The protest psychosis

An ad for the drug Haldol from the 'Archives of General Psychiatry,' 1974, shows an angry African American man alongside the text 'Cooperation often begins with Haldol.' The association of schizophrenia with anger and blackness in the 1960s was a significant change from the original association of the illness with frail, nervous white women.
A prominent story appeared on the front page of the Washington Post on June 28, 2005. "Racial Disparities Found in Pinpointing Mental Illness" read the headline above an article that was at once shocking and sadly familiar. Researchers had examined the largest American registry of psychiatric patient records looking for "ethnic trends" in schizophrenia diagnoses. As the Post described it, schizophrenia, "a disorder that often portends years of powerful brain-altering drugs, social ostracism and forced hospitalizations…has been shown to affect all ethnic groups at the same rate."

"Racial schizophrenia" arose not from individual racism, but from cultural shifts that defined the thoughts, actions and even politics of black men as insane.
And yet, the large government study uncovered striking categorical differences in its analysis of 134,523 case files: doctors diagnosed schizophrenia in African American patients, and particularly African American men, four times as often as in white patients. The Post cited the study's lead author, John Zeber, who explained that doctors overdiagnosed schizophrenia in African American men even though the research team uncovered no evidence that "black patients were any sicker than whites." According to Zeber, "the only factor that was truly important was race."

Paradoxically, we live in an era when the opposite is supposed to be the case: race should be entirely unimportant to psychiatric diagnosis. Present-day psychiatry believes that mental illness results from disordered brain biology at levels that are presumably the same in people of all races and ethnic backgrounds. And psychiatrists consider schizophrenia to be the most biologically based of the mental illnesses. Textbooks routinely claim that, as a biological disorder, schizophrenia should occur in one percent of any given population, or one out of every hundred persons regardless of where they live, how they dress, who they know, or what type of music they happen to prefer.

Yet, in the real world, one percent is a delusion. Not only do stories such as the Post article appear with regularity—they persist over time. For instance, throughout the 1980s and 1990s, a host of articles from leading psychiatric and medical journals showed that African American patients were "significantly more likely" than white patients to receive schizophrenia diagnoses, and "significantly less likely" than white patients to receive diagnoses for other mental illnesses such as depression or bipolar disorder.

My research tells the story of how these race-based imbalances came to be. I look closely at changing twentieth-century American assumptions about race and schizophrenia through sources including American medical journals, newspapers, popular magazines, pharmaceutical advertisements, and medical charts. What I find, surprisingly, is that the very idea of "racial schizophrenia" came about only in the 1960s and 1970s. And, that far from resulting from the racist intentions of individual doctors or the symptoms of specific patients, racial schizophrenia resulted from a much wider set of cultural shifts that defined the thoughts, actions, and even the politics of black men as being inherently insane.

For instance between the 1920s to the 1950s, mainstream American medical and popular opinion often assumed that patients with schizophrenia were largely white, and generally harmless to society. Psychiatric textbooks depicted schizophrenia as an exceedingly broad, general condition, manifest by "emotional disharmony," that negatively impacted white people's abilities to "think and feel." Authors of research articles in leading psychiatric journals described patients with schizophrenia, and, all too often, their "schizophrenogenic mothers," as "native-born Americans" or immigrants of "white European ancestry."

Leading mainstream American newspapers in the 1920s to the 1950s similarly described schizophrenia as an illness that occurred "in the seclusive, sensitive person with few friends who has been the model of behavior in childhood," or that afflicted white women or intellectuals. In 1935, for instance, the New York Times described how many white poets and novelists demonstrated a symptom called "grandiloquence," a propensity toward flower prose believed to be "one of the telltale phrases of schizophrenia, the mild form of insanity known as split personality." Meanwhile, popular magazines such as Ladies' Home Journal and Better Homes and Gardens wrote of unhappily married, middle-class white women whose schizophrenic mood swings were suggestive of "Doctor Jekyll and Mrs. Hyde."

A series of transformations occurred during the American civil rights era of the 1960s and 1970s. During this vital period, new clinical ways of defining mental illness unintentionally combined with growing cultural anxieties about social change. Meanwhile, reports about new "psychochemical" technologies of control merged with concerns about the "uncontrolled" nature of urban unrest. As these historical contingencies evolved, the American public, and at times members of the scientific community, increasingly described schizophrenia as a violent social disease—even as psychiatry took its first steps toward defining schizophrenia as a disorder of biological brain function.

As but one example, in 1968, psychiatry published the second edition of the "Diagnostic and Statistical Manual" (DSM)—the "official" source of psychiatric diagnoses. That text recast the paranoid subtype of schizophrenia as a disorder of masculinized belligerence. "The patient's attitude is frequently hostile and aggressive," the DSM-II claimed, "and his behavior tends to be consistent with his delusions." My evidence shows that growing numbers of research articles used this language to cast schizophrenia as a disorder of racialized aggression. In the worst cases, psychiatric authors conflated the schizophrenic symptoms of African American patients with the perceived schizophrenia of civil rights protests, particularly those organized by Black Power, Black Panthers, Nation of Islam, or other activist groups. Advertisements for new pharmaceutical treatments for schizophrenia in the 1960s and 1970s depicted similar themes. An Archives of General Psychiatry ad for the antipsychotic drug Haldol showed an angry black man with a clenched, Black Power fist whose symptoms of social belligerence required chemical management (see illustration above).

Meanwhile, mainstream white newspapers described schizophrenia as a condition of angry black masculinity, or warned of crazed, black, schizophrenic killers on the loose.

Changing notions of schizophrenic illness in the 1960s impacted persons of many different racial and ethnic backgrounds. Some patients became schizophrenic because of changes in diagnostic criteria rather than in their clinical symptoms. Others saw their diagnoses changed to depression, anxiety, or other conditions because they did not manifest hostility or aggression. Emerging understandings of the illness shaped American cultural fears about mental illness more broadly, particularly regarding cultural stereotypes of persons with schizophrenia as being unduly hostile or violent.

In no way is my research meant to suggest that schizophrenia is a socially fabricated disease, or, worse, that people's suffering is somehow inauthentic. As a psychiatrist, I have seen the tragic ways in which hallucinations, delusions, and other symptoms can rupture lives, careers, families, and dreams in profoundly material ways. I know that such symptoms afflict persons of many different social, economic, and racial backgrounds, most all of whom are deeply aware of the sense of loss that their disease represents. I also strongly believe that persons diagnosed with schizophrenia and other mental illnesses benefit from various forms of treatment or social support, and that our society should invest more in the care and well-being of the severely mentally ill.

At the same time, I believe that the material reality of schizophrenia is shaped by social, political, and, ultimately, institutional factors in addition to chemical or biological ones. And, I believe that well-intentioned efforts to correct present-day stigmatizations and racial imbalances are at times undermined by the still-present past. Findings such as those from the Washington Post reflect the ongoing salience of American racial history, and the ongoing need for doctors, patients, policymakers, and others, to better understand this history in order to create better conditions in the present-day.

Far from being static or timeless, stigmatizations of mental illness change over time, and reflect anxieties about race, gender, and class in addition to anxieties about mental illness. Only during the civil-rights era did emerging scientific understandings of schizophrenia become enmeshed in a set of historical currents that marked particular bodies, and particular psyches, as crazy in particular ways. The tensions of that era then changed the associations that many Americans made about persons with schizophrenia. Ultimately, recent American racial history altered more than the meaning of mental illness: it changed the meaning of mental health as well.

This essay is adapted from Jonathan Metzl's book The Protest Psychosis: How Schizophrenia Became a Black Disease (Beacon Press, 2010). He is associate professor of psychiatry and women's studies, and director of the Culture, Health, and Medicine Program at the University of Michigan. He is also the author of the book "Prozac on the Couch."

Technology, revisited.

Earlier this week, I wrote about how too much technology could be bad for your brain. I made the comment that there was no real reason any child under 16 needed a cell phone – if the argument for cell phones is safety. I’ve been handily challenged via comments and other methods to reconsider that blanket statement. After consideration, I concede that maybe children at the age of middle school might need a cell phone for safety. Under that age, it seriously seems that hands-on parenting is what should be providing the safety for that child.
However, even if parents do believe their young ones need a cell phone, thought must be given to the negatives (cognitive development, bullying via texting, the inability to “disconnect”, decreased ability to connect with anyone not tethered to a texting machine, the cost, the ability of creepers to track where your kid is by the fact they have a phone, the unknown effect of holding a battery to your head or in your front pocket all day, the decidedly unsafe practice of texting/talking by teens while driving) versus the positives (reaching your kid, tracking your kid with those creepy tracking devices, talking via text to a teen who won’t talk in person, safety).
If you think your child needs a cell phone, give him one. But as the grownup, perhaps you should consider setting limits on usage of that phone. If it truly is for safety, he doesn’t need it once he gets home – turn the thing off and turn on face-to-face interactions. Then again, many parents are just as addicted to their devices as their children are. Awhile ago, I saw a family of four at a restaurant. Mom and Dad were both reading/using their smart phones, the baby was propped in front of a tiny video device watching a kid-vid, and the young boy, who looked to be about 8, was saying, “And then, when my teacher told me ….” while his parents stared at their phones and said, “Uh-huh, hmm” and other grunts of feined interest. The sad thing is, this isn’t a rare sight and personally, I’m not sure this is all that great for family development.
I know the risks of being over-wired. When I first discovered instant messaging about 15 years ago (after succumbing to begging from my family to get the Internet in our house), I was instantly addicted. It was like a drug – all this real-time connection with people all over the place. Now, I have to fight wasting 30 minutes here and 40 minutes there reading Twitter feeds or Facebook updates – and don’t even get me started on what happens to my morning if I start searching blogs for a particular teacher topic! I really want a smart phone, but I’m fairly certain if I get it I’ll not be able to control my insatiable need-to-know what is happening right this minute in Japan, New York, the Middle East. Right now, if I leave my computer, I’m off the connection web. If I were to have a smart phone, Lord only knows what might happen.
Do you think someone who is 10 years old knows the risks of over-connection? Does a 16 year old understand what she’s missing in real relationships as she feeds her virtual ones online? We’ve all seen the interviews with tweens who say they can’t sleep if they aren’t holding their phones. Should we just accept this as normal or should we use are critical thinking skills and question it? Should we poo-poo what the the research in the story Monday was showing or maybe give it a little thought? Or should we wonder that wiring up our kids at birth may be one of the reasons college students today are showing 40 percent less empathy than students did just a decade ago?
I’m not saying we should all go back to the unwired dark ages. There is so much potential for good out there in the wired world. I’m saying we should not all march like lemmings to bow at the altar of technology without thinking about it longer than five minutes, especially when young children, young brains and young relationships are involved.

Virus infection may trigger unusual immune cells to attack nerves in multiple sclerosis

A virus infection can incite the body to attack its own nerve tissue by activating unusual, disease-fighting cells with receptors for both viral and nerve proteins. The dual-receptor observation suggests a way brain and spinal cord nerve damage might be triggered in susceptible young adults afflicted with multiple sclerosis (MS). University of Washington Department of Immunology scientists Qingyong "John" Ji, Antoine Perchellet, and Joan M. Goverman conducted the study, which was published June 6 in Nature Immunology.
This is thought to be the first study to reveal a mechanism for autoimmune disease that depends on destroyer immune cells expressing dual receptors for a normal protein made by the body and a pathogen.
Multiple sclerosis is one of many autoimmune disorders in which the body's lines of defense become misguided and start damaging normal tissue. In the case of multiple sclerosis, the protective sheath around major nerves -- the myelin -- in the brain and spinal cord disintegrates. Like a frayed electrical cord, the nerves no longer transmit a clear signal.
People with multiple sclerosis might lose their ability to see, walk, or use their arms, depending on which nerves are affected. The symptoms can appear, disappear, and re-appear. The disease is more common in women than in men.
In healthy people, the immune system is kept in check to tolerate the usual proteins and cells in the body, much like an eager watch dog is put on a leash and trained to ignore friends and neighbors, yet still protect the family.
"Autoimmunity is believed to arise from an accidental breakdown in this tolerance of the body's own proteins. This breakdown is triggered by something in the environment, most likely a pathogen," noted Goverman, professor and acting chair of immunology whose research concentrates on the origins of autoimmune disease. Her lab is studying mechanisms that maintain tolerance, as well as the "tripping" mechanisms that defeat it.
In their most recently published study, her research team genetically engineered mice that over-produce a certain type of white blood cell from a group known as killer T cells. The normal function of killer cells is to attack tumor cells or cells infected with viruses or other pathogens. These T cells have receptors that recognize specific proteins that infected cells display to them, much like holding up a target in a window.
The specific killer T cells examined in this study were CD8+ T cells. The Goverman lab engineered mice to over-produce CD8+cells that recognized myelin basic protein, a predominant protein in the myelin sheath that covers nerves. The major question investigated in the study was whether the genetically engineered mice would exhibit a disease that resembled multiple sclerosis.
The researchers infected the mice with a virus that has itself been engineered to produce myelin basic protein. This infection should activate the CD8+T cells to first attack the virally infected cells making myelin basic protein to eliminate the virus, then kill other cells that make myelin basic protein to wrap around nerves. Killing those cells would destroy the myelin sheath.
As expected, the mice developed a multiple sclerosis-like disease. But the researchers were surprised when viruses lacking the myelin basic protein also triggered the disease.
Additional cross-breeding experiments revealed the existence of two receptors on a few of the CD8+T cells. These cells, engineered specifically to bind to myelin basic protein, also built their own receptors for viruses, and could recognize both. When exposed to cells infected with viruses, they would bind to and destroy them using one receptor. Geared up as if they were beserk, some of these double-agent cells then would head elsewhere to bind their other receptor to cells producing myelin basic protein and ruin the coats on nerve cells.
"These results," the authors noted, "demonstrate a role for dual-receptor cells in autoimmunity." The study also points to why a ubiquitous viral infection could leave most people without any lasting effects, but trigger autoimmunity in genetically predisposed individuals.
The findings open a new perspective on the proposal that multiple sclerosis is virally induced, despite the inability to detect infectious virus in the central nervous system of multiple sclerosis patients. Data from other studies show that CD8+T cells can cross the blood-brain barrier, and also that multiple sclerosis patients have more central nervous system protein-specific CD8+T cells, compared to healthy people.
In the dual-receptor model, the autoimmune activity against nerve protein can continue after the virus is wiped out. Multiple sclerosis patients usually have high levels of antibodies indicating past infectious from several common viruses, but a live virus associated with multiple sclerosis has not been consistently observed. Therefore, to date, no specific virus has been confirmed as a causative agent for multiple sclerosis.
The authors explained that it's possible that multiple viruses could influence susceptibility to multiple sclerosis. The ability of any particular virus to contribute to the disease could depend on an individual's own repertoire of other predisposing genes, exposure to other predisposing environmental factors, and the random chance that T cells had been generated that recognize a myelin protein and a pathogen.
Receptors on T cells are randomly generated during their development. This observation helps explain why multiple sclerosis is partly a matter of chance. Some people with a genetic predisposition and environmental exposure develop the disease, while others with similar genetic predisposition and environmental exposure do not.
It's uncertain how common these dual-receptor T cells are, according to the researchers, although there are reports that up to one-third of human T cells express dual receptors. Goverman and her group plan to test samples from multiple sclerosis patients and see how many have dual-receptor T-cells.

A Different Story About Desire

With an FDA hearing looming for pharmaceutical manufacturer Boehringer Ingelheim about their experimental sex drug Flibanserin, they are ramping up their marketing efforts, softening up all of us to accept their particular story about female desire, which is that it's gone, but if they tweak the brain it'll come back.
Where did it go, you ask? Do all younger women report higher levels of desire and then suddenly at a certain age it just disappears, you wonder? These are good questions. One of the responses you hear is that we don't know. That there's no good research about female sexuality. But that's part of the same story, the one that ends with a pill and a simple answer. Because the more complicated answer is that there's actually quite a bit of research on female sexuality. And some of it includes the actual voices of women, talking about sexuality.
In an effort to present the possibility of a different narrative than the one being marketed by a for profit drug company, members of the New View Campaign have put together an easy to read summary of 27 studies which offer different narratives about female sexuality and desire. There are actually many more studies they could have included, but to provide a reasonable point of comparison they stuck with mainly empirical studies. It seems to me that whatever your current opinion is on the value of taking a brain drug to address a sexual problem, why wouldn't you want to get more information about the way that sexual problems are constructed in the first place, and how other researchers have approached addressing them.

Wine, Food and Funds for Children's Brain Tumor Research

A benefit for a foundation dedicated to funding children's gliomas research
 

ROCKY RIVER, Ohio, June 11--Uncork the Cure – a festival involving wine, food and music – will contribute funds for research into the causes of and cure for children's gliomas or brain tumors.
On Saturday, July 24, from 1-8 p.m., representatives from award-winning wineries will be pouring choice vintages from stations located up and down Rocky River's Linda Street, which is near the city's eastern border.

WHAT:	Uncork the Cure
WHEN:	1-8 p.m., Sat., July 24
WHERE:	Linda Street, Rocky River
WHO:	Prayers from Maria Foundation
WHY:	Funding research into the causes, prevention, treatments, and cure for children's glioma or brain tumors
TICKETS:	$30/ea.(prior) @ www.PrayersFromMaria.org

Michael Chiarello Vineyards, Groth, Duckhorn, Loosen Brothers, Clarendon Hills, Penfold, William Hill and Neiman Cellars are just some of the twenty renowned wineries that will be present and serving at the festival.

The event also offers gourmet cheese and meats stations, a limited 32-team bocce tournament sponsored by Peroni Beer, and an 8 p.m. concert, The Oak Barrel Bash; its center stage will be occupied by Shucking Bubba Deluxe, a cover band from Columbus.
The fundraising event is benefiting The Prayers from Maria Foundation, which is dedicated to funding global research into the causes, prevention, treatments, and cure for children's gliomas.
Advanced tickets are $30/each and can be secured at the Prayers From Maria website, www.PrayersFromMaria.org.  Otherwise, tickets can be purchased for $40/each at the event.

New entry effective in deep brain surgery

BALTIMORE, June 10 (UPI) -- U.S. surgeons say they've developed a safe, effective and less invasive entry method to use in skull and deep brain surgical procedures.
Surgeons at Johns Hopkins University in Baltimore report safely entering into the brains of a dozen patients by making a small incision through the natural creases of an eyelid.
They said access to the skull and brain through either lid, formally known as a transpalpebral orbitofrontal craniotomy, sharply contrasts with the more laborious, physically damaging and invasive, traditional means of entry -- opening of the top half of the skull.
"Going through the eyelid offers a simpler, more direct route to the middle and front regions of the brain than traditional skull-based surgery," said Dr. Kofi Boahene, who led the research. He said the approach eliminates the need for shaving the patient's hair, pulling up the scalp, opening the top half of the skull and moving aside whole outer sections of the brain in order to operate on the organ's neurological tissue.
The Johns Hopkins team said it believes the findings mark the first published case studies of the procedure.
The research appears in two reports -- one in the June issue of the Journal of Otolaryngology and the other to appear in the July issue of the journal Skull Base.

Chicago pioneer of laser brain surgery plans more milestones

Northshore University Hospital
Dr. Leonard Cerullo is widely considered one of the pioneers of laser surgery across the globe.

Leaning back in his office chair at Northshore University Hospital in Skokie, Dr. Leonard Cerullo wants to make one thing clear.
“I’m not a scientific-type person.”
Behind him on the wall is a framed magazine cover showing the mustachioed doctor holding a model of a brain in an area of medicine he helped remap.
It’s difficult to imagine a man who’s practiced neurosurgery for 40 years - an early pioneer using lasers in the operating room - as "not a scientific-type.”
But the 66-year-old says it’s always been more important to understand how to use a laser as an alternative to opening up a person’s head in surgery rather than understanding all the technology behind it.
“You’ve got to understand the physics a little bit, but understand the application a big bit,” Cerullo says. “[Surgery] boils down to how good are your hands, how good is your judgment?”
Cerullo has taught and practiced across the world and performed the first laser neurosurgeries in Argentina and Brazil. His trailblazing laser surgery and his work in diagnosing and operating on brain tumors is highly regarded in the medical community. He has been featured several times in Chicago Magazine’s Top Doctors issues.
The subject of several news and magazine articles, and a major source in many books on surgery and medicine, Cerullo has been in the public eye for most of his career. And while some have called him a self-promoter, Cerullo said he simply feels obligated to inform.
“I’m doing something I think people should know about, and if I don’t let people know about it, than morally, I’m not cutting it,” he says. “I want people to know that there might be a better way to take care of your hemorrhoids than having someone stick their hand up your ass.”
He’s been performing and developing laser surgery since the 1970s and is the founder and medical director of the Chicago Institute of Neurosurgery and Neuroresearch is likely to discuss.
“You don’t need to know a lot of science to go to medical school,” he says.
After studying English at Georgetown University, Cerullo decided to go to Northwestern University for medical school in the 1970s, where he would later teach. He made the switch because, at the time, med students got more dates, he jokes. But eventually, after standing in on his first surgery almost by mistake, Cerullo realized neurosurgery was for him. As he so often says, “The rest is history.”
Dr. Edward Mkrdichian trained under Cerullo, and credited him for being one of the forefathers of using new, innovative technologies in surgery.
“He was one of the first people involved, and he has been a front man in technology,” “He brought up a lot of people who used innovative technologies.”
Cerullo began working in medicine during a time of major technological advance. As a practicing surgeon he saw the operating microscope, the ultrasonic aspirator and image guidance find their way into the operating room.
And when he began working with lasers and non-invasive surgeries in the 1970s, few were certain what effects lasers might have on sensitive nerve tissue, in places such as the eye, the spine or the brain. But coming of age in a time of such accelerated technological advance made working with cutting-edge technology the norm of Cerullo.
Based on its wavelength, a laser can penetrate and precisely target tissue. This allows surgeons to avoid making incisions and allows for easier surgery on particularly sensitive areas such as the eyes.

“It can be a very powerful, and very dangerous instrument if not used properly,” he says. “So we would try to get these various different lasers and use them on various different tissues and try to discover what the immediate short term and long term effects were.”
The danger of non-invasive surgery lies as much in the hands of the surgeon as it does with the immense power emitted by a laser. Cerullo spent years conducting over 100 practice and experimental surgeries on animals before he finally had what he called “an intimate knowledge” with the laser.
“One of the things you give up with lasers is the tactile input of the tissue to your fingers, and in surgery, that’s really important,” he says. “Your vision and your tactile senses are what allow a surgeon to do what they do.”
Cerullo continued operating until about a year ago. But he still sees patients from across the world everyday and much of his time is spent on the last self-assigned challenge of his career - helping to create a neuroscience institute the serve the entire Midwest.
When he isn’t working, Cerullo spends time with his wife Cheryl and dons his chef's apron as an avid cook. And while he no longer uses his hands to carefully operate a laser, he’s still putting a career’s worth of dexterity to the test.

“I’m just getting decent at typing,” he jokes.

A gym for the brain? Go figure

LOFTY LOGO – Bridget Summers, owner of the “Mathnasium” franchise that opened last week in Hyannis, points to the company logo, which also happens to be a goal of the serious student.

“Mathnasium” sums up path to learning

There’s a new gym in town but you will hear less about abs, biceps and bench presses than you will about square roots, quotients, and finding unknown quantities.

It is called “Mathnasium” and it opened last week at 16 Sea St., Hyannis, between South and Main streets under the direction of local franchise owner Bridget Summers of Osterville.

 “You join like you would a gymnasium,” Summers said, “and you drop in at your  convenience, as you would a fitness center, to exercise your mind in mathematics, from second grade all the way up to pre-calculus.”

“Mathnasium” is a franchise operation with 202 offices nationwide and three, including this one, in Massachusetts, helping fulfill the national desire to produce more students with the solid math skills required in most 21st century business and science applications, or “apps” as the young ’uns call them these days.

Here’s how it works. A student signs up as he or she would a fitness center. The student, or client, receives a comprehensive assessment via “sophisticated techniques” to determine “with great accuracy” what a student or client knows and does not know about mathematics.   

Then a personalized learning program is prescribed, with clients following their own prescription for mathematical success with the help of specially trained “Mathnasium” teachers who provide individual instruction and “warm encouragement.”

The site is arranged with a number of L-shaped tables, each with a teacher on one side, and up to four or six students on the other, each of them following their prescribed program at their own pace and with the help of the teacher at their elbow

 “The students can stop by any time and as often as they wish,” Summers said. “There are always teachers here. We suggest they work out at least twice a week for an hour.”

While “Mathnasium’s” logo is a big red “A+,” that grade in school is not guaranteed, Summers quips. The student has a lot to do with success. But for proof of progress, “Mathnasium” relies on student report cards, independent tests and parent testimony, all intended to measure the speed and magnitude of improvements in math skills, numerical thinking and attitude.

 “We offer parents an alternative to private in-home tutoring, which can be very expensive. It decreases the cost by about half,” Summers said.

Summers, on the Cape since 1994, commuted to and graduated from U-Mass, Dartmouth, with a degree in biology following high school in her native New Jersey. She confesses she had difficulty with mathematics as a young student. “I had to do a lot of catch-up in college and ultimately found joy in math.”

Her own experience is what directed her entrepreneurial bent toward buying into the franchise even while she is in the process of completing her MBA. She will be handling the business end while teachers tend to student training.  

She said “Mathnasium” isn’t only for students who may have fallen behind in math, but for those who are good at it and seek enrichment.

“We’re having a grand opening July 3 and an open house July 4 to accommodate interested parents and students who may walk by before and after the July 4 parade,” Summers said.

Dakim Introduces the Only Clinically Tested Brain Fitness Software Created for People Over 60

Decades of medical research confirms that long-term participation in broad-based rigorous cognitive exercise is associated with as much as a 63% reduced risk of dementia-the greatest threat to the quality of life of the over 50 million Americans, age 60 and above. Dakim, is introducing the first brain fitness software designed specifically for people over age 60 to use on their home computers.
Santa Monica (PRWEB) June 11, 2010 -- In response to the growing number of individuals concerned about maintaining their brain health and fighting the threat of dementia, Dakim, Inc. a leader in the development and marketing of computer-based brain fitness products announced today that its Dakim BrainFitness Software, the first brain fitness software created specifically for people over age 60, is now available for sale via a select group of retailers as well as on its own website.
To date, Dakim's clinically tested Dakim BrainFitness has only been sold to senior living providers, and only as part of its turnkey, integrated hardware/software system that incorporates a touch screen computer. This system, over the past three years, has earned the reputation as the Gold Standard of brain fitness for seniors, and become the #1 brand of brain fitness products in the long-term care market.

People over age 60 are most at risk for the development of dementia, and they know that getting the most out of life depends on keeping their minds sharp

The new Dakim BrainFitness Software, a DVD package containing a prodigious 6.5GB worth of content, helps maintain mental acuity with entertaining, scientifically based brain games designed specifically to appeal to people over age 60. Dakim's software is valued at $349.95 but the company is introducing it for $249.95, which includes one user license and a full year of updates to Dakim's award-winning content. Fight Mental Decline in 20 Fun Minutes a Day
Drawing on medical research conducted over the past two decades that shows that brain training is most effective when the program is varied and stimulates multiple functions, Dakim's approach to brain fitness centers on a regimen of cross-training the brain in six cognitive domains, short- as well as long-term memory, critical thinking, visuospatial orientation, calculation and language for a thorough brain workout. Unlike other brain fitness products that use simple, cartoon-like flash animation for its exercises, Dakim transforms standardized neurological exercises and tests into sophisticated and richly produced interactive brain games reminiscent of a TV game show, complete with live-action videos, music, newsreels, story exercises, colorful graphics, humor and variety to maintain interest long-term.
The cognitive activities self-adjust across five levels of challenge ranging from normal brain function to moderate dementia, automatically increasing or decreasing difficulty levels in real time based on user performance. New brain games are automatically updated almost daily via the Internet to keep users coming back for more. The have-fun design encourages consistent long-term use in keeping with medical research indicating that ongoing mental stimulation is associated with a more than 60% reduced risk of dementia.
Activities range from anagrams and word association games to interactive puzzles, visual comparisons and grocery-store math challenges. ‘Keep Your Eyes Open,' for example, trains short-term memory by showing old movie clips and then questioning users about what they saw. ‘Phunny Phrases,' on the other hand, exercises language and deductive reasoning by presenting nonsense words and asking users to add the correct letters to turn them into real phrases.
Top Choice of Senior Living Communities
Originally designed for use in senior living communities, Dakim BrainFitness is the best-selling product in the industry with adoption by more than 400 independent retirement, assisted living and skilled nursing communities, adult day care centers and senior centers across the U.S. That dominance stems from compelling and continually updated multimedia activities that keep users engaged, as well as a community package that utilizes a touchscreen computer requiring no mouse, keyboard or computer skills. The touchscreen form factor enables use by individuals who have never used a computer or those with arthritis, Parkinson's or fine motor impairment issues, while also reducing or eliminating the need for caregiver assistance.
The new software-only edition extends the brain-building benefits to home users on their personal computers, providing an enjoyable cognitive stimulation program specifically designed to help users fight or slow the development of dementia symptoms.
"People over age 60 are most at risk for the development of dementia, and they know that getting the most out of life depends on keeping their minds sharp," said Dakim CEO Dan Michel. "Given years of medical research showing that long-term participation in cognitive stimulation is associated with as much as a 63% reduced risk of dementia, regular brain workouts are the most promising strategy available for preserving brain health. We have spent nearly a decade developing Dakim BrainFitness for people over age 60, specifically for that purpose, and now anyone with a computer can use it to help maintain brain health and to build their defenses against mental decline."
Availability
Dakim BrainFitness Software is available at select retailers as well as www.dakim.com. It is compatible with Windows 7/XP/Vista and Mac OS X 10.5 or higher, as well as touchscreen computer/monitor platforms.
About Dakim, Inc.
Dakim Inc., the Brain Fitness Company, is the leading provider of brain fitness programs for people over 60 that offer rigorous cognitive stimulation to help reduce the risk of memory loss and dementia as well as expedite the process of regaining cognitive function after a stroke or traumatic brain injury. The company's flagship product, Dakim BrainFitness, offers an entertaining multimedia cross-training brain workout that is available as a software product for home use and also packaged on a touchscreen computer for senior living communities. The hardware-based version is the #1 brain fitness program in the senior living market. The company is headquartered in Santa Monica, CA. For more information, visit www.dakim.com.

Panel explores ethics, effectiveness of 'brain doping'

The full effect of "cogs" is unknown
It's 2:00 a.m. the morning before the midterm. Eager to ward off sleep, a student pops a couple of modafinils, a drug originally designed to help those suffering from narcolepsy to stay awake.
While many college students, truck drivers and even executives swear by it, might the drug cause long-term harm? Perhaps more significantly, does it even work the way its users believe it does?

A panel hosted by the National Institute on Drug Abuse at the American Psychiatric Association's annual meeting last month in New Orleans sought to produce hard data where now exists mostly dorm-room and back-office anecdotes about drugs known as "cogs," or cognitive enhancers--prescription drugs whose labeled purpose treats neurological conditions but which moonlight, often illegally, as brain boosters.

"The main thrust is really to look at the science behind medications that have the potential to be used as cogs," Dr. Ruben Buehler, an organizer of the panel, The Challenge of Cognitive Enhancers in Medicine, told DOTmed News. "Usually, a lot of information about alternative or non-medical uses for the drugs out there that have potential at least as cog enhancers is without much science."

The practice of using cogs is widespread, even among the scientific elite. According to a 2008 survey by Nature, one in five of that magazine's readers use some form of cognitive enhancing drug.

"We try to understand as best as we can, the science-based benefits for other populations, even normal populations," Buehler said, such as "asymptomatic housewives that just want to better remember phone numbers."

In one of the talks, researchers discussed a drug that assists with up-take of serotonin, and is used for schizophrenia; some think it might also help alleviate mild cognitive impairment in aging brains. The drug could help raise levels of the neurotransmitter acetylcholine, implicated in both schizophrenia and Alzheimer's. But there's not a lot of hard evidence for its cognitive improvement effects, Dr. Buehler said.

"Acetylcholine, in particular, facilitates flow from one [neural] circuit to another. Not much more than that is really known," he said.

Surprisingly, the results so far for many of these nootropic, or cognitive enhancing drugs, at least in aiding student cram sessions, are pretty thin, Buehler said. "The evidence so far doesn't suggest they're particularly effective for performing better in the long-term in schools," Buehler said.

What does work? Exercise.

"Exercise I think is one of the best known [ways] to raise many of the neurotransmitters naturally," Buehler said. "In the presence of things like this we know are so good for the brain in a natural way, it seems silly to focus on pharmacological agents."

Controlling the brain with light

Genetically encoded tools enable activation and silencing of neurons with light, revealing how the brain works and facilitating potential new therapies.

Our brains mediate everything we perceive, feel, decide, and do. This is accomplished by an incredibly densely packed network of hundreds of billions of neurons, which fall into perhaps hundreds of different classes, defined by their shape and the molecules they contain. Each computes in concert with thousands of others, its activity dynamically changing on the millisecond timescale. In many diseases, specific computations mediated by the brain are thrown into disarray when specific classes of neuron are compromised. Such neurological and psychiatric disorders affect billions of people worldwide and are some of the most intractable medical needs of our time. To treat these diseases, we need to understand how the elements of a neural circuit work together. This requires the ability to selectively perturb the activity of specific neurons within the circuit, observing the resultant impact on neural computation and behavior.

Until now, the ability to test the causal role of specific neuron types in emergent brain functions was limited. Lesions and pharmacological agents can eliminate the activity of neurons in a region, but the effects would apply to all cell classes in a region and would be long-lasting or even permanent, preventing researchers from analyzing when a given set of cells made its critical contribution. Stimulation of brain tissue with electrodes or magnetic fields enables temporally precise driving of neural activity, but such methods affect all neuron classes located within a region, including projection pathways entering or passing through the region. Accordingly, we have developed a series of molecular tools that enable activation or silencing of genetically specified neurons.

These are proteins encoded by genes from natural species of algae, fungi, and archaebacteria. These ‘optogenetic’ proteins can be thought of as tiny, genetically encoded solar panels: they sit, embedded, in the membranes of cells such as neurons and respond to light by altering the voltage of the cell. Since neurons are themselves electrical devices, using a virus to express these genes in neurons enables activation or silencing of the latter by different colors of light.

We have shown that the algal gene channelrhodopsin-2 (ChR2), which encodes a light-gated ion channel, can be inserted into neurons to activate them by brief pulses of blue light.¹ In addition, my group has found that a halorhodopsin (Halo/NpHR), a light-gated chloride pump, can be used to silence neurons by yellow/red light.² ChR2 and Halo can be used together in the same cell to activate and quiet neural activity with two different colors of light, enabling precise perturbations of the timing of electrical signals in the brain.³

More recently, we found a new reagent, nicknamed Arch (see Figure 1), that offers order-of-magnitude improvements in silencing power and recovery kinetics over halorhodopsins and enables near-digital switching off of neurons in the awake-behaving brain in response to yellow-green light.⁴ We also identified a reagent that we nicknamed Mac, a blue-light-driven neural silencer, opening up the ability to silence (alongside Arch or Halo) two different populations of neurons with different colors of light (see Figure 2).

Figure 1. A neuron expressing the Arch gene and generating light-activated proteins that are then localized to the outside of the neuron, where they can control the neuron's activity in response to pulses of light. Scale bar: 20 μm.⁴

Note that these reagents can be expressed in practically any cell type. Given that cardiac, immune, pancreatic, and other kinds of cells can be electrically modulated, we can perform ‘synthetic physiology’ on these cells, controlling their state to assess how they contribute to organism or system-level functions.

Figure 2. Demonstration of multicolor silencing of two different neurons. One neuron expresses Mac and is thus silenceable by blue but not by red light, while the second neuron expresses Halo and is thus silenceable by red but not by blue light.⁴

In summary, we have identified optogenetic proteins that act as molecular tools to make neurons controllable with pulses of colored light. We are now developing high-count arrays of optical fibers that enable perturbation of activity in distributed and complexly shaped neural circuits, in order to open up systematic analysis of brain circuits. By revealing the neural substrates that can most powerfully control and correct aberrant neural computations, these tools will lead to better therapies for treating brain disorders such as post-traumatic stress disorder, epilepsy, and Parkinson's disease. New drugs can be generated that target these control circuits but not other unrelated ones, presenting more efficacy and fewer side effects. They may also present new targets for neuromodulation therapies such as deep-brain and transcranial magnetic stimulation. The ability to optically control cells may directly enable a new generation of optical prostheses, which can precisely control aspects of patient physiology using temporally precise pulses of light.

ESB acknowledges funding by the National Institutes of Health (NIH) Director's New Innovator Award (DP2 OD002002-01), NIH Challenge Grant 1RC1MH088182-01, NIH Grand Opportunities Grant 1RC2DE020919-01, NIH 1R01NS067199-01, National Science Foundation (grants 0835878 and 0848804), the McGovern Institute Neurotechnology Award Program, the Department of Defense Congressionally Directed Medical Research Programs Post Traumatic Stress Disorder Program, the National Alliance for Research on Schizophrenia and Depression (since recently known by the business name NARSAD), the Alfred P. Sloan Foundation, Jerry and Marge Burnett, the Society for Neuroscience Research Award for Innovation in Neuroscience, the Massachusetts Institute of Technology Media Lab, the Benesse Foundation, and the Wallace H. Coulter Foundation.

Virus infection may trigger unusual immune cells to attack the brain and spinal cord in multiple sclerosis

A virus infection can incite the body to attack its own nerve tissue by activating rare, disease-fighting cells with receptors for both viral and nerve proteins. The dual-receptor observation suggests a way nerve damage might be triggered in susceptible young adults afflicted with multiple sclerosis (MS).
University of Washington Department of Immunology scientists Qingyong "John" Ji, Antoine Perchellet, and Joan M. Goverman conducted the study, which was published this week in Nature Immunology.
This is thought to be the first study to reveal a mechanism for autoimmune disease that depends on destroyer immune cells expressing dual receptors for a normal protein made by the body and a pathogen.
Multiple sclerosis is one of many autoimmune disorders in which the body's lines of defense become misguided and start damaging normal tissue. In the case of multiple sclerosis, the protective sheath around major nerves -- the myelin -- in the brain and spinal cord disintegrates. Like a frayed electrical cord, the nerves no longer transmit a clear signal.
People with multiple sclerosis might lose their ability to see, walk, or use their arms, depending on which nerves are affected. The symptoms can appear, disappear, and re-appear. The disease is more common in women than in men.
In healthy people, the immune system is kept in check to tolerate the usual proteins and cells in the body, much like an eager watch dog is put on a leash and trained to ignore friends and neighbors, yet still protect the family.
"Autoimmunity is believed to arise from an accidental breakdown in this tolerance of the body's own proteins. This breakdown is triggered by something in the environment, most likely a pathogen," noted Goverman, professor and acting chair of immunology whose research concentrates on the origins of autoimmune disease. Her lab is studying mechanisms that maintain tolerance, as well as the "tripping" mechanisms that defeat it.
In their most recently published study, her research team genetically engineered mice that over-produce a certain type of white blood cell from a group known as killer T cells. The normal function of killer cells is to attack tumor cells or cells infected with viruses or other pathogens. These T cells have receptors that recognize specific proteins that infected cells display to them, much like holding up a target in a window.
The specific killer T cells examined in this study were CD8+ T cells. The Goverman lab engineered mice to over-produce CD8+cells that recognized myelin basic protein, a predominant protein in the myelin sheath that covers nerves. The major question investigated in the study was whether the genetically engineered mice would exhibit a disease that resembled multiple sclerosis.
The researchers infected the mice with a virus that has itself been engineered to produce myelin basic protein. This infection should activate the CD8+T cells to first attack the virally infected cells making myelin basic protein to eliminate the virus, then kill other cells that make myelin basic protein to wrap around nerves. Killing those cells would destroy the myelin sheath.
As expected, the mice developed a multiple sclerosis-like disease. But the researchers were surprised when viruses lacking the myelin basic protein also triggered the disease.
Additional cross-breeding experiments revealed the existence of two receptors on a few of the CD8+T cells. These cells, engineered specifically to bind to myelin basic protein, also built their own receptors for viruses, and could recognize both. When exposed to cells infected with viruses, they would bind to and destroy them using one receptor. Geared up as if they were beserk, some of these double-agent cells then would head elsewhere to bind their other receptor to cells producing myelin basic protein and ruin the coats on nerve cells.
"These results," the authors noted, "demonstrate a role for dual-receptor cells in autoimmunity." The study also points to why a ubiquitous viral infection could leave most people without any lasting effects, but trigger autoimmunity in genetically predisposed individuals.
The findings open a new perspective on the proposal that multiple sclerosis is virally induced, despite the inability to detect infectious virus in the central nervous system of multiple sclerosis patients. Data from other studies show that CD8+T cells can cross the blood-brain barrier, and also that multiple sclerosis patients have more central nervous system protein-specific CD8+T cells, compared to healthy people.
In the dual-receptor model, the autoimmune activity against nerve protein can continue after the virus is wiped out. Multiple sclerosis patients usually have high levels of antibodies indicating past infectious from several common viruses, but a live virus associated with multiple sclerosis has not been consistently observed. Therefore, to date, no specific virus has been confirmed as a causative agent for multiple sclerosis.
The authors explained that it's possible that multiple viruses could influence susceptibility to multiple sclerosis. The ability of any particular virus to contribute to the disease could depend on an individual's own repertoire of other predisposing genes, exposure to other predisposing environmental factors, and the random chance that T cells had been generated that recognize a myelin protein and a pathogen.
Receptors on T cells are randomly generated during their development. This observation helps explain why multiple sclerosis is partly a matter of chance. Some people with a genetic predisposition and environmental exposure develop the disease, while others with similar genetic predisposition and environmental exposure do not.
It's uncertain how common these dual-receptor T cells are, according to the researchers, although there are reports that up to one-third of human T cells express dual receptors. Goverman and her group plan to test samples from multiple sclerosis patients and see how many have dual-receptor T-cells.
A grant from the National Institutes of Health supported the study.

Traumatic Brain Injury Could Also Mean Poor Sleep

Traumatic brain injury could also mean poor sleep, say Australian researchers.

Scientists with the Monash University's School of Psychology and Psychiatry measured in a laboratory setting the sleep of 23 patients with Traumatic Brain Injury (TBI) with 23 healthy people who had not suffered trauma.

Study leader, Associate Professor Shantha Rajaratnam said patients with TBI showed increased sleep disturbance and reported poorer sleep quality, and higher anxiety and depressive symptoms than healthy volunteers.

"These results suggest that TBI may disrupt the brain structures that regulate sleep, including the production of melatonin. Patients with TBI showed decreased sleep efficiency and increased periods of being awake after trying to sleep," Associate Professor Rajaratnam said.

Study co-author, Professor Jennie Ponsford, said injury-related damage to sleep-wake regulating centres and associated pathways or neurotransmitter systems was the most likely cause of such disturbances.

The study also revealed that TBI patients spent more time in a stage of sleep called slow wave sleep or deep sleep (after controlling for anxiety and depression). They were also awake more after initially falling asleep, averaging 62 minutes per night awake compared to 27 minutes for the healthy group.

The study also revealed that patients with TBI had significantly lower levels of evening melatonin production. Melatonin is a hormone produced by the pineal gland in the brain, and is known to be involved in the regulation of sleep.

The results suggest that there are at least two factors contributing to sleep disturbances in patients with TBI. Elevated depression is associated with reduced sleep quality, and increased slow wave sleep is attributed to the effects of mechanical brain damage.

Using a cooling blanket to prevent brain damage in newborn babies

Cooling blanket therapy can help newborns deprived of oxygen

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A recent 18-month study has shown that the use of a cooling blanket can save the lives of babies that experienced oxygen deprivation at birth. This new procedure, called brain cooling, will help newborns suffering from moderate brain damage caused by lack of oxygen.
In this simple procedure, the newborn infant is placed on top of the cooling blanket. The blanket, which has cold water flowing through it via tubes, will cool the baby for 72 hours, lowering the body temperature to 91° Fahrenheit. As the body cools its systems also slow down causing a reduction in swelling around the brain thus preventing further damage from taking place.
Study results look promising with a shown decrease in seizure activity, cerebral palsy, and death. There was also an improvement noted in the mental scores, motor skills and vision of babies who received this type of therapy. Candidates for the use of a cooling blanket must be less than six hours old and born at 36 weeks gestation or older.
The following video explains this wonderful new therapy and shows what a big difference it made for one little girl and her family.

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*The Infant Health Examiner’s articles are meant to be used for education purposes only. Your pediatrician should always be consulted when you have questions regarding the health of your child.*

New Brain Death Guidelines Issued

The American Academy of Neurology has released new guidelines for determining brain death in adults. Updated for the first time in 15 years, the recommendations provide step-by-step instructions to help guide clinical decision making. "The brain death diagnosis can be made only after a comprehensive clinical evaluation and often involves more than 25 separate assessments," lead author Eelco Wijdicks, MD, from the Mayo Clinic in Rochester, Minnesota, said in a news release.
The guidelines are published in the June 8 issue of Neurology.
The authors report that new data have confirmed the effectiveness of earlier recommendations. They saw no evidence of recovery of neurologic function after a diagnosis of brain death using the criteria from the 1995 practice parameter.
"To correctly diagnose brain death, it is essential clinicians adhere to a uniform framework," coauthor Gary Gronseth, MD, from the University of Kansas, Kansas City, said in an interview.
"We wanted to provide useful tools to help clinicians," Dr. Gronseth said, "but many factors will still need to be based on clinical judgment."
The authors report insufficient evidence to determine the minimally acceptable observation period to ensure that neurologic functions have ceased irreversibly.
"I think some people will be disappointed that we weren't able to nail this down," Dr. Gronseth said, "but this will be highly variable patient to patient, and there is no general rule."
These new guidelines focus on patients 18 years and older. Another group is currently working on new brain death recommendations for children. Those recommendations are expected to be released in a couple of months. Some predict those guidelines will include a prescribed observation period.
"Different groups take different approaches," Dr. Gronseth noted. "We felt the evidence was lacking."
Single Exam Sufficient
Some clinicians may also be surprised to see that more than 1 exam is not required in the new brain death guidelines. "The original guideline did not require this either, but I think it was a common misconception that 2 exams are necessary. This is not the case," Dr. Gronseth said. "Some people may object, but we found that 1 exam was sufficient."
The authors point out that complex-spontaneous motor movements and false-positive triggering of the ventilator may occur in patients who are brain dead.
Oxygenation diffusion to determine apnea is safe, they report, but there is insufficient evidence to determine the comparative benefit of the various techniques used for apnea testing.
There is also insufficient evidence to determine whether newer ancillary tests accurately confirm the cessation of function of the entire brain.

To correctly diagnose brain death, it is essential clinicians adhere to a uniform framework.

Asked by Medscape Neurology to comment on the new guidelines, James Bernat, MD, from Dartmouth-Hitchcock Medical Center in Lebanon, New Hampshire, said he hopes these recommendations will help address the often wide variation among hospitals.
In 2008, guideline senior author David Greer, MD, from Massachusetts General Hospital, in Boston, reported substantial differences in approaches to brain death among leading neurological institutions in the United States.
That study, published in Neurology, prompted this guideline update because the authors felt more detail was needed to help physicians (2008;70;284-289).
"The new recommendations are encouraging uniformity and thoroughness among institutions," Dr. Bernat said.
"Moving forward, I'd like to see a national registry to track brain death, so we can get an idea of how we're doing," Dr. Gronseth said. "This registry should be voluntary. A lot of studies are done this way."
The American Academy of Neurology will be hosting an online conference about the new guidelines Monday, June 21. The authors will present at the session and take questions. The registration deadline for continuing medical education credit is June 16. Clinicians wanting to participate will need a computer with Microsoft Office Powerpoint and a telephone. For more information and to access the audio conference, visit the academy's Web site.
Dr. Gronseth reports receiving financial support from Boehringer Ingelheim. Dr. Greer also receives funding from Boehringer Ingelheim. In addition, he reports royalties from the publication of Acute Ischemic Stroke: An Evidence-Based Approach and has served as a consultant in a medico-legal case. Coauthor Dr. Panayiotis Varelas serves on a scientific advisory board for Gift of Life of Michigan. Dr. Varelas has received funding from the Medicines Company and Alsius and receives royalties from the publication of Seizures in the ICU.

Mind Over Mass Media

NEW forms of media have always caused moral panics: the printing press, newspapers, paperbacks and television were all once denounced as threats to their consumers’ brainpower and moral fiber.
So too with electronic technologies. PowerPoint, we’re told, is reducing discourse to bullet points. Search engines lower our intelligence, encouraging us to skim on the surface of knowledge rather than dive to its depths. Twitter is shrinking our attention spans.
But such panics often fail basic reality checks. When comic books were accused of turning juveniles into delinquents in the 1950s, crime was falling to record lows, just as the denunciations of video games in the 1990s coincided with the great American crime decline. The decades of television, transistor radios and rock videos were also decades in which I.Q. scores rose continuously.
For a reality check today, take the state of science, which demands high levels of brainwork and is measured by clear benchmarks of discovery. These days scientists are never far from their e-mail, rarely touch paper and cannot lecture without PowerPoint. If electronic media were hazardous to intelligence, the quality of science would be plummeting. Yet discoveries are multiplying like fruit flies, and progress is dizzying. Other activities in the life of the mind, like philosophy, history and cultural criticism, are likewise flourishing, as anyone who has lost a morning of work to the Web site Arts & Letters Daily can attest.
Critics of new media sometimes use science itself to press their case, citing research that shows how “experience can change the brain.” But cognitive neuroscientists roll their eyes at such talk. Yes, every time we learn a fact or skill the wiring of the brain changes; it’s not as if the information is stored in the pancreas. But the existence of neural plasticity does not mean the brain is a blob of clay pounded into shape by experience.
Experience does not revamp the basic information-processing capacities of the brain. Speed-reading programs have long claimed to do just that, but the verdict was rendered by Woody Allen after he read “War and Peace” in one sitting: “It was about Russia.” Genuine multitasking, too, has been exposed as a myth, not just by laboratory studies but by the familiar sight of an S.U.V. undulating between lanes as the driver cuts deals on his cellphone.
Moreover, as the psychologists Christopher Chabris and Daniel Simons show in their new book “The Invisible Gorilla: And Other Ways Our Intuitions Deceive Us,” the effects of experience are highly specific to the experiences themselves. If you train people to do one thing (recognize shapes, solve math puzzles, find hidden words), they get better at doing that thing, but almost nothing else. Music doesn’t make you better at math, conjugating Latin doesn’t make you more logical, brain-training games don’t make you smarter. Accomplished people don’t bulk up their brains with intellectual calisthenics; they immerse themselves in their fields. Novelists read lots of novels, scientists read lots of science.
The effects of consuming electronic media are also likely to be far more limited than the panic implies. Media critics write as if the brain takes on the qualities of whatever it consumes, the informational equivalent of “you are what you eat.” As with primitive peoples who believe that eating fierce animals will make them fierce, they assume that watching quick cuts in rock videos turns your mental life into quick cuts or that reading bullet points and Twitter postings turns your thoughts into bullet points and Twitter postings.
Yes, the constant arrival of information packets can be distracting or addictive, especially to people with attention deficit disorder. But distraction is not a new phenomenon. The solution is not to bemoan technology but to develop strategies of self-control, as we do with every other temptation in life. Turn off e-mail or Twitter when you work, put away your Blackberry at dinner time, ask your spouse to call you to bed at a designated hour.
And to encourage intellectual depth, don’t rail at PowerPoint or Google. It’s not as if habits of deep reflection, thorough research and rigorous reasoning ever came naturally to people. They must be acquired in special institutions, which we call universities, and maintained with constant upkeep, which we call analysis, criticism and debate. They are not granted by propping a heavy encyclopedia on your lap, nor are they taken away by efficient access to information on the Internet.
The new media have caught on for a reason. Knowledge is increasing exponentially; human brainpower and waking hours are not. Fortunately, the Internet and information technologies are helping us manage, search and retrieve our collective intellectual output at different scales, from Twitter and previews to e-books and online encyclopedias. Far from making us stupid, these technologies are the only things that will keep us smart.

Steven Pinker, a professor of psychology at Harvard, is the author of “The Stuff of Thought.”

Brain paintings

An artist and a neuroscientist are plumbing the depths of human perception to create works of art that explore quirks in how we view the world

Artists have found inspiration in love, pain, landscape, death, and history, but it's safe to say Mariano Molina is one of the first to find his muse in neuroscience.

Molina, an artist well known in his homeland of Argentina for paintings that bend perception, spent five months working to better understand how people perceive art with Rodrigo Quian Quiroga, an Argentine neuroscientist at the University of Leicester in the United Kingdom. "There are so many things artists have known for centuries that neuroscience is just beginning to know," Quian Quiroga says. "Artists have an intuition that scientists simply don't have."

Binocular Rivalry Hands By Mariano Molina

In 2008 Quian Quiroga collaborated with University of Leicester social anthropologist Sandra Dudley and David Barrie, former director of the Art Fund in the UK, to investigate the "wow factor" that some experience when looking at a piece of art in a museum. They wanted to understand how the eyes and brain react to the fluid strokes of a Georiga O'Keefe flower, or the thick, chucky globs of paint in Vincent van Gogh's "Starry Night." Could the lighting in the museum or the knowledge of the artist's fame affect an individual's reaction?

From November 2009 to April 2010, Molina was a resident artist in Quian Quiroga's lab. Molina says his visit began with a lot of reading about the neuroscience of visual perception. After a couple of months, Quian Quiroga introduced Molina to the eye tracker, a camera used in neuroscience that looks into the eye, detects slight movements in the retina, and correlates them to the location of the gaze on a picture.

"When you look at something," says Quian Quiroga, "your eyes move around looking at different pieces of the picture at a time, and then your brain reconstructs the whole image. With the eye tracker, Molina was able to see what parts of his painting people were paying the most attention to." If an observer's eyes concentrated on sections of the painting Molina felt were most important, his technique had worked; if not, he could highlight or dull certain areas, and try the eye tracker again to see if the changes made a difference.

Molina says the eye tracker fascinated him because "it was like people were painting with their eyes."

In "The Center of Gaze," Molina blurs the painting to a center point where figures of people can be seen cheering and smiling. When Molina tested the effectiveness of his technique with the eye tracker, people's eyes spent most of their time on the clear center, the response he had hoped to achieve. Without any prior knowledge of how the brain perceives images, Molina was aware of the response he was creating in people, says Quian Quiroga.

An example of the data generated by the eye tracker

The Center of Gaze By Mariano Molina

Quian Quiroga introduced Molina to theories in neuroscience that inspired other paintings. The aptly named "Binocular Rivalry Hands" applies a theory in neuroscience called binocular rivalry. When a different image is presented to each eye with blue-red 3D glasses, the brain creates a psychedelic picture that alternates from the image seen in the left eye to the image seen in the right. Binocular rivalry is one of many optical illusions that Molina plans to use in his artwork.

Molina's knowledge of the art world also helped Quian Quiroga to further his project with Dudley and Barrie. Molina suggested certain painters to present to test subjects over others because, he says, using famous artists wouldn't invoke an objective response to technique. He proposed lesser-known substitutes to painters like Picasso, Miro, and Monet that Quian Quiroga could use in his study.

Throughout his career, Quian Quiroga has witnessed the accuracy of an artist's intuition. He recently published an opinion article in Nature about his visit to the private library of Jorge Luis Borges, a famous Argentinean writer and author of "Funes the Memorious." Borges' library, says Quian Quiroga, revealed the author's fascination with memory and neuroscience. "In the story of Funes," Quian Quiroga wrote, "Borges described very precisely the problems of distorted memory capacities well before neuroscience caught up." So when Quian Quiroga turned his research to the visual perception of art, he thought having an artist on board would bring a different and highly valuable perspective.

The main point of Molina's five-month stay, however, was not for Quian Quiroga to publish another paper. Instead, they are looking for a museum or gallery interested in displaying Molina's art accompanied by explanations of the neuroscience theories the paintings illustrate.

They are applying for a grant that would allow Molina to stay as a resident artist for up to three years. Then, says Quian Quiroga, a paper might be possible. "With science, you have to be very specific and you have to aim to prove just one point," he says. "If you put the word 'art' in the title of the paper, it takes a lot more for people to take it seriously. When you mix art and science, it's not so easy to get published."

But Quian Quiroga is not deterred by the bias that exists in his field. He says he has a feeling that the alliance of art and science could open a door to a new way of looking at research. "Ten years from now," he says, "there will be a lot of more of this going on. It's just too exciting to avoid."

Berries for the brain

Can a cup of strawberries a day prevent dementia? Some researchers think so. The Chicago Health and Aging Project (CHAP) has been studying cognitive decline in 10,000 south Chicago residents for the last 15 years. Data from this ongoing study suggests that frequent consumption of strawberries may help prevent dementia, a loss of cognitive function. Alzheimer's disease is the most common form of dementia.

Tufts University researchers are investigating this same berry-brain connection. In animal studies, they found strawberries and other berries improved memory. Human studies are next. Nutritionists suggest it is the antioxidants in berries that help power our brain and nervous system. Beyond promising brain health, the antioxidants in strawberries may contribute to heart health and cancer prevention.

It's strawberry season in Iowa, so eat up! One cup of strawberries contains 50 calories and provides 2 grams of fiber and 100 percent of your daily need for vitamin C.

Medanta Medicity Launches Brain Suite system

Tumour fluorescence can help detect small bits and pieces of tumour that may otherwise be likely to be left behind

The neurosciences service at Medanta has started using advanced Brain Suite system in Asia-Pacific. This system permits the neurosurgeon to have an MRI study on the patient during surgery, and if tumour has remained which was hidden to the human eye, can be detected by special MRI sequences, and can be targeted using neuronavigation (which works on the same principle as the GPS system). Further, tumour fluorescence can help detect small bits and pieces of tumour that may otherwise be likely to be left behind. All this while, the microscope display digitally outlines the critical brain areas, critical nerve fibers, and also the outline of the tumour. This has permitted an aggressive removal of highly malignant brain tumours, which will enhance the survival.

Modern medicine is rapidly moving away from standardised approaches, basically the 'one size fits all' approach. The revolutionary concept of personalised medicine is here to stay. There are two important aspects, as far as brain tumours are concerned.

First, molecular medicine has shown that any two tumours looking the same on imaging do not look the same at surgery or even under the microscope when being examined by a pathologist. Further, two tumours looking similar on the microscope do not look alike, when examined for their molecular signatures. Some of these molecular signatures have the potential to indicate the likely response a tumour would have to radiation and chemotherapy.

Second, there is general agreement in medical literature that the attempt has to be to remove the brain tumour totally, or almost totally, within limits of preserving important brain functions like movements of limbs, speech, language and vision. This requires a quantum leap in surgical technology that enables the neurosurgeon to peel away the entire tumour, while not damaging critical brain areas. Such a technology is being unveiled at Medanta Medicity in Gurgaon.

Dr AN Jha, who is a pioneer in the MRI guided brain tumour surgery in the country, said, "The surgical methods have themselves undergone a silent revolution. At Medanta, a team approach helps us neurosurgeons and oncologists working together to determine the best approach for a particular patient. For example, some patients may require microsurgery for removal of the tumour. Others may require an endoscopic approach, or a stereotactic biopsy. Certain tumours can be treated with single session precisely delivered radiation, called as radio surgery. We are privileged to have a multi-disciplinary team with several neurosurgeons who are known experts in all these approaches."

The success stories are many. Take the case of a patient who developed a large tumour in his pituitary gland. This tumour was removed by a team comprising of an ENT surgeon and two neurosurgeons. Using a combination of approaches, the tumour was thought to have been removed. An intraoperative MRI revealed a part remaining on the right side, which was removed, resulting in total removal of the tumour.

Another patient, a 60-year old gentleman, developed forgetfulness and headache. MRI showed a large malignant brain tumour. He was subsequently operated, and BrainSuite helped in the total removal of the tumour. He looks forward to an extended survival, and is currently on appropriate chemotherapy and radiation therapy guided by a molecular analysis of his tumour specimen.

Dr Jha said, "We want to emphasise that true team-based use of appropriate technology is the only way to achieve world-class patient outcomes, and we are glad that Medanta provides us with the means of pursuing this dream."

The key advances in the Miyabi Brain Suite:

* Two-room concept enables us to do scan one day before and do detailed planning (in earlier machine patient would need to come inside OT, compromising sterility) as this is in separate but adjoining room.

* Latest MR scanner, enabling high-resolution images in as little as 5 minutes, helping saving time and reducing infection.

* Larger bore magnet allowing intraoperative MRI in different positions of the patient.

* Ability to perform a complete range of MRI sequences.

* Advanced patient head rest allowing larger variety of surgical procedures.

* Digital projection of tumour and nerve fibre tracks onto microscope view.

* Advanced Pentero microscope with tumour fluorescence capability.

Alzheimer’s brain protein may provide target for treating mental retardation

From the perspective of neuroscientists, Alzheimer’s disease and Down syndrome have at least one thing in common: patients with both diseases have an accumulation of β-amyloid protein in their brains. Rockefeller University scientists now provide evidence that drugs which help reduce the level of β-amyloid in the brains of Alzheimer’s patients may also work to treat mental retardation in Down syndrome.

The study was led by Paul Greengard, head of the Laboratory of Molecular and Cellular Neuroscience and 2000 Nobel laureate in Physiology or Medicine, and William Netzer, a research associate in Greengard’s laboratory. Their research on Down syndrome grew out of the group’s interest in Alzheimer’s disease, which is the most common form of dementia affecting elderly populations worldwide.

“The buildup of β-amyloid is a central feature in Alzheimer’s disease and also in elderly Down syndrome patients who go on to develop Alzheimer’s, but it was not known whether β-amyloid contributes to mental retardation in Down syndrome children,” says Greengard, Vincent Astor Professor and director of the Fisher Center for Alzheimer’s Disease Research at Rockefeller. “Our study suggests that β-amyloid may be a contributing factor in mental retardation, and that gives us hope that it might be possible to improve cognitive abilities in these children.”

The accumulation of β-amyloid in the brain is believed to initiate the pathological cascade leading to neuronal dysfunction, cell death and dementia. β-amyloid is derived from a protein called the amyloid precursor protein (APP) as a result of that protein’s metabolism by enzymes called secretases, and β-amyloid levels are elevated in Alzheimer’s disease patients as well as in both children and adults with Down syndrome. Down syndrome is a complex genetic disorder that’s caused by the triplication of more than 100 genes on human chromosome 21, including the gene that encodes APP; the extra APP, scientists believe, results in extra β-amyloid.

Researchers in the Greengard laboratory were aware that nearly all individuals with Down syndrome progress to Alzheimer’s dementia by the fifth or sixth decade of life. Though β-amyloid is believed to be responsible for the high prevalence of Alzheimer’s in Down syndrome adults, it was not known whether elevated β-amyloid levels influence mental retardation in children with Down syndrome.

The Rockefeller scientists postulated that elevated levels of β-amyloid might influence mental retardation in children with Down syndrome, and that by lowering β-amyloid levels with drugs, cognitive ability in these children might be improved. In other words, mental retardation, which has historically been seen as an irreversible developmental defect, might in fact be treatable with drugs that lower β-amyloid.

“Our study was designed to test our hypothesis that drugs that reduce levels of β-amyloid might improve learning and memory in children with Down syndrome,” says Netzer, lead author of the study, which was published in the June issue of PLoS ONE.

Using a mouse model of Down syndrome, the researchers tested a drug-like compound called DAPT, which is a secretase inhibitor known to suppress production of β-amyloid. Mice treated with DAPT not only had a rapid reduction in β-amyloid levels but also a significant improvement in their ability to learn to navigate a water maze and remember where important features were located. The behavior of normal siblings used as a control group was unaffected by DAPT.

Netzer cautions that current compounds used experimentally to lower β-amyloid generally have very toxic side effects. Several years ago, Greengard and his colleagues discovered that the anti-cancer drug Gleevec, used to treat a form of leukemia, lowered β-amyloid without the same side effects as other secretase inhibitors. Although Gleevec does not remain in the brain long enough to treat either Alzheimer’s disease or Down syndrome, it may provide a model for developing new anti-amyloid drugs, says Greengard.

Karen Duff, an Alzheimer’s researcher from Columbia University Medical Center, also took part in the study; behavioral tests were conducted by Craig Powell’s lab at University of Texas Southwestern Medical Center.