes that have already been shown to be linked to bipolar disorder, including glycogen synthase kinase 3 beta (GSK3β), FK506 binding protein 5 (FKBP5), and Ankyrin 3 (ANK3).

Going forward, says McInnis, cell culture studies will be critical to studying how medications for bipolar disorder work, and to screen new molecules as potential new medications.

New gene variant may explain psychotic features in bipolar disorder

Researchers at Karolinska Institutet have found an explanation for why the level of kynurenic acid (KYNA) is higher in the brains of people with schizophrenia or bipolar disease with psychosis. The study, which is published in the scientific periodical Molecular Psychiatry, identifies a gene variant associated with an increased production of KYNA.

The discovery contributes to the further understanding of the link between inflammation and psychosis, and might pave the way for improved therapies. Kynurenic acid (KYNA) is a substance that affects several signalling pathways in the brain and that is integral to cognitive function. Earlier studies of cerebrospinal fluid have shown that levels of KYNA are elevated in the brains of patients with schizophrenia or bipolar diseases with psychotic features. The reason for this has, however, not been fully understood.

KMO is an enzyme involved in the production of KYNA, and the Karolinska Institutet team has now shown that some individuals have a particular genetic variant of KMO that affects its quantity, resulting in higher levels of KYNA. The study also shows that patients with bipolar disease who carry this gene variant had almost twice the chance of developing psychotic episodes.

KYNA is produced in inflammation, such as when the body is exposed to stress and infection. It is also known that stress and infection may trigger psychotic episodes. The present study provides a likely description of this process, which is more likely to occur in those individuals with the gene variant related to higher production of KYNA. The researchers also believe that the discovery can help explain certain features of schizophrenia or development of other psychotic conditions.

"Psychosis related to bipolar disease has a very high degree of heredity, up to 80 per cent, but we don’t know which genes and which mechanisms are involved," says Martin Schalling, Professor of medical genetics at Karolinska Institutet’s Department of Molecular Medicine and Surgery, also affiliated to the Center for Molecular Medicine (CMM). "This is where our study comes in, with a new explanation that can be linked to signal systems activated by inflammation. This has consequences for diagnostics, and paves the way for new therapies, since there is a large arsenal of already approved drugs that modulate inflammation."

Brain imaging identifies bipolar risk

Researchers from the Black Dog Institute and University of NSW have used brain imaging technology to show that young people with a known genetic risk of bipolar but no clinical signs of the condition have clear and quantifiable differences in brain activity when compared to controls.

“We found that the young people who had a parent or sibling with bipolar disorder had reduced brain responses to emotive faces, particularly a fearful face. This is an extremely promising breakthrough,” says study leader Professor Philip Mitchell.

Affecting around 1 in 75 Australians, bipolar disorder involves extreme and often unpredictable fluctuations in mood. The mood swings and associated behaviours such as disinhibited behaviour, aggression and severe depression, have a significant impact on day-to-day life, careers and relationships. Bipolar has the highest suicide rate of all psychiatric disorders.

“We know that bipolar is primarily a biological illness with a strong genetic influence but triggers are yet to be understood. Being able to identify young people at risk will enable implementation of early intervention programs, giving them the best chance for a long and happy life,” says Prof Mitchell.

Researchers used functional MRI to visualise brain activity when participants were shown pictures of happy, fearful or calm (neutral) human faces. Results showed that those with a genetic risk of bipolar displayed significantly reduced brain activity in a specific part of the brain known to regulate emotional responses.

“Our results show that bipolar disorder may be linked to a dysfunction in emotional regulation and this is something we will continue to explore,” Professor Mitchell said.

“And we now have an extremely promising method of identifying children and young people at risk of bipolar disorder.”

 “We expect that early identification will significantly improve outcomes for people that go on to develop bipolar disorder, and possibly even prevent onset in some people.”

Results are published this week in Biological Psychiatry and come from the NHMRC-funded ‘Kids and Sibs study’, the biggest research study in the world focusing on genetic and environmental aspects of bipolar disorder. Based at the Black Dog Institute, the trial is still recruiting.

Replicating Risk Genes in Bipolar Disorder

One of the biggest challenges in psychiatric genetics has been to replicate findings across large studies.

Scientists at King’s College London, Institute of Psychiatry have now performed one of the largest ever genetic replication studies of bipolar affective disorder, with 28,000 subjects recruited from 36 different research centers. Their findings provide compelling evidence that the chromosome 3p21.1 locus contains a common genetic risk for bipolar disorder, the PBRM1 gene.

The locus at 3p21.1 has also been previously associated with depression and schizophrenia. Using a separate dataset of over 34,000 subjects, they did not confirm association of this same variant with schizophrenia.

Thus, they replicated the association of the marker with bipolar disorder, but not with schizophrenia. This is an interesting finding, in that it distinguishes the heritable risk for bipolar disorder and schizophrenia. It contrasts with the majority of studies that have found that schizophrenia risk genes also contribute to the risk for bipolar disorder.

"This study adds to the recent rapid progress in identifying genes for mental illness. The last few years have seen the identification of about two dozen genetic loci for bipolar disorder and schizophrenia," commented first author Evangelos Vassos. "About half of these are shared between these two disorders, indicating they share some, but not all, genetic causes."

Due to the conflicting results, it is clear that more work is needed to determine the role this locus plays in psychosis, but the evidence seems solid that it is associated with bipolar disorder.