Addiction as a disorder of decision-making
New research shows that craving drugs such as nicotine can be visualized in specific regions of the brain that are implicated in determining the value of actions, in planning actions and in motivation. Dr. Alain Dagher, from McGill University, suggests abnormal interactions between these decision-making brain regions could underlie addiction. These results were presented at the 2013 Canadian Neuroscience Meeting, the annual meeting of the Canadian Association for Neuroscience - Association Canadienne des Neurosciences (CAN-ACN).
Neuroeconomics is a field of research which seeks to explain decision making in humans based on calculating costs and likely rewards or benefits of choices individuals make. Previous studies have suggested addicted individuals place greater value on immediate rewards (cigarette smoking) over delayed rewards (health benefits). Research done by Dr. Dagher and colleagues show how the value of the drug, which is indicated by the degree of craving, varies based on drug availability, decision to quit and other factors. He also shows that this perceived value of the drug at a given time can be visualized in the brains of addicted individuals by functional Magnetic Resonance Imaging (fMRI), and that imaging results can be used to predict subsequent consumption.
Dr. Dagher showed that a specific brain region called the dorsolateral prefrontal cortex (abbreviated DLPFC) regulates cigarette craving in response to drug cues - seeing people smoke, or smelling cigarettes - and that these induced cravings could be altered by inactivating the DLPFC by Transcranial Magnetic Stimulation (TMS). He suggests addiction may result from abberrant connections between the DLFPC and other brain region in susceptible individuals. These results could provide a rational basis for novel interventions to reduce cravings in addicted individuals, such as cognitive behavioral therapy or transcranial stimulation of the DLFPC.
Concluding quote from Dr. Dagher: “Policy debates have often centred on whether addictive behaviour is a choice or a brain disease. This research allows us to view addiction as a pathology of choice. Dysfunction in brain regions that assign value to possible options may lead to choosing harmful behaviours.”
Autism Linked with Excess of Neurons in Prefrontal Cortex
health.ucsd.eduA study by researchers at the University of California, San Diego Autism Center of Excellence shows that brain overgrowth in boys with autism involves an abnormal, excess number of neurons in areas of the brain associated with social, communication and cognitive development.
The scientists discovered a 67 percent excess of cortical cells – a type of brain cell only made before birth – in children with autism. The findings suggest that the disorder may arise from prenatal processes gone awry, according to lead researcher Eric Courchesne, PhD, professor of neurosciences at the UC San Diego School of Medicine and director of the Autism Center of Excellence.
Relying on meticulous, direct cell counting, the study – to be published November 9 by the Journal of the American Medical Society (JAMA) and funded in part by the National Institutes of Health – confirms a relatively recent theory about possible causes of autism.
Connectivity of prefrontal cortex predicts cognitive control and intelligence
mindblog.dericbownds.netby Deric Bownds
From Cole et al.:
Control of thought and behavior is fundamental to human intelligence. Evidence suggests a frontoparietal brain network implements such cognitive control across diverse contexts. We identify a mechanism—global connectivity—by which components of this network might coordinate control of other networks. A lateral prefrontal cortex (LPFC) region’s activity was found to predict performance in a high control demand working memory task and also to exhibit high global connectivity. Critically, global connectivity in this LPFC region, involving connections both within and outside the frontoparietal network, showed a highly selective relationship with individual differences in fluid intelligence. These findings suggest LPFC is a global hub with a brainwide influence that facilitates the ability to implement control processes central to human intelligence.
Figure - Cognitive control regions, as defined by successful cognitive control. A, Regions of Interest (ROIs) were defined based on brain activity during successful N-back task performance. The following highly selective criteria were used: preferential activation for trials requiring flexible control (lures), correct > incorrect trials, positive correlation with accuracy across participants. All 3 of these regions were hubs (in top 10% connectivity in the brain).
Do compulsive/pathological liars have different brain structure?
The answer is yes. Numerous studies have converged in designating prefrontal white matter as the likely culprit behind all the lies. This increase in prefrontal white matter is also found in individuals that lie, cheat and manipulate others. Sounds bad…
Back in 2005, Yang et. al found an abnormal prefrontal white matter increase in the brains of pathological liars. The group postulated that perhaps this increase resulted in a predisposition towards lying. In 2007, the group examined white matter differences in four prefrontal areas by using structural magnetic resonance imaging (MRI).
Prefrontal areas exhibiting increased white matter (in the liars’ brains) were:
- Orbitofrontal cortex (22-26% increase)
- Inferior frontal cortex (32-36% increase)
- Middle frontal cortex (28-32% increase)
So how does one explain these differences?
There are many options. Among the ones I find most interesting are:
- This pre-existing variation of prefrontal structures may render individuals susceptible to pathological lying.
- Excessive and repetitive lying activates the prefrontal circuitry underlying pathological lying.
Another thing that I find very fascinating is that these prefrontal regions also happen to be implicated in executive functions essential for deception like decision-making and moral reasoning!
Other studies from nonhuman primates have suggested a role for larger neocortices in the act of deception.
References:
Yang, Yaling, et. al. 2007. Localisation of increased prefrontal white matter in pathological liars. British Journal of Psychiatry. 190: 174-175.
Top-down control in action
charbonniers.orgby Janet Kwazniak
The prefrontal cortex can select a rule to deploy in a particular situation. How is this done? The group of neurons that deploy a rule oscillate in synchrony when that rule is to be used. This synchrony explanation is becoming quite common. Synchrony is what produces functioning groups of neurons. Buschman at al have looked at rule selection in detail. However, I cannot access their paper. Fortunately two reviews of the paper are available (see citations).
Buschman used monkeys with electrodes implanted in their dorsolateral prefrontal cortex. They were taught to respond to the colour of a target and to the orientation of a target. They were presented with coloured targets that had an orientation. The decision for the monkey was which rule to use: colour or orientation discrimination. The monkeys were given a cue before the target that instructed them to use one rule or the other. In this way the researchers could see the events of choosing the rule.
The results -
The authors found that the local field potentials (LFPs) of a subset of the electrodes synchronized in the higher beta band (19–40 Hz) around stimulus onset when the color rule was applied. When the orientation rule was applied, LFPs from a different set of electrodes synchronized in the same frequency band. Crucially, when the more difficult color rule was applied, the researchers observed pre-stimulus synchronization in the alpha band (6–16 Hz) for electrodes showing a preference for the orientation rule.
The oscillatory activity had consequences for behavior: especially stronger alpha-band synchronization allowed the monkeys to perform the task faster. In line with the behavioral effects, the higher the anticipatory alpha power for the orientation ensemble, the higher the spike rate of the color-rule ensemble during stimulus presentation. Additionally it was demonstrated that neuronal spiking was phase-locked to beta oscillations. … The strong phase- locking between spikes and LFPs demonstrates that the timing of neuronal action potentials is determined by the phase of ongoing oscillations. As such, oscillations are intimately involved in controlling the dynamics underlying neuronal computations. Oscillations might not only be important for creating neuronal ensembles within regions, but also for communication between distant regions.
This is interpreted to mean that the executive functioning in rule selection involves beta wave synchrony. This synchrony gathers together what is needed for the use of that rule in a discrimination. The alpha synchrony appears to suppress the default (orientation) rule so that the non-default rule (colour) is easier to deploy.
This seems to be what top-down control looks like.
For those of you that can access it, the Buschman paper is also listed below.
Jensen, O., & Bonnefond, M. (2012). Prefrontal alpha- and beta-band oscillations are involved in rule selection Trends in Cognitive Sciences DOI: 10.1016/j.tics.2012.11.002
Engel, A. (2012). Rules Got Rhythm Neuron, 76 (4), 673-676 DOI: 10.1016/j.neuron.2012.11.003
Buschman TJ, Denovellis EL, Diogo C, Bullock D, & Miller EK (2012). Synchronous oscillatory neural ensembles for rules in the prefrontal cortex. Neuron, 76 (4), 838-46 PMID: 23177967
I have access to the paper if anyone wants it.
Gene Expression Abnormalities in Autism Identified
health.ucsd.eduGenetic studies find dysregulation in pathways that govern development of the prefrontal cortex in young patients with autism
A study led by Eric Courchesne, PhD, director of the Autism Center of Excellence at the University of California, San Diego School of Medicine has, for the first time, identified in young autism patients genetic mechanisms involved in abnormal early brain development and overgrowth that occurs in the disorder. The findings suggest novel genetic and molecular targets that could lead to discoveries of new prevention strategies and treatment for the disorder.
The study to be published on March 22 in PLoS Genetics uncovered differences in gene expression between brain tissue from young (2 to14 years old) and adult individuals with autism syndrome disorder, providing important clues why brain growth and development is abnormal in this disorder.
Courchesne first identified the link between early brain overgrowth and autism in a landmark study published by the Journal of the American Medical Association (JAMA) in 2003. Next, he tested the possibility that brain overgrowth might result from an abnormal excess of brain cells. In November 2011, his study, also published in JAMA, discovered a 67 percent excess of brain cells in a major region of the brain, the prefrontal cortex – a part of the brain associated with social, communication and cognitive development.
“Our next step was to see whether there might be abnormalities of genetic functioning in that same region that might give us insight into why there are too many cells and why that specific region does not develop normally in autism,” said Courchesne.
In the new study, the researchers looked towards genes for answers, and showed that genetic mechanisms that normally regulate the number of cortical neurons are abnormal. “The genes that control the number of brain cells did not have the normal functional expression, and the level of gene expression that governs the pattern of neural organization across the prefrontal cortex is turned down. There are abnormal numbers and patterns of brain cells, and subsequently the pattern is disturbed,” Courchesne said. “This probably leads to too many brain cells in some locations, such as prefrontal cortex, but perhaps too few in other regions of cortex as well.”
In addition, the scientists discovered a turning down of the genetic mechanisms responsible for detecting DNA defects and correcting or removing affected cells during periods of rapid prenatal development.
What makes a psychopath's brain different?
io9.com“There’s no neurological disorder quite as infamous as psychopathy, and yet figuring out exactly what goes on in a psychopath’s brain is extraordinarily difficult. We’ve now got an answer…and all it took was scanning the brains of forty medium-security prisoners.”
on Attention Deficit Hyperactivity Disorder
I’m not going to argue whether or not this is a real disorder - the science and my own personal experiences lead me to very much know it’s a Real Thing and not just some thing made up by doctors to push amphetamines onto children. Not that that doesn’t happen, but it’s not a negation of the condition itself. Rather, what I intend to do is give you a little insight into what exactly it is like for someone with ADHD, how they perceive the world, and what phenomenological reality is like for them. I say this as someone who has been diagnosed with ADHD. I have been diagnosed only after submitting to numerous mental and physical health evaluations.
I also don’t claim to speak for anyone but myself. It’s very well possible someone else with ADHD might feel differently or experience different things, and that’s fine. However, something leads me to believe that what I’m going to write will resonate with a lot of individuals. Regardless of that, this is just me personally - it’s not indicative of how everyone else experiences it.
There are numerous aspects to ADHD that most neurotypical people cannot relate to. Obviously, our attention span is severely decreased. It’s hard for us to focus. We have trouble staying on task. Etc etc - you know the basic story. But, digging deeper than that, what is the experience of life like for person with ADHD? What of our percetions, our interpretations, our way we view the world? How does that differ?
I never really noticed this until I was critiqued during a public speaking seminar, but in person I am an extremely fast talker. I sound like I”m rambling about a million words per minute. Ask anyone on this site who has met me in person, and I’m sure they will agree (unless I’m stoned/drunk/nodding-off) with that. I asked Kate about it, and that’s what she told me.
That got me thinking: why do I talk fast? From my own point of view, whn I am talking to someone in person, I don’t feel like I’m talking fast. In fact, I think the opposite: I think that the other person is slow. Even though they might be normal compared to everyone else, for me normal = slow.
That got me thinking even more. And when I sat down and finally thought things out, I came to a conclusion:individuals who have ADHD perceive each individual unit of time on a smaller scale than a neurotypical/non-ADHD person does.
To explain, consider the following. Let us take a neurotypical person, call them X. The minimum threshold under which X can notice any sort of change is 1 second. In other words,it takes X one second - on average - to notice a change in their environment. Now consider a person Y. For Y, this time is 1/2 of a second. Y, who is diagnosed with ADHD, can perceive changes in their environment within 1/2 of a second after they occur. The ratio doesn’t matter so much as it is the fact that an individual with ADHD is more “sensitive to time” than a neurotypical individual.
I think this explains a lot about ADHD. We get disatracted easily. Why is that? Well, we perceive more than you do. Not necessarily more, but rather because we perceive a more fine level of detail in change of time, our attention naturally matches our enhanced time-sensitivity. And that enhanced sensitivity to time causes us to notice more things, and thus get distracted.
There’s a lot more to ADHD than just time-sensitivity. A LOT more, for sure. But I haven’t seen this sort of detail written about in the literature. Coming from someone who has been diagnosed with ADHD for over 10 years, this is one way in which I feel ADHD affects the brain.
It’s not necessarily a negative thing. It absolutely can have repercussions, but there are also benefits. I’m not saying it’s a bad thing - it’s simply not the norm.
Chimpanzee's born with immature frontal lobes, Like Humans.
On August 11, 2011, Current Biology are the firs to track the development of the chimpanzee brain to the human brain in comparison.
Tetsuro Matsuzawa of Kyoto University in Japan says “One of the most marked evolutionary changes underlying human-specific cognitive traits is a greatly enlarged prefrontal cortex. It is also one of the latest-developing brain regions of the cerebrum.”
He also says, “Both humans and chimpanzees need to render their neural network and brain function more suspectible to the influence of postnatal experience.”
Chimps and humans both enjoy close relationships between their young and adults, like smiles and mutual gazes. But, the greater prefrontal expansion in the human brain may give a role in development of language, complex social infrastructure, and other abilities that make us unique.
Matsuzawa’s team made the discovery of this by magnetic reasonance imaging (MRI) studies of 3 growing chimpanzees from the age of 6 months to 6 years. Chimpanezee’s reach pre-puberty at the age of 6 years old.
In the last ancestor of chimpanzees and humans, the studies suggest that they were less mature and more protracted on their neural connection in the prefrontal portions of the brain. The last ancestor to human and chimps were called, macaques.
Matsuzawa says that his group was interested in exploring the development of the brain over evolution. The team was hoping to compare the humans and chimps brains into the young adulthood. They noted that chimps also enter late puberty at the age of 11-years old.
