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Brain Site for Depression Symptoms
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NEW YORK (Reuters) -- Abnormally high glucose metabolism in a region at the
center of the brain may cause many of the emotional symptoms associated
with depression, according to a new study.

The almond-sized brain region is the amygdala, known to be important in
emotional behavior and in learning the emotional significance of
situations, explains Dr. Wayne Drevets, associate professor of psychiatry
and radiology at the University of Pittsburgh Medical Center, Pittsburgh,
Pennsylvania.

The new findings were based on overlays of positron emission tomography
(PET) scans on magnetic resonance imaging (MRI) brain scans of depressed
and non-depressed individuals.

In presenting the study this week at the Society for Neuroscience Annual
Meeting in New Orleans, Louisiana, Drevets said the findings may improve
our understanding of how antidepressant and mood-stabilizing treatments work.

They may also lead to better treatments for people with major depression
and those who suffer mood changes associated with bipolar disorder (manic
depression).

"In a previous study of depressed patients, we had found increased blood
flow in the amygdala, and increased blood flow would go along with
increased amount of communication between cells in the structure," Drevets
says. "So the amygdala was overly active in depression."

In the new study, "we used a much higher resolution PET scanner and so we
were able to confirm that there is, in fact, increased glucose metabolism
also in this region," the researcher explains, adding that the findings
were similar "in people who had bipolar illness, who were either depressed
or manic."

The study used PET images of glucose metabolism and MRI images of brain
structure in 32 people with major depressive disorder or bipolar disorder.
"We also had a control group of 15 subjects who neither had episodes of
major depression themselves nor had family histories of depression,"
Drevets says.

The researcher notes the study also linked abnormal amygdala metabolism
with elevated cortisol in depression -- including in bipolar depressed
patients.

"It's been known for about 30 years that depressed people release too much
of a stress hormone called cortisol," he says.

"There's sort of a chemical cascade in the body that's responsible for
releasing cortisol. That cascade is called the
hypothalamic-pituitary-adrenal-axis.

"That axis is overly active in depression, and our study is the first to
suggest that the overactive amygdala might be the explanation for this
effect."

Drevets explains that the amygdala helps the brain learn the emotional
significance of sensory signals, such as situations that present a threat,
and organizes the way those signals are expressed, from rapid heart beat to
facial expressions.

Because of the amygdala's key role in producing such experiences as fear,
malaise (dysphoria), and sometimes vivid recall of past emotionally charged
events, its abnormal activity may be responsible for anxiety, panic
attacks, and many symptoms of depression, Drevets says.

"When neurosurgeons have electrically stimulated the amygdala in humans
during operations, people report feeling anxiety, fear, dysphoria, and some
of them may vividly recall emotionally charged events that happened 20
years ago," Drevets says.

"So when you think of our PET scans showing this overactive amygdala in
depressed people, that might account for why they feel quite anxious.

"In major depression, anxiety is sometimes more prominent than the
depressed mood itself."

And depressed people are prone to be preoccupied with memories of negative
life events, he adds.

"If you are taking antidepressant treatment and it's not successful at
either restoring your amygdala activity to normal or dropping the
hypothalamic--pituitary-adrenal axis activity to normal, then you're at a
very high risk to relapse -- even though you continue the treatment,"
Drevets says.

"What we now know suggests that if we can develop drugs that more
effectively reduce metabolism in this structure, we may be able to better
treat or prevent depression as well as mania."


1997, Reuters Health eLine
<http://www.medscape.com/reuters/mon/t1031-6f.html>
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