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Use of antipsychotic medication has been linked to a significantly reduced risk of psychiatric patients committing violent crime, according to new research published in The Lancet. The study also records an association between mood-stabilizing drugs for people with bipolar disorder and a reduced rate of violent crime.

People with schizophrenia or bipolar disorder are most likely to use antipsychotic treatments such as clozapine or risperidone, or mood-stabilizing drugs such as lithium and carbamazepine. These increasingly popular drugs are known to put psychiatric patients at less risk of relapse and rehospitalization.

However, there has been little research examining how these drugs influence potential adverse outcomes in the community, such as violent behavior.

Violent behavior, the new study notes, is one of the most important adverse outcomes for patients with psychiatric disorders. Previous research has shown that the relative risk of violence against others is four times higher in schizophrenia patients than in the general population.

The risk of interpersonal violence in people with bipolar disorder, meanwhile, is “substantially increased” when the patient is misusing substances.

Studying the influence drugs have on violence risk is difficult, because aggressive patients are less likely to be recruited or give consent to be in a study, and they are less likely to remain enrolled in a study than patients without violent traits. As such, the evidence for antipsychotic drugs to prevent violence in patients is described as “weak or inconclusive.”

medication capsules
When participants were using their medication, there was a 45% fall in violent crime among people taking antipsychotics and a 24% decrease in violence among patients using mood stabilizers.

For the new study, researchers in the UK and Sweden analyzed the psychiatric diagnoses and any subsequent criminal convictions of more than 80,000 patients recorded in Swedish health registries. This group were all prescribed either antipsychotic and/or mood-stabilizing medication at some point between 2006 and 2009.

Over the 3-year study period, 6.5% (2,657) of the men and 1.4% (604) of the women in the study were convicted of a violent crime.

Importantly, the researchers compared the periods when individual participants were not using medication with when they were.

Analyzing the results, the study found that when participants were using their medication, there was a 45% fall in violent crime among people taking antipsychotics and a 24% decrease in violence among patients using mood stabilizers.

Antipsychotics and mood stabilizers are often prescribed together, but the study did not find any further decrease in violence when the drugs were combined. Also, the researchers found that mood stabilizers were only associated with reductions in violent crime among male bipolar disorder patients.

Study can prove link between antipsychotics and reduced violence but not cause

The study was not able to make any conclusions about causality from their findings, because the researchers did not investigate how the associations between medication and violent crime are mediated.

For instance, patients with psychiatric disorders who are using medication may receive more support from family or carers, and this could make them less likely to commit violent crime, rather than the effects of the medication itself.

However, the authors point out that this would also mean that people who take mood stabilizers are equally less likely to commit violent crime as people who take antipsychotics, since they would both receive a similar level of support. Instead, the study found that people who took antipsychotics were significantly less likely to engage in violent crime than those who only took mood stabilizers.

Lead researcher Dr. Seena Fazel, of Oxford University in the UK, concludes:

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Researchers from Harvard Medical School in Boston, MA, investigating the pathophysiology of psychotic disorders have found that patients with these disorders have a reduced brain volume in the hippocampus.

The pathophysiology of psychotic disorders has been studied for more than a hundred years but still remains unclear.

Previous research has suggested that alterations in the medial temporal lobe (MTL), hippocampus, parahippocampal gyrus and entorhinal cortex are indicators of schizophrenia.

The extent to which these alterations are found in patients with other psychotic disorders has been inconclusive, however. In bipolar disorder, for instance, most studies show either little or no change in the MTL.

Some research also found no reduction in the hippocampal volumes of patients with bipolar disorder who were taking lithium.

To investigate this further, the Harvard researchers – who publish their findings in JAMA Psychiatry – conducted a neuroimaging study in healthy volunteers and patients with schizophrenia, schizoaffective disorder and psychotic bipolar disorder.

Consistent with previous research, the MTL appeared reduced in volume in patients with schizophrenia and schizoaffective disorder, but not in patients with psychotic bipolar disorder.

diagram depicting the location of the hippocampus in the brain
This study is one of the largest and most technologically sophisticated to analyze the role the hippocampus plays in psychotic disorders.

But the researchers did find volume reductions in the hippocampus across all three groups of patients with psychotic disorders, compared with the healthy volunteers.

Each psychotic disorder also demonstrated hippocampal alterations specific to that condition.

However, although the correlations between psychotic symptoms and reduced volumes in different areas of the hippocampus were statistically significant and consistent with other recent research, the authors admit that the association in their study is still weak.

This could be because there was not much variation in psychotic symptoms in their study participants, as the patients were stable and using antipsychotic medication.

“Yes, the association between hippocampal volume is weak,” study author Dr. Matcheri S. Keshavan told Medical News Today. “It is possible that measures of hippocampal physiology and neurochemistry are more sensitive in detecting relationships to clinical features such as psychosis.”

The researchers also found the reductions in hippocampal volume to be associated with the severity of psychosis, declarative memory and overall cognitive performance.

Different variations may account for different symptoms. For instance, although the hippocampus is involved in encoding new memories – and psychotic disorders are thought to arise from an inability to discriminate between present and past memory experiences – different areas of the hippocampus may play distinct roles in encoding or retrieving memories.

Further investigation of unmedicated patients and bipolar subtypes is required

As the patients in this study were mostly medicated with antipsychotics, the authors suggest that future studies should examine the hippocampal alterations in patients before and after beginning treatment with antipsychotics.

Also, this study did not include patients with non-psychotic bipolar disorder, so the researchers are unable to generalize their findings to patients with this condition.

But because this study assessed 549 patients with psychotic disorders (including 188 psychotic bipolar disorder patients) as well as 336 healthy volunteer subjects, the researchers think that the relatively large sample size lends credibility to their findings. They suggest this addresses the previous inconsistencies in smaller studies looking at hippocampal alterations in psychotic bipolar disorder patients.

Also, compared with other research, this study used the most sophisticated technology for analyzing the hippocampus to date.

Explaining why the Harvard study is important, Dr. Keshavan told us:

“This study demonstrated the ability to investigate smaller substructures within the hippocampus in a large sample of individuals with a spectrum of psychotic disorders, including schizophrenia and psychotic bipolar disorders. Our observations suggest that changes in the hippocampus, a key brain region related to how we create, store, process and retrieve memories, may not be confined to schizophrenia alone, but are seen across a spectrum of psychotic disorders.”

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Bipolar disorder (BD) is among the 10 most burdensome medical conditions, according to the World Health Organization. The disorder is known for its dramatic highs of extreme euphoria, racing thoughts and decreased need for sleep, as well as its profound lows of sadness and despair.

Because it is also associated with a heightened risk of suicide, substance abuse, hypersexuality, familial discord and aggressive behaviour, BD affects not just those suffering from it, but also those around them – especially their children.

While previous research has shown that children of parents with BD are at a greater risk of developing psychiatric disorders, the psychosocial implications of being raised by parents with BD has been ignored – until now.

A new study conducted by Mark Ellenbogen, a psychology professor at Concordia University, and Rami Nijjar, a graduate student, reveals that children of parents with BD are more susceptible to psychosocial problems, most notably risky sexual behaviour. The study was published in the Journal of Affective Disorders.

Using a longitudinal approach, the researchers followed children of parents with bipolar disorder and children from families without mental disorder from ages four to 12 until early adulthood.

They assessed:
◾ Suicidal behaviour
◾ Self-harm
◾ Smoking
◾ Delinquent or criminal behaviour
◾ Risky sexual behaviour (sexual activity before age 16, unprotected sex, abortions)

For both genders, the researchers saw the biggest group difference in the last category, which can be seen as an extension of other tendencies.

“Risky sexual behaviour falls along the spectrum of general externalizing behaviours, like delinquency and aggression. We know it is predicted by externalizing behaviours in middle childhood,” says Ellenbogen, who is also a member of Concordia’s Centre for Research in Human Development.

What can concerned parents with BD do?

To prevent the offspring of parents with BD from engaging in risky behaviour, doctors need to look beyond the patient and give the entire family, including the children, the coping skills they need to live with the disorder. “In psychiatry, we tend to treat the patient – there’s never any evaluation of their family or kids or partners. Across my career, I’ve been saying that’s the wrong way of looking at the issues,” Ellenbogen says. “The children of BD patients are at high risk of developing a number of psychiatric and psychosocial problems. We need to think about interventions that will work for all members of the family.”

A new pilot prevention program that is open to the public

Ellenbogen is now working to establish the first prevention program for children of parents with BD. Entitled Reducing Unwanted Stress in the Home (RUSH), the intervention will consist of 12 sessions of group therapy, with one group to teach children effective coping strategies and another to teach their parents the skills to manage stress, family discord and children. The pilot program, open to families in the Montreal area, will launch this summer. It will operate in groups of five to six families.

Ellenbogen and his team will monitor the behaviour, hormone levels and mental health of the children before and after the intervention in order to assess the effectiveness of the RUSH program.

“These parents need additional help in organizing family life, parenting, dealing with spouses and coping with stress,” Ellenbogen says. “The ultimate goal is to reduce the levels of stress in the family, which we believe will then reduce negative outcomes in their children.”

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Researchers from Tufts have gained new insight into a protein associated with bipolar disorder. The study, published in Science Signaling, reveals that calcium channels in resting neurons activate the breakdown of Sp4, which belongs to a class of proteins called transcription factors that regulate gene expression.

This study, led by Grace Gill, identifies a molecular mechanism regulating Sp4 activity. Her previous research had determined that reduced levels of Sp4 in the brain are associated with bipolar disorder. Her work overall suggests that misregulation of Sp4 may contribute to the development of bipolar disorder.

“Understanding how transcription factors like Sp4 are regulated may provide us with ways to change neuronal gene expression to treat symptoms of mental illness, including bipolar disorder,” said Gill, Ph.D., an associate professor in the department of developmental, molecular & chemical biology at Tufts University School of Medicine and member of the neuroscience; genetics; and cell, molecular and developmental biology program faculties at the Sackler School of Graduate Biomedical Sciences at Tufts.

The main goal of the study was to determine whether a specific type of calcium channel – store-operated calcium channels – drive the breakdown of Sp4 protein. Along the way, however, the research team also discovered that signaling by these calcium channels is most active in the so-called “off” or “resting” phase.

“The calcium-signaling regulation of Sp4 during the resting phase was unexpected and suggests two things: resting neurons are more active than we had thought and calcium signaling influences gene expression in both active and resting neurons,” Gill said.

“We tend to think about cells being “on” or “off,” but the reality of the biology is far more complex. Cells are always busy,” she continued.

In neurons – cells that can be stimulated by electrical signals – transcription factors are regulated by calcium entry that is initiated when the cell depolarizes. Depolarization occurs when the overall voltage of the cell is increased. This is the “on” or “active” state for the cell. In contrast, when the cell’s voltage is decreased, hyperpolarization occurs. This is called the “off” or “resting” phase for the cell.

Store-operated calcium channels (SOCC) are a type of calcium channel found in all cells. These channels are activated when stores of calcium inside the cell are reduced. A calcium sensor called stromal interaction molecule 1 (STIM1) is responsible for calcium entry into the cell through SOCCs.

To determine whether STIM1 controlled Sp4 breakdown, the researchers reduced STIM1 levels in cells and measured Sp4 levels. A control group of cells contained normal levels of STIM1, while a comparison group contained reduced STIM1 levels. Both cell groups were placed in a solution for 60 minutes to place them into their “resting” state.

The cells in the control group displayed significantly less Sp4 when at rest while, in contrast, cells in the comparison group – those with reduced STIM1 levels – had higher Sp4 levels.

“These findings provide evidence that STIM1 is required for the breakdown of Sp4 when the cell hyperpolarizes, which tell us the presence of STIM1 directly influences Sp4 levels in neurons,” said first author, Jasmin Lalonde, Ph.D., a former postdoctoral fellow in Gill’s lab and now a research fellow at the Center for Human Genetic Research and the department of neurology at the Massachusetts General Hospital.

This is ongoing work by Gill to understand the role of Sp4 in bipolar disorder. Some of Gill’s previous research, performed in collaboration with researchers from Spain, found that Sp4 levels were lower in two areas of the brain in postmortem samples from patients with bipolar disorder. In a study published in May of this year in the Journal of Neurochemistry, she and her team determined that one mechanism of Sp4 regulation is a glutamate receptor called the NMDA receptor.

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