New Technology Puts Guilty Verdict to the Test

An academic at the University of Sheffield has used groundbreaking technology to investigate the potential innocence of a woman convicted of poisoning a child in her care.

Professor Sean Spence, who has pioneered the use of functional Magnetic Resonance Imaging (fMRI) to detect lies, carried out groundbreaking experiments on the woman who, despite protesting her innocence, was sentenced to four years in prison. His results have now been published for the first time in the journal European Psychiatry.

Using the technology, Spence examined the woman´s brain activity as she alternately confirmed her account of events and that of her accusers. The tests demonstrated that when she agreed with her accusers´ account of events she activated extensive regions of her frontal lobes and also took significantly longer to respond – these findings have previously been found to be consistent with false or untrue statements.

Although the technology has previously been claimed to be 90% accurate - far better than polygraph tests – its use has also been open to debate. Lie detection tests are already used regularly in parts of the US justice system, as well as by businesses. But these are the first brain scanning tests of their kind, carried out on a real-life case, reported in the world literature.

Spence says: "This research provides a fresh opportunity for the British legal system as it has the potential to reduce the number of miscarriages of justice. However, it is important to note that, at the moment, this research doesn´t prove that this woman is innocent. Instead, what it clearly demonstrates is that her brain responds as if she were innocent."

"If proved to be accurate, and these findings replicated, this technology could be used alongside other factors to address questions of guilt versus innocence."

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Study: Health Supplement May Curb Addiction of Problem Gamblers

University of Minnesota researchers have discovered that a common amino acid, available as a health food supplement, may help curb pathological gamblers’ addiction.

In a recent eight-week trial, 27 people were given increasing doses of the amino acid, N-acetyl cysteine, which has an impact on the chemical glutamate – often associated with reward in the brain. At the end of the trial, 60 percent of the participants reported fewer urges to gamble. The research will be published in the Sept.15, 2007 issue of Biological Psychiatry.

“It looks very promising,” says Jon Grant, a University of Minnesota associate professor of psychiatry and principal investigator of the study. “We were able to reduce people’s urges to gamble.”

Those who responded well in the first round of the study were asked to continue to participate in a double-blind study – a testing method where neither the researcher nor subjects know who is in the control group until the study is finished.

Of the 16 who responded to the amino acid the first time around, 13 agreed to continue in the double-blind study (three didn’t want to risk quitting the drug) for an additional six weeks.

About 83 percent who received the supplement, continued to report fewer urges to gamble. Nearly 72 percent of those who took the placebo went back to gambling.

Similar studies using N-acetyl cysteine have shown its ability to curb drug addictions in animals, and a current University of Minnesota study conducted by Grant is investigating whether the drug could help methamphetamine users quit.

“This research could be encouraging for a lot of addictions,” Grant says.

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Faster-acting Antidepressants Closer to Becoming Reality

A new study has revealed more about how the medication ketamine, when used experimentally for depression, relieves symptoms of the disorder in hours instead of the weeks or months it takes for current antidepressants to work. While ketamine itself probably won’t come into use as an antidepressant because of its side effects, the new finding moves scientists considerably closer to understanding how to develop faster-acting antidepressant medications – among the priorities of the National Institute of Mental Health (NIMH), part of the National Institutes of Health.

Ketamine blocks a receptor called NMDA on brain cells, an earlier NIMH study in humans had shown, but the new study in mice shows that this is an intermediate step. It turns out that blocking NMDA increases the activity of another receptor, AMPA, and that this boost in AMPA is crucial for ketamine’s rapid antidepressant actions. The study was reported online in Biological Psychiatry on July 23, by NIMH researchers Husseini K. Manji, MD, Guang Chen, MD, PhD, Carlos Zarate, MD, and colleagues.

“Our research is showing us how to develop medications that get at the biological roots of depression. This new finding is a major step toward learning how to improve treatment for the millions of Americans with this debilitating disorder; toward eliminating the weeks of suffering and uncertainty they have to endure while they wait for their medications to work,” says NIH Director Elias Zerhouni, M.D.

Almost 15 million American adults have a depressive disorder. During the long wait to begin feeling the effects of conventional medications, patients may worsen, raising the risk of suicide for some. Depressive disorders also affect children and adolescents.

By aiming new medications at more direct molecular targets, such as NMDA or AMPA, scientists may be able to bypass some of the steps through which current antidepressants indirectly exert their effects – a roundabout route that accounts for the long time it takes for patients to begin feeling better with the conventional medications.

While ketamine appears to achieve this, it is an unlikely candidate to become a new treatment for depression, because of the side effects it can cause in humans, including hallucinations. It is approved as an anesthetic by the Food and Drug Administration at much higher doses than those given in the study, but its use is limited because it may cause hallucinations during recovery from anesthesia.

Both NMDA and AMPA are receptors for the neurotransmitter glutamate, one of the chemical messengers that enable brain cells to communicate with each other. The glutamate system has been implicated in depression recently, leading to efforts to unravel its molecular machinery in search of abnormalities and of better targets for antidepressant medications.

This focus on the glutamate system is a departure from the thinking that led to currently available antidepressants, which are thought to relieve depression through a lengthy trickle-down process of biochemical reactions that affect the circuitry underlying depression.

The fact that NMDA and AMPA receptors are part of the glutamate system and that targeting them directly led to such rapid, sustained relief of depression-like behaviors in this study – and that a single dose of ketamine did the same in humans in the earlier study – suggests that they are probably the key targets for antidepressant medications.

“In any other illness of depression’s magnitude, patients aren’t expected to just accept that their treatments won’t start helping them for weeks or months. The value of our research on compounds like ketamine is that it tells us where to look for more precise targets for new kinds of medications that can close the gap,” says NIMH Director Thomas Insel, MD. “We’re making tremendous progress.”

To conduct the new study, researchers induced depression-like behaviors in mice; for example, the mice gave up after being forced to engage in hopeless tasks, such as prolonged swimming. A dose of ketamine reversed the depression-like behaviors for at least two weeks.

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Suicide Attempts Decline After Depression Treatment

In a study of more than 100,000 patients treated for depression, suicide attempts declined during the first month of treatment—whether that treatment consisted of medication, psychotherapy, or both. The findings, published by Group Health researchers in the July American Journal of Psychiatry, show a similar pattern for populations of adolescents and young adults (up to age 24) as for older adults.

The study sheds new light on the “black box” advisory that the U.S. Food and Drug Administration (FDA) placed in 2004 and has revised since then, said Greg Simon, MD, MPH, the Group Health psychiatrist who led the study. The advisory—which has concerned many patients, families, and care providers—warns that suicidal behavior may emerge soon after people younger than 25 start treatment with newer antidepressant medications called selective serotonin reuptake inhibitors (SSRIs). It was spurred by randomized placebo-controlled trials showing that starting to take an SSRI can make thoughts of suicide more common among some teens and young adults.

Dr. Simon’s study is the first published research to compare the risk of suicide attempts before and after the start of treatment with not only antidepressants but also psychotherapy. It is based on computerized medical and pharmacy records for more than 109,000 patients who started treatment for depression at Group Health from 1996 to 2005.

In the study, suicide attempts were about twice as common among patients up to age 24 as among older adults. However, the time pattern was the same for both age groups, regardless of the type of treatment they received: Suicide attempts were most likely during the month before treatment started, falling by at least 50 percent in the month after treatment began, with steady declines thereafter.

At all time points—up to three months before and six months after starting treatment—patients who received their antidepressant prescription from a psychiatrist tended to be most likely to attempt suicide. Those who received it from their primary care doctor were least likely to attempt suicide, with levels in between for those who got individual psychotherapy from a therapist other than a psychiatrist. “That’s not because seeing a psychiatrist makes you want to kill yourself,” says Dr. Simon. Rather, he suggests, these results reflect the fact that people with severe depression, who tend to be more suicidal, are more likely to be referred to psychiatrists, while those with milder depression stick with their primary doctors.

“Our study indicates that there’s nothing specific to antidepressant medications that would either make large populations of people with depression start trying to kill themselves—or protect them from suicidal thoughts,” says Dr. Simon. “Instead, we think that, on average, starting any type of treatment—medication, psychotherapy, or both—helps most people of any age have fewer symptoms of depression, including thinking about suicide and attempting it.” That said, he likened population-based studies—both observational studies such as this one and randomized controlled trials of medications—to “circumstantial evidence” about what happens to individual patients.

Like other psychiatrists, Dr. Simon has seen a few depressed patients start having suicidal thoughts while taking antidepressant medication despite never having thought about suicide before then. He hypothesizes that subgroups of people may be vulnerable to becoming more agitated or suicidal after taking these drugs. “We hope to learn how to identify these people in advance,” he says.

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