Image: Eleven areas of the brain are showing differential activity levels in a Dartmouth study using functional MRI to measure how humans manipulate mental imagery. Credited to Alex Schlegel, Dartmouth College

Researchers discover how and where imagination occurs in human brains

New insights into ‘mental workspace’ may help advance artificial intelligence

Philosophers and scientists have long puzzled over where human imagination comes from. In other words, what makes humans able to create art, invent tools, think scientifically and perform other incredibly diverse behaviors?

The answer, Dartmouth researchers conclude in a new study, lies in a widespread neural network — the brain’s “mental workspace” — that consciously manipulates images, symbols, ideas and theories and gives humans the laser-like mental focus needed to solve complex problems and come up with new ideas.

Their findings, titled “Network structure and dynamics of the mental workspace,” appear the week of Sept. 16 in the Proceedings of the National Academy of Sciences.

"Our findings move us closer to understanding how the organization of our brains sets us apart from other species and provides such a rich internal playground for us to think freely and creatively," says lead author Alex Schlegel, a graduate student in the Department of Psychological and Brain Sciences. "Understanding these differences will give us insight into where human creativity comes from and possibly allow us to recreate those same creative processes in machines."

Scholars theorize that human imagination requires a widespread neural network in the brain, but evidence for such a “mental workspace” has been difficult to produce with techniques that mainly study brain activity in isolation. Dartmouth researchers addressed the issue by asking: How does the brain allow us to manipulate mental imagery? For instance, imagining a bumblebee with the head of a bull, a seemingly effortless task but one that requires the brain to construct a totally new image and make it appear in our mind’s eye.

In the study, 15 participants were asked to imagine specific abstract visual shapes and then to mentally combine them into new more complex figures or to mentally dismantle them into their separate parts. Researchers measured the participants’ brain activity with functional MRI and found a cortical and subcortical network over a large part of the brain was responsible for their imagery manipulations. The network closely resembles the “mental workspace” that scholars have theorized might be responsible for much of human conscious experience and for the flexible cognitive abilities that humans have evolved.

Children’s Computation of Complex Linguistic Forms: A Study of Frequency and Imageability Effects

This study investigates the storage vs. composition of inflected forms in typically-developing children. Children aged 8–12 were tested on the production of regular and irregular past-tense forms. Storage (vs. composition) was examined by probing for past-tense frequency effects and imageability effects – both of which are diagnostic tests for storage – while controlling for a number of confounding factors. We also examined sex as a factor. Irregular inflected forms, which must depend on stored representations, always showed evidence of storage (frequency and/or imageability effects), not only across all children, but also separately in both sexes. In contrast, for regular forms, which could be either stored or composed, only girls showed evidence of storage. This pattern is similar to that found in previously-acquired adult data from the same task, with the notable exception that development affects which factors influence the storage of regulars in females: imageability plays a larger role in girls, and frequency in women. Overall, the results suggest that irregular inflected forms are always stored (in children and adults, and in both sexes), whereas regulars can be either composed or stored, with their storage a function of various item- and subject-level factors.

Brainhack 2013

We are thrilled to draw your attention on the upcoming Brainhack 2013, which is being held from October 23-26 at the Centre International d’Études Pédagogiques, Sèvres, France (just outside of Paris).

Brainhack 2013 is a unique workshop with the goals of fostering interdisciplinary collaboration and open neuroscience. The structure builds from the concepts of an unconference and hackathon: The term “unconference” refers to the fact that most of the content will be dynamically created by the participants — a “hackathon” is an event where participants collaborate
intensively on projects.

Participants interested in neuroimaging from any discipline are welcome. Ideal participants span in range from graduate students to professors across any disciplines willing to contribute (e.g., mathematics, computer
science, engineering, neuroscience, psychology, psychiatry, neurology, medicine, art, etc…). The primary requirement is a desire to work in close collaborations with people outside of your specialization in order to
address neuroscience questions that are beyond the expertise of a single discipline.

One should come to brainhack ready to engage into collaborative projects, and with some material (slides, ideas, data, tools) ready to start a project or a discussion panel. Brainhack will build on the successful techniques used in other unconferences to keep the meeting focused and productive. It is possible to start a project and build a team as early as today. Please have a look at the website for information on the conference and a sample of projects (from Brainhack 2012).

The Preliminary Schedule for Brainhack 2013 is available here.

***NEW*** We will be accepting and publishing Brainhack 2013 abstracts. Abstracts should be submitted when you register.

Registration is now open here

DNA damage may cause ALS

New study finds link between neurons’ inability to repair DNA and neurodegeneration.

Amyotrophic lateral sclerosis (ALS) — also known as Lou Gehrig’s disease — is a neurodegenerative disease that destroys the neurons that control muscle movement. There is no cure for ALS, which kills most patients within three to five years of the onset of symptoms, and about 5,600 new cases are diagnosed in the United States each year.

MIT neuroscientists have found new evidence that suggests that a failure to repair damaged DNA could underlie not only ALS, but also other neurodegenerative disorders such as Alzheimer’s disease. These findings imply that drugs that bolster neurons’ DNA-repair capacity could help ALS patients, says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory and senior author of a paper describing the ALS findings in the Sept. 15 issue of Nature Neuroscience.

Neurons are some of the longest-living cells in the human body. While other cells are frequently replaced, our neurons are generally retained throughout our lifetimes. Consequently, neurons can accrue a lot of DNA damage and are especially vulnerable to its effects.

“Our genome is constantly under attack and DNA strand breaks are produced all the time. Fortunately, they are not a worry because we have the machinery to repair it right away. But if this repair machinery were to somehow become compromised, then it could be very devastating for neurons,” Tsai says.

Lead authors of the paper are Picower Institute postdoc Wen-Yuan Wang and research scientist Ling Pan.

Impaired repair

Tsai’s group has been interested in understanding the importance of DNA repair in neurodegenerative processes for several years. In a study published in 2008, they reported that DNA double-strand breaks precede neuronal loss in a mouse model that undergoes Alzheimer’s disease-like neurodegeneration and identified a protein, HDAC1, which prevents neuronal loss under these conditions. 

HDAC1 is a histone deacetylase, an enzyme that regulates genes by modifying chromatin, which consists of DNA wrapped around a core of proteins called histones. HDAC1 activity normally causes DNA to wrap more tightly around histones, preventing gene expression. However, it turns out that cells, including neurons, also exploit HDAC1’s ability to tighten up chromatin to stabilize broken DNA ends and promote their repair.

In a paper published earlier this year in Nature Neuroscience, Tsai’s team reported that HDAC1 works cooperatively with another deacetylase called SIRT1 to repair DNA and prevent the accumulation of damage that could promote neurodegeneration.

When a neuron suffers double-strand breaks, SIRT1 migrates within seconds to the damaged sites, where it soon recruits HDAC1 and other repair factors. SIRT1 also stimulates the enzymatic activity of HDAC1, which allows the broken DNA ends to be resealed.

SIRT1 itself has recently gained notoriety as the protein that promotes longevity and protects against diseases including diabetes and Alzheimer’s disease, and Tsai’s group believes that its role in DNA repair contributes significantly to the protective effects of SIRT1.

In an attempt to further unveil other partners that work with HDAC1 to repair DNA, Tsai and colleagues stumbled upon a protein called Fused In Sarcoma (FUS). This finding was intriguing, Tsai says, because the FUS gene is one of the most common sites of mutations that cause inherited forms of ALS.

The MIT team found that FUS appears at the scene of DNA damage very rapidly, suggesting that FUS is orchestrating the repair response. One of its roles is to recruit HDAC1 to the DNA damage site. Without it, HDAC1 does not appear and the necessary repair does not occur. Tsai believes that FUS may also be involved in sensing when DNA damage has occurred.

Linking mutation and disease

At least 50 mutations in the FUS gene have been found to cause ALS. The majority of these mutations occur in two sections of the FUS protein. The MIT team mapped the interactions between FUS and HDAC1 and found that these same two sections of the FUS protein bind to HDAC1.

They also generated four FUS mutants that are most commonly seen in ALS patients. When they replaced the normal FUS with these mutants, they found that the interaction with HDAC1 was impaired and DNA damage was significantly increased. This suggests that those mutations prevent FUS from recruiting HDAC1 when DNA damage occurs, allowing damage to accumulate and eventually leading to ALS.

The researchers also analyzed brain tissue samples from ALS patients harboring FUS mutations and found that the amount of DNA damage in neurons in motor cortex was about double that found in normal brain tissue.

ALS patients with FUS mutations usually develop the disease early, before age 40. Only one of a person’s two copies of the FUS gene needs to be mutated to produce the disease. Tsai says that early in life, having one copy of the normal FUS gene may be enough to keep DNA repair going. “With aging, eventually the machinery is compromised and it contributes to neuronal demise,” she says.

The findings suggest that drugs that promote DNA damage repair, including activators of HDAC1 and SIRT1, could help combat the effects of ALS. SIRT1 activators are now being developed and have entered clinical trials to treat diabetes.

“There are numerous human inherited DNA-repair deficiency syndromes, many of which show neurodegeneration or other neurological defects. This new study now extends the spectrum of neuropathology caused by defects in DNA maintenance to include ALS,” says Peter McKinnon, a professor of genetics at St. Jude Children’s Research Hospital who was not part of the research team. “This study offers new avenues to explore in the quest for treatment strategies.”

Tsai’s lab is now studying whether there is a direct relationship between FUS and SIRT1. She also wants to determine whether the DNA damage that occurs in ALS patients after FUS is lost occurs in certain “hotspots” or is random. “I would speculate that there’s got to be hotspots in terms of where the DNA is damaged. But right now it remains speculation,” she says. “We really need to do the experiments and demonstrate whether that’s the case.”

Research Points to Promising Treatment for Macular Degeneration

Experiments show promising results for a drug that could lead to a lasting treatment for millions of Americans with macular degeneration.

Researchers at the University of North Carolina School of Medicine have published new findings in the hunt for a better treatment for macular degeneration. In studies using mice, a class of drugs known as MDM2 inhibitors proved highly effective at regressing the abnormal blood vessels responsible for the vision loss associated with the disease.

“We believe we may have found an optimized treatment for macular degeneration,” said senior study author Sai Chavala, MD, director of the Laboratory for Retinal Rehabilitation and assistant professor of Ophthalmology and Cell Biology & Physiology at the UNC School of Medicine. “Our hope is that MDM2 inhibitors would reduce the treatment burden on both patients and physicians.”

The research appeared Sept. 9, 2013 in the Journal of Clinical Investigation.

As many as 11 million Americans have some form of macular degeneration, which is the most common cause of central vision loss in the western world. Those with the disease find many daily activities such as driving, reading and watching TV increasingly difficult.

Currently, the best available treatment for macular degeneration is an antibody called anti-VEGF that is injected into the eye. Patients must visit their doctor for a new injection every 4-8 weeks, adding up to significant time and cost.

“The idea is we’d like to have a long-lasting treatment so patients wouldn’t have to receive as many injections,” said Chavala. “That would reduce their overall risk of eye infections, and also potentially lower the economic burden of this condition by reducing treatment costs.” Chavala practices at the Kittner Eye Center at UNC Health Care in Chapel Hill and New Bern.

All patients with age-related macular degeneration start out with the “dry” form of the disease, which can cause blurred vision or blind spots. In about 20 percent of patients, the disease progresses to its “wet” form, in which abnormal blood vessels form in the eye and begin to leak fluid or blood, causing vision loss.

While anti-VEGF works by targeting the growth factors that lead to leaky blood vessels, MDM2 inhibitors target the abnormal blood vessels themselves causing them to regress — potentially leading to a lasting effect.

Chavala and his colleagues investigated the effects of MDM2 inhibitors in cell culture and in a mouse model of macular degeneration. They found that the drug abolishes the problematic blood vessels associated with wet macular degeneration by activating a protein known as p53. “p53 is a master regulator that determines if a cell lives or dies. By activating p53, we can initiate the cell death process in these abnormal blood vessels,” said Chavala.

MDM2 inhibitors also have conceivable advantages over another treatment that is currently being investigated in several clinical trials: the use of low-dose radiation for wet macular degeneration. Radiation works by causing DNA damage in cells leading to an increase in p53 and cell death. MDM2 inhibitors activate p53 without causing DNA damage. Also, MDM2 inhibitors can be given by eye injection, which is advantageous over some forms of radiation treatment that require surgery to administer.

Electro-shock therapy sees a resurgence

The procedure is widely accepted by the medical community, although it lingers in the public imagination as a crude medical holdover.

The patients are rolled on gurneys into a small screened-off area at Park Royal Hospital every 15 minutes with assembly line regularity.

One is a woman in her 60s, who, like the others, gets a momentary jolt of electricity sent through her head, causing a brain seizure and her body to tense for several seconds. The hope: That this treatment — the electroconvulsive, or “electro-shock,” therapy — will ease the symptoms of her bipolar disorder that has so far not responded well to drugs.

The procedure, one of thousands performed at Park Royal since the 76-bed hospital opened last year, has worked on the woman in the past, says Dr. Ivan Mazzorana, who performs all of them on patients here. And, he said, it’s likely to do so again.

These days, the treatment goes by its more clinical-sounding acronym, “ECT.”

"When you bring it up, most people say, ‘Oh my God! Not ECT, that’s something from the past,’" Mazzorana said. "It’s a very simple procedure, safer, and it’s a lot quicker than the medication."

Electroconvulsive therapy today is a procedure widely accepted by the medical community and one, absent a rare court order, that is done with patient consent. But it is also a treatment that lingers in the public imagination as a crude medical holdover almost as dated as bloodletting. Many outside of psychiatry are surprised to learn that the procedure still exists at all.

Despite that, ECT has seen a resurgence at many health centers in recent decades, experts say.

Park Royal, the only inpatient psychiatric hospital in Lee County, Fla., has already treated nearly 200 people with ECT, most receiving multiple treatments. The number represents roughly 10 percent of all of Park Royal’s admissions since it opened in early 2012.

The hospital is a for-profit facility owned by the Tennessee-based Acadia Healthcare Co.

Most of those who have received ECT at Park Royal — patient ages have ranged from 18 years to those in their 90s — suffer from severe depression or bi-polar disorders. About 90 percent are inpatients. Others are referred from other parts of Florida, according to the hospital. A few are snowbirds who come in for ETC “maintenance” treatments.

The Mayo Clinic calls the treatment, which has a reported success rate of 70 percent to 80 percent, the “gold standard” treatment for severe depression. The most common side effect, according to proponents, is temporary short-term memory loss.

"I was afraid, to be honest with you," said Ron Spesia, a 71-year-old Fort Myers Beach retiree who suffered a deep, multiyear depression that did not respond to medication. He had 12 treatments and said he started feeling better after the third. "Then one day I decided, ‘Hey, you know what? It’s time to put the big boy pants on and pursue this.’ Smartest move I ever made."

Still, ECT has its critics. Some, including patients of decades past and anti-ECT groups, say it is little more than intentional brain damage. This, despite the psychiatric community’s endorsement of it and positive testimonials from many of the estimated 100,000 Americans who get the treatment each year.

A Fort Myers News-Press reporter was recently allowed to witness about a half dozen such procedures at Park Royal.

But even hospital administrators remain sensitive to the ECT stigma. Though a patient agreed to be photographed during one such procedure, and to have it recorded on video, the hospital overruled that consent.

The hospital also prohibited patient interviews inside the building, though other medical facilities routinely allow such interactions if patients are willing. David Edson, Park Royal’s director of business development, cited concerns about privacy and “the very delicate nature of the ECT treatment.”

Despite that, Mazzorana said he wants to demystify the treatment and those who get it.

"It seems like an extreme, dramatic treatment," Mazzorana said. "It’s a matter of really educating the psychiatric community, so then we can educate patients."

Mundane process

The treatments at Park Royal begin at 7 a.m. Mondays, Wednesdays and Fridays, and continue throughout the mornings. Staff usually see up to 10 ECT patients on these days.

The process bears little resemblance to its horrific depictions in popular culture. At Park Royal, it starts when patients come to a medical preparation area adjacent to the ECT treatment room, where staff hook them up to IVs — they will eventually get medication to paralyze their muscles during the treatment — as well as heart and brain monitors attached to their skin.

After a quick chat with medical staff, who assess their conditions, patients bite down on foam “bite blocks” before they are put fully under.

Flashlight-shaped paddles coated with a blue conductive gel are placed on each temple (bilateral treatment) or one goes on the right temple and one on the top of the head (unilateral treatment), depending on the type of ECT the patients need. Bilateral ECT is recommended in more severe cases of mental illness and may produce more memory loss, experts say.

Following a quick buzzing sound, patients’ bodies tense for about five seconds. Patients typically wake a minute or so after the procedure and are sent off to a recovery area until the anesthesia fully wears off. They remember nothing of the treatment itself.

New patients must typically stay in the hospital for the first half of the standard dozen ECT treatments.

Spesia, the former ECT patient, said the IV injection was the most painful part of the process. The most unpleasant, he said was the hospital stay. Now, months after the process, he said the only lingering side effect has been some short-term memory loss.

"All I can remember is them giving me the rubber bite block and then them putting the (anesthesia) mask on and telling me to breathe deeply." he said. "Absolutely painless."

Nancy Kish, a 74-year-old Fort Myers resident who has received dozens of treatments over the years, said her memory of treatments from years past is fuzzy but her mind is otherwise as sharp as it has ever been. She said the treatment is a better alternative to the high doses of medication she otherwise took, drugs that largely left her bed-ridden.

"I feel pretty good," said Kish. "I get upset easy, and I get anxiety attacks. But other than that, I’m better than what I was."

Much like the therapeutic mystery behind anti-depressant medication experts are not exactly sure why ECT works for some patients.

Mazzorana said two theories dominate: One says that electroconvulsive therapy enhances certain beneficial brain chemicals that are lacking in different parts of the brain. Another states that it causes the release of hormones that have a beneficial effect on mood and promote the growth of healthy brain cells, he said. Other recent research suggests that ECT works by reducing “hyper-connectivity” in the minds of severely depressed patients.

Endorsements

Whatever the exact mechanism, ECT’s endorsements include the American Psychiatric Association, the American Medical Association, and the U.S. Surgeon General.

"When you raise ECT, people’s eyes always roll up in their heads and their family says, ‘Oh my God, you’re a monster!’" said Fort Myers psychiatrist Steve Machlin, who performed the procedure more than a decade ago. "There’s always going to be people on the outside who say it’s not proven but, if you’ve looked at the science, it’s been proven to be effective."

Another Southwest Florida psychiatrist and researcher, Fred Schaerf, said opposition to the treatment is largely anti-psychiatry bias and from the treatment’s early days, when it was performed without anesthesia.

"I think there is a misconception about the treatment — that it’s barbaric, cruel," Schaerf said. "It has to do with that stigma and people’s belief system with psychiatry."

Most insurance, including Medicare, covers the treatment.

Edson, the Park Royal Hospital business development director, said the health center generally charge insurers $500 a treatment, though that does not include the costs of the anesthesiologist and hospital stay. Mazzorana said the total cost is about $1,000.

Opposition

Medical and patient endorsements aside, some patient groups believe it does little more than cause brain damage. A quick Internet search turns up a long list of anti-ECT websites, many of which include testimonials from people claiming to have suffered negative effects from the treatments.

Among the most vocal opponents is the Philadelphia-based National Mental Health Consumers’ Self Help Clearinghouse, which urged the U.S. Food and Drug Administration in 2011 not to reduce federal oversight of ECT devices. It also sharply criticized the Surgeon General’s endorsement of ECT in 1999.

The group points to published studies suggesting that ECT leads to memory loss and may be far more dangerous for the elderly than medication alone. Susan Rogers, the organization’s director, said patients aren’t warned enough about the risks.

"People are not given the opportunity for truly informed consent," said Rogers, who has not had the procedure herself. "People are not advised of the enormous risks as well as the benefits. They’re given a whitewashed version of the facts. They’re not told it might cause permanent cognitive impairment, and I think that’s wrong."

She said she is not opposed to the treatment itself.

"Apparently about 100,000 people a year receive ECT in the United States and, I’m sure for many of those people, they’re satisfied with those results," she said. "There are also many people who feel that ECT has destroyed their lives."

The psychiatric community commonly uses the one in 10,000 patients mortality figure (or one per 80,000 treatments), figures anti-ECT groups say dramatically under-estimate the risk, particularly among older patients. A 1995 USA TODAY investigation found that it may have been as high as one in 200 among elderly patients, based on some state reports at the time and some earlier studies.

A recent Department of Veterans Affairs review of ECT between 1999 and 2010 found no ECT deaths at VA hospitals during that period. It placed the mortality risk at one per 14,000 patients, or one per 73,400 treatments.

Florida does not closely track ECT usage. But Texas, which does, reported that none of the 2,079 patients receiving ECT last year died during the procedure. Two died shortly after treatment in 2012, the state report noted, but neither case was related to the treatment.

Five years of reports show that roughly 2 percent of patients experience some level of memory loss shortly after treatment.

None of Park Royal’s ECT patients have died during the procedure, said Christina Brownwood, the hospital’s ECT coordinator. Nor have any needed emergency medical care immediately after a treatment, she said.

Sleep Better, Look Better? New Research Says Yes

First scientific look at how sleep apnea treatment affects appearance — alertness, youthfulness & attractiveness — may help patients stick with care

Getting treatment for a common sleep problem may do more than help you sleep better – it may help you look better over the long term, too, according to a new research study from the University of Michigan Health System and Michigan Technological University.

The findings aren’t just about “looking sleepy” after a late night, or being bright-eyed after a good night’s rest.

It’s the first time researchers have shown specific improvement in facial appearance after at-home treatment for sleep apnea, a condition marked by snoring and breathing interruptions. Sleep apnea affects millions of adults – most undiagnosed — and puts them at higher risk for heart-related problems and daytime accidents.

Using a sensitive “face mapping” technique usually used by surgeons, and a panel of independent appearance raters, the researchers detected changes in 20 middle-aged apnea patients just a few months after they began using a system called CPAP to help them breathe better during sleep and overcome chronic sleepiness.

While the research needs to be confirmed by larger studies, the findings may eventually give apnea patients even more reason to stick with CPAP treatment – a challenge for some because they must wear a breathing mask in bed. CPAP is known to stop snoring, improve daytime alertness and reduce blood pressure.

Sleep neurologist Ronald Chervin, M.D., M.S., director of the U-M Sleep Disorders Center, led the study, which was funded by the Covault Memorial Foundation for Sleep Disorders Research and published in the Journal of Clinical Sleep Medicine.

Putting anecdote to the test

Chervin says the study grew out of the anecdotal evidence that sleep center staff often saw in sleep apnea patients when they came for follow-up visits after using CPAP. The team, including research program manager Deborah Ruzicka, R.N., Ph.D., sought a more scientific way to assess appearance before and after sleep treatment.

“The common lore, that people ‘look sleepy’ because they are sleepy, and that they have puffy eyes with dark circles under them, drives people to spend untold dollars on home remedies,” notes Chervin, the Michael S. Aldrich Collegiate Professor of Sleep Medicine and professor of Neurology at the U-M Medical School. “We perceived that our CPAP patients often looked better, or reported that they’d been told they looked better, after treatment. But no one has ever actually studied this.”

They teamed with U-M plastic and reconstructive surgeon Steven Buchman, M.D., to use a precise face-measuring system called photogrammetry to take an array of images of the patients under identical conditions before CPAP and a few months after. Capable of measuring tiny differences in facial contours, the system helps surgeons plan operations and assess their impact.

“One of the breakthroughs in plastic surgery over the last decade has been our aim to get more objective in our outcomes,” says Buchman. “The technology used in this study demonstrates the real relationship between how you look and how you really are doing, from a health perspective.”

The research team also included longtime collaborators at the Michigan Tech Research Institute, led by signal analysis expert and engineer Joseph W. Burns, Ph.D., who developed a way to precisely map the colors of patients’ facial skin before and after CPAP treatment.

The researchers also used a subjective test of appearance: 22 independent raters were asked to look at the photos, without knowing which were the “before” pictures and which the “after” pictures of each patient. The raters were asked to rank attractiveness, alertness and youthfulness – and to pick which picture they thought showed the patient after sleep apnea treatment.

Results show improvement

About two-thirds of the time, the raters stated that the patients in the post-treatment photos looked more alert, more youthful and more attractive. The raters also correctly identified the post-treatment photo two-thirds of the time.

Meanwhile, the objective measures of facial appearance showed that patients’ foreheads were less puffy, and their faces were less red, after CPAP treatment. The redness reduction was especially visible in 16 patients who are Caucasian, and was associated with the independent raters’ tendency to say a patient looked more alert in the post-treatment photo. The researchers also perceived, but did not have a way to measure, a reduction in forehead wrinkles after treatment.

However, the researchers note, they didn’t see a big change in facial characteristics that popular lore associates with sleepiness. “We were surprised that our approach could not document any improvement, after treatment, in tendency to have dark blue circles or puffiness under the eyes,” says Chervin. “Further research is needed, to assess facial changes in more patients, and over a longer period of CPAP treatment.”

He notes that this initial study wouldn’t have been possible without the generosity of donors who have supported U-M sleep research as a way of honoring the memory of Jonathan Covault, a promising attorney who died young, and whose undertreated sleep apnea may have contributed to his premature death. The Covault family was aware of the research study, and of the importance of research that might encourage others to seek and stay with apnea treatment.

Chervin and his colleagues hope to continue to study the effect of sleep apnea treatment on many aspects of a person’s life, including further research on appearance. “We want sleep to be on people’s minds, and to educate them about the importance of getting enough sleep and getting attention for sleep disorders,” he says.

Think twice, speak once: Bilinguals process both languages

Bilingual speakers can switch languages seamlessly, likely developing a higher level of mental flexibility than monolinguals, according to Penn State linguistic researchers.

"In the past, bilinguals were looked down upon," said Judith F. Kroll, Distinguished Professor of Psychology, Linguistics and Women’s Studies. "Not only is bilingualism not bad for you, it may be really good. When you’re switching languages all the time it strengthens your mental muscle and your executive function becomes enhanced."

Fluent bilinguals seem to have both languages active at all times, whether both languages are consciously being used or not, the researchers report in a recent issue of Frontiers in Psychology. Both languages are active whether either was used only seconds earlier or several days earlier.

Bilinguals rarely say a word in the unintended language, which suggests that they have the ability to control the parallel activity of both languages and ultimately select the intended language without needing to consciously think about it.

The researchers conducted two separate but related experiments. In the first, 27 Spanish-English bilinguals read 512 sentences, written in either Spanish or English — alternating language every two sentences. Participants read the sentences silently until they came across a word displayed in red, at which point they were instructed to read the red word out loud, as quickly and accurately as possible. About half of the red words were cognates — words that look and sound similar and have the same meaning in both languages.

"Cognate words were processed more quickly than control words," said Jason W. Gullifer, a graduate student in psychology, suggesting that both languages are active at the same time.

Participants in the second experiment performed the same tasks as those in the first experiment, but this time were presented one language at a time. The second experiment’s results were similar to the first, suggesting that context does not influence word recognition.

"The context of the experiment didn’t seem to matter," said Gullifer. "If you look at bilinguals there seems to be some kind of mechanistic control."