Brain's 'Radio Stations' Have Much to Tell Scientists

Like listeners adjusting a high-tech radio, scientists at Washington University School of Medicine in St. Louis have tuned in to precise frequencies of brain activity to unleash new insights into how the brain works.

"Analysis of brain function normally focuses on where brain activity happens and when," says Eric C. Leuthardt, MD. "What we've found is that the wavelength of the activity provides a third major branch of understanding brain physiology."

Researchers used electrocorticography, a technique for monitoring the brain with a grid of electrodes temporarily implanted directly on the brain's surface. Clinically, Leuthardt and other neurosurgeons use this approach to identify the source of persistent, medication-resistant seizures in patients and to map those regions for surgical removal. With the patient's permission, scientists can also use the electrode grid to experimentally monitor a much larger spectrum of brain activity than they can via conventional brainwave monitoring.

Scientists normally measure brainwaves with a process called electroencephalography (EEG), which places electrodes on the scalp. Brainwaves are produced by many neurons firing at the same time; how often that firing occurs determines the activity's frequency or wavelength, which is measured in hertz, or cycles per second. Neurologists have used EEG to monitor consciousness in patients with traumatic injuries, and in studies of epilepsy and sleep.

In contrast to EEG, electrocorticography records brainwave data directly from the brain's surface.

"We get better signals and can much more precisely determine where those signals come from, down to about one centimeter," Leuthardt, assistant professor of neurosurgery, of neurobiology and of biomedical engineering, says. "Also, EEG can only monitor frequencies up to 40 hertz, but with electrocorticography we can monitor activity up to 500 hertz. That really gives us a unique opportunity to study the complete physiology of brain activity."

Leuthardt and his colleagues have used the grids to watch consciousness fade under surgical anesthesia and return when the anesthesia wears off. They found each frequency gave different information on how different circuits changed with the loss of consciousness, according to Leuthardt.

"Certain networks of brain activity at very slow frequencies did not change at all regardless of how deep under anesthesia the patient was," Leuthardt says. "Certain relationships between high and low frequencies of brain activity also did not change, and we speculate that may be related to some of the memory circuits."

Their results also showed a series of changes that occurred in a specific order during loss of consciousness and then repeated in reverse order as consciousness returned. Activity in a frequency region known as the gamma band, which is thought to be a manifestation of neurons sending messages to other nearby neurons, dropped and returned as patients lost and regained consciousness.

The results appeared in December in the Proceedings of the National Academy of Sciences.

In another paper that will publish Feb. 9 in The Journal of Neuroscience, Leuthardt and his colleagues have shown that the wavelength of brain signals in a particular region can be used to determine what function that region is performing at that time. They analyzed brain activity by focusing on data from a single electrode positioned over a number of different regions involved in speech. Researchers could use higher-frequency bands of activity in this brain area to tell whether patients:

• had heard a word or seen a word
• were preparing to say a word they had heard or a word they had seen
• were saying a word they had heard or a word they had seen.

"We've historically lumped the frequencies of brain activity that we used in this study into one phenomenon, but our findings show that there is true diversity and non-uniformity to these frequencies," he says. "We can obtain a much more powerful ability to decode brain activity and cognitive intention by using electrocorticography to analyze these frequencies."
Source: Daily Science

Traffic Jam In Brain Causes Schizophrenia Symptoms

Schizophrenia waits silently until a seemingly normal child becomes a teenager or young adult. Then it swoops down and derails a young life.

Scientists have not understood what causes the severe mental disorder, which affects up to 1 percent of the population and results in hallucinations, memory loss and social withdrawal.

But new research from the Northwestern University Feinberg School of Medicine has revealed how schizophrenia works in the brain and provided a fresh opportunity for treatment. In a new, genetically engineered mouse model, scientists have discovered the disease symptoms are triggered by a low level of a brain protein necessary for neurons to talk to one another.

A Traffic Jam in Brain

In human and mouse brains, kalirin is the brain protein needed to build the dense network of highways, called dendritic spines, which allow information to flow from one neuron to another. Northwestern scientists have found that without adequate kalirin, the frontal cortex of the brain of a person with schizophrenia only has a few narrow roads. The information from neurons gets jammed up like rush hour traffic on an interstate highway squeezed to a single lane.

"Without enough pathways, the information takes much longer to travel between neurons and much of it will never arrive," said Peter Penzes, assistant professor of physiology at the Feinberg School. He is senior author of a paper reporting the findings published in a recent issue of the Proceedings of the National Academy of Science. Michael Cahill, a Feinberg doctoral student in neuroscience, is the lead author.

First Mouse Model to Develop Disease as a Teenager

Penzes discovered the kalirin effect after he created the mouse model, which was the first to have a low level of kalirin and the first to develop symptoms of schizophrenia as an adolescent (two months old in mouse time). This mimics the delayed onset of the disease in humans. In normal development, the brain ramps up the production of kalirin as it begins to mature in adolescence.

New Direction for Treatment

"This discovery opens a new direction for treating the devastating cognitive symptoms of schizophrenia," Penzes said. "There is currently no treatment for that. It suggests that if you can stimulate and amplify the activity of the protein kalirin that remains in the brain, perhaps we can help the symptoms."

Currently the only drug treatment for schizophrenia is an antipsychotic. "The drugs address the hallucinations and calm down the patient, but they don't improve their working memory (the ability of the brain to temporarily store and manage information required for complex mental tasks such as learning and reasoning) or their ability to think or their social behavior," Penzes said. "So you end up with patients who still can't integrate into society. Many attempt suicide."

Brain Difference In Psychopaths Identified

Professor Declan Murphy and colleagues Dr Michael Craig and Dr Marco Catani from the Institute of Psychiatry at King's College London have found differences in the brain which may provide a biological explanation for psychopathy.

The research investigated the brain biology of psychopaths with convictions that included attempted murder, manslaughter, multiple rape with strangulation and false imprisonment. Using a powerful imaging technique (DT-MRI) the researchers have highlighted biological differences in the brain which may underpin these types of behaviour and provide a more comprehensive understanding of criminal psychopathy.

Dr Michael Craig said: 'If replicated by larger studies the significance of these findings cannot be underestimated. The suggestion of a clear structural deficit in the brains of psychopaths has profound implications for clinicians, research scientists and the criminal justice system.'

While psychopathy is strongly associated with serious criminal behaviour (eg rape and murder) and repeat offending, the biological basis of psychopathy remains poorly understood. Also some investigators stress mainly social reasons to explain antisocial behaviours. To date, nobody has investigated the 'connectivity' between the specific brain regions implicated in psychopathy.

Earlier studies had suggested that dysfunction of specific brain regions might underpin psychopathy. Such areas of the brain were identified as the amygdale, ie the area associated with emotions, fear and aggression, and the orbitofrontal cortex (OFC), the region which deals with decision making. There is a white matter tract that connects the amygdala and OFC, which is called the uncinate fasciculus (UF). However, nobody had ever studied the UF in psychopaths. The team from King's used an imaging method called in vivo diffusion tensor magnetic resonance imaging (DT-MRI) tractography to analyse the UF in psychopaths.

They found a significant reduction in the integrity of the small particles that make up the structure of the UF of psychopaths, compared to control groups of people with the same age and IQ. Also, the degree of abnormality was significantly related to the degree of psychopathy. These results suggest that psychopaths have biological differences in the brain which may help to explain their offending behaviours.

Dr Craig added: 'This study is part of an ongoing programme of research into the biological basis of criminal psychopathy. It highlights that exciting developments in brain imaging such as DT-MRI now offer neuroscientists the potential to move towards a more coherent understanding of the possible brain networks that underlie psychopathy, and potentially towards treatments for this mental disorder.'