Saturday, October 30, 2010

In children, hallucinations are not always a sign of psychosis

Current Psychiatry
Vol. 9, No. 10 / October 2010

Although hallucinations frequently are considered synonymous with psychotic disorders, in children this rare. Neurobiologic studies (fMRI) of adults show activation of Broca’s area (left inferior frontal gyrus) seconds before patients perceive auditory verbal hallucinations, which suggests that auditory hallucinations may be misidentified self-talk.a,b According to Piaget,c children age <7 may have difficulty distinguishing between events occurring while dreaming and awake. He further theorized that nonpathologic hallucinations could become pathologic when combined with trauma such as abuse. Straussd suggested that psychosis might lie on a continuum with normal phenomenon. In a case series, Wilking and Paulie described how developmental difficulties, deprivation, sociocultural conditions, and family relationships could contribute to impaired reality testing. Imaginary friends or companions are common among all children. Children who have imaginary friends are more likely to report hearing “voices.”f Imaginary friends: * appear, function, and disappear at the wish of the child * pose no threat and often are a source of comfort * often can be described in detail * are not ego-dystonic Also, children with imaginary friends will not show evidence of a thought disorder.

Full text: http://www.currentpsychiatry.com/article_pages.asp?aid=8973

Brain Molecule May Offer Key to Erasing Fearful Memories

by Jon Hamilton

Scientists have discovered a molecule in the brain that may help erase the fearful memories that afflict people with post-traumatic stress disorder.

The substance, described in an online edition of the journal Science, was found in mice. But it's part of a memory system that seems to work the same way in people.

Roger Clem and Richard Huganir of the Johns Hopkins University School of Medicine made the discovery while studying mice conditioned to associate a particular sound with an electric shock.

"If they hear the tone the next day, or even weeks later, the mouse will freeze" because it will bring up the fearful memory of the shock, Huganir tells Shots.

Clem and Huganir wanted to understand how that fearful memory is created.

So they studied the brains of mice that had just gone through fear conditioning. And they noticed that an unusual protein appeared in the amygdala, a part of the brain involved in emotions.

That molecule remained for only a few days and appeared to strengthen the brain circuit responsible for maintaining the fearful memory.

But when the researchers eliminated the protein during this period, mice lost their fearful memory. Forever.

The trick was to eliminate the protein soon after a fearful incident, Huganir says.

"Maybe this is a window of time when behavioral therapy would work much better," Huganir says, adding that it may also be possible to eliminate the protein with drugs.

And he says research on people suggests that it may be possible to create a new window for treatment by having people deliberately recall a fearful memory.

Researchers from New York University found that when people did that, there was a 6-hour window in which the original memory could be altered permanently through behavioral techniques.

Experiments in rodents suggest that's because the molecule involved in fear memories appears once again in the amygdala, Huganir says.

If so, he says, it may be possible to eliminate a person's unwanted memory during the critical period by giving a drug that interferes with the fear molecule.

Source link: http://www.npr.org/blogs/health/2010/10/29/130913234/brain-molecule-may-offer-key-to-erasing-fearful-memories-treating-ptsd?ft=1&f=1007

Thursday, October 28, 2010

Reversal of Depressed Behaviors in Mice by p11 Gene Therapy in the Nucleus Accumbens

Sci Transl Med 20 October 2010:  Vol. 2, Issue 54, p. 54ra76
ABSTRACT

The etiology of major depression remains unknown, but dysfunction of serotonergic signaling has long been implicated in the pathophysiology of this disorder. p11 is an S100 family member recently identified as a serotonin 1B [5-hydroxytryptamine 1B (5-HT1B)] and serotonin 4 (5-HT4) receptor–binding protein. Mutant mice in which p11 is deleted show depression-like behaviors, suggesting that p11 may be a mediator of affective disorder pathophysiology. Using somatic gene transfer, we have now identified the nucleus accumbens as a key site of p11 action. Reduction of p11 with adeno-associated virus (AAV)–mediated RNA interference in the nucleus accumbens, but not in the anterior cingulate, of normal adult mice resulted in depression-like behaviors nearly identical to those seen in p11 knockout mice. Restoration of p11 expression specifically in the nucleus accumbens of p11 knockout mice normalized depression-like behaviors. Human nucleus accumbens tissue shows a significant reduction of p11 protein in depressed patients when compared to matched healthy controls. These results suggest that p11 loss in rodent and human nucleus accumbens may contribute to the pathophysiology of depression. Normalization of p11 expression within this brain region with AAV-mediated gene therapy may be of therapeutic value.

Source link: http://stm.sciencemag.org/content/2/54/54ra76.abstract

Full Text: http://stm.sciencemag.org/content/2/54/54ra76.full

Tuesday, October 26, 2010

Nature Neuroscience: November 2010, Volume 13 No 11 pp1299-1440

Meridia (sibutramine): Market Withdrawal Due to Risk of Serious Cardiovascular Events

FDA U.S. Food and Drug Administration

AUDIENCE: Primary Care, Consumers

ISSUE: Abbott Laboratories and FDA notified healthcare professionals and patients about the voluntary withdrawal of Meridia (sibutramine), an obesity drug, from the U.S. market because of clinical trial data indicating an increased risk of heart attack and stroke.

BACKGROUND: Meridia was approved November 1997 for weight loss and maintenance of weight loss in obese people, as well as in certain overweight people with other risks for heart disease. The approval was based on clinical data showing that more people receiving sibutramine lost at least 5 percent of their body weight than people on placebo who relied on diet and exercise alone. FDA has now requested market withdrawal after reviewing data from the Sibutramine Cardiovascular Outcomes Trial (SCOUT). SCOUT is part of a postmarket requirement to look at cardiovascular safety of sibutramine after the European approval of the drug. The trial demonstrated a 16 percent increase in the risk of serious heart events, including non-fatal heart attack, non-fatal stroke, the need to be resuscitated once the heart stopped, and death, in a group of patients given sibutramine compared with another given placebo. There was a small difference in weight loss between the placebo group and the group that received sibutramine.

RECOMMENDATION: Physicians are advised to stop prescribing Meridia to their patients, and patients should stop taking this medication. Patients should talk to their health care provider about alternative weight loss and weight loss maintenance programs.

Source link: http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm228830.htm

Mortality Hazard Associated With Anxiolytic and Hypnotic Drug Use in the National Population Health Survey

The Canadian Journal of Psychiatry, vol 55, no 9, septembre 2010
Geneviève Belleville, PhD


Objective: Although widely used in the general population, sleeping pills and minor tranquilizers, also known as antianxiety agents, have been associated with undesirable outcomes. Reports about the association of these drugs with an elevated mortality rate are inconsistent and controversial. This study was designed to assess the mortality hazard associated with anxiolytic and hypnotic drug use in the National Population Health Survey in
Canada. It was hypothesized that anxiolytic and hypnotic drug use would be associated with
an elevated mortality hazard.
Method: A population-based sample of 14 117 people aged 18 to 102 years participated in a longitudinal panel survey, with data collected every second year from 1994 to 2007. The primary outcome measures reported in this study are self-report use of anxiolytic and hypnotic drugs, and death.
Results: For respondents who reported anxiolytic or hypnotic drug use in the past month the odds of mortality were 3.22 times more (95% CI 2.70 to 3.84) than for those who did not use anxiolytic or hypnotic drugs in the past month. After controlling for confounding sociodemographic, lifestyle, and health factors (including depression), the odds ratio was reduced to 1.36 (95% CI 1.09 to 1.70) but remained significant.
Conclusion: Sedative drug use is associated with a small but significant increase in mortality risk. Further research is required to confirm the mechanisms by which sedative drug use increases mortality risk. Where possible, physicians should systematically consider possibilities for nonpharmacological treatment of sleep disturbances and anxiety.

Can J Psychiatry. 2010;55(9):558–567.

View full text: http://publications.cpa-apc.org/media.php?mid=1018