Study Explains How Shock Therapy Might Ease Severe Depression

Clickbank Products Study Explains How Shock Therapy Might Ease Severe Depression



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By Carina Storrs
HealthDay Reporter

MONDAY, March 19 (HealthDay News) -- A small new study gives insight into how electroshock therapy, an effective yet poorly understood treatment for severe depression, affects the brains of depressed people.

Researchers used functional MRI scans to look at brain activity in nine adults with severe depression before and after electroshock therapy. The investigators found that electroshock, or electroconvulsive therapy (ECT), dampens the connections between different areas of the brain in depressed people.

"With our study we were able to confirm that there is hyperconnectivity [in depression], and in addition we could show that treatment removes it," said study co-author Christian Schwarzbauer, a professor of neuroimaging at the University of Aberdeen in Scotland.

Although it may seem counterintuitive that people with severe depression, who are often also lethargic, would have brains on overdrive, one explanation could be that they have too much internal brain activity and cannot deal as well with external stimulation, Schwarzbauer said.

This study could point to ways to improve electroshock therapy's effectiveness and safety, he added. In its 76-year history, the treatment has met with opposition from doctors because of concerns of its side effects, such as memory loss.

Electroshock therapy is typically only used for patients who have not responded to antidepressants or other types of treatment and are at risk of hurting themselves or others.

"I think the fact that now there's more of an explanation, I think that's reassuring to the clinician as well as the patient," said Jennifer Perrin, who is a research fellow at the University of Aberdeen and lead author of the study published online March 19 in the Proceedings of the National Academy of Sciences.

For the study, nine severely depressed participants underwent functional MRI scans of their whole brain before and after a series of electroshock therapy. They received the treatment twice a week until their symptoms, including sadness and fatigue, subsided.

The participants had not responded to antidepressant drugs before the study or received electroshock therapy in the past six months, although four of the patients were taking antipsychotic medications.

The researchers zeroed in on an area in the front of the brain called the dorsolateral prefrontal cortex. It had fewer and less intense connections with a number of other areas of the brain following electroshock therapy, the scans showed.

This particular part of the brain is involved in cognition [thought processes] and social behavior and has been implicated in depression, so this finding is not surprising, said Tony Tang, an adjunct professor of psychology at Northwestern University. What is surprising, he said, is that none of the many other brain areas that have been associated with depression were found to have cut-off lines of communication following electroshock therapy.

"ECT is a rather invasive, drastic procedure and you see a lot of changes in patients, so we would probably speculate that there would be some sort of widespread brain connectivity changes," Tang said. This study "found it to be localized, and I found that to be rather amazing."

During electroshock treatment, clinicians place electrodes on the scalp and, while the patient is under anesthesia, deliver enough electric current to induce a seizure. The therapy is more effective when electrodes are on both sides of the head, as opposed to just one, but unfortunately this also carries greater risk of side effects.

Having electrodes on both sides of the head may be more effective because it triggers a more widespread seizure, but the current findings suggest another possibility, Tang said: When clinicians put electrodes just on one side of the scalp, they usually put them over the right half of the brain because it is less dominant (for right-handed people). However, according to this study, the dorsolateral prefrontal cortex, in the left side of the brain, could be the crucial area to target.

"Most localized forms of stimulation we've tried so far don't work as well [as having electrodes on both sides], but this type of study could potentially point to the right direction," Tang said.

Looking at brain connections in people with severe depression could help clinicians predict who will benefit from electroshock therapy as well as who will relapse after treatment, Schwarzbauer suggested. Between about 60 percent and 80 percent of people become depressed again, usually within six months of the treatment.

Beyond depression, functional MRI of the entire brain could offer insights into other conditions that could be related to changes in brain networks, including autism, schizophrenia and dementia, Schwarzbauer said.

Copyright © 2012 HealthDay. All rights reserved. SOURCES: Christian Schwarzbauer, Ph.D., chair, neuroimaging, University of Aberdeen, Aberdeen, Scotland; Jennifer Perrin, Ph.D., research fellow, University of Aberdeen, Scotland; Tony Tang, Ph.D., adjunct professor, psychology, Weinberg College of Arts & Sciences, Northwestern University, Chicago; March 19, 2012, Proceedings of the National Academy of Sciences, online

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Study Might Explain Brain Overgrowth Seen in Autism

Clickbank Products Study Might Explain Brain Overgrowth Seen in Autism



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By Jenifer Goodwin
HealthDay Reporter

FRIDAY, March 23 (HealthDay News) -- Researchers report that they have identified abnormalities in the DNA and RNA of cells in the prefrontal cortex of the brains of autistic children.

The findings may help to explain the underlying mechanism for the brain "overgrowth" that prior reports have documented in autistic children. Those studies have found that the brains of young children with autism are larger than the brains of non-autistic children, particularly in the prefrontal cortex. The prefrontal cortex is key to complex thoughts and behaviors, including language, social behavior and decision-making.

This growth abnormality likely contributes significantly to the social,communication, and emotional deficits common among people with autism, the researchers said.

In the new study, researchers analyzed tissue from the prefrontal cortexes of 33 postmortem brain samples from autistic and non-autistic people aged 2 to 56.

In addition to DNA differences known as copy number variations, researchers also did genome-wide RNA profiling and found differences in RNA between the autistic and non-autistic brains. RNA (ribonucleic acid) plays crucial roles within cells, serving as an intermediary between DNA, the blueprints for genetic information, and the production of proteins that carry out a vast array of vital activities in cells.

The RNA abnormalities appear to be involved with genes that code for proteins regulating cellular growth, the researchers said.

"What we found was the networks that are supposed to regulate the genesis of brain cells and develop them were abnormal. The networks that were supposed to regulate DNA repair were turned down. And the networks supposed to regulate neuron removal and survival were abnormal," said study author Eric Courchesne, director of the Autism Center of Excellence at the University of California, San Diego (UCSD) School of Medicine.

The study is published in the March 22 issue of PLoS Genetics.

How might these differences fit into the autistic picture?

Preliminary research by the UCSD team found that an excessive amount of neurons, or brain cells, might account for the overgrowth. While typically developing kids had about 0.88 billion neurons in the prefrontal cortex, autistic children had about 1.57 billion.

According to the researchers, the copy number variations along with the RNA abnormalities may disrupt the cell cycle and may explain the underlying mechanism driving the overgrowth.

"We found DNA defects, or copy number variations, in a variety of genes that regulate cell production and cell survival," Courchesne said. "To us, that suggests the explanation for why there are an abnormal number of neurons in the prefrontal cortex. Those genes fall into networks that control the number of neurons generated and the number that survive in prenatal life."

Researchers also noted that the RNA differences vary, depending on the age of the brain, with children and adults having different RNA profiles.

Courchesne said that the way the brain responds to that overgrowth of neurons -- in other words, what's happening in those repair pathways -- may help to explain why people with autism may have different trajectories, with some seeming to regress and others continuing to learn new skills throughout their lifetime.

"In adulthood, we see individuals that continue to improve, and continue to gain more and more skills and abilities," Courchesne said. "Then there are others that don't show that continued, ongoing improvement or show the opposite. My best guess is the trajectory has less to do with the original cause of the autism, than with an individual's specific composition of genes, or the available genes to remodel the brain."

Robert Ring, vice president for translational research at Autism Speaks, said researchers offer up a provocative and plausible theory. However, he noted that while brain overgrowth is well-established, only one, small study has shown that the explanation for it is too many neurons.

"What's valuable about the approach this group has taken is that they've gone directly to the tissue of interest, and have asked, 'Is there any evidence there are abnormalities in the expression of genes that correlate with the neuro-anatomic or cellular findings that have been reported?'" Ring said.

"What they're reporting is there is indeed some evidence that particular pathways might be disregulated in the autistic brain vs. the control brain, and some of these pathways, when you look at their function, may be a plausible explanation for the increased growth and increased cell number."

The study, Ring added, offers up new clues for researchers to pursue, but nothing is proven. "There is an enormous amount of work needed to confirm this," he said.

Copyright © 2012 HealthDay. All rights reserved. SOURCES: Eric Courchesne, Ph.D., director, Autism Center of Excellence, University of California, San Diego School of Medicine; Robert Ring, Ph.D., vice president, translational research, Autism Speaks; March 22, 2012, PLoS Genetics

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