2 chapter 2 learning

Tuesday, July 29, 2008

Before I start my reading for this topic of PTSD, I want to note that I suspect PTSD and problems with associational learning, or associative learning are connected, and that this connection reflects in the smaller hippocampus size for trauma survivors.

I also think it is connected to dissociation – dis-association.  If we can’t learn, every time we are presented with an opportunity that would require a normal person to learn, or allow them to do so, or enable to do so – and we can’t take advantage of these opportunities because something is “screwed up,” we are suffering a learning dis-ability.

This has to do with memory complications

There is nothing in Scaer’s trauma resiliency book in the index on association or associational learning

How can they consider dissociation without considering association?  I don’t get it.

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Sunday, August 17, 2008

As an aside, because I have no idea how this fits in – They called me yesterday and told me my disability has been approved.  Today I am aware that this changes things in my life – but my cognition does not seem able to follow exactly what changes when one thing changes – how to hold anything constant?  Is everything that relative?  That interdependent, or overly dependent on one thing – like there’s no internal consistency – I can’t accurately judge what is “the same” and what is “different.”  It is all scary, threatening – as if all change has the potential to destroy – never assuming that change is for the best, even when logically I know it is in this case – but what about the impact of the changes that occur in connection with this change?  How does the brain hold one thing constant in a world where everything is continually changing as we move from the past into the future.  Nothing is guaranteed, nothing is truly ever safe and secure.  And if life is not safe, then there is no middle ground for me – it is dangerous.  So danger and threat become automatically activated when change happens anywhere in “the system.”

I think this is directly related to not having a strong central self component that orchestrates the whole mess of things – prioritizes, determines what is constant and what is not given a reasonable assumption that the world is safe in the moment and in the near future – enough that one can “go on being” with reasonable certainty. To me, it’s as IF this one thing changes and then everything else has to change at the same time.

For me, it’s like IF one thing changes then everything falls apart – or is a WHEN one thing changes?  – like in the game of pick up sticks – the stress and anxiety part of PTSD – especially when it is built into the circuitry of the brain, is that nothing is constant so therefore nothing can be predicted – there is no safety of the known or the dependable or the constant.  The whole choice, reward, decision, conflict parts of the brain do not work correctly – and panic is always on the scene or very near to it…  What IF the brain is predicated upon a working IF system:  IF this happens then that will happen; IF I do this then that will happen; IF only this or that: what IF this or that – a powerful little tiny word:  IF – what IF this is the fulcrum point of the brain?

IF

Function:conjunction

Etymology:Middle English, from Old English gif; akin to Old High German ibu if

Date:before 12th century

1 a : in the event that  b : allowing that  c : on the assumption that  d : on condition that

2 : WHETHER  *asked if the mail had come*  *I doubt if I’ll pass the course*

3 –  used as a function word to introduce an exclamation expressing a wish  *if it would only rain*

4 : even though  : although perhaps  *an interesting if untenable argument*

5 : and perhaps not even  *few if any changes are expected* –  often used with not  *difficult if not impossible*

-if anything : on the contrary even  : perhaps even  *if anything, you ought to apologize*

Or, maybe alternatively this is about me introducing unnecessary drama into my life – like I have to MAKE everything else change just because this one thing has changed….in such a case I need to be very careful…..

What do I want, what can I have?  I love the landscape here, the mountains, this area exactly – but I hate this situation with Ernie, I hate being alone, I hate not being near family – I hate that my children live in a place I cannot tolerate living in.  I know I will not have a mate in this lifetime.  I know I probably do not have that much longer to live before this cancer is back to claim my life.  What is the best compromise that I can make?  Is it to go live in those subsidized apartments in Earth, TX – mostly to be in a quiet calm and peaceful place but with a chance for Jaydn and Kenna to come and spend some time with me?  So that I could be a part of their remembered life?  Would that cause complications in Faith’s life, and/or in Cindy’s should she decide to move back there?  How would I feel about being in TX, about being in such a flat place, about being remote – not that I can afford to drive anywhere here because I can’t.  Mostly it’s about being able to write, and having access to whatever simple pleasures I can have – kind of like being in a womb while this book is growing – at the same time knowing that if I can give birth to this book before I die and am myself called to move into a different world – at least I can lessen all my surrounding “lonelinesses” in some way…

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Ridley 2004

Sunday, August 10, 2008

I propose that traumas have always plagued our species.  Our interaction with them has enabled us to adapt, to learn, to grow in ability and capacity.

Our brain’s growth and development occurs in an experience-dependent fashion.  We are used to overcoming challenges.  Our ability to do so has enabled us to “conquer the world.”

Not everyone who experiences trauma develops PTSD.  Research is attempting to clarify the complexities of variables that determine who gets it, who doesn’t, and why.

I propose that those of us who develop PTSD have an evolutionary adaptive advantage in that we not only survived the traumas, but are poised on the brink of learning something vital to the continued survival of our species.

That we are captured and captivated in this poised condition indicates to me that there is no available context for the new possibilities contained in new learnings to manifest themselves in our individual lives or in the ongoing life of our species.

This frozen status of being poised on the verge of new learning is what kills us.  The same spectrum or continuum of brain plasticity that allows us to learn has on its other end neurotoxicity and neuronal death due to over excitation that results from being stuck at the learning threshold.  Our bodies are left with implicit awareness based on our exposure to traumas, but that information is not being processed on a cognitive, semantic level that allows the new learnings to become integrated into life – on the particular as well as on the general level.

PTSD literature describes three symptom matrixes:  avoidance, reexperiencing, and hyperarousal.  I propose that all three of these matrixes are interrelated feedback-feedforward loops that are involved with the potential to learn important new responses to the environment.  Our species is still here only because we have the ability to learn.

I propose that we need to reconnect our experiences of trauma that lead to PTSD as a species so that we can learn together what our bodies are trying to teach us.  Research on the global level includes complicating factors both toward the development of PTSD and towards its solution.  We have to connect what happens to the individual with what happens to the species.  As long was we force an arbitrary disconnection of the process of survival for the individual and the survival of our species we are robbing all of us with information that life deems important for us to have.

Nowhere in the literature have I seen any reference to what I suspect is the truth.  People who develop PTSD after exposure to trauma contain a genetic connection to the gift of our species that has allowed us to survive trauma, to endure, and to thrive on this planet.  We are the learners.  We are driven to learn.  We are predisposed to learn.  We are hardwired to learn.  We are required by the mystery and the history of human DNA to learn.

It is not the commonality of our human gene pool that offers us the best hope of being able to adapt to crisis-laden changing situations of life.

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Ridley 2004

P 27

“When a cell reproduces, its DNA and genes are physically replicated.  Normally an exact copy of the parental DNA is produced, but sometimes a copying error happens.  The set of enzymes that replicate the DNA include proof-reading and repair enzymes.  These enzymes detect and correct most of the copying errors, but some errors persist even after proofreading and repair  These errors are called mutations.  The new sequence of (27) DNA that results from a mutation may code for a form of protein with different properties from the original.  Mutations can happen in any cell, but the most important mutations, for the theory of evolution, are those occurring in the production of the gametes.  These mutations are passed on to the offspring, who may differ from their parents because of the mutation.”  (28)

“All cellular life forms, including bacteria and human beings, have a similar set of proof-reading and repair enzymes…”  31

“Whole chromosomes may fuse, as has happened in human evolution; chips and gorillas (our closest living relatives) have 24 pairs of chromosomes whereas we have 23.”  30

evolution, to me, is learning.

p 558

part of the human genome that codes for genes….contains abut 30,000 genes….genes that code for proteins..code for RNA molecules that re not translated into protein and are excluded from this analysis, concentrating on protein genome = full et of proteins in an organism …

humans share 21% of the genes with all cellular life forms, are “housekeeping” gene of each cell t regulate basic cellular machinery

oldest fossil cells are 3-.5 billion years old, probably most or all of housekeeping gene have evolved by then…most evolve slowly and copied with very little change for billion of years…

our DNA has probably been copied 10-100 times a year on average since our bacterial

ancestors….housekeeping genes reverberate with “deep time” in all our DNA molecules

32% of our genes in common the eukaryotes (greater complexity of cellular metabolism)  but not with bacteria – also housekeeping

next stage, animals – 24% shared with other animals, including genes that control development

another 22% of our genes only shared with vertebrates, 500 or more million years old, include genes that operate in the immune system and nervous system

flies and worms have 10 genes coding for the immune system where humans have 10

probably only 1% or less of human genes not shared with other vertebrates – at least not with mice!

“coding part of human DNA for genes that regulate, build and defend our bodies makes up les than 5%of our genome, rest is noncoding p 567

p 573

evolutionary development – study of called informally “evo-devo”

p 577 morphology – heterchrony

580

HOX gene (switch on other specific sets of genes to cause the right structure to develop in different body regions)  -genes that regulate development probably evolved once when animals that required development first originated and has been conserved ever since

545

“Humans are primates, and our ancestors from about 60 (or more) million years ago to about 5 – 10 million years ago were tree-dwelling primates.  Some of the trends we see in human evolution began in these ancestors.”

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Wade 2005

2 genes involved in determining size of human brain have undergone substantial evolution in last 60,000 years – science does not yet know how or why they were selected or what these alleles are actually doing in the brain….surprising discovery that the brain is still undergoing rapid evolution….it was assumed that human evolution “more or less stopped 50,000 years ago.”

Genes, or alleles as scientists call them…these brain genes are more common in some populations that others….reported by Bruce T. Lahn of University of Chicago and colleagues…

2 genes:  microcephalin and ASPM

disease of microcephaly people born with smaller brains “that seems to be a throwback to when the human brain was a fraction of its present size.”

Have identified 20 genes associated with the brain….with microcephalin a new allele arouse about 37,000 eyars ago, though could have appeared as early as 60,000 years or as late as 14,000 years ago, 70% of people in most European and East Asian populations carry this allele of the gene but rarer in most sub-Saharan Africans….

ASPM, new allele emerged 15,100 to 500 years ago, favor a midway date of 5,800 years ago, has gained a frequency of about 50% in populatons of Middle East and Europe is less common in East Asia found at low frequency in some sub-Saharan African peoples

Chicago team suggest new version of microcephalin allele may have arisen in Eurasia or as first humans emigrated from Africa some 50,000 years ago….the new ASPM allele emerged about the same time as spread of agriculture in Middle East 10,000 years ago and emergence of civilizations in Middle East 5,000 years ago, but connection is not yet clearbrain function.”

Dr. Lahn noted that there is “a reluctance to acknowledge that selection could affect a trait as controversial as brain function.”

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Evolution is meant to advance us and move us forward through learning and adaptation.  PTSD represents an inability to access new learnings that can be applied, and the result is de-evolution.

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Wade 2006

Evidence that humans are still evolving…researchers have detected 700 regions of human genome where genes appear to have been reshaped by natural selection within last 5,000 to 15,000 years

Include some [functional] genes responsible for “senses of taste and smell, digestion [like gene to digest lactose in milk among Europeans who kept cattle], bone structure [from forager/hunters to farmers], skin color and brain function” and hair texture

Hunting to agriculture well underway in Europe and parts of East Asia 5,000 years ago….selections may be due to pressures from these changes….

Three populations studied:  Africans, East Asians and Europeans……based on HapMap decoding of human genome in 2003 ….agriculture spread about 6,000 to 7,000 years ago…few skeletons older than 10,000 years found in Europe that look like modern Europeans….

Dr. Johathan Pritchard, a population geneticist at the University of Chicago -“Each gene has a story of some pressure we adapted to.”

First modern humans to arrive in Europe 45,000 years ago were probably dark, they know 5 genes …selected pressure…that contributed to lightening of the skin to admit more vitamin D, seem to be selected only 6,600 years ago….happened in Japan and China thousands of years earlier, signal of selection is no longer visible with current tests….

Selection in brain genes, Pritchard found include group known as microcephaly genes when disrupted result in unusually small brains…probably genes related to selective pressure for larger brains…continued into recent human past…another brain gene, SNTG1 was under heavy selective pressure in all three populations in recent history…function of the gene is not yet understood….

Few overlaps found in selected gene regions of the genome:  206 under selection in Africa, 185 in East Asians, 188 in Europeans

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SHANKS 1995

Associative learning

I believe that there has to be a connection between associative learning and dissociative behaviors and states.  I don’t see anybody addresses this, and while I am not qualified in my understanding of all the implications, I need to at least try, for myself, to rule out that they are NOT connected.

We have to be able to learn new things associated with the context we learn them in.  The ability to adapt behavior is a result of “acquiring information about associations or contingencies that exist between events…” in our environment.  Shanks 1995 p 2

from learning predicative relationships between reliable signals and searching out rewards and avoiding threats

adaptive ability, flexible learning equated with intelligence

causal relationships where one even or sets of events are followed by another – press switch, light comes on

structural – can predict something from presence of other features that regularly occur with it – sound of water is good index of sight of it [early hunters were able to learn this – tracks plus follow tracks equals finding food]

[Broca’s area could do this before language gene took hold, this region had to be established and developed before we could use it for words]

we classify sounds into words based on their structure of feature or property

humans are capable of abstracting general rules (no other species can do this)

multiple sources of knowledge, can learn sequential prediction unconsciously

implicit/explicit learning – is there a dissociation between the two? P 14

do we have distinct learning systems? P 16

associations and dissociations between performance and report measures – what we have learned, what we know of what we have learned, what we know of the rules we used – we don’t always know what the rules are that we went by, they can be implicit

“To the extent that people only learn associative relationships where they indeed exist, and do not believe events to be related when they are not, we can say that the system is well adapted.  But how exactly are we to know whether a pair or set of events are objectively related.  Clearly, we require some procedure or norm for specifying when events are truly related.  In short, we need a normative theory which gives us a yardstick against which to compare human behaviour.  The statistical concept called ‘contingency’ provides just such a yardstick,, and the best-developed current theory of the objective relatedness of events relies on this notion of contingency.”  Shanks 1995 p 20

“The world provides a number of informational clues concerning associative relationships….perhaps the most fundamental of these…the degree of correlation or contingency over time between events.  From a statistical perspective, associative learning simply requires the calculation of the degree to which a pair of events covary…..For continuous variables, the term correlation is used to describe relatedness, while for discrete variables, the term contingency is used.  It is now well-known that variations in correlation or contingency [represented as binary] affect associative learning, and this is…a fundamental property of learning….”  Shanks 1995 p 21

“…in causal prediction we are interested only in the question of whether the outcome is dependent on the cue….”  Shanks 1995 p 22

phobias…conditioned response to associated stimuli – extinction can be used to reduce or eliminate the connection between the phobic stimulus and anxiety… shank 1995, 35

phobias tend to develop to some stimuli objects and not others – usually not to a flower, but yes to a spider – “…it seems very unlikely that the distribution of phobias is in general related to objective threat.  For instance, aversive events probably do not occur in the presence of fear-relevant stimuli such as spiders any more often than in the presence of fear-irrelevant stimuli such as flowers;  in fact, spiders are rarely signals of objective threat at all.”  36

could be during our evolutionary history so our species developed a rapid tendency to fear reactions, more probable it is cultural…

“…it is rarely (if ever) the case that potentially predictive cues appear in isolation; instead, we are often confronted with a set of potential cues that co-occur with one another, and we have to pick out the one (or ones) that is (are) truly predictive.”  Shank 1995 40

cue-outcome

“Without changing the objective contingency between a cue and an outcome, in some circumstances the cue may be selected for association with the outcome and in other circumstances not, depending on the presence and status of other cues.  Such selection effects have been regarded in a number of different ways:  at one extreme has been the view that they are signs of the fundamental irrationality of human learning, while at the other has been the view that they represent the near-perfect adaptiveness of the human learning mechanism to the environment.”  Shank 1995 42

“…the very notion of varying the degree of contingency between a cue and outcome presupposes that outcomes may occur in the absence of the cue, which in turn requires that some third event must be present to have actually caused the outcome.”  Shanks 1995 p 43

what is the contingency between two events when the background varies? – probabilistic contrast model…”appropriate normative theory for causal or associative relationships….that human behaviour is closely matched to it.” P 45 …can be a conjunction of cue and background…hard to guarantee that a cue is the sole cause of an outcome if the background varies….compute contingency conditionally…action or cue is an interactive cause when combined with background.

Trauma gives us “new” background information that no matter what the cues were originally, they are now different/changed

“The key idea, of course, is that the evaluation of a cue must be based on a contrast between what happens when it is present versus what happens when it is absent, all else being held constant [as in scientific experiments where they hold constant all but the variables]….”  Shank 1995 p 45

“People appear to select amongst predictive cues:  when the unconditional contingency between a target cue and an outcome is held constant, the extent to which the cue and outcome are associated depends on the status of other cues that are concurrently present.  If these other cues are themselves highly predictive of the outcome, then the target cue will be to some extent ignored, while if the other cues are not especially informative, the target event will receive a normal association with the outcome.”  Shank 1995 50

I keep thinking of a newborn and how complex the environment is as its brain is forming – and how vulnerable to confusion when everything is out of control.  How is an infant supposed to then learn predictable contingencies?

“…assuming that the associative learning mechanism has been shaped by evolution to detect statistical contingency…like visual illusions, deviations from the prescriptions of the normative theory are likely to be understood by examining the specific mechanism that underlies learning.  One can either interpret illusions as evidence that perception is inherently biased, or as the result of a system that has to provide a true picture of the world given the constraints of the processing machinery of the brain.  I suggest that the latter is more plausible.  The system often has to operate under severe pressure and so may yield inaccurate results; nevertheless, the system as a whole is designed to operate veridically [truthfully, not an illusion].”  Shank 1995 50

there are fairly clear biases in learning:

task must provide sufficient information about contrasts to be able to distinguish relationships – so relevant computation can be made….”…there appear to be circumstances in which insufficient evidence is provided for the relevant contrasts to be made, but where subjects have no difficulty making associative judgments.”  Shank 1995 52

trial order does in some circumstances have an affect on associative learning – “The effect of trial order seems to occur because the different trial types are presented in separate blocks…Presenting trials in distinct blocks seems to allow biases in associative judgments to appear, and perhaps this is not surprising.  If the learning mechanism needs prolonged exposure to a set of relationships in order to determine where the true predictive relationships lie, then this can only be achieved by continually repeating the various trial types in an intermixed fashion until learning is complete.”  Shanks 1995 54

This makes me think of PTSD in that once a trauma occurs, it happens out of context as a “separate block” from other experiences – it is not a part of normalizing “prolonged exposure to a set of relationships” – so there’s no way to tell “where the true predictive relationships lie” – it is normally the nature of trauma that they are not part of the “continually repeating” patterns of life events, and they do not become “intermixed” so that learning can be completed

(associationist theories posit a close relationship between surprise and learning – see his chapt 4)

“…it is important to note that contingency is not the only informational clue that the environment provides about associative relationships, and biases may emerge via the manipulation of other types of information.  Temporal organization is just such an alternative source of information….events close together in time are more likely to be related than ones separated in time.”  Shanks 1995 54

insertion of a delay between the action and outcome reduces judgments – increased delay causes a reduction in associative learning…in studies a 4 s action-outcome delay causes subjects to no longer be sensitive to the instrumental associative relationship.

“Thus in this sort of task, people only appear to be able to detect a relationship between their actions and the outcome when the delay between them is less than about 4 s.  It should be emphasized, of course, that much longer delays can certainly be tolerated in other situations.  The slope of the contiguity function is likely to be highly task-specific.”  Shanks 1995 55

is this in any way connected to the finding that the sooner traumas are processed, the less chance there is for PTSD to develop?

“…there is a small amount of evidence that spatial as well as temporal contiguity may influence learning….”  Shanks 1995, 57

overall action-outcome contingency but differing in precise temporal patterning of events….”…judgments depended on whether or not each outcome was preceded by a temporally-isolated response or not” shanks 1995 58….cannot ignore the local characteristics of action-outcome pairings….

“Outside the field of phobias, it is known that cues can differ in terms of the ease with which they can be associated with a given outcome, the best-known example being taste-a version learning.  Animals readily associate gastric illness, induced by an injection of lithium chloride, with a novel food that they have eaten some hours earlier, but they find it difficult to learn an association between a tone and illness.  In contrast, a tone will be (58) far more readily associated with shock than will a novel food (Domjan and Wilson, 1972).  There is clearly something in the nature of the stimuli themselves that operates in addition to contingency and contiguity.  For example, the internal or external nature of a stimulus may be relevant:  stimuli may be easy to associate when they are both internal (food and illness) or external (tone and shock), but not otherwise.  As yet, such factors have not been widely studied in humans.”  Shanks, 1995, 59

“The environment provides us with a number of hints that events are causally or structurally related, amongst which contingency is the most obvious.  Perhaps it is not surprising that humans have evolved to be quite finely sensitive (under ideal conditions) to this factor…the demonstration in humans of such sensitivity not only establishes the adaptiveness of the learning system, but also provides a fundamental empirical phenomenon against which theories of associative learning may be compared.”  Shanks, 1995, 59

Why, then, would it be such a stretch to say that dissociation, as a rule, exemplifies instances when associational learning has gone awry?  When something is NOT learned – that in different circumstances, or different situations would enable associational learning to occur – that dissociation results when necessary learning situations are present but there are factors that interfere with completion of the act of learning?

What happens in situations where there is an interference between the normal stimulus – cue – target action cycle so that associational learning that should occur cannot? How could there not be some circumstances in which interferes interrupt the learning?  If one is considering that dissociation can be seen in 12 month old infants, what it actually is must be very basic.  If infants are learning in associational contexts from birth, then their dissociation has to be a part of that continuum.  It can’t just be a mysterious “something else” entirely different.  When Liotti calls dissociation in infants an unconscious coping strategy some children use to cope with traumatic experiences, this, to me, is a form of anthropomorphizing – it is suggesting that if they were as advanced as others their age they would be doing something else? What, exactly, are their options at that age?

“…there plainly are situations in which biased judgments may be obtained.  In situations where the conditional probabilities cannot be assessed across an unchanging background, but where subjects have no difficulty making associative judgments, the predictions of the account become unclear.  When trials are presented in blocks rather than intermixed, effects of trial order can occur which are outside the scope of the theory, and biases can also be induced by varying the schedule relating the action to the outcome.  Finally, I have argued that in some situations, particularly those involving manipulations of contiguity, the normative theory can come close to being undefined.”  Shanks 1995, 59

concept of similarity:  “…it has become commonplace to interpret similarity in terms of distance in a psychological space.”  Shanks, 1995, 61

“Essentially, prototype and instance theories assume that some mental representation is formed as a result of exposure to a set of training stimuli, with responding to further stimuli being a function of their similarity to the represented stimuli.”  Shanks 1995, 61

“Nosofsky (1992) has noted in a recent review, the idea of a psychological space and the development of accompanying techniques for analyzing such spaces have proven to be amongst the most significant advances made in cognitive psychology in the last 40 years, since they allow us to discover regularities about that apace that are distinct from regularities holding in physical space.”  Shanks, 1995, 62

“…stimuli represented in the mind of an observer in a way that reflects his or her perceptual as well as cognitive capacities, with the representations of the stimuli not necessarily corresponding to their physical descriptions….In order to discover how stimuli are represented in psychological space, we need to use a statistical method such as multidimensional scaling (MDS), which is one of a family of techniques for recovering the psychological structure inherent in a class of stimuli (Shepard, 1980).”  Shanks, 1995, 62

“…stimuli judged most similar appear close together in the spatial solution, and those judged most dissimilar appear furthest apart.”  Shanks, 1995, 64

“Similarity ratings have been the most common type of proximity measures for pairs of stimuli, but another measure that is of more relevance to associative learning involves identification learning….two stimuli far apart in psychological space are less likely to be confused….identification confusion data…can be interpreted in terms of similarities between points in a multidimensional space….points…are such that if the distances between all pairs of points are computed and rank ordered, then that rank ordering will very closely match the rank-ordering of confusion frequencies.”  Shanks, 1995, 64

identification learning

improvement of classification accuracy, lessen distortions of patterns, become more discriminating, so-called perceptual learning

Forgetting – “Experimental evidence suggests that the extent to which information is genuinely lost or unlearned is negligible, and instead, forgetting is almost entirely attributable to retrieval failure.”  Shanks, 1995, 93

“…forgetting is not in the main due to real unlearning or fragmentation of memory traces but is instead due to the fact that later information blocks the retrieval of earlier information….blocking of the target items by subsequent items only occurs when the latter are active in memory…..It appears that the behavioural phenomenon of forgetting is not due to a genuine loss of stored memory traces.  Hence it is not as implausible as it might seem to suppose that people have implicit access to stored instances.”  Shanks, 1995, 95

“…the only way in which information is transmitted in an adaptive network are via the excitatory or inhibitory influence of one unit on another, and of course these are precisely the processes by which neural activity is propagated in the brain.”  Shanks, 1995, 105

“…connectionist networks are by their nature parallel processing devices, in that the connectivity of individual units allows parallel sources of information from other units simultaneously to influence the state of activation of any given unity.  The appeal of such parallel processing comes from the following observation.  People are extremely good at retrieving stored knowledge from partial cues, even when some of the cues are inappropriate.  For instance, a friend can often be recognized even if part of their face is occluded or if they are wearing an unfamiliar pair of glasses, a word can be made out even if poorly enunciated, and so on.  This kind of memory is called content-addressable, because part of the content of the memory is used as the cue for retrieving the whole item, and it is particularly easy to achieve in parallel systems (and correspondingly difficult to achieve in conventional non-parallel ones).”  Shanks, 1995, 105

OK, I see here he is going to talk about something I was writing about this weekd – feedforward loops – he is calling networks.

“Imagine that memories are stored as patterns of activation across a large number of units.  When at a later point some subset of those units is reactivated in parallel to represent the retrieval situation, the connections between the units will allow excitation and inhibition to spread such that the entire original pattern of activation is recreated.  Even if some units are inappropriately activated, the original pattern may still be recreated if it represents the best ‘solution’ to the current set of input cues.  Essentially, connections can be seen as constraints that exist on the spread of excitation and inhibition through the system.”  Shanks, 1995, 105

This is where the plasticity-toxicity problem lies when the neurons in the hippocampus become toxic through over excitation – and in my thinking, this is related to the brain being geared up to learn something it cannot learn.  If the suggestion is correct that cognition is continued evolution within the brain, and if evolution is the natural forward movement of life, and if the brain needs to learn continually, to associate continually, and if we are in traumatic situations that are beyond the brain’s capacity to learn from (due to pressure of limitations that either can or cannot be accounted for and worked around within the brain) – then the continual hyperarousal of PTSD, the inability to integrate memory, is the brain’s reaction, along with the body, of a process that is really de-evolution – resources are not enabling forward movement – meaning entropy has the reins.  The brain reacts by killing itself – neuronal death referred to as suicide – it has no choice – unless we see what is happening and find a REAL way to ameliorate the difficulties – not just throw drugs at the brain and call it good enough.  We have to use Superman vision, Superwoman vision – what is going on on the inside???  I wrote about this earlier in the week – what happens between the feedforward and feedback loops when interrupted in flow by trauma….

“…feature of adaptive connectionist networks is that knowledge is distributed across very many connections.  Each connection represents a relationship between a pair of what we might best call micro-features, and hence it requires a large number of connections to represent memory for a complex object such as a face.  At the same time, any given connection can contribute to many different memories.  In short, a network can store a large number of superimposed patterns with each one being distributed across the network and with each connection contributing in a small way to very many memories.  As a consequence, networks tend to demonstrate considerable resilience in the face of degradation.  If some connections are removed or if noise is added to them, there is still a possibility that useful information may be retrieved from the system – again, a characteristic shared by real brains.”  Shanks, 1995, 107

connectionist models – connectionist learning rules — THE DELTA RULE –

FEEDFORWARD NETWORKS OR PATTERN ASSOCIATORS

a feedforward network – “A homogeneous layer of input units is connected in parallel to a layer of output units.  The connections between the units have modifiable weights.  When a pattern of activation (representing the input stimulus) is applied to the input units, activation spreads to the output units via the weighted links between the units.  A learning algorithm adjusts the weights on a trail-by-trail basis until the correct pattern of activation is obtained on the output units…..an autoassociator. Here, there is only a single layer of units dealing with both input and output.  Each unit provides an input to every other unity but not to itself”  Figure 4.1 shanks, 1995, page 106

“Suppose we have a large set of potential cues or actions and an equally large number of possible outcomes or categories.  We assume that each of the cues is represented by a unit in a homogeneous input layer of a large, highly interconnected network such as that shown in the left panel of Figure 4.1 [see above for notations].  Each output is also represented by a unit in a separate output layer, and each input unit is connected to each output unit with a modifiable connection (for the moment, we ignore possible ). (107)  Networks of this form are called feedforward networks or pattern associators.  In reality, each cue and each outcome would be represented not by a single unity, but by a large collection of units corresponding to the elements (or microfeatures) of the stimulus, and the subject would have to learn structural associations amongst the elements of the cue, amongst the elements of the outcome, as well as the association between the cue and outcome.”  Shanks, 1995, 108

“Using one type of network for between-stimulus associations and another or within-stimulus associations [autoassociator] may seem unjustified, but in fact the differences between feedforward and autoassociative networks are more apparent than real.   An autoassociator can be considered as a feedforward network in which the input…and output patterns…are identical and where the connections between an input unit and the corresponding output unit…are deleted….The removal of these connections means that the network is forced to predict a given element of the output pattern on the basis of different elements of the input pattern….The system is therefore forced to learn about the internal structure of the set of elements making up the cue.”  Shanks, 1995, 109

“…many feedforward connectionist models incorporate a layer of ‘hidden’ units that intervene between the input and output units…The development of multilayer networks using this generalized version of the delta rule has provided a major contribution to recent connectionist modeling since phenomena such as learning of nonlinear classifications that are impossible for single-layer networks can be easily dealt with by (129) multilayer networks.”  Shanks, 1995, 130

“…backpropagation networks [model] can learn essentially any mapping between a set of input and output patterns that one cares to construct.”  Shanks, 1995, 130

can’t learn what humans do, learn a nonlinear classification of stimuli as fast as a linear one

“…whereas genuine unlearning seems to play a rather minor role in normal human forgetting, it appears that backpropagation networks are extremely prone to unlearning; indeed, they seem to suffer from an effect known as ‘catastrophic interference’, whereby target information is almost entirely overwritten or unlearned by later interfering information in a way quite uncharacteristic of human performance.”  Shanks, 1995, 132

“It is very difficult for such a network to maintain a record of a set of information in the face of some new information that has to be learned.”  Shanks, 1995, 133 ..does not provide a good model of human behavior 135

What is the human process of integrating something already learned so that something new can be learned?  These backpropagation networks  erase all learning of a first stimuli while they are learning about the second one – not sure what that means…

Selective attention process

“A typical learning task will therefore entail two processes, one (135) whereby stimuli come to be associated with outcomes and one which alters the perceived inter-stimulus similarities.”  Shank, 1995,137

they are trying to construct an adaptive network model of learning….has to sa something about how selective attention is to be dealt with

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associative learning

Suzuki, Wendy A. 2005

“…novel information is first acquired, and if strengthened through a process called consolidation, is eventually stored in long-term memory.  The structures of the medial temporal lobe are essential for this ability to acquire new long-term memories for facts and events. [bolding mine]  This kind of memory is called declarative memory in humans and relational memory in animals….the key medial temporal lobe structures important for declarative/relational memory include the hippocampus together with the surrounding entorhinal, perirhinal and parahippocampal cortices…. it is clear that the structures of the medial temporal lobe are essential for the acquisition of new declarative/relational memories….”

“…my laboratory has recorded the activity of individual neurons in the hippocampus as monkeys perform various memory demanding tasks.  We have focused on one particular form of declarative/relational memory, called associative memory, which is defined as the ability to learn and remember the relationship between unrelated items such as the name of someone we have just met or the aroma of a particular perfume.  Specifically, we examined the patterns of activity in hippocampal neurons as monkeys are in the process of forming new associations in memory…..Our long-term goal is to understand the evolution of learning-related signals throughout the medial temporal lobe as memories are initially established, strengthened and eventually stored in long-term memory.”

“…medial temporal lobe participates importantly in the normal performance…[of the] ability to learn new location-scene associations (Brasted et.al., 2003….).

new location-scene associations: I could see that this is disturbed in trauma.  For me, with all the trauma I experienced, there was no predict and control, so how could associations be connected to one another correctly?  Hence, dissociation?  I can also see that the person begins to limit their exposure to learning, to limit their exposure to stimuli, and this, too, would limit our opportunities to learn.  Yet I still say that there as so much going on in my family, particularly the moves, that we were forced to learn new active coping skills continually to cope with these new location-scenes – new schools, new houses, etc.  I think it helped us to compensate somehow for the insanity in the home.

“…the hippocampus, a medial temporal lobe structure long implicated in associative learning and memory….”

They found in their monkey study that 18% of the total population of hippocampal cells recorded “…exhibited changes in neural activity across trials that were significantly correlated with the animal’s behavioral learning curve for a particular scene.  We called these cells “changing cells.”  Two categories of changing cells were observed.”

“Sustained changing cells (54% of the population of changing cells) signaled learning with a change in neural activity that was maintained for as long as we were able to hold the cell (typically 30 min to 1 hour).  Many of these cells exhibited dramatic increases in neural activity that paralleled the  animals’ behavioral learning curve for that association….Importantly, these learning signals were highly selective in that a changing cell would typically only change its activity for one particular learned scene while the responses to other learned scenes did not change over time…..changing cells typically responded with little or no activity to the reference scene with the same rewarded target location.  These findings support the idea that the changing activity is related to learning of a new association between a scene and a target/eye movement and not learning of a particular motor response….changing cells identified in the first set of learned location-scene associations never signaled learning of a second novel set of location-scene association even when the rewarded target location was the same….”

“The remaining 45% of changing cells exhibited a different pattern of learning-related activity.  These changing cells started out with a scene-selective response during either the scene or delay period of the task early in the session well before the animal learned the association.  These cells signaled learning by returning to baseline activity and this return to baseline was typically anti-correlated with the animal’s learning curve for that particular scene….We called these cells baseline sustained changing cells.  Importantly, the changes in neural activity seen in the baseline sustained cells were as selective for a particular learned scene as the sustained changing cells.  Similar patterns of activity were never seen for the reference scene with the corresponding rewarded target location suggesting that these signals were not motor-driven.”

“Thus, both sustained changing cells and baseline sustained changing cells provide a highly selective signal for when a particular scene is learned.  We hypothesize that these selective increases and decreases in neural activity that occur across the hippocampal population may constitute a hippocampal network learning signal.”

“We found that hippocampal changing cells could both precede…parallel…and lag…behavioral learning….These finding [sic] suggest that the hippocampus participate in all states of the learning process from several trails before behavioral learning is expressed, when the observed activity may be involved in driving the behavioral changes that underlie learning to several trials after learning, when the activity may be involved in strengthening the newly formed association.”

“We showed that cells in the hippocampus provide strong learning-related patterns of neural activity that participate in the initial formation of new associative memories.  Because these changes can occur before, at the same time, or after learning, these findings suggest that there may be a gradual recruitment of a network of hippocampal neurons during the formation of new associative memories.”

“Previous studies have shown that in addition to the hippocampus, cells in several other brain areas including the prefrontal cortex (Asaad et al, 1998), frontal motor-related areas (Brasted and Wise, 2004….), and striatum (Brasted and Wise, 2004) exhibit similar patterns of learning-related activity during similar associative learning tasks.  An important long-term goal will be to understand how all these brain areas from the hippocampus to the motor related areas of the frontal lobe and striatum may work together to underlie the initial formation as well as the early strengthening and consolidation of new associative learning.”

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Tucker, 2001

KINDLING

Cortex….cognitive organization….”framework for reasoning between connectivity and function….

“…improved methods of characterizing the anatomical networks of the cortex have for the first time detailed the connectivity of the primate brain that must form the substrate for distributed cognitive representation (Barbas, 1995; Pandya and Yeterian, 1984).”  Tucker, 2001, 125

“hemispheric asymmetry for global versus local perceptual and cognitive representation…difference may map directly onto the anatomical differences between right and left hemispheric patterns of cortical network architecture…”  Tucker, 2001, 125

“The more densely interconnected right hemisphere may support more global cognitive processing.  This structural isomorphism of cognition and cortex may also be important in understanding hemispheric asymmetries for emotion….The right hemisphere’s capacity for interpreting nonverbal emotional communication may draw on its holistic representational skills, integrating sensory data and interoceptive responses within a single conceptual framework….”  Tucker, 2001, 125

“…the cortex is not a complete organ.  It is dependent on subcortical mechanisms not only for motivational control, but for the most fundamental cognitive operation, memory.”  Tucker, 2001, 125

“In this chapter, I will consider the primary mechanisms of subcortical control of the operations of memory in cortical networks….I will suggest that we need a new theoretical model of the cortex, what might be called a ‘core-and-shell’ model.  At the limbic core of the cortex are motivational mechanisms, centered on the hypothalamus.  Forming the shell or interface with the environment are the sensory and motor neocortical networks.  Memory is organized through reentrant arbitration, creating a functional resonance between the paralimbic networks of the core and the neocortical networks of the shell.”  Tucker, 2001, 125

model of the functional bases of the cortex  Tucker, 2001, 125

hypothalamic projections to paralimbic cortices

“…speculation on the evolutionary origins of mammalian neocortex from the reptilian and avian external striatum.” Tucker, 2001, 126

core-and-shell model is fundamentally a speculative theory of cortical evolution, useful role in neuropsychology of emotion

“It serves to organize the several lines of evidence on the adaptive self-regulation of cognition that must be explained by any theory…”  Tucker, 2001, 126

“…the most typical emotional response to left hemisphere brain lesions is a depressive-catastrophic reaction….” Tucker, 2001, 126

“…the core-and-shell model may help to explain how the right hemisphere’s dense interconnectivity may actually reflect the close integration of its neocortical networks with the paralimbic core of the cortex.”  Tucker, 2001, 126

core-and-shell….”based on a classical evolutionary-developmental analysis….and with the recognition that embryological development recapitulates evolution….”  Tucker, 2001, 126

“I will…consider two key issues in neuropsychological theory:  the hierarchic organization of human neuroanatomy and the physiological control of memory consolidation in the cortex.  Considering the architecture of corticolimbic anatomy (the patterns and density of cortical connections) and the mechanisms of memory consolidation (the physiological excitability that seems integral to neural plasticity) leads directly to the core-and-shell model.  Cognition emerges when the homeostatic, adaptive, and integrative core negotiates with the shell of sensorimotor networks representing the current flux of the environmental interface.”  Tucker, 2001, 126  [bolding mine]

“The core-and-shell architecture of limbic-cortical networks is positioned at the top of a hierarchy of diencephalic and lower brainstem systems.  Adaptive functioning requires vertical integration of these multiple evolutionary structures.”  Tucker, 2001, 126

“Within the anatomical structure of both brainstem and cortical networks, the nature of neurophysiological control is defined by mechanisms of activation and inhibition.  By framing the general principles of hierarchic anatomy and neurophysiological control, it may be possible to improve our theoretical understanding of basic problems such as hemispheric specialization for emotion and frontal lobe contributions to self-regulation.  The key functional question may be the adaptive control of memory.”  Tucker, 2001, 127

“…a full account of the detailed structure of neuroanatomy, and of its neurophysiological control, must be informed by research on neural plasticity that is still formative and controversial at the beginning of the 21^st Century…..the basic mechanisms of neural plasticity in ontogenesis are only now being worked out, the evidence is growing that there are new opportunities for general insights into adaptive development.”  Tucker, 2001, 127

not sure what the following means, is also true during all the postnatal development of the brain’s architecture, as well, perhaps this is a “behind the scenes” meaning archaic perspective he is voicing below.

“The mechanisms of arousal and motivation that guide an animal’s behavior are also integral to the activity-dependent specification of the brain’s connectional architecture in embryonic development (Tucker, 1992; Von de Malsburg and Singer, 1988).”  Tucker, 2001, 127

“The fine structure of cortical anatomy is differentiated by the self-organization of tissue excitability.  For humans, because our neural ontogenetic process is highly neotenic (retarded), the morphogenesis of cortical connectivity continues throughout life.”  Tucker, 2001, 127

“By framing the issues of hierarchic anatomy and adaptive neural plasticity in broad terms, it may be possible to create a theoretical basis for understanding how complex cognitive operations of the human brain are dependent on the effective organization of elementary mechanisms of arousal and motivation.”  Tucker, 2001, 127

They are also dependent on these regions of the brain having been formed correctly during their windows of opportunity in the first place.  If they don’t form right through caregiver-infant interactions, this whole system is not going to work right later on.

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“…general organization of the mammalian brain retraces several major phases of vertebrate neural evolution.  Each later stage is added to, and modifies the function of, the previous one.”  Tucker, 2001, 127

[mentions rest, but this one below is important as are implicated as flawed in borderlines]

“…the diencephalic structures of the neuraxis, including the thalamus and hypothalamus, are fairly stereotyped across vertebrate species.”  Tucker, 2001, 127

“The telencephalic structures comprising the cerebral hemispheres of higher mammals, including the striatum, limbic system, and cortex, have taken unique paths of differentiation for reptile, avian, and the various mammalian brains (Sarnat and Netsky, 1974).”  Tucker, 2001, 127

“…species variations are added at the end of the root program of ontogenetic specification….progression through terminal additions is the rule, even when the exceptions are definitive.  It is the rule because mutations of the root program are almost always fatal.  Selection therefore operates most freely on the terminal ontogenetic programs, such as those shaping the vertebrate telencephalon.”  Tucker, 2001, 127

“…because ontogeny recapitulates phylogeny, the vertical integration across the evolved forms of the neuraxis is a critical issue for explaining the behavior of the individual as well as that of the species.”  Tucker, 2001, 127

Is he talking of phenotypes for the individual, or just genotypes?  Phenotypes influence who survives and who doesn’t, so must affect evolution in the long run….have to look into this.

Ok, and below—-  this is in the best case scenarios!  If the experience that the infant has that develops its brain is anti-life, makes a mess of things!

“The essential principle for understanding ontogenesis may also be that development is continuous.  This continuity seems to extend from the self-organization of neuroanatomy in the embryo to the self-organization of each psychological process.  Because the mechanisms of neural plasticity are the same processes of activity-dependent specification of neural connectivity that organize the architecture of the cortex in embryology.  (Von de Malsburg and Singer, 1988), cognition appears to be an form of extended morphogenesis.”  Tucker, 2001, 128

So we are not robbed of the process of genesis – positive entropy of cognition – a word which is a female word, btw – ours is just different, and I assume negatively so unless I can “prove” otherwise.  It is not of the norm, and Teicher calls it a malevolent brain…..but any cognitive ability is positive — !

“The process of cognition results in the formation of connections in the cortex through activity-dependent mechanisms of neural plasticity that are essentially embryological (Tucker, 1992).  In this way, microgeny (the development of each idea) appears to extend the process of embryological morphogenesis, and is thus an act of anatomical articulation.” Tucker, 2001, 128

“Because the mechanisms of memory must recruit the controls on neural arousal from each level of the evolved neural hierarchy (Brown, 1977), each cognition can be seen as an act of motivated evolutionary anatomy.”  Tucker, 2001, 128

“…root structures of the brainstem…cannot retain their primordial functional roles, but must be subordinated to support the new functional capacities of a varied and complex telencephalon….The basic principle of this subordination…is hierarchic inhibition:  each higher system adds a level of complexity to the overall brain that requires suppression of, or at least modulation of, the reflex-like operation of lower circuits….[i.e.} the disappearance of primitive reflexes, such as the root-and-suck reflex, as an infant matures.  Yet the disappearance does not mean the reflex is lost; if the adult brain is damaged the root-and-suck reflex may reappear, apparently disinhibited as a result of the lesion.”  Tucker, 2001, 128

This makes me think of the reflexive nature of PTSD reactions…..fast, instantaneous, and bypasses the cortex

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“[studied vocalizations in squirrel monkeys]  At the level of the neocortex, Ploog observed the capacity for ‘voluntary call formation’, in which the animal is able to select the vocalization deliberately, rather than in the more spontaneous cries seen with only limbic control.  In considering human cognition, Ploog (1992) emphasized that language capacity engaging the neocortex may allow volitional cognition that is relative [sic] free of motivational constraints.”  Tucker, 2001, 129

“James [1890] began with Meynert’s dictum, that subcortical structures are capable of fixed actions in response to stimuli, and that only at the level of the cerebral hemisphere can there be adaptive, goal-oriented, organization of flexible responses to a stimulus condition.”  Tucker, 2001, 129

describes this evolutionarily different brain that Teicher talks about, I see that now.  I can also see that PTSD is a fixed action pattern rather than adaptive – the goal only be for the body to survive

“A key issue for increasing adaptive flexibility is temporal span:  the higher networks provide motivational control over a longer interval of time, whereas the lower networks provide more reflexive, immediate response to internal states and external stimuli (Derryberry and Tucker, 1990; Tucker, Derryberry and Luu, 2000).  In fact, it can be seen that the need for motivation as an organismic function only arises when the control system operates with memory capacity, i.e., when it can span an extended interval of time.  When the response is reflexive, there is no memory of the adaptive problem, no directed action plan, and thus no motivation needed.  The cybernetics are immediate and integral to the reflex arc.  However, as coping extends over an increasing span of time, motivation becomes necessary to direct ongoing behavior in relation to the continuing, remembered, adaptive problem (Tucker et.al., 2000).”  Tucker, 2001, 129

Interesting….this describes the PTSD reaction process.  There is a disturbance of memory and of a sense of time with trauma—   perhaps not restored if the cycle cannot complete itself.  In my case, it never got built into the brain in the first place.

I believe that’s partly where attachment fits into this.  An infant’s needs are tied to the coming and going of its caregiver.  Rupture and repair on a basic level, but begins, with prediction and satisfaction, to establish patterns in the brain that span time –

“For example, immediate responses to threat stimuli are organized within the rostral brainstem, in the periaqueductal gray (PAG) area.  This integrative region of the mesencephalic brainstem incorporates connectivity to sensory, autonomic, and motor functions, as well as to the controls on arousal modulation traditionally associated with the reticular activating system.  These packaged assemblies of defensive behavior patterns appear similar to the stereotyped brainstem vocalizations described by Ploog (1981).” Tucker, 2001, 129

packaged, huh?  Like fast food responses rather than slower considered ones

“The anatomical location of the PAG, adjacent to the cerebral aqueduct, is particularly significant in light of vertebrate evolution.  In early vertebrates…the neural tube was open to the sea, and integrative neurons evolved adjacent to elementary chemosensory receptors that sampled properties of seawater.  When the neural tube closed, some periventricular sensory functions (e.g. interoception [stimuli arousing/in trunk of body] of sex hormones) were conserved, but now restricted to the internal medium of cerebrospinal fluid.  Evidencing the importance of the lower brainstem to all vertebrate behavior, the PAG retains a full complement of adaptive controls in the mammalian brain (Luu et al., 1999; Tucker et al., 2000).”  Tucker, 2001, 129

“In defensive behavior, for example, one network of the PAG regulates an integrated pattern of autonomic, pain, and motor control for fighting; another network regulates a different integrated pattern for fleeing, and still another network regulates a pattern for freezing.”  Tucker, 2001, 129

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HYPOTHALAMUS

Panic vs anxiety

“At the higher, diencephalic, level, the ventromedial hypothalamus exerts inhibitory control over these PAG defensive responses, as the hypothalamus provides a more complex tuning of defensive behavior through its integration of sensory data with the organism’s internal state (Risold et al., 1997).  In turn, the hypothalamus is regulated by multiple telencephalic structures that are concerned with defense, including the amygdala, ventral striatum, and orbital frontal cortex.  The increased temporal span (129) of the higher networks of the neural hierarchy is clearly illustrated in the case of defensive behavior.  Whereas the hypothalamic recruitment of the PAG patterns is essential to the response to immediate danger, often termed panic, the amygdala and striatal networks mediate a more extended state of defensive preparation, which could be termed anxiety (Tucker et. al., 2000).”  Tucker, 2001, 130

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insert

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Bhattacharya 2006

Actual level of preference is encoded in two regions – important role in learning – ventral striatum and the ventral midbrain – referring to work led by John O’Doherty, Caltech in Pasadena – we use these prior experience preferences in making future decisions – conditioned response related to like or not like – evolutionary advantage programming related to the environment – related to food poisoning

[Feedback – feedforward]

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Biello 2006

Choosing between familiar and unknown – Nathaniel Daw and John O’Doherty of University College London – “Scientists call the behavior of utilizing a known resource exploitation; the term they give to the behavior of seeking an even better resource is exploration.  Although exploitation seems the safe bet, survival can depend on judicious use of exploration.” – balanced, richest option against desire to choose less familiar option that might serve us better – usually seamless switching between the two [as per gambling] –

“They found that human exploration follows the so-called softmax mathematical rule, in which subjects choose whether to explore or not based on the probability of a better payout.  In other words, if you determine your reward at a given machine will be small, you are more likely to change…..The fMRI showed that the frontopolar cortex and sulcus of a given subject strongly activated when they chose to explore.  Other studies have implicated these regions in behavioral control and decision making…but this is the first time neuroscientists have marked these areas of the brain as associated with investigating the unknown.  Exploration turns out to be a controlled gamble after all.”

This is making me think of young children, especially during their theta brain wave phase particularly 3-6 when they are developing their theory of mind, trying to learn the rules and apply the rules – but suffer betrayal trauma [see ref on this under attachment] that breaks all the rules – and perhaps shuts down their exploratory process so that a breach is formed and an alternative direction is taken – where this attachment betrayal implies implicit danger in their environment such that further exploration is considered by the brain to be unwise – exploitation (as the child has been exploited) comes through a different motivational circuit than does attachment – activates the competition circuit – side swipes the future caretaking circuit – enables “revenge” based on childhood rule interpretation – the big rule has been broken, the big rule (adult) is obviously what matters – how can a child’s attempts to understand all the fine-tuned rules that govern our interactions in a balanced theory of mind begin to measure up against the big rules?

It has to all be related to basic human processes.  When an infant “hatches” and first slides off of its caregiver’s lap into the big world, it has no idea of the risk or of the dangers, but it learns quickly.  All these learnings from these experiences are built into the brain – and my guess is that somehow they are formulated into what we could call rules.

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“…the cortex normally modulates and inhibits the hemisphere’s subcortical (limbic and striatal) responsivity.”  Tucker, 2001, 130

“…human motivational and emotional mechanisms incorporate a hierarchy of neural networks crossing the multiple levels of the neuraxis.  Inhibitory control of higher over lower levels appears to be a key principle of operation.  However, this inhibitory control must be complex, involving sophisticated processes of recruitment and subordination of the lower, more reflexive mechanisms, rather than simple suppression.  In addition, the direction of control is not only top-down, but bottom-up as well:  the higher networks of the telencephalon appear to be critically dependent upon diencephalic and mesencephalic circuits for regulation of arousal and activation.” Tucker, 2001, 130

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“By articulating memory through consolidating synaptic architecture, cognition continues morphogenesis.”  Tucker, 2001, 130

“the quickening” – “…the first movements that the mother feels in her womb…the spontaneous, spasmodic motor activity of the fetus is highly functional, providing the self-activation of neural circuits that organizes the connections of the vertebrate brain through activity-dependent specification (Hamburger, 1977).  Through a process of exuberant synaptogenesis, mammalian embryology prepares for specification of the connectivity of the cortex through a substractive elimination (use it or lose it) rule (Greenough and Black, 1992; Merzenich and Sameshima, 1993).  Activity-dependent articulation of cortical anatomy is thus determined by neural activity in whatever form it takes, not only that caused by environmental stimulation, but perhaps more fundamentally that caused by the animal’s self-regulation of activation.”  Tucker, 2001, 130

“For humans, the extended neural plasticity of adult learning continues to be supported by the multiple levels of regulating activation across the neuraxis.”  Tucker, 2001, 130

“For mammals, the reticular activating system (RAS) now is subordinated to serve a more elementary integrative control, monitoring curde features of sensory inputs (loudness, abruptness, nearness) and translating these into levels of activation to apply to higher brain centers (Moruzzi and Magoun, 1949)…..the projection systems from the mesencephalic RAS to the diencephalons and telencephalon are chemically specific, with each neuromodulator (acetylcholine, norepinephrine, dopamine, serotonin) applying a unique, and as yet poorly understood, form of control in its projections to widespread regions of the forebrain.”  Tucker, 2001, 130

“The key sensory agenda for the hypothalamus is the internal bodily state, represented as multiple parameters including hunger, thirst, and sexual drive.  Represented in this way, the hypothalamus appears to provide reference or set points to guide activating mechanisms as a function of need states….the hypothalamus exerts important regulatory influences over telencephalic processes that appear to represent the diencephalic extension of the mesencephalic reticular formation….”   Tucker, 2001, 130

“In contrast to the internal regulatory operations of the hypothalamus, the thalamus can be seen to achieve the representative functions of the diencephalons, organized for specific sensory and motor nuclei that represent the patterns of perception and behavior.  In mammals, the massive cortex subordinates these sensorimotor representative functions, and the thalamus is often described as a relay for the sensory and motor pathways to the cortex.”  Tucker, 2001, 130

“…the reticular networks of the hypothalamus that regulate the brain’s response to the internal state have important diencephalic counterparts in the reticula of the thalamus.  Essential controls over the activation of the cortex are exerted through the ‘non-specific’ thalamic nuclei, sometimes termed the diffuse thalamic projection system.  A remarkable control structure is the reticular nucleus of the thalamus, a neural network forming a sheet around the anterior thalamus and gating the traffic from thalamus to cortex as a function of both cortical and striatal inputs…..At the diencephalic level, these thalamic reticula can be seen to integrate the representative functions in parallel to the hypothalamic integration of the regulatory functions.”  Tucker, 2001, 130

“Thus from the earliest levels of vertebrate neural organization, the regulatory functions have been achieved by reticular networks, web-like organizations that organize multiple inputs and outputs into matrices of neurons capable of integrative processing.  In mammals, a massive and highly ordered reticulum appeared in the form of the cerebral cortex. ”  Tucker, 2001, 130

“Through integrating top-down projections from the cortex and other telencephalic structures, activity control centers such as the brainstem reticular activating system or the reticular nucleus of the thalamus provide the mechanism for self-regulation of the brain’s activation level through higher cognitive representations.  Fundamentally, the integrative reticula achieve control through regulating the mechanisms of neural activation and arousal.  These control mechanisms have been recognized by neurophsychologists as critical not only to elementary motivation and arousal processes, but also to the most complex executive processes of self-control (Luria and Homskaya, 1970).”  Tucker, 2001, 130

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“Because the brain’s connectional anatomy is achieved through activity-dependent synaptic differentiation, the regulatory (activity) controls remain the essential determinants of the representative (memory) functions of the continually developing brain.”  Tucker, 2001, 131

“In humans, the limbic and brainstem circuits are modulated by complex and largely inhibitory controls from the massive cortex, with the result that human motivation, and human awareness, may extend over spans of time that are unknown in the rest of the animal world.”  Tucker, 2001, 131

“Key roles in both architecture and physiology are played by the limbic nuclei of the telencephalon, including the amygdala, hippocampus, and septal nuclei, structures which occupy pivotal roles in the connectivity of the neocortex and in the funneling of cortical connections to the diencephalons and lower brainstem.  In addition, the other major nuclei of the telencephalon, the basal ganglia, play critical roles in regulating cortical function, not only for motor control but for sequencing and organizing attention, memory, and cognition.” Tucker, 2001, 131

regulatory core and representative shell

growth rings of the brain, ripples from evolution – “…each wave of neocortical differentiation took shape interior to the existing rings (Romanski et al., 1999), forming a new, architectonically more complex island within the more primitive general cortex…..we can understand the evolution of the sensory shell as each new island network took up the thalamic projection that had previously gone to the adjacent, now concentric, ring (Tucker, 1992).”  Tucker, 2001, 135

“Each primary sensory cortex is a cytoarchitectonically homogeneous island, connected only to a ring of adjacent secondary sensory cortex (Romanaski et al., 1999).  That network is connected to another ring, and so on through five architectonic network layers, the last of which is limbic cortex, i.e. either archicortex or paleocortex (Mesulam, 1985).”  Tucker, 2001, 135

“Thus, the global pattern of cortical connectivity is a ‘fan-in’ from sensory cortices toward the paralimbic cortex.  These fan-in or ‘limbipetal’ connections have a systematic projection pattern….This gives the impression that the thalamic input…is relayed to the layer…of progressive processing networks until it reaches limbic cortex, as if the sensory data is being integrated and modeled at each stage (Tucker, 1992).  Tucker, 2001, 135

“Although the functional implications of this highly ordered network organization are not yet understood, we can surmise that they must be critical in some way to the bidirectional corticolimbic traffic necessary to support memory consolidation (Tucker, 1992).”  Tucker, 2001, 135

“Furthermore, the density of intercortical, and callosal, projections increases for each network closer to the paralimbic cortex (Pandya and Yeterian, 1984), creating a pattern of cortical connectivity in which global integration must be achieved by the more generic, primitive, fully interconnected paralimbic networks, and local sensory or motor processing must be achieved by the more differentiated neocortical island networks (Tucker, 1992).”  Tucker, 2001, 135

“With our massive frontal and parietal cortices, we humans are of course at the apex of associating….But it was not obvious until the detailed studies of Pandya and associates that the core-brain paralimbic cortices must be the integrative centers of the brain, receiving the (135) terminal projections of cortical sensory networks and originating the source projections of the cortical motor networks.”  Tucker, 2001, 136

“The remarkable implication of this architecture is that the neocortex performs specialized modular processing for sensory and motor operations, whereas the primitive, fully interconnected, paralimbic cortex must perform the more general, abstract, cognitive functions.”  Tucker, 2001, 136

“…it is reasonable to conclude that the motivational constraints, intrinsic to paralimbic cortex may also be intrinsic to the global semantic integration provided by the paralimbic regions (Tucker, 1992).  With its close connection to limbic nuclei (amygdala, hippocampus), neostriatum (caudate, putamen, pallidum), and the diencephalons (thalamus, hypothalamus, mammilary bodies), the limbic cortex is pivotal for the motivational control of the cognitive and attentional operations of the cortex (Mesulam, 1985).”  Tucker, 2001, 136

“…it is in the paralimbic networks at the core of the brain that we must find the integration of semantic representations with intrinsic adaptive controls (Derryberry and Tucker, 1990).  This neural architecture may be consistent with cognitive analyses that have found elementary dimensions of evaluation, activity, and potency to form the basis for semantic judgments (Osgood, Suci and Tannenbaum, 1957).”  Tucker, 2001, 136

“The behavioral specialization of the ventral pathway appears to be object perception and memory….Although the differing memory specializations of the archicortical and peleocortical pathways…appear to extend to the organization of spatial and object working memory, respectively, in frontal lobe….”  Tucker, 2001, 136

“…each of the two major roots of cortical evolution appears to have unique connectivity with subcortical as well as cortical structures, thus providing a specialized mode of integrating cortical representative functions with subcortical regulatory functions.”  Tucker, 2001, 136

“Given its importance to spatial cognition, the dorsal cortical pathway may draw upon its cingulate roots to provide the capacity for emotional evaluation to direct attentional orienting (Bear, 1983).  Consistent with this is the evidence that the parietal (dorsal pathway) functions of spatial attention are linked with the posterior cingulate gyrus representation of motivational values and expectancies (Mesulam, 1981).  The growoing data on the role of the anterior cingulate gyrus in effort and self-control provides further evidence of the archicortical basis of the psychological operations of the dorsal pathway….Although it has been considered to be primitive, paralimbic cortex, the cingulate gyrus has recently been found to contain a class of neurons, spindle cells, that are unique to pongids and hominids (Nimchinsky et al., 199).  The spindle cells are not seen in monkeys, are sparse in common chimps, are more dense in bonobos, and are organized in dense clusters in humans (Nimchinsky et al, 199).   Thus, although the general progression of mammalian cortical evolution has been toward neocortical differentiation from the paralimbic roots, complementary evolution of the cingulate base of the dorsal pathway appears to have conferred some advantages in the evolution of the big apes.”  Tucker, 2001, 137

“With strong interconnections with the amygdala and ventral striatum, the paleocortical ventral pathway must bring the specific motivational functions of the ventral limbic circuits to regulate the object perception and memory operations of the ventral cortical trend.  Tucker and Derryberry (1992) proposed that the extension of the ventral pathway to the orbital frontal love would allow object working memory to be modulated by the vigilance and anxiety integral to the flight-flight modes of the ventral limbic circuits.  Although this ventral limbic circuitry, together with its associated cortico-striatal networks, has been implicated in the pathological attentional and cognitive constraints of anxiety and obsessive-compulsive disorders, it may be integral to effective attention as well.  When it is appropriately modulated, anxiety may focus and sustain working memory adaptively, allowing the ventral corebrain motivational mechanisms to direct the substantial capacities of the frontal neocortex in action planning (Luu et al., 1999; Tucker and Derryberry, 1992).”  Tucker, 2001, 137

++

connectionist modeling…pattern of connections ….interpret the functional architecture of a newural network (McClelland et al., 1995; Rumelhart and McClelland, 1986)

functional architecture of the telencephalon, dominated in humans by the massive cortex of the cerebral hemispheres.

“The evolution of the cortex has elaborated the contrasting influences of two poles, one regulatory and one representative, each anchored in its diencephalic roots.”  Tucker, 2001, 137

“At the medial core of the hemisphere is the paralimbic cortex…the paralimbic cortex elaborates the operations of the limbic structures, which in turn represent the telencephalic extension of the hypothalamic regulatory function.  At this core, the regulatory function is closely linked with the evaluative monitoring operation of the hypothalamus.  The insular cortex reflects the visceral state, and the cingulate cortex reflects the hedonic evaluation of ongoing sensory and cognitive processes and their implicit implication for action (Luu, Flaish and Tucker, 2000b; Mesulam, 1985).”  Tucker, 2001, 137

“The continuity with the integrative reticula of the brainstem is seen in the way that the paralimbic core controls arousal mechanisms at the same time that it monitors the bodily state.  Just as the hypothalamus forms the diencephalic extension of the mesencephalic reticular formation, the paralimbic cortex is the telencephalic extension of the hypothalamus (and limbic thalamic nuclei), feeding back to both diencephalic and brainstem networks to adjust specific, neuromodulator-mediated modes of brain arousal in response to current motivational demands (Gabriel, 1990; Gabriel et al., 1986).”  Tucker, 2001, 137

“Forming a shell of environmental interface networks, the neo cortex provides models of sensory (137) and motor data that are relatively isolated, through multiple cortical network maps, from the regulatory limbic constraints.  Because of this, higher mammals have gained sensorimotor and cognitive capacities that have greater separation from immediate adaptive constraints, i.e. greater working memory, than is the case for lower animals.  As each growth ring differentiated to form a new thalamic model, interposing itself between the thalamus and the previous corticothalamic model (Tucker, 1992), the architecture of the cortex gained a new complexity, in which there was increasing separation of the representative shell from the regulatory core.”  Tucker, 2001, 138

“This separation gave rise to cognition that spans increased domains of sensation and action, and to behavior that spans increased intervals of time.  In addition, the separation of the core and the shell required continual network processing to arbitrate across the layered networks, negotiating the enduring core of the bodily self with the fluid shell of the sensorimotor interface.  In this negotiation, complex representational forms (ideas and personalities) are achieved by the process of memory consolidation.”  Tucker, 2001, 138

++

“Throughout the vertical hierarchy of the neuraxis, a functional division is maintained between homeostatic, regulatory networks and sensorimotor, representative networks. This division appears to have been maintained in the progressive differentiation of the sensorimotor neocortices from the primitive general cortex of the paralimbic core.”  Tucker, 2001, 138

“Adaptive cognition thus emerges as memory consolidation continually weaves the web of multileveled representations, linked across the progressive, reentrant transformations from the bodily core to the environmental shell.”  Tucker, 2001, 138

++

MEMORY

“The fact that motivational significant events strongly engage the mechanisms of memory, whereas insignificant events do so weakly if at all, indicates that this process of consolidation must be under control of the brain’s adaptive mechanisms (Derryberry and Tucker, 1994).”  Tucker, 2001, 138

PTSD must interfere with this natural order of things.  Does the body decide that the experiences of trauma are insignificant for attention – because it is not possible to find a way to adapt to them, anyway?

“…the mechanisms of memory consolidation require time (Squire and Zola-Morgan, 1988).

“Research on the neurophysiology of the limbic system and cortex has provided evidence of excitable circuits in the limbic system and paralimbic cortex that are integral to the synaptic modifications of memory.  The excitability of these circuits appears directly related to the organism’s state of emotional arousal.  More specifically, the excitability that supports corticolimbic consolidation is dependent on effective vertical integration throughout the neuraxis, as the key limbic and striatal circuits require both diencephalic (thalamic and hypothalamic) and lower brainstem (reticular network neuromodulator) support in order to achieve effective control over the synaptic modification of cortical networks.”  Tucker, 2001, 138

“For both the dorsal and ventral cortical pathways, the connections between neocortex and paralimbic cortex have been found to be essential to allow the neurophysiological mechanisms of memory formation (Squire, 1986, 1992).  Brain lesions that disrupt (138) the normal connections between neocortex and its limbic target result in retrograde amnesia, in which memory is impaired in a graded fashion for the events hours, days, or even years prior to the lesion (Squire, 1986, 1992).”  Tucker, 2001, 139

“The storage is not localized within the limbic structures (amygdala, septal nucleus, and hippocampus), but is distributed across the multiple corticolimbic networks.  However, because disconnection within the pathway disrupts memory formation, and often retrieval as well, the mechanism of memory consolidation appears to require an extended participation of the multiple levels of the corticolimbic hierarchy (Tucker, 1992).”  Tucker, 2001, 139

research efforts o “understand the specific limbic circuitry in memory…”  Tucker, 2001, 139

“The importance of the hippocampus to episodic memory generally, and to spatial memory specifically, seems clear.  The anatomical connectivity of archicortex with the hippocampus is extensive, although the paleocortex may also provide substantial input to the hippocampus as well….Mishkin (1982) has proposed that the amygdala and ventral limbic networks organize an object-based, categorical memory system that is a complement to the hippocampal location memory system.  To the extent that the temporal pole and orbital frontal cortex provide the cortical elaboration of the extended amygdala (Alheid and Heimer, 1988), we can expect the amygdala’s regulation of emotional responsiveness to be integrated with the memory and cognition of the ventral division of the cortex (Tucker and Derrberry, 1992).”  Tucker, 2001, 139

“…many researchers in human cognitive neuroscience seem to assume that memory is in the cognitive domain, whereas motivational and emotional processes are in some other domain….However, given that the emotional facilitation was proportional to the residual memory ability, it could also be concluded that emotion is essential to memory, because whatever memory capacity remains in the amnesic remains responsive to emotional control.”  Tucker, 2001, 139

++

“Memories appear to be formed through modification of the connectivity of neurons in cortical networks…An important model for how this occurs is long-term potentiation in the hippocampus (Malenka and Nicoll, 1999).  If a neuron is made active (through titanic stimulation) at the same time as it receives afferent input, it becomes more responsive (potentiated) to that afferent input, permanently (Teyler, 1986).”  Tucker, 2001, 139

“The primary control on synaptic change appears to be the activity level of the postsynaptic neuron (Gustafsson and Wigstrom, 1988).  Therefore, neuromodulator controls on neural activity appear to be important to setting the context for Hebbian learning.  Although long-term potentiation is typically related to learning in the adult animal, the process of activity-dependent neural plasticity appears to be the same whether it mediates new learning in the adult animal or the specification of cortical connectivity in the embryonic brain.  In both cases, activity controls are integral to synaptic differentiation.”  Tucker, 2001, 140

critical period of plasticity of some systems, structural formation is dependent upon input, is dependent upon normal control by brain neuromodulators

“Given the complexities of neuromodulation with each target neural circuit, it is difficult to predict how global controls on behavioral arousal are related to the control of plasticity and learning…..evidence shows that the excitability of paralimbic cortex is integral to cortical plasticity of learning, and that this excitability is controlled neuromodulator-specific controls on organismic arousal.  These controls on arousal are relevant to motivational mechanisms, including both the effects of stimulant drugs and the effects of environmental stress.  The arousal controls regulate not just the simple quantity of neural activity, but qualitative aspects of neural function, including sensitization and habituation.  Although sensitization and habituation have traditionally been considered as primitive, ‘non-associative’ forms of learning, they may be integral mechanisms to the control of associative learning as well.”  Tucker, 2001, 140

AROUSAL, KINDLING, AND MEMORY

“Limbic cortex may be critical to memory formation not only because of its pivotal connectional architecture, but because of an intrinsic excitability that is integral to the physiology of memory.”  Tucker, 2001, 140

“If electrical stimulation is applied to a region of cortex, producing an afterdischarge, subsequent applications of the same stimulation may produce an increasing afterdischarge (Doane and Livingston, 1986).  At a certain point, no stimulation is necessary:  the corticolinmbic network begins to show spontaneous seizures, as if the intrinsic physiological mechanisms are capable of maintaining the kindling process.  Kindling appears to reflect a synaptic modification that is essentially the same as that seen in long-term potentiation (Lopes da Silva, Kamphus, Titulaer et al., 1995) and perhaps normal learning.” Tucker, 2001, 140

“Importantly, kindling occurs preferentially in paralimbic cortex.  Electrical stimulation anywhere in the cortex is likely to result in a kindled response from the electrically excitable paralimbic cortex (Doane and Livingston, 1986).  Thus, whereas long-term potentiation provides a model learning mechanism for a well-studied hippocampal circuitry, kindling provides insight into the learning mechanism of the cortex as a whole, in which the fan-in connectivity from neocortical regions to paralimbic networks is associated with a particular excitability of those paralimbic networks.”  Tucker, 2001, 140

stress and psychological stress:

“It seems likely that this excitability of paralimbic networks is important to the process of consolidation that allows significant experiences to be instantiated across the multiple network representations of the corticolimbic pathway.  One motivational control that sensitizes the kindling process is psychological stress.  A stressor such as pain shows cross-tolerance with a kindling stimulus, such that the (140) stressor increases the likelihood of that [sic] a subsequent stimulus will produce kindling  (Adamec and Stark-Adamec, 1983).  From this evidence we can infer that normal motivational conditions regulate corticolimbic excitability.  In addition, augmenting neural arousal with a stimulant drug such as amphetamine or cocaine also shows cross-sensitization for kindling with both electrical stimulation and with psychological stress  (Adamec and Stark-Adamec, 1983).  This finding suggests that the key factor is the excitability of the corticolimbic pathway, and the effects of stress are likely mediated through an increase in the control exerted by neuromodulator-specific projections from brainstem reticular formation.”  Tucker, 2001, 141

“Recognizing the similarity between the increasing vulnverability of limbic excitability in kindling and the increasing vulnerability to emotional disorder in chronic manic-depression, Post and his associates have proposed thatkindling may provide a useful analogy for the progressive vulnerability to relaps seen in affective disorder (Post and Weiss, 1998; Post, Weisss, Smith et al., 1995).”  Tucker, 2001, 141

“Considering the cross-sensitization of kindling with stress, Harkness and Tucker (2000) have argued that, for conditions such as post-traumatic stress disorder (PTSD), kindling may be more than an analogy.  The sensitization of corticolimbic networks by a traumatic stressor may be responsible for the emotional hypervigilance, temporal-limbic brain dysfunction, and memory deficits that are observed in PTSD (Harkness and Tucker, 2000).”  Tucker, 2001, 141

Ah, Ha!  Here it is.  I knew this had to be connected, just had to keep going through all of this information to find it!  Yes!

“The sensitization of kindling produced by stress, or that produced by stimulant drugs, would be described as non-associative learning, in that there is a change in the brain’s response but there is no specificity of this response in association with a particular environmental stimulus.  However, the effect itself (kindling) can be expected to alter the neural substrate for memory and thus the process of associative learning.  An interesting demonstration of associative learning of the kindling response itself was provided my Janowsky, Laxer and Rushmer (1980).  After a kindling stimulus had been paired with a tone, the tone by itself was able to elicit the kindled seizure response.  Interestingly, it was necessary to allow several seconds for the tone to be consolidated in memory before the seizure response was elicited on the conditioning trials, suggesting that the normal corticolimbic memory mechanism were necessary to condition the pathological corticolimbic discharges of the seizure.”  Tucker, 2001, 141

Unfortunately for me, the “tone” was conditioned for me to be people!  Like I say, I am allergic to my own species

HORMONES

“One way to link limbic physiology to cognition is to speculate that kindling represents the pathological recruitment of the normal processes of memory consolidation.  The close relation of arousal and memory is shown by the sensitivity of memory processes to circulating hormones, such as adrenaline (McGaugh, 1983, 1990, 2000).  Reflecting the periventricular heritage of the core regulatory networks, both the hippocampus and the amygdala are sensitive to hormonal influences, and they appear to regulate activity in limbic circuitry.  This limbic circuit activity, such as indexed by hippocampal theta, is directly predictive of the effectiveness of memory consolidation (McGaugh, 2000).”  Tucker, 2001, 141

for some reason this brings to mind mother’s fire story, like in the end she couldn’t remember how the story was supposed to end, or that the end of the story was lost as surely as the people in her story were still lost at the end.

“In addition to the limbic circuits, the subcortical telencephalon includes the basal ganglia.  For many years these nuclei have been known to be important to the organization [sic] motor sequences, and recent research has recognized their contributions to learning and cognition more generally….In both cases, the modulation of excitability appears integral to neural plasticity and learning.”  Tucker, 2001, 141

++

“Drawing from input from each of the five regions of the frontal lobe, the striatum does not reciprocate projections to the cortex, but rather projects to the globus pallidum, which in turn exerts inhibitory control over specific motor nuclei of the thalamus, which then project to each of the originating cortical territories. Each loop is reentrant, in that the originating region of cortex is also the target of the loop.”  Tucker, 2001, 141

“The five loops are remarkably separate, such that interactions among them must occur through corticocortical connections, or within the striatum itself.”  Tucker, 2001, 142

“Given the specificity of the cortico-striatal circuitry, we can surmise that each circuit plays a specific role in habit memory and probabilistic classification….key role in the motivational control of habit learning…The DA [dopamine] neurons appear particularly responsive when a reward stimulus is unpredictably good, unaffected when it as good as expected, and show a depressed response when the reward is not as good as expected (Schultz et al., 1998)….striatal neurons may show greater specificity than dopamine neurons, by adapting reward expectancy to new stimulus conditions.  At a more complex level of representation and regulation, neurons of the orbital frontal cortex may code specific preferred rewards differentially.”  Tucker, 2001, 142

“Considering this evidence, an important question becomes the extent to which the cortico-striatal organization of probabilistic, automatic prediction is integrated with the corticolimbic organization of episodic memory.”  Tucker, 2001, 142

attachment disorders show a pattern of incoherency, or faults with episodic memory.  So also does PTSD affect coherence of memory

“Although it may be useful to recognize the separate neural substrates of these memory systems (Squire, 1998), in the normal brain they may develop to function in an integrated fashion.”  Tucker, 2001, 142

key phrase, in the normal brain

“The importance of striatal circuitry to psychiatric disorders is widely appreciated.  In obsessive-compulsive disorder, for example, the unusual repetitive actions suggest exaggerated control from cortico-striatal reentrance, and are reminiscent of behavioral stereotypy in animals given large does of stimulant drugs….The stereotyped actions in OCD are often associated with hypervigilance and anxiety, suggesting a close integration of affective state, attention, and motor control….it seems likely that the cross-sensitization of stress and stimulant drugs seen for limbic kindling is relevant to the sensitization of cortico-striatal mechanisms of habit memory as well.  As a result, the motivational control of arousal state may alter the excitability of limbic and striatal circuits, thereby influencing learning and memory in multiple neural systems simultaneously.”  Tucker, 2001, 142

“The kindling model provides evidence that neural excitability and synaptic control are regulated not just in the frontal lobe, but at multiple levels of the neuraxis.”  Tucker, 2001, 143

“In experimental kindled seizures, it is the excitability of limbic structures and paralimbic cortex that alters the reactivity of extensive networks of the cortex (Doane and Livingston, 1986).”  Tucker, 2001, 143

“The progressive recruitment of limbic, hypothalamic, and mesencephalic reticular networks in the development of seizures is consistent with the anatomical continuity of these regulatory networks, and it may provide important insight into the control of memory as well;”  Tucker, 2001, 143

circuits:

limbic – hippocampus, cingulate

diencephalic – thalamus, mammillary bodies

“It may be relevant that the kindling of seizures requires intact dopamine projections…Both NE and 5-HT appear to exert anticonvulsant actions (Kooy, 1987).  Such effects on neural excitability may be important to memory in the same way they are important to the control of neural plasticity (Singer, 1987).”  Tucker, 2001, 144

specificity of plasticity regulation

the affective quality of the dopaminergic redundancy bias is anxiety

“From a psychological perspective, the proposal is that, as limbic and brainstem mechanisms are recruited, the control of memory is achieved by modulating the continuous levels of anxiety and elation.  The excitability of paralimbic representations may be mediated through the recruitment of brainstem activation and arousal controls, such that an experience gains a purchase in memory to the extent that it resonates with the paralimbic core.  Through this limbic resonance, brainstem pro- (144) jections are engaged, such that the experience generates the anxiety and/or elation required to achieve effective corticolimbic consolidation.”  Tucker, 2001, 145

“Studies of consolidation in rat learning experiments have shown that the amount of EEG theta following practice predicts later retrieval….the amount of hippocampal theta closely predicted the effectiveness of memory consolidation.  Electrical stimulation of the hippocampus also enhanced memory consolidation, and this was directly paralleled by increased corticolimbic theta (Landfield, Tusa and McGaugh, 1973)”  Tucker, 2001, 145

“Although it remains poorly understood the process of consolidation seems to be a key to understanding adaptive self-regulation (McGaugh, 2000).  Although hippocampal theta is not readily observed in humans with scalp EEG, theta oscillations in the EEG are often observed to predict memory performance (Klimesch, 1996).  Theta oscillations over midline frontal regions (reflecting the anterior cingulate gyrus and associated networks) were found to alternate phases of the theta rhythm with motor cortex (Luu and Tucker, 2001).  When subjects made an error on the task, and were aware of their error, the midline frontal theta increased in amplitude, and its correlation with theta over the motor cortex increased, suggesting a functional coupling of the paralimbic (anterior cingulate) with neocortical (motor cortex) networks (Luu and Tucker, 20010.”  Tucker, 2001, 145

++

“Thus, the paralimbic cortices at the core of the hemisphere appear to be highly excitable, both in terms of physiological reactivity as seen in kindling and in terms of degree of plasticity.  In contrast, the neocortical networks forming the shell of the environmental interface appear to be more stable.  An important theoretical question s the implication of these differences for the adaptive control of cognition.”  Tucker, 2001, 145

“…process of myelination signals maturation and a corresponding reduction of neural plasticity….”  Tucker, 2001, 146

“This maturational gradient [of different regions of the brain] appears to reflect a fundamental evolutionary strategy, at least for the big primates, yet it may not be apparent why any loss of plasticity is an advantage.  Why not have all cortical networks retain maximal plasticity to adapt to changing environmental conditions?”  Tucker, 2001, 146

“At the shell, the rigidity of the fully myelinated sensorimotor neocortices allows these networks to model the ephemeral environmental flux (with percepts and motor plans), without themselves being adapted in the process.  At the core, the fluid constructions integrate environmental events with the animal’s motivational state.  Given the stability-plasticity complementarity, the result is a dynamic, evolving concept of the self-in-context. As the core and shell communicate, through the negotiated process of memory consolidation, linked representations are formed which capture features of both the environmental state and the organismic, adaptive significance of that state.”  Tucker, 2001, 147

historical self

“Because they are rigid, the sensorimotor neocortices are able to reflect the continual flux of environmental events and coping actions, while retaining the network patterns formed early in development.  Because they are plastic, the paralimbic cortices hold a single, cumulative, historical concept that, because of the stability-plasticity complementarity, is irreversibly altered by each experience.  From this perspective, memory consolidation must be regulated not just to create a store of experience, but to achieve a strategic balance of stability and plasticity across the multileveled corticolimbic hierarchy (Grossberg, 1984; McClelland et al., 1995).  For each experience, the choice is either new learning or the continuity of the historical self (Tucker and Desmond, 1998).”  Tucker, 2001, 147

interesting implications to think about regarding impossible traumas.  How necessary is it to us to preserve this “self” in any given situation?

“In reviewing the evidence of extended plasticity in paralimbic networks, Barbas (1995) speculated that this developmental outcome may leave the human brain vulnerable to disorganization, such as seen in psychiatric disorders.  The balance between limbic and neocortical contributions to psychological functioning has been an important question in neuropsychological approaches to psychiatric disorders for many years….psychiatric disorders may involve a disrupted balance between neocortical and paralimbic networks, particularly within the frontal lobes.”  Tucker, 2001, 147

“Frontal inhibition of emotional responsivity was observed when Johansson, Gustafson, Passant et al. (1998), examined the cerebral blood flow of spider phobics as they watched a video of spider activity.  Those patients who reported being in control of their fear showed increased right frontal blood flow, whereas those who reported panic during the procedure showed decreased right frontal blood flow.  Other research has observed that frontal (neocortical and intermediate corticolimbic networks) activity may be inversely correlated with paralimbic activity.”  Tucker, 2001, 147

spindle cell

“Given the radical neoteny of human ontogenesis, a major feature seems to have been the extended plasticity of the core networks (Barbas, 1995).  The retarded morphogenesis of these networks may have facilitated the novel cytoarchitectonic mutation of the cingulate spindle cells (Nimchinsky et al, 1999).”  Tucker, 2001, 148

“The extended plasticity and excitability of the human core networks must be complemented by regulation by the complex representational capacities of the multileveled neocortex.”  Tucker, 2001, 148

“The shell appears specialized to reflect and interface with the changing environment.  The core appears specialized to maintain the adaptive, historical base.  Cognition then takes form as a five-leveled construct to span these informational constraints.”  Tucker, 2001, 148

++++

“Although the mechanisms remain to be understood, memory appears to require some form of consolidation, in which processing over time integrates an experience within the architecture of the cortex.  The critical role of limbic circuits in memory suggests that some form of excitability in paralimbic cortex results in a physiologic process operating across the linked corticolimbic networks to integrate and stabilize the multiple levels of representation.  Clues to the nature of this excitability are given by the mechanisms of long-term potentiation and kindling.  The cortico-striatal circuits appear to play parallel roles to limbic circuits in organizing action patterns, and they appear to be modulated b similar brainstem neuromodulator projection systems.” Tucker, 2001, 148

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Stover et al 2007

“Preclinical studies of the effects of stress suggest a minimum of three mechanisms through which hippocampal atrophy may result:  neuronal atrophy, neurotoxicity, and disruption of neurogenesis.  In animals, 3 weeks of exposure to stress and/or stress levels of glucocorticoids can cause neuronal atrophy in the CA3 region of the hippocampus (28,29).  At this level, glucocorticoids produce a reversible decrease in number of apical dendritic branch points and length of apical dendrites of sufficient magnitude to impair hippocampal-dependent cognitive processes (28).  More sustained stress and/or glucocorticoids exposure can lead to neurotoxicity – actual permanent loss of hippocampal neurons through binding of glutamate to N-methyl-D-aspartate (NMDA) receptors….Evidence of stress-induced neurotoxicity of cells in this region has been reported in nonhuman primates….Reductions in hippocampal volume may also be affected by decreases in neurogenesis, which results from decreased expression of Brain Derived Factor (BDNF) caused by elevated glucocorticoids (33).  The granule cells in the dentate gyrus of the hippocampus continue to proliferate into adulthood, and neurogenesis in this region is markedly reduced by stress.”  Stover et al 2007, 705

“…studies have failed to detect hippocampal atrophy in children with PTSD (36-39).”  Stover 2007, 705

mentions Child-Parent Psychotherapy (CPP) 52-week dyadic treatment -based on following premises:  1) the attachment system is the main organizer of children’s responses to danger and safety in the first years of life; 2) early mental health problems should be addressed in the context of the child’s primary attachment relationships; 3) child outcomes emerge in the context of transactions between the child and environmental protective and risk factors; 4) interpersonal violence is a traumatic stressor with pathogenic repercussions on its witnesses as well as its recipients; 5) the therapeutic relationship is a key mutative factor in early mental health treatment; and 6) cultural values must be incorporated into treatment (104).”  Stover et al 2007, 707

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Smith 2001

Organizational learning conceptualized by Chris Argyris

Models he developed with Donald Schon of single-loop and double-loop learning

[this ties in with my thinking about feedback and feedforward circuits in the brain, how the neurotoxicity on the extreme end of neuro plasticity must relate to the interaction of body and brain in adapting in situations that require new learning – that becomes impossible in trauma – only the body remembers – holds the memory on implicit level enabling body to re-act from its own informational base should another extreme trauma arise – traumas that don’t fit the logic of the ordinary world – how do we learn from them, as I believe it is this not able to learn part that keeps the trauma recycling through us – we cannot exorcise it, it has a purpose, but that is tied to the big organization of the evolution and survival of our species, not to the individual, hence no semantic memories – experience remains unintegrated in conscious memory or autobiography]

[we have no provisions – or very little and of weak structure – that allows the greater organization of our species to learn anything from our individual traumatic experiences – our encounters with life threatening experiences.  We have little frame of reference to converse about trauma – either personally or socially – we need the language, and I am looking toward theories that exist on some level to aid me in my conceptualizing of what I suspect might be going on with PTSD….]

concern with human reasoning, not just behavior

[how do we find the reason in trauma?  It is unreasonable – not reason-able and we cannot make sense our of it using our ordinary mental processes – trauma is beyond the ordinary]

REFLECTION IN ACTION

Subtle patterns of reasoning underlie our behavior – mental models in action

[this is exactly how they describe attachment learning and action]

how are our mental models operating?

[my “theory” is that with BPD – trauma onset on top of flawed attachment system – the theory of mind is damaged and the “learned rules” are broken before their order can become properly connected in the brain – hence severe damage to operational self]

how do we engage with others, “make links with the general and the particular” – explore basic orientations and values  (2)

“…people have mental maps with regard to how to act in situations.  This involves the way they plan, implement and review their actions.”  (2)

these maps guide people’s actions

[much of it is implicit, built into the brain before we had semantic recall for memories – traumas revert back to this level of non-verbal – connected to a not-verbal part of our brain-bodies]

[I think these “mental maps” relate to the rules we learn and live by – more than just moral rules, but fundamental rules, like the rules of grammar which correspond with the innate syntax ability in humans – corresponding to an innate ability to choreograph our life as social beings based on rules like a social version of syntax rules]

split between two contrasting theories of action

theories in use/action

implicit

govern actual behavior

related to action

tacit [implied but not spoken] structures

“they contain assumptions about self, others and environment”

[are a microcosm of applied “life”]

espoused theory

words we use to convey what we do or want others to think we do

theory of action we give allegiance to, whether we live by it or not

do our inner feelings become expressed in actions?

Are the two congruent?  Congruence between the two results in effectiveness

“A key role of reflection we could argue, is to reveal the theory-in-use and to explore the nature of the ‘fit’  Much of supervision… is concerned with the gulf between espoused theory and theory-in-use or in bringing the later to the surface.  This gulf is no bad thing.  If it gets too wide then there is clearly a difficulty.  But provided the two remain connected then the gap creates a dynamic for reflection and for dialogue.” (3)

model of processes involved with theory-in-use

is there a match between intention and outcome?  Consequences may not be intended

“They [intention and outcome?] may also not match, or work against, the person’s governing values.”  (4)

single-loop and double-loop learning

learning involves the detection and correction of error [but not mistakes?]

single-loop learning

“Where something goes wrong, it is suggested, an initial port of call for many people is to look for another strategy that will address and work within the governing variables.  In other words, given or chosen goals, values, plans and rules are operationalized rather than questioned.”  (4)

quoting Argyris and Schon (1978; 2-3)
“When the error detected and corrected permits the organization to carry on its present policies or achieve its present objectives, then that error-and-correction process is single-loop learning.  Single-loop learning is like a thermostat that learns when it is too hot or too cold and turns the heat on or off.  The thermostat can perform this task because it can receive information (the temperature of the room) and take corrective action.  Double-loop learning occurs when error is detected and corrected in ways that involve the modification of an organization’s underlying norms, policies and objectives.”  (4)

[single-loop is based on past learning and structure being used in the present – double-loop requires modification of what lies underneath – to me, this is making something new for the future because what was in the past is not working —  I consider this in a transitional and historical perspective, both in terms of what has worked in the past for us as individuals, and what has worked for us as a species.]

I think single-loop learning supports the status quo

“Single-loop learning seems to be present when goals, values, frameworks and, to a significant extent, strategies are taken for granted.”  (5)

emphasis is on techniques [that have worked in the past] and making these techniques more efficient – any reflection is geared toward making these techniques more effective

follows preset plan and routines, affords less risk and greater control [if it works!!]

alternative contrasting response

double-loop learning

question governing variables themselves, to subject them to critical scrutiny

leads to an alteration in the governing variables

thus to a shift in the way in which strategies and consequences are framed  (4)

involves questioning frameworks and learning systems that underlie the goals and strategies

more creative and reflexive [which does not read easier! My guess is, only relied upon in new situations where the old simply doesn’t work – is in our CNS, ANS response as well in crisis situations]

Reflection are more fundamental — basic assumptions behind ideas or policies are confronted and questioned – hypothesis are tested –

Necessary in changing and uncertain contexts

How to increase capacity for double-loop learning?

We tend to most frequently use a model based on assumptions and inferences about other’s behavior without checking to see if they are valid assumptions or not

[this is efficient – something we “learn” from birth – is usually implicit and works most of the time if we had adequate social experiences in the first place.  We have specialized brain circuits that help us understand other’s intentions and we take this short cut to understanding whenever possible – it is species specific within our culture – they move from this brain-built ability to our theory of mind that evolves as we grow in early childhood through adolescence – corresponding to the developing hemispheres and cortex]

“The theories-in-use are shaped by an implicit disposition to winning (and to avoid embarrassment).  The primary action strategy looks to the unilateral control of the environment and task plus the unilateral protection of self and others….leads to often deeply entrenched defensive routines…and these can operate at individual, group and organizational levels.  Exposing actions, thoughts and feelings can make people vulnerable to the reaction of others.”  (6)

acting defensively is usually about moving away from something –

“If our actions are driven by moving away from something then our actions are controlled and defined by whatever it is we are moving away from, not by us and what we would like to be moving towards.  Therefore our potential for growth and learning is seriously impaired.  If my behaviour is driven by my not wanting to be seen as incompetent, this may lead me to hide things from myself and others, in order to avoid feelings of incompetence.  For example, if my behavior is driven by wanting to be competent, honest evaluation of my behavior by myself and others would be welcome and useful (Anderson, 1997).”  (6)

“It is only by interrogating and changing the governing values, the argument goes, is it possible to produce new action strategies that can address changing circumstances.”  (6)

[trauma is certainly an instance of changing circumstances]

his theory describes a “Model II” in which the views and experiences of participants are included rather than trying to impose a view upon the situation that may not be relevant

[I see this as a need to include the body in the conversation!]

Theories should be made explicit and tested, positions should be reasoned and open to exploration by others….dialogical….shared leadership

[how willing are we to share leadership of our lives with our bodies in our culture? – as ludicrous at it sounds NOT to do that!]

need to emphasize common goals and mutual influence, encourage open communication, to publicly test assumptions and beliefs [get feedback], combine advocacy with inquiry (7)

should result in high choice of freedom [degrees of freedom do not originate from stuck traumas] minimally defensive relationship [in PTSD the body is defending itself and we do not honor this – nor that it has a wisdom that is keeping its factual information from us so as to not complicate the situation further than the “self” can handle] – and increased likelihood of double-loop learning

while not being asked to relinquish control altogether, do need to share control

[I am considering this in light of disorganized attachment – need to find ways to improve organization within and in response to environment] –

active process of organizing is a cognitive process – problem with PTSD is that body has taken reins away from cortex

“Individual members are continually engaged in attempting to know the organization, and to know themselves in the context of the organization.  At the same time, their continuing efforts to know and to test their knowledge represent the object of their inquiry.  Organizing is reflexive inquiry. (9)

“There must be public representations of organizational theory-in-use to which individuals can refer.  This is the function of organizational maps.  These are the shared descriptions of the organization which individuals jointly construct and use to guide their own inquiry….”  (Argyris and Schon 1978; 16-17  [this is one of the major unfortunate implications of trauma – it is considered trauma because it is not ordinarily encountered – though in the formed-in-trauma brains it is integral – though in both cases it is not talked about and shared in a common format – there is a division between those familiar with it and those who are not – even though on some level as many as 70% in the general public have experience with at least one traumatic encounter….find the reference on this]

“By looking at the way that people jointly construct maps it is then possible to talk about organizational learning (involving the detection and correction of error) and organizational theory-in-use.  For organizational learning to occur, ‘learning agents’, discoveries, inventions, and evaluations must be embedded in organizational memory’ (Aryris and Schon 1978; 19)”

individual learning must become a part of the joint maps people create so that the images are encoded on both levels [the particular and the general] – [my idea being that traumas belong more to the general than to the individual and are in many ways imbedded in our group memory, e.g. tooth grinding, etc]

“the organization itself can begin to function in ways that act against its long-term interests.  Indeed, in a very real sense systems can begin to malfunction.”  (10)

yet the alternative is a “rare phenomenon”

Smith states:  “…I think we need to be distrustful of bipolar models….They tend to set up an ‘either-or’ orientation.  They are useful as teaching or sensitizing devices, alerting us to different and important aspects of organizational life, but the area between the models (and beyond them) might well yield interesting alternatives.” (11)

[I think PTSD is already a bipolar condition between approach and avoid – equals stuck – this is an interruption, an infraction, of the balance of wholeness and flexible, productive organization

[how do we “learn our way out” of PTSD? – rework the experiential learning cycle –

trauma is not a learn by trial and error situation – we either survive it or we don’t – there is no mistake that we made – yet how do we continue to learn once PTSD becomes entrenched?  How do we prevent this state from taking hold?]

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

Cunningham 2004

[PTSD robs people of their lives on every level.  Disorganized attachment, as an underlying complication to many cases of PTSD, does the same.  How do we measure the cost and the toll – on all levels?]

Is our concern more than manipulating behavior to improve “performance” and “yield?”  [and to lessen costs/expenses?]

How do we take a “macro-historical” view that can conceptualize the worker [individual], the organization [from the family up to the species – society], and the entity (capitol) into an “accountability framework that privileges quality of life of citizens….?

[PTSD on all levels is a quality of life issue and concern and fundamentally it is about learning – pedagogy – art and science of teaching – who can teach us of trauma’s rules and trauma’s ways?

++++

Martin & Chao, 2001

Semantic memory

“The domain of semantic memory consists of stored information about the features and attributes that define concepts and the processes that allow us to efficiently retrieve, act upon and produce this information in the service of thought and language.”  Martin & chao, 2001, 194

two brain regions, particularly in left hemisphere

……….left prefrontal cortex (LPC) – general and critical role – retrieves lexical [words, vocabulary] and semantic information

……..temporal lobes – object-specific characteristics

broadly defined areas from early functional imaging of semantic processes (now revealing specific functions and processes subserved by smaller regions in these areas):

broad expanses of the left prefrontal, parietal and posterior temporal lobes, commonly including ventral and lateral regions of temporal cortex

“…greater activity in the left posterior middle temporal gyrus during action word generation to visually and auditorily presented words and pictures….tested across a wide variety of native languages…as well as to bilingual individuals responding in their native and second languages…Taken together, these word generation data are consistent with the idea that information about object-specific features may be stored within the same neural systems that are active during perception.”  Martin & chao, 2001, 194

object concepts may be represented by distributed feature networks

“Evidence is accumulating that suggests that all object categories elicit distinct patterns of neural activity in regions that mediate perception of object form (the ventral occipitotemporal cortex).  Moreover, the locations of these category-related activations, especially for objects defined primarily by their visual form-related features such as animals, faces and landmarks, appear to be consistent across individual subjects and processing tasks.”  Martin & chao, 2001, 195

access to additional features may be required to identify certain unique entities in categories such as man-made objects such as tools – need more than just information about how they move through space and patterns of movement

“…naming and identifying objects with motion-related attributes activate areas close to regions that mediate perception of object motion (the posterior region of the lateral temporal lobe), with different patterns of activity associated with biological and man-made objects.  Similarly, naming manipulable man-made objects selectively activates areas close to regions active during object manipulation.  Finally, these regions are active not only when objects are viewed and named:  answering written questions and imagining them also elicits activity in these regions…these activations reflect retrieval of stored information about object-specific attributes and features.”  Martin & chao, 2001, 195 [all bold is mine]

“…distinct regions of ventral temporal cortex show differential responses to different object categories….greater activity in the lateral region of the fusiform gyrus for animal than for tool stimuli…In contrast, the medial fusiform gyrus was more active for tools than for animals….A similar, but not identical pattern of activation was found for viewing faces (in the lateral fusiform) relative to viewing houses (the medial fusiform)….face-related activity in the lateral region of the fusiform gyrus…and house-related activity in more medial regions, including the fusiform and lingual gyri…and parahippocampal cortex (especially for landmarks…).”  Martin & chao, 2001, 195

“Fine-grained distinctions were documented between each of these categories (i.e. animals, tools, houses, and faces…activations associated with animate objects or living things (i.e. animals, faces) cluster in the more lateral aspect of the fusiform gyrus, whereas activations associated with inanimate or man-made objects (i.e. tools, houses) cluster in the more medial aspect of the fusiform gyrus…..(i.e. in the medial fusiform region, more active for houses than faces, and more active for tools than animals), the main peak of activity for chairs was lateral to the face-responsive area, falling in the inferior temporal gyrus.”  Martin & chao, 2001, 196

“…different object categories elicit activity in different regions of the ventral temporal cortex, as defined by the location of their peak activation….it is important to note that activity associated with each object category was not limited to one region, but rather involved a relatively large expanse of ventral cortex.  Moreover, rather than a single peak, this activity was best characterized by a complex pattern of peaks and valleys distributed over much of ventral temporal and, as discussed below, occipital cortex as well.  This suggests that the representations of different object categories are distributed and overlapping.”  Martin & chao, 2001, 196

“…

activation of medial and ventrolateral occipital cortex for animals compared with tools….patients with unilateral lesions of the medial and ventral occipital cortex are more impaired at recognizing animals than tools and famous faces.  Because the activations occurred so earl in the visual-processing stream, we suggested that they might reflect top-down activation from more anterior sites.  This may occur whenever detailed information about visual features is needed to identify a specific object.  However, evidence about the onset times of occipital and temporal activity will be needed to determine whether these occipital activations represent bottom-up or top-down effects….”  Martin & chao, 2001, 196

As an infant is learning what all these objects are and begins to name them with language, the corresponding regions of the brain are growing and forming

Distributed nature of object representations in the ventral temporal cortex — recorded from the medial temporal cortex (i.e. the entorhinal cortex, hippocampus and amygdala), which receives major inputs from the ventral temporal regions – neurons identified that show highly selective responses to different object categories including animals, faces, and houses…responses of the neurons are category-specific rather than stimulus-specific, animal-responsive cells respond to all pictures of animals, rather than to one picture or a select few

“Studies reporting similar patterns of activation when subjects view and imagine objects from different object categories provide further support that the responses in these regions are driven by stored object information…same regions …active when subjects both viewed and imagined famous faces and known landmarks…correspondence between the brain regions active during viewing and imagining faces, houses and chairs…majority of category-selective neurons (88%) …also responded selectively when the patients were asked to imagine these objects.”  Martin & chao, 2001, 196  [talking about several different study results here]

“…ventral occipitotemporal cortex may be best viewed not as a mosaic of discrete category-specific areas, but rather as a lumpy feature-space, representing stored information about features of object form shared by members of a category…A feature-based model can accommodate the observation that an arbitrary category such as chairs elicited a pattern of neural activity distinct from other object categories (i.e. faces and houses).  Clearly, it would be difficult, as well as unwise, to argue that there is a ‘chair area’ in the brain.  There are simply too many categories, and too little neural space to accommodate discrete, category-specific modules for every category.  In fact, there is no limit on the number of object categories.  Feature-based models can provide the flexibility needed to represent an infinite variety of objects.  How this feature space is organized, and why its topological arrangement is so consistent from one subject to another, are critical questions for future investigations.”  Martin & chao, 2001, 196

lateral temporal cortex and representation of object motion

“…tools elicit greater activity in the left posterior middle temporal gyrus than animas and other object categories….Moreover, the active region is just anterior to area MT (middle temporal) and slightly posterior to, or overlapping with, the region active in … verb-generation studies….Damage to this region has been reported to selectively impair tool recognition and naming.”  Martin & chao, 2001, 196

“…naming animals…and viewing faces…elicits greater activity in the superior temporal sulcus in approximately half the subjects (196) tested…association with the perception of biological motion in monkeys….”  Martin & chao, 2001, 197  [what about the other half of subjects?  And why this finding?  A mystery?]

“…greater activation of left ventral premotor cortex has been found for naming tools relative to naming animals…viewing pictures of tools compared with viewing pictures of animals, faces and houses…and generating action words to tools…As with studies of object form and object color, mental imagery (e.g. imaging manipulating objects with the right hand) also results in ventral premotor activation….studies have identified cells in monkey ventral premotor cortex that respond not only when objects are grasped, but also when the animals view objects that they have previously manipulated…The ventral premotor activation noted in the human neuroimaging studies may reflect a similar process.  Alternatively, this activation may reflect action-planning.”  Martin & chao, 2001, 197

basic level object categories (i.e. house, face, chair, dog, hammer) – subordinate or unique-object level investigations typically seen to activate anterior middle temporal gyrus and temporal pole…this activity in anterior temporal regions may extend to other classes of objects, both basic and subordinate…Damasio asserted “…that the anterior regions of the temporal lobes are critical for retrieving information about unique entities…why this should be so is not clear….one possibility is that the temporal lobe object representation system is organized hierarchically, with increasing convergence and integration of information occurring along its poster to anterior axis…”  Martin & chao, 2001, 197

WORKING WITH SEMANTIC REPRESENTATIONS

“…performing semantic tasks commonly activates a wide expanse of left lateral prefrontal cortex.  More recently, evidence has accumulated suggesting that an anterior and inferior prefrontal region (roughly equivalent to Broadmann’s Area BA 47 and the inferior aspect of BA 45) may be involved selectively in semantic processing.  Specifically, as suggested by Gabrieli and co-workers, and Wagner [70, 71, 72*] this region may serve as a ‘semantic working memory system’ responsible for retrieving, maintaining, monitoring and manipulating semantic representations stored elsewhere…studies showing that the left inferior prefrontal cortex (LIPC) is more active when subjects make semantic judgements [sic] to words than when they make nonsemantic judgements to the same words….”  Martin & chao, 2001, 197

“Whereas the studies mentioned above define semantic processing by abstract/concrete classification of single words, a recent study [76] has extended the selective activation of the LIPC to sentence-level semantic processing as well.  Specifically, judging whether pairs of sentences have the same meaning activates LIPC when meaning is determined by synonyms (e.g. the car is in the garage; the auto is in the garage) relative to when meaning is determined by syntax (e.g. the pool is behind the gate; behind the gate is the pool).”  Martin & chao, 2001, 197

LIPC activity is modulated by selection demands…patients with LIPC lesions are impaired when required to generate verbs to nouns with high, but not low, selection demand

“Because high-selection-demand tasks also place greater demands on retrieval, these findings may reflect retrieval demands, rather than selection demands per se….the location of the selection-related LIPC activity is actually in the dorsal aspect of BA 44, lacing it posterior and superior to the semantic working memory region…[suggesting] that the process of selecting among competing alternatives may occur in a different cortical region than other working memory processes.”  Martin & chao, 2001, 197

“…recent evidence suggests that the polar region of the left temporal lobe may also contribute to the overall functioning of a semantic working memory system….normal functioning of the polar region of the left temporal lobe may provide top-down modulatory input necessary for successful retrieval of semantic representations stored in posterior regions….”  Martin & chao, 2001, 197

conclusions

“Distributed networks of discrete cortical regions are active during object processing.  The distribution of these regions varies as a function of semantic [semantic meaning meaning] category.  The same regions are active, at least in part, when objects from a category are recognized, named, imagined, and when reading and answering questions about them.”  Martin & chao, 2001, 199

“Critical questions for future research will be to clarify the precise role of these regions in object semantics and how are they influenced by experience.  In addition, it has yet to be determined how the lexicon is organized and how lexical representations are linked to the semantic feature networks described here.  Finally, little is known about the neural representations of nonfeatural semantic object information and abstract concepts.”  Martin & chao, 2001, 199

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

To me, the idea of a self is an abstract concept.  I still do not believe that I was very aware of having a self, even by age 18.  I was not raised to BE a self.  I suspect that to the degree a person does not have information about a self they remain in a category if not of object, than at least perhaps of animal.  An animal does not think of itself as separate from a rock or a blade of grass.  I have to still consider the “vision” I had at 14-15 – I had the experience of oneness at that time – more than I had the experience of separateness.

We take it fore granted in our culture that people grow up to automatically become a self.  This is not true.  If we have the capacity to adapt, we will take on the mantle of a self at some point because everyone acts like we are one and have one – even though we will truly never know what that means – the felt self as the developmental experts call it.

Attachment experiences create this sense of the felt self.  It does not happen automatically.  I believe that I perhaps share more with autistic people than I do with normal people in this regard.  Another aspect is the self-as-agent, which must be a concept tied to the action part of the brain – but how is it tied to the animal or object perception in the brain?

Brains grow throughout life in an experience-dependent fashion which we like to call learning.

What does that word mean?  What are the semantics of this abstract concept?

LEARN

Function:verb

Etymology:Middle English lernen, from Old English leornian; akin to Old High German lern*n to learn, Old English last footprint, Latin lira furrow, track

Date:before 12th century

1 a (1) : to gain knowledge or understanding of or skill in by study, instruction, or experience  *learn a trade*  (2) : MEMORIZE  *learn the lines of a play*  b : to come to be able  *learn to dance*  c : to come to realize  *learned that honesty paid*

2 a nonstandard   : TEACH  b obsolete   : to inform of something

3 : to come to know  : HEAR  *we just learned that he was ill*

intransitive verb   : to acquire knowledge or skill or a behavioral tendency

synonyms see DISCOVER

usage Learn in the sense of *teach* dates from the 13th century and was standard until at least the early 19th  *made them drunk with true Hollands*and then learned them the art of making bargains – Washington Irving*. But by Mark Twain’s time it was receding to a speech form associated chiefly with the less educated  *never done nothing for three months but set in his back yard and learn that frog to jump – Mark Twain*. The present-day status of learn has not risen. This use persists in speech, but in writing it appears mainly in the representation of such speech or its deliberate imitation for effect.

When a mother terribly abuses an infant, she is treating the infant as an object.  We must remember that it was first the society for the prevention of cruelty to animals that helped the little girl stabbed with scissors.

We can learn the words for things that we have no real understanding of, no personal experience with.  I know the word “frigate,” but not because I have seen one.  I wonder sometimes if that is not how having a “self” is for me.  Sort of my self by default – there’s nobody else in this body, and it seems to be mine – I am attached to it —  there seems to be a vacancy and people aren’t standing in line to move in to it – so it and me are I.

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

Hampton & O’Doherty, 2007

Reward-related decision making

“Decision making is a neural process that intervenes between the processing of a stimulus input and the generation of an appropriate motor output.  Motor responses are often performed to obtain reward, and the obligation of a decision-making mechanism is to ensure that appropriate responses are selected to maximize available reward.”  Hampton & O’Doherty, 2007,1377

this study decoded “…on a trial by trial basis subjects’ behavior or subjective states directly from their neural activity….many of our target regions of interest have been found to show global signal changes related to behavioral choice, that is, large spatially extended cluster areas of activation…in addition to testing for global signals, we also tested for the presence of locally distributed signals relevant to behavioral decision making in each of our areas of interest.  For this, we separated out global and local signals within each region and explored the separate contributions of signals at these two different spatial scales.  We then extend this technique to the multiregion level to determine the contribution of interactions between brain areas in reward-related decision making.”  Hampton & O’Doherty, 2007,1377

subjects needed to “…take into account the history of outcomes received to make decisions about what choices to make in the future.”  Hampton & O’Doherty, 2007,1377

nine regions of interest chosen from previous research:

medial and lateral orbitofrontal cortex and adjacent mPFC –  “These regions have been shown to encode expected reward values, as well as the reward value of outcomes…signals in these regions have been found to relate to behavioral choice, whereby activity increases in mPFC on trials when subjects maintain their current choices on subsequent trials compared with when they switch…”  Hampton & O’Doherty, 2007,1378

ACC – “…engaged when subjects switch their choice of stimulus on reversal learning tasks…suggesting that signals there relate to behavioral choice….region has also been argued to mediate action selection under situations involving conflict between competing responses…and action selection between responses with different reward contingencies…also been suggested to play a role in monitoring errors in behavioral responding or even in decoding when these errors might occur…have in common is that they posit an intervening role for this area between the processing of a stimulus input and the generation of an appropriate behavioral response…”  Hampton & O’Doherty, 2007,1378

Insular cortex – “…has been shown to respond during uncertainty in action choice, as well as under situations involving risk or ambiguity…correlated with whether subjects will make a risk-seeking or risk-aversive choice in a risky decision-making paradigm.”  Hampton & O’Doherty, 2007,1378

Ventral striatum – “…where activity is linked to errors in prediction of future reward…”  Hampton & O’Doherty, 2007,1378

Dorsal striatum –   “…which is argued to mediate stimulus-response learning and goal-directed action selection…”  Hampton & O’Doherty, 2007,1378

Amygdala – “…has been implicated in learning of stimulus-reward or stimulus-punisher associations….”  Hampton & O’Doherty, 2007,1378

Contribution of global vs. local signals in the encoding of behavioral choice – switch vs. stay decisions

Regions can decode whether a subject is going to switch or note:

…ACC 64%, anterior insula 52%, DLPFC 60%

“…decisions can be decoded before subjects are aware of the specific action that needs to be performed to realize them …[suggesting] that decision signals can be encoded in the brain at an abstract level, independently of the actual physical action with which they are ultimately linked…our decoding technique…is likely to be picking up both the decision itself and the consequence of the decision.  In other words, once a decision to switch is computed, a change in stimulus-response mapping is going to be initiated, and the activity being detected in our analysis may also reflect this additional process.”  Hampton & O’Doherty, 2007,1380

“…the decision to switch or maintain current response set may be initiated as soon as the information needed to compute the decision is available, rather than being implemented only when required on the subsequent trial.”  Hampton & O’Doherty, 2007,1380

“…within each region of interest, local signals do convey important information regarding behavioral choice over and above that conveyed by the global signals….the presence of global and local information relevant to behavioral decision making strongly covaries within areas.”  Hampton & O’Doherty, 2007,1380

“…our findings suggest that reward-related decision processes might be better understood as a product of computations performed across a distributed network of brain regions, rather than being the purview of any one single brain area.”  Hampton & O’Doherty, 2007,1381

“Nevertheless, our results do suggest that some regions are more important than others….activity in a specific subset of our regions of interest accounted for the maximum accuracy of our classifier; namely, the ACC, mPFC, and ventral striatum.  Each of these regions has been identified previously as playing a role in decision making and behavioral choice…Out of these, one region in particular stood out as contributing the most:  dorsal ACC.  Our results…{suggest] that this region is playing a key role in implementing the behavioral decision itself.”  Hampton & O’Doherty, 2007,1381

“…decision making is best thought of as an emergent property of interactions between a distributed network of brain areas rather than being computed in any one single brain region.  Of all of the regions we studied, we found that a subset of three regions seemed to contain information that was sufficient to decode behavioral decision making:  ACC, mPFC, and ventral striatum.”  Hampton & O’Doherty, 2007,1381

Evidently the brain LIKES making choices and decisions, and at the same time my guess is that gray matter shows a corresponding increase.  Trauma takes away our ability to choose, or at least has an interaction with it.

There is a difference between learning based on the option of choice and one that runs closer to habit – both are necessary in their own way – but choice and the ability to make decisions is a good thing.

++++

I have no idea how the following fits in, but this abstract is persistently demanding inclusion at this point

Perhaps related to evolution, or how a small damage in the brain can result in an obvious behavioral manifestation that is not subject to intervention by learning

Anderson, Damasio and Damasio, 2005

abstract

[Telencephalon – the cerebral hemispheres – largest of the divisions of the human brain]

collecting behavior is commonplace in normal population

Mesial prefrontal cortices – system – found through a lesion study that abnormal collecting characterized by “massive disruptive accumulation of useless objects…abnormality of collecting behaviour was severe and persisted despite attempted interventions and obvious negative consequences” —  “All subjects with pathological collecting behaviour had damage to the mesial frontal region (including the right polar sector and the anterior cingulate)….The evidence suggests that damage to the mesial frontal region disrupts a mechanism which normally modulates subcortically driven predispositions to acquire and collect, and adjusts these predispositions to environmental context.”

Here again something is creating an obstruction in the brain between an activity that has been and is biologically essential to survival and a person’s control over the activity of providing for themselves and their loved ones.  A choice is no longer possible.  Evidently this can result from something other than a lesion to the brain…..

++++

Rubia et al 2003

London

Abstract:  “Inhibitory control and error detection are among the highest evolved human self-monitoring functions….Different brain regions in inferior, mesial, and dorsolateral prefrontal cortices and parietal and temporal lobes have been related to inhibitory control in go/no-go and stop tasks.  The widespread activation reflects the fact that the designs used so far have commeasured additional noninhibitory cognitive functions such as selective attention, response competition, decision making, target detection, and inhibition failure…..”

“This design allowed to elegantly separate brain activation related to successful motor response inhibition and to inhibition failure or error detection.  Brain activation correlating with successful inhibitory control in 20 healthy volunteers could be isolated in right inferior prefrontal cortex.  Failure to inhibit was associated with activation in mesial frontopolar and bilateral inferior parietal cortices, presumably reflecting an attention network for error detection.”

An out-of-control parent who is abusing a child obviously has a problem somewhere related to these brain regions —  that the successful inhibition of control would be in the right brain, the early developing experience-dependent right brain, probably means this area is part of the emotional control system as well…..?

Problems with inhibitory control would seem to me to be connected to a “de-evolved” brain, if having these abilities is related to the “highest evolved human self-monitoring functions”

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

Sailer et al 2008

Altered reward processing in nucleus accumbens and mesial prefrontal cortex PTSD

(mesial prefrontal cortex is mentioned in empathy section also)

abstract found on page 2836

“Posttraumatic stress disorder (PTSD) is known to be associated with altered medial prefrontal activation in response to threatening stimuli and with behavioural deficits in prefrontal functions such as working memory and attention.  Given the importance of these areas and processes for decision-making, this functional magnetic resonance imaging study investigated whether decision-making is altered in patients with PTSD.  In particular, the neural response to gain and loss feedback was evaluated in a decision-making task in which subjects could maximize their number of points total by learning a particular response pattern.”

“Behaviourally, controls learned the correct response pattern faster than patients.  Functionally, patients and controls differed in their neural response to gains, but not in their response to losses.  During the processing of gains in the late phase of learning, PTSD patients as compared to controls showed lower activation in the nucleus accumbens and the mesial PFC, critical structures in the reward pathway.  This reduced activation was not due to different rates of learning, since it was similarly present in patients with unimpaired learning performance.”

“These findings suggest that positive outcome information lost its salience for patients with PTSD.  This may reflect decreasing motivation as the task progressed.”  Sailer et al 2008, 2836

++

“The medial PFC includes the anterior cingulate cortex (ACC), subcallosal cortex and medial frontal gyrus.

It is closely connected to the “fear system”, particularly the amygdala….Via downward projections, the medial PFC can inhibit activation of the amygdala….[blocking the extinction of conditioned fear in rats with lesions in the medial PFC]….

insufficient level of potentiation in the medial PFC during the extinction of learned fear leads to persistent fear response (Herry & Garcia, 2002).

Acute stress may lead to the depression of synaptic excitability in the medial PFC which could cause long-lasting affective changes in vulnerable individuals (Herry & Garcia, 2002….)…

failure of medial prefrontal networks to regulate amygdala activity may thus result in hyper-reactivity to threatening stimuli ….

or a more general inability to dealing with emotional conflict….”  Sailer et al 2008, 2836

++

“Structurally, PTSD patients have smaller ACC volumes than trauma-exposed individuals without PTSD…[lists refs]…

.It even seems that the smaller the ACC volume, the worse is the severity of PTSD symptoms [lists refs]….

Functionally, ACC activation in PTSD (2836) patients was found to be reduced not only under exposure to trauma-related stimuli [lists refs]…but also under neutral (rest) conditions (Semple et al., 2000).

On the other hand, extinction of PTSD symptoms following pharmacologic treatment led to increased blood flow in the medial PFC (Fernandez et al., 2001).”  Sailer et al 2008, 2837

++

“This hypoactivity of the medial PFC is in some studies coupled to a hyperactive amygdala….r

educed ACC activation to pictures of fearful versus happy faces was associated with an increased activation of the amygdala (Shin et al., 2005).

Similarly, a reduced medial PFC and enhanced amygdala response occurred to targets in a non-emotional auditory oddball task (Bryant et al., 2005).

These results suggest that the medial prefrontal-amygdala dysregulation in PTSD is not specific to emotional or trauma-related stimuli, but generalizes to other categories of salient stimuli.”

++

“…PTSD patients are impaired in a range of non-trauma related executive tasks relying on prefrontal functioning [lists refs]

such as tasks involving sustained attention, working memory, and initial learning of verbal information (Vasterline et al., 2002)….

impaired problem-solving in PTSD when it was associated with other psychiatric diagnoses [lists refs].

It has also been suggested that error monitoring and the sensitivity to errors or other signals of nonreward are altered in individuals with PTSD (Casada & Roache, 2005) as well as in anxious individuals without PTSD (Compton et al, 2007….).

All these abilities are crucial for optimal decision-making.  Thus, there is reason to assume that decision-making is impaired in PTSD.”  Sailer et al 2008, 2837

++

Medial PFC – critical structure for decision-making

………………known to be affected in PTSD

…………activated during error detection, hypothesis testing,

…………conflict monitoring – related to internal cognitive representations guiding a choice or to evaluation of emotion-related aspects of choice  Sailer et al 2008, 2837

This alone makes me think of dissociation – what it feels like from the inside, and perhaps related to what the say is “dissociative like behaviors” of the disorganized infant at 12 months of age in the strange situation test.  If we can’t evaluate the emotional aspects of a situation so that a choice can be made, we are stuck in limbo -there has been too much conflict between the infant and its caregiver and the situations created so that the “unsolvable paradox” means that no appropriate choice is available.  Given enough of this, it seems to me the brain matter and circuitry in the medial PFC would be damaged.

It is unfortunate that researchers are not required to administer an attachment measure every time they are doing research on PTSD so that we could begin to disentangle the causes and correlations of what they are seeing.  If having dissociated prior to a later trauma is one of the main predictors of onset of PTSD after the later trauma, then what they are seeing when they test adult PTSD might very well have originated in early traumas that changed the way all these brain regions have been operating all along since infancy.  We have been operating the best we can with these deficits, in effect hiding them from ourselves and from others by the adjustments we have made toward “trying to be normal.”

A situation of extreme trauma takes away our choices.  The resulting emotions overwhelm the conflict-monitoring abilities of our brain – evidently especially the medial PFC. The PFC has detected an “error” that the individual cannot respond to in any other way except to survive it.  But then what do we do with this overwhelming information?  Nobody else wants it!

Humans are faced with millions of choices in a day’s time.  That is what life is.  Unbearable traumas rob the individual of the right to choose, and it makes sense that the result would be deterioration of the part of the brain that is designed to orchestrate choice.

++

“Thus, both the cognitive impairments of PTSD patients and the altered brain activation in decision-relevant areas hit at decision-making processes being altered in these patients.”  Sailer et al 2008, 2837

++

authors designed a decision-making learning study based on gain or loss in relation to negative outcomes as determined by a particular pattern designed into the study – investigated the neural response to feedback of gains and losses

13 PTSD-diagnosed women matched with and compared to 38 healthy female subjects

MOTIVATION MEASUREMENTS

PTSD were much lower than controls on measurement of motivation to put effort into completing the task, and tended to set their aspiration level lower than controls

……………… – yet their measure of motivation stemming from setting their own goals or the motivation through competition was no different than controls

BEHAVIOR DATA

Learning was impaired in PTSD patients who also achieved a lower percentage of correct responses compared to controls in the later stage of learning – thus controls were able to increase their performance with learning to a larger extent than PTSD patients

“Across all conditions, brain activation was different in a number of areas following gains compared to losses….”  Sailer et al 2008, 2839

…………….main effect of feedback – “When considering the experiment as a whole, there was no difference in the way patients and controls reacted to gain and loss feedback….Activation was larger following losses compared to gains in several temporal areas, none of which was related to our hypothesis….There were no areas in which activation was larger following gains than losses.”  Sailer et al 2008, 2840

“In the early phase as compared to the late phase, gain and loss feedback both elicited larger activation in the dorsolateral prefrontal and orbitofrontal cortices, the intraparietal sulcus, and a number of visual areas….In contrast, activation in the superior temporal gyrus and the inferior frontal gyrus was larger in the late than in the early phase.”  Sailer et al 2008, 2840

“Overall, i.e. across both early and late phases, there were no differences in the processing of gains and losses between controls and patients….However, the brain activation during the processing of gains and losses differed with the experimental phase the subjects were in.”  Sailer et al 2008, 2840

“During the early phase, activation in the dorsomedial prefrontal cortex, the supramarginal area and the posterior cingulate of controls was larger following losses than gains….This difference in the processing of gains and losses in controls disappeared in the late phase.  Thus, different processing of gains and losses was only evident early during learning in controls.”  Sailer et al 2008, 2840

“Patients showed the reverse pattern:  during the early phase, gains and losses were not processed differently.  However, in the late phase, activation was larger (i.e deactivation was smaller…following losses than gains in the left postcentral gyrus.  Thus, in patients, different processing of gains and losses was only evident during the late phase of the experiment.”  Sailer et al 2008, 2840

“Feedback-related brain activation was also different for patients and controls….This was particularly the case following gains….Patients and controls were not different when processing losses in the early or late phase.  However, in response to gains, patients displayed more brain activation than controls in the (2840) early phase, and less than controls in the late phase of the experiment….larger activation in patients than controls when processing such early gains in the dorsomedial PFC and supramarginal area….Quite the reverse, during the late phase, gain-related activation was larger in controls than in patients in the nucleus accumbens (NAcc), thalamus and mesial PFC….”  Sailer et al 2008, 2841

“Learners and non-learners [in the late experimental phase] generally exhibited similar brain activation….However, this was only the case for controls.  In patients, learners displayed larger activation in the hippocampal gyrus [BA 28]…and the left premotor cortex…than non-learners.”  Sailer et al 2008, 2841

“A generally larger activation for controls than for patients in the group of learners and non-learners…was further qualified by an interaction between group and performance.  In both learners and non-learners, controls showed larger activation than patients in the mesial PFC and the NAcc….In the group of non-learners, controls had larger activation in the hippocampal gyrus and the DLPFC.”  Sailer et al 2008, 2842

“…controls were consistently found to activate the nucleus accumbens and the mesial prefrontal cortex (BA 10) following gains in the late phase to a larger extent than patients….at least in these regions – the observed differences between patients and controls during the processing of gain feedback in the late experimental phase are not simply caused by differences in learning.”  Sailer et al 2008, 2842

DISCUSSION

“The present study investigated the neural response to feedback of gains and losses in a decision-making task.  By deriving a particular response pattern, healthy subjects and patients with PTSD could learn to make correct responses only.  However, losses were unavoidable even when all the responses were correct.  This allowed us to examine the reaction to gains and losses both during an early and a late stage of learning.”  Sailer et al 2008, 2842

learning performance was slightly impaired in patients with PTSD

early phase learning in both:  activation in left dorsolateral prefrontal and orbitofrontal cortices and in visual areas  — [these activations lower in later phase]

two areas with larger activation in late phase:  right inferior frontal gyrus [not expected by authors, may be related to memory retrieval – “Early studies of verbal episodic retrieval reported activations in right rather than left frontal cortex” – speculative on this issue]

[stupid, they don’t say what the second area was!]

“In contrast to our second hypothesis, however, patients and controls processed losses in a similar way, both during the early and the late phase of the experiment.  Furthermore, there was no evidence for the ACC being differently activated in patients and controls under any of the conditions investigated.”  Sailer et al 2008, 2842

“Patients and controls differed, however, in the way they processed gains particularly in the late phase:  during the early phase, there was no difference in activation in reward-related areas.  However, during the late phase, patients showed lower activation in the nucleus accumbens and the mesial PFC (BA 10) than controls.  This difference in the late phase was not due to different rates of learning, because the pattern was the same among patients and controls who had both learned the task.  It thus seems rather to be related to the PTSD.”  Sailer et al 2008, 2842

“The nucleus accumbens (NAcc) and the mesial PFC are linked via the mesocortical dopaminergic system, which is central to the brain’s reward circuit.  Within this circuit, dopamine appears to promote reward-related learning, mediating the binding between the hedonic evaluation of stimuli and the assignment of these hedonic values to objects or actions (Berridge & Robinson, 1998).”  Sailer et al 2008, 2842

……………….lists studies that have shown the NAcc and the mesial PFC – one or both when subjects obtain or expect monetary reward

“The fact that the striatal activation to positive stimuli which is typically found in controls…was decreased in PTSD patients of our study can be interpreted as rewards being less salient to these patients….Interestingly, this pattern occurred only for gains in the late phase.  One interpretation of this finding could be reduced attention to positive (2842) feedback that occurs with time.  This interpretation is also supported by the fact that activation in the thalamus of PTSD patients following late gains was similarly reduced.”  Sailer et al 2008, 2843

“An alternative explanation for the differences in brain activation in the late experimental phase is differences in the level of motivation between patients and controls.  The patients may have lost motivation – i.e. faster than the controls – as the experiment progressed….NAcc and mesial PFC….The role of the mesolimbic circuit in appetitive motivation to approach a stimulus has been highlighted previously in animal research (e.g. Panksepp, 1998; Salamone, 1994).”  Sailer et al 2008, 2843

authors mention other studies where depressed patients failed to activate the NAcc in response to positive words….

……………mention that in this present study the same pattern was seen in the PTSD pattern of brain activation without a depression diagnosis

………..deficits in reaction to positive but not in response to negative stimuli, impairment in processing of positive stimuli with no presence of trauma cues

“Overall, our data extend the findings of studies with trauma-related material that show functional abnormalities in brain circuits resulting emotion and motivation.  The patients’ decreased response to positive outcomes in reward-related regions in the late phase of the experiment may be related to a loss of task-related motivation.”  Sailer et al 2008, 2843

Personally, I think that this finding is related to the overall level of overwhelming level of sadness and lack of a sense of well-being that trauma can steal from its victims.

We cannot take pleasure in our own accomplishments, then, or our own successes.  It is like that circuit is broken or has been disconnected – perhaps dissociated?

How can this not be related to an overall sense of helplessness and hopelessness?  Interesting that in this area there is an overlap between PTSD and depression – and yet it is not referred to as a hypoactivation of involvement of the reward system circuitry?  Is it about loss and losing – that we see no way to win?  That somehow this winning process has been so overwhelmed in us by trauma that winning in the little things of life holds no weight compared to losing in the huge things?  A different take to the win-lose, lose-lose scenarios – we lose even when we win!  Maybe even lose BECAUSE we win.  Maybe it really doesn’t matter in our brain if we win or lose – we just “go on being.”  Does this have anything to do with disappointment in the nervous system as with early shame reaction and later trauma reactions in the nervous system that are necessarily the same process?

Do we use a different value scale as a result of trauma exposure so that relevancy and comparison are changed [or saturation] – a comparative alteration – you might think it’s a bad thing if you get a sliver under your fingernail.  But not in comparison to getting both legs cut off in an accident.  That is one of the consequences of trauma, exposure to extremes which changes awareness of what is possible, and what is important.  It is entirely possible that it would take a totally different magnitude of reward, or kind of reward, to cause the same kind of reward reaction between PTSD subjects and controls.  To us, the question, “How big a deal is it?” has changed everything about us and in us and in our lives and in our interactions – both positively and negatively.  (We have experienced an abundance-overabundance paradigm – overabundance of trauma, under-abundance of coping skills in comparison to demands on our abilities)

Our set point was altered from birth if the trauma began that early, and is altered at a later stage if the trauma occurs later – but trauma alters set points for equilibrium within the nervous system, including the brain.  Life will not fool us again in to thinking this is a safe and positive world – why would a little reward motivate us the same as a normal person?  How do we decide what competence is, or if we have it, or if we have enough of it?

++++

Sailer et al 2007

Austria

Feedforward – feedback

“Learning from the outcome of decisions can be expected not only to change future decisions, but also our reaction to future outcomes.”  Sailer et al, 2007, 1474

“Being able to learn from the consequences of previous decisions and to adapt behaviour accordingly is critical for maximizing reward in a variety of situations.  However, it seems likely that learning to make correct choices will change the evaluation of the very outcomes upon which it is based.  For example, in the course of acquiring a successful response strategy, outcomes become more and more predictable.  Thus, as subjects can rely more on internal predictive information, external feedback becomes less informative and it might be expected that it is evaluated and processed differently.”  Sailer et al, 2007, 1474

“The goal of the present study was to investigate how the processing of outcome information, in particular the processing of gains and losses, changes with the acquisition of a correct response strategy.”  Sailer et al, 2007, 1474

There is nothing predictable about trauma.  And, when trauma is built into the brain because of the faults of an inadequately predictable environment, those connections in the brain are already flawed.  There is no chance of “acquiring a successful response strategy” with trauma.  Then if we cannot grow to rely more and more on internal predictive information, external feedback would constantly be required because we need more external information, not less, to predict possible trauma in the future.  Perhaps this is related to our hypersensitivity to external cues and stimuli, related to our hyperarousal.  A constant scanning for something useful “out there” to help us survive – knowing that it is not possible to have enough information “in here.”

In addition, I suspect that trauma survivors, certainly those of us with altered brain development and/or later forming PTSD, have an energy and attention investment in constantly scanning every situation for an escape route should danger loom – and if need be, dissociation gives us that “break” even when we don’t wish it intentionally…..we have an extremely low threshold for stimulation, always being in or near a state of “too muchness,” near a state of being threatened to tip over into a state of chaos.

Practicing tasks – local learning processes occurring in brain regions which handle task-specific information = “are assumed to be regulated by more general control processes that deploy working memory, attentional selection, and performance monitoring….It is assumed that these controlled processing resources determine behaviour to a lesser and lesser extent as learning progresses.  Thus, learning causes a transition from a controlled to an automatic mode of processing,  characterized by efficient and low-effort behaviour.  Such a decreased reliance on controlled processes in the course of learning is reflected by reduced activation in certain distributed brain areas across a number of different perceptual, verbal and manual learning tasks…These areas include the medial frontal (pre-SMA (BA 6), anterior cingulate (BA 32), dorsolateral prefrontal (BA 9, 44, 46), posterior parietal (BA 7, 39, 40), and occipital (BA 18,19) cortices.”  Sailer et al, 2007, 1474

“…reduction in activation is to some extent task-dependent.  For example, reward-based learning of probabilities has primarily been associated with reduced activation in the caudate nucleus….The caudate, (1474) together with the anterior cingulate cortex (ACC), has also been found to be activated during sequence and passive avoidance learning (e.g. Aizenstein et al., 2004 and Kossen et al., 2006, respectively).”  Sailer et al, 2007, 1475

“In this investigation, we analysed how neuronal activation during the processing of feedback about the outcome of a choice differs before and after ascertaining and learning a correct response strategy.”  Sailer et al, 2007, 1475

“Nieuwenhuis et al. (2004) demonstrated that emphasising [sic] either the utilitarian aspect of the feedback in terms of gains and losses, or the performance aspect of the feedback in terms of correct and wrong responses, led to a similar medial frontal negative event-related potential component, the so-called error-related negativity (ERN).  Thus, the ERN was sensitive to whichever aspect of the feedback was salient.”  Sailer et al, 2007, 1475

……performance feedback – right or wrong – more subjects show consistent response to this aspect

…..utilitarian feedback – gains and losses

predictions of this study:

“…feedback processing before learning the pattern would preferentially recruit limbic structures such as the striatum and orbitofrontal cortex relative to after learning, because these regions are involved in forming and updating associations between environmental stimuli and rewards….”  Sailer et al, 2007, 1475

“…activation in the ACC would be greater before learning than after because the ACC is involved in conflict processing….and conflict about which of two response alternatives is – or was – correct should diminish during the course of learning”  Sailer et al, 2007, 1475

………assumed activation in ACC [shown in other studies to be larger for negative than for positive outcomes] would be associated with losses more than gains across the task

“…activation in prefrontal structures engaged in working memory, particularly the dorsolateral prefrontal cortex (DLPFC), would be higher before learning than after because cognitive demands are reduced and/or processing is more efficient as performance becomes more automatic.”  Sailer et al, 2007, 1475

“Furthermore, we explored how the processing of gains and losses changes with learning.  Due to the striatum’s role in reward, we expected the hypothesized decreased activation in the striatum with learning to be greater for gains than losses.”  Sailer et al, 2007, 1475

38 female subjects (subgroup was also involved with the PTSD study)

“In accordance with a learning phase classification in motor learning (Sailer et al., 2005), we assumed that subjects would start with an exploratory phase in which they generated and tested hypotheses about successful strategies, followed by a phase of strategy acquisition in which performance improved rapidly, and finally, a proficiency phase in which they refined the learned strategy.”  Sailer et al, 2007, 1478

………….model-conform learners, fast learners and slow learners [who never attained proficiency]

RESULTS

Based on utilitarian feedback:

……..higher activation after gains than losses in the orbitofrontal cortex (OFC; BA 45, BA 11), the caudate nucleus and the frontopolar area (BA 10)

Based on performance feedback:

…..brain activation also higher following correct than wrong performance feedback in the OFC, precuneus and dorsolateral prefrontal cortex (DLPFC)

This study was set up so that losses were unavoidable even when all the choices were made correctly

“There was also an interaction between performance and utilitarian feedback in a number of areas….(1478)  This interaction indicated that the different feedback types could be grouped into ambiguous, i.e., correct loss and wrong win, versus unambiguous, i.e. correct gain and wrong loss, feedback.  Except for one area, the inferior temporal area, activation in all areas was either larger or smaller following both types of ambiguous feedback versus both types of unambiguous feedback….”  Sailer et al, 2007, 1479

“In the pre-supplementary motor area (pre-SMA) and prefrontal regions (the frontopolar area and DLPFC) as well as parietally in the precuneus and supramarginal area activation was larger following unambiguous than ambiguous feedback.

In the remaining areas such as the ACC the middle temporal area, caudate, insula and the OFC, activation was larger following ambiguous than unambiguous feedback.

Only activation in the inferior temporal area (BA 20) showed a different pattern with lower activation following correct gains compared to the other three types of feedback.”  Sailer et al, 2007, 1479

“In general, unambiguous feedback led to more pronounced neural responses than ambiguous feedback.  This implies that the observed main effects are mainly due to the effects of the unambiguous factor levels.  For example, the main effect for utilitarian feedback in the caudate is primarily due to the larger activation after correct gains compared to after wrong losses.”  Sailer et al, 2007, 1479

“…in all these areas, activation was larger for gains in the exploratory phase than for all the other conditions….Importantly, the response to gains changed to a larger extent with learning than did the response to losses.  Activation following gains was larger in the exploratory phase than in the proficiency phase in the left lateral OFC, the right OFC, the putamen and the frontopolar area.  In contrast, activation following losses was somewhat lower in the exploratory phase than in the proficiency phase both in the lateral OFC and the putamen.  Learning-related activation changes in the right OFC and the frontopolar area only occurred during the processing of gain, not loss feedback.”  Sailer et al, 2007, 1479

COMPARISON OF MODEL-CONFORM WITH SLOW LEARNERS:

“There were no areas in which model-conform learners showed larger activation than slow learners, neither in the exploratory nor in the proficiency phase.

In contrast, slow learners showed more activation in the precuneus (BA 7…) than model-conform learners did in the exploratory phase.  Slow learners also showed more activation in the precuneus…and in the inferior parietal cortex (supramarginal area, BA 40…and BA 39…) than model-conform learners did in the proficiency phase.  Thus, the larger parietal activation throughout the experiment distinguished slow from model-conform learners.”  Sailer et al, 2007, 1479

COMPARISON OF MODEL-CONFORM LEARNERS WITH FAST LEARNERS:

“There were no areas which were activated to a larger extent in fast learners than in model-conform learners.

Moreover, there was no difference in brain activation for model-conform and fast learners in the proficiency phase; that phase in which both groups already had acquired the correct response strategy.

However, fast learners showed less brain activation in the supramarginal area (BA 40…), the caudate…and the superior temporal (1479) area bilaterally…than model-conform learners did in the exploratory phase.”  Sailer et al, 2007, 1480

DISCUSSION

“We investigated how the processing of feedback about choice outcomes changes before and after learning a response strategy that led to correct choices only.  Learning this strategy did not prevent the subjects from experiencing losses, however, allowing differential changes in activation associated with experiencing gains and losses to be analysed.”  Sailer et al, 2007, 1480

“With the exception of a decrease in ACC activation following losses, our hypotheses were confirmed.  Additionally, lower activation following learning occurred not only within subjects across learning phases, but also between subjects with different learning speed.”  Sailer et al, 2007, 1480

LEARNING-RELATED ACTIVATION CHANGES

“The OFC is thought to code for the incentive value of both sensory (e.g. taste or touch) and abstract (money or game points) rewarding stimuli…particularly when the contingencies between reward and behaviour change….

The incentive value encoded in the OFC is linked to specific cues particularly when this information is relevant to the rules that guide task performance….

The OFC and the dorsal striatum are prominent target areas of dopamine neurons.  They are connected via the mesolimbic dopamine system which is postulated to function as a reward system.  It arises in the substantia nigra and ventral tegmental area of the midbrain and terminates in the ventral striatum, dorsal (1480) striatum (caudate and putamen) and the prefrontal cortex…

The crucial role that both the OFC and the putamen play in reward-related behavior is stressed by human neuroimaging studies that identified prediction error signals…in these regions.  Such signals indicate that an event is better or worse than expected….”  Sailer et al, 2007, 1481

“The putamen and OFC are thus both involved in evaluating or establishing contingencies between stimuli, rewards and behaviours as is required in the exploratory [learning] phase.  It seems that what is tracked are rather rewards than punishments, since activation of the OFC and putamen was larger for gains than for any of the other (1481) outcomes in the exploratory phase.  Along these lines, it has been reported previously that the putamen is activated primarily in response to unexpected primary rewards…and following positive than negative feedback….Since the putamen has traditionally been associated with motor-related activities…it could be tentatively assumed that the putamen activation observed in our task is more related to aspects of the behavioural adjustments to be made, whereas OFC activation may rather reflect the affective aspects of rewards.”  Sailer et al, 2007, 1482

“There is also significant functional connectivity between the putamen and the DLPFC….Consistent with our hypothesis, activation in the DLPFC after both gains and losses decreased with learning.  Thus, the automatisation of task performance, and therefore, the decrease in cognitive requirements on working memory was reflected in a decrease in prefrontal activation.  It has been suggested that working memory for novel stimuli requires the additional recruitment of parahippocampal regions….The increased parahippocampal activation observed in the exploratory phase of our task may be explained in this way, because in this phase, a sequence of novel stimuli has to be maintained, whereas the stimuli were already familiar in the proficiency phase.”  Sailer et al, 2007, 1482

“Additional structures not covered by our hypotheses that showed reduced activation after learning following both gains and losses were the middle and inferior temporal area, the peristriate area, the precuneus and the pre-SMA (BA 6).  The middle temporal area is involved in language and semantic memory processing….Activation in this region may be larger in the exploratory phase because subjects try to verbalise and/or extract semantic knowledge about the correct response sequence.  Similarly, the middle temporal area has been reported to be activated during uncertain vs. certain decisions when the task employed words….At the same time, the middle temporal area seems to be involved in processing of losses, for example, following losses as compared to gains in risky decision-making (Dickhaut et al., 2003), following streaks of losses (Atitsuki et al., 2003) and following an outcome that as more negative than the alternative outcome (Coricelli et al., 2005).  A smiliar pattern was observed in our task where activation in the middle temporal area was smaller for correct gains than for any of the other outcomes.”  Sailer et al, 2007, 1482

“An interesting question arising from the different roles of this structure described in the literature is whether the increased activation in this area following both losses, ambiguous feedback and during the exploratory phase is associated with disappointment, as understood by Coricelli et al (2005), or with a kind of sense-making of the provided feedback.”  Sailer et al, 2007, 1482

precuneus

I need to copy all of this into my working section on the self and the precuneus

“Learning-related decreases in the precuneus have been described previously using working memory (modified Sternberg task; Koch et al., 2006) and decision-making tasks (Ernst et al, 2002).  Interestingly, precuneus activation was also what distinguished slow learners from model-conform learners both during the exploratory and the proficiency phase.  The precuneus is closely connected to the DLPFC and has – among others – been ascribed a role in shifting attention between different targets and object features (Cavanna and Trimble, 2006).  For example, in a set-shifting task that required to change the sorting criterion in response to incorrect feedback, a transient increase of activation occurred in the precuneus and the pre-SMA which was time locked with attention shifts (Nagahama et al., 1999). The precuneus is also activated during risky decision-making (Dickaut et al, 2003; Paulus et al., 2003; Krain et al., 2006; Ernst et al., 2004) which may also be explained by the attentional requirements involved in tracking contingencies and supplying alternative response strategies in the presence of uncertainty (Paulus et al., 2001).”  Sailer et al, 2007, 1483

“Similarly, differing set- and attention-shifting requirements can explain why precuneus activation was larger in the exploratory phase than in the proficiency phase, why it was noticeably larger following ambiguous than unambiguous feedback in the exploratory phase, and finally, why it was also larger in slow learners than in model-conform learners.

As slow learners fail to grasp and automatise the correct response strategy, they may feel a greater need to adjust their response strategy and to pay more attention to the task than model-conform learners from the beginning of the task up to its end.”  Sailer et al, 2007, 1483

I can see a “self” putting great effort into trying to get it right – applying oneself to the task – effortful control!!  Self as agent – paying attention – I think it is related to trying to learn the rules and apply them.  This describes a difficult life process!!

I see the description of the model-conform learners to be like those who learn about themselves and the world in a secure attachment, safe environment.  The slow learners have been, then, forced to continue to try to learn what was easy for the MC learners

They don’t talk about the precuneus being the seat of mental images – but I get the picture of Dorothy wanting to go back to Kansas, the center that was her home – the tornado of life transported her from one center to another – into the world of drama and adventure – home being an earlier place, though she had no family and was evidently an orphan…

I feel like an orphan.  Maybe the precuneus is the place we are at in the world, alone – born alone, die alone – meet the challenges alone, ultimately – maybe this is our orphan place, the center of our wheel of effort, of trying, from beginning to end.  Maybe we trauma survivors know this place better than others, having been overwhelmed, having been challenged past what was ours to give to the task – and still we survived, but it is like getting home early, too early – before the whole of our life was completed – dropped on the other side of the finish line before we got to run our race one foot in front of the other – trauma tripped us up.

It stole from us our “right” to run the race of our lives our way – we constantly have to try to assert ourselves over the survival will of our bodies so that we, as a self, can participate in our lives as more than some fractured illusion of a self.  When one rule does not grow in an orderly fashion from the preceding rule, attached to the next forthcoming rule, in an orderly and predictable fashion – what’s left?

Maybe when we dissociate the precuneus is the place we go to.

++

“This difference in attentional involvement is particularly pronounced during the proficiency phase, when slow learners also activated other attention-related areas such as the supramarginal area to a larger extent than model-conform learners.  In fact, activation in the supramarginal area also distinguished fast learners from model-conform learners.  This probably reflects the fact that attentional and working memory demands are reduced for fast learners who lack the initial exploratory phase and – as they start off with the correct sequence at once – do not have to work and try out different response strategies.”  Sailer et al, 2007, 1483

“A further structure that plays a role in working memory…and shows reduced activation after learning is the pre-SMA.  The pre-SMA has also been implicated in decision-making under conditions of uncertainty….This applies to our task, in which correct responses and outcomes are uncertain in the exploratory, but not in the proficiency phase.  Moreover, pre-SMA activation was larger with unambiguous than ambiguous feedback which also supports a role of the pre-SMA in uncertainty management…..uncertainty cannot be related to the question of which alternative to choose, but rather to the way to interpret the feedback given or to evaluate the consequences of an uncertain choice.  Consistent with this view, activation in the pre-SMA has been previously found to decrease during the learning of arbitrary stimulus-response associations….”  Sailer et al, 2007, 1483

“In contrast with our expectation, activation in the ACC did not change with learning….ACCs role in error detection…conflict detection…and the evaluation of emotion-related aspects of the choice or outcome….The fact that the ACC was activated more strongly after ambiguous than unambiguous feedback supports its role in resolving conflict….A different explanation for the lacking decrease in ACC activation with learning could e that the ACC serves a more general role than conflict detection alone, namely updating control states in tasks that require following a course of mental activity that comprises several steps….one could argue that the control demand in the present experiment is constant…Thus, the number of mental operations did not change in the course of the experiment, which could explain why ACC activity did not change either.”  Sailer et al, 2007, 1483

LEARNING-RELATED ACTIVATION CHANGES SPECIFIC TO GAINS & LOSSES

“There were no areas which were specific for processing either gains or losses across learning phases.  This suggests that losses and gains are coded by the same brain regions.  Within these regions, however, the activation following gains and losses changed differentially with learning.  Whereas the activation following losses increased with learning in the left lateral OFC and the putamen, the activation following gains decreased in those same area and additionally in the right OFC (BA 11) and the frontopolar area.  In general, the effect of learning on brain activation was larger for gains than for losses.”  Sailer et al, 2007, 1483

“…positive reward prediction errors being more sensitive to increased reward probability than negative reward prediction errors.”  Sailer et al, 2007, 1483

UTILITARIAN VS. PERFORMANCE FEEDBACK

“The distinction that most clearly affects brain activation is between ambiguous and unambiguous feedback.  In general, unambiguous feedback, that is correct gains and wrong losses, yielded the strongest responses.  The reason for this result may be that unambiguous feedback represents the clearest indication for a good or a bad outcome.”  Sailer et al, 2007, 1484

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How often do we stop and be grateful for our brains?  Do we remember to thank all our ancestors who engaged their brains so that our species could continue to exist up to our present day?

In the early days of our species we were getting along like riding a bike with training wheels on it.  Much of what we have choice over now used to be governed by hormones and instinct. We constantly and continually used our brains to the maximum, and were ready for each mutation that allowed us to do things better and more effectively and efficiently.  We used our brains so that when the mutation came along that allowed us to grow a bigger brain, we were ready to make use of these new opportunities.  As a result of all the work we did with our brains as a species, when the genetic mutation came along on the FOXP2 gene, we were ready for that one too, and we began talking up a storm.  As circuits and networks in our brains grew through experience and use, we were able to interact with one another and with our environment in wider and wider circles until our migrations allowed us to encircle the planet.

If someone gives you a gift and you never use it, it probably means you don’t need the gift – if you needed it you would like it and use it.  How many of us think for the sheer pleasure of it?  Like if we woke tomorrow morning and found that we could fly easily and well.  How many of us would be stuck here on the ground with a gift like that at our disposal?  And yet with the wonder of our brain, how many of us understand it, or use it past anything more than mundane necessity?

I believe that what lead us forward through evolution in a continual process of expanded adaptation was related to our desire for the novel experience, our desire to “go on being,” our desires – period.  Our drive – drove us forward and enabled us to make good use of every “tool” handed to us by the forces of the biophysical world of which we are a part – not apart from, but a part of.

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Friday, August 22, 2008

Thinking about the epigenetic transgenerational disease transmission – like the human species as a single body sloughing off dead cells of the skin – or how we menstruate each month and release blood that is not needed….we are passing on destruction to our progeny as a result of exposing ourselves to toxic environments.  I suppose the evolution of our species doesn’t think we need to survive through our offspring if we are so at risk, put ourselves so at risk – nature would sooner get rid of us….

The truth is coming through tome, down to me.  The truth that exists in the academic world that has to travel so far before it reaches those of us here down below where the ordinary people live.  Like a leak that starts in someone’s roof, first a few small drops of water, growing into a cascade.  The body learns.  Cells remember.  The instructional process that determines how our DNA shows itself in our bodies responds to its memories of having once lived in a malevolent world.  And we need to call this by its name.  It is toxic.  Whether the toxins were due to famine and starvation in a Swedish fishing village that meant the epigenetic transgenerational weight of alterations in the body now means that the descendants of those people suffer from metabolism disorders.  Of in the generations of descendants of the Holocaust or in those exposed to pesticides.  We the descendants are suffering the results of those alterations, of that genetic memory.

So learning DOES happen in our cells, and this learning IS passed down through the generations and it DOES change things for us, the ones that are left behind.  It’s like we continue to burn down people’s houses and then treat the burn victims for generations afterwards.

Standing under the leak in the roof with my tin cup before the roof falls in with a gush….dripping blood in the dishpan.

Micro macro personal general transmission of information about the environment – experience-dependent learning that goes right into our genetic pool

Those of us standing too close to the epicenter have epigenetic alterations that mean nature has deemed that we are too damaged but gives us a chance to reproduce another generation that MIGHT make it before we have to leave this world ourselves.  Like operating in computer safety mode, we are given a time of reprieve to amend our ways, for our environment to eliminate the toxins so that we can be restored to our original DNA. Redemption – but things cannot remain the way they are without something permanent and irrevocable happening as a result.

This is rupture and repair on the molecular level – that’s how deep the threat to our species is becoming.  If we let toxicity and trauma become the norm?  Nature will do its best to establish well being and equilibrium.  How much time do we have to make changes before it all comes tumbling down upon and around us?  The sky IS falling.  And it is doing so inside our own bodies and within our own and our children’s lives.

Our bodies will take over the driving and become response-able to the environment.  When does this all reach a climax of critical mass?  Epigenetics provides a flexible, adaptive response to human interaction with a toxic environment.  That the “somehow in our genes” adaptation allows us to survive the unsurvivable, and moves from the vague to the specific, from the general to the individual, should not surprise us.

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Panksepp 2003

“…consciousness is a resource-intensive and “limited-bandwidth” system, and…the brain works endlessly to offload as much of its processing as possible to unconscious processes.  Novel tasks that initially demand the resources of consciousness are quickly learned and become increasingly supported in basal ganglia and cerebellar systems that underwrite the consolidation of habits, procedural memories, and complex motor skills, thus allowing consciousness the luxury, so to speak, of focusing on the most essential and novel adaptive demands facing the organism.”  Panksepp 2003, p 81

FEED BACK, FEEDFORWARD:

“…consciousness is not an al-or-nothing phenomenon…it is built through organizational hierarchies in the brain that feed back and forward, integrating the processing performed by many systems.”  Panksepp 2003, p 82

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flooding and exposure TREATMENT

“”For traumatic reminders to lose their emotional valence, patients must be able to experience new information that contradicts the rigid traumatic memory, such as feeling physically safe, [nearly impossible for those abused from birth] while thinking about the event, not feeling they are to blame, and feeling able to cope with similar events in the future.  The critical issue in treatment is reexposure to traumatic imprints, and at the same time experiencing sensations (of mastery, safety, etc.) that are incompatible with the fear and terror associated with the trauma.”  Panksepp 2003, 338

“Flooding and exposure are by no means harmless treatment techniques:  Exposure to information consistent with a traumatic memory can be expected to strengthen anxiety (i.e., sensitize and thereby aggravating PTSD symptomatology).  Excessive arousal may make the PTSD patient worse by interfering with the acquisition of new information.  When that occurs, the traumatic memories will not be corrected, but merely confirmed:  Instead of promoting habituation, it may accidentally foster sensitization.”  Panksepp 2003, 338

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Watkins 2008

Article

Repetitive thought (RT) – can have positive and negative consequences – unconstructive or constructive —

constructive consequence of recovery from upsetting and traumatic events – necessary part of “coming to terms” OR can lead to depression and poor recovery from upsetting/traumatic events – adjustment or maladjustment – article has detailed description of major thought type categories

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LATENT INHIBITION – relates to de novo art info in well-being chapter

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Carson, Peterson & Higgins 2003

Abstract – Department of Psychology, Harvard University, Cambridge, Massachusetts 02138, USA. carson@wjh.harvard.edu

Reductions in latent inhibition (LI), the

capacity to screen from conscious awareness

stimuli previously experienced as irrelevant,

have been generally associated with the tendency towards psychosis.

However, “failure” to screen out previously irrelevant stimuli might also hypothetically contribute to original thinking, particularly in combination with high IQ.

Meta-analysis of two studies, conducted on youthful high-IQ samples. demonstrated that

high lifetime creative achievers had significantly lower LI scores than low creative achievers …

Eminent creative achievers (participants under 21 years who reported unusually high scores in a single domain of creative achievement) were 7 times more likely to have low rather than high LI scores, …

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Razumnikova, Vol’f & Tarasova 2007

Abstract – article in Russian

Effect of extrinsic motivation stimulating the most original problem solving during verbal and figurative divergent thinking was studied by EEG mapping. The righthanded university students (27 males and 26 females) participated in the experiments. An instruction “to create the most original solution” as compared to condition with an instruction “to create any solution” induced an increase in the baseline power of the alpha 1 and alpha 2 rhythms most pronounced in the posterior cortex. Task-related desynchronization of the alpha rhythms was higher but the beta-2 synchronization was lower after the former than after the latter instruction.

Differences in the asymmetry of the alpha 1 and alpha 2 rhythms in the parietal and temporal regions of hemispheres suggested the right hemisphere dominance in intrinsic alertness and evoked activation related to

divergent thinking

The findings were common and gender-independent in both figurative and verbal tasks suggesting a generalized influence of extrinsic motivation on creative activity. There was no reward, just the suggestion which by itself was the motivation – so reward is not an issue here, but motivation is.

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Nelson & Rawlings 2008

Abstract – 2ORYGEN Research Centre, University of Melbourne, 35 Poplar Road (Locked Bag 10), Parkville, Victoria 3052, Australia.

Introduction: Although a considerable amount of research has addressed psychopathological and personality correlates of creativity, the relationship between these characteristics and the phenomenology of creativity has been neglected. Relating these characteristics to the phenomenology of creativity may assist in clarifying the precise nature of the relationship between psychopathology and creativity. The current article reports on an empirical study of the relationship between the phenomenology of the creative process and psychopathological and personality characteristics in a sample of artists. Method: A total of 100 artists (43 males, 57 females, mean age = 34.69 years) from a range of disciplines completed the Experience of Creativity Questionnaire and measures of “positive” schizotypy, affective disturbance, mental boundaries, and normal personality. Results: The sample of artists was found to be elevated on “positive” schizotypy, unipolar affective disturbance, thin boundaries, and the personality dimensions of Openness to Experience and Neuroticism, compared with norm data. Schizotypy was found to be the strongest predictor of a range of creative experience scales (Distinct Experience, Anxiety, Absorption, Power/Pleasure), suggesting a strong overlap of schizotypal and creative experience.

Discussion: These findings indicate that “positive” schizotypy is associated with central features of “flow”-type experience, including distinct shift in phenomenological experience, deep absorption, focus on present experience, and sense of pleasure.

The neurologically based construct of latent inhibition

may be a mechanism that facilitates entry into flow-type states for schizotypal individuals.

This may occur by reduced latent inhibition

providing a “fresh” awareness and therefore

a greater absorption in present experience,

thus leading to flow-type states.

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Miller et al 2000

Abstract – Department of Neurology, University of California at San Francisco School of Medicine, USA. brucem@email.his.ucsf.edu

BACKGROUND: The emergence of new skills in the setting of dementia suggests that loss of function in one brain area can release new functions elsewhere. AIMS: To characterize 12 patients with frontotemporal dementia (FTD) who acquired, or sustained, new musical or visual abilities despite progression of their dementia. METHOD: Twelve patients with FTD who acquired or maintained musical or artistic ability were compared with 46 patients with FTD in whom new or sustained ability was absent. RESULTS: The group with musical or visual ability performed better on visual, but worse on verbal tasks than did the other patients with FTD. Nine had asymmetrical left anterior dysfunction. Nine showed the temporal lobe variant of FTD. CONCLUSION: Loss of function in the left anterior temporal lobe may lead to facilitation of artistic or musical skills. Patients with the left-sided temporal lobe variant of FTD offer an unexpected window into the neurological mediation of visual and musical talents.

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Gal et al 2005

Abstract – Shalvata Mental Health Center, Hod Hasharon, P.O. Box 94, Israel.

Learned irrelevance (LIrr) is a pre-exposure effect in which uncorrelated presentations of a conditioned stimulus (CS) and an unconditioned stimulus (US) retard subsequent CS-US association.  I still don’t understand this, really.

LIrr is closely related to the phenomenon of latent inhibition (LI). LI refers to the retarding effects of inconsequential stimulus pre-exposure on subsequent conditioning to that stimulus, and is considered to reflect the organism’s capacity to ignore irrelevant stimuli.

LI is disrupted in schizophrenia patients, due to faster learning of the association between the preexposed CS and the US. A new within-subject target-recognition LIrr procedure was applied. The target was either cued by a priming signal or appeared at random, and priming signals were novel or preexposed cues. Schizophrenia patients were compared to age- and sex-matched control subjects.

Normal subjects (n = 24) have shown robust LIrr, namely, faster cue-target associations of novel compared to preexposed cues.

Schizophrenia patients at the early stages of their first episode (n = 7) showed LIrr disruption, namely, cue-target associations to preexposed cues were as fast as for novel cues. Chronic patients during an acute phase (n = 18) did not show LIrr as they failed to learn the cue-target association. In addition to the LIrr paradigm the same subjects were tested in a covert-orientation task. No differences were observed between the groups on this task. The possible advantages of the new LIrr paradigm are discussed.

I still suspect that when abuse begins early, or from birth, there’s no cause and effect logic to learning – and there are interactions that are complex and beyond the abilities of the forming brain to dis-integrate.

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Vaitl et al 2002

Abstract – Department of Clinical and Physiological Psychology, University of Giessen, Otto-Behaghel-Str. 10, D-35394 Giessen, Germany. dieter.vaitl@psychol.uni-giessen.de

Latent inhibition (LI) is an important model for understanding cognitive deficits in schizophrenia. Disruption of LI is thought to result from an inability to ignore irrelevant stimuli. The study investigated LI in schizophrenic patients by using Pavlovian conditioning of electrodermal responses in a complete within-subject design. Thirty-two schizophrenic patients (16 acute, unmedicated and 16 medicated patients) and 16 healthy control subjects (matched with respect to age and gender) participated in the study. The experiment consisted of two stages: preexposure and conditioning. During preexposure two visual stimuli were presented. one of which served as the to-be-conditioned stimulus (CSp + ) and the other one was the not-to-be-conditioned stimulus (CSp – ) during the following conditioning ( = acquisition). During acquisition, two novel visual stimuli(CSn + and CSn – ) were introduced. A reaction time task was used as the unconditioned stimulus (US). LI was defined as the difference in response differentiation observed between preexposed and non-preexposed sets of CS + and CS – . During preexposure, the schizophrenic patients did not differ in electrodermal responding from the control subjects, neither concerning the extent of orienting nor the course of habituation. The exposure to novel stimuli at the beginning of the acquisition elicited reduced orienting responses in unmedicated patients compared to medicated patients and control subjects. LI was observed in medicated schizophrenic patients and healthy controls, but not in acute unmedicated patients. Furthermore LI was found to be correlated with the duration of illness: it was attenuated in patients who had suffered their first psychotic episode.

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Metzger & Riccio 2008

Abstract – Ashland University, 401 College Avenue, Ashland, OH, 44805, USA.

Numerous studies have demonstrated that the forgetting of stimulus attributes is a common occurrence; that is,

organisms forget the specific characteristics of training stimuli over long retention intervals, while retaining general information of the training stimuli themselves. This sounds like it’s related to semantic memory – remembering the facts – to one degree or another, not always with context, which belongs more to declarative or autobiographical memory.

In PTSD we remember the specific characteristics of the “training stimuli” over long retention intervals – when I guess we “should” forget them and just remember something general – but I think evolution intervenes – either the specifics are too terrible to either integrate or forget, or nature has us hold onto the specifics for some time in the future when they might be useful.

Perhaps the same thing happens with depression – the things that hurt us, compared with the things, also, that we remember details of that scare us

However, most studies have examined this effect after a learning episode, and there have been virtually no accounts to test whether the forgetting of attributes occurs for stimuli presented prior to training. Therefore, this experiment was designed to test that possibility, and it examined whether the forgetting of stimulus attributes occurred prior to training for the flavor stimulus in a conditioned taste aversion (CTA) procedure. Specifically, a latent inhibition (LI) procedure was used to measure the extent of forgetting for a pre-exposed flavor over short and long retention intervals. The results indicate that rats forgot the specific characteristics of the flavor stimulus (CS) while retaining memory for pre-exposure sessions over a long retention interval. That is, subjects pre-exposed and conditioned with different concentrations of sucrose showed no LI effect with a 1-day delay between pre-exposure and training, but demonstrated a generalized LI with an 8-day delay between pre-exposure and conditioning. This experiment provides further evidence for the robustness of the forgetting of stimulus attributes, and demonstrates that this specific type of forgetting also occurs prior to the learning of a CTA task.

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Rodriguez & Hall 2008

Abstract – Department of Psychology, University of York, York, UK.

Rats were given exposure either to an odor (almond) or a compound of odor plus taste (almond plus saline), prior to training in which the odor served as the conditioned stimulus. It was found, for both appetitive and aversive procedures, that conditioning was retarded by preexposure (a latent inhibition effect), and the extent of the retardation was greater in rats preexposed to the compound (i.e., latent inhibition to the odor was potentiated by the presence of the taste).

In contrast, the presence of the taste during conditioning itself overshadowed learning about the odor. We argue that the presence of the salient taste in compound with the odor enhances the rate of associative learning, producing a rapid loss in the associability of the odor. This loss of associability will generate both overshadowing and the potentiation of latent inhibition that is observed after preexposure to the compound.

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Geuze et al 2008b

Abstract – Research Centre – Military Mental Health, Ministry of Defense, PO Box 90.000, 3509AA Utrecht, The Netherlands. s.g.geuze@umcutrecht.nl

Impaired attention and memory are symptoms frequently associated with posttraumatic stress disorder (PTSD).

Although patients with PTSD frequently report memory difficulties and empirical research provides support for a memory deficit in PTSD, as of yet, no fMRI study has adequately investigated the neural correlates of learning and memory of neutral (i.e. not trauma related) material in patients with PTSD compared to controls. Twelve male veterans with PTSD, and twelve male veterans without PTSD, were recruited, and matched for age, region and year of deployment. Encoding and retrieval of 12 word-pair associates was assessed during fMRI in both experimental groups. Compared to controls veterans with

PTSD revealed underactivation of the frontal cortex, and

overactivation of the temporal cortex

during the encoding phase.

PTSD retrieval of the paired associates resulted in

underactivation of right frontal cortex,

bilateral middle temporal gyri, and the

left posterior hippocampus/parahippocampal gyrus

Deficits in memory performance in PTSD appear to be related to altered activity in fronto-temporal areas during both the encoding and retrieval phase of memory processing.

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Yap & Richardson 2005

Abstract – School of Psychology, University of New South Wales, Sydney 2052, Australia. c.yap@student.unsw.edu.au

Latent inhibition (LI) refers to the reduction in conditioned responding when the conditioned stimulus (CS) is preexposed prior to CS-unconditioned stimulus pairings. Experiment 1a demonstrated that preexposure to an odor CS prior to odor-shock pairings markedly reduced conditioned freezing in 25-day-old rats; however, this LI effect was observed only if odor preexposure and odor-shock pairings occurred in the same context (i.e., LI was context-specific at this age). The results of Experiment 1b showed that 18-day-olds also exhibited LI, but this effect was not context-specific at this age. In Experiment 2, rats were preexposed to the odor at 18 days of age and given odor-shock pairings at 25 days of age. These rats exhibited context-specific latent inhibition, suggesting that 18-day-old rats encoded the preexposure context. In Experiment 3, all parameters were identical to Experiment 2, with the exception that odor-shock pairings were given at approximately PN18 and testing occurred at approximately PN25. These rats exhibited latent inhibition at test, but this effect was not context-specific. The results of this study suggest that (a) PN18 rats can exhibit latent inhibition, and (b) the expression of context-specific latent inhibition depends on the age at which conditioning occurs.

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Moran & Moser 1992

Abstract – Marion Merrell Dow Research Institute, Strasbourg, France.

Latent inhibition (LI) is a behavioral model of selective attention that has been used to study the attentional deficits seen in schizophrenia. In the present study, we examined the effect of 5-hydroxytryptamine3

(5-HT3) receptor

blockade on LI using the conditioned emotional response (CER) procedure. Prior exposure to 20, 30, or 40 stimulus presentations significantly, and almost completely, inhibited the CER to that stimulus. This LI effect was much weaker when only 10 preexposures were given. 1H-indole-3-carboxylic acid, trans-octahydro-3-oxo-2,6-methano-2H-quinolizin-8-yl ester methanesulfonate (MDL 73,147EF), a selective 5-HT3 receptor antagonist, significantly facilitated the LI effect observed after 10 preexposures at 0.1 mg/kg but not at 0.01 mg/kg. The magnitude of this effect was comparable to that observed with the classical neuroleptic haloperidol (0.1 mg/kg). Neither MDL 73,147EF nor haloperidol affected the CER in animals not preexposed to the stimulus. These results strongly corroborate suggestions that 5-HT3 receptor antagonists will be of use in the treatment of schizophrenia.

I suspect that latent inhibition plays a role in PTSD – and probably this receptor, as well.  Child abuse loads us with conditioned emotional responses – to nearly everything (in my case) having to do with people.  These patterns, based on experience, were built into my brain.  I cannot simply make them go away as extraneous – which is what latent inhibition seems to be about.

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Order cDNA clone, Links

HTR3E

Official Symbol HTR3E and Name: 5-hydroxytryptamine (serotonin) receptor 3, family member E [Homo sapiens]

Other Aliases: 5-HT3c1, MGC120035, MGC120036, MGC120037

Other Designations: 5-HT3 receptor subunit E splice variant HTR3Ea; 5-hydroxytryptamine receptor 3 subunit E; serotonin receptor 3 subunit E

Chromosome: 3; Location: 3q27.1

Annotation: Chromosome 3, NC_000003.10 (185300661..185307477)

MIM: 610123

GeneID: 285242

5-HT3c1; MGC120035; MGC120036; MGC120037

Summary

The product of this gene belongs to the ligand-gated ion channel receptor superfamily. This gene encodes a subunit E of the type 3 receptor for 5-hydroxytryptamine (serotonin), a biogenic hormone that functions as a neurotransmitter, a hormone, and a mitogen. This receptor causes fast, depolarizing responses in neurons after activation. Genes encoding subunits C, D and E form a cluster on chromosome 3. An alternative splice variant has been described but its full length sequence has not been determined. [provided by RefSeq]

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Harrell & Allan 2003

Abstract – University of New Mexico School of Medicine, Health Sciences Center, Department of Neurosciences, Albuquerque, New Mexico 87131 USA.

The 5-HT3 receptor for serotonin is expressed within limbic structures and is known to modulate neurotransmitter release, suggesting that this receptor may influence learning and memory.

Perturbations in serotonergic neurotransmission lead to changes in the ability to attend, learn, and remember.

To examine the role of 5-HT3 receptors in learning, memory, and attention, 5-HT3 receptor overexpressing (5-HT3-OE) transgenic mice and their wild-type littermates (WT) were tested in Pavlovian contextual and cued fear conditioning, fear extinction, and latent inhibition (LI) paradigms. Prepulse inhibition (PPI) was assessed to reveal changes in sensorimotor gating. Additionally, anxious behaviors, shock sensitivity, and reactions to novel stimuli were evaluated. 5-HT3-OE mice displayed enhanced contextual conditioning, whereas cued conditioning remained the same as that of WT mice. 5-HT3-OE mice did not differ from WT in extinction rates to either the context or cue. LI was enhanced for 5-HT3-OE mice compared to WT. PPI remained unchanged. No differences in sensitivity to footshock or startle were found. However, 5-HT3-OE mice demonstrated heightened exploratory behavior in response to novel environmental stimuli and decreased anxiety as measured in the elevated plus-maze. Results indicate that

overexpression of the 5-HT3 receptor in mouse forebrain results in enhanced hippocampal-dependent learning and attention.

Enhanced inspective behavior in response to novelty may contribute to the observed improvements in learning, memory, and attention due to 5-HT3 receptor overexpression.

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