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What is the neurological basis for 'daredevil' behaviour?

What is the neurological basis for 'daredevil' behaviour?



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What is the neurological basis for people being seemingly fearless and engaging in risk-taking and daredevil behaviour?

I am talking about those that frequently perform or participate in activities that are often described by a lot of people as reckless and life-threateningly dangerous.


Dopamine receptor agonists related to reckless driving and gambling

There are three case reports provided by Reactions Weekly (2010) demonstrating correlations between treatment with dopamine receptor agonists and reckless driving:

Reckless driving occurred in three patients during treatment with dopamine receptor agonists (DA)… DA are associated with impulse control disorders, and may alter how the brain perceives and avoids risk. DA-associated impulse control disorders include pathological gambling and hypersexuality. Reckless driving may be another manifestation of DA-associated impulse control disorders.

Some further evidence is provided to suggest neurological correlates between dopamine receptor agonist and risky choices in a gambling task (Riba et al., 2008):

In summary, the present findings indicate that the dopamine D2/D3 receptor agonist pramipexole is capable of blocking reward-related activations in the rostral basal ganglia and midbrain and may lead to a behavioral disinhibition characterized by increases in risky choices in a gambling task.

Neurological correlates between voluntary and involuntary risk taking in the brain

A study used functional magnetic resonance imaging (fMRI) and administered a modified BART with an active choice mode and a passive no-choice mode in order to examine the neural correlates of voluntary and involuntary risk taking in the human brain (Rao et al., 2008):

In summary, the present study modified the BART in both active and passive modes for use during fMRI and the findings provide direct visualization of voluntary and involuntary risk processing in the human brain. Regardless of the involvement of voluntary decision making, risk in this task is processed in visual pathway regions in the occipital and parietal lobes. However, during active decision-making, risk is associated with additional robust activation in dopamine rich mesolimbic (VTA-striatum) and frontal regions (insula, ACC/MFC, and DLPFC). Voluntary decision making per se, is associated with activation in the right DLPFC, which is absent in the involuntary no-choice condition. These results contribute to understanding the neural basis of normal and high risk behavior. Extending this paradigm to pathological populations characterized by impaired decisionmaking, such as patients with drug addition and compulsive gambling, may allow the specific neural components of impaired risk behavior to be distinguished, and may ultimately inform more effective clinical treatment interventions.

References

  • Reactions Weekly. (2010). Dopamine receptor agonists: reckless driving: 3 case reports.(Adverse Reaction Case Reports)(Case study)(Brief article), 1300, 18(1)
  • Riba, J., Kramer, U.M., Heldmann, M., Richter, S. & Munte, T.F. (2008). Dopamine agonist increases risk taking but blunts reward-related brain activity. PLoS One, 3(6)
  • Rao, H. Korczykowski, M., Pluta, J., Hoang, A. & Detre, J.A. (2008). Neural correlates of voluntary and involuntary risk taking in the human brain: An fMRI study of the Balloon Analog Risk Task (BART). Neuroimage, 42, 902-910

Sensation Seeking behaviour:

Sensation Seeking behaviour, is a better description of the type of extreme dare devil or extreme sport type of behaviour, as opposed to risk taking generally. Reckless risk taking is associated with a variety of psychological conditions that do not necessarily display this specific style of risk taking. There are gender differences with sensation seeking behaviour (and risk taking generally), with more men exhibiting this type of behaviour. From an evolutionary perspective, it makes sense that men, classically the hunters and protectors, would be more inclined to take risks.

Type T personality:

People who are high on the sensation seeking scale, are not necessarily anti social, but a personality type, which propels them to push the limits of life. The best description I have of this type of personality is the description of being a Type T personality. Channeled positively, this type of personality has the potential to be a high achiever.

The Type T personality has been described as a personality dimension referring to individual differences in stimulation seeking, excitement seeking, thrill seeking, arousal seeking, and risk taking. (1)

Physiological differences:

Sensation seekers have notable physiological differences from individual's with average risk taking profiles. Their orienting reflex (OR) works in reverse to other individuals. In brief, OR is a creatures natural response to external stimuli, change in environment. An event that would, usually, cause a stressful response in the autonomic nervous system will trigger an entirely different response in this type of personality. Physiologically this personality type is primed for adventure.

One study found that when subjects with high disinhibition scores were presented with a moderate-intensity tone, their heart-rates slowed down on the first exposure, while the heart rates of low sensation-seekers quickened.
Another of his studies, published in the Journal of Personality (Vol. 58, No. 1, pages 313-345) in 1990, indicates that the differences between high and low sensation-seekers extend to the cortex of the brain, with high sensation-seekers showing an "augmenting" electrochemical reaction, or increasing amplitude of cortical-evoked potentials (EPs) in response to increasing intensities of stimulation. Low sensation-seekers, however, demonstrate a reducing reaction, showing little EP increase in relation to increasing stimulus intensity, and sometimes showing a reduction in EP amplitudes at the highest intensities of stimulation. (2)

Monoamine oxidase (MAO) is needed for the chemical cascade in the release of dopamine. The brain chemistry is also deficit in MAO, which could explain the need for a self induced high, from thrill seeking, to increase the release of dopamine.

Conclusion:

In conclusion these extremists, may be an evolutionary necessity for the species. As mentioned in one of the articles, it is this drive to push the boundaries that has caused the species to explore the earth and, even, outer space.


References:

  • Gender differences in risk taking: A meta-analysis.
    Byrnes, James P,et al doi: 10.1037/0033-2909.125.3.367

  • Type T personality and the Jungian classification system.
    Morehouse RE, et al PMID: 2313544 (1)

  • Risk taking in Extreme Sports: A phenomenological perspective
    Brymer, Eric PDF

  • Frisky, but more risky
    Christopher Munsey, American Psychological Association (2)

  • Higher Nervous Functions: The Orienting Reflex
    E N Sokolov DOI: 10.1146/annurev.ph.25.030163.002553

  • Natural selective attention: Orienting and emotion
    Margaret M. Bradley DOI: 10.1111/j.1469-8986.2008.00702.x

  • Risk taking: A study in cognition and personality.
    Kogan, Nathan; Wallach, Michael A, Oxford, England: Holt, Rinehart & Winston. (1964)

  • Motivational determinants of risk-taking behavior. Atkinson, John W doi: 10.1037/h0043445

  • The life attitudes schedule: a scale to assess adolescent life-enhancing and life-threatening behaviors.
    Lewinsohn PM, et al

All supporting evidence for all my claims are within these references


Conclusions

Convergent data from neuroimaging, neuropsychology, genetics and neurochemical studies consistently point to the involvement of the frontostriatal network as a likely contributor to the pathophysiology of ADHD. This network involves the lateral prefrontal cortex, the dorsal anterior cingulate cortex and the caudate nucleus and putamen [39]. Functional neuroimaging has provided new ways to examine the pathophysiology of ADHD, has shown widespread dysfunction in neural systems involving the prefrontal, striatal, and parietal brain regions, and has led to a brain model of deficits in multiple developmental pathways [72]. Molecular genetic studies support dysregulation of neurotransmitter systems as the basis of genetic susceptibility to the disorder, and it is becoming clear that the genotype may influence the response to medications [73]. Hopefully, advances in understanding the underlying neurobiology of ADHD will contribute to identifying more specific and targeted pharmacotherapies, and will help child neurologists to better manage their patients.


The greater the volume of the prefrontal cortex, the less aggressive behavior

Already in the late 1990s, it was suggested that increased activity in the amygdala led to greater negative behaviors, including greater aggression, as opposed to decreased activity of the prefrontal cortex offered less ability to control his emotions.

It was a study by Whittle et al. (2008) in adolescents, who ultimately concluded that the greater the volume of the prefrontal cortex, the less aggressive behavior was perceived in boys and unlike in the case of the amygdala, a larger volume responded to both more aggressive and reckless behaviors.

When Anthony Hopkins plays the character of Hannibal lecter a The Silence of the Lambs, shows an unusual temperament for a murderer, far from conveying an impulsive and emotional personality which is distinguished by a profile, calculating, cold and extremely rational, which escapes the explanation that we propose.

White matter in the prefrontal cortex and its relationship to aggression

So far, we have seen how an increase in amygdala activity and a decrease in the prefrontal cortex is ideal for describing a personality that is more impulsive, thoughtless and even with little ability in emotional management but how to explain typical characteristics. Hannibal?

In 2005, Yang et al. found that a decrease in white matter in the prefrontal cortex responded to a decrease in one’s own cognitive resources, Both to persuade or manipulate other people and to make decisions at specific times. Keeping the white matter intact would explain why Hannibal and other assassins with the same characteristics are able to control their behavior so masterfully, to make appropriate decisions in complex situations, always for their own benefit and to the point of achieving a fictitious authority.

Serotonin is the key to understanding aggressive behavior

As we said at the beginning, serotonin also plays a key role in this problem, in particular, a decrease in their activity is directly linked to the aggression and with the implementation of risky behavior. In 2004, New et al. showed that treatment with SSRIs (selective serotonin reuptake inhibitors) increased the activity of the prefrontal cortex, and that at the end of the year, the aggressive behavior of individuals was significantly reduced.

In summary, one can notice how an increase in serotonergic activity would increase the activity of the prefrontal cortex, which would cause an inhibition of the activity of the amygdala and consequently aggressive behaviors.

We are not slaves to our biology

Although knowing that the brain is not decisive in modulating aggression and these behaviors on its own, it is thanks to advances and numerous studies that we can explain its mechanism with regard to the neurological process. Guido Frank, scientist and physicist at the University of California points out that biology and behavior are subject to change and that by combining a good therapeutic process and adequate individualized control, the progress of each individual can be changed.

Ultimately, as neurologist Craig Ferris of Northeastern University in Boston, USA points out, we have to keep in mind that “we are not completely slaves to our biology.”


A Neuroscientist Uncovers A Dark Secret

Fallon with his wife, daughters and son. When he compared the brain scans of his family — including his wife, siblings, children and mother — his was the only one that resembled the brain of a pyschopath. Courtesy of Jim Fallon hide caption

Fallon with his wife, daughters and son. When he compared the brain scans of his family — including his wife, siblings, children and mother — his was the only one that resembled the brain of a pyschopath.

The criminal brain has always held a fascination for James Fallon. For nearly 20 years, the neuroscientist at the University of California-Irvine has studied the brains of psychopaths. He studies the biological basis for behavior, and one of his specialties is to try to figure out how a killer's brain differs from yours and mine.

About four years ago, Fallon made a startling discovery. It happened during a conversation with his then 88-year-old mother, Jenny, at a family barbecue.

"I said, 'Jim, why don't you find out about your father's relatives?' " Jenny Fallon recalls. "I think there were some cuckoos back there."

"There's a whole lineage of very violent people -- killers," he says.

One of his direct great-grandfathers, Thomas Cornell, was hanged in 1667 for murdering his mother. That line of Cornells produced seven other alleged murderers, including Lizzy Borden. "Cousin Lizzy," as Fallon wryly calls her, was accused (and controversially acquitted) of killing her father and stepmother with an ax in Fall River, Mass., in 1882.

Explore The Series

A little spooked by his ancestry, Fallon set out to see whether anyone in his family possesses the brain of a serial killer. Because he has studied the brains of dozens of psychopaths, he knew precisely what to look for. To demonstrate, he opened his laptop and called up an image of a brain on his computer screen.

"Here is a brain that's not normal," he says. There are patches of yellow and red. Then he points to another section of the brain, in the front part of the brain, just behind the eyes.

"Look at that -- there's almost nothing here," Fallon says.

This is the orbital cortex, the area that Fallon and other scientists believe is involved with ethical behavior, moral decision-making and impulse control.

"People with low activity [in the orbital cortex] are either free-wheeling types or sociopaths," he says.

Fallon's Scans

He's clearly oversimplifying, but Fallon says the orbital cortex puts a brake on another part of the brain called the amygdala, which is involved with aggression and appetites. But in some people, there's an imbalance -- the orbital cortex isn't doing its job -- perhaps because the person had a brain injury or was born that way.

"What's left? What takes over?" he asks. "The area of the brain that drives your id-type behaviors, which is rage, violence, eating, sex, drinking."

Fallon's brain (on the right) has dark patches in the orbital cortex, the area just behind the eyes. This is the area that Fallon and other scientists say is involved with ethical behavior, moral decision-making and impulse control. The normal scan on the left is his son's. Courtesy of Jim Fallon hide caption

Fallon says nobody in his family has real problems with those behaviors. But he wanted to be sure. Conveniently, he had everything he needed: Previously, he had persuaded 10 of his close relatives to submit to a PET brain scan and give a blood sample as part of a project to see whether his family had a risk for developing Alzheimer's disease.

After learning his violent family history, he examined the images and compared them with the brains of psychopaths. His wife's scan was normal. His mother: normal. His siblings: normal. His children: normal.

"And I took a look at my own PET scan and saw something disturbing that I did not talk about," he says.

What he didn't want to reveal was that his orbital cortex looks inactive.

"If you look at the PET scan, I look just like one of those killers."

Fallon cautions that this is a young field. Scientists are just beginning to study this area of the brain -- much less the brains of criminals. Still, he says the evidence is accumulating that some people's brains predispose them toward violence and that psychopathic tendencies may be passed down from one generation to another.

The Three Ingredients

And that brings us to the next part of Jim Fallon's family experiment. Along with brain scans, Fallon also tested each family member's DNA for genes that are associated with violence. He looked at 12 genes related to aggression and violence and zeroed in on the MAO-A gene (monoamine oxidase A). This gene, which has been the target of considerable research, is also known as the "warrior gene" because it regulates serotonin in the brain. Serotonin affects your mood -- think Prozac -- and many scientists believe that if you have a certain version of the warrior gene, your brain won't respond to the calming effects of serotonin.

Fallon calls up another slide on his computer. It has a list of family members' names, and next to them, the results of the genotyping. Everyone in his family has the low-aggression variant of the MAO-A gene, except for one person.

"You see that? I'm 100 percent. I have the pattern, the risky pattern," he says, then pauses. "In a sense, I'm a born killer."

Fallon was prompted to study his brain after his mother, Jenny, told him his ancestry was full of alleged murderers. Courtesy of Jim Fallon hide caption

Fallon was prompted to study his brain after his mother, Jenny, told him his ancestry was full of alleged murderers.

Fallon's being tongue-in-cheek -- sort of. He doesn't believe his fate or anyone else's is entirely determined by genes. They merely tip you in one direction or another.

And yet: "When I put the two together, it was frankly a little disturbing," Fallon says with a laugh. "You start to look at yourself and you say, 'I may be a sociopath.' I don't think I am, but this looks exactly like [the brains of] the psychopaths, the sociopaths, that I've seen before."

I asked his wife, Diane, what she thought of the result.

"I wasn't too concerned," she says, laughing. "I mean, I've known him since I was 12."

Diane probably does not need to worry, according to scientists who study this area. They believe that brain patterns and genetic makeup are not enough to make anyone a psychopath. You need a third ingredient: abuse or violence in one's childhood.

"And fortunately, he wasn't abused as a young person," Diane says, "so I've lived to be a ripe old age so far."

The New World of 'Neurolaw'

Jim Fallon says he had a terrific childhood he was doted on by his parents and had loving relationships with his brothers and sisters and entire extended family. Significantly, he says this journey through his brain has changed the way he thinks about nature and nurture. He once believed that genes and brain function could determine everything about us. But now he thinks his childhood may have made all the difference.

"We'll never know, but the way these patterns are looking in general population, had I been abused, we might not be sitting here today," he says.

As for the psychopaths he studies, Fallon feels some compassion for these people who, he says, got "a bad roll of the dice."

"It's an unlucky day when all of these three things come together in a bad way, and I think one has to empathize with what happened to them," he says.

But what about people who rape and murder -- should we feel empathy for them? Should they be allowed to argue in court that their brains made them do it? Enter the new world of "neurolaw" -- in which neuroscience is used as evidence in the courtroom.


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A neurological basis for the lack of empathy in psychopaths

IMAGE: This is response in the right amygdala across groups of low (L), medium (M) and high (H) psychopathy participants, when they adopted an imagine-self and an imagine-other affective perspective. view more

Credit: Decety. J, Chenyi. C, Harenski. C, and Kiehl. K, A. Frontiers in Human Neuroscience, 2013.

When individuals with psychopathy imagine others in pain, brain areas necessary for feeling empathy and concern for others fail to become active and be connected to other important regions involved in affective processing and decision-making, reports a study published in the open-access journal Frontiers in Human Neuroscience.

Psychopathy is a personality disorder characterized by a lack of empathy and remorse, shallow affect, glibness, manipulation and callousness. Previous research indicates that the rate of psychopathy in prisons is around 23%, greater than the average population which is around 1%.

To better understand the neurological basis of empathy dysfunction in psychopaths, neuroscientists used functional magnetic resonance imaging (fMRI) on the brains of 121 inmates of a medium-security prison in the USA.

Participants were shown visual scenarios illustrating physical pain, such as a finger caught between a door, or a toe caught under a heavy object. They were by turns invited to imagine that this accident happened to themselves, or somebody else. They were also shown control images that did not depict any painful situation, for example a hand on a doorknob.

Participants were assessed with the widely used PCL-R, a diagnostic tool to identify their degree of psychopathic tendencies. Based on this assessment, the participants were then divided in three groups of approximately 40 individuals each: highly, moderately, and weakly psychopathic.

When highly psychopathic participants imagined pain to themselves, they showed a typical neural response within the brain regions involved in empathy for pain, including the anterior insula, the anterior midcingulate cortex, somatosensory cortex, and the right amygdala. The increase in brain activity in these regions was unusually pronounced, suggesting that psychopathic people are sensitive to the thought of pain.

But when participants imagined pain to others, these regions failed to become active in high psychopaths. Moreover, psychopaths showed an increased response in the ventral striatum, an area known to be involved in pleasure, when imagining others in pain.

This atypical activation combined with a negative functional connectivity between the insula and the ventromedial prefrontal cortex may suggest that individuals with high scores on psychopathy actually enjoyed imagining pain inflicted on others and did not care for them. The ventromedial prefrontal cortex is a region that plays a critical role in empathetic decision-making, such as caring for the wellbeing of others.

Taken together, this atypical pattern of activation and effective connectivity associated with perspective taking manipulations may inform intervention programs in a domain where therapeutic pessimism is more the rule than the exception. Altered connectivity may constitute novel targets for intervention. Imagining oneself in pain or in distress may trigger a stronger affective reaction than imagining what another person would feel, and this could be used with some psychopaths in cognitive-behavior therapies as a kick-starting technique, write the authors.

Prof Jean Decety
Department of Psychology and Department of Psychiatry and Behavioral Neuroscience
University of Chicago, USA
E-mail: [email protected]

To request a copy of the embargoed paper, please contact Gozde Zorlu: [email protected]

Please cite "Frontiers in Human Neuroscience" as the publication and include a link to the paper, which will become available on the following active URL: http://94. 236. 98. 240/ human_neuroscience/ 10. 3389/ fnhum. 2013. 00489/ abstract

Article title: An fMRI study of affective perspective taking in individuals with psychopathy: imagining another in pain does not evoke empathy
Journal: Frontiers in Human Neuroscience
DOI: 10.3389/fnhum.2013.00489

List of authors: Jean Decety, Chenyi Chen, Carla Harenski and Kent A. Kiehl.

Frontiers is a community driven open-access publisher and research networking platform. Launched and run by scientists since 2007, Frontiers empowers researchers to advance the way science is evaluated communicated, and shared in the digital era. Frontiers joined the Nature Publishing Group family in 2013.

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The Neural Basis of Learning

Learning is a process by which we integrate new knowledge generated as a result of experiences. The product of such experiences is converted into memories stored in our brain. There is basically no learning without memories.

There are essentially two ways in which learning occurs: one is called classical conditioning and the other instrumental conditioning. Both ways modify brain structure and brain chemistry, but they do so with varying degree of awareness or self-control. Classical conditioning pertains to situations in which we tend to respond automatically, based on the severity or repetition of a stimulus. The amygdala is involved in regulating many of our autonomic, fight or flight type responses.

For instrumental conditioning, more brain structures appear to take an active role in encoding and reinforcing a learned behavior. For instance when we learn driving, the repetition or rehearsal of that behavior will involve the perceptual and motor systems as well as the frontal lobes. As the behavior is memorized, it is managed by the basal ganglia. People who have lesions in the basal ganglia have severe deficits in their capacity to learn via instrumental conditioning. The process by which we learn new behaviors is also largely influence by specific neurotransmitters, especially dopamine which is known to reinforce or reward specific behaviors by making us feel good about it.

Memory is typically described as either short or long-term. Short term memory is also called working memory and can last from several minutes to a few hours. The front lobes are known to play a very important role in the short term memorization while the hippocampus is critical in consolidating information into long term storage.

To understand the anatomical changes that are happening in the brain as a result of learning or the creation of memories, we need to go back to the basis of brain functioning: synaptic connections.

The Neurological Basis of Learning and Memory

Though we now recognize that there are different forms of learning such as classical conditioning and instrumental conditioning and several types of memory from short term to long term, all these processes in our brain depend on our ability to detect, decode and respond to a change captured by our perceptual systems. For instance, a visual stimulus triggers a response that results in the formation of thousands of synapses in our brain. Our eyes capture photons that our visual neural pathway converts into electrical signals reaching different receptors in the brain via the optic nerve. The stimulus ultimately generates action potentials among thousands of neurons responsible for processing the signal and triggering a response. The signal is either amplified or minimized based on the intensity of the stimulation –the intensity of the light for instance–, its frequency and the presence or absence of the many molecules involved in exciting or inhibiting the chemical exchange in the synaptic cleft such as hormones, neurotransmitters and neuropeptides.

The process of learning and memorization develops neural efficiency by making new synaptic connections or by reinforcing the strength of existing ones. When neurons fire together, they wire together. Neuroscientists call this phenomenon synaptic plasticity.

Understanding Synaptic Plasticity

A considerable amount of brain research has been produced on learning and memorization over the last decade. We understand that learning is produced when the nature and structure of synaptic connections change, especially when postsynaptic neurons are affected by anatomical and biochemical alterations inflicted on axons. Early studies on learning used electrical stimulation within the hippocampal formation, a brain structure known to play a critical role in memory formation. Those studies revealed that the stimulation produced more long term potentiation (LPT). The discovery of LPT proved what Donald Hebb (1949) suggested over 50 years ago while trying to describe a law that would explain the process by which we remember in our brain. Hebb proposed that “if a synapse repeatedly becomes active at about the same time the postsynaptic neuron fires, changes will take place in the structure or chemistry of the synapse that will strengthen it (Carlson, 2008: p 432). More recent research reveals that the process of LPT is largely governed by chemical reactions between important receptors such as NMDA and AMPA receptors. NMDA receptors can actually block LTP by making it impossible for calcium ions to enter dentritic spines, a chemical process that is necessary to strengthen synapses between neurons while AMPA facilitates the release of glutamate which can amplify a post synaptic potential.

The study of structural changes in the brain as a result of learning and memorization has received a considerable boost since neuroscientists have used imaging technology such as fMRI in the mid 90s. With fMRI, scientist can see the brain at work, specifically they can map which areas of the brain are most active in given circ***tances by tracking blood flood. For instance, research conducted by Bogdan Draganski and his colleagues of the Department of Neurology of the University of Regensbug Germany (Draganski &, 2006) demonstrated that gray matter volume increases as a result of learning. The process by which we generate new neurons is called neurogenesis and is the condition that makes it possible for us to increase our capacity to learn and memorize.

Though it is still very difficult for Neuroscientists to crack the neural code of both learning and memory, we do know that the production of new neurons is primarily possible in the hypothalamus, the brain area mostly responsible for creating and maintaining our long term memories. We also know that we do produce new neurons as a result of learning activities at any age, which is why additional research in this area is so critical to the future of neuroscience.

Christophe is a co-founder of SalesBrain, and the co-author The Persuasion Code (2018) and Neuromarketing (2002/2007). With over 30 years of marketing and business development experience, he is passionate about understanding and predicting consumer behavior using neuroscience.

Christophe holds an MBA from Bowling Green State University, and an MA and PhD in Media Psychology from Fielding Graduate University, where he is currently an adjunct faculty member. Christophe has received multiple awards from Vistage International and from the Advertising Research Foundation (ARF). He served as a board member of the Neuromarketing Science and Business Association (NMSBA) from 2011-2016.

Follow Christophe on LinkedIn, Facebook, and Instagram: @ChristopheMorinPhD, and on Twitter: @ChristopheMorin


Treatments for neurological disorders

There are multiple treatments for neurological disorders, which can vary depending on the condition. Normally, the main treatment consists of neurorehabilitation, which aims to restore, minimise or compensate functional deficits that the patient may have, but setting realistic expectations as to what is possible.

In some cases it is possible to mitigate some symptoms with medication or surgery.

Overall, treatment aims to improve the quality of life of patients suffering from a neurological disorder, so that they can have the greatest possible independence.

In all neurological disorders, an early diagnosis is vital, so that the specialist can establish the most appropriate treatment in each case.

Ask a top neurologist: what is vascular neurology?

By Professor Hedley Emsley
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We were fortunate to speak to one of our leading vascular neurologists Professor Hedley Emsley about his specialty, including the conditions he treats, such as stroke and transient ischaemic attack. Read more on the topic of vascular neurology and cerebrovascular disease here. See more

Women and epilepsy (part 1): hormones, periods and contraception

By Professor Matthew Walker
2021-06-23

The female body can have a profound effect on epilepsy. Unbeknownst to many, hormones, menstrual cycles and contraception measures play a part in the management of the condition. Matthew Walker, a leading specialist and researcher in the field of epilepsy, explains the connection between women and epilepsy. See more


A neurological basis for the lack of empathy in psychopaths

IMAGE: This is response in the right amygdala across groups of low (L), medium (M) and high (H) psychopathy participants, when they adopted an imagine-self and an imagine-other affective perspective. view more

Credit: Decety. J, Chenyi. C, Harenski. C, and Kiehl. K, A. Frontiers in Human Neuroscience, 2013.

When individuals with psychopathy imagine others in pain, brain areas necessary for feeling empathy and concern for others fail to become active and be connected to other important regions involved in affective processing and decision-making, reports a study published in the open-access journal Frontiers in Human Neuroscience.

Psychopathy is a personality disorder characterized by a lack of empathy and remorse, shallow affect, glibness, manipulation and callousness. Previous research indicates that the rate of psychopathy in prisons is around 23%, greater than the average population which is around 1%.

To better understand the neurological basis of empathy dysfunction in psychopaths, neuroscientists used functional magnetic resonance imaging (fMRI) on the brains of 121 inmates of a medium-security prison in the USA.

Participants were shown visual scenarios illustrating physical pain, such as a finger caught between a door, or a toe caught under a heavy object. They were by turns invited to imagine that this accident happened to themselves, or somebody else. They were also shown control images that did not depict any painful situation, for example a hand on a doorknob.

Participants were assessed with the widely used PCL-R, a diagnostic tool to identify their degree of psychopathic tendencies. Based on this assessment, the participants were then divided in three groups of approximately 40 individuals each: highly, moderately, and weakly psychopathic.

When highly psychopathic participants imagined pain to themselves, they showed a typical neural response within the brain regions involved in empathy for pain, including the anterior insula, the anterior midcingulate cortex, somatosensory cortex, and the right amygdala. The increase in brain activity in these regions was unusually pronounced, suggesting that psychopathic people are sensitive to the thought of pain.

But when participants imagined pain to others, these regions failed to become active in high psychopaths. Moreover, psychopaths showed an increased response in the ventral striatum, an area known to be involved in pleasure, when imagining others in pain.

This atypical activation combined with a negative functional connectivity between the insula and the ventromedial prefrontal cortex may suggest that individuals with high scores on psychopathy actually enjoyed imagining pain inflicted on others and did not care for them. The ventromedial prefrontal cortex is a region that plays a critical role in empathetic decision-making, such as caring for the wellbeing of others.

Taken together, this atypical pattern of activation and effective connectivity associated with perspective taking manipulations may inform intervention programs in a domain where therapeutic pessimism is more the rule than the exception. Altered connectivity may constitute novel targets for intervention. Imagining oneself in pain or in distress may trigger a stronger affective reaction than imagining what another person would feel, and this could be used with some psychopaths in cognitive-behavior therapies as a kick-starting technique, write the authors.

Prof Jean Decety
Department of Psychology and Department of Psychiatry and Behavioral Neuroscience
University of Chicago, USA
E-mail: [email protected]

To request a copy of the embargoed paper, please contact Gozde Zorlu: [email protected]

Please cite "Frontiers in Human Neuroscience" as the publication and include a link to the paper, which will become available on the following active URL: http://94. 236. 98. 240/ human_neuroscience/ 10. 3389/ fnhum. 2013. 00489/ abstract

Article title: An fMRI study of affective perspective taking in individuals with psychopathy: imagining another in pain does not evoke empathy
Journal: Frontiers in Human Neuroscience
DOI: 10.3389/fnhum.2013.00489

List of authors: Jean Decety, Chenyi Chen, Carla Harenski and Kent A. Kiehl.

Frontiers is a community driven open-access publisher and research networking platform. Launched and run by scientists since 2007, Frontiers empowers researchers to advance the way science is evaluated communicated, and shared in the digital era. Frontiers joined the Nature Publishing Group family in 2013.

The "Frontiers in" series of journals publish around 500 peer-reviewed articles every month, which receive 5 million monthly views and are supported by 30,000 editors and reviewers around the world. Frontiers has partnerships with international organizations such as the Max Planck Society and the International Union of Immunological Societies (IUIS). For more information, please visit: http://www. frontiersin. org

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Watch the video: 610 . Lecture No. 1. L. A (August 2022).