Judgment and decision-making: brain activity indicates there is more than meets the eye

Published today in PLOS ONE, the study is the first in the world to show that it is possible to predict abstract judgments from brain waves, even though people were not conscious of making such judgments. The study also increases our understanding of impulsive behaviours and how to regulate it. 



It found that researchers could predict from participants’ brain activity how exciting they found a particular image to be, and whether a particular image made them think more about the future or the present. This is true even though the brain activity was recorded before participants knew they were going to be asked to make these judgments.


Lead authors Dr Stefan Bode from the Melbourne School of Psychological Sciences and Dr Carsten Murawski from the University of Melbourne Department of Finance said these findings illustrated there was more information encoded in brain activity than previously assumed.


“We have found that brain activity when looking at images can encode judgments such as time reference, even when the viewer is not aware of making such judgments. Moreover, our results suggest that certain images can prompt a person to think about the present or the future,” they said.


The authors said the results contributed to our understanding of impulsive behaviours, especially where those behaviours were caused by ‘prompts’ in the world around us. 



“For instance, consider someone trying to quit gambling who sees a gambling advertisement on TV. Our results suggest that even if this person is trying to ignore the ad, their brain may be unconsciously processing it and making it more likely that they will relapse,” he said. 


The researchers used electroencephalography technology (EEG) to measure the electrical activity of people’s brains while they looked at different pictures. The pictures displayed images of food, social scenes or status symbols like cars and money. 



After the EEG, researchers showed participants the same pictures again and asked questions about each image, such as how exciting they thought the image was or how strongly the image made them think of either the present or the future.

A statistical ‘decoding’ technique was then used to predict the judgments participants made about each of the pictures from the EEG brain activity that was recorded.

Co-author Daniel Bennett said just as certain prompts might cause impulsive behaviour, images could be used to prompt people to be more patient by regulating impulse control.


“Our results suggest that prompting people with images related to the future might cause processing outside awareness that could make it easier to think about the future. In theory, this could make people less impulsive and more likely to make healthy long-term decisions. These are hypotheses we will try to test in the future,” he said. 

The research was done in collaboration with the University of Cologne, Germany.

Sleep twitches light up the brain

A University of Iowa study has found twitches made during sleep activate the brains of mammals differently than movements made while awake.

Researchers say the findings show twitches during rapid eye movement (REM) sleep comprise a different class of movement and provide further evidence that sleep twitches activate circuits throughout the developing brain. In this way, twitches teach newborns about their limbs and what they can do with them.

“Every time we move while awake, there is a mechanism in our brain that allows us to understand that it is we who made the movement,” says Alexandre Tiriac, a fifth-year graduate student in psychology at the UI and first author of the study, which appeared this month in the journal Current Biology. “But twitches seem to be different in that the brain is unaware that they are self-generated. And this difference between sleep and wake movements may be critical for how twitches, which are most frequent in early infancy, contribute to brain development.”

Mark Blumberg, a psychology professor at the UI and senior author of the study, says this latest discovery is further evidence that sleep twitches— whether in dogs, cats or humans—are connected to brain development, not dreams.

“Because twitches are so different from wake movements,” he says, “these data put another nail in the coffin of the ‘chasing rabbits’ interpretation of twitches.”

For this study, Blumberg, Tiriac and fellow graduate student Carlos Del Rio-Bermudez studied the brain activity of unanesthetized rats between 8 and 10 days of age. They measured the brain activity while the animals were awake and moving and again while the rats were in REM sleep and twitching.

What they discovered was puzzling, at first.

“We noticed there was a lot of brain activity during sleep movements but not when these animals were awake and moving,” Tiriac says.

The researchers theorized that sensations coming back from twitching limbs during REM sleep were being processed differently in the brain than awake movements because they lacked what is known as “corollary discharge.”

First introduced by researchers in 1950, corollary discharge is a split-second message sent to the brain that allows animals—including rats, crickets, humans and more—to recognize and filter out sensations generated from their own actions. This filtering of sensations is what allows animals to distinguish between sensations arising from their own movements and those from stimuli in the outside world.

So, when the UI researchers noticed an increase in brain activity while the newborn rats were twitching during REM sleep but not when the animals were awake and moving, they conducted several follow-up experiments to determine whether sleep twitching is a unique self-generated movement that is processed as if it lacks corollary discharge.

The experiments were consistent in supporting the idea that sensations arising from twitches are not filtered: And without the filtering provided by corollary discharge, the sensations generated by twitching limbs are free to activate the brain and teach the newborn brain about the structure and function of the limbs.

“If twitches were like wake movements, the signals arising from twitching limbs would be filtered out,” Blumberg says. “That they are not filtered out suggests again that twitches are special—perhaps special because they are needed to activate developing brain circuits.”

The UI researchers were initially surprised to find the filtering system functioning so early in development.

“But what surprised us even more,” Blumberg says, “was that corollary discharge appears to be suspended during sleep in association with twitching, a possibility that – to our knowledge – has never before been entertained.”

No sedative necessary: Scientists discover new “sleep node” in the brain

A sleep-promoting circuit located deep in the primitive brainstem has revealed how we fall into deep sleep. Discovered by researchers at Harvard School of Medicine and the University at Buffalo School of Medicine and Biomedical Sciences, this is only the second “sleep node” identified in the mammalian brain whose activity appears to be both necessary and sufficient to produce deep sleep.

Published online in August in Nature Neuroscience, the study demonstrates that fully half of all of the brain’s sleep-promoting activity originates from the parafacial zone (PZ) in the brainstem. The brainstem is a primordial part of the brain that regulates basic functions necessary for survival, such as breathing, blood pressure, heart rate and body temperature.

“The close association of a sleep center with other regions that are critical for life highlights the evolutionary importance of sleep in the brain,” says Caroline E. Bass, assistant professor of Pharmacology and Toxicology in the UB School of Medicine and Biomedical Sciences and a co-author on the paper.

The researchers found that a specific type of neuron in the PZ that makes the neurotransmitter gamma-aminobutyric acid (GABA) is responsible for deep sleep. They used a set of innovative tools to precisely control these neurons remotely, in essence giving them the ability to turn the neurons on and off at will.

 “These new molecular approaches allow unprecedented control over brain function at the cellular level,” says Christelle Ancelet, postdoctoral fellow at Harvard School of Medicine. “Before these tools were developed, we often used ‘electrical stimulation’ to activate a region, but the problem is that doing so stimulates everything the electrode touches and even surrounding areas it didn’t. It was a sledgehammer approach, when what we needed was a scalpel.”

“To get the precision required for these experiments, we introduced a virus into the PZ that expressed a ‘designer’ receptor on GABA neurons only but didn’t otherwise alter brain function,” explains Patrick Fuller, assistant professor at Harvard and senior author on the paper. “When we turned on the GABA neurons in the PZ, the animals quickly fell into a deep sleep without the use of sedatives or sleep aids.”

How these neurons interact in the brain with other sleep and wake-promoting brain regions still need to be studied, the researchers say, but eventually these findings may translate into new medications for treating sleep disorders, including insomnia, and the development of better and safer anesthetics.

“We are at a truly transformative point in neuroscience,” says Bass, “where the use of designer genes gives us unprecedented ability to control the brain. We can now answer fundamental questions of brain function, which have traditionally been beyond our reach, including the ‘why’ of sleep, one of the more enduring mysteries in the neurosciences.”

(Image caption: These figures show lagged maturation of connections in ADHD between the default mode network, involved in internally-directed thought (i.e., daydreaming) and shown on the left of each figure, and two brain networks involved in externally-focused attention, shown on the right of each figure. The width of each arc represents the number of lagged connections between two regions within each network. Connections that normally increase with age and that are hypoconnected in ADHD are shown in blue; connections that normally decrease with age and that are hyperconnected in ADHD are shown in red.)

Slow to mature, quick to distract: ADHD brain study finds slower development of key connections

A peek inside the brains of more than 750 children and teens reveals a key difference in brain architecture between those with attention deficit hyperactivity disorder and those without.

Kids and teens with ADHD, a new study finds, lag behind others of the same age in how quickly their brains form connections within, and between, key brain networks.

The result: less-mature connections between a brain network that controls internally-directed thought (such as daydreaming) and networks that allow a person to focus on externally-directed tasks. That lag in connection development may help explain why people with ADHD get easily distracted or struggle to stay focused.

What’s more, the new findings, and the methods used to make them, may one day allow doctors to use brain scans to diagnose ADHD — and track how well someone responds to treatment. This kind of neuroimaging “biomarker” doesn’t yet exist for ADHD, or any psychiatric condition for that matter.

The new findings come from a team in the University of Michigan Medical School’s Department of Psychiatry. They used highly advanced computing techniques to analyze a large pool of detailed brain scans that were publicly shared for scientists to study. Their results are published in the Proceedings of the National Academy of Sciences.

Lead author Chandra Sripada, M.D., Ph.D., and colleagues looked at the brain scans of 275 kids and teens with ADHD, and 481 others without it, using “connectomic” methods that can map interconnectivity between networks in the brain.

The scans, made using function magnetic resonance imaging (fMRI) scanners, show brain activity during a resting state. This allows researchers to see how a number of different brain networks, each specialized for certain types of functions, were “talking” within and amongst themselves.

The researchers found lags in development of connection within the internally-focused network, called the default mode network or DMN, and in development of connections between DMN and two networks that process externally-focused tasks, often called task-positive networks, or TPNs. They could even see that the lags in connection development with the two task-related networks — the frontoparietal and ventral attention networks — were located primarily in two specific areas of the brain.

The new findings mesh well with what other researchers have found by examining the physical structure of the brains of people with and without ADHD in other ways.

Such research has already shown alterations in regions within DMN and TPNs. So, the new findings build on that understanding and add to it. 

The findings are also relevant to thinking about the longitudinal course of ADHD from childhood to adulthood. For instance, some children and teens “grow out” of the disorder, while for others the disorder persists throughout adulthood. Future studies of brain network maturation in ADHD could shed light into the neural basis for this difference.

“We and others are interested in understanding the neural mechanisms of ADHD in hopes that we can contribute to better diagnosis and treatment,” says Sripada, an assistant professor and psychiatrist who holds a joint appointment in the U-M Philosophy department and is a member of the U-M Center for Computational Medicine and Bioinformatics. “But without the database of fMRI images, and the spirit of collaboration that allowed them to be compiled and shared, we would never have reached this point.”  

Sripada explains that in the last decade, functional medical imaging has revealed that the human brain is functionally organized into large-scale connectivity networks. These networks, and the connections between them, mature throughout early childhood all the way to young adulthood. “It is particularly noteworthy that the networks we found to have lagging maturation in ADHD are linked to the very behaviors that are the symptoms of ADHD,” he says. 

Studying the vast array of connections in the brain, a field called connectomics, requires scientists to be able to parse through not just the one-to-one communications between two specific brain regions, but the patterns of communication among thousands of nodes within the brain. This requires major computing power and access to massive amounts of data – which makes the open sharing of fMRI images so important.

“The results of this study set the stage for the next phase of this research, which is to examine individual components of the networks that have the maturational lag,” he says. “This study provides a coarse-grained understanding, and now we want to examine this phenomenon in a more fine-grained way that might lead us to a true biological marker, or neuromarker, for ADHD.”

Sripada also notes that connectomics could be used to examine other disorders with roots in brain connectivity – including autism, which some evidence has suggested stems from over-maturation of some brain networks, and schizophrenia, which may arise from abnormal connections. Pooling more fMRI data from people with these conditions, and depression, anxiety, bipolar disorder and more could boost connectomics studies in those fields.

(Image caption: Shown are fMRI scans across all subjects in the study. The yellow and red areas in Section A represent parts of the brain that are activated while subjects are forming “gist memories” of pictures viewed. Section B represents areas of increased activation, shown in yellow and red, as detailed memories are being formed. Credit: Image courtesy of Jagust Lab)

Researchers find neural compensation in people with Alzheimer’s-related protein

The human brain is capable of a neural workaround that compensates for the buildup of beta-amyloid, a destructive protein associated with Alzheimer’s disease, according to a new study led by UC Berkeley researchers.

The findings, published today (Sunday, Sept. 14) in the journal Nature Neuroscience, could help explain how some older adults with beta-amyloid deposits in their brain retain normal cognitive function while others develop dementia.

“This study provides evidence that there is plasticity or compensation ability in the aging brain that appears to be beneficial, even in the face of beta-amyloid accumulation,” said study principal investigator Dr. William Jagust, a professor with joint appointments at UC Berkeley’s Helen Wills Neuroscience Institute, the School of Public Health and Lawrence Berkeley National Laboratory.

Previous studies have shown a link between increased brain activity and beta-amyloid deposits, but it was unclear whether the activity was tied to better mental performance.

The study included 22 healthy young adults and 49 older adults who had no signs of mental decline. Brain scans showed that 16 of the older subjects had beta-amyloid deposits, while the remaining 55 adults did not.

The researchers used functional magnetic resonance imaging (fMRI) to track the brain activity of subjects in the process of memorizing pictures of various scenes. Afterwards, the researchers tested the subjects’ “gist memory” by asking them to confirm whether a written description of a scene – such as a boy doing a handstand – corresponded to a picture previously viewed. Subjects were then asked to confirm whether specific written details of a scene – such as the color of the boy’s shirt – were true.

“Generally, the groups performed equally well in the tasks, but it turned out that for people with beta-amyloid deposits in the brain, the more detailed and complex their memory, the more brain activity there was,” said Jagust. “It seems that their brain has found a way to compensate for the presence of the proteins associated with Alzheimer’s.”

What remains unclear, said Jagust, is why some people with beta-amyloid deposits are better at using different parts of their brain than others. Previous studies suggest that people who engage in mentally stimulating activities throughout their lives have lower levels of beta-amyloid.

“I think it’s very possible that people who spend a lifetime involved in cognitively stimulating activity have brains that are better able to adapt to potential damage,” said Jagust.