Posts tagged brain
Articles and news from the latest research reports.
Research on multisensory speech perception in recent years has helped revolutionize our understanding of how the brain organizes the information it receives from our many different senses, UC Riverside psychology professor Lawrence D. Rosenblum writes in the January 2013 issue of Scientific American.
“Neuroscientists and psychologists have largely abandoned early ideas of the brain as a Swiss Army knife, in which many distinct regions are dedicated to different senses,” he says. “Instead scientists now think that the brain has evolved to encourage as much cross talk as possible between the senses — that the brain’s sensory regions are physically intertwined.”
The article, “A Confederacy of Senses,” explains how research in the past 15 years has demonstrated that no sense works alone. An abstract of the article can be read here.
“The multisensory revolution is also suggesting new ways to improve devices for the blind and deaf, such as cochlear implants,” Rosenblum writes. This research also has improved speech-recognition software, he says.
Researchers have discovered that the brain “does not channel visual information from the eyes into one neural container and auditory information from the ears into another, discrete, container as though it were sorting coins,” Rosenblum writes. “Rather our brains derive meaning from the world in as many ways as possible by blending the diverse forms of sensory perception.”
Rosenblum is the author of “See What I’m Saying: The Extraordinary Powers of Our Five Senses” (Norton, 2010), and has spent two decades studying multisensory perception, lipreading and hearing. His research has been supported by the National Science Foundation and the National Institutes of Health. He is known internationally for his research on risks the inaudibility of hybrid cars pose for blind and other pedestrians.
Mild brain cooling after head injury prevents epileptic seizures in lab study
Mild cooling of the brain after a head injury prevents the later development of epileptic seizures, according to an animal study reported this month in the Annals of Neurology.
Epilepsy can result from genetics or brain damage. Traumatic head injury is the leading cause of acquired epilepsy in young adults. It is often difficult to manage with antiepileptic drugs. The mechanisms behind the onset of epileptic seizures after brain injury are not known . There is currently no treatment to cure it, prevent it, or even limit its severity.
The multi-institutional research team used a rodent model of acquired epilepsy in which animals develop chronic spontaneous recurrent seizures -the hallmark of epilepsy- after a contusive head injury similar to that causing epilepsy in humans. The rats were randomized to either mock-cooling or cooling of the contused brain by no more than 2 Celsius degrees. This degree of cooling, the authors explained, is known to be safe and to decrease mortality of patients with head injury. The rats were then monitored for four months after injury and epilepsy was evaluated by intracranial EEG. The contused brain was cooled continuously with special headsets engineered to passively dissipate heat. No Peltier cells or other power sources for refrigeration were needed.
The investigators report that cooling by just 2 degrees celsius for 5 weeks beginning 3 days after injury virtually abolished the later development of epileptic seizure activity. This effect persisted through the end of the study. The treatment induced no additional pathology or inflammation, and restored neuronal activity depressed by the injury.
“These findings demonstrate for the first time that prevention of epileptic seizures after traumatic brain brain injury is possible, and that epilepsy prophylaxis in patients could be achieved more easily than previously thought, said the lead author of the study, Raimondo D’Ambrosio, UW associate professor of neurological surgery. He added that a clinical trial is required to verify the findings in head injury patients.
Many causes for learning lags in tumor disorder
The causes of learning problems associated with an inherited brain tumor disorder are much more complex than scientists had anticipated, researchers at Washington University School of Medicine in St. Louis report.
The disorder, neurofibromatosis 1 (NF1), is among the most common inherited pediatric brain cancer syndromes. Children born with NF1 can develop low-grade brain tumors, but their most common problems are learning and attention difficulties.
“While one of our top priorities is halting tumor growth, it’s also important to ensure that these children don’t have the added challenges of living with learning and behavioral problems,” says senior author David H. Gutmann, MD, PhD, the Donald O. Schnuck Family Professor of Neurology. “Our results suggest that learning problems in these patients can be caused by more than one factor. Successful treatment depends on identifying the biological reasons underlying the problems seen in individual patients with NF1.”
The study appears online in Annals of Neurology.
According to Gutmann, who is director of the Washington University Neurofibromatosis Center, scientists are divided when considering the basis for NF1-associated learning abnormalities and attention deficits.
Mutations in the Nf1 gene can disrupt normal regulation of an important protein called RAS in the hippocampus, a brain region critical for learning. Initial work from other investigators had shown that increased RAS activity due to defective Nf1 gene function impairs memory and attention in some Nf1 mouse models.
However, earlier studies by Gutmann and collaborator David F. Wozniak, PhD, research professor in psychiatry, showed that a mutation in the Nf1 gene lowers levels of dopamine, a neurotransmitter involved in attention. In this Nf1 mouse model, Gutmann and his colleagues found that the branches of dopamine-producing nerve cells were unusually short, limiting their ability to make and distribute dopamine and leading to reduced attention in those mice.
The new research suggests that both sides may be right.
In the latest study, postdoctoral fellow Kelly Diggs-Andrews, PhD, found that the branches of dopamine-producing nerve cells that normally extend into the hippocampus are shorter in Nf1 mice. As a result, dopamine levels are lower in that part of the brain.
Charles F. Zorumski, MD, the Samuel B. Guze Professor and head of the Department of Psychiatry, showed that the low dopamine levels disrupts the ability of nerve cells in the hippocampus to modulate the way they communicate with each other. These communication adjustments are a primary way the brain creates memories.
Researchers then found that giving Nf1 mice L-DOPA, which increases dopamine levels, restored their nerve cell branch lengths to normal and corrected the hippocampal communication defect. L-DOPA also eliminated the memory and learning deficits in these mice.
“These results and the earlier findings suggest that there are a variety of ways that NF1 may cause cognitive dysfunction in people,” Gutmann says. “Some may have problems caused only by increased RAS function, others may be having problems attributable to reduced dopamine, and a third group may be having difficulties caused by both RAS and dopamine abnormalities.”
To customize patient therapy, Gutmann and his colleagues are now working to develop ways to quantify the contributions of dopamine and RAS to NF1-related learning disorders.
(Source: news.wustl.edu)
Re-tuning responses in the visual cortex
New research led by Shigeru Tanaka of the University of Electro-Communications and visiting scientist at the RIKEN Brain Science Institute has shown that the responses of cells in the visual cortex can be ‘re-tuned’ by experience.
Experiments on kittens in the 1960s showed that the primary visual cortex contains neurons that fire selectively to straight lines of specific orientations. These cells are organized into alternating columns that receive inputs from the left or right eye. The kitten experiments also showed that proper brain development is highly dependent on sensory information. Closing one eye altered the organization of the columns, so that those that should have received inputs from the closed eye were reduced in width, whereas those that received inputs from the open eye were much wider than normal.
The normal columnar organization can be restored if the closed eye is re-opened within a critical period of brain development. The effect of sensory experience on the orientation selectivity of neurons in the primary visual cortex is, however, unknown.
To investigate, Tanaka and his colleagues reared mice and fitted them with specially designed goggles through which they can only perceive vertically oriented visual stimuli, for a one-week period, between 3 and 15 weeks of age. Immediately after removing the goggles, they created a ‘window’ in the skull bone lying over the visual cortex to examine the cell response under the microscope.
Rearing the mice in this way had a significant effect on the properties of neurons in the primary visual cortex. The researchers found that the number of cells responding to vertical orientation increased, while the number responding to other orientation decreased. They also found that the extent of these changes depended on the age at which they fitted the animals with the goggles. Mice fitted with the goggles between 4 and 7 weeks of age had more cells that were sensitive to the experienced (vertical) orientation than those fitted later.
These findings show that there is a critical period of plasticity between 4 and 7 weeks, during which cells in the primary visual cortex are particularly sensitive to sensory experience and that plasticity persists in older animals, albeit to a lesser extent. They also suggest that plasticity in younger and older animals involves different mechanisms.
“When we put similar goggles on kittens, the age at which we started goggle rearing determined the reversibility of orientation selectivity,” says Tanaka. “We would now like to clarify the differences and commonalities of the mechanisms in cats and mice.”
Research offers new targets for stroke treatments
New research from the University of Georgia identifies the mechanisms responsible for regenerating blood vessels in the brain.
Looking for ways to improve outcomes for stroke patients, researchers led by the UGA College of Pharmacy assistant dean for clinical programs Susan Fagan used candesartan, a commonly prescribed medication for lowering blood pressure, to identify specific growth factors in the brain responsible for recovery after a stroke.
The results were published online Dec. 4 in the Journal of Pharmacology and Experimental Therapeutics
Although candesartan has been shown to protect the brain after a stroke, its use is generally avoided because lowering a person’s blood pressure quickly after a stroke can cause problems-like decreasing much-needed oxygen to the brain-during the critical period of time following a stroke.
"The really unique thing we found is that candesartan can increase the secretion of brain derived neurotrophic factor, and the effect is separate from the blood pressure lowering effect," said study coauthor Ahmed Alhusban, who is a doctoral candidate in the College of Pharmacy. "This will support a new area for treatments of stroke and other brain injury."
Alhusban and Fagan worked with Anna Kozak, a research scientist in the college, and Adviye Ergul, a professor and director of the physiology graduate program at Georgia Health Sciences University. They are the first to show that the positive effects of candesartan on brain blood vessel growth are caused by brain derived neurotrophic factor, or BDNF.
The research shows that when candesartan blocks the angiotensin II type 1 receptor, which lowers blood pressure, it stimulates the AT2 receptor and increases the secretion of BDNF, which encourages brain repair through the growth of new blood vessels.
"BDNF is a key player in learning and memory," said Fagan, the Albert W. Jowdy Professor. "A reduction of BDNF in the brain has been associated with Alzheimer’s disease and depression, so increasing this growth factor with a common medication is exciting."
AT2 is a brain receptor responsible for angiogenesis, or the growth of new blood vessels from pre-existing vessels. Angiogenesis is a normal and vital process in human growth and development-as well as in healing.
(Image: iStock)
Will we ever… have cyborg brains?
For the first time in over 15 years, Cathy Hutchinson brought a coffee to her lips and smiled. Cathy had suffered from the paralysing effects of a stroke, but when neurosurgeons implanted tiny recording devices in her brain, she could use her thought patterns to guide a robot arm that delivered her hot drink. This week, it was reported that Jan Scheuermann, who is paralysed from the neck down, could grasp and move a variety of objects by controlling a robotic arm with her mind.
In both cases the implants convert brain signals into digital commands that a robotic device can follow. It’s a remarkable achievement, one that could transform the lives of people debilitated through illness.
Yet it’s still a far cry from the visions of man fused with machine, or cyborgs, that grace computer games or sci-fi. The dream is to create the type of brain augmentations we see in fiction that provide cyborgs with advantages or superhuman powers. But the ones being made in the lab only aim to restore lost functionality – whether it’s brain implants that restore limb control, or cochlear implants for hearing.
Creating implants that improve cognitive capabilities, such as an enhanced vision “gadget” that can be taken from a shelf and plugged into our brain, or implants that can restore or enhance brain function is understandably a much tougher task. But some research groups are being to make some inroads.
For instance, neuroscientists Matti Mintz from Tel Aviv University and Paul Verschure from Universitat Pompeu Fabra in Barcelona, Spain, are trying to develop an implantable chip that can restore lost movement through the ability to learn new motor functions, rather than regaining limb control. Verschure’s team has developed a mathematical model that mimics the flow of signals in the cerebellum, the region of the brain that plays an important role in movement control. The researchers programmed this model onto a circuit and connected it with electrodes to a rat’s brain. If they tried to teach the rat a conditioned motor reflex – to blink its eye when it sensed an air puff – while its cerebellum was “switched off” by being anaesthetised, it couldn’t respond. But when the team switched the chip on, this recorded the signal from the air puff, processed it, and sent electrical impulses to the rat’s motor neurons. The rat blinked, and the effect lasted even after it woke up.
How the mind can map negative spaces around the body
The brain’s perception of space can determine whether a part of a body which occupies that space is either healthy or “neglected”.
Lorimer Moseley, Chair in Physiotherapy and Professor of Clinical Neurosciences at the University of South Australia, describes recent outcomes of research into spatial perception of people with complex regional pain syndrome (CRPS) as “profound”.
CRPS is a disorder that can develop after a minor injury occurs to a limb and results in abnormal or severe pain developing out of proportion to the nature of the injury. Other problems also result, for example blood flow problems in which the painful arm or leg goes cold and blue, grows too much hair and stays swollen.
In a series of experiments using thermal imaging cameras, changes in the temperature of the hands of people with CRPS were recorded as they moved them across their body midline.
When only the affected hand was crossed over the midline, it became warmer and when only the healthy hand was crossed over the midline, it became cooler.
The temperature change of either hand was positively related to its distance from the body midline and crossing the affected hand over the body midline had small but significant effects on both spontaneous pain (which was reduced) and the sense of ownership over the hand (which was increased).
Professor Moseley said the results of this research indicated that CRPS involves more complex neurological dysfunction than has previously been considered.
“We conclude that impaired spatial perception modulated temperature of the limbs, tactile processing, spontaneous pain and the sense of ownership over the hands.
“This means that the problem that is occurring with the limb relates to the brain process that maps something into a space. It’s almost as though the brain has rejected the space which the limb inhabits.
"In strokes it’s called spatial neglect. This problem with space affects the way blood is sent to the body. If you remove the hand or limb away from that side of space it warms up.
“When you put a healthy hand into the negative space it cools down; the map of space is influencing the rules by which blood flows. Our current finding is clear evidence of the autonomic nervous system being influenced by the brain’s map of space.
“The space itself has adopted the signature of the disorder. This is a profound discovery, it’s a clear physiological phenomena.
“This midline effect changes how much the patient feels the arm belongs to them and how much it hurts.”
(Source: unisa.edu.au)
Study reveals how the brain categorizes thousands of objects and actions
Humans perceive numerous categories of objects and actions, but where are these categories represented spatially in the brain?
Researchers reporting in the December 20 issue of the Cell Press journal Neuron present their study that undertook the remarkable task of determining how the brain maps over a thousand object and action categories when subjects watched natural movie clips. The results demonstrate that the brain efficiently represents the diversity of categories in a compact space. Instead of having a distinct brain area devoted to each category, as previous work had identified, for some but not all types of stimuli, the researchers uncovered that brain activity is organized by the relationship between categories.
"Humans can recognize thousands of categories. Given the limited size of the human brain, it seems unreasonable to expect that every category is represented in a distinct brain area," says first author Alex Huth, a graduate student working in Dr. Jack Gallant’s laboratory at the University of California, Berkeley. The authors proposed that perhaps a more efficient way for the brain to represent object and action categories would be to organize them into a continuous space that reflects the similarity between categories.
To test this hypothesis, they used blood oxygen level-dependent functional magnetic resonance imaging (BOLD fMRI) to measure human brain activity evoked by natural movies in five people. They then mapped out how 1,705 distinct object and action categories are represented across the surface of the cortex of the brain. Their results show that categories are organized as smooth gradients that cover much of the surface of the visual as well as nonvisual cortex, such that similar categories are located next to each other, and notably, this organization was shared across the individuals imaged.
"Discovering the feature space that the brain uses to represent information helps us to recover functional maps across the cortical surface. The brain probably uses similar mechanisms to map other kinds of information across the cortical surface, so our approach should be widely applicable to other areas of cognitive neuroscience," says Dr. Gallant.
The empathy machine
…Let’s dwell for a moment on ‘Silver Blaze’ (1892), Arthur Conan Doyle’s story of the gallant racehorse who disappeared, and his trainer who was found dead, just days before a big race. The hapless police are stumped, and Sherlock Holmes is called in to save the day. And save the day he does — by putting himself in the position of both the dead trainer and the missing horse. Holmes speculates that the horse is ‘a very gregarious creature’. Surmising that, in the absence of its trainer, it would have been drawn to the nearest town, he finds horse tracks, and tells Watson which mental faculty led him there. ‘See the value of imagination… We imagined what might have happened, acted upon that supposition, and find ourselves justified.’
Holmes takes an imaginative leap, not only into another human mind, but into the mind of an animal. This perspective-taking, being able to see the world from the point of view of another, is one of the central elements of empathy, and Holmes raises it to the status of an art.
Usually, when we think of empathy, it evokes feelings of warmth and comfort, of being intrinsically an emotional phenomenon. But perhaps our very idea of empathy is flawed. The worth of empathy might lie as much in the ‘value of imagination’ that Holmes employs as it does in the mere feeling of vicarious emotion. Perhaps that cold rationalist Sherlock Holmes can help us reconsider our preconceptions about what empathy is and what it does.
Though the scientific literature on empathy is complex, a recent review in Nature Neuroscience by a team of researchers from Harvard and Columbia including Jamil Zaki and Kevin Ochsner has distilled the phenomenon into three central stages. The first stage is ‘experience sharing’, or feeling someone else’s emotions as if they were your own — scared when they are scared, happy when they are happy, and so on. The second stage is ‘mentalising’, or consciously considering those states and their sources, and trying to work through understanding them. The final stage is ‘prosocial concern’, or being motivated to act — wanting, for example, to reach out to someone in pain. However, you don’t need all three to experience empathy. Instead, you can view these as three points on an empathetic continuum: first, you feel; then, you feel and you understand; and finally, you feel, understand, and are compelled to act on your understanding. It seems that the defining thing here is the feeling that accompanies all those stages.
MRIs Reveal Signs of Brain Injuries Not Seen in CT Scans
Hospital MRIs may be better at predicting long-term outcomes for people with mild traumatic brain injuries than CT scans, the standard technique for evaluating such injuries in the emergency room, according to a clinical trial led by researchers at UCSF and the San Francisco General Hospital and Trauma Center (SFGH).
Published this month in the journal Annals of Neurology, the study led by UCSF neuroradiologist Esther Yuh, MD, PhD, followed 135 people treated for mild traumatic brain injuries over the past two years at one of three urban hospitals with level-one trauma centers: SFGH, the University of Pittsburgh Medical Center and University Medical Center Brackenridge in Austin, Texas. The study was called the NIH-funded TRACK-TBI (Transforming Research and Clinical Knowledge in Traumatic Brain Injury).
All 135 patients with mild traumatic brain injuries received CT scans when they were first admitted, and all were given MRIs about a week later. Most of them (99) had no detectable signs of injury on a CT scan, but more than a quarter (27/99) who had a “normal” CT scans also had detectable spots on their MRI scans called “focal lesions,” which are signs of microscopic bleeding in the brain.
Spotting these focal lesions helped the doctors predict whether the patients were likely to suffer persistent neurological problems. About 15 percent of people who have mild traumatic brain injuries do suffer long-term neurological consequences, but doctors currently have no definitive way of predicting whether any one patient will or not.
“This work raises questions of how we’re currently managing patients via CT scan,” said the study’s senior author Geoff Manley, MD, PhD, the chief of neurosurgery at SFGH and vice-chair of the Department of Neurological Surgery at UCSF. “Having a normal CT scan doesn’t, in fact, say you’re normal,” he added.
Better Precision Tools Needed for Head Injuries
At least 1.7 million Americans seek medical attention every year for acute head injuries, and three-quarters of them have mild traumatic brain injuries – which generally do not involve skull fractures, comas or severe bleeding in the brain but have a variety of more mild symptoms, such as temporary loss of consciousness, vomiting or amnesia.
The U.S. Centers for Disease Control and Prevention estimates that far more mild traumatic brain injuries may occur each year in the United States but the true number is unknown because only injuries severe enough to bring someone to an emergency room are counted.
Most of those who do show up at emergency rooms are treated and released without being admitted to the hospital. In general, most people with mild traumatic brain injuries recover fully, but about one in six go on to develop persistent, sometimes permanent, disability.
The problem, Manley said, is that there is no way to tell which patients are going to have the poor long-term outcomes. Some socioeconomic indicators can help predict prolonged disability, but until now there were no proven imaging features, or blood tests for predicting how well or how fast a patient will recover. Nor is there a consensus on how to treat mild traumatic brain injuries.
“The treatment’s all over the place – if you’re getting treatment at all,” Manley said.
The new work is an important step toward defining a more quantitative way of assessing patients with mild traumatic brain injuries and developing more precision medical tools to detect, monitor and treat them, he added.
If doctors knew which patients were at risk of greater disabilities, they could be followed more closely. Being able to identify patients at risk of long-term consequences would also speed the development of new therapeutics because it would allow doctors to identify patients who would benefit the most from treatment and improve their ability to test potential new drugs in clinical trials.