More on emotions and population data

[From Bill Powers (2010.02.08.1145 MST)]
It feels as if a great chunk of something has suddenly started to make
sense. I hear David Goldstein saying “individual differences.”
I think of Casting Nets and Testing Specimens. I think of being a rather
violent child who got into fights. I think of Panksepp stimulating
midbrains and seeing stereotyped signs of emotions in decorticate animals
yuck. I think of Hess’s cats showing stereotyped configurations of the
body upon brain stimulation, also stereotyped movements.
What I realized about getting into fights is that fighting is a very
sterotyped behavior. Make a fist and propel it outward to make hard
contact with someone. Grab, push, pull, and twist. Just as stereotyped as
a cat baring its teeth, squinting its eyes, hissing, standing the hair on
its back up. A dog attacking in a sudden flurry of slashing teeth, or
seizing and grinding or wrenching from side to side. I start to see sense
in what Bruce Abbott has been saying about “emotion
systems.”
These are all lower-level systems from relationships down through events,
transitions, and configurations. The stereotypical behavior we see shows
that (1) the means available for violent action is similar across members
of a species (I can’t wreak havoc with my teeth the way a dog does), and
(2) there are probably some inherited control systems that used these
means in species-specific ways, though under electrical stimulation
they’re not used for any higher-level purposes. When higher goals are
frustrated and efforts begin to escalate, sooner or later the animal
sends reference signals to these inherited control systems which act
similarly in most members of a species. So in normal emotions, the same
lower-order appearances are generated, plus the higher-order cognitive
aspects of emotion.
This all fits in with my theory of emotions in that when these inherited
systems come into action, that somatic branch I speak of does alter the
physiological state, which does create sensations of all kinds, providing
the feeling part of an emotion. But along with that feeling part,
inherited behavioral systems are also involved; a good deal of an
emotional experience comes from the cognitive conflict inherent in NOT
letting those systems act as they are organized to act. I haven’t been
thinking of those lower-level inherited behavioral systems as being part
of emotions.
One fact seems probably true: Panksepp is wrong in thinking emotions are
strictly bottom-up. He was fooled by seeing those emotional-looking
actions and body configurations when he stimulated the midbrain or
thereabouts. What he was doing was supply reference signals like those
that normally would come from higher-level control systems, including
cognitive systems. He rejected the idea that emotions originate in the
cortex, which was a mistake. The goal component of an emotion comes from
higher systems; the feeling part from the systems Panksepp was
stimulating. He was seeing only part of an emotion, and mistook it for
the whole thing.
Individual differences. The problem with using population data to
investigate the behavior of organisms is that it leads to what I call the
universal principle of mass behavior: “Some do and some don’t.”
This is why correlations are so low in such studies. If the
generalizations drawn from such studies were general in the same sense as
the General Theory of Gravitation, they would be true of all but a small
handful of members of the population. Correlations would be in the high
nineties. But they are not true of all members of the population: large
numbers of subjects behave contrary to the hypothesis, but statistics
still allow you to say “Mothers hold their babies on the left,”
which is true of a little more than half of the population of mothers, a
statistically significant but otherwise unimportant majority.
Now why does this come up now? Because I realized that if we simply asked
what the difference is between those who do and those who don’t, we could
create subpopulations in which a much greater fraction do than don’t. We
might, in fact, find real predictable subpopulations in which practically
everyone behaves the same way: keeping the lost wallet or returning
it; paying more with a credit card than with cash, or vice versa,
banging on people with fists when in extrema, or avoiding them or
using other nonviolent means. After all, the first round of an
investigation using population statistics very handily separates those
who do from those who don’t. Why not then study those subpopulations to
see what is different about them? David G., is this what you’ve been
trying to get through my thick skull by talking in jargon about
Individual Difference Variables?

What we might then find are subpopulations who have evolved a little
differently, inheriting different stereotyped emotions, strategies, ways
of walking or running, likes and dislikes for foods, and so forth. I
assume they would all have the same levels of perception and control, but
if that’s not true we could discover the differences there, too.

Am I the last one to realize all this?

Best,

Bill P.

[From David Goldstein (2010.02.09.0712 EST)]

[About Bill Powers (2010.02.08.1145 MST)]

BP: David G., is this what you’ve been trying to get through my thick skull by talking in jargon about Individual Difference Variables?

DG: I think that you have expressed very well the reasons why Psychologists have taken the individual differences approach.

Knowing how we are the same, as well as how we are different, will likely result in the most complete picture. PCT focuses

on the former, which is what attracts me. MOL is based on the latter, which is what attracts me. In therapy, each person is approached as

an individual.

The book by Plutchik “Emotions and Life” is the best summary I have come across, which includes a description of Panksepp. Have you

been able to obtain it yet?

David

···

----- Original Message -----

From:
Bill Powers

To: CSGNET@LISTSERV.ILLINOIS.EDU

Sent: Tuesday, February 09, 2010 2:44 AM

Subject: More on emotions and population data

[From Bill Powers (2010.02.08.1145 MST)]
It feels as if a great chunk of something has suddenly started to make sense. I hear David Goldstein saying “individual differences.” I think of Casting Nets and Testing Specimens. I think of being a rather violent child who got into fights. I think of Panksepp stimulating midbrains and seeing stereotyped signs of emotions in decorticate animals yuck. I think of Hess’s cats showing stereotyped configurations of the body upon brain stimulation, also stereotyped movements.
What I realized about getting into fights is that fighting is a very sterotyped behavior. Make a fist and propel it outward to make hard contact with someone. Grab, push, pull, and twist. Just as stereotyped as a cat baring its teeth, squinting its eyes, hissing, standing the hair on its back up. A dog attacking in a sudden flurry of slashing teeth, or seizing and grinding or wrenching from side to side. I start to see sense in what Bruce Abbott has been saying about “emotion systems.”
These are all lower-level systems from relationships down through events, transitions, and configurations. The stereotypical behavior we see shows that (1) the means available for violent action is similar across members of a species (I can’t wreak havoc with my teeth the way a dog does), and (2) there are probably some inherited control systems that used these means in species-specific ways, though under electrical stimulation they’re not used for any higher-level purposes. When higher goals are frustrated and efforts begin to escalate, sooner or later the animal sends reference signals to these inherited control systems which act similarly in most members of a species. So in normal emotions, the same lower-order appearances are generated, plus the higher-order cognitive aspects of emotion.
This all fits in with my theory of emotions in that when these inherited systems come into action, that somatic branch I speak of does alter the physiological state, which does create sensations of all kinds, providing the feeling part of an emotion. But along with that feeling part, inherited behavioral systems are also involved; a good deal of an emotional experience comes from the cognitive conflict inherent in NOT letting those systems act as they are organized to act. I haven’t been thinking of those lower-level inherited behavioral systems as being part of emotions.
One fact seems probably true: Panksepp is wrong in thinking emotions are strictly bottom-up. He was fooled by seeing those emotional-looking actions and body configurations when he stimulated the midbrain or thereabouts. What he was doing was supply reference signals like those that normally would come from higher-level control systems, including cognitive systems. He rejected the idea that emotions originate in the cortex, which was a mistake. The goal component of an emotion comes from higher systems; the feeling part from the systems Panksepp was stimulating. He was seeing only part of an emotion, and mistook it for the whole thing.
Individual differences. The problem with using population data to investigate the behavior of organisms is that it leads to what I call the universal principle of mass behavior: “Some do and some don’t.” This is why correlations are so low in such studies. If the generalizations drawn from such studies were general in the same sense as the General Theory of Gravitation, they would be true of all but a small handful of members of the population. Correlations would be in the high nineties. But they are not true of all members of the population: large numbers of subjects behave contrary to the hypothesis, but statistics still allow you to say “Mothers hold their babies on the left,” which is true of a little more than half of the population of mothers, a statistically significant but otherwise unimportant majority.
Now why does this come up now? Because I realized that if we simply asked what the difference is between those who do and those who don’t, we could create subpopulations in which a much greater fraction do than don’t. We might, in fact, find real predictable subpopulations in which practically everyone behaves the same way: keeping the lost wallet or returning it; paying more with a credit card than with cash, or vice versa, banging on people with fists when in extrema , or avoiding them or using other nonviolent means. After all, the first round of an investigation using population statistics very handily separates those who do from those who don’t. Why not then study those subpopulations to see what is different about them? David G., is this what you’ve been trying to get through my thick skull by talking in jargon about Individual Difference Variables?

What we might then find are subpopulations who have evolved a little differently, inheriting different stereotyped emotions, strategies, ways of walking or running, likes and dislikes for foods, and so forth. I assume they would all have the same levels of perception and control, but if that’s not true we could discover the differences there, too.

Am I the last one to realize all this?

Best,

Bill P.

[From Bruce Abbott
(2010.02.08.1320 EST)

Bill Powers (2010.02.08.1145 MST)

···

BP: It feels as if a great chunk of something has
suddenly started to make sense. I hear David Goldstein saying “individual
differences.” I think of Casting Nets and Testing Specimens. I think of
being a rather violent child who got into fights. I think of Panksepp
stimulating midbrains and seeing stereotyped signs of emotions in decorticate
animals yuck. I think of Hess’s cats showing stereotyped configurations of
the body upon brain stimulation, also stereotyped movements.

BP: What I realized about getting into fights is that fighting is a very
sterotyped behavior. Make a fist and propel it outward to make hard contact
with someone. Grab, push, pull, and twist. Just as stereotyped as a cat baring
its teeth, squinting its eyes, hissing, standing the hair on its back up. A dog
attacking in a sudden flurry of slashing teeth, or seizing and grinding or
wrenching from side to side. I start to see sense in what Bruce Abbott has been
saying about “emotion systems.”

BP: These are all lower-level systems from relationships down through events,
transitions, and configurations. The stereotypical behavior we see shows that
(1) the means available for violent action is similar across members of a
species (I can’t wreak havoc with my teeth the way a dog does), and (2) there
are probably some inherited control systems that used these means in
species-specific ways, though under electrical stimulation they’re not used for
any higher-level purposes. When higher goals are frustrated and efforts begin
to escalate, sooner or later the animal sends reference signals to these
inherited control systems which act similarly in most members of a species. So
in normal emotions, the same lower-order appearances are generated, plus the
higher-order cognitive aspects of emotion.

BP: This all fits in with my theory of emotions in that when these inherited
systems come into action, that somatic branch I speak of does alter the
physiological state, which does create sensations of all kinds, providing the
feeling part of an emotion. But along with that feeling part, inherited
behavioral systems are also involved; a good deal of an emotional experience
comes from the cognitive conflict inherent in NOT letting those systems act as
they are organized to act. I haven’t been thinking of those lower-level
inherited behavioral systems as being part of emotions.

BP: One fact seems probably true: Panksepp is wrong in thinking emotions are
strictly bottom-up. He was fooled by seeing those emotional-looking actions and
body configurations when he stimulated the midbrain or thereabouts. What he was
doing was supply reference signals like those that normally would come from
higher-level control systems, including cognitive systems. He rejected the idea
that emotions originate in the cortex, which was a mistake. The goal component
of an emotion comes from higher systems; the feeling part from the systems
Panksepp was stimulating. He was seeing only part of an emotion, and mistook it
for the whole thing.

Relying
on second-hand descriptions of someone’s theory always carries the risk
of getting it wrong, or only partly right, so I’d like to interject a few
things that Jaak Panksepp wrote in his book Affective Neuroscience that
may apply here. The following is from Chapter 10, which covers rage and anger.

Varieties of ESB-Induced Aggression and Their Affective
Consequences

Distinctions
among neural pathways for aggression have been effectively made by the careful
psychobehavioral analysis of aggressive sequences evoked by direct electrical
stimulation of the brain (ESB). The fact that coherent patterns of aggression
can be produced in this way is remarkable in itself. If, as many scientists
used to believe, aggression is largely a learned response rather than an
intrinsic potential of the nervous system . . ., it would be unlikely
that localized ESB could evoke attack behaviors. However, since Walter Hess’s
work in the 1930’s . . ., it has been clear that rage can be precipitously
provoked by ESB administered to specific brain areas.

My
own initial experience with this technique was especially revealing. When I
first applied ESB to a cat that had been surgically prepared with an indwelling
electrode in the medial hypothalamus, within the first few seconds of ESB the
peaceful animal was emotionally transformed. It leaped viciously toward me with
claws unsheathed, fangs bared, hissing and spitting. It could have pounced in
many different directions, but its arousal was directed right at my head.
Fortunately a Plexiglas wall separated me from the enraged beast. Within a
fraction of a minute after terminating the stimulation, the cat was again
relaxed and peaceful, and could be petted without further retribution.

.
. .at present three distinct kinds of aggression can be aroused by applying ESB
to slightly different brain zones: (1) predatory aggression, (2) angry rage-like
aggression, and perhaps (3) intermale aggression, even though the last may also
have strong components of the other two. It is the second of these systems that
will be the center of attention in the remainder of this chapter, even though I
will summarize selected issues related to the other two.

Several
investigators called aggressive displays induced by ESB “sham rage,”
based on the assumption that the animals were not experiencing true affect.
This seemed plausible because some of the subjects could be petted even while
they were hissing and snarling. However, such sites appear to be quite low in
the brain stem and in the minority. Now it seems more likely that most
electrode placements above the mesencephalon do evoke a central state
indistinguishable from normal anger (except perhaps for the fact that
stimulation-induced rage is not sustained for a long time after ESB offset,
perhaps because of the sudden release of an opponent process). Perhaps the most
compelling evidence that ESB evokes a true affective feeling is that humans
stimulated at such brain sites have reported experiencing a feeling of intense
rage.

It
is clear from the above that Panksepp distinguishes the midbrain manifestations
of the motor components of emotions from the fuller expression of an affective
state elicited by stimulation above the midbrain.

A
little earlier in the same chapter, Panksepp says this:

Although
anger appears to have several obvious precipitating stimuli in the environment,
the emotion is not created out of environmental events but represents the
ability of certain types of stimuli to access the neural circuitry of RAGE
within the brain. For instance, a human baby typically becomes enraged if its
freedom of action is restricted simply by holding its arms to its sides. This
highlights a general and lifelong principle. Anything that restricts our
freedom will be viewed as an irritant deserving our anger, contempt, and
revolutionary intent. Of course, restriction of freedom is not the only
precipitant of our anger and scorn. The same response emerges when one’s
body surface is repeatedly irritated or when one does not receive expected
rewards, namely, when one is frustrated. To take a trivial example: Who has not
experienced a brief flash of frustration-induced anger when a vending machine
takes one’s money without dispensing any goods? Most can shrug off the
feeling rapidly with cognitive intervention, especially if one is not too
hungry and still has sufficient coins available to try again elsewhere. This
simple observation suggests that unfulfilled expectancies within the SEEKING
system activate the neural patterns of frustration, probably in frontal
cortical areas which compute reward contingencies. As will be explained in detail
alter, reward and expectation mismatches may promote anger by downward neural
influences that arouse RAGE circuits.

Such
cognitive precipitants of anger would, of course, require prior learning. By
contrast, a young baby who becomes enraged because it is prevented from moving
may not initially conceptualize the external source of its anger, but with
social development and insights into the nature of social dynamics, it rapidly
learns to appraise the sources of the irritations and frustrations in its
world. And then the neural paths have been prepared for retributions.

Indeed,
human brains are evolutionarily “prepared” to externalize the
causes of anger and to “blame” others for the evoked feelings
rather than the evolutionary heritage that created the potential for anger in
the first place. Of course, this makes adaptive sense. The aim of anger is to
increase the probability of success in the pursuit of one’s ongoing
desires and competition for resources. But this is also the dilemma that
therapists commonly highlight when they exhort their clients “to take
responsibility for their feelings.” Other people do not cause anger; they
merely trigger certain emotional circuits into action. Ultimately, our feelings
come from within, and perhaps only humans have a substantive opportunity,
through emotional education or willpower, to choose which stimuli they allow to
trigger their emotional circuits into full-blown arousal. Animals, because of
their limited ability to conceptualize the nature of emotions and intentions,
do not appear to have such options.

(Note:
Panksepp’s use of all capitals in the words “RAGE” and “SEEKING”
refer to the neural circuitry that he theorizes supports these
behavioral/emotional states.)

Although
there is much room in the above description for a reinterpretation in HPCT
(rather than stimulus) terms, Panksepp clearly is aware that these emotion
systems do not operate in a strictly bottom-up mode. In another paragraph he
notes further that, once such a system becomes active, it can also change how
one perceives the situation; thus inputs at the cognitive level can influence
the activity of the emotion systems and, once active, the emotion systems can
influence processing of information at the cognitive level.

Be
aware that one would have to read much more of Affective Neuroscience
than I have quoted here to get a full, accurate picture of Panksepp’s
theory and the evidence he provides to support it. One of the more refreshing aspects
of this presentation is that Panksepp is not afraid to admit when he’s
speculating beyond his data, and uses those opportunities to point out where
further research needs to be undertaken.

By
the way, I’m copying from a prepublication version of Affective
Neuroscience
that Jaak sent me some years ago, so I am not able to give
page numbers for the above as they appear in the published book, and there is
always the possibility that some of it may have been revised during the editing
process.

Bruce
A.

[From Bill Powers (2010.02.10.0845 MST)]

Bruce Abbott (2010.02.08.1320 EST) –

BA: Relying on second-hand
descriptions of someone’s theory always carries the risk of getting it
wrong, or only partly right, so I’d like to interject a few things that
Jaak Panksepp wrote in his book Affective Neuroscience that may
apply here. The following is from Chapter 10, which covers rage and
anger.

Varieties of ESB-Induced Aggression and Their Affective
Consequences

Distinctions among neural pathways for aggression have been effectively
made by the careful psychobehavioral analysis of aggressive sequences
evoked by direct electrical stimulation of the brain (ESB). The fact that
coherent patterns of aggression can be produced in this way is remarkable
in itself. If, as many scientists used to believe, aggression is largely
a learned response rather than an intrinsic potential of the nervous
system . . ., it would be unlikely that localized ESB could evoke
attack behaviors. However, since Walter Hess’s work in the 1930’s . . .,
it has been clear that rage can be precipitously provoked by ESB
administered to specific brain areas.

BP: Thinking about this for several days has reminded me of where I
started with this subject. What I started with (in the back of my mind)
was a scale of emotion sort of like this: distraction, annoyance,
irritation, exasperation, antagonism, anger, fury, rage, destructive
violence. That’s how emotions seem to me: not on-off, but on a scale of
magnitude. And that scale starts at the high end of a physical
preparedness scale that starts at zero.

This is what suggested the link between error signals and emotion, and
what led me to see emotion simply as one extreme on a continuous scale of
normal control behavior. As disturbances increase, more action is
required to oppose their effects; as more action is required, more energy
is expended; as more energy is expended, demands on the life support
systems increase, depleting reserves; as reserves are depleted, the
physiological systems gear up to replace and maintain them. So we end up
gasping and sweating, with the heart racing and muscles swelling and
capillaries dilating and maximum effort being produced as we strain to
overcomed the threat, glucose pouring into the bloodstream, ATP being
shoveled frantically into the muscles, muscles contracting violently,
pulling their attachments toward each other with with half a ton of
force.

Emotion is not an either-or process. It’s not a “response” that
either occurs or doesn’t occur. It’s a state of body and mind that ranges
over a continuum from peacefully dozing in a hammock to charging an
opponent, all restraint removed, with the intent to kill. To get from one
extreme to the other, it passes through all the intermediate states. Only
in pathological cases does it snap from nothing at all to the maximum
possible degree.

Pathological cases – and ESB. Electrical stimulation is usually on-off,
and it tends to be violent. If the current or the frequency of stimulus
spikes were gradually reduced, the animal would be seen to pass smoothly
from the high extreme back down to the lowest level of arousal, or so I
would predict. I would not predict that as the stimulation is reduced,
the animal would continue throwing itself at the bars of the cage without
regard to pain or exhaustion, trying to kill the experimenter, and then
at some threshold level, suddenly relax, curling up and purring itself to
sleep.

In your description, there is one variable you don’t mention:

BA: My own
initial experience with this technique was especially revealing. When I
first applied ESB to a cat that had been surgically prepared with an
indwelling electrode in the medial hypothalamus, within the first few
seconds of ESB the peaceful animal was emotionally transformed. It leaped
viciously toward me with claws unsheathed, fangs bared, hissing and
spitting. It could have pounced in many different directions, but its
arousal was directed right at my head. Fortunately a Plexiglas wall
separated me from the enraged beast. Within a fraction of a minute after
terminating the stimulation, the cat was again relaxed and peaceful, and
could be petted without further retribution.

BP: That certain sounds like an on-off reaction: either the animal was
viciously attacking you, or it was relaxed and peaceful. But you don’t
mention how the stimulation was applied. I would guess that the ESB was
turned on and off by a switch, so the signal was either zero or maximum.
When on, the magnitude of the ESB was evidently large enough to drive the
reference signals hard against their maximum values. What would have
happened if instead of an on-off switch, you had had a knob with which
you could gradually increase the stimulation from zero? Do you suppose
that at the first picoampere of current, the animal would have charged
you in all-out rage? I rather doubt that. If you know different I would
be wrong, but I’ll bet that was not tried.

Of course it’s possible that the stimulation wasn’t confined to reference
signals. I’d be surprised, in fact, if it didn’t disturb a lot of
different kinds of signals at various places in the control loop. If
perceptual signals were generated, and it’s hard to imagine how that
could be avoided, those signals follow paths that bifurcate, going not
only into the comparators at the same level but passing upward into the
perceptual input functions of higher-level systems. This means that
disturbances would appear in higher-level control systems, possibly quite
extreme disturbances as the perceptual world was suddenly altered by
large amounts. Considering that as many as 1000 neurons can be found in
one cubic millimeter of brain tissue (and many more than that in a cat,
where, I’ve read, the neurons are a tenth the size of human neurons), and
that the geometric details of neural function vary widely from animal to
animal, it seems highly unlikely that placement of electrodes by
stereotaxis could aim the stimulation at a precisely known neural
function without spilling over into relatively large volumes of brain
tissue. Also, we mustn’t forget, electricity flows through closed paths,
so the current at the tip of an electrode flows on through all sorts of
other structures after it has done its job where the experimenter aimed
it.

The sudden cessation of the aggressive-looking action is a clue to
something else. How often have you had a really strong emotion, realized
it was based on a mistaken perception, and instantly returned to a normal
calm state? I would guess never. Strong emotions taper off as the
adrenaline gradually dissipates or is metabolized; the heart pounds on
for more than few second or minutes; the breathing gradually slows down;
the trembling in the limbs gradually lessens and smoothes out. The mental
upsetness slowly departs. Emotions don’t simply switch on and off; the
physiological changes can’t be reversed that quickly. A small fraction of
a minute isn’t long enough to recover from all the physiological changes
involved, especially if the emotion is violent rage.

So I am led to suspect that what you saw was “behavioral
emotion” – that is, the visually-observable configurations,
transitions, events, and relationships typical of high-error situations,
but without the somatic changes that normally accompany emotional
activity. I don’t see how a complete recovery from an extreme emotional
state could occur so fast: " Within a fraction of a minute after
terminating the stimulation, the cat was again relaxed and peaceful, and
could be petted without further retribution." That makes even
higher-order involvement unlikely; the attack is more like a stickleback
attacking any red blob. The cat attacked a moving object; you shouldn’t
take it personally.

I’d guess that using the electrode, you were hijacking the same means of
control that the cat’s higher-order systems would operate under normal
conditions, but without the normal higher-order control going on (other
than resisting disturbances), and without the normal somatic changes that
accompany strong emotions. An actor can produce the appearance of emotion
that way without necessarily experiencing the whole emotion at all the
levels that are normally involved. Even actors may require a little time
to recover, since the good ones do feel some of the physiological
changes, and some have problems with shedding the persona for a long time
afterward. But it’s nothing like a complete emotion.

Several
investigators called aggressive displays induced by ESB “sham rage,”
based on the assumption that the animals were not experiencing true
affect. This seemed plausible because some of the subjects could be
petted even while they were hissing and snarling. However, such sites
appear to be quite low in the brain stem and in the minority. Now it
seems more likely that most electrode placements above the mesencephalon
do evoke a central state indistinguishable from normal anger (except
perhaps for the fact that stimulation-induced rage is not sustained for a
long time after ESB offset, perhaps because of the sudden release of an
opponent process).

No, I don’t buy it. Everything points to sham rage, by which I would mean
the production of visual and auditory configurations, transitions, and
relationships (observable by a human experimenter) without the normal
higher-order motivation or the normal lower order physiological changes.
I don’t think you can draw correct conclusions simply by watching a cat
from outside its skin. I can’t prove the rage isn’t “real”,
whatever that means, but you can’t prove it is.

Perhaps the most compelling
evidence that ESB evokes a true affective feeling is that humans
stimulated at such brain sites have reported experiencing a feeling of
intense rage.

That strongly suggests that there are higher-level perceptions disturbed
by the stimulation of lower systems as I conjectured above, and that the
perceptions are recognizeable as emotions. The implication is that in the
cats as well as the humans, you were disturbing a lot more than the
mesencephalon. It would be interesting to know whether, in the human
beings, the intense feeling of rage ceased instantly when the current was
switched off, or if there were continuing jitters from adrenaline,
pounding of the heart, rapid breathing, and so on. If those things didn’t
happen (and I should think they would be mentioned if they did), then the
perception of rage was false, being the result of electrical stimulation
of the same higher-order perceptual pathway that would have been
stimulated by such physiological changes. The subjects experience
rage-ness, but not rage.

I really think that all this so-called information about emotions is just
too sketchy and superficial to be taken seriously. You didn’t know
anything about PCT when you conducted the experiment with the cat; you
can’t be blamed for not having any ideas about subtler possibilities, or
for taking the appearances for granted. Neither can the others, though I
do wonder why some of these considerations were not brought up. It’s as
if everyone is used to taking superficial appearances as “prima
facie” evidence when in fact they aren’t evidence at all, but
illusions.

I think I am reaching the level of irritation, and as I scan down through
more reports about Panksepp’s free-wheeling interpretations the level
seems to be increasing, so I think I’ll pause for your
commentary.

Best,

Bill P.

[From
Bruce Abbott (2010.02.10.1810 EST)]

Bill Powers (2010.02.10.0845 MST)

···

Bruce Abbott (2010.02.08.1320 EST)

BA: Relying on second-hand descriptions of someone’s
theory always carries the risk of getting it wrong, or only partly right, so
I’d like to interject a few things that Jaak Panksepp wrote in his book Affective
Neuroscience
that may apply here. The following is from Chapter 10, which
covers rage and anger.

BP: Emotion is not an either-or process.
It’s not a “response” that either occurs or doesn’t occur. It’s a
state of body and mind that ranges over a continuum from peacefully dozing in a
hammock to charging an opponent, all restraint removed, with the intent to
kill. To get from one extreme to the other, it passes through all the
intermediate states. Only in pathological cases does it snap from nothing at
all to the maximum possible degree.

BP: Pathological cases – and ESB.
Electrical stimulation is usually on-off, and it tends to be violent. If the
current or the frequency of stimulus spikes were gradually reduced, the animal
would be seen to pass smoothly from the high extreme back down to the lowest
level of arousal, or so I would predict. I would not predict that as the
stimulation is reduced, the animal would continue throwing itself at the bars
of the cage without regard to pain or exhaustion, trying to kill the
experimenter, and then at some threshold level, suddenly relax, curling up and
purring itself to sleep.

BP: In your description, there is one
variable you don’t mention:

In
my previous post, I indicated the sections quoted from Panksepp’s Affective
Neuroscience
by (1) introducing them in the immediately preceding
paragraph, and (2) Using indents rather than spaces to separate the paragraphs
of the quoted text from one-another. The block of quoted material was then
separated from my own comments by a space. [Perhaps this wasn’t clear to
you, in which case I accept the blame if you became confused as to whose
writing was whose.]

The paragraph immediately below, attributed to me,
was written by Panksepp.

BA:
My own initial experience with this technique was especially revealing. When I
first applied ESB to a cat that had been surgically prepared with an indwelling
electrode in the medial hypothalamus, within the first few seconds of ESB the
peaceful animal was emotionally transformed. It leaped viciously toward me with
claws unsheathed, fangs bared, hissing and spitting. It could have pounced in
many different directions, but its arousal was directed right at my head.
Fortunately a Plexiglas wall separated me from the enraged beast. Within a
fraction of a minute after terminating the stimulation, the cat was again
relaxed and peaceful, and could be petted without further retribution.

BP: That certain sounds like an on-off reaction: either the animal was
viciously attacking you, or it was relaxed and peaceful. But you don’t mention
how the stimulation was applied. I would guess that the ESB was turned on and
off by a switch, so the signal was either zero or maximum. When on, the
magnitude of the ESB was evidently large enough to drive the reference signals
hard against their maximum values. What would have happened if instead of an
on-off switch, you had had a knob with which you could gradually increase the
stimulation from zero? Do you suppose that at the first picoampere of current,
the animal would have charged you in all-out rage? I rather doubt that. If you
know different I would be wrong, but I’ll bet that was not tried.

I
haven’t done any of this ESB research, but my impression from reading
about it is that lower levels of stimulation produce lower levels of
activation, just as you suggest. At low levels, you might see the cat hiss and
bare its teeth, but not leap at someone’s face.

Of course it’s possible that the stimulation wasn’t confined to reference
signals. I’d be surprised, in fact, if it didn’t disturb a lot of different
kinds of signals at various places in the control loop. If perceptual signals
were generated, and it’s hard to imagine how that could be avoided, those
signals follow paths that bifurcate, going not only into the comparators at the
same level but passing upward into the perceptual input functions of
higher-level systems. This means that disturbances would appear in higher-level
control systems, possibly quite extreme disturbances as the perceptual world
was suddenly altered by large amounts. Considering that as many as 1000 neurons
can be found in one cubic millimeter of brain tissue (and many more than that
in a cat, where, I’ve read, the neurons are a tenth the size of human neurons),
and that the geometric details of neural function vary widely from animal to
animal, it seems highly unlikely that placement of electrodes by stereotaxis
could aim the stimulation at a precisely known neural function without spilling
over into relatively large volumes of brain tissue. Also, we mustn’t forget,
electricity flows through closed paths, so the current at the tip of an
electrode flows on through all sorts of other structures after it has done its
job where the experimenter aimed it.

Panksepp
and everyone else who has done ESB research is aware of the potential spread of
stimulation well beyond the intended target. That’s why other, more
localized techniques have been developed, such as delivering pico-amounts of a
specific neurotransmitter, blocking agent, etc. to specific brain locations. These
techniques allow one to zero in on specific target neurons; however, I don’t
know what work has been done using these techniques to refine or refute the
conclusions Panksepp draws from the ESB data.

The sudden cessation of the aggressive-looking action is a clue to something
else. How often have you had a really strong emotion, realized it was based on
a mistaken perception, and instantly returned to a normal calm state? I would
guess never. Strong emotions taper off as the adrenaline gradually dissipates
or is metabolized; the heart pounds on for more than few second or minutes; the
breathing gradually slows down; the trembling in the limbs gradually lessens
and smoothes out. The mental upsetness slowly departs. Emotions don’t simply
switch on and off; the physiological changes can’t be reversed that quickly. A
small fraction of a minute isn’t long enough to recover from all the
physiological changes involved, especially if the emotion is violent rage.

So I am led to suspect that what you saw was “behavioral emotion” –
that is, the visually-observable configurations, transitions, events, and
relationships typical of high-error situations, but without the somatic changes
that normally accompany emotional activity. I don’t see how a complete recovery
from an extreme emotional state could occur so fast: " Within a fraction
of a minute after terminating the stimulation, the cat was again relaxed and
peaceful, and could be petted without further retribution." That makes
even higher-order involvement unlikely; the attack is more like a stickleback
attacking any red blob. The cat attacked a moving object; you shouldn’t take it
personally.

I
agree that the observations are open to that possible interpretation, although it’s
just as speculative as the possibility that Panksepp offered. After all, nobody
measured the cat’s heart rate or circulating levels of adrenalin; the cat
may have appeared to be relaxed while still experiencing elevated levels of
these.

I’d guess that using the electrode, you were hijacking the same means of control
that the cat’s higher-order systems would operate under normal conditions, but
without the normal higher-order control going on (other than resisting
disturbances), and without the normal somatic changes that accompany strong
emotions. An actor can produce the appearance of emotion that way without
necessarily experiencing the whole emotion at all the levels that are normally
involved. Even actors may require a little time to recover, since the good ones
do feel some of the physiological changes, and some have problems with shedding
the persona for a long time afterward. But it’s nothing like a complete
emotion.

That’s exactly how I would
interpret it, except that I have no problem imagining that it’s the whole
“rage” emotion system that’s been artificially brought into
action, either by over-riding a reference or producing a disturbance that the
system would act to counter. Why do you insist that it can’t be the
complete emotion that is brought into play?

Several investigators called aggressive displays induced by ESB “sham
rage,” based on the assumption that the animals were not experiencing
true affect. This seemed plausible because some of the subjects could be petted
even while they were hissing and snarling. However, such sites appear to be
quite low in the brain stem and in the minority. Now it seems more likely that
most electrode placements above the mesencephalon do evoke a central state
indistinguishable from normal anger (except perhaps for the fact that
stimulation-induced rage is not sustained for a long time after ESB offset,
perhaps because of the sudden release of an opponent process).

No, I don’t buy it. Everything points to sham rage, by which I would mean the
production of visual and auditory configurations, transitions, and
relationships (observable by a human experimenter) without the normal
higher-order motivation or the normal lower order physiological changes. I
don’t think you can draw correct conclusions simply by watching a cat from
outside its skin. I can’t prove the rage isn’t “real”, whatever that
means, but you can’t prove it is.

Everything points to sham rage? We can’t get into the cat’s
head to know what it was experiencing, so all we have are the cat’s
behaviors to go by. According to the description, everything one might expect
to go with genuine rage was present. What points to sham rage is only the
relatively quick recovery of an apparently docile state once the stimulation
ceased. That could point to shame rage, but other explanations are possible.

Perhaps the most compelling evidence that ESB evokes a true
affective feeling is that humans stimulated at such brain sites have reported
experiencing a feeling of intense rage.

That strongly suggests that there are higher-level perceptions disturbed by the
stimulation of lower systems as I conjectured above, and that the perceptions
are recognizeable as emotions. The implication is that in the cats as well as
the humans, you were disturbing a lot more than the mesencephalon.

I’m
having difficulty parsing your meaning here. The stimulation that produces
feelings of rage is at the level of the medial hypothalamus (and certain other
structures of the limbic system that feed into it). So yes, the stimulation at
that level was disturbing (or changing references for) a lot more than the
mesencephalon. Electrodes in the latter produce only certain components of the
reaction. It’s just what one might expect to find if there’s a
hierarchy of levels of control.

It would be interesting to know whether, in the human
beings, the intense feeling of rage ceased instantly when the current was
switched off, or if there were continuing jitters from adrenaline, pounding of
the heart, rapid breathing, and so on. If those things didn’t happen (and I
should think they would be mentioned if they did), then the perception of rage
was false, being the result of electrical stimulation of the same higher-order
perceptual pathway that would have been stimulated by such physiological
changes. The subjects experience rage-ness, but not rage.

The human case that Panksepp
referred to was reported in another paper by another researcher. I’ll see
if I can find it. But if the person cannot distinguish “rage” from “rage-ness,”
where is this distinction getting us? Is it somehow crucial to the PCT-based
theory of emotions that it not be true rage? I must confess that I don’t
see it that way.

I really think that all this so-called information about emotions is just too
sketchy and superficial to be taken seriously. You didn’t know anything about
PCT when you conducted the experiment with the cat; you can’t be blamed for not
having any ideas about subtler possibilities, or for taking the appearances for
granted. Neither can the others, though I do wonder why some of these
considerations were not brought up. It’s as if everyone is used to taking
superficial appearances as “prima facie” evidence when in fact they
aren’t evidence at all, but illusions.

Again,
those were Panksepp’s observations, conclusions, and speculations, not
mine. I agree that they cry out for reinterpretation in control-theoretic terms.
However, I have a bit more faith in the soundness of the observations (and
their interpretation in terms of an innately-organized emotion system) than you
do.

Bruce

[From Bill Powers (2010.02.10.1645 MST)]

Bruce Abbott (2010.02.10.1810 EST) –

BA: The block of quoted material
was then separated from my own comments by a space. [Perhaps this wasn’t
clear to you, in which case I accept the blame if you became confused as
to whose writing was whose.]

The paragraph immediately below, attributed to me, was written by
Panksepp.

BP: Sorry, I didn’t catch that.

···

BA: Panksepp and everyone else
who has done ESB research is aware of the potential spread of stimulation
well beyond the intended target. That’s why other, more localized
techniques have been developed, such as delivering pico-amounts of a
specific neurotransmitter, blocking agent, etc. to specific brain
locations. These techniques allow one to zero in on specific target
neurons; however, I don’t know what work has been done using these
techniques to refine or refute the conclusions Panksepp draws from the
ESB data.

BP: That takes care of unwanted direct effects of the administered doses
of electricity or chemicals, but it doesn’t do away with the normal
hierarchical connections on the afferent side. Those are part of every
level in the brain: there are collaterals going from the sensory nuclei
over to the output nuclei at every level, and those signals all bifurcate
sending copies to the sensory inputs of higher systems. If the treatment
affects perceptual signals at one level, it will affect perceptual
signals in any intact higher levels, too. The only way to prevent that is
to interrupt the upgoing neural pathways, as in decortication.

Also, as soon as there is some behavior pattern developing, the animal
can sense it at all levels in the normal way, though it sees the behavior
from inside rather than outside. If what is sensed disturbs anything the
animal is controlling at higher levels, those levels will start adjusting
the reference signals going to lower levels. With the brain intact, that
will result in alterations of the reference signal going to the lower
levels where stimulation is taking place; PCT would lead us to assume
that the reference signals would be changing in whatever way will tend to
oppose the effects of the stimulation.

I think the interpretations offered by Panksepp and others look weaker
and weaker the more we go into the details. The observers are assuming a
certain kind of system, and assuming that the effects they see are being
produced by that kind of system – just as we are. But just in general I
think we have a lot more evidence in favor of our interpretation than
they have in favor of theirs. Because of our model, we ask questions they
didn’t think of asking.


BP earlier: The sudden cessation
of the aggressive-looking action is a clue to something … So I am led
to suspect that what you saw was “behavioral emotion” – that
is, the visually-observable configurations, transitions, events, and
relationships typical of high-error situations, but without the somatic
changes that normally accompany emotional activity. I don’t see how a
complete recovery from an extreme emotional state could occur so fast:
" Within a fraction of a minute after terminating the stimulation,
the cat was again relaxed and peaceful, and could be petted without
further retribution." That makes even higher-order involvement
unlikely; the attack is more like a stickleback attacking any red blob.
The cat attacked a moving object; you shouldn’t take it personally.

BA: I agree that the observations are open to that possible
interpretation, although it’s just as speculative as the possibility that
Panksepp offered. After all, nobody measured the cat’s heart rate or
circulating levels of adrenalin; the cat may have appeared to be relaxed
while still experiencing elevated levels of these.

BP: Yes, that would have to be the case to argue that it was a normal
emotion. But since there is no common sense or personal experience
arguing for the other side, and no meaasurements were taken, our case is
the stronger at the moment. At least we have a case for saying such
measurements are needed before any convincing conclusions can be
reached.

BP earlier: I’d guess that using
the electrode, you were hijacking the same means of control that the
cat’s higher-order systems would operate under normal conditions, but
without the normal higher-order control going on (other than resisting
disturbances), and without the normal somatic changes that accompany
strong emotions. An actor can produce the appearance of emotion that way
without necessarily experiencing the whole emotion at all the levels that
are normally involved. Even actors may require a little time to recover,
since the good ones do feel some of the physiological changes, and some
have problems with shedding the persona for a long time afterward. But
it’s nothing like a complete emotion.

BA: That’s exactly how I would interpret it, except that I have no
problem imagining that it’s the whole “rage” emotion system that’s been
artificially brought into action, either by over-riding a reference or
producing a disturbance that the system would act to counter. Why do you
insist that it can’t be the complete emotion that is brought into
play?

I don’t insist; it seems to me that the preponderance of evidence and
reasonable assumptions leads to the conclusions that not all the
components of a normal emotional state were present: cognitive goals (and
error signals), physiological preparedness, and now a third component,
inherited low-order behavior patterns. The third component is mainly what
is observed, with the other two components being – possibly – missing.

BA/Panksepp: Several investigators called aggressive displays induced by ESB “sham
rage,” based on the assumption that the animals were not experiencing
true affect. This seemed plausible because some of the subjects could be
petted even while they were hissing and snarling. However, such sites
appear to be quite low in the brain stem and in the minority. Now it
seems more likely that most electrode placements above the mesencephalon
do evoke a central state indistinguishable from normal anger (except
perhaps for the fact that stimulation-induced rage is not sustained for a
long time after ESB offset, perhaps because of the sudden release of an
opponent process).
BP: I don’t buy it. Everything points to sham rage, by which I would
mean the production of visual and auditory configurations, transitions,
and relationships (observable by a human experimenter) without the normal
higher-order motivation or the normal lower order physiological changes.
I don’t think you can draw correct conclusions simply by watching a cat
from outside its skin. I can’t prove the rage isn’t “real”,
whatever that means, but you can’t prove it is.

Everything points to sham rage? We can’t get into the cat’s head
to know what it was experiencing, so all we have are the cat’s
behaviors to go by.

Yes, but we also experience emotions, and there is experimental evidence
about experimental subjects being stimulated in similar ways and
reporting emotions, and there are observations of immediate recovery
after emotional displays that do not support the idea that the
physiological changes were present. If all we know about the cat is what
we observe and recognize from outside the cat, then we can immediately
conclude that we did not see an emotion, because the other parts of a
genuine or complete emotion were not observable. If you want to see a
complete emotion, you have to imagine that there was some higher-level
error and that there was physiological preparedness going on. If you
don’t want to see a complete emotion, or don’t care, you don’t imagine
those things. It’s optional.

BA: According to the
description, everything one might expect to go with genuine rage was
present.

BP: No it wasn’t. Only the externally visible and audible appearances
that accompany emotions were observed to be present.

BA: What points to sham
rage is only the relatively quick recovery of an apparently docile state
once the stimulation ceased. That could point to sham rage, but other
explanations are possible.

BP: Yes, and as long as we can’t rule sham rage out, and there are any
suggestions that the Panksepp, or common-sense, explanations was wrong,
we can’t conclude that all the components of an emotion were
present.

BA: Perhaps the most compelling
evidence that ESB evokes a true affective feeling is that humans
stimulated at such brain sites have reported experiencing a feeling of
intense rage.

BP: That strongly suggests that there are higher-level perceptions
disturbed by the stimulation of lower systems as I conjectured above, and
that the perceptions are recognizeable as emotions. The implication is
that in the cats as well as the humans, you were disturbing a lot more
than the mesencephalon.

BA: I’m having difficulty parsing your meaning here. The stimulation that
produces feelings of rage is at the level of the medial hypothalamus (and
certain other structures of the limbic system that feed into it). So yes,
the stimulation at that level was disturbing (or changing references for)
a lot more than the mesencephalon. Electrodes in the latter produce only
certain components of the reaction. It’s just what one might expect to
find if there’s a hierarchy of levels of control.

BP: That’s what I’m saying, too: there’s a hierarchy of perception and
control, and a natural emotion involves more that one level. Without the
cognitive goal, the posturing and actions are empty of meaning. They
amount to going through the motions of an emotion.

Note, also, that if you inject a signal into a perceptual pathway at a
level that would normally carry a perceptual signal when real rage was
going on, the result can be an imagined experience of rage with none of
the actual rage phenomena going on.

BP earlier: It would be
interesting to know whether, in the human beings, the intense feeling of
rage ceased instantly when the current was switched off, or if there were
continuing jitters from adrenaline, pounding of the heart, rapid
breathing, and so on. If those things didn’t happen (and I should think
they would be mentioned if they did), then the perception of rage was
false, being the result of electrical stimulation of the same
higher-order perceptual pathway that would have been stimulated by such
physiological changes. The subjects experience rage-ness, but not
rage.

The human case that Panksepp referred to was reported in another paper by
another researcher. I’ll see if I can find it. But if the person cannot
distinguish “rage” from “rage-ness,” where is this distinction getting
us? Is it somehow crucial to the PCT-based theory of emotions that it not
be true rage? I must confess that I don’t see it that
way.

BP: The distinction is the same as the distinction between real and
remembered or imagined perceptions. Above the level where imagination is
in effect, the perceptual result is the same. But the actual state of the
system below that level is not the state being experienced by the higher
levels.

Overall, what I’m trying to say is that there is nothing special about
emotion; it’s simply a point on a scale running from no affect to maximum
affect. It’s the way we categorize all the consequences of having large
errors that remain, for a while, uncorrected. All behaviors involve large
parts of the hierarchy, and include systems from highest to lowest.
Emotion is just a way of categorizing normal perception and control when
errors are unusually large. I think we will eventually see how that works
for positive emotions, too.

When experimenters stick electrodes into this hierarchy, they have no
idea of what they’re actually doing to it. It’s highly unlikely that the
results will be anything but confusing, because the organization of the
hierarchy is being circumvented and we’re not seeing the system in its
natural state. Injecting an arbitrary signal into this highly-organized
system will disturb it in myriad unknown ways. We might see fragments of
familiar behaviors, but they will be out of context and make no sense –
like a cat showing threatening postures, sounds, and actions, while
allowing the person it is threatening to pet it. If Panksepp could reach
out and touch the cat, why didn’t it sink its teeth into his hand if it
was really threatening him? Panksepp was seeing a cat which had the
ability to threaten and attack, but this ability had been taken over by
an electric current and quite likely did not reflect any actual intent to
threaten or attack, especially considering that the cat allowed the
petting. That’s what I mean by an incomplete pattern of emotion. A real
emotion is organized at all the levels from the level where the primary
error is down to the physiological systems.

BP earlier: I really think that
all this so-called information about emotions is just too sketchy and
superficial to be taken seriously. You didn’t know anything about PCT
when you conducted the experiment with the cat; you can’t be blamed for
not having any ideas about subtler possibilities, or for taking the
appearances for granted. Neither can the others, though I do wonder why
some of these considerations were not brought up. It’s as if everyone is
used to taking superficial appearances as “prima facie”
evidence when in fact they aren’t evidence at all, but
illusions.

Again, those were Panksepp’s observations, conclusions, and speculations,
not mine.

BP: OK, pretend I was talking to Panksepp.

BA: I agree that they cry out
for reinterpretation in control-theoretic terms. However, I have a bit
more faith in the soundness of the observations (and their interpretation
in terms of an innately-organized emotion system) than you
do.

BP: That appears to be true.

But I like you anyway.

Best,

Bill P.

[Martin Taylor 2010.02.23.14.05]

[From Bill Powers (2010.02.10.0845 MST)] to

Bruce Abbott (2010.02.08.1320 EST) --

BP: Thinking about this for several days has reminded me of where I started with this subject [emotion: MMT]. What I started with (in the back of my mind) was a scale of emotion sort of like this: distraction, annoyance, irritation, exasperation, antagonism, anger, fury, rage, destructive violence. That's how emotions seem to me: not on-off, but on a scale of magnitude. And that scale starts at the high end of a physical preparedness scale that starts at zero.

This is what suggested the link between error signals and emotion, and what led me to see emotion simply as one extreme on a continuous scale of normal control behavior. ...

Forgive me if this is covered in B:CP's new edition or elsewhere in your writings, but in CSGnet discussions, every thread about emotions has dealt only with what are colloquially called "negative" emotions. Could you expand on how you see the other side of the scale, such as mild amusement, enjoyment, gaiety, ecstacy, and the like? Or point me to the appropriate pages in some volume to which I am likely to have access?

Martin