Category: Neuropsychiatric Disease

More evidence that mindfullness meditation can help with anxiety, depression and pain

On By A.P.In Allan Goroll, Andrew M. Seaman, Anxiety, Depression, Harvard Medical School, JAMA Internal Medicine, Johns Hopkins University, Madhav Goyal, mantra meditation, Medicine, Meditation, mindfullness, mindfulness meditation, Neuropsychiatric Disease, Pain, ScienceLeave a comment

mindfulness-meditation

By Andrew M. Seaman

Mindfulness meditation may be useful in battles against anxiety, depression and pain, according to a fresh look at past research.

Using data from 47 earlier studies, researchers found moderate evidence to support the use of mindfulness meditation to treat those conditions. Meditation didn’t seem to affect mood, sleep or substance use.

“Many people have the idea that meditation means just sitting quietly and doing nothing,” wrote Dr. Madhav Goyal in an email to Reuters Health. “That is not true. It is an active training of the mind to increase awareness, and different meditation programs approach this in different ways.”

Goyal led the study at The Johns Hopkins University in Baltimore.

He and his colleagues write in JAMA Internal Medicine that meditation techniques emphasize mindfulness and concentration.

So-called mindfulness meditation is aimed at allowing the mind to pay attention to whatever thoughts enter it, such as sounds in the environment, without becoming too focused. Mantra meditation, on the other hand, involves focusing concentration on a particular word or sound.

Approximately 9 percent of people in the U.S. reported meditating in 2007, according to the National Institutes of Health. About 1 percent said they use meditation as some sort of treatment or medicine.

For the new report, the researchers searched several electronic databases that catalog medical research for trials that randomly assigned people with a certain condition – such as anxiety, pain or depression – to do meditation or another activity. These randomized controlled trials are considered the gold standard of medical research.

The researchers found 47 studies with over 3,500 participants that met their criteria.

After combining the data, Goyal said his team found between a 5 and 10 percent improvement in anxiety symptoms among people who took part in mindfulness meditation, compared to those who did another activity.

There was also about a 10 to 20 percent improvement in symptoms of depression among those who practiced mindfulness meditation, compared to the other group.

“This is similar to the effects that other studies have found for the use of antidepressants in similar populations,” Goyal said.

Mindfulness meditation was also tied to reduced pain. But Goyal said it’s hard to know what kind of pain may be most affected by meditation.

The benefits of meditation didn’t surpass what is typically associated with other treatments, such as drugs and exercise, for those conditions.

“As with many therapies, we try to get a moderate level of confidence that the therapy works before we prescribe it,” Goyal said. “If we have a high level of confidence, it is much better.”

But he noted that the researchers didn’t find anything more than moderate evidence of benefit from meditation for anxiety, depression and pain.

There was some suggestion that meditation may help improve stress and overall mental health, but the evidence supporting those findings was of low quality.

There was no clear evidence that meditation could influence positive mood, attention, substance use, eating habits, sleep or weight.

“Clinicians should be prepared to talk with their patients about the role that meditation programs could have in addressing psychological stress, particularly when symptoms are mild,” Goyal said.

Dr. Allan Goroll, who wrote an editorial accompanying the new study, told Reuters Health the analysis is an example of an area of much-needed scientific study, because many people make treatment decisions based on beliefs – not data.

“That is particularly the case with alternative and complimentary approaches to treating medical problems,” he said. “It ranges from taking vitamins to undergoing particular procedures for which the scientific evidence is very slim but people’s beliefs are very great.”

Goroll is professor at Harvard Medical School and Massachusetts General Hospital in Boston.

Goyal said people should remember that meditation was not conceived to treat any particular health problem.

“Rather, it is a path we travel on to increase our awareness and gain insight into our lives,” he wrote. “The best reason to meditate is to gain this insight. Improvements in health conditions are really a side benefit, and it’s best to think of them that way.”

SOURCE: bit.ly/WiwDtv JAMA Internal Medicine, online January 6, 2014.

Durham man with ALS achieves Krispy Kreme dream

On By A.P.In A Krispy Kreme Heist, ALS, amyotrophic lateral sclerosis, Anna Rosati, Chris Rosati, donut, Dr. Goldman, Duke University Medical Center, Durham, Durham Academy, Facebook, Flexible Starliner, generosity, Inspire MEdia, Krispy Kreme, Krispy Kreme Cruiser, Medicine, Megan Brock, mischief, Neuropsychiatric Disease, North Carolina, Original Glazed, random acts of kindness, Robin Hood, Winston-SalemLeave a comment

Vhris

krispy-kreme-cruiser

In a speech a few weeks ago at Durham Academy, his high-school alma mater, Chris Rosati told students about a sweet dream of his.

He wanted to hijack a Krispy Kreme doughnut delivery truck and, with the cops chasing him, drive around tossing out free confections and cheer. Robin Hood, with baked goods.

The normally jaded teens embraced the idea with such enthusiasm that Rosati – already inclined to mischief – became determined to make it happen.

But every successful dreamer is also a realist, and Rosati knew his chances of getting away with a loaded doughnut truck were pretty slim, especially since he was diagnosed three years ago with amyotrophic lateral sclerosis. He can still walk, with assistance, but the degenerative neuromuscular disorder, which is ultimately fatal, has slowed him down.

He would need some help.

Rosati, a self-employed marketing consultant, knew what to do. He set up a Facebook page called A Krispy Kreme Heist, where he described his plan. He solicited “likes,” in the hopes that eventually, Winston-Salem-based Krispy Kreme would hear about it, lend him a truck and driver, and give him some doughnuts to give away.

Since he got sick, he explained, “I’m more open than ever to chasing my dreams … even odd ones like this.”

His story traveled like the scent of Original Glazed hot off the line. Within eight hours, Krispy Kreme corporate officials heard about Rosati’s idea.

“We got in touch with Chris and told him, ‘Don’t steal one of our trucks,’” said Megan Brock, directer of marketing. “We’ll give you the Krispy Kreme Cruiser and a thousand doughnuts.”

The Cruiser is a 1960 Flexible Starliner bus restored and christened last year for the company’s 75th anniversary. Krispy Kreme likes to say it’s one sweet ride that travels the country for promotional events.

Tuesday, its route was chosen by Rosati, who had the driver go to Duke University Medical Center, where he visited a cancer treatment center, a bone marrow transplant facility and the clinic where he gets treatment for his ALS.

After that, it was on to Durham Academy, where 400 high-schoolers had been assembled on the sidewalk without knowing why.

They figured it out when the Cruiser rolled into the parking lot, with its trademark green polka dots and Krispy Kreme bow-tie logo. They screamed and hooted.

“I told y’all to live out your dreams, as dumb as they may be sometimes,” he told the students as he got off the bus.

They would each get a doughnut, he promised, but then he asked a favor. Would some of them take a box, go out into the community and give them away just to see people smile?

“You get 12 chances in that box to make somebody happy,” he said.

Rosati’s wife, Anna, said the couple would use video of the day’s events to inspire others toward random acts of kindness through Rosati’s nonprofit, called Inspire MEdia. Eventually, Anna Rosati said, the couple hope the foundation will be able to help people fund their own uplifting projects.

http://www.journalnow.com/news/state_region/article_8a8f4da8-5fb0-11e3-ad14-001a4bcf6878.html

Thanks to Dr. Goldman for bringing this to the It’s Interesting community.

‘Jumping Genes’ Linked to Schizophrenia

On By A.P.In DNA, Dr. Rajadhyaksha, gene, Japan, jumping gene, line element, Medicine, mental health, mental illness, neural activity, neurogenesis, neurologist, Neurology, Neuron, neuroplasticity, Neuropsychiatric Disease, Neuroscience, neuroscientist, neurotransmitter, RIKEN Brain Science Institute, schizophrenia, Science, Tadafumi KatoLeave a comment

sn-schizophrenia

Roaming bits of DNA that can relocate and proliferate throughout the genome, called “jumping genes,” may contribute to schizophrenia, a new study suggests. These rogue genetic elements pepper the brain tissue of deceased people with the disorder and multiply in response to stressful events, such as infection during pregnancy, which increase the risk of the disease. The study could help explain how genes and environment work together to produce the complex disorder and may even point to ways of lowering the risk of the disease, researchers say.

Schizophrenia causes hallucinations, delusions, and a host of other cognitive problems, and afflicts roughly 1% of all people. It runs in families—a person whose twin sibling has the disorder, for example, has a roughly 50-50 chance of developing it. Scientists have struggled to define which genes are most important to developing the disease, however; each individual gene associated with the disorder confers only modest risk. Environmental factors such as viral infections before birth have also been shown to increase risk of developing schizophrenia, but how and whether these exposures work together with genes to skew brain development and produce the disease is still unclear, says Tadafumi Kato, a neuroscientist at the RIKEN Brain Science Institute in Wako City, Japan and co-author of the new study.

Over the past several years, a new mechanism for genetic mutation has attracted considerable interest from researchers studying neurological disorders, Kato says. Informally called jumping genes, these bits of DNA can replicate and insert themselves into other regions of the genome, where they either lie silent, doing nothing; start churning out their own genetic products; or alter the activity of their neighboring genes. If that sounds potentially dangerous, it is: Such genes are often the culprits behind tumor-causing mutations and have been implicated in several neurological diseases. However, jumping genes also make up nearly half the current human genome, suggesting that humans owe much of our identity to their audacious leaps.

Recent research by neuroscientist Fred Gage and colleagues at the University of California (UC), San Diego, has shown that one of the most common types of jumping gene in people, called L1, is particularly abundant in human stem cells in the brain that ultimately differentiate into neurons and plays an important role in regulating neuronal development and proliferation. Although Gage and colleagues have found that increased L1 is associated with mental disorders such as Rett syndrome, a form of autism, and a neurological motor disease called Louis-Bar syndrome, “no one had looked very carefully” to see if the gene might also contribute to schizophrenia, he says.

To investigate that question, principal investigator Kazuya Iwamoto, a neuroscientist; Kato; and their team at RIKEN extracted brain tissue of deceased people who had been diagnosed with schizophrenia as well as several other mental disorders, extracted DNA from their neurons, and compared it with that of healthy people. Compared with controls, there was a 1.1-fold increase in L1 in the tissue of people with schizophrenia, as well as slightly less elevated levels in people with other mental disorders such as major depression, the team reports today in Neuron.

Next, the scientists tested whether environmental factors associated with schizophrenia could trigger a comparable increase in L1. They injected pregnant mice with a chemical that simulates viral infection and found that their offspring did, indeed, show higher levels of the gene in their brain tissue. An additional study in infant macaques, which mimicked exposure to a hormone also associated with increased schizophrenia risk, produced similar results. Finally, the group examined human neural stem cells extracted from people with schizophrenia and found that these, too, showed higher levels of L1.

The fact that it is possible to increase the number of copies of L1 in the mouse and macaque brains using established environmental triggers for schizophrenia shows that such genetic mutations in the brain may be preventable if such exposures can be avoided, Kato says. He says he hopes that the “new view” that environmental factors can trigger or deter genetic changes involved in the disease will help remove some of the disorder’s stigma.

Combined with previous studies on other disorders, the new study suggests that L1 genes are indeed more active in the brain of patients with neuropsychiatric diseases, Gage says. He cautions, however, that no one yet knows whether they are actually causing the disease. “Now that we have multiple confirmations of this occurring in humans with different diseases, the next step is to determine if possible what role, if any, they play.”

One tantalizing possibility is that as these restless bits of DNA drift throughout the genomes of human brain cells, they help create the vibrant cognitive diversity that helps humans as a species respond to changing environmental conditions, and produces extraordinary “outliers,” including innovators and geniuses such as Picasso, says UC San Diego neuroscientist Alysson Muotri. The price of such rich diversity may be that mutations contributing to mental disorders such as schizophrenia sometimes emerge. Figuring out what these jumping genes truly do in the human brain is the “next frontier” for understanding complex mental disorders, he says. “This is only the tip of the iceberg.”

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

http://news.sciencemag.org/biology/2014/01/jumping-genes-linked-schizophrenia

Alexandra Wolff: 1 of 55 people in the U.S. with highly superior autobiographical memory.

On By A.P.In Alexandra Wolff, brain, Depression, highly superior autobiographical memory, HSAM, memory, Neurology, Neuropsychiatric Disease, NeuroscienceLeave a comment

alexandra_custom-dd75c71966d9515cea210d91d68ce7aff737e3a5-s6-c85

On Feb. 21, Alexandra Wolff ate steak, mashed potatoes and broccoli for dinner. Later that night, sitting in her room, she spent 20 minutes scanning pictures in InStyle magazine.

She remembers those things, just as she remembers that on Aug. 2 she stopped at Target and bought Raisin Bran; and on April 17 she wore a white button-down shirt; and on Oct. 2 she went to TGI Fridays and spoke to the hostess, who was wearing black leather flats with small bows on them.

Alexandra Wolff has what’s known as highly superior autobiographical memory. She is one of only 55 people in the U.S. who have been identified with this ability. All of these people can remember details about their lives that the rest of us couldn’t hope to remember: the strangers they pass on the street, the first thing they saw when they woke up seven months ago.

And though it’s not clear why the brains of people with HSAM can do what they do, what is clear is that this ability gives them an access to the past that’s profoundly different from you and me.

If you think of 2013, probably only a handful of memories stand out. The day-by-day is a blur.

We forget most of our lives.

But Alexandra says that remembering even an inconsequential trip to Target is an almost physical experience for her. She says she sees what she saw that day, hears what she heard, and emotionally feels what she felt at the time.

“Right down to getting sick to my stomach or getting a headache,” she says. “It’s almost like time travel.”

But being unable to forget can affect your relationship to the present, people with this form of memory say.

Alexandra is 22 and lives with her mother in a long brick ranch house in southern Maryland. She has dark hair and beautifully balanced features, but hasn’t really dated and seems to have few of the preoccupations of most 22-year-olds. She blames her memory for this, saying it separates her from other people her age because they can’t understand why she’s so focused on things that have already happened.

Alexandra often feels frustrated with her preoccupation with the past. “It seems like you hold onto everything, and it seems like you’re just stuck in the past all the time,” she says.

It really bothers her. For one, Alexandra says, in her life there are no fresh days, no clean slates without association. Every morning when she wakes up, details of that date from years before are scrolling through her mind, details that can profoundly affect the new day she’s in.

For example, the day before we spoke was a day when years ago in middle school a boy bullied her in one of her classes.

“I didn’t mention it to anyone,” she says, “but I mean, still in the back of my mind I kept thinking and thinking about it. It knocked some of my confidence down.”

Because the past is so viscerally right there, so available, she finds that when the present gets overwhelming, it’s hard not to retreat to the past.

Even though she’s only 22, she says she spends huge amounts of time in her room with her eyes closed, reliving the past in her mind, particularly this one day a decade ago.

It was July 8, 2004. She spent that day in a bathing suit by a pool laughing and playing with her 10-year-old cousin. They ate macaroni and cheese, and swam. It was an easy, innocent time.

She says she probably takes herself through that day in her mind four times a week. Over the past couple of years, she estimates, she’s probably spent close to 2,000 hours reliving that one day.

“I mean, I definitely say it’s a huge temptation. I could, if I didn’t have stuff to do all day, I could probably live in the past 24/7.”
Scientists think there’s a reason why we forget.

“It has long been believed by research scientists that forgetting is adaptive,” says James McGaugh, the University of California, Irvine neurobiologist who first documented highly superior autobiographical memory.

McGaugh discovered HSAM by accident. He got an email out of the blue from a woman named Jill Price who said she had a serious memory problem: She couldn’t seem to forget anything, and like Alexandra, this bothered her.

“The emotions evoked by remembering bad things troubled her,” McGaugh says.

And so McGaugh started studying first Price and then other people with this kind of memory. He found ultimately that there are differences in the brains of people with HSAM, though it’s not clear whether the differences are the cause or the consequence of this ability.

But it is clear that it’s specifically this issue of forgetting that’s different. If you were asked to recall what happened to you earlier this morning, you’d remember roughly the same amount as someone like Alexandra. But if asked about this morning three months from now, for you it would probably be gone, while for her it’s as fresh as it is for you today.

“So it’s not that they’re superior learners,” McGaugh says, “it’s that they are very poor at forgetting.”
The emotional effects of not being able to forget aren’t clear, says McGaugh. No one, including McGaugh, has studied it. His sense is that there is variation in the group of 55.

“The effects of having this ability depends on the kind of experiences people have had in the past as well as their present circumstances,” he says.

But Bill Brown, another person with HSAM, says that he’s been in touch with most of the people in the group, and that everyone he has spoken to has struggled with depression. He says that very few of them have been able to maintain a long-term marriage — the rumor is only 2 out of the 55.
Brown himself, though a pretty jolly guy, recently separated from his wife.

And talking to him, you do get the sense that the difference in his memory has led to misunderstandings in his relationships.

“Just because I remember something that you did wrong doesn’t mean that I still hold it against you,” he says. “But it’s taken me a long while to realize that folks without my ability probably don’t understand that distinction. Because after all, if you’re bringing it up, the logic from the other side would be: You must still hold it against me.”

This is not, in fact, the case, he says. “It has more to do with wanting you to be honest in your dealings.”

What he eventually realized was that most of the people he talks to are being as honest as they know how to be. “They just don’t necessarily remember.”
Brown says it’s easier for him now, because over time he’s learned how to manage the memories, not to focus on the bad stuff, and instead use his memory to entertain himself.

“But you know,” he says, “life’s rough, and there’s so much bad that’s kinda there.”

Sometimes, he says, he thinks it might be nice to forget.

http://www.npr.org/blogs/health/2013/12/18/255285479/when-memories-never-fade-the-past-can-poison-the-present

Could Pot Help Veterans With PTSD? Brain Scientists Say Maybe

On By A.P.In Andrew Holmes, anxiety circuitry, Atlanta, brain, cannabinoids, cannabis, Cannabis sativa, Drugs, Emory University, Emory University School of Medicine, extinction therapy, fear circuitry, Georgia, Jon Hamilton, Kerry Ressler, marijuana, Medicine, military, National Institute of Mental Health, National Institute on Alcohol Abuse and Alcoholism, National Institute on Drug Abuse, Neuropsychiatric Disease, Neuroscience, neuroscientist, post-traumatic stress disorder, pot, psychiatrist, Psychiatry, psychology, psychotherapy, PTSD, Science, tetrahydrocannabinol, THC, VeteransLeave a comment

pot

by Jon Hamilton

Veterans who smoke marijuana to cope with post-traumatic stress disorder may be onto something. There’s growing evidence that pot can affect brain circuits involved in PTSD.

Experiments in animals show that tetrahydrocannabinol, the chemical that gives marijuana its feel-good qualities, acts on a system in the brain that is “critical for fear and anxiety modulation,” says Andrew Holmes, a researcher at the National Institute on Alcohol Abuse and Alcoholism. But he and other brain scientists caution that marijuana has serious drawbacks as a potential treatment for PTSD.

The use of marijuana for PTSD has gained national attention in the past few years as thousands of traumatized veterans who fought in Iraq and Afghanistan have asked the federal government to give them access to the drug. Also, Maine and a handful of other states have passed laws giving people with PTSD access to medical marijuana.

But there’s never been a rigorous scientific study to find out whether marijuana actually helps people with PTSD. So lawmakers and veterans groups have relied on anecdotes from people with the disorder and new research on how both pot and PTSD works in the brain.

An Overactive Fear System

When a typical person encounters something scary, the brain’s fear system goes into overdrive, says Dr. Kerry Ressler of Emory University. The heart pounds, muscles tighten. Then, once the danger is past, everything goes back to normal, he says.

But Ressler says that’s not what happens in the brain of someone with PTSD. “One way of thinking about PTSD is an overactivation of the fear system that can’t be inhibited, can’t be normally modulated,” he says.

For decades, researchers have suspected that marijuana might help people with PTSD by quieting an overactive fear system. But they didn’t understand how this might work until 2002, when scientists in Germany published a mouse study showing that the brain uses chemicals called cannabinoids to modulate the fear system, Ressler says.

There are two common sources of cannabinoids. One is the brain itself, which uses the chemicals to regulate a variety of brain cells. The other common source is Cannabis sativa, the marijuana plant.

So in recent years, researchers have done lots of experiments that involved treating traumatized mice with the active ingredient in pot, tetrahydrocannabinol (THC), Ressler says. And in general, he says, the mice who get THC look “less anxious, more calm, you know, many of the things that you might imagine.”

Problems with Pot

Unfortunately, THC’s effect on fear doesn’t seem to last, Ressler says, because prolonged exposure seems to make brain cells less sensitive to the chemical.

Another downside to using marijuana for PTSD is side effects, says Andrew Holmes at the National Institute on Alcohol Abuse and Alcoholism. “You may indeed get a reduction in anxiety,” Holmes says. “But you’re also going to get all of these unwanted effects,” including short-term memory loss, increased appetite and impaired motor skills.

So for several years now, Holmes and other scientists have been testing drugs that appear to work like marijuana, but with fewer drawbacks. Some of the most promising drugs amplify the effect of the brain’s own cannabinoids, which are called endocannabinoids, he says. “What’s encouraging about the effects of these endocannabinoid-acting drugs is that they may allow for long-term reductions in anxiety, in other words weeks if not months.”

The drugs work well in mice, Holmes says. But tests in people are just beginning and will take years to complete. In the meantime, researchers are learning more about how marijuana and THC affect the fear system in people.

At least one team has had success giving a single dose of THC to people during something called extinction therapy. The therapy is designed to teach the brain to stop reacting to something that previously triggered a fearful response.

The team’s study found that people who got THC during the therapy had “long-lasting reductions in anxiety, very similar to what we were seeing in our animal models,” Holmes says. So THC may be most useful when used for a short time in combination with other therapy, he says.

As studies continue to suggest that marijuana can help people with PTSD, it may be unrealistic to expect people with the disorder to wait for something better than marijuana and THC, Ressler says. “I’m a pragmatist,” he says. “I think if there are medications including drugs like marijuana that can be used in the right way, there’s an opportunity there, potentially.”

http://www.npr.org/blogs/health/2013/12/23/256610483/could-pot-help-veterans-with-ptsd-brain-scientists-say-maybe

Sleep therapy becoming increasingly important in depression treatment

On By A.P.In Aaron T. Beck, American Psychological Association, Anxiety, brain, CBT, CBT-I, cognitive behavioral therapy, cognitive behavioral therapy for insomnia, Colleen Carney, Department of Veterans Affairs, Depression, insomnia, John M. Oldham, Johns Hopkins University, Johns Hopkins University School of Medicine, Medicine, Menninger Clinic, Michael T. Smith, Montefiore Medical Center, Neuropsychiatric Disease, psychiatrist, Psychiatry, psychology, psychotherapy, Ryerson University, Shelby Harris, Sleep, sleep psychology, Society of Behavioral Sleep Medicine2 Comments

Insomnia-Electronic-Cigarettes

An insomnia therapy that scientists just reported could double the effectiveness of depression treatment is not widely available nor particularly well understood by psychiatrists or the public. The American Board of Sleep Medicine has certified just 400 practitioners in the United States to administer it, and they are sparse, even in big cities.

That may change soon, however. Four rigorous studies of the treatment are nearing completion and due to be reported in coming months. In the past year, the American Psychological Association recognized sleep psychology as a specialty, and the Department of Veterans Affairs began a program to train about 600 sleep specialists. So-called insomnia disorder is defined as at least three months of poor sleep that causes problems at work, at home or in relationships.

The need is great: Depression is the most common mood disorder, affecting some 18 million Americans in any given year, and most have insomnia.

“I think it’s increasingly likely that this kind of sleep therapy will be used as a possible complement to standard care,” said Dr. John M. Oldham, chief of staff at the Menninger Clinic in Houston. “We are the court of last resort for the most difficult-to-treat patients, and I think sleep problems have been extremely underrecognized as a critical factor.”

The treatment, known as cognitive behavioral therapy for insomnia, or CBT-I, is not widely available. Most insurers cover it, and the rates for private practitioners are roughly the same as for any psychotherapy, ranging from $100 to $250 an hour, depending on the therapist.

“There aren’t many of us doing this therapy,” said Shelby Harris, the director of the behavioral sleep medicine program at Montefiore Medical Center in the Bronx, who also has a private practice in Tarrytown, N.Y. “I feel like we all know each other.”

According to preliminary results, one of the four studies has found that when CBT-I cures insomnia — it does so 40 percent to 50 percent of the time, previous work suggests — it powerfully complements the effect of antidepressant drugs.

“There’s been a huge recognition that insomnia cuts across a wide variety of medical disorders, and there’s a need to address it,” said Michael T. Smith, a professor at the Johns Hopkins School of Medicine and president of the Society of Behavioral Sleep Medicine.

The therapy is easy to teach, said Colleen Carney, director of the sleep and depression lab at Ryerson University in Toronto, whose presentation at a conference of the Association for Behavioral and Cognitive Therapies in Nashville on Saturday raised hopes for depression treatment. “In the study we did, I trained students to administer the therapy,” she said in an interview, “and the patients in the study got just four sessions.”

CBT-I is not a single technique but a collection of complementary ideas. Some date to the 1970s, others are more recent. One is called stimulus control, which involves breaking the association between being in bed and activities like watching television or eating. Another is sleep restriction: setting a regular “sleep window” and working to stick to it. The therapist typically has patients track their efforts on a standardized form called a sleep diary. Patients record bedtimes and when they wake up each day, as well as their perceptions about quality of sleep and number of awakenings. To this the therapist might add common-sense advice like reducing caffeine and alcohol intake, and making sure the bedroom is dark and quiet.

Those three elements — stimulus control, restriction and common sense — can do the trick for many patients. For those who need more, the therapist applies cognitive therapy — a means of challenging self-defeating assumptions. Patients fill out a standard questionnaire that asks how strongly they agree with statements like: “Without an adequate night’s sleep, I can hardly function the next day”; “I believe insomnia is the result of a chemical imbalance”; and “Medication is probably the only solution to sleeplessness.” In sessions, people learn to challenge those beliefs, using evidence from their own experiences.

“If someone has the belief that if they don’t sleep, they’ll somehow fail the next day, I’ll ask, ‘What does failure mean? You’ll be slower at work, not get everything done, not make dinner?’ ” Dr. Harris said. “Then we’ll look at the 300 nights they didn’t sleep well over the past few years and find out they managed; it might not have been as pleasant as they liked, but they did not fail. That’s how we challenge those kinds of thoughts.”

Dr. Aaron T. Beck, an emeritus professor of psychiatry at the University of Pennsylvania who is recognized as the father of cognitive therapy for mental disorders, said the techniques were just as applicable to sleep problems. “In fact, I have used it myself when I occasionally have insomnia,” he said by email.

In short-term studies of a month or two, CBT-I has been about as effective as prescription sleeping pills. But it appears to have more staying power. “There’s no data to show that if you take a sleeping pill — and then stop taking it — that you’ll still be good six months later,” said Jack Edinger, a professor at National Jewish Health in Denver and an author, with Dr. Carney, of “Overcoming Insomnia: A Cognitive-Behavioral Therapy Approach.”

“It might happen, but those certainly aren’t the people who come through my door,” he said.

Dr. Edinger and others say that those who respond well to CBT-I usually do so quickly — in an average of four sessions, and rarely more than eight. “You’re not going to break the bank doing this stuff; it’s not a marriage,” he said. “You do it for a fixed amount of time, and then you’re done. Once you’ve got the skills, they don’t go away.”

Electric brain stimulation in a specific area discovered to induce a sense of determination

On By A.P.In aMCC, anterior midcingulate cortex, brain, Depression, determination, epilepsy, Josef Parvizi, Kebmodee, motivation, neural activity, neural prosthetics, neurologist, Neurology, Neuron, neuroplasticity, neuroprosthetic device, Neuropsychiatric Disease, Neuropsychopharmacology, Neuroscience, neuroscientist, neurosurgeon, neurosurgery, neurotransmitter, neurotrophin, Stanford, The FutureLeave a comment

Doctors in the US have induced feelings of intense determination in two men by stimulating a part of their brains with gentle electric currents.

The men were having a routine procedure to locate regions in their brains that caused epileptic seizures when they felt their heart rates rise, a sense of foreboding, and an overwhelming desire to persevere against a looming hardship.

The remarkable findings could help researchers develop treatments for depression and other disorders where people are debilitated by a lack of motivation.

One patient said the feeling was like driving a car into a raging storm. When his brain was stimulated, he sensed a shaking in his chest and a surge in his pulse. In six trials, he felt the same sensations time and again.

Comparing the feelings to a frantic drive towards a storm, the patient said: “You’re only halfway there and you have no other way to turn around and go back, you have to keep going forward.”

When asked by doctors to elaborate on whether the feeling was good or bad, he said: “It was more of a positive thing, like push harder, push harder, push harder to try and get through this.”

A second patient had similar feelings when his brain was stimulated in the same region, called the anterior midcingulate cortex (aMCC). He felt worried that something terrible was about to happen, but knew he had to fight and not give up, according to a case study in the journal Neuron.

Both men were having an exploratory procedure to find the focal point in their brains that caused them to suffer epileptic fits. In the procedure, doctors sink fine electrodes deep into different parts of the brain and stimulate them with tiny electrical currents until the patient senses the “aura” that precedes a seizure. Often, seizures can be treated by removing tissue from this part of the brain.

“In the very first patient this was something very unexpected, and we didn’t report it,” said Josef Parvizi at Stanford University in California. But then I was doing functional mapping on the second patient and he suddenly experienced a very similar thing.”

“Its extraordinary that two individuals with very different past experiences respond in a similar way to one or two seconds of very low intensity electricity delivered to the same area of their brain. These patients are normal individuals, they have their IQ, they have their jobs. We are not reporting these findings in sick brains,” Parvizi said.

The men were stimulated with between two and eight milliamps of electrical current, but in tests the doctors administered sham stimulation too. In the sham tests, they told the patients they were about to stimulate the brain, but had switched off the electical supply. In these cases, the men reported no changes to their feelings. The sensation was only induced in a small area of the brain, and vanished when doctors implanted electrodes just five millimetres away.

Parvizi said a crucial follow-up experiment will be to test whether stimulation of the brain region really makes people more determined, or simply creates the sensation of perseverance. If future studies replicate the findings, stimulation of the brain region – perhaps without the need for brain-penetrating electrodes – could be used to help people with severe depression.

The anterior midcingulate cortex seems to be important in helping us select responses and make decisions in light of the feedback we get. Brent Vogt, a neurobiologist at Boston University, said patients with chronic pain and obsessive-compulsive disorder have already been treated by destroying part of the aMCC. “Why not stimulate it? If this would enhance relieving depression, for example, let’s go,” he said.

http://www.theguardian.com/science/2013/dec/05/determination-electrical-brain-stimulation

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

New research shows that sleep functions to allow the brain to eliminate toxins that accumulate while we are awake

On By A.P.In Alzheimer's disease, beta amyloid, brain, brain cleaning, Kebmodee, Maiken Nedergaard, Medicine, mental concentration, mental health, mental illness, National Institute of Neurological Disorders and Stroke, neurologist, Neurology, Neuropsychiatric Disease, Neuroscience, NINDS, Randall Bateman, Science, University of Rochester, Washington UniversityLeave a comment

sleepingbrain_wide-e40290d47221863e13990f78f86b983781d5673e-s40-c85

While the brain sleeps, it clears out harmful toxins, a process that may reduce the risk of Alzheimer’s, researchers say.

During sleep, the flow of cerebrospinal fluid in the brain increases dramatically, washing away harmful waste proteins that build up between brain cells during waking hours, a study of mice found.

“It’s like a dishwasher,” says Dr. Maiken Nedergaard, a professor of neurosurgery at the University of Rochester and an author of the study in Science.

The results appear to offer the best explanation yet of why animals and people need sleep. If this proves to be true in humans as well, it could help explain a mysterious association between sleep disorders and brain diseases, including Alzheimer’s.

Nedergaard and a team of scientists discovered the cleaning process while studying the brains of sleeping mice. The scientists noticed that during sleep, the system that circulates cerebrospinal fluid through the brain and nervous system was “pumping fluid into the brain and removing fluid from the brain in a very rapid pace,” Nedergaard says.

The team discovered that this increased flow was possible in part because when mice went to sleep, their brain cells actually shrank, making it easier for fluid to circulate. When an animal woke up, the brain cells enlarged again and the flow between cells slowed to a trickle. “It’s almost like opening and closing a faucet,” Nedergaard says. “It’s that dramatic.”

Nedergaard’s team, which is funded by the National Institute of Neurological Disorders and Stroke, had previously shown that this fluid was carrying away waste products that build up in the spaces between brain cells.

The process is important because what’s getting washed away during sleep are waste proteins that are toxic to brain cells, Nedergaard says. This could explain why we don’t think clearly after a sleepless night and why a prolonged lack of sleep can actually kill an animal or a person, she says.

So why doesn’t the brain do this sort of housekeeping all the time? Nedergaard thinks it’s because cleaning takes a lot of energy. “It’s probably not possible for the brain to both clean itself and at the same time [be] aware of the surroundings and talk and move and so on,” she says.

The brain-cleaning process has been observed in rats and baboons, but not yet in humans, Nedergaard says. Even so, it could offer a new way of understanding human brain diseases including Alzheimer’s. That’s because one of the waste products removed from the brain during sleep is beta amyloid, the substance that forms sticky plaques associated with the disease.

That’s probably not a coincidence, Nedergaard says. “Isn’t it interesting that Alzheimer’s and all other diseases associated with dementia, they are linked to sleep disorders,” she says.

Researchers who study Alzheimer’s say Nedergaard’s research could help explain a number of recent findings related to sleep. One of these involves how sleep affects levels of beta amyloid, says Randall Bateman, a professor of neurology Washington University in St. Louis who wasn’t involved in the study.

“Beta amyloid concentrations continue to increase while a person is awake,” Bateman says. “And then after people go to sleep that concentration of beta amyloid decreases. This report provides a beautiful mechanism by which this may be happening.”

The report also offers a tantalizing hint of a new approach to Alzheimer’s prevention, Bateman says. “It does raise the possibility that one might be able to actually control sleep in a way to improve the clearance of beta amyloid and help prevent amyloidosis that we think can lead to Alzheimer’s disease.”

http://www.npr.org/blogs/health/2013/10/17/236211811/brains-sweep-themselves-clean-of-toxins-during-sleep

http://m.sciencemag.org/content/342/6156/373.abstract

Thanks to Kebmodee for bringing this to the It’s Interesting community.

New research shows that drug for Parkinson’s disease (benztropine) may also treat multiple sclerosis

On By A.P.In benztropine, cogentin, fingolimod, interferon beta, MS, multiple sclerosis, myelin, Nature, Neurology, Neuropsychiatric Disease, Neuropsychopharmacology, Neuroscience, oligodendrocyte, Parkinson's diseaseLeave a comment

benzotropine

A drug that treats Parkinson’s disease might also work against multiple sclerosis, or MS.

In MS patients, an aberrant immune onslaught degrades the fatty myelin sheaths that coat nerve fibers, causing blurred vision, weakness, loss of coordination and other symptoms.

Luke Lairson of the Scripps Research Institute in La Jolla, Calif., and colleagues tested a host of compounds to see which might boost regeneration of oligodendrocytes, the brain cells that make myelin and which are often lacking in MS. Using the cells’ forerunners, nascent brain cells called oligodendrocyte precursor cells, from rats and mice, the researchers found that benztropine proved adept at steering these cells to become myelin-making oligodendrocytes.

The researchers then induced in mice a disease that mimics MS and gave some of the animals benztropine, others a standard MS drug (fingolimod or interferon beta) and some no drug at all. Whether given before or after disease onset, benztropine reduced symptom severity and prevented relapses better than other MS drugs. Mice getting no drug fared the poorest, according to results appearing October 9 in Nature.

A cell count of brain tissue revealed that mice getting benztropine had substantially more mature oligodendrocytes than mice getting no drug. Further analyses suggested the animals’ symptom improvement with benztropine resulted from a rebuilding of the myelin sheaths, not from suppressing the animals’ immune systems. The researchers think the drug, if approved for use in MS, might work in concert with immune-suppressing drugs.

Old drug may have new trick

How Exercise Beefs Up the Brain

On By A.P.In Alzheimer's disease, Barbara Hempstead, BDNF, Boston, brain derived neurotrophic factor, brown fat, Bruce Spiegelman, Cell Metabolism, Christiane Wrann, Dementia, diabetes, Dr. Rajadhyaksha, Exercise, FNDC5, Harvard Medical School, hippocampus, irisin, Karolinska Institute in Sweden, Medicine, Nature, neurologist, Neurology, Neuropsychiatric Disease, Neuroscience, neuroscientist, neurotrophin, Obesity, Parkinson's disease, PGC-1α, Pontus Boström, Science, The Brain, Weill Cornell Medical College, white fatLeave a comment

exercise

New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules.

While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain.

Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.)

While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons.

Spiegelman and his colleagues suspected that FNDC5 (and the irisin created from it) was responsible for exercise-induced benefits to the brain—in particular, increased levels of a crucial protein called brain-derived neurotrophic factor (BDNF), which is essential for maintaining healthy neurons and creating new ones. These functions are crucial to staving off neurological diseases, including Alzheimer’s and Parkinson’s. And the link between exercise and BDNF is widely accepted. “The phenomenon has been established over the course of, easily, the last decade,” says neuroscientist Barbara Hempstead of Weill Cornell Medical College in New York City, who was not involved in the new work. “It’s just, we didn’t understand the mechanism.”

To sort out that mechanism, Spiegelman and his colleagues performed a series of experiments in living mice and cultured mouse brain cells. First, they put mice on a 30-day endurance training regimen. They didn’t have to coerce their subjects, because running is part of a mouse’s natural foraging behavior. “It’s harder to get them to lift weights,” Spiegelman notes. The mice with access to a running wheel ran the equivalent of a 5K every night.

Aside from physical differences between wheel-trained mice and sedentary ones—“they just look a little bit more like a couch potato,” says co-author Christiane Wrann, also of Harvard Medical School, of the latter’s plumper figures—the groups also showed neurological differences. The runners had more FNDC5 in their hippocampus, an area of the brain responsible for learning and memory.

Using mouse brain cells developing in a dish, the group next showed that increasing the levels of the co-activator PGC-1α boosts FNDC5 production, which in turn drives BDNF genes to produce more of the vital neuron-forming BDNF protein. They report these results online today in Cell Metabolism. Spiegelman says it was surprising to find that the molecular process in neurons mirrors what happens in muscles as we exercise. “What was weird is the same pathway is induced in the brain,” he says, “and as you know, with exercise, the brain does not move.”

So how is the brain getting the signal to make BDNF? Some have theorized that neural activity during exercise (as we coordinate our body movements, for example) accounts for changes in the brain. But it’s also possible that factors outside the brain, like those proteins secreted from muscle cells, are the driving force. To test whether irisin created elsewhere in the body can still drive BDNF production in the brain, the group injected a virus into the mouse’s bloodstream that causes the liver to produce and secrete elevated levels of irisin. They saw the same effect as in exercise: increased BDNF levels in the hippocampus. This suggests that irisin could be capable of passing the blood-brain barrier, or that it regulates some other (unknown) molecule that crosses into the brain, Spiegelman says.

Hempstead calls the findings “very exciting,” and believes this research finally begins to explain how exercise relates to BDNF and other so-called neurotrophins that keep the brain healthy. “I think it answers the question that most of us have posed in our own heads for many years.”

The effect of liver-produced irisin on the brain is a “pretty cool and somewhat surprising finding,” says Pontus Boström, a diabetes researcher at the Karolinska Institute in Sweden. But Boström, who was among the first scientists to identify irisin in muscle tissue, says the work doesn’t answer a fundamental question: How much of exercise’s BDNF-promoting effects come from irisin reaching the brain from muscle cells via the bloodstream, and how much are from irisin created in the brain?

Though the authors point out that other important regulator proteins likely play a role in driving BDNF and other brain-nourishing factors, they are focusing on the benefits of irisin and hope to develop an injectable form of FNDC5 as a potential treatment for neurological diseases and to improve brain health with aging.

http://news.sciencemag.org/biology/2013/10/how-exercise-beefs-brain

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.