Useful information:
 The readings are from 2 text
books: 1) Carlson “Physiology of
Behavior” latest (10th) edition
(2009) and 2) Andreassi
“Psychophysiology” 5th edition
(2007).
 Other readings and most class
notes are on my web site:
To get to web site….
 Google J Peter Rosenfeld
 On list that GOOGLE brings up , you’ll see
Rosenfeld Lab Home Page
Find out about current research in the Rosenfeld lab.Get
information on
groups.psych.northwestern.edu/rosenfeld/home.html
*Click it. You’ll see:

Note the buttons
 Clicking “publications” or
“classes” gets you where you
need to be for this course.
If you took 312-1…..
 Then clicking “classes” then “312-2”
and “Publications” gets you to all nontext assigned readings. That’s all you
need to know.
 Otherwise, you may want to
click”classes”, then “312-1” and go to
bottom of page for powerpoint
presentations, and review the one
called, “2. EEG,ERPs, & relation to single
neuronal activity.” and check out the first
29 slides.
If, from “Classes,” you go to the
312-2 site…
….You’ll see the texts, the syllabus,
lists of papers, chapters and
powerpoint presentations
(including this very presentation!)
which go with this course. Let’s do
for real…
Topic 1: Continuation of Neural
Coding from 312-1
 You may recall that we previously
subdivided this topic into 3
subtopics:
 1) Sensory coding, 2) Motor coding,
3) Coding of Psychological Events.
 We saw that the brain represents
sensory events in terms of neuronal
firing patterns. Remember the
following?
Or what about this?
These are neural representations
of somatic sensory sensations…
 Of course you read in 312-1 about
neuronal representation of visual
and auditory events. These are
sensory codes. There are also codes
for motor events, that is, firing
patterns in the motor cortex and
elsewhere that correlate with
muscle action leading to body
movements. These are motor codes.
Now for the almost unmanageably complex
and largely unknown neural representations
of “pure” psychological events….
 ….such as cognitions associated
with emotions(love, hate, sexual
arousal, perceptions), memories
(real and false), learning (classicalautomatic and instrumental),
deceptions (altruistic and selfserving), and so on… This giant topic
started out with the title, “Neural
Coding of Behavior” in the 1950s.
We now refer to this effort also as
“Neural Correlates of Behavior.”
 Note that word, “Behavior…”
(rather than “cognition” which is a
much broader and more sensible
term). That’s because the 1950s
was the heyday at most
universities of the Psychological
Movement known as
“Behaviorism” that dominated
academic Psychology.
In case you forgot, here is the
Wikipedia definition:
 Behaviorism (or behaviourism), also called the learning
perspective (where any physical action is a behavior), is a
philosophy of psychology based on the proposition that all
things that organisms do—including acting, thinking and
feeling—can and should be regarded as behaviors.[1] The
behaviorist school of thought maintains that behaviors as
such can be described scientifically without recourse either
to internal physiological events or to hypothetical
constructs such as the mind.[2] Behaviorism comprises the
position that all theories should have observational
correlates but that there are no philosophical differences
between publicly observable processes (such as actions)
and privately observable processes (such as thinking and
feeling).[3]
Now this was crazy, and has been largely
replaced by Cognitive Psychology…
 But a convenient thing about
behaviorism was its simplification of
psychological things to observable
behavior (omitting invisible thoughts
and such). So if you wanted to study
the neural substrates of learning, all
you had to do was study the “neural
correlates of observable behavior,”
which is where that term came from.
So the typical experiment in Neural
Correlates of Behavior went like this:
 OK, you are interested in learning,
so pick a standard learning protocol
(paradigm): Training animals like
cats to run down a maze to get food.
1. Get them hungry via food
deprivation. 2. Put them at the ‘start’
end with the food many feet away at
the ‘goal’. 3. Define ‘learning’ as the
state obtained when they can run
through the maze at top speed 5
times in a row with no wrong turns.
How do you study the neural
coding of this process?
 What neural events do you study?
That was easy to answer: There was no
method back in the 50s to record action
potentials from single neurons in freely
moving animals. (It is still not so easy to
do.) So you have to study population
neural activity such as EEG (spontaneous
brain waves) recorded from “chronically
implanted” animals.
From Carlson
From my chapter:
OK, so back in 50’s we could record
EEG from freely moving animals…
 But a bigger question is: “From
where do you record the EEG?”
Well this is a learning experiment
so just put the electrodes in the
learning center(s). Where’s that?
There’s the problem: In the 50’s
 We didn’t know what or where the
learning center(s) is (are) and how
they connect or how they interact. If
we knew that we wouldn't need to
do these experiments. So how did
the neural correlators in the 50s
proceed? They used reason. They
reasoned that learning must involve
association (ala John Stuart Mill and
the British Associationists)..
So clearly, one needed record from
places where associations are formed.
 Such as association cortices…2-3
in each side?
The special thing about association
areas are that in those places…
 Different sensory pathways come
together and “talk to each other”
(synapse on the same neurons), so
that one can form an association
between say the tone CS and the
smell of food as in Pavlovian
conditioning—or between bar press
and food in Skinnerian conditioning.
Any other such places? (Class?)
Yes, reticular formation, so we should
put a few electrodes up and down the
r.f. too, maybe 4 or 6? (So far, 16 sites)
 But learning also involves motivation
and reinforcement, so we probably
need 2 more on each side of
hypothalamus. (total now 20.)
 Animals have to see & hear stimuli
and smell food, so in those sensory
systems, figure to add 12 more to
cover thalamus and cortex,
bilaterally. We might be now up to
40! Why the exclamation point?
Well 40 wires coming from the
animal’s recording socket is a lot.
 Rats like this with just 6 wires are not big enough, one
must use a cat or dog. In 50’s these head preamps were
unavailable. One had to use wires
embedded with mercury powder.
Very Heavy. A cat with 40 of them
would “run” down the maze with
head tilted over. But that’s what
they did! (Not terribly natural.)
Besides the question of how many
electrodes and where to put them..
 ..was
the question of what neural
events to analyze from the
ongoing EEG.
 What would a page of ongoing
EEG look like, taken from a live
subject like a cat?
Here’s page of 14 site’s worth in
about 30 sec…
This actually is
unusually pretty
This is more realistic---but I digress
In the old days, there were no FFTs
etc..
 Just amplitude and frequency.
 So the old neural correlators of the
1950s would plot amplitude and
frequency for each of the 40 brain
sites during, say, pre-learning, early
learning, mid-learning, asymptote
learning, and extinction. The results
read like this: “In early learning, the
visual cortex amplitude is high but
the frequency is low, but the …..etc”
It was like the stock market:
“In January, Boeing was up but…
Microsoft was low, but Apple was
up, but GE was middling while
Exxon and ATT were
recovering…etc, etc…. In Spring,
however, Boeing and Exxon
crashed, while Microsoft and GE
reached new historic highs….etc
etc…”
If every lab got the same results,
no matter how complex, well OK.
 But in 1961, there were 2 well-known
review papers that summarized the
neural correlates literature: One:
High nervous functions: brain functions
and learning ER John - Annual Review of
Physiology,
 The other:
Electrophysiological contributions to the
neural basis of learning F Morrell Physiological Reviews, 1961
These papers both summarized
over a thousand studies….
 They both should have ended the
neural correlates literature,
because both essentially noted
the same thing, namely, that no
labs replicated themselves, let
alone others!!!
 The literature did taper off,
producing 2 reactions, and 2 new
literatures:
The reactions:
 1) The Operant Controlled Neural Event
(“OCNE”) approach: Operant
Conditioning of ERP components.
 2) The Cognitive Psychophysiology
literature: The less radical and longer
lasting carefully controlled scientific
study of ERP indicators of psychological
events.
 (We’ll start with the first reaction now)
The “OCNE” approach began with a
paper* outlining this first reaction. The
paper involved 3 things:
 1. A systematic critique of the
neural correlates literature.
 2. The rather ambitious program
outlined in reaction (Note title):
3. An empirical description and
demonstration of the method.
*The paper was by Fox & Rudell (1968)
Science, and is on 312-2 web page, article 9
1. The critique:
 A) F&R cited the replicability issues as noted
by John and Morrell in the ‘61 reviews.
 B) problem of choosing electrode sites and
neural parameters for study.
 C) Correlation approach: let animals do their
own thing and see what neural events from
what sites correlate. That’s not controlled
science.
 D) Time base issues: Learning takes days vs.
EEG, ERPs, action potentials that are
measured in milliseconds. One cannot make
laws connecting things measured in such
different units. (The “reduction problem”—see
Bergmann, “The Philosophy of Science.” 1966
The OCNE approach was supposed
to solve all these problems…
 We’ll see if it did (and how) later,
after we consider OCNE’s empirical
approach, which went something
like this: “The old neural correlators
wanted to see systematic & reliable
brain wave changes by training
behavior and looking for brain wave
correlates. Why bother? If you want
see a brain wave change, TRAIN IT
DIRECTLY.”
That is, specify a brain wave variable from
some brain site, and operantly condition it
like a bar press, by rewarding its occurence.
 The following figure, from the F&R
‘68 paper, shows 2 sets of
superimposed photic erps (visual
eps) elicited by a light flash,
recorded from chronically
installed electrodes in a freely
moving Cat’s visual area 19
(tertiary visual cortex). (Why
there? It’s convenient on top.)
The cats had been operated on and
electrodes as well as a milk tube
…had been installed. They were
recovered and each one was run
in a chamber (former hollowed out
‘fridge) as the strobe lights
flashed every 3 seconds, evoking
the eps.
The 2 sets of waves shown next are
during baseline (A) and training (B)
within one day:
The area between the lines had been
pre-selected as the critical area, i.e.,
 F&R had decided that the cat was to
lower the amplitude of the EP
amplitude between the lines. (They
saw that in the naïve cat, this was a
variable amplitude.) Every time the
cat did so, a computer (6’x3’x3’)
detected this and caused a relay to
close, delivering ~ 1cc milk through
the tube implanted that ended in the
roof of the hungry cat’s mouth.
So F & R decided to treat a deviant ERP
amplitude like a bar press and give the
cat a reward for making them.
 These EP amplitudes varied
within a bell curve, and F&R
rewarded deviant samples in
the blue tail at left. They
chose rare but occasionally
occurring samples with a finite
probability (.16) of occurrence.
Of course the cats were able to do
it, increasing negativity:
Of course the naysayers said, “well, it’s
simply the effect of milk on the EP…”
 i.e., the non-contingent or non-
associative or unconditional effect
of reinforcement. It isn’t learning.
 There was evidence. Others had
shown that food or shock affects
ERPs. I did myself with
Routtenberg. But then how do you
explain the following?
Now the cats are making the
criterion segment go UP. they are
increasing positivity
The naysayers can’t have it both
ways….
 If the unconditional/non-
associative effect of milk is
making wave go up then the down
effects are learning
 If the unconditional/nonassociative effect of milk is
making wave go down then the up
effects are learning
So we do have the learning of
something going on here…
 But what, exactly? In other words, the
naysayers were not done complaining. Before
we get there, however, what did Fox say was
the importance of the demonstration?
 1. OCNE solves problem of choosing
electrode sites and neural parameters for
study. Well that’s sort of true. You pre-specify
what brain wave variable you train, and from
where you record it. In this first
demonstration, convenience and common
sense guided the choice….(continued)
In other words,
 As noted, site was chosen for surgical
convenience and familiarity to Fox, who
knew that at the segment chosen (170190 ms post stimulus), the EP amplitude
was typically variable, high to low
values. He intuited that the variability
was tied to some behavioral state which
he hoped could be operantly conditioned.
(The tricky, slippery part is identifying
that state. We never have. We still don’t
know the significance of the effect.)
Fox also concluded
 The neural correlate approach was not
controlled science. The OCNE
approach makes the neural event the
independent variable, not the
dependent variable.
 This was bogus. It is the reinforcement
contingency which is directly
manipulated as the independent
variable. As just noted, we still don’t
know its behavioral correlate.
He also stated:
 OCNE solves the time base
incompatibility problem that learning
takes days, as opposed to EEG, ERPs,
action potentials that are measured in
milliseconds.
 Not exactly. The OCNE method simply
treats an EP segment like a behavior
but since it is already neural, it is
forced onto a compatible time base. It’s
not a behavior like a CR paw lift is.
There are some incontrovertible
benefits of OCNE that Fox didn’t
mention (& maybe didn’t appreciate!):
 1. Replication was not a problem:
Hundreds of cats, rats, humans have
been trained to self-control all sorts of
ERPs as we’ll see.
 2. Obvious clinical applications? (If you
change a visual EP, do you change
vision? We’ll come back to this.
 3. OCNE uniquely can work out neural
code/mechanisms of voluntary
movement in an unrestrained animal (vs.
Mountcastle’s curarized,sedated cats).
This too is shown later…(continued)…
A final, most important benefit:
 4. Operant neural conditioning offers a
method of testing the generality of
putative laws of learning, (of which there
are precious few known). This because it
may be a new response system. (Laws
Theories that account for phenomena
like learning.)
 A fellow named John Garcia showed
how critical novel response systems are
in his now classical taste aversion
conditioning studies in dogs.
From the 40s to the 60s, the king of
learning theory was not Skinner (who
opposed theories), but Kenneth Spence
 …the head of Psychology at Iowa
(one reason I went there).
 Spence had found what he regarded
as a law of classical conditioning (a
learning protocol), stating that the
ideal CS-UCS interval was about ½
second. This was developed with
human blink conditioning, rat eye-lid
conditioning, and rabbit nictitating
membrane conditioning in rabbits.
Here was the typical supportive
datum:
Then Garcia showed that if you
exposed a dog to a food….
…followed immediately by xirradiation, 3-5 hours later he got
terribly sick and vomited the day
away (radiation sickness).
Thereafter, the dog would never
touch that particular food again.
Other dogs could be similarly
trained to avoid different foods.
Which are CS, UCS, UCR, CR ?
Well here is a classically
conditioned avoidance response…
 Involving a 3-5 hour CS-UCS
interval. Not = .5 sec.
 Garcia showed that the response
system determined the optimal
CS-UCS interval, and that
Spence’s putative learning law
was not general. Physiological
explanations based on .5sec
would be wrong.
OCNE could also be a novel
response system …
 …with which to test putative
operant conditioning laws
(magnitude of reinforcement
effect, acquisition/extinction law,
etc.)
 BUT…first you have to show that
operantly conditioned learning
laws were not trivially mediated
by known motor systems.
Best example of Trivial Mediation…
 …is what the naysayers said:
 “All the cats are learning is to move
their heads oriented towards the
light flash to make big wave, and
away to make small wave. That is,
they are learning certain movements
and resulting receptor orientations.
Learning movements is not novel,
not independent of skeletal motor
systems involved in, say, bar
pressing.”
Another example, time-locked
movements feedback into visual EP
 That is, a cat can flex his elbow
joint at just the right time so that
the somatic sensory feedback can
get to cortex and influence the
criterion segment (Rosenfeld &
Fox, 1972). (Yes all sensory
systems can get all over cortex,
directly, and/or via reticular
formation, strange as it seems…)
Also, non-time-locked movements
 Which means running around a lot
or holding still. Bures & Buresova
had shown in Czechoslavia in
early 70’s that such behavior in
rats affected all components of
flash-evoked potential. If that’s
what F & R’s cats were doing, no
big deal, not a novel learned
behavior.
There were attempts to partially
control trivial mediation…
 …but less than satisfactory. F&R painted
chambers white and regular ITI as well as
latish component latency (170 ms) allowed for
timelocked movements to occur.
 In 1969 (Science) I ran humans with
earphones to control for receptor orientation
(and also to ask how) but nothing else was
controlled and the asking of how was not
helpful. Until Hetzler’s PhD study, there was
no simultaneous control of all possible trivial
mediation. So let’s go there … ppt #4 on web
site for 312-2.
OK—we have inadvertently
opened topic of Biofeedback…
…in the process of concluding
“Neural Coding.”
So what is Biofeedback? It means
feeding back to a biological
organism (e.g., a patient)
information about a sick system to
which he ordinarily has no
conscious access: high blood
pressure, for example.
How is this done?
 …Usually by recording the
physiological activity with a
transducer with an electrical
output to a display.
 How did Biofeedback start? Was it
originally a clinical development?
 No. It had a dual origin:
First origin was…
…the psychophysiologists who
believed that mental problems had
external physiological correlates,
so that if one could control the
‘outside’—e.g., heart rate--- one
could then control the inside
mental problem—anxiety(!) This
bass ackwards anti-Freudian
approach had minimal influence.
The much more important
influence was that of Neal Miller..
… a major psychologist from the HullSpence learning theoretical
background at Yale. Miller was
wrestling with a question in learning
theory: Is there more than one
fundamental learning process? One
for each form of learning: operant
vs. Pavlovian conditioning? Or is
there only one fundamental
mechanism—association?
At the time in 50s,60s, most people
were 2 process theorists.
Evidence?
Operant conditioning seems to
work best with voluntary
responses mediated by skeletal
muscles (bar presses, mazes, key
pecks) whereas Autonomic (ANS)
responses (salivation, heart rate
changes) seem to work best with
Pavlov’s CS-UCS pairing (classical,
Pavlovian conditioning).
Besides, they reasoned…
 It was obviously impossible to
voluntarily control heart rate (for
example): Try it. Lower it. See, you
can’t do it.
 Miller didn’t buy this, reasoning
that “absence of evidence is not
evidence of absence.” Maybe you
didn’t look hard enough in the
haystack for the needle.
The one common denominator in
both forms of learning was
association.
 CS-UCS association in Pavlovian
Conditioning…
Response-Reinforcer association
in Operant (Skinnerian)
conditioning.
* Maybe, voluntary control of ANS
responses (= Biofeedback) is
harder and takes longer.
There were good reasons to
suspect so: voluntary muscle route
is more direct:
So Miller & DiCara proceeded to
train Curarized rats to alter HR
…for Lat. Hyoth. Stim reward.
• Why curare? What to do with
trivial mediation? Why not reward
with rat chow?
• Why bidirectional training?
• What were results?
First Results: Heart Rate
Next: Operant control of Salivation,
formerly Pavlov’s property (Note it
takes time):
Next: Intestinal motility: Rats not
supposed to have much because
they can’t vomit like dogs ca!
Next: Urine formation rate!
The Newsweek photo of one ear
red, the other white:
One more critical example: Blood
Pressure control…
All these Results…
 Made clear that Autonomic
responses could be operantly
conditioned = voluntarily
controlled. So much for 2 process
theories of learning. Miller made
major evidence evaporate.
 Perhaps more important,
incredible clinical potential.
So much so that Miller’s new lab at
Rockefeller U/Cornell Med became a
Mecca
 And then, during the Vietnam war,
other folks became interested. At a
CIA (we think) sponsored meeting in
DC, after Surwit described his
method of training folks to control
skin temperature, a shady character
in dark glasses (in darkened room)
and trench coat asked, “So with this
method, a guy could stay in freezing
water a bit longer if the pick-up
submarine was late?”
But then it came toppling down
Actual graph from Miller--
 Visceral learning: Recent
difficulties with curarized rats and
significant problems for human
research.
 NE Miller… - 1974 – In
Cardiovascular Psychophysiology,
ed. By Obrist et al., Aldine Press
Miller started bad-mouthing Leo Di
Cara, who could get no grants, grads….
 Neither could the rest of us doing
research in biofeedback …
 Di Cara committed suicide.
…and then Miller ran into a
urologist named Lapides at a
Rockefeller cocktail party, and
told the story of failure to
replicate.
Lapides in turn told Miller of the
1957(!) demo in J. Urology …
 …in which a batch of med student
“volunteers” offered to be
curarized and were then asked to
urinate, using only the visceral
muscles of the bladder, as the
skeletal abdominal muscles were
blocked. They were easily able to
do this, to turn both off and on a
urine stream while curarized.
In other words,
 Lapides et al. (1957) had shown
that it was indeed possible to
voluntarily command (operantly
condition) autonomically
controlled visceral muscle, thus
having accomplished Miller’s main
research goal before Miller ever
got started with the first rat
studies in the 1960s!
This accomplishment had two
effects:
 (1) It validated Miller’s one
process learning theory (from left
field).
 (2) It made Biofeedback an ok
clinical and research endeavor
again.
Examples of Clinical success stories with
“lower body” biofeedback(BF):
 1. Fecal Incontinence: NIH issued
a consensus opinion (1993) that
BF is the treatment of choice.
 2. Asthma and breathing
disorders.
 3. Headache: tension and
migraine.
 4. Reynaud’s Syndrome.
More…
 (5) Stroke rehab with motor unit
control.
 (6) As for cardiovascular BF, is it “a
promise unfulfilled with only
statistical not clinical effects”? BP
was until Steptoe’s interbeat interval
BF; and HR can only be clinically
significantly speeded, but there is an
application in PVC control.
Clinical BF “above the neck” called
Neurofeedback, or brainwave BF
 Most is bogus, but there are 3-4
promising applications:
(1) Sterman and epilepsy with SMR
EEG control.
This started accidentally as he
was a sleep researcher studying
vets---ultimately cats, and training
increased changes in SMR (1213Hz) EEG spindle bursts.
Ultimately, to prove he wasn’t
capitalizing on his charm..
 He ran cats induced to have grand mal
seizures with the toxic drug,
monomethylhydrazine.
 After training, cats injected with a dose
sufficient to cause instant grand mal
seizures (sometimes, death) in most cats
in control group, had no grand mal
seizures and latencies were delayed by
hours for petit mal effects. 3 had no
symptoms at all! It was time to move to
humans.
A human patient after months of
training:
Changes in power spectra with SMR
training also led to reduced seizure
occurrence.
(2) Lubar’s Theta Beta ratio for
ADD.
 He trained AD(H)D boys to
increase the Beta(10-30Hz)-to
Theta (5-8Hz) ratio. This was
based on the finding that ADD
was associated with too much
theta and not enough Beta—
compared to age cohort
normals.
Lubar et al., 1995:
By 2002, Monastra et al. showed
neurofeedback to be better than
Ritalin—and longer lasting.
(3) (?) R-L alpha asymmetry
training for depression
Results (Rosenfeld 2000)
(4.)A heroic application:
Birbaumer:
 “Locked in” patients with high
spinal cord lesions lack all ability
to communicate. Birbaumer has
trained them to generate DC
potentials in patterns
corresponding to letters so they
can communicate.
http://www.innovationmagazine.com/innov
ation/volumes/v4n3/features2.shtml
Brain-Computer Interface
Wolpaw, Birbaumer et al. Clin.Neurophysiol.(2002)
The patient shown….
…eventually wrote a
thank-you note to
Birbaumer with BCI
device.
Dear Mr Birbaumer,
Hopefully you will come to visit me
once you have received this letter.
I cordially thank you and your
team, particularly Ms Kuebler, for
making me a good pupil who often
knows the correct letters
(meaning teaching me to write).
Ms Kuebler has an artistic skill in
motivating people. Without her
this letter would never had been
written. This has to be celebrated.
I would therefore like to invite you
and your team very cordially at the
earliest opportunity.
With best regards,
Hans Peter Salzmann
Biofeedback has one big pro and
one big con:
 The pro is that it has no bad side
effects ever reported.
 The con is that most of the
studies have not been verified
with large “double blind” placebo
controls.
OK, where are we?
Remember the next slide?
The reactions:
 1) The Operant Controlled Neural Event
(“OCNE”) approach: Operant
Conditioning of ERP components.
 2) The Cognitive Psychophysiology
literature: The less radical and longer
lasting carefully controlled scientific
study of ERP indicators of psychological
events.
 (We’ll start with the first reaction now)
This last slide followed the lecture
some weeks ago….
 …in which we discussed that after the
neural correlators failed, there were 2
reactions. One was OCNE which led to
biofeedback, which we are now done
with.
 The other reaction: The Cognitive
Psychophysiology literature: The less
radical and longer lasting carefully
controlled scientific study of ERP
indicators of psychological events. This
involves some repetition from 312-1.
So go to 312-1 web site
 The second powerpoint
presentation, starting at slide
14….and finishing with slide 29.
 Then go to powerpoint presentation
2
# 1 on 312site for example of
applied psychophysiology in
Detection of Deception: the oldest
and still very lively sub-field. BUT
FIRST------
Based for openers
on Polygraph.
Polygraph:
 Does not mean “lie detector.”
 Means a machine with many
(poly) channels of visually
presented (graphical) information;
in inked paper or laptop display
format.
 A Polygraph machine can be and
is used in many fields of
Psychophysiology
2 Major Protocols currently used :
 Comparison (“Control”) Question Test
(CQT)-- beloved by enforcers, ‘cuz it’s
easy to use (“Didja do it?”) and tends to
elicit confessions—but hated by
academics who prefer the
 Guilty Knowledge Test (GKT better
known as the Concealed Information
Test (CIT), since knowledge can’t be
guilty (just perps.)
 Both utilize autonomic arousal.
Why do us professors frown on
CQT?
 Pre-test interview cannot be
standardized.
 It compares arousal responses to
relevants. & “controls.”There can
never be true comparison control
questions in the scientific sense of
control.(Yet there could be better
versions.)
 High false positive rate (which CIA
et al. don’t care about….)
Why do we love CIT?
 It compares arousal (?) responses to critical
(probe) and non-critical (irrelevant) stimuli.
 There are usually 6 or more multiple choice
questions with 1 + 5 choices per question. (Throw
away 1st.) Thus for each item, the P(chance hit) =
1/5=.2
 For 6 INDEPENDENT items, probability of subject
hitting on all 6 by chance =P = .2^6 = .2 x .2 x .2 x
.2 x .2 x .2. Use Bernoulli for chance hits on < 6.
Thus you can reduce the false positive P as low as
you like by adding independent items (not always
so easy).
Problems with these tests:
 They are not very accurate:
estimated hit rates vary from .5 to
.85, CIT is better.
 CQT has very high false positive
rate.
 CIT has high false negative rate.
 Both vulnerable to CMs. So we
went to P300-based tests in late
‘80s. (Rosenfeld et al., 1987,1988.)
OK, now:
 go to powerpoint presentation # 1 on
312-
2 site for example of applied
psychophysiology in Detection of
Deception:
New Topic:
 The method of ablation or experimental
lesions.
 One usually makes them with electrolysis
(DC applied to brain).
 But residues are left at cathode. These
can become stimulative or epileptogenic.
So AC (RF) lesions also done. KCL can
make a reversible lesion.
 Best lesions are cell or axon specific.
(Kainic Acid for neurons.)
The first topic to which lesions were
applied was the most complex:
Learning & Memory.
 This was a mistake. But for the first
lesion maker, Lashley, the father of
modern neuroscience, it was ok,
because he was the first.
 He used all kinds of paradigms
especially brightness
discriminations and mazes to see
how cortical (eventually, sub
cortical) asperation lesions affected
learning, memory, post-op retention,
re-learning.
He found 2 major principles-Mass Action: the more
damage, the greater the
deficit.
Equipotentiality: One piece
of cortex can replace the
function of another. His
major study used mazes at
3 difficulty levels:
Mass action is shown in the following
slides: The first shows difficulty effect:
Here is pure mass action:
Here is model integrating
complexity and mass action
interaction:
..and here is equipotentiality:
That should have been the end of the
lesion/stimulation method applied to
higher cognitive phenomena..
 It was not, and many years were
spent repeating Lashley in other
sensory cortices. So then people
looked at emotion and more than
2000 papers on limbic system lesionstimulation effects were done up to
the 1980s, and probably still going
on at some places. Self stimulation
story (rats press for brain stim)
wasted a lot of time.
Now, besides brain
wave types, people
are trying to localize
higher cognitive
function with fMRI,
and are (some of
them) making similar
mistakes. (See the
November 2010 issue
of Psychological
Science.)
Lesions have been useful as long as one
examines location for simple functions
and necessity of those loci…
 An example is in the study of the
recently discovered endogenous
opiate system.
 Liebeskind & Mayer 1972-3
discovered that VCG stimulation
inhibits pain.
Then, following M&L’s work, I
stumbled in..
 Mayer’s thesis: 1) effects of applied
opiates (stimulation)
 (2) cross tolerance(stim & opiates)
studies and extensive study of sites
in brain supporting self stimulation
and/or analgesia…
 Go to powerpoint # 5 on 312-2 web page.
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Psychology 312-1 - Northwestern University