Posts tagged magnetoencephalography
Articles and news from the latest research reports.
Detecting Autism From Brain Activity
Neuroscientists from Case Western Reserve University School of Medicine and the University of Toronto have developed an efficient and reliable method of analyzing brain activity to detect autism in children. Their findings appear today in the online journal PLOS ONE.
The researchers recorded and analyzed dynamic patterns of brain activity with magnetoencephalography (MEG) to determine the brain’s functional connectivity – that is, its communication from one region to another. MEG measures magnetic fields generated by electrical currents in neurons of the brain.
Roberto Fernández Galán, PhD, an assistant professor of neurosciences at Case Western Reserve and an electrophysiologist seasoned in theoretical physics led the research team that detected autism spectrum disorder (ASD) with 94 percent accuracy. The new analytic method offers an efficient, quantitative way of confirming a clinical diagnosis of autism.
“We asked the question, ‘Can you distinguish an autistic brain from a non-autistic brain simply by looking at the patterns of neural activity?’ and indeed, you can,” Galán said. “This discovery opens the door to quantitative tools that complement the existing diagnostic tools for autism based on behavioral tests.”
In a study of 19 children—nine with ASD—141 sensors tracked the activity of each child’s cortex. The sensors recorded how different regions interacted with each other while at rest, and compared the brain’s interactions of the control group to those with ASD. Researchers found significantly stronger connections between rear and frontal areas of the brain in the ASD group; there was an asymmetrical flow of information to the frontal region, but not vice versa.
The new insight into the directionality of the connections may help identify anatomical abnormalities in ASD brains. Most current measures of functional connectivity do not indicate the interactions’ directionality.
“It is not just who is connected to whom, but rather who is driving whom,” Galán said.
Their approach also allows them to measure background noise, or the spontaneous input driving the brain’s activity while at rest. A spatial map of these inputs demonstrated there was more complexity and structure in the control group than the ASD group, which had less variety and intricacy. This feature offered better discrimination between the two groups, providing an even stronger measure of criteria than functional connectivity alone, with 94 percent accuracy.
Case Western Reserve’s Office of Technology Transfer has filed a provisional patent application for the analysis’ algorithm, which investigates the brain’s activity at rest. Galán and colleagues hope to collaborate with others in the autism field with emphasis on translational and clinical research.
(Image: SPL)
Why crying babies are so hard to ignore: Study suggests the sound of a baby crying activates primitive parts of the brain involved in fight-or-flight responses
Ever wondered why it is so difficult to ignore the sound of a crying baby when you are trapped aboard a train or aeroplane? Scientists have found that our brains are hard-wired to respond strongly to the sound, making us more attentive and priming our bodies to help whenever we hear it – even if we’re not the baby’s parents.
"The sound of a baby cry captures your attention in a way that few other sounds in the environment generally do," said Katie Young of the University of Oxford, who led the study looking at how the brain processes a baby’s cries.
She scanned the brains of 28 people while they listened to the sound of babies and adults crying and sounds of animal distress including cats meowing and dogs whining.
Using a very fast scanning technique, called magnetoencephalography, Young found an early burst of activity in the brain in response to the sound of a baby cry, followed by an intense reaction after about 100 milliseconds. The reaction to other sounds was not as intense. “This was primarily in two regions of the brain,” said Young. “One is the middle temporal gyrus, an area previously implicated in emotional processing and speech; the other area is the orbitofrontal cortex, an area well-known for its role in reward and emotion processing.”
Young and her colleague, Christine Parsons, presented their findings this week at the annual meeting of the Society for Neuroscience in New Orleans.
Brain signal ID’s responders to fast-acting antidepressant
August 3, 2012
Scientists have discovered a biological marker that may help to identify which depressed patients will respond to an experimental, rapid-acting antidepressant. The brain signal, detectable by noninvasive imaging, also holds clues to the agent’s underlying mechanism, which are vital for drug development, say National Institutes of Health researchers.
Dr. Zarate views subject in MEG scanner from scanner control room.
The signal is among the latest of several such markers, including factors detectable in blood, genetic markers, and a sleep-specific brain wave, recently uncovered by the NIH team and grantee collaborators. They illuminate the workings of the agent, called ketamine, and may hold promise for more personalized treatment.
"These clues help focus the search for the molecular targets of a future generation of medications that will lift depression within hours instead of weeks," explained Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health (NIMH). "The more precisely we understand how this mechanism works, the more narrowly treatment can be targeted to achieve rapid antidepressant effects and avoid undesirable side effects."
Zarate, Brian Cornwell, Ph.D., and NIMH colleagues report on their brain imaging study online in the journal Biological Psychiatry.
Previous research had shown that ketamine can lift symptoms of depression within hours in many patients. But side effects hamper its use as a first-line medication. So researchers are studying its mechanism of action in hopes of developing a safer agent that works similarly.
Ketamine works through a different brain chemical system than conventional antidepressants. It initially blocks a protein on brain neurons, called the NMDA receptor, to which the chemical messenger glutamate binds. However, it is not known if the drug’s rapid antidepressant effects are a direct result of this blockage or of downstream effects triggered by the blockage, as suggested by animal studies.
To tease apart ketamine’s workings, the NIMH team imaged depressed patients’ brain electrical activity with magnetoencephalography (MEG). They monitored spontaneous activity while subjects were at rest, and activity evoked by gentle stimulation of a finger, before and 6.5 hours after an infusion of ketamine.
It was known that by blocking NMDA receptors, ketamine causes an increase in spontaneous electrical signals, or waves, in a particular frequency range in the brain’s cortex, or outer mantle. Hours after ketamine administration— in the timeframe in which ketamine relieves depression — spontaneous electrical activity in people at rest was the same whether or not the drug lifted their depression.
Electrical activity evoked by stimulating a finger, however, was different in the two groups. MEG imaging made it possible to monitor excitability of the somatosensory cortex, the part of the cortex that registers sensory stimulation. Those who responded to ketamine showed an increased response to the finger stimulation, a greater excitability of the neurons in this part of the cortex.
Such a change in excitability is likely to result, not from the immediate effects of blocking the receptor, but from other processes downstream, in the cascade of effects set in motion by NMDA blockade, say the researchers. Evidence points to changes in another type of glutamate receptor, the AMPA receptor, raising questions about whether the blocking of NMDA receptors is even necessary for ketamine’s antidepressant effect. If NMDA blockade is just a trigger, then targeting AMPA receptors may prove a more direct way to effect a lifting of depression.