New directions in applied psychophysiology

Biofeedback and Self-Regulation, VoL 17, No. 2, 1992

New Directions in Applied Psychophysiology 1 J. Peter Rosenfeld 2 Northwestern University

About last January (1991), the AAPB office called and asked me for a title of my upcoming presidential address to be given two months later at our annual meeting. I hadn't really had a chance to think about it so far ahead of time, so I came up with the very general "New Directions in Applied Psychophysiology," figuring that it wouldn't be hard to make any talk compatible with so nonspecific a title. It never occurred to me at the time that the talk I'd ultimately give (and on which this article is based) would be a polemic, because despite my AAPB presidency, I just don't ordinarily think of myself as a political animal with a messianic mission. A month or so later, however, when I finally sat down to write the address, I recalled the title I had supplied, and had to think about what the "new directions in applied psychophysiology" actually were. This effort then led me to think about what many of the leading researchers in AAPB are doing in their labs lately, and it occurred to me that much of the recent research activity is broader than - - though sometimes inclusive of, and always related to - - the simple biofeedback demonstrations we had been doing 10-20 years ago. After pondering it for awhile I realized that I really do have a two-part message to deliver after all, and that I might as well deliver it up front: (1) It's time to change the name of the organization again (from AAPB to AAP, as if you didn't know!). (2) It's long past time to change the name of our journal. Since the March meeting, I have come to feel much more strongly about the urgency of our need to make a journal name change than our need to change the organization's name again. I'll get to why I think so later. 1This paper is based on the Presidential Address given at the AAPB meeting in Dallas, Texas, March, 1991. 2Address correspondence to Department of Psychology, Evanston, Illinois 60208. 77 0363-3586/92/0600-0077506.50/0 © 1992 PlenumPublishingCorporation

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I really will be shortly talking about "New Directions in Applied Psychophysiology" in this article, but please let me say first just a couple of things more about the message: The point is practical; (what else would you expect of an applied psychophysiologist?) Thus if there are any real untoward or negative consequences of further name changes, I'll be the first to say: let's forget it! For example, if a name change from AAPB to AAP threatens insurance reimbursements, let's keep AAPB as our name. (I also depend on reimbursements for a part of my living!) If no real world adverse consequences of a name change can be demonstrated, what then is a good positive reason to change the name of the association again? Let's first recall why we changed the name of the organization just a few years ago to AAPB (from BSA): The main reason was related to our wanting to broaden our base to include not only people doing biofeedback, a discipline in which organisms learn to regulate their psychophysiology, but also people doing diagnostic psychophysiology, a closely related (maybe inseparable) discipline in which the meanings of psychophysiological signs, from brain to gut, are worked out. I ~hink - - I would hope - - it is still true that we would like a broad base of people in our organization. Many of us now are clinicians who use biofeedback. From an idealistic point of view, it is hard to argue that it would do the pure clinicians among us anything but good to have more and more solid scientists around to keep new ideas and facts before us. The original name of our organization was the Biofeedback Research Society, after all, and I think we all still agree we need biofeedback researchers in our midst to keep us abreast of what the best kind of feedback is, what the best electrode locations are, what length of training session is best, etc. Certainly we also need researchers to keep

us informed about what novel physiological modalities we might utilize for clinical benefits. But people doing research in biofeedback efficacy, mechanisms, parametric optimization, and the like might very well not be the workers who will give us novel modalities. More likely, the worker who discovers a novel modality will be the nonclinician, applied or basic psychophysiologist who studies the meaning of physiological correlates of psychological events. Indeed (to get back to the title of this article), newly understood physiological expressions of psychological phenomena are the signposts for new directions in applied psychophysiology, and their discoverers are people from whom we should always be learning. Idealism aside, as a practical matter we want such people among us, at our meetings, publishing in our journal. Later on I will try to persuade you all that many such individuals would have b e e n unlikely to belong to a B i o f e e d b a c k Association of America, and are more likely to join AAPB, and would be

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most likely to join an AAP. I will also argue that such people cannot afford to publish in Biofeedback and Self-Ret,ulation, but might very well publish in (and perhaps even subscribe to and join the editorial board of) Journal of Aoolied Psvchoohvsioloev. Another crucial practical matter that has been with us from the beginning concerns our r e p u t a t i o n and the seriousness with which biofeedback therapy is taken outside the world of biofeedback. Very simply, if our membership were to restrict itself (even de facto) to nonresearcher clinicians and/or to nondoctorals, referrals from medical colleagues and other mainstream health care workers would go to zero, as would thirdparty reimbursements! We must have scientists around, and our name, and especially our journal name, are highly relevant to this aim. 2 That's enough message for a while. So what specifically are some "new directions in applied psychophysiology?" To best get at this, we should quickly consider what the already established directions are, and more basically, what does "Applied Psychophysiology" mean? "Psychophysiology" refers to the study of how the mind's mental cont e n t s - cognition, perception, emotion, affect, e t c . - express themselves in a body function that anybody (with the right equipment) can measure. "Body," these days, is not restricted to what is below the neck, but certainly includes brain. "Applied Psychophysiology," obviously, refers to using psychophysiological knowledge to benefit humanity. It has always been the case that there are two main branches of applied psychophysiology: (1) diagnostics and (2) therapeutics. Many of the older directions of applied diagnostic psychophysiology served mostly a heuristic value. The best known (if most controversial) diagnostic applications were in the physiological detection of deception; "lie detection." The diagnostic categories were dichotomous: guilty or innocent. Proponents of this approach argued that the act of lying led to emotional concomitants expressed by the peripheral actions of autonomic nervous system (ANS). Thus two kinds of deception tests were devised using polygraphic ANS indexes of emotion, the "guilty knowledge" test and the "control question test;" (Ekman, 1985). The former is established as an accurate diagnostic test in laboratory and field situations; however, it has two critical limitations. (1) It cannot be used when details of the crime have been published (e.g., in the news) or if for any other reasons an innocent person has acquired the critical guilty knowledge upon whose recognition and concomitant ANS reactions this guilty-knowledge test depends. (2) As its leading proponent has noted, the guilty knowledge test also requires that 2The recent Time cover story lumped us in the alternative care bag with some very dubious practices. Solid scientists in our midst are the only remedy for this kind of publicity.

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much investigation and care must be invested to develop a unique test in each case (Lykken, 1981), and the resulting required amount of time and resources are typically more than most agencies have available. Thus the "control question" polygraph test has been offered as an alternative that does not depend on developing a critical guilty knowledge data base (e.g., a set of crime scene details), but which puts simple, direct questions to subjects, e.g., "Do you use cocaine?" Some clever researchers have developed objective, computerized versions of this test, and have provided supportive data in laboratory ("mock crime") models of criminal investigations, (e.g., Raskin, Kircher, Horowitz, & Honts, 1989), however, there have been few controlled studies of the method in the criminal field and only one in the pre-employment situation. (This is partly why most preemployment polygraph tests were banned in the U.S. in 1985.) The diagnostic success rate, and thus the method itself, have been highly controversial (e.g., Furedy, 1986; Ekman, 1985; Lykken, 1981) and critics have suggested that a 50% (chance)hit rate is typical of the results with innocent persons. Thus what I call "lower body" (ANS) lie detection m e t h o d s which have involved some of the most creative minds in psychophysiology have not really given us a solid application, though they have given us a powerfully influential heuristic push. What the bottom line of the ANS polygraphic lie detection story reveals (for me) is the essence of the difference between the older and the newer directions in applied psychophysiology: Lying may involve emotional reactions in some individuals- it doesn't in others, e.g., in psychopaths, who ironically comprise the most prominent criminal s u b p o p u l a t i o n - but even when there are emotions, they probably vary across individuals, which follows from the Laceys' (1958) principle of response specificity. A specific pattern of ANS signs of "guilty" emotions across all persons is probably nonexistent. This is surely related to the general nonacceptance of ANS polygraph methods by psychophysiologists. If we think about what lying is, it is not surprising that lower body (ANS-based) methods have not provided a satisfying answer to the deception-detection question. Lying is saying something that one knows to be untrue. The word "knows" was emphasized, because lying is more directly a matter of cognition (knowing) than of emotion; i.e. it is more specifically related to knowing than to emoting. In the 1940s and 1950s when ANS polygraphy was first developed, ANS indices were the best physiological indicators of emotion (or cognition) we had, so it was reasonable at that time to explore the utility of these measurements for various applications, including lie detection. Now however, we know of much more specific and recently discovered indicators of c o g n i t i o n - cognitive event-related brain potentials. These


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have been recently used with increasing success in detection of deception (see Rosenfeld, Angell, Johnson, & Qian, 1991) as well as in other applications (e.g., Kramer, Sirevaag, & Braune, 1987) where we need a specific physiological indicator of a cognitive event. After all, cognition must happen first in the brain, well before secondary accompanying ANS signs are generated. Cognitive event related brain potentials are direct brain recordings; it is no wonder that they would appear to have more promise for providing cognition signs than do lower body signs. The above arguments thus point to two major new directions in applied psychophysiology: (1) the tendency for increased utilization of brain-index-based measures of cognition and (2) the tendency toward utilization of increasingly specific indicators of various physiological conditions. I noted before the existence of two major branches of applied psychophysiology: diagnostic and therapeutic. I haven't yet talked about the latter, but it is the one more closely related to the interests of biofeedback practitioners and researchers. I believe that in therapeutic applications, as in diagnostic applications, the new direction is also toward increasingly specific parameters. It actually started that way in the 1960s when biofeedback came on the scene. We were very ambitious and inspired by Neal Miller's animal studies (Miller, 1969) to go after increasingly specific physiological changes, e.g., differential, simultaneous increases and decreases in venous pressure in contralateral ears. Unfortunately, there were problems not only in the transfer of paradigms from lab to clinic [see Blanchard and Young's pessimistic (1973) assessment of cardiovascular biofeedback as "a promise unfulfilled"], but also in simple replication of some of the basic animal studies (Miller & Dworkin, 1974). Meanwhile, other clinicians were finding and increasingly utilizing effective methods of biofeedback-based stress management utilizing multimodal (and thus nonspecific) approaches. This has been and continues to be an older but solid - - direction in applied clinical psychophysiology. But in the 1980s and up to the present, new methods have become increasingly specific and effective. For example, Freedman (1989) has had great success with hand temperature training but not autogenic training in the treatment of Raynaud's disease, a specifically cold hand disease. Another example: Rich Sherman (Glaros, 1991) recently described a fascinating example of biofeedback specificity in our newsletter: We eventuallydiscovered that burning and tingling phantom limb pain is related to decreased blood flow in the residual limb and the most effectivebiofeedback for that is temperature biofeedback. EMG biofeedbackis not particularlyeffective because there is not anythingwrongwith the muscle tension in the limb. Conversely, temperature biofeedback isn't particularly effectivewith cramping descriptions of phantom pain because what the people are trying to do is learn to recognize tiny,

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tiny cramps that you can't normally feel or you wouldn't normally notice and stop them which is best done with the EMG biofeedback.

A final example: I recently attended the Second International Conference on Biobehavioral Self-Regulation and Health in Munich (organized by Ron Siefert and Jack Carlson), where I had the pleasure of hearing none o t h e r than one of o u r most scientifically rigorous past-presidents, Bernie Engel, state in a wonderfully matter-of-fact and utterly persuasive tone that "Biofeedback is the treatment of choice for fecal incontinence." Of course this was not simply a bald assertion; it was based on a wealth of foregoing, transparently convincing evidence of the rapid, powerful effect of the specific, sphincter training procedures, as presented in the first part of Engel's talk. (The data he presented on biobehavioral treatment of urinary incontinence promise the same conclusion regarding this problem in the future.) I believe that when we find the right (specific) measurements to make, many of the early promises will be fulfilled for a variety of conditions. These methods will not always be easy to find. Mother Nature is not promiscuous with her secrets. It will take relentless, tenacious p u r s u e r s - basic and applied psychophysiological researchers. In the therapeutic branch of applied psychophysiology also, I see an increasing tendency toward utilization of brain modalities, particularly when the problem involves cognitive (i.e., brain-specific) signs. Pain, the most ubiquitous sign of many impending or ongoing pathologies, may of course be often attributable to peripheral injuries, and we know there are many effective EMG-based biofeedback treatments for peripheral conditions. Again, these treatments represent older but established directions in applied psychophysiology. Nevertheless, the conscious experience of pain is mediated by multiple loci in the brain, often working in a complex ensemble (Rosenfeld, Huang, & Xia, 1990b). With this in mind, our group at Northwestern has worked for a long time in an effort to develop a novel biofeedback modality based on the central representation of the pain experience in the somatosensory evoked E E G potential (SEP). Our first efforts along these lines were in rats, and as this story has been previously reviewed in several places (Rosenfeld, Dowman, Heinricher, & Silvia, 1984; 1985; Rosenfeld, 1990; Dowman & Rosenfeld, 1985), I will not dwell on it here. Suffice it to say that Bob Dowman and I were able to demonstrate that as a rat learns (through simple rewarding of successful trials) to alter the size of the brain wave elicited in cortical pain systems by neutral stimuli, his responsiveness to pain changes predictably and significantly. Also important were our collateral findings that these effects show great specificity in that (1) only the one side of the body represented in the one side of the brain we trained showed changes (other brain and body areas didn't


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change); (2) only the pain submodality of somatic sensation (i.e., not innocuous submodalities such as light touch) were affected by the brain wave biofeedback; (3) The biofeedback-produced analgesia was probably specifically m e d i a t e d by p-opioid systems since it was naloxone-reversible Dowman & Rosenfeld, 1985). We have recently extended these findings to normal humans in experimentally induced pain (Rosenfeld, Silvia, Weitkunat, & Dowman, 1985) and are in the process of testing them on clinical pain patient populations. The component (i.e., wave peak) in the series of components comprising the SEP that we have worked with in humans is the P200 component (so-called because it is of positive polarity and occurs about 200 milliseconds poststimulus). It has been reported by various workers (including ourselves: Rosenfeld, Diaz-Clark, & Olson, 1983) to be a good pain correlate. However it has also been shown by the group that has done the most work with it that this correlation is disruptable (Chapman, Colpitts, Mayeno, & Gagliardi, 1981). Probably the reason many of us have been unable to discover a pure brain indicator of pain is that the various SEP components we've studied have multiple functional brain sources. Thus P200 sometimes can represent pain, but it can also represent other psychological events under different conditions. This has led my group to look, more recently, for an indirect pain index in P300 (rather than P200), a different, later evoked EEG component, which can be found in event-related potentials (ERPs, what we used to call "evoked potentials") elicited by any stimuli: visual, acoustic, and somatosensory. In fact P300 can be elicited by no stimulus at all! If I were to present, every two seconds, a series of tones to y o u - beep, beep, beep, beep, beep, , beep, beep [ e t c . ] - P300 would appear in response to the one I omitted. The fact that the disappointed expectancy of a stimulus, but not the stimulus itself, evokes P300 points up the psychological significance of P300, rather than its possible sensory coding qualities (which are actually quite dubious). No doubt P300 has multiple determinants also, but there is no doubt that it can be reliably used as an attention index in the following way: I present a series of randomly alternating high and low tones to you; the highs have an 80% probability, and the rarer lows have a 20% probability. I also ask you to keep a silent count of the oddball low tones w h e n e v e r you hear them. This is the classic " o d d b a l l " paradigm (Duncan-Johnson & Donchin, 1977) most often used to elicit P300 which appears in response to the task-relevant, oddball low tones but not to the high tones. 3 P300 is evoked by the oddballs because the subject is attending to them. If you burden him with a second task (e.g., a video game, simulated 3There can be a much reduced though not absent P300 to the non-oddballs.

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flight, listening to a story) performed concurrently with the oddball task, his attention will be divided, which predicts that the P300 response to the previously fully attended oddballs will be reduced (and also delayed). Kramer and colleagues (1987) have, in fact, utilized this P300-based dual-task paradigm to assess task difficulty in human engineering situations, and at Northwestern, we have utilized this dual-task paradigm as the indirect pain index I alluded to above: Very simply, we conceptualize the pain e x p e r i e n c e as a s e c o n d a r y t a s k which will c o m p e t e for attentional-cognitive processing resources represented by oddball-evoked P300 waves. Moreover it works. P300 amplitude inversely indexes pain level and distinguishes real and feigned pain subjects (Rosenfeld and Kim, 1991; Johnson et al., 1991). We have also used this approach in distinguishing movies of differential interestingness (Rosenfeld et al., 1990a, Rosenfeld, Bhat, Johnson, & Miltenberger, 1992). We do not, however, plan to have P300 replace Siskel and Ebert or Kroll and Ansen. The intent of this first demonstration - - P 3 0 0 as film c r i t i c - was with an eye toward a diagnostic psychopathology instrument. The idea is that some diagnostic subcategories should find some kinds of films more engaging than others, and P300 could measure this. We have had some preliminary success with depressed individuals (Leiphart & Rosenfeld, 1991). I have reviewed these recent efforts not only because it is probably expected that I do so in the context of this article. As I noted above, I believe that some of the newer directions in applied psychophysiology involve increased use of brain indices, and it was easy to illustrate this with reference to my own work since I know it better than I know others' efforts. But there are ample other examples: Barry Sterman has recently utilized EEG measures of attention to get at some of the same flight cockpit phenomena that Kramer et al. (1987) attack with the P300-based dual task situation. Niels Birbaumer's Tiibingen group is also using sophisticated EEG measurements to assess human attention and activation. I expect that as those of us who are working at development of brain indices of cognitive attentional processes are able to get on with our work, the indices we settle on may become novel biofeedback modalities. Wouldn't it be helpful to have such modalities in the treatment of the many pathologies with cognitive symptoms? Joel Lubar, as some of you may know, is already working in this area with specific EEG-biofeedback parameters (see Mann, Lubar, Zimmerman, Miller, & Muenchen, 1992, in press). In conclusion, I want to get back to the message: there are too many people outside AAPB who belong there with us, namely, the researchers who are looking for the presently unknown psychological meanings of


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physiological events, the people who are taking us in the new directions in applied psychophysiology. An important way to begin involving them may be to get them reading and publishing in our journal. I have been lobbying very hard lately among my colleagues to change the journal name to a title that will reflect new directions in applied psychophysiology. I recently sent a letter to the AAPB board that details the arguments for a journal name change. I'd like to close by paraphrasing this letter here, so that the readers of this journal whose support we want, can hear the key arguments for a new journal name: What name? If I had my druthers it would beApplied Psychophysiology or Journal of Applied Psychophysiology (AP or JAP). The reason I like a name along these lines is that while no former contributors to Biofeedback and Self-Regulation (BSR) ought to feel inhibited by names like AP or JAP (biofeedback and self-regulation are to my mind simply two examples of applied psychophysiology) there are many new potential quality contributors to our journal out there who can't now contribute to a journal with the name BSR. Why not? Let me illustrate with my own research because I am obviously very familiar with it, and I know it illustrates others' problems. I've already published some of my work in BSR, specifically, the work that is clearly biofeedback and that I am desirous of and happy to bring to the attention of fellow biofeedbackers. But there's other work that I do (described above) which involves psychophysiological diagnostic measures of pain, psychopathology, personality, and attention. I am reluctant to publish it in a journal with the restrictive name, BSR, because many people with interests outside biofeedback but in psychophysiology whom I want to see this work would not ordinarily read a journal named BSR, nor see it in a place like Current Contents, since this name (BSR) does not suggest diagnostic psychophysiological contents. I know personally many others in and out of AAPB who feel exactly as I do: I believe these are good people whose presence in our journal as reviewers as well as contributors can only enhance our journal's standing. Moreover, I have the distinct impression that most of those AAPB people who want a journal name change are those very people who typically publish a lot (in BSR and elsewhere) and who, in general, are the experimentalists who mostly read and write journal articles and who thus constitute a major pillar in the research/credibility edifice of AAPB. Beyond my impressions, which could surely be biased, let me share with you some relevant data of which I am aware: Bob Freedman recently polled the editorial board of BSR and found that 15 people wanted a name like Applied Psychophysiology, 8 more liked Applied Psychophysiology and

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Biofeedback, and the remaining minority of 8 wanted no change. This means that already a 2/3 majority of the editorial board (who presumably represent that pillar noted above) wants a change, differing only in the specific nature of the change. The majority of this majority (the plurality of the editorial board) wants Applied Psychophysiology. I am aware that there may be good friends and first class scientists out there who are in the minority, who want to keep things as they are. It's really to you that I'm speaking now: From my perspective, it can't hurt you to publish in a Journal of Applied Psychophysiology or something of the sort, because this title conceptually includes biofeedback (or any other therapeutic) research. Moreover, everyone in AAPB will know that biofeedback studies are published in the new journal, so you all can't lose any audience! (Moreover, we can state the journal's continued strong association with biofeedback in the standard, repeatedly published journal policy statement.) On the other hand, as I noted earlier, those of us who may feel strongly associated with AAPB but whose careers depend upon continuing exposure and visibility to o t h e r r e s e a r c h w o r l d s (e.g., pain, psychophysiology, physiology, psychopathology, personality disorders, neuroscience, human engineering, etc.), cannot restrict our published presence to a purely biofeedback journal; our work wouldn't get seen by key people and that would hurt us! Finally, Bob Freedman recently (October, 1991) told me yet one more new relevant fact, which should be even more persuasive: He surveyed the last 4 issues of BSR and counted 26 articles. Of these, only 8 were on biofeedback and 3 of these were review articles; i.e., the two-thirds-plus majority of papers were on other topics in applied psychophysiology. The journal's recent content has mostly not been biofeedback. Other considerations aside, shouldn't this fact alone be reflected in a new and content-appropriate journal title? REFERENCES Blanchard, E. G., & Young, L. D. (1973). Self-control of cardiac functioning: A promise as yet unfulfilled. Psychological Bulletin, 79, 145-163. Chapman, C. R., Colpitts, Y. H., Mayeno, J. K., & Gagliardi, G. J. (1981). Rate of stimulus repetition changes evoked potential amplitude: Dental and auditory modalities compared. Experimental Brain Research, 43, 240-252. Dowman, R., & Rosenfeld, J. P. (1985). Operant conditioning of somatosensory evoked potential (SEP) in rats. I. Specific changes in SEP amplitude and a naloxone-reversible, somatotypically specific change in facial nociception. Brain Research, 333, 201-212. Duncan-Johnson, C. C., & Donchin, E. (1977). On quantifying surprise: The variation of event-related potentials with subjective probability. Psychophysiology, 14, 456-467. Ekman, P. (1985). Telling lies. New York: Norton. Freedman, R. R. (1989). Quantitative measurements of finger blood flow during behavioral treatments for Raynaud's Disease. Psychophysiology, 26, 437-441.


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Furedy, J. J. (1986). Lie detection as psychophysiological differentiation. In G. Coles et al. (Eds.), Psychophysiology: Systems, processes, and applications (pp. 683-701). New York: Guilford Press. Glaros, A. (1991). Interview with Richard Sherman, Ph.D. Biofeedback, 19, 22-26. Johnson, M. M., Rosenfeld, J. P., Goldbloom, E., Pirnazar, R., and Clark, J. (1991). P300 Amplitude as an indirect index of pain, Psychophysiology, 28, Suppl. $32. Kramer, A., Sirevaag, E., & Braune, R. (1987). A psychophysiological assessment of operator workload during simulated flight missions. Human Factors, 29, 145-160. Lacey, J. I., & Lacey, B. (1958). Verification and extension of the principle of autonomic response stereotypy. American Journal of Psychology, 71, 50-73. Leiphart, J. W., & Rosenfeld, J. P. (1991). Study of Depression using P300. Psychophysiology, 28, Suppl. $37. Lykken, D. T. (1981). A "tremor in the blood. New York: McGraw-Hill. Mann, C., Lubar, J., Zimmerman, A., Miller, C., & Muenchen, R. (1992). Quantitative analysis of EEG in boys with attention deficit disorder. Pediatric Neurology, in press. Miller, N. E. (1969). Learning of visceral and glandular responses. Science, 163, 434-445. Miller, N. & Dworkin, B. (1974). Visceral learning: Recent difficulties with curarized rats. In Obrist et al. (Eds.), Cardiovascular Psychophysiology, (pp. 312-331) Chicago: Aldine. Raskin, D. C., KJrcher, J. C., Horowitz, S. W., & Honts, C. R. (1989). Recent laboratory techniques and field research on polygraph techniques. In J. C. Yuille (Ed.) Credibility Assessment (pp. 1-24). Dordrect; Netherlands: Kluwer Academic Publishers. Rosenfeld, J. P. (1990). Applied psychophysiology and biofeedback of event-related potentials (brain waves): Historical perspective, review, future directions. Biofeedback and Self-Regulation, 15, 99-120. Rosenfeld, J. P., Angell, A., Johnson, M., & Qian, J. (1991). An ERP-based control-question lie detector analog: Algorithms for discriminating effects within individual waveforms. Psychophysiology, 28, 320-336. Rosenfeld, J. P., Bhat, K., Johnson, M., & Miltenberger, A. (1992). ERPs in the dual task paradigm: P300 discriminates engaging and non-engaging films when film-viewing is the primary task. International Journal of Psychophysiology, in press. Rosenfeld, J. P., Diaz-Clark, A., & Olson, R. E. (1983). Response to painful electrical stimulation in MPD Syndrome Patients. Journal of Dental Research, 62, 259-260. Rosenfeld, J. P., Dowman, R., Heinricher, M., & Silvia, R. (1984). Operantly controlled somatosensory evoked potentials: Specific effects on pain processes. In B. Ruckstroh, T. Elbert, W. Lutzenberger, and N. Birbaumer (Eds.), Self-regulation of the brain and behavior (pp. 164-179). Berlin: Springer-Verlag (1985). Rosenfeld, J. P., Huang, K. H., & Xia, L. Y. (1990b). Effects of single and simultaneous combined nanoinjections of met-enkephalin into rat midbrain and medulla on activity of differentially noci-responsive ventral medullary neurons. Brain Research, 508, 199-209. Rosenfeld, J. P., & Kim, M. (1991). Ongoing pain as a mental workload indexed by P300 depression: Discrimination of real and feigned pain conditions. Psychophysiology, 28, 336-343. Rosenfeld, J. P., Silvia, R., Weitkunat, R., & Dowman, R. Operant control of human somatosensory evoked response alters experimental pain perception. Advances in Neurology, 9, 343-348. Rosenfeld, J. P., Bhat, K., Johnson, M., and Miltenberger, A. (1990a). P3 in the dual task paradigm: Film-viewing. Psychophysiology, 27. Suppl. $60.