What's New in Neurofeedback
A Monthly Summary of News and Events

Vol. 10 No. 10 - October 2007

This newsletter is sponsored by EEG Spectrum Intl Inc,
a leader in providing clinical service and training
professionals. Past issues available at
http://start.eegspectrum.com/Newsletter/
To subscribe or cancel, see newsletter's end.
Opinions related in this newsletter reflect
author's only. Copyright (C) 2007 by EEG Spectrum
Intl, Inc. or David Kaiser. All rights reserved.
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Announcements - News
In the Spotlight - Applied social psychophysiology
News & Reviews - Books & journal papers
Events & Locations - Conferences, courses
Last Word - Placebo-resistant disorders
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Announcements

-Bad Memories Stick Better Than Good
-Breakthrough drug for schizophrenia
-Roots of Fearful Memories

All links at: news.yahoo.com/fc/Science/Brain_Research
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In the Spotlight
Applied Social Psychophysiology

Humans are mind readers. We are able to adjust our
communication to match our audience's knowledge and
adjust our behaviors to the intentions of a friend,
stranger, or rival. How we are able to perceive the
behavior of other minds has been under scientific
investigation for decades, but only recently have we
strapped electrodes onto head or body to study its
physical basis.

Social psychophysiology melds social sciences with
psychophysiology, relating brain activity to social
cognition and social behavior. Interactive
biofeedback -- applied social psychophysiology --
promises new means to improve social competence and
function.

There are social and non-social behaviors, and of the
social, we have competitive and cooperative forms.
Competitive behaviors attempt to exclude others from
obtaining resources while cooperative behaviors
include others in the acquisition and distribution of
resources. Our ability to mind-read evolved from
competitive impulses, interestingly. In fact,
chimpanzees fail on theory of mind tests when
cooperation is the goal, but act like mind-reading
humans in competitive situations (Povinelli et al
1990).

Joint attention, or co-perception, is a foundation of
social cognition. Joint attention produces not only a
shared perception but a shared reality: we become
aware of the other person's current state of mind, if
only for a moment. A child advances along his or her
two- decade-long journey of enculturation --
acquiring beliefs, practices and values of a culture
-- through joint attention and other social cognitive
developments (cf. Vygotsky, 1962).

A long time ago in a galaxy not so far away I
collected EEG from a two dozen people while they
watched a slew of bad, good, and mediocre film
previews. The goal was to identify EEG correlates of
perceptual and emotional integration of cinematic
content. In addition to entire previews, I linked
moment-to-moment changes in EEG to fluctuation of
audience engagement. I thought such a technology
would let movie execs know which scene in a video
killed and which was dead weight and should be
killed, where did audience interest wax in their
product and at what point exactly did it flounder.

Such a technology was the end stage of
deconstructionism, a movement in literary criticism
in which an author's point of view is completely
eliminated from her work of art; voided, creation
divorced from creator intent. Had this technology
matured, directors would provide raw material
(scenes) but no integration, not even when to stop or
start a scene. All narrative motion would be
determined by audience brain response. Rank,
rearrange, reorganize to maximize studio product.
What an enemies list I would have created had a
single Hollywood exec understood a word I said.

You can understand it. We measured group cohesion
with electrodes, and by indexing group cohesion
during film watching, we actually measured how well a
stimulus engages an audience.

So considering EEG, we all know that EEG
desynchronizes when we attend to stimuli (e.g., alpha
activity diminishes) and it generally synchronizes
when we don't. Films aren't simple stimuli, however;
they span and build across time. They are narrative
content, so interest in a film cannot be computed by
counting up engagements and subtracting
disengagements. Story interest is a function of
surprise, meaning and surprise. High-surprise story
endings are more interesting than low-surprise story
endings as long as post- surprise incongruity is
resolved (Iran-Nejad & Cecil, 1992). The more
surprises, the better, as long as they are all
relevant. When the unfamiliar is suddenly,
surprisingly familiar, that is meaning. And surprise
is more emotion than cognition, release of all
instead of containment (cognition).

When we process narratives, we seek release.
Engagement is a reasonable mix of containment and
release, as Shakespeare and wordsmiths realized long
ago. Narratives consists of arousal-release cycles,
nothing more, emotional and cognitive tension
building to unbearability .... to be released. The
more thorough, expansive, and all-encompassing the
tension, the greater the release when it is all
resolved. A story bangs our head against the wall
because it feels so good to us when it stops.

We couldn't estimate accurately when tension was
building or releasing in our film previews, but we
could determine when a group acted as one, compared
to when it acted as many. We measured how similar
members of a group responded to each film preview.

The assumption was that when an individual was
interested by a stimulus (scene in a film), his or
her attentional state was likely to be guided by
narrative events and changes. When individuals are
engaged by a film, their brains swim together,
tensing up and releasing together. When a film bores
an audience, they swim apart, going off on
independently tangents.

Simultaneous patterns of engagement and disengagement
for a group is what I call attentional synchrony, and
we believe attentional synchrony should manifest in
EEG as converging alpha activity in response to
stimulation.

Between-subject variance of alpha magnitude at
relevant cortical sites was measured. We chose site
Pz for two reasons: 1) parietal engagement indicated
interest better than other brain areas in a general
analysis, and 2) we chose midline Pz in order to
minimize differences caused by cognitive style
(interhemispheric differences).

Large variance of the group's alpha activity was
expected to occur when some of the audience were more
engaged that other members of the audience. Some
could be entirely disengaged when others were rapt.
On the other hand, large variance of the group's
alpha activity could only occur when alpha magnitudes
were similar across individuals -- that is, when
people were all doing the same thing, be it engaged
or not.

Online are examples of smoothed (10 s) alpha activity
of five individuals during eyes open rest, a low
interest preview, and one rated high in interest.
Individuals respond similarly as the high interest
film progresses.
(start.eegspectrum.com/Newsletter/oct2007.htm

Another way to depict brains swimming together or
swimming apart is by summarizing group dynamics. To
the right, a high-low graph presents mean alpha
magnitude at each epoch plus or minus 1 standard
deviation for 20 individuals. Each vertical line
signifies the group's range out to one standard
deviation. The wider the range, the more various were
psychophysiological responses at any given moment in
time. As you can see, low engagement -- eyes open
rest baseline -- produced high group variance and
high interest restricted vertical line length, with
low interest films resulting in moderate group
variance.

Finally, we correlated our index of attentional
synchrony (between-subject standard deviation, the
height of each vertical line, divided by two) to
subjective interest ratings of a film preview. Each
film preview was rated on interest level by our
subjects as well as by an independent group. Three
replications of eyes open rest are numbered and
plotted to the left as states of very low interest,
what should indicate nearly random associations
between individuals. As you can see, we found a
robust relationship between group psychophysiology
and group subjective ratings. Interesting stimuli
apparently cohese a group.

An argument might be made that low group alpha
variance is due to a floor effect in alpha magnitude:
lower values tend to show low variability. And alpha
magnitude and subjective interest ratings were
correlated (r =-.42), but not as strongly as ratings
with group alpha variance (r =-.80). In fact trends
of group alpha variance occasionally acted opposite
of trends of alpha magnitude within some film
previews.

The one drawback to this index of attentional
synchrony, which is perhaps true for any measure from
social psychophysiology, is that it cannot be
determined for an individual but requires a group.

Functional neuroimaging will eventually intervene in
the creative process, especially given enormous
budgets and high risk involved in feature film
production. But I would suggest they start not with
scene selection or editing but with score. Whenever
attentional synchrony of an audience's right
hemisphere drops during a movie, add some music to
your production.

--References

Hare B, Brown M, Williamson C, & Tomasello M.
(2002).The domestication of social cognition in dogs.
Science, 298, 1634-6.

Iran-Nejad, A., & Cecil, C. (1992). Interest and
learning: A biofunctional perspective. In K.A.
Renninger, S. Hidi, A. Krapp (Eds), The role of
interest in learning and development pp. 297-332.
Hillsdale, NJ: Lawrence Erlbaum Associates, Inc.

Kaiser, D.A. (1994, unpubl dissertation.) Interest in
films as measured by ratings and topographic EEG.
UCLA, co-chairs, MB Sterman & E Zaidel.

Pack, A & Herman, LM (2006). Dolphin social cognition
and joint attention: Our current understanding.
Aquatic Mammals, 32, 443- 460.

Povinelli DJ, Nelson KE & Boysen ST (1990).
Inferences about guessing and knowing by chimpanzees
(Pan troglodytes). Journal of Comparative Psychology,
104, 203-210.

Vygotsky LS (1962) Thought and language. Cambridge,
MA: MIT Press.

-DK
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News & Reviews

NEW BOOKS

Frontal Subcortical Circuits Psychiatric Neurological Disorders
by David G. Lichter
Extensive review of frontal circuitry
--www.amazon.com/exec/obidos/ASIN/1572306238/eegspectrum

Utterly Unique Celebrating Strengths High Functioning
by Vivian Strand
Discusses strengths of Asperger Syndrome children.
--www.amazon.com/exec/obidos/ASIN/1931282897/eegspectrum

Awareness Deficit after Brain Injury
by George P. Prigatano
Describes treatment and condition of loss of awareness after TBI
--www.amazon.com/exec/obidos/ASIN/0195059417/eegspectrum

Dancing with Fear: Overcoming Anxiety in a World of Stress & Uncertainty
by Paul Foxman
Biological as well as holistic perspective on anxiety.
--www.amazon.com/exec/obidos/ASIN/0765701502/eegspectrum

Codependent No More Controlling Yourself
by Melody Beattie
Assistance in recovery from codependency.
--www.amazon.com/exec/obidos/ASIN/0894864025/eegspectrum

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JOURNAL PAPERS

Long-acting methylphenidate has effect on aggressive behavior in ADHD
: Oppositional-defiant and mild aggressive behavior are improved by this drug.
www.ncbi.nlm.nihgov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17822338

Psychosocial and emotional outcomes 10 years following TBI
: Anxiety, depression, fatigue, and alcohol use must be addressed for TBI
recovery.
www.ncbi.nlm.nihgov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17878769

Orbitofrontal Cortex Function and Structure in Depression.
: Antidepressant treatment may reduce activity in orbitofrontal cortex.
www.ncbi.nlm.nihgov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17872395

Clinical neurophysiology of aging brain
: Neurophysiological techniques (EEG, ERP, MEG, TMS) can assess loss of brain
function with aging.
www.ncbi.nlm.nihgov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17870229

Impact of substance use disorder on ADHD and its treatment.
One in 5 adults with ADHD suffer from a substance use disorder.
www.ncbi.nlm.nihgov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17876905
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Events & Locations

Upcoming Courses

A Pathway to Brain Regulation - Neurofeedback helps improve
neuroregulation. It's used by health care professionals for ADHD,
depression, anxiety disorders, LD, mood disorders, and behavioral
problems. This 4-day course, Neurofeedback in a Clinical Practice,
provides the basis for using Neurofeedback clinically. - *28 CEs

4-Day Comprehensive Course Dates (subject to change)

* San Antonio TX Nov 29-Dec 2
* Glendale CA Dec 13-16
* Portland OR Jan 17-20

Our course is a hands-on experience right from the start. Attendees
consistently say this format is a very good way to learn
Neurofeedback.

"Neurofeedback should be viewed as one of the three essential or
primary forms of intervention - psychotherapy, psychopharmacology,
and Neurofeedback. In my experience, neurofeedback is every bit as
important and powerful as the other two forms of treatment." - Dr.
Laurence Hirshberg of Brown University Medical School, a
psychologist specializing in Developmental Disorders and Autism.

Contact Karie Kramer, our training coordinator, for more information
818-789-3456 ext 847 or see www.eegspectrum.com/ Training

*EEG Spectrum International, Inc. is approved by the APA to offer
continuing education to psychologists. ESII maintains responsibility
for the program.


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Conferences for Clinicians & Researchers

CONFERENCE LOCATION DATES

AAPB - www.aapb.org Daytona Beach, FL May 13-18, 2008
SABA - www.skiltopo.com/saba Tampa Bay area, FL Apr 28-May 1, 2008

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Last Word

Placebo-resistant disorders

It dawn on me, while revising an article of epilepsy
and neurofeedback, how we have been mislabelling
epilepsy and other disorders studied in this field.
People enroll in neurofeedback programs as a latter
option, especially for seizure disorder, having
already undergone months or years of the best Western
medicine has to offer. Medication was ineffective in
controlling seizures so not only do these individuals
provide a historical control against which clinical
improvement ought to be evaluated, we mustn't
overlook a failed placebo effect in all of these
cases. All epilepsy patients undergo lengthy
unsuccessful medication therapies, some even
neurosurgies, spending hundreds of hours in
well-diploma'd medical clinics with men and women in
labcoats scurrying nearby.

The placebo effect had its chance. It ran its course.
As the placebo effect had minimal impact in previous
treatments, its presence in neurofeedback training is
highly unlikely, negligible if you want to quantify it,
and more important to scientific investigation,
it is more conservative to assume a placebo effect
was present in the current post-treatment outcome,
which is the state usually just prior to neurofeedback.
Either that, or Western medicine was
so ineffective it couldn't even elicit a placebo
effect. Or Western medicine harmed the patient but
the placebo effect balanced off the harm. I believe
pills and scalpels are the most powerful placebo
devices yet devised. So when you describe epilepsy
patients who undergo neurofeedback, we need to
clearly labelled them as suffering from both
medication-resistant and placebo-resistant seizure.

That said, here is a slight revision of a piece I
wrote years ago on the Placebo Effect. Be warned --
it goes in a new direction.

When Freud gave a name to Darkness, calling it Our
Unconscious, he set loose a process of distrust in
ourselves and others that is difficult to transcend.
From his infernal creation descends a ray of hope,
the placebo effect, the notion that mind heals itself
if only we can get out of the way. Healing through
interaction with a clinician, regardless of the tools
the clinician brings. A clinician can shake a rattle
or inject an inactive serum, yet we will heal. It's a
powerful idea -- because it works.

Or does it?

Henry K. Beecher's influential 1955 paper "The
Powerful Placebo," published in JAMA, the Journal of
the American Medical Association, was the first to
quantify the magnitude of a placebo effect. From this
paper derives the ubiquitous citation of 35% or one-
third improvement associated with placebo. According
to Beecher, 35% of 1082 patients were "satisfactorily
relieved" by placebo alone, a value never meant to be
carved in stone. It was a mathematical mean from 15
clinical trials that involved numerous diseases, with
a range of improvement from 21 to 58 %.

Forty years later, Kienle and Kiene (1997) reexamined
Beecher's paper and concluded that "no evidence was
found of any placebo effect in any of the studies
cited by (Beecher)."

One hundred percent off the mark - tying a record
with the best of 'em. Instead of a placebo effect,
Kienle and Kiene (1997) concluded that improvements
from these 15 studies could be accounted for by:
spontaneous improvement or recovery (that one is
questionable for eliminating placebo), symptom
fluctuation, regression to mean, concomitant
treatments, scaling bias, obliging reports by
patients, irrelevant response variables, experimental
subordination, conditioned answers, psychosomatic
phenomena, and other factors including an "active
placebo" also known as an (active) treatment. Not one
factor listed by these authors incorporated a concept
of psychological anticipation for well-being, what I
consider the agency of a placebo.

The same authors later wondered whether the placebo
effect was largely illusory. Gotzsche (1995) argued
that the placebo concept should be discarded
altogether. But others disagree and continue to argue
that psychological mechanisms underlay nonspecific
effects (Kirsch, 1997), perhaps because of their lack
of study of the mind. Some researchers sling the
P-term around like mud at anything they do not own
patent rights to. Perhaps with hindsight, Kienle and
Kiene (1997) warned that "the placebo topic seems to
invite sloppy methodological thinking." And sloppy
thinking is the immediate label thrusted upon any
treatment modality which successfully outcompetes the
current standard.

A placebo effect in mental health should have
neurobiological mechanisms underlying it. What are
they? What are the neuroanatomical and
neurophysiological systems involved? We should
observe duration and dose curves with placebo if it
exists.

I can think of three reasons why placebo controls are
desirable in research:

To evaluate absolute efficacy: Placebo controls
determine whether a new treatment is better than
placebo (e.g., nothing).

To avoid difficult decisions about treatment
effectiveness: Differences in cost, unintended side
effects, drug interactions, and other factors may
make comparisons between treatments of similar
efficacy inexact and subjective.

To bolster statistical significance: As any grad
student knows, it is much easier to detect
statistical significance between a placebo and an
active treatment than between two active treatments.

Ignoring the ethics of requiring placebo controls, or
even the phenomenological argument of whether placebo
effects exist at all, I realize that one can define
an active treatment by a set of criteria that
placebos will not meet. This will provide the needed
unfalsifiability of a scientific hypothesis, which is
missing in most arguments about the impact of
placebo.

Specificity: its use impacts a single functional
domain. (This is a weak requirement, allowing domain
to be redefined and ignoring cascading effects.)

Toxicity: its use worsen symptoms in some patients.

Long Duration: Changes associated with its use endure
for weeks, months, or years.

Dose-dependence: Changes reflect an accumulation of
doses. (We should be able to plot at least 2 or 3
points on a dose-response curve between asymptotes.)

Time-dependence: Changes occur in response to a
time-line which can be manipulated in research. ABA.

-DK
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