+EMPATHY

8 chapter 8

empathy

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Emotions are a part of empathy.  We experience empathy with ourselves and with our own bodies through the experience of emotions.  They arise in interaction between our bodies and our environment.

It really is pretty simple.  As humans we only have 5 basic emotions, and from these five we learn to differentiate all the other shades of the emotions we identify as we mature.  Four of these five emotions – disgust, fear, sadness and anger – lie in the older limbic right hemisphere of our brains.  These emotions are the ones that kept us alive.  The fifth emotion, joy, is in our newer left hemisphere.  Our right hemisphere develops earlier from the time of our birth than does our left hemisphere.

We can coin and propagate all the quote “positive thinking” techniques, including meditation, that we want to.  But thinking does not always “make it so.”  Facts are facts.  The facts are that if an infant is not allowed joy and happiness in a safe, loving and secure environment from birth, the left joy center will not develop to its capacity.  The early experiences prior to age 2 tell the brain as it develops what to do.  If there is not adequate joy interactions, the neurons that COULD have formed themselves in the joy center simply leave the scene, and they do not come back.  The brain is very efficient, and this region is one that demands experience to build it.  Without enough happy experiences before age 2, this part of the brain will be smaller than it should be, without as many neurons as it could have had, and it will remain so for the rest of a person’s life.

Neurons are cell bodies that happen to have limbs – think of them as legs, arms, fingers and toes.  Neurons in the happy center, even if they are a very limited collection allowed to develop birth to age 2, can later on add multiple limbs.  So I am not saying that exercising the happy center is useless.  But we must also realize the limitations.  Never again will new neurons attach themselves, or include themselves in the joyful community part of the left brain.  This means that biologically, physiologically, some people have to work much, much harder at being happy and may never get to the same level of joy that some people take for granted because they were loved and not abused and neglected from birth.

The flip side of this lack of early joy experiences is that at the same time these infants were not happy, they were experiencing terrifying and painful experiences that DID contribute to increase in the capacity for fear, anxiety and anguish.  They were pushing their little shopping carts, as it were, through a completely different part of the store and had them filled with traumas and difficulties, not pleasure and happiness.

We must understand that as these varieties of experiences are happening to the little ones as their brains are developing, every part of their being and body is being altered as well.  As we will explore in this text, they end up having an entirely different life because they ended up getting an entire different body – including nervous system, brain, and immune system.  Their adaptive genetic potentials made sure this was so, because to all practical appearances, these little people were having to develop a brain that would serve them in a completely toxic, traumatic, dangerous and malevolent world.

When we flush our toilets or let the water out of our bathtubs north of the equator, the water swirls in one direction.  If we perform these actions south of the equator, the waters circle in the opposite direction.  I believe our bodies have evolved to form themselves in equally distinct opposite ways, depending on whether we were prepared for a safe or a dangerous world.  This preparation begins with the stress level of the mother altering her hormones so that the communication has already begun before conception, and hence begins to program the offspring for the world from the start.

This is not unlike a long line of train tracks with switches that are flipped every step of the developmental journey, fine tuning adaptation to either a benevolent or a malevolent world, and sending the fetus and the infant off on an anticipated trajectory like an arrow into the future – be it toxic or be it not.  Pointing at any individual and blaming either them or their genes for the long term consequence is neglecting the basic facts of life.  Nature provides us with the miraculous ability to make the best of any situation to the best of our abilities.  When we witness people with less than perfect lives we need to understand their beginnings and their journey to understand what types of adaptations were called into play along the way.

So on the simplest level the easiest place to begin to look for the directional input of our early genetic programming is to determine what the overall emotion of our current lives is – when we are medication free.  There are just the five basic choices:  happy, sad, disgusted, angry or scared.  I disagree with the “personality experts” that these emotions are simply a reflection of our personality type.  We need to know what both the genes and the experiences of our ancestors were to know what those interactions determined for them in the same way we need to know what ours were before we can ever begin to simply assign our emotional tone to our “innate” personalities.

This isn’t about personality so much as it is about what the environment has communicated to our genetic material about the state of the world we are being formed to fit into.  I do not believe that “enlightenment” is so much about feeling blissful as it is about becoming informed about the facts of our existence as interactional, evolved and evolving beings in relationship with our environment.  This in-forming is worth more than all the bliss in the world because it will reflect a state of fact in reality that THEN becomes something we can being to consciously moderate toward a different end – within reason and within bounds.

When we look back on our cave dwelling, stone age history we see that originally we survived using very few tools.  In my book, I will say that we have a club in one hand and a spear with a large stone tip point in the other.  Once we determine what our basic emotional overriding emotional tone is, that can be our spear.  The nature of our club is equally as simple to determine:  Where do we fall on the spectrum or continuum of sensitivity?

Just as we know that our overall emotional tone was completely influenced by the interaction of our genetic self with our environmental influences, so too was our natural sensitivity alignment equally influenced.  But even though our natural sensitivity was influenced by our experience, we naturally all fall more toward one end than the other.  Do we detect only the largest disturbances we encounter, or do we notice the tiniest variations in our environment?  It’s that simple.  Do we notice what LOOMS or do we notice what FLUTTERS?

I refer to this continuum as being our club because I believe the whole spectrum of variation in human types is simply a reflection of our place in the energy give-and-take as it developed in our species through time in relation to a vital, necessary, efficient division of labor based on who had what kind of proficiency potential.  It quite being  possible for everyone to be equally as capable at performing all the kinds of jobs that needed to be done within our groups a long, long time ago.  Some were the hunters with the big stick clubs to bash and bring down the big game.  Others were provided with the more delicate sticks that allowed us to poke around in the bushes and dirt to find the plants.

I would much rather think about all the degrees of differences and similarities between myself in relation to others not in “psychiatric” terms but in the practical terms of who is better prepared to interact with the environment in what ways, using which abilities, to contribute what kind of energy to the whole?  Are we, most simply put, hunters or gathers?  Are we animal chasing clubbing people or are we find the vital plants in the right season in the right place people?  Are we plant people or are we animal people?

I like thinking about who we are as individuals in these terms because it makes me smile.  It provides me with all sorts of comedic visuals that are connected to the most ancient, ancient experiences of my species.  I can entertain myself with the visuals of fishing, say, that would have required a unique combinations of skills perhaps having been developed very well within a group of people who were on the middle of the loom-flutter range.  I can imagine the frustration, the desperation, the detached-point-of-view humor of me today imagining situations in the past when someone whose constitution allowed them to bring down the lion or the mammoth stomping through a meadow trying to find a delicate plant needed to heal a particular ailment, not knowing what to look for or where, stomping to death a wide path full of vital life and ending up empty handed.  I can imagine the tiny relationship plant people with their fist full of willow sticks trying to swat a bison to death and being knocked flat on their hind end or worse, again ending up empty handed.

Empty handed never suited either the survival or the advancement of our species.  Our genes have conspired over thousands and thousands of generations to create in each of us a unique combination of potentials to provide for the good of ourselves and our species.  Although we may be separated from our ancient ancestors by thousands upon thousands of years and miles of migrations, we each contain within ourselves a particular combination of assets.  What we must realize is that the state of the world we were being prepared to enter from before our conception in the body of our mother has been communicated to our genes so that they could best continue to combine and recombine themselves in the best way possible to allow us the success of completing our missions.

Our first responsibility toward adju8sting ourselves consciously to a world so complicated that scientists will spend the rest of eternity trying to unravel its secrets and will never be able to complete that task, is to understand that we all have behind the scenes adjustments to the ongoing operation and manifestation of our genetic codes throughout our lifetimes that happened and continue to happen in response to degrees of threat or of safety. Being human today means that, except in the rarest of circumstances, we can enlighten ourselves through learning and education about our own bodies and our own responses within our environment so that we can exercise increasing levels of control over how we ARE in the world.  It starts, in my humble opinion, by understanding who we are on as many levels as possible.

I suspect that all information about our place in our environment enters our body as a degree of stress – great or small.  We are all geared in our own particular ways both to notice it and to respond to it.  I believe that everything we detect in our environment that requires us to make some kind of an adjustment in response to threat – large or small – so that we can get back to balanced homeostasis, is processed through our immune system.  Taken literally, even our emotions are immune system responses.  Life is an ongoing interactive information gathering and response process.  Every reaction that goes on inside our bodies involves signaling and communication.

Is it friend or is it foe?  Is it going to eat me?  How humbling might it be to realize that every response we automatically make within our environment is based on a detection of where we are in the food chain at any given instant of time?  Do we fight, run, freeze?  What alerts us and what do we do about it?  That is the question.

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de Vigenmont & Singer 2006

My thought is that empathy proper is a cognitive operation

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contextual approach, several modulatory factors

discovery of mirror neurons in 1996 in monkeys

“Brain imaging studies have shown overlapping brain activation patterns when subjects feel their own emotions and observe the same emotions in others….It has been suggested that:

(i)                 shared affective neuronal networks explain how we feel the emotions of others as if they were our own and

(ii)               these networks are activated automatically whenever we observe others displaying emotion.  But is empathy really automatically triggered every time we observe someone else displaying emotion?”  de Vigenmont & Singer, 2006, 435

narrowed definition of empathy –

There is empathy if:

(i) one is in an affective state;

(ii)               this state is isomorphic [identical, similar, alike] to another person’s affective state;

(iii)             this state is elicited by the observation or imagination of another person’s affective state;

(iv)              one knows that the other person is the source of one’s own affective state.”  de Vigenmont & Singer, 2006, 435

this definition related to the neuronal basis of empathy — enables us to distinguish empathy from other related phenomena – such as …cognitive perspective-taking — making inferences based on what we know of a person but don’t feel the feeling ourselves

…emotional contagion – involves affect sharing but does not meet the condition of self-other distinction – not aware that the other is the cause of our feeling the same as other

..sympathy – an affective state related to the other but we are not having the feeling the same – I feel sorry for you because you feel jealous, angry or depressed but I don’t feel jealous, angry or depressed myself

“…observing another person’s emotional state activates parts of the neuronal network involved in processing that same state in oneself….”  de Vigenmont & Singer, 2006, 435

WHEN DO WE EMPATHIZE?

“In real life, we constantly witness people displaying contradictory emotions.  If we were to consciously feel what they feel all the time, we would be in permanent emotional (436)turmoil, leaving no room for our own emotions.”  de Vigenmont & Singer, 2006, 437

Some caregivers create just this situation for infants – caregiver attacking infant, or not clearly mirroring back the infant’s own emotions “properly” (or not at all) – caregiver overwhelming infant with adult’s emotions unrelated to infant’s, etc.

“We now provide neuroscientific evidence suggesting that empathy is not merely the consequence of the passive observation of emotional cues but that it is subject to contextual appraisal and modulation.”  de Vigenmont & Singer, 2006, 437

infants have no contextual appraisal and modulation abilities – they are the ones that are supposed to be on the receiving end of this in the beginning, or their brains won’t grow right so they will be able to do this on their own later one

MODULATION OF THE EMPATHIC BRAIN

“Recently, neuroscientists have started investigating whether activity in shared emotional networks can be modulated.  Evidence for a modulatory role of saliency and intensity of pain stimulus was observed by Aglioti’s group, who only saw an empathy-related reduction in motor excitability in the observer’s hand when a needle deeply penetrated the model’s muscle but not when the needle merely pricked the hand  [21].”  de Vigenmont & Singer, 2006, 437

“Singer et al. [22] found modulation as a function of the affective link between the empathizer and the person in pain.  de Vigenmont & Singer, 2006, 437  [fair play vs unfair play, empathy-related activation in the anterior cingulate cortex (ACC) and anterior insula (AI) for both genders when they liked a fair player who was in pain –men but not women showed absence of such empathic activity when perceiving unfair player in pain – instead on average men showed increase in activity in areas associated with reward (nucleus accumbens) positively correlated with expressed desire for revenge]

Lamm et al. [23] subjects had smaller empathic response in pain-related areas when told the pain other was feeling was justified to cure them

Is this related to parents who think hurting a child is deserved and for their own good?

All suggesting empathic brain responses are prone to modulation

CONTEXTUAL APPROACH

Authors “…propose a contextual approach to empathy….that;

(i)                 empathy is modulated by appraisal processes and

(ii)                this modulation is present even at the subpersonal [?] level of a neural empathic response, and can be fast, and implicit.”  de Vigenmont & Singer, 2006, 437

leaves lots of room with those who have distorted cognitions – like my theory of the childhood broken-rule people

authors distinguish between two types of modulation of empathy

…”..one can modulate one’s empathy voluntarily, using the control one has over one’s emotional responses..”  de Vigenmont & Singer, 2006, 437

which those of us with inadequate infant brain development cannot easily do (regulate emotions)

…mentions Buddhist monk, I would say also like chemo doctors’ “functional empathy”, like professionals – journalists EMT, cops, etc

……also, earned secure attachment would fit here – we changed the way we experience empathy from the way we were treated ourselves

…:empathy can be modulated by implicit appraisal processes, which might strongly influence the magnitude of empathic responses.”  de Vigenmont & Singer, 2006, 437

these would be the unconscious ones

four main categories of modulatory factors:

intrinsic features of the shared emotions:  intensity, saliency [striking point or feature] and valence (positive versus negative) of the emotion might have great influence on empathy of the perceiver of another’s emotions

…………….it might be easier to empathize with primary emotions such as fear, happiness or sadness rather than with secondary emotions such as jealousy

….relationship  between characteristics of people involved

……..gender, personality, age, past experiences of empathizer

……..if empathizer does not have the specific experiences of the other, can use cognitive perspective taking, but cannot empathize

……..this is especially relevant, to me, in regard to traumas, authors use example of vertigo

..context of situation

………judgment as to if the other’s emotion is justified in situation

………..does other’s reaction make sense to us in the situation

………..empathy difficult if there is more than one person present each expressing different emotions

Past history of trauma is a major factor in empathy modulation.  The first place to look for its effects are in the roles we are triggered to take in relation to the emotional world of human interactions we participate in.  The role of perpetrator, victim or rescuer will manifest in all emotional reactions because emotion is intimately tied to the human aspect of drama that operates in our interactions with each other.

If there is emotional drama, we need to carefully be aware (beware) of which role we are in at the time we are perceiving another’s emotional state because our role will influence our reactions.

Without the interacting force of past trauma infiltrating our current emotional state, equality and facts will dominate.  The facts of a situation can only be assessed through objectivity.  This is difficult because of the subjective nature of the emotional realities we live in.  How can we be objective about emotions when the very existence of emotions entails a subjective perspective?

We are not machines.  Yet we are also not educated and do not usually have factual knowledge about our emotions.  What causes them and what purpose do they have in our lives?  Do they exist only because of drama, or can we have emotional reactions – including empathetic reactions – that are not tied deeply into drama?

If the basis in our bodies of emotions is tied to our inner point of homeostatic equilibrium, and if that set point was formed in traumatic interactions with a malevolent caregiver situation, we have to understand that our point of “being equal,” our point of non-traumatic dramatic interaction will mislead us.  Not only is this “resting place” of centered balance without emotion not set right in the first place for us, but the switch that goes off to alert us of an emotional complication that we need to react to, is not set at a “secure base” place, either.

We grow up doing the best we can to stand on our own two feet, not being told that the boat we are standing in is not safe in the first place, and that we are in an inadequate boat that is itself  in extremely dangerous turbulent waters.  How are we to keep our balance, or even to experience that center point of balanced calmness if we have never had it in the first place?

People who were raised from infancy in a secure environment have a center point of balanced equilibrium – and that point is calmness.  That is the point from which the degree of drama can be measured.  That is the point that the cortex can come from so that it can realistically (!) assess the degree of drama in a situation or interaction so that the maximum “degrees of freedom” are possible in order than health-promoting, wellness of being choices and decisions can be made.

These choices include the amount of empathy we are going to allow ourselves to experience in any situation.  If we are not consciously aware of our own background as it has built itself into our nervous system, including the brain, then any automatic reaction that we have – implicit reaction – cannot be counted upon to take us in directions that is best for us, either in the short or in the long run.

We are being asked to play a game in an unfair circumstance where others with a secure history (of attachment) have the unfair advantage over us.  In addition, we are not told the game rules.  Everyone assumes that secure history game rules should apply equally to everyone, while the reality is that at best only 60 – 65% of the population were raised in a secure enough environment that these rules in fact apply.

Because the majority of the population starts with a calm ground zero built within their bodies – nervous system and brain – everyone assumes that “mind” and therefore the operational theory of mind that all operate with and from is the same and equal.  This is not so.  And for every degree that our center point was not set at calmness due to the trauma that we were exposed to, we lose corresponding degrees of freedom to operate from a place of well being in our own preservation of self interest.   (That is, if we even know who and where and what our self is in the first place.)

We have to understand that the emotional regulation and modulatory circuits in the brain are built from birth in an experience-dependent fashion and are well in place before we are a year old.  Those “rules” and our ability to use them are thus well out of our conscious awareness and control.  They place us in a reactive position rather than in an active or proactive position for the rest of our lives.  Only to the degree that we can, in adulthood, obtain conscious knowledge about ourselves and apply this information in an aware and self-reflective manner can we hope to change these patterns so that we have a choice  not remain caught in trauma drama as being victims, perpetrators or rescuers for the rest of our lives.

There is no better arena to assess our basic homeostatic center in relation to calm or chaos than in our empathetic relationships to others of our species.  This is where we will see the degree of “pathetic” or “pathos” that is operating on the stage of our lives.  To the exact degree that our center point was not set at calm equilibrium from birth (or before), our automatic reactions coming from our BODY will determine the course of our lives.  And in no other place will this be truer than if we suffer from PTSD.

………..”Some of the modulatory factors can be partly explained by the role they have in increasing or decreasing attention to the emotion-eliciting stimulus (e.g. cue saliency and intensity; empathizer’s mood and level of arousal; empathizer and target’s familiarity with and similarity to each other; target’s intention to communicate that he wants the empathizer to share his emotions).  However, the modulation of empathy cannot solely be explained by attention….future research will have to determine the relative importance of these factors and investigate their complex interplay in modulating empathic brain responses.”  de Vigenmont & Singer, 2006, 438

WHEN DOES MODULATION OCCUR

Which stage of empathic processing does the modulation occur?  Do appraisal processes happen before onset of or during empathic response?

It is interesting to see the change that is occurring as researchers begin to actually see from inside the brain how empathy is actually orchestrated.  In describing how experts used to believe empathy operates, they are describing how it DOES usually operate for those of us with trauma built into our bodies.  When they describe NOW what they see –I believe they are describing an ideal that operates for people who do NOT have trauma build into their bodies.  They are describing a reality where choice is an option.  For those of us with PTSD built into our bodies, our body makes the choice for us – informed consent is by default obliterated by the survival reactivity of the body who understands that the world is an extremely dangerous place that threatens it with immanent extinction.

The body will never allow the slower route through the cortex to be taken if it thinks destruction is the immediate goal and reality of life.  In other words, by fact as well as by definition – in reality – empathy only happens when and where choice is an option.  If we have no ability to choose, empathy is not an option in our reality.  Thus is was so with my mother.  Once we understand that we are not biologically designed – even in the best of circumstances – to respond with empathy, we can begin to explore all the possible intervening factors that might prevent empathy from being a possibility in somebody’s life.  It is the difference between “an empathic response WILL be elicited” and “an empathic response MIGHT be elicited.”  And, as yet, the jury is out……science cannot yet tell us which model is the fact and which is not…..

Resonance and appraisal in tandem and automatic:

“According to the late appraisal model, the empathic response is directly and automatically activated by the perception of an emotional cue.  The default rule is that there is always an empathic response.”  de Vigenmont & Singer, 2006, 438

…………this prior empathic response can be modulated or inhibited “at a later stage”

…………information about context, general and personal, is processed in parallel

…………outcome of this contextual appraisal process leads to modulation of the empathic response

……”This modulation can either be achieved by top-down inhibitory or excitatory processes or by horizontal competition between different motivational processes.”  de Vigenmont & Singer, 2006, 438

……..”…in this model, there are two independent systems working in parallel, empathic resonance and appraisal processes.”  de Vigenmont & Singer, 2006, 438

evaluated in context of information and not automatic

“According to the early appraisal model, the empathic response is not directly and automatically activated by the perception of an emotional cue.  Rather, the emotional cue is evaluated in the context of external and internal information.  Whether an empathic response is elicited depends on the outcome of the contextual appraisal process.  Thus, the default rule is that an empathic response is not automatically activated but an empathic response might be elicited as the outcome of the appraisal process (Jacob and Jeannerod [29] have a similar view of mirror neurons).”  de Vigenmont & Singer, 2006, 438

This internal information can be implicit – perhaps it is usually implicit – so that our reactions seem automatic.

“Current neuroscientific studies on empathy cannot yet distinguish between these two proposed routes.”  de Vigenmont & Singer, 2006, 438

………..sometimes contextual processing precedes activation of shared networks

……….future studies need to be designed that can distinguish between these two proposed routes

………see info on mirror neurons

….see Jacob & Jeannerod

…need improved analysis of effective connectivity, dynamics of cause, to determine “…whether the decrease in empathy-related activation in the ACC and AI in men observing unfair as compared with fair players in pain was causally preceded by an increase in activation in the dorsolateral prefrontal cortex, an area that has been associated with emotional control and inhibition [31, 32].”  de Vigenmont & Singer, 2006, 439 [Oschner et al 2002; Anderson et al 2004]

WHY DO WE EMPATHIZE

Why has evolution selected empathy?

………adaptive function of empathy – studies of other species

…”Shared emotional representations could have evolved as a byproduct of more general associative learning mechanisms….” de Vigenmont & Singer, 2006, 439

…….understanding of evolutionary roles is merely speculative at this point

What is its role now that it has emerged?

..role in everyday life, studied by disturbances in empathy and in social and developmental psychology

………has two main advantages

“First, as compared with cognitive perspective-taking, it might not be the more direct route to understanding other people’s emotions but it is a faster route for prediction of their subsequent behavior.  We propose that empathy provides a more precise and direct estimate of other people’s further actions because shared emotional networks also directly elicit the activation of associated relevant motivational and action systems.  By sharing the emotional state of others, we also share their emotional and motivational significance…However, it should be noted that prediction accuracy depends on the similarity between the empathizer’s and the target’s experiential repertoires….”  de Vigenmont & Singer, 2006, 439

“Second, empathy provides knowledge about important environmental properties.  For instance, by seeing someone being burnt by a machine, we attach a negative ‘avoidance’ value to the machine, without first having to experience the pain ourselves….In this sense, empathy is an efficient computation tool for acquiring knowledge about the values of the world around us…”  de Vigenmont & Singer, 2006, 439

SOCIAL ROLE

Empathy has “…been related to moral sense, altruism, justice, prosocial behavior and cooperation….people help others more when they report having empathized with them, whether they help to alleviate their own personal distress or because they care for the other person….However, it remains to be shown whether individual differences in empathic brain responses also predict subsequent prosocial behavior.”  de Vigenmont & Singer, 2006, 439

“…is empathy a necessary and sufficient condition for these prosocial behaviors to arise?”  de Vigenmont & Singer, 2006, 439

“…we suggest that empathy per se does not suffice to induce prosocial behavior but that empathy has to be turned into sympathy to motivate helping.  By contrast, empathic responses might also result in personal distress and thereby motivate self-related behavior, such as avoidance and withdrawal, instead of other-related prosocial behavior….Clearly, neuroscientific research is still in its infancy.  As for questions concerning the interplay between empathy, sympathy and prosocial behavior, we need a better understanding of the neural signature underlying specific emotion and empathy before we can distinguish between empathic and sympathetic affective brain response.:  de Vigenmont & Singer, 2006, 440

“Finally, we propose that the ability to share other people’s emotional experiences and to react to them in a fine-tuned manner might facilitate social communication and create social coherence.  For example, in action imitation, the chameleon effect – the tendency to adapt other people’s postures, gestures and mannerisms – was found to create affiliation and fondness….[also has been shown to be stronger in people who rate higher on empathy scores]…Similarly, perceiving another person’s empathy for oneself is likely to increase affiliation and strengthen the emotional bond with that person.”  de Vigenmont & Singer, 2006, 440

“The development of simultaneous recording techniques between multiple brains might be a promising step for future neuroscientific research in this domain.”  de Vigenmont & Singer, 2006, 440

CONCLUSION

we share someone else’s emotions “…by means of shared affective neural networks, which are activated when we feel our own emotions, as well as when we observe others feeling emotions…empathic brain responses are modulated by appraisal processes which take into account information about the emotional stimuli, their situative context, characteristics of the empathizer and his/her relationship with the target….two major roles of empathy:  one epistemological and one social.  Empathy might enable us to make faster and more accurate predictions of other people’s needs and actions and discover salient aspects of our environment.  Furthermore, empathy might serve as the origin of the motivation for altruistic behavior and cooperation.  Finally, it might have a crucial role in human communications.”  de Vigenmont & Singer, 2006, 440

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Simmons et al 2008

Abstract – Laboratory of Biological Dynamics and Theoretical Medicine, USA. ansimmons@ucsd.edu

Intolerance of uncertainty correlates with insula activation during affective ambiguity.

Intolerance of uncertainty (IU),

or the increased affective response

to situations with uncertain outcomes,

is an important component process of anxiety disorders.

Increased IU is observed in panic disorder (PD), obsessive compulsive disorder (OCD) and generalized anxiety disorder (GAD), and is thought to relate to dysfunctional behaviors and thought patterns in these disorders.

Identifying what brain systems are associated with IU would contribute to a comprehensive model of anxiety processing, and increase our understanding of the neurobiology of anxiety disorders. Here, we used a behavioral task, Wall of Faces (WOFs), during functional magnetic resonance imaging (fMRI), which probes both affect and ambiguity, to examine the neural circuitry of IU in 14 (10 females) college age (18.8 years) subjects. All subjects completed the Intolerance of Uncertainty Scale (IUS), Anxiety Sensitivity Index (ASI), and a measure of neuroticism (i.e. the NEO-N).

Uncertainty Scale (IUS) scores

but neither Anxiety Sensitivity Index (ASI)nor measure of neuroticism (i.e. the NEO-N).scores,

correlated positively with activation in bilateral insula during affective ambiguity.

Thus, the experience of IU

during certain types of emotion processing may relate to the degree to which

bilateral insula processes uncertainty.

Previously observed

insula hyperactivity

in anxiety disorder individuals may therefore be directly linked to

altered processes of uncertainty.

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Krain et al 2008

Abstract – New York University Child Study Center, New York University School of Medicine, New York, NY 10016, USA. amy.krain@med.nyu.edu

A functional magnetic resonance imaging investigation of uncertainty in adolescents with anxiety disorders.

Pediatric anxiety disorders, although highly prevalent, are understudied with little known about their pathophysiology.

Intolerance of uncertainty (IU) is a trait associated with worry, a key characteristic of these disorders.

Neural responses to uncertainty in healthy subjects involve the same frontal-limbic circuits that are hyper-responsive in pediatric anxiety.

As such, the present study examines the relationship between IU and neural responses to uncertainty in anxious adolescents. METHODS: Sixteen adolescents (ages 13-17) diagnosed with generalized anxiety disorder and/or social phobia (ANX) and 13 non-anxious control subjects completed a decision-making task while functional magnetic resonance imaging scans were acquired. RESULTS: The ANX group endorsed greater task-related anxiety and less certainty than control subjects on a post-task questionnaire.

Compared with control subjects, the ANX group did not demonstrate hyper-responsivity of brain regions as hypothesized.

Across groups, IU was positively correlated with activity in several frontal and limbic regions.

Further analyses identified subgroups within the ANX group: those with high IU activated frontal/limbic regions,

whereas those with low IU and less anxiety during the task deactivated the same regions in response to uncertainty.

CONCLUSIONS: Results substantiate the hypothesized link between IU and neural responses to uncertainty in some adolescents with anxiety disorders. Our findings, if replicated, suggest that trait measures, such as IU, can significantly improve our understanding of the neurobiological basis of pediatric anxiety disorders.

I believe these same responses are probably linked to attachment disorders [preoccupied and disorganized?] and corresponding reductions in empathy abilities.

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Kugel et al 2008

Abstract – Department of Clinical Radiology, University of Münster, Münster, Germany.

Alexithymic features and automatic amygdala reactivity to facial emotion.

Alexithymic individuals

have difficulties in identifying

and verbalizing their emotions.

The amygdala is known to play a central role in processing emotion stimuli and in generating emotional experience. In the present study automatic amygdala reactivity to facial emotion was investigated as a function of alexithymia (as assessed by the 20-Item Toronto Alexithymia Scale). The Beck-Depression Inventory (BDI) and the State-Trait-Anxiety Inventory (STAI) were administered to measure participants’ depressivity and trait anxiety. During 3T fMRI scanning, pictures of faces bearing sad, happy, and neutral expressions masked by neutral faces were presented to 21 healthy volunteers. The amygdala was selected as the region of interest (ROI) and voxel values of the ROI were extracted, summarized by mean and tested among the different conditions. A detection task was applied to assess participants’ awareness of the masked emotional faces shown in the fMRI experiment.

Masked sad and happy facial emotions led to greater right amygdala activation than masked neutral faces. [see Baas, Aleman & Kahn 2004

– says left amygdala most often active]

The alexithymia feature difficulties identifying feelings was negatively correlated with the neural response of the right amygdala to masked sad faces, even when controlling for depressivity and anxiety.

Reduced automatic amygdala responsivity

may contribute to problems in identifying one’s emotions in everyday life.

Low spontaneous reactivity of the amygdala to sad faces could implicate less engagement in the encoding of negative emotional stimuli.

Is this true for angry and fearful faces, as well?  Do they consider this a defense mechanism, a form of automatic detachment?

++++

Costafreda et al 2008

Abstract – Institute of Psychiatry, King’s College London, UK. s.costafreda@iop.kcl.ac

Predictors of amygdala activation during the processing of emotional stimuli: a meta-analysis of 385 PET and fMRI studies.

Although amygdala activity has been purported to be modulated by affective and non-affective factors, considerable controversy remains on its precise functional nature. We conducted a meta-analysis of 385 functional neuroimaging studies of emotional processing, examining the effects of experimental characteristics on the probability of detecting amygdala activity.

All emotional stimuli were associated with higher probability of amygdala activity than neutral stimuli. Comparable effects were observed for most negative and positive emotions, however there was a

higher probability of activation for fear and disgust relative to happiness.

The level of attentional processing affected amygdala activity,

as passive processing was associated with a higher probability of activation than active task instructions.

Gustatory-olfactory and visual stimulus modalities increased the probability of activation relative to internal stimuli.

Aversive learning increased the probability of amygdala activation as well.

There was some evidence of hemispheric specialization

with a relative left-lateralization for stimuli containing language and a relative right-lateralization for masked stimuli.

Methodological variables, such as type of analysis and magnet strength, were also independent predictors of amygdala activation.

++++

Sergerie, Chochol & Armony 2008

Abstract – Douglas Mental Health University Institute, McGill University, 6875 LaSalle Boulevard, Montreal, Quebec, Canada H4H 1R3. karine.sergerie@douglas.mcgill.ca

The role of the amygdala in emotional processing: a quantitative meta-analysis of functional neuroimaging studies.

Functional neuroimaging studies have provided strong support for a critical role of the amygdala in emotional processing. However, several controversies remain in terms of whether different factors-such as sex, valence and stimulus type-have an effect on the magnitude and lateralization of amygdala responses. Handedness would also be a factor, few take into consideration

To address these issues, we conducted a meta-analysis of functional neuroimaging studies of visual emotional perception that reported amygdala activation. Critically, unlike previous neuroimaging meta-analyses, we took into account the magnitude (effect size) and reliability (variance) associated with each of the activations.

Our results confirm that the amygdala responds to both positive and negative stimuli, with a preference for faces depicting emotional expressions.

We did not find evidence for amygdala lateralization as a function of sex or valence.

Instead, our findings provide strong support for a functional dissociation between left and right amygdala in terms of temporal dynamics.

But of course I don’t know what the temporal dynamics are without the article!

Taken together, results from this meta-analysis shed new light on several of the models proposed in the literature regarding the neural basis of emotional processing.

++++

Dannlowski et al 2007

Abstract – Department of Psychiatry, University of Münster, Albert-Schweitzer-Str. 11, 48149 Münster, Germany. dannlow@uni-muenster.de

Amygdala reactivity predicts automatic negative evaluations for facial emotions.

The amygdala is a key structure in a limbic circuit involved in the rapid and unconscious processing of facial emotions.

In the present study, the role of the amygdala in automatic, involuntary appraisal processes, which are believed to be a crucial component of emotion processing, was investigated in 23 healthy subjects.

Amygdala activity was recorded in response to masked displays of angry, sad, and happy facial expressions using functional magnetic resonance imaging (fMRI). In a subsequent experiment, the subjects performed a masked affective priming task that characterizes automatic emotion processing by investigating the biasing effect of subliminally presented emotional faces on evaluative ratings to subsequently presented neutral stimuli. In the affective priming task, significant valence-congruent evaluation manipulation was observed. Subjects rated neutral targets more positively if they were primed by happy faces.

Significant correlations were found between

amygdala responses to masked negative facial expressions and negative evaluation shifts elicited by the corresponding emotion quality in the affective priming task.

Spontaneous amygdala reactivity to facial emotions appears to be a determinant of automatic negative evaluative response tendencies.

This finding might shed some light on how amygdala hyperresponsivity contributes to negative cognitive biases commonly observed in affective disorders.

++++

Ohrmann et al 2007

Abstract – Department of Psychiatry, University of Münster, Albert-Schweitzer-Street 11, 48149, Muenster, Germany. ohrmann@uni-muenster.de

Threat sensitivity as assessed by automatic amygdala response to fearful faces predicts speed of visual search for facial expression.

It has been argued that the amygdala represents an integral component of a vigilance system that is primarily involved in the perception of ambiguous stimuli of biological relevance.

The present investigation was conducted to examine the relationship between automatic amygdala responsivity to fearful faces which may be interpreted as an index of trait-like threat sensitivity and spatial processing characteristics of facial emotions. During 3T fMRI scanning, pictures of human faces bearing fearful, angry, and happy expressions were presented to 20 healthy volunteers using a backward masking procedure based on neutral facial expressions. Subsequently, a computer-based face-in-the-crowd task using schematic face stimuli was administered.

The neural response of the (right) amygdala to masked fearful faces correlated consistently with response speed to negative and neutral faces. Neither amygdala activation during the masked presentation of angry faces nor amygdala activation during the presentation of happy faces was correlated with any of the response latencies in the face-in-the-crowd task. Our results suggest that

amygdala responsivity to masked facial expression is differentially related to the general visual search speed for facial expression.

Neurobiologically defined threat sensitivity seems to represent an important determinant of visual scanning behavior.

++++

Killgore & Yurgelun-Todd 2004

Abstract – Cognitive Neuroimaging Laboratory, McLean Hospital/Harvard Medical School, Belmont, MA 02478, USA. william.d.killgore@us.army.mil

Activation of the amygdala and anterior cingulate during nonconscious processing of sad versus happy faces.

Previous functional neuroimaging studies have demonstrated that the amygdala activates in response to fearful faces presented below the threshold of conscious visual perception. Using a backward masking procedure similar to that of previous studies, we used functional magnetic resonance imaging (fMRI) to study the amygdala and anterior cingulate gyrus during preattentive presentations of sad and happy facial affect. Twelve healthy adult females underwent blood oxygen level dependent (BOLD) fMRI while viewing sad and happy faces, each presented for 20 ms and “masked” immediately by a neutral face for 100 ms. Masked happy faces were associated with significant bilateral activation within the anterior cingulate gyrus and amygdala, whereas masked sadness yielded only limited activation within the left anterior cingulate gyrus.

In a direct comparison, masked happy faces yielded significantly greater activation in the anterior cingulate and amygdala relative to identically masked sad faces. Conjunction analysis showed that masked affect perception, regardless of emotional valence, was associated with greater activation within the left amygdala and left anterior cingulate. Findings suggest that the

amygdala and anterior cingulate are important components of a network involved in detecting and discriminating affective information presented below the normal threshold of conscious visual perception.

++++

Burnett et al 2008

Abstract – 1University College London, UK, 2National Institutes of Health, Bethesda, MD.

Abstract In this fMRI study, we investigated the development between adolescence and adulthood of the neural processing of social emotions.

Unlike basic emotions (such as disgust and fear),

social emotions (such as guilt and embarrassment)

require the representation of another’s mental states.

Nineteen adolescents (10-18 years) and 10 adults (22-32 years) were scanned while thinking about scenarios featuring either social or basic emotions.

In both age groups, the anterior rostral medial prefrontal cortex (MPFC) was activated during social versus basic emotion.

However, adolescents activated a lateral part of the MPFC for social versus basic emotions, whereas adults did not.

Relative to adolescents, adults showed higher activity in the left temporal pole for social versus basic emotions.

These results show that, although the MPFC is activated during social emotion in both adults and adolescents, adolescents recruit anterior (MPFC) regions more than do adults, and adults recruit posterior (temporal) regions more than do adolescents.

++++

Blakemore et al 2007

Abstract – Institute of Cognitive Neuroscience, University College London, 17 Queen Square, London WC1N 3AR, UK.

In this fMRI study, we investigated the development during adolescence of the neural network underlying thinking about intentions. A total of 19 adolescent participants (aged 12.1-18.1 years), and 11 adults (aged 22.4-37.8 years), were scanned using fMRI. A factorial design was employed with between-subjects factor age group and within-subjects factor causality (intentional or physical).

In both adults and adolescents, answering questions about intentional causality vs physical causality activated the medial prefrontal cortex (PFC), superior temporal sulcus (STS), temporal poles and precuneus bordering with posterior cingulate cortex.

In addition, there was a significant interaction between group and task in the medial PFC. During intentional relative to physical causality, adolescents activated part of the medial PFC more than did adults and adults activated part of the right STS more than did adolescents.

These results suggest that the neural strategy for thinking about intentions changes between adolescence and adulthood. Although the same neural network is active, the relative roles of the different areas change, with activity moving from anterior (medial prefrontal) regions to posterior (temporal) regions with age.

++++

Vollm et al 2006

Abstract – Neuroscience and Psychiatry Unit, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK. birgit.vollm@man.ac.uk

Theory of Mind (ToM), the ability to attribute mental states to others, and empathy, the ability to infer emotional experiences, are important processes in social cognition.

Brain imaging studies in healthy subjects have described a brain system involving medial prefrontal cortex, superior temporal sulcus and temporal pole in ToM processing.

Studies investigating networks associated with empathic responding also suggest involvement of temporal and frontal lobe regions. In this fMRI study, we used a cartoon task derived from Sarfati et al. (1997) [Sarfati, Y., Hardy-Bayle, M.C., Besche, C., Widlocher, D. 1997. Attribution of intentions to others in people with schizophrenia: a non-verbal exploration with comic strips. Schizophrenia Research 25, 199-209.]with both ToM and empathy stimuli in order to allow comparison of brain activations in these two processes. Results of 13 right-handed, healthy, male volunteers were included. Functional images were acquired using a 1.5 T Phillips Gyroscan.

Our results confirmed that

ToM and empathy stimuli are associated with overlapping but distinct neuronal networks.

Common areas of activation included the

medial prefrontal cortex,

temporoparietal junction and

temporal poles.

Compared to the empathy condition, ToM stimuli revealed increased activations in

lateral orbitofrontal cortex,

middle frontal gyrus,

cuneus and

superior temporal gyrus.

Empathy, on the other hand, was associated with enhanced activations of

paracingulate,

anterior and

posterior cingulate and

amygdala.

We therefore suggest that ToM and empathy both rely on networks associated with making inferences about mental states of others.

However, empathic responding requires the additional recruitment of networks involved in emotional processing.

These results have implications for our understanding of disorders characterized by impairments of social cognition, such as autism and psychopathy.

It seems that there might be a dissociation possible between these brain areas – my suspicion that RULE LEARNING is involved with both, going bad, leading to, among other problems, BPD

++++

Kim et al 2005

Abstract – Department of Psychiatry, College of Medicine, Konyang University Hospital, 685 Gasoowon-Dong, Seo-Gu, Daejeon, Republic of Korea. cortex@konyang.ac.kr

Questions regarding the appropriateness of facial expressions in particular situations arise ubiquitously in everyday social interactions.

To determine the appropriateness of facial affect, first of all,

we should represent our own or the other’s emotional state

as induced by the social situation.

Then, based on these representations,

we should infer the possible affective response of the other person.

In this study, we identified the brain mechanism mediating special types of social evaluative judgments of facial affect in which the internal reference is related to theory of mind (ToM) processing. Many previous ToM studies have used non-emotional stimuli, but, because so much valuable social information is conveyed through nonverbal emotional channels, this investigation used emotionally salient visual materials to tap ToM. Fourteen right-handed healthy subjects volunteered for our study. We used functional magnetic resonance imaging to examine brain activation during the judgmental task for the appropriateness of facial affects as opposed to gender matching tasks.

We identified activation of a brain network, which includes

both medial frontal cortex,

left temporal pole,

left inferior frontal gyrus, and

left thalamus during the judgmental task for appropriateness of facial affect compared to the gender matching task.

The results of this study suggest that the brain system involved in ToM plays a key role in judging the appropriateness of facial affect in an emotionally laden situation.

In addition, our result supports that common neural substrates are involved in performing diverse kinds of ToM tasks irrespective of perceptual modalities and the emotional salience of test materials.

++++

den Ouden et al 2005

abstract – Institute of Cognitive Neuroscience, Department of Psychology, University College London, UK.

In this fMRI study, we investigated the convergence of underlying neural networks in thinking about a scenario involving one’s own intentional action and its consequences and setting up and holding in mind an intention to act. A factorial design was employed comprising two factors: i. Causality (intentional or physical events) and ii. Prospective Memory (present or absent). In each condition, subjects answered questions about various hypothetical scenarios, which related either to the link between the subject’s own intentions and consequential actions (Intentional Causality) or to the link between a natural, physical event and its consequences (Physical Causality). A prospective memory task was embedded in half the blocks. In this task, subjects were required to keep in mind an intention (to press a key on seeing a red stimulus background) whilst carrying out the ongoing Causality task.

Answering questions about intentional causality

versus physical causality activated a network of regions

that have traditionally been associated with Theory of Mind,

including the medial prefrontal cortex (mPFC), the superior temporal sulcus and the temporal poles bilaterally.

In addition, the

precuneus bordering with posterior cingulate cortex,

an area involved in self-awareness and self-related processing, was activated more when thinking about intentional causality.

In the prospective memory task, activations were found in the

right parietal cortex,

frontopolar cortex (BA 10) and

precuneus.

Different subregions within the

precuneus/posterior cingulate cortex

were activated in both main effects of intentional causality and prospective memory.

Therefore, the precuneus/posterior cingulate cortex

subserves separately

thinking about one’s own intentions and consequent actions

and bearing in mind an intention to make an action.

Previous studies have shown that prospective memory,

requiring the formation of an intention

and the execution of a corresponding action,

is associated with decreased activation in the dorsal mPFC,

close to the region activated in Theory of Mind tasks.

Future memory?

And of course looking at empathy has to eventually involve the self – precuneus?

Here, we found that holding in mind an intention to act

and at the same time thinking about an intentional action

led to reduced activity in a dorsal section of the mPFC.

This was a different region from a more anterior, inferior dorsal mPFC region that responded to intentional causality.

This suggests that different regions of mPFC play different roles in thinking about intentions.

++++

Saturday, July 19, 2008

Empathy and pain and mirror brain regions

“The human mirror system is formed by a cortical network composed of the rostral part of the inferior parietal lobule, by the caudal sector (pars opercularis) of the inferior frontal gyrus, as well as by parts of the premotor cortex.”  Decety & Lamm, 2006, p 1149

“…the anterior insula gets activated in response to the sight of disgusted facial expressions of others as well as by the first-hand experience of disgust [19].”  Decety & Lamm, 2006, p 1149

“…when participants are required to observe or to imitate facial expressions of various emotions, increased neurodynamic activity is detected in the superior temporal sulcus, the anterior insula, and the amygdala, as well as in areas of the premotor cortex corresponding to the representation of faces [20].”  Decety & Lamm, 2006, p 1149

+++++++++++++++++++++++++

“The first-hand experience of pain resulted in the activation of the somatosensory cortex, which encodes the sensory-discriminative dimension of a noxious (1149) stimulus such as its bodily location and intensity….[pain to self and to other]…[activated]…the anterior medial cingulate cortex (ACC), the anterior insula, and the cerebellum….”  Decety & Lamm, 2006, p 1150

“…these regions contribute to the affective and motivational processing of noxious stimuli, i.e., aspects of pain that pertain to desires, urges, or impulses to avoid or terminate a painful experience.”  Decety & Lamm, 2006, p 1150

When I go back to study Singer’s article, I will again pay attention to the fact that additional areas are activated in perception of pain to others besides the areas involved in processing pain to self

+++

Another study ( Morrison et al 2004) involving pain prick to self or watching to other…….”Both conditions resulted common hemodynamic activity in a pain-related area in the right dorsal ACC.  Common activities in response to noxious tactile and to visual stimulation were restricted to the right inferior Brodmann’s area 24b.  In contrast, the primary somatosensory cortex showed significant activations in response to noxious tactile, but not to visual, stimuli.  The different response patterns in the two areas are consistent with the ACC’s role in coding the motivational-affective dimension of pain, which is associated with the preparation of behavioral responses to aversive events.”  Decety & Lamm, 2006, p 1150

+++

shown still photographs of painful situations and imagining the level of pain produced …notably the ACC, the thalamus, and the anterior insula — activation in these regions “involved in the affective aspect of pain processing.”  Decety & Lamm, 2006, p 1150

no signal change in the somatosensory cortex

because there was no behavioral response?

Moreover, the level of activation within the ACC was strongly correlated with subjects’ ratings of pain attributed to the different situations.” Decety & Lamm, 2006, p 1150

++++

“…observation of pain can involve sensorimotor representations…in the somatosensory cortex during the perception of pain in others [22.23.24].  Decety & Lamm, 2006, p 1150

another study [26] when participants were asked to focus attention on the location of the painful stimulus there was “…increased regional cerebral blood flow in the contralateral primary somatosensory cortex.”  Decety & Lamm, 2006, p 1150

++++

“Neuroimaging studies of first-hand experience and perception of pain in others indicate a partial overlap in the ACC and anterior insula, but also in specific nonoverlapping areas belonging to the pain matrix [27] [Jackson 2006].

First-hand experience of pain is associated with more caudal activations (BA24), consistent with spinothalamic nociceptive [responds to pain or noxious stimuli] projections,

while perception of pain in others is represented in more rostral (and dorsal; BA32) regions, closer to the prefrontal pathways.

A similar rostrocaudal organization is observed in the insula, in which

pain-specific responses are observed in more medial-posterior parts,

while observation of pain leads to increases in anterior insula [28] [Ostrowsky 2006].

This pattern of activation is also consistent with data collected using direct nonpainful and painful electrical stimulation of the insular cortex in neurological patients [29] [Ostrowsky 2002].

Painful sensations could only be evoked by stimulating the posterior part of the insula,

while application of electrical currents to the anterior insula did not result in pain reports.

Interestingly, the localizations of painful and nonpainful somaesthetic stimulations overlapped considerably, indicating a nonspecific role of the insula in the first-hand experience of pain.”  Decety & Lamm, 2006, p 1150

+++++++++++++++

the neural network involved in the perception of pain in others (ACC and anterior insula) is not specific to pain processing.  This network is also implicated in disgust and more generally in situations that can put individuals at risk, and which trigger visceral and somatosensory responses.”  Decety & Lamm, 2006, p 1151

++++

“Similarly, activation in the mid-ACC in conjunction with the pre-supplementary motor area (SMA)

is not necessarily specific to the (either vicarious or first-hand) emotional experience of pain,

but is related to other processes, such as somatic monitoring, negative stimulus evaluation, and the selection of appropriate skeletomuscular movements of aversion [30] [Isomura & Takada 2004].

Thus, it seems likely that the shared neural representations in the affective-motivational part of the pain matrix are not specific to the sensory qualities of pain, but are associated with the more general survival mechanisms such as aversion and withdrawal.”  Decety & Lamm, 2006, p 1151

++++

“…when individuals are asked to adopt the perspective of others, common neural circuits are activated both for the self and the other.  However, taking the perspective of the other results in specific activation of parts of the frontal cortex that are implicated in executive control. It has been hypothesized that the role of the frontal lobes could be to hold separate perspectives, or to resist interference from one’s own perspective [36] [Decety, J. and Grezes, J. (2006) “The power of simulation:  Imagining one’s own and other’s behavior” Brain Res 1079, 4-14].”

++++

[study, imagine if someone opens bathroom door on you, or on your mother]

“Neurodynamic changes were detected in the frontopolar cortex, the ventromedial prefrontal cortex, the medial prefrontal cortex, and the right inferior parietal lobule when the participants adopted the perspective of their mother, regardless of the affective content of the situations depicted [neutral or shame, pride, etc.].  Cortical regions that are involved in emotional processing activated in the conditions that involved emotion-laden situations, including the amygdala and the temporal poles.”  Decety & Lamm, 2006, p 1151

++++

“Both the self-perspective and the other-perspective were associated with activation in the neural network involved in pain processing, including the parietal operculum, ACC, and the anterior insula.  These results reveal the similarities in neural networks representing first- and third-person information, which is consistent with the shared representations account of social interaction [38].”  Decety & Lamm, 2006, p 1152

“However, the self-perspective yielded higher pain ratings and involved the pain matrix more extensively in the secondary somatosensory cortex, the posterior part of the ACC, and the middle insula.  Thus, these results highlight important differences between the self- and other-perspectives.  For instance, while the anterior insula and the ACC are activated both when participants imagine their own and when they imagine another’s pain, the self-perspective is specifically associated with nonoverlapping clusters within the middle insula, another division of the ACC, and the right parietal cortex.”  Decety & Lamm, 2006, p 1152

++++

The self-perspective evoked stronger hemodynamic responses in brain regions involved in coding the motivational-affective dimensions of pain, including bilateral insular cortices and anterior medial cingulate cortex (aMCC).  In addition, the self-perspective was associated with stronger activation in the amygdala.  This limbic structure plays a critical role in fear-related behaviors, such as the evaluation of actual or potential threats [41].  Interestingly, the amygdala receives nociceptive information from the spino-parabrachial pain system and the insula, and its activity appears closely tied to the context and level of aversiveness of the perceived stimuli [42].  Imagining oneself to be in a painful or potentially dangerous situation thus triggers a stronger fearful and/or aversive response than imagining someone else to be in the same situation.  Alternatively and less specifically, the stronger involvement of the amygdala might also reflect a general increase of arousal evoked by imagining oneself to be in a painful situation.  Regarding the insular activation, it is worth noting that it was located in the mid-dorsal section of this area….”  Decety & Lamm, 2006, p 1152

“This part of the insula [mid-dorsal section] plays a role in coding the sensorimotor aspects of painful stimulation and it has strong connections with the basal ganglia…in which activity was also higher when adopting the self-perspective.  Taken together, activity in this portion of the insula possible reflects the simulation of the sensory aspects of the painful experience.  Such a simulation might both lead to the mobilization of motor areas (including the SMA) in order to prepare defensive or withdrawal behaviors [fight or flight], and to interoceptive monitoring associated with autonomic changes evoked by this simulation process [44].”  Decety & Lamm, 2006, p 1152

++++

There’s a photograph on p 1153

“Dissociation of activation in the anterior and middle insular cortex elicited by perspective-taking instructions.  Participants watched videos of patients undergoing painful medical treatment.  The cluster in the anterior part of the insula…whose activation irrespective of the perspective adopted by the study participants.  The cluster in the mid-insula…reflects higher signal change when participants adopted a first-person perspective as compared to adapting the perspective of the patient.  It is worth noting that both perspectives activated the anterior insula, whereas the posterior cluster was specifically associated with the self-perspective….”  Decety & Lamm, 2006, p 1153

++++

“…the right inferior parietal cortex, at the junction with the posterior temporal cortex (temporoparietal junction, TPJ), plays a critical role in comparing signals arising from self-produced actions with signals from the environment [53,54].  The TPJ is a heteromodal association cortex that integrates input from the lateral and posterior thalamus, as well as visual, auditory, somaesthetic, and limbic areas.  It has reciprocal connections to the prefrontal cortex and to the temporal lobes.  Because of these anatomical characteristics, this region is a pivotal neural locus for self-processing that is involved in multisensory body-related information processing, as well as in the processing of phenomenological and cognitive aspects of the self [55].  Damage of this cortical area can produce a variety of disorders associated with body knowledge and self-awareness….Blanke and collaborators [57] demonstrated that out-of-body experiences (i.e., the experience that one’s self is located outside of one’s own body) can be induced by electrical stimulation of the TPJ in neurological patients.”  Decety & Lamm, 2006, p 1154

+++++++++++++++

AGENCY

“…involvement of the inferior parietal lobule in the experience of agency.  Attribution of action to another agent, which crucially requires distinguishing between behavior of the self and the other, has been associated with specifically increased activity in the right inferior parietal lobe.”  Decety & Lamm, 2006, p 1154

“…being aware of causing an action was associated with activation in the anterior insula, whereas being aware of not causing the action and attributing it to another person was associated with activation in the right inferior parietal cortex.”  Decety & Lamm, 2006, p 1154  [study on driving a circle – they or the experimenter?]

“…Uddin and colleagues [61] recently demonstrated selective impairment of self-other distinction when repetitive TMS [transcranial magnetic stimulation] was applied over the right inferior parietal lobule when participants performed a perceptual task involving discrimination between self-faces and other familiar faces.  This latter study provides direct evidence for a causal role for this region in self-other discrimination.”  Decety & Lamm, 2006, p 1154

++++

“…studies on imitation have documented the involvement of right inferior parietal cortex/TPJ during reciprocal imitation in which it may be difficult to keep track of agency [62,63].  When participants imitated the other, the left TPJ was strongly engaged, whereas greater activation was detected (1154) in the right TPJ when they were being imitated…..results provide strong arguments for the implication of the right TPJ in the process of agency by demonstrating a clear dissociation between left and right TPJ.”  Decety & Lamm, 2006, p 1155

++++

“…even mental simulation of one’s own and others’ behavior recruits a similar seld-other discrimination mechanism….Both perspectives were associated with signal increases in cortical regions involved in motor representations, including the premotor and left parietal lobule.  Specific activation in the right inferior parietal cortex/TPJ was detected when participants mentally simulated actions from someone else’s perspective [64]….participants were required to imagine an action….this area is not simply involved in associating actions and their sensory consequences, but, in general, contributes to distinguishing the self from others [38,65].”  Decety & Lamm, 2006, p 1155

++++

“Such findings point to the similarity of the neural mechanisms that account for the correct attribution of actions, emotions, and thoughts to their respective agents when one mentally simulates actions or experiences emotions for oneself or for another individual….activity in the inferior parietal cortex was negatively associated with the degree of overlap between self and other, and that less self-other overlap led to increased accuracy during social perception [68].”  Decety & Lamm, 2006, p 1155
++++

“…role of the right TPJ…studies on visual attention and the detection of uncertainty and of change…it has been demonstrated that the right TPJ is specifically activated when subjects focusing their attention on a certain screen location are presented with a stimulus at a nonattended location, representing a violation of their expectancy and requiring them to redirect their attention.  Decety & Lamm, 2006, p 1155

“…right (and left) TPJs are crucial aspects of a multimodal cortical network for the detection of changes in the sensory environment.  Thus, the higher activation in the TPJ region during studies on self-other discrimination and agency might reflect the higher uncertainty associated with the often unpredictable behaviors of our conspecifics.”  Decety & Lamm, 2006, p 1155

I would think abuse drives this part of the brain into hyper or hypo drive…..

“These data also suggest that elementary computational operations performed by the TPJ contribute to higher (social) levels of social interaction.” Decety & Lamm, 2006, p 1155

++++

“Distraction is another powerful mechanism to exert attentional control, as it increases cognitive load and thus reduces the attentional resources available for stimulus perception and processing.  In everyday situations, distractive strategies might play an important role if the cost of empathizing is to high….it is well known that distraction can effectively reduce and even eliminate the personal reaction to aversive painful stimulation [78].  [like the Buddhist’s pain meditations?]  A rostral region in medial prefrontal cortex (MPFC) seems to play an important role in this modulation [79], as activation in this region during painful stimulation was considerably reduced under higher attentional workload.  In addition, the importance of the MPFC in regulating painful responses was recently corroborated by an fMRI study demonstrating that anxiety triggered by the anticipation of electric shocks is significantly reduced by the concurrent performance of a working memory task [80].”  Decety & Lamm, 2006, p 1156

++++

“…selectively focusing on specific sensory cues (such as facial expression or language prosody) conveying emotional state of another may trigger different emotional responses in the observer.…the amygdala is differentially involved when participants are instructed to attend to or to actively ignore fearful or happy faces as compared to houses [77].  Amygdala activation differed according to the valence of the facial expression and the category of the attended stimulus.  For happy faces, activity in the amygdala was greater in the attend-face than in the attend-house condition, whereas for fearful faces, activity was greater in the attend-house than in the attend-face condition.”  Decety & Lamm, 2006, p 1156 [I have the abstract for this study]

“Distraction is another powerful mechanism to exert attentional control, as it increases cognitive load and thus reduces the attentional resources available for stimulus perception and processing.  In everyday situations, distractive strategies might play an important role if the cost of empathizing is to high….it is well known that distraction can effectively reduce and even eliminate the personal reaction to aversive painful stimulation [78].  [like the Buddhist’s pain meditations?]  A rostral region in medial prefrontal cortex (MPFC) seems to play an important role in this modulation [79], as activation in this region during painful stimulation was considerably reduced under higher attentional workload.  In addition, the importance of the MPFC in regulating painful responses was recently corroborated by an fMRI study demonstrating that anxiety triggered by the anticipation of electric shocks is significantly reduced by the concurrent performance of a working memory task [80].”  Decety & Lamm, 2006, p 1156

++++

“…selectively attending to certain aspects of a painful experience can increase (i.e., up-regulate its aversiveness.  This process recruits specific functional neural networks…(1156)…focusing on the unpleasantness of noxious stimuli resulted in stronger activation in the medial pain system.  This system includes the insula and medial cingulate cortices [81] and codes the affective and motivational dimensions of pain.”  Decety & Lamm, 2006, p 1157

++++

“Recent fMRI studies have identified a limited number of regions in the anterolateral prefrontal and medial prefrontal cortices that mediate such function [generating an image of the observing self – maintaining a neutral perspective on the target] .  For instance, participants instructed to imagine being in a safe, comfortable place showed reduced behavioral and physiological markers of anxiety related to the anticipation of painful stimulation [82].  This condition was accompanied by a modulation of activation in medial prefrontal/cingulate and anterolateral prefrontal cortex. While the former [medial prefrontal/cingulate] region seems to reflect the change in affective experience evoked by the emotion regulation strategy, activation changes in the latter [anterolateral prefrontal cortex] are seen as their source, as this brain region has repeatedly been identified during emotion regulation by reappraisal.”  Decety & Lamm, 2006, p 1157

++++

“Brain activation was modulated in two subregions of the orbitofrontal cortex (OFC) and the rostral part of aMCC.  The OFC plays an important role in the evaluation of positive and negative reinforcements [83], and it is also involved in emotion reappraisal.  For instance, attending to negatively valenced pictures evokes stronger activity in ventromedial OFC than reappraising these pictures in a way that they no longer elicit a negative response [84].  Activity in the OFC may thus reflect the requirement to evaluate the overall positive and negative aspects of the presented stimuli.  Interestingly, watching effectively vs. noneffectively treated patients did neither modulate the hemodynamic activity in the visual-sensory areas nor in the insula.  This suggests that both patient groups triggered an emotional reaction and that top-down mechanisms did not operate on perceptual processing at an early stage.”  Decety & Lamm, 2006, p 1157

+++

“Overall, the capacity to regulate emotions is an important aspect of our ability to interact appropriately with other people.  The prefrontal cortex is highly differentiated in terms of cell structures (1157) and patterns of interconnectivity with other cortical subsystems….specific systems interact in generating emotion regulation.”  Decety & Lamm, 2006, p 1158

++++

“…Lamm and colleagues [39] demonstrated significantly increased activation in insular and cingulate cortices in participants with higher self-reported empathy during the observation of others in pain.”  Decety & Lamm, 2006, p 1158

++++

“…mothers viewing their offspring vs. a familiar child showed stronger response in a (para)limbic brain network and in posterior superior temporal sulcus (STS), possibly reflecting the more intense attachment that mothers have to their own offspring.”  Decety & Lamm, 2006, p 1159

++++

reward-related areas (i.e., nucleus accumbens and ventral striatum… Decety & Lamm, 2006, p 1159

++++++++++++++++++++

+++++++++++++++++++++++++++++++++++++++++

++++++++++++++++++++++++++++++++++++

need to print

from effortful control article

Reactive processes seem to originate primarily in subcortical systems (Gray, 1991)

whereas executive attention, the basis of effortful control, is believed to be situated primarily in the cortex (e.g., the anterior cingulated, lateral ventral, and prefrontal cortex; see Posner & Rothbart, 2007).

+++++

Farrow et al, 2001

“Both empathic and forgivability judgments [sic] activated left superior frontal gyrus, orbitofrontal gyrus and precuneus.  Empathic judgments also activated left anterior middle temporal and left inferior frontal gyri, while forgivability judgments activated posterior cingulate gyrus.  Empathic and forgivability judgements activate specific regions of the human brain, which we propose contribute to social cohesion.”  Farrow, abstract

++++

Ray, et al, 2008

Abstract

“…we observed that dissociative experiences are associated with slow abnormal brain waves generated in left ventrolateral frontal cortex.  Given that focal slow waves often result from depriving neural networks of major input, the present results may indicate decoupling of frontal affective processors from left cortical language areas.  This interpretation is consistent with the fact that disturbed access to structured verbal memory concerning traumatic events is a core feature of the dissociative experience.”  Ray et al 2008 abstract

if the events were never recorded in memory in the first place, it would be impossible to retrieve them in any fashion, certainly including verbally

(also, speech as an external representation as per Zelazo 2001)

++++++++++

Saturday, July 19, 2008

Decety & Lamm, 2006

+++++++++++++++

Important to remember that empathy is a social psychological concept that does not necessarily correspond to neuronal processes….. Decety & Lamm, 2006, p 1149

Empathy is the ability to experience and understand what others feel without confusion between oneself and others.”  Decety & Lamm, 2006, p 1146

interesting, considering the contagion aspects, when one person is sad and pupil shrinks and the other perceives this and then their pupil mimics and shrinks also

“In this paper, we articulate evidence from social psychology and cognitive neuroscience, and argue that empathy involves both emotion sharing (bottom-up information processing) and executive control to regulate and modulate this experience (top-down information processing), underpinned by specific and interacting neural systems.”  Decety & Lamm, 2006, p 1146

Interesting reference to bottom up and top down, which is what I have been saying about my book – in this case, the emotion sharing part would be the bottom-up, a source of information that is personal, while perhaps other books are written from the top-down information processing model that is based on executive control, i.e. what they know based on reading, studies, guesses, etc.

“Furthermore, awareness of a distinction between the experiences of the self and others constitutes a crucial aspect of empathy.”  Decety & Lamm, 2006, p 1146

This makes me wonder about the importance/relevance on research about body awareness, etc.

Perception of pain in others – neurological processes

…highlight the role of different neural mechanisms that underpin the experience of empathy, including emotion sharing, perspective taking, and emotion regulation.”  Decety & Lamm, 2006, p 1146

I say that I don’t think I have the experience of empathy, which I would think connects to ToM – I am numb here, like I don’t have the capacity to feel this or feel being connected to others – is that the sharing part, or the perspective taking part – AND the regulation part?  I guess, must read on….

Empathy:

“sense of similarity between the feelings one experiences and those expressed by others….

an interaction between any two individuals, with one experiencing and sharing the feeling of the other.  Yet, the

sharing of feelings is not sufficient to elicit empathy.  Many scholars view

empathy as an other-oriented social emotion….

the social and emotional situations that elicit empathy can become quite complex depending on the feelings experienced by the observer and the relationship of the target to the observer….studies have documented that

empathy plays a central role in moral reasoning, motivates prosocial behaviors, and inhibits aggression toward others….

Empathic concern is defined as an emotional reaction characterized by such feelings as compassion, tenderness, softheartedness, and sympathy.” Decety & Lamm, 2006, p 1146

+++++++++++

TABLE 1

Various Definitions of Empathy*

+ the ability to put oneself into the mental shoes of another person to understand his or her emotions and feelings [a form of simulation, or inner imitation] [4]

+ A complex form of psychological inference in which observation, memory, knowledge, and reasoning are combined to yield insights into the thoughts and feelings of others [5]

how is this different from theory of mind?

+ An affective response more appropriate to someone else’s situation than to one’s own [6]

+ An other-oriented emotional response congruent with the other’s perceived welfare [7]

+ An affective response that stems from the apprehension or comprehension of another’s emotional state or condition, and which is similar to what the other person is feeling or would be expected to feel in the given situation [8]

*Note that these definitions point to an emotional experience that is more congruent with another’s situation than with one’s own.  Another important aspect of the construct of empathy is that it must involve some self-other differentiation, which makes it distinct from related reactions such as emotional contagion and personal distress

++++  Decety & Lamm, 2006, p 1147

I have the info from that child study on empathy, probably applies with this

Reading this now, I don’t think I have empathy.  I know earlier in my life I certainly thought I did – how much of this is connected to even caring, or having the extra resources available to care about another – I don’t know where empathy leaves off and compassion begins.

And how is it different from theory of mind?

++++

task of social neuroscience is to bridge evolutionary, cognitive neuroscience and social psychology  Decety & Lamm, 2006, p 1147

Overarching conceptual framework:

“…accounts for a sense of similarity in the feelings experienced by self and other (such translations go both ways, from other-to-self and from self-to-other), without confusion between the two agents.

“The experience of empathy often (but not always) results in sympathy (concern for another based on the apprehension or comprehension of the other’s emotional sate or condition), although it also can lead to

empathic overarousal (or personal distress, an aversive, self-focused emotional reaction to the apprehension or comprehension of another’s emotional state or condition).

Seems to me that this is about projection, possibly working the other way around where one takes on into themselves aspects of  the other person/situation that is not theirs, probably activating defense mechanisms or “short circuits”

Our model of empathy involves both bottom-up and top-down information processing.  Furthermore, it combines representational aspects, i.e., memories that are localized in distributed neural networks that encode information and, when temporarily activated, enable access to this stored information, as well as processes, i.e., computational procedures that are localized and are independent of the nature or modality of the stimulus that is being processed.  Decety & Lamm, 2006, p 1147

Seems to me that these are the perfect bifurcation points for the entry of unresolved traumas, trauma memories and their reenactments – like worm holes between parallel universes of past and present, where time boundaries slip away

Just like empathy requires that one know the self-other parameters, it might well require also the past-present parameters, the TIME parameters, the when as well as the who and the what.

It seems understandably likely that those of us who cannot process empathy properly would seek and find others like ourselves because of our “sameness”

Processing empathy normally is not normal for us.  Our normalcy is NOT being able to process empathy

I also suppose that if one looks at the initial operation of an infant’s opioid system’s functioning, that empathy is the process that makes it all work – the infant is hungry, the mother empathizes and feeds it and all is well!

I would also want to know how emotions like fear, triggered in the interactions we have with one another, send the process off in other directions.

This is all stuff I need to know because it so affects my life.  When I am done, and if I do it right, people will flock to buy the book because it will help them, as well.  Like, the main reason my mother couldn’t mother me was because her empathy capacity was broken!  Maybe that’s the same reason Ernie can’t empathize with me – because I don’t think he can – and it makes me sad.  That doesn’t change the fact that I miss him – uniquely him.

But I have to write this, anyway…trying to see that there’s a rightness and a necessity to my having to be without him.

++++++++

EVOLUTIONARY ROOTS OF EMPATHY

“Preston and de Waal [9] convincingly argued that empathy is not an all-or-nothing phenomenon, and many intermediate forms of empathy exist between the extremes of mere agitation at the distress of another and full understanding of their predicament.”  Decety & Lamm, 2006, p 1147

comparative psychologists

“…empathy as a kind of induction process by which emotions, both positive and negative, are shared, and by which the probabilities of similar behaviors are increased in the observers.”  Decety & Lamm, 2006, p 1147

probabilities of what?  The emotions as behaviors or some other kind of not specified behaviors?  What if the emotions cannot be shared by the other, as in my mother’s case?  Are these kinds of people automatically eliminated from consideration like the 3 subjects in Harrison’s study because they score negatively?  Does that make these people like ANTI-MATTER transmitters when around empathy issues?

WHAT IF?  What if their emotional circuits aren’t working right, their emitters aren’t working right, their receivers are broken along with their translators?

“While certain nonhuman primates may share feelings between individuals, humans are uniquely able to intentionally feel for and act on behalf of other people whose experiences may differ greatly from their own [3].  Such a capacity may help to explain why empathic concern is often associated with prosocial behaviors such as helping akin, and has been considered crucial for altruism.”  Decety & Lamm, 2006, p 1147

What about when bottlenose dolphins save humans from sharks?  In New Zealand, the swam circles around 4 people for 40 minutes until the shark lost interest and left so the people could get to shore. And August 2007 in Monterey when a surfer was saved from am attacking great white shark?  Is this an intentional altruistic action on the part of the dolphins?  We don’t know, can we ask them?  Is it a mothering instinct, where the dolphins females?  There are over 50 reported incidents of dolphins saving humans.

“Evolutionary biologists suggest that empathic helping behavior has evolved because of its contribution to genetic fitness (kin selection).  Decety & Lamm, 2006, p 1147

mothering

“In humans and other mammals, an (1147) impulse to care for offspring is almost certainly genetically hard wired.”  Decety & Lamm, 2006, p 1148

I have this info in the evolutionary article on well being

“The emergence of altruism, of empathizing with and caring for those who are not kin, is not easily explained within the framework of neo-Darwinian theories of natural selection, and thus social learning explanations of kinship patterns in human helping behavior are highly plausible.  Indeed, one of the most striking aspects of human empathy is that it can be felt for virtually any target, even targets of a different species.” Decety & Lamm, 2006, p 1148

Why must we be so exclusive rather than inclusive in our thinking?  Obviously dolphins can feel it and act on it – it is NOT unique to humans.  We see and believe what we want to.

This would also match up with the Chinese biophysics position on cooperation and communication within the holistic entity/organism of life, not just about competition, or even mainly about it.

“hypothesis that advanced levels of social cognition may have arisen as an emergent property of powerful executive functioning assisted by the representational properties of language [11]…these higher levels operate on previous levels of organization, and should not be seen as independent or conflicting with one another.”  Decety & Lamm, 2006, p 1148

What if the foundation is faulty???

“ Evolution has constructed layers of increasing complexity, from nonrepresentational to representational and metarepresentational mechanisms, which need to be taken into account for a full understanding of human empathy.  Decety & Lamm, 2006, p 1148

Representations, in this context, are defined as parallel distributed patterns of activation that reliably fire in response to a given stimulus.  These neural networks encode information and, when temporarily activated, enable access to this stored information.”  Decety & Lamm, 2006, p 1148

Representations – involving access to stored information – what about trauma memories that are either strictly implicit, or just not processed due to PTSD mechanisms?

+++++++++

From table:

Interrelated levels of information processes involved in empathy

Bottom-up….direct matching between perception and action – automatically activated unless inhibited by perpetual input = emotion sharing “which leads to implicit recognition that others are like us.” Decety & Lamm, 2006, p 1148

Top-down…..regulation and control

++++++++++++++

“…social psychological concepts, such as empathy, do not necessarily correspond to neuronal processes. Decety & Lamm, 2006, p 1149

SHARED NEURAL CIRCUITS BETWEEN SELF AND OTHER

“Prosocial behaviors may abound due to synchronizing representations between self and other.”  Decety & Lamm, 2006, p 1149

“The initial component that precedes empathy draws on the somatic mimicry also known as emotion contagion, i.e., the tendency to automatically mimic and synchronize facial expressions [see below, also known as the chameleon effect], vocalizations, postures, and movements with those of another person, and consequently to converge emotionally [13].”  Decety & Lamm, 2006, p 1149

When a caregiver cannot do this with an infant, for example, when they are preoccupied with another time and place or even with their emotions in the present so that they are not responding to the infant as a separate self, or cannot go the extra mile with an infant which is to STAGE and EXAGERATE THEATRICALLY the mimic of the infant’s state –things in the infant’s brain do not get built right – as Schore describes.

Research shows that people automatically are triggered by others’ facial expressions to respond with mimic expressions on their own faces, even without conscious (nonconscious – implicit – automatic) “recognition of the stimulus.”  Decety & Lamm, 2006, p 1149

Speculation that this ability evolved to help us communicate

“…leading to more smooth interactions and increased liking….people with higher levels of dispositional empathy [don’t forget, this is not about dispositional, this is about how the brain was MADE!] show this so-called chameleon effect to a greater extent.”  Decety & Lamm, 2006, p 1149

“It has also been demonstrated that nonconscious behavioral mimicry increases affiliation, which serves to foster relationships with others [16].”  Decety & Lamm, 2006, p 1149

This is what I was writing about in pupil size notes……if we weren’t given the ability to do this, it keeps us isolated and alone – and also interferes with our own ability to communicate, first of all, with our own self….

It would also seem to me that this mimicry also in some way preserves the status quo and moderates expectations so that we remain more equal somehow in our interactions.

But what happens when people fall out of this normal range for one reason or another?  Say excess of creativity or intelligence even, so that they are outside the normal range?  Cultures and societies attempt to keep this cohesiveness – maybe coherency?  Does it keep things in systems from becoming too chaotic?  From changing too fast?

This would be tied to moderation and modulation

“The human mirror system is formed by a cortical network composed of the rostral part of the inferior parietal lobule, by the caudal sector (pars opercularis) of the inferior frontal gyrus, as well as by parts of the premotor cortex.”  Decety & Lamm, 2006, p 1149

This is “…an automatic perception-action mechanism” which “has adaptive value for the survival of individuals.”  Decety & Lamm, 2006, p 1149

“…observing fearful body expressions not only produces increased activity in brain areas associated with emotional processes, but also in areas linked with representation of action and movement [18].  Thus, the mechanism of fear contagion automatically prepares the brain for action.”  Decety & Lamm, 2006, p 1149

Evidence is mounting “…that similar neural circuits are stimulated when humans experience emotions and when they perceive others expressing emotions.  For instance, the anterior insula gets activated in response to the sight of disgusted facial expressions of others as well as by the first-hand experience of disgust [19].”  Decety & Lamm, 2006, p 1149

This also has to be tied to attachment disorders such as the “detached” parent not only does not express their own emotions, but does not notice and respond to the infant’s emotions either.

It also must be involved when depressed people do not see happy people’s signals —  and then not in their infant’s either.

“One fMRI experiment demonstrates that when participants are required to observe or to imitate facial expressions of various emotions, increased neurodynamic activity is detected in the superior temporal sulcus, the anterior insula, and the amygdala, as well as in areas of the premotor cortex corresponding to the representation of faces [20].”  Decety & Lamm, 2006, p 1149

“Another study showed that the observation of everyday hand and face actions performed with an emotion

recruits regions involved in the perception and the experience of emotion and/or communication [21].”  Decety & Lamm, 2006, p 1149

“The authors of that study speculate that,

in addition to inducing resonance in the motor program necessary to execute an action,

watching an action performed with emotion

induces a resonance in the emotional system

responsible for the affective modulation of the motor program.

Such a mechanism could also be a key to understanding how the other person feels and to his or her associated intentions.”  Decety & Lamm, 2006, p 1149

+++++++++++++

action-perception coupling mechanisms

pain

The action-perception coupling mechanisms apparent in emotion contagion also seems to contribute to our ability to perceive and understand others’ pain.”  Decety & Lamm, 2006, p 1149

“…brain areas implicated in processing the affective and motivational aspects of pain mediate the observation of pain in others.”  Decety & Lamm, 2006, p 1149

I have this study — Singer 2004 study

“The first-hand experience of pain resulted in the activation of the somatosensory cortex, which encodes the sensory-discriminative dimension of a noxious (1149) stimulus such as its bodily location and intensity….[pain to self and to other]…[activated]…the anterior medial cingulate cortex (ACC), the anterior insula, and the cerebellum….”  Decety & Lamm, 2006, p 1150

“…these regions contribute to the affective and motivational processing of noxious stimuli, i.e., aspects of pain that pertain to desires, urges, or impulses to avoid or terminate a painful experience.”  Decety & Lamm, 2006, p 1150

When I go back to study Singer’s article, I will again pay attention to the fact that additional areas are activated in perception of pain to others besides the areas involved in processing pain to self

I thought they also said that there were no mirror neurons in one of the responding brain regions

Another study ( Morrison et al 2004) involving pain prick to self or watching to other…….”Both conditions resulted common hemodynamic activity in a pain-related area in the right dorsal ACC.  Common activities in response to noxious tactile and to visual stimulation were restricted to the right inferior Brodmann’s area 24b.  In contrast, the primary somatosensory cortex showed significant activations in response to noxious tactile, but not to visual, stimuli.  The different response patterns in the two areas are consistent with the ACC’s role in coding the motivational-affective dimension of pain, which is associated with the preparation of behavioral responses to aversive events.”  Decety & Lamm, 2006, p 1150

++

shown still photographs of painful situations and imagining the level of pain produced …notably the ACC, the thalamus, and the anterior insula — activation in these regions “involved in the affective aspect of pain processing.”  Decety & Lamm, 2006, p 1150

no signal change in the somatosensory cortex

because there was no behavioral response?

Is it possible that no possibility of escape creates this same inactivation of the somatosensory cortex over time – or in times of dissociation/freeze?

“Moreover, the level of activation within the ACC was strongly correlated with subjects’ ratings of pain attributed to the different situations.” Decety & Lamm, 2006, p 1150

++++

“…observation of pain can involve sensorimotor representations…in the somatosensory cortex during the perception of pain in others [22.23.24].  Decety & Lamm, 2006, p 1150

another study [26] when participants were asked to focus attention on the location of the painful stimulus there was “…increased regional cerebral blood flow in the contralateral primary somatosensory cortex.”  Decety & Lamm, 2006, p 1150 – pain to their own hand, not someone else’s

this makes me think about mother beating me –what parts of her brain were working and which ones weren’t?  I doubt she was focusing on my pain

Yet is seems to be a given that borderlines have a very high pain threshold, so the part of her brain that should have registered my pain was perhaps not able to – related to the fact that she could not feel her own

I still wonder if there’s a point where someone just has too much pain and literally dissociates from it – as any animal will if severely wounded and in the freeze response – when endogenous opioids kick in as a part of the stress response so they don’t feel the pain????

++

“Current evidence thus suggests that merely observing another individual in a painful situation yields pain-related responses in the neural network associated with the coding of the motivational-affective dimension of pain in oneself, and may include the somatosensory cortex….”  Decety & Lamm, 2006, p 1150

what if this is where the dissociation occurs, between the affective dimension of the pain, which is intolerable and overwhelming – and the motivational aspect which came from being completely helpless (without adequate ability to compete, be competent, utilize an active coping skill) to get away from the pain – escape – or to fight back.

If you can’t fight or run, you freeze – and an uncompleted trauma cycle leads to dissociation, I think

“The finding of a strong overlap between first-hand experiences of pain and the perception of pain in others seems to suggest total congruence between self and other phenomenal experience.  However, this assumption is superficial, as we do not literally feel the pain of others in such situations.”  Decety & Lamm, 2006, p 1150

“Neuroimaging studies of first-hand experience and perception of pain in others indicate a partial overlap in the ACC and anterior insula, but also in specific nonoverlapping areas belonging to the pain matrix [27] [Jackson 2006].

First-hand experience of pain is associated with more caudal activations (BA24), consistent with spinothalamic nociceptive [responds to pain or noxious stimuli] projections,

while perception of pain in others is represented in more rostral (and dorsal; BA32) regions, closer to the prefrontal pathways.

A similar rostrocaudal organization is observed in the insula, in which

pain-specific responses are observed in more medial-posterior parts,

while observation of pain leads to increases in anterior insula [28] [Ostrowsky 2006].

This pattern of activation is also consistent with data collected using direct nonpainful and painful electrical stimulation of the insular cortex in neurological patients [29] [Ostrowsky 2002].

Painful sensations could only be evoked by stimulating the posterior part of the insula,

while application of electrical currents to the anterior insula did not result in pain reports.

Interestingly, the localizations of painful and nonpainful somaesthetic stimulations overlapped considerably, indicating a nonspecific role of the insula in the first-hand experience of pain.”  Decety & Lamm, 2006, p 1150

+++++++++++++++

“…the neural network involved in the perception of pain in others (ACC and anterior insula) is not specific to pain processing.  This network is also implicated in disgust and more generally in situations that can put individuals at risk, and which trigger visceral and somatosensory responses.”  Decety & Lamm, 2006, p 1151

Might this also be tied to borderline, that mother couldn’t tell when she put me at risk, maybe because in a borderline’s brain – as with self injury and suicide – there is something not working right in the risk part of the brain?

++++

“Similarly, activation in the mid-ACC in conjunction with the pre-supplementary motor area (SMA)

is not necessarily specific to the (either vicarious or first-hand) emotional experience of pain,

but is related to other processes, such as somatic monitoring, negative stimulus evaluation, and the selection of appropriate skeletomuscular movements of aversion [30] [Isomura & Takada 2004].

Thus, it seems likely that the shared neural representations in the affective-motivational part of the pain matrix

are not specific to the sensory qualities of pain, but

are associated with the more general survival mechanisms such as aversion and withdrawal.”  Decety & Lamm, 2006, p 1151

My point exactly, that when a child’s system is overwhelmed with unbearable pain and there is no survival mechanism possible except freeze/dissociate, and no possibility of acting against the aversion or withdrawing – or fighting, something has to happen in these networks. I think the brain goes in a different direction, and that this adaptation is appropriate considering the nature of the trauma

Again, that what we might call a “bad” phenotype is a good one.

++++++++++++++++++++++++++++++++

PERSPECTIVE TAKING AND EMPATHY

“By means of imagination, we come to experience sensations, which are generally similar to, although typically weaker than, those of the other person.”  Decety & Lamm, 2006, p 1151

This capacity to engage in role taking has been theoretically linked to the development of empathy, moral reasoning, and more generally, prosocial behavior.”  Decety & Lamm, 2006, p 1151

This naturally makes me think of trauma dramas and reenactments.

Interesting to find that this might be one of the basic neural substrates of the human brain.

Unlike the motor mimicry and emotional contagion aspect of empathy, perspective taking develops later, possibly because it heavily draws on the maturation of executive resources (i.e., the processes that serve to monitor and control thought and actions, including self-regulation, planning, cognitive flexibility, response inhibition, and resistance to interference) of the prefrontal cortex, which continues to mature from birth to adolescence.”  Decety & Lamm, 2006, p 1151

and, boy, can there be troubles with this one!

development of self and other mental state understanding

interesting – so this sounds like a circle thought – development of self, self being a mental state, is just one of many – all influencing one another every step of the way

interactive, choose your own ending and your own process, but everything effects everything else

“…the development of self and other mental state understanding is functionally linked to that of executive functions [31, 32] [ 32 is Zelazo 2004 The development of conscious control in childhood, Trends Cogn. Sci 8, 12-17]”  Decety & Lamm, 2006, p 1151

“There is increasingly clear evidence of a specific developmental link between theory-of-mind development and improved self-control at around the age of 4 [33] [Perner, J. and Lang, B. (1999) Development of theory of mind and executive control.  Trends Cogn Sci, 3, 337-344].”  Decety & Lamm, 2006, p 1151

contribution of executive functions, especially inhibitory control

“Perspective-taking ability allows us to overcome our usual egocentrism, tailor our behaviors to others’ expectations, and thus make satisfying interpersonal relations possible [35].”  Decety & Lamm, 2006, p 1151

“…when individuals are asked to adopt the perspective of others, common neural circuits are activated both for the self and the other.  However, taking the perspective of the other results in specific activation of parts of the frontal cortex that are implicated in executive control. It has been hypothesized that the role of the frontal lobes could be to hold separate perspectives, or to resist interference from one’s own perspective [36] [Decety, J. and Grezes, J. (2006) “The power of simulation:  Imagining one’s own and other’s behavior” Brain Res 1079, 4-14].”  Decety & Lamm, 2006, p 1151

++++

[study, imagine if someone opens bathroom door on you, or on your mother] [37] [Ruby, P. and Decety, J. (2004) How would you feel versus how do you think she would feel?  A neuroimaging study of perspective taking with social emotions.  J. Cogn. Neurosci, 19, 988-999]

“Neurodynamic changes were detected in the frontopolar cortex, the ventromedial prefrontal cortex, the medial prefrontal cortex, and the right inferior parietal lobule when the participants adopted the perspective of their mother, regardless of the affective content of the situations depicted [neutral or shame, pride, etc.].  Cortical regions that are involved in emotional processing activated in the conditions that involved emotion-laden situations, including the amygdala and the temporal poles.”  Decety & Lamm, 2006, p 1151

++

another study

“Both the self-perspective and the other-perspective were associated with activation in the neural network involved in pain processing, including the parietal operculum, ACC, and the anterior insula.  These results reveal the similarities in neural networks representing first- and third-person information, which is consistent with the shared representations account of social interaction [38].”  Decety & Lamm, 2006, p 1152

“However, the self-perspective yielded higher pain ratings and involved the pain matrix more extensively in the secondary somatosensory cortex, the posterior part of the ACC, and the middle insula.  Thus, these results highlight important differences between the self- and other-perspectives.  For instance, while the anterior insula and the ACC are activated both when participants imagine their own and when they imagine another’s pain, the self-perspective is specifically associated with nonoverlapping clusters within the middle insula, another division of the ACC, and the right parietal cortex.”  Decety & Lamm, 2006, p 1152

++

imagine the other and imagine oneself.

“…the former may evoke empathic concern (defined as an other-oriented response congruent with the perceived distress of the person in need),

while the latter induces both empathic concern and personal distress (i.e., a self-oriented aversive emotional response such as anxiety or discomfort).

If perceiving another person in an emotionally or physically painful circumstance elicits personal distress, then the observer may tend not to attend fully to the other’s experience and as a result lack sympathetic behaviors.”  Decety & Lamm, 2006, p 1152

Boy, does this implicate a lot!!

++++

Sunday, July 20, 2008

++++

“…the distinction between empathic concern and personal distress….demonstrated that depending on the adopted perspective, observing other people in pain will trigger either empathic concern or personal distress….this other- vs. self-oriented response engages distinct neural networks.”  Decety & Lamm, 2006, p 1152

“…projecting oneself [“imagine self”] into an aversive situation leads to higher personal distress and lower empathic concern, while focusing on the emotional and behavioral reactions of another’s [“imagine other”] plight is accompanied by higher empathic concern and lower personal distress….”  Decety & Lamm, 2006, p 1152

This is the way it is supposed to work.  But what if a situation triggers unresolved past memories which then transplant themselves into the present, and then the watcher is suddenly immersed in their own version of the pain which overrides concern for the other, or even awareness of the other’s pain?

“The self-perspective evoked stronger hemodynamic responses in brain regions involved in coding the motivational-affective dimensions of pain, including bilateral insular cortices and anterior medial cingulate cortex (aMCC).  In addition, the self-perspective was associated with stronger activation in the amygdala.  This limbic structure plays a critical role in fear-related behaviors, such as the evaluation of actual or potential threats [41].  Interestingly, the amygdala receives nociceptive information from the spino-parabrachial pain system and the insula, and its activity appears closely tied to the context and level of aversiveness of the perceived stimuli [42].  Imagining oneself to be in a painful or potentially dangerous situation thus triggers a stronger fearful and/or aversive response than imagining someone else to be in the same situation.  Alternatively and less specifically, the stronger involvement of the amygdala might also reflect a general increase of arousal evoked by imagining oneself to be in a painful situation.  Regarding the insular activation, it is worth noting that it was located in the mid-dorsal section of this area….”  Decety & Lamm, 2006, p 1152

++++

“This part of the insula [mid-dorsal section] plays a role in coding the sensorimotor aspects of painful stimulation and it has strong connections with the basal ganglia…in which activity was also higher when adopting the self-perspective.  Taken together, activity in this portion of the insula possible reflects the simulation of the sensory aspects of the painful experience.  Such a simulation might both lead to the mobilization of motor areas (including the SMA) in order to prepare defensive or withdrawal behaviors [fight or flight], and to interoceptive monitoring associated with autonomic changes evoked by this simulation process [44].”  Decety & Lamm, 2006, p 1152

+++

“…similarities in affective representations of self and other, stemming from shared neural circuits that can be activated by the act of perspective taking.  These data also fit neatly with simulation theory, which states that behavior can be simulated by activating the same neural resources for acting and perceiving [45,46].  However, there are also some important differences in the activated neural systems involved in first-and third-person perspectives, which run counter to the suggestion of a complete merging between self and other.  In the case of perception of pain in others, executive control may be necessary to inhibit distress experienced by the self and allow for the full, though nonegocentric and self-regulated, consideration of the other’s situation.”  Decety & Lamm, 2006, p 1153

If there are flaws with the executive control mechanism, the distress of self is not modulated and the concern for the other cannot become activated, I would guess

This also makes me wonder about pruned neurons in adolescence – the don’t use will lose neuronal death – less gray matter, ineffective cortical involvement – can’t use this ability, don’t develop it, vicious cycle

++++

SELF-OTHER AWARENESS AND EMPATHY

“Given commensurability between self and other action representations,

whether these representations are activated through bottom-up processing (emotion sharing) or when adopting the subjective perspective of another individual,

self-awareness and the sense of being an agent constitute key additional processes that are necessary for successful social interactions.”  Decety & Lamm, 2006, p 1153

“The prerequisite for social communication, including the experience of empathy, is that the two agents can preserve their individuality.  Social cognition relies both on similarities and differences between individuals.”  Decety & Lamm, 2006, p 1153

“…in the case of emotion sharing, a complete overlap between self and other representations would induce emotional distress (a self-oriented aversive (1153) emotional response), or empathic overarousal, which is not the goal of empathy [7].”  Decety & Lamm, 2006, p 1154

this has massive implications for parenting, brain building

“In fact, in the experience of empathy, individuals must be able to disentangle their own feelings from the feelings shared with others to attribute mental states to the target.  Self-awareness is a necessary condition for making inference about the mental states in others [47].”  Decety & Lamm, 2006, p 1154

I just read the theory of mind article that articulates important aspects of the process of acquiring a tom

++++

“…”agency” is a crucial aspect for successfully navigating shared representations between self and other….

agency plays a pivotal role in cognitive development, including the first stage of self-awareness (or pretheoretical experience of one’s own mentality), which scaffolds theory of mind capacities [51]

…..the ability to recognize oneself as the agent of a behavior is the way one builds as an entity independent from the external world [52].

In the case of empathy, affective sharing must be modulated and monitored by the sense of whose feelings belong to whom [36], and thus,

agency is a crucial aspect that enables a selfless regard for the other rather than a selfish desire to escape aversive arousal.”  Decety & Lamm, 2006, p 1154

wow, this is really at the core….I sense such a value judgment in this last sentence, is that just me?  When one considers how complex the process really is to get this agency, and considers how vulnerable we are to all the forces – all of the out of our control – that determine if we get an adequate self or we don’t.

I would read “selfish” as absolutely desperate to survive unsurvivable circumstances in a malevolent environment.  This is the crucial “place” for all future brain development, the place that determines who and how we are going to be in the world for the rest of our lives.  It is built into the brain.

Sense of whose feelings belong to whom – this is built on the assumption that we literally even know what time it is – is this not only about the other person, but is it about the present or the past or both?  It must be a key place for dissociation to occur, and for memory to intervene and obliterate any chance of obtaining this supposedly “higher” selfless perspective

Oh, dear!

It is inaccurate to use the word “selfish” in this context.  Selfish assumes that there is a SELF!  This is about the absence of even having a self.  If a person has agency that means that they have a self.  Otherwise, selfish is being used inaccurately.  It is the absence of self, which came from having no agency, that created the problem of not being “self-less” in the first place.

You have to have something before you can set it aside, choose to disregard it, or give it away – really to have any informed choices built on agency in the first place.

I read arrogance in that last sentence, and a total and complete lack of appreciation and gratitude for having a self in the first place on the part of writers who write such trash!

They are the haves, not the have-nots.  They don’t appreciate this, don’t realize it, don’t value it, and then turn around and call us names like SELFISH!  Shame on them!  Shame on you, Decety and Lamm!

If you are going to condemn us, at least recognize that we are the condemned from birth!  Our self, our agency, our lives have been robbed from us.  We will never have what you have, and what you take so for granted.  Do you think this is about divine right?  That you somehow deserved to have agency and a self so you can choose to be self-less while we never even had this chance?

Yes, I feel scathing.  THIS is what writing from the bottom and not from the top is all about.  It is a sort of revolution that leads to revelation, like turning the tables in a card game.  Let me write from THIS perspective, the perspective of not having agency – or from having to guess what that is.

When I make choices I don’t make them with the same coherent background, or in or with the same benevolent brain.  I have to work all the harder (you up there cannot imagine) to get anything right!

++++++++++++++

“…the right inferior parietal cortex, at the junction with the posterior temporal cortex (temporoparietal junction, TPJ), plays a critical role in comparing signals arising from self-produced actions with signals from the environment [53,54].  The TPJ is a heteromodal association cortex that integrates input from the lateral and posterior thalamus, as well as visual, auditory, somaesthetic, and limbic areas.  It has reciprocal connections to the prefrontal cortex and to the temporal lobes.  Because of these anatomical characteristics, this region is a pivotal neural locus for self-processing that is involved in multisensory body-related information processing, as well as in the processing of phenomenological and cognitive aspects of the self [55].  Damage of this cortical area can produce a variety of disorders associated with body knowledge and self-awareness….Blanke and collaborators [57] demonstrated that out-of-body experiences (i.e., the experience that one’s self is located outside of one’s own body) [they had no control of their bodies actions, no sense of being able to see their “other” body – not the same thing as OBE] can be induced by electrical stimulation of the TPJ in neurological patients.”  Decety & Lamm, 2006, p 1154

++++

AGENCY

“…involvement of the inferior parietal lobule in the experience of agency.  Attribution of action to another agent, which crucially requires distinguishing between behavior of the self and the other, has been associated with specifically increased activity in the right inferior parietal lobe.”  Decety & Lamm, 2006, p 1154

“…being aware of causing an action was associated with activation in the anterior insula, whereas being aware of not causing the action and attributing it to another person was associated with activation in the right inferior parietal cortex.”  Decety & Lamm, 2006, p 1154  [study on driving a circle – they or the experimenter?]

“…Uddin and colleagues [61] recently demonstrated selective impairment of self-other distinction when repetitive TMS [transcranial magnetic stimulation] was applied over the right inferior parietal lobule when participants performed a perceptual task involving discrimination between self-faces and other familiar faces.  This latter study provides direct evidence for a causal role for this region in self-other discrimination.”  Decety & Lamm, 2006, p 1154

++++

“…studies on imitation have documented the involvement of right inferior parietal cortex/TPJ during reciprocal imitation in which it may be difficult to keep track of agency [62,63].  When participants imitated the other, the left TPJ was strongly engaged, whereas greater activation was detected (1154) in the right TPJ when they were being imitated…..results provide strong arguments for the implication of the right TPJ in the process of agency by demonstrating a clear dissociation between left and right TPJ.”  Decety & Lamm, 2006, p 1155

++++

“…even mental simulation of one’s own and others’ behavior recruits a similar self-other discrimination mechanism….Both perspectives were associated with signal increases in cortical regions involved in motor representations, including the premotor and left parietal lobule.  Specific activation in the right inferior parietal cortex/TPJ was detected when participants mentally simulated actions from someone else’s perspective [64]….participants were required to imagine an action….this area is not simply involved in associating actions and their sensory consequences, but, in general, contributes to distinguishing the self from others [38,65].”  Decety & Lamm, 2006, p 1155

++++

“….this region is also involved in empathy [36] and in theory of mind, i.e. the awareness that others like the self possess mental states that can be similar or different from oneself [66,67].  For instance, the right TPJ is specifically involved when participants imagine how another person would feel in everyday-life situations that elicit social emotions [37] or in painful experiences, but not when they imagine these situations for themselves [27,39].  Decety & Lamm, 2006, p 1155

++++

“Such findings point to the similarity of the neural mechanisms that account for the correct attribution of actions, emotions, and thoughts to their respective agents when one mentally simulates actions or experiences emotions for oneself or for another individual….activity in the inferior parietal cortex was negatively associated with the degree of overlap between self and other, and that less self-other overlap led to increased accuracy during social perception [68].”  Decety & Lamm, 2006, p 1155
++++

“…role of the right TPJ…studies on visual attention and the detection of uncertainty and of change…it has been demonstrated that the right TPJ is specifically activated when subjects focusing their attention on a certain screen location are presented with a stimulus at a nonattended location, representing a violation of their expectancy and requiring them to redirect their attention.  Decety & Lamm, 2006, p 1155

“…right (and left) TPJs are crucial aspects of a multimodal cortical network for the detection of changes in the sensory environment.  Thus, the higher activation in the TPJ region during studies on self-other discrimination and agency might reflect the higher uncertainty associated with the often unpredictable behaviors of our conspecifics.”  Decety & Lamm, 2006, p 1155

I would think abuse drives this part of the brain into hyper or hypo drive…..

“These data also suggest that elementary computational operations performed by the TPJ contribute to higher (social) levels of social interaction.” Decety & Lamm, 2006, p 1155

++++

summary

“To sum up, self-awareness and the sense of agency play pivotal roles in empathy and significantly contribute to social interaction.  These important aspects are likely to be at play in distinguishing emotional contagion, which heavily relies on the automatic link between perception of the emotions expressed by the other and one’s own experience of the same emotion, and empathy that necessitates a more detached relation.  We suggest that the nonoverlap in the neural response between self and other frees up processing capacity in the brain for unfolding appropriate future action towards the other.  Further, being aware of one’s own feelings, and being able to regulate consciously one’s own emotions may be what allows us to distinguish empathic responses to others from our own personal distress, with only the former leading to prosocial behavior.”  Decety & Lamm, 2006, p 1155

It is important to note that these functions happen in areas that Schore specifically describes as damaged in malevolent early brain-building circumstances

This description elucidates how that early brain formation will disturb long range functioning of an individual.  No amount of magical thinking on anyone’s part is going to change this fact.

It’s like holding onto both ends of a piece of string, one end being birth and infant brain-building experiences, and the other one being the adult consequences.  Passage of time will not repair the structural and operational damages that happened early.  No magic to this, only predictable and understandable logical consequences. What went wrong IS wrong.

++++

EMOTION REGULATION

Emotion regulation construct:  “…defined as the process of initiating, avoiding, inhibiting, maintaining, or modulating  the occurrence, form, intensity, or duration of internal feeling states, emotion-related physiological processes, emotion-related goals, and/or behavioral concomitants of emotion, generally in the service of accomplishing one’s goal [72].”  Decety & Lamm, 2006, p 1156

Distress

Emotion regulation is also important for modulation of one’s own vicarious emotion so that it is not experienced as aversive….emotion regulation positively relates to feelings of concern for the other person [73].  In contrast, people who experience their emotions intensely, especially negative emotions, are prone to personal distress, i.e., an aversive emotional reaction, such as anxiety or discomfort based on the recognition of another’s emotional state or condition [74].  Emotional distress may shift priorities toward the immediate present and therefore promotes a short-term focus; for instance, feeling better and getting relief from a painful situation, which may be in conflict with a motivation to feel for the other.  In the case of empathy, the best response to other’s distress may not be distress, but efforts to soothe that distress.”  Decety & Lamm, 2006, p 1156

this ties in with feeling distressed when others might feel just stressed

shifting priorities in the immediate present – what about when the way past trauma is right there in the present – so the focus really is on the past – like preoccupied styles

or avoidant, avoiding the feelings all together

++

In our model of empathy, we consider that emotion regulation, under voluntary control (top-down processing), which taps into executive function resources, operates in conjunction with other neural mechanisms to carry out specific cognitive and emotional computations required for the experience of feelings for the other.  Such computations include the selection of appropriate response and the inhibition of other less-appropriate responses.” Decety & Lamm, 2006, p 1156

+++

“Cognitive top-down mechanisms can either function to down-regulate (i.e., reduce) or up-regulate (i.e., promote) emotions.  Although down-regulation seems to be more prevalent in the case of empathy, both processes play an important role when responding to others in need.  In the case of perception of others in pain, the ability for down-regulation of emotion is prominent if the distress of the target becomes overwhelming for the observer.”  Decety & Lamm, 2006, p 1156

too often for insecure attachment, the down-regulation is defensive – especially in personality disorders

CHANGE

They are actually advocating conscious control in which a person intentionally utilizes aspects of insecure attachment styles, like shifting attention and being preoccupied elsewhere, being detached

“Various strategies have been identified to regulate emotions by means of top-down cognitive control [75].  Heuristically, these processes have been arranged on a continuum from attentional control to cognitive change [76].  While attentional control mainly affects the type and the amount of sensory information that is perceived and, hence, processed by the observer, cognitive change strategies predominantly tap into re-evaluating or reappraising external or internal affective information.”  Decety & Lamm, 2006, p 1156

is it possible for these to be any other than Band-Aid solutions when the damage is in the structure of the brain and nervous system?

+++

this is interesting in light of my language processing disabilities – I think the hearing and the visual share some circuitry, so that if I am in an emotional state I cannot hear the words – am assessing the emotional component of the face and prosody instead – can’t do all at the same time

“…selectively focusing on specific sensory cues (such as facial expression or language prosody) conveying emotional state of another may trigger different emotional responses in the observer.…the amygdala is differentially involved when participants are instructed to attend to or to actively ignore fearful or happy faces as compared to houses [77].  Amygdala activation differed according to the valence of the facial expression and the category of the attended stimulus.  For happy faces, activity in the amygdala was greater in the attend-face than in the attend-house condition, whereas for fearful faces, activity was greater in the attend-house than in the attend-face condition.”  Decety & Lamm, 2006, p 1156 [I have the abstract for this study]

“Distraction is another powerful mechanism to exert attentional control, as it increases cognitive load and thus reduces the attentional resources available for stimulus perception and processing.  In everyday situations, distractive strategies might play an important role if the cost of empathizing is to high….it is well known that distraction can effectively reduce and even eliminate the personal reaction to aversive painful stimulation [78].  [like the Buddhist’s pain meditations?]  A rostral region in medial prefrontal cortex (MPFC) seems to play an important role in this modulation [79], as activation in this region during painful stimulation was considerably reduced under higher attentional workload.  In addition, the importance of the MPFC in regulating painful responses was recently corroborated by an fMRI study demonstrating that anxiety triggered by the anticipation of electric shocks is significantly reduced by the concurrent performance of a working memory task [80].”  Decety & Lamm, 2006, p 1156

this must tie in with the article on attentional blindness

we use all kinds of “addictions” to distract ourselves – also that OCD from evolution article is about the reward rather than motivational system – if we can distract ourselves from distressing emotions then what we use to do that must become a rewarding activity for us

it all takes energy resources!

++++

“…selectively attending to certain aspects of a painful experience can increase (i.e., up-regulate its aversiveness.  This process recruits specific functional neural networks…(1156)…focusing on the unpleasantness of noxious stimuli resulted in stronger activation in the medial pain system.  This system includes the insula and medial cingulate cortices [81] and codes the affective and motivational dimensions of pain.”  Decety & Lamm, 2006, p 1157

++++++++++

“Cognitive change strategies are an alternative and/or complementary way to regulate emotions.  Denying the relevance of an emotion-eliciting stimulus is an example for such a strategy.  Taking a detached observer position by consciously or unconsciously generating an image of the observing self is known to reduce the subjective experience of anxiety, sympathetic arousal, and pain reactivity.  Such a detachment likely plays an important role in empathy in order to maintain a neutral perspective on the target; for example, in the interaction between a psychotherapist and his or her client.”  Decety & Lamm, 2006, p 1157

How is this different from dissociating?

Also, reminds me of the FUNCTIONAL EMPATHY perspective in that other article

Also, what about beta-blockers they give therapists before they go into war zones?  What are they doing in the process of emotional regulation?

++

“Recent fMRI studies have identified a limited number of regions in the anterolateral prefrontal and medial prefrontal cortices that mediate such function [generating an image of the observing self – maintaining a neutral perspective on the target] .  For instance, participants instructed to imagine being in a safe, comfortable place showed reduced behavioral and physiological markers of anxiety related to the anticipation of painful stimulation [82].  This condition was accompanied by a modulation of activation in medial prefrontal/cingulate and anterolateral prefrontal cortex. While the former [medial prefrontal/cingulate] region seems to reflect the change in affective experience evoked by the emotion regulation strategy, activation changes in the latter [anterolateral prefrontal cortex] are seen as their source, as this brain region has repeatedly been identified during emotion regulation by reappraisal.”  Decety & Lamm, 2006, p 1157

+++

emotion reappraisal

“Emotion reappraisal involves reinterpreting the valence [good or bad] of a stimulus in order to change the way in which we respond to it.  It can either be intentionally achieved (e.g., in the attempt to react differently than usual to another’s distress) or it can be based on additional external information provided about the emotion-eliciting stimulus.”  Decety & Lamm, 2006, p 1157

cognitive appraisal

I would relate to informed compassion!?!

“Brain activation was modulated in two subregions of the orbitofrontal cortex (OFC) and the rostral part of aMCC.  The OFC plays an important role in the evaluation of positive and negative reinforcements [83], and it is also involved in emotion reappraisal.  For instance, attending to negatively valenced pictures evokes stronger activity in ventromedial OFC than reappraising these pictures in a way that they no longer elicit a negative response [84].  Activity in the OFC may thus reflect the requirement to evaluate the overall positive and negative aspects of the presented stimuli.  Interestingly, watching effectively vs. noneffectively treated patients did neither modulate the hemodynamic activity in the visual-sensory areas nor in the insula.  This suggests that both patient groups triggered an emotional reaction and that top-down mechanisms did not operate on perceptual processing at an early stage.”  Decety & Lamm, 2006, p 1157

++

“Overall, the capacity to regulate emotions is an important aspect of our ability to interact appropriately with other people.  The prefrontal cortex is highly differentiated in terms of cell structures (1157) and patterns of interconnectivity with other cortical subsystems….specific systems interact in generating emotion regulation.”  Decety & Lamm, 2006, p 1158

++++

MODULATION OF EMPATHY

Interesting concept – I would think one would be lucky to just have it at all!

“…empathy partly relies on bottom-up information processing, which is automatic and unconscious….”  Decety & Lamm, 2006, p 1158

empathy costs

“….we do not always respond in prosocial ways.  This seems to be counterintuitive to lay conceptions that consider empathy as an automatic response that should be promoted without restrictions.  However, despite the obvious advantages of understanding another person’s thoughts and feelings, empathy does not come without costs [85].  Besides, empathy has evolved as an in-group phenomena [9].  Several intra-and interpersonal factors have been identified that facilitate or inhibit the occurrence and the degree of empathic responses, and thus allow modulation of their associated expenses.”  Decety & Lamm, 2006, p 1158

“…neural mechanisms underlying such modulations.  Background affective state, prior experience with a situation, and the ability to cope with the distress of others (which relies, among others, on emotion regulation capabilities) are just a few examples of various intrapersonal factors that can impact the experience of empathy.”  Decety & Lamm, 2006, p 1158

“…induced emotional states affect the ability of observers to recognize the facial display of emotion [86].  Depressive mood is also known to affect our perception of the world, including the expression of emotions by others [including happy signals in others – and in infants]…” Decety & Lamm, 2006, p 1158

“…potential neural substrates of such a modulation.  Limbic structures such as the amygdala and the nucleus accumbens became hyperactive when participants with pediatric bipolar disorder attended to the facial expression of emotion.  Similarly, patients with generalized social phobia…show increased amygdala activation when exposed to angry or contemptuous faces [87]….emotional priming (i.e., the brief presentation of negatively or positively valenced stimuli before presenting a target stimulus) enhances early visual processing in normal volunteers [88].  This, in turn, might affect the visual perception of emotional cues, such as the subtle changes in the facial expression of emotion.”  Decety & Lamm, 2006, p 1158

“Prior experience is another factor that affects our emotional resonance with others.”  Decety & Lamm, 2006, p 1158

“…Lamm and colleagues [39] demonstrated significantly increased activation in insular and cingulate cortices in participants with higher self-reported empathy during the observation of others in pain.”  Decety & Lamm, 2006, p 1158

++++

“…mothers viewing their offspring vs. a familiar child showed stronger response in a (para)limbic brain network and in posterior superior temporal sulcus (STS), possibly reflecting the more intense attachment that mothers have to their own offspring.”  Decety & Lamm, 2006, p 1159

++++

competitive vs cooperation

“…affective dispositions, or attitudes, differ depending on whether the other is seen as a competitor or a cooperator, and in turn influence whether we react with a congruent or a  noncongruent emotion to another’s affect.”  Decety & Lamm, 2006, p 1159

“Lanzetta and coworkers [94,95] investigated the psychophysiological, behavioral, and psychological effects of attitudes on interpersonal interaction.  Their main finding is that competitive relationships lead to asymmetric affective (counterempathic) responses, while cooperative settings result in symmetric vicarious emotions.  For instance, psychophysiological measures indicated that participants reacted to a painful shock of competitors with little arousal and distress, but got distressed when seeing them in joy.  The reverse pattern was obtained for cooperators.  These findings reflect an important and often ignored aspect of empathy, namely that this ability can also be used in a malevolent way as when knowledge about the emotional or cognitive state of competitors is used to harm them….”  Decety & Lamm, 2006, p 1159

My mother was like this with me and I wrote a year ago about this, that she viewed me as a competitor, for what I don’t really know

“…neural correlates of such counterempathinc responding.  Singer and colleagues [91]….observing fair players replicated earlier findings of increased activation in brain areas coding the affective aspect of pain, such as the anterior insula and medial/anterior cingulate cortex.  Of particular interest, activation in these brain regions was significantly reduced when participants in the scanner observed unfair players in pain.  This effect, however, was detected in male participants only, who also showed a concurrent increase of activation in reward-related areas (i.e., nucleus accumbens and ventral striatum).  The specific reduction of activity in the neural network processing the affective dimension of pain is in contrast with the results with the results from the neuroimaging studies that investigated the modulation of affective responses (vicarious or direct) to pain by means of emotion regulation…different mechanisms are at play when empathy is modulated due to inter- or intrapersonal factors.  Liking/disliking somebody might determine whether an affective empathic response is generated at all, while responding to the distress of neutral others might require regulation of an evoked emotional response.”  Decety & Lamm, 2006, p 1159

+++

conclusion

“…adopting a self-perspective when observing others in pain results in stronger feelings of personal distress and activates the pain matrix to a larger extent, as well as the amygdala.  Such a complete self-other merging seems to be detrimental to empathic concern.  Indeed, the best response to another person’s plight may not be distress, but efforts to soothe that distress.  Conversely, when participants take the other’s perspective, there is less overlap between the neural circuits involved in the processing of first-hand experience of pain, and they indeed report more feelings of empathic concern…it can be concluded that empathy relies both on bottom-up information processing (shared neural systems between first-hand emotional experience and the perception or imagination of the other’s experience), as well as top-down information processing that allows modulation and self-regulation.  Without self regulation, information processing would lose flexibility and would become primarily bound to external stimulations.”  Decety & Lamm, 2006, p 1160

++++

Thursday, July 17, 2008

Harrison et al, 2007

++++

“Communication of affective and motivational signals between individuals guides adaptive social behavior.  Arguably, visual cues expressed on our faces represent the most salient of these emotional signals….psychological and neural mechanisms that support the processing of emotional facial expressions…research in affective neuroscience….implicate discrete, partially overlapping, neural substrates for processing facial emotional signals observed in others….explicit facial expressions generated through the (voluntary or automatic) action of the facial musculature….” Harrison et al, 2007, 724

set of core motor expressions that have the same affective meaning and are “fundamental” across cultures and societies……………….paraphrasing Harrison et al, 2007, 724

there are “autonomic responses” that “also contribute to affective communication, where information conveyed or betrayed by facial autonomic changes may indicate specific emotional states…..Many autonomic facial signals are identifiable across species and have evolutionary origins in homeostatic control mechanisms (Darwin, 1872).  [ The expression of the emotions in man and animals, London, Murray]  Harrison et al, 2007, 724

amygdala

superior temporal sulcus

automatic signals

“nonmuscular aspects of facial expression”

“influence the perception of another’s emotional state”  Harrison et al, 2007, 724

“Emotional arousal, regardless of valence” Harrison et al, 2007, 724

[good or bad attributions/observations]

observed pupil size, is “an exclusively autonomic facial physiological signal”  Harrison et al, 2007, 724

“influences the perceived intensity and valence of expression of sadness (Harrison, 2006)”  Harrison et al, 2007, 724

Harrison, N.A., Singer, T., Rotshtein, P., Dolan, RlJl, Critchley, H.D. (2206).  Pupillary contagion:  Central mechanisms engaged in sadness processing.  Social Cognitive and Affective Neuroscience, 1, 5-17

I probably should get this one, not sure yet

“We also demonstrated that this interaction between pupil size and (facial muscular) expression induces corresponding “contagious” pupil response in the viewer.”  Harrison et al, 2007, 724

note:  as in other article, this is not the mirror neuron system if this is empathy, need to compare brain regions specified in each article

“…we showed these effects to be associated with neural activity changes in regions that process salient social cues, including amygdala and superior temporal sulcus.”  Harrison et al, 2007, 724

they found that pupil size  only influenced specifically the emotion perception of sadness

Harrison et al, 2007, 724

  1. “…pupil size was not observed to modulate ratings of the perceived intensity and valence of neutral, happy, or angry facial expressions.”  Harrison et al, 2007, 725   They are not saying in this sentence anything about the pure recognition of the existence of sadness or any other of the emotions, just mentioning intensity and valence/value

“Expression, perception, communication and even contagion of emotional signals contribute to adaptive social behavior and empathic understanding of others’ emotional states (De Vignemont, in press).”  Harrison et al, 2007, 725

empathic understanding – expression, perception, communication, contagion of emotional signals

adaptive social behavior – this must include mothering!

“…in clinical disorders of empathy, including autism and psychopathy, deficits in discriminatory identification of facial expressions may be subtle (Dolan & Fullman, 2006; Grossman, Klin, Carter, & Vokmar, 2000), indicating a need for more objective, perhaps nonlinguistic, indices of empathy.  Thus, individuals who score highly on personality measures of emotional empathy are more sensitive to subliminally presented emotional face stimuli (Martin, Berry, Dobranski, & Horne, 1996) and show enhanced mimicry and contagion of emotional facial (muscular expressions (Sonnby-Borgstrom, 2002).  No study to date has examined whether personality measures of empathy also correlate with sensitivity to facial autonomic signals, yet our previous study demonstrated a specific mirroring of pupil size in the context of perceived sadness.”   Harrison et al, 2007, 725

I wish they would include some kind of attachment measurement in their studies.  I would certainly think that those who are more sensitive might rank higher as securely attached which would mean that their limbic emotional structures have been more perfectly formed.

Happy

Angry

Neutral

Sad

Fear

Disgust

Surprise

“…clinical need for an objective index of emotional empathy, we examine the relationship between the affective sensitivity to pupil size and individual differences in social emotional behavior, which we measured using the Mehbrabian Balanced Emotional Empathy Score (BEES; Mehrabian, & Epstein, 1972).”  Harrison et al, 2007, 725

18 female, 15 male, screened for neurological or psychiatric illnesses

color digital photographs of faces

sad

fearful

disgusted

surprised

rated:

intensity

valence (good or bad)

attractiveness  Harrison et al, 2007, 725

“We also tested how Interindividual differences in emotional sensitivity to pupil size (in the context of sadness) related to scores on a rating scale of emotional empathy.  Subjects who scored negatively on the BEES were excluded from this analysis (3 subjects).´ Harrison et al, 2007, 726

“…whether high empathy was associated with a sensitivity to an increase or decrease in pupil size was explored.”  Harrison et al, 2007, 726  [31 subjects from earlier study, Harrison et al., 2006]

RESULTS

“The size of pupils incidentally perceive on the face stimuli size modulated the ratings of emotional facial expression….across all four emotional expressions and three pupil sizes for ratings of emotional intensity showed a significant main effect of pupil size…with faces with small pupils rated as more intense.”  Harrison et al, 2007, 726

“Notably, there was also a significant interaction between pupil size and emotional (facial muscular) expression, driven by effects of pupil size in the context of sad facial expression….Subjects rated facial expressions of sadness with small pupils as significantly more intense…so that decreasing pupil size linearly modulated ratings of perceived intensity….Observed pupil size did not affect intensity ratings for expressions of fear…or surprise….However both large…and small…pupil areas were rated as significantly more intense than midsized pupils in expression of disgust….”  Harrison et al, 2007, 726

“When judging the emotional valence of facial expressions, there was no significant main effect of pupil size.”  Harrison et al, 2007, 726

“There was a trend in the interaction between pupil size and emotional expression…again driven by effects of pupil size on sadness ratings.”  Harrison et al, 2007, 726

“Analysis of the effects of observed pupil size on ratings of specific emotional expressions confirmed our previous findings that sad face stimuli with small…pupils are also rated as significantly more negative…than sad face stimuli with large…pupils.”  Harrison et al, 2007, 726

“Observed pupil size in facial expressions of fear, surprise, and disgust had no effect on valence ratings….It is noteworthy that, at debriefing, subjects reported a lack of awareness of differences in pupil size across the stimuli when explicitly questioned.”  Harrison et al, 2007, 726  [so this was an implicit reaction]

correlation with empathy scores

“Subjects who were more sensitive to changes in pupil size in the context of sadness were rated as having significantly higher empathy scores on ratings of intensity of emotional expression…valency ratings…and a composite score combining both ratings.”  Harrison et al, 2007, 726

“….significant predictive relationship between scores on the BEES and sensitivity to a reduction in pupil size….”  Harrison et al, 2007, 726

discussion

“This study confirmed a salient influence of pupil size on the processing of sad expressions and showed that individual differences in the magnitude of this effect reflect differences in empathy score.”  Harrison et al, 2007, 726

“These data complement an earlier investigation describing a selective effect of pupil size on sadness perception that did not occur when viewing happy, angry, or neutral facial expressions [in Harrison 2006 earlier investigation]….The present study extends these observations to all “basic” emotional facial expressions by examining the influence of pupil on perception of fear, disgust, and surprise.  The further finding that emotional sensitivity to pupil size in the context of sadness predicts an individual’s empathy score is noteworthy.”  Harrison et al, 2007, 726

“In an earlier study, we showed an automatic unconscious mirroring of pupil size in the context of sad expressions, present even when attention was directed at nonemotional aspects of faces, where the observer’s pupil constricts more when viewing small pupils on a sad face than when viewing larger pupils (no such mimicry of pupil size accompanies perception of happy, angry, or neutral faces; Harrison et al, 2006).  Harrison et al, 2007, 726

“Together, these observations reinforce the notion that effective communication of emotional feelings engages visceral autonomic reactions underlying feeling states.  [I don’t know how they can generalize past just sad emotional feelings based on these studies – the other feelings do not generate this effect]’”  Harrison et al, 2007, 726

“Speculatively, these automatic responses provide a potential basis for the development of objective (and perhaps nonlinguistic) screening tools for disorders of emotional empathy, such as autism and psychopathy.”  Harrison et al, 2007, 726

attachment disorders, other personality disorders, too

“Our findings provide further empirical validation for emotional specificity of patterns of autonomic physiological responses….”  Harrison et al, 2007, 726

“Emotional specificity of physiological responses across individuals has remained surprisingly contentious, particularly when (276) measuring single autonomic responses….Nevertheless, despite high individual variability, there is increasing empirical evidence for patterned autonomic responses associated with different emotional states in humans ….[lists refs]….In addition, autonomic responses have evolved as salient signals for the perception and recognition of emotions (Darwin, 1872):  Thus, psychophysiological changes in the face, such as flushing in anger or blanching in fear, may contribute to signaling an individual’s emotional state.”  Harrison et al, 2007, 727

“Why pupil size is salient only for expressions of sadness remains unclear….central contribution of the eye region to successful recognition of facial expressions of sadness.  Nevertheless, pupillary changes are subtle, vary with ambient light, and may only be perceived at close range.  However, sadness is an affiliative emotion that can draw individuals together and inhibit interpersonal conflict (Blair, 2001).  Speculatively, the communication of sadness intensity through pupil size may have evolved to act over short distances, in contrast to emotions such as anger, which may lead to the “withdrawal” of the observing party.”  Harrison et al, 2007, 728

FEAR

Sympathetic arousal

“The visual signaling and perception of fear is also linked to perception of the eyes, in particular the sclerae (whites of the eyes).  It was therefore surprising to find no effect of pupil size on intensity or valence ratings for fearful facial expressions.  Moreover, fear is associated with sympathetic arousal, which causes both pupillary dilatation and eyelid retraction (Adolphs & Tranel, 2004) and perhaps also facial vasoconstriction.  Hence, we anticipated that perceived (sympathetic) pupillary dilatation would enhance ratings of fearful expressions.  The fact that we did not observe this effect perhaps emphasizes the degree of organ specificity within emotion-specific autonomic responses patterns.  Alternatively, it may indicate a redundancy of pupillary arousal responses in a context where other facial signs of sympathetic arousal predominate.”  Harrison et al, 2007, 728

are they saying that sadness is a sympathetic arousal?  I wish they specified that here

small and large, but not medium pupil size affected “the perceived intensity of disgust facial expressions”  Harrison et al, 2007, 728

“Perhaps the most clinically relevant finding is the correlation between an individual’s tendency to respond empathically and the same individual’s sensitivity to pupillary signals…. Harrison et al, 2007, 728

“Heuristically, enhanced sensitivity to socially salient signals is anticipated in more empathic individuals.  Indeed, subjects who score highly on the rating scales of emotional empathy have reduced visual thresholds for identifying emotional expressions presented for brief periods (Martin et al., 1996) and show the strongest degree of automatic mimicry (in their facial muscles) of observed facial emotional expressions …. [has refs here]”  Harrison et al, 2007, 728

“The mechanism that specifically links empathy ratings to enhanced sensitivity to pupils during sadness perception remains a topic for future empirical studies.  It is, however, noteworthy that the identification of sadness in others is selectively impaired in psychopaths (Blair, Colledge, Murray, & Mitchell, 2001; Dolarn & Fullam, 2006) and in normal individuals after the administration of propranolol, a drug that blocks peripheral and central beta-adrenergic receptors (Harmer, Perrett, Cowen, & Goodwin, 2001).  Harrison et al, 2007, 729

beta blockers?

“In summary, reduced pupil size, perceived without conscious awareness, selectively enhances the subjective intensity and negativity attributed to sad facial expressions.  Individual differences in the extent to which pupils influence sadness perception reflect, or predict, individual differences in emotional empathy score.  Together, these observations highlight the existence of emotion-specific autonomic signal in affective communication that may potentially contribute to screening tools for clinical disorders of empathy.”  Harrison et al, 2007, 729

++++++++++++++++++++++++++

Chakrabarti, Bullmore & Baron-Cohen 2006b

Abstract – Department of Psychiatry, University of Cambridge, Cambridge, Cambridgeshire, UK. bc249@cam.ac.uk

Empathizing is a quantitative trait involving understanding another’s mental state (including their emotion) and responding to this with an appropriate emotion. A reliable, behaviorally validated self-report questionnaire measure of this is the Empathy Quotient (EQ), which is continuously distributed across the general population. The “discrete emotions” model posits that each “basic” emotion has a relatively independent evolutionary antecedent and social-communicative function and is subserved by a discrete neural system. In this study, we investigate if and how empathy influences the perception of basic emotions. Twenty-five volunteers (13 female, 12 male) selected across Empathy Quotient (EQ space participated in a correlational design 3T fMRI study. The stimuli were presented in a box-car design, where 5 blocks (each containing 4 video clips of any one of happy, sad, angry, disgust or neutral expressions from different actors) and a low-level baseline were presented in pseudo-random order. Using an exploratory analysis,

we found different brain regions correlated with Empathy Quotient (EQ, depending on which emotion was being perceived.

In particular, the ventral striatal response to happy faces correlated positively with EQ,

while the ventral striatal response to sad faces was negatively correlated with EQ.

The precuneus and lateral prefrontal cortical response to angry faces correlated positively with EQ.

The response of the insula and the superior temporal gyrus cortex to disgust faces were negatively correlated with EQ.

These results are discussed in the light of the postulated evolutionary function of each emotion. Using a hypothesis-driven conjunction analysis, we found that a region in the left dorsal inferior frontal gyrus/premotor cortex was positively correlated to the EQ across all four emotions. This region could therefore constitute a biomarker for trait empathy across emotions.

We conclude that there are common regions underlying empathy across different emotions, and there are regions that show an emotion-specific correlation with empathy. This pattern of results is interpreted using a modification of Haxby et al.’s model of face perception.

++++

Nomi et al 2008

Abstract – Department of Neurology, University Hospital Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany. seitz@neurologie.uni-duesseldorf.de.

Human emotional expressions serve an important communicatory role allowing the rapid transmission of valence information among individuals. We aimed at exploring the neural networks mediating the recognition of and empathy with human facial expressions of emotion. METHODS: A principal component analysis was applied to event-related functional magnetic imaging (fMRI) data of 14 right-handed healthy volunteers (29 +/- 6 years). During scanning, subjects viewed happy, sad and neutral face expressions in the following conditions: emotion recognition, empathizing with emotion, and a control condition of simple object detection. Functionally relevant principal components (PCs) were identified by planned comparisons at an alpha level of p < 0.001. RESULTS: Four PCs revealed significant differences in variance patterns of the conditions, thereby revealing

distinct neural networks:

mediating facial identification (PC 1),

identification of an expressed emotion (PC 2),

attention to an expressed emotion (PC 12), and

sense of an emotional state (PC 27). CONCLUSION: Our findings further the notion that the

appraisal of human facial expressions involves

multiple neural circuits that process highly differentiated cognitive aspects of emotion.

++++

++++++++

Friday, July 18, 2008

Pupil size comments

I just finished watching “I Am Legend,” and it struck me that as alone as Will Smith was in that movie, I am always that alone.  Those of us whose brains do not process the recognition of emotional communication in the normal way are sealed off from being human and will never truly know what it would be like to join as a member of our species.

It is one thing for researchers to stack and pile up the numbers, but they can never describe this from the inside.

I can be around people in the body, be with their bodies, but I always alone.  Maybe everyone always is alone, but there is something so special and unique about being able to communicate with one another that we as humans can forget how alone we really are.

I spent thousands and thousands of hours alone as a child with the monster lurking, never far away.  She controlled all access to me, except at school, but the time I was there was like a frozen time; already I was so alone everywhere, but nobody knew it.

I have spent most of my adult life not knowing how alone I am, too.  It is as if the pretend walls of contact have tipped over like dominoes and fallen away, and it is clear in all directions around me that I am alone.  Everything that has to do with people is in another world, like the Mexican party music I can hear tonight from the other side of the wall.  I am not there.  That is not my place.  Another country.  And me, a species of one.

Our brains were created in that void and for that void, as if there never would be another human so there was no way to develop the brain one needs to be with others.  My brain had no way to know that this isolation would ever end.  The brain can’t just build itself for the hopeful chance that someday it would be able to connect to someone else.  That’s not how it works……

If a brain is built in a void of violence, that IS all it will ever know – at least intimately, on a feeling level.  There’s no magic to this brain building process.  What you get is what you get, like a strange deviant prize out of a cracker jack box.  There’s no turning it in for a new one, no trading.

I guess I have to physically be this alone right now so that I can know what I know.  A tiny ship set out to sea, nobody visible in sight all the way out to the circle of horizon.

++++++++++++++++

There is no magic wand.  Magic thinking is not going to change anything.  The reality of our condition is created in our bodies.  Our nervous system developed without the proper contact with another (or other) humans.  The brain is a part of the nervous system.

Because our nervous system including our ANS and brain were built this way, and because nothing can change it, we will always be alone even when we are with others.  No matter how “healthy” a mate I might have, I can never feel that connection.  So maybe that’s why I say, “Why bother?  It doesn’t matter who I try to be in relationship with, it really won’t make any difference in the end, or even in the middle.”

This gives a perpetual edge to everything I do.  It is present when I am alone and when I am in the presence of another.  My brain cannot connect to another, like a cord with the plug permanently severed, cut off.  This makes being with others a distraction and a disturbance of what is normal for us – being alone.  That is our normal state.

Do not believe that this being alone is necessarily a pleasant experience.  It creates a sense of unreality of the world, as if it is a dream, and reality of being alone is like being in a prison, the prison of life.  We are imprisoned, alone, in our bodies and have been since the moment of our birth.  The construction and operation of our brains reflect this reality.

There is no trust built into our brains.  If anyone ever shows us affection, we will not be able to truly recognize and experience, we will not trust this, either.  The part of our brains that was supposed to evolve to tell us who to trust and who not to trust, did not develop.  People around us, who do have their communication equipment relatively intact, must be able to sense this about us, that we have some debilitation in regard to being able to communicate fluently with them.  They must sense that we cannot “hear” them, and they must sense that they cannot get through to us.  I don’t think this endears us to them.  It can lead to such a subtle (sometimes it’s obvious) form of shunning that nobody can even see it without sophisticated camera equipment.  It is about the kind of nearly instantaneous signal transmission patterns that he identifies as occurring between infants and mothers.

I think it can lead to children being picked on without anyone knowing why.  It can leave us being rejected and abandoned, and we don’t know why.  We are like our own species, but nobody tells us the facts.  It’s a part of our suffering, and it’s time we figured it out.  It’s no different than the lesion primates in the compounds ….

+++++++++++++++++++

+++++++++++++++++++++++++

Harrison et al, 2007

Communication of affective and motivational signals between individuals guides adaptive social behavior” Harrison et al, 2007, 724

It guides it from birth.  Infant’s attempt to meet their needs by interacting with their caregivers to the best of their capabilities from birth – even if that first communication is only to be a cry.  Nature has carved a niche in motherly biological reactions throughout evolution so that their signal for assistance is not met with disregard.

“Arguably, visual cues expressed on our faces represent the most salient of these emotional signals….psychological and neural mechanisms that support the processing of emotional facial expressions…research in affective neuroscience….implicate discrete, partially overlapping, neural substrates for processing facial emotional signals observed in others….explicit facial expressions generated through the (voluntary or automatic) action of the facial musculature….” Harrison et al, 2007, 724

set of core motor expressions that have the same affective meaning and are “fundamental” across cultures and societies……………….paraphrasing Harrison et al, 2007, 724

there are “autonomic responses” that “also contribute to affective communication, where information conveyed or betrayed by facial autonomic changes may indicate specific emotional states…..Many autonomic facial signals are identifiable across species and have evolutionary origins in homeostatic control mechanisms (Darwin, 1872).  [ The expression of the emotions in man and animals, London, Murray]  Harrison et al, 2007, 724

amygdala

superior temporal sulcus

automatic signals

“nonmuscular aspects of facial expression”

“influence the perception of another’s emotional state”  Harrison et al, 2007, 724

“Emotional arousal, regardless of valence” Harrison et al, 2007, 724

[good or bad attributions/observations]

observed pupil size, is “an exclusively autonomic facial physiological signal”  Harrison et al, 2007, 724

“influences the perceived intensity and valence of expression of sadness (Harrison, 2006)”  Harrison et al, 2007, 724

Harrison, N.A., Singer, T., Rotshtein, P., Dolan, RlJl, Critchley, H.D. (2206).  Pupillary contagion:  Central mechanisms engaged in sadness processing.  Social Cognitive and Affective Neuroscience, 1, 5-17

I probably should get this one, not sure yet

“We also demonstrated that this interaction between pupil size and (facial muscular) expression induces corresponding “contagious” pupil response in the viewer.”  Harrison et al, 2007, 724

note:  as in other article, this is not the mirror neuron system if this is empathy, need to compare brain regions specified in each article

“…we showed these effects to be associated with neural activity changes in regions that process salient social cues, including amygdala and superior temporal sulcus.”  Harrison et al, 2007, 724

they found that pupil size  only influenced specifically the emotion perception of sadness

Harrison et al, 2007, 724

  1. “…pupil size was not observed to modulate ratings of the perceived intensity and valence of neutral, happy, or angry facial expressions.”  Harrison et al, 2007, 725   They are not saying in this sentence anything about the pure recognition of the existence of sadness or any other of the emotions, just mentioning intensity and valence/value

“Expression, perception, communication and even contagion of emotional signals contribute to adaptive social behavior and empathic understanding of others’ emotional states (De Vignemont, in press).”  Harrison et al, 2007, 725

empathic understanding – expression, perception, communication, contagion of emotional signals

adaptive social behavior – this must include mothering!

“…in clinical disorders of empathy, including autism and psychopathy, deficits in discriminatory identification of facial expressions may be subtle (Dolan & Fullman, 2006; Grossman, Klin, Carter, & Vokmar, 2000), indicating a need for more objective, perhaps nonlinguistic, indices of empathy.  Thus, individuals who score highly on personality measures of emotional empathy are more sensitive to subliminally presented emotional face stimuli (Martin, Berry, Dobranski, & Horne, 1996) and show enhanced mimicry and contagion of emotional facial (muscular expressions (Sonnby-Borgstrom, 2002).  No study to date has examined whether personality measures of empathy also correlate with sensitivity to facial autonomic signals, yet our previous study demonstrated a specific mirroring of pupil size in the context of perceived sadness.”   Harrison et al, 2007, 725

I wish they would include some kind of attachment measurement in their studies.  I would certainly think that those who are more sensitive might rank higher as securely attached which would mean that their limbic emotional structures have been more perfectly formed.

Happy

Angry

Neutral

Sad

Fear

Disgust

Surprise

“…clinical need for an objective index of emotional empathy, we examine the relationship between the affective sensitivity to pupil size and individual differences in social emotional behavior, which we measured using the Mehbrabian Balanced Emotional Empathy Score (BEES; Mehrabian, & Epstein, 1972).”  Harrison et al, 2007, 725

18 female, 15 male, screened for neurological or psychiatric illnesses

color digital photographs of faces

sad

fearful

disgusted

surprised

rated:

intensity

valence (good or bad)

attractiveness  Harrison et al, 2007, 725

“We also tested how Interindividual differences in emotional sensitivity to pupil size (in the context of sadness) related to scores on a rating scale of emotional empathy.  Subjects who scored negatively on the BEES were excluded from this analysis (3 subjects).´ Harrison et al, 2007, 726

“…whether high empathy was associated with a sensitivity to an increase or decrease in pupil size was explored.”  Harrison et al, 2007, 726  [31 subjects from earlier study, Harrison et al., 2006]

RESULTS

“The size of pupils incidentally perceive on the face stimuli size modulated the ratings of emotional facial expression….across all four emotional expressions and three pupil sizes for ratings of emotional intensity showed a significant main effect of pupil size…with faces with small pupils rated as more intense.”  Harrison et al, 2007, 726

“Notably, there was also a significant interaction between pupil size and emotional (facial muscular) expression, driven by effects of pupil size in the context of sad facial expression….Subjects rated facial expressions of sadness with small pupils as significantly more intense…so that decreasing pupil size linearly modulated ratings of perceived intensity….Observed pupil size did not affect intensity ratings for expressions of fear…or surprise….However both large…and small…pupil areas were rated as significantly more intense than midsized pupils in expression of disgust….”  Harrison et al, 2007, 726

“When judging the emotional valence of facial expressions, there was no significant main effect of pupil size.”  Harrison et al, 2007, 726

“There was a trend in the interaction between pupil size and emotional expression…again driven by effects of pupil size on sadness ratings.”  Harrison et al, 2007, 726

“Analysis of the effects of observed pupil size on ratings of specific emotional expressions confirmed our previous findings that sad face stimuli with small…pupils are also rated as significantly more negative…than sad face stimuli with large…pupils.”  Harrison et al, 2007, 726

“Observed pupil size in facial expressions of fear, surprise, and disgust had no effect on valence ratings….It is noteworthy that, at debriefing, subjects reported a lack of awareness of differences in pupil size across the stimuli when explicitly questioned.”  Harrison et al, 2007, 726  [so this was an implicit reaction]

correlation with empathy scores

“Subjects who were more sensitive to changes in pupil size in the context of sadness were rated as having significantly higher empathy scores on ratings of intensity of emotional expression…valency ratings…and a composite score combining both ratings.”  Harrison et al, 2007, 726

“….significant predictive relationship between scores on the BEES and sensitivity to a reduction in pupil size….”  Harrison et al, 2007, 726

discussion

“This study confirmed a salient influence of pupil size on the processing of sad expressions and showed that individual differences in the magnitude of this effect reflect differences in empathy score.”  Harrison et al, 2007, 726

“These data complement an earlier investigation describing a selective effect of pupil size on sadness perception that did not occur when viewing happy, angry, or neutral facial expressions [in Harrison 2006 earlier investigation]….The present study extends these observations to all “basic” emotional facial expressions by examining the influence of pupil on perception of fear, disgust, and surprise.  The further finding that emotional sensitivity to pupil size in the context of sadness predicts an individual’s empathy score is noteworthy.”  Harrison et al, 2007, 726

“In an earlier study, we showed an automatic unconscious mirroring of pupil size in the context of sad expressions, present even when attention was directed at nonemotional aspects of faces, where the observer’s pupil constricts more when viewing small pupils on a sad face than when viewing larger pupils (no such mimicry of pupil size accompanies perception of happy, angry, or neutral faces; Harrison et al, 2006).  Harrison et al, 2007, 726

“Together, these observations reinforce the notion that effective communication of emotional feelings engages visceral autonomic reactions underlying feeling states.  [I don’t know how they can generalize past just sad emotional feelings based on these studies – the other feelings do not generate this effect]’”  Harrison et al, 2007, 726

“Speculatively, these automatic responses provide a potential basis for the development of objective (and perhaps nonlinguistic) screening tools for disorders of emotional empathy, such as autism and psychopathy.”  Harrison et al, 2007, 726

attachment disorders, other personality disorders, too

“Our findings provide further empirical validation for emotional specificity of patterns of autonomic physiological responses….”  Harrison et al, 2007, 726

“Emotional specificity of physiological responses across individuals has remained surprisingly contentious, particularly when (276) measuring single autonomic responses….Nevertheless, despite high individual variability, there is increasing empirical evidence for patterned autonomic responses associated with different emotional states in humans ….[lists refs]….In addition, autonomic responses have evolved as salient signals for the perception and recognition of emotions (Darwin, 1872):  Thus, psychophysiological changes in the face, such as flushing in anger or blanching in fear, may contribute to signaling an individual’s emotional state.”  Harrison et al, 2007, 727

“Why pupil size is salient only for expressions of sadness remains unclear….central contribution of the eye region to successful recognition of facial expressions of sadness.  Nevertheless, pupillary changes are subtle, vary with ambient light, and may only be perceived at close range.  However, sadness is an affiliative emotion that can draw individuals together and inhibit interpersonal conflict (Blair, 2001).  Speculatively, the communication of sadness intensity through pupil size may have evolved to act over short distances, in contrast to emotions such as anger, which may lead to the “withdrawal” of the observing party.”  Harrison et al, 2007, 728

FEAR

Sympathetic arousal

“The visual signaling and perception of fear is also linked to perception of the eyes, in particular the sclerae (whites of the eyes).  It was therefore surprising to find no effect of pupil size on intensity or valence ratings for fearful facial expressions.  Moreover, fear is associated with sympathetic arousal, which causes both pupillary dilatation and eyelid retraction (Adolphs & Tranel, 2004) and perhaps also facial vasoconstriction.  Hence, we anticipated that perceived (sympathetic) pupillary dilatation would enhance ratings of fearful expressions.  The fact that we did not observe this effect perhaps emphasizes the degree of organ specificity within emotion-specific autonomic responses patterns.  Alternatively, it may indicate a redundancy of pupillary arousal responses in a context where other facial signs of sympathetic arousal predominate.”  Harrison et al, 2007, 728

are they saying that sadness is a sympathetic arousal?  I wish they specified that here

small and large, but not medium pupil size affected “the perceived intensity of disgust facial expressions”  Harrison et al, 2007, 728

“Perhaps the most clinically relevant finding is the correlation between an individual’s tendency to respond empathically and the same individual’s sensitivity to pupillary signals…. Harrison et al, 2007, 728

“Heuristically, enhanced sensitivity to socially salient signals is anticipated in more empathic individuals.  Indeed, subjects who score highly on the rating scales of emotional empathy have reduced visual thresholds for identifying emotional expressions presented for brief periods (Martin et al., 1996) and show the strongest degree of automatic mimicry (in their facial muscles) of observed facial emotional expressions …. [has refs here]”  Harrison et al, 2007, 728

“The mechanism that specifically links empathy ratings to enhanced sensitivity to pupils during sadness perception remains a topic for future empirical studies.  It is, however, noteworthy that the identification of sadness in others is selectively impaired in psychopaths (Blair, Colledge, Murray, & Mitchell, 2001; Dolarn & Fullam, 2006) and in normal individuals after the administration of propranolol, a drug that blocks peripheral and central beta-adrenergic receptors (Harmer, Perrett, Cowen, & Goodwin, 2001).  Harrison et al, 2007, 729

beta blockers?

“In summary, reduced pupil size, perceived without conscious awareness, selectively enhances the subjective intensity and negativity attributed to sad facial expressions.  Individual differences in the extent to which pupils influence sadness perception reflect, or predict, individual differences in emotional empathy score.  Together, these observations highlight the existence of emotion-specific autonomic signal in affective communication that may potentially contribute to screening tools for clinical disorders of empathy.”  Harrison et al, 2007, 729

++++

Singer et al, 2006

Pain network – Pain-related empathic response observed in anterior insula/fronto-insular cortex (AI/FI) and the anterior cingulate cortex (ACC) – pain in oneself and when observing pain in someone else

Studied if liking or disliking someone modulated empathic responses for pain

“The comparison of brain activity associated with painful and nonpainful trials in the ‘self’ condition for men and women revealed an expected increase in the ‘pain network’, including activity in AI and ACC….Moreover, we observed pain-related empathic responses in both genders in bilateral AI extending into FI and brainstem when seeing an unfamiliar but likeable person in pain….The activation in ACC was significant in women…but was borderline in men…Furthermore, we extended previous findings by showing that men, as well as women, who scored higher on standard empathy scales had higher empathy-related brain activity in ACC and AI/FI….”  Singer et al, 2006, 466

“…less empathic activity was elicited by the knowledge that an unfair player was in pain.  However, there was also a marked difference between the sexes.  In women this reduction in activity was very small, whereas in men the knowledge that an unfair player was in receipt of pain elicited no increase in empathic activity in FI.  And indeed, formal analysis revealed no significant difference for women when comparing painful trials for fair versus unfair players in empathy-related pain regions.  However, men showed significantly enhanced activation in bilateral FI when observing fair compared with unfair players in pain….women but not men displayed significant activation in bilateral AI/FI and ACC in all three conditions.”  Singer et al, 2006, 467

“We next sought evidence of increases in brain activity in regions associated with reward processing (ventral striatum/nucleus accumbens and orbito-frontal cortex) when observing an unfair player receiving painful stimulation…we observed increased activation in left ventral striatum/nucleus accumbens for men, but not for women, in the comparison of painful trials in the unfair and the fair condition (pain in unfair – pain in fair) as well as in the interaction ((pain – no pain) unfair – (pain – no pain) fair).  This latter comparison also revealed increased activation in left orbito-frontal cortex….the direct gender comparison for painful trials in the unfair and the fair condition ((pain in unfair-pain in fair) men – (pain in unfair – pain in fair) women) revealed that men showed significantly higher activation than women in left nucleus accumbens….”  Singer et al, 2006, 467

“…men, but not women, who expressed a stronger desire for revenge showed greater activation in nucleus accumbens when they perceived an unfair player receiving painful stimuli than when they perceived a fair player in pain….”  Singer et al, 2006, 467

Unfortunately, this makes me think of both of my parents.  Was there some twisted interaction in their brains that I deserved what happened to me?

++++

This whole concept of revenge must operate somehow in interaction with perceived rules that govern the perception and judgment of fair versus unfair rules.

“Our data provide neurobiological evidence on how fairness in social interactions shapes the nature of the affective link between people.  Our findings indicate that cooperation nourishes this link, but selfish behavior that is detrimental to others effectively compromises this link (at least with males), such that empathic responses in the brain are diminished or abolished.”  Singer et al, 2006, 467

“These findings complement those of a previous imaging study that reported enhanced activation in dorsal striatum (caudate nucleus) when individuals punished defectors….in a sequential Prisoner’s Dilemma game.  In the present study we observed activation correlated with revenge in ventral striatum.  This difference in evoked activity in dorsal and ventral regions of the striatum is likely to reflect the different nature of the tasks used.  In the previous study subjects were required to select an action to administer punishment, whereas in the present study subjects passively observed a cue indicating that a defector was receiving pain.  These findings are consistent with the different functions associated with distinct regions of the striatum:  afferent projections to dorsal striatum are thought to be crucial for learning correct actions so as to maximize reward, whereas projections to ventral striatum, including nucleus accumbens, have a key function in reward prediction and pavolovian learning….The findings of enhanced activation in ventral striatum to a signal indicating that a defector is receiving pain are in agreement with the hypothesis that humans derive satisfaction simply from seeing justice administered, even if the instrument of punishment is out of their control.”  Singer et al, 2006, 467

“Our results suggest a neural foundation for theories of social preferences.  These theories suggest that people value the gains of others positively if they are perceived to behave fairly, but value (467) others’ gains negatively if they behave unfairly.  This pattern of preferences implies that people like cooperating with fair opponents but also like punishing unfair opponents.  Our corresponding neurobiological observations were more prominent in men, although further experiments are needed to confirm the gender specificity of the effect….these findings could indicate a predominant role for males in the maintenance of justice and punishment of norm violation in human societies.”  Singer et al, 2006, 468

++++

++++

Valentin, Dickinson & O’Doherty, 2007

goal-directed learning

“Instrumental conditioning involves learning to perform a particular action in response to a stimulus to obtain rewards or avoid punishments.  Evidence from animal learning studies suggests that this operates via two distinct processes, a goal-directed component that involves learning of associations between responses and the incentive value of outcomes (response-outcome or stimulus-response-outcome learning), and a habit learning component that involves learning associations between stimuli (or context) and responses (stimulus-response learning)….”  Valentin, Dickinson & O’Doherty, 2007, 4019

study to differentiate between the neural systems involved in goal-directed or habit learning in humans

focused on the orbitofrontal cortex and amygdala “…because these regions have been implicated previously in mediating instrumental outcome devaluation effects in nonhuman primates….”  Valentin, Dickinson & O’Doherty, 2007, 4020

“Decreased responding to the action associated with the devalued outcome compared with the action associated with the valued outcome is the indication of goal-directed performance.”  Valentin, Dickinson & O’Doherty, 2007, 4021

regions of interest – orbital and medial prefrontal cortex, dorsolateral prefrontal cortex, anterior cingulate cortex, ventral and dorsal striatum and amygdala – these areas implicated in reward-related processing and learning  Valentin, Dickinson & O’Doherty, 2007, 4022

brain regions involved in mediating the goal-directed component of instrumental conditioning – significant effects in the medial OFC, right central OFC, and anrea in left lateral OFC bordering on the inferior prefrontal cortex

medial and central OFC “…showed an increase in activity when subjects chose the high-probability action in the valued condition, but a decrease in activity when subjects chose the high-probability action in the devalued condition, suggesting that these regions are sensitive to the incentive value of the associated outcomes associated with particular instrumental actions (even in extinction).  Moreover, these areas showed an increase in activity on trials in which subjects chose the low-probability action in the devalued condition, suggesting that the incentive value of the alternative action that was not associated with the devalued outcome was increased as a result of the devaluation process.”  Valentin, Dickinson & O’Doherty, 2007, 4023

“…activity in the medial OFC is not specific to the extinction context during test, but rather is involved in goal-directed instrumental action selection more generally.”  Valentin, Dickinson & O’Doherty, 2007, 4023

How can a terribly abused child, from birth, build goal-directed parts of their brain when the only known goal is to stay alive?  How can they build reliable circuitry when there is no prediction between choice and either reward or punishment?  How can a child stop doing whatever it is that adults devalue that results in punishment when the children have no clue what the rules are that lead to the consequences in an unpredictable environment?

And we wonder about corresponding reductions in brain mass in abused children?  How can we learn in a toxic learning environment?

Region of far posterior caudate (tail of caudate) suggestive of a possible contribution of this area to the habit learning component…..did not reach significance..

“…both medial and lateral regions of the orbitofrontal cortex show neural responses during performance of instrumental actions that reflect the incentive value of an associated outcome….[authors were able to] disambiguate goal-directed response-outcome (or stimulus-response-outcome) learning processes from stimulus-response learning.  The finding that responses in the orbitofrontal cortex are sensitive to the incentive value of instrumental actions indicates that this region is likely to be involved in the goal-directed component of instrumental learning.”  Valentin, Dickinson & O’Doherty, 2007, 4024

consistent with other findings “of a role for the ventromedial prefrontal cortex in behavioral choice in humans…”  Valentin, Dickinson & O’Doherty, 2007, 4024

flexible adapting – instrumental responding after reinforcer devaluation

“O’Doherty et al. (2003) showed that activity in this region [orbitofrontal cortex] in this region is significantly enhanced when subjects are performing instrumental actions to obtain reward as opposed to passively receiving rewards (thereby involving only stimulus-outcome associations)….increased activity in medial orbitofrontal cortex during a menu preference task in which subjects had to choose specific high incentive menu items from the menu as opposed to passively viewing these items…..the orbitofrontal cortex contributes to instrumental as well as pavolovian learning processes.”  Valentin, Dickinson & O’Doherty, 2007, 4025

Good reasons for the “new” parenting that encourages children to make choices whenever possible – builds these brain networks!  But what if choice is not an option, and the connection between stimuli and response is insane, as it was in my childhood?

Authors “…found significant effects of instrumental devaluation in both central, lateral, and medial areas.”  Valentin, Dickinson & O’Doherty, 2007, 4025

Anatomical connectivity of these areas in which lateral and central areas of OFC (Broadmann areas 12/47, 11, and 13) receive input primarily from sensory areas, consistent with a role for these areas in stimulus-stimulus learning, whereas the medial OFC (areas 14 and 25) receives input primarily from structures on the adjacent medial wall of prefrontal cortex such as cingulate cortex, an area often implicated in response selection and/or reward-based action choice….  Valentin, Dickinson & O’Doherty, 2007, 4025

“[results strongly suggest that]…the orbitofrontal cortex (especially its medial aspect) plays a role in the goal-directed component of instrumental choice.”  Valentin, Dickinson & O’Doherty, 2007, 4025

“…when the actions are trained in the context of a choice between different outcomes, as in the present experiment, performance remains goal-directed even in the case of extensive overtraining [and does not become habituated]…” Valentin, Dickinson & O’Doherty, 2007, 4025

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MIRROR NEURONS

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Fecteau, Pascual-Leone & Theoret 2008

Abstract – Center for Non-Invasive Brain Stimulation, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.

Recent advances in social neuroscience suggest

a link between empathy

and the mirror neuron system (MNS).

Impaired empathy

is one of the core diagnostic features

of psychopathic personality disorder.

In the present study, we investigated whether psychopathic personality traits in a non-psychiatric sample were related to MNS function. Healthy participants viewed short videos known to activate the sensorimotor MNS for pain (a needle penetrating a human hand) while transcranial magnetic stimulation (TMS) -induced motor evoked potentials (MEP) were recorded as a measure of motor cortex excitability. Individual psychopathic personality traits were assessed using the Psychopathic Personality Inventory (PPI) and correlated with the MEP findings. Consistent with previous data,

observation of the painful stimulus

was associated with

a significant reduction in the amplitude

of the transcranial magnetic stimulation (TMS) -induced motor evoked potentials (MEP).

Interestingly, the level of corticospinal excitability modulation was positively correlated with individual scores on the coldheartedness subscale of the PPI, such that

individuals with the greatest motor evoked potentials (MEP) reduction were the ones scoring highest on the

coldheartedness measure.

These data suggest the

existence of a functional link between ‘motor empathy’

and psychopathy.

It would seem, then, that coldheartedness is a response to the observation of painful stimuli – a defense against feeling the corresponding pain in oneself or a protection against the painful stimulus potential for oneself?

I am thinking about Schore’s statement that all insecure attachments comprise an empathy pathology.  There is a direct link between insecure attachment and empathy reductions – if I can pinpoint it – somehow, somewhere.  We need not then be surprised at the way some people treat others – they do it because they can, because they were built that way?  And what, then, is the connection between the empathy operation of the motor system and oxytocin and vasopressin, both a part of the social behavioral spectrum and with degrees of anxiety measurement?

One might ask how is psychopathy and language directly related to one another?  Through the operation of the mirror neuron system in the motor cortex.  Interesting that right here, where mirror neurons meet empathy comes a direct connection to the evolution of language – which, of course, I must now move over to the language chapter.

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Rizzolatti et al 1999

Abstract – Istituto di Fisiologia Umana, Università di Parma, Italy.

This article is subdivided into two parts. In the first part we review the properties of a particular class of premotor neurons, the “mirror” neurons. With this term we define neurons that discharge both when the monkey makes a particular action and when it observes another individual (monkey or human) making a similar action.

The second part is an attempt to give a neurophysiological account of the mechanisms underlying behaviors where an individual reproduces, overtly or internally, movements or actions made by another individual.

We will refer to these behaviors as “resonance behaviors“. We distinguish two types of resonance behavior.

The first type is characterized by imitation, immediate or with delay, of movements made by other individuals. Examples of resonance behavior of this type are the “imitative” behaviors observed in birds, young infants and patients with frontal lesions.

The second type of resonance behavior is characterized by the occurrence, at the observation of an action, of a neural pattern, which, when internally generated, determines the making of the observed action. In this type of resonance behavior the observed action is, typically, not repeated (overtly).

We argue that resonance behavior of the second type is at the basis of the understanding of actions made by others. At the end of the article we review evidence of mirror mechanisms in humans and discuss their anatomical localizations.

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Ferrari, Rozzi & Fogassi 2005

Abstract – Università di Parma, Italy.

In the present study, we describe a new type of visuomotor neurons, named tool-responding mirror neurons, which are found in the lateral sector of monkey ventral premotor area F5.

Tool-responding mirror neurons discharge when the monkey observes actions performed by an experimenter with a tool (a stick or a pair of pliers). This response is stronger than that obtained when the monkey observes a similar action made with a biological effector (the hand or the mouth).

These neurons respond also when the monkey executes actions with both the hand and the mouth.

The visual and the motor responses of each neuron

are congruent in that they share the same general goal,

that is, taking

possession of an object and

modifying its state.

It is hypothesized that after a relatively long visual exposure to tool actions, a visual association between the hand and the tool is created, so that the tool becomes as a kind of prolongation of the hand.

Is this where we are vulnerable to possession of material objects as extensions of ourselves – as part of the way our brain works – objects being things we naturally want, want to manipulate, take possession of – and that we see as extensions of our self?

We propose that tool-responding mirror neurons

enable the observing monkey

to extend action-understanding capacity

to actions that do not strictly correspond

to its motor representations.

Our findings support the notion that the motor cortex plays a crucial role in understanding action goals.

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Järveläinen, Schürmann & Hari 2004

Abstract – Brain Research Unit, Low Temperature Laboratory, Helsinki University of Technology FIN-02015 HUT Espoo, Finland.

Tool use is a characteristic human trait, requiring motor skills that are largely learned by imitation. A neural system that supports imitation and action understanding by directly matching observed actions and their motor counterparts has been found in the human premotor and motor cortices. To test whether this “mirror-neuron system” (MNS) would be activated by observation of tool use, we recorded neuromagnetic oscillatory activity from the primary motor cortex of 10 healthy subjects while they observed the experimenter to use chopsticks in a goal-directed and non-goal-directed manner. The left and right median nerves were stimulated alternatingly, and the poststimulus rebounds of the approximately 20-Hz motor-cortex rhythms were quantified. Compared with the rest condition, the level of the approximately 20-Hz rhythm was suppressed during observation of both types of tool use, indicating activation of the primary motor cortex. The suppression was on average 15-17% stronger during observation of goal-directed than non-goal-directed tool use, and this difference correlated positively with the frequency of subjects’ chopstick use during the last year. These results support the view that the motor-cortex activation is related to the observer’s ability to understand and imitate motor acts.

++++

Leslie, Johnson-Frey & Grafton 2004

Abstract – Department of Psychological and Brain Sciences and Center for Cognitive Neurosciences, Dartmouth College, Hanover NH 03755, USA. kleslie@dartmouth.edu

Empathy

requires the ability to map the feelings of others

onto our own nervous system.

Until recently, there was no plausible mechanism to explain how such a mapping might occur.

The discovery of mirror neurons, however, suggests that the

nervous system is capable of mapping the observed actions

of others onto the premotor cortex of the self,

at least for reaching and grasping movements.

Is there a mirroring system for emotive actions,

such as facial expression?

Subjects (N = 15; all right-handed; eight men, seven women) watched movies of facial expressions (smile or frown) and hand movements (move index or middle finger) while brain activity was imaged using functional magnetic resonance imaging (fMRI). Subjects watched the movies under three different conditions: passive viewing, active imitation, and an active motor control. Subjects also performed a verb generation task to functionally identify language-processing areas. We found evidence for

a common cortical imitation circuit for

both face and hand imitation, consisting of

Broca’s area,

bilateral dorsal and

ventral premotor areas,

right superior temporal gyrus (STG),

supplementary motor area,

posterior temporo-occipital cortex, and

cerebellar areas.

For faces, passive viewing led to significant activation in the

right ventral premotor area,

whereas imitation produced bilateral activation.

This result is consistent with evidence for right hemisphere (RH) dominance for emotional processing, and suggests that

there may be a right hemisphere mirroring system

that could provide a neural substrate for empathy.

This is an overlap of mirror neurons and empathy – I knew the two had to be related.  This is 2004 research.  I need to find where the research has gone since then.  It also shows how hard it is to keep the information about processing facial expressions separate from both mirror neurons and empathy.  I suspect that pain processing areas are also involved – like in BPD where pain processing is altered, and so, therefore, empathy abilities and capacities also must be altered.  I must also keep in mind what Schore says that all insecure attachment systems lead to empathy pathologies to one degree or another.

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Schulte-Ruther et al 2007

Abstract – Research Center Jülich, Germany. m.schulte@fz-juelich.de

Schulte-Ruther, et al, 2007

Study of empathy

Empathy is the way we are supposed to be able to make “psychological inference” about other people’s “mental states and feelings in social contexts.”

An infant is created by and born into a social context.  The building of empathic understanding begins before birth.  Empathy is an interactive process and is part of the experience-dependent growth process of the brain throughout our entire existence in a physical body.

Empathy happens in context.  That context, we assume, involves a social process at least in a dyad, as Schore would say.

What happens when we are in consultation with only our self, which seems to be a major occupation of the precuneus?  Is that not also a social context, being in fact the genesis point for all of our concerns throughout our lifespan?

How do we become a self when our self is not adequately or appropriately mirrored back to us from birth?  How does our developing sense of self fill in the blanks when we are left as infants and young children alone, isolated, abandoned and neglected – not even considering the erroneous information that is fed to us by “crazy people” in some of the gaps in between – which include violent, terrifying abusive assaults on our tiny bodies?

How are we to make sense of “mental states” before we have a mind to have our own mental states with?  Does the resting activity of the precuneus region reflect our continual adjustments of ourselves to a world beginning before birth?

Is this the part of the brain that tries to make sense out of dysregulated input, trying to find a way to fit the self into the patterns?  Is a dysregulated self ever the same thing as a regulated self?  Is it a requisite that a self be regulated to even be a self – by definition?

At what point and how does a self define itself as being separate from the patterns of mirrored interactions that it experiences?  Is it something like learning a song, humming along with the tune, and then at some point feeling confident and competent enough in ability to say, “OK, now.  I’ve got it.  I can hum it by myself?”

If this part of the brain, the precuneus, is especially activated in difficult locomotion, is it like learning to walk in the beginning when we have to hold our caregiver’s hand or move from stable object to stable object until we have the ability to  walk alone by ourselves?

If we are expected to do anything before we have the resources available, or to do it completely without resources, we fall flat on our faces.  In cases of PTSD, our resources were completely overwhelmed.  We are expected by biological design to learn something from these experiences that can help our species later on should the need arise for the information, but we are in today’s world, left completely alone to deal with the trauma when it happens (which is really what makes it a trauma in the first place), and are left alone in the learning and resolution stage.  This probably makes about as much sense to our brains as it would to tell an infant before it is ready to get right on up there and run.

We cannot even stand up under the burden of our traumas.  We certainly cannot crawl with them, or stand with them, or run with them.  And putting them down and leaving them behind is simply not an option, I believe, by evolutionary species-survival design.

Our physiology is designed to recognize the challenges in trauma.  When there is a challenge there is either an opportunity to use what we have learned in the past that will work in this situation, or it is an opportunity to learn something new.

How can these “obstacle learnings” be processed in the precuneus and integrated into our self if there is no mirroring taking place in the context we find ourselves in?  We cannot isolate the individual from the demands of the species!  Don’t leave us alone and expect us to do alone what is impossible to do alone.  Don’t turn your backs.  And, no, pills are not the solution!

Which neural mechanisms are shared in common and which are different in the “self” vs the “other” in “related attribution of emotional states?”

FMRI – self-task and other-task

Common networks activated for both:

Left lateral orbito-frontal cortical region

Medial prefrontal cortical region (MPFC)

Bilateral inferior frontal cortices

Superior temporal sulci

Temporal poles

Right cerebellum

Subset of these regions showed neural activity correlated with empathic abilities

Self- (relative to the other-) task differentially activated:

MPFC (medial prefrontal cortex)

Posterior cingulate cortex (PCC)/precuneus

Temporo-parietal junction bilaterally (both hemispheres)

Brain areas involved in mirror neuron and theory-of-mind (ToM) were recruited in the empathy-related processing of emotional facial expressions

The differential engagement of the MPFC, the PCC/precuneus, and temporo-parietal regions in the self-task indicates that these structures act as key players in the evaluation of one’s own emotional state during empathic face-to-face interaction.”

This is where, in the beginning as the regions of the brain are forming, it is crucial that a caregiver exaggerates in almost a theatrical way the mirroring to the infant of the infant’s – and not the adult’s – emotional state.  This is where the infant begins to define itself as a self, and as a self not overwhelmed by or confused with, the caregiver.

I am beginning to form my own version of a hierarchy regarding which of these implicated brain regions end up being the most important in my consideration of the impact and consequences of severe trauma that is not resolved on the individual self – its formation and maintenance in reaction to and in combination with not only all the ordinary interactions and experiences of life, but most importantly for our considerations in, through and with interactions of severe traumatic content.

Brain scientists do not seem to differentiate a specific hierarchy of response – they can tell and do note which regions are interacting or active at a given time – and they compare this information with “normal, healthy subjects.”  But it is entirely possible that what they are seeing as deviant in us is actually perfectly normal considering the situations we have had to adjust and adapt to – both those of us abused from birth and those who experience abuse around age 5 – and those who have normal brains and are faced with adapting to insurmountable trauma at later, older ages.

Activation of mirror neurons in a task relying on empathic abilities without explicit task-related motor components supports the view that mirror neurons are not only involved in motor cognition but also in emotional interpersonal cognition.”

How does an infant begin to process terrifying interactions with caregivers from birth?  How do those interactions alter the development of self?

An interplay between ToM and mirror neuron mechanisms may hold for the maintenance of self-other distinction during empathic interpersonal face-to-face interactions.”

What does the individual self do with:  the external reality of the “threator” as other,  the actual experiencing of the threat itself, and the process dealing from within with the threator, the experience of the threat, the integration of the meaning of the threat, etc.?

Why would we not look first at this region of the brain when considering borderlines when we describe them as “lost in the mirrors?”

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Schulte-Ruther et al 2008

Abstract – Cognitive Neurology Section, Institute of Neuroscience and Biophysics (INB3-Medicine), Research Center Jülich, Leo-Brand Str. 5, 52425 Jülich, Germany. m.schulte@fz-juelich.de

Females frequently score higher on standard tests of empathy, social sensitivity, and emotion recognition than do males. It remains to be clarified, however, whether these gender differences are associated with gender specific neural mechanisms of emotional social cognition. We investigated gender differences in an emotion attribution task using functional magnetic resonance imaging. Subjects either focused on their own emotional response to emotion expressing faces (SELF-task) or evaluated the emotional state expressed by the faces (OTHER-task). Behaviorally, females rated SELF-related emotions significantly stronger than males.

Across the sexes,

SELF- and OTHER-related processing of facial expressions activated a network of medial and lateral prefrontal, temporal, and parietal [does this include the precuneus?] brain regions involved in emotional perspective taking.

During SELF-related processing, females recruited the right inferior frontal cortex and superior temporal sulcus stronger than males.

In contrast, there was increased neural activity in the left temporoparietal junction in males (relative to females).

When performing the OTHER-task, females showed increased activation of the right inferior frontal cortex while there were no differential activations in males.

The data suggest that females recruit areas

containing mirror neurons to a higher degree than males

during both SELF- and OTHER-related processing

in empathic face-to-face interactions.

This may underlie facilitated emotional “contagion” in females. Very handy for mothering interactions with infants – no way to tell from this article if this is innate and genetic or if it is socially conditioned

Together with the observation that males differentially rely on the left temporoparietal junction (an area mediating the distinction between the SELF and OTHERS)

the data suggest that females and males rely on different strategies when assessing their own emotions in response to other people.

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Information is also making a wide swing now over to language, with the brain’s processing of mirror neurons in sound, connected to talking faces.  It is strange that the research had to evolve our understanding of how things are working in the brain before I would be able to write this book.

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