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Neuroscience

Behavioral Science, Complementary Medicine, Neuroscience, NIH, Patient Care, Research

“Tranceformation:” David Spiegel on how hypnosis can change your brain’s perception of your body

4254170454_4f55755317_zWhen we think of cognitive function, we usually think of having the power to alter our reasoning, while we passively respond to our perceptions. What if we could do the inverse: manipulate our perception, while merely responding to reasoning and language? That is the basic neurological explanation of hypnosis, says David Spiegel, MD, director of the Center on Stress and Health and medical director of the Center for Integrative Medicine.

Spiegel spoke on new research in hypnosis yesterday morning during the Integrative Medicine Research Lecture Series presented by the National Center for Complementary and Integrative Health (NCCIH). Despite its Greek etymology, hypnosis does not involve going to sleep; it’s more like a narrowing of attention. “Hypnosis is to consciousness what a telephoto lens is to a camera,” Spiegel explained.

When hypnotized, you put outside of awareness what would normally be in consciousness (dissociation), and become less likely to judge what people tell you (suggestibility). The idea of this often makes people nervous, because we’re evolved to respond to nuanced social cues. But a growing body of scientific evidence suggests that overcoming this nervousness can yield a wealth of health benefits.

Hypnosis can be an effective method for managing pain, and treating anxiety and stress-related disorders. Past studies have shown that people hypnotized before operative care have a shorter procedure time and a significant reduction in intraprocedural complications, such as hypoxemia and vomiting. One study showed that in select cases “hypnosis as sole anesthesia works extremely well,” Spiegel said.

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Neuroscience, Patient Care

My dance with dystonia

My dance with dystonia

We’ve partnered with Inspire, a company that builds and manages online support communities for patients and caregivers, to launch a patient-focused series here on Scope. Once a month, patients affected by serious and often rare diseases share their unique stories; this month’s column comes from a patient advocate who describes herself as a “battle-clever dystonia damsel.”

4704705307_3dd45d8ed2_zMy dance with dystonia, a rare neurological movement disorder, has been a mangled cha-cha-cha with a wayward partner. Seems I keep taking steps forward then back — ever shifting my center of gravity — while engaging in a never-ending battle over who assumes the lead. In terms of mechanics, think of dystonia as a travesty of muscular timing orchestrated by the brain and executed by body parts moving off tempo. Imagine trying to master a new dance routine and your feet fly over the dance floor in scattered disarray. That’s dystonia.

Life took its unexpected turn when I was 8 and various body parts began to assert minds of their own. First my right arm insisted on straying off course when I wrote. Then the chaos spread to my left leg. In a creeping progression that eventually stabilized, a degree of unrest extended to all my limbs. Articulatory challenges gradually manifested. While dystonia is a game changer, over the years it’s become my second skin. I find it hard to recall time before dystonia.

When I was diagnosed in the 1970s, patients and their families exhibited far greater reluctance to broadcast their health conditions, especially when a disorder struck early in life. Disability was all too absent from the landscape, especially living in a small suburban town. We’d yet to witness the proliferation of the Internet let alone a grid of online media breaking down barriers and opening up lines of communication.

I didn’t encounter a soul with dystonia until my mid 20s. Often, I felt apart and alone. It was a challenge viewing my condition with any kind of perspective. How I wished there was someone out there who understood.

How far we’ve progressed over 40+ years. Accessing health information is as easy as a trip to Google to enter a superhighway, rife with two-way traffic. Significantly, information flows from patients as well as to them. Abundant resources have ushered in an era of patient empowerment where the scientific community no longer holds a monopoly on medical explanation. In this era of cyber-connection, patients have stepped forward to educate themselves, chronicle their stories and support one another. Health activism burgeons across the Web. Online support networks abound, even for a rare condition like dystonia.

Launching my own dystonia blog (Chronicles of a Dystonia Muse) seemed a rash step until I found myself amid a veritable revolution of personal sites and health communities steering disability and chronic illness into the light.

As for me, it’s the same cha-cha-cha – stepping forward, then back. But in this age of openness, I’ve moved on to a better place deep inside myself, traveling untold miles along the road to self-acceptance. The fellow patients I encounter serve as an unending reminder that I’m not alone in my health struggles and lend me critical perspective. I may not move like everyone else but at my core I’m just like everyone else.

Pamela Sloate is a health activist who is involved in an array of awareness efforts. She moderates a patient support group, advocates for the dystonia community, and advances fundraising. She holds degrees from Brown University and NYU School of Law, and her career spans law, marketing and non-profit administration. Her blog is Chronicles Of A Dystonia Muse.
Photo by Dominic Alves

Chronic Disease, Immunology, Infectious Disease, Neuroscience, Research, Stanford News

ME/CFS/SEID: It goes by many aliases, but its blood-chemistry signature is a giveaway

ME/CFS/SEID: It goes by many aliases, but its blood-chemistry signature is a giveaway

signature

It’s the disease that dare not speak its name without tripping over one of its other names. Call it what you will – chronic fatigue syndrome (CFS), myalgic encephalomyelitis (ME) or its latest, Institute of Medicine-sanctioned designation, systemic exertion intolerance disease (SEID). It’s very real, affecting between 1 million and 4 million people in the United States alone, according to Stanford infectious-disease sleuth Jose Montoya, MD, who has closely followed more than 200 SEID patients for several years and done extensive testing on these patients in an effort to find out what’s causing their condition.

Different authorities have quoted different numbers regarding those with SEID. The name-calling and number-assigning squishiness stems from the fact that beyond its chief defining symptom – overwhelming, unremitting exhaustion lasting for six months or longer – it’s tough to pin down. Additional symptoms can range from joint and muscle pain, incapacitating headaches or food intolerance to sore throat, lymph-node enlargement, gastrointestinal problems, abnormal blood-pressure or hypersensitivity to light, noise or other sensations.

Research into the hows and whys of SEID has been plagued by the inability to establish any characteristic biochemical or neuroanatomical underpinnings of the disorder. Although many viral suspects have been interrogated, no accused microbial culprit has been indicted. To this day, there are no valid laboratory tests for diagnosing SEID.

But a burst of insight into SEID’s physiological substrate came only months ago when Stanford neuroradiologist Mike Zeineh, MD, PhD, working with patients from Montoya’s registry, found that they shared a pattern of white-matter loss in specific parts of the brain. The discovery drew a great deal of attention in the press as well as the CFS community. (See our news release about that study for details.)

Now a high-profile, multi-institution team including Montoya has published a study in Science Advances showing yet another physiological basis for a diagnosis of SEID: a characteristic pattern, or “signature,” consisting of elevated levels of various circulating immune-signaling substances in the blood.

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Imaging, Neuroscience, Research, Videos

Exploring the science of decision making

Exploring the science of decision making

Every day we make decisions that affect our work, personal relationships and health. With stakes this high, it’s no wonder many of us dread decision-making and wish we knew how to make better choices.

The first step towards making better decisions is to understand how the process works. This animation from Worldview Stanford’s upcoming course, The Science of Decision Making, shows the regions of the brain that are activated as we evaluate information.

Enrollment is now open for this interdisciplinary course, which explores and applies the nitty-gritty science of making a choice. If you’re unable to participate in the class, but you’d like to learn more about how to make better decisions, you can visit the Worldview Stanford blog for a sample of animations, videos and content from this course and their other offerings (.pdf).

Previously: Exploring the intelligence-gathering and decision-making processes of infantsIs there a connection between consuming mass media and making healthy choices?Genetics may influence financial risk-takingStanford neurobiologist Bill Newsome: Seeking gains for the brain and How does the brain plan movement? Stanford grad students explain in a video

Neuroscience, Research, Sleep, Stanford News

Stumbling upon circadian rhythms

Stumbling upon circadian rhythms

PrintIn my job as a science writer, I get to hear lots of amazing stories of discovery. In some cases, researchers have worked diligently to solve one question for decades. Others I talk to describe exciting Eureka! moments where their data suddenly made sense. But some of my favorite stories are those where a scientist is studying one thing, only to make an off-the-cuff observation that leads them in a totally new direction.

In researching circadian rhythms for the latest issue of Stanford Medicine magazine, I heard lots of this last kind of story. There are many obvious ways that circadian rhythms influence biology: our sleep cycles, the way our stomachs start to grumble for lunch at the same time every day, and how many plants close their flowers each night. But scientists are also starting to reveal lots of hidden, unexpected ways that circadian rhythms – the natural cycles in living organisms – affect us. Over just the past few years, researchers in disparate fields have made chance observations that have made them think twice about the timing of their experiments; daily circadian cycles in our bodies can affect everything from how we metabolize drugs to how our immune system acts, they’ve found.

Craig Heller, PhD, who co-directs the Stanford Down Syndrome Research Center, told me about how he was testing a new drug to improve memory in mice with Down syndrome. During the course of his experiments, he noticed that mice who received the drug at night didn’t respond the same way as mice that received a dose in the morning. It led him to start investigating the link between learning, memory, and daily sleep cycles. What he discovered doesn’t just have implications for Down syndrome, but for learning and memory more broadly.

Then, sleep researcher Emmanuel Mignot, MD, PhD, of the Stanford Center for Narcolepsy, walked me through the story of how he and other scientists discovered a link between the immune system and narcolepsy. It all started, he explained, after an odd epidemiological observation: narcolepsy was more often diagnosed in the spring than in the fall.

Of course, lots of what we know about how circadian clocks tick along inside our bodies, keeping time with the world around us, comes from tireless, carefully planned out benchwork, and that can’t be discredited. But some of the most surprising new links I describe in my feature come from scientists taking leaps across fields to explain something they found curious. Check out my feature, “Hacking the Biological Clock,” to learn more about what Heller, Mignot, and other scientists have found on these journeys of discovery.

Sarah C.P. Williams is a freelance science writer based in Hawaii.

Previously: Stanford Medicine magazine reports on time’s intersection with health, Study shows altered circadian rhythms in the brains of depressed people and Narcolepsy = autoimmune disease
Illustration by Harry Campbell

Aging, Chronic Disease, In the News, Media, Neuroscience, Women's Health

Science Friday explores women’s heightened risk for Alzheimer’s

Science Friday explores women's heightened risk for Alzheimer's

More than two-thirds of the Americans living with Alzheimer’s are women — some like the character Alice in the movie “Still Alice,” who suffers from an early onset form of the disease.

Science Friday tackled that topic Friday, with guests Michael Greicius, MD, MPH, associate professor of neurology and director of the Stanford Center for Memory Disorders, and Roberta Diaz Brinton, PhD, professor of pharmacology at the University of Southern California. The two quickly disputed the belief that more women get Alzheimer’s disease because they live longer.

“The way women age puts them at risk,” Brinton said. As they transition through menopause, some women develop cognitive symptoms such as insomnia, depression and short-term memory loss, leaving them at greater risk for Alzheimer’s, she explained.

Women who have a form of a gene called APOE-e4 are particularly at risk, although it doesn’t seem to affect men, Greicius said. The gene interacts with estrogen.

Scientists are continuing to decipher the link between estrogen and Alzheimer’s and the possibility of hormone therapies, as well as the connection — if any — between pregnancy and Alzheimer’s risk, the scientists told listeners.

The 18-minute segment is available here.

Previously: Blocking a receptor on brain’s immune cells counters Alzheimer’s in mice, The state of Alzheimer’s research: A conversation with Stanford neurologist Michael Greicius, Having a copy of ApoE4 gene variant doubles Alzheimer’s risk for women but not for men and The toll of Alzheimer’s on caretakers

Aging, Genetics, In the News, Mental Health, Neuroscience, Research, Women's Health

Are women at greater risk for Alzheimer’s? Stanford expert to discuss on today’s Science Friday

Are women at greater risk for Alzheimer’s? Stanford expert to discuss on today's Science Friday

2187905205_158290644d_zConfession: I named my parents’ cat (who died recently) Watson after listening to Ira Flatow interview James Watson, PhD, while driving cross country with my dad in 2000. Both before and after the all-critical cat-name-inspiring program, Science Friday has been a part of my Friday as often as I can squeeze it in.

So I was happy to hear that today’s program (which airs locally from 11 a.m. to 1 p.m. on KQED) will feature Stanford’s Michael Greicius, MD, MPH. He’ll be talking about Alzheimer’s disease and why the disease affects men and women differently.

Greicius, medical director of the Stanford Center for Memory Disorders, has worked with the gene variant known as ApoE4 – the largest single genetic risk factor for Alzheimer’s, particularly for women. Last spring, he published a study showing that healthy ApoE4-positive women were twice as likely to contract the disease as their ApoE4-negative counterparts.

Greicius is expected to be on in the second hour, from 12 to 1 p.m. Pacific time.

Previously: Blocking a receptor on brain’s immune cells counters Alzheimer’s in mice, Examining the potential of creating new synapses in old or damaged brains, The state of Alzheimer’s research: A conversation with Stanford neurologist Michael Greicius and Having a copy of ApoE4 gene variant doubles Alzheimer’s risk for women but not for men
Photo by *Ann Gordon

Biomed Bites, Mental Health, Neuroscience, Research, Videos

A visual deluge may provide clues to ADHD treatment

A visual deluge may provide clues to ADHD treatment

It’s time for Biomed Bites, a weekly feature that introduces readers to some of Stanford’s most innovative researchers.

Looking out my window, I see a man dressed in red sweats on a bike. There’s my neighbor’s white truck parked in the street. A tree just starting to bud. A fire hydrant. A woman fertilizing roses. Closer, there’s my grey-and-white cat, Grizzly, bathing in the sun. My glass of ice water. My phone. Scattered papers.

And that’s probably only one-thousandth of the things I see right now. (I didn’t even mention the computer.) How do I make sense of that visual onslaught? How do I navigate, perceive threats, respond to changing conditions?

Well, that’s part of the puzzle Stanford neurobiologist Tirin Moore, PhD, is working to figure out.

“I’m a systems-level neurobiologist, which means I study how networks of neurons combine to either process sensory information or to control complex behaviors,” Moore explains in the video above.

How do we filter out what’s important – seeing the dog darting across the street in front of our car, but not focusing on the bird in the tree?

This process is most obvious when it breaks down, such as in patients with Attention Deficit Hyperactivity Disorder, or other attention disorders that affect from 3 to 8 percent of the population, Moore said:

At present, disorders such as ADHD are treatable, but their underlying neural basis is still very much a mystery… Our hope is that by understanding disorders of attention at the level of the neurocircuitry we will be able to arrive at more effective treatments…

Stay tuned to see what he, and his team, figures out.

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.

Aging, In the News, Neuroscience, Research

The distinctly different brains of “SuperAgers”

The distinctly different brains of “SuperAgers”

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Scientists are gaining insights into the cognitive abilities of “SuperAgers” and why their memories are more resilient against the ravages of time than are other older people’s. ABC News reports today on new research:

The SuperAgers were picked to be studied because all were over age 80 and had the memory capability of a person 20 to 30 years their junior according to the study recently published in the Journal of Neurology.

To understand how SuperAgers managed to keep their mental ability intact, researchers performed a battery of tests on them, including MRI scans on 12 SuperAgers and post-mortem studies on five other SuperAgers to understand the make-up of their brains.

“The brains of the SuperAgers are either wired differently or have structural differences when compared to normal individuals of the same age,” Changiz Geula, a study senior author and a research professor at the Cognitive Neurology and Alzheimer’s Disease Center, said in a prepared statement. “It may be one factor, such as expression of a specific gene, or a combination of factors that offers protection.”

The article goes on to explain that participants’ unusual brain signature had three common components in comparison to normal people of similar ages: notably fewer tangles (a primary marker of Alzheimer’s disease), a thicker region of the cortex and a significant supply of a neuron called von Economo, which is linked to higher social intelligence.

Previously: What brain scans reveal about “super agers”, The secret to living longer? It’s all in the ‘tude and Healthy aging the focus of Stanford study
Photo by Fiona Shields

Imaging, Mental Health, Neuroscience, NIH, Research, Stanford News

Study: Major psychiatric disorders share common deficits in brain’s executive-function network

Study: Major psychiatric disorders share common deficits in brain's executive-function network

marble brainPsychiatric disorders, traditionally distinguished from one another based on symptoms, may in reality not be as discrete as we think.

In a huge meta-analysis just published in JAMA Psychiatry, Stanford neuroscientist and psychiatrist Amit Etkin, MD, PhD, and his colleagues pooled the results from 193 different studies. This allowed them to compare brain images from 7,381 patients diagnosed with any of six conditions – schizophrenia, bipolar disorder, major depression, addiction, obsessive-compulsive disorder, and a cluster of anxiety syndromes – to one another, as well as to brain images from 8,511 healthy patients.

Compared with healthy brains, patients in all six psychiatric categories showed a loss of gray matter in each of three separate brain structures. These three areas, along with others, tend to fire in synchrony and are known to participate in the brain’s so-called “executive-function network,” which is associated with high-level functions including planning, decision-making, task-switching, concentrating in the face of distractions, and damping counterproductive impulses.

The findings call into question a longstanding tendency to distinguish psychiatric disorders chiefly by their symptoms

(“Gray matter” refers to information-processing nerve-cell concentrations in the brain, as opposed to the “white matter” tracts that, like connecting cables, shuttle information from one part of the brain to another.)

As Etkin told me when I interviewed him for the news release we issued on this study, “these three structures can be viewed as the alarm system for the brain.” More from our release:

“They work together, signaling to other brain regions when reality deviates from expectations – that something important and unpredicted has happened, or something important has failed to happen.” That signaling guides future behavior in directions more likely to obtain desired results.

The studies of psychiatric patients that Etkin’s team employed all used a technique that yields high-resolution images of the brain’s component structures but can say nothing about how or when these structures work or interact with one another. However, that kind of imaging data was available for the healthy subjects. And, on analysis, those healthy peoples’ performance on classic tests of executive-function (such as  asking the test-taker to note the color of the word “blue,” displayed in a color other than blue, after seeing it briefly flashed on a screen) correlated strongly with the volume of gray matter in the three suspect brain areas, supporting the idea that the anatomical loss in psychiatric patients was physiologically meaningful.

The findings call into question a longstanding tendency to distinguish psychiatric disorders chiefly by their symptoms rather than their underlying brain pathology – and, by implication, suggest that disparate conditions may be amenable to some common remedy.

As National Institute of Mental Health Director Thomas Insel, MD, told me in an interview about the study, the Stanford investigators “have stepped back from the trees to look at the forest and see a pattern in that forest that wasn’t apparent when you just look at the trees.”

Previously: Hope for the globby thing inside our skulls, Brain study offers intriguing clues toward new therapies for psychiatric disorders and Study shows abnormalities in brains of anxiety-disorder patients
Photo by Philippe Put

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