Posts tagged psychology
Articles and news from the latest research reports.
Combat Stress in Afghanistan Could Alter Soldiers’ Long-term Neural Makeup
Some soldiers who serve in Afghanistan or other war-torn countries return home with visible injuries: concussions, broken bones or amputated limbs. Many others, though, suffer from injuries we can’t visibly see. The daily strain of being exposed to armed combat, enemy fire and unpredictable explosions can lead to a range of behavioral symptoms, including fatigue, slower reaction times and a difficulty in connecting to one’s immediate surroundings.
A new study of soldiers returning home from Afghanistan, published today online in the Proceedings of the National Academy of Sciences, hints at the underlying cause for these behavioral changes. Researchers from the Netherlands and elsewhere used neurological exams and MRI scanning techniques to examine 33 soldiers before and after a four-month deployment in NATO’s International Security Assistance Force, and compared them to a control group of 26 soldiers who were never deployed.
The results were sobering—and indicate that a relatively short period of combat stress can alter an individual’s neurological circuitry for a long time.
You already know it’s hard to balance your checkbook while simultaneously reflecting on your past. Now, investigators at the Stanford University School of Medicine — having done the equivalent of wire-tapping a hard-to-reach region of the brain — can tell us how this impasse arises.
The researchers showed that groups of nerve cells in a structure called the posterior medial cortex, or PMC, are strongly activated during a recall task such as trying to remember whether you had coffee yesterday, but just as strongly suppressed when you’re engaged in solving a math problem.
The PMC, situated roughly where the brain’s two hemispheres meet, is of great interest to neuroscientists because of its central role in introspective activities.
“This brain region is famously well-connected with many other regions that are important for higher cognitive functions,” said Josef Parvizi, MD, PhD, associate professor of neurology and neurological sciences and director of Stanford’s Human Intracranial Cognitive Electrophysiology Program. “But it’s very hard to reach. It’s so deep in the brain that the most commonly used electrophysiological methods can’t access it.”
Ιn a study published online Sept. 3 in Proceedings of the National Academy of Sciences, Parvizi and his Stanford colleagues found a way to directly and sensitively record the output from this ordinarily anatomically inaccessible site in human subjects. By doing so, the researchers learned that particular clusters of nerve cells in the PMC that are most active when you are recalling details of your own past are strongly suppressed when you are performing mathematical calculations.
Even in normal range, high blood sugar linked to brain shrinkage
September 3, 2012
People whose blood sugar is on the high end of the normal range may be at greater risk of brain shrinkage that occurs with aging and diseases such as dementia, according to new research published in the September 4, 2012, print issue of Neurology, the medical journal of the American Academy of Neurology.
"Numerous studies have shown a link between type 2 diabetes and brain shrinkage and dementia, but we haven’t known much about whether people with blood sugar on the high end of normal experience these same effects," said study author Nicolas Cherbuin, PhD, with Australian National University in Canberra.
The study involved 249 people age 60 to 64 who had blood sugar in the normal range as defined by the World Health Organization. The participants had brain scans at the start of the study and again an average of four years later.
Those with higher fasting blood sugar levels within the normal range and below 6.1 mmol/l (or 110 mg/dL) were more likely to have a loss of brain volume in the areas of the hippocampus and the amygdala, areas that are involved in memory and cognitive skills, than those with lower blood sugar levels. A fasting blood sugar level of 10.0 mmol/l (180 mg/dL) or higher was defined as diabetes and a level of 6.1 mmol/l (110 mg/dL) was considered impaired, or prediabetes.
After controlling for age, high blood pressure, smoking, alcohol use and other factors, the researchers found that blood sugar on the high end of normal accounted for six to 10 percent of the brain shrinkage.
"These findings suggest that even for people who do not have diabetes, blood sugar levels could have an impact on brain health," Cherbuin said. "More research is needed, but these findings may lead us to re-evaluate the concept of normal blood sugar levels and the definition of diabetes."
Source: medicalxpress.com
Obesity and Metabolic Syndrome Associated With Impaired Brain Function in Adolescents
ScienceDaily (Sep. 3, 2012) — A new study by researchers at NYU School of Medicine reveals for the first time that metabolic syndrome (MetS) is associated with cognitive and brain impairments in adolescents and calls for pediatricians to take this into account when considering the early treatment of childhood obesity.
The study, funded by the National Institutes of Health under award number DK083537, and in part by award number 1ULIRR029892, from the National Center for Research Resources, appears online September 3 in Pediatrics.
As childhood obesity has increased in the U.S., so has the prevalence of metabolic syndrome — a constellation of three or more of five defined health problems, including abdominal obesity, low HDL (good cholesterol), high triglycerides, high blood pressure and pre-diabetic insulin resistance. Lead investigator Antonio Convit, MD, professor of psychiatry and medicine at NYU School of Medicine and a member of the Nathan Kline Research Institute, and colleagues have shown previously that metabolic syndrome has been linked to neurocognitive impairments in adults, but this association was generally thought to be a long-term effect of poor metabolism. Now, the research team has revealed even worse brain impairments in adolescents with metabolic syndrome, a group absent of clinically-manifest vascular disease and likely shorter duration of poor metabolism.
"The prevalence of MetS parallels the rise in childhood obesity," Dr. Convit said. "There are huge numbers of people out there who have problems with their weight. If those problems persist long enough, they will lead to the development of MetS and diabetes. As yet, there has been very little information available about what happens to the brain in the setting of obesity and MetS and before diabetes onset in children."
Vaughan Bell: how simulating dementia can help map our minds
Electrodes inside the skull can temporarily mimic brain disease – and so allow us to find out more about the way we work
Second thoughts: electrodes are inserted into a patient’s brain. Photograph: University of Utah Department of Neurosurgery
The first person to electrically stimulate the brain of a living human during surgery was the 19th-century British neurosurgeon Sir Victor Horsley. The operation was to treat a deformation called an encephalocele, where the bones of the skull do not close properly in the womb, causing the brain to protrude from the head. Horsely applied a weak electrical current to the surgically exposed brain tissue, making the patient’s eyes swivel to the side, which told the surgeon that the out-of-place area was the top of the midbrain – normally a deeply embedded neural structure essential for directing vision.
The technique was later picked up to treat epilepsy as it became clear that removing the part of the brain that triggered seizures could be an effective treatment, even if identifying it could be tricky. Small, clearly identified points of damage or localised tumours could often trigger seizures but sometimes the errant waves of epileptic activity would start far away from the original point of visible injury. Horsley used the electrical stimulation technique while patients were awake to find the sensitive area and remove it. Not bad for 1886.
Although initially invented for medical reasons, this surgical technique began to throw up some curious scientific data. In the 1930s the Canadian neurosurgeon Wilder Penfield asked patients undergoing epilepsy surgery if he could perform brief experiments while they were being operated on. He found that stimulating parts of the brain could cause a range of reactions from tingling to weeping to a “desire to move” – providing crucial evidence that activity in specific brain areas could trigger surprisingly complex behaviours.
People with epilepsy have remained an important part of our quest to understand ourselves as they have regularly volunteered to take part in neuroscience experiments while undergoing open-brain operations. Even though these experiments are a relatively brief pause in the procedure, they still require people to offer some of their time while their skull has been opened and their brain exposed, and we know much more about the brain thanks to their generosity.
As surgical techniques have moved on, so has the science. The starting points of some seizures are not easily located in the relatively short period available during surgery. To compensate for this, neurosurgeons have taken to implanting electrodes in the brains of people with epilepsy before the skull is replaced and the skin sewn up, which allows the medical team to record brain activity as the patients go about their daily life. One form of this “in brain” recording, known as electrocorticography, involves surgically inserting a grid of electrodes over the surface of the brain.
This has allowed neuroscientists to measure the brain at work in the real world via cables that go from the brain into a small digital recorder. A study published last year in the Journal of Neurosurgery mapped the main language areas of the cortex, the brain’s outer layer, using an implanted electrode grid and a simple word task that took an average of just 47 seconds. More than 100 other studies have used this technique with similarly impressive results.
One innovation is particularly mind-boggling. After years of using implanted electrode grids to read from the brain, neuroscientists have begun to use the electrodes to write to it – in other words, to alter the function of the brain through the same electrodes that record its activity. “By having a grid of electrodes in place,” says Matthew Lambon Ralph, professor of cognitive neuroscience at Manchester University, “it is possible to probe many different regions rather than just one.”
The precision is such that the Lambon Ralph team and a team at Kyoto University Medical School, led by Riki Matsumoto, have used an implanted grid to temporarily simulate characteristics of a brain disease called semantic dementia. Like Alzheimer’s, semantic dementia is a degenerative disorder, but one in which brain cells that specifically support our understanding of meaning rapidly decline. Studies of patients with semantic dementia have taught us a great deal about how memory is organised in the brain but the disorder is swift and unpredictable, and a method that can mimic the effects while recording directly from the cortex is a powerful tool.
The technique is safe and reversible, as we know from a simple version that is often done pre-neurosurgery to ensure that no tissue that supports key mental functions is removed during the operation. Using it as a way of briefly simulating more complex cognitive difficulties is an exciting development. “Stimulation is injected in one part of a grid and the evoked response across other grids is measured. It’s a direct measure of functional connectivity,” explains Lambon Ralph, highlighting how these sorts of studies can allow the brain’s function, in terms of thinking skills, to be closely linked to its physical connections.
The research was presented at the British Neuropsychological Society spring conference by UK-based team member Taiji Ueno. The main findings are still being prepared for peer review but the use of implant grids in neuroscience research is sure to become more common as the surgical procedure becomes more widely used.
These procedures are only done for medical reasons, and researchers get no say about how and on whom they are performed. But, as ever, patients have been generous with their time. From 1886 until now, these exciting discoveries have been made possible by people on the operating table.
(Source: Guardian)
A pain map of the brain being developed by scientists could finally put an end to the debate about whether women suffer more pain than men.
Using brain scanning technology, neuroscientists have been able to see how the brain responds to pain and map the signals to different parts of the body. They have also been able to measure how much pain someone is in from the signals in the brain.
Scientists have restored the sense of smell in mice through gene therapy for the first time — a hopeful sign for people who can’t smell anything from birth or lose it due to disease.
The achievement in curing congenital anosmia — the medical term for lifelong inability to detect odors — may also aid research on other conditions that also stem from problems with the cilia. Those tiny hair-shaped structures on the surfaces of cells throughout the body are involved in many diseases, from the kidneys to the eyes.
The new findings, published online in Nature Medicine, come from a team at the University of Michigan Medical School and their colleagues at several other institutions.
Doctors have long recognized a link between alcoholism and anxiety disorders such as post-traumatic stress disorder (PTSD). Those who drink heavily are at increased risk for traumatic events like car accidents and domestic violence, but that only partially explains the connection. New research using mice reveals heavy alcohol use actually rewires brain circuitry, making it harder for alcoholics to recover psychologically following a traumatic experience.
“There’s a whole spectrum to how people react to a traumatic event,” said study author Thomas Kash, PhD, assistant professor of pharmacology at the University of North Carolina School of Medicine. “It’s the recovery that we’re looking at — the ability to say ‘this is not dangerous anymore.’ Basically, our research shows that chronic exposure to alcohol can cause a deficit with regard to how our cognitive brain centers control our emotional brain centers.”
The study, which was published online on Sept. 2, 2012 by the journal Nature Neuroscience, was conducted by scientists at the National Institute on Alcohol Abuse and Alcoholism (NIAAA) and UNC’s Bowles Center for Alcohol Studies.
Flying High: Researchers Decipher Manic Gene
ScienceDaily (Sep. 1, 2012) — Flying high, or down in the dumps — individuals suffering from bipolar disorder alternate between depressive and manic episodes. Researchers from the University of Bonn and the Central Institute of Mental Health in Mannheim have now discovered, based on patient data and animal models, how the NCAN gene results in the manic symptoms of bipolar disorder.
(Credit: © Bastos / Fotolia)
The results have been published in the current issue of The American Journal of Psychiatry.
Individuals with bipolar disorder are on an emotional roller coaster. During depressive phases, they suffer from depression, diminished drive and often, also from suicidal thoughts. The manic episodes, however, are characterized by restlessness, euphoria, and delusions of grandeur. The genesis of this disease probably has both hereditary components as well as psychosocial environmental factors.
The NCAN gene plays a major part in how manias manifest
"It has been known that the NCAN gene plays an essential part in bipolar disorder," reports Prof. Dr. Markus M. Nöthen, Director of the Institute of Human Genetics at the University of Bonn. "But until now, the functional connection has not been clear." In a large-scale study, researchers led by the University of Bonn and the Central Institute of Mental Health in Mannheim have now shown how the NCAN gene contributes to the genesis of mania. To do so, they evaluated the genetic data and the related descriptions of symptoms from 1218 patients with differing ratios between the manic and depressive components of bipolar disorder.
Comprehensive data from patients and animal models
Using the patients’ detailed clinical data, the researchers tested statistically which of the symptoms are especially closely related to the NCAN gene. “Here it became obvious that the NCAN gene is very closely and quite specifically correlated with the manic symptoms,” says Prof. Dr. Marcella Rietschel from the Central Institute of Mental Health in Mannheim. According to the data the gene is, however, not responsible for the depressive episodes in bipolar disorder.
Manic mice drank from sugar solution with abandon
A team working with Prof. Dr. Andreas Zimmer, Director of the Institute of Molecular Psychiatry at the University of Bonn, examined the molecular causes effected by the NCAN gene. The researchers studied mice in which the gene had been “knocked out.” “It was shown that these animals had no depressive component in their behaviors, only manic ones,” says Prof. Zimmer. These knockout mice were, e.g., considerably more active than the control group and showed a higher level of risk-taking behavior. In addition, they tended to exhibit increased reward-seeking behavior, which manifested itself by their unrestrained drinking from a sugar solution offered by the researchers.
Lithium therapy also effective against hyperactivity in mice
Finally, the researchers gave the manic knockout mice lithium — a standard therapy for humans. “The lithium dosage completely stopped the animals’ hyperactive behavior,” reports Prof. Zimmer. So the results also matched for lithium; the responses of humans and mice regarding the NCAN gene were practically identical. It has been known from prior studies that knocking out the NCAN gene results in a developmental disorder in the brain due to the fact that the production of the neurocan protein is stopped. “As a consequence of this molecular defect, the individuals affected apparently develop manic symptoms later,” says Prof. Zimmer.
Opportunity for new therapies
Now the scientists want to perform further studies of the molecular connections of this disorder — also with a view towards new therapies. “We were quite surprised to see how closely the findings for mice and the patients correlated,” says Prof. Nöthen. “This level of significance is very rare.” With a view towards mania, the agreement between the findings opens up the opportunity to do further molecular studies on the mouse model, whose results will very likely also be applicable to humans. “This is a great prerequisite for advancing the development of new drugs for mania therapy,” believes Prof. Rietschel.
Source: Science Daily
When she was 9 years old, Camilla would entertain her friends by jumping off her bed and landing directly on her knees. She said she liked to hear the crunching sound they made—just like popcorn.
Another time, Camilla spent an entire school recess period walking around on a broken leg, without so much as a whimper, says neuroscientist India Morrison of the University of Gothenburg in Sweden. The child’s teachers didn’t believe Camilla when she said something was wrong, because she wasn’t sobbing or wailing in pain. Her father thought perhaps her leg needed massaging, but quickly realized the situation was much worse.