A Monthly Summary of News and Events
Vol. 10 No. 10 - October 2007
This newsletter is sponsored by EEG Spectrum International Intl, Inc.,
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Past issues are available at start.eegspectrum.com/Newsletter/
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The opinions related in this newsletter reflect those of the author only.
Copyright (C) 2007 by David Kaiser or ESII. All rights reserved.
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All links at: news.yahoo.com/fc/Science/Brain_Research
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 unique 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.
Below, to the left, are examples of smoothed alpha activity of five individuals during eyes open rest, a low interest preview, and one rated high in interest [10 s smooth]. Individuals respond similarly as the high interest film progresses.
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 variety of psychophysiological responses going on at any given moment. As you can see, low engagement -- eyes open rest baseline -- produced the highest group variance and high interest the least, the most restricted vertical line length. Low interest films showed group variance in between.
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.
This work was completed in Sterman's lab, 1994.
-DK
News & Reviews
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Long-acting methylphenidate has an effect on aggressive behavior in ADHD
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Oppositional-defiant and mild aggressive behavior are improved by this drug.
Psychosocial and emotional outcomes 10 years following traumatic brain injury.
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Anxiety, depression, fatigue, and alcohol use must be addressed for TBI recovery.
Orbitofrontal Cortex Function and Structure in Depression.
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Antidepressant treatment may reduce activity in orbitofrontal cortex.
Clinical neurophysiology of aging brain: From normal aging to neurodegeneration.
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Neurophysiological techniques (EEG, ERP, MEG, TMS) can assess loss of brain function with aging.
Impact of substance use disorder on ADHD and its treatment.
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One in 5 adults with ADHD suffer from a substance use disorder.
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Conferences for Neurofeedback Clinicians & Researchers | ||
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| CONFERENCE | LOCATION | DATES |
| AAPB - www.aapb.org | Daytona Beach, FL | May 13-18, 2008 |
| SABA - www.skiltopo.com/saba | Tampa Bay area, FL | April 28-May 1, 2008 |
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 label them as suffering from medication-resistant and placebo-resistant seizure.
That said, here is a brief article on the Placebo Effect, written awhile back, which goes in a slightly new direction.
When Freud gave a name to Darkness, calling it 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 one mind can heal another, if only we can get out of their way. Healing may come about through interaction with a clinician, regardless of his or her tools and techniques. A clinician can shake a rattle or inject inactive serum and we will heal.
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% -- 1 in 3 -- 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 the mean of a sample, 15 clinical trials over numerous diseases with improvement ranging 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 due to interaction with a healer, what I consider a placebo's source of agency.
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.
I can think of three reasons why placebo controls are desirable in research:
To compare effect of tool presence: An interaction with a healer who uses his or her typical tools can be compared to interactions where s/he does not use his tools.
Comparisons between different tools or techniques are difficult: Differences in cost, side effects, therapy interactions, make comparisons between known treatments inexact and subjective.
To bolster our stats: As any math student knows, if we can set one variable to zero, we can usually solve for the other. (Set placebo to 0 and x becomes a constant.)
Ignoring the ethics of requiring placebo controls, or even a phenomenological argument of whether placebo effects exist as advertised, I realize that one can define an active treatment by a set of criteria that placebos will not meet, which provides a needed falsifiability for a scientific hypothesis, currently lacking in evaluating the placebo effect.
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 using ABA and like designs.
-DK