- A chapter from the Textbook of Neurofeedback, EEG
Biofeedback and Brain Self Regulation
-
edited by Rob Kall, Joe Kamiya and Gary Schwartz
- The E-book is Available on CD
Rom
|
Biofeedback
of Brain Wave Activity: models, mechanisms, effects
by Peter Rosenfeld
- J.P. Rosenfeld,Ph.D.
- Department of Psychology
- Northwestern University
- Evanston, IL, USA 60208
- phone:847-491-3629
- fax: 847-491-7859
- email: jp-rosenfeld@nwu.edu
Acknowledgment. I am grateful to a succession of talented Collaborators over the
years, especially Karl Diedrichs, Bruce Hetzler, Paul Birkel, and Bob Dowman. I am also
grateful to Steve Fox and Al Rudell for Early inspiration.
_________________________________________________________________
Abstract: The present chapter discusses theoretical and methodological
implications of the process of voluntary control of brain activity. Clinical applications
are discussed which deal with modification of 1) pain perception, and 2) affective
disorders, using brain-wave biofeedback. |
1. Uniqueness of Brain Wave Biofeedback In some
ways, brain wave feedback (BWB) is like other
biofeedback, but in many other ways, BWB is unique. In general, biofeedback
methodology presents to a subject's conscious perceptual sensorium a representation of
the activity of a given organ-system, of with the subject is ordinarily unaware. For
example, one usually has no innate awareness of his moment-to-moment blood pressure, but
it can be recorded and displayed for conscious perception. If it is pathologically high,
the subject needs to be able to know its value on a moment-to-moment basis in order to
become aware of which of his cognitions and/or behaviors cause it to move in a healthy
direction. Some BWB is perfectly analogous. Epileptic seizure activity and seizure-related
activity, for example, is directly represented in scalp-recorded brain waves (EEG). It may
represent pathological brain activity, exactly as recorded blood pressure represents
pathological cardiovascular activity. Moreover, as Sterman, Lubar, Finley, and others have
shown (in other chapters of this volume), BWB can be used to represent pathological EEG to
a subject, who is (ordinarily) unaware of his EEG frequency spectrum, so that he may learn
to generate those cognitions/emotions/behaviors whose effects tend to normalize
the EEG. In this example in which BWB is like other biofeedback, the
fed-back EEG information directly represents the action of the diseased
organ-system, i.e., the central nervous system.
However the fact that, more generally, the central nervous system (CNS)controls and/or
represents the activities of most(if not all) peripheral systems, voluntary (biofeedback)
control of CNS activity has futuristic-sounding but logically real implications for
control of many other systems in a more direct manner than that afforded by more familiar,
direct, peripheral biofeedback methods. Equally important and fascinating is the fact that
since psychological functions -- cognition, emotion, perception -- are probably uniquely
mediated by brain systems, BWB must afford the most direct and perhaps the only method for
drug-free therapeutic management of psychological disorders, or for tuning and improving
normal psychology.
2. Trivial Mediation
There is another side of this potentially valuable coin, however: Since
the CNS is probably connected to all other behavioral-peripheral systems,
in order to make the case that there is the potential for unique effects of
BWB, one has to demonstrate that various instances of BWB do not involve mere central
representations of known peripheral phenomena. This is known as the "trivial
mediation" issue, and an example of it may be found by briefly re-considering our
demonstrations years ago that ensory-evoked EEG potentials can be voluntarily controlled
(see, e.g., Rosenfeld & Hetzler, 1979). We trained cats, people, and rats to both
increase and decrease the size of components of cortical EEG potentials evoked by
stroboscopic light flashes or electric shocks presented about every 3-5 seconds. The
subjects were readily able to alter the evoked potentials (EPs), but how did they do so?
More precisely we needed to rule out possible trivial things that they could have done
which would result in altered EPs. For example, since the size of flash EPs is a monotonic
though noisy function of light intensity impinging on subjects eyes, subjects could
increase flash Eps by orienting to the light source, or decrease EPs by facing away, or by
closing eyes. Also, it is known (from some of our own work, e.g., Rosenfeld & Fox,
1972) that voluntary movement generates somatic sensory neuronal activity which ascends
the CNS and affects cortical activity in widespread cortical and subcortical areas. Thus,
our test animals could alter flash-EPs by altering receptor orientation and/or by moving
in such a way as to affect EP amplitude size. We have previously detailed a 10 year long
series of experiments designed to rule out such trivial mediation (reviewed by Rosenfeld
et al. 1985; Rosenfeld 1974, 1977), and it is not appropriate to review all these
experiments here. I will describe just one study (Rosenfeld, Hetzler, Birkel,
Antoinetti,
& Kowatch, 1976) which went a long way in terms of ruling out trivial mediation of
visual EP-BWB in visual cortex.
First, the visual EPs (in rats) were evoked by non-painful electrical stimuli to the
visual pathways via electrodes implanted in optic tracts. The rats were run in total
darkness. The EP component specified for alteration appeared .07 seconds (70 milliseconds)
after the electrical stimulation applications, which were delivered at intervals randomly
varying between 3 and 5 seconds. Movement of subjects was monitored at all times by a
highly sensitive transducer mounted directly on the rats. Beginning 300 milliseconds after
a visual stimulus for a successful trial, the rats were rewarded with a brain stimulation
in the lateral hypothalamic "pleasure center.
Clearly, the highly successful rats could not have been altering their orientations to
the stimuli, which were delivered at electrodes fixed in their brains to activate the same
optic tract location on each trial, every day. Altering orientation to background light
was prevented by the running of rats in total darkness. Discrete movements timelocked to
the interstimulus intervals were impossible because these intervals randomly varied. The
timuli themselves could not serve as timing cues for timelocked movements because the
latency of the EP component specified for change was (at 70 milliseconds) significantly
less than behavioral reaction time to the stimuli. It was possible to rule out neural
effects of non-timelocked movements as trivial mediators of the BWB in two ways: First,
the changes observed in the EPs were highly specific, i.e., usually localized to the one
late component of the EP prespecified for training, whereas ongoing body movements are
known to affect all components of the visual evoked potential. Second, a detailed analysis
of the recorded ongoing movements showed no differences between the movement patterns
associated with BWB-trained increases in EPs and the movements associated with trained
decreases in the EPs (see also Hetzler, Rosenfeld & Birkel, 1978).
The inescapable conclusion is that the rats were probably learning to produce specific
mental activitiesthe rat versions of thoughts or feelingswhich altered the
cortical synaptic organizations where the specified EP components were generated.
Moreover, there were no outward signs (behaviors) of the particular cognitive activities.
It should be noted that Dowman & Rosenfeld (1985), later demonstrated the same effects
using a completely different sensory system (the trigeminal tract) as a stimulation site,
an EP recorded from somatosensory as opposed to visual cortex, and a multilevel behavioral
analysis.
Voluntary control of brain activity with no immediate outward signs may sound far
fetched, however, it can be easily rationalized and made intuitively obvious by pointing
out that such is what happens all the time as humans sit, quietly thinking, reacting
internally to stimuli, processing information, experiencing emotions, and so forth.
Indeed, in another line of research, we have shown that certain "endogenous"
evoked EEG waves (or "Event-Related Potentials, ERPs) can be used as mind-reading lie
detectors in subjects motivated to show no outward signs of their recognition of key
stimuli (Rosenfeld, Angell, Johnson, & Quian, 1991; Rosenfeld, Sweet & Ellwanger,
1994). Indeed, we have come to believe that BWB in our hands involves production of neural
responses well within the normal repertoire of neuronal activity (although see Rosenfeld
& Hetzler, 1973). We believe this because the criteria we define for successful trials
(hits) are based on the normal distribution of neuronal responses prior to training. E.g.,
we collect the pre-training amplitude distribution and define a hit as an amplitude value
greater than .5 to 1 standard deviation(s) from the pre-training mean. Thus a successful
subject is simply generating more instances of a normal event which had a lower
probability of occurrence prior to training.
Is it always necessary to go to great lengths to prove that a given instance of BWB is
free of trivial mediation? The answer to this question depends on the aims of the
BWB.
Clearly if one wants to make a claim that there is something unique and novel about a BWB
effect, it would seem incumbent upon one to show that the BWB was unmediated by something
previously known and familiar. For example, we have argued (Rosenfeld &
Hetzler, 1979)
that EP biofeedback may provide a novel (motor-free) response system with which to test
the generality of putative learning laws. It becomes obviously essential, given this aim,
to demonstrate clearly that the BWB is indeed unmediated by the familiar voluntary motor
behavior traditionally utilized in conditioning research. On the other hand, if ones
aim is mostly clinical-therapeutic, one is less interested in mediation mechanisms than in
positive clinical results. Sometimes, however, it would seem that a strong, positive
clinical effect
of BWB on a pathological condition previously refractory to all kinds of
alternative interventions, is itself the best argument for the novelty of
the BWB utilized.
3. Delayed Effects of BWB: Clinical Effects, BWB and Pain
It was stated above that some instances of non-trivially mediated BWB would involve CNS
changes with no immediate outward signs. On the other hand, a positive clinical effect by
definition must involve an outwardly expressed, measurable effect at some point. This
could simply be a verbalized expression of inner experiences"I feel less
pain" or "I am less depressed." Or it could involve a change in measurable
behavior such as spastic activity, convulsions, gait, etc. It is well known that simply
causing a change in activity at a given CNS locus can affect the manner in which synaptic
organizations at that locus transmit neural information in the future. Experimental models
of this effect include Long Term Potentiation (LTP) and Post-Tetanic
Potentiation, (Bliss
& Lynch, 1988; Colley & Routtenberg, 1993). In LTP, for example, a nerve fiber
bundle afferent to rat hippocampus is electrically stimulated repeatedly. The synapses
involved are subsequently found to have a lower activation threshold than prior to
stimulation. This effect, which has been shown to have membrane structural-biochemical
correlates, has been suggested as a simple model of learning, defined as a change in
behavior produced by experience (Bliss, & Lynch, 1988; Colley, &
Routtenberg,
1993). It is not a bad model for clinical effects of BWB, either. Of course, in the case
of BWB, it is the learned alteration in EEG, rather than brain stimulation which is
hypothesized to effect the synaptic change.
For example, we performed several studies in rats and in humans, in which we trained
subjects to change EPs evoked by non-aversive electric pulses applied to the somatosensory
system; the trigeminal tract in rats or the skin surface (back of hand or forearm) in
humans. The human subjects confirmed verbally that the stimuli felt like just noticeable
(and certainly not painful) skin taps. We inferred the painlessness of the stimuli in rats
from the fact that they would not stop eating during stimulation. Indeed, they mostly
showed no outward signs at all of the stimulative experience, and our only way of knowing
for certain that the stimuli were activating the CNS was via observation of the
stimulus-evoked cortical potentials. In rats, the EPs were monopolarly recorded from
electrodes placed directly over the primary somatic sensory cortex; the reference and
grounds were in the frontal sinus. In humans, EPs were recorded from the vertex
(Cz), a
site over human sensorimotor cortex, referenced to linked mastoids, with the forehead
grounded. We expected and confirmed (Rosenfeld et al., 1985; Dowman & Rosenfeld,
1985a, 1985b; Rosenfeld, Dowman, Heinricher, & Silva, 1984) that the effects of this
BWB of somatic-sensory evoked cortical potentials would involve changes in subjects
pain sensitivities (measured after BWB), even though the EPs were not evoked themselves by
painful stimuli. Our expectation was based on the fact that the same somatic-sensory
cortical neurons subserving non-noxious somatic sensory submodalities (e.g., touch) also
respond to painful stimuli. (These well studied cells are commonly referred to as
"WDR" cells wide dynamic range neurons; see Rosenfeld et al., 1984.)
The changes in pain sensitivity we actually did observe were quite sizeable; equivalent
to the effects of moderate doses of morphine. They were probably also somatotopically
specificonly the side of the face represented in the conditioned side of the cortex
showed effects. They were also related to endogenous opioids (Enkephalin, Endorphin,
etc.), since naloxone antagonized the BWB effects on pain perception. We reasoned that all
these dramatic observations occurred because by conditioning WDR neurons responses
to innocuous stimuli, we effected an alteration in their responsiveness to noxious (i.e.,
painful) stimuli with which they were challenged following the 33 minute conditioning
blocks of 500 trials each.
Incidentally, it should be appreciated that although the Eps are evoked by electrical
stimuli of constant intensity, the BWB-produced changes in the EPs are effected
endogenously (by the subject). The protocol in humans was as follows: An evoking stimulus
(see above) was presented every 4 seconds. The Cz-recorded EPs were led to a PDP8
minicomputer via a Digital Equipment Corporation A/D converter, after amplification with a
Grass P5J amplifier set to pass signals between 3 and 300 Hz. The A/D sampled at 1 KHz. On
a baseline day, in which 250 trials (stimulus presentations) occurred, the average
monopolar EP at Cz referenced to mastoids, was computed. In particular, the average of a
100 msec segment (criterion segment) of EP occurring in a positive component peaking at
about 200 msec post-stimulus was determined on each trial, and these segment averages were
then averaged over all trials. The standard deviation (SD) of the criterion segment was
also computed. In subsequent training days, a reward tone was presented immediately
following hit trials, defined as those on which the criterion segment was .7 SDs greater
than the pre-training mean. (This protocol has since been implemented on an MS-DOS-based
PC clone; interested readers are welcome to contact me for further information.)
BWB Alpha Asymmetry Effects of Emotion and Depression
Our working model for very recent work in BWB with possible applications for depression
is related, but not similar, to the model we used in our just described pain-related BWB.
The approach to be now described has as its conceptual foundation the work of Davidson and
colleagues (Davidson, 1992). This research has elegantly extended earlier
neuropsychological data suggesting that there are emotion-relevant systems in the frontal
cortical areas of brain. In particular the right frontal cortex seems to contain a system
which mediates avoidance reactions associated with negative emotional experience and, in
contrast, the left frontal cortex appears to contain a system specializing in elaborating
approach reactions facilitating positive experience. Thus relative increased right frontal
activation, which can be indexed by reduced right alpha activity, would be expected to go
with negative reactions, whereas enhanced left frontal activation, expressed in reduced
left alpha power would go with positive experience. (Note activation is inversely related
to alpha activity.) Although it is possible to distinctly record left and right alpha, for
technical reasons beyond the scope of this chapter, Davidson and colleagues have utilized
a right-minus-left log alpha power index (called "ZA" here) as an indicator of
emotion. Thus if ZA is high, there is relatively greater left frontal (approach)
activation than right frontal (avoid) activation, and the corresponding emotional state
would be positive. By parallel reasoning, low ZA would be expected to go with negative
emotional states. The Davidson group has confirmed these expectations in many ways (see
Davidson, 1992, for a review), but most relevant to present concerns, they have shown that
currently and previously depressed individuals have resting ZA scores on the low end of
the ZA population distribution, whereas non-depressed individuals have moderate to higher
levels of ZA (Henriques & Davidson, 1990). Davidson (1992) has argued that although
some of his other work indicated that ZA can index temporary states induced by
experimental emotional manipulations, the fact that previously depressed (but then
successfully treated and currently non-depressed) persons still show the
characteristically lower ZA scores indicaates that ZA may be a stable marker of the
lifelong trait of vulnerability to depression.
There are obvious clinical implications here of subjecting ZA to BWB. Our view is that
such BWB might be a beneficial and non-intrusive intervention for depressive disorders,
with none of the unpleasant side effects which can accompany traditional treatments for
depression such as ECT and pharmacotherapies. I suspect though that future research will
show that the best time to intervene with BWB of ZA will not be in the depths of
depression, but when known vulnerable individuals are in stressful periods which often
bring on depressive episodes. (This notion is based on the often-expressed view that
severe depression is a counterindication for any biofeedback; (Schwartz, 1987, p.170). BWB
of ZA might even be a useful regular prophylactic activity. This, of course, is looking
far ahead into the future. What is the status of this project now?
We have done three studies of five normal subjects each, mostly to learn 1) whether or
not such ZA training is possible, 2) how readily achievable (or how difficult) it is, and
3) what some of the training parameters should be (Rosenfeld, 1994, 1995, Rosenfeld et
al., 1993). Our first study was done by using active filters to extract and index alpha
power. Our more recent work has utilized Fast Fourier Transforms to do the alpha
powerextraction and BWB (with our own software running on a PC386 clone running at 40 MHZ
and equipped with a mathematics co-processor). We have found that half to two-thirds of
our normal subjects are able to learn to increase ZA. Our mastery criterion for learning
was a doubling of mean hit-rate from that achieved during the first training day. I hasten
to note here that, due to limited resources, we could utilize only three (one hour)
training sessions following a baseline and exploration session in each subject. Since
other clinical BWB paradigms involve typically more than ten times this number of training
sessions, we would expect a higher percentage of trainable persons in the future when we
too can utilize multiple sessions. Our sessions consists of 400 "trials," i.e.,
FFT epochs of 1 second of analysis. Also, our method of reinforcement so far has been
quite primitive (sounding high tones of one fixed frequency when the trial has been a
failure, sounding low tones of another fixed frequency for hits, and no sounds during
artifact trials). The protocol will probably work much better when we give
moment-to-moment feedback such that either volume or pitch continuously changes in
proportion to the instantaneous asymmetry score, with "hit trials" additionally
signaled with a chime. We have recently reported success with one clinical patient using
continuously variable tone volume and 26 training sessions (Rosenfeld, Baehr, & Baehr,
1995). We also need to further explore appropriate epoch (trial) durations, intertrial
intervals, and so on, before the potential of the paradigm can be fully realized.
Nevertheless, our success
rate, given our preliminary conditions, is encouraging.
Two other results should also be noted: 1) Although until recently, we have not
systematically explored behavioral-affective changes, associated with BWB of
ZA, recent
informal monitoring of two recent subjects on closed circuit TV during training revealed
profound emotional changes confirmed by post-training debriefing. The changes appear
paradoxically puzzlinggrief and tears accompanied increased ZA production which, in
Davidsons hands, indexes positive emotional effects. It is tempting to speculate
from these data about possible rebound effects as complex emotional phenomena, but at this
stage of the research, I feel it is more appropriate to devote energy to more empirical
work. 2) Changing ZA, logically, can result from three effects: increased right alpha
power, reduced left alpha power, simultaneously increased right and decreased left power.
We have seen all three of these effects in various subjects. Most important: some subjects
start with a "depressed" ZA score, i.e., more left than right alpha power, but
after training, show more right than left alpha power. In other words, in the course of
training, the left and right power curves cross one another going in opposite directions.
Such subjects both reduce left alpha and enhance right alpha power at the same time. This
bodes well for working with depressed patients in the future, for it suggests that people
can go from a depressed to a normal asymmetry profile via BWB.
Another implication of our preliminary results (that it is possible to voluntarily
control ZA) is the possibility of testing to what extent ZA is a trait marker of
vulnerability to depression. If long term changes in ZA, resulting from BWB, can be
demonstrated, and if these correlate with emotional changes, then ZA and/or vulnerability
to depression may not be stable traits, which is good. On the other hand, if further
research reveals that non-depressed but low baseline ZA subjects cannot modify ZA as
readily as baseline-high ZA subjects, the trait hypothesis will receive strong support.
Our model of the ZA-BWB is of necessity different than that described earlier regarding
our pain studies. This is because whereas the neural events altered in the pain studies
involved evoked activities, the neural events from which ZA is extracted are ongoing,
spontaneous EEG waves. Nevertheless it is still possible that increased ZA events
occurring during BWB facilitate such events happening in the future via some potentiation
process (like LTP). This view will become problematic, however, if we continue to see
negative emotional concomitants of increased ZA in training, followed by later rebounds in
the direction of positive affect. Such results might suggest a receptor regulation-based
process (as happens in pharmacotherapy with depressed persons) involving a slow build-up
or rebound of neurotransmitter receptors and/or substances related to synaptic
transmission. These notions approach the borderline of wild speculation, but hopefully
have some heuristic value in suggesting very much needed future research. Finally, it may
be noted that most biofeedback protocols are not pure when they reach clinical maturity.
They may then include ancillary or supplementary procedures such as cognitive and
behavioral training, relaxation procedures, and so on. It is not unexpected that such will
also be the case for the BWB protocols described here.
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- Florence S. Sales
- Graduate Admissions Coordinator
- Northwestern University
- Department of Psychology
- Evanston, IL 60208
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- J.P. Rosenfeld,Ph.D.
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